An updated review of new brominated flame retardant decabromodiphenyl ethane (DBDPE): environmental fate, toxicokinetics, toxicity, and mechanisms based on adverse outcome pathway framework.

Decabromodiphenyl ethane (DBDPE), a novel brominated flame retardant (NBFR) widely adopted as a primary replacement for banned decabromodiphenyl ether (BDE-209), now permeates global environmental matrices. Emerging evidence indicates DBDPE elicits biota toxicity and poses human health risks. This review synthesizes current knowledge on DBDPE's environmental distribution, contamination characteristics, and toxicokinetic profiles-including absorption, distribution, metabolism, and excretion (ADME) in vivo. We critically evaluate its multi-system toxicity (neurological, thyroid, hepatic, intestinal, reproductive, cardiovascular, endocrine) and associated mechanisms. Evidence indicates DBDPE is ubiquitously detected in air, indoor/outdoor dust, soil, water, sediments, and wastewater sludge, with manufacturing emissions and waste disposal identified as dominant pollution sources. Urbanization metrics (population density, city size) correlate significantly with environmental concentrations. Post-absorption, DBDPE bioaccumulates in lipid-rich tissues (adipose, brain, liver, gonads), driving organ-specific toxicity. Finally, an adverse outcome pathway (AOP) framework was constructed to elucidate DBDPE toxicity, synthesizing evidence that identifies reactive oxygen species (ROS) formation as the primary molecular initiating event (MIE). This MIE triggers key cellular events, including oxidative stress, mitochondrial dysfunction, DNA damage, and programmed cell death pathways, culminating in inflammation, multi-organ injury, and heightened human health risks. Future research should prioritize developing strategies to reduce environmental DBDPE levels, creating interventions to mitigate its toxicity informed by established toxicological mechanisms, and conducting human health risk assessments.