Dioxin-like polychlorinated biphenyls (DL-PCBs) are persistent environmental pollutants known to induce oxidative stress and inflammation, which may accelerate telomere shortening and affect neurodevelopment. We hypothesized that DL-PCB exposure contributes to cognitive deficits in children by accelerating telomere attrition, which in turn impairs brain function. We analyzed serum DL-PCB levels, leukocyte telomere length (LTL), and cognitive performance in 1756 primary school children (aged 7–10 years) from Shenyang, China. Twelve DL-PCB congeners were measured, and cognitive outcomes were assessed using a standardized test battery, including the n-back task (Two-Back and Three-Back) and the Attentional Network Test (ANT). LTL was quantified via qRT-PCR. Linear mixed models, mixture analyses (Quartile g-computation analysis (g-comp), Generalized Weighted Quantile Sum regression (gWQS), Bayesian Kernel Machine Regression (BKMR) ), and mediation analysis were applied, adjusting for relevant covariates. Serum concentrations of PCB77, PCB126, and PCB189 were significantly associated with shorter LTL after Bonferroni correction (β = −0.041 for PCB189 per IQR increase, adjusted p = 0.001). PCB81 and PCB189 showed robust negative associations with superior working memory (Three-Back task; adjusted p < 0.05), while basic working memory (Two-Back) exhibited no significant associations. Inattentiveness (HRT-SE) was negatively associated with PCB157, PCB167, PCB169, and PCB189 in crude models, but these associations were attenuated after correction. Mixture analyses confirmed that DL-PCB mixtures were strongly associated with shorter LTL (g-comp β = −0.104, p < 0.001; gWQS β = −0.055, p < 0.001), as well as poorer superior working memory and inattentiveness. Mediation analysis revealed that LTL explained approximately 5–10
Wildland fires are a significant source of pollution that can cause sudden changes in ground-level ambient fine particulate matter (PM2.5), an exposure that has been associated with gestational blood pressure increases. However, estimating the health risks specific to wildland fire smoke PM2.5 is often encumbered by limitations to smoke plume modeling. We utilized a novel approach to estimate and characterize wildland fire smoke PM2.5 in Reno, Nevada, USA, an area prone to seasonal smoke from wildland fires. Daily, 24-h averaged, plume-specific wildland fire smoke PM2.5 concentrations were estimated at two air quality monitoring stations, and each plume was categorized by both the intensity of the source fire (high vs. low intensity) and the primary fuel type (forest, shrub/scrub, grassland, and other). Using electronic medical records (2012–2019), we identified a set of healthcare encounters of pregnant individuals, assigned these encounters to the air quality monitor closest to the maternal residential address at the time of the encounter and estimated the acute effects (0 to 3 day lag periods) of wildland fire smoke PM2.5 on maternal systolic and diastolic blood pressure measures across gestational periods using a multi-level linear regression model. We evaluated 132,570 clinical encounters with a blood pressure measurement over 22,399 pregnancies (median 4.0 measures per pregnancy). Overall, we found null associations between wildland fire smoke PM2.5 and maternal blood pressure, regardless of the lag period. However, there was evidence that suggested associations could differ between gestational exposure periods, as positive associations not meeting statistical significance criteria were observed for almost all first trimester exposures. Associations did not differ by fire intensity or fuel type. We did not find evidence for short-term associations between wildland fire smoke PM2.5 and maternal blood pressure. Similar to other studies in the field, challenges to modeling smoke plumes and subjects altering their behavior during smoke events may be impacting the analyses.
Abstract Background Plasma per- and polyfluoroalkyl substances (PFAS) are associated with immune dysfunction, including childhood antibody response. We evaluated whether first trimester maternal plasma PFAS concentrations are associated with mid-childhood MMR (measles, mumps, rubella) and DTaP (diphtheria, tetanus, pertussis) antibody titers. Methods We measured six PFAS (EtFOSSA, MeFOSSA, PFHxS, PFNA, PFOA, PFOS) in first trimester plasma from participants in the longitudinal Project Viva cohort, recruited 1999–2002 in eastern Massachusetts. We measured mid-childhood plasma MMR and DTaP antibody titers. We restricted the analytical sample to children fully vaccinated, according to 2007 United States Center for Disease Control guidelines and used covariate-adjusted quantile g-computation and regression analyses to estimate associations ( n = 333–416). Results Median [interquartile range (IQR)] age at antibody titer blood draw was 7.7 years (7.4, 8.4), and children received their most recent MMR or DTaP dose at median (IQR) 4.3 years (4.1, 5.0). The PFAS mixture was associated with lower antibody titers, except for measles, although none of the associations reached statistical significance. A one unit (ng/mL) increase in EtFOSSA was associated with higher measles antibody titers [β = 0.02, 95% confidence interval (CI) = 0.01, 0.04 antibody (Ab) index]. A one ng/mL increase in MeFOSSA was associated with − 6.8% (95% CI: -11.9, -1.3) lower pertussis antibody titers. There was evidence of effect modification by infant sex for prenatal PFOS and childhood pertussis antibody titers, with higher prenatal PFOS associated with lower antibody titers in females and higher in males, although neither association reached statistical significance. Conclusions While the prenatal PFAS mixture was not significantly associated with childhood antibody titers in our cohort, we observed individual associations between EtFOSSA and higher measles antibody titers and MeFOSSA and lower pertussis antibody titers. Overall, we found limited evidence of associations between first trimester plasma PFAS and mid-childhood antibody titers in our cohort. Trial registration Clinical trial number: not applicable.
Bisphenol A (BPA) is a high production volume chemical that has been used for decades in numerous consumer and industrial applications. Daily exposure to BPA is likely; it is readily detected in >90
Childhood lead exposure remains a significant public health concern, particularly in urban settings with persistent socioeconomic disadvantage. Although prior studies have linked lead exposure to adverse neurodevelopmental outcomes, evidence using clinically diagnosed neurobehavioral disorders at contemporary low blood lead levels (BLLs) is limited. We conducted a retrospective cohort study of children aged 11 years or younger who received care through the Temple University Health System in Philadelphia, Pennsylvania, between 2010 and 2020. BLLs were obtained from electronic health records and analyzed as continuous measures and dichotomized at 3.5 µg/dL. Attention-deficit/hyperactivity disorder (ADHD) and conduct disorders were identified using international classification diagnoses (ICD) codes, and only incident diagnoses occurring after blood lead measurement were considered. Multivariable logistic regression models were fit adjusted for individual- and neighborhood-level sociodemographic factors selected using a directed acyclic graph framework. Sex-stratified analyses were conducted to assess effect modification. Among 13,989 children included in the ADHD analysis, 751 (5.4
