Hygroscopic properties of particulate matter and effects of their interactions with weather on visibility.
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ABSTRACT:
SUBMITTER: Won WS
PROVIDER: S-EPMC8361198 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:In order to study effects of ambient particulate matter (PM) it was previously necessary to have access to a comprehensive air monitoring network. However, there are locations in the world where PM levels are above generally accepted exposure standards but lack a monitoring infrastructure. This is true in Iraq and other locations in Southwest Asia and Afghanistan where U.S. and other coalition troops were deployed beginning in 2001. Since aerosol optical depth (AOD), determined by satellite, and visibility are both highly related to atmospheric PM2.5 (particulate matter with an aerodynamic diameter ?2.5 ?m) concentrations, we employed a novel approach that took advantage of historic airport visibility measurements to calibrate the AOD-visibility relationship and determine visibility spatially and temporally (2006-2007) over an approximately 17,000 km2 region of Iraq. We obtained daily visibility predictions that were highly associated with satellite-based 1x1 km AOD daily observations (R2=0.87). Based on a previously derived calibration between PM2.5 and visibility, we were able to predict spatially and temporally resolved PM2.5 concentrations. Variability of PM2.5 among sites was high, with daily concentrations differing by as much as ~30 ?g/m3. This study demonstrates the feasibility of characterizing historic PM2.5 exposures in Iraq and other locations in Southwest Asia and Afghanistan with similar climate characteristics. This is of utility for epidemiologists seeking to assess the potential health effects related to PM2.5 exposures among previously deployed military personnel and of the population of the region. IMPLICATIONS:This study demonstrates the ability to utilize aerosol optical depth to successfully estimate visibility spatially and temporally in Southwest Asia and Afghanistan. This enables for the estimation of spatially resolved PM2.5 concentrations in the region. The ability to caracterize PM2.5 concentrations in Southwest Asia and Afghanistan is highly important for epidemiologists investigating the relationship between chronic exposure to PM2.5 and respiratory diseases among military personnel deployed to the region. This information will better position policy makers to draft meaningful legislation relating to military health.
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Project description:ImportanceOutdoor particulate matter 2.5 μm or less in diameter (PM2.5) is a ubiquitous environmental neurotoxicant that may affect the developing brain. Little is known about associations between PM2.5 and white matter connectivity.ObjectivesTo assess associations between annual residential PM2.5 exposure and white matter microstructure health in a US sample of children 9 to 10 years of age and to examine whether associations are specific to certain white matter pathways or vary across neuroimaging diffusion markers reflective of intracellular and extracellular microstructural processes.Design, setting, and participantsThis cross-sectional study, the Adolescent Brain and Cognitive Development (ABCD) Study, was composed of 21 study sites across the US and used baseline data collected from children 9 to 10 years of age from September 1, 2016, to October 15, 2018. Data analysis was performed from September 15, 2020, to June 30, 2021.ExposuresAnnual mean PM2.5 exposure estimated by ensemble-based models and assigned to the primary residential addresses at baseline.Main outcomes and measuresDiffusion-weighted imaging (DWI) and tractography were used to delineate white matter tracts. The biophysical modeling technique of restriction spectrum imaging (RSI) was implemented to examine total hindered diffusion and restricted isotropic and anisotropic intracellular diffusion in each tract. Hierarchical mixed-effects models with natural splines were used to analyze the associations between PM2.5 exposure and DWI.ResultsIn a study population of 7602 children (mean [SD] age, 119.1 [7.42] months; 3955 [52.0%] female; 160 [ 21.%] Asian, 1025 [13.5%] Black, 1616 [21.3%] Hispanic, 4025 [52.9%] White, and 774 [10.2%] other [identified by parents as American Indian/Native American or Alaska Native; Native Hawaiian, Guamanian, Samoan, other Pacific Islander; Asian Indian, Chinese, Filipino, Japanese, Korean, Vietnamese, or other Asian; or other race]), associations were seen between annual ambient PM2.5 and hemispheric differences in white matter microstructure. Hemisphere-stratified models revealed significant associations between PM2.5 exposure and restricted isotropic intracellular diffusion in the left cingulum, in the left superior longitudinal fasciculus, and bilaterally in the fornix and uncinate fasciculus. In tracts with strong positive associations, a PM2.5 increase from 8 to 12 μg/m3 was associated with increases of 2.16% (95% CI, 0.49%-3.84%) in the left cingulum, 1.95% (95% CI, 0.43%-3.47%) in the left uncinate, and 1.68% (95% CI, 0.01%-3.34%) in the right uncinate. Widespread negative associations were observed between PM2.5 and mean diffusivity.Conclusions and relevanceThe findings of this cross-sectional study suggest that annual mean PM2.5 exposure during childhood is associated with increased restricted isotropic diffusion and decreased mean diffusivity of specific white matter tracts, potentially reflecting differences in the composition of white matter microarchitecture.
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Project description:Particulate matter (PM), which is the primary contributor to air pollution, has become a pervasive global health threat. When PM enters into a respiratory tract, the first body tissues to be directly exposed are the cells of respiratory tissues and pulmonary surfactant. Pulmonary surfactant is a pivotal component to modulate surface tension of alveoli during respiration. Many studies have proved that PM would interact with pulmonary surfactant to affect the alveolar activity, and meanwhile, pulmonary surfactant would be adsorbed to the surface of PM to change the toxic effect of PM. This review focuses on recent studies of the interactions between micro/nanoparticles (synthesized and environmental particles) and pulmonary surfactant (natural surfactant and its models), as well as the health effects caused by PM through a few significant aspects, such as surface properties of PM, including size, surface charge, hydrophobicity, shape, chemical nature, etc. Moreover, in vitro and in vivo studies have shown that PM leads to oxidative stress, inflammatory response, fibrosis, and cancerization in living bodies. By providing a comprehensive picture of PM-surfactant interaction, this review will benefit both researchers for further studies and policy-makers for setting up more appropriate regulations to reduce the adverse effects of PM on public health.
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Project description:Air pollution is a complex mixture of gaseous and particulate components, each of which has detrimental effects on human health. While the composition of air pollution varies greatly depending on the source, studies from across the world have consistently shown that air pollution is an important modifiable risk factor for significantly increased morbidity and mortality. Moreover, clinical studies have generally shown a greater impact of particulate matter (PM) air pollution on health than the gaseous components. PM has wide-ranging deleterious effects on human health, particularly on the cardiovascular system. Both acute and chronic exposure to PM air pollution is associated with increased risk of death from cardiovascular diseases including ischemic heart disease, heart failure, and ischemic/thrombotic stroke. Particulate matter has also been shown to be an important endocrine disrupter, contributing to the development of metabolic diseases such as obesity and diabetes mellitus, which themselves are risk factors for cardiovascular disease. While the epidemiological evidence for the deleterious effects of PM air pollution on health is increasingly accepted, newer studies are shedding light on the mechanisms by which PM exerts its toxic effects. A greater understanding of how PM exerts toxic effects on human health is required in order to prevent and minimize the deleterious health effects of this ubiquitous environmental hazard. Air pollution is a growing public health problem and mortality due to air pollution is expected to double by 2050. Here, we review the epidemiological evidence for the cardiovascular effects of PM exposure and discuss current understanding about the biological mechanisms, by which PM exerts toxic effects on cardiovascular system to induce cardiovascular disease.
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Project description:BackgroundEstimating the causal effect of pollution on human health is integral for evaluating returns to pollution regulation, yet separating out confounding factors remains a perennial challenge.MethodsWe use a quasi-experimental design to investigate the causal relationship between regulation of particulate matter smaller than 2.5 micrograms per cubic meter (PM2.5) and mortality among those 65 years of age and older. We exploit regulatory changes in the Clean Air Act Amendments (CAAA). Regulation in 2005 impacted areas of the United States differentially based on pre-regulation air quality levels for PM2.5. We use county-level mortality data, extracted from claims data managed by the Centers for Medicare & Medicaid Services, merged to county-level average PM2.5 readings and attainment status as classified by the Environmental Protection Agency.ResultsBased on estimates from log-linear difference-in-differences models, our results indicate after the CAAA designation for PM2.5 in 2005, PM2.5 levels decreased 1.59 micrograms per cubic meter (95% CI = 1.39, 1.80) and mortality rates among those 65 and older decreased by 0.93% (95% CI = 0.10%, 1.77%) in nonattainment counties, relative to attainment ones. Results are robust to a series of alternate models, including nearest-neighbor matching based on propensity score estimates.ConclusionThis analysis suggests large health returns to the 2005 PM2.5 designations, and provides evidence of a causal association between pollution and mortality among the Medicare population.
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