Search

Low birthweight and reduced height gain during infancy (stunting) may arise at least in part from adverse early life environments that trigger epigenetic reprogramming that may favor survival. We examined differential DNA methylation patterns using targeted methyl sequencing of regions regulating gene activity in groups of rural Gambian infants: (a) low and high birthweight (DNA from cord blood (n = 16 and n = 20, respectively), from placental trophoblast tissue (n = 21 and n = 20, respectively), and DNA from peripheral blood collected from infants at 12 months of age (n = 23 and n = 17, respectively)), and, (b) the top 10% showing rapid postnatal length gain (high, n = 20) and the bottom 10% showing slow postnatal length gain (low, n = 20) based on z score change between birth and 12 months of age (LAZ) (DNA from peripheral blood collected from infants at 12 months of age). Using BiSeq analysis to identify significant methylation marks, for birthweight, four differentially methylated regions (DMRs) were identified in trophoblast DNA, compared to 68 DMRs in cord blood DNA, and 54 DMRs in 12‐month peripheral blood DNA. Twenty‐five DMRs were observed to be associated with high and low length for age (LAZ) at 12 months. With the exception of five loci (associated with two different genes), there was no overlap between these groups of methylation marks. Of the 194 CpG methylation marks contained within DMRs, 106 were located to defined gene regulatory elements (promoters, CTCF‐binding sites, transcription factor‐binding sites, and enhancers), 58 to gene bodies (introns or exons), and 30 to intergenic DNA. Distinct methylation patterns associated with birthweight between comparison groups were observed in DNA collected at birth (at the end of intrauterine growth window) compared to those established by 12 months (near the infancy/childhood growth transition). The longitudinal differences in methylation patterns may arise from methylation adjustments, changes in cellular composition of blood or both that continue during the critical postnatal growth period, and in response to early nutritional and infectious environmental exposures with impacts on growth and longer‐term health outcomes. [ABSTRACT FROM AUTHOR]

The goal of this article is to consider data solutions to investigate the differential pathways that connect climate/weather variability to child health outcomes. We apply several measures capturing different aspects of climate/weather variability to different time periods of in utero exposure. The measures are designed to capture the complexities of climate-related risks and isolate their impacts based on the timing and duration of exposure. Specifically, we focus on infant birth weight in Mali and consider local weather and environmental conditions associated with the three most frequently posited potential drivers of adverse health outcomes: disease (malaria), heat stress, and food insecurity. We focus this study on Mali, where seasonal trends facilitate the use of measures specifically designed to capture distinct aspects of climate/weather conditions relevant to the potential drivers. Results indicate that attention to the timing of exposures and employing measures designed to capture nuances in each of the drivers provides important insight into climate and birth weight outcomes, especially in the case of factors impacted by precipitation. Results also indicate that high temperatures and low levels of agricultural production are consistently associated with lower birth weights, and exposure to malarious conditions may increase likelihood of nonlive birth outcomes. [ABSTRACT FROM AUTHOR]

Background: Changing environmental factors are likely responsible for the rising prevalence of allergic diseases in children. However, whether environmental exposures induce allergen sensitizations, and which allergen sensitization is related to the development of allergic diseases, is not clear. The study is aimed to investigate the association between environmental exposure, allergen sensitization, and the development of allergic diseases for further preventive intervention. Methods: We conducted the Taiwan Childhood Environment and Allergic diseases Study (TCEAS) in kindergarten children in Taiwan. Skin prick tests for 6 allergens were performed. Information on the development of allergic diseases and environmental exposure was collected using standardized questionnaires. Multiple logistic regressions were used to estimate the association between environmental factors, allergen sensitization, and the development of allergic diseases. Results: A total of 3192 children were recruited. 485 (15.2%) children had atopic dermatitis (AD), 1126 (35.3%) had allergic rhinitis (AR), and 552 (17.3%) had asthma. Children with environmental tobacco smoke exposure and fungi on the house wall had a higher risk of asthma, with ORs (95% CIs) of 1.25 (1.03–1.52) and 1.22 (1.01–1.47), respectively. The mite sensitization rate was found to be the highest. Mite sensitization was associated with significant increases in the risks of AD, AR, and asthma, with ORs (95% CIs) of 2.15 (1.53–3.03), 1.94 (1.46–2.58), and 2.31 (1.63–3.29), respectively. Cockroach sensitization also increased the risk of asthma, with an OR (95% CI) of 2.38 (1.01–5.61). Mite sensitization was associated with carpet in the home and fungi on the house wall, and milk sensitization was associated with breastfeeding duration. Conclusion: Environmental exposures play a role in the development of allergic diseases. Allergen sensitizations were associated with certain environmental exposures. Early environmental interventions are urgently needed to prevent the development of childhood allergic diseases.

The Integrated Clinical and Environmental Exposures Service (ICEES) provides regulatory-compliant open access to sensitive patient data that have been integrated with public exposures data. ICEES was designed initially to support dynamic cohort creation and bivariate contingency tests. The objective of the present study was to develop an open approach to support multivariate analyses using existing ICEES functionalities and abiding by all regulatory constraints. We first developed an open approach for generating a multivariate table that maintains contingencies between clinical and environmental variables using programmatic calls to the open ICEES application programming interface. We then applied the approach to data on a large cohort (N = 22,365) of patients with asthma or related conditions and generated an eight-feature table. Due to regulatory constraints, data loss was incurred with the incorporation of each successive feature variable, from a starting sample size of N = 22,365 to a final sample size of N = 4,556 (20.4%), but data loss was < 10% until the addition of the final two feature variables. We then applied a generalized linear model to the subsequent dataset and focused on the impact of seven select feature variables on asthma exacerbations, defined as annual emergency department or inpatient visits for respiratory issues. We identified five feature variables—sex, race, obesity, prednisone, and airborne particulate exposure—as significant predictors of asthma exacerbations. We discuss the advantages and disadvantages of ICEES open multivariate analysis and conclude that, despite limitations, ICEES can provide a valuable resource for open multivariate analysis and can serve as an exemplar for regulatory-compliant informatic solutions to open patient data, with capabilities to explore the impact of environmental exposures on health outcomes.

Determining the etiologic basis of the mutations that are responsible for cancer is one of the fundamental challenges in modern cancer research. Different mutational processes induce different types of DNA mutations, providing ‘mutational signatures’ that have led to key insights into cancer etiology. The most widely used signatures for assessing genomic data are based on unsupervised patterns that are then retrospectively correlated with certain features of cancer. We show here that supervised machine-learning techniques can identify signatures, called SuperSigs, that are more predictive than those currently available. Surprisingly, we found that aging yields different SuperSigs in different tissues, and the same is true for environmental exposures. We were able to discover SuperSigs associated with obesity, the most important lifestyle factor contributing to cancer in Western populations.

Epigenetic information is transmitted from one generation to the next, modulating the phenotype of offspring non-genetically in organisms ranging from plants to mammals. For intergenerational non-genetic inheritance to occur, epigenetic information must accumulate in germ cells. The three main carriers of epigenetic information—histone post-translational modifications, DNA modifications, and RNAs—all exhibit dynamic patterns of regulation during germ cell development. For example, histone modifications and DNA methylation are extensively reprogrammed and often eliminated during germ cell maturation and after fertilization during embryogenesis. Consequently, much attention has been given to RNAs, specifically small regulatory RNAs, as carriers of inherited epigenetic information. In this review, we discuss examples in which microRNAs have been implicated as key players in transmitting paternal epigenetic information intergenerationally.

BackgroundHousehold pesticide use is widespread in the USA. Since the 1970s, organophosphorus chemicals (OPs) have been common active ingredients in these products. Parkinson's disease (PD) has been linked to pesticide exposures but little is known about the contributions of chronic exposures to household pesticides. Here we investigate whether long-term use of household pesticides, especially those containing OPs, increases the odds of PD.MethodsIn a population-based case-control study, we assessed frequency of household pesticide use for 357 cases and 807 controls, relying on the California Department of Pesticide Regulation product label database to identify ingredients in reported household pesticide products and the Pesticide Action Network pesticide database of chemical ingredients. Using logistic regression we estimated the effects of household pesticide use.ResultsFrequent use of any household pesticide increased the odds of PD by 47% [odds ratio (OR)=1.47, (95% confidence interval (CI): 1.13, 1.92)]; frequent use of products containing OPs increased the odds of PD more strongly by 71% [OR=1.71, (95% CI: 1.21, 2.41)] and frequent organothiophosphate use almost doubled the odds of PD. Sensitivity analyses showed that estimated effects were independent of other pesticide exposures (ambient and occupational) and the largest odds ratios were estimated for frequent OP users who were carriers of the 192QQ paraoxonase genetic variant related to slower detoxification of OPs.ConclusionsWe provide evidence that household use of OP pesticides is associated with an increased risk of developing PD.

BackgroundThere is interest in using residential dust to estimate human exposure to environmental contaminants.ObjectivesWe aimed to characterize the sources of variability for polycyclic aromatic hydrocarbons (PAHs) in residential dust and provide guidance for investigators who plan to use residential dust to assess exposure to PAHs.MethodsWe collected repeat dust samples from 293 households in the Northern California Childhood Leukemia Study during two sampling rounds (from 2001 through 2007 and during 2010) using household vacuum cleaners, and measured 12 PAHs using gas chromatography-mass spectrometry. We used a random- and a mixed-effects model for each PAH to apportion observed variance into four components and to identify sources of variability.ResultsMedian concentrations for individual PAHs ranged from 10 to 190 ng/g of dust. For each PAH, total variance was apportioned into regional variability (1-9%), intraregional between-household variability (24-48%), within-household variability over time (41-57%), and within-sample analytical variability (2-33%). Regional differences in PAH dust levels were associated with estimated ambient air concentrations of PAH. Intraregional differences between households were associated with the residential construction date and the smoking habits of residents. For some PAHs, a decreasing time trend explained a modest fraction of the within-household variability; however, most of the within-household variability was unaccounted for by our mixed-effects models. Within-household differences between sampling rounds were largest when the interval between dust sample collections was at least 6 years in duration.ConclusionsOur findings indicate that it may be feasible to use residential dust for retrospective assessment of PAH exposures in studies of health effects.

Nongenetic, environmental factors contribute to maternal morbidity and mortality through chemical exposures via air, water, soil, food, and consumer products. Pregnancy represents a particularly sensitive window of susceptibility during which physiological changes to every major organ system increase sensitivity to chemicals that can impact a woman's long-term health. Nonchemical stressors, such as low socioeconomic status, may exacerbate the effects of chemical exposures on maternal health. Racial/ethnic minorities are exposed disproportionately to both chemicals and nonchemical stressors, which likely contribute to the observed health disparities for maternal morbidities and mortality. Epidemiological studies linking exposures to adverse maternal health outcomes underscore the importance of environmental health impacts, and mechanistic studies in model systems reveal how chemicals perturb biological pathways and processes. Environmental stressors are associated with a variety of immediate maternal health impacts, including hypertensive disorders of pregnancy, fibroids, and infertility, as well as long-term maternal health impacts, such as higher risk of breast cancer and metabolic disorders. Identifying and reducing a pregnant woman's environmental exposures is not only beneficial to her offspring but also important to preserve her short- and long-term health. [ABSTRACT FROM AUTHOR]

Although Crohn's disease (CD) and ulcerative colitis (UC) have been considered as disorders that affect individuals of European ancestry, the epidemiology of the inflammatory bowel diseases (IBDs) is changing. Coupled with the increasing incidence of IBD in previously low-incidence areas, the population demographics of IBD in the United States are also changing, with increases among non-White races and ethnicities. It is therefore important to fully understand the epidemiology and progression of IBD in different racial and ethnic groups, and the effects of race and ethnicity on access to care, use of resources, and disease-related outcomes. We review differences in IBD development and progression among patients of different races and ethnicities, discussing the effects of factors such as access to care, delays in diagnosis, and health and disease perception on disparities in IBD care and outcomes. We identify research priorities for improving health equity among minority patients with IBD. [ABSTRACT FROM AUTHOR]

Historical functional linear models (HFLMs) quantify associations between a functional predictor and functional outcome where the predictor is an exposure variable that occurs before, or at least concurrently with, the outcome. Prior work on the HFLM has largely focused on estimation of a surface that represents a time-varying association between the functional outcome and the functional exposure. This existing work has employed frequentist and spline-based estimation methods, with little attention paid to formal inference or adjustment for multiple testing and no approaches that implement wavelet bases. In this work, we propose a new functional regression model that estimates the time-varying, lagged association between a functional outcome and a functional exposure. Building off of recently developed function-on-function regression methods, the model employs a novel use the wavelet-packet decomposition of the exposure and outcome functions that allows us to strictly enforce the temporal ordering of exposure and outcome, which is not possible with existing wavelet-based functional models. Using a fully Bayesian approach, we conduct formal inference on the time-varying lagged association, while adjusting for multiple testing. We investigate the operating characteristics of our wavelet-packet HFLM and compare them to those of two existing estimation procedures in simulation. We also assess several inference techniques and use the model to analyze data on the impact of lagged exposure to particulate matter finer than 2.5 μ g, or PM 2.5 , on heart rate variability in a cohort of journeyman boilermakers during the morning of a typical day’s shift. [ABSTRACT FROM AUTHOR]

Copyright of Ankara Review of European Studies (ARES) / Ankara Avrupa Çalışmaları Dergisi (AAÇD) is the property of Ankara University European Union Research Centre and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Air pollution and noise exposure may synergistically contribute to increased cardiometabolic disorders; however, few studies have examined this potential interaction nor considered exposures beyond residential location. This study investigates the combined impact of dynamic air pollution and transportation noise on cardiometabolic disorders in San Diego County. Using the Community of Mine Study (2014-2017), 602 ethnically diverse participants were assessed for obesity, dyslipidemia, hypertension, and metabolic syndrome (MetS) using anthropometric measurements and biomarkers from blood samples. Time-weighted measures of exposure to PM2.5, NO2, road and aircraft noise were calculated using global positioning system (GPS) mobility data and Kernel Density Estimation. Generalized estimating equation models were used to analyze associations. Interactions were assessed on the multiplicative and additive scales using relative excess risk due to interaction (RERI). We found that air pollution and noise interact to affect metabolic disorders on both multiplicative and additive scales. The effect of noise on obesity and MetS was higher when air pollution was higher. The RERI of aircraft noise and NO2 on obesity and MetS were 0.13 (95%CI 0.03, 0.22) and 0.13 (95%CI 0.02, 0.25), respectively. This finding suggests that aircraft noise and air pollution may have synergistic effects on obesity and MetS., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health.)

Background: Maternal nutrient intake may moderate associations between environmental exposures and children's neurodevelopmental outcomes, but few studies have assessed joint effects. We aimed to evaluate whether prenatal nutrient intake influences the association between air pollutants and autism-related trait scores., Methods: We included 126 participants from the EARLI (Early Autism Risk Longitudinal Investigation, 2009-2012) cohort, which followed US pregnant mothers who previously had a child with autism. Bayesian kernel machine regression and traditional regression models were used to examine joint associations of prenatal nutrient intake (vitamins D, B12, and B6; folate, choline, and betaine; and total omega 3 and 6 polyunsaturated fatty acids, reported via food frequency questionnaire), air pollutant exposure (particulate matter <2.5 μm [PM 2.5 ], nitrogen dioxide [NO 2 ], and ozone [O 3 ], estimated at the address level), and children's autism-related traits (measured by the Social Responsiveness Scale [SRS] at 36 months)., Results: Most participants had nutrient intakes and air pollutant exposures that met US standards. Bayesian kernel machine regression mixture models and traditional regression models provided little evidence of individual or joint associations of nutrients and air pollutants with SRS scores or of an association between the overall mixture and SRS scores., Conclusion: In this cohort with a high familial likelihood of autism, we did not observe evidence of joint associations between air pollution exposures and nutrient intake with autism-related traits. Future work should examine the use of these methods in larger, more diverse samples, as our results may have been influenced by familial liability and/or relatively high nutrient intakes and low air pollutant exposures., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2024 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)

This study aims to evaluate the association between social determinants, environmental exposure metrics, and the risk of asthma emergency department (ED) visits in the New York State (NYS) Medicaid population using small-area analysis. Traffic densities for each census tract in NYS were calculated using the length of road segments within each tract and total area of the tract to produce a measure of average number of vehicles per square meter per day. Data on social determinants of health including internal and external environments and other demographic factors were obtained from various sources. Poisson regression analyses were conducted to identify significant factors associated with asthma ED visits in Medicaid claim and encounter data for years 2005-2015. High traffic density in NYS excluding New York City (NYC) correlated with increased risk of asthma ED visits (RR 1.69; 95% CI: 1.42, 2.00), mitigated by adjusting for environmental and social determinants (RR 1.00; 95% CI: 0.85, 1.19). Similar trends were observed in NYC only (RR 1.19; 95% CI: 1.00, 1.41), with the adjusted risk remaining elevated (RR 1.14; 95% CI: 0.98, 1.33) albeit not statistically significant. Living in census tracts with high concentrated disadvantage index, high proportions of minorities, and less green space predicted higher asthma ED visits. We mapped predicted rates and model residuals to identify areas of high risk. Our results support previous findings that environmental and social risk factors in poor and urban areas contribute to asthma exacerbations in the NYS Medicaid population, even if they may not necessarily contribute to its development., Competing Interests: The authors have declared no conflicts of interest., (© 2024 The Authors.)

BackgroundExposure to chemicals during fetal development can increase the risk of adverse health effects, and while biomonitoring studies suggest pregnant women are exposed to chemicals, little is known about the extent of multiple chemicals exposures among pregnant women in the United States.ObjectiveWe analyzed biomonitoring data from the National Health and Nutritional Examination Survey (NHANES) to characterize both individual and multiple chemical exposures in U.S. pregnant women.MethodsWe analyzed data for 163 chemical analytes in 12 chemical classes for subsamples of 268 pregnant women from NHANES 2003-2004, a nationally representative sample of the U.S. population. For each chemical analyte, we calculated descriptive statistics. We calculated the number of chemicals detected within the following chemical classes: polybrominated diphenyl ethers (PBDEs), perfluorinated compounds (PFCs), organochlorine pesticides, and phthalates and across multiple chemical classes. We compared chemical analyte concentrations for pregnant and nonpregnant women using least-squares geometric means, adjusting for demographic and physiological covariates.ResultsThe percentage of pregnant women with detectable levels of an individual chemical ranged from 0 to 100%. Certain polychlorinated biphenyls, organochlorine pesticides, PFCs, phenols, PBDEs, phthalates, polycyclic aromatic hydrocarbons, and perchlorate were detected in 99-100% of pregnant women. The median number of detected chemicals by chemical class ranged from 4 of 12 PFCs to 9 of 13 phthalates. Across chemical classes, median number ranged from 8 of 17 chemical analytes to 50 of 71 chemical analytes. We found, generally, that levels in pregnant women were similar to or lower than levels in nonpregnant women; adjustment for covariates tended to increase levels in pregnant women compared with nonpregnant women.ConclusionsPregnant women in the U.S. are exposed to multiple chemicals. Further efforts are warranted to understand sources of exposure and implications for policy making.

Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) represents a heterogeneous group of rare diseases characterised by necrotising inflammation of the small blood vessels and the presence of ANCA with specificity for proteinase-3 or myeloperoxidase. Genetic susceptibility along with malignancy, drug exposure, and environmental exposures to infectious agents and silica are involved in disease progression. To date, growing evidence has revealed that ANCA specificity defines homogeneous groups of patients more effectively than clinical diagnosis, since proteinase-3 ANCA and myeloperoxidase-ANCA are linked with different genetic backgrounds and epidemiologies. This review presents current and updated knowledge on the central aetiopathogenic role of genetic associations and environmental exposures in AAV; discusses the main mechanisms of ANCA immunogenesis; and highlights the value of ANCA specificity for future classification criteria.

Abstract Background Increasing evidence suggests that welding fume exposure is associated with systemic inflammation. Although celluar metabolites may be associated with inflammation, there is limited information on metabolomic changes during welding fume exposure. Such changes may play an important role in the occurrence, development, and prevention of metal-associated diseases. We aim to investigate human metabolomics changes pre- and post-welding fume exposure. Methods This study included 52 boilermakers totally. We collected plasma samples pre- and post-shift welding fume exposure and prepared samples using the automated MicroLab STAR® system. Metabolite concentrations were measured using ultra performance liquid chromatography - tandem mass spectrometer (UPLC-MS/MS) methods. Two-way analysis of variance was used to test the significance of metabolite changes with false discovery rate correction. Results Analysis detected several metabolic changes after welding fume exposure, mainly involved in the lipid pathway [glucocorticoid class (cortisol, corticosterone, and cortisone), acylcarnitine class, and DiHOME species (9,10-DiHOME and 12,13-DiHOME)], amino acid utilization (isoleucine, proline and phenylalanine), and S-(3-hydroxypropyl) mercapturic acid (3-HPMA). These compounds are all associated with inflammation according to previous studies. Further, additive interaction effects linked smoking and 3-HPMA levels. In the metabolite set enrichment analysis for diseases, the top two disease-associated metabolite pathways were systemic inflammation-related diseases including rheumatoid arthritis and systemic lupus erythematosus. Conclusions This global metabolomics study shows evidence that metabolite changes during welding fume exposure are closely associated with systemic inflammation. The altered metabolites detected may be potential health monitoring biomarkers for boilermakers, especially for inflammation-related disease prevention.

Some of the recent publications have reported a decline in semen quality in the last few decades. This phenomenon is associated with environmental factors, particularly with exposure to endocrine disrupting chemicals (EDCs). The aim of this publication is to critically review the literature on exposure to the following 6 ubiquitous environmental non-persistent EDCs: bisphenol A, triclosan, parabens, synthetic pyrethroids, organophosphate pesticides and phthalates, and on their influence on semen quality measured as sperm concentration, sperm volume, total sperm count, motility, total motile count, morphology, sperm motion, sperm DNA damage (comet extent, tail length, tail distributed moment, percent of DNA located in the tail (tail%), DNA fragmentation index, high DNA stainability, X:Y ratio and aneuploidy. Several electronic databases were systematically searched until 31 August 2016. Studies were qualified for the review if they: linked environmental exposure to non-persistent EDCs to semen quality outcomes, were published in English after 2006 (and, in the case of phthalates, if they were published after 2009) and were conducted in the case of humans. Out of the 970 references, 45 articles were included in the review. This review adds to the body of evidence that exposure to non-persistent EDCs may affect semen quality parameters and decrease semen quality. Int J Occup Med Environ Health 2018;31(4):377–414

Abstract Background Growing evidence demonstrates that exposure to organophosphate flame retardants (PFRs) is widespread and that these chemicals can alter thyroid hormone regulation and function. We investigated the relationship between PFR exposure and thyroid cancer and whether individual or temporal factors predict PFR exposure. Methods We analyzed interview data and spot urine samples collected in 2010–2013 from 100 incident female, papillary thyroid cancer cases and 100 female controls of a Connecticut-based thyroid cancer case-control study. We measured urinary concentrations of six PFR metabolites with mass spectrometry. We estimated odds ratios (OR) and 95% confidence intervals (95% CI) for continuous and categories (low, medium, high) of concentrations of individual and summed metabolites, adjusting for potential confounders. We examined relationships between concentrations of PFR metabolites and individual characteristics (age, smoking status, alcohol consumption, body mass index [BMI], income, education) and temporal factors (season, year) using multiple linear regression analysis. Results No PFRs were significantly associated with papillary thyroid cancer risk. Results remained null when stratified by microcarcinomas (tumor diameter ≤ 1 cm) and larger tumor sizes (> 1 cm). We observed higher urinary PFR concentrations with increasing BMI and in the summer season. Conclusions Urinary PFR concentrations, measured at time of diagnosis, are not linked to increased risk of thyroid cancer. Investigations in a larger population or with repeated pre-diagnosis urinary biomarker measurements would provide additional insights into the relationship between PFR exposure and thyroid cancer risk.

Abstract Background Triclosan is an antimicrobial agent that may affect the gut microbiome and endocrine system to influence adiposity. However, little data from prospective studies examining prenatal and childhood exposures exist. We investigated the relationship between multiple, prospective early life measure of triclosan exposure and child adiposity. Methods In a prospective cohort of 220 mother-child pairs from Cincinnati, OH (enrolled 2003–2006), we quantified triclosan in urine samples collected twice during pregnancy, annually from 1 to 5 years of age, and once at 8 years. We assessed child adiposity at age 8 years using body mass index (BMI), waist circumference, and bioelectric impedance. We estimated covariate-adjusted associations of child adiposity with a 10-fold increase in average prenatal, average early childhood (average of 1–5 years), and 8-year triclosan concentrations. Results Among all children, there was no association between triclosan and child adiposity. While urinary triclosan concentrations at all three time periods were weakly, imprecisely, and inversely associated with all three measures of adiposity among girls, these associations did not differ significantly from those in boys (sex x triclosan p-values> 0.35). Among girls, the strongest associations were generally observed for prenatal triclosan when we adjusted for all three triclosan concentrations and covariates in the same model; BMI z-score (β: -0.13; 95% CI: -0.42, 0.15), waist circumference (β: − 1.7 cm; 95% CI: -4.2, 0.7), and percent body fat (β :-0.6; 95% CI: -2.7, 1.3). In contrast, the associations between triclosan concentrations and adiposity measures were inconsistent among boys. Conclusion We did not observe evidence of an association of repeated urinary triclosan concentrations during pregnancy and childhood with measures of child adiposity at age 8 years in this cohort.

Abstract Background The developing fetus is susceptible to environmental insults. Studying the effects of environmental exposures on fetal growth is essential for understanding the causal pathway between prenatal exposures and pregnancy outcomes. Here we describe the Haifa Pregnancy Cohort Study (HPCS) and discuss challenges and opportunities in applying “big data” paradigm. Methods Maccabi Healthcare Services (MHS), is the second largest Israeli health maintenance organization (HMO) providing care services to two million beneficiaries. The HPCS cohort potentially includes ~750,000 newborns born between 1998 and 2017. We will estimate daily exposures to air pollutants, temperature and greenness, using satellite-based data and models. We hypothesize that residents of Haifa have higher exposures to environmental pollutants and that in pregnant women this higher exposure is associated with poorer fetal growth. We will evaluate outcomes such as birth-weight, head-circumference and gestational age at birth. We will adjust for pregnancy complications such as pre-eclampsia and gestational diabetes and parental variables, such as maternal weight, age and smoking habits as potential confounders. In addition, we will conduct a multi-tiered field study, nested within this population, among 150 pregnant women residing in two geographical regions-one in the polluted Haifa area, and one in a relatively unpolluted area in central Israel. Blood and urinary samples will be collected, as well as personal and indoor exposure to air pollution. Discussion Evaluating environmental exposures of pregnant women and assessing in utero growth over the course of the pregnancy during different exposure windows, is of great scientific and public health interest. Recent advances in data collection and analysis pose great promise to provide insights into contribution of environment to the health of the developing fetus, but also pose major challenges and pitfalls, such as data management, proper statistical framework and integration of data in the population-based study and selectiveness in the nested field study. Yet the continuing follow-up of the study cohort, integrating data from different services, health-promotion, and eventually, application later in real life of our main promises. Our study aims to meet these challenges and to provide evidence of the environmental exposures associated with fetal growth.

Inorganic arsenic (iAs/As2O32−) is an environmental toxicant found in watersheds around the world including in densely populated areas. iAs is a class I carcinogen known to target the skin, lungs, bladder, and digestive organs, but its role as a primary breast carcinogen remains controversial. Here, we examined a different possibility: that exposure to iAs promotes the transition of well‐differentiated epithelial breast cancer cells characterized by estrogen and progesterone receptor expression (ER+/PR+), to more basal phenotypes characterized by active proliferation, and propensity to metastasis in vivo. Our results indicate two clear phenotypic responses to low‐level iAs that depend on the duration of the exposure. Short‐term pulses of iAs activate ER signaling, consistent with its reported pseudo‐estrogen activity, but longer‐term, chronic treatments for over 6 months suppresses both ER and PR expression and signaling. In fact, washout of these chronically exposed cells for up to 1 month failed to fully reverse the transcriptional and phenotypic effects of prolonged treatments, indicating durable changes in cellular physiologic identity. RNA‐seq studies found that chronic iAs drives the transition toward more basal phenotypes characterized by impaired hormone receptor signaling despite the conservation of estrogen receptor expression. Because treatments for breast cancer patients are largely designed based on the detection of hormone receptor expression, our results suggest greater scrutiny of ER+ cancers in patients exposed to iAs, because these tumors may spawn more aggressive phenotypes than unexposed ER+ tumors, in particular, basal subtypes that tend to develop therapy resistance and metastasis. [ABSTRACT FROM AUTHOR]

Background: Extensive literature in human and animal models has documented an association between maternal smoking during pregnancy and externalizing behavior in offspring. It remains unclear; however, the extent to which postnatal environmental smoke exposure is associated with behavioral development, particularly for children whose mothers did not smoke during pregnancy. The present study examined whether magnitude of exposure to environmental smoke across the first four years of life demonstrated a linear association with later externalizing symptoms. Methods: Exposure was quantified through salivary cotinine measured when children were 6, 15, 24, and 48 months of age, providing a more accurate quantification of realized exposure than can be estimated from parental report of cigarettes smoked. Data were available for n = 1,096 (50% male; 44% African American) children recruited for the Family Life Project, a study of child development in areas of rural poverty. Results: Analyses indicate a linear association between cotinine and children's symptoms of hyperactivity and conduct problems. This association remained significant after controlling for family poverty level, parental education, parental history of ADHD, hostility, depression, caregiver IQ, and obstetric complications. Furthermore, this association was unchanged when excluding mothers who smoked during pregnancy from the model. Conclusions: Findings are consistent with animal models demonstrating an effect of environmental exposure to nicotine on ongoing brain development in regions related to hyperactivity and impulsivity, and highlight the importance of mitigating children's exposure to environmental smoke, including sources that extend beyond the parents. [ABSTRACT FROM AUTHOR]

Copyright of Giornale Italiano di Medicina del Lavoro ed Ergonomia is the property of Giornale Italiano di Medicina del Lavoro ed Ergonomia Editorial Board and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: While the maternal risk factors on congenital heart defects (CHDs) have often been assessed, paternal contribution to CHDs, especially the joint effects of paternal risk factors on CHDs remain unknown. This study examined the major impacts of paternal alcohol consumption and its interaction (on multiplicative and additive scales) with paternal socioeconomic status (SES) and environmental exposures on CHDs in China. Methods: A population‐based case–control study involving 4,726 singleton CHDs cases and 4,726 controls (without any malformation and matched on hospital, gender, and gestational age) was conducted in Guangdong, China, 2004–2014. Information on parental demographics, behavioral patterns, disease/medication, and environmental exposures (3 months before pregnancy) was collected through face‐to‐face interviews. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) while controlling for all parental factors. Results: Paternal alcohol consumption was associated with an increased OR of CHDs (adjusted OR = 2.87, 95% CI: 2.25–3.65). Additionally, paternal smoking, industry occupation, organic solvent contact, virus infection and antibiotic use, living in rural areas, low household income, and migrant status were significantly associated with CHDs (ORs ranged: 1.42–4.44). Significant additive or multiplicative interactions were observed between paternal alcohol consumption and paternal smoking, industrial occupation, and low income on any CHDs (interaction contrast ratio [ICR] = 4.72, 95% CI: 0.96–8.47] and septal defects (ICRs ranged from 2.04 to 2.79, p <.05). Conclusions: Paternal alcohol consumption and multiple paternal factors were significantly associated with CHDs in China. Paternal smoking and low SES factors modified paternal alcohol consumption–CHDs relationships. Further studies are needed to confirm these findings. [ABSTRACT FROM AUTHOR]

Prior to Hurricane Maria, Puerto Rico already had 200+ hazardous waste sites, significant contamination of water resources, and among the highest rates of preterm birth in the USA. To address these issues, the Puerto Rico Testsite for Exploring Contamination Threats (PROTECT) Center was formed in 2010 to investigate prenatal environmental exposures, particularly phthalates, and adverse birth outcomes. Recent work from the PROTECT study confirms that in utero exposure to certain phthalates is associated with shorter gestation and increased risk of preterm birth. However, previous research also suggests that pregnant women who experience a natural disaster such as Hurricane Maria are at higher risk of adverse birth outcomes, but it is unknown whether this is due to stress, hazardous exposures, or a combination of factors. Thus, the aim of this analysis was to characterize hurricane-related changes in phthalate exposures and experiences within the PROTECT cohort. Among 176 participants who were pregnant during or within 5 months after Maria, 122 completed a questionnaire on hurricane-related experiences. Questionnaire results and biomarkers of exposure suggest that participants did not have regular access to fresh foods and water during hurricane recovery, and almost half reported structural damage to their home. In addition, biomarker concentrations of phthalates commonly used in food packaging were higher among participants post-hurricane, while phthalates commonly used in personal care products were lower compared to pre-hurricane levels. Hurricane-related increases in phthalate exposure, as well as widespread structural damage, food and water shortages, and long-term absence of electricity and cell phone service, likely increased the risk of adverse birth outcomes among this already vulnerable population. [ABSTRACT FROM AUTHOR]

This article describes environmental exposures of adult participants in the Moving to Opportunity (MTO) for Fair Housing experiment over a four to seven year period from baseline to the interim evaluation. The MTO experiment randomized participants living in public housing or private assisted housing at baseline into experimental and control groups and provided a housing voucher for experimental group participants to move to neighbourhoods with less than 10% of the population below the poverty line. However, few studies have examined how this move affected exposures to health promoting environments. We used data on residential locations of MTO participants and archival data on the built and food environment to construct environmental exposure variables. MTO participants in the experimental and Section 8 groups lived in neighbourhoods with higher food prices, less high intensity development and more open space relative to the control group. The findings suggest that housing policies can have potential health consequences by altering health-related environmental exposures. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: Type 1 diabetes is an autoimmune disease affecting ~400,000 people across the UK. It is likely that environmental factors trigger the disease process in genetically susceptible individuals. We assessed the associations between a wide range of environmental factors and childhood type 1 diabetes incidence in England, using an agnostic, ecological environment-wide association study (EnWAS) approach, to generate hypotheses about environmental triggers. Methods: We undertook analyses at the local authority district (LAD) level using a national hospital episode statistics-based incident type 1 diabetes dataset comprising 13,948 individuals with diabetes aged 0–9 years over the period April 2000 to March 2011. We compiled LAD level estimates for a range of potential demographic and environmental risk factors including meteorological, land use and environmental pollution variables. The associations between type 1 diabetes incidence and risk factors were assessed via Poisson regression, disease mapping and ecological regression. Results: Case counts by LAD varied from 1 to 236 (median 33, interquartile range 24–46). Overall type 1 diabetes incidence was 21.2 (95% CI 20.9, 21.6) per 100,000 individuals. The EnWAS and disease mapping indicated that 15 out of 53 demographic and environmental risk factors were significantly associated with diabetes incidence, after adjusting for multiple testing. These included air pollutants (particulate matter, nitrogen dioxide, nitrogen oxides, carbon monoxide; all inversely associated), as well as lead in soil, radon, outdoor light at night, overcrowding, population density and ethnicity. Disease mapping revealed spatial heterogeneity in type 1 diabetes risk. The ecological regression found an association between type 1 diabetes and the living environment domain of the Index of Multiple Deprivation (RR 0.995; 95% credible interval [CrI] 0.991, 0.998) and radon potential class (RR 1.044; 95% CrI 1.015, 1.074). Conclusions/interpretation: Our analysis identifies a range of demographic and environmental factors associated with type 1 diabetes in children in England. [ABSTRACT FROM AUTHOR]

Long INterspersed element (LINE‐1, L1) retrotransposons are the most abundant transposable elements in the human genome, constituting approximately 17%. They move by a "copy‐paste" mechanism, involving reverse transcription of an RNA intermediate and insertion of its cDNA copy at a new site in the genome. L1 retrotransposition (L1‐RTP) can cause insertional mutations, alter gene expression, transduce exons, and induce epigenetic dysregulation. L1‐RTP is generally repressed; however, a number of observations collected over about 15 years revealed that it can occur in response to environmental stresses. Moreover, emerging evidence indicates that L1‐RTP can play a role in the onset of several neurological and oncological diseases in humans. In recent years, great attention has been paid to the exposome paradigm, which proposes that health effects of an environmental factor should be evaluated considering both cumulative environmental exposures and the endogenous processes resulting from the biological response. L1‐RTP could be an endogenous process considered for this application. Here, we summarize the current understanding of environmental factors that can affect the retrotransposition of human L1 elements. Evidence indicates that L1‐RTP alteration is triggered by numerous and various environmental stressors, such as chemical agents (heavy metals, carcinogens, oxidants, and drugs), physical agents (ionizing and non‐ionizing radiations), and experiential factors (voluntary exercise, social isolation, maternal care, and environmental light/dark cycles). These data come from in vitro studies on cell lines and in vivo studies on transgenic animals: future investigations should be focused on physiologically relevant models to gain a better understanding of this topic. [ABSTRACT FROM AUTHOR]

The gut microbiota is a vast, complex, and fascinating ecosystem of microorganisms that resides in the human gastrointestinal tract. As an integral part of the microbiota–gut–brain axis, it is now being recognized that the microbiota is a modulator of brain and behavior, across species. Intriguingly, periods of change in the microbiota coincide with the development of other body systems and particularly the brain. We hypothesize that these times of parallel development are biologically relevant, corresponding to 'sensitive periods' or 'critical windows' in the development of the microbiota–gut–brain axis. Specifically, signals from the microbiota during these periods are hypothesized to be crucial for establishing appropriate communication along the axis throughout the life span. In other words, the microbiota is hypothesized to act like an expected input to calibrate the development of the microbiota–gut–brain axis. The absence or disruption of the microbiota during specific developmental windows would therefore be expected to have a disproportionate effect on specific functions or potentially for regulation of the system as a whole. Evidence for microbial modulation of neurocognitive development and neurodevelopmental risk is discussed in light of this hypothesis, finishing with a focus on the challenges that lay ahead for the future study of the microbiota–gut–brain axis during development. Read the Commentary on this article at doi: 10.1111/jcpp.13192 [ABSTRACT FROM AUTHOR]

Objective: The study investigated the associations between fine particulate matter (PM2.5; <2.5 μm in diameter), indoor environment, pulmonary function, and healthcare utilization in a vulnerable group of elderly persons with asthma. We hypothesized that environmental conditions were associated with adverse pulmonary health outcomes. Methods: The study involved elderly (n = 76; mean age 64.6 years; 48 women) vulnerable persons in Detroit, Michigan, USA, with physician-diagnosed asthma. Exposure variables included measured outdoor PM2.5, self-rated outdoor and household environmental pollutants. Outcome variables were self-rated and measured pulmonary function, and asthma-related healthcare utilization. Results: Mean ambient PM2.5 concentrations during the study was 14.14 ± (S.D. 6.36) µg/m3 during the summer and 14.20 (6.33) during the winter (p = 0.95). In multiple regression analyses, adjusting for age and gender, mean 6-month concentration of PM2.5 was related to shortness of breath (SHOB; standardized β = 0.26, p = 0.02) and inversely with self-rated respiratory health (SRRH; β = 0.28, p = 0.02). However, PM2.5 did not predict lung function (FEV1% predicted and FEV1/FVC). However, PM2.5 was related to use of asthma controller drugs (β = 0.38, p = 0.001). Participants' air pollution ratings predicted total healthcare utilization (β = 0.33, p = 0.01). Conclusions: In elderly persons with asthma, living near heavy industry and busy highways, objective and perceived environmental pollution relate to participants' respiratory health and healthcare utilization. Importantly, air pollution might increase use of asthma controller drugs containing corticosteroids with implication for elderly persons' risk to develop osteoporosis and cardiovascular disease. [ABSTRACT FROM AUTHOR]

Background: Low and middle-income countries like India with a large youth population experience a different environment from that of high-income countries. The Consortium on Vulnerability to Externalizing Disorders and Addictions (cVEDA), based in India, aims to examine environmental influences on genomic variations, neurodevelopmental trajectories and vulnerability to psychopathology, with a focus on externalizing disorders. Methods: cVEDA is a longitudinal cohort study, with planned missingness design for yearly follow-up. Participants have been recruited from multi-site tertiary care mental health settings, local communities, schools and colleges. 10,000 individuals between 6 and 23 years of age, of all genders, representing five geographically, ethnically, and socio-culturally distinct regions in India, and exposures to variations in early life adversity (psychosocial, nutritional, toxic exposures, slum-habitats, socio-political conflicts, urban/rural living, mental illness in the family) have been assessed using age-appropriate instruments to capture socio-demographic information, temperament, environmental exposures, parenting, psychiatric morbidity, and neuropsychological functioning. Blood/saliva and urine samples have been collected for genetic, epigenetic and toxicological (heavy metals, volatile organic compounds) studies. Structural (T1, T2, DTI) and functional (resting state fMRI) MRI brain scans have been performed on approximately 15% of the individuals. All data and biological samples are maintained in a databank and biobank, respectively. Discussion: The cVEDA has established the largest neurodevelopmental database in India, comparable to global datasets, with detailed environmental characterization. This should permit identification of environmental and genetic vulnerabilities to psychopathology within a developmental framework. Neuroimaging and neuropsychological data from this study are already yielding insights on brain growth and maturation patterns. [ABSTRACT FROM AUTHOR]

The prevalence of allergic diseases differs in urban and rural populations. We sought to assess associations between environmental and dietary factors with allergic diseases in urban and rural South African children. Toddlers aged 12 to 36 months were assessed for food allergen and aeroallergen sensitization, atopic dermatitis, allergic rhinitis, asthma, and challenge-proved food allergy. Information was collected on family history of allergic diseases, household size, socioeconomic status, delivery mode, antibiotic and probiotic use, exposure to fermented and unpasteurized milk, antihelminth treatment, sunlight exposure, pet and farm animal exposure, cigarette smoke, and household cooking and heating fuels. Antenatal exposures to pets, livestock, and cigarette smoke were assessed. A subsection completed questions on consumption of fruits and vegetables, fast foods, soft drinks/fruit juices, and fried/microwaved meat. Risk and protective factors differed between urban and rural settings. Exposure to farm animals in infants and their mothers during pregnancy was protective against allergic outcomes in the rural population. Consumption of unpasteurized milk is uncommon in this group of rural children and is unlikely to be an important factor in rural protection. In urban children birth by cesarean section is associated with food allergy, and consumption of fermented milk products is associated with reduced asthma and atopic dermatitis. In both cohorts antenatal maternal smoking and environmental smoking exposure were predominantly associated with asthma, and consumption of fast foods and fried meats were associated with allergy. In this rural environment exposure to livestock is the strongest protective factor. In urban communities, where animal contact is rare, risk factors include cesarian section, and protective factors include consumption of fermented milk products. Modifiable risk factors urgently require interventions to prevent increasing allergy rates in countries undergoing rapid urbanization. [ABSTRACT FROM AUTHOR]

Household settings are high risk for COVID-19 transmission. Understanding transmission factors associated with environmental dwelling characteristics is important in informing public health and building design recommendations. We aimed to develop a directed acyclic graph (DAG) to inform a novel analytical study examining the effect of dwelling environmental characteristics on household transmission of COVID-19. Key demographic, behavioural and environmental dwelling characteristics were identified by a multidisciplinary team. Using the DAG to visually display risk factors, and using expert knowledge of available datasets we reached a consensus on the factors included and directionality of relationships to build the final conceptual framework. Factors were displayed as nodes and relationships as pathways. Of 34 potential factors, 16 were included in the DAG, with 13 causal and three biasing pathways. Three variables were not measurable using retrospective datasets. The DAG enabled us to select data sources for the pilot study period and to inform the analysis plan. Key exposure nodes were energy efficiency or dwelling age; dwelling type or number of storeys; and dwelling size. We determined direct and proxy confounders which we could adjust for, potential interactions terms we could test in model building, and co-linear variables to omit in the same model. The DAG helped identify key variables and datasets. It prioritised key nodes and pathways to formalise complex relationships between variables. It was pivotal in identifying unobserved variables, confounders, co-linearity and potential interactions. It has supported data selection and design of a retrospective pilot study analysis plan. • Directed acyclic graphs (DAGs) can inform variable and data source selection. • Multidisciplinary teams should use DAGs to visualise complex conceptual frameworks. • DAGs should be used to build complex models to inform analytical study design. • DAGs should be taught in epidemiological training programmes. • DAGs can be used as a tool in developing multidisciplinary consensus. [ABSTRACT FROM AUTHOR]