Ambient particulate air pollution and circulating C-reactive protein level: A systematic review and meta-analysis

Ambient particulate air pollution is a major threat to the cardiovascular health of people. Inflammation is an important component of the pathophysiological process that links air pollution and cardiovascular disease (CVD). A classical marker of inflammation—C-reactive protein (CRP), has been recognized as an independent predictor of CVD risk. Exposure to ambient particulate matter (PM) may cause systemic inflammatory response but its association with CRP has been inconsistently reported. To estimate the potential effects of short-term and long-term exposures to ambient particulate air pollution on circulating CRP level based on previous epidemiological studies. A systematic literature search of PubMed, Web of Science, Embase, and Scopus databases for publications up to January 2018 was conducted for studies reporting the association between ambient PM (PM2.5 or PM10, or both) and circulating CRP level. We performed a meta-analysis for the associations reported in individual studies using a random-effect model and evaluated the effect modification by major potential modifiers. This meta-analysis comprised data from 40 observational studies conducted on 244,681 participants. These included 32 (27 PM2.5 studies and 13 PM10 studies) and 11 (9 PM2.5 studies and 5 PM10 studies) studies that investigated the associations of CRP with short-term and long-term exposure to particulate air pollution, respectively. A 10 μg/m3 increase in short-term exposure to PM2.5 and PM10 was associated with increases of 0.83 % (95% CI: 0.30%, 1.37%) and 0.39% (95% CI: -0.04%, 0.82%) in CRP level, respectively, and a 10 μg/m3 increase in long-term exposure to PM2.5 and PM10 was associated with much higher increases of 18.01% (95% CI: 5.96%, 30.06%) and 5.61% (95% CI: 0.79%, 10.44%) in CRP level, respectively. The long-term exposure to particulate air pollution was more strongly associated with CRP level than short-term exposure and PM2.5 had a greater effect on CRP level than PM10. Exposure to ambient particulate air pollution is associated with elevated circulating CRP level suggesting an activated systemic inflammatory state upon exposure, which may explain the association between particulate air pollution and CVD risk.