The effects of prenatal PM2.5 oxidative potential exposure on feto-placental vascular resistance and fetal weight: A repeated-measures study.

BACKGROUND: Feto-placental hemodynamic deterioration is a critical contributing factor to fetal growth restriction. Whether PM2.5 oxidative potential (OP) affects feto-placental hemodynamics and what impact is on estimated fetal weight (EFW) have not been fully elucidated. We sought to evaluate the association of PM2.5 OP with EFW and to explore whether feto-placental vascular impedance hemodynamic change is a possible mediator in this association. METHODS: A repeated-measures study was conducted involving sixty pregnant women with at least 26 weeks of follow-up during pregnancy in Guangzhou, China, from September 2017 to October 2018. Daily filter-based PM2.5 samples were prospectively collected from ground monitors, and estimates of OP for PM2.5 and its metallic (OPv-metal) and non-metallic constituents (OPv-nonmental) were determined by dithiothreitol assay. Ultrasound data of fetal growth and umbilical arterial resistance, including estimated fetal weight (EFW), pulsatility index, resistance index, and systolic-to-diastolic ratio, were also obtained during gestation. Generalized estimating equations and polynomial distribution lag models were applied to analyze the associations of maternal exposure to PM2.5 OP with EFW and umbilical artery indices. Causal mediation analysis was used to evaluate the mediating role of umbilical arterial resistance. RESULTS: Prenatal exposure to ambient PM2.5 OP was significantly inversely associated with EFW. The magnitudes of effects of OPv-nonmetal on EFW were larger than those of OPv-metal. Significant mediation for the relationship between PM2.5-related OP and EFW by increased impedance in the umbilical artery was observed, with the estimated percent mediated ranging from 31% to 61%. The estimated percent mediated for OPv-nonmetal was higher than those for OPv-metal. CONCLUSIONS: Findings suggest that increased impedance in the umbilical artery may be one of the potential mediators of the relationship between PM2.5 oxidative potential exposure and low fetal weight.

Role of antenatal anxiety in the relationship between maternal exposure to nitrogen dioxide and small for gestational age: A birth cohort study.

BACKGROUND: Both Nitrogen dioxide (NO2) exposure and antenatal anxiety have individually been associated with small for gestational age (SGA). Little is known, however, about whether there is effect modification of antenatal anxiety on NO2-related SGA. METHODS: The prospective birth cohort study included 1823 mother-newborn pairs in Guangzhou, China, from January 2017 to April 2020. Exposure to NO2 during the pre-conceptional and prenatal periods was estimated using an inverse distance weighted method. Antenatal anxiety was assessed by Trait Anxiety Inventory. SGA was determined by the Chinese gestational age- and sex-specific birthweight standards. Cox proportional hazards regression models was used to estimate hazard ratios (HRs) and 95 % confidence intervals (CIs) for SGA as per 10 µg/m3 increase in NO2. Modifying effects of trait anxiety on NO2-related SGA were identified by stratified analyses, and three-dimensional response surface plots and two-dimensional heat maps. RESULTS: Each 10 µg/m3 increase in NO2 exposure during the third trimester was significantly associated with SGA risk among overall participants (HR = 1.221, 95 % CI: 1.014-1.471) and primipara (HR = 1.271, 95 % CI: 1.023-1.579). We found significant effect modification of anxiety level for NO2-related SGA in the third trimester (Pinteraction < 0.05). Pregnant women with higher levels of trait anxiety were more likely to deliver SGA newborns, particularly for those with high trait anxiety (HR = 1.781, 95 % CI: 1.007-2.945). Primiparous women were more susceptible. CONCLUSIONS: This study provides evidence that antenatal trait anxiety may modify the effects of maternal NO2 exposure on SGA risk. The third trimester could be a critical window of susceptibility.

Insights into the source-specific health risk of ambient particle-bound metals in the Pearl River Delta region, China.

Quantification of source-specific health risks of PM2.5 plays an essential role in health-oriented air pollution control. However, there is limited evidence supporting the source-based risk apportionment of particle-bound metals. In this study, source-specific cancer and non-cancer risk characterization of 12 particle-bound metals was performed in the Pearl River Delta (PRD) region, China. A combination of health risk assessment model and receptor-based source apportionment modeling with positive matrix factorization (PMF) was applied for characterizing the spatial-temporal patterns for inhalation health risks of particle-bound metals in three main city clusters, inland area and coastal area in the region from December 2014 through July 2016. Results showed that the carcinogenic risk of particle-bound metals for adults (4.13 × 10-5) was higher than that for children (9.53 × 10-6) in the PRD region. The highest and significant non-carcinogenic risk was found in the northwest city cluster. Industrial emission (63.3%) were the dominant contributors to the cancer risk, while the main contributors to the non-cancer risk were the vehicle emission source (33.2%) in the dry season and industrial emission (30.8%) in the wet season. Our results provide important evidence for spatial source-specific health risks with temporal characteristics of particle-bound metals in most densely populated areas in the southern China, and suggest that reduction of industrial and vehicle emissions could facilitate more cost-effective PM2.5 control measures to improve human health.