Metabolism of Oxybenzone and Dioxybenzone to Phototoxins in Human Skin Cells

Recent research indicated that exposure of sea anemones in full-spectrum sunlight to the UV filter, oxybenzone, induced increased mortality attributable to the production of phototoxic glucoside metabolites. This study evaluated whether exposure of oxybenzone and dioxybenzone to human skin cell models formed analogous glucuronide conjugates and induced a reduction in cell viability under full-spectrum sunlight. In dose–response evaluations with two human skin cell models, increasing doses of oxybenzone or dioxybenzone (up to 0.1%) or increasing exposure times (up to 24 h) were associated with decreasing skin cell viability. Approximately 20–25% of both UV filters were metabolized to their corresponding glucuronide metabolites during permeation through the skin cell models. The masses of UV filters and their metabolites both were correlated with decreasing skin cell viability. While residual UV filters at the skin surface could shield against such phototoxic effects, these results suggest a benefit to identifying novel sunscreen components that avoid potentially phototoxic glucuronide metabolites.