Ultra-high-resolution mapping of ambient fine particulate matter to estimate human exposure in Beijing.
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ABSTRACT:
SUBMITTER: Wang Y
PROVIDER: S-EPMC7615407 | biostudies-literature | 2023 Dec
REPOSITORIES: biostudies-literature
Publications
Ultra-high-resolution mapping of ambient fine particulate matter to estimate human exposure in Beijing.
Wang Yongyue Y Li Qiwei Q Luo Zhenyu Z Zhao Junchao J Lv Zhaofeng Z Deng Qiuju Q Liu Jing J Ezzati Majid M Baumgartner Jill J Liu Huan H He Kebin K
Communications earth & environment 20231201
With the decreasing regional-transported levels, the health risk assessment derived from fine particulate matter (PM<sub>2.5</sub>) has become insufficient to reflect the contribution of local source heterogeneity to the exposure differences. Here, we combined the both ultra-high-resolution PM<sub>2.5</sub> concentration with population distribution to provide the personal daily PM<sub>2.5</sub> internal dose considering the indoor/outdoor exposure difference. A 30-m PM<sub>2.5</sub> assimilatin ...[more]
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Project description:Ambient air pollution of fine particulate matter with diameters less than 2.5 μm (PM2.5) is associated with millions of premature deaths per year, recognized as a leading global health concern. The dose-response relation between ambient PM2.5 exposure and mortality risk is the most fundamental information for assessments of the health effects of PM2.5. The existing dose-response relations were generally developed based on the assumption of equal contribution to toxicity from various sources. However, the sources of PM2.5 may significantly influence health effects. In this study, we conducted an ecological study to investigate the global long-term correlation between source-specific PM2.5 exposure and cause-specific mortality risk (SPECM) based on the regional aggregate data of the publically available official health databases from 528 regions worldwide with a total registered population of 3.2 billion. The results provided preliminary epidemiological evidence for differing chronic health effects across various sources. The relative mortality risks of lung cancer and circulatory diseases were closely correlated with the primary emissions from industrial and residential combustion sources. Chronic lower respiratory diseases were mostly associated with the mass concentration of particulate matter.
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Project description:BackgroundAmbient fine particulate matter (PM2.5) exposure adversely impacts child airway health; however, research on prenatal PM2.5 exposure, and child lung function is limited. We investigated these associations in the ECHO-PATHWAYS Consortium, focusing on the role of exposure timing during different phases of fetal lung development.MethodsWe included 675 children in the CANDLE cohort born between 2007 and 2011 in Memphis, TN, USA. Prenatal exposure to ambient PM2.5 was estimated using a spatiotemporal model based on maternal residential history and averaged over established prenatal periods of lung development. Forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC) were measured by spirometry at age 8-9 years. We used linear regression and Bayesian Distributed Lag Interaction Models (BDLIM) to estimate associations between exposure and lung function z-scores, adjusting for maternal/child characteristics, prenatal/postnatal tobacco exposure, and birth year/season, and evaluating effect modification by child sex and allergic sensitization.ResultsThe average ambient concentration of PM2.5 during pregnancy was 11.1 µg/m3 (standard deviation:1.0 µg/m3). In the adjusted linear regression and BDLIM models, adverse, but not statistically significant, associations were observed between exposure during the pseudoglandular (5-16 weeks of gestation) and saccular (24-36 weeks) phases of lung development and FEV1 and FVC. The strongest association was between a 2 μg/m3 higher concentration of PM2.5 during the saccular phase and FEV1 z-score (-0.176, 95% Confidence Interval [CI]: -0.361, 0.010). The FEV1/FVC ratio was not associated with PM2.5 in any exposure window. No effect modification by child sex or allergic sensitization was observed.ConclusionsWe did not find strong evidence of associations between prenatal ambient PM2.5 exposure and child lung function in a large, well-characterized study sample. However, there was a suggested adverse association between FEV1 and exposure during late pregnancy. The saccular phase of lung development might be an important window for exposure to PM2.5.
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Project description:BackgroundChronic kidney disease (CKD) is a serious global public health challenge, but there is limited information on the connection between air pollution and risk of CKD.ObjectiveThe aim of this study was to investigate the association between long-term exposure to particulate matter (PM) with an aerodynamic diameter of less than [Formula: see text] ([Formula: see text]) and the development of CKD in a large cohort.MethodsA total of 100,629 nonCKD Taiwanese residents age 20 y or above were included in this study between 2001 and 2014. Ambient [Formula: see text] concentration was estimated at each participant's address using a satellite-based spatiotemporal model. Incident CKD cases were identified by an estimated glomerular filtration rate (eGFR) of less than [Formula: see text]. We collected information on a wide range of potential confounders/modifiers during the medical examinations. Cox proportional hazard regression was applied to calculate hazard ratios (HRs).ResultsDuring the follow-up, 4,046 incident CKD cases were identified, and the incidence rate was 6.24 per 1,000 person-years. In contrast with participants with the first quintile exposure of [Formula: see text], participants with the fourth and fifth quintiles exposure of [Formula: see text] had increased risk of CKD development, adjusting for age, sex, educational level, smoking, drinking, body mass index, systolic blood pressure, fasting glucose, total cholesterol, and self-reported heart disease or stroke, with an HR [95% confidence interval (CI)] of 1.11 (1.02, 1.22) and 1.15 (1.05, 1.26), respectively. A significant concentration-response trend was observed ([Formula: see text]). Every [Formula: see text] increment in the [Formula: see text] concentration was associated with a 6% higher risk of developing CKD (HR: 1.06, 95% CI: 1.02, 1.10). Sensitivity and stratified analyses yielded similar results.ConclusionsLong-term exposure to ambient [Formula: see text] was associated with an increased risk of CKD development. Our findings reinforce the urgency to develop global strategies of air pollution reduction to prevent CKD. https://doi.org/10.1289/EHP3304.
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