Abstract
This panel study attempted to assess the effects of ambient fine particulate matter (PM2.5) 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 PM2.5 was recorded from the China National Environmental Monitoring Center. Linear mixed-effects regression models were used to investigate the relationships of ambient PM2.5 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 PM2.5 was the highest in spring, with a median of 151 μg/m3. 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/m3 increase in lag4 PM2.5 exposure. Furthermore, we detected a significant association in cytokines. Lag4 PM2.5 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 PM2.5 exposure is most likely to occur at lag 4 days. Ambient PM2.5 aggravates asthma by systemic oxidative stress and inflammation, in which JAK/STAT signal molecules may be involved.
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Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.
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Acknowledgements
We are grateful to all staffs from three Community Healthcare Centers for their assistance in the investigation of asthmatic patients. We like to thank all the participants and investigators for their contribution to the study.
Funding
This study was supported by grants from the National Natural Science Foundation of China (81872589, 81072261), Scientific Research Foundation for Returned Scholars of Ministry of Education (2013-1792), and Research Funding Project for Returned Overseas Students in Shanxi Province (2013-057, 2017-060).
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NL conducted the analyses and drafted the manuscript; XM, JW, HG, BY, JH, GQ, and HL were involved in investigating the population and obtaining the data. LL, JT, XW, CW, DW, and HS revised the draft versions. ZZ designed this study and provided advice on the analyses and interpretation of the data, and revised the draft version of the manuscript. All authors read and approved the final manuscript.
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All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. The research proposal was approved by the Medical Ethics committee of Shanxi Medical University (2012033).
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Highlights
• Exposure to PM2.5 in asthmatic patients disrupts the oxidation-antioxidant system balance and leads to increase of inflammatory cytokines.
• Mediating effect analyses show that JAK/STAT signaling molecules are involved in systemic oxidative stress and inflammation induced by PM2.5 exposure.
• The correlations between lag4 PM2.5 exposure and lung function index, systemic oxidative stress, systemic inflammation, and JAK/STAT signaling molecules are most remarkable.
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Liu, N., Ma, X., Wang, J. et al. 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. Air Qual Atmos Health 15, 403–414 (2022). https://doi.org/10.1007/s11869-021-01139-y
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DOI: https://doi.org/10.1007/s11869-021-01139-y