Effects of particulate matter on inflammatory markers in the general adult population.

TitreEffects of particulate matter on inflammatory markers in the general adult population.
Publication TypeJournal Article
Year of Publication2012
AuthorsTsai, D-H, Amyai, N, Marques-Vidal, P, Wang, J-L, Riediker, M, Mooser, V, Paccaud, F, Waeber, G, Vollenweider, P, Bochud, M
JournalPart Fibre Toxicol
Date Published2012
Mots-clésAdult, Aged, Air Pollutants, Biological Markers, C-Reactive Protein, Cardiovascular Diseases, Cytokines, Female, Humans, Inflammation, Inhalation Exposure, Interleukin-1beta, Interleukin-6, Male, Middle Aged, Particulate Matter, Risk Factors, Tumor Necrosis Factor-alpha

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 PM(10) (on the day of examination visit) with continuous circulating serum levels of high-sensitive C-reactive protein (hs-CRP), interleukin 1-beta (IL-1β), interleukin 6 (IL-6), and tumor-necrosis-factor alpha (TNF-α) by robust linear regressions, controlling for potential confounding factors and assessing effect modification.

RESULTS: In adjusted analyses, for every 10 μg/m(3) elevation in PM(10), IL-1ß 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-α by 0.024 (0.013-0.035) pg/mL, whereas no significant association was found with hs-CRP levels.

CONCLUSIONS: Short-term exposure to PM(10) was positively associated with higher levels of circulating IL-1ß, IL-6 and TNF-α 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 PM(10) to cardiovascular risk.

Alternate URL


Alternate JournalPart Fibre Toxicol
Citation Key / SERVAL ID3275
PubMed ID22769230
PubMed Central IDPMC3464812


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