Bisphenol P activates hormonal genes and introduces developmental outcomes in Chironomus tentans

The endocrine disrupting properties of bisphenol A (BPA) discharged to the environment have been newly identified by the European Chemicals Agency, increasing the need to assess the environmental endocrine disrupting potentials of its alternatives with which it shares close structural features. However, few investigations of the environmental endocrine disrupting functions of BPA analogs have been conducted to date. In this study, the endocrine disrupting effects of a BPA analog of bisphenol P (BPP) were investigated in the nonbiting midge (Chironomus tentans), a model organism in ecotoxicology. An initial ex vivo test using salivary gland cells explanted from the larvae and a subsequent in vivo test using embryos and larvae revealed the upregulatory effects of BPP on ecdysone receptor genes encoding the ecdysone receptor (EcR) and the early responsive gene E74, with a similar temporal pattern of gene activation. Partial life cycle and full life cycle toxicity tests demonstrated BPP altered embryo hatching, larval emergence, and adult sex ratio at concentrations close to the effective concentrations for hormonal genetic endpoints in embryos and larvae after 48 h of exposure. Although embryos appeared to be more sensitive to BPP than the fourth instar larvae, the impact on neither life stage seemed enough to estimate the developmental impairment of the insects. These results demonstrate the ecdysone pathway is a target of BPP, and that long-term exposure could cause apical effects on the development of C. tentans. The endocrine disrupting effects towards aquatic organisms, as well as the high persistence and bioconcentration potential, indicate an urgent need to assess the environmental risks associated with BPP.