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OP X – 3 C-reactive protein (crp) and long-term air pollution with a focus on ultrafine particles
  1. Regina Rückerl1,
  2. Veronika Pilz1,
  3. Kathrin Wolf1,
  4. Susanne Breitner1,
  5. Wolfgang Koenig2,
  6. Wolfgang Rathmann3,
  7. Annette Peters1,4,
  8. Alexandra Schneider1
  1. 1Helmholtz Zentrum München, Epidemiology II, München, Germany
  2. 2Deutsches Herzzentrum München, Klinik für Herz-and Kreislauferkrankungen, München, Germany
  3. 3Deutsches Diabetes-Zentrum, Institute of Biometry and Epidemiology, Düsseldorf, Germany
  4. 4German Centre for Diabetes Research (DZD e.V.), München, Germany


Background/aim Long-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.

Methods A 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.

Results The 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).

Conclusion Our 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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