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Household air pollution (HAP) is of public health concern, with ~3 billion people worldwide (including >15 million in the US) exposed. HAP from coal use is a human lung carcinogen, yet the epidemiological evidence on carcinogenicity of HAP from biomass use, primarily wood, is not conclusive. To robustly assess biomass’s carcinogenic potential, prospective studies of individuals experiencing a variety of HAP exposures are needed. We have built a global consortium of 13 prospective cohorts (HAPCO: Household Air Pollution Consortium) that have site- and disease-specific mortality and solid fuel use data, for a combined sample size of 587,257 participants and 57,483 deaths. HAPCO provides a novel opportunity to assess the association of HAP with lung cancer death while controlling for important confounders such as tobacco and outdoor air pollution exposures. HAPCO is also uniquely positioned to determine the risks associated with cancers other than lung as well as nonmalignant respiratory and cardiometabolic outcomes, for which prospective epidemiologic research is limited. HAPCO will facilitate research to address public health concerns associated with HAP-attributed exposures by enabling investigators to evaluate sex-specific and smoking status-specific effects under various exposure scenarios.

Context:Clinical toxicologists may be called upon to determine the appropriateness of medical monitoring following documented or purported exposures to toxicants in the occupational, environmental, and medical settings. Methods:We searched the MEDLINE database using the Ovid®search engine for the following terms cross-referenced to the MeSH database: (“occupational exposures” OR “environmental exposures”) AND (“physiologic monitoring” OR “population surveillance”). The titles and abstracts of the resulted articles were reviewed for relevance. We expanded our search to include non-peer-reviewed publications and gray literature and resources using the same terms as utilized in the MEDLINE search. There were a total of 48 relevant peer-reviewed and non-peer-reviewed publications. Publications excluded contained no information relevant to medical monitoring following potentially harmful toxicologic exposures, discussed only worker screening/surveillance and/or population biomonitoring, contained redundant information, or were superseded by more recent information. Approaches to medical monitoring:A consensus exists in the peer-reviewed medical literature, legal literature, and government publications that for medical monitoring to be a beneficial public health activity, careful consideration must be given to potential benefits and harms of the program. Characteristics of the exposure, the adverse human health effect, the screening test, and the natural history of the disease are important in determining whether an exposed population will reap a net benefit or harm from a proposed monitoring program. Broader interpretations of medical monitoring:Some have argued that medical monitoring programs should not be limited to exposure-related outcomes but should duplicate general preventive medicine efforts to improve public health outcomes although an overall reduction of morbidity, mortality and disability by modifying correctable risk factors and disease conditions. This broader approach is inconsistent with the targeted approach advocated by the Agency for Toxic Substances and Disease Registry and the United States Preventive Services Task Force and the bulk of the peer-reviewed medical literature. Medical monitoring in legal contexts:Numerous medical monitoring actions have been litigated. Legal rationales for allowing medical monitoring claims often incorporate some of the scientific criteria for the appropriateness of monitoring programs. In the majority of cases in which plaintiffs were awarded medical monitoring relief, plaintiffs were required to demonstrate both that the condition for which medical monitoring was sought could be detected early, and that early detection and treatment will improve morbidity and mortality. However, the treatment of medical monitoring claims varies significantly depending upon jurisdiction. Examples of large-scale, comprehensive medical monitoring programs:Large-scale, comprehensive medical monitoring programs have been implemented, such as the Fernald Medical Monitoring Program and the World Trade Center Health Program, both of which exceeded the scope of medical monitoring typically recommended in the peer-reviewed medical literature and the courts. The Fernald program sought to prevent death and disability due to non-exposure-related conditions in a manner similar to general preventive medicine. The World Trade Center Health Program provides comprehensive medical care for World Trade Center responders and may be viewed as a large-scale, federally--funded research effort, which distinguishes it from medical monitoring in a medico-legal context. Synthesis of public health approaches to medical monitoring:Medical monitoring may be indicated following a hazardous exposure in limited circumstances. General causation for a specific adverse health effect must be either established by scientific consensus through a formal causal analysis using a framework such as the Bradford–Hill criteria. The exposure must be characterized and must be of sufficient severity that the exposed population has a significantly elevated risk of an adverse health effect. Monitoring must result in earlier detection of the condition than would otherwise occur and must confer a benefit in the form of primary, secondary or tertiary prevention. Outcome tables may be of use in describing the potential benefits and harms of a proposed monitoring program. Conclusions:In the context of litigation, plaintiffs may seek medical monitoring programs after documented or putative exposures. The role of the clinical toxicologist, in this setting, is to evaluate the scientific justifications and medical risks and assist the courts in determining whether monitoring would be expected to result in a net public health benefit. [ABSTRACT FROM PUBLISHER]

Background Environmental exposures are contributing factors to prostate cancer etiology, but these remain unclear. We aimed to document the associations between environmental risk factors and prostate cancer in Chinese, with special reference to bisphenol A (BPA). Methods We recruited 431 newly diagnosed prostate cancer cases and 402 age-matched controls from Prince of Wales Hospital in Hong Kong. We obtained each participant's clinical data and epidemiological information on chronic BPA exposure and other environmental risk factors (e.g., dietary habits, occupation and shift work) using a standard questionnaire. A new assessment tool of environmental BPA exposure was developed and replicated. Multiple logistic regression analysis was performed to examine odds ratio (OR) and 95% confidence interval (95% CI) for the association of prostate cancer with a novel cumulative BPA exposure index (CBPAI) and other environmental risk factors. Results Weekly consumption of deep fried food (OR = 1.85, 95% CI: 1.15–2.95) and pickled vegetable (OR = 1.87, 95% CI: 1.07–3.28) was significantly associated with excessive prostate cancer risk. Prostate cancer was positively associated with nightshift work (OR = 1.76, 95% CI: 1.07–2.89) and it was negatively associated with green tea drinking (OR = 0.56, 95% CI: 0.34–0.91). There was a positive exposure-response relationship between CBPAI and prostate cancer, with the greatest and significant risk in the high versus reference category (OR = 1.57, 95% CI: 1.01–2.44). Conclusions Frequent consumption of deep fried food and pickled vegetable, non-habitual green tea drinking and nightshift work are the contributing risk factors to prostate cancer in Hong Kong Chinese. More importantly, this study provides the first epidemiological evidence on carcinogenicity of BPA on the human prostate. [ABSTRACT FROM AUTHOR]

Background Environmental chemical exposures have been implicated in pediatric kidney disease. No appraisal of the available evidence has been conducted on this topic. Methods We performed a systematic review of the epidemiologic studies that assessed association of environmental exposures with measures of kidney function and disease in pediatric populations. The search period went through July 2016. Results We found 50 studies that met the search criteria and were included in this systematic review. Environmental exposures reviewed herein included lead, cadmium, mercury, arsenic, fluoride, aflatoxin, melamine, environmental tobacco, bisphenol A, dental procedures, phthalates, ferfluorooctanoic acid, triclosan, and thallium/uranium. Most studies assessed environmental chemical exposure via biomarkers but four studies assessed exposure via proximity to emission source. There was mixed evidence of association between metal exposures, and other non-metal environmental exposures and pediatric kidney disease and other kidney disease biomarkers. The evaluation of causality is hampered by the small numbers of studies for each type of environmental exposure, as well as lack of study quality and limited prospective evidence. Conclusion There is a need for well-designed epidemiologic studies of environmental chemical exposures and kidney disease outcomes. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study has been to assess ambient bisphenol A (BPA) levels in workplaces and urine levels of workers and to establish a BPA database for different populations in Malaysia.Material and Methods: Urine samples were collected from plastic factory workers and from control subjects after their shift. Air samples were collected using gas analyzers from 5 sampling positions in the injection molding unit work area and from ambient air. The level of BPA in airborne and urine samples was quantified by the gas chromatography mass spectrometry - selected ion monitoring (GCMS-SIM) analysis.Results: Bisphenol A was detected in the median range of 8-28.3 ng/m³ and 2.4-3.59 ng/m³ for the 5 sampling points in the plastic molding factory and in the ambient air respectively. The median urinary BPA concentration was significantly higher in the workers (3.81 ng/ml) than in control subjects (0.73 ng/ml). The urinary BPA concentration was significantly associated with airborne BPA levels (ρ = 0.55, p < 0.01).Conclusions: Our findings provide the first evidence that workers in a molding factory in Malaysia are occupationally exposed to BPA. Int J Occup Med Environ Health 2017;30(5):743-750. [ABSTRACT FROM AUTHOR]

Introduction: Arsenic is one of the heavy metals known to be a cause of cancer and many other serious human health problems. The International Agency for Research on Cancer (IARC), has classified arsenic as a Group 1 carcinogen. Studies were performed in different populations to investigate the association between arsenic and breast cancer and the present paper attempts to review these studies.Methods and Materials: Accessible electronic resources including, PubMed, Web of Knowledge, Science Direct and Scopus and Google Scholar were searched, with relevant phrases up to October 30, 2016. All articles were reviewed by two people separately and among them, original epidemiologic studies that investigated the association between breast cancer and exposure to arsenic were included.Results: Eventually seven articles were selected from 126 retrieved articles. Although three studies (one case-control and two ecological) were not able to show a significant affect, others provide some evidence of a relation between arsenic and breast cancer in specific subgroups.Conclusion: Exposure to arsenic may increase the risk of breast cancer. The strength of this relation can vary due to regional and individual differences. [ABSTRACT FROM AUTHOR]

BACKGROUND: Outdoor air pollution has been considered as one of the most serious health concerns over the last decade. This study aimed to investigate the association between ambient air pollution and cardiovascular hospital admissions. METHODS: This investigation was carried out from January 1, 2010 to December 31, 2015, in the urban population of Arak, Iran. Daily records of concentrations of air pollutants including particulate matter less than 10 μm (PM10), nitrogen dioxide (NO2), particulate matter less than 2.5 μm (PM2.5), ozone (O3), carbon monoxide (CO), and sulfur dioxide (SO2) as well as the daily number of hospital admissions due to cardiovascular disease were inquired from the Arak Department of Environment and two major hospitals, respectively. Time-series regression analysis was used to evaluate the effect of the pollutants on cardiovascular hospital admissions with different lag structures, controlling for weather variables, seasonality and long-term time trends, and day of the week. RESULTS: Each 10 μg/m3 increase in PM10 and NO2 and 1 mg/m3 increase in CO concentrations at lag 0 (day) were significantly associated with an increase of 0.7%(P = 0.004), 3.3% (P = 0.006), and 9.4% (P < 0.001), respectively in overall cardiovascular hospital admissions. The elderly were more susceptible than those under 60 years to exposure to the pollutants (especially NO2) with regard to cardiovascular hospital admission. CONCLUSION: The results of this study showed that hospital admission for cardiovascular disease is partly related to the levels of ambient air pollutions in Arak. Susceptibility to air pollutants varies by age groups and sex. [ABSTRACT FROM AUTHOR]

Research on workplace injuries and exposures in ocean safety personnel remains limited. Despite increasing beach attendance and reliance on lifeguards for protection, the most common types of injuries, equipment resulting in injuries, and environmental exposures remains unknown. This study reviewed OSHA 300 logs summarizing workers' compensation claims from 2007–2012 to identify common body parts injured, action at time of injury, equipment causing injury, and environmental exposures. A secondary phase consisted of a cross-sectional anonymous survey to determine demographics, body part injured, equipment causing injury, sun and environmental exposures, action at time of injury, and proportion of injuries reported to the department. During the 6-year period, 304 claims from the OSHA logs were reviewed, finding the lower extremity was most commonly injured with 2921 (31.9%) cumulative lost work days (104 reported injured, 34.2%) followed by the back with 1679 (18.4%) lost work days (39 reported injuries, 12.8%). Of the 304 occupational injury claims from OSHA logs, 108 incidents (35.5%) occurred during rescues, 87 (28.6%) during normal duties, and 31 (10.2%) during training. Of survey participants, 22/52 sustained an injury, with 14 filling a worker's compensation claim. The rescueboard resulted in 7/22 injuries (31.8%) while 17 (32.7%) of respondents sought care for a sun related concern with a mean of 9.3 days lost. Occupational injuries in ocean safety personnel are largely unknown. In this study, lower extremity and back injuries were the most common musculoskeletal injuries providers encountered. Rescues and moving equipment were common actions at the time of injury. With this preliminary information, jurisdictions may develop training directed at rescue techniques and safer options for moving heavy equipment. [ABSTRACT FROM PUBLISHER]

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 disease. [ABSTRACT FROM AUTHOR]

Exposure to environmental stressors, toxicants, and nutrient deficiencies can affect DNA in several ways. Some exposures cause damage and alter the structure of DNA, but there is increasing evidence that the same or other environmental exposures, including those that occur during fetal development in utero, can cause epigenetic effects that modulate DNA function and gene expression. Some epigenetic changes to DNA that affect gene transcription are at least partially reversible (i.e., they can be enzymatically reversed after cessation of exposure to environmental agents), but some epigenetic modifications seem to persist, even for decades. To explain the effects of early life experiences (such as famine and exposures to other stressors) on the long‐term persistence of specific patterns of epigenetic modifications, such as DNA methylation, we propose an analogy with immune memory. We propose that an epigenetic memory can be established and maintained in self‐renewing stem cell compartments. We suggest that the observations on early life effects on adult diseases and the persistence of methylation changes in smokers support our hypothesis, for which a mechanistic basis, however, needs to be further clarified. We outline a new model based on methylation changes. Although these changes seem to be mainly adaptive, they are also implicated in the pathogenesis and onset of diseases, depending on individual genotypic background and types of subsequent exposures. Elucidating the relationships between the adaptive and maladaptive consequences of the epigenetic modifications that result from complex environmental exposures is a major challenge for current and future research in epigenetics.—Vineis, P., Chatziioannou, A., Cunliffe, V. T., Flanagan, J. M., Hanson, M., Kirsch‐Volders, M., Kyrtopoulos, S. Epigenetic memory in response to environmental stressors. FASEB J. 31, 2241–2251 (2017). www.fasebj.org [ABSTRACT FROM AUTHOR]

In France, preterm births concern about 5.5% of pregnancies. Preterm births are associated with increased risk of mortality and morbidity, during either the perinatal period or the later life. Among the possible causes reported in the literature, several intrauterine chemical exposures were reported, especially air pollution, some organochlorine pesticides, lead, and some phthalates. However, the panel of compounds studied remains limited regarding the amount of chemicals that can be found in the environment. [ABSTRACT FROM AUTHOR]

Background Current exposure assessment research does not sufficiently address multi-pollutant exposure and their correlations in human media. Understanding the extent of chemical exposure in reproductive-aged women is of particular concern due to the potential for in utero exposure and fetal susceptibility. Objectives The objectives of this study were to characterize concentrations of chemical biomarkers during preconception and examine correlations between and within chemical classes. Methods We examined concentrations of 135 biomarkers from 16 chemical classes in blood and urine from 73 women aged 18–40 enrolled in Snart Foraeldre/Milieu, a prospective cohort study of pregnancy planners in Denmark (2011–2014). We compared biomarker concentrations with United States similarly-aged, non-pregnant women who participated in the National Health and Nutrition Environmental Survey (NHANES) and with other international biomonitoring studies. We performed principal component analysis to examine biomarker correlations. Results The mean number of biomarkers detected in the population was 92 (range: 60–108). The most commonly detected chemical classes were phthalates, metals, phytoestrogens and polycyclic aromatic hydrocarbons. Except blood mercury, urinary barium and enterolactone, geometric means were higher in women from NHANES. Chemical classes measured in urine generally did not load on a single component, suggesting high between-class correlation among urinary biomarkers, while there is high within-class correlation for biomarkers measured in serum and blood. Conclusions We identified ubiquitous exposure to multiple chemical classes in reproductive-aged Danish women, supporting the need for more research on chemical mixtures during preconception and early pregnancy. Inter- and intra-class correlation between measured biomarkers may reflect common exposure sources, specific lifestyle factors or shared metabolism pathways. [ABSTRACT FROM AUTHOR]

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition with lifelong impacts. Genetic and environmental factors contribute to ASD etiology, which remains incompletely understood. Research on ASD epidemiology has made significant advances in the past decade. Current prevalence is estimated to be at least 1.5% in developed countries, with recent increases primarily among those without comorbid intellectual disability. Genetic studies have identified a number of rare de novo mutations and gained footing in the areas of polygenic risk, epigenetics, and gene-by-environment interaction. Epidemiologic investigations focused on nongenetic factors have established advanced parental age and preterm birth as ASD risk factors, indicated that prenatal exposure to air pollution and short interpregnancy interval are potential risk factors, and suggested the need for further exploration of certain prenatal nutrients, metabolic conditions, and exposure to endocrine-disrupting chemicals. We discuss future challenges and goals for ASD epidemiology as well as public health implications. [ABSTRACT FROM AUTHOR]

Objective: Low to moderate inorganic arsenic (iAs) exposure is independently associated with cardiovascular disease (CVD), particularly for patients with diabetes mellitus (DM). The mechanism of increased CVD risk from iAs exposure in DM has not been adequately characterized. We evaluated whether increasing concentrations of glucose enhance the effects of iAs on platelet and megakaryocyte activity, key steps in atherothrombosis.Methods: Healthy donor whole blood was prepared in a standard fashion and incubated with sodium arsenite in a range from 0 to 10 µM. iAs-induced platelet activation was assessed by platelet receptor CD62P (P-selectin) expression and monocyte-platelet and leukocyte-platelet aggregation (MPA and LPA, respectively) in the presence of increasing sodium arsenite and glucose concentrations. Megakaryocyte (Meg-01) cell adhesion and gene expression was assessed after incubation with or without iAs and increasing concentrations of D-glucose.Results: Platelet activity markers increased significantly with 10 vs. 0 µM iAs (P < 0.05 for all) and with higher D-glucose concentrations. Platelet activity increased significantly following co incubation of 1 and 5 µM iAs concentrations with hyperglycemic D-glucose (P < 0.01 for both) but not after incubation with euglycemic D-glucose. Megakaryocyte adhesion was more pronounced after co incubation with iAs and hyperglycemic than euglycemic D-glucose, while gene expression increased significantly to iAs only after co incubation with hyperglycemic D-glucose.Conclusion: We demonstrate that glucose concentrations common in DM potentiate the effect of inorganic arsenic exposure on markers of platelet and megakaryocyte activity. Our results support recent observational cohort data that DM enhances the vasculotoxic effects of arsenic exposure, and suggest that activation of the platelet-megakaryocyte hemostatic axis is a pathway through which inorganic arsenic confers atherothrombotic risk, particularly for patients with DM. [ABSTRACT FROM AUTHOR]

Objectives: On January 9, 2014, approximately 10000 gallons of a mixture of 4-methylcyclohexanemethanol and propylene glycol phenyl ether spilled into West Virginia's Elk River, contaminating the potable water supply of about 300000 West Virginia residents. This study sought to describe acute health effects after the chemical spill. Methods: We conducted a descriptive analysis using 3 complementary data sources: (1) medical records of patients who visited an emergency department during January 9-23,2014, with illness potentially related to the spill; (2) West Virginia Poison Center caller records coded as "contaminated water" during January 9-23,2014; and (3) answers to household surveys about health effects from a Community Assessment for Public Health Emergency Response (CASPER) questionnaire administered 3 months after the spill. Results: In the 2 weeks after the spill, 2000 people called the poison center reporting exposure to contaminated water, and 369 people visited emergency departments in the affected area with reports of exposure and symptoms potentially related to the spill. According to CASPER weighted cluster analyses, an estimated 25 623 households (21.7%; 95% confidence interval [CI], 14.4%-28.9%) had ≥ 1 person with symptoms who felt that they were related to the spill in the 3 months after it. Reported health effects across all 3 data sources included mild skin, respiratory, and gastrointestinal symptoms that resolved with no or minimal treatment. Conclusions: Medical records, poison center data, and CASPER household surveys were inexact but useful data sources to describe overall community health effects after a large-scale chemical spill. Analyzing multiple data sources could inform epidemiologic investigations of similar events. [ABSTRACT FROM AUTHOR]

The Developmental Origins of Health and Disease (DOHaD) scientific field investigates the influence of early life environmental stressors on later life health outcomes. Environmental chemical exposures are a particular focus area within this field. Although the DOHaD hypothesis originated in the 1990s, the data evaluating this hypothesis in environmental epidemiology has not been comprehensively summarized. We conducted a scoping literature review to describe the human evidence for the DOHaD hypothesis and to identify, 1) where there may be reasonable data to draw conclusions, and 2) areas warranting further research. Using PubMed and Web of Science we identified 425 publications through 2014 that met our criteria for evaluating the DOHaD hypothesis in environmental epidemiology. These publications covered 60 different chemicals. The majority of publications focused on neurological/cognitive outcomes, followed by cancer, and respiratory outcomes. We note areas ready for more detailed review, those requiring more data and ideas for future directions. [ABSTRACT FROM AUTHOR]

In 2013-2015, a consortium of European scientists - NEWDANUBE - was established to prepare a birth cohort in the Danube region, including most of the countries with the highest air pollution in Europe, the area being one-fifth of the European Union's (EU's) territory, including 14 countries (nine EU member states), over 100 million inhabitants, with numerous challenges: big socioeconomic disparities, and a region-specific environmental pollution. The consortium reflects the EU Strategy for the Danube Region Strategy (2010), which identified 11 thematic Priority Areas - one of which is the environmental risks. Birth cohorts have been established in all other areas of Europe and collaborative efforts in promoting maternal and fetal health by minimizing the environmental exposures have been initiated with national, European, and international financial support. A birth cohort in the Danube area could apply the established methodologies for prenatal exposure and birth outcome measurements and establish a platform for targeted health promotion in couples planning pregnancies. The consortium included a strong socioeconomic part focusing on the participant's active registration of exposures to environmental toxicants and health indicators of disease and wellbeing, combined with investigation of their risk-reducing behavior and interventions to change their lifestyle to avoid the adverse health risks. Willingness to pay for reducing the health risks in children is also proposed to be estimated. Further collaboration and networking is encouraged as the Danube region has several decades of experience and expertise in biomonitoring adult populations exposed environmentally or occupationally. Additionally, some countries in the Danube region launched small-scale birth cohorts encouraged by participation in several ongoing research projects. [ABSTRACT FROM AUTHOR]

Rationale: The heterogeneity of asthma phenotypes may explain inconsistencies in observed associations with environmental exposures.Objectives: To identify trajectories of childhood asthma and to characterize the potential impact of residential greenness and air pollution on asthma trajectory subgroups.Methods: Linked administrative databases of medical visits were used to define the occurrence and recurrence of asthma over a 10-year follow-up period within a population-based birth cohort of more than 65,000 children. Group-based trajectory modeling was used to identify unique asthma trajectories. Weighted multinomial regression was used to assess the relationship between asthma trajectories and risk factors, including environmental exposures.Measurements and Main Results: Group-based trajectory modeling distinguished four trajectories: one with no asthma representing 88.8% of the cohort, one with transient asthma (5.6% of the cohort), and two trajectories with chronic asthma with early (<1 yr; 1.5%) and late (<3 yr; 4.1%) onset during early childhood. These trajectories differed with respect to socioeconomic markers and modifiable risk factors, including maternal smoking and breastfeeding initiation. After accounting for sex, parity, breastfeeding, term birth weight, household income, maternal education, delivery mode, and smoking, an interquartile increase in nitrogen dioxide exposure increased the risk of membership in the early and late-onset chronic asthma trajectories, relative to subjects without asthma, by 50% and 20%, respectively (weighted risk ratio, 1.5 and 1.2; 95% confidence interval, 1.2-1.9 and 1.0-1.4). Greenness was not associated with any of the asthma trajectories.Conclusions: Traffic-related air pollution increased the probability of a chronic asthma trajectory. [ABSTRACT FROM AUTHOR]

The field of Developmental Origins of Health and Disease (DOHaD) seeks to understand the relationships between early-life environmental exposures and long-term health and disease. Until recently, the molecular mechanisms underlying these phenomena were poorly understood; however, epigenetics has been proposed to bridge the gap between the environment and phenotype. Epigenetics involves the study of heritable changes in gene expression, which occur without changes to the underlying DNA sequence. Different types of epigenetic modifications include DNA methylation, post-translational histone modifications and non-coding RNAs. Increasingly, changes to the epigenome have been associated with early-life exposures in both humans and animal models, offering both an explanation for how the environment may programme long-term health, as well as molecular changes that could be developed as biomarkers of exposure and/or future disease. As such, epigenetic studies in DOHaD hold much promise; however, there are a number of factors which should be considered when designing and interpreting such studies. These include the impact of the genome on the epigenome, the tissue-specificity of epigenetic marks, the stability (or lack thereof) of epigenetic changes over time and the importance of associating epigenetic changes with changes in transcription or translation to demonstrate functional consequences. In this review, we discuss each of these key concepts and provide practical strategies to mitigate some common pitfalls with the aim of providing a useful guide for future epigenetic studies in DOHaD. [ABSTRACT FROM PUBLISHER]

Intercellular communication has been transformed by the discovery of extracellular vesicles (EVs) and their cargo, including microRNAs (miRNAs), which play crucial roles in intercellular signaling. These EVs were previously disregarded as cellular debris but are now recognized as vital mediators of biological information transfer between cells. Furthermore, they respond not only to internal stimuli but also to environmental and lifestyle factors. Identifying EV-borne oncomiRs, a subset of miRNAs implicated in cancer development, could revolutionize our understanding of how environmental and lifestyle exposures contribute to oncogenesis. To investigate this, we studied the plasma levels of EV-borne oncomiRs in a population of 673 women and 238 men with a body mass index > 25 kg/m 2 (SPHERE population). The top fifty oncomiRs associated with the three most common cancers in women (breast, colorectal, and lung carcinomas) and men (lung, prostate, and colorectal carcinomas) were selected from the OncomiR database. Only oncomiRs expressed in more than 20% of the population were considered for statistical analysis. Using a Multivariate Adaptive Regression Splines (MARS) model, we explored the interactions between environmental/lifestyle exposures and EV oncomiRs to develop optimized predictor combinations for each EV oncomiR. This innovative approach allowed us to better understand miRNA regulation in response to multiple environmental and lifestyle influences. By uncovering non-linear relationships among variables, we gained valuable insights into the complexity of miRNA regulatory networks. Ultimately, this research paves the way for comprehensive exposome studies in the future.

Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

'The clock to type 1 diabetes has started when islet antibodies are first detected', commented George Eisenbarth with regard to the pathogenesis of type 1 diabetes. This review focuses on 'starting the clock', i.e. the initiation of pre-symptomatic islet autoimmunity/the first appearance of islet autoantibodies. In particular, this review addresses why susceptibility to developing islet autoimmunity is greatest in the first 2 years of life and why beta cells are a frequent target of the immune system during this fertile period. A concept for the development of beta cell autoimmunity in childhood is discussed and three factors are highlighted that contribute to this early predisposition: (1) high beta cell activity and potential vulnerability to stress; (2) high rates of and first exposures to infection; and (3) a heightened immune response, with a propensity for T helper type 1 (Th1) immunity. Arguments are presented that beta cell injury, accompanied by activation of an inflammatory immune response, precedes the initiation of autoimmunity. Finally, the implications for strategies aimed at primary prevention for a world without type 1 diabetes are discussed., (© 2023. The Author(s).)

The exposome is the cumulative measure of environmental influences and associated biological responses throughout lifespan, including exposures from the environment, diet, behavior and endogenous processes. Much of the direct interaction of an individual′s exposome involves redox biology as the body responds to environmental, dietary and behavioral risk factors of disease. The present commentary addresses this critical interface and the need for redox biologists to lead development of concepts and strategies to sequence the exposome.

The combined effects of multiple environmental toxicants and social stressor exposures are widely recognized as important public health problems, likely contributing to health inequities. However, US policy makers at state and federal levels typically focus on one stressor exposure at a time and have failed to develop comprehensive strategies to reduce multiple co-occurring exposures, mitigate cumulative risks and prevent harm. This research aimed to move from considering disparate environmental stressors in isolation to mapping the links between environmental, economic, social and health outcomes as a dynamic complex system using children's exposure to neurodevelopmental toxicants as an illustrative example. Such a model can be used to support a broad range of child developmental and environmental health policy stakeholders in improving their understanding of cumulative effects of multiple chemical, physical, biological and social environmental stressors as a complex system through a collaborative learning process. We used system dynamics (SD) group model building to develop a qualitative causal theory linking multiple interacting streams of social stressors and environmental neurotoxicants impacting children's neurodevelopment. A 2 1/2-day interactive system dynamics workshop involving experts across multiple disciplines was convened to develop the model followed by qualitative survey on system insights. The SD causal map covered seven interconnected themes: environmental exposures, social environment, health status, education, employment, housing and advocacy. Potential high leverage intervention points for reducing disparities in children's cumulative neurotoxicant exposures and effects were identified. Workshop participants developed deeper level of understanding about the complexity of cumulative environmental health risks, increased their agreement about underlying causes, and enhanced their capabilities for integrating diverse forms of knowledge about the complex multi-level problem of cumulative chemical and non-chemical exposures. Group model building using SD can lead to important insights to into the sociological, policy, and institutional mechanisms through which disparities in cumulative impacts are transmitted, resisted, and understood. • Children are exposed to multiple chemical and other stressors that are neurotoxic. • Chemical by chemical approach to environmental policy leaves children underprotected • Multiple chemical and nonchemical exposures represent a complex system. • System dynamics (SD) examines complex behaviors of organizational and social systems. • Group model building using SD can better inform policies to protect children's health. [ABSTRACT FROM AUTHOR]

Throughout life individuals are exposed to a large array of diverse environmental exposures (exposome). Hair analyses can assess chronic exposure to a large number of chemicals with less intra-variability than urine and blood. This is essential for studies that aim to achieve a global vision of the exposome. We aimed at characterizing the adult exposome by describing 175 environmental exposures and correlation patterns between and within exposure groups. A subsample of participants of the European Health Examination Survey, covering information on exposure to chemical pollutants in hair samples, were included in the present analysis (N = 442). Concentrations of micronutrients, lifestyle, home environment and socioeconomic information completed the exposome description and were obtained through blood analyses and questionnaires. We detected 29 persistent and non-persistent chemical pollutants in more than 70% of hair samples. Compared to women, men had higher concentrations of pesticides, lower concentrations of micronutrients (with the exception of vitamin A), and presented higher alcohol consumption. Across all exposures, a low median absolute correlation was found, 0.05 (5th − 95th centiles = 0.10, 0.20). We observed higher correlations and median correlations within exposure groups than between groups of exposure. The highest median correlation was observed between plasticizers (bisphenol A and S) in both men (0.50) and women (0.31). A 70% and 95% of cumulative variance was explained by 37 and 73 principal components respectively. We found a wide range of chemical exposures in hair samples of men and women. The adult exposome was complex and multidimensional. Future exposome studies should include hair as a matrix for characterizing exposure to multiple environmental chemicals. [ABSTRACT FROM AUTHOR]

The exposome is the cumulative measure of environmental influences and associated biological responses throughout the lifespan, including those from the environment, diet, behaviour, and endogenous processes. The exposome concept and the 2030 Agenda for the Sustainable Development Goals (SDGs) from the United Nations are the basis for understanding the aetiology and consequences of non-communicable diseases, including gestational diabetes mellitus (GDM). Pregnancy may be developed in an environment with adverse factors part of the immediate internal medium for fetus development and the external medium to which the pregnant woman is exposed. The placenta is the interface between maternal and fetal compartments and acts as a protective barrier or easing agent to transfer exposome from mother to fetus. Under and over-nutrition in utero, exposure to adverse environmental pollutants such as heavy metals, endocrine-disrupting chemicals, pesticides, drugs, pharmaceuticals, lifestyle, air pollutants, and tobacco smoke plays a determinant role in the development of GDM. This phenomenon is worsened by metabolic stress postnatally, such as obesity which increases the risk of GDM and other diseases. Clinical risk factors for GDM development include its aetiology. It is proposed that knowledge-based interventions to change the potential interdependent ecto -exposome and endo -exposome could avoid the occurrence and consequences of GDM. • Pregnancy may develop under permanent exposure to an adverse exposome. • Endo- and ecto-exposome increase the risk of gestational diabetes mellitus (GDM). • Exposome factors contribute to fetoplacental endothelial dysfunction in GDM. • Knowledge-based interventions could avoid GDM occurrence and consequences. [ABSTRACT FROM AUTHOR]

Interest is growing in neighborhood effects on health beyond individual's home locations. However, few studies accounted for selective daily mobility bias. Selective mobility of 470 older adults (aged 67-94) living in urban and suburban areas of Luxembourg, was measured through detour percentage between their observed GPS-based paths and their shortest paths. Multilevel negative binomial regression tested associations between detour percentage, trips characteristics and environmental exposures. Detour percentage was higher for walking trips (28%) than car trips (16%). Low-speed areas and connectivity differences between observed and shortest paths vary by transport mode, indicating a potential selective daily mobility bias. The positive effects of amenities, street connectivity, low-speed areas and greenness on walking detour reinforce the existing evidence on older adults' active transportation. Urban planning interventions favoring active transportation will also promote walking trips with longer detours, helping older adults to increase their physical activity levels and ultimately promote healthy aging. • Among older adults, walkers compared to car drivers make higher detour percentage. • Environmental characteristics of observed vs. shortest path vary by transport mode. • Walkers seek walking-friendly areas with more street connectivity and low-speed areas. • More access to greenness and amenities entices older adults to make longer detour. [ABSTRACT FROM AUTHOR]

Environmental exposures are implicated in diabetes etiology, but are poorly understood due to disease heterogeneity, complexity of exposures, and analytical challenges. Machine learning and data mining are artificial intelligence methods that can address these limitations. Despite their increasing adoption in etiology and prediction of diabetes research, the types of methods and exposures analyzed have not been thoroughly reviewed. We aimed to review articles that implemented machine learning and data mining methods to understand environmental exposures in diabetes etiology and disease prediction. We queried PubMed and Scopus databases for machine learning and data mining studies that used environmental exposures to understand diabetes etiology on September 19th, 2022. Exposures were classified into specific external, general external, or internal exposures. We reviewed machine learning and data mining methods and characterized the scope of environmental exposures studied in the etiology of general diabetes, type 1 diabetes, type 2 diabetes, and other types of diabetes. We identified 44 articles for inclusion. Specific external exposures were the most common exposures studied, and supervised models were the most common methods used. Well-established specific external exposures of low physical activity, high cholesterol, and high triglycerides were predictive of general diabetes, type 2 diabetes, and prediabetes, while novel metabolic and gut microbiome biomarkers were implicated in type 1 diabetes. The use of machine learning and data mining methods to elucidate environmental triggers of diabetes was largely limited to well-established risk factors identified using easily explainable and interpretable models. Future studies should seek to leverage machine learning and data mining to explore the temporality and co-occurrence of multiple exposures and further evaluate the role of general external and internal exposures in diabetes etiology. • AI is poised to elucidate complex environmental exposures in diabetes etiology. • Current approaches were limited to well-established risk factors using traditional models. • Future work should leverage AI's full potential while maintaining explainability. • Studies exploring temporality, sequences & co-occurrence of environmental exposures are needed. [ABSTRACT FROM AUTHOR]

Background: Lung cancer remains a major health problem world-wide. Environmental exposure to lung cancer carcinogens can affect lung cancer incidence. We investigated the association between lung cancer incidence and an air toxics hazard score of environmental carcinogen exposures derived previously under the exposome concept., Methods: Lung cancer cases diagnosed in Philadelphia and the surrounding counties between 2008 and 2017 were identified from the Pennsylvania Cancer Registry. Age-adjusted incidence rates at the ZIP code level were calculated based on the residential address at diagnosis. The air toxics hazard score, an aggregate measure for lung cancer carcinogen exposures, was derived using the criteria of toxicity, persistence, and occurrence. Areas with high incidence or hazard score were identified. Spatial autoregressive models were fitted to evaluate the association, with and without adjusting for confounders. Stratified analysis by smoking prevalence was performed to examine potential interactions., Results: We observed significantly higher age-adjusted incidence rates in ZIP codes that had higher air toxics hazard score values after controlling for demographic variables, smoking prevalence, and proximity to major highways. Analyzes stratified by smoking prevalence suggested that exposure to environmental lung carcinogens had a larger effect on cancer incidence in locations with higher smoking prevalence., Conclusion: The positive association between the multi-criteria derived air toxics hazard score and lung cancer incidence provides the initial evidence to validate the hazard score as an aggregate measure of carcinogenic exposures in the environment. The hazard score can be used to supplement the existing risk factors in identifying high risk individuals. Communities with higher incidence/hazard score may benefit from greater awareness of lung cancer risk factors and targeted screening programs., Competing Interests: AV reports personal fees as a scientific advisor to the Lung Cancer Initiative at Johnson & Johnson and grants to his institution from MagArray, Inc. and Precyte, Inc. outside of the submitted work. AV is an advisory board member of the Lungevity Foundation (unpaid). The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Zhu, McWilliams, McKeon, Vachani, Penning and Hwang.)