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Evaluation of PM_2.5 air pollution sources and cardiovascular health.

ABSTRACT: Long-term air pollution exposure, notably fine particulate matter, is a global contributor to morbidity and mortality and a known risk factor for coronary artery disease (CAD) and myocardial infarctions (MI). Knowledge of impacts related to source-apportioned PM_2.5 is limited. New modeling methods allow researchers to estimate source-specific long-term impacts on the prevalence of CAD and MI. The Catheterization Genetics (CATHGEN) cohort consists of patients who underwent a cardiac catheterization at Duke University Medical Center between 2002 and 2010. Severity of coronary blockage was determined by coronary angiography and converted into a binary indicator of clinical CAD. History of MI was extracted from medical records. Annual averages of source specific PM_2.5 were estimated using an improved gas-constrained source apportionment model for North Carolina from 2002 to 2010. We tested six sources of PM_2.5 mass for associations with CAD and MI using mixed effects multivariable logistic regression with a random intercept for county and multiple adjustments. PM_2.5 fractions of ammonium bisulfate and ammonium nitrate were associated with increased prevalence of CAD (odds ratio [OR] 1.20; 95% CI = 1.11, 1.22 and OR 1.18; 95% CI = 1.05, 1.32, respectively). PM_2.5 from ammonium bisulfate and ammonium nitrate were also associated with increased prevalence of MI (OR 1.20; 95% CI = 1.10, 1.29 and OR 1.35; 95% CI = 1.20, 1.53, respectively). Greater PM_2.5 concentrations of ammonium bisulfate and ammonium nitrate are associated with greater MI and CAD prevalence. The association with bisulfate suggests aerosol acidity may play a role. Our findings suggest analyses of source specific PM_2.5 mass can reveal novel associations.

SUBMITTER: Slawsky E

PROVIDER: S-EPMC8196100 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundAir pollution is the greatest environmental threat to human health in the world today and is responsible for an estimated 7-9 million deaths annually. One of the most damaging air pollutants is PM2.5 pollution, fine airborne particulate matter under 2.5 microns in diameter. Exposure to PM2.5 pollution can cause premature death, heart disease, lung cancer, stroke, diabetes, asthma, low birthweight, and IQ loss. To avoid these adverse health effects, the WHO recommends that PM2.5 levels not exceed 5 μg/m3.MethodsThis study estimates the negative health impacts of PM2.5 pollution in Texas in 2016. Local exposure estimates were calculated at the census tract level using the EPA's BenMAP-CE software. In BenMAP, a variety of exposure-response functions combine air pollution exposure data with population data and county-level disease and death data to estimate the number of health effects attributable to PM2.5 pollution for each census tract. The health effects investigated were mortality, low birthweight, stroke, new onset asthma, new onset Alzheimer's, and non-fatal lung cancer.FindingsThis study found that approximately 26.7 million (98.9%) of the 27.0 million people living in Texas in 2016 resided in areas where PM2.5 concentrations were above the WHO recommendation of 5 μg/m3, and that 2.6 million people (9.8%) lived in areas where the average PM2.5 concentration exceeded 10 μg/m3. This study estimates that there were 8,405 (confidence interval [CI], 5,674-11,033) premature deaths due to PM2.5 pollution in Texas in 2016, comprising 4.3% of all deaths. Statewide increases in air-pollution-related morbidity and mortality were seen for stroke (2,209 - CI: [576, 3,776]), low birthweight (2,841 - CI: [1,696, 3,925]), non-fatal lung cancers (636 - CI: [219, 980]), new onset Alzheimer's disease (24,575 - CI: [20,800, 27,540]), and new onset asthma (7,823 - CI: [7,557, 8,079]).ConclusionThis study found that air pollution poses significant risks to the health of Texans, despite the fact that pollution levels across most of the state comply with the EPA standard for PM2.5 pollution of 12 μg/m3. Improving air quality in Texas could save thousands of lives from disease, disability, and premature death.

Project description:Air pollution, via ambient PM2.5, is a big threat to public health since it associates with increased hospitalisation, incidence rate and mortality of cardiopulmonary injury. However, the potential mediators of pulmonary injury in PM2.5 -induced cardiovascular disorder are not fully understood. To investigate a potential cross talk between lung and heart upon PM2.5 exposure, intratracheal instillation in vivo, organ culture ex vivo and human bronchial epithelial cells (Beas-2B) culture in vitro experiments were performed respectively. The exposed supernatants of Beas-2B were collected to treat primary neonatal rat cardiomyocytes (NRCMs). Upon intratracheal instillation, subacute PM2.5 exposure caused cardiac dysfunction, which was time-dependent secondary to lung injury in mice, thereby demonstrating a cross-talk between lungs and heart potentially mediated via small extracellular vesicles (sEV). We isolated sEV from PM2.5 -exposed mice serum and Beas-2B supernatants to analyse the change of sEV subpopulations in response to PM2.5 . Single particle interferometric reflectance imaging sensing analysis (SP-IRIS) demonstrated that PM2.5 increased CD63/CD81/CD9 positive particles. Our results indicated that respiratory system-derived sEV containing miR-421 contributed to cardiac dysfunction post-PM2.5 exposure. Inhibition of miR-421 by AAV9-miR421-sponge could significantly reverse PM2.5 -induced cardiac dysfunction in mice. We identified that cardiac angiotensin converting enzyme 2 (ACE2) was a downstream target of sEV-miR421, and induced myocardial cell apoptosis and cardiac dysfunction. In addition, we observed that GW4869 (an inhibitor of sEV release) or diminazene aceturate (DIZE, an activator of ACE2) treatment could attenuate PM2.5 -induced cardiac dysfunction in vivo. Taken together, our results suggest that PM2.5 exposure promotes sEV-linked miR421 release after lung injury and hereby contributes to PM2.5 -induced cardiac dysfunction via suppressing ACE2.

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Evaluation of PM_2.5 air pollution sources and cardiovascular health.

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Evaluation of PM2.5 air pollution sources and cardiovascular health.

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OmicsDI is part of the ELIXIR infrastructure

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Evaluation of PM_2.5 air pollution sources and cardiovascular health.