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Polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) were measured in air (using PUF disk passive samplers) in 31 homes, 33 offices, 25 cars, and 3 public microenvironments. Average concentrations of sigmaBDE (273 pg m(-3)) and sigmaPCB (8920 pg m(-3)) were an order of magnitude higher than those previously reported for outdoor air. Cars were the most contaminated microenvironment for sigmaBDE (average = 709 pg m(-3)), but the least for sigmaPCB (average = 1391 pg m(-3)). Comparison with data from a previous spatially consistent study, revealed no significant decline in concentrations of sigmaPCB in indoor air since 1997-98. Concentrations in indoor dust from 8 homes were on average 215.2 ng sigmaBDE g(-1), slightly higher than other European dust samples, but twenty times lower than Canadian samples. Inhalation makes an important contribution (between 4.2 and 63% for adults) to overall UK exposure to sigmaPCB. For sigmaBDE, dust ingestion makes a significant but--in contrast to Canada-a not overwhelming contribution (up to 37% for adults, and 69% for toddlers). Comparison of UK and Canadian estimates of absolute exposure to sigmaBDE suggest that differences in dust contamination are the likely cause of higher PBDE body burdens in North Americans compared to Europeans.

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Hexabromocyclododecanes (alpha-, beta-, and gamma-HBCDs) and tetrabromobisphenol-A (TBBP-A) were determined in indoor air from homes (n=33; median concentrations sigma HBCDs = 180 pg m(-3); TBBP-A = 15 pg m(-3)), offices (n=25; 170; 11), public microenvironments (n=4; 900; 27) and outdoor air (n=5; 37; 1). HBCDs and TBBP-A were also determined in dust from homes (n=45; median concentrations sigma HBCDs = 1300 ng g(-1); TBBP-A = 62 ng g(-1)), offices (n=28; 760; 36), cars (n=20; 13,000; 2), and public microenvironments (n=4; 2700; 230). While sigma HBCDs in car dust significantly exceeded (p < 0.05) those in homes and offices, TBBP-A in car dust was significantly lower (p < 0.05) than that in homes and offices. No significant differences were observed between sigma HBCDs and TBBP-A in air or dust from homes and offices. Compared to dietary and inhalation exposures, dust ingestion constitutes an important pathway of exposure to HBCDs and TBBP-A for the UK population. Specifically, using average dust ingestion rates and concentrations in dust, dust ingestion constitutes for adults 34% (TBBP-A) and 24% (HBCDs) of overall exposure, and for toddlers 90% (TBBP-A) and 63% (HBCDs). Inhalation appears a minor exposure pathway to both HBCDs and TBBP-A. On average, dust is 33% alpha-, 11% beta-, and 56% gamma-HBCD, while air is 22% alpha-, 11% beta-, and 65% gamma-HBCD.