Polybrominated diphenyl ether (PBDE) flame retardants are ubiquitous in the environment and in humans. A decabromodiphenyl ether mixture (deca-BDE) is the dominating commercial PBDE product today. Deca-BDE is degraded by UV to PBDEs with fewer bromines. We hypothesized that photodegradation of deca-BDE results in the formation of free radicals. We employed electron paramagnetic resonance (EPR) with spin trap agents to examine the free radicals formed from UV irradiation of a deca-BDE mixture (DE-83R). The activating wavelength for deca-BDE photochemistry was in the UVA to UVB range. The yields of radicals from irradiated deca-BDE in tetrahydrofuran (THF), dimethylformamide (DMF), and toluene were about 9-, 4-, and 7-fold higher, respectively, than from irradiated solvent alone. Radical formation increased with deca-BDE concentration and irradiation time. The quantum yield of radical formation of the deca-BDE mixture was higher than with an octa-BDE mixture (DE-79; ~2-fold), decabromobiphenyl (PBB 209; ~2-fold), decachlorobiphenyl (PCB 209; ~3-fold), and diphenylether (DE; ~6-fold), indicating the positive effects of bromine and an ether bond on radical formation. Analysis of hyperfine splittings of the spin adducts suggests that radical formation is initiated or significantly enhanced by debromination paired with hydrogen abstraction from the solvents. To our knowledge this is the first report that uses EPR to demonstrate the formation of free radicals during the photolytic degradation of PBDEs. Our findings strongly suggest the potential of negative consequences due to radical formation during UV exposure of PBDEs in biological systems.

Decabromodiphenylether (deca-BDE) and triclosan (2,4,4'-trichloro-2'hydroxydiphenylether) are used in consumer products as flame retardant and bactericide, respectively. Dermal contact is a major human exposure pathway. Deca-BDE and triclosan are known to be photolytically degraded to compounds like lower-BDEs and dioxins. My hypothesis is that photolysis of deca-BDE and triclosan generates free radicals and degradation products which cause toxic effects including cytotoxicity, growth inhibition, oxidative stress and genotoxicity in skin. To test this hypothesis radical formation and photolytic products of deca-BDE and toxic effects of deca-BDE and triclosan alone/with UV-exposure were determined using immortal human keratinocytes (HaCaT) and primary human skin fibroblasts (HSF). My electron paramagnetic resonance and GC-MS studies indicate that deca-BDE is photoreactive and UV irradiation of deca-BDE in organic solvents generates free radicals and lower-BDEs. The free radical formation is wavelength-dependent and positively related to the irradiation time and deca-BDE concentration. In structure-activity relationship studies with deca-BDE, octa-BDE, PBB 209, PCB 209 and diphenyl ether, the presence of halogen atoms (Br > Cl), and/or an ether bond enhance free radical formation. Debromination and hydrogen abstraction from the solvents are the mechanism of radical formation with deca-BDE, which raises concerns about possible toxic effects in UV-exposed skin. In cell culture experiments high levels of triclosan plus UV irradiation and repetitive deca-BDE and UV exposures caused synergistic cytotoxicity in HaCaT. However, neither triclosan nor deca-BDE can be regarded as a phototoxicant following the OECD test and evaluation guidelines. In HSF, no synergistic cytotoxicity was observed, although HSF were more sensitive to deca-BDE and triclosan alone than HaCaT. Contrary to expectations, the photodegradation products of triclosan were less vi Methods .