OP X – 3 C-reactive protein (crp) and long-term air pollution with a focus on ultrafine particles

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Background/aimLong-term exposure to ambient air pollution contributes to the burden of disease and particularly affects cardiovascular (CV) causes of death. We investigated the association between particle number concentration (PNC), a marker for ultrafine particles (UFP), and other air pollutants and high sensitivity C-reactive protein (hs-CRP) as a potential link between air pollution and CV disease.MethodsA cross-sectional analysis was performed on data of the second follow-up of the KORA S4 survey in Augsburg, Germany (2013–2014). Residential long-term exposure to PNC, particulate matter <10 µm and <2.5 µm in aerodynamic diameter (PM10 and PM2.5, respectively), PMcoarse (2.5–10 µm), absorbance of PM2.5 (PM2.5abs), nitrogen dioxide (NO2) and nitrogen oxides (NOx) was estimated by land-use regression models. Associations between annual air pollution concentration and hs-CRP were modelled in 2252 participants using linear regression adjusting for confounders. Possible effect-modifiers were examined by interaction terms. Two-pollutant models were calculated for pollutants with Spearman inter-correlation <0.70.ResultsThe results pointed to a positive association between PNC, PM10, PMcoarse, PM2.5abs, NO2 and NOx and hs-CRP. For PNC, an interquartile-range (IQR, 2000 particles/cm3) increase was associated with a 3.63% [95% confidence interval (CI): −0.86% to 8.33%] increase in hs-CRP. Effect estimates were higher for women, non-obese and participants without history of CVD. Effect modification was also seen for participants without diabetes with the highest effect estimate of 14.71% [95% CI: 5.47% to 24.77%] for an IQR increase of 2.1 µg/m³ in PM10. In two-pollutant models, adjustment for PM2.5 strengthened the effect estimates for PNC and PM10 (increase per IQR 6.31% [95% CI: 0.42% to 12.53%] and 7.34% [95%CI: 0.40% to 14.77%], respectively).ConclusionOur results highlight the role of UFP within the complex mixture of ambient air pollution and their inflammatory potential and help fill a research gap since studies on chronic exposure to ultrafine particles are still scarce.

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