Disrupted biomineralization in zebra mussels after exposure to bisphenol-A: Potential implications for molar-incisor hypomineralization

•Biomineralization in mussels could be a model for screening potential MIH-related factors.•Potential MIH-causative chemicals disrupted shell mineralization.•BPA could be a potential causative factor of MIH in humans. The aetiology of molar-incisor hypomineralization (MIH) is currently unclear. A major hurdle in MIH research is the lack of adequate model systems. The study investigated the feasibility of zebra mussel (Dreissena polymorpha) as a novel model to screen potential MIH-related factors. In four experiments with overall 46 groups (n = 7 mussels/group), six groups per experiment were incubated with 100 mg/l calcein (mineralization marker) solution for 96 h to evaluate the dynamics of shell biomineralization, another six groups with tap water only (controls). Then zebra mussels with and without calcein pre-incubation were exposed to cadmium sulfate hydrate (3CdSO4•8H2O) (positive control; 0, 0.01, 0.1, 1, 10 and 100 mg/l), possible aetiological factors of MIH including bisphenol-A (BPA; 0, 0.02, 0.2, 2, 20 and 200 mg/l) and erythromycin (0, 0.1, 1, 10, 100 and 1000 mg/l) as mineralization “disruptors”, and doxycycline (0, 0.1, 1, 10, 100 and 1000 mg/l) for 96 h, respectively. After two weeks, the mussels were sacrificed and shells were embedded in methylmethacrylate for fluorescence intensity analysis. Mortality rate was 100% after 20, 200 mg/l BPA and 10, 100 mg/l 3CdSO4•8H2O exposure. Thereby, the median lethal concentration (96 h-LC50) of BPA was 6.3 mg/l (95% CI, 1.3–34.4 mg/l), and that of cadmium was 3.1 mg/l (95% CI, 0.7–10.5 mg/l). Notably, calcein fluorescence in shells significantly decreased (p