The relationship between particulate matter (PM) pollution exposure and lung cancer incidence has been well established. However, the association between PM exposure and immunosurveillance, which indirectly controls tumor growth and progression, remains limited. In this study, we investigated the effect of urban particulate matter (UPM) on modulating the cancer microenvironment, particularly its impact on immunosurveillance functions. Exposure of non-small cell lung cancer (NSCLC) cell lines, A549 and NCI-H1975, to UPM induced the expression of the immune checkpoint molecule programmed cell death ligand 1 (PD-L1) in a dose-dependent manner. Additionally, UPM exposure upregulated the mRNA expression of transforming growth factor-beta (TGF-β), an immunosuppressive cytokine. The alteration in the cytokine profile upon UPM exposure impaired dendritic cell maturation, as evidenced by the retention of the CD14 monocyte marker after monocytes were exposed to UPM-treated cancer cell supernatant during the maturation process. Autologous T cells activated by UPM-treated dendritic cells exhibited reduced anti-tumor activity compared to those activated by untreated dendritic cells. This was demonstrated by the lower cancer cell death observed in cancer-T cell co-culture assays. However, there were no significant changes in immune cell populations, including CD4+ T lymphocytes, CD8+ T lymphocytes, and CD3-negative cells, between the UPM-treated dendritic cell group and the conventional dendritic cell group. This suggests that UPM affects immune function primarily in terms of quality rather than quantity. In conclusion, our findings indicate that PM exposure promotes cancer progression by altering the tumor microenvironment and impairing immunosurveillance function.

Fine particulate matter (PM2.5) is a major air pollutant linked to lung cancer progression. In Southeast Asia, seasonal smoke-haze produces biomass-derived PM2.5, yet its acute effects on genetically diverse lung tumours remain unclear. We investigate how Chiang Mai haze-derived PM2.5 impacts oxidative stress and gene expression in three non-small-cell lung cancer (NSCLC) cell lines: A549 (KRAS-mutant), NCI-H1975 (EGFR-mutant), and NCI-H460 (KRAS/PIK3CA-mutant). Cells were exposed to PM2.5 (0–200 µg/mL) and assessed for viability (MTT), reactive oxygen species (ROS; H₂O₂, •OH) and malondialdehyde (MDA) levels, mitochondrial-associated fluorescence, and whole-transcriptome responses. Acute exposure caused dose- and time-dependent viability loss, with A549 and NCI-H1975 more sensitive than NCI-H460. ROS profiling normalized to viable cells revealed genotype-specific oxidative patterns: cumulative increases in A549, sharp reversible spikes in NCI-H1975, and modest changes in NCI-H460. MitoTracker intensity trended downward without significance, with subtle fluorescence changes and particulate uptake. RNA-seq identified robust induction of xenobiotic metabolism (CYP1A1, CYP1B1), oxidative/metabolic stress mediators (GDF15, TIPARP), and tumour-associated genes (FOSB, VGF), alongside repression of tumour suppressors (FAT1, LINC00472). Pathway enrichment analyses highlighted oxidative stress, IL-17, NF-κB, and immune checkpoint signaling. Together, biomass haze-derived PM2.5 from Northern Thailand drives genotype-dependent oxidative stress and transcriptional remodeling in NSCLC cells.