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Associations between long-term air pollution exposure and the incidence of cardiovascular diseases among American older adults
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- Persistent URL
- Last modified
- 09/26/2025
- Type of Material
- Authors
- Language
- English
- Date
- 2022-10-22
- Publisher
- PERGAMON-ELSEVIER SCIENCE LTD
- Publication Version
- Copyright Statement
- © 2022 The Authors. Published by Elsevier Ltd.
- License
- Final Published Version (URL)
- Title of Journal or Parent Work
- Volume
- 170
- Start Page
- 107594
- End Page
- 107594
- Grant/Funding Information
- This study was supported by the United States Environmental Protection Agency (grant number RD-83587201 received by JS, https://www.epa.gov/) and the National Institutes of Health (grant number R01 ES032418 received by JS, R01 AG074357 received by LS, R21 ES032606 received by LS, https://www.nih.gov/). The contents of this publication are solely the responsibility of the grantee and do not necessarily represent the official views of the US EPA. Further, the US EPA does not endorse the purchase of any commercial products or services mentioned in the publication. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
- Supplemental Material (URL)
- Abstract
- Background & aim: Numerous studies have linked air pollution with cardiovascular diseases. Fewer studies examined the associations at low concentration levels or assessed potential modifiers. Some investigations only examined hospitalizations, which can miss incident cases. This study aims to address these gaps through a nationwide cohort study of Medicare enrollees. Methods: Our study cohort comprise all Medicare enrollees (≥65 years old) continuously enrolled in the fee-for-service program and both Medicare part A and B across the contiguous U.S. from 2000 to 2016. We examined the associations of population-weighted ZIP code-level annual average PM2.5, NO2, and warm-season O3 (May-October), with the first diagnoses of atrial fibrillation (AF), congestive heart failure (CHF), and stroke. We fit multi-pollutant Cox proportional hazards models adjusted for individual demographic characteristics and area-level covariates. We further examined these associations at low pollutant concentration levels and the potential effect modifications by race/ethnicity and comorbidities (diabetes, hypertension, hyperlipidemia). Results: Elevated PM2.5 and NO2 levels were associated with increased incidence of AF, CHF, and stroke. For each 1 μg/m3 increase in annual PM2.5, hazard ratios (HRs) were 1.0059 (95%CI: 1.0054-1.0064), 1.0260 (95%CI: 1.0256-1.0264), and 1.0279 (95%CI: 1.0274-1.0284), respectively. For each1 ppb increase in annual NO2, HRs are 1.0057 (95%CI: 1.0056-1.0059), 1.0112 (95%CI: 1.0110-1.0113), and 1.0095 (95%CI: 1.0093-1.0096), respectively. For warm-season O3, each 1 ppb increase was associated with increased incidence of CHF (HR=1.0035, 95%CI: 1.0033–1.0037) and stroke (HR=1.0026, 95%CI: 1.0023–1.0028). Larger magnitudes of HRs were observed when restricted to pollutants levels lower than NAAQS standards. Generally higher risks were observed for Black people and diabetics. Conclusions: Long-term exposure to PM2.5, NO2, and warm-season O3 were associated with increased incidence of cardiovascular diseases, even at low pollutant concentration levels. Black people and people with diabetes were found to be vulnerable populations.
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