The chronic toxicity of bisphenol A to Caenorhabditis elegans after long-term exposure at environmentally relevant concentrations

To investigate biological effects of bisphenol A (BPA) over the long term, the model animal Caenorhabditis elegans was used to conduct the chronic exposure. C. elegans were exposed to BPA (0.0001–10 μM) from L4 larvae to day-10 adult in the present chronic toxicity assay system. Multiple endpoints at the physiological (growth, locomotion behaviors and lifespan), biochemical (lipofuscin accumulation), molecular (stress-related genes expressions), and population (population size) levels were examined. At the physiological level, BPA exposure induced significant negative effects on the indicators. Among the endpoints, head thrash was most sensitive and the detection limit was 0.001 μM. At the biochemical level, BPA exposure induced no significant effects on lipofuscin accumulation. At the molecular level, BPA induced strong stress responses in vivo. At the population level, the population size was significantly decreased in the treatment groups from 0.1 to 10 μM. Compared to the previous short-term toxicity evaluation, long-term exposure to BPA induced a more obvious response at the same concentration, and the phenomenon might be due to cumulative toxic effects. By the Pearson correlation analyses, cep-1 was speculated to act as an important role in BPA-induced chronic toxicity on C. elegans. [Display omitted] •Long-term exposure was conducted to evaluate chronic toxicity of BPA on Caenorhabditis elegans.•Long-term exposure significantly decreased the head thrash frequency at 0.001 μM.•Chronic exposure induced a stronger stress response than prolonged exposure.•The gene cep-1 might act as an important role in BPA-induced chronic toxicity.