US EPA

4168585 

Journal Article 

Acute Inflammation Following Personal Exposure to Fine-particulate Air Pollution 

Wang, C; Chen, R; Shi, M; Cai, J; Shi, J; Yang, C; Li, H; Lin, Z; Meng, X; Liu, C; Niu, Y; Xia, Y; Zhao, Z; Kan, H; Weinberg, CR 

2017 

Yes 

American Journal of Epidemiology
ISSN: 0002-9262
EISSN: 1476-6256 

187 

3 

484-493 

English 

29020142 

10.1093/aje/kwx277 

WOS:000426812300012 

Air pollution may increase cardiovascular and respiratory risk through inflammatory pathways, but evidence for acute effects has been weak and indirect. We enrolled 36 healthy nonsmoking college students for a panel study in Shanghai, China, a city with highly variable levels of air pollution, between December 2014 and July 2015. We measured personal exposure to fine particulate matter (PM2.5) continuously for 72-hour preceding each of four clinical visits that included phlebotomy. We measured four inflammation proteins and DNA methylation at nearby regulatory CpG loci. We applied linear mixed-effect models to examine associations over various lag times. When results suggested mediation, we evaluated methylation as mediator. Increased PM2.5 was positively associated with all four inflammation proteins, and negatively associated with DNA methylation at regulatory loci for tumor necrosis factor alpha (TNFα) and soluble intercellular adhesion molecule-1. A 10 μg/m3 increase in average PM2.5 during the 24 hours preceding blood draw corresponded to a 4.4% increase in TNFα and a statistically significant decrease in methylation at one of the two studied candidate CpG loci for TNFα. Epigenetics may play an important role in mediating effects of PM2.5 on inflammatory pathways.