With the increasingly serious problem of environmental pollution, the health problems caused by PM2.5 are gradually coming into our line of sight. Previous researches have indicated that air pollution is nearly related to various diseases, but few studies have focused on the exact function mediated by particulate matter less than 2.5 (PM2.5) in these diseases. PM2.5 is known to induce multiple ways of cell death, including autophagy, necrosis, apoptosis, pyroptosis and ferroptosis. Therefore, it is of much importance to understand the different ways of cell death caused by PM2.5 in the pathogenesis and treatment of PM2.5-related diseases. This present review is an insight of multiple ways of PM2.5‑induced cell death in different diseases.

Epidemiologic studies have reported the association between fine particles (aerodynamic diameter ≤ 2.5 μm; PM2.5) and health effects, but the immunological mechanisms are not clear. To investigate the dose and time-dependent role of toll-like receptor (TLR) and Th1/Th2 shift in local and systemic inflammation induced by PM2.5, mice were subjected to intratracheal instillation of 2.5, 5, or 10 mg/kg PM2.5 in this study. After 24 h, 72 h, 7 days, and 14 days, mice were sacrificed to measure TLR2 and TLR4 expressions and Th1/Th2 related cytokines in bronchoalveolar lavage fluid (BALF) and peripheral blood. Histopathological changes in lung were also examined. Inflammatory infiltration and macrophages with engulfed particles were found by lung histopathology after PM2.5 exposure. TLR4 positive cells decreased in BALF but increased in blood at 24 h after the exposure. The low percentage of TLR4 positive cells continued to day 14 in BALF, but recovered at day 7 and decreased further to lower than the control value at day 14 in blood. TLR2 positive cell changed similar to TLR4 in BALF on the dose effects. In BALF at 24 h after the exposure, the Th2 related cytokines IL-5 and IL-10 increased dose-dependently; and in blood, the Th2 related cytokines IL-4, IL-5, and IL-10 also increased. These results suggest that acute exposure of PM2.5 leads to acute inflammatory responses locally and systemically in mice. TLR2 and TLR4 are involved in this process and PM2.5 can drive a Th2-biased immune response.

Air pollutants are associated with cardiovascular death; however, there is limited evidence of the effects of different pollutants on out-of-hospital cardiac arrests (OHCAs) in Beijing, China. We aimed to investigate the associations of OHCAs with the air pollutants PM_2.5–10 (coarse particulate matter), PM_2.5 (particles ≤2.5 μm in aerodynamic diameter), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), carbon monoxide (CO), and ozone (O₃) between 2013 and 2015 using a time-stratified case-crossover study design. We obtained health data from the nationwide emergency medical service database; 4720 OHCA cases of cardiac origin were identified. After adjusting for relative humidity and temperature, the highest odds ratios of OHCA for a 10 μg/m³ increase in PM_2.5 were observed at Lag Day 1 (1.07; 95% confidence interval (CI): 1.04–1.10), with strong associations with advanced age (aged ≥70 years) (1.09; 95% CI: 1.05–1.13) and stroke history (1.11; 95% CI: 1.06–1.16). PM_2.5–10 and NO₂ also showed significant associations with OHCAs, whereas SO₂, CO, and O₃ had no effects. After simultaneously adjusting for NO₂ and SO₂ in a multi-pollutant model, PM_2.5 remained significant. The effects of PM_2.5 in the single-pollutant models for cases with hypertension, respiratory disorders, diabetes mellitus, and heart disease were higher than those for cases without these complications; however, the differences were not statistically significant. The results support that elevated PM_2.5 exposure contributes to triggering OHCA, especially in those who are advanced in age and have a history of stroke.