Reesepope6957

Background We previously reported chronic respiratory effects in children who were then 7-17 years of age in Matlab, Bangladesh. One group of children had been exposed to high concentrations of arsenic in drinking water in utero and early childhood (average 436 µg/L), and the other group of children were never known to have been exposed to >10 µg/L. The exposed children, both males and females, had marked increases in chronic respiratory symptoms. Methods The current study involves a further follow-up of these children now 14-26 years of age with 463 located and agreeing to participate. They were interviewed for respiratory symptoms and lung function was measured. Data were collected on smoking, body mass index (BMI), and number of rooms in the house as a measure of socioeconomic status. Results Respiratory effects were still present in males but not females. In the high exposure group (>400 µg/L in early life) the odds ratio (OR) among male participants for dry cough in the last 12 months was 2.36 (95% confidence interval [CI] = 1.21, 4.63, P = 0.006) and for asthma OR = 2.51 (95% CI = 1.19, 5.29, P = 0.008). Forced vital capacity (FVC) was reduced in males in the early life high-exposure group compared with those never exposed (-95ml, P = 0.04), but not in female participants. Conclusions By the age range 14-26, there was little remaining evidence of chronic respiratory effects in females but pronounced effects persisted in males. Mechanisms for the marked male female differences warrant further investigation along with further follow-up to see if respiratory effects continue in males. Background Studies have identified associations between air pollution and lipid levels in adults, suggesting a mechanism by which air pollution contributes to cardiovascular disease. However, little is known about the association between early life air pollution exposure and lipid levels in children. Methods Participants included 465 mother-child pairs from a prospective birth cohort in Mexico City. Daily particulate matter less then 2.5 µm in diameter (PM2.5) predictions were estimated using a satellite-based exposure model and averaged over trimesters, the entire pregnancy, and the first year of life. We assessed associations with several lipid measures at 4-6 years of age, including total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), non-HDL-C, high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG). Linear regression models were used to estimate change in lipid levels with each interquartile range increase in PM2.5. We additionally assessed if associations between PM2.5 and lipid levels varied across lipid quantiles using quantile regression. Models were adjusted for maternal education, body mass index, and age, child's age at study visit, prenatal environmental tobacco smoke, and season of conception. Results PM2.5 exposure during the third trimester was associated with increases in childhood total cholesterol, LDL-C, and non-HDL-C, and decreases in HDL-C and triglycerides. There was additionally an increasing trend in the effect estimate across higher quantiles of total cholesterol, LDL-C, and non-HDL-C during the third trimester and entire pregnancy period. There were no consistent associations for first year of life exposures. Conclusion In this longitudinal birth cohort in Mexico City, associations between prenatal PM2.5 and childhood lipid (total cholesterol, LDL-C, non-HDL-C) levels were greater for children at higher lipid quantiles. Background Black men with prostate cancer (CaP) experience excess mortality compared with White men. Residential greenness, a health promoting contextual factor, could explain racial disparities in mortality among men with CaP. Methods We identified Pennsylvania Cancer Registry cases diagnosed between January 2000 and December 2015. Totally, 128,568 participants were followed until death or 1 January 2018, whichever occurred first. Residential exposure at diagnosis was characterized using the Normalized Difference Vegetation Index (NDVI) with 250 m resolution. We estimated hazard ratios (HRs) using Cox models, adjusting for area-level socioeconomic status, geographic healthcare access, and segregation. To determine whether increasing residential greenness could reduce racial disparities, we compared standardized 10-year mortality Black-White risk differences under a hypothetical intervention fixing NDVI to the 75th percentile of NDVI experienced by White men. Results We observed 29,978 deaths over 916,590 person-years. Comparing men in the highest to lowest NDVI quintile, all-cause (adjusted HR [aHR] 0.88, 95% confidence interval [CI] 0.84, 0.92, P trend less then 0.0001), prostate-specific (aHR 0.88, 95% CI 0.80, 0.99, P trend= 0.0021), and cardiovascular-specific (aHR 0.82, 95% CI 0.74, 0.90, P trend less then 0.0001) mortality were lower. Inverse associations between an interquartile range increase in NDVI and cardiovascular-specific mortality were observed in White (aHR 0.90, 95% CI 0.86, 0.93) but not Black men (aHR 0.97, 95% CI 0.89, 1.06; P het = 0.067). Hypothetical interventions to increase NDVI led to nonsignificant reductions in all-cause (-5.3%) and prostate-specific (-23.2%), but not cardiovascular-specific mortality disparities (+50.5%). Discussion Residential greenness was associated with lower mortality among men with CaP, but findings suggest that increasing residential greenness would have limited impact on racial disparities in mortality. selleck chemicals llc Background Arsenic exposure affects >100 million people globally and increases risk for chronic diseases. One possible toxicity mechanism is epigenetic modification. Previous epigenome-wide association studies (EWAS) have identified associations between arsenic exposure and CpG-specific DNA methylation. To provide additional evidence that observed associations represent causal relationships, we examine the association between genetic determinants of arsenic metabolism efficiency (percent dimethylarsinic acid, DMA%, in urine) and DNA methylation among individuals from the Health Effects of Arsenic Longitudinal Study (n = 379) and Bangladesh Vitamin E and Selenium Trial (n = 393). Methods We used multivariate linear models to assess the association of methylation at 221 arsenic-associated CpGs with DMA% and measures of genetically predicted DMA% derived from three SNPs (rs9527, rs11191527, and rs61735836). We also conducted two-sample Mendelian randomization analyses to estimate the association between arsenic metabolism efficiency and CpG methylation.