Bart Ostro1, Brian Malig2, Rachel Broadwin2, Rupa Basu2, Ellen B Gold3, Joyce T Bromberger4, Carol Derby5, Steven Feinstein6, Gail A Greendale7, Elizabeth A Jackson8, Howard M Kravitz6, Karen A Matthews4, Barbara Sternfeld9, Kristin Tomey10, Robin R Green11, Rochelle Green2. 1. Office of Environmental Health Hazard Assessment, 1515 Clay St, 16th Floor, Oakland, CA, USA. Electronic address: Bart.Ostro@oehha.ca.gov. 2. Office of Environmental Health Hazard Assessment, 1515 Clay St, 16th Floor, Oakland, CA, USA. 3. University of California, Davis, CA, USA. 4. University of Pittsburgh, Pittsburgh, PA, USA. 5. Albert Einstein College of Medicine, New York, NY, USA. 6. Rush University Medical Center, Chicago, IL, USA. 7. Geffen School of Medicine at UCLA, Los Angeles, CA, USA. 8. University of Michigan Hospital and Health Systems, Ann Arbor, MI, USA. 9. Kaiser Permanente, Oakland, CA, USA. 10. School of Public Health, University of Michigan, Ann Arbor, MI, USA. 11. Albert Einstein College of Medicine, Yeshiva University, Jersey City, NJ, USA.
Abstract
BACKGROUND: Several cohort studies report associations between chronic exposure to ambient fine particles (PM2.5) and cardiovascular mortality. Uncertainty exists about biological mechanisms responsible for this observation, but systemic inflammation has been postulated. In addition, the subgroups susceptible to inflammation have not been fully elucidated. METHODS: We investigated whether certain subgroups are susceptible to the effects of long-term exposure to PM2.5 on C-reactive protein (CRP), a marker of inflammation directly linked to subsequent cardiovascular disease. We used data from the SWAN cohort of 1923 mid-life women with up to five annual repeated measures of CRP. Linear mixed and GEE models accounting for repeated measurements within an individual were used to estimate the effects of prior-year PM2.5 exposure on CRP. We examined CRP as a continuous and as binary outcome for CRP greater than 3mg/l, a level of clinical significance. RESULTS: We found strong associations between PM2.5 and CRP among several subgroups. For example a 10 µg/m(3) increase in annual PM2.5 more than doubled the risk of CRP greater than 3mg/l in older diabetics, smokers and the unmarried. Larger effects were also observed among those with low income, high blood pressure, or who were using hormone therapy, with indications of a protective effects for those using statins or consuming moderate amounts of alcohol. CONCLUSIONS: In this study, we observed significant associations between long-term exposure to PM2.5 and CRP in several susceptible subgroups. This suggests a plausible pathway by which exposure to particulate matter may be associated with increased risk of cardiovascular disease.
BACKGROUND: Several cohort studies report associations between chronic exposure to ambient fine particles (PM2.5) and cardiovascular mortality. Uncertainty exists about biological mechanisms responsible for this observation, but systemic inflammation has been postulated. In addition, the subgroups susceptible to inflammation have not been fully elucidated. METHODS: We investigated whether certain subgroups are susceptible to the effects of long-term exposure to PM2.5 on C-reactive protein (CRP), a marker of inflammation directly linked to subsequent cardiovascular disease. We used data from the SWAN cohort of 1923 mid-life women with up to five annual repeated measures of CRP. Linear mixed and GEE models accounting for repeated measurements within an individual were used to estimate the effects of prior-year PM2.5 exposure on CRP. We examined CRP as a continuous and as binary outcome for CRP greater than 3mg/l, a level of clinical significance. RESULTS: We found strong associations between PM2.5 and CRP among several subgroups. For example a 10 µg/m(3) increase in annual PM2.5 more than doubled the risk of CRP greater than 3mg/l in older diabetics, smokers and the unmarried. Larger effects were also observed among those with low income, high blood pressure, or who were using hormone therapy, with indications of a protective effects for those using statins or consuming moderate amounts of alcohol. CONCLUSIONS: In this study, we observed significant associations between long-term exposure to PM2.5 and CRP in several susceptible subgroups. This suggests a plausible pathway by which exposure to particulate matter may be associated with increased risk of cardiovascular disease.
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