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Updated: Jan 26, 2026

In Vivo Assessment of Alveolar Macrophage Efferocytosis Following Ozone Exposure
Published on: October 22, 2019
Long-term ozone exposures and cause-specific mortality in a US Medicare cohort
Fatemeh Kazemiparkouhi1, Ki-Do Eum2, Bingyu Wang3
1Department of Civil and Environmental Engineering, Tufts University, Medford, MA, USA. fkazem01@tufts.edu.
Abstract:
We examined the association of long-term, daily 1-h maximum O3 (ozone) exposures on cause-specific mortality for 22.2 million US Medicare beneficiaries between 2000-2008. We modeled the association between O3 and mortality using age-gender-race stratified log-linear regression models, adjusted for state of residence. We examined confounding by (1) adjusting for PM2.5 (particles with aerodynamic diameters <2.5 μm) and NO2 (nitrogen dioxide) exposures, temperature, and neighborhood-level characteristics and behaviors, and (2) decomposing O3 into its temporal and spatio-temporal components and comparing estimated risk ratios. We also examined sensitivity of our results to alternate exposure measures based on warm-season 8-h daily maximum and 24-h average exposures. We found increased risks from long-term O3 exposures to be strongest and most consistent for mortality from respiratory disease (1.030, 95% CI: 1.027, 1.034) (including COPD (chronic obstructive pulmonary disease)), CHF (congestive heart failure), and lung cancer (1.015, 95% CI: 1.010, 1.020), with no evidence of confounding by PM2.5, NO2, and temperature and with results similar across O3 exposure measures. While significant, associations between long-term O3 exposures and CVD (cardiovascular)-related mortality (1.005, 95% CI: 1.003, 1.007) were confounded by PM2.5 and varied with the exposure measure, with associations no longer significantly positive when warm-season 8-h maximum or 24-h average O3 was used to assess exposures. In this large study, we provide strong evidence that O3 exposure is associated with mortality from respiratory-related causes and for the first-time, lung cancer, but raise questions regarding O3-related impacts on CVD mortality. Our findings demonstrate the need to further identify potential confounders.
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