An updated weight of evidence approach to the aquatic hazard assessment of Bisphenol A and the derivation a new predicted no effect concentration (Pnec) using a non-parametric methodology

Abstract

An aquatic hazard assessment establishes a derived predicted no effect concentration (PNEC) below which it is assumed that aquatic organisms will not suffer adverse effects from exposure to a chemical. An aquatic hazard assessment of the endocrine disruptor Bisphenol A [BPA; 2, 2-bis (4-hydroxyphenyl) propane] was conducted using a weight of evidence approach, using the ecotoxicological endpoints of survival, growth and development and reproduction. New evidence has emerged that suggests that the aquatic system may not be sufficiently protected from adverse effects of BPA exposure at the current PNEC value of 100 μg/L. It is with this background that; 1) An aquatic hazard assessment for BPA using a weight of evidence approach, was conducted, 2) A PNEC value was derived using a non parametric hazardous concentration for 5% of the specie (HC 5) approach and, 3) The derived BPA hazard assessment values were compared to aquatic environmental concentrations for BPA to determine, sufficient protectiveness from BPA exposure for aquatic species. A total of 61 studies yielded 94 no observed effect concentration (NOEC) and a toxicity dataset, which suggests that the aquatic effects of mortality, growth and development and reproduction are most likely to occur between the concentrations of 0.0483 μg/L and 2280 μg/L. This finding is within the range for aquatic adverse estrogenic effects reported in the literature. A PNEC of 0.06 μg/L was calculated. The 95% confidence interval was found to be (0.02, 3.40) μg/L. Thus, using the weight of evidence approach based on repeated measurements of these endpoints, the results indicate that currently observed BPA concentrations in surface waters exceed this newly derived PNEC value of 0.06 μg/L. This indicates that some aquatic receptors may be at risk for adverse effects on survival, growth and development and reproduction from BPA exposure at environmentally relevant concentrations.