Environmental tobacco smoke exposure and children's health.

NARCIS (Netherlands)

Polanska, K.; Hanke, W.; Ronchetti, R.; Hazel, P.J. van den; Zuurbier, M.; Koppe, J.G.; Bartonova, A.

2006-01-01

Almost half of the child population is involuntarily exposed to environmental tobacco smoke (ETS). The ETS exposure gives rise to an excessive risk of several diseases in infancy and childhood, including sudden infant death syndrome, upper and lower respiratory infections, asthma and middle ear

Fetal programming and environmental exposures ...

Science.gov (United States)

Fetal programming is an enormously complex process that relies on numerous environmental inputs from uterine tissue, the placenta, the maternal blood supply, and other sources. Recent evidence has made clear that the process is not based entirely on genetics, but rather on a delicate series of interactions between genes and the environment. It is likely that epigenctic (“above the genome”) changes are responsible for modifying gene expression in the developing fetus, and these modifications can have long-lasting health impacts. Determining which epigenetic regulators are most vital in embryonic development will improve pregnancy outcomes and our ability to treat and prevent disorders that emerge later in life. “Fetal Programming and Environmental Exposures: Implications for Prenatal Care and Preterm Birth’ began with a keynote address by Frederick vom Saal, who explained that low-level exposure to endocrine disrupting chemicals (EDCs) perturbs hormone systems in utero and can have negative effects on fetal development. vom Saal presented data on the LOC bisphenol A (BPA), an estrogen-mimicking compound found in many plastics. He suggested that low-dose exposure to LOCs can alter the development process and enhance chances of acquiring adult diseases, such as breastcancer, diabetes, and even developmental disorders such as attention deficit disorder (ADHD).’ Fetal programming is an enormously complex process that relies on numerous environmental inputs

Human exposure, health hazards, and environmental regulations

International Nuclear Information System (INIS)

Steinemann, Anne

2004-01-01

United States environmental regulations, intended to protect human health, generally fail to address major sources of pollutants that endanger human health. These sources are surprisingly close to us and within our control, such as consumer products and building materials that we use within our homes, workplaces, schools, and other indoor environments. Even though these indoor sources account for nearly 90% of our pollutant exposure, they are virtually unregulated by existing laws. Even pollutant levels found in typical homes, if found outdoors, would often violate federal environmental standards. This article examines the importance of human exposure as a way to understand and reduce effects of pollutants on human health. Results from exposure studies challenge traditional thinking about pollutant hazards, and reveal deficiencies in our patchwork of laws. And results from epidemiological studies, showing increases in exposure-related diseases, underscore the need for new protections. Because we cannot rely solely on regulations to protect us, and because health effects from exposures can develop insidiously, greater efforts are needed to reduce and prevent significant exposures before they occur. Recommendations include the development and use of safer alternatives to common products, public education on ways to reduce exposure, systematic monitoring of human exposure to pollutants, and a precautionary approach in decision-making

Calculation of the disease burden associated with environmental chemical exposures

DEFF Research Database (Denmark)

Grandjean, Philippe; Bellanger, Martine

2017-01-01

neurotoxicants, air pollution, and endocrine disrupting chemicals, where sufficient data were available to determine dose-dependent adverse effects. Environmental exposure information allowed cost estimates for the U.S. and the EU, for OECD countries, though less comprehensive for industrializing countries...

Protective influence of healthful nutrition on mechanisms of environmental pollutant toxicity and disease risks.

Science.gov (United States)

Hoffman, Jessie B; Hennig, Bernhard

2017-06-01

Human exposures to environmental contaminants around the world contribute to the global burden of disease and thus require urgent attention. Exploring preventive measures against environmental exposure and disease risk is essential. While a sedentary lifestyle and/or poor dietary habits can exacerbate the deleterious effects resulting from exposure to toxic chemicals, much emerging evidence suggests that positive lifestyle changes (e.g., healthful nutrition) can modulate and/or reduce the toxicity of environmental pollutants. Our work has shown that diets high in anti-inflammatory bioactive food components (e.g., phytochemicals or polyphenols) are possible strategies for modulating and reducing the disease risks associated with exposure to toxic pollutants in the environment. Thus, consuming healthy diets rich in plant-derived bioactive nutrients may reduce the vulnerability to diseases linked to environmental toxic insults. This nutritional paradigm in environmental toxicology requires further study in order to improve our understanding of the relationships between nutrition and other lifestyle modifications and toxicant-induced diseases. © 2017 New York Academy of Sciences.

Children's Exposure to Environmental Contaminants: An Editorial Reflection of Articles in the IJERPH Special Issue Entitled, "Children's Exposure to Environmental Contaminants".

Science.gov (United States)

Ferguson, Alesia; Solo-Gabriele, Helena

2016-11-09

Children are at increased vulnerability to many environmental contaminants compared to adults due to their unique behavior patterns, increased contaminant intake per body weight, and developing biological systems. Depending upon their age, young children may crawl on the floor and may practice increased hand to mouth activity that may increase their dose-intake of specific contaminants that accumulate in dust and other matrices. Children are also smaller in size than adults, resulting in a greater body burden for a given contaminant dose. Because children undergo rapid transitions through particular developmental stages they are also especially vulnerable during certain growth-related time windows. A Special Issue was organized focused on the latest findings in the field of children's environmental exposure for these reasons. This editorial introduces articles in this Special Issue and emphasizes their main findings in advancing the field. From the many articles submitted to this Special Issue from around the world, 23 were accepted and published. They focus on a variety of research areas such as children's activity patterns, improved risk assessment methods to estimate exposures, and exposures in various contexts and to various contaminants. The future health of a nation relies on protecting the children from adverse exposures and understanding the etiology of childhood diseases. The field of children's environmental exposures must consider improved and comprehensive research methods aimed at introducing mitigation strategies locally, nationally, and globally. We are happy to introduce a Special Issue focused on children's environmental exposure and children's health and hope that it contributes towards improved health of children.

Evaluation of environmental radiation exposure

International Nuclear Information System (INIS)

Imai, Kazuhiko

1974-01-01

The environmental radiation exposure due to radioactive rare gases is most important both at the time of reactor accidents and also in the long-term normal operation of reactor plants. The exposure dose is usually calculated by means of computers. The procedure of the calculation on environmental exposure dose is divided in several consecutive steps. The calculational formulae frequently used and those proposed recently are given with the explanation on released radionuclides, release to the atmosphere, concentration in the atmosphere, β-ray exposure, γ-ray exposure, and calculation of long-term exposure dose. (Mori, K.)

Effects of Prenatal Methylmercury Exposure: From Minamata Disease to Environmental Health Studies.

Science.gov (United States)

Sakamoto, Mineshi; Itai, Takaaki; Murata, Katsuyuki

2017-01-01

Methylmercury, the causative agent of Minamata disease, can easily penetrate the brain, and adult-type Minamata disease patients showed neurological symptoms according to the brain regions where the neurons, mainly in the cerebrum and cerebellum, were damaged. In addition, fetuses are exposed to methylmercury via the placenta from maternal fish consumption, and high-level exposure to methylmercury causes damage to the brains of infants. Typical patients with fetal-type Minamata disease (i.e., serious poisoning caused by in utero exposure to methylmercury) were born during the period of severe methylmercury pollution in 1955-1959, although they showed no abnormality during gestation nor at delivery. However, they showed difficulties in head control, sitting, and walking, and showed disturbances in mental development, these symptoms that are similar to those of cerebral palsy, during the growth periods after birth. The impaired development of fetal-type Minamata disease patients was one of the most tragic and characteristic feature of Minamata disease. In this review, we first summarize 1) the effects of prenatal methylmercury exposure in Minamata disease. Then, we introduce the studies that were conducted mainly by Sakamoto et al. as follows: 2) a retrospective study on temporal and regional variations of methylmercury pollution in Minamata area using preserved umbilical cord methylmercury, 3) decline in male sex ratio observed in Minamata area, 4) characteristics of hand tremor and postural sway in fetal-type Minamata disease patients, 5) methylmercury transfer from mothers to infants during gestation and lactation (the role of placenta), 6) extrapolation studies using rat models on the effects of prenatal methylmercury exposure on the human brain, and 7) risks and benefits of fish consumption.

Developmental origin of immune diseases-Environmental influences

DEFF Research Database (Denmark)

Strom, M.; Halldorsson, T. I.; Hansen, S.

2015-01-01

(PCBs), organochlorine pesticides, andmorerecently perfluoroalkyl substances (PFAS). Developmental exposures to PCBs have, for example, been associated with both otitis media and lower respiratory infections. Evidence regarding asthma and allergic disease is less well established, partly due to lack......Experimental studies have shown that developmental exposures to environmental chemicals may have long lasting adverse consequences for the development of the immune system. In humans such findings have mostly been explored for persistent organic pollutants (POPs) including polychlorinated biphenyls...... years of age we have examined the long term consequences of in utero exposure to POPs on offspring use of asthma medication and biomarkers of allergic airway disease. Using registry based information on offspring use of asthma medication until 20 years of age, prenatal exposures to PCB-118...

Environmental Issues in Thyroid Diseases.

Science.gov (United States)

Ferrari, Silvia Martina; Fallahi, Poupak; Antonelli, Alessandro; Benvenga, Salvatore

2017-01-01

Environmental factors are determinant for the appearance of autoimmune thyroid diseases (AITD) in susceptible subjects. Increased iodine intake, selenium, and vitamin D deficiency, exposure to radiation, from nuclear fallout or due to medical radiation, are environmental factors increasing AITD. Cigarette smoking is associated with Graves' disease and Graves' ophthalmopathy, while it decreases the risk of hypothyroidism and thyroid autoimmunity. Viral infections are important environmental factors in the pathogenesis of AITD, too, particularly human parvovirus B19 (EVB19) and hepatitis C virus. Among the many chemical contaminants, halogenated organochlorines and pesticides variably disrupt thyroid function. Polychlorinated biphenyls and their metabolites and polybrominated diethyl ethers bind to thyroid transport proteins, such as transthyretin, displace thyroxine, and disrupt thyroid function. Among drugs, interferon- and iodine-containing drugs have been associated with AITD. Moreover intestinal dysbiosis causes autoimmune thyroiditis. To reduce the risk to populations and also in each patient, it is necessary to comprehend the association between environmental agents and thyroid dysfunction.

Environmental monitoring of secondhand smoke exposure

Science.gov (United States)

Apelberg, Benjamin J; Hepp, Lisa M; Avila-Tang, Erika; Gundel, Lara; Hammond, S Katharine; Hovell, Melbourne F; Hyland, Andrew; Klepeis, Neil E; Madsen, Camille C; Navas-Acien, Ana; Repace, James; Samet, Jonathan M

2013-01-01

The complex composition of secondhand smoke (SHS) provides a range of constituents that can be measured in environmental samples (air, dust and on surfaces) and therefore used to assess non-smokers' exposure to tobacco smoke. Monitoring SHS exposure (SHSe) in indoor environments provides useful information on the extent and consequences of SHSe, implementing and evaluating tobacco control programmes and behavioural interventions, and estimating overall burden of disease caused by SHSe. The most widely used markers have been vapour-phase nicotine and respirable particulate matter (PM). Numerous other environmental analytes of SHS have been measured in the air including carbon monoxide, 3-ethenylpyridine, polycyclic aromatic hydrocarbons, tobacco-specific nitrosamines, nitrogen oxides, aldehydes and volatile organic compounds, as well as nicotine in dust and on surfaces. The measurement of nicotine in the air has the advantage of reflecting the presence of tobacco smoke. While PM measurements are not as specific, they can be taken continuously, allowing for assessment of exposure and its variation over time. In general, when nicotine and PM are measured in the same setting using a common sampling period, an increase in nicotine concentration of 1 μg/m3 corresponds to an average increase of 10 μg/m3 of PM. This topic assessment presents a comprehensive summary of SHSe monitoring approaches using environmental markers and discusses the strengths and weaknesses of these methods and approaches. PMID:22949497

Environmental chemical exposures and breast cancer

Directory of Open Access Journals (Sweden)

E. Stanley

2016-02-01

Full Text Available As a hormone-sensitive condition with no single identifiable cause, breast cancer is a major health problem. It is characterized by a wide range of contributing factors and exposures occurring in different combinations and strengths across a lifetime that may be amplified during periods of enhanced developmental susceptibility and impacted by reproductive patterns and behaviours. The vast majority of cases are oestrogen-receptor positive and occur in women with no family history of the disease suggesting that modifiable risk factors are involved. A substantial body of evidence now links oestrogen-positive breast cancer with environmental exposures. Synthetic chemicals capable of oestrogen mimicry are characteristic of industrial development and have been individually and extensively assessed as risk factors for oestrogen-sensitive cancers. Existing breast cancer risk assessment tools do not take such factors into account. In the absence of consensus on causation and in order to better understand the problem of escalating incidence globally, an expanded, integrated approach broadening the inquiry into individual susceptibility breast cancer is proposed. Applying systems thinking to existing data on oestrogen-modulating environmental exposures and other oestrogenic factors characteristic of Westernisation and their interactions in the exposure, encompassing social, behavioural, environmental, hormonal and genetic factors, can assist in understanding cancer risks and the pursuit of prevention strategies. A new conceptual framework based on a broader understanding of the “system” that underlies the development of breast cancer over a period of many years, incorporating the factors known to contribute to breast cancer risk, could provide a new platform from which government and regulators can promulgate enhanced and more effective prevention strategies.

Environmental source of arsenic exposure.

Science.gov (United States)

Chung, Jin-Yong; Yu, Seung-Do; Hong, Young-Seoub

2014-09-01

Arsenic is a ubiquitous, naturally occurring metalloid that may be a significant risk factor for cancer after exposure to contaminated drinking water, cigarettes, foods, industry, occupational environment, and air. Among the various routes of arsenic exposure, drinking water is the largest source of arsenic poisoning worldwide. Arsenic exposure from ingested foods usually comes from food crops grown in arsenic-contaminated soil and/or irrigated with arsenic-contaminated water. According to a recent World Health Organization report, arsenic from contaminated water can be quickly and easily absorbed and depending on its metabolic form, may adversely affect human health. Recently, the US Food and Drug Administration regulations for metals found in cosmetics to protect consumers against contaminations deemed deleterious to health; some cosmetics were found to contain a variety of chemicals including heavy metals, which are sometimes used as preservatives. Moreover, developing countries tend to have a growing number of industrial factories that unfortunately, harm the environment, especially in cities where industrial and vehicle emissions, as well as household activities, cause serious air pollution. Air is also an important source of arsenic exposure in areas with industrial activity. The presence of arsenic in airborne particulate matter is considered a risk for certain diseases. Taken together, various potential pathways of arsenic exposure seem to affect humans adversely, and future efforts to reduce arsenic exposure caused by environmental factors should be made.

Environmental Source of Arsenic Exposure

Directory of Open Access Journals (Sweden)

Jin-Yong Chung

2014-09-01

Full Text Available Arsenic is a ubiquitous, naturally occurring metalloid that may be a significant risk factor for cancer after exposure to contaminated drinking water, cigarettes, foods, industry, occupational environment, and air. Among the various routes of arsenic exposure, drinking water is the largest source of arsenic poisoning worldwide. Arsenic exposure from ingested foods usually comes from food crops grown in arsenic-contaminated soil and/or irrigated with arsenic-contaminated water. According to a recent World Health Organization report, arsenic from contaminated water can be quickly and easily absorbed and depending on its metabolic form, may adversely affect human health. Recently, the US Food and Drug Administration regulations for metals found in cosmetics to protect consumers against contaminations deemed deleterious to health; some cosmetics were found to contain a variety of chemicals including heavy metals, which are sometimes used as preservatives. Moreover, developing countries tend to have a growing number of industrial factories that unfortunately, harm the environment, especially in cities where industrial and vehicle emissions, as well as household activities, cause serious air pollution. Air is also an important source of arsenic exposure in areas with industrial activity. The presence of arsenic in airborne particulate matter is considered a risk for certain diseases. Taken together, various potential pathways of arsenic exposure seem to affect humans adversely, and future efforts to reduce arsenic exposure caused by environmental factors should be made.

Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease

OpenAIRE

Balmes John; Eisner Mark D; Katz Patricia P; Trupin Laura; Yelin Edward H; Blanc Paul D

2005-01-01

Abstract Background Exposure to environmental tobacco smoke (ETS), which contains potent respiratory irritants, may lead to chronic airway inflammation and obstruction. Although ETS exposure appears to cause asthma in children and adults, its role in causing COPD has received limited attention in epidemiologic studies. Methods Using data from a population-based sample of 2,113 U.S. adults aged 55 to 75 years, we examined the association between lifetime ETS exposure and the risk of developing...

Compensation for environmental asbestos-related diseases in South Africa: a neglected issue.

Science.gov (United States)

Ndlovu, Ntombizodwa; Naude, Jim teWater; Murray, Jill

2013-01-24

Environmentally acquired asbestos-related diseases (ARDs) are of concern globally. In South Africa, there is widespread contamination of the environment due to historical asbestos mining operations that were poorly regulated. Although the law makes provision for the compensation of occupationally acquired ARDs, compensation for environmentally acquired ARDs is only available through the Asbestos Relief Trust (ART) and Kgalagadi Relief Trust, both of which are administered by the ART. This study assessed ARDs and compensation outcomes of environmental claims submitted to the Trusts. The personal details, medical diagnoses, and exposure information of all environmental claims considered by the Trusts from their inception in 2003 to April 2010 were used to calculate the numbers and proportions of ARDs and compensation awards. There were 146 environmental claimants of whom 35 (23.9%) had fibrotic pleural disease, 1 (0.7%) had lung cancer, and 77 (52.7%) had malignant mesothelioma. 53 (36.3%) claimants were compensated: 20 with fibrotic pleural disease and 33 with mesothelioma. Of the 93 (63.7%) claimants who were not compensated, 33 had no ARDs, 18 had fibrotic pleural disease, 1 had lung cancer, and 44 had mesothelioma. In addition to having ARDs, those that were compensated had qualifying domestic (33; 62.2%) or neighbourhood (20; 37.8%) exposures to asbestos. Most of the claimants who were not compensated had ARDs but their exposures did not meet the Trusts' exposure criteria. This study demonstrates the environmental impact of asbestos mining on the burden of ARDs. Mesothelioma was the most common disease diagnosed, but most cases were not compensated. This highlights that there is little redress for individuals with environmentally acquired ARDs in South Africa. To stop this ARD epidemic, there is a need for the rehabilitation of abandoned asbestos mines and the environment. These issues may not be unique to South Africa as many countries continue to mine and use

Effect of environmental air pollution on cardiovascular diseases.

Science.gov (United States)

Meo, S A; Suraya, F

2015-12-01

Environmental air pollution has become a leading health concern especially in the developing countries with more urbanization, industrialization and rapidly growing population. Prolonged exposure to air pollution is a risk factor for cardiovascular diseases. The present study aimed to investigate the effects of environmental air pollution on progression of cardiovascular problems. In this study, we identified 6880 published articles through a systematic database including ISI-Web of Science, PubMed and EMBASE. The allied literature was searched by using the key words such as environmental pollution, air pollution, particulate matter pollutants PM 2.5 μm-PM 10 μm. Literature in which environmental air pollution and cardiac diseases were discussed was included. Descriptive information was retrieved from the selected literature. Finally, we included 67 publications and remaining studies were excluded. Environmental pollution can cause high blood pressure, arrhythmias, enhanced coagulation, thrombosis, acute arterial vasoconstriction, atherosclerosis, ischemic heart diseases, myocardial infarction and even heart failure. Environmental air pollution is associated with increased risk of cardiovascular diseases. Environmental pollution exerts its detrimental effects on the heart by developing pulmonary inflammation, systemic inflammation, oxidative stress, endothelial dysfunction and prothrombotic changes. Environmental protection officials must take high priority steps to minimize the air pollution to decrease the prevalence of cardiovascular diseases.

Children’s Exposure to Environmental Contaminants: An Editorial Reflection of Articles in the IJERPH Special Issue Entitled, “Children’s Exposure to Environmental Contaminants”

Directory of Open Access Journals (Sweden)

Alesia Ferguson

2016-11-01

Full Text Available Children are at increased vulnerability to many environmental contaminants compared to adults due to their unique behavior patterns, increased contaminant intake per body weight, and developing biological systems. Depending upon their age, young children may crawl on the floor and may practice increased hand to mouth activity that may increase their dose-intake of specific contaminants that accumulate in dust and other matrices. Children are also smaller in size than adults, resulting in a greater body burden for a given contaminant dose. Because children undergo rapid transitions through particular developmental stages they are also especially vulnerable during certain growth-related time windows. A Special Issue was organized focused on the latest findings in the field of children’s environmental exposure for these reasons. This editorial introduces articles in this Special Issue and emphasizes their main findings in advancing the field. From the many articles submitted to this Special Issue from around the world, 23 were accepted and published. They focus on a variety of research areas such as children’s activity patterns, improved risk assessment methods to estimate exposures, and exposures in various contexts and to various contaminants. The future health of a nation relies on protecting the children from adverse exposures and understanding the etiology of childhood diseases. The field of children’s environmental exposures must consider improved and comprehensive research methods aimed at introducing mitigation strategies locally, nationally, and globally. We are happy to introduce a Special Issue focused on children’s environmental exposure and children’s health and hope that it contributes towards improved health of children.

Occupational and environmental exposures and cancers in developing countries.

Science.gov (United States)

Hashim, Dana; Boffetta, Paolo

2014-01-01

Over the past few decades, there has been a decline in cancers attributable to environmental and occupational carcinogens of asbestos, arsenic, and indoor and outdoor air pollution in high-income countries. For low- to middle-income countries (LMICs), however, these exposures are likely to increase as industrialization expands and populations grow. The aim of this study was to review the evidence on the cancer risks and burdens of selected environmental and occupational exposures in less-developed economies. A causal association has been established between asbestos exposure and mesothelioma and lung cancer. For arsenic exposure, there is strong evidence of bladder, skin, lung, liver, and kidney cancer effects. Women are at the highest risk for lung cancer due to indoor air pollution exposure; however, the carcinogenic effect on the risk for cancer in children has not been studied in these countries. Cancer risks associated with ambient air pollution remain the least studied in LMICs, although reported exposures are higher than World Health Organization, European, and US standards. Although some associations between lung cancer and ambient air pollutants have been reported, studies in LMICs are weak or subject to exposure misclassification. For pulmonary cancers, tobacco smoking and respiratory diseases have a positive synergistic effect on cancer risks. A precise quantification of the burden of human cancer attributable to environmental and occupational exposures in LMICs is uncertain. Although the prevalence of carcinogenic exposures has been reported to be high in many such countries, the effects of the exposures have not been studied due to varying country-specific limitations, some of which include lack of resources and government support. Copyright © 2014 Icahn School of Medicine at Mount Sinai. Published by Elsevier Inc. All rights reserved.

Challenges to studying the health effects of early life environmental chemical exposures on children's health.

Science.gov (United States)

Braun, Joseph M; Gray, Kimberly

2017-12-01

Epidemiological studies play an important role in quantifying how early life environmental chemical exposures influence the risk of childhood diseases. These studies face at least four major challenges that can produce noise when trying to identify signals of associations between chemical exposure and childhood health. Challenges include accurately estimating chemical exposure, confounding from causes of both exposure and disease, identifying periods of heightened vulnerability to chemical exposures, and determining the effects of chemical mixtures. We provide recommendations that will aid in identifying these signals with more precision.

Risk assessment for heart disease and workplace ETS exposure among nonsmokers.

OpenAIRE

Steenland, K

1999-01-01

In 1994 the U.S. Occupational Health and Safety Administration (OSHA) published a study of risk assessment for heart disease and lung cancer resulting from workplace exposure to environmental tobacco smoke (ETS) among nonsmokers. This assessment is currently being revised. The present article considers different possible approaches to a risk assessment for heart disease among nonsmokers resulting from workplace ETS exposure, reviews the approach taken by OSHA in 1994, and suggests some modifi...

Environmental exposure assessment in European birth cohorts

DEFF Research Database (Denmark)

Gehring, Ulrike; Casas, Maribel; Brunekreef, Bert

2013-01-01

of the environmental exposure and health data in these studies was made as part of the ENRIECO (Environmental Health Risks in European Birth Cohorts) project. The focus with regard to exposure was on outdoor air pollution, water contamination, allergens and biological organisms, metals, pesticides, smoking and second...... hand tobacco smoke (SHS), persistent organic pollutants (POPs), noise, radiation, and occupational exposures. The review lists methods and data on environmental exposures in 37 European birth cohort studies. Most data is currently available for smoking and SHS (N=37 cohorts), occupational exposures (N......Environmental exposures during pregnancy and early life may have adverse health effects. Single birth cohort studies often lack statistical power to tease out such effects reliably. To improve the use of existing data and to facilitate collaboration among these studies, an inventory...

Mercury Exposure and Heart Diseases

Science.gov (United States)

Genchi, Giuseppe; Sinicropi, Maria Stefania; Carocci, Alessia; Lauria, Graziantonio; Catalano, Alessia

2017-01-01

Environmental contamination has exposed humans to various metal agents, including mercury. It has been determined that mercury is not only harmful to the health of vulnerable populations such as pregnant women and children, but is also toxic to ordinary adults in various ways. For many years, mercury was used in a wide variety of human activities. Nowadays, the exposure to this metal from both natural and artificial sources is significantly increasing. Recent studies suggest that chronic exposure, even to low concentration levels of mercury, can cause cardiovascular, reproductive, and developmental toxicity, neurotoxicity, nephrotoxicity, immunotoxicity, and carcinogenicity. Possible biological effects of mercury, including the relationship between mercury toxicity and diseases of the cardiovascular system, such as hypertension, coronary heart disease, and myocardial infarction, are being studied. As heart rhythm and function are under autonomic nervous system control, it has been hypothesized that the neurotoxic effects of mercury might also impact cardiac autonomic function. Mercury exposure could have a long-lasting effect on cardiac parasympathetic activity and some evidence has shown that mercury exposure might affect heart rate variability, particularly early exposures in children. The mechanism by which mercury produces toxic effects on the cardiovascular system is not fully elucidated, but this mechanism is believed to involve an increase in oxidative stress. The exposure to mercury increases the production of free radicals, potentially because of the role of mercury in the Fenton reaction and a reduction in the activity of antioxidant enzymes, such as glutathione peroxidase. In this review we report an overview on the toxicity of mercury and focus our attention on the toxic effects on the cardiovascular system. PMID:28085104

Mercury Exposure and Heart Diseases.

Science.gov (United States)

Genchi, Giuseppe; Sinicropi, Maria Stefania; Carocci, Alessia; Lauria, Graziantonio; Catalano, Alessia

2017-01-12

Environmental contamination has exposed humans to various metal agents, including mercury. It has been determined that mercury is not only harmful to the health of vulnerable populations such as pregnant women and children, but is also toxic to ordinary adults in various ways. For many years, mercury was used in a wide variety of human activities. Nowadays, the exposure to this metal from both natural and artificial sources is significantly increasing. Recent studies suggest that chronic exposure, even to low concentration levels of mercury, can cause cardiovascular, reproductive, and developmental toxicity, neurotoxicity, nephrotoxicity, immunotoxicity, and carcinogenicity. Possible biological effects of mercury, including the relationship between mercury toxicity and diseases of the cardiovascular system, such as hypertension, coronary heart disease, and myocardial infarction, are being studied. As heart rhythm and function are under autonomic nervous system control, it has been hypothesized that the neurotoxic effects of mercury might also impact cardiac autonomic function. Mercury exposure could have a long-lasting effect on cardiac parasympathetic activity and some evidence has shown that mercury exposure might affect heart rate variability, particularly early exposures in children. The mechanism by which mercury produces toxic effects on the cardiovascular system is not fully elucidated, but this mechanism is believed to involve an increase in oxidative stress. The exposure to mercury increases the production of free radicals, potentially because of the role of mercury in the Fenton reaction and a reduction in the activity of antioxidant enzymes, such as glutathione peroxidase. In this review we report an overview on the toxicity of mercury and focus our attention on the toxic effects on the cardiovascular system.

Mercury Exposure and Heart Diseases

Directory of Open Access Journals (Sweden)

Giuseppe Genchi

2017-01-01

Full Text Available Environmental contamination has exposed humans to various metal agents, including mercury. It has been determined that mercury is not only harmful to the health of vulnerable populations such as pregnant women and children, but is also toxic to ordinary adults in various ways. For many years, mercury was used in a wide variety of human activities. Nowadays, the exposure to this metal from both natural and artificial sources is significantly increasing. Recent studies suggest that chronic exposure, even to low concentration levels of mercury, can cause cardiovascular, reproductive, and developmental toxicity, neurotoxicity, nephrotoxicity, immunotoxicity, and carcinogenicity. Possible biological effects of mercury, including the relationship between mercury toxicity and diseases of the cardiovascular system, such as hypertension, coronary heart disease, and myocardial infarction, are being studied. As heart rhythm and function are under autonomic nervous system control, it has been hypothesized that the neurotoxic effects of mercury might also impact cardiac autonomic function. Mercury exposure could have a long-lasting effect on cardiac parasympathetic activity and some evidence has shown that mercury exposure might affect heart rate variability, particularly early exposures in children. The mechanism by which mercury produces toxic effects on the cardiovascular system is not fully elucidated, but this mechanism is believed to involve an increase in oxidative stress. The exposure to mercury increases the production of free radicals, potentially because of the role of mercury in the Fenton reaction and a reduction in the activity of antioxidant enzymes, such as glutathione peroxidase. In this review we report an overview on the toxicity of mercury and focus our attention on the toxic effects on the cardiovascular system.

Compensation for environmental asbestos-related diseases in South Africa: a neglected issue

Directory of Open Access Journals (Sweden)

Ntombizodwa Ndlovu

2013-01-01

Full Text Available Background: Environmentally acquired asbestos-related diseases (ARDs are of concern globally. In South Africa, there is widespread contamination of the environment due to historical asbestos mining operations that were poorly regulated. Although the law makes provision for the compensation of occupationally acquired ARDs, compensation for environmentally acquired ARDs is only available through the Asbestos Relief Trust (ART and Kgalagadi Relief Trust, both of which are administered by the ART. This study assessed ARDs and compensation outcomes of environmental claims submitted to the Trusts. Methods: The personal details, medical diagnoses, and exposure information of all environmental claims considered by the Trusts from their inception in 2003 to April 2010 were used to calculate the numbers and proportions of ARDs and compensation awards. Results: There were 146 environmental claimants of whom 35 (23.9% had fibrotic pleural disease, 1 (0.7% had lung cancer, and 77 (52.7% had malignant mesothelioma. 53 (36.3% claimants were compensated: 20 with fibrotic pleural disease and 33 with mesothelioma. Of the 93 (63.7% claimants who were not compensated, 33 had no ARDs, 18 had fibrotic pleural disease, 1 had lung cancer, and 44 had mesothelioma. In addition to having ARDs, those that were compensated had qualifying domestic (33; 62.2% or neighbourhood (20; 37.8% exposures to asbestos. Most of the claimants who were not compensated had ARDs but their exposures did not meet the Trusts’ exposure criteria. Conclusions: This study demonstrates the environmental impact of asbestos mining on the burden of ARDs. Mesothelioma was the most common disease diagnosed, but most cases were not compensated. This highlights that there is little redress for individuals with environmentally acquired ARDs in South Africa. To stop this ARD epidemic, there is a need for the rehabilitation of abandoned asbestos mines and the environment. These issues may not be unique to

Harnessing genomics to identify environmental determinants of heritable disease

Science.gov (United States)

Yauk, Carole Lyn; Argueso, J. Lucas; Auerbach, Scott S.; Awadalla, Philip; Davis, Sean R.; DeMarini, David M.; Douglas, George R.; Dubrova, Yuri E.; Elespuru, Rosalie K.; Glover, Thomas W.; Hales, Barbara F.; Hurles, Matthew E.; Klein, Catherine B.; Lupski, James R.; Manchester, David K.; Marchetti, Francesco; Montpetit, Alexandre; Mulvihill, John J.; Robaire, Bernard; Robbins, Wendie A.; Rouleau, Guy A.; Shaughnessy, Daniel T.; Somers, Christopher M.; Taylor, James G.; Trasler, Jacquetta; Waters, Michael D.; Wilson, Thomas E.; Witt, Kristine L.; Bishop, Jack B.

2012-01-01

Next-generation sequencing technologies can now be used to directly measure heritable de novo DNA sequence mutations in humans. However, these techniques have not been used to examine environmental factors that induce such mutations and their associated diseases. To address this issue, a working group on environmentally induced germline mutation analysis (ENIGMA) met in October 2011 to propose the necessary foundational studies, which include sequencing of parent–offspring trios from highly exposed human populations, and controlled dose–response experiments in animals. These studies will establish background levels of variability in germline mutation rates and identify environmental agents that influence these rates and heritable disease. Guidance for the types of exposures to examine come from rodent studies that have identified agents such as cancer chemotherapeutic drugs, ionizing radiation, cigarette smoke, and air pollution as germ-cell mutagens. Research is urgently needed to establish the health consequences of parental exposures on subsequent generations. PMID:22935230

Health assessment of environmental pollutants: proliferative and degenerative diseases

International Nuclear Information System (INIS)

Stuart, B.O.

1988-01-01

In order to achieve a balanced approach to risk assessment between carcinogenic and non-carcinogenic health effects one must examine the risk of disease or death in the general population exposed to a particular air pollutant that can be related quantitatively to intensity and duration of exposures (National Academy of Sciences, 1983). Such risk assessment should be based upon careful evaluation of scientific findings of dose-response relationships in the chronically exposed population. Quantitative assessment of environmentally produced disease in man has proven to be complex and demanding. A variety of factors play important roles in this task. As an example, there are induction-latency periods for chronic diseases, including cancer, which may range from five to twenty-five years. The diseases themselves, whether proliferative or degenerative, may follow several stages of progression. There is only sparse epidemiological data on serious health effects that may be due to environmental as compared to occupational exposures. Exposures to chemical or radiological air contaminants do not occur singly but to a multiplicity of agents, and disease processes are frequently markedly affected by the interaction of a variety of factors, particularly that of cigarette smoking. There is growing recognition of potentially sensitive subpopulations, including the elderly and the very young, but adequate techniques for assessing the magnitude of increased risks to these groups have not yet been developed

Influences of large sets of environmental exposures on immune responses in healthy adult men.

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Yi, Buqing; Rykova, Marina; Jäger, Gundula; Feuerecker, Matthias; Hörl, Marion; Matzel, Sandra; Ponomarev, Sergey; Vassilieva, Galina; Nichiporuk, Igor; Choukèr, Alexander

2015-08-26

Environmental factors have long been known to influence immune responses. In particular, clinical studies about the association between migration and increased risk of atopy/asthma have provided important information on the role of migration associated large sets of environmental exposures in the development of allergic diseases. However, investigations about environmental effects on immune responses are mostly limited in candidate environmental exposures, such as air pollution. The influences of large sets of environmental exposures on immune responses are still largely unknown. A simulated 520-d Mars mission provided an opportunity to investigate this topic. Six healthy males lived in a closed habitat simulating a spacecraft for 520 days. When they exited their "spacecraft" after the mission, the scenario was similar to that of migration, involving exposure to a new set of environmental pollutants and allergens. We measured multiple immune parameters with blood samples at chosen time points after the mission. At the early adaptation stage, highly enhanced cytokine responses were observed upon ex vivo antigen stimulations. For cell population frequencies, we found the subjects displayed increased neutrophils. These results may presumably represent the immune changes occurred in healthy humans when migrating, indicating that large sets of environmental exposures may trigger aberrant immune activity.

Environmental exposure to benzene: an update.

OpenAIRE

Wallace, L

1996-01-01

During the 1990s, several large-scale studies of benzene concentrations in air, food, and blood have added to our knowledge of its environmental occurrence. In general, the new studies have confirmed the earlier findings of the U.S. Environmental Protection Agency Total Exposure Assessment Methodology (TEAM) studies and other large-scale studies in Germany and the Netherlands concerning the levels of exposure and major sources. For example, the new studies found that personal exposures exceed...

Geocoding accuracy and the recovery of relationships between environmental exposures and health

Directory of Open Access Journals (Sweden)

Zimmerman Dale L

2008-04-01

Full Text Available Abstract Background This research develops methods for determining the effect of geocoding quality on relationships between environmental exposures and health. The likelihood of detecting an existing relationship – statistical power – between measures of environmental exposures and health depends not only on the strength of the relationship but also on the level of positional accuracy and completeness of the geocodes from which the measures of environmental exposure are made. This paper summarizes the results of simulation studies conducted to examine the impact of inaccuracies of geocoded addresses generated by three types of geocoding processes: a addresses located on orthophoto maps, b addresses matched to TIGER files (U.S Census or their derivative street files; and, c addresses from E-911 geocodes (developed by local authorities for emergency dispatch purposes. Results The simulated odds of disease using exposures modelled from the highest quality geocodes could be sufficiently recovered using other, more commonly used, geocoding processes such as TIGER and E-911; however, the strength of the odds relationship between disease exposures modelled at geocodes generally declined with decreasing geocoding accuracy. Conclusion Although these specific results cannot be generalized to new situations, the methods used to determine the sensitivity of results can be used in new situations. Estimated measures of positional accuracy must be used in the interpretation of results of analyses that investigate relationships between health outcomes and exposures measured at residential locations. Analyses similar to those employed in this paper can be used to validate interpretation of results from empirical analyses that use geocoded locations with estimated measures of positional accuracy.

Lipid and Creatinine Adjustment to Evaluate Health Effects of Environmental Exposures.

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O'Brien, Katie M; Upson, Kristen; Buckley, Jessie P

2017-03-01

Urine- and serum-based biomarkers are useful for assessing individuals' exposure to environmental factors. However, variations in urinary creatinine (a measure of dilution) or serum lipid levels, if not adequately corrected for, can directly impact biomarker concentrations and bias exposure-disease association measures. Recent methodological literature has considered the complex relationships between creatinine or serum lipid levels, exposure biomarkers, outcomes, and other potentially relevant factors using directed acyclic graphs and simulation studies. The optimal measures of urinary dilution and serum lipids have also been investigated. Existing evidence supports the use of covariate-adjusted standardization plus creatinine adjustment for urinary biomarkers and standardization plus serum lipid adjustment for lipophilic, serum-based biomarkers. It is unclear which urinary dilution measure is best, but all serum lipid measures performed similarly. Future research should assess methods for pooled biomarkers and for studying diseases and exposures that affect creatinine or serum lipids directly.

Chronic Kidney Disease and Exposure to Nephrotoxic Metals

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Orr, Sarah E.; Bridges, Christy C.

2017-01-01

Chronic kidney disease (CKD) is a common progressive disease that is typically characterized by the permanent loss of functional nephrons. As injured nephrons become sclerotic and die, the remaining healthy nephrons undergo numerous structural, molecular, and functional changes in an attempt to compensate for the loss of diseased nephrons. These compensatory changes enable the kidney to maintain fluid and solute homeostasis until approximately 75% of nephrons are lost. As CKD continues to progress, glomerular filtration rate decreases, and remaining nephrons are unable to effectively eliminate metabolic wastes and environmental toxicants from the body. This inability may enhance mortality and/or morbidity of an individual. Environmental toxicants of particular concern are arsenic, cadmium, lead, and mercury. Since these metals are present throughout the environment and exposure to one or more of these metals is unavoidable, it is important that the way in which these metals are handled by target organs in normal and disease states is understood completely. PMID:28498320

Children?s Health in Latin America: The Influence of Environmental Exposures

OpenAIRE

Laborde, Amalia; Tomasina, Fernando; Bianchi, Fabrizio; Brun?, Marie-Noel; Buka, Irena; Comba, Pietro; Corra, Lilian; Cori, Liliana; Duffert, Christin Maria; Harari, Raul; Iavarone, Ivano; McDiarmid, Melissa A.; Gray, Kimberly A.; Sly, Peter D.; Soares, Agnes

2014-01-01

Background Chronic diseases are increasing among children in Latin America. Objective and Methods To examine environmental risk factors for chronic disease in Latin American children and to develop a strategic initiative for control of these exposures, the World Health Organization (WHO) including the Pan American Health Organization (PAHO), the Collegium Ramazzini, and Latin American scientists reviewed regional and relevant global data. Results Industrial development and urbanization are pr...

Exposure to environmental tobacco smoke and sensitisation in children.

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Lannerö, E; Wickman, M; van Hage, M; Bergström, A; Pershagen, G; Nordvall, L

2008-02-01

Exposure to environmental tobacco smoke (ETS) increases the risk of respiratory illness in children but data are inconclusive regarding the risk of IgE sensitisation. To elucidate whether exposure to smoking prenatally and/or postnatally is related to IgE sensitisation in children at 4 years of age. As part of a prospective birth cohort study (BAMSE), a total of 4089 families with children answered questionnaires when the child was 2 months, 1, 2 and 4 years old on environmental factors and symptoms of allergic disease. Blood collected at age 4 years from 2614 children was analysed for IgE antibodies to common inhalant and food allergens. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using logistic regression with adjustments for potential confounders. There was no evident association between maternal smoking during pregnancy and risk of IgE sensitisation. In contrast, a dose-response effect was found for exposure to ETS from parental smoking during the first few months of life and IgE sensitisation. There was an increased risk of sensitisation to inhalant and/or food allergens (OR(adj) 1.28 (95% CI 1.01 to 1.62)) among children exposed to ETS at 2 months of age. The risk appeared particularly elevated for indoor inhalant allergens, such as cat (OR(adj) 1.96 (95% CI 1.28 to 2.99)) and for food allergens (OR(adj) 1.46 (95% CI 1.11 to 1.93)). The IgE sensitising effect of ETS seemed to be confined to infants of parents without allergic diseases and to ETS exposure during early infancy. Our data indicate that exposure in early infancy to ETS increases the risk of IgE sensitisation to indoor inhalant and food allergens.

A global perspective on the influence of environmental exposures on the nervous system

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Tshala-Katumbay, Desire; Mwanza, Jean-Claude; Rohlman, Diane S.; Maestre, Gladys; Oriá, Reinaldo B.

2016-01-01

Economic and social transitions in the era of globalization warrant a fresh look at the neurological risks associated with environmental change. These are driven by industrial expansion, transfer and mobility of goods, climate change and population growth. In these contexts, risk of both infectious and non-infectious diseases are shared across geographical boundaries. In low- and middle-income countries, the risk of environmentally mediated brain disease is augmented several-fold by lack of infrastructure, poor health and safety regulations, and limited measures for environmental protection. Neurological disorders may occur as a result of direct exposure to chemical and/or non-chemical stressors such as ultrafine particulate matters. Individual susceptibilities to exposure-related diseases are modified by genetic, epigenetic and metagenomic factors. The existence of several uniquely exposed populations, including those in the areas surrounding the Niger Delta or north western Amazon oil operations; those working in poorly regulated environments, such as artisanal mining industries; or those, mostly in sub-Saharan Africa, relying on cassava as a staple food, offers invaluable opportunities to advance the current understanding of brain responses to environmental challenges. Increased awareness of the brain disorders that are prevalent in low- and middle-income countries and investments in capacity for further environmental health-related research are positive steps towards improving human health. PMID:26580326

Using environmental forensic microscopy in exposure science.

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Millette, James R; Brown, Richard S; Hill, Whitney B

2008-01-01

Environmental forensic microscopy investigations are based on the methods and procedures developed in the fields of criminal forensics, industrial hygiene and environmental monitoring. Using a variety of microscopes and techniques, the environmental forensic scientist attempts to reconstruct the sources and the extent of exposure based on the physical evidence left behind after particles are exchanged between an individual and the environments he or she passes through. This article describes how environmental forensic microscopy uses procedures developed for environmental monitoring, criminal forensics and industrial hygiene investigations. It provides key references to the interdisciplinary approach used in microscopic investigations. Case studies dealing with lead, asbestos, glass fibers and other particulate contaminants are used to illustrate how environmental forensic microscopy can be very useful in the initial stages of a variety of environmental exposure characterization efforts to eliminate some agents of concern and to narrow the field of possible sources of exposure.

Environmental and occupational exposures in immigrant health.

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Eamranond, Pracha P; Hu, Howard

2008-09-23

Immigrants comprise vulnerable populations that are frequently exposed to a multitude of environmental and occupational hazards. The historical context behind state and federal legislation has helped to foster an environment that is particularly hostile toward caring for immigrant health. Current hazards include toxic exposures, air and noise pollution, motor vehicle accidents, crowded living and work environments with inadequate ventilation, poor sanitation, mechanical injury, among many others. Immigrants lack the appropriate training, materials, health care access, and other resources to reduce their exposure to preventable environmental and occupational health risks. This dilemma is exacerbated by current anti-immigrant sentiments, miscommunication between native and immigrant populations, and legislation denying immigrants access to publicly funded medical care. Given that current health policy has failed to address immigrant health appropriately and political impetus is lacking, efforts should also focus on alternative solutions, including organized labor. Labor unions that serve to educate workers, survey work environments, and defend worker rights will greatly alleviate and prevent the burden of disease incurred by immigrants. The nation's health will benefit from improved regulation of living and workplace environments to improve the health of immigrants, regardless of legal status.

Environmental and Occupational Exposures in Immigrant Health

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Pracha P. Eamranond

2008-01-01

Full Text Available Immigrants comprise vulnerable populations that are frequently exposed to a multitude of environmental and occupational hazards. The historical context behind state and federal legislation has helped to foster an environment that is particularly hostile toward caring for immigrant health. Current hazards include toxic exposures, air and noise pollution, motor vehicle accidents, crowded living and work environments with inadequate ventilation, poor sanitation, mechanical injury, among many others. Immigrants lack the appropriate training, materials, health care access, and other resources to reduce their exposure to preventable environmental and occupational health risks. This dilemma is exacerbated by current anti-immigrant sentiments, miscommunication between native and immigrant populations, and legislation denying immigrants access to publicly funded medical care. Given that current health policy has failed to address immigrant health appropriately and political impetus is lacking, efforts should also focus on alternative solutions, including organized labor. Labor unions that serve to educate workers, survey work environments, and defend worker rights will greatly alleviate and prevent the burden of disease incurred by immigrants. The nation’s health will benefit from improved regulation of living and workplace environments to improve the health of immigrants, regardless of legal status.

Biological markers in animals can provide information on exposure and bioavailability of environmental contaminants

International Nuclear Information System (INIS)

Shugart, L.R.; Adams, S.M.; Jimenez, B.D.; Talmage, S.S.; McCarthy, J.F.

1987-01-01

Epidemiologic studies of agents present in the environment seek to identify the extent to which they contribute to the causation of a specific toxic, clinical, or pathological endpoint. The multifactorial nature of disease etiology, long latency periods and the complexity of exposure, all contribute to the difficulty of establishing associations and casual relationships between a specific exposure and an adverse outcome. These barriers to studies of exposures and subsequent risk assessment cannot generally be changed. However, the appropriate use of biological markers in animal species living in a contaminated habitat can provide a measure of potential damage from that exposure and, in some instances, act as a surrogate for human environmental exposures. Quantitative predictivity of the effect of exposure to environmental pollutants is being approached by employing an appropriate array of biological end points. 34 refs., 1 fig., 6 tabs

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.

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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.

Disease and Health Inequalities Attributable to Air Pollutant Exposure in Detroit, Michigan

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Sheena E. Martenies

2017-10-01

Full Text Available The environmental burden of disease is the mortality and morbidity attributable to exposures of air pollution and other stressors. The inequality metrics used in cumulative impact and environmental justice studies can be incorporated into environmental burden studies to better understand the health disparities of ambient air pollutant exposures. This study examines the diseases and health disparities attributable to air pollutants for the Detroit urban area. We apportion this burden to various groups of emission sources and pollutants, and show how the burden is distributed among demographic and socioeconomic subgroups. The analysis uses spatially-resolved estimates of exposures, baseline health rates, age-stratified populations, and demographic characteristics that serve as proxies for increased vulnerability, e.g., race/ethnicity and income. Based on current levels, exposures to fine particulate matter (PM2.5, ozone (O3, sulfur dioxide (SO2, and nitrogen dioxide (NO2 are responsible for more than 10,000 disability-adjusted life years (DALYs per year, causing an annual monetized health impact of $6.5 billion. This burden is mainly driven by PM2.5 and O3 exposures, which cause 660 premature deaths each year among the 945,000 individuals in the study area. NO2 exposures, largely from traffic, are important for respiratory outcomes among older adults and children with asthma, e.g., 46% of air-pollution related asthma hospitalizations are due to NO2 exposures. Based on quantitative inequality metrics, the greatest inequality of health burdens results from industrial and traffic emissions. These metrics also show disproportionate burdens among Hispanic/Latino populations due to industrial emissions, and among low income populations due to traffic emissions. Attributable health burdens are a function of exposures, susceptibility and vulnerability (e.g., baseline incidence rates, and population density. Because of these dependencies, inequality

Life-Long Implications of Developmental Exposure to Environmental Stressors: New Perspectives.

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Grandjean, Philippe; Barouki, Robert; Bellinger, David C; Casteleyn, Ludwine; Chadwick, Lisa H; Cordier, Sylvaine; Etzel, Ruth A; Gray, Kimberly A; Ha, Eun-Hee; Junien, Claudine; Karagas, Margaret; Kawamoto, Toshihiro; Paige Lawrence, B; Perera, Frederica P; Prins, Gail S; Puga, Alvaro; Rosenfeld, Cheryl S; Sherr, David H; Sly, Peter D; Suk, William; Sun, Qi; Toppari, Jorma; van den Hazel, Peter; Walker, Cheryl L; Heindel, Jerrold J

2015-10-01

The Developmental Origins of Health and Disease (DOHaD) paradigm is one of the most rapidly expanding areas of biomedical research. Environmental stressors that can impact on DOHaD encompass a variety of environmental and occupational hazards as well as deficiency and oversupply of nutrients and energy. They can disrupt early developmental processes and lead to increased susceptibility to disease/dysfunctions later in life. Presentations at the fourth Conference on Prenatal Programming and Toxicity in Boston, in October 2014, provided important insights and led to new recommendations for research and public health action. The conference highlighted vulnerable exposure windows that can occur as early as the preconception period and epigenetics as a major mechanism than can lead to disadvantageous "reprogramming" of the genome, thereby potentially resulting in transgenerational effects. Stem cells can also be targets of environmental stressors, thus paving another way for effects that may last a lifetime. Current testing paradigms do not allow proper characterization of risk factors and their interactions. Thus, relevant exposure levels and combinations for testing must be identified from human exposure situations and outcome assessments. Testing of potential underpinning mechanisms and biomarker development require laboratory animal models and in vitro approaches. Only few large-scale birth cohorts exist, and collaboration between birth cohorts on a global scale should be facilitated. DOHaD-based research has a crucial role in establishing factors leading to detrimental outcomes and developing early preventative/remediation strategies to combat these risks.

Time series models of environmental exposures: Good predictions or good understanding.

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Barnett, Adrian G; Stephen, Dimity; Huang, Cunrui; Wolkewitz, Martin

2017-04-01

Time series data are popular in environmental epidemiology as they make use of the natural experiment of how changes in exposure over time might impact on disease. Many published time series papers have used parameter-heavy models that fully explained the second order patterns in disease to give residuals that have no short-term autocorrelation or seasonality. This is often achieved by including predictors of past disease counts (autoregression) or seasonal splines with many degrees of freedom. These approaches give great residuals, but add little to our understanding of cause and effect. We argue that modelling approaches should rely more on good epidemiology and less on statistical tests. This includes thinking about causal pathways, making potential confounders explicit, fitting a limited number of models, and not over-fitting at the cost of under-estimating the true association between exposure and disease. Copyright © 2017 Elsevier Inc. All rights reserved.

Can exposure to environmental chemicals increase the risk of diabetes type 1 development?

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Bodin, Johanna; Stene, Lars Christian; Nygaard, Unni Cecilie

2015-01-01

Type 1 diabetes mellitus (T1DM) is an autoimmune disease, where destruction of beta-cells causes insulin deficiency. The incidence of T1DM has increased in the last decades and cannot entirely be explained by genetic predisposition. Several environmental factors are suggested to promote T1DM, like early childhood enteroviral infections and nutritional factors, but the evidence is inconclusive. Prenatal and early life exposure to environmental pollutants like phthalates, bisphenol A, perfluorinated compounds, PCBs, dioxins, toxicants, and air pollutants can have negative effects on the developing immune system, resulting in asthma-like symptoms and increased susceptibility to childhood infections. In this review the associations between environmental chemical exposure and T1DM development is summarized. Although information on environmental chemicals as possible triggers for T1DM is sparse, we conclude that it is plausible that environmental chemicals can contribute to T1DM development via impaired pancreatic beta-cell and immune-cell functions and immunomodulation. Several environmental factors and chemicals could act together to trigger T1DM development in genetically susceptible individuals, possibly via hormonal or epigenetic alterations. Further observational T1DM cohort studies and animal exposure experiments are encouraged.

Can Exposure to Environmental Chemicals Increase the Risk of Diabetes Type 1 Development?

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Johanna Bodin

2015-01-01

Full Text Available Type 1 diabetes mellitus (T1DM is an autoimmune disease, where destruction of beta-cells causes insulin deficiency. The incidence of T1DM has increased in the last decades and cannot entirely be explained by genetic predisposition. Several environmental factors are suggested to promote T1DM, like early childhood enteroviral infections and nutritional factors, but the evidence is inconclusive. Prenatal and early life exposure to environmental pollutants like phthalates, bisphenol A, perfluorinated compounds, PCBs, dioxins, toxicants, and air pollutants can have negative effects on the developing immune system, resulting in asthma-like symptoms and increased susceptibility to childhood infections. In this review the associations between environmental chemical exposure and T1DM development is summarized. Although information on environmental chemicals as possible triggers for T1DM is sparse, we conclude that it is plausible that environmental chemicals can contribute to T1DM development via impaired pancreatic beta-cell and immune-cell functions and immunomodulation. Several environmental factors and chemicals could act together to trigger T1DM development in genetically susceptible individuals, possibly via hormonal or epigenetic alterations. Further observational T1DM cohort studies and animal exposure experiments are encouraged.

OBGYN screening for environmental exposures: A call for action

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Allshouse, A. A.; Jungheim, E.; Powell, T. L.; Jansson, T.; Polotsky, A. J.

2018-01-01

Background Prenatal exposures have known adverse effects on maternal and neonatal outcomes. Professional societies recommend routine screening for environmental, occupational, and dietary exposures to reduce exposures and their associated sequelae. Objective Our objective was to determine the frequency of environmental exposure screening by obstetricians and gynecologists (OBGYNs) at initial patient visits. Study design Practicing OBGYNs were approached at the University of Colorado and by social media. The survey instrument queried demographics, environmental literacy, and screening practices. Statistical analysis was performed using Chi-square and two-sample t-test. Results We received 312 online survey responses (response rate of 12%). Responding OBGYNs were predominantly female (96%), board-certified (78%), generalists (65%) with a mean age of 37.1 years. Fewer than half of physicians screened for the following factors: occupational exposures, environmental chemicals, air pollution, pesticide use, personal care products, household cleaners, water source, use of plastics for food storage, and lead and mercury exposure. Eighty five percent of respondents reported that they did not feel comfortable obtaining an environmental history and 58% respondents reported that they performed no regular screening of environmental exposures. A higher frequency of screening was associated with > 4 years of practice (p = 0.001), and having read the environmental committee opinion (p = <0.001). Conclusion The majority of OBGYNs did not incorporate screening for known environmental exposures into routine practice. Reading the environmental committee opinions was strongly and significantly associated with a higher rate of screening. Improving physician comfort in counseling patients may enhance screening for exposures that affect reproductive health. PMID:29768418

OBGYN screening for environmental exposures: A call for action.

Science.gov (United States)

Grindler, N M; Allshouse, A A; Jungheim, E; Powell, T L; Jansson, T; Polotsky, A J

2018-01-01

Prenatal exposures have known adverse effects on maternal and neonatal outcomes. Professional societies recommend routine screening for environmental, occupational, and dietary exposures to reduce exposures and their associated sequelae. Our objective was to determine the frequency of environmental exposure screening by obstetricians and gynecologists (OBGYNs) at initial patient visits. Practicing OBGYNs were approached at the University of Colorado and by social media. The survey instrument queried demographics, environmental literacy, and screening practices. Statistical analysis was performed using Chi-square and two-sample t-test. We received 312 online survey responses (response rate of 12%). Responding OBGYNs were predominantly female (96%), board-certified (78%), generalists (65%) with a mean age of 37.1 years. Fewer than half of physicians screened for the following factors: occupational exposures, environmental chemicals, air pollution, pesticide use, personal care products, household cleaners, water source, use of plastics for food storage, and lead and mercury exposure. Eighty five percent of respondents reported that they did not feel comfortable obtaining an environmental history and 58% respondents reported that they performed no regular screening of environmental exposures. A higher frequency of screening was associated with > 4 years of practice (p = 0.001), and having read the environmental committee opinion (p = counseling patients may enhance screening for exposures that affect reproductive health.

Seeking environmental causes of neurodegenerative disease and envisioning primary prevention.

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Spencer, Peter S; Palmer, Valerie S; Kisby, Glen E

2016-09-01

Pathological changes of the aging brain are expressed in a range of neurodegenerative disorders that will impact increasing numbers of people across the globe. Research on the causes of these disorders has focused heavily on genetics, and strategies for prevention envision drug-induced slowing or arresting disease advance before its clinical appearance. We discuss a strategic shift that seeks to identify the environmental causes or contributions to neurodegeneration, and the vision of primary disease prevention by removing or controlling exposure to culpable agents. The plausibility of this approach is illustrated by the prototypical neurodegenerative disease amyotrophic lateral sclerosis and parkinsonism-dementia complex (ALS-PDC). This often-familial long-latency disease, once thought to be an inherited genetic disorder but now known to have a predominant or exclusive environmental origin, is in the process of disappearing from the three heavily affected populations, namely Chamorros of Guam and Rota, Japanese residents of Kii Peninsula, Honshu, and Auyu and Jaqai linguistic groups on the island of New Guinea in West Papua, Indonesia. Exposure via traditional food and/or medicine (the only common exposure in all three geographic isolates) to one or more neurotoxins in seed of cycad plants is the most plausible if yet unproven etiology. Neurotoxin dosage and/or subject age at exposure might explain the stratified epidemic of neurodegenerative disease on Guam in which high-incidence ALS peaked and declined before that of PD, only to be replaced today by a dementing disorder comparable to Alzheimer's disease. Exposure to the Guam environment is also linked to the delayed development of ALS among a subset of Chamorro and non-Chamorro Gulf War/Era veterans, a summary of which is reported here for the first time. Lessons learned from this study and from 65 years of research on ALS-PDC include the exceptional value of initial, field-based informal investigation of

Is exposure to cyanobacteria an environmental risk factor for amyotrophic lateral sclerosis and other neurodegenerative diseases?

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Bradley, Walter G.; Borenstein, Amy R.; Nelson, Lorene M.; Codd, Geoffrey A.; Rosen, Barry H.; Stommel, Elijah W.; Cox, Paul Alan

2013-01-01

There is a broad scientific consensus that amyotrophic lateral sclerosis (ALS) is caused by gene-environment interactions. Mutations in genes underlying familial ALS (fALS) have been discovered in only 5–10% of the total population of ALS patients. Relatively little attention has been paid to environmental and lifestyle factors that may trigger the cascade of motor neuron death leading to the syndrome of ALS, although exposure to chemicals including lead and pesticides, and to agricultural environments, smoking, certain sports, and trauma have all been identified with an increased risk of ALS. There is a need for research to quantify the relative roles of each of the identified risk factors for ALS. Recent evidence has strengthened the theory that chronic environmental exposure to the neurotoxic amino acid β-N-methylamino-L-alanine (BMAA) produced by cyanobacteria may be an environmental risk factor for ALS. Here we describe methods that may be used to assess exposure to cyanobacteria, and hence potentially to BMAA, namely an epidemiologic questionnaire and direct and indirect methods for estimating the cyanobacterial load in ecosystems. Rigorous epidemiologic studies could determine the risks associated with exposure to cyanobacteria, and if combined with genetic analysis of ALS cases and controls could reveal etiologically important gene-environment interactions in genetically vulnerable individuals.

Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease

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Balmes John

2005-05-01

Full Text Available Abstract Background Exposure to environmental tobacco smoke (ETS, which contains potent respiratory irritants, may lead to chronic airway inflammation and obstruction. Although ETS exposure appears to cause asthma in children and adults, its role in causing COPD has received limited attention in epidemiologic studies. Methods Using data from a population-based sample of 2,113 U.S. adults aged 55 to 75 years, we examined the association between lifetime ETS exposure and the risk of developing COPD. Participants were recruited from all 48 contiguous U.S. states by random digit dialing. Lifetime ETS exposure was ascertained by structured telephone interview. We used a standard epidemiologic approach to define COPD based on a self-reported physician diagnosis of chronic bronchitis, emphysema, or COPD. Results Higher cumulative lifetime home and work exposure were associated with a greater risk of COPD. The highest quartile of lifetime home ETS exposure was associated with a greater risk of COPD, controlling for age, sex, race, personal smoking history, educational attainment, marital status, and occupational exposure to vapors, gas, dusts, or fumes during the longest held job (OR 1.55; 95% CI 1.09 to 2.21. The highest quartile of lifetime workplace ETS exposure was also related to a greater risk of COPD (OR 1.36; 95% CI 1.002 to 1.84. The population attributable fraction was 11% for the highest quartile of home ETS exposure and 7% for work exposure. Conclusion ETS exposure may be an important cause of COPD. Consequently, public policies aimed at preventing public smoking may reduce the burden of COPD-related death and disability, both by reducing direct smoking and ETS exposure.

Environmental Stressors and Their Impact on Health and Disease with Focus on Oxidative Stress.

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Münzel, Thomas; Daiber, Andreas

2018-03-20

Epidemiological, preclinical and interventional clinical studies have demonstrated that environmental stressors are associated with health problems, namely cardiovascular diseases. According to estimations of the World Health Organization (WHO), environmental risk factors account for an appreciable part of global deaths and life years spent with disability. This Forum addresses the impact of the environmental risk factors such as traffic noise exposure, air pollution by particulate matter (PM), mental stress/loneliness, and the life style risk factor (water-pipe) smoking on health and disease with focus on the cardiovascular system. We will critically discuss the use of observatory/modifiable biomarkers of oxidative stress and inflammation in environmental research on the aforementioned risk factors highlighting the need of exposome studies. Another focus will be on the epigenetic regulation via microRNAs in environmental stress upon exposure to noise and toxins/heavy metals as well as mental stress conditions, providing mechanistic insights into the modulation of microRNA signaling by oxidative stress, and vice versa the contribution of microRNAs to oxidative stress conditions. We will also provide an in-depth overview on the mechanistic pathways that lead to health problems (e.g., cardiovascular diseases) in response to environmental psychosocial stress, air pollution exposure in the form of ambient PM and diesel exhaust, traffic noise exposure, and the life style drug (water-pipe) smoking. Almost all stressors share the activation of the hypothalamic-pituitary-adrenocortical axis and of the sympathetic nervous system with subsequent onset of inflammation and oxidative stress, defining the here proposed therapeutic (antioxidant and exercise) strategies. Antioxid. Redox Signal. 28, 735-740.

The Pregnancy Exposome: Multiple Environmental Exposures in the INMA-Sabadell Birth Cohort.

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Robinson, Oliver; Basagaña, Xavier; Agier, Lydiane; de Castro, Montserrat; Hernandez-Ferrer, Carles; Gonzalez, Juan R; Grimalt, Joan O; Nieuwenhuijsen, Mark; Sunyer, Jordi; Slama, Rémy; Vrijheid, Martine

2015-09-01

The "exposome" is defined as "the totality of human environmental exposures from conception onward, complementing the genome" and its holistic approach may advance understanding of disease etiology. We aimed to describe the correlation structure of the exposome during pregnancy to better understand the relationships between and within families of exposure and to develop analytical tools appropriate to exposome data. Estimates on 81 environmental exposures of current health concern were obtained for 728 women enrolled in The INMA (INfancia y Medio Ambiente) birth cohort, in Sabadell, Spain, using biomonitoring, geospatial modeling, remote sensors, and questionnaires. Pair-wise Pearson's and polychoric correlations were calculated and principal components were derived. The median absolute correlation across all exposures was 0.06 (5th-95th centiles, 0.01-0.54). There were strong levels of correlation within families of exposure (median = 0.45, 5th-95th centiles, 0.07-0.85). Nine exposures (11%) had a correlation higher than 0.5 with at least one exposure outside their exposure family. Effectively all the variance in the data set (99.5%) was explained by 40 principal components. Future exposome studies should interpret exposure effects in light of their correlations to other exposures. The weak to moderate correlation observed between exposure families will permit adjustment for confounding in future exposome studies.

Environmental health: an opportunity for health promotion and disease prevention.

Science.gov (United States)

Chalupka, Stephanie

2005-01-01

Variance in personal susceptibility to environmental hazards may be attributable to age, gender, previous or concomitant exposure, economic status, race, or genetic endowment. Water pollution sources can be either point sources (a well-defined source, e.g., factory waste water discharge) or non-point sources (more diffuse sources including agricultural, industrial, and urban runoff, domestic lawn care, and air pollution). Pollutants can migrate from disposal sites, underground injection wells, or underground storage systems and contaminate ground and surface drinking water sources. The annual cost of human exposure to outdoor air pollutants from all sources is estimated to be between $40 to $50 billion. The death toll from exposure to particulate air pollution generated by motor vehicles, burning coal, fuel oil, and wood is estimated to be responsible for as many as 100,000 fatalities annually in the United States. Through the identification of individuals and groups at greater risk, occupational and environmental health nurses can use primary and secondary prevention activities to protect susceptible individuals and communities from adverse exposures and environmentally related disease.

Environmental Determinants of Chronic Disease and Medical Approaches: Recognition, Avoidance, Supportive Therapy, and Detoxification

International Nuclear Information System (INIS)

Sears, M.E.; Sears, M.E.; Genuis, S.J.

2012-01-01

The World Health Organization warns that chronic, non communicable diseases are rapidly becoming epidemic worldwide. Escalating rates of neuro cognitive, metabolic, autoimmune and cardiovascular diseases cannot be ascribed only to genetics, lifestyle, and nutrition; early life and ongoing exposures, and bio accumulated toxicants may also cause chronic disease. Contributors to ill health are summarized from multiple perspectives biological effects of classes of toxicants, mechanisms of toxicity, and a synthesis of toxic contributors to major diseases. Health care practitioners have wide-ranging roles in addressing environmental factors in policy and public health and clinical practice. Public health initiatives include risk recognition and chemical assessment then exposure reduction, remediation, monitoring, and avoidance. The complex web of disease and environmental contributors is amenable to some straightforward clinical approaches addressing multiple toxicants. Widely applicable strategies include nutrition and supplements to counter toxic effects and to support metabolism; as well as exercise and sweating, and possibly medication to enhance excretion. Addressing environmental health and contributors to chronic disease has broad implications for society, with large potential benefits from improved health and productivity.

Human exposure assessment to environmental chemicals using biomonitoring.

Science.gov (United States)

Calafat, Antonia M; Ye, Xiaoyun; Silva, Manori J; Kuklenyik, Zsuzsanna; Needham, Larry L

2006-02-01

In modern societies, humans may be exposed to a wide spectrum of environmental chemicals. Although the health significance of this exposure for many chemicals is unknown, studies to investigate the prevalence of exposure are warranted because of the chemicals' potential harmful health effects, as often indicated in animal studies. Three tools have been used to assess exposure: exposure history/questionnaire information, environmental monitoring, and biomonitoring (i.e. measuring concentrations of the chemicals, their metabolites, or their adducts in human specimens). We present an overview on the use of biomonitoring in exposure assessment using phthalates, bisphenol A and other environmental phenols, and perfluorinated chemicals as examples. We discuss some factors relevant for interpreting and understanding biomonitoring data, including selection of both biomarkers of exposure and human matrices, and toxicokinetic information. The use of biomonitoring in human risk assessment is not discussed.

Improving Environmental Health Literacy and Justice through Environmental Exposure Results Communication

Directory of Open Access Journals (Sweden)

Monica D. Ramirez-Andreotta

2016-07-01

Full Text Available Understanding the short- and long-term impacts of a biomonitoring and exposure project and reporting personal results back to study participants is critical for guiding future efforts, especially in the context of environmental justice. The purpose of this study was to evaluate learning outcomes from environmental communication efforts and whether environmental health literacy goals were met in an environmental justice community. We conducted 14 interviews with parents who had participated in the University of Arizona’s Metals Exposure Study in Homes and analyzed their responses using NVivo, a qualitative data management and analysis program. Key findings were that participants used the data to cope with their challenging circumstances, the majority of participants described changing their families’ household behaviors, and participants reported specific interventions to reduce family exposures. The strength of this study is that it provides insight into what people learn and gain from such results communication efforts, what participants want to know, and what type of additional information participants need to advance their environmental health literacy. This information can help improve future report back efforts and advance environmental health and justice.

Transgenerational Exposure to Environmental Tobacco Smoke

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Xavier Joya

2014-07-01

Full Text Available Traditionally, nicotine from second hand smoke (SHS, active or passive, has been considered the most prevalent substance of abuse used during pregnancy in industrialized countries. Exposure to environmental tobacco smoke (ETS is associated with a variety of health effects, including lung cancer and cardiovascular diseases. Tobacco is also a major burden to people who do not smoke. As developing individuals, newborns and children are particularly vulnerable to the negative effects of SHS. In particular, prenatal ETS has adverse consequences during the entire childhood causing an increased risk of abortion, low birth weight, prematurity and/or nicotine withdrawal syndrome. Over the last years, a decreasing trend in smoking habits during pregnancy has occurred, along with the implementation of laws requiring smoke free public and working places. The decrease in the incidence of prenatal tobacco exposure has usually been assessed using maternal questionnaires. In order to diminish bias in self-reporting, objective biomarkers have been developed to evaluate this exposure. The measurement of nicotine and its main metabolite, cotinine, in non-conventional matrices such as cord blood, breast milk, hair or meconium can be used as a non-invasive measurement of prenatal SMS in newborns. The aim of this review is to highlight the prevalence of ETS (prenatal and postnatal using biomarkers in non-conventional matrices before and after the implementation of smoke free policies and health effects related to this exposure during foetal and/or postnatal life.

Probabilistic integrated risk assessment of human exposure risk to environmental bisphenol A pollution sources.

Science.gov (United States)

Fu, Keng-Yen; Cheng, Yi-Hsien; Chio, Chia-Pin; Liao, Chung-Min

2016-10-01

Environmental bisphenol A (BPA) exposure has been linked to a variety of adverse health effects such as developmental and reproductive issues. However, establishing a clear association between BPA and the likelihood of human health is complex yet fundamentally uncertain. The purpose of this study was to assess the potential exposure risks from environmental BPA among Chinese population based on five human health outcomes, namely immune response, uterotrophic assay, cardiovascular disease (CVD), diabetes, and behavior change. We addressed these health concerns by using a stochastic integrated risk assessment approach. The BPA dose-dependent likelihood of effects was reconstructed by a series of Hill models based on animal models or epidemiological data. We developed a physiologically based pharmacokinetic (PBPK) model that allows estimation of urinary BPA concentration from external exposures. Here we showed that the daily average exposure concentrations of BPA and urinary BPA estimates were consistent with the published data. We found that BPA exposures were less likely to pose significant risks for infants (0-1 year) and adults (male and female >20 years) with human long-term BPA susceptibility in relation to multiple exposure pathways, and for informing the public of the negligible magnitude of environmental BPA pollution impacts on human health.

Potential role of reduced environmental UV exposure as a driver of the current epidemic of atopic dermatitis

DEFF Research Database (Denmark)

Thyssen, Jacob P; Zirwas, Matthew J; Elias, Peter M

2015-01-01

The basis for the sudden and dramatic increase in atopic dermatitis (AD) and related atopic diseases in the second half of the 20th century is unclear. The hygiene hypothesis proposes that the transition from rural to urban living leads to reduced childhood exposure to pathogenic microorganisms....... Hence instead of having the normal TH1 bias and immune tolerance because of repeated exposure to pathogens, urban dwellers have TH2 cell immune activity and atopic disease in a more sterile environment. Various other environmental exposures have been implicated in the explosion of AD (and atopic...

Exposure-response relationships for environmental use

NARCIS (Netherlands)

Miedema, H.M.E.

2007-01-01

This paper presents an overview of the following exposure-response relationships that can be used for assessing the impact of environmental noise: • Lden - annoyance relationships from the EU Position Paper on exposure-response relationships for transportation noise annoyance (EC-WG/2 2002; Env.

Alternative Testing Methods for Predicting Health Risk from Environmental Exposures

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Annamaria Colacci

2014-08-01

Full Text Available Alternative methods to animal testing are considered as promising tools to support the prediction of toxicological risks from environmental exposure. Among the alternative testing methods, the cell transformation assay (CTA appears to be one of the most appropriate approaches to predict the carcinogenic properties of single chemicals, complex mixtures and environmental pollutants. The BALB/c 3T3 CTA shows a good degree of concordance with the in vivo rodent carcinogenesis tests. Whole-genome transcriptomic profiling is performed to identify genes that are transcriptionally regulated by different kinds of exposures. Its use in cell models representative of target organs may help in understanding the mode of action and predicting the risk for human health. Aiming at associating the environmental exposure to health-adverse outcomes, we used an integrated approach including the 3T3 CTA and transcriptomics on target cells, in order to evaluate the effects of airborne particulate matter (PM on toxicological complex endpoints. Organic extracts obtained from PM2.5 and PM1 samples were evaluated in the 3T3 CTA in order to identify effects possibly associated with different aerodynamic diameters or airborne chemical components. The effects of the PM2.5 extracts on human health were assessed by using whole-genome 44 K oligo-microarray slides. Statistical analysis by GeneSpring GX identified genes whose expression was modulated in response to the cell treatment. Then, modulated genes were associated with pathways, biological processes and diseases through an extensive biological analysis. Data derived from in vitro methods and omics techniques could be valuable for monitoring the exposure to toxicants, understanding the modes of action via exposure-associated gene expression patterns and to highlight the role of genes in key events related to adversity.

Clinical and pathological manifestations of cardiovascular disease in rat models: the influence of acute ozone exposure

Science.gov (United States)

This paper shows that rat models of cardiovascular diseases have differential degrees of underlying pathologies at a young age. Rodent models of cardiovascular diseases (CVD) and metabolic disorders are used for examining susceptibility variations to environmental exposures. How...

Efficient prion disease transmission through common environmental materials.

Science.gov (United States)

Pritzkow, Sandra; Morales, Rodrigo; Lyon, Adam; Concha-Marambio, Luis; Urayama, Akihiko; Soto, Claudio

2018-03-02

Prion diseases are a group of fatal neurodegenerative diseases associated with a protein-based infectious agent, termed prion. Compelling evidence suggests that natural transmission of prion diseases is mediated by environmental contamination with infectious prions. We hypothesized that several natural and man-made materials, commonly found in the environments of wild and captive animals, can bind prions and may act as vectors for disease transmission. To test our hypothesis, we exposed surfaces composed of various common environmental materials ( i.e. wood, rocks, plastic, glass, cement, stainless steel, aluminum, and brass) to hamster-adapted 263K scrapie prions and studied their attachment and retention of infectivity in vitro and in vivo Our results indicated that these surfaces, with the sole exception of brass, efficiently bind, retain, and release prions. Prion replication was studied in vitro using the protein misfolding cyclic amplification technology, and infectivity of surface-bound prions was analyzed by intracerebrally challenging hamsters with contaminated implants. Our results revealed that virtually all prion-contaminated materials transmitted the disease at high rates. To investigate a more natural form of exposure to environmental contamination, we simply housed animals with large contaminated spheres made of the different materials under study. Strikingly, most of the hamsters developed classical clinical signs of prion disease and typical disease-associated brain changes. Our findings suggest that prion contamination of surfaces commonly present in the environment can be a source of disease transmission, thus expanding our understanding of the mechanisms for prion spreading in nature. © 2018 by The American Society for Biochemistry and Molecular Biology, Inc.

Environmental exposure to pesticides and respiratory health

Directory of Open Access Journals (Sweden)

Ali Mamane

2015-09-01

Full Text Available Respiratory effects of environmental exposure to pesticides are debated. Here we aimed to review epidemiological studies published up until 2013, using the PubMed database. 20 studies dealing with respiratory health and non-occupational pesticide exposure were identified, 14 carried out on children and six on adults. In four out of nine studies in children with biological measurements, mothers' dichlorodiphenyldichloroethylene (DDE blood levels during pregnancy were associated with asthma and wheezing in young children. An association was also found between permethrin in indoor air during pregnancy and wheezing in children. A significant association between asthma and DDE measured in children's blood (aged 7–10 years was observed in one study. However, in three studies, no association was found between asthma or respiratory infections in children and pesticide levels in breast milk and/or infant blood. Lastly, in three out of four studies where post-natal pesticide exposure of children was assessed by parental questionnaire an association with respiratory symptoms was found. Results of the fewer studies on pesticide environmental exposure and respiratory health of adults were much less conclusive: indeed, the associations observed were weak and often not significant. In conclusion, further studies are needed to confirm whether there is a respiratory risk associated with environmental exposure to pesticides.

Dose-response relationships for environmentally mediated infectious disease transmission models.

Directory of Open Access Journals (Sweden)

Andrew F Brouwer

2017-04-01

Full Text Available Environmentally mediated infectious disease transmission models provide a mechanistic approach to examining environmental interventions for outbreaks, such as water treatment or surface decontamination. The shift from the classical SIR framework to one incorporating the environment requires codifying the relationship between exposure to environmental pathogens and infection, i.e. the dose-response relationship. Much of the work characterizing the functional forms of dose-response relationships has used statistical fit to experimental data. However, there has been little research examining the consequences of the choice of functional form in the context of transmission dynamics. To this end, we identify four properties of dose-response functions that should be considered when selecting a functional form: low-dose linearity, scalability, concavity, and whether it is a single-hit model. We find that i middle- and high-dose data do not constrain the low-dose response, and different dose-response forms that are equally plausible given the data can lead to significant differences in simulated outbreak dynamics; ii the choice of how to aggregate continuous exposure into discrete doses can impact the modeled force of infection; iii low-dose linear, concave functions allow the basic reproduction number to control global dynamics; and iv identifiability analysis offers a way to manage multiple sources of uncertainty and leverage environmental monitoring to make inference about infectivity. By applying an environmentally mediated infectious disease model to the 1993 Milwaukee Cryptosporidium outbreak, we demonstrate that environmental monitoring allows for inference regarding the infectivity of the pathogen and thus improves our ability to identify outbreak characteristics such as pathogen strain.

Human Environmental Disease Network: A computational model to assess toxicology of contaminants.

Science.gov (United States)

Taboureau, Olivier; Audouze, Karine

2017-01-01

During the past decades, many epidemiological, toxicological and biological studies have been performed to assess the role of environmental chemicals as potential toxicants associated with diverse human disorders. However, the relationships between diseases based on chemical exposure rarely have been studied by computational biology. We developed a human environmental disease network (EDN) to explore and suggest novel disease-disease and chemical-disease relationships. The presented scored EDN model is built upon the integration of systems biology and chemical toxicology using information on chemical contaminants and their disease relationships reported in the TDDB database. The resulting human EDN takes into consideration the level of evidence of the toxicant-disease relationships, allowing inclusion of some degrees of significance in the disease-disease associations. Such a network can be used to identify uncharacterized connections between diseases. Examples are discussed for type 2 diabetes (T2D). Additionally, this computational model allows confirmation of already known links between chemicals and diseases (e.g., between bisphenol A and behavioral disorders) and also reveals unexpected associations between chemicals and diseases (e.g., between chlordane and olfactory alteration), thus predicting which chemicals may be risk factors to human health. The proposed human EDN model allows exploration of common biological mechanisms of diseases associated with chemical exposure, helping us to gain insight into disease etiology and comorbidity. This computational approach is an alternative to animal testing supporting the 3R concept.

Environmental factors in a population-based inception cohort of inflammatory bowel disease patients in Europe

DEFF Research Database (Denmark)

Burisch, J; Pedersen, Natalia; Cukovic-Cavka, S

2014-01-01

BACKGROUND AND AIMS: The incidence of inflammatory bowel disease (IBD) is increasing in Eastern Europe possibly due to changes in environmental factors towards a more "westernised" standard of living. The aim of this study was to investigate differences in exposure to environmental factors prior ...... and Western European patients differed in environmental factors prior to diagnosis. Eastern European patients exhibited higher occurrences of suspected risk factors for IBD included in the Western lifestyle.......BACKGROUND AND AIMS: The incidence of inflammatory bowel disease (IBD) is increasing in Eastern Europe possibly due to changes in environmental factors towards a more "westernised" standard of living. The aim of this study was to investigate differences in exposure to environmental factors prior...... to diagnosis in Eastern and Western European IBD patients. METHODS: The EpiCom cohort is a population-based, prospective inception cohort of 1560 unselected IBD patients from 31 European countries covering a background population of 10.1 million. At the time of diagnosis patients were asked to complete an 87...

Designing exposure registries for improved tracking of occupational exposure and disease.

Science.gov (United States)

Arrandale, Victoria H; Bornstein, Stephen; King, Andrew; Takaro, Timothy K; Demers, Paul A

2016-06-27

Registries are one strategy for collecting information on occupational exposure and disease in populations. Recently leaders in the Canadian occupational health and safety community have shown an interest in the use of occupational exposure registries. The primary goal of this study was to review a series of Canadian exposure registries to identify their strengths and weaknesses as a tool for tracking occupational exposure and disease in Canada. A secondary goal was to identify the features of an exposure registry needed to specifically contribute to prevention, including the identification of new exposure-disease relationships. A documentary review of five exposure registries from Canada was completed. Strengths and limitations of the registries were compared and key considerations for designing new registries were identified. The goals and structure of the exposure registries varied considerably. Most of the reviewed registries had voluntary registration, which presents challenges for the use of the data for either surveillance or epidemiology. It is recommended that eight key issues be addressed when planning new registries: clear registry goal(s), a definition of exposure, data to be collected (and how it will be used), whether enrolment will be mandatory, as well as ethical, privacy and logistical considerations. When well constructed, an exposure registry can be a valuable tool for surveillance, epidemiology and ultimately the prevention of occupational disease. However, exposure registries also have a number of actual and potential limitations that need to be considered.

Drinking water exposure to cadmium, an environmental contaminant, results in the exacerbation of autoimmune disease in the murine model

International Nuclear Information System (INIS)

Leffel, Elizabeth K.; Wolf, Carl; Poklis, Alphonse; White, Kimber L.

2003-01-01

Cadmium is a pervasive environmental contaminant. The primary route of exposure to the general population occurs via contaminated drinking water or food supplies. Our hypothesis was that cadmium could be a trigger for inducing autoimmune disease (AD) in genetically predisposed populations. Therefore, New Zealand Black/White F1 (NZBW) mice were exposed to cadmium via drinking water. Mice were exposed to: 0, 3, 30, 3000 or 10000 parts per billion (ppb) of cadmium in tap water for 2, 4, 28, or 31 weeks. After 4 weeks of exposure, in the group of mice exposed to 10000 ppb cadmium, there was an increased incidence of antinuclear antibodies (ANA). There was also deposition of immune complexes in all groups after 4 weeks of exposure. After 31 weeks, there were increases in IgG2a in mice exposed to low doses of cadmium. In an attempt to establish the progression from an autoimmune reaction to the development of AD, the biological marker for AD, proteinuria, was assessed. Onset of proteinuria was exacerbated by 11 weeks in mice exposed to cadmium. This data suggests that short-term exposure may result in a type of autoimmune reaction since the mice are beginning to produce ANA after only 4 weeks of exposure and there is immune-complex deposition in the kidney. Long-term exposure to cadmium appears to result in the exacerbation of AD as indicated by the development of proteinuria and continued presence of immune complexes in the kidney. The mechanism may involve the increased production of IgG2a, which is capable of forming immune complexes and causing autoimmune glomerulonephritis

A review of the epidemiologic literature on the role of environmental arsenic exposure and cardiovascular diseases

International Nuclear Information System (INIS)

Wang, C.-H.; Hsiao, C.K.; Chen, C.-L.; Hsu, L.-I; Chiou, H.-Y.; Chen, S.-Y.; Hsueh, Y.-M.; Wu, M.-M.; Chen, C.-J.

2007-01-01

Cardiovascular disease is the leading cause of mortality worldwide. Arsenic is a ubiquitous metalloid in the crust of the earth. Chronic arsenic poisoning is becoming an emerging epidemic in Asia. Epidemiological studies have shown that chronic arsenic poisoning through ingestion of arsenic-contaminated water is associated with various cardiovascular diseases in dose-response relationships. These cardiovascular disorders include carotid atherosclerosis detected by ultrasonography, impaired microcirculation, prolonged QT interval and increased QT dispersion in electrocardiography, and clinical outcomes such as hypertension, blackfoot disease (a unique peripheral vascular disease endemic in southwestern Taiwan), coronary artery disease and cerebral infarction. Chronic arsenic poisoning is an independent risk factor for cardiovascular disease. The adverse cardiovascular effects of long-term arsenic exposure may be persistent and/or irreversible. Arsenic-induced cardiovascular diseases in human population may result from the interaction among genetic, environment and nutritional factors. The major adverse cardiovascular effect of chronic arsenic poisoning has been established qualitatively and quantitatively in the high arsenic exposure areas, but the low-dose effect of arsenic on cardiovascular diseases remains to be explored. Cardiovascular death is the major cause of mortality worldwide, and a small increased risk may imply a large quantity of excess mortality

NEURODEVELOPMENTAL EFFECTS OF ENVIRONMENTAL EXPOSURES

Science.gov (United States)

Neurodevelopmental Effects of Environmental ExposuresSherry G. Selevan, Pauline Mendola, Deborah C. Rice (US EPA, Washington,DC) The nervous system starts development early in gestation and continues to develop through adolescence. Thus, critical windows of vuln...

Parental tobacco smoke exposure: Epigenetics and the developmental origins of health and disease

Science.gov (United States)

Epigenetic programming is an important mechanism underlying the Developmental Origins of Health and Disease (DOHaD). Much of the research in this area has focused on maternal nutrition. Parental smoking has emerged as a prime example of how exposure to environmental toxicants dur...

Integrated Environmental Assessment Part III: ExposureAssessment

Energy Technology Data Exchange (ETDEWEB)

McKone, Thomas E.; Small, Mitchell J.

2006-06-01

Human exposure assessment is a key step in estimating the environmental and public health burdens that result chemical emissions in the life cycle of an industrial product or service. This column presents the third in a series of overviews of the state of the art in integrated environmental assessment - earlier columns described emissions estimation (Frey and Small, 2003) and fate and transport modeling (Ramaswami, et al., 2004). When combined, these first two assessment elements provide estimates of ambient concentrations in the environment. Here we discuss how both models and measurements are used to translate ambient concentrations into metrics of human and ecological exposure, the necessary precursors to impact assessment. Exposure assessment is the process of measuring and/or modeling the magnitude, frequency and duration of contact between a potentially harmful agent and a target population, including the size and characteristics of that population (IPCS, 2001; Zartarian, et al., 2005). Ideally the exposure assessment process should characterize the sources, routes, pathways, and uncertainties in the assessment. Route of exposure refers to the way that an agent enters the receptor during an exposure event. Humans contact pollutants through three routes--inhalation, ingestion, and dermal uptake. Inhalation occurs in both outdoor environments and indoor environments where most people spend the majority of their time. Ingestion includes both water and food, as well as soil and dust uptake due to hand-to-mouth activity. Dermal uptake occurs through contacts with consumer products; indoor and outdoor surfaces; the water supply during washing or bathing; ambient surface waters during swimming or boating; soil during activities such as work, gardening, and play; and, to a lesser extent, from the air that surrounds us. An exposure pathway is the course that a pollutant takes from an ambient environmental medium (air, soil, water, biota, etc), to an exposure medium

Secondhand tobacco exposure is associated with nonalcoholic fatty liver disease in children

International Nuclear Information System (INIS)

Lin, Connie; Rountree, Carl B.; Methratta, Sosamma; LaRusso, Salvatore; Kunselman, Allen R.; Spanier, Adam J.

2014-01-01

Background: Nonalcoholic fatty liver disease (NAFLD) is the leading cause of liver disease in children in the United States, and prevalence rates are rising. Smoking is associated with NAFLD, but the association of secondhand smoke exposure with NAFLD is unknown. Aims: To investigate the association of secondhand tobacco exposure with NAFLD in children. Methods: We surveyed parents/guardians of 304 children aged 3–12 years who had received an abdominal ultrasound at Penn State Hershey Medical Center. The survey addressed demographics, medical history, secondhand tobacco exposure, activity level, screen viewing time and other environmental exposures. A pediatric radiologist and sonographer reviewed the ultrasounds to grade the presence of bight liver compatible with NAFLD. We conducted logistic regression analysis to assess the association of secondhand tobacco exposure and NAFLD. Results: 54% of eligible potential participants responded to the survey. Fatty liver was present in 3% of the children. Increasing child age was associated with increased odds of NAFLD (OR 1.63 95% CI 1.1, 2.4). Reported child obesity was associated with increased odds of NAFLD (OR 44.5 95% CI 5.3, 371.7). The rate of NAFLD was higher in the smoke exposed group (6.7% vs. 1.7%). For every extra pack per day smoked at home, the odds of a child having NAFLD increased 1.8 times (AOR 1.8, 95% CI 1.2, 2.8), and any exposure increased a child's odds of NAFLD four-fold (AOR 4.0, 95% CI 1.02, 15.8). Conclusion: We found an association of secondhand smoke exposure and NAFLD in children. This may represent an area for future prevention efforts. - Highlights: • We evaluated the relation of tobacco exposure with nonalcoholic fatty liver disease. • Tobacco smoke exposure was associated with nonalcoholic fatty liver disease. • Tobacco smoke exposure may be an addressable risk factor

Secondhand tobacco exposure is associated with nonalcoholic fatty liver disease in children

Energy Technology Data Exchange (ETDEWEB)

Lin, Connie [College of Medicine, Penn State University Hershey Medical Center, 500 University Drive, PO Box 850, Hershey, PA 17033-0850 (United States); Rountree, Carl B. [Department of Pediatrics, Penn State University Hershey Medical Center, 500 University Drive, PO Box 850, Hershey, PA 17033-0850 (United States); Department of Pediatrics, Bon Secour St. Mary' s Hospital, 5801 Bremo Rd, Richmond, VA 23226 (United States); Methratta, Sosamma [Department of Pediatrics, Penn State University Hershey Medical Center, 500 University Drive, PO Box 850, Hershey, PA 17033-0850 (United States); Department of Radiology, Penn State University Hershey Medical Center, 500 University Drive, PO Box 850, Hershey, PA 17033-0850 (United States); LaRusso, Salvatore [Department of Radiology, Penn State University Hershey Medical Center, 500 University Drive, PO Box 850, Hershey, PA 17033-0850 (United States); Kunselman, Allen R. [Department of Public Health Sciences, Penn State University Hershey Medical Center, 500 University Drive, PO Box 850, Hershey, PA 17033-0850 (United States); Spanier, Adam J., E-mail: aspanier@hmc.psu.edu [Department of Pediatrics, Penn State University Hershey Medical Center, 500 University Drive, PO Box 850, Hershey, PA 17033-0850 (United States); Department of Public Health Sciences, Penn State University Hershey Medical Center, 500 University Drive, PO Box 850, Hershey, PA 17033-0850 (United States)

2014-07-15

Background: Nonalcoholic fatty liver disease (NAFLD) is the leading cause of liver disease in children in the United States, and prevalence rates are rising. Smoking is associated with NAFLD, but the association of secondhand smoke exposure with NAFLD is unknown. Aims: To investigate the association of secondhand tobacco exposure with NAFLD in children. Methods: We surveyed parents/guardians of 304 children aged 3–12 years who had received an abdominal ultrasound at Penn State Hershey Medical Center. The survey addressed demographics, medical history, secondhand tobacco exposure, activity level, screen viewing time and other environmental exposures. A pediatric radiologist and sonographer reviewed the ultrasounds to grade the presence of bight liver compatible with NAFLD. We conducted logistic regression analysis to assess the association of secondhand tobacco exposure and NAFLD. Results: 54% of eligible potential participants responded to the survey. Fatty liver was present in 3% of the children. Increasing child age was associated with increased odds of NAFLD (OR 1.63 95% CI 1.1, 2.4). Reported child obesity was associated with increased odds of NAFLD (OR 44.5 95% CI 5.3, 371.7). The rate of NAFLD was higher in the smoke exposed group (6.7% vs. 1.7%). For every extra pack per day smoked at home, the odds of a child having NAFLD increased 1.8 times (AOR 1.8, 95% CI 1.2, 2.8), and any exposure increased a child's odds of NAFLD four-fold (AOR 4.0, 95% CI 1.02, 15.8). Conclusion: We found an association of secondhand smoke exposure and NAFLD in children. This may represent an area for future prevention efforts. - Highlights: • We evaluated the relation of tobacco exposure with nonalcoholic fatty liver disease. • Tobacco smoke exposure was associated with nonalcoholic fatty liver disease. • Tobacco smoke exposure may be an addressable risk factor.

[Amyotrophic lateral sclerosis and exposure to metals and other occupational/environmental hazardous materials: state of the art].

Science.gov (United States)

Garzillo, Elpidio Maria; Miraglia, Nadia; Pedata, Paola; Feola, Daniela; Sannolo, Nicola; Lamberti, Monica

2015-01-01

In recent years, scientific literature has been giving more and more importance to the study of the occupational/environmental exposure to risk agents related to the onset of Amyotrophic Lateral Sclerosis (ALS), a neurodegenerative disease characterized by progressive muscular paralysis reflecting degeneration of motor neurons in the primary motor cortex. Aim of this work is to verify the state of art about the eventual role of occupational/environmental exposure to risk agents. Selected articles, on the basis of keywords, year of publication and topics, are related to occupational and environmental exposure to xenobiotics, and, in particular, to the exposure to heavy metals that could lead to neuronal damage mechanisms involved in ALS onset. The review shows that although the scientific production has increased the interest in the evaluation of extra-genetic causes of ALS onset, there are still few studies concerning the careful study of the work activities of the individual patient, and the inferences that can be drawn to date about the possible connection between occupational exposure to risk factors and the onset of ALS are still lacking.

Demographic, genetic, and environmental factors that modify disease course.

Science.gov (United States)

Marrie, Ruth Ann

2011-05-01

As with susceptibility to disease, it is likely that multiple factors interact to influence the phenotype of multiple sclerosis and long-term disease outcomes. Such factors may include genetic factors, socioeconomic status, comorbid diseases, and health behaviors, as well as environmental exposures. An improved understanding of the influence of these factors on disease course may reap several benefits, such as improved prognostication, allowing us to tailor disease management with respect to intensity of disease-modifying therapies and changes in specific health behaviors, in the broad context of coexisting health issues. Such information can facilitate appropriately adjusted comparisons within and between populations. Elucidation of these factors will require careful study of well-characterized populations in which the roles of multiple factors are considered simultaneously. Copyright © 2011 Elsevier Inc. All rights reserved.

[Difficulties of the methods for studying environmental exposure and neural tube defects].

Science.gov (United States)

Borja-Aburto, V H; Bermúdez-Castro, O; Lacasaña-Navarro, M; Kuri, P; Bustamante-Montes, P; Torres-Meza, V

1999-01-01

To discuss the attitudes in the assessment of environmental exposures as risk factors associated with neural tube defects, and to present the main risk factors studied to date. Environmental exposures have been suggested to have a roll in the genesis of birth defects. However, studies conducted in human populations have found difficulties in the design and conduction to show such an association for neural tube defects (anencephaly, espina bifida and encephalocele) because of problems raised from: a) the frequency measures used to compare time trends and communities, b) the classification of heterogeneous malformations, c) the inclusion of maternal, paternal and fetal factors as an integrated process and, d) the assessment of environmental exposures. Hypothetically both maternal and paternal environmental exposures can produce damage before and after conception by direct action on the embryo and the fetus-placenta complex. Therefore, in the assessment of environmental exposures we need to take into account: a) both paternal and maternal exposures; b) the critical exposure period, three months before conception for paternal exposures and one month around the conceptional period for maternal exposures; c) quantitatively evaluate environmental exposures when possible, avoiding a dichotomous classification; d) the use of biological markers of exposure is highly recommended as well as markers of genetic susceptibility.

The impact of environmental conditions on human performance: A handbood of environmental exposures. Volume 1

International Nuclear Information System (INIS)

Echeverria, D.; Barnes, V.; Bittner, A.

1994-09-01

A comprehensive review of the technical literature was conducted regarding the impact of environmental conditions on hyman performance applicable to nuclear power plant workers. The environmental conditions considered were vibration, noise, heat, cold, and light. Research staff identified potential human performance deficits (e.g., decreased dexterity, impaired vision, hearing loss, memory deficiency) along a continuum of increasing occupational exposure, ranging from exposures that result in no deficit to exposures that resulted in significant performance problems. Specific deficits were included in the report if there was sound scientific evidence that environmental exposure resulted in those performance deficits. The levels associated with each deficit were then compared to the protection afforded by existing occupational exposure standards. Volume 1 is a handbook for use by NRC inspectors to help them determine the impact of specific environmental conditions on licensee personnel performance. it discusses the units used to measure each condition, discusses the effects of the condition on task performance, presents an example of the assessment of each condition in a nuclear power plant, and discusses potential methods for reducing the effects of

Chromosomal abnormalities and environmental exposures in acute nonlymphocytic leukemia

International Nuclear Information System (INIS)

Crane, M.M.; Keating, M.J.; Trujillo, J.M.; Labarthe, D.R.

1988-01-01

Chromosomal abnormalities are present in bone marrow of approximately 50% of newly diagnostic acute nonlymphatic leukemia (ANLL) patients, but their etiologic significance, if any, is unclear. The frequency of environmental exposures, gathered by questionnaire from patients or relatives, was compared in 127 newly diagnosed ANLL patients with marrow abnormalities (AA) and 109 ANLL patients with cytogenetically normal marrow. These represented 73% of de novo patients treated at M. D. Anderson Hospital between 1976 and 1983. AA patients were more likely than NN patients to: report cytotoxic treatment for prior medical conditions, smoke cigarettes, drink alcoholic beverages, and work at occupations with possible exposure to mutagens. No statistically significant associations between aneuploidy and use of other tobacco, avocational exposure to chemicals or exposure to animals were present. Associations between specific abnormalities and prior cytotoxic therapy (deletion of chromosome 7), smoking (extra chromosome 8, inversion chromosome 16), and occupation at the time of diagnosis (translocation between chromosomes 8 and 21) were noted. No association between occupational exposure to benzene or ionizing radiation and the 6 most common chromosomal abnormalities in ANLL patients were noted, although these agents are known to be leukemogenic. Problems with interpreting the above associations, including the high nonresponse rate, a high proportion of surrogate respondents, and the large number of significance tests that were performed, are discussed. These results are consistent with those from previously reported series, and suggest that tumor-specific markers may be present for some exposures in this disease

The effects of indoor environmental exposures on pediatric asthma: a discrete event simulation model

Directory of Open Access Journals (Sweden)

Fabian M Patricia

2012-09-01

Full Text Available Abstract Background In the United States, asthma is the most common chronic disease of childhood across all socioeconomic classes and is the most frequent cause of hospitalization among children. Asthma exacerbations have been associated with exposure to residential indoor environmental stressors such as allergens and air pollutants as well as numerous additional factors. Simulation modeling is a valuable tool that can be used to evaluate interventions for complex multifactorial diseases such as asthma but in spite of its flexibility and applicability, modeling applications in either environmental exposures or asthma have been limited to date. Methods We designed a discrete event simulation model to study the effect of environmental factors on asthma exacerbations in school-age children living in low-income multi-family housing. Model outcomes include asthma symptoms, medication use, hospitalizations, and emergency room visits. Environmental factors were linked to percent predicted forced expiratory volume in 1 second (FEV1%, which in turn was linked to risk equations for each outcome. Exposures affecting FEV1% included indoor and outdoor sources of NO2 and PM2.5, cockroach allergen, and dampness as a proxy for mold. Results Model design parameters and equations are described in detail. We evaluated the model by simulating 50,000 children over 10 years and showed that pollutant concentrations and health outcome rates are comparable to values reported in the literature. In an application example, we simulated what would happen if the kitchen and bathroom exhaust fans were improved for the entire cohort, and showed reductions in pollutant concentrations and healthcare utilization rates. Conclusions We describe the design and evaluation of a discrete event simulation model of pediatric asthma for children living in low-income multi-family housing. Our model simulates the effect of environmental factors (combustion pollutants and allergens

Occupational exposure to organic solvents: a risk factor for pulmonary veno-occlusive disease.

Science.gov (United States)

Montani, David; Lau, Edmund M; Descatha, Alexis; Jaïs, Xavier; Savale, Laurent; Andujar, Pascal; Bensefa-Colas, Lynda; Girerd, Barbara; Zendah, Inès; Le Pavec, Jerome; Seferian, Andrei; Perros, Frédéric; Dorfmüller, Peter; Fadel, Elie; Soubrier, Florent; Sitbon, Oliver; Simonneau, Gérald; Humbert, Marc

2015-12-01

Pulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension characterised by predominant remodelling of pulmonary venules. Bi-allelic mutations in the eukaryotic translation initiation factor 2α kinase 4 (EIF2AK4) gene were recently described as the major cause of heritable PVOD, but risk factors associated with PVOD remain poorly understood. Occupational exposures have been proposed as a potential risk factor for PVOD, but epidemiological studies are lacking.A case-control study was conducted in consecutive PVOD (cases, n=33) and pulmonary arterial hypertension patients (controls, n=65). Occupational exposure was evaluated via questionnaire interview with blinded assessments using an expert consensus approach and a job exposure matrix (JEM).Using the expert consensus approach, PVOD was significantly associated with occupational exposure to organic solvents (adjusted OR 12.8, 95% CI 2.7-60.8), with trichloroethylene being the main agent implicated (adjusted OR 8.2, 95% CI 1.4-49.4). JEM analysis independently confirmed the association between PVOD and trichloroethylene exposure. Absence of significant trichloroethylene exposure was associated with a younger age of disease (54.8±21.4 years, p=0.037) and a high prevalence of harbouring bi-allelic EIF2AK4 mutations (41.7% versus 0%, p=0.015).Occupational exposure to organic solvents may represent a novel risk factor for PVOD. Genetic background and environmental exposure appear to influence the phenotypic expression of the disease. Copyright ©ERS 2015.

Performance of GPS-devices for environmental exposure assessment.

Science.gov (United States)

Beekhuizen, Johan; Kromhout, Hans; Huss, Anke; Vermeulen, Roel

2013-01-01

Integration of individual time-location patterns with spatially resolved exposure maps enables a more accurate estimation of personal exposures to environmental pollutants than using estimates at fixed locations. Current global positioning system (GPS) devices can be used to track an individual's location. However, information on GPS-performance in environmental exposure assessment is largely missing. We therefore performed two studies. First, a commute-study, where the commute of 12 individuals was tracked twice, testing GPS-performance for five transport modes and two wearing modes. Second, an urban-tracking study, where one individual was tracked repeatedly through different areas, focused on the effect of building obstruction on GPS-performance. The median error from the true path for walking was 3.7 m, biking 2.9 m, train 4.8 m, bus 4.9 m, and car 3.3 m. Errors were larger in a high-rise commercial area (median error=7.1 m) compared with a low-rise residential area (median error=2.2 m). Thus, GPS-performance largely depends on the transport mode and urban built-up. Although ~85% of all errors were 50 m. Modern GPS-devices are useful tools for environmental exposure assessment, but large GPS-errors might affect estimates of exposures with high spatial variability.

Systematic correlation of environmental exposure and physiological and self-reported behaviour factors with leukocyte telomere length.

Science.gov (United States)

Patel, Chirag J; Manrai, Arjun K; Corona, Erik; Kohane, Isaac S

2017-02-01

It is hypothesized that environmental exposures and behaviour influence telomere length, an indicator of cellular ageing. We systematically associated 461 indicators of environmental exposures, physiology and self-reported behaviour with telomere length in data from the US National Health and Nutrition Examination Survey (NHANES) in 1999-2002. Further, we tested whether factors identified in the NHANES participants are also correlated with gene expression of telomere length modifying genes. We correlated 461 environmental exposures, behaviours and clinical variables with telomere length, using survey-weighted linear regression, adjusting for sex, age, age squared, race/ethnicity, poverty level, education and born outside the USA, and estimated the false discovery rate to adjust for multiple hypotheses. We conducted a secondary analysis to investigate the correlation between identified environmental variables and gene expression levels of telomere-associated genes in publicly available gene expression samples. After correlating 461 variables with telomere length, we found 22 variables significantly associated with telomere length after adjustment for multiple hypotheses. Of these varaibales, 14 were associated with longer telomeres, including biomarkers of polychlorinated biphenyls([PCBs; 0.1 to 0.2 standard deviation (SD) increase for 1 SD increase in PCB level, P  environmental exposures and chronic disease-related risk factors may play a role in telomere length. Our secondary analysis found no evidence of association between PCBs/smoking and gene expression of telomere-associated genes. All correlations between exposures, behaviours and clinical factors and changes in telomere length will require further investigation regarding biological influence of exposure. © The Author 2016. Published by Oxford University Press on behalf of the International Epidemiological Association

Environmental radioactivity and radiation exposure

International Nuclear Information System (INIS)

1976-01-01

The environmental radioactivity in the Federal Republic of Germany was almost as high in 1976 as in 1975. It only increased temporarily in autumn 1976 as a result of the above-ground nuclear weapons test of the People's Republic of China on September 29th 1976 and then returned to its previous level. The radioactivity in food had a slight decreasing trend in 1976, apart from a temporary increase in the radioactivity in milk also caused by the nuclear weapons test mentioned. The population exposure remains basically unchanged in 1976 compared with 1975. The artificial radiation exposure is about half as high as the natural radiation exposure to which man has always been exposed. The former is based to 83% on using X-rays in medicine, particularly for X-ray diagnostic purposes. The population exposure due to nuclear power plants and other nuclear plants is still well below 1% of the natural radiation exposure although in 1976 three new nuclear power plants were put into operation. This is also true for the average radiation exposure within an area of 3 km around the nuclear plant. (orig.) [de

Environmental lead exposure increases micronuclei in children

DEFF Research Database (Denmark)

Kapka, Lucyna; Baumgartner, Adolf; Siwińska, Ewa

2007-01-01

The objective of this pilot study was to investigate the contribution of environmental exposures to lead in the development of cytogenetic damage detected as the frequency of micronuclei (MN) in children. The other aim was to apply the MN assay in combination with fluorescence in situ hybridization...... age from an unexposed recreational area. Exposure to lead was assessed by determination of lead concentrations in blood (PbB) by atomic absorption spectrophotometry, whereas the level of selenium (Se) in serum was detected by using graphite furnace atomic-absorption spectrometry. The frequency of MN...... was determined by the cytokinesis-block MN assay and fluorescence in situ hybridization performed using a specific pan-centromeric probe. Environmental exposure to lead resulted in significantly increased levels of PbB (5.29 +/- 2.09 versus 3.45 +/- 1.20 microg/dl in controls), although the average level...

Data Sources Available for Modeling Environmental Exposures in Older Adults

Science.gov (United States)

This report, “Data Sources Available for Modeling Environmental Exposures in Older Adults,” focuses on information sources and data available for modeling environmental exposures in the older U.S. population, defined here to be people 60 years and older, with an emphasis on those...

Blood-borne biomarkers and bioindicators for linking exposure to health effects in environmental health science.

Science.gov (United States)

Wallace, M Ariel Geer; Kormos, Tzipporah M; Pleil, Joachim D

2016-01-01

Environmental health science aims to link environmental pollution sources to adverse health outcomes to develop effective exposure intervention strategies that reduce long-term disease risks. Over the past few decades, the public health community recognized that health risk is driven by interaction between the human genome and external environment. Now that the human genetic code has been sequenced, establishing this "G × E" (gene-environment) interaction requires a similar effort to decode the human exposome, which is the accumulation of an individual's environmental exposures and metabolic responses throughout the person's lifetime. The exposome is composed of endogenous and exogenous chemicals, many of which are measurable as biomarkers in blood, breath, and urine. Exposure to pollutants is assessed by analyzing biofluids for the pollutant itself or its metabolic products. New methods are being developed to use a subset of biomarkers, termed bioindicators, to demonstrate biological changes indicative of future adverse health effects. Typically, environmental biomarkers are assessed using noninvasive (excreted) media, such as breath and urine. Blood is often avoided for biomonitoring due to practical reasons such as medical personnel, infectious waste, or clinical setting, despite the fact that blood represents the central compartment that interacts with every living cell and is the most relevant biofluid for certain applications and analyses. The aims of this study were to (1) review the current use of blood samples in environmental health research, (2) briefly contrast blood with other biological media, and (3) propose additional applications for blood analysis in human exposure research.

Risk-based indicators of Canadians' exposures to environmental carcinogens.

Science.gov (United States)

Setton, Eleanor; Hystad, Perry; Poplawski, Karla; Cheasley, Roslyn; Cervantes-Larios, Alejandro; Keller, C Peter; Demers, Paul A

2013-02-12

Tools for estimating population exposures to environmental carcinogens are required to support evidence-based policies to reduce chronic exposures and associated cancers. Our objective was to develop indicators of population exposure to selected environmental carcinogens that can be easily updated over time, and allow comparisons and prioritization between different carcinogens and exposure pathways. We employed a risk assessment-based approach to produce screening-level estimates of lifetime excess cancer risk for selected substances listed as known carcinogens by the International Agency for Research on Cancer. Estimates of lifetime average daily intake were calculated using population characteristics combined with concentrations (circa 2006) in outdoor air, indoor air, dust, drinking water, and food and beverages from existing monitoring databases or comprehensive literature reviews. Intake estimates were then multiplied by cancer potency factors from Health Canada, the United States Environmental Protection Agency, and the California Office of Environmental Health Hazard Assessment to estimate lifetime excess cancer risks associated with each substance and exposure pathway. Lifetime excess cancer risks in excess of 1 per million people are identified as potential priorities for further attention. Based on data representing average conditions circa 2006, a total of 18 carcinogen-exposure pathways had potential lifetime excess cancer risks greater than 1 per million, based on varying data quality. Carcinogens with moderate to high data quality and lifetime excess cancer risk greater than 1 per million included benzene, 1,3-butadiene and radon in outdoor air; benzene and radon in indoor air; and arsenic and hexavalent chromium in drinking water. Important data gaps were identified for asbestos, hexavalent chromium and diesel exhaust in outdoor and indoor air, while little data were available to assess risk for substances in dust, food and beverages. The ability to

Acrolein and Human Disease: Untangling the Knotty Exposure Scenarios Accompanying Several Diverse Disorders.

Science.gov (United States)

Burcham, Philip C

2017-01-17

Acrolein is a highly toxic electrophile that participates in many diseases, yet efforts to delineate its precise mechanistic contributions to specific conditions are complicated by its wide distribution within human environments. This Perspective develops the proposal that due to its mixed status as environmental pollutant, metabolic byproduct, and endotoxicant which forms via ubiquitous pathophysiological processes, many diseases likely involve acrolein released from multiple sources. Although the category boundaries are indistinct, at least four identifiable exposure scenarios are identifiable. First, in some syndromes, such as those accompanying chronic or acute intoxication with smoke, whatever role acrolein plays in disease pathogenesis mainly traces to exogenous sources such as the combustion of tobacco or other organic matter. A second exposure category involves xenobiotics that undergo metabolism within the body to release acrolein. Still other health conditions, however, involve acrolein that forms via several endogenous pathways, some of which are activated upon intoxication with xenobiotics (i.e., Exposure Category 3), while still others accompany direct physical trauma to body tissues (Exposure Category 4). Further complicating efforts to clarify the role of endogenous acrolein in human disease is the likelihood that many such syndromes are complex phenomena that resemble "chemical mixture exposures" by involving multiple toxic substances simultaneously. This Perspective contends that while recent decades have witnessed much progress in describing the deleterious effects of acrolein at the cellular and molecular levels, more work is needed to define the contributions of different acrolein sources to "real-world" health conditions in human subjects.

Environmental stress, ageing and glial cell senescence: a novel mechanistic link to Parkinson's disease?

Science.gov (United States)

Chinta, S J; Lieu, C A; Demaria, M; Laberge, R-M; Campisi, J; Andersen, J K

2013-05-01

Exposure to environmental toxins is associated with a variety of age-related diseases including cancer and neurodegeneration. For example, in Parkinson's disease (PD), chronic environmental exposure to certain toxins has been linked to the age-related development of neuropathology. Neuronal damage is believed to involve the induction of neuroinflammatory events as a consequence of glial cell activation. Cellular senescence is a potent anti-cancer mechanism that occurs in a number of proliferative cell types and causes the arrest of proliferation of cells at risk of malignant transformation following exposure to potentially oncogenic stimuli. With age, senescent cells accumulate and express a senescence-associated secretory phenotype (SASP; that is the robust secretion of many inflammatory cytokines, growth factors and proteases). Whereas cell senescence in peripheral tissues has been causally linked to a number of age-related pathologies, little is known about the induction of cellular senescence and the SASP in the brain. On the basis of recently reported findings, we propose that environmental stressors associated with PD may act in part by eliciting senescence and the SASP within non neuronal glial cells in the ageing brain, thus contributing to the characteristic decline in neuronal integrity that occurs in this disorder. © 2013 The Association for the Publication of the Journal of Internal Medicine.

Environmental exposure to arsenic and chromium in an industrial area

OpenAIRE

Vimercati, Luigi; Gatti, Maria F; Gagliardi, Tommaso; Cuccaro, Francesco; De Maria, Luigi; Caputi, Antonio; Quarato, Marco; Baldassarre, Antonio

2017-01-01

Arsenic and chromium are widespread environmental contaminants that affect global health due to their toxicity and carcinogenicity. To date, few studies have investigated exposure to arsenic and chromium in a population residing in a high-risk environmental area. The aim of this study is to evaluate the exposure to arsenic and chromium in the general population with no occupational exposure to these metals, resident in the industrial area of Taranto, Southern Italy, through biological monitor...

Assessment of chemical exposures: calculation methods for environmental professionals

National Research Council Canada - National Science Library

Daugherty, Jack E

1997-01-01

... on by scientists, businessmen, and policymakers. Assessment of Chemical Exposures: Calculation Methods for Environmental Professionals addresses the expanding scope of exposure assessments in both the workplace and environment...

Environmentally toxicant exposures induced intragenerational transmission of liver abnormalities in mice

Directory of Open Access Journals (Sweden)

Mohamed A. Al-Griw

2017-08-01

Full Text Available Environmental toxicants such as chemicals, heavy metals, and pesticides have been shown to promote transgenerational inheritance of abnormal phenotypes and/or diseases to multiple subsequent generations following parental and/ or ancestral exposures. This study was designed to examine the potential transgenerational action of the environmental toxicant trichloroethane (TCE on transmission of liver abnormality, and to elucidate the molecular etiology of hepatocyte cell damage. A total of thirty two healthy immature female albino mice were randomly divided into three equal groups as follows: a sham group, which did not receive any treatment; a vehicle group, which received corn oil alone, and TCE treated group (3 weeks, 100 μg/kg i.p., every 4th day. The F0 and F1 generation control and TCE populations were sacrificed at the age of four months, and various abnormalities histpathologically investigated. Cell death and oxidative stress indices were also measured. The present study provides experimental evidence for the inheritance of environmentally induced liver abnormalities in mice. The results of this study show that exposure to the TCE promoted adult onset liver abnormalities in F0 female mice as well as unexposed F1 generation offspring. It is the first study to report a transgenerational liver abnormalities in the F1 generation mice through maternal line prior to gestation. This finding was based on careful evaluation of liver histopathological abnormalities, apoptosis of hepatocytes, and measurements of oxidative stress biomarkers (lipid peroxidation, protein carbonylation, and nitric oxide in control and TCE populations. There was an increase in liver histopathological abnormalities, cell death, and oxidative lipid damage in F0 and F1 hepatic tissues of TCE treated group. In conclusion, this study showed that the biological and health impacts of environmental toxicant TCE do not end in maternal adults, but are passed on to offspring

Interleukin-24 as a target cytokine of environmental aryl hydrocarbon receptor agonist exposure in the lung

Energy Technology Data Exchange (ETDEWEB)

Luo, Yueh-Hsia; Kuo, Yu-Chun; Tsai, Ming-Hsien; Ho, Chia-Chi; Tsai, Hui-Ti; Hsu, Chin-Yu; Chen, Yu-Cheng; Lin, Pinpin, E-mail: pplin@nhri.org.tw

2017-06-01

Exposure to environmental aryl hydrocarbon receptor (AhR) agonists, such as halogenated aromatic hydrocarbons and polycyclic aromatic hydrocarbons (PAHs), has great impacts on the development of various lung diseases. As emerging molecular targets for AhR agonists, cytokines may contribute to the inflammatory or immunotoxic effects of environmental AhR agonists. However, general cytokine expression may not specifically indicate environmental AhR agonist exposure. By comparing cytokine and chemokine expression profiles in human lung adenocarcinoma cell line CL5 treated with AhR agonists and the non-AhR agonist polychlorinated biphenyl (PCB) 39, we identified a target cytokine of environmental AhR agonist exposure of in the lungs. Thirteen cytokine and chemokine genes were altered in the AhR agonists-treated cells, but none were altered in the PCB39-treated cells. Interleukin (IL)-24 was the most highly induced gene among AhR-modulated cytokines. Cotreatment with AhR antagonist completely prevented IL-24 induction by AhR agonists in the CL5 cells. Knockdown AhR expression with short-hairpin RNA (shRNA) significantly reduced benzo[a]pyrene (BaP)-induced IL-24 mRNA levels. We further confirmed that gene transcription, but not mRNA stability, was involved in IL-24 upregulation by BaP. Particulate matter (PM) in the ambient air contains some PAHs and is reported to activate AhR. Oropharyngeal aspiration of PM significantly increased IL-24 levels in lung epithelia and in bronchoalveolar lavage fluid of mice 4 weeks after treatment. Thus, our data suggests that IL-24 is a pulmonary exposure target cytokine of environmental AhR agonists. - Graphical abstract: (A) Cytokine and chemokine gene expressions were examined in CL5 cells treated with AhR and non-AhR agonists. Thirteen cytokines and chemokines genes were altered in the AhR agonist-treated cells, but not in the non-AhR agonist-treated cells. IL-24 was the most highly induced gene among the AhR-modulated cytokines. (B

A review of the cohorts with environmental and occupational mineral fiber exposure.

Science.gov (United States)

Metintas, Selma; Ak, Guntulu; Metintas, Muzaffer

2018-04-20

The aim of the study was to examine factors associated with Malignant Mesothelioma (MM) incidence rate of the groups with occupational asbestos and environmental asbestos or erionite exposure in rural area. In this ecological study, a total of 21 cohort datasets (8 environmental and 13 occupational) were evaluated. Data were analyzed using a multiple linear regression analysis model. In environmental cohorts, the risk of MM incidence was higher in women and people exposed to erionite. In this cohort, the incidence rate of MM increased as the median exposure time increased, while the incidence decreased as the median cumulative exposure dose increased. In occupational cohorts, the incidence rate of MM was positively correlated with the median cumulative exposure dose. The risk of mesothelioma was lower in those exposed to tremolite than others. Environmental asbestos exposure is as important as occupational exposure to develop MM, and it has its own unique exposure features on the risk of MM.

Metabolic profiling detects early effects of environmental and lifestyle exposure to cadmium in a human population

Directory of Open Access Journals (Sweden)

Ellis James K

2012-06-01

Full Text Available Abstract Background The 'exposome' represents the accumulation of all environmental exposures across a lifetime. Top-down strategies are required to assess something this comprehensive, and could transform our understanding of how environmental factors affect human health. Metabolic profiling (metabonomics/metabolomics defines an individual's metabolic phenotype, which is influenced by genotype, diet, lifestyle, health and xenobiotic exposure, and could also reveal intermediate biomarkers for disease risk that reflect adaptive response to exposure. We investigated changes in metabolism in volunteers living near a point source of environmental pollution: a closed zinc smelter with associated elevated levels of environmental cadmium. Methods High-resolution 1H NMR spectroscopy (metabonomics was used to acquire urinary metabolic profiles from 178 human volunteers. The spectral data were subjected to multivariate and univariate analysis to identify metabolites that were correlated with lifestyle or biological factors. Urinary levels of 8-oxo-deoxyguanosine were also measured, using mass spectrometry, as a marker of systemic oxidative stress. Results Six urinary metabolites, either associated with mitochondrial metabolism (citrate, 3-hydroxyisovalerate, 4-deoxy-erythronic acid or one-carbon metabolism (dimethylglycine, creatinine, creatine, were associated with cadmium exposure. In particular, citrate levels retained a significant correlation to urinary cadmium and smoking status after controlling for age and sex. Oxidative stress (as determined by urinary 8-oxo-deoxyguanosine levels was elevated in individuals with high cadmium exposure, supporting the hypothesis that heavy metal accumulation was causing mitochondrial dysfunction. Conclusions This study shows evidence that an NMR-based metabolic profiling study in an uncontrolled human population is capable of identifying intermediate biomarkers of response to toxicants at true environmental

Accommodating the ecological fallacy in disease mapping in the absence of individual exposures.

Science.gov (United States)

Wang, Feifei; Wang, Jian; Gelfand, Alan; Li, Fan

2017-12-30

In health exposure modeling, in particular, disease mapping, the ecological fallacy arises because the relationship between aggregated disease incidence on areal units and average exposure on those units differs from the relationship between the event of individual incidence and the associated individual exposure. This article presents a novel modeling approach to address the ecological fallacy in the least informative data setting. We assume the known population at risk with an observed incidence for a collection of areal units and, separately, environmental exposure recorded during the period of incidence at a collection of monitoring stations. We do not assume any partial individual level information or random allocation of individuals to observed exposures. We specify a conceptual incidence surface over the study region as a function of an exposure surface resulting in a stochastic integral of the block average disease incidence. The true block level incidence is an unavailable Monte Carlo integration for this stochastic integral. We propose an alternative manageable Monte Carlo integration for the integral. Modeling in this setting is immediately hierarchical, and we fit our model within a Bayesian framework. To alleviate the resulting computational burden, we offer 2 strategies for efficient model fitting: one is through modularization, the other is through sparse or dimension-reduced Gaussian processes. We illustrate the performance of our model with simulations based on a heat-related mortality dataset in Ohio and then analyze associated real data. Copyright © 2017 John Wiley & Sons, Ltd.

Assessing Health Outcomes After Environmental Exposures Associated With Open Pit Burning in Deployed US Service Members.

Science.gov (United States)

Rohrbeck, Patricia; Hu, Zheng; Mallon, Col Timothy M

2016-08-01

This study assessed the long-term health impact of environmental exposures associated with open pit burning in deployed US service members. Two hundred individuals deployed to Balad, Iraq, and Bagram, Afghanistan, with known exposure to open pits, were matched to 200 non-deployed service members. Both cohorts were observed for adverse health outcomes after returning from deployment. Slight increased risks were observed for respiratory diseases in the Bagram cohort (adj RR: 1.259), and for cardiovascular disease in the Balad cohort (adj RR: 1.072), but the findings were not significant. The combined deployed cohort showed lower risks for adverse health outcomes, suggesting a healthy deployer effect. In conclusion, this study did not find significantly increased risks for selected health outcomes after burn pit exposure during deployment among two deployed cohorts compared with a non-deployed cohort.

Critical disease windows shaped by stress exposure alter allocation trade-offs between development and immunity.

Science.gov (United States)

Kirschman, Lucas J; Crespi, Erica J; Warne, Robin W

2018-01-01

Ubiquitous environmental stressors are often thought to alter animal susceptibility to pathogens and contribute to disease emergence. However, duration of exposure to a stressor is likely critical, because while chronic stress is often immunosuppressive, acute stress can temporarily enhance immune function. Furthermore, host susceptibility to stress and disease often varies with ontogeny; increasing during critical developmental windows. How the duration and timing of exposure to stressors interact to shape critical windows and influence disease processes is not well tested. We used ranavirus and larval amphibians as a model system to investigate how physiological stress and pathogenic infection shape development and disease dynamics in vertebrates. Based on a resource allocation model, we designed experiments to test how exposure to stressors may induce resource trade-offs that shape critical windows and disease processes because the neuroendocrine stress axis coordinates developmental remodelling, immune function and energy allocation in larval amphibians. We used wood frog larvae (Lithobates sylvaticus) to investigate how chronic and acute exposure to corticosterone, the dominant amphibian glucocorticoid hormone, mediates development and immune function via splenocyte immunohistochemistry analysis in association with ranavirus infection. Corticosterone treatments affected immune function, as both chronic and acute exposure suppressed splenocyte proliferation, although viral replication rate increased only in the chronic corticosterone treatment. Time to metamorphosis and survival depended on both corticosterone treatment and infection status. In the control and chronic corticosterone treatments, ranavirus infection decreased survival and delayed metamorphosis, although chronic corticosterone exposure accelerated rate of metamorphosis in uninfected larvae. Acute corticosterone exposure accelerated metamorphosis increased survival in infected larvae. Interactions

Differential environmental exposure among non-Indigenous Canadians as a function of sex/gender and race/ethnicity variables: a scoping review.

Science.gov (United States)

Chakravartty, Dolon; Wiseman, Clare L S; Cole, Donald C

2014-11-21

To determine the extent, range and types of studies of differential environmental chemical exposures among non-Indigenous Canadians as a function of sex/gender and race/ethnicity. Computerized database searches were performed from November to December 2013 using Medline, Embase, CAB Abstracts, Proquest and Scopus to identify relevant studies of environmental exposures among non-Indigenous adults aged ≥18 years in Canada published between 1993 and 2013. Articles were identified for full-text review based on a screening of titles and abstracts and were excluded during this initial review if they focused on environmental exposures in the following populations: 1) Indigenous populations, 2) individuals <15 years of age, 3) pregnant women and associated negative birth outcomes, or 4) non-Canadian populations. Articles were also excluded if the primary focus was on exposures to environmental tobacco smoke, non-chemical occupational hazards, infectious diseases, noise and/or radiation. A full-text review of 78 identified articles systematically assessed how sex/gender and race/ethnicity were considered. Although 59% of studies stratified results by sex, less than half of these offered any explanation of differential exposures. Eighteen of the 78 studies (23%) used terms related to race/ethnicity in their participant descriptions. Of the studies that conducted subgroup analyses of exposure results by race/ethnicity (n=15), a total of 8 also included subgroup analysis by sex. Overall, 3 of the 78 (3%) articles reviewed analyzed environmental exposures as a function of sex/gender and race/ethnicity. The role of sex/gender and race/ethnicity in influencing environmental exposure levels among non-Indigenous Canadians has not been adequately addressed to date.

Circulating mitochondrial DNA as biomarker linking environmental chemical exposure to early preclinical lesions elevation of mtDNA in human serum after exposure to carcinogenic halo-alkane-based pesticides.

Directory of Open Access Journals (Sweden)

Lygia T Budnik

Full Text Available There is a need for a panel of suitable biomarkers for detection of environmental chemical exposure leading to the initiation or progression of degenerative diseases or potentially, to cancer. As the peripheral blood may contain increased levels of circulating cell-free DNA in diseased individuals, we aimed to evaluate this DNA as effect biomarker recognizing vulnerability after exposure to environmental chemicals. We recruited 164 individuals presumably exposed to halo-alkane-based pesticides. Exposure evaluation was based on human biomonitoring analysis; as biomarker of exposure parent halo-methanes, -ethanes and their metabolites, as well as the hemoglobin-adducts methyl valine and hydroxyl ethyl valine in blood were used, complemented by expert evaluation of exposure and clinical intoxication symptoms as well as a questionnaire. Assessment showed exposures to halo alkanes in the concentration range being higher than non-cancer reference doses (RfD but (mostly lower than the occupational exposure limits. We quantified circulating DNA in serum from 86 individuals with confirmed exposure to off-gassing halo-alkane pesticides (in storage facilities or in home environment and 30 non-exposed controls, and found that exposure was significantly associated with elevated serum levels of circulating mitochondrial DNA (in size of 79 bp, mtDNA-79, p = 0.0001. The decreased integrity of mtDNA (mtDNA-230/mtDNA-79 in exposed individuals implicates apoptotic processes (p = 0.015. The relative amounts of mtDNA-79 in serum were positively associated with the lag-time after intoxication to these chemicals (r = 0.99, p<0.0001. Several months of post-exposure the specificity of this biomarker increased from 30% to 97% in patients with intoxication symptoms. Our findings indicate that mitochondrial DNA has a potential to serve as a biomarker recognizing vulnerable risk groups after exposure to toxic/carcinogenic chemicals.

Epidemiologic studies of fatal and nonfatal cardiovascular disease and ETS exposure from spousal smoking.

OpenAIRE

Thun, M; Henley, J; Apicella, L

1999-01-01

This article reviews the epidemiologic studies of the association of ischemic heart disease risk and environmental tobacco smoke (ETS) exposure from a spouse who smokes. Seventeen studies (nine cohort, eight case-control) comprising more than 485,000 lifelong nonsmokers and 7,345 coronary heart disease (CHD) events were included in a meta-analysis. Together, these studies include 36% more CHD events and 58% more study subjects than were available for review by the U. S. Occupational Safety an...

Environmental stress, ageing and glial cell senescence: a novel mechanistic link to Parkinson’s disease?

Science.gov (United States)

Chinta, Shankar J; Lieu, Christopher A; DeMaria, Marco; Laberge, Remi-Martin; Campisi, Judith; Andersen, Julie K

2013-01-01

Exposure to environmental toxins is associated with a variety of age-related diseases including cancer and neurodegeneration. For example, in Parkinson’s disease (PD), chronic environmental exposure to certain toxins has been linked to the age-related development of neuropathology. Neuronal damage is believed to involve the induction of neuroinflammatory events as a consequence of glial cell activation. Cellular senescence is a potent anti-cancer mechanism that occurs in a number of proliferative cell types and causes the arrest of proliferation of cells at risk of malignant transformation following exposure to potentially oncogenic stimuli. With age, senescent cells accumulate and express a senescence-associated secretory phenotype (SASP; i.e. the robust secretion of many inflammatory cytokines, growth factors and proteases). Whereas cell senescence in peripheral tissues has been causally linked to a number of age-related pathologies, little is known about the induction of cellular senescence and the SASP in the brain. Based on recently reported findings, we propose that environmental stressors associated with PD may act in part by eliciting senescence and the SASP within non-neuronal glial cells in the ageing brain, thus contributing to the characteristic decline in neuronal integrity that occurs in this disorder. PMID:23600398

The Penobscot River and environmental contaminants: Assessment of tribal exposure through sustenance lifeways

Science.gov (United States)

Marshall, Valerie; Kusnierz, Daniel; Hillger, Robert; Ferrario, Joseph; Hughes, Thomas; Diliberto, Janet; Orazio, Carl E.; Dudley, Robert W.; Byrne, Christian; Sugatt, Richard; Warren, Sarah; DeMarini, David; Elskus, Adria; Stodola, Steve; Mierzykowski, Steve; Pugh, Katie; Culbertson, Charles W.

2015-01-01

EPA in collaboration with the Penobscot Indian Nation, U.S. Geological Survey (USGS), Agency for Toxic Substances and Disease Registry (ATSDR), and the U.S. Fish and Wildlife Service (USF&WS) collectively embarked on a four year research study to evaluate the environmental health of the riverine system by targeting specific cultural practices and using traditional science to conduct a preliminary contaminant screening of the flora and fauna of the Penobscot River ecosystem. This study was designed as a preliminary screening to determine if contaminant concentrations in fish, eel, snapping turtle, wood ducks, and plants in Regions of the Penobscot River relevant to where PIN tribal members hunt, fish and gather plants were high enough to be a health concern. This study was not designed to be a statistically validated assessment of contaminant differences among study sites or among species. The traditional methodology for health risk assessment used by the U. S. Environmental Protection Agency (EPA) is based on the use of exposure assumptions (e.g. exposure duration, food ingestion rate, body weight, etc.) that represent the entire American population, either as a central tendency exposure (e.g. average, median) or as a reasonable maximum exposure (e.g. 95% upper confidence limit). Unfortunately, EPA lacked exposure information for assessing health risks for New England regional tribes sustaining a tribal subsistence way of life. As a riverine tribe, the Penobscot culture and traditions are inextricably tied to the Penobscot River watershed. It is through hunting, fishing, trapping, gathering and making baskets, pottery, moccasins, birch-bark canoes and other traditional practices that the Penobscot culture and people are sustained. The Penobscot River receives a variety of pollutant discharges leaving the Penobscot Indian Nation (PIN) questioning the ecological health and water quality of the river and how this may affect the practices that sustain their way of life

Occupational and environmental exposures to radon: A perspective for mitigators

International Nuclear Information System (INIS)

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

1989-01-01

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

Gender differences in asbestos exposure and disease location in 327 patients with mesothelioma

DEFF Research Database (Denmark)

Panou, Vasiliki; Weinreich, Ulla Moller; Bak, Jens

2017-01-01

Introduction: The Region of North Denmark has a high incidence of malignant mesothelioma (MM) of 6.2/100.000 for men and 1/100.000 for women mainly due to large-scale use of chrysotile asbestos.Aims: The aim of the study is to investigate gender differences in asbestos exposure and disease location...... workers; domestic, referring to patients living with an asbestos worker; environmental, defined as living or working within 10.000 meters from asbestos emitting location; unknown, where no source of asbestos exposure could be identified. MM location was classified as pleural (MPM) or peritoneal (MAM...

Perspectives for integrating human and environmental exposure assessments.

Science.gov (United States)

Ciffroy, P; Péry, A R R; Roth, N

2016-10-15

Integrated Risk Assessment (IRA) has been defined by the EU FP7 HEROIC Coordination action as "the mutual exploitation of Environmental Risk Assessment for Human Health Risk Assessment and vice versa in order to coherently and more efficiently characterize an overall risk to humans and the environment for better informing the risk analysis process" (Wilks et al., 2015). Since exposure assessment and hazard characterization are the pillars of risk assessment, integrating Environmental Exposure assessment (EEA) and Human Exposure assessment (HEA) is a major component of an IRA framework. EEA and HEA typically pursue different targets, protection goals and timeframe. However, human and wildlife species also share the same environment and they similarly inhale air and ingest water and food through often similar overlapping pathways of exposure. Fate models used in EEA and HEA to predict the chemicals distribution among physical and biological media are essentially based on common properties of chemicals, and internal concentration estimations are largely based on inter-species (i.e. biota-to-human) extrapolations. Also, both EEA and HEA are challenged by increasing scientific complexity and resources constraints. Altogether, these points create the need for a better exploitation of all currently existing data, experimental approaches and modeling tools and it is assumed that a more integrated approach of both EEA and HEA may be part of the solution. Based on the outcome of an Expert Workshop on Extrapolations in Integrated Exposure Assessment organized by the HEROIC project in January 2014, this paper identifies perspectives and recommendations to better harmonize and extrapolate exposure assessment data, models and methods between Human Health and Environmental Risk Assessments to support the further development and promotion of the concept of IRA. Ultimately, these recommendations may feed into guidance showing when and how to apply IRA in the regulatory decision

Exposure information in environmental health research: Current opportunities and future directions for particulate matter, ozone, and toxic air pollutants

Energy Technology Data Exchange (ETDEWEB)

McKone, Thomas E.; Ryan, P. Barry; Ozkaynak, Haluk

2007-02-01

Understanding and quantifying outdoor and indoor sources of human exposure are essential but often not adequately addressed in health-effects studies for air pollution. Air pollution epidemiology, risk assessment, health tracking and accountability assessments are examples of health-effects studies that require but often lack adequate exposure information. Recent advances in exposure modeling along with better information on time-activity and exposure factors data provide us with unique opportunities to improve the assignment of exposures for both future and ongoing studies linking air pollution to health impacts. In September 2006, scientists from the US Environmental Protection Agency (EPA) and the Centers for Disease Control and Prevention (CDC) along with scientists from the academic community and state health departments convened a symposium on air pollution exposure and health in order to identify, evaluate, and improve current approaches for linking air pollution exposures to disease. This manuscript presents the key issues, challenges and recommendations identified by the exposure working group, who used cases studies of particulate matter, ozone, and toxic air pollutant exposure to evaluate health-effects for air pollution. One of the over-arching lessons of this workshop is that obtaining better exposure information for these different health-effects studies requires both goal-setting for what is needed and mapping out the transition pathway from current capabilities to meeting these goals. Meeting our long-term goals requires definition of incremental steps that provide useful information for the interim and move us toward our long-term goals. Another over-arching theme among the three different pollutants and the different health study approaches is the need for integration among alternate exposure assessment approaches. For example, different groups may advocate exposure indicators, biomonitoring, mapping methods (GIS), modeling, environmental media

Environmental and occupational exposures as a cause of male infertility.

Science.gov (United States)

Wijesekara, G U S; Fernando, D M S; Wijerathna, S; Bandara, N

2015-06-01

To determine the association between environmental and occupational exposures, semen parameters and lead (Pb) and cadmium (Cd) levels in seminal plasma of men investigated for infertility. Data were collected from 300 men investigated for infertility using an interviewer administered questionnaire. Seminal fluid analysis and classification was done according to WHO guidelines. Positive exposure was defined as environmental or occupational exposure to agro or industrial chemicals, heavy metals and living in areas within 50 m of potential sources of pollution for three months or more. Seminal plasma lead and cadmium levels were estimated by graphite furnace atomic absorption spectrophotometry after digestion with nitric acid. The means of sperm parameters, Pb and Cd concentrations between exposed and non exposed groups were compared using t-test. Mean age was 34.8 (95% CI 34.2-35.4) years BMI was 24.3 (95% CI 23.8-24.7) kg/m2 and duration of the infertility was 45.7 (41.7-49.6) months. In this study, 54.6% were exposed to toxins through environmental or occupational sources. All sperm parameters were lower in the exposed group when compared to the non exposed. Lead and cadmium were detected in 38.3% and 23% of men respectively. The distance from the source of possible environmental or occupational exposure was negatively correlated to seminal plasma Pb (r=0.06, p>0.05) and Cd (r=0.26, pEnvironmental and occupational exposures were associated with reduced sperm count motility, viability, normal forms and detectable levels of lead and cadmium in seminal plasma.

Air Quality and Indoor Environmental Exposures: Clinical ...

Science.gov (United States)

Indoor air quality (IAQ) is a term which refers to the air quality within and around buildings and homes as it relates to the health and comfort of the occupants. Many ambient (outdoor) air pollutants readily permeate indoor spaces. Because indoor air can be considerably more polluted than ambient air, the USEPA lists poor IAQ as a major environmental concern. In the sections that follow, health effects associated with commonly encountered ambient air pollutants and indoor contaminants will be broken down by agent class. In some cases, exposure may be acute, with one or more pets (and owners) experiencing signs within a relatively short period. However, most exposures are episodic or chronic, making it difficult to definitively link poor IAQ to respiratory or other adverse health outcomes. Age or underlying immunologic, cardiac, or respiratory disease may further complicate the clinical picture, as those patients may be more sensitive to (and affected by) lower concentrations than prove problematic for healthy housemates. Because pets, like their owners, spend most of their lives indoors, we will discuss how certain home conditions can worsen indoor air quality and will briefly discuss measures to improve IAQ for owners and their pets. In this overview presentation, health effects associated with commonly encountered ambient air pollutants and indoor contaminants will be broken down by agent class. Because pets, like their owners, spend most of their lives indoo

Environmental exposure assessment in European birth cohorts: results from the ENRIECO project

Directory of Open Access Journals (Sweden)

Gehring Ulrike

2013-01-01

Full Text Available Abstract Environmental exposures during pregnancy and early life may have adverse health effects. Single birth cohort studies often lack statistical power to tease out such effects reliably. To improve the use of existing data and to facilitate collaboration among these studies, an inventory of the environmental exposure and health data in these studies was made as part of the ENRIECO (Environmental Health Risks in European Birth Cohorts project. The focus with regard to exposure was on outdoor air pollution, water contamination, allergens and biological organisms, metals, pesticides, smoking and second hand tobacco smoke (SHS, persistent organic pollutants (POPs, noise, radiation, and occupational exposures. The review lists methods and data on environmental exposures in 37 European birth cohort studies. Most data is currently available for smoking and SHS (N=37 cohorts, occupational exposures (N=33, outdoor air pollution, and allergens and microbial agents (N=27. Exposure modeling is increasingly used for long-term air pollution exposure assessment; biomonitoring is used for assessment of exposure to metals, POPs and other chemicals; and environmental monitoring for house dust mite exposure assessment. Collaborative analyses with data from several birth cohorts have already been performed successfully for outdoor air pollution, water contamination, allergens, biological contaminants, molds, POPs and SHS. Key success factors for collaborative analyses are common definitions of main exposure and health variables. Our review emphasizes that such common definitions need ideally be arrived at in the study design phase. However, careful comparison of methods used in existing studies also offers excellent opportunities for collaborative analyses. Investigators can use this review to evaluate the potential for future collaborative analyses with respect to data availability and methods used in the different cohorts and to identify potential partners

Environmental Exposure and Accelerated Testing of Rubber-to-Metal Vulcanized Bonded Assemblies

Science.gov (United States)

1974-11-01

btadiene/acrylonitrile ( NBR ) rubber -to-metat -. canized bonded assemblies at the two exposure sites are shown in Table 5. After exposure for one year...AD-A0-17 368 EN~VIRONMENTAL EXPOSURE AND ACCELERATED TESTING OF RUBBER -TO-METAL VULCANIZED BONDED ASSEMBLIES John A. WilliamsI Rock Island Arseital...COMMERCE 325116 1AD R-TR-75-013 ENViRONMENTAL EXPOSURE AND ACCELERATED TESTING OF RUBBER -TO-METAL VULCANIZED BONDED ASSEMBLIES by __ John A. Williams

Environmental lead exposure is associated with visit-to-visit systolic blood pressure variability in the US adults.

Science.gov (United States)

Faramawi, Mohammed F; Delongchamp, Robert; Lin, Yu-Sheng; Liu, Youcheng; Abouelenien, Saly; Fischbach, Lori; Jadhav, Supriya

2015-04-01

The association between environmental lead exposure and blood pressure variability, an important risk factor for cardiovascular disease, is unexplored and unknown. The objective of the study was to test the hypothesis that lead exposure is associated with blood pressure variability. American participants 17 years of age or older from National Health and Nutrition Examination Survey III were included in the analysis. Participants' blood lead concentrations expressed as micrograms per deciliter were determined. The standard deviations of visit-to-visit systolic and diastolic blood pressure were calculated to determine blood pressure variability. Multivariable regression analyses adjusted for age, gender, race, smoking and socioeconomic status were employed. The participants' mean age and mean blood lead concentration were 42.72 years and 3.44 mcg/dl, respectively. Systolic blood pressure variability was significantly associated with environmental lead exposure after adjusting for the effect of the confounders. The unadjusted and adjusted means of visit-to-visit systolic blood pressure variability and the β coefficient of lead exposure were 3.44, 3.33 mcg/dl, β coefficient = 0.07, P variability. Screening adults with fluctuating blood pressure for lead exposure could be warranted.

Healthcare utilisation prior to the diagnosis of inflammatory bowel diseases and the influence of livestock exposure: a longitudinal case-control study.

NARCIS (Netherlands)

Star, B.J. van der; Dijk, C.E. van; Zock, J.P.; Smit, L.A.M.; Baliatsas, C.; Heerderik, D.J.; Yzermans, C.J.

2018-01-01

An increased prevalence of the inflammatory bowel diseases, ulcerative colitis and Crohn's disease, was found amongst residents in a livestock dense area. We hypothesised that exposure to livestock farms might be a substantial environmental factor that contributes to the development of these

Clarifying and simplifying the management of environmental exposures under different exposure situations

International Nuclear Information System (INIS)

Pentreath, R.J.

2012-01-01

The International Commission on Radiological Protection recognises three different exposure situations: planned, existing, and emergency. In all three situations, the release of radionuclides into the natural environment leads to exposures of non-human species, as well as having the potential for exposures of the general public. Each release may therefore need separate evaluations of these two consequences in order to clarify the relevant objectives of protection, their compliance with various legal requirements, and how these objectives can be achieved. However, the need to meet more than one objective should not necessarily lead to a more complicated regulatory system. Indeed, with regard to low-level routine discharges from most nuclear plants, there would appear to be scope for simplifying the entire system, to protect both humans and biota, by using discharge consent and specified radionuclide environmental quality standards for water, soil, and air in a manner similar to that used to regulate other major, non-nuclear industries. In contrast, different objectives for humans and the environment need to be set and evaluated independently for existing exposure situations. For emergency situations, the separate consequences of different management options for humans and the environment should be made clear. Should an emergency occur, it is important to have meaningful environmental criteria in order to communicate clearly with the public at large as events unfold.

Current knowledge of environmental exposure in children during the sensitive developmental periods

Directory of Open Access Journals (Sweden)

Norma Helena Perlroth

2017-01-01

Full Text Available Objective: This study aims to identify the scientific evidence on the risks and effects of exposure to environmental contaminants in children during sensitive developmental periods. Data source: The search was performed in the Bireme database, using the terms: children's health, environmental exposure, health vulnerability, toxicity pathways and developmental disabilities in the LILACS, MEDLINE and SciELO systems. Data synthesis: Children differ from adults in their unique physiological and behavioral characteristics and the potential exposure to risks caused by several threats in the environment. Exposure to toxic agents is analyzed through toxicokinetic processes in the several systems and organs during the sensitive phases of child development. The caused effects are reflected in the increased prevalence of congenital malformations, diarrhea, asthma, cancer, endocrine and neurological disorders, among others, with negative impacts throughout adult life. Conclusion: To identify the causes and understand the mechanisms involved in the genesis of these diseases is a challenge for science, as there is still a lack of knowledge on children's susceptibility to many environmental contaminants. Prevention policies and more research on child environmental health, improving the recording and surveillance of environmental risks to children's health, should be an ongoing priority in the public health field. Resumo: Objetivo: O presente estudo busca identificar as evidências científicas sobre os riscos e efeitos da exposição de contaminantes ambientais no organismo infantil durante os períodos sensíveis de seu desenvolvimento. Fonte de dados: As pesquisas foram realizadas pelo banco de dados da Bireme, com os termos children's health, environmental exposure, health vulnerability, toxicity pathways and developmental disabilities nos sistemas LILACS, MEDLINE e SciELO. Síntese de dados: A criança difere do adulto por suas características singulares

Environmental exposures of trace elements assessed using keratinized matrices from patients with chronic kidney diseases of uncertain etiology (CKDu) in Sri Lanka.

Science.gov (United States)

Diyabalanage, Saranga; Fonseka, Sanjeewani; Dasanayake, D M S N B; Chandrajith, Rohana

2017-01-01

An alarming increase in chronic kidney disease with unknown etiology (CKDu) has recently been reported in several provinces in Sri Lanka and chronic exposures to toxic trace elements were blamed for the etiology of this disease. Keratinized matrices such as hair and nails were investigated to determine the possible link between CKDu and toxic element exposures. Elements Li, B, Al, Cr, Mn, Fe, Co, Ni, Cu, Zn, As, Se, Sr, Mo, Cd, Ba, Hg and Pb of hair and nails of patients and age that matched healthy controls were determined with Inductively Coupled Plasma Mass Spectrometry (ICP-MS). The results showed that trace element contents in the hair of patients varies in the order of Zn>Fe>Al>Mn>Cu>Ba>Sr>Ni>Pb>Cr>B>Hg>Se>Mo>Co>As>Li>Cd while Fe>Al>Zn>Ni>Cu>Mn>Cr>Ba>Sr>B>Pb>Se>Mo>Co>Hg>Li>As>Cd in nail samples. The hair As levels of 0.007-0.165μgg -1 were found in CKDu subjects. However, no significant difference was observed between cases and controls. The total Se content in hair of CKDu subjects ranged from 0.043 to 0.513μgg -1 while it was varied from 0.031 to 1.15μgg -1 in controls. Selenium in nail samples varied from 0.037μgg -1 to 4.10μgg -1 in CKDu subjects and from 0.042μgg -1 to 2.19μgg -1 in controls. This study implies that substantial proportions of Sri Lankan population are Se deficient irrespective of gender, age and occupational exposure. Although some cutaneous manifestations were observed in patient subjects, chemical analyses of hair and nails indicated that patients were not exposed to toxic levels of arsenic or the other studied toxic elements. Therefore the early suggested causative factors such as exposure to environmental As and Cd, can be ruled out. Copyright © 2016 Elsevier GmbH. All rights reserved.

Metal working fluid exposure and diseases in Switzerland.

Science.gov (United States)

Koller, Michael F; Pletscher, Claudia; Scholz, Stefan M; Schneuwly, Philippe

2016-07-01

Exposure to metal working fluids (MWF) is common in machining processes worldwide and may lead to diseases of the skin and the respiratory tract. The aim of the study was to investigate exposure and diseases due to MWF in Switzerland between 2004 and 2013. We performed descriptive statistics including determination of median and 90th percentile values of MWF concentrations listed in a database of Suva. Moreover, we clustered MWF-induced occupational diseases listed in a database from the Swiss Central Office for Statistics in Accident Insurance, and performed linear regression over time to investigate temporal course of the illnesses. The 90th percentile for MWF air concentration was 8.1 mg (aerosol + vapor)/m 3 and 0.9 mg aerosol/m 3 (inhalable fraction). One thousand two hundred and eighty skin diseases and 96 respiratory diseases were observed. This is the first investigation describing exposure to and diseases due to MWF in Switzerland over a timeframe of 10 years. In general, working conditions in the companies of this investigation were acceptable. Most measured MWF concentrations were below both the Swiss and most international occupational exposure limits of 2014. The percentage of workers declared unfit for work was 17% compared to the average of other occupational diseases (12%).

Molecular epidemiology of acute leukemia in children: causal model, interaction of three factors-susceptibility, environmental exposure and vulnerability period.

Science.gov (United States)

Mejía-Aranguré, Juan Manuel

Acute leukemias have a huge morphological, cytogenetic and molecular heterogeneity and genetic polymorphisms associated with susceptibility. Every leukemia presents causal factors associated with the development of the disease. Particularly, when three factors are present, they result in the development of acute leukemia. These phenomena are susceptibility, environmental exposure and a period that, for this model, has been called the period of vulnerability. This framework shows how the concepts of molecular epidemiology have established a reference from which it is more feasible to identify the environmental factors associated with the development of leukemia in children. Subsequently, the arguments show that only susceptible children are likely to develop leukemia once exposed to an environmental factor. For additional exposure, if the child is not susceptible to leukemia, the disease does not develop. In addition, this exposure should occur during a time window when hematopoietic cells and their environment are more vulnerable to such interaction, causing the development of leukemia. This model seeks to predict the time when the leukemia develops and attempts to give a context in which the causality of childhood leukemia should be studied. This information can influence and reduce the risk of a child developing leukemia. Copyright © 2016 Hospital Infantil de México Federico Gómez. Publicado por Masson Doyma México S.A. All rights reserved.

Environmental exposures to agrochemicals in the Sierra Nevada mountain range

Science.gov (United States)

LeNoir, J.; Aston, L.; Data, S.; Fellers, G.; McConnell, L.; Sieber, J.

2000-01-01

The release of pesticides into the environment may impact human and environmental health. Despite the need for environmental exposure data, few studies quantify exposures in urban areas and even fewer determine exposures to wildlife in remote areas. Although it is expected that concentrations in remote regions will be low, recent studies suggest that even low concentrations may have deleterious effects on wildlife. Many pesticides are known to interfere with the endocrine systems of humans and wildlife, adversely affecting growth, development, and behavior. This chapter reviews the fate and transport of pesticides applied in the Central Valley of California and quantifies their subsequent deposition into the relatively pristine Sierra Nevada Mountain Range.

Housing and health: intersection of poverty and environmental exposures.

Science.gov (United States)

Rauh, Virginia A; Landrigan, Philip J; Claudio, Luz

2008-01-01

The importance of adequate housing for the maintenance of health and well-being has long been a topic of scientific and public health policy discussion, but the links remain elusive. Here we explore the role of the residential environment in the etiology of illness (specifically asthma) and the persistence of socioeconomic health disparities. Housing conditions, shaped by social forces, affect exposure to physical and chemical "toxicants," thereby translating social adversities into individual illness and population health disparities. We discuss the mediating role of housing in determining health outcomes at multiple levels (social-structural, neighborhood, and individual family). To date, little attention has been paid by most environmental health scientists to the social-structural conditions underlying gross inequities in the distribution of toxic exposures, with even less attention to the processes whereby these social conditions may directly affect susceptibility to the toxic exposures themselves. This chapter goes beyond traditional medical and environmental science models to incorporate a range of social and physical determinants of environmental pollutions, illustrating how these conditions result in health and illness. We focus here on childhood asthma as an example of a serious public health problem that has been associated with low income, minority status, and characteristics of the home environment. We end the chapter with a discussion of the environmental justice movement and the role of housing as a potential agent of change and focus of interventions aimed to reduce the harmful effects of environmental pollutants.

Brief Report: Association of Myositis Autoantibodies, Clinical Features, and Environmental Exposures at Illness Onset With Disease Course in Juvenile Myositis.

Science.gov (United States)

Habers, G Esther A; Huber, Adam M; Mamyrova, Gulnara; Targoff, Ira N; O'Hanlon, Terrance P; Adams, Sharon; Pandey, Janardan P; Boonacker, Chantal; van Brussel, Marco; Miller, Frederick W; van Royen-Kerkhof, Annet; Rider, Lisa G

2016-03-01

To identify early factors associated with disease course in patients with juvenile idiopathic inflammatory myopathies (IIMs). Univariable and multivariable multinomial logistic regression analyses were performed in a large juvenile IIM registry (n = 365) and included demographic characteristics, early clinical features, serum muscle enzyme levels, myositis autoantibodies, environmental exposures, and immunogenetic polymorphisms. Multivariable associations with chronic or polycyclic courses compared to a monocyclic course included myositis-specific autoantibodies (multinomial odds ratio [OR] 4.2 and 2.8, respectively), myositis-associated autoantibodies (multinomial OR 4.8 and 3.5), and a documented infection within 6 months of illness onset (multinomial OR 2.5 and 4.7). A higher overall clinical symptom score at diagnosis was associated with chronic or monocyclic courses compared to a polycyclic course. Furthermore, severe illness onset was associated with a chronic course compared to monocyclic or polycyclic courses (multinomial OR 2.1 and 2.6, respectively), while anti-p155/140 autoantibodies were associated with chronic or polycyclic courses compared to a monocyclic course (multinomial OR 3.9 and 2.3, respectively). Additional univariable associations of a chronic course compared to a monocyclic course included photosensitivity, V-sign or shawl sign rashes, and cuticular overgrowth (OR 2.2-3.2). The mean ultraviolet index and highest ultraviolet index in the month before diagnosis were associated with a chronic course compared to a polycyclic course in boys (OR 1.5 and 1.3), while residing in the Northwest was less frequently associated with a chronic course (OR 0.2). Our findings indicate that myositis autoantibodies, in particular anti-p155/140, and a number of early clinical features and environmental exposures are associated with a chronic course in patients with juvenile IIM. These findings suggest that early factors, which are associated with poorer

Environmental exposure to carcinogens in northwestern Cameroon ...

African Journals Online (AJOL)

African Health Sciences ... Humans can prevent themselves from a number of workplace and environmental carcinogens. ... Methods: A structured questionnaire was used to collect information on carcinogen exposure in the workplace and environment through trained field staff from volunteers after gaining informed ...

Exposure of hospitality workers to environmental tobacco smoke

Science.gov (United States)

Bates, M; Fawcett, J; Dickson, S; Berezowski, R; Garrett, N

2002-01-01

Objective: To determine quantitatively the extent of exposure of hospitality workers to environmental tobacco smoke (ETS) exposure during the course of a work shift, and to relate these results to the customer smoking policy of the workplace. Subjects: Three categories of non-smoking workers were recruited: (1) staff from hospitality premises (bars and restaurants) that permitted smoking by customers; (2) staff from smokefree hospitality premises; and (3) government employees in smokefree workplaces. All participants met with a member of the study team before they began work, and again at the end of their shift or work day. At each meeting, participants answered questions from a standardised questionnaire and supplied a saliva sample. Main outcome measures: Saliva samples were analysed for cotinine. The difference between the first and second saliva sample cotinine concentrations indicated the degree of exposure to ETS over the course of the work shift. Results: Hospitality workers in premises allowing smoking by customers had significantly greater increases in cotinine than workers in smokefree premises. Workers in hospitality premises with no restrictions on customer smoking were more highly exposed to ETS than workers in premises permitting smoking only in designated areas. Conclusions: Overall, there was a clear association between within-shift cotinine concentration change and smoking policy. Workers in premises permitting customer smoking reported a higher prevalence of respiratory and irritation symptoms than workers in smokefree workplaces. Concentrations of salivary cotinine found in exposed workers in this study have been associated with substantial involuntary risks for cancer and heart disease. PMID:12035005

Parkinson disease and Alzheimer disease: environmental risk factors.

Science.gov (United States)

Campdelacreu, J

2014-01-01

The purpose of this review is to update and summarise available evidence on environmental risk factors that have been associated with risk of Parkinson disease (PD) or Alzheimer disease (AD) and discuss their potential mechanisms. Evidence consistently suggests that a higher risk of PD is associated with pesticides and that a higher risk of AD is associated with pesticides, hypertension and high cholesterol levels in middle age, hyperhomocysteinaemia, smoking, traumatic brain injury and depression. There is weak evidence suggesting that higher risk of PD is associated with high milk consumption in men, high iron intake, chronic anaemia and traumatic brain injury. Weak evidence also suggests that a higher risk of AD is associated with high aluminium intake through drinking water, excessive exposure to electromagnetic fields from electrical grids, DM and hyperinsulinaemia, obesity in middle age, excessive alcohol consumption and chronic anaemia. Evidence consistently suggests that a lower risk of PD is associated with hyperuricaemia, tobacco and coffee use, while a lower risk of AD is associated with moderate alcohol consumption, physical exercise, perimenopausal hormone replacement therapy and good cognitive reserve. Weak evidence suggests that lower risk of PD is associated with increased vitamin E intake, alcohol, tea, NSAIDs, and vigorous physical exercise, and that lower risk of AD is associated with the Mediterranean diet, coffee and habitual NSAID consumption. Several environmental factors contribute significantly to risk of PD and AD. Some may already be active in the early stages of life, and some may interact with other genetic factors. Population-based strategies to modify such factors could potentially result in fewer cases of PD or AD. Copyright © 2012 Sociedad Española de Neurología. Published by Elsevier Espana. All rights reserved.

Human Scalp Hair as an Indicator of Exposure to the Environmental Toxin β-N-Methylamino-l-alanine

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Simoné Downing

2017-12-01

Full Text Available Dietary or aerosol exposure to the environmental neurotoxin β-N-methylamino-l-alanine (BMAA is a putative risk factor for the development of sporadic neurodegenerative disease. There are many potential sources of BMAA in the environment, but BMAA presence and quantities are highly variable. It has been suggested that BMAA in human hair may serve as an indicator of exposure. We sought to evaluate the use of the BMAA content of human scalp hair as an indicator of exposure, as well as the correlation between specific lifestyle or dietary habits, reported as hypothesised exposure risk factors, and BMAA in hair. Scalp hair samples and questionnaires were collected from participants in a small residential village surrounding a freshwater impoundment renowned for toxic cyanobacterial blooms. Data suggested a positive correlation between hair BMAA content and consumption of shellfish, and possibly pork. No statistically significant correlations were observed between hair BMAA content and residential proximity to the water or any other variable. Hair BMAA content was highly variable, and in terms of exposure, probably reflects primarily dietary exposure. However, the BMAA content of human hair may be affected to a great extent by several other factors, and as such, should be used with caution when evaluating human BMAA exposure, or correlating exposure to neurodegenerative disease incidence.

Environmental radiation and exposure to radiation

International Nuclear Information System (INIS)

1981-02-01

Compared to 1977 the exposure to radiation of the population of the Federal Republic of Germany from both natural and artificial radiation sources has not greatly charged. The amin part of exposure to natural radiation is caused by environmental radiation and by the absorption of naturally radioactive substances into the body. Artificial exposure to radiation of the population is essentially caused by the use of ionizing rays and radioactive substances in medicine. When radioactive materials are released from nuclear facilities the exposure to radiation of the population is only very slightly increased. The real exposure to radiation of individual people can even in the worst affected places, have been at most fractions of a millirem. The exposure to radiation in the worst afected places in the area of a hard-coal power station is higher than that coming from a nuclear power station of the same capacity. The summation of all contributions to the exposure of radiation by nuclear facilities to the population led in 1978 in the Federal Republic of Germany to a genetically significant dose of clearly less than 1 millerem per year. The medium-ranged exposure to radiation by external radiation effects through professional work was in 1978 at 80 millirems. No difference to 1977. The contribution of radionuclide from the fallout coming from nuclear-weapon tests and which has been deposited in the soil, to the whole-body dose for 1978 applies the same as the genetically significant dose of the population with less than 1 millirem. (orig./HP) [de

Exposure to and risk awareness of environmental tobacco smoke ...

African Journals Online (AJOL)

Background: Many students in higher institutions tend to be exposed to environmental tobacco smoke. This work was designed to survey the exposure to environmental tobacco smoke and awareness of the dangers associated with it among undergraduates of university of Ilorin. Method: It was a cross-sectional study ...

Associations between environmental factors and hospital admissions for sickle cell disease

Science.gov (United States)

Piel, Frédéric B.; Tewari, Sanjay; Brousse, Valentine; Analitis, Antonis; Font, Anna; Menzel, Stephan; Chakravorty, Subarna; Thein, Swee Lay; Inusa, Baba; Telfer, Paul; de Montalembert, Mariane; Fuller, Gary W.; Katsouyanni, Klea; Rees, David C.

2017-01-01

sometimes confusing. This study shows that environmental factors do explain some of the variations in rates of admission to hospital with acute symptoms in sickle cell disease, but the associations are complex, and likely to be specific to different environments and the individual’s exposure to them. Furthermore, this study highlights the need for prospective studies with large numbers of patients and standardized protocols across Europe. PMID:27909222

Wind turbines and idiopathic symptoms: The confounding effect of concurrent environmental exposures.

Science.gov (United States)

Blanes-Vidal, Victoria; Schwartz, Joel

2016-01-01

Whether or not wind turbines pose a risk to human health is a matter of heated debate. Personal reactions to other environmental exposures occurring in the same settings as wind turbines may be responsible of the reported symptoms. However, these have not been accounted for in previous studies. We investigated whether there is an association between residential proximity to wind turbines and idiopathic symptoms, after controlling for personal reactions to other environmental co-exposures. We assessed wind turbine exposures in 454 residences as the distance to the closest wind turbine (Dw) and number of wind turbines turbines and agricultural odor exposure, we did not observe a significant relationship between residential proximity to wind turbines and symptoms and the parameter estimates were attenuated toward zero. Wind turbines-health associations can be confounded by personal reactions to other environmental co-exposures. Isolated associations reported in the literature may be due to confounding bias. Copyright © 2016 Elsevier Inc. All rights reserved.

Environmental radiation exposure: Regulation, monitoring, and assessment

International Nuclear Information System (INIS)

Chen, S.Y.; Yu, C.; Hong, K.J.

1991-01-01

Radioactive releases to the environment from nuclear facilities constitute a public health concern. Protecting the public from such releases can be achieved through the establishment and enforcement of regulatory standards. In the United States, numerous standards have been promulgated to regulate release control at nuclear facilities. Most recent standards are more restrictive than those in the past and require that radioactivity levels be as low as reasonably achievable (ALARA). Environmental monitoring programs and radiological dose assessment are means of ensuring compliance with regulations. Environmental monitoring programs provide empirical information on releases, such as the concentrations of released radioactivity in environmental media, while radiological dose assessment provides the analytical means of quantifying dose exposures for demonstrating compliance

Developmental Bisphenol A Exposure Modulates Immune-Related Diseases

Science.gov (United States)

Xu, Joella; Huang, Guannan; Guo, Tai L.

2016-01-01

Bisphenol A (BPA), used in polycarbonate plastics and epoxy resins, has a widespread exposure to humans. BPA is of concern for developmental exposure resulting in immunomodulation and disease development due to its ability to cross the placental barrier and presence in breast milk. BPA can use various mechanisms to modulate the immune system and affect diseases, including agonistic and antagonistic effects on many receptors (e.g., estrogen receptors), epigenetic modifications, acting on cell signaling pathways and, likely, the gut microbiome. Immune cell populations and function from the innate and adaptive immune system are altered by developmental BPA exposure, including decreased T regulatory (Treg) cells and upregulated pro- and anti-inflammatory cytokines and chemokines. Developmental BPA exposure can also contribute to the development of type 2 diabetes mellitus, allergy, asthma and mammary cancer disease by altering immune function. Multiple sclerosis and type 1 diabetes mellitus may also be exacerbated by BPA, although more research is needed. Additionally, BPA analogs, such as bisphenol S (BPS), have been increasing in use, and currently, little is known about their immune effects. Therefore, more studies should be conducted to determine if developmental exposure BPA and its analogs modulate immune responses and lead to immune-related diseases. PMID:29051427

Developmental Bisphenol A Exposure Modulates Immune-Related Diseases

Directory of Open Access Journals (Sweden)

Joella Xu

2016-09-01

Full Text Available Bisphenol A (BPA, used in polycarbonate plastics and epoxy resins, has a widespread exposure to humans. BPA is of concern for developmental exposure resulting in immunomodulation and disease development due to its ability to cross the placental barrier and presence in breast milk. BPA can use various mechanisms to modulate the immune system and affect diseases, including agonistic and antagonistic effects on many receptors (e.g., estrogen receptors, epigenetic modifications, acting on cell signaling pathways and, likely, the gut microbiome. Immune cell populations and function from the innate and adaptive immune system are altered by developmental BPA exposure, including decreased T regulatory (Treg cells and upregulated pro- and anti-inflammatory cytokines and chemokines. Developmental BPA exposure can also contribute to the development of type 2 diabetes mellitus, allergy, asthma and mammary cancer disease by altering immune function. Multiple sclerosis and type 1 diabetes mellitus may also be exacerbated by BPA, although more research is needed. Additionally, BPA analogs, such as bisphenol S (BPS, have been increasing in use, and currently, little is known about their immune effects. Therefore, more studies should be conducted to determine if developmental exposure BPA and its analogs modulate immune responses and lead to immune-related diseases.

Environmental Chemical Exposures and Autism Spectrum Disorders: A Review of the Epidemiological Evidence

Science.gov (United States)

Kalkbrenner, Amy E.; Schmidt, Rebecca J.; Penlesky, Annie C.

2016-01-01

In the past decade, the number of epidemiological publications addressing environmental chemical exposures and autism has grown tremendously. These studies are important because it is now understood that environmental factors play a larger role in causing autism than previously thought and because they address modifiable risk factors that may open up avenues for the primary prevention of the disability associated with autism. In this review, we covered studies of autism and estimates of exposure to tobacco, air pollutants, volatile organic compounds and solvents, metals (from air, occupation, diet, dental amalgams, and thimerosal-containing vaccines), pesticides, and organic endocrine-disrupting compounds such as flame retardants, non-stick chemicals, phthalates, and bisphenol A. We included studies that had individual-level data on autism, exposure measures pertaining to pregnancy or the 1st year of life, valid comparison groups, control for confounders, and adequate sample sizes. Despite the inherent error in the measurement of many of these environmental exposures, which is likely to attenuate observed associations, some environmental exposures showed associations with autism, especially traffic-related air pollutants, some metals, and several pesticides, with suggestive trends for some volatile organic compounds (e.g., methylene chloride, trichloroethylene, and styrene) and phthalates. Whether any of these play a causal role requires further study. Given the limited scope of these publications, other environmental chemicals cannot be ruled out, but have not yet been adequately studied. Future research that addresses these and additional environmental chemicals, including their most common routes of exposures, with accurate exposure measurement pertaining to several developmental windows, is essential to guide efforts for the prevention of the neurodevelopmental damage that manifests in autism symptoms. PMID:25199954

Incorporating exposure to pitch canker disease to support management decisions of Pinus pinaster Ait. in the face of climate change.

Science.gov (United States)

Serra-Varela, María Jesús; Alía, Ricardo; Pórtoles, Javier; Gonzalo, Julián; Soliño, Mario; Grivet, Delphine; Raposo, Rosa

2017-01-01

Climate change is gravely affecting forest ecosystems, resulting in large distribution shifts as well as in increasing infection diseases and biological invasions. Accordingly, forest management requires an evaluation of exposure to climate change that should integrate both its abiotic and biotic components. Here we address the implications of climate change in an emerging disease by analysing both the host species (Pinus pinaster, Maritime pine) and the pathogen's (Fusarium circinatum, pitch canker) environmental suitability i.e. estimating the host's risk of habitat loss and the disease`s future environmental range. We constrained our study area to the Spanish Iberian Peninsula, where accurate climate and pitch canker occurrence databases were available. While P. pinaster is widely distributed across the study area, the disease has only been detected in its north-central and north-western edges. We fitted species distribution models for the current distribution of the conifer and the disease. Then, these models were projected into nine Global Climate Models and two different climatic scenarios which totalled to 18 different future climate predictions representative of 2050. Based on the level of agreement among them, we created future suitability maps for the pine and for the disease independently, which were then used to assess exposure of current populations of P. pinaster to abiotic and biotic effects of climate change. Almost the entire distribution of P. pinaster in the Spanish Iberian Peninsula will be subjected to abiotic exposure likely to be driven by the predicted increase in drought events in the future. Furthermore, we detected a reduction in exposure to pitch canker that will be concentrated along the north-western edge of the study area. Setting up breeding programs is recommended in highly exposed and productive populations, while silvicultural methods and monitoring should be applied in those less productive, but still exposed, populations.

Additional Burden of Diseases Associated with Cadmium Exposure: A Case Study of Cadmium Contaminated Rice Fields in Mae Sot District, Tak Province, Thailand

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Nisarat Songprasert

2015-08-01

Full Text Available The cadmium (Cd contaminated rice fields in Mae Sot District, Tak Province, Thailand has been one of the major environmental problems in Thailand for the last 10 years. We used disability adjusted life years (DALYs to estimate the burden of disease attributable to Cd in terms of additional DALYs of Mae Sot residents. Cd exposure data included Cd and β2–microglobulin (β2-MG in urine (as an internal exposure dose and estimated cadmium daily intake (as an external exposure dose. Compared to the general Thai population, Mae Sot residents gained 10%–86% DALYs from nephrosis/nephritis, heart diseases, osteoporosis and cancer depending on their Cd exposure type and exposure level. The results for urinary Cd and dietary Cd intake varied according to the studies used for risk estimation. The ceiling effect was observed in results using dietary Cd intake because of the high Cd content in rice grown in the Mae Sot area. The results from β2-MG were more robust with additional DALYs ranging from 36%–86% for heart failure, cerebral infraction, and nephrosis/nephritis. Additional DALYs is a useful approach for assessing the magnitude of environmental Cd exposure. The Mae Sot population lost more healthy life compared to populations living in a non- or less Cd polluted area. This method should be applicable to various types of environmental contamination problems if exposure assessment information is available.

Environmental exposure assessment framework for nanoparticles in solid waste

Science.gov (United States)

Boldrin, Alessio; Hansen, Steffen Foss; Baun, Anders; Hartmann, Nanna Isabella Bloch; Astrup, Thomas Fruergaard

2014-06-01

Information related to the potential environmental exposure of engineered nanomaterials (ENMs) in the solid waste management phase is extremely scarce. In this paper, we define nanowaste as separately collected or collectable waste materials which are or contain ENMs, and we present a five-step framework for the systematic assessment of ENM exposure during nanowaste management. The framework includes deriving EOL nanoproducts and evaluating the physicochemical properties of the nanostructure, matrix properties and nanowaste treatment processes as well as transformation processes and environment releases, eventually leading to a final assessment of potential ENM exposure. The proposed framework was applied to three selected nanoproducts: nanosilver polyester textile, nanoTiO2 sunscreen lotion and carbon nanotube tennis racquets. We found that the potential global environmental exposure of ENMs associated with these three products was an estimated 0.5-143 Mg/year, which can also be characterised qualitatively as medium, medium, low, respectively. Specific challenges remain and should be subject to further research: (1) analytical techniques for the characterisation of nanowaste and its transformation during waste treatment processes, (2) mechanisms for the release of ENMs, (3) the quantification of nanowaste amounts at the regional scale, (4) a definition of acceptable limit values for exposure to ENMs from nanowaste and (5) the reporting of nanowaste generation data.

Female non-smokers' environmental tobacco smoking exposure by public transportation mode.

Science.gov (United States)

Kim, Seyoung; Park, Jin-Soo; Park, Minkyu; Kim, Yeji; Lim, Sinye; Lee, Hye-Eun

2018-01-01

This study aimed to analyze environmental tobacco smoking exposure in female nonsmokers by public transportation mode using representative data of Koreans. Data from the Second Korean National Environmental Health Survey (2012-2014) were analyzed. Urine cotinine was analyzed by public transport behavior, secondhand smoke exposure, socioeconomic factors, and health-related factors. Participants were 1322 adult females; those with the top 75% urine cotinine concentrations were assigned to the high exposure group. A logistic regression analysis was performed considering appropriate weights and stratification according to the sample design of the Second Korean National Environmental Health Survey. The geometric mean of urine cotinine concentrations differed according to public transportation modes: subway (1.66 μg/g creatinine) bus (1.77 μg/g creatinine), and taxi (1.94 μg/g creatinine). The odds ratio [OR] was calculated for the high exposure group. The OR of the taxi (2.39; 95% confidence interval, 1.00-5.69) was statistically significantly higher than the subway value (reference), and marginally significant after adjusted with life style, sociodemographic factors and involuntary smoking frequency (2.42, 95% confidence interval, 0.97-6.04). The odds ratio of passengers who mainly used taxis was marginally significantly higher than those of passengers who used subways and buses after adjusted with life style and sociodemographic factors. Implementation of supplementary measures and further studies on exposure to environmental tobacco smoking in taxis are warranted.

Potential for occupational and environmental exposure to ten carcinogens in Toronto

Energy Technology Data Exchange (ETDEWEB)

Muller, P. [ToxProbe Inc., Toronto, ON (Canada)

2002-03-01

A study was conducted in which several contaminants were assessed for their toxicological properties, potencies and occupational and environmental exposures in the city of Toronto. The contaminants included 1,3-butadiene, asbestos, benzene, cadmium, chromium, dioxins, formaldehyde, polycyclic aromatic hydrocarbons (PAHs), tetrachloroethylene, and trichloroethylene. The International Agency for Research on Cancer, the United States Environmental Protection Agency, and Health Canada have classified 9 of the 10 substances as human carcinogens. Tetrachloroethylene was classified as a probable human carcinogen. It was noted that there is no level of exposure for these chemicals that is without some risk. The information on the levels of selected contaminants in the workplace were obtained from existing literature. The sectors with the highest number of potentially exposed workers to these contaminants include the textiles industry, footwear manufacturing, wood products manufacturing, rubber products manufacturing, non-metallic mineral products manufacturing, fabricated metal products manufacturing, construction, land transport, and household services. The report discussed sources of emissions, routes and pathways of exposures and environmental levels, including outdoor air levels water concentrations, soil concentrations, and food concentrations. The report does not estimate the actual risk to Toronto residents due to environmental exposure to these carcinogens because data are insufficient to conduct such an assessment. However, some previous studies have indicated that exposure from ambient and indoor air has the greatest impact on human health. It is recommended that the city of Toronto remain up to date on the regulatory status of these chemicals. refs., tabs., figs., appendices.

Perceived Vulnerability to Disease Predicts Environmental Attitudes

Science.gov (United States)

Prokop, Pavol; Kubiatko, Milan

2014-01-01

Investigating predictors of environmental attitudes may bring valuable benefits in terms of improving public awareness about biodiversity degradation and increased pro-environmental behaviour. Here we used an evolutionary approach to study environmental attitudes based on disease-threat model. We hypothesized that people vulnerable to diseases may…

Recruitment and Retention Strategies for Environmental Exposure Studies: Lessons from the Detroit Exposure and Aerosol Research Study

Science.gov (United States)

The Environmental Protection Agency’s Detroit Exposure and Aerosol Research Study (DEARS) was a complex 3-year personal exposure study. The six geographically defined areas in the Detroit (Wayne County), Michigan, area used as study locations are ethnically diverse; the majority ...

Renal and blood pressure effects from environmental cadmium exposure in Thai children

International Nuclear Information System (INIS)

Swaddiwudhipong, Witaya; Mahasakpan, Pranee; Jeekeeree, Wanpen; Funkhiew, Thippawan; Sanjum, Rungaroon; Apiwatpaiboon, Thitikarn; Phopueng, Ittipol

2015-01-01

Very few studies have shown renal and blood pressure effects from environmental cadmium exposure in children. This population study examined associations between urinary cadmium excretion, a good biomarker of long-term cadmium exposure, and renal dysfunctions and blood pressure in environmentally exposed Thai children. Renal functions including urinary excretion of β 2 -microglobulin, calcium (early renal effects), and total protein (late renal effect), and blood pressure were measured in 594 primary school children. Of the children studied, 19.0% had urinary cadmium ≥1 μg/g creatinine. The prevalence of urinary cadmium ≥1 μg/g creatinine was significantly higher in girls and in those consuming rice grown in cadmium-contaminated areas. The geometric mean levels of urinary β 2 -microglobulin, calcium, and total protein significantly increased with increasing tertiles of urinary cadmium. The analysis did not show increased blood pressure with increasing tertiles of urinary cadmium. After adjusting for age, sex, and blood lead levels, the analysis showed significant positive associations between urinary cadmium and urinary β 2 -microglobulin and urinary calcium, but not urinary total protein nor blood pressure. Our findings provide evidence that environmental cadmium exposure can affect renal functions in children. A follow-up study is essential to assess the clinical significance and progress of renal effects in these children. - Highlights: • Few studies show renal effects from environmental cadmium exposure in children. • We report renal and blood pressure effects from cadmium exposure in Thai children. • Urinary β 2 -microglobulin and calcium increased with increasing urinary cadmium. • The study found no association between urinary cadmium levels and blood pressure. • Environmental cadmium exposure can affect renal functions in children

The role of early life environmental risk factors in Parkinson disease: what is the evidence?

Science.gov (United States)

Logroscino, Giancarlo

2005-09-01

Parkinson disease (PD) is of unknown but presumably multifactorial etiology. Neuropathologic studies and animal models show that exposure to environmental neurotoxicants can determine progressive damage in the substantia nigra many years before the onset of clinical parkinsonism. Therefore, PD, like other neurologic diseases related to aging, may be determined by exposures present in the environment early during the life span or even during pregnancy. Recent epidemiologic studies have focused on the possible role of environmental risk factors present during adult life or aging. Smoking and coffee drinking have consistently been identified to have protective associations, whereas roles of other risk factors such as pesticide and infections have been reported in some studies but not replicated in others. Both genetic inheritance and sharing of common environment in the same family explain the increased risk of PD of relatives of PD cases compared with relatives of controls in familial aggregation studies. Much evidence indicates that risk factors that have a long latency or a slow effect could be important for late-onset PD. Further epidemiologic studies are warranted in this area.

An assessment of residential exposure to environmental noise at a shipping port.

Science.gov (United States)

Murphy, Enda; King, Eoin A

2014-02-01

The World Health Organisation has recently acknowledged that contrary to the trend for other environmental stressors, noise exposure is increasing in Europe. However, little research has been conducted on environmental noise exposure to handling activity at shipping ports. This paper reports on research examining the extent of noise exposure for residents within the vicinity of Dublin Port, Ireland using the nation's largest port terminal as a proxy for port noise. In order to assess the level of exposure in the area, long-term measurements were undertaken at the most exposed residential façade for a period of 45days to determine the extent of night-time exposure that was above levels recommended by the World Health Organisation. The indicators L90, Leq and LMax were used to determine exposure levels. The results show that exposure is above night-time guideline limits set down by the WHO, above Irish levels for the assessment of noise mitigation and highlight the extent to which port noise can be a significant environmental stressor. The research also investigated the extent of low-frequency noise (which is associated with greater health issues) from night-time port handling activity and found a significant low-frequency component indicating the negative health issues that might arise from port noise exposure more generally. We also undertook semi-structured interviews with residents to qualitatively assess the self-reported impact of prolonged night-time noise exposure for local residents. Copyright © 2013 Elsevier Ltd. All rights reserved.

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.

Epigenetic: a molecular link between testicular cancer and environmental exposures.

Science.gov (United States)

Vega, Aurelie; Baptissart, Marine; Caira, Françoise; Brugnon, Florence; Lobaccaro, Jean-Marc A; Volle, David H

2012-01-01

In the last decades, studies in rodents have highlighted links between in utero and/or neonatal exposures to molecules that alter endocrine functions and the development of genital tract abnormalities, such as cryptorchidism, hypospadias, and impaired spermatogenesis. Most of these molecules, called endocrine disrupters exert estrogenic and/or antiandrogenic activities. These data led to the hypothesis of the testicular dysgenesis syndrome which postulates that these disorders are one clinical entity and are linked by epidemiological and pathophysiological relations. Furthermore, infertility has been stated as a risk factor for testicular cancer (TC). The incidence of TC has been increasing over the past decade. Most of testicular germ cell cancers develop through a pre-invasive carcinoma in situ from fetal germ cells (primordial germ cell or gonocyte). During their development, fetal germ cells undergo epigenetic modifications. Interestingly, several lines of evidence have shown that gene regulation through epigenetic mechanisms (DNA and histone modifications) plays an important role in normal development as well as in various diseases, including TC. Here we will review chromatin modifications which can affect testicular physiology leading to the development of TC; and highlight potential molecular pathways involved in these alterations in the context of environmental exposures.

Cognitive Function Related to Environmental Exposure to Manganese

Science.gov (United States)

Background: The towns of Marietta and East Liverpool (EL), Ohio, have been identified as having elevated manganese (Mn) in air due to industrial pollution. Objectives: To evaluate relationships between environmental Mn (Mn-air) exposure and distance from the source and cognitive...

Early Life Stress, Air Pollution, Inflammation, and Disease: An Integrative Review and Immunologic Model of Social-Environmental Adversity and Lifespan Health.

Science.gov (United States)

Olvera Alvarez, Hector A; Kubzansky, Laura D; Campen, Matthew J; Slavich, George M

2018-06-03

Socially disadvantaged individuals are at greater risk for simultaneously being exposed to adverse social and environmental conditions. Although the mechanisms underlying joint effects remain unclear, one hypothesis is that toxic social and environmental exposures have synergistic effects on inflammatory processes that underlie the development of chronic diseases, including cardiovascular disease, diabetes, depression, and certain types of cancer. In the present review, we examine how exposure to two risk factors that commonly occur with social disadvantage-early life stress and air pollution-affect health. Specifically, we identify neuroimmunologic pathways that could link early life stress, inflammation, air pollution, and poor health, and use this information to propose an integrated, multi-level model that describes how these factors may interact and cause health disparity across individuals based on social disadvantage. This model highlights the importance of interdisciplinary research considering multiple exposures across domains and the potential for synergistic, cross-domain effects on health, and may help identify factors that could potentially be targeted to reduce disease risk and improve lifespan health. Copyright © 2018. Published by Elsevier Ltd.

The Impact of Environmental Mn Exposure on Insect Biology

Directory of Open Access Journals (Sweden)

Yehuda Ben-Shahar

2018-03-01

Full Text Available Manganese (Mn is an essential trace element that acts as a metal co-factor in diverse biochemical and cellular functions. However, chronic environmental exposure to high levels of Mn is a well-established risk factor for the etiology of severe, atypical parkinsonian syndrome (manganism via its accumulation in the basal ganglia, pallidum, and striatum brain regions, which is often associated with abnormal dopamine, GABA, and glutamate neural signaling. Recent studies have indicated that chronic Mn exposure at levels that are below the risk for manganism can still cause behavioral, cognitive, and motor dysfunctions via poorly understood mechanisms at the molecular and cellular levels. Furthermore, in spite of significant advances in understanding Mn-induced behavioral and neuronal pathologies, available data are primarily for human and rodents. In contrast, the possible impact of environmental Mn exposure on brain functions and behavior of other animal species, especially insects and other invertebrates, remains mostly unknown both in the laboratory and natural habitats. Yet, the effects of environmental exposure to metals such as Mn on insect development, physiology, and behavior could also have major indirect impacts on human health via the long-term disruptions of food webs, as well as direct impact on the economy because of the important role insects play in crop pollination. Indeed, laboratory and field studies indicate that chronic exposures to metals such as Mn, even at levels that are below what is currently considered toxic, affect the dopaminergic signaling pathway in the insect brain, and have a major impact on the behavior of insects, including foraging activity of important pollinators such as the honey bee. Together, these studies highlight the need for a better understanding of the neuronal, molecular, and genetic processes that underlie the toxicity of Mn and other metal pollutants in diverse animal species, including insects.

The Relationship between Environmental Tobacco Smoke Exposure and Cardiovascular Disease and the Potential Modifying Effect of Diet in a Prospective Cohort among American Indians: The Strong Heart Study

Directory of Open Access Journals (Sweden)

Sarah Rajkumar

2017-05-01

Full Text Available American Indians experience high rates of cardiovascular diseases (CVD. Environmental tobacco smoke (ETS has been linked to CVD, possibly due to pro-inflammatory and oxidative stress pathways. We examined the relationship between self-reported exposure to ETS and fatal and nonfatal CVD incidence using Cox proportional hazards models among 1843 non-smoking American Indians participating in the Strong Heart Study. We also evaluated potential modifying effects of several dietary nutrients high in anti-inflammatory and anti-oxidant properties with ETS exposure on fatal and nonfatal CVD by creating interaction terms between ETS exposure and the dietary variable. Participants exposed to ETS had a higher hazard (hazard ratio: 1.22; 95% confidence interval, 1.03 to 1.44 for developing CVD compared to persons not exposed. Interaction analyses suggested stronger effects of ETS on CVD incidence among those consuming diets lower in vitamin E as compared to those consuming higher amounts, particularly on the additive scale. Additional research is recommended to clarify whether public health prevention strategies should simultaneously target reductions in ETS exposures and improvements in diets that may exceed the expected benefits of targeting these risk factors separately.

Prion Disease: Learn the Facts. Avoid Exposure.

Centers for Disease Control (CDC) Podcasts

2011-05-23

This podcast discusses prion diseases and the risk of exposure associated with some common activities.  Created: 5/23/2011 by National Center for Emerging and Zoonotic Infectious Diseases (NCEZID).   Date Released: 5/23/2011.

Environmental Factors Influencing White-Tailed Deer (Odocoileus virginianus Exposure to Livestock Pathogens in Wisconsin.

Directory of Open Access Journals (Sweden)

Shelli Dubay

Full Text Available White-tailed deer (Odocoileus virginianus are commonly exposed to disease agents that affect livestock but environmental factors that predispose deer to exposure are unknown for many pathogens. We trapped deer during winter months on two study areas (Northern Forest and Eastern Farmland in Wisconsin from 2010 to 2013. Deer were tested for exposure to six serovars of Leptospira interrogans (grippotyphosa, icterohaemorrhagiae, canicola, bratislava, pomona, and hardjo, bovine viral diarrhea virus (BVDV-1 and BVDV-2, infectious bovine rhinotracheitis virus (IBR, and parainfluenza 3 virus (PI3. We used logistic regression to model potential intrinsic (e.g., age, sex and extrinsic (e.g., land type, study site, year, exposure to multiple pathogens variables we considered biologically meaningful to exposure of deer to livestock pathogens. Deer sampled in 2010-2011 did not demonstrate exposure to BVDV, so we did not test for BVDV in subsequent years. Deer had evidence of exposure to PI3 (24.7%, IBR (7.9%, Leptospira interrogans serovar pomona (11.7%, L. i. bratislava (1.0%, L. i. grippotyphosa (2.5% and L. i. hardjo (0.3%. Deer did not demonstrate exposure to L. interrogans serovars canicola and icterohaemorrhagiae. For PI3, we found that capture site and year influenced exposure. Fawns (n = 119 were not exposed to L. i. pomona, but land type was an important predictor of exposure to L. i. pomona for older deer. Our results serve as baseline exposure levels of Wisconsin white-tailed deer to livestock pathogens, and helped to identify important factors that explain deer exposure to livestock pathogens.

Renal and blood pressure effects from environmental cadmium exposure in Thai children

Energy Technology Data Exchange (ETDEWEB)

Swaddiwudhipong, Witaya, E-mail: swaddi@hotmail.com [Department of Community and Social Medicine, Mae Sot General Hospital, Tak 63110 (Thailand); Mahasakpan, Pranee [Department of Community and Social Medicine, Mae Sot General Hospital, Tak 63110 (Thailand); Jeekeeree, Wanpen [Department of Medical Technology, Mae Sot General Hospital, Tak 63110 (Thailand); Funkhiew, Thippawan [Department of Community and Social Medicine, Mae Sot General Hospital, Tak 63110 (Thailand); Sanjum, Rungaroon; Apiwatpaiboon, Thitikarn [Department of Medical Technology, Mae Sot General Hospital, Tak 63110 (Thailand); Phopueng, Ittipol [Department of Community and Social Medicine, Mae Sot General Hospital, Tak 63110 (Thailand)

2015-01-15

Very few studies have shown renal and blood pressure effects from environmental cadmium exposure in children. This population study examined associations between urinary cadmium excretion, a good biomarker of long-term cadmium exposure, and renal dysfunctions and blood pressure in environmentally exposed Thai children. Renal functions including urinary excretion of β{sub 2}-microglobulin, calcium (early renal effects), and total protein (late renal effect), and blood pressure were measured in 594 primary school children. Of the children studied, 19.0% had urinary cadmium ≥1 μg/g creatinine. The prevalence of urinary cadmium ≥1 μg/g creatinine was significantly higher in girls and in those consuming rice grown in cadmium-contaminated areas. The geometric mean levels of urinary β{sub 2}-microglobulin, calcium, and total protein significantly increased with increasing tertiles of urinary cadmium. The analysis did not show increased blood pressure with increasing tertiles of urinary cadmium. After adjusting for age, sex, and blood lead levels, the analysis showed significant positive associations between urinary cadmium and urinary β{sub 2}-microglobulin and urinary calcium, but not urinary total protein nor blood pressure. Our findings provide evidence that environmental cadmium exposure can affect renal functions in children. A follow-up study is essential to assess the clinical significance and progress of renal effects in these children. - Highlights: • Few studies show renal effects from environmental cadmium exposure in children. • We report renal and blood pressure effects from cadmium exposure in Thai children. • Urinary β{sub 2}-microglobulin and calcium increased with increasing urinary cadmium. • The study found no association between urinary cadmium levels and blood pressure. • Environmental cadmium exposure can affect renal functions in children.

Diversity of allergen exposure: implications for the efficacy of environmental control.

Science.gov (United States)

Segundo, Gesmar Rodrigues Silva; Sopelete, Mônica Camargo; Terra, Sílvia Azevedo; Pereira, Fernando Lourenço; Justino, Caroline Morais; Silva, Deise Aparecida de Oliveira; Taketomi, Ernesto Akio

2009-01-01

The prevalence of allergic diseases such as asthma, rhinitis, allergic conjunctivitis and atopic dermatitis has increased in the last decades. The relationship between allergen exposure, atopic sensitization and development of allergic diseases is widely described in the literature. To evaluate measures for reducing allergen exposure as part of the treatment of allergic diseases. An analysis was made of previous studies on allergen exposure done with a similar methodology in the central region of Brazil; the study included homes, hotels, cinemas, cars, taxis, buses and scholar transportation. High levels of Der p 1 and Der f 1 mite allergens were found in a large proportion of the sample in most of the environments included in those studies; there were higher levels of pet allergens in cars and school transportation vehicles. The diversity of allergen exposure demonstrates the need for education about allergic diseases for patients and their families, as well as measures of reducing allergens in homes. This should be part of a global strategy of the management of allergic diseases, given that individuals live in society, not only in their houses.

Environmental exposures as a risk factor for fibrolamellar carcinoma.

Science.gov (United States)

Graham, Rondell P; Craig, John R; Jin, Long; Oliveira, Andre M; Bergquist, John R; Truty, Mark J; Mounajjed, Taofic; Greipp, Patricia T; Torbenson, Michael S

2017-06-01

Fibrolamellar carcinoma was first described in 1956. Subsequent large studies failed to identify cases before 1939 (the start of the World War II). This finding, combined with the presence of aryl hydrocarbon receptors on the tumor cells, have suggested that fibrolamellar carcinomas may be caused by environmental exposures that are new since World War II. To investigate this possibility, the surgical pathology files before 1939 were reviewed for hepatocellular carcinomas resected in young individuals. Two cases of fibrolamellar carcinoma were identified, from 1915 to 1924. The diagnosis of fibrolamellar carcinoma was confirmed at the histologic, ultrastructural and proteomic levels. These two fibrolamellar carcinoma cases clarify a key aspect of fibrolamellar carcinoma biology, reducing the likelihood that these tumors result exclusively from post World War II environmental exposures.

Environmental Influences on the Epigenome: Exposure- Associated DNA Methylation in Human Populations.

Science.gov (United States)

Martin, Elizabeth M; Fry, Rebecca C

2018-04-01

DNA methylation is the most well studied of the epigenetic regulators in relation to environmental exposures. To date, numerous studies have detailed the manner by which DNA methylation is influenced by the environment, resulting in altered global and gene-specific DNA methylation. These studies have focused on prenatal, early-life, and adult exposure scenarios. The present review summarizes currently available literature that demonstrates a relationship between DNA methylation and environmental exposures. It includes studies on aflatoxin B 1 , air pollution, arsenic, bisphenol A, cadmium, chromium, lead, mercury, polycyclic aromatic hydrocarbons, persistent organic pollutants, tobacco smoke, and nutritional factors. It also addresses gaps in the literature and future directions for research. These gaps include studies of mixtures, sexual dimorphisms with respect to environmentally associated methylation changes, tissue specificity, and temporal stability of the methylation marks.

Biomass fuel exposure and respiratory diseases in India.

Science.gov (United States)

Prasad, Rajendra; Singh, Abhijeet; Garg, Rajiv; Giridhar, Giridhar B

2012-10-01

One half of the world's population relies on biomass fuel as the primary source of domestic energy. Biomass fuel exposure causes a high degree of morbidity and mortality in humans. This is especially true in the context of developing countries, which account for 99% of the world's biomass fuel use. Biomass fuel consists of fire wood, dung cakes, agricultural crop residues such as straw, grass, and shrubs, coal fuels and kerosene. Together, they supply 75% of the domestic energy in India. An estimated three-quarters of Indian households use biomass fuel as the primary means for domestic cooking. Ninety percent of rural households and 32% of urban households cook their meals on a biomass stove. There are wide variations between the rural and urban households regarding the specific type of biomass fuel used. Globally, almost 2 million deaths per year are attributable to solid fuel use, with more than 99% of these occurring in developing countries. Biomass fuel accounts for 5-6% of the national burden of disease. Burning biomass fuels emits toxic fumes into the air that consist of small solid particles, carbon monoxide, polyorganic and polyaromatic hydrocarbons, and formaldehyde. Exposure to biomass fuels has been found to be associated with many respiratory diseases such as acute lower respiratory infections, chronic obstructive pulmonary disease, lung cancer, pulmonary tuberculosis, and asthma. Biomass fuel exposure is closely related to the burden of disease in India. Hopes are that future studies will examine the morbidity associated with biomass exposure and seek to prevent it. Concerted efforts to improve stove design and transition to high-efficiency low-emission fuels may reduce respiratory disease associated with biomass fuel exposure.

Environmental radioactivity and radiation exposure in 2013; Umweltradioaktivitaet und Strahlenbelastung im Jahr 2013

Energy Technology Data Exchange (ETDEWEB)

NONE

2013-07-01

The report on the environmental radioactivity and radiation exposure in 2013 covers the natural radiation exposure due to radon, food, cosmic and terrestric radiation and the radiation exposure due to nuclear medicine nuclear facilities, mining, industry household and fallout. Special issues are the occupational radiation exposure the medical radiation exposure and the exposure to non-ionizing radiation.

Exposure to environmental tobacco smoke among adolescents in ...

African Journals Online (AJOL)

Objective: To estimate the prevalence of environmental tobacco smoke (ETS) inside or outside the home among school-going adolescents in Kampala, Uganda. Methods: Data from the Kampala Global Youth Tobacco Survey (GYTS) of 2002 was used. We estimated frequencies and proportions of self reported exposure to ...

Contaminant mixtures and repoductive health: Developmental toxicity effects in rats after mixed exposure to environmentally relevant endocrine disrupting chemicals, with focus on effects in females

DEFF Research Database (Denmark)

Jacobsen, Pernille Rosenskjold; Christiansen, Sofie; Hass, Ulla

proposed that a similar syndrome, called the ovarian dysgenesis syndrome (ODS), exists for females. This syndrome encompasses alterations in reproductive development caused by chemical exposure in sensitive windows of development that may result in fecundity impairments, gravid diseases, gynecological...... disorders or later onset adult diseases. However, experimental evidence on the effects of developmental exposure to environmentally relevant endocrine disrupting chemicals in females has been missing attention. Since chemical exposure can affect female reproductive development it is important to investigate......, mixtures were modeled based on high end human intakes, and the project involved two developmental mixture studies in rats, called Contamed 1 and 2. In these studies 13 chemicals where data on in vivo endocrine disrupting effects and information on human exposures was available, were selected. The tested...

Exposure to modern, widespread environmental endocrine disrupting chemicals and their effect on the reproductive potential of women: an overview of current epidemiological evidence.

Science.gov (United States)

Karwacka, Anetta; Zamkowska, Dorota; Radwan, Michał; Jurewicz, Joanna

2017-07-31

Growing evidence indicates that exposure to widespread, environmental contaminants called endocrine disruptors (EDCs) negatively affects animal and human reproductive health and has been linked to several diseases including infertility. This review aims to evaluate the impact of environmental exposure to endocrine disrupting chemicals [phthalates, parabens, triclosan, bisphenol A (BPA), organochlorine (PCBs) and perfluorinated (PFCs) compounds] on the reproductive potential among women, by reviewing most recently published literature. Epidemiological studies focusing on EDCs exposure and reproductive potential among women for the last 16 years were identified by a search of the PUBMED, MEDLINE, EBSCO and TOXNET literature databases. The results of the presented studies show that exposure to EDCs impacts the reproductive potential in women, measured by ovarian reserve and by assisted reproductive technology outcomes. Exposure to environmental endocrine disrupting chemicals decrease: (i) oestradiol levels (BPA); (ii) anti-Müllerian hormone concentrations (PCBs); (iii) antral follicle count (BPA, parabens, phthalates); (iv) oocyte quality (BPA, triclosan, phthalates, PCBs); (v) fertilization rate (PFCs, PCBs); (vi) implantation (BPA, phthalates, PCBs); (vii) embryo quality (triclosan, PCBs, BPA); (viii) rate of clinical pregnancy and live births (parabens, phthalates). The studies were mostly well-designed and used prospective cohorts with the exposure assessment based on the biomarker of exposure. Considering the suggested health effects, more epidemiological data is urgently needed to confirm the presented findings.

Clinical Relevance of Environmental Factors in the Pathogenesis of Autoimmune Thyroid Disease

Directory of Open Access Journals (Sweden)

Wilmar M. Wiersinga

2016-06-01

Full Text Available Genetic factors contribute for about 70% to 80% and environmental factors for about 20% to 30% to the pathogenesis of autoimmune thyroid disease (AITD. Relatives of AITD patients carry a risk to contract AITD themselves. The 5-year risk can be quantified by the so-called Thyroid Events Amsterdam-score, based on serum thyroid-stimulating hormone, thyroid peroxidase (TPO-antibodies and family history. Subjects at risk may ask what they can do to prevent development of AITD. This review summarizes what is known about modulation of exposure to environmental factors in terms of AITD prevention. To stop smoking decreases the risk on Graves disease but increases the risk on Hashimoto disease. Moderate alcohol intake provides some protection against both Graves and Hashimoto disease. Low selenium intake is associated with a higher prevalence of thyroid autoimmunity, but evidence that selenium supplementation may lower TPO antibodies and prevent subclinical hypothyroidism remains inconclusive. Low serum vitamin D levels are associated with a higher prevalence of TPO antibodies, but intervention studies with extra vitamin D have not been done yet. Stress may provoke Graves hyperthyroidism but not Hashimoto thyroiditis. Estrogen use have been linked to a lower prevalence of Graves disease. The postpartum period is associated with an increased risk of AITD. Taking together, preventive interventions to diminish the risk of AITD are few, not always feasible, and probably of limited efficacy.

Measuring and modeling exposure from environmental radiation on tidal flats

International Nuclear Information System (INIS)

Gould, T.J.; Hess, C.T.

2005-01-01

To examine the shielding effects of the tide cycle, a high pressure ion chamber was used to measure the exposure rate from environmental radiation on tidal flats. A theoretical model is derived to predict the behavior of exposure rate as a function of time for a detector placed one meter above ground on a tidal flat. The numerical integration involved in this derivation results in an empirical formula which implies exposure rate ∝tan-1(sint). We propose that calculating the total exposure incurred on a tidal flat requires measurements of only the slope of the tidal flat and the exposure rate when no shielding occurs. Experimental results are consistent with the model

Somatic mutation in peripheral blood lymphocytes among Metro Manila residents: indicator of exposure to environmental pollution

International Nuclear Information System (INIS)

Yulo-Nazarea, M.T.; Cobar, M.L.C.; Endriga, M.A.; Sta Maria, E.J.; Nato, A.Q.; Eduardo, J.; Dy, R.

1994-01-01

Metro Manila is ranked as one of the world's most polluted cities where air quality levels are 2-3 times higher than the levels set by WHO. Development of diseases could be alleviated if early warning signs as occurrence of gene mutations are detected early enough. The adapted hypoxanthine guanine phosphoribosyl transferase (HGPRT) mutation assay measures the degree of mutation on the HGPRT gene and allows rapid evaluation of the occurrence of mutation in an individual exposed to radiation or mutagens within six months after exposure. The objective of the project is to (1) assay exposure of Metro Manila residents exposed to environmental pollution, (2) determine population groups significantly affected by pollutants and (3) construct an environmental baseline HGPRT mutation data bank specific to area in Metro Manila. A composite table of personal information of donors against mutation index in two barangays in Venezuela is presented. About 30% of the total samples are shown to have mutation index greater than 0.5. So far, the data show a slightly higher mutation rate among donors who are smokers with more than 5 hours outdoor exposure to pollutants per day than the corresponding class of non-smokers. (author). 5 refs.; 5 tabs

The Environmental Protection Agency's Community-Focused Exposure and Risk Screening Tool (C-FERST) and its potential use for environmental justice efforts.

Science.gov (United States)

Zartarian, Valerie G; Schultz, Bradley D; Barzyk, Timothy M; Smuts, Marybeth; Hammond, Davyda M; Medina-Vera, Myriam; Geller, Andrew M

2011-12-01

Our primary objective was to provide higher quality, more accessible science to address challenges of characterizing local-scale exposures and risks for enhanced community-based assessments and environmental decision-making. After identifying community needs, priority environmental issues, and current tools, we designed and populated the Community-Focused Exposure and Risk Screening Tool (C-FERST) in collaboration with stakeholders, following a set of defined principles, and considered it in the context of environmental justice. C-FERST is a geographic information system and resource access Web tool under development for supporting multimedia community assessments. Community-level exposure and risk research is being conducted to address specific local issues through case studies. C-FERST can be applied to support environmental justice efforts. It incorporates research to develop community-level data and modeled estimates for priority environmental issues, and other relevant information identified by communities. Initial case studies are under way to refine and test the tool to expand its applicability and transferability. Opportunities exist for scientists to address the many research needs in characterizing local cumulative exposures and risks and for community partners to apply and refine C-FERST.

Epigenetic: a molecular link between testicular cancer and environmental exposures?

Directory of Open Access Journals (Sweden)

Aurelie eVega

2012-11-01

Full Text Available In the last decades, studies in rodents have highlighted links between in utero and/or neonatal exposures to molecules that alter endocrine functions and the development of genital tract abnormalities, such as cryptorchidism, hypospadias, and impaired spermatogenesis. Most of these molecules, called endocrine disrupters (EDs exert estrogenic and/or antiandrogenic activities. These data led to the hypothesis of the Testicular Dysgenesis Syndrome which postulates that these disorders are one clinical entity and are linked by epidemiological and pathophysiological relations. Futhermore, infertility has been stated as a risk factor for testicular cancer. The incidence of testicular cancer has been increasing over the past decades. Most of testicular germ cell cancers develop through a pre-invasive carcinoma in situ (CIS from fetal germ cells (primordial germ cell or gonocyte. During their development, fetal germ cells undergo epigenetic modifications. Interestingly, several lines of evidence have shown that gene regulation through epigenetic mechanisms (DNA and histone modifications plays an important role in normal development as well as in various diseases, including testicular cancer.Here we will review chromatin modifications which can affect testicular physiology leading to the development of testicular cancer; and highlight potential molecular pathways involved in these alterations in the context of environmental exposures.

The role of gene-environment interplay in occupational and environmental diseases: current concepts and knowledge gaps.

Science.gov (United States)

Kwo, Elizabeth; Christiani, David

2017-03-01

The interplay between genetic susceptibilities and environmental exposures in the pathogenesis of a variety of diseases is an area of increased scientific, epidemiologic, and social interest. Given the variation in methodologies used in the field, this review aims to create a framework to help understand occupational exposures as they currently exist and provide a foundation for future inquiries into the biological mechanisms of the gene-environment interactions. Understanding of this complex interplay will be important in the context of occupational health, given the public health concerns surrounding a variety of occupational exposures. Studies found evidence that suggest genetics influence the progression of disease postberyllium exposure through genetically encoded major histocompatibility complex, class II, DP alpha 2 (HLA-DP2)-peptide complexes as it relates to T-helper cells. This was characterized at the molecular level by the accumulation of Be-responsive CD4 T cells in the lung, which resulted in posttranslational change in the HLA-DPB1 complex. These studies provide important evidence of gene-environment association, and many provide insights into specific pathogenic mechanisms. The following includes a review of the literature regarding gene-environment associations with a focus on pulmonary diseases as they relate to the workplace.

Agent Orange exposure and prevalence of self-reported diseases in Korean Vietnam veterans.

Science.gov (United States)

Yi, Sang-Wook; Ohrr, Heechoul; Hong, Jae-Seok; Yi, Jee-Jeon

2013-09-01

The aim of this study was to evaluate the association between Agent Orange exposure and self-reported diseases in Korean Vietnam veterans. A postal survey of 114 562 Vietnam veterans was conducted. The perceived exposure to Agent Orange was assessed by a 6-item questionnaire. Two proximity-based Agent Orange exposure indices were constructed using division/brigade-level and battalion/company-level unit information. Adjusted odds ratios (ORs) for age and other confounders were calculated using a logistic regression model. The prevalence of all self-reported diseases showed monotonically increasing trends as the levels of perceived self-reported exposure increased. The ORs for colon cancer (OR, 1.13), leukemia (OR, 1.56), hypertension (OR, 1.03), peripheral vasculopathy (OR, 1.07), enterocolitis (OR, 1.07), peripheral neuropathy (OR, 1.07), multiple nerve palsy (OR, 1.14), multiple sclerosis (OR, 1.24), skin diseases (OR, 1.05), psychotic diseases (OR, 1.07) and lipidemia (OR, 1.05) were significantly elevated for the high exposure group in the division/brigade-level proximity-based exposure analysis, compared to the low exposure group. The ORs for cerebral infarction (OR, 1.08), chronic bronchitis (OR, 1.05), multiple nerve palsy (OR, 1.07), multiple sclerosis (OR, 1.16), skin diseases (OR, 1.05), and lipidemia (OR, 1.05) were significantly elevated for the high exposure group in the battalion/company-level analysis. Korean Vietnam veterans with high exposure to Agent Orange experienced a higher prevalence of several self-reported chronic diseases compared to those with low exposure by proximity-based exposure assessment. The strong positive associations between perceived self-reported exposure and all self-reported diseases should be evaluated with discretion because the likelihood of reporting diseases was directly related to the perceived intensity of Agent Orange exposure.

Information by the German Federal Government. Environmental radioactivity and radiation exposure in 2010

International Nuclear Information System (INIS)

2010-01-01

The information by the German Federal Government on the environmental radioactivity and radiation exposure in 2010 includes five chapters. (I) Natural radiation exposure: radiation sources, contributions from cosmic radiation, contaminated construction materials, food and drinking water, and radon, evaluation of the different components of natural radiation exposure. (II) Civilization caused radiation exposure: nuclear power plants, research centers, nuclear fuel processing plants, other nuclear facilities (interim storage facilities, repositories); summarizing evaluation for nuclear facilities; environmental radioactivity due to mining; radioactive materials in research, technology and households; industrial and mining residues; fall-out as a consequence of the Chernobyl reactor accident and nuclear weapon testing. (III) Occupational radiation exposure: civil radiation sources, natural radiation sources, special events. (IV) Medical radiation exposure; X-ray diagnostics; nuclear medicine; radiotherapy using ionizing radiation; radiotherapy using open radioactive materials; evaluation of radiotherapy. (V) Non-ionizing radiation: electromagnetic fields; optical radiation; certification of solaria.

Developmental effects of exposures to environmental factors: the Polish Mother and Child Cohort Study.

Science.gov (United States)

Polanska, Kinga; Hanke, Wojciech; Sobala, Wojciech; Trzcinka-Ochocka, Malgorzata; Ligocka, Danuta; Brzeznicki, Slawomir; Strugala-Stawik, Halina; Magnus, Per

2013-01-01

This paper estimates the effects of exposure to environmental factors, including lead, mercury, environmental tobacco smoke (ETS), and polycyclic aromatic hydrocarbons (PAH), on child psychomotor development. The study population consists of mother-child pairs in the Polish Mother and Child Cohort Study. Prenatal and postnatal exposure to environmental factors was determined from biomarker measurements as follows: for lead exposure--cord blood lead level, for mercury--maternal hair mercury level, for ETS--cotinine level in saliva and urine, and for PAH--1-hydroxypyrene (1-HP) in urine. At the age of 12 (406 subjects) and 24 months (198 subjects) children were assessed using Bayley Scales of Infant and Toddler Development. There were no statistically significant effects of prenatal exposure to mercury or 1-HP on child psychomotor development. After adjusting for potential confounders, adverse effects of prenatal exposure to ETS on motor development ( β = -2.6; P = 0.02) and postnatal exposure to ETS on cognitive ( β = -0.2; P = 0.05) and motor functions ( β = -0.5; P = 0.01) were found. The adverse effect of prenatal lead exposure on cognitive score was of borderline significance ( β = -6.2; P = 0.06). The study underscores the importance of policies and public health interventions that aim to reduce prenatal and postnatal exposure to lead and ETS.

Problems in evaluating health effects of occupational and environmental exposures

International Nuclear Information System (INIS)

Gilbert, E.S.

1981-01-01

The assessment of health effects from low-level exposure to radiation is a matter of considerable controversy. Existing standards for exposure are based primarily on estimates of health effects obtained by extrapolation from effects of high-level exposures such as those experienced at Hiroshima and Nagasaki. Occupational and environmental exposures provide one source of data for this task. A number of studies of populations exposed in this manner have attracted recent attention. Because of the size of most of the groups and the magnitude of the exposures received, the amount that can be learned from such populations is severely limited. A number of the problems involved in analyzing and interpreting such data are addressed. Many of these problems are illustrated by a current study of the effects on mortality of occupational exposure to radiation at the Hanford plant

Genome-Wide Locations of Potential Epimutations Associated with Environmentally Induced Epigenetic Transgenerational Inheritance of Disease Using a Sequential Machine Learning Prediction Approach

OpenAIRE

Haque, M. Muksitul; Holder, Lawrence B.; Skinner, Michael K.

2015-01-01

Environmentally induced epigenetic transgenerational inheritance of disease and phenotypic variation involves germline transmitted epimutations. The primary epimutations identified involve altered differential DNA methylation regions (DMRs). Different environmental toxicants have been shown to promote exposure (i.e., toxicant) specific signatures of germline epimutations. Analysis of genomic features associated with these epimutations identified low-density CpG regions (

Zebrafish in Toxicology and Environmental Health.

Science.gov (United States)

Bambino, Kathryn; Chu, Jaime

2017-01-01

As manufacturing processes and development of new synthetic compounds increase to keep pace with the expanding global demand, environmental health, and the effects of toxicant exposure are emerging as critical public health concerns. Additionally, chemicals that naturally occur in the environment, such as metals, have profound effects on human and animal health. Many of these compounds are in the news: lead, arsenic, and endocrine disruptors such as bisphenol A have all been widely publicized as causing disease or damage to humans and wildlife in recent years. Despite the widespread appreciation that environmental toxins can be harmful, there is limited understanding of how many toxins cause disease. Zebrafish are at the forefront of toxicology research; this system has been widely used as a tool to detect toxins in water samples and to investigate the mechanisms of action of environmental toxins and their related diseases. The benefits of zebrafish for studying vertebrate development are equally useful for studying teratogens. Here, we review how zebrafish are being used both to detect the presence of some toxins as well as to identify how environmental exposures affect human health and disease. We focus on areas where zebrafish have been most effectively used in ecotoxicology and in environmental health, including investigation of exposures to endocrine disruptors, industrial waste byproducts, and arsenic. © 2017 Elsevier Inc. All rights reserved.

Modeling approaches for characterizing and evaluating environmental exposure to engineered nanomaterials in support of risk-based decision making.

Science.gov (United States)

Hendren, Christine Ogilvie; Lowry, Michael; Grieger, Khara D; Money, Eric S; Johnston, John M; Wiesner, Mark R; Beaulieu, Stephen M

2013-02-05

As the use of engineered nanomaterials becomes more prevalent, the likelihood of unintended exposure to these materials also increases. Given the current scarcity of experimental data regarding fate, transport, and bioavailability, determining potential environmental exposure to these materials requires an in depth analysis of modeling techniques that can be used in both the near- and long-term. Here, we provide a critical review of traditional and emerging exposure modeling approaches to highlight the challenges that scientists and decision-makers face when developing environmental exposure and risk assessments for nanomaterials. We find that accounting for nanospecific properties, overcoming data gaps, realizing model limitations, and handling uncertainty are key to developing informative and reliable environmental exposure and risk assessments for engineered nanomaterials. We find methods suited to recognizing and addressing significant uncertainty to be most appropriate for near-term environmental exposure modeling, given the current state of information and the current insufficiency of established deterministic models to address environmental exposure to engineered nanomaterials.

ENVIRONMENTAL PCB AND PESTICIDE EXPOSURE AND RISK OF ENDOMETRIOSIS

Science.gov (United States)

Environmental PCB and Pesticide Exposure and Risk of EndometriosisGermaine M. Buck1, John M. Weiner2, Hebe Greizerstein3, Brian Whitcomb1, Enrique Schisterman1, Paul Kostyniak3, Danelle Lobdell4, Kent Crickard5, and Ralph Sperrazza51Epidemiology Branch, Division o...

Environmental exposure assessment framework for nanoparticles in solid waste

DEFF Research Database (Denmark)

Boldrin, Alessio; Hansen, Steffen Foss; Baun, Anders

2014-01-01

Information related to the potential environmental exposure of engineered nanomaterials (ENMs) in the solid waste management phase is extremely scarce. In this paper, we define nanowaste as separately collected or collectable waste materials which are or contain ENMs, and we present a five...... transformation during waste treatment processes, (2) mechanisms for the release of ENMs, (3) the quantification of nanowaste amounts at the regional scale, (4) a definition of acceptable limit values for exposure to ENMs from nanowaste and (5) the reporting of nanowaste generation data....

Measuring combined exposure to environmental pressures in urban areas: an air quality and noise pollution assessment approach.

Science.gov (United States)

Vlachokostas, Ch; Achillas, Ch; Michailidou, A V; Moussiopoulos, Nu

2012-02-01

This study presents a methodological scheme developed to provide a combined air and noise pollution exposure assessment based on measurements from personal portable monitors. Provided that air and noise pollution are considered in a co-exposure approach, they represent a significant environmental hazard to public health. The methodology is demonstrated for the city of Thessaloniki, Greece. The results of an extensive field campaign are presented and the variations in personal exposure between modes of transport, routes, streets and transport microenvironments are evaluated. Air pollution and noise measurements were performed simultaneously along several commuting routes, during the morning and evening rush hours. Combined exposure to environmental pollutants is highlighted based on the Combined Exposure Factor (CEF) and Combined Dose and Exposure Factor (CDEF). The CDEF takes into account the potential relative uptake of each pollutant by considering the physical activities of each citizen. Rather than viewing environmental pollutants separately for planning and environmental sustainability considerations, the possibility of an easy-to-comprehend co-exposure approach based on these two indices is demonstrated. Furthermore, they provide for the first time a combined exposure assessment to these environmental pollutants for Thessaloniki and in this sense they could be of importance for local public authorities and decision makers. A considerable environmental burden for the citizens of Thessaloniki, especially for VOCs and noise pollution levels is observed. The material herein points out the importance of measuring public health stressors and the necessity of considering urban environmental pollution in a holistic way. Copyright © 2011 Elsevier Ltd. All rights reserved.

EPA's Research at the Cutting Edge of Exposure Science

Science.gov (United States)

EPA’s National Exposure Research Laboratory (NERL) serves as the lead for exposure science across U.S. Federal agencies. Exposure science has gained importance with increased appreciation of environmental influences on population disease burden. At a time when population ...

The die is cast - Arsenic exposure in early life and disease susceptibility

Science.gov (United States)

Abstract Early life exposure to arsenic in humans and mice produces similar patterns of disease in later life. Given the long interval between exposure and effect, epigenetic effects of early life exposure to arsenic may account for development and progression of disease in bo...

Self and environmental exposures to drinking, smoking, gambling or video game addiction are associated with adult hypertension, heart and cerebrovascular diseases, allergy, self-rated health and happiness: Japanese General Social Survey, 2010.

Science.gov (United States)

Shiue, Ivy

2015-02-15

It was aimed to study the relationships between addiction behaviors and human health and well-being in East Asians in a national and population-based setting. Data were retrieved from Japanese General Social Survey, 2010. Information on demographics, lifestyle factors, addiction behaviors and self-reported health conditions and well-being in Japanese adults was obtained by household interview. Analysis included chi-square test, logistic and multi-nominal regression modeling. Of 5003 Japanese adults (aged 20-89) included in the study cohort, 13.8%, 14.7%, 4.8% and 5.5% were addicted to drinking, smoking, gambling and video games, respectively while 10.6%, 13.8%, 4.3% and 11.4% were exposed to co-residing family member's drinking, smoking, gambling and video game addiction behaviors, respectively. People who reported addiction to drinking had poor self-rated health, hypertension and food allergy. People who reported addiction to smoking had fair to poor self-rated health, unhappiness, cerebrovascular disease and itchy skin. People who reported addiction to gambling had fair to poor self-rated health and unhappiness. People who reported addiction to video games had poor self-rated health and heart disease. People who were exposed to addiction to drinking, smoking, gambling and video games from co-residing family member(s) also reported hay fever, poor self-rated health and unhappiness. Self and environmental exposures to drinking, smoking, gambling or video game addiction are associated with adult hypertension, heart and cerebrovascular diseases, allergy, self-rated health and happiness. Future public health programs continuing to minimize self and environmental exposures to addiction behaviors tackling health concerns would still be encouraged. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

Infectious Disease risks associated with exposure to stressful environments

Science.gov (United States)

Meehan, Ichard T.; Smith, Morey; Sams, Clarence

1993-01-01

Multiple environmental factors asociated with space flight can increase the risk of infectious illness among crewmembers thereby adversely affecting crew health and mission success. Host defences can be impaired by multiple physiological and psychological stressors including: sleep deprivation, disrupted circadian rhythms, separation from family, perceived danger, radiation exposure, and possibly also by the direct and indirect effects of microgravity. Relevant human immunological data from isolated or stressful environments including spaceflight will be reviewed. Long-duration missions should include reliable hardware which supports sophisticated immunodiagnostic capabilities. Future advances in immunology and molecular biology will continue to provide therapeutic agents and biologic response modifiers which should effectively and selectively restore immune function which has been depressed by exposure to environmental stressors.

The U.S. National Health and Nutrition Examination Survey and human exposure to environmental chemicals.

Science.gov (United States)

Calafat, Antonia M

2012-02-01

Researchers are increasingly interested in using human biomonitoring - the measurement of chemicals, their metabolites or specific reaction products in biological specimens/body fluids - for investigating exposure to environmental chemicals. General population human biomonitoring programs are useful for investigating human exposure to environmental chemicals and an important tool for integrating environment and health. One of these programs, the National Health and Nutrition Examination Survey (NHANES), conducted in the United States is designed to collect data on the health and nutritional status of the noninstitutionalized, civilian U.S. population. NHANES includes a physical examination, collecting a detailed medical history, and collecting biological specimens (i.e., blood and urine). These biological specimens can be used to assess exposure to environmental chemicals. NHANES human biomonitoring data can be used to establish reference ranges for selected chemicals, provide exposure data for risk assessment, and monitor exposure trends. Published by Elsevier GmbH.

Concurrent Fetal Exposure to Multiple Environmental Chemicals along the U.S.—Mexico Border: An Exploratory Study in Brownsville, Texas

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Ken Sexton

2014-09-01

Full Text Available There is mounting concern that cumulative exposure to diverse chemicals in the environment may contribute to observed adverse health outcomes in the Lower Rio Grande Valley of Texas. To investigate this situation, biomarker concentrations of organochlorine (OC pesticides/metabolites, polychlorinated biphenyls (PCBs, and polycyclic aromatic hydrocarbons (PAHs were measured in maternal and umbilical cord blood from pregnant Hispanic women in Brownsville, TX. Results show that both mothers and fetuses were exposed concurrently to a variety of relatively low-level, hazardous environmental chemicals. Approximately 10% of the blood specimens had comparatively high concentrations of specific OC pesticides, PCBs and PAHs. Because many pregnant women in Brownsville live in socioeconomically-disadvantaged and environmentally-challenging circumstances, there is appropriate concern that exposure to these exogenous substances, either individually or in combination, may contribute to endemic health problems in this population, including cardiovascular disease, obesity, and diabetes.  The challenge is to identify individuals at highest comparative risk and then implement effective programs to either prevent or reduce cumulative exposures that pose significant health-related threats.

Children's Environmental Health Indicators in Australia.

Science.gov (United States)

Sly, J Leith; Moore, Sophie E; Gore, Fiona; Brune, Marie Noel; Neira, Maria; Jagals, Paul; Sly, Peter D

2016-01-01

Adverse environmental exposures in early life increase the risk of chronic disease but do not attract the attention nor receive the public health priority warranted. A safe and healthy environment is essential for children's health and development, yet absent in many countries. A framework that aids in understanding the link between environmental exposures and adverse health outcomes are environmental health indicators-numerical estimates of hazards and outcomes that can be applied at a population level. The World Health Organization (WHO) has developed a set of children's environmental health indicators (CEHI) for physical injuries, insect-borne disease, diarrheal diseases, perinatal diseases, and respiratory diseases; however, uptake of steps necessary to apply these indicators across the WHO regions has been incomplete. A first indication of such uptake is the management of data required to measure CEHI. The present study was undertaken to determine whether Australia has accurate up-to-date, publicly available, and readily accessible data on each CEHI for indigenous and nonindigenous Australian children. Data were not readily accessible for many of the exposure indicators, and much of the available data were not child specific or were only available for Australia's indigenous population. Readily accessible data were available for all but one of the outcome indicators and generally for both indigenous and nonindigenous children. Although Australia regularly collects data on key national indicators of child health, development, and well-being in several domains mostly thought to be of more relevance to Australians and Australian policy makers, these differ substantially from the WHO CEHI. The present study suggests that the majority of these WHO exposure and outcome indicators are relevant and important for monitoring Australian children's environmental health and establishing public health interventions at a local and national level and collection of appropriate

ENVIRONMENTAL PCB EXPOSURE AND RISK OF ENDOMETRIOSIS

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BACKGROUND: Hormonally active environmental agents recently have been associated with the development of endometriosis. METHODS: We undertook a study to assess the relation between endometriosis, an estrogen dependent gynecologic disease, and 62 individual polychlorinated biphe...

Early Exposure to Environmental Chaos and Children's Physical and Mental Health.

Science.gov (United States)

Coley, Rebekah Levine; Lynch, Alicia Doyle; Kull, Melissa

Environmental chaos has been proposed as a central influence impeding children's health and development, with the potential for particularly pernicious effects during the earliest years when children are most susceptible to environmental insults. This study evaluated a high-risk sample, following 495 low-income children living in poor urban neighborhoods from infancy to age 6. Longitudinal multilevel models tested the main tenets of the ecobiodevelopmental theory, finding that: (1) numerous distinct domains of environmental chaos were associated with children's physical and mental health outcomes, including housing disorder, neighborhood disorder, and relationship instability, with no significant results for residential instability; (2) different patterns emerged in relation to the timing of exposure to chaos, with more proximal exposure most strongly associated with children's functioning; and (3) the intensity of chaos also was a robust predictor of child functioning. Contrary to expectations, neither biological vulnerability (proxied through low birth weight status), maternal sensitivity, nor maternal distress moderated the role of chaos. Rather, maternal psychological distress functioned as a pathway through which environmental chaos was associated with children's functioning.

Human exposure to bisphenol A by biomonitoring: Methods, results and assessment of environmental exposures

International Nuclear Information System (INIS)

Dekant, Wolfgang; Voelkel, Wolfgang

2008-01-01

Human exposure to bisphenol A is controversially discussed. This review critically assesses methods for biomonitoring of bisphenol A exposures and reported concentrations of bisphenol A in blood and urine of non-occupationally ('environmentally') exposed humans. From the many methods published to assess bisphenol A concentrations in biological media, mass spectrometry-based methods are considered most appropriate due to high sensitivity, selectivity and precision. In human blood, based on the known toxicokinetics of bisphenol A in humans, the expected very low concentrations of bisphenol A due to rapid biotransformation and the very rapid excretion result in severe limitations in the use of reported blood levels of bisphenol A for exposure assessment. Due to the rapid and complete excretion of orally administered bisphenol A, urine samples are considered as the appropriate body fluid for bisphenol A exposure assessment. In urine samples from several cohorts, bisphenol A (as glucuronide) was present in average concentrations in the range of 1-3 μg/L suggesting that daily human exposure to bisphenol A is below 6 μg per person (< 0.1 μg/kg bw/day) for the majority of the population

[Behavioral-cognitive disorders due to chronic exposure to industrial and environmental toxic substances].

Science.gov (United States)

Mangone, Carlos A; Genovese, Osvaldo; Abel, Carlos

2006-01-01

A review of neurotoxics is made, given the low tendency to investigate for chronic exposure to environmental and industrial potential central nervous system toxic substances (heavy metals, insecticides, organic solvents and carbon monoxide) in the history of a patient consulting for behavioral - cognitive complains, and considering the potential overturn of the disease if a correct diagnosis and early treatment is made. to determine the onset of the cognitive - behavioral features, presentation pattern, diagnosis and treatment of such neurotoxics (NT). systematized search in Cochrane and Medline reviews, Embase and Lilacs. chronic exposure to neurotoxics can produce personality changes (sleeping problems, excitation, depression, delusions and hallucinations) as well as cognitive problems (memory, learning, language and cognitive reaction problems). NT may cause changes in the neuron morphology and its sub cellular structures, affecting its normal biochemistry and physiology (proteins and neurotransmitters synthesis). The clinical history, diagnosis and treatment of each neurotoxic are discussed. The NT must be taken in consideration among the possible different etiologies when a patient with a bizarre behavioral cognitive syndrome is examined.

Alcohol, drugs, caffeine, tobacco, and environmental contaminant exposure: reproductive health consequences and clinical implications.

Science.gov (United States)

Sadeu, J C; Hughes, Claude L; Agarwal, Sanjay; Foster, Warren G

2010-08-01

Reproductive function and fertility are thought to be compromised by behaviors such as cigarette smoking, substance abuse, and alcohol consumption; however, the strength of these associations are uncertain. Furthermore, the reproductive system is thought to be under attack from exposure to environmental contaminants, particularly those chemicals shown to affect endocrine homeostasis. The relationship between exposure to environmental contaminants and adverse effects on human reproductive health are frequently debated in the scientific literature and these controversies have spread into the lay press drawing increased public and regulatory attention. Therefore, the objective of the present review was to critically evaluate the literature concerning the relationship between lifestyle exposures and adverse effects on fertility as well as examining the evidence for a role of environmental contaminants in the purported decline of semen quality and the pathophysiology of subfertility, polycystic ovarian syndrome, and endometriosis. The authors conclude that whereas cigarette smoking is strongly associated with adverse reproductive outcomes, high-level exposures to other lifestyle factors are only weakly linked with negative fertility impacts. Finally, there is no compelling evidence that environmental contaminants, at concentrations representative of the levels measured in contemporary biomonitoring studies, have any effect, positive or negative, on reproductive health in the general population. Further research using prospective study designs with robust sample sizes are needed to evaluate testable hypotheses that address the relationship between exposure and adverse reproductive health effects.

Environmental tobacco smoke exposure among casino dealers.

Science.gov (United States)

Achutan, Chandran; West, Christine; Mueller, Charles; Bernert, John T; Bernard, Bruce

2011-04-01

This study quantified casino dealers' occupational exposure to environmental tobacco smoke (ETS). We measured casino dealers' exposure to ETS components by analyzing full-shift air and preshift and postshift urine samples. Casino dealers were exposed to nicotine, 4-vinyl pyridine, benzene, toluene, naphthalene, formaldehyde, acetaldehyde, solanesol, and respirable suspended particulates. Levels of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) in urine increased significantly during an 8-hour work shift both with and without adjustment for creatinine clearance. Creatinine-unadjusted cotinine significantly increased during the 8-hour shift, but creatinine-adjusted cotinine did not increase significantly. Casino dealers at the three casinos were exposed to airborne ETS components and absorbed an ETS-specific component into their bodies, as demonstrated by detectable levels of urinary NNAL. The casinos should ban smoking on their premises and offer employee smoking cessation programs.

The effects of low environmental cadmium exposure on bone density

Energy Technology Data Exchange (ETDEWEB)

Trzcinka-Ochocka, M., E-mail: ochocka@imp.lodz.pl [Department of Chemical Hazards, Laboratory of Biomonitoring, Nofer Institute of Occupational Medicine, Lodz (Poland); Jakubowski, M. [Department of Chemical Hazards, Laboratory of Biomonitoring, Nofer Institute of Occupational Medicine, Lodz (Poland); Szymczak, W. [Department of Environmental Epidemiology, Nofer Institute of Occupational Medicine, Lodz (Poland); Insitute of Psychology, University of Lodz (Poland); Janasik, B.; Brodzka, R. [Department of Chemical Hazards, Laboratory of Biomonitoring, Nofer Institute of Occupational Medicine, Lodz (Poland)

2010-04-15

Recent epidemiological data indicate that low environmental exposure to cadmium, as shown by cadmium body burden (Cd-U), is associated with renal dysfunction as well as an increased risk of cadmium-induced bone disorders. The present study was designed to assess the effects of low environmental cadmium exposure, at the level sufficient to induce kidney damage, on bone metabolism and mineral density (BMD). The project was conducted in the area contaminated with cadmium, nearby a zinc smelter located in the region of Poland where heavy industry prevails. The study population comprised 170 women (mean age=39.7; 18-70 years) and 100 men (mean age=31.9; 18-76 years). Urinary and blood cadmium and the markers of renal tubular dysfunction ({beta}{sub 2}M-U RBP, NAG), glomerular dysfunction (Alb-U and {beta}{sub 2}M-S) and bone metabolism markers (BAP-S, CTX-S) as well as forearm BMD, were measured. The results of this study based on simple dose-effect analysis showed the relationship between increasing cadmium concentrations and an increased excretion of renal dysfunction markers and decreasing bone density. However, the results of the multivariate analysis did not indicate the association between exposure to cadmium and decrease in bone density. They showed that the most important factors that have impact on bone density are body weight and age in the female subjects and body weight and calcium excretion in males. Our investigation revealed that the excretion of low molecular weight proteins occurred at a lower level of cadmium exposure than the possible loss of bone mass. It seems that renal tubular markers are the most sensitive and significant indicators of early health effects of cadmium intoxication in the general population. The correlation of urinary cadmium concentration with markers of kidney dysfunction was observed in the absence of significant correlations with bone effects. Our findings did not indicate any effects of environmental cadmium exposure on bone

Environmental tobacco smoke exposure among non-smoking waiters: measurement of expired carbon monoxide levels

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Ronaldo Laranjeira

2000-07-01

Full Text Available CONTEXT: Exposure to environmental tobacco smoke is a health risk that is of concern to patrons and of particular concern to employees of restaurants and bars. OBJECTIVE: To assess environmental tobacco smoke exposure (using expired carbon monoxide levels in non-smoking waiters before and after a normal day's shift and to compare pre-exposure levels with non-smoking medical students. DESIGN: An observational study. SETTING: Restaurants with more than 50 tables or 100 places in São Paulo. SUBJECTS: 100 non-smoking restaurant waiters and 100 non-smoking medical students in São Paulo, Brazil. MAIN MEASUREMENTS: Levels of expired carbon monoxide, measured with a Smokerlyser (Bedfont EC 50 Scientific, before and after a normal day's work. RESULTS: Waiters' pre-exposure expired carbon monoxide levels were similar to those of medical students, but after a mean of 9 hours exposure in the workplace, median levels more than doubled (2.0 ppm vs. 5.0 ppm, P <0.001. Post-exposure carbon monoxide levels were correlated with the number of tables available for smokers (Kendall's tau = 0.2, P <0.0001. CONCLUSIONS: Exposure to environmental tobacco smoke is the most likely explanation for the increase in carbon monoxide levels among these non-smoking waiters. These findings can be used to inform the ongoing public health debate on passive smoking.

Developmental Effects of Exposures to Environmental Factors: The Polish Mother and Child Cohort Study

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Kinga Polanska

2013-01-01

Full Text Available This paper estimates the effects of exposure to environmental factors, including lead, mercury, environmental tobacco smoke (ETS, and polycyclic aromatic hydrocarbons (PAH, on child psychomotor development. The study population consists of mother-child pairs in the Polish Mother and Child Cohort Study. Prenatal and postnatal exposure to environmental factors was determined from biomarker measurements as follows: for lead exposure—cord blood lead level, for mercury—maternal hair mercury level, for ETS—cotinine level in saliva and urine, and for PAH—1-hydroxypyrene (1-HP in urine. At the age of 12 (406 subjects and 24 months (198 subjects children were assessed using Bayley Scales of Infant and Toddler Development. There were no statistically significant effects of prenatal exposure to mercury or 1-HP on child psychomotor development. After adjusting for potential confounders, adverse effects of prenatal exposure to ETS on motor development (β = −2.6; P=0.02 and postnatal exposure to ETS on cognitive (β = −0.2; P=0.05 and motor functions (β = −0.5; P=0.01 were found. The adverse effect of prenatal lead exposure on cognitive score was of borderline significance (β = −6.2; P=0.06. The study underscores the importance of policies and public health interventions that aim to reduce prenatal and postnatal exposure to lead and ETS.

Environmental Exposure to Manganese in Air: Associations ...

Science.gov (United States)

Manganese (Mn), an essential element, can be neurotoxic in high doses. This cross-sectional study explored the oognitive function of adults residing in two towns (Marietta and East Liverpool, Ohio, USA) identified as having high levels of environmental airborne Mn from industrial sources. Air-Mn site surface emissions method modeling for total suspended particulate (TSP) ranged from 0.03 to 1.61 µg/m(3) in Marietta and 0.01-6.32 µg/m(3) in East Liverpool. A comprehensive screening test battery of cognitive function, including the domains of abstract thinking, attention/concentration, executive function and memory was administered. The mean age of the participants was 56 years (±10.8 years). Participants were mostly female (59.1) and primarily white (94.6%). Significant relationships (pworking and visuospatial memory (e.g., Rey-0 Immediate B3=0.19, Rey-0 Delayed B3=0.16) and verbal skills (e.g., Similarities B3=0.19). Using extensive cognitive testing and computer modeling of 10-plus years of measured air monitoring data, this study suggests that long-term environmental exposure to high levels of air-Mn, the exposure metric of this paper, may result in mild deficits of cognitive function in adult populations. This study addresses research questions under Sustainable and Healthy Communities (2.2.1.6 lessons learned, best practices and stakeholder feedback from community and tribal participa

Advances in environmental and occupational diseases 2004.

Science.gov (United States)

Frew, Anthony J

2005-06-01

2004 was another good year for publications on environmental and occupational disorders in our journal. The major focus is clearly on the environment and particularly on environmental risk factors for sensitization and asthma. There is a growing consensus that exposure to pets is good, provided there is enough of it. Low levels enhance sensitization, and higher levels protect against the consequences of that sensitization. Following on from previous work on cockroaches, we now see allergy to feral mice as an emergent problem--at least we now have the tools to study this properly. Emphasis seems to be swinging away from the outdoor environment as a cause of allergic disease and toward the indoor environment, which is, after all, where most of us spend most of our lives. New techniques for studying isocyanate allergy might kindle a revival of interest in the mechanisms of occupational asthma caused by low-molecular-weight compounds. But for all types of occupational allergy, prevention remains key, and it is good to see that comprehensive programs of allergen reduction can pay off in reduced rates of latex allergy in health care workers. Further work in the area of recombinant allergens is welcome but needs soon to be translated into new diagnostic and therapeutic strategies. This sector of allergy research remains vibrant, and the editors will continue to welcome outstanding contributions in this area.

Developmental Exposure to an Environmental PCB Mixture ...

Science.gov (United States)

Developmental PCB exposure impairs hearing and induces brainstem audiogenic seizures in adult offspring. The degree to which this enhanced susceptibility to seizure is manifest in other brain regions has not been examined. Thus, electrical kindling of the amygdala was used to evaluate the effect of developmental exposure to an environmentally relevant PCB mixture on seizure susceptibility in the rat. Female Long-Evans rats were dosed orally with 0 or 6 mg/kg/day of the PCB mixture dissolved in corn oil vehicle during the perinatal period. On postnatal day (PND) 21, pups were weaned, and two males from each litter were randomly selected for the kindling study. As adults, the male rats were implanted bilaterally with electrodes in the basolateral amygdala. For each animal, afterdischarge (AD) thresholds in the amygdala were determined on the first day of testing followed by once daily stimulation at a standard 200 µA stimulus intensity until three stage 5 generalized seizures (GS) ensued. Developmental PCB exposure did not affect the AD threshold or total cumulative AD duration, but PCB exposure did increase the latency to behavioral manifestations of seizure propagation. PCB exposed animals required significantly more stimulations to reach stage 2 seizures compared to control animals, indicating an attenuated focal (amygdala) excitability. A delay in kindling progression from a focally stimulated limbic site stands in contrast to our previous finding of increase

Racial Differences in Perceptions of Air Pollution Health Risk: Does Environmental Exposure Matter?

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Jayajit Chakraborty

2017-01-01

Full Text Available This article extends environmental risk perception research by exploring how potential health risk from exposure to industrial and vehicular air pollutants, as well as other contextual and socio-demographic factors, influence racial/ethnic differences in air pollution health risk perception. Our study site is the Greater Houston metropolitan area, Texas, USA—a racially/ethnically diverse area facing high levels of exposure to pollutants from both industrial and transportation sources. We integrate primary household-level survey data with estimates of excess cancer risk from ambient exposure to industrial and on-road mobile source emissions of air toxics obtained from the U.S. Environmental Protection Agency. Statistical analysis is based on multivariate generalized estimation equation models which account for geographic clustering of surveyed households. Our results reveal significantly higher risk perceptions for non-Hispanic Black residents and those exposed to greater cancer risk from industrial pollutants, and also indicate that gender influences the relationship between race/ethnicity and air pollution risk perception. These findings highlight the need to incorporate measures of environmental health risk exposure in future analysis of social disparities in risk perception.

Does low to moderate environmental exposure to noise and air pollution influence preterm delivery in medium-sized cities?

Science.gov (United States)

Barba-Vasseur, Marie; Bernard, Nadine; Pujol, Sophie; Sagot, Paul; Riethmuller, Didier; Thiriez, Gérard; Houot, Hélène; Defrance, Jérôme; Mariet, Anne-Sophie; Luu, Vinh-Phuc; Barbier, Alice; Benzenine, Eric; Quantin, Catherine; Mauny, Frédéric

2017-12-01

Preterm birth (PB) is an important predictor of childhood morbidity and educational performance. Beyond the known risk factors, environmental factors, such as air pollution and noise, have been implicated in PB. In urban areas, these pollutants coexist. Very few studies have examined the effects of multi-exposure on the pregnancy duration. The objective of this study was to analyse the relationship between PB and environmental chronic multi-exposure to noise and air pollution in medium-sized cities. A case-control study was conducted among women living in the city of Besançon (121 671 inhabitants) or in the urban unit of Dijon (243 936 inhabitants) and who delivered in a university hospital between 2005 and 2009. Only singleton pregnancies without associated pathologies were considered. Four controls were matched to each case in terms of the mother's age and delivery location. Residential noise and nitrogen dioxide (NO2) exposures were calculated at the mother's address. Conditional logistic regression models were applied, and sensitivity analyses were performed. This study included 302 cases and 1204 controls. The correlation between noise and NO2 indices ranged from 0.41 to 0.59. No significant differences were found in pollutant exposure levels between cases and controls. The adjusted odds ratios ranged between 0.96 and 1.08. Sensitivity analysis conducted using different temporal and spatial exposure windows demonstrated the same results. The results are in favour of a lack of connection between preterm delivery and multi-exposure to noise and air pollution in medium-sized cities for pregnant women without underlying disease. © The Author 2017; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association

Theoretical determination of spectrum-exposure rate conversion operator of HPGe detector and its application to the measurement of environmental gamma-ray exposure rate

International Nuclear Information System (INIS)

Park, Ch.M.; Choi, B.I.; Kwak, S.S.; Ji, P.K.; Kim, T.W.; Park, Y.W.; Yoon, B.K.

1993-01-01

A conversion operator between spectrum and exposure rate, using a portable HPGe detector for environmental radiation monitoring, was determined theoretically under the assumption of uniform distribution of radiation source on the ground surface. The measurement results were compared with those of a pressurized ionization chamber. The results obtained with the HPGe detector were slightly lower. The method can be easily applied to any gamma ray detector to obtain a spectrum - exposure-rate conversion factor for computing the exposure rate of environmental gamma radiation. (N.T.) 15 refs.; 6 figs.; 3 tabs

Celiac Disease Genomic, Environmental, Microbiome, and Metabolomic (CDGEMM Study Design: Approach to the Future of Personalized Prevention of Celiac Disease

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Maureen M. Leonard

2015-11-01

Full Text Available In the past it was believed that genetic predisposition and exposure to gluten were necessary and sufficient to develop celiac disease (CD. Recent studies however suggest that loss of gluten tolerance can occur at any time in life as a consequence of other environmental stimuli. Many environmental factors known to influence the composition of the intestinal microbiota are also suggested to play a role in the development of CD. These include birthing delivery mode, infant feeding, and antibiotic use. To date no large-scale longitudinal studies have defined if and how gut microbiota composition and metabolomic profiles may influence the loss of gluten tolerance and subsequent onset of CD in genetically-susceptible individuals. Here we describe a prospective, multicenter, longitudinal study of infants at risk for CD which will employ a blend of basic and applied studies to yield fundamental insights into the role of the gut microbiome as an additional factor that may play a key role in early steps involved in the onset of autoimmune disease.

Environmental Influences on Reproductive Health, the Importance of Chemical Exposures

Science.gov (United States)

Wang, Aolin; Padula, Amy; Sirota, Marina; Woodruff, Tracey J.

2016-01-01

Unstructured Abstract Chemical exposures during pregnancy can have a profound and life-long impact on human health. Due to the omnipresence of chemicals in our daily life, there is continuous contact with chemicals in food, water, air and consumer products. Consequently, human biomonitoring studies show that pregnant women around the globe are exposed to a variety of chemicals. In this review, we provide a summary of current data on maternal and fetal exposure as well as health consequences from these exposures. We review several chemical classes including polychlorinated biphenyls (PCBs), perfluoroalkyl substances (PFAS), polybrominated diphenyl ethers (PBDEs), phenols, phthalates, pesticides, and metals. Additionally, we discuss environmental disparities and vulnerable populations, and future research directions. We conclude by providing some recommendations for prevention of chemical exposure and its adverse reproductive health consequences. PMID:27513554

Primary Paediatric Bronchial Airway Epithelial Cell in Vitro Responses to Environmental Exposures

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Neil McInnes

2016-03-01

Full Text Available The bronchial airway epithelial cell (BAEC is the site for initial encounters between inhaled environmental factors and the lower respiratory system. Our hypothesis was that release of pro inflammatory interleukins (IL-6 and IL-8 from primary BAEC cultured from children will be increased after in vitro exposure to common environmental factors. Primary BAEC were obtained from children undergoing clinically indicated routine general anaesthetic procedures. Cells were exposed to three different concentrations of lipopolysaccharide (LPS or house dust mite allergen (HDM or particulates extracted from side stream cigarette smoke (SSCS. BAEC were obtained from 24 children (mean age 7.0 years and exposed to stimuli. Compared with the negative control, there was an increase in IL-6 and IL-8 release after exposure to HDM (p ≤ 0.001 for both comparisons. There was reduced IL-6 after higher compared to lower SSCS exposure (p = 0.023. There was no change in BAEC release of IL-6 or IL-8 after LPS exposure. BAEC from children are able to recognise and respond in vitro with enhanced pro inflammatory mediator secretion to some inhaled exposures.

Cadmium Exposure is Associated with the Prevalence of Dyslipidemia

OpenAIRE

Zhou Zhou; Yong-hui Lu; Hui-feng Pi; Peng Gao; Min Li; Lei Zhang; Li-ping Pei; Xiang Mei; Lin Liu; Qi Zhao; Qi-Zhong Qin; Yu Chen; Yue-ming Jiang; Zhao-hui Zhang; Zheng-ping Yu

2016-01-01

Background: Cadmium is a widespread environmental and occupational pollutant that accumulates in human body with a biological half-life exceeding 10 years. Cadmium exposure has been demonstrated to increase rates of cardiovascular diseases. Whether occupational cadmium exposure is associated with the increase in the prevalence of dyslipidemia and hence contributes to the risk of cardiovascular diseases is still equivocal. To test the hypothesis that exposure to cadmium is related to the preva...

[Impact of the Spanish smoking laws on the exposure to environmental tobacco smoke in Galicia (2005-2011)].

Science.gov (United States)

Pérez-Ríos, Mónica; Santiago-Pérez, María Isolina; Malvar, Alberto; Jesús García, María; Seoane, Bernardo; Suanzes, Jorge; Hervada, Xurxo

2014-01-01

Prevalence of exposure to environmental tobacco smoke is a valuable index to assess the impact of the laws for tobacco control. The objective of this work is to analyse variations in the prevalence of exposure to environmental tobacco smoke in Galicia (Spain) between 2005, before the Law 28/2005, and 2011, after the law 42/2010. Data were obtained from five population-based independent cross-sectional studies, telephone surveys, developed in Galicia between 2005 and 2011 among population aged 16 to 74 (n=34.419). Self-reported exposure among population aged between 16 and 74 was analysed by setting and tobacco consumption by prevalence with 95% confidence intervals. Environmental tobacco smoke exposure decreased dramatically in Galicia between 2005 and 2011. In 2005, before the Law 28/2005, 95% of the population reported exposure to environmental tobacco smoke compared to 28% in 2011, after the Law 42/2010. Decrease was greater in workplaces in 2006 and in leisure time venues in 2011. After an initial decrease in 2006, exposure at home remains unchanged. An important reduction in self-reported exposure to environmental tobacco smoke occurred in Galicia in the period 2005-2011, specially after the introduction of Laws 28/2005 and 42/2010. Nevertheless, one in four of the population aged 16 to 74 remained exposed in 2011. Copyright © 2013 SESPAS. Published by Elsevier Espana. All rights reserved.

The die is cast: arsenic exposure in early life and disease susceptibility.

Science.gov (United States)

Thomas, David J

2013-12-16

Early life exposure to arsenic in humans and mice produces similar patterns of disease in later life. Given the long interval between exposure and effect, epigenetic effects of early life exposure to arsenic may account for the development and progression of disease in both species. Mode of action and dosimetric studies in the mouse may help assess the role of age at exposure as a factor in susceptibility to the toxic and carcinogenic effects of arsenic in humans.

Life-Long Implications of Developmental Exposure to Environmental Stressors

DEFF Research Database (Denmark)

Grandjean, Philippe; Barouki, Robert; Bellinger, David C

2015-01-01

The Developmental Origins of Health and Disease (DOHaD) paradigm is one of the most rapidly expanding areas of biomedical research. Environmental stressors that can impact on DOHaD encompass a variety of environmental and occupational hazards as well as deficiency and oversupply of nutrients and ...

Environmental radioactivity and radiation exposure in 2015; Umweltradioaktivitaet und Strahlenbelastung im Jahr 2015

Energy Technology Data Exchange (ETDEWEB)

NONE

2017-07-20

The information of the German Federal Government on the environmental radioactivity and radiation exposure in 2015 covers the following issues: selected topics of radiation protection, natural radiation exposure; civilizing (artificial) radiation exposure: nuclear power plants and other nuclear facilities, uranium mine recultivation, radioactive materials in industry and households, fallout from nuclear weapon testing and reactor accidents; occupational radiation exposure: exposed personnel in nuclear facilities, aviation personnel, radiation accidents; medical radiation exposure: nuclear medical diagnostics and therapy; non-ionizing radiation: electromagnetic fields, UV radiation, optical radiation.

Validity and Reliability of Asbestos Knowledge and Awareness Questionnaire for Environmental Asbestos Exposure in Rural Areas

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Selma Metintaş

2017-04-01

Full Text Available Objective: There is no treatment for asbestos–related diseases, but they can be prevented. One of the first interventions is to improve the knowledge level of people in order to protect people from asbestos and asbestos–related diseases. The present study was conducted to develop a questionnaire for measuring the knowledge and awareness level of asbestos and also assess its validity and reliability in a rural population that is exposed to asbestos environmentally. Methods: A questionnaire, interviewer–administered, that included 37 items was employed on a convenient sample consisting of adult persons who attended a tertiary teaching hospital in Eskişehir where asbestos exposure is widespread in its rural areas. After assessment of validity and reliability of the results, the questionnaire was refined to 19 items and one subscale. Results: A total of 760 participants were included in this study. The mean age of participants was 53.2±15.1 years and 51.6% of them were male. The discrimination and difficulty indices of the asbestos knowledge and awareness questionnaire ranged between 20.0–60.5% and 0.39–0.98, respectively. Cronbach’s alpha coefficient was 0.951 for overall items. The median (min–max and mean (SD score of the study population were 30 (19–56 and 33.9 (11.9, respectively. The score increased correspondingly with greater knowledge levels. Conclusion: This questionnaire is a practical and easy tool to apply with acceptable reliability and validity on high-risk adults in rural areas with environmental asbestos exposure.

Association between NOx exposure and deaths caused by respiratory diseases in a medium-sized Brazilian city

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A. C. G. César

2015-12-01

Full Text Available Exposure to nitrogen oxides (NOx emitted by burning fossil fuels has been associated with respiratory diseases. We aimed to estimate the effects of NOx exposure on mortality owing to respiratory diseases in residents of Taubaté, São Paulo, Brazil, of all ages and both sexes. This time-series ecological study from August 1, 2011 to July 31, 2012 used information on deaths caused by respiratory diseases obtained from the Health Department of Taubaté. Estimated daily levels of pollutants (NOx, particulate matter, ozone, carbon monoxide were obtained from the Centro de Previsão de Tempo e Estudos Climáticos Coupled Aerosol and Tracer Transport model to the Brazilian developments on the Regional Atmospheric Modeling System. These environmental variables were used to adjust the multipollutant model for apparent temperature. To estimate association between hospitalizations owing to asthma and air pollutants, generalized additive Poisson regression models were developed, with lags as much as 5 days. There were 385 deaths with a daily mean (±SD of 1.05±1.03 (range: 0-5. Exposure to NOx was significantly associated with mortality owing to respiratory diseases: relative risk (RR=1.035 (95% confidence interval [CI]: 1.008-1.063 for lag 2, RR=1.064 (95%CI: 1.017-1.112 lag 3, RR=1.055 (95%CI: 1.025-1.085 lag 4, and RR=1.042 (95%CI: 1.010-1.076 lag 5. A 3 µg/m3 reduction in NOx concentration resulted in a decrease of 10-18 percentage points in risk of death caused by respiratory diseases. Even at NOx concentrations below the acceptable standard, there is association with deaths caused by respiratory diseases.

CT Characteristics of Pleural Plaques Related to Occupational or Environmental Asbestos Exposure from South Korean Asbestos Mines.

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Kim, Yookyung; Myong, Jun-Pyo; Lee, Jeong Kyong; Kim, Jeung Sook; Kim, Yoon Kyung; Jung, Soon-Hee

2015-01-01

This study evaluated the CT characteristics of pleural plaques in asbestos-exposed individuals and compared occupational versus environmental exposure groups. This study enrolled 181 subjects with occupational exposure and 98 with environmental exposure from chrysotile asbestos mines, who had pleural plaques confirmed by a chest CT. The CT scans were analyzed for morphological characteristics, the number and distribution of pleural plaques and combined pulmonary fibrosis. Furthermore, the CT findings were compared between the occupational and environmental exposure groups. Concerning the 279 subjects, the pleural plaques were single in 2.2% and unilateral in 3.6%, and showed variable widths (range, 1-20 mm; mean, 5.4 ± 2.7 mm) and lengths (5-310 mm; 72.6 ± 54.8 mm). The chest wall was the most commonly involved (98.6%), with an upper predominance on the ventral side (upper, 77.8% vs. lower, 55.9%, p occupational exposure group (p environmentally exposed individuals.

Combat exposure severity as a moderator of genetic and environmental liability to post-traumatic stress disorder.

Science.gov (United States)

Wolf, E J; Mitchell, K S; Koenen, K C; Miller, M W

2014-05-01

Twin studies of veterans and adults suggest that approximately 30-46% of the variance in post-traumatic stress disorder (PTSD) is attributable to genetic factors. The remaining variance is attributable to the non-shared environment, which, by definition, includes combat exposure. This study used a gene by measured environment twin design to determine whether the effects of genetic and environmental factors that contribute to the etiology of PTSD are dependent on the level of combat exposure. The sample was drawn from the Vietnam Era Twin Registry (VETR) and included 620 male-male twin pairs who served in the US Military in South East Asia during the Vietnam War era. Analyses were based on data from a clinical diagnostic interview of lifetime PTSD symptoms and a self-report measure of combat exposure. Biometric modeling revealed that the effects of genetic and non-shared environment factors on PTSD varied as a function of level of combat exposure such that the association between these factors and PTSD was stronger at higher levels of combat exposure. Combat exposure may act as a catalyst that augments the impact of hereditary and environmental contributions to PTSD. Individuals with the greatest exposure to combat trauma were at increased risk for PTSD as a function of both genetic and environmental factors. Additional work is needed to determine the biological and environmental mechanisms driving these associations.

Exposure to mobile phone radiation opens new horizons in Alzheimer's disease treatment.

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Mortazavi, Sar; Shojaei-Fard, Mb; Haghani, M; Shokrpour, N; Mortazavi, Smj

2013-09-01

Alzheimer's disease, the most common type of dementia and a progressive neurodegenerative disease, occurs when the nerve cells in the brain die. Although there are medications that can help delay the development of Alzheimer's disease, there is currently no cure for this disease. Exposure to ionizing and non-ionizing radiation may cause adverse health effects such as cancer.  Looking at the other side of the coin, there are reports indicating stimulatory or beneficial effects after exposure to cell phone radiofrequency radiation. Mortazavi et al. have previously reported some beneficial cognitive effects such as decreased reaction time after human short-term exposure to cell phone radiation or occupational exposure to radar microwave radiation. On the other hand, some recent reports have indicated that RF radiation may have a role in protecting against cognitive impairment in Alzheimer's disease. Although the majority of these data come from animal studies that cannot be easily extrapolated to humans, it can be concluded that this memory enhancing approach may open new horizons in treatment of cognitive impairment in Alzheimer disease.

Integrated Bioinformatics, Environmental Epidemiologic and Genomic Approaches to Identify Environmental and Molecular Links between Endometriosis and Breast Cancer

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Deodutta Roy

2015-10-01

Full Text Available We present a combined environmental epidemiologic, genomic, and bioinformatics approach to identify: exposure of environmental chemicals with estrogenic activity; epidemiologic association between endocrine disrupting chemical (EDC and health effects, such as, breast cancer or endometriosis; and gene-EDC interactions and disease associations. Human exposure measurement and modeling confirmed estrogenic activity of three selected class of environmental chemicals, polychlorinated biphenyls (PCBs, bisphenols (BPs, and phthalates. Meta-analysis showed that PCBs exposure, not Bisphenol A (BPA and phthalates, increased the summary odds ratio for breast cancer and endometriosis. Bioinformatics analysis of gene-EDC interactions and disease associations identified several hundred genes that were altered by exposure to PCBs, phthalate or BPA. EDCs-modified genes in breast neoplasms and endometriosis are part of steroid hormone signaling and inflammation pathways. All three EDCs–PCB 153, phthalates, and BPA influenced five common genes—CYP19A1, EGFR, ESR2, FOS, and IGF1—in breast cancer as well as in endometriosis. These genes are environmentally and estrogen responsive, altered in human breast and uterine tumors and endometriosis lesions, and part of Mitogen Activated Protein Kinase (MAPK signaling pathways in cancer. Our findings suggest that breast cancer and endometriosis share some common environmental and molecular risk factors.

Environmental exposure to manganese and motor function of children in Mexico.

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Hernández-Bonilla, D; Schilmann, A; Montes, S; Rodríguez-Agudelo, Y; Rodríguez-Dozal, S; Solís-Vivanco, R; Ríos, C; Riojas-Rodríguez, H

2011-10-01

Occupational manganese (Mn) exposure has been associated with motor deficits in adult workers, but data on the potential effects of environmental exposure to Mn on the developing motor function for a children population is scarce. The aim of this study was to evaluate the association between exposure to Mn and motor function of school aged children. We conducted a cross-sectional study selecting 195 children (100 exposed and 95 unexposed) between 7 and 11 years old. The following tests were used to evaluate the motor function: Grooved pegboard, finger tapping, and Santa Ana test. Mn exposure was assessed by blood (MnB) and hair concentrations (MnH). We constructed linear regression models to evaluate the association between exposure to Mn and the different test scores adjusting for age, sex, maternal education, hemoglobin and blood lead. The median concentration of MnH and MnB was significantly higher in exposed (12.6 μg/g and 9.5 μg/L) compared to unexposed children (0.6 μg/g and 8.0 μg/L). The exposed children on average performed the grooved pegboard test faster, but made more errors, although these results did not reach statistical significance with neither one of the Mn exposure biomarkers. MnB showed an inverse association on the execution of the finger tapping test (average in 5 trials β -0.4, p=0.02), but no association was observed with MnH. A subtle negative association of Mn exposure on motor speed and coordination was shown. In adults, the main effect of environmental Mn exposure has been associated with motor skills, but these results suggest that such alterations are not the main effect on children. Copyright © 2011 Elsevier Inc. All rights reserved.

Health effects of subchronic exposure to environmental levels of diesel exhaust.

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Reed, M D; Gigliotti, A P; McDonald, J D; Seagrave, J C; Seilkop, S K; Mauderly, J L

2004-04-01

Diesel exhaust is a public health concern and contributor to both ambient and occupational air pollution. As part of a general health assessment of multiple anthropogenic source emissions conducted by the National Environmental Respiratory Center (NERC), a series of health assays was conducted on rats and mice exposed to environmentally relevant levels of diesel exhaust. This article summarizes the study design and exposures, and reports findings on several general indicators of toxicity and carcinogenic potential. Diesel exhaust was generated from a commonly used 2000 model 5.9-L, 6-cylinder turbo diesel engine operated on a variable-load heavy-duty test cycle burning national average certification fuel. Animals were exposed to clean air (control) or four dilutions of whole emissions based on particulate matter concentration (30, 100, 300, and 1000 microg/m(3)). Male and female F344 rats and A/J mice were exposed by whole-body inhalation 6 h/day, 7 days/wk, for either 1 wk or 6 mo. Exposures were characterized in detail. Effects of exposure on clinical observations, body and organ weights, serum chemistry, hematology, histopathology, bronchoalveolar lavage, and serum clotting factors were mild. Significant exposure-related effects occurring in both male and female rats included decreases in serum cholesterol and clotting Factor VII and slight increases in serum gamma-glutamyl transferase. Several other responses met screening criteria for significant exposure effects but were not consistent between genders or exposure times and were not corroborated by related parameters. Carcinogenic potential as determined by micronucleated reticulocyte counts and proliferation of adenomas in A/J mice were unaffected by 6 mo of exposure. Parallel studies demonstrated effects on cardiac function and resistance to viral infection; however, the results reported here show few and only modest health hazards from subchronic or shorter exposures to realistic concentrations of

Sunlight exposure is important for preventing hip fractures in patients with Alzheimer's disease, Parkinson's disease, or stroke.

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Iwamoto, J; Takeda, T; Matsumoto, H

2012-04-01

Hypovitaminosis D as a result of malnutrition or sunlight deprivation, increased bone resorption, low bone mineral density (BMD), or an increased risk of falls may contribute to an increased risk of hip fractures in patients with neurological diseases, including Alzheimer's disease, Parkinson's disease, and stroke. The purpose of this study was to clarify the efficacy of sunlight exposure for reducing the risk of hip fractures in patients with such neurological diseases. The English literature was searched using PubMed, and randomized controlled trials evaluating the efficacy of sunlight exposure for reducing the risk of hip fractures in patients with Alzheimer's disease, Parkinson's disease, and stroke were identified. The relative risk and the 95% confidence interval were calculated for individual randomized controlled trials, and a pooled data analysis (meta-analysis) was performed. Three randomized controlled trials were identified. Sunlight exposure improved hypovitaminosis D and increased the BMD. The relative risk (95% confidence interval) of hip fractures was 0.22 (0.05, 1.01) for Alzheimer's disease, 0.27 (0.08, 0.96) for Parkinson's disease, and 0.17 (0.02, 1.36) for stroke. The relative risk (95% confidence interval) calculated for the pooled data analysis was 0.23 (0.10, 0.56) (P = 0.0012), suggesting a significant risk reduction rate of 77%. The present meta-analysis added additional evidence indicating the efficacy of sunlight exposure for reducing the risk of hip fractures in patients with Alzheimer's disease, Parkinson's disease, and stroke. © 2011 John Wiley & Sons A/S.

Abnormal environmental light exposure in the intensive care environment.

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Fan, Emily P; Abbott, Sabra M; Reid, Kathryn J; Zee, Phyllis C; Maas, Matthew B

2017-08-01

We sought to characterize ambient light exposure in the intensive care unit (ICU) environment to identify patterns of light exposure relevant to circadian regulation. A light monitor was affixed to subjects' bed at eye level in a modern intensive care unit and continuously recorded illuminescence for at least 24h per subject. Blood was sampled hourly and measured for plasma melatonin. Subjects underwent hourly vital sign and bedside neurologic assessments. Care protocols and the ICU environment were not modified for the study. A total of 67,324 30-second epochs of light data were collected from 17 subjects. Light intensity peaked in the late morning, median 64.1 (interquartile range 19.7-138.7) lux. The 75th percentile of light intensity exceeded 100lx only between 9AM and noon, and never exceeded 150lx. There was no correlation between melatonin amplitude and daytime, nighttime or total light exposure (Spearman's correlation coefficients all 0.5). Patients' environmental light exposure in the intensive care unit is consistently low and follows a diurnal pattern. No effect of nighttime light exposure was observed on melatonin secretion. Inadequate daytime light exposure in the ICU may contribute to abnormal circadian rhythms. Copyright © 2017 Elsevier Inc. All rights reserved.

Using Geographic Information Systems for Exposure Assessment in Environmental Epidemiology Studies

OpenAIRE

Nuckols, John R.; Ward, Mary H.; Jarup, Lars

2004-01-01

Geographic information systems (GIS) are being used with increasing frequency in environmental epidemiology studies. Reported applications include locating the study population by geocoding addresses (assigning mapping coordinates), using proximity analysis of contaminant source as a surrogate for exposure, and integrating environmental monitoring data into the analysis of the health outcomes. Although most of these studies have been ecologic in design, some have used GIS in estimating enviro...

Environmental toxicants, incidence of degenerative diseases, and therapies from the epigenetic point of view.

Science.gov (United States)

Hodjat, Mahshid; Rahmani, Soheila; Khan, Fazlullah; Niaz, Kamal; Navaei-Nigjeh, Mona; Mohammadi Nejad, Solmaz; Abdollahi, Mohammad

2017-07-01

Epigenotoxicology is an emerging field of study that investigates the non-genotoxic epigenetic effects of environmental toxicants resulting in alteration of normal gene expression and disruption of cell function. Recent findings on the role of toxicant-induced epigenetic modifications in the development of degenerative diseases have opened up a promising research direction to explore epigenetic therapy approaches and related prognostic biomarkers. In this review, we presented comprehensive data on epigenetic alterations identified in various diseases, including cancer, autoimmune disorders, pulmonary conditions as well as cardiovascular, gastrointestinal and bone disease. Although data on abnormalities of DNA methylation and their role in the development of diseases are abundant, less is known about the impact of histone modifications and microRNA expressions. Further, we discussed the effects of selected common environmental toxicants on epigenetic modifications and their association with particular abnormalities. A number of different environmental toxicants have been identified for their role in aberrant DNA methylation, histone modifications, and microRNA expression. Such epigenetic effects were shown to be tissue-type specific and highly associated with the level and duration of exposure. Finally, we described present and future therapeutic strategies, including medicines and dietary compounds for combating the toxicant-induced epigenetic alterations. There are currently seven histone deacetylase inhibitors and two DNA methyltransferase inhibitors approved for clinical use and many other promising candidates are in preclinical and clinical testing. Dietary compounds are thought to be the effective and safe strategies for treating and prevention of epigenetic pathophysiological conditions. Still more concentrated epigenetic researches are required for evaluation of chemical toxicity and identifying the causal association between key epigenetic alteration and

Skewed riskscapes and gentrified inequities: environmental exposure disparities in Seattle, Washington.

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Abel, Troy D; White, Jonah

2011-12-01

Few studies have considered the sociohistorical intersection of environmental injustice and gentrification; a gap addressed by this case study of Seattle, Washington. This study explored the advantages of integrating air toxic risk screening with gentrification research to enhance proximity and health equity analysis methodologies. It was hypothesized that Seattle's industrial air toxic exposure risk was unevenly dispersed, that gentrification stratified the city's neighborhoods, and that the inequities of both converged. Spatial characterizations of air toxic pollution risk exposures from 1990 to 2007 were combined with longitudinal cluster analysis of census block groups in Seattle, Washington, from 1990 to 2000. A cluster of air toxic exposure inequality and socioeconomic inequity converged in 1 area of south central Seattle. Minority and working class residents were more concentrated in the same neighborhoods near Seattle's worst industrial pollution risks. Not all pollution was distributed equally in a dynamic urban landscape. Using techniques to examine skewed riskscapes and socioeconomic urban geographies provided a foundation for future research on the connections among environmental health hazard sources, socially vulnerable neighborhoods, and health inequity.

TRP channels and traffic-related environmental pollution-induced pulmonary disease.

Science.gov (United States)

Akopian, Armen N; Fanick, E Robert; Brooks, Edward G

2016-05-01

Environmental pollutant exposures are major risk factors for adverse health outcomes, with increased morbidity and mortality in humans. Diesel exhaust (DE) is one of the major harmful components of traffic-related air pollution. Exposure to DE affects several physiological systems, including the airways, and pulmonary diseases are increased in highly populated urban areas. Hence, there are urgent needs to (1) create newer and lesser polluting fuels, (2) improve exhaust aftertreatments and reduce emissions, and (3) understand mechanisms of actions for toxic effects of both conventional and cleaner diesel fuels on the lungs. These steps could aid the development of diagnostics and interventions to prevent the negative impact of traffic-related air pollution on the pulmonary system. Exhaust from conventional, and to a lesser extent, clean fuels, contains particulate matter (PM) and more than 400 additional chemical constituents. The major toxic constituents are nitrogen oxides (NOx) and polycyclic aromatic hydrocarbons (PAHs). PM and PAHs could potentially act via transient receptor potential (TRP) channels. In this review, we will first discuss the associations between DE from conventional as well as clean fuel technologies and acute and chronic airway inflammation. We will then review possible activation and/or potentiation of TRP vanilloid type 1 (TRPV1) and ankyrin 1 (TRPA1) channels by PM and PAHs. Finally, we will discuss and summarize recent findings on the mechanisms whereby TRPs could control the link between DE and airway inflammation, which is a primary determinant leading to pulmonary disease.

Early Exposure to Environmental Chaos and Children’s Physical and Mental Health

Science.gov (United States)

Coley, Rebekah Levine; Lynch, Alicia Doyle; Kull, Melissa

2015-01-01

Environmental chaos has been proposed as a central influence impeding children’s health and development, with the potential for particularly pernicious effects during the earliest years when children are most susceptible to environmental insults. This study evaluated a high-risk sample, following 495 low-income children living in poor urban neighborhoods from infancy to age 6. Longitudinal multilevel models tested the main tenets of the ecobiodevelopmental theory, finding that: (1) numerous distinct domains of environmental chaos were associated with children’s physical and mental health outcomes, including housing disorder, neighborhood disorder, and relationship instability, with no significant results for residential instability; (2) different patterns emerged in relation to the timing of exposure to chaos, with more proximal exposure most strongly associated with children’s functioning; and (3) the intensity of chaos also was a robust predictor of child functioning. Contrary to expectations, neither biological vulnerability (proxied through low birth weight status), maternal sensitivity, nor maternal distress moderated the role of chaos. Rather, maternal psychological distress functioned as a pathway through which environmental chaos was associated with children’s functioning. PMID:25844016

The environmental injustice of beauty: framing chemical exposures from beauty products as a health disparities concern.

Science.gov (United States)

Zota, Ami R; Shamasunder, Bhavna

2017-10-01

The obstetrics-gynecology community has issued a call to action to prevent toxic environmental chemical exposures and their threats to healthy human reproduction. Recent committee opinions recognize that vulnerable and underserved women may be impacted disproportionately by environmental chemical exposures and recommend that reproductive health professionals champion policies that secure environmental justice. Beauty product use is an understudied source of environmental chemical exposures. Beauty products can include reproductive and developmental toxicants such as phthalates and heavy metals; however, disclosure requirements are limited and inconsistent. Compared with white women, women of color have higher levels of beauty product-related environmental chemicals in their bodies, independent of socioeconomic status. Even small exposures to toxic chemicals during critical periods of development (such as pregnancy) can trigger adverse health consequences (such as impacts on fertility and pregnancy, neurodevelopment, and cancer). In this commentary, we seek to highlight the connections between environmental justice and beauty product-related chemical exposures. We describe racial/ethnic differences in beauty product use (such as skin lighteners, hair straighteners, and feminine hygiene products) and the potential chemical exposures and health risks that are associated with these products. We also discuss how targeted advertising can take advantage of mainstream beauty norms to influence the use of these products. Reproductive health professionals can use this information to advance environmental justice by being prepared to counsel patients who have questions about toxic environmental exposures from beauty care products and other sources. Researchers and healthcare providers can also promote health-protective policies such as improved ingredient testing and disclosure for the beauty product industry. Future clinical and public health research should consider beauty

Dealing with uncertainties in environmental burden of disease assessment

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van der Sluijs Jeroen P

2009-04-01

Full Text Available Abstract Disability Adjusted Life Years (DALYs combine the number of people affected by disease or mortality in a population and the duration and severity of their condition into one number. The environmental burden of disease is the number of DALYs that can be attributed to environmental factors. Environmental burden of disease estimates enable policy makers to evaluate, compare and prioritize dissimilar environmental health problems or interventions. These estimates often have various uncertainties and assumptions which are not always made explicit. Besides statistical uncertainty in input data and parameters – which is commonly addressed – a variety of other types of uncertainties may substantially influence the results of the assessment. We have reviewed how different types of uncertainties affect environmental burden of disease assessments, and we give suggestions as to how researchers could address these uncertainties. We propose the use of an uncertainty typology to identify and characterize uncertainties. Finally, we argue that uncertainties need to be identified, assessed, reported and interpreted in order for assessment results to adequately support decision making.

Issues in environmental control data used in DD ampersand ER worker dose exposures

International Nuclear Information System (INIS)

White, M.G.

1995-01-01

Sites for decontamination and decommissioning (DD) or environmental remediation (ER) are often from US DOE operations that began during and shortly after World War II. This paper discusses selected problems in the use of environmental data for DD and ER worker dose exposure calculations

Biochar physico-chemical properties as affected by environmental exposure

International Nuclear Information System (INIS)

Sorrenti, Giovambattista; Masiello, Caroline A.; Dugan, Brandon; Toselli, Moreno

2016-01-01

To best use biochar as a sustainable soil management and carbon (C) sequestration technique, we must understand the effect of environmental exposure on its physical and chemical properties because they likely vary with time. These properties play an important role in biochar's environmental behavior and delivery of ecosystem services. We measured biochar before amendment and four years after amendment to a commercial nectarine orchard at rates of 5, 15 and 30 t ha −1 . We combined two pycnometry techniques to measure skeletal (ρ s ) and envelope (ρ e ) density and to estimate the total pore volume of biochar particles. We also examined imbibition, which can provide information about soil hydraulic conductivity. Finally, we investigated the chemical properties, surface, inner layers atomic composition and C1s bonding state of biochar fragments through X-ray photoelectron spectroscopy (XPS). Ageing increased biochar skeletal density and reduced the water imbibition rate within fragments as a consequence of partial pore clogging. However, porosity and the volume of water stored in particles remained unchanged. Exposure reduced biochar pH, EC, and total C, but enhanced total N, nitrate-N, and ammonium-N. X-ray photoelectron spectroscopy analyses showed an increase of O, Si, N, Na, Al, Ca, Mn, and Fe surface (0–5 nm) atomic composition (at%) and a reduction of C and K in aged particles, confirming the interactions of biochar with soil inorganic and organic phases. Oxidation of aged biochar fragments occurred mainly in the particle surface, and progressively decreased down to 75 nm. Biochar surface chemistry changes included the development of carbonyl and carboxylate functional groups, again mainly on the particle surface. However, changes were noticeable down to 75 nm, while no significant changes were measured in the deepest layer, up to 110 nm. Results show unequivocal shifts in biochar physical and chemical properties/characteristics over short (~ years

Chronic arsenic exposure and its adverse health effects in Taiwan: A paradigm for management of a global environmental problem

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Cheng-Che Lan

2011-09-01

Full Text Available It was estimated that, nearly 100 million people are at risk for drinking arsenic (As-contaminated drinking water. Although the WHO guideline recommends that levels of As in drinking water should not exceed 10 μm/L, it was estimated that more than 30 million people drink As-containing water at levels more than 50 μm/L in Bangladesh and India alone. Therefore, the adverse health effects resulting from chronic As exposure pose a global threat. In Taiwan, studies focusing on the health effects resulting from chronic As exposure through contaminated drinking water have been ongoing for more than 50 years. During the past half century, it was recognized that the impact of high As exposure on human health is much more complicated than originally anticipated. Chronic As exposure resulted in infamous blackfoot disease, which is unique to As endemic areas in Taiwan, and various diseases including cancers and non-cancers. Although the potential-biological outcomes have been well-documented, the pathomechanisms leading from As exposure to occurrence and development of the diseases remain largely unclear. One of the major obstacles that hindered further understanding regarding the adverse health effect resulting from chronic As exposure is documentation of cumulative As exposure from the distant past, which remains difficult as the present technologies mostly document relatively recent As exposure. Furthermore, the susceptibility to As exposure appears to differ between different ethnic groups and individuals and is modified by lifestyle factors including smoking habits and nutrition status. No consensus data has yet been reached even after comparing the study results obtained from different parts of the world focusing on associations between human As toxicity and genetic polymorphisms in terms of cellular detoxification enzymes, tumor suppressor proteins, and DNA repair pathway. With the availability of the new powerful “OMIC” technologies, it may

Foetal exposure to food and environmental carcinogens in human beings.

Science.gov (United States)

Myöhänen, Kirsi; Vähäkangas, Kirsi

2012-02-01

Exposure to many different chemicals during pregnancy through maternal circulation is possible. Transplacental transfer of xenobiotics can be demonstrated using human placental perfusion. Also, placental perfusion can give information about the placental kinetics as well as metabolism and accumulation in the placenta because it retains the tissue structure and function. Although human placental perfusion has been used extensively to study the transplacental transfer of drugs, the information on food and environmental carcinogens is much more limited. This review deals with the foetal exposure to food and environmental carcinogens in human beings. In particular, human transplacental transfer of the food carcinogens such as acrylamide, glycidamide and nitrosodimethylamine are in focus. Because these carcinogens are genotoxic, the functional capacity of human placenta to induce DNA adduct formation or metabolize these above mentioned CYP2E1 substrates is of interest in this context. © 2011 The Authors. Basic & Clinical Pharmacology & Toxicology © 2011 Nordic Pharmacological Society.

Immune-mediated diseases and microbial exposure in early life

DEFF Research Database (Denmark)

Bisgaard, H; Bønnelykke, K; Stokholm, Jacob

2014-01-01

The non-communicable disease pandemic includes immune-mediated diseases such as asthma and allergy, which are likely originating in early life where the immature immune system is prone to alterations caused by the exposome. The timing of exposure seems critical for the developing immune system...

Mercury Exposure and Risk of Cardiovascular Disease in Two U.S. Cohorts

Science.gov (United States)

Mozaffarian, Dariush; Shi, Peilin; Morris, J. Steven; Spiegelman, Donna; Grandjean, Philippe; Siscovick, David S.; Willett, Walter C.; Rimm, Eric B.

2011-01-01

BACKGROUND Exposure to methylmercury from fish consumption has been linked to a potentially increased risk of cardiovascular disease, but evidence from prior studies is equivocal. Beneficial effects of the ingestion of fish and selenium may also modify such effects. METHODS Among subjects from two U.S. cohorts (a total of 51,529 men and 121,700 women) whose toenail clippings had been stored, we prospectively identified incident cases of cardiovascular disease (coronary heart disease and stroke) in 3427 participants and matched them to risk-set–sampled controls according to age, sex, race, and smoking status. Toenail mercury and selenium concentrations were assessed with the use of neutron-activation analysis. Other demographic characteristics, cardiovascular risk factors, fish consumption, and lifestyle habits were assessed by means of validated questionnaires. Associations between mercury exposure and incident cardiovascular disease were evaluated with the use of conditional logistic regression. RESULTS Median toenail mercury concentrations were 0.23 µg per gram (interdecile range, 0.06 to 0.94) in the case participants and 0.25 µg per gram (interdecile range, 0.07 to 0.97) in the controls. In multivariate analyses, participants with higher mercury exposures did not have a higher risk of cardiovascular disease. For comparisons of the fifth quintile of mercury exposure with the first quintile, the relative risks were as follows: coronary heart disease, 0.85 (95% confidence interval [CI], 0.69 to 1.04; P = 0.10 for trend); stroke, 0.84 (95% CI, 0.62 to 1.14; P = 0.27 for trend); and total cardiovascular disease, 0.85 (95% CI, 0.72 to 1.01; P = 0.06 for trend). Findings were similar in analyses of participants with low selenium concentrations or low overall fish consumption and in several additional sensitivity analyses. CONCLUSIONS We found no evidence of any clinically relevant adverse effects of mercury exposure on coronary heart disease, stroke, or total

Incidence of nephrolithiasis in relation to environmental exposure to lead and cadmium in a population study

Energy Technology Data Exchange (ETDEWEB)

Hara, Azusa; Yang, Wen-Yi; Petit, Thibault; Zhang, Zhen-Yu; Gu, Yu-Mei; Wei, Fang-Fei; Jacobs, Lotte [Studies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences, University of Leuven, Leuven (Belgium); Odili, Augustine N. [Studies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences, University of Leuven, Leuven (Belgium); Department of Internal Medicine, Faculty of Clinical Sciences, College of Health Sciences University of Abuja (Nigeria); Thijs, Lutgarde [Studies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences, University of Leuven, Leuven (Belgium); Nawrot, Tim S. [Centre for Environmental Sciences, University of Hasselt (Belgium); Staessen, Jan A., E-mail: jan.staessen@med.kuleuven.be [Studies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences, University of Leuven, Leuven (Belgium); R& D Group VitaK, Maastricht University, Maastricht (Netherlands)

2016-02-15

Whether environmental exposure to nephrotoxic agents that potentially interfere with calcium homeostasis, such as lead and cadmium, contribute to the incidence of nephrolithiasis needs further clarification. We investigated the relation between nephrolithiasis incidence and environmental lead and cadmium exposure in a general population. In 1302 participants randomly recruited from a Flemish population (50.9% women; mean age, 47.9 years), we obtained baseline measurements (1985–2005) of blood lead (BPb), blood cadmium (BCd), 24-h urinary cadmium (UCd) and covariables. We monitored the incidence of kidney stones until October 6, 2014. We used Cox regression to calculate multivariable-adjusted hazard ratios for nephrolithiasis. At baseline, geometric mean BPb, BCd and UCd was 0.29 µmol/L, 9.0 nmol/L, and 8.5 nmol per 24 h, respectively. Over 11.5 years (median), nephrolithiasis occurred in 40 people. Contrasting the low and top tertiles of the distributions, the sex- and age-standardized rates of nephrolithiasis expressed as events per 1000 person-years were 0.68 vs. 3.36 (p=0.0016) for BPb, 1.80 vs. 3.28 (p=0.11) for BCd, and 1.65 vs. 2.95 (p=0.28) for UCd. In continuous analysis, with adjustments applied for sex, age, serum magnesium, and 24-h urinary volume and calcium, the hazard ratios expressing the risk associated with a doubling of the exposure biomarkers were 1.35 (p=0.015) for BPb, 1.13 (p=0.22) for BCd, and 1.23 (p=0.070) for UCd. In conclusion, our results suggest that environmental lead exposure is a risk factor for nephrolithiasis in the general population. - Highlights: • Prevalence and incidence rates of nephrolithiasis are increasing worldwide. • Lead and cadmium interfere with calcium homeostasis and might cause nephrolithiasis. • Environmental exposure to lead, not cadmium, predicts nephrolithiasis in the population. • Safety standards for environmental lead exposure need to account for nephrolithiasis. • Reducing environmental

Complications in autopsy cases of Hashimoto's disease with special reference to A-bomb exposure

International Nuclear Information System (INIS)

Asano, Masahide; Kato, Hiroo

1978-01-01

To clarify a relationship between A-bomb exposure and Hashimoto's disease and that between Hashimoto's disease and carcinoma of the thyroid gland, autopsy cases of Hashimoto's disease (112 cases in Hiroshima and 43 cases in Nagasaki) were examined. Incidence of Hashimoto's disease was not related to exposure doses and ages at the time of exposure. Incidence of carcinoma of the thyroid gland from Hashimoto's disease was 1.3% (2 cases), and there was no relationship between them. Incidence of ovarian cancer as cancer accompanied with Hashimoto's disease was significantly high, but that of stomach cancer was significantly low. Incidence of total cancer from Hashimoto's disease was also significantly low. Incidences of rheumatic fever and rheumatoid arthritis which were collagen diseases and diseases similar to them complicated by Hashimoto's disease was significantly high. (Tsunoda, M.)

Human exposure to environmental health concern by types of urban environment: The case of Tel Aviv

International Nuclear Information System (INIS)

Schnell, Izhak; Potchter, Oded; Yaakov, Yaron; Epstein, Yoram

2016-01-01

This study classifies urban environments into types characterized by different exposure to environmental risk factors measured by general sense of discomfort and Heart Rate Variability (HRV). We hypothesize that a set of environmental factors (micro-climatic, CO, noise and individual heart rate) that were measured simultaneously in random locations can provide a better understanding of the distribution of human exposure to environmental loads throughout the urban space than results calculated based on measurements from close fixed stations. We measured micro-climatic and thermal load, CO and noise, individual Heart Rate, Subjective Social Load and Sense of Discomfort (SD) were tested by questionnaire survey. The results demonstrate significant differences in exposure to environmental factors among 8 types of urban environments. It appears that noise and social load are the more significant environmental factors to enhance health risks and general sense of discomfort. - Highlights: • Indoor and outdoor environments were classified by exposure to health concern. • Measurements taken by people provide better knowledge than fixed stations. • Social stress and noise are more stressing factors than Thermal load and CO. • The most stressful places are crowded ones like markets etc. • Short visit in green spaces are effective in reducing levels of stress.

Webinar Presentation: Environmental Exposures and Health Risks in California Child Care Facilities: First Steps to Improve Environmental Health where Children Spend Time

Science.gov (United States)

This presentation, Environmental Exposures and Health Risks in California Child Care Facilities: First Steps to Improve Environmental Health where Children Spend Time, was given at the NIEHS/EPA Children's Centers 2016 Webinar Series: Exposome.

Environmental radioactivity: the importance of controlling exposure of the public: some experiences in Cuba

International Nuclear Information System (INIS)

Fernandez Gomez, Isis Maria

2008-01-01

The nuclear power is offering considerable advantages, it is considering the option to produce energy and the economy has moved in favour of the nuclear power. Therefore, the security is important within of the industry because ensures the control of public exposure and the environment and it plays a crucial role. Public exposure refers to exposure that is not of the direct work with ionizing radiation or the application of nuclear techniques in medical treatment and diagnosis. There are potential sources of discharges into the environment as the spent fuel and the waste disposal. Some of the routes of exposure are atmospheric discharge, liquid discharge, irrigation, environment, decomposition of the rain, food chains, etc. International regulations on subject of radiological safety are set by the IAEA and have a hierarchical order: fundamentals, requirements and guidelines. The International Commission of Radiological Protection and the Committee of the General Assembly of the United Nations are described in the research. The action is exposed in Cuba with regard to nuclear programs that have been realized or that are executed in relation to the control of the exposure of the public in existing applications. It mentions the centralized management of radioactive rights generated, the control of other sources of exposure, and the Red Nacional de Vigilancia Radiologica Ambiental. It also includes numerical data of studies realized on the extent of the sources of public exposure, the external doses received by the Cuban population product of environmental sources of radiation, the estimating of the doses received by the Cuban population by the incorporation of radionuclides present in the water and food. Likewise, the radioactive environmental funds; the phosphate mining; the protection and extraction of oil and the presence of radon inside the house are shown. The exposure to gamma radiation in thermal spas; the exposure to environmental sources of radiation

Impact of environmental exposures on the mutagenicity/carcinogenicity of heterocyclic amines

Energy Technology Data Exchange (ETDEWEB)

Felton, James S; Knize, Mark G; Bennett, L Michelle; Malfatti, Michael A; Colvin, Michael E; Kulp, Kristen S

2004-05-20

Carcinogenic heterocyclic amines are produced from overcooked foods and are highly mutagenic in most short-term test systems. One of the most abundant of these amines, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), induces breast, colon and prostate tumors in rats. Human dietary epidemiology studies suggest a strong correlation between either meat consumption or well-done muscle meat consumption and cancers of the colon, breast, stomach, lung and esophagus. For over 20 years our laboratory has helped define the human exposure to these dietary carcinogens. In this report we describe how various environmental exposures may modulate the risk from exposure to heterocyclic amines, especially PhIP. To assess the impact of foods on PhIP metabolism in humans, we developed an LC/MS/MS method to analyze the four major PhIP urinary metabolites following the consumption of a single portion of grilled chicken. Adding broccoli to the volunteers' diet altered the kinetics of PhIP metabolism. At the cellular level we have found that PhIP itself stimulates a significant estrogenic response in MCF-7 cells, but even more interestingly, co-incubation of the cells with herbal teas appear to enhance the response. Numerous environmental chemicals found in food or the atmosphere can impact the exposure, metabolism, and cell proliferation response of heterocyclic amines.

Impact of environmental exposures on the mutagenicity/carcinogenicity of heterocyclic amines

International Nuclear Information System (INIS)

Felton, James S.; Knize, Mark G.; Bennett, L. Michelle; Malfatti, Michael A.; Colvin, Michael E.; Kulp, Kristen S.

2004-01-01

Carcinogenic heterocyclic amines are produced from overcooked foods and are highly mutagenic in most short-term test systems. One of the most abundant of these amines, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), induces breast, colon and prostate tumors in rats. Human dietary epidemiology studies suggest a strong correlation between either meat consumption or well-done muscle meat consumption and cancers of the colon, breast, stomach, lung and esophagus. For over 20 years our laboratory has helped define the human exposure to these dietary carcinogens. In this report we describe how various environmental exposures may modulate the risk from exposure to heterocyclic amines, especially PhIP. To assess the impact of foods on PhIP metabolism in humans, we developed an LC/MS/MS method to analyze the four major PhIP urinary metabolites following the consumption of a single portion of grilled chicken. Adding broccoli to the volunteers' diet altered the kinetics of PhIP metabolism. At the cellular level we have found that PhIP itself stimulates a significant estrogenic response in MCF-7 cells, but even more interestingly, co-incubation of the cells with herbal teas appear to enhance the response. Numerous environmental chemicals found in food or the atmosphere can impact the exposure, metabolism, and cell proliferation response of heterocyclic amines

Exposure to Mobile Phone Radiation Opens New Horizons in Alzheimer’s Disease Treatment

Science.gov (United States)

Mortazavi, SAR; Shojaei-Fard, MB; Haghani, M; Shokrpour, N; Mortazavi, SMJ

2013-01-01

Alzheimer’s disease, the most common type of dementia and a progressive neurodegenerative disease, occurs when the nerve cells in the brain die. Although there are medications that can help delay the development of Alzheimer’s disease, there is currently no cure for this disease. Exposure to ionizing and non-ionizing radiation may cause adverse health effects such as cancer.  Looking at the other side of the coin, there are reports indicating stimulatory or beneficial effects after exposure to cell phone radiofrequency radiation. Mortazavi et al. have previously reported some beneficial cognitive effects such as decreased reaction time after human short-term exposure to cell phone radiation or occupational exposure to radar microwave radiation. On the other hand, some recent reports have indicated that RF radiation may have a role in protecting against cognitive impairment in Alzheimer’s disease. Although the majority of these data come from animal studies that cannot be easily extrapolated to humans, it can be concluded that this memory enhancing approach may open new horizons in treatment of cognitive impairment in Alzheimer disease. PMID:25505755

Exposure to Mobile Phone Radiation Opens New Horizons in Alzheimer’s Disease Treatment

Directory of Open Access Journals (Sweden)

Mortazavi SAR

2013-09-01

Full Text Available Alzheimer’s disease, the most common type of dementia and a progressive neurodegenerative disease, occurs when the nerve cells in the brain die. Although there are medications that can help delay the development of Alzheimer’s disease, there is currently no cure for this disease. Exposure to ionizing and non-ionizing radiation may cause adverse health effects such as cancer. Looking at the other side of the coin, there are reports indicating stimulatory or benefcial effects after exposure to cell phone radiofrequency radiation. Mortazavi et al. have previously reported some benefcial cognitive effects such as decreased reaction time after human short-term exposure to cell phone radiation or occupational exposure to radar microwave radiation. On the other hand, some recent reports have indicated that RF radiation may have a role in protecting against cognitive impairment in Alzheimer’s disease. Although the majority of these data come from animal studies that cannot be easily extrapolated to humans, it can be concluded that this memory enhancing approach may open new horizons in treatment of cognitive impairment in Alzheimer disease.

Metabolic profiling detects early effects of environmental and lifestyle exposure to cadmium in a human population

OpenAIRE

Ellis, James K; Athersuch, Toby J; Thomas, Laura DK; Teichert, Friederike; Pérez-Trujillo, Miriam; Svendsen, Claus; Spurgeon, David J; Singh, Rajinder; Järup, Lars; Bundy, Jacob G; Keun, Hector C

2012-01-01

Background: The ‘exposome’ represents the accumulation of all environmental exposures across a lifetime. Topdown strategies are required to assess something this comprehensive, and could transform our understanding of how environmental factors affect human health. Metabolic profiling (metabonomics/metabolomics) defines an individual’s metabolic phenotype, which is influenced by genotype, diet, lifestyle, health and xenobiotic exposure, and could also reveal intermediate biomarkers...

The effects of exposure to environmental factors on Heart Rate Variability: An ecological perspective

International Nuclear Information System (INIS)

Schnell, Izhak; Potchter, Oded; Epstein, Yoram; Yaakov, Yaron; Hermesh, Hagai; Brenner, Shmuel; Tirosh, Emanuel

2013-01-01

The impact of human exposure to environmental factors on Heart Rate Variability (HRV) was examined in the urban space of Tel-Aviv-Jaffa. Four environmental factors were investigated: thermal and social loads; CO concentrations and noise. Levels of HRV are explained mainly by subjective social stresses, noise and CO. The most interesting result is the fact that while subjective social stress and noise increase HRV, low levels of CO are reducing HRV to some extent moderating the impact of subjective social stress and noise. Beyond the poisoning effect of CO and the fact that extremely low levels of HRV associated with high dozes of CO increase risk for life, low levels of CO may have a narcotic effect, as it is measured by HRV. The effects of thermal loads on HRV are negligible probably due to the use of behavioral means in order to neutralize heat and cold effects. -- Highlights: ► The impact of human exposure to environmental factors on Heart Rate Variability (HRV) was examined. ► Previous studies measured human exposure to pollution by fixed monitoring stations. ► This study measured actual personal exposure by mini sensors. ► High level of subjective social load and noise increase HRV. ► Low levels of CO may have a narcotic effect, as it is measured by HRV. -- The research focuses on the effects of environmental factors; noise, subjective social stress, thermal load and CO on Heart Rate Variability

Environmental exposure at day care centres: are our children at risk?

CSIR Research Space (South Africa)

John, J

2005-09-01

Full Text Available This study aimed to characterize the exposure of 5-year old children attending preschool facilities in Pretoria to lead (as an example of an environmental pollutant) in air and surface soil, specifically in relation to their activity patterns....

Responses to occupational and environmental exposures in the U.S. military--World War II to the present.

Science.gov (United States)

Richards, Erin E

2011-07-01

Since the Civil War, a proportion of U.S. service members continues to return from war with new health problems and continues to reference battlefield exposures as the cause. Hence, one of the most pressing public health debates in military policy, the determination of causality and linking of battlefield exposures to health outcomes in veterans, continues. The advances in military environmental and occupational epidemiologic research and Department of Defense policy concerning battlefield exposures are summarized and examples from World War II through the first Gulf War are provided. The limitations associated with the unique battlefield environment, multiple environmental exposures, and the inherent stresses of war, beget challenges for researchers responsible for determining causality. In light of these difficulties, six strategies for addressing environmental exposures and their possible impact on veterans were recommended by the Institute of Medicine post Operation Desert Storm. These strategies, along with their respective progress and remaining gaps, are addressed.

Modelling exposure opportunities

DEFF Research Database (Denmark)

Sabel, Clive E.; Gatrell, Anthony C.; Löytönen, Markku

2000-01-01

This paper addresses the issues surrounding an individual's exposure to potential environmental risk factors, which can be implicated in the aetiology of a disease. We hope to further elucidate the 'lag' or latency period between the initial exposure to potential pathogens and the physical...... boundaries.We use kernel estimation to model space-time patterns. Raised relative risk is assessed by adopting appropriate adjustments for the underlying population at risk, with the use of controls. Significance of the results is assessed using Monte Carlo simulation, and comparisons are made with results...

Solid fuel smoke exposure and risk of obstructive airways disease

Directory of Open Access Journals (Sweden)

Qorbani Mostafa

2012-10-01

Full Text Available Abstract This study was designed to investigate whether there is an association between Obstructive Airways Disease (OAD and indoor exposure to baking home-made bread smoke (BHBS in ground oven at home. In this hospital-based case–control study, 83 patients with OAD (cases were compared with 72 patients without any known pulmonary diseases from the surgical ward (controls who were frequently matched with cases on age. The interview was performed using the modified questionnaire recommended by the "American Thoracic Society". The questionnaire comprised of demographic information, occupational history, cigarette smoking and indoor exposure to BHBS in ground oven at home. The exposure to BHBS was considered both as a dichotomous and quantitative variable (number of years being exposed to smoke and the population attributable fraction (PAF was estimated due to BHBS exposure. The percentage of indoor exposure to BHBS was measured as 51.8% and 30.6% in the cases and the controls, respectively. The average years of exposure to BHBS was 20.46 years (SD: 11.60 for the cases and 15.38 years (SD: 13.20 for the controls. The univariate analysis comparing the cases and the controls showed that exposure to BHBS (as a binary variable and occupational exposure to dust was significantly associated with OAD. In the multivariate model, only exposure to BHBS was associated with OAD (OR=2.22, 95%CI = 1.14-4.35. Duration of exposure to BHBS (as a quantitative variable was significantly associated with OAD in the univariate model. In the multivariate model, only the duration of exposure to BHBS (years showed a significant association with OAD (OR=1.04, 95% CI=1.01-1.08. Population attributable risk due to BHBS exposure was equal to 28.5%.

Early life exposure to antibiotics and the risk of childhood allergic diseases: an update from the perspective of the hygiene hypothesis.

Science.gov (United States)

Kuo, Chang-Hung; Kuo, Hsuan-Fu; Huang, Ching-Hua; Yang, San-Nan; Lee, Min-Sheng; Hung, Chih-Hsing

2013-10-01

The prevalence of allergic diseases has been growing rapidly in industrial countries during recent decades. It is postulated that growing up with less microbial exposure may render the immune system susceptible to a T helper type 2 (Th2)-predominant allergic response-also known as the hygiene hypothesis. This review delineates recent epidemiological and experimental evidence for the hygiene hypothesis, and integrates this hypothesis into the association between early life exposure to antibiotics and the development of allergic diseases and asthma. Several retrospective or prospective epidemiological studies reveal that early exposure to antibiotics may be positively associated with the development of allergic diseases and asthma. However, the conclusion is inconsistent. Experimental studies show that antibiotics may induce the Th2-skewed response by suppressing the T helper type 1 (Th1) response through inhibition of Th1 cytokines and disruption of the natural course of infection, or by disturbing the microflora of the gastrointestinal (GI) tract and therefore jeopardizing the establishment of oral tolerance and regulatory T cell immune responses. The hygiene hypothesis may not be the only explanation for the rapid increase in the prevalence of allergic diseases and asthma. Further epidemiological and experimental studies addressing the issue of the impact of environmental factors on the development of allergic diseases and the underlying mechanisms may unveil novel strategies for the prevention and treatment of allergic diseases in the future. Copyright © 2013. Published by Elsevier B.V.

[Monitoring of hematogenous occupational exposure in medical staff in infectious disease hospital].

Science.gov (United States)

Xie, Manxia; Zhou, Jin; Wang, Yimei

2015-10-01

To investigate the status and risk factors for hematogenous occupational exposure in medical staff in an infectious disease hospital, and to provide a scientific basis for targeted preventive and control measures. The occupational exposure of 395 medical workers in our hospital was monitored from January 2012 to December 2014, among whom 79 individuals with occupational exposure were subjected to intervention and the risk factors for occupational exposure were analyzed. The high-risk group was mainly the nursing staff (69.6%). The incidence of hematogenous occupational exposure was high in medical personnel with a working age under 3 years, aged under 25 years, and at the infection ward, accounting for 63.3%, 72.1%, and 72.2%, respectively. Hepatitis B virus, hepatitis C virus, Treponema pallidum, and human immunodeficiency virus were the primary exposure sources. Sharp injury was the major way of injury (91.1%), with needle stick injury accounting for the highest proportion (86.1%). Injury occurred on the hand most frequently (91.1%). The high-risk links were improper disposal during or after pulling the needle, re-capturing the needle, and processing waste, accounting for 46.8%, 17.7%, and 12.7%, respectively. Seventy-nine professionals with occupational exposure were not infected. The main risk factor for hematogenous occupational exposure in medical staff in the infectious disease hospital is needle stick injury. Strengthening the occupational protection education in medical staff in infectious disease hospital, implementing protective measures, standardizing operating procedures in high-risk links, and enhancing the supervision mechanism can reduce the incidence of occupational exposure and infection after exposure.

Air pollution and the fetal origin of disease: A systematic review of the molecular signatures of air pollution exposure in human placenta.

Science.gov (United States)

Luyten, Leen J; Saenen, Nelly D; Janssen, Bram G; Vrijens, Karen; Plusquin, Michelle; Roels, Harry A; Debacq-Chainiaux, Florence; Nawrot, Tim S

2018-06-13

Fetal development is a crucial window of susceptibility in which exposure-related alterations can be induced on the molecular level, leading to potential changes in metabolism and development. The placenta serves as a gatekeeper between mother and fetus, and is in contact with environmental stressors throughout pregnancy. This makes the placenta as a temporary organ an informative non-invasive matrix suitable to investigate omics-related aberrations in association with in utero exposures such as ambient air pollution. To summarize and discuss the current evidence and define the gaps of knowledge concerning human placental -omics markers in association with prenatal exposure to ambient air pollution. Two investigators independently searched the PubMed, ScienceDirect, and Scopus databases to identify all studies published until January 2017 with an emphasis on epidemiological research on prenatal exposure to ambient air pollution and the effect on placental -omics signatures. From the initial 386 articles, 25 were retained following an a priori set inclusion and exclusion criteria. We identified eleven studies on the genome, two on the transcriptome, five on the epigenome, five on the proteome category, one study with both genomic and proteomic topics, and one study with both genomic and transcriptomic topics. Six studies discussed the triple relationship between exposure to air pollution during pregnancy, the associated placental -omics marker(s), and the potential effect on disease development later in life. So far, no metabolomic or exposomic data discussing associations between the placenta and prenatal exposure to air pollution have been published. Integration of placental biomarkers in an environmental epidemiological context enables researchers to address fundamental questions essential in unraveling the fetal origin of disease and helps to better define the pregnancy exposome of air pollution. Copyright © 2018 Elsevier Inc. All rights reserved.

Fetal Exposure to Environmental Neurotoxins in Taiwan

OpenAIRE

Jiang, Chuen-Bin; Hsi, Hsing-Cheng; Fan, Chun-Hua; Chien, Ling-Chu

2014-01-01

Mercury (Hg), lead (Pb), cadmium (Cd), and arsenic (As) are recognized neurotoxins in children that particularly affect neurodevelopment and intellectual performance. Based on the hypothesis that the fetal basis of adult disease is fetal toxic exposure that results in adverse outcomes in adulthood, we explored the concentrations of key neurotoxins (i.e., Hg, Pb, Cd, and As) in meconium to identify the risk factors associated with these concentrations. From January 2007 to December 2009, 545 m...

Gestational diabetes and offspring birth size at elevated environmental pollutant exposures

DEFF Research Database (Denmark)

Valvi, Damaskini; Oulhote, Youssef; Weihe, Pal

2017-01-01

examined whether GDM may mediate or modify the associations between maternal environmental pollutant exposures and offspring birth size measures. METHODS: We analyzed 604 Faroese pregnant women and their offsprings born in 1997-2000. Maternal pregnancy serum concentrations of organochlorine compounds (OCs...... circumference in boys, and positive or null associations in girls. None of the environmental pollutants was associated with offspring length. GDM neither modified nor mediated the associations with birth size measures. CONCLUSIONS: We found associations with GDM and offspring birth size to be specific...... to the environmental pollutant or pollutant group. Associations with birth size measures appear to be independent of GDM occurrence....

Biochar physico-chemical properties as affected by environmental exposure

Energy Technology Data Exchange (ETDEWEB)

Sorrenti, Giovambattista, E-mail: g.sorrenti@unibo.it [Department of Agricultural Sciences, University of Bologna, viale G. Fanin 44, 40127 Bologna (Italy); Masiello, Caroline A., E-mail: masiello@rice.edu [Departments of Earth Science, BioSciences, and Chemistry, Rice University, Houston, TX 77005 (United States); Dugan, Brandon, E-mail: dugan@rice.edu [Department of Earth Science, Rice University, Houston, TX 77005 (United States); Toselli, Moreno, E-mail: moreno.toselli@unibo.it [Department of Agricultural Sciences, University of Bologna, viale G. Fanin 44, 40127 Bologna (Italy)

2016-09-01

To best use biochar as a sustainable soil management and carbon (C) sequestration technique, we must understand the effect of environmental exposure on its physical and chemical properties because they likely vary with time. These properties play an important role in biochar's environmental behavior and delivery of ecosystem services. We measured biochar before amendment and four years after amendment to a commercial nectarine orchard at rates of 5, 15 and 30 t ha{sup −1}. We combined two pycnometry techniques to measure skeletal (ρ{sub s}) and envelope (ρ{sub e}) density and to estimate the total pore volume of biochar particles. We also examined imbibition, which can provide information about soil hydraulic conductivity. Finally, we investigated the chemical properties, surface, inner layers atomic composition and C1s bonding state of biochar fragments through X-ray photoelectron spectroscopy (XPS). Ageing increased biochar skeletal density and reduced the water imbibition rate within fragments as a consequence of partial pore clogging. However, porosity and the volume of water stored in particles remained unchanged. Exposure reduced biochar pH, EC, and total C, but enhanced total N, nitrate-N, and ammonium-N. X-ray photoelectron spectroscopy analyses showed an increase of O, Si, N, Na, Al, Ca, Mn, and Fe surface (0–5 nm) atomic composition (at%) and a reduction of C and K in aged particles, confirming the interactions of biochar with soil inorganic and organic phases. Oxidation of aged biochar fragments occurred mainly in the particle surface, and progressively decreased down to 75 nm. Biochar surface chemistry changes included the development of carbonyl and carboxylate functional groups, again mainly on the particle surface. However, changes were noticeable down to 75 nm, while no significant changes were measured in the deepest layer, up to 110 nm. Results show unequivocal shifts in biochar physical and chemical properties/characteristics over

Chronic exposure to environmental levels of tribromophenol impairs zebrafish reproduction

International Nuclear Information System (INIS)

Deng Jun; Liu Chunsheng; Yu Liqin; Zhou Bingsheng

2010-01-01

Tribromophenol (2,4,6-TBP) is ubiquitously found in aquatic environments and biota. In this study, we exposed zebrafish embryos (F 0 ; 2'''' days post-fertilization, dpf) to environmental concentration (0.3 μg/L) and a higher concentration (3.0 μg/L) of TBP and assessed the impact of chronic exposure (120 dpf) on reproduction. TBP exposure did not cause a significant increase in the malformation and reduction in the survival in the F 0 -generation fish. After TBP exposure, the plasma testosterone and estradiol levels significantly increased in males and decreased in females. The transcription of steroidogenic genes (3β-HSD, 17β-HSD, CYP17, CYP19A, CYP19B) was significantly upregulated in the brain and testes in males and downregulated in the brain and ovary in females. TBP exposure significantly downregulated and upregulated the expression of VTG in the liver of female and male fish, respectively. Meanwhile, TBP exposure altered the sex ratio toward a male-dominant state. The F 1 -generation larvae exhibited increased malformation, reduced survival, and retarded growth, suggesting that TBP in the aquatic environment has significant adverse effects on fish population.

Normal mere exposure effect with impaired recognition in Alzheimer's disease

OpenAIRE

Willems, Sylvie; Adam, Stéphane; Van der Linden, Martial

2002-01-01

We investigated the mere exposure effect and the explicit memory in Alzheimer's disease (AD) patients and elderly control subjects, using unfamiliar faces. During the exposure phase, the subjects estimated the age of briefly flashed faces. The mere exposure effect was examined by presenting pairs of faces (old and new) and asking participants to select the face they liked. The participants were then presented with a forced-choice explicit recognition task. Controls subjects exhibited above-ch...

Determining the validity of exposure models for environmental epidemiology : predicting electromagnetic fields from mobile phone base stations

NARCIS (Netherlands)

Beekhuizen, Johan|info:eu-repo/dai/nl/34472641X

2014-01-01

One of the key challenges in environmental epidemiology is the exposure assessment of large populations. Spatial exposure models have been developed that predict exposure to the pollutant of interest for large study sizes. However, the validity of these exposure models is often unknown. In this

Exposure to Environmental Toxicants and Pathogenesis of Amyotrophic Lateral Sclerosis: State of the Art and Research Perspectives

Directory of Open Access Journals (Sweden)

Maria Rosaria Monsurrò

2013-07-01

Full Text Available There is a broad scientific consensus that amyotrophic lateral sclerosis (ALS, a fatal neuromuscular disease, is caused by gene-environment interactions. In fact, given that only about 10% of all ALS diagnosis has a genetic basis, gene-environmental interaction may give account for the remaining percentage of cases. However, relatively little attention has been paid to environmental and lifestyle factors that may trigger the cascade of motor neuron degeneration leading to ALS, although exposure to chemicals—including lead and pesticides—agricultural environments, smoking, intense physical activity, trauma and electromagnetic fields have been associated with an increased risk of ALS. This review provides an overview of our current knowledge of potential toxic etiologies of ALS with emphasis on the role of cyanobacteria, heavy metals and pesticides as potential risk factors for developing ALS. We will summarize the most recent evidence from epidemiological studies and experimental findings from animal and cellular models, revealing that potential causal links between environmental toxicants and ALS pathogenesis have not been fully ascertained, thus justifying the need for further research.

Prenatal exposure to environmental chemical contaminants and asthma and eczema in school-age children

DEFF Research Database (Denmark)

Smit, Lidwien A M; Lenters, Virissa; Høyer, Birgit Bjerre

2015-01-01

BACKGROUND: Emerging evidence suggests that prenatal or early-life exposures to environmental contaminants may contribute to an increased risk of asthma and allergies in children. We aimed to the explore associations of prenatal exposures to a large set of environmental chemical contaminants...... asthma, eczema, and wheeze. We applied principal components analysis (PCA) to sixteen contaminants in maternal serum sampled during pregnancy, including perfluoroalkyl substances (PFASs), metabolites of diethylhexyl (DEHP) and diisononyl (DiNP) phthalates, PCB-153, and p,p'-DDE. Scores of five principal...... components (PCs) explaining 70% of the variance were included in multiple logistic regression models. RESULTS: In a meta-analysis that included both populations, the PC2 score, reflecting exposure to DiNP, was negatively associated with current eczema (OR 0.71, 95% CI 0.52-0.96). Other associations were...

The Matthew Effect and widely prescribed pharmaceuticals lacking environmental monitoring: case study of an exposure-assessment vulnerability.

Science.gov (United States)

Daughton, Christian G

2014-01-01

Assessing ambient exposure to chemical stressors often begins with time-consuming and costly monitoring studies to establish environmental occurrence. Both human and ecological toxicology are currently challenged by the unknowns surrounding low-dose exposure/effects, compounded by the reality that exposure undoubtedly involves mixtures of multiple stressors whose identities and levels can vary over time. Long absent from the assessment process, however, is whether the full scope of the identities of the stressors is sufficiently known. The Matthew Effect (a psychosocial phenomenon sometimes informally called the "bandwagon effect" or "iceberg effect," among others) may adversely bias or corrupt the exposure assessment process. The Matthew Effect is evidenced by decisions that base the selection of stressors to target in environmental monitoring surveys on whether they have been identified in prior studies, rather than considering the possibility that additional, but previously unreported, stressors might also play important roles in an exposure scenario. The possibility that the Matthew Effect might influence the scope of environmental stressor research is explored for the first time in a comprehensive case study that examines the preponderance of "absence of data" (in contrast to positive data and "data of absence") for the environmental occurrence of a very large class of potential chemical stressors associated with ubiquitous consumer use - active pharmaceutical ingredients (APIs). Comprehensive examination of the published data for an array of several hundred of the most frequently used drugs for whether their APIs are environmental contaminants provides a prototype example to catalyze discussion among the many disciplines involved with assessing risk. The findings could help guide the selection of those APIs that might merit targeting for environmental monitoring (based on the absence of data for environmental occurrence) as well as the prescribing of those

The role of environmental tobacco exposure and Helicobacter pylori infection in the risk of chronic tonsillitis in children

Directory of Open Access Journals (Sweden)

Chen Li’e

Full Text Available ABSTRACT CONTEXT AND OBJECTIVE: Helicobacter pylori (H. pylori is a chronic infectious pathogen with high prevalence. This study investigated the interaction between environmental tobacco exposure and H. pylori infection on the incidence of chronic tonsillitis in Chinese children. DESIGN AND SETTING: Cross-sectional study performed in an outpatient clinic in China. METHODS: Pediatric patients with chronic tonsillitis were enrolled. H. pylori infection was determined according to the presence of H. pylori CagA IgG antibodies. Serum cotinine levels and environmental tobacco smoke (ETS exposure were determined for all participants. RESULTS: There was no significant difference in H. pylori infection between the children with chronic tonsillitis and children free of disease, but there was a significant difference in ETS between the two groups (P = 0.011. We next studied the association between ETS and chronic tonsillitis based on H. pylori infection status. In the patients with H. pylori infection, there was a significant difference in ETS distribution between the chronic tonsillitis and control groups (P = 0.022. Taking the participants without ETS as the reference, multivariate logistic regression analysis showed that those with high ETS had higher susceptibility to chronic tonsillitis (adjusted OR = 2.33; 95% CI: 1.67-3.25; adjusted P < 0.001. However, among those without H. pylori infection, ETS did not predispose towards chronic tonsillitis. CONCLUSION: Our findings suggest that tobacco exposure should be a putative mediator risk factor to chronic tonsillitis among children with H. pylori infection.

Palivizumab Exposure and the Risk of Autoimmune Disease

DEFF Research Database (Denmark)

Haerskjold, Ann; Linder, Marie; Henriksen, Lonny

2016-01-01

of autoimmune disease were diagnosed among palivizumab-exposed children during the period of observation. Among the children exposed to palivizumab, one child in Denmark developed inflammatory bowel disease; in Sweden, children developed juvenile arthritis (one child), diabetes mellitus (two children), celiac......BACKGROUND: Treatment with biologic pharmaceuticals may be associated with an increased risk of immune-mediated disease. Palivizumab is a humanized monoclonal antibody designed to provide passive immunity against respiratory syncytial virus infection. Palivizumab is primarily used in preterm...... children known to be immunologically immature. The long-term effect of palivizumab in terms of autoimmune diseases has not yet been investigated. AIM: Our objective was to investigate whether exposure to palivizumab was associated with the development of autoimmune diseases in children. METHODS...

[Allergy - an environmental disease].

Science.gov (United States)

Traidl-Hoffmann, Claudia

2017-06-01

The increase in allergies is a phenomenon that is being observed in all fast-developing countries. For a long time, science has taken as a starting point that solely a genetic predisposition is a precondition for the development of an allergy. Today, knowledge of environmental factors that can alter genes or the transcription of genes in the cells, has improved. Epidemiological studies have meanwhile identified several environmental factors that have a protective or supporting effect on allergy development. The environmental microbiome has recently gained central interest. A common theme in most of the studies is diversity: reduced diversity is correlated with enhanced risk for chronic inflammatory diseases and allergy.It is now of great interest for research to further analyze such environment-gene and/or environment-human interactions on all levels - from organs to cells to small and microstructures such as genes. For immunologists, it is specifically about understanding the influencing factors and effector pathways of allergens, and to apply thereby obtained insights in the follow-up for the ultimate goal of allergy research - prevention.

Serum metabolome biomarkers associate low-level environmental perfluorinated compound exposure with oxidative /nitrosative stress in humans.

Science.gov (United States)

Wang, Xiaofei; Liu, Liangpo; Zhang, Weibing; Zhang, Jie; Du, Xiaoyan; Huang, Qingyu; Tian, Meiping; Shen, Heqing

2017-10-01

Previous in vivo and in vitro studies have linked perfluorinated compound (PFC) exposure with metabolic interruption, but the inter-species difference and high treatment doses usually make the results difficult to be extrapolated to humans directly. The best strategy for identifying the metabolic interruption may be to establish the direct correlations between monitored PFCs data and metabolic data on human samples. In this study, serum metabolome data and PFC concentrations were acquired for a Chinese adult male cohort. The most abundant PFCs are PFOA and PFOS with concentration medians 7.56 and 12.78 nM, respectively; in together they count around 81.6% of the total PFCs. PFC concentration-related serum metabolic profile changes and the related metabolic biomarkers were explored by using partial least squares-discriminant analysis (PLS-DA). Respectively taking PFOS, PFOA and total PFC as the classifiers, serum metabolome can be differentiated between the lowest dose group (1st quartile PFCs) and the highest PFC dose group (4th quartile PFCs). Ten potential PFC biomarkers were identified, mainly involving in pollutant detoxification, antioxidation and nitric oxide (NO) signal pathways. These suggested that low-level environmental PFC exposure has significantly adverse impacts on glutathione (GSH) cycle, Krebs cycle, nitric oxide (NO) generation and purine oxidation in humans. To the best of our knowledge, this is the first report investigating the association of environmental PFC exposure with human serum metabolome alteration. Given the important biological functions of the identified biomarkers, we suggest that PFC could increase the metabolism syndromes risk including diabetes and cardiovascular diseases. Copyright © 2017 Elsevier Ltd. All rights reserved.

Exposure to Mobile Phone Radiation Opens New Horizons in Alzheimer’s Disease Treatment

OpenAIRE

Mortazavi SAR; Shojaei-Fard MB; Haghani M; Shokrpour N; Mortazavi SMJ

2013-01-01

Alzheimer’s disease, the most common type of dementia and a progressive neurodegenerative disease, occurs when the nerve cells in the brain die. Although there are medications that can help delay the development of Alzheimer’s disease, there is currently no cure for this disease. Exposure to ionizing and non-ionizing radiation may cause adverse health effects such as cancer.  Looking at the other side of the coin, there are reports indicating stimulatory or beneficial effects after exposure t...

Confirmation of childhood acute lymphoblastic leukemia variants, ARID5B and IKZF1, and interaction with parental environmental exposures.

Directory of Open Access Journals (Sweden)

Tiffany-Jane Evans

Full Text Available Genome wide association studies (GWAS have established association of ARID5B and IKZF1 variants with childhood acute lymphoblastic leukemia (ALL. Epidemiological studies suggest that environmental factors alone appear to make a relatively minor contribution to disease risk. The polygenic nature of childhood ALL predisposition together with the timing of environmental triggers may hold vital clues for disease etiology. This study presents results from an Australian GWAS of childhood ALL cases (n = 358 and population controls (n = 1192. Furthermore, we utilised family trio (n = 204 genotypes to extend our investigation to gene-environment interaction of significant loci with parental exposures before conception, and child's sex and age. Thirteen SNPs achieved genome wide significance in the population based case/control analysis; ten annotated to ARID5B and three to IKZF1. The most significant SNPs in these regions were ARID5B rs4245595 (OR 1.63, CI 1.38-1.93, P = 2.13×10(-9, and IKZF1 rs1110701 (OR 1.69, CI 1.42-2.02, p = 7.26×10(-9. There was evidence of gene-environment interaction for risk genotype at IKZF1, whereby an apparently stronger genetic effect was observed if the mother took folic acid or if the father did not smoke prior to pregnancy (respective interaction P-values: 0.04, 0.05. There were no interactions of risk genotypes with age or sex (P-values >0.2. Our results evidence that interaction of genetic variants and environmental exposures may further alter risk of childhood ALL however, investigation in a larger population is required. If interaction of folic acid supplementation and IKZF1 variants holds, it may be useful to quantify folate levels prior to initiating use of folic acid supplements.

Ambient air pollution exposure and the incidence of related health effects among racial/ethnic minorities

Energy Technology Data Exchange (ETDEWEB)

Nieves, L.A.; Wernette, D.R.

1997-02-01

Differences among racial and ethnic groups in morbidity and mortality rates for diseases, including diseases with environmental causes, have been extensively documented. However, documenting the linkages between environmental contaminants, individual exposures, and disease incidence has been hindered by difficulties in measuring exposure for the population in general and for minority populations in particular. After briefly discussing research findings on associations of common air pollutants with disease incidence, the authors summarize recent studies of radial/ethnic subgroup differences in incidence of these diseases in the US. They then present evidence of both historic and current patterns of disproportionate minority group exposure to air pollution as measured by residence in areas where ambient air quality standards are violated. The current indications of disproportionate potential exposures of minority and low-income populations to air pollutants represent the continuation of a historical trend. The evidence of linkage between disproportionate exposure to air pollution of racial/ethnic minorities and low-income groups and their higher rates of some air pollution-related diseases is largely circumstantial. Differences in disease incidence and mortality rates among racial/ethnic groups are discussed for respiratory diseases, cancers, and lead poisoning. Pollutants of concern include CO, Pb, SO{sub 2}, O{sub 3}, and particulates.

Final report on the Project Research 'Assessment of Human Exposure to Environmental Radiation'

International Nuclear Information System (INIS)

1989-03-01

This is the final report of the Project Research, 'Assessment of Human Exposure to Environmental Radiation', which has been conducted during the period 1983-1988. With the objective of assessing risk of environmental radioactivity to the population, the Project was divided into the following five research groups: (1) research for establishing calculation models and parameters in transfer of radionuclides from crop species through the human body; (2) research for analyzing transfer of radionuclides in the ocean and their contributions to exposure doses in the human body; (3) research for surveying accuracy of exposure models for the external body and respiratory organ and the influential factors; (4) research for determining uptake and biokinetics of radionuclides in the body; and (5) research for estimating and evaluating physical and physiological characteristics of reference Japanese man and the populaltion doses. Effluents from nuclear power plants and reprocessing plants were regarded as radionuclide sources in the water and atmosphere. (N.K.)

Child's play : investigating the exposure potential of environmental contaminants in soil

International Nuclear Information System (INIS)

Pearce, D.C.; Dowling, K.; Waldron, H.; Garnett, D.

2005-01-01

Arsenic and chromium have been identified as soil contaminants from smelting, industrial and mining activities. The potential for human uptake of these elements from soil has been established with highest concentrations found in children, who are particularly susceptible to environmental exposure. This study explores the exposure potential of selected soil trace elements in rural Victoria, Australia, by investigating the relationship between uptake, measured using toenail clippings as the biomarker of exposure, and soil concentrations in two communities: one near current and historic gold mining, the other an agricultural community. We report the preliminary findings of a cross-sectional survey, in which toenail clippings were obtained from 12 children in the former community, and 16 children in the latter. (author). 26 refs., 3 tabs

A Review of Environmental Occurrence, Fate, Exposure, and Toxicity of Benzothiazoles.

Science.gov (United States)

Liao, Chunyang; Kim, Un-Jung; Kannan, Kurunthachalam

2018-05-01

Benzothiazole and its derivatives (BTs) are high production volume chemicals that have been used for several decades in a large number of industrial and consumer products, including vulcanization accelerators, corrosion inhibitors, fungicides, herbicides, algicides, and ultraviolet (UV) light stabilizers. Several benzothiazole derivatives are used commercially, and widespread use of these chemicals has led to ubiquitous occurrence in diverse environmental compartments. BTs have been reported to be dermal sensitizers, respiratory tract irritants, endocrine disruptors, carcinogens, and genotoxicants. This article reviews occurrence and fate of a select group of BTs in the environment, as well as human exposure and toxicity. BTs have frequently been found in various environmental matrices at concentrations ranging from sub-ng/L (surface water) to several tens of μg/g (indoor dust). The use of BTs in a number of consumer products, especially in rubber products, has resulted in widespread human exposure. BTs undergo chemical, biological, and photolytic degradation in the environment, creating several transformation products. Of these, 2-thiocyanomethylthio-benzothiazole (2-SCNMeS-BTH) has been shown to be the most toxic. Epidemiological studies have shown excess risks of cancers, including bladder cancer, lung cancer, and leukemia, among rubber factory workers, particularly those exposed to 2-mercapto-benzothiazole (2-SH-BTH). Human exposure to BTs continues to be a concern.

Environmental proxies of antigen exposure explain variation in immune investment better than indices of pace of life.

Science.gov (United States)

Horrocks, Nicholas P C; Hegemann, Arne; Ostrowski, Stéphane; Ndithia, Henry; Shobrak, Mohammed; Williams, Joseph B; Matson, Kevin D; Tieleman, B I

2015-01-01

Investment in immune defences is predicted to covary with a variety of ecologically and evolutionarily relevant axes, with pace of life and environmental antigen exposure being two examples. These axes may themselves covary directly or inversely, and such relationships can lead to conflicting predictions regarding immune investment. If pace of life shapes immune investment then, following life history theory, slow-living, arid zone and tropical species should invest more in immunity than fast-living temperate species. Alternatively, if antigen exposure drives immune investment, then species in antigen-rich tropical and temperate environments are predicted to exhibit higher immune indices than species from antigen-poor arid locations. To test these contrasting predictions we investigated how variation in pace of life and antigen exposure influence immune investment in related lark species (Alaudidae) with differing life histories and predicted risks of exposure to environmental microbes and parasites. We used clutch size and total number of eggs laid per year as indicators of pace of life, and aridity, and the climatic variables that influence aridity, as correlates of antigen abundance. We quantified immune investment by measuring four indices of innate immunity. Pace of life explained little of the variation in immune investment, and only one immune measure correlated significantly with pace of life, but not in the predicted direction. Conversely, aridity, our proxy for environmental antigen exposure, was predictive of immune investment, and larks in more mesic environments had higher immune indices than those living in arid, low-risk locations. Our study suggests that abiotic environmental variables with strong ties to environmental antigen exposure can be important correlates of immunological variation.

Disease awareness advertising - women's intentions following exposure.

Science.gov (United States)

Hall, Danika; Jones, Sandra; Iverson, Don

2011-03-01

In Australia, where direct to consumer advertising of prescription medicines is prohibited, pharmaceutical companies can sponsor disease awareness advertising targeting consumers. This study examined the impact of disease awareness advertising exposure on older women's reported behavioural intentions. Women were approached in a shopping centre and randomly assigned mock advertisements for two health conditions. Disease information and sponsors were manipulated. Two hundred and forty-one women responded to 466 advertisements. Almost half reported an intention to ask their doctor for a prescription or referral as a result of seeing the advertisement, but more reported they would talk to their doctor and ask about treatments and tests. Participants were more likely to report an intention to ask for prescriptions if they perceived the health condition to be severe and themselves susceptible or if they had viewed advertisements containing limited information on the disease. Disease awareness advertising may stimulate demand for prescription medicine products. This has serious implications for general practitioners and regulators.

Environmental and occupational health research and training needs in Colombia: A Delphi study.

Science.gov (United States)

Rodríguez-Villamizar, Laura A; González, Beatriz Elena; Vera, Lina María; Patz, Jonathan; Bautista, Leonelo E

2015-08-01

Environmental factors contribute with 16% of the burden of disease in Colombia. A main obstacle in implementing national and regional environmental and occupational health policies is the limited knowledge on the local ability to study and control the impact of harmful exposures on health. To identify needs for research and training in environmental and occupational health in Colombia. We conducted a three-round hybrid Delphi study. A group of environmental and occupational health Colombian experts (n=16) from government agencies, universities, and research centers was recruited to participate in the study. Expert´s opinions on research and training needs were gathered through online questionnaires, followed by an in-person meeting. The percentage of agreement and the coefficient of variation were used to measure consensus. Air pollution and chemical products were considered the most important environmental and occupational exposures, due to their significant impact on chronic non-communicable diseases, such as respiratory diseases, cardiovascular diseases, and cancer. Research on the effects of outdoor air pollution on cardiovascular and respiratory diseases was considered of the greatest importance. Priority training areas included environmental and occupational health risk assessment, exposure modeling, advanced statistical methods, urban planning, occupational safety and hygiene, and epidemiology and toxicology. These findings provide a valuable input for the definition and implementation of national environmental and occupational health policies and for the development of a regional hub aimed at strengthening the capacity for research and training in Colombia.

Environmental and occupational health research and training needs in Colombia: A Delphi study

Science.gov (United States)

Rodríguez-Villamizar, Laura A.; González, Beatriz Elena; Vera, Lina María; Patz, Jonathan; Bautista, Leonelo E.

2015-01-01

Introduction Environmental factors contribute with 16% of the burden of disease in Colombia. A main obstacle in implementing national and regional environmental and occupational health policies is the limited knowledge on the local ability to study and control the impact of harmful exposures on health. Objective To identify needs for research and training in environmental and occupational health in Colombia. Materials and methods We conducted a three-round hybrid Delphi study. A group of environmental and occupational health Colombian experts (n=16) from government agencies, universities, and research centers was recruited to participate in the study. Expert’s opinions on research and training needs were gathered through online questionnaires, followed by an in-person meeting. The percentage of agreement and the coefficient of variation were used to measure consensus. Results Air pollution and chemical products were considered the most important environmental and occupational exposures, due to their significant impact on chronic non-communicable diseases, such as respiratory diseases, cardiovascular diseases, and cancer. Research on the effects of outdoor air pollution on cardiovascular and respiratory diseases was considered of the greatest importance. Priority training areas included environmental and occupational health risk assessment, exposure modeling, advanced statistical methods, urban planning, occupational safety and hygiene, and epidemiology and toxicology. Conclusions These findings provide a valuable input for the definition and implementation of national environmental and occupational health policies and for the development of a regional hub aimed at strengthening the capacity for research and training in Colombia. PMID:26535742

Nature exposure sufficiency and insufficiency: The benefits of environmental preservation.

Science.gov (United States)

Reddon, John R; Durante, Salvatore B

2018-01-01

Increasing industrialization, urbanization, and a failure of many world leaders to appreciate the consequences of climate change are deleteriously impacting quality of life as well as diminishing the prospects for long term survival. Economic competitiveness and corporate profitability often pre-empt environmental concerns. The calving of an iceberg in Antarctica and the hurricane activity in the Caribbean during 2017 are unfortunate illustrations of the continuing escalation of environmental issues. We provide historical and current evidence for the importance of Nature Exposure (NE) and introduce the continuum Nature Exposure Sufficiency (NES) and Insufficiency (NEI). Insufficiency includes impoverished environments (e.g., slums and prisons) where nature exposure is very limited. Nature Exposure Sufficiency (NES) is an optimal amount of exposure to nature where many benefits such as reinvigoration can be obtained by everyone. NES also has several benefits for individuals with various health conditions such as arthritis, dementia, or depression. The benefits of NE are not just derivable from parks, forests, and other natural settings. Interiors of buildings and homes can be enhanced with plants and even pictures or objects from nature. Additionally, there is abundant evidence indicating that virtual and artificial environments depicting nature can provide substantial NE and therefore contribute to general wellbeing. Besides the difficulty in achieving cooperation amongst nations, corporations, and other collectives in developing and implementing long range plans to deal with climate change, there is also sometimes an aversion at the individual level whereby people are unwilling to experience nature due to insects and other discomforts. Such individuals are often averse to supplanting the comforts of home, even temporarily, with inadequate facilities that are seemingly less pleasant than their typical dwellings. We propose using the term Nature Exposure Aversion

Conceptualization and measurement of environmental exposure in epidemiology: accounting for activity space related to daily mobility.

Science.gov (United States)

Perchoux, Camille; Chaix, Basile; Cummins, Steven; Kestens, Yan

2013-05-01

A considerable body of literature has investigated how environmental exposures affect health through various pathways. These studies have generally adopted a common approach to define environmental exposures, focusing on the local residential environment, using census tracts or postcodes to delimit exposures. However, use of such administrative units may not be appropriate to evaluate contextual effets on health because they are generally not a 'true' representation of the environments to which individuals are exposed. Recent work has suggested that advances may be made if an activity-space approach is adopted. The present paper investigates how various disciplines may contribute to the refinement of the concept of activity space for use in health research. In particular we draw on seminal work in time geography, which provides a framework to describe individual behavior in space and time, and can help the conceptualization of activity space. In addition we review work in environmental psychology and social networks research, which provides insights on how people and places interact and offers new theories for improving the spatial definition of contextual exposures. Copyright © 2013 Elsevier Ltd. All rights reserved.

Workshop. Assessment of Occupational and Environmental Exposure to Genotoxic Substances - a Methodological Approach

International Nuclear Information System (INIS)

2000-01-01

During the workshop various works concerning radiobiology, environmental and occupational medicine were presented. Exposure to genotoxic and carcinogenic agents, like ionizing radiation, aromatic hydrocarbons, herbicides, pesticides was investigated

Modern environmental health hazards: a public health issue of increasing significance in Africa.

Science.gov (United States)

Nweke, Onyemaechi C; Sanders, William H

2009-06-01

Traditional hazards such as poor sanitation currently account for most of Africa's environmentally related disease burden. However, with rapid development absent appropriate safeguards for environment and health, modern environmental health hazards (MEHHs) may emerge as critical contributors to the continent's disease burden. We review recent evidence of human exposure to and health effects from MEHHs, and their occurrence in environmental media and consumer products. Our purpose is to highlight the growing significance of these hazards as African countries experience urbanization, industrial growth, and development. We reviewed published epidemiologic, exposure, and environmental studies of chemical agents such as heavy metals and pesticides. The body of evidence demonstrates ongoing environmental releases of MEHHs and human exposures sometimes at toxicologically relevant levels. Several sources of MEHHs in environmental media have been identified, including natural resource mining and processing and automobile exhaust. Biomonitoring studies provided direct evidence of human exposure to metals such as mercury and lead and pesticides such as p,p'-dichlorodiphenyltrichloroethane (DDT) and organophosphates. Land and water resource pollution and industrial air toxics are areas of significant data gaps, notwithstanding the presence of several emitting sources. Unmitigated MEHH releases and human exposure have implications for Africa's disease burden. For Africans encumbered by conditions such as malnutrition that impair resilience to toxicologic challenges, the burden may be higher. A shift in public health policy toward accommodating the emerging diversity in Africa's environmental health issues is necessary to successfully alleviate the burden of avoidable ill health and premature death for all its communities now and in the future.

The Adverse Effects of Environmental Noise Exposure on Oxidative Stress and Cardiovascular Risk

Science.gov (United States)

Sørensen, Mette; Schmidt, Frank; Schmidt, Erwin; Steven, Sebastian; Kröller-Schön, Swenja; Daiber, Andreas

2018-01-01

Abstract Epidemiological studies have provided evidence that traffic noise exposure is linked to cardiovascular diseases such as arterial hypertension, myocardial infarction, and stroke. Noise is a nonspecific stressor that activates the autonomous nervous system and endocrine signaling. According to the noise reaction model introduced by Babisch and colleagues, chronic low levels of noise can cause so-called nonauditory effects, such as disturbances of activity, sleep, and communication, which can trigger a number of emotional responses, including annoyance and subsequent stress. Chronic stress in turn is associated with cardiovascular risk factors, comprising increased blood pressure and dyslipidemia, increased blood viscosity and blood glucose, and activation of blood clotting factors, in animal models and humans. Persistent chronic noise exposure increases the risk of cardiometabolic diseases, including arterial hypertension, coronary artery disease, diabetes mellitus type 2, and stroke. Recently, we demonstrated that aircraft noise exposure during nighttime can induce endothelial dysfunction in healthy subjects and is even more pronounced in coronary artery disease patients. Importantly, impaired endothelial function was ameliorated by acute oral treatment with the antioxidant vitamin C, suggesting that excessive production of reactive oxygen species contributes to this phenomenon. More recently, we introduced a novel animal model of aircraft noise exposure characterizing the underlying molecular mechanisms leading to noise-dependent adverse oxidative stress-related effects on the vasculature. With the present review, we want to provide an overview of epidemiological, translational clinical, and preclinical noise research addressing the nonauditory, adverse effects of noise exposure with focus on oxidative stress. Antioxid. Redox Signal. 28, 873–908. PMID:29350061

Widespread covariation of early environmental exposures and trait-associated polygenic variation.

Science.gov (United States)

Krapohl, E; Hannigan, L J; Pingault, J-B; Patel, H; Kadeva, N; Curtis, C; Breen, G; Newhouse, S J; Eley, T C; O'Reilly, P F; Plomin, R

2017-10-31

Although gene-environment correlation is recognized and investigated by family studies and recently by SNP-heritability studies, the possibility that genetic effects on traits capture environmental risk factors or protective factors has been neglected by polygenic prediction models. We investigated covariation between trait-associated polygenic variation identified by genome-wide association studies (GWASs) and specific environmental exposures, controlling for overall genetic relatedness using a genomic relatedness matrix restricted maximum-likelihood model. In a UK-representative sample ( n = 6,710), we find widespread covariation between offspring trait-associated polygenic variation and parental behavior and characteristics relevant to children's developmental outcomes-independently of population stratification. For instance, offspring genetic risk for schizophrenia was associated with paternal age ( R 2 = 0.002; P = 1e-04), and offspring education-associated variation was associated with variance in breastfeeding ( R 2 = 0.021; P = 7e-30), maternal smoking during pregnancy ( R 2 = 0.008; P = 5e-13), parental smacking ( R 2 = 0.01; P = 4e-15), household income ( R 2 = 0.032; P = 1e-22), watching television ( R 2 = 0.034; P = 5e-47), and maternal education ( R 2 = 0.065; P = 3e-96). Education-associated polygenic variation also captured covariation between environmental exposures and children's inattention/hyperactivity, conduct problems, and educational achievement. The finding that genetic variation identified by trait GWASs partially captures environmental risk factors or protective factors has direct implications for risk prediction models and the interpretation of GWAS findings.

Exposure calculations for the FRG isotopic heat source project environmental assessment

International Nuclear Information System (INIS)

Metcalf, I.L.

1997-01-01

The report documents the maximum exposure for transfer of the Federal Republic of Germany (FRG) Isotopic Heat Sources from the 324 Building and placed in interim storage at the Central Waste Complex (CWC). These results are to be reported in the Environmental Assessment DOE-EA- 1 21 1

Cardiovascular disease hospitalizations in relation to exposure to the September 11, 2001 World Trade Center disaster and posttraumatic stress disorder.

Science.gov (United States)

Jordan, Hannah T; Stellman, Steven D; Morabia, Alfredo; Miller-Archie, Sara A; Alper, Howard; Laskaris, Zoey; Brackbill, Robert M; Cone, James E

2013-10-24

A cohort study found that 9/11-related environmental exposures and posttraumatic stress disorder increased self-reported cardiovascular disease risk. We attempted to replicate these findings using objectively defined cardiovascular disease hospitalizations in the same cohort. Data for adult World Trade Center Health Registry enrollees residing in New York State on enrollment and no cardiovascular disease history (n = 46,346) were linked to a New York State hospital discharge-reporting system. Follow-up began at Registry enrollment (2003-2004) and ended at the first cerebrovascular or heart disease (HD) hospitalization, death, or December 31, 2010, whichever was earliest. We used proportional hazards models to estimate adjusted hazard ratios (AHRs) for HD (n = 1151) and cerebrovascular disease (n = 284) hospitalization during 302,742 person-years of observation (mean follow-up, 6.5 years per person), accounting for other factors including age, race/ethnicity, smoking, and diabetes. An elevated risk of HD hospitalization was observed among women (AHR 1.32, 95% CI 1.01 to 1.71) but not men (AHR 1.16, 95% CI 0.97 to 1.40) with posttraumatic stress disorder at enrollment. A high overall level of World Trade Center rescue and recovery-related exposure was associated with an elevated HD hospitalization risk in men (AHR 1.82, 95% CI 1.06 to 3.13; P for trend = 0.05), but findings in women were inconclusive (AHR 3.29, 95% CI 0.85 to 12.69; P for trend = 0.09). Similar associations were observed specifically with coronary artery disease hospitalization. Posttraumatic stress disorder increased the cerebrovascular disease hospitalization risk in men but not in women. 9/11-related exposures and posttraumatic stress disorder appeared to increase the risk of subsequent hospitalization for HD and cerebrovascular disease. This is consistent with findings based on self-reported outcomes.

An Agent-Based Modeling Framework for Simulating Human Exposure to Environmental Stresses in Urban Areas

Directory of Open Access Journals (Sweden)

Liang Emlyn Yang

2018-04-01

Full Text Available Several approaches have been used to assess potential human exposure to environmental stresses and achieve optimal results under various conditions, such as for example, for different scales, groups of people, or points in time. A thorough literature review in this paper identifies the research gap regarding modeling approaches for assessing human exposure to environment stressors, and it indicates that microsimulation tools are becoming increasingly important in human exposure assessments of urban environments, in which each person is simulated individually and continuously. The paper further describes an agent-based model (ABM framework that can dynamically simulate human exposure levels, along with their daily activities, in urban areas that are characterized by environmental stresses such as air pollution and heat stress. Within the framework, decision-making processes can be included for each individual based on rule-based behavior in order to achieve goals under changing environmental conditions. The ideas described in this paper are implemented in a free and open source NetLogo platform. A basic modeling scenario of the ABM framework in Hamburg, Germany, demonstrates its utility in various urban environments and individual activity patterns, as well as its portability to other models, programs, and frameworks. The prototype model can potentially be extended to support environmental incidence management through exploring the daily routines of different groups of citizens, and comparing the effectiveness of different strategies. Further research is needed to fully develop an operational version of the model.

Exposure to environmental noise and risk for male infertility: A population-based cohort study

International Nuclear Information System (INIS)

Min, Kyoung-Bok; Min, Jin-Young

2017-01-01

Background: Noise is associated with poor reproductive health. A number of animal studies have suggested the possible effects of exposure to high noise levels on fertility; to date, a little such research has been performed on humans. Objectives: We examined an association between daytime and nocturnal noise exposures over four years (2002–2005) and subsequent male infertility. Methods: We used the National Health Insurance Service-National Sample Cohort (2002–2013), a population-wide health insurance claims dataset. A total of 206,492 males of reproductive age (20–59 years) with no history of congenital malformations were followed up for an 8-year period (2006–2013). Male infertility was defined as per ICD-10 code N46. Data on noise exposure was obtained from the National Noise Information System. Exposure levels of daytime and night time noise were extrapolated using geographic information systems and collated with the subjects' administrative district code, and individual exposure levels assigned. Results: During the study period, 3293 (1.6%) had a diagnosis of infertility. Although there was no association of infertility with 1-dB increments in noise exposure, a non-linear dose-response relationship was observed between infertility and quartiles of daytime and night time noise after adjustment for confounding variables (i.e., age, income, residential area, exercise, smoking, alcohol drinking, blood sugar, body mass index, medical histories, and particulate pollution). Based on WHO criteria, adjusted odds for infertility were significantly increased (OR = 1.14; 95% CI, 1.05–1.23) in males exposed to night time noise ≥ 55 dB. Conclusion: We found a significant association between exposure to environmental noise for four years and the subsequent incidence of male infertility, suggesting long-term exposure to noise has a role in pathogenesis of male infertility. - Highlights: • Noise is widespread and imposes auditory and non-auditory health

CUMEX: a cumulative hazard index for assessing limiting exposures to environmental pollutants

International Nuclear Information System (INIS)

Walsh, P.J.; Killough, G.G.; Parzyck, D.C.; Rohwer, P.S.; Rupp, e.M.; Whitfield, B.L.; Booth, R.S.; Raridon, R.J.

1977-04-01

A hazard index methodology called CUMEX has been developed for limiting human exposure to environmental pollutants. Hazard index is defined as Q/Q/sub L/ where Q is exposure or dose to total-body, organ or tissue from all environmental pathways and Q/sub L/ is a limit which should not be exceeded because of health risk to humans. Mathematical formulations for hazard indices are developed for each sampling medium corresponding to each effluent type. These hazard indices are accumulated into composite indices such that total human intake or dose would not exceed the health risk limit. Mathematical formulation for composite hazard indices or CUMEX indices for multiple pollutants are presented. An example CUMEX application to cadmium release from a smelter complex in East Helena, Montana demonstrates details of the methodology for a single pollutant where human intake occurs through inhalation and ingestion

Environmental exposure to human carcinogens in teenagers and the association with DNA damage

International Nuclear Information System (INIS)

Franken, Carmen; Koppen, Gudrun; Lambrechts, Nathalie; Govarts, Eva; Bruckers, Liesbeth; Den Hond, Elly; Loots, Ilse; Nelen, Vera; Sioen, Isabelle; Nawrot, Tim S.; Baeyens, Willy; Van Larebeke, Nicolas; Boonen, Francis; Ooms, Daniëlla; Wevers, Mai; Jacobs, Griet; Covaci, Adrian; Schettgen, Thomas; Schoeters, Greet

2017-01-01

Background: We investigated whether human environmental exposure to chemicals that are labeled as (potential) carcinogens leads to increased (oxidative) damage to DNA in adolescents. Material and methods: Six hundred 14–15-year-old youngsters were recruited all over Flanders (Belgium) and in two areas with important industrial activities. DNA damage was assessed by alkaline and formamidopyrimidine DNA glycosylase (Fpg) modified comet assays in peripheral blood cells and analysis of urinary 8-hydroxydeoxyguanosine (8-OHdG) levels. Personal exposure to potentially carcinogenic compounds was measured in urine, namely: chromium, cadmium, nickel, 1-hydroxypyrene as a proxy for exposure to other carcinogenic polycyclic aromatic hydrocarbons (PAHs), t,t-muconic acid as a metabolite of benzene, 2,5-dichlorophenol (2,5-DCP), organophosphate pesticide metabolites, and di(2-ethylhexyl) phthalate (DEHP) metabolites. In blood, arsenic, polychlorinated biphenyl (PCB) congeners 118 and 156, hexachlorobenzene (HCB), dichlorodiphenyltrichloroethane (DDT) and perfluorooctanoic acid (PFOA) were analyzed. Levels of methylmercury (MeHg) were measured in hair. Multiple linear regression models were used to establish exposure-response relationships. Results: Biomarkers of exposure to PAHs and urinary chromium were associated with higher levels of both 8-OHdG in urine and DNA damage detected by the alkaline comet assay. Concentrations of 8-OHdG in urine increased in relation with increasing concentrations of urinary t,t-muconic acid, cadmium, nickel, 2,5-DCP, and DEHP metabolites. Increased concentrations of PFOA in blood were associated with higher levels of DNA damage measured by the alkaline comet assay, whereas DDT was associated in the same direction with the Fpg-modified comet assay. Inverse associations were observed between blood arsenic, hair MeHg, PCB 156 and HCB, and urinary 8-OHdG. The latter exposure biomarkers were also associated with higher fish intake. Urinary nickel

Environmental exposure to human carcinogens in teenagers and the association with DNA damage

Energy Technology Data Exchange (ETDEWEB)

Franken, Carmen, E-mail: carmen.franken@vito.be [Flemish Institute for Technological Research (VITO), Mol (Belgium); Department of Biomedical Sciences, University of Antwerp, Antwerp (Belgium); Koppen, Gudrun; Lambrechts, Nathalie; Govarts, Eva [Flemish Institute for Technological Research (VITO), Mol (Belgium); Bruckers, Liesbeth [Interuniversity Institute for Biostatistics and Statistical Bioinformatics, Hasselt University, Hasselt (Belgium); Den Hond, Elly [Flemish Institute for Technological Research (VITO), Mol (Belgium); Loots, Ilse [Political and Social Sciences, University of Antwerp, Antwerp (Belgium); Nelen, Vera [Provincial Institute for Hygiene, Antwerp (Belgium); Sioen, Isabelle [Department of Public Health, Ghent University, Ghent (Belgium); Department of Food Safety and Food Quality, Ghent University, Ghent (Belgium); Nawrot, Tim S. [Centre for Environmental Sciences, Hasselt University, Diepenbeek (Belgium); Department of Public Health & Primary Care, Leuven University, Leuven (Belgium); Baeyens, Willy [Department of Analytical and Environmental Chemistry, Vrije Universiteit Brussel, Brussels (Belgium); Van Larebeke, Nicolas [Department of Analytical and Environmental Chemistry, Vrije Universiteit Brussel, Brussels (Belgium); Department of Radiotherapy and Experimental Cancerology, Ghent University, Ghent (Belgium); Boonen, Francis; Ooms, Daniëlla; Wevers, Mai; Jacobs, Griet [Flemish Institute for Technological Research (VITO), Mol (Belgium); Covaci, Adrian [Toxicological Centre, Department of Pharmaceutical Sciences, University of Antwerp, Antwerp (Belgium); Schettgen, Thomas [Department of Occupational and Social Medicine, RWTH Aachen University, Aachen (Germany); Schoeters, Greet [Flemish Institute for Technological Research (VITO), Mol (Belgium); Department of Biomedical Sciences, University of Antwerp, Antwerp (Belgium); University of Southern Denmark, Institute of Public Health, Department of Environmental Medicine, Odense (Denmark)

2017-01-15

Background: We investigated whether human environmental exposure to chemicals that are labeled as (potential) carcinogens leads to increased (oxidative) damage to DNA in adolescents. Material and methods: Six hundred 14–15-year-old youngsters were recruited all over Flanders (Belgium) and in two areas with important industrial activities. DNA damage was assessed by alkaline and formamidopyrimidine DNA glycosylase (Fpg) modified comet assays in peripheral blood cells and analysis of urinary 8-hydroxydeoxyguanosine (8-OHdG) levels. Personal exposure to potentially carcinogenic compounds was measured in urine, namely: chromium, cadmium, nickel, 1-hydroxypyrene as a proxy for exposure to other carcinogenic polycyclic aromatic hydrocarbons (PAHs), t,t-muconic acid as a metabolite of benzene, 2,5-dichlorophenol (2,5-DCP), organophosphate pesticide metabolites, and di(2-ethylhexyl) phthalate (DEHP) metabolites. In blood, arsenic, polychlorinated biphenyl (PCB) congeners 118 and 156, hexachlorobenzene (HCB), dichlorodiphenyltrichloroethane (DDT) and perfluorooctanoic acid (PFOA) were analyzed. Levels of methylmercury (MeHg) were measured in hair. Multiple linear regression models were used to establish exposure-response relationships. Results: Biomarkers of exposure to PAHs and urinary chromium were associated with higher levels of both 8-OHdG in urine and DNA damage detected by the alkaline comet assay. Concentrations of 8-OHdG in urine increased in relation with increasing concentrations of urinary t,t-muconic acid, cadmium, nickel, 2,5-DCP, and DEHP metabolites. Increased concentrations of PFOA in blood were associated with higher levels of DNA damage measured by the alkaline comet assay, whereas DDT was associated in the same direction with the Fpg-modified comet assay. Inverse associations were observed between blood arsenic, hair MeHg, PCB 156 and HCB, and urinary 8-OHdG. The latter exposure biomarkers were also associated with higher fish intake. Urinary nickel

Evaluation of the diseases associated with occupational exposure to ionizing radiation

International Nuclear Information System (INIS)

Frometa Suarez, I.

1998-01-01

Medical monitoring of workers occupationally exposed to ionizing radiation enables evaluation of their state of health, as well as early detection of general or somatic diseases which are considered as a criterion of unfitness for work, and which may or may not be related to the exposure conditions. A retrospective study is presented of all the cases of workers suspected to be suffering from radiation-related diseases which were referred for specialized study to the Institute of Occupational Medicine (IMT) during 1990-95. The incidence of the diseases and affected tissues is described, as well as the relationship between the time of manifestation and the type of source, the exposure time and the recorded dose levels. Diseases of the haemolymphopoietic system predominated, being observed in individuals exposed to medical radiodiagnostic sources. (author)

Occupational exposures are associated with worse morbidity in patients with chronic obstructive pulmonary disease.

Science.gov (United States)

Paulin, Laura M; Diette, Gregory B; Blanc, Paul D; Putcha, Nirupama; Eisner, Mark D; Kanner, Richard E; Belli, Andrew J; Christenson, Stephanie; Tashkin, Donald P; Han, MeiLan; Barr, R Graham; Hansel, Nadia N

2015-03-01

Links between occupational exposures and morbidity in individuals with established chronic obstructive pulmonary disease (COPD) remain unclear. To determine the impact of occupational exposures on COPD morbidity. A job exposure matrix (JEM) determined occupational exposure likelihood based on longest job in current/former smokers (n = 1,075) recruited as part of the Subpopulations and Intermediate Outcomes in COPD Study, of whom 721 had established COPD. Bivariate and multivariate linear regression models estimated the association of occupational exposure with COPD, and among those with established disease, the occupational exposure associations with 6-minute-walk distance (6MWD), the Modified Medical Research Council Dyspnea Scale (mMRC), the COPD Assessment Test (CAT), St. George's Respiratory Questionnaire (SGRQ), 12-item Short-Form Physical Component (SF-12), and COPD exacerbations requiring health care utilization, adjusting for demographics, current smoking status, and cumulative pack-years. An intermediate/high risk of occupational exposure by JEM was found in 38% of participants. In multivariate analysis, those with job exposures had higher odds of COPD (odds ratio, 1.44; 95% confidence interval, 1.04-1.97). Among those with COPD, job exposures were associated with shorter 6MWDs (-26.0 m; P = 0.006); worse scores for mMRC (0.23; P = 0.004), CAT (1.8; P = 0.003), SGRQ (4.5; P = 0.003), and SF-12 Physical (-3.3; P Accounting for smoking, occupational exposure was associated with COPD risk and, for those with established disease, shorter walk distance, greater breathlessness, worse quality of life, and increased exacerbation risk. Clinicians should obtain occupational histories from patients with COPD because work-related exposures may influence disease burden.

The perception of exposure to environmental risks

International Nuclear Information System (INIS)

Pautard, Eric

2014-10-01

This publication reports and comments the results of a survey performed every 6 years on the perception of exposure to environmental risks. It notably comments the evolution between 2007 and 2013 of the perception of exposure to different types of risks: seismic risks, terrorism, major industrial risks, flooding risks, nuclear risks, food-related risks, risks related to climate change, unemployment, air pollution, and cancer. The perceptions of inhabitants of cities exposed or not exposed to some risks (industrial, climate, flooding) are compared. Risks are ranked from very important to not important at all. The influence of the existence of a risk when choosing to settle in a dwelling is also assessed, as well as the already lived consequences of catastrophes, the level of concern about possible consequences of a catastrophe, the respective roles of the State and citizen in the field of risk prevention, the opinions on law efficiency to protect people and goods, the knowledge of prevention arrangements against natural and technological risk, the level of confidence in public action regarding risks to which interviewed people are actually exposed (industrial risks, risks related to climate, flooding)

Clinical-epidemiological features of contact dermatitis in rural and urban communities in northern Ethiopia: correlation with environmental or occupational exposure.

Science.gov (United States)

Morrone, Aldo; Bordignon, Valentina; Barnabas, Gebre Ab; Dassoni, Federica; Latini, Ottavio; Padovese, Valeska; Ensoli, Fabrizio; Cristaudo, Antonio

2014-08-01

The widespread diffusion of low-quality products as well as the local cultural habits could be a relevant cause of allergic diseases in developing countries. In the present observational study, we explored the prevalence of allergic contact dermatitis in both rural and urban settings in northern Ethiopia, where skin diseases represent a frequent cause of morbidity. Clinical features and specific reactivities in association with environmental or occupational exposure were investigated. We patch tested 480 consecutive patients, visited at the Mekele IDC, exhibiting symptoms of contact dermatitis. A detailed medical history of each patient was collected. A positive patch-test response was observed in 50% of subjects; nickel was the most frequent sensitizer (26.2%), followed by p-tert-butylphenol formaldehyde resin (10%), fragrance mix (7.1%), potassium dichromate (5.4%), cobalt chloride (4.6%), disperse blue (2.3%), and p-phenylenediamine (1.7%). Gender-related differences were analyzed for single allergen. Eczema represented the most common manifestation, affecting the head and neck as primary skin areas. While reactivity to nickel interested almost all the occupational categories, sensitization to other allergens could be ascribed to working habits or environmental exposure. The results gathered from this study, the first one conducted within the Tigray region in Ethiopia, confirm the need to take appropriate measures to limit the nickel rate in metal objects and may be useful to design allergenic series suitable for patch testing in those geographical settings. © 2013 The International Society of Dermatology.

Environmental radioactivity and radiation exposure

International Nuclear Information System (INIS)

1980-01-01

In 1977 population exposure in the Federal Republic of Germany has not changed as compared to the previous years. The main share of the total exposure, nearly two thirds, is attributed to natural radioactive substances and cosmic radiation. The largest part (around 85%) of the artificial radiation exposure is caused by X-ray diagnostics. In comparison to this, radiation exposure from application of ionizing radiation in medical therapy, use of radioactive material in research and technology, or from nuclear facilities is small. As in the years before, population exposure caused by nuclear power plants and other nuclear facilities is distinctly less than 1% of the natural radiation exposure. This is also true for the average radiation exposure within a radius of 3 km around nuclear facilities. On the whole, the report makes clear that the total amount of artificial population exposure will substantially decrease only if one succeeds in reducing the high contribution to the radiation exposure caused by medical measures. (orig.) [de

Evaluation of diseases associated to occupational exposure to ionizing radiations

International Nuclear Information System (INIS)

Suarez, Ileana Frometa

1997-01-01

A retrospective investigation of all cases of radiation workers with diseases and injuries, considered as occupational diseases caused by ionizing radiation is presented. The investigation includes all cases registered in the Institute of Occupational Health over five years period (1990-1995). The incidence of that diseases are studied, as well as the correlation between each type of source, time of exposure and annual average equivalent individual dose

Gray wolf exposure to emerging vector-borne diseases in Wisconsin with comparison to domestic dogs and humans

Science.gov (United States)

Jara, Rocio F.; Wydeven, Adrian P.; Samuel, Michael D.

2016-01-01

World-wide concern over emerging vector-borne diseases has increased in recent years for both animal and human health. In the United Sates, concern about vector-borne diseases in canines has focused on Lyme disease, anaplasmosis, ehrlichiosis, and heartworm which infect domestic and wild canids. Of these diseases, Lyme and anaplasmosis are also frequently diagnosed in humans. Gray wolves (Canis lupus) recolonized Wisconsin in the 1970s, and we evaluated their temporal and geographic patterns of exposure to these four vector-borne diseases in Wisconsin as the population expanded between 1985 and 2011. A high proportion of the Wisconsin wolves were exposed to the agents that cause Lyme (65.6%) and anaplasma (47.7%), and a smaller proportion to ehrlichiosis (5.7%) and infected with heartworm (9.2%). Wolf exposure to tick borne diseases was consistently higher in older animals. Wolf exposure was markedly higher than domestic dog (Canis familiaris) exposure for all 4 disease agents during 2001–2013. We found a cluster of wolf exposure to Borrelia burgdorferi in northwestern Wisconsin, which overlaps human and domestic dog clusters for the same pathogen. In addition, wolf exposure to Lyme disease in Wisconsin has increased, corresponding with the increasing human incidence of Lyme disease in a similar time period. Despite generally high prevalence of exposure none of these diseases appear to have slowed the growth of the Wisconsin wolf population.

Ecohealth approach to urban waste management: exposure to environmental pollutants and health risks in Yamoussoukro, Côte d'Ivoire.

Science.gov (United States)

Kouamé, Parfait K; Dongo, Kouassi; Nguyen-Viet, Hung; Zurbrügg, Christian; Lüthi, Christoph; Hattendorf, Jan; Utzinger, Jürg; Biémi, Jean; Bonfoh, Bassirou

2014-10-02

Poor waste management is a key driver of ill-health in urban settlements of developing countries. The current study aimed at assessing environmental and human health risks related to urban waste management in Yamoussoukro, the political capital of Côte d'Ivoire. We undertook trans-disciplinary research within an Ecohealth approach, comprised of a participatory workshop with stakeholders and mapping of exposure patterns. A total of 492 randomly selected households participated in a cross-sectional survey. Waste deposit sites were characterised and 108 wastewater samples were subjected to laboratory examinations. The physico-chemical parameters of the surface water (temperature, pH, conductivity, potential oxidise reduction, BOD5, COD, dissolved oxygen, nitrates, ammonia and total Kendal nitrogen) did not comply with World Health Organization standards of surface water quality. Questionnaire results showed that malaria was the most commonly reported disease. Diarrhoea and malaria were associated with poor sanitation. Households having dry latrines had a higher risk of diarrhoea (odds ratio (OR) = 1.8, 95% confidence interval (CI) 1.2-2.7) compared to latrines with septic tanks and also a higher risk for malaria (OR = 1.9, 95% (CI) 1.1-3.3). Our research showed that combining health and environmental assessments enables a deeper understanding of environmental threats and disease burdens linked to poor waste management. Further study should investigate the sanitation strategy aspects that could reduce the environmental and health risks in the study area.

Ecohealth Approach to Urban Waste Management: Exposure to Environmental Pollutants and Health Risks in Yamoussoukro, Côte d’Ivoire

Directory of Open Access Journals (Sweden)

Parfait K. Kouamé

2014-10-01

Full Text Available Poor waste management is a key driver of ill-health in urban settlements of developing countries. The current study aimed at assessing environmental and human health risks related to urban waste management in Yamoussoukro, the political capital of Côte d’Ivoire. We undertook trans-disciplinary research within an Ecohealth approach, comprised of a participatory workshop with stakeholders and mapping of exposure patterns. A total of 492 randomly selected households participated in a cross-sectional survey. Waste deposit sites were characterised and 108 wastewater samples were subjected to laboratory examinations. The physico-chemical parameters of the surface water (temperature, pH, conductivity, potential oxidise reduction, BOD5, COD, dissolved oxygen, nitrates, ammonia and total Kendal nitrogen did not comply with World Health Organization standards of surface water quality. Questionnaire results showed that malaria was the most commonly reported disease. Diarrhoea and malaria were associated with poor sanitation. Households having dry latrines had a higher risk of diarrhoea (odds ratio (OR = 1.8, 95% confidence interval (CI 1.2–2.7 compared to latrines with septic tanks and also a higher risk for malaria (OR = 1.9, 95% (CI 1.1–3.3. Our research showed that combining health and environmental assessments enables a deeper understanding of environmental threats and disease burdens linked to poor waste management. Further study should investigate the sanitation strategy aspects that could reduce the environmental and health risks in the study area.

Transplacental exposure to environmental carcinogens: Association with childhood cancer risks and the role of modulating factors.

Science.gov (United States)

Fucic, A; Guszak, V; Mantovani, A

2017-09-01

Biological responses to carcinogens from environmental exposure during adulthood are modulated over years or decades. Conversely, during transplacental exposure, the effects on the human foetus change within weeks, intertwining with developmental mechanisms: even short periods of transplacental exposure may be imprinted in the organism for a lifetime. The pathways leading to childhood and juvenile cancers, such as leukaemias, neuroblastoma/brain tumours, hepatoblastoma, and Willm's tumour involve prenatally-induced genomic, epigenomic and/or non-genomic effects caused by xenobiotics. Pregnant women most often live in complex environmental settings that cause transplacental exposure of the foetus to xenobiotic mixtures. Mother-child biomonitoring should integrate the analysis of chemicals/radiation present in the living and workplace environment with relevant risk modulators related to life style. The interdisciplinary approach for transplacental cancer risk assessment in high-pressure areas should be based on an integrated model for mother-child exposure estimation via profiling the exposure level by water quality analysis, usage of emission grids, and land use maps. Copyright © 2017. Published by Elsevier Inc.

Wildlife disease and environmental health in Alaska

Science.gov (United States)

Van Hemert, Caroline; Pearce, John; Oakley, Karen; Whalen, Mary

2013-01-01

Environmental health is defined by connections between the physical environment, ecological health, and human health. Current research within the U.S. Geological Survey (USGS) recognizes the importance of this integrated research philosophy, which includes study of disease and pollutants as they pertain to wildlife and humans. Due to its key geographic location and significant wildlife resources, Alaska is a critical area for future study of environmental health.

Spatial Modelling Tools to Integrate Public Health and Environmental Science, Illustrated with Infectious Cryptosporidiosis.

Science.gov (United States)

Lal, Aparna

2016-02-02

Contemporary spatial modelling tools can help examine how environmental exposures such as climate and land use together with socio-economic factors sustain infectious disease transmission in humans. Spatial methods can account for interactions across global and local scales, geographic clustering and continuity of the exposure surface, key characteristics of many environmental influences. Using cryptosporidiosis as an example, this review illustrates how, in resource rich settings, spatial tools have been used to inform targeted intervention strategies and forecast future disease risk with scenarios of environmental change. When used in conjunction with molecular studies, they have helped determine location-specific infection sources and environmental transmission pathways. There is considerable scope for such methods to be used to identify data/infrastructure gaps and establish a baseline of disease burden in resource-limited settings. Spatial methods can help integrate public health and environmental science by identifying the linkages between the physical and socio-economic environment and health outcomes. Understanding the environmental and social context for disease spread is important for assessing the public health implications of projected environmental change.

Spatial Modelling Tools to Integrate Public Health and Environmental Science, Illustrated with Infectious Cryptosporidiosis

Directory of Open Access Journals (Sweden)

Aparna Lal

2016-02-01

Full Text Available Contemporary spatial modelling tools can help examine how environmental exposures such as climate and land use together with socio-economic factors sustain infectious disease transmission in humans. Spatial methods can account for interactions across global and local scales, geographic clustering and continuity of the exposure surface, key characteristics of many environmental influences. Using cryptosporidiosis as an example, this review illustrates how, in resource rich settings, spatial tools have been used to inform targeted intervention strategies and forecast future disease risk with scenarios of environmental change. When used in conjunction with molecular studies, they have helped determine location-specific infection sources and environmental transmission pathways. There is considerable scope for such methods to be used to identify data/infrastructure gaps and establish a baseline of disease burden in resource-limited settings. Spatial methods can help integrate public health and environmental science by identifying the linkages between the physical and socio-economic environment and health outcomes. Understanding the environmental and social context for disease spread is important for assessing the public health implications of projected environmental change.

Physiochemical basis of human degenerative disease.

Science.gov (United States)

Zeliger, Harold I; Lipinski, Boguslaw

2015-03-01

The onset of human degenerative diseases in humans, including type 2 diabetes, cardiovascular disease, neurological disorders, neurodevelopmental disease and neurodegenerative disease has been shown to be related to exposures to persistent organic pollutants, including polychlorinated biphenyls, chlorinated pesticides, polybrominated diphenyl ethers and others, as well as to polynuclear aromatic hydrocarbons, phthalates, bisphenol-A and other aromatic lipophilic species. The onset of these diseases has also been related to exposures to transition metal ions. A physiochemical mechanism for the onset of degenerative environmental disease dependent upon exposure to a combination of lipophilic aromatic hydrocarbons and transition metal ions is proposed here. The findings reported here also, for the first time, explain why aromatic hydrocarbons exhibit greater toxicity than aliphatic hydrocarbons of equal carbon numbers.

Physiochemical basis of human degenerative disease

Directory of Open Access Journals (Sweden)

Zeliger Harold I.

2015-03-01

Full Text Available The onset of human degenerative diseases in humans, including type 2 diabetes, cardiovascular disease, neurological disorders, neurodevelopmental disease and neurodegenerative disease has been shown to be related to exposures to persistent organic pollutants, including polychlorinated biphenyls, chlorinated pesticides, polybrominated diphenyl ethers and others, as well as to polynuclear aromatic hydrocarbons, phthalates, bisphenol-A and other aromatic lipophilic species. The onset of these diseases has also been related to exposures to transition metal ions. A physiochemical mechanism for the onset of degenerative environmental disease dependent upon exposure to a combination of lipophilic aromatic hydrocarbons and transition metal ions is proposed here. The findings reported here also, for the first time, explain why aromatic hydrocarbons exhibit greater toxicity than aliphatic hydrocarbons of equal carbon numbers.

Occupational and environmental risk factors for chronic rhinosinusitis: a systematic review.

Science.gov (United States)

Sundaresan, Agnes S; Hirsch, Annemarie G; Storm, Margaret; Tan, Bruce K; Kennedy, Thomas L; Greene, J Scott; Kern, Robert C; Schwartz, Brian S

2015-11-01

Chronic rhinosinusitis (CRS) is a prevalent and disabling paranasal sinus disease, with a likely multifactorial etiology potentially including hazardous occupational and environmental exposures. We completed a systematic review of the occupational and environmental literature to evaluate the quality of evidence of the role that hazardous exposures might play in CRS. We searched PubMed for studies of CRS and following exposure categories: occupation, employment, work, industry, air pollution, agriculture, farming, environment, chemicals, roadways, disaster, and traffic. We abstracted information from the final set of articles across 6 primary domains: study design; population; exposures evaluated; exposure assessment; CRS definition; and results. We identified 41 articles from 1080 manuscripts: 37 occupational risk papers, 1 environmental risk paper, and 3 papers studying both categories of exposures. None of the 41 studies used a CRS definition consistent with current diagnostic guidelines. Exposure assessment was generally dependent on self-report or binary measurements of exposure based on industry of employment. Only grain, dairy, and swine operations among farmers were evaluated by more than 1 study using a common approach to defining CRS, but employment in these settings was not consistently associated with CRS. The multiple other exposures did not meet quality standards for reporting associations or were not evaluated by more than 1 study. The current state of the literature allows us to make very few conclusions about the role of hazardous occupational or environmental exposures in CRS, leaving a critical knowledge gap regarding potentially modifiable risk factors for disease onset and progression. © 2015 ARS-AAOA, LLC.

In utero and early life arsenic exposure in relation to long-term health and disease

Energy Technology Data Exchange (ETDEWEB)

Farzan, Shohreh F.; Karagas, Margaret R. [Children' s Environmental Health and Disease Prevention Research Center at Dartmouth, Hanover, NH 03755 (United States); Section of Biostatistics and Epidemiology, Department of Community and Family Medicine and Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, Lebanon, NH 03756 (United States); Chen, Yu, E-mail: yu.chen@nyumc.org [Department of Population Health, New York University School of Medicine, New York, NY 10016 (United States)

2013-10-15

Background: There is a growing body of evidence that prenatal and early childhood exposure to arsenic from drinking water can have serious long-term health implications. Objectives: Our goal was to understand the potential long-term health and disease risks associated with in utero and early life exposure to arsenic, as well as to examine parallels between findings from epidemiological studies with those from experimental animal models. Methods: We examined the current literature and identified relevant studies through PubMed by using combinations of the search terms “arsenic”, “in utero”, “transplacental”, “prenatal” and “fetal”. Discussion: Ecological studies have indicated associations between in utero and/or early life exposure to arsenic at high levels and increases in mortality from cancer, cardiovascular disease and respiratory disease. Additional data from epidemiologic studies suggest intermediate effects in early life that are related to risk of these and other outcomes in adulthood. Experimental animal studies largely support studies in humans, with strong evidence of transplacental carcinogenesis, atherosclerosis and respiratory disease, as well as insight into potential underlying mechanisms of arsenic's health effects. Conclusions: As millions worldwide are exposed to arsenic and evidence continues to support a role for in utero arsenic exposure in the development of a range of later life diseases, there is a need for more prospective studies examining arsenic's relation to early indicators of disease and at lower exposure levels. - Highlights: • We review in utero and early-life As exposure impacts on lifelong disease risks. • Evidence indicates that early-life As increases risks of lung disease, cancer and CVD. • Animal work largely parallels human studies and may lead to new research directions. • Prospective studies and individual exposure assessments with biomarkers are needed. • Assessing intermediary

In utero and early life arsenic exposure in relation to long-term health and disease

International Nuclear Information System (INIS)

Farzan, Shohreh F.; Karagas, Margaret R.; Chen, Yu

2013-01-01

Background: There is a growing body of evidence that prenatal and early childhood exposure to arsenic from drinking water can have serious long-term health implications. Objectives: Our goal was to understand the potential long-term health and disease risks associated with in utero and early life exposure to arsenic, as well as to examine parallels between findings from epidemiological studies with those from experimental animal models. Methods: We examined the current literature and identified relevant studies through PubMed by using combinations of the search terms “arsenic”, “in utero”, “transplacental”, “prenatal” and “fetal”. Discussion: Ecological studies have indicated associations between in utero and/or early life exposure to arsenic at high levels and increases in mortality from cancer, cardiovascular disease and respiratory disease. Additional data from epidemiologic studies suggest intermediate effects in early life that are related to risk of these and other outcomes in adulthood. Experimental animal studies largely support studies in humans, with strong evidence of transplacental carcinogenesis, atherosclerosis and respiratory disease, as well as insight into potential underlying mechanisms of arsenic's health effects. Conclusions: As millions worldwide are exposed to arsenic and evidence continues to support a role for in utero arsenic exposure in the development of a range of later life diseases, there is a need for more prospective studies examining arsenic's relation to early indicators of disease and at lower exposure levels. - Highlights: • We review in utero and early-life As exposure impacts on lifelong disease risks. • Evidence indicates that early-life As increases risks of lung disease, cancer and CVD. • Animal work largely parallels human studies and may lead to new research directions. • Prospective studies and individual exposure assessments with biomarkers are needed. • Assessing intermediary endpoints may

Occupational exposures and chronic obstructive pulmonary disease (COPD): comparison of a COPD-specific job exposure matrix and expert-evaluated occupational exposures.

Science.gov (United States)

Kurth, Laura; Doney, Brent; Weinmann, Sheila

2017-03-01

To compare the occupational exposure levels assigned by our National Institute for Occupational Safety and Health chronic obstructive pulmonary disease-specific job exposure matrix (NIOSH COPD JEM) and by expert evaluation of detailed occupational information for various jobs held by members of an integrated health plan in the Northwest USA. We analysed data from a prior study examining COPD and occupational exposures. Jobs were assigned exposure levels using 2 methods: (1) the COPD JEM and (2) expert evaluation. Agreement (Cohen's κ coefficients), sensitivity and specificity were calculated to compare exposure levels assigned by the 2 methods for 8 exposure categories. κ indicated slight to moderate agreement (0.19-0.51) between the 2 methods and was highest for organic dust and overall exposure. Sensitivity of the matrix ranged from 33.9% to 68.5% and was highest for sensitisers, diesel exhaust and overall exposure. Specificity ranged from 74.7% to 97.1% and was highest for fumes, organic dust and mineral dust. This COPD JEM was compared with exposures assigned by experts and offers a generalisable approach to assigning occupational exposure. 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/.

Environmental exposures in the US electric utility industry

International Nuclear Information System (INIS)

Repetto, R.; Henderson, J.

2003-01-01

Quantitative analysis of 47 US investor-owned electric utilities' environmental exposures to impending air quality and climate policies shows potentially material and highly differentiated financial impacts. For many companies the minimized compliance costs of a four-pollutant cap-and-trade regulatory regime would be less than those of a three-pollutant regime that omitted controls on carbon dioxide emissions. Fragmented regulatory requirements would have the highest compliance costs. The companies studied vary considerably in the adequacy of their financial reporting of these potential impacts. Greater transparency would benefit investors and the most favorably positioned companies. (author)

Risk of ischemic heart disease following occupational exposure to welding fumes

DEFF Research Database (Denmark)

Mocevic, Emina; Kristiansen, Pernille; Bonde, Jens Peter

2015-01-01

PURPOSE: Air pollution has been linked to an increased risk of ischemic heart disease (IHD), but less is known about occupational exposure to welding fumes and the risk of IHD. The objective of this paper was to review the epidemiological evidence on causal links between welding fume exposure...

Gray Wolf Exposure to Emerging Vector-Borne Diseases in Wisconsin with Comparison to Domestic Dogs and Humans.

Directory of Open Access Journals (Sweden)

Rocio F Jara

Full Text Available World-wide concern over emerging vector-borne diseases has increased in recent years for both animal and human health. In the United Sates, concern about vector-borne diseases in canines has focused on Lyme disease, anaplasmosis, ehrlichiosis, and heartworm which infect domestic and wild canids. Of these diseases, Lyme and anaplasmosis are also frequently diagnosed in humans. Gray wolves (Canis lupus recolonized Wisconsin in the 1970s, and we evaluated their temporal and geographic patterns of exposure to these four vector-borne diseases in Wisconsin as the population expanded between 1985 and 2011. A high proportion of the Wisconsin wolves were exposed to the agents that cause Lyme (65.6% and anaplasma (47.7%, and a smaller proportion to ehrlichiosis (5.7% and infected with heartworm (9.2%. Wolf exposure to tick borne diseases was consistently higher in older animals. Wolf exposure was markedly higher than domestic dog (Canis familiaris exposure for all 4 disease agents during 2001-2013. We found a cluster of wolf exposure to Borrelia burgdorferi in northwestern Wisconsin, which overlaps human and domestic dog clusters for the same pathogen. In addition, wolf exposure to Lyme disease in Wisconsin has increased, corresponding with the increasing human incidence of Lyme disease in a similar time period. Despite generally high prevalence of exposure none of these diseases appear to have slowed the growth of the Wisconsin wolf population.

Pleuroparenchymal Lung Disease Secondary to Nonoccupational Exposure to Vermiculite

Directory of Open Access Journals (Sweden)

Fahad Al-Ghimlas

2007-01-01

Full Text Available An unusual case of pleuroparenchymal lung disease caused by the inhalation of vermiculite dust, presumably containing asbestos fibers is described. The uniqueness of the case lies in the very indirect nature of exposure – the wife of a factory owner, rather than a worker exposed to asbestos, whose factory manufactured vermiculite. The present case illustrates the importance of taking careful occupational histories of all household members when presented with a patient whose chest radiograph exhibits features consistent with asbestos exposure.

Preconception care: caffeine, smoking, alcohol, drugs and other environmental chemical/radiation exposure.

Science.gov (United States)

Lassi, Zohra S; Imam, Ayesha M; Dean, Sohni V; Bhutta, Zulfiqar A

2014-09-26

As providing health education, optimizing nutrition, and managing risk factors can be effective for ensuring a healthy outcome for women and her yet un-conceived baby, external influences play a significant role as well. Alcohol, smoking, caffeine use and other similar lifestyle factors, have now become an integral part of the daily life of most men and women, who use/misuse one or more of these harmful substances regularly despite knowledge of their detrimental effects. The adverse health outcomes of these voluntary and involuntary exposures are of even greater concern in women of child bearing age where the exposure has the potential of inflicting harm to two generations. This paper is examining the available literature for the possible effects of caffeine consumption, smoking, alcohol or exposure to chemicals may have on the maternal, newborn and child health (MNCH). A systematic review and meta-analysis of the evidence was conducted to ascertain the possible impact of preconception usage of caffeine, tobacco, alcohol and other illicit drugs; and exposure to environmental chemicals and radiant on MNCH outcomes. A comprehensive strategy was used to search electronic reference libraries, and both observational and clinical controlled trials were included. Cross-referencing and a separate search strategy for each preconception risk and intervention ensured wider study capture. Heavy maternal preconception caffeine intake of >300 mg/d significantly increase the risk of a subsequent fetal loss by 31% (95% CI: 8-58%). On the other hand, preconception alcohol consumption leads to non-significant 30% increase in spontaneous abortion (RR 1.30; 95% CI: 0.85-1.97). Preconception counselling can lead to a significant decrease in the consumption of alcohol during the first trimester (OR 1.79; 95% CI: 1.08-2.97). Periconception smoking, on the other hand, was found to be associated with an almost 3 times increased risk of congenital heart defects (OR 2.80; 95% CI 1

Quality assurance of external exposure measurement for national survey of environmental natural radioactive level

International Nuclear Information System (INIS)

Yue Qingyu

1995-01-01

This paper summarizes the quality assurance work of external exposure measurement for national survey of environmental natural radioactive level. It mainly introduces instrumentation used in external exposure measurement and its properties, the measurement results of three times of national in-site intercomparison, and in-site sample check results of measurement results from 29 provinces, cities and autonomous regions and Wuhan, Baotou cities

Parental Concern about Environmental Chemical Exposures and Children's Urinary Concentrations of Phthalates and Phenols.

Science.gov (United States)

Pell, Tripler; Eliot, Melissa; Chen, Aimin; Lanphear, Bruce P; Yolton, Kimberly; Sathyanarayana, Sheela; Braun, Joseph M

2017-07-01

To examine whether parents' concerns about environmental chemical exposures were associated with urinary phthalate and phenol concentrations in their school-age children. In a prospective cohort of 218 mother-child pairs from Cincinnati, Ohio (2010-2014), we measured 11 phthalate metabolites and 5 phenols in urine samples when children were age 8 years and used questionnaire data from caregivers. We estimated the covariate-adjusted percent difference in phthalates and phenols among children of parents who expressed concern about environmental chemical exposures compared with children whose parents did not. Concentrations of 4 phthalates, bisphenol S, and bisphenol A were lower among children whose parents expressed concern about environmental chemicals (n = 122) compared with those who did not (n = 96). Di-2-ethylhexyl phthalate metabolites, bisphenol S, and bisphenol A concentrations were 23% (95% CI -38, -5), 37% (95% CI -49, -21), and 13% (95% CI -26, 3) lower, respectively, among children whose parents expressed concern compared with those whose parents did not. Triclosan concentrations were 35% greater (95% CI -2, 87) among children whose parents expressed concern compared with children whose parents did not. Parental concern about environmental chemicals was associated with lower childhood urine concentrations of several phthalates and phenols; unexpectedly, parental concern was associated with greater triclosan concentrations. These results suggest that parental concern may be an important factor in mitigating children's phthalate and phenol exposures. Copyright © 2017 Elsevier Inc. All rights reserved.

Airway Epithelial Barrier Dysfunction in Chronic Obstructive Pulmonary Disease: Role of Cigarette Smoke Exposure.

Science.gov (United States)

Aghapour, Mahyar; Raee, Pourya; Moghaddam, Seyed Javad; Hiemstra, Pieter S; Heijink, Irene H

2018-02-01

The epithelial lining of the airway forms the first barrier against environmental insults, such as inhaled cigarette smoke, which is the primary risk factor for the development of chronic obstructive pulmonary disease (COPD). The barrier is formed by airway epithelial junctions, which are interconnected structures that restrict permeability to inhaled pathogens and environmental stressors. Destruction of the epithelial barrier not only exposes subepithelial layers to hazardous agents in the inspired air, but also alters the normal function of epithelial cells, which may eventually contribute to the development of COPD. Of note, disruption of epithelial junctions may lead to modulation of signaling pathways involved in differentiation, repair, and proinflammatory responses. Epithelial barrier dysfunction may be particularly relevant in COPD, where repeated injury by cigarette smoke exposure, pathogens, inflammatory mediators, and impaired epithelial regeneration may compromise the barrier function. In the current review, we discuss recent advances in understanding the mechanisms of barrier dysfunction in COPD, as well as the molecular mechanisms that underlie the impaired repair response of the injured epithelium in COPD and its inability to redifferentiate into a functionally intact epithelium.

Exposure to environmental tobacco smoke from husband more strongly impacts on the airway obstruction of nonsmoking women

Directory of Open Access Journals (Sweden)

Suyama K

2017-12-01

Full Text Available Kazuaki Suyama, Ryo Kozu, Takako Tanaka, Yuji Ishimatsu, Terumitsu Sawai Department of Cardiopulmonary Rehabilitation Science, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan Background: The impact of airway obstruction of nonsmoking women caused by their husband’s smoking is unclear, despite the association between environmental tobacco smoke (ETS exposure at home and obstructive pulmonary diseases among nonsmoking women. The aim of this study was to provide evidence that ETS exposure from the husband at home has a more significant influence on the airway obstruction of nonsmoking women than other housemates. Participants and methods: Nonsmoking women aged 40 years or older were recruited from the health checkup during May 2015–December 2016, Japan. They answered structured questionnaires, including ETS exposure from their husbands and other housemates (parents, siblings and dependants, and performed spirometry. We categorized the women with any history of ETS exposure from housemates into three groups (A = husband, B = others and C = both of husband and others and defined the control group as those with no ETS exposure from housemates. Results: A total of 811 nonsmoking women completed questionnaires and spirometry. The proportion of nonsmoking women who had airway obstruction (forced expiratory volume in 1 second [FEV1]/forced vital capacity [FVC] <70% among Group A (7.5% was significantly higher than those in the control group (1.1%, p<0.01 and Group B (0.8%, p<0.01. The proportion of airway obstruction in Group C (6.4% was also higher than that in the control group (p<0.05 and Group B (p<0.05. ETS exposure from husband (odds ratio [OR], 3.53; 95% confidence interval [CI], 1.48–8.42 remained strongly associated with airway obstruction after multiple logistic regression analysis, adjusting for age, housemate’s smoking habits, family history and ETS exposure in childhood and at work. Conclusion: Nonsmoking

Mercury exposure and risk of cardiovascular disease in two U.S. cohorts

DEFF Research Database (Denmark)

Mozaffarian, Dariush; Shi, Peilin; Morris, J Steven

2011-01-01

Exposure to methylmercury from fish consumption has been linked to a potentially increased risk of cardiovascular disease, but evidence from prior studies is equivocal. Beneficial effects of the ingestion of fish and selenium may also modify such effects.......Exposure to methylmercury from fish consumption has been linked to a potentially increased risk of cardiovascular disease, but evidence from prior studies is equivocal. Beneficial effects of the ingestion of fish and selenium may also modify such effects....

Integrated indoor and outdoor exposure assessment framework for fine particulate matter pollution

DEFF Research Database (Denmark)

McKone, Thomas E; Hodas, Natasha; Apte, Joshua S.

2016-01-01

The 2010 Global Burden of Disease report demonstrates that fine particulate matter (PM2.5) pollution is the major environmental contributor to mortality. Exposures outdoors (ambient) and indoors (household) contribute almost qually to this burden. Unfortunately, the health impacts from exposure t...

Inter-individual susceptibility to environmental toxicants-A current assessment

International Nuclear Information System (INIS)

Nebert, Daniel W.

2005-01-01

Virtually all diseases have an environmental component. The two most important factors affecting your unique risk of an environmental disease (toxicity or cancer) are (a) your exposure to the environmental agent and (b) your genes. Epidemiologists have found ways to calculate inter-individual risk-if the exposure to environmental agents is sufficiently high and can be documented (e.g., years of cigarette smoking, taking prescribed drugs, drinking alcohol, or exposure to radon or other radioactive material, etc.). If the dose of environmental agents is lower and more ambiguous (e.g., exposure to chemicals on the job, herbicides sprayed on a golf course, outdoor or indoor air pollution, endocrine disruptors in cans of food, living near a toxic waste dump site, etc.), however, calculations of inter-individual risk become much more difficult. Highly accurate DNA tests for genetic susceptibility to toxicity and cancer have been sought in order to identify individuals at increased risk; this type of research represents the leading edge of phenotype-genotype association studies and is the major goal of most public health and preventive medicine programs. The task, however, has turned out to be far more challenging than anticipated. The major stumbling block has been the difficulty in determining an unequivocal phenotype or an unequivocal genotype. We were quite optimistic 5-10 years ago that this would be easy, but now we are beginning to appreciate how difficult it is to determine an unequivocal phenotype or genotype with certainty. For many reasons set forth in this overview, it appears that DNA testing alone, to predict and prevent environmental disease on an individual basis, may be virtually impossible with current knowledge and technologies and will require novel insights before major practical applications will evolve

Environmental monitoring through the use of exposure panels

International Nuclear Information System (INIS)

Hillman, R.E.

1975-01-01

Exposure panels made of white pine with a transite facing are useful for assessing population and community changes in both polluted and unpolluted waters. Their uniform size and shape and the ease with which they can be handled makes them ideal for sampling a wide variety of sessile plants and animals, and those motile forms usually associated with sessile communities. Data from an ecological study at Millstone Point are used as examples of the kinds of information provided through the use of exposure panels as environmental monitors. Species diversity indexes for both algal and annelid populations as they occurred on panels from 1968 through 1973 were calculated. Regression analyses over time showed increases in diversity indexes since the program began, indicating possible changes in water quality. For the period of October 1971 through September 1972, the number of phyla found on panels exposed at Millstone Point, New Haven Harbor, and Stamford Harbor were not significantly different, but far more species were found on the Millstone Point panels. (U.S.)

Occupational exposure to pesticides and endotoxin and Parkinson disease in the Netherlands

NARCIS (Netherlands)

van der Mark, Marianne; Vermeulen, Roel; Nijssen, Peter C. G.; Mulleners, Wim M.; Sas, Antonetta M. G.; van Laar, Teus; Brouwer, Maartje; Huss, Anke; Kromhout, Hans

2014-01-01

Objectives Previous research has indicated that occupational exposure to pesticides and possibly airborne endotoxin may increase the risk of developing Parkinson disease (PD). We studied the associations of PD with occupational exposure to pesticides, specifically to the functional subclasses

Linking high resolution mass spectrometry data with exposure and toxicity forecasts to advance high-throughput environmental monitoring

Data.gov (United States)

U.S. Environmental Protection Agency — There is a growing need in the field of exposure science for monitoring methods that rapidly screen environmental media for suspect contaminants. Measurement and...

The TERRA framework: conceptualizing rural environmental health inequities through an environmental justice lens.

Science.gov (United States)

Butterfield, Patricia; Postma, Julie

2009-01-01

The deleterious consequences of environmentally associated diseases are expressed differentially by income, race, and geography. Scientists are just beginning to understand the consequences of environmental exposures under conditions of poverty, marginalization, and geographic isolation. In this context, we developed the TERRA (translational environmental research in rural areas) framework to explicate environmental health risks experienced by the rural poor. Central to the TERRA framework is the premise that risks exist within physical-spatial, economic-resources, and cultural-ideologic contexts. In the face of scientific and political uncertainty, a precautionary risk reduction approach has the greatest potential to protect health. Conceptual and technical advances will both be needed to achieve environmental justice.

Environmental chemicals and autoimmune disease: cause and effect

International Nuclear Information System (INIS)

Hess, Evelyn V.

2002-01-01

Many important clues have been provided by the relationship of certain medications to lupus and other autoimmune syndromes. These are temporary conditions that resolve when the medication is removed. There are now over 70 such medications which have been reported related to these autoimmune conditions. Interest continues to grow in the potential for environmental substances to cause these syndromes. Among those under suspicion are hydrazines, tartrazines, hair dyes, trichloroethylene, industrial emissions and hazardous wastes. Other possible associations include silica, mercury, cadmium, gold and L canavanine. Two recognised outbreaks include 'toxic oil syndrome' related to contaminated rape seed oil in Spain in 1981 and exposure to a contaminated environmental substance associated with an autoimmune attack on muscle tissue in 1989. Recently, there have been proposals made for the definition and identification of environmentally associated immune disorders. The World Health Organisation (WHO) has also provided recent publications for other environmentally related problems. All these aspects will be presented and reviewed in detail

Physical Activity, a Critical Exposure Factor of Environmental Pollution in Children and Adolescents Health Risk Assessment.

Science.gov (United States)

Dong, Jingmei; Zhang, Su; Xia, Li; Yu, Yi; Hu, Shuangshuang; Sun, Jingyu; Zhou, Ping; Chen, Peijie

2018-01-23

It is an extremely urgent problem that physical fitness promotion must face not only the increasing air pollution but also the decline of physical activity level of children and adolescents worldwide at present, which is the major reason that forms an inactive lifestyle and does harm to adolescents' health. Thus, it is necessary to focus on the exposure factor in environmental health risk assessment (EHRA) which conducts supervision of environmental pollution and survey of adolescents' activity patterns according to the harmful characteristics of air pollutant and relationship between dose and response. Some countries, such as USA, Canada and Australia, regard both respiratory rate and physical activity pattern as main exposure factors for adolescents in both air pollution health risk assessment and exercise risk assessment to forecast a safe exposing condition of pollutant for adolescents while they are doing exercise outdoors. In addition, it suggests that the testing indexes and testing methods of these two exposure factors, such as investigating the time of daily physical activity, strength, and characteristic of frequency, help to set up the quantitative relationship between environmental pollution index and the time, strength, frequency of daily activities, and formulate children's and adolescents' activity instructions under different levels of environmental pollutions. As smog becomes increasingly serious at present, it is meaningful to take physical activity as a critical composition of exposure factor and establish physical activity guideline, so as to reduce the risk of air pollution, and promote physical health of children and adolescents effectively.

Blood miRNAs as sensitive and specific biological indicators of environmental and occupational exposure to volatile organic compound (VOC).

Science.gov (United States)

Song, Mi-Kyung; Ryu, Jae-Chun

2015-10-01

To date, there is still shortage of highly sensitive and specific minimally invasive biomarkers for assessment of environmental toxicants exposure. Because of the significance of microRNA (miRNA) in various diseases, circulating miRNAs in blood may be unique biomarkers for minimally invasive prediction of toxicants exposure. We identified and validated characteristic miRNA expression profiles of human whole blood in workers exposed to volatile organic compounds (VOCs) and compared the usefulness of miRNA indicator of VOCs with the effectiveness of the already used urinary biomarkers of occupational exposure. Using a microarray based approach we screened and detected deregulated miRNAs in their expression in workers exposed to VOCs (toluene [TOL], xylene [XYL] and ethylbenzene [EBZ]). Total 169 workers from four dockyards were enrolled in current study, and 50 subjects of them were used for miRNA microarray analysis. We identified 467 miRNAs for TOL, 211 miRNAs for XYL, and 695 miRNAs for XYL as characteristic discernible exposure indicator, which could discerned each VOC from the control group with higher accuracy, sensitivity, and specificity than urinary biomarkers. Current observations from this study point out that the altered levels of circulating miRNAs can be a reliable novel, minimally invasive biological indicator of occupational exposure to VOCs. Copyright © 2015 Elsevier GmbH. All rights reserved.

Interactions of GST Polymorphisms in Air Pollution Exposure and Respiratory Diseases and Allergies.

Science.gov (United States)

Bowatte, Gayan; Lodge, Caroline J; Perret, Jennifer L; Matheson, Melanie C; Dharmage, Shyamali C

2016-11-01

The purpose of this review is to summarize the evidence from recently published original studies investigating how glutathione S-transferase (GST) gene polymorphisms modify the impact of air pollution on asthma, allergic diseases, and lung function. Current studies in epidemiological and controlled human experiments found evidence to suggest that GSTs modify the impact of air pollution exposure on respiratory diseases and allergies. Of the nine articles included in this review, all except one identified at least one significant interaction with at least one of glutathione S-transferase pi 1 (GSTP1), glutathione S-transferase mu 1 (GSTM1), or glutathione S-transferase theta 1 (GSTT1) genes and air pollution exposure. The findings of these studies, however, are markedly different. This difference can be partially explained by regional variation in the exposure levels and oxidative potential of different pollutants and by other interactions involving a number of unaccounted environment exposures and multiple genes. Although there is evidence of an interaction between GST genes and air pollution exposure for the risk of respiratory disease and allergies, results are not concordant. Further investigations are needed to explore the reasons behind the discordancy.

Environmental, life-style, and physical precursors of clinical Parkinson's disease: recent findings from the Honolulu-Asia Aging Study.

Science.gov (United States)

Abbott, Robert D; Ross, G Webster; White, Lon R; Sanderson, Wayne T; Burchfiel, Cecil M; Kashon, Michael; Sharp, Dan S; Masaki, Kamal H; Curb, J David; Petrovitch, Helen

2003-10-01

Increased westernization with Japanese migration to the U. S. in the early 20(th) century is thought to have altered the risk of cardiovascular disease. Whether similar effects include changes in the risk of Parkinson's disease (PD) is not clear. This report describes the relations between environmental, life-style, and physical attributes and the incidence of PD that have been observed in the Honolulu-Asia Aging Study. Beginning in 1965, environmental, life-style, and physical attributes were recorded at selected examinations in a cohort of 8,006 Japanese-American men. Subjects were followed for clinical PD. During 30 years of follow- up, PD was observed in 137 men. Overall incidence (7.1/10,000 person-years) was generally higher than in Asia and similar to rates observed in Europe and the U. S. Precursors of PD included constipation, adiposity, years worked on a sugar or pineapple plantation, years of exposure to pesticides, and exposure to sugar cane processing. Factors showing an inverse association with PD included coffee intake and cigarette smoking. Among dietary factors, carbohydrates increased the risk of PD while the intake of polyunsaturated fats appeared protective. Total caloric intake, saturated and monounsaturated fats, protein, niacin, riboflavin, beta-carotene, vitamins A, B, and C, dietary cholesterol, cobalamin, alpha-tocopherol, and pantothenic acid showed no clear relation with clinical PD. Findings suggest that several environmental, life-style, and physical attributes appear to be precursors of PD. Whether patterns of precursors can be used to identify individuals at high risk of future PD or can broaden the scope of early interventions or recruitment into neuroprotective trials warrants further study.

U.S. Geological Survey environmental health science strategy: Providing environmental health science for a changing world

Science.gov (United States)

Bright, Patricia R.; Buxton, Herbert T.; Balistrieri, Laurie S.; Barber, Larry B.; Chapelle, Francis H.; Cross, Paul C.; Krabbenhoft, David P.; Plumlee, Geoffrey S.; Sleeman, Jonathan M.; Tillitt, Donald E.; Toccalino, Patricia L.; Winton, James R.

2013-01-01

America has an abundance of natural resources. We have bountiful clean water, fertile soil, and unrivaled national parks, wildlife refuges, and public lands. These resources enrich our lives and preserve our health and wellbeing. These resources have been maintained because of our history of respect for their value and an enduring commitment to their vigilant protection. Awareness of the social, economic, and personal value of the health of our environment is increasing. The emergence of environmentally driven diseases caused by exposure to contaminants and pathogens is a growing concern worldwide. New health threats and patterns of established threats are affected by both natural and anthropogenic changes to the environment. Human activities are key drivers of emerging (new and re-emerging) health threats. Societal demands for land and natural resources, quality of life, and economic prosperity lead to environmental change. Natural earth processes, climate trends, and related climatic events will compound the environmental impact of human activities. These environmental drivers will influence exposure to disease agents, including viral, bacterial, prion, and fungal pathogens, parasites, synthetic chemicals and substances, natural earth materials, toxins, and other biogenic compounds.

Normal mere exposure effect with impaired recognition in Alzheimer's disease.

Science.gov (United States)

Willems, Sylvie; Adam, Stéphane; Van der Linden, Martial

2002-02-01

We investigated the mere exposure effect and the explicit memory in Alzheimer's disease (AD) patients and elderly control subjects, using unfamiliar faces. During the exposure phase, the subjects estimated the age of briefly flashed faces. The mere exposure effect was examined by presenting pairs of faces (old and new) and asking participants to select the face they liked. The participants were then presented with a forced-choice explicit recognition task. Controls subjects exhibited above-chance preference and recognition scores for old faces. The AD patients also showed the mere exposure effect but no explicit recognition. These results suggest that the processes involved in the mere exposure effect are preserved in AD patients despite their impaired explicit recognition. The results are discussed in terms of Seamon et al.'s (1995) proposal that processes involved in the mere exposure effect are equivalent to those subserving perceptual priming. These processes would depend on extrastriate areas which are relatively preserved in AD patients.

Climate change and occupational allergies: an overview on biological pollution, exposure and prevention.

Science.gov (United States)

D'Ovidio, Maria Concetta; Annesi-Maesano, Isabella; D'Amato, Gennaro; Cecchi, Lorenzo

2016-01-01

Climate change, air pollution, temperature increase and other environmental variables are modifying air quality, contributing to the increase of prevalence of allergic respiratory diseases. Allergies are complex diseases characterized by multilevel interactions between individual susceptibility, response to immune modulation and environmental exposures to physical, chemical and biological agents. Occupational allergies introduce a further complexity to these relationships by adding occupational exposure to both the indoor and outdoor ones in the living environment. The aim of this paper is to overview climate-related allergy affecting environmental and occupational health, as literature data are scanty in this regard, and to suggest a management model of this risk based on a multidisciplinary approach, taking the case of biological pollution, with details on exposure and prevention. The management of climate-related occupational allergy should take into account preventive health strategies, environmental, public and occupational interventions, as well as to develop, implement, evaluate, and improve guidelines and standards protecting workers health under changing climatic conditions; new tools and strategies based on local conditions will have to be developed. Experimental studies and acquisition of environmental and personal data have to be matched to derive useful information for the scope of occupational health and safety.

Cardiovascular Mortality Caused by Exposure to Radon

International Nuclear Information System (INIS)

Johnson, J. R.; Duport, P.

2004-01-01

Cardiovascular diseases (CVD) are reported as the cause of morbidity and mortality in humans exposed to (high) therapeutic doses of radiation, A-bomb explosions, accidental (Chernobyl liquidators) and occupational level of radiation while CVD risk does not appear to be elevated in other populations exposed to radiation CVD mortality also appears to be elevated, proportionally with radon progeny exposure in Newfoundland fluorspar miners. In addition, radiation exposure does not seem to increase and may indeed decrease CVD mortality or morbidity in mammals exposed to radiation in the laboratory. We have calculated the doses to blood and coronary artery wall from radon and progeny, and have concluded radon exposure may indeed increase the incidence of cardiovascular diseases and that a thorough investigation of that risk is justified, even at environmental and occupational levels. These contradictory observations suggest that radiation may be considered as one of many risk factors for cardiovascular diseases. As such, it may be necessary to reduce not only other risk factors as far as possible, but also to minimize exposures to radiation to further reduce the burden of cardiovascular diseases in the population. (Author) 27 refs

Exposure to environmental tobacco smoke measured by cotinine 125I-radioimmunoassay

International Nuclear Information System (INIS)

Knight, G.J.; Palomaki, G.E.; Lea, D.H.; Haddow, J.E.

1989-01-01

We describe a polyclonal-antiserum-based 125 I-radioimmunoassay for cotinine that is suitable for measuring nonsmokers' passive exposure to tobacco smoke in the environment. The standard curve ranged from 0.25 to 12.0 micrograms/L, with an estimated lower limit of sensitivity of 0.2 microgram/L (95% B/Bo = 0.2 microgram/L; 50% B/Bo = 4.0 micrograms/L). The median within-assay CVs for patients' samples with cotinine values from 0.4 to 1.3, 1.4 to 2.4, 2.5 to 4.6, and 4.7 to 15.6 micrograms/L were 13.9%, 7.2%, 5.1%, and 5.7%, respectively. Between-assay CVs for two quality-control sera with average values of 1.53 and 3.68 micrograms/L were 14.3% and 7.8%, respectively. Analytical recoveries of cotinine from smokers' sera diluted in zero calibrant ranged from 91% to 116%. Cotinine values determined on 79 paired sera and urines from nonsmokers showed significant correlation with self-reported exposure to environmental tobacco smoke (r = 0.49, P less than 0.001 for sera; r = 0.57, P less than 0.001 for urine). The log of the values for serum and urine cotinine were also significantly correlated (r = 0.85, P less than 0.001). Evidently, polyclonal antiserum can be used to develop a cotinine assay for measuring exposure to environmental tobacco smoke that compares well with that described for monoclonal-based assays

Skin diseases associated with Agent Orange and other organochlorine exposures.

Science.gov (United States)

Patterson, Andrew T; Kaffenberger, Benjamin H; Keller, Richard A; Elston, Dirk M

2016-01-01

Organochlorine exposure is an important cause of cutaneous and systemic toxicity. Exposure has been associated with industrial accidents, intentional poisoning, and the use of defoliants, such as Agent Orange in the Vietnam War. Although long-term health effects are systematically reviewed by the Institute of Medicine, skin diseases are not comprehensively assessed. This represents an important practice gap as patients can present with cutaneous findings. This article provides a systematic review of the cutaneous manifestations of known mass organochlorine exposures in military and industrial settings with the goal of providing clinically useful recommendations for dermatologists seeing patients inquiring about organochlorine effects. Patients with a new diagnosis of chloracne, porphyria cutanea tarda, cutaneous lymphomas (non-Hodgkin lymphoma), and soft-tissue sarcomas including dermatofibrosarcoma protuberans and leiomyosarcomas should be screened for a history of Vietnam service or industrial exposure. Inconclusive evidence exists for an increased risk of other skin diseases in Vietnam veterans exposed to Agent Orange including benign fatty tumors, melanomas, nonmelanoma skin cancers, milia, eczema, dyschromias, disturbance of skin sensation, and rashes not otherwise specified. Affected veterans should be informed of the uncertain data in those cases. Referral to Department of Veterans Affairs for disability assessment is indicated for conditions with established associations. Copyright © 2015 American Academy of Dermatology, Inc. All rights reserved.

Chronic obstructive pulmonary disease and long-term exposure to traffic-related air pollution: a cohort study

DEFF Research Database (Denmark)

Andersen, Zorana J; Hvidberg, Martin; Jensen, Steen S

2011-01-01

Short-term exposure to air pollution has been associated with exacerbation of chronic obstructive pulmonary disease (COPD), whereas the role of long-term exposures on the development of COPD is not yet fully understood.......Short-term exposure to air pollution has been associated with exacerbation of chronic obstructive pulmonary disease (COPD), whereas the role of long-term exposures on the development of COPD is not yet fully understood....

Prenatal diethylstilbestrol exposure and self-reported immune-related diseases

NARCIS (Netherlands)

Vingerhoets, A. J.; Assies, J.; Goodkin, K.; van Heck, G. L.; Bekker, M. H.

1998-01-01

To compare self-reports of immune-related diseases in diethylstilbestrol (DES) daughters and controls. Prenatal exposure to DES has been associated with several malformations in the lower genital tract, a higher prevalence of adenosis, and increased risk of clear cell adenocarcinoma, and

Impacts of environment on human diseases: a web service for the human exposome

Science.gov (United States)

Karssenberg, Derek; Vaartjes, Ilonca; Kamphuis, Carlijn; Strak, Maciek; Schmitz, Oliver; Soenario, Ivan; de Jong, Kor

2017-04-01

The exposome is the totality of human environmental exposures from conception onwards. Identifying the contribution of the exposome to human diseases and health is a key issue in health research. Examples include the effect of air pollution exposure on cardiovascular diseases, the impact of disease vectors (mosquitos) and surface hydrology exposure on malaria, and the effect of fast food restaurant exposure on obesity. Essential to health research is to disentangle the effects of the exposome and genome on health. Ultimately this requires quantifying the totality of all human exposures, for each individual in the studied human population. This poses a massive challenge to geoscientists, as environmental data are required at a high spatial and temporal resolution, with a large spatial and temporal coverage representing the area inhabited by the population studied and the time span representing several decades. Then, these data need to be combined with space-time paths of individuals to calculate personal exposures for each individual in the population. The Global and Geo Health Data Centre is taking this challenge by providing a web service capable of enriching population data with exposome information. Our web service can generate environmental information either from archived national (up to 5 m spatial and 1 h temporal resolution) and global environmental information or generated on the fly using environmental models running as microservices. On top of these environmental data services runs an individual exposure service enabling health researchers to select different spatial and temporal aggregation methods and to upload space-time paths of individuals. These are then enriched with personal exposures and eventually returned to the user. We illustrate the service in an example of individual exposures to air pollutants calculated from hyper resolution air pollution data and various approaches to estimate space-time paths of individuals.

Concentrations of environmental organic contaminants in meat and meat products and human dietary exposure: A review.

Science.gov (United States)

Domingo, José L

2017-09-01

Meat and meat products is one of the most relevant food groups in an important number of human diets. Recently, the IARC, based on results of a number of epidemiological studies, classified the consumptions of red meat and processed meat as "probably carcinogenic to humans" and as "carcinogenic to humans", respectively. It was suggested that the substances responsible of the potential carcinogenicity would be mainly generated during meat processing, such as curing and smoking, or when meat is heated at high temperatures. However, the exposure to environmental pollutants through meat consumption was not discussed. The purpose of the present paper was to review recent studies reporting the concentrations of PCDD/Fs, DL-PCBs and PAHs in meat and meat products, as well as the human exposure to these pollutants through the diet. It is concluded that the health risks derived from exposure to carcinogenic environmental contaminants must be considered in the context of each specific diet, which besides meat and meat products, includes other foodstuffs containing also chemical pollutants, some of them with carcinogenic potential. Anyhow, meat and meat products are not the main food group responsible of the dietary exposure to carcinogenic (or probably carcinogenic) environmental organic pollutants. Copyright © 2017 Elsevier Ltd. All rights reserved.

Immunogenetic basis of environmental lung disease: Lessons from the berylliosis model

International Nuclear Information System (INIS)

Saltini, C.; Richeldi, L.; Amicosante, M.; Franchi, A.; Lombardi, G.

1998-01-01

The role of genetic factors has been hypothesized in the pathogenesis of a number of chronic inflammatory lung diseases. The genes of the major histocompatibility complex (MHC) locus on human chromosome 6 have been identified as important determinants in diseases caused both by inorganic and organic compounds such as beryllium, gold, acid anhydrides, isocyanates and grass pollens. Since many environmental factors are the determinants of the immunopathogenesis of asthma, pulmonary granulomatous disorders, hypersensitivity pneumonitis and fibrotic lung disorders, an understanding of the interaction between environmental factors is crucial to epidemiology, prevention and treatment of these disorders. Berylliosis is an environmental chronic inflammatory disorder of the lung caused by inhalation of beryllium dusts. A human leukocyte antigen class II marker (HLA-DP Glu69) has been found to be strongly associated with the disease. In in vitro studies, the gene has been shown to play a direct role in the immunopathogenesis of the disease. In human studies, the gene has been shown to confer increased susceptibility to beryllium in exposed workers, thus suggesting that HLA gene markers may be used as epidemiological probes to identify population groups at higher risk of environmental lung diseases, to identify environmental levels of lung immunotoxicants that would be safe for the entire population and the prevent disease risk associated with occupation, manufactured products and the environment. Studies on the associations between human leukocyte antigens and chronic inflammatory lung disorders are reviewed in the context of the berylliosis model. (au)

The association between phthalate exposure and asthma

Directory of Open Access Journals (Sweden)

Ming-Ju Tsai

2012-07-01

Full Text Available Asthma is a chronic inflammatory disorder of the airway, characterized by airway hyperresponsiveness. It is a disabling disease with an increasing prevalence, resulting in heavy social and economic burdens worldwide. Humans are extensively exposed to phthalates, and many epidemiological studies have shown a relationship between phthalate exposure and asthma in recent decades. Earlier experimental studies focused on inflammatory cells, demonstrating the adjuvant effects, immunomodulatory effects, or immunosuppressive effects related to phthalate exposure. Recent studies have shown that phthalates may have a direct effect on airway epithelial cells and contribute to airway remodeling, which is the cardinal pathologic characteristic of chronic asthma, with a high correlation with disease severity. Through these efforts, phthalates have been recognized as important environmental factors in the pathogenesis of asthma, but further studies are still required to elucidate the detailed mechanism. This review discusses the current status of human exposure to phthalates in Taiwan and summarizes the epidemiological and experimental evidence related to the roles of phthalate exposure in the development of asthma and associated diseases.

Environmental exposure to mineral fibers in New Caledonia: an ecological study

Science.gov (United States)

Baumann, F.; Ambrosi, J.

2013-05-01

Inhalation of asbestos and other fibrous minerals causes lung cancer and other malignancies, specifically malignant mesothelioma (MM). MM is an aggressive pleural tumor that presents with a median latency period of 30-40 years from initial fiber exposure. Due to occupational exposure, MM incidence is 4-8 times higher in men as compared to women. In New Caledonia (NC), very high incidences of MM and lung cancer were observed in both men and women, suggesting an environmental origin of exposure. Although nickel mining and the traditional use of tremolite-containing whitewash were suspected causes of MM, numerous MM cases have been observed in areas lacking these risk factors. We carried out an ecological study of MM incidence in NC and identified a study area that included those counties having the highest MM incidences as well as counties lacking MM. We conducted epidemiological and environmental investigations for each of the 100 tribes living within this area. Residential history was assessed for each MM case, and samples of each quarry, road, and whitewash were analyzed to determine the nature of any mineral fibers. We analyzed the environmental determinants of MM, including geology, mineralogy, plant cover, land shape and human activities as well as use of whitewash, by using two univariate and multivariate statistical methods: 1) a logistic regression to compare tribes with and without MM cases and calculate the odds ratios, (OR) 2) the Poisson regression to calculate incidence rate ratios (IRR) for each factor. While most MM cases among Caucasians were observed in men with a mean age of 72, indicating occupational exposure, Melanesians exhibited elevated MM incidence in both men and women at a mean age of 60. A sex ratio close to 1 compounded with the relatively young ages of MM cases confirmed environmental causation within the Melanesian population. We found one significant and two secondary spatial clusters of MM in tribal areas. No temporal cluster was

Managing health effects of beryllium exposure

National Research Council Canada - National Science Library

Committee on Beryllium Alloy Exposures; Committee on Toxicology; National Research Council; Division on Earth and Life Studies; National Research Council

2008-01-01

... to its occurrence in exposed people. Despite reduced workplace exposure, chronic beryllium disease continues to occur. In addition, beryllium has been classified as a likely human carcinogen by several agencies, such as the International Agency for Research on Cancer, the National Toxicology Program, and the U.S. Environmental Protection Agency. Thos...

Environmental exposure to arsenic and chromium in children is associated with kidney injury molecule-1

International Nuclear Information System (INIS)

Cárdenas-González, M.; Osorio-Yáñez, C.; Gaspar-Ramírez, O.; Pavković, M.; Ochoa-Martínez, A.; López-Ventura, D.

2016-01-01

Environmental hazards from natural or anthropological sources are widespread, especially in the north-central region of Mexico. Children represent a susceptible population due to their unique routes of exposure and special vulnerabilities. In this study we evaluated the association of exposure to environmental kidney toxicants with kidney injury biomarkers in children living in San Luis Potosi (SLP), Mexico. A cross-sectional study was conducted with 83 children (5–12 years of age) residents of Villa de Reyes, SLP. Exposure to arsenic, cadmium, chromium, fluoride and lead was assessed in urine, blood and drinking water samples. Almost all tap and well water samples had levels of arsenic (81.5%) and fluoride (100%) above the permissible levels recommended by the World Health Organization. Mean urine arsenic (45.6 ppb) and chromium (61.7 ppb) were higher than the biological exposure index, a reference value in occupational settings. Using multivariate adjusted models, we found a dose-dependent association between kidney injury molecule-1 (KIM-1) across chromium exposure tertiles [(T1: reference, T2: 467 pg/mL; T3: 615 pg/mL) (p-trend=0.001)]. Chromium upper tertile was also associated with higher urinary miR-200c (500 copies/μl) and miR-423 (189 copies/μL). Arsenic upper tertile was also associated with higher urinary KIM-1 (372 pg/mL). Other kidney injury/functional biomarkers such as serum creatinine, glomerular filtration rate, albuminuria, neutrophil gelatinase-associated lipocalin and miR-21 did not show any association with arsenic, chromium or any of the other toxicants evaluated. We conclude that KIM-1 might serve as a sensitive biomarker to screen children for kidney damage induced by environmental toxic agents. - Highlights: • Children living in Mexico had exceedingly high arsenic and chromium exposure. • Arsenic and chromium exposure was significantly associated with urinary KIM-1. • KIM-1 might serve as a sensitive biomarker to evaluate kidney

Environmental exposure to arsenic and chromium in children is associated with kidney injury molecule-1

Energy Technology Data Exchange (ETDEWEB)

Cárdenas-González, M. [Laboratory of Systems Pharmacology, Harvard Program in Therapeutic Sciences, Harvard Medical School, Boston, MA (United States); Osorio-Yáñez, C. [Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA (United States); Gaspar-Ramírez, O. [Centro de Investigación y Asistencia en Tecnología y Diseño del Estado de Jalisco, Unidad Noreste (CIATEJ), Nuevo Leon (Mexico); Pavković, M. [Laboratory of Systems Pharmacology, Harvard Program in Therapeutic Sciences, Harvard Medical School, Boston, MA (United States); Renal Division, Department of Medicine, Brigham and Women' s Hospital, Boston, MA (United States); Ochoa-Martínez, A. [Laboratorio de Toxicología Molecular, Centro de Investigación Aplicada en Ambiente y Salud (CIAAS), Coordinación para la Innovación y Aplicación de la Ciencia y la Tecnología (CIACYT), Universidad Autónoma de San Luis Potosí, San Luis Potosí (Mexico); López-Ventura, D. [Departamento de Toxicología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV), México City (Mexico); and others

2016-10-15

Environmental hazards from natural or anthropological sources are widespread, especially in the north-central region of Mexico. Children represent a susceptible population due to their unique routes of exposure and special vulnerabilities. In this study we evaluated the association of exposure to environmental kidney toxicants with kidney injury biomarkers in children living in San Luis Potosi (SLP), Mexico. A cross-sectional study was conducted with 83 children (5–12 years of age) residents of Villa de Reyes, SLP. Exposure to arsenic, cadmium, chromium, fluoride and lead was assessed in urine, blood and drinking water samples. Almost all tap and well water samples had levels of arsenic (81.5%) and fluoride (100%) above the permissible levels recommended by the World Health Organization. Mean urine arsenic (45.6 ppb) and chromium (61.7 ppb) were higher than the biological exposure index, a reference value in occupational settings. Using multivariate adjusted models, we found a dose-dependent association between kidney injury molecule-1 (KIM-1) across chromium exposure tertiles [(T1: reference, T2: 467 pg/mL; T3: 615 pg/mL) (p-trend=0.001)]. Chromium upper tertile was also associated with higher urinary miR-200c (500 copies/μl) and miR-423 (189 copies/μL). Arsenic upper tertile was also associated with higher urinary KIM-1 (372 pg/mL). Other kidney injury/functional biomarkers such as serum creatinine, glomerular filtration rate, albuminuria, neutrophil gelatinase-associated lipocalin and miR-21 did not show any association with arsenic, chromium or any of the other toxicants evaluated. We conclude that KIM-1 might serve as a sensitive biomarker to screen children for kidney damage induced by environmental toxic agents. - Highlights: • Children living in Mexico had exceedingly high arsenic and chromium exposure. • Arsenic and chromium exposure was significantly associated with urinary KIM-1. • KIM-1 might serve as a sensitive biomarker to evaluate kidney

Environmental exposure to asbestos and other inorganic fibres using animal lung model

Energy Technology Data Exchange (ETDEWEB)

Fornero, Elisa [Dipartimento di Scienze dell' Ambiente e della Vita, Universita del Piemonte Orientale ' A. Avogadro' , Via Bellini 25/g, 15100 Alessandria (Italy); Centro Interdipartimentale per lo Studio degli Amianti e di altri Particolati Nocivi ' Giovanni Scansetti' , Universita degli Studi di Torino, Torino (Italy)], E-mail: elisa.fornero@mfn.unipmn.it; Belluso, Elena [Dipartimento di Scienze Mineralogiche e Petrologiche, Universita degli Studi di Torino, Via V. Caluso 35, 10125 Torino (Italy); Istituto di Geoscienze e Georisorse, CNR-Unita di Torino, Via V. Caluso 35, 10125 Torino (Italy); Centro Interdipartimentale per lo Studio degli Amianti e di altri Particolati Nocivi ' Giovanni Scansetti' , Universita degli Studi di Torino, Torino (Italy); Capella, Silvana [Dipartimento di Scienze Mineralogiche e Petrologiche, Universita degli Studi di Torino, Via V. Caluso 35, 10125 Torino (Italy); Centro Interdipartimentale per lo Studio degli Amianti e di altri Particolati Nocivi ' Giovanni Scansetti' , Universita degli Studi di Torino, Torino (Italy); Bellis, Donata [Servizio di Anatomia, Istologia Patologica e Citodiagnostica, Azienda Ospedaliera San Giovanni Bosco, ASLTO2 Piazza Donatori del Sangue 3, 10154 Torino (Italy); Centro Interdipartimentale per lo Studio degli Amianti e di altri Particolati Nocivi ' Giovanni Scansetti' , Universita degli Studi di Torino, Torino (Italy)

2009-01-15

Professional exposure to asbestos fibres is widely recognized as very dangerous to human health and for this reason many countries have banned their commercial uses. People, nevertheless, continue to be exposed to low dose of asbestos from natural and anthropogenic sources still in loco, for which the potential hazard is unknown. The aim of this research is to assess environmental exposure in an area with outcropping serpentinite rocks, which bear asbestos mineralizations, using sentinel animals which are a non-experimental animal model. We studied the burden of inorganic fibres in cattle lungs which come from two areas in Italy's Western Alps bearing serpentinitic outcrops: Susa Valley with a heavy anthropization and Lanzo Valleys, with a minor human impact. The identification and quantification of inorganic fibres were performed by Scanning Electron Microscope (SEM) and Energy Dispersive Spectrometer (EDS). In comparison to humans, studies of animals have some advantages, such as no occupational exposure or history of smoking and, in the case of cattle, a sedentary life restricted to one region. Results spotlight that over than 35% of inorganic fibres found both in Susa and Lanzo valleys, belong to asbestos mineralogical species (asbestos tremolite/actinolite, chrysotile s.s., asbestos grunerite, crocidolite). We also observed a higher concentration of artificial fibrous products in Susa samples showing a correlation with the level of anthropization. These results confirm that sentinel animals are an excellent model to assess breathable environmental background because it is possible to eliminate some variables, such as unknown occupational exposure.

Environmental exposure to asbestos and other inorganic fibres using animal lung model

International Nuclear Information System (INIS)

Fornero, Elisa; Belluso, Elena; Capella, Silvana; Bellis, Donata

2009-01-01

Professional exposure to asbestos fibres is widely recognized as very dangerous to human health and for this reason many countries have banned their commercial uses. People, nevertheless, continue to be exposed to low dose of asbestos from natural and anthropogenic sources still in loco, for which the potential hazard is unknown. The aim of this research is to assess environmental exposure in an area with outcropping serpentinite rocks, which bear asbestos mineralizations, using sentinel animals which are a non-experimental animal model. We studied the burden of inorganic fibres in cattle lungs which come from two areas in Italy's Western Alps bearing serpentinitic outcrops: Susa Valley with a heavy anthropization and Lanzo Valleys, with a minor human impact. The identification and quantification of inorganic fibres were performed by Scanning Electron Microscope (SEM) and Energy Dispersive Spectrometer (EDS). In comparison to humans, studies of animals have some advantages, such as no occupational exposure or history of smoking and, in the case of cattle, a sedentary life restricted to one region. Results spotlight that over than 35% of inorganic fibres found both in Susa and Lanzo valleys, belong to asbestos mineralogical species (asbestos tremolite/actinolite, chrysotile s.s., asbestos grunerite, crocidolite). We also observed a higher concentration of artificial fibrous products in Susa samples showing a correlation with the level of anthropization. These results confirm that sentinel animals are an excellent model to assess breathable environmental background because it is possible to eliminate some variables, such as unknown occupational exposure

Just who is at risk? The ethics of environmental regulation.

Science.gov (United States)

Simon, Ted

2011-08-01

The willingness to view risk as part of daily life has vanished. A risk-averse mindset among environmental regulators engenders confusion between the ethics of intention and the ethics of consequence, leading to the elevation of the precautionary principle with unintended and often unfortunate outcomes. Environmental risk assessment is conservative, but the actual level of conservatism cannot be determined. High-end exposure assumptions and current toxicity criteria from the USEPA, based on linear extrapolation for carcinogens and default uncertainty factors for systemic toxicants, obscure the degree of conservatism in risk assessments. Ideally, one could choose a percentile of the target population to include within environmental standards, but this choice is complicated by the food, pharmaceutical and advertising industries, whose activities, inadvertent or not, often promote maladaptive and unhealthy lifestyle choices. There has lately been much discussion about background exposures and disease processes and their potential to increase the risk from environmental chemicals. Should these background exposures or disease processes, especially those associated with maladaptive individual choices, be included as part of a regulatory risk evaluation? A significant ethical question is whether environmental regulation should protect those pursuing a self-destructive lifestyle that may add to or synergize with otherwise innocuous environmental exposures. Choosing a target percentile of protection would provide an increased level of transparency and the flexibility to choose a higher or lower percentile if such a choice is warranted. Transparency and flexibility will lead to more responsive environmental regulation that balances protection of public health and the stewardship of societal resources.

Current knowledge of environmental exposure in children during the sensitive developmental periods

Directory of Open Access Journals (Sweden)

Norma Helena Perlroth

2017-01-01

Conclusion: To identify the causes and understand the mechanisms involved in the genesis of these diseases is a challenge for science, as there is still a lack of knowledge on children's susceptibility to many environmental contaminants. Prevention policies and more research on child environmental health, improving the recording and surveillance of environmental risks to children's health, should be an ongoing priority in the public health field.

[Hospitality workers' exposure to environmental tobacco smoke before and after implementation of smoking ban in public places: a review of epidemiological studies].

Science.gov (United States)

Polańska, Kinga; Hanke, Wojciech; Konieczko, Katarzyna

2011-01-01

Environmental tobacco smoke (ETS) exposure induces serious negative health consequences, of which the increased risk of cardiovascular diseases, cancer, respiratory symptoms and poor pregnancy outcomes appear to be most important. Taking into account those health consequences of ETS exposure most countries have introduced legislation to ban or restrict smoking in public places. In this paper the effectiveness of the introduced legislation was analyzed with regard to the protection of hospitality workers from ETS exposure in the workplace. The analysis of 12 papers published after 2000 covered the year of publication, type of legislation, study population, hospitality venue (pub, bar, restaurant, disco) and type of markers or self-reported perception of exposure to ETS. The analysis indicates that the legislation to ban smoking in hospitality venues protects workers from ETS exposure when the venues are 100% tobacco smoke free. The reduction of the cotinine level in biological samples after the implementation of smoke free law was 57-89%, comparing to the biomarker level in the samples taken before the new law was introduced. About 90% of reduction in nicotine and PM levels was also noted. In addition, the positive self perception reported by workers proved the effectiveness of new legislation protecting them from ETS exposure.

USGS Environmental health science strategy: providing environmental health science for a changing world: public review release

Science.gov (United States)

Bright, Patricia R.; Buxton, Herbert T.; Balistrieri, Laurie S.; Barber, Larry B.; Chapelle, Francis H.; Cross, Paul C.; Krabbenhoft, David P.; Plumlee, Geoffrey S.; Sleeman, Jonathan M.; Tillitt, Donald E.; Toccalino, Patricia L.; Winton, James R.

2012-01-01

America has an abundance of natural resources. We have bountiful clean water, fertile soil, and unrivaled national parks, wildlife refuges, and public lands. These resources enrich our lives and preserve our health and wellbeing. These resources have been maintained because of our history of respect for their value and an enduring commitment to their vigilant protection. Awareness of the social, economic, and personal value of the health of our environment is increasing. The emergence of environmentally driven diseases caused by environmental exposure to contaminants and pathogens is a growing concern worldwide. New health threats and patterns of established threats are affected by both natural and anthropogenic changes to the environment. Human activities are key drivers of emerging (new and re-emerging) health threats. Societal demands for land and natural resources, a better quality of life, improved economic prosperity, and the environmental impacts associated with these demands will continue to increase. Natural earth processes, climate trends, and related climatic events will add to the environmental impact of human activities. These environmental drivers will influence exposure to disease agents, including viral, bacterial, prion, and fungal pathogens, parasites, natural earth materials, toxins and other biogenic compounds, and synthetic chemicals and substances. The U.S. Geological Survey (USGS) defines environmental health science broadly as the interdisciplinary study of relations among the quality of the physical environment, the health of the living environment, and human health. The interactions among these three spheres are driven by human activities, ecological processes, and natural earth processes; the interactions affect exposure to contaminants and pathogens and the severity of environmentally driven diseases in animals and people. This definition provides USGS with a framework for synthesizing natural science information from across the Bureau

Validity of self-reported intensity of exposure to second-hand smoke at home against environmental and personal markers.

Science.gov (United States)

Martínez-Sánchez, José M; González-Marrón, Adrián; Martín-Sánchez, Juan Carlos; Sureda, Xisca; Fu, Marcela; Pérez-Ortuño, Raúl; Lidón-Moyano, Cristina; Galán, Iñaki; Pascual, José Antonio; Fernández, Esteve

2017-11-02

The objective of this study was to assess the validity of two questions about the perception of intensity of exposure to secondhand smoke (SHS) at home using as a reference environmental markers (airborne nicotine and benzene) and biomarkers of exposure (cotinine in saliva and urine). This was a cross-sectional study in a convenience sample of 49 non-smoking volunteers. We found a high correlation between self-reported SHS exposure and airborne nicotine (r sp =0.806, p0.05). In conclusion, the significant correlation of the two questions proposed with environmental markers and personal markers indicates their potential validity to assess exposure to SHS at home. Copyright © 2017 SESPAS. Publicado por Elsevier España, S.L.U. All rights reserved.

Reducing Environmental Allergic Triggers: Policy Issues.

Science.gov (United States)

Abramson, Stuart L

The implementation of policies to reduce environmental allergic triggers can be an important adjunct to optimal patient care for allergic rhinitis and allergic asthma. Policies at the local level in schools and other public as well as private buildings can make an impact on disease morbidity. Occupational exposures for allergens have not yet been met with the same rigorous policy standards applied for exposures to toxicants by Occupational Safety and Health Administration. Further benefit may be obtained through policies by local, county, state, and national governments, and possibly through international cooperative agreements. The reduction of allergenic exposures can and should be affected by policies with strong scientific, evidence-based derivation. However, a judicious application of the precautionary principle may be needed in circumstances where the health effect of inaction could lead to more serious threats to vulnerable populations with allergic disease. This commentary covers the scientific basis, current implementation, knowledge gaps, and pro/con views on policy issues in reducing environmental allergic triggers. Copyright © 2017 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.

The role of epigenetics in genetic and environmental epidemiology.

Science.gov (United States)

Ladd-Acosta, Christine; Fallin, M Daniele

2016-02-01

Epidemiology is the branch of science that investigates the causes and distribution of disease in populations in order to provide preventative measures and promote human health. The fields of genetic and environmental epidemiology primarily seek to identify genetic and environmental risk factors for disease, respectively. Epigenetics is emerging as an important piece of molecular data to include in these studies because it can provide mechanistic insights into genetic and environmental risk factors for disease, identify potential intervention targets, provide biomarkers of exposure, illuminate gene-environment interactions and help localize disease-relevant genomic regions. Here, we describe the importance of including epigenetics in genetic and environmental epidemiology studies, provide a conceptual framework when considering epigenetic data in population-based studies and touch upon the many challenges that lie ahead.

Isotopically modified silver nanoparticles to assess nanosilver bioavailability and toxicity at environmentally relevant exposures

Science.gov (United States)

Croteau, Marie-Noële; Dybowska, Agnieszka D.; Luoma, Samuel N.; Misra, Superb K.; Valsami-Jones, Eugenia

2014-01-01

A major challenge in understanding the environmental implications of nanotechnology lies in studying nanoparticle uptake in organisms at environmentally realistic exposure concentrations. Typically, high exposure concentrations are needed to trigger measurable effects and to detect accumulation above background. But application of tracer techniques can overcome these limitations. Here we synthesised, for the first time, citrate-coated Ag nanoparticles using Ag that was 99.7 % 109Ag. In addition to conducting reactivity and dissolution studies, we assessed the bioavailability and toxicity of these isotopically modified Ag nanoparticles (109Ag NPs) to a freshwater snail under conditions typical of nature. We showed that accumulation of 109Ag from 109Ag NPs is detectable in the tissues of Lymnaea stagnalis after 24-h exposure to aqueous concentrations as low as 6 ng L–1 as well as after 3 h of dietary exposure to concentrations as low as 0.07 μg g–1. Silver uptake from unlabelled Ag NPs would not have been detected under similar exposure conditions. Uptake rates of 109Ag from 109Ag NPs mixed with food or dispersed in water were largely linear over a wide range of concentrations. Particle dissolution was most important at low waterborne concentrations. We estimated that 70 % of the bioaccumulated 109Ag concentration in L. stagnalis at exposures –1 originated from the newly solubilised Ag. Above this concentration, we predicted that 80 % of the bioaccumulated 109Ag concentration originated from the 109Ag NPs. It was not clear if agglomeration had a major influence on uptake rates.

Chronic Toxic Metal Exposure and Cardiovascular Disease: Mechanisms of Risk and Emerging Role of Chelation Therapy.

Science.gov (United States)

Aneni, Ehimen C; Escolar, Esteban; Lamas, Gervasio A

2016-12-01

Over the last few decades, there has been a growing body of epidemiologic evidence linking chronic toxic metal exposure to cardiovascular disease-related morbidity and mortality. The recent and unexpectedly positive findings from a randomized, double-blind, multicenter trial of metal chelation for the secondary prevention of atherosclerotic cardiovascular disease (Trial to Assess Chelation Therapy (TACT)) have focused the discussion on the role of chronic exposure to toxic metals in the development and propagation of cardiovascular disease and the role of toxic metal chelation therapy in the secondary prevention of cardiovascular disease. This review summarizes the most recent evidence linking chronic toxic metal exposure to cardiovascular disease and examines the findings of TACT.

Physical Activity, a Critical Exposure Factor of Environmental Pollution in Children and Adolescents Health Risk Assessment

Science.gov (United States)

Zhang, Su; Xia, Li; Yu, Yi; Hu, Shuangshuang; Sun, Jingyu; Zhou, Ping; Chen, Peijie

2018-01-01

It is an extremely urgent problem that physical fitness promotion must face not only the increasing air pollution but also the decline of physical activity level of children and adolescents worldwide at present, which is the major reason that forms an inactive lifestyle and does harm to adolescents’ health. Thus, it is necessary to focus on the exposure factor in environmental health risk assessment (EHRA) which conducts supervision of environmental pollution and survey of adolescents’ activity patterns according to the harmful characteristics of air pollutant and relationship between dose and response. Some countries, such as USA, Canada and Australia, regard both respiratory rate and physical activity pattern as main exposure factors for adolescents in both air pollution health risk assessment and exercise risk assessment to forecast a safe exposing condition of pollutant for adolescents while they are doing exercise outdoors. In addition, it suggests that the testing indexes and testing methods of these two exposure factors, such as investigating the time of daily physical activity, strength, and characteristic of frequency, help to set up the quantitative relationship between environmental pollution index and the time, strength, frequency of daily activities, and formulate children’s and adolescents’ activity instructions under different levels of environmental pollutions. As smog becomes increasingly serious at present, it is meaningful to take physical activity as a critical composition of exposure factor and establish physical activity guideline, so as to reduce the risk of air pollution, and promote physical health of children and adolescents effectively. PMID:29360730

Physical Activity, a Critical Exposure Factor of Environmental Pollution in Children and Adolescents Health Risk Assessment

Directory of Open Access Journals (Sweden)

Jingmei Dong

2018-01-01

Full Text Available It is an extremely urgent problem that physical fitness promotion must face not only the increasing air pollution but also the decline of physical activity level of children and adolescents worldwide at present, which is the major reason that forms an inactive lifestyle and does harm to adolescents’ health. Thus, it is necessary to focus on the exposure factor in environmental health risk assessment (EHRA which conducts supervision of environmental pollution and survey of adolescents’ activity patterns according to the harmful characteristics of air pollutant and relationship between dose and response. Some countries, such as USA, Canada and Australia, regard both respiratory rate and physical activity pattern as main exposure factors for adolescents in both air pollution health risk assessment and exercise risk assessment to forecast a safe exposing condition of pollutant for adolescents while they are doing exercise outdoors. In addition, it suggests that the testing indexes and testing methods of these two exposure factors, such as investigating the time of daily physical activity, strength, and characteristic of frequency, help to set up the quantitative relationship between environmental pollution index and the time, strength, frequency of daily activities, and formulate children’s and adolescents’ activity instructions under different levels of environmental pollutions. As smog becomes increasingly serious at present, it is meaningful to take physical activity as a critical composition of exposure factor and establish physical activity guideline, so as to reduce the risk of air pollution, and promote physical health of children and adolescents effectively.

Assessing and evaluating the health impact of environmental exposures

NARCIS (Netherlands)

Hollander, Augustinus Ernst Maria de

2004-01-01

Never in our Western-European history we have been as healthy as we are now. Until the 20th century the (physical) environment was the source of 70-80 percent of disease burden, nowadays, environmental factors probably contribute less than 5%, while life-style is responsible for the bulk of the

Agent Orange exposure and disease prevalence in Korean Vietnam veterans: the Korean veterans health study.

Science.gov (United States)

Yi, Sang-Wook; Hong, Jae-Seok; Ohrr, Heechoul; Yi, Jee-Jeon

2014-08-01

Between 1961 and 1971, military herbicides were used by the United States and allied forces for military purposes. Agent Orange, the most-used herbicide, was a mixture of 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-trichlorophenoxyacetic acid, and contained an impurity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Many Korean Vietnam veterans were exposed to Agent Orange during the Vietnam War. The aim of this study was to evaluate the association between Agent Orange exposure and the prevalence of diseases of the endocrine, nervous, circulatory, respiratory, and digestive systems. The Agent Orange exposure was assessed by a geographic information system-based model. A total of 111,726 Korean Vietnam veterans were analyzed for prevalence using the Korea National Health Insurance claims data from January 2000 to September 2005. After adjusting for covariates, the high exposure group had modestly elevated odds ratios (ORs) for endocrine diseases combined and neurologic diseases combined. The adjusted ORs were significantly higher in the high exposure group than in the low exposure group for hypothyroidism (OR=1.13), autoimmune thyroiditis (OR=1.93), diabetes mellitus (OR=1.04), other endocrine gland disorders including pituitary gland disorders (OR=1.43), amyloidosis (OR=3.02), systemic atrophies affecting the nervous system including spinal muscular atrophy (OR=1.27), Alzheimer disease (OR=1.64), peripheral polyneuropathies (OR=1.09), angina pectoris (OR=1.04), stroke (OR=1.09), chronic obstructive pulmonary diseases (COPD) including chronic bronchitis (OR=1.05) and bronchiectasis (OR=1.16), asthma (OR=1.04), peptic ulcer (OR=1.03), and liver cirrhosis (OR=1.08). In conclusion, Agent Orange exposure increased the prevalence of endocrine disorders, especially in the thyroid and pituitary gland; various neurologic diseases; COPD; and liver cirrhosis. Overall, this study suggests that Agent Orange/2,4-D/TCDD exposure several decades earlier may increase morbidity