Parental co-exposure to bisphenol A and nano-TiO2 causes thyroid endocrine disruption and developmental neurotoxicity in zebrafish offspring

Abstract

The coexistence of organic toxicants and nanoparticles in the environment influences pollutant bioavailability and toxicity. Using chronic co-exposure to an adult zebrafish model, this study investigated the transfer kinetics and transgenerational effects of bisphenol A (BPA) and titanium dioxide nanoparticles (n-TiO₂) exposure in F1 offspring. When single and combined exposure to BPA (0, 2, and 20 μg/L) and n-TiO₂ (100 μg/L) were compared, combined exposure was found to reciprocally facilitate bioaccumulation in adult fish while enhancing maternal transfer to offspring. Thyroid endocrine disruption and developmental neurotoxicity were observed in larval offspring by parental exposure to BPA alone or in combination with n-TiO₂. Exposure to 20 μg/L BPA significantly decreased the thyroxine (T4) concentration in adult plasma, leading to less transfer into the eggs. The presence of 20 μg/L BPA with n-TiO₂ further decreased the level of T4 compared to BPA exposure alone. Additionally, offspring larvae derived from exposed parents exhibited lethargic swimming behavior. Overall, this study examined the interactions of BPA and n-TiO₂ with regard to their bioaccumulation, maternal transfer, and developmental effects, which highlighted that co-exposure dynamics are important and need to be considered for accurate environmental risk assessment.

Keywords: Bisphenol A; Chronic co-exposure; Developmental neurotoxicity and thyroid disruption; Maternal transfer; Zebrafish; n-TiO(2).