Association of prenatal exposure to PM2.5 and its chemical constituents with early childhood obesity: A population-based study.

Associations of early-life exposure to PM2.5 mass and its components with childhood anemia: A cross-sectional study in China, India, and Africa.

Childhood anemia remains a major public health concern, but evidence regarding the associations of early-life exposure to PM2.5 mass and its components with childhood anemia across regions remains limited. We conducted a cross-sectional study of 449,894 children under 5 years from China, India, and 26 African countries. Prenatal, postnatal, and cumulative exposures to PM2.5 and five components, including black carbon, organic carbon, sulfate, dust, and sea salt, were estimated using NASA's MERRA-2 reanalysis data. The prevalence of childhood anemia was 26.9% in China, 62.6% in India, and 64.5% in Africa. In multivariable logistic regression models, each 1 μg/m3 increase in cumulative PM2.5 exposure was associated with higher odds of childhood anemia in China (odds ratio [OR] = 1.019, 95% confidence interval [CI]: 1.009, 1.028), India (OR = 1.009, 95% CI: 1.008, 1.009), and Africa (OR = 1.001, 95% CI: 1.000, 1.002). Organic carbon and dust also showed positive associations across all three regions. The population attributable fractions (PAFs) for cumulative PM2.5 exposure were 28.46% in China, 10.64% in India, and 0.69% in Africa. Among the individual components, organic carbon and black carbon had the largest positive PAF estimates in China, dust had the largest estimate in India, and organic carbon and dust had the largest positive estimates in Africa. Overall, our findings highlight the potential value of region-specific air-quality strategies that address total PM2.5 mass while prioritizing locally relevant components, particularly carbonaceous aerosols in China, dust-related PM2.5 in India, and organic carbon and dust in Africa.

Prenatal bisphenols and ambient air pollutants are differentially associated with early childhood length and weight from birth to 36 months: a multi-domain mixture analysis in a Korean birth cohort.

Prenatal exposure to environmental chemicals has been implicated in impaired fetal and early childhood growth. However, most previous studies have focused on single exposure domains, limiting understanding of the combined effects of co-occurring chemical mixtures. We investigated the joint effects of a prenatal multi-domain chemical mixture comprising endocrine-disrupting chemicals (EDCs), heavy metals, and ambient air pollutants on infant growth from birth to 36 months using data from the Korean Children's Environmental Health Study (Ko-CHENS), a nationwide prospective birth cohort of 5,056 mother-child pairs. We applied weighted quantile sum (WQS) regression and Bayesian kernel machine regression (BKMR) to estimate mixture effects and identify key contributing exposures, WQS and BKMR were fitted separately at each of five assessment ages, and a latent class mixed model (LCMM) was used to characterize prenatal exposure trajectory subgroups, whose association with repeated growth measures was then evaluated in a linear mixed model. Ten mixture-outcome tests (two outcomes x five ages) were pre-specified as primary and were corrected for multiplicity using the Benjamini-Hochberg false discovery rate (FDR) procedure. WQS regression identified a significant inverse association between the prenatal chemical mixture and infant length-for-age z-scores at birth and 6 months, with late-pregnancy BPF and BPS consistently emerging as the top-weighted contributors; both associations remained below a 5% FDR threshold. Overall mixture effects estimated by BKMR were null at every assessment age, although BKMR suggested nonlinear and exposure-specific dose-response relationships involving bisphenol analogues and ambient air pollutants across multiple assessment time points. No significant associations were observed between LCMM-derived exposure trajectory class and longitudinal growth outcomes through 36 months. Domain-specific patterns were observed across both analyses: bisphenol analogues showed more consistent associations with length outcomes, whereas ambient air pollutants were more frequently identified as key contributors in weight-related models. These exploratory findings suggest that prenatal exposure to bisphenol analogues and ambient air pollutants may be associated with early childhood growth and warrants further investigation. They support the use of mixture-based approaches in environmental health research but should not be interpreted as evidence of causal effects.

The association between prenatal PM2.5 constituent exposure and gestational diabetes mellitus: Exploratory analysis of the potential modifying role of thyroid hormones.

The associations of PM2.5 constituents with blood glucose and GDM remain unclear, and the interplay between PM2.5 exposure and thyroid hormone levels in relation to GDM has not been well characterized. This retrospective cohort study included 1314 pregnant women with data collected through multiple methods. A generalized linear model analyzed PM2.5-glucose links, logistic regression assessed pollutant-GDM associations, and stratified analyses explored these relationships at different thyroid hormone levels. In the study population, first-trimester exposure to SO42- and BC correlated positively with FBG, as did PM2.5 and its components in the second trimester. First-trimester SO4²⁻ exposure (OR=1.26, 95% CI: 1.06, 1.51) and second-trimester exposures to PM2.5 (OR=1.67, 95% CI: 1.19, 2.35), NO3⁻ (OR=1.34, 95% CI: 1.06, 1.68), and NH4⁺ (OR=1.33, 95% CI: 1.06, 1.65) were associated with increased GDM risk. Stratified analyses showed that second-trimester BC and OM were positively correlated with FBG in the high-TSH and low-FT4 strata, respectively. In addition, first-trimester exposure to SO42- (high TSH: OR = 1.42, 95% CI: 1.10, 1.84; low FT4: OR = 1.35, 95% CI: 1.05, 1.74) and to PM2.5 (high TSH: OR = 1.93, 95% CI: 1.14, 3.27; low FT4: OR = 1.82, 95% CI: 1.46, 2.25) in the second trimester were associated with higher odds of GDM. These findings show that PM2.5 exposure was associated with glucose dysregulation and GDM in pregnant women differently by trimester and component. Across the separate TSH- and FT4-stratified analyses, women in the high-TSH and low-FT4 strata, respectively, appeared to show greater susceptibility to air pollution-related GDM. These subgroup findings should therefore be interpreted as exploratory and require validation in future studies.

Maternal exposure to particulate matter during pregnancy and offspring liver function.

Air pollution is associated with hepatic dysfunction, but the evidence in the early childhood remains limited. This study aimed to explore the associations between maternal exposure to particulate matter and offspring liver function, as indicated by serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in children aged 1-2 years. Based on the Fujian Birth Cohort Study (FJBCS), a total of 1046 mother-offspring pairs were analyzed in this study. Maternal mean exposures to PM1, PM2.5 and PM10 were calculated for the entire gestational period and each of the three trimesters. Linear regression models were used and restricted cubic spline (RCS) models were further applied to explore the exposure-response relationships. Distributed lag models (DLMs) were conducted to examine the weekly associations throughout pregnancy. Results show that positive associations were found between maternal exposure and offspring enzyme levels in the entire pregnancy as well as the second trimester alone. After adjustment, an interquartile range (IQR) increment in PM1, PM2.5 and PM10 in the second trimester was associated with increases in ALT by 1.42 (0.82-2.03) U/L, 1.41 (0.77-2.05) U/L, 0.91 (0.35-1.46) U/L, and in AST by 1.64 (1.00-2.29) U/L, 1.56 (0.88-2.23) U/L and 0.80 (0.21-1.39) U/L, respectively. DLM analyses further indicated that the associations were the most pronounced during the second trimester. Our findings suggest that maternal exposure to particulate matter is positively associated with increased levels of ALT and AST in offspring, with the second trimester representing a potentially sensitive period.

Prenatal and childhood exposure to mixtures of endocrine-disrupting chemicals in association with measures of adiposity in childhood and adolescence.

BACKGROUND Childhood obesity is a global public health crisis. Endocrine-disrupting chemicals (EDCs) - widespread pollutants that interfere with hormonal and metabolic systems - may contribute to excessive adiposity. The combined, long-term, and mechanistic effects of multi-class EDC mixtures remain unexplored. METHODS We analyzed 1301 mother-child pairs from the Human Early Life Exposome (HELIX) project, spanning six European cohorts. Prenatal and childhood exposures to 45 EDCs across nine chemical classes were measured in maternal and child biospecimens. Thirty-six plasma proteins were quantified in childhood using targeted proteomic panels. Adiposity outcomes in childhood (6-11 years) and adolescence (12-18 years) included BMI z-scores, waist circumference, and body fat percentage. We applied penalized Lasso-type Bayesian Weighted Quantile Sum Regression to assess mixtures, a signed iterative random forest for interactions, and mediation analyses for biological pathways. RESULTS Prenatal metal and organochlorine pesticide mixtures were associated with higher BMI z-scores in childhood and adolescence and 47-48 % higher odds of overweight. Prenatal PFAS exposure was associated with higher body-fat percentage in both periods. Childhood phenol and high-molecular-weight phthalate exposures were associated with higher adolescent zBMI, whereas parabens and persistent compounds showed inverse associations. Childhood metal exposures were associated with higher body-fat percentage and overweight odds. An inflammatory-metabolic protein pattern mediated ∼ 30 % of the prenatal metal-adolescent zBMI association. CONCLUSIONS Early-life exposure to EDC mixtures may reprogram metabolic and inflammatory pathways, predisposing children to obesity that persists into adolescence. These findings provide mechanistic evidence linking chemical exposures to the global obesity epidemic and underscore the urgent need for policies preventing EDC exposure during critical developmental periods.

Prenatal exposure to PM2.5 components and fetal growth: identifying critical gestational weeks and key toxic components in a Chinese birth cohort.