Abstract
Fine particulate matter 2.5 (PM2.5) is linked to rising cases of respiratory, cardiovascular, and immune-mediated diseases and increased hospitalizations in non-respiratory patients. Chiang Mai Province in Northern Thailand, faces seasonal severe PM2.5 pollution, but its impact on immune responses in human remains poorly characterized. This study aimed to investigate the association between air pollution and non-communicable diseases in Chiang Mai and to assess how PM2.5 collected in Chiang Mai (CM-PM2.5) during the peak of poor air quality in 2020 affected the innate immune responses of primary human monocytes. PM2.5, PM10, NO2, and O3 air quality index (AQI) levels concurrently increased throughout the year. Notably, PM2.5 and NO2 AQI levels were positively correlated with the incidence of chronic obstructive pulmonary disease (COPD) in Chiang Mai. Transcriptomic profiling of primary human monocytes stimulated with CM-PM2.5 (5 and 20 μg/ml) for 24 h indicated a dose-dependent effect on gene expression profiles. Alterations in pyrimidine ribonucleotide metabolism were observed at both CM-PM2.5 concentrations. Upregulation of key metabolic genes (CYP1B1, HK2, and XYLT1) and suppression of glycolytic activity were observed with treatment of 20 μg/ml of CM-PM2.5. This study provides strong evidence that exposure to PM2.5 disrupts metabolism and alters responses of human innate immune cells which may contribute to increased severity of respiratory diseases.