Effect of Co-Exposure to Temperature and Fine Particulate Matter on Metabolomic and Immune Processes among Chinese Women of Childbearing Age

Short-term exposures to temperature and fine particulate matter (PM2.5) have been associated with metabolomic perturbations. However, their combined effect on the metabolome has not been evaluated. We investigated the effect of short-term coexposure to temperature and PM2.5 on metabolomic signatures and the potential roles of serum lipids and biomarkers using a repeated-measures study among Chinese women of childbearing age. We performed untargeted metabolomic profiling to quantify plasma metabolites. Data on temperature and PM2.5 exposures were estimated using a fused estimator. Serum lipids and biomarkers of oxidative stress and inflammation were detected. The independent and combined effects of temperature and PM2.5 were estimated using a linear mixed-effect model and quantile-based g-computation, respectively. Pathway analysis was conducted to identify perturbed metabolic pathways. Ten women provided 46 blood samples, from which 139 metabolites were quantified. Temperature and PM2.5 had independent effects on several metabolites and pathways. The largest positive and negative combined effects were observed for benzyl sulfate [β = 1.460, 95% confidence interval (CI): 0.438, 2.481] and chenodeoxycholic acid glycine conjugate (β = −1.933, 95% CI: −3.473, −0.392), respectively. Co-exposure to temperature and PM2.5 perturbed four pathways, including biosynthesis of unsaturated fatty acids; phenylalanine, tyrosine and tryptophan biosynthesis; linoleic acid metabolism; and phenylalanine metabolism. The metabolomic perturbations were mainly related to oxidative stress and the inflammatory response. We observed a positive combined effect of temperature and PM2.5 on interleukin-8. Our findings demonstrate that the metabolic mechanisms induced by temperature and PM2.5 involve oxidative stress and the inflammatory response and suggest that these metabolomic perturbations might promote an inflammatory response via release of interleukin-8.