Responses of serum chemokines to dramatic changes of air pollution
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Background: Chemokines are critical component of systemic inflammation. Accumulating in vitro and in vivo evidence suggested that chemokines might act as inflammatory mediators through which air pollution induces various adverse health effects, however human evidence is lacking. In addition, little is known if levels of chemokines are affected by certain lifestyle and demographic factors and if possible associations exist between chemokines and oxidative stress, especially among the healthy adults. Aims: This study aims to examine (1) associations between age, sex and lifestyle factors and levels of serum chemokines; (2) the relationships between changes in air pollution levels and serum chemokines; and (3) the cross-sectional relationships between chemokines and oxidative stress biomarkers. Methods: Temporary air quality control measures during the Beijing Olympics led to a drastic decline in air pollution levels, followed by an elevation to the usual levels after the Games. We conducted a panel study among 180 healthy Beijing adults and collected bio-specimens in periods of pre-, during and post-Olympics. Using a subset of serum samples collected from 104 participants, we measured a suite of chemokines consisting of CXCL-1 (GRO-α), CXCL-8 (IL-8), CXCL-10 (IP-10), CCL-2 (MCP-1), CCL-5 (RANTES), CCL-8 (MCP-2), CCL-11 (Eotaxin-1) and CCL-17 (TARC). We used linear mixed-effect models to evaluate changes of serum chemokine levels across the Olympics. Using the baseline data of this panel study, we assessed cross-sectional associations of age, sex, smoking, alcohol consumption and body mass index with chemokines levels. We also assessed the cross-sectional correlations of chemokines with total antioxidant status (TAS) and lipid peroxidation markers malondialdehyde (MDA) and thiobarbituric acid-reactive substances (TBARS). Results: In the baseline data, we found higher levels of serum MCP-1 in alcohol drinkers, higher Eotaxin-1 in older individuals and elevated TARC in smokers. Serum RANTES, MCP-2, and TARC decreased by 25.84%, 20.88% and 35.30% respectively (P<0.0001) from the before to the during-Olympic period and then increased by 45.84%, 34.92% and 61.53% respectively (P<0.0001) after the air pollution control measures ceased. Significant decreases in GRO-α and IL-8 were found from pre- to during-Olympics, but their levels increased non-significantly after the Olympics. For Eotaxin-1, non-significant decrease was found from pre- to during-Olympics, while significant increase was found from during to post-Olympics. TAS showed positive correlations with MCP-1 (r=0.19606, p=0.0518), MCP-2 (r=0.30958, p= 0.0018), Eotaxin-1 (r=0.27219, p=0.007) and TARC (r=0.21458, p=0.0329). TBARS and MDA showed no significant associations with any chemokine. Conclusion: Our findings suggest that chemokines might act as important mediators in the inflammatory pathway induced by air pollution exposure. Levels of chemokines are affected by some demographic and lifestyle factors. Correlations between chemokines and oxidative stress biomarkers exist in this healthy general population.