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Sample records for radon-induced rat lung

  1. Involvement of growth factors and their receptors in radon-induced rat lung tumors

    International Nuclear Information System (INIS)

    Leung, F.C.; Dagle, G.E.; Cross, F.T.

    1992-01-01

    In this paper we examine the role of growth factors (GF) and their receptors (GFR) in radon-induced rat lung tumors. Inhalation exposure of radon and its daughters induced lung tumors in rats, but the molecule/cellular mechanisms are not known. Recent evidence suggests that GF/GFR play a critical role in the growth and development of lung cancer in humans and animals. We have developed immunocytochemical methods for identifying sites of production and action of GF/GFR at the cellular level; for example, the avidin-biotin horseradish peroxidase technique. In radon-induced rat epidermoid carcinomas, epidermal growth factor (EGF), EGF-receptors (EGF-R), transforming growth factor alpha (TGF-α), and bombesin were found to be abnormally expressed. These abnormal expressions, mainly associated with epidermoid carcinomas of the lung, were not found in any other lung tumor types. Our data suggest that EGF, EGF-R, TGF-α, and bombesin are involved in radon oncogenesis in rat lungs, especially in epidermoid carcinomas, possibly through the autocrine/paracrine pathway

  2. Molecular and cytogenetic characterization of radon-induced lung tumors in the rat

    International Nuclear Information System (INIS)

    Dano, Laurent

    2000-01-01

    Radon is a natural radioactive gas. This radioelement, which is an α-particle emitter, is omnipresent in the environment. Inhalation of atmospheric radon is the major exposure route in man of natural radioactivity which results in respiratory tract contamination. An increased lung cancer risk associated with radon inhalation has been shown both in humans and animals by epidemiological and experimental studies, respectively. In rats, characterization of dose-effect relationships has led to the construction of statistical models that may help theoretically in the prediction of human health involvements of both occupational and domestic chronic exposure to radon. However, little is known about the cellular and molecular mechanisms of radon-induced lung carcinogenesis. In the laboratory, a model of lung cancers induced in rats after radon inhalation is available. This model represents a good tool to identify and characterize the genetic events contributing to the development of radon-induced lung tumors. Carrying out a global approach based on the combined use of classical and molecular cytogenetic methods, the analysis of 17 neoplasms allowed the identification of chromosomal regions frequently altered in these tumors. Numerous similarities have been found between our results and the cytogenetic data for human lung cancers, suggesting common underlying genetic molecular mechanisms for lung cancer development in both species. Moreover, our study has allowed to point to tumor suppressor genes and proto-oncogenes potentially involved in radon-induced lung carcinogenesis. Thus, our results may aid further molecular studies aimed either at confirming the role of these candidate genes or at demonstrating the involvement of yet to be identified genes. (author) [fr

  3. Molecular characterization of radon-induced rat lung tumors

    International Nuclear Information System (INIS)

    Guillet Bastide, K.

    2008-11-01

    The radon gas is a well known lung carcinogenic factor in human at high doses but the cancer risk at low doses is not established. Indeed, epidemiological studies at low doses are difficult to conduct because of the human exposure to other lung carcinogenic factors. These data underlined the necessity to conduct experiments on lung tumors developed on animal model. The aim of this work was to characterize rat lung tumors by working on a series of radon-induced tumors that included adenocarcinomas (A.C.), squamous cell carcinomas (S.C.C.) and adeno-squamous carcinomas (A.S.C.), that are mixed tumors with both A.C. and S.C.C. cellular components. A C.G.H. analysis of the three types of tumors allowed us to define chromosomal recurrent unbalances and to target candidate genes potentially implicated in lung carcinogenesis, as p16Ink4a, p19Arf, Rb1, K-Ras or c-Myc. A more precise analysis of the p16Ink4a/Cdk4/Rb1 and p19Arf/Mdm2/Tp53 pathways was performed and indicated that the Rb1 pathway was frequently inactivated through an absence of p16 Ink4a protein expression, indicating that it has a major role in rat lung carcinogenesis. Finally, a comparative transcriptomic analysis of the three types of tumors allowed us to show for the first time that the complex tumors A.S.C. have a transcriptomic profile in accordance with their mixed nature but that they also display their own expression profiles specificities. This work allowed us to find molecular characteristics common to murine and human lung tumors, indicating that the model of lung tumors in rat is pertinent to search for radiation-induced lung tumors specificities and to help for a better molecular identification of this type of tumors in human. (author)

  4. Stochastic rat lung dosimetry for inhaled radon progeny: a surrogate for the human lung for lung cancer risk assessment

    Energy Technology Data Exchange (ETDEWEB)

    Winkler-Heil, R.; Hofmann, W. [University of Salzburg, Division of Physics and Biophysics, Department of Materials Research and Physics, Salzburg (Austria); Hussain, M. [University of Salzburg, Division of Physics and Biophysics, Department of Materials Research and Physics, Salzburg (Austria); Higher Education Commission of Pakistan, Islamabad (Pakistan)

    2015-05-15

    Laboratory rats are frequently used in inhalation studies as a surrogate for human exposures. The objective of the present study was therefore to develop a stochastic dosimetry model for inhaled radon progeny in the rat lung, to predict bronchial dose distributions and to compare them with corresponding dose distributions in the human lung. The most significant difference between human and rat lungs is the branching structure of the bronchial tree, which is relatively symmetric in the human lung, but monopodial in the rat lung. Radon progeny aerosol characteristics used in the present study encompass conditions typical for PNNL and COGEMA rat inhalation studies, as well as uranium miners and human indoor exposure conditions. It is shown here that depending on exposure conditions and modeling assumptions, average bronchial doses in the rat lung ranged from 5.4 to 7.3 mGy WLM{sup -1}. If plotted as a function of airway generation, bronchial dose distributions exhibit a significant maximum in large bronchial airways. If, however, plotted as a function of airway diameter, then bronchial doses are much more uniformly distributed throughout the bronchial tree. Comparisons between human and rat exposures indicate that rat bronchial doses are slightly higher than human bronchial doses by about a factor of 1.3, while lung doses, averaged over the bronchial (BB), bronchiolar (bb) and alveolar-interstitial (AI) regions, are higher by about a factor of about 1.6. This supports the current view that the rat lung is indeed an appropriate surrogate for the human lung in case of radon-induced lung cancers. Furthermore, airway diameter seems to be a more appropriate morphometric parameter than airway generations to relate bronchial doses to bronchial carcinomas. (orig.)

  5. Genetic and molecular analysis of radon-induced rat lung tumours

    International Nuclear Information System (INIS)

    Guilly, M.N.; Joubert, Ch.; Levalois, C.; Dano, L.; Chevillard, S.

    2002-01-01

    We have a model of radon-induced rat lung tumours, which allow us to analyse the cytogenetic and molecular alterations of the tumours. The aim is to better understand the mechanisms of radio-induced carcinogenesis and to define if it exists a specificity of radio-induced genetic alterations as compared to the genetic alterations found in the sporadic tumours. We have started our analysis by developing global cytogenetic and molecular approaches. We have shown that some alterations are recurrent. The genes that are potentially involved are the oncogene MET and the tumour suppressor Bene p16, which are also frequently altered in human lung tumours. Simultaneously, we have focussed our analysis by targeting the search of mutation in the tumour suppressor gene TP3. We have found that 8 of 39 tumours were mutated by deletion in the coding sequence of TP53. This high frequency of deletion, which is not observed in the human p53 mutation database could constitute a signature of radio-induced alterations. On this assumption, this type of alteration should not be only found on TP53 Bene but also in other suppressor genes which are inactivated by a mutation such as p16 for example. The work we are carrying out on radio-induced tumours among humans and animals is directed to this end. (author)

  6. Radon-induced bronchiolo-alveolar tumors in rats: cytologic and microinvasive characteristics

    International Nuclear Information System (INIS)

    Busch, R.H.; Cross, R.; Bair, W.

    1983-07-01

    A series of 39 rat lung tumors induced by radon and radon daughters alone or in conjunction with uranium ore dust exposure were studied by light microscopy, transmission electron microscopy, and scanning electron microscopy. Using absence of appreciable mucus, mucuos granules, tonofibrils, and desmosomes, and the presence of alveolar Type II cell inclusions as criteria, all were confirmed as bronchiolo-alveolar (B-A) tumors with predominantly Type II cell characteristics

  7. An experimental two-stage rat model of lung carcinoma initiated by radon exposure

    International Nuclear Information System (INIS)

    Poncy, J.L.; Laroque, P.; Fritsch, P.; Monchaux, G.; Masse, R.; Chameaud, J.

    1992-01-01

    We present the results of a two-stage biological model of lung carcinogenesis in rats. The histogenesis of these tumors was examined, and DNA content of lung cells was measured by flow cytometry during the evolving neoplastic stage. Tumors were induced in rat lungs after radon inhalation (1600 WLM) followed by a promoter treatment; six intramuscular injections of 5,6-benzoflavone (25 mg/kg of body weight/injection) every 2 wk. Less than 3 mo after the first injection of benzoflavone, squamous cell carcinoma was observed in the lungs of all rats exposed to radon. The preneoplastic lesions gradually developed as follows: hyperplastic bronchiolar-type cells migrated to the alveoli from cells that proliferated in bronchioles and alveolar ducts; initial lesions were observed in almost all respiratory bronchioles. From some hyperplasias, epidermoid metaplasias arose distally, forming nodular epidermoid lesions in alveoli, which progressed to form squamous papilloma and, finally, epidermoid carcinomas. The histogenesis of these experimentally induced epidermoid carcinomas showed the bronchioloalveolar origin of the tumor. This factor must be considered when comparing these with human lesions; in humans, lung epidermoid carcinomas are thought to arise mainly in the first bronchial generations. The labeling index of pulmonary tissue after incorporation of 3 H-thymidine by the cells was 0.2% in control rats. This index reached a value of 1 to 2% in the hyperplastic area of the bronchioles and 10 to 15% in epidermoid nodules and epidermoid tumors, respectively. DNA cytometric analysis was performed on cell suspensions obtained after enzymatic treatment of paraffin sections of lungs from rats sacrificed during different stags of neoplastic transformations. Data showed the early appearance of a triploid cell population that grew during the evolution of nodular epidermoid lesions to epidermoid carcinomas

  8. Sex and smoking sensitive model of radon induced lung cancer

    Energy Technology Data Exchange (ETDEWEB)

    Zhukovsky, M.; Yarmoshenko, I. [Institute of Industrial Ecology of Ural Branch of Russian Academy of Sciences, Yekaterinburg (Russian Federation)

    2006-07-01

    Radon and radon progeny inhalation exposure are recognized to cause lung cancer. Only strong evidence of radon exposure health effects was results of epidemiological studies among underground miners. Any single epidemiological study among population failed to find reliable lung cancer risk due to indoor radon exposure. Indoor radon induced lung cancer risk models were developed exclusively basing on extrapolation of miners data. Meta analyses of indoor radon and lung cancer case control studies allowed only little improvements in approaches to radon induced lung cancer risk projections. Valuable data on characteristics of indoor radon health effects could be obtained after systematic analysis of pooled data from single residential radon studies. Two such analyses are recently published. Available new and previous data of epidemiological studies of workers and general population exposed to radon and other sources of ionizing radiation allow filling gaps in knowledge of lung cancer association with indoor radon exposure. The model of lung cancer induced by indoor radon exposure is suggested. The key point of this model is the assumption that excess relative risk depends on both sex and smoking habits of individual. This assumption based on data on occupational exposure by radon and plutonium and also on the data on external radiation exposure in Hiroshima and Nagasaki and the data on external exposure in Mayak nuclear facility. For non-corrected data of pooled European and North American studies the increased sensitivity of females to radon exposure is observed. The mean value of ks for non-corrected data obtained from independent source is in very good agreement with the L.S.S. study and Mayak plutonium workers data. Analysis of corrected data of pooled studies showed little influence of sex on E.R.R. value. The most probable cause of such effect is the change of men/women and smokers/nonsmokers ratios in corrected data sets in North American study. More correct

  9. Sex and smoking sensitive model of radon induced lung cancer

    International Nuclear Information System (INIS)

    Zhukovsky, M.; Yarmoshenko, I.

    2006-01-01

    Radon and radon progeny inhalation exposure are recognized to cause lung cancer. Only strong evidence of radon exposure health effects was results of epidemiological studies among underground miners. Any single epidemiological study among population failed to find reliable lung cancer risk due to indoor radon exposure. Indoor radon induced lung cancer risk models were developed exclusively basing on extrapolation of miners data. Meta analyses of indoor radon and lung cancer case control studies allowed only little improvements in approaches to radon induced lung cancer risk projections. Valuable data on characteristics of indoor radon health effects could be obtained after systematic analysis of pooled data from single residential radon studies. Two such analyses are recently published. Available new and previous data of epidemiological studies of workers and general population exposed to radon and other sources of ionizing radiation allow filling gaps in knowledge of lung cancer association with indoor radon exposure. The model of lung cancer induced by indoor radon exposure is suggested. The key point of this model is the assumption that excess relative risk depends on both sex and smoking habits of individual. This assumption based on data on occupational exposure by radon and plutonium and also on the data on external radiation exposure in Hiroshima and Nagasaki and the data on external exposure in Mayak nuclear facility. For non-corrected data of pooled European and North American studies the increased sensitivity of females to radon exposure is observed. The mean value of ks for non-corrected data obtained from independent source is in very good agreement with the L.S.S. study and Mayak plutonium workers data. Analysis of corrected data of pooled studies showed little influence of sex on E.R.R. value. The most probable cause of such effect is the change of men/women and smokers/nonsmokers ratios in corrected data sets in North American study. More correct

  10. Risk of lung cancer in animals following low exposures to Radon-222 progeny

    International Nuclear Information System (INIS)

    Duport, P.; Monchaux, G.; Morlier, J.P.

    1997-01-01

    Owing to the facts that a) large uncertainties affect the epidemiology of radon progeny-induced lung cancer in humans (especially at low exposures), and b) the rat is a good model for studying the carcinogenicity of radon progeny in humans, the risk of lung cancer following low exposures to low concentrations of radon progeny can be estimated from data obtained in the laboratory on rats exposed under controlled conditions. From the limited set of laboratory data on the induction of lung cancer in laboratory rats it appears that, at low exposures, the risk of lung cancer decreases with decreasing concentration, and that exposures of the order of 25 WLM, at an exposure rate of 2 WL do not produce any excess lung cancers. Since 20 WLM is a lifetime exposure comparable to those expected in occupational or indoors conditions and 2 WL is an exposure rate about 20 times higher dm current occupational exposures rates and 100 times higher than indoor ones, these observations may be indicative of threshold conditions for the induction of lung cancer by radon progeny. (author)

  11. Lung cancer incidence after exposure of rats to low doses of radon: influence of dose rate

    Energy Technology Data Exchange (ETDEWEB)

    Morlier, J.P.; Morin, M.; Monchaux, G.; Fritsch, P.; Lafuma, J.; Masse, R. [CEA Centre d`Etudes Nucleaires de Fontenay-aux-Roses, 92 (France). Dept. de Protection Technique; Pineau, J.F. [ALGADE, Bessines (France); Chameaud, J. [Compagnie Generale des Matieres Nucleaires (COGEMA), 87 - Razes (France)

    1994-12-31

    To study the effect on lung cancer incidence of a long exposure to low levels of radon, 500 male 3-months-old Sprague-Dawley rats, were exposed to a cumulative dose of 25 WLM of radon and its daughters, 6 hours a day, 5 days a week, during 18 months. Exposure conditions were controlled in order to maintain a defined PAEC: 42 x 10{sup 6} J.m{sup -3} (2 WL), in the range of domestic and environmental exposures. Animals were kept until they died or given euthanasia when moribund. Mean survival times were similar in both irradiated and control groups: 828 days (SD = 169) and 830 days (SD = 137), as well as lung cancer incidence, 0.60% at 25 WLM and 0.63% for controls. The incidence of lung lesions was compared statistically with controls and those previously obtained at cumulative exposures of 25 and 50 WLM delivered over a 4-6 month period, inducing a significant increase of lung cancer, 2.2% and 3.8% respectively. Such a comparison showed a decreased lung cancer incidence related to a decrease in the dose rate for low levels of radon exposure. (author).

  12. Lung cancer incidence after exposure of rats to low doses of radon: influence of dose rate

    International Nuclear Information System (INIS)

    Morlier, J.P.; Morin, M.; Monchaux, G.; Fritsch, P.; Lafuma, J.; Masse, R.; Chameaud, J.

    1994-01-01

    To study the effect on lung cancer incidence of a long exposure to low levels of radon, 500 male 3-months-old Sprague-Dawley rats, were exposed to a cumulative dose of 25 WLM of radon and its daughters, 6 hours a day, 5 days a week, during 18 months. Exposure conditions were controlled in order to maintain a defined PAEC: 42 x 10 6 J.m -3 (2 WL), in the range of domestic and environmental exposures. Animals were kept until they died or given euthanasia when moribund. Mean survival times were similar in both irradiated and control groups: 828 days (SD = 169) and 830 days (SD = 137), as well as lung cancer incidence, 0.60% at 25 WLM and 0.63% for controls. The incidence of lung lesions was compared statistically with controls and those previously obtained at cumulative exposures of 25 and 50 WLM delivered over a 4-6 month period, inducing a significant increase of lung cancer, 2.2% and 3.8% respectively. Such a comparison showed a decreased lung cancer incidence related to a decrease in the dose rate for low levels of radon exposure. (author)

  13. Canadian population risk of radon induced lung cancer variation range assessment based on various radon risk models

    International Nuclear Information System (INIS)

    Chen, Jing

    2017-01-01

    To address public concerns regarding radon risk and variations in risk estimates based on various risk models available in the literature, lifetime lung cancer risks were calculated with five well-known risk models using more recent Canadian vital statistics (5-year averages from 2008 to 2012). Variations in population risk estimation among various models were assessed. The results showed that the Canadian population risk of radon induced lung cancer can vary from 5.0 to 17% for men and 5.1 to 18% for women based on different radon risk models. Averaged over the estimates from various risk models with better radon dosimetry, 13% of lung cancer deaths among Canadian males and 14% of lung cancer deaths among Canadian females were attributable to long-term indoor radon exposure. (authors)

  14. The protective effect of propolis on damage to lung and blood in rats by inhaled radioactive radon and its progeny

    International Nuclear Information System (INIS)

    Ding Jiansong; Nie Jihua; Tong Jian

    2006-01-01

    Twenty-eight male wistar rats were randomly divided into seven groups, i.e. the radon groups (3), the propolis+radon groups (3) and the control (1). The propolis+radon groups were fed intragastrically with propolis 0.2 g/kg, before exposing them, together with the radon groups, to radon and its progeny with the cumulative dose up to 30, 67 and 111 working level month (WLM), respectively. The levels of SOD (superoxide dismutase) and MDA (Malonic dialdehyde) in blood and lung tissue were determined. The SOD level of in blood and lung tissues of the radon groups decreased significantly and the MDA level increased. The MDA level in lung tissue of the 30 WLM propolis+radon group was significantly higher than the 30 WLM radon group. The SOD level in lung tissue of the 67 WLM propolis+radon group was significantly higher, but the MDA level was significantly lower, than the 67 WLM radon group. Both the SOD and MDA levels in blood and lung tissue of the 111 WLM propolis+radon group were significantly higher than the 111 WLM radon group. In conclusion, the inhalation of radon and its progeny can lead to persistent disturbance of the redox state in rats. Propolis show some protective effects on the redox damage under the experimental conditions. (authors)

  15. Canadian individual risks of radon-induced lung cancer for different exposure profiles.

    Science.gov (United States)

    Chen, Jing

    2005-01-01

    Indoor radon has been determined to be the second leading cause of lung cancer after tobacco smoking. There is an increasing need among radiation practitioners to have numerical values of lung cancer risks for men and women, ever-smokers and never-smokers exposed to radon in homes. This study evaluates individual risks for the Canadian population exposed to radon in homes at different radon concentrations and for different periods of their lives. Based on the risk model developed recently by U.S. Environmental Protection Agency (EPA), individual risks of radon-induced lung cancers are calculated with Canadian age-specific rates for overall and lung cancer mortalities (1996-2000) as well as the Canadian smoking prevalence data in 2002. Convenient tables of lifetime relative risks are constructed for lifetime exposures and short exposures between any two age intervals from 0 to 110, and for various radon concentrations found in homes from 50 to 1000 Bq/m3. The risk of developing lung cancer from residential radon exposure increases with radon concentration and exposure duration. For short exposure periods, such as 10 or 20 years, risks are higher in middle age groups (30-50) compared especially to the later years. Individuals could lower their risks significantly by reducing radon levels earlier in life. The tables could help radiation protection practitioners to better communicate indoor radon risk to members of the public.

  16. Radon exposure and lung cancer

    International Nuclear Information System (INIS)

    Planinic, J.; Vukovic, B.; Faj, Z.; Radolic, V.; Suveljak, B.

    2003-01-01

    Although studies of radon exposure have established that Rn decay products are a cause of lung cancer among miners, the lung cancer risk to the general population from indoor radon remains unclear and controversial. Our epidemiological investigation of indoor radon influence on lung cancer incidence was carried out for 201 patients from the Osijek town. Ecological method was applied by using the town map with square fields of 1 km 2 and the town was divided into 24 fields. Multiple regression study for the lung cancer rate on field, average indoor radon exposure and smoking showed a positive linear double regression for the mentioned variables. Case-control study showed that patients, diseased of lung cancer, dwelt in homes with significantly higher radon concentrations, by comparison to the average indoor radon level of control sample. (author)

  17. Lung cancer risks from residential radon among smokers and non-smokers

    International Nuclear Information System (INIS)

    Enflo, Anita

    2002-01-01

    Primary lung cancer occurs mainly among elderly smokers. Smoking and radon are generally considered to be the main causes of lung cancer. By simply studying the age dependence of all primary lung cancer incidences it seems plausible to suggest that the risk for obtaining lung cancer from domestic radon is low for children. In addition, as there are few non-smoking primary lung cancer cases at older ages, it seems plausible to suggest that most of the radon-induced lung cancer cases are to be found among the smoking population. Reduction of smoking habits would appear to be the most cost effective method to reduce lung cancer cases. (author)

  18. Prediction of lung cells oncogenic transformation for induced radon progeny alpha particles using sugarscape cellular automata.

    Science.gov (United States)

    Baradaran, Samaneh; Maleknasr, Niaz; Setayeshi, Saeed; Akbari, Mohammad Esmaeil

    2014-01-01

    Alpha particle irradiation from radon progeny is one of the major natural sources of effective dose in the public population. Oncogenic transformation is a biological effectiveness of radon progeny alpha particle hits. The biological effects which has caused by exposure to radon, were the main result of a complex series of physical, chemical, biological and physiological interactions. The cellular and molecular mechanisms for radon-induced carcinogenesis have not been clear yet. Various biological models, including cultured cells and animals, have been found useful for studying the carcinogenesis effects of radon progeny alpha particles. In this paper, sugars cape cellular automata have been presented for computational study of complex biological effect of radon progeny alpha particles in lung bronchial airways. The model has included mechanism of DNA damage, which has been induced alpha particles hits, and then formation of transformation in the lung cells. Biomarkers were an objective measure or evaluation of normal or abnormal biological processes. In the model, the metabolism rate of infected cell has been induced alpha particles traversals, as a biomarker, has been followed to reach oncogenic transformation. The model results have successfully validated in comparison with "in vitro oncogenic transformation data" for C3H 10T1/2 cells. This model has provided an opportunity to study the cellular and molecular changes, at the various stages in radiation carcinogenesis, involving human cells. It has become well known that simulation could be used to investigate complex biomedical systems, in situations where traditional methodologies were difficult or too costly to employ.

  19. Review of radon and lung cancer risk

    International Nuclear Information System (INIS)

    Samet, J.M.; Hornung, R.W.

    1990-01-01

    Radon, a long-established cause of lung cancer in uranium and other underground miners, has recently emerged as a potentially important cause of lung cancer in the general population. The evidence for widespread exposure of the population to radon and the well-documented excess of lung cancer among underground miners exposed to radon decay products have raised concern that exposure to radon progeny might also be a cause of lung cancer in the general population. To date, epidemiological data on the lung cancer risk associated with environmental exposure to radon have been limited. Consequently, the lung cancer hazard posed by radon exposure in indoor air has been addressed primarily through risk estimation procedures. The quantitative risks of lung cancer have been estimated using exposure-response relations derived from the epidemiological investigations of uranium and other underground miners. We review five of the more informative studies of miners and recent risk projection models for excess lung cancer associated with radon. The principal models differ substantially in their underlying assumptions and consequently in the resulting risk projections. The resulting diversity illustrates the substantial uncertainty that remains concerning the most appropriate model of the temporal pattern of radon-related lung cancer. Animal experiments, further follow-up of the miner cohorts, and well-designed epidemiological studies of indoor exposure should reduce this uncertainty. 18 references

  20. Radon and radiation biology of the lung

    International Nuclear Information System (INIS)

    Crameri, R.; Burkart, W.

    1989-01-01

    The main papers presented at the meeting dealt with the behaviour of radon and the indoor environment, radiation biology of the lung, lung dosis and the possible cancer risk caused by radon in homes, contamination of the room air. A series of special papers treated the radon problem in detail: sources and transport mechanisms of radon, geological aspects of the radon radiation burden in Switzerland, radon in homes, search for radon sources, and the Swiss radon-programme RAPROS. 67 figs., 13 tabs., 75 refs

  1. Lung tumors and radon inhalation in over 2000 rats: Approximate linearity across a wide range of doses and potentiation by tobacco smoke

    International Nuclear Information System (INIS)

    Gray, R.G.; Lafuma, J.; Parish, S.E.; Peto, R.; CEA Centre d'Etudes Nucleaires de Fontenay-aux-Roses

    1986-01-01

    More than 2000 rats were exposed to cumulative doses of up to 28,000 WLMs of radon gas. More than 300 pulmonary tumors were induced by this exposure, most being nonfatal lesions detected only at autopsy of animals that had died of unrelated causes. Above 6000 WLMs rats suffered increasingly from life shortening due to radiation-induced nonneoplastic causes and so had less time in which to develop tumors. When adjusted for these competing causes of death, the hazard function for the excess risk of developing pulmonary tumors was approximately linearly related to dose throughout the range of doses studied. This suggests that some previously reported high-dose ''reductions'' in radiogenic tumor-induction rates may chiefly have involved the killing of rats rather than the killing of precursor cells. Rats exposed to radon and then to six months of inhalation of tobacco smoke had a four times greater age-specific prevalence of pulmonary tumors than rats exposed to an identical radon dose either alone or preceded by tobacco smoke inhalation. This suggests that tobacco smoke may accelerate the carcinogenic process by acting as a promoter of radiation-induced somatic damage. These data suggest that, for assessing human risk from exposure to radon, the linear model should be assumed, but that the WLM is not on its own an adequate index of carcinogenic insult. 7 refs., 2 figs., 4 tabs

  2. Gene alterations in radiation-induced F344 rat lung tumors

    International Nuclear Information System (INIS)

    Kelly, G.; Hahn, F.F.

    1994-01-01

    The p53 tumor suppressor gene is frequently altered in all major histopathologic types of human lung tumors. Reported p53 mutations include base substitutions, allelic loss, rearrangements, and deletions. Point mutations resulting in base substitutions are clustered within a highly conserved region of the gene encoding exons 508, and mutations in this region substantially extend the half-life of the p53 protein. In addition to its prominent importance in lung carcinogenesis, the p53 gene plays a critical role in the cellular response to genetic damage caused by radiation. Specifically, the protein product of p53 induces a pause or block at the G 1 to S boundary of the cell cycle following radiation-caused DNA damage. This G 1 block may allow the cell time to repair the damaged DNA prior to replication. Cells lacking a functional p53 protein fail to pause for repair and consequently accumulate mutations in the genome at an accelerated rate. p53 has also been implicated as a controlling factor in apoptosis or in programmed cell death induced by DNA-damaging agents, such as ionizing radiation. The p53 gene is mutated in approximately 50% of squamous cell carcinomas from uranium miners who inhaled high doses of radon daughters. The purpose of the present study was to determine if a similar percentage of squamous cell carcinomas with p53 mutations developed in the lungs of rats exposed to aerosols of 239 PuO 2

  3. Experimental study of the combined effects of inhalation of radon daughter products and tobacco smoke

    International Nuclear Information System (INIS)

    Chameaud, J.; Perraud, R.; Chretien, J.; Masse, R.; Lafuma, J.

    1979-01-01

    For 10 years, over 500 lung cancers have been induced in rats by inhalations of radon daughter products at various concentrations and cumulated doses. Considering several points and the dose-effect relationship especially, such cancers can be compared with human cancers. This type of experiments, fully mastered, has made it possible to undertake under good conditions the study of the co-carcinogenic effect of various inhaled pollutants such as tobacco smoke. In a first experiment, 100 rats were exposed to a 4000WLM cumulated dose of radon daughter products, knowing that this level induces some 30% of lung cancers. 50 animals were then administered tobacco smoke by inhalation in a fume box during 5 months (350 h.) In the group inhaling radon only, 17 cancers appeared; in the radon -tobacco group 32 cancers bigger and more invasive were observed. Under the same conditions, tobacco smoke was inhaled by rats previously exposed to lower doses of radon daughter products (2 groups of 30 rats, 500 and 100 WLM respectively). Again, the number of cancers observed was higher that the number of cancers expected if the rats had inhaled radon only. This co-carcinogenic and potentiating action of tobacco was clearly demonstrated. Further experiments are considered in order to determine the processes involved

  4. American Lung Association's radon public information program

    International Nuclear Information System (INIS)

    McCurdy, L.E.

    1992-01-01

    The American Lung Association (ALA), the nation's oldest voluntary health organization, is dedicated to the conquest of lung disease and the promotion of lung health. The objective of the ALA Radon Public Information Program is to reduce public exposure to elevated indoor radon levels through implementing grassroots-based radon public awareness campaigns by 22 local ALA groups. The program, which is funded by a grant from the US Environmental Protection Agency (EPA), was initiated in December 1989; the first phase will continue until May, 1991. Activities of local Lung Associations include distribution of free or reduced-cost radon kits; presenting programs in elementary and secondary schools; presenting information on TV news series and talk shows, and on radio Public Service Announcements and talk shows; presenting articles and feature stories in the print media; holding conferences, workshops, and displays at fairs and other exhibitions; distributing radon fact sheets through libraries and utility company mailings; and distributing videos through video chains and libraries. The local Lung Associations also serve as promoters for the EPA/Advertising Council Radon Public Service Announcement Campaign. We will highlight the activities of the groups in communicating radon health risks to the public; we will describe the results obtained and will attempt to evaluate the merits of the various approaches on the basis of the initial results

  5. Concentration and distribution of 210Po in rats exposed to radon

    International Nuclear Information System (INIS)

    Pan Peng; Yang Zhanshan; Wang Tianchang; Tong Jian; Zhou Jianwei

    2007-01-01

    Objective: To study the concentration and distribution of 210 Po in rats exposed to radon and its daughters. Methods: Fifteen male wistar rats were randomly divided into three groups, including one control group and two radon exposed groups with the cumulative doses of 100 WLM (low dose) and 200 WLM (high dose), respectively. Tissue samples containing 210 Po were spontaneously deposited onto silvery discs with the diameter of 20 mm by means of wet ashing and electrodeposition. The concentration of 210 Po in tissues were measured by α spectroscopy, and tissue burden were calculated. Results: The concentrations of 210 Po were significantly different among the three dose groups in femur, liver, sex gland and hair (P 210 Po were different between the exposed groups and the control group in lung and soleus muscle (P 210 Po in lung, spleen and hair were higher than that in liver, bone and sex gland, the lowest was in intestine. The tissue burdens of liver, bone and sex gland were significantly different from those in other organs or tissues. Conclusions: 210 Po was mainly distributed in lung, liver, spleen, femur and sex gland. The concentrations of 210 Po in organs or tissues and the tissue burdens were correspondingly increased with the exposure dose of radon and its daughters. The results of this experiment provide a dosimetric basis for further studies on the carcinogenic effect of radon and its daughters. (authors)

  6. Human Lung Cancer Risks from Radon – Part III - Evidence of Influence of Combined Bystander and Adaptive Response Effects on Radon Case-Control Studies - A Microdose Analysis

    Science.gov (United States)

    Leonard, Bobby E.; Thompson, Richard E.; Beecher, Georgia C.

    2012-01-01

    Since the publication of the BEIR VI (1999) report on health risks from radon, a significant amount of new data has been published showing various mechanisms that may affect the ultimate assessment of radon as a carcinogen, in particular the potentially deleterious Bystander Effect (BE) and the potentially beneficial Adaptive Response radio-protection (AR). The case-control radon lung cancer risk data of the pooled 13 European countries radon study (Darby et al 2005, 2006) and the 8 North American pooled study (Krewski et al 2005, 2006) have been evaluated. The large variation in the odds ratios of lung cancer from radon risk is reconciled, based on the large variation in geological and ecological conditions and variation in the degree of adaptive response radio-protection against the bystander effect induced lung damage. The analysis clearly shows Bystander Effect radon lung cancer induction and Adaptive Response reduction in lung cancer in some geographical regions. It is estimated that for radon levels up to about 400 Bq m−3 there is about a 30% probability that no human lung cancer risk from radon will be experienced and a 20% probability that the risk is below the zero-radon, endogenic spontaneous or perhaps even genetically inheritable lung cancer risk rate. The BEIR VI (1999) and EPA (2003) estimates of human lung cancer deaths from radon are most likely significantly excessive. The assumption of linearity of risk, by the Linear No-Threshold Model, with increasing radon exposure is invalid. PMID:22942874

  7. Lung vagal afferent activity in rats with bleomycin-induced lung fibrosis.

    Science.gov (United States)

    Schelegle, E S; Walby, W F; Mansoor, J K; Chen, A T

    2001-05-01

    Bleomycin treatment in rats results in pulmonary fibrosis that is characterized by a rapid shallow breathing pattern, a decrease in quasi-static lung compliance and a blunting of the Hering-Breuer Inflation Reflex. We examined the impulse activity of pulmonary vagal afferents in anesthetized, mechanically ventilated rats with bleomycin-induced lung fibrosis during the ventilator cycle and static lung inflations/deflations and following the injection of capsaicin into the right atrium. Bleomycin enhanced volume sensitivity of slowly adapting stretch receptors (SARs), while it blunted the sensitivity of these receptors to increasing transpulmonary pressure. Bleomycin treatment increased the inspiratory activity, while it decreased the expiratory activity of rapidly adapting stretch receptors (RARs). Pulmonary C-fiber impulse activity did not appear to be affected by bleomycin treatment. We conclude that the fibrosis-related shift in discharge profile and enhanced volume sensitivity of SARs combined with the increased inspiratory activity of RARs contributes to the observed rapid shallow breathing of bleomycin-induced lung fibrosis.

  8. Smoking cessation programmes in radon affected areas: can they make a significant contribution to reducing radon-induced lung cancers?

    International Nuclear Information System (INIS)

    Denman, A.R.; Groves-Kirkby, C.J.; Timson, K.; Shield, G.; Rogers, S.; Phillips, P.S.

    2008-01-01

    Domestic radon levels in parts of the UK are sufficiently high to increase the risk of lung cancer in the occupants. Public health campaigns in Northamptonshire, a designated radon affected area with 6.3% of homes having average radon levels over the UK action level of 200 Bq m -3 , have encouraged householders to test for radon and then to carry out remediation in their homes, but have been only partially successful. Only 40% of Northamptonshire houses have been tested, and only 15% of householders finding raised levels proceed to remediate. Of those who did remediate, only 9% smoked, compared to a countywide average of 28.8%. This is unfortunate, since radon and smoking combine to place the individual at higher risk by a factor of around 4, and suggests that current strategies to reduce domestic radon exposure are not reaching those most at risk. During 2004-5, the NHS Stop Smoking Services in Northamptonshire assisted 2,808 smokers to quit to the 4-week stage, with some 30% of 4-week quitters remaining quitters at 1 year. We consider whether smoking cessation campaigns make significant contributions to radon risk reduction on their own, by assessing individual occupants' risk of developing lung cancer from knowledge of their age, gender, and smoking habits, together with he radon level in their house. The results demonstrate that smoking cessation programmes have significant added value in radon affected areas, and contribute a greater health benefit than reducing radon levels in the smokers' homes, whilst they remain smokers. Additionally, results are presented from a questionnaire-based survey of quitters, addressing their reasons for seeking help in quitting smoking, and whether knowledge of radon risks influenced this decision. The impact of these findings on future public health campaigns to reduce the impact of radon and smoking are discussed. (author)

  9. Influence of radon daughter exposure rate, unattachment fraction, and disequilibrium on occurrence of lung tumours

    International Nuclear Information System (INIS)

    Cross, F.T.; Palmer, R.F.; Dagle, G.E.; Busch, R.H.; Buschbom, R.L.

    1984-01-01

    Groups of male, specific-pathogen-free (SPF), Wistar rats were exposed to several concentrations of radon daughters and uranium ore dust to clarify the roles of exposure rate, unattached RaA daughters, and the degree of radon daughter disequilibrium, in the development of respiratory system disease. Modelled, human dosimetric data indicate that the dose to sensitive tissues of the respiratory tract increases with increasing radon daughter unattachment fraction and degree of disequilibrium. Data bearing on these developments as well as updated results of experiments designed to test the role of radon daughter exposure rate on lung tumour incidence are reported. (author)

  10. The bystander effect in experimental systems and compatibility with radon-induced lung cancer in humans

    International Nuclear Information System (INIS)

    Little, M.P.; Wakeford, R.

    2002-01-01

    Bystander effects following exposure to α-particles have been observed in C3H 10T 1/2 cells and in other experimental systems, and imply that linearly extrapolating low-dose risks from high-dose data might materially underestimate risk. The ratio of lung cancer risk among persons exposed to low and high doses of radon daughters is 2.4-4.0, with an upper 95% confidence limit (CL) of about 14. Assuming that the bystander effect observed in the C3H 10T 1/2 data applies to human lung cells in vivo, the epidemiological data imply that the number of neighbouring cells that can contribute to the bystander effect is between 0 and 1, with an upper 95% CL of about 7. As a consequence, the bystander effect observed in the C3H 10T 1/2 system probably does not play a large part in the process of radon-induced lung carcinogenesis in humans. Other experimental data relating to the bystander effect after α-particle exposure are surveyed; some of these data are more compatible with the epidemiological data. (author)

  11. Radon-induced lung cancer in smokers and non-smokers: risk implications using a two-mutation carcinogenesis model

    International Nuclear Information System (INIS)

    Leenhouts, H.P.

    1999-01-01

    Three sets of data (population statistics in non-smokers, data from an investigation of the smoking habits of British doctors and a study of Colorado uranium miners) were used to analyse lung cancer in humans as a function of exposure to radon and smoking. One of the aims was to derive implications for radon risk estimates. The data were analysed using a two-mutation radiation carcinogenesis model and a stepwise determination of the model parameters. The basic model parameters for lung cancer were derived from the age dependence fit of the spontaneous lung cancer incidence in non-smokers. The effect of smoking was described by two additional parameters and, subsequently, the effect of radon by three other parameters; these five parameters define the dependence of the two mutation steps on smoking and exposure to radon. Using this approach, a consistent fit and comprehensive description of the three sets of data have been achieved, and the parameters could, at least partly, be related to cellular radiobiological data. The model results explain the different effect of radon on non-smokers and smokers as seen in epidemiological data. Although the analysis was only applied to a limited number of populations, lung cancer incidence as a result of radon exposure is estimated to be about ten times higher for people exposed at the age of about 15 than at about 50, although this effect is masked (especially for smokers) by the high lung cancer incidence from smoking. Using the model to calculate the lung cancer risks from lifetime exposure to radon, as is the case for indoor radon, higher risks were estimated than previously derived from epidemiological studies of the miners' data. The excess absolute risk per unit exposure of radon is about 1.7 times higher for smokers of 30 cigarettes per day than for non-smokers, even though, as a result of the low spontaneous tumour incidence in the non-smokers, the excess relative risk per unit exposure for the smokers is about 20 times

  12. Cyclin D expression in plutonium-induced lung tumors in F344 rats

    Energy Technology Data Exchange (ETDEWEB)

    Hahn, F.F.; Kelly, G. [SouthWest Scientific Resources, Inc., Albuquerque, NM (United States)

    1995-12-01

    The genetic mechanisms responsible for {alpha}-radiation-induced lung cancer in rats following inhalation of {sup 239}Pu is an ongoing area of research in our laboratory. Previous studies have examined the status of the p53 gene by immunohistochemistry. Only two tumors (2/26 squamous cell carcinomas) exhibited detectable levels of p53 products. Both were the result of mutations in codons 280 and 283. More recent studies of X-ray-induced lung tumors in rats showed a similar lack of involvement of p53. In conclusion, we found that {alpha}-radiation-induced rat lung tumors have a high incidence (31 of 39) of cyclin D{sub 1} overexpression.

  13. Lung dose and lung cancer risk by inhalation of radon daughters

    International Nuclear Information System (INIS)

    Jacobi, W.

    1983-01-01

    The inhalation of short-lived radon daughters constitutes the most important occupational radiation exposure in mines, particularly in uranium mines. Among some groups of miners exposed in the past to relatively high radon levels, an excess lung cancer incidence has been observed. In addition to this occupational hazard, the observed radon levels in domestic houses indicate that the inhalation of short-lived radon daughters seems to be the most important component of the radiation exposure of the population from natural sources. For the quantification and judgment of the radiological impact by inhalation of radon daughters in mines as well as in houses, it is necessary to estimate the relationships between the inhaled activity or potential alpha (α) energy of these radionuclides, the dose to target tissues in the lung, and the possible associated lung cancer (LC) risk. It is the purpose of this paper to give a condensed review of our present knowledge in this field and to indicate the main gaps and uncertainties where future research seems necessary

  14. Combined effects of inhalation of Radon daughter products and tobacco smoke

    International Nuclear Information System (INIS)

    Chameaud, J.; Perraud, R.; Chretien, J.; Masse, R.; Lafuma, J.

    1980-01-01

    Over the last 10 years, more than 500 lung cancers have been induced in rats by inhalations of radon daughter products at various concentrations and cumulated doses. These cancers were compared with human cancers. Another study examines the cocarcinogenic effect of tobacco smoke. In the first experiment, 100 rats were exposed to a 4000-WLM (working level month) cumulated dose of radon daughter products. Fifty animals were then administered tobacco smoke by inhalation in a fume box during 5 months (i.e., for a total of 352 hr). In the group inhaling radon only, 17 cancers appeared; in the radon-tobacco group, 32 cancers were observed, many of them larger and more invasive than those seen in animals exposed to radon only. Under the same conditions tobacco smoke was inhaled by rats previously exposed to lower doses of radon daughter products (two groups of 30 rats each, at 500 and 100 WLM, respectively). Again, the number of cancers observed was greater than the number of cancers expected if the rats had inhaled radon only. The carcinogenic and potentiating action of tobacco smoke was clearly demonstrated

  15. Radon, smoking and human papilloma virus as risk factors for lung cancer in an environmental epidemiological study

    Directory of Open Access Journals (Sweden)

    G. P. Malinovsky

    2017-01-01

    Full Text Available The aim of the study: to analyze the risk of lung cancer caused by exposure to indoor radon using an environmental study, taking into account recent data on the possible effect of Human Papillomavirus, based on lung cancer mortality and radon exposure in the Russian regions.Materials and methods: in the analysis, linear dependencies of lung cancer against influencing factors were used. The average radon concentration for the regions of Russia was earlier reconstructed on the basis of the annual reports of the form 4-DOZ. Information on morbidity and mortality from malignant neoplasms in Russia was obtained from annual reports issued by the Р. Hertsen Moscow Oncology Research Institute. As a surrogate of the level of infection with Human Papillomavirus, the incidence of cervix cancer was used. The smoking prevalence was estimated applying data on the incidence of tongue cancer.Results: taking into account smoking and infection with Human Papillomavirus, it is possible to obtain estimates of lung cancer excess relative risk when induced by radon in dwellings consistent with the results of case-control studies.Conclusion: the analysis of regionally aggregated data on deaths from lung cancer in Russia, the average level of indoor radon concentrations and significant risk factors for lung cancer confirms the linear threshold-free concept of radiation-induced carcinogenesis.

  16. Indoor Radon and Lung Cancer Risk in Osijek

    International Nuclear Information System (INIS)

    Planinic, J.; Vukovic, B.; Faj, Z.; Radolic, V.; Culo, D.; Smit, G.; Suveljak, B.; Stanic, D.; Faj, D.

    2001-01-01

    Full text: Although studies of radon exposure have established that Rn decay products are a cause of lung cancer among miners, the lung cancer risk to the general population from indoor radon remains unclear. Our investigation of indoor radon influence on lung cancer incidence was carried out for 188 cases of the disease appeared in Osijek town during last five years. Radon concentration was measured in homes of the patients as well as for a control group. An ecologic method was applied by using the town map with square fields of 1,1km2 and the town was divided into 24 fields. For indoor radon level in the fields and belonging number of the diseases, a positive correlation coefficient was obtained, that was statistically significant, and a linear regression equation of cancer mortality rates was determined. In the mentioned population of the patients, subgroups of smokers and nonsmokers, males and females were also particularly investigated. (author)

  17. Radon and lung cancer among New Jersey women

    International Nuclear Information System (INIS)

    Schoenberg, J.; Klotz, J.; Wilcox, H.; Nicholls, G.

    1990-01-01

    An epidemiologic study previously conducted in New Jersey women was extended to examine the association of lung cancer with radon exposure. The substudy included 433 cases and 402 controls who lived in a single index residence for 10+ years during the period 10--30 years prior to diagnosis or selection. Lung cancer risks showed a significant trend (p = 0.04) with increasing year-round living area radon concentrations (based on alpha track measurements), and a weaker (p = 0.09) trend with estimated cumulative radon exposure. The relative risk coefficient of 3.4% per working level month (WLM) was consistent with the range of 0.5--4%/WLM generally reported for underground miners. This paper results must be interpreted cautiously due to the small number of subjects with high radon exposures and the possibility of selection biases. Nevertheless, the study suggests that findings of radon-related lung cancer in miners can be applied to the residential setting

  18. Comparative toxicity in rats vs hamsters of inhaled radon daughters with and without uranium ore dust

    International Nuclear Information System (INIS)

    Gaven, J.C.; Palmer, R.F.; McDonald, K.E.; Lund, J.E.; Stuart, B.O.

    1977-01-01

    Simultaneous exposures of rats and hamsters to inhaled radon daughters, with and without uranium ore dust, were performed daily for five months. Pulmonary pathology developing in 6 to 13 mo after cessation of daily exposures included interstitial fibrosis, emphysema, epithelial hyperplasia, squamous metaplasia, and malignant neoplasia. Rats showed a greater variety and more severe response to these uranium mine inhalation exposures than did hamsters. Inhalation of radon daughters with uranium ore dust displayed the site of greatest damage, including squamous carcinoma, from the nasopharynx to the lungs. Sixty percent of the rats exposed to radon daughters with ore dust developed primary pulmonary carcinomas, providing an appropriate short-term experimental animal model for investigation of respiratory tract carcinogenesis in uranium miners

  19. Residential radon and lung cancer incidence in a Danish cohort

    Energy Technology Data Exchange (ETDEWEB)

    Braeuner, Elvira V., E-mail: ole@cancer.dk [Diet, Genes and Environment, Danish Cancer Society Research Centre, Copenhagen (Denmark); Danish Building Research Institute, Aalborg University (Denmark); Andersen, Claus E. [Center for Nuclear Technologies, Radiation Research Division, Riso National Laboratory for Sustainable Energy, Technical University of Denmark, Roskilde (Denmark); Sorensen, Mette [Diet, Genes and Environment, Danish Cancer Society Research Centre, Copenhagen (Denmark); Jovanovic Andersen, Zorana [Diet, Genes and Environment, Danish Cancer Society Research Centre, Copenhagen (Denmark); Center for Epidemiology Screening, Department of Public Health, University of Copenhagen (Denmark); Gravesen, Peter [Geological Survey of Denmark and Greenland, Copenhagen (Denmark); Ulbak, Kaare [National Institute of Radiation Protection, Herlev (Denmark); Hertel, Ole [Department of Environmental Science, Aarhus University, Aarhus (Denmark); Pedersen, Camilla [Diet, Genes and Environment, Danish Cancer Society Research Centre, Copenhagen (Denmark); Overvad, Kim [Department of Epidemiology, School of Public Health, Aarhus University, Aarhus (Denmark); Tjonneland, Anne; Raaschou-Nielsen, Ole [Diet, Genes and Environment, Danish Cancer Society Research Centre, Copenhagen (Denmark)

    2012-10-15

    High-level occupational radon exposure is an established risk factor for lung cancer. We assessed the long-term association between residential radon and lung cancer risk using a prospective Danish cohort using 57,053 persons recruited during 1993-1997. We followed each cohort member for cancer occurrence until 27 June 2006, identifying 589 lung cancer cases. We traced residential addresses from 1 January 1971 until 27 June 2006 and calculated radon at each of these addresses using information from central databases regarding geology and house construction. Cox proportional hazards models were used to estimate incidence rate ratios (IRR) and 95% confidence intervals (CI) for lung cancer risk associated with residential radon exposure with and without adjustment for sex, smoking variables, education, socio-economic status, occupation, body mass index, air pollution and consumption of fruit and alcohol. Potential effect modification by sex, traffic-related air pollution and environmental tobacco smoke was assessed. Median estimated radon was 35.8 Bq/m{sup 3}. The adjusted IRR for lung cancer was 1.04 (95% CI: 0.69-1.56) in association with a 100 Bq/m{sup 3} higher radon concentration and 1.67 (95% CI: 0.69-4.04) among non-smokers. We found no evidence of effect modification. We find a positive association between radon and lung cancer risk consistent with previous studies but the role of chance cannot be excluded as these associations were not statistically significant. Our results provide valuable information at the low-level radon dose range.

  20. Residential radon and lung cancer incidence in a Danish cohort

    International Nuclear Information System (INIS)

    Bräuner, Elvira V.; Andersen, Claus E.; Sørensen, Mette; Jovanovic Andersen, Zorana; Gravesen, Peter; Ulbak, Kaare; Hertel, Ole; Pedersen, Camilla; Overvad, Kim; Tjønneland, Anne; Raaschou-Nielsen, Ole

    2012-01-01

    High-level occupational radon exposure is an established risk factor for lung cancer. We assessed the long-term association between residential radon and lung cancer risk using a prospective Danish cohort using 57,053 persons recruited during 1993–1997. We followed each cohort member for cancer occurrence until 27 June 2006, identifying 589 lung cancer cases. We traced residential addresses from 1 January 1971 until 27 June 2006 and calculated radon at each of these addresses using information from central databases regarding geology and house construction. Cox proportional hazards models were used to estimate incidence rate ratios (IRR) and 95% confidence intervals (CI) for lung cancer risk associated with residential radon exposure with and without adjustment for sex, smoking variables, education, socio-economic status, occupation, body mass index, air pollution and consumption of fruit and alcohol. Potential effect modification by sex, traffic-related air pollution and environmental tobacco smoke was assessed. Median estimated radon was 35.8 Bq/m 3 . The adjusted IRR for lung cancer was 1.04 (95% CI: 0.69–1.56) in association with a 100 Bq/m 3 higher radon concentration and 1.67 (95% CI: 0.69–4.04) among non-smokers. We found no evidence of effect modification. We find a positive association between radon and lung cancer risk consistent with previous studies but the role of chance cannot be excluded as these associations were not statistically significant. Our results provide valuable information at the low-level radon dose range.

  1. Pathomorphologic observation on treatment of radiation-induced lung damage in rats with

    International Nuclear Information System (INIS)

    Ye Jiangfeng; Qi Haowen; Zhao Feng; Fan Fengyun; Shi Mei; Zhao Yiling; Meng Yulin

    2004-01-01

    Objective: To inquire into the means of preventing lung damage induced by thoracic irradiation. Methods: SD rats were divided randomly into 3 groups: normal control, irradiated control (Group IC) and irradiated and fluvastatin (Flu)-treated group (Group F). The later two groups of rats were irradiated with X-rays at a dose of 20 Gy thoracically. Beginning from the seventh day before irradiation the rats in the Group F were treated with Flu at a dose of 20 mg per day by garaging until the end of the experiment. Animals from each group were sacrificed on days 5, 15, 30, 60 respectively after irradiation. Sections of lung were examined with light microscopy, electron microscopy and morphometry. Results: The rats in the Group IC suffered from typical radiation pneumonitis (P<0.01). Electron microscopy indicated type II pneumonocytes and capillary endothelial cells were injured in rats of Group IC on days 30, 60. There were increase of collagen and a great quantity of mast cells in irradiated control rats. In rats of the Group F there was slight reaction in the lung. Conclusion: Fluvastatin could reduce radiation pneumonitis and inhibit increase of collagen. The treatment and prevention of radiation-induced lung injury in rats with fluvastatin is effective

  2. Lung pathology and exposure to radon daughters

    International Nuclear Information System (INIS)

    Saccomanno, G.

    1980-01-01

    The data presented suggest that the primary carcinogen of lung cancer in uranium miners is cigarette smoking because the incidence of lung cancer in noncigarette smokers is insignificant. In cigarette-smoking uranium miners, however, the incidence of cancer in those exposed to significant amounts of radon daughters is higher than in the smoking, nonmining population. This suggests that radon is an additive carcinogen if the lung has been injured by the cigarette-smoking carcinogen. Preliminary studies measuring DNA, T cells, and rosette inhibition immunological studies indicate closer monitoring of uranium miners' health during this occupation may be justified

  3. Lung dosimetry for inhaled radon progeny in smokers

    International Nuclear Information System (INIS)

    Baias, P. F.; Hofmann, W.; Winkler-Heil, R.; Cosma, C.; Duliu, O. G.

    2010-01-01

    Cigarette smoking may change the morphological and physiological parameters of the lung. Thus the primary objective of the present study was to investigate to what extent these smoke-induced changes can modify deposition, clearance and resulting doses of inhaled radon progeny relative to healthy non-smokers (NSs). Doses to sensitive bronchial target cells were computed for four categories of smokers: (1) Light, short-term (LST) smokers, (2) light, long-term (LLT) smokers, (3) heavy, short-term (HST) smokers and (4) heavy, long-term (HLT) smokers. Because of only small changes of morphological and physiological parameters, doses for the LST smokers hardly differed from those for NSs. For LLT and HST smokers, even a protective effect could be observed, caused by a thicker mucus layer and increased mucus velocities. Only in the case of HLT smokers were doses higher by about a factor of 2 than those for NSs, caused primarily by impaired mucociliary clearance, higher breathing frequency, reduced lung volume and airway obstructions. These higher doses suggest that the contribution of inhaled radon progeny to the risk of lung cancer in smokers may be higher than currently assumed on the basis of NS doses. (authors)

  4. Assessment of lung cancer risk from radon in five provinces of Iran

    International Nuclear Information System (INIS)

    Baradaran, S.; Taheri, M.; Setayeshi, S.

    2010-01-01

    Radon is a natural radioactive gas which is produced by decay of the Uranium and emanates from the ground. According to EPA and WHO studies, Radon is the second largest cause of lung cancer after smoking. According to the registered information report of cancer cases from 1985 till now, lung cancer is the second most common death cause in all cancers (after stomach cancer) in Iran. Based on the report of the National Institute of Cancer and the Iranian Ministry of Health, the total death due to lung cancer were estimated to be 5.7%, 4.82%, 4.48% 3.76%, 9% in mentioned provinces. An investigation was made on the relation between lung cancer risk and radon levels. The risk for smoking, the first leading cause of lung cancer, is more greater than for radon, the second leading cause. The results show that there is no direct relation between increased risk of lung cancer from indoor radon exposure, but it cannot be ignored that indoor radon should be considered as a cause of lung cancer in the general population

  5. Estimating lung cancer risks of indoor radon: applications for prevention

    International Nuclear Information System (INIS)

    Klotz, J.B.

    1986-01-01

    The epidemiologic evidence for a serious lung cancer hazard from radon exposure is very strong, and cumulative exposures accrued in residences may frequently overlap those accrued in underground miners. However, many uncertainties exist in extrapolating from mining to indoor risks because of differences in the populations, in radon exposure variables, and in other exposures. Risks are also considered for indoor radon exposures outside the home. There is already suggestive evidence of an association of lung cancer with radon levels in community settings, and several large-scale investigations are in progress. Some important questions regarding quantifying risk may not be approached, however; some further research needs are outlined including development of techniques for preventing or postponing lung cancer in individuals previously exposed to high radon levels. 31 references, 2 tables

  6. Residential radon and lung cancer incidence in a Danish cohort

    DEFF Research Database (Denmark)

    Bräuner, Elvira Vaclavik; Andersen, Claus Erik; Sørensen, Mette

    2012-01-01

    High-level occupational radon exposure is an established risk factor for lung cancer. We assessed the long-term association between residential radon and lung cancer risk using a prospective Danish cohort using 57,053 persons recruited during 1993–1997. We followed each cohort member for cancer...... occurrence until 27 June 2006, identifying 589 lung cancer cases. We traced residential addresses from 1 January 1971 until 27 June 2006 and calculated radon at each of these addresses using information from central databases regarding geology and house construction. Cox proportional hazards models were used...... to estimate incidence rate ratios (IRR) and 95% confidence intervals (CI) for lung cancer risk associated with residential radon exposure with and without adjustment for sex, smoking variables, education, socio-economic status, occupation, body mass index, air pollution and consumption of fruit and alcohol...

  7. Czech studies of lung cancer and radon

    International Nuclear Information System (INIS)

    Tomasek, L.

    2002-01-01

    According to the International Agency for Research on Cancer, there is a significant evidence to classify radon as a carcinogen. Using extrapolations from occupational studies, it can be shown that for some countries environmental exposure to radon is the second most important cause of lung cancer in the general population after cigarette smoking. Czech studies among uranium miners, established in 1970 by Josef Sevc, and in the general population aim to contribute to knowledge on the risk from radon, particularly by evaluating temporal factors and interaction of radon exposure and smoking

  8. Indoor radon exposure in Norway and lung cancer risk

    International Nuclear Information System (INIS)

    Sanner, T.; Dybing, E.

    1990-01-01

    The risk for lung cancer due to indoor radon in Norway was estimated. The risk factor recommended by the World Health Organization was used. Corrections were made for time not spent at home and type of activity. On the basis of measurements by the Norwegian National Institute for Radiation Hygiene in 7,500 homes, Strand et al estimated that the average concentration of radon daughters in the bedroom of Norwegian dwellings was 26.5 Bq/m 3 (EER). The level of exposure during time spent outside the home was assumed to be 10% of that at home. It was calculated that indoor radon exposure may cause 75-225 lung cancer deaths per year. This corresponds to about 5-15% of all lung cancer deaths in Norway. The risk for lung cancer death per 1,000 deaths at an indoor radon decay product level of 100 Bq/m 3 was calculated on the basis of various reports in the paper. The results show that the present risk estimate is lower than most of the other estimates

  9. Lung doses from radon in dwellings and influencing factors

    International Nuclear Information System (INIS)

    Stranden, E.

    1980-01-01

    The radon concentration in Norwegian dwellings and the lung doses received by the Norwegian population are reported. The biological effects of these doses are discussed. The mean value of radon-daughters in Norwegian dwellings was found to be about 7x10 -3 WL (working levels). This corresponds to an annual exposure of about 0.3 WLM (working level months). From studies of the lung cancer statistics of Norway, this exposure may account for about 10% of the annual lung cancer cases in Norway. The variations in the radon concentration inside dwellings are discussed, and the influence of exhalation, ventilation and meteorological parameters upon the respiratory dosage is studied. From the risk estimates performed, the consequences of an increased indoor radon concentration due to reduced ventilation or introduction of building materials with high radium concentrations are discussed. From comparison of the population doses from different sources of radiation, it is evident that a possible future increase in the radon concentration in dwellings is one of the most serious radiation protection problems of our time. (author)

  10. Radon in dwellings and lung cancer - a discussion

    International Nuclear Information System (INIS)

    Stranden, E.

    1980-01-01

    A discussion of the lung cancer risk associated with radon exposure inside dwellings is presented. The risk factors found for miners are discussed and modified according to the lower mean breathing rates inside dwellings and the differences in atmosphere. Statistical information on the lung cancer incidence in the Norwegian population indicates that a 'doubling exposure rate' of radon daughters inside dwellings may be about 2-3 WLM/yr. This corresponds to a radon concentration of about 10-15 pCi/l. These values are used in a discussion of the consequences of a future reduction of the mean ventilation rates in modern houses. (author)

  11. Radon-induced cancer: a cell-based model of tumorigenesis due to protracted exposures

    International Nuclear Information System (INIS)

    Elkind, M.M.

    1994-01-01

    In 1982, results with C3H mouse embryo cells showed that the frequency of neoplastic transformation was enhanced when exposures to fission-spectrum neutrons were protracted in time. This finding was unexpected because the opposite was found with low-LET radiations. Similar neutron enhancements were reported with normal life-span Syrian hamster embryo cells, and with human hybrid cells. Because other studies did not confirm the preceding, in 1990 - at a conference convened by the US Armed Forces Radiobiological Research Institute - a biophysical model was proposed to explain the basis for the enhancement observed in some experiments but not in others. The model attributed special sensitivities, related to killing and neoplastic transformation, to cells in and around mitosis. Subsequently, it was shown that late G 2 /M phase cells constituted this window of sensitivity. In the instance of tumorigenesis, the model predicted that protracted exposures to a high-LET radiation would result in enhanced frequencies of transformation providing that susceptible cells were cycling or could be induced to cycle. The model explained data on lung tumour induction in rats breathing radon at different concentrations, and uranium miners working in atmospheres containing different concentrations of radon. The model also explains the anomalous finding that lung cancer deaths are often sublinearly correlated with indoor radon concentration. (author)

  12. Inhibition of acid-induced lung injury by hyperosmolar sucrose in rats.

    Science.gov (United States)

    Safdar, Zeenat; Yiming, Maimiti; Grunig, Gabriele; Bhattacharya, Jahar

    2005-10-15

    Acid aspiration causes acute lung injury (ALI). Recently, we showed that a brief intravascular infusion of hyperosmolar sucrose, given concurrently with airway acid instillation, effectively blocks the ensuing ALI. The objective of the present study was to determine the extent to which intravascular infusion of hyperosmolar sucrose might protect against acid-induced ALI when given either before or after acid instillation. Our studies were conducted in anesthetized rats and in isolated, blood-perfused rat lungs. We instilled HCl through the airway, and we quantified lung injury in terms of the extravascular lung water (EVLW) content, filtration coefficient (Kfc), and cell counts and protein concentration in the bronchoalveolar lavage. We infused hyperosmolar sucrose via the femoral vein. In anesthetized rats, airway HCl instillation induced ALI as indicated by a 52% increase of EVLW and a threefold increase in Kfc. However, a 15-min intravenous infusion of hyperosmolar sucrose given up to 1 h before or 30 min after acid instillation markedly blunted the increases in EVLW, as well as the increases in cell count, and in protein concentration in the bronchoalveolar lavage. Hyperosmolar pretreatment also blocked the acid-induced increase of Kfc. Studies in isolated perfused lungs indicated that the protective effect of hyperosmolar sucrose was leukocyte independent. We conclude that a brief period of vascular hyperosmolarity protects against acid-induced ALI when the infusion is administered shortly before, or shortly after, acid instillation in the airway. The potential applicability of hyperosmolar sucrose in therapy for ALI requires consideration.

  13. Radon and lung cancer in Bangalore Metropolitan, India

    International Nuclear Information System (INIS)

    Sathish, L.A.; Nethravathi, K.S.; Ramachandran, T.V.

    2012-01-01

    Radon is a radioactive gas released from the normal decay of 238 U in rocks and soil. It is an invisible, odorless, tasteless gas that seeps up through the ground and diffuses into the air. In a few areas, depending on local geology, radon dissolves into ground water and can be released into the air when the water is used. Radon gas usually exists at very low levels outdoors. However, in areas without adequate ventilation, such as underground mines, radon can accumulate to levels that substantially increase the risk of lung cancer. Radon decays quickly, giving off tiny radioactive particles. When inhaled, these radioactive particles can damage the cells that line the lung. Long-term exposure to radon can lead to lung cancer, the only cancer proven to be associated with inhaling radon. Public interest in radon has been occasionally piqued by articles in the general press. Considerable attention has been given to the high radon levels that were uncovered in the Reading Prong region of Pennsylvania, following the discovery in late 1984 of extremely high levels in one home. Several epidemiological study programmes in different countries are in progress to estimate the population exposures due to natural radiation with a view to obtain the radiation risk coefficients at low dose rate levels. In this regard, radiation surveys in high background areas (HBRAs) can provide excellent settings for epidemiological studies relating to the effects of low doses of radiation. In view of these, a comprehensive estimate of the natural inhalation dose requires both 222 Rn and 220 Rn levels in the indoor atmosphere. In this outlook an attempt is made to investigate the 222 Rn and 220 Rn levels in dwellings of Bangalore Metropolitan, India. Three year results shows that the activity concentrations of 226 Ra, 232 Th, radon in ground water, the concentrations 222 Rn and 220 Rn and the dose rate (mSvy -1 ) are at alarming levels for the environment of Bangalore Metropolitan, India. The

  14. Risk of Lung Cancer and Indoor Radon Exposure in France

    International Nuclear Information System (INIS)

    Baysson, H.; Tirmarche, M.; Tymen, G.; Ducloy, F.; Laurier, D.

    2004-01-01

    It is well established that radon exposure increases risks of lung cancer among underground miners. to estimate the lung cancer risk linked to indoor radon exposure, a hospital based case-control study was carried out in France, With a focus on precise reconstruction of past indoor radon exposure over the 30 years preceding the lung cancer diagnosis. The investigation rook place from 1992 to 1998 in four regions of France: Auvergne, Brittany, Languedoc and Limousin. During face-to-face interviews a standardized questionnaire was used to ascertain demographic characteristics, information on active and passive smoking, occupational exposure, medical history as well as extensive details on residential history. Radon concentrations were measured in the dwellings where subjects had lived at least one year during the 5-30 year period before interview. Measurements of radon concentrations were performed during a 6-month period, using two Kodalpha LR 115 detectors, one in the living room and one in the bedroom. The time-weighted average (TWA) radon concentration for a subject during the 5-30 year period before interview was based on radon concentrations over all addresses occupied by the subject weighted by the number of years spent at each address. For the time intervals without available measurements, we imputed the region-specific arithmetic average of radon concentrations for measured addresses of control subjects. Lung cancer risk was examined in relation to indoor radon exposure after adjustment for age, sex, region, cigarette smoking and occupational exposure. The estimated relative a risk per 100 Bq/m''3 was 1.04, at the borderline of statistical significance (95 percent Confidence Interval: 0.99, 1..1). These results are in agreement with results from other indoor radon case-control studies and with extrapolations from underground miners studies. (Author) 31 refs

  15. Case-control study of radon and lung cancer in New Jersey

    International Nuclear Information System (INIS)

    Wilcox, H. B.; Al-Zoughool, M.; Garner, M. J.; Jiang, H.; Klotz, J. B.; Krewski, D.; Nicholson, W. J.; Schoenberg, J. B.; Villeneuve, P. J.; Zielinski, J. M.

    2008-01-01

    Radon is known to cause lung cancer in humans; however, there remain uncertainties about the effects associated with residential exposures. This case-control study of residential radon and lung cancer was conducted in five counties in New Jersey and involved 561 cases and 740 controls. A yearlong α-track detector measurement of radon was completed for ∼93% of all residences lived in at the time of interview (a total of 2063). While the odds ratios (ORs) for whole data were suggestive of an increased risk for exposures >75 Bq m -3 , these associations were not statistically significant. The adjusted excess OR (EOR) per 100 Bq m -3 was -0.13 (95% CI: -0.30 to 0.44) for males, 0.29 (95% CI: -0.12 to 1.70) for females and 0.05 (95% CI: -0.14 to 0.56) for all subjects combined. An analysis of radon effects by histological type of lung cancer showed that the OR was strongest for small/oat cell carcinomas in both males and females. There was no statistical heterogeneity of radon effects by demographic factors (age at disease occurrence, education level and type of respondent). Analysis by categories of smoking status, frequency or duration did not modify the risk estimates of radon on lung cancer. The findings of this study are consistent with an earlier population-based study of radon and lung cancer among New Jersey women, and with the North American pooling of case control radon seven studies, including the previous New Jersey study. Several uncertainties regarding radon measurements and assumptions of exposure history may have resulted in underestimation of a true exposure-response relationship. (authors)

  16. Occupational studies of radon daughters and lung cancer

    International Nuclear Information System (INIS)

    Hornung, R.W.; Ballew, M.A.

    1988-01-01

    The relationship between exposure to radon daughters and lung cancer mortality has been established. The purpose of this paper is to review some of the major studies of the health effects due to exposure to the decay products of radon gas and to discuss their potential implications with regard to risk associated with indoor radon. There has been much recent interest in the health hazards associated with radon largely motivated by the discovery of high levels of this radioactive gas in the Reading Prong (a geological area in Pennsylvania and New Jersey) and subsequently throughout the United States. Although at least three studies in the U.S. have been initiated to better estimate the lung cancer risks from low level indoor radon exposure, the results will not be known for several years. Consequently, present knowledge concerning such risks is almost entirely derived from studies of underground exposure to miners. Those studies effectively exclude women and children; therefore, assumptions must be made with regard to risk to a large segment of the population. Before discussing current health studies of radon daughter exposure, some background information is presented

  17. Histomorphologic change of radiation pneumonitis in rat lungs: captopril reduces rat lung injury induced by irradiation

    International Nuclear Information System (INIS)

    Kim, Jin Hee

    1999-01-01

    To assess the histomorphologic changes in the rat lung injury induced by radiation, to determine whether captopril reduces the rat lung injury and to evaluate change in TNF-α and TGF β and rat lung damage by radiation and captopril. Right lungs in male Sprague-Dawley rats were divided irradiation alone (10, 20, 30 Gy) or radiation (same dose with radiation alone group) with captopril (500 mg/L). Radiation alone group were sacrificed at twelve hours and eleven weeks after radiation and radiation with captopril group (captopril group) were sacrificed at eleven weeks after radiation with captopril. We examined the light microscope and electron microscopic features in the groups. In radiation alone group, there were patch parenchymal collapse and consolidation at twelve hours after radiation. The increase of radiation dose shows more prominent the severity and broader the affected areas. Eleven weeks after radiation, the severity and areas of fibrosis had increased in proportion to radiation dose given in the radiation alone group. There was notable decrease of lung fibrosis in captopril group than in radiation alone group. The number of mast cells rapidly increased with increase of radiation dose in radiation alone group and the degree of increase of mast cell number and severity of collagen accumulation more decreased in captopril group than in radiation alone group. In radiation alone group expression of TNF-α and TGF-β] increased according to increase of radiation dose at twelve hours after radiation in both group. At eleven weeks after radiation, expression of TGF- P increased according to increase of radiation dose in radiation group but somewhat decreased in captopril group. In the captopril group the collagen deposition increased but less dense than those of radiation alone group. The severity of perivascular thickening, capillary change, the number and degranulation of mast cells more decreased in the captopril group than in the radiation alone group. It

  18. Hesperidin as radioprotector against radiation-induced lung damage in rat: A histopathological study

    Directory of Open Access Journals (Sweden)

    Gholam Hassan Haddadi

    2017-01-01

    Full Text Available Reactive oxygen species (ROS are generated by ionizing radiation, and one of the organs commonly affected by ROS is the lung. Radiation-induced lung injury including pneumonia and lung fibrosis is a dose-limiting factor in radiotherapy (RT of patients with thorax irradiation. Administration of antioxidants has been proved to protect against ROS. The present study was aimed to assess the protective effect of hesperidin (HES against radiation-induced lung injury of male rats. Fifty rats were divided into three groups. G1: Received no HES and radiation (sham. G2: Underwent γ-irradiation to the thorax. G3: Received HES and underwent γ-irradiation. The rats were exposed to a single dose of 18 Gy using cobalt-60 unit and were administered HES (100 mg/kg for 7 days before irradiation. Histopathological analysis was performed 24 h and 8 weeks after RT. Histopathological results in 24 h showed radiation-induced inflammation and presence of more inflammatory cells as compared to G1 (P < 0.05. Administration of HES significantly decreased such an effect when compared to G2 (P < 0.05. Histopathological evaluation in 8 weeks showed a significant increase in mast cells, inflammation, inflammatory cells, alveolar thickness, vascular thickness, pulmonary edema, and fibrosis in G2 when compared to G1 (P < 0.05. HES significantly decreased inflammatory response, fibrosis, and mast cells when compared to G2 (P < 0.05. Administration of HES resulted in decreased radiation pneumonitis and radiation fibrosis in the lung tissue. Thus, the present study showed HES to be an efficient radioprotector against radiation-induced damage in the lung of tissue rats.

  19. Lung cancer mortality and indoor radon concentrations in 18 Canadian cities

    International Nuclear Information System (INIS)

    Letourneau, E.G.; Mao, Y.; McGregor, R.G.; Semenciw, R.; Smith, M.H.; Wigle, D.T.

    1983-01-01

    Indoor radon and radon daughter concentrations were measured in a survey of 14,000 homes in 18 Canadian cities conducted in the summers of 1978 through 1980. Mortality and population data for the period 1966 through 1979 were retrieved for the geographic areas surveyed in each city. The results of analysis of the relation between lung cancer and radon daughter concentration, smoking habits and socioeconomic indicators for each city showed no detectable association between radon daughter concentrations and lung cancer mortality rates with or without adjustment for differences in smoking habits between cities

  20. Effect of radon and its progeny on the expression and mutation of p53 in lung tissues of mice

    International Nuclear Information System (INIS)

    Piao Chunnan; Tian Mei; Liu Jianxiang; Ruan Jianlei; Su Xu

    2010-01-01

    Objective: To explore the effect of radon and its progeny on the expression and mutations of p53 in lung tissue of mouse model. Methods: Apoptosis was detected by terminal deoxynucleotidy transferase-mediated dUTP-biotin nick end labeling. The expression of p53 gene was analyzed by immunohistochemistry, Western blot and realtime-PCR. PCR-SSCP was used to detect the mutation of p53 in lung tissues. Results: Compared with those in the control group, the apoptotic index were increased significantly in 30 WLM and 60 WLM groups (t=18.11, -10.30, P<0.05). The p53 protein was increased significantly (t=-11.08, P<0.05; t=-7.00, P<0.05) in 30 WLM and 60 WLM groups. The mutation of p53 gene was not detected in lungs of radon-exposure mice. Conclusions: Lung and bronchus might be the targets of radon and its progeny, and p53 gene plays an important role in the progression of radon-induced lung injury. (authors)

  1. Residential radon and lung cancer: a cohort study in Galicia, Spain

    Directory of Open Access Journals (Sweden)

    Raquel Barbosa-Lorenzo

    Full Text Available Case-control studies show an association between residential radon and lung cancer. The aim of this paper is to investigate this association through a cohort study. We designed an ambispective cohort study using the Galician radon map, Spain, with controls drawn from a previous case-control study. Subjects were recruited between 2002 and 2009. The data were cross-checked to ascertain lung cancer incidence and then analysed using a Cox regression model. A total of 2,127 subjects participated; 24 lung cancer cases were identified; 76.6% of subjects were drawn from the radon map. The adjusted hazard ratio was 1.2 (95%CI: 0.5-2.8 for the category of subjects exposed to 50Bq/m3 or more. This risk rose when subjects from the case-control study were analyzed separately. In conclusion, we did not observe any statistically significant association between residential radon exposure and lung cancer; however, it appears that with a sample of greater median age (such as participants from the case-control study, the risk of lung cancer would have been higher.

  2. Iron supplementation at high altitudes induces inflammation and oxidative injury to lung tissues in rats

    Energy Technology Data Exchange (ETDEWEB)

    Salama, Samir A., E-mail: salama.3@buckeyemail.osu.edu [High Altitude Research Center, Taif University, Al-Haweiah, Taif 21974 (Saudi Arabia); Department of Biochemistry, Faculty of Pharmacy, Al-Azhar University, Cairo 11751 (Egypt); Department of Pharmacology and GTMR Unit, College of Clinical Pharmacy, Taif University, Al-Haweiah, Taif 21974 (Saudi Arabia); Omar, Hany A. [Department of Pharmacology, Faculty of Pharmacy, Beni-Suef University, Beni-Suef 62514 (Egypt); Maghrabi, Ibrahim A. [Department of Clinical Pharmacy, College of Clinical Pharmacy, Taif University, Al-Haweiah, Taif 21974 (Saudi Arabia); AlSaeed, Mohammed S. [Department of Surgery, College of Medicine, Taif University, Al-Haweiah, Taif 21974 (Saudi Arabia); EL-Tarras, Adel E. [High Altitude Research Center, Taif University, Al-Haweiah, Taif 21974 (Saudi Arabia)

    2014-01-01

    Exposure to high altitudes is associated with hypoxia and increased vulnerability to oxidative stress. Polycythemia (increased number of circulating erythrocytes) develops to compensate the high altitude associated hypoxia. Iron supplementation is, thus, recommended to meet the demand for the physiological polycythemia. Iron is a major player in redox reactions and may exacerbate the high altitudes-associated oxidative stress. The aim of this study was to explore the potential iron-induced oxidative lung tissue injury in rats at high altitudes (6000 ft above the sea level). Iron supplementation (2 mg elemental iron/kg, once daily for 15 days) induced histopathological changes to lung tissues that include severe congestion, dilatation of the blood vessels, emphysema in the air alveoli, and peribronchial inflammatory cell infiltration. The levels of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), lipid peroxidation product and protein carbonyl content in lung tissues were significantly elevated. Moreover, the levels of reduced glutathione and total antioxidant capacity were significantly reduced. Co-administration of trolox, a water soluble vitamin E analog (25 mg/kg, once daily for the last 7 days of iron supplementation), alleviated the lung histological impairments, significantly decreased the pro-inflammatory cytokines, and restored the oxidative stress markers. Together, our findings indicate that iron supplementation at high altitudes induces lung tissue injury in rats. This injury could be mediated through excessive production of reactive oxygen species and induction of inflammatory responses. The study highlights the tissue injury induced by iron supplementation at high altitudes and suggests the co-administration of antioxidants such as trolox as protective measures. - Highlights: • Iron supplementation at high altitudes induced lung histological changes in rats. • Iron induced oxidative stress in lung tissues of rats at high altitudes. • Iron

  3. Iron supplementation at high altitudes induces inflammation and oxidative injury to lung tissues in rats

    International Nuclear Information System (INIS)

    Salama, Samir A.; Omar, Hany A.; Maghrabi, Ibrahim A.; AlSaeed, Mohammed S.; EL-Tarras, Adel E.

    2014-01-01

    Exposure to high altitudes is associated with hypoxia and increased vulnerability to oxidative stress. Polycythemia (increased number of circulating erythrocytes) develops to compensate the high altitude associated hypoxia. Iron supplementation is, thus, recommended to meet the demand for the physiological polycythemia. Iron is a major player in redox reactions and may exacerbate the high altitudes-associated oxidative stress. The aim of this study was to explore the potential iron-induced oxidative lung tissue injury in rats at high altitudes (6000 ft above the sea level). Iron supplementation (2 mg elemental iron/kg, once daily for 15 days) induced histopathological changes to lung tissues that include severe congestion, dilatation of the blood vessels, emphysema in the air alveoli, and peribronchial inflammatory cell infiltration. The levels of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), lipid peroxidation product and protein carbonyl content in lung tissues were significantly elevated. Moreover, the levels of reduced glutathione and total antioxidant capacity were significantly reduced. Co-administration of trolox, a water soluble vitamin E analog (25 mg/kg, once daily for the last 7 days of iron supplementation), alleviated the lung histological impairments, significantly decreased the pro-inflammatory cytokines, and restored the oxidative stress markers. Together, our findings indicate that iron supplementation at high altitudes induces lung tissue injury in rats. This injury could be mediated through excessive production of reactive oxygen species and induction of inflammatory responses. The study highlights the tissue injury induced by iron supplementation at high altitudes and suggests the co-administration of antioxidants such as trolox as protective measures. - Highlights: • Iron supplementation at high altitudes induced lung histological changes in rats. • Iron induced oxidative stress in lung tissues of rats at high altitudes. • Iron

  4. Indoor radon and risk of lung cancer: an epidemiological study in Finland

    International Nuclear Information System (INIS)

    Ruosteenoja, E.

    1991-03-01

    The main aim of the present study was to establish whether high radon concentrations in dwellings in Finland had increased the risk of lung cancer. Previous studies had shown an association between the α-active radon daughters and elevated lung cancer risk among miners. Convincing evidence of the risk among the general population exposed to radon indoors was, however, lacking. A descriptive analysis was first conducted in an area in southern Finland with high indoor radon exposure. In 18 rural municipalities this analysis yielded no significant correlation between the average radon exposure and incidence of male lung cancer. A case-control study within a cohort of the same rural population was then designed. The data included 238 male cases of lung cancer diagnosed in 1980-85 and 434 controls (390 smokers and 44 nonsmokers) from the male population. Radon exposure was measured, when possible, in all the dwellings occupied by a case or control in 1950-1975. Measurements were available for the total 25-year period, or for a proportion of it, for 164 cases and 334 controls; for the rest only estimates were available. In spite of the fact that the controls were mainly selected among smokers, the amount smoked still appeared to be the most important lung cancer risk factor in the data, the risk increasing linearly with the quantity of cigarettes smoked in a lifetime. The risk of lung cancer was not associated with the radon exposure level when the whole data were studied. In heavy smokers, however, a positive though not significant, effect on the risk from radon exposure was found. In the range of uncertainty the findings do not conflict with most of those observed among miners or the general population so far. (orig.)

  5. Riboflavin attenuates lipopolysaccharide-induced lung injury in rats.

    Science.gov (United States)

    Al-Harbi, Naif O; Imam, Faisal; Nadeem, Ahmed; Al-Harbi, Mohammed M; Korashy, Hesham M; Sayed-Ahmed, Mohammed M; Hafez, Mohamed M; Al-Shabanah, Othman A; Nagi, Mahmoud N; Bahashwan, Saleh

    2015-01-01

    Riboflavin (vitamin B2) is an easily absorbed micronutrient with a key role in maintaining health in humans and animals. It is the central component of the cofactors flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN) and is therefore required by all flavoproteins. Riboflavin also works as an antioxidant by scavenging free radicals. The present study was designed to evaluate the effects of riboflavin against acute lungs injury induced by the administration of a single intranasal dose (20 μg/rat) of lipopolysaccharides (LPS) in experimental rats. Administration of LPS resulted in marked increase in malondialdehyde (MDA) level (p riboflavin in a dose-dependent manner (30 and 100 mg/kg, respectively). Riboflavin (100 mg/kg, p.o.) showed similar protective effects as dexamethasone (1 mg/kg, p.o.). Administration of LPS showed marked cellular changes including interstitial edema, hemorrhage, infiltration of PMNs, etc., which were reversed by riboflavin administration. Histopathological examinations showed normal morphological structures of lungs tissue in the control group. These biochemical and histopathological examination were appended with iNOS and CAT gene expression. The iNOS mRNA expression was increased significantly (p riboflavin significantly (p riboflavin caused a protective effect against LPS-induced ALI. These results suggest that riboflavin may be used to protect against toxic effect of LPS in lungs.

  6. High Radon Areas and lung cancer prevalence: Evidence from Ireland.

    Science.gov (United States)

    Dempsey, Seraphim; Lyons, Seán; Nolan, Anne

    2018-02-01

    This paper examined the relationship between radon risk and lung cancer prevalence using a novel dataset combining spatially-coded survey data with a radon risk map. A logit model was employed to test for significant associations between a high risk of indoor radon and lung cancer prevalence using data on 5590 people aged 50+ from The Irish Longitudinal Study on Ageing (TILDA) and radon risk data from Ireland's Environmental Protection Agency (EPA). The use of data at the individual level allowed a wide range of potentially confounding factors (such as smoking) to be included. Results indicate that those who lived in an area in which 10%-20% of households were above the national reference level (200 Bq/m 3 ) were 2.9-3.1 times more likely to report a lung cancer diagnosis relative to those who lived in areas in which less than 1% of households were above the national reference level. Copyright © 2017 Elsevier Ltd. All rights reserved.

  7. Using bosentan to treat paraquat poisoning-induced acute lung injury in rats.

    Directory of Open Access Journals (Sweden)

    Zhongchen Zhang

    Full Text Available BACKGROUND: Paraquat poisoning is well known for causing multiple organ function failure (MODS and high mortality. Acute lung injury and advanced pulmonary fibrosis are the most serious complications. Bosentan is a dual endothelin receptor antagonist. It plays an important role in treating PF. There is no related literature on the use of bosentan therapy for paraquat poisoning. OBJECTIVE: To study the use of bosentan to treat acute lung injury and pulmonary fibrosis as induced by paraquat. METHOD: A total of 120 adult Wister male rats were randomly assigned to three groups: the paraquat poisoning group (rats were intragastrically administered with paraquat at 50 mg/kg body weight once at the beginning; the bosentan therapy group (rats were administered bosentan at 100 mg/kg body weight by intragastric administration half an hour after paraquat was administered, then the same dose was administered once a day; and a control group (rats were administered intragastric physiological saline. On the 3rd, 7th, 14th, and 21st days following paraquat exposure, rats were sacrificed, and samples of lung tissue and venous blood were collected. The levels of transforming growth factor-β1 (TGF-β1, endothelin-1 (ET-1, and hydroxyproline (HYP in the plasma and lung homogenate were determined. Optical and electronic microscopes were used to examine pathological changes. RESULT: The TGF-β1, ET-1, and HYP of the paraquat poisoning group were significantly higher than in the control group, and they were significantly lower in the 21st day therapy group than in the paraquat poisoning group on the same day. Under the optical and electronic microscopes, lung tissue damage was observed to be more severe but was then reduced after bosentan was administered. CONCLUSION: Bosentan can reduce inflammation factor release. It has a therapeutic effect on acute lung injury as induced by paraquat.

  8. Establishment and evaluation of a rat model of inhalation lung injury induced by ship smog

    Directory of Open Access Journals (Sweden)

    Xin-xin DUAN

    2018-03-01

    Full Text Available Objective To establish and evaluate a rat model of inhalation lung injury induced by ship smog. Methods A rat model of inhalation lung injury was established by analyzing the composition of ship materials after combustion. Forty- two healthy male Wistar rats were randomly divided into normal control group and 2, 6, 12, 24, 48 and 72h groups (6 eachafter inhalation, these rats were killed at each time point, and the changes of arterial blood gas, coagulation function, the lung water content (% were detected. Macroscopic and microscopic changes in lung tissues were observed to judge the degree of lung injury. Results The main components after combustion of 7 kinds of nonmetal materials on ship included CO, CO2, H2S, NOx and other harmful gases in this study, AIKE in one gas detector was used to monitor O2, CO, CO2 and H2S, and their concentrations remained relatively stable within 15 minutes, and the injury time was 15 minutes. The rats presented with shortness of breath and mouth breathing. Smoke inhalation caused a significant hypoxemia, the concentration of blood COHb reached a peak value 2h and the lung water content (% did 6h after inhalation (P<0.05. It is metabolic acidosis in the early stage after inhalation, but metabolic acidosis combined with respiratory acidosis in the later period. Histopathological observation showed diffuse hemorrhage, edema and inflammatory cell infiltration in the lung tissue as manifestations of lung injury, and the injury did not recover at 72h after inhalation, the change of blood coagulation function was not statistically significant. Conclusion A rat model of inhalation lung injury induced by ship smog has been successfully established, and has the advantages of easy replication, stability and reliability, thus can be used to research and treat inhalation lung injury induced by ship smog in naval war environment and other cases. DOI: 10.11855/j.issn.0577-7402.2018.03.14

  9. Mechanisms of radon injury

    International Nuclear Information System (INIS)

    Cross, F.T.

    1988-01-01

    In this new project, they conduct molecular, cellular and whole-animal research relevant to understanding the inhalation toxicology of radon and radon-daughter exposures. The work specifically addresses the exposure-rate effect in radon-daughter carcinogenesis; the induction-promotion relationships associated with exposure to radon and cigarette-smoke mixtures; the role of oncogenes in radon-induced cancers; the effects of radon on DNA as well as on DNA repair processes; and the involvement of growth factors and their receptors in radon-induced carcinogenesis. Preliminary experiments showed that oncogenes are activated in radon-induced lung tumors. They have therefore begun further exposures pertinent to the oncogene and growth-factor studies. An in vitro radon cellular-exposure system was designed, and cell exposures were initiated. Initiation-promotion-initiation studies with radon and cigarette-smoke mixtures have also begun; and they are compiling a radon health-effects bibliography

  10. Effects of radon in indoor air studied

    International Nuclear Information System (INIS)

    Auvinen, A.

    1994-01-01

    Radon is an odorless, tasteless and colourless radioactive noble gas that enters indoor air from the ground. Radon causes lung cancer. A committee set up to evaluate the health risks of chemical substances has been drafting a report on radon, which will compile the major research findings on the lung cancer risk posed by radon. Animal tests have shown that even small doses of radon can cause lung cancer. Smokers seem to contract radon-induced lung cancer more readily than non-smokers. Because research findings have been conflicting, however, it is not known exactly how high the risk of lung cancer caused by indoor radon exposure really is. Several major research projects are under way to obtain increasingly accurate risk assessments. An on-going European joint project brings together several studies - some already finished, some still being worked on. In this way it will be possible to get more accurate risk assessments than from individual studies. In order to prevent lung cancer, it is important to continue the work of determining and reducing radon connects and to combat smoking. (orig.)

  11. Evidence of the cause of radon in the incidence of lung cancer

    International Nuclear Information System (INIS)

    Aljaralla, M. I.

    2008-01-01

    Lung cancer Develops slowly among the general public and its symptoms typically appear only in later stages. The air pollution or radon gas is the major cause of lung cancer after smoking. Incidence of lung cancer is spread among miners. Studies demonstrated a direct relationship between radiation exposure and the incidence of lung cancer in miners. Studies were conducted on laboratory animals to determine the impact of radioactive materials on these animals and the anatomical changes that appear on them. There is a positive relationship between radiation dose and effects. The disease is classified by the type of lung cancer cells in which it occurs. The scientists tried to devise the impact of radon on the inhabitants of houses from the studies on the effect of gas on the miners. The medication can be by exposure to radon where thousands of people go every year to radon springs for treatment. The interpretation that defenders of that medication say is that low-dose radiation stimulates the body's cells to the reform process and increases the body's immune.

  12. A combined analysis of North American case-control studies of residential radon and lung cancer.

    Science.gov (United States)

    Krewski, Daniel; Lubin, Jay H; Zielinski, Jan M; Alavanja, Michael; Catalan, Vanessa S; Field, R William; Klotz, Judith B; Létourneau, Ernest G; Lynch, Charles F; Lyon, Joseph L; Sandler, Dale P; Schoenberg, Janet B; Steck, Daniel J; Stolwijk, Jan A; Weinberg, Clarice; Wilcox, Homer B

    2006-04-01

    Cohort studies have consistently shown underground miners exposed to high levels of radon to be at excess risk of lung cancer, and extrapolations based on those results indicate that residential radon may be responsible for nearly 10-15% of all lung cancer deaths per year in the United States. However, case-control studies of residential radon and lung cancer have provided ambiguous evidence of radon lung cancer risks. Regardless, alpha-particle emissions from the short-lived radioactive radon decay products can damage cellular DNA. The possibility that a demonstrated lung carcinogen may be present in large numbers of homes raises a serious public health concern. Thus, a systematic analysis of pooled data from all North American residential radon studies was undertaken to provide a more direct characterization of the public health risk posed by prolonged radon exposure. To evaluate the risk associated with prolonged residential radon exposure, a combined analysis of the primary data from seven large scale case-control studies of residential radon and lung cancer risk was conducted. The combined data set included a total of 4081 cases and 5281 controls, representing the largest aggregation of data on residential radon and lung cancer conducted to date. Residential radon concentrations were determined primarily by a-track detectors placed in the living areas of homes of the study subjects in order to obtain an integrated 1-yr average radon concentration in indoor air. Conditional likelihood regression was used to estimate the excess risk of lung cancer due to residential radon exposure, with adjustment for attained age, sex, study, smoking factors, residential mobility, and completeness of radon measurements. Although the main analyses were based on the combined data set as a whole, we also considered subsets of the data considered to have more accurate radon dosimetry. This included a subset of the data involving 3662 cases and 4966 controls with a-track radon

  13. Human Lung Cancer Risks from Radon – Part II – Influence from Combined Adaptive Response and Bystander Effects – A Microdose Analysis

    Science.gov (United States)

    Leonard, Bobby E.; Thompson, Richard E.; Beecher, Georgia C.

    2010-01-01

    In the prior Part I, the potential influence of the low level alpha radiation induced bystander effect (BE) on human lung cancer risks was examined. Recent analysis of adaptive response (AR) research results with a Microdose Model has shown that single low LET radiation induced charged particles traversals through the cell nucleus activates AR. We have here conducted an analysis based on what is presently known about adaptive response and the bystander effect (BE) and what new research is needed that can assist in the further evaluation human cancer risks from radon. We find that, at the UNSCEAR (2000) worldwide average human exposures from natural background and man-made radiations, the human lung receives about a 25% adaptive response protection against the radon alpha bystander damage. At the UNSCEAR (2000) minimum range of background exposure levels, the lung receives minimal AR protection but at higher background levels, in the high UNSCEAR (2000) range, the lung receives essentially 100% protection from both the radon alpha damage and also the endogenic, spontaneously occurring, potentially carcinogenic, lung cellular damage. PMID:22461760

  14. On the radiation dose to lung tissues from radon daughters

    International Nuclear Information System (INIS)

    Wise, K.N.

    1980-04-01

    The work of Harley and Pasternak on calculating dose conversion factors for radon daughters is re-examined. It is found that their estimates of the deposit of radon daughters on the lung airways are too low and the factor for converting from equilibrium activity of radon daughters on the airways to dose to basal cells is too high; these are re-calculated. However, it is shown that inter-subject variability of the depth of the basal cells leads to considerable uncertainty in the individual dose. Finally average dose conversion factors are re-calculated for atmospheres which may be charactersitic of underground mines; the dose conversion factors range from 8 mGy/WLM to 40 mGy/WLM as calculated from the Weibel lung model and from 3 mGy/WLM to 17 mGy/WLM as calculated from the Landahl lung model

  15. Experimental study of the combined effect of cigarette smoke and an active burden of radon-222

    International Nuclear Information System (INIS)

    Chameaud, J.; Perraud, R.; Chretien, J.; Masse, R.; Lafuma, J.

    1978-01-01

    Previous studies on the carcinogenic effect of radon-222 derivatives have yielded accurate relationships, for each radon dose, between the dose value and the frequencies and latency times of lung cancers. In the present work, one hundred rats were subjected, over one-and-a-half months, to a total dose of 3600 WLM, chosen because it corresponds to a 30% occurrence of cancers. Fifty of these animals then inhaled cigarette smoke during 50 ten-minute sessions per week. The total time for these inhalations was 350 hours spread over about six months. In the 'radon' group (50 rats), 17 animals were found to have lung cancer. In the 'radon + tobacco' group (50 rats), 32 cancers were observed; moreover, the tumours in this group were much more extensive, multifocal and invasive. Animals subjected to cigarette smoke alone have never shown lung cancer. The effect of tobacco as a co-factor in carcinogenesis has thus been varified experimentally, although inhaled cigarette smoke alone is not carcinogenic in rats. (author)

  16. Lung cancer mortality among nonsmoking uranium miners exposed to radon daughters

    International Nuclear Information System (INIS)

    Roscoe, R.J.; Steenland, K.; Halperin, W.E.; Beaumont, J.J.; Waxweiler, R.J.

    1989-01-01

    Radon daughters, both in the workplace and in the household, are a continuing cause for concern because of the well-documented association between exposure to radon daughters and lung cancer. To estimate the risk of lung cancer mortality among nonsmokers exposed to varying levels of radon daughters, 516 white men who never smoked cigarettes, pipes, or cigars were selected from the US Public Health Service cohort of Colorado Plateau uranium miners and followed up from 1950 through 1984. Age-specific mortality rates for nonsmokers from a study of US veterans were used for comparison. Fourteen deaths from lung cancer were observed among the nonsmoking miners, while 1.1 deaths were expected, yielding a standardized mortality ratio of 12.7 with 95% confidence limits of 8.0 and 20.1. These results confirm that exposure to radon daughters in the absence of cigarette smoking is a potent carcinogen that should be strictly controlled

  17. Lung cancer mortality among nonsmoking uranium miners exposed to radon daughters

    International Nuclear Information System (INIS)

    Roscoe, R.J.; Stenland, K.; Halperin, W.E.; Waxweiler, R.J.

    1990-01-01

    This paper reports on radon daughters, both in the workplace and in the household, that are a continuing cause of concern because of the well-documented association between exposure to radon daughters and lung cancer. To estimate the risk of lung cancer mortality among nonsmokers exposed to varying levels of radon daughters, 516 white men who never smoked cigarettes, pipes, or cigars were selected from the U.S. Public Health Service cohort of Colorado Plateau uranium miners and followed up from 1950 through 1984. Age-specific mortality rates for nonsmokers from a study of U.S. veterans were used for comparison. Fourteen deaths from lung cancer were observed among the nonsmoking miners, while 1.1 deaths were expected, yielding a standardized mortality radio of 12.7 with 95% confidence limits of 8.0 and 20.1. These results confirm that exposure to radon daughters in the absence of cigarette smoking is a potent carcinogen that should be strictly controlled

  18. Residential Radon Exposure and Lung Cancer: Evidence of an Inverse Association in Washington State.

    Science.gov (United States)

    Neuberger, John S.; And Others

    1992-01-01

    Presents results of a descriptive study of lung cancer death rates compared to county levels of radon in Washington State. Age-specific death rates were computed for white female smokers according to radon exposure. A significant lung cancer excess was found in lowest radon counties. No significant difference was found between the proportion of…

  19. Predictions of lung cancer based on county averages for indoor radon versus the historic incidence of regional lung cancer

    International Nuclear Information System (INIS)

    Mose, D.G.; Chrosniak, C.E.; Mushrush, G.W.

    1992-01-01

    After a decade of effort to determine the health risk associated with indoor radon, the efforts of the US Environmental Protection Agency have prevailed in the US, and 4 pCi/1 is commonly used as an Action Level. Proposals by other groups supporting lower or higher Action Levels have failed, largely due to paucity of information supporting any particular level of indoor radon. The authors' studies have compared indoor radon for zip code and county size areas with parameters such as geology, precipitation and home construction. Their attempts to verify the relative levels of lung cancer using US-EPA estimates of radon-vs-cancer have not been supportive of the EPA risk estimates. In general, when they compare the number of lung cancer cases in particular geological or geographical areas with the indoor radon levels in that area, they find the EPA predicted number of lung cancer cases to exceed the total number of lung cancer cases from all causes. Comparisons show a correlation between the incidence of lung cancer and indoor radon, but the level of risk is about 1/10 that proposed by the US-EPA. Evidently the assumptions used in their studies are flawed. Even though they find lower risk estimates using many counties in several states, fundamental flaws must be present in this type of investigation. Care must be taken in presenting health risks to the general population in cases, such as in indoor radon, where field data do not support risk estimates obtained by other means

  20. RADON AND CARCINOGENIC RISK IN MOSCOW

    Directory of Open Access Journals (Sweden)

    S. M. Golovanev

    2015-01-01

    Full Text Available Objective: comparative evaluation of carcinogenic risk inMoscowfrom radon in indoor and atmospheric pollutants.Materials and methods: the lung cancer incidence in Moscow; radiation-hygienic passport of the territory; .U.S. EPA estimated average age at all and radon induced deaths, years of life lost; Report of UNSCEAR 2006 and WHO handbook on indoor radon, 2009. Trend analysis of incidence; evaluation of the excess relative risk; assessment of ratio radon-induced population risk and published values оf total population carcinogenic risk from chemical carcinogens.Results: it is shown that the 304 cases of lung cancer per year (1. 85 10-3 on average from 2006 to 2011 (21280diseases for 70 years in addition to background level induced by radon; the differences in average trends of all lungcancer incidence in the districts can exceed 25%.Conclusion. The potential of risk reduction by measures of mitigation radon concentration exceeds 5 times the cost efficiency to reduce emissions from vehicles and can reduce cancer incidence, on average 236 cases per year; population risk 16520 cases over 70 years or save not less than 2832 person-years of life per year. The annual effect of reducing losses from not-survival of 12 years as a result of radon-induced lung cancer deaths exceeds 14160000 dollars. The evaluating of the carcinogenic risk from radon in accordance with the definition of population risk increases the predictive evaluation of the effectiveness of preventive measures more than twice.

  1. Calculation of lung cancer incidence in the Netherlands by smoking and radon exposure. Implications for the effect of radon

    International Nuclear Information System (INIS)

    Leenhouts, H.P.; Brugmans, J.P.

    2001-01-01

    Although the main cause of lung cancer is smoking cigarettes, part of the cases are subscribed to radon exposure, in particular α-radiation from daughter products. However, the relation between lung cancer and radon exposure is rather insecure. Based on international reports (e.g. BEIR VI) and extrapolation of lung cancer incidence in uranium mine workers to the population of the USA and subsequently to the Netherlands, the number of lung cancer cases in the Netherlands is estimated to be circa 800 per year, varying between 200-2000. Results of the analysis are summarized in this article. 10 refs

  2. Pooled Bayesian analysis of 28 studies on radon induced lung cancers

    International Nuclear Information System (INIS)

    Fornalski, K.W.; Dobrzyński, L.

    2010-01-01

    The influence of ionizing radiation of radon-222 and its daughters on the lung cancer incidence and mortality published in 28 papers was reanalyzed, for two ranges of low annual radiation dose of below 70 mSv per year (391 Bq m -3 ) and 150 mSv per year (838 Bq m -3 ). The seven popular models of dose-effect relationship were tested. The assumption-free Bayesian statistical methods were used for all curve fittings. Also the Model Selection algorithm was used to verify the relative probability of all seven models. The results of the analysis demonstrate that in this ranges of doses (below 70 and 150 mSv/ year) the published data do not show the presence of a risk of lung cancer induction. The most probable dose-effect relationship is constant one (risk ratio, RR=1). The statistical analysis shows that there is no basis for increase the risk of lung cancer in low dose area. The final conclusion results from the fact that the model assuming no dependence of the lung cancer induction on the radiation doses is at least 100 times more likely than six other models tested, including the Linear No-Threshold (LNT) model

  3. The use of track registration detectors to reconstruct contemporary and historical airborne radon ( sup 2 sup 2 sup 2 Rn) and radon progeny concentrations for a radon-lung cancer epidemiologic study

    CERN Document Server

    Steck, D J

    1999-01-01

    Epidemiologic studies that investigate the relationship between radon and lung cancer require accurate estimates for the long-term average concentrations of radon progeny in dwellings. Year-to-year and home-to-home variations of radon in domestic environments pose serious difficulties for reconstructing an individual's long-term radon-related exposure. The use of contemporary radon gas concentrations as a surrogate for radon-related dose introduces additional uncertainty in dose assessment. Studies of glass exposed in radon chambers and in a home show that radon progeny deposited on, and implanted in, glass hold promise for reconstructing past radon concentrations in a variety of atmospheres. We developed an inexpensive track registration detector for the Iowa Radon Lung Cancer Study (IRLCS) that simultaneously measures contemporary airborne radon concentrations, surface deposited alpha activity density, and implanted sup 2 sup 1 sup 0 Po activity density. The implanted activity is used to reconstruct the cum...

  4. St. Joachimstal: pitchblende, uranium and radon-induced lung cancer

    International Nuclear Information System (INIS)

    Robison, R. F.; Mould, R. F.

    2006-01-01

    This article is based on a presentation given at the 2005 annual meeting of the Radiological Society of North America. Without the mining of pitchblende at St. Joachimstal at the end of the 19 ch century, and its availability to the Curies, the discovery of radium would have been delayed. The uranium bearing are carnotide in Colorado and Utah only became available after World War I and in any event this ore was far less uranium-rich than the St. Joachimstal pitchblende. Pitchblende deposits in the Belgian Congo (now Zaire), were only processed for radium by the Union Miniere du Haut Katanga in the early 1920 s. This article briefly describes the mining activities at St. Joachimstal. Uranium are was first mined at the end of the 16 th century although lead mining had occurred since the 12 th century. By 1959 the mines were essentially depleted of pitchblende and in 1981 all but one, the Concordia mine which was then sill open, were flooded. The miners disease first recorded in the 16 th century was eventually identified as radon-induced lung cancer. Finally, speculations is made with regard to who might have discovered radium if the Curies did not, because enough pitchblende was just not available to them in Paris in the late 1890 s. (author)

  5. Protective effects of ghrelin in ventilator-induced lung injury in rats.

    Science.gov (United States)

    Li, Guang; Liu, Jiao; Xia, Wen-Fang; Zhou, Chen-Liang; Lv, Li-Qiong

    2017-11-01

    Ghrelin has exhibited potent anti-inflammatory effects on various inflammatory diseases. The aim of this study was to investigate the potential effects of ghrelin on a model of ventilator-induced lung injury (VILI) established in rats. Male Sprague-Dawley rats were randomly divided into three groups: low volume ventilation (LV, Vt=8ml/kg) group, a VILI group (Vt=30ml/kg), and a VILI group pretreated with ghrelin (GH+VILI). For the LV group, for the VILI and GH+VILI groups, the same parameters were applied except the tidal volume was increased to 40ml/kg. After 4h of MV, blood gas, lung elastance, and levels of inflammatory mediators, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and (MIP)-2 and total protein in bronchoalveolar lavage fluid (BALF) were analyzed. Myeloperoxidase (MPO), (TLR)-4, and NF-κB, were detected in lung tissues. Water content (wet-to-dry ratio) and lung morphology were also evaluated. The VILI group had a higher acute lung injury (ALI) score, wet weight to dry ratio, MPO activity, and concentrations of inflammatory mediators (TNF-α, IL-6, IL-1β, and MIP-2) in BALF, as well as higher levels of TLR4 and NF-κB expression than the LV group (Pghrelin pretreatment (PGhrelin pretreatment also decreased TLR4 expression and NF-κB activity compared with the VILI group (PGhrelin pretreatment attenuated VILI in rats by reducing MV-induced pulmonary inflammation and might represent a novel therapeutic candidate for protection against VILI. Copyright © 2017 Elsevier B.V. All rights reserved.

  6. Relationship between indoor radon and lung cancer: a study of feasibility of an epidemiological study. Final report

    Energy Technology Data Exchange (ETDEWEB)

    Rasmussen, S.; Neuberg, D.; DuMouchel, W.; Kleitman, D.; Chernoff, H.

    1981-01-01

    This report describes a study to assess the feasibility of an epidemiologic investigation of the relationship between residential radon exposure and lung cancer. Field measurements of residential radon levels in the State of Maine are described. Using these radon measurements and BEIR, 1980 risk assessments, it is estimated that at most 10% of lung cancers in Maine can be considered attributable to residential radon exposure. Calculations are made of sample sizes necessary for a case-control study of radon and lung cancer, for several levels of radon and smoking health effects. The effects of misclassification of exposure variables on the probability of detecting a radon health effect are discussed. A comparison is made of three different mathematical models which could be used for sample size estimation. Dollar cost estimates are given for conducting an epidemiologic case-control study of the relationship between residential radon exposure and lung cancer.

  7. Relationship between indoor radon and lung cancer: a study of feasibility of an epidemiological study. Final report

    International Nuclear Information System (INIS)

    Rasmussen, S.; Neuberg, D.; DuMouchel, W.; Kleitman, D.; Chernoff, H.

    1981-01-01

    This report describes a study to assess the feasibility of an epidemiologic investigation of the relationship between residential radon exposure and lung cancer. Field measurements of residential radon levels in the State of Maine are described. Using these radon measurements and BEIR, 1980 risk assessments, it is estimated that at most 10% of lung cancers in Maine can be considered attributable to residential radon exposure. Calculations are made of sample sizes necessary for a case-control study of radon and lung cancer, for several levels of radon and smoking health effects. The effects of misclassification of exposure variables on the probability of detecting a radon health effect are discussed. A comparison is made of three different mathematical models which could be used for sample size estimation. Dollar cost estimates are given for conducting an epidemiologic case-control study of the relationship between residential radon exposure and lung cancer

  8. Study of lung cancer and residential radon in the Czech Republic

    International Nuclear Information System (INIS)

    Tomasek, L.; Mueller, T.; Kunz, E.; Heribanova, A.; Matzner, J.; Placek, V.; Burian, I.; Holecek, J.

    2001-01-01

    The lung cancer mortality study was designed as a follow-up study of the population (N = 12,004) in a radon-prone area in the Czech Republic, covering the 1960-1999 period. Information on the vital status and causes of death was mostly obtained from local authorities and extracted from the national population registry. Exposure estimates were based on one-year measurements of radon progeny in the majority of houses within the study area (74 %). Exposures outside the area (16%) were based on radon mapping of the Czech Republic. The mean concentration, 509 Bq/m 3 , is five-fold higher than the country-wide average. By 1999, a total of 210 lung cancers had been observed, which is somewhat more than the nationally expected value (O/E = 1.10), as compared to the generally low numbers regarding cancer types other than lung cancer (O/E = 0.81). The excess relative risk for the standard radon concentration (100 Bq/m 3 ) was 0.087 (90 % CI: 0.017-0.208), which is consistent with the risk coefficients derived from other indoor studies. The increased lung cancer incidence was found to depend linearly on exposure in terms of the mean radon concentration during the past 5-34 years. The estimate was not affected appreciably by adjustment to smoking; although the risk coefficient was higher for non-smokers than for smokers (0.130 vs 0.069), the difference was not statistically significant

  9. Human umbilical cord mesenchymal stem cells reduce systemic inflammation and attenuate LPS-induced acute lung injury in rats

    Directory of Open Access Journals (Sweden)

    Li Jianjun

    2012-09-01

    Full Text Available Abstract Background Mesenchymal stem cells (MSCs possess potent immunomodulatory properties and simultaneously lack the ability to illicit immune responses. Hence, MSCs have emerged as a promising candidate for cellular therapeutics for inflammatory diseases. Within the context of this study, we investigated whether human umbilical cord-derived mesenchymal stem cells (UC-MSCs could ameliorate lipopolysaccharide- (LPS- induced acute lung injury (ALI in a rat model. Methods ALI was induced via injection of LPS. Rats were divided into three groups: (1 saline group(control, (2 LPS group, and (3 MSC + LPS group. The rats were sacrificed at 6, 24, and 48 hours after injection. Serum, bronchoalveolar lavage fluid (BALF, and lungs were collected for cytokine concentration measurements, assessment of lung injury, and histology. Results UC-MSCs increased survival rate and suppressed LPS-induced increase of serum concentrations of pro-inflammatory mediators TNF-α, IL-1β, and IL-6 without decreasing the level of anti-inflammatory cytokine IL-10. The MSC + LPS group exhibited significant improvements in lung inflammation, injury, edema, lung wet/dry ratio, protein concentration, and neutrophil counts in the BALF, as well as improved myeloperoxidase (MPO activity in the lung tissue. Furthermore, UC-MSCs decreased malondialdehyde (MDA production and increased Heme Oxygenase-1 (HO-1 protein production and activity in the lung tissue. Conclusion UC-MSCs noticeably increased the survival rate of rats suffering from LPS-induced lung injury and significantly reduced systemic and pulmonary inflammation. Promoting anti-inflammatory homeostasis and reducing oxidative stress might be the therapeutic basis of UC-MSCs.

  10. Lung cancer attributable to indoor radon exposure in France using different risk models

    International Nuclear Information System (INIS)

    Catelinois, O.C.; Laurier, D.L.; Rogel, A.R.; Billon, S.B.; Tirmarche, M.T.; Hemon, Dh.; Verger, P.V.

    2006-01-01

    Full text of publication follows: Radon exposure is omnipresent for the general public, but at variable levels, because radon mainly comes from granitic and volcanic subs oils as well as from certain construction materials. Inhalation of radon is the main source of exposure to radioactivity in the general population of most countries. In 1988, the International Agency for Research on Cancer declared radon to be carcinogenic for humans (lung cancer): radon is classed in the group 1. The exposure of the overall general population to a carcinogenic component led scientists to assess the lung cancer risk associated to indoor radon. The aim of this work is to provide the first lung cancer risk assessment associated with indoor radon exposure in France, using all available epidemiological results and performing an uncertainty analysis. The number of lung cancer deaths potentially associated with radon in houses is estimated for the year 1999 according to several dose-response relationships which come from either cohorts of miners or joint analysis of residential case-controls studies. The variability of indoor radon exposure in France and uncertainties related to each of the dose-response relationships are considered. The assessment of lung cancer risk associated with domestic radon exposure considers 10 dose-response relationships resulting from miners cohorts and case-control studies in the general population. A critical review of available data on smoking habits has been performed and allowed to consider the interaction between radon and tobacco. The exposure data come from measurements campaigns carried out since the beginning of the 1980's by the Institute for Radiation protection and Nuclear Safety and the Health General Directory in France. The French lung cancer mortality data are provided by the INSERM. Estimates of the number of attributable cancers are carried out for the whole country, stratified by 8 large regions and b y 96 departments for the year 1999

  11. Temporal Patterns of Lung Cancer Risk from Radon, Smoking and their Interaction

    International Nuclear Information System (INIS)

    Tomasek, L.; Urban, S.; Kubik, A.; Zatloukal, P.

    2004-01-01

    Studies of uranium miners conducted since the late 1960s demonstrated that the risk depends on cumulated exposure in terms of working level months (WLM) integrating both duration of exposure and concentration of radon. It has been also demonstrated that the risk from radon decreases with time since exposure. The objective of the work is to study temporal patterns of lung cancer risk from occupational and residential radon and from smoking. The present analysis of temporal changes of relative risk is based on a model, where the total individual exposure is partitioned into components in dependence on time. Exposure to radon is studied in a cohort of 9411 Czech uranium miners with 766 cases of lung cancer and in a residential study of 1 803 inhabitants exposed to radon in houses with 218 cases. Temporal patterns of smoking are analyzed in a case-control study of patients from a major Prague hospital including 566 cases. for both carcinogens, the relative risk decreases with time since exposure. In comparison to period with exposure before 5-19 years, the risk from exposures before 20-34 years is 36% and 34% for smoking and randon, respectively. The effect of exposures from more distant periods 35-49 is only 5% for smoking and 14% for radon in comparison to 5-19 years. Combined effect of smoking and radon is studied by a nested case-control approach including 434 cases and 962 controls. Analyses of the joint effects of smoking and radon, conducted in the occupational and the residential studies, suggest a sub-multiplicative interaction. The relative risk from radon among non-smokers is higher by a factor of 2-3 in comparison to smokers, suggesting different patterns of lung deposition and clearance among smokers and non-smokers. (Author) 13 refs

  12. Temporal Patterns of Lung Cancer Risk from Radon, Smoking and their Interaction

    Energy Technology Data Exchange (ETDEWEB)

    Tomasek, L.; Urban, S.; Kubik, A.; Zatloukal, P.

    2004-07-01

    Studies of uranium miners conducted since the late 1960s demonstrated that the risk depends on cumulated exposure in terms of working level months (WLM) integrating both duration of exposure and concentration of radon. It has been also demonstrated that the risk from radon decreases with time since exposure. The objective of the work is to study temporal patterns of lung cancer risk from occupational and residential radon and from smoking. The present analysis of temporal changes of relative risk is based on a model, where the total individual exposure is partitioned into components in dependence on time. Exposure to radon is studied in a cohort of 9411 Czech uranium miners with 766 cases of lung cancer and in a residential study of 1 803 inhabitants exposed to radon in houses with 218 cases. Temporal patterns of smoking are analyzed in a case-control study of patients from a major Prague hospital including 566 cases. for both carcinogens, the relative risk decreases with time since exposure. In comparison to period with exposure before 5-19 years, the risk from exposures before 20-34 years is 36% and 34% for smoking and randon, respectively. The effect of exposures from more distant periods 35-49 is only 5% for smoking and 14% for radon in comparison to 5-19 years. Combined effect of smoking and radon is studied by a nested case-control approach including 434 cases and 962 controls. Analyses of the joint effects of smoking and radon, conducted in the occupational and the residential studies, suggest a sub-multiplicative interaction. The relative risk from radon among non-smokers is higher by a factor of 2-3 in comparison to smokers, suggesting different patterns of lung deposition and clearance among smokers and non-smokers. (Author) 13 refs.

  13. Carvacrol and Pomegranate Extract in Treating Methotrexate-Induced Lung Oxidative Injury in Rats

    Science.gov (United States)

    Şen, Hadice Selimoğlu; Şen, Velat; Bozkurt, Mehtap; Türkçü, Gül; Güzel, Abdulmenap; Sezgi, Cengizhan; Abakay, Özlem; Kaplan, Ibrahim

    2014-01-01

    Background This study was designed to evaluate the effects of carvacrol (CRV) and pomegranate extract (PE) on methotrexate (MTX)-induced lung injury in rats. Material/Methods A total of 32 male rats were subdivided into 4 groups: control (group I), MTX treated (group II), MTX+CRV treated (group III), and MTX+PE treated (group IV). A single dose of 73 mg/kg CRV was administered intraperitoneally to rats in group III on Day 1 of the investigation. To group IV, a dose of 225 mg/kg of PE was administered via orogastric gavage once daily over 7 days. A single dose of 20 mg/kg of MTX was given intraperitoneally to groups II, III, and IV on Day 2. The total duration of experiment was 8 days. Malondialdehyde (MDA), total oxidant status (TOS), total antioxidant capacity (TAC), and oxidative stress index (OSI) were measured from rat lung tissues and cardiac blood samples. Results Serum and lung specimen analyses demonstrated that MDA, TOS, and OSI levels were significantly greater in group II relative to controls. Conversely, the TAC level was significantly reduced in group II when compared to the control group. Pre-administering either CRV or PE was associated with decreased MDA, TOS, and OSI levels and increased TAC levels compared to rats treated with MTX alone. Histopathological examination revealed that lung injury was less severe in group III and IV relative to group II. Conclusions MTX treatment results in rat lung oxidative damage that is partially counteracted by pretreatment with either CRV or PE. PMID:25326861

  14. Reliability of up-to-date risk factor between residential radon and lung cancer

    International Nuclear Information System (INIS)

    Tokonami, Shinji; Ishikawa, Tetsuo; Sorimachi, Atsuyuki; Kobayashi, Yosuke; Yoshinaga, Shinji; Quanfu, Sun; Akiba, Suminori

    2008-01-01

    Full text: The WHO launched an international radon project in January, 2005 because two major scientific articles on the residential-radon-and-lung-cancer risk have been published. Furthermore, the ICRP has just issued a new recommendation (Publ. 103). In the publication, radon issues have been mentioned using these references. They show that there is a significant correlation between radon exposures and lung cancer risks even with a somewhat lower radon concentration than an internationally recommended level (200 Bq m -3 ). In most cases, residential radon concentrations were measured by passive integrating radon monitors based on the alpha track detection techniques in their studies. We examined detection responses for the presence of thoron with some typical alpha track detectors (Kf K: Germany, Radtrak: USA and NRPB: UK), which were widely used in many epidemiological studies. In addition, we measured indoor radon and thoron concentrations in cave dwellings in Gansu Province, China, in which the National Cancer Institute (NCI) conducted a large-scale epidemiological study. The NCI concluded that there was also a significant correlation between the two aforementioned parameters, which was a similar value to recently acceptable one. However, our results on radon concentrations were obviously different from them because there was much thoron in that area. The present study demonstrates whether these risk factors are really correct throughout our data or not. Tokonami (2005) has pointed out that some of popular alpha track detectors are sensitive to thoron ( 220 Rn). This finding implies that radon readings will be overestimated and consequently may lead to biased estimates of lung cancer risk. The present study describes thoron interference on accurate radon measurements from the viewpoint of both experimental studies and field experiences. (author)

  15. Indoor radon and lung cancer in the radium dial workers

    International Nuclear Information System (INIS)

    Neuberger, J.S.; Rundo, J.

    1996-01-01

    Internally deposited radium has long been known to have tumorigenic effects in the form of sarcomas of the bone and carcinomas of the paranasal sinuses and mastoid air cells. However, the radium dial workers were also exposed to radiation hazards other than that occurring from ingestion of the radium paint, viz., external gamma radiation and elevated concentrations of airborne radon. The uranium miners were also exposed to high concentrations of radon in the 1950s and later, and numerous cases of lung cancer have occurred in that population. However, unlike the atmosphere in the uranium mines, the air in the dial painting plants was probably rather clean and perhaps not much different from the air in many houses. In view of the current concern over the possibility of lung cancer fin the general population being caused by radon (progeny) in houses, it is important to examine the mortality due to this usually fatal disease in the dial workers and to attempt to relate it to their exposure to radon, to the extent that this is possible

  16. Niacinamide mitigated the acute lung injury induced by phorbol myristate acetate in isolated rat's lungs.

    Science.gov (United States)

    Lin, Chia-Chih; Hsieh, Nan-Kuang; Liou, Huey Ling; Chen, Hsing I

    2012-03-01

    Phorbol myristate acetate (PMA) is a strong neutrophil activator and has been used to induce acute lung injury (ALI). Niacinamide (NAC) is a compound of B complex. It exerts protective effects on the ALI caused by various challenges. The purpose was to evaluate the protective effects of niacinamide (NAC) on the PMA-induced ALI and associated changes. The rat's lungs were isolated in situ and perfused with constant flow. A total of 60 isolated lungs were randomized into 6 groups to received Vehicle (DMSO 100 μg/g), PMA 4 μg/g (lung weight), cotreated with NAC 0, 100, 200 and 400 mg/g (lung weight). There were 10 isolated lungs in each group. We measured the lung weight and parameters related to ALI. The pulmonary arterial pressure and capillary filtration coefficient (Kfc) were determined in isolated lungs. ATP (adenotriphosphate) and PARP [poly(adenosine diphophate-ribose) polymerase] contents in lung tissues were detected. Real-time PCR was employed to display the expression of inducible and endothelial NO synthases (iNOS and eNOS). The neutrophil-derived mediators in lung perfusate were determined. PMA caused increases in lung weight parameters. This agent produced pulmonary hypertension and increased microvascular permeability. It resulted in decrease in ATP and increase in PARP. The expression of iNOS and eNOS was upregulated following PMA. PMA increased the neutrophil-derived mediators. Pathological examination revealed lung edema and hemorrhage with inflammatory cell infiltration. Immunohistochemical stain disclosed the presence of iNOS-positive cells in macrophages and endothelial cells. These pathophysiological and biochemical changes were diminished by NAC treatment. The NAC effects were dose-dependent. Our results suggest that neutrophil activation and release of neutrophil-derived mediators by PMA cause ALI and associated changes. NO production through the iNOS-producing cells plays a detrimental role in the PMA-induced lung injury. ATP is beneficial

  17. Niacinamide mitigated the acute lung injury induced by phorbol myristate acetate in isolated rat's lungs

    Directory of Open Access Journals (Sweden)

    Lin Chia-Chih

    2012-03-01

    Full Text Available Abstract Background Phorbol myristate acetate (PMA is a strong neutrophil activator and has been used to induce acute lung injury (ALI. Niacinamide (NAC is a compound of B complex. It exerts protective effects on the ALI caused by various challenges. The purpose was to evaluate the protective effects of niacinamide (NAC on the PMA-induced ALI and associated changes. Methods The rat's lungs were isolated in situ and perfused with constant flow. A total of 60 isolated lungs were randomized into 6 groups to received Vehicle (DMSO 100 μg/g, PMA 4 μg/g (lung weight, cotreated with NAC 0, 100, 200 and 400 mg/g (lung weight. There were 10 isolated lungs in each group. We measured the lung weight and parameters related to ALI. The pulmonary arterial pressure and capillary filtration coefficient (Kfc were determined in isolated lungs. ATP (adenotriphosphate and PARP [poly(adenosine diphophate-ribose polymerase] contents in lung tissues were detected. Real-time PCR was employed to display the expression of inducible and endothelial NO synthases (iNOS and eNOS. The neutrophil-derived mediators in lung perfusate were determined. Results PMA caused increases in lung weight parameters. This agent produced pulmonary hypertension and increased microvascular permeability. It resulted in decrease in ATP and increase in PARP. The expression of iNOS and eNOS was upregulated following PMA. PMA increased the neutrophil-derived mediators. Pathological examination revealed lung edema and hemorrhage with inflammatory cell infiltration. Immunohistochemical stain disclosed the presence of iNOS-positive cells in macrophages and endothelial cells. These pathophysiological and biochemical changes were diminished by NAC treatment. The NAC effects were dose-dependent. Conclusions Our results suggest that neutrophil activation and release of neutrophil-derived mediators by PMA cause ALI and associated changes. NO production through the iNOS-producing cells plays a detrimental

  18. Role of macrophages and oxygen radicals in IgA induced lung injury in the rat

    International Nuclear Information System (INIS)

    Johnson, K.J.; Ward, P.A.; Kunkel, R.G.; Wilson, B.S.

    1986-01-01

    Acute lung injury in the rat has been induced by the instillation of affinity-purified mouse monoclonal IgA antibody with specific reactivity to dinitrophenol (DNP) coupled to albumin. This model of lung injury requires an intact complement system but not neutrophils, and evidence suggests that pulmonary macrophages are the critical effector cell. Macrophages retrievable from the lungs of the IgA immune complex treated rats are considerably increased in number as compared to control animals which received only the antibody. In addition these cells show evidence of activation in vivo with greater spontaneous generation of the superoxide anion (O 2 - ) as well as significantly enhanced O 2 - response in the presence of a second stimulus. Inhibition studies in vivo suggest that the lung injury is mediated by oxygen radical generation by the pulmonary macrophages. Pretreatment of rats with superoxide dismutase (SOD), catalase, the iron chelator deferoxamine or the hydroxyl radical scavenger dimethyl sulfoxide (DMSO) all markedly suppressed the development of the lung injury. In summary, these studies suggest that IgA immune complex injury in the rat lung is mediated by oxygen radical formation from pulmonary macrophages

  19. Contribution of radon and radon daughters to respiratory cancer

    International Nuclear Information System (INIS)

    Harley, N.; Samet, J.M.; Cross, F.T.; Hess, T.; Muller, J.; Thomas, D.

    1986-01-01

    This article reviews studies on the contribution of radon and radon daughters to respiratory cancer and proposes recommendations for further research, particularly a national radon survey. The steady-state outdoor radon concentration averages 200 pCi/m3, and indoor levels are about 4 times higher. The primary source of radon in homes is the underlying soil; entry depends on multiple variables and reduced ventilation for energy conservation increases indoor radon levels. Occupational exposures are expressed in units of radon daughter potential energy concentration or working level (WL). Cumulative exposure is the product of the working level and the time exposed. The unit for cumulative exposure is the working level month (WLM). The occupational standard for radon exposure is 4 WLM/year, and 2 WLM/year has been suggested as a guideline for remedial action in homes. Epidemiologic studies show that miners with cumulative radon daughter exposures somewhat below 100 WLM have excess lung cancer mortality. Some 3% to 8% of miners studied have developed lung cancer attributable to radon daughters. All of the underground mining studies show an increased risk of lung cancer with radon daughter exposure. All cell types of lung cancer increased with radon exposure. If radon and smoking act in a multiplicative manner, then the risk for smokers could be 10 times that for nonsmokers. The potential risk of lung cancer appears to be between 1 and 2 per 10,000/WLM, which yields a significant number of lung cancers as some 220 million persons in the United States are exposed on average to 10 to 20 WLM/lifetime

  20. Prevention of cigarette smoke induced lung cancer by low let ionizing radiation

    Energy Technology Data Exchange (ETDEWEB)

    Sanders, Charles L. [Korea Advanced Institute of Science and Technology, Daejeon (Korea, Republic of)

    2008-12-15

    Lung cancer is the most prevalent global cancer, {approx}90% of which is caused by cigarette smoking. The LNT hypothesis has been inappropriately applied to estimate lung cancer risk due to ionizing radiation. A threshold of {approx}1 Gy for lung cancer has been observed in never smokers. Lung cancer risk among nuclear workers, radiologists and diagnostically exposed patients was typically reduced by {approx}40% following exposure to <100 mSv low LET radiation. The consistency and magnitude of reduced lung cancer in nuclear workers and occurrence of reduced lung cancer in exposed non-worker populations could not be explained by the HWE. Ecologic studies of indoor radon showed highly significant reductions in lung cancer risk. A similar reduction in lung cancer was seen in a recent well designed case-control study of indoor radon, indicating that exposure to radon at the EPA action level is associated with a decrease of {approx}60% in lung cancer. A cumulative whole-body dose of {approx}1 Gy gamma rays is associated with a marked decrease in smoking-induced lung cancer in plutonium workers. Low dose, low LET radiation appears to increase apoptosis mediated removal of {alpha}-particle and cigarette smoke transformed pulmonary cells before they can develop into lung cancer.

  1. Prevention of cigarette smoke induced lung cancer by low let ionizing radiation

    International Nuclear Information System (INIS)

    Sanders, Charles L.

    2008-01-01

    Lung cancer is the most prevalent global cancer, ∼90% of which is caused by cigarette smoking. The LNT hypothesis has been inappropriately applied to estimate lung cancer risk due to ionizing radiation. A threshold of ∼1 Gy for lung cancer has been observed in never smokers. Lung cancer risk among nuclear workers, radiologists and diagnostically exposed patients was typically reduced by ∼40% following exposure to <100 mSv low LET radiation. The consistency and magnitude of reduced lung cancer in nuclear workers and occurrence of reduced lung cancer in exposed non-worker populations could not be explained by the HWE. Ecologic studies of indoor radon showed highly significant reductions in lung cancer risk. A similar reduction in lung cancer was seen in a recent well designed case-control study of indoor radon, indicating that exposure to radon at the EPA action level is associated with a decrease of ∼60% in lung cancer. A cumulative whole-body dose of ∼1 Gy gamma rays is associated with a marked decrease in smoking-induced lung cancer in plutonium workers. Low dose, low LET radiation appears to increase apoptosis mediated removal of α-particle and cigarette smoke transformed pulmonary cells before they can develop into lung cancer

  2. Does granulocyte colony-stimulating factor exacerbate radiation-induced acute lung injury in rats?

    International Nuclear Information System (INIS)

    Miura, Gouji; Awaya, Hitomi; Matsumoto, Tsuneo; Tanaka, Nobuyuki; Matsunaga, Naofumi

    2000-01-01

    Radiation pneumonitis (RP) frequently occurs as a complication of thoracic irradiation. However, the mechanism of RP is not well known. Activated neutrophils are a possible pathogenesis of RP. Neutrophil activation induced by granulocyte colony-stimulating factor (G-CSF) may exacerbate RP. We studied the effects of recombinant human G-CSF on acute lung injury induced by thoracic irradiation using rats. Animals were divided into three groups: sham irradiation with saline control, irradiation alone, and irradiation with G-CSF. Actual irradiation was given as a single fraction of 16 Gy delivered to the right hemithorax. G-CSF at a dose of 12 μg/body was administered subcutaneously once a day from 14 to 18 days after actual irradiation. Lung injury was evaluated 21 days after irradiation by bronchoalveolar lavage (BAL) fluid findings and the lung wet/dry weight (W/D) ratio. Neutrophil and lymphocyte counts in BAL fluid and the W/D ratio were significantly increased in the irradiation alone and the irradiation with G-CSF groups compared with those of the sham irradiation+saline control group. However, there was no significant difference observed between the irradiation alone and irradiation with G-CSF groups. In conclusion, this study suggests that postradiation administration of G-CSF does not exacerbate acute lung injury induced by thoracic irradiation in rats. (author)

  3. Does granulocyte colony-stimulating factor exacerbate radiation-induced acute lung injury in rats?

    Energy Technology Data Exchange (ETDEWEB)

    Miura, Gouji; Awaya, Hitomi; Matsumoto, Tsuneo; Tanaka, Nobuyuki; Matsunaga, Naofumi [Yamaguchi Univ., Ube (Japan). School of Medicine

    2000-08-01

    Radiation pneumonitis (RP) frequently occurs as a complication of thoracic irradiation. However, the mechanism of RP is not well known. Activated neutrophils are a possible pathogenesis of RP. Neutrophil activation induced by granulocyte colony-stimulating factor (G-CSF) may exacerbate RP. We studied the effects of recombinant human G-CSF on acute lung injury induced by thoracic irradiation using rats. Animals were divided into three groups: sham irradiation with saline control, irradiation alone, and irradiation with G-CSF. Actual irradiation was given as a single fraction of 16 Gy delivered to the right hemithorax. G-CSF at a dose of 12 {mu}g/body was administered subcutaneously once a day from 14 to 18 days after actual irradiation. Lung injury was evaluated 21 days after irradiation by bronchoalveolar lavage (BAL) fluid findings and the lung wet/dry weight (W/D) ratio. Neutrophil and lymphocyte counts in BAL fluid and the W/D ratio were significantly increased in the irradiation alone and the irradiation with G-CSF groups compared with those of the sham irradiation+saline control group. However, there was no significant difference observed between the irradiation alone and irradiation with G-CSF groups. In conclusion, this study suggests that postradiation administration of G-CSF does not exacerbate acute lung injury induced by thoracic irradiation in rats. (author)

  4. Quantification of the lung cancer risk from radon daughter exposure in dwellings - an epidemiological approach

    International Nuclear Information System (INIS)

    Edling, C.; Wingren, G.; Axelson, O.

    1986-01-01

    Some epidemiological studies have suggested a relationship between the concentration of decay products from radon, i.e., radon daughter exposure, in dwellings and lung cancer. Further experiences made from radon measurements have indicated that both building material and particularly the radioactivity in the ground is of importance for the leakage of radon into the houses. In Sweden, a survey is now ongoing in 15 municipalities with alum shale deposits, and in one area a case-referent evaluation has been made, considering building materials, ground conditions and smoking habits. The size of the study is small, but the results suggest that a risk is at hand and that there is a multiplicative effect from smoking and radon daughter exposure. About 30% of the lung cancers in the studied population might be attributable to elevated and potentially avoidable exposure to radon and radon daughters. (author)

  5. Radon: possible links with leukaemia and other non-lung cancers

    International Nuclear Information System (INIS)

    Henshaw, D.L.; Eatough, J.P.

    1993-01-01

    The evidence for possible links between domestic radon exposure and incidence of leukaemia and other non-lung cancers is reviewed. Recent calculations of the radon derived dose to red bone marrow suggests that if background radiation is linked to leukaemia in the general population then radon exposure may be a causative factor. Accordingly, statistically significant geographical correlations between domestic radon exposure and incidence of leukaemia have been observed in several data sets. In a preliminary study the level of hprt mutation in peripheral blood of individuals has been found to correlate with radon concentration in their homes. Geographical associations have also been observed between domestic radon exposure and certain other cancers. A model has been developed which predicts the possible carcinogenic effect of simultaneous exposure to alpha particles and gamma radiation and to radon and cigarette smoke, reflecting the nature of natural exposures. The model is used to suggest a mechanism for an antagonistic effect of radon and smoking at domestic levels but a synergistic effect at higher dose rates such as in uranium miners. (orig.)

  6. Effects of FTY720 on Lung Injury Induced by Hindlimb Ischemia Reperfusion in Rats

    Directory of Open Access Journals (Sweden)

    Liangrong Wang

    2017-01-01

    Full Text Available Background. Sphingosine-1-phosphate (S1P is a biologically active lysophospholipid mediator involved in modulating inflammatory process. We investigated the effects of FTY720, a structural analogue of S1P after phosphorylation, on lung injury induced by hindlimb ischemia reperfusion (IR in rats. Methods. Fifty Sprague-Dawley rats were divided into groups SM, IR, F3, F5, and F10. Group SM received sham operation, and bilateral hindlimb IR was established in group IR. The rats in groups F3, F5, and F10 were pretreated with 3, 5, and 10 mg/kg/d FTY720 for 7 days before IR. S1P lyase (S1PL, sphingosine kinase (SphK 1, and SphK2 mRNA expressions, wet/dry weight (W/D, and polymorphonuclear/alveolus (P/A in lung tissues were detected, and the lung injury score was evaluated. Results. W/D, P/A, and mRNA expressions of S1PL, SphK1, and SphK2 were higher in group IR than in group SM, while these were decreased in both groups F5 and F10 as compared to IR (p<0.05. The lung tissue presented severe lesions in group IR, which were attenuated in groups F5 and F10 with lower lung injury scores than in group IR (p<0.05. Conclusions. FTY720 pretreatment could attenuate lung injury induced by hindlimb IR by modulating S1P metabolism and decreasing pulmonary neutrophil infiltration.

  7. Residential radon exposure and lung cancer risk in Misasa, Japan. A case-control study

    International Nuclear Information System (INIS)

    Sobue, Tomotaka; Lee, Valerie S.; Ye, Weimin; Tanooka, Hiroshi; Mifune, Masaaki; Suyama, Akihiko; Koga, Taeko; Morishima, Hiroshige; Kondo, Sohei

    2000-01-01

    In order to investigate an association between residential radon exposure and risk of lung cancer, a case-control study was conducted in Misasa Town, Tottori Prefecture, Japan. The case series consisted of 28 people who had died of lung cancer in the years 1976-96 and 36 controls chosen randomly from the residents in 1976, matched by sex and year of birth. Individual residential radon concentrations were measured for 1 year with alpha track detectors. The average radon concentration was 46 Bq/m 3 for cases and 51 Bq/m 3 for controls. Compared to the level of 24 or less Bq/m 3 , the adjusted odds ratios of lung cancer associated with radon levels of 25-49, 50-99 and 100 or more Bq/m 3 , were 1.13 (95% confidence interval; 0.29-4.40), 1.23 (0.16-9.39) and 0.25 (0.03-2.33), respectively. None of the estimates showed statistical significance, due to small sample size. When the subjects were limited to only include residents of more than 30 years, the estimates did not change substantially. This study did not find that the risk pattern of lung cancer, possibly associated with residential radon exposure, in Misasa Town differed from patterns observed in other countries. (author)

  8. Multi-stratified multiple regression tests of the linear/no-threshold theory of radon-induced lung cancer

    International Nuclear Information System (INIS)

    Cohen, B.L.

    1992-01-01

    A plot of lung-cancer rates versus radon exposures in 965 US counties, or in all US states, has a strong negative slope, b, in sharp contrast to the strong positive slope predicted by linear/no-threshold theory. The discrepancy between these slopes exceeds 20 standard deviations (SD). Including smoking frequency in the analysis substantially improves fits to a linear relationship but has little effect on the discrepancy in b, because correlations between smoking frequency and radon levels are quite weak. Including 17 socioeconomic variables (SEV) in multiple regression analysis reduces the discrepancy to 15 SD. Data were divided into segments by stratifying on each SEV in turn, and on geography, and on both simultaneously, giving over 300 data sets to be analyzed individually, but negative slopes predominated. The slope is negative whether one considers only the most urban counties or only the most rural; only the richest or only the poorest; only the richest in the South Atlantic region or only the poorest in that region, etc., etc.,; and for all the strata in between. Since this is an ecological study, the well-known problems with ecological studies were investigated and found not to be applicable here. The open-quotes ecological fallacyclose quotes was shown not to apply in testing a linear/no-threshold theory, and the vulnerability to confounding is greatly reduced when confounding factors are only weakly correlated with radon levels, as is generally the case here. All confounding factors known to correlate with radon and with lung cancer were investigated quantitatively and found to have little effect on the discrepancy

  9. Radon and Lung Cancer Case-Control Study in Middle Ural

    International Nuclear Information System (INIS)

    Kirdin, I.A.; Lezhnin, V.L.; Yarmoshenko, I.V.; Ekidin, A.

    2001-01-01

    Full text: The pilot phase of radon and lung cancer case-control study has been performed in Karpinsk and Pervouralsk towns of Middle Ural region of Russia. The case group consists of 341 persons with lung cancer and living in that towns at least five previous years. The lung cancer diagnoses were carefully verified by instrumental techniques and 70% of its were morphologically validated. The persons for the control group (448) were chosen from the population living in that towns at least five years taking into account the age and sex. The special epidemiological questionnaire was developed which includes the items by the groups of factors as follow: clinical data, social factors, chronic lung diseases, life habit, tobacco smoking, alcohol drinking, diet preference etc. The epidemiological questionnaires were fulfilled for each member of case and control groups. Radon gas concentration and thoron equilibrium equivalent concentration measurements had been performed using nuclear track detectors and grab sampling accordingly in the dwellings of case and control groups members. By preliminary estimation the odds ratios are 1, 0.91, 1.2, 1.1 in the ranges of radon and thoron equilibrium equivalent concentration 0-6, 3-13, 13-36 and 36-370 Bq/m 3 respectively. The deeper and more rigorous analysis as well as different independent approaches will be discussed in the paper.(author)

  10. Lung cancer incidence after smoking and exposure to radon using a two-mutation model

    International Nuclear Information System (INIS)

    Leenhouts, H.P.

    1997-01-01

    A study to analyze lung cancer in humans as a function of exposure to radon and smoking, used three types of data: population statistics in non-smokers habits of British radiologists and radon exposure of the Colorado uranium miners. Using a simplified two-mutation carcinogenesis model and only six unknown variables yielded a coherent description of lung cancer dependence on exposure to radon and smoking. For risk estimates the radiation effect of radon can be concluded to be highly dependent on smoking habits, e.g. the radiation effect differs (in absolute terms) by a factor of about 7 between non-smokers, but the relative risk is much higher in non-smokers than in smokers. The results to data justify a thorough investigation of the analysis method to realize improved radon risk estimates. (author)

  11. Lung cancer incidence after smoking and exposure to radon using a two-mutation model

    Energy Technology Data Exchange (ETDEWEB)

    Leenhouts, H.P. [RIVM, Bilthoven (Netherlands)

    1997-03-01

    A study to analyze lung cancer in humans as a function of exposure to radon and smoking, used three types of data: population statistics in non-smokers habits of British radiologists and radon exposure of the Colorado uranium miners. Using a simplified two-mutation carcinogenesis model and only six unknown variables yielded a coherent description of lung cancer dependence on exposure to radon and smoking. For risk estimates the radiation effect of radon can be concluded to be highly dependent on smoking habits, e.g. the radiation effect differs (in absolute terms) by a factor of about 7 between non-smokers, but the relative risk is much higher in non-smokers than in smokers. The results to data justify a thorough investigation of the analysis method to realize improved radon risk estimates. (author)

  12. Shelter and indoor air in the twenty-first century: Radon, smoking and lung cancer risks

    International Nuclear Information System (INIS)

    Fabrikant, J.I.

    1988-04-01

    This document describes the relationship between indoor radon exposure, cigarette smoking, and lung cancer. The author explains the sources of radon, the tissues at risk, the human populations most likely to be affected, and the estimates of lung cancer in the population. 6 refs., 2 tabs

  13. Ethanolic Extract of Marsdenia condurango Ameliorates Benzo[a]pyrene-induced Lung Cancer of Rats

    Directory of Open Access Journals (Sweden)

    Sikdar Sourav

    2014-06-01

    Full Text Available Objectives:Condurango is widely used in various systems of complementary and alternative medicines (CAM against oesophageal and stomach ailments including certain types of cancer. However, until now no systematic study has been conducted to verify its efficacy and dose with proper experimental support. Therefore, we examined if ethanolic extract of Condurango could ameliorate benzo[a]pyrene (BaP-induced lung cancer in rats, in vivo to validate its use as traditional medicine. Methods:Fifteen male and 15 female Sprague-Dawley (SD rats were treated with 0.28 mg/kg of Sweet Bee Venom (SBV (high-dosage group and the same numbers of male and female SD rats were treated with 0.2 mL/kg of normal saline (control group for 13 weeks. We selected five male and five female SD rats from the high-dosage group and the same numbers of male and female SD rats from the control group, and we observed these rats for four weeks. We conducted body-weight measurements, ophthalmic examinations, urinalyses and hematology, biochemistry, histology tests. Results:A histological study revealed gradual progress in lung tissue-repair activity in Condurango-fed cancer-bearing rats, showing gradual tissue recovery after three months of drug administration. Condurango has the capacity to generate reactive oxygen species (ROS, which may contribute to a reduction in anti-oxidative activity and to an induction of oxidative stress-mediated cancer cell-death. Condurango-activated pro-apoptotic genes (Bax, caspase-3, caspase-9, p53, cytochrome-c, apaf-1, ICAD and PARP and down-regulated antiapoptotic-Bcl-2 expression were noted both at mRNA and protein levels. Studies on caspase-3 activation and PARP cleavage by western blot analysis revealed that Condurango induced apoptosis through a caspase-3-dependent pathway. Conclusion:The anticancer efficacy of an ethanolic extract of Condurango for treating BaP-induced lung cancer in rats lends support for its use in various traditional

  14. Methanolic extract of Moringa oleifera leaf and low doses of gamma radiation alleviated amiodarone-induced lung toxicity in albino rats

    Directory of Open Access Journals (Sweden)

    Hasan Hesham F.

    2016-01-01

    Full Text Available This study aimed to evaluate the effects of methanolic extract of Moringa oleifera (MO and/or low doses of gamma radiation (LDR on amiodarone (AMD-induced lung toxicity in rats. AMD administered to female albino rats (100 mg/kg body weight for 10 consecutive days. Rats received methanolic extract of MO (250 mg/kg bwt for 15 successive days and/or were exposed to whole body LDR (0.25Gy on the 1st and 10th days, up to a total dose of 0.5Gy. MO administration induced a significant decrease in serum tumor necrosis factor-alpha (TNF-α and transforming growth factor-beta (TGF-β levels as well as lactate dehydrogenase (LDH activity. Also, the content of malondialdehyde (MDA and hydroxyproline (HYP was significantly decreased in lung tissue. Furthermore, MO significantly increased reduced glutathione (GSH content in lung tissue as compared with AMD. The histopathological investigation of lung tissue revealed the appearance of interstitial pneumonia in rats treated with AMD. The oral administration of MO and/or exposure to LDR reversed the biochemical and histopathological alterations induced by AMD. It can be posited that MO and LDR might have a considerable role in the prevention of lung toxicity induced by AMD.

  15. High-LET alpha-emitters: Radon, lung cancer and smoking

    International Nuclear Information System (INIS)

    Fabrikant, J.I.

    1988-11-01

    The National Academy of Sciences BEIR IV Report deals with the health effects in human populations exposed to internally-deposited alpha-emitting radionuclides and their decay products. Quantitative risk estimates for cancer induction are derived, mainly from analyses of epidemiological data. The Report addresses the health outcomes of exposure to radon and its daughters, primarily lung cancer risks of worker exposure to radon progeny in underground mines and in the general public in indoor domestic environments. An excess relative risk model of lung cancer mortality and exposure to radon progeny is developed; this models the excess risk per Working Level Month in terms of time intervals prior to an attained age, and is dependent on time-since-exposure and age at risk. Risk projections are presented and cover exposure situations of current public health concern. For example, lifetime exposure to 1 WLM y/sup /minus/1/ is estimated to increase the number of deaths due to lung cancer by a factor of about 1.5 over the current rate for both males and females in a population having the current prevalence of cigarette-smoking. Occupational exposure to 4 WLM y/sup /minus/1/ from ages 20 y to 40 y is projected to increase lung cancer deaths by a factor of 1.6 over the current rate of this age cohort in the general population. In all of these cases, most of the increased risk occurs to smokers for whom the risk is up to ten times greater than for non-smokers. 8 refs., 1 tab

  16. Exercise training attenuated chronic cigarette smoking-induced up-regulation of FIZZ1/RELMα in lung of rats.

    Science.gov (United States)

    Ma, Wan-li; Cai, Peng-cheng; Xiong, Xian-zhi; Ye, Hong

    2013-02-01

    FIZZ/RELM is a new gene family named "found in inflammatory zone" (FIZZ) or "resistin-like molecule" (RELM). FIZZ1/RELMα is specifically expressed in lung tissue and associated with pulmonary inflammation. Chronic cigarette smoking up-regulates FIZZ1/RELMα expression in rat lung tissues, the mechanism of which is related to cigarette smoking-induced airway hyperresponsiveness. To investigate the effect of exercise training on chronic cigarette smoking-induced airway hyperresponsiveness and up-regulation of FIZZ1/RELMα, rat chronic cigarette smoking model was established. The rats were treated with regular exercise training and their airway responsiveness was measured. Hematoxylin and eosin (HE) staining, immunohistochemistry and in situ hybridization of lung tissues were performed to detect the expression of FIZZ1/RELMα. Results revealed that proper exercise training decreased airway hyperresponsiveness and pulmonary inflammation in rat chronic cigarette smoking model. Cigarette smoking increased the mRNA and protein levels of FIZZ1/RELMα, which were reversed by the proper exercise. It is concluded that proper exercise training prevents up-regulation of FIZZ1/RELMα induced by cigarette smoking, which may be involved in the mechanism of proper exercise training modulating airway hyperresponsiveness.

  17. Protective Effects of Erythropoietin and N-Acetylcysteine on Methotrexate-Induced Lung Injury in Rats

    Directory of Open Access Journals (Sweden)

    Hasan Kahraman

    2013-03-01

    Full Text Available Objective: Methotrexate (MTX is known to have deleterious side effects on lung tissue. We aimed to investigate the effects of erythropoietin (EPO and N-acetyl-cysteine (NAC on MTX-induced lung injury in rats. Study Design: Animal experiment. Material and Methods: Twenty-six female Sprague-Dawley rats were divided into 4 groups. Sham group, 0.3 mL saline; MTX group, 5 mg/kg MTX; EPO group, 5mg/kg MTX and 2000 IU/kg EPO; NAC group, 5 mg/kg MTX and 200 mg/kg NAC were administered once daily for 4 consecutive days. Malondialdehyde (MDA, superoxide dismutase (SOD, catalase (CAT and inflammation and congestion scores in lung tissues were evaluated. Results: In MTX group MDA were significantly higher, CAT and SOD were significantly lower than in sham, EPO and NAC groups (p0.005. In group MTX both scores were significantly higher than in sham (p<0.005. The congestion score of group MTX was significantly higher than those of group EPO and NAC (p<0.005. Conclusion: EPO and NAC have significant preventive effects on MTX-induced lung injury in rats. Decreased antioxidant capacity and increased MDA level may cause the oxidative damage in MTX group. Also, higher antioxidant capacity and lower MDA level may be a response to oxidative stress in EPO and NAC groups.

  18. Quantitative aspects of radon daughter exposure and lung cancer in underground miners

    International Nuclear Information System (INIS)

    Edling, C.; Axelson, O.

    1983-01-01

    Epidemiological studies have shown an excessive incidence of lung cancer in miners with exposure to radon daughters. The various risk estimates have ranged from six to 47 excess cases per 10 6 person years and working level month, but the effect of smoking has not been fully evaluated. A group of iron ore miners was studied in an attempt to obtain quantitative information about the risk of lung cancer due to radon and its daughters among smoking and non-smoking miners. The results show a considerable risk for miners to develop lung cancer; even non-smoking miners seem to be at a rather high risk. An additive effect of smoking and exposure to radon daughters is indicated and an estimate of about 30-40 excess cases per 10 6 person years and working level month seems to apply on a life time basis to both smoking and non-smoking miners aged over 50. (author)

  19. Calculation of lung cancer incidence in the Netherlands by smoking and radon exposure. Implications for the effect of radon; Berekening van de longkankerincidentie in Nederland door roken en blootstelling aan radon. Implicaties voor het effect van radon

    Energy Technology Data Exchange (ETDEWEB)

    Leenhouts, H.P.; Brugmans, J.P. [Laboratorium voor Stralingsonderzoek, Rijksinstituut voor Volksgezondheid en Milieu RIVM, Bilthoven (Netherlands)

    2001-09-01

    Although the main cause of lung cancer is smoking cigarettes, part of the cases are subscribed to radon exposure, in particular {alpha}-radiation from daughter products. However, the relation between lung cancer and radon exposure is rather insecure. Based on international reports (e.g. BEIR VI) and extrapolation of lung cancer incidence in uranium mine workers to the population of the USA and subsequently to the Netherlands, the number of lung cancer cases in the Netherlands is estimated to be circa 800 per year, varying between 200-2000. Results of the analysis are summarized in this article. 10 refs.

  20. Effect of ozone oxidative preconditioning in preventing early radiation-induced lung injury in rats

    Energy Technology Data Exchange (ETDEWEB)

    Bakkal, B.H. [Department of Radiation Oncology, School of Medicine, Bulent Ecevit University, Kozlu, Zonguldak (Turkey); Gultekin, F.A. [Department of General Surgery, School of Medicine, Bulent Ecevit University, Kozlu, Zonguldak (Turkey); Guven, B. [Department of Biochemistry, School of Medicine, Bulent Ecevit University, Kozlu, Zonguldak (Turkey); Turkcu, U.O. [Mugla School of Health Sciences, Mugla Sitki Kocman University, Mugla (Turkey); Bektas, S. [Department of Pathology, School of Medicine, Bulent Ecevit University, Kozlu, Zonguldak (Turkey); Can, M. [Department of Biochemistry, School of Medicine, Bulent Ecevit University, Kozlu, Zonguldak (Turkey)

    2013-09-27

    Ionizing radiation causes its biological effects mainly through oxidative damage induced by reactive oxygen species. Previous studies showed that ozone oxidative preconditioning attenuated pathophysiological events mediated by reactive oxygen species. As inhalation of ozone induces lung injury, the aim of this study was to examine whether ozone oxidative preconditioning potentiates or attenuates the effects of irradiation on the lung. Rats were subjected to total body irradiation, with or without treatment with ozone oxidative preconditioning (0.72 mg/kg). Serum proinflammatory cytokine levels, oxidative damage markers, and histopathological analysis were compared at 6 and 72 h after total body irradiation. Irradiation significantly increased lung malondialdehyde levels as an end-product of lipoperoxidation. Irradiation also significantly decreased lung superoxide dismutase activity, which is an indicator of the generation of oxidative stress and an early protective response to oxidative damage. Ozone oxidative preconditioning plus irradiation significantly decreased malondialdehyde levels and increased the activity of superoxide dismutase, which might indicate protection of the lung from radiation-induced lung injury. Serum tumor necrosis factor alpha and interleukin-1 beta levels, which increased significantly following total body irradiation, were decreased with ozone oxidative preconditioning. Moreover, ozone oxidative preconditioning was able to ameliorate radiation-induced lung injury assessed by histopathological evaluation. In conclusion, ozone oxidative preconditioning, repeated low-dose intraperitoneal administration of ozone, did not exacerbate radiation-induced lung injury, and, on the contrary, it provided protection against radiation-induced lung damage.

  1. Effect of ozone oxidative preconditioning in preventing early radiation-induced lung injury in rats

    International Nuclear Information System (INIS)

    Bakkal, B.H.; Gultekin, F.A.; Guven, B.; Turkcu, U.O.; Bektas, S.; Can, M.

    2013-01-01

    Ionizing radiation causes its biological effects mainly through oxidative damage induced by reactive oxygen species. Previous studies showed that ozone oxidative preconditioning attenuated pathophysiological events mediated by reactive oxygen species. As inhalation of ozone induces lung injury, the aim of this study was to examine whether ozone oxidative preconditioning potentiates or attenuates the effects of irradiation on the lung. Rats were subjected to total body irradiation, with or without treatment with ozone oxidative preconditioning (0.72 mg/kg). Serum proinflammatory cytokine levels, oxidative damage markers, and histopathological analysis were compared at 6 and 72 h after total body irradiation. Irradiation significantly increased lung malondialdehyde levels as an end-product of lipoperoxidation. Irradiation also significantly decreased lung superoxide dismutase activity, which is an indicator of the generation of oxidative stress and an early protective response to oxidative damage. Ozone oxidative preconditioning plus irradiation significantly decreased malondialdehyde levels and increased the activity of superoxide dismutase, which might indicate protection of the lung from radiation-induced lung injury. Serum tumor necrosis factor alpha and interleukin-1 beta levels, which increased significantly following total body irradiation, were decreased with ozone oxidative preconditioning. Moreover, ozone oxidative preconditioning was able to ameliorate radiation-induced lung injury assessed by histopathological evaluation. In conclusion, ozone oxidative preconditioning, repeated low-dose intraperitoneal administration of ozone, did not exacerbate radiation-induced lung injury, and, on the contrary, it provided protection against radiation-induced lung damage

  2. Design issues in studies of radon and lung cancer: Implications of the joint effect of smoking and radon

    International Nuclear Information System (INIS)

    Upfal, M.; Divine, G.; Siemiatycki, J.

    1995-01-01

    Many case-control studies have been undertaken to assess whether and to what extent residential radon exposure is a risk factor for lung cancer. Nearly all these studies have been conducted in populations including smokers and nonsmokers. In this paper, we show that, depending on the nature of the joint effect of radon and tobacco on lung cancer risk, it may be very difficult to detect a main effect due to radon in mixed smoking and nonsmoking populations. If the joint effect is closer to additive than multiplicative, the most cost-effective way to achieve adequate statistical power may be to conduct a study among never-smokers. Because the underlying joint effect is unknown, and because many studies have been carried out among mixed smoker and nonsmoker populations, it would be desirable to conduct some studies with adequate power among never-smokers only. 30 refs., 4 figs., 2 tabs

  3. Assessment of radon-induced health risk for occupants of a house built on uranium ore residue

    International Nuclear Information System (INIS)

    Clero, E.; Marie, L.; Challeton-De Vathaire, C.; Laurier, D.; Rannou, A.

    2016-01-01

    At the request of French public authorities, the Institute of Radiological Protection and Nuclear Safety has assessed the radiological situation of a house built on uranium ore residues in Haute-Vienne and the health risks induced from exposure to radon for all occupants. Classified as a lung carcinogen by the World Health Organization, radon is a proven cause of lung cancer in case of regular inhalation over a long period, and the risk increases with cumulative exposure. Radon exposure was reconstructed for various standard profiles of house occupancy. A risk model derived from a European epidemiological study was used to calculate the lifetime probability of death from lung cancer according to these standard profiles. Risk assessment of the occupants of the house highlighted the following main findings. For a resident school child having been exposed to radon from birth to the age of 7, the lifetime relative risk (LRR) was estimated at 5. For last adult and young adult residents having lived more than 10 years in the house, the probability of death from lung cancer was in the same order of magnitude as that of a regular cigarette smoker, with a LRR from 10 to 13 and a lifetime probability of death from lung cancer between 3 and 4%. If these individuals smoked regularly, in addition to being exposed to radon, this probability would be between 6 and 32% (supposing an additive or multiplicative interaction). For former occupants (non-smokers) having been exposed 10 years during childhood, the LRR was two-fold lower. For children having been in day care in the house, the increased probability of death from lung cancer was low, with a LRR lower than 2. Supposing, as in adults, that the risk decreases beyond 30 years after the end of radon exposure, the increase was almost zero for former occupants exposed during childhood and during day care, with a LRR close to 1. (authors)

  4. Quantitative evaluation of the lung cancer deaths attributable to residential radon: A simple method and results for all the 21 Italian Regions

    International Nuclear Information System (INIS)

    Bochicchio, F.; Antignani, S.; Venoso, G.; Forastiere, F.

    2013-01-01

    Pooled analyses of epidemiological case-control studies on lung cancer and residential radon have shown that radon exposure in dwellings increases lung cancer risk, and that the increase is statistically significant also for prolonged exposures to low-medium level of radon concentration, i.e. levels commonly found in many dwellings. In this paper, a simple method to evaluate the health burden due to the presence of radon in homes (i.e. the number of lung cancer deaths attributable to radon exposure in dwellings) was presented. This method is based on the following parameters: i) the excess relative risk per unit of exposure evaluated in case-control studies; ii) the average radon concentration that can be considered representative of population exposure in dwellings; iii) the total number of lung cancer deaths occurring each year. Moreover, the interaction between radon and cigarette smoking is needed to be taken into account: in fact, although most of the persons are non-smokers, most of the lung cancer deaths attributed to radon are actually due to the multiplicative effect of radon and cigarette smoking. To show this effect, the number of radon related lung cancer deaths estimated to occur among current, former and never smokers was calculated separately for males and females, taking into account the relative risk of lung cancer for the different smoking categories and the prevalence of smoking habits. The methodology described in this work was applied to all the 21 Italian Regions in order to illustrate it. The overall fraction of lung cancer deaths attributable to radon in Italy is about 10%, with values in individual Regions ranging from 4% to 16%. The greater part of the lung cancers attributable to radon is estimated to occur among current smokers for both males and females (72% and 60%, respectively, at national level). This is due to the synergistic effects of radon and cigarette smoking, which should therefore be taken into account in policies aimed to

  5. Radon and risk of cancer

    International Nuclear Information System (INIS)

    Rootwelt, K.

    1988-01-01

    The article reviews present knowledge on the possible detriment to health of radon in homes. It is concluded that inducement of lung cancer has neither been proved nor disproved. Large-scale epidemiological studies are in progress. Until the results of these studies have been reported, frightening anti-radon propaganda should be discouraged

  6. Pathological studies on carcinoma of the lung in rats induced by external x-ray irradiation

    International Nuclear Information System (INIS)

    Kodama, Tetsuro

    1978-01-01

    Lung tumors in Wistar rats were induced by administration of various doses of external irradiation through the anterior chest wall. Pulmonary fibrosis following external irradiation was observed in 13 of 17 rats (76.4%) in Group I (800R/day for 5 days), in 26 of 36 rats (78.8%) in Group II (800R/WK for 5 WKs), and in 6 of 18 rats (35.3%) in Group III (500R/WK for 4 WKs). The degree of pulmonary fibrosis was greater each time in the rats given 4,000R than in the rats given 2,000R. In Groups I and II 5 pulmonary tumors (2 squamous cell carcinomas, 1 adenocarcinoma, and 2 adenomas) were observed in 3 of 16 rats (17.6%), and 10 pulmonary tumors (4 squamous cell carcinomas, 1 adenocarcinoma, 4 adenomas, and 1 fibrosarcoma) were observed in 9 of 33 rats (24.2%), respectively. In Group III only 1 case of pulmonary adenoma was observed among 17 rats (6.8%). The first case of epithelial tumor of the lung was found in a rat in Group I. Histological findings during the course of the experiment revealed that the earliest changes following irradiation were those of radiation pneuminitis, characterized by engorged capillaries and edema in collapsed alveoli, with lymphocytic and plasma cell infiltrations. In addition, the nuclei of the lining cells of the alveoli and bronchioles were enlarged and atypical. From the 10th through the 20th experimental week, fibrosis of the alveolar septum and adenomatous hyperplasia of the alveolar lining became extensive, particularly in the bronchiolo-alveolar areas of the periphery of the lung. Atypical adenomatous hyperplasia occurred within the fibrotic lesion or in proximity to it. It was frequently followed by carcinoma, suggesting that carcinoma in the present experiment arose in atypical epithelium, induced by irradiation of the bronchiolo-alveolar epithelial lining

  7. Pathological studies on carcinoma of the lung in rats induced by external x-ray irradiation

    Energy Technology Data Exchange (ETDEWEB)

    Kodama, T [Hiroshima Univ. (Japan). School of Medicine

    1978-08-01

    Lung tumors in Wistar rats were induced by administration of various doses of external irradiation through the anterior chest wall. Pulmonary fibrosis following external irradiation was observed in 13 of 17 rats (76.4%) in Group I (800R/day for 5 days), in 26 of 36 rats (78.8%) in Group II (800R/WK for 5 WKs), and in 6 of 18 rats (35.3%) in Group III (500R/WK for 4 WKs). The degree of pulmonary fibrosis was greater each time in the rats given 4,000R than in the rats given 2,000R. In Groups I and II 5 pulmonary tumors (2 squamous cell carcinomas, 1 adenocarcinoma, and 2 adenomas) were observed in 3 of 16 rats (17.6%), and 10 pulmonary tumors (4 squamous cell carcinomas, 1 adenocarcinoma, 4 adenomas, and 1 fibrosarcoma) were observed in 9 of 33 rats (24.2%), respectively. In Group III only 1 case of pulmonary adenoma was observed among 17 rats (6.8%). The first case of epithelial tumor of the lung was found in a rat in Group I. Histological findings during the course of the experiment revealed that the earliest changes following irradiation were those of radiation pneuminitis, characterized by engorged capillaries and edema in collapsed alveoli, with lymphocytic and plasma cell infiltrations. In addition, the nuclei of the lining cells of the alveoli and bronchioles were enlarged and atypical. From the 10th through the 20th experimental week, fibrosis of the alveolar septum and adenomatous hyperplasia of the alveolar lining became extensive, particularly in the bronchiolo-alveolar areas of the periphery of the lung. Atypical adenomatous hyperplasia occurred within the fibrotic lesion or in proximity to it. It was frequently followed by carcinoma, suggesting that carcinoma in the present experiment arose in atypical epithelium, induced by irradiation of the bronchiolo-alveolar epithelial lining.

  8. Study of epidemiological risk of lung cancer in Mexico due indoor radon exposure

    Science.gov (United States)

    Ángeles, A.; Espinosa, G.

    2014-07-01

    In this work the lifetime relative risks (LRR) of lung cancer due to exposure to indoor 222Rn on the Mexican population is calculated. Cigarette smoking is the number one risk factor for lung cancer (LC), because that, to calculate the number of cases of LC due to exposure to 222Rn is necessary considers the number of cases of LC for smoking cigarette. The lung cancer mortality rates published by the "Secretaría de Salud" (SSA), the mexican population data published by the "Consejo Nacional de Población" (CONAPO), smoking data in the mexican population, published by the "Comisión Nacional Contra las Adicciones" (CONADIC), the "Organización Panamericana de la Salud" (OPS) and indoor 222Rn concentrations in Mexico published in several recent studies are used. To calculate the lifetime relative risks (LRR) for different segments of the Mexican population, firstly the Excess Relative Risk (ERR) is calculated using the method developed by the BEIR VI committee and subsequently modified by the USEPA and published in the report "EPA Assessment of Risks from Radon in Homes". The excess relative risks were then used to calculate the corresponding lifetime relative risks, again using the method developed by the BEIR VI committee. The lifetime relative risks for Mexican male and female eversmokers and Mexican male and female never-smokers were calculated for radon concentrations spanning the range found in recent studies of indoor radon concentrations in Mexico. The lifetime relative risks of lung cancer induced by lifetime exposure to the mexican average indoor radon concentration were estimated to be 1.44 and 1.40 for never-smokers mexican females and males respectively, and 1.19 and 1.17 for ever-smokers Mexican females and males respectively. The Mexican population LRR values obtained in relation to the USA and Canada LRR published values in ever-smokers for both gender are similar with differences less than 4%, in case of never-smokers in relation with Canada

  9. Radon in homes and risk of lung cancer: 13 collaborative analyses of individual data from European case-control studies

    International Nuclear Information System (INIS)

    Darby, S.; Hill, D.; Doll, R.; Auvinen, A.; Barros Dios, J.M.; Ruano Ravina, A.; Baysson, H.; Tirmarche, M.; Bochicchio, F.; Deo, H.; Falk, R.; Forastiere, F.; Hakama, M.; Heid, I.; Schaffrath Rosario, A.; Wichmann, H.E.; Kreienbrock, L.; Kreuzer, M.; Lagarde, F.; Pershagen, G.; Makelainen, I.; Ruosteenoja, E.; Muirhead, C.; Oberaigner, W.; TomaBek, L.; Whitley, E.

    2007-01-01

    Objective: To determine the risk of lung cancer associated with exposure at home to the radioactive disintegration products of naturally occurring radon gas. Design: Collaborative analysis of individual data from 13 case-control studies of residential radon and lung cancer. Setting: Nine European countries. Subjects: 7148 cases of lung cancer and 14 208 controls. Main outcome measures: Relative risks of lung cancer and radon gas concentrations in homes inhabited during the previous 5-34 years measured in becquerels (radon disintegrations per second) per cubic metre (Bq/m3) of household air. Results: The mean measured radon concentration in homes of people in the control group was 97 Bq/m3, with 11% measuring > 200 and 4% measuring > 400 Bq/m3. For cases of lung cancer the mean concentration was 104 Bq/m3. The risk of lung cancer increased by 8.4% (95% confidence interval 3.0% to 15.8%) per 100 Bq/m3 increase in measured radon (P=0.0007). This corresponds to an increase of 16% (5% to 31%) per 100 Bq/m3 increase in usual radon- that is, after correction for the dilution caused by random uncertainties in measuring radon concentrations. The dose-response relation seemed to be linear with no threshold and remained significant (P = 0.04) in analyses limited to individuals from homes with measured radon < 200 Bq/m3. The proportionate excess risk did not differ significantly with study, age, sex, or smoking. In the absence of other causes of death, the absolute risks of lung cancer by age 75 years at usual radon concentrations of 0, 100, and 400 Bq/m3 would be about 0.4%, 0.5%, and 0.7%, respectively, for lifelong non-smokers, and about 25 times greater (10%, 12%, and 16%) for cigarette smokers. Conclusions: Collectively, though not separately, these studies show appreciable hazards from residential radon, particularly for smokers and recent ex-smokers, and indicate that it is responsible for about 2% of all deaths from cancer in Europe. (author)

  10. Models for comparing lung-cancer risks in radon- and plutonium-exposed experimental animals

    International Nuclear Information System (INIS)

    Gilbert, E.S.; Cross, F.T.; Sanders, C.L.; Dagle, G.E.

    1990-10-01

    Epidemiologic studies of radon-exposed underground miners have provided the primary basis for estimating human lung-cancer risks resulting from radon exposure. These studies are sometimes used to estimate lung-cancer risks resulting from exposure to other alpha- emitters as well. The latter use, often referred to as the dosimetric approach, is based on the assumption that a specified dose to the lung produces the same lung-tumor risk regardless of the substance producing the dose. At Pacific Northwest Laboratory, experiments have been conducted in which laboratory rodents have been given inhalation exposures to radon and to plutonium ( 239 PuO 2 ). These experiments offer a unique opportunity to compare risks, and thus to investigate the validity of the dosimetric approach. This comparison is made most effectively by modeling the age-specific risk as a function of dose in a way that is comparable to analyses of human data. Such modeling requires assumptions about whether tumors are the cause of death or whether they are found incidental to death from other causes. Results based on the assumption that tumors are fatal indicate that the radon and plutonium dose-response curves differ, with a linear function providing a good description of the radon data, and a pure quadratic function providing a good description of the plutonium data. However, results based on the assumption that tumors are incidental to death indicate that the dose-response curves for the two exposures are very similar, and thus support the dosimetric approach. 14 refs., 2 figs., 6 tabs

  11. Lower radiation weighting factor for radon indicated in mechanistic modelling of human lung cancer

    International Nuclear Information System (INIS)

    Brugmans, M.J.P.; Leenhouts, H.P.

    2002-01-01

    A two-mutation carcinogenesis (TMC) model was fitted to the age-dependent lung cancer incidence in a cohort of Dutch Hodgkin patients treated with radiotherapy. Employing the results of previous TMC analyses of lung cancer due to smoking (by British doctors) and due to exposure to radon (for Colorado miners) a model fit was obtained with an estimate for the low LET radiation effect at the cellular level. This allows risk calculations for lung cancer from low LET radiation. The excess absolute risks are in tune with the values reported in the literature, the excess relative risks differ among the exposed groups. Comparing the cellular radiation coefficients for radon and for low LET radiation leads to an estimated radiation weighting factor for radon of 3 (0.1-6). (author)

  12. Bio-mathematical models for radon daughters inhalation. The ModeLung software

    International Nuclear Information System (INIS)

    Tomulescu, Vlad C.; Rusu, Mircea

    2002-01-01

    Radon and its decay daughters are the most important sources for natural irradiation of population. ModeLung software is based on the human respiratory tract compartment model and is computing radiation doses on several internal organs and tissues for subjects inhaling radon daughters attached to aerosols. Radiation doses are presented for several subjects performing different types of activity under specific environmental conditions. (authors)

  13. Mineral dusts and radon in uranium mines

    International Nuclear Information System (INIS)

    Abelson, P.H.

    1991-01-01

    The Environmental Protection Agency (EPA) continues to assert that radon is a major cause of lung cancer in this country. EPA is fostering a radon program that could entail huge financial and emotional costs while yielding negligible benefits to public health. Justification for the program was the occurrence of lung cancer in men exposed to huge amounts of radon, mineral dusts, and other lung irritants in uranium mines on the Colorado Plateau. Lung cancer has been reported in about 356 cigarette smokers and in about 25 nonsmokers. During the era of high radon levels, monitoring was sporadic. Conditions in only a small fraction of the mines were measured, and that on a few separate occasions. Later, cumulative exposure to radon was calculated on the basis of measurements involving only a tiny fraction of the miners. Some were exposed to more than 15,000 pCi/liter of radon and its products. The level in the average home is about 1.5 pCi/liter. In making extrapolations from mine to home, the assumption is made that residents are in their dwellings most of the time and that miners spend only 170 hours a month in the mine. Two major questionable assumptions are involved in extrapolations from high doses of radon in the mines to low doses in homes. One is that no threshold is involved; that is, that humans have no remediation mechanism for α particle damages. There is evidence to the contrary. The most unrealistic assumption is that heavy exposure to silica has no effect on inducing lung cancer. Many studies have shown that silica dust causes lung cancer in animals. Exposure of human culture cells to silica has resulted in formation of neoplastic tissue. EPA has no solid evidence that exposures to 4 pCi/liter of radon causes lung cancer in either smokers or nonsmokers. Indeed, there is abundant evidence to the contrary in the fact that in states with high levels of radon, inhabitants have less lung cancer than those in states with low levels

  14. Relation of radon exposure and tobacco use to lung cancer among tin miners in Yunnan Province, China

    International Nuclear Information System (INIS)

    Qiao, Y.L.; Taylor, P.R.; Yao, S.X.; Schatzkin, A.; Mao, B.L.; Lubin, J.; Rao, J.Y.; McAdams, M.; Xuan, X.Z.; Li, J.Y.

    1989-01-01

    We studied the relation of radon exposure and tobacco use to lung cancer among tin miners in Yunnan Province in the People's Republic of China. Interviews were conducted in 1985 with 107 living tin miners with lung cancer and an equal number of age-matched controls from among tin miners without lung cancer to obtain information on lung cancer risk factors including a detailed history of employment and tobacco use. Occupational history was combined with extensive industrial hygiene data to estimate cumulative working level months (WLM) of radon daughter exposure. Similar data were also used to estimate arsenic exposure for control in the analysis. Results indicate an increased risk of lung cancer for water pipe smoking, a traditional form of tobacco use practiced in 91% of cases and 85% of controls. The use of water pipes was associated with a twofold elevation in risk when compared with tobacco abstainers, and a dose-response relation was observed with increasing categories of pipe-year (dose times duration) usage. Estimated WLM of radon exposure varied from 0 to 1,761 among subjects but averaged 515 in cases versus only 244 in controls. Analyses indicated that the persons in the highest quarter of the radon exposure distribution had an odds ratio (OR) = 9.5 (95% confidence interval = 2.7-33.1) compared to persons without radon exposure after controlling for arsenic exposure and other potential confounders. Examination of duration and rate of radon exposure indicated higher risk associated with long duration as opposed to high rate of exposure. Cross-categorizations of radon exposure and tobacco use suggest greater risk associated with radon exposure than tobacco in these workers

  15. Risk of radiation-induced pneumonitis after helical and static-port tomotherapy in lung cancer patients and experimental rats

    International Nuclear Information System (INIS)

    Zhang, Xianglan; Shin, You Keun; Zheng, Zhenlong; Zhu, Lianhua; Lee, Ik Jae

    2015-01-01

    Radiotherapy (RT) is one of the major non-operative treatment modalities for treating lung cancer. Tomotherapy is an advanced type of intensity-modulated radiotherapy (IMRT) in which radiation may be delivered in a helical fashion. However, unexpected pneumonitis may occur in patients treated with tomotherapy, especially in combination with chemotherapy, as a result of extensive low-dose radiation of large lung volumes. The aim of our study was to investigate the risk of radiation-induced pneumonitis after helical-mode and static-mode tomotherapy in patients with lung cancer and in an animal model. A total of 63 patients with primary lung cancer who were treated with static or helical tomotherapy with or without concurrent chemoradiotherapy (CCRT) were analyzed. Additionally, rats with radiation-induced pulmonary toxicity, which was induced by the application of helical or static tomography with or without CCRT, were evaluated. Helical-mode tomotherapy resulted in a significantly higher rate of late radiation pneumonitis in lung cancer patients than static-mode tomotherapy when evaluated by the Radiation Therapy Oncology Group (RTOG) and National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE) scoring system. In the animal model, helical tomotherapy alone induced significantly higher expression of interleukin (IL)-1α, IL-1β, IL-6, and transforming growth factor (TGF)-β in lung specimens, especially on the untreated side, compared to static tomotherapy alone. Additionally, rats treated with helical tomotherapy and CCRT demonstrated significantly higher expression of inflammatory cytokines compared to those treated with static tomotherapy and CCRT. Rat models treated with tomotherapy with or without CCRT could present similar patterns of pulmonary toxicity to those shown in lung cancer patients. The models can be used in further investigations of radiation induced pulmonary toxicity

  16. Strategy for the reduction of radon exposure in Norway

    Energy Technology Data Exchange (ETDEWEB)

    NONE

    2010-05-15

    Elevated indoor radon concentrations are a more extensive problem in Norway than in many other countries. It has been estimated that indoor radon causes approximately 300 deaths from lung cancer each year in Norway. On average, avoiding lung cancer increases life expectancy by 14 to 18 years. Radon is a radioactive noble gas formed continually is a decay product from uranium. Uranium is a natural constituent existing in varying concentrations in bedrock, minerals and soils. For this reason, both the soil air and groundwater contain radon. Radon in buildings normally originates from the soil air in the underlying ground. Indoor air pressure is often low, so that radon-containing air from the surrounding ground gets sucked in through cracks in the building foundations. Elevated indoor radon concentrations can be due to household water drawn from groundwater wells, and radon gas can also be emitted from building materials such as certain types of stone or concrete containing high levels of natural radioactivity. Norway, Sweden and Finland are among the the countries in the world with the highest average indoor radon concentrations. Geological conditions and the cool climate pose a big challenge, but the radon problem can be solved in a cost-effective way. Radon is the most common cause of lung cancer after active smoking. At a radon concentration of 100 Bq/m3, which is not far from the estimated average for Norwegian housing, the risks of dying of radon-induced lung cancer before the age of 75 are 0.1 % for non-smokers and 2 % for smokers, respectively. Many buildings in Norway have radon levels that exceed this. The most important health impact of radon exposure is the increased risk of lung cancer. This increase in risk is assumed to be linear in relation to radon concentration (i.e., the risk is 10 times higher at 1000 Bq/m3 compared to 100 Bq/m3). The risk also increases linearly with exposure time, i.e. there is a tenfold greater risk of contracting lung cancer

  17. Strategy for the reduction of radon exposure in Norway

    International Nuclear Information System (INIS)

    2010-05-01

    Elevated indoor radon concentrations are a more extensive problem in Norway than in many other countries. It has been estimated that indoor radon causes approximately 300 deaths from lung cancer each year in Norway. On average, avoiding lung cancer increases life expectancy by 14 to 18 years. Radon is a radioactive noble gas formed continually is a decay product from uranium. Uranium is a natural constituent existing in varying concentrations in bedrock, minerals and soils. For this reason, both the soil air and groundwater contain radon. Radon in buildings normally originates from the soil air in the underlying ground. Indoor air pressure is often low, so that radon-containing air from the surrounding ground gets sucked in through cracks in the building foundations. Elevated indoor radon concentrations can be due to household water drawn from groundwater wells, and radon gas can also be emitted from building materials such as certain types of stone or concrete containing high levels of natural radioactivity. Norway, Sweden and Finland are among the the countries in the world with the highest average indoor radon concentrations. Geological conditions and the cool climate pose a big challenge, but the radon problem can be solved in a cost-effective way. Radon is the most common cause of lung cancer after active smoking. At a radon concentration of 100 Bq/m3, which is not far from the estimated average for Norwegian housing, the risks of dying of radon-induced lung cancer before the age of 75 are 0.1 % for non-smokers and 2 % for smokers, respectively. Many buildings in Norway have radon levels that exceed this. The most important health impact of radon exposure is the increased risk of lung cancer. This increase in risk is assumed to be linear in relation to radon concentration (i.e., the risk is 10 times higher at 1000 Bq/m3 compared to 100 Bq/m3). The risk also increases linearly with exposure time, i.e. there is a tenfold greater risk of contracting lung cancer

  18. Measuring your radon risk

    International Nuclear Information System (INIS)

    Mackmurdo, R.

    1994-01-01

    In its annual report for 1992/93, the NRPB has warned that tens of thousands of UK employees may be exposed to high levels of radon at work. In addition to those who work underground, employees at risk of radon-induced lung cancer are typically those who spend long periods indoors. This article reviews the implications for all employers especially those in low or unknown levels of radon who resist taking measurements in the belief that by not measuring, they are not liable. (UK)

  19. Lung cancer risk from radon and smoking - additive or multiplicative effect?

    International Nuclear Information System (INIS)

    Tomasek, L.

    2016-01-01

    The aim of the work is to evaluate the risk of lung cancer when combined radon and smoking exposure. Methodologically the evaluation is based on case and control study nested in two cohort studies, including 11,000 miners and 12,000 residents exposed to high concentrations of radon in homes. Radon exposure in individuals is complemented by information on smoking gained personally from them or from their relatives. The study is based on 1,073 cases of lung cancer among miners and 372 cases in population study. Control subjects were randomly selected in each study based on gender, year of birth and age achieved. The combined effect of smoking and radon is evaluated using the so-called geometric mixed models, whose special case is an additive or multiplicative model. The resulting model of the risk is closer to additive interaction (parameter of mixed model 0.2). The consequences of the model in the study of population are illustrated by estimates of lifetime risk in a hypothetical population of smokers and nonsmokers. Compared to the multiplicative risk model, the lifetime risk significantly increased according to the best geometric mixed model, especially in the population of non-smokers. (author)

  20. The potential for bias in Cohen's ecological analysis of lung cancer and residential radon

    International Nuclear Information System (INIS)

    Lubin, Jay H.

    2002-01-01

    Cohen's ecological analysis of US lung cancer mortality rates and mean county radon concentration shows decreasing mortality rates with increasing radon concentration (Cohen 1995 Health Phys. 68 157-74). The results prompted his rejection of the linear-no-threshold (LNT) model for radon and lung cancer. Although several authors have demonstrated that risk patterns in ecological analyses provide no inferential value for assessment of risk to individuals, Cohen advances two arguments in a recent response to Darby and Doll (2000 J. Radiol. Prot. 20 221-2) who suggest Cohen's results are and will always be burdened by the ecological fallacy. Cohen asserts that the ecological fallacy does not apply when testing the LNT model, for which average exposure determines average risk, and that the influence of confounding factors is obviated by the use of large numbers of stratification variables. These assertions are erroneous. Average dose determines average risk only for models which are linear in all covariates, in which case ecological analyses are valid. However, lung cancer risk and radon exposure, while linear in the relative risk, are not linearly related to the scale of absolute risk, and thus Cohen's rejection of the LNT model is based on a false premise of linearity. In addition, it is demonstrated that the deleterious association for radon and lung cancer observed in residential and miner studies is consistent with negative trends from ecological studies, of the type described by Cohen. (author)

  1. Simvastatin mitigates functional and structural impairment of lung and right ventricle in a rat model of cigarette smoke-induced COPD.

    Science.gov (United States)

    Wang, Yajie; Jiang, Xue; Zhang, Lihai; Wang, Lihong; Li, Zhu; Sun, Wuzhuang

    2014-01-01

    This study is conducted to investigate an effect of simvastatin on cigarette smoke-induced COPD. Rats were exposed to air (control) and cigarette smoke (smoking) in presence and absence of simvastatin. Heart and lung tissues were harvested for histopathologic and morphometric analysis. Body weight of rat, mean liner intercept (MLI), mean alveolar number (MAN), lung function test, mean pulmonary artery pressure (mPAP), right ventricular hypertrophy index (RVHI) and 5-HTT level in serum and BALF were examined in experimental rats, respectively. Application of simvastatin mitigated peribronchiolar inflammation and pulmonary bullae formed in the smoke-exposed lungs with weight gain as compared to the smoking rats (P reversal of lung function decline (all P reverses lung function decline and attenuates structural impairments of lung and right ventricle possibly through reducing 5-HTT content in the model of COPD.

  2. Fluoxetine protects against methamphetamine‑induced lung inflammation by suppressing oxidative stress through the SERT/p38 MAPK/Nrf2 pathway in rats.

    Science.gov (United States)

    Wang, Yun; Gu, Yu-Han; Liu, Ming; Bai, Yang; Wang, Huai-Liang

    2017-02-01

    Methamphetamine (MA) abuse is a major public health and safety concern throughout the world and a growing burden on healthcare costs. The purpose of the present study was to investigate the protective effect of fluoxetine against MA‑induced chronic pulmonary inflammation and to evaluate the potential role of nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidative stress. Wistar rats were divided into control, MA and two fluoxetine‑treated groups. Rats in the MA and the two fluoxetine‑treated groups were treated daily with intraperitoneal injection of 10 mg/kg MA twice daily. Rats in the two fluoxetine‑treated groups were injected intragastrically with fluoxetine (2 and 10 mg/kg) once daily, respectively. After 5 weeks, the rats were euthanized and hematoxylin and eosin staining, immunohistochemistry, western blot analysis and redox assay were performed. It was demonstrated that chronic exposure to MA can induce pulmonary inflammation in rats, with the symptoms of inflammatory cell infiltration, crowded lung parenchyma, thickened septum and a reduced number of alveolar sacs. Fluoxetine attenuated pulmonary inflammation and the expression of interleukin‑6 and tumor necrosis factor‑α in rat lungs. Fluoxetine inhibited MA‑induced increases in the expression levels of serotonin transporter (SERT) and p‑p38 mitogen‑activated protein kinase (MAPK), and reversed the MA‑induced decrease in nuclear Nrf2 and human heme oxygenase‑1 in lungs. Fluoxetine at 10 mg/kg significantly reversed the reduced glutathione (GSH) level, the ratio of GSH/oxidized glutathione, and the reactive oxygen species level in rat lungs from the MA group. These findings suggested that fluoxetine, a SERT inhibitor, has a protective effect against MA‑induced lung inflammation by suppressing oxidative stress through the SERT/p38 MAPK/Nrf2 pathway in rats.

  3. Cigarette use and the estimation of lung cancer attributable to radon in the United States

    International Nuclear Information System (INIS)

    Lubin, J.H.; Steindorf, K.

    1995-01-01

    Residential exposure to radioactive radon and its decay products has been estimated to account for 10-12% of all lung cancer deaths in the US. It has been difficult to evaluate fully the impact of cigarette smoking, the most important cause of lung cancer, on this estimate, because factors for patterns of tobacco use have not been included in the risk models, since risk models are derived from studies of underground miners exposed to radon and detailed data on smoking are limited. Lung cancer risk estimates for exposure to radon progeny in smoker and non-smoker populations are obtained by applying the same risk model to each population group, thereby assuming the joint effects of smoking and exposure to radon progeny are multiplicative. However, in miners, joint relative risks (RR) for the two exposures are most consistent with an intermediate relationship between multiplicative and additive, so that the present approach likely results in an overestimate of risk in smokers and an underestimate of risk in nonsmokers. One approach for adjusting risk models to incorporate smoking status is based on the relative magnitude of the effects of radon progeny in smokers and nonsmokers and therefore may not be applicable to non-miner populations if the proportion of smokers and the RR for smoking differ. We show that the modification can be derived explicitly by assuming an arithmetic mixture model for the joint RR for smoking and exposure to radon progeny. In this way, smoking parameters in the population of interest (the proportion of smokers and the RR of smoking) can be used directly to adjust radon progeny risk models and obtain risk estimates that are specific for smokers and nonsmokers. With an intermediate RR relationship for smoking and radon progeny, the attributable percentage of lung cancer deaths from residential radon may be twofold greater in nonsmokers than in smokers. 20 refs., 1 fig., 3 tabs

  4. Radon and lung cancer: an epidemiological study in Norway

    International Nuclear Information System (INIS)

    Stranden, E.; Strand, T.; Magnus, K.; James, A.C.; Green, B.M.R.

    1988-01-01

    The objectives and strategy of an epidemiological study on the effects of exposure to radon in Norwegian dwellings is presented. The study is a cooperation between the National Institute of Radiation Hygiene and the Norwegian Cancer Registry in Norway and the National Radiological Protection Board of the United Kingdom, with funding by the Norwegian Cancer Society. Measurements of radon are being made in 10,000 dwellings representing all Norwegian municipalities. The potential for detecting an effect of radon exposure by such a study in Norway is unique because: (1) Radon concentrations are high and there are large regional variations. (2) Data from the Norwegian Cancer Registry is of high quality: all cancers have been subject to compulsory reporting since 1955. These data can be broken down according to municipality, sex and age. (3) In 1964/1965 a large scale survey of smoking habits was carried out in Norway. These data can also be broken down according to municipality, sex and age, and by types of smoking and smoking rate. It is intended to examine the correlation between lung cancer incidence and geographical variation in radon levels after making allowance for smoking habits. Radon measurements were started in early 1987 and the results of the study are expected to be published in 1989. (author)

  5. Small area mapping of domestic radon, smoking prevalence and lung cancer incidence – A case study in Northamptonshire, UK

    International Nuclear Information System (INIS)

    Denman, Antony R.; Rogers, Stephen; Ali, Akeem; Sinclair, John; Phillips, Paul S.; Crockett, Robin G.M.; Groves-Kirkby, Christopher J.

    2015-01-01

    Smoking and radon both cause lung cancer, and together the risk is significantly higher. UK public health campaigns continue to reduce smoking prevalence, and other initiatives identify houses with raised radon (radon-222) levels and encourage remedial action. Smoking prevalence and radon levels in the UK have been mapped at Primary Care Trust level. This paper extends that work, using a commercial socio-demographic database to estimate smoking prevalence at the postcode sector level, and to predict the population characteristics at postcode sector level for 87 postcode sectors in Northamptonshire. Likely smoking prevalence in each postcode sector is then modelled from estimates of the smoking prevalence in the different socio-economic groups used by the database. Mapping estimated smoking prevalence, radon potential and average lung cancer incidence for each postcode sector suggested that there was little correlation between smoking prevalence and radon levels, as radon potential was generally lower in urban areas in Northamptonshire, where the estimates of smoking prevalence were highest. However, the analysis demonstrated some sectors where both radon potential and smoking prevalence were moderately raised. This study showed the potential of this methodology to map estimated smoking prevalence and radon levels to inform locally targeted public health campaigns to reduce lung cancer incidence. - Highlights: • We use a commercial socio-demographic database to estimate smoking prevalence in small areas in Northamptonshire, UK. • We map the estimated smoking prevalence and average domestic radon levels in these small areas. • We estimate annual average lung cancer incidence in these small areas. • The methodology is useful to evaluate and plan localised public health campaigns to reduce lung cancer incidence.

  6. Potential role of Saudi red propolis in alleviating lung damage induced by methicillin resistant Staphylococcus aureus virulence in rats.

    Science.gov (United States)

    Saddiq, Amna Ali; Mohamed, Azza Mostafa

    2016-07-01

    The aim of this study was to explore the protective impact of aqueous extract of Saudi red propolis against rat lung damage induced by the pathogenic bacteria namely methicillin resistant Staphylococcus aureus (MRSA) ATCC 6538 strain. Infected rats were received a single intraperitoneal (i.p.) injection of bacterial suspension at a dose of 1 X 10(6) CFU / 100g body weight. Results showed that oral administration of an aqueous extract of propolis (50mg/100g body weight) daily for two weeks to infected rats simultaneously with bacterial infection, effectively ameliorated the alteration of oxidative stress biomarker, malondialdehyde (MDA), as well as the antioxidant markers, glutathione peroxidase (GPx) and superoxide dismutase (SOD), in lungs of infected rats compared with infected untreated ones. Also, the used propolis extract successfully modulated the alterations in proinflammatory mediators, tumor necrosis factor-α (TNF- α) and vascular endothelial growth factor (VEGF) in serum. In addition, the propolis extract successfully modulated the oxidative DNA damage and the apoptosis biomarker, caspase 3, in lungs of S aureus infected rats compared with infected untreated animals. The biochemical results were supported by histo-pathological observation of lung tissues. In conclusion, the beneficial prophylactic role of the aqueous extract of Saudi red propolis against lung damage induced by methicillin resistant S aureus may be related to the antioxidant, anti-inflammatory, immunomodulatory and antiapoptosis of its active constituents.

  7. An assessment of ecological and case-control methods for estimating lung cancer risk due to indoor radon

    International Nuclear Information System (INIS)

    Stidley, C.A.; Samet, J.M.

    1992-01-01

    Studies of underground miners indicate that indoor radon is an important cause of lung cancer. This finding has raised concern that exposure to radon also causes lung cancer in the general population. Epidemiological studies, including both case-control and ecological approaches, have directly addressed the risks of indoor residential radon; many more case-control studies are in progress. Ecological studies that associate lung-cancer rates with typical indoor radon levels in various geographic areas have not consistently shown positive associations. The results of purportedly negative ecological studies have been used as a basis for questioning the hazards of indoor radon exposure. Because of potentially serious methodologic flaws for testing hypotheses, we examined the ecological method as a tool for assessing lung-cancer risk from indoor radon exposure. We developed a simulation approach that utilizes the Environmental Protection Agency (EPA) radon survey data to assign exposures to individuals within counties. Using the computer-generated data, we compared risk estimates obtained by ecological regression methods with those obtained from other regression methods and with the open-quotes trueclose quotes risks used to generate the data. For many of these simulations, the ecological models, while fitting the summary data well, gave risk estimates that differed considerably from the true risks. For some models, the risk estimates were negatively correlated with exposure, although the assumed relationship was positive. Attempts to improve the ecological models by adding smoking variables, including interaction terms, did not always improve the estimates of risk, which are easily affected by model misspecification. Because exposure situations used in the simulations are realistic, our results show that ecological methods may not accurately estimate the lung-cancer risk associated with indoor radon exposure

  8. Radon, cigarette smoke, and lung cancer: A re-analysis of the Colorado Plateau uranium miners' data [see comments

    International Nuclear Information System (INIS)

    Moolgavkar, S.H.; Luebeck, E.G.; Krewski, D.; Zielinski, J.M.

    1993-01-01

    Much of our knowledge regarding the interaction of radon and tobacco smoke in the etiology of human lung cancer derives from studies of uranium miners. In this article, we present a re-analysis of lung cancer mortality in the Colorado Plateau miners' cohort within the framework of the two-mutation clonal expansion model of carcinogenesis. This analysis takes into account the patterns of exposure to radon and cigarette smoke experienced by individuals in the cohort. A simultaneous re-analysis of the British doctors' cohort indicated that those model parameters relating to the effects of tobacco were comparable in the two data sets. We found no evidence of interaction between radon and tobacco smoke with respect to their joint effect on the first or second stage mutation rates or on the rate of proliferation of initiated cells. The age-specific relative risks associated with joint exposure to radon and cigarette smoke, however, were supra-additive but submultiplicative. The analysis also confirmed that fractionation of radon exposures leads to higher lung cancer risks. Finally, we present some estimates of lung cancer risk from environmental radon exposure for non-smokers and smokers

  9. An overview of PNL radon experiments with reference to epidemiological data

    International Nuclear Information System (INIS)

    Cross, F.T.; Palmer, R.F.; Busch, R.H.; Dagle, G.E.; Filipy, R.E.; Ragan, H.A.

    1986-01-01

    Biological effects observed in dogs and rodents after the inhalation of radon and radon daughters have included, primarily, respiratory carcinoma, pulmonary fibrosis, emphysema, and life-span shortening. Extrapulmonary lesions observed are not considered significant except for certain hematological effects. In this paper we present biological effects data resulting from chronic exposures of hamsters, rats, and beagle dogs. Emphasis is placed on the carcinogenic effects of radon and radon daughters, including the influences of radon-daughter exposure rate, unattachment fraction, and disequilibrium and of concomitant exposure to other pollutants. These data are correlated with results from human epidemiological studies. Plausible values for the radon (radon-daughter) lifetime lung-cancer risk coefficient are provided. 30 refs., 3 tabs

  10. On Academician Behounek's paper ''Lung cancer induced by ionizing radiation''

    International Nuclear Information System (INIS)

    Thomas, J.

    1979-01-01

    The significance and scientific contribution are discussed of the paper ''Lung Cancer Induced by Ionizing Radiation'' submitted by Academician Frantisek Behounek to the nation-wide workshop of the Czechoslovak Society of Pneumology and Oncology in Prague, October 3 and 4, 1952 and published in the Proceedings in 1953. The paper discussed the problem which still remains topical, ie., lung exposure to radon daughters, which Academician Behounek considered to be the true cause of lung cancer in Jachymov miners. (B.S.)

  11. A case of lung cancer in a miner - An estimation of radon exposure and discussion of probable causes

    International Nuclear Information System (INIS)

    Snihs, J.O.; Walinder, Gunnar.

    1977-01-01

    One particular lung cancer case which was brought before the National Swedish Social Insurance Board as a possible case of industrial injury due to exposure to radon is described. The man concerned had worked in two mines during the period 1917-1944 and he was found to be suffering from lung cancer in 1961 when he was 69 years of age. He had been a moderate smoker for the previous 20 years, he had a healed lung tuberculosis and confirmed silicosis in stage 1. The mines in which he worked have been out of use for many years and they have bot been accessible for measurements of radon concentrations. The estimation of the radon concentrations is discussed on the basis of experience of the causes of radon occurrence in other mines with regard to their geology, ventilation and depth and the extent to which mine water was present. The estimated exposure was 600 WLM. With the given conditions there is a discussion on the partial and combined probabilities of lung cancer in the above case taking into account the type of lung cancer, the estimated exposure to radon and his smoking, silicosis, tuberculosis and age

  12. 4-Hydroxyphenylacetic Acid Attenuated Inflammation and Edema via Suppressing HIF-1α in Seawater Aspiration-Induced Lung Injury in Rats

    Science.gov (United States)

    Liu, Zhongyang; Xi, Ronggang; Zhang, Zhiran; Li, Wangping; Liu, Yan; Jin, Faguang; Wang, Xiaobo

    2014-01-01

    4-Hydroxyphenylacetic acid (4-HPA) is an active component of Chinese herb Aster tataricus which had been widely used in China for the treatment of pulmonary diseases. The aim of this study is to investigate the effect of 4-HPA on seawater aspiration-induced lung injury. Pulmonary inflammation and edema were assessed by enzyme-linked immunosorbent assay (ELISA), bronchoalveolar lavage fluid (BALF) white cell count, Evans blue dye analysis, wet to dry weight ratios, and histology study. Hypoxia-inducible factor-1α (HIF-1α) siRNA and permeability assay were used to study the effect of 4-HPA on the production of inflammatory cytokines and monolayer permeability in vitro. The results showed that 4-HPA reduced seawater instillation-induced mortality in rats. In lung tissues, 4-HPA attenuated hypoxia, inflammation, vascular leak, and edema, and decreased HIF-1α protein level. In primary rat alveolar epithelial cells (AEC), 4-HPA decreased hypertonicity- and hypoxia-induced HIF-1α protein levels through inhibiting the activations of protein translational regulators and via promoting HIF-1α protein degradation. In addition, 4-HPA lowered inflammatory cytokines levels through suppressing hypertonicity- and hypoxia-induced HIF-1α in NR8383 macrophages. Moreover, 4-HPA decreased monolayer permeability through suppressing hypertonicity and hypoxia-induced HIF-1α, which was mediated by inhibiting vascular endothelial growth factor (VEGF) in rat lung microvascular endothelial cell line (RLMVEC). In conclusion, 4-HPA attenuated inflammation and edema through suppressing hypertonic and hypoxic induction of HIF-1α in seawater aspiration-induced lung injury in rats. PMID:25050781

  13. Modeling of lung cancer risk due to radon exhalation of granite stone in dwelling houses

    Directory of Open Access Journals (Sweden)

    Akbar Abbasi

    2017-01-01

    Conclusions: The estimated numbers of lung cancer deaths attributable to indoor radon due to granite stones in 2013 were 145 (3.33% and 103 (2.37% for poor and normal ventilation systems, respectively. According to our estimations, the values of 3.33% and 2.37% of lung cancer deaths in 2013 are attributed to radon exhalation of granite stones with poor and normal ventilation systems, respectively.

  14. Environmentally persistent free radicals induce airway hyperresponsiveness in neonatal rat lungs

    Directory of Open Access Journals (Sweden)

    Lominiki Slawo

    2011-03-01

    Full Text Available Abstract Background Increased asthma risk/exacerbation in children and infants is associated with exposure to elevated levels of ultrafine particulate matter (PM. The presence of a newly realized class of pollutants, environmentally persistent free radicals (EPFRs, in PM from combustion sources suggests a potentially unrecognized risk factor for the development and/or exacerbation of asthma. Methods Neonatal rats (7-days of age were exposed to EPFR-containing combustion generated ultrafine particles (CGUFP, non-EPFR containing CGUFP, or air for 20 minutes per day for one week. Pulmonary function was assessed in exposed rats and age matched controls. Lavage fluid was isolated and assayed for cellularity and cytokines and in vivo indicators of oxidative stress. Pulmonary histopathology and characterization of differential protein expression in lung homogenates was also performed. Results Neonates exposed to EPFR-containing CGUFP developed significant pulmonary inflammation, and airway hyperreactivity. This correlated with increased levels of oxidative stress in the lungs. Using differential two-dimensional electrophoresis, we identified 16 differentially expressed proteins between control and CGUFP exposed groups. In the rats exposed to EPFR-containing CGUFP; peroxiredoxin-6, cofilin1, and annexin A8 were upregulated. Conclusions Exposure of neonates to EPFR-containing CGUFP induced pulmonary oxidative stress and lung dysfunction. This correlated with alterations in the expression of various proteins associated with the response to oxidative stress and the regulation of glucocorticoid receptor translocation in T lymphocytes.

  15. Experimental study of gene expression in lung and bronchus of radon-exposed mice

    International Nuclear Information System (INIS)

    Guo Zhiying; Tian Mei; Liu Jianxiang; Ruan Jianlei; Piao Chunnan; Su Xu

    2008-01-01

    Objective: To construct and identify differentially expressed cDNA library in lung and bronchus of mice exposed to radon. Methods: 2 week old, weighing (18-22)g, male BALB/c mice were placed in a SR-NIM02 radon chamber. One group of mice was exposed to radon, which was equivalent to the accumulative dose of 30 WLM. The control group was about 0.02 WLM. To construct a subtracted cDNA library enriched with differentially expressed genes, the Super SMART technique and the suppression subtractive hybridization (SSH) were performed. The obtained forward and reverse cDNA fragments were directly inserted into pGEM-T-easy vector and transformed into E. coli DH5α. The inserts in plasmid were amplified by nested polymerase chain reaction (PCR), and some of which were sequenced. In the end these sequences were BLASTed with GeneBank. Results: 146 of 460 clones obtained randomly were positive clones contained (1000-1500)bp inserted cDNA fragments. The forward and reverse subtracted cDNA library in lung and bronchus of mice exposed to radon was constructed, and 48 up-regulation and 61 down-regulation cDNA sequences selected were homologous with GeneBank in different extent. Conclusions: The subtracted cDNA library in lung and bronchus of mice exposed to radon is successfully constructed, and genes that differentially expressed are identified. Some genes might have relation with the immunity, cell cycle and apoptosis. (authors)

  16. Low tidal volume ventilation ameliorates left ventricular dysfunction in mechanically ventilated rats following LPS-induced lung injury.

    Science.gov (United States)

    Cherpanath, Thomas G V; Smeding, Lonneke; Hirsch, Alexander; Lagrand, Wim K; Schultz, Marcus J; Groeneveld, A B Johan

    2015-10-07

    High tidal volume ventilation has shown to cause ventilator-induced lung injury (VILI), possibly contributing to concomitant extrapulmonary organ dysfunction. The present study examined whether left ventricular (LV) function is dependent on tidal volume size and whether this effect is augmented during lipopolysaccharide(LPS)-induced lung injury. Twenty male Wistar rats were sedated, paralyzed and then randomized in four groups receiving mechanical ventilation with tidal volumes of 6 ml/kg or 19 ml/kg with or without intrapulmonary administration of LPS. A conductance catheter was placed in the left ventricle to generate pressure-volume loops, which were also obtained within a few seconds of vena cava occlusion to obtain relatively load-independent LV systolic and diastolic function parameters. The end-systolic elastance / effective arterial elastance (Ees/Ea) ratio was used as the primary parameter of LV systolic function with the end-diastolic elastance (Eed) as primary LV diastolic function. Ees/Ea decreased over time in rats receiving LPS (p = 0.045) and high tidal volume ventilation (p = 0.007), with a lower Ees/Ea in the rats with high tidal volume ventilation plus LPS compared to the other groups (p tidal volume ventilation without LPS (p = 0.223). A significant interaction (p tidal ventilation and LPS for Ees/Ea and Eed, and all rats receiving high tidal volume ventilation plus LPS died before the end of the experiment. Low tidal volume ventilation ameliorated LV systolic and diastolic dysfunction while preventing death following LPS-induced lung injury in mechanically ventilated rats. Our data advocates the use of low tidal volumes, not only to avoid VILI, but to avert ventilator-induced myocardial dysfunction as well.

  17. Prevention of lung cancer by remediation of residential exposure to radon daughters

    International Nuclear Information System (INIS)

    Mahaffey, J.A.; Cross, F.T.; Johnson, J.R.; Baechler, M.C.

    1991-01-01

    The United States Bonneville Power Administration (BPA), as part of an energy conservation programme in the states of Washington, Oregon, Idaho, Wyoming, and Montana, has collected over 36,000 residential radon concentration measurements. Data were collected between 1983 and 1989 with ambient α etched track dosemeters. Based on the linear risk coefficient from the BEIR IV report for lifetime lung cancer in smokers and non-smokers, numbers of lung cancer cases attributable to radon exposure were predicted. Numbers of baseline lung cancer cases and numbers of these that were preventable by remediation were also estimated. Remediation to 10 pCi.1 -1 , to 4 pCi.1 -1 , and to outdoor levels were considered. With vital statistics data, results were extrapolated to populations in the states represented by the BPA data. Costs of remediation were estimated. Results were evaluated in terms of cost per cancer saved and per cent reduction in fatal lung cancer cases from the baseline estimate. (author)

  18. BEIR VI report. Public summary: the health effects of exposure to indoor radon

    International Nuclear Information System (INIS)

    1998-01-01

    For centuries it has been known that some underground miners suffered from higher rates of lung cancer than the general population. In recent decades, a growing body of evidence has casually linked their lung cancers to exposure to high levels of radon and also to cigarette smoking. The connection between radon and lung cancer in miners has raised concern that radon in homes might be causing lung cancer in the general population, although the radon levels in most homes are much lower than in most mines. The National Research Council study, which has been carried out by the sixth Committee on Biological Effects of Ionizing Radiations (BEIR VI), has used the most recent information available to estimate the risks posed by exposure to radon in homes. The most direct way to assess the risks posed by radon in homes is to measure radon exposures among people who have lung cancer and compare them with exposures among people who have not developed lung cancer. Several such studies have been completed, and several are under way. The studies have not produced a definitive answer, primarily because the risk is likely to be very small at the low exposure encountered from most homes and because it is difficult to estimate radon exposures that people have received over their lifetimes. In addition, it is clear that far more lung cancers are caused by smoking that are caused by radon. The risk of lung cancer caused by smoking is much higher than the risk of lung cancer caused by indoor radon. Most of the radon-related deaths among smokers would not have occurred if the victims had not smoked. Furthermore, there is evidence for a synergistic interaction between smoking and radon. In other words, the number of cancers induced in ever-smokers by radon is greater than one would expect from the additive effects of smoking along and radon alone. Nevertheless, the estimated 15400 or 21800 deaths attributed to radon in combination with cigarette-smoking and radon alone in never

  19. Erythropoietin Pretreatment Attenuates Seawater Aspiration-Induced Acute Lung Injury in Rats.

    Science.gov (United States)

    Ji, Mu-Huo; Tong, Jian-Hua; Tan, Yuan-Hui; Cao, Zhen-Yu; Ou, Cong-Yang; Li, Wei-Yan; Yang, Jian-Jun; Peng, Y G; Zhu, Si-Hai

    2016-02-01

    Seawater drowning-induced acute lung injury (ALI) is a serious clinical condition characterized by increased alveolar-capillary permeability, excessive inflammatory responses, and refractory hypoxemia. However, current therapeutic options are largely supportive; thus, it is of great interest to search for alternative agents to treat seawater aspiration-induced ALI. Erythropoietin (EPO) is a multifunctional agent with antiinflammatory, antioxidative, and antiapoptotic properties. However, the effects of EPO on seawater aspiration-induced ALI remain unclear. In the present study, male rats were randomly assigned to the naive group, normal saline group, seawater group, or seawater + EPO group. EPO was administered intraperitoneally at 48 and 24 h before seawater aspiration. Arterial blood gas analysis was performed with a gas analyzer at baseline, 30 min, 1 h, 4 h, and 24 h after seawater aspiration, respectively. Histological scores, computed tomography scan, nuclear factor kappa B p65, inducible nitric oxide synthase, caspase-3, tumor necrosis factor-alpha, interleukin (IL)-1β, IL-6, IL-10, wet-to-dry weight ratio, myeloperoxidase activity, malondialdehyde, and superoxide dismutase in the lung were determined 30 min after seawater aspiration. Our results showed that EPO pretreatment alleviated seawater aspiration-induced ALI, as indicated by increased arterial partial oxygen tension and decreased lung histological scores. Furthermore, EPO pretreatment attenuated seawater aspiration-induced increase in the expressions of pulmonary nuclear factor kappa B p65, inducible nitric oxide synthase, caspase-3, tumor necrosis factor-alpha, IL-1β, myeloperoxidase activity, and malondialdehyde when compared with the seawater group. Collectively, our study suggested that EPO pretreatment attenuates seawater aspiration-induced ALI by down-regulation of pulmonary pro-inflammatory cytokines, oxidative stress, and apoptosis.

  20. Occupational and environmental exposures to radon: A perspective for mitigators

    International Nuclear Information System (INIS)

    Sanchez, D.C.; Messing, M.; Saum, D.

    1989-01-01

    This paper compares normal environmental and occupational exposures to radon and radon decay products for the occupational group, including radon mitigators and diagnosticians. Occupational exposures to radon and radon decay products and the associated high incidence of radiation-induced lung cancer form the basis for current concern for limiting exposures to radon. While it is now known that radon is a ubiquitous environmental pollutant and estimates exist as to what this means in terms of cancer risk to the general population, similar estimates are not available for radon mitigators and diagnosticians

  1. Radon and lung cancer in the Ardennes and Eifel region

    International Nuclear Information System (INIS)

    Wichmann, H.E.; Poffijn, C.

    1993-01-01

    The objectives of the project are to perform epidemiological studies on the role of radon in the etiology of lung cancer in the Ardennes-Eifel region and in Brittany. In each of the participating countries, Belgium, France, Germany and Luxemburg cases and controls were collected in a series of hospitals. The radon exposure for the last 35 years was reconstructed through 6 months measurements in the living and bedrooms of the different dwellings. The objectives and results of the eight contributions to the project for the reporting period are presented. (R.P.) 1 ref

  2. Role for macrophage inflammatory protein-2 in lipopolysaccharide-induced lung injury in rats

    DEFF Research Database (Denmark)

    Schmal, H; Shanley, T P; Jones, M L

    1996-01-01

    Macrophage inflammatory protein-2 (MIP-2) is a C-X-C chemokine that possesses chemotactic activity for neutrophils. Rat MIP-2 was cloned and expressed as a 7.9-kDa peptide that exhibited dose-dependent neutrophil chemotactic activity at concentrations from 10 to 250 nM. Rabbit polyclonal Ab to th...... instillation of LPS was found to be MIP-2-dependent. These data indicate that MIP-2 plays a significant role in LPS-induced inflammatory response in rat lungs and is required for the full recruitment of neutrophils....

  3. Protecting People and Families from Radon: A Federal Action Plan for Saving Lives

    Science.gov (United States)

    This strategy for radon action outlines actions federal agencies can take within existing resources and program capacities to advance the Healthy People 2020 radon objectives and launch a national effort to end all avoidable radon-induced lung cancer death

  4. The unattached fraction of radon decay products: Potential effects of in-home air cleaners on lung cancer risk

    International Nuclear Information System (INIS)

    Brady, P.A.

    1991-01-01

    Radon decay products are a factor in the development of lung cancer. Because of their efficient deposition within the lung, the fraction of decay products not attached to particulate (i.e., the unattached fraction) is very important in lung dosimetry. This study simulated the use of two in-home air cleaning devices to reduce airborne particulate concentrations, measure the effect on the unattached fraction, and estimate the radon lung cancer risk. Radon was released into a chamber having a volume-to-surface-area ratio similar to a small home. At radon-decay product equilibrium, radon and airborne particle concentrations were measured, and the concentration of the unattached fraction was estimated. The effect of particle concentration on the unattached fraction was then determined. The average unattached fractions corresponding to the particle concentration ranges expected for the air cleaning devices were used to calculate the annual alpha radiation dose and annual radon lung cancer for men, women and children at rest and under light activity. The annual doses and related risks were compared to those used in the models published by the Environmental Protection Agency. For particulate concentrations of a home with no particulate generating activities (e.g., smoking, cooking), the electronic air cleaner is predicted to reduce the unattached fraction from seven percent (the value used by the NCRP and confirmed in this study) to four percent. These conditions represent the maximum reduction in the unattached fraction. The decrease in the unattached fraction is tentatively attributed to an increase in plateout. Based on these results, a reduction of less than ten percent in the calculated annual lung cancer risk is found in all cases

  5. Integrating microRNA and mRNA expression profiles in response to radiation-induced injury in rat lung

    International Nuclear Information System (INIS)

    Xie, Ling; Zhou, Jundong; Zhang, Shuyu; Chen, Qing; Lai, Rensheng; Ding, Weiqun; Song, ChuanJun; Meng, XingJun; Wu, Jinchang

    2014-01-01

    Exposure to radiation provokes cellular responses, which are likely regulated by gene expression networks. MicroRNAs are small non-coding RNAs, which regulate gene expression by promoting mRNA degradation or inhibiting protein translation. The expression patterns of both mRNA and miRNA during the radiation-induced lung injury (RILI) remain less characterized and the role of miRNAs in the regulation of this process has not been studied. The present study sought to evaluate miRNA and mRNA expression profiles in the rat lung after irradiation. Male Wistar rats were subjected to single dose irradiation with 20 Gy using 6 MV x-rays to the right lung. (A dose rate of 5 Gy/min was applied). Rats were sacrificed at 3, 12 and 26 weeks after irradiation, and morphological changes in the lung were examined by haematoxylin and eosin. The miRNA and mRNA expression profiles were evaluated by microarrays and followed by quantitative RT-PCR analysis. A cDNA microarray analysis found 2183 transcripts being up-regulated and 2917 transcripts down-regulated (P ≤ 0.05, ≥2.0 fold change) in the lung tissues after irradiation. Likewise, a miRNAs microarray analysis indicated 15 miRNA species being up-regulated and 8 down-regulated (P ≤ 0.05). Subsequent bioinformatics anal -yses of the differentially expressed mRNA and miRNAs revealed that alterations in mRNA expression following irradiation were negatively correlated with miRNAs expression. Our results provide evidence indicating that irradiation induces alterations of mRNA and miRNA expression in rat lung and that there is a negative correlation of mRNA and miRNA expression levels after irradiation. These findings significantly advance our understanding of the regulatory mechanisms underlying the pathophysiology of radiation-induced lung injury. In summary, RILI does not develop gradually in a linear process. In fact, different cell types interact via cytokines in a very complex network. Furthermore, this study suggests that

  6. Factors modifying the risk of lung cancer associated to radon in the french cohort of uranium miners

    International Nuclear Information System (INIS)

    Vacquier, B.; Rogel, A.; Laurier, D.; Caer, S.; Acker, A.

    2008-01-01

    The radon is classified lung carcinogen for man, but questions stay about the effects for low doses irradiation.The results of the analysis radon-lung cancer and the factors modifying on this relationship in the French cohort of miners followed until to 1999 is reported. This analysis confirms that the risk lung cancer is different according the period of exposure. A best precision in the measurement of exposure after 1956 could explain this difference. (N.C.)

  7. Caffeine Mitigates Lung Inflammation Induced by Ischemia-Reperfusion of Lower Limbs in Rats

    Directory of Open Access Journals (Sweden)

    Wei-Chi Chou

    2015-01-01

    Full Text Available Reperfusion of ischemic limbs can induce inflammation and subsequently cause acute lung injury. Caffeine, a widely used psychostimulant, possesses potent anti-inflammatory capacity. We elucidated whether caffeine can mitigate lung inflammation caused by ischemia-reperfusion (IR of the lower limbs. Adult male Sprague-Dawley rats were randomly allocated to receive IR, IR plus caffeine (IR + Caf group, sham-operation (Sham, or sham plus caffeine (n=12 in each group. To induce IR, lower limbs were bilaterally tied by rubber bands high around each thigh for 3 hours followed by reperfusion for 3 hours. Caffeine (50 mg/kg, intraperitoneal injection was administered immediately after reperfusion. Our histological assay data revealed characteristics of severe lung inflammation in the IR group and mild to moderate characteristic of lung inflammation in the IR + Caf group. Total cells number and protein concentration in bronchoalveolar lavage fluid of the IR group were significantly higher than those of the IR + Caf group (P<0.001 and P=0.008, resp.. Similarly, pulmonary concentrations of inflammatory mediators (tumor necrosis factor-α, interleukin-1β, and macrophage inflammatory protein-2 and pulmonary myeloperoxidase activity of the IR group were significantly higher than those of the IR + Caf group (all P<0.05. These data clearly demonstrate that caffeine could mitigate lung inflammation induced by ischemia-reperfusion of the lower limbs.

  8. Allicin Protects against Lipopolysaccharide-Induced Acute Lung ...

    African Journals Online (AJOL)

    Purpose: To investigate the effect of allicin, an active component of garlic, on lipopolysaccharide (LPS)- induced acute lung injury. Methods: Wistar rats were subjected to LPS intravenous injection with or without allicin treatment to induce acute lung injury (ALI) model. Also, A549 cells were stimulated with LPS in the ...

  9. Effects of ICRF-187 and L-Carnitine on bleomycin-induced lung toxicity in rats

    International Nuclear Information System (INIS)

    Shouman, Samia A.; Abdel-Hamid, M.A.; Hassan, Zeinab A.; Mansour, Heba H.

    2002-01-01

    The possible modulatory effects of ICRF-187 and L-carnitine against bleomycin-induced pulmonary toxicity in male rats were investigated. Repeated administration of bleomycin (10 mg/kg, twice weekly for 6 consecutive weeks) produced significant lung toxicity. The toxicity was manifested by significant increase in normal contents of lipid peroxide (LPO, 91.7%) reduced glutathione (GSH, 73.2%) and oxidized glutathione (GSSG, 135.4%) as well as the activity of superoxide dismutase (SOD, 222.7%). Thirty minutes prior to bleomycin treatment, other groups of rats received either ICRF-187 (95 mg/kg) or L-carnitine (500 mg/kg) adopting the same schedule of treatment as in bleomycin-treated group. L-carnitine decreased bleomycin-induced elevations in SOD activity, GSH and GSSG contents, however, it failed to suppress the increase in LPO level. On the other hand, treatment with ICRF-187 returned back all the elevated biochemical parameters induced by bleomycin to nearly normal levels. In conclusion, the results of this study showed a potential capability of ICRF-187 to mitigate the bleomycin-induced lung injury. Moreover, despite the inability of L-carnitine to change the elevated LPO content, it was able however, to decrease the elevated endogenous antioxidant parameters. (author)

  10. Nitric oxide mediates lung injury induced by ischemia-reperfusion in rats.

    Science.gov (United States)

    Kao, Shang Jyh; Peng, Tai-Chu; Lee, Ru Ping; Hsu, Kang; Chen, Chao-Fuh; Hung, Yu-Kuen; Wang, David; Chen, Hsing I

    2003-01-01

    Nitric oxide (NO) has been reported to play a role in lung injury (LI) induced by ischemia-reperfusion (I/R). However, controversy exists as to the potential beneficial or detrimental effect of NO. In the present study, an in situ, perfused rat lung model was used to study the possible role of NO in the LI induced by I/R. The filtration coefficient (Kfc), lung weight gain (LWG), protein concentration in the bronchoalveolar lavage (PCBAL), and pulmonary arterial pressure (PAP) were measured to evaluate the degree of pulmonary hypertension and LI. I/R resulted in increased Kfc, LWG, and PCBAL. These changes were exacerbated by inhalation of NO (20-30 ppm) or 4 mM L-arginine, an NO precursor. The permeability increase and LI caused by I/R could be blocked by exposure to 5 mM N omega-nitro-L-arginine methyl ester (L-NAME; a nonspecific NO synthase inhibitor), and this protective effect of L-NAME was reversed with NO inhalation. Inhaled NO prevented the increase in PAP caused by I/R, while L-arginine had no such effect. L-NAME tended to diminish the I/R-induced elevation in PAP, but the suppression was not statistically significant when compared to the values in the I/R group. These results indicate that I/R increases Kfc and promotes alveolar edema by stimulating endogenous NO synthesis. Exogenous NO, either generated from L-arginine or delivered into the airway, is apparently also injurious to the lung following I/R. Copyright 2003 National Science Council, ROC and S. Karger AG, Basel

  11. Post-irradiation dietary vitamin E does not affect the development of radiation-induced lung damage in rats

    International Nuclear Information System (INIS)

    Wiegman, Erwin M.; Gameren, Mieke M. van; Kampinga, Harm H.; Szabo, Ben G.; Coppes, Rob P.

    2004-01-01

    The purpose of this study was to investigate whether application of post-irradiation vitamin E, an anti-oxidant, could prevent the development of radiation induced lung damage. Wistar rats were given vitamin E enriched or vitamin E deprived food starting from 4 weeks after 18 Gy single dose irradiation of the right thorax. Neither breathing frequencies nor CT density measurements revealed differences between the groups. It is concluded that post-irradiation vitamin E does not influence radiation-induced fibrosis to the lung

  12. Induced hypernatraemia is protective in acute lung injury.

    Science.gov (United States)

    Bihari, Shailesh; Dixon, Dani-Louise; Lawrence, Mark D; Bersten, Andrew D

    2016-06-15

    Sucrose induced hyperosmolarity is lung protective but the safety of administering hyperosmolar sucrose in patients is unknown. Hypertonic saline is commonly used to produce hyperosmolarity aimed at reducing intra cranial pressure in patients with intracranial pathology. Therefore we studied the protective effects of 20% saline in a lipopolysaccharide lung injury rat model. 20% saline was also compared with other commonly used fluids. Following lipopolysaccharide-induced acute lung injury, male Sprague Dawley rats received either 20% hypertonic saline, 0.9% saline, 4% albumin, 20% albumin, 5% glucose or 20% albumin with 5% glucose, i.v. During 2h of non-injurious mechanical ventilation parameters of acute lung injury were assessed. Hypertonic saline resulted in hypernatraemia (160 (1) mmol/l, mean (SD)) maintained through 2h of ventilation, and in amelioration of lung oedema, myeloperoxidase, bronchoalveolar cell infiltrate, total soluble protein and inflammatory cytokines, and lung histological injury score, compared with positive control and all other fluids (p ≤ 0.001). Lung physiology was maintained (conserved PaO2, elastance), associated with preservation of alveolar surfactant (p ≤ 0.0001). Independent of fluid or sodium load, induced hypernatraemia is lung protective in lipopolysaccharide-induced acute lung injury. Copyright © 2016 Elsevier B.V. All rights reserved.

  13. Relationship of radioactive radon daughters and cigarette smoking in the genesis of lung cancer in uranium miners

    International Nuclear Information System (INIS)

    Saccomanno, G.; Huth, G.C.; Auerbach, O.; Kuschner, M.

    1988-01-01

    This article documents the study of 383 cases of lung cancer in uranium miners and presents for the first time the relationship of radioactive radon gas and cigarette smoking. There is evidence that alpha radiation from radon gas at exposure levels above 465 working level months (WLM) is a strong contributor to the development of lung cancer. Cigarette smoking plays the most significant role in causing lung tumor; this is also noticed in nonminers who smoke cigarettes. A synergistic or additive effect of these two carcinogens is strongly suggested. The data indicate that small cell tumors develop in younger nonsmoking miners exposed to radon levels above 465 WLM. Lung cancers develop in smoking miners at lower levels of radon exposure than in nonsmoking miners. Based on an average mining experience of 15 years, there is substantial evidence that the present maximum allowable limit of 0.3 working levels (WL), or 4 working level months (WLM) per year, is safe, representing a margin of safety of approximately 10:1. Furthermore, a comparison of these data with the radon levels in some homes, averaging in the neighborhood of 0.025 WL, would indicate that health risks at these levels are negligible. It is suggested that 20 picocuries/liter, which equals 0.10 WL, be the maximum allowable level in homes

  14. Sodium butyrate protects against severe burn-induced remote acute lung injury in rats.

    Directory of Open Access Journals (Sweden)

    Xun Liang

    Full Text Available High-mobility group box 1 protein (HMGB1, a ubiquitous nuclear protein, drives proinflammatory responses when released extracellularly. It plays a key role as a distal mediator in the development of acute lung injury (ALI. Sodium butyrate, an inhibitor of histone deacetylase, has been demonstrated to inhibit HMGB1 expression. This study investigates the effect of sodium butyrate on burn-induced lung injury. Sprague-Dawley rats were divided into three groups: 1 sham group, sham burn treatment; 2 burn group, third-degree burns over 30% total body surface area (TBSA with lactated Ringer's solution for resuscitation; 3 burn plus sodium butyrate group, third-degree burns over 30% TBSA with lactated Ringer's solution containing sodium butyrate for resuscitation. The burned animals were sacrificed at 12, 24, and 48 h after burn injury. Lung injury was assessed in terms of histologic changes and wet weight to dry weight (W/D ratio. Tumor necrosis factor (TNF-α and interleukin (IL-8 protein concentrations in bronchoalveolar lavage fluid (BALF and serum were measured by enzyme-linked immunosorbent assay, and HMGB1 expression in the lung was determined by Western blot analysis. Pulmonary myeloperoxidase (MPO activity and malondialdehyde (MDA concentration were measured to reflect neutrophil infiltration and oxidative stress in the lung, respectively. As a result, sodium butyrate significantly inhibited the HMGB1 expressions in the lungs, reduced the lung W/D ratio, and improved the pulmonary histologic changes induced by burn trauma. Furthermore, sodium butyrate administration decreased the TNF-α and IL-8 concentrations in BALF and serum, suppressed MPO activity, and reduced the MDA content in the lungs after severe burn. These results suggest that sodium butyrate attenuates inflammatory responses, neutrophil infiltration, and oxidative stress in the lungs, and protects against remote ALI induced by severe burn, which is associated with inhibiting HMGB1

  15. Lifetime loss through lung cancer in Denmark and Sweden in relation to radon levels

    International Nuclear Information System (INIS)

    Gjorup, H.L.; Hansen, H.J.M.

    1987-01-01

    Radon levels in Swedish houses are 2.1 times higher than in Danish. Results show no positive correlation with cumulative lifetime loss due to lung cancer for the period 1972-1978, which in Denmark was 2.0 times that in Sweden. Neither do they show any positive correlation with lifetime loss due to leukemia, which was the same in Sweden and Denmark, or with lifetime loss due to total neoplasms. Lung cancer mortality figures resemble those for bronchitis, asthma and emphysema. The authors thus see no special radiogenic effect of the high Swedish radon levels. (author)

  16. Temporal patterns of lung cancer risk from radon and smoking - consequences to remediation measures

    International Nuclear Information System (INIS)

    Tomasek, L.

    2004-01-01

    Studies of uranium miners conducted since the late 1960s demonstrated that the risk depends on cumulated exposure in terms of working level months (WLM) integrating both duration of exposure and concentration of radon. It has been also demonstrated that the risk from radon decreases with time since exposure. The present analysis of temporal changes of relative risk is based on a model where the total individual exposure is partitioned into components in dependence on time. Exposure to radon is studied in a cohort of 9411 Czech uranium miners with 766 cases of lung cancer and in a residential study of 11 803 inhabitants exposed to radon in houses with 218 cases. In addition, temporal patterns of the risk from smoking are analyzed in a case-control study of patients from a major Prague hospital including 566 cases. For both carcinogens, the relative risk decreases with time since exposure. The risk from exposures before 20-34 years is 36% and 34% in comparison to period 5-19 for smoking and radon, respectively. The effect of exposures from more distant periods 35-49 is only 5% for smoking and 14% for radon in comparison to 5-19 years. This substantial decrease of relative risk with time may contribute to a better evaluation of remediation measures taken in houses and in the cost effectiveness of remediation. Combined effect of smoking and radon is studied by a nested case-control approach including 434 cases and 962 controls. Analyses of the joint effects of smoking and radon, conducted in the occupational and the residential studies, suggest a sub-multiplicative interaction. The relative risk from radon among non-smokers is higher by a factor of 2-3 in comparison to smokers, suggesting different patterns of lung deposition and clearance among smokers and non-smokers. (author)

  17. Preventive effects of dexmedetomidine on the liver in a rat model of acid-induced acute lung injury.

    Science.gov (United States)

    Sen, Velat; Güzel, Abdulmenap; Şen, Hadice Selimoğlu; Ece, Aydın; Uluca, Unal; Söker, Sevda; Doğan, Erdal; Kaplan, İbrahim; Deveci, Engin

    2014-01-01

    The aim of this study was to examine whether dexmedetomidine improves acute liver injury in a rat model. Twenty-eight male Wistar albino rats weighing 300-350 g were allocated randomly to four groups. In group 1, normal saline (NS) was injected into the lungs and rats were allowed to breathe spontaneously. In group 2, rats received standard ventilation (SV) in addition to NS. In group 3, hydrochloric acid was injected into the lungs and rats received SV. In group 4, rats received SV and 100 µg/kg intraperitoneal dexmedetomidine before intratracheal HCl instillation. Blood samples and liver tissue specimens were examined by biochemical, histopathological, and immunohistochemical methods. Acute lung injury (ALI) was found to be associated with increased malondialdehyde (MDA), total oxidant activity (TOA), oxidative stress index (OSI), and decreased total antioxidant capacity (TAC). Significantly decreased MDA, TOA, and OSI levels and significantly increased TAC levels were found with dexmedetomidine injection in group 4 (P < 0.05). The highest histologic injury scores were detected in group 3. Enhanced hepatic vascular endothelial growth factor (VEGF) expression and reduced CD68 expression were found in dexmedetomidine group compared with the group 3. In conclusion, the presented data provide the first evidence that dexmedetomidine has a protective effect on experimental liver injury induced by ALI.

  18. Effects of puerarin combined with edaravone on inhalation lung injury induced by black gunpowder smog in rats

    Directory of Open Access Journals (Sweden)

    Zheng-guan WANG

    2015-04-01

    Full Text Available Objective To explore the protective effects of puerarin combined with edaravone on inhalation lung injury induced by black gunpowder smog in rats. Methods Forty healthy male Wistar rats were randomly divided into normal control group (group N, inhalation group (group X, puerarin group (group P, edaravone group (group E and edaravone combined with puerarin group (group L, with 8 rats in each group. Rat model of inhalation lung injury was reproduced by a self-made smoke generator. Rats in group E were given intraperitoneal injections of edaravone (9 mg/kg at 30 minutes and 1 day after modeling (twice totally. Rats in group P were given intraperitoneal injections of puerarin (100 mg/kg at 30 minutes and 1, 2, 3, 4, 5 days after modeling (6 times totally. Rats in group L were treated the way of both group E and P. The rats in group N and group X were given intraperitoneal injections of normal saline (12 ml/kg at the time-points above. The animals were sacrificed 6 days after modeling, and the blood samples were collected from abdominal aorta to assess arterial blood gas values, meanwhile the serum levels of tumor necrosis factor-α (TNF-α, interleukin-6 (IL-6, interleukin-10 (IL-10 were determined by ELISA. Lung tissue homogenates were prepared to determine the protein content and myeloperoxidase (MPO activity. The pathological changes in the lung tissue with HE staining were observed under light microscope. Results Arterial blood gas analysis revealed that the PaO2 levels in groups P, E and L were higher than that in group X (P<0.05, and the PaO2 levels in groups E and L were higher than that in group P (P<0.05, while the PaCO2 level in group L was lower than that in groups X and E (P<0.05. The TNF-α, IL-6 and IL-10 levels in serum, the protein content and MPO activity in lung tissue homogenate in groups P, E and L were lower than those of group X (P<0.05. The TNF-α and IL-6 levels in serum and protein content and MPO activity in lung

  19. The value of 99Tcm-HSA in monitoring acute lung injury induced by lipopolysaccharide in rats

    International Nuclear Information System (INIS)

    Fu Zhanli; Zhang Chunli; Wang Rongfu; Zhang Shengsuo; Xue Yun

    2005-01-01

    To evaluate the value of 99 Tc m labeled human serum albumin ( 99 Tc m -HSA) in monitoring acute lung injury (ALI) induced by lipopolysaccharide (LPS) in rats, twenty adult Wistar rats are given 99 Tc m -HSA intravenously, and are randomly divided into four groups 30 min later. The control and LPS group are given intravenous injection of 0.9% saline and LPS 8 mg/kg respectively. The ketamine and aminoguanidine group are given intraperitoneal injection of ketamine 4 mg/kg and aminoguanidine 20 mg/kg respectively just 30 min after administration of LPS 8 mg/kg. All of the four group rats are killed by blood letting at 3 h post-injection of 99 Tc m -HSA. Pulmonary permeability index (PPI) and the ratio of lung wet weight and dry weight (W/D) is calculated. The results of PPI and W/D in control and LPS group are 95.58 ± 11.32 and 5.38 ± 0.24, 6.61 ± 0.18 and 4.19 ± 0.11, respectively. The PPI and W/D in LPS group are much higher than that in the control group (P 0.05). So 99 tc m -HSA is an effective tracer in monitoring ALI induced by LPS in rats. (authors)

  20. Air pollution, environmental tobacco smoke, radon, and lung cancer

    International Nuclear Information System (INIS)

    Crawford, W.A.

    1988-01-01

    The health of populations in industrialized societies has been affected for many years by ambient air pollutants presenting a threat of chronic bronchitis and lung cancer. In the 1980s indoor pollutants received much needed investigation to assess their hazards to health. Exposure to environmental tobacco smoke and radon is now the subject of much research and concern. This review attempts to put some perspective on lung cancer that is attributable to lifetime exposure to airborne pollutants. The view is expressed that air pollution control authorities have played and are playing a major role in health improvement

  1. Lung dosimetry for inhaled radon progeny

    International Nuclear Information System (INIS)

    Hofmann, W.

    1986-01-01

    Lung cancer risk assessment for inhaled radon progeny requires a detailed knowledge of the dose distribution pattern throughout the human respiratory tract. Current lung dosimetry models take into acocunt aerosol deposition in a formalized airway structrue, modification of the initial deposition pattern by clearance mechanisms, and the energy deposited by alpha particles in sensitive cells of the bronchial epithelium. The resulting dose distribution pattern depends on the characteristics of the inhaled aerosol and the breathing pattern. Special emphasis has been laid on the age dependency of the anatomical structure of the human lung and the resulting doses, as well as on the rediological significance of enhanced aerosol deposition at bronchial bifuraction. The biological variability inherent in all morphometric, physiological and histological parameters involved in lung dosimetry suggests the application of stochastic modelling techniques. Examples for the use of Monte Carlo methods presented here are the random walk of inhaled particles through a random airway geometry, and the influence of the intra-subject variability of radiation doses on radiation protection standards. At the cellular level the concept of absorbed dose loses its significance and has to be replaced by microdosimetric concepts, such as internal microdosimtry or track structure theory. An image-analysis model allows us to construct specific energy distributions in sensitive lung cells. Application of a track structure model of alpha particle interaction with bronchial epithelial cells permits the calculation of probabilities for inactivation, transformation, and tumor induction. The latter has been used to analyse lung cancer risk at low doses in Chinese high background areas

  2. Lung cancer risk, exposure to radon and tobacco consumption in a nested case-control study of French uranium miners

    International Nuclear Information System (INIS)

    Leuraud, K.; Billon, S.; Bergot, D.; Tirmarche, M.; Laurier, D.; Caer, S.; Quesne, B.

    2006-01-01

    tobacco effect, the estimated lung cancer risk coefficient obtained for radon exposure is close to that obtained from the French miners cohort and coherent with results from other miners cohorts. As the information came from three different sources, complementary analyses are necessary to investigate a possible induced bias. Nevertheless, some limiting features of the study have to be underlined: the categorization of smoking status in only two levels, the moderate percentage of missing data and the low number of never smoker cases (only 6 never smokers among cases), which limit the statistical power of further analyses. In the framework of a European project on the quantification of risks associated with multiple radiation exposures named Alpha-Risk, a collaborative work including these data and large data sets from German and Czech partners should allow a more powerful analysis of radon exposure and tobacco consumption effects on lung cancer risk among uranium miners. (authors)

  3. Lung cancer from radon and smoking: a multistage model for the WISMUT uranium miners

    International Nuclear Information System (INIS)

    Dillen, Teun van; Bijwaard, Harmen; Schnelzer, Maria; Kreuzer, Michaela; Grosche, Bernd

    2008-01-01

    Full text: In the world's third-largest uranium-mining province located in areas of Saxony and Thuringia in the former German Democratic Republic, the WISMUT Company conducted extensive uranium mining starting in 1946. Up to 1990, when mining activities were discontinued, most of the 400,000 employees had been exposed to uranium ore dust and radon and its progeny. It is well established that, besides smoking, such exposures are associated with an increased risk of lung cancer. From about 130,000 known miners a huge cohort of 59,000 miners has been formed and in an epidemiological analysis lung cancer risks have been evaluated (Grosche et al., 2006). We will present an alternative approach using a biologically-based multistage carcinogenesis model quantifying the lung-cancer risk related to both the exposure to radon and smoking habits. This mechanistic technique allows for extrapolation to the low exposures that are important for present-day radiation protection purposes and the transfer of risk across populations. The model is applied to a sub-cohort of about 35,000 persons who were employed at WISMUT after 1955, with known annual exposures estimated from the job-exposure matrix (Lehmann et al., 2004). Unfortunately, detailed information on smoking is missing for most miners. However, this information has been retrieved in two case-control studies, one of which was nested in the cohort while the other was not (Brueske-Hohlfeld et al., 2006). For these studies, the relevant smoking parameters are assembled in so-called smoking spectra that are next projected onto the entire cohort using a Monte-Carlo sampling method. Individual smoking habits that are randomly assigned to the cohort members, together with the information on annual exposure to radon, is used as an input for the multistage model. Model parameters related to radon and tobacco exposure are fitted with a maximum-likelihood technique. We will show results of the observed and expected lung

  4. Risk of lung cancer by radon, disagreement in international regulation

    International Nuclear Information System (INIS)

    Balcazar, M.; Pena, P.; Villamares, A.; Avelar, J. R.

    2013-10-01

    Diverse international organizations have evaluated the risk of lung cancer starting from epidemic studies in miners of uranium mines, where the corresponding effective dose was determined relating with the dose received by the population during Hiroshima and Nagasaki events. Alternately, the equivalent dose has been calculated by means of based models on the energy deposited by the breathable radon fractions and its decay products in the breathing ducts. A unique factor agreed by the diverse organizations that allows converting radon concentration to effective dose does not exist. Neither an agreement exists among the different countries on which duty to be the value of the maximum concentration of radon, in interiors starting from which an intervention is required and if this intervention is standardized, recommended or nonexistent. In this work study cases in Mexico are presented and their interpretation alternative based on the international agreements absence. (Author)

  5. Creation of lung-targeted dexamethasone immunoliposome and its therapeutic effect on bleomycin-induced lung injury in rats.

    Directory of Open Access Journals (Sweden)

    Xue-Yuan Chen

    Full Text Available OBJECTIVE: Acute lung injury (ALI, is a major cause of morbidity and mortality, which is routinely treated with the administration of systemic glucocorticoids. The current study investigated the distribution and therapeutic effect of a dexamethasone(DXM-loaded immunoliposome (NLP functionalized with pulmonary surfactant protein A (SP-A antibody (SPA-DXM-NLP in an animal model. METHODS: DXM-NLP was prepared using film dispersion combined with extrusion techniques. SP-A antibody was used as the lung targeting agent. Tissue distribution of SPA-DXM-NLP was investigated in liver, spleen, kidney and lung tissue. The efficacy of SPA-DXM-NLP against lung injury was assessed in a rat model of bleomycin-induced acute lung injury. RESULTS: The SPA-DXM-NLP complex was successfully synthesized and the particles were stable at 4°C. Pulmonary dexamethasone levels were 40 times higher with SPA-DXM-NLP than conventional dexamethasone injection. Administration of SPA-DXM-NLP significantly attenuated lung injury and inflammation, decreased incidence of infection, and increased survival in animal models. CONCLUSIONS: The administration of SPA-DXM-NLP to animal models resulted in increased levels of DXM in the lungs, indicating active targeting. The efficacy against ALI of the immunoliposomes was shown to be superior to conventional dexamethasone administration. These results demonstrate the potential of actively targeted glucocorticoid therapy in the treatment of lung disease in clinical practice.

  6. Evaluation of radon induced lung cancer risk in occupants of the old and new dwellings of the Dera Ismail Khan City, Pakistan

    International Nuclear Information System (INIS)

    Tabassum Nasir; Muhammad Khalil; Naveed Anwar; Matiullah; Muhammad Rafique; Saeed Ur Rahman

    2014-01-01

    In order to carry out indoor radon measurement in new and old buildings of the Dera Ismail Khan city, CR-39 based radon detectors were installed in bed rooms and sitting rooms/TV lounges in 25 (each) old and new houses and were exposed to indoor radon for 90 days. After processing, mean weighted average indoor radon concentrations in old and new houses were found to be 275 ± 33 and 86 ± 18 Bq m -3 whereas mean annual effective doses expected to be received by the occupants were 6.86 ± 0.79 and 2.1 ± 0.43 mSv year -1 , respectively. From the measured weighted average indoor radon concentration, excess relative risk factor was calculated using the risk model of BEIR VI for the age group of 35 and 55 years. Average excess lung cancer risk was found to be 1.63 ± 0.19 and 1.35 ± 0.16 and 0.5 ± 0.10 and 0.4 ± 0.08 for old and new houses, respectively. (author)

  7. Evaluation of radon induced lung cancer risk in occupants of the old and new dwellings of the Dera Ismail Khan City, Pakistan

    Energy Technology Data Exchange (ETDEWEB)

    Nasir, Tabassum; Khalil, Muhammad; Anwar, Naveed [Gomal University, Dera Ismail Khan (Pakistan). Department of Physics; Matiullah, [PINSTECH, Islamabad (Pakistan). Directorate of Systems and Services; Rafique, Muhammad [University of Azad Jammu and Kashmir, Azad Kashmir (Pakistan). Department of Physics; Rahman, Saeed Ur [Nuclear Medicine, Oncology and Radiotherapy Institute, Islamabad (Pakistan). Department of Medical Physics

    2014-06-15

    In order to carry out indoor radon measurement in new and old buildings of the Dera Ismail Khan city, CR-39 based radon detectors were installed in bed rooms and sitting rooms/TV lounges in 25 (each) old and new houses and were exposed to indoor radon for 90 days. After processing, mean weighted average indoor radon concentrations in old and new houses were found to be 275 ± 33 and 86 ± 18 Bq m{sup -3} whereas mean annual effective doses expected to be received by the occupants were 6.86 ± 0.79 and 2.1 ± 0.43 mSv year{sup -1}, respectively. From the measured weighted average indoor radon concentration, excess relative risk factor was calculated using the risk model of BEIR VI for the age group of 35 and 55 years. Average excess lung cancer risk was found to be 1.63 ± 0.19 and 1.35 ± 0.16 and 0.5 ± 0.10 and 0.4 ± 0.08 for old and new houses, respectively. (author)

  8. Angiotensin-(1?7) inhibits inflammation and oxidative stress to relieve lung injury induced by chronic intermittent hypoxia in rats

    OpenAIRE

    Lu, W.; Kang, J.; Hu, K.; Tang, S.; Zhou, X.; Yu, S.; Li, Y.; Xu, L.

    2016-01-01

    Obstructive sleep apnea is associated with inflammation and oxidative stress in lung tissues and can lead to metabolic abnormalities. We investigated the effects of angiotensin1–7 [Ang-(1–7)] on lung injury in rats induced by chronic intermittent hypoxia (CIH). We randomly assigned 32 male Sprague-Dawley rats (180–200 g) to normoxia control (NC), CIH-untreated (uCIH), Ang-(1–7)-treated normoxia control (N-A), and Ang-(1–7)-treated CIH (CIH-A) groups. Oxidative stress biomarkers were measured ...

  9. Risk assessment of exposure to radon decay products

    Energy Technology Data Exchange (ETDEWEB)

    Monchaux, G

    1999-07-01

    The aim of this project was to assess the risk due to inhalation of radon and its decay products using an horizontal approach across a large scale research programme. The central objective was the assessment of human risk which requires combination of several topics involving a multidisciplinary approach. In the Aerosol Studies Group, progress was achieved in improvement, calibration and automation of experimental techniques for continuous and integrated measurements of the unattached fraction f{sub p}- and equilibrium factor F- values. Measurements were performed to determine the variation of size distributions of unattached and aerosol-associated radon decay products under typical living conditions. All aerosol groups performed controlled chamber studies to understand the basic behaviour of airborne activity concentrations. Measurements were performed to determine neutralisation rates of {sup 218}Po, to understand the cluster growth with residence time and to understand the hygroscopic growth of aerosol particles. In the Modelling Group, the programme RADEP has been developed to calculate the weighted committed equivalent lung dose per unit exposure of radon progeny (H{sub w}/P{sub p}) which implements the ICRP Publication 66 Human Respiratory Tract Model (HRTM). The stochastic deposition model (IDEAL) has been compared with the deposition model used by the HRTM, and the agreement between the two deposition models was excellent. A deterministic radon progeny dosimetry model (RADOS) has been developed. This model includes all bronchial airway generations compared with the HRTM that groups the 16 airway generations into three regions. Initial calculations with RADOS show that the basal and secretory cell doses are slightly smaller compared with that of the HRTM. A sensitivity analysis has been performed that has identified those HRTM model parameters that most affect the Hw/Pp. A stochastic rat deposition model (RALMO) and a clearance model for the rat based on the

  10. Risk assessment of exposure to radon decay products

    International Nuclear Information System (INIS)

    Monchaux, G.

    1999-01-01

    The aim of this project was to assess the risk due to inhalation of radon and its decay products using an horizontal approach across a large scale research programme. The central objective was the assessment of human risk which requires combination of several topics involving a multidisciplinary approach. In the Aerosol Studies Group, progress was achieved in improvement, calibration and automation of experimental techniques for continuous and integrated measurements of the unattached fraction f p - and equilibrium factor F- values. Measurements were performed to determine the variation of size distributions of unattached and aerosol-associated radon decay products under typical living conditions. All aerosol groups performed controlled chamber studies to understand the basic behaviour of airborne activity concentrations. Measurements were performed to determine neutralisation rates of 218 Po, to understand the cluster growth with residence time and to understand the hygroscopic growth of aerosol particles. In the Modelling Group, the programme RADEP has been developed to calculate the weighted committed equivalent lung dose per unit exposure of radon progeny (H w /P p ) which implements the ICRP Publication 66 Human Respiratory Tract Model (HRTM). The stochastic deposition model (IDEAL) has been compared with the deposition model used by the HRTM, and the agreement between the two deposition models was excellent. A deterministic radon progeny dosimetry model (RADOS) has been developed. This model includes all bronchial airway generations compared with the HRTM that groups the 16 airway generations into three regions. Initial calculations with RADOS show that the basal and secretory cell doses are slightly smaller compared with that of the HRTM. A sensitivity analysis has been performed that has identified those HRTM model parameters that most affect the Hw/Pp. A stochastic rat deposition model (RALMO) and a clearance model for the rat based on the HRTM have been

  11. Reply to 'Explaining the lung cancer versus radon exposure data for USA counties'

    International Nuclear Information System (INIS)

    Darby, S.; Doll, R.

    2000-01-01

    Full text: Professor Cohen states in his letter that his analysis 'encompasses all of the Doll suggestions'. It is, however, logically impossible for it to have done so using data at the level of counties. This is because the effect of cigarette smoking on the relationship between residential radon and individual lung cancer risk will be determined by the relationship between smoking status and lung cancer among the individuals within each county. Unless smoking is irrelevant to lung cancer risk (which we know to be untrue) or smoking status and residential radon are uncorrelated within each county (which seems unlikely), the relationship between residential radon and lung cancer at the county level will differ from that at the level of the individual in a way that cannot be overcome by including corrections for smoking habits at the county level, even if these corrections correctly represent the smoking habits of the individuals within each county. The difference in the relationship between a risk factor and a disease rate at the level of the individual and at an area level is the ecologic fallacy and is described in detail by Greenland and Robins (1994) and Morgenstern (1998). Lubin (1998) has also demonstrated that biases caused by the ecologic fallacy can be of any magnitude from minus infinity to plus infinity. In two recent studies (Lagarde and Pershagen 1999, Darby et al 2000), parallel individual and ecological analyses have been carried out of identical data from case-control studies of residential radon (Peshagen et al 1994, Darby et al 1998). These analyses have shown that, in addition to any bias caused by the ecological fallacy, ecological studies of residential radon and lung cancer are also prone to biases caused by determinants of lung cancer risk that vary at the level of the ecological unit concerned. In these two examples, the additional variables were latitude and urban/rural status respectively. The explanation of these variables is not yet

  12. Analysis of radon-induced lung cancer risk by a stochastic state-vector model of radiation carcinogenesis

    International Nuclear Information System (INIS)

    Crawford-Brown, Douglas J.; Hofmann, Werner

    2002-01-01

    A biologically based state-vector model (SVM) of radiation carcinogenesis has been extended to incorporate stochasticity of cellular transitions and specific in vivo irradiation conditions in the lungs. Dose-rate-dependent cellular transitions related to the formation of double-stranded DNA breaks, repair of breaks, interactions (translocations) between breaks, fixation of breaks, cellular inactivation, stimulated mitosis and promotion through loss of intercellular communication are simulated by Monte Carlo methods. The stochastic SVM has been applied to the analysis of lung cancer incidence in uranium miners exposed to alpha-emitting radon progeny. When incorporating in vivo features of cell differentiation, stimulated cell division and heterogeneity of cellular doses into the model, excellent agreement between epidemiological data and modelling results could be obtained. At low doses, the model predicts a non-linear dose-response relationship; e.g., computed lung cancer risk at 20 WLM is about half of current lung cancer estimates based on the linear hypothesis. The model also predicts a slight dose rate effect; e.g., at a cumulative exposure of 20 WLM, calculated lung cancer incidence for an exposure rate 0.27 WLM/year (assuming an exposure time of 73 years) is smaller by a factor of 1.2 than that for an exposure rate of 10 WLM/year. (author)

  13. Concentrations of indoor radon and thoron in cave-dwellings with discussions on risk estimation of lung cancer

    International Nuclear Information System (INIS)

    Sun Quanfu; Hou Changsong; Zhang Shouzhi; Nie Xiaoqian; Shang Bing

    2005-01-01

    Objective: To explore a residential area with elevated indoor radon exposure for conducting epidemiological studies on indoor radon and lung cancer. Methods: Two hundred and two cave-dwellings (CD) including loess CD, brick CD, stone CD, and ordinary house in twenty villages were selected from Yan'an and Lvliang in the Chinese loess plateau. Indoor levels of thoron and its progeny as well as radon were measured with passive radon-thoron discriminative detectors and thoron progeny deposition rate devices. The exposure period covered from August 2001 through August 2002. Results: Loess CD was one of the most common type of dwelling caves in both areas. The indoor radon concentrations in loess CD ranged from 17 to 179 Bq/m 3 ; thoron varied sub-stantially depending upon the distance from the device to the wall, ranged from 10 to 760 Bq/m 3 . Geometric means of indoor radon, thoron and thoron's progeny (EEC Tn ) of loess caves in Yan'an area were estimated to be 71, 185 and 2.2 Bq/m 3 , respectively, and the corresponding figures were 73, 145 and 116 Bq/m 3 in Lvliang area. Possible contamination of thoron on radon measurement in a previous case-control study on lung caner was discussed. The study revealed that the indoor air pollution in Yan'an area was slight compared with that in Lvliang area. Migration was very low. Eighty-six percent of the investigated persons have had no migration in Yan'an area, and 90 percent of the cave-dwellings where the subjects once resided were available to our measurements. Two million people have been living in cave-dwellings over several generations. Conclusion: The investigated cave-dwelling area in Yan'an is suitable for conducting epidemiological study on residential thoron and radon exposure and lung cancer.(authors)

  14. Preventive Effects of Dexmedetomidine on the Liver in a Rat Model of Acid-Induced Acute Lung Injury

    Directory of Open Access Journals (Sweden)

    Velat Şen

    2014-01-01

    Full Text Available The aim of this study was to examine whether dexmedetomidine improves acute liver injury in a rat model. Twenty-eight male Wistar albino rats weighing 300–350 g were allocated randomly to four groups. In group 1, normal saline (NS was injected into the lungs and rats were allowed to breathe spontaneously. In group 2, rats received standard ventilation (SV in addition to NS. In group 3, hydrochloric acid was injected into the lungs and rats received SV. In group 4, rats received SV and 100 µg/kg intraperitoneal dexmedetomidine before intratracheal HCl instillation. Blood samples and liver tissue specimens were examined by biochemical, histopathological, and immunohistochemical methods. Acute lung injury (ALI was found to be associated with increased malondialdehyde (MDA, total oxidant activity (TOA, oxidative stress index (OSI, and decreased total antioxidant capacity (TAC. Significantly decreased MDA, TOA, and OSI levels and significantly increased TAC levels were found with dexmedetomidine injection in group 4 (P<0.05. The highest histologic injury scores were detected in group 3. Enhanced hepatic vascular endothelial growth factor (VEGF expression and reduced CD68 expression were found in dexmedetomidine group compared with the group 3. In conclusion, the presented data provide the first evidence that dexmedetomidine has a protective effect on experimental liver injury induced by ALI.

  15. Isoproterenol attenuates high vascular pressure-induced permeability increases in isolated rat lungs.

    Science.gov (United States)

    Parker, J C; Ivey, C L

    1997-12-01

    To separate the contributions of cellular and basement membrane components of the alveolar capillary barrier to the increased microvascular permeability induced by high pulmonary venous pressures (Ppv), we subjected isolated rat lungs to increases in Ppv, which increased capillary filtration coefficient (Kfc) without significant hemorrhage (31 cmH2O) and with obvious extravasation of red blood cells (43 cmH2O). Isoproterenol (20 microM) was infused in one group (Iso) to identify a reversible cellular component of injury, and residual blood volumes were measured to assess extravasation of red blood cells through ruptured basement membranes. In untreated lungs (High Ppv group), Kfc increased 6.2 +/- 1.3 and 38.3 +/- 15.2 times baseline during the 31 and 43 cmH2O Ppv states. In Iso lungs, Kfc was 36.2% (P Kfc increases at moderate Ppv, possibly because of an endothelial effect, but it did not affect red cell extravasation at higher vascular pressures.

  16. Lowering the UK domestic radon action level to reduce radiation-induced lung cancer in general population: when and where is it cost effective?

    International Nuclear Information System (INIS)

    Denman, A.R.; Phillips, P.S.

    2008-01-01

    Case studies have shown that radon gas can be present within domestic properties at sufficiently high levels that it can significantly increase the risk of lung cancer in occupants. Recently, Darby et al. (2006) have shown that this risk exists at radon concentrations as low as 100 Bq·m -3 , which is below the UK domestic Action Level of 200 Bq·m -3 . As a result, there have been suggestions that national domestic Action Levels should be reduced. This paper considers the benefits and costs of the domestic radon remediation programmes in the UK, when a range of Action Levels from 125 Bq·m -3 to 600 Bq·m -3 are applied. The variations of total cost, cost-effectiveness, dose reduction and lung cancers saved for each proposed action level, and the proportion of houses over the proposed action level, were estimated. The study shows that, for an Action Level above 200 Bq·m -3 , a completed domestic radon remediation programme in Northamptonshire, where 6.3% of existing houses have initial radon levels over 200 Bq·m -3 , will cost less and will target those most at risk, but will be less cost effective. In addition, a higher Action Level leaves a higher residual dose and greater risk of cancer in the population living in unremediated homes. Reducing the Action Level below 200 Bq·m -3 will prevent more cancers, but at significantly higher cost. It will be less cost-effective, because a significant number of houses with moderate radon levels will be remediated with modest health benefit to occupants. The study suggests that a completed radon remediation programme is most cost-effective with an action level of around 250 to 300 Bq·m -3 . The finding appears to be independent of the percentage of houses over the Action Level. This has clear implications for future health policy. (author)

  17. Radon in coal power plant areas

    International Nuclear Information System (INIS)

    Mauna, Traian; Mauna, Andriesica

    2006-01-01

    Radon, the radioactive colourless and inodorous noble gas, represents more than 55% of the natural average radioactivity. It is permanently released from the soil and majority of building materials, it builds up in the mine galleries, in dwelling houses and in other closed rooms. Radon gained increasingly in importance, particularly after 1990 when was doubtless identified as the second cause of lung cancer if a given concentration threshold is surpassed. This threshold is established differentially by each country as a function of the particular site and generally ranges between 150 Bq.m -3 and 600 Bq.m -3 . The telluric radon consists of two isotopes, 222 Rn, a daughter of radium descending from uranium, which induces 90% of the effects, and 220 Rn from thorium series which have too short a lifetime to count in the risk assessments of radon inhalation. The interest of the authorities and population for diminishing the radon effects was illustrated by specific studies which in USA were managed by the National Counsel of Research, the BEIR VI committee of which has issued a report concerning the lung cancer produced by radon and its descendants. Coal mining, the transport, processing, burning, slag and ash disposal are activities entailing radon release. The miners' dwellings are placed in areas with the high radon potential. The local building materials have a high content of radioactive elements from the uranium or thorium series so that radon can build up in the closed rooms of these buildings. Hence the social responsible authorities in the coal power industry zones should consider this aspect long time ignored in the Balkans macro zone so far. The radon issue must be differentially approached in different areas hence a zonal mapping of the radon emission should be first done. It is worth to underline that the gaseous radioactive emission from operational nuclear power plants amounts up to a few percents of the radon natural emissions what entails a

  18. Protective Effects of Alpha-Lipoic Acid on Oleic Acid-Induced Acute Lung Injury in Rats

    Directory of Open Access Journals (Sweden)

    Funda Gülcü Bulmuş

    2013-09-01

    Full Text Available Background: Oxidative stress is believed to be an important factor in the pathogenesis of acute lung injury (ALI. Aims: The aim of this study was to investigate the possible protective role of alpha-lipoic acid (α-LA on oleic acid (OA-induced ALI in rats. Study Design: Animal experiment. Methods: A total of thirty-five rats were divided into five groups in the study. Group 1 served as a control group. Rats in Group 2 (α-LA were administered α-LA intraperitoneally at a dose of 100 mg/kg body weight (BW. Rats in Group 3 (OA were administered OA intravenously at a dose of 100 mg/kg BW. In Group 4 (pre-OA-α-LA, α-LA was given 15 minutes prior to OA infusion, and in Group 5 (post-OA-α-LA, α-LA was given two hours after OA infusion. Four hours after the OA infusion, rats were decapitated. Blood samples were collected to measure serum levels of malondialdehyde (MDA and glutathione (GSH, and the levels of activity for superoxide dismutase (SOD, catalase (CAT and glutathione peroxidase (GSH-Px. Lung tissue samples were taken for histopathological examination. Results: Exposure to OA resulted in increases in serum MDA levels (p<0.001, as well as histopathological lesions in lung tissue, and decreases in CAT (p<0.05, GSH-Px (p<0.05 activities and GSH (p<0.05 levels. On the other hand, MDA levels were decreased significantly (p<0.001, while CAT (p<0.05, GSH-Px (p<0.01 activities and GSH (p<0.05 levels were increased significantly in the pre-OA-α-LA group compared with the OA group. Conclusion: α-LA was found to lessen oxidative stress and to have positive effects on antioxidants in cases of OA-induced ALI. In conclusion, α-LA appears to have protective effects against ALI and potential for the prevention of ALI.

  19. Radon and energy efficient homes

    International Nuclear Information System (INIS)

    Burkart, W.

    1981-09-01

    Radon and its daughters in indoor air are presently responsible for dose equivalents of about 31 mSv/year (3 rem/year) to parts of the respiratory tract. Linear extrapolation from the dose response values of uranium miners heavily exposed to radon and its decay products would suggest that almost all lung cancers in the non-smoking population are caused by environmental 222 Rn. Using epidemiological data on the types of lung cancer found in non-smokers of the general public as compared to the miners, a smaller effect of low level radon exposure is assumed, which would result in a lung cancer mortality rate due to radon of about 10 deaths per year and million or 25% of the non-smoker rate. Higher indoor radon concentrations in energy efficient homes mostly caused by reduced air exchange rates will lead to a several fold increase of the lung cancer incidence from radon. Based on the above assumption, about 100 additional lung cancer deaths/year-million will result both from an increase in radionuclide concentrations in indoor air and a concomitant rise in effectiveness of radiation to cause cancer with higher exposure levels. Possibilities to reduce indoor radon levels in existing buildings and costs involved are discussed. (Auth.)

  20. Radon Research Program, FY 1992

    International Nuclear Information System (INIS)

    1993-04-01

    The United States Department of Energy, Office of Health and Environmental Research (DOE/OHER) is the principal federal agency conducting basic research related to indoor radon. The scientific information being sought in this program encompasses research designed to determine radon availability and transport outdoors, modeling transport into and within buildings, physics and chemistry of radon and radon progeny, dose response relationships, lung cancer risk, and mechanisms of radon carcinogenesis. There still remains a significant number of uncertainties in the currently available knowledge that is used to estimate lung cancer risk from exposure to environmental levels of radon and its progeny. The main goal of the DOE/OHER Radon Research Program is to develop information to reduce these uncertainties and thereby provide an improved health risk estimate of exposure to radon and its progeny and to identify and understand biological mechanisms of lung cancer development and required copollutants at low levels of exposure. Information useful in radon control strategies is also provided by the basic science undertaken in this program

  1. Indoor radon

    International Nuclear Information System (INIS)

    1997-12-01

    The radon, a natural radioactive gas, is present almost everywhere on the earth's surface. It can be accumulated at high concentration in confined spaces (buildings, mines, etc). In the last decades many studies conducted in several countries showed that inhaling important amounts of radon rises the risk of lung cancer. Although, the radon is a naturally appearing radioactive source, it may be the subject of a human 'enhancement' of concentration. The increasing radon concentration in professional housing constitutes an example of enhanced natural radioactivity which can induce health risks on workers and public. Besides, the radon is present in the dwelling houses (the domestic radon). On 13 May 1996, the European Union Council issued the new EURATOM Instruction that establishes the basic standards of health protection of population and workers against the ionizing radiation hazards (Instruction 96/29/EURATOM, JOCE L-159 of 29 June 1996). This instruction does not apply to domestic radon but it is taken into consideration by another EURATOM document: the recommendation of the Commission 90/143/EURATOM of 21 February 1990 (JOCE L-80 of 27 March 1990). The present paper aims at establishing in accordance to European Union provisions the guidelines for radon risk management in working places, as well as in dwelling houses, where the implied risk is taken into account. This document does not deal with cases of high radon concentration on sites where fabrication, handling or storage of radium sources take place. These situations must be treated by special studies

  2. Experimental chronic kidney disease attenuates ischemia-reperfusion injury in an ex vivo rat lung model.

    Directory of Open Access Journals (Sweden)

    Chung-Kan Peng

    Full Text Available Lung ischemia reperfusion injury (LIRI is one of important complications following lung transplant and cardiopulmonary bypass. Although patients on hemodialysis are still excluded as lung transplant donors because of the possible effects of renal failure on the lungs, increased organ demand has led us to evaluate the influence of chronic kidney disease (CKD on LIRI. A CKD model was induced by feeding Sprague-Dawley rats an adenine-rich (0.75% diet for 2, 4 and 6 weeks, and an isolated rat lung in situ model was used to evaluate ischemia reperfusion (IR-induced acute lung injury. The clinicopathological parameters of LIRI, including pulmonary edema, lipid peroxidation, histopathological changes, immunohistochemistry changes, chemokine CXCL1, inducible nitric oxide synthase (iNOS, proinflammatory and anti-inflammatory cytokines, heat shock protein expression, and nuclear factor-κB (NF-κB activation were determined. Our results indicated that adenine-fed rats developed CKD as characterized by increased blood urea nitrogen and creatinine levels and the deposition of crystals in the renal tubules and interstitium. IR induced a significant increase in the pulmonary arterial pressure, lung edema, lung injury scores, the expression of CXCL1 mRNA, iNOS level, and protein concentration of the bronchial alveolar lavage fluid (BALF. The tumor necrosis factor-α levels in the BALF and perfusate; the interleukin-10 level in the perfusate; and the malondialdehyde levels in the lung tissue and perfusate were also significantly increased by LIRI. Counterintuitively, adenine-induced CKD significantly attenuated the severity of lung injury induced by IR. CKD rats exhibited increased heat shock protein 70 expression and decreased activation of NF-κB signaling. In conclusion, adenine-induced CKD attenuated LIRI by inhibiting the NF-κB pathway.

  3. Pistacia chinensis: A Potent Ameliorator of CCl4 Induced Lung and Thyroid Toxicity in Rat Model

    Directory of Open Access Journals (Sweden)

    Kiran Naz

    2014-01-01

    Full Text Available In the current study protective effect of ethanol extract of Pistacia chinensis bark (PCEB was investigated in rats against CCl4 induced lung and thyroid injuries. PCEB dose dependently inhibited the rise of thiobarbituric acid-reactive substances, hydrogen peroxide, nitrite, and protein content and restored the levels of antioxidant enzymes, that is, catalase, peroxidase, superoxide dismutase, glutathione-S-transferase, glutathione reductase, glutathione peroxidase, γ-glutamyl transpeptidase, and quinone reductase in both lung and thyroid tissues of CCl4 treated rats. Decrease in number of leukocytes, neutrophils, and hemoglobin and T3 and T4 content as well as increase in monocytes, eosinophils, and lymphocytes count with CCl4 were restored to normal level with PCEB treatment. Histological study of CCl4 treated rats showed various lung injuries like rupture of alveolar walls and bronchioles, aggregation of fibroblasts, and disorganized Clara cells. Similarly, histology of CCl4 treated thyroid tissues displayed damaged thyroid follicles, hypertrophy, and colloidal depletion. However, PCEB exhibited protective behaviour for lungs and thyroid, with improved histological structure in a dose dependant manner. Presence of three known phenolic compounds, that is, rutin, tannin, and gallic acid, and three unknown compounds was verified in thin layer chromatographic assessment of PCEB. In conclusion, P. chinensis exhibited antioxidant activity by the presence of free radical quenching constituents.

  4. Relation between radiation-induced whole lung functional loss and regional structural changes in partial irradiated rat lung

    International Nuclear Information System (INIS)

    Luijk, Peter van; Novakova-Jiresova, Alena; Faber, Hette; Steneker, Marloes N.J.; Kampinga, Harm H.; Meertens, Haarm; Coppes, Robert P.

    2006-01-01

    Purpose: Radiation-induced pulmonary toxicity is characterized by dose, region, and time-dependent severe changes in lung morphology and function. This study sought to determine the relation between the structural and functional changes in the irradiated rat lung at three different phases after irradiation. Materials and Methods: Six groups of animals were irradiated to 16-22 Gy to six different lung regions, each containing 50% of the total lung volume. Before and every 2 weeks after irradiation, the breathing rate (BR) was measured, and at Weeks 8, 26, and 38 CT was performed. From the computed tomography scans, the irradiated lung tissue was delineated using a computerized algorithm. A single quantitative measure for structural change was derived from changes of the mean and standard deviation of the density within the delineated lung. Subsequently, this was correlated with the BR in the corresponding phase. Results: In the mediastinal and apex region, the BR and computed tomography density changes did not correlate in any phase. After lateral irradiation, the density changes always correlated with the BR; however, in all other regions, the density changes only correlated significantly (r 2 = 0.46-0.85, p < 0.05) with the BR in Week 26. Conclusion: Changes in pulmonary function correlated with the structural changes in the absence of confounding heart irradiation

  5. Ischemia and reperfusion of the lung tissues induced increase of lung permeability and lung edema is attenuated by dimethylthiourea (PP69).

    Science.gov (United States)

    Chen, K H; Chao, D; Liu, C F; Chen, C F; Wang, D

    2010-04-01

    This study sought to determine whether oxygen radical scavengers of dimethylthiourea (DMTU), superoxide dismutase (SOD), or catalase (CAT) pretreatment attenuated ischemia-reperfusion (I/R)-induced lung injury. After isolation from a Sprague-Dawley rat, the lungs were perfused through the pulmonary artery cannula with rat whole blood diluted 1:1 with a physiological salt solution. An acute lung injury was induced by 10 minutes of hypoxia with 5% CO2-95% N2 followed by 65 minutes of ischemia and then 65 minutes of reperfusion. I/R significantly increased microvascular permeability as measured by the capillary filtration coefficient (Kfc), lung weight-to-body weight ratio (LW/BW), and protein concentration in bronchoalveolar lavage fluid (PCBAL). DMTU pretreatment significantly attenuated the acute lung injury. The capillary filtration coefficient (P<.01), LW/BW (P<.01) and PCBAL (P<.05) were significantly lower among the DMTU-treated rats than hosts pretreated with SOD or CAT. The possible mechanisms of the protective effect of DMTU in I/R-induced lung injury may relate to the permeability of the agent allowing it to scavenge intracellular hydroxyl radicals. However, whether superoxide dismutase or catalase antioxidants showed protective effects possibly due to their impermeability of the cell membrane not allowing scavenging of intracellular oxygen radicals. Copyright (c) 2010 Elsevier Inc. All rights reserved.

  6. Simulation model of lung cancer incidence related to smoking and radon daughter exposure

    International Nuclear Information System (INIS)

    Stolowijk, J.A.J.

    1990-01-01

    A mathematical model of lung cancer and radon daughter exposure is presented. It is aimed to provide a quantitative estimate in the form of dose-effect relationship. The nature of the cigarette smoking and radon exposure interaction it is shown to be a multiplicative or sub-multiplicative function rather than a simpler model in which the effect of the two exposures would be summed. The model was written in the SAS programming language. An annotated listing of the program is given. 4 refs

  7. Mechanistic study on lung cancer mortality after radon exposure in the Wismut cohort supports important role of clonal expansion in lung carcinogenesis

    Energy Technology Data Exchange (ETDEWEB)

    Zaballa, I.; Eidemueller, M. [Helmholtz Zentrum Muenchen, Institute of Radiation Protection, Neuherberg (Germany)

    2016-08-15

    Lung cancer mortality after radon exposure in the Wismut cohort was analyzed using the two-stage clonal expansion (TSCE) model. A total of 2996 lung cancer deaths among the 58,695 male workers were observed during the follow-up period between 1946 and 2003. Adjustment to silica exposure was performed to find a more accurate estimation of the risk of radon exposure. An additional analysis with the descriptive excess relative risk (ERR) model was carried out for comparison. The TSCE model that best describes the data is nonlinear in the clonal expansion with radon exposure and has a saturation level at an exposure rate of d{sub r} ≅ 100 WLM/yr. The excess relative risk decreases with age and shows an inverse exposure rate effect. In comparison with the ERR model, the TSCE model predicts a considerably larger risk for low exposures rates below 50 WLM/yr. Comparison to other mechanistic studies of lung cancer after exposure to alpha particles using the TSCE model reveals an extraordinary consistency in the main features of the exposure response, given the diversity in the characteristics of the cohorts and the exposure across different studies. This suggests that a nonlinear response mechanism in the clonal expansion, with some level of saturation at large exposure rates, may be playing a crucial role in the development of lung cancer after alpha particle irradiation. (orig.)

  8. Effects of repeated cycles of starvation and refeeding on lungs of growing rats.

    Science.gov (United States)

    Sahebjami, H; Domino, M

    1992-12-01

    Adult male rats were subjected to four cycles of mild starvation (2 wk) and refeeding (1 wk) and were compared with a fed group. Starvation was induced by giving rats one-third of their measured daily food consumption. During each starvation cycle, rats lost approximately 20% of their body weight. Despite catch-up growth and overall weight gain, starved rats had lower final body weight than fed rats. Lung dry weight and lung volumes were also reduced in the starved group. The mechanical properties of air- and saline-filled lungs did not change significantly with repeated cycles of starvation. Mean linear intercept was similar in the two groups, but alveolar surface area was reduced in the starved rats. Total content of crude connective tissue and concentration per lung dry weight of hydroxyproline and crude connective tissue were reduced in starved rats. We conclude that lung growth is retarded in growing rats subjected to repeated cycles of mild starvation and refeeding, as manifested by smaller lung volume and reduced alveolar surface area. Because alveolar size is unchanged, a reduced number of alveoli is most likely responsible for decreased lung volumes.

  9. Occupational exposure to radon for underground tourist routes in Poland: Doses to lung and the risk of developing lung cancer

    Directory of Open Access Journals (Sweden)

    Katarzyna Walczak

    2017-10-01

    Full Text Available Objectives: Radon concentrations for 31 Polish underground tourist routes were analyzed. The equivalent dose to the lung, the effective dose and the relative risk were calculated for employees of the analyzed routes on the grounds of information on radon concentrations, work time, etc. Material and Methods: The relative risk for lung cancers was calculated using the Biological Effects of Ionizing Radiation (BEIR VI Committee model. Equivalent doses to the lungs of workers were determined using the coefficients calculated by the Kendall and Smith. The conversion coefficient proposed by the International Atomic Energy Agency (IAEA in the report No. 33 was used for estimating the effective doses. Results: In 13 routes, the effective dose was found to be above 1 mSv/year, and in 3 routes, it exceeded 6 mSv/year. For 5 routes, the equivalent dose to lungs was higher than 100 mSv/year, and in 1 case it was as high as 490 mSv/year. In 22.6% of underground workplaces the risk of developing lung cancer among employees was about 2 times higher than that for the general population, and for 1 tourist route it was about 5 times higher. The geometric mean of the relative risk of lung cancer for all workers of underground tourist routes was 1.73 (95% confidence interval (CI: 1.6–1.87. Routes were divided into: caves, mines, post-military underground constructions and urban underground constructions. Conclusions: The difference between levels of the relative risk of developing lung cancer for all types of underground tourist routes was not found to be significant. If we include the professional group of the employees of underground tourist routes into the group of occupational exposure, the number of persons who are included in the Category A due to occupational exposure may increase by about 3/4. The professional group of the employees of underground tourist routes should be monitored for their exposure to radon. Int J Occup Med Environ Health 2017;30(5:687

  10. Experimental pulmonary carcinogenesis by radon and its daughters

    International Nuclear Information System (INIS)

    Sato, Fumiaki

    1989-01-01

    Information on experimental pulmonary carcinogenesis by radon and its daughters has come mostly from experiments carried out in France and United States of America. In rats a dose response relation was estimated to be linear with dose at low dose region. Studies of rats exposed daily to radon and radon daughters indicated that the frequency of pulmonary cancer at total exposure greater than 3000 WLM was greater when the exposure rates were low. At low total exposures the dose-rate effect was less apparent. Cigarette smoke increased the pulmonary cancer in rats but decreased in dogs. The decrease may be due to a decrease of absorbed doses with increased secretion of mucus and to an enhancement of mucociliary clearance. After inhalation of 222 Ru at equilibrium with radon daughters, rats were inoculated intrapleurally with asbestos fibres or glass fibres. The additive co-carcinogenic effects of this type of insult were demonstrated by the increased incidence of malignant thoracic tumours. As for species differences, dogs and hamsters are relatively resistant to cancer induction and rats are sensitive. While bronchogenic carcinomas are the most frequently observed radiation-induced pulmonary cancer in humans, bronchioloalveolar carcinomas are the most frequent type in most animal species. (author)

  11. Post-irradiation dietary vitamin E does not affect the development of radiation-induced lung damage in rats

    NARCIS (Netherlands)

    Wiegman, EA; van Gameren, MA; Kampinga, HH; Szabo, BG; Coppes, RP

    The purpose of this study was to investigate whether application of post-irradiation vitamin E, an anti-oxidant, could prevent the development of radiation induced lung damage. Wistar rats were given vitamin E enriched or vitamin E deprived food starting from 4 weeks after 18 Gy single dose

  12. Estimating the risk of lung cancer from inhalation of radon daughters indoors: review and evaluation. Final report, October 1986-April 1988

    International Nuclear Information System (INIS)

    Borak, T.B.; Johnson, J.A.

    1988-06-01

    A review of the dosimetric models and epidemiological studies with regard to the relation between indoor radon exposure and lung cancer indicates that the Working Level is an appropriate unit for indoor radon exposure; that the uncertainty in applying risk estimates derived from uranium miner data may be reduced by determining nose vs. mouth breathing ratios, residential aerosol characteristics, and lung cancer risk vs. age at exposure; that there is persuasive evidence of an association between radon exposure indoors and lung cancer; and that epidemiological studies in progress may provide a basis for revision or validation of current models but only is experimental designs are employed that will permit pooling of data to obtain greater statistical power

  13. Bone-marrow-derived mesenchymal stem cells inhibit gastric aspiration lung injury and inflammation in rats.

    Science.gov (United States)

    Zhou, Jing; Jiang, Liyan; Long, Xuan; Fu, Cuiping; Wang, Xiangdong; Wu, Xiaodan; Liu, Zilong; Zhu, Fen; Shi, Jindong; Li, Shanqun

    2016-09-01

    Gastric aspiration lung injury is one of the most common clinical events. This study investigated the effects of bone-marrow-derived mesenchymal stem cells (BMSCs) on combined acid plus small non-acidified particle (CASP)-induced aspiration lung injury. Enhanced green fluorescent protein (EGFP(+) ) or EGFP(-) BMSCs or 15d-PGJ2 were injected via the tail vein into rats immediately after CASP-induced aspiration lung injury. Pathological changes in lung tissues, blood gas analysis, the wet/dry weight ratio (W/D) of the lung, levels of total proteins and number of total cells and neutrophils in bronchoalveolar lavage fluid (BALF) were determined. The cytokine levels were measured using ELISA. Protein expression was determined by Western blot. Bone-marrow-derived mesenchymal stem cells treatment significantly reduced alveolar oedema, exudation and lung inflammation; increased the arterial partial pressure of oxygen; and decreased the W/D of the lung, the levels of total proteins and the number of total cells and neutrophils in BALF in the rats with CASP-induced lung injury. Bone-marrow-derived mesenchymal stem cells treatment decreased the levels of tumour necrosis factor-α and Cytokine-induced neutrophil chemoattractant (CINC)-1 and the expression of p-p65 and increased the levels of interleukin-10 and 15d-PGJ2 and the expression of peroxisome proliferator-activated receptor (PPAR)-γ in the lung tissue in CASP-induced rats. Tumour necrosis factor-α stimulated BMSCs to secrete 15d-PGJ2 . A tracking experiment showed that EGFP(+) BMSCs were able to migrate to local lung tissues. Treatment with 15d-PGJ2 also significantly inhibited CASP-induced lung inflammation and the production of pro-inflammatory cytokines. Our results show that BMSCs can protect lung tissues from gastric aspiration injury and inhibit lung inflammation in rats. A beneficial effect might be achieved through BMSC-derived 15d-PGJ2 activation of the PPAR-γ receptor, reducing the production of

  14. Biological basis of inhalation exposure of radon and its daughters

    International Nuclear Information System (INIS)

    Matsuoka, Osamu

    1989-01-01

    Since inhalation exposure by radon and its daughters is very specific type of internal exposure, it is necessary to understand its characteristic nature. The specificity originates from the nuclear feature of radon daughters and the biological micro-environment in the respiratory tract. Inhaled radon and its daughters exist in the respiratory tract as ions attached to air dusts and deposit on the mucus surface of the respiratory tract by various mechanisms such as impaction, sedimentation and diffusion. Deposition of radon daughters is predominant around the site of the fourth generation according to Weibel's model. Deposited particles with radon daughters are cleared by muco-ciliary transportation. Its speed is estimated to be about 1.0 cm/min, at the upper region. Alpha decay will happen during transportation in the respiratory tract. Radon has no tissue affinity metabolically. Therefore, the irradiation is limited to the epithelial cells of respiratory tract. The cell components within 30-70 micron in depth are irradiated with alpha particle. Biological effectiveness of alpha radiation is very high compared with beta or gamma radiation. The target cell for carcinogenesis by radon exposure is considered to be the basal cell of epithelium. Lung cancer induced by radon inhalation is recognized to be squamous cell carcinoma, small cell carcinoma, or oat-cell carcinoma and adenocarcinoma. The modification factors which influence the effect of radon exposure are co-inhalation of ore dust and smoking habit. According to epidemiological studies on lung cancer which occurred in uranium miners, it is suggested that the smoking habit strongly promotes lung cancer induction. (author)

  15. Health effects of radon

    International Nuclear Information System (INIS)

    Easterly, C.

    1994-01-01

    Exposure of people to radon has taken on increased interest during the last decade because of the understanding that buildings can serve to trap radon and its daughters, and thereby build up undesirable concentrations of these radioactive elements. Numerous studies of underground miners (often uranium miners) have shown an increased risk of lung cancer in comparison with nonexposed populations. Laboratory animals exposed to radon daughters also develop lung cancer. The abundant epidemiological and experimental data have established the carcinogenicity of radon progeny. Those observations are of considerable importance, because uranium, from which radon and its progeny arise, is ubiquitous in the earth's crust, including coal mines. Risk estimates of the health effects of long-term exposures at relatively low levels require continued development, especially to address the potential health effects of radon and radon daughters in homes and occupational settings where the exposure levels are less than levels in underground uranium and other metal mines that have been the subject of epidemiological studies. Two approaches can be used to characterize the lung-cancer risks associated with radon-daughter exposure: mathematical representations of the respiratory tract that model radiation doses to target cells and epidemiological investigation of exposed populations, mainly underground uranium miners. The mathematically-based dosimetric approach provides an estimate of lung cancer risk related to radon-daughter exposure based specifically on modeling of the dose to target cells. The various dosimetric models all require assumptions, some of which are not subject to direct verification, as to breathing rates; the deposition of radon daughters in the respiratory tract; and the type, nature, and location of the target cells for cancer induction. The most recent large committee effort drawn together to evaluate this issue was sponsored by the National Research Council

  16. Boron absorption imaging in rat lung colon adenocarcinoma metastases

    Energy Technology Data Exchange (ETDEWEB)

    Altieri, S [Dipartimento di Fisica Nucleare e Teorica Universita degli Studi di Pavia (Italy); Bortolussi, S [Dipartimento di Fisica Nucleare e Teorica Universita degli Studi di Pavia (Italy); Bruschi, P [Dipartimento di Fisica Nucleare e Teorica Universita degli Studi di Pavia (Italy); Fossati, F [Dipartimento di Fisica Nucleare e Teorica Universita degli Studi di Pavia (Italy); Vittor, K [Dipartimento di Fisica Nucleare e Teorica Universita degli Studi di Pavia (Italy); Nano, R [Dipartimento di Biologia Animale Universita degli Studi di Pavia (Italy); Facoetti, A [Dipartimento di Biologia Animale Universita degli Studi di Pavia (Italy); Chiari, P [Dipartimento di Fisica Nucleare e Teorica Universita degli Studi di Pavia (Italy); Bakeine, J [Dipartimento di Scienze Biomediche e Biotecnologie Universita degli Studi di Brescia (Italy); Clerici, A [Dipartimento di Chirurgia Universita degli Studi di Pavia (Italy); Ferrari, C [Dipartimento di Chirurgia Universita degli Studi di Pavia (Italy); Salvucci, O [Dipartimento di Scienze Biomediche e Biotecnologie Universita degli Studi di Brescia (Italy)

    2006-05-15

    Given the encouraging results from our previous work on the clinical application of BNCT on non-resectable, chemotherapy resistant liver metastases, we explore the possibility to extend our technique to lung metastases. A fundamental requirement for BNCT is achieving higher {sup 10}B concentrations in the metastases compared to those in healthy tissue. For this reason we developed a rat model with lung metastases in order to study the temporal distribution of {sup 10}B concentration in tissues and tumoral cells. Rats with induced lung metastases from colon adenocarcinoma were sacrificed two hours after intraperitoneal Boronphenylalanine infusion. The lungs were harvested, frozen in liquid nitrogen and subsequently histological sections underwent neutron autoradiography in the nuclear reactor Triga Mark II, University of Pavia. Our findings demonstrate higher Boron uptake in tumoral nodules compared to healthy lung parenchyma 2 hours after Boronphenylalanine infusion.

  17. MODERN APPROACHES TO PUBLIC PROTECTION AGAINST INDOOR RADON. INTERNATIONAL REGULATORY EXPERIENCE

    Directory of Open Access Journals (Sweden)

    S. M. Kiselev

    2014-01-01

    Full Text Available Intensive worldwide researches of the public exposure to radon are carried out for over 30 years. According to numerous studies being performed in many countries, radon and its progenies contribute significantly in total dose to the public. At that, dose due to inhalation of radon and its progenies is higher than that induced by other radiation sources, including sources used in medicine and those occurring in the environment due to the nuclear fuel cycle activities. Prolonged internal exposure to the human‘s body induced by the radon decay products is one of the key factors in the development of the lung cancer pathology. The recent results of global epidemiological studies, aimed at the risk assessment of indoor radon-induced lung cancer, have initiated the need to improve approaches to the regulation of this problem. International organizations (such as WHO, IAEA, ICRP proposed a strategy of the public radiation protection against radon exposure and adapted this strategy to the up-to-date realities. The recent recommendations not only correct the radon activity concentration being limited in dwellings, but also change its status through converting the action level to the reference one. The strategies for limitation of the public exposure due to this component of natural radiation should be revised at the national level and an action plan for their implementation in the long term perspective should be developed. This paper deals with the key provisions of the recent international recommendations including approaches to regulate the public protection against radon exposure.

  18. Radon reference levels and priority areas considering optimisation and avertable lung cancers

    International Nuclear Information System (INIS)

    Bochicchio, F.; Venoso, G.; Antignani, S.; Carpentieri, C.

    2017-01-01

    Protection from radon exposure in workplaces and dwellings, as included in the latest relevant international regulations and recommendations, is based on the new concept of 'reference level' whose meaning is significantly different from that of previous 'action level' concept. In fact, whereas remedial actions had to be considered only for radon concentrations above the action level, actions to optimise radon exposure are requested with priority above reference level but optimisation should be applied also for radon concentrations below reference level. Similar considerations can be applied to the usually called 'Rn-prone' areas, which are here proposed to be regulated as 'priority' areas. The main implication of these new challenging concepts is a substantial increase of avertable lung cancer deaths, as it will be shown using Italian data. Some practical examples of possible policy actions fitting an approach based on these new concepts will also be given, which could be useful for the implementation of the Council Directive 2013/59/Euratom. (authors)

  19. Living with radon and uncertainty

    International Nuclear Information System (INIS)

    Frame, P.W.

    1990-01-01

    Lung cancer is the second leading cause of death in the United States, heart disease is the first. In 1990 an estimated 142,000 will die form lung cancer and approximately 157,000 new cases will be reported. Of the latter, only 20,000 are expected to survive beyond five years. For all practical purposes lung cancer is 100% fatal. This paper reports that he Environmental Protection Agency has predicted that 8,400-43,000 lung caner deaths each year can be attributed to radon with their best estimate at 21,600. If the EPA's estimate of 21,600 is correct, radon is responsible for 15% of lung cancer deaths. It would also be responsible for approximately the same number of deaths as homicides, the various diseases of infancy, and leukemia. Radon has also been cited in several recent reports as a possible cause of leukemia, cancer of the kidney and melanoma. It is no wonder that radon is widely considered the most hazardous indoor air pollutant

  20. Puerarin Attenuates Ovalbumin-Induced Lung Inflammation and Hemostatic Unbalance in Rat Asthma Model

    Directory of Open Access Journals (Sweden)

    Feng Dong

    2014-01-01

    Full Text Available Aim. We aimed to investigate and evaluate the preventive activity of puerarin on the ovalbumin-induced asthma rat model. Materials and Methods. Male Wistar rats were sensitized intraperitoneally on days 0, 7, and 14 and challenged to ovalbumin intratracheally on day 21. Groups of sensitized rats were treated randomly either with placebo, puerarin, dexamethasone, or puerarin combined with dexamethasone, from days 15 to 20. Inflammatory markers, including cell counts in bronchoalveolar lavage fluid (BALF, inflammatory cytokines, histopathology, and coagulation parameters, such as coagulation tests and the activity of coagulation factors, were analyzed. Results. Puerarin significantly inhibited the recruitment of inflammatory cells in BALF and lung tissue. At the same time, the release of IL-4, IL-10, and IFN-γ in serum and the expression of mRNAs in lung tissue homogenate were changed by puerarin. Administration of puerarin also effectively rectified the coagulation disorder in asthmatic rats, such as prothrombin time (PT (P<0.01, thrombin time (TT (P<0.05, fibrinogen (FIB (P<0.01,the activity of factor II (FII (P<0.01, the activity of factor V (FV (P<0.05, the activity of factor VII (FVII (P<0.05, the activity of factor X (FX (P<0.05, the activity of factor VIII (FVIII (P<0.01, the activity of factor IX (FIX (P<0.05, and the activity of factor XII (FXII (P<0.05. Conclusions. Our results provide a clue that puerarin was useful for the preventive of allergic airway disease in rodents.

  1. Radon as a risk factor in mines and dwellings

    Energy Technology Data Exchange (ETDEWEB)

    Axelson, O [Yrkesmedicinska kliniken, Regionsjukhuset, Linkoeping (Sweden)

    1985-03-01

    In mines, exposure to radon and radon daughters is the most important factor for the initiation of lung cancer. Tobacco smoke probably acts as a lung cancer promotor, but the relationship between minework, smoking and lung cancer is complicated. It is suggested that smokers may have a relative protection from a mucous sheet covering their basal cells. There is a connection between radon exposure in dwellings and lung cancer. Radon in buildings comes from the building material or the ground. The risk for developing lung cancer seems to be enhanced considerably by smoking. Tobacco contains some radioactivity itself (Lead 210 and Polonium 210), but tobacco smoke also adsorb electrically charged radon daughters and keeps them floating in the breathing air. Measurements show a doubling of radon daughter concentration in a room of normal size if 3-4 cigarettes are burnt out in it. A raised risk for lung cancer has been observed in connection with passive smoking. The relative risk for lung cancer is 2-3 for passive smokers and 5-6 for active smoking women. Children of smoking mothers who start smoking themselves develop lung cancer more easily than other groups. There seems to be a connection between early exposure to radon daughters, passive smoking and lung cancer.

  2. Uranium induces oxidative stress in lung epithelial cells

    International Nuclear Information System (INIS)

    Periyakaruppan, Adaikkappan; Kumar, Felix; Sarkar, Shubhashish; Sharma, Chidananda S.; Ramesh, Govindarajan T.

    2007-01-01

    Uranium compounds are widely used in the nuclear fuel cycle, antitank weapons, tank armor, and also as a pigment to color ceramics and glass. Effective management of waste uranium compounds is necessary to prevent exposure to avoid adverse health effects on the population. Health risks associated with uranium exposure includes kidney disease and respiratory disorders. In addition, several published results have shown uranium or depleted uranium causes DNA damage, mutagenicity, cancer and neurological defects. In the current study, uranium toxicity was evaluated in rat lung epithelial cells. The study shows uranium induces significant oxidative stress in rat lung epithelial cells followed by concomitant decrease in the antioxidant potential of the cells. Treatment with uranium to rat lung epithelial cells also decreased cell proliferation after 72 h in culture. The decrease in cell proliferation was attributed to loss of total glutathione and superoxide dismutase in the presence of uranium. Thus the results indicate the ineffectiveness of antioxidant system's response to the oxidative stress induced by uranium in the cells. (orig.)

  3. Expression of Angiotensin II and Aldosterone in Radiation-induced Lung Injury

    OpenAIRE

    Cao, Shuo; Wu, Rong

    2012-01-01

    Objective Radiation-induced lung injury (RILI) is the most common, dose-limiting complication in thoracic malignancy radiotherapy. Considering its negative impact on patients and restrictions to efficacy, the mechanism of RILI was studied. Methods Wistar rats were locally irradiated with a single dose of 0, 16, and 20 Gy to the right half of the lung to establish a lung injury model. Two and six months after irradiation, the right half of the rat lung tissue was removed, and the concentration...

  4. Measurements of indoor radon and radon progeny in Mexico City

    International Nuclear Information System (INIS)

    Cheng, Y.S.; Rodriguez, G.P.

    1996-01-01

    Indoor radon has been a public concern associated with increased lung cancer risks. Radon decay products interact with indoor aerosols to form progeny with different size distributions, which may influence the lung dosimetry when the progeny are inhaled. Air pollution in Mexico City is a serious problems with high particulate concentrations, but there are few reports of indoor radon measurement. The purposes of this study were to measure the aerosol concentration, radon concentration, and radon activity size distribution in the living area of three houses in Mexico City. The radon concentration was monitored by a RGM-3 radon gas monitor (Eberline, Inc., Santa Fe, NM). A graded diffusion battery was used to determine the progeny concentration and activity size distribution. The concentration and size distribution of the indoor aerosols were monitored by a quartz, crystal microbalance cascade impactor. Our measurements showed high concentrations of indoor aerosols (20-180 gg m -3 ). However, the radon concentrations-were low ( -1 ), but showed a clear diurnal pattern with peak concentrations from 2-10 AM. The activity size distributions of radon progeny were trimodal, with peaks of 0.6 nm, 4-5 nm, and 100 rim. Most activities were associated with large particle sizes. Our results indicated that indoor radon concentration was not high, due in part to a relatively high air exchange with outdoor air. The high aerosol concentration may also play an important part in the activity size distribution of radon progeny

  5. Simulation of lifetime radon exposures using observation data

    International Nuclear Information System (INIS)

    Janssen, I.; Stebbings, J.H.

    1990-01-01

    The frequency distribution of lifetime risk of radon-induced lung cancer is a function of the frequency distribution of lifetime radon exposure, which differs from the frequency distribution of radon in homes because of residential mobility. Cumulative personal exposures are averages of a variable number of house radon values, weighted according to duration of occupancy and recency of residence. We simulated a distribution of individual, cumulative Working Level Month (WLM) exposures using observed residence histories from lung cancer cases from Eastern Pennsylvania and (basement) Working Levels (WL) from a survey of Reading Prong, Pennsylvania. The measurements for basement-level houses have a higher skewed distribution, well-approximated by a Gamma distribution with small shape parameter for this high-radon area, where 30% of the houses have basement radon levels that exceed 9 pCi/ell. Using the BEIR IV model and assuming a 50% occupancy factor, we assigned either lifetime residence in a single house or a real residence history at random for women randomly selected from the age distribution of female lung cancer cases. Averaging over houses reduces the exposure of the most highly exposed 5% of the population but increases it for 95%: the upper 25% attains lifetime exposure of ≥ 74 WLM, yielding a relative risk (RR) ≥ 2.1. Ignoring mobility and basing the calculations on the distribution of radon in houses, the corresponding values would be 48.0 WLM and a RR of 1.7. The 50th percentile of the population has an estimated WLM exposure of 34.6 (RR = 1.5); this estimate would be 16.8 (RR = 1.2) if we assume one house per lifetime

  6. Risk of lung cancer by radon, disagreement in international regulation; Riesgo de cancer pulmonar por radon, discordancia en reglamentacion internacional

    Energy Technology Data Exchange (ETDEWEB)

    Balcazar, M.; Pena, P.; Villamares, A.; Avelar, J. R., E-mail: miguel.balcazar@inin.gob.mx [ININ, Carretera Mexico-Toluca s/n, 52750 Ocoyoacac, Estado de Mexico (Mexico)

    2013-10-15

    Diverse international organizations have evaluated the risk of lung cancer starting from epidemic studies in miners of uranium mines, where the corresponding effective dose was determined relating with the dose received by the population during Hiroshima and Nagasaki events. Alternately, the equivalent dose has been calculated by means of based models on the energy deposited by the breathable radon fractions and its decay products in the breathing ducts. A unique factor agreed by the diverse organizations that allows converting radon concentration to effective dose does not exist. Neither an agreement exists among the different countries on which duty to be the value of the maximum concentration of radon, in interiors starting from which an intervention is required and if this intervention is standardized, recommended or nonexistent. In this work study cases in Mexico are presented and their interpretation alternative based on the international agreements absence. (Author)

  7. Radon measurement and its risk in the development of lung cancer in indoor spaces at the historical center of Quito, Ecuador

    International Nuclear Information System (INIS)

    Suarez, Omar

    2006-01-01

    In Ecuador, as in other countries around the world, the presence of radon is eminent. This study compiles some information about the effects that radon has over human beings, its incidence in lung cancer and the methodologies used to determine radon. High concentrations of radon, superior to international limits have been found in indoor sites in the center of Quito and Cuenca Ecuador. (The author)

  8. Evidence of lung cancer risk from animal studies

    International Nuclear Information System (INIS)

    Cross, F.T.

    1988-03-01

    Human epidemiological data provide the most important basis for assessing risks of radon exposures. However, additional insight into the nature of exposure-response relationships is provided by animal experimentation and dosimetric determinations. Animal studies have now been conducted for more than 50 years to examine the levels of pollutants in underground mines that were responsible for the respiratory effects observed among miners. This work has emphasized respiratory cancer and the interaction of radon with other agents, such as ore dust, diesel-engine-exhaust fumes and cigarette smoke. The more recent data on radon-daughter inhalation exposures were provided by two American research centers, The University of Rochester (UR) and the Pacific Northwest Laboratory (PNL), and by the Compagnie Generale des Matieres Nucleaires (COGEMA) laboratory in France. Approximately 2000 mice, 100 rats and 80 dogs were employed in the completed UR studies, begun in the mid 1950s; 800 hamsters, 5000 rats and 100 dogs in the ongoing PNL studies, begun in the late 1960s; and 10,000 rats in the ongoing COGEMA studies, also begun in the late 1960s. More complete updated biological effects, data resulting from chronic radon-daughter inhalation exposures of mice, hamsters, rats and beagle dogs were examined. Emphasis on the carcinogenic effects of radon-decay product exposure, including the influences of radon-daughter exposure rate, unattached fraction and disequilibrium, and co-exposures to other pollutants. Plausible values for the radon (radon-daughter) lifetime lung-cancer risk coefficients are also provided. 13 refs., 1 fig., 1 tab

  9. Measurement of radon concentration in dwellings in the region of highest lung cancer incidence in India

    International Nuclear Information System (INIS)

    Zoliana, B.; Rohmingliana, P.C.; Sahoo, B.K.; Mayya, Y.S.

    2015-01-01

    Monitoring of radon exhalation from soil and its concentration in indoor is found to be helpful in many investigations such as health risk assessment and others as radiation damage to bronchial cells which eventually can be the second leading cause of lung cancer next to smoking. The fact that Aizawl District, Mizoram, India has the highest lung cancer incidence rates among males and females in Age Adjusted Rate (AAR) in India as declared by Population Based Cancer Registry Report 2008 indicates the need for quantification of radon and its anomalies attached to it. Measurement of radon concentration had been carried out inside the dwellings in Aizawl district, Mizoram. A time integrated method of measurement was employed by using a solid state nuclear track detector (SSNTD) type (LR-115 films) kept in a twin cup dosimeter for measurement of concentration of radon and thoron. The dosimeters were suspended over bed rooms or living rooms in selected dwellings. They were deployed for a period of about 120 days at a time in 63 houses which were selected according to their place of location viz. fault region, places where fossil remains were found and geologically unidentified region. After the desired period of exposure, the detectors were retrieved and chemically etched which were then counted by using a spark counter. The recorded nuclear tract densities are then converted into air concentrations of Radon and Thoron

  10. Sarcandra glabra combined with lycopene protect rats from lipopolysaccharide induced acute lung injury via reducing inflammatory response.

    Science.gov (United States)

    Liu, Tian-Yin; Chen, Shi-Biao

    2016-12-01

    Sarcandra glabra (Chinese name, Zhongjiefeng) is an important herb widely used in traditional Chinese medicine. Lycopene has been shown to be a powerful antioxidant. This study aims to test the hypothesis that Sarcandra glabra combined with lycopene protect rats from lipopolysaccharide (LPS) induced acute lung injury (ALI). Metabolomics approach combined with pathological inspection, serum biochemistry examination, enzyme-linked immunosorbent assay and western blotting were used to explore the protective effects of Sarcandra glabra and lycopene on LPS-induced ALI, and to elucidate the underlying mechanisms. Results showed that Sarcandra glabra and lycopene could significantly ameliorate LPS-induced histopathological injuries, improve the anti-oxidative activities of rats, decrease the levels of TNF-α and IL-6, suppress the activations of MAPK and transcription factor NF-κB and reverse the disturbed metabolism towards the normal status. Taken together, this integrated study revealed that Sarcandra glabra combined with lycopene had great potential in protecting rats from LPS-induced ALI, which would be helpful to guide the clinical medication. Copyright © 2016 Elsevier Masson SAS. All rights reserved.

  11. Occupational exposure to radon for underground tourist routes in Poland: Doses to lung and the risk of developing lung cancer.

    Science.gov (United States)

    Walczak, Katarzyna; Olszewski, Jerzy; Politański, Piotr; Zmyślony, Marek

    2017-07-14

    Radon concentrations for 31 Polish underground tourist routes were analyzed. The equivalent dose to the lung, the effective dose and the relative risk were calculated for employees of the analyzed routes on the grounds of information on radon concentrations, work time, etc. The relative risk for lung cancers was calculated using the Biological Effects of Ionizing Radiation (BEIR) VI Committee model. Equivalent doses to the lungs of workers were determined using the coefficients calculated by the Kendall and Smith. The conversion coefficient proposed by the International Atomic Energy Agency (IAEA) in the report No. 33 was used for estimating the effective doses. In 13 routes, the effective dose was found to be above 1 mSv/year, and in 3 routes, it exceeded 6 mSv/year. For 5 routes, the equivalent dose to lungs was higher than 100 mSv/year, and in 1 case it was as high as 490 mSv/year. In 22.6% of underground workplaces the risk of developing lung cancer among employees was about 2 times higher than that for the general population, and for 1 tourist route it was about 5 times higher. The geometric mean of the relative risk of lung cancer for all workers of underground tourist routes was 1.73 (95% confidence interval (CI): 1.6-1.87). Routes were divided into: caves, mines, post-military underground constructions and urban underground constructions. The difference between levels of the relative risk of developing lung cancer for all types of underground tourist routes was not found to be significant. If we include the professional group of the employees of underground tourist routes into the group of occupational exposure, the number of persons who are included in the Category A due to occupational exposure may increase by about 3/4. The professional group of the employees of underground tourist routes should be monitored for their exposure to radon. Int J Occup Med Environ Health 2017;30(5):687-694. This work is available in Open Access model and licensed under a CC

  12. Unattached radon daughter atoms and radon daughter equilibrium ratios in uranium mines. Final report

    International Nuclear Information System (INIS)

    Holaday, D.A.

    1972-01-01

    Uranium mines in Colorado and New Mexico were surveyed for airborne concentrations of radon (10043922) and radon daughters. A procedure for measuring individual daughters and the fraction of each existing as free atoms was developed and used for field monitoring. Samples were taken in working areas and particle counts were made. The data was analyzed to determine the ratio of radon to radon daughters as well as the ratios among the radon daughters. The author concludes that since the radon to working level ratios have not changed much in 20 years, using the ratio as the basis for estimating relative biological hazard is just as uncertain now as then. The large number of daughters present as free atoms indicate that the lung radiation doses calculated using any of the lung models need reexamination

  13. Cases study of lung cancer deaths and analysis of radon levels in house-room of Mexicali, B. C

    International Nuclear Information System (INIS)

    Lopez B, G.; Reyna C, M. A.

    2009-10-01

    The lung cancer is a case of health of more importance as much in women as in men, with more frequency that the cancer of mamma, colon and prostate on the whole. A factor that influences in the cancer generation originating serious complications it is the exposition to radioactive substances in closed places, as house-room. In the investigation study, levels of radon concentration were measured in interiors of Mexicali homes, to study the relationship that this gas could have with the death cases by lung cancer into population. The gas radon is radioactive and it adheres easily to particles that remain suspended in air; when inhaling them small explosions take place inside the alveoli, changing the DNA of cells and lung cancer is generated. The meteorological, geographical and urban characteristics of Mexicali, favor conditions so that certain areas of the city present high indexes of suspended particles in atmosphere. One sample of gas radon inside 100 house-rooms, the analysis was made by paved and not paved colonies and for sex, to establish if the death cases by lung cancer had relationship with the genus and/or with some of two groups of colonies. The study found that the major number of deaths it was presented in colonies in which lacked the paving service and always happened with more frequency in women; and that in homes of having died by lung cancer the radon concentrations were more high that the homes where there was not death cases, with significant differences that go from 9.2% to 70%. This investigation project is presented as a cases study in the Mexicali City. (Author)

  14. Inhibitory Effects of Pretreatment with Radon on Acute Alcohol-Induced Hepatopathy in Mice

    Directory of Open Access Journals (Sweden)

    Teruaki Toyota

    2012-01-01

    Full Text Available We previously reported that radon inhalation activates antioxidative functions in the liver and inhibits carbon tetrachloride-induced hepatopathy in mice. In addition, it has been reported that reactive oxygen species contribute to alcohol-induced hepatopathy. In this study, we examined the inhibitory effects of radon inhalation on acute alcohol-induced hepatopathy in mice. C57BL/6J mice were subjected to intraperitoneal injection of 50% alcohol (5 g/kg bodyweight after inhaling approximately 4000 Bq/m3 radon for 24 h. Alcohol administration significantly increased the activities of glutamic oxaloacetic transaminase (GOT, glutamic pyruvic transaminase (GPT in serum, and the levels of triglyceride and lipid peroxide in the liver, suggesting acute alcohol-induced hepatopathy. Radon inhalation activated antioxidative functions in the liver. Furthermore, pretreatment with radon inhibited the depression of hepatic functions and antioxidative functions. These findings suggested that radon inhalation activated antioxidative functions in the liver and inhibited acute alcohol-induced hepatopathy in mice.

  15. Radon progeny exposure and lung cancer risk: Analyses of a cohort of Newfoundland fluorspar miners

    International Nuclear Information System (INIS)

    Morrison, H.I.; Villeneuve, P.J.

    1995-07-01

    A cohort study of the mortality experience (1950-1990) of 1744 underground miners and 321 millers or surface workers has been conducted. Excess mortality among underground miners was noted for cancers of the lung, buccal cavity, pharynx and mouth, urinary tract and for silicosis and pneumoconioses. A highly statistically significant relationship was noted between radon daughter exposure and risk of dying of lung cancer; the small numbers of buccal cavity/pharynx cancers (n = 6) precluded meaningful analysis of exposure-response. No statistically significant excess was found for any cause of death among surface workers. The exposure-response data for lung cancer were fitted to various mathematical models. The model selected included terms for attained age, cumulative dose, dose rate and time since last exposure. Because risk varies according to each of these factors, a single summary risk estimate was felt to be misleading. The joint effects of radon and smoking could not be adequately assessed using this cohort. (author). 46 refs., 16 tabs., 1 fig

  16. Beta Adrenergic Regulation of Intrapulmonary Arteriovenous Anastomoses in Intact Rat and Isolated Rat Lungs

    Directory of Open Access Journals (Sweden)

    Melissa L. Bates

    2017-04-01

    Full Text Available Intrapulmonary arteriovenous anastomoses (IPAVA allow large diameter particles of venous origin to bypass the pulmonary capillary bed and embolize the systemic arterial circulation. IPAVA have been routinely observed in healthy humans with exercise, hypoxia, and catecholamine infusion, but the mechanism by which they are recruited is not well-defined. We hypothesized that beta-adrenergic receptor stimulation recruits IPAVA and that receptor blockade would limit hypoxia-induced IPAVA recruitment. To test our hypothesis, we evaluated the transpulmonary passage of microspheres in intact rats and isolated rats lung infused with the beta-adrenergic receptor agonist isoproterenol. We also evaluated IPAVA recruitment in intact rats with hypoxia and the beta-adrenergic receptor blocker propranolol. We found that IPAVA are recruited in the intact rat by isoproterenol and their recruitment by hypoxia can be minimized by propranolol, suggesting a role for the adrenergic system in the recruitment of IPAVA by hypoxia. IPAVA recruitment is completely abolished by ventilation with 100% oxygen. Isoproterenol also recruits IPAVA in isolated rat lungs. The fact that isoproterenol can recruit IPAVA in isolated lungs, without increased pulmonary flow, suggests that elevated cardiac output is not required for IPAVA recruitment.

  17. Workshop on dosimetry for radon and radon daughters

    International Nuclear Information System (INIS)

    Turner, J.E.; Holoway, C.F.; Loebl, A.S.

    1978-05-01

    Emphasis is placed on the dosimetry for radon and daughters, rather than on monitoring and instrumentation. The objectives of the meeting were to exchange scientific information, to identify problem areas in radon-daughter dosimetry, and to make any observations or recommendations by the participants through issuance of this report. The discussion topics included the history of dosimetry for radon and daughters, human data, aerosols, deposition and movement in the respiratory tract, dose calculations, dose-to-working-level-month (WLM) conversion factors, animal experiments, and the development of regulations and remedial criteria for reducing population exposures to radon daughters. This report contains a summary of Workshop discussions plus individual statements contributed by several of the participants. The outstanding problem areas from the standpoint of dosimetry appear to involve the appropriate lung organ mass to be used (average lung-tissue dose vs. high-level local dose); recognition of the discrete, rather than continuous, structure of the mucus; lack of knowledge about lung clearance; the variability of dose with the degree of disequilibrium and the unattached fraction of radon daughters for a given WLM; and questions about the character of uranium mine atmospheres actually breathed in the older mines from which much of the epidemiological information originates. The development of criteria for taking remedial action to reduce exposures involves additional concerns of basing long-term risk assessment on short-term sampling and applying WLM data for miners to general populations

  18. Evaluation of lung cancer risk from radon in homes. Smoking plays the important part; Bewertung des Lungenkrebsrisikos durch Wohnungsradon. Lungenkrebsrisiko ausschliesslich durch Rauchen verursacht

    Energy Technology Data Exchange (ETDEWEB)

    Schuettmann, W.

    1999-07-01

    Studies of lung cancer risk from the beginning of the century until today are investigated and evaluated. The result shows that the risk in homes with Radon exposure is determined exclusively by the amount of smoking. Further studies of the lung cancer risk from Radon therefore should exclusively treat with non-smokers. (orig.) [German] Studien zum Lungenkrebsrisiko durch Radon vom Anfang dieses Jahrhunderts bis heute werden untersucht und bewertet. Das Ergebnis zeigt, dass das Lungenkrebsrisiko in Wohnungen mit Radonexpositionen ausschliesslich durch den Umfang des Zigarettenrauchens bestimmt wird. Untersuchungen zur Bewertung des Lungenkrebsrisikos durch Radon sollten daher ausschliesslich bei Nichtrauchern durchgefuehrt werden. (orig.)

  19. Dosimetry of inhaled radon and thoron progeny

    International Nuclear Information System (INIS)

    James, A.C.

    1994-06-01

    This chapter reviews recent developments in modeling doses received by lung tissues, with particular emphasis on application of ICRP's new dosimetric model of the respiratory tract for extrapolating to other environments the established risks from exposure to radon progeny in underground mines. Factors discussed include: (1) the influence of physical characteristics of radon progeny aerosols on dose per unit exposure, e.g., the unattached fraction, and the activity-size distributions of clustered and attached progeny; (2) the dependence of dose on breathing rate, and on the exposed subject (man, woman or child); (3) the variability of dose per unit exposure in a home when exposure is expressed in terms of potential α energy or radon gas concentration; (4) the comparative dosimetry of thoron progeny; and (5) the effects of air-cleaning on lung dose. Also discussed is the apparent discrepancy between lung cancer risk estimates derived purely from dosimetry and the lung cancer incidence observed in the epidemiological studies of radon-exposed underground miners. Application of ICRP's recommended risk factors appears to overestimate radon lung-cancer risk for miners by a factor of three. ''Normalization'' of the calculated effective dose is therefore needed, at least for α dose from radon and thoron progeny, in order to obtain a realistic estimate of lung cancer risk

  20. Czech miner studies of lung cancer risk from radon

    International Nuclear Information System (INIS)

    Tomasek, L.

    2002-01-01

    Epidemiological evidence of lung cancer risk from radon is based mainly on studies of miners. Two such studies among Czech uranium miners were established in 1970 and 1980. A subcohort of 5002 miners and a nested-in case-control study contribute to a joint European project. In this paper, the subcohort of miners with 495 lung cancers is described. The excess relative risk depends linearly on cumulative exposure incurred more than 5 years before. The relative effect from exposures in the distant past decreases by 62% per decade. Simultaneously, the excess relative risk is lower by 43% per decade in dependence on age at exposure. The effect of smoking, partly analysed in the study, suggests a twofold elevation in the relative risk coefficient among non-smokers, but this difference is not significant. (author)

  1. Prevention of reperfusion lung injury by lidocaine in isolated rat lung ventilated with higher oxygen levels.

    Directory of Open Access Journals (Sweden)

    Das K

    2003-01-01

    Full Text Available BACKGROUND: Lidocaine, an antiarrhythmic drug has been shown to be effective against post-ischaemic reperfusion injury in heart. However, its effect on pulmonary reperfusion injury has not been investigated. AIMS: We investigated the effects of lidocaine on a postischaemic reperfused rat lung model. MATERIALS AND METHODS: Lungs were isolated and perfused at constant flow with Krebs-Henseilet buffer containing 4% bovine serum albumin, and ventilated with 95% oxygen mixed with 5% CO2. Lungs were subjected to ischaemia by stopping perfusion for 60 minutes followed by reperfusion for 10 minutes. Ischaemia was induced in normothermic conditions. RESULTS: Postischaemic reperfusion caused significant (p < 0.0001 higher wet-to-dry lung weight ratio, pulmonary arterial pressure and peak airway pressure compared to control lungs. Lidocaine, at a dose of 5mg/Kg b.w. was found to significantly (p < 0.0001 attenuate the increase in the wet-to-dry lung weight ratio, pulmonary arterial pressure and peak airway pressure observed in post-ischaemic lungs. CONCLUSION: Lidocaine is effective in preventing post-ischaemic reperfusion injury in isolated, perfused rat lung.

  2. Cordycepin alleviates lipopolysaccharide-induced acute lung injury via Nrf2/HO-1 pathway.

    Science.gov (United States)

    Qing, Rui; Huang, Zezhi; Tang, Yufei; Xiang, Qingke; Yang, Fan

    2018-04-24

    The present study is to investigate the protective effect of cordycepin on inflammatory reactions in rats with acute lung injury (ALI) induced by lipopolysaccharide (LPS), as well as the underlying mechanism. Wistar rat model of ALI was induced by intravenous injection of LPS (30 mg/kg body weight). One hour later, intravenous injection of cordycepin (1, 10 or 30 mg/kg body weight) was administered. The wet-to-dry weight ratio of lung tissues and myeloperoxidase activity in the lung tissues were measured. The contents of nitrite and nitrate were measured by reduction method, while chemiluminescence was used to determine the content of superoxide. Quantitative real-time polymerase chain reaction and Western blotting were used to determine the expression of mRNA and protein, respectively. Colorimetry was performed to determine the enzymatic activity of heme oxygenase-1 (HO-1). Nuclear translocation of Nrf2 was identified by Western blotting. The plasma contents of cytokines were measured by enzyme-linked immunosorbent assay. Cordycepin enhanced the expression and enzymatic activity of HO-1 in ALI rats, and activated Nrf2 by inducing the translocation of Nrf2 from cytoplasm to nucleus. In addition, cordycepin regulated the secretion of TNF-α, IL-6 and IL-10 via HO-1, and suppressed inflammation in lung tissues of ALI rats by inducing the expression of HO-1. HO-1 played important roles in the down-regulation of superoxide levels in lung tissues by cordycepin, and HO-1 expression induced by cordycepin affected nitrite and nitrate concentrations in plasma and iNOS protein expression in lung tissues. Cordycepin showed protective effect on injuries in lung tissues. The present study demonstrates that cordycepin alleviates inflammation induced by LPS via the activation of Nrf2 and up-regulation of HO-1 expression. Copyright © 2018. Published by Elsevier B.V.

  3. Evaluation of fifteen epidemiologic studies examining the lung cancer mortality of underground miners

    International Nuclear Information System (INIS)

    1985-01-01

    A group of 15 epidemiologic studies was identified in which researchers reported excess lung cancer deaths among underground miners who worked in mines where radon (10043922) progeny were present. Several other studies demonstrated a dose response relationship existing between radon progeny exposure and mortality from lung cancer. Two recent studies indicated excess numbers of cases of lung cancer deaths resulting from mean cumulative radon progeny exposures below 100 Working Level Months (WLM). In the mining environment exposure can also occur to other substances such as arsenic (1332214), diesel exhaust, smoking, chromium (7440473), nickel (7440020), and radiation, which can affect the lung cancer risk resulting from exposure to radon progeny. Not much was available in the literature which deals with the results of these combined exposures except the finding that a combined exposure to radon progeny and cigarette smoke resulted in a higher risk than exposure to either substance alone. X-ray surveillance and sputum cytology appeared to be ineffective in preventing radon progeny induced lung cancers in individual miners. There does not appear to be any particular association between one specific lung cancer cell type and radon progeny exposure

  4. Health effects of exposure to indoor radon and its decay products

    International Nuclear Information System (INIS)

    Mustafa, A.A.; Vasisht, C.M.

    1987-01-01

    Estimates of possible incidence of lung cancer associated with present exposure to natural indoor radon are assessed for Kuwait. Several dosimetric models were used and their results are compared. Some models took into consideration individual differences in sex, life-style and age. The UNSCEAR model gives life-time risk values of 2-4.5 x 10 -4 per WLM for miners. Taking into account a factor of 0.6 between the mean breathing rate of workers in the model and non-miners, and the population of Kuwait as 1.7 million, the model gives 46-105 lung cancer cases per year induced by radon and its decay products. Since these models are developed for smokers they tend to overestimate the actual incidence rates. Assuming that 20% of the population in Kuwait are smokers, the incidence rates range will be reduced to 30-63 cases per year which is about 9-20% of the observed lung cancer incidence in 1982. The energy conservation programme is expected to increase average indoor radon concentrations, and consequently bring about higher lung cancer incidence. (author)

  5. Sequence analysis of LACI mutations obtained from lung cells of control and radon-exposed Big Blue trademark transgenic mice

    International Nuclear Information System (INIS)

    Jostes, R.F.; Cross, F.T.; Stillwell, L.

    1995-01-01

    We have exposed Stratagene Big Blue trademark transgenic mice by inhalation to 310, 640 and 960 Working Level Months (WLM) of radon progency. Twelve LacI mutations have been isolated from the lung tissue of a mouse from the 960-WLM group and the LacI gene sequenced. Mutations are scored only if they occur unambiguously in both strands of the mutant gene; the entire gene is evaluated. In addition, sixteen LacI mutations were isolated from the lung tissue of a mouse from the 640-WLM group; seven have been completely sequenced. Nine LacI mutations from the lung tissue of unirradiated control mice have been sequenced. Sequence data from the unirradiated mice are similar to that found in lung tissue at Stratagene; predominately G:C to A:T transitions in the protein associated region. The mutation spectrum from radon-irradiated mice is markedly different from that obtained with the control, unirradiated mice. Small deletions and insertions compromise 53% of the mutations in the irradiated mice. No multiple events have been noted in the spontaneous mutations; six of the mutations obtained from radon-irradiated mice (26%) have multiple events within the gene. In some, deletions, insertions are base changes occur together. The mutational events in the irradiated mice are approximately equally distributed throughout the gene. The breakpoint rejoining regions of large deletions obtained from the radon-irradiated mice are being studied at the University of California, San Francisco

  6. Tualang Honey Protects the Rat Midbrain and Lung against Repeated Paraquat Exposure

    Directory of Open Access Journals (Sweden)

    Suk Peng Tang

    2017-01-01

    Full Text Available Paraquat (PQ is a dopaminergic neurotoxin and a well-known pneumotoxicant that exerts its toxic effect via oxidative stress-mediated cellular injuries. This study investigated the protective effects of Tualang honey against PQ-induced toxicity in the midbrain and lungs of rats. The rats were orally treated with distilled water (2 mL/kg/day, Tualang honey (1.0 g/kg/day, or ubiquinol (0.2 g/kg/day throughout the experimental period. Two weeks after the respective treatments, the rats were injected intraperitoneally with saline (1 mL/kg/week or PQ (10 mg/kg/week once per week for four consecutive weeks. After four weekly exposures to PQ, the glutathione peroxidase activity and the number of tyrosine-hydroxylase immunopositive neurons in the midbrain were significantly decreased in animals from group PQ (p<0.05. The lungs of animals from group PQ showed significantly decreased activity of superoxide dismutase and glutathione-S-transferase. Treatment with Tualang honey ameliorated the toxic effects observed in the midbrain and lungs. The beneficial effects of Tualang honey were comparable to those of ubiquinol, which was used as a positive control. These findings suggest that treatment with Tualang honey may protect against PQ-induced toxicity in the rat midbrain and lung.

  7. Correlation between the radon levels and the lung cancer mortality rates - experimental and theoretical problems

    International Nuclear Information System (INIS)

    Tran Dai Nghiep; Vo Thi Anh

    2003-01-01

    Radon is a radioactive gas and is present in the most earth materials such as soil, stone, air, water and others. Comprehensive and scientifically rigorous studies found a low lung cancer mortality rates in high radon areas. It is opposite to the linear no-threshold hypothesis (LNTH), which is a popular theory in the field of radiation safety. The fact is explained by the theory of energy transfer model, that takes accounts of the competitive processes arising in material during irradiation.(author)

  8. Influence of radon-daughter exposure rate and uranium ore dust concentration on occurrence of lung tumors

    International Nuclear Information System (INIS)

    Cross, F.T.; Palmer, R.F.; Busch, R.H.

    1980-01-01

    Groups of male SPF Wistar rats were exposed concurrently to several levels of radon daughters and uranium ore dust to study the effect of these variables on pulmonary disease states. Clinical pathology data at 1 yr postexposure indicate no significant differences among exposed animals when compared with controls. Preliminary histopathologic data suggest a trend toward increasing lung tumor risk as the exposure rate is decreased (constant total dose), but the differences are not statistically significant at the 0.05 level. A similar trend occurs with decrease in ore dust concentration (except for the 2560-WLM exposure group), but these differences are also not significant at the 0.05 level. The tumor risk is significantly (0.05 level) increased as the exposure level increases from approximately 320 and 640 WLM to 2560 WLM at the high ore dust concentration

  9. Lung cancer and inhaled uranium ore dust in rats

    International Nuclear Information System (INIS)

    Mitchel, R.E.J.; Jackson, J.S.

    1997-01-01

    Using a nose only inhalation system, 187 nine week old male Sprague-Dawley rats were exposed to two different concentrations of natural uranium ore dust aerosol (44% U) without significant radon content. Inhalation exposures averaged about 4.2 h/day, 5 days/week for 65 weeks at which point lung uranium burdens in the two groups averaged 0.9 and 1.9 mg/g dry weight. Animals (63) exposed to the air stream without dust served as controls. After inhalation exposure ceased, the rats were allowed to live for their natural lifetime, a maximum of about 900 days after the start of dust inhalation. Lung uranium burdens were measured at the time of death of each animal. Lung burdens were found to decline exponentially after dust inhalation ceased, and the rate of decline was independent of the initial lung burden. All lungs were examined at necropsy and histologically for lung tumors. Lung tumors of lung origin were observed in both exposed groups and in the control group. The frequency of primary malignant lung tumors was 0.016, 0.175 and 0.328 and primary non-malignant lung tumors 0.016, 0.135 and 0.131 in the control low and high aerosol exposed groups respectively. Absorbed dose to the lung was calculated for each animal in the study. The average maximum doses for all the animals exposed to the low or high concentration of dust aerosol were 0.87 Gy and 1.64 Gy respectively. The average risk of malignant lung tumors from inhaled natural uranium ore dust was therefore about 0.20 tumors/animal/Gy. For animals with lung tumors, the average doses were 0.98 and 1.90 in the exposed groups. In both exposed groups, the frequency of primary malignant or non-malignant lung tumors was significantly greater than in the control group (p < 0.02) and the frequency of primary malignant lung tumors in the two exposed group were significantly different from each other (p = 0.05). The frequency of primary lung tumors (malignant and non-malignant) was calculated as a function of dose

  10. LIFETIME LUNG CANCER RISKS ASSOCIATED WITH INDOOR RADON EXPOSURE BASED ON VARIOUS RADON RISK MODELS FOR CANADIAN POPULATION.

    Science.gov (United States)

    Chen, Jing

    2017-04-01

    This study calculates and compares the lifetime lung cancer risks associated with indoor radon exposure based on well-known risk models in the literature; two risk models are from joint studies among miners and the other three models were developed from pooling studies on residential radon exposure from China, Europe and North America respectively. The aim of this article is to make clear that the various models are mathematical descriptions of epidemiologically observed real risks in different environmental settings. The risk from exposure to indoor radon is real and it is normal that variations could exist among different risk models even when they were applied to the same dataset. The results show that lifetime risk estimates vary significantly between the various risk models considered here: the model based on the European residential data provides the lowest risk estimates, while models based on the European miners and Chinese residential pooling with complete dosimetry give the highest values. The lifetime risk estimates based on the EPA/BEIR-VI model lie within this range and agree reasonably well with the averages of risk estimates from the five risk models considered in this study. © Crown copyright 2016.

  11. Radon in workplaces

    International Nuclear Information System (INIS)

    Gooding, Tracy

    1995-01-01

    The naturally occurring radioactive gas radon has been found at excessive levels in many workplaces other than mines throughout the country. Prolonged exposure to radon and its decay products increases the risk of developing lung cancer, and controls to protect employees from excessive exposure are included in the Ionising Radiations Regulations 1985. The control of occupational exposure to radon is discussed here. (author)

  12. Detection of radiation induced lung injury in rats using dynamic hyperpolarized 129Xe magnetic resonance spectroscopy

    International Nuclear Information System (INIS)

    Fox, Matthew S.; Ouriadov, Alexei; Hegarty, Elaine; Thind, Kundan; Wong, Eugene; Hope, Andrew; Santyr, Giles E.

    2014-01-01

    Purpose: Radiation induced lung injury (RILI) is a common side effect for patients undergoing thoracic radiation therapy (RT). RILI can lead to temporary or permanent loss of lung function and in extreme cases, death. Combining functional lung imaging information with conventional radiation treatment plans may lead to more desirable treatment plans that reduce lung toxicity and improve the quality of life for lung cancer survivors. Magnetic Resonance Imaging of the lung following inhalation of hyperpolarized 129 Xe may provide a useful nonionizing approach for probing changes in lung function and structure associated with RILI before, during, or after RT (early and late time-points). Methods: In this study, dynamic 129 Xe MR spectroscopy was used to measure whole-lung gas transfer time constants for lung tissue and red blood cells (RBC), respectively (T Tr-tissue and T Tr-RBC ) in groups of rats at two weeks and six weeks following 14 Gy whole-lung exposure to radiation from a 60 Co source. A separate group of six healthy age-matched rats served as a control group. Results: T Tr-tissue values at two weeks post-irradiation (51.6 ± 6.8 ms) were found to be significantly elevated (p < 0.05) with respect to the healthy control group (37.2 ± 4.8 ms). T Tr-RBC did not show any significant changes between groups. T Tr-tissue was strongly correlated with T Tr-RBC in the control group (r = 0.9601 p < 0.05) and uncorrelated in the irradiated groups. Measurements of arterial partial pressure of oxygen obtained by arterial blood sampling were found to be significantly decreased (p < 0.05) in the two-week group (54.2 ± 12.3 mm Hg) compared to those from a representative control group (85.0 ± 10.0 mm Hg). Histology of a separate group of similarly irradiated animals confirmed the presence of inflammation due to radiation exposure with alveolar wall thicknesses that were significantly different (p < 0.05). At six weeks post-irradiation, T Tr-tissue returned to values (35

  13. Development of a data base on radon in US homes and applications

    Energy Technology Data Exchange (ETDEWEB)

    Cohen, B.L.

    1991-01-01

    This research led to the development of the compilation of data on radon in homes which is included in this document. This research also contributed to the development of two papers analyzing the results. These are a case control study test and tests of the liner no-threshold theory for lung cancer induced by exposure to radon in residential buildings.

  14. Measurement of simulated lung deposition of radon daughters

    International Nuclear Information System (INIS)

    Jonassen, N.; Jensen, B.

    1992-01-01

    A measurement system for the lung deposition of radon daughters based on respiratory models was suggested by Hopke et al. By choosing suitable mesh size and flow velocities it is possible to design a multiple-wire screen sampler simulating deposition in the respiratory tract of aerosols over the size range 0.5-1000 nm. This paper describes a preliminary investigation where simulated deposition in the nasal tract and in the bronchii (for mouth breathing as well as nasal breathing) is determined. The measurements were performed in atmospheres where the normalised exposure rate (equilibrium factor) was varied by changing the aerosol loading of the air as well as by enhanced electrostatic plateout. The general results of the measurements are that the energy deposited in the nose with nasal breathing and in the bronchii with mouth breathing varies as the calculated dose while the energy deposited in the bronchii with nasal breathing follows the exposure. It is also demonstrated that the energy deposited for a fixed value of the radon concentration may vary by a factor of 2-7 depending on the treatment of the air. (author)

  15. Radon - The management of the risk related to radon

    International Nuclear Information System (INIS)

    2010-01-01

    This leaflet briefly explains what radon is, where it comes from, and what it becomes. It indicates and briefly comments its concentrations in French departments, describes how radon can affect our health (lung cancer), describes how the risk can be reduced in buildings, and indicates the existing regulatory provisions

  16. Ischemia postconditioning and mesenchymal stem cells engraftment synergistically attenuate ischemia reperfusion-induced lung injury in rats.

    Science.gov (United States)

    Chen, Shuchen; Chen, Liangwan; Wu, Xiaonan; Lin, Jiangbo; Fang, Jun; Chen, Xiangqi; Wei, Shijin; Xu, Jianxin; Gao, Qin; Kang, Mingqiang

    2012-11-01

    It has been reported that ischemic postconditioning (IPO) or mesenchymal stem cell (MSC) engraftment could protect organs from ischemia/reperfusion (I/R) injury. We investigated the synergetic effects of combined treatment on lung injury induced by I/R. Adult Sprague-Dawley rats were randomly assigned to one of the following groups: sham-operated control, I/R, IPO, MSC engraftment, and IPO plus MSC engraftment. Lung injury was assessed by arterial blood gas analysis, the wet/dry lung weight ratio, superoxide dismutase level, malondialdehyde content, myeloperoxidase activity, and tissue histologic changes. Cytokine expression was detected using real-time polymerase chain reaction, Western blotting, and enzyme-linked immunosorbent assay. Cell apoptosis was determined by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end assay and annexin V staining. MSC engraftment or IPO alone markedly attenuated the lung wet/dry weight ratio, malondialdehyde and myeloperoxidase production, and lung pathologic injury and enhanced arterial partial oxygen pressure, superoxide dismutase content, inhibited pro-inflammatory cytokine levels, and decreased cell apoptosis in lung tissue, compared with the I/R group. In contrast, IPO pretreatment enhanced the protective effects of MSC on I/R-induced lung injury compared with treatment alone. Moreover, in the combined treatment group, the number of MSC engraftments in the lung tissue was increased, associated with enhanced survival of MSCs compared with MSC treatment alone. Additional investigation showed that IPO treatment increased expression of vascular endothelial growth factor and stromal cell-derived factor-1 in I/R lung tissue. IPO might contribute to the homing and survival of transplanted MSCs and enhance their therapeutic effects through improvement of the microenvironment of I/R injury. Copyright © 2012 Elsevier Inc. All rights reserved.

  17. NF-κB inhibition is involved in tobacco smoke-induced apoptosis in the lungs of rats

    International Nuclear Information System (INIS)

    Zhong Caiyun; Zhou Yamei; Pinkerton, Kent E.

    2008-01-01

    Apoptosis is a vital mechanism for the regulation of cell turnover and plays a critical role in tissue homeostasis and development of many disease processes. Previous studies have demonstrated the apoptotic effect of tobacco smoke; however, the molecular mechanisms by which tobacco smoke triggers apoptosis remain unclear. In the present study we investigated the effects of tobacco smoke on the induction of apoptosis in the lungs of rats and modulation of nuclear factor-kappa B (NF-κB) in this process. Exposure of rats to 80 mg/m 3 tobacco smoke significantly induced apoptosis in the lungs. Tobacco smoke resulted in inhibition of NF-κB activity, noted by suppression of inhibitor of κB (IκB) kinase (IKK), accumulation of IκBα, decrease of NF-κB DNA binding activity, and downregulation of NF-κB-dependent anti-apoptotic proteins, including Bcl-2, Bcl-xl, and inhibitors of apoptosis. Initiator caspases for the death receptor pathway (caspase 8) and the mitochondrial pathway (caspase 9) as well as effector caspase 3 were activated following tobacco smoke exposure. Tobacco smoke exposure did not alter the levels of p53 and Bax proteins. These findings suggest the role of NF-κB pathway in tobacco smoke-induced apoptosis

  18. Captopril reduces collagen and mast cell accumulation in irradiated rat lung

    International Nuclear Information System (INIS)

    Ward, W.F.; Molteni, A.; Ts'ao, C.H.; Hinz, J.M.

    1990-01-01

    The angiotensin converting enzyme inhibitor captopril ameliorates radiation-induced pulmonary endothelial dysfunction in rats. The present study determined whether captopril also reduces collagen (hydroxyproline) accumulation in the lungs of rats sacrificed 2 months after a range of single doses (0-30 Gy) of 60Co gamma rays to the right hemithorax. Captopril was administered in the feed at a regimen of 0, 25, or 50 mg/kg/day continuously after irradiation. Mast cell counts also were obtained from lungs of all animals exposed to 30 Gy. In rats receiving no captopril, there was a radiation dose-dependent increase in right lung hydroxyproline (HP) content and in HP concentration per g wet weight. Captopril produced a drug dose-dependent suppression in this radiation-induced HP accumulation. At a dose of 50 mg/kg/d, captopril reduced the slope of the radiation dose response curve for lung HP content by a factor of 1.7, and completely prevented the increase in HP concentration. At an isoeffect level of 550 micrograms HP per right superior lobe, this dose of captopril exhibited a DRF of 1.7 +/- 0.2. In rats exposed to 30 Gy, moreover, the number of mast cells per mm2 of alveolar cross-sectional surface area decreased from 105 +/- 8 to 100 +/- 7 and 59 +/- 5 in the groups given 0, 25 or 50 mg/kg/d of captopril, respectively, (vs none in sham-irradiated rats). These data are the first to demonstrate that the ACE inhibitor captopril might provide a novel intervention in the pathogenesis of radiation fibrosis

  19. Developmental toxicology of radon exposures

    International Nuclear Information System (INIS)

    Sikov, M.R.; Cross, F.T.; Mast, T.J.; Palmer, H.E.; James, A.C.; Thrall, K.D.

    1992-01-01

    Concerns about hazards associated with radon exposure in dwellings may be especially relevant to pregnant women, many of whom spend substantial amounts of time in their homes. There are few data concerning the placental transfer and fetoplacental distribution of inhaled radon and decay products or their effects on the conceptus. We performed a study in rats to determine if prenatal effects could be produced by prolonged inhalation exposures to high concentrations of radon throughout gestation. A group of 43 pregnant rats was exposed 18 h d -1 , at a rate of 124 working level months (WLM) per day, from 6 to 19 days of gestation (dg), of radon and daughters adsorbed onto ore dust. A group of 26 pregnant rats from the same shipment was exposed to a filtered-air atmosphere as controls. At 20 dg, the rats were removed from the chambers, killed, and necropsied. The fetuses were evaluated for the presence of toxic effects, which included detailed teratology protocols. These exposures did not produce detectable reproductive toxicity nor teratogenic change. Two other rats were removed from the radon chambers during the last day of exposure, and their tissues were analyzed to determine the distribution of radioactivity and for dosimetry. Samples from these rats suggested that the dose rates to the placenta were roughly threefold those to the fetus but were similar to those to the liver and femur of the pregnant rats. These data indicate that the dose to the conceptus from the decay of placentally transferred radon and its progeny is more important than the contribution of translocated decay products. Translocated radon decay products are an important source of radiation doses to placental structures, however, and may have most of the radioactivity content at birth

  20. Comparisons of indoor radon to other radiation hazards

    International Nuclear Information System (INIS)

    Bodansky, D.; Jackson, K.L.; Geraci, J.P.

    1987-01-01

    The significance of radon as a cause of cancer can be put into perspective by a comparison with other causes of cancer. Lung cancer is fatal in about 90% of the cases and therefore in assessing radon exposures it is pertinent to make a comparison in terms of mortality figures. There is a broad range of estimates for the U.S. lung cancer mortality from indoor radon, extending from well below 5,000 to above 20,000 per year. For simplicity in making comparisons, the authors use an intermediate estimate of 10,000 per year, although one needs to bear in mind this number is uncertain. Given approximately 480,000 fatal cancers in the United States per year and 136,000 fatal lung cancers, this estimate corresponds to indoor radon being responsible for 2% of all cancer mortality and 7% of lung cancer mortality. It is estimated that 83% of lung cancers are due to smoking, corresponding to about 113,000 deaths per year. Overall, therefore, smoking is far more important than indoor radon as a cause of lung cancer. Despite the authors' concentration on it, radon is a relatively small contributor in the perspective of cancer as a whole or even of lung cancer alone. It is a more dominant contributor in considering average exposures to ionizing radiation

  1. Some comments on the feasibility of an epidemiological study on incidence of lung cancer due to exposure to radon daughters

    International Nuclear Information System (INIS)

    Elsasser, U.

    1988-01-01

    For two different designs of a study - cohort and case control study - estimates of required sample size have been made on the basis of lung cancer risk assessment data for exposure to radon and radon daughters. The estimates have shown that a cohort study is not feasible for reasons of unjustifiably high requirements. A case control study, however, may contribute to clarifying the lung cancer risk, especially if the basic overall entity is limited to the population group of over 50 years of age. (orig.) [de

  2. Combined effect of radon exposure and smoking on lung cancer risk - result of a case-control study among Czech miners

    International Nuclear Information System (INIS)

    Tomasek, Ladislav

    2010-01-01

    Because of the predominant role of cigarette smoking as a cause of lung cancer, an understanding of the joint effect of smoking and radon exposure is needed for the assessment of the risk from radon. The aim of the present work is to verify differences in smoking specific risk coefficients observed earlier (BEIR VI). The present study includes two cohorts of uranium miners in west and central Bohemia and one cohort of burnt clay miners exposed to radon. In the nested study, for each case of lung cancer (observed in 1954-2007) with smoking data up to three controls were selected from all cohort members matched by year of birth, age, and the cohort. Data on smoking in the study were collected from subjects in person, from medical records, and from relatives. The statistical assessment of the study was based on conditional logistic regression with linear dependence of estimated relative risk on radon exposure

  3. How dangerous is radon in buildings? - Some reflections from Europe

    International Nuclear Information System (INIS)

    Becker, K.

    1994-01-01

    ICRP published recommendations on indoor radon in 1987. Based on the suggested action levels for new and existing houses of 200 and 400 Bq/m 3 , various countries established levels of their own which vary between 150 Bq/m 3 in the United States, and 200-250 in most European countries. In 1989, the ICRP Task Group responsible for radon proposed another increase of the risk factors by about a factor of three. This would imply more radon-induced lung cancers in certain nonsmoking population groups than are totally observed. On the other hand, there is an increasing number of scientists who seriously question the validity of the ICRP assumptions, and all the more or less official governmental actions based on them -- including the substantial socioeconomic impact of remedial measures which would be required in high-radon areas. In this editorial the author discusses some cases in which people have exposed themselves to radon for its supposedly therapeutic effects and have not apparently suffered an increase in health problems as would have been expected based on data of lung cancer in uranium miners. The author discusses the complexity of determining the health hazards of radon gas and the associated problems of establishing safe exposure limits. 11 refs

  4. Evaluation of different radon guideline values based on characterization of ecological risk and visualization of lung cancer mortality trends in British Columbia, Canada.

    Science.gov (United States)

    Branion-Calles, Michael C; Nelson, Trisalyn A; Henderson, Sarah B

    2015-11-19

    There is no safe concentration of radon gas, but guideline values provide threshold concentrations that are used to map areas at higher risk. These values vary between different regions, countries, and organizations, which can lead to differential classification of risk. For example the World Health Organization suggests a 100 Bq m(-3)value, while Health Canada recommends 200 Bq m(-3). Our objective was to describe how different thresholds characterized ecological radon risk and their visual association with lung cancer mortality trends in British Columbia, Canada. Eight threshold values between 50 and 600 Bq m(-3) were identified, and classes of radon vulnerability were defined based on whether the observed 95(th) percentile radon concentration was above or below each value. A balanced random forest algorithm was used to model vulnerability, and the results were mapped. We compared high vulnerability areas, their estimated populations, and differences in lung cancer mortality trends stratified by smoking prevalence and sex. Classification accuracy improved as the threshold concentrations decreased and the area classified as high vulnerability increased. Majority of the population lived within areas of lower vulnerability regardless of the threshold value. Thresholds as low as 50 Bq m(-3) were associated with higher lung cancer mortality, even in areas with low smoking prevalence. Temporal trends in lung cancer mortality were increasing for women, while decreasing for men. Radon contributes to lung cancer in British Columbia. The results of the study contribute evidence supporting the use of a reference level lower than the current guideline of 200 Bq m(-3) for the province.

  5. Tualang Honey Protects the Rat Midbrain and Lung against Repeated Paraquat Exposure.

    Science.gov (United States)

    Tang, Suk Peng; Kuttulebbai Nainamohamed Salam, Sirajudeen; Jaafar, Hasnan; Gan, Siew Hua; Muzaimi, Mustapha; Sulaiman, Siti Amrah

    2017-01-01

    Paraquat (PQ) is a dopaminergic neurotoxin and a well-known pneumotoxicant that exerts its toxic effect via oxidative stress-mediated cellular injuries. This study investigated the protective effects of Tualang honey against PQ-induced toxicity in the midbrain and lungs of rats. The rats were orally treated with distilled water (2 mL/kg/day), Tualang honey (1.0 g/kg/day), or ubiquinol (0.2 g/kg/day) throughout the experimental period. Two weeks after the respective treatments, the rats were injected intraperitoneally with saline (1 mL/kg/week) or PQ (10 mg/kg/week) once per week for four consecutive weeks. After four weekly exposures to PQ, the glutathione peroxidase activity and the number of tyrosine-hydroxylase immunopositive neurons in the midbrain were significantly decreased in animals from group PQ ( p honey ameliorated the toxic effects observed in the midbrain and lungs. The beneficial effects of Tualang honey were comparable to those of ubiquinol, which was used as a positive control. These findings suggest that treatment with Tualang honey may protect against PQ-induced toxicity in the rat midbrain and lung.

  6. Tualang Honey Protects the Rat Midbrain and Lung against Repeated Paraquat Exposure

    Science.gov (United States)

    Sulaiman, Siti Amrah

    2017-01-01

    Paraquat (PQ) is a dopaminergic neurotoxin and a well-known pneumotoxicant that exerts its toxic effect via oxidative stress-mediated cellular injuries. This study investigated the protective effects of Tualang honey against PQ-induced toxicity in the midbrain and lungs of rats. The rats were orally treated with distilled water (2 mL/kg/day), Tualang honey (1.0 g/kg/day), or ubiquinol (0.2 g/kg/day) throughout the experimental period. Two weeks after the respective treatments, the rats were injected intraperitoneally with saline (1 mL/kg/week) or PQ (10 mg/kg/week) once per week for four consecutive weeks. After four weekly exposures to PQ, the glutathione peroxidase activity and the number of tyrosine-hydroxylase immunopositive neurons in the midbrain were significantly decreased in animals from group PQ (p honey ameliorated the toxic effects observed in the midbrain and lungs. The beneficial effects of Tualang honey were comparable to those of ubiquinol, which was used as a positive control. These findings suggest that treatment with Tualang honey may protect against PQ-induced toxicity in the rat midbrain and lung. PMID:28127418

  7. The significance of radon in radioactive pollution of environment. Pt. 2. Radon effect on living organism

    International Nuclear Information System (INIS)

    Kossakowski, S.; Dziura, A.; Kossakowski, A.

    1998-01-01

    Authors review the history of radon monitoring. Epidemiological studies of lung cancer and its correlation to radon concentration in mines and buildings are described. The influence of radon on animals living in the buildings built from waste materials is described. Authors review plans concerning creation of radon monitoring system in Poland. The necessity of monitoring influence of radon on animals is described

  8. Health effects of radon in air

    International Nuclear Information System (INIS)

    Cohen, B.L.

    1988-01-01

    Widely accepted risk estimates for exposure to radon in homes are derived largely from studies of miners. These include large groups of US Czechoslovakian, and Canadian uranium miners, Newfoundland fluorspar miners, and Swedish iron, lead, and zinc miners, all of which give roughly consistent results, with the excess risk of lung cancer increasing linearly with the exposure to radon. The authors have studied correlations between average radon levels and lung cancer rates in counties of the US. One study based on 50,000 purchased measurements in the main living areas of houses in which there have been no previous measurements involves 310 counties. It gives a weak but statistically significant negative correlation between mean radon levels and lung cancer rates for both females and males, whereas the usual risk estimates predict a large positive correlation

  9. Changes in the rat lung after exposure to radon and its progeny: Effects on incorporation of bromodeoxyuridine in epithelial cells and on the incidence of nuclear aberrations in Alveolar macrophages

    International Nuclear Information System (INIS)

    Taya, A.; Morgan, A.; Baker, S.T.; Humphreys, J.A.H.; Collier, C.G.; Bisson, M.

    1994-01-01

    The aim of this study was to investigate some responses of cells in the rat respiratory tract as a function of time after inhalation exposure to various levels of radon and its progeny. Rats were exposed to a constant concentration of radon and its progeny to give cumulative exposure levels of 120, 225, 440 and 990 working level months (WLM). An additional unexposed group of rats served as controls. The end points selected for investigation were (a) the incorporation of bromodeoxyuridine (BrdU) in epithelial cells of the conducting airways and of the alveolar region of the respiratory tract and (b) the incidence of alveolar macrophages with nuclear aberrations. After exposure, the incidence of epithelial cells incorporating BrdU-the labeling index-increased in all regions of the respiratory tract examined, but the increase occurred later in alveolar than in airway epithelial cells. The highest labeling index was found in bronchial epithelial cells, which probably received the highest radiation dose. After an initial induction period, the incidence of alveolar macrophages with nuclear aberrations also increased. The possibility of using the labeling index of alveolar and airway epithelial cells, and/or the incidence of nuclear aberrations in alveolar macrophages, to estimate the radiation dose to various regions of the respiratory tract after exposure of rats to radon and its progeny is discussed. 22 refs., 3 figs., 1 tab

  10. Epigallocatechin-3-gallate Ameliorates Seawater Aspiration-Induced Acute Lung Injury via Regulating Inflammatory Cytokines and Inhibiting JAK/STAT1 Pathway in Rats

    Science.gov (United States)

    Liu, Wei; Dong, Mingqing; Bo, Liyan; Li, Congcong; Liu, Qingqing; Li, Yanyan; Ma, Lijie; Xie, Yonghong; Fu, Enqing; Mu, Deguang; Pan, Lei; Jin, Faguang; Li, Zhichao

    2014-01-01

    Signal transducers and activators of transcriptions 1 (STAT1) play an important role in the inflammation process of acute lung injury (ALI). Epigallocatechin-3-gallate (EGCG) exhibits a specific and strong anti-STAT1 activity. Therefore, our study is to explore whether EGCG pretreatment can ameliorate seawater aspiration-induced ALI and its possible mechanisms. We detected the arterial partial pressure of oxygen, lung wet/dry weight ratios, protein content in bronchoalveolar lavage fluid, and the histopathologic and ultrastructure staining of the lung. The levels of IL-1, TNF-α, and IL-10 and the total and the phosphorylated protein level of STAT1, JAK1, and JAK2 were assessed in vitro and in vivo. The results showed that EGCG pretreatment significantly improved hypoxemia and histopathologic changes, alleviated pulmonary edema and lung vascular leak, reduced the production of TNF-α and IL-1, and increased the production of IL-10 in seawater aspiration-induced ALI rats. EGCG also prevented the seawater aspiration-induced increase of TNF-α and IL-1 and decrease of IL-10 in NR8383 cell line. Moreover, EGCG pretreatment reduced the total and the phosphorylated protein level of STAT1 in vivo and in vitro and reduced the phosphorylated protein level of JAK1 and JAK2. The present study demonstrates that EGCG ameliorates seawater aspiration-induced ALI via regulating inflammatory cytokines and inhibiting JAK/STAT1 pathway in rats. PMID:24692852

  11. Lung Cancer Mortality and Radon Concentration in a Chronically Exposed Neighborhood in Chihuahua, Mexico: A Geospatial Analysis

    Science.gov (United States)

    Hinojosa de la Garza, Octavio R.; Sanín, Luz H.; Montero Cabrera, María Elena; Serrano Ramirez, Korina Ivette; Martínez Meyer, Enrique; Reyes Cortés, Manuel

    2014-01-01

    This study correlated lung cancer (LC) mortality with statistical data obtained from government public databases. In order to asses a relationship between LC deaths and radon accumulation in dwellings, indoor radon concentrations were measured with passive detectors randomly distributed in Chihuahua City. Kriging (K) and Inverse-Distance Weighting (IDW) spatial interpolations were carried out. Deaths were georeferenced and Moran's I correlation coefficients were calculated. The mean values (over n = 171) of the interpolation of radon concentrations of deceased's dwellings were 247.8 and 217.1 Bq/m3, for K and IDW, respectively. Through the Moran's I values obtained, correspondingly equal to 0.56 and 0.61, it was evident that LC mortality was directly associated with locations with high levels of radon, considering a stable population for more than 25 years, suggesting spatial clustering of LC deaths due to indoor radon concentrations. PMID:25165752

  12. Human Lung Cancer Risks from Radon – Part I - Influence from Bystander Effects - A Microdose Analysis

    Science.gov (United States)

    Leonard, Bobby E.; Thompson, Richard E.; Beecher, Georgia C.

    2010-01-01

    Since the publication of the BEIR VI report in 1999 on health risks from radon, a significant amount of new data has been published showing various mechanisms that may affect the ultimate assessment of radon as a carcinogen, at low domestic and workplace radon levels, in particular the Bystander Effect (BE) and the Adaptive Response radio-protection (AR). We analyzed the microbeam and broadbeam alpha particle data of Miller et al. (1995, 1999), Zhou et al. (2001, 2003, 2004), Nagasawa and Little (1999, 2002), Hei et al. (1999), Sawant et al. (2001a) and found that the shape of the cellular response to alphas is relatively independent of cell species and LET of the alphas. The same alpha particle traversal dose response behavior should be true for human lung tissue exposure to radon progeny alpha particles. In the Bystander Damage Region of the alpha particle response, there is a variation of RBE from about 10 to 35. There is a transition region between the Bystander Damage Region and Direct Damage Region of between one and two microdose alpha particle traversals indicating that perhaps two alpha particle “hits” are necessary to produce the direct damage. Extrapolation of underground miners lung cancer risks to human risks at domestic and workplace levels may not be valid. PMID:21731539

  13. Effect of radon inhalations on certain oxyda-reductive enzymes in adrenols of white rats

    International Nuclear Information System (INIS)

    Robaczynski, J.; Kaplonska, J.; Lozinska, E.

    1974-01-01

    Histochemical investigations were carried out on adrenals of white rats after radon inhalations from inhalers in Swieradow-spa. Increased reactions of oxydo-reductive enzymes: NAD tetrazolium reductase, succinic dehydrogenase and glucose-6-phosphate dehydrogenase were observed in the adrenal cortex, particularly in the zona reticularis which was hypertrophied. Raised activity of oxydo-reductive enzymes in the cells of adrenal cortex evidences increased metabolism in these cells which may reflect increased production of hormones. Finding of stimulation of adrenocortical cells after radon inhalations is of essential importance for explanation of the biological mechanism of action of radon used in balneotherapy. (author)

  14. Estimation of the Radon-induced Dose for Russia's Population: Methods and Results

    International Nuclear Information System (INIS)

    Marenny, A.M.; Savkin, M.N.; Shinkarev, S.M.

    2000-01-01

    A model is proposed for inferring the radon-induced annual average collective and personal doses, as well as the dose distribution of the population, all over Russia from selective radon monitoring in some regions of Russia. The model assumptions and the selective radon monitoring results that underlie the numerical estimates obtained for different population groups are presented. The current estimate of the collective radon-induced dose received by the population of Russia (148,100,000 as of 1996) is about 130,000 man Sv, of which 55,000 man Sv is for the rural population (27% of the total population) and 75,000 man Sv for the urban population (73% of the total). The average radon-induced personal dose in Russia is estimated to be about 0.87 mSv. About 1,000,000 people receive annual doses above 10 mSv, including some 200,000 people who receive doses above 20 mSv annually. The ways of making the current estimates more accurate are outlined. (author)

  15. Telomere elongation protects heart and lung tissue cells from fatal damage in rats exposed to severe hypoxia.

    Science.gov (United States)

    Wang, Yaping; Zhao, Zhen; Zhu, Zhiyong; Li, Pingying; Li, Xiaolin; Xue, Xiaohong; Duo, Jie; Ma, Yingcai

    2018-02-17

    The effects of acute hypoxia at high altitude on the telomere length of the cells in the heart and lung tissues remain unclear. This study aimed to investigate the change in telomere length of rat heart and lung tissue cells in response to acute exposure to severe hypoxia and its role in hypoxia-induced damage to heart and lung tissues. Forty male Wistar rats (6-week old) were randomized into control group (n = 10) and hypoxia group (n = 30). Rats in control group were kept at an altitude of 1500 m, while rats in hypoxia group were exposed to simulated hypoxia with an altitude of 5000 m in a low-pressure oxygen chamber for 1, 3, and 7 days (n = 10). The left ventricular and right middle lobe tissues of each rat were collected for measurement of telomere length and reactive oxygen species (ROS) content, and the mRNA and protein levels of telomerase reverse transcriptase (TERT), hypoxia-inducible factor1α (HIF-1α), and hypoxia-inducible factor1α (HIF-2α). Increased exposure to hypoxia damaged rat heart and lung tissue cells and increased ROS production and telomere length. The mRNA and protein levels of TERT and HIF-1α were significantly higher in rats exposed to hypoxia and increased with prolonged exposure; mRNA and protein levels of HIF-2α increased only in rats exposed to hypoxia for 7 days. TERT was positively correlated with telomere length and the levels of HIF-1α but not HIF-2α. Acute exposure to severe hypoxia causes damage to heart and lung tissues due to the production of ROS but promotes telomere length and adaptive response by upregulating TERT and HIF-1α, which protect heart and lung tissue cells from fatal damage.

  16. Maternal deprivation decelerates postnatal morphological lung development of F344 rats.

    Science.gov (United States)

    Hupa, Katharina Luise; Schmiedl, Andreas; Pabst, Reinhard; Von Hörsten, Stephan; Stephan, Michael

    2014-02-01

    Intensive medical care at premature born infants is often associated with separation of neonates from their mothers. Here, early artificial prolonged separation of rat pups from their dams (Maternal Deprivation, MD) was used to study potential impact on morphological lung maturation. Furthermore, we investigated the influence of an endogenous deficiency of the neuropeptide-cleaving dipeptidyl peptidase IV (DPP4), since the effects of MD are known to be partly mediated via neuropeptidergic effects, hypothesizing that MD will lead to a retardation of postnatal lung development, DPP4-dependendly. We used wild type and CD26/DPP4 deficient rats. For MD, the dam was placed each day into a separate cage for 2 h, while the pups remained in the nest on their own. Morphological lung maturation and cell proliferation at the postnatal days 7, 10, 14, and 21 were determined morphometrically. Maternally deprived wild types showed a retarded postnatal lung development compared with untreated controls in both substrains. During alveolarization, an increased thickness of alveolar septa and a decreased surface of septa about 50% were found. At the end of the morphological lung maturation, the surface of the alveolar septa was decreased at about 25% and the septal thickness remained increased about 20%. The proliferation rate was also decreased about 50% on day 14. However, the MD induced effects were less pronounced in DPP4-deficient rats, due to a significant deceleration already induced by DPP4-deficiency. Thus, MD as a model for postnatal stress experience influences remarkably postnatal development of rats, which is significantly modulated by the DPP4-system. Copyright © 2013 Wiley Periodicals, Inc.

  17. Bioactive Components from Qingwen Baidu Decoction against LPS-Induced Acute Lung Injury in Rats

    Directory of Open Access Journals (Sweden)

    Qi Zhang

    2017-04-01

    Full Text Available Qingwen Baidu Decoction (QBD is an extraordinarily “cold” formula. It was traditionally used to cure epidemic hemorrhagic fever, intestinal typhoid fever, influenza, sepsis and so on. The purpose of this study was to discover relationships between the change of the constituents in different extracts of QBD and the pharmacological effect in a rat model of acute lung injury (ALI induced by lipopolysaccharide (LPS. The study aimed to discover the changes in constituents of different QBD extracts and the pharmacological effects on acute lung injury (ALI induced by LPS. The results demonstrated that high dose and middle dose of QBD had significantly potent anti-inflammatory effects and reduced pulmonary edema caused by ALI in rats (p < 0.05. To explore the underlying constituents of QBD, we assessed its influence of six different QBD extracts on ALI and analyzed the different constituents in the corresponding HPLC chromatograms by a Principal Component Analysis (PCA method. The results showed that the pharmacological effect of QBD was related to the polarity of its extracts, and the medium polarity extracts E2 and E5 in particular displayed much better protective effects against ALI than other groups. Moreover, HPLC-DAD-ESI-MSn and PCA analysis showed that verbascoside and angoroside C played a key role in reducing pulmonary edema. In addition, the current study revealed that ethyl gallate, pentagalloylglucose, galloyl paeoniflorin, mudanpioside C and harpagoside can treat ALI mainly by reducing the total cells and infiltration of activated polymorphonuclear leukocytes (PMNs.

  18. Health hazards due to radon and its daughters

    International Nuclear Information System (INIS)

    Khan, H.A.; Qureshi, I.E.; Tufail, M.

    1993-01-01

    The health hazards liked to radon and its daughters have become a matter of great public concern. When inhaled, a fraction of radon is dissolved into the lung fluid, from where it is transported to other parts of the body. The radiation damage is caused to the lungs due to alpha decay of radon during its transit time within the respiratory tract. Radon daughters are found to be even more dangerous than radon itself. These daughters attach themselves to dust particles present in the air. Some of the aerosols so produced enter the lungs and enter the blood stream. It has now been confirmed that radon and its daughters contribute about 70% of the internal dose received by an individual from natural radiation sources. The danger of indoor radon and its daughters is even higher for energy-saving houses and those having poor ventilation systems. This paper briefly describes the health hazards due to radon and its daughters. Different methods employed for the measurement of concentrations of radon and their daughters are described. The experience gained from the nation-wide surveys carried out in different countries is also given. (author). 18 refs, 3 figs, 1 tab

  19. Radon: implications for the health professional

    International Nuclear Information System (INIS)

    Romano, C.A.

    1990-01-01

    Radon is a colorless, odorless gas formed by radioactive decay of radium and uranium, which are naturally present in the earth's crust. When concentrated indoors, this invisible gas becomes a potential health hazard. The Environmental Protection Agency estimates that up to 20,000 lung cancer deaths annually can be attributed to prolonged radon exposure. Radon is an important health issue that should be understood by all health care professionals. This paper discusses some of the important issues regarding radon, such as the incidences of lung cancer believed to be attributable to radon, the high-risk areas in the United States, federal safety guidelines, and public apathy. These issues and their impact on the health care required by professionals, especially nurse practitioners, are discussed

  20. Experimental studies on lung carcinogenesis and their relationship to future research on radiation-induced lung cancer in humans

    International Nuclear Information System (INIS)

    Cross, F.T.

    1991-03-01

    The usefulness of experimental systems for studying human lung carcinogenesis lies in the ease of studying components of a total problem. As an example, the main thrust of attack on possible synergistic interactions between radiation, cigarette smoke, and other irritants must be by means of research on animals. Because animals can be serially sacrificed, a systematic search can be made for progressive lung changes, thereby improving our understanding of carcinogenesis. The mechanisms of radiation-induced carcinogenesis have not yet been delineated, but modern concepts of molecular and cellular biology and of radiation dosimetry are being increasingly applied to both in vivo and in vitro exposure to determine the mechanisms of radiation-induced carcinogenesis, to elucidate human data, and to aid in extrapolating experimental animal data to human exposures. In addition, biologically based mathematical models of carcinogenesis are being developed to describe the nature of the events leading to malignancy; they are also an essential part of a rational approach to quantitative cancer risk assessment. This paper summarizes recent experimental and modeling data on radon-induced lung cancer and includes the confounding effects of cigarette-smoke exposures. The applicability of these data to understanding human exposures is emphasized, and areas of future research on human radiation-induced carcinogenesis are discussed. 7 refs., 2 figs., 3 tabs

  1. Solar radon reduction at six homes in northeast Iowa

    International Nuclear Information System (INIS)

    Rhoads, H.E.; Hoekje, P.L.

    1995-01-01

    Growing concern about radon lung cancer risks, carbon monoxide poisoning, and the sick building syndrome have increased demand for improved indoor air quality. Through solar pre-heating of ventilation air, the Solar Radon Reduction System (SRRS) provides energy benefits with lower installation costs than conventional air-to-air heat exchangers and sub-slab suction approaches. Indoor air quality is improved through dilution, combustion appliance make-up air, pressurization, and reduced radon infiltration through induced-draft solar air collectors drawing supply air from outdoors. Installed at six homes in Waterloo and Cedar Falls, Iowa, the SRRS was found to significantly reduce radon concentrations in all houses with energy benefits and improved overall indoor comfort. Up to 73% reductions from closed house levels as high as 20.9 pCi/L were achieved

  2. Radon in Africa: South African Lessons Learnt

    International Nuclear Information System (INIS)

    Simanga, A.T.

    2010-01-01

    Radon remained a chemical curiosity for decades, promoted at some stage as a health giving gas. Mining related history: (based on ICRP 65) dating back to 15 Century when high mortality from lung cancer was observed among miners in Schneeberg. After the Curies had extracted Radium from Jachymov ores (1898), radon was identified. When measurements were done in Schneeberger and Jachymov mines high concentrations of radon were found. Initially a link was assumed between lung cancer and high radon concentration based on the measurements. (The assumption was not generally accepted).In 1953 William F. Bale indicated that the causative agents of lung cancer was the radon progeny and not radon gas. A possible lung cancer risk to members of the public was discovered very recently (first published results were based on the indoor measurements done in Sweden in a study initiated by Rolf Sievert) Much attention has been given to radon as a radiological health hazard: Recently human exposure to radon progeny in buildings has emerged as an important issue. Lung cancer is the principal concern associated with Rn exposure. The principal concern is associated with radon progeny. These species are chemically reactive, and may be deposited on respiratory tract tissues when inhaled. Subsequent alpha particle decay may damage cells near the deposition site, contributing to increased risk of lung cancer Radon: In Occupational Exposure Protection against Rn Exposure is a Techno-Legal Legal Aspects: There has to be a national legislative framework for the protection of workers against radon The legal framework should entail, inter alia: - Set up of regulator, development of regulations and standards to enable compliance assurance and other protection issues, training of technical people. 10 Legislative Framework in South Africa National Nuclear Regulatory Act (1999) Enables the regulator (NNR) to exercise oversight for Rn protection Occupational Exposure is mainly in Mining and Mineral

  3. Scopingreport radon

    International Nuclear Information System (INIS)

    Blaauboer, R.O.; Vaas, L.H.; Hesse, J.M.; Slooff, W.

    1989-09-01

    This report contains general information on radon concerning the existing standards, sources and emissions, the exposure levels and effect levels. lt serves as a basis for the discussion during the exploratory melting to be held in November/December 1989, aimed at determining the contents of the Integrated Criteria Document Radon. Attention is focussd on Rn-222 (radon) and Rn-220 (thoron), presently of public interest because of radon gas pollution in private homes. In the Netherlands air quality standards nor product standards for the exhalation rate of building materials have been recommended. The major source of radon in the Netherlands is the soil gas (> 97%), minor sources are phosphate residues and building materials (> 2% in total). Hence, the major concern is the transfer through the inhalation of air, the lung being the most critical organ at risk to develop cancer. Compared to risks for humans, the risks of radon and its daughters for aquatic and terrestric organisms, as well as for agricultural crops and livestock, are assumed to be limited. In the Netherlands the average dose for man due to radon and thoron progeny is appr. 1.2 mSv per year, the estimated dose range being 0.1-3.5 mSv per year. This dose contributes for about 50% to rhe total exposure due to all sources of ionizing radiation. Of this dose respectively 80% is caused by radon and about 90% is received indoor. The estimated dose for the general population corresponds to a risk for inducing fatal cancers of about 15 x 10-6 per year, ranging from 1.2 x 10-6 to 44 x 10-6 which exceeds the risk limit of 1 x 10-6 per year -as defined in the standardization policy in the Netherlands for a single source of ionizing radiation-with a factor 15 (1- 44). Reduction of exposure is only possible in the indoor environment. Several techniques have been described to reduce the indoor dose, resulting from exhalation of the soil and building materials. )aut- hor). 37 refs.; 3 figs.; 8 tabs

  4. A perspective on risks from radon

    International Nuclear Information System (INIS)

    Higson, D. J.

    2010-10-01

    In its Statement on Radon (November 2009), the International Commission on Radiological Protection (ICRP) has reduced the upper reference level for radon gas in dwellings to 300 Bq m -3 . The recommended level for workplaces is 1000 Bq m -3 . A risk coefficient of 8 x 10 -10 per Bq h m -3 is recommended without reference to smoking habits. On the basis of these figures: 1) The estimated risk of fatal cancer from exposure to radon at home and at work could be greater than the observed risk of accidental death from travelling by car, which would be surprising if true. 2) The estimated risk of lung cancer from radon could be greater than the observed risk of lung cancer from all causes, which is actually known to be dominated by smoking. The author is not aware of any direct evidence of risks from inhaling radon in Australian dwellings, 99% of which have radon levels below 50 Bq m -3 . Evidence available from other countries shows that: 1) The effects of radon in the incidences of lung cancer are uncertain at levels less then about 50-100 Bq m -3 . 2) The estimation of risks at levels below 200 Bq m -3 depends on extrapolation from risks observed at higher levels. 3) Risks to non-smokers from radon are 25 times less than risks to smokers. Its concluded that the ICRP Statement on Radon and radon policies in the US and UK have the potential to cause unwarranted concern. Some people may be made to feel they need to spend money modifying their homes and workplaces to protect occupants from exposure to radon when there is no compelling reason to show that this is necessary. The vast majority of non-smokers do not need to be protected from radon. (Author)

  5. A perspective on risks from radon

    International Nuclear Information System (INIS)

    Higson, D.J.

    2011-01-01

    In its Statement on Radon (November 2009), the ICRP has reduced the upper reference level for radon gas in dwellings to 300 Bq m -3 . The recommended level for workplaces is 1000 Bq m -3 . A risk coefficient of 8x10 -10 per Bq h m is recommended without reference to smoking habits. On the basis of these figures,the estimated risk of fatal cancer from exposure to radon at home and at work could be greater than the observed risk of accidental death from travelling by car, which would be surprising if true. Also the estimated risk of lung cancer from radon could be greater than the observed risk of lung cancer from all causes, which is actually known to be dominated by smoking. The author is not aware of any direct evidence of risks from inhaling radon in Australian dwellings, 99% of which have radon levels below 50 Bq m -3 . Evidence available from other countries shows that: effects on the incidences of lung cancer are uncertain at radon levels below 100 Bq m -3 ; the estimation of risks at levels below 200 Bq m -3 depends on extrapolation from risks observed at higher levels, and risks to non-smokers from radon are 25 times less than risks to smokers. It is concluded that the ICRP Statement on Radon and radon policies in the US and UK have the potential to cause unwarranted concern. Some people may be made to feel they need to spend money modifying their homes and workplaces to protect occupants from exposure to radon when there is no compelling reason to show that this is necessary. The vast majority of non-smokers do not need to be protected from radon.

  6. A perspective on risks from radon

    Energy Technology Data Exchange (ETDEWEB)

    Higson, D. J., E-mail: higsond@bigpond.net.a [Australasian Radiation Protection Society, PO Box 7108, Upper Ferntree Gully, Victoria 3156 (Australia)

    2010-10-15

    In its Statement on Radon (November 2009), the International Commission on Radiological Protection (ICRP) has reduced the upper reference level for radon gas in dwellings to 300 Bq m{sup -3}. The recommended level for workplaces is 1000 Bq m{sup -3}. A risk coefficient of 8 x 10{sup -10} per Bq h m{sup -3} is recommended without reference to smoking habits. On the basis of these figures: 1) The estimated risk of fatal cancer from exposure to radon at home and at work could be greater than the observed risk of accidental death from travelling by car, which would be surprising if true. 2) The estimated risk of lung cancer from radon could be greater than the observed risk of lung cancer from all causes, which is actually known to be dominated by smoking. The author is not aware of any direct evidence of risks from inhaling radon in Australian dwellings, 99% of which have radon levels below 50 Bq m{sup -3}. Evidence available from other countries shows that: 1) The effects of radon in the incidences of lung cancer are uncertain at levels less then about 50-100 Bq m{sup -3}. 2) The estimation of risks at levels below 200 Bq m{sup -3} depends on extrapolation from risks observed at higher levels. 3) Risks to non-smokers from radon are 25 times less than risks to smokers. Its concluded that the ICRP Statement on Radon and radon policies in the US and UK have the potential to cause unwarranted concern. Some people may be made to feel they need to spend money modifying their homes and workplaces to protect occupants from exposure to radon when there is no compelling reason to show that this is necessary. The vast majority of non-smokers do not need to be protected from radon. (Author)

  7. Alveolar macrophages have a dual role in a rat model for trimellitic anhydride-induced occupational asthma

    International Nuclear Information System (INIS)

    Valstar, Dingena L.; Schijf, Marcel A.; Nijkamp, Frans P.; Storm, Gert; Arts, Josje H.E.; Kuper, C. Frieke; Bloksma, Nanne; Henricks, Paul A.J.

    2006-01-01

    Occupational exposure to low molecular weight chemicals, like trimellitic anhydride (TMA), can result in occupational asthma. Alveolar macrophages (AMs) are among the first cells to encounter inhaled compounds. These cells can produce many different mediators that have a putative role in asthma. In this study, we examined the role of AMs in lung function and airway inflammation of rats exposed to TMA. Female Brown Norway rats were sensitized by dermal application of TMA or received vehicle alone on days 0 and 7. One day before challenge, rats received intratracheally either empty or clodronate-containing liposomes to deplete the lungs of AMs. On day 21, all rats were challenged by inhalation of TMA in air. Lung function parameters were measured before, during, within 1 h after, and 24 h after challenge. IgE levels and parameters of inflammation and tissue damage were assessed 24 h after challenge. Sensitization with TMA led to decreased lung function parameters during and within 1 h after challenge as compared to non-sensitized rats. AM depletion alleviated the TMA-induced drop in lung function parameters and induced a faster recovery compared to sham-depleted TMA-sensitized rats. It also decreased the levels of serum IgE 24 h after challenge, but did not affect the sensitization-dependent increase in lung lavage fluid IL-6 and tissue TNF-α levels. In contrast, AM depletion augmented the TMA-induced tissue damage and inflammation 24 h after challenge. AMs seem to have a dual role in this model for TMA-induced occupational asthma since they potentiate the immediate TMA-induced decrease in lung function but tended to dampen the TMA-induced inflammatory reaction 24 h later

  8. Edaravone prevents lung injury induced by hepatic ischemia-reperfusion.

    Science.gov (United States)

    Uchiyama, Munehito; Tojo, Kentaro; Yazawa, Takuya; Ota, Shuhei; Goto, Takahisa; Kurahashi, Kiyoyasu

    2015-04-01

    Lung injury is a major clinical concern after hepatic ischemia-reperfusion (I/R), due to the production of reactive oxygen species in the reperfused liver. We investigated the efficacy of edaravone, a potent free-radical scavenger, for attenuating lung injury after hepatic I/R. Adult male Sprague-Dawley rats were assigned to sham + normal saline (NS), I/R + NS, or I/R + edaravone group. Rats in the I/R groups were subjected to 90 min of partial hepatic I/R. Five minutes before reperfusion, 3 mg/kg edaravone was administered to the I/R + edaravone group. After 6 h of reperfusion, we evaluated lung histopathology and wet-to-dry ratio. We also measured malondialdehyde (MDA), an indicator of oxidative stress, in the liver and the lung, as well as cytokine messenger RNA expressions in the reperfused liver and plasma cytokine concentrations. Histopathology revealed lung damages after 6 h reperfusion of partial ischemic liver. Moreover, a significant increase in lung wet-to-dry ratio was observed. MDA concentration increased in the reperfused liver, but not in the lungs. Edaravone administration attenuated the lung injury and the increase of MDA in the reperfused liver. Edaravone also suppressed the reperfusion-induced increase of interleukin-6 messenger RNA expressions in the liver and plasma interleukin-6 concentrations. Edaravone administration before reperfusion of the ischemic liver attenuates oxidative stress in the reperfused liver and the subsequent lung injury. Edaravone may be beneficial for preventing lung injury induced by hepatic I/R. Copyright © 2015 Elsevier Inc. All rights reserved.

  9. Caspase 3 activity in isolated fetal rat lung fibroblasts and rat periodontal ligament fibroblasts: cigarette smoke-induced alterations

    Directory of Open Access Journals (Sweden)

    James Elliot Scott

    2016-03-01

    Full Text Available Background Cigarette smoking is the leading cause of preventable death in the world. It has been implicated in the pathogenesis of pulmonary, oral and systemic diseases. Smoking during pregnancy is clearly a risk factor for the developing fetus and may be a major cause of infant mortality. Moreover, the oral cavity is the first site of exposure to cigarette smoke and may be a possible source for the spread of toxins to other organs of the body. Fibroblasts in general are morphologically heterogeneous connective tissue cells with diverse functions. Apoptosis or programmed cell death is a crucial process during embryogenesis and for the maintenance of homeostasis throughout life. Deregulation of apoptosis has been implicated in abnormal lung development in the fetus and disease progression in adults. Caspases, are proteases which belong to the family of cysteine aspartic acid proteases and are the key components for the downstream amplification of intra-cellular apoptotic signals. Of the 14 caspases known, caspase-3 is the key executioner of apoptosis. Fetal rat lung fibroblasts but not PDL viability is reduced by exposure to CSE. In addition Caspase 3 activity is elevated after CSE exposure in fetal lung fibroblasts but not in PDLs. Expression of caspase 3 is induced in CSE exposed lung fibroblasts but not in PDLs. Caspase 3 was localized to the cytoplasm in both cell types.

  10. Mitigation of radiation-induced lung fibrosis by angiotensin converting enzyme inhibitors

    International Nuclear Information System (INIS)

    Kma, Lakhan; Gao, Feng; Jacobs, Elizabeth R.; Medhora, Meetha; Fish, Brian L.; Moulder, John E.

    2014-01-01

    The aim of this study was to test the mitigating potential of angiotensin converting enzyme inhibitors (ACEi) against radiation-induced pulmonary fibrosis, which could result from accidental exposure or radiological terrorism. Rats (WAG/RijCmcr) were exposed to a single dose of 13 Gy of X-irradiation to the whole thorax, at the dose rate of 1.43 Gy/min. Three structurally-different ACEi's, captopril (145-207 mg/m 2 /day), enalapril (19-28 mg/m 2 /day) and fosinopril (19-28 mg/m 2 /day) were administered in drinking water beginning 1 week after whole thoracic irradiation. Rats that survived acute pneumonitis (6-12 weeks) were accessed monthly after irradiation for the effects on lung structure and function. Endpoints included breathing rate, wet:dry weight ratio, collagen content and histolopathological studies. Treatment with captopril or enalapril, but not fosinopril, beginning 1 week after 13 Gy X-irradiation improved survival of rats. Mortality of 30-35% was observed with administration of captopril or enalapril compared to 70% for 13 Gy alone. All three ACEi's attenuated radiation-induced lung fibrosis at 7 months after irradiation based on histological indices and measurement of lung collagen. After whole-thoracic irradiation, ACEi's mitigate radiation induced pulmonary fibrosis based on histological and biochemical endpoints. These treatments were effective even when administration was not started until one week after irradiation. Our findings support the therapeutic potential of ACEi's against chronic radiation induced lung injury. (author)

  11. Acute respiratory changes and pulmonary inflammation involving a pathway of TGF-β1 induction in a rat model of chlorine-induced lung injury

    Energy Technology Data Exchange (ETDEWEB)

    Wigenstam, Elisabeth; Elfsmark, Linda; Koch, Bo [Swedish Defence Research Agency, CBRN Defence and Security, Umeå (Sweden); Bucht, Anders [Swedish Defence Research Agency, CBRN Defence and Security, Umeå (Sweden); Department of Public Health and Clinical Medicine, Unit of Respiratory Medicine, Umeå University, Umeå (Sweden); Jonasson, Sofia, E-mail: sofia.jonasson@foi.se [Swedish Defence Research Agency, CBRN Defence and Security, Umeå (Sweden)

    2016-10-15

    We investigated acute and delayed respiratory changes after inhalation exposure to chlorine (Cl{sub 2}) with the aim to understand the pathogenesis of the long-term sequelae of Cl{sub 2}-induced lung-injury. In a rat model of nose-only exposure we analyzed changes in airway hyperresponsiveness (AHR), inflammatory responses in airways, expression of pro-inflammatory markers and development of lung fibrosis during a time-course from 5 h up to 90 days after a single inhalation of Cl{sub 2}. A single dose of dexamethasone (10 mg/kg) was administered 1 h following Cl{sub 2}-exposure. A 15-min inhalation of 200 ppm Cl{sub 2} was non-lethal in Sprague-Dawley rats. At 24 h post exposure, Cl{sub 2}-exposed rats displayed elevated numbers of leukocytes with an increase of neutrophils and eosinophils in bronchoalveolar lavage (BAL) and edema was shown both in lung tissue and the heart. At 24 h, the inflammasome-associated cytokines IL-1β and IL-18 were detected in BAL. Concomitant with the acute inflammation a significant AHR was detected. At the later time-points, a delayed inflammatory response was observed together with signs of lung fibrosis as indicated by increased pulmonary macrophages, elevated TGF-β expression in BAL and collagen deposition around airways. Dexamethasone reduced the numbers of neutrophils in BAL at 24 h but did not influence the AHR. Inhalation of Cl{sub 2} in rats leads to acute respiratory and cardiac changes as well as pulmonary inflammation involving induction of TGF-β1. The acute inflammatory response was followed by sustained macrophage response and lack of tissue repair. It was also found that pathways apart from the acute inflammatory response contribute to the Cl{sub 2}-induced respiratory dysfunction. - Highlights: • Inhalation of Cl{sub 2} leads to acute lung inflammation and airway hyperreactivity. • Cl{sub 2} activates an inflammasome pathway of TGF-β induction. • Cl{sub 2} leads to a fibrotic respiratory disease. • Treatment

  12. Active Oxygen Metabolites and Thromboxane in Phorbol Myristate Acetate Toxicity to the Isolated, Perfused Rat Lung.

    Science.gov (United States)

    Carpenter, Laurie Jean

    When administered intravenously or intratracheally to rats, rabbits and sheep, phorbol myristate acetate (PMA) produces changes in lung morphology and function are similar to those seen in humans with the adult respiratory distress syndrome (ARDS). Therefore, it is thought that information about the mechanism of ARDS development can be gained from experiments using PMA-treated animals. Currently, the mechanisms by which PMA causes pneumotoxicity are unknown. Results from other studies in rabbits and in isolated, perfused rabbit lungs suggest that PMA-induced lung injury is mediated by active oxygen species from neutrophils (PMN), whereas studies in sheep and rats suggest that PMN are not required for the toxic response. The role of PMN, active oxygen metabolites and thromboxane (TxA_2) in PMA-induced injury to isolated, perfused rat lungs (IPLs) was examined in this thesis. To determine whether PMN were required for PMA to produce toxicity to the IPL, lungs were perfused for 30 min with buffer containing various concentrations of PMA (in the presence or absence of PMN). When concentrations >=q57 ng/ml were added to medium devoid of added PMN, perfusion pressure and lung weight increased. When a concentration of PMA (14-28 ng/ml) that did not by itself cause lungs to accumulate fluid was added to the perfusion medium containing PMN (1 x 10 ^8), perfusion pressure increased, and lungs accumulated fluid. These results indicate that high concentrations of PMA produce lung injury which is independent of PMN, whereas injury induced by lower concentrations is PMN-dependent. To examine whether active oxygen species were involved in mediating lung injury induced by PMA and PMN, lungs were coperfused with the oxygen radical scavengers SOD and/or catalase. Coperfusion with either or both of these enzymes totally protected lungs against injury caused by PMN and PMA. These results suggest that active oxygen species (the hydroxyl radical in particular), mediate lung injury in

  13. Radiation-induced mesotheliomas in rats

    International Nuclear Information System (INIS)

    Hahn, F.F.; Haley, P.J.; Hubbs, A.F.; Hoover, M.D.; Lundgren, D.L.

    1990-01-01

    Mesotheliomas have been reported in rats that inhaled plutonium, but these tumors have not been extensively studied. To investigate a possible role for inhaled radionuclides in the induction of mesotheliomas, four life-span studies conducted at the Inhalation Toxicology Research Institute are reviewed. A total of 3076 F344 rats were exposed by inhalation to aerosols of 239 PuO 2 , mixed uranium-plutonium oxide, or 144 CeO 2 . Results showed that a low incidence of pleural mesotheliomas was induced by either alpha- or beta-emitting radionuclides deposited and retained in the lung. Chronic alpha irradiation was more effective per unit dose in producing mesotheliomas than chronic beta irradiation of the lung by a factor of 15. 7 refs., 1 tab., 7 figs

  14. Elevated indoor radon levels and elevated incidence of lung cancer in Columbus and Franklin County, Ohio: Cause or coincidence?

    International Nuclear Information System (INIS)

    Grafton, H.E.; West, D.R.

    1992-01-01

    Columbus, and Franklin County, Ohio, have been identified as having elevated residential radon levels. Research by the Columbus Health Department, the Ohio Department of Health, and the US Environmental Protection Agency has shown that average screening measurements for the county range from 63% to 73% above 148 Bq m -3 , 23% to 27% above 370 Bq m -3 , and 1% above 1850 Bq m -3 , for both males and females, respectively. The observed cancer rate per 100,000 persons for the period 1979-1986 for the City of Columbus was 62.8 and for the State of Ohio, 49.3, for the bronchi, lungs, and trachea. The reliability of residential radon data, the effect of smoking, mobility of residents, and other confounding factors are referenced. We suggest that while current evidence is insufficient to demonstrate a causal or coincidental relationship between elevated radon levels and higher-than-average rates of lung cancer, the measurement data suggest that Franklin County, Ohio, is an appropriate site for such research

  15. Radon: Detection and treatment

    International Nuclear Information System (INIS)

    Loken, S.; Loken, T.

    1989-01-01

    Within the last few years, natural radon exposure in non-industrial settings, primarily homes, has become a health concern. Research has demonstrated that many homes throughout the United States have radon concentrations much higher than the legal federal limits set for miners. Thousands of unsuspecting people are being exposed to high levels of radiation. It is estimated that up to 15 percent of lung cancers are caused from radon. This is a significant health risk. With basic knowledge of the current information on radon, a primary health care provider can address patients' radon concerns and make appropriate referrals

  16. Glucose utilisation in the lungs of septic rats

    International Nuclear Information System (INIS)

    Hansson, L.; Jeppsson, B.; Ohlsson, T.; Sandell, A.; Valind, S.; Luts, A.; Wollmer, P.

    1999-01-01

    Sequestration and degranulation of leucocytes in the pulmonary microcirculation is considered to be a key event in the development of acute respiratory distress syndrome in patients with sepsis. Glucose serves as the main source of energy in activated leucocytes. The aim of this study was to assess whether glucose utilisation in the lungs can be used as an indicator of pulmonary leucocyte accumulation in an experimental model of sepsis of intra-abdominal origin. Sepsis was induced in rats by abdominal implantation of a gelatine capsule containing bacteria and rat colonic contents. Empty gelatine capsules were implanted in control animals. Animals were studied 6 and 12 h after sepsis induction. Glucose utilisation was measured as the tissue uptake of fluorine-18-fluorodeoxyglucose ( 18 FDG) 1 h after intravenous injection of the tracer. Micro-autoradiography was also performed after injection of tritiated deoxyglucose. We found increased uptake of 18 FDG in the lungs of septic animals. The uptake also increased with time after sepsis induction. 18 FDG uptake in circulating leucocytes was increased in septic animals compared with controls, and micro-autoradiography showed intense accumulation of deoxyglucose in leucocytes in the lungs of septic animals. We conclude that glucose utilisation is increased in the lungs of septic rats. Measurements of pulmonary glucose utilisation as an index of leucocyte metabolic activity may open new possibilities for studies of the pathophysiology of sepsis and for evaluation of therapeutic interventions. (orig.)

  17. Health effects of inhaled radon progeny

    International Nuclear Information System (INIS)

    Monchaux, G.

    1997-01-01

    The relationship between an increased risk of lung cancer and exposure to radon progeny has been studied in eleven cohorts of underground workers, both in uranium and non uranium mines as well as in experimental animals. Risk estimates derived from miners studies are used to assess the risk of lung cancer in relation to exposure to indoor radon progeny. Human and animal experimental data are reviewed in the perspective of risk assessment for low exposure to radon progeny, in the conditions of the contemporary working environment as well as the indoor domestic environment. (authors)

  18. Radon and cancer

    International Nuclear Information System (INIS)

    2011-01-01

    This publication proposes an overview on what is known about the carcinogenic effect of radon. It recalls the origin of radon, its presence in the environment, and its radioactivity. It comments data on the relationship between exposure to radon and lung cancer, and with other forms of cancer. It discusses the role of the exposure level, and the cases of professional and domestic exposure with respect to these risks. It indicates the hazardous areas in France which are well identified, outlines that smokers are more likely victims of risks related to radon, that this risk is still underrated and underestimated (notably by the public). It gives an overview of existing regulations regarding exposure to radon, of public health policies and national plans concerning radon, and recalls some WHO recommendations

  19. Protective effect of U74500A on phorbol myristate acetate-induced acute lung injury.

    Science.gov (United States)

    Chu, Shi-Jye; Chang, Deh-Ming; Wang, David; Lin, Hen-I; Lin, Shih-Hua; Hsu, Kang

    2004-08-01

    1. The present study was designed to determine whether U74500A could ameliorate acute lung injury (ALI) induced by phorbol myristate acetate (PMA) in our rat isolated lung model compared with any amelioration induced by dimethylthiourea (DMTU), superoxide dismutase (SOD) and catalase. 2. Acute lung injury was induced successfully by PMA during 60 min of observation. At 2 microg/kg, PMA elicited a significant increase in microvascular permeability (measured using the capillary filtration coefficient Kfc), lung weight gain, the lung weight/bodyweight ratio, pulmonary arterial pressure and protein concentration of the bronchoalveolar lavage fluid. 3. Pretreatment with 1.5 mg/kg U74500A significantly attenuated ALI; there was no significant increase in any parameters measured, except for pulmonary arterial pressure. The protective effect of U74500A was approximately the same as that of 600 mg/kg DMTU. However, 6000 U/kg SOD, 50,000 U/kg catalase and 6000 U/kg SOD + 50,000 U/kg catalase had no protective effect. 4. These experimental data suggest that U74500A significantly ameliorates ALI induced by PMA in rats.

  20. Antioxidant effects of selenium on lung injury in paraquat intoxicated rats

    Science.gov (United States)

    Kim, K.S.; Suh, G.J.; Kwon, W.Y.; Kwak, Y.H.; Lee, Kenneth; Lee, H.J.; Jeong, K.Y.; Lee, M.W.

    2012-01-01

    CONTEXT: Paraquat (PQ) causes lethal intoxication by inducing oxidant injury to the lung. Selenium is a cofactor for glutathione peroxidase (GPx), which is one of the major endogenous antioxidant enzymes. OBJECTIVE: To determine whether selenium post-treatment activates GPx, decreases lung injury, and improves survival in PQ intoxicated rats. MATERIALS AND METHODS: Male Spraque-Dawley rats were categorized into three groups: sham (n = 6), PQ (n = 12), and PQ + Se (n = 12). In the PQ and PQ + Se groups, 50 mg/kg of PQ was administered intraperitoneally. After 10 minutes, 60 μg/kg of Se (PQ + Se) or saline (PQ) was administered via the tail vein. Six rats per group were euthanized 6 hours or 24 hours later. Lung tissues were harvested for the measurement of GPx activity, reduced glutathione (GSH), glutathione disulfide (GSSG) and malondialdehyde (MDA) and for histological analysis. Using separated set of rats, survival of PQ (n = 10) and PQ + Se (n = 10) were observed for 72 hours. RESULTS: GPx activity in the PQ group at the 6-hour and 24-hour time points was lower than in the sham group (p CONCLUSION: Single dose of selenium post-treatment activates GPx and attenuates lipid peroxidation and lung injury early after paraquat intoxication, but does not improve 72 hours of survival.

  1. Development of a data base on radon in US homes and applications. Final technical report

    Energy Technology Data Exchange (ETDEWEB)

    Cohen, B.L.

    1991-12-31

    This research led to the development of the compilation of data on radon in homes which is included in this document. This research also contributed to the development of two papers analyzing the results. These are a case control study test and tests of the liner no-threshold theory for lung cancer induced by exposure to radon in residential buildings.

  2. Health hazards from radon daughters in dwellings in Sweden

    International Nuclear Information System (INIS)

    Axelson, O.; Edling, C.

    1980-01-01

    To clarify the possible etiological role for lung cancer from exposure to the low levels of radon and its daughters in dwellings, a case-control study was made, comparing cases of lung cancer with controls with respect to residency in different types of houses. This pilot study was restricted to include only people who lived in typically rural areas. The results support the hypothesis that radon and radon daughter exposure in dwellings is pertinent to the question of the etiology of lung cancer

  3. Detection of radiation induced lung injury in rats using dynamic hyperpolarized {sup 129}Xe magnetic resonance spectroscopy

    Energy Technology Data Exchange (ETDEWEB)

    Fox, Matthew S. [Department of Physics and Astronomy, Western University, London, Ontario, N6A 3K7, Canada and Imaging Research Laboratories, Robarts Research Institute, Western University, London, Ontario, N6A 5B7 (Canada); Ouriadov, Alexei; Hegarty, Elaine [Imaging Research Laboratories, Robarts Research Institute, Western University, London, Ontario, N6A 5B7 (Canada); Thind, Kundan [Department of Medical Biophysics, Western University, London, Ontario, N6A 5C1, Canada and Imaging Research Laboratories, Robarts Research Institute, Western University, London, Ontario, N6A 5B7 (Canada); Wong, Eugene [Department of Physics and Astronomy, Western University, London, Ontario, N6A 3K7, Canada and London Regional Cancer Program, London, Ontario, N6C 2R6 (Canada); Hope, Andrew [Department of Radiation Oncology, University of Toronto, Toronto, Ontario, M5S 3E2, Canada and Radiation Medicine Program, Princess Margaret Hospital, Toronto, Ontario, M5T 2M9 (Canada); Santyr, Giles E., E-mail: gsantyr@robarts.ca [Department of Medical Biophysics, Western University, London, Ontario, N6A 5C1 (Canada); Imaging Research Laboratories, Robarts Research Institute, Western University, London, Ontario, N6A 5B7 (Canada); Department of Medical Imaging, Western University, London, Ontario, N6A 5B7 (Canada)

    2014-07-15

    Purpose: Radiation induced lung injury (RILI) is a common side effect for patients undergoing thoracic radiation therapy (RT). RILI can lead to temporary or permanent loss of lung function and in extreme cases, death. Combining functional lung imaging information with conventional radiation treatment plans may lead to more desirable treatment plans that reduce lung toxicity and improve the quality of life for lung cancer survivors. Magnetic Resonance Imaging of the lung following inhalation of hyperpolarized{sup 129}Xe may provide a useful nonionizing approach for probing changes in lung function and structure associated with RILI before, during, or after RT (early and late time-points). Methods: In this study, dynamic{sup 129}Xe MR spectroscopy was used to measure whole-lung gas transfer time constants for lung tissue and red blood cells (RBC), respectively (T{sub Tr-tissue} and T{sub Tr-RBC}) in groups of rats at two weeks and six weeks following 14 Gy whole-lung exposure to radiation from a {sup 60}Co source. A separate group of six healthy age-matched rats served as a control group. Results: T{sub Tr-tissue} values at two weeks post-irradiation (51.6 ± 6.8 ms) were found to be significantly elevated (p < 0.05) with respect to the healthy control group (37.2 ± 4.8 ms). T{sub Tr-RBC} did not show any significant changes between groups. T{sub Tr-tissue} was strongly correlated with T{sub Tr-RBC} in the control group (r = 0.9601 p < 0.05) and uncorrelated in the irradiated groups. Measurements of arterial partial pressure of oxygen obtained by arterial blood sampling were found to be significantly decreased (p < 0.05) in the two-week group (54.2 ± 12.3 mm Hg) compared to those from a representative control group (85.0 ± 10.0 mm Hg). Histology of a separate group of similarly irradiated animals confirmed the presence of inflammation due to radiation exposure with alveolar wall thicknesses that were significantly different (p < 0.05). At six weeks post

  4. Human umbilical cord-derived mesenchymal stem cells protect from hyperoxic lung injury by ameliorating aberrant elastin remodeling in the lung of O2-exposed newborn rat.

    Science.gov (United States)

    Hou, Chen; Peng, Danyi; Gao, Li; Tian, Daiyin; Dai, Jihong; Luo, Zhengxiu; Liu, Enmei; Chen, Hong; Zou, Lin; Fu, Zhou

    2018-01-08

    The incidence and mortality rates of bronchopulmonary dysplasia (BPD) remain very high. Therefore, novel therapies are imminently needed to improve the outcome of this disease. Human umbilical cord-derived mesenchymal stem cells (UC-MSCs) show promising therapeutic effects on oxygen-induced model of BPD. In our experiment, UC-MSCs were intratracheally delivered into the newborn rats exposed to hyperoxia, a well-established BPD model. This study demonstrated that UC-MSCs reduce elastin expression stimulated by 90% O 2 in human lung fibroblasts-a (HLF-a), and inhibit HLF-a transdifferentiation into myofibroblasts. In addition, the therapeutic effects of UC-MSCs in neonatal rats with BPD, UC-MSCs could inhibit lung elastase activity and reduce aberrant elastin expression and deposition in the lung of BPD rats. Overall, this study suggested that UC-MSCs could ameliorate aberrant elastin expression in the lung of hyperoxia-induced BPD model which may be associated with suppressing increased TGFβ1 activation. Copyright © 2017. Published by Elsevier Inc.

  5. New aspects of the etiology of lung carcinomas in respect to radon 222

    International Nuclear Information System (INIS)

    Merkel, K.

    1984-01-01

    Radon is the reason for the high cancer risk of uran miners. It also is present in building materials and therefore in the air inside houses. In the last year the radium content in houses increased because of the use of other row materials for building materials and because of a better isolation of the houses. This may increase the risc of lung cancer. (P.W.)

  6. Pulmonary gallium uptake in rats with granulomatosis induced by complete Freund adjuvant

    International Nuclear Information System (INIS)

    Stanislas-Leguern, G.; Masse, R.; Jaubert, F.; Chretien, J.; Huchon, G.

    1988-01-01

    To investigate the mechanism of gallium-67 uptake in lung granulomatosis, we studied 13 rats in which lung granulomatosis was induced by injection of complete Freund adjuvant (CFA) and 14 controls. Gallium uptake was assessed in bronchoalveolar lavage fluid and lavaged lung. The cells responsible for gallium uptake were identified by latent image activation autoradiography. Gallium activity in both lavaged lungs and bronchoalveolar cells (BAC) was higher in CFA-treated animals than in controls [172,205 +/- 134,783 DPM versus 44,456 +/- 14,486 DPM +/- SD (p less than 0.05) and 40,083 +/- 16,350 DPM versus 9100 +/- 4114 DPM (p less than 0.05), respectively]. In control rats, about two-thirds of total lung gallium was located in the interstitium, whereas in CFA-treated rats it was found in the mononuclear cells of lung granulomas. Gallium tracks were more numerous in the alveolar macrophages (AM) of CFA-treated rats than in control AM (28.4 +/- 10.0/field versus 8.4 +/- 3.8/field, p less than 0.001) but the number of tracks was proportional to the number of AM (52.4 +/- 18.7 versus 12.2 +/- 4.3, respectively; p less than 0.001). It is concluded that in rats with CFA-induced lung granulomatosis 1) pulmonary gallium uptake increases, 2) mononuclear cells are responsible for this uptake in both granulomas and AM, and 3) the increased uptake is due to the increased number of mononuclear cells

  7. Interaction of radon Exposure and cigarette smoking on cells

    International Nuclear Information System (INIS)

    Zhu, Maoxiang; Wei, Han; Yang, Zhihua; Pan, Xiujie; Cao, Zhenshan

    2008-01-01

    Full text: Environmental radon and its progenies is important lung carcinogen both in occupational underground miners and in the general population. Exposure to radon often occurs combined with smoking, another most important lung carcinogen. The join biological effects of alpha- particle radiation and cigarette smoke condense (CSC) were investigated here in order to provide experimental base for medical protection from lung cancer inducing by joint exposure of radon and smoking. Immortalized human bronchial epithelial cells (BEP2D) were divided into 5 groups, namely normal control group (NC), alpha particles irradiation group (0.25 Gy,α), CSC administration group (1μg/ml, CSC), CSC administration (1μg/ml) before (CSC + α) and after (α + CSC) alpha particles irradiation (0.25 Gy) group. On the 35 th passage after treated by alpha particles irradiation and CSC singly or jointly, only α + CSC cells showed malignant transformation characteristics, representing anchor growing independently, losing contact inhibition, and cell cycle disordering, whereas, there were no distinct difference between cells of other groups and normal cells. Moreover, comparison to the groups treated alone with alpha particles radiation or CSC administration, in the groups of joint exposure to alpha particles radiation and CSC treatment, cell survival fractions markedly decreased, intracellular ROS levels, frequencies of comet cell generation significantly increase, and could found that cell survival fractions of group CSC administration after α particle radiation was significantly higher than that of group CSC administration before alpha particles irradiation, suggesting that interaction of radon and smoking associated with their exposure sequence. In summary, interaction of radon and smoking was synergistic effect, and which was impacted by the order of exposure. (author)

  8. Radiation-induced lung damage in rats: The influence of fraction spacing on effect per fraction

    International Nuclear Information System (INIS)

    Haston, C.K.; Hill, R.P.; Newcomb, C.H.; Van Dyk, J.

    1994-01-01

    When the linear-quadratic model is used to predict fractionated treatments which are isoeffective, it is usually assumed that each (equal size) treatment fraction has an equal effect, independent of the time at which it was delivered during a course of treatment. Previous work has indicated that this assumption may not be valid in the context of radiation-induced lung damage in rats. Consequently the authors tested directly the validity of the assumption that each fraction has an equal effect, independent of the time it is delivered. An experiment was completed in which fractionated irradiation was given to whole thoraces of Sprague-Dawley rats. All treatment schedules consisted of eleven equal dose fractions in 36 days given as a split course, with some groups receiving the bulk of the doses early in the treatment schedule, before a 27-day gap, and others receiving most of the dose toward the end of the treatment schedule, after the time gap. To monitor the incidence of radiation-induced damage, breathing rate and lethality assays were used. The maximum differences in the LD 50 s and breathing rate ED 50 s for the different fractionation schedules were 4.0% and 7.7% respectively. The lethality data and breathing rate data were consistent with results expected from modelling using the linear-quadratic model with the inclusion of an overall time factor, but not the generalized linear-quadratic model which accounted for fraction spacing. For conventional daily fractionation, and within the range of experimental uncertainties, the results indicate that the effect of a treatment fraction does not depend on the time at which it is given (its position) in the treatment. The results indicate no need to extend isoeffect formulae to consider the effect of each fraction separately for radiation-induced lung damage. 21 refs., 6 figs., 3 tabs

  9. Angiotensin-(1–7 inhibits inflammation and oxidative stress to relieve lung injury induced by chronic intermittent hypoxia in rats

    Directory of Open Access Journals (Sweden)

    W. Lu

    2016-01-01

    Full Text Available Obstructive sleep apnea is associated with inflammation and oxidative stress in lung tissues and can lead to metabolic abnormalities. We investigated the effects of angiotensin1–7 [Ang-(1–7] on lung injury in rats induced by chronic intermittent hypoxia (CIH. We randomly assigned 32 male Sprague-Dawley rats (180–200 g to normoxia control (NC, CIH-untreated (uCIH, Ang-(1–7-treated normoxia control (N-A, and Ang-(1–7-treated CIH (CIH-A groups. Oxidative stress biomarkers were measured in lung tissues, and expression of NADPH oxidase 4 (Nox4 and Nox subunits (p22phox, and p47phox was determined by Western blot and reverse transcription-polymerase chain reaction. Pulmonary pathological changes were more evident in the uCIH group than in the other groups. Enzyme-linked immunosorbent assays and immunohistochemical staining showed that inflammatory factor concentrations in serum and lung tissues in the uCIH group were significantly higher than those in the NC and N-A groups. Expression of inflammatory factors was significantly higher in the CIH-A group than in the NC and N-A groups, but was lower than in the uCIH group (P<0.01. Oxidative stress was markedly higher in the uCIH group than in the NC and N-A groups. Expression of Nox4 and its subunits was also increased in the uCIH group. These changes were attenuated upon Ang-(1–7 treatment. In summary, treatment with Ang-(1-7 reversed signs of CIH-induced lung injury via inhibition of inflammation and oxidative stress.

  10. Emphysema induced by elastase enhances acute inflammatory pulmonary response to intraperitoneal LPS in rats.

    Science.gov (United States)

    da Fonseca, Lídia Maria Carneiro; Reboredo, Maycon Moura; Lucinda, Leda Marília Fonseca; Fazza, Thaís Fernanda; Rabelo, Maria Aparecida Esteves; Fonseca, Adenilson Souza; de Paoli, Flavia; Pinheiro, Bruno Valle

    2016-12-01

    Abnormalities in lungs caused by emphysema might alter their response to sepsis and the occurrence of acute lung injury (ALI). This study compared the extension of ALI in response to intraperitoneal lipopolysaccharide (LPS) injection in Wistar rats with and without emphysema induced by elastase. Adult male Wistar rats were randomized into four groups: control, emphysema without sepsis, normal lung with sepsis and emphysema with sepsis. Sepsis was induced, and 24 h later the rats were euthanised. The following analysis was performed: blood gas measurements, bronchoalveolar lavage (BAL), lung permeability and histology. Animals that received LPS showed significant increase in a lung injury scoring system, inflammatory cells in bronchoalveolar lavage (BAL) and IL-6, TNF-α and CXCL2 mRNA expression in lung tissue. Animals with emphysema and sepsis showed increased alveolocapillary membrane permeability, demonstrated by higher BAL/serum albumin ratio. In conclusion, the presence of emphysema induced by elastase increases the inflammatory response in the lungs to a systemic stimulus, represented in this model by the intraperitoneal injection of LPS. © 2016 The Authors. International Journal of Experimental Pathology © 2016 International Journal of Experimental Pathology.

  11. Protein synthesis in the growing rat lung

    International Nuclear Information System (INIS)

    Kelley, J.; Chrin, L.

    1986-01-01

    Developmental control of protein synthesis in the postnatal growth of the lung has not been systematically studied. In male Fischer 344 rats, lung growth continues linearly as a function of body weight (from 75 to 450 g body weight). To study total protein synthesis in lungs of growing rats, we used the technique of constant intravenous infusion of tritiated leucine, an essential amino acid. Lungs of sacrificed animals were used to determine the leucine incorporation rate into newly synthesized protein. The specific radioactivity of the leucine associated with tRNA extracted from the same lungs served as an absolute index of the precursor leucine pool used for lung protein synthesis. On the basis of these measurements, we were able to calculate the fractional synthesis rate (the proportion of total protein destroyed and replaced each day) of pulmonary proteins for each rat. Under the conditions of isotope infusion, leucyl-tRNA very rapidly equilibrates with free leucine of the plasma and of the extracellular space of the lung. Infusions lasting 30 minutes or less yielded linear rates of protein synthesis without evidence of contamination of lung proteins by newly labeled intravascular albumin. The fractional synthesis rate is considerably higher in juvenile animals (55% per day) than in adult rats (20% per day). After approximately 12 weeks of age, the fractional synthesis rate remains extremely constant in spite of continued slow growth of the lung. It is apparent from these data that in both young and adult rats the bulk of total protein synthesis is devoted to rapidly turning over proteins and that less than 4 percent of newly made protein is committed to tissue growth

  12. Analysis of the joint effects of radon exposure and smoking on lung cancer risk in three nested case-control studies in Europe

    International Nuclear Information System (INIS)

    Leuraud, Klervi; Laurier, Dominique; Schnelzer, Maria; Grosche, Bernd; Tomasek, Ladislav

    2008-01-01

    Full text: Objectives: Three case-control studies nested in the French (Fr), German (Ge) and Czech (Cz) cohorts of uranium miners were conducted in the frame of a European research Project, named Alpha-Risk, on the quantification of risks associated with multiple radiation exposures. These case-control studies aimed at assessing the effect of protracted radon exposure on lung cancer risk taking into account individual tobacco consumption. Material and methods: In the three case-control studies, cases were miners of the corresponding cohort who died of lung cancer (100, 704, 672 cases for the Fr, Ge and Cz study, respectively). For each case, controls were randomly matched on birth period and attained age at the time of death of the corresponding case (500, 1398 and 1491 controls for the Fr, Ge and Cz study, respectively). Cumulated radon exposure during employment was obtained from ambient and individual measurements for the Fr and Cz studies, and from a job exposure matrix for the Ge study. Smoking habits were retrospectively determined from medical archives and questionnaires applied in face-to-face interviews, phone calls or mailings. Analysis was performed by conditional logistic regression using a linear excess relative risk (ERR) model. A multiplicative model was fitted to assess the joint effect of radon exposure and smoking on lung cancer risk. Results: Smoking status was established for 62, 421, and 672 cases and 320, 620, and 1491 controls for the Fr, Ge, and Cz study, respectively. Two categories ('ever smokers' vs. 'never smokers') were defined. The percentages of 'ever-smokers' were 90%, 95%, and 92% for the cases and 73%, 75%, and 73% for the controls, for the Fr, Ge and Cz study, respectively. Mean five-year lagged cumulated radon exposures were 115, 717 and 174 working level months (WLM) for the cases, and 71, 505 and 118 WLM for the controls, for the Fr, Ge and Cz study, respectively. The excess relative risk per WLM (ERR/WLM) was 0.98% with a 95

  13. Lung Deposition And Biological Effects Of Inhaled Radon Progenies

    International Nuclear Information System (INIS)

    Balashazy, I.; Farkas, A.; Szoke, I.; Moustafa, M.; Kudela, G.

    2010-01-01

    Inhaled radon progenies provide more than the half of natural radiation exposure. There is increasing evidence that the cellular distribution of radiation burden is an important factor regarding the biological response to ionisation radiation, thus, one of our tasks was the characterisation of the distribution of cellular exposure. Histological studies of former uranium miners presented strong correlation between primer deposition hot spots and neoplastic lesions. Most of these lesions were located along the carinal regions of the large bronchial airways. In the present work, computational fluid dynamics (CFD) approaches have been applied to simulate the deposition distribution of inhaled radon progenies along central human airways. The geometry and the cellular structure of epithelial lung tissue were numerically reconstructed based on anatomical and histological data. Single and multiple ha-hit and cellular dose distributions have been computed applying Monte Carlo modelling techniques at different breathing conditions. Figure 1. Deposition enhancement factor (EF) of inhaled radon progenies on a central airway bifurcation in airway generations 4-5 during light physical activity breathing condition. Size of scanning surface element is a 45μm side triangle. Left panel: EF max=1400,Dp=200 nm (attached). Right panel: EF max1290, Dp= 1 nm (unattached). Values of local per average deposition densities, that is, enhancement factors (Figure 1), hit probabilities and doses may be up to two-three orders of magnitude higher in the deposition hot spots than the average values. Dose calculations revealed that some cell clusters may receive high doses even at low exposure conditions. Applying the model to different radiation exposure conditions useful relations can be received regarding the linear-non threshold hypothesis

  14. Prototype exposure chamber of radon for animal experiments

    Energy Technology Data Exchange (ETDEWEB)

    Yamada, Yuji; Koizumi, Akira; Yonehara, Hidenori; Shimo, Michikuni; Inaba, Jiro [National Institute of Radiological Sciences, Chiba (Japan)

    1998-12-31

    To evaluate a dose conversion factor from the `Working Level of Month` (WLM) of radon to the absorbed dose (mGy), the quality of radon and its progeny was assessed, and exposures controlled for each deposition region were planed as follows: 1) exposure of radon gas to the entire respiratory tract, 2) exposure of `unattached` fractions to the upper respiratory tract, 3) exposure of `attached` fractions onto ultrafine particles to the deep lung, 4) exposure of `attached` fractions onto fine particles to the lower respiratory tract, 5) exposure of `attached` fractions onto coarse particles to the upper respiratory tract. In this preliminary study, a prototype exposure system of radon and its progeny for small rodents was designed. A whole body exposure chamber with a volume of about 0.5 m{sup 3} was used, which it held 20 rats. The aging and mixing chamber separated by the exposure chamber had a volume of about 1 m{sup 3}. As career aerosols of radon progeny, carnauba wax aerosols as solid particles, DOS aerosols as liquid particles and NaCl aerosols as hygroscopic particles were selected. These aerosols generated using a vaporization-condensation method and/or an electrical classification method were almost monodisperse with {sigma}{sub g} of <1.2. The monitoring data on biologically related gases showed an importance in the oxygen injection system and the carbon dioxide absorption system. (author)

  15. Lowering the UK domestic radon Action Level to prevent more lung cancers-is it cost-effective?

    International Nuclear Information System (INIS)

    Denman, A R; Groves-Kirkby, C J; Coskeran, T; Phillips, P S; Crockett, R G M; Tornberg, R

    2008-01-01

    Case studies have shown that radon gas can accumulate within domestic properties at sufficiently high levels that it can cause lung cancer, and recent studies have suggested that this risk remains significant below the UK domestic Action Level of 200 Bq m -3 . Raised radon levels can be reduced by engineering measures, and it has been shown that domestic radon remediation programmes in UK Affected Areas can result in reduced risks to the population and can be cost-effective. We consider here the benefits and costs of the domestic radon remediation programme in Northamptonshire, UK, and consider the implications for that programme of reducing the UK Action Level below its present value. A radon remediation programme based on an Action Level above 200 Bq m -3 will cost less and will target those most at risk, but will be less cost-effective and will lead to higher residual dose and greater risk of cancer in the remaining population. Reducing the Action Level below 200 Bq m -3 will prevent more cancers, but at significantly higher cost. It will also be less cost-effective, because remediation of a significant number of houses with moderate radon levels will provide only a modest health benefit to occupants. Overall, a completed radon remediation programme of the type implemented in Northamptonshire is most cost-effective for an Action Level between 200 and 300 Bq m -3 . The implications for future health policy are discussed

  16. Radiation-induced mesotheliomas in rats

    Energy Technology Data Exchange (ETDEWEB)

    Hahn, F.F.; Haley, P.J.; Hubbs, A.F.; Hoover, M.D.; Lundgren, D.L.

    1990-01-01

    Mesotheliomas have been reported in rats that inhaled plutonium, but these tumors have not been extensively studied. To investigate a possible role for inhaled radionuclides in the induction of mesotheliomas, four life-span studies conducted at the Inhalation Toxicology Research Institute are reviewed. A total of 3076 F344 rats were exposed by inhalation to aerosols of {sup 239}PuO{sub 2}, mixed uranium-plutonium oxide, or {sup 144}CeO{sub 2}. Results showed that a low incidence of pleural mesotheliomas was induced by either alpha- or beta-emitting radionuclides deposited and retained in the lung. Chronic alpha irradiation was more effective per unit dose in producing mesotheliomas than chronic beta irradiation of the lung by a factor of 15. 7 refs., 1 tab., 7 figs. (MHB)

  17. Modeling the potential impacts of different radon policies for the U.S. housing stock

    International Nuclear Information System (INIS)

    Peterson, M.D.; Ritchie, I.M.

    1995-01-01

    According to the Environmental Protection Agency (EPA) and other public health agencies in the United States, radon may be the leading cause (along with passive smoking) of lung cancer deaths among nonsmokers. Radon is estimated to be the second leading cause of lung cancer death in smokers behind smoking-related lung cancer. EPA estimates that 7,000 to 30,000 lung cancer deaths each year are due to radon exposure. (It is implied that radon-related lung cancer deaths can be prevented by reducing radon levels below EPA's guideline levels). Current EPA radon policy is based on a strategy of education, the transfer of testing and remediation technologies to the public and private sectors, and recently proposed radon-resistant construction standards for new homes. This paper models the effectiveness of current proposed, and alternative policies for reducing radon risks in U.S. residential construction. The results of our analysis suggest that EPS's projections of 2,200 'lives saved annually' as a result of its current action level of 4 pCi/l will not be achieved with its current policy in the near future. Overall, the response of radon-related mortality to most policy options is delayed and flat due in part to the large number of houses with low radon levels and the long latency period between radon exposure and the development of cancer. The modeling results suggest that more aggressive smoking reduction programs may yield greater benefits in overall lung cancer mortality (but not reduced radon exposure) than most radon-related policies. (au)

  18. Radon in the indoor environment

    International Nuclear Information System (INIS)

    Vanmarcke, H.

    1998-01-01

    A precise retrospective assessment of long-term radon exposures in dwellings is essential for estimating lung-cancer risks. The objectives of this research are (1) to investigate the deposition of radon progeny in the human respiratory tract by means of direct measurements as a function of aerosol conditions, (2) to assess the radon concentrations in buildings retrospectively with volume traps

  19. Regulatory Strategy to Control Radon Exposure in Pakistan

    International Nuclear Information System (INIS)

    Younus, Irfan; Cho, Kun Woo

    2012-01-01

    Pakistan Nuclear Regulatory Authority (PNRA) was established in 2001 with one of the objectives to ensure the protection of workers, general public and the environment from the harmful effects of naturally occurring and artificially produced ionizing radiations by formulating and implementing the effective regulations. Radon is a naturally occurring odorless, colorless, tasteless, imperceptible to senses and chemically inert radioactive gas which is produced continuously from the natural decay of U-238, U-235 and Th-232 in most soils, rocks and water all over the earth. High levels of radon in the soil and rock are primarily responsible for indoor radon problems. Therefore when inhaled with air, there much probability that radon decay products will stay and decay in the lungs. If stayed in the lungs, the radiation may damage the cells causing lung cancer. Hence the radon problems have been taken seriously in most of the developed countries of the world. Radon reference levels for dwellings and workplaces have been set and the general public has been made alert of radon through newspapers and electronic media. In Pakistan, neither publicity campaign nor radon measurement and control programmes have been started countrywide. Rather small individual efforts for the sake of interest have been done to investigate the radon in some specific area or institution. This paper presents the regulatory strategy to control radon exposure for the sake of radiation protection of public and workers in Pakistan

  20. Radon inhalation suppresses nephropathy in streptozotocin-induced type-1 diabetic mice

    International Nuclear Information System (INIS)

    Nishiyama, Yuichi; Kataoka, Takahiro; Yamato, Keiko; Etani, Reo; Taguchi, Takehito; Yamaoka, Kiyonori

    2016-01-01

    In this study, we investigated the suppressive effects of radon inhalation against nephropathy in C57BL/6J mice with type-1 diabetes induced by intraperitoneal injection of streptozotocin (50 mg/kg weight, given five times). Four weeks after diabetes induction, the diabetic mice were continuously treated with inhaled radon-222 of 2000 Bq/m3 or air only (sham) for four weeks. The results showed that radon inhalation did not affect type-1 diabetic symptoms such as body weight loss, hyperglycemia, and hypoinsulinemia. However, diabetic mice treated with radon showed lower urinary albumin excretion and fibrotic change in renal glomeruli compared with diabetic mice not treated with radon. Furthermore, renal superoxide dismutase activity and glutathione content were significantly higher in diabetic mice treated with radon than in diabetic mice not treated with radon. These findings suggested that radon inhalation enhanced renal antioxidants activities, resulting in the suppression of diabetic nephropathy. This study may contribute to the development of a novel approach in the treatment of nephropathy for diabetic patients. (author)

  1. Prolonged mechanical ventilation induces cell cycle arrest in newborn rat lung.

    Directory of Open Access Journals (Sweden)

    Andreas A Kroon

    Full Text Available RATIONALE: The molecular mechanism(s by which mechanical ventilation disrupts alveolar development, a hallmark of bronchopulmonary dysplasia, is unknown. OBJECTIVE: To determine the effect of 24 h of mechanical ventilation on lung cell cycle regulators, cell proliferation and alveolar formation in newborn rats. METHODS: Seven-day old rats were ventilated with room air for 8, 12 and 24 h using relatively moderate tidal volumes (8.5 mL.kg⁻¹. MEASUREMENT AND MAIN RESULTS: Ventilation for 24 h (h decreased the number of elastin-positive secondary crests and increased the mean linear intercept, indicating arrest of alveolar development. Proliferation (assessed by BrdU incorporation was halved after 12 h of ventilation and completely arrested after 24 h. Cyclin D1 and E1 mRNA and protein levels were decreased after 8-24 h of ventilation, while that of p27(Kip1 was significantly increased. Mechanical ventilation for 24 h also increased levels of p57(Kip2, decreased that of p16(INK4a, while the levels of p21(Waf/Cip1 and p15(INK4b were unchanged. Increased p27(Kip1 expression coincided with reduced phosphorylation of p27(Kip1 at Thr¹⁵⁷, Thr¹⁸⁷ and Thr¹⁹⁸ (p<0.05, thereby promoting its nuclear localization. Similar -but more rapid- changes in cell cycle regulators were noted when 7-day rats were ventilated with high tidal volume (40 mL.kg⁻¹ and when fetal lung epithelial cells were subjected to a continuous (17% elongation cyclic stretch. CONCLUSION: This is the first demonstration that prolonged (24 h of mechanical ventilation causes cell cycle arrest in newborn rat lungs; the arrest occurs in G₁ and is caused by increased expression and nuclear localization of Cdk inhibitor proteins (p27(Kip1, p57(Kip2 from the Kip family.

  2. Penconazole alters redox status, cholinergic function and lung's histoarchitecture of adult rats: Reversal effect of vitamin E.

    Science.gov (United States)

    Chaâbane, Mariem; Elwej, Awatef; Ghorbel, Imen; Chelly, Sabrine; Mnif, Hela; Boudawara, Tahia; Ellouze Chaabouni, Semia; Zeghal, Najiba; Soudani, Nejla

    2018-06-01

    The present study pertains to the possible adverse effects of penconazole exposure on the lung of adult rats, and to the potential ability of vitamin E (Vit E) in mitigating the toxicity induced by this fungicide. Male Wistar rats were divided into four groups of six animals each: Group I (Controls): rats drank distilled water; Group II (PEN): rats received, by gavage, 50 mg/kg body weight (1/40 LD 50 ) of penconazole every 2 days during 10 days; Group III (Vit E): rats received daily 100 mg α-tocopherol acetate/kg body weight during 10 days by gavage; and Group IV (Vit E + PEN): rats received both vitamin E (100 mg α-tocopherol acetate/kg body weight) and penconazole (50 mg/kg body weight), being vitamin E given as a daily dosage and penconazole every 2 days, by gavage during 10 days. Results showed that penconazole induced oxidative stress in the lung demonstrated by an increase in malondialdehyde (+77%), hydrogen peroxide (+58%) and advanced oxidation protein product (+22%) levels, as compared to the controls. Furthermore, a decrease in the activities of catalase (-41%), superoxide dismutase (-45%), glutathione peroxidase (-23%) and acetylcholinesterase (-67%), and an increase in the levels of non-protein thiols (+17%), glutathione (+7%) and vitamin C (+44%) were registered. Abnormalities in lung histological sections such as alveolar edema, infiltration of inflammatory cells (leukocytes) and emphysema, were also observed following penconazole exposure. Vitamin E ameliorated the biochemical parameters, as well as the histological impairments induced by this fungicide. In conclusion, our study demonstrated that vitamin E, a natural antioxidant, was effective in alleviating penconazole-induced lung damage in Wistar rats. Copyright © 2018 Elsevier Masson SAS. All rights reserved.

  3. Environmental Radon Gas and Degenerative Conditions An Overview

    International Nuclear Information System (INIS)

    Groves-Kirkby, C.J.; Denman, A.R.; Woolridge, A.C.; Phillips, P.S.; Phillips, C.

    2006-01-01

    Radon, a naturally occurring radioactive gas, has variable distribution in the environment as a decay product of uranium occurring in a wide range of rocks, soils and building materials. Although radon dissipates rapidly in outdoor air, it concentrates in the built environment, and inhalation of 222 Rn and its progeny 218 Po and 214 Po is believed to provide the majority of the radioactive dose to the respiratory system. While the connection between radon and lung cancer has long been recognised and investigated, recent studies have highlighted potential links between radon and other conditions, among them Multiple Sclerosis, Alzheimer and Parkinson Diseases, and Paget Disease of Bone. A strong case exists for clarifying the relationship between radon and these other conditions, not least since radon remediation to reduce lung cancer may conceivably have additional benefits hitherto unrecognized. The present status of the postulated links between environmental radon gas and degenerative conditions is reviewed, and recommendations for further research into levering current anti-radon campaigns are made. (authors)

  4. Heme oxygenase-1 mediates the protective effects of ischemic preconditioning on mitigating lung injury induced by lower limb ischemia-reperfusion in rats.

    Science.gov (United States)

    Peng, Tsui-Chin; Jan, Woan-Ching; Tsai, Pei-Shan; Huang, Chun-Jen

    2011-05-15

    Lower limb ischemia-reperfusion (I/R) imposes oxidative stress, elicits inflammatory response, and subsequently induces acute lung injury. Ischemic preconditioning (IP), a process of transient I/R, mitigates the acute lung injury induced by I/R. We sought to elucidate whether the protective effects of IP involve heme oxygenase-1 (HO-1). Adult male rats were randomized to receive I/R, I/R plus IP, I/R plus IP plus the HO-1 inhibitor tin protoporphyrin (SnPP) (n = 12 in each group). Control groups were run simultaneously. I/R was induced by applying rubber band tourniquet high around each thigh for 3 h followed by reperfusion for 3 h. To achieve IP, three cycles of bilateral lower limb I/R (i.e., ischemia for 10 min followed by reperfusion for 10 min) were performed. IP was performed immediately before I/R. After sacrifice, degree of lung injury was determined. Histologic findings, together with assays of leukocyte infiltration (polymorphonuclear leukocytes/alveoli ratio and myeloperoxidase activity) and lung water content (wet/dry weight ratio), confirmed that I/R induced acute lung injury. I/R also caused significant inflammatory response (increases in chemokine, cytokine, and prostaglandin E(2) concentrations), imposed significant oxidative stress (increases in nitric oxide and malondialdehyde concentrations), and up-regulated HO-1 expression in lung tissues. IP significantly enhanced HO-1 up-regulation and, in turn, mitigated oxidative stress, inflammatory response, and acute lung injury induced by I/R. In addition, the protective effects of IP were counteracted by SnPP. The protective effects of IP on mitigating acute lung injury induced by lower limb I/R are mediated by HO-1. Copyright © 2011 Elsevier Inc. All rights reserved.

  5. Exposure to unusually high indoor radon levels

    International Nuclear Information System (INIS)

    Rasheed, F.N.

    1993-01-01

    Unusually high indoor radon concentrations were reported in a small village in western Tyrol, Austria. The authors have measured the seasonal course of indoor radon concentrations in 390 houses of this village. 71% of houses in winter and 33% in summer, showed radon values on the ground floor above the Austrian action level of 400 Bq/cm 3 . This proportion results in an unusually high indoor radon exposure of the population. The radon source was an 8,700-year-old rock slide of granite gneiss, the largest of the alpine crystalline rocks. It has a strong emanating power because its rocks are heavily fractured and show a slightly increased uranium content. Previous reports show increased lung cancer mortality, myeloid leukemia, kidney cancer, melanoma, and prostate cancer resulting from indoor radon exposure. However, many studies fail to provide accurate information on indoor radon concentrations, classifying them merely as low, intermediate, and high, or they record only minor increases in indoor radon concentrations. Mortality data for 1970-91 were used to calculate age and sex standardized mortality rates (SMR) for 51 sites of carcinoma. The total population of Tyrol were controls. A significantly higher risk was recorded for lung cancer. The high SMR for lung cancer in female subjects is especially striking. Because the numbers were low for the other cancer sites, these were combined in one group to calculate the SMR. No significant increase in SMR was found for this group

  6. Radon Measurements in Vojvodina

    International Nuclear Information System (INIS)

    Bikit, I.; Bikit, K.; Forkapic, S.; Mrda, D.; Nikolov, J.; Todorovic, N.; Veskovic, M.

    2013-01-01

    Recent analyses of epidemiological studies of lung cancer risk from residential exposures demonstrate a statistically significant increase per unit of exposure below average annual concentrations of about 200 Bq/m 3 . Indoor radon measurements performed in Novi Sad in about 400 houses and flats are presented and discussed in this paper. By measuring gamma-activity of radon daughters, radon activity concentration was determined to be 50 Bq/m 3 . In Vojvodina region indoor radon levels were measured by alpha track detectors CR-39 on about 3000 locations during the winter seasons in the period of three years (2003-2005). The main aim of the present study was to explore the critical group of population for radon exposure and to estimate maximal annual doses. Existing radon maps which identify regions with elevated radon levels will improve data collection and analysis for the future radon campaigns. Collaboration on the JRC program of European indoor radon map and implementation of grid system are also discussed.(author)

  7. Controlling exposure to radon, France, December 2006

    International Nuclear Information System (INIS)

    Godet, J.L.; Perrin, M.L.; Dechaux, E.; Pineau, C.

    2007-01-01

    Controlling exposure to radon, France, December 2006 Exposure to radon, along with medical exposure, is the leading source of the French population exposure to ionizing radiation. Radon is a confirmed cause of lung cancer in man (classified in group I by the international Agency for research on Cancer (I.A.R.C.)). According to available estimates, the numbers of lung cancers attributable to radon exposure in France are far fewer than those caused by tobacco. However, according to a recent European study, around 9% of lung cancers in Europe may be caused by radon. Thus, due to the number of people exposed, radon has become a public health issue which calls for action, considering that exposure can be significantly reduced by implementing measures which are often simple. Since 2002, the Nuclear Safety Authority (Asn) has proceeded in implementing a new regulatory framework for the risk management related to the presence of radon in public places. The new system is now fully operational. In addition, based on the initiatives adopted by the government in June 2004 in the context of the National Health and Environment Plan (P.N.S.E.), the Asn drew up a plan in 2005, in collaboration with the Ministry for Urban Planning and Construction, to coordinate the actions of various national bodies involved in this field. This three-pronged strategy is as follows: - Creation of a new risk management policy related to the presence of radon in existing homes and in new buildings; - Supporting and controlling the implementation of regulations for managing radon related risks in public places; - Improvement and dissemination of knowledge on radon exposure and its related risks. (author)

  8. Working towards residential Radon survey in South America

    International Nuclear Information System (INIS)

    Zielinski, Jan M.; University of Ottawa, ON; Canoba, Analia C.; Shilnikova, Natalia S.; Veiga, Lene H. S.

    2008-01-01

    Information about residential radon levels in low and middle income countries is very sparse. In response to the World Health Organization initiative in the International Radon Project, we propose a research project that will address this knowledge gap in South America by conducting a residential radon survey. Following initial in vitro and in vivo studies of radon and studies of uranium miners exposed to radon, over twenty large case-control studies of lung cancer risk from exposure to residential radon have been completed worldwide by year 2004. Recently pooled data from these individual studies have been analyzed. These collaborative analyses of the indoor studies in Europe, North America, and China provide strong direct evidence that radon is causing a substantial number of lung cancers in the general population. To reduce radon lung cancer risk, national authorities must have methods and tools based on solid scientific evidence to develop sound public health policies. We propose to conduct a survey in ten South American countries using the distribution and analysis of passive alpha tracking detectors in houses selected at random in pre-selected cities in each participating country. We also present an approach to estimate the cost of carrying out such a survey and the radon laboratory infrastructure needed. The results of the proposed survey will allow to conduct assessment of the exposure to residential radon in the populations of South American countries and to assess the health impact of this exposure. The results of the project will also help national health authorities in developing national residential radon action levels and regulations, as well as provide public health guidance for radon awareness and mitigation. (author)

  9. Characterization of rat lung ICAM-1

    DEFF Research Database (Denmark)

    Beck-Schimmer, B; Schimmer, R C; Schmal, H

    1998-01-01

    studies, rat pulmonary artery endothelial cells (RPAEC), rat alveolar macrophages and aortic rings were stimulated (as described below) and evaluated for ICAM-1 expression. TREATMENT: RPAEC and macrophages were stimulated with lipopolysaccharide (LPS) and recombinant murine tumour necrosis factor alpha...... peaked at 4 h, while lung ICAM- I protein peaked at 6 h. CONCLUSIONS: Quantitation of ICAM-1 expression in vitro and in vivo suggests that ICAM-1 plays a central role in two lung inflammatory models. Furthermore, lung ICAM-1 upregulation involves at least two cell types: vascular endothelial cells...

  10. Cyclooxygenase-2-dependent bronchoconstriction in perfused rat lungs exposed to endotoxin.

    Science.gov (United States)

    Uhlig, S; Nüsing, R; von Bethmann, A; Featherstone, R L; Klein, T; Brasch, F; Müller, K M; Ullrich, V; Wendel, A

    1996-05-01

    Lipopolysaccharides (LPS), widely used to study the mechanisms of gram-negative sepsis, increase airway resistance by constriction of terminal bronchioles. The role of the cyclooxygenase (COX) isoenzymes and their prostanoid metabolites in this process was studied. Pulmonary resistance, the release of thromboxane (TX) and the expression of COX-2 mRNA were measured in isolated blood-free perfused rat lungs exposed to LPS. LPS induced the release of TX and caused increased airway resistance after about 30 min. Both TX formation and LPS-induced bronchoconstriction were prevented by treatment with the unspecific COX inhibitor acetyl salicylic acid, the specific COX-2 inhibitor CGP-28238, dexamethasone, actinomycin D, or cycloheximide. LPS-induced bronchoconstriction was also inhibited by the TX receptor antagonist BM-13177. The TX-mimetic compound, U-46619, increased airway resistance predominantly by constricting terminal bronchioles. COX-2-specific mRNA in lung tissue was elevated after LPS exposure, and this increase was attenuated by addition of dexamethasone or of actinomycin D. In contrast to LPS, platelet-activating factor (PAF) induced immediate TX release and bronchoconstriction that was prevented by acetyl salicylic acid, but not by CGP-28238. LPS elicits the following biochemical and functional changes in rat lungs: (i) induction of COX-2; (ii) formation of prostaglandins and TX; (iii) activation of the TX receptor on airway smooth muscle cells; (iv) constriction of terminal bronchioles; and (v) increased airway resistance. In contrast to LPS, the PAF-induced TX release is likely to depend on COX-1.

  11. [The effects of postconditioning with propofol on Toll-like receptor 4 expression in the lung tissue of rat with acute lung injury].

    Science.gov (United States)

    Li, Guo-Fu; Tong, Xin; Luan, Ting; Zang, Bin

    2012-10-01

    To investigate the effect of postconditioning with propofol on Toll-like receptor 4 (TLR4) expression in the lung tissue in lipopolysaccharide (LPS)-induced acute lung injury (ALI) rats. Thirty Sprague-Dawley (SD) rats were randomly assigned to control group, ALI group, and propofol postcondition group (each n=10). The model of ALI was reproduced by intravenous injection of LPS (8 mg/kg for 30 minutes) into the rats, equivalent normal saline was injected into the rats of control group. The rats were postconditioned with propofol injected intravenously by 20 mg/kg bolus dose and then continuously by 40 mg×kg(-1)×h(-1) with a constant speed for 1 hour. The rats were sacrificed 6 hours after drug injection. Lung wet/dry weight (W/D) ratio and lung permeability index (LPI) was taken. Tumor necrosis factor-α (TNF-α) level in bronchoalveolar lavage fluid (BALF) was detected using enzyme linked immunosorbent assay (ELISA) method and TLR4 mRNA expression in lung tissue was assessed by reverse transcription-polymerase chain reaction (RT-PCR). The lung W/D ratio, LPI, TLR4 mRNA and TNF-α in BALF were all increased in ALI group compared with control group [lung W/D ratio: 5.30±0.28 vs. 4.21±0.14, LPI (×10(-3)): 8.7±2.2 vs. 3.3±2.0, TLR4 mRNA: 2.451±0.028 vs. 0.998±0.021, TNF-α: 643.46±62.31 ng/L vs. 120.43±12.65 ng/L, all Pwaterfall-like inflammatory reaction.

  12. Radon problems

    International Nuclear Information System (INIS)

    Cohen, B.L.

    1985-01-01

    This chapter examines the health hazards resulting from the release of naturally occurring radioactive gas derived from the decay of uranium. It is estimated that random inhalation is now causing about 10,000 fatal lung cancers per year in the US. Radon is constantly being generated in rocks and soils (in which uranium is naturally present) and in materials produced from them (e.g., brick, stone, cement, plaster). It is emphasized that radon levels in buildings are typically 5 times higher than outdoors because radon diffusing up from the ground below or out of bricks, stone, cement, or plaster is trapped inside for a relatively long time

  13. Smoking produced mucus and clearance of particulates in the lung

    International Nuclear Information System (INIS)

    Sterling, T.D.; Poland, T.M.

    1992-01-01

    Some studies of miners have shown a lesser relative lung-cancer risk for smokers than for nonsmokers. For example, experiments by Cross and associates with dogs have shown an apparent protective effect of cigarette smoke against radon-daughter and dust exposure. One reason for these changes may be the thickened mucus layer in the tracheobronchial region of smokers. Physiological changes in the lung due to smoking may decrease the effects of radioactive particles in cancers in the bronchial region by apparently promoting faster clearance, in that region, of radioactive particles and by decreasing the radiation dose through reduced penetration to the sensitive basal epithelial cells. Because of the short half-life of radon daughters, even if there is possible tobacco-related delay of particle clearance from the alveolar region it cannot affect radon clearance. Therefore, the possible mitigating effect of tobacco on radon-produced cancer appears to be limited to the tracheobronchial region. It would be of value to a number of occupations if the same changes in the lungs due to smoking could be produced in exposed workers in the absence of cigarette-smoking. Beta-carotene and vitamin A, which affect maintenance and secretion of the mucosal lining, appear to thicken mucus, thereby providing protection against radon-induced lung cancers that is similar to smoking-related changes in the lung

  14. Meta-analysis of thirty-two case-control and two ecological radon studies of lung cancer.

    Science.gov (United States)

    Dobrzynski, Ludwik; Fornalski, Krzysztof W; Reszczynska, Joanna

    2018-03-01

    A re-analysis has been carried out of thirty-two case-control and two ecological studies concerning the influence of radon, a radioactive gas, on the risk of lung cancer. Three mathematically simplest dose-response relationships (models) were tested: constant (zero health effect), linear, and parabolic (linear-quadratic). Health effect end-points reported in the analysed studies are odds ratios or relative risk ratios, related either to morbidity or mortality. In our preliminary analysis, we show that the results of dose-response fitting are qualitatively (within uncertainties, given as error bars) the same, whichever of these health effect end-points are applied. Therefore, we deemed it reasonable to aggregate all response data into the so-called Relative Health Factor and jointly analysed such mixed data, to obtain better statistical power. In the second part of our analysis, robust Bayesian and classical methods of analysis were applied to this combined dataset. In this part of our analysis, we selected different subranges of radon concentrations. In view of substantial differences between the methodology used by the authors of case-control and ecological studies, the mathematical relationships (models) were applied mainly to the thirty-two case-control studies. The degree to which the two ecological studies, analysed separately, affect the overall results when combined with the thirty-two case-control studies, has also been evaluated. In all, as a result of our meta-analysis of the combined cohort, we conclude that the analysed data concerning radon concentrations below ~1000 Bq/m3 (~20 mSv/year of effective dose to the whole body) do not support the thesis that radon may be a cause of any statistically significant increase in lung cancer incidence.

  15. Endothelial Semaphorin 7A promotes inflammation in seawater aspiration-induced acute lung injury.

    Science.gov (United States)

    Zhang, Minlong; Wang, Li; Dong, Mingqing; Li, Zhichao; Jin, Faguang

    2014-10-28

    Inflammation is involved in the pathogenesis of seawater aspiration-induced acute lung injury (ALI). Although several studies have shown that Semaphorin 7A (SEMA7A) promotes inflammation, there are limited reports regarding immunological function of SEMA7A in seawater aspiration-induced ALI. Therefore, we investigated the role of SEMA7A during seawater aspiration-induced ALI. Male Sprague-Dawley rats were underwent seawater instillation. Then, lung samples were collected at an indicated time for analysis. In addition, rat pulmonary microvascular endothelial cells (RPMVECs) were cultured and then stimulated with 25% seawater for indicated time point. After these treatments, cells samples were collected for analysis. In vivo, seawater instillation induced lung histopathologic changes, pro-inflammation cytokines release and increased expression of SEMA7A. In vitro, seawater stimulation led to pro-inflammation cytokine release, cytoskeleton remodeling and increased monolayer permeability in pulmonary microvascular endothelial cells. In addition, knockdown of hypoxia-inducible factor (HIF)-1α inhibited the seawater induced increase expression of SEMA7A. Meanwhile, knockdown of SEMA7A by specific siRNA inhibited the seawater induced aberrant inflammation, endothelial cytoskeleton remodeling and endothelial permeability. These results suggest that SEMA7A is critical in the development of lung inflammation and pulmonary edema in seawater aspiration-induced ALI, and may be a therapeutic target for this disease.

  16. Radiation Protection for Radon in Dwellings - Consequences of the ICRP Publication 115

    International Nuclear Information System (INIS)

    Azzam, Jai T.; Breckow, J.; Grimm, V.; Grund, A.

    2013-01-01

    In the last decade several epidemiological studies on risk estimations due to exposure to radon in dwellings revealed higher risks to radon exposure than estimated previously. Thus, in ICRP Publication 115 (ICRP, 2011) a revised nominal probability coefficient for radon and its progeny-induced lung cancer was propounded. Based on the results of the exposure from residential studies and underground miners, the risk of lung cancer was estimated as 5x10 -4 per WLM (lifetime excess absolute risk, LEAR) and 8x10 -1 0 per Bqxh/m 3 , respectively. In the former Publication 65 (ICRP, 1993), the coefficient has been 2.83x10 -4 per WLM and 4x10 -1 0 per Bqxh/m 3 , respectively. Typical radon activity concentration in dwellings is about 60 Bq/m? in many parts of Europe. According to the ICRP Publication 65-dose coefficients, this concentration leads to a mean annual effective dose of 1.2 mSv. If the new nominal risk coefficient from ICRP Publication 115 is applied, the effective dose due to radon in dwellings increases to approximately 2.3 mSv per year. Referring the reference level of 10 mSv/a for radon exposure in dwellings in ICRP Publication 103 (ICRP, 2007) and based on the new recommendations in ICRP Publication 115, actions have to be taken to reduce the upper reference level for radon gas in dwellings from 600 Bq/m 3 to 300 Bq/m 3 .(author)

  17. Aerosol properties of indoor radon decay products

    International Nuclear Information System (INIS)

    Martell, E.A.

    1984-01-01

    Lung cancer risks attributable to indoor radon are highly dependent on the properties of radon progeny aerosols which, in turn, are dependent on the nature and concentration of small particles in indoor air. In clean filtered air, radon progeny are attached to small hygroscopic particles of high mobility which are rapidly deposited on surfaces. By contrast, radon progeny attached to cigarette smoke are on large particles of low mobility which persist in air. Radon progeny ingaled by smokers are largely associated with smoke particles from 0.5 to 4.0 μm diameter. Such particles are selectively deposited at bronchial bifurcations and are highly resistant to dissolution. The attached radon progeny undergo a substantial degree of radioactive decay at deposition sites before clearance which gives rise to large alpha radiation doses in small volumes of bronchial epithelium. These processes provide new insights on mechanisms of bronchial cancer induction and on relative risks of lung cancer in smokers, passive smokers, and other non-smokers. (Author)

  18. Assessment of radiation exposure to miners due to radon and radon daughters

    International Nuclear Information System (INIS)

    Przyborowski, S.

    1979-01-01

    An overview is given of the basic considerations regarding the establishment of lung limits for miners exposed to radon and radon daughters. Problems associated with the practical conduct of radiation protection monitoring are also dealt with, for example, the implications of temporal and local variations in activity levels to the mode of sampling and the interpretation of results. (author)

  19. Shelter and indoor air in the twenty-first century--radon, smoking, and lung cancer risks

    International Nuclear Information System (INIS)

    Fabrikant, J.I.

    1990-01-01

    Recognition that radon and its daughter products may accumulate to high levels in homes and in the workplace has led to concern about the potential lung cancer risk resulting from indoor domestic exposure. While such risks can be estimated with current dosimetric and epidemiological models for excess relative risks, it must be recognized that these models are based on data from occupational exposure and from underground miners' mortality experience. Several assumptions are required to apply risk estimates from an occupational setting to the indoor domestic environment. Analyses of the relevant data do not lead to a conclusive description of the interaction between radon daughters and cigarette smoking for the induction of lung cancer. The evidence compels the conclusion that indoor radon daughter exposure in homes represents a potential life-threatening public health hazard, particularly in males, and in cigarette smokers. Resolution of complex societal interactions will require public policy decisions involving the governmental, scientific, financial, and industrial sectors. These decisions impact the home, the workplace, and the marketplace, and they extend beyond the constraints of science. Risk identification, assessment, and management require scientific and engineering approaches to guide policy decisions to protect the public health. Mitigation and control procedures are only beginning to receive attention. Full acceptance for protection against what could prove to be a significant public health hazard in the twenty-first century will certainly involve policy decisions, not by scientists, but rather by men and women of government and law

  20. Radon Research Program, FY 1991

    International Nuclear Information System (INIS)

    1992-03-01

    The scientific information being sought in this program encompasses research designed to determine radon availability and transport outdoors, modeling transport into and within buildings, physics and chemistry of radon and radon progeny, dose response relationships, lung cancer risk, and mechanisms of radon carcinogenesis. The main goal of the DOE/OHER Radon Research Program is to develop information to reduce these uncertainties and thereby provide an improved health risk estimate of exposure to radon and its progeny as well as to provide information useful in radon control strategies. Results generated under the Program were highlighted in a National Research Council report on radon dosimetry. The study concluded that the risk of radon exposure is 30% less in homes than in mines. This program summary of book describes the OHER FY-1991 Radon Research Program. It is the fifth in an annual series of program books designed to provide scientific and research information to the public and to other government agencies on the DOE Radon Research Program

  1. Synergy of radon inhalation and tobacco smoking in the induction of lung cancer

    International Nuclear Information System (INIS)

    Sedlak, Antonin

    2010-01-01

    The problem of contribution of tobacco smoking to the induction of lung cancer in persons living in environments with the enhanced radon concentrations is treated. An attempt is made to interpret the sub-multiplicative mechanism of the synergy of the two factors, i.e. a situation where the contribution of the two factors acting jointly is larger than their simple addition but lower than their multiplication, as currently assumed to hold. (P.A.)

  2. Effects of Physalis peruviana L on Toxicity and Lung Cancer Induction by Nicotine Derived Nitrosamine Ketone in Rats.

    Science.gov (United States)

    El-Kenawy, Ayman El-Meghawry; Elshama, Said Said; Osman, Hosam-Eldin Hussein

    2015-01-01

    Nicotine-derived nitrosamine ketone (NNK) is considered a key tobacco smoke carcinogen inducing lung tumors. Physalis peruviana L (harankash) is considered one plant with marked health benefits. This study aimed to evaluate Physalis peruviana L effect on the toxic effect of NNK induced lung cancer in the rats by using pulmonary histopathological, immunohistochemical and DNA flow cytometric analyses. Sixty adult male rats were divided into four groups, each consisting of fifteen animals. The first group received saline, the second received two successive toxic doses of NNK only while the third received two successive toxic doses of NNK with a single daily dose of Physalis peruviana L. The fourth group received a single daily dose of Physalis peruviana L only. Toxic doses of NNK induced hyperplasia and adenocarcinoma in the lung and positive immunoreactivity for Ki-67 and p53 staining with disturbance of the lung DNA content. Administration of Physalis peruviana L with NNK led to a mild pulmonary hyperplasia and weak expression of Ki-67 and p53 with an improvement in the lung DNA content. Physalis peruviana L may protect against NNK induced lung carcinogenesis due to its antioxidant and anti-proliferative effects.

  3. Lung structure-respiratory function relationships in experimentally-induced bronchiolitis, bronchopneumonia and interstitial pneumonia in rats

    Energy Technology Data Exchange (ETDEWEB)

    Mauderly, J L; Madron, E de; Harkema, J R

    1988-12-01

    Histopathology and respiratory function of rats with three different types and distributions of lower lung inflammation were compared to better understand lung structure-function relationships. Rats were exposed 21 h/day for 7 days to 0.8 ppm ozone (O{sub 3}), sham-exposed as controls, or given 5 mg/kg bacterial endotoxin either intratracheally (ITE) or intraperitoneally (IPE). Respiratory function was measured 24 h after the end of treatment, than the rats were sacrificed and the distribution of inflammation was evaluated morphometrically. Chronic centriacinar inflammation with formation of new respiratory bronchioles caused an obstructive functional impairment in the O{sub 3} rats, which was clearly distinguished from the restrictive impairments resulting from acute inflammation in ITE and IPE rats. Only the magnitudes of changes related to the distribution of inflammation differentiated the ITE and IPE groups. Flow parameters previously thought sensitive to large airway resistance were changed in the O{sub 3} rats. Alveolar luminal inflammatory exudate affected quasistatic compliance more than septal inflammation in ITE and IPE rats. Quasistatic chord compliance was the most sensitive of three indices of pressure-volume relationships. The findings in this study improve the basis for interpreting respiratory function changes of rats. (author)

  4. Another bogus radiation scare - radon in homes. Letter to the editor

    International Nuclear Information System (INIS)

    Cuttler, J.

    2012-01-01

    This article discusses Health Canada's research that radon in homes is causing unnecessary lung cancer deaths. Health Canada has carried out a cross-Canada survey of radon-concentrations in homes (Health Canada 2012). The aims of their study were to obtain an estimate of the proportion of the Canadian population living in homes, with radon gas levels above the guideline of 200 Bq/m to identify new areas of this health risk. Their results indicate that 6.9% of Canadians are in 3 such homes (similar to their 1970 results). The authors state that their results can be used by governments and health professionals to help prioritize radon outreach and education efforts, and testing and remediation. Their next step is to correlate radon level and home characteristics, and also develop radon mapping methods. Several sentences in the introduction link radon with lung cancer, based on early studies of uranium miners and later studies in homes. It is estimated that about 10% of all lung cancers worldwide are related to radon exposure.

  5. House in Bessine-sur-Gartempe (87) built on uranium ore waste rocks and residues. Assessment of radon contents of the indoor air and induced health risks for dwellers

    International Nuclear Information System (INIS)

    2014-01-01

    After having recalled the origin of radon and how characterization measurements of exposure pathways are performed, this document reports an expertise investigation of the exposure to radon of dwellers of a house. It presents the main results of environmental radiological measurements: exposure to beta/gamma radiation and to radon, assessment of average radon concentrations in the house (measurement strategy, interpretation of average values). It reports the assessment of annual exposures to radon. It discusses the assessment of risks: status of knowledge of impacts of radon on health (radon and risk of lung cancer, other potential health effects of radon), risk assessment based on the efficient dose, method and results of assessment of the risk of lung cancer, impact of tobacco on this assessment, assessment of the risk of leukaemia

  6. Interactions of ozone and antineoplastic drugs on rat lung fibroblasts and Walker rat carcinoma cells

    International Nuclear Information System (INIS)

    Wenzel, D.G.; Morgan, D.L.

    1983-01-01

    Cultured rat lung fibroblasts (F-cells) and Walker rat carcinoma cells (WRC-cells) labeled with 51 Cr were exposed to the following antitumor drugs alone or with O 3 : carmustine (BCNU), doxorubicin (Dox), cisplatin (CPt), mitomycin C (Mit C) or vitamin K 3 (Vit K). Release of 51 Cr (cell injury) was greater for F-cells than WRC-cells with any single treatment. Pretreatment with any drug (400 microM), except for Vit K with WRC-cells, did not significantly increase O 3 -induced loss of 51 Cr. Co-exposure of F-cells to drugs and O 3 resulted in a marked potentiation of O 3 -induced injury with Vit K, and an inhibition with Dox

  7. Dexmedetomidine protects from post-myocardial ischaemia reperfusion lung damage in diabetic rats

    Science.gov (United States)

    Kip, Gülay; Çelik, Ali; Bilge, Mustafa; Alkan, Metin; Kiraz, Hasan Ali; Özer, Abdullah; Şıvgın, Volkan; Erdem, Özlem; Arslan, Mustafa; Kavutçu, Mustafa

    2015-01-01

    Objective Diabetic complications and lipid peroxidation are known to have a close association. Lipid peroxidation commonly occurs at sites exposed to ischaemia, but distant organs and tissues also get damaged during ischaemia/reperfusion (I/R). Some of these targets are vital organs, such as the lung, liver, and kidney; the lung is the most frequently affected. The aim of our study was to investigate the effects of dexmedetomidine on I/R damage in lung tissue and on the oxidant/anti-oxidant system in diabetic rats. Material and methods Diabetes was induced with streptozotocin (55 mg/kg) in 18 Wistar Albino rats, which were then randomly divided into three groups (diabetes control (DC), diabetes plus ischaemia-reperfusion (DIR), and diabetes plus dexmedetomidine-ischaemia/reperfusion (DIRD)) after the effects of diabetes were clearly evident. The rats underwent a left thoracotomy and then ischaemia was produced in the myocardium muscle by a left anterior descending artery ligation for 30 min in the DIR and DIRD groups. I/R was performed for 120 min. The DIRD group received a single intraperitoneal dose of dexmedetomidine (100 µg/kg); the DIR group received no dexmedetomidine. Group DC was evaluated as the diabetic control group and also included six rats (C group) in which diabetes was not induced. These mice underwent only left thoracotomy and were closed without undergoing myocardial ischaemia. Histopathological changes, activities of catalase (CAT) and glutathione-S-transferase anti-oxidant enzymes, and malondialdehyde (MDA) levels were evaluated in the lung tissues of all rats. Results Neutrophil infiltration/aggregation was higher in the DIR group than in the C, DC, and DIRD groups (p=0.001, p=0.013, and p=0.042, respectively). The lung injury score was significantly higher in the DIR group than in the C and DC groups (p<0.0001 and p=0.024, respectively). The levels of MDA were significantly higher in the DIR group than in the C and DIRD groups. CAT activity

  8. Dexmedetomidine protects from post-myocardial ischaemia reperfusion lung damage in diabetic rats

    Directory of Open Access Journals (Sweden)

    Gülay Kip

    2015-09-01

    Full Text Available Objective: Diabetic complications and lipid peroxidation are known to have a close association. Lipid peroxidation commonly occurs at sites exposed to ischaemia, but distant organs and tissues also get damaged during ischaemia/reperfusion (I/R. Some of these targets are vital organs, such as the lung, liver, and kidney; the lung is the most frequently affected. The aim of our study was to investigate the effects of dexmedetomidine on I/R damage in lung tissue and on the oxidant/anti-oxidant system in diabetic rats. Material and methods: Diabetes was induced with streptozotocin (55 mg/kg in 18 Wistar Albino rats, which were then randomly divided into three groups (diabetes control (DC, diabetes plus ischaemia-reperfusion (DIR, and diabetes plus dexmedetomidine-ischaemia/reperfusion (DIRD after the effects of diabetes were clearly evident. The rats underwent a left thoracotomy and then ischaemia was produced in the myocardium muscle by a left anterior descending artery ligation for 30 min in the DIR and DIRD groups. I/R was performed for 120 min. The DIRD group received a single intraperitoneal dose of dexmedetomidine (100 µg/kg; the DIR group received no dexmedetomidine. Group DC was evaluated as the diabetic control group and also included six rats (C group in which diabetes was not induced. These mice underwent only left thoracotomy and were closed without undergoing myocardial ischaemia. Histopathological changes, activities of catalase (CAT and glutathione-S-transferase anti-oxidant enzymes, and malondialdehyde (MDA levels were evaluated in the lung tissues of all rats. Results: Neutrophil infiltration/aggregation was higher in the DIR group than in the C, DC, and DIRD groups (p=0.001, p=0.013, and p=0.042, respectively. The lung injury score was significantly higher in the DIR group than in the C and DC groups (p<0.0001 and p=0.024, respectively. The levels of MDA were significantly higher in the DIR group than in the C and DIRD groups. CAT

  9. Environmental Radon Gas and Degenerative Conditions An Overview

    Energy Technology Data Exchange (ETDEWEB)

    Groves-Kirkby, C.J. [Medical Physics Department, Northampton General Hospital, Northampton NN1 5BD (United Kingdom)]|[School of Health, University of Northampton, Northampton NN2 7AL (United Kingdom); Denman, A.R. [Medical Physics Department, Northampton General Hospital, Northampton NN1 5BD (United Kingdom); Woolridge, A.C. [School of Health, University of Northampton, Northampton NN2 7AL (United Kingdom)]|[School of Applied Sciences, University of Northampton, Northampton NN2 7AL (United Kingdom); Phillips, P.S. [School of Applied Sciences, University of Northampton, Northampton NN2 7AL (United Kingdom); Phillips, C. [School of Health, University of Northampton, Northampton NN2 7AL (United Kingdom)

    2006-07-01

    Radon, a naturally occurring radioactive gas, has variable distribution in the environment as a decay product of uranium occurring in a wide range of rocks, soils and building materials. Although radon dissipates rapidly in outdoor air, it concentrates in the built environment, and inhalation of {sup 222}Rn and its progeny {sup 218}Po and {sup 214}Po is believed to provide the majority of the radioactive dose to the respiratory system. While the connection between radon and lung cancer has long been recognised and investigated, recent studies have highlighted potential links between radon and other conditions, among them Multiple Sclerosis, Alzheimer and Parkinson Diseases, and Paget Disease of Bone. A strong case exists for clarifying the relationship between radon and these other conditions, not least since radon remediation to reduce lung cancer may conceivably have additional benefits hitherto unrecognized. The present status of the postulated links between environmental radon gas and degenerative conditions is reviewed, and recommendations for further research into levering current anti-radon campaigns are made. (authors)

  10. Tualang Honey Protects the Rat Midbrain and Lung against Repeated Paraquat Exposure

    OpenAIRE

    Tang, Suk Peng; Kuttulebbai Nainamohamed Salam, Sirajudeen; Jaafar, Hasnan; Gan, Siew Hua; Muzaimi, Mustapha; Sulaiman, Siti Amrah

    2017-01-01

    Paraquat (PQ) is a dopaminergic neurotoxin and a well-known pneumotoxicant that exerts its toxic effect via oxidative stress-mediated cellular injuries. This study investigated the protective effects of Tualang honey against PQ-induced toxicity in the midbrain and lungs of rats. The rats were orally treated with distilled water (2?mL/kg/day), Tualang honey (1.0?g/kg/day), or ubiquinol (0.2?g/kg/day) throughout the experimental period. Two weeks after the respective treatments, the rats were i...

  11. A cost-effect analysis of an intervention against radon in homes

    Directory of Open Access Journals (Sweden)

    Hein Stigum

    2009-10-01

    Full Text Available Background  Key words  : Radon exposure, lung cancer, cost-effect analysis, attributable risk, models-mathematical: Radon is a radioactive gas that may leak into buildings from the ground. Radon exposure is a risk factor for lung cancer. An intervention against radon exposure in homes may consist of locating homes with high radon exposure (above 200 Bq m-3 and improving these, and of protecting future houses. The purpose of this paper is to calculate the costs and the effects of this intervention. Methods: We performed a cost-effect analysis from the perspective of the society, followed by an uncertainty and sensitivity analysis. The distribution of radon levels in Norwegian homes is lognormal with mean=74.5 Bq/m3, and 7.6% above 200 Bq/m3. Results: The preventable attributable fraction of radon on lung cancer was 3.8% (95% uncertainty interval: 0.6%, 8.3%. In cumulative present values the intervention would cost $238 (145, 310 million and save 892 (133, 1981 lives, each life saved costs $0.27 (0.09, 0.9 million. The cost-effect ratio was sensitive to the radon risk, the radon exposure distribution, and the latency period of lung cancer. Together these three parameters explained 90% of the variation in the cost-effect ratio. Conclusions: Reducing the radon concentration in present and future homes to below 200 Bq/m3 will cost $0.27 (0.09, 0.9 million per life saved. The uncertainty in the estimated cost per life is large, mainly due to uncertainty in the risk of lung cancer from radon. Based on estimates from road construction, the Norwegian society has been willing to pay $1 million to save a life. We therefore conclude that the intervention against radon in homes is justifiable. The willingness to pay is also larger that the upper uncertainty limit of the cost per life. Our conclusion is therefore robust against the uncertainties in the parameters.

  12. Draft of „National Radon Programme” 2013-2017

    International Nuclear Information System (INIS)

    Ivanova, K.; Badulin, V.; Georgieva, R.

    2013-01-01

    The World Health Organization defines radon as the second most important causal factor for lung cancer after smoking and the number one factor for people who have never smoked. The draft of the new European Directive takes accounts the latest ICRP Recommendations for reducing radon exposure in buildings. The Directive requires Member States to bring into force the laws, regulations and administrative provisions. The main goal of „National Radon Programme” is establishment and implementation of long-term policy to reduce and prevent risks of public health resulting from exposure to high concentrations of indoor radon in buildings. To achieve this are required: – to establish an appropriate system; – to carry out national survey and mapping of areas with radon background; – to establish radon prevention strategies in newly constructed buildings and radon mitigation strategies in existing buildings; – to improve public awareness; – to lay down a system for protection against radon in workplaces. The implementation of the program will contribute to reducing the public exposure due to indoors due to radon. Along with the reduction of smoking, it will directly and indirectly improve the prevention of lung cancer risks. (author)

  13. Peripheral 5-HT7 receptors as a new target for prevention of lung injury and mortality in septic rats.

    Science.gov (United States)

    Cadirci, Elif; Halici, Zekai; Bayir, Yasin; Albayrak, Abdulmecit; Karakus, Emre; Polat, Beyzagul; Unal, Deniz; Atamanalp, Sabri S; Aksak, Selina; Gundogdu, Cemal

    2013-10-01

    Sepsis is a complex pathophysiological event involving metabolic acidosis, systemic inflammatory response syndrome, tissue damage and multiple organ dysfunction syndrome. Although many new mechanisms are being investigated to enlighten the pathophysiology of sepsis, there is no effective treatment protocol yet. Presence of 5-HT7 receptors in immune tissues prompted us to hypothesize that these receptors have roles in inflammation and sepsis. We investigated the effects of 5-HT7 receptor agonists and antagonists on serum cytokine levels, lung oxidative stress, lung histopathology, nuclear factor κB (NF-κB) positivity and lung 5-HT7 receptor density in cecal ligation and puncture (CLP) induced sepsis model of rats. Agonist administration to septic rats increased survival time; decreased serum cytokine response against CLP; decreased oxidative stress and increased antioxidant system in lungs; decreased the tissue NF-κB immunopositivity, which is high in septic rats; and decreased the sepsis-induced lung injury. In septic rats, as a result of high inflammatory response, 5-HT7 receptor expression in lungs increased significantly and agonist administration, which decreased inflammatory response and related mortality, decreased the 5-HT7 receptor expression. In conclusion, all these data suggest that stimulation of 5-HT7 receptors may be a new therapeutic target for prevention of impaired inflammatory response related lung injury and mortality. Copyright © 2013 Elsevier GmbH. All rights reserved.

  14. Mortality and indoor radon daughter concentrations in 13 Canadian cities

    International Nuclear Information System (INIS)

    Letourneau, E.G.; Wigle, D.T.

    1980-01-01

    A study was carried out to determine if lung cancer and general mortality rates in 13 Canadian cities were significantly correlated with average indoor radon daughter concentrations. The radon daughter measurements were obtained from a study of 10,000 homes chosen in a statistically valid grab sample basis. Cancer deaths by year of death, sex, age, and cause were retrieved for each of the cities for the period 1957-1976. Age specific and age standardized mortality rates were calculated. The results showed no evidence of any substantial association between general or lung cancer mortality rates and indoor radon daughter concentrations. The limitations of this study and the feasibility of a common international program of epidemiology of radon daughter exposure are discussed. A proposal is made for the use of case control studies of lung cancer to assess the relative importance of smoking, occupational and domestic exposure to radon daughters

  15. Crocin attenuates hemorrhagic shock-induced oxidative stress and organ injuries in rats.

    Science.gov (United States)

    Yang, Long; Dong, Xiujuan

    2017-06-01

    We aimed to evaluate the effect of natural antioxidant crocin in alleviating hemorrhagic shock (HS)-induced organ damages. HS rats were treated with crocin during resuscitation. Mortality at 12h and 24h post resuscitation was documented. HS and resuscitation induced organ injuries, as characterized by elevated wet/dry ratio, quantitative assessment ratio, blood urea nitrogen, creatinine, aspartate aminotransferase and alanine aminotransferase, whereas rats received crocin treatment demonstrated improvements in all the above characteristics. This protective effect coincided with reduced malondialdehyde and increased glutathione in both serum and lung tissues, indicating attenuated oxidative stress in crocin-treated rats. Myeloperoxide levels in lung, kidney and liver were also reduced. Crocin can potentially be used to protect organs from HS-induced damages during resuscitation due to its anti-oxidative role. Copyright © 2017 Elsevier B.V. All rights reserved.

  16. Nanosized zinc oxide particles do not promote DHPN-induced lung carcinogenesis but cause reversible epithelial hyperplasia of terminal bronchioles.

    Science.gov (United States)

    Xu, Jiegou; Futakuchi, Mitsuru; Alexander, David B; Fukamachi, Katsumi; Numano, Takamasa; Suzui, Masumi; Shimizu, Hideo; Omori, Toyonori; Kanno, Jun; Hirose, Akihiko; Tsuda, Hiroyuki

    2014-01-01

    Zinc oxide (ZnO) is known to induce lung toxicity, including terminal bronchiolar epithelial hyperplasia, which gives rise to concerns that nanosized ZnO (nZnO) might lead to lung carcinogenesis. We studied the tumor promoting activity of nZnO by an initiation-promotion protocol using human c-Ha-ras proto-oncogene transgenic rats (Hras128 rats). The rats were given 0.2 % N-nitrosobis(2-hydroxypropyl)amine (DHPN) in the drinking water for 2 weeks and then treated with 0.5 ml of 250 or 500 μg/ml nZnO suspension by intra-pulmonary spraying once every 2 weeks for a total of 7 times. Treatment with nZnO particles did not promote DHPN-induced lung carcinogenesis. However, nZnO dose-dependently caused epithelial hyperplasia of terminal bronchioles (EHTB) and fibrosis-associated interstitial pneumonitis (FAIP) that were independent of DHPN treatment. Tracing the fate of EHTB lesions in wild-type rats indicated that the hyperplastic lesions almost completely disappeared within 12 weeks after the last nZnO treatment. Since nZnO particles were not found in the lung and ZnCl2 solution induced similar lung lesions and gene expression profiles, the observed lesions were most likely caused by dissolved Zn(2+). In summary, nZnO did not promote carcinogenesis in the lung and induced EHTB and FAIP lesions that regressed rapidly, probably due to clearance of surplus Zn(2+) from the lung.

  17. Radon concentration in a house of Calvados

    International Nuclear Information System (INIS)

    Leleyter, L.; Riffault, B.; Mazenc, B.

    2010-01-01

    Recent studies indicate a link between the risk of lung cancer and residential radon exposure. However, in France, awareness of this problem was made relatively late. Accordingly this study examines the radon concentration in a private home in Calvados (Normandy region). Findings show that the presence of a fireplace in a house can accelerate radon convective transfer, and that simple adjustments to interior and exterior accommodation can significantly reduce radon concentrations in the home. (authors)

  18. Expression of Angiotensin II and Aldosterone in Radiation-induced Lung Injury.

    Science.gov (United States)

    Cao, Shuo; Wu, Rong

    2012-12-01

    Radiation-induced lung injury (RILI) is the most common, dose-limiting complication in thoracic malignancy radiotherapy. Considering its negative impact on patients and restrictions to efficacy, the mechanism of RILI was studied. Wistar rats were locally irradiated with a single dose of 0, 16, and 20 Gy to the right half of the lung to establish a lung injury model. Two and six months after irradiation, the right half of the rat lung tissue was removed, and the concentrations of TGF-β1, angiotensin II, and aldosterone were determined via enzyme-linked immunosorbent assay. Statistical differences were observed in the expression levels of angiotensin II and aldosterone between the non-irradiation and irradiation groups. Moreover, the expression level of the angiotensin II-aldosterone system increased with increasing doses, and the difference was still observed as time progressed. Angiotensin II-aldosterone system has an important pathophysiological function in the progression of RILI.

  19. Expression of Angiotensin II and Aldosterone in Radiation-induced Lung Injury

    International Nuclear Information System (INIS)

    Cao, Shuo; Wu, Rong

    2012-01-01

    Radiation-induced lung injury (RILI) is the most common, dose-limiting complication in thoracic malignancy radiotherapy. Considering its negative impact on patients and restrictions to efficacy, the mechanism of RILI was studied. Wistar rats were locally irradiated with a single dose of 0, 16, and 20 Gy to the right half of the lung to establish a lung injury model. Two and six months after irradiation, the right half of the rat lung tissue was removed, and the concentrations of TGF-β1, angiotensin II, and aldosterone were determined via enzyme-linked immunosorbent assay. Statistical differences were observed in the expression levels of angiotensin II and aldosterone between the non-irradiation and irradiation groups. Moreover, the expression level of the angiotensin II-aldosterone system increased with increasing doses, and the difference was still observed as time progressed. Angiotensin II-aldosterone system has an important pathophysiological function in the progression of RILI

  20. N-Methyl-D-aspartate Receptor Excessive Activation Inhibited Fetal Rat Lung Development In Vivo and In Vitro

    Directory of Open Access Journals (Sweden)

    Zhengchang Liao

    2016-01-01

    Full Text Available Background. Intrauterine hypoxia is a common cause of fetal growth and lung development restriction. Although N-methyl-D-aspartate receptors (NMDARs are distributed in the postnatal lung and play a role in lung injury, little is known about NMDAR’s expression and role in fetal lung development. Methods. Real-time PCR and western blotting analysis were performed to detect NMDARs between embryonic days (E 15.5 and E21.5 in fetal rat lungs. NMDAR antagonist MK-801’s influence on intrauterine hypoxia-induced retardation of fetal lung development was tested in vivo, and NMDA’s direct effect on fetal lung development was observed using fetal lung organ culture in vitro. Results. All seven NMDARs are expressed in fetal rat lungs. Intrauterine hypoxia upregulated NMDARs expression in fetal lungs and decreased fetal body weight, lung weight, lung-weight-to-body-weight ratio, and radial alveolar count, whereas MK-801 alleviated this damage in vivo. In vitro experiments showed that NMDA decreased saccular circumference and area per unit and downregulated thyroid transcription factor-1 and surfactant protein-C mRNA expression. Conclusions. The excessive activation of NMDARs contributed to hypoxia-induced fetal lung development retardation and appropriate blockade of NMDAR might be a novel therapeutic strategy for minimizing the negative outcomes of prenatal hypoxia on lung development.

  1. Dynamic evolution characteristics of mining-induced fractures in overlying strata detected by radon

    International Nuclear Information System (INIS)

    Zhang Wei; Ma Liqiang; Wang Xufeng; Fang Gangwei; Zhang Dongsheng

    2011-01-01

    For environment protection in mining areas in northwest China, we developed a CTSRM (comprehensive test system by radon measurement) to measure radon radioactivity and detect dynamic evolution characteristics of mining-induced fractures in overlying strata. It was used to simulate the relationship between the dynamic evolution characteristics and radon concentrations of No. 33201 coalface at Bulianta coal mine in Inner Mongolia, and feasibility of the method was validate. (authors)

  2. Indoor radon epidemiological study

    Energy Technology Data Exchange (ETDEWEB)

    Kunz, E; Tomasek, L; Mueller, T [National Radiation Protection Institute, Prague (Czech Republic); Placek, V [Inst. for Expertises and Emergencies, Pribram-Kamenna (Czech Republic); Matzner, J; Heribanova, A [State Office for Nuclear Safety, Prague (Czech Republic)

    1996-12-31

    The study is a long-term prospective cohort study of lung cancer and possibility other causes of death. The study population includes inhabitants of the area, who had resided there for at three years and at least one of these between 1.1.1960 and 21.12.1989. A total of 11865 inhabitants satisfied these criteria. The cumulative exposure of each respondent is being assessed on the basis of measurements in dwellings, time spent there and estimation of previous exposure levels by a model accounting for constructional changes in buildings. One year lasting measurements of radon daughter products by integral dosimeters (Kodak film LR 115) were performed in practically all dwellings of the specified area. Radon measurements in houses in term of equilibrium concentration are compared with the results of a pilot study in Petrovice in 1990-91 which gave the stimulus for the epidemiological study. The distribution of death causes and ratio of observed (O) to expected (E) cases among collected death cases in the cohort, generally, somewhat lower ratios than one reflect the non-industrial character of the region, with the exception of lung cancer in man. The differences in the O/E ratios for lung cancer among the separate communities indicate that even in the situation of generally lower mortality, the dependence of lung cancer mortality on radon.

  3. Hydrogen-rich saline inhibits tobacco smoke-induced chronic obstructive pulmonary disease by alleviating airway inflammation and mucus hypersecretion in rats.

    Science.gov (United States)

    Liu, Zibing; Geng, Wenye; Jiang, Chuanwei; Zhao, Shujun; Liu, Yong; Zhang, Ying; Qin, Shucun; Li, Chenxu; Zhang, Xinfang; Si, Yanhong

    2017-09-01

    Chronic obstructive pulmonary disease induced by tobacco smoke has been regarded as a great health problem worldwide. The purpose of this study is to evaluate the protective effect of hydrogen-rich saline, a novel antioxidant, on chronic obstructive pulmonary disease and explore the underlying mechanism. Sprague-Dawley rats were made chronic obstructive pulmonary disease models via tobacco smoke exposure for 12 weeks and the rats were treated with 10 ml/kg hydrogen-rich saline intraperitoneally during the last 4 weeks. Lung function testing indicated hydrogen-rich saline decreased lung airway resistance and increased lung compliance and the ratio of forced expiratory volume in 0.1 s/forced vital capacity in chronic obstructive pulmonary disease rats. Histological analysis revealed that hydrogen-rich saline alleviated morphological impairments of lung in tobacco smoke-induced chronic obstructive pulmonary disease rats. ELISA assay showed hydrogen-rich saline lowered the levels of pro-inflammatory cytokines (IL-8 and IL-6) and anti-inflammatory cytokine IL-10 in bronchoalveolar lavage fluid and serum of chronic obstructive pulmonary disease rats. The content of malondialdehyde in lung tissue and serum was also determined and the data indicated hydrogen-rich saline suppressed oxidative stress reaction. The protein expressions of mucin MUC5C and aquaporin 5 involved in mucus hypersecretion were analyzed by Western blot and ELISA and the data revealed that hydrogen-rich saline down-regulated MUC5AC level in bronchoalveolar lavage fluid and lung tissue and up-regulated aquaporin 5 level in lung tissue of chronic obstructive pulmonary disease rats. In conclusion, these results suggest that administration of hydrogen-rich saline exhibits significant protective effect on chronic obstructive pulmonary disease through alleviating inflammation, reducing oxidative stress and lessening mucus hypersecretion in tobacco smoke-induced chronic obstructive pulmonary disease rats

  4. Risks from Radon: Reconciling Miner and Residential Epidemiology

    International Nuclear Information System (INIS)

    Chambers, Douglas B.; Harley, Naomi H.

    2008-01-01

    Everyone is exposed to radon, an inert radioactive gas that occurs naturally and is present everywhere in the atmosphere. The annual dose from radon and its (short-lived) decay products is typically about one-half of the dose received by members of the public from all natural sources of ionizing radiation. Data on exposures and consequent effects have recently been reviewed by the National Council on Radiation Protection and Measurements (NCRP) and the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR). Studies of underground miners provides a well-established basis for estimating risks from occupational exposures to radon and for studying factors that may affect the dose response relationship such as the reduction of risk (coefficients) with increasing time since exposure. Miners' studies previously formed the basis for estimating risks to people exposed to radon at home, with downward extrapolation from exposures in mines to residential levels of radon. Presently, the risk estimates from residential studies are adequate to estimate radon risks in homes. Although there are major uncertainties in extrapolating the risks of exposure to radon from the miner studies to assessing risks in the home, there is remarkably good agreement between the average of risk factors derived from miner studies and those from pooled residential case-control studies. There are now over 20 analytical studies of residential radon and lung cancer. These studies typically assess the relative risk from exposure to radon based on estimates of residential exposure over a period of 25 to 30 years prior to diagnosis of lung cancer. Recent pooled analyses of residential case-control studies support a small but detectable lung cancer risk from residential exposure, and this risk increases with increasing concentrations. The excess relative risk of lung cancer from long-term residential exposure is about the same for both smokers and non-smokers; however, because the

  5. Scanning electron microscopy of rat throat and trachea following the effects of radon decay products

    International Nuclear Information System (INIS)

    Rode, J.; Vaupotic, J.; Kobal, I.; Draslar, K.

    1996-01-01

    In two preliminary experiments, five laboratory rats were exposed in a small chamber to radon-rich air. In both experiments the exposure was about 0.9 WLM. The surface of throat and trachea was examined by scanning electron microscope. (author)

  6. Analysis of the K-ras and p53 pathways in x-ray-induced lung tumors in the rat

    Energy Technology Data Exchange (ETDEWEB)

    Belinsky, S.A.; Middleton, S.K.; Hahn, F.F.; Nikula, K.J. [Inhalation Toxicology Research Inst., Albuquerque, NM (United States); Picksley, S.M. [Medical Sciences Inst., Dundee (United Kingdom)

    1996-04-01

    The risk from exposure to low-dose radiation in conjunction with cigarette smoking has not been estimated due in part to lmited knowledge surrounding the molecular mechanisms underlying radiation-induced cancers. The purpose of this investigation was to determine the frequency for alterations in genes within the K-ras and p53 signal and cell cycle regulatory pathways, respectively, in X-ray-induced lung tumors in the F344/N rat. These tumors were examined for genetic alterations in the K-ras, c-raf-1, p53, mdm2 and cip1 genes. No K-ras mutations were detected by sequencing in 18 squamous cell carcinomas (SCCs) or 17 adenocarcinomas. However, using a K-ras codon 12 mutation selection assay, a codon 12 GGT {r_arrow} GAT mutation was detected in one SCC, suggesting that activation of the K-ras proto-oncogene is both a rare and late event. Single-strand conformation polymorphism (SSCP) analysis of the kinase-binding domain of the c-raf-1 gene did not detect any polymorphisms. Three of 18 SCCs but none of the adenocarcinomas showed p53 nuclear immunoreactivity. Single-strand conformation polymorphism analysis of exons 4-9 of the p53 gene detected only an exon 9 mutation in one SCC. Mutations were not detected in the three SCCs with immunoreactive p53 protein. No amplification of the mdm2 gene was detected; however, nuclear mdm2 immunoreactivity was present in one of the three SCCs that stained positive for the p53 protein. The complete cDNA of the rat cip1 gene comprising 810 bases was cloned and sequenced. The frequency of somatic mutations in exon 2 of the cip1 gene was determined by SSCP analysis. No alterations in electrophoretic mobility were detected. The results of this investigation indicate that alterations in the K-ras and p53 pathways do not play a major role in the genesis of X-ray-induced lung tumors in the rat. 49 refs., 5 figs.

  7. Rapamycin attenuates bleomycin-induced pulmonary fibrosis in rats and the expression of metalloproteinase-9 and tissue inhibitors of metalloproteinase-1 in lung tissue.

    Science.gov (United States)

    Jin, Xiaoguang; Dai, Huaping; Ding, Ke; Xu, Xuefeng; Pang, Baosen; Wang, Chen

    2014-01-01

    Idiopathic pulmonary fibrosis (IPF) is the most common and devastating form of interstitial lung disease (ILD) in the clinic. There is no effective therapy except for lung transplantation. Rapamycin is an immunosuppressive drug with potent antifibrotic activity. The purpose of this study was to examine the effects of rapamycin on bleomycin-induced pulmonary fibrosis in rats and the relation to the expression of metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1). Sprague-Dawley rats were treated with intratracheal injection of 0.3 ml of bleomycin (5 mg/kg) in sterile 0.9% saline to make the pulmonary fibrosis model. Rapamycin was given at a dose of 0.5 mg/kg per gavage, beginning one day before bleomycin instillation and once daily until animal sacrifice. Ten rats in each group were sacrificed at 3, 7, 14, 28 and 56 days after bleomycin administration. Alveolitis and pulmonary fibrosis were semi-quantitatively assessed after HE staining and Masson staining under an Olympus BX40 microscope with an IDA-2000 Image Analysis System. Type I and III collagen fibers were identified by Picro-sirius-polarization. Hydroxyproline content in lung tissue was quantified by a colorimetric-based spectrophotometric assay, MMP-9 and TIMP-1 were detected by immunohistochemistry and by realtime quantitative reverse transcriptase polymerase chain reaction (RT-PCR). Bleomycin induced alveolitis and pulmonary fibrosis of rats was inhibited by rapamycin. Significant inhibition of alveolitis and hydroxyproline product were demonstrated when daily administration of rapamycin lasted for at least 14 days. The inhibitory efficacy on pulmonary fibrosis was unremarkable until rapamycin treatment lasted for at least 28 days (P pulmonary fibrosis, which is associated with decreased expression of MMP-9 and TIMP-1.

  8. Comparative study on the inhibitory effects of antioxidant vitamins and radon on carbon tetrachloride-induced hepatopathy

    International Nuclear Information System (INIS)

    Kataoka, Takahiro; Nishiyama, Yuichi; Yamato, Keiko; Teraoka, Junichi; Morii, Yuji; Taguchi, Takehito; Yamaoka, Kiyonori; Sakoda, Akihiro; Ishimori, Yuu

    2012-01-01

    We have previously reported that radon inhalation activates anti-oxidative functions and inhibits carbon tetrachloride (CCl 4 )-induced hepatopathy. It has also been reported that antioxidant vitamins can inhibit CCl 4 -induced hepatopathy. In the current study, we examined the comparative efficacy of treatment with radon, ascorbic acid and α-tocopherol on CCl 4 -induced hepatopathy. Mice were subjected to intraperitoneal injection of CCl 4 after inhaling approximately 1000 or 2000 Bq/m 3 radon for 24 h, or immediately after intraperitoneal injection of ascorbic acid (100, 300, or 500 mg/kg bodyweight) or α-tocopherol (100, 300, or 500 mg/kg bodyweight). We estimated the inhibitory effects on CCl 4 -induced hepatopathy based on hepatic function-associated parameters, oxidative damage-associated parameters and histological changes. The results revealed that the therapeutic effects of radon inhalation were almost equivalent to treatment with ascorbic acid at a dose of 500 mg/kg or α-tocopherol at a dose of 300 mg/kg. The activities of superoxide dismutase, catalase, and glutathione peroxidase in the liver were significantly higher in mice exposed to radon than in mice treated with CCl 4 alone. These findings suggest that radon inhalation has an anti-oxidative effect against CCl 4 -induced hepatopathy similar to the anti-oxidative effects of ascorbic acid or α-tocopherol due to the induction of anti-oxidative functions. (author)

  9. Indoor radon level in schools of Shillong, Meghalaya

    International Nuclear Information System (INIS)

    Saxena, A.; Sharma, Y.; Maibam, D.; Walia, D.; Diengdoh, E.

    2010-01-01

    Radon ( 222 Rn) in the atmosphere is the most important contributor to human exposure from natural sources. Radon is a noble inert gas; and it decays to radionuclides that are chemically active and relatively short lived. Inhalation of the short lived radon progeny imparts a radiation dose to the lung, to which an increased risk of lung cancer is attributed due to the alpha particle irradiation of the secretory and basal cells of the respiratory tract. The indoor radon concentration is dependent on the texture, porosity, permeability, water content of the soil underlying the structure and the radon behaviour in soils on aspects of geology and climate. The direct cause of high radon entry rates into structures exhibiting high indoor radon concentrations are fractures in bedrock formations, cracks in the soil, and similar inhomogeneities in the materials of the foundation of the structures. Other factors influencing indoor radon concentration includes exhalations from the walls and ceilings, building design and material, cracks and openings in the foundation of the buildings. The geological factors in the study area promote radon accumulation especially in buildings and dwellings. The world average annual effective dose in the indoor environments is 1.01 mSv.y -1 . The importance of radon level measurements in school buildings is of interest as children are more sensitive to radon exposure than adults. Hence, radon measurements in 10 schools have been undertaken in the present study

  10. Stimulation of alveolar macrophages by BCG vaccine enhances the process of lung fibrosis induced by bleomycin.

    Science.gov (United States)

    Chyczewska, E; Chyczewski, L; Bańkowski, E; Sułkowski, S; Nikliński, J

    1993-01-01

    It was found that the BCG vaccine injected subcutaneously to the rats enhances the process of lung fibrosis induced by bleomycin. Pretreatment of rats with this vaccine results in accumulation of activated macrophages in lung interstitium and in the bronchoalveolar spaces. It may be suggested that the activated macrophages release various cytokines which may stimulate the proliferation of fibroblasts and biosynthesis of extracellular matrix components.

  11. [The influnence of dachengqi tang on acute lung injury and intra abdominal hypertension in rats with acute pancreatitis].

    Science.gov (United States)

    Wan, Mei-Hua; Li, Juan; Tang, Wen-Fu; Gong, Han-Lin; Chen, Guang-Yuan; Xue, Ping; Zhao, Xian-Lin; Xia, Qing

    2011-09-01

    To test the hypothesis "lung and large intestine are interior exteriorly related" through investgating into the effect of Dacheng qi tang (DCQT) on intra abdominal hypertension (IAH) and acute lung injury (ALI) in rats with acute pancreatitis. Male SD rats were randomly divided into three groups with ten rats for each group: rats with sham-operations (SO); rats with acute necrosis pancreatitis (ANP); rats with ANP plus DCQT treatment. ANP was induced by retrograde infusion of 5% taurocholic acid into pancreatic duct. Two hours after operations, 10 mL/kg of normal saline was orally adminstered to the rats in both SO and ANP groups, whereas 10 mL/kg DCQT was adminstered to the rats in the treatment group. Aterial blood, pancreas and lung tissues were collected for biomarkers and histopathology 24 hours after operations. Intra-abdominal pressure and intestinal propulsion rate were also measured. RESULTS; DCQT treatment reduced intra-abdominal pressure and improved intestinal propulsion rate compared with those treated with saline (P 0.05). Only two rats in the ANP group died. DCQT can effectively relieve IAH and cure ALI at the same time in rats with acute pancreatitis. The result provides evidence to support the hypothesis "lung and large intestine are interior exteriorly related".

  12. Lessons from radon

    International Nuclear Information System (INIS)

    Nichols, M.

    1993-01-01

    At EPA there is a public outreach program that the Office of Air and Radiation (OAR) has developed for radon. To meet the difficult challenge radon presented, OAR's Radon Division developed working relationships with national nonprofit groups who share a mission. These groups have well-established communication networks with their memberships for advancing their goals. Such diverse groups as the American Lung Association, the Advertising Council, the National Association of Counties (NACo), the Consumer Federation of America, the National Association of Homebuilders, and the National Safety Council have joined with EPA to reduce radon health risks. Through this alliance, EPA has been able to take advantage of communication channels that it could never replicate on tis own. Every group working with EPA disseminates the radon message through its own established channels to reach its constituency. These partners wield authority in their fields and are ideal for addressing the concerns of their audiences

  13. Radon level and radon effective dose rate determination in Moroccan dwellings using SSNTDs

    International Nuclear Information System (INIS)

    Oufni, L.; Misdaq, M.A.; Amrane, M.

    2005-01-01

    Inhalation of radon ( 222 Rn) and its daughter product are a major source of natural radiation exposure. The measurement of radon activity in dwelling is assuming ever increasing importance. It is known from recent surveys in many countries that radon and its progeny contribute significantly to total inhalation dose and it is fairly established that radon when inhaled in large quantity causes lung disorder. Keeping this in view, the indoor radon activity level and radon effective dose rate were carried out in the dwellings of Beni-Mellal, Khouribgra and Ben Guerir cities, Morocco, using the solid state nuclear track detectors (SSNTD) technique. Assuming an indoor occupancy factor of 0.8 and 0.4 for the equilibrium factor of radon indoors, we found that the 222 Rn effective dose rate in the studied dwellings ranges from 1.01 to 7.90mSvy -1 . The radon activity in the corresponding dwellings was found to vary from 40 to 532Bqm -3 . The radon activity has not only been found to vary with seasonal changes, but also with the age, the construction mode of houses, the ventilation conditions and with specific sites and geological materials

  14. Inhaled tobacco sterols: uptake by the lungs and disposition to selected organs of rats

    International Nuclear Information System (INIS)

    Holden, W.E.; Maier, J.M.; Liebler, J.M.; Malinow, M.R.

    1988-01-01

    Tobacco sterols (cholesterol, beta-sitosterol, campesterol, and stigmasterol) are present in tobacco smoke and appear in plasma of mammals exposed to cigarette smoke. Because tobacco sterols may be important in the pathogenesis of smoking-induced lung and vascular diseases, we studied the pattern of deposition of cigarette sterols in the lungs and appearance of cigarette sterols in plasma and body organs of rats. After exposure to twenty 5 ml puffs of smoke from tobacco labeled with [4- 14 C]cholesterol or beta-[4- 14 C]sitosterol, rats were killed just after exposure (day 0) and on days 2, 5, 8, 11, 15, and 30, and the lungs and selected body organs analyzed for activity. We found that cigarette sterols are associated with particulates in cigarette smoke, deposited mostly in distal airspaces and parenchyma of the lungs, and appear in plasma and several body organs for more than 30 days after this single exposure to cigarette smoke. Bronchoalveolar lavage fluid contained relatively small amounts of radiolabel for only the first few days, suggesting that most of the sterols were rapidly incorporated in lung parenchyma. Because disorders of sterol metabolism have been implicated in a variety of diseases including atherosclerosis and cancer, the significance of tobacco sterols to human smoking-induced diseases deserves further study

  15. Influence of random daughter exposure rate, unattachment fraction, and disequilibrium on occurrence of lung tumors

    International Nuclear Information System (INIS)

    Cross, F.T.; Palmer, R.F.; Dagle, G.E.; Busch, R.H.; Buschbom, R.L.

    1983-10-01

    Groups of male, specific-pathogen-free (SPF), Wistar rats were exposed to several concentrations of radon daughters and uranium ore dust to clarify the roles of exposure rate, unattached RaA daughters, and the degree of radon daughter disequilibrium, in the development of respiratory system disease. Modeled, human-dosimetric data indicate that the dose to sensitive tissues of the respiratory tract increases with increasing radon-daughter unattachment fraction and degree of disequilibrium. Experimental verification of these dose-effect relationships is needed to protect the health of workers and of the public exposed to radon-daughter environments. Data bearing on these relationships as well as updated results of experiments designed to test the role of radon-daughter exposure rate on lung-tumor incidence are reported. 13 references, 3 tables

  16. Effect of the number of cigarettes smoked and of radon exposure on the lung cancer risk

    International Nuclear Information System (INIS)

    Boehm, R.; Holy, K.; Sedlak, A.

    2012-01-01

    The relation between the extent of cigarette smoking and the lung cancer risk in people exposed to radon was examined. The changes in the airway geometry due to an increased production of mucus caused by smoking were taken into account. The mucous layer protects the target cells from the effects of ionizing radiation. The radiation risk per unit exposure decreases with the number of cigarettes smoked, in contrast to the total risk, which increases to stagnate in the range of extensive daily cigarette smoking. Lung damage in chronic smokers should be taken into account, though. (orig.)

  17. Proteomic Analysis of Lung Tissue in a Rat Acute Lung Injury Model: Identification of PRDX1 as a Promoter of Inflammation

    Directory of Open Access Journals (Sweden)

    Dongdong Liu

    2014-01-01

    Full Text Available Acute respiratory distress syndrome (ARDS remains a high morbidity and mortality disease entity in critically ill patients, despite decades of numerous investigations into its pathogenesis. To obtain global protein expression changes in acute lung injury (ALI lung tissues, we employed a high-throughput proteomics method to identify key components which may be involved in the pathogenesis of ALI. In the present study, we analyzed lung tissue proteomes of Pseudomonas aeruginosa-induced ALI rats and identified eighteen proteins whose expression levels changed more than twofold as compared to normal controls. In particular, we found that PRDX1 expression in culture medium was elevated by a lipopolysaccharide (LPS challenge in airway epithelial cells in vitro. Furthermore, overexpression of PRDX1 increased the expression of proinflammatory cytokines interleukin-6 (IL-6, interleukin-8 (IL-8, and tumor necrosis factor-α (TNF-α, whereas knockdown of PRDX1 led to downregulated expression of cytokines induced by LPS. In conclusion, our findings provide a global alteration in the proteome of lung tissues in the ALI rat model and indicate that PRDX1 may play a critical role in the pathogenesis of ARDS by promoting inflammation and represent a novel strategy for the development of new therapies against ALI.

  18. A correlation study between high resolution CT appearances and expression of transforming growth factor-β, tumor necrosis factor-α in radiation-induced lung injury of rats

    International Nuclear Information System (INIS)

    Guo Lili; Cheng Guangjun; Li Shaodong; Xu Kai

    2008-01-01

    Objective: To study the correlation between high resolution computed tomography manifestations and expression of transforming growth factor beta, tumor necrosis factor alpha in radiation- induced lung injury of rats, and to investigate the values of cytokine detection and HRCT scanning for the prediction and early diagnosis of radiation-induced lung injury. Methods: Forty-eight Sprague-Dawley (SD) rats were randomly divided into eight groups, group A was normal control group, and group B- H were irradiated with a single dose of 15 Gy to the lungs. HRCT scanning was performed before and 1 week, 2, 4, 8, 12, 16, 24 weeks after radiation in group A-H respectively. The expression of TGF-beta and TNF-alpha were detected with ELISA. All the rats were killed to observe pathological changes of their lungs. HRCT signs, levels of cytokine were simultaneously compared and analyzed. The t-test and Spearman rank correlation were used for the statistics. Results: Four HRCT signs were observed during the 24 weeks after radiation, including ground-glass opacity (1 case), patchy consolidation (8 cases), massive consolidation (7 cases) and fibrosis (3 cases). The average levels of TGF-beta in group B-H [(3.33± 0.47), (3.20±0.65), (3.12±0.45), (3.54±0.80), (3.30±1.13), (2.49±0.67), (4.19± 0.22) μg/L, respectively] were higher than the control group [(0.45±0.14) μg/L, P 0.05). There were no rank correlations between HRCT manifestations and expression of TGF-beta and TNF-alpha (r s = 0.5570 and 0.1013,P>0.05). HRCT signs were correlated with pathological changes. Conclusions: The monitoring of TGF-beta and TNF-alpha in the serum after irradiation can predict the development of radiation-induced lung injury. There are no rank correlations between HRCT manifestations and expression of TGF-beta and TNF-alpha. (authors)

  19. Effects of sevoflurane on ventilator induced lung injury in a healthy lung experimental model.

    Science.gov (United States)

    Romero, A; Moreno, A; García, J; Sánchez, C; Santos, M; García, J

    2016-01-01

    Ventilator-induced lung injury (VILI) causes a systemic inflammatory response in tissues, with an increase in IL-1, IL-6 and TNF-α in blood and tissues. Cytoprotective effects of sevoflurane in different experimental models are well known, and this protective effect can also be observed in VILI. The objective of this study was to assess the effects of sevoflurane in VILI. A prospective, randomized, controlled study was designed. Twenty female rats were studied. The animals were mechanically ventilated, without sevoflurane in the control group and sevoflurane 3% in the treated group (SEV group). VILI was induced applying a maximal inspiratory pressure of 35 cmH2O for 20 min without any positive end-expiratory pressure for 20 min (INJURY time). The animals were then ventilated 30 min with a maximal inspiratory pressure of 12 cmH2O and 3 cmH2O positive end-expiratory pressure (time 30 min POST-INJURY), at which time the animals were euthanized and pathological and biomarkers studies were performed. Heart rate, invasive blood pressure, pH, PaO2, and PaCO2 were recorded. The lung wet-to-dry weight ratio was used as an index of lung edema. No differences were found in the blood gas analysis parameters or heart rate between the 2 groups. Blood pressure was statistically higher in the control group, but still within the normal clinical range. The percentage of pulmonary edema and concentrations of TNF-α and IL-6 in lung tissue in the SEV group were lower than in the control group. Sevoflurane attenuates VILI in a previous healthy lung in an experimental subclinical model in rats. Copyright © 2015 Sociedad Española de Anestesiología, Reanimación y Terapéutica del Dolor. Publicado por Elsevier España, S.L.U. All rights reserved.

  20. Experimental study of the protective effects of Zhongfei decoction on radiation-induced pneumonia in rats

    International Nuclear Information System (INIS)

    Wang Yuezhen; Ma Shenglin; Zhang Aiqin; Feng Jianguo; Fang Xianhua; Sun Xiaojiang; Bao Yejiang

    2007-01-01

    Objective: To investigate the protective effect and its possible mechanism of ZhongFei Decoction on radiation-induced pneumonia in rats. Methods: Single irradiation was given at two thorax of female Wistar rats with 30 Gy of 6 MV X irradiation. Sixty rats were randomly divided into the control group, radiation group, radiation plus DXM and ZhongFei Decoction plus radiation group. On days 14 and 28 after treatment, 5 rats of each group were sacrificed, and their lungs were harvested for measurement of the lung index, the difference of the histopathology change, the concentration of hydroxyproline (hyp), and expression of transforming growth factor-β1 in lungs were analyzed by HE stain, biochemical method and immunohistochemical method, respectively. Results: The pathological study showed marked lung injury in the radiation group while only slight hyperemia hemorrhage, exudation and thickness of alveolar walls in the lungs of ZhongFei Decoction plus radiation group, the concentration of hydroxyproline and expression of TGF-β1 in the radiation lungs increased compared with that in the control group and reduced in the ZhongFei Decoction plus radiation group compared with that in the radiation group. Conclusions: ZhongFei Decoction could have protective effects on the radiation-induced pneumonia and the mechanism of its may be related with down-regulating the expression of TGF-β1 in the irritated lung tissue. (authors)

  1. Lung response to ultrafine Kevlar aramid synthetic fibrils following 2-year inhalation exposure in rats.

    Science.gov (United States)

    Lee, K P; Kelly, D P; O'Neal, F O; Stadler, J C; Kennedy, G L

    1988-07-01

    Four groups of 100 male and 100 female rats were exposed to ultrafine Kevlar fibrils at concentrations of 0, 2.5, 25, and 100 fibrils/cc for 6 hr/day, 5 days/week for 2 years. One group was exposed to 400 fibrils/cc for 1 year and allowed to recover for 1 year. At 2.5 fibrils/cc, the lungs had normal alveolar architecture with a few dust-laden macrophages (dust cell response) in the alveolar airspaces. At 25 fibrils/cc, the lungs showed a dust cell response, slight Type II pneumocyte hyperplasia, alveolar bronchiolarization, and a negligible amount of collagenized fibrosis in the alveolar duct region. At 100 fibrils/cc, the same pulmonary responses were seen as at 25 fibrils/cc. In addition, cystic keratinizing squamous cell carcinoma (CKSCC) was found in 4 female rats, but not in male rats. Female rats had more prominent foamy alveolar macrophages, cholesterol granulomas, and alveolar bronchiolarization. These pulmonary lesions were related to the development of CKSCC. The lung tumors were derived from metaplastic squamous cells in areas of alveolar bronchiolarization. At 400 fibrils/cc following 1 year of recovery, the lung dust content, average fiber length, and the pulmonary lesions were markedly reduced, but slight centriacinar emphysema and minimal collagenized fibrosis were found in the alveolar duct region. One male and 6 female rats developed CKSCC. The lung tumors were a unique type of experimentally induced tumors in the rats and have not been seen as spontaneous tumors in man or animals. Therefore, the relevance of this type of lung tumor to the human situation is minimal.

  2. Low power infrared laser modifies the morphology of lung affected with acute injury induced by sepsis

    Science.gov (United States)

    Sergio, L. P. S.; Trajano, L. A. S. N.; Thomé, A. M. C.; Mencalha, A. L.; Paoli, F.; Fonseca, A. S.

    2018-06-01

    Acute lung injury (ALI) is a potentially fatal disease characterized by uncontrolled hyperinflammatory responses in the lungs as a consequence of sepsis. ALI is divided into two sequential and time-dependent phases, exudative and fibroproliferative phases, with increased permeability of the alveolar barrier, causing edema and inflammation. However, there are no specific treatments for ALI. Low-power lasers have been successfully used in the resolution of acute inflammatory processes. The aim of this study was to evaluate the effects of low-power infrared laser exposure on alveolus and interalveolar septa of Wistar rats affected by ALI-induced by sepsis. Laser fluences, power, and the emission mode were those used in clinical protocols for the treatment of acute inflammation. Adult male Wistar rats were randomized into six groups: control, 10 J cm‑2, 20 J cm‑2, ALI, ALI  +  10 J cm‑2, and ALI  +  20 J cm‑2. ALI was induced by intraperitoneal Escherichia coli lipopolysaccharide (LPS). Lungs were removed and processed for hematoxylin–eosin staining. Morphological alterations induced by LPS in lung tissue were quantified by morphometry with a 32-point cyclic arcs test system in Stepanizer. Data showed that exposure to low-power infrared laser in both fluences reduced the thickening of interalveolar septa in lungs affected by ALI, increasing the alveolar space; however, inflammatory infiltrate was still observed. Our research showed that exposure to low-power infrared laser improves the lung parenchyma in Wistar rats affected by ALI, which could be an alternative approach for treatment of inflammatory lung injuries.

  3. Radon and radon daughters in South African underground mines

    International Nuclear Information System (INIS)

    Rolle, R.

    1980-01-01

    Radon and the radon daughters are the radionuclides which primarily determine the level of the radiation hazard in underground uranium mines and to a smaller extent in non-uranium mines. Radon is a gas, and its daughters adsorb on aerosol particles which are of respirable size. The hazard thus arises from the alpha decay of radon and its daughters in contact with lung tissue. Radon is itself part of the uranium decay chain. The major radionuclide, 238 U, decays successively through thirteen shorter-lived radionuclides to 206 Pb. Radon is the only gaseous decay product at room temperature; the other twelve are solids. The main hazard presented by the uranium decay chain is normally determined by the radon concentration because gaseous transport can bring alpha emitters close to sensitive tissue. There is no such transport route for the other alpha emitters, and the level of beta and gamma radiation caused by the uranium decay chain generally presents a far lower external radiation hazard. Radon itself is the heaviest of the noble gases, which are He, Ne, Ar, Kr, Xe and Rn. Its chemical reactions are of no concern in regard to its potential hazard in mines as it may be considered inert. It does, however, have a solubility ten times higher than oxygen in water, and this can play a significant part in assisting the movement of the gas from the rock into airways. Radon continuously emanates into mine workings from uranium ores and from the uranium present at low concentrations in practically any rock. It has been found that the control of the exposure level is most effectively achieved by sound ventilation practices. In South African mines the standard of ventilation is generally high and exposure to radon and radon daughters is at acceptably low levels

  4. Carcinogenesis and low-level ionizing radiation with special reference to lung cancer and exposure to radon daughters

    International Nuclear Information System (INIS)

    Fabrikant, J.I.

    1982-06-01

    The quantitative estimation of the carcinogenic risk of low-dose, high-LET radiation in the case of exposure to radon daughters and lung-cancer is subject to numerous uncertainties. The greatest of these concerns the parametric values of the dose-response curve. We lack knowledge and an understanding of the dosimetry and the distribution of aggregates of radioactivity that remain localized as hot spots in specific regions of the lungs and the influence on greater or lesser risk of lung cancer per average lung dose than uniformly deposited radiation (NRC76). We have only a limited understanding of the response to exposure to high-LET radiations, such as alpha particles, for which linear risk estimates for low doses are less likely to overestimate the risk, and may, in fact, underestimate the risk (BEIR80). Other uncertainties include the length of the latency period, the RBE for alpha radiation relative to gamma radiation, the period during which the radiation risk is expressed, the risk projection model used - whether absolute or relative - for projecting risk beyond the period of observation, the effect of dose rate and protraction of dose, and the influence of differences in the natural incidence of lung cancer in different populations. In addition, uncertainties are introduced by the biological and life-style risk characteristics of humans, for example, the effect of sex, the effect of age at the time of irradiation and at the time of appearance of the cancer, the influence of length of observation or follow-up of the study populations, and the influence of perhaps the most important confounding bias, cigarette-smoking. The collective influence of these uncertainties is such as to deny great credibility to any estimate of human lung cancer risk and other cancer risk that can be made for low-dose, high-LET radon daughter radiation exposure

  5. Carcinogenesis and low-level ionizing radiation with special reference to lung cancer and exposure to radon daughters

    Energy Technology Data Exchange (ETDEWEB)

    Fabrikant, J.I.

    1982-06-01

    The quantitative estimation of the carcinogenic risk of low-dose, high-LET radiation in the case of exposure to radon daughters and lung-cancer is subject to numerous uncertainties. The greatest of these concerns the parametric values of the dose-response curve. We lack knowledge and an understanding of the dosimetry and the distribution of aggregates of radioactivity that remain localized as hot spots in specific regions of the lungs and the influence on greater or lesser risk of lung cancer per average lung dose than uniformly deposited radiation (NRC76). We have only a limited understanding of the response to exposure to high-LET radiations, such as alpha particles, for which linear risk estimates for low doses are less likely to overestimate the risk, and may, in fact, underestimate the risk (BEIR80). Other uncertainties include the length of the latency period, the RBE for alpha radiation relative to gamma radiation, the period during which the radiation risk is expressed, the risk projection model used - whether absolute or relative - for projecting risk beyond the period of observation, the effect of dose rate and protraction of dose, and the influence of differences in the natural incidence of lung cancer in different populations. In addition, uncertainties are introduced by the biological and life-style risk characteristics of humans, for example, the effect of sex, the effect of age at the time of irradiation and at the time of appearance of the cancer, the influence of length of observation or follow-up of the study populations, and the influence of perhaps the most important confounding bias, cigarette-smoking. The collective influence of these uncertainties is such as to deny great credibility to any estimate of human lung cancer risk and other cancer risk that can be made for low-dose, high-LET radon daughter radiation exposure.

  6. Concentration en radon dans une maison du Calvados

    Science.gov (United States)

    Leleyter, Lydia; Riffault, Benoit; Mazenc, Bernard

    2010-03-01

    Recent studies indicate a link between the risk of lung cancer and residential radon exposure. However, in France, awareness of this problem was made relatively late. Accordingly this study examines the radon concentration in a private home in Calvados. Findings show that the presence of a fireplace in a house can accelerate radon convective transfer, and that simple adjustments to interior and exterior accommodation can significantly reduce radon concentrations in the home.

  7. Studies on spatial distribution of indoor radon concentration at Mysore city, India

    International Nuclear Information System (INIS)

    Pruthvi Rani, K.S.; Chandrashekara, M.S.; Paramesh, L.

    2016-01-01

    Radon is a radioactive inert gas, with a half life of 3.82 days. Radium present in soil rocks and building material are the sources of atmospheric radon. Radon and its short-lived decay products ( 218 Po, 214 Pb, 214 Bi, and 214 Po) can be deposited in the lung tissues and give rise to higher radiation doses. Radon is now recognized as the second most important cause of lung cancer after smoking in the general population. In the present investigation a systematic study of the distribution of radon concentration has been carried out in a small room at different co-ordinates and time scales

  8. Environmental assessment of indoor radon gas exposure health hazards and some of its public risks

    International Nuclear Information System (INIS)

    Hussein, Abd El-Razik. Z.; Ibrahim, M.Se.; Ragab, M.H.; El-Bukhari, M.S.

    2005-01-01

    This study examine the relationship between indoor radon gas exposure and the cancer risk and housing characteristics in lung cancer risk houses (CRH) compared to non lung cancer risk houses (NCRH). Mean radon concentrations measured by active method were significantly higher among CRH compared to NCRH, 9:93 pCi/L versus 4.56 pCi/L, respectively. There was no statistically significant diurnal variation as regards radon levels in all examined houses. Indoor radon concentrations show statistically significance in houses with bad ventilation (low air change rate) compared to houses with good ventilation (high air change rate). Houses with floor material of tiles, had statistically significant higher radon concentrations. Neither finishing wall material nor indoor gas source shows statistically significance as regard radon levels. Radon levels > 4 pCi/L (US EPA action level) were statistically significance higher in bed rooms compared levels in living rooms. High radon concentrations were reported in lung cane risk houses and in houses with bad ventilation

  9. Cost effectiveness of reducing radon exposure in Spanish dwellings

    International Nuclear Information System (INIS)

    Colgan, P.A.; Gutierrez, J.

    1996-01-01

    Published information on the distribution of radon levels in Spanish single family dwellings is used to evaluate the cost-effectiveness of three different intervention scenarios: remediation of existing dwellings, radon proofing of all future dwellings and the targetting of areas with higher than average indoor radon concentrations. Analysis is carried out on the basis of a Reference Level of 400 Bq m -3 for the existing housing stock and 200 Bq m -3 for new dwellings. Certain assumptions are made about the effectiveness and durability of the measures applied and annualised costs are used to calculate the costs per lung cancer death averted. The results reveal that targetting future housing is a more cost-effective option than remediation of existing dwellings with radon concentrations above the Reference Level -the costs per lung cancer death averted are typically $145000. In high-risk areas, these costs can be considerably less, depending on the percentage of dwellings expected to exceed the Reference Level and the average savings in exposure as a result of the intervention. The costs of intervention to reduce lung cancer deaths following exposure to radon compare favourably with those of other health programmes in other countries. (Author)

  10. Morphologic and biochemical changes in male rat lung after surgical and pharmacological castration

    Directory of Open Access Journals (Sweden)

    M.S. Ojeda

    2000-03-01

    Full Text Available The morphology of the rat lung was studied by light microscopy in different situations: after surgical and pharmacological castration and after administration of testosterone to the castrated rat to determine if the androgen is required to maintain the normal morphology of the lung. We also determined the effect of flutamide on the phospholipid composition of both the surfactant and microsomes of the lung. Rats were separated into five groups: I - control non-castrated rats, II - castrated rats sacrificed 21 days after castration, III - castrated rats that received testosterone daily from day 2 to day 21 after castration, IV - castrated rats that received testosterone from day 15 to day 21 after castration, and V - control rats injected with flutamide for 7 days. The amount of different phospholipids in the surfactant and microsomes of the lung was measured in group I and V rats. At the light microscopy level, the surgical and pharmacological castration provoked alterations in the morphology of the lung, similar to that observed in human lung emphysema. The compositions of surfactant and microsomes of the lung were similar to those previously reported by us for the surgically castrated rats. These results indicate that androgens are necessary for the normal morphology as well as for some metabolic aspects of the lung.

  11. The conversion of exposures due to radon into the effective dose: the epidemiological approach

    Energy Technology Data Exchange (ETDEWEB)

    Beck, T.R. [Federal Office for Radiation Protection, Berlin (Germany)

    2017-11-15

    The risks and dose conversion coefficients for residential and occupational exposures due to radon were determined with applying the epidemiological risk models to ICRP representative populations. The dose conversion coefficient for residential radon was estimated with a value of 1.6 mSv year{sup -1} per 100 Bq m{sup -3} (3.6 mSv per WLM), which is significantly lower than the corresponding value derived from the biokinetic and dosimetric models. The dose conversion coefficient for occupational exposures with applying the risk models for miners was estimated with a value of 14 mSv per WLM, which is in good accordance with the results of the dosimetric models. To resolve the discrepancy regarding residential radon, the ICRP approaches for the determination of risks and doses were reviewed. It could be shown that ICRP overestimates the risk for lung cancer caused by residential radon. This can be attributed to a wrong population weighting of the radon-induced risks in its epidemiological approach. With the approach in this work, the average risks for lung cancer were determined, taking into account the age-specific risk contributions of all individuals in the population. As a result, a lower risk coefficient for residential radon was obtained. The results from the ICRP biokinetic and dosimetric models for both, the occupationally exposed working age population and the whole population exposed to residential radon, can be brought in better accordance with the corresponding results of the epidemiological approach, if the respective relative radiation detriments and a radiation-weighting factor for alpha particles of about ten are used. (orig.)

  12. The conversion of exposures due to radon into the effective dose: the epidemiological approach

    International Nuclear Information System (INIS)

    Beck, T.R.

    2017-01-01

    The risks and dose conversion coefficients for residential and occupational exposures due to radon were determined with applying the epidemiological risk models to ICRP representative populations. The dose conversion coefficient for residential radon was estimated with a value of 1.6 mSv year -1 per 100 Bq m -3 (3.6 mSv per WLM), which is significantly lower than the corresponding value derived from the biokinetic and dosimetric models. The dose conversion coefficient for occupational exposures with applying the risk models for miners was estimated with a value of 14 mSv per WLM, which is in good accordance with the results of the dosimetric models. To resolve the discrepancy regarding residential radon, the ICRP approaches for the determination of risks and doses were reviewed. It could be shown that ICRP overestimates the risk for lung cancer caused by residential radon. This can be attributed to a wrong population weighting of the radon-induced risks in its epidemiological approach. With the approach in this work, the average risks for lung cancer were determined, taking into account the age-specific risk contributions of all individuals in the population. As a result, a lower risk coefficient for residential radon was obtained. The results from the ICRP biokinetic and dosimetric models for both, the occupationally exposed working age population and the whole population exposed to residential radon, can be brought in better accordance with the corresponding results of the epidemiological approach, if the respective relative radiation detriments and a radiation-weighting factor for alpha particles of about ten are used. (orig.)

  13. Mesenchymal Stem Cells Adopt Lung Cell Phenotype in Normal and Radiation-induced Lung Injury Conditions.

    Science.gov (United States)

    Maria, Ola M; Maria, Ahmed M; Ybarra, Norma; Jeyaseelan, Krishinima; Lee, Sangkyu; Perez, Jessica; Shalaby, Mostafa Y; Lehnert, Shirley; Faria, Sergio; Serban, Monica; Seuntjens, Jan; El Naqa, Issam

    2016-04-01

    Lung tissue exposure to ionizing irradiation can invariably occur during the treatment of a variety of cancers leading to increased risk of radiation-induced lung disease (RILD). Mesenchymal stem cells (MSCs) possess the potential to differentiate into epithelial cells. However, cell culture methods of primary type II pneumocytes are slow and cannot provide a sufficient number of cells to regenerate damaged lungs. Moreover, effects of ablative radiation doses on the ability of MSCs to differentiate in vitro into lung cells have not been investigated yet. Therefore, an in vitro coculture system was used, where MSCs were physically separated from dissociated lung tissue obtained from either healthy or high ablative doses of 16 or 20 Gy whole thorax irradiated rats. Around 10±5% and 20±3% of cocultured MSCs demonstrated a change into lung-specific Clara and type II pneumocyte cells when MSCs were cocultured with healthy lung tissue. Interestingly, in cocultures with irradiated lung biopsies, the percentage of MSCs changed into Clara and type II pneumocytes cells increased to 40±7% and 50±6% at 16 Gy irradiation dose and 30±5% and 40±8% at 20 Gy irradiation dose, respectively. These data suggest that MSCs to lung cell differentiation is possible without cell fusion. In addition, 16 and 20 Gy whole thorax irradiation doses that can cause varying levels of RILD, induced different percentages of MSCs to adopt lung cell phenotype compared with healthy lung tissue, providing encouraging outlook for RILD therapeutic intervention for ablative radiotherapy prescriptions.

  14. Doses and affects of radon and its daughters

    International Nuclear Information System (INIS)

    Snihs, J.O.

    1982-01-01

    Radon and its short-lived daughters are one of the main contributors to the natural exposures of ionizing radiation to man. Their sources, levels and characteristics are described. By inhalation of radon and its daughters tissues in the lung are irritated by α-particles leading to an increased risk of lung cancer. Methods of calculation of doses and risks using the dosimetric approach and the epidemiological approach are described and discussed. (Author)

  15. Attenuation of cigarette smoke-induced airway mucus production by hydrogen-rich saline in rats.

    Directory of Open Access Journals (Sweden)

    Yunye Ning

    Full Text Available BACKGROUND: Over-production of mucus is an important pathophysiological feature in chronic airway disease such as chronic obstructive pulmonary disease (COPD and asthma. Cigarette smoking (CS is the leading cause of COPD. Oxidative stress plays a key role in CS-induced airway abnormal mucus production. Hydrogen protected cells and tissues against oxidative damage by scavenging hydroxyl radicals. In the present study we investigated the effect of hydrogen on CS-induced mucus production in rats. METHODS: Male Sprague-Dawley rats were divided into four groups: sham control, CS group, hydrogen-rich saline pretreatment group and hydrogen-rich saline control group. Lung morphology and tissue biochemical changes were determined by immunohistochemistry, Alcian Blue/periodic acid-Schiff staining, TUNEL, western blot and realtime RT-PCR. RESULTS: Hydrogen-rich saline pretreatment attenuated CS-induced mucus accumulation in the bronchiolar lumen, goblet cell hyperplasia, muc5ac over-expression and abnormal cell apoptosis in the airway epithelium as well as malondialdehyde increase in the BALF. The phosphorylation of EGFR at Tyr1068 and Nrf2 up-regulation expression in the rat lungs challenged by CS exposure were also abrogated by hydrogen-rich saline. CONCLUSION: Hydrogen-rich saline pretreatment ameliorated CS-induced airway mucus production and airway epithelium damage in rats. The protective role of hydrogen on CS-exposed rat lungs was achieved at least partly by its free radical scavenging ability. This is the first report to demonstrate that intraperitoneal administration of hydrogen-rich saline protected rat airways against CS damage and it could be promising in treating abnormal airway mucus production in COPD.

  16. Hypoxia-preconditioned mesenchymal stem cells ameliorate ischemia/reperfusion-induced lung injury.

    Directory of Open Access Journals (Sweden)

    Yung-Yang Liu

    Full Text Available Hypoxia preconditioning has been proven to be an effective method to enhance the therapeutic action of mesenchymal stem cells (MSCs. However, the beneficial effects of hypoxic MSCs in ischemia/reperfusion (I/R lung injury have yet to be investigated. In this study, we hypothesized that the administration of hypoxic MSCs would have a positive therapeutic impact on I/R lung injury at molecular, cellular, and functional levels.I/R lung injury was induced in isolated and perfused rat lungs. Hypoxic MSCs were administered in perfusate at a low (2.5×105 cells and high (1×106 cells dose. Rats ventilated with a low tidal volume of 6 ml/kg served as controls. Hemodynamics, lung injury indices, inflammatory responses and activation of apoptotic pathways were determined.I/R induced permeability pulmonary edema with capillary leakage and increased levels of reactive oxygen species (ROS, pro-inflammatory cytokines, adhesion molecules, cytosolic cytochrome C, and activated MAPK, NF-κB, and apoptotic pathways. The administration of a low dose of hypoxic MSCs effectively attenuated I/R pathologic lung injury score by inhibiting inflammatory responses associated with the generation of ROS and anti-apoptosis effect, however this effect was not observed with a high dose of hypoxic MSCs. Mechanistically, a low dose of hypoxic MSCs down-regulated P38 MAPK and NF-κB signaling but upregulated glutathione, prostaglandin E2, IL-10, mitochondrial cytochrome C and Bcl-2. MSCs infused at a low dose migrated into interstitial and alveolar spaces and bronchial trees, while MSCs infused at a high dose aggregated in the microcirculation and induced pulmonary embolism.Hypoxic MSCs can quickly migrate into extravascular lung tissue and adhere to other inflammatory or structure cells and attenuate I/R lung injury through anti-oxidant, anti-inflammatory and anti-apoptotic mechanisms. However, the dose of MSCs needs to be optimized to prevent pulmonary embolism and thrombosis.

  17. Inhalation exposure to chloramine T induces DNA damage and inflammation in lung of Sprague-Dawley rats.

    Science.gov (United States)

    Shim, Ilseob; Seo, Gyun-Baek; Oh, Eunha; Lee, Mimi; Kwon, Jung-Taek; Sul, Donggeun; Lee, Byung-Woo; Yoon, Byung-Il; Kim, Pilje; Choi, Kyunghee; Kim, Hyun-Mi

    2013-01-01

    Chloramine T has been widely used as a disinfectant in many areas such as kitchens, laboratories and hospitals. It has been also used as a biocide in air fresheners and deodorants which are consumer products; however, little is known about its toxic effects by inhalation route. This study was performed to identify the subacute inhalation toxicity of chloramine T under whole-body inhalation exposure conditions. Male and female groups of rats were exposed to chloramine T at concentrations of 0.2, 0.9 and 4.0 mg/m³ for 6 hr/day, 5 days/week during 4 weeks. After 28-day repeated inhalation of chloramine T, there were dose-dependently significant DNA damage in the rat tissues evaluated and inflammation was histopathologically noted around the terminal airways of the lung in both genders. As a result of the expression of three types of antioxidant enzymes (SOD-2, GPx-1, PRX-1) in rat's lung after exposure, there was no significant change of all antioxidant enzymes in the male and female rats. The results showed that no observed adverse effect level (NOAEL) was 0.2 mg/m³ in male rats and 0.9 mg/m³ in female rats under the present experimental condition.

  18. The role of thymus-dependent T cells in hexachlorobenzene-induced inflammatory skin and lung lesions

    NARCIS (Netherlands)

    Michielsen, CCPPC; Bloksma, N; Klatter, FA; Rozing, J; Vos, JG; van Dijk, JE

    1999-01-01

    The involvement of thymus-dependent T cells in the inflammatory skin and lung lesions and spleen effects induced by hexachlorobenzene (HCB) was investigated by using genetically athymic and euthymic WAG/Rij rats and Brown Norway (BN) rats with or without depletion of T cells by adult thymectomy,

  19. Effect of nuclear factor kappa B on intercellular adhesion molecule-1 expression and neutrophil infiltration in lung injury induced by intestinal ischemia/reperfusion in rats

    Science.gov (United States)

    Tian, Xiao-Feng; Yao, Ji-Hong; Li, Ying-Hua; Zhang, Xue-Song; Feng, Bing-An; Yang, Chun-Ming; Zheng, Shu-Sen

    2006-01-01

    AIM: To investigate the role of nuclear factor kappa B (NF-κB) in the pathogenesis of lung injury induced by intestinal ischemia/reperfusion (I/R), and its effect on intercellular adhesion molecule-1 (ICAM-1) expression and neutrophil infiltration. METHODS: Twenty-four Wistar rats were divided randomly into control, I/R and pyrrolidine dithiocarbamate (PDTC) treatment groups, n = 8 in each. I/R group and PDTC treatment group received superior mysenteric artery (SMA) occluding for 1 h and reperfusion for 2 h. PDTC group was administrated with intraperitoneal injection of 2% 100 mg/kg PDTC 1 h before surgery. Lung histology and bronchia alveolus lung fluid (BALF) protein were assayed. Serum IL-6, lung malondialdehyde (MDA) and myeloperoxidase (MPO) as well as the expression level of NF-κB and ICAM-1 were measured. RESULTS: Lung injury induced by intestinal I/R, was characterized by edema, hemorrhage and neutrophil infiltration as well as by the significant rising of BALF protein. Compared to control group, the levels of serum IL-6 and lung MDA and MPO increased significantly in I/R group (P = 0.001). Strong positive expression of NF-κB p65 and ICAM-1 was observed. After the administration of PDTC, the level of serum IL-6, lung MDA and MPO as well as NF-κB and ICAM-1 decreased significantly (P < 0.05) when compared to I/R group. CONCLUSION: The activation of NF-κB plays an important role in the pathogenesis of lung injury induced by intestinal I/R through upregulating the neutrophil infiltration and lung ICAM-1 expression. PDTC as an inhibitor of NF-κB can prevent lung injury induced by intestinal I/R through inhibiting the activity of NF-κB. PMID:16489637

  20. Phosphotyrosine phosphatase and tyrosine kinase inhibition modulate airway pressure-induced lung injury.

    Science.gov (United States)

    Parker, J C; Ivey, C L; Tucker, A

    1998-11-01

    We determined whether drugs which modulate the state of protein tyrosine phosphorylation could alter the threshold for high airway pressure-induced microvascular injury in isolated perfused rat lungs. Lungs were ventilated for successive 30-min periods with peak inflation pressures (PIP) of 7, 20, 30, and 35 cmH2O followed by measurement of the capillary filtration coefficient (Kfc), a sensitive index of hydraulic conductance. In untreated control lungs, Kfc increased by 1.3- and 3.3-fold relative to baseline (7 cmH2O PIP) after ventilation with 30 and 35 cmH2O PIP. However, in lungs treated with 100 microM phenylarsine oxide (a phosphotyrosine phosphatase inhibitor), Kfc increased by 4.7- and 16.4-fold relative to baseline at these PIP values. In lungs treated with 50 microM genistein (a tyrosine kinase inhibitor), Kfc increased significantly only at 35 cmH2O PIP, and the three groups were significantly different from each other. Thus phosphotyrosine phosphatase inhibition increased the susceptibility of rat lungs to high-PIP injury, and tyrosine kinase inhibition attenuated the injury relative to the high-PIP control lungs.

  1. Radon Monitoring in Army Stand-Alone Housing Units

    Science.gov (United States)

    1990-04-01

    damage lung tissue and lead I to increased risk of developing lang cancer . Your risk of developing lung cancer from exposure to radon depends upon the...of developing lung cancer than exposure to a significantly elevated level for a short time. In general, your risk increases as the level of radon and...000mm 0Mmm *000 OOO 0 0w 0 0 000 -0-0 *4 0 880 mama 0 0000000000 000 000Eca ( el cN) 00 9 ’ qqO .00 1(10 0 -U M w co SEE wSS SEES NSEwESO m v MM O v mm

  2. Expression of transforming growth factor alpha and epidermal growth factor receptor in rat lung neoplasms induced by plutonium-239

    International Nuclear Information System (INIS)

    Stegelmeier, B.L.; Gillett, N.A.; Hahn, F.F.; Kelly, G.; Rebar, A.H.

    1994-01-01

    Ninety-two rat lung proliferative lesions and neoplasms induced by inhaled 239 PuO 2 were evaluated for aberrant expression of transforming growth factor alpha (TGF-α) and epidermal growth factor receptor (EGFR). Expression of TGF-α protein, measured by immunohistochemistry, was higher in 94% of the squamous cell carcinomas and 87% of the foci of alveolar epithelial squamous metaplasia than that exhibited by the normal-appearing, adjacent lung parenchyma. In contrast, only 20% of adenocarcinomas and foci of epithelial hyperplasia expressed elevated levels of TGF-α. Many neoplasms expressing TGF-α also expressed excessive levels of EGFR mRNA. Southern and DNA slot blot analyses showed that the elevated EGFR expression was not due to amplification of the EGFR gene. These data suggest that increased amounts of TGF-α were early alterations in the progression of plutonium-induced squamous cell carcinoma, and these increases may occur in parallel with overexpression of the receptor for this growth factor. Together, these alterations create a potential autocrine loop for sustaining clonal expansion of cells initiated by high-LET radiation. 44 refs., 4 figs., 1 tab

  3. Carbonic anhydrase inhibitor attenuates ischemia-reperfusion induced acute lung injury.

    Directory of Open Access Journals (Sweden)

    Chou-Chin Lan

    Full Text Available Ischemia-reperfusion (IR-induced acute lung injury (ALI is implicated in several clinical conditions including lung transplantation, cardiopulmonary bypass surgery, re-expansion of collapsed lung from pneumothorax or pleural effusion and etc. IR-induced ALI remains a challenge in the current treatment. Carbonic anhydrase has important physiological function and influences on transport of CO2. Some investigators suggest that CO2 influences lung injury. Therefore, carbonic anhydrase should have the role in ALI. This study was undertaken to define the effect of a carbonic anhydrase inhibitor, acetazolamide (AZA, in IR-induced ALI, that was conducted in a rat model of isolated-perfused lung with 30 minutes of ischemia and 90 minutes of reperfusion. The animals were divided into six groups (n = 6 per group: sham, sham + AZA 200 mg/kg body weight (BW, IR, IR + AZA 100 mg/kg BW, IR + AZA 200 mg/kg BW and IR+ AZA 400 mg/kg BW. IR caused significant pulmonary micro-vascular hyper-permeability, pulmonary edema, pulmonary hypertension, neutrophilic sequestration, and an increase in the expression of pro-inflammatory cytokines. Increases in carbonic anhydrase expression and perfusate pCO2 levels were noted, while decreased Na-K-ATPase expression was noted after IR. Administration of 200mg/kg BW and 400mg/kg BW AZA significantly suppressed the expression of pro-inflammatory cytokines (TNF-α, IL-1, IL-6 and IL-17 and attenuated IR-induced lung injury, represented by decreases in pulmonary hyper-permeability, pulmonary edema, pulmonary hypertension and neutrophilic sequestration. AZA attenuated IR-induced lung injury, associated with decreases in carbonic anhydrase expression and pCO2 levels, as well as restoration of Na-K-ATPase expression.

  4. Rating radon through the looking glass

    International Nuclear Information System (INIS)

    Anon.

    1993-01-01

    Radon emerged as a health threat in the last five years as studies showed that exposure to high levels in the home can cause lung cancer. But many families move so often that its difficult to determine their exposure over a lifetime. Now, Battelle Memorial Institute scientists at the Energy Dept.'s Pacific Northwest Lab in Richland, Wash., have devised a clever way to do so. They tape a 2-inch-square piece of clear plastic polymer to the glass on an old mirror or framed picture. Such items as wedding photos are easily datable and normally carried from home to home. As radon decays over the years, it emits alpha particles, which embed themselves in glass. The particles leave tracks in the polymer. By analyzing these tracks, scientists can estimate a person's average annual exposure to indoor radon over 20 years or more. Starting in May, the technique will be used in a three-year National Cancer Institute study that examines radon, smoking, and diet as co-factors in the risk of lung cancer

  5. Human disease from radon exposures: the impact of energy conservation in buildings

    International Nuclear Information System (INIS)

    Budnitz, R.J.; Berk, J.V.; Hollowell, C.D.; Nazaroff, W.W.; Nero, A.V.; Rosenfeld, A.H.

    1978-01-01

    The level of radon and its daughters inside conventional buildings is often higher than the ambient background level. Interest in conserving energy is motivating home-owners and builders to reduce the rate of infiltration of fresh air into homes, and hence to increase the concentration of indoor air contaminants, including radon. It is unlikely, but possible, that the present radiation levels from radon daughters account for much of the lung cancer rate in non-smokers. In any event, it is likely that some increased lung cancer risk would result from increased radon exposures; hence, it is desirable not to allow radon concentrations to rise significantly. There are several ways to circumvent the increased risk without compromising energy conservation considerations

  6. Measurements of indoor radon concentration in Libyan cities

    International Nuclear Information System (INIS)

    Elarabiy, S. F.; Khalifa, M.; Misrati, N.; Chahboune, N.; Ahmed, M.

    2012-12-01

    Studies confirm that the risk of exposure to indor radon is attributable to lung cancer worldwide. The relationship between radon exposure and cancer is a linear one which necessitates for need for measurements of indoor radon concentration. This paper presents the results of measurements of indoor radon in several libya cities using CR-39 plastic. The results showed that the average radon concentration in the cities of Tripoli, Al-harcha and Alrajaban were 48.8 Bg/m 3 , 51.4 Bg/m 3 and 55.5 Bg/m 3 respectively. The average indoor radon concentration in Libya is low comparing with other studies. (Author)

  7. Ghrelin ameliorates acute lung injury induced by oleic acid via inhibition of endoplasmic reticulum stress.

    Science.gov (United States)

    Tian, Xiuli; Liu, Zhijun; Yu, Ting; Yang, Haitao; Feng, Linlin

    2018-03-01

    Acute lung injury (ALI) is associated with excessive mortality and lacks appropriate therapy. Ghrelin is a novel peptide that protects the lung against ALI. This study aimed to investigate whether endoplasmic reticulum stress (ERS) mediates the protective effect of ghrelin on ALI. We used a rat oleic acid (OA)-induced ALI model. Pulmonary impairment was detected by hematoxylin and eosin (HE) staining, lung mechanics, wet/dry weight ratio, and arterial blood gas analysis. Plasma and lung content of ghrelin was examined by ELISA, and mRNA expression was measured by quantitative real-time PCR. Protein levels were detected by western blot. Rats with OA treatment showed significant pulmonary injury, edema, inflammatory cellular infiltration, cytokine release, hypoxia and CO 2 retention as compared with controls. Plasma and pulmonary content of ghrelin was reduced in rats with ALI, and mRNA expression was downregulated. Ghrelin (10nmol/kg) treatment ameliorated the above symptoms, but treatment with the ghrelin antagonists D-Lys 3 GHRP-6 (1μmol/kg) and JMV 2959 (6mg/kg) exacerbated the symptoms. ERS induced by OA was prevented by ghrelin and augmented by ghrelin antagonist treatment. The ERS inducer, tunicamycin (Tm) prevented the ameliorative effect of ghrelin on ALI. The decreased ratio of p-Akt and Akt induced by OA was improved by ghrelin treatment, and was further exacerbated by ghrelin antagonists. Ghrelin protects against ALI by inhibiting ERS. These results provide a new target for prevention and therapy of ALI. Copyright © 2017 Elsevier Inc. All rights reserved.

  8. Rosmarinic acid potentiates carnosic acid induced apoptosis in lung fibroblasts.

    Directory of Open Access Journals (Sweden)

    Sana Bahri

    Full Text Available Pulmonary fibrosis is characterized by over-population and excessive activation of fibroblasts and myofibroblasts disrupting normal lung structure and functioning. Rosemary extract rich in carnosic acid (CA and rosmarinic acid (RA was reported to cure bleomycin-(BLM-induced pulmonary fibrosis. We demonstrate that CA decreased human lung fibroblast (HLF viability with IC50 value of 17.13±1.06 μM, while RA had no cytotoxic effect. In the presence of 50 μM of RA, dose-response for CA shifted to IC50 value of 11.70±1.46 μM, indicating synergic action. TGFβ-transformed HLF, rat lung fibroblasts and L929 cells presented similar sensitivity to CA and CA+RA (20μM+100μM, respectively treatment. Rat alveolar epithelial cells died only under CA+RA treatment, while A549 cells were not affected. Annexin V staining and DNA quantification suggested that HLF are arrested in G0/G1 cell cycle phase and undergo apoptosis. CA caused sustained activation of phospho-Akt and phospho-p38 expression and inhibition of p21 protein.Addition of RA potentiated these effects, while RA added alone had no action.Only triple combination of inhibitors (MAPK-p38, pan-caspase, PI3K/Akt/autophagy partially attenuated apoptosis; this suggests that cytotoxicity of CA+RA treatment has a complex mechanism involving several parallel signaling pathways. The in vivo antifibrotic effect of CA and RA was compared with that of Vitamine-E in BLM-induced fibrosis model in rats. We found comparable reduction in fibrosis score by CA, RA and CA+RA, attenuation of collagen deposition and normalization of oxidative stress markers. In conclusion, antifibrotic effect of CA+RA is due to synergistic pro-apoptotic action on lung fibroblasts and myofibroblasts.

  9. Expression of cyclin D{sub 1} during endotoxin-induced aleveolar type II cell hyperplasia in rat lung and the detection of apoptotic cells during the remodeling process

    Energy Technology Data Exchange (ETDEWEB)

    Tesfaigzi, J.; Wood, M.B.; Johnson, N.F.

    1995-12-01

    Our studies have shown that endotoxin intratracheally instilled into the rat lung induces proliferation of alveolar type II cells. In that study, the alveolar type II cells. In that study, the alveolar type II cell hyperplasia occurred 2 d after instillation of endotoxin and persisted for a further 2 d. After hyperplasia, the lung remodeled and returned to a normal state within 24-48 h. Understanding the mechanisms involved in the remodeling process of this transient hyperplasia may be useful to identify molecular changes that are altered in neoplasia. The purpose of the present study was to corroborate induction of epithelial cell hyperplasia by endotoxin and to delineate mechanisms involved in tissue remodeling after endotoxin-induced alveolar type II cell hyperplasia. In conclusion, immonostaining with cyclin D1 and cytokeratin shows that endotoxin induced epithelial cell proliferation and resulted in hyperplasia in the lung which persisted through 4 d post-instillation.

  10. Residential radon exposure, diet and lung cancer: a case-control study in a Mediterranean region.

    Science.gov (United States)

    Bochicchio, Francesco; Forastiere, Francesco; Farchi, Sara; Quarto, Maria; Axelson, Olav

    2005-05-10

    We performed a case-control study in Lazio, a region in central Italy characterized by high levels of indoor radon, Mediterranean climate and diet. Cases (384) and controls (404) aged 35-90 years were recruited in the hospital. Detailed information regarding smoking, diet and other risk factors were collected by direct interview. Residential history during the 30-year period ending 5 years before enrollment was ascertained. In each dwelling, radon detectors were placed in both the main bedroom and the living room for 2 consecutive 6-month periods. We computed odds ratios (ORs) and 95% confidence intervals (CIs) for time-weighted radon concentrations using both categorical and continuous unconditional logistic regression analysis and adjusting for smoking, diet and other variables. Radon measurements were available from 89% and 91% of the time period for cases and controls, respectively. The adjusted ORs were 1.30 (1.03-1.64), 1.48 (1.08-2.02), 1.49 (0.82-2.71) and 2.89 (0.45-18.6) for 50-99, 100-199, 200-399 and 400+ Bq/m(3), respectively, compared with 0-49 Bq/m(3) (OR = 1; 0.56-1.79). The excess odds ratio (EOR) per 100 Bq/m(3) was 0.14 (-0.11, 0.46) for all subjects, 0.24 (-0.09, 0.70) for subjects with complete radon measurements and 0.30 (-0.08, 0.82) for subjects who had lived in 1 or 2 dwellings. There was a tendency of higher risk estimates among subjects with low-medium consumption of dietary antioxidants (EOR = 0.32; -0.19, 1.16) and for adenocarcinoma, small cell and epidermoid cancers. This study indicates an association, although generally not statistically significant, between residential radon and lung cancer with both categorical and continuous analyses. Subjects with presumably lower uncertainty in the exposure assessment showed a higher risk. Dietary antioxidants may act as an effect modifier.

  11. Low Level Laser Therapy Reduces the Development of Lung Inflammation Induced by Formaldehyde Exposure.

    Directory of Open Access Journals (Sweden)

    Cristiane Miranda da Silva

    Full Text Available Lung diseases constitute an important public health problem and its growing level of concern has led to efforts for the development of new therapies, particularly for the control of lung inflammation. Low Level Laser Therapy (LLLT has been highlighted as a non-invasive therapy with few side effects, but its mechanisms need to be better understood and explored. Considering that pollution causes several harmful effects on human health, including lung inflammation, in this study, we have used formaldehyde (FA, an environmental and occupational pollutant, for the induction of neutrophilic lung inflammation. Our objective was to investigate the local and systemic effects of LLLT after FA exposure. Male Wistar rats were exposed to FA (1% or vehicle (distillated water during 3 consecutive days and treated or not with LLLT (1 and 5 hours after each FA exposure. Non-manipulated rats were used as control. 24 h after the last FA exposure, we analyzed the local and systemic effects of LLLT. The treatment with LLLT reduced the development of neutrophilic lung inflammation induced by FA, as observed by the reduced number of leukocytes, mast cells degranulated, and a decreased myeloperoxidase activity in the lung. Moreover, LLLT also reduced the microvascular lung permeability in the parenchyma and the intrapulmonary bronchi. Alterations on the profile of inflammatory cytokines were evidenced by the reduced levels of IL-6 and TNF-α and the elevated levels of IL-10 in the lung. Together, our results showed that LLLT abolishes FA-induced neutrophilic lung inflammation by a reduction of the inflammatory cytokines and mast cell degranulation. This study may provide important information about the mechanisms of LLLT in lung inflammation induced by a pollutant.

  12. Late changes in lungs of rats irradiated with 6.5 Gy of X-rays

    International Nuclear Information System (INIS)

    Mazanowska, A.M.; Jelenska, M.M.; Dancewicz, A.M.

    1978-01-01

    1, 3, 6 and 9 months after exposure of mature male rats to 650 rads of X-rays, the composition of isolated lung collagen has been estimated and the distribution of fatty acids in lipids of lung wash analyzed. The results obtained indicate that during the development of lung fibrosis proportion of type I to type III collagen in this organ increases. At the same period increases proportion of saturated fatty acids in lipids isolated from lung wash. Thus, radiation-induced fibrosis is accompanied not only by collagen accumulation but also by an essential change in the type of collagen produced. It seems that also the increased saturation of fatty acids in lung surfactant contributes to the impairment of function of fibrotic lung. (orig./AJ) [de

  13. Indoor exposure to radon and its health effects

    International Nuclear Information System (INIS)

    Loskiewicz, J.

    1997-10-01

    Radon (Rn-222) is a noble radioactive gas which originates during U-238 series decay. As a noble gas it is not reacting with soils and building materials and therefore is showing large mobility due to its half-life of 3.82 days. It decays through alpha emission and is producing other radioactive isotopes (Po-218, Bi-214 etc.) which are solid. The migration of radon and its decay products can be in unattached form or attached to aerosols. The size of aerosol particles is important for adhesion coefficient value and for inhalation probability by human respiratory system. The unattached radon is penetrating more easily into lung space and there it may decay into radioactive and alpha emitting solid isotopes. The emitted alpha particle can damage sensitive cells. An alpha particle that penetrates that epithelial cells can deposit enough energy in a cell to kill or transform it. The transformed cell, alone or through interaction with some other agent, has the potential to develop eventually into a lung cancer. The data on risk of a lung cancer occurrence for high and medium concentrations of radon in the air will also be presented. (author)

  14. Indoor radon concentrations in Vushtrri, Kosovo

    International Nuclear Information System (INIS)

    Xhafa, B.; Jonuzaj, A.; ); Bekteshi, S.; Ahmetaj, S.; Kabashi, S.; )

    2009-01-01

    Indoor air radon concentration was measured by exposing trac ketch detectors in the two elementary schools, one high school, a kindergarten and the hospital in the city of Vushtrri. Measurements were performed with the radon monitor PRM-145, which uses alpha scintillation cells and serves to determine the current concentration of radon. The results we obtained are in the range between the average values of radon for the interior spaces, and values that pose a potential risk for lung cancer. Measuring the concentration of radon was done in total of 34 rooms and came up with values which are between 28Bqm -3 and 398Bqm -3 . In order to reduce the concentration of radon, we have built a ventilation pump, then we performed repeated measurements and finally came with results between 130-145Bqm -3 .

  15. Effect of sildenafil on acrolein-induced airway inflammation and mucus production in rats.

    Science.gov (United States)

    Wang, T; Liu, Y; Chen, L; Wang, X; Hu, X-R; Feng, Y-L; Liu, D-S; Xu, D; Duan, Y-P; Lin, J; Ou, X-M; Wen, F-Q

    2009-05-01

    Airway inflammation with mucus overproduction is a distinguishing pathophysiological feature of many chronic respiratory diseases. Phosphodiesterase (PDE) inhibitors have shown anti-inflammatory properties. In the present study, the effect of sildenafil, a potent inhibitor of PDE5 that selectively degrades cyclic guanosine 3',5'-monophosphate (cGMP), on acrolein-induced inflammation and mucus production in rat airways was examined. Rats were exposed to acrolein for 14 and 28 days. Sildenafil or distilled saline was administered intragastrically prior to acrolein exposure. Bronchoalveolar lavage fluid (BALF) was acquired for cell count and the detection of pro-inflammatory cytokine levels. Lung tissue was examined for cGMP content, nitric oxide (NO)-metabolite levels, histopathological lesion scores, goblet cell metaplasia and mucin production. The results suggested that sildenafil pretreatment reversed the significant decline of cGMP content in rat lungs induced by acrolein exposure, and suppressed the increase of lung NO metabolites, the BALF leukocyte influx and pro-inflammatory cytokine release. Moreover, sildenafil pretreatment reduced acrolein-induced Muc5ac mucin synthesis at both mRNA and protein levels, and attenuated airway inflammation, as well as epithelial hyperplasia and metaplasia. In conclusion, sildenafil could attenuate airway inflammation and mucus production in the rat model, possibly through the nitric oxide/cyclic guanosine 3',5'-monophosphate pathway, and, thus, might have a therapeutic potential for chronic airway diseases.

  16. Contribution of waterborne radon to home air quality

    International Nuclear Information System (INIS)

    Deb, A.K.

    1994-01-01

    Radon-222 is a member of the uranium decay chain and is formed from the decay of radium-226. Radon and its decay products emit alpha particles during the decay process. If radon is inhaled, alpha particles emitted from inhaled radon and its daughters increase the risk of lung cancer. Radon is soluble in water; thus when radon comes in contact with groundwater it dissolves. The radon concentration in groundwater may range from 100 pCi/L to 1,000,000 pCi/L. When water with a high radon level is used in the home, radon is released from the water to the air and thus can increase indoor air radon concentration. Considering the estimated health risk from radon in public water supply systems, EPA has proposed a maximum contaminant level (MCL) of 300 pCi/L for radon in public drinking water supplies. To address the health risks of radon in water and the proposed regulations, the American Water Works Association Research Foundation (AWWARF) initiated a study to determine the contribution of waterborne radon to radon levels in indoor household air

  17. Men and radon - a noble gas of many disguise - Part I and Part II

    International Nuclear Information System (INIS)

    Momcilovic, B.; Lykken, G. I.

    2005-01-01

    Radon-induced lung cancer can be traced back to the 16th century miners in Europe, but recently there has been a world wide concern that elevated radon progeny levels in dwellings may also be implicated in lung cancer. Historical and experimental evidence is presented to document how inhaled radon is distributed throughout the body and stored in fats and lipids. Background counts in a steel room using a human whole-body counter (HWBC) progressively decreased throughout the day, which is attributed to a lowering of radon as subjects entered the steel room. The observed increases in potassium-40 (4 0K ) counts in marathon runners was attributed to inhalation of environmental radon, and radon progeny was verified by measuring contributions to the 4 0K photopeak by 2 14B i in cyclists and an untrained subject who exercised in a room with radon-laden air. Effective half-lives and regional 2 14B i emissions were found to be the highest in the areas of the head (brain) and stomach (omentum) when filtered radon-laden air was inhaled. These observations prompted analyses for radon progeny (2 10B i and 2 10P o) from brain tissues of persons who suffered from Alzheimer's and Parkinson's Diseases (AD and PD). Protein in AD and lipids in PD were high in these progeny relative to the control tissues. Whole body counts (2 14B i emissions) of subjects over a period of 24 years were analysed for radon body content (Rn-conc). Statistically significant correlations were found between total body fat and Rn-conc in women and between seasonal home radon concentrations and seasonal Rn-conc in subjects participating in community-based studies. It is concluded that environmental radon is indeed stored in the body, that body concentration correlates with body fat in women, and that these reflect seasonal concentrations in their dwellings. Radon decay products include a number of alpha and beta particle emitters. These emissions produce a radiation risk and may play a role in multiple

  18. Lung transplantation in the rat. III. Functional studies in iso- and allografts

    International Nuclear Information System (INIS)

    Marck, K.W.; Prop, J.; Wildevuur, C.R.

    1983-01-01

    Recently a microsurgical technique for orthotopic left lung transplantation in the rat was developed. The aim of this study was to investigate the influence of the operation itself and of an unmodified rejection reaction on the function of the transplanted rat lung. Orthotopic left lung transplantation was performed in 59 rats (34 isografts and 25 allografts). Isografts demonstrated a mean left lung perfusion of 23.1% in the first two postoperative weeks. Seven out of the 10 animals, subjected to a repeated scintigraphy 5-10 weeks later, had an increased graft perfusion, resulting in an almost normal mean left lung perfusion of 34.8%. At that time chest roentgenography revealed a good aeration of the grafts, that at autopsy had a normal aspect. Allografts showed an initial mean left lung perfusion (24.6%) similar to the isografts, which, however, declined sharply a few days later (4.3%). At that time chest roentgenography revealed totally opalescent grafts that at autopsy had the hepatized aspect characteristic of lung allograft rejection. These results of isogeneic and allogeneic lung transplantation in the rat were comparable with those of canine auto- and allotransplantation. For immunogenetic and economical reasons lung transplantation in the rat is a good alternative animal model in lung transplantation research

  19. Protective effects of lipoic acid against oxidative stress induced by lead acetate and gamma-irradiation in the kidney and lung in albino rats

    International Nuclear Information System (INIS)

    Rezk, R.G.; Abdel-Rahman, N.A.

    2013-01-01

    Lipoic acid is widely used as antioxidant that protects tissues against a range of oxidative stress. The present study was designed to determine the protective effect of lipoic acid against oxidative organ damage induced by lead intoxication and/or gamma-irradiation. Rats were treated daily intrapritonealy (i. p.) with lipoic acid( 200 mg/kg/b.w.) for 15 consecutive days before lead acetate injection(30 mg/kg/b.w) i.p. for 5 days and/ or whole body. gamma-irradiation (3 Gy). Animals were sacrificed on the 3rd day post the last treatment. Histological examination of kidney and lung tissues through light microscope showed that lead acetate injection and/or exposure to gamma radiation has provoked severe architectural damage in both tissues as necrotic lesions, atrophoid glomerulei and degenerated proximal and distal convoluted tubules, severe bronchiole fibrosis, decreased ciliated bronchioles and dilated and widened pulmonary artery. Histological damage was associated with significant biochemical. changes as increase in lead, copper, iron, zinc and calcium levels in both kidney and lung tissues. Kidney and lung of rats treated with lipoic acid before lead intoxication and/or gamma-irradiation showed significant regenerated glomerulei structure, well-defined structure of proximal and distal convoluted tubules, regenerated ciliated bronchiole structure and improved pulmonary artery. Tissue regeneration was associated with significant decrease in Pb, Cu, Fe, Zn, and Ca levels in kidney and lung and prevented the accumulation of metals in these organs. It could be concluded that lipoic acid administration before lead and/or whole body gamma-irradiation might be capable to attenuate lead and/or gamma radiation induced organ injury and organ metals disruption

  20. Effect of lung resection and sham surgery on the frequency of infection in alloxan-diabetic rats

    Directory of Open Access Journals (Sweden)

    A.C. Seidel

    2003-03-01

    Full Text Available The present study was carried out in order to determine the effect of lung resection on the frequency of infections in alloxan-diabetic rats. Adult female Wistar rats were injected with alloxan (40 mg/kg, iv to induce diabetes mellitus (group D; N = 45 or with vehicle (1.0 ml/kg, iv to be used as controls (group C; N = 45. Thirty-six days after receiving alloxan both groups were randomly divided into three subgroups: no operation (NO; N = 15, sham operation (SO; N = 15, and left pneumonectomy (PE; N = 15. The rats were sacrificed 36 days after surgery and their lungs were examined microscopically and macroscopically. The occurrence of thoracic wall infection, thoracic wall abscess, lung abscess and pleural empyema was similar in groups D and C. In contrast, the overall infection rate was higher (P<0.05 in the diabetic rats (SO-D and PE-D subgroups, but not in the NO-D subgroup. Considering that the overall infection rate was similar in the SO-D and PE-D subgroups, we suggest that surgery but not pneumonectomy was related to the higher prevalence of infection in diabetic rats.

  1. Glycyrrhizic acid alleviates bleomycin-induced pulmonary fibrosis in rats

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    Lili eGao

    2015-10-01

    Full Text Available Idiopathic pulmonary fibrosis is a progressive and lethal form of interstitial lung disease that lacks effective therapies at present. Glycyrrhizic acid (GA, a natural compound extracted from a traditional Chinese herbal medicine Glycyrrhiza glabra, was recently reported to benefit lung injury and liver fibrosis in animal models, yet whether GA has a therapeutic effect on pulmonary fibrosis is unknown. In this study, we investigated the potential therapeutic effect of GA on pulmonary fibrosis in a rat model with bleomycin (BLM-induced pulmonary fibrosis. The results indicated that GA treatment remarkably ameliorated BLM-induced pulmonary fibrosis and attenuated BLM-induced inflammation, oxidative stress, epithelial-mesenchymal transition and activation of tansforming growth factor-beta signaling pathway in the lungs. Further, we demonstrated that GA treatment inhibited proliferation of 3T6 fibroblast cells, induced cell cycle arrest and promoted apoptosis in vitro, implying that GA-mediated suppression of fibroproliferation may contribute to the anti-fibrotic effect against BLM-induced pulmonary fibrosis. In summary, our study suggests a therapeutic potential of GA in the treatment of pulmonary fibrosis.

  2. Depressed glucose utilization in lungs of BB wistar spontaneously diabetic rats

    International Nuclear Information System (INIS)

    Uhal, B.D.; Moxley, M.A.; Longmore, W.J.

    1986-01-01

    Lungs of BB wistar spontaneously diabetic rats were perfused with [ 14 C(U)]glucose in modified Krebs Ringer bicarbonate medium for 1.5 hours. Lungs from non-diabetic BB Wistar rats were perfused simultaneously and served as controls. The perfusions were terminated by rapid freezing of the tissue in liquid N 2 followed by separation of surfactant and residual lung fractions. The rates of glucose incorporation into surfactant DSPC, PG, and PE were decreased 4.7, 2.4 and 2.5-fold, respectively, in lungs of spontaneously diabetic rats when expressed as final product specific activities. The rate of glucose incorporation into residual PC was also reduced by 2.3-fold. Expressed as moles incorporated per gram wet weight of lung, incorporations into surfactant DSPC, PG and residual PC were also reduced by 4.1, 6.3 and 3.8-fold respectively. These data; (1) agree with previous studies of the lungs of streptozotocin and alloxan-diabetic rats; (2) show that the depressed glucose utilization for lipid synthesis observed previously is not due to streptozotocin or alloxan toxicity; (3) suggest that the BB Wistar rat will provide a useful model for the study of the effects of insulin-dependent diabetes on lung metabolism

  3. Post-cancer Treatment with Condurango 30C Shows Amelioration of Benzo[a]pyrene-induced Lung Cancer in Rats Through the Molecular Pathway of Caspa- se-3-mediated Apoptosis Induction

    Directory of Open Access Journals (Sweden)

    Sikdar Sourav

    2013-09-01

    Full Text Available Objectives: The present investigation aimed at examining if post-cancer treatment with a potentized homeopathic drug, Condurango 30C, which is generally used to treat oesophageal cancer, could also show an ameliorating effect through apoptosis induction on lung cancer induced by benzo[a]pyrene (BaP in white rats (Rattus norvegicus. Methods: Lung cancer was induced after four months by chronic feeding of BaP to rats through gavage at a dose of 50 mg/kg body weight for one month. After four months, the lung-cancer-bearing rats were treated with Condurango 30C for the next one (5th, two (5th-6th and three (5th-7th months, respectively, and were sacrificed at the corresponding time- points. The ameliorating effect, if any, after Condurango 30C treatment for the various periods was evaluated by using protocols such as histology, scanning electron microscopy (SEM, annexinV-FITC/PI assay, flow cytometry of the apoptosis marker, DNA fragmentation, reverse transcriptase-polymerase chain reaction (RT-PCR, immunohistochemistry, and western blot analyses of lung tissue samples. Results: Striking recovery of lung tissue to a near normal status was noticed after post-cancerous drug treatment, as evidenced by SEM and histology, especially after one and two months of drug treatment. Data from the annexinV-FITC/PI and DNA fragmentation assays revealed that Condurango 30C could induce apoptosis in cancer cells after post-cancer treatment. A critical analysis of signalling cascade, evidenced through a RT-PCR study, demonstrated up-regulation and down-regulation of different pro- and anti-apoptotic genes, respectively, related to a caspase-3-mediated apoptotic pathway, which was especially discernible after one-month and two- month drug treatments. Correspondingly, Western blot and immunohistochemistry studies confirmed the ameliorative potential of Condurango 30C by its ability to down-regulate the elevated epidermal growth factor receptor (EGFR expression, a

  4. Explaining the lung cancer versus radon exposure data for USA counties

    International Nuclear Information System (INIS)

    Cohen, B.L.

    2000-01-01

    Our study of lung cancer mortality rates, m, versus average radon levels in homes, r, for 1601 USA counties (Cohen 1995) found a very strong negative correlation. In a recent exchange (Cohen 1999), Sir Richard Doll suggested that these discrepancies may be due to lack of consideration of details on smoking habits, specifically 'the amount smoked, the proportion of ex-smokers who have stopped for different periods, the proportion of smokers who smoked cigarettes, cigars or pipes, and the age at which those smoking in different ways began'. The purpose of this letter is to explore these Doll suggestions. Our analysis is performed for males because the data are of better quality, but the results would be quite similar for females. Letter-to-the-editor

  5. The Effects of Dexmedetomidine on Secondary Acute Lung and Kidney Injuries in the Rat Model of Intra-Abdominal Sepsis

    Directory of Open Access Journals (Sweden)

    Uğur Koca

    2013-01-01

    Full Text Available In the present study, the effects of dexmedetomidine on secondary lung and kidney injuries were studied in the rat model of intra-abdominal sepsis by immunohistological and biochemical examinations. We measured serum creatinine, kidney tissue malondialdehide and plasma neutrophil gelatinase-associated lipocalin levels. In order to evaluate tissue injury we determined kidney tissue mononuclear cell infiltration score, alveolar macrophage count, histological kidney and lung injury scores and kidney and lung tissue immunoreactivity scores. We demonstrated that dexmedetomidine attenuates sepsis-induced lung and kidney injuries and apoptosis in the rat model of sepsis. There is still need for comparative studies in order to determine the effects of dexmedetomidine on organ functions in early human sepsis.

  6. Formation of cigarette smoke-induced DNA adducts in the rat lung and nasal mucosa

    International Nuclear Information System (INIS)

    Gupta, R.C.; Sopori, M.L.; Gairola, C.G.

    1989-01-01

    The formation of DNA adducts in the nasal, lung, and liver tissues of rats exposed daily to fresh smoke from a University of Kentucky reference cigarette (2R1) for up to 40 weeks was examined. The amount of smoke total particulate matter (TPM) inhaled and the blood carboxyhemoglobin (COHb) values averaged 5-5.5 mg smoke TPM/day/rat and 5.5%, respectively. The pulmonary AHH activity measured at the termination of each experiment showed an average increase of about two- to threefold in smoke-exposed groups. These observations suggested that animals effectively inhaled both gaseous and particulate phase constituents of cigarette smoke. DNAs from nasal, lung, and liver tissue were extracted and analyzed by an improved 32 P-postlabeling procedure. The data demonstrate the DNA-damaging potential of long term fresh cigarette smoke exposure and suggest the ability of the tissue to partially recover from such damage following cessation of the exposure

  7. Prevention of chinese green tea on 3,4-benzopyrene-induced lung cancer and its mechanism in animal model

    Directory of Open Access Journals (Sweden)

    Qihua GU

    2008-08-01

    Full Text Available Background and objective Chinese green tea is one of the daily consumption beverages in the world and is considered a promising cancer chemopreventive agent. In the present study, we investigate the role of lung cancer prevention by green tea and its mechanism. Methods Three groups of female SD rats were kept with the same feed. Rats in group A were administrated with 1% green tea drinking, while in group B and group C with water only. Animals in group A and group B were given 3,4-benzopyrene-corn oil mixture pulmonary injection fortnightly for 4 times, while in group C corn oil only. Rats were sacrificed 1 year after the first injection under narcotism. Lung tumors and lung tissues were performed H&E staining for cancer identification. Each case of lung cancer was examined for expression of p53 and Bcl-2 with in situ hybridization analysis and immunohistochemistry staining. Results No cancer was found in rats in group C. However, in group B, 15 out of 20 rats were found generating lung cancer, and in group A, 6 out of 20 rats inducing lung cancer were recorded. The rate of lung carcinogenesis in rats was decreased from 75% to 30% by 1% chinese green tea oral administration (χ2=8.12, P0.05. However, significantly lower level of Bcl-2 expression was found in lung cancer tissues of group A than that of group B (P<0.05. Conclusion The results indicate that chinese green tea inhibits lung carcinogenesis. Chinese green tea can slightly upregulate expression of p53, but significantly downregulate expression of Bcl-2 in lung cancer, and this may be related to the mechanism of lung cancer prevention.

  8. Radon therapy; Radon in der Therapie

    Energy Technology Data Exchange (ETDEWEB)

    Spruck, Kaija [Technische Hochschule Mittelhessen, Giessen (Germany). Inst. fuer Medizinische Physik und Strahlenschutz

    2017-04-01

    Radon therapies are used since more than 100 years in human medicine. Today this method is controversially discussed due to the possible increase of ionizing radiation induced tumor risk. Although the exact mode of biological radiation effect on the cell level is still not known new studies show the efficiency of the radon therapy without side effect for instance for rheumatic/inflammatory or respiratory disorders.

  9. Early and late effects of prenatal corticosteroid treatment on the microRNA profiles of lung tissue in rats

    Science.gov (United States)

    YU, HONG-REN; LI, SUNG-CHOU; TSENG, WAN-NING; TAIN, YOU-LIN; CHEN, CHIH-CHENG; SHEEN, JIUNN-MING; TIAO, MAO-MENG; KUO, HO-CHANG; HUANG, CHAO-CHENG; HSIEH, KAI-SHENG; HUANG, LI-TUNG

    2016-01-01

    Glucocorticoids have been administered to mothers at risk of premature delivery to induce maturation of preterm fetal lungs and prevent the development of respiratory distress syndrome. Micro (mi)RNAs serve various crucial functions in cell proliferation, differentiation and organ development; however, few studies have demonstrated an association between miRNAs and lung development. The aim of the present study was to investigate alterations in the miRNA profiles of rat lung tissue following prenatal glucocorticoid therapy for fetal lung development. The differences in miRNA expression profiles were compared between postnatal days 7 (D7) and 120 (D120) rat lung tissues, followed by validation using reverse transcription-quantitative polymerase chain reaction. The miRNA profiles of rat lung tissues following prenatal dexamethasone (DEX) therapy were also investigated. miRNAs with 2-fold changes were selected for further analysis. At D120, 6 upregulated and 6 downregulated miRNAs were detected, compared with D7. Among these differentially expressed miRNAs, miR-101-3p and miR-99b-5p were associated with the lowest and highest expressions of miRNA at D7, respectively. A limited impact on the miRNA profiles of rat lung tissues was observed following prenatal DEX treatment, which may help to further clarify the mechanisms underlying normal lung development. However, the results of the present study cannot entirely elucidate the effects of prenatal DEX treatment on the lung development of premature infants, and further studies investigating the impact of prenatal corticosteroids on fetal lung miRNA profiles are required. PMID:26997989

  10. Combined effects of radon inhalation and antioxidant vitamin administration on acute alcohol-induced hepatopathy in mice

    International Nuclear Information System (INIS)

    Etani, Reo; Kataoka, Takahiro; Nishiyama, Yuichi; Takata, Yuji; Yamaoka, Kiyonori

    2015-01-01

    It has been reported that radon inhalation activates antioxidative functions in liver and has an antioxidative effect against hepatopathy similar to that of the antioxidative effects of ascorbic acid (VC) or α-tocopherol (VE). In this study, we examined the combined effects of radon inhalation and antioxidant vitamin administration on acute alcohol-induced hepatopathy in mice. ICR mice were subjected to intraperitoneal (i.p.) administration of alcohol after pretreating with air only (sham) or radon at a concentration of approximately 2000 Bq/m 3 for 24 hours and i.p. administration of VC (300 mg/kg body weight) or VE (300 mg/kg body weight). In mice injected with alcohol, the combined radon and antioxidant vitamins treatment significantly decreased the activities of glutamic oxaloacetic transaminase in serum compared to not only the alcohol-administered group (sham group), but also the radon inhalation with alcohol administration group or the vitamin and alcohol administration group. In addition, radon inhalation significantly increased the antioxidant level, in such as the catalase activity and the total glutathione content in liver compared to the sham group. These results suggested that the combined radon and antioxidant vitamin treatment could effectively inhibit alcohol-induced hepatopathy in mice without any antagonizing action. (author)

  11. Therapeutic Effects of Procainamide on Endotoxin-Induced Rhabdomyolysis in Rats.

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    Chih-Chin Shih

    Full Text Available Overt systemic inflammatory response is a predisposing mechanism for infection-induced skeletal muscle damage and rhabdomyolysis. Aberrant DNA methylation plays a crucial role in the pathophysiology of excessive inflammatory response. The antiarrhythmic drug procainamide is a non-nucleoside inhibitor of DNA methyltransferase 1 (DNMT1 used to alleviate DNA hypermethylation. Therefore, we evaluated the effects of procainamide on the syndromes and complications of rhabdomyolysis rats induced by lipopolysaccharide (LPS. Rhabdomyolysis animal model was established by intravenous infusion of LPS (5 mg/kg accompanied by procainamide therapy (50 mg/kg. During the experimental period, the changes of hemodynamics, muscle injury index, kidney function, blood gas, blood electrolytes, blood glucose, and plasma interleukin-6 (IL-6 levels were examined. Kidneys and lungs were exercised to analyze superoxide production, neutrophil infiltration, and DNMTs expression. The rats in this model showed similar clinical syndromes and complications of rhabdomyolysis including high levels of plasma creatine kinase, acute kidney injury, hyperkalemia, hypocalcemia, metabolic acidosis, hypotension, tachycardia, and hypoglycemia. The increases of lung DNMT1 expression and plasma IL-6 concentration were also observed in rhabdomyolysis animals induced by LPS. Treatment with procainamide not only inhibited the overexpression of DNMT1 but also diminished the overproduction of IL-6 in rhabdomyolysis rats. In addition, procainamide improved muscle damage, renal dysfunction, electrolytes disturbance, metabolic acidosis, hypotension, and hypoglycemia in the rats with rhabdomyolysis. Moreover, another DNMT inhibitor hydralazine mitigated hypoglycemia, muscle damage, and renal dysfunction in rhabdomyolysis rats. These findings reveal that therapeutic effects of procainamide could be based on the suppression of DNMT1 and pro-inflammatory cytokine in endotoxin-induced rhabdomyolysis.

  12. Therapeutic Effects of Procainamide on Endotoxin-Induced Rhabdomyolysis in Rats.

    Science.gov (United States)

    Shih, Chih-Chin; Hii, Hiong-Ping; Tsao, Cheng-Ming; Chen, Shiu-Jen; Ka, Shuk-Man; Liao, Mei-Hui; Wu, Chin-Chen

    2016-01-01

    Overt systemic inflammatory response is a predisposing mechanism for infection-induced skeletal muscle damage and rhabdomyolysis. Aberrant DNA methylation plays a crucial role in the pathophysiology of excessive inflammatory response. The antiarrhythmic drug procainamide is a non-nucleoside inhibitor of DNA methyltransferase 1 (DNMT1) used to alleviate DNA hypermethylation. Therefore, we evaluated the effects of procainamide on the syndromes and complications of rhabdomyolysis rats induced by lipopolysaccharide (LPS). Rhabdomyolysis animal model was established by intravenous infusion of LPS (5 mg/kg) accompanied by procainamide therapy (50 mg/kg). During the experimental period, the changes of hemodynamics, muscle injury index, kidney function, blood gas, blood electrolytes, blood glucose, and plasma interleukin-6 (IL-6) levels were examined. Kidneys and lungs were exercised to analyze superoxide production, neutrophil infiltration, and DNMTs expression. The rats in this model showed similar clinical syndromes and complications of rhabdomyolysis including high levels of plasma creatine kinase, acute kidney injury, hyperkalemia, hypocalcemia, metabolic acidosis, hypotension, tachycardia, and hypoglycemia. The increases of lung DNMT1 expression and plasma IL-6 concentration were also observed in rhabdomyolysis animals induced by LPS. Treatment with procainamide not only inhibited the overexpression of DNMT1 but also diminished the overproduction of IL-6 in rhabdomyolysis rats. In addition, procainamide improved muscle damage, renal dysfunction, electrolytes disturbance, metabolic acidosis, hypotension, and hypoglycemia in the rats with rhabdomyolysis. Moreover, another DNMT inhibitor hydralazine mitigated hypoglycemia, muscle damage, and renal dysfunction in rhabdomyolysis rats. These findings reveal that therapeutic effects of procainamide could be based on the suppression of DNMT1 and pro-inflammatory cytokine in endotoxin-induced rhabdomyolysis.

  13. Health effects and radiation dose from exposure to radon indoors

    International Nuclear Information System (INIS)

    Swedjemark, G.A.

    1998-01-01

    Radon exposure has been declared a health hazard by several organisations, for example the International Commission on Radiological Protection (ICRP) and the World Health Organisation (WHO). The basis for the risk estimate has been the results from epidemiological studies on miners exposed to radon, supported by the results of residential epidemiology. Only few of the many residential epidemiological studies carried out hitherto have a design applicable for a risk estimate. The largest is the Swedish national study but several large well designed studies are ongoing. An excess risk has also been found in animal research. The model describes smoking and radon exposure as between additive and multiplicative, found in both miners and residential studies. The relatively few non-smokers among the miners and also among the residents give a problem at estimating the radon risk for these groups. It would also be desirable to know more about the importance of the age and the time period at exposure. Lung dose calculations from radon exposure are not recommended by ICRP in their publication 66. For comparison with other radiation sources the ICRP recommends the concept 'dose conversion convention' obtained as the risk estimate divided by the detriment. Other effects of radon exposure than lung cancer have not been shown epidemiologically, but dose calculations indicate an excess risk of about 5% of the excess lung cancer risk. (author)

  14. A Cohort Study on Risk Factors of Lung Cancer in Yunnan Tin Miners

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    Yong JIANG

    2013-04-01

    Full Text Available Background and objective Smoking is a major cause of lung cancer. Studies of lung cancer among miners have shown that occupational exposure also played an important role. The aim of this study is to investigate radon, cigarette use and other risk factors of lung cancer in Yunnan tin miners and to provide a scientific basis for the prevention and control of occupational lung cancer. Methods A prospective cohort study was conducted among Yunnan tin miners, the associations between potential risk factors for lung cancer were analyzed by multivariate Cox regression model. Effects of age at first radon exposure and radon exposure rate on lung cancer risk were analyzed. The relationship between cumulative working level month and lung cancer was analyzed according to smoking status. The joint effect of tobacco use and cumulative radon exposure was analyzed based on additive and multiplicative models. Results Increased risk of lung cancer was associated with age at enrollment, tobacco use, prior bronchitis, and cu