Journal
PARTICLE AND FIBRE TOXICOLOGY
Volume 9, Issue -, Pages -Publisher
BIOMED CENTRAL LTD
DOI: 10.1186/1743-8977-9-24
Keywords
High-sensitive C-reactive protein (hs-CRP); Interleukin 1-beta (IL-1 beta); Interleukin 6 (IL-6); Tumor-necrosis-factor alpha (TNF-alpha); Air pollution
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Funding
- GlaxoSmithKline
- Faculty of Biology and Medicine of Lausanne, Switzerland
- Swiss National Science Foundation [33CSCO-122661]
- National Science Council, Taiwan [NSC100-2917-I-564-009]
- Swiss School of Public Health + (SSPH+)
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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 beta), interleukin 6 (IL-6), and tumor-necrosis-factor alpha (TNF-alpha) by robust linear regressions, controlling for potential confounding factors and assessing effect modification. Results: In adjusted analyses, for every 10 mu g/m(3) elevation in PM10, IL-1 beta 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-a 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 beta, IL-6 and TNF-alpha 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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