Format

Send to

Choose Destination
Biomarkers. 2019 Nov;24(7):712-719. doi: 10.1080/1354750X.2019.1658803. Epub 2019 Sep 15.

Responses of serum chemokines to dramatic changes of air pollution levels, a panel study.

Author information

1
Department of Epidemiology and Environmental Health, State University of New York at Buffalo , Buffalo , NY , USA.
2
Department of Biotechnical and Clinical Laboratory Sciences, State University of New York at Buffalo , Buffalo , NY , USA.
3
Department of Environmental Health, Peking University Health Science Center , Beijing , China.
4
Department of Biostatistics, State University of New York at Buffalo , Buffalo , NY , USA.
5
Nicholas School of the Environment, Duke University , Durham , NC , USA.

Abstract

Background: Despite the in vitro and in vivo evidence, studies are limited in evaluating whether chemokines are potential inflammatory mediators in response to air pollution exposure in humans. Methods: We conducted a panel study coinciding with the Beijing Olympics, when temporary air pollution controls were implemented. We measured a suite of serum chemokines among healthy adults before, during and after the Olympics, respectively. Linear mixed-effect models were used to evaluate changes in chemokine levels over the three time periods. Results: In response to the 50% drop in air pollution levels during the games, levels of RANTES, MCP-2, and TARC decreased by 25.8%, 20.9% and 35.3%, respectively (p < 0.001) from pre-Olympics, and then increased by 45.8%, 34.9% and 61.5%, respectively (p < 0.001) after the games when air pollution levels went up again. Similar patterns were observed in subgroup analyses by sex, age, smoking and body mass index. GRO-α and IL-8 decreased significantly during the games (22.5% and 30.4%), and increased non-significantly after the games. Eotaxin-1 only increased significantly from during- to post-games. Conclusions: The strongest associations with air pollution levels were observed among RANTES, TARC and MCP-2. Those chemokines may play important roles in the air pollution-induced inflammatory pathway.

KEYWORDS:

Air pollution; biological mechanism; chemokines; inflammation; panel study

Supplemental Content

Full text links

Icon for Taylor & Francis
Loading ...
Support Center