Exposure to metal mixtures and telomere length in Bangladeshi children.

Telomere length is associated with chronic diseases and in younger populations, may represent a biomarker of disease susceptibility. As growing evidence suggests that environmental factors, including metals, may impact telomere length, we investigated the association between 17 metals measured in toenail samples and leukocyte relative telomere length (RTL), among 472 five- to seven-year-old children enrolled in the Bangladesh Environmental Research in Children's Health (BiRCH) cohort. In single exposure linear regression models, a doubling of arsenic (As) and mercury (Hg) (µg/g) were associated with a -0.21 (95%CI: -0.032, -0.010; p=0.0005) and -0.017 (95%CI: -0.029, -0.004; p=0.006) difference in RTL, respectively. In Bayesian Kernel Machine Regression (BKMR) mixture models, the overall metal mixture was inversely associated with RTL (P-for-trend <0.001). Negative associations with RTL were observed with both log2-As and log2-Hg, while an inverted U-shaped association was observed for log2-zinc (Zn) with RTL. We found little evidence of interaction among metals. Sex-stratification identified stronger associations of the overall mixture and log2-As with RTL among females, compared to males. Our study suggests that As and Hg may independently influence RTL in mid-childhood. Further studies are needed to investigate potential long-term impacts of metal-associated telomere shortening in childhood on health outcomes in adult life.

Maternal educational attainment in pregnancy and epigenome-wide DNA methylation changes in the offspring from birth until adolescence.

Maternal educational attainment (MEA) shapes offspring health through multiple potential pathways. Differential DNA methylation may provide a mechanistic understanding of these long-term associations. We aimed to quantify the associations of MEA with offspring DNA methylation levels at birth, in childhood and in adolescence. Using 37 studies from high-income countries, we performed meta-analysis of epigenome-wide association studies (EWAS) to quantify the associations of completed years of MEA at the time of pregnancy with offspring DNA methylation levels at birth (n = 9 881), in childhood (n = 2 017), and adolescence (n = 2 740), adjusting for relevant covariates. MEA was found to be associated with DNA methylation at 473 cytosine-phosphate-guanine sites at birth, one in childhood, and four in adolescence. We observed enrichment for findings from previous EWAS on maternal folate, vitamin-B12 concentrations, maternal smoking, and pre-pregnancy BMI. The associations were directionally consistent with MEA being inversely associated with behaviours including smoking and BMI. Our findings form a bridge between socio-economic factors and biology and highlight potential pathways underlying effects of maternal education. The results broaden our understanding of bio-social associations linked to differential DNA methylation in multiple early stages of life. The data generated also offers an important resource to help a more precise understanding of the social determinants of health.

Association between maternal cigarette smoking cessation and risk of preterm birth in Western New York.

BACKGROUND: Although many studies suggested the benefit of smoking cessation among pregnant women in reducing the risk of preterm birth (PTB), the timing of the effect of the cessation remains inconclusive. OBJECTIVES: To examine the association of trimester-specific smoking cessation behaviours with PTB risk. METHODS: We included 199,453 live births in Western New York between 2004 and 2018. Based on self-reported cigarette smoking during preconception and in each trimester, we created six mutually exclusive groups: non-smokers, quitters in each trimester, those who smoked throughout pregnancy, and inconsistent smokers. Risk ratios (RRs) and 95% confidence intervals (CIs) were estimated using Poisson regression to examine the association between smoking cessation and PTB. Effect modification by illegal drug use, maternal age, race and ethnicity and pre-pregnancy body mass index (BMI) was investigated multiplicatively by ratio of relative risk and additively by relative excess risk due to interaction (RERI). RESULTS: Overall, 6.7% of women had a PTB; 14.1% smoked throughout pregnancy and 3.4%, 1.8% and 0.8% reported quitting smoking during the first, second and third trimesters, respectively. Compared to non-smokers, third-trimester cessation (RR 1.20, 95% CI 1.01, 1.43) and smoking throughout pregnancy (RR 1.27, 95% CI 1.21, 1.33) were associated with a higher PTB risk, while quitting smoking during the first or second trimester, or inconsistent smoking was not associated with PTB. A positive additive interaction was identified for maternal age and late smoking cessation or smoking throughout pregnancy on PTB risk (RERI 0.17, 95% CI 0.00, 0.36), and a negative interaction was observed for pre-pregnancy BMI ≥30 kg/m2 (ratio of relative risk 0.70, 95% CI 0.63, 0.78; RERI -0.42, 95% CI -0.56, -0.30). CONCLUSION: Compared to non-smokers, smoking throughout pregnancy and third-trimester smoking cessation are associated with an increased risk of PTB, while quitting before the third trimester may not increase PTB risk.

Do small effects matter more in vulnerable populations? an investigation using Environmental influences on Child Health Outcomes (ECHO) cohorts.

BACKGROUND: A major challenge in epidemiology is knowing when an exposure effect is large enough to be clinically important, in particular how to interpret a difference in mean outcome in unexposed/exposed groups. Where it can be calculated, the proportion/percentage beyond a suitable cut-point is useful in defining individuals at high risk to give a more meaningful outcome. In this simulation study we compute differences in outcome means and proportions that arise from hypothetical small effects in vulnerable sub-populations. METHODS: Data from over 28,000 mother/child pairs belonging to the Environmental influences on Child Health Outcomes Program were used to examine the impact of hypothetical environmental exposures on mean birthweight, and low birthweight (LBW) (birthweight < 2500g). We computed mean birthweight in unexposed/exposed groups by sociodemographic categories (maternal education, health insurance, race, ethnicity) using a range of hypothetical exposure effect sizes. We compared the difference in mean birthweight and the percentage LBW, calculated using a distributional approach. RESULTS: When the hypothetical mean exposure effect was fixed (at 50, 125, 167 or 250g), the absolute difference in % LBW (risk difference) was not constant but varied by socioeconomic categories. The risk differences were greater in sub-populations with the highest baseline percentages LBW: ranging from 3.1-5.3 percentage points for exposure effect of 125g. Similar patterns were seen for other mean exposure sizes simulated. CONCLUSIONS: Vulnerable sub-populations with greater baseline percentages at high risk fare worse when exposed to a small insult compared to the general population. This illustrates another facet of health disparity in vulnerable individuals.

Meta-Analysis on Associations of Timing of Maternal Smoking Cessation Before and During Pregnancy With Childhood Overweight and Obesity.

INTRODUCTION: There is a lack of comprehensive review on associations of maternal smoking cessation (versus nonsmokers) with childhood overweight and obesity. AIMS AND METHODS: We conducted a systematic review and meta-analysis of existing evidence in this field. Within PubMed, EMBASE, and CENTRAL databases, we identified and screened 1147 abstracts. We reviewed full-texts and extracted related information from 10 eligible articles. We pooled odds ratios for overweight/obesity and mean differences in BMI z-scores by maternal smoking status around pregnancy. RESULTS: Among 10 eligible studies, 71 393 children were included from ages 2 to 18 years. Compared to children of nonsmokers, the pooled unadjusted odds ratio (OR) for overweight was 1.36 (95% Confidence Interval CI: 1.14, 1.62) in children of quitters and 1.44 (1.27, 1.64) in children of continued smokers. The pooled unadjusted OR for obesity was 1.65 (1.17, 2.32) in children of quitters and 1.94 (1.38, 2.73) in children of continued smokers. The pooled unadjusted mean difference in BMI z-score was 0.51 (0.41, 0.61) in children of quitters and 0.64 (0.58, 0.70) in children of continued smokers. The pooled unadjusted OR for overweight in children of mothers quitting before pregnancy was 1.46 (1.15, 1.85), during the first trimester was 1.52 (1.27, 1.82), and during pregnancy (mixed timing, mostly first trimester) was 0.97 (0.79, 1.20). CONCLUSION: The risk of offspring overweight and obesity was moderately higher for quitters during pregnancy compared to nonsmokers, although it might not be as high as continued smokers. IMPLICATIONS: Maternal smoking during pregnancy is an established risk factor of childhood overweight and obesity. Based on our systematic review, intervention to help mothers quit smoking has the potential to reduce the risk of childhood overweight and obesity in offspring related to prenatal tobacco exposure. Quitting before pregnancy is ideal, but quitting in early pregnancy is still helpful for reducing risk.

Sex-specific effects of prenatal organophosphate ester (OPE) metabolite mixtures and adverse infant birth outcomes in the maternal and developmental risks from environmental and social stressors (MADRES) pregnancy cohort.

BACKGROUND: Organophosphate esters (OPEs) are used as flame retardants and plasticizers in various consumer products. Limited prior research suggests sex-specific effects of prenatal OPE exposures on fetal development. We evaluated overall and sex-specific associations between prenatal OPE exposures and gestational age (GA) at birth and birthweight for gestational age (BW for GA) z-scores among the predominately low-income, Hispanic MADRES cohort. METHODS: Nine OPE metabolite concentrations were measured in 421 maternal urine samples collected during a third trimester visit (GA = 31.5 ± 2.0 weeks). We examined associations between single urinary OPE metabolites and GA at birth and BW for GA z-scores using linear regression models and Generalized Additive Models (GAMs) and effects from OPE mixtures using Bayesian Kernel Machine Regression (BKMR). We also assessed sex-specific differences in single metabolite analyses by evaluating statistical interactions and stratifying by sex. RESULTS: We did not find significant associations between individual OPE metabolites and birth outcomes in the full infant sample; however, we found that higher bis(1,3-dichloro-2-propyl) phosphate (BDCIPP) was associated with earlier GA at birth among male infants (p = 0.04), and a nonlinear, inverted U-shape association between the sum of dibutyl phosphate and di-isobutyl phosphate (DNBP + DIBP) and GA at birth among female infants (p = 0.03). In mixtures analysis, higher OPE metabolite mixture exposures was associated with lower GA at birth, which was primarily driven by female infants. No associations were observed between OPE mixtures and BW for GA z-scores. CONCLUSION: Higher BDCIPP and DNBP + DIBP concentrations were associated with earlier GA at birth among male and female infants, respectively. Higher exposure to OPE mixtures was associated with earlier GA at birth, particularly among female infants. However, we saw no associations between prenatal OPEs and BW for GA. Our results suggest sex-specific impacts of prenatal OPE exposures on GA at birth.

Associations between area-level arsenic exposure and adverse birth outcomes: An Echo-wide cohort analysis.

BACKGROUND: Drinking water is a common source of exposure to inorganic arsenic. In the US, the Safe Drinking Water Act (SDWA) was enacted to protect consumers from exposure to contaminants, including arsenic, in public water systems (PWS). The reproductive effects of preconception and prenatal arsenic exposure in regions with low to moderate arsenic concentrations are not well understood. OBJECTIVES: This study examined associations between preconception and prenatal exposure to arsenic violations in water, measured via residence in a county with an arsenic violation in a regulated PWS during pregnancy, and five birth outcomes: birth weight, gestational age at birth, preterm birth, small for gestational age (SGA), and large for gestational age (LGA). METHODS: Data for arsenic violations in PWS, defined as concentrations exceeding 10 parts per billion, were obtained from the Safe Drinking Water Information System. Participants of the Environmental influences on Child Health Outcomes Cohort Study were matched to arsenic violations by time and location based on residential history data. Multivariable, mixed effects regression models were used to assess the relationship between preconception and prenatal exposure to arsenic violations in drinking water and birth outcomes. RESULTS: Compared to unexposed infants, continuous exposure to arsenic from three months prior to conception through birth was associated with 88.8 g higher mean birth weight (95% CI: 8.2, 169.5), after adjusting for individual-level confounders. No statistically significant associations were observed between any preconception or prenatal violations exposure and gestational age at birth, preterm birth, SGA, or LGA. CONCLUSIONS: Our study did not identify associations between preconception and prenatal arsenic exposure, defined by drinking water exceedances, and adverse birth outcomes. Exposure to arsenic violations in drinking water was associated with higher birth weight. Future studies would benefit from more precise geodata of water system service areas, direct household drinking water measurements, and exposure biomarkers.

Prenatal exposures to organophosphate ester metabolite mixtures and children's neurobehavioral outcomes in the MADRES pregnancy cohort.

BACKGROUND: Evidence suggests organophosphate esters (OPEs) are neurotoxic; however, the epidemiological literature remains scarce. We investigated whether prenatal exposures to OPEs were associated with child neurobehavior in the MADRES cohort. METHODS: We measured nine OPE metabolites in 204 maternal urine samples (gestational age at collection: 31.4 ± 1.8 weeks). Neurobehavior problems were assessed among 36-month-old children using the Child Behavior Checklist's (CBCL) three composite scales [internalizing, externalizing, and total problems]. We examined associations between tertiles of prenatal OPE metabolites (> 50% detection) and detect/non-detect categories (< 50% detection) and CBCL composite scales using linear regression and generalized additive models. We also examined mixtures for widely detected OPEs (n = 5) using Bayesian kernel machine regression. RESULTS: Maternal participants with detectable versus non-detectable levels of bis(2-methylphenyl) phosphate (BMPP) had children with 42% (95% CI: 4%, 96%) higher externalizing, 45% (-2%, 114%) higher internalizing, and 35% (3%, 78%) higher total problems. Participants in the second versus first tertile of bis(butoxethyl) phosphate (BBOEP) had children with 43% (-1%, 109%) higher externalizing scores. Bis(1-chloro-2-propyl) phosphate (BCIPP) and child sex had a statistically significant interaction in internalizing (p = 0.02) and total problems (p = 0.03) models, with 120% (23%, 295%) and 57% (6%, 134%) higher scores in the third versus first BCIPP tertile among males. Among females, detectable vs non-detectable levels of prenatal BMPP were associated with 69% higher externalizing scores (5%, 170%) while the third versus first tertile of prenatal BBOEP was associated with 45% lower total problems (-68%, -6%). Although the metabolite mixture and each CBCL outcome had null associations, we observed marginal associations between di-n-butyl phosphate and di-isobutyl phosphate (DNBP + DIBP) and higher internalizing scores (0.15; 95% CrI: -0.02, 0.32), holding other metabolites at their median. CONCLUSIONS: Our results generally suggest adverse and sex-specific effects of prenatal exposure to previously understudied OPEs on neurobehavioral outcomes in 36-month children, providing evidence of potential OPE neurotoxicity.

Alcohol Consumption and Mental Health during the COVID-19 Pandemic.

AIMS: To examine the association between alcohol consumption and mental health during the COVID-19 pandemic. METHODS: An anonymous online survey was distributed among US adults during May-August 2020 through social networks and ResearchMatch. We collected information on demographic, lifestyles and mental health symptoms including anxiety, depression, stress and post-traumatic stress disorder. Logistic regression models were used to examine the cross-sectional association between alcohol consumption and mental health symptoms. We also examined effect modification by race, age, gender, social support, financial insecurity and quarantine status. RESULTS: The analytical sample consists of 3623 adults. Stable drinking habits and regular drinking behaviors were found to co-exist with better mental health status. Participants who increased their alcohol use had higher odds of developing mental health disorders than those who maintained their pre-pandemic drinking habits. Additionally, participants who engaged in binge drinking during the pandemic had higher odds of depression and stress than those who did not. The associations regarding increased drinking and binge drinking in relation to adverse mental health outcomes were stronger among females, racial minorities, and individuals with financial concerns, poor social support and restricted quarantine status than their counterparts. CONCLUSIONS: During the early stage of the COVID-19 pandemic, increased alcohol use and binge drinking are cross-sectionally associated with higher odds of mental health disorders, which highlighted the need for targeted intervention to address the mental health needs of individuals who have engaged in these behaviors, especially among females, minorities, those with insecurities or with restricted quarantine status.

Personal exposure to benzene, toluene, ethylbenzene, and xylenes (BTEXs) mixture and telomere length: a cross-sectional study of the general US adult population.

BACKGROUND: Benzene, Toluene, Ethylbenzene, and Xylenes (BTEXs) are a group of aromatic air pollutants from fossil fuels. There is no research on associations of the BTEXs mixture with telomere length (TL), a marker of cellular aging, in the general population. METHODS: We analyzed a subsample of 549 US adults aged 20-59 years from the National Health and Nutrition Examination Survey 1999-2000. BTEXs samples were collected by passive exposure badges worn by participants for 48-72 h. Levels of BTEXs were measured with gas chromatography/mass spectrometry. Leukocyte TL was measured with qPCR. We used Bayesian Kernel Machine Regression (BKMR) to examine the effect of the BTEXs mixture on TL adjusting for potential confounders. Analyses were stratified by tobacco smoking status (serum cotinine≥10 ng/mL vs. <10 ng/mL). RESULTS: Levels of personal exposure to BTEXs were detectable in most participants and were relatively higher in the 150 smokers than in the 399 nonsmokers. The BTEXs were moderately or strongly intercorrelated (0.5 < r ≤ 0.9, P < 0.05). All chemicals had weak, inverse correlations with TL (-0.1 0.05). In BKMR models among the nonsmokers, the BTEXs mixture was significantly inversely associated with TL at a low range of the BTEXs (20th-65th percentile) but was not associated with TL at a higher range (>65th percentile). Also, we found a U-shape association of benzene and a positive association of ethylbenzene with TL independent of other BTEXs. Among smokers, neither the BTEXs mixture nor any individual BTEXs were significantly associated with TL. CONCLUSION: Within a low-to-middle range, exposure to the BTEXs mixture may be associated with shorter telomere length in the general nonsmoking population.

Association of ambient fine particulate matter exposure with gestational diabetes mellitus and blood glucose levels during pregnancy.

BACKGROUND: Previous studies have examined the associations between ambient fine particulate matter (PM2.5) exposure and gestational diabetes mellitus (GDM). However, limited studies explored the relationships between PM2.5 exposure and blood glucose levels during pregnancy, especially in highly polluted areas. OBJECTIVES: To examine the associations of prenatal ambient PM2.5 exposure with GDM and blood glucose levels, and to identify the sensitive exposure windows in a highly air-polluted area. METHODS: From July 2016 to October 2017, a birth cohort study was conducted in Beijing, China. Participants were interviewed in each trimester regarding demographics, lifestyle, living and working environment, and medical conditions. Participant's daily ambient PM2.5 levels from 3 m before last menstrual period (LMP) to the third trimester was estimated by a hybrid spatiotemporal model. Indoor air quality index was calculated based on environmental tobacco smoke, ventilation, cooking, painting, pesticide, and herbicide use. Distributed lag non-linear model was applied to explore the sensitive weeks of PM2.5 exposure. RESULTS: Of 165 pregnant women, 23 (13.94%) developed GDM. After adjusting for potential confounders, PM2.5 exposure during the 1st trimester was associated with higher odds of GDM (10 µg/m3 increase: OR = 1.89, 95% CI: 1.04-3.49). Each 10 µg/m3 increase in PM2.5 during the 2nd trimester was associated with 17.70% (2.21-33.20), 15.99% (2.96-29.01), 18.82% (4.11-33.52), and 17.10% (3.28-30.92) increase in 1-h, 2-h, Δ1h-fasting (1-h minus fasting), and Δ2h-fasting (2-h minus fasting) blood glucose levels, respectively. PM2.5 exposure at 24th-27th weeks after LMP was associated with increased GDM risk. We identified sensitive exposure windows of 21st-24th weeks for higher 1-h and 2-h blood glucose levels and of 20th-22nd weeks for increased Δ1h-fasting and Δ2h-fasting. CONCLUSIONS: Ambient PM2.5 exposure during the second trimester was associated with higher odds of GDM and higher blood glucose levels. Avoiding exposure to high air pollution levels during the sensitive windows might prevent women from developing GDM.

Identifying pre-conception and pre-natal periods in which ambient air pollution exposure affects fetal growth in the predominately Hispanic MADRES cohort.

BACKGROUND: It is well documented that persons of color experience disproportionate exposure to environmental contaminants, including air pollution, and have poorer pregnancy outcomes. This study assessed the critical windows of exposure to ambient air pollution on in utero fetal growth among structurally marginalized populations in urban Los Angeles. METHODS: Participants (N = 281) from the larger ongoing MADRES pregnancy cohort study were included in this analysis. Fetal growth outcomes were measured on average at 32 [Formula: see text] 2 weeks of gestation by a certified sonographer and included estimated fetal weight, abdominal circumference, head circumference, biparietal diameter and femur length. Daily ambient air pollutant concentrations were estimated for four pollutants (particulate matter less than 2.5 µm (PM2.5) and less than 10 µm (PM10) in aerodynamic diameter, nitrogen dioxide (NO2), and 8-h maximum ozone (O3)) at participant residences using inverse-distance squared spatial interpolation from ambient monitoring data. Weekly gestational averages were calculated from 12 weeks prior to conception to 32 weeks of gestation (44 total weeks), and their associations with growth outcomes were modeled using adjusted distributed lag models (DLMs). RESULTS: Participants were on average 29 years [Formula: see text] 6 old and predominately Hispanic (82%). We identified a significant sensitive window of PM2.5 exposure (per IQR increase of 6 [Formula: see text]3) between gestational weeks 4-16 for lower estimated fetal weight [Formula: see text] averaged4-16 = -8.7 g; 95% CI -16.7, -0.8). Exposure to PM2.5 during gestational weeks 1-23 was also significantly associated with smaller fetal abdominal circumference ([Formula: see text] averaged1-23 = -0.6 mm; 95% CI -1.1, -0.2). Additionally, prenatal exposure to PM10 (per IQR increase of 13 [Formula: see text]3) between weeks 6-15 of pregnancy was significantly associated with smaller fetal abdominal circumference ([Formula: see text] averaged6-15 = -0.4 mm; 95% CI -0.8, -0.1). DISCUSSION: These results suggest that exposure to particulate matter in early to mid-pregnancy, but not preconception or late pregnancy, may have critical implications on fetal growth.

Low-level exposure to lead, mercury, arsenic, and cadmium, and blood pressure among 8-17-year-old participants of the 2009-2016 National Health and Nutrition Examination Survey.

BACKGROUND: Dysregulation of systolic, diastolic blood pressure (SBP, DBP), and pulse pressure (PP) in children may predict elevated blood pressure (BP) in adulthood. Toxicant exposure is widely studied as a risk factor for high BP in adults, but not in children. We assessed the joint associations between lead (Pb), mercury (Hg), arsenic (As), and cadmium (Cd) exposure and SBP, DBP, and PP among 8-17 year-old participants (n = 1642) of the 2009-2016 National Health and Nutrition Examination Survey (NHANES). METHODS: Participants with at least two BP measures were included. Urinary As and Cd were adjusted for urinary creatinine concentrations. Blood Pb, Hg, and urinary As, Cd were natural log-transformed. Bayesian Kernel Machine Regression (BKMR) analyses were conducted to assess the associations between the toxicant mixture and BP measures. Multivariable regression models assessed the associations between individual toxicants, and the four toxicants simultaneously with each of the outcomes. Interactions with sodium intake were tested. RESULTS: Exposure to all toxicants was low, with median (5%, 95%) level: Pb, 0.57 (0.26, 1.60) µg/dL; Hg, 0.37 (0.19, 2.12) µg/L; As, 5.61 (1.37, 33.2) µg/g creatinine, Cd, 0.06 (0.03, 0.23) µg/g creatinine. Toxicant mixture showed a statistically significant, inverse association with DBP, but not other BP measures. Linear regressions revealed no association between toxicants, individually or together, and BP measures. No evidence of interaction of sodium intake with any of the toxicants was observed. CONCLUSIONS: In a nationally representative sample of 8-17 year-olds, we found suggestive inverse association of the mixture of low-level Pb, Hg, As, and Cd, with DBP. Longitudinal studies with multiple toxicants are needed to understand the interactive effects of toxicants on children's BP.

Changes in arachidonic acid (AA)- and linoleic acid (LA)-derived hydroxy metabolites and their interplay with inflammatory biomarkers in response to drastic changes in air pollution exposure.

BACKGROUND: Untargeted metabolomics analyses have indicated that fatty acids and their hydroxy derivatives may be important metabolites in the mechanism through which air pollution potentiates diseases. This study aimed to use targeted analysis to investigate how metabolites in arachidonic acid (AA) and linoleic acid (LA) pathways respond to short-term changes in air pollution exposure. We further explored how they might interact with markers of antioxidant enzymes and systemic inflammation. METHODS: This study included a subset of participants (n = 53) from the Beijing Olympics Air Pollution (BoaP) study in which blood samples were collected before, during, and after the Beijing Olympics. Hydroxy fatty acids were measured by liquid chromatography/mass spectrometry (LC/MS). Native total fatty acids were measured as fatty acid methyl esters (FAMEs) using gas chromatography. A set of chemokines were measured by ELISA-based chemiluminescent assay and antioxidant enzyme activities were analyzed by kinetic enzyme assays. Changes in levels of metabolites over the three time points were examined using linear mixed-effects models, adjusting for age, sex, body mass index (BMI), and smoking status. Pearson correlation and repeated measures correlation coefficients were calculated to explore the relationships of metabolites with levels of serum chemokines and antioxidant enzymes. RESULTS: 12-hydroxyeicosatetraenoic acid (12-HETE) decreased by 50.5% (95% CI: -66.5, -34.5; p < 0.0001) when air pollution dropped during the Olympics and increased by 119.4% (95% CI: 36.4, 202.3; p < 0.0001) when air pollution returned to high levels after the Olympics. In contrast, 13-hydroxyoctadecadienoic acid (13-HODE) elevated significantly (p = 0.023) during the Olympics and decreased nonsignificantly after the games (p = 0.104). Interleukin 8 (IL-8) correlated with 12-HETE (r = 0.399, BH-adjusted p = 0.004) and 13-HODE (r = 0.342, BH-adjusted p = 0.014) over the three points; it presented a positive and moderate correlation with 12-HETE during the Olympics (r = 0.583, BH-adjusted p = 0.002) and with 13-HODE before the Olympics (r = 0.543, BH-adjusted p = 0.008). CONCLUSION: AA- and LA-derived hydroxy metabolites are associated with air pollution and might interact with systemic inflammation in response to air pollution exposure.

Adolescents' Depressive Symptom Experience Mediates the Impact of Long-Term Exposure to Maternal Depression Symptoms on Adolescents' Body Mass Index.

BACKGROUND: Obesity is a cardiovascular disease risk factor and affects approximately 13.7 million U.S. children and adolescents between the ages 2 and 19 years old in 2015-2016. PURPOSE: To determine the relationship between children's average long-term exposure to maternal depressive symptoms age 1 month to Grade 6 and adolescents' body mass index (BMI) z-score at age 15 mediated by the adolescents' depressive symptom experience. METHODS: A total of 1,364 infants and their families from the Eunice Kennedy Shriver National Institute of Child Health and Human Development Study of Early Child Care and Youth Development were recruited. RESULTS: Mediation analyses revealed a significant relationship between children's average long-term exposure to maternal depressive symptoms from age 1 month to Grade 6 and adolescents' BMI z-score at age 15 (total effect = 0.015, p = .013, 95% confidence interval (CI): 0.0032, 0.027). The adolescents' experience of depressive symptoms significantly mediated this relationship (indirect effect = 0.0021, bias-corrected bootstrapped 95% CI: 0.0004, 0.0044), with this mediated relationship more pronounced in girls. CONCLUSIONS: Findings indicate the possible existence of a mediating role of adolescents' depressive symptoms experience in the pathway from average long-term exposure to maternal depressive symptoms during children's early life to adolescents' elevated BMI.

The relation between Helicobacter pylori immunoglobulin G seropositivity and leukocyte telomere length in US adults from NHANES 1999-2000.

BACKGROUND: Helicobacter pylori (H pylori) immunoglobulin G (IgG) seropositivity is prevalent but its relation with leukocyte telomere length (LTL), a cellular aging biomarker, is unclear. METHODS: Among 3,472 participants from the National Health and Nutrition Examination Survey (NHANES) cycle 1999-2000, LTL was measured with the quantitative polymerase chain reaction. H pylori IgG was measured by enzyme-linked immunosorbent assays and defined as seropositivity with an immune status ratio score > 0.9. We used linear regression models to examine the relation of H pylori IgG seropositivity with continuous LTL and logistic regression for the relation with short LTL (<10th percentile of the population distribution) adjusting for potential confounders. We stratified the analyses by a priori selected variables. RESULTS: Population prevalence of H pylori IgG seropositivity was 31.5% in the overall population with higher prevalence found in those with older age, other races than non-Hispanic whites, lower education, and being born out of the United States. Continuous LTL was non-significantly shorter in those with H Pylori IgG seropositivity versus seronegativity (mean difference = -40.3 bp, 95% CI: -112.4, 31.9). This difference was not significant after adjusting for potential confounders nor stratifying by potential effect modifiers. H Pylori IgG seropositivity was significantly associated with short LTL among the elderly (55-75 years, adjusted OR: 3.06, 95% CI: 1.17, 7.99), but not in the overall population (OR: 1.28, 95% CI: 0.81-2.02). CONCLUSION: H Pylori IgG seropositivity was not associated with continuous LTL in the general population but may be associated with an excessively short LTL in the elderly.

Adverse Birth Outcomes and Birth Telomere Length: A Systematic Review and Meta-Analysis.

OBJECTIVES: To synthesize previous findings on the difference in birth telomere length between newborns with and without intrauterine growth restriction (IUGR) or with and without preterm birth. STUDY DESIGN: We systematically searched 3 databases (PubMed, Embase, and Web of Science) for publications that examined the relationships of IUGR or preterm birth with birth telomere length. We conducted meta-analysis to pool the estimated difference in birth telomere length either between IUGR and non-IUGR or between preterm birth and full-term birth. Subgroup analyses were conducted by tissues (newborn blood vs placenta) and techniques used for telomere length measurement (quantitative polymerase chain reaction [qPCR] vs telomere restriction fragment). RESULTS: We included 11 articles on comparing birth telomere length between IUGR (combined n = 227) and non-IUGR (n = 1897) and 7 articles on comparing birth telomere length between preterm birth (n = 182) and full-term birth (n = 1320). We found IUGR was associated with shorter birth telomere length only when birth telomere length was measured in placenta (pooled standardized mean difference [SMD] = -0.85; 95% CI -1.13 to -0.57; IUGR/non-IUGR n = 87/173), but not in newborn blood (pooled SMD = 0.00, 95% CI -0.18 to 0.19; IUGR/non-IUGR n = 148/1733). Birth telomere length was significantly longer in preterm birth than in full-term birth when birth telomere length was measured by qPCR (pooled SMD = 0.40, 95% CI 0.18-0.63; preterm birth/full-term birth n = 137/682) but not by telomere restriction fragment (pooled SMD = 0.05, 95% CI -0.29 to 0.38; preterm birth/full-term birth n = 44/444). CONCLUSIONS: IUGR is associated with shorter placental telomere length and preterm birth is associated with longer birth telomere length measured by qPCR.

Family functioning, moods, and binge eating among urban adolescents.

This study builds upon prior research on associations between moods, family functioning, and binge eating, using ecological momentary assessment to examine moderating effects of family functioning on associations between moods and binge eating. This study was conducted among a nonclinical sample of urban adolescents. Family functioning was assessed using five constructs adopted from the FACES-IV measure: 'family cohesion,' 'family flexibility' 'family communication,' 'family satisfaction,' and 'family balance.' Mood data was gathered using 13 items from a daily affect scale. Binge eating was assessed using two subscales from the Eating Disorder Diagnostic Scale-binge eating associated with 'embarrassment' (BE1), and binge eating associated with a sense of 'loss of control' (BE2). A multilevel modeling approach was employed to examine how associations between momentary moods and binge eating behaviors were moderated by family functioning. Results indicated that measures of negative affect, stress/frustration, and tiredness/boredom were significantly and positively associated with two measures of binge eating (BE1 and BE2; p values ≤ 0.05), and that multiple factors of family functioning buffered the positive predictive effects of moods on binge eating. Findings indicate the importance of inclusion of family functioning in the development of eating behavior interventions for adolescents.

Impact of childhood parent-child relationships on cardiovascular risks in adolescence.

This study aims to determine prospective effects of the childhood parent-child relationships on the development of cardiovascular risks in adolescence. Using available 917 parent-child dyads from the Study of Early Child Care and Youth Development (1991 to 2006), we analyzed the prospective effects of childhood parent-child relationships of Conflict and Closeness, as well as their categorized combinations (Harmonic, Dramatic, Hostile, and Indifferent) on the development of subscapular and triceps skinfold thickness (SST/TST), body mass index (BMI), systolic and diastolic blood pressure (SBP/DBP), and heart rate (HR) during adolescence. We found that higher levels of Conflict in the relationship with mothers (slope=0.05, P<0.001) and fathers (slope=0.04, P=0.03) increased the growth rate of TST among girls during adolescence, but not among boys. The maternal-girl dyadic with higher Conflict scores also increased girl's growth rate of BMI percentile (slope=0.10, P=0.02), though the paternal-boy dyadic with higher Conflict scores decreased boy's growth rate of BMI percentile (slope=-0.13, P=0.04). A Hostile maternal-son relationship lowered boy's growth rate of SBP (slope=-3.15, P<0.001) and DBP (slope=-4.42, P<0.001). A Dramatic maternal-son relationship increased boy's growth rate of SST (slope=0.89, P<0.001) and TST (slope=0.64, P=0.03). Hostile paternal-daughter relationships were positively associated with the growth rate of TST (slope=0.28, P=0.03). Overall, there was a significant influence of childhood parent-child relationships on the development of cardiovascular risks during adolescence, and the effect was further modified by both parents' and child's gender.