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Background: Experimental studies have shown that disinfection byproducts (DBPs) including haloacetic acids (HAAs) can cause liver toxicity, but evidence linking this association in humans is sparse. Objectives: We aimed to explore the associations between HAA exposures and liver injury. Methods: We included 922 women between December 2018 and January 2020 from the Tongji Reproductive and Environmental (TREE) cohort study in Wuhan, China. Urinary HAA concentrations including trichloroacetic acid (TCAA) and dichloroacetic acid (DCAA) and serum indicators of liver function, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma- glutamyltransferase (GGT) were measured. Liver injury was defined as if any of serum indicator levels were above the 90th percentile. Multivariate logistic and linear regression models were fitted to assess the associations of urinary HAA concentrations with the risk of liver injury and liver function indicators. Stratified analyses by age, body mass index (BMI), alcohol use, and passive smoking were also applied to evaluate the potential effect modifiers. RESULTS: There is little evidence of associations of urinary TCAA concentrations with liver injury risk and liver function indicators. However, urinary DCAA concentrations were associated with a higher risk of liver injury [odds ratios (OR) for 1-interquartile range (IQR) increase in natural log (ln) transformed DCAA concentrations: 1.45; 95% confidence interval (CI): 1.07, 1.98]. This association was observed only among nondrinkers (pinteraction =0.058). We also found that a 1-IQR increase in ln-transformed DCAA concentrations was positively associated with ALT levels (percentage change = 6.06%; 95% CI: 0.48%, 11.95%) and negatively associated with AST/ALT (percentage change = - 4.48%; 95% CI: -7.80%, -1.04%). In addition, urinary DCAA concentrations in relation to higher GGT levels was observed only among passive smokers (Pmtcnaitm = 0.040). Conclusion: Our findings suggest that exposure to DCAA but not TCAA is associated with liver injury among women undergoing assisted reproductive technology. https://doi.org/10.1289/EHP13386, Introduction Nonalcoholic fatty liver disease (NAFLD), whose pathogenesis is linked with liver injury commonly measured by alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gammaglutamyltransferase (GGT), is the most common chronic [...]

Byline: S. Sujatha, Asha. Iyengar, S. Pruthvish, Radhaprashanth, Ravleen. Nagi Tobacco use is one of the major public health problems in India and also the single most important remediable public [...]

BACKGROUND: Chemical and nonchemical environmental exposures are increasingly suspected to influence the development of obesity, especially during early life, but studies mostly consider single exposure groups. OBJECTIVES: Our study aimed to systematically assess the association between a wide array of early-life environmental exposures and childhood obesity, using an exposome-wide approach. METHODS: The HELIX (Human Early Life Exposome) study measured child body mass index (BMI), waist circumference, sMnfold thickness, and body fat mass in 1,301 children from six European birth cohorts age 6-11 y. We estimated 77 prenatal exposures and 96 childhood exposures (cross-sectionally), including indoor and outdoor air pollutants, built environment, green spaces, tobacco smoking, and biomarkers of chemical pollutants (persistent organic pollutants, metals, phthalates, phenols, and pesticides). We used an exposure-wide association study (ExWAS) to screen all exposure-outcome associations independently and used the deletion-substitution-addition (DSA) variable selection algorithm to build a final multiexposure model. RESULTS: The prevalence of overweight and obesity combined was 28.8%. Maternal smoking was the only prenatal exposure variable associated with higher child BMI (z-score increase of 0.28, 95% confidence interval: 0.09, 0.48, for active vs. no smoking). For childhood exposures, the multiexposure model identified particulate and nitrogen dioxide air pollution inside the home, urine cotinine levels indicative of secondhand smoke exposure, and residence in more densely populated areas and in areas with fewer facilities to be associated with increased child BMI. Child blood levels of copper and cesium were associated with higher BMI, and levels of organochlorine pollutants, cobalt, and molybdenum were associated with lower BMI. Similar results were found for the other adiposity outcomes. DISCUSSION: This first comprehensive and systematic analysis of many suspected environmental obesogens strengthens evidence for an association of smoking, air pollution exposure, and characteristics of the built environment with childhood obesity risk. Cross-sectional biomarker results may suffer from reverse causality bias, whereby obesity status influenced the biomarker concentration. https://doi.org/10.1289/EHP5975, Introduction Rates of childhood obesity are increasing at alarming rates across the globe, with some leveling-off of this trend reported in Europe and high-income English-speaking regions [NCD Risk Factor Collaboration [...]

Background: Lead can adversely affect maternal and child health across a wide range of exposures; developing fetuses and breastfeeding infants may be particularly vulnerable. We describe the distribution of blood lead levels (BLLs) in U.S. women of childbearing age and associations with sociodemographic, reproductive, smoking, and housing characteristics over a 40-y period. Methods: Data from the National Health and Nutrition Examination Survey (NHANES) II, NHANES III Phase I and Phase II, and 1999-2016 continuous NHANES were used to describe the distribution of BLLs (given in micrograms per deciliter; 1 [micro]g/dL = 0.0483 [micro]mol/L) in U.S. women 15-49 years of age between 1976 and 2016. For all women with valid BLLs (n = 22,408), geometric mean (GM) BLLs and estimated prevalence of BLLs >5 [micro]g/dL were calculated overall and by selected demographic characteristics. For NHANES II, estimated prevalence of BLLs [greater than or equal to] 10 and [greater than or equal to] 20 [micro]g/dL were also calculated. Results: The most recent GM BLLs (2007-2010 and 2011-2016, respectively) were 0.81 [micro]g/dL [95% confidence interval (CI): 0.79, 0.84] and 0.61 [micro]g/dL (95% CI: 0.59, 0.64). In comparison, GM BLLs in earlier periods (1976-1980, 1988-1991, and 1991-1994) were 10.37 [micro]g/dL (95% CI: 9.95, 10.79), 1.85 [micro]g/dL (95% CI: 1.75, 1.94), and 1.53 [micro]g/dL (95% CI: 1.45, 1.60), respectively. In 2011-2016, 0.7% of women of childbearing age had BLLs >5 [micro]g/dL, and higher BLLs were associated with older age, other race/ethnicity, birthplace outside the United States, four or more live births, exposure to secondhand tobacco smoke, and ever pregnant or not currently pregnant. Discussion: Lead exposure in U.S. women of childbearing age is generally low and has substantially decreased over this 40-y period. However, based on these estimates, there are still at least 500,000 U.S. women being exposed to lead at levels that may harm developing fetuses or breastfeeding infants. Identifying high-risk women who are or intend to become pregnant remains an important public health issue. https://doi.org/10.1289/EHP5925, Introduction Despite overall declines in environmental sources, lead exposure remains an important public health problem for certain groups, including women of childbearing age, due to the potential exposure to the [...]

Background: Maternal tobacco smoke exposure has been associated with altered DNA methylation. However, previous studies largely used methylation arrays, which cover a small fraction of CpGs, and focused on whole cord blood. Objectives: The current study examined the impact of in utero exposure to maternal tobacco smoke on the cord blood [CD4.sup.+] DNA methylome. Methods: The methylomes of 20 Hispanic white newborns (n = 10 exposed to any maternal tobacco smoke in pregnancy; n = 10 unexposed) from the Maternal and Child Health Study (MACHS) were profiled by whole-genome bisulfite sequencing (median coverage: 6.5 X). Statistical analyses were conducted using the Regression Analysis of Differential Methylation (RADMeth) program because it performs well on low-coverage data (minimizes false positives and negatives). Results: We found that 10,381 CpGs were differentially methylated by tobacco smoke exposure [neighbor-adjusted p-values that are additionally corrected for multiple testing based on the Benjamini-Hochberg method for controlling the false discovery rate (FDR) ([p.sub.FDR]) Conclusions: Maternal tobacco smoke exposure in pregnancy is associated with cord blood [CD4.sup.+] DNA methylation in key regulatory regions, including enhancers. While we used a method that performs well on low-coverage data, we cannot exclude the possibility that some results may be false positives. However, we identified a differentially methylated CpG in amino acid transporter SLC7A8 that is highly reproducible, which may be sensitive to cigarette smoke in both cord blood and adult [CD4.sup.+] cells. https://doi.org/10.1289/EHP3398, Introduction Maternal smoking during pregnancy is one of the most prevalent and modifiable risk factors affecting newborn health (Curtin and Matthews 2016). In the United States, >8% of women smoke [...]

There is a general consensus among policymakers that raising tobacco taxes reduces cigarette consumption. However, evidence that tobacco taxes reduce adult smoking is relatively sparse. In this paper, we extend the literature in two ways: using data from the Current Population Survey Tobacco Use Supplements we focus on recent, large tax changes, which provide the best opportunity to empirically observe a response in cigarette consumption, and employ a novel paired difference-in-differences technique to estimate the association between tax increases and cigarette consumption. Estimates indicate that, for adults, the association between cigarette taxes and either smoking participation or smoking intensity is negative, small and not usually statistically significant. Our evidence suggests that increases in cigarette taxes are associated with small decreases in cigarette consumption and that it will take sizable tax increases, on the order of 100%, to decrease smoking by as much as 5%. (JEL I18, I12), I. INTRODUCTION There is a general consensus among policymakers that raising tobacco taxes reduces cigarette consumption. (1) However, evidence that tobacco taxes reduce adult smoking is relatively sparse (Gallet and [...]