RESUMO
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. PM2.5 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 PM2.5 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 PM2.5. 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.
RESUMO
Although numerous studies have investigated that atmospheric fine particulate matter (PM2.5) can be toxic to environmental organisms, the research on the reproductive toxicity of PM2.5 is limited, and the key toxic components and underlying mechanisms remain unknown. In this work, PM2.5 samples of four seasons in Nanjing from March 1, 2021, to February 28, 2022 were collected and the chemical components were analyzed. Caenorhabditis elegans (C. elegans) was employed to conduct the toxicological testing. The reproductive toxicity of PM2.5 to C. elegans in different seasons was evaluated by multiple reproductive endpoints. Exposure to high concentrations of PM2.5 significantly decreased the brood size and the number of fertilized eggs in utero. PM2.5 exposure also increased the number of germ cell corpses and caused abnormal expression of apoptosis-related genes (ced-9, ced-4, and ced-3), which confirmed that PM2.5 induced germline apoptosis. In addition, PM2.5 exposure significantly increased the production of reactive oxygen species (ROS) in C. elegans and the fluorescence intensity of HUS-1 protein in of transgenic strain WS1433. Meanwhile, the expression of genes related to DNA damage (cep-1, clk-2, egl-1, and hus-1) and oxidative stress (mev-1, isp-1, and gas-1) also significantly altered in C. elegans, suggesting induction of DNA damage and oxidative stress. According to Pearson correlation analyses, DNA damage and oxidative stress were significantly correlated with multiple reproductive endpoints in C. elegans. Thus, it was speculated that PM2.5 caused reproductive dysfunction and germ cell apoptosis in C. elegans may be by inducing ROS and DNA damage. In addition, heavy metals in PM2.5 were significantly correlated with multiple endpoints at physiological and biochemical, suggesting that the heavy metals might be an important contributor to the reproductive toxicity induced by PM2.5.
