Toxicity and endocrine-disrupting potential of PM2.5: Association with particulate polycyclic aromatic hydrocarbons, phthalate esters, and heavy metals

The adverse effects of fine atmospheric particulate matter with aerodynamic diameters of ≤2.5 μm (PM2.5) are closely associated with particulate chemicals. In this study, PM2.5 samples were collected from highway and industry sites in Hangzhou, China, during the autumn and winter, and their cytotoxicity and pulmonary toxicity and endocrine-disrupting potential (EDP) were evaluated in vitro and in vivo; the particulate polycyclic aromatic hydrocarbons (PAHs), phthalate esters (PAEs), and heavy metals were then characterized. The toxicological results suggested that the PM2.5 from highway site induced higher cytotoxicity (cell viability inhibition, intracellular oxidative stress, and cell membrane injury) and pulmonary toxicity (inflammatory response (IR) and oxidative stress (OS)) than the samples from industry site, while the PM2.5 from industry site exhibited higher EDP (estrogenic and anti-androgenic activity). The cytotoxicity and pulmonary toxicity of PM2.5 in the winter were higher than those in the autumn, while no seasonal difference in the endocrine-disrupting potential was observed (p > 0.05). The Pearson correlation analysis between the biological effects and particulate chemicals revealed that the PM2.5-induced inflammatory response and oxidative stress were closely associated with the particulate PAHs and heavy metals (Pearson correlation coefficients: rIR, PAHs = 0.822-0.988, rIR, heavy metals = 0.895-0.971, rOS, PAHs = 0.843-0.986, and rOS, heavy metals = 0.887-0.933), while particulate di (2-ethylhexyl)phthalate (DEHP) substantially contributed to the EDP of PM2.5 (rEDP, DEHP = 0.981). This study indicated that the toxicity and EDP of PM2.5 could vary with the surrounding environment and season, which was closely associated with the variations of particulate chemicals. Further studies are needed to clarify the associations between the harmful effects of PM2.5 and other contributing factors.