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Polychlorinated biphenyls (PCBs) have been detected at relatively high concentrations in harbor seals, apex predators in the northwest Atlantic. As part of an ongoing assessment of the effects of PCBs on population health, we analyzed tri- to deca-PCBs in the liver of 56 harbor seals (6 adult males, 50 pups) and in 11 blubber samples (4 adult males, 7 pups) and examined tissue-specific accumulation patterns, biomagnification potential, and toxic implications of current PCB concentrations. Hepatic ?30PCB concentrations (overall mean ± standard deviation: 76,860 ± 111,800 ng/g lipid weight, lw) were higher than blubber concentrations (48,180 ± 69,420 ng/g lw). Regional trends were suggestive of fresh PCB inputs from the industrialized, densely populated southern coast of New England versus the rural north. The lack of temporal trends confirmed that tissue concentrations of PCBs have plateaued since the early 1990s. Tissue distribution of PCBs varied significantly by age and, surprisingly by gender among the pups. Principal Component Analysis (PCA) revealed that lighter PCBs are selectively transferred from mother to pup blubber in relation to lipid solubility (log Kow), but heavier PCBs may be efficiently transferred during late lactation from mother to pup liver. Biomagnification factors (BMFs) for ?6PCBs from prey fish to adult male seals ranged from 90 to 547 in the liver and 88 to 532 in the blubber, and suggested that molecular structure and metabolic capacity were more important influences than log Kow on the retention of PCBs. Blubber concentrations of ?30PCBs in 87% of the pups were an order of magnitude higher than recent toxic reference values (TRVs) calculated for ?154PCBs in nursing harbor seals, suggesting that the pups are at risk for PCB-mediated toxicity at a vulnerable stage of development. Given the recurring pattern of epizootics in these seals, the health of the population is of concern.

Scope: The aim of this study was to i) characterize dietary polychlorinated biphenyls (PCBs) and dioxin exposure in consumers of fish from the PCB contaminated Lake Mjosa in Norway ii) examine the influence of demographic factors on blood concentrations and congener composition of dioxins and PCBs, iii) characterize dietary sources and possible exposures above tolerable intake. Methods and results: Blood samples were analysed for dioxin-like (dl) compounds (PCDD/Fs and dl-PCBs) and non-dl-PCBs (ndl-PCBs). Dietary exposures were calculated using food frequency questionnaires (n=64). Men had higher median intake of dl-compounds than women (1.2 and 0.85 pg TEQ/kg bw/day), but similar blood concentrations (23.3 and 25.8, pg TEQ/g lipid weight (lw)). For non-dl-PCBs, intakes (6.5 and 4.5 ng/kg bw/day) and blood concentrations (381 and 224 ng/g lw) were higher in men than in women. Blood concentrations correlated with dietary intakes in men only. Increasing BMI and age elevated blood concentrations mainly in women. Men and women had different blood congener profiles, with a higher share of PCB-126 in women, despite similar dietary congener profiles. Eleven participants exceeded the tolerable intake for dl-compounds. Fish from Lake Mjosa was the main dietary source. Conclusion: The higher influence of BMI and age for women than for men may have implications for risk assessment.

Objectives The objective of this article is to extend our previous studies of persistent organic pollutant (POP) contamination of U.S. food by measuring perfluorinated compounds (PFCs), organochlorine pesticides, and polychlorinated biphenyls (PCBs) in composite food samples. This study is part of a larger study reported in two articles, the other of which reports levels of polybrominated diphenyl ethers and hexabromocyclododecane brominated flame retardants in these composite foods [Schecter et al. 2010. Polybrominated diphenyl ethers (PBDEs) and hexabromocyclodecane (HBCD) in composite U.S. food samples, Environ Health Perspect 118:357–362]. Methods In this study we measured concentrations of 32 organochlorine pesticides, 7 PCBs, and 11 PFCs in composite samples of 31 different types of food (310 individual food samples) purchased from supermarkets in Dallas, Texas (USA), in 2009. Dietary intake of these chemicals was calculated for an average American. Results Contamination varied greatly among chemical and food types. The highest level of pesticide contamination was from the dichlorodiphenyltrichloroethane (DDT) metabolite p,p′- dichlorodiphenyldichloroethylene, which ranged from 0.028 ng/g wet weight (ww) in whole milk yogurt to 2.3 ng/g ww in catfish fillets. We found PCB congeners (28, 52, 101, 118, 138, 153, and 180) primarily in fish, with highest levels in salmon (PCB-153, 1.2 ng/g ww; PCB-138, 0.93 ng/g ww). For PFCs, we detected perfluorooctanoic acid (PFOA) in 17 of 31 samples, ranging from 0.07 ng/g in potatoes to 1.80 ng/g in olive oil. In terms of dietary intake, DDT and DDT metabolites, endosulfans, aldrin, PCBs, and PFOA were consumed at the highest levels. Conclusion Despite product bans, we found POPs in U.S. food, and mixtures of these chemicals are consumed by the American public at varying levels. This suggests the need to expand testing of food for chemical contaminants.

Levels of polybrominated diphenyl ether (PBDE) flame retardants have been increasing in humans and the environment for the past few decades. Human levels are markedly higher in the US than Europe. Although food appears to be a significant route of intake, food PBDE levels are not substantially higher in the US than Europe. House and office dust appear to be major routes of exposure with air believed to usually provide a lesser route of intake. Because there are very few measurements of airborne PBDE that have been performed in relevant microenvironments in the US, increased efforts to assess airborne PBDE in the US as sources of exposure are needed. This study reports, for the first time from a Southwestern US city in Texas, the results of measurements of airborne PBDE in multiple locations, two outdoor and six indoor (residential and office) from active air sampling with collection of a combination of both vapor- and particulate-phase PBDE. Higher PBDE levels were measured in indoor than outdoor air, whi...

Objectives This study was designed to update previous U.S. market basket surveys of levels and polybrominated diphenyl ether (PBDE) dietary intake calculations. This study also quantifies hexabromocyclododecane (HBCD) levels in U.S.-purchased foods for the first time and estimates U.S. dietary intake of HBCD. This is part of a larger market basket study reported in two companion articles, of current levels of certain persistent organic pollutants (POPs) PBDEs, HBCD, perfluorinated compounds, polychlorinated biphenyls, and pesticides in composite food samples collected in 2008–2009. Methods In this study, we measured concentrations of 24 PBDE congeners and total HBCD in composite samples of 31 food types (310 samples). U.S. dietary intake of PBDEs and HBCD was estimated referencing the most current U.S. Department of Agriculture loss-adjusted food availability report. Results Total PBDE concentrations in food varied by food type, ranging from 12 pg/g wet weight (ww) in whole milk to 1,545 pg/g ww in canned sardines and 6,211 pg/g ww in butter. Total HBCD concentrations also varied substantially within and among food groups, ranging from 23 pg/g in canned beef chili to 593 pg/g in canned sardines. HBCD was not detected in any dairy samples. Dietary intake of all PBDE congeners measured was estimated to be 50 ng/day, mostly from dairy consumption but also from meat and fish. HBCD intake was estimated at 16 ng/day, primarily from meat consumption. Conclusion PBDEs and HBCDs currently contaminate some food purchased in the United States, although PBDE intake estimated in this study is lower than reported in our previous market basket surveys. HBCD is in food at higher levels than expected based on previously reported levels in milk and blood compared with PBDE levels and is comparable to European levels.

Polybrominated diphenyl ether (PBDE) flame retardants have been increasing exponentially in the US general population in recent decades. PBDEs are persistent organic pollutants (POPs) and thus are toxic, persistent, and bioaccumulative. Levels in human blood and milk are markedly higher in North America than Europe. Food is a major route of intake. Typically higher levels of PBDEs are found in food of animal origin including fish, meat, and dairy products. Currently, there are no published data on the levels of PBDE in US fruits, vegetables, or food of vegetable origin. This study was conducted to study PBDE contamination in US fruits, vegetables, and food of vegetable origin; compare with levels in US fish, meat, and dairy products and with levels in vegetables in other countries. This is a follow-up study of our previously reported studies on PBDE levels in US food of animal origin. Of 14 food samples collected in Dallas, Texas, the total sum of five PBDE congeners, Σ5 PBDE, ranged from 2.6 to 90 pg g−1...

Seven species of teleost fishes comprising major prey of northwest Atlantic harbor seals were analyzed for polybrominated diphenyl ethers (PBDEs). PBDE concentrations in whole fish samples (n = 87) were compared with those measured previously in harbor seal blubber to evaluate the transfer of PBDEs from prey to predator. Hexabromocyclododecane (HBCD) concentrations were measured in three fish species to provide an initial estimation of HBCD contamination in this ecosystem. HBCD was detected in 87% of the fish samples at concentrations ranging from 2.4 to 38.1 ng/g, lw (overall mean 17.2 ± 10.2 ng/g, lw). ∑PBDE concentrations in fish ranged from 17.9 to 94 ng/g, lw (overall mean 62 ± 34 ng/g, lw). ∑PBDE concentrations in the harbor seals were two orders of magnitude higher than levels in the fish. Biomagnification factors (BMFs) from fish to seals averaged from 17 to 76, indicating that tetra- to hexa-BDEs are highly biomagnified in this marine food web. BDE-47 was the dominant congener in all samples, suggesting exposure to the penta-BDE mixture. The presence of higher brominated congeners including BDE-209 at measurable levels in fish and seal tissue, along with the very high biomagnification of BDE-153, as well as − 155, and − 154, suggests recent exposure to the octa- and deca-BDE formulations in this US coastal marine food web, as well as the additional contribution of BDE-209 debromination in fish to the loading of persistent PBDEs in the seals. This is the first study to report the occurrence of BDE-209 and other higher BDEs in commercially important marine fishes from the northwest Atlantic.

For analysis of organochlorine contaminants in human tissue, the "gold standard" for preservation, storage, and shipping is usually freezing. However, this method can be difficult, if samples are taken in remote areas, and costly, when the samples must be shipped on dry ice. Therefore, a more simple and cost effective method of preservation is essential for remote field work. Potassium dichromate (K(2)Cr(2)O(7)) has been successfully employed in the preservation of human and cows' milk as well as chicken eggs. Our previous studies described the use of potassium dichromate for preservation of whole blood for analysis of dioxins, dibenzofurans, and PCBs. Potassium dichromate was found to successfully preserve blood at room temperature for 34 d with no significant differences in the measured concentrations of chemical contaminants or blood lipid level when compared to frozen samples. However, in a follow-up study, 3 months and 6 months of potassium dichromate preservation proved inadequate to preserve the samples for organic pollutant analysis. We noted that the lipid portion of the blood in the chemically preserved samples was declining in level or degrading, while the persistent organic pollutants remained intact at the same levels on a whole weight basis. To narrow down the window of efficacy for the use of potassium dichromate to preserve blood samples for analysis, the present study compared chemical preservation to freezing for an intermediate time period, 2 months. Similar to our previous findings at 3 and 6 months, at 2 months significant lipid degradation was observed in the chemically preserved samples. Chemically preserved samples had significantly higher levels of organochlorine contaminants (dioxins, dibenzofurans, and PCBs) when measured on a blood lipid basis but not on a wet weight basis compared to frozen samples. While 2 months of potassium dichromate preservation was not useful for obtaining accurate measure of dioxins, furans, and PCBs on a lipid basis, previous studies found this method of preservation to be useful for at least one month (Schecter, A., Pavuk, M., Päpke, O., Malisch, R., 2004. The use of potassium dichromate and ethyl alcohol as blood preservatives for analysis of organochlorine contaminants. Chemosphere 57, 1-7). However blood stored at -70 degrees C and at 22 degrees C with potassium dichromate gave similar results when expressed on a wet weight basis.

Seven polybrominated diphenyl ether (PBDE) congeners were measured in the particulate fraction (

Previous studies have identified elevated levels of polychlorinated dibenzo-p-dioxins (PCDDs) in sediments and megafauna (dugongs and green turtles) in the marine environment of southeast Queensland, Australia. Little information exists, however, regarding the levels of PCDDs, polychlorinated dibenzofurans (PCDFs) and related polychlorinated biphenyls (PCBs) in seafood from this area. This study aims to establish baseline information on PCDD/F and PCB contamination in a range of seafood species from Moreton Bay and to investigate contaminant variability due to harvesting season, size, habitat location and trophic level. In addition, different seafood extraction methods were tested to evaluate their impact on lipid yields and contaminant concentration. Overall, the median TEQ(DFPCB) levels in seafood from Moreton Bay were elevated compared to background levels in Australian marine/estuarine and retail fish. However, TEQ(DFPCB) levels of most seafood analysed were below the respective EU maximum limits. High inter- and intraspecies variability was observed, which could be partially attributed to differences in trophic level, season harvested and habitat location.

The Greenland shark (Somniosus microcephalus) is a high-trophic fish species present in Arctic waters. The present study aimed to determine concentrations of polychlorinated dibenzo-p-dioxins and furans (PCDDs/Fs), dioxin-like (DL) PCBs and six non-dioxin-like (NDL) PCBs in muscle and liver from 10 female Greenland sharks collected between 2001 and 2003 from Icelandic waters. The mean total concentrations of PCDDs/Fs were 13 and 530pg/g fat for muscle and liver, respectively, and show enrichment in the liver. Concentrations of DL-non-ortho PCBs were also higher in liver compared to muscle with mean concentrations of 7.8 and 0.36ng/g fat, respectively. No enrichment in the liver was found for DL-mono-ortho- and NDL-PCBs. No correlation was found between the size range studied and total concentrations of the compounds analyzed. Total WHO-TEQs (PCDDs/Fs and DL-PCBs) ranged between 7.1-70 and 54-1500pg/g fat in muscle and liver, respectively.

In utero exposure to polybrominated diphenyl ethers (PBDEs) reduces the number of ovarian follicles in rat females and causes permanent effects on rat males. Little data have been gathered on the associations between PBDEs exposure and birth outcome and female menstruation characteristics in both epidemiological and animal studies. The aim of this study was to examine how PBDEs in breast milk are associated with infant birth outcome and maternal menstruation characteristics. Study participants were healthy women recruited from central Taiwan between December 2000 and November 2001. Twelve congener levels of PBDEs (BDE-17, 28, 47, 66, 85, 99, 100, 138, 153, 154, 183, 209) in 20 breast milk samples were measured by gas chromatography with high resolution mass spectrometer. The mean level of PBDEs in breast milk was 3.93±1.74 ng/g lipid. The estimated PBDE daily intake for a breastfed infant was 20.6 ng/kg b.w./day after delivery. After maternal age, pre-pregnant BMI, and parity were adjusted, increased PBDEs in breast milk was related with decreased birth outcome, particularly for birth weight and length, chest circumference, and Quetelet's index of infants. No significant differences in PBDEs were found between the two groups of menstrual cycle length higher and lower than 30 days after we adjusted for maternal age, pre-pregnant BMI, and parity. In utero exposure to low doses of PBDEs may result in lower birth weight and short or birth length. Our findings are limited based on the low doses of PBDEs and the small sampling size. Keywords: Polybrominated diphenyl ethers, Breast milk, Breastfeeding, Infants, Reproductive effects, Menstruation, Birth outcome, Birth weight, Daily intake

The aim was to determine the body burden of dioxins and polychlorinated biphenyls (PCBs) and whether they are associated with variables influencing reproduction. Our subjects were healthy women (mean age of 29 [SD=4.5]) from central Taiwan. The congeners of dioxins and dioxin-like PCBs in placentas (n=119) were identified using gas chromatography/high resolution mass spectrometry. The median levels of polychlorinated dibenzo-p-dioxins/dibenzofurans and PCBs were 10.2 (geometric mean [GM]: 9.8, 95% confidence interval [95% CI]: 8.8-10.9) and 2.7 (GM: 2.7, 95% CI: 2.3-3.1) pg WHO-TEQ/g lipid, respectively. Total TEQ level in placentas was significantly correlated with mothers' arm circumference (r=0.22, p=0.043). Increased body fat percentage was associated with higher total TEQ level in placentas. After adjustment for maternal age, pre-pregnant body mass index (BMI), and parity, placental dioxin-TEQ level higher in women (age 19 years) with irregular menstrual cycle than in those (age

Mussel samples were collected monthly between October-2010 and October-2011 from four stations (Bosphorus, Bandirma, Gelibolu, Tekirdag) in the Marmara Sea. Two consecutive months’ samples were homogenized and combined as a single group for analysis. Mussel samples were analyzed for Organochlorine pesticides (OCPs); (total-DDT, total-HCH, Endrin, α-Endosulfan, β-Endosulfan, Heptachlor) and Polychlorinated biphenyls (PCBs); (PCB 28, PCB 52, PCB 138, PCB 153, and PCB 180). All analyses were done according to Eurofins house method in ERGO Laboratory in Germany. Concentrations of α-endosulfan and heptachlor in mussel tissues were below method detection limits. The annual average OCPs concentrations among the stations ranged between 0.02 and 1.45 ng/g (wet weight), 1.9–99.75 ng/g (lipid weight) whereas the annual average PCBs concentrations among the stations ranged between 0.03 and 0.40 ng/g (wet weight), 1.71–26.48 ng/g (lipid weight), respectively. There was no relation between fat content of mussels and residues of the contaminants. PCB 138 and PCB 153 were the most predominant PCBs, while total-DDT and total-HCH were the most predominant OCPs in the mussels. Total-DDT concentrations were higher compared to total-HCH and PCBs isomers. Measured levels were below the national and international committees’ and institutions’ limits for human consumption and protection of aquatic biota.

Polybrominated diphenyl ether (PBDE) brominated flame retardants have recently been found to contaminate humans in the United States and other countries. U.S. human breast milk and blood levels of PBDEs are presently the highest in the world. U.S. cord blood samples tested positive for PBDEs, but until now there have been no peer-reviewed published data concerning levels of PBDEs in human tissue prior to and immediately after birth. Liver tissues were obtained from 4 stillborn fetuses and 7 liveborn infants, ranging from 20.5 to 39 wk gestational age; only 2 of the liveborn infants lived longer than 4 h and none were formula-fed or nursed, so tissue levels reflect intrauterine PBDE intake only. All samples were contaminated with PBDEs. Levels varied from 4 to 98 ppb, lipid. The mean level was 23.1 and the median 15.2 ppb, lipid. PBDE levels did not increase with gestational age. These data document the transfer of PBDEs from maternal to fetal tissue. PBDE concentrations are somewhat lower than those reported in adult blood or breast milk. The health consequences of prenatal contamination are not clear at present.

Polybrominated diphenyl ethers (PBDEs), persistent and bioaccumulative flame retardants, are of concern because they are ubiquitous in the United States, are potentially toxic, and have been found at rapidly rising levels in humans during the past few decades (Birnbaum and Staskal 2004; Hites 2004; Schecter et al. 2005b; Sjodin et al. 2004; Webster et al. 2005). The high level of PBDE contamination in the U.S. population and food is cause for concern because these compounds are chemically similar to polychlorinated biphenyls (PCBs) and have been shown in laboratory animal studies to be toxic in a number of ways. These include cancer in high-dose studies [National Toxicology Program (NTP) 1986], reproductive and developmental toxicity (Stoker et al. 2004), endocrine disruption (Hallgren and Darnerud 2002), and central nervous system effects (Eriksson et al. 2002; Viberg et al. 2003). PBDEs can be found in some textiles, electronics, (e.g., computers, televisions), plastics, and furniture such as sofas, chairs, and mattresses. Unlike dioxins and PCBs, these chemicals are primarily indoor pollutants and are found at high levels in household vacuum dust and other home and workplace environmental samples (Schecter et al. 2005a; Stapleton et al. 2005). Very high levels of PBDEs have recently been found in the United States in mothers’ milk (Schecter et al. 2003, 2005b), blood (Mazdai et al. 2003; Morland et al. 2005; Schecter et al. 2004, 2005b; Sjodin et al. 2004), food (Schecter et al. 2004), and adipose tissue (Johnson-Restrepo et al. 2005; She et al. 2002). U.S. blood and milk concentrations were 10- to 20-fold higher than the levels found in Europe (Bocio et al. 2003; Meironyte et al. 1999; Noren and Meironyte 2000; Ohta et al. 2002). Although levels of dioxins, dibenzofurans, and PCBs in human tissues are declining, PBDEs have been increasing substantially in blood levels in the United States during the past two to three decades (Schecter et al. 2005b; Sjodin et al. 2004). The penta-BDE and octa-BDE commercial PBDE mixtures are no longer being produced or sold in the United States, whereas deca-BDE continues to be manufactured and sold in the United States as well as worldwide. Furthermore, because these compounds are persistent in the environment, reservoir sources are likely to be present for substantial periods of time. These reservoir sources may continue to contaminate food and dust, both of which are believed to contribute substantially to human intake of these compounds (Birnbaum and Staskal 2004; Jones-Otazo et al. 2005; Webster et al. 2005). Even though studies have begun to estimate PBDE intake from ingestion and inhalation, the amount and percent of intake from food in the U.S. general population have not been well characterized nor have the amounts of intake from dust ingestion and inhalation been well defined (Jones-Otazo et al. 2005; Stapleton et al. 2005; Webster et al. 2005). The present study expands and complements our previous U.S. market basket survey (Schecter et al. 2004) and also estimates dietary PBDE exposure by age and sex from birth through ≥60 years of age. The food sample size is approximately twice the size of the earlier study and includes previously unpublished congener data from that study (Schecter et al. 2004). For the first time, we characterize the U.S. population’s PBDE intake from food.

Workers at an electronics recycling plant have previously been shown to have elevated serum levels of polybrominated diphenyl ethers (PBDEs) compared to referents without occupational PBDE exposure. Subsequent structural changes and industrial hygiene measures at the plant were applied to improve the work environment. The present study aims to assess the impact of these work environment changes on the occupational exposure to PBDEs. Blood were drawn from the workers and analyzed at two different laboratories, and serum concentrations of several PBDE congeners were determined by GC/MS or GC/HRMS. Cross-sectional studies were performed prior to (in 1997; N=19) and after (in 2000; N=27) workplace improvements. Longitudinal studies were performed on twelve of the workers that were sampled at both occasions. Even though the amount of processed goods had doubled in 2000 as compared to 1997, there was a significant decrease in the serum levels of BDE-183 and BDE-209. For BDE-209 the levels observed in year 2000 were even lower than in referents with no occupational exposure. In contrast to the decrease of higher brominated diphenyl ethers, the concentrations of BDE-47 did not significantly change. For BDE-153, the cross-sectional study indicated no change, whereas the longitudinal follow up indicated a significant increase. This study shows that the industrial hygiene improvements clearly reduced the occupational exposure to BDE-183 and BDE-209 at the plant. Still, the levels of hexa- to nonaBDEs but not BDE-209 were elevated, compared to referents with no occupational exposure.

Food surveys for levels of toxic chemicals frequently report the levels on an uncooked basis. It is known that cooking may in some conditions decrease the amount of dioxins and related chemicals in food. Surveys of polybrominated diphenyl ether (PBDE) levels in food to date show data from uncooked food only. In this article, it was shown that broiling, with fat dripped from the foods reported here, ground beef, ground lamb, catfish, trout, and salmon, reduces the amount of PBDEs in these foods. This suggests that calculations of food intake need to take into consideration levels in the cooked food rather than in the uncooked food.

The objective of this study was to find sites in Vietnam where there was human exposure from Agent Orange herbicide sprayed between 1962 and 1971, as determined by congener-specific measurement of dioxins, including 2,3,7,8-tetrachlorodibenzodioxin (TCDD), the dioxin that contaminated Agent Orange, in blood.Blood was collected from residents of eight heavily sprayed regions in the south of Vietnam and analyzed for TCDD and in some cases the dioxin-like dibenzofurans and dioxin-like PCBs.Six of the eight newly studied sites did not show substantial or any elevated TCDD in blood. Marked elevation of TCDD in Vietnamese blood was found in one new location with a suggestion of slightly elevated TCDD in a second location.In newly studied locations in Vietnam, we found some persons with elevation of TCDD consistent with exposure to dioxin from Agent Orange. In our previous studies, we found PCBs, PCDDs, and PCDFs as well as pesticides in human milk, blood, or in food. Health effects from Agent Orange need to be differentiated from effects caused by chemicals other than TCDD from Agent Orange.

Polybrominated diphenyl ethers (PBDEs) are brominated flame retardants (BFRs) which have recently been detected in human blood and milk in the USA, and presently these PBDE levels are found to be the highest globally. On a population basis, individual blood and individual milk analyses show similar congener patterns and levels. Until now, there has not been a study comparing PBDE levels in milk and blood of the same individuals. This study is the first to report these levels for PBDEs, though partitioning between blood and milk has been done previously for dioxins and polychlorinated biphenyls (PCBs). Twelve congeners in 11 nursing mothers’ blood and milk were found and the data describe partitioning ratios between blood and milk. The data suggest it may be easier for smaller, less brominated congeners to move from blood to milk.

Intake of many persistent organic pollutants (POPs) including dioxins, dibenzofurans and PCBs is almost exclusively from gastrointestinal ingestion of animal fats in the diet. With polybrominated diphenyl ether (PBDE) brominated flame retardants (BFRs), no consensus exists at present as to the extent of intake from food, from indoor dust or other routes of intake. Vegans, or pure vegetarians, were previously found to have low body burden of dioxins and dibenzofurans in blood. Data reported here for the first time show a trend towards lower PBDE levels with longer time periods without ingestion of food of animal origin in 8 adult residents of the United States. A stronger relationship between lower PBDE levels and time without meat, specifically, is consistent with substantial PBDE intake from meat relative to fish or dairy products in Americans. These vegans had somewhat lower PBDE levels with a range 12.4–127 and a median 23.9 ppb than published reports of US general population samples which had a range ...

Previous studies described the use of potassium dichromate (K2Cr2O7) to successfully preserve whole blood for up to 34 days at room temperature (20–22°C) for analysis of chlorinated dioxins, dibenzofurans and PCBs. Potassium dichromate has been successfully employed as a preservative for cows’ milk and in a World Health Organization study of human milk. The use of two 100 mg tablets in 40 to 100 mL of whole blood in anticoagulant was found to provide almost identical levels of dioxins, dibenzofurans, PCBs and lipids as found in frozen comparison blood at −70°C which is generally regarded as the gold standard for blood preservation. Potassium dichromate was found to be preferable to 20 and 40% ethyl alcohol for this preservation. This finding opens opportunities for preservation under field conditions in developing countries where neither electricity nor dry ice is available. Not having to use dry ice for shipping also allows more flexibility in the choice of commercial carriers for transporting blood to a...

The aim of this study is to examine the association between transplacental exposure to dioxins/polychlorinated biphenyls (PCBs) and thyroid and growth hormones in newborns. We recruited 118 pregnant women, between 25 and 34 years of age, at the obstetric clinic. Personal data collected included reproductive and medical histories and physical factors. Clinicians gathered placental and umbilical cord serum upon delivery and carefully scored the 118 newborns, making both structural and functional assessments. We analyzed placentas for 17 polychlorinated dibenzo-p-dioxins and dibenzofurans and 12 dioxin-like PCB congeners with the World Health Organization–defined toxic equivalent factors, and six indicator PCBs by high-resolution gas chromatography and high-resolution mass spectrometry. We analyzed thyroid and growth hormones from cord serum using radioimmunoassay. Insulin-like growth factor (IGF)-1, IGF-binding globulin-3, and thyroxine × yroid-stimulating hormone (T4 × TSH) were significantly associated with increased placental weight and Quetelet index (in kilograms per square meter; correlation coefficient r = 0.2–0.3; p < 0.05). Multivariate analyses showed independently and significantly decreased free T4 (FT4) × TSH with increasing non-ortho PCBs (r = −0.2; p < 0.05). We suggest that significant FT4 feedback alterations to the hypothalamus result from in utero exposure to non-ortho PCBs. Considering the vast existence of bioaccumulated dioxins and PCBs and the resultant body burden in modern society, we suggest routine screening of both thyroid hormone levels and thyroid function in newborns.

Postnatal exposure to dioxins in breastfed infants occurs mainly during breast-feeding. The exposure to a substantial amount of endocrine disruptors in the early days of life may cause long-term health effects. Test subjects were healthy and primiparous mothers with a mean age of 28 (S.D. = 3.8) in 2001. The PCDD/F congeners were analyzed in the breast milk using gas chromatograph/high resolution mass spectrometry. The mean level of PCDD/Fs was 7.4 pg-WHO-TEQ/g lipid, which is significantly lower than the level found in individuals from other countries. The total PCDD WHO-TEQ levels in breast milk had a significant positive association with maternal age and a slightly negative association with perinatal BMI (body mass index of the period before and after the delivery). The estimated daily intake of 10.5 pg-WHO-TEQ/kg/day from individual breast milk was predicted for a breastfed infant at 6 months of age with proper assumption of 8 kg body weight, 854 g milk per day of consumption, 95% of dioxin absorption rate, and linear decline of dioxin during lactation. Based on the lower WHO-TEQ levels in the breast milk, breast-feeding should still be encouraged and continued in Taiwan.

Brominated flame retardants have come into common use in the United States during the past 3 decades. This study reports levels of polybrominated diphenyl ether (PBDE) flame retardants in blood from the U.S. population at the present time and 30 years previously and also current human milk levels. This is also the first study to report measured congeners and dioxin toxic equivalents (TEQs) of dioxins, dibenzofurans, and dioxin-like polychlorinated biphenyls (PCBs) from archived, 1973, blood and compare them with current levels. The findings indicate there have been significant changes in levels of each class of these persistent organic pollutants (POPs) in U.S. human blood. Although dioxin, dibenzofuran, and PCB levels are markedly higher in the 1973 blood, the opposite is true for PBDEs. Furthermore, unlike dioxins, dibenzofurans, and PCBs, which increase with age, there was no significant correlation found in our study between PBDE levels and age. Current total PBDE levels in U.S. blood are the highest reported worldwide to date, with 2 pooled samples (N = 100 each) measuring 61.7 and 79.7 parts per billion (ppb) lipid, and in a series of 39 individual analyses, the range was 4.6 to 365.5 ppb with a median of 29 ppb and a mean of 52.6 ppb. The median for women in this study was 43.3 ppb, and for men it was 25.1 ppb. Although women have a higher level of PBDEs in blood than men, in our study, this is not statistically significant. Blood levels are similar to levels in U.S. human milk from 59 women, 6.2 to 418.8 ppb lipid. Levels of PBDE in pooled 2003 serum are far higher at 61.7 ppb than in 1973 archived pooled serum in which almost no PBDEs were quantified, although the estimated level using half the detection limit for nondetects was 0.77 ppb. Although no human health studies have been conducted on PBDEs, they are of concern because in vivo and in vitro animal studies show nervous system, reproductive, developmental, and endocrine effects, as well as cancer in high-dose studies.

Blood samples of 152 residents (male 75 and female 77) aged 20–60 years in Fukuoka, Japan, were analyzed for dioxin toxic compounds of polychlorinated dibenzo- p -dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), non- ortho polychlorinated biphenyls (non- ortho PCBs) and mono- ortho polychlorinated biphenyls (mono- ortho PCBs) as well as 35 PCB congeners and 12 chlorinated pesticides by high-resolution gas chromatography/high-resolution mass spectrometry. Average concentrations of dioxin toxic equivalents (TEQ) from PCDDs, PCDFs, non- ortho PCBs, mono- ortho PCBs and their total in the blood of 152 residents were 10.28, 5.56, 7.75, 4.57 and 28.15 ppt in lipid, respectively. These total TEQ levels were comparable to the blood TEQ levels of normal Japanese ( n = 735). Lipid basis total TEQ levels progressively increased in the males from 17.1 ppt at age 20s to 47.5 ppt at age 50s and in the females from 19.5 ppt at age 20s to 54.5 ppt at age 50s. Dioxin toxic contribution of PCBs to total TEQ was increased from 31% at age 20s to 55% at age 50s. Average concentrations of total 35 PCBs and total 12 pesticides in the blood of 151 residents were 386 and 1079 ppb in lipid, respectively. Average concentrations (ppb in lipid) of total PCBs and total pesticides also progressively increased in the males from 213 and 444 at age 20s to 868 and 2140 at age 50s, respectively, and in the females from 199 and 588 at age 20s to 550 and 1977 at age 50s, respectively. The levels of TEQ, PCBs, hexachlorobenzene, beta-hexachlorocyclohexane, dieldrin, p , p ′-dichlorodiphenyldichloroethylene, p , p ′-dichlorodiphenyltrichloroethane, trans -nonachlor and cis -nonachlor were positively correlated with each other in most of the combinations, and the highest correlations ( r > 0.8) were observed between total TEQ and PCBs in both sexes.

This paper gives an overview on the determination of PBDEs in biological tissues, such as human blood and milk, cow's milk and fish with special emphasis on quality control and assurance measures which are mandatory and a prerequisite for a reliable determination of environmental pollutants at trace levels. First experiences in the determination of PBDEs have been gained nearly 20 years ago. Due to great progress in the development of analytical instrumentation, the applied GC/MS methods resulted in very low detection limits. Furthermore, because of unexpected findings in biological tissues, the determination of PBDEs became of growing importance in the past few years. The analysis of hundreds of samples demonstrated the need for extensive quality control/quality assurance (QC/QA) measures which will be reported in detail in the following.

Forest fires are suggested as a potential and significant source of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/Fs), even though no studies to date provide sufficient evidence to confirm forest fires as a source of PCDD/Fs. Recent investigations in Queensland, Australia have identified a widespread contamination of PCDDs (in particular OCDD) in soils and sediments in the coastal region from an unknown source of PCDD/Fs. Queensland is predominately rural; it has few known anthropogenic sources of PCDD/Fs, whereas forest fires are a frequent occurrence. This study was conducted to assess forest fires as a potential source of the unknown PCDD/F contamination in Queensland. A combustion experiment was designed to assess the overall mass of PCDD/Fs before and after a simulated forest fire. The results from this study did not identify an increase in sigmaPCDD/Fs or OCDD after the combustion process. However, specific non-2,3,7,8 substituted lower chlorinated PCDD/Fs were elevated after the combustion process, suggesting formation from a precursor. The results from this study indicate that forest fires are unlikely to be the source of the unknown PCDD contamination in Queensland, rather they are a key mechanism for the redistribution of PCDD/Fs from existing sources and precursors.

Recently, elevated dioxin levels, over 5 parts per trillion (ppt) 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), from Agent Orange was reported in 95% of 43 selected residents of Bien Hoa City, a city in southern Vietnam near a former air base used for Agent Orange-spraying missions. Agent Orange herbicide, contaminated with TCDD, was sprayed in Vietnam between 1962 and 1971 primarily for use as a defoliant. Typical blood TCCD levels are 2 ppt in Vietnamese, but levels are as high as 413 ppt in Bien Hoa City. Elevated TCDD was found in children born many years after Agent Orange spraying ended and in immigrants from non-Agent Orange-sprayed parts of Vietnam, which documented new exposures. Extremely elevated soil TCDD samples, over 1 million ppt, and elevated TCDD in sediment were found in some nearby areas such as Bien Hung Lake. The primary route of intake of almost all dioxins in humans is food. However, in our prior studies in Bien Hoa, food was unavailable for dioxin analysis so the route of intake was not confirmed. In the 1970s, while Agent Orange was still being sprayed, elevated human milk TCDD levels as high as 1850 were detected in milk from Vietnamese people living in Agent Orange-sprayed areas where consumption of fish was high. Furthermore, also in the 1970s, elevated TCDD levels (up to 810 ppt) were found in fish and shrimp from the same area as the milk donors. In the 1980s, we found elevated TCDD and also other organohalogen levels in human tissue, pork, fish, a turtle, and a snake in Southern Vietnam. For these reasons, we recently collected food from Bien Hoa and analyzed it for dioxins, polychlorinated biphenyls (PCBs), DDT and its metabolites, and other organochlorines. We found marked elevation of TCDD, the dioxin characteristic of Agent Orange, in some of the food products, including ducks with 276 ppt and 331 ppt wet weight, chickens from 0.031-15 ppt wet weight, fish from 0.063-65 ppt wet weight, and a toad with 56 ppt wet weight. Usual TCDD levels in food are less than 0.1 ppt. Total TEQ for ducks was from 286-343 ppt wet weight or 536 ppt and 550 ppt lipid; for chickens from 0.35-48 ppt wet weight or 0.95-74 ppt lipid, for fish from 0.19-66 ppt wet weight or 3.2 ppt and 15,349 ppt lipid, and the toad was 80 ppt wet weight and 11,765 ppt lipid. Interestingly, this study did not find elevated levels of TCDD in the pork and beef samples. Clearly, food, including duck, chicken, some fish, and a toad, appears responsible for elevated TCDD in residents of Bien Hoa City, even though the original Agent Orange contamination occurred 30-40 years before sampling. Elevated levels of PCBs and DDT and its metabolites were found in some food samples. Furthermore, measurable levels of hexachlorocyclohexanes (HCH) and hexachlorobenzene (HCB) were found in a wide range of measurable levels. All of the 11 dioxin-like PCBs measured and presented plus 6 dioxins in addition to TCDD and 10 dibenzofurans contributed to the total dioxin toxicity (TEQ). However, when elevated, TCDD frequently contributed most of the TEQ. Thirty-six congeners from 7 classes of chemicals were measured in each of the 16 specimens providing a total of 576 congener levels.

Agent Orange, a phenoxyherbicide contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), was used by American military forces during the United States-Vietnam war between 1962 and 1971 primarily as a defoliant to destroy forests where enemy troops might find cover. Agent Orange was used mainly in Vietnam, but also to a lesser extent in Laos and Cambodia. In Laos, there have been no prior studies of TCDD contamination from Agent Orange, despite known defoliation and documented records of Agent Orange spraying. This article presents findings of TCDD in human blood and milk from two geographic areas in Laos: Vientiane, a nonsprayed area, and Sepone, an Agent Orange-sprayed area. German and Canadian laboratories used high-resolution gas chromatography-mass spectrometry to measure 7 dioxin, 10 dibenzofuran, and 4 non-ortho or coplanar polychlorinated biphenyls in Laotian blood and milk samples. Most subjects tested in this Laos Ministry of Health Study showed low dioxin and dibenzofuran levels, consistent with what would be expected in a primarily rural nonindustrial country. These findings are consistent with relatively low dioxin and dibenzofuran levels recently found in food from these same areas. The chemically and toxicologically related non-ortho PCBs were measured but were found at low levels compared to specimens from other countries, presumably because of less industrialization and industrial pollution in Laos.

No previous reports exist on polybrominated diphenyl ether (PBDE) congeners in human milk from individual U.S. mothers. This article on PBDEs is an extension of our previous studies on concentrations of dioxins, dibenzofurans, polychlorinated biphenyls, and other chlorinated organic compounds in human milk in a number of countries. PBDE commercial products are used as flame retardants in flexible polyurethane foam (penta-BDE), in acrylonitrile-butadiene-styrene resins (octa-BDE), and in high-impact polystyrene resins (deca-BDE). Their use is permitted in the United States but is banned in some European countries because of presumed toxicity, demonstrated persistence, and bioaccumulation. Different commercial products can be found in various consumer products such as television sets, computers, computer monitors and printers, carpets, and upholstery. Analyses of human levels of these compounds suggest low but rising levels in European human milk, which may have peaked, at least in Sweden, in the late 1990s. Very few data exist on levels of PBDEs in humans in the United States, and none from milk from individual nursing mothers. To address this issue, we analyzed 47 individual milk samples from nursing mothers, 20-41 years of age, from a milk bank in Austin, Texas, and a community women's health clinic in Dallas, Texas. Up to 13 PBDE congeners were measured. The concentrations of the sum of PBDE congeners varied from 6.2 to 419 ng/g (or parts per billion) lipid, with a median of 34 ng/g and a mean of 73.9 ng/g lipid. The PBDE levels in breast milk from Texas were similar to levels found in U.S. blood and adipose tissue lipid from California and Indiana and are 10-100 times greater than human tissue levels in Europe. Their detection in breast milk raises concern for potential toxicity to nursing infants, given the persistence and bioaccumulative nature of some of the PBDE congeners. These results indicate a need for more detailed investigation of the levels of PBDE in people and food, as well as determining if animal fat in food is the major route of exposure of the general U.S. population. Other routes of intake may also be significant.

Concentrations of 2,3,7,8-substituted polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) were determined in 14 sediment samples collected from four sites in the Mai Po Marshes Nature Reserve (within a RAMSAR Site) and from another six sites in Victoria Harbour and along the Hong Kong coastline. Elevated levels of PCDDs, and particularly OCDD, were detectable in all samples collected from the Mai Po Marshes and five of the six sites. In contrast to PCDDs, PCDFs were mainly found in sediment samples collected from industrial areas (Kwun Tong and To Kwa Wan) in Victoria Harbour. PCDD/F levels and congener profiles in the samples from the Mai Po Marshes Nature Reserve in particular show strong similarities to those reported in studies which have attributed similar elevated PCDD concentrations to nonanthropogenic PCDD sources. (C) 2002 Elsevier Science Ltd. All rights reserved.

Recent findings of elevated PCDDs from an unknown source in the coastal marine environment of Queensland, Australia has instigated further investigations into the distribution of, and environments associated with the PCDD contamination. This study presents data for OCDD concentrations in the coastal, mountainous and inland environment of Queensland. Additionally, full 2,3,7,8-substituted polychlorinated dibenzo-p-dioxins and dibenzofuran (PCDD/F) profiles from different land-use types and environments in the coastal region were analysed. Distinct east-west gradients were detected in topsoil collected from various bushland regions with elevated OCDD concentrations confined to the coastal region. However, PCDD/F results from topsoil and river sediments collected in the Queensland coastal region suggest that elevated OCDD concentrations cannot be attributed to any of the environments, land-use or industry types investigated. PCDD/F congener profiles from select samples were remarkably similar to those previously described in marine sediments collected along the entire Queensland coastline. In addition, kaolinite clay samples from Queensland exhibited elevated OCDD concentrations, and PCDD/F profiles in these samples were similar to those detected in kaolinite clays elsewhere. Natural formation processes have been hypothesised as the source of elevated PCDDs in Queensland and other locations, where similar PCDD/F profiles and the general lack of anthropogenic sources are evident. This study presents additional data supporting this hypothesis and provides further information that may assist in the identification of the processes involved in the natural formation of PCDDs.

Dioxin and PCB monitoring programs for food and feeding stuff in most countries of the world, including many European Countries are currently inadequate. Better control of food production lines and food processing procedures is needed to minimize entry of dioxin to the food chain and will help to avoid dioxin contamination accidents. This would also improve the ability to trace back a possible contamination to its source. European guidelines for monitoring programs should be established to ensure comparable and meaningful results. These guidelines should define the minimum requirements for the design of monitoring programs, analytical methods, and quality assurance. Though data from Northern Europe shows that the general population exposure to dioxin and PCB has decreased during the last ten years these compounds continue to be a risk of accidental contamination of the food chain. The most prominent recent example is the Belgian dioxin contamination of feeding stuff in 1999. The Belgian dioxin contamination was not detected due to dioxin monitoring programs but by their direct biological effects seen in animals. Four other cases of dioxin contamination have been detected in Europe since 1997 due to local monitoring programs. One of them (citrus pulp pellets 1998) was in a much larger scale than the Belgian dioxin contamination. The general population's exposure to dioxins and PCBs is still in the same range (1-4 pg WHO-TEQ/kg body weight and day) as the recently revised WHO tolerable daily intake (TDI). There is concern that short-term high level exposure to dioxins, furans, and PCB may cause biological effects on the human fetal development and further research is required. Further actions to control sources building on considerable advances already made in many countries may need to be supplemented by measures to prevent direct contamination of feeding stuff or food to reduce general population exposure further.

Nine samples of butter from producers in various states of Australia were analysed for polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). Detectable concentrations of 2,3,7,8-chlorine substituted PCDD/Fs were found in all samples. The mean PCDD/F concentration expressed as 2,3,7,8-TCDD equivalents (TEQs) was 0.19 pg TEQ g−1 fat. The highest concentration (0.46 pg TEQ g−1 fat) was observable in a sample from Victoria which is the most densely populated state. Overall the results indicate that PCDD/F concentrations in dairy products from Australia are low in comparison to the levels in dairy products of industrialized countries on the Northern Hemisphere. As expected, this study provides evidence that the environmental and consequently the human body burden of PCDD/ Fs to be relatively low in Australia.

This paper presents new data on the levels of polybrominated diphenyl ethers (PBDEs) in American airline workers. This pilot study did not find elevated total PBDEs in the blood of nine flight attendants and one aircraft pilot who have worked in airplanes for at least the past 5 years. These findings are not consistent with the findings of elevated blood levels of PBDEs from the 2008 Christiansson et al. publication "Polybrominated diphenyl ethers in aircraft cabins - A source of human exposure?" We agree that more research needs to be done on larger, more representative samples of airline workers to better characterize exposure of airline workers and other frequent flyers to PBDEs.

A digestive tract mass balance was performed on six men with high body burdens of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs). Intake via food was measured by analyzing duplicate portions of the food consumed by the volunteers and excretion via feces was determined by quantitative collection and analysis of the feces. Blood samples were taken to determine the current body burden. The results showed that the quantity of non-metabolized chemical excreted in the feces clearly exceeded the uptake via food for all of the 2,3,7,8-substituted PCDDs and some of the PCDFs, indicating a significant clearance across the gastrointestinal tract. The concentrations of these PCDD/F congeners in blood and feces were highly correlated (r > 0.8), demonstrating that the fecal PCDD/F content was determined by the body burden. The half lives in the test persons due to fecal clearance of non-metabolized chemical were estimated from the excretion rate and the current body burden and ranged between 10 years (Cl8DD) and 33 years (2,3,4,7,8-Cl5DF). These were compared with the overall contaminant half-lives due to all clearance processes which were calculated from the body burden and the decrease in blood concentrations measured over several years. The fecal clearance of non-metabolized PCDD/F contributed on average between 37% (2,3,7,8-Cl4DD) and 90% (Cl8DD) to the total elimination. This indicates that the gastrointestinal pathway plays a decisive role in the clearance of most 2,3,7,8-subsituted PCDD/F congeners.

PCDD/PCDF/PCB concentrations were measured in samples from four mothers (at delivery and during lactation) and their infants (at birth and the end of first year of life). For two of these mothers it was the second delivery and breast-feeding period, and additional data were available from first lactation period and the first-born infant at the age of 11 to 12 months. Five of the six infants were fully breast-fed for at least 17 weeks. In four of them a distinct PCDD/PCDF/PCB accumulation was observed at the end of the first year of life: concentrations in blood fat were 1.5 to 3.6 times higher than maternal levels measured at the same time. Due to decreasing maternal body burdens during lactation, PCDD/PCDF concentrations at 11 to 12 months of life were only about half as high in the second infant as in the first one at the same age. During second pregnancy, no important change of the concentrations was observed in maternal blood.

The primary source of dioxins (PCDDs), dibenzofurans (PCDFs) and coplanar PCBs for the general population is food, especially meat, fish, and dairy products. However, most data on the levels of these chemicals is from food in the raw or uncooked state. We report here the effect of one type of cooking (broiling) on the levels of PCDDs, PCDFs, and coplanar PCBs in ground beef (hamburger), bacon and catfish. Samples of hamburger, bacon, and catfish were broiled and compared to uncooked samples in order to measure changes in the amounts of dioxins in cooked food. The total amount of PCDD, PCDF, and coplanar PCB TEQ decreased by approximately 50% on average for each portion as a result of broiling the hamburger, bacon and catfish specimens. The mean concentration (pg TEQ/kg, wet weight) of PCDDs, PCDFs, and coplanar PCBs, however, remained the same in the hamburger, increased by 83% in the bacon, and decreased by 34% in the catfish. On average, the total measured concentration (pg/kg) of the congeners of PCDDs, PCDFs, and coplanar PCBs increased 14% in the hamburger, increased 29% in the bacon, and decreased 33% in the catfish.

This paper presents measured dioxin, dibenzofuran, PCB, DDE and HCB blood and milk levels and estimated body burdens in a mother who nursed twins for thirty-eight months. A total of thirteen milk samples and three blood samples were collected and analyzed. Measured PCDD and PCDF levels in milk decreased from 309 and 21 ng/kg (ppt) to 173 and 9 ng/kg, respectively, between March 1993 and September 1995. Based on the decrease in breast milk dioxin levels, we estimate that the nursing mother reduced her dioxin body burden from 310 to 96 ng dioxin toxic equivalents (TEQs), or approximately 69%. In two and one half years the level of HCB in the mother's milk decreased from 10.7 to less than 1.8 ng/g (ppb), the level of DDE decreased from 246 to 46 ng/g and the total level of non-coplanar PCBs decreased from 285 to 63 ng/g, on a lipid basis. We estimate that the twin's consumption of dioxins, dibenzofurans, and coplanar PCBs from breast feeding was approximately 115 ng TEQ per twin.

Yusho blood and control serum were collected in around 1991 and analyzed for congeners of PCDDs, PCDFs and PCBs. In Yusho blood, TEQ was mainly contributed by 2,3,4,7,8-penta-CDF (77-248 ppt), 1,2,3,4,7,8-hexa-CDF (15-37 ppt) and 2,3,3',4,4',5-hexa-CB (16-77 ppt). Total TEQ in Yusho blood (185-441 ppt) was only 3-14 times higher than that of control serum (31-61 ppt). It is notable that the concentrations of 3,3',4,4',5-, 2,3,3',4,4'- and 2,3',4,4',5-penta-CBs in Yusho blood were comparable to or lower up to 3-5 times than those in control blood.

Animal models suggest that dioxins have a negative effect on the level of expression of the epidermal growth factor receptor in cells. In vivo the level of expression in tissue of the epidermal growth factor receptor can be monitored by assaying for the extracellular domain in blood using an enzyme linked immunosorbent assay. We have determined the levels of the extracellular domain of the epidermal growth factor receptor in the plasma of 30 individuals: 10 with high blood dioxin levels (TEQ range = 318–673 ppt), 10 with medium blood dioxin levels (TEQ range = 16–60 ppt), and 10 with low background blood dioxin levels (TEQ range = 3–10 ppt). The levels of the epidermal growth factor receptor extracellular domain were lower in the high blood dioxin group (mean ± SD = 45 ± 26 fmol/ml) and the medium blood dioxin group (mean ± SD = 41 ± 23 fmol/ml) compared with the low blood dioxin group (mean ± SD = 73 ± 43 fmol/ml). These results suggest that the extracellular domain of the epidermal growth factor receptor may be a marker of the biological effect of dioxin exposure. Am. J. Ind. Med. 34:1–5, 1998. © 1998 Wiley-Liss, Inc.

A cross-sectional study was performed to examine the internal exposure of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDF) in former workers in a nonferrous metal recycling facility. Liver enzymes, lipid parameters, and thyroid hormones were measured to check possible biologic effects. Compared to background levels, the international toxicity equivalent levels of exposed workers were slightly elevated (median 42 ppt, range 13-281 ppt). The workers also had higher total PCDF concentrations (median 128 ppt, range 30-1138 ppt). Correlation analyses demonstrate significant associations with only one liver enzyme, alanine aminotransferase. There were no such associations with serum cholesterol levels or with serum thyroid hormones. Because of the cross-sectional design of the study, firm conclusions cannot be drawn. For further evaluation, a follow-up examination appears necessary. Images Figure 1

This paper gives an overview of the development of the environmental or background exposure of humans to polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) in Germany. To determine the background exposure, adipose tissue, human milk, or blood can be used. The good comparability of the matrices analyzed is demonstrated. The daily consumption of low-level contaminated food, mainly of animal origin, leads to the accumulation of PCDDs/PCDFs in the human adipose reservoir. The influence of factors such as various eating habits, severe weight loss, age, and nursing (women only) on the human body burden is discussed. Because of decreasing emission of PCDDs/PCDFs into the environment, a decline of these components in humans could be observed over a time span of 10 years. Images Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 7 Figure 8 Figure 9 Figure 11

To assess toxicokinetics of polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs), oral intake and fecal excretion were measured in two breast-fed infants and one formula-fed infant during the 1st y of life. The intake of these compounds was up to 50 times higher in the breast-fed infants. In these children, fecal excretion of the main tetra- to hexachlorinated congeners was less than 9% of the intake at age of 1 and 5 mo, indicating almost complete intestinal absorption during breast-feeding. In contrast, distinctly higher fecal excretion rates were observed for the hepta- and octachlorinated compounds. Despite much lower PCDD/PCDF intake after weaning, concentrations in stool fat did not decrease substantially. We conclude that concentrations in fecal fat more or less reflect those in body fat. Additionally, PCDD/PCDF concentrations were measured in blood fat of all infants (and in a second formula-fed baby) at the age of 11 mo. International toxicity equivalent (I-TEq) concentrations in the formula-fed infants were less than 25% of maternal values and about 10 times lower than in the infants breast-fed for 6-7 mo. In the latter, a distinct accumulation was found for the tetra- to hexachlorinated congeners compared with maternal concentrations. We conclude that accumulation of PCDDs and PCDFs in infants is as high as expected on the basis of intake data and assuming complete absorption and negligible elimination during the 1st y of life.

Large amounts of the powerful pesticide sodium pentachlorophenol (Na-PCP) salt have been sprayed over vast areas in central China to control schistosomiasis, a parasitic disease of epidemic proportions. Approximately 6000 tons of Na-PCP are produced in China annually. Dioxins, a class of toxic, persistent compounds, are found as impurities in commercial Na-PCP products. These contaminants are released into the environment and significantly contribute to human exposure to dioxins in China. This study was carried out to determine dioxin levels in environmental and human tissue samples from one schistosomiasis area to evaluate the health risks associated with exposure to Na-PCP. Na-PCP pesticide was applied in 1972, 1973, and again in 1978. A total of approximately 454 tons and 902 tons of 5-ppm Na-PCP in water were sprayed over large land and lake problem schistosomiasis areas, respectively. The groups studied were (1) sprayers or handlers of Na-PCP, (2) persons living in the sprayed areas, and (3) persons living in unsprayed areas 300 km north of the sprayed lake located in a city in the Jiangxi province. Individual whole-blood and breast-milk samples were collected and later pooled for dioxin analysis. Also, a sample of commercial Na-PCP was collected. In addition, sediment samples from the lake where Na-PCP was sprayed were collected from four different sites and one control sample was collected from a non-schistosomiasis area. All of the samples were analyzed by high-resolution gas chromatography/mass spectrometry. A sample of Na-PCP used in schistosomiasis regions was analyzed and levels of 2,3,7,8-substituted dibenzodioxin (PCDD) and dibenzofuran (PCDF) congeners were measured. In addition, the international dioxin toxic equivalent (I-TEQ) value of this sample was calculated. Total I-TEQ of 162 parts per billion (ppb) was found in the Chinese Na-PCP product. A pooled breast-milk sample from mothers, female agricultural workers who were born in the schistosomiasis areas where large amounts of Na-PCP were sprayed, had an I-TEQ of 5,4 parts per trillion (ppt), lipid, which was about double that of mothers from control regions, women born in areas not sprayed with Na-PCP (2.6 ppt, lipid). The dioxin I-TEQ values in human blood ranged from 9.0 (subjects 15 to 19 years of age) to 16.3 ppt, lipid (subjects 35 to 70 years of age) in the whole-blood samples from Na-PCP exposed persons, whereas the general population's whole-blood I-TEQs were 4.8 and 6.4 ppt, lipid, respectively. The PCDD/F congener distribution patterns in four sediment samples from schistosomiasis areas were similar to that of Na-PCP. By comparison of specific "fingerprint" congeners (higher chlorinated dioxins and the closely related dibenzofurans) in Na-PCP, human tissues, and sediment samples, we conclude that the chemical pesticide Na-PCP is a source of environmental and human dioxin exposure in the Chinese schistosomiasis area studied. Although human PCDD/F tissue levels in China are low compared with those in more industrialized countries, the elevated I-TEQ levels in exposed persons are cause for concern.

This study addresses the issue of breast-feeding and its reduction of maternal dioxin body burden. Nursing is also a source of infant dioxin exposure. This study extends our previous efforts to investigate a nursing mother's milk and blood dioxin levels. We report polychlorinated dibenzo-p-dioxin (PCDD) and polychlorinated dibenzofuran (PCDF) dioxin toxic equivalents (TEQs) in milk (M) and blood (B) both before and also after two years of nursing twins to be 16.9 ppt (M), 14.9 ppt (B), and 3.1 ppt (M) and 4.9 ppt (B), respectively. The ratios of measured congeners comparing milk to whole blood from a nursing mother taken initially and after two years of nursing vary from 0.36 to 8.40 in 1992 and 0.17 to 1.0 in 1994. The mother's body burden was initially calculated to be 329 ng TEQ from milk levels and 291 ng TEQ from blood levels using samples taken in February 1992 and decreased to 60.1 ng TEQ from milk and 96 ng TEQ from measured blood using samples collected in December 1994. We calculate that the excretion of dioxin TEQ by the mother through breast-feeding is 269 ng TEQ, which is similar to the 303 ng TEQ estimated total dioxin intake by the twins over two years. The average daily dioxin intake from nursing is 66 pg TEQ/kg-BW/day for each twin over the two years.

Food, especially meat, milk, and fish, is the immediate source of almost all polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and dioxinlike compounds in the general population. To estimate intake of these highly toxic compounds, we performed congener-specific dioxin analyses for the first time on U.S. food for 18 dairy meat, and fish samples from a supermarket in upstate New York. 2,3,7,8 Tetrachlorodibenzo-p-dioxin (TCDD, "dioxin") toxic equivalents (TEqs) on a wet weight basis for the dairy products ranged for 0.04 to 0.7 ppt, meat TEqs ranged from 0.03 to 1.5 ppt, and fish TEqs ranged from 0.02 to 0.13 ppt. Previous human breast milk and infant formula analyses were used with the current preliminary food data to estimate a range of dioxin intake for Americans. Average daily food intake of TEqs for an adult weighing 65 kg was estimated to be between 0.3 and 3.0 pg/kg body weight, for a total of 18-192 pg TEq, using 1986 American consumption rates. Due to the relatively high level of PCDDs and PCDFs commonly found in human breast milk from American women and from women in other industrial countries, a nursing infant may consume an average of 35-53 pg TEq/kg body weight/day in its first year of life. This may be compared with the current U.S. EPA virtually safe dose of 0.006 pg TCDD/kg body weight per day over a 70-year lifetime based on an upper limit cancer risk of 10(-6), or the 10 pg/kg/day used by some European government agencies.

Polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) are unwanted by-products formed in a variety of industrial and thermal processes. Humans may become contaminated with PCDD/PCDFs through environmental, occupational or accidental exposure.In summary, a broad spectrum of biomarkers have been analysed in human populations highly exposed to dioxins. These include changes in liver enzymes, blood lipids, thyroid and steroid hormones, and glucose tolerance. None of these markers can be considered to be specific for dioxin exposure because they can be elicited by a broad spectrum of diseases and/or exposures to other types of chemicals. Even chloracne, one of the most reliable marker/diseases observed after high exposure to dioxins in humans, can be caused by other chemicals.Among the biomarkers closely related to arylhydrocarbon receptor (AhR) activation, cytochrome P (CYP) induction plays the most prominent role. It is usually measured as a change in caffeine metabolism. In addition, these markers are not absolutely specific for dioxin exposure but can also result from exposure to certain polycyclicaromatic hydrocarbons (PAHs), e.g., in workers or in smokers. Furthermore, CYP activity measurements in peripheral blood lymphocytes have been reported to be highly variable, even in among individuals without evidence for different exposure.Taken together, biomarkers of dioxin exposure can be useful in combination with chemical analysis of dioxins in blood, adipose tissue, etc. Here, they can provide a suitable tool for the follow-up of intoxication cases or after local high exposure of certain populations in order to obtain information on biological responses over time. As an isolated tool for exposure or risk assessment of dioxins they should not be used.For a number of years a decreasing trend in dioxins has been observed in the environment and in humans. Despite this declining PCDD/PCDF trend, the exposure of babies during the breast-feeding period is still a matter of concern and justifies taking measures to reduce PCDD/PCDF emissions into the environment.