Faculty Bibliography

Prior to this study, reports of occurrence of polycyclic musks and polychlorinated naphthalenes (PCNs) in human tissues from Italy were not available. In this study, concentrations of PCNs and polycyclic musks were determined in human adipose tissue from Italy collected during 2005-2006; for comparison, legacy organohalogen pollutants such as organochlorine pesticides (OCPs), polychlorinated biphenyls (PCBs), and polybrominated diphenyl ethers (PBDEs) were determined. SigmaPCN concentrations ranged from 0.5 to 14 ng/g lipid wt (lw). Polycyclic musks such as HHCB and AHTN were found in 92% and 83% of the human samples, respectively. Concentrations of PBDEs in Italian adipose tissue ranged between 3.2 and 35.6 ng/g lw.

Chlorinated polycyclic aromatic hydrocarbons (ClPAHs) are widespread environmental pollutants in the urban environment. Nevertheless, there is little information available regarding the occurrence and profiles of ClPAHs in environmental matrices. In this study, residual concentrations and profiles of 20 individual ClPAHs and 16 US EPA-priority PAHs were determined using high- resolution gas chromatography-high-resolution mass spectrometry in sediments from water bodies near industrialized areas: Tokyo Bay, Japan; the Saginaw River watershed, Michigan, USA; a former chlor-alkali plant, Georgia, USA; and the New Bedford Harbor Superfund site, Massachusetts, USA. A sediment core from Tokyo Bay showed temporal patterns in the distribution of ClPAHs from the 1950s through 2004. The fluxes of ClPAHs and 16 priority PAHs in Tokyo Bay sediment core were 0.029-0.57 ng/cm(2)/year and 85-609 ng/cm(2)/year, respectively; fluxes were lowest in the 1950s and highest in 1989-1990. In the United States, a high mean concentration of ClPAHs was found in sediment collected near a former chlor-alkali plant [8820 pg/g dry weight (dry wt)], and lower mean concentrations were found for New Bedford Harbor (1880 pg/g dry wt) and the Saginaw River watershed (1140 pg/g dry wt). Among individual ClPAHs, 6-ClBaP and 1-ClPyr were the dominant compounds in sediments; this pattern is similar to the pattern reported in the literature for waste incineration and ambient urban air samples. Significant correlation between SigmaClPAH concentrations and Sigmaparent-PAH concentrations in Tokyo Bay sediment implies that the sources and distribution of ClPAHs are directly related to those of parent PAHs. We also analyzed ClPAHs and parent PAHs in blue mussels from New Bedford Harbor. The mean concentration of ClPAHs in mussels from New Bedford Harbor was 21 ng/g lipid weight, a concentration three orders of magnitude lower than the mean concentration of parent PAHs. Low-molecular-weight ClPAHs predominated in mussel tissues. Toxic equivalents (TEQs) of ClPAHs analyzed in sediment ranged between 1.1 fg TEQ/g dry wt (Tokyo Bay) and 2.4 fg TEQ/g dry wt (Saginaw River watershed). The dioxinlike toxicity contributed by ClPAHs in sediment from contaminated areas was five orders of magnitude lower than that previously reported for dioxins.

Polybrominated diphenyl ethers (PBDEs) have been widely used as flame retardants. The structurally related hydroxylated PBDEs (OH-PBDEs) and methoxylated PBDEs (MeO-PBDEs) occur in precipitation, surface water, wildlife, and humans. The formation of OH-PBDEs in wildlife and humans is of considerable concern due to their greater toxicities relative to PBDEs and MeO-PBDEs. Research to date suggests that OH-PBDEs are formed by hydroxylation of PBDEs, and MeO-PBDEs are then formed by methylation of the OH-PBDEs. Here we show significant metabolic production of OH-PBDEs from MeO-PBDEs while hydroxylation of synthetic PBDEs to OH-PBDEs was negligible. Concentrations of PBDEs, OH-PBDEs, and MeO-PBDEs were analyzed in tuna, albatross, and polar bears collected from marine environments worldwide, and we found a closer relationship between OH-PBDEs and MeO-PBDEs than had been previously reported. Furthermore, for the first time the metabolic relationships between PBDEs, OH-PBDEs, and MeO-PBDEs were elucidated in vitro using rainbow trout, chicken, and rat microsomes. We propose the production of OH-PBDEs from naturally occurring MeO-PBDEs as a previously unidentified mechanism that could be an important contributor for the occurrence of OH-PBDEs found in wildlife from remote areas. Our results suggest that risk assessment paradigms for PBDEs and their metabolites need reevaluation and that human exposure to MeO-PBDEs that occur naturally in marine organisms should be considered.

The formation and release of polybrominated dibenzo-p-dioxins and dibenzofurans (PBDD/Fs) from the incineration of electronic wastes (e-waste) that contain brominated flame retardants (BFRs) are a concern. However, studies on the determination of PBDD/Fs in environmental samples collected from e-waste recycling facilities are scarce. In this study, 11 2,3,7,8-substituted PBDD/Fs and 10 polybrominated diphenyl ether (PBDE) congeners were determined in electronic shredder waste, workshop-floor dust soil, and leaves (of plants on the grounds of the facility) from a large-scale e-waste recycling facility and in surface soil from a chemical-industrial complex (comprising a coke-oven plant, a coal-fired power plant, and a chlor-alkali plant) as well as agricultural areas in eastern China. Total PBDD/F concentrations in environmental samples were in the range of 113-818 pg/g dry wt (dw) for leaves, 392-18500 pg/g dw for electronic shredder residues, 716-800000 pg/g dw for soil samples, and 89600-pg/g dw for workshop-floor dust from the e-waste recycling facility and in a range from nondetect (ND) to 427 pg/g dw in soil from the chemical-industrial complex. The highest mean concentrations of total PBDD/Fs were found in soil samples and workshop-floor dust from the e-waste recycling facility. The dioxin-like toxic equivalent (measured as TEQ) concentrations of PBDD/Fs were greater than the TEQs of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) reported in our previous study for the same set of samples. The concentrations of PBDFs were several orders of magnitude higher than the concentrations of PBDDs in samples from the e-waste facility or from soil from the chemical-industrial complex. A significant correlation was found between the concentrations of sigmaPBDD/Fs and sigmaPBDEs (r = 0.769, p < 0.01) and between sigmaPBDD/Fs and the previously reported sigmaPCDD/F concentrations (r = 0.805, p < 0.01). The estimated daily human intakes of TEQs contributed by PBDD/Fs via soil/dust ingestion and dermal exposures in e-waste recycling facilities were higher than the intakes of TEQs contributed by PCDD/ Fs, calculated in our previous study.

Despite the concern over widespread distribution of perfluorinated compounds (PFCs) even in sparsely populated regions of the world, few studies have reported their occurrence in South America. In this study, PFCs were measured in Rio de Janeiro State in southeast Brazil: in drinking water from various districts in the State, in river water and tucuxi dolphins from the Paraiba do Sul River, several species of fish from the State, and mussels from Guanabara Bay. Liver, kidney, and muscle from fishes were analyzed to enable an understanding of the tissue distribution of PFCs. PFOS, PFOA, and PFHxS were detected in all drinking water samples in concentration ranges of 0.58-6.70, 0.35-2.82, and 0.15-1.00 ng L(-1), respectively. The profiles of PFCs in drinking water from Brazil (with PFOS concentrations comparable to or higher than those of PFOA) were different from the profiles that have been reported for other countries. In fish, concentrations of PFOS were, in general, higher in liver than in muscle. Concentrations of PFOA in livers of fish were similar to or lower than fish muscle tissue concentrations. PFOS and PFOA were found in brown mussels from Guanabara Bay. Bioconcentration factors (BCFs) of PFOA calculated for mussels were higher than the BCFs calculated for fishes. Elevated concentrations of PFUnDA (mean: 109+/-17.4 ng g(-1) wet weight) were found in mussels from certain locations within Guanabara Bay. Although PFCs were detected in all types of samples analyzed, the concentrations were generally lower than the concentrations reported for Japan and the USA.

Perfluorooctanesulfonamides, such as N-ethyl perfluorooctanesulfonamidoethanol (N-EtFOSE), are large scale industrial chemicals but their disposition and toxicity are poorly understood despite significant human exposure. The hypothesis that subacute exposure to N-EtFOSE, a weak peroxisome proliferator, causes a redox imbalance in vivo was tested using the known peroxisome proliferator, ciprofibrate, as a positive control. Female Sprague-Dawley rats were treated orally with N-EtFOSE, ciprofibrate or corn oil (vehicle) for 21 days, and levels of N-EtFOSE and its metabolites as well as markers of peroxisome proliferation and oxidative stress were assessed in serum, liver and/or uterus. The N-EtFOSE metabolite profile in liver and serum was in good agreement with reported in vitro biotransformation pathways in rats and the metabolite levels decreasing in the order perfluorooctanesulfonate > perfluorooctanesulfonamide ~ N-ethyl perfluorooctanesulfonamidoacetate > perfluorooctanesulfonamidoethanol approximately N-EtFOSE. Although N-EtFOSE treatment significantly decreased the growth rate, increased relative liver weight and activity of superoxide dismutases (SOD) in liver and uterus (total SOD, CuZnSOD and MnSOD), a metabolic study revealed no differences in the metabolome in serum from N-EtFOSE-treated and control animals. Ciprofibrate treatment increased liver weight and peroxisomal acyl Co-A oxidase activity in the liver and altered antioxidant enzyme activities in the uterus and liver. According to NMR metabolomic studies, ciprofibrate treated animals had altered serum lipid profiles compared to N-EtFOSE-treated and control animals, whereas putative markers of peroxisome proliferation in serum were not affected. Overall, this study demonstrates the biotransformation of N-EtFOSE to PFOS in rats that is accompanied by N-EtFOSE-induced alterations in antioxidant enzyme activity.

The perchlorate anion (ClO(4)(-),MW=99) is present in food, drinking water, groundwater, and surface waters. Exposure to perchlorate is of concern, due to the ability of the anion to disrupt the function of the thyroid gland, and affect the synthesis of thyroid hormones. In this study, liquid chromatography - tandem mass spectrometry (LC-MS/MS) method has been optimized to analyze for perchlorate in blood sera and plasma samples from 84 US donors. In addition, 15 volunteers provided saliva and serum samples concurrently, to enable assessment of the ratio of perchlorate in these two matrices. Recoveries of perchlorate from fortified blanks and from serum/plasma samples were between 92% and 97%. Replicate analysis of blood-matrix spikes had a relative standard deviation (RSD) of <3%, and the relative percent difference (RPD) of repeat analysis of samples was <4%. Perchlorate concentrations in serum and plasma ranged from below the limit of quantitation (0.05ngmL(-1)) to a maximum of 7.7ngmL(-1). Perchlorate concentrations in serum and plasma were log-normally distributed. The mean and median concentrations of perchlorate in 84 serum and plasma samples were 0.32 and 0.17ngmL(-1), respectively. No significant difference existed in perchlorate concentrations between serum and plasma. Analysis of paired saliva and serum samples showed a significant positive correlation for log-normalized perchlorate concentrations (r(2)=0.60) and perchlorate concentrations themselves (r(2)=0.86). The mean saliva:serum concentration ratio of perchlorate was 14:1 (after exclusion of two pairs of outliers). This is the first report to provide measurement data for perchlorate in blood sera and plasma of populations in the US.

The recent development of a sensitive and accurate analytical method for the analysis of 20 perfluorinated compounds (PFCs), including several short-chain PFCs, has enabled their quantification in tap water collected in China, Japan, India, the United States, and Canada between 2006 and 2008. Of the PFCs measured, PFOS, PFHxS, PFBS, PFPrS, PFEtS, PFOSA, N-EtFOSAA, PFDoDA, PFUnDA, PFDA, PFNA, PFHpA, PFHxA, PFPeA, PFBA, and PFPrA were found at detectable concentrations in the tap water samples. The water samples from Shanghai (China) contained the greatest concentrations of total PFCs (arithmetic mean = 130 ng/L), whereas those from Toyama (Japan) contained only 0.62 ng/L. In addition to PFOS and PFOA, short-chain PFCs such as PFHxS, PFBS, PFHxA, and PFBA were found to be prevalent in drinking water. According to the health-based values (HBVs) and advisory guidelines derived for PFOS, PFOA, PFBA, PFHxS, PFBS, PFHxA, and PFPeA by the U.S.EPA and the Minnesota Department of Health, tap water may not pose an immediate health risk to consumers.

Polybrominated diphenyl ethers (PBDEs) are ubiquitous in the indoor environment, owing to their use in consumer products ranging from electronics to mattresses, furniture, and carpets. People are exposed to PBDEs through inhalation of indoor air and ingestion, and dermal absorption of dust particles present in the air. In this study, concentrations of PBDEs were determined in indoor air and house dust collected from homes in Albany, New York, USA. Based on the measured concentrations of PBDEs in indoor air and dust, we estimated daily exposure dose (DED) of PBDEs. In addition, we used previously published PBDE concentrations reported for breast milk from Massachusetts, USA [Johnson-Restrepo, B., Addink, R., Wong, C., Arcaro, K., Kannan, K., 2007. Polybrominated diphenyl ethers and organochlorine pesticides in human breast milk from Massachusetts. USA. J. Environ. Monitor. 9, 1205-1212] and foodstuffs collected from Texas and Florida, USA [Schecter, A., Päpke, O., Harris, T.R., Tung, K.C., Musumba, A., Olson, J., Birnbaum, L., 2006. Polybrominated diphenyl ether (PBDE) levels in an expanded market basket survey of U.S. food and estimated PBDE dietary intake by age and sex. Environ. Health Perspect. 114, 1515-1520, Johnson-Restrepo, B., Kannan, K., Addink, R., Adams, D.H., 2005b. Polybrominated diphenyl ethers and polychlorinated biphenyls in a marine foodweb of coastal Florida. Environ. Sci. Technol. 39, 8243-8250], in an estimation of dietary exposure to PBDEs. The exposure assessment was performed for five age groups: infants (<1yr), toddlers (1-5yr), children (6-11yr), teenagers (12-19yr), and adults (20yr). The dust ingestion and air inhalation factors that we used were the US Environmental Protection Agency's (EPA) exposure factors, while the daily food intake rates (g/day) were derived from the US Department of Agriculture's (USDA) food intake surveys. The total DED of PBDEs was calculated by summation of the exposures from diet, indoor air, and house dust. The average estimated DED of PBDEs was the highest for breastfed infants (86.4ng/kg-bw/day), contributed primarily (91%) from the consumption of breast milk. The average DED of PBDEs for toddlers, children, teenagers, and adults was respectively, 13.3, 5.3, 3.5, and 2.9ng/kg-bw/day. Ingestion and dermal absorption of house dust are the major pathways of PBDE exposure in toddlers, children, teenagers, and adults accounting for, on average, 56-77% of the total PBDE intake.