Early pregnancy PM2.5 exposure and its inorganic constituents affect fetal growth by interrupting maternal thyroid function.

Early pregnancy is crucial for fetal growth. Maternal thyroid hormone is critical for fetal growth and can be disturbed under exogenous exposure. However, it's uncertain whether exposure to PM2.5 and inorganic constituents during early pregnancy can affect TH and fetal growth. We focused on the associations of early-pregnancy PM2.5 and inorganic constituents with fetal growth and maternal THs. PM2.5 concentration was estimated using a satellite-based spatiotemporal model. Fetal biparietal diameter (BPD), head circumference (HC), femur length (FL), and humerus length (HL) were measured by ultrasonography at median 15.6, 22.2, and 33.1 gestational weeks. Levels of 28 PM2.5 constituents were measured in a sub-group of 329 pregnancies. Maternal serum free thyroxine (fT4), free triiodothyronine, and thyroid-stimulating hormone levels were measured at 14 weeks of gestation. Mixed-effect models and multiple linear regression were applied to evaluate the associations of PM2.5 and its constituents with fetal growth measures. Mediation analysis was used to examine the mediating role of the THs. Results showed that each 10 µg/m3 increase in PM2.5 was associated with 0.20 mm reductions in BPD (95%CI: 0.33, -0.01), 0.27 mm decreases in FL (95%CI: 0.40, -0.13), and 0.36 decreases in HL (95%CI: 0.49, -0.23). Per 10 µg/m3 increment in PM2.5 was correlated with 5.82% decreases in the fT4 level (95% CI: 8.61%, -2.96%). FT4 accounted for 14.3% of PM2.5 exposure-induced change in BPD at first follow-up. Al (ß = -2.91, 95%CI: 5.17, -0.66), Si (ß = -1.20, 95%CI: 2.22, -0.19), K (ß = -3.09, 95%CI: 5.41, -0.77), Mn (ß = -47.20, 95%CI: 83.68, -10.79) and Zn (ß = -3.02, 95%CI: 5.55, -0.49) were associated with decreased fetal BPD, especially in first follow-up. Zn (ß = -38.12%, 95% CI: 58.52%, -8.61%) was also associated with decreased fT4 levels. Overall, early pregnancy exposure to PM2.5 and its constituents was associated with fetal growth restriction and decreased maternal fT4 levels might mediate the effect of PM2.5.

Prenatal exposure to ambient fine particulate matter and early childhood neurodevelopment: A population-based birth cohort study.

Although previous studies have reported the adverse effect of air pollution exposure during pregnancy on neurodevelopment in children, epidemiological evidence is limited, and the results are inconsistent. This study aimed to explore the association between prenatal ambient fine particulate matter (PM2.5) exposure and early childhood neurodevelopment in a large birth cohort study of 4009 maternal-child pairs. Prenatal daily PM2.5 exposure concentrations at 1 km spatial revolution were estimated using high-performance machine-learning models. Neurodevelopmental outcomes of children at ages 2, 6, 12, and 24 months were assessed using the Ages and Stages Questionnaire (ASQ). Distributed lag nonlinear models were used to identify critical windows of prenatal PM2.5 exposure. General linear mixed models with binomially distributed errors were used to estimate the effect of prenatal PM2.5 exposure on suspected developmental delay (SDD) in five developmental domains based on the longitudinal design. Prenatal PM2.5 exposure was significantly associated with decreased scores for all neurodevelopmental domains of children at ages 2, 6, and 24 months. Each 10-µg/m3 increase in PM2.5 exposure was significantly associated with increased risk of SDD for all subjects (RR: 1.52 95% CI: 1.19, 2.03), specifically, in problem-solving domain for girls (RR: 2.23, 95% CI: 1.22, 4.35). Prenatal PM2.5 exposure in weeks 18 to 34 was significantly associated with both ASQ scores and SDDs. Our study proposed that prenatal PM2.5 exposure affected early childhood neurodevelopment evaluated with the ASQ scale. PM2.5 exposure might increase the risk of SDD for boys and girls, specifically in the problem-solving domain for girls.

[Exposure Levels, Sources, and Health Risks of Heavy Metal Components of PM2.5 in Housewives in Rural Shanghai].

To investigate exposure characteristics and potential health risk of PM2.5-bound heavy metals in housewives in rural areas, 265 personal exposure samples from 143 subjects were collected in the Songjiang district, Shanghai from February 2017 to June 2018. Mass concentrations of 13 elements in PM2.5 were determined by energy-dispersive X-ray fluorescence spectrometry (ED-XRF). The sources of heavy metal components in PM2.5 were analyzed using positive matrix factorization (PMF). The inhalation health risks of exposure to Ni, V, Cr, Mn, As, and Pb were analyzed using the US EPA health risk assessment model. The results showed that the average concentration of personal exposure to PM2.5 was 40.61 µg·m-3 in housewives, which was higher than the concentration at peripheral monitoring stations. The carcinogenic risks of Cr(Ⅵ)and As exceeded the acceptable risk level (10-6). The non-carcinogenic risks of V, Cr(Ⅵ), Mn, Ni, and As were all below the safety threshold, while the total non-carcinogenic risks of these five elements were higher than the safety threshold (>1). The results of PMF indicated that resuspended dust and indoor dust(43.8%), the metallurgy industry(34.6%), coal combustion(14.5%), and fossil-fuel combustion(7.2%)were the major sources of ten elements (Al, Ti, V, Cr, Mn, Fe, Ni, Zn, As, and Pb) in PM2.5. Based on the results of health risk assessment of pollution sources, control measures on the metallurgy industry and fossil-fuel combustion should be further strengthened.

Personal exposure to PM2.5 constituents associated with gestational blood pressure and endothelial dysfunction.

Ambient fine particulate matter (PM2.5) pollution has been implicated in the development of hypertensive disorders of pregnancy. However, evidence on the effects of PM2.5-derived chemical constituents on gestational blood pressure (BP) is limited, and the potential mechanisms underlying the association remain unclear. In this study, we repeated three consecutive 72-h personal air sampling and BP measurements in 215 pregnant women for 590 visits during pregnancy. Individual PM2.5 exposure level was assessed by gravimetric method and 28 PM2.5 chemical constituents were analyzed by ED-XRF method. Plasma biomarkers of endothelial function and inflammation were measured using multiplexed immunoassays. Robust multiple linear regression models were used to estimate the associations among personal PM2.5 exposure and chemical constituents, BP changes (compared with pre-pregnancy BP) and plasma biomarkers. Mediation analyses were performed to evaluate underlying potential pathways. Result showed that exposure to PM2.5 was significantly associated with increases in systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) in the early second trimester. Meanwhile, elevated concentration of lead (Pb) constituent in PM2.5 was significant associated with increases in DBP and MAP after adjusting for PM2.5 total mass. PM2.5 and Pb constituent also presented positive associations with plasma biomarkers of endothelial function (ET-1, E-selectin, ICAM-1) and inflammation (IL-1ß, IL-6, TNFα) significantly. After multiple adjustment, elevated ET-1 and IL-6 were significantly correlated with increased gestational BP, and respectively mediated 1.24%-25.06% and 7.01%-10.69% of the increased BP due to PM2.5 and Pb constituent exposure. In conclusion, our results suggested that personal exposure to PM2.5 and Pb constituent were significantly associated with increased BP during pregnancy, and the early second trimester might be the sensitive window of PM2.5 exposure. The endothelial dysfunction and elevated inflammation partially mediated the effect of PM2.5 and Pb constituent on BP during pregnancy.