An interagency comparison of screening-level risk assessment approaches.

Approaches to risk assessment have been shown to vary among regulatory agencies and across jurisdictional boundaries according to the different assumptions and justifications used. Approaches to screening-level risk assessment from six international agencies were applied to an urban case study focusing on benzo[a]pyrene (B[a]P) exposure and compared in order to provide insight into the differences between agency methods, assumptions, and justifications. Exposure estimates ranged four-fold, with most of the dose stemming from exposure to animal products (8-73%) and plant products (24-88%). Total cancer risk across agencies varied by two orders of magnitude, with exposure to air and plant and animal products contributing most to total cancer risk, while the air contribution showed the greatest variability (1-99%). Variability in cancer risk of 100-fold was attributed to choices of toxicological reference values (TRVs), either based on a combination of epidemiological and animal data, or on animal data. The contribution and importance of the urban exposure pathway for cancer risk varied according to the TRV and, ultimately, according to differences in risk assessment assumptions and guidance. While all agency risk assessment methods are predicated on science, the study results suggest that the largest impact on the differential assessment of risk by international agencies comes from policy and judgment, rather than science.

Is house dust the missing exposure pathway for PBDEs? An analysis of the urban fate and human exposure to PBDEs.

Polybrominated diphenyl ether (PBDE) body burdens in North America are 20 times that of Europeans and some "high accumulation" individuals have burdens up to 1-2 orders of magnitude higher than median values, the reasons for which are not known. We estimated emissions and fate of sigma PBDEs (minus BDE-209) in a 470 km2 area of Toronto, Canada, using the Multi-media Urban Model (MUM-Fate). Using a combination of measured and modeled concentrations for indoor and outdoor air, soil, and dust plus measured concentrations in food, we estimated exposure to sigma PBDEs via soil, dust, and dietary ingestion and indoor and outdoor inhalation pathways. Fate calculations indicate that 57-85% of PBDE emissions to the outdoor environment originate from within Toronto and that the dominant removal process is advection by air to downwind locations. Inadvertent ingestion of house dust is the largest contributor to exposure of toddlers through to adults and is thus the main exposure pathway for all life stages other than the infant, including the nursing mother, who transfers PBDEs to her infant via human milk. The next major exposure pathway is dietary ingestion of animal and dairy products. Infant consumption of human milk is the largest contributor to lifetime exposure. Inadvertent ingestion of dust is the main exposure pathway for a scenario of occupational exposure in a computer recycling facility and a fish eater. Ingestion of dust can lead to almost 100-fold higher exposure than "average" for a toddler with a high dust intake rate living in a home in which PBDE concentrations are elevated.