Is House Dust the Missing Exposure Pathway for PBDEs? An Analysis of the Urban Fate and Human Exposure to PBDEs

Abstract

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.

Quantified outdoor micro-activity data for children aged 7–12-years old

“…Incidental ingestion is a primary route of exposure for pesticides, metals including lead and arsenic, flame retardants and microbes (Chisolm Jr and Harrison, 1956;Aung et al, 2004;Jones-Otazo et al, 2005;Zartarian et al, 2006;De Miguel et al, 2007;Morgan et al, 2007;Nicas and Best, 2008). Furthermore clean-up decisions and appropriate risk mitigation actions for hazardous waste sites, including Superfund sites, are based on estimates of the incidental ingestion and dermal exposure pathways (US EPA, 2004).…”

“…Non-dietary ingestion exposure has continued to be the primary route for lead and other heavy metal exposure in children (Chisolm Jr and Harrison, 1956;Aung et al, 2004;Zartarian et al, 2006;De Miguel et al, 2007), and is the primary contribution to the polybromindated diphenyl ether body burden of toddlers through adults (Jones-Otazo et al, 2005). Furthermore, non-dietary ingestion exposure is the primary means of transmission for certain infectious diseases like the influenza virus, where exposure occurs through the hand and mouthing contacts with fomites (Nicas and Best, 2008).…”

Developmental neurotoxicity of polybrominated diphenyl ether (PBDE) flame retardants

“…For example, with regard to occupational exposure, in a group of computer dismantlers, serum levels of PBDEs were 26 ng/g, compared to 3.3 ng/g in a reference group of hospital cleaners (Sjodin et al 1999). Among foods, fish has the highest content of PBDEs, followed by meat and diary products, with meat estimated to be the major source of PBDEs in the U.S. diet (Schecter et al 2004;Hites et al 2004;Jones-Otazo et al 2005;Schecter et al 2006a). In a small study, vegetarians (vegans) were found to have somewhat lower plasma levels of PBDEs (range 12.4 -127 ng/g lipid) than the general U.S. population (4 -366 ng/g lipid) (Schecter et al 2006b).…”

“…Given the high levels found in breast milk, it has been estimated that a breastfed infant would be exposed to approximately 306 ng/kg/day of PBDE, as compared to about 1 ng/kg/day for adults (Schecter et al 2006a; see also Table 4). Although PBDE contamination of food is currently higher in the USA than in other countries, diet alone cannot explain the higher levels of PBDEs in the general U.S. population (Jones-Otazo et al 2005;Wilford et al 2005;Schecter et al 2006a;Fischer et al 2006;Lorber, 2007). Several studies have indicated that house dust is a major source of exposure to PBDEs (Jones-Otazo et al 2005;Schecter et al 2005b;Wu et al 2007).…”

Evaluating Indoor Exposure Modeling Alternatives for LCA: A Case Study in the Vehicle Repair Industry

“…Consequently, inhalation intake fractions of indoor emissions can exceed those of outdoor emissions by several orders of magnitude [1][2][3]. For example, in vehicle repair shops, solvents in "aerosol" cans are used in large quantities during tasks such as engine repair, brake cleaning, oil changes, etc [4,5].…”