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Pilz, Veronika; Wolf, Kathrin; Breitner, Susanne; Rückerl, Regina; König, Wolfgang; Rathmann, Wolfgang; Cyrys, Josef; Peters, Annette; Schneider, Alexandra (2018): C-reactive protein (CRP) and long-term air pollution with a focus on ultrafine particles. In: International Journal of Hygiene and Environmental Health, Vol. 221, No. 3: pp. 510-518
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Background: Long-term exposure to ambient air pollution contributes to the global burden of disease by particularly affecting cardiovascular (CV) causes of death. We investigated the association between particle number concentration (PNC), a marker for ultrafine particles, and other air pollutants and high sensitivity C-reactive protein (hs-CRP) as a potential link between air pollution and CV disease. Methods: We cross-sectionally analysed data from the second follow up (2013 and 2014) of the German KORA baseline survey which was conducted in 1999-2001. Residential long-term exposure to PNC and various other size fractions of particulate matter (PM10 with size of < 10 mu m in aerodynamic diameter, PMcoarse, 2.5-10 mu m or PM2.5 < 2.5 mu m, respectively), soot (PM(2.5)abs: absorbance of PM2.5), nitrogen oxides (nitrogen dioxide NO2 or oxides NOx, respectively) and ozone (O-3) were estimated by land-use regression models. Associations between annual air pollution concentrations and hs-CRP were modeled in 2252 participants using linear regression models adjusted for several confounders. Potential effect-modifiers were examined by interaction terms and two pollutant models were calculated for pollutants with Spearman inter-correlation < 0.70. Results: Single pollutant models for PNC, PM10 PMcoarse, PM(2.5)abs, NO2 and NOx showed positive but nonsignificant associations with hs-CRP. For PNC, an interquartile range (2000 particles/cm(3)) increase was associated with a 3.6% (95% CI: -0.9%, 8.3%) increase in hs-CRP. A null association was found for PM2.5. Effect estimates were higher for women, non-obese participants, for participants without diabetes and without a history of cardiovascular disease whereas ex-smokers showed lower estimates compared to smokers or non-smokers. For O-3, the dose-response function suggested a non-linear relationship. In two-pollutant models, adjustment for PM2.5 strengthened the effect estimates for PNC and PM10 (6.3% increase per 2000 particles/cm(3) [95% CI: 0.4%;12.5%] and 7.3% per 16.5 mu g/m(3) [95% CI: 0.4%;14.8%], respectively). Conclusion: This study adds to a scarce but growing body of literature showing associations between long-term exposure to ultrafine particles and hs-CRP, one of the most intensely studied blood biomarkers for cardiovascular health. Our results highlight the role of ultrafine particles within the complex mixture of ambient air pollution and their inflammatory potential.