Particulate matter 2.5 induced inflammatory responses and metabolic alterations in human monocytes

Fine particulate matter 2.5 (PM_2.5) 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 PM_2.5 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 PM_2.5 collected in Chiang Mai (CM-PM_2.5) during the peak of poor air quality in 2020 affected the innate immune responses of primary human monocytes. PM_2.5, PM₁₀, NO₂, and O₃ air quality index (AQI) levels concurrently increased throughout the year. Notably, PM_2.5 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-PM_2.5 (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-PM_2.5 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-PM_2.5. This study provides strong evidence that exposure to PM_2.5 disrupts metabolism and alters responses of human innate immune cells which may contribute to increased severity of respiratory diseases.