Gene-environment interactions linking air pollution and inflammation in Parkinson's disease

• Published in: Environmental research 2016-11, Vol.151, p.713-720
• Main Authors: Lee, Pei-Chen, Raaschou-Nielsen, Ole, Lill, Christina M., Bertram, Lars, Sinsheimer, Janet S., Hansen, Johnni, Ritz, Beate
• Format: Article
• Language: English
• Subjects: Air Pollutants - analysis; Air Pollutants - toxicity; Case-Control Studies; Denmark; Female; Gene-Environment Interaction; Genetic Predisposition to Disease; Genotype; Geographic Information Systems; Humans; Inflammation; Interleukin-1beta - genetics; Male; Middle Aged; Nitrogen Dioxide - analysis; Nitrogen Dioxide - toxicity; Odds Ratio; Parkinson Disease - etiology; Parkinson Disease - genetics; Parkinson Disease - immunology; Parkinson's disease; Particulate Matter - analysis; Particulate Matter - toxicity; Polymorphism, Single Nucleotide; Traffic-related air pollution; Tumor Necrosis Factor-alpha - genetics
• ISSN: 0013-9351; 1096-0953
• DOI: 10.1016/j.envres.2016.09.006

Both air pollution exposure and systemic inflammation have been linked to Parkinson's disease (PD). In the PASIDA study, 408 incident cases of PD diagnosed in 2006–2009 and their 495 population controls were interviewed and provided DNA samples. Markers of long term traffic related air pollution measures were derived from geographic information systems (GIS)-based modeling. Furthermore, we genotyped functional polymorphisms in genes encoding proinflammatory cytokines, namely rs1800629 in TNFα (tumor necrosis factor alpha) and rs16944 in IL1B (interleukin-1β). In logistic regression models, long-term exposure to NO2 increased PD risk overall (odds ratio (OR)=1.06 per 2.94μg/m3 increase, 95% CI=1.00–1.13). The OR for PD in individuals with high NO2 exposure (≧75th percentile) and the AA genotype of IL1B rs16944 was 3.10 (95% CI=1.14–8.38) compared with individuals with lower NO2 exposure (