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.