Alicia J. Fraser

Exposure to PBDEs in the office environment: evaluating the relationships between dust, handwipes, and serum.

Background: Polybrominated diphenyl ethers (PBDEs) have been widely used as flame retardants in consumer products and are ubiquitous in residential indoor air and dust. However, little is known about exposure in the office environment. Objectives: We examined relationships between PBDE concentrations in the office environment and internal exposure using concurrent measurements of PBDEs in serum, handwipes, and office dust. Methods: We collected serum, dust, and handwipe samples from 31 participants who spent at least 20 hr/week in an office. We used a questionnaire to collect information about work and personal habits. Results: We found positive associations between PBDEs in room dust, handwipes (a measure of personal exposure), and serum. PBDE office dust concentrations were weakly correlated with measurements in handwipes: r = 0.35 (p = 0.06) for pentaBDE (sum of BDE congeners 28/33, 47, 99, 100, and 153) and 0.33 (p = 0.07) for BDE-209. Hand washing also predicted pentaBDE levels in handwipes: low hand-washers had 3.3 times the pentaBDE levels in their handwipes than did high hand-washers (p = 0.02). PentaBDE in handwipes predicted pentaBDE levels in serum (p = 0.03): Serum concentrations in the highest handwipe tertile were on average 3.5 times the lowest handwipe tertile. The geometric mean concentration of pentaBDEs in serum was 27 ng/g lipid. We detected BDE-209 in 20% of serum samples, at levels ranging from < 4.8 to 9.7 ng/g lipid. Conclusion: Our research suggests that exposure to pentaBDE in the office environment contributes to pentaBDE body burden, with exposure likely linked to PBDE residues on hands. In addition, hand washing may decrease exposure to PBDEs.

Diet contributes significantly to the body burden of PBDEs in the general U.S. population.

BACKGROUND Exposure of the U.S. population to polybrominated diphenyl ethers (PBDEs) is thought to be via exposure to dust and diet. However, little work has been done to empirically link body burdens of these compounds to either route of exposure. OBJECTIVES The primary goal of this research was to evaluate the dietary contribution to PBDE body burdens in the United States by linking serum levels to food intake. METHODS We used two dietary instruments--a 24-hr food recall (24FR) and a 1-year food frequency questionnaire (FFQ)--to examine food intake among participants of the 2003-2004 National Health and Nutrition Examination Survey. We regressed serum concentrations of five PBDEs (BDE congeners 28, 47, 99, 100, and 153) and their sum (Sigma PBDE) against diet variables while adjusting for age, sex, race/ethnicity, income, and body mass index. RESULTS Sigma PBDE serum concentrations among vegetarians were 23% (p = 0.006) and 27% (p = 0.009) lower than among omnivores for 24FR and 1-year FFQ, respectively. Serum levels of five PBDE congeners were associated with consumption of poultry fat: Low, medium, and high intake corresponded to geometric mean Sigma PBDE concentrations of 40.6, 41.9, and 48.3 ng/g lipid, respectively (p = 0.0005). We observed similar trends for red meat fat, which were statistically significant for BDE-100 and BDE-153. No association was observed between serum PBDEs and consumption of dairy or fish. Results were similar for both dietary instruments but were more robust using 24FR. CONCLUSIONS Intake of contaminated poultry and red meat contributes significantly to PBDE body burdens in the United States.

Predictors of tris(1,3-dichloro-2-propyl) phosphate metabolite in the urine of office workers.

Tris(1,3-dichloro-2-propyl) phosphate (TDCPP) is a flame retardant widely used in furniture containing polyurethane foam. It is a carcinogen, endocrine disruptor, and potentially neurotoxic. Our objectives were to characterize exposure of adult office workers (n=29) to TDCPP by measuring its primary metabolite, bis(1,3-dichloro-2-propyl) phosphate (BDCPP), in their urine; measuring TDCPP in dust from their homes; offices and vehicles; and assessing possible predictors of exposure. We identified TDCPP in 99% of dust (GM=4.43μg/g) and BDCPP in 100% of urine samples (GM=408pg/mL). Concentrations of TDCPP were significantly higher in dust from vehicles (GM=12.5μg/g) and offices (GM=6.06μg/g) than in dust from the main living area (GM=4.21μg/g) or bedrooms (GM=1.40μg/g) of worker homes. Urinary BDCPP concentrations among participants who worked in a new office building were 26% of those who worked in older buildings (p=0.01). We found some evidence of a positive trend between urinary BDCPP and TDCPP in office dust that was not observed in the other microenvironments and may be related to the timing of urine sample collection during the afternoon of a workday. Overall our findings suggest that exposure to TDCPP in the work environment is one of the contributors to the personal exposure for office workers. Further research is needed to confirm specific exposure sources (e.g., polyurethane foam), determine the importance of exposure in other microenvironments such as homes and vehicles, and address the inhalation and dermal exposure pathways.

Impact of dust from multiple microenvironments and diet on PentaBDE body burden

Our objectives were to determine relative contributions of diet and dust exposure from multiple microenvironments to PentaBDE body burden, and to explore the role of handwipes as a measure of personal exposure to PentaBDE. We administered a food frequency questionnaire and collected serum, dust (office, main living area, bedroom, and vehicle), and handwipe samples from 31 participants. ΣPentaBDEs (sum of BDE 28/33, 47, 99, 100, and 153) in handwipes collected in the office environment were weakly correlated with dust collected from offices (r = 0.35, p = 0.06) and bedrooms (r = 0.39, p = 0.04), but not with dust from main living areas (r = -0.05, p = 0.77) or vehicles (r = 0.17, p = 0.47). ΣPentaBDEs in serum were correlated with dust from main living areas (r = 0.42, p = 0.02) and bedrooms (r = 0.49, p = 0.008), but not with dust from offices (r = 0.22, p = 0.25) or vehicles (r = 0.20, p = 0.41). Our final regression model included variables for main living area dust and handwipes, and predicted 55% of the variation in serum ΣPentaBDE concentrations (p = 0.0004). Diet variables were not significant predictors of ΣPentaBDEs in serum. Our research suggests that exposure to dust in the home environment may be the most important factor in predicting PentaBDE body burden in North Americans, and potential exposure pathways may involve PBDE residues on hands.

Polyfluorinated Compounds in Serum Linked to Indoor Air in Office Environments

We aimed to investigate the role of indoor office air on exposure to polyfluorinated compounds (PFCs) among office workers. Week-long, active air sampling was conducted during the winter of 2009 in 31 offices in Boston, MA. Air samples were analyzed for fluorotelomer alcohols (FTOHs), sulfonamides (FOSAs), and sulfonamidoethanols (FOSEs). Serum was collected from each participant (n = 31) and analyzed for 12 PFCs including PFOA and PFOS. In air, FTOHs were present in the highest concentrations, particularly 8:2-FTOH (GM = 9920 pg/m(3)). FTOHs varied significantly by building with the highest levels observed in a newly constructed building. PFOA in serum was significantly correlated with air levels of 6:2-FTOH (r = 0.43), 8:2-FTOH (r = 0.60), and 10:2-FTOH (r = 0.62). Collectively, FTOHs in air significantly predicted PFOA in serum (p < 0.001) and explained approximately 36% of the variation in serum PFOA concentrations. PFOS in serum was not associated with air levels of FOSAs/FOSEs. In conclusion, FTOH concentrations in office air significantly predict serum PFOA concentrations in office workers. Variation in PFC air concentrations by building is likely due to differences in the number, type, and age of potential sources such as carpeting, furniture, and/or paint.

Associations between PBDEs in Office Air, Dust, and Surface Wipes

Increased use of flame-retardants in office furniture may increase exposure to PBDEs in the office environment. However, partitioning of PBDEs within the office environment is not well understood. Our objectives were to examine relationships between concurrent measures of PBDEs in office air, floor dust, and surface wipes. We collected air, dust, and surface wipe samples from 31 offices in Boston, MA. Correlation and linear regression were used to evaluate associations between variables. Geometric mean (GM) concentrations of individual BDE congeners in air and congener specific octanol-air partition coefficients (Koa) were used to predict GM concentrations in dust and surface wipes and compared to the measured concentrations. GM concentrations of PentaBDEs in office air, dust, and surface wipes were 472pg/m(3), 2411ng/g, and 77pg/cm(2), respectively. BDE209 was detected in 100% of dust samples (GM=4202ng/g), 93% of surface wipes (GM=125pg/cm(2)), and 39% of air samples. PentaBDEs in dust and air were moderately correlated with each other (r=0.60, p=0.0003), as well as with PentaBDEs in surface wipes (r=0.51, p=0.003 for both dust and air). BDE209 in dust was correlated with BDE209 in surface wipes (r=0.69, p=0.007). Building (three categories) and PentaBDEs in dust were independent predictors of PentaBDEs in both air and surface wipes, together explaining 50% (p=0.0009) and 48% (p=0.001) of the variation respectively. Predicted and measured concentrations of individual BDE congeners were highly correlated in dust (r=0.98, p<0.0001) and surface wipes (r=0.94, p=002). BDE209 provided an interesting test of this equilibrium partitioning model as it is a low volatility compound. Associations between PentaBDEs in multiple sampling media suggest that collecting dust or surface wipes may be a convenient method of characterizing exposure in the indoor environment. The volatility of individual congeners, as well as physical characteristics of the indoor environment, influence relationships between PBDEs in air, dust, and surface wipes.