Effects of particulate matter on inflammatory markers in the general adult population |
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Authors: | Dai-Hua Tsai Nadia Amyai Pedro Marques-Vidal Jia-Lin Wang Michael Riediker Vincent Mooser Fred Paccaud Gerard Waeber Peter Vollenweider Murielle Bochud |
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Affiliation: | 1. Institute of Social and Preventive Medicine (IUMSP), Lausanne University Hospital (CHUV), Biop?le 2, Route de la Corniche 10, CH-1010, Lausanne, Switzerland 2. Department of Chemistry, National Central University, Jhong-Li, 32001, Taiwan 3. Department of Medicine, Internal Medicine, CHUV, Lausanne, Switzerland 4. Institute for Work and Health (IST), Lausanne, Switzerland 5. Department of Genetics, GlaxoSmithKline, Philadelphia, PA, USA
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Abstract: | Background Particulate air pollution is associated with increased risk of cardiovascular disease and stroke. Although the precise mechanisms underlying this association are still unclear, the induction of systemic inflammation following particle inhalation represents a plausible mechanistic pathway. Methods We used baseline data from the CoLaus Study including 6183 adult participants residing in Lausanne, Switzerland. We analyzed the association of short-term exposure to PM10 (on the day of examination visit) with continuous circulating serum levels of high-sensitive C-reactive protein (hs-CRP), interleukin 1-beta (IL-1??), interleukin 6 (IL-6), and tumor-necrosis-factor alpha (TNF-??) by robust linear regressions, controlling for potential confounding factors and assessing effect modification. Results In adjusted analyses, for every 10???g/m3 elevation in PM10, IL-1? increased by 0.034 (95?% confidence interval, 0.007-0.060) pg/mL, IL-6 by 0.036 (0.015-0.057) pg/mL, and TNF-?? by 0.024 (0.013-0.035) pg/mL, whereas no significant association was found with hs-CRP levels. Conclusions Short-term exposure to PM10 was positively associated with higher levels of circulating IL-1?, IL-6 and TNF-?? in the adult general population. This positive association suggests a link between air pollution and cardiovascular risk, although further studies are needed to clarify the mechanistic pathway linking PM10 to cardiovascular risk. |
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