The health of humans has been negatively impacted by PM_2.5 exposure, but the chemical composition and toxicity of PM_2.5 might vary depending on its source. To investigate the toxic effects of particulate matter from different sources on lung epithelial cells (A549), PM_2.5 samples were collected from residential, industrial, and transportation areas in Nanjing, China. The chemical composition of PM_2.5 was analyzed, and toxicological experiments were conducted. The A549 cells were exposed using an air–liquid interface (ALI) exposure system, and the cytotoxic indicators of the cells were detected. The research results indicated that acute exposure to different sources of particulate matter at the air–liquid interface caused damage to the cells, induced the production of ROS, caused apoptosis, inflammatory damage, and DNA damage, with a dose–effect relationship. The content of heavy metals and PAHs in PM_2.5 from the traffic source was relatively high, and the toxic effect of the traffic–source samples on the cells was higher than that of the industrial– and residential–source samples. The cytotoxicity of particulate matter was mostly associated with water–soluble ions, carbon components, heavy metals, PAHs, and endotoxin, based on the analysis of the Pearson correlation. Oxidative stress played an important role in PM_2.5–induced biological toxicity.

PM_2.5 is an air pollutant with complex components. After entering the body through respiration, PM_2.5 can not only cause respiratory diseases, but also break through the blood–testis barrier and influence the reproductive system. PM_2.5 with different components may result in different toxic effects. In the first five years of Nanjing Jiangbei New Area, industrial transformation would change the concentration and chemical fraction of PM_2.5 in the local environment to a certain extent. In this study, PM_2.5 collected in Nanjing Jiangbei New Area every autumn and winter from 2015 to 2019 was analyzed. PM_2.5 concentration generally decreased year by year. The large proportion of secondary inorganic ions indicated the presence of secondary pollution at the sampling site. PM_2.5 was mainly emitted from fossil fuel combustion and vehicle exhaust. The cytotoxicity of PM_2.5 samples was evaluated by PM_2.5 exposure to mouse spermatocytes (GC-2spd(ts) cells). Cell viability was relatively low in 2016 and 2018, and relatively high in 2017 and 2019. Reactive oxygen species levels and DNA damage levels followed similar trends, with an overall annual decrease. The cytotoxicity of PM_2.5 on GC-2spd(ts) cells was significantly correlated with water-soluble ions, water-soluble organic carbon, heavy metals and polycyclic aromatic hydrocarbons (p < 0.01). According to principal component analysis and multiple linear regression, fossil fuel combustion, secondary transformation of pollutants and construction dust were identified as the major contributors to cytotoxic effects, contributing more than 50%.

While numerous studies have demonstrated the adverse effects of fine particulate matter (PM) on human health, little attention has been paid to its impact on offspring health. The multigenerational toxic effects on Caenorhabditis elegans (C. elegans) were investigated by acute exposure. PM_2.5 and PM₁ samples were collected and analysed for their chemical composition (inorganic ions, metals, OM, PAHs) in different seasons from April 2019 to January 2020 in Lin’an, China. A higher proportion of organic carbon components (34.3%, 35.9%) and PAHs (0.0144%, 0.0200%) occupied the PM_2.5 and PM₁ samples in winter, respectively. PM₁ in summer was enriched with some metal elements (2.7%). Exposure to fine PM caused developmental slowing and increased germ cell apoptosis, as well as inducing intestinal autofluorescence and reactive oxygen species (ROS) production. PM₁ caused stronger toxic effects than PM_2.5. The correlation between PM component and F0 generation toxicity index was analysed. Body length, germ cell apoptosis and intestinal autofluorescence were all highly correlated with Cu, As, Pb, OC and PAHs, most strongly with PAHs. The highest correlation coefficients between ROS and each component are SO₄²⁻ (R = 0.743), Cd (R = 0.816) and OC (R = 0.716). The results imply that OC, PAHs and some transition metals play an important role in the toxicity of fine PM to C. elegans, where the organic fraction may be the key toxicogenic component. The multigenerational studies show that PM toxicity can be passed from parent to offspring, and gradually returns to control levels in the F3–F4 generation with germ cell apoptosis being restored in the F4 generation. Therefore, the adverse effects of PM on reproductive damage are more profound.

Although the health risks associated with the use of biomass fuels have received widespread attention, there has been insufficient detailed research conducted on the toxic effects and toxicity generation mechanisms of PM_2.5 produced by the use of different sources of solid organic fuels. In this study, the synchronized L4-stage Caenorhabditis elegans (C. elegans) were exposed to the suspensions of the PM_2.5 samples collected from incomplete combustion products of rice straw, wheat straw, peanut straw, rapeseed straw and the branch of poplar and paulownia. Body length, the number of fertilized eggs, accumulation of lipofuscin, and levels of reactive oxygen species (ROSs) were measured to characterize developmental toxicity, reproductive toxicity, intestinal damage, and oxidative stress. The types and mass proportions of organic carbon (OC), elemental carbon (EC), water-soluble inorganic ions, and polycyclic aromatic hydrocarbons (PAHs) in PM_2.5 were determined. The results show that PM_2.5 generated from the combustion of the straw of oilseed crops such as peanuts and rapeseed has the most severe toxic effects on C. elegans. The toxicological mechanism was mainly mediated by severe oxidative stress and excessive generation of ROSs. The chemical characteristics of PM_2.5 have strong source-specificity, and its toxic effects are closely related to the high content of lipid-soluble PAHs in PM_2.5 from oilseed crop sources.