RESUMEN
The oxidative potential (OP) of particulate matter (PM) is a major driver of PM-associated health effects. In India, the emission sources defining PM-OP, and their local/regional nature, are yet to be established. Here, to address this gap we determine the geographical origin, sources of PM, and its OP at five Indo-Gangetic Plain sites inside and outside Delhi. Our findings reveal that although uniformly high PM concentrations are recorded across the entire region, local emission sources and formation processes dominate PM pollution. Specifically, ammonium chloride, and organic aerosols (OA) from traffic exhaust, residential heating, and oxidation of unsaturated vapors from fossil fuels are the dominant PM sources inside Delhi. Ammonium sulfate and nitrate, and secondary OA from biomass burning vapors, are produced outside Delhi. Nevertheless, PM-OP is overwhelmingly driven by OA from incomplete combustion of biomass and fossil fuels, including traffic. These findings suggest that addressing local inefficient combustion processes can effectively mitigate PM health exposure in northern India.
RESUMEN
A comprehensive chemical characterization of fine particulate matter (PM2.5) was conducted at an urban site in one of the most densely populated cities of Vietnam, Hanoi. Chemical analysis of a series of 57 daily PM2.5 samples obtained in 2019-2020 included the quantification of a detailed set of chemical tracers as well as the oxidative potential (OP), which estimates the ability of PM to catalyze reactive oxygen species (ROS) generation in vivo as an initial step of health effects due to oxidative stress. The PM2.5 concentrations ranged from 8.3 to 148 µg m-3, with an annual average of 40.2 ± 26.3 µg m-3 (from September 2019 to December 2020). Our results obtained by applying the Positive Matrix Factorization (PMF) source-receptor apportionment model showed the contribution of nine PM2.5 sources. The main anthropogenic sources contributing to the PM mass concentrations were heavy fuel oil (HFO) combustion (25.3 %), biomass burning (20 %), primary traffic (7.6 %) and long-range transport aerosols (10.6 %). The OP activities were evaluated for the first time in an urban site in Vietnam. The average OPv levels obtained in our study were 3.9 ± 2.4 and 4.5 ± 3.2 nmol min-1 m-3 for OPDTT and OPAA, respectively. We assessed the contribution to OPDTT and OPAA of each PM2.5 source by applying multilinear regression models. It shows that the sources associated with human activities (HFO combustion, biomass burning and primary traffic) are the sources driving OP exposure, suggesting that they should be the first sources to be controlled in future mitigation strategies. This study gives for the first time an extensive and long-term chemical characterization of PM2.5, providing also a link between emission sources, ambient concentrations and exposure to air pollution at an urban site in Hanoi, Vietnam.
RESUMEN
BACKGROUND: Fine particulate matter (PM2.5) has been found to be detrimental to respiratory health of children, but few studies have examined the effects of prenatal PM2.5 oxidative potential (OP) on lung function in infants and preschool children. OBJECTIVES: We estimated the associations of personal exposure to PM2.5 and OP during pregnancy on offspring objective lung function parameters and compared the strengths of associations between both exposure metrics. METHODS: We used data from 356 mother-child pairs from the SEPAGES cohort. PM filters collected twice during a week were analyzed for OP, using the dithiothreitol (DTT) and the ascorbic acid (AA) assays, quantifying the exposure of each pregnant woman. Lung function was assessed with tidal breathing analysis (TBFVL) and nitrogen multiple-breath washout (N2MBW) test, performed at 6 wk, and airwave oscillometry (AOS) performed at 3 y. Associations of prenatal PM2.5 mass and OP with lung function parameters were estimated using multiple linear regressions. RESULTS: In neonates, an interquartile (IQR) increase in OPvDTT (0.89 nmol/min/m3) was associated with a decrease in functional residual capacity (FRC) measured by N2MBW [ß=-2.26mL; 95% confidence interval (CI): -4.68, 0.15]. Associations with PM2.5 showed similar patterns in comparison with OPvDTT but of smaller magnitude. Lung clearance index (LCI) and TBFVL parameters did not show any clear association with the exposures considered. At 3 y, increased frequency-dependent resistance of the lungs (Rrs7-19) from AOS tended to be associated with higher OPvDTT (ß=0.09 hPa×s/L; 95% CI: -0.06, 0.24) and OPvAA (IQR=1.14 nmol/min/m3; ß=0.12 hPa×s/L; 95% CI: -0.04, 0.27) but not with PM2.5 (IQR=6.9 µg/m3; ß=0.02 hPa×s/L; 95% CI: -0.13, 0.16). Results for FRC and Rrs7-19 remained similar in OP models adjusted on PM2.5. DISCUSSION: Prenatal exposure to OPvDTT was associated with several offspring lung function parameters over time, all related to lung volumes. https://doi.org/10.1289/EHP11155.
