Exploring the adverse effect of fine particulate matter (PM2.5) on wildland firefighters’ pulmonary function and DNA damage

Abstract Chiang Mai encounters severe pollution during the wildfire season. Wildland firefighters encounter various hazards while engaged in fire suppression operations, which encompass significant exposure to elevated concentrations of air pollutants resulting from combustion, especially particulate matter. The adverse effects of wildfire smoke on respiratory health are a significant concern. The objective of this study was to examine the potential adverse effects of PM 2.5 exposure on the respiratory function and DNA damage of wildland firefighters. This prospective cohort study conducted in Chiang Mai from January to May 2022 planned to evaluate the health status of wildland firefighters during the pre-peak, peak, and post-peak ambient air pollution seasons. The measurement of PM2.5 was done at every forest fire station, as well as utilizing data from the Pollution Control Department. Participants received general health examinations, spirometry evaluations, and blood tests for DNA damage analysis. Pair t -tests and multiple regression models were used to examine the connection between pulmonary function parameters (FVC, FEV 1 ) and PM 2.5 concentration, with a significance level of P 15%. Multiple regression analysis showed a negative association between PM 2.5 exposure and FVC% predicted (− 2.81%, 95% CI − 5.27 to − 0.34%, P = 0.027) and a marginally significant negative correlation with FVC (− 114.38 ml, 95% CI − 230.36 to 1.59 ml, P = 0.053). The remaining pulmonary measures showed a statistically insignificant decline. There were no significant changes in DNA damage detected. Wildland firefighters suffered a significant decline in pulmonary function associated with PM 2.5 exposure. Spirometry is crucial for monitoring and promptly identifying respiratory issues that occur during wildfire seasons. Further research is recommended to explore DNA damage alterations and their potential association with PM2.5.