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.
Ethical approval
The current study was approved by the institutional review boards of the State University of New York at Buffalo (SPM1080708E) and Peking University Health Science Center (IRB00001052-08057).
Consent to participate
Written inform consent was obtained from all study participants.
Author’s contributions
Dr. Li analyzed data and drafted the manuscript; Dr. Bonner helped the study design and interpreted the data; Dr. Browne helped with laboratory design, quality control and results interpretation; Dr. Deng oversaw the field work; Dr. Tian helped with model building and data analysis; Dr. Zhang contributed to the data analysis; Mrs. Swanson helped with data management and initial analysis; Dr. Rittenhouse-Olson was involved in the original study design and manuscript revision; Ms. Farhat helped with the interpretation of the data; Dr. Mu oversaw the entire study.
Acknowledgements
The authors acknowledge Matt Groll and Sara Call from Quansys Bioscience for their help in developing and validating the chemokines assays and conducting the laboratory analysis for the current study.
Disclosure statement
We disclose that no conflict interest is involved in the submitted work. We declare that the work has not been published previously and it is not under consideration for publication elsewhere.
Data availability statement
The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.