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.