Short-term Ozone Exposure is Associated With Elevated C-Reactive Protein Levels Among Older Adults

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TM6-O-07 Introduction: Ozone (O3), not just particulate matter (PM), has been associated with increased risk of hospitalization and mortality from respiratory and cardiovascular causes. One mechanistic hypothesis for these effects centers on oxidative stress and airway inflammatory processes that can translate into systemic inflammation and hemostatic changes. Elevated blood levels of C-reactive protein (CRP) have been identified as a risk factor for acute cardiovascular events; this effect may be mediated by altered atherosclerotic plaque stability. As part of our study on the subclinical and clinical effects of short- and long-term air pollution exposures in a cohort of older women and men (age ≥65 years), we evaluated the impact of short-term O3 exposure on CRP levels, and effect modification by prevalent chronic respiratory disease (CRD). Methods: The population-based sample was recruited (June 1989 through May 1990) from one western and 2 eastern United States counties (approximately 1300 participants/county). Blood samples were obtained at baseline. CRP was measured by competitive immunoassay at a central laboratory. Ozone and meteorologic data were from existing national databases. Sex-specific single-pollutant linear regression models were used to evaluate effects of 24-hour average pollutant concentrations averaged over exposure periods (EAP) of 2 days (day of exam and previous day (L01) or 7 days (day of exam and previous 6 days). A natural log transformation of CRP was used in all analyses. Various time-dependent potential confounders were evaluated; final models were adjusted for age at exam, community, 24-hour average temperature (L01), and 24-hour average dew point (L01). Prevalent CRD was defined as a diagnosis of current asthma or chronic bronchitis or emphysema at baseline. Potential confounding by PM was evaluated. Results: After adjustment for covariates, a 2-day average 10-ppb increase in 24-hour average O3 was associated with a 6.6% (95% CI, 0.34% to 12.9%) increase in CRP for all women combined; no significant O3-related changes were observed among men. In stratified analyses, a 7-day average 10-ppb increase in O3 was associated with notably higher levels of CRP among women (13.4%; 95% CI, −0.53% to 27.4%) and men (20.8%: 95% CI, 0.83% to 40.8%) with CRD. Discussion and Conclusions: These results provide further epidemiologic evidence that respiratory exposure to a potent oxidant, O3, can translate to increased CRP levels in blood, a marker of systemic inflammation, and that persons with CRD have a heightened response. The elevation in CRP provides a plausible link to the extrapulmonary effects, including acute cardiovascular events, especially among persons with CRD.