Effects of ambient fine particulate matter on oxidative stress, inflammation, and janus kinase/signal transducer and activator of transcription signal molecules: a panel study of asthmatic adults in Taiyuan, China

This panel study attempted to assess the effects of ambient fine particulate matter (PM 2.5 ) exposure on oxidative stress, inflammation, and janus kinase (JAK)/signal transducer and activator of transcription (STAT) signal molecules. Twenty-nine nonsmoking adults with asthma were followed up for three seasons. Lung function was measured four times and peripheral blood was collected one time per season. The markers of oxidative stress, inflammation, and JAK/STAT were detected. Daily concentration of ambient PM 2.5 was recorded from the China National Environmental Monitoring Center. Linear mixed-effects regression models were used to investigate the relationships of ambient PM 2.5 with the index of lung function, oxidative stress, inflammation, and JAK/STAT. Mediation analyses were used to explore the mediation effect of JAK. The concentration of PM 2.5 was the highest in spring, with a median of 151 μg/m 3 . In the analyses of oxidative stress, the malonaldehyde (MDA) increased by 3.80% (95% CI: 2.43 to 5.17%; p <0.001) for each 10 μg/m 3 increase in lag4 PM 2.5 exposure. Furthermore, we detected a significant association in cytokines. Lag4 PM 2.5 exposure was associated with an increased interleukin-4 (IL-4) by 3.00% (95% CI: 0.26 to 5.74%; p <0.05). Besides, we found mediation of JAK2 in the associations between superoxide dismutase (SOD)/IL-12 and STAT4, JAK3 in the association between MDA and STAT6. The injury of pulmonary function in asthmatic adults induced by ambient PM 2.5 exposure is most likely to occur at lag 4 days. Ambient PM 2.5 aggravates asthma by systemic oxidative stress and inflammation, in which JAK/STAT signal molecules may be involved. Graphical abstract