Tomographic and functional findings in severe COPD: comparison between the wood smoke-related and smoking-related disease

Energy Technology Data Exchange (ETDEWEB)

Gonzalez-Garcia, Mauricio; Maldonado Gomez, Dario; Torres-Duque, Carlos A.; Barrero, Margarita; Jaramillo Villegas, Claudia; Perez, Juan Manuel; Varon, Humberto [Colombian Pulmonology Foundation, Bogota (Colombia); Department of Radiology and Diagnostic Imaging, Children' s Cardiology Foundation, Cardiology Institute, Bogota (Colombia)

2013-11-01

Objective: Wood smoke exposure is a risk factor for COPD. For a given degree of airway obstruction, the reduction in DLCO is smaller in individuals with wood smoke-related COPD than in those with smoking-related COPD, suggesting that there is less emphysema in the former. The objective of this study was to compare HRCT findings between women with wood smoke-related COPD and women with smoking-related COPD. Methods: Twenty-two women with severe COPD (FEV1/FVC ratio < 70% and FEV1 < 50%) were divided into two groups: those with wood smoke-related COPD (n = 12) and those with smoking-related COPD (n = 10). The two groups were compared regarding emphysema scores and airway involvement (as determined by HRCT); and functional abnormalities-spirometry results, DLCO, alveolar volume (VA), the DLCO/VA ratio, lung volumes, and specific airway resistance (sRaw). Results: There were no significant differences between the two groups in terms of FEV1, sRaw, or lung hyperinflation. Decreases in DLCO and in the DLCO/VA ratio were greater in the smoking-related COPD group subjects, who also had higher emphysema scores, in comparison with the wood smoke-related COPD group subjects. In the wood smoke-related COPD group, HRCT scans showed no significant emphysema, the main findings being peribronchial thickening, bronchial dilation, and subsegmental atelectasis. Conclusions: Female patients with severe wood smoke-related COPD do not appear to develop emphysema, although they do show severe airway involvement. The reduction in DLCO and VA, with a normal DLCO/VA ratio, is probably due to severe bronchial obstruction and incomplete mixing of inspired gas during the determination of single-breath DLCO. (author)

Tomographic and functional findings in severe COPD: comparison between the wood smoke-related and smoking-related disease

International Nuclear Information System (INIS)

Gonzalez-Garcia, Mauricio; Maldonado Gomez, Dario; Torres-Duque, Carlos A.; Barrero, Margarita; Jaramillo Villegas, Claudia; Perez, Juan Manuel; Varon, Humberto

2013-01-01

Objective: Wood smoke exposure is a risk factor for COPD. For a given degree of airway obstruction, the reduction in DLCO is smaller in individuals with wood smoke-related COPD than in those with smoking-related COPD, suggesting that there is less emphysema in the former. The objective of this study was to compare HRCT findings between women with wood smoke-related COPD and women with smoking-related COPD. Methods: Twenty-two women with severe COPD (FEV1/FVC ratio < 70% and FEV1 < 50%) were divided into two groups: those with wood smoke-related COPD (n = 12) and those with smoking-related COPD (n = 10). The two groups were compared regarding emphysema scores and airway involvement (as determined by HRCT); and functional abnormalities—spirometry results, DLCO, alveolar volume (VA), the DLCO/VA ratio, lung volumes, and specific airway resistance (sRaw). Results: There were no significant differences between the two groups in terms of FEV1, sRaw, or lung hyperinflation. Decreases in DLCO and in the DLCO/VA ratio were greater in the smoking-related COPD group subjects, who also had higher emphysema scores, in comparison with the wood smoke-related COPD group subjects. In the wood smoke-related COPD group, HRCT scans showed no significant emphysema, the main findings being peribronchial thickening, bronchial dilation, and subsegmental atelectasis. Conclusions: Female patients with severe wood smoke-related COPD do not appear to develop emphysema, although they do show severe airway involvement. The reduction in DLCO and VA, with a normal DLCO/VA ratio, is probably due to severe bronchial obstruction and incomplete mixing of inspired gas during the determination of single-breath DLCO. (author)

Smoking water pipe is injurious to lungs

DEFF Research Database (Denmark)

Sivapalan, Pradeesh; Ringbæk, Thomas; Lange, Peter

2014-01-01

This review describes the pulmonary consequences of water pipe smoking. Smoking water pipe affects the lung function negatively, is significantly associated with chronic obstructive pulmonary disease and increases the risk of lung infections. Case reports suggest that regular smokers of water pipe...

Wnt5a Is Associated with Cigarette Smoke-Related Lung Carcinogenesis via Protein Kinase C

OpenAIRE

Whang, Young Mi; Jo, Ukhyun; Sung, Jae Sook; Ju, Hyun Jung; Kim, Hyun Kyung; Park, Kyong Hwa; Lee, Jong Won; Koh, In Song; Kim, Yeul Hong

2013-01-01

Wnt5a is overexpressed during the progression of human non-small cell lung cancer. However, the roles of Wnt5a during smoking-related lung carcinogenesis have not been clearly elucidated. We investigated the associations between Wnt5a and the early development of cigarette smoke related lung cancer using human bronchial epithelial (HBE) cells (NHBE, BEAS-2B, 1799, 1198 and 1170I) at different malignant stages established by exposure to cigarette smoke condensate (CSC). Abnormal up-regulation ...

SEGEL: A Web Server for Visualization of Smoking Effects on Human Lung Gene Expression.

Science.gov (United States)

Xu, Yan; Hu, Brian; Alnajm, Sammy S; Lu, Yin; Huang, Yangxin; Allen-Gipson, Diane; Cheng, Feng

2015-01-01

Cigarette smoking is a major cause of death worldwide resulting in over six million deaths per year. Cigarette smoke contains complex mixtures of chemicals that are harmful to nearly all organs of the human body, especially the lungs. Cigarette smoking is considered the major risk factor for many lung diseases, particularly chronic obstructive pulmonary diseases (COPD) and lung cancer. However, the underlying molecular mechanisms of smoking-induced lung injury associated with these lung diseases still remain largely unknown. Expression microarray techniques have been widely applied to detect the effects of smoking on gene expression in different human cells in the lungs. These projects have provided a lot of useful information for researchers to understand the potential molecular mechanism(s) of smoke-induced pathogenesis. However, a user-friendly web server that would allow scientists to fast query these data sets and compare the smoking effects on gene expression across different cells had not yet been established. For that reason, we have integrated eight public expression microarray data sets from trachea epithelial cells, large airway epithelial cells, small airway epithelial cells, and alveolar macrophage into an online web server called SEGEL (Smoking Effects on Gene Expression of Lung). Users can query gene expression patterns across these cells from smokers and nonsmokers by gene symbols, and find the effects of smoking on the gene expression of lungs from this web server. Sex difference in response to smoking is also shown. The relationship between the gene expression and cigarette smoking consumption were calculated and are shown in the server. The current version of SEGEL web server contains 42,400 annotated gene probe sets represented on the Affymetrix Human Genome U133 Plus 2.0 platform. SEGEL will be an invaluable resource for researchers interested in the effects of smoking on gene expression in the lungs. The server also provides useful information

Relative preservation of peripheral lung function in smoking-related pulmonary emphysema: assessment with {sup 99m}Tc-MAA perfusion and dynamic {sup 133}Xe SPET

Energy Technology Data Exchange (ETDEWEB)

Suga, Kazuyoshi; Kume, Norihiko; Matsunaga, Naofumi; Ogasawara, Nobuhiko; Motoyama, Kazumi; Hara, Akiko; Matsumoto, Tsuneo [Department of Radiology, Yamaguchi University School of Medicine, Ube, Yamaguchi (Japan)

2000-07-01

In this study the cross-sectional functional differences between the central and peripheral lung in smokers with pulmonary emphysema were evaluated by lung perfusion and dynamic xenon-133 single-photon emission tomography (SPET). The subjects were 81 patients with a long-term smoking history and relatively advanced emphysema, 17 non-smoker patients with non-obstructive lung diseases and six healthy non-smokers. Regional lung functional difference between the peripheral and central lung was assessed in the upper, middle and lower lung zones by technetium-99m macroaggregated albumin SPET and dynamic {sup 133}Xe SPET. The distribution of emphysematous changes was assessed by density-mask computed tomography (CT) images which depicted abnormally low attenuation areas (LAAs) of less than -960 Hounsfield units. Two hundred and eighty-eight (59.2%) lung zones of 63 (77.7%) patients with pulmonary emphysema showed relative preservation of lung function in the peripheral lung, with a curvilinear band of normal perfusion (a stripe sign) and a significantly faster {sup 133}Xe half-clearance time (T{sub 1/2}) than in central lung (P<0.0001). Of these lung zones, 256 (88.8%) showed central-dominant LAA distributions on density-mask CT images, but the remaining 32 zones did not show any regional preference in LAA distribution. Conversely, 117 (24.0%) lung zones of 19 (23.4%) patients showed periphery-dominant perfusion defects and LAA distributions, with significantly prolonged T{sub 1/2} in the peripheral lung area (P<0.0001). The remaining 81 lung zones of the patients with pulmonary emphysema and all the lung zones of the healthy subjects and patients with non-obstructive lung diseases did not show a stripe sign, and no differences were observed in T{sub 1/2} values and LAA distributions between the central and peripheral lung. Relative preservation of peripheral lung function seems to be a characteristic feature in smoking-related pulmonary emphysema, and may indicate a

Mortality in women and men in relation to smoking

DEFF Research Database (Denmark)

Prescott, Eva; Osler, Merete; Andersen, Per Kragh

1998-01-01

characteristics differed considerably with gender, particularly in the older subjects. Overall mortality rates in smokers were approximately twice those in people who never smoked. Positive associations with smoking in both men and women were confirmed for all-cause mortality as well as mortality from respiratory...... disease, vascular disease, lung cancer, and other tobacco-related cancers. Despite large gender differences in age at smoking debut, total and cause-specific relative mortality in smokers was similar in men and women. After excluding non-inhalers, relative risks associated with smoking for respiratory......BACKGROUND: Mortality from smoking-related diseases in women is increasing worldwide. Studies comparing hazards associated with smoking in women and men based on a sufficient number of heavy smokers of both genders are lacking. METHODS: We used pooled data from three prospective population studies...

Wnt5a is associated with cigarette smoke-related lung carcinogenesis via protein kinase C.

Science.gov (United States)

Whang, Young Mi; Jo, Ukhyun; Sung, Jae Sook; Ju, Hyun Jung; Kim, Hyun Kyung; Park, Kyong Hwa; Lee, Jong Won; Koh, In Song; Kim, Yeul Hong

2013-01-01

Wnt5a is overexpressed during the progression of human non-small cell lung cancer. However, the roles of Wnt5a during smoking-related lung carcinogenesis have not been clearly elucidated. We investigated the associations between Wnt5a and the early development of cigarette smoke related lung cancer using human bronchial epithelial (HBE) cells (NHBE, BEAS-2B, 1799, 1198 and 1170I) at different malignant stages established by exposure to cigarette smoke condensate (CSC). Abnormal up-regulation of Wnt5a mRNA and proteins was detected in CSC-exposed transformed 1198 and tumorigenic 1170I cells as compared with other non-CSC exposed HBE cells. Tumor tissues obtained from smokers showed higher Wnt5a expressions than matched normal tissues. In non-CSC exposed 1799 cells, treatment of recombinant Wnt5a caused the activations of PKC and Akt, and the blockage of Wnt5a and PKC significantly decreased the viabilities of CSC-transformed 1198 cells expressing high levels of Wnt5a. This reduced cell survival rate was associated with increased apoptosis via the down-regulation of Bcl2 and the induction of cleaved poly ADP-ribose polymerase. Moreover, CSC-treated 1799 cells showed induction of Wnt5a expression and enhanced colony-forming capacity. The CSC-induced colony forming efficiency was suppressed by the co-incubation with a PKC inhibitor. In conclusion, these results suggest that cigarette smoke induces Wnt5a-coupled PKC activity during lung carcinogenesis, which causes Akt activity and anti-apoptosis in lung cancer. Therefore, current study provides novel clues for the crucial role of Wnt5a in the smoking-related lung carcinogenesis.

Wnt5a is associated with cigarette smoke-related lung carcinogenesis via protein kinase C.

Directory of Open Access Journals (Sweden)

Young Mi Whang

Full Text Available Wnt5a is overexpressed during the progression of human non-small cell lung cancer. However, the roles of Wnt5a during smoking-related lung carcinogenesis have not been clearly elucidated. We investigated the associations between Wnt5a and the early development of cigarette smoke related lung cancer using human bronchial epithelial (HBE cells (NHBE, BEAS-2B, 1799, 1198 and 1170I at different malignant stages established by exposure to cigarette smoke condensate (CSC. Abnormal up-regulation of Wnt5a mRNA and proteins was detected in CSC-exposed transformed 1198 and tumorigenic 1170I cells as compared with other non-CSC exposed HBE cells. Tumor tissues obtained from smokers showed higher Wnt5a expressions than matched normal tissues. In non-CSC exposed 1799 cells, treatment of recombinant Wnt5a caused the activations of PKC and Akt, and the blockage of Wnt5a and PKC significantly decreased the viabilities of CSC-transformed 1198 cells expressing high levels of Wnt5a. This reduced cell survival rate was associated with increased apoptosis via the down-regulation of Bcl2 and the induction of cleaved poly ADP-ribose polymerase. Moreover, CSC-treated 1799 cells showed induction of Wnt5a expression and enhanced colony-forming capacity. The CSC-induced colony forming efficiency was suppressed by the co-incubation with a PKC inhibitor. In conclusion, these results suggest that cigarette smoke induces Wnt5a-coupled PKC activity during lung carcinogenesis, which causes Akt activity and anti-apoptosis in lung cancer. Therefore, current study provides novel clues for the crucial role of Wnt5a in the smoking-related lung carcinogenesis.

Marijuana and Lung Disease.

Science.gov (United States)

Tashkin, Donald P

2018-05-17

As marijuana smoking prevalence increases in the U.S. concern regarding its potential risks to lung health has also risen, given the general similarity in the smoke contents between marijuana and tobacco. Most studies have found a significant association between marijuana smoking and chronic bronchitis symptoms after adjustment for tobacco. While reports are mixed regarding associations between marijuana smoking and lung function, none has shown a relationship to decrements in forced expired volume in 1 sec (FEV1) and few have found a relationship to a decreased ratio of FEV1 to forced vital capacity (FVC), possibly related to an association between marijuana and an increased FVC. A few studies have found a modest reduction in specific airway conductance in relation to marijuana, probably reflecting endoscopic evidence of bronchial mucosal edema among habitual marijuana smokers. Diffusing capacity in marijuana smokers has been normal and two studies of thoracic high-resolution computed tomography (HRCT) have not shown any association of marijuana smoking with emphysema. Although bronchial biopsies from habitual marijuana smokers have shown precancerous histopathological changes, a large cohort study and a pooled analysis of six well-designed case-control studies have not found evidence of a link between marijuana smoking and lung cancer. The immunosuppressive effects of delta-9 tetrahydrocannabinol raise the possibility of an increased risk of pneumonia, but further studies are needed to evaluate this potential risk. Several cases series have demonstrated pneumothoraces/pneumomediastinum, as well as bullous lung disease, in marijuana smokers, but these associations require epidemiologic studies for firmer evidence of possible causality. Copyright © 2018. Published by Elsevier Inc.

Smoking Marijuana and the Lungs

Science.gov (United States)

... C O P Y PATIENT EDUCATION | INFORMATION SERIES Smoking Marijuana and the Lungs Marijuana, also known as ... a safe way to smoke marijuana. How can smoking marijuana damage my lungs? Tobacco smoke of any ...

Effect of smoking on lung function, respiratory symptoms and respiratory diseases amongst HIV-positive subjects: a cross-sectional study

Directory of Open Access Journals (Sweden)

Thabane Lehana

2010-03-01

Full Text Available Abstract Background Smoking prevalence in human immunodeficiency virus (HIV positive subjects is about three times of that in the general population. However, whether the extremely high smoking prevalence in HIV-positive subjects affects their lung function is unclear, particularly whether smoking decreases lung function more in HIV-positive subjects, compared to the general population. We conducted this study to determine the association between smoking and lung function, respiratory symptoms and diseases amongst HIV-positive subjects. Results Of 120 enrolled HIV-positive subjects, 119 had an acceptable spirogram. Ninety-four (79% subjects were men, and 96 (81% were white. Mean (standard deviation [SD] age was 43.4 (8.4 years. Mean (SD of forced expiratory volume in one second (FEV1 percent of age, gender, race and height predicted value (%FEV1 was 93.1% (15.7%. Seventy-five (63% subjects had smoked 24.0 (18.0 pack-years. For every ten pack-years of smoking increment, %FEV1 decreased by 2.1% (95% confidence interval [CI]: -3.6%, -0.6%, after controlling for gender, race and restrictive lung function (R2 = 0.210. The loss of %FEV1 in our subjects was comparable to the general population. Compared to non-smokers, current smokers had higher odds of cough, sputum or breathlessness, after adjusting for highly active anti-retroviral therapy (HAART use, odds ratio OR = 4.9 (95% CI: 2.0, 11.8. However respiratory symptom presence was similar between non-smokers and former smokers, OR = 1.0 (95% CI: 0.3, 2.8. All four cases of COPD (chronic obstructive pulmonary disease had smoked. Four of ten cases of restrictive lung disease had smoked (p = 0.170, and three of five asthmatic subjects had smoked (p = 1.000. Conclusions Cumulative cigarette consumption was associated with worse lung function; however the loss of %FEV1 did not accelerate in HIV-positive population compared to the general population. Current smokers had higher odds of respiratory symptoms

Bidi smoking and lung cancer.

Science.gov (United States)

Prasad, Rajendra; Singhal, Sanjay; Garg, Rajiv

2009-04-01

This article discusses the role of bidi smoking as a risk factor for lung cancer. A review of the documented evidence is presented. The literature from Pubmed has been searched using the key words 'beedi smoking', 'bidi smoking' and 'lung cancer'. The bibliographies of all papers found were further searched for additional relevant articles. After this thorough search, eight studies were found. The evidence suggests that bidi smoking poses a higher risk for lung cancer than cigarette smoking and risk further increases with both the length of time and amount of bidi smoking. The focus of tobacco control programs should be expanded to all types of tobacco use, including bidis, to reduce the increasing problem of lung cancer.

[Burden of smoking-related disease and potential impact of cigarette price increase in Peru].

Science.gov (United States)

Bardach, Ariel E; Caporale, Joaquín E; Alcaraz, Andrea; Augustovski, Federico; Huayanay-Falconí, Leandro; Loza-Munarriz, Cesar; Hernández-Vásquez, Akram; Pichon-Riviere, Andrés

2016-01-01

. To calculate the burden of smoking-related disease and evaluate the potential economic and health impact of tax-induced cigarette price increase in Peru. A microsimulation model was used to estimate smoking-attributable impact on mortality, quality of life, and costs associated with heart and cerebrovascular disease, chronic obstructive pulmonary disease, pneumonia, lung cancer, and another nine cancers. Three scenarios, involving increased taxes, were evaluated. . A yearly total of 16,719 deaths, 6,926 cancer diagnoses, 7,936 strokes, and 7,548 hospital admissions due to cardiovascular disease can be attributed to smoking in Peru. Similarly, 396,069 years of life are lost each year from premature death and disability, and the cost of treating smoking-attributable health issues rises to 2,500 million soles (PEN 2015). Currently, taxes on tobacco cover only 9.1% of this expense. If cigarette prices were to increase by 50% over the next 10 years, 13,391 deaths, 6,210 cardiovascular events, and 5,361 new cancers could be prevented, representing an economic benefit of 3,145 million (PEN) in savings in health costs and increases in tax revenues. . Smoking-attributable burden of disease and costs to the health system are very high in Peru. Higher cigarette taxes could have substantial health and economic benefits for the country.

Cigarette smoke alters the secretome of lung epithelial cells.

Science.gov (United States)

Mossina, Alessandra; Lukas, Christina; Merl-Pham, Juliane; Uhl, Franziska E; Mutze, Kathrin; Schamberger, Andrea; Staab-Weijnitz, Claudia; Jia, Jie; Yildirim, Ali Ö; Königshoff, Melanie; Hauck, Stefanie M; Eickelberg, Oliver; Meiners, Silke

2017-01-01

Cigarette smoke is the most relevant risk factor for the development of lung cancer and chronic obstructive pulmonary disease. Many of its more than 4500 chemicals are highly reactive, thereby altering protein structure and function. Here, we used subcellular fractionation coupled to label-free quantitative MS to globally assess alterations in the proteome of different compartments of lung epithelial cells upon exposure to cigarette smoke extract. Proteomic profiling of the human alveolar derived cell line A549 revealed the most pronounced changes within the cellular secretome with preferential downregulation of proteins involved in wound healing and extracellular matrix organization. In particular, secretion of secreted protein acidic and rich in cysteine, a matricellular protein that functions in tissue response to injury, was consistently diminished by cigarette smoke extract in various pulmonary epithelial cell lines and primary cells of human and mouse origin as well as in mouse ex vivo lung tissue cultures. Our study reveals a previously unrecognized acute response of lung epithelial cells to cigarette smoke that includes altered secretion of proteins involved in extracellular matrix organization and wound healing. This may contribute to sustained alterations in tissue remodeling as observed in lung cancer and chronic obstructive pulmonary disease. © 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Surfactant Protein D is a candidate biomarker for subclinical tobacco smoke-induced lung damage

DEFF Research Database (Denmark)

Lock Johansson, Sofie; Tan, Qihua; Holst, Rene

2014-01-01

Variation in Surfactant Protein D (SP-D) is associated with lung function in tobacco smoke-induced chronic respiratory disease. We hypothesized that the same association exists in the general population and could be used to identify individuals sensitive to smoke-induced lung damage. The associat......Variation in Surfactant Protein D (SP-D) is associated with lung function in tobacco smoke-induced chronic respiratory disease. We hypothesized that the same association exists in the general population and could be used to identify individuals sensitive to smoke-induced lung damage...... or haplotypes, and expiratory lung function were assessed using twin study methodology and mixed-effects models. Significant inverse associations were evident between sSP-D and the forced expiratory volume in 1 second and forced vital capacity in the presence of current tobacco smoking but not in non...... with lung function measures in interaction with tobacco smoking. The obtained data suggest sSP-D as a candidate biomarker in risk assessments for subclinical tobacco smoke-induced lung damage. The data and derived conclusion warrant confirmation in a longitudinal population following chronic obstructive...

Effects of marijuana smoking on the lung.

Science.gov (United States)

Tashkin, Donald P

2013-06-01

Regular smoking of marijuana by itself causes visible and microscopic injury to the large airways that is consistently associated with an increased likelihood of symptoms of chronic bronchitis that subside after cessation of use. On the other hand, habitual use of marijuana alone does not appear to lead to significant abnormalities in lung function when assessed either cross-sectionally or longitudinally, except for possible increases in lung volumes and modest increases in airway resistance of unclear clinical significance. Therefore, no clear link to chronic obstructive pulmonary disease has been established. Although marijuana smoke contains a number of carcinogens and cocarcinogens, findings from a limited number of well-designed epidemiological studies do not suggest an increased risk for the development of either lung or upper airway cancer from light or moderate use, although evidence is mixed concerning possible carcinogenic risks of heavy, long-term use. Although regular marijuana smoking leads to bronchial epithelial ciliary loss and impairs the microbicidal function of alveolar macrophages, evidence is inconclusive regarding possible associated risks for lower respiratory tract infection. Several case reports have implicated marijuana smoking as an etiologic factor in pneumothorax/pneumomediastinum and bullous lung disease, although evidence of a possible causal link from epidemiologic studies is lacking. In summary, the accumulated weight of evidence implies far lower risks for pulmonary complications of even regular heavy use of marijuana compared with the grave pulmonary consequences of tobacco.

Smoking cessation and lung cancer screening

DEFF Research Database (Denmark)

Pedersen, Jesper Johannes Holst; Tønnesen, Philip; Ashraf, Haseem

2016-01-01

Smoking behavior may have a substantial influence on the overall effect of lung cancer screening. Non-randomized studies of smoking behavior during screening have indicated that computer tomography (CT) screening induces smoking cessation. Randomized studies have further elaborated that this effect...... and decrease smoking relapse rate. Also low smoking dependency and high motivation to quit smoking at baseline predicted smoking abstinence in screening trials. Lung cancer screening therefore seems to be a teachable moment for smoking cessation. Targeted smoking cessation counselling should be an integrated...... part of future lung cancer screening trials....

Accelerated decline in lung function in smoking women with airway obstruction: SAPALDIA 2 cohort study

Directory of Open Access Journals (Sweden)

Zemp Elisabeth

2005-05-01

Full Text Available Abstract Background The aim was to determine if effects from smoking on lung function measured over 11 years differ between men and women. Methods In a prospective population based cohort study (Swiss Study on Air Pollution and Lung Diseases in Adults current smokers in 1991 (18 – 60 yrs were reassessed in 2002 (n = 1792. Multiple linear regression was used to estimate effects from pack-years of cigarettes smoked to 1991 and mean packs of cigarettes smoked per day between 1991 and 2002 on change in lung volume and flows over the 11 years. Results In both sexes, packs smoked between assessments were related to lung function decline but pack-years smoked before 1991 were not. Mean annual decline in FEV1 was -10.4 mL(95%CI -15.3, -5.5 per pack per day between assessments in men and -13.8 mL(95%CI-19.5,-8.1 in women. Decline per pack per day between 1991 and 2002 was lower in women who smoked in 1991 but quit before 2002 compared to persistent smokers (-6.4 vs -11.6 mL, p = 0.05 but this was not seen in men (-14.3 vs -8.8 mL p = 0.49. Smoking related decline was accelerated in men and women with airway obstruction, particularly in women where decline in FEV1 was three fold higher in participants with FEV1/FVC Conclusion There are differences in effects from smoking on lung function between men and women. Lung function recovers faster in women quitters than in men. Women current smokers with airway obstruction experience a greater smoking related decline in lung function than men.

Risks for heart disease and lung cancer from passive smoking by workers in the catering industry.

Science.gov (United States)

Hedley, Anthony J; McGhee, Sarah M; Repace, James L; Wong, Lai-Chin; Yu, Marcus Y S; Wong, Tze-Wai; Lam, Tai-Hing

2006-04-01

Workers in the catering industry are at greater risk of exposure to secondhand smoke (SHS) when smoke-free workplace policies are not in force. We determined the exposure of catering workers to SHS in Hong Kong and their risk of death from heart disease and lung cancer. Nonsmoking catering workers were provided with screening at their workplaces and at a central clinic. Participants reported workplace, home, and leisure time exposure to SHS. Urinary cotinine was estimated by enzyme immunoassay. Catering facilities were classified into three types: nonsmoking, partially restricted smoking (with nonsmoking areas), and unrestricted smoking. Mean urinary cotinine levels ranged from 3.3 ng/ml in a control group of 16 university staff through 6.4 ng/ml (nonsmoking), 6.1 ng/ml (partially restricted), and 15.9 ng/ml (unrestricted smoking) in 104 workers who had no exposures outside of work. Workers in nonsmoking facilities had exposures to other smoking staff. We modeled workers' mortality risks using average cotinine levels, estimates of workplace respirable particulates, risk data for cancer and heart disease from cohort studies, and national (US) and regional (Hong Kong) mortality for heart disease and lung cancer. We estimated that deaths in the Hong Kong catering workforce of 200,000 occur at the rate of 150 per year for a 40-year working-lifetime exposure to SHS. When compared with the current outdoor air quality standards for particulates in Hong Kong, 30% of workers exceeded the 24-h and 98% exceeded the annual air quality objectives due to workplace SHS exposures.

Lung Microbiota Is Related to Smoking Status and to Development of Acute Respiratory Distress Syndrome in Critically Ill Trauma Patients.

Science.gov (United States)

Panzer, Ariane R; Lynch, Susan V; Langelier, Chaz; Christie, Jason D; McCauley, Kathryn; Nelson, Mary; Cheung, Christopher K; Benowitz, Neal L; Cohen, Mitchell J; Calfee, Carolyn S

2018-03-01

Cigarette smoking is associated with increased risk of acute respiratory distress syndrome (ARDS) in patients after severe trauma; however, the mechanisms underlying this association are unknown. To determine whether cigarette smoking contributes to ARDS development after trauma by altering community composition of the lung microbiota. We studied the lung microbiota of mechanically ventilated patients admitted to the ICU after severe blunt trauma. To do so, we used 16S ribosomal RNA gene amplicon sequencing of endotracheal aspirate samples obtained on ICU admission (n = 74) and at 48 hours after admission (n = 30). Cigarette smoke exposure (quantified using plasma cotinine), ARDS development, and other clinical parameters were correlated with lung microbiota composition. Smoking status was significantly associated with lung bacterial community composition at ICU admission (P = 0.007 by permutational multivariate ANOVA [PERMANOVA]) and at 48 hours (P = 0.03 by PERMANOVA), as well as with significant enrichment of potential pathogens, including Streptococcus, Fusobacterium, Prevotella, Haemophilus, and Treponema. ARDS development was associated with lung community composition at 48 hours (P = 0.04 by PERMANOVA) and was characterized by relative enrichment of Enterobacteriaceae and of specific taxa enriched at baseline in smokers, including Prevotella and Fusobacterium. After severe blunt trauma, a history of smoking is related to lung microbiota composition, both at the time of ICU admission and at 48 hours. ARDS development is also correlated with respiratory microbial community structure at 48 hours and with taxa that are relatively enriched in smokers at ICU admission. The data derived from this pilot study suggest that smoking-related changes in the lung microbiota could be related to ARDS development after severe trauma.

Radioaerosol lung scanning in chronic obstructive pulmonary disease (COPD) and related disorders

International Nuclear Information System (INIS)

Yong Whee Bahk; Soo Kyo Chung

1994-01-01

As a coordinated research project of the International Atomic Energy Agency (IAEA), a multicentre joint study on radioaerosol lung scan using the BARC nebulizer has prospectively been carried out during 1988-1992 with the participation of 10 member countries in Asia [Bangladesh, China, India, Indonesia, Japan, Korea, Pakistan, Philippines, Singapore and Thailand]. The study was designed so that it would primarily cover chronic obstructive pulmonary disease (COPD) and the other related and common pulmonary diseases. The study also included normal controls and asymptomatic smokers. The purposes of this presentation are three fold: firstly, to document the usefulness of the nebulizer and the validity of user's protocol in imaging COPD and other lung diseases; secondly, to discuss scan features of the individual COPD and other disorders studied and thirdly, to correlate scan alterations with radiographic findings. Before proceeding with a systematic analysis of aerosol scan patterns in the disease groups, we documented normal pattern. The next step was the assessment of scan features in those who had been smoking for more than several years but had no symptoms or signs referable to airways. The lung diseases we analyzed included COPD [emphysema, chronic bronchitis, asthma and bronchiectasis], bronchial obstruction, compensatory overinflation and other common lung diseases such as lobar pneumonia, tuberculosis, interstitial fibrosis, diffuse panbronchiolitis, lung edema and primary and metastatic lung cancers. Lung embolism, inhalation bums and glue-sniffer's lung are separately discussed by Dr. Sundram of Singapore elsewhere in this book. The larger portion of this chapter is allocated to the discussion of COPD with a special effort made in sorting out differential scan features. Diagnostic criteria in individual COPD were defined for each category of disease and basic clinical symptoms and signs and pertinent laboratory data as well as radiographic manifestations are

Radioaerosol lung scanning in chronic obstructive pulmonary disease (COPD) and related disorders

Energy Technology Data Exchange (ETDEWEB)

Bahk, Yong Whee [Departments of Radiology and Nuclear Medicine, Kangnam St. Mary' s Hospital, Catholic University Medical College, Seoul (Korea, Republic of); Chung, Soo Kyo [Department of Nuclear Medicine, Kangnam St. Mary' s Hospital, Catholic University Medical College, Seoul (Korea, Republic of)

1994-07-01

As a coordinated research project of the International Atomic Energy Agency (IAEA), a multicentre joint study on radioaerosol lung scan using the BARC nebulizer has prospectively been carried out during 1988-1992 with the participation of 10 member countries in Asia [Bangladesh, China, India, Indonesia, Japan, Korea, Pakistan, Philippines, Singapore and Thailand]. The study was designed so that it would primarily cover chronic obstructive pulmonary disease (COPD) and the other related and common pulmonary diseases. The study also included normal controls and asymptomatic smokers. The purposes of this presentation are three fold: firstly, to document the usefulness of the nebulizer and the validity of user's protocol in imaging COPD and other lung diseases; secondly, to discuss scan features of the individual COPD and other disorders studied and thirdly, to correlate scan alterations with radiographic findings. Before proceeding with a systematic analysis of aerosol scan patterns in the disease groups, we documented normal pattern. The next step was the assessment of scan features in those who had been smoking for more than several years but had no symptoms or signs referable to airways. The lung diseases we analyzed included COPD [emphysema, chronic bronchitis, asthma and bronchiectasis], bronchial obstruction, compensatory overinflation and other common lung diseases such as lobar pneumonia, tuberculosis, interstitial fibrosis, diffuse panbronchiolitis, lung edema and primary and metastatic lung cancers. Lung embolism, inhalation bums and glue-sniffer's lung are separately discussed by Dr. Sundram of Singapore elsewhere in this book. The larger portion of this chapter is allocated to the discussion of COPD with a special effort made in sorting out differential scan features. Diagnostic criteria in individual COPD were defined for each category of disease and basic clinical symptoms and signs and pertinent laboratory data as well as radiographic manifestations are

Impact of Cigarette Smoke on the Human and Mouse Lungs : A Gene-Expression Comparison Study

NARCIS (Netherlands)

Morissette, Mathieu C.; Lamontagne, Maxime; Berube, Jean-Christophe; Gaschler, Gordon; Williams, Andrew; Yauk, Carole; Couture, Christian; Laviolette, Michel; Hogg, James C.; Timens, Wim; Halappanavar, Sabina; Stampfli, Martin R.; Bosse, Yohan

2014-01-01

Cigarette smoke is well known for its adverse effects on human health, especially on the lungs. Basic research is essential to identify the mechanisms involved in the development of cigarette smoke-related diseases, but translation of new findings from pre-clinical models to the clinic remains

Second Hand Smoke Exposure and Excess Heart Disease and Lung Cancer Mortality among Hospital Staff in Crete, Greece: A Case Study

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Anthony Kafatos

2008-09-01

Full Text Available Exposure to secondhand smoke (SHS is a serious threat to public health, and a significant cause of lung cancer and heart disease among non-smokers. Even though Greek hospitals have been declared smoke free since 2002, smoking is still evident. Keeping the above into account, the aim of this study was to quantify the levels of exposure to environmental tobacco smoke and to estimate the attributed lifetime excess heart disease and lung cancer deaths per 1000 of the hospital staff, in a large Greek public hospital. Environmental airborne respirable suspended particles (RSP of PM2.5 were performed and the personnel’s excess mortality risk was estimated using risk prediction formulas. Excluding the intensive care unit and the operating theatres, all wards and clinics were polluted with environmental tobacco smoke. Mean SHS-RSP measurements ranged from 11 to 1461 μg/m3 depending on the area. Open wards averaged 84 μg/m3 and the managing wards averaged 164 μg/m3 thus giving an excess lung cancer and heart disease of 1.12 (range 0.23-1.88 and 11.2 (range 2.3–18.8 personnel in wards and 2.35 (range 0.55-12.2 and 23.5 (range 5.5–122 of the managing staff per 1000 over a 40-year lifespan, respectively. Conclusively, SHS exposure in hospitals in Greece is prevalent and taking into account the excess heart disease and lung cancer mortality risk as also the immediate adverse health effects of SHS exposure, it is clear that proper implementation and enforcement of the legislation that bans smoking in hospitals is imperative to protect the health of patients and staff alike.

Prediction of the effect of indoor smoking on the lung cancer risk

International Nuclear Information System (INIS)

Böhm, Radoslav; Holý, Karol; Sedlák, Antonín

2018-01-01

Inhalation of tobacco smoke leads to hyperproduction of mucus, which acts as a radioprotective layer for the target cells. On the other hand, long-term smoking affects adversely the lungs function, damages the lung tissue and frequently leads to the chronic obstructive pulmonary disease: This serious disease results in the accumulation of radon progeny in the lung tissue and hence, in an increased radiation dose to the target cells. The aim of this work was to quantify the effect of such changes on the bronchial dose and radon risk for current population. (orig.)

Maternal smoking and the retinoid pathway in the developing lung

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Manoli Sara E

2012-06-01

Full Text Available Abstract Background Maternal smoking is a risk factor for pediatric lung disease, including asthma. Animal models suggest that maternal smoking causes defective alveolarization in the offspring. Retinoic acid signaling modulates both lung development and postnatal immune function. Thus, abnormalities in this pathway could mediate maternal smoking effects. We tested whether maternal smoking disrupts retinoic acid pathway expression and functioning in a murine model. Methods Female C57Bl/6 mice with/without mainstream cigarette smoke exposure (3 research cigarettes a day, 5 days a week were mated to nonsmoking males. Cigarette smoke exposure continued throughout the pregnancy and after parturition. Lung tissue from the offspring was examined by mean linear intercept analysis and by quantitative PCR. Cell culture experiments using the type II cell-like cell line, A549, tested whether lipid-soluble cigarette smoke components affected binding and activation of retinoic acid response elements in vitro. Results Compared to tobacco-naïve mice, juvenile mice with tobacco toxin exposure had significantly (P  Conclusions A murine model of maternal cigarette smoking causes abnormal alveolarization in association with altered retinoic acid pathway element expression in the offspring. An in vitro cell culture model shows that lipid-soluble components of cigarette smoke decrease retinoic acid response element activation. It is feasible that disruption of retinoic acid signaling contributes to the pediatric lung dysfunction caused by maternal smoking.

Cost Effectiveness of Free Access to Smoking Cessation Treatment in France Considering the Economic Burden of Smoking-Related Diseases.

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Cadier, Benjamin; Durand-Zaleski, Isabelle; Thomas, Daniel; Chevreul, Karine

2016-01-01

In France more than 70,000 deaths from diseases related to smoking are recorded each year, and since 2005 prevalence of tobacco has increased. Providing free access to smoking cessation treatment would reduce this burden. The aim of our study was to estimate the incremental cost-effectiveness ratios (ICER) of providing free access to cessation treatment taking into account the cost offsets associated with the reduction of the three main diseases related to smoking: lung cancer, chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD). To measure the financial impact of such a measure we also conducted a probabilistic budget impact analysis. We performed a cost-effectiveness analysis using a Markov state-transition model that compared free access to cessation treatment to the existing coverage of €50 provided by the French statutory health insurance, taking into account the cost offsets among current French smokers aged 15-75 years. Our results were expressed by the incremental cost-effectiveness ratio in 2009 Euros per life year gained (LYG) at the lifetime horizon. We estimated a base case scenario and carried out a Monte Carlo sensitivity analysis to account for uncertainty. Assuming a participation rate of 7.3%, the ICER value for free access to cessation treatment was €3,868 per LYG in the base case. The variation of parameters provided a range of ICER values from -€736 to €15,715 per LYG. In 99% of cases, the ICER for full coverage was lower than €11,187 per LYG. The probabilistic budget impact analysis showed that the potential cost saving for lung cancer, COPD and CVD ranges from €15 million to €215 million at the five-year horizon for an initial cessation treatment cost of €125 million to €421 million. The results suggest that providing medical support to smokers in their attempts to quit is very cost-effective and may even result in cost savings.

Smoking and Lung Cancer: A Geo-Regional Perspective.

Science.gov (United States)

Rahal, Zahraa; El Nemr, Shaza; Sinjab, Ansam; Chami, Hassan; Tfayli, Arafat; Kadara, Humam

2017-01-01

Lung cancer is the leading cause of cancer-related deaths worldwide. Non-small cell lung cancer (NSCLC) represents the most frequently diagnosed subtype of this morbid malignancy. NSCLC is causally linked to tobacco consumption with more than 500 million smokers worldwide at high risk for this fatal malignancy. We are currently lagging in our knowledge of the early molecular (e.g., genomic) effects of smoking in NSCLC pathogenesis that would constitute ideal markers for early detection. This limitation is further amplified when considering the variable etiologic factors in NSCLC pathogenesis among different regions around the globe. In this review, we present our current knowledge of genomic alterations arising during early stages of smoking-induced lung cancer initiation and progression, including discussing the premalignant airway field of injury induced by smoking. The review also underscores the wider spectra and higher age-adjusted rates of tobacco (e.g., water-pipe smoke) consumption, along with elevated environmental carcinogenic exposures and relatively poorer socioeconomic status, in low-middle income countries (LMICs), with Lebanon as an exemplar. This "cocktail" of carcinogenic exposures warrants the pressing need to understand the complex etiology of lung malignancies developing in LMICs such as Lebanon.

Smoking and Lung Cancer: A Geo-Regional Perspective

Directory of Open Access Journals (Sweden)

Zahraa Rahal

2017-09-01

Full Text Available Lung cancer is the leading cause of cancer-related deaths worldwide. Non-small cell lung cancer (NSCLC represents the most frequently diagnosed subtype of this morbid malignancy. NSCLC is causally linked to tobacco consumption with more than 500 million smokers worldwide at high risk for this fatal malignancy. We are currently lagging in our knowledge of the early molecular (e.g., genomic effects of smoking in NSCLC pathogenesis that would constitute ideal markers for early detection. This limitation is further amplified when considering the variable etiologic factors in NSCLC pathogenesis among different regions around the globe. In this review, we present our current knowledge of genomic alterations arising during early stages of smoking-induced lung cancer initiation and progression, including discussing the premalignant airway field of injury induced by smoking. The review also underscores the wider spectra and higher age-adjusted rates of tobacco (e.g., water-pipe smoke consumption, along with elevated environmental carcinogenic exposures and relatively poorer socioeconomic status, in low-middle income countries (LMICs, with Lebanon as an exemplar. This “cocktail” of carcinogenic exposures warrants the pressing need to understand the complex etiology of lung malignancies developing in LMICs such as Lebanon.

Recommendations to improve smoking cessation outcomes from people with lung conditions who smoke

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Sarah Masefield

2016-04-01

Full Text Available This study aimed to gain insight into the impact of lung conditions on smoking behaviour and smoking cessation, and identify recommendations for smoking cessation and professional-patient communications. The study was led by the European Lung Foundation in collaboration with the European Respiratory Society Task Force on “Statement on smoking cessation on COPD and other pulmonary diseases and in smokers with comorbidities who find it difficult to quit”. A web-based observational cross-sectional questionnaire was developed from a patient-centered literature review. Topics covered were: cohort characteristics; perspectives on smoking cessation; interactions with healthcare professionals; and recommendations to improve cessation outcomes. The questionnaire was disseminated via existing patient and professional networks and social media channels. The survey was available online for a period of 4 months in 16 languages. The data were analysed as a whole, not by country, with thematic analysis of the open responses. Common characteristics were: male (54%; age 40–55 years (39%; 11–20 cigarettes a day (39%; smokes within 30 min of waking (61%; and has made 1–5 cessation attempts in the previous 12 months (54%. 59% had tried cessation treatments, but, of these, 55% had not found any treatments helpful. Recommendations were: earlier intervention; discussion of the patient's smoking beliefs, behaviours and motivation; giving constructive advice; understanding addiction; informed decision-making; and treatment options. Areas for new and further research have been highlighted through exploring the smoking cessation perspectives and recommendations of people with lung conditions in Europe who smoke.

Rapid fall in lung density following smoking cessation in COPD.

Science.gov (United States)

Shaker, Saher B; Stavngaard, Trine; Laursen, Lars Christian; Stoel, Berend C; Dirksen, Asger

2011-02-01

Whether smoking-induced lung inflammation subsides after smoking cessation is currently a matter of debate. We used computed tomography (CT) to evaluate the effect of smoking cessation on lung density in patients with COPD. Thirty-six patients quit smoking out of 254 current smokers with COPD who were followed with annual CT and lung function tests (LFT) for 2?4 years as part of a randomised placebo-controlled trial of the effect of inhaled budesonide on CT-lung density. Lung density was expressed as the 15th percentile density (PD15) and relative area of emphysema below -910 HU (RA-910). From the time-trends in the budesonide and placebo groups the expected CT-lung densities at the first visit after smoking cessation were calculated by linear regression and compared to the observed densities. Following smoking cessation RA-910 increased by 2.6% (p = 0.003) and PD15 decreased by -4.9 HU (p = 0.0002). Furthermore, changes were larger in the budesonide group than the placebo group (PD15: -7.1 vs -2.8 HU. RA-910 3.7% vs 1.7%). These differences were, however, not statistically significant. The LFT parameters (FEV(1) and diffusion capacity) were not significantly influenced by smoking cessation. Inflammation partly masks the presence of emphysema on CT and smoking cessation results in a paradoxical fall in lung density, which resembles rapid progression of emphysema. This fall in density is probably due to an anti-inflammatory effect of smoking cessation.

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

Marijuana and lung diseases.

Science.gov (United States)

Joshi, Manish; Joshi, Anita; Bartter, Thaddeus

2014-03-01

Cannabis sativa (marijuana) is used throughout the world, and its use is increasing. In much of the world, marijuana is illicit. While inhalation of smoke generated by igniting dried components of the plant is the most common way marijuana is used, there is concern over potential adverse lung effects. The purpose of this review is to highlight recent studies that explore the impact upon the respiratory system of inhaling marijuana smoke. Smoking marijuana is associated with chronic bronchitis symptoms and large airway inflammation. Occasional use of marijuana with low cumulative use is not a risk factor for the development of chronic obstructive pulmonary disease. The heavy use of marijuana alone may lead to airflow obstruction. The immuno-histopathologic and epidemiologic evidence in marijuana users suggests biological plausibility of marijuana smoking as a risk for the development of lung cancer; at present, it has been difficult to conclusively link marijuana smoking and cancer development. There is unequivocal evidence that habitual or regular marijuana smoking is not harmless. A caution against regular heavy marijuana usage is prudent. The medicinal use of marijuana is likely not harmful to lungs in low cumulative doses, but the dose limit needs to be defined. Recreational use is not the same as medicinal use and should be discouraged.

[Cannabis smoking and lung cancer].

Science.gov (United States)

Underner, M; Urban, T; Perriot, J; de Chazeron, I; Meurice, J-C

2014-06-01

Cannabis is the most commonly smoked illicit substance in the world. It can be smoked alone in plant form (marijuana) but it is mainly smoked mixed with tobacco. The combined smoking of cannabis and tobacco is a common-place phenomenon in our society. However, its use is responsible for severe pulmonary consequences. The specific impact of smoking cannabis is difficult to assess precisely and to distinguish from the effect of tobacco. Marijuana smoke contains polycyclic aromatic hydrocarbons and carcinogens at higher concentration than tobacco smoke. Cellular, tissue, animal and human studies, and also epidemiological studies, show that marijuana smoke is a risk factor for lung cancer. Cannabis exposure doubles the risk of developing lung cancer. This should encourage clinicians to identify cannabis use and to offer patients support in quitting. Copyright © 2014 SPLF. Published by Elsevier Masson SAS. All rights reserved.

Cannabis Smoking in 2015: A Concern for Lung Health?

Science.gov (United States)

Biehl, Jason R; Burnham, Ellen L

2015-09-01

Recent legislative successes allowing expanded access to recreational and medicinal cannabis have been associated with its increased use by the public, despite continued debates regarding its safety within the medical and scientific communities. Despite legislative changes, cannabis is most commonly used by smoking, although alternatives to inhalation have also emerged. Moreover, the composition of commercially available cannabis has dramatically changed in recent years. Therefore, developing sound scientific information regarding its impact on lung health is imperative, particularly because published data conducted prior to widespread legalization are conflicting and inconclusive. In this commentary, we delineate major observations of epidemiologic investigations examining cannabis use and the potential associated development of airways disease and lung cancer to highlight gaps in pulmonary knowledge. Additionally, we review major histopathologic alterations related to smoked cannabis and define specific areas in animal models and human clinical translational investigations that could benefit from additional development. Given that cannabis has an ongoing classification as a schedule I medication, federal funding to support investigations of modern cannabis use in terms of medicinal efficacy and safety profile on lung health have been elusive. It is clear, however, that the effects of inhaled cannabis on lung health remain uncertain and given increasing use patterns, are worthy of further investigation.

Smoked marijuana as a cause of lung injury.

Science.gov (United States)

Tashkin, D P

2005-06-01

In many societies, marijuana is the second most commonly smoked substance after tobacco. While delta9-tetrahydrocannabinol (THC) is unique to marijuana and nicotine to tobacco, the smoke of marijuana, like that of tobacco, consists of a toxic mixture of gases and particulates, many of which are known to be harmful to the lung. Although far fewer marijuana than tobacco cigarettes are generally smoked on a daily basis, the pulmonary consequences of marijuana smoking may be magnified by the greater deposition of smoke particulates in the lung due to the differing manner in which marijuana is smoked. Whereas THC causes modest short-term bronchodilation, regular marijuana smoking produces a number of long-term pulmonary consequences, including chronic cough and sputum, histopathologic evidence of widespread airway inflammation and injury and immunohistochemical evidence of dysregulated growth of respiratory epithelial cells, that may be precursors to lung cancer. The THC in marijuana could contribute to some of these injurious changes through its ability to augment oxidative stress, cause mitochondrial dysfunction, and inhibit apoptosis. On the other hand, physiologic, clinical or epidemiologic evidence that marijuana smoking may lead to chronic obstructive pulmonary disease or respiratory cancer is limited and inconsistent. Habitual use of marijuana is also associated with abnormalities in the structure and function of alveolar macrophages, including impairment in microbial phagocytosis and killing that is associated with defective production of immunostimulatory cytokines and nitric oxide, thereby potentially predisposing to pulmonary infection. In view of the growing interest in medicinal marijuana, further epidemiologic studies are needed to clarify the true risks of regular marijuana smoking on respiratory health.

Protocols to Evaluate Cigarette Smoke-Induced Lung Inflammation and Pathology in Mice.

Science.gov (United States)

Vlahos, Ross; Bozinovski, Steven

2018-01-01

Cigarette smoking is a major cause of chronic obstructive pulmonary disease (COPD). Inhalation of cigarette smoke causes inflammation of the airways, airway wall remodelling, mucus hypersecretion and progressive airflow limitation. Much of the disease burden and health care utilisation in COPD is associated with the management of its comorbidities and infectious (viral and bacterial) exacerbations (AECOPD). Comorbidities, in particular skeletal muscle wasting, cardiovascular disease and lung cancer markedly impact on disease morbidity, progression and mortality. The mechanisms and mediators underlying COPD and its comorbidities are poorly understood and current COPD therapy is relatively ineffective. Many researchers have used animal modelling systems to explore the mechanisms underlying COPD, AECOPD and comorbidities of COPD with the goal of identifying novel therapeutic targets. Here we describe a mouse model that we have developed to define the cellular, molecular and pathological consequences of cigarette smoke exposure and the development of comorbidities of COPD.

Identification of nuclear phosphoproteins as novel tobacco markers in mouse lung tissue following short-term exposure to tobacco smoke

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Kanako Niimori-Kita

2014-01-01

Full Text Available Smoking is a risk factor for lung diseases, including chronic obstructive pulmonary disease and lung cancer. However, the molecular mechanisms mediating the progression of these diseases remain unclear. Therefore, we sought to identify signaling pathways activated by tobacco-smoke exposure, by analyzing nuclear phosphoprotein expression using phosphoproteomic analysis of lung tissue from mice exposed to tobacco smoke. Sixteen mice were exposed to tobacco smoke for 1 or 7 days, and the expression of phosphorylated peptides was analyzed by mass spectrometry. A total of 253 phosphoproteins were identified, including FACT complex subunit SPT16 in the 1-day exposure group, keratin type 1 cytoskeletal 18 (K18, and adipocyte fatty acid-binding protein, in the 7-day exposure group, and peroxiredoxin-1 (OSF3 and spectrin β chain brain 1 (SPTBN1, in both groups. Semi-quantitative analysis of the identified phosphoproteins revealed that 33 proteins were significantly differentially expressed between the control and exposed groups. The identified phosphoproteins were classified according to their biological functions. We found that the identified proteins were related to inflammation, regeneration, repair, proliferation, differentiation, morphogenesis, and response to stress and nicotine. In conclusion, we identified proteins, including OSF3 and SPTBN1, as candidate tobacco smoke-exposure markers; our results provide insights into the mechanisms of tobacco smoke-induced diseases.

Smoking, health-related quality of life and economic evaluation.

Science.gov (United States)

López-Nicolás, Ángel; Trapero-Bertran, Marta; Muñoz, Celia

2018-06-01

The economic evaluation of tobacco control policies requires the adoption of assumptions about the impact of changes in smoking status on health-related quality of life (HRQoL). Estimates for such impacts are necessary for different populations. This paper aims to test whether smoking status has an independent effect on HRQoL over and above the effect derived from the increased likelihood of suffering a tobacco related disease, and to calculate utility values for the Spanish population. Using data from the Spanish Encuesta Nacional de Salud of 2011-12, we estimate statistical models for HRQoL as measured by the EQ-5D-5L instrument as a function of smoking status. We include a comprehensive set of controls for biological, clinical, lifestyle and socioeconomic characteristics. Smoking status has an independent, statistically significant effect on HRQoL. However, the size of the effect is small. The typical smoking related diseases, such as lung cancer, are associated with a reduction in HRQoL about 5 times larger than the difference between current smokers and never smokers. Attributing substantive HRQoL gains to quitting smoking as well as accounting for the concomitant HRQoL gain derived from a smaller likelihood of contracting tobacco related diseases might lead to an overestimation of the benefits of tobacco control policies. Nonetheless, the relatively large drops in HRQoL associated with being diagnosed with diseases that might be causally linked to tobacco suggest that such diseases should not be omitted from the economic evaluations of tobacco control policies.

Patient's lung cancer diagnosis as a cue for relatives' smoking cessation: evaluating the constructs of the teachable moment.

Science.gov (United States)

McBride, Colleen M; Blocklin, Michelle; Lipkus, Isaac M; Klein, William M P; Brandon, Thomas H

2017-01-01

To understand whether patient-reported experiences with lung cancer may create teachable moments (TM) for their relatives as evidenced by shifts in their risk perceptions, affective response, and self-image and in turn, motivation to quit smoking. Patients at a comprehensive cancer center (n = 152) completed a survey within 6 months of lung cancer diagnosis to assess their cancer-related symptoms and openness and enumerated relatives who were smokers. Relative smokers (n = 218) then completed a survey assessing their risk perceptions, affective response, and self-image as a smoker related to the patient's diagnosis (TM mechanisms), and their motivation to quit smoking. Cross-sectional mediation and moderation analyses were conducted to explore the links between patient-reported experiences, and relatives' TM mechanisms, and motivation to quit smoking. Relative-reported affect was a significant mediator of the association between patient-reported symptoms and relative smoker's desire to quit. Relatives' self-image was a significant moderator of the association between patient-reported symptoms and relative smoker's desire to quit, such that patients' reported symptoms were associated with relatives' desire to quit only when the relative smoker reported a generally positive self-image as a smoker. No evidence was found for moderated mediation. However, the link between symptoms and negative affect was moderated by perceptions of risk. Whether smokers experience a family member's lung cancer as a TM is influenced by multiple interrelated cognitive and affective factors that warrant further exploration. Clearer understanding of these factors could inform how to re-invigorate and sustain this motivation to promote concrete actions toward smoking cessation. Copyright © 2015 John Wiley & Sons, Ltd. Copyright © 2015 John Wiley & Sons, Ltd.

Will chronic e-cigarette use cause lung disease?

OpenAIRE

Rowell, Temperance R.; Tarran, Robert

2015-01-01

Chronic tobacco smoking is a major cause of preventable morbidity and mortality worldwide. In the lung, tobacco smoking increases the risk of lung cancer, and also causes chronic obstructive pulmonary disease (COPD), which encompasses both emphysema and chronic bronchitis. E-cigarettes (E-Cigs), or electronic nicotine delivery systems, were developed over a decade ago and are designed to deliver nicotine without combusting tobacco. Although tobacco smoking has declined since the 1950s, E-Cig ...

Systematic review with meta-analysis of the epidemiological evidence in the 1900s relating smoking to lung cancer

Science.gov (United States)

2012-01-01

, earlier starting age, tar level and fraction smoked and decreased with time quit. Relationships were strongest for small and squamous cell, intermediate for large cell and weakest for adenocarcinoma. Covariate-adjustment little affected RR estimates. Conclusions The association of lung cancer with smoking is strong, evident for all lung cancer types, dose-related and insensitive to covariate-adjustment. This emphasises the causal nature of the relationship. Our results quantify the relationships more precisely than previously. PMID:22943444

[Smoking fewer cigarettes per day may determine a significant risk reduction in developing smoking attributable diseases? Is there a risk reduction for e-cigarette users?].

Science.gov (United States)

Pieri, Luca; Chellini, Elisabetta; Gorini, Giuseppe

2014-01-01

Among Italian smokers--about 10 millions in 2013--about 600,000 began using electronic cigarettes (e-cigs) in last years. About 10% of e-cig users quitted smoking tobacco, whereas the 90% was dual users. Among them, about three out of four decreased the number of cigarettes smoked per day (cig/day), but did not quit. How many fewer cigarettes a smoker has to smoke to obtain significant health benefits? Is there a threshold? In order to observe a significant 27% reduction in the risk of developing lung cancer, a smoker must reduce the number of cig/day by at least 50%, while for the other smoking-related diseases (acute myocardial infarction - AMI, stroke, chronic obstructive pulmonary diseases), halving the number of cig/day did not drive to a significant risk reduction. Even smoking 5 cig/day increases the risk of AMI, whereas it significantly lowers the risk of lung cancer. Obviously, quitting smoking is the best choice to highly reduce risks for all smoking-related diseases. Therefore, in order to achieve significant risk reductions, e-cig users should quit smoking as first choice, or, if they feel it is impossible to them, reduce the consumption of traditional cigarettes to less than 5 cig/day.

HIV infection is associated with an increased risk for lung cancer, independent of smoking.

Science.gov (United States)

Kirk, Gregory D; Merlo, Christian; O' Driscoll, Peter; Mehta, Shruti H; Galai, Noya; Vlahov, David; Samet, Jonathan; Engels, Eric A

2007-07-01

Human immunodeficiency virus (HIV)-infected persons have an elevated risk for lung cancer, but whether the increase reflects solely their heavy tobacco use remains an open question. The Acquired Immunodeficiency Syndrome (AIDS) Link to the Intravenous Experience Study has prospectively observed a cohort of injection drug users in Baltimore, Maryland, since 1988, using biannual collection of clinical, laboratory, and behavioral data. Lung cancer deaths were identified through linkage with the National Death Index. Cox proportional hazards regression was used to examine the effect of HIV infection on lung cancer risk, controlling for smoking status, drug use, and clinical variables. Among 2086 AIDS Link to the Intravenous Experience Study participants observed for 19,835 person-years, 27 lung cancer deaths were identified; 14 of the deaths were among HIV-infected persons. All but 1 (96%) of the patients with lung cancer were smokers, smoking a mean of 1.2 packs per day. Lung cancer mortality increased during the highly active antiretroviral therapy era, compared with the pre-highly active antiretroviral therapy period (mortality rate ratio, 4.7; 95% confidence interval, 1.7-16). After adjusting for age, sex, smoking status, and calendar period, HIV infection was associated with increased lung cancer risk (hazard ratio, 3.6; 95% confidence interval, 1.6-7.9). Preexisting lung disease, particularly noninfectious diseases and asthma, displayed trends for increased lung cancer risk. Illicit drug use was not associated with increased lung cancer risk. Among HIV-infected persons, smoking remained the major risk factor; CD4 cell count and HIV load were not strongly associated with increased lung cancer risk, and trends for increased risk with use of highly active antiretroviral therapy were not significant. HIV infection is associated with significantly increased risk for developing lung cancer, independent of smoking status.

New insights into lung diseases using hyperpolarized gas MRI.

Science.gov (United States)

Flors, L; Altes, T A; Mugler, J P; de Lange, E E; Miller, G W; Mata, J F; Ruset, I C; Hersman, F W

2015-01-01

Hyperpolarized (HP) gases are a new class of contrast agents that permit to obtain high temporal and spatial resolution magnetic resonance images (MRI) of the lung airspaces. HP gas MRI has become important research tool not only for morphological and functional evaluation of normal pulmonary physiology but also for regional quantification of pathologic changes occurring in several lung diseases. The purpose of this work is to provide an introduction to MRI using HP noble gases, describing both the basic principles of the technique and the new information about lung disease provided by clinical studies with this method. The applications of the technique in normal subjects, smoking related lung disease, asthma, and cystic fibrosis are reviewed. Copyright © 2014 SERAM. Published by Elsevier España, S.L.U. All rights reserved.

Lung cancer development in patients with connective tissue disease-related interstitial lung disease: A retrospective observational study.

Science.gov (United States)

Enomoto, Yasunori; Inui, Naoki; Yoshimura, Katsuhiro; Nishimoto, Koji; Mori, Kazutaka; Kono, Masato; Fujisawa, Tomoyuki; Enomoto, Noriyuki; Nakamura, Yutaro; Iwashita, Toshihide; Suda, Takafumi

2016-12-01

Previous studies have reported that patients with idiopathic pulmonary fibrosis occasionally develop lung cancer (LC). However, in connective tissue disease (CTD)-related interstitial lung disease (ILD), there are few data regarding the LC development. The aim of the present study was to evaluate the clinical significance of LC development in patients with CTD-ILD. A retrospective review of our database of 562 patients with ILD between 2000 and 2014 identified 127 patients diagnosed with CTD-ILD. The overall and cumulative incidences of LC were calculated. In addition, the risk factors and prognostic impact of LC development were evaluated. The median age at the ILD diagnosis was 63 years (range 37-84 years), and 73 patients (57.5%) were female. The median follow-up period from the ILD diagnosis was 67.4 months (range 10.4-322.1 months). During the period, 7 out of the 127 patients developed LC (overall incidence 5.5%). The cumulative incidences at 1, 3, and 5 years were 0.0%, 1.8%, and 2.9%, respectively. The risk of LC development was significantly higher in patients with higher smoking pack-year (odds ratio [OR] 1.028; 95% confidence interval [CI] 1.008-1.049; P = 0.007) and emphysema on chest high-resolution computed tomography (OR 14.667; 95% CI 2.871-74.926; P = 0.001). The median overall survival time after developing LC was 7.0 months (95% CI 4.9-9.1 months), and the most common cause of death was LC, not ILD. According to the Cox proportional hazard model analysis with time-dependent covariates, patients who developed LC showed significantly poorer prognosis than those who did not (hazard ratio 87.86; 95% CI 19.56-394.67; P < 0.001). In CTD-ILD, clinicians should be careful with the risk of LC development in patients with a heavy smoking history and subsequent emphysema. Although not so frequent, the complication could be a poor prognostic determinant.

Rapid fall in lung density following smoking cessation in COPD

DEFF Research Database (Denmark)

Shaker, Saher B; Stavngaard, Trine; Laursen, Lars Christian

2011-01-01

Whether smoking-induced lung inflammation subsides after smoking cessation is currently a matter of debate. We used computed tomography (CT) to evaluate the effect of smoking cessation on lung density in patients with COPD.......Whether smoking-induced lung inflammation subsides after smoking cessation is currently a matter of debate. We used computed tomography (CT) to evaluate the effect of smoking cessation on lung density in patients with COPD....

Endoplasmic reticulum stress in lung disease

Directory of Open Access Journals (Sweden)

Stefan J. Marciniak

2017-06-01

Full Text Available Exposure to inhaled pollutants, including fine particulates and cigarette smoke is a major cause of lung disease in Europe. While it is established that inhaled pollutants have devastating effects on the genome, it is now recognised that additional effects on protein folding also drive the development of lung disease. Protein misfolding in the endoplasmic reticulum affects the pathogenesis of many diseases, ranging from pulmonary fibrosis to cancer. It is therefore important to understand how cells respond to endoplasmic reticulum stress and how this affects pulmonary tissues in disease. These insights may offer opportunities to manipulate such endoplasmic reticulum stress pathways and thereby cure lung disease.

Cigarettes, lung cancer, and coronary heart disease: the effects of inhalation and tar yield.

Science.gov (United States)

Higenbottam, T; Shipley, M J; Rose, G

1982-06-01

Ten-year mortality rates for lung cancer and coronary heart disease have been related to cigarette smoking habits in 17 475 male civil servants aged 40-64 and in sample of 8089 male British residents aged 35-69. Both diseases were more frequent in smokers. Lung cancer rates were higher overall for "non-inhalers", particularly in heavy smokers. Tar yield correlated with the risk of lung cancer in non-inhalers but less so in inhalers. Conversely, coronary deaths were more common among inhalers, and the effect of tar/nicotine yield (such as it was) was confined to inhalers. It appears that there are subtle interactions between the amount smoked, the tar/nicotine yield of the cigarette, and the style of smoking. Thus the effects of a change in cigarette characteristics are hard to predict, and they may be different for respiratory and cardiovascular disease.

IgG4-related lung disease presenting as interstitial lung disease with bronchiolitis: A case report.

Science.gov (United States)

Chen, Chiu-Fan; Chu, Kuo-An; Tseng, Yen-Chiang; Wu, Chang-Che; Lai, Ruay-Sheng

2017-12-01

IgG4-related disease is a rare and novel disease entity that tends to involve multiple organs. The pulmonary manifestation of this disease is highly variable and may mimic lung cancer, pneumonia, interstitial lung disease (ILD), sarcoidosis, and so forth. Small airway disease is rarely reported in IgG4-related lung disease (IgG4-RLD). In the current study, we describe a rare case of IgG4-RLD with patterns of ILD and bronchiolitis. A 43-year-old man had chronic cough and dyspnea on exertion for 4 years. Initial chest radiography showed diffuse interstitial infiltration. Follow-up chest computed tomography 4 years later revealed bilateral diffuse centrilobular nodules with tree-in-bud pattern, bronchial wall thickening, and mediastinal lymph nodes. Bilateral diffuse multifocal ground-glass opacities and mosaic attenuation were also observed. Pulmonary function test revealed mixed restrictive and obstructive ventilatory impairment. Video-assisted thoracoscopic surgery (VATS) lung biopsy showed interstitial fibrosis with lymphoplasmacytic infiltration rich in IgG4-positive plasma cells. Serum IgG4 level also showed remarkable elevation. Therefore, IgG4-RLD is confirmed. VATS wedge resection of right upper lobe and mediastinal lymph node. The patient responded well to steroid and immunosuppression therapy, and was regular followed-up in outpatient clinic. IgG4-RLD should be considered not only in ILD, but also in small airway disease. Serum IgG4 level may be a useful tool for screening.

Cannabis smoking and lung cancer risk: Pooled analysis in the International Lung Cancer Consortium

OpenAIRE

Zhang, L.R.; Morgenstern, H.; Greenland, S.; Chang, S.C.; Lazarus, P.; Teare, M.D.; Woll, P.J.; Orlow, I.; Cox, B.; Brhane, Y.; Liu, G.; Hung, R.J.

2015-01-01

To investigate the association between cannabis smoking and lung cancer risk, data on 2,159 lung cancer cases and 2,985 controls were pooled from 6 case-control studies in the US, Canada, UK, and New Zealand within the International Lung Cancer Consortium. Study-specific associations between cannabis smoking and lung cancer were estimated using unconditional logistic regression adjusting for sociodemographic factors, tobacco smoking status and pack-years; odds-ratio estimates were pooled usin...

Exploring smoking, mental health and smoking-related disease in a nationally representative sample of older adults in Ireland - A retrospective secondary analysis.

Science.gov (United States)

Burns, Annette; Strawbridge, Judith D; Clancy, Luke; Doyle, Frank

2017-07-01

Smoking is the leading preventable cause of death among individuals with mental health difficulties (MHD). The aim of the current study was to determine the impact of smoking on the physical health of older adults with MHD in Ireland and to explore the extent to which smoking mediated or moderated associations between MHD and smoking-related diseases. Cross-sectional analysis of a nationally representative sample of 8175 community-dwelling adults aged 50 and over from The Irish Longitudinal Study on Ageing (TILDA) was undertaken. Multivariate adjusted logistic regression models were used to assess the association between MHD, smoking (current/past/never) and smoking-related diseases (respiratory disease, cardiovascular disease, smoking-related cancers). A number of variables were employed to identify individuals with MHD, including prescribed medication, self-reported diagnoses and self-report scales. MHD was associated with current (RRRs ranging from 1.84 [1.50 to 2.26] to 4.31 [2.47 to 7.53]) and former (RRRs ranging from 1.26 [1.05 to 1.52] to 1.99 [1.19 to 3.33]) smoking and also associated with the presence of smoking-related disease (ORs ranging from 1.24 [1.01 to 1.51] to 1.62 [1.00 to 2.62]). Smoking did not mediate and rarely moderated associations between MHD and smoking-related disease. Older adults in Ireland with MHD are more likely to smoke than those without such difficulties. They also experience higher rates of smoking-related disease, although smoking had no mediating and no consistent moderating role in these analyses. Findings underscore the need for attention to the physical health of those with MHD including support in smoking cessation. Copyright © 2017 Elsevier Inc. All rights reserved.

Exposure to secondhand tobacco smoke and lung cancer by histological type: a pooled analysis of the International Lung Cancer Consortium (ILCCO)

Science.gov (United States)

Kim, Claire H; Lee, Yuan-Chin Amy; Hung, Rayjean J; McNallan, Sheila R; Cote, Michele L; Lim, Wei-Yen; Chang, Shen-Chih; Kim, Jin Hee; Ugolini, Donatella; Chen, Ying; Liloglou, Triantafillos; Andrew, Angeline S; Onega, Tracy; Duell, Eric J; Field, John K; Lazarus, Philip; Le Marchand, Loic; Neri, Monica; Vineis, Paolo; Kiyohara, Chikako; Hong, Yun-Chul; Morgenstern, Hal; Matsuo, Keitaro; Tajima, Kazuo; Christiani, David C; McLaughlin, John R; Bencko, Vladimir; Holcatova, Ivana; Boffetta, Paolo; Brennan, Paul; Fabianova, Eleonora; Foretova, Lenka; Janout, Vladimir; Lissowska, Jolanta; Mates, Dana; Rudnai, Peter; Szeszenia-Dabrowska, Neonila; Mukeria, Anush; Zaridze, David; Seow, Adeline; Schwartz, Ann G; Yang, Ping; Zhang, Zuo-Feng

2014-01-01

While the association between exposure to secondhand smoke and lung cancer risk is well established, few studies with sufficient power have examined the association by histological type. In this study, we evaluated the secondhand smoke-lung cancer relationship by histological type based on pooled data from 18 case-control studies in the International Lung Cancer Consortium (ILCCO), including 2,504 cases and 7,276 controls who were never smokers and 10,184 cases and 7,176 controls who were ever smokers. We used multivariable logistic regression, adjusting for age, sex, race/ethnicity, smoking status, pack-years of smoking, and study. Among never smokers, the odds ratios (OR) comparing those ever exposed to secondhand smoke with those never exposed were 1.31 (95% CI: 1.17–1.45) for all histological types combined, 1.26 (95% CI: 1.10–1.44) for adenocarcinoma, 1.41 (95% CI: 0.99–1.99) for squamous cell carcinoma, 1.48 (95% CI: 0.89–2.45) for large cell lung cancer, and 3.09 (95% CI: 1.62–5.89) for small cell lung cancer. The estimated association with secondhand smoke exposure was greater for small cell lung cancer than for non-small cell lung cancers (OR=2.11, 95% CI: 1.11–4.04). This analysis is the largest to date investigating the relation between exposure to secondhand smoke and lung cancer. Our study provides more precise estimates of the impact of secondhand smoke on the major histological types of lung cancer, indicates the association with secondhand smoke is stronger for small cell lung cancer than for the other histological types, and suggests the importance of intervention against exposure to secondhand smoke in lung cancer prevention. PMID:24615328

Exposure to secondhand tobacco smoke and lung cancer by histological type: a pooled analysis of the International Lung Cancer Consortium (ILCCO).

Science.gov (United States)

Kim, Claire H; Lee, Yuan-Chin Amy; Hung, Rayjean J; McNallan, Sheila R; Cote, Michele L; Lim, Wei-Yen; Chang, Shen-Chih; Kim, Jin Hee; Ugolini, Donatella; Chen, Ying; Liloglou, Triantafillos; Andrew, Angeline S; Onega, Tracy; Duell, Eric J; Field, John K; Lazarus, Philip; Le Marchand, Loic; Neri, Monica; Vineis, Paolo; Kiyohara, Chikako; Hong, Yun-Chul; Morgenstern, Hal; Matsuo, Keitaro; Tajima, Kazuo; Christiani, David C; McLaughlin, John R; Bencko, Vladimir; Holcatova, Ivana; Boffetta, Paolo; Brennan, Paul; Fabianova, Eleonora; Foretova, Lenka; Janout, Vladimir; Lissowska, Jolanta; Mates, Dana; Rudnai, Peter; Szeszenia-Dabrowska, Neonila; Mukeria, Anush; Zaridze, David; Seow, Adeline; Schwartz, Ann G; Yang, Ping; Zhang, Zuo-Feng

2014-10-15

While the association between exposure to secondhand smoke and lung cancer risk is well established, few studies with sufficient power have examined the association by histological type. In this study, we evaluated the secondhand smoke-lung cancer relationship by histological type based on pooled data from 18 case-control studies in the International Lung Cancer Consortium (ILCCO), including 2,504 cases and 7,276 control who were never smokers and 10,184 cases and 7,176 controls who were ever smokers. We used multivariable logistic regression, adjusting for age, sex, race/ethnicity, smoking status, pack-years of smoking, and study. Among never smokers, the odds ratios (OR) comparing those ever exposed to secondhand smoke with those never exposed were 1.31 (95% CI: 1.17-1.45) for all histological types combined, 1.26 (95% CI: 1.10-1.44) for adenocarcinoma, 1.41 (95% CI: 0.99-1.99) for squamous cell carcinoma, 1.48 (95% CI: 0.89-2.45) for large cell lung cancer, and 3.09 (95% CI: 1.62-5.89) for small cell lung cancer. The estimated association with secondhand smoke exposure was greater for small cell lung cancer than for nonsmall cell lung cancers (OR=2.11, 95% CI: 1.11-4.04). This analysis is the largest to date investigating the relation between exposure to secondhand smoke and lung cancer. Our study provides more precise estimates of the impact of secondhand smoke on the major histological types of lung cancer, indicates the association with secondhand smoke is stronger for small cell lung cancer than for the other histological types, and suggests the importance of intervention against exposure to secondhand smoke in lung cancer prevention. © 2014 UICC.

Lung cancer in never smokers: disease characteristics and risk factors.

Science.gov (United States)

Pallis, Athanasios G; Syrigos, Konstantinos N

2013-12-01

It is estimated that approximately 25% of all lung cancer cases are observed in never-smokers and its incidence is expected to increase due to smoking prevention programs. Risk factors for the development of lung cancer described include second-hand smoking, radon exposure, occupational exposure to carcinogens and to cooking oil fumes and indoor coal burning. Other factors reported are infections (HPV and Mycobacterium tuberculosis), hormonal and diatery factors and diabetes mellitus. Having an affected relative also increases the risk for lung cancer while recent studies have identified several single nucleotide polymorphisms associated with increased risk for lung cancer development in never smokers. Distinct clinical, pathology and molecular characteristics are observed in lung cancer in never smokers; more frequently is observed in females and adenocarcinoma is the predominant histology while it has a different pattern of molecular alterations. The purpose of this review is to summarize our current knowledge of this disease. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

Resolvin D1 prevents smoking-induced emphysema and promotes lung tissue regeneration.

Science.gov (United States)

Kim, Kang-Hyun; Park, Tai Sun; Kim, You-Sun; Lee, Jae Seung; Oh, Yeon-Mok; Lee, Sang-Do; Lee, Sei Won

2016-01-01

Emphysema is an irreversible disease that is characterized by destruction of lung tissue as a result of inflammation caused by smoking. Resolvin D1 (RvD1), derived from docosahexaenoic acid, is a novel lipid that resolves inflammation. The present study tested whether RvD1 prevents smoking-induced emphysema and promotes lung tissue regeneration. C57BL/6 mice, 8 weeks of age, were randomly divided into four groups: control, RvD1 only, smoking only, and smoking with RvD1 administration. Four different protocols were used to induce emphysema and administer RvD1: mice were exposed to smoking for 4 weeks with poly(I:C) or to smoking only for 24 weeks, and RvD1 was injected within the smoking exposure period to prevent regeneration or after completion of smoking exposure to assess regeneration. The mean linear intercept and inflammation scores were measured in the lung tissue, and inflammatory cells and cytokines were measured in the bronchoalveolar lavage fluid. Measurements of mean linear intercept showed that RvD1 significantly attenuated smoking-induced lung destruction in all emphysema models. RvD1 also reduced smoking-induced inflammatory cell infiltration, which causes the structural derangements observed in emphysema. In the 4-week prevention model, RvD1 reduced the smoking-induced increase in eosinophils and interleukin-6 in the bronchoalveolar lavage fluid. In the 24-week prevention model, RvD1 also reduced the increased neutrophils and total cell counts induced by smoking. RvD1 attenuated smoking-induced emphysema in vivo by reducing inflammation and promoting tissue regeneration. This result suggests that RvD1 may be useful in the prevention and treatment of emphysema.

Is Previous Respiratory Disease a Risk Factor for Lung Cancer?

Science.gov (United States)

Denholm, Rachel; Schüz, Joachim; Straif, Kurt; Stücker, Isabelle; Jöckel, Karl-Heinz; Brenner, Darren R.; De Matteis, Sara; Boffetta, Paolo; Guida, Florence; Brüske, Irene; Wichmann, Heinz-Erich; Landi, Maria Teresa; Caporaso, Neil; Siemiatycki, Jack; Ahrens, Wolfgang; Pohlabeln, Hermann; Zaridze, David; Field, John K.; McLaughlin, John; Demers, Paul; Szeszenia-Dabrowska, Neonila; Lissowska, Jolanta; Rudnai, Peter; Fabianova, Eleonora; Dumitru, Rodica Stanescu; Bencko, Vladimir; Foretova, Lenka; Janout, Vladimir; Kendzia, Benjamin; Peters, Susan; Behrens, Thomas; Vermeulen, Roel; Brüning, Thomas; Kromhout, Hans

2014-01-01

Rationale: Previous respiratory diseases have been associated with increased risk of lung cancer. Respiratory conditions often co-occur and few studies have investigated multiple conditions simultaneously. Objectives: Investigate lung cancer risk associated with chronic bronchitis, emphysema, tuberculosis, pneumonia, and asthma. Methods: The SYNERGY project pooled information on previous respiratory diseases from 12,739 case subjects and 14,945 control subjects from 7 case–control studies conducted in Europe and Canada. Multivariate logistic regression models were used to investigate the relationship between individual diseases adjusting for co-occurring conditions, and patterns of respiratory disease diagnoses and lung cancer. Analyses were stratified by sex, and adjusted for age, center, ever-employed in a high-risk occupation, education, smoking status, cigarette pack-years, and time since quitting smoking. Measurements and Main Results: Chronic bronchitis and emphysema were positively associated with lung cancer, after accounting for other respiratory diseases and smoking (e.g., in men: odds ratio [OR], 1.33; 95% confidence interval [CI], 1.20–1.48 and OR, 1.50; 95% CI, 1.21–1.87, respectively). A positive relationship was observed between lung cancer and pneumonia diagnosed 2 years or less before lung cancer (OR, 3.31; 95% CI, 2.33–4.70 for men), but not longer. Co-occurrence of chronic bronchitis and emphysema and/or pneumonia had a stronger positive association with lung cancer than chronic bronchitis “only.” Asthma had an inverse association with lung cancer, the association being stronger with an asthma diagnosis 5 years or more before lung cancer compared with shorter. Conclusions: Findings from this large international case–control consortium indicate that after accounting for co-occurring respiratory diseases, chronic bronchitis and emphysema continue to have a positive association with lung cancer. PMID:25054566

Smoking is Associated with Higher Disease-related Costs and Lower Health-related Quality of Life in Inflammatory Bowel Disease

NARCIS (Netherlands)

Severs, M.; Mangen, M.J.; Valk, M.E. van der; Fidder, H.H.; Dijkstra, G.; Have, M. van der; Bodegraven, A.A. van; Jong, D.J. de; Woude, C.J. van der; Romberg-Camps, M.J.; Clemens, C.H.; Jansen, J.M.; Meeberg, P.C. van de; Mahmmod, N.; Ponsioen, C.Y.; Vermeijden, J.R.; Jong, A E F de; Pierik, M.; Siersema, P.D.; Oldenburg, B.

2017-01-01

Background and Aims: Smoking affects the course of inflammatory bowel disease [IBD]. We aimed to study the impact of smoking on IBD-specific costs and health-related quality-of-life [HrQoL] among adults with Crohn's disease [CD] and ulcerative colitis [UC]. Methods: A large cohort of IBD patients

Chronic cigarette smoke exposure adversely alters 14C-arachidonic acid metabolism in rat lungs, aortas and platelets

International Nuclear Information System (INIS)

Lubawy, W.C.; Valentovic, M.A.; Atkinson, J.E.; Gairola, G.C.

1983-01-01

Male rats were exposed to freshly generated cigarette smoke once daily, 5 times a week for 10 weeks. Inhalation of smoke was verified by elevated carboxyhemoglobin in blood sampled immediately after smoke exposure and by increased lung aryl hydrocarbon hydroxylase activity 24 hours after the last smoke exposure. Aortic rings isolated from smoke-exposed rats synthesized less prostacyclin (PGI2) from 14 C-arachidonic acid than rings from sham rats. Platelets from smoke-exposed rats synthesized more thromboxane (TXA2) from 14 C-arachidonic acid than platelets from room controls but not those from sham rats. Lung microsomes from smoke-exposed rats synthesized more TXA2 and had a lower PGI2/TXA2 ratio than lung microsomes from room controls and shams. It is concluded that chronic cigarette smoke exposure alters arachidonic acid metabolism in aortas, platelets and lungs in a manner resulting in decreased PGI2 and increased TXA2, thereby creating a condition favoring platelet aggregation and a variety of cardiovascular diseases

Gender difference in smoking effects on lung function and risk of hospitalization for COPD

DEFF Research Database (Denmark)

Prescott, E; Bjerg, A M; Andersen, P K

1997-01-01

Recent findings suggest that females may be more susceptible than males to the deleterious influence of tobacco smoking in developing chronic obstructive pulmonary disease (COPD). This paper studies the interaction of gender and smoking on development of COPD as assessed by lung function and hosp......Recent findings suggest that females may be more susceptible than males to the deleterious influence of tobacco smoking in developing chronic obstructive pulmonary disease (COPD). This paper studies the interaction of gender and smoking on development of COPD as assessed by lung function.......7-50.9) in females, and 3.2 (1.1-9.1), 5.7 (2.2-14.3) and 8.4 (3.3-21.6) in males) but the interaction term gender x pack-years did not reach significance (p=0.08). Results were similar in the GPS. After adjusting for smoking in more detail, females in both cohorts had an increased risk of hospitalization for COPD...

Enhancement of lung cancer by cigarette smoking in uranium and other miners

International Nuclear Information System (INIS)

Archer, V.E.

1985-01-01

There are substantial animal and epidemiological data related to cigarette smoking and lung cancer among miners exposed to elevated levels of radon daughters that appears to be in disagreement. An hypothesis is advanced that explains most of this disagreement as being derived from temporal differences of cancer expression. The hypothesis is that a given radiation exposure induced a finite number of lung cancers, which have shorter latent periods due to the cancer promotion activity of smoke among cigarette smokers. According to this hypothesis, the life-shortening effect is greater among smoking miners than nonsmoking miners, and the ultimate number of lung cancers among smoking miners will be only a little larger than among nonsmokers. The greater number will derive from the additive effect of radiation and smoking, plus the greater force of competing causes of death among elderly nonsmokers

Cystic lung disease: Achieving a radiologic diagnosis

Energy Technology Data Exchange (ETDEWEB)

Trotman-Dickenson, Beatrice, E-mail: btrotmandickenson@partners.org

2014-01-15

Diffuse cystic lung disease represents a diverse group of uncommon disorders with characteristic appearance on high resolution CT imaging. The combination of imaging appearance with clinical features and genetic testing where appropriate permits a confident and accurate diagnosis in the majority of the diseases without recourse for open lung biopsy. The mechanism of cyst development disease is unclear but in some disorders appears to be related to small airways obstruction. These diseases are incurable, with the exception of Langerhans cell histiocytosis which may spontaneously remit or resolve on smoking cessation. Disease progression is unpredictable; in general older patients have a more benign disease, while young patients may progress rapidly to respiratory failure. An understanding of the complications of cystic lung disease and the appearance of disease progression is essential for the management of these patients. A number of these disorders are associated with malignancy, recognition of the potential tumors permits appropriate imaging surveillance. Due to the widespread use of CT, pulmonary cysts are increasingly discovered incidentally in an asymptomatic individual. The diagnostic challenge is to determine whether these cysts represent an early feature of a progressive disease or have no clinical significance. In the elderly population the cysts are unlikely to represent a progressive disease. In individuals <50 years further evaluation is recommended.

Cystic lung disease: Achieving a radiologic diagnosis

International Nuclear Information System (INIS)

Trotman-Dickenson, Beatrice

2014-01-01

Diffuse cystic lung disease represents a diverse group of uncommon disorders with characteristic appearance on high resolution CT imaging. The combination of imaging appearance with clinical features and genetic testing where appropriate permits a confident and accurate diagnosis in the majority of the diseases without recourse for open lung biopsy. The mechanism of cyst development disease is unclear but in some disorders appears to be related to small airways obstruction. These diseases are incurable, with the exception of Langerhans cell histiocytosis which may spontaneously remit or resolve on smoking cessation. Disease progression is unpredictable; in general older patients have a more benign disease, while young patients may progress rapidly to respiratory failure. An understanding of the complications of cystic lung disease and the appearance of disease progression is essential for the management of these patients. A number of these disorders are associated with malignancy, recognition of the potential tumors permits appropriate imaging surveillance. Due to the widespread use of CT, pulmonary cysts are increasingly discovered incidentally in an asymptomatic individual. The diagnostic challenge is to determine whether these cysts represent an early feature of a progressive disease or have no clinical significance. In the elderly population the cysts are unlikely to represent a progressive disease. In individuals <50 years further evaluation is recommended

Cigarette smoking and risk of lung metastasis from esophageal cancer.

Science.gov (United States)

Abrams, Julian A; Lee, Paul C; Port, Jeffrey L; Altorki, Nasser K; Neugut, Alfred I

2008-10-01

Whereas extensive research has explored the effect of environmental factors on the etiology of specific cancers, the influence of exposures such as smoking on risk of site-specific metastasis is unknown. We investigated the association of cigarette smoking with lung metastasis in esophageal cancer. We conducted a case-control study of esophageal cancer patients from two centers, comparing cases with lung metastases to controls without lung metastases. Information was gathered from medical records on smoking history, imaging results, site(s) of metastasis, and other patient and tumor characteristics. We used logistic regression to assess association. We identified 354 esophageal cancer cases; smoking status was known in 289 (82%). Among patients with lung metastases, 73.6% (39 of 53) were ever smokers, versus 47.8% (144 of 301) of patients without lung metastases [P=0.001; summary odds ratio (OR), 2.52; 95% confidence interval (95% CI), 1.17-5.45; stratified by histology]. Smoking was associated with a nonsignificant increased adjusted odds of lung metastasis (OR, 1.89; 95% CI, 0.80-4.46). Upper esophageal subsite (OR, 4.71; 95% CI, 1.20-18.5), but not histology (squamous OR 0.65,95% CI 0.27-1.60), was associated with lung metastasis. Compared with the combined never/unknown smoking status group, smoking was associated with a significantly increased odds of lung metastasis (OR, 2.35; 95% CI, 1.11-4.97). There was no association between liver metastasis and smoking (OR, 0.88; 95% CI, 0.42-1.83). Smoking is associated with increased odds of lung metastasis from esophageal cancer, and this relationship seems to be site specific. Future studies are needed to determine whether smoking affects the tumor cell or the site of metastasis, and whether this changes the survival outcome.

Smoking cessation results in a clinical lung cancer screening program.

Science.gov (United States)

Borondy Kitts, Andrea K; McKee, Andrea B; Regis, Shawn M; Wald, Christoph; Flacke, Sebastian; McKee, Brady J

2016-07-01

Lung cancer screening may provide a "teachable moment" for promoting smoking cessation. This study assessed smoking cessation and relapse rates among individuals undergoing follow-up low-dose chest computed tomography (CT) in a clinical CT lung screening program and assessed the influence of initial screening results on smoking behavior. Self-reported smoking status for individuals enrolled in a clinical CT lung screening program undergoing a follow-up CT lung screening exam between 1st February, 2014 and 31st March, 2015 was retrospectively reviewed and compared to self-reported smoking status using a standardized questionnaire at program entry. Point prevalence smoking cessation and relapse rates were calculated across the entire population and compared with exam results. All individuals undergoing screening fulfilled the National Comprehensive Cancer Network Clinical Practice Guidelines in Oncology: Lung Cancer Screening v1.2012(®) high-risk criteria and had an order for CT lung screening. A total of 1,483 individuals underwent a follow-up CT lung screening exam during the study interval. Smoking status at time of follow-up exam was available for 1,461/1,483 (98.5%). A total of 46% (678/1,461) were active smokers at program entry. The overall point prevalence smoking cessation and relapse rates were 20.8% and 9.3%, respectively. Prior positive screening exam results were not predictive of smoking cessation (OR 1.092; 95% CI, 0.715-1.693) but were predictive of reduced relapse among former smokers who had stopped smoking for 2 years or less (OR 0.330; 95% CI, 0.143-0.710). Duration of program enrollment was predictive of smoking cessation (OR 0.647; 95% CI, 0.477-0.877). Smoking cessation and relapse rates in a clinical CT lung screening program rates are more favorable than those observed in the general population. Duration of participation in the screening program correlated with increased smoking cessation rates. A positive exam result correlated with reduced

Collagenolytic Matrix Metalloproteinases in Chronic Obstructive Lung Disease and Cancer

Energy Technology Data Exchange (ETDEWEB)

Woode, Denzel; Shiomi, Takayuki; D’Armiento, Jeanine, E-mail: jmd12@cumc.columbia.edu [Department of Anesthesiology, Columbia University, College of Physicians and Surgeons, New York, NY 10033 (United States)

2015-02-05

Chronic obstructive pulmonary disease (COPD) and lung cancer result in significant morbidity and mortality worldwide. In addition to the role of environmental smoke exposure in the development of both diseases, recent epidemiological studies suggests a connection between the development of COPD and lung cancer. Furthermore, individuals with concomitant COPD and cancer have a poor prognosis when compared with individuals with lung cancer alone. The modulation of molecular pathways activated during emphysema likely lead to an increased susceptibility to lung tumor growth and metastasis. This review summarizes what is known in the literature examining the molecular pathways affecting matrix metalloproteinases (MMPs) in this process as well as external factors such as smoke exposure that have an impact on tumor growth and metastasis. Increased expression of MMPs provides a unifying link between lung cancer and COPD.

Collagenolytic Matrix Metalloproteinases in Chronic Obstructive Lung Disease and Cancer

International Nuclear Information System (INIS)

Woode, Denzel; Shiomi, Takayuki; D’Armiento, Jeanine

2015-01-01

Chronic obstructive pulmonary disease (COPD) and lung cancer result in significant morbidity and mortality worldwide. In addition to the role of environmental smoke exposure in the development of both diseases, recent epidemiological studies suggests a connection between the development of COPD and lung cancer. Furthermore, individuals with concomitant COPD and cancer have a poor prognosis when compared with individuals with lung cancer alone. The modulation of molecular pathways activated during emphysema likely lead to an increased susceptibility to lung tumor growth and metastasis. This review summarizes what is known in the literature examining the molecular pathways affecting matrix metalloproteinases (MMPs) in this process as well as external factors such as smoke exposure that have an impact on tumor growth and metastasis. Increased expression of MMPs provides a unifying link between lung cancer and COPD

Ascorbate attenuates pulmonary emphysema by inhibiting tobacco smoke and Rtp801-triggered lung protein modification and proteolysis.

Science.gov (United States)

Gupta, Indranil; Ganguly, Souradipta; Rozanas, Christine R; Stuehr, Dennis J; Panda, Koustubh

2016-07-19

Cigarette smoking causes emphysema, a fatal disease involving extensive structural and functional damage of the lung. Using a guinea pig model and human lung cells, we show that oxidant(s) present in tobacco smoke not only cause direct oxidative damage of lung proteins, contributing to the major share of lung injury, but also activate Rtp801, a key proinflammatory cellular factor involved in tobacco smoke-induced lung damage. Rtp801 triggers nuclear factor κB and consequent inducible NOS (iNOS)-mediated overproduction of NO, which in combination with excess superoxide produced during Rtp801 activation, contribute to increased oxido-nitrosative stress and lung protein nitration. However, lung-specific inhibition of iNOS with a iNOS-specific inhibitor, N6-(1-iminoethyl)-L-lysine, dihydrochloride (L-NIL) solely restricts lung protein nitration but fails to prevent or reverse the major tobacco smoke-induced oxidative lung injury. In comparison, the dietary antioxidant, ascorbate or vitamin C, can substantially prevent such damage by inhibiting both tobacco smoke-induced lung protein oxidation as well as activation of pulmonary Rtp801 and consequent iNOS/NO-induced nitration of lung proteins, that otherwise lead to increased proteolysis of such oxidized or nitrated proteins by endogenous lung proteases, resulting in emphysematous lung damage. Vitamin C also restricts the up-regulation of matrix-metalloproteinase-9, the major lung protease involved in the proteolysis of such modified lung proteins during tobacco smoke-induced emphysema. Overall, our findings implicate tobacco-smoke oxidant(s) as the primary etiopathogenic factor behind both the noncellular and cellular damage mechanisms governing emphysematous lung injury and demonstrate the potential of vitamin C to accomplish holistic prevention of such damage.

'Biomass lung': primitive biomass combustion and lung disease

International Nuclear Information System (INIS)

Baris, Y. I.; Seyfikli, Z.; Demir, A.; Hoskins, J. A.

2002-01-01

Domestic burning of biomass fuel is one of the most important risk factors for the development of respiratory diseases and infant mortality. The fuel which causes the highest level of disease is dung. In the rural areas of developing countries some 80% of households rely on biomass fuels for cooking and often heating as well and so suffer high indoor air pollution. Even when the fire or stove is outside the home those near it are still exposed to the smoke. In areas where the winters are long and cold the problem is aggravated since the fire or stove is indoors for many months of the year. The consequence of biomass burning is a level of morbidity in those exposed to the smoke as well as mortality. The rural areas of Turkey are among many in the world where biomass is the major fuel source. In this case report 8 patients from rural areas, particularly Anatolia, who used biomass are presented. Many of these are non-smoking, female patients who have respiratory complaints and a clinical picture of the chronic lung diseases which would have been expected if they had been heavy smokers. Typically patients cook on the traditional 'tandir' stove using dung and crop residues as the fuel. Ventilation systems are poor and they are exposed to a high level of smoke pollution leading to cough and dyspnoea. Anthracosis is a common outcome of this level of exposure and several of the patients developed lung tumours. The findings from clinical examination of 8 of these patients (2 M, 6 F) are presented together with their outcome where known. (author)

Primary Care Provider-Delivered Smoking Cessation Interventions and Smoking Cessation Among Participants in the National Lung Screening Trial.

Science.gov (United States)

Park, Elyse R; Gareen, Ilana F; Japuntich, Sandra; Lennes, Inga; Hyland, Kelly; DeMello, Sarah; Sicks, JoRean D; Rigotti, Nancy A

2015-09-01

The National Lung Screening Trial (NLST) found a reduction in lung cancer mortality among participants screened with low-dose computed tomography vs chest radiography. In February 2015, Medicare announced its decision to cover annual lung screening for patients with a significant smoking history. These guidelines promote smoking cessation treatment as an adjunct to screening, but the frequency and effectiveness of clinician-delivered smoking cessation interventions delivered after lung screening are unknown. To determine the association between the reported clinician-delivered 5As (ask, advise, assess, assist [talk about quitting or recommend stop-smoking medications or recommend counseling], and arrange follow-up) after lung screening and smoking behavior changes. A matched case-control study (cases were quitters and controls were continued smokers) of 3336 NLST participants who were smokers at enrollment examined participants' rates and patterns of 5A delivery after a lung screen and reported smoking cessation behaviors. Prevalence of the clinician-delivered 5As and associated smoking cessation after lung screening. Delivery of the 5As 1 year after screening were as follows: ask, 77.2%; advise, 75.6%; assess, 63.4%; assist, 56.4%; and arrange follow-up, 10.4%. Receipt of ask, advise, and assess was not significantly associated with quitting in multivariate models that adjusted for sociodemographic characteristics, medical history, screening results, nicotine dependence, and motivation to quit. Assist was associated with a 40% increase in the odds of quitting (odds ratio, 1.40; 95% CI, 1.21-1.63), and arrange was associated with a 46% increase in the odds of quitting (odds ratio, 1.46; 95% CI, 1.19-1.79). Assist and arrange follow-up delivered by primary care providers to smokers who were participating in the NLST were associated with increased quitting; less intensive interventions (ask, advise, and assess) were not. However, rates of assist and arrange

Genetic ancestry-smoking interactions and lung function in African Americans: a cohort study.

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Melinda C Aldrich

Full Text Available BACKGROUND: Smoking tobacco reduces lung function. African Americans have both lower lung function and decreased metabolism of tobacco smoke compared to European Americans. African ancestry is also associated with lower pulmonary function in African Americans. We aimed to determine whether African ancestry modifies the association between smoking and lung function and its rate of decline in African Americans. METHODOLOGY/PRINCIPAL FINDINGS: We evaluated a prospective ongoing cohort of 1,281 African Americans participating in the Health, Aging, and Body Composition (Health ABC Study initiated in 1997. We also examined an ongoing prospective cohort initiated in 1985 of 1,223 African Americans in the Coronary Artery Disease in Young Adults (CARDIA Study. Pulmonary function and tobacco smoking exposure were measured at baseline and repeatedly over the follow-up period. Individual genetic ancestry proportions were estimated using ancestry informative markers selected to distinguish European and West African ancestry. African Americans with a high proportion of African ancestry had lower baseline forced expiratory volume in one second (FEV₁ per pack-year of smoking (-5.7 ml FEV₁/ smoking pack-year compared with smokers with lower African ancestry (-4.6 ml in FEV₁/ smoking pack-year (interaction P value  = 0.17. Longitudinal analyses revealed a suggestive interaction between smoking, and African ancestry on the rate of FEV(1 decline in Health ABC and independently replicated in CARDIA. CONCLUSIONS/SIGNIFICANCE: African American individuals with a high proportion of African ancestry are at greater risk for losing lung function while smoking.

“Lung age” - a motivational smoking cessation tool in smokers with chronic obstructive pulmonary disease

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Antigona Trofor

2018-03-01

“Lung age” measurement, used together with lung function and exhaled CO testing, adds value to proving impact of tobacco exposure on COPD patients and helps increasing motivation to quit smoking in this difficult to treat category of patients.

Rapid fall in lung density following smoking cessation in COPD

DEFF Research Database (Denmark)

Shaker, Saher B; Stavngaard, Trine; Laursen, Lars Christian

2011-01-01

Whether smoking-induced lung inflammation subsides after smoking cessation is currently a matter of debate. We used computed tomography (CT) to evaluate the effect of smoking cessation on lung density in patients with COPD....

Collagenolytic Matrix Metalloproteinases in Chronic Obstructive Lung Disease and Cancer

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Denzel Woode

2015-02-01

Full Text Available Chronic obstructive pulmonary disease (COPD and lung cancer result in significant morbidity and mortality worldwide. In addition to the role of environmental smoke exposure in the development of both diseases, recent epidemiological studies suggests a connection between the development of COPD and lung cancer. Furthermore, individuals with concomitant COPD and cancer have a poor prognosis when compared with individuals with lung cancer alone. The modulation of molecular pathways activated during emphysema likely lead to an increased susceptibility to lung tumor growth and metastasis. This review summarizes what is known in the literature examining the molecular pathways affecting matrix metalloproteinases (MMPs in this process as well as external factors such as smoke exposure that have an impact on tumor growth and metastasis. Increased expression of MMPs provides a unifying link between lung cancer and COPD.

Multiple independent loci at chromosome 15q25.1 affect smoking quantity: a meta-analysis and comparison with lung cancer and COPD.

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Nancy L Saccone

2010-08-01

Full Text Available Recently, genetic association findings for nicotine dependence, smoking behavior, and smoking-related diseases converged to implicate the chromosome 15q25.1 region, which includes the CHRNA5-CHRNA3-CHRNB4 cholinergic nicotinic receptor subunit genes. In particular, association with the nonsynonymous CHRNA5 SNP rs16969968 and correlates has been replicated in several independent studies. Extensive genotyping of this region has suggested additional statistically distinct signals for nicotine dependence, tagged by rs578776 and rs588765. One goal of the Consortium for the Genetic Analysis of Smoking Phenotypes (CGASP is to elucidate the associations among these markers and dichotomous smoking quantity (heavy versus light smoking, lung cancer, and chronic obstructive pulmonary disease (COPD. We performed a meta-analysis across 34 datasets of European-ancestry subjects, including 38,617 smokers who were assessed for cigarettes-per-day, 7,700 lung cancer cases and 5,914 lung-cancer-free controls (all smokers, and 2,614 COPD cases and 3,568 COPD-free controls (all smokers. We demonstrate statistically independent associations of rs16969968 and rs588765 with smoking (mutually adjusted p-values<10(-35 and <10(-8 respectively. Because the risk alleles at these loci are negatively correlated, their association with smoking is stronger in the joint model than when each SNP is analyzed alone. Rs578776 also demonstrates association with smoking after adjustment for rs16969968 (p<10(-6. In models adjusting for cigarettes-per-day, we confirm the association between rs16969968 and lung cancer (p<10(-20 and observe a nominally significant association with COPD (p = 0.01; the other loci are not significantly associated with either lung cancer or COPD after adjusting for rs16969968. This study provides strong evidence that multiple statistically distinct loci in this region affect smoking behavior. This study is also the first report of association between rs588765

Combined Pulmonary Fibrosis and Emphysema Syndrome: A New Phenotype within the Spectrum of Smoking-Related Interstitial Lung Disease

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Karina Portillo

2012-01-01

Full Text Available Combined pulmonary fibrosis and emphysema (CPFE is a recently defined syndrome, in which centrilobular and/or paraseptal emphysemas in upper lung zones coexist with pulmonary fibrosis in lower lobes in individuals. These patients have a characteristic lung function profile, with unexpected subnormal dynamic and static lung volumes, contrasting with a significant reduction of carbon monoxide transfer (DLco and exercise hypoxemia. Pulmonary hypertension is highly prevalent in CPFE and is the leading determinant of death. Tobacco smoking has been proposed as the main factor in its etiology, though the pathophysiology and its natural history remain to be determined. High-resolution computed axial tomography is the mandatory tool to confirm the diagnosis. Currently, there is no consensus about its treatment since those published to date on this issue are limited to well-characterised series of cases; hence, a better understanding of this entity may help in the development of future therapeutic approaches.

Effect of smoking reduction on lung cancer risk

DEFF Research Database (Denmark)

Godtfredsen, Nina S; Prescott, Eva; Osler, Merete

2005-01-01

Many smokers are unable or unwilling to completely quit smoking. A proposed means of harm reduction is to reduce the number of cigarettes smoked per day. However, it is not clear whether this strategy decreases the risk for tobacco-related diseases.......Many smokers are unable or unwilling to completely quit smoking. A proposed means of harm reduction is to reduce the number of cigarettes smoked per day. However, it is not clear whether this strategy decreases the risk for tobacco-related diseases....

Lung cancer, genetic predisposition and smoking

DEFF Research Database (Denmark)

Hjelmborg, Jacob; Korhonen, Tellervo; Holst, Klaus

2017-01-01

Background: We aimed to disentangle genetic and environmental causes in lung cancer while considering smoking status. Methods: Four Nordic twin cohorts (43 512 monozygotic (MZ) and 71 895 same sex dizygotic (DZ) twin individuals) had smoking data before cancer diagnosis. We used time...

Pulmonary microRNA profiling: implications in upper lobe predominant lung disease

OpenAIRE

Armstrong, David A.; Nymon, Amanda B.; Ringelberg, Carol S.; Lesseur, Corina; Hazlett, Haley F.; Howard, Louisa; Marsit, Carmen J.; Ashare, Alix

2017-01-01

Background Numerous pulmonary diseases manifest with upper lobe predominance including cystic fibrosis, smoking-related chronic obstructive pulmonary disease, and tuberculosis. Zonal hypoxia, characteristic of these pulmonary maladies, and oxygen stress in general is known to exert profound effects on various important aspects of cell biology. Lung macrophages are major participants in the pulmonary innate immune response and regional differences in macrophage responsiveness to hypoxia may co...

Will chronic e-cigarette use cause lung disease?

Science.gov (United States)

Rowell, Temperance R; Tarran, Robert

2015-12-15

Chronic tobacco smoking is a major cause of preventable morbidity and mortality worldwide. In the lung, tobacco smoking increases the risk of lung cancer, and also causes chronic obstructive pulmonary disease (COPD), which encompasses both emphysema and chronic bronchitis. E-cigarettes (E-Cigs), or electronic nicotine delivery systems, were developed over a decade ago and are designed to deliver nicotine without combusting tobacco. Although tobacco smoking has declined since the 1950s, E-Cig usage has increased, attracting both former tobacco smokers and never smokers. E-Cig liquids (e-liquids) contain nicotine in a glycerol/propylene glycol vehicle with flavorings, which are vaporized and inhaled. To date, neither E-Cig devices, nor e-liquids, are regulated by the Food and Drug Administration (FDA). The FDA has proposed a deeming rule, which aims to initiate legislation to regulate E-Cigs, but the timeline to take effect is uncertain. Proponents of E-Cigs say that they are safe and should not be regulated. Opposition is varied, with some opponents proposing that E-Cig usage will introduce a new generation to nicotine addiction, reversing the decline seen with tobacco smoking, or that E-Cigs generally may not be safe and will trigger diseases like tobacco. In this review, we shall discuss what is known about the effects of E-Cigs on the mammalian lung and isolated lung cells in vitro. We hope that collating this data will help illustrate gaps in the knowledge of this burgeoning field, directing researchers toward answering whether or not E-Cigs are capable of causing disease. Copyright © 2015 the American Physiological Society.

[Vaping: a new strategy to prevent smoking-related diseases?].

Science.gov (United States)

Polosa, Riccardo

2014-01-01

By quitting, smokers of all ages can gain substantial health benefits. No other single effort of public health is able to achieve an advantage comparable to smoking cessation on a large scale. However, conventional approaches to smoking cessation require tobacco users to completely abstain, and many smokers are unable - or have not the willingness - to achieve this goal, and then continue to smoke despite the looming negative consequences for health. But it is possible to consider another option: the reduction of harm caused by tobacco smoking (tobacco harm reduction) through the intake of nicotine from alternative sources safer than tobacco smoke, such as the electronic cigarette (e-cig). It is a promising product for the reduction of harm caused by tobacco smoking. In addition to providing nicotine through the vapour without the typical toxic and carcinogenic substances derived from combustion, the e-cig is also a good substitute for the rituals associated with the behaviour of the smoker. In this article, the author suggests that the wide dissemination of vaping behaviour can become a successful strategy to reduce smoking and preventing smoking-related diseases, advancing on how to succeed with this matter.

A case of immunoglobulin G-4 related sclerosing disease mimicking lung cancer

International Nuclear Information System (INIS)

Kwon, Soo Hee; Lee, Young Kyung; Shim, Mi Suk; Lee, Hyang Im

2013-01-01

Immunoglobulin (Ig) G4-related sclerosing disease is a recently described systemic fibro-inflammatory disease associated with an elevated circulating level of IgG4 and extensive IgG4-positive lymphoplasmacytic infiltration, resulting in sclerosing inflammation involving various body organs. We experienced one case where surgery confirmed IgG4-related sclerosing disease as a solitary lung mass mimicking lung cancer. We report radiologic findings including chest computed tomography and positron emission tomography computed tomography, with clinical manifestations of IgG4-related sclerosing disease.

Cigarette smoke induces an unfolded protein response in the human lung: a proteomic approach.

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Kelsen, Steven G; Duan, Xunbao; Ji, Rong; Perez, Oscar; Liu, Chunli; Merali, Salim

2008-05-01

Cigarette smoking, which exposes the lung to high concentrations of reactive oxidant species (ROS) is the major risk factor for chronic obstructive pulmonary disease (COPD). Recent studies indicate that ROS interfere with protein folding in the endoplasmic reticulum and elicit a compensatory response termed the "unfolded protein response" (UPR). The importance of the UPR lies in its ability to alter expression of a variety of genes involved in antioxidant defense, inflammation, energy metabolism, protein synthesis, apoptosis, and cell cycle regulation. The present study used comparative proteomic technology to test the hypothesis that chronic cigarette smoking induces a UPR in the human lung. Studies were performed on lung tissue samples obtained from three groups of human subjects: nonsmokers, chronic cigarette smokers, and ex-smokers. Proteomes of lung samples from chronic cigarette smokers demonstrated 26 differentially expressed proteins (20 were up-regulated, 5 were down-regulated, and 1 was detected only in the smoking group) compared with nonsmokers. Several UPR proteins were up-regulated in smokers compared with nonsmokers and ex-smokers, including the chaperones, glucose-regulated protein 78 (GRP78) and calreticulin; a foldase, protein disulfide isomerase (PDI); and enzymes involved in antioxidant defense. In cultured human airway epithelial cells, GRP78 and the UPR-regulated basic leucine zipper, transcription factors, ATF4 and Nrf2, which enhance expression of important anti-oxidant genes, increased rapidly (< 24 h) with cigarette smoke extract. These data indicate that cigarette smoke induces a UPR response in the human lung that is rapid in onset, concentration dependent, and at least partially reversible with smoking cessation. We speculate that activation of a UPR by cigarette smoke may protect the lung from oxidant injury and the development of COPD.

Effect of cannabis smoking on lung function and respiratory symptoms: a structured literature review

Science.gov (United States)

Ribeiro, Luis IG; Ind, Philip W

2016-01-01

As cannabis use increases, physicians need to be familiar with the effects of both cannabis and tobacco on the lungs. However, there have been very few long-term studies of cannabis smoking, mostly due to legality issues and the confounding effects of tobacco. It was previously thought that cannabis and tobacco had similar long-term effects as both cause chronic bronchitis. However, recent large studies have shown that, instead of reducing forced expiratory volume in 1 s and forced vital capacity (FVC), marijuana smoking is associated with increased FVC. The cause of this is unclear, but acute bronchodilator and anti-inflammatory effects of cannabis may be relevant. Bullous lung disease, barotrauma and cannabis smoking have been recognised in case reports and small series. More work is needed to address the effects of cannabis on lung function, imaging and histological changes. PMID:27763599

Gene expression signature of cigarette smoking and its role in lung adenocarcinoma development and survival.

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Maria Teresa Landi

2008-02-01

Full Text Available Tobacco smoking is responsible for over 90% of lung cancer cases, and yet the precise molecular alterations induced by smoking in lung that develop into cancer and impact survival have remained obscure.We performed gene expression analysis using HG-U133A Affymetrix chips on 135 fresh frozen tissue samples of adenocarcinoma and paired noninvolved lung tissue from current, former and never smokers, with biochemically validated smoking information. ANOVA analysis adjusted for potential confounders, multiple testing procedure, Gene Set Enrichment Analysis, and GO-functional classification were conducted for gene selection. Results were confirmed in independent adenocarcinoma and non-tumor tissues from two studies. We identified a gene expression signature characteristic of smoking that includes cell cycle genes, particularly those involved in the mitotic spindle formation (e.g., NEK2, TTK, PRC1. Expression of these genes strongly differentiated both smokers from non-smokers in lung tumors and early stage tumor tissue from non-tumor tissue (p1.5, for each comparison, consistent with an important role for this pathway in lung carcinogenesis induced by smoking. These changes persisted many years after smoking cessation. NEK2 (p<0.001 and TTK (p = 0.002 expression in the noninvolved lung tissue was also associated with a 3-fold increased risk of mortality from lung adenocarcinoma in smokers.Our work provides insight into the smoking-related mechanisms of lung neoplasia, and shows that the very mitotic genes known to be involved in cancer development are induced by smoking and affect survival. These genes are candidate targets for chemoprevention and treatment of lung cancer in smokers.

Lung diseases in the elderly. Pathogenetic significance of pollutants and environmental factors

Energy Technology Data Exchange (ETDEWEB)

Heitz, M; Herzog, H

1984-05-03

In the elderly pneumoconioses due to anorganic or organic dusts are not very common. The incidence of mesothelioma is increasing also in the elderly population. Mesothelioma has become the most frequent occupational malignancy. There is also evidence that mesothelioma can be produced by other fibers than asbestos particles. The paper discusses further the effect of passive smoking, where there is new evidence that passive-smokers are exposed to a higher risk for bronchial cancer than non-smokers. The interactions between smoking and air pollution and morbidity of chronic bronchitis are illustrated. New aspects of pathogenesis and pathophysiology of chronic obstructive lung disease and pulmonary emphysema due to smoking as the most frequent environmental lung disease in the elderly are further discussed. A brief overview of the therapeutical approach to chronic obstructive lung disease including new forms of treatment of cor pulmonale is finally given.

Longitudinal follow-up study of smoking-induced emphysema progression in low-dose CT screening of lung cancer

Science.gov (United States)

Suzuki, H.; Matsuhiro, M.; Kawata, Y.; Niki, N.; Nakano, Y.; Ohmatsu, H.; Kusumoto, M.; Tsuchida, T.; Eguchi, K.; Kaneko, Masahiro; Moriyama, N.

2014-03-01

Chronic obstructive pulmonary disease is a major public health problem that is predicted to be third leading cause of death in 2030. Although spirometry is traditionally used to quantify emphysema progression, it is difficult to detect the loss of pulmonary function by emphysema in early stage, and to assess the susceptibility to smoking. This study presents quantification method of smoking-induced emphysema progression based on annual changes of low attenuation volume (LAV) by each lung lobe acquired from low-dose CT images in lung cancer screening. The method consists of three steps. First, lung lobes are segmented using extracted interlobar fissures by enhancement filter based on fourdimensional curvature. Second, LAV of each lung lobe is segmented. Finally, smoking-induced emphysema progression is assessed by statistical analysis of the annual changes represented by linear regression of LAV percentage in each lung lobe. This method was applied to 140 participants in lung cancer CT screening for six years. The results showed that LAV progressions of nonsmokers, past smokers, and current smokers are different in terms of pack-year and smoking cessation duration. This study demonstrates effectiveness in diagnosis and prognosis of early emphysema in lung cancer CT screening.

Cigarette smoke-induced blockade of the mitochondrial respiratory chain switches lung epithelial cell apoptosis into necrosis

NARCIS (Netherlands)

van der Toorn, Marco; Slebos, Dirk-Jan; de Bruin, Harold G.; Leuvenink, Henri G.; Bakker, Stephan J. L.; Gans, Rijk O. B.; Koeter, Gerard H.; van Oosterhout, Antoon J. M.; Kauffman, Henk F.

Increased lung cell apoptosis and necrosis occur in patients with chronic obstructive pulmonary disease ( COPD). Mitochondria are crucially involved in the regulation of these cell death processes. Cigarette smoke is the main risk factor for development of COPD. We hypothesized that cigarette smoke

Confronting the effects of smoking and air quality on the development of chronic respiratory diseases

Energy Technology Data Exchange (ETDEWEB)

Jedrychowski, W; Krzyzanowski, M W; Wojtyniak, B

1985-08-01

The main purpose of the paper was to compare the effects of outdoor and indoor air quality on the development of chronic respiratory diseases measured in the prospective study of chronic chest diseases among the inhabitants of Cracow, Poland. The 5-year follow-up study covered a probability sample of 4355 adult inhabitants. Data on respiratory symptoms and lung function in addition to variables related to environmental and socioeconomic factors were included. To assess the separate and joint effects of the chosen environmental factors on chronic chest problems, the multiple logistic regression analysis has been carried out. As expected, smoking habit was the strongest single of the factors related to the persistence of the respiratory symptoms. The effect of smoking was more marked in men than in women and this can be attributed to longer duration of smoking and more cigarettes smoked daily by men. Out of all considered adverse occupational factors only chemicals increased the risk of chronic bronchitis in men while dust increased the risk of exacerbations in women. The data showed a significant decrease in risk of exacerbations among the women who used a gas stove for cooking. The study also confirmed the harmful effect of smoking on lung function. Against this particular background the importance of variable temperature combined with ambient air pollution appeared to have rather strong detrimental biologic impact.

Racial and ethnic differences in smoking changes after chronic disease diagnosis among middle-aged and older adults in the United States.

Science.gov (United States)

Quiñones, Ana R; Nagel, Corey L; Newsom, Jason T; Huguet, Nathalie; Sheridan, Paige; Thielke, Stephen M

2017-02-08

Middle-aged and older Americans from underrepresented racial and ethnic backgrounds are at risk for greater chronic disease morbidity than their white counterparts. Cigarette smoking increases the severity of chronic illness, worsens physical functioning, and impairs the successful management of symptoms. As a result, it is important to understand whether smoking behaviors change after the onset of a chronic condition. We assessed the racial/ethnic differences in smoking behavior change after onset of chronic diseases among middle-aged and older adults in the US. We use longitudinal data from the Health and Retirement Study (HRS 1992-2010) to examine changes in smoking status and quantity of cigarettes smoked after a new heart disease, diabetes, cancer, stroke, or lung disease diagnosis among smokers. The percentage of middle-aged and older smokers who quit after a new diagnosis varied by racial/ethnic group and disease: for white smokers, the percentage ranged from 14% after diabetes diagnosis to 32% after cancer diagnosis; for black smokers, the percentage ranged from 15% after lung disease diagnosis to 40% after heart disease diagnosis; the percentage of Latino smokers who quit was only statistically significant after stoke, where 38% quit. In logistic models, black (OR = 0.43, 95% CI: 0.19-0.99) and Latino (OR = 0.26, 95% CI: 0.11-0.65) older adults were less likely to continue smoking relative to white older adults after a stroke, and Latinos were more likely to continue smoking relative to black older adults after heart disease onset (OR = 2.69, 95% CI [1.05-6.95]). In models evaluating changes in the number of cigarettes smoked after a new diagnosis, black older adults smoked significantly fewer cigarettes than whites after a new diagnosis of diabetes, heart disease, stroke or cancer, and Latino older adults smoked significantly fewer cigarettes compared to white older adults after newly diagnosed diabetes and heart disease. Relative to black

A Case-control Study on Non-smoking Primary Lung Cancers in Sichuan, China

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Feifei LIU

2010-05-01

Full Text Available Background and objective The incidence of lung cancer in non-smokers is increasing in recent years. The aim of this investigation is to explore main risk factors of non-smoking primary lung cancers in Sichuan province in order to provide more accurate data for clinical. Methods One hundred and fourty-five non-smoking pairs of cases and 145 of controls were matched by age and sex. The patients were newly-diagnosed definitely as primary lung cancer at West China Hospital of Sichuan University from March to December 2009. Results Seventeen exposure factors were explored as epidemic agents for non-smoking lung cancer in Sichuan by using univariate analysis; mutivariate conditional Logistic regression analysis showed that passive smoking, moved into newly renovated homes over the past 10 years, family cancer history from second/third-degree relatives, lack of emotion regulation, heavy work pressure and poor quality of sleep were main risk agents for the non-smoking lung cancer incidence with OR 2.267 (95%CI: 1.231-4.177, 5.080 (95%CI: 1.632-15.817, 7.937 (95%CI: 1.815-34.705, 2.491 (95%CI: 1.230-4.738, 5.769 (95%CI: 2.030-16.396, 2.538 (95%CI: 1.277-4.861, respectively. While higher body mass index, eating fruit and vegetable and regular participating in physical exercise might be protective factors with OR 0.419 (95%CI: 0.226-0.779, 0.344 (95%CI: 0.155-0.762, 0.507 (95%CI: 0.274-0.937, respectively. Conclusion The occurrence of non-smoking primary lung cancer associated with a variety of exposure factors including passive smoking, history of exposure to harmful environmental, family cancer history, mental and psychological factors in Sichuan Province.

Gender differences in first and secondhand smoke exposure, spirometric lung function and cardiometabolic health in the old order Amish: A novel population without female smoking.

Science.gov (United States)

Reed, Robert M; Dransfield, Mark T; Eberlein, Michael; Miller, Michael; Netzer, Giora; Pavlovich, Mary; Pollin, Toni I; Scharf, Steven M; Shuldiner, Alan R; Sin, Don; Mitchell, Braxton D

2017-01-01

Due to their relatively homogeneous lifestyle and living environment, the Amish offer a novel opportunity to study the health associations of tobacco smoke exposure, particularly secondhand smoke. We hypothesized that secondhand smoke exposure is associated with worse pulmonary and cardiometabolic health. We examined cross-sectional data on 3568 Amish study participants, including tobacco use and secondhand smoke exposure from family members included in the study. Thirty-four percent of Amish men reported ever smoking. Of this proportion, 64% used cigars, 46% cigarettes, and 21% pipes. Less than 1% of women reported ever smoking. Smoking was associated with lower spirometric lung function, higher body mass index, lower HDL cholesterol, higher heart rate, lower ankle-brachial index, and larger aortic diameter in men. A greater number of sources of secondhand smoke exposure (defined from the total of spouses, parents, and siblings who smoke) was associated with higher body mass index (p = 0.03) and with higher fasting glucose in men (p = 0.01), but not in women (p = 0.007 for sex*secondhand smoke interaction). Secondhand smoke exposure was also associated with reduced HDL cholesterol only in women (p = 0.002) and a lower heart rate only in men (p = 0.006). Smoking habits among the Old Order Amish are notable for the absence of female participation and a high proportion of cigar and pipe use. Smoking is associated with decreased spirometric indices of lung function and increased cardiovascular risk in this population and secondhand smoke exposure is associated with a greater burden of risk factors for cardiovascular disease. Sex differences in correlations could reflect differences in exposure patterns, mechanisms, or susceptibilities.

Modelling lung cancer due to radon and smoking in WISMUT miners: Preliminary results

International Nuclear Information System (INIS)

Bijwaard, H.; Dekkers, F.; Van Dillen, T.

2011-01-01

A mechanistic two-stage carcinogenesis model has been applied to model lung-cancer mortality in the largest uranium-miner cohort available. Models with and without smoking action both fit the data well. As smoking information is largely missing from the cohort data, a method has been devised to project this information from a case-control study onto the cohort. Model calculations using 256 projections show that the method works well. Preliminary results show that if an explicit smoking action is absent in the model, this is compensated by the values of the baseline parameters. This indicates that in earlier studies performed without smoking information, the results obtained for the radiation parameters are still valid. More importantly, the inclusion of smoking-related parameters shows that these mainly influence the later stages of lung-cancer development. (authors)

Effects of occupational exposures and smoking on lung function in tile factory workers.

Science.gov (United States)

Jaakkola, Maritta S; Sripaiboonkij, Penpatra; Jaakkola, Jouni J K

2011-02-01

The aims of this study were to investigate the relations of occupational exposures in tile industry to lung function and to evaluate potential interaction between smoking and tile dust exposure containing silica. A cross-sectional study of 232 workers (response rate 100%) in a tile factory and 76 office workers (response rate 73%) from four factories in Thailand was conducted in 2006-2007. Participants answered a questionnaire and performed spirometry. Factory workers had lower spirometric functions than office workers, especially those with high dust exposure. There was a dose-response relation between duration of dust exposure and FEV1 and FVC, the adjusted effect of ≥ 21 years of exposure on FEV1 being -240 ml (-100 to -380) and on FVC -300 ml (-140 to -460). The adverse effect of dust on lung function was larger in current smokers suggesting synergism between smoking and tile dust exposure. This study provides evidence that long-term exposure to dust in tile industry is related to lung function reduction. There was a suggestion of synergistic effect between dust exposure and smoking. Tile factories should consider measures to reduce dust exposure and arrange spirometry surveillance for workers with such exposure. Smoking cessation should be promoted to prevent harmful effects of occupational tile dust exposure.

Diagnostic Imaging of Lung Cancer

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Kemal Kara

2012-12-01

Full Text Available Lung cancer is the most common cause of cancer related death in men and women. It is frequently seen among men than in women and male-female ratio is 1.5:1. Common epidemiological factors that increase risk of lung cancer is smoking. Early age to start smoking, high number of smoking cigarettes per a day and depth of inhalation increase risk of lung cancer. 25% of patients with lung cancer are nonsmokers that passively exposed to cigarette smoke. Occupational exposure to substances such as asbestos, arsenic, nickel, beryllium, mustard gas increases the risk of lung cancer. The well defined risk factor is exposure to asbestos. In addition advanced age, diffuse pulmonary fibrosis, chronic obstructive pulmonary disease (COPD and genetic predisposition are the risk factors that increases lung cancer. [TAF Prev Med Bull 2012; 11(6.000: 749-756

SHORT COMMUNICATION: Reduction of Spirometric Lung Function Tests in Habitually Smoking Healthy Young Adults: It’s Correlation with Pack Years

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Sumangala M Patil

2012-01-01

Full Text Available Background: Adolescent smoking and the subsequent health problems are a major concern today. However there are very few studies done on spirometric lung functions and its relation with pack years in young adult habitual smokers who are apparently healthy. Aims and Objectives: The present study is undertaken to assess the change in lung functions in apparently healthy young adult habitual smokers compared to their age matched controls. Materials and Methods: A random sample of apparently healthy young adult habitual smokers (n=40 and nonsmokers (n=40 between age group17-35 years with history suggesting of pack years of 2-10 years were selected from students & employee’s of B.L.D.E.U’s Sri B.M. Patil Medical College,Hospital & Research Centre Bijapur (Karnataka, India. Spirometric lung functions recorded were forced expiratory volume in one second (FEV1, FEV1%, Peak expiratory flow rate (PEFR and Maximal expiratory pressure (MEP. Results: The results suggested that inapparently healthy habitual smokers there was significant decrease in FEV1 (L (-13.34%, p<0.001, FEV1 % (-10.76%, p<0.001, PEFR (-45.26%, p<0.0001 and MEP (-35.51%, p<0.0001 compared to nonsmokers and decrease in FEV1 was negatively correlated withpack years in smokers (r2=0.063, p=0.001. Reduced lung functions and negative correlation to pack years may be attributed todecreased airway diameter & reflex broncho- constriction in response to inhaled smoke particles. Conclusions: In conclusion young adulthabitual smokers who were apparently healthy are more prone for respiratory dysfunction than their nonsmoker counterparts. FEV1 reduction in relation to pack years acts as an important determinant for detecting lung dysfunction in the early stage of the disease. As the risk of having smoking related diseases depends mainly on number of pack years, it is suggested that quitting smoking earliest helps to get greatest health benefits in apparently healthy young adult habitual smokers.

Medical care costs incurred by patients with smoking-related non-small cell lung cancer treated at the National Cancer Institute of Mexico.

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Arrieta, Oscar; Quintana-Carrillo, Roger Humberto; Ahumada-Curiel, Gabriel; Corona-Cruz, Jose Francisco; Correa-Acevedo, Elma; Zinser-Sierra, Juan; de la Mata-Moya, Dolores; Mohar-Betancourt, Alejandro; Morales-Oyarvide, Vicente; Reynales-Shigematsu, Luz Myriam

2014-01-01

Smoking is a public health problem in Mexico and worldwide; its economic impact on developing countries has not been well documented. The aim of this study was to assess the direct medical costs attributable to smoking incurred by lung cancer patients treated at the National Cancer Institute of Mexico (INCan). The study was conducted at INCan in 2009. We carried out a cost of illness (COI) methodology, using data derived from an expert panel consensus and from medical chart review. A panel of experts developed a diagnostic-therapeutic guide that combined the hospital patient pathways and the infrastructure, human resources, technology, and services provided by the medical units at INCan. Cost estimates in Mexican pesos were adjusted by inflation and converted into US Dollars using the 2013 FIX exchange rate for foreign transactions (1 USD = 13.06 Mexican pesos). A 297 incident cases diagnosed with any type of lung cancer were analyzed. According to clinical stage, the costs per patient were 13,456; 35,648; 106,186; and 144,555 USD, for lung cancer stages I, II, III, and IV respectively. The weighted average annual cost/patient was and 139,801 USD and the average annual cost/patient that was attributable to smoking was 92,269 USD. This cost was independent of the clinical stage, with stage IV representing 96% of the annual cost. The total annual cost of smoking-related lung cancer at INCan was 19,969,781 USD. The medical care costs of lung cancer attributable to smoking represent a high cost both for INCan and the Mexican health sector. These costs could be reduced if all provisions established in the Framework Convention of Tobacco Control of the World Health Organization were implemented in Mexico.

Physicians’ views on the role of smoking in smoking-related diseases: findings from cross-sectional studies from 1982–2014 in Estonia

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Kersti Pärna

2017-07-01

From 1982 to 2014, physicians’ attitudes towards the health risks of smoking improved in Estonia. However, their assessment of a causal role of smoking in smoking-related diseases was related to their own smoking habits and ethnicity. A further decline in smoking among Estonian physicians would require special efforts targeted at physicians. Societal pressure from a national policy could support a further decline in the social acceptability of smoking in Estonia and developments in medical education could provide continuing evidence-based information about the health effects of smoking to Estonian physicians.

Andrographolide protects against cigarette smoke-induced oxidative lung injury via augmentation of Nrf2 activity

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Guan, SP; Tee, W; Ng, DSW; Chan, TK; Peh, HY; Ho, WE; Cheng, C; Mak, JC; Wong, WSF

2013-01-01

Background and Purpose Cigarette smoke is a major cause for chronic obstructive pulmonary disease (COPD). Andrographolide is an active biomolecule isolated from the plant Andrographis paniculata. Andrographolide has been shown to activate nuclear factor erythroid-2-related factor 2 (Nrf2), a redox-sensitive antioxidant transcription factor. As Nrf2 activity is reduced in COPD, we hypothesize that andrographolide may have therapeutic value for COPD. Experimental Approach Andrographolide was given i.p. to BALB/c mice daily 2 h before 4% cigarette smoke exposure for 1 h over five consecutive days. Bronchoalveolar lavage fluid and lungs were collected for analyses of cytokines, oxidative damage markers and antioxidant activities. BEAS-2B bronchial epithelial cells were exposed to cigarette smoke extract (CSE) and used to study the antioxidant mechanism of action of andrographolide. Key Results Andrographolide suppressed cigarette smoke-induced increases in lavage fluid cell counts; levels of IL-1β, MCP-1, IP-10 and KC; and levels of oxidative biomarkers 8-isoprostane, 8-OHdG and 3-nitrotyrosine in a dose-dependent manner. Andrographolide promoted inductions of glutathione peroxidase (GPx) and glutathione reductase (GR) activities in lungs from cigarette smoke-exposed mice. In BEAS-2B cells, andrographolide markedly increased nuclear Nrf2 accumulation, promoted binding to antioxidant response element (ARE) and total cellular glutathione level in response to CSE. Andrographolide up-regulated ARE-regulated gene targets including glutamate-cysteine ligase catalytic (GCLC) subunit, GCL modifier (GCLM) subunit, GPx, GR and heme oxygenase-1 in BEAS-2B cells in response to CSE. Conclusions Andrographolide possesses antioxidative properties against cigarette smoke-induced lung injury probably via augmentation of Nrf2 activity and may have therapeutic potential for treating COPD. PMID:23146110

[The role of spirometry in encouraging smoking cessation in general practice. A pilot study using "lung age"].

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Lorenzo, A; Noël, F; Lorenzo, M; Van Den Broucke, J

2017-09-01

Our aim was to investigate whether spirometry, performed in general practitioners' offices would change non-motivated smokers' attitudes toward smoking cessation. We performed an interventional, prospective, before-after single-center study, approved by a research ethics committee. We included 74 smokers older than 18years old, who reported no intention to quit smoking, whatever they were visiting general practitioners for. We performed spirometry and gave them their results, FEV 1 /FVC and lung age together with a comment on it. Nine months later, we called them for another assessment. Fifty-six percent were women with an average-age of 46.5, who smoked 26.3 pack-years. Eighty-two percent of them had normal FEV 1 /FVC but lung age was pathological among 38% of them. Nine months later, 61.1% reported an increased motivation to quit smoking. They smoked 10.9 cigarettes per day versus 13,3 at baseline (P=0.0254). Increase in motivation was not statistically related to age, gender, previous smoking cessations, daily smoking, nicotine dependence or an abnormal FEV 1 /VC ratio (P>0.75) but was significantly related to the presence of an abnormal lung age status (Pspirometry in general practice, combined with the determination of the lung age, may increase motivation towards smoking cessation in smokers who lack motivation. Copyright © 2016 SPLF. Published by Elsevier Masson SAS. All rights reserved.

Final data of an Italian multicentric survey about counseling for smoking cessation in patients with diagnosis of a respiratory disease.

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Capelletto, Enrica; Rapetti, Simonetta Grazia; Demichelis, Sara; Galetta, Domenico; Catino, Annamaria; Ricci, Donata; Moretti, Anna Maria; Bria, Emilio; Pilotto, Sara; Bruno, Arianna; Valmadre, Giuseppe; Bandelli, Gian Piero; Trisolini, Rocco; Gianetta, Martina; Pacchiana, Maria Vittoria; Vallone, Stefania; Novello, Silvia

2018-03-01

Smoking is the major risk factor for cancer and several respiratory diseases. Quitting smoking at any point of life may increase the effectiveness of treatments and improve prognosis of patients with any pulmonary disease, including lung cancer. However, few institutions in Europe offer to patients adequate counseling for smoking cessation. Aim of this study was to investigate the level of counseling for smoking cessation offered by healthcare professionals to patients and their appreciation towards the intervention itself. Between January 2013 and February 2016, 490 patients, diagnosed with a respiratory diseases, were prospectively evaluated with an anonymous survey developed by WALCE (Women Against Lung Cancer in Europe). The majority of patients enrolled (76%) declared to have stopped smoking after the diagnosis of a respiratory disease, 17% to smoke less, 7% to continue smoking. Patients who reported to have never received any counseling for smoking cessation were 38%. Almost 73% of the other patients reported a positive judgment about the quality of healthcare's intervention. Despite these favorable considerations, 83% of patients have disclosed they simply quit smoking overnight without help, 5% have used electronic cigarettes, 5% nicotine replacement treatments, 4% dedicated books, 3% have attended a referral clinic. Considering all the smoking-related side effects, greater efforts should be made in order to better support patients in smoking cessation. Smoking should be considered as a real physical disorder and similar surveys should be encouraged with the aim to fight the 'stigma' of smoking that still exists among patients. © 2017 John Wiley & Sons Ltd.

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

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.

Expiratory CT in cigarette smokers: correlation between areas of decreased lung attenuation, pulmonary function tests and smoking history

Energy Technology Data Exchange (ETDEWEB)

Verschakelen, J.A.; Scheinbaum, K.; Bogaert, J.; Baert, A.L. [Department of Radiology, University Hospitals, Leuven (Belgium); Demedts, M.; Lacquet, L.L. [Department of Pneumology, University Hospitals, Leuven (Belgium)

1998-10-01

The aim of this study was to determine the correlation between cigarette-smoke-related bronchial disease and air trapping as assessed by expiratory high-resolution CT (HRCT) scans. Thirty healthy subjects (11 non-smokers, 7 ex-smokers for > 2 years, 12 current smokers; age range 35-55 years) with a smoking history between 0 and 28.5 pack-years underwent pulmonary function tests (PFT) and HRCT in inspiration and expiration in supine and prone position. The extent of air trapping was scored in ventral and dorsal aspects of the upper, middle and lower lung portions. In 24 subjects (7 non-smokers, 7 ex-smokers, 10 current smokers) areas of focal air trapping were found, and were present significantly more often in dependent lung portions (p < 0.05) compared with non-dependent portions. No significant differences were found between apical and basal lung zones. Scores of focal air trapping were not significantly different between smokers and ex-smokers, but were significantly lower (p < 0.05) in non-smokers and showed a significant (p < 0.0005) correlation with pack-years. The degree of air trapping was also associated with several lung function tests, especially RV, DLCO, FRC, FEV1 and FEV1/VC. Air trapping is seen in smokers with normal PFT and correlates with the severity of the smoking history, independently of current smoking status. (orig.) (orig.) With 4 figs., 4 tabs., 59 refs.

Identification of Oxidative Stress Related Proteins as Biomarkers for Lung Cancer and Chronic Obstructive Pulmonary Disease in Bronchoalveolar Lavage

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Amancio Carnero

2013-02-01

Full Text Available Lung cancer (LC and chronic obstructive pulmonary disease (COPD commonly coexist in smokers, and the presence of COPD increases the risk of developing LC. Cigarette smoke causes oxidative stress and an inflammatory response in lung cells, which in turn may be involved in COPD and lung cancer development. The aim of this study was to identify differential proteomic profiles related to oxidative stress response that were potentially involved in these two pathological entities. Protein content was assessed in the bronchoalveolar lavage (BAL of 60 patients classified in four groups: COPD, COPD and LC, LC, and control (neither COPD nor LC. Proteins were separated into spots by two dimensional polyacrylamide gel electrophoresis (2D-PAGE and examined by matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF/TOF. A total of 16 oxidative stress regulatory proteins were differentially expressed in BAL samples from LC and/or COPD patients as compared with the control group. A distinct proteomic reactive oxygen species (ROS protein signature emerged that characterized lung cancer and COPD. In conclusion, our findings highlight the role of the oxidative stress response proteins in the pathogenic pathways of both diseases, and provide new candidate biomarkers and predictive tools for LC and COPD diagnosis.

An immune basis for lung parenchymal destruction in chronic obstructive pulmonary disease and emphysema.

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Sandra Grumelli

2004-10-01

Full Text Available Chronic obstructive pulmonary disease and emphysema are a frequent result of long-term smoking, but the exact mechanisms, specifically which types of cells are associated with the lung destruction, are unclear.We studied different subsets of lymphocytes taken from portions of human lungs removed surgically to find out which lymphocytes were the most frequent, which cell-surface markers these lymphocytes expressed, and whether the lymphocytes secreted any specific factors that could be associated with disease. We found that loss of lung function in patients with chronic obstructive pulmonary disease and emphysema was associated with a high percentage of CD4+ and CD8+ T lymphocytes that expressed chemokine receptors CCR5 and CXCR3 (both markers of T helper 1 cells, but not CCR3 or CCR4 (markers of T helper 2 cells. Lung lymphocytes in patients with chronic obstructive pulmonary disease and emphysema secrete more interferon gamma--often associated with T helper 1 cells--and interferon-inducible protein 10 and monokine induced by interferon, both of which bind to CXCR3 and are involved in attracting T helper 1 cells. In response to interferon-inducible protein 10 and monokine induced by interferon, but not interferon gamma, lung macrophages secreted macrophage metalloelastase (matrix metalloproteinase-12, a potent elastin-degrading enzyme that causes tissue destruction and which has been linked to emphysema.These data suggest that Th1 lymphoctytes in the lungs of people with smoking-related damage drive progression of emphysema through CXCR3 ligands, interferon-inducible protein 10, and monokine induced by interferon.

Persistence of smoking-induced dysregulation of miRNA expression in the small airway epithelium despite smoking cessation.

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Guoqing Wang

Full Text Available Even after quitting smoking, the risk of the development of chronic obstructive pulmonary disease (COPD and lung cancer remains significantly higher compared to healthy nonsmokers. Based on the knowledge that COPD and most lung cancers start in the small airway epithelium (SAE, we hypothesized that smoking modulates miRNA expression in the SAE linked to the pathogenesis of smoking-induced airway disease, and that some of these changes persist after smoking cessation. SAE was collected from 10th to 12th order bronchi using fiberoptic bronchoscopy. Affymetrix miRNA 2.0 arrays were used to assess miRNA expression in the SAE from 9 healthy nonsmokers and 10 healthy smokers, before and after they quit smoking for 3 months. Smoking status was determined by urine nicotine and cotinine measurement. There were significant differences in the expression of 34 miRNAs between healthy smokers and healthy nonsmokers (p1.5, with functions associated with lung development, airway epithelium differentiation, inflammation and cancer. After quitting smoking for 3 months, 12 out of the 34 miRNAs did not return to normal levels, with Wnt/β-catenin signaling pathway being the top identified enriched pathway of the target genes of the persistent dysregulated miRNAs. In the context that many of these persistent smoking-dependent miRNAs are associated with differentiation, inflammatory diseases or lung cancer, it is likely that persistent smoking-related changes in SAE miRNAs play a role in the subsequent development of these disorders.

Relation between small airways disease and parenchymal destruction in surgical lung specimens.

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Willems, L N; Kramps, J A; Stijnen, T; Sterk, P J; Weening, J J; Dijkman, J H

1990-01-01

The relation between small airways disease and parenchymal destruction was investigated in lungs and lobes removed at surgery from 27 patients aged 15-70 years. Eight of the 27 patients were life-long non-smokers. The degree of small airways disease was assessed by semi-quantitative grading (SAD score) and by measuring diameter and wall thickness of membranous bronchioles. Parenchymal destruction was measured in three ways. Firstly, the number of alveolar attachments on membranous bronchioles per millimetre of circumference (AA/mm) was counted; the number of broken attachments was subtracted from the total AA/mm to give the numbers of intact attachments (normal AA/mm). Secondly, a point counting technique was used to give a destructive index (DI). Thirdly, the mean linear intercept (Lm) was determined. Total and normal AA/mm correlated negatively with the SAD score of membranous bronchioles (rs = -0.48 and -0.51) and with wall thickness (rs = -0.37 and -0.45) and DI correlated with wall thickness (rs = 0.5) and with the SAD score of respiratory bronchioles (rs = 0.53). Lm did not correlate with indices of small airway disease and total and normal AA/mm did not correlate with diameter. Multiple regression analyses showed that the correlation of total AA/mm with the SAD score of membranous and respiratory bronchioles and with wall thickness were not confounded by age or smoking. It is concluded that small airways disease is related to destruction of peribronchiolar alveoli, and it is postulated that small airways disease has a direct role in the causation of centrilobular emphysema. PMID:2315880

Egr-1 regulates autophagy in cigarette smoke-induced chronic obstructive pulmonary disease.

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Zhi-Hua Chen

2008-10-01

Full Text Available Chronic obstructive pulmonary disease (COPD is a progressive lung disease characterized by abnormal cellular responses to cigarette smoke, resulting in tissue destruction and airflow limitation. Autophagy is a degradative process involving lysosomal turnover of cellular components, though its role in human diseases remains unclear.Increased autophagy was observed in lung tissue from COPD patients, as indicated by electron microscopic analysis, as well as by increased activation of autophagic proteins (microtubule-associated protein-1 light chain-3B, LC3B, Atg4, Atg5/12, Atg7. Cigarette smoke extract (CSE is an established model for studying the effects of cigarette smoke exposure in vitro. In human pulmonary epithelial cells, exposure to CSE or histone deacetylase (HDAC inhibitor rapidly induced autophagy. CSE decreased HDAC activity, resulting in increased binding of early growth response-1 (Egr-1 and E2F factors to the autophagy gene LC3B promoter, and increased LC3B expression. Knockdown of E2F-4 or Egr-1 inhibited CSE-induced LC3B expression. Knockdown of Egr-1 also inhibited the expression of Atg4B, a critical factor for LC3B conversion. Inhibition of autophagy by LC3B-knockdown protected epithelial cells from CSE-induced apoptosis. Egr-1(-/- mice, which displayed basal airspace enlargement, resisted cigarette-smoke induced autophagy, apoptosis, and emphysema.We demonstrate a critical role for Egr-1 in promoting autophagy and apoptosis in response to cigarette smoke exposure in vitro and in vivo. The induction of autophagy at early stages of COPD progression suggests novel therapeutic targets for the treatment of cigarette smoke induced lung injury.

Smoking habits in lung cancer patients: a hospital based case ...

African Journals Online (AJOL)

This retrospective, hospital based case-control study was designed to investigate the cigarette smoking history, the relationship between cigarette smoking and the risk of lung cancer in KHMC-Jordan. Six hundred cases with lung cancer (576 males, 24 females) and 600 controls were included in the study. The majority of ...

Cigarette Smoke Decreases the Maturation of Lung Myeloid Dendritic Cells.

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Elena Arellano-Orden

Full Text Available Conflicting data exist on the role of pulmonary dendritic cells (DCs and their maturation in patients with chronic obstructive pulmonary disease (COPD. Herein, we investigated whether disease severity and smoking status could affect the distribution and maturation of DCs in lung tissues of patients undergoing elective pneumectomy or lobectomy for suspected primary lung cancer.A total of 75 consecutive patients were included. Spirometry testing was used to identify COPD. Lung parenchyma sections anatomically distant from the primary lesion were examined. We used flow cytometry to identify different DCs subtypes-including BDCA1-positive myeloid DCs (mDCs, BDCA3-positive mDCs, and plasmacytoid DCs (pDCs-and determine their maturation markers (CD40, CD80, CD83, and CD86 in all participants. We also identified follicular DCs (fDCs, Langerhans DCs (LDCs, and pDCs in 42 patients by immunohistochemistry.COPD was diagnosed in 43 patients (16 current smokers and 27 former smokers, whereas the remaining 32 subjects were classified as non-COPD (11 current smokers, 13 former smokers, and 8 never smokers. The number and maturation of DCs did not differ significantly between COPD and non-COPD patients. However, the results of flow cytometry indicated that maturation markers CD40 and CD83 of BDCA1-positive mDCs were significantly decreased in smokers than in non-smokers (P = 0.023 and 0.013, respectively. Immunohistochemistry also revealed a lower number of LDCs in COPD patients than in non-COPD subjects.Cigarette smoke, rather than airflow limitation, is the main determinant of impaired DCs maturation in the lung.

[Promissing role of probiotics in prevention of smoking-related diseases].

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Hozyasz, Kamil K

2008-01-01

Humans are highly adapted to consuming probiotics. Trehalose ("mushroom" sugar) is probably an important reserve compound and stress-responsible metabolite (increases bile and gastric acid resistance) of probiotic bacteria's and trehalase activity, in contrast to lactase activity, is preserved in all human populations, even those not consuming mushrooms. Among traditional Melanesian horticulturists, of whom 4/5 are daily smokers, the diet is rich in pre- and probiotics and there is absence of cancer and cardiovascular disease. Indoor air pollution is an important cancer risk factor. Over thousands of years, the controlled use of fire for preparing meals has resulted in exposure to smoke pollution (biomass fuels produce up to 100 times more respirable particles compared to gas ovens). Simultaneously, up until the 20th century, the only commonly available and inexpensive way of preserving food was fermentation and drying. Probiotics may protect the detoxification function of the kidney and liver. Furthermore, it can be speculated that probiotics may help in adaptation to smoke pollution generated during cooking, heating but also tobacco smoking. Smoking is the most important lifestyle risk factor for bladder cancer and the consumption of probiotic foods reduces the risk of this cancer in humans. Probiotics may restore natural killer cell activity which is lowered in smokers. In one study it was observed that a diet supplemented with Lactobacillus plantarum could be also useful in the prevention of cardiovascular disease in smokers. There is no sufficient data from clinical trials to recommend the routine use of probiotics in prevention of smoking-related diseases. More research is needed to investigate the role of probiotics in this area.

[The association of lung cancer and atheromatous arterial disease].

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Lamour, A; Azorin, J; Tchandjou Ngoko, L E; Valeyre, D; Morère, F; Destable, M D; de Saint-Florent, G

1989-01-01

This work is based on the retrospective study of the case history of 26 patients who were treated between September 1979 and January 1987 in the department of thoracic and vascular surgery at the Avicenne Hospital--and who were all suffering from both lung cancer and atheromatous arterial disease. It is now well established by all the epidemiologic research that the link between lung cancer and atheromatous arterial disease is smoking tobacco. The risks involved in the misunderstanding of such an association are not without danger for the patient, particularly the risk of severe complication of possible coronary or carotid lesions, threatening survival; from this derives the necessity to decide automatically for a minimum of pre-surgery vascular investigations in the case of patients suffering from lung cancer. The therapeutic strategy in this association must be thorough, considering that there are three priorities in the vascular field which must absolutely be treated before the lung itself: --the coronary and carotid lesions which are likely to be complicated cancer after surgery and any state of emergency in the other vascular territories. The fight against tobacco smoking must also be considered as a priority aim.

meta-analysis of the Relationship between Passive Smoking Population in China and Lung Cancer

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Hui ZHAO

2010-06-01

Full Text Available Background and objective Studies of passive smoking exposure in China however are of particular interest, because of the high lung cancer rate in people who are mostly non-smokers. The aim of this study is to explore the relationship between passive smoking and lung cancer among non-smoking Chinese. Methods By searching Medline, PubMed, CENTRAL (the Cochrane central register of controlled trials, CBM, CNKI and VIP, et al, we collected both domestic and overseas published documents between 1987 and 2007 on passive smoking and lung cancer among non-smoking Chinese. Random or fixed effect models were applied to conduct meta-analysis on the case control study results, and the combined odds ratio (OR and the 95% confidence interval (CI were calculated as well. Results Sixteen documents were included into the combined analysis, which indicated that there was statistical significance between passive smoking and lung cancer (OR=1.13, 95%CI: 1.05-1.21, P=0.001. It was significant of lung cancer among non-smoking subjects associated with amount of tobacco passively smoked more than 20 cigarettes daily, with life period in adulthood passive smoking exposure, with gender female, and with exposure to workplace. The P value, OR and 95%CI were P=0.000 3, OR=1.78, 95%CI: 1.30-2.43; P=0.000 1, OR=1.50, 95%CI: 1.23-1.83; P=0.000 7, OR=1.50, 95%CI: 1.19-1.90; P<0.000 1, OR=1.41, 95%CI: 1.19-1.66; respectively. And there was no significant difference between passive smoking and lung cancer with amount of tobacco passively smoked within 20 cigarettes daily, with life period in childhood passive smoking exposure, with gender male and with exposure to spouse and parents. Conclusion Passive smoking is an important risk factor of lung cancer among non-smoking Chinese, and for non-smoking women who expose to environment tobacco smoke in a long period of time have a close relationship with lung cancer risk.

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.)

Hydrogen-rich saline inhibits tobacco smoke-induced chronic obstructive pulmonary disease by alleviating airway inflammation and mucus hypersecretion in rats.

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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

Smoking and atherosclerosis: mechanisms of disease and new therapeutic approaches.

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Siasos, Gerasimos; Tsigkou, Vasiliki; Kokkou, Eleni; Oikonomou, Evangelos; Vavuranakis, Manolis; Vlachopoulos, Charalambos; Verveniotis, Alexis; Limperi, Maria; Genimata, Vasiliki; Papavassiliou, Athanasios G; Stefanadis, Christodoulos; Tousoulis, Dimitris

2014-01-01

It has been clear that at least 1 billion adults worldwide are smokers and at least 700 million children are passive smokers at home. Smoking exerts a detrimental effect to many organ systems and is responsible for illnesses such as lung cancer, pneumonia, chronic obstructive pulmonary disease, cancer of head and neck, cancer of the urinary and gastrointestinal tract, periodontal disease, cataract and arthritis. Additionally, smoking is an important modifiable risk factor for the development of cardiovascular disease such as coronary artery disease, stable angina, acute coronary syndromes, sudden death, stroke, peripheral vascular disease, congestive heart failure, erectile dysfunction and aortic aneurysms via initiation and progression of atherosclerosis. A variety of studies has proved that cigarette smoking induces oxidative stress, vascular inflammation, platelet coagulation, vascular dysfunction and impairs serum lipid pro-file in both current and chronic smokers, active and passive smokers and results in detrimental effects on the cardiovascular system. The aim of this review is to depict the physical and biochemical properties of cigarette smoke and, furthermore, elucidate the main pathophysiological mechanisms of cigarette-induced atherosclerosis and overview the new therapeutic approaches for smoking cessation and augmentation of cardiovascular health.

Deterioration of lung function is associated with presence of IgM rheumatoid factor and smoking in patients with systemic sclerosis

DEFF Research Database (Denmark)

Broholm, B.; Ullman, S.; Halberg, P.

2008-01-01

of patients with systemic sclerosis (SSc) the influence of smoking and IgM RF on the lung function was calculated. One hundred fifty-five persons with SSc had vital capacity (VC) and diffusing capacity (DLco) measured at least twice with at least 1-year interval as percents of predicted values according......Smoking is a known risk factor for the development of several lung diseases, autoimmune diseases, and IgM rheumatoid factor (RF) in nonrheumatic persons. In patients with rheumatoid arthritis and IgM RF the diffusion capacity is decreased in smokers but not in nonsmokers. In the present study......M RF was found only in smokers or previous smokers, P = 0.007 and P = 0.01, respectively. These findings were confirmed by means of multiple regression analyses. The presence of IgM RF in smoking SSc patients is associated with deteriorating lung function. Whether this is a causal association...

Diferencias tomográficas y funcionales entre la EPOC severa relacionada con humo de leña y con cigarrillo Tomographic and functional findings in severe COPD: comparison between the wood smoke-related and smoking-related disease

Directory of Open Access Journals (Sweden)

Mauricio González-García

2013-04-01

Full Text Available OBJETIVO: La exposición a humo de leña es factor de riesgo para EPOC. A diferencia de la EPOC por cigarrillo (EPOC-C, para un mismo nivel de obstrucción, en la EPOC por leña (EPOC-L, la DLCO está menos disminuida, sugiriendo menos enfisema. Por tanto, el objetivo de este estudio fue comparar los hallazgos en la TCAR en mujeres con EPOC-L y con EPOC- C. MÉTODOS: Veintidós mujeres con EPOC severa (VEF1/CVF OBJECTIVE: Wood smoke exposure is a risk factor for COPD. For a given degree of airway obstruction, the reduction in DLCO is smaller in individuals with wood smoke-related COPD than in those with smoking-related COPD, suggesting that there is less emphysema in the former. The objective of this study was to compare HRCT findings between women with wood smoke-related COPD and women with smoking-related COPD. METHODS: Twenty-two women with severe COPD (FEV1/FVC ratio < 70% and FEV1 < 50% were divided into two groups: those with wood smoke-related COPD (n = 12 and those with smoking-related COPD (n = 10. The two groups were compared regarding emphysema scores and airway involvement (as determined by HRCT; and functional abnormalities-spirometry results, DLCO, alveolar volume (VA, the DLCO/VA ratio, lung volumes, and specific airway resistance (sRaw. Results: There were no significant differences between the two groups in terms of FEV1, sRaw, or lung hyperinflation. Decreases in DLCO and in the DLCO/VA ratio were greater in the smoking-related COPD group subjects, who also had higher emphysema scores, in comparison with the wood smoke-related COPD group subjects. In the wood smoke-related COPD group, HRCT scans howed no significant emphysema, the main findings being peribronchial thickening, bronchial dilation, and subsegmental atelectasis. CONCLUSIONS: Female patients with severe wood smoke-related COPD do not appear to develop emphysema, although they do show severe airway involvement. The reduction in DLCO and VA, with a normal DLCO

Cost of tobacco-related diseases, including passive smoking, in Hong Kong.

Science.gov (United States)

McGhee, S M; Ho, L M; Lapsley, H M; Chau, J; Cheung, W L; Ho, S Y; Pow, M; Lam, T H; Hedley, A J

2006-04-01

Costs of tobacco-related disease can be useful evidence to support tobacco control. In Hong Kong we now have locally derived data on the risks of smoking, including passive smoking. To estimate the health-related costs of tobacco from both active and passive smoking. Using local data, we estimated active and passive smoking-attributable mortality, hospital admissions, outpatient, emergency and general practitioner visits for adults and children, use of nursing homes and domestic help, time lost from work due to illness and premature mortality in the productive years. Morbidity risk data were used where possible but otherwise estimates based on mortality risks were used. Utilisation was valued at unit costs or from survey data. Work time lost was valued at the median wage and an additional costing included a value of USD 1.3 million for a life lost. In the Hong Kong population of 6.5 million in 1998, the annual value of direct medical costs, long term care and productivity loss was USD 532 million for active smoking and USD 156 million for passive smoking; passive smoking accounted for 23% of the total costs. Adding the value of attributable lives lost brought the annual cost to USD 9.4 billion. The health costs of tobacco use are high and represent a net loss to society. Passive smoking increases these costs by at least a quarter. This quantification of the costs of tobacco provides strong motivation for legislative action on smoke-free areas in the Asia Pacific Region and elsewhere.

Lung emphysema induced by cigarette smoke: Studies in mice

NARCIS (Netherlands)

Eijl, Teunis Jan Ahasuerus van

2006-01-01

The experiments described in this thesis were designed to shed some more light on the mechanisms underlying cigarette smoke-induced lung emphysema. We used elastase instillation to induce lung emphysema, and subsequently perfused the lungs ex-vivo with buffer at a range of flows to measure changes

Work-relatedness of lung cancer by smoking and histologic type in Korea.

Science.gov (United States)

Lee, Young-Il; Lee, Sang-Gil; Kang, Dong-Mug; Kim, Jong-Eun; Kim, Young-Ki; Leem, Jong-Han; Kim, Hwan-Cheol

2014-01-01

This study investigated the distribution of causative agents related to occupational lung cancer, their relationships with work, and associations between work-relatedness and the histologic type of lung cancer. We used data from the occupational surveillance system in Korea in 2013. In addition, data from 1,404 participants diagnosed with lung cancer were collected through interviews. We included the patients' longest-held job in the analysis. Work-relatedness was categorized as "definite," "probable," "possible," "suspicious," "none," or "undetermined." Among the subjects, 69.3% were men and 30.7% were women. Regarding smoking status, current smokers were the most prevalent (35.5%), followed by non-smokers (32.3%), ex-smokers (32.2%). Regarding the causative agents of lung cancer, asbestos (1.0%) and crystalline silica (0.9%) were the most common in definite work-related cases, while non-arsenical insecticide (2.8%) was the most common in probable cases followed by diesel engine exhaust (1.9%) and asbestos (1.0%). Regarding histologic type, adenocarcinoma was the most common (41.7%), followed by squamous cell carcinoma (21.2%). Among current smokers, squamous cell carcinoma was the most common among definite and probable cases (13.4%), while non-small cell lung cancer was the least common (7.1%). Among non-smokers, squamous cell carcinoma was the most common (21.4%), while the least common was adenocarcinoma (1.6%). Approximately, 9.5% of all lung cancer cases in Korea are occupational-related lung cancer. Well-known substances associated with lung cancer, such as crystalline silica, asbestos, and diesel engine exhaust, are of particular concern. However, the histologic types of lung cancer related to smoking were inconsistent with previous studies when work-relatedness was taken into account. Future studies are required to clarify the incidence of occupational lung cancer in agricultural workers exposed to non-arsenical insecticides and the associations between

Chronic obstructive pulmonary disease in patients with lung cancer: prevalence, impact and management challenges

Directory of Open Access Journals (Sweden)

Spyratos D

2017-08-01

Full Text Available Dionisios Spyratos, Eleni Papadaki, Sofia Lampaki, Theodoros Kontakiotis Pulmonary Department, Lung Cancer Oncology Unit, Aristotle University of Thessaloniki, G. Papanicolaou Hospital, Thessaloniki, Greece Abstract: Chronic obstructive pulmonary disease (COPD and lung cancer share a common etiological factor (cigarette smoking and usually coexist in everyday clinical practice. The prevalence of COPD among newly diagnosed patients with lung cancer sometimes exceeds 50%. COPD is an independent risk factor (2–4 times higher than non-COPD subjects for lung cancer development.The presence of emphysema in addition to other factors (e.g., smoking history, age could be incorporated into risk scores in order to define the most appropriate target group for lung cancer screening using low-dose computed tomography. Clinical management of patients with coexistence of COPD and lung cancer requires a multidisciplinary oncology board that includes a pulmonologist. Detailed evaluation (lung function tests, cardiopulmonary exercise test and management (inhaled drugs, smoking cessation, pulmonary rehabilitation of COPD should be taken into account for lung cancer treatment (surgical approach, radiotherapy. Keywords: lung cancer, COPD, coexistence, risk factor, therapy decisions 

Effect of smoking reduction on lung cancer risk

DEFF Research Database (Denmark)

Godtfredsen, Nina S; Prescott, Eva; Osler, Merete

2005-01-01

Many smokers are unable or unwilling to completely quit smoking. A proposed means of harm reduction is to reduce the number of cigarettes smoked per day. However, it is not clear whether this strategy decreases the risk for tobacco-related diseases....

Mast cell density in isolated monkey lungs on exposure to cigarette smoke.

OpenAIRE

Walter, A; Walter, S

1982-01-01

The density and percentage of degranulated cells of the mast cell population were studied in the isolated lungs of 25 monkeys (Macaca radiata radiata) before and after acute exposure to cigarette smoke. In each animal one lung was used as the test lung while the other lung was used as its control. In the control lungs the total mean mast cell count was 9.5/mm2 and the proportion of degranulated cells was 9.7%. In the lungs exposed to smoke the total counts were lower (7.3/mm2) and the percent...

Donor Smoking and Older Age Increases Morbidity and Mortality After Lung Transplantation

DEFF Research Database (Denmark)

Schultz, H H; Møller, C H; Zemtsovski, M

2017-01-01

survival as well as CLAD-free survival was significantly lower with donors ≥55 years. CONCLUSIONS: Donor smoking history and older donor age impact lung function, mortality, and CLAD-free survival after transplantation. Because of a shortage of organs, extended donor criteria may be considered while taking......BACKGROUND: The lack of lung transplant donors has necessitated the use of donors with a smoking history and donors of older age. We have evaluated the effects of donor smoking history and age on recipient morbidity and mortality with baseline values of pulmonary function and survival free...... of chronic lung allograft dysfunction (CLAD) as morbidity variables. METHODS: This is a retrospective analysis of 588 consecutive lung transplant recipients and their corresponding 454 donors. Donors were divided into three groups: group 1 included smokers, group 2 nonsmokers, and group 3 had unknown smoking...

A DRD1 polymorphism predisposes to lung cancer among those exposed to secondhand smoke during childhood.

Science.gov (United States)

Robles, Ana I; Yang, Ping; Jen, Jin; McClary, Andrew C; Calhoun, Kara; Bowman, Elise D; Vähäkangas, Kirsi; Greathouse, K Leigh; Wang, Yi; Olivo-Marston, Susan; Wenzlaff, Angela S; Deng, Bo; Schwartz, Ann G; Ryan, Bríd M

2014-12-01

Lung cancer has a familial component which suggests a genetic contribution to its etiology. Given the strong evidence linking smoking with lung cancer, we studied miRNA-related loci in genes associated with smoking behavior. CHRNA, CHRNB gene families, CYP2A6, and DRD1 (dopamine receptor D1) were mined for SNPs that fell within the seed region of miRNA binding sites and then tested for associations with risk in a three-stage validation approach. A 3'UTR (untranslated region) SNP in DRD1 was associated with a lower risk of lung cancer among individuals exposed to secondhand smoke during childhood [OR, 0.69; 95% confidence interval (CI), 0.60-0.79; P secondhand smoke and heterogeneity between individuals in regard to their susceptibility to the effects of secondhand smoke, our data show an interaction between an SNP in the 3'UTR of DRD1 and exposure to secondhand smoke during childhood. Further work is needed to explore the mechanistic underpinnings of this SNP and the nature of the interaction between DRD1 and exposure to secondhand smoke during childhood. ©2014 American Association for Cancer Research.

Smoking habits of patients with newly diagnosed stage IIIA/IIIB non-small cell lung cancer

International Nuclear Information System (INIS)

Sloan, J.; Bonner, J.A.; McGinnis, W.L.; Stella, P.; Marks, R.

1997-01-01

pack per day throughout the course of the trial. The median follow-up time for these 35 patients was 6.9 months. Conclusions: The results of this study provide initial estimates for smoking patterns of lung cancer patients entered onto clinical trials. The data suggested that many patients who had recently entered a clinical trial for locally advanced non-small cell lung cancer had quit smoking within one month of study entry and almost half had quit during the 8 months prior to entry on the study. It is possible that early symptoms related to the lung cancer prompted this smoking cessation pattern. Also, a majority of patients who were smoking at the time of entry on the study quit smoking during subsequent visits. There remains, however, a small minority of patients who continue to smoke despite a diagnosis of lung cancer and complications due to treatment interventions

The effects of drugs, other foreign compounds, and cigarette smoke on the synthesis of protein by lung slices

International Nuclear Information System (INIS)

Hellstern, K.; Curtis, C.G.; Powell, G.M.; Upshall, D.G.

1990-01-01

The incorporation of 14 C-leucine into rabbit lung slices was monitored in the absence and presence of selected drugs and chemicals relevant to the perturbation of lung function and the development of lung disease. Known inhibitors of protein synthesis (cycloheximide and ricin) inhibited the incorporation of 14 C-leucine. Marked inhibition was also recorded with the lung toxins paraquat and 4-ipomeanol. By contrast, orciprenaline, salbutamol, and terbutaline were without effect although some response was recorded with isoprenaline. The filtered gas phase of cigarette smoke and acrolein, one of its components, were inhibitory but protection was afforded by N-acetylcysteine. It is suggested that the inhibitory effects of cigarette smoke may be due to its acrolein content. It is further suggested that the use of lung slices and measurements of 14 C-leucine incorporation provide valuable means for monitoring potential pulmonary toxins

Respiratory disease mortality among uranium miners as related to height, radiation, smoking, and latent period

International Nuclear Information System (INIS)

Archer, V.E.; Gillam, J.D.; James, L.A.

1975-11-01

A prospective mortality study using a life table method was done on 3366 white underground uranium miners, and 1231 surface workers. Observed deaths were found to exceed those expected from respiratory cancer, pneumoconiosis and related diseases, and accidents related to work. Exposure - response relationships with radiation varied with cigarette smoking and with height of workers. Of four factors involved in both malignant and nonmalignant respiratory diseases (height, free silica, cigarette smoking and alpha radiation), radiation was considered to be most important

Cigarette smoke induces molecular responses in respiratory tissues of ApoE−/− mice that are progressively deactivated upon cessation

International Nuclear Information System (INIS)

Boué, Stéphanie; De León, Héctor; Schlage, Walter K.; Peck, Michael J.; Weiler, Horst; Berges, An; Vuillaume, Grégory; Martin, Florian; Friedrichs, Baerbel; Lebrun, Stefan

2013-01-01

Cigarette smoking is the primary etiology of chronic obstructive pulmonary disease (COPD) and a risk factor for both lung and cardiovascular (CV) diseases, which are rarely investigated concomitantly. Although smoking cessation shows clear CV risk benefit, lung-related disease risk remains higher in former smokers than in never smokers. We sought to determine the differential molecular responses of murine respiratory tissues to better understand the toxicity pathways involved in smoking-related disease risk and those related to the benefits of smoking cessation. ApoE −/− mice were exposed to mainstream cigarette smoke (CS) or a smoking cessation-mimicking protocol for up to 6 months and transcriptomics analysis of nasal epithelium and lung parenchyma performed. We supported our gene expression profiling approach with standard lung histopathology and bronchoalveolar lavage fluid (BALF) analysis. Many BALF analytes involved in functions ranging from inflammation to cell proliferation and tissue remodeling were found elevated in BALF. Gene expression levels of these molecules were also increased in lung tissue, suggesting that the inflammatory response was the result of local tissue activation and the contribution of recruited inflammatory cells. Gene set enrichment analysis (GSEA) of expression data from murine lungs and nasal epithelium showed distinct activation patterns of inflammation, complement, and xenobiotic metabolism pathways during CS exposure that were deactivated upon smoking cessation. Pathways involved in cell proliferation and tissue remodeling were activated by CS and progressively deactivated upon smoke exposure cessation. Differential CS-mediated responses of pulmonary and nasal tissues reflect common mechanisms but also the varying degrees of epithelial functional specialization and exposure along the respiratory tract

What Are Asbestos-Related Lung Diseases?

Science.gov (United States)

... asbestosis include: Fibrotic lung disease Pneumoconiosis (NOO-mo-ko-ne-O-sis) Interstitial (in-ter-STISH-al) ... tissue samples. One way is through bronchoscopy (bron-KOS-ko-pee). For this procedure, your doctor will ...

The Impact of Smoking Status on the Efficacy of Erlotinib in Patients with Advanced Non-small Cell Lung Cancer

Directory of Open Access Journals (Sweden)

Yilong WU

2009-12-01

Full Text Available Background and objective Erlotinib is a targeted treatment for advanced non-small cell lung cancer. Smoking status may be one of influencing factors of the efficacy of erlotinib. The aim of this study is to explore the impact of smoking status on the efficacy of erlotinib in patients with advanced non-small cell lung cancer. Methods Patients with nonsmall cell lung cancer who had been previously treated with at least one course of platinum based chemotherapy received 150 mg oral doses of erlotinib once daily until disease progression. Response rate, progression-free survival, overall survival were analyzed in the different smoking status groups. Kaplan-Meier method was used to analyze the survival rate. Results Fortyeight patients were enrolled into the study from December 2005 to September 2006. We followed up these patients until 28th December, 2008. Median follow up time was 30 months. The compliance rate was 100%. The response rate was 32.1% in the smoking group and 35% in the never smoking group (P=0.836; The median progression-free survival was 3 months and 9 months, respectively (P=0.033. The median overall survival was 5 months and 17 months, respectively (P=0.162. Conclusion Erlotinib is an effective drug for advanced non-small cell lung cancer patients with different smoking status. Progressionfree survival is better in the never smoking patients than the smoking patients.

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

Interactions between ethanol and cigarette smoke in a mouse lung carcinogenesis model

International Nuclear Information System (INIS)

Balansky, Roumen; Ganchev, Gancho; Iltcheva, Marietta; Nikolov, Manasi; La Maestra, S.; Micale, Rosanna T.; Steele, Vernon E.; De Flora, Silvio

2016-01-01

Highlights: • Cigarette smoke and ethanol are known to synergize in the upper aerodigestive tract. • Their interactions in the lower respiratory tract have poorly been explored. • Prenatal and postnatal treatments of mice with ethanol caused pulmonary alterations. • However, ethanol attenuated smoke-induced preneoplastic and neoplastic lesions in lung. • The interaction between smoke and alcohol depends on life stage and target tissue. - Abstract: Both ethanol and cigarette smoke are classified as human carcinogens. They can synergize, especially in tissues of the upper aerodigestive tract that are targeted by both agents. The main objective of the present study was to evaluate the individual and combined effects of ethanol and smoke in the respiratory tract, either following transplacental exposure and/or postnatal exposure. We designed two consecutive studies in mouse models by exposing Swiss H mice to oral ethanol and/or inhaled mainstream cigarette smoke for up to 4 months, at various prenatal and postnatal life stages. Clastogenic effects and histopathological alterations were evaluated after 4 and 8 months, respectively. Ethanol was per se devoid of clastogenic effects in mouse peripheral blood erythrocytes. However, especially in mice exposed both transplacentally throughout pregnancy and in the postnatal life, ethanol administration was associated not only with liver damage but also with pro-angiogenetic effects in the lung by stimulating the proliferation of blood vessels. In addition, these mice developed pulmonary emphysema, alveolar epithelial hyperplasias, microadenomas, and benign tumors. On the other hand, ethanol interfered in the lung carcinogenesis process resulting from the concomitant exposure of mice to smoke. In fact, ethanol significantly attenuated some smoke-related preneoplastic and neoplastic lesions in the respiratory tract, such as alveolar epithelial hyperplasia, microadenomas, and even malignant tumors. In addition, ethanol

Antioxidant intervention of smoking-induced lung tumor in mice by vitamin E and quercetin

International Nuclear Information System (INIS)

Yang, Jie; Li, Jun-Wen; Wang, Lu; Chen, Zhaoli; Shen, Zhi-Qiang; Jin, Min; Wang, Xin-Wei; Zheng, Yufei; Qiu, Zhi-Gang; Wang, Jing-feng

2008-01-01

Epidemiological and in vitro studies suggest that antioxidants such as quercetin and vitamin E (VE) can prevent lung tumor caused by smoking; however, there is limited evidence from animal studies. In the present study, Swiss mouse was used to examine the potential of quercetin and VE for prevention lung tumor induced by smoking. Our results suggest that the incidence of lung tumor and tumor multiplicity were 43.5% and 1.00 ± 0.29 in smoking group; Quercetin has limited effects on lung tumor prevention in this in vivo model, as measured by assays for free radical scavenging, reduction of smoke-induced DNA damage and inhibition of apoptosis. On the other hand, vitamin E drastically decreased the incidence of lung tumor and tumor multiplicity which were 17.0% and 0.32 ± 0.16, respectively (p < 0.05); and demonstrated prominent antioxidant effects, reduction of DNA damage and decreased cell apoptosis (p < 0.05). Combined treatment with quercetin and VE in this animal model did not demonstrate any effect greater than that due to vitamin E alone. In addition, gender differences in the occurrence of smoke induced-lung tumor and antioxidant intervention were also observed. We conclude that VE might prevent lung tumor induced by smoking in Swiss mice

Gender and smoking-related risk of lung cancer. The Copenhagen Center for Prospective Population Studies

DEFF Research Database (Denmark)

Prescott, E; Osler, M; Hein, H O

1998-01-01

Our aim was to compare risk of lung cancer associated with smoking by gender and histologic type. A total of 30,874 subjects, 44% women, from three prospective population-based studies with initial examinations between 1964 and 1992 were followed until 1994 through the National Cancer Registry...

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.

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

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

The effect of cigarette smoking on neutrophil kinetics in human lungs [see comments

International Nuclear Information System (INIS)

MacNee, W.; Wiggs, B.; Belzberg, A.S.; Hogg, J.C.

1989-01-01

Neutrophils may play a part in the pathogenesis of the centrilobular emphysema associated with cigarette smoking. The capillary bed of the lungs concentrates neutrophils approximately 100-fold with respect to erythrocytes, producing a large pool of marginated cells. We examined the effect of cigarette smoking on the kinetics of this pool of cells, using 99mTc-labeled erythrocytes to measure regional blood velocity and 111In-labeled neutrophils to measure the removal of neutrophils during the first passage through the pulmonary circulation, their subsequent washout from the lungs, and the effect of local blood velocity on the number of neutrophils retained in each lung region. We observed no difference in these measurements between subjects who had never smoked (n = 6) and smokers who did not smoke during the study (n = 12). However, subjects who did smoke during the study (n = 12) had a significantly slower rate of washout of radiolabeled neutrophils from the lung (0.08 +/- 0.04 of the total per minute, as compared with 0.13 +/- 0.06 in smokers who did not smoke during the experiment and 0.14 +/- 0.08 in non-smokers) (P = 0.02). We also observed an increase in the regional retention of labeled neutrophils with respect to blood velocity in 5 of the 12 subjects who smoked during the study, but in none of the other subjects. We conclude that the presence of cigarette smoke in the lungs of some subjects increases the local concentration of neutrophils, and suggest that the lesions that characterize emphysema may be a result of the destruction of lung tissue by neutrophils that remain within pulmonary microvessels

Exposure of Human Lung Cells to Tobacco Smoke Condensate Inhibits the Nucleotide Excision Repair Pathway.

Directory of Open Access Journals (Sweden)

Nathaniel Holcomb

Full Text Available Exposure to tobacco smoke is the number one risk factor for lung cancer. Although the DNA damaging properties of tobacco smoke have been well documented, relatively few studies have examined its effect on DNA repair pathways. This is especially true for the nucleotide excision repair (NER pathway which recognizes and removes many structurally diverse DNA lesions, including those introduced by chemical carcinogens present in tobacco smoke. The aim of the present study was to investigate the effect of tobacco smoke on NER in human lung cells. We studied the effect of cigarette smoke condensate (CSC, a surrogate for tobacco smoke, on the NER pathway in two different human lung cell lines; IMR-90 lung fibroblasts and BEAS-2B bronchial epithelial cells. To measure NER, we employed a slot-blot assay to quantify the introduction and removal of UV light-induced 6-4 photoproducts and cyclobutane pyrimidine dimers. We find a dose-dependent inhibition of 6-4 photoproduct repair in both cell lines treated with CSC. Additionally, the impact of CSC on the abundance of various NER proteins and their respective RNAs was investigated. The abundance of XPC protein, which is required for functional NER, is significantly reduced by treatment with CSC while the abundance of XPA protein, also required for NER, is unaffected. Both XPC and XPA RNA levels are modestly reduced by CSC treatment. Finally, treatment of cells with MG-132 abrogates the reduction in the abundance of XPC protein produced by treatment with CSC, suggesting that CSC enhances proteasome-dependent turnover of the protein that is mediated by ubiquitination. Together, these findings indicate that tobacco smoke can inhibit the same DNA repair pathway that is also essential for the removal of some of the carcinogenic DNA damage introduced by smoke itself, increasing the DNA damage burden of cells exposed to tobacco smoke.

Mechanisms of protein misfolding in conformational lung diseases.

LENUS (Irish Health Repository)

McElvaney, N G

2012-08-01

Genetic or environmentally-induced alterations in protein structure interfere with the correct folding, assembly and trafficking of proteins. In the lung the expression of misfolded proteins can induce a variety of pathogenetic effects. Cystic fibrosis (CF) and alpha-1 antitrypsin (AAT) deficiency are two major clinically relevant pulmonary disorders associated with protein misfolding. Both are genetic diseases the primary causes of which are expression of mutant alleles of the cystic fibrosis transmembrane conductance regulator (CFTR) and SERPINA1, respectively. The most common and best studied mutant forms of CFTR and AAT are ΔF508 CFTR and the Glu342Lys mutant of AAT called ZAAT, respectively. Non-genetic mechanisms can also damage protein structure and induce protein misfolding in the lung. Cigarette-smoke contains oxidants and other factors that can modify a protein\\'s structure, and is one of the most significant environmental causes of protein damage within the lung. Herein we describe the mechanisms controlling the folding of wild type and mutant versions of CFTR and AAT proteins, and explore the consequences of cigarette-smoke-induced effects on the protein folding machinery in the lung.

Lung cancer in Hodgkin's disease: association with previous radiotherapy

International Nuclear Information System (INIS)

List, A.F.; Doll, D.C.; Greco, F.A.

1985-01-01

Seven cases of lung cancer were observed in patients with Hodgkin's disease (HD) since 1970. The risk ratio for the development of lung cancer among HD patients was 5.6 times that expected in the general population. The pertinent clinical data from these patients are described and compared to 28 additional patients reported from other institutions. Small-cell lung cancer represented the predominant histologic type of lung cancer encountered in both smoking and nonsmoking patients with HD, accounting for 42% of cases overall and greater than 55% of cases reported in reviews of second malignancies. Tobacco use was noted in only 53% of patients. Twenty-eight (94%) of 30 patients developing metachronous lung cancer received supradiaphragmatic irradiation as primary therapy for HD. Nineteen (68%) of these patients received subsequent chemotherapy salvage. The median age at diagnosis of HD and lung cancer was 39 and 45 years, respectively. The interval between diagnosis of HD and metachronous lung cancer averaged seven years but appeared to vary inversely with age. HD patients treated with supradiaphragmatic irradiation or combined modality therapy may be at increased risk for developing lung cancer. The high frequency of in-field malignancies that the authors observed and the prevalence of small-cell lung cancer in both smoking and nonsmoking patients suggests that chest irradiation may influence the development of metachronous lung cancer in these patients. The finding of a mean latent interval in excess of seven years emphasizes the need for close long-term observation

Stimulating high impact HIV-related cardiovascular research: recommendations from a multidisciplinary NHLBI Working Group on HIV-related heart, lung, and blood disease.

Science.gov (United States)

Shah, Monica R; Cook, Nakela; Wong, Renee; Hsue, Priscilla; Ridker, Paul; Currier, Judith; Shurin, Susan

2015-02-24

The clinical challenges confronting patients with human immunodeficiency virus (HIV) have shifted from acquired immunodeficiency syndrome (AIDS)-related illnesses to chronic diseases, such as coronary artery disease, chronic lung disease, and chronic anemia. With the growing burden of HIV-related heart, lung, and blood (HLB) disease, the National Heart, Lung, and Blood Institute (NHLBI) recognizes it must stimulate and support HIV-related HLB research. Because HIV offers a natural, accelerated model of common pathological processes, such as inflammation, HIV-related HLB research may yield important breakthroughs for all patients with HLB disease. This paper summarizes the cardiovascular recommendations of an NHLBI Working Group, Advancing HIV/AIDS Research in Heart, Lung, and Blood Diseases, charged with identifying scientific priorities in HIV-related HLB disease and developing recommendations to promote multidisciplinary collaboration among HIV and HLB investigators. The working group included multidisciplinary sessions, as well as HLB breakout sessions for discussion of disease-specific issues, with common themes about scientific priorities and strategies to stimulate HLB research emerging in all 3 groups. Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

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

Lung cancer trends: smoking, obesity, and sex assessed in the Staten Island University’s lung cancer patients

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Gupta S

2014-07-01

Full Text Available Shilpi Gupta,1 Samer Hassan,1 Vijaya R Bhatt,2 Houssein Abdul Sater,1 Asma Dilawari31Hematology-Oncology, Staten Island University Hospital, Staten Island, NY, USA; 2Hematology-Oncology, Nebraska Medical Ctr, Omaha, NE, USA; 3Hematology-Oncology, MedStar Georgetown University Hospital, Olney, Maryland, USAIntroduction: The incidence of lung cancer in the United States decreased by 1.8% from 1991 to 2005 while it increased by 0.5% in females. We assessed whether nonsmokers afflicted with lung cancer at Staten Island University Hospital are disproportionately female in comparison to national averages. We also evaluated different factors including race, histology, and body mass index (BMI in correlation with smoking history.Methods: A retrospective chart review was conducted from 2005 to 2011 on 857 patients. Patients were divided into two groups according to their smoking status: current or ever-smokers, and former or never-smokers. A chi-square test for categorical data and multivariate logistic regression analyses was used to study the relation between BMI and the other clinical and demographic data.Results: Forty-nine percent of patients were men and 51% were women with a mean age at diagnosis of 67.8 years. Current smokers were most common (50.2% followed by ever-smokers (18.2%, former smokers (15.8% and never-smokers (15.6%. Forty eight percent had stage IV lung cancer upon presentation. Never-smokers with lung cancer were 24 times more likely to be females. However, the proportion of female former smokers (31.6% was lower than the proportion of male former smokers (68.4% (P=0.001. There was no significant association between American Joint Committee on Cancer (AJCC stage, sex, race, and histological type in the two smoking groups. Current/ever-smokers tended to be younger at age of diagnosis (P=0.0003. BMI was lower in the current/ever-smokers (26.8 kg/m2 versus former/never-smokers (28.8 in males (P=0.0005. BMI was significantly higher in

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.

Evolution of emphysema in relation to smoking

International Nuclear Information System (INIS)

Bellomi, Massimo; Rampinelli, Cristiano; Veronesi, Giulia; Harari, Sergio; Lanfranchi, Federica; Raimondi, Sara; Maisonneuve, Patrick

2010-01-01

We have little knowledge about the evolution of emphysema, and relatively little is understood about its evolution in relation to smoking habits. This study aims to assess the evolution of emphysema in asymptomatic current and former smokers over 2 years and to investigate the association with subjects' characteristics. The study was approved by our Ethics Committee and all participants provided written informed consent. We measured emphysema by automatic low-dose computed tomography densitometry in 254 current and 282 former smokers enrolled in a lung-cancer screening. The measures were repeated after 2 years. The association between subjects' characteristics, smoking habits and emphysema were assessed by chi-squared and Wilcoxon tests. Univariate and multivariate odds ratios (OR) with 95% confidence intervals (CI) were calculated for the risk of emphysema worsening according to subjects' characteristics. We assessed the trend of increasing risk of emphysema progression by smoking habits using the Mantel-Haenszel chi-squared test. The median percentage increase in emphysema over a 2-year period was significantly higher in current than in former smokers (OR 1.8; 95% CI 1.3-2.6; p < 0.0001). The risk of worsening emphysema (by 30% in 2 years) in current smokers increased with smoking duration (p for trend <0.02). As emphysema is a known risk factor for lung cancer, its evaluation could be used as a potential factor for identification of a high-risk population. The evaluation of emphysema progression can be added to low-dose CT screening programmes to inform and incite participants to stop smoking. (orig.)

Evolution of emphysema in relation to smoking

Energy Technology Data Exchange (ETDEWEB)

Bellomi, Massimo [European Institute of Oncology, Department of Radiology, Milan (Italy); University of Milan - IT, School of Medicine, Milan (Italy); Rampinelli, Cristiano [European Institute of Oncology, Department of Radiology, Milan (Italy); Veronesi, Giulia [European Institute of Oncology, Department of Thoracic Surgery, Milan (Italy); Harari, Sergio [Fatebenefratelli-Milanocuore, Pneumology Operative Unit, San Giuseppe Hospital, Milan (Italy); Lanfranchi, Federica [University of Milan - IT, School of Medicine, Milan (Italy); Raimondi, Sara; Maisonneuve, Patrick [European Institute of Oncology, Department of Epidemiology and Biostatistics, Milan (Italy)

2010-02-15

We have little knowledge about the evolution of emphysema, and relatively little is understood about its evolution in relation to smoking habits. This study aims to assess the evolution of emphysema in asymptomatic current and former smokers over 2 years and to investigate the association with subjects' characteristics. The study was approved by our Ethics Committee and all participants provided written informed consent. We measured emphysema by automatic low-dose computed tomography densitometry in 254 current and 282 former smokers enrolled in a lung-cancer screening. The measures were repeated after 2 years. The association between subjects' characteristics, smoking habits and emphysema were assessed by chi-squared and Wilcoxon tests. Univariate and multivariate odds ratios (OR) with 95% confidence intervals (CI) were calculated for the risk of emphysema worsening according to subjects' characteristics. We assessed the trend of increasing risk of emphysema progression by smoking habits using the Mantel-Haenszel chi-squared test. The median percentage increase in emphysema over a 2-year period was significantly higher in current than in former smokers (OR 1.8; 95% CI 1.3-2.6; p < 0.0001). The risk of worsening emphysema (by 30% in 2 years) in current smokers increased with smoking duration (p for trend <0.02). As emphysema is a known risk factor for lung cancer, its evaluation could be used as a potential factor for identification of a high-risk population. The evaluation of emphysema progression can be added to low-dose CT screening programmes to inform and incite participants to stop smoking. (orig.)

CHRNA3 genotype, nicotine dependence, lung function and disease in the general population

DEFF Research Database (Denmark)

Kaur-Knudsen, Diljit; Nordestgaard, Børge G; Bojesen, Stig E

2012-01-01

The CHRNA3 rs1051730 polymorphism has been associated to chronic obstructive pulmonary disease (COPD), lung cancer and nicotine dependence in case-control studies with high smoking exposure; however, its influence on lung function and COPD severity in the general population is largely unknown. We...... genotyped 57,657 adult individuals from the Copenhagen General Population Study, of whom 34,592 were ever-smokers. Information on spirometry, hospital admissions, smoking behaviour and use of nicotinic replacement therapy was recorded. In homozygous (11%), heterozygous (44%) and noncarrier (45%) ever...

Secondhand smoke exposure and risk of lung cancer in Japan: a systematic review and meta-analysis of epidemiologic studies.

Science.gov (United States)

Hori, Megumi; Tanaka, Hirokazu; Wakai, Kenji; Sasazuki, Shizuka; Katanoda, Kota

2016-10-01

Systematic evaluation of the association between secondhand smoke exposure and lung cancer in Japan has yet to be conducted. Here, we performed a systematic review and meta-analysis of the relationship between secondhand smoke and lung cancer in Japanese non-smokers. Relevant studies were collected from the MEDLINE and Ichushi Web databases using a combination of search terms and Medical Subject Headings. Eligible studies were identified, and relative risks or odds ratios were extracted to calculate pooled risk estimates. This procedure was performed independently by at least two authors. Stratified analyses were carried out according to study design, publication year, and whether or not potential confounding variables were accounted for. The presence of publication bias was assessed via funnel plots. We identified four cohort studies and five case-control studies. Quantitative synthesis was conducted only for secondhand smoke exposure in the home during adulthood. Of the 12 populations included in meta-analysis, positive secondhand smoke exposure-lung cancer associations were observed in 11, whereas an inverse association was found in the remaining 1. The pooled relative risk of lung cancer associated with secondhand smoke exposure was 1.28 (95% confidence interval: 1.10-1.48). We found no evidence of publication bias, and a significant association remained even when potentially missing studies were included (pooled relative risk: 1.26; 95% confidence interval: 1.09-1.46). The results were stable across different subgroup analyses, including by study design, publication year, and when adjusting for confounding variables. Secondhand smoke exposure in the home during adulthood results in a statistically significant increase in the risk of lung cancer. © The Author 2016. Published by Oxford University Press.

The mediation of social influences on smoking cessation and awareness of the early signs of lung cancer.

Science.gov (United States)

Chatwin, John; Povey, Andrew; Kennedy, Anne; Frank, Tim; Firth, Adam; Booton, Richard; Barber, Phil; Sanders, Caroline

2014-10-07

Whilst there has been no clear consensus on the potential for earlier diagnosis of lung cancer, recent research has suggested that the time between symptom onset and consultation can be long enough to plausibly affect prognosis. In this article, we present findings from a qualitative study involving in-depth interviews with patients who had been diagnosed with lung cancer (n = 11), and people who were at heightened risk of developing the disease (n = 14). A grounded theory methodology was drawn upon to conduct thematic and narrative based approaches to analysis. The paper focuses on three main themes which emerged from the study: i) fatalism and resignation in pathways to help-seeking and the process of diagnosis; ii) Awareness of smoking risk and response to cessation information and advice. iii) The role of social and other networks on help-seeking. Key findings included: poor awareness among participants of the symptoms of lung cancer; ambivalence about the dangers of smoking; the perception of lung cancer as part of a homogenisation of multiple illnesses; close social networks as a key trigger in help-seeking. We suggest that future smoking cessation and lung cancer awareness campaigns could usefully capitalise on the influence of close social networks, and would benefit from taking a 'softer' approach.

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.

Effects of cooking fuel smoke on respiratory symptoms and lung function in semi-rural women in Cameroon.

Science.gov (United States)

Mbatchou Ngahane, Bertrand Hugo; Afane Ze, Emmanuel; Chebu, Cyrille; Mapoure, Njankouo Yacouba; Temfack, Elvis; Nganda, Malea; Luma, Namme Henry

2015-01-01

Indoor air pollution is a major health problem in the developing world. In sub-Saharan Africa more than 90% of people rely on biomass to meet their domestic energy demands. Pollution from biomass fuel ranks 10th among preventable risk factors contributing to the global burden of diseases. The present study aimed to determine the prevalence of respiratory symptoms and the factors associated with reduced lung function in a population of women exposed to cooking fuel smoke. A cross-sectional study was conducted in a semi-rural area in Cameroon. We compared forced respiratory volume between women using wood (n = 145) and women using alternative sources of energy (n = 155) for cooking. Chronic bronchitis was found in 7·6% of the wood smoke group and 0·6% in the alternative fuels group. We observed two cases of airflow obstruction in the wood smoke group. Factors associated with lung function impairment were chronic bronchitis, use of wood as cooking fuel, age, and height. Respiratory symptoms and reduced lung function are more pronounced among women using wood as cooking fuel. Improved stoves technology should be developed to reduce the effects of wood smoke on respiratory health.

Effects of smoking on lung uptake of 201Tl during exercise myocardial perfusion imaging

International Nuclear Information System (INIS)

Ouyang Wei; He Guorong; Liu Jinhua

2004-01-01

Objective: To investigate the influence of smoking on lung uptake of 201 Tl during myocardial perfusion imaging. Methods: Ninety-two healthy subjects, with normal 201 Tl myocardial perfusion imaging findings but no evidence of left ventricular hypertrophy and pulmonary disease, were divided into three groups, smoker, nonsmoker and quitted smoker groups. Exercise/delay 201 Tl myocardial perfusion imaging was performed on all subjects included. Lung/heart ratio was defined on the anterior planar image obtained during exercise tomography. Results: Both the lung/heart ratios during exercise in smoker (0.40 ± 0.07, F=10.635, P 201 Tl lung/heart ratios in smokers are higher than in nonsmokers and this must be kept in mind when 201 Tl lung/heart ratios are used clinically, even in quitted smokers

[Study on smoking attributed death and effects of smoking cessation in residents aged 35-79 years in Tianjin, 2016].

Science.gov (United States)

Li, W; Wang, D Z; Zhang, H; Xu, Z L; Xue, X D; Jiang, G H

2017-11-10

Objective: To analyze the influence of smoking on deaths in residents aged 35-79 years and the effects of smoking cessation in Tianjin. Methods: The data of 39 499 death cases aged 35-79 years in 2016 in Tianjin were collected, the risks for deaths caused by smoking related diseases and excess deaths as well as effects of smoking cessation were analyzed after adjusting 5 year old age group, education level and marital status. Results: Among the 39 499 deaths cases, 1 589 (13.56%) were caused by smoking, the percentage of the excess mortality of lung cancer caused by smoking was highest (47.60%); the risk of death due to lung cancer in smokers was 2.75 times higher than that in non-smokers (95 %CI : 2.47-3.06). Among the female deaths, 183 (7.29%) were caused by smoking, the percentage of the excess mortality of lung cancer was highest (28.90%); and the risk of death of lung cancer in smokers was 4.04 times higher than that in non-smokers (95 %CI : 3.49-4.68). The OR for disease in ex-smokers was 0.80 compared with 1.00 in smokers (95 %CI : 0.72-0.90). The OR in males who had quitted smoking for ≥10 years was lower (0.74, 95 %CI : 0.63-0.86) than that in those who had quitted smoking for 1-9 years (0.85, 95 %CI : 0.74-0.98), but the difference was not significant. Conclusion: Smoking is one of the most important risk factors for deaths in residents in Tianjin. Smoking cessation can benefit people's health.

A case of IgG4-related lung disease complicated by asymptomatic chronic Epstein-Barr virus infection.

Science.gov (United States)

Kotetsu, Yasuaki; Ikegame, Satoshi; Takebe-Akazawa, Keiko; Koga, Takaomi; Okabayashi, Kan; Takata, Shohei

2017-11-01

IgG4-related disease is characterized by IgG4-positive plasmacyte infiltration into various organs, but its etiology is not unknown. To elucidate the etiology of IgG4-related disease. We experienced an interesting case of IgG4-related lung disease complicated by chronic EB virus infection. A 70-year-old male visited our hospital due to failure of pneumonia treatment. Chest computed tomography (CT) showed consolidation in the right middle field and slight mediastinal lymphadenopathy in the subcarinal region. Lung consolidation improved with antibiotics; subcarinal lymphadenopathy progressed after 4 months. Malignant lymphoma was suspected given elevated sIL2-R levels (1862 U/mL). Patchy ground glass opacities appeared in the bilateral lung field just before surgical biopsy. He was diagnosed with IgG4-related lung disease after inspection of a pathological specimen obtained from the right upper lung and right hilar lymph node. EB virus-infected cells were also detected in the lymph node. Blood examination revealed EB virus viremia, but the patient did not present with symptoms or organ involvement. This led to a diagnosis of asymptomatic chronic EB virus infection. Recent studies have suggested an association between EB virus infection and IgG4-related diseases in the pathological exploration of surgically resected lymph nodes. Our case is the first case of IgG4-related lung disease in which EB virus infection was both pathologically and clinically proved. The present case is of particular interest in view of this newly reported association, and may serve as a fundamental report for future studies connecting EB virus infection with IgG4-related diseases. © 2016 John Wiley & Sons Ltd.

Acute cigarette smoke exposure causes lung injury in rabbits treated with ibuprofen

Energy Technology Data Exchange (ETDEWEB)

Witten, M.L.; Lemen, R.J.; Quan, S.F.; Sobonya, R.E.; Magarelli, J.L.; Bruck, D.C.

1987-01-01

We studied lung clearance of aerosolized technetium-labeled diethylenetriamine pentaacetic acid (/sup 99m/TcDTPA), plasma concentrations of 6-keto-PGF1 alpha and thromboxane B2, and pulmonary edema as indices of lung injury in rabbits exposed to cigarette smoke (CSE). Forty-six rabbits were randomly assigned to 4 groups: control sham smoke exposure (SS, N = 9), sham smoke exposure ibuprofen-pretreated (SS-I, N = 10), CSE (N = 9), sham smoke exposure ibuprofen-pretreated (SS-I, N = 10), CSE (N = 9), and CSE ibuprofen-pretreated (CSE-I, N = 19). Ibuprofen (cyclooxygenase eicosanoid inhibitor) was administered as a single daily intramuscular injection (25 mg/kg) for 7 days before the experiment. Cigarette or sham smoke was delivered by syringe in a series of 5, 10, 20, and 30 tidal volume breaths with a 15-min counting period between each subset of breaths to determine /sup 99m/TcDTPA biological half-life (T1/2). In the ibuprofen pretreated group, CSE caused significant decreases in /sup 99m/TcDTPA T1/2 and dynamic lung compliance. Furthermore, these changes in lung function were accompanied by severe injury to type I alveolar cell epithelium, pulmonary edema, and frequently death of the rabbits. These findings suggest that inhibition of the cyclooxygenase pathway before CSE exacerbates lung injury in rabbits.

Acute cigarette smoke exposure causes lung injury in rabbits treated with ibuprofen

International Nuclear Information System (INIS)

Witten, M.L.; Lemen, R.J.; Quan, S.F.; Sobonya, R.E.; Magarelli, J.L.; Bruck, D.C.

1987-01-01

We studied lung clearance of aerosolized technetium-labeled diethylenetriamine pentaacetic acid (/sup 99m/TcDTPA), plasma concentrations of 6-keto-PGF1 alpha and thromboxane B2, and pulmonary edema as indices of lung injury in rabbits exposed to cigarette smoke (CSE). Forty-six rabbits were randomly assigned to 4 groups: control sham smoke exposure (SS, N = 9), sham smoke exposure ibuprofen-pretreated (SS-I, N = 10), CSE (N = 9), sham smoke exposure ibuprofen-pretreated (SS-I, N = 10), CSE (N = 9), and CSE ibuprofen-pretreated (CSE-I, N = 19). Ibuprofen (cyclooxygenase eicosanoid inhibitor) was administered as a single daily intramuscular injection (25 mg/kg) for 7 days before the experiment. Cigarette or sham smoke was delivered by syringe in a series of 5, 10, 20, and 30 tidal volume breaths with a 15-min counting period between each subset of breaths to determine /sup 99m/TcDTPA biological half-life (T1/2). In the ibuprofen pretreated group, CSE caused significant decreases in /sup 99m/TcDTPA T1/2 and dynamic lung compliance. Furthermore, these changes in lung function were accompanied by severe injury to type I alveolar cell epithelium, pulmonary edema, and frequently death of the rabbits. These findings suggest that inhibition of the cyclooxygenase pathway before CSE exacerbates lung injury in rabbits

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)

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)

The role of endotoxin in grain dust-induced lung disease.

Science.gov (United States)

Schwartz, D A; Thorne, P S; Yagla, S J; Burmeister, L F; Olenchock, S A; Watt, J L; Quinn, T J

1995-08-01

To identify the role of endotoxin in grain dust-induced lung disease, we conducted a population-based, cross-sectional investigation among grain handlers and postal workers. The study subjects were selected by randomly sampling all grain facilities and post offices within 100 miles of Iowa City. Our study population consisted of 410 grain workers and 201 postal workers. Grain workers were found to be exposed to higher concentrations of airborne dust (p = 0.0001) and endotoxin (p = 0.0001) when compared with postal workers. Grain workers had a significantly higher prevalence of work-related (cough, phlegm, wheezing, chest tightness, and dyspnea) and chronic (usual cough or phlegm production) respiratory symptoms than postal workers. Moreover, after controlling for age, gender, and cigarette smoking status, work-related respiratory symptoms were strongly associated with the concentration of endotoxin in the bioaerosol in the work setting. The concentration of total dust in the bioaerosol was marginally related to these respiratory problems. After controlling for age, gender, and cigarette smoking status, grain workers were found to have reduced spirometric measures of airflow (FEV1, FEV1/FVC, and FEF25-75) and enhanced airway reactivity to inhaled histamine when compared with postal workers. Although the total dust concentration in the work environment appeared to have little effect on these measures of airflow obstruction, higher concentrations of endotoxin in the bioaerosol were associated with diminished measures of airflow and enhanced bronchial reactivity. Our results indicate that the concentration of endotoxin in the bioaerosol may be particularly important in the development of grain dust-induced lung disease.

Systematic Review of Studies of Workplace Exposure to Environmental Tobacco Smoke and Lung Cancer Risk

Directory of Open Access Journals (Sweden)

Xinzhuo WANG

2011-04-01

Full Text Available Background and objective It has been reported that there was a close relationship between lung cancer risk and environmental tobacco smoke at workplace. The aim of this study is to explore the relationship between workplace environmental tobacco smoke exposure and lung cancer risk among non-smoking subjects. Methods By searching Medline, CENTRAL (the Cochrane central register of controlledtrials, EMBASE, CBM, CNKI and VIP et al, we collected both domestic and overseas published documents on workplace environmental tobacco smoke exposure and lung cancer risk. Random or fixed effect models were applied to conduct systematic review on the study results, the combined odds ratio (OR and the 95% confidence interval (CI were calculated as well. Results 22 reports were included into the combined analysis, which indicated that 25% lung cancer risk was increased by exposing to workplace environment tobacco smoke (OR=1.25, 95%CI: 1.13-1.39, P < 0.001. For female the increased risk was 22% (OR=1.22, 95%CI: 1.05-1.42, P=0.011. For male the increased risk was 54%, but it does not reach the statistical significance (OR=1.54, 95%CI: 0.74-3.18, P=0.247. Conclusion Workplace environmental tobacco smoke exposure is an important risk factor of lung cancer risk among non-smoking subjects. Especially for non-smoking women who expose to workplace environment tobacco smoke have a close relationship with lung cancer.

Smoky coal, tobacco smoking, and lung cancer risk in Xuanwei, China

NARCIS (Netherlands)

Kim, Christopher; Chapman, Robert S.; Hu, Wei; He, Xingzhou; Hosgood, H. Dean; Liu, Larry Z.; Lai, Hong; Chen, Wei; Silverman, Debra T.; Vermeulen, Roel; Tian, Linwei; Bassig, Bryan; Shen, Min; Zhang, Yawei; Ma, Shuangge; Rothman, Nathaniel; Lan, Qing

2014-01-01

Objectives: Lung cancer rates in Xuanwei are the highest in China. In-home use of smoky coal has been associated with lung cancer risk, and the association of smoking and lung cancer risk strengthened after stove improvement. Here, we explored the differential association of tobacco use and lung

Cannabis Smoking and Risk of Lung Cancer - A Systematic Review and Meta-Analysis

Directory of Open Access Journals (Sweden)

khalid BOUTI

2014-12-01

Full Text Available Background: Cannabis is the illicit psychoactive substance the most consumed in the world. Little is known about the association between the use of cannabis and the risk of lung cancer.Objective:The objective of this meta-analysis is to determine whether use of cannabis is a risk factor for lung cancer.Methods: We conducted a systematic review and meta-analyses of all languages articles using relevant computerised databases. MEDLINE (online PubMed, Web of knowledge, Embase, EBSCO CINAHL, ScienceDirect, Scopus, Cochrane Library, and Directory of Open Access Journals were searched to September 2014 for cohorts and case-control studies that assessed the risk of lung cancer associated with cannabis smoking.  The literature search was performed with a combination of medical subject headings terms, "cannabis" and "lung neoplasms". Data extraction: Two investigators independently analysed and extracted results from eligible studies.Our study's registration number on PROSPERO is  CRD42014008872.Results: The search strategy identified 2476 citations. 13 studies were eligible for inclusion: 2 pooled analysis of 9 case-control studies, one case-control study and 3 cohorts.The cumulative analysis for all the studies under a fixed-effects model showed that cannabis smoking determined an increased risk of developing lung cancer in the future (relative risk 1.22, 95% confidence interval 0.999–1.5; p=0.051, with no evidence of heterogeneity across the studies (I2: 34%; p¼0.01.Conclusions: The use of cannabis with or without tobacco smoking is associated with an increased risk for lung cancer.

Nontypeable Haemophilus influenzae in chronic obstructive pulmonary disease and lung cancer

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Seyed Javad Moghaddam

2011-01-01

Full Text Available Seyed Javad Moghaddam1, Cesar E Ochoa1,2, Sanjay Sethi3, Burton F Dickey1,41Department of Pulmonary Medicine, the University of Texas MD Anderson Cancer Center, Houston, TX, USA; 2Tecnológico de Monterrey School of Medicine, Monterrey, Nuevo León, Mexico; 3Department of Medicine, University at Buffalo, State University of New York, Buffalo, NY, USA; 4Center for Inflammation and Infection, Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, TX, USAAbstract: Chronic obstructive pulmonary disease (COPD is predicted to become the third leading cause of death in the world by 2020. It is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles and gases, most commonly cigarette smoke. Among smokers with COPD, even following withdrawal of cigarette smoke, inflammation persists and lung function continues to deteriorate. One possible explanation is that bacterial colonization of smoke-damaged airways, most commonly with nontypeable Haemophilus influenzae (NTHi, perpetuates airway injury and inflammation. Furthermore, COPD has also been identified as an independent risk factor for lung cancer irrespective of concomitant cigarette smoke exposure. In this article, we review the role of NTHi in airway inflammation that may lead to COPD progression and lung cancer promotion.Keywords: COPD, NTHi, inflammation

Factors related to knowledge and perception of women about smoking: a cross sectional study from a developing country

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Taj Fawad

2011-05-01

Full Text Available Abstract Background Smoking rates among women are currently low, but they are the fastest growing segment of cigarette smoking population in developing countries. We aimed to assess the knowledge and perceptions towards smoking and to identify the factors related with level of knowledge and perceptions among adult women in urban slums. Methods This was a cross sectional study conducted on 250 adult (≥18 years of age women attending primary care clinics in three slums of Karachi, Pakistan. A pre-tested and structured, interviewer administered questionnaire was used for data collection. Factors associated with level of understanding about smoking were analyzed with chi-square test. Results Most of the women knew that smoking has adverse effects on women and children's health but the knowledge of specific health effects was limited. About one third of the women knew that active smoking can cause lung disease, but only a small percentage (7% knew that it could lead to heart disease. None of the women were aware that smoking contributes to infertility and osteoporosis. A small proportion of women were aware that smoking can lead to low birth weight (7%, congenital anomalies (5% and less than 1% of women knew that it contributes to pregnancy loss, still birth and preterm delivery. The understanding of passive smoking affecting children's lung was low (20% and a similar proportion voiced concern about the bad influence of maternal smoking on children. Educated women had better knowledge of health effects of smoking. Education was associated with having better knowledge about effects on women health in general (p = 0.02 and specific effects like lung (p = 0.03 and reproductive health effects (p Conclusions This study reveals that women are aware of the general ill effects of smoking but fail to identify smoking to be associated with female maladies particularly those who were illiterate and had lower levels of education. Understanding and attitudes

Mixture randomized item-response modeling: a smoking behavior validation study

NARCIS (Netherlands)

Fox, Gerardus J.A.; Avetisyan, Marianna; van der Palen, Jacobus Adrianus Maria

2013-01-01

Misleading response behavior is expected in medical settings where incriminating behavior is negatively related to the recovery from a disease. In the present study, lung patients feel social and professional pressure concerning smoking and experience questions about smoking behavior as sensitive

A DRD1 Polymorphism Predisposes to Lung Cancer among those Exposed to Secondhand smoke during Childhood

OpenAIRE

Robles, Ana I.; Yang, Ping; Jen, Jin; McClary, Andrew C.; Calhoun, Kara; Bowman, Elise D.; Vähäkangas, Kirsi; Greathouse, K. Leigh; Wang, Yi; Olivo-Marston, Susan; Wenzlaff, Angela S.; Deng, Bo; Schwartz, Ann G.; Ryan, Bríd M.

2014-01-01

Lung cancer has a familial component which suggests a genetic contribution to its etiology. Given the strong evidence linking smoking with lung cancer, we studied miRNA-related loci in genes associated with smoking behavior. CHRNA, CHRNB gene families, CYP2A6 and DRD1 were mined for single nucleotide polymorphisms (SNPs) that fell within the seed region of miRNA binding sites and then tested for associations with risk in a three-stage validation approach. A 3’UTR SNP in DRD1 (Dopamine Recepto...

Management of Myositis-Related Interstitial Lung Disease.

Science.gov (United States)

Morisset, Julie; Johnson, Cheilonda; Rich, Eric; Collard, Harold R; Lee, Joyce S

2016-11-01

Interstitial lung disease (ILD) is a frequent pulmonary manifestation and an important cause of morbidity and mortality in patients with idiopathic inflammatory myopathy. Myositis-related ILD presents a therapeutic challenge for clinicians, as there are no available guidelines to help with management decisions. This review covers the existing evidence on the pharmacologic and nonpharmacologic management of myositis-related ILD, highlighting the lack of randomized controlled data to guide treatment. Given the absence of existing guidelines to inform treatment decisions, we provide a comprehensive summary, including dosing, side effects, and suggested monitoring of the commonly used immunosuppressive agents and a proposed treatment algorithm based on the existing literature. Copyright © 2016 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

Pulmonary adenocarcinoma mutation profile in smokers with smoking-related interstitial fibrosis

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Primiani A

2014-05-01

Full Text Available Andrea Primiani,1 Dora Dias-Santagata,1 A John Iafrate,1 Richard L Kradin1,2 1Pathology Service, 2Pulmonary Medicine/Critical Care Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA Abstract: Cigarette smoking is an established cause of lung cancer. However, pulmonary fibrosis is also an independent risk factor for the development of lung cancer. Smoking-related interstitial fibrosis (SRIF has recently been reported. We hypothesized that adenocarcinomas in lungs with SRIF might show distinct molecular changes and examined the molecular phenotype of 168 resected lung adenocarcinomas in lungs with and without SRIF. The diagnosis of SRIF was determined by histological examination, based on the presence of alveolar septal thickening, due to pauci-inflamed, hyalinized, “ropy” collagen, in areas of lung greater than 1 cm away from the tumor. Tumors were concomitantly examined genotypically for mutations in genes frequently altered in cancer, including EGFR and KRAS, by SNaPshot and by fluorescence in situ hybridization for possible ALK rearrangements. Fluorescence in situ hybridization for ROS1 rearrangement (n=36 and/or MET amplification (n=31 were performed when no mutation was identified by either SNaPshot or ALK analysis. Sixty-five cases (38.7% showed SRIF, which was distributed in all lobes of the lungs examined. No differences were observed in sex, average age, or smoking history in patients with and without SRIF. There was no difference in either the percent or types of adenocarcinoma genetic mutations in patients with SRIF versus those without. This data suggests that SRIF does not represent an independent risk factor for the development of the major known and targeted mutations seen in pulmonary adenocarcinoma. However, additional research is required to investigate the potential significance of SRIF in the pathogenesis of lung cancer. Keywords: lung, cancer, smoking, SRIF

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

Buccal Epithelium, Cigarette Smoking, and Lung Cancer: Review of the Literature.

Science.gov (United States)

Saba, Raya; Halytskyy, Oleksandr; Saleem, Nasir; Oliff, Ira A

2017-01-01

Lung cancer is currently the leading cause of cancer-related mortality among men and women in the United States, and optimal screening methods are still lacking. The field effect is a well-supported phenomenon wherein a noxious stimulus triggers genetic, epigenetic and molecular changes that are widespread throughout the entire exposed organ system. The buccal epithelium is an easily accessible part of the respiratory tree that has good potential of yielding a surrogate marker for the field effect in cigarette smokers, and thus, a noninvasive, reliable lung cancer screening method. Herein, we review the literature on the relationship between the buccal epithelium, cigarette smoking, and lung cancer. © 2017 S. Karger AG, Basel.

The Risk of Hypertension and Other Chronic Diseases: Comparing Smokeless Tobacco with Smoking

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Ankit Anand

2017-09-01

Full Text Available BackgroundIn the past, studies have compared smokeless tobacco and non-tobacco users for the risk of various chronic diseases. The differences in the risk of chronic diseases between smokeless tobacco user and smokers have not been explored. The objective of this study is to estimate the risk of chronic diseases among smokeless tobacco users compared to smokers.MethodsThe data were used from the Study on Global Ageing and Adult Health (SAGE Wave-1, conducted in 2007–2008 in India. The study sample is the respondents who reported consuming any form of tobacco in last 1 month. The total sample size was 4,038 respondents. The odds ratio of chronic morbidities was estimated taking smokers as the reference category.ResultsThe odds ratios for (self-reported diabetes, asthma, and hypertension were not significant for smokeless tobacco user compared to smoked tobacco users. The odds ratio of chronic lung diseases (CLDs was significantly lower among smokeless tobacco users compared to smoked tobacco users. The odds ratio of hypertension (measured combined with low education and belonging to lowest wealth quintiles were not significant for smokeless tobacco users compared to smoked tobacco users. Duration of the use of smokeless tobacco and quantity of use was found to have no significant relation with risk of chronic diseases as compared to smoking.ConclusionThis study did not find the significantly higher risk of chronic morbidities except for CLD for smokeless tobacco users compared to smoked tobacco users. The study suggests that the use of any form of tobacco may have a similar risk of chronic diseases.

Up-Regulation of Claudin-6 in the Distal Lung Impacts Secondhand Smoke-Induced Inflammation

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Joshua B. Lewis

2016-10-01

Full Text Available It has long been understood that increased epithelial permeability contributes to inflammation observed in many respiratory diseases. Recently, evidence has revealed that environmental exposure to noxious material such as cigarette smoke reduces tight junction barrier integrity, thus enhancing inflammatory conditions. Claudin-6 (Cldn6 is a tetraspanin transmembrane protein found within the tight junctional complex and is implicated in maintaining lung epithelial barriers. To test the hypothesis that increased Cldn6 ameliorates inflammation at the respiratory barrier, we utilized the Tet-On inducible transgenic system to conditionally over-express Clnd6 in the distal lung. Cldn6 transgenic (TG and control mice were continuously provided doxycycline from postnatal day (PN 30 until euthanasia date at PN90. A subset of Cldn6 TG and control mice were also subjected to daily secondhand tobacco smoke (SHS via a nose only inhalation system from PN30-90 and compared to room air (RA controls. Animals were euthanized on PN90 and lungs were harvested for histological and molecular characterization. Bronchoalveolar lavage fluid (BALF was procured for the assessment of inflammatory cells and molecules. Quantitative RT-PCR and immunoblotting revealed increased Cldn6 expression in TG vs. control animals and SHS decreased Cldn6 expression regardless of genetic up-regulation. Histological evaluations revealed no adverse pulmonary remodeling via Hematoxylin and Eosin (H&E staining or any qualitative alterations in the abundance of type II pneumocytes or proximal non-ciliated epithelial cells via staining for cell specific propeptide of Surfactant Protein-C (proSP-C or Club Cell Secretory Protein (CCSP, respectively. Immunoblotting and qRT-PCR confirmed the differential expression of Cldn6 and the pro-inflammatory cytokines TNF-α and IL-1β. As a general theme, inflammation induced by SHS exposure was influenced by the availability of Cldn6. These data reveal

Waterpipe smoking induces epigenetic changes in the small airway epithelium.

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Matthew S Walters

Full Text Available Waterpipe (also called hookah, shisha, or narghile smoking is a common form of tobacco use in the Middle East. Its use is becoming more prevalent in Western societies, especially among young adults as an alternative form of tobacco use to traditional cigarettes. While the risk to cigarette smoking is well documented, the risk to waterpipe smoking is not well defined with limited information on its health impact at the epidemiologic, clinical and biologic levels with respect to lung disease. Based on the knowledge that airway epithelial cell DNA methylation is modified in response to cigarette smoke and in cigarette smoking-related lung diseases, we assessed the impact of light-use waterpipe smoking on DNA methylation of the small airway epithelium (SAE and whether changes in methylation were linked to the transcriptional output of the cells. Small airway epithelium was obtained from 7 nonsmokers and 7 light-use (2.6 ± 1.7 sessions/wk waterpipe-only smokers. Genome-wide comparison of SAE DNA methylation of waterpipe smokers to nonsmokers identified 727 probesets differentially methylated (fold-change >1.5, p<0.05 representing 673 unique genes. Dominant pathways associated with these epigenetic changes include those linked to G-protein coupled receptor signaling, aryl hydrocarbon receptor signaling and xenobiotic metabolism signaling, all of which have been associated with cigarette smoking and lung disease. Of the genes differentially methylated, 11.3% exhibited a corresponding significant (p<0.05 change in gene expression with enrichment in pathways related to regulation of mRNA translation and protein synthesis (eIF2 signaling and regulation of eIF4 and p70S6K signaling. Overall, these data demonstrate that light-use waterpipe smoking is associated with epigenetic changes and related transcriptional modifications in the SAE, the cell population demonstrating the earliest pathologic abnormalities associated with chronic cigarette smoking.

Smoking cessation, lung function, and weight gain : a follow-up study

NARCIS (Netherlands)

Chinn, S; Jarvis, D; Melotti, R; Luczynska, C; Ackermann-Liebrich, U; Anto, JM; Cerveri, [No Value; de Marco, R; Gislason, T; Heinrich, J; Janson, C; Kunzli, N; Leynaert, B; Neukirch, F; Schouten, J; Sunyer, J; Svanes, C; Vermeire, P; Wjst, M; Burney, P

2005-01-01

Background Only one population-based study in one country has reported effects of smoking cessation and weight change on lung function, and none has reported the net effect. We estimated the net benefit of smoking cessation, and the independent effects of smoking and weight change on change in

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)

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

Evaluating the impacts of screening and smoking cessation programmes on lung cancer in a high-burden region of the USA: a simulation modelling study.

Science.gov (United States)

Tramontano, Angela C; Sheehan, Deirdre F; McMahon, Pamela M; Dowling, Emily C; Holford, Theodore R; Ryczak, Karen; Lesko, Samuel M; Levy, David T; Kong, Chung Yin

2016-02-29

While the US Preventive Services Task Force has issued recommendations for lung cancer screening, its effectiveness at reducing lung cancer burden may vary at local levels due to regional variations in smoking behaviour. Our objective was to use an existing model to determine the impacts of lung cancer screening alone or in addition to increased smoking cessation in a US region with a relatively high smoking prevalence and lung cancer incidence. Computer-based simulation model. Simulated population of individuals 55 and older based on smoking prevalence and census data from Northeast Pennsylvania. Hypothetical lung cancer control from 2014 to 2050 through (1) screening with CT, (2) intensified smoking cessation or (3) a combination strategy. Primary outcomes were lung cancer mortality rates. Secondary outcomes included number of people eligible for screening and number of radiation-induced lung cancers. Combining lung cancer screening with increased smoking cessation would yield an estimated 8.1% reduction in cumulative lung cancer mortality by 2050. Our model estimated that the number of screening-eligible individuals would progressively decrease over time, indicating declining benefit of a screening-only programme. Lung cancer screening achieved a greater mortality reduction in earlier years, but was later surpassed by smoking cessation. Combining smoking cessation programmes with lung cancer screening would provide the most benefit to a population, especially considering the growing proportion of patients ineligible for screening based on current recommendations. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/

Pulmonary microRNA profiling: implications in upper lobe predominant lung disease.

Science.gov (United States)

Armstrong, David A; Nymon, Amanda B; Ringelberg, Carol S; Lesseur, Corina; Hazlett, Haley F; Howard, Louisa; Marsit, Carmen J; Ashare, Alix

2017-01-01

Numerous pulmonary diseases manifest with upper lobe predominance including cystic fibrosis, smoking-related chronic obstructive pulmonary disease, and tuberculosis. Zonal hypoxia, characteristic of these pulmonary maladies, and oxygen stress in general is known to exert profound effects on various important aspects of cell biology. Lung macrophages are major participants in the pulmonary innate immune response and regional differences in macrophage responsiveness to hypoxia may contribute in the development of lung disease. MicroRNAs are ubiquitous regulators of human biology and emerging evidence indicates altered microRNA expression modulates respiratory disease processes. The objective of this study is to gain insight into the epigenetic and cellular mechanisms influencing regional differences in lung disease by investigating effect of hypoxia on regional microRNA expression in the lung. All studies were performed using primary alveolar macrophages ( n  = 10) or bronchoalveolar lavage fluid ( n  = 16) isolated from human subjects. MicroRNA was assayed via the NanoString nCounter microRNA assay. Divergent molecular patterns of microRNA expression were observed in alternate lung lobes, specifically noted was disparate expression of miR-93 and miR-4454 in alveolar macrophages along with altered expression of miR-451a and miR-663a in bronchoalveolar lavage fluid. Gene ontology was used to identify potential downstream targets of divergent microRNAs. Targets include cytokines and matrix metalloproteinases, molecules that could have a significant impact on pulmonary inflammation and fibrosis. Our findings show variant regional microRNA expression associated with hypoxia in alveolar macrophages and BAL fluid in the lung-upper vs lower lobe. Future studies should address whether these specific microRNAs may act intracellularly, in a paracrine/endocrine manner to direct the innate immune response or may ultimately be involved in pulmonary host-to-pathogen trans

Epidemiology of Lung Cancer.

Science.gov (United States)

Schwartz, Ann G; Cote, Michele L

2016-01-01

Lung cancer continues to be one of the most common causes of cancer death despite understanding the major cause of the disease: cigarette smoking. Smoking increases lung cancer risk 5- to 10-fold with a clear dose-response relationship. Exposure to environmental tobacco smoke among nonsmokers increases lung cancer risk about 20%. Risks for marijuana and hookah use, and the new e-cigarettes, are yet to be consistently defined and will be important areas for continued research as use of these products increases. Other known environmental risk factors include exposures to radon, asbestos, diesel, and ionizing radiation. Host factors have also been associated with lung cancer risk, including family history of lung cancer, history of chronic obstructive pulmonary disease and infections. Studies to identify genes associated with lung cancer susceptibility have consistently identified chromosomal regions on 15q25, 6p21 and 5p15 associated with lung cancer risk. Risk prediction models for lung cancer typically include age, sex, cigarette smoking intensity and/or duration, medical history, and occupational exposures, however there is not yet a risk prediction model currently recommended for general use. As lung cancer screening becomes more widespread, a validated model will be needed to better define risk groups to inform screening guidelines.

Kids and Smoking (For Parents)

Science.gov (United States)

... can cause cancer, heart disease, and lung disease. E-cigarettes , vape pens, and hookahs (water pipes) , which have ... and Asthma Nicotine: What Parents Need to Know E-Cigarettes Secondhand Smoke What Are the Risks of Smoking ...

Interaction of smoking and urban air pollution in the etiology of lung cancer

Energy Technology Data Exchange (ETDEWEB)

Jedrychowski, W

1983-01-01

Surveillance of lung cancer incidence based on mortality was carried out over 6 years in Cracow. It appeared that lung cancer death rates among Cracow inhabitants were higher than average rate in the population of Poland but this difference in the large extent could be explained by the greater prevalence of smoking habit in Cracow than in whole Poland. Very intriguing was a substantial excess of lung cancer deaths only in male residents of the city center having the highest level of the air pollution. Since this excess in the lung cancer deaths could not be exclusively explained by smoking or occupational hazards the air pollution should be assumed as a responsible factor. Lack of the similar phenomenon in females living in the city center can be explained by the fact that the air pollution alone is not sufficient cause in the etiology of lung cancer but that in combination with other adverse factors like smoking or occupational hazards it develops its carcinogenic effect.

Role of aberrant WNT signalling in the airway epithelial response to cigarette smoke in chronic obstructive pulmonary disease

NARCIS (Netherlands)

Heijink, Hilde; de Bruin, Harold G.; van den Berge, Maarten; Bennink, Lisa J. C.; Brandenburg, Simone M.; Gosens, Reinoud; van Oosterhout, Antoon J.; Postma, Dirkje S.

Background WNT signalling is activated during lung tissue damage and inflammation. We investigated whether lung epithelial expression of WNT ligands, receptors (frizzled; FZD) or target genes is dysregulated on cigarette smoking and/or in chronic obstructive pulmonary disease (COPD). Methods We

Prevalence of chronic obstructive pulmonary disease according to BTS, ERS, GOLD and ATS criteria in relation to doctor's diagnosis, symptoms, age, gender, and smoking habits.

Science.gov (United States)

Lindberg, Anne; Jonsson, Ann-Christin; Rönmark, Eva; Lundgren, Rune; Larsson, Lars-Gunnar; Lundbäck, Bo

2005-01-01

Guidelines and standards for diagnosis and management of chronic obstructive pulmonary disease (COPD) have been presented by different national and international societies, but the spirometric criteria for COPD differ between guidelines. To estimate prevalence of COPD using the guidelines of the British Thoracic Society (BTS), the European Respiratory Society (ERS), the Global Initiative for Chronic Obstructive Lung Disease (GOLD), and the American Thoracic Society (ATS). Further, to evaluate reported airway symptoms, contacts with health care providers, and physician diagnosis of COPD in relation to the respective criteria, and gender differences. In 1992 a postal questionnaire was sent to a random sample of adults aged 20-69 years, 4,851 (85%) out of 5,681 subjects responded. In 1994-1995 a random sample of the responders, 970 subjects, were invited to a structured interview and a lung function test; 666 (69%) participated. The prevalence of COPD was 7.6, 14.0, 14.1, 12.2 and 34.1% according to BTS, ERS, GOLD, clinical ATS (with symptoms or physician diagnosis), and spirometric ATS criteria, respectively. Prevalent COPD was related to age, smoking habits and family history of obstructive airway disease but not to gender. Physician diagnosis of chronic bronchitis or emphysema was only reported by 16.3, 12.2, 11.0, 23.4 and 8.2% of subjects fulfilling the respective criteria, though a majority reported airway symptoms. The main determinants for prevalent COPD were age, smoking habits and spirometric criteria of COPD. Though a majority reported airway symptoms and contact with health care providers due to respiratory complaints, only a minority was diagnosed as having COPD, indicating a large underdiagnosis. Copyright (c) 2005 S. Karger AG, Basel.

Cigarette smoking and pulmonary diffusion defects in rheumatoid arthritis.

Science.gov (United States)

Westedt, M L; Hazes, J M; Breedveld, F C; Sterk, P J; Dijkman, J H

1998-01-01

The pathogenesis of lung disease in rheumatoid arthritis (RA) has still to be defined. Risk factors associated with lung involvement in RA were investigated by means of pulmonary function studies in 40 RA patients without apparent lung disease. A decreased carbon monoxide (CO) diffusion capacity indicative of interstitial lung disease (ILD) was the main pulmonary function defect found in the first 20 patients. The occurrence was associated with current cigarette smoking. This association was confirmed in a case control study performed subsequently. These data suggest that ILD in RA is stimulated by smoking and provide an additional argument that modification of smoking behaviour in RA patients might lead to less severe complications.

Estimating mortality due to cigarette smoking

DEFF Research Database (Denmark)

Brønnum-Hansen, H; Juel, K

2000-01-01

We estimated the mortality from various diseases caused by cigarette smoking using two methods and compared the results. In one method, the "Prevent" model is used to simulate the effect on mortality of the prevalence of cigarette smoking derived retrospectively. The other method, suggested by R....... Peto et al (Lancet 1992;339:1268-1278), requires data on mortality from lung cancer among people who have never smoked and among smokers, but it does not require data on the prevalence of smoking. In the Prevent model, 33% of deaths among men and 23% of those among women in 1993 from lung cancer...... are small and appear to be explicable. The Prevent model can be used for more general scenarios of effective health promotion, but it requires more data than the Peto et al method, which can be used only to estimate mortality related to smoking....

Tobacco smoke exposure suppresses radiation-induced inflammation in the lung

International Nuclear Information System (INIS)

Bjermer, L.; Cai, Y.; Nilsson, K.; Hellstroem, S.; Henriksson, R.

1993-01-01

Previous studies on patients with breast cancer, who received postsurgical irradiation, displayed a markedly suppressed inflammatory response in the lung of smoking patients compared to nonsmokers. The aim of the present study was to investigate further the effect of exposure to tobacco smoke on the development of irradiation-induced pneumonitis in the rat. Four groups of animals were used: controls (C); those exposed to tobacco smoke (S); those irradiated but not exposed to smoke (RNS); and those irradiated and exposed to tobacco smoke (RS). The rats were exposed to a diluted main stream of cigarette smoke, at a concentration of about 0.4 mgxl -1 , in a nose-only exposure system for 1 hxday -1 , 5 daysxweek -1 for 10 weeks. Exposure to tobacco smoke started 3 weeks before irradiation. The basal one third of both lungs was exposed to a single radiation dose of 28 Gy (6 MeV photons). All animals were killed 7 weeks after irradiation. We compared findings in bronchoalveolar lavage (BAL) and tissue morphology. The alveolar tissue showed less inflammation in the RS-group than in the RNS-group. Most strikingly, mast cells were increased one hundredfold in the lung interstitium and thirty fold in the peribronchial area in the RNS-group, whereas no increase was found in the RS-group or in the controls. The alveolar septa of the RNS-group were thickened, with occurrence of inflammatory cells and mast cells, whereas the RS-group displayed no difference as compared to the non-irradiated, nonsmoking group (C). There was a marked discrepancy between the findings in BAL and tissue of the alveolar space or lung interstitium. In BAL, neutrophils, and to a lesser extent lymphocytes, were increased both in the RS- and RNS-group; however, with significantly higher numbers in the RNS-group. In contrast, the cells in the alveolar space and interstitium were dominated by mononuclear cells, mainly macrophages. Moreover, a more than twenty fold increase in total cells in the alveolar

Multimodal e-Health Services for Smoking Cessation and Public Health: The SmokeFreeBrain Project Approach.

Science.gov (United States)

Bamidis, Panagiotis D; Paraskevopoulos, Evangelos; Konstantinidis, Evdokimos; Spachos, Dimitris; Billis, Antonis

2017-01-01

Smoking is the largest avoidable cause of preventable morbidity worldwide. It causes most of the cases of lung cancer and chronic obstructive pulmonary disease (COPD) and contributes to the development of other lung diseases. SmokeFreeBrain aims to address the effectiveness of a multi-level variety of interventions aiming at smoking cessation in high risk target groups within High Middle Income Countries (HMIC) such as unemployed young adults, COPD and asthma patients, and within the general population in Low-Middle Income Countries (LMIC). The project addresses existing approaches aimed to prevent lung diseases caused by tobacco while developing new treatments and evaluating: (i) Public Service Announcement (PSA) against smoking, (ii) the use of electronic cigarettes, (iii) neurofeedback protocols against smoking addiction, (iv) a specifically developed intervention protocol based on behavioral therapy, social media/mobile apps and short text messages (sms) and (v) pharmacologic interventions. Emphasis in this paper, however, is placed on the e-heath, m-health, open (big) data, mobile game and neuroscientific challenges and developments upon facilitating the aforementioned interventions.

Smoking and skin disease

DEFF Research Database (Denmark)

Thomsen, S F; Sørensen, L T

2010-01-01

Tobacco smoking is a serious and preventable health hazard that can cause or exacerbate a number of diseases and shorten life expectancy, but the role of smoking as an etiologic factor in the development of skin disease is largely unknown. Although epidemiological evidence is sparse, findings...... suggest that tobacco smoking is a contributing factor in systemic lupus erythematosus, psoriasis, palmoplantar pustulosis, cutaneous squamous cell carcinoma, hidradenitis suppurativa, and genital warts. In contrast, smoking may confer some protective effects and mitigate other skin diseases, notably...... pemphigus vulgaris, pyoderma gangrenosum, aphthous ulcers, and Behçet's disease. Various degenerative dermatologic conditions are also impacted by smoking, such as skin wrinkling and dysregulated wound healing, which can result in post-surgical complications and delayed or even arrested healing of chronic...

Solely lung-involved IgG4-related disease : a case report and review of the literature.

Science.gov (United States)

Zhang, Xiao-Qin; Chen, Guo-Ping; Wu, Sheng-Chang; Yu, Sa; Wang, Hong; Chen, Xuan-Yi; Ren, Zhuo-Chao

2016-12-23

By analyzing the clinical data of 1 case of IgG4-related lung disease(IgG4-RLD) and the review of literature, the author investigated the clinical characteristics of IgG4-RLD. IgG4-RLD is a rare disease characterized by significant elevation of serum IgG4 and infiltration of a large number of IgG4+ plasma cells. The clinical manifestations of the disease were nonspecific, and the imaging features were mixed with several types. The disease can only be involved in the lung, but also multiple organ involvement. Solely lung-involved IgG4-RD is not only extremely rare but also easily misdiagnosed as tuberculosis, lung cancer, lymphoma and other common pulmonary diseases. Histopathological examination is the key to the diagnosis of the disease. Corticosteroids are the first choice of treatment, and the overall prognosis is good.

Effects of smoking cessation on hypoxia and its potential impact on radiation treatment effects in lung cancer patients

Energy Technology Data Exchange (ETDEWEB)

Nieder, C. [Radiation Oncology Unit, Medical Dept., Nordlandssykehuset HF, Bodo (Norway); Inst. of Clinical Medicine, Faculty of Medicine, Univ. of Tromso (Norway); Bremnes, R.M. [Inst. of Clinical Medicine, Faculty of Medicine, Univ. of Tromso (Norway); Dept. of Oncology, Univ. Hospital of North Norway, Tromso (Norway)

2008-11-15

Background and purpose: smoking cessation is often attempted in the context of a lung cancer diagnosis. If cessation causes slowly continuing changes of total lung capacity and vital capacity, this may have consequences for lung volume, results of dose-volume histogram (DVH) analysis and targeting precision, in addition to changes in oxygenation, tumor biology (gene expression) and prognosis. Methods: to address the impact of smoking cessation on radiation treatment of lung cancer, a literature review was performed. Results: smoking cessation is associated with important benefits such as improved lung function and a better general health and performance status. In surgically and radiation treated patients, smoking cessation might lead to longer survival and reduced complications. Early data indicate that hypoxia in non-small cell lung cancer should be considered a poor prognostic factor. Yet, specific human data on how hypoxia is influenced by smoking status are not available. The influence of smoking history on the pneumonitis risk is not entirely clear. However, it appears that other factors outweigh the influence of smoking. The short-term effects of smoking cessation on lung function do not appear to cause relevant errors in treatment planning or targeting precision. Yet, no prospective study formally addressing this question was identified. Conclusion: smoking cessation appears to be prognostically beneficial. The role of hypoxia in this context requires more detailed evaluation. (orig.)

[Motivations and obstacles to occupational disease claims in lung cancer patients: an exploratory psychosocial study].

Science.gov (United States)

Britel, Manon; Pérol, Olivia; Blois Da Conceiçao, Stéphanie; Ficty, Manon; Brunet, Houria; Avrillon, Virginie; Charbotel, Barbara; Fervers, Béatrice

2017-10-02

The proportion of lung cancers with an occupational origin has been estimated to be between 10 and 20%. They are largely under-reported, as 60% are not compensated as occupational disease. Although most patients are not familiar with the process of compensation, other factors could explain this under-reporting. The aim of this study was to identify psychosocial factors that could impact patients with occupational lung cancer to claim for compensation. We conducted a case study involving semi-structured interviews with eight lung cancer patients enrolled in a cohort designed to systematically screen occupational exposures and propose claims for compensation to work-related cancer patients. Seven interviewed patients were familiar with occupational cancers, but most of them did not believe that past exposure could be related to their current disease. Patients associated compensation claims with a long and complex procedure for an abstract purpose. Several patients expressed a certain attachment to their employers. Interviewed patients often considered compensation claims to be a grievance procedure against the employers whom they did not consider to be responsible for their disease. Lung cancer is itself an obstacle to compensation considering the aggressive treatments and related adverse events, the poor medium-term prognosis and the predominant role of smoking in the etiology of the disease. Patients mentioned the financial compensation and the role of healthcare professionals as key elements to motivate them to claim for compensation.

Perinatal exposure to environmental tobacco smoke is associated with changes in DNA methylation that precede the adult onset of lung disease in a mouse model.

Science.gov (United States)

Cole, Elizabeth; Brown, Traci A; Pinkerton, Kent E; Postma, Britten; Malany, Keegan; Yang, Mihi; Kim, Yang Jee; Hamilton, Raymond F; Holian, Andrij; Cho, Yoon Hee

2017-08-01

Prenatal and early-life environmental tobacco smoke (ETS) exposure can induce epigenetic alterations associated with inflammation and respiratory disease. The objective of this study was to address the long-term epigenetic consequences of perinatal ETS exposure on latent respiratory disease risk, which are still largely unknown. C57BL/6 mice were exposed to prenatal and early-life ETS; offspring lung pathology, global DNA, and gene-specific methylation were measured at two adult ages. Significant alterations in global DNA methylation and promoter methylation of IFN-γ and Thy-1 were found in ETS-exposed offspring at 10-12 and 20 weeks of age. These sustained epigenetic alterations preceded the onset of significant pulmonary pathologies observed at 20 weeks of age. This study suggests that perinatal ETS exposure induces persistent epigenetic alterations in global DNA, as well as IFN-γ and Thy-1 promoter methylation that precede the adult onset of fibrotic lung pathology. These epigenetic findings could represent potential biomarkers of latent respiratory disease risk.

Effects of cigarette smoking on I-123 IMP clearance from the lung

International Nuclear Information System (INIS)

Katoh, Kunihiko; Takahashi, Tsuneo

1990-01-01

N-isopropyl-p-I-123-iodoamphetamine (I-123 IMP), originally developed as a brain scanning agent, is also taken up by the lung. To evaluate the cigarette smoking on the uptake of IMP by the lung, we studied I-123 IMP clearance from the lung on 14 volunteers; 5 non-smokers and 9 smokers. After the injection of 111 MBq (3mCi) of I-123 IMP into the medial cubital vein, the time-activity curve for 60 minutes and the regional activity using 1 frame per minute and a 64 x 64 matrix was obtained. I-123 IMP clearance curve was described as follows: C(t)=A 1 e -k1t +A 2 e -k2t (A 1 , A 2 : intercepts, and k 1 , k 2 : slopes of the exponential components). I-123 IMP clearance was delayed in smokers, and k 2 was smaller in smokers. Also a significant correlations between k 1 , k 2 , and the number of cigarettes smoked per day were found. In conclusion, this study suggests that the delayed clearance and retention of I-123 IMP in the lung indicate the lung metabolic disorders due to cigarette smoking. (author)

Smoking Cessation and the Microbiome in Induced Sputum Samples from Cigarette Smoking Asthma Patients.

Directory of Open Access Journals (Sweden)

Christian Munck

Full Text Available Asthma is a common disease causing cough, wheezing and shortness of breath. It has been shown that the lung microbiota in asthma patients is different from the lung microbiota in healthy controls suggesting that a connection between asthma and the lung microbiome exists. Individuals with asthma who are also tobacco smokers experience more severe asthma symptoms and smoking cessation is associated with improved asthma control. In the present study we investigated if smoking cessation in asthma patients is associated with a change in the bacterial community in the lungs, examined using induced sputum. We found that while tobacco smokers with asthma have a greater bacterial diversity in the induced sputum compared to non-smoking healthy controls, smoking cessation does not lead to a change in the microbial diversity.

Are generic and disease-specific health related quality of life correlated? The case of chronic lung disease due to sulfur mustard

Directory of Open Access Journals (Sweden)

Shervin Assari

2009-09-01

Full Text Available

• BACKGROUND: The aim of this study was to investigate the association between the two most commonly used generic and disease specific health-related quality of life (HRQoL measures in patients with chronic lung disease due to SM: Medical Outcomes Study Short Form 36-Item (SF-36 and St George's Respiratory Questionnaire (SGRQ.
• METHODS: This is a secondary analysis of Iranian Chemical Warfare Victims Health Assessment Study (ICWVHAS during October 2007 in Isfahan, Iran. In that survey, conducted in an outpatient setting, 292 patients with chronic lung disease due to SM were selected from all provinces in Iran. The total score and sub scores of correlations of SGRQ and SF-36 were assessed. Correlation of quality-of-life scores were evaluated using Pearson’s coefficient.
• RESULTS: Samples were 276 patients who were selected for our analysis. No significant correlation was found between the total score or sub scores of SF-36 and the total score or sub scores of SGRQ (p > 0.05.
• CONCLUSIONS: In patients with chronic lung disease due to SM, the SF-36 and SGRQ assess different aspects of HRQoL. Therefore applying both of them together, at least in the research setting is suggested.
• KEYWORDS: Chronic Lung Disease, Health Related Quality of Life, Generic Health Related Quality of Life, Disease Specific Health Related Quality of Life, Sulfur Mustard.

Risk of chronic bronchitis in twin pairs discordant for smoking

DEFF Research Database (Denmark)

Meteran, Howraman; Thomsen, Simon Francis; Harmsen, Lotte

2012-01-01

It is well known that smoking is a major risk factor for lung disease and respiratory symptoms. We examined the association between smoking and the risk of chronic bronchitis in a large twin sample.......It is well known that smoking is a major risk factor for lung disease and respiratory symptoms. We examined the association between smoking and the risk of chronic bronchitis in a large twin sample....

Cigarette smoking and radiation exposure in relation to cancer mortality, Hiroshima and Nagasaki

International Nuclear Information System (INIS)

Prentice, R.L.; Yoshimoto, Yasuhiko; Mason, M.W.

1983-05-01

Cancer mortality among 40,498 Hiroshima and Nagasaki residents was examined in relation to cigarette smoking habits and estimated atomic bomb radiation exposure. Relative risk models that are either multiplicative or additive in the two exposures (smoking radiation) were emphasized. Most analyses were directed toward all nonhematologic cancer, stomach cancer, lung cancer, or digestive cancer other than stomach, for which there were, respectively, 1,725, 658, 281, and 338 deaths in the follow-up period of this study. Persons heavily exposed to both cigarette smoke and radiation were found to have significantly lower cancer mortality than multiplcative relative risk models would suggest for all nonhematologic cancer, stomach cancer, and digestive cancer other than stomach. Surprisingly, the relative risk function appeared not only to be submultiplicative for these cancer sites, but to be subadditive as well. The lung cancer relative risk function could not be distinguished from either a multiplicative or an additive form. The number of deaths was sufficient to permit some more detailed study of all nonhematologic cancer mortality: Relative risk functions appeared to be consistent between males and females though a paucity of heavy smoking females limits the precision of this comparison. (author)

The role of proteases, endoplasmic reticulum stress and SERPINA1 heterozygosity in lung disease and alpha-1 anti-trypsin deficiency.

LENUS (Irish Health Repository)

Greene, Catherine M

2012-02-01

The serine proteinase inhibitor alpha-1 anti-trypsin (AAT) provides an antiprotease protective screen throughout the body. Mutations in the AAT gene (SERPINA1) that lead to deficiency in AAT are associated with chronic obstructive pulmonary diseases. The Z mutation encodes a misfolded variant of AAT that is not secreted effectively and accumulates intracellularly in the endoplasmic reticulum of hepatocytes and other AAT-producing cells. Until recently, it was thought that loss of antiprotease function was the major cause of ZAAT-related lung disease. However, the contribution of gain-of-function effects is now being recognized. Here we describe how both loss- and gain-of-function effects can contribute to ZAAT-related lung disease. In addition, we explore how SERPINA1 heterozygosity could contribute to smoking-induced chronic obstructive pulmonary diseases and consider the consequences.

OP36 Decisions about smoking in patients screened with the early cdt-lung test for the early detection of lung cancer: a qualitative study

OpenAIRE

Young, Ben; Vedhara, Kavita; Robertson, John; das Nair, Roshan

2017-01-01

Background: \\ud Routine screening for lung cancer in high risk groups (characterised by age and smoking history) is recommended in the USA and may be implemented elsewhere. It is unclear whether being screened for lung cancer promotes smoking cessation or conversely provides false reassurance and a ‘license to smoke’. This study aimed to understand how experiences of lung cancer screening influence individual decision making about smoking.\\ud \\ud Methods:\\ud Thirty one people in Scotland, age...

Cellular and molecular mechanisms of cigarette smoke-induced lung damage and prevention by vitamin C

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Roy Siddhartha

2008-11-01

Full Text Available Abstract Background Cigarette smoke-induced cellular and molecular mechanisms of lung injury are not clear. Cigarette smoke is a complex mixture containing long-lived radicals, including p-benzosemiquinone that causes oxidative damage. Earlier we had reported that oxidative protein damage is an initial event in smoke-induced lung injury. Considering that p-benzosemiquinone may be a causative factor of lung injury, we have isolated p-benzosemiquinone and compared its pathophysiological effects with cigarette smoke. Since vitamin C is a strong antioxidant, we have also determined the modulatory effect of vitamin C for preventing the pathophysiological events. Methods Vitamin C-restricted guinea pigs were exposed to cigarette smoke (5 cigarettes/day; 2 puffs/cigarette for 21 days with and without supplementation of 15 mg vitamin C/guinea pig/day. Oxidative damage, apoptosis and lung injury were assessed in vitro, ex vivo in A549 cells as well as in vivo in guinea pigs. Inflammation was measured by neutrophilia in BALF. p-Benzosemiquinone was isolated from freshly prepared aqueous extract of cigarette smoke and characterized by various physico-chemical methods, including mass, NMR and ESR spectroscopy. p-Benzosemiquinone-induced lung damage was examined by intratracheal instillation in guinea pigs. Lung damage was measured by increased air spaces, as evidenced by histology and morphometric analysis. Oxidative protein damage, MMPs, VEGF and VEGFR2 were measured by western blot analysis, and formation of Michael adducts using MALDI-TOF-MS. Apoptosis was evidenced by TUNEL assay, activation of caspase 3, degradation of PARP and increased Bax/Bcl-2 ratio using immunoblot analysis and confocal microscopy. Results Exposure of guinea pigs to cigarette smoke resulted in progressive protein damage, inflammation, apoptosis and lung injury up to 21 days of the experimental period. Administration of 15 mg of vitamin C/guinea pig/day prevented all these

Exposure to neonatal cigarette smoke causes durable lung changes but does not potentiate cigarette smoke–induced chronic obstructive pulmonary disease in adult mice

Science.gov (United States)

McGrath-Morrow, Sharon; Malhotra, Deepti; Lauer, Thomas; Collaco, J. Michael; Mitzner, Wayne; Neptune, Enid; Wise, Robert; Biswal, Shyam

2016-01-01

The impact of early childhood cigarette smoke (CS) exposure on CS-induced chronic obstructive pulmonary disease (COPD) is unknown. This study was performed to evaluate the individual and combined effects of neonatal and adult CS exposure on lung structure, function, and gene expression in adult mice. To model a childhood CS exposure, neonatal C57/B6 mice were exposed to 14 days of CS (Neo CS). At 10 weeks of age, Neo CS and control mice were exposed to 4 months of CS. Pulmonary function tests, bronchoalveolar lavage, and lung morphometry were measured and gene expression profiling was performed on lung tissue. Mean chord lengths and lung volumes were increased in neonatal and/or adult CS-exposed mice. Differences in immune, cornified envelope protein, muscle, and erythrocyte genes were found in CS-exposed lung. Neonatal CS exposure caused durable structural and functional changes in the adult lung but did not potentiate CS-induced COPD changes. Cornified envelope protein gene expression was decreased in all CS-exposed mice, whereas myosin and erythrocyte gene expression was increased in mice exposed to both neonatal and adult CS, suggesting an adaptive response. Additional studies may be warranted to determine the utility of these genes as biomarkers of respiratory outcomes. PMID:21649527

Gene and metabolite time-course response to cigarette smoking in mouse lung and plasma.

Directory of Open Access Journals (Sweden)

Mikaela A Miller

Full Text Available Prolonged cigarette smoking (CS causes chronic obstructive pulmonary disease (COPD, a prevalent serious condition that may persist or progress after smoking cessation. To provide insight into how CS triggers COPD, we investigated temporal patterns of lung transcriptome expression and systemic metabolome changes induced by chronic CS exposure and smoking cessation. Whole lung RNA-seq data was analyzed at transcript and exon levels from C57Bl/6 mice exposed to CS for 1- or 7 days, for 3-, 6-, or 9 months, or for 6 months followed by 3 months of cessation using age-matched littermate controls. We identified previously unreported dysregulation of pyrimidine metabolism and phosphatidylinositol signaling pathways and confirmed alterations in glutathione metabolism and circadian gene pathways. Almost all dysregulated pathways demonstrated reversibility upon smoking cessation, except the lysosome pathway. Chronic CS exposure was significantly linked with alterations in pathways encoding for energy, phagocytosis, and DNA repair and triggered differential expression of genes or exons previously unreported to associate with CS or COPD, including Lox, involved in matrix remodeling, Gp2, linked to goblet cells, and Slc22a12 and Agpat3, involved in purine and glycerolipid metabolism, respectively. CS-induced lung metabolic pathways changes were validated using metabolomic profiles of matched plasma samples, indicating that dynamic metabolic gene regulation caused by CS is reflected in the plasma metabolome. Using advanced technologies, our study uncovered novel pathways and genes altered by chronic CS exposure, including those involved in pyrimidine metabolism, phosphatidylinositol signaling and lysosome function, highlighting their potential importance in the pathogenesis or diagnosis of CS-associated conditions.

Impact of Neuro-Psychological Factors on Smoking-Associated Lung Cancer

Energy Technology Data Exchange (ETDEWEB)

Schuller, Hildegard M. [Experimental Oncology Laboratory, Department of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, 2407 River Drive, Knoxville, TN 37996 (United States)

2014-03-13

Smoking has been extensively documented as a risk factor for all histological types of lung cancer and tobacco-specific nitrosamines and polycyclic aromatic hydrocarbons reproducibly cause lung cancer in laboratory rodents. However, the most common lung cancer, non-small cell lung cancer (NSCLC), frequently develops in never smokers and is particularly common in women and African Americans, suggesting that factors unrelated to smoking significantly impact this cancer. Recent experimental investigations in vitro and in animal models have shown that chronic psychological stress and the associated hyperactive signaling of stress neurotransmitters via β-adrenergic receptors significantly promote the growth and metastatic potential of NSCLC. These responses were caused by modulation in the expression and sensitization state of nicotinic acetylcholine receptors (nAChRs) that regulate the production of stress neurotransmitters and the inhibitory neurotransmitter γ-aminobutyric acid (GABA). Similar changes in nAChR-mediated neurotransmitter production were identified as the cause of NSCLC stimulation in vitro and in xenograft models by chronic nicotine. Collectively, these data suggest that hyperactivity of the sympathetic branch of the autonomic nervous system caused by chronic psychological stress or chronic exposure to nicotinic agonists in cigarette smoke significantly contribute to the development and progression of NSCLC. A recent clinical study that reported improved survival outcomes with the incidental use of β-blockers among patients with NSCLC supports this interpretation.

Impact of Neuro-Psychological Factors on Smoking-Associated Lung Cancer

International Nuclear Information System (INIS)

Schuller, Hildegard M.

2014-01-01

Smoking has been extensively documented as a risk factor for all histological types of lung cancer and tobacco-specific nitrosamines and polycyclic aromatic hydrocarbons reproducibly cause lung cancer in laboratory rodents. However, the most common lung cancer, non-small cell lung cancer (NSCLC), frequently develops in never smokers and is particularly common in women and African Americans, suggesting that factors unrelated to smoking significantly impact this cancer. Recent experimental investigations in vitro and in animal models have shown that chronic psychological stress and the associated hyperactive signaling of stress neurotransmitters via β-adrenergic receptors significantly promote the growth and metastatic potential of NSCLC. These responses were caused by modulation in the expression and sensitization state of nicotinic acetylcholine receptors (nAChRs) that regulate the production of stress neurotransmitters and the inhibitory neurotransmitter γ-aminobutyric acid (GABA). Similar changes in nAChR-mediated neurotransmitter production were identified as the cause of NSCLC stimulation in vitro and in xenograft models by chronic nicotine. Collectively, these data suggest that hyperactivity of the sympathetic branch of the autonomic nervous system caused by chronic psychological stress or chronic exposure to nicotinic agonists in cigarette smoke significantly contribute to the development and progression of NSCLC. A recent clinical study that reported improved survival outcomes with the incidental use of β-blockers among patients with NSCLC supports this interpretation

Genome-wide association analysis identifies new lung cancer susceptibility loci in never-smoking women in Asia.

NARCIS (Netherlands)

Lan, Q.; Hsiung, C.A.; Matsuo, K.; Hong, Y.C.; Seow, A.; Wang, Z.; Hosgood, H.D.; Chen, K.; Wang, J.C.; Chatterjee, N.; Hu, W.; Wong, M.P.; Zheng, W.; Caporaso, N.; Park, J.Y.; Chen, C.J.; Kim, Y.H.; Kim, Y.T.; Landi, M.T.; Shen, H.; Lawrence, C.; Burdett, L.; Yeager, M.; Yuenger, J.; Jacobs, K.B.; Chang, I.S.; Mitsudomi, T.; Kim, H.N.; Chang, G.C.; Bassig, B.A.; Tucker, M.; Wei, F.; Yin, Y.; Wu, C.; An, S.J.; Qian, B.; Lee, V.H.; Lu, D.; Liu, J.; Jeon, H.S.; Hsiao, C.F.; Sung, J.S.; Kim, J.H.; Gao, Y.T.; Tsai, Y.H.; Jung, Y.J.; Guo, H.; Hu, Z.; Hutchinson, A.; Wang, W.C.; Klein, R.; Chung, C.C.; Oh, I.J.; Chen, K.Y.; Berndt, S.I.; He, X.; Wu, W.; Chang, J.; Zhang, X.C.; Huang, M.S.; Zheng, H.; Wang, J.; Zhao, X.|info:eu-repo/dai/nl/413577805; Li, Y.; Choi, J.E.; Su, W.C.; Park, K.H.; Sung, S.W.; Shu, X.O.; Chen, Y.M.; Liu, L.; Kang, C.H.; Hu, L.; Chen, C.H.; Pao, W.; Kim, Y.C.; Yang, T.Y.; Xu, J.; Guan, P.; Tan, W.; Su, J.; Wang, C.L.; Li, H.; Sihoe, A.D.; Zhao, Z.|info:eu-repo/dai/nl/304120995; Chen, Y.; Choi, Y.Y.; Hung, J.Y.; Kim, J.S.; Yoon, H.I.; Cai, Q.; Lin, C.C.; Park, I.K.; Xu, P.; Dong, J.; Kim, C.; He, Q; Perng, R.P.; Kohno, T.; Kweon, S.S.; Chen, C.Y.; Vermeulen, R.|info:eu-repo/dai/nl/216532620; Wu, J.; Lim, W.Y.; Chen, K.C.; Chow, W.H.; Ji, B.T.; Chan, J.K.; Chu, M.; Li, Y.J.; Yokota, J.; Li, J.; Chen, H.; Xiang, Y.B.; Yu, C.J.; Kunitoh, H.; Wu, G.; Jin, L.; Lo, Y.L.; Shiraishi, K.; Chen, Y.H.; Lin, H.C.; Wu, T.; WU, Y.; Yang, P.C.; Zhou, B.; Shin, M.H.; Fraumeni, J.F.; Lin, D.; Chanock, S.J.; Rothman, N.

2012-01-01

To identify common genetic variants that contribute to lung cancer susceptibility, we conducted a multistage genome-wide association study of lung cancer in Asian women who never smoked. We scanned 5,510 never-smoking female lung cancer cases and 4,544 controls drawn from 14 studies from mainland

The Relations Between False Positive and Negative Screens and Smoking Cessation and Relapse in the National Lung Screening Trial: Implications for Public Health.

Science.gov (United States)

Clark, Melissa A; Gorelick, Jeremy J; Sicks, JoRean D; Park, Elyse R; Graham, Amanda L; Abrams, David B; Gareen, Ilana F

2016-01-01

Lung screening is an opportunity for smoking cessation and relapse prevention, but smoking behaviors may differ across screening results. Changes in smoking were evaluated among 18 840 current and former smokers aged 55-74 scheduled to receive three annual lung screenings. Participants were randomized to low-dose computed tomography or single-view chest radiography in the American College of Radiology/National Lung Screening Trial. Outcome measures included point and sustained (6-month) abstinence and motivation to quit among smokers; and relapse among smokers who quit during follow-up, recent quitters (quit < 6 months), and long-term former smokers (quit ≥ 6 months). During five years of follow-up, annual point prevalence quit rates ranged from 11.6%-13.4%; 48% of current smokers reported a quit attempt and 7% of long-term former smokers relapsed. Any false positive screening result was associated with subsequent increased point (multivariable hazard ratio HR = 1.23, 95% CI = 1.13, 1.35) and sustained (HR = 1.28, 95% CI = 1.15, 1.43) abstinence among smokers. Recent quitters with ≥1 false positive screen were less likely to relapse (HR = 0.72, 95% CI = 0.54, 0.96). Screening result was not associated with relapse among long-term former smokers or among baseline smokers who quit during follow-up. A false positive screen was associated with increased smoking cessation and less relapse among recent quitters. Consistently negative screens were not associated with greater relapse among long-term former smokers. Given the Affordable Care Act requires most health plans to cover smoking cessation and lung screening, the impact and cost-effectiveness of lung screening could be further enhanced with the addition of smoking cessation interventions. © The Author 2015. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Modulation by metformin of molecular and histopathological alterations in the lung of cigarette smoke-exposed mice

International Nuclear Information System (INIS)

Izzotti, Alberto; Balansky, Roumen; D'Agostini, Francesco; Longobardi, Mariagrazia; Cartiglia, Cristina; Micale, Rosanna T; La Maestra, Sebastiano; Camoirano, Anna; Ganchev, Gancho; Iltcheva, Marietta; Steele, Vernon E; De Flora, Silvio

2014-01-01

The anti-diabetic drug metformin is endowed with anti-cancer properties. Epidemiological and experimental studies, however, did not provide univocal results regarding its role in pulmonary carcinogenesis. We used Swiss H mice of both genders in order to detect early molecular alterations and tumors induced by mainstream cigarette smoke. Based on a subchronic toxicity study, oral metformin was used at a dose of 800 mg/kg diet, which is 3.2 times higher than the therapeutic dose in humans. Exposure of mice to smoke for 4 months, starting at birth, induced a systemic clastogenic damage, formation of DNA adducts, oxidative DNA damage, and extensive downregulation of microRNAs in lung after 10 weeks. Preneoplastic lesions were detectable after 7.5 months in both lung and urinary tract along with lung tumors, both benign and malignant. Modulation by metformin of 42 of 1281 pulmonary microRNAs in smoke-free mice highlighted a variety of mechanisms, including modulation of AMPK, stress response, inflammation, NFκB, Tlr9, Tgf, p53, cell cycle, apoptosis, antioxidant pathways, Ras, Myc, Dicer, angiogenesis, stem cell recruitment, and angiogenesis. In smoke-exposed mice, metformin considerably decreased DNA adduct levels and oxidative DNA damage, and normalized the expression of several microRNAs. It did not prevent smoke-induced lung tumors but inhibited preneoplastic lesions in both lung and kidney. In conclusion, metformin was able to protect the mouse lung from smoke-induced DNA and microRNA alterations and to inhibit preneoplastic lesions in lung and kidney but failed to prevent lung adenomas and malignant tumors induced by this complex mixture

Secondhand tobacco smoke, arterial stiffness, and altered circadian blood pressure patterns are associated with lung inflammation and oxidative stress in rats.

Science.gov (United States)

Gentner, Nicole J; Weber, Lynn P

2012-02-01

Chronic smoking and secondhand tobacco smoke exposure are major risk factors for cardiovascular disease that are known to adversely alter the structural and mechanical properties of arteries. The objective of this study was to determine the effects of subchronic secondhand tobacco smoke exposure on circadian blood pressure patterns, arterial stiffness, and possible sources of oxidative stress in conscious, unsedated radiotelemetry-implanted rats. Pulse wave change in pressure over time (dP/dt) was used an indicator of arterial stiffness and was compared with both structural (wall thickness) and functional (nitric oxide production and bioactivity and endothelin-1 levels) features of the arterial wall. In addition, histology of lung, heart, and liver was examined as well as pulmonary and hepatic detoxifying enzyme activity (cytochrome P450, specifically CYP1A1). Subchronic secondhand tobacco smoke exposure altered the circadian pattern of heart rate and blood pressure, with a loss in the normal dipping pattern of blood pressure during sleep. Secondhand tobacco smoke exposure also increased pulse wave dP/dt in the absence of any structural modifications in the arterial wall. Furthermore, although nitric oxide production and endothelin-1 levels were not altered by secondhand tobacco smoke, there was increased inactivation of nitric oxide as indicated by peroxynitrite production. Increased lung neutrophils or pulmonary CYP1A1 may be responsible for the increase in oxidative stress in rats exposed to secondhand tobacco smoke. In turn, this may be related to the observed failure of blood pressure to dip during periods of sleep and a possible increase in arterial stiffness.

Whole exome re-sequencing implicates CCDC38 and cilia structure and function in resistance to smoking related airflow obstruction.

Directory of Open Access Journals (Sweden)

Louise V Wain

2014-05-01

Full Text Available Chronic obstructive pulmonary disease (COPD is a leading cause of global morbidity and mortality and, whilst smoking remains the single most important risk factor, COPD risk is heritable. Of 26 independent genomic regions showing association with lung function in genome-wide association studies, eleven have been reported to show association with airflow obstruction. Although the main risk factor for COPD is smoking, some individuals are observed to have a high forced expired volume in 1 second (FEV1 despite many years of heavy smoking. We hypothesised that these "resistant smokers" may harbour variants which protect against lung function decline caused by smoking and provide insight into the genetic determinants of lung health. We undertook whole exome re-sequencing of 100 heavy smokers who had healthy lung function given their age, sex, height and smoking history and applied three complementary approaches to explore the genetic architecture of smoking resistance. Firstly, we identified novel functional variants in the "resistant smokers" and looked for enrichment of these novel variants within biological pathways. Secondly, we undertook association testing of all exonic variants individually with two independent control sets. Thirdly, we undertook gene-based association testing of all exonic variants. Our strongest signal of association with smoking resistance for a non-synonymous SNP was for rs10859974 (P = 2.34 × 10(-4 in CCDC38, a gene which has previously been reported to show association with FEV1/FVC, and we demonstrate moderate expression of CCDC38 in bronchial epithelial cells. We identified an enrichment of novel putatively functional variants in genes related to cilia structure and function in resistant smokers. Ciliary function abnormalities are known to be associated with both smoking and reduced mucociliary clearance in patients with COPD. We suggest that genetic influences on the development or function of cilia in the bronchial

SMOKING AS A RISK FACTOR OF CARDIOVASCULAR AND CEREBROVASCULAR DISEASES: PREVALENCE, IMPACT ON PROGNOSIS, POSSIBLE SMOKING CESSATION STRATEGIES AND THEIR EFFECTIVENESS. Part 1. Smoking Prevalence and Impact on Prognosis

Directory of Open Access Journals (Sweden)

O. D. Ostroumova

2017-01-01

Full Text Available The prevalence of smoking in the Russian Federation is 27.7%. Losses of potential years of life in working age associated with premature death due to smoking in Russia on average are 9 years for men, for women – 5.6 years. Tobacco use is a risk factor for 6 of 8 main causes of death in the world: ischemic heart disease (IHD; cerebral circulation disorders; lower respiratory tract infection; chronic obstructive pulmonary disease; tuberculosis; trachea, bronchus, and lung cancer. The risk of developing IHD in smoking patients is increased by 2-4 times in men and women and in any age group. Myocardial infarction occurs in smoking patients at a younger age, and they have a similar risk of coronary events with patients of older age groups. The increased risk of recurrent coronary events persists with the continuation of smoking in the patient after myocardial infarction. Smoking is associated with a double risk of ischemic stroke and a 2-4-fold increase in the risk of subarachnoid hemorrhage. The risk of peripheral arteries diseases in smokers is increased 3-6 times than this in non-smokers. The mechanisms of development of acute cardiovascular events during smoking include the activation of inflammation, platelet aggregation/thrombogenesis, the sympathetic nervous system, and the development of endothelial dysfunction due to exposure to tobacco smoke components.

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

Smoking rate and periodontal disease prevalence: 40-year trends in Sweden 1970-2010.

Science.gov (United States)

Bergstrom, Jan

2014-10-01

To investigate the relationship between smoking rate and periodontal disease prevalence in Sweden. National smoking rates were found from Swedish National Statistics on smoking habits. Based on smoking rates for the years 1970-2010, periodontal disease prevalence estimates were calculated for the age bracket 40-70 years and smoking-associated relative risks between 2.0 and 20.0. The impact of smoking on the population was estimated according to the concept of population attributable fraction. The age-standardized smoking rate in Sweden declined from 44% in 1970 to 15% in 2010. In parallel with the smoking decline the calculated prevalence estimate of periodontal disease dropped from 26% to 12% assuming a 10-fold smoking-associated relative risk. Even at more moderate magnitudes of the relative risk, e.g. 2-fold or 5-fold, the prevalence decrease was quite tangible, suggesting that the current prevalence in Sweden is about 20-50% of the level 40 years ago. The population attributable fraction, estimating the portion of the disease that would have been avoided in the absence of smoking, was 80% in 1970 and 58% in 2010 at a ten-fold relative risk. Calculated estimates of periodontal disease prevalence are closely related to real changes in smoking rate. As smoking rate drops periodontal disease prevalence will drop. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Mortality Risk Prediction in Scleroderma-Related Interstitial Lung Disease: The SADL Model.

Science.gov (United States)

Morisset, Julie; Vittinghoff, Eric; Elicker, Brett M; Hu, Xiaowen; Le, Stephanie; Ryu, Jay H; Jones, Kirk D; Haemel, Anna; Golden, Jeffrey A; Boin, Francesco; Ley, Brett; Wolters, Paul J; King, Talmadge E; Collard, Harold R; Lee, Joyce S

2017-11-01

Interstitial lung disease (ILD) is an important cause of morbidity and mortality in patients with scleroderma (Scl). Risk prediction and prognostication in patients with Scl-ILD are challenging because of heterogeneity in the disease course. We aimed to develop a clinical mortality risk prediction model for Scl-ILD. Patients with Scl-ILD were identified from two ongoing longitudinal cohorts: 135 patients at the University of California, San Francisco (derivation cohort) and 90 patients at the Mayo Clinic (validation cohort). Using these two separate cohorts, a mortality risk prediction model was developed and validated by testing every potential candidate Cox model, each including three or four variables of a possible 19 clinical predictors, for time to death. Model discrimination was assessed using the C-index. Three variables were included in the final risk prediction model (SADL): ever smoking history, age, and diffusing capacity of the lung for carbon monoxide (% predicted). This continuous model had similar performance in the derivation (C-index, 0.88) and validation (C-index, 0.84) cohorts. We created a point scoring system using the combined cohort (C-index, 0.82) and used it to identify a classification with low, moderate, and high mortality risk at 3 years. The SADL model uses simple, readily accessible clinical variables to predict all-cause mortality in Scl-ILD. Copyright © 2017 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

Differential effects of smoking on lung cancer mortality before and after household stove improvement in Xuanwei, China

Energy Technology Data Exchange (ETDEWEB)

Lee, K.M.; Chapman, R.S.; Shen, M.; Lubin, J.H.; Silverman, D.T.; He, X.; Hosgood, H.D.; Chen, B.E.; Rajaraman, P.; Caporaso, N.E.; Fraumeni, J.F.; Blair, A.; Lan, Q. [NCI, Bethesda, MD (USA)

2010-08-24

In Xuanwei County, Yunnan Province, China, lung cancer mortality rates in both males and females are among the highest in China. We evaluated differential effects of smoking on lung cancer mortality before and after household stove improvement with chimney to reduce exposure to smoky coal emissions in the unique cohort in Xuanwei, China. Effects of independent variables on lung cancer mortality were measured as hazard ratios and 95% confidence intervals using a multivariable Cox regression model that included separate time-dependent variables for smoking duration (years) before and after stove improvement. We found that the effect of smoking on lung cancer risk becomes considerably stronger after chimney installation and consequent reduction of indoor coal smoke exposure.

The effect of cigarette smoke on the metabolism of arachidonic acid in isolated hamster lungs

International Nuclear Information System (INIS)

Maennistoe, J.; Toivonen, H.; Hartiala, J.; Bakhle, Y.S.; Uotila, P.

1981-01-01

The effects of cigarette smoke on the metabolism of exogenous arachidonic acid (AA) were investigated in isolated hamster lungs. Arachidonate was injected into the pulmonary circulation and the metabolites were analysed from the nonrecirculating perfusion effluent by thin layer chromatography. After the pulmonary injection of 66 nmol of 14C-AA about 20% of the injected radioactivity appeared in the perfusion effluent mostly as metabolites in six minutes. When isolated lungs were ventilated with cigarette smoke during the perfusion, the amounts of PGF2 alpha, PGE2 and two unidentified metabolite groups increased in the lung effluent. In two other experimental series hamsters were exposed to cigarette smoke before the lung perfusion either once for 30 min or during one hour daily for ten consecutive days. Neither pre-exposures caused any changes in the amounts of arachidonate metabolites in the lung effluent

Statistical Measure Of Association Between Smoking And Lung ...

African Journals Online (AJOL)

Statistical Measure Of Association Between Smoking And Lung Cancer In Abakaliki, Ebonyi State Nigeria. ... East African Journal of Public Health ... To investigate the havoc caused by all these on people, questionnaire was distributed among smokers and non smokers in various areas of specialization and habitations.

A case of proteinase 3 anti-neutrophil cytoplasmic antibody (PR3-ANCA positive/IgG4-related lung disease

Directory of Open Access Journals (Sweden)

Hirokazu Touge

2017-01-01

Full Text Available IgG4-related lung disease (IgG4-RLD is a rare and chronic progressive autoimmune disease. We report a case of IgG4-related inflammatory pseudo-tumor of the lung that was seropositive for proteinase 3 anti-neutrophil cytoplasmic antibody (PR3-ANCA. A 61-year-old male had a mass lesion in the right lower lung field in chest X-ray. Transbronchial lung biopsy resulted in a pathological diagnosis of IgG4-RLD. The condition was improved by hormonal therapy.

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)

Lung cancer risk in welders and foundry workers with a history of heavy smoking in the USA: The National Lung Screening Trial.

Science.gov (United States)

Wong, Jason Y Y; Bassig, Bryan A; Seow, Wei Jie; Hu, Wei; Ji, Bu-Tian; Blair, Aaron; Silverman, Debra T; Lan, Qing

2017-06-01

Foundry work is a risk factor for lung cancer; however, the association with welding is unclear, as smoking is common among metalworkers and may mask the relationship. We evaluated whether history of welding and foundry work, independently and jointly, and employment duration were associated with lung cancer risk in heavy smokers. We analysed data from the National Lung Screening Trial, a prospective randomised trial of 53 454 heavy smokers (>30 pack-years) in the USA. Cox regression models were used to estimate the HRs and 95% CIs of medically/histologically confirmed incident lung cancer during the follow-up period (2002-2009) in relation to history and duration of welding and foundry work assessed via questionnaires, adjusted for screening arm, component study, sex, age, race/ethnicity, education, smoking status and pack-years, body mass index and personal/family medical history. There were 2034 incident lung cancer cases throughout the follow-up. Increasing years of employment in welding (p-trend =0.039) and foundry work (p-trend =0.005) were related to increased lung cancer risk among heavy smokers. Having ever been employed (≥1 yr) as either a welder or foundry worker alone was associated with non-significant increased risks of lung cancer (HR=1.12 (95% CI 0.91 to 1.37) and HR=1.09 (95% CI 0.85 to 1.39), respectively). Further, there was a joint-effect in that those who were ever employed in both occupations had significantly increased risks (HR=1.48 (95% CI 1.08 to 2.04)). Our findings provide further evidence that exposure to welding/metal fumes may be associated with elevated lung cancer risk. NCT00047385. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.

Quantification of neutrophil migration into the lungs of patients with chronic obstructive pulmonary disease

Energy Technology Data Exchange (ETDEWEB)

Ruparelia, Prina; Summers, Charlotte; Chilvers, Edwin R [University of Cambridge School of Clinical Medicine, Department of Respiratory Medicine, Cambridge (United Kingdom); Szczepura, Katherine R [University of Cambridge School of Clinical Medicine, Department of Radiology, Cambridge (United Kingdom); Solanki, Chandra K; Balan, Kottekkattu [Cambridge University Hospitals NHS Foundation Trust, Nuclear Medicine, Addenbrooke' s Hospital, Cambridge (United Kingdom); Newbold, Paul [AstraZeneca R and D Charnwood, Loughborough (United Kingdom); Bilton, Diana [Papworth Hospital NHS Foundation Trust, Cystic Fibrosis and Lung Defence Unit, Papworth Everard (United Kingdom); Peters, A M [University of Cambridge School of Clinical Medicine, Department of Radiology, Cambridge (United Kingdom); Brighton Sussex Medical School, Brighton (United Kingdom)

2011-05-15

To quantify neutrophil migration into the lungs of patients with chronic pulmonary obstructive disease (COPD). Neutrophil loss via airways was assessed by dedicated whole-body counting 45 min, 24 h and 2, 4, 7 and 10 days after injection of very small activities of {sup 111}In-labelled neutrophils in 12 healthy nonsmokers, 5 healthy smokers, 16 patients with COPD (of whom 7 were ex-smokers) and 10 patients with bronchiectasis. Lung accumulation of {sup 99m}Tc-labelled neutrophils was assessed by sequential SPECT and Patlak analysis in six COPD patients and three healthy nonsmoking subjects. Whole body {sup 111}In counts, expressed as percentages of 24 h counts, decreased in all subjects. Losses at 7 days (mean {+-} SD) were similar in healthy nonsmoking subjects (5.5 {+-} 1.5%), smoking subjects (6.5 {+-} 4.4%) and ex-smoking COPD patients (5.8 {+-} 1.5%). In contrast, currently smoking COPD patients showed higher losses (8.0 {+-} 3.0%) than healthy nonsmokers (p = 0.03). Two bronchiectatic patients lost 25% and 26%, indicating active disease; mean loss in the remaining eight was 6.9 {+-} 2.5%. The rate of accumulation of {sup 99m}Tc-neutrophils in the lungs, determined by sequential SPECT, was increased in COPD patients (0.030-0.073 min{sup -1}) compared with healthy nonsmokers (0-0.002 min{sup -1}; p = 0.02). In patients with COPD, sequential SPECT showed increased lung accumulation of {sup 99m}Tc-labelled neutrophils, while whole-body counting demonstrated subsequent higher losses of {sup 111}In-labelled neutrophils in patients who continued to smoke. Sequential SPECT as a means of quantifying neutrophil migration deserves further evaluation. (orig.)

Quantification of neutrophil migration into the lungs of patients with chronic obstructive pulmonary disease

International Nuclear Information System (INIS)

Ruparelia, Prina; Summers, Charlotte; Chilvers, Edwin R.; Szczepura, Katherine R.; Solanki, Chandra K.; Balan, Kottekkattu; Newbold, Paul; Bilton, Diana; Peters, A.M.

2011-01-01

To quantify neutrophil migration into the lungs of patients with chronic pulmonary obstructive disease (COPD). Neutrophil loss via airways was assessed by dedicated whole-body counting 45 min, 24 h and 2, 4, 7 and 10 days after injection of very small activities of 111 In-labelled neutrophils in 12 healthy nonsmokers, 5 healthy smokers, 16 patients with COPD (of whom 7 were ex-smokers) and 10 patients with bronchiectasis. Lung accumulation of 99m Tc-labelled neutrophils was assessed by sequential SPECT and Patlak analysis in six COPD patients and three healthy nonsmoking subjects. Whole body 111 In counts, expressed as percentages of 24 h counts, decreased in all subjects. Losses at 7 days (mean ± SD) were similar in healthy nonsmoking subjects (5.5 ± 1.5%), smoking subjects (6.5 ± 4.4%) and ex-smoking COPD patients (5.8 ± 1.5%). In contrast, currently smoking COPD patients showed higher losses (8.0 ± 3.0%) than healthy nonsmokers (p = 0.03). Two bronchiectatic patients lost 25% and 26%, indicating active disease; mean loss in the remaining eight was 6.9 ± 2.5%. The rate of accumulation of 99m Tc-neutrophils in the lungs, determined by sequential SPECT, was increased in COPD patients (0.030-0.073 min -1 ) compared with healthy nonsmokers (0-0.002 min -1 ; p = 0.02). In patients with COPD, sequential SPECT showed increased lung accumulation of 99m Tc-labelled neutrophils, while whole-body counting demonstrated subsequent higher losses of 111 In-labelled neutrophils in patients who continued to smoke. Sequential SPECT as a means of quantifying neutrophil migration deserves further evaluation. (orig.)

Smoking and Tobacco Use Health Effects

Science.gov (United States)

... respiratory infections, middle ear disease, more severe asthma, respiratory symptoms, and slowed lung growth. CANCER Tobacco use increases the risk for many types of cancer, such as lung cancer. More HEART DISEASE Studies show a direct link between cigarette smoking ...

Worldwide burden of disease from exposure to second-hand smoke: a retrospective analysis of data from 192 countries.

Science.gov (United States)

Oberg, Mattias; Jaakkola, Maritta S; Woodward, Alistair; Peruga, Armando; Prüss-Ustün, Annette

2011-01-08

Exposure to second-hand smoke is common in many countries but the magnitude of the problem worldwide is poorly described. We aimed to estimate the worldwide exposure to second-hand smoke and its burden of disease in children and adult non-smokers in 2004. The burden of disease from second-hand smoke was estimated as deaths and disability-adjusted life-years (DALYs) for children and adult non-smokers. The calculations were based on disease-specific relative risk estimates and area-specific estimates of the proportion of people exposed to second-hand smoke, by comparative risk assessment methods, with data from 192 countries during 2004. Worldwide, 40% of children, 33% of male non-smokers, and 35% of female non-smokers were exposed to second-hand smoke in 2004. This exposure was estimated to have caused 379,000 deaths from ischaemic heart disease, 165,000 from lower respiratory infections, 36,900 from asthma, and 21,400 from lung cancer. 603,000 deaths were attributable to second-hand smoke in 2004, which was about 1·0% of worldwide mortality. 47% of deaths from second-hand smoke occurred in women, 28% in children, and 26% in men. DALYs lost because of exposure to second-hand smoke amounted to 10·9 million, which was about 0·7% of total worldwide burden of diseases in DALYs in 2004. 61% of DALYs were in children. The largest disease burdens were from lower respiratory infections in children younger than 5 years (5,939,000), ischaemic heart disease in adults (2,836,000), and asthma in adults (1,246,000) and children (651,000). These estimates of worldwide burden of disease attributable to second-hand smoke suggest that substantial health gains could be made by extending effective public health and clinical interventions to reduce passive smoking worldwide. Swedish National Board of Health and Welfare and Bloomberg Philanthropies. Copyright © 2011 Elsevier Ltd. All rights reserved.

Cigarette Smoke Exposure during Pregnancy Alters Fetomaternal Cell Trafficking Leading to Retention of Microchimeric Cells in the Maternal Lung

Science.gov (United States)

Vogelgesang, Anja; Scapin, Cristina; Barone, Caroline; Tam, Elaine

2014-01-01

Cigarette smoke exposure causes chronic oxidative lung damage. During pregnancy, fetal microchimeric cells traffic to the mother. Their numbers are increased at the site of acute injury. We hypothesized that milder chronic diffuse smoke injury would attract fetal cells to maternal lungs. We used a green-fluorescent-protein (GFP) mouse model to study the effects of cigarette smoke exposure on fetomaternal cell trafficking. Wild-type female mice were exposed to cigarette smoke for about 4 weeks and bred with homozygote GFP males. Cigarette smoke exposure continued until lungs were harvested and analyzed. Exposure to cigarette smoke led to macrophage accumulation in the maternal lung and significantly lower fetal weights. Cigarette smoke exposure influenced fetomaternal cell trafficking. It was associated with retention of GFP-positive fetal cells in the maternal lung and a significant reduction of fetal cells in maternal livers at gestational day 18, when fetomaternal cell trafficking peaks in the mouse model. Cells quickly clear postpartum, leaving only a few, difficult to detect, persisting microchimeric cells behind. In our study, we confirmed the postpartum clearance of cells in the maternal lungs, with no significant difference in both groups. We conclude that in the mouse model, cigarette smoke exposure during pregnancy leads to a retention of fetal microchimeric cells in the maternal lung, the site of injury. Further studies will be needed to elucidate the effect of cigarette smoke exposure on the phenotypic characteristics and function of these fetal microchimeric cells, and confirm its course in cigarette smoke exposure in humans. PMID:24832066

Smoking, epidemiology and e-cigarettes

OpenAIRE

Raschke RA

2013-01-01

No abstract available. Article truncated at 150 words. “The true face of smoking is disease, death and horror - not the glamour and sophistication the pushers in the tobacco industry try to portray.” - David Byrne In our fellows’ conference we recently reviewed the evolution of the science of clinical epidemiology as it relates to the association of smoking and lung cancer and the concurrent history of tobacco marketing in the United States. This story begins in 1950, when Richard Doll and A...

Modulation of cigarette smoke-related end-points in mutagenesis and carcinogenesis

International Nuclear Information System (INIS)

De Flora, Silvio; D'Agostini, Francesco; Balansky, Roumen; Camoirano, Anna; Bennicelli, Carlo; Bagnasco, Maria; Cartiglia, Cristina; Tampa, Elena; Longobardi, Maria Grazia; Lubet, Ronald A.; Izzotti, Alberto

2003-01-01

The epidemic of lung cancer and the increase of other tumours and chronic degenerative diseases associated with tobacco smoking have represented one of the most dramatic catastrophes of the 20th century. The control of this plague is one of the major challenges of preventive medicine for the next decades. The imperative goal is to refrain from smoking. However, chemoprevention by dietary and/or pharmacological agents provides a complementary strategy, which can be targeted not only to current smokers but also to former smokers and passive smokers. This article summarises the results of studies performed in our laboratories during the last 10 years, and provides new data generated in vitro, in experimental animals and in humans. We compared the ability of 63 putative chemopreventive agents to inhibit the bacterial mutagenicity of mainstream cigarette smoke. Modulation by ethanol and the mechanisms involved were also investigated both in vitro and in vivo. Several studies evaluated the effects of dietary chemopreventive agents towards smoke-related intermediate biomarkers in various cells, tissues and organs of rodents. The investigated end-points included metabolic parameters, adducts to haemoglobin, bulky adducts to nuclear DNA, oxidative DNA damage, adducts to mitochondrial DNA, apoptosis, cytogenetic damage in alveolar macrophages, bone marrow and peripheral blood erytrocytes, proliferation markers, and histopathological alterations. The agents tested in vivo included N-acetyl-L-cysteine, 1,2-dithiole-3-thione, oltipraz, phenethyl isothiocyanate, 5,6-benzoflavone, and sulindac. We started applying multigene expression analysis to chemoprevention research, and postulated that an optimal agent should not excessively alter per se the physiological background of gene expression but should be able to attenuate the alterations produced by cigarette smoke or other carcinogens. We are working to develop an animal model for the induction of lung tumours following exposure

Statement on smoking cessation in COPD and other pulmonary diseases and in smokers with comorbidities who find it difficult to quit

DEFF Research Database (Denmark)

Jiménez-Ruiz, Carlos A; Andreas, Stefan; Lewis, Keir E

2015-01-01

Chronic obstructive pulmonary disease (COPD), lung cancer, asthma and pulmonary tuberculosis are common pulmonary diseases that are caused or worsened by tobacco smoking. Growing observational evidence suggests that symptoms and prognosis of these conditions improve upon smoking cessation. Despite...... increasing numbers of (small) randomised controlled trials suggesting intensive smoking cessation treatments work in people with pulmonary diseases many patients are not given specific advice on the benefits or referred for intensive cessation treatments and, therefore, continue smoking.This is a qualitative...... review regarding smoking cessation in patients with COPD and other pulmonary disorders, written by a group of European Respiratory Society experts. We describe the epidemiological links between smoking and pulmonary disorders, the evidence for benefits of stopping smoking, how best to assess tobacco...

Influenza Virus-Induced Lung Inflammation Was Modulated by Cigarette Smoke Exposure in Mice

Science.gov (United States)

Han, Yan; Ling, Man To; Mao, Huawei; Zheng, Jian; Liu, Ming; Lam, Kwok Tai; Liu, Yuan; Tu, Wenwei; Lau, Yu-Lung

2014-01-01

Although smokers have increased susceptibility and severity of seasonal influenza virus infection, there is no report about the risk of 2009 pandemic H1N1 (pdmH1N1) or avian H9N2 (H9N2/G1) virus infection in smokers. In our study, we used mouse model to investigate the effect of cigarette smoke on pdmH1N1 or H9N2 virus infection. Mice were exposed to cigarette smoke for 21 days and then infected with pdmH1N1 or H9N2 virus. Control mice were exposed to air in parallel. We found that cigarette smoke exposure alone significantly upregulated the lung inflammation. Such prior cigarette smoke exposure significantly reduced the disease severity of subsequent pdmH1N1 or H9N2 virus infection. For pdmH1N1 infection, cigarette smoke exposed mice had significantly lower mortality than the control mice, possibly due to the significantly decreased production of inflammatory cytokines and chemokines. Similarly, after H9N2 infection, cigarette smoke exposed mice displayed significantly less weight loss, which might be attributed to lower cytokines and chemokines production, less macrophages, neutrophils, CD4+ and CD8+ T cells infiltration and reduced lung damage compared to the control mice. To further investigate the underlying mechanism, we used nicotine to mimic the effect of cigarette smoke both in vitro and in vivo. Pre-treating the primary human macrophages with nicotine for 72 h significantly decreased their expression of cytokines and chemokines after pdmH1N1 or H9N2 infection. The mice subcutaneously and continuously treated with nicotine displayed significantly less weight loss and lower inflammatory response than the control mice upon pdmH1N1 or H9N2 infection. Moreover, α7 nicotinic acetylcholine receptor knockout mice had more body weight loss than wild-type mice after cigarette smoke exposure and H9N2 infection. Our study provided the first evidence that the pathogenicity of both pdmH1N1 and H9N2 viruses was alleviated in cigarette smoke exposed mice, which might

Influenza virus-induced lung inflammation was modulated by cigarette smoke exposure in mice.

Directory of Open Access Journals (Sweden)

Yan Han

Full Text Available Although smokers have increased susceptibility and severity of seasonal influenza virus infection, there is no report about the risk of 2009 pandemic H1N1 (pdmH1N1 or avian H9N2 (H9N2/G1 virus infection in smokers. In our study, we used mouse model to investigate the effect of cigarette smoke on pdmH1N1 or H9N2 virus infection. Mice were exposed to cigarette smoke for 21 days and then infected with pdmH1N1 or H9N2 virus. Control mice were exposed to air in parallel. We found that cigarette smoke exposure alone significantly upregulated the lung inflammation. Such prior cigarette smoke exposure significantly reduced the disease severity of subsequent pdmH1N1 or H9N2 virus infection. For pdmH1N1 infection, cigarette smoke exposed mice had significantly lower mortality than the control mice, possibly due to the significantly decreased production of inflammatory cytokines and chemokines. Similarly, after H9N2 infection, cigarette smoke exposed mice displayed significantly less weight loss, which might be attributed to lower cytokines and chemokines production, less macrophages, neutrophils, CD4+ and CD8+ T cells infiltration and reduced lung damage compared to the control mice. To further investigate the underlying mechanism, we used nicotine to mimic the effect of cigarette smoke both in vitro and in vivo. Pre-treating the primary human macrophages with nicotine for 72 h significantly decreased their expression of cytokines and chemokines after pdmH1N1 or H9N2 infection. The mice subcutaneously and continuously treated with nicotine displayed significantly less weight loss and lower inflammatory response than the control mice upon pdmH1N1 or H9N2 infection. Moreover, α7 nicotinic acetylcholine receptor knockout mice had more body weight loss than wild-type mice after cigarette smoke exposure and H9N2 infection. Our study provided the first evidence that the pathogenicity of both pdmH1N1 and H9N2 viruses was alleviated in cigarette smoke exposed

Interaction in COPD experiment (ICE): a hazardous combination of cigarette smoking and bronchodilation in chronic obstructive pulmonary disease.

Science.gov (United States)

van Dijk, W D; Heijdra, Y; Scheepers, P T J; Lenders, J W M; van Weel, C; Schermer, T R J

2010-02-01

Chronic obstructive pulmonary disease (COPD) is a highly prevalent disease, characterised by poorly reversible, obstructive airflow limitation. Alongside other comorbidities, COPD is associated with increased morbidity and mortality resulting from cardiovascular disease - mainly heart failure and ischemic heart disease. Both diseases share an important risk factor, namely, smoking. About 50% of COPD patients are active cigarette smokers. Bronchodilation is the cornerstone of pharmaceutical treatment for COPD symptoms, and half of all COPD patients use long-acting bronchodilating agents. Discussion about these agents is currently focusing on the association with overall mortality and morbidity in COPD patients, of cardiovascular origin in particular. Bronchodilation diminishes the hyperinflated state of the lung and facilitates the pulmonary deposition of cigarette smoke by deeper inhalation into the smaller airways. Smaller particles, as in smoke, tend to penetrate and depose more in these small airways. In addition, bronchodilation indeed increases carbon monoxide uptake in the lungs, an important gaseous compound of cigarette smoke. Since the number of cigarettes smoked is positively correlated to mortality from cardiac events, we therefore hypothesise that chronic bronchodilation increases cardiovascular disease and mortality in COPD patients who continue smoking by increasing pulmonary retention of pathogenic smoke constituents. Indeed, a recent meta-analysis is suggestive that long-acting anticholinergics might increase cardiovascular disease if patients exceed a certain number of cigarettes smoked. To demonstrate the fundamental mechanism of this pathogenic interaction we will perform a randomised placebo-controlled cross-over trial to investigate the effect of maximum bronchodilation on the retention of cigarette smoke constituents. In 40 moderate to severe COPD patients we measure the inhaled and exhaled amount of tar and nicotine, as well during maximum

Apocynin and ebselen reduce influenza A virus-induced lung inflammation in cigarette smoke-exposed mice.

Science.gov (United States)

Oostwoud, L C; Gunasinghe, P; Seow, H J; Ye, J M; Selemidis, S; Bozinovski, S; Vlahos, R

2016-02-15

Influenza A virus (IAV) infections are a common cause of acute exacerbations of chronic obstructive pulmonary disease (AECOPD). Oxidative stress is increased in COPD, IAV-induced lung inflammation and AECOPD. Therefore, we investigated whether targeting oxidative stress with the Nox2 oxidase inhibitors and ROS scavengers, apocynin and ebselen could ameliorate lung inflammation in a mouse model of AECOPD. Male BALB/c mice were exposed to cigarette smoke (CS) generated from 9 cigarettes per day for 4 days. On day 5, mice were infected with 1 × 10(4.5) PFUs of the IAV Mem71 (H3N1). BALF inflammation, viral titers, superoxide production and whole lung cytokine, chemokine and protease mRNA expression were assessed 3 and 7 days post infection. IAV infection resulted in a greater increase in BALF inflammation in mice that had been exposed to CS compared to non-smoking mice. This increase in BALF inflammation in CS-exposed mice caused by IAV infection was associated with elevated gene expression of pro-inflammatory cytokines, chemokines and proteases, compared to CS alone mice. Apocynin and ebselen significantly reduced the exacerbated BALF inflammation and pro-inflammatory cytokine, chemokine and protease expression caused by IAV infection in CS mice. Targeting oxidative stress using apocynin and ebselen reduces IAV-induced lung inflammation in CS-exposed mice and may be therapeutically exploited to alleviate AECOPD.

Non-smoking Chronic Obstructive Pulmonary Disease Attributed to Occupational Exposure to Silica Dust.

Science.gov (United States)

Tsuchiya, Kazuo; Toyoshima, Mikio; Kamiya, Yosuke; Nakamura, Yutaro; Baba, Satoshi; Suda, Takafumi

2017-01-01

An 85-year-old, never-smoking man presented with exertional dyspnea. He had been exposed to silica dust in the work place. Chest computed tomography revealed bronchial wall thickening without emphysema. A pulmonary function test showed airflow obstruction without impaired gas transfer. Airway hyperresponsiveness and reversibility were not evident. A transbronchial lung biopsy showed findings suggestive of mineral dust exposure, such as fibrosis and slight pigmentation of bronchioles. He was diagnosed with non-smoking chronic obstructive pulmonary disease (COPD) due to occupational exposure to silica dust. His symptoms were improved using an inhaled long-acting bronchodilator. The clinical characteristics of non-smoking COPD are discussed in this report.

Simvastatin inhibits smoke-induced airway epithelial injury: implications for COPD therapy.

Science.gov (United States)

Davis, Benjamin B; Zeki, Amir A; Bratt, Jennifer M; Wang, Lei; Filosto, Simone; Walby, William F; Kenyon, Nicholas J; Goldkorn, Tzipora; Schelegle, Edward S; Pinkerton, Kent E

2013-08-01

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death. The statin drugs may have therapeutic potential in respiratory diseases such as COPD, but whether they prevent bronchial epithelial injury is unknown. We hypothesised that simvastatin attenuates acute tobacco smoke-induced neutrophilic lung inflammation and airway epithelial injury. Spontaneously hypertensive rats were given simvastatin (20 mg·kg(-1) i.p.) daily for either 7 days prior to tobacco smoke exposure and during 3 days of smoke exposure, or only during tobacco smoke exposure. Pretreatment with simvastatin prior to and continued throughout smoke exposure reduced the total influx of leukocytes, neutrophils and macrophages into the lung and airways. Simvastatin attenuated tobacco smoke-induced cellular infiltration into lung parenchymal and airway subepithelial and interstitial spaces. 1 week of simvastatin pretreatment almost completely prevented smoke-induced denudation of the airway epithelial layer, while simvastatin given only concurrently with the smoke exposure had no effect. Simvastatin may be a novel adjunctive therapy for smoke-induced lung diseases, such as COPD. Given the need for statin pretreatment there may be a critical process of conditioning that is necessary for statins' anti-inflammatory effects. Future work is needed to elucidate the mechanisms of this statin protective effect.

Cigarette smoking prior to first cancer and risk of second smoking-associated cancers among survivors of bladder, kidney, head and neck, and stage I lung cancers.

Science.gov (United States)

Shiels, Meredith S; Gibson, Todd; Sampson, Joshua; Albanes, Demetrius; Andreotti, Gabriella; Beane Freeman, Laura; Berrington de Gonzalez, Amy; Caporaso, Neil; Curtis, Rochelle E; Elena, Joanne; Freedman, Neal D; Robien, Kim; Black, Amanda; Morton, Lindsay M

2014-12-10

Data on smoking and second cancer risk among cancer survivors are limited. We assessed associations between smoking before first cancer diagnosis and risk of second primary smoking-associated cancers among survivors of lung (stage I), bladder, kidney, and head/neck cancers. Data were pooled from 2,552 patients with stage I lung cancer, 6,386 with bladder cancer, 3,179 with kidney cancer, and 2,967 with head/neck cancer from five cohort studies. We assessed the association between prediagnostic smoking and second smoking-associated cancer risk with proportional hazards regression, and compared these estimates to those for first smoking-associated cancers in all cohort participants. Compared with never smoking, current smoking of ≥ 20 cigarettes per day was associated with increased second smoking-associated cancer risk among survivors of stage I lung (hazard ratio [HR] = 3.26; 95% CI, 0.92 to 11.6), bladder (HR = 3.67; 95% CI, 2.25 to 5.99), head/neck (HR = 4.45; 95% CI, 2.56 to 7.73), and kidney cancers (HR = 5.33; 95% CI, 2.55 to 11.1). These estimates were similar to those for first smoking-associated cancer among all cohort participants (HR = 5.41; 95% CI, 5.23 to 5.61). The 5-year cumulative incidence of second smoking-associated cancers ranged from 3% to 8% in this group of cancer survivors. Understanding risk factors for second cancers among cancer survivors is crucial. Our data indicate that cigarette smoking before first cancer diagnosis increases second cancer risk among cancer survivors, and elevated cancer risk in these survivors is likely due to increased smoking prevalence. The high 5-year cumulative risks of smoking-associated cancers among current smoking survivors of stage I lung, bladder, kidney, and head/neck cancers highlight the importance of smoking cessation in patients with cancer. © 2014 by American Society of Clinical Oncology.

Health-related quality of life is related to COPD disease severity

Directory of Open Access Journals (Sweden)

Rönmark Eva

2005-09-01

Full Text Available Abstract Background The aim of this study was to evaluate the association between health-related quality of life (HRQL and disease severity using lung function measures. Methods A survey was performed in subjects with COPD in Sweden. 168 subjects (70 women, mean age 64.3 years completed the generic HRQL questionnaire, the Short Form 36 (SF-36, the disease-specific HRQL questionnaire; the St George's Respiratory Questionnaire (SGRQ, and the utility measure, the EQ-5D. The subjects were divided into four severity groups according to FEV1 per cent of predicted normal using two clinical guidelines: GOLD and BTS. Age, gender, smoking status and socio-economic group were regarded as confounders. Results The COPD severity grades affected the SGRQ Total scores, varying from 25 to 53 (GOLD p = 0.0005 and from 25 to 45 (BTS p = 0.0023. The scores for SF-36 Physical were significantly associated with COPD severity (GOLD p = 0.0059, BTS p = 0.032. No significant association were noticed for the SF-36, Mental Component Summary scores and COPD severity. Scores for EQ-5D VAS varied from 73 to 37 (GOLD I-IV p = 0.0001 and from 73 to 50 (BTS 0-III p = 0.0007. The SGRQ Total score was significant between age groups (p = 0.0047. No significant differences in HRQL with regard to gender, smoking status or socio-economic group were noticed. Conclusion The results show that HRQL in COPD deteriorates with disease severity and with age. These data show a relationship between HRQL and disease severity obtained by lung function.

Smoking control: challenges and achievements

Directory of Open Access Journals (Sweden)

Luiz Carlos Corrêa da Silva

Full Text Available ABSTRACT Smoking is the most preventable and controllable health risk. Therefore, all health care professionals should give their utmost attention to and be more focused on the problem of smoking. Tobacco is a highly profitable product, because of its large-scale production and great number of consumers. Smoking control policies and treatment resources for smoking cessation have advanced in recent years, showing highly satisfactory results, particularly in Brazil. However, there is yet a long way to go before smoking can be considered a controlled disease from a public health standpoint. We can already perceive that the behavior of our society regarding smoking is changing, albeit slowly. Therefore, pulmonologists have a very promising area in which to work with their patients and the general population. We must act with greater impetus in support of health care policies and social living standards that directly contribute to improving health and quality of life. In this respect, pulmonologists can play a greater role as they get more involved in treating smokers, strengthening anti-smoking laws, and demanding health care policies related to lung diseases.

Smoking control: challenges and achievements

Science.gov (United States)

da Silva, Luiz Carlos Corrêa; de Araújo, Alberto José; de Queiroz, Ângela Maria Dias; Sales, Maria da Penha Uchoa; Castellano, Maria Vera Cruz de Oliveira

2016-01-01

ABSTRACT Smoking is the most preventable and controllable health risk. Therefore, all health care professionals should give their utmost attention to and be more focused on the problem of smoking. Tobacco is a highly profitable product, because of its large-scale production and great number of consumers. Smoking control policies and treatment resources for smoking cessation have advanced in recent years, showing highly satisfactory results, particularly in Brazil. However, there is yet a long way to go before smoking can be considered a controlled disease from a public health standpoint. We can already perceive that the behavior of our society regarding smoking is changing, albeit slowly. Therefore, pulmonologists have a very promising area in which to work with their patients and the general population. We must act with greater impetus in support of health care policies and social living standards that directly contribute to improving health and quality of life. In this respect, pulmonologists can play a greater role as they get more involved in treating smokers, strengthening anti-smoking laws, and demanding health care policies related to lung diseases. PMID:27832238

Transcriptomic Analysis of Lung Tissue from Cigarette Smoke-Induced Emphysema Murine Models and Human Chronic Obstructive Pulmonary Disease Show Shared and Distinct Pathways.

Science.gov (United States)

Yun, Jeong H; Morrow, Jarrett; Owen, Caroline A; Qiu, Weiliang; Glass, Kimberly; Lao, Taotao; Jiang, Zhiqiang; Perrella, Mark A; Silverman, Edwin K; Zhou, Xiaobo; Hersh, Craig P

2017-07-01

Although cigarette smoke (CS) is the primary risk factor for chronic obstructive pulmonary disease (COPD), the underlying molecular mechanisms for the significant variability in developing COPD in response to CS are incompletely understood. We performed lung gene expression profiling of two different wild-type murine strains (C57BL/6 and NZW/LacJ) and two genetic models with mutations in COPD genome-wide association study genes (HHIP and FAM13A) after 6 months of chronic CS exposure and compared the results to human COPD lung tissues. We identified gene expression patterns that correlate with severity of emphysema in murine and human lungs. Xenobiotic metabolism and nuclear erythroid 2-related factor 2-mediated oxidative stress response were commonly regulated molecular response patterns in C57BL/6, Hhip +/- , and Fam13a -/- murine strains exposed chronically to CS. The CS-resistant Fam13a -/- mouse and NZW/LacJ strain revealed gene expression response pattern differences. The Fam13a -/- strain diverged in gene expression compared with C57BL/6 control only after CS exposure. However, the NZW/LacJ strain had a unique baseline expression pattern, enriched for nuclear erythroid 2-related factor 2-mediated oxidative stress response and xenobiotic metabolism, and converged to a gene expression pattern similar to the more susceptible wild-type C57BL/6 after CS exposure. These results suggest that distinct molecular pathways may account for resistance to emphysema. Surprisingly, there were few genes commonly modulated in mice and humans. Our study suggests that gene expression responses to CS may be largely species and model dependent, yet shared pathways could provide biologically significant insights underlying individual susceptibility to CS.

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.

Disparities in Smoking-Related Mortality Among American Indians/Alaska Natives.

Science.gov (United States)

Mowery, Paul D; Dube, Shanta R; Thorne, Stacy L; Garrett, Bridgette E; Homa, David M; Nez Henderson, Patricia

2015-11-01

Smoking-related disparities continue to be a public health problem among American Indian/Alaska Native (AI/AN) population groups and data documenting the health burden of smoking in this population are sparse. The purpose of this study was to assess mortality attributable to cigarette smoking among AI/AN adults relative to non-Hispanic white adults (whites) by calculating and comparing smoking-attributable fractions and mortality. Smoking-attributable fractions and mortality among AI/ANs (n=1.63 million AI/ANs) and whites were calculated for people living in 637 Indian Health Service Contract Health Service Delivery Area counties in the U.S., from mortality data collected during 2001-2009. Differences in smoking-attributable mortality between AI/ANs and whites for five major causes of smoking-related deaths were examined. All data analyses were carried out in 2013-2014. Overall, from 2001 to 2009, age-adjusted death rates, smoking-attributable fractions, and smoking-attributable mortality for all-cause mortality were higher among AI/ANs than among whites for adult men and women aged ≥35 years. Smoking caused 21% of ischemic heart disease, 15% of other heart disease, and 17% of stroke deaths in AI/AN men, compared with 15%, 10%, and 9%, respectively, for white men. Among AI/AN women, smoking caused 18% of ischemic heart disease deaths, 13% of other heart diseases deaths, and 20% of stroke deaths, compared with 9%, 7%, and 10%, respectively, among white women. These findings underscore the need for comprehensive tobacco control and prevention efforts that can effectively reach and impact the AI/AN population to prevent and reduce smoking. Copyright © 2015 American Journal of Preventive Medicine. All rights reserved.

Stratification for smoking in case-cohort studies of genetic polymorphisms and lung cancer

DEFF Research Database (Denmark)

Sørensen, Mette; López, Ana García; Andersen, Per Kragh

2009-01-01

and adjustment for smoking on the estimated effect of polymorphisms on lung cancer risk was explored in the case-cohort design. We used an empirical and a statistical simulation approach. The stratification strategies were: no smoking stratification, stratification for smoking status and stratification......The risk estimates obtained in studies of genetic polymorphisms and lung cancer differ markedly between studies, which might be due to chance or differences in study design, in particular the stratification/match of comparison group. The effect of different strategies for stratification...... for smoking duration. The study base was a prospective follow-up study with 57,053 participants. In the simulation approach the glutathione S-transferase T1 null polymorphism, as a model of any polymorphism, was added to simulated data in two different ways, assuming either absence or presence of association...

Quantitative proteomics analysis using 2D-PAGE to investigate the effects of cigarette smoke and aerosol of a prototypic modified risk tobacco product on the lung proteome in C57BL/6 mice.

Science.gov (United States)

Elamin, Ashraf; Titz, Bjoern; Dijon, Sophie; Merg, Celine; Geertz, Marcel; Schneider, Thomas; Martin, Florian; Schlage, Walter K; Frentzel, Stefan; Talamo, Fabio; Phillips, Blaine; Veljkovic, Emilija; Ivanov, Nikolai V; Vanscheeuwijck, Patrick; Peitsch, Manuel C; Hoeng, Julia

2016-08-11

Smoking is associated with several serious diseases, such as lung cancer and chronic obstructive pulmonary disease (COPD). Within our systems toxicology framework, we are assessing whether potential modified risk tobacco products (MRTP) can reduce smoking-related health risks compared to conventional cigarettes. In this article, we evaluated to what extent 2D-PAGE/MALDI MS/MS (2D-PAGE) can complement the iTRAQ LC-MS/MS results from a previously reported mouse inhalation study, in which we assessed a prototypic MRTP (pMRTP). Selected differentially expressed proteins identified by both LC-MS/MS and 2D-PAGE approaches were further verified using reverse-phase protein microarrays. LC-MS/MS captured the effects of cigarette smoke (CS) on the lung proteome more comprehensively than 2D-PAGE. However, an integrated analysis of both proteomics data sets showed that 2D-PAGE data complement the LC-MS/MS results by supporting the overall trend of lower effects of pMRTP aerosol than CS on the lung proteome. Biological effects of CS exposure supported by both methods included increases in immune-related, surfactant metabolism, proteasome, and actin cytoskeleton protein clusters. Overall, while 2D-PAGE has its value, especially as a complementary method for the analysis of effects on intact proteins, LC-MS/MS approaches will likely be the method of choice for proteome analysis in systems toxicology investigations. Quantitative proteomics is anticipated to play a growing role within systems toxicology assessment frameworks in the future. To further understand how different proteomics technologies can contribute to toxicity assessment, we conducted a quantitative proteomics analysis using 2D-PAGE and isobaric tag-based LC-MS/MS approaches and compared the results produced from the 2 approaches. Using a prototypic modified risk tobacco product (pMRTP) as our test item, we show compared with cigarette smoke, how 2D-PAGE results can complement and support LC-MS/MS data, demonstrating

The association between combined non-cystic fibrosis bronchiectasis and lung cancer in patients with chronic obstructive lung disease

Directory of Open Access Journals (Sweden)

Kim YW

2015-05-01

Full Text Available Yeon Wook Kim,1 Kwang-Nam Jin,2 Eun Young Heo,3 Sung Soo Park,3 Hee Soon Chung,3 Deog Kyeom Kim31Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea; 2Department of Radiology, Seoul National University College of Medicine, Seoul Metropolitan Government-Seoul National University Boramae Medical Center, Seoul, Republic of Korea; 3Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University College of Medicine, Seoul Metropolitan Government-Seoul National University Boramae Medical Center, Seoul, Republic of KoreaBackground: Whereas the epidemiological association between lung cancer and chronic obstructive pulmonary disease (COPD, a chronic inflammatory respiratory disease, is well known, limited studies have examined the association between lung cancer and non-cystic fibrosis bronchiectasis, a representative chronic airway inflammatory disease. This study evaluated the association between bronchiectasis and lung cancer in patients with COPD.Methods: A matched case–control study was conducted in a referral hospital in South Korea. Among COPD patients with moderate to very severe airflow limitation (forced expiratory volume in one second/forced vital capacity <0.7 and forced expiratory volume in one second ≤70% [% predicted] who underwent chest computed tomography (CT between January 1, 2010 and May 30, 2013, patients with lung cancer and controls matched for age, sex, and smoking history were selected. The risk of lung cancer was assessed according to the presence of underlying bronchiectasis confirmed by chest CT.Results: The study enrolled 99 cases and 198 controls. Combined bronchiectasis on chest CT was inversely associated with the risk of lung cancer compared with controls (odds ratio [OR] 0.25, 95% confidence interval [CI] 0.12–0.52, P<0.001. Significant associations were found in

Burden of total and cause-specific mortality related to tobacco smoking among adults aged ≥ 45 years in Asia: a pooled analysis of 21 cohorts.

Directory of Open Access Journals (Sweden)

Wei Zheng

2014-04-01

Full Text Available Tobacco smoking is a major risk factor for many diseases. We sought to quantify the burden of tobacco-smoking-related deaths in Asia, in parts of which men's smoking prevalence is among the world's highest.We performed pooled analyses of data from 1,049,929 participants in 21 cohorts in Asia to quantify the risks of total and cause-specific mortality associated with tobacco smoking using adjusted hazard ratios and their 95% confidence intervals. We then estimated smoking-related deaths among adults aged ≥45 y in 2004 in Bangladesh, India, mainland China, Japan, Republic of Korea, Singapore, and Taiwan-accounting for ∼71% of Asia's total population. An approximately 1.44-fold (95% CI = 1.37-1.51 and 1.48-fold (1.38-1.58 elevated risk of death from any cause was found in male and female ever-smokers, respectively. In 2004, active tobacco smoking accounted for approximately 15.8% (95% CI = 14.3%-17.2% and 3.3% (2.6%-4.0% of deaths, respectively, in men and women aged ≥45 y in the seven countries/regions combined, with a total number of estimated deaths of ∼1,575,500 (95% CI = 1,398,000-1,744,700. Among men, approximately 11.4%, 30.5%, and 19.8% of deaths due to cardiovascular diseases, cancer, and respiratory diseases, respectively, were attributable to tobacco smoking. Corresponding proportions for East Asian women were 3.7%, 4.6%, and 1.7%, respectively. The strongest association with tobacco smoking was found for lung cancer: a 3- to 4-fold elevated risk, accounting for 60.5% and 16.7% of lung cancer deaths, respectively, in Asian men and East Asian women aged ≥45 y.Tobacco smoking is associated with a substantially elevated risk of mortality, accounting for approximately 2 million deaths in adults aged ≥45 y throughout Asia in 2004. It is likely that smoking-related deaths in Asia will continue to rise over the next few decades if no effective smoking control programs are implemented. Please see later in the article for

Impact of active smoking on survival of patients with metastatic lung adenocarcinoma harboring an epidermal growth factor receptor (EGFR) mutation.

Science.gov (United States)

Erdogan, Bulent; Kodaz, Hilmi; Karabulut, Senem; Cinkaya, Ahmet; Tozkir, Hilmi; Tanriverdi, Ozgur; Cabuk, Devrim; Hacioglu, Muhammed Bekir; Turkmen, Esma; Hacibekiroglu, Ilhan; Uzunoglu, Sernaz; Cicin, Irfan

2016-11-10

Lung cancer in smokers and non-smokers demonstrates distinct genetic profiles, and cigarette smoking affects epidermal growth factor receptor (EGFR) function and causes secondary EGFR tyrosine kinase resistance. We evaluated the effect of active smoking in patients with metastatic lung adenocarcinoma. A total of 132 metastatic lung adenocarcinoma patients, diagnosed between 2008 and 2013, with known EGFR mutation status, were evaluated retrospectively. Among these patients, 40 had an activating EGFR mutation. Patients who continued smoking during the treatment were defined as active smokers. Former smokers and never smokers were together defined as non-smokers. The outcomes of the treatment in relation to the EGFR mutation and smoking status were evaluated. The median follow-up time was 10.5 months. The overall response rate for the first-line therapy was significantly higher among the EGFR-mutant patients (p = 0.01), however, smoking status had no impact on the response rate (p = 0.1). The EGFR-mutant active smokers progressed earlier than the non-smokers (p non-smokers and patients treated with erlotinib was significantly longer (p = 0.02 and p = 0.01, respectively). Smoking status did not affect the OS in EGFR wild type tumors (p = 0.49) but EGFR-mutant non-smokers had a longer OS than the active smokers (p = 0.01).The active smokers treated with erlotinib had poorer survival than the non-smokers (p = 0.03). Multivariate analysis of EGFR-mutant patients showed that erlotinib treatment at any line and non-smoking were independent prognostic factors for the OS (p = 0.04 and p = 0.01, respectively). Smoking during treatment is a negative prognostic factor in metastatic lung adenocarcinoma with an EGFR mutation.

Epidemiology of Lung Cancer

Science.gov (United States)

Brock, Malcolm V.; Ford, Jean G.; Samet, Jonathan M.; Spivack, Simon D.

2013-01-01

Background: Ever since a lung cancer epidemic emerged in the mid-1900s, the epidemiology of lung cancer has been intensively investigated to characterize its causes and patterns of occurrence. This report summarizes the key findings of this research. Methods: A detailed literature search provided the basis for a narrative review, identifying and summarizing key reports on population patterns and factors that affect lung cancer risk. Results: Established environmental risk factors for lung cancer include smoking cigarettes and other tobacco products and exposure to secondhand tobacco smoke, occupational lung carcinogens, radiation, and indoor and outdoor air pollution. Cigarette smoking is the predominant cause of lung cancer and the leading worldwide cause of cancer death. Smoking prevalence in developing nations has increased, starting new lung cancer epidemics in these nations. A positive family history and acquired lung disease are examples of host factors that are clinically useful risk indicators. Risk prediction models based on lung cancer risk factors have been developed, but further refinement is needed to provide clinically useful risk stratification. Promising biomarkers of lung cancer risk and early detection have been identified, but none are ready for broad clinical application. Conclusions: Almost all lung cancer deaths are caused by cigarette smoking, underscoring the need for ongoing efforts at tobacco control throughout the world. Further research is needed into the reasons underlying lung cancer disparities, the causes of lung cancer in never smokers, the potential role of HIV in lung carcinogenesis, and the development of biomarkers. PMID:23649439

Classical patterns of interstitial lung diseases

International Nuclear Information System (INIS)

Mueller-Mang, C.

2014-01-01

High resolution computed tomography (HRCT) is the most important non-invasive tool in the diagnostics and follow-up of patients with interstitial lung disease (ILD). A systematic review of the HRCT patterns of ILD was carried out and the most relevant differential diagnoses are discussed in order to provide a road map for the general radiologist to successfully navigate the complex field of ILD. Using HRCT four basic patterns of ILD can be identified: linear and reticular patterns, the nodular pattern, the high attenuation and low attenuation patterns. These patterns can be further differentiated according to their localization within the secondary pulmonary lobule (SPL), e.g. centrilobular or perilymphatic and their distribution within the lungs (e.g. upper or lower lobe predominance). Relevant clinical data, such as smoking history and course of the disease provide useful additional information in the diagnosis of ILD. On the basis of the pattern and anatomical distribution on HRCT, an accurate diagnosis can be achieved in some cases of ILD; however, due to morphological and clinical overlap the final diagnosis of many ILDs requires close cooperation between clinicians, radiologists and pathologists. (orig.) [de

Vanishing Lung Syndrome: Compound Effect of Tobacco and Marijuana Use on the Development of Bullous Lung Disease – A Joint Effort

OpenAIRE

Wiesel, Shimshon; Siddiqui, Faraz; Khan, Tahir; Hossri, Sami; El-Sayegh, Dany

2017-01-01

Marijuana use has been increasing across the United States due to its legalization as both a medicinal and recreational product. A small number of case reports have described a pathological entity called vanishing lung syndrome (VLS), which is a rare bullous lung disease usually caused by tobacco smoking. Recent case reports have implicated marijuana in the development of VLS. We present a case of a 47-year-old man, who presented to our hospital with shortness of breath, fevers and a producti...

Lung Cancer

International Nuclear Information System (INIS)

Maghfoor, Irfan; Perry, M.C.

2005-01-01

Lung cancer is the leading cause of cancer-related mortality. Since tobacco smoking is the cause in vast majority of cases, the incidence of lung cancer is expected to rise in those countries with high or rising incidence of tobacco smoking. Even though population at a risk of developing lung cancer are easily identified, mass screening for lung cancer is not supported by currently available evidence. In case of non-small cell lung cancer, a cure may be possible with surgical resection followed by post-operative chemotherapy in those diagnosed at an early stage. A small minority of patients who present with locally advanced disease may also benefit from preoperative chemotherapy and/or radiation therapy to down stage the tumor to render it potentially operable. In a vast majority of patients, however, lung cancer presents at an advanced stage and a cure is not possible with currently available therapeutic strategies. Similarly small cell lung cancer confined to one hemi-thorax may be curable with a combination of chemotherapy and thoracic irradiation followed by prophylactic cranial irradiation, if complete remission is achieved at the primary site. Small cell lung cancer that is spread beyond the confines of one hemi-thorax is however, considered incurable. In this era of molecular targeted therapies, new agents are constantly undergoing pre-clinical and clinical testing with the aim of targeting the molecular pathways thought to involved in etiology and pathogenesis of lung cancer. (author)

Polonium in cigarette smoke and radiation exposure of lungs

International Nuclear Information System (INIS)

Carvalho, F.P.; Oliveira, J.M.

2006-01-01

Polonium ( 210 Po), the most volatile of naturally-occurring radionuclides in plants, was analysed in three common brands of cigarettes produced in Portugal. The analyses were carried out on the unburned tobacco contained in cigarettes, on the ashes and butts of smoked cigarettes and on the mainstream smoke. 210 Po in tobacco displays concentrations ranging from 3 to 37 mBq g -1 , depending upon the cigarette brand. The 210 Po activity remaining in the solid residue of a smoked cigarette varied from 0.3 to 4.9 mBq per cigarette, and the 210 Po in the inhaled smoke varied from 2.6 to 28.9 mBq. In all brands of cigarettes tested, a large fraction of the 210 Po content is not inhaled by the smoker and it is released into the atmosphere. Part of it may be inhaled by passive smokers. Depending upon the commercial brand and upon the presence or absence of a filter in the cigarette, 5 to 37 % of the 210 Po in the cigarette can be inhaled by the smoker. Taking into account the average 210 Po in surface air, the smoker of one pack of twenty cigarettes per day may inhale 50 times more 210 Po than a non smoker. Cigarette smoke contributes with 1.5 % to the daily rate of 210 Po absorption into the blood, 0.39 Bq d -1 , and, after systemic circulation it gives rise to a whole body radiation dose in the same proportion. However, in the smoker the deposition of 210 Po in the lungs is much more elevated than normal and may originate an enhanced radiation exposure. Estimated dose to the lungs is presented and radiobiological effects of cigarette smoke are discussed. (author)

Lung volumes and emphysema in smokers with interstitial lung abnormalities.

Science.gov (United States)

Washko, George R; Hunninghake, Gary M; Fernandez, Isis E; Nishino, Mizuki; Okajima, Yuka; Yamashiro, Tsuneo; Ross, James C; Estépar, Raúl San José; Lynch, David A; Brehm, John M; Andriole, Katherine P; Diaz, Alejandro A; Khorasani, Ramin; D'Aco, Katherine; Sciurba, Frank C; Silverman, Edwin K; Hatabu, Hiroto; Rosas, Ivan O

2011-03-10

Cigarette smoking is associated with emphysema and radiographic interstitial lung abnormalities. The degree to which interstitial lung abnormalities are associated with reduced total lung capacity and the extent of emphysema is not known. We looked for interstitial lung abnormalities in 2416 (96%) of 2508 high-resolution computed tomographic (HRCT) scans of the lung obtained from a cohort of smokers. We used linear and logistic regression to evaluate the associations between interstitial lung abnormalities and HRCT measurements of total lung capacity and emphysema. Interstitial lung abnormalities were present in 194 (8%) of the 2416 HRCT scans evaluated. In statistical models adjusting for relevant covariates, interstitial lung abnormalities were associated with reduced total lung capacity (-0.444 liters; 95% confidence interval [CI], -0.596 to -0.292; Ppulmonary disease (COPD) (odds ratio, 0.53; 95% CI, 0.37 to 0.76; P<0.001). The effect of interstitial lung abnormalities on total lung capacity and emphysema was dependent on COPD status (P<0.02 for the interactions). Interstitial lung abnormalities were positively associated with both greater exposure to tobacco smoke and current smoking. In smokers, interstitial lung abnormalities--which were present on about 1 of every 12 HRCT scans--were associated with reduced total lung capacity and a lesser amount of emphysema. (Funded by the National Institutes of Health and the Parker B. Francis Foundation; ClinicalTrials.gov number, NCT00608764.).

Ventilatory Function and Cigarette Smoking in Cement Handlers in ...

African Journals Online (AJOL)

Introduction: Occupational exposure to dust and cigarette smoking play important roles in the pathogenesis of lung diseases, particularly in developing countries. To determine the effects of outdoor cement dust exposure and cigarette smoking on lung health, we compared ventilatory function in cement handlers (smokers ...

Th17/Treg immunoregulation and implications in treatment of sulfur mustard gas-induced lung diseases.

Science.gov (United States)

Iman, Maryam; Rezaei, Ramazan; Azimzadeh Jamalkandi, Sadegh; Shariati, Parvin; Kheradmand, Farrah; Salimian, Jafar

2017-12-01

Sulfur mustard (SM) is an extremely toxic gas used in chemical warfare to cause massive lung injury and death. Victims exposed to SM gas acutely present with inhalational lung injury, but among those who survive, some develop obstructive airway diseases referred to as SM-lung syndrome. Pathophysiologically, SM-lung shares many characteristics with smoking-induced chronic obstructive pulmonary disease (COPD), including airway remodeling, goblet cell metaplasia, and obstructive ventilation defect. Some of the hallmarks of COPD pathogenesis, which include dysregulated lung inflammation, neutrophilia, recruitment of interleukin 17A (IL -17A) expressing CD4 + T cells (Th17), and the paucity of lung regulatory T cells (Tregs), have also been described in SM-lung. Areas covered: A literature search was performed using the MEDLINE, EMBASE, and Web of Science databases inclusive of all literature prior to and including May 2017. Expert commentary: Here we review some of the recent findings that suggest a role for Th17 cell-mediated inflammatory changes associated with pulmonary complications in SM-lung and suggest new therapeutic approaches that could potentially alter disease progression with immune modulating biologics that can restore the lung Th17/Treg balance.

Smoking, epidemiology and e-cigarettes

Directory of Open Access Journals (Sweden)

Raschke RA

2013-07-01

Full Text Available No abstract available. Article truncated at 150 words. “The true face of smoking is disease, death and horror - not the glamour and sophistication the pushers in the tobacco industry try to portray.” - David Byrne In our fellows’ conference we recently reviewed the evolution of the science of clinical epidemiology as it relates to the association of smoking and lung cancer and the concurrent history of tobacco marketing in the United States. This story begins in 1950, when Richard Doll and Austin Bradford Hill published their landmark case control study demonstrating the association between smoking and lung cancer (1. This study was performed with methodological standards that have rarely been matched in the 63 years since. Exhaustive analysis of possible confounders, a multi-stage evaluation of study blinding, determination of dose-effect, and the use of multiple analyses to establish consistency are among many examples of superb attention to detail exercised by Doll and Hill in this study. The …

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

Biomarkers of Induced Active and Passive Smoking Damage

Directory of Open Access Journals (Sweden)

2009-02-01

Full Text Available In addition to thewell-known link between smoking and lung cancer, large epidemiological studies have shown a relationship between smoking and cancers of the nose, oral cavity, oropharynx, larynx, esophagus, pancreas, bladder, kidney, stomach, liver, colon and cervix, as well as myeloid leukemia. Epidemiological evidence has reported a direct link between exposure of non-smokers to environmental tobacco smoke and disease, most notably, lung cancer. Much evidence demonstrates that carcinogenic-DNA adducts are useful markers of tobacco smoke exposure, providing an integrated measurement of carcinogen intake, metabolic activation, and delivery to the DNA in target tissues. Monitoring accessible surrogate tissues, such as white blood cells or bronchoalveolar lavage (BAL cells, also provides a means of investigating passive and active tobacco exposure in healthy individuals and cancer patients. Levels of DNA adducts measured in many tissues of smokers are significantly higher than in non-smokers. While some studies have demonstrated an association between carcinogenic DNA adducts and cancer in current smokers, no association has been observed in ex or never smokers. The role of genetic susceptibility in the development of smoking related-cancer is essential. In order to establish whether smoking-related DNA adducts are biomarkers of tobacco smoke exposure and/or its carcinogenic activity we summarized all data that associated tobacco smoke exposure and smoking-related DNA adducts both in controls and/or in cancer cases and studies where the effect of genetic polymorphisms involved in the activation and deactivation of carcinogens were also evaluated. In the future we hope we will be able to screen for lung cancer susceptibility by using specific biomarkers and that subjects of compared groups can be stratified for multiple potential modulators of biomarkers, taking into account various confounding factors.

A Study on adverse effect of smoke/flue on lung functions of glass factory workers of Firozabad district

Directory of Open Access Journals (Sweden)

Santosh Kumar Sant

2014-03-01

Full Text Available The pulmonary function impairment is the most common respiratory problem in industrial plants and their vicinity. Therefore, the purpose was to study the effects of furnace smoke and flue and its duration of exposure on lung function. This was a matched cross-sectional study of Spirometry in 100 bangle workers with age range 20 – 60 years, who worked without the benefit of smoke control ventilation or respiratory protective devices. Pulmonary function test was performed by using Digital Spirometer (Spiro-excel. Significant reduction was observed in the mean values of Forced Vital Capacity (FVC, Forced Expiratory Volume in one second (FEV1, Forced Expiratory Ratio (FEV1/FVC, Forced Expiratory Flow (25%-75% and Peak Expiratory Flow Rate (PEFR in bangle workers relative to their matched controls. This impairment was increased with the duration of exposure to fumes in bangle industries. It is concluded that lung function in bangle workers is impaired and stratification of results shows a dose-response effect of years of smoke and flue exposure on lung function. 

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.

Black lung: the social production of disease.

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Smith, B E

1981-01-01

The black lung movement that erupted in West Virginia in 1968 was not simply a struggle for recognition of an occupational disease; it grew into a bitter controversy over who would control the definition of that disease. This article examines the historical background and medical politics of that controversy, arguing that black lung was socially produced and defined on several different levels. As a medical construct, the changing definitions of this disease can be traced to major shifts in the political economy of the coal industry. As an occupational disease, the history of black lung is internally related to the history of the workplace in which it is produced. As the object of a mass movement, black lung acquired a political definition that grew out of the collective experience of miners and their families. The definition of disease with which black lung activists challenged the medical establishment has historical roots and justification; their experience suggests that other health advocates may need to redefine the diseases they hope to eradicate.

Smoking-attributable medical expenditures by age, sex, and smoking status estimated using a relative risk approach☆

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Maciosek, Michael V.; Xu, Xin; Butani, Amy L.; Pechacek, Terry F.

2015-01-01

Objective To accurately assess the benefits of tobacco control interventions and to better inform decision makers, knowledge of medical expenditures by age, gender, and smoking status is essential. Method We propose an approach to distribute smoking-attributable expenditures by age, gender, and cigarette smoking status to reflect the known risks of smoking. We distribute hospitalization days for smoking-attributable diseases according to relative risks of smoking-attributable mortality, and use the method to determine national estimates of smoking-attributable expenditures by age, sex, and cigarette smoking status. Sensitivity analyses explored assumptions of the method. Results Both current and former smokers ages 75 and over have about 12 times the smoking-attributable expenditures of their current and former smoker counterparts 35–54 years of age. Within each age group, the expenditures of formers smokers are about 70% lower than current smokers. In sensitivity analysis, these results were not robust to large changes to the relative risks of smoking-attributable mortality which were used in the calculations. Conclusion Sex- and age-group-specific smoking expenditures reflect observed disease risk differences between current and former cigarette smokers and indicate that about 70% of current smokers’ excess medical care costs is preventable by quitting. PMID:26051203

Smoking and the eye: what Québec teenagers know and fear.

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Brûlé, Julie; Tousignant, Benoît; Marcotte, Stéphanie; Moreau, Marie-Christelle

2018-01-01

Although most people associate smoking with lung cancer and heart disease, few are aware of the impact of smoking on ocular health. Studies have suggested a better knowledge of this association might promote higher quit rates, particularly in teenagers. The purpose of our study was to determine the knowledge of teenagers about the effects of smoking on ocular health and the fear associated with several tobacco-related health conditions. A self-administered questionnaire was distributed to 180 high school students aged 14 to 17 years. Measured variables included socio-economic demographics, smoking status, knowledge of the effects of smoking on general and ocular health, and level of fear as well as level of motivation to quit smoking associated with the following tobacco-related conditions: lung cancer, cardiovascular disease, heart attack, blindness and deafness. Response rate was 100 per cent. Eleven per cent of responders were smokers. The proportion of smokers who thought smoking could cause blindness was 64.3 per cent while it was 13.5 per cent for non-smokers. The proportion of smokers fearing blindness was 30 per cent, as opposed to 69.8 per cent for non-smokers. The proportion of respondents who thought the presented conditions were 'extremely' or 'very good' reasons to quit were similarly high for all smoking-associated conditions. These findings suggest teenagers are unaware of the impact smoking can have on ocular health. Smokers did not seem more concerned about vision loss compared to other tobacco-related diseases, as opposed to non-smokers. Our findings suggest vision loss would be a strong motivator to prevent initiation, but not very effective regarding cessation in this group. However, optometrists should be aware teenagers seem receptive to the message that 'smoking can cause blindness' and use this strategy in order to prevent smoking initiation. © 2017 Optometry Australia.

HRCT findings in the lungs of non-smokers with neurofibromatosis

International Nuclear Information System (INIS)

Oikonomou, Anastasia; Vadikolias, Konstantinos; Birbilis, Theodosios; Bouros, Demosthenes; Prassopoulos, Panos

2011-01-01

Purpose: Interstitial lung disease in neurofibromatosis (NF) has been disputed and attributed to smoking-related changes. The aim of this study was to describe HRCT findings in the lungs of non-smokers with NF. Materials and methods: Six never-smokers with NF underwent lung HRCT. Two radiologists evaluated the HRCT scans and a final decision was reached by consensus. The HRCT scans were analyzed with regard to the number, size, location (upper, middle or lower lung zone) and distribution (peripheral and central) of lung cysts and the presence of ground-glass density centrilobular micronodules. Results: All patients with NF had small (2–18 mm) thin wall cysts and upper-lobe predominant patchy areas of ground-glass density centrilobular micronodules. In five cases, there were 3–17 cysts and in one there were numerous (>100). Lung cysts were central (1), subpleural (1) and in both locations (4). Conclusion: Interstitial lung disease in NF is not associated with smoking and may be entirely asymptomatic. HRCT may reveal small cysts, with barely perceptible walls therefore not representing emphysema and occasionally a minimal micronodular pattern of ground glass opacity. There was no radiologic evidence of lung fibrosis, honeycombing or severe bullous disease.

Secondhand Tobacco Smoke Exposure and Lung Adenocarcinoma In Situ/Minimally Invasive Adenocarcinoma (AIS/MIA).

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Kim, Claire H; Lee, Yuan-Chin Amy; Hung, Rayjean J; Boffetta, Paolo; Xie, Dong; Wampfler, Jason A; Cote, Michele L; Chang, Shen-Chih; Ugolini, Donatella; Neri, Monica; Le Marchand, Loic; Schwartz, Ann G; Morgenstern, Hal; Christiani, David C; Yang, Ping; Zhang, Zuo-Feng

2015-12-01

The aim of this study was to estimate the effect of exposure to secondhand tobacco smoke on the incidence of lung adenocarcinoma in situ/minimally invasive adenocarcinoma (AIS/MIA). Data from seven case-control studies participating in the International Lung Cancer Consortium (ILCCO) were pooled, resulting in 625 cases of AIS/MIA and 7,403 controls, of whom 170 cases and 3,035 controls were never smokers. Unconditional logistic regression was used to estimate adjusted ORs (ORadj) and 95% confidence intervals (CI), controlling for age, sex, race, smoking status (ever/never), and pack-years of smoking. Study center was included in the models as a random-effects intercept term. Ever versus never exposure to secondhand tobacco smoke was positively associated with AIS/MIA incidence in all subjects (ORadj = 1.48; 95% CI, 1.14-1.93) and in never smokers (ORadj = 1.45; 95% CI, 1.00-2.12). There was, however, appreciable heterogeneity of ORadj across studies (P = 0.01), and the pooled estimates were largely influenced by one large study (40% of all cases and 30% of all controls). These findings provide weak evidence for an effect of secondhand tobacco smoke exposure on AIS/MIA incidence. Further studies are needed to assess the impact of secondhand tobacco smoke exposure using the newly recommended classification of subtypes of lung adenocarcinoma. ©2015 American Association for Cancer Research.

The Assessment of Health-Related Quality of Life in Scleroderma-Interstitial Lung Disease

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Shahrzad M Lari

2014-05-01

Full Text Available Introduction: Pulmonary involvement is the most common cause of mortality and disability in patients with systemic sclerosis and it significantly affects the quality of life in these patients. Therefore, early diagnosis and treatment of pulmonary involvement seems necessary in patients with SSc. In this study, we aimed to assess the health-related quality of life (HRQoL in patients with Scleroderma-Interstitial Lung Disease (SSc-ILD and its relationship with pulmonary function parameters. Materials and Methods: Considering the inclusion and exclusion criteria, 25 patients with SSc-ILD were enrolled in this cross-sectional study from April 2012 to June 2013. Full tests of lung function, including body plethysmography and diffusing capacity of the lungs for carbon monoxide (DLCO, 6-minute walk distance (6MWD, and pulse oximetry were performed. The HRQoL was assessed using St. George’s and CAT questionnaires; also, dyspnea was evaluated for all the patients, using modified medical research council (MMRC scale. Afterwards, the relationship between the total scores of HRQoL questionnaires and the severity of lung disease was analyzed, based on the recorded variables. Results: The mean age of the patients was 40.36±9.50 years and the mean duration of the disease was 7.16±4.50 years. A statistically significant inverse correlation was observed between 6MWD (r=-0.50, P=0.01, DLCO (r=-0.67, P

Impact of active smoking on survival of patients with metastatic lung adenocarcinoma harboring an epidermal growth factor receptor (EGFR mutation

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Bulent Erdogan

2016-11-01

Full Text Available Lung cancer in smokers and non-smokers demonstrates distinct genetic profiles, and cigarette smoking affects epidermal growth factor receptor (EGFR function and causes secondary EGFR tyrosine kinase resistance. We evaluated the effect of active smoking in patients with metastatic lung adenocarcinoma. A total of 132 metastatic lung adenocarcinoma patients, diagnosed between 2008 and 2013, with known EGFR mutation status, were evaluated retrospectively. Among these patients, 40 had an activating EGFR mutation. Patients who continued smoking during the treatment were defined as active smokers. Former smokers and never smokers were together defined as non-smokers. The outcomes of the treatment in relation to the EGFR mutation and smoking status were evaluated. The median follow-up time was 10.5 months. The overall response rate for the first-line therapy was significantly higher among the EGFR-mutant patients (p = 0.01, however, smoking status had no impact on the response rate (p = 0.1. The EGFR-mutant active smokers progressed earlier than the non-smokers (p < 0.01. The overall survival (OS of the non-smokers and patients treated with erlotinib was significantly longer (p = 0.02 and p = 0.01, respectively. Smoking status did not affect the OS in EGFR wild type tumors (p = 0.49 but EGFR-mutant non-smokers had a longer OS than the active smokers (p = 0.01.The active smokers treated with erlotinib had poorer survival than the non-smokers (p = 0.03. Multivariate analysis of EGFR-mutant patients showed that erlotinib treatment at any line and non-smoking were independent prognostic factors for the OS (p = 0.04 and p = 0.01, respectively. Smoking during treatment is a negative prognostic factor in metastatic lung adenocarcinoma with an EGFR mutation.

[Elevated expression of endothelin 2 in lung tissues of asthmatic rats after exposed to cigarette smoke and its mechanism].

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Han, Fangfang; Zhu, Shuyang; Chen, Bi; Li, Jingjing

2017-08-01

ET-2, JNK1/2, MDA and GSH decreased in the lung tissues of the dexamethasone treated group, bosentan treated group, and dexamethasone-bosentan treated group. Airway inflammation was attenuated and the staining intensity of ET-2 in the lung tissue was reduced in the dexamethasone treated group, bosentan treated group, and dexamethasone-bosentan treated group, which were more obvious in the dexamethasone-bosentan treated group. Conclusion Cigarette smoke exposure obviously aggravates airway inflammation in asthmatic rats, and bosentan can effectively alleviate the airway inflammation. The mechanism of the inflammation may be related to ET-2 and JNK1/2 signaling pathway.

Bronchial hyperresponsiveness in women with chronic obstructive pulmonary disease related to wood smoke

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Jaramillo C

2012-06-01

Full Text Available Mauricio González-García,1,2 Carlos A Torres-Duque,1,2 Adriana Bustos,1 Claudia Jaramillo,1 Darío Maldonado1,21Fundación Neumológica Colombiana, 2Universidad de la Sabana, Bogotá, ColombiaPurpose: Chronic obstructive pulmonary disease (COPD related to wood smoke exposure is characterized by important inflammation of the central and peripheral airways without significant emphysema. The objective of this study is to describe the bronchial hyperresponsiveness (BHR level in women with COPD related to wood smoke exposure and to compare it with the BHR in women with COPD related to tobacco smoking.Materials and methods: Two groups of women with stable COPD were studied: (1 wood smoke exposed (WS-COPD; and (2 tobacco smoke exposed (TS-COPD. A methacholine challenge test (MCT was performed in all patients according to American Thoracic Society criteria. BHR levels were compared using the methacholine concentration, which caused a 20% fall in the FEV1 (PC20.Results: Thirty-one patients, 19 with WS-COPD and 12 with TS-COPD, were included. There were no significant differences between the groups in baseline FVC, FEV1, IC, FEF25–75, and FEF25–75/FVC. All 31 patients had a positive MCT (PC20 , <16 mg/mL and the fall in the FEV1 and IC was similar in both groups. The severity of BHR was significantly higher in the WS-COPD patients (PC20: 0.39 mg/mL than in the TS-COPD patients (PC20: 1.24 mg/mL (P = 0.028. The presence of cough, phlegm, and dyspnea during the test were similar in both groups.Conclusion: We found moderate to severe BHR in women with WS-COPD, which was more severe than in the TS-COPD women with similar age and airflow obstruction. This paper suggests that the structural and inflammatory changes induced by the chronic exposure to wood smoke, described in other studies, can explain the differences with TS-COPD patients. Future studies may clarify our understanding of the impact of BHR on COPD physiopathology, phenotypes, and treatment

Smoking habits in the randomised Danish Lung Cancer Screening Trial with low-dose CT

DEFF Research Database (Denmark)

Ashraf, Haseem; Saghir, Zaigham; Dirksen, Asger

2014-01-01

BACKGROUND: We present the final results of the effect of lung cancer screening with low-dose CT on the smoking habits of participants in a 5-year screening trial. METHODS: The Danish Lung Cancer Screening Trial (DLCST) was a 5-year screening trial that enrolled 4104 subjects; 2052 were randomised...... to annual low-dose CT (CT group) and 2052 received no intervention (control group). Participants were current and ex-smokers (≥4 weeks abstinence from smoking) with a tobacco consumption of ≥20 pack years. Smoking habits were determined annually. Missing values for smoking status at the final screening...... round were handled using two different models. RESULTS: There were no statistically significant differences in annual smoking status between the CT group and control group. Overall the ex-smoker rates (CT + control group) significantly increased from 24% (baseline) to 37% at year 5 of screening (p

Smoking, Stress, and Coronary Heart Disease.

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Epstein, Leonard H.; Perkins, Kenneth A.

1988-01-01

Focuses on the interrelation between stressors and smoking, and on its potential impact on coronary heart disease risk beyond that due to stressors or to smoking alone. Reviews evidence supporting the stress-smoking interrelationship, its relevance to the risk of heart disease, and mechanisms explaining why smokers smoke more during stress and why…

Impact of a smoking and alcohol intervention programme on lung and breast cancer incidence in Denmark: An example of dynamic modelling with Prevent

DEFF Research Database (Denmark)

Soerjomataram, Isabelle; de Vries, Esther; Engholm, Gerda

2010-01-01

Prevent v.3.01 to assess the changes in incidence as a result of risk factor changes. Incidence of lung and breast cancer until 2050 was predicted under two scenarios: ideal (total elimination of smoking and reduction of alcohol intake to maximum 1units/d for women) and optimistic (decreasing prevalence......PURPOSE: Among the known risk factors, smoking is clearly related to the incidence of lung cancer and alcohol consumption is to breast cancer. In this manuscript we modelled the potential benefits of reductions in smoking or alcohol prevalence for the burden of these cancers. METHOD: We used...... of risk factors because of a 10% increase in cigarette and alcohol beverage price, repeated every 5years). Danish data from the household surveys, cancer registration and Eurostat were used. RESULTS: Up to 49% less new lung cancer cases can be expected in 2050 if smoking were to be completely eliminated...

[Prevention of coronary heart disease: smoking].

Science.gov (United States)

Heitzer, T; Meinertz, T

2005-01-01

Smoking is the leading preventable cause of illness and premature death in Germany, claiming over 110,000 lives a year because it directly increases the risk of dying from heart disease, stroke, emphysema and a variety of cancers. The overwhelming majority of smokers begin tobacco use before they reach adulthood. Among those young people who smoke, the average age is now 13-14. In Germany, about 39% of male and 31% of female adults (age 18-60 years) continue to smoke, despite information about the unequivocally negative health consequences of smoking. The exact mechanisms of smoking-related vascular disease are not yet known. Smoking causes acute hemodynamic alterations such as increase in heart rate, systematic and coronary vascular resistance, myocardial contractility, and myocardial oxygen demand. These short-term effects could lower the ischemic threshold in smokers with coronary artery disease and contribute to the increased risk for acute cardiovascular events. Endothelial damage is thought to be an initiating event in atherosclerosis and early studies have demonstrated that long-term smoking has direct toxic effects with structural changes of human endothelial cells. Recent research has shown the importance of the functional role of the endothelium in regulating vascular tone, platelet-endothelial interactions, leukocyte adhesion and smooth muscle cell proliferation via synthesis and release of a variety of substances such as nitric oxide. There is strong evidence that smoking leads to endothelial dysfunction mainly by increased inactivation of nitric oxide by oxygen-derived free radicals. Smoking also increases oxidative modification of LDL and is associated with lower HDL plasma levels. Smoking induces a systemic inflammatory response with increased leukocyte count and elevation of the C-reactive protein level. Importantly, the prothrombotic effects of smoking have been repeatedly demonstrated to cause alterations in platelet function, imbalance of

Women and Smoking: Global Challenge

Directory of Open Access Journals (Sweden)

Taru Kinnunen

2016-03-01

Full Text Available Global tobacco control has led to a reduction in smoking prevalence and mortality in men, while the rates among women have not followed the same declining rates or patterns. Tobacco-induced diseases, including those unique to women (reproductive complications, cervical and breast cancer are becoming increasingly prevalent among women. Unfortunately, many tobacco control policies and cessation programs have been found to be less effective for women than men. This is alarming as disease risk for lung cancer, CVD, osteoporosis, and COPD, associated with smoking, is higher among women. Women are also more likely to be exposed to secondhand tobacco smoke and subsequent morbidity. Finally, quitting smoking appears to be harder for women than men. Current tobacco control and surveillance data come primarily from high resource countries. WHO estimates that in 2030, in low and medium resource countries, 7 out of 10 deaths will be smoking-related. While the prevalence of smoking in women is relatively low in these countries, more information is needed regarding their patterns of tobacco use uptake, and subsequent health outcomes, as theirs differ from men. Tobacco use in women is greatly influenced by social, cultural and political determinants, and needs to be conceptualized within an intersectional framework.

AN INSTITUTION STUDENTS OF KNOWLEDGE OF HIGHER EDUCATION ON THE SMOKING AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Directory of Open Access Journals (Sweden)

Adriana Ponte Carneiro de Matos

2015-09-01

Full Text Available To evaluate the knowledge of an academic institution of higher education on smoking and chronic obstructive pulmonary disease. This descriptive, field, exploratory and cross conducted from February to April 2010, the two offices of a higher education institution in Fortaleza / CE. They evaluated 100 students, the courses in law, accounting, physical education and physiotherapy. The average age was 26.7 ± 9.38 years. It was observed that 45% (n = 45 of the sample neverheard about the disease, 66% (n = 66 did not know their causes, 69% (n = 69 did not know the symptoms, 69% (n = 69 did not know the treatment, 71% (n = 71 did not know how the diagnosis was made and 87% (n = 87 reported not knowing anyone with the disease. When asked about their knowledge of the harm caused by smoking, 92% (n = 92 said they knew, and 96% (n = 96 considered passive smoking as responsible for diseases of the lungs. Showed up little knowledge of COPD, its causes, symptoms, treatment and association with smoking among students assessed.

Radiation factors and smoking interaction at lung cancer incidence for workers at a nuclear enterprise

International Nuclear Information System (INIS)

Tokarskaya, Z.B.; Khokhryakov, V.T.; Okladnikova, N.D.; Belyaeva, Z.D.; Zhuntova, G.V.; Fleck, C.M.; Schollnberger, H.; Drozhko, E.G.

1998-01-01

A study is reported which is a continuation of a previous investigation of lung cancer incidence in workers at a nuclear enterprise and its relation to three basic etiological factors: the body burden due to 239 Pu, chronic external gamma irradiation, and smoking. Whereas previously each of the factors was assessed separately, in the present study the attempt was made to assess the interaction of the factors. A statistical analysis of the data revealed that for the following pairs of factors a superposition effect could be seen: external gamma irradiation and 239 Pu body burden; external gamma irradiation and a medium level of smoking; and 239 Pu body burden and a medium level of smoking. (A.K.)

Persistent smoking rate after coronary revascularization and factors related to smoking cessation in Turkey.

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Keskin, Kudret; Sezai Yildiz, Süleyman; Çetinkal, Gökhan; Çetin, Sükrü; Sigirci, Serhat; Kilci, Hakan; Aksan, Gökhan; Helvaci, Füsun; Gürdal, Ahmet; Balaban Kocas, Betül; Arslan, Sükrü; Orta Kiliçkesmez, Kadriye

2017-11-22

Although smoking is an established risk factor for coronary artery disease, smoking cessation efforts, as part of a lifestyle change, have been disappointing so far. Therefore, assessing current smoking trends and identifying patients who are at risk of smoking continuation is of paramount importance. In this study, our aim was to assess current smoking rates after coronary revascularization as of 2017, and to define factors that potentially affect smoking cessation. Overall, 350 patients who had undergone coronary revascularization, either by percutaneous coronary intervention or bypass surgery were included in this cross-sectional, observational study. Patients were queried for various sociodemographic characteristics and smoking habits. Disease related data were obtained from the hospital archives. The overall smoking rate was 57% after coronary revascularization. Age, bypass surgery and the occurrence of in-hospital adverse events were found to be independent predictors of smoking cessation in multivariate analysis. Despite efforts, smoking rates after coronary intervention remain substantially high. Therefore, a multidisciplinary approach to smoking cessation that incorporates cardiac rehabilitation programs and medications should be implemented in clinical practice. © The Author 2017. Published by Oxford University Press on behalf of Faculty of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com

Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure.

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Lewis, Joshua B; Hirschi, Kelsey M; Arroyo, Juan A; Bikman, Benjamin T; Kooyman, David L; Reynolds, Paul R

2017-03-17

Approximately 1 billion people smoke worldwide, and the burden placed on society by primary and secondhand smokers is expected to increase. Smoking is the leading risk factor for myriad health complications stemming from diverse pathogenic programs. First- and second-hand cigarette smoke contains thousands of constituents, including several carcinogens and cytotoxic chemicals that orchestrate chronic inflammatory responses and destructive remodeling events. In the current review, we outline details related to compromised pulmonary and systemic conditions related to smoke exposure. Specifically, data are discussed relative to impaired lung physiology, cancer mechanisms, maternal-fetal complications, cardiometabolic, and joint disorders in the context of smoke exposure exacerbations. As a general unifying mechanism, the receptor for advanced glycation end-products (RAGE) and its signaling axis is increasingly considered central to smoke-related pathogenesis. RAGE is a multi-ligand cell surface receptor whose expression increases following cigarette smoke exposure. RAGE signaling participates in the underpinning of inflammatory mechanisms mediated by requisite cytokines, chemokines, and remodeling enzymes. Understanding the biological contributions of RAGE during cigarette smoke-induced inflammation may provide critically important insight into the pathology of lung disease and systemic complications that combine during the demise of those exposed.

Nano-based theranostics for chronic obstructive lung diseases: challenges and therapeutic potential.

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Vij, Neeraj

2011-09-01

The major challenges in the delivery and therapeutic efficacy of nano-delivery systems in chronic obstructive airway conditions are airway defense, severe inflammation and mucous hypersecretion. Chronic airway inflammation and mucous hypersecretion are hallmarks of chronic obstructive airway diseases, including asthma, COPD (chronic obstructive pulmonary disease) and CF (cystic fibrosis). Distinct etiologies drive inflammation and mucous hypersecretion in these diseases, which are further induced by infection or components of cigarette smoke. Controlling chronic inflammation is at the root of treatments such as corticosteroids, antibiotics or other available drugs, which pose the challenge of sustained delivery of drugs to target cells or tissues. In spite of the wide application of nano-based drug delivery systems, very few are tested to date. Targeted nanoparticle-mediated sustained drug delivery is required to control inflammatory cell chemotaxis, fibrosis, protease-mediated chronic emphysema and/or chronic lung obstruction in COPD. Moreover, targeted epithelial delivery is indispensable for correcting the underlying defects in CF and targeted inflammatory cell delivery for controlling other chronic inflammatory lung diseases. We propose that the design and development of nano-based targeted theranostic vehicles with therapeutic, imaging and airway-defense penetrating capability, will be invaluable for treating chronic obstructive lung diseases. This paper discusses a novel nano-theranostic strategy that we are currently evaluating to treat the underlying cause of CF and COPD lung disease.

Comparison of in vitro toxicological effects of biomass smoke from different sources of animal dung.

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McCarthy, Claire E; Duffney, Parker F; Wyatt, Jeffrey D; Thatcher, Thomas H; Phipps, Richard P; Sime, Patricia J

2017-09-01

Worldwide, over 4 million premature deaths each year are attributed to the burning of biomass fuels for cooking and heating. Epidemiological studies associate household air pollution with lung diseases, including chronic obstructive pulmonary disease, lung cancer, and respiratory infections. Animal dung, a biomass fuel used by economically vulnerable populations, generates more toxic compounds per mass burned than other biomass fuels. The type of animal dung used varies widely depending on local agro-geography. There are currently neither standardized experimental systems for dung biomass smoke research nor studies assessing the health impacts of different types of dung smoke. Here, we used a novel reproducible exposure system to assess outcomes related to inflammation and respiratory infections in human airway cells exposed to six different types of dung biomass smoke. We report that dung biomass smoke, regardless of species, is pro-inflammatory and activates the aryl hydrocarbon receptor and JNK transcription factors; however, dung smoke also suppresses interferon responses after a challenge with a viral mimetic. These effects are consistent with epidemiological data, and suggest a mechanism by which the combustion of animal dung can directly cause lung diseases, promote increased susceptibility to infection, and contribute to the global health problem of household air pollution. Copyright © 2017. Published by Elsevier Ltd.

The contribution of DNA apurinic/apyrimidinic endonuclease genotype and smoking habit to Taiwan lung cancer risk.

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Chen, Wei-Chun; Tsai, Chia-Wen; Hsia, Te-Chun; Chang, Wen-Shin; Lin, Liang-Yi; Liang, Shinn-Jye; Tu, Chih-Yen; Cheng, Wei-Erh; Chen, Hung-Jen; Wang, Shu-Ming; Bau, da-Tian

2013-06-01

To evaluate the association and interaction of genotypic polymorphism the gene for DNA-apurinic/apyrimidinic endonuclease (APEX1) with personal smoking habit and lung cancer risk in Taiwan, the polymorphic variants of APEX1, Asp(148)Glu (rs1130409), were analyzed in association with lung cancer risk, and their joint effect with personal smoking habits on lung cancer susceptibility was discussed. In this hospital-based case-control study, 358 patients with lung cancer and 716 cancer-free controls, frequency-matched by age and sex, were recruited and genotyped by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). The results showed that the percentages of TT, TG and GG APEX1 Asp(148)Glu genotypes were not significantly different at 43.0%, 41.1% and 15.9% in the lung cancer patient group and 39.9%, 46.1% and 14.0% in non-cancer control group, respectively. We further analyzed the genetic-lifestyle effects on lung cancer risk and found the contribution of APEX1 Asp(148)Glu genotypes to lung cancer susceptibility was neither enhanced in the cigarette smokers nor in the non-smokers (p=0.3550 and 0.8019, respectively). Our results provide evidence that the non-synonymous polymorphism of APEX1 Asp(148)Glu may not be directly associated with lung cancer risk, nor enhance the effects of smoking habit on lung cancer development.

Smoking and Passive Smoking

OpenAIRE

Russell V. Luepker, MD, MS

2016-01-01

Objective: To review the literature on associations between cardiovascular diseases and tobacco use, including recent trends in smoking behaviors and clinical approaches for cessation of smoking. Methods: A literature review of recent scientific findings for smoking and cardiovascular diseases and recommendations for obtaining cessation. Results: Tobacco smoking is causally related to cardiovascular disease, with nearly a half million deaths annually attributed to cigarette smoking in the Uni...

Chronic interstitial lung disease in children

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Matthias Griese

2018-02-01

Full Text Available Children's interstitial lung diseases (chILD are increasingly recognised and contain many lung developmental and genetic disorders not yet identified in adult pneumology. Worldwide, several registers have been established. The Australasian Registry Network for Orphan Lung Disease (ARNOLD has identified problems in estimating rare disease prevalence; focusing on chILD in immunocompetent patients, a period prevalence of 1.5 cases per million children and a mortality rate of 7% were determined. The chILD-EU register highlighted the workload to be covered per patient included and provided protocols for diagnosis and initial treatment, similar to the United States chILD network. Whereas case reports may be useful for young physicians to practise writing articles, cohorts of patients can catapult progress, as demonstrated by recent studies on persistent tachypnoea of infancy, hypersensitivity pneumonitis in children and interstitial lung disease related to interferonopathies from mutations in transmembrane protein 173. Translational research has linked heterozygous mutations in the ABCA3 transporter to an increased risk of interstitial lung diseases, not only in neonates, but also in older children and adults. For surfactant dysfunction disorders in infancy and early childhood, lung transplantation was reported to be as successful as in adult patients. Mutual potentiation of paediatric and adult pneumologists is mandatory in this rapidly extending field for successful future development. This brief review highlights publications in the field of paediatric interstitial lung disease as reviewed during the Clinical Year in Review session presented at the 2017 European Respiratory Society (ERS Annual Congress in Milan, Italy. It was commissioned by the ERS and critically presents progress made as well as drawbacks.

Radiation factors and smoking interaction at lung cancer incidence for workers at a nuclear enterprise

International Nuclear Information System (INIS)

Tokarskaya, Z.B.; Khokhryakov, V.F.; Okladnikova, N.D.; Belyaeva, Z.D.; Zhuntova, G.V.

1997-01-01

It was shown on the basis of retrospective investigation of 500 workers at a nuclear enterprise (162 cases of lung cancer, 338 persons as matching control) that the interaction of external gamma-irradiation (> 2.0 Gy) and the body - burden of 239 Pu (> 9.3 kBq) at lung cancer is characterized as the multiplicative effect. Combined influence of smoking and radiation factors dependent on smoking index (SI): it changed from additive up to multiplicative and than to antagonistic with the increase of the smoking effect. The received results could be explained on the basis of a two - mutation model of radiation carcinogenesis

The combined effects of plutonium and cigarette smoke on the production of lung tumours

International Nuclear Information System (INIS)

Priest, N.D.; Moores, S.R.; Black, A.; Talbot, R.; Morgan, A.

1989-01-01

An experiment was conducted to determine the effect of exposure to cigarette smoke on the incidence of plutonium induced lung tumours in mice. Approximately 130 female CBA/H mice were used. These were exposed to plutonium-239 dioxide to give an initial alveolar deposit of 100 Bq, then treated in one of three ways. One third received no further treatment and were held for a period of 18 months. The remainder were either sham-exposed or exposed to mainstream cigarette smoke for one year then held for a further 6 months. After this all the animals were killed. The control mice - that had received only plutonium -contained more tumours than mice that were also either sham-exposed or exposed to cigarette smoke. The lowest number of tumours was found in the group exposed to smoke. These results indicate that, under some circumstances, the effects of cigarette smoke and of alpha-irradiation of the lung can be antagonistic, contrasting with a common expectation of synergy. (author)

Indirectly estimated absolute lung cancer mortality rates by smoking status and histological type based on a systematic review

International Nuclear Information System (INIS)

Lee, Peter N; Forey, Barbara A

2013-01-01

National smoking-specific lung cancer mortality rates are unavailable, and studies presenting estimates are limited, particularly by histology. This hinders interpretation. We attempted to rectify this by deriving estimates indirectly, combining data from national rates and epidemiological studies. We estimated study-specific absolute mortality rates and variances by histology and smoking habit (never/ever/current/former) based on relative risk estimates derived from studies published in the 20 th century, coupled with WHO mortality data for age 70–74 for the relevant country and period. Studies with populations grossly unrepresentative nationally were excluded. 70–74 was chosen based on analyses of large cohort studies presenting rates by smoking and age. Variations by sex, period and region were assessed by meta-analysis and meta-regression. 148 studies provided estimates (Europe 59, America 54, China 22, other Asia 13), 54 providing estimates by histology (squamous cell carcinoma, adenocarcinoma). For all smoking habits and lung cancer types, mortality rates were higher in males, the excess less evident for never smokers. Never smoker rates were clearly highest in China, and showed some increasing time trend, particularly for adenocarcinoma. Ever smoker rates were higher in parts of Europe and America than in China, with the time trend very clear, especially for adenocarcinoma. Variations by time trend and continent were clear for current smokers (rates being higher in Europe and America than Asia), but less clear for former smokers. Models involving continent and trend explained much variability, but non-linearity was sometimes seen (with rates lower in 1991–99 than 1981–90), and there was regional variation within continent (with rates in Europe often high in UK and low in Scandinavia, and higher in North than South America). The indirect method may be questioned, because of variations in definition of smoking and lung cancer type in the

Indirectly estimated absolute lung cancer mortality rates by smoking status and histological type based on a systematic review

Science.gov (United States)

2013-01-01

Background National smoking-specific lung cancer mortality rates are unavailable, and studies presenting estimates are limited, particularly by histology. This hinders interpretation. We attempted to rectify this by deriving estimates indirectly, combining data from national rates and epidemiological studies. Methods We estimated study-specific absolute mortality rates and variances by histology and smoking habit (never/ever/current/former) based on relative risk estimates derived from studies published in the 20th century, coupled with WHO mortality data for age 70–74 for the relevant country and period. Studies with populations grossly unrepresentative nationally were excluded. 70–74 was chosen based on analyses of large cohort studies presenting rates by smoking and age. Variations by sex, period and region were assessed by meta-analysis and meta-regression. Results 148 studies provided estimates (Europe 59, America 54, China 22, other Asia 13), 54 providing estimates by histology (squamous cell carcinoma, adenocarcinoma). For all smoking habits and lung cancer types, mortality rates were higher in males, the excess less evident for never smokers. Never smoker rates were clearly highest in China, and showed some increasing time trend, particularly for adenocarcinoma. Ever smoker rates were higher in parts of Europe and America than in China, with the time trend very clear, especially for adenocarcinoma. Variations by time trend and continent were clear for current smokers (rates being higher in Europe and America than Asia), but less clear for former smokers. Models involving continent and trend explained much variability, but non-linearity was sometimes seen (with rates lower in 1991–99 than 1981–90), and there was regional variation within continent (with rates in Europe often high in UK and low in Scandinavia, and higher in North than South America). Conclusions The indirect method may be questioned, because of variations in definition of smoking and

Comparison of clinical and pathological features of lung lesions of systemic IgG4-related disease and idiopathic multicentric Castleman's disease.

Science.gov (United States)

Terasaki, Yasuhiro; Ikushima, Soichiro; Matsui, Shoko; Hebisawa, Akira; Ichimura, Yasunori; Izumi, Shinyu; Ujita, Masuo; Arita, Machiko; Tomii, Keisuke; Komase, Yuko; Owan, Isoko; Kawamura, Tetsuji; Matsuzawa, Yasuo; Murakami, Miho; Ishimoto, Hiroshi; Kimura, Hiroshi; Bando, Masashi; Nishimoto, Norihiro; Kawabata, Yoshinori; Fukuda, Yuh; Ogura, Takashi

2017-06-01

The lung lesion [immunoglobulin (Ig)G4-L] of IgG4-related disease (IgG4-RD) is a condition that occurs together with IgG4-RD and often mimics the lung lesion [idiopathic multicentric Castleman's disease (iMCD-L)] of idiopathic multicentric Castleman's disease (iMCD). Because no clinical and pathological studies had previously compared features of these diseases, we undertook this comparison with clinical and histological data. Nine patients had IgG4-L (high levels of serum IgG4 and of IgG4 + cells in lung specimens; typical extrapulmonary manifestations). Fifteen patients had iMCD-L (polyclonal hyperimmunoglobulinaemia, elevated serum interleukin-6 levels and polylymphadenopathy with typical lymphadenopathic lesions). Mean values for age, serum haemoglobin levels and IgG4/IgG ratios were higher in the IgG4-L group and C-reactive protein levels were higher in the iMCD-L group. All IgG4-RD lung lesions showed myxomatous granulation-like fibrosis (active fibrosis), with infiltration of lymphoplasmacytes and scattered eosinophils within the perilymphatic stromal area, such as interlobular septa and pleura with obstructive vasculitis. All 15 lung lesions of iMCD, however, had marked accumulation of polyclonal lymphoplasmacytes in lesions with lymphoid follicles and dense fibrosis, mainly in the alveolar area adjacent to interlobular septa and pleura without obstructive vasculitis. Although both lesions had lymphoplasmacytic infiltration, lung lesions of IgG4-RD were characterized by active fibrosis with eosinophilic infiltration within the perilymphatic stromal area with obstructive vasculitis, whereas lung lesions of iMCD had lymphoplasmacyte proliferating lesions mainly in the alveolar area adjacent to the perilymphatic stromal area. These clinicopathological features may help to differentiate the two diseases. © 2017 John Wiley & Sons Ltd.

Smoking habit and benign breast disease

International Nuclear Information System (INIS)

Dziewulska-Bokiniec, A.

1995-01-01

The possible association between cigarette smoking and the risk of benign breast disease (BBD) was assessed in a case-control study conducted in Gdansk, Poland, between 1990 and 1994. The study compared 160 women with newly diagnosed BBD admitted to the Gdansk Cancer Outpatients Clinic and 160 controls, women from outpatients clinics at the Medical University of Gdansk. There was no convincing evidence of an association, either positive or negative, between various indicators of smoking habit (smoking status, number of cigarettes smoked per day, duration of smoking) and the risk of BBD. Slightly lower relative risk (RRs) of BBD in ex-smokers of 10 or more cigarettes per day (RR = 0.9; 95% confidence interval, CI: 0.4-2.2), and with duration of smoking >= (RR = 0.1-3.4), were also observed in current smokers (RR = 0.8; 95% CI: 0.4-1.5), and (RR = 0.8; 95% CI: 0.1-3.4), but these findings were not statistically significant. (author)

Long-Term Benefits of Smoking Cessation on Gastroesophageal Reflux Disease and Health-Related Quality of Life.

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Yukie Kohata

Full Text Available Smoking is associated with gastroesophageal reflux disease (GERD. Varenicline, a nicotinic receptor partial agonist, is used to aid smoking cessation. The purpose of this study was to prospectively examine the long-term benefits of smoking cessation on GERD and health-related quality of life (HR-QOL.Patients treated with varenicline were asked to fill out a self-report questionnaire about their smoking habits, gastrointestinal symptoms, and HR-QOL before and 1 year after smoking cessation. The prevalence of GERD, frequency of symptoms, and HR-QOL scores were compared. We also investigated associations between clinical factors and newly-developed GERD.A total of 141 patients achieved smoking cessation (success group and 50 did not (failure group at 1 year after the treatment. The GERD improvement in the success group (43.9% was significantly higher than that in the failure group (18.2%. The frequency of reflux symptoms significantly decreased only in the success group. There were no significant associations between newly developed GERD and clinical factors including increased body mass index and successful smoking cessation. HR-QOL significantly improved only in the success group.Smoking cessation improved both GERD and HR-QOL. Smoking cessation should be recommended for GERD patients.

Effects of cigarette smoking on iodine 123 N-isopropyl-f-iodoamphetamine clearance from the lung

International Nuclear Information System (INIS)

Kato, Kunihiko; Harada, Satoshi; Takahashi, Tsuneo; Katsuragawa, Shigehiko; Yanagisawa, Toru

1991-01-01

Iodine 123 N-isopropyl-p-iodoamphetamine ( 123 I-IMP), originally developed as a brain scanning agent, is also taken up by the lung. To evaluate the effects of cigarette smoking on the kinetics of IMP in the lung, we studied 123 I-IMP clearance from the lung in 18 volunteers (8 non-smokers and 10 smokers). After the injection of 111 MBq of 123 I-IMP into the medial cubital vein, the time-activity curve for 60 min and the regional activity using 1 frame per minute and a 64x64 matrix were obtained. The 123 I-IMP clearance curve was described as follows: C(t)=A 1 e ( -k 1 t)+A 2 e ( -k 2 t)(A 1 , A 2 : intercepts, and k 1 , k 2 : slopes of the exponential components). 123 I-IMP clearance was delayed in smokers, and k 2 was smaller in smokers. Also, a correlation between k 1 , k 2 , and the number of cigarettes smoked per day was found (r=-0.65, r=-0.74, respectively, P 123 I-IMP in the lung indicate lung metabolic disorders due to cigarette smoking. (orig.)

Cancer, coronary artery disease and smoking: a preliminary report on differences in incidence between Seventh-day Adventists and others.

Science.gov (United States)

WYNDER, E L; LEMON, F R

1958-10-01

A study was made of the incidence of certain types of disease among Seventh-day Adventists, a religious group of special interest because they refrain from smoking and drinking. Epidermoid cancer of the lung, previously shown to be related to smoking, was 10 times less common among Seventh-day Adventists than among the general population, even among those Seventh-day Adventists living in the Los Angeles area where all are exposed to smog. Similarly, cancers of the mouth, larynx, and esophagus, previously shown to be related not only to smoking but also to heavy drinking, were at least 10 times less common among Seventh-day Adventist men than among men of the general population. All other types of cancer, with the exception of cancer of the bladder and cervix, occurred among Seventh-day Adventists with the same frequency as in the general population. The latter occurred slightly less than in the general population. Myocardial infarction in Seventh-day Adventist males was less frequent and occurred at a later age than among males in the general population; while the age distribution of the disease among the Seventh-day Adventist females was similar to that of females in the general population.

Cigarette smoke exposure inhibits extracellular MMP-2 (gelatinase A activity in human lung fibroblasts

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Cappello Francesco

2007-03-01

Full Text Available Abstract Background Exposure to cigarette smoke is considered a major risk factor for the development of lung diseases, since its causative role has been assessed in the induction and maintenance of an inflamed state in the airways. Lung fibroblasts can contribute to these processes, due to their ability to produce proinflammatory chemotactic molecules and extracellular matrix remodelling proteinases. Among proteolytic enzymes, gelatinases A and B have been studied for their role in tissue breakdown and mobilisation of matrix-derived signalling molecules. Multiple reports linked gelatinase deregulation and overexpression to the development of inflammatory chronic lung diseases such as COPD. Methods In this study we aimed to determine variations in the gelatinolytic pattern of human lung fibroblasts (HFL-1 cell line exposed to cigarette smoke extract (CSE. Gelatinolytic activity levels were determined by using gelatin zymography for the in-gel detection of the enzymes (proenzyme and activated forms, and the subsequent semi-quantitative densitometric evaluation of lytic bands. Expression of gelatinases was evaluated also by RT-PCR, zymography of the cell lysates and by western blotting. Results CSE exposure at the doses used (1–10% did not exert any significant cytotoxic effects on fibroblasts. Zymographic analysis showed that CSE exposure resulted in a linear decrease of the activity of gelatinase A. Control experiments allowed excluding a direct inhibitory effect of CSE on gelatinases. Zymography of cell lysates confirmed the expression of MMP-2 in all conditions. Semi-quantitative evaluation of mRNA expression allowed assessing a reduced transcription of the enzyme, as well as an increase in the expression of TIMP-2. Statistical analyses showed that the decrease of MMP-2 activity in conditioned media reached the statistical significance (p = 0.0031 for 24 h and p = 0.0012 for 48 h, while correlation analysis showed that this result was

Cigarette smoke promotes dendritic cell accumulation in COPD; a Lung Tissue Research Consortium study

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Yi Eunhee S

2010-04-01

Full Text Available Abstract Background Abnormal immune responses are believed to be highly relevant in the pathogenesis of chronic obstructive pulmonary disease (COPD. Dendritic cells provide a critical checkpoint for immunity by their capacity to both induce and suppress immunity. Although evident that cigarette smoke, the primary cause of COPD, significantly influences dendritic cell functions, little is known about the roles of dendritic cells in the pathogenesis of COPD. Methods The extent of dendritic cell infiltration in COPD tissue specimens was determined using immunohistochemical localization of CD83+ cells (marker of matured myeloid dendritic cells, and CD1a+ cells (Langerhans cells. The extent of tissue infiltration with Langerhans cells was also determined by the relative expression of the CD207 gene in COPD versus control tissues. To determine mechanisms by which dendritic cells accumulate in COPD, complimentary studies were conducted using monocyte-derived human dendritic cells exposed to cigarette smoke extract (CSE, and dendritic cells extracted from mice chronically exposed to cigarette smoke. Results In human COPD lung tissue, we detected a significant increase in the total number of CD83+ cells, and significantly higher amounts of CD207 mRNA when compared with control tissue. Human monocyte-derived dendritic cells exposed to CSE (0.1-2% exhibited enhanced survival in vitro when compared with control dendritic cells. Murine dendritic cells extracted from mice exposed to cigarette smoke for 4 weeks, also demonstrated enhanced survival compared to dendritic cells extracted from control mice. Acute exposure of human dendritic cells to CSE induced the cellular pro-survival proteins heme-oxygenase-1 (HO-1, and B cell lymphoma leukemia-x(L (Bcl-xL, predominantly through oxidative stress. Although activated human dendritic cells conditioned with CSE expressed diminished migratory CCR7 expression, their migration towards the CCR7 ligand CCL21 was not

Polonium in cigarette smoke and radiation exposure of lungs

International Nuclear Information System (INIS)

Carvalho, F.P.; Oliveira, J.M.

2006-01-01

210 Po was analysed in three common brands of cigarettes produced in Portugal. The analyses of polonium were performed using 209 Po as an internal isotopic tracer. Samples were dissolved with acids, polonium plated on a silver disc and measured by alpha spectrometry using silicon surface barrier detectors. The analyses were carried out on the unburned tobacco contained in the cigarettes, on the ashes of smoked cigarettes and on the mainstream smoke inhaled by the smoker. 210 Po in the tobacco display concentrations ranging from 3 to 37 mBq/g, depending upon the cigarette brand. The 210 Po remaining in the solid residue of a smoked cigarette varied between 0.3 to 4.9 mBq per cigarette, and the 210 Po in the inhaled smoke from one cigarette varied from 2.6 to 28.9 mBq. In all brands of cigarettes tested, about 50 % of the 210 Po content is not inhaled by the smoker and it is released into the atmosphere. Part of it may be inhaled by passive smokers. Depending upon the commercial brand and upon the presence or absence of a filter in the cigarette, 5 to 37 % of the 210 Po in the cigarette can be inhaled by the smoker. Taking into account the average 210 Po and 210 Pb in surface air, the smoker of one pack of twenty cigarettes per day may inhale 50 times more 210 Po than a non smoker. The average absorption of 210 Po into the blood taking all pathways into account is 0.39 Bq d -1 . This includes, namely, the ingestion of water and beverages, the ingestion of food, the inhalation of air and cigarette smoke. Cigarette smoke contributes with 1.5 % to this rate of 210 Po absorption into the blood and, after circulating in all organs, gives rise to a whole body radiation dose in the same proportion. However, in the smoker the deposition of 210 Po in the lungs is much more elevated than normal and may originate an enhanced radiation exposure of this organ. Estimated dose to the lungs is presented and radiobiological effects of cigarette smoking are discussed. (author)

Epidemiology, aetiology, diagnosis and screening of lung cancer

International Nuclear Information System (INIS)

Berzinec, P.

2006-01-01

Lung cancer is the leading cause of cancer death globally. Smoking causes about 90 % of all lung cancer cases. Passive, i.e. involuntary smoking has been confirmed to enhance the risk of lung cancer in exposed people. Individual susceptibility is one of important factors in lung cancer formation. New knowledge in epidemiology and aetiology of lung cancer gives new possibilities in diagnostic and screening of this disease. Results of large randomised trials aimed at new technologies in lung cancer screening will be available in a few years. (author)

Pulmonary hypertension associated with lung diseases and hypoxemia.

Science.gov (United States)

Cuttica, Michael J

2016-05-01

Pulmonary hypertension that develops in the setting of underlying lung diseases such as COPD or idiopathic pulmonary fibrosis (IPF) is associated with decreased functional status, worsening hypoxemia and quality of life, and increased mortality. This complication of lung disease is complex in its origin and carries a unique set of diagnostic and therapeutic issues. This review attempts to provide an overview of mechanisms associated with the onset of pulmonary hypertension in COPD and IPF, touches on appropriate evaluation, and reviews the state of knowledge on treating pulmonary hypertension related to underlying lung disease.

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

Pathologic Cellular Events in Smoking-Related Pancreatitis

Energy Technology Data Exchange (ETDEWEB)

Thrower, Edwin [Department of Internal Medicine, Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT 06520 (United States); Veterans Affairs Connecticut Healthcare, West Haven, CT 06516 (United States)

2015-04-29

Pancreatitis, a debilitating inflammatory disorder, results from pancreatic injury. Alcohol abuse is the foremost cause, although cigarette smoking has recently surfaced as a distinct risk factor. The mechanisms by which cigarette smoke and its toxins initiate pathological cellular events leading to pancreatitis, have not been clearly defined. Although cigarette smoke is composed of more than 4000 compounds, it is mainly nicotine and the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), which have been extensively studied with respect to pancreatic diseases. This review summarizes these research findings and highlights cellular pathways which may be of relevance in initiation and progression of smoking-related pancreatitis.

Anti-proline-glycine-proline or antielastin autoantibodies are not evident in chronic inflammatory lung disease.

LENUS (Irish Health Repository)

Greene, Catherine M

2010-01-01

In patients with chronic inflammatory lung disease, pulmonary proteases can generate neoantigens from elastin and collagen with the potential to fuel autoreactive immune responses. Antielastin peptide antibodies have been implicated in the pathogenesis of tobacco-smoke-induced emphysema. Collagen-derived peptides may also play a role.

Smoking at workplace – Legislation and health aspect of exposure to second-hand tobacco smoke

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Agnieszka Lipińska-Ojrzanowska

2015-12-01

Full Text Available Tobacco smoke contains thousands of xenobiotics harmful to human health. Their irritant, toxic and carcinogenic potential has been well documented. Passive smoking or exposure to second-hand smoke (SHS in public places, including workplace, poses major medical problems. Owing to this fact there is a strong need to raise workers’ awareness of smoking-related hazards through educational programs and to develop and implement legislation aimed at eliminating SHS exposure. This paper presents a review of reports on passive exposure to tobacco smoke and its impact on human health and also a review of binding legal regulations regarding smoking at workplace in Poland. It has been proved that exposure to tobacco smoke during pregnancy may lead to, e.g., preterm delivery and low birth weight, sudden infant death syndrome, lung function impairment, asthma and acute respiratory illnesses in the future. Exposure to tobacco smoke, only in the adult age, is also considered as an independent risk factor of cardiovascular diseases, acute and chronic respiratory diseases and cancer. Raising public awareness of tobacco smoke harmfulness should be a top priority in the field of workers’ health prevention. Occupational medicine physicians have regular contacts with occupationally active people who smoke. Thus, occupational health services have a unique opportunity to increase employees and employers’ awareness of adverse health effects of smoking and their prevention. Med Pr 2015;66(6:827–836

Magnetic resonance imaging biomarkers of chronic obstructive pulmonary disease prior to radiation therapy for non-small cell lung cancer

International Nuclear Information System (INIS)

Sheikh, Khadija; Capaldi, Dante P.I.; Hoover, Douglas A.; Palma, David A.; Yaremko, Brian P.; Parraga, Grace

2015-01-01

•Three imaging phenotypes of COPD and ventilation heterogeneity.•We examine relationships for non-tumour lobe ventilation voids and clinical tests.•Smoking history and airflow obstruction were diagnostics for imaging phenotypes. Three imaging phenotypes of COPD and ventilation heterogeneity. We examine relationships for non-tumour lobe ventilation voids and clinical tests. Smoking history and airflow obstruction were diagnostics for imaging phenotypes. In this prospectively planned interim-analysis, the prevalence of chronic obstructive lung disease (COPD) phenotypes was determined using magnetic resonance imaging (MRI) and X-ray computed tomography (CT) in non-small-cell-lung-cancer (NSCLC) patients. Stage-III-NSCLC patients provided written informed consent for pulmonary function tests, imaging and the 6-min-walk-test. Ventilation defect percent (VDP) and CT lung density (relative-of-CT-density-histogram <−950, RA 950 ) were measured. Patients were classified into three subgroups based on qualitative and quantitative COPD and tumour-specific imaging phenotypes: (1) tumour-specific ventilation defects (TSD), (2) tumour-specific and other ventilation defects without emphysema (TSD V ), and, (3) tumour-specific and other ventilation defects with emphysema (TSD VE ). Seventeen stage-III NSCLC patients were evaluated (68 ± 7 years, 7 M/10 F, mean FEV 1 = 77% pred ) including seven current and 10 ex-smokers and eight patients with a prior lung disease diagnosis. There was a significant difference for smoking history (p = .02) and FEV 1 /FVC (p = .04) for subgroups classified using quantitative imaging. Patient subgroups classified using qualitative imaging findings were significantly different for emphysema (RA 950 , p < .001). There were significant relationships for whole-lung VDP (p < .05), but not RECIST or tumour-lobe VDP measurements with pulmonary function and exercise measurements. Preliminary analysis for non-tumour burden ventilation abnormalities

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

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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.

Histological findings and lung dust analysis as the basis for occupational disease compensation in asbestos-related lung cancer in Germany.

Science.gov (United States)

Feder, Inke Sabine; Theile, Anja; Tannapfel, Andrea

2018-01-15

This study has researched the significance of histologically raised findings and lung dust analyses in the context of claiming the recognition of and thus compensation for an asbestos-associated occupational disease. For this approach, all findings from the German Mesothelioma Register in 2015 that included lung dust analyses were evaluated and were compared with information on asbestos fiber exposure at work based on fiber years, and with the results of radiological findings. For 68 insured persons, recognition of an asbestos-induced lung disease according to Section 4104 of the German Ordinance on Occupational Diseases (Berufskrankheitenverordnung - BKV) could be recommended solely on the basis of the histological examinations of lung tissues and complementary lung dust analyses. Neither did the calculation of the cumulative asbestos dust exposure at work yield 25 fiber years, nor could bridge findings (e.g., plaques) be identified. In addition, the autopsies of 12 patients revealed plaques that had not been diagnosed during radiological examinations. These results show that - irrespective of the prescribed working techniques and radiological diagnosis - pathological/anatomical and histological diagnostics are often the only way for the insureds to demonstrate the causal connection between asbestos and their disease. Even after long intervals of up to 40 years post last exposure, the asbestos fibers would still be easily detectable in the lung tissues evaluated. Whenever suitable tissue is available, it should be examined for mild asbestosis with the aid of a lung dust analysis. Otherwise there is a risk that an occupational disease is wrongfully rejected. In the context of health insurance, the lung dust analysis and the resulting proof of the presence of asbestosis often constitute one option of providing evidence of an occupational disease. Int J Occup Med Environ Health 2018;31(3):293-305. This work is available in Open Access model and licensed under a CC BY

German EstSmoke: estimating adult smoking-related costs and consequences of smoking cessation for Germany.

Science.gov (United States)

Sonntag, Diana; Gilbody, Simon; Winkler, Volker; Ali, Shehzad

2018-01-01

We compared predicted life-time health-care costs for current, never and ex-smokers in Germany under the current set of tobacco control polices. We compared these economic consequences of the current situation with an alternative in which Germany were to implement more comprehensive tobacco control policies consistent with the World Health Organization (WHO) Framework Convention for Tobacco Control (FCTC) guidelines. German EstSmoke, an adapted version of the UK EstSmoke simulation model, applies the Markov modelling approach. Transition probabilities for (re-)currence of smoking-related diseases were calculated from large German disease-specific registries and the German Health Update (GEDA 2010). Estimations of both health-care costs and effect sizes of smoking cessation policies were taken from recent German studies and discounted at 3.5%/year. Germany. German population of prevalent current, never and ex-smokers in 2009. Life-time cost and outcomes in current, never and ex-smokers. If tobacco control policies are not strengthened, the German smoking population will incur €41.56 billion life-time excess costs compared with never smokers. Implementing tobacco control policies consistent with WHO FCTC guidelines would reduce the difference of life-time costs between current smokers and ex-smokers by at least €1.7 billion. Modelling suggests that the life-time healthcare costs of people in Germany who smoke are substantially greater than those of people who have never smoked. However, more comprehensive tobacco control policies could reduce health-care expenditures for current smokers by at least 4%. © 2017 Society for the Study of Addiction.

Tobacco related knowledge and support for smoke-free policies among community pharmacists in Lagos state, Nigeria

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Poluyi EO

2015-03-01

Full Text Available Background: There are no safe levels of exposure to second hand smoke and smoke-free policies are effective in reducing the burden of tobacco-related diseases and death. Pharmacists, as a unique group of health professionals, might be able to play a role in the promotion of smoke-free policies. Objective: To determine the tobacco-related knowledge of community pharmacists and assess their support for smoke-free policies in Lagos state, Nigeria. Methods: A cross-sectional descriptive study design using both quantitative and qualitative methods was employed. Two hundred and twelve randomly selected community pharmacists were surveyed using a pre-tested self-administered questionnaire. In addition, one focus group discussion was conducted with ten members of the Lagos state branch of the Association of Community Pharmacists of Nigeria. Results: The quantitative survey revealed that the majority (72.1% of the respondents were aged between 20 and 40 years, predominantly male (60.8%, Yoruba (50.2% or Igbo (40.3% ethnicity and had been practicing pharmacy for ten years or less (72.2%. A majority (90.1% of respondents were aware that tobacco is harmful to health. Slightly less (75.8% were aware that second hand smoke is harmful to health. Among the listed diseases, pharmacists responded that lung (84.4% and esophageal (68.9% cancers were the most common diseases associated with tobacco use. Less than half of those surveyed associated tobacco use with heart disease (46.9%, chronic obstructive pulmonary disease (27.8%, bladder cancer (47.2%, peripheral vascular disease (35.8% and sudden death (31.1%. Only 51.9% had heard of the World Health Organization Framework Convention on Tobacco Control (WHO FCTC. A little over half of the respondents (53.8% were aware of any law in Nigeria controlling tobacco use. The majority of respondents supported a ban on smoking in homes (83.5%, in public places (79.2%, and in restaurants, nightclubs and bars (73.6%. For

Smoking in Africa: the coming epidemic.

Science.gov (United States)

Taha, A; Ball, K

1982-01-01

success. Smoking-related diseases have already made their appearance in Africa. The 2 most common types of cancer in the Natal Bantu are lung and esophageal tumors. Lung cancer in Natal men has increased 6-fold and in women about 5-fold over the past 11 years. Other studies from southern Africa show much higher smoking rates in patients with lung cancer than in controls. The incidence of esophageal cancer in blacks in Durban, South Africa, and Zimbabwe is among the highest in the world. Other suggestive associations with cigarette smoking in African subjects are bladder cancer, myocardial infarction, and chronic bronchitis. Many Western governments and health authorities now try to persuade people not to smoke, and in some developed countries consumption has already begun to fall. As a result, tobacco companies have started to diversify and intensify promotion of cigarettes and the growth of tobacco in the 3rd world.

South African tobacco smoking cessation clinical practice guideline ...

African Journals Online (AJOL)

Smokers have an increased risk of cancer (i.e. lung, throat, bladder), chronic obstructive pulmonary disease (COPD), tuberculosis and cardiovascular disease (i.e. stroke, heart attack). Smoking affects unborn babies, children and others exposed to second hand smoke. Stopping or 'quitting' is not easy. Nicotine is highly ...

The association of systemic microvascular changes with lung function and lung density: a cross-sectional study.

Directory of Open Access Journals (Sweden)

Bianca Harris