Medium term moderate to low-level air pollution exposure is associated with higher C-reactive protein among healthy Danish blood donors.

Air pollution is a significant contributor to the global burden of disease with a plethora of associated health effects such as pulmonary and systemic inflammation. C-reactive protein (CRP) is associated with a wide range of diseases and is associated with several exposures. Studies on the effect of air pollution exposure on CRP levels in low to moderate pollution settings have shown inconsistent results. In this cross-sectional study high sensitivity CRP measurements on 18,463 Danish blood donors were linked to modelled air pollution data for NOx, NO2, O3, CO, SO2, NH3, mineral dust, black carbon, organic carbon, sea salt, secondary inorganic aerosols and its components, primary PM2.5, secondary organic aerosols, total PM2.5, and total PM10 at their residential address over the previous month. Associations were analysed using ordered logistic regression with CRP quartile as individuals outcome and air pollution exposure as scaled deciles. Analyses were adjusted for health related and socioeconomic covariates using health questionnaires and Danish register data. Exposure to different air pollution components was generally associated with higher CRP (odds ratio estimates ranging from 1.11 to 1.67), while exposure to a few air pollution components was associated with lower CRP. For example, exposure to NO2 increased the odds of high CRP 1.32-fold (95%CI 1.16-1.49), while exposure to NH3 decreased the odds of high CRP 0.81-fold (95%CI 0.73-0.89). This large study among healthy individuals found air pollution exposure to be associated with increased levels of CRP even in a setting with low to moderate air pollution levels.

A comparison of neighbourhood level variation and risk factors for affective versus non-affective psychosis.

BACKGROUND: Studies typically highlight area level variation in the incidence of non-affective but not affective psychoses. We compared neighbourhood-level variation for both types of disorder, and the specific effects of neighbourhood urbanicity and ethnic density, using Danish national registry data. METHODS: Population based cohort (2,224,464 people) followed from 1980 to 2013 with neighbourhood exposure measured at age 15 and incidence modelled using multilevel Poisson regression. RESULTS: Neighbourhood variation was similar for both disorders with an adjusted median risk ratio of 1.37 (95% CI 1.34-1.39) for non-affective psychosis and 1.43 (1.38-1.49) for affective psychosis. Associations with neighbourhood urbanicity differed: living in the most compared to the least urban quintile at age 15 was associated with a minimal increase in subsequent affective psychosis, IRR 1.13 (1.01-1.27) but a substantial increase in rates of non-affective psychosis, IRR 1.66 (1.57-1.75). Mixed results were found for neighbourhood ethnic density: for Middle Eastern migrants there was an increased average incidence of both affective, IRR 1.54 (1.19-1.99), and non-affective psychoses, 1.13 (1.04-1.23) associated with each decrease in ethnic density quintile, with a similar pattern for African migrants, but for European migrants ethnic density appeared to be associated with non-affective psychosis only. CONCLUSIONS: While overall variation and the effect of neighbourhood ethnic density were similar for both types of disorder, associations with urbanicity were largely confined to non-affective psychosis. This may reflect differences in aetiological pathways although the mechanism behind these differences remains unknown.