Exposure to dioxin-like pollutants via different food commodities in Swedish children and young adults

The dietary intake of polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs) and biphenyls (PCBs) in terms of toxic equivalents (TEQs) was investigated in Swedish children and young adults. Exposure was estimated from concentration data of six groups of individual food commodities (meat, fish, dairy products, egg, edible fats and other foodstuff) combined with food intake data from a 7-day record book obtained from 670 individuals aged 1–24 years. The results showed that Swedish boys and girls, up to the age of ten, had a median TEQ intake that exceeded the tolerable daily intake (TDI) of 2 pg TEQ/kg body weight. Children exceeding the TDI varied from almost all individuals among the youngest children to about 20% among young men and women. Dairy and fish products were the main sources of exposure for the average child, accounting for 59% of the total TEQ intake. The individuals most highly exposed were, on the other hand, characterized by a high consumption of fish. Since children constitute a vulnerable group, results obtained from the present study show that it is essential to perform age specific dietary intake assessments of pollutants and more carefully consider sensitive and/or highly exposed groups in the population in the risk management processes.     

Levels and congener profiles of polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) and polychlorinated biphenyls (PCBs) in sheep milk from an industrialised area of Sardinia,Italy

Concentrations of 7 polychlorinated dibenzo-p-dioxins (PCDDs), 10 polychlorinated dibenzofurans (PCDFs) and 22 polychlorinated biphenyls (PCBs), including 12 dioxin like-PCBs (non- and mono-ortho PCBs) were measured in 80 sheep milk samples from farms located in an industrialized area of Sardinia, Italy. PCDDs and PCDFs mean concentrations were 2.45 and 3.69 pg g⁻¹ fat basis, respectively. The mean dl-PCB concentration was 2.01 ng g⁻¹ fat basis, while cumulative ndl-PCB levels ranged from 1.02 to 20.42, with a mean of 4.92 ng g⁻¹ fat. The results expressed in pg WHO-TEQ/g fat showed that contamination level of milk was below the limit values for human consumption established by EC legislation. In the same way, all the investigated milk exhibited PCDD/Fs concentrations below EU action levels, while dl-PCBs concentrations exceeded the action level of 2.0 pg WHO-TEQ/g fat. These findings point to the need to continue to conduct general monitoring programmes, including also milk samples from areas not close to the contaminant-emitting industries, in order to better evaluate the impact of industrial activities on surrounding environment.     

A sensitivity analysis using alternative toxic equivalency factors to estimate U.S. dietary exposures to dioxin-like compounds

EPA recommends sensitivity analyses when applying the toxic equivalency factor (TEF) method to evaluate exposures to dioxin-like compounds (DLCs). Applying the World Health Organization’s (WHO) 2005 TEF values and estimating average U.S. daily dietary intakes of 25 DLCs from eight food categories, we estimate a toxic equivalency (TEQ) intake of 23 pg/day. Among DLCs, PCB 126 (26%) and 1,2,3,7,8-PeCDD (23%) dominate TEQ intakes. Among food categories, milk (14%), other dairy (28%), beef (25%), and seafood (18%) most influenced TEQ intakes. We develop two approaches to estimate alternative TEF values. Based on WHO’s assumption regarding TEF uncertainty, Approach1 estimates upper and lower TEFs for each DLC by multiplying and dividing, respectively, its individual TEF by ± half a log. Based on compiled empirical ranges of relative potency estimates, Approach2 uses percentile values for individual TEFs. Total TEQ intake estimates using the lower and upper TEFs based on Approach1 were 8 and 68 pg TEQ/day, respectively. The 25th and 75th percentile TEFs from Approach2 yielded 12 and 28 pg TEQ/day, respectively. The influential DLCs and food categories remained consistent across alternative TEFs, except at the 90th percentile using Approach2. We highlight the need for developing underlying TEF probability distributions.     

Teratogenic potency of 2,3,4,7,8-pentachlorodibenzofuran and of three mixtures of polychlorinated dibenzo-p-dioxins and dibenzofurans in mice. Problems with risk assessment using TCDD toxic-equivalency factors

The potency of 2,3,4,7,8-pentachlorodibenzofuran (P5CDF) and of three defined 2,3,7,8-TCDD-free mixtures of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDDs/PCDFs) to induce cleft palates in NMRI mice was studied. The data were compared with a dose-response curve for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The slope of the dose-response curve for P5CDF was the same as for TCDD. However, application of the International-TCDD-Toxic-Equivalency (I-TE) factor (NATO/CCMS 1988) of 0.5 overestimated the potency of the pentachlorinated congener about 2.5-fold under these experimental conditions, suggesting 0.2 as a TE factor. When assessing the cleft palate frequency on the basis of I-TEs and the weight of the substances, the potencies of the two PCDF mixtures studied were also clearly overestimated. This result was not substantially changed when using the TE factor of 0.2 for P5CDF. For the PCDD mixture studied, the cleft palate-inducing potency found largely agreed with the prediction when applying the I-TE factors. According to our data, the use of TE factors as calculated by the UBA/BGA (1985) or the NATO/CCMS (1988) are both conservative when attempting to assess the cleft palate incidence induced by PCDF mixtures in mice.     

Significant decreasing trend in human dietary exposure to PCDD/PCDFs and PCBs in Catalonia, Spain

The concentrations of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/PCDFs), and 18 polychlorinated biphenyls (PCBs) were determined in samples of foodstuffs widely consumed by the population of Catalonia, Spain. The dietary intake of PCDD/PCDFs and dioxin-like (DL)-PCBs was subsequently estimated for the population of this Spanish region. These results were compared with those of a previous survey performed during 2000. For PCDD/PCDFs, the highest WHO-TEQ values corresponded to oils and fats (0.223 ng/kg), followed by fish and seafood (0.131 ng/kg) and dairy products (0.057 ng/kg), while the lowest levels were found in fruits (0.003 ng/kg), as well as in vegetables and milk (0.009 ng/kg). For DL-PCBs the highest WHO-TEQ values corresponded to the groups of fish and seafood (0.761 ng/kg) followed by oils and fats (0.169 ng/kg), and dairy products (0.039 ng/kg), while the lowest values were observed in fruits (0.004 ng/kg), and vegetables (0.005 ng/kg) and tubers (0.006 ng/kg). The current dietary intakes of PCDD/PCDFs, DL-PCBs, and PCDD/PCDFs plus DL-PCBs were estimated to be 25.7, 52.4, and 78.1 pg WHO-TEQ/day vs. 95.4, 150.1, and 245.5 pg WHO-TEQ/day found in our previous survey. It means reductions of 73%, 65%, and 68%, for PCDD/PCDFs, DL-PCBs, and PCDD/PCDFs plus DL-PCBs, respectively. The current estimated intake for an adult male, 1.12 pg WHO-TEQ/kg body weight per day, is lower than most intakes recently reported in a number of countries over the world.     

Comparison of Intake and Systemic Relative Effect Potencies of Dioxin-like Compounds in Female Mice after a Single Oral Dose

Background: Risk assessment for mixtures of polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) is performed using the toxic equivalency factor (TEF) approach. These TEF values are derived mainly from relative effect potencies (REPs) linking an administered dose to an in vivo toxic or biological effect, resulting in “intake” TEFs. At present, there is insufficient data available to conclude that intake TEFs are also applicable for systemic concentrations (e.g., blood and tissues).Objective: We compared intake and systemic REPs of 1,2,3,7,8-pentachlorodibenzodioxin (PeCDD), 2,3,4,7,8-pentachlorodibenzofuran (4-PeCDF), 3,3´,4,4´,5-pentachlorobiphenyl (PCB-126), 2,3´,4,4´,5-pentachlorobiphenyl (PCB-118), and 2,3,3´,4,4´,5-hexachlorobiphenyl (PCB-156) in female C57BL/6 mice 3 days after a single oral dose.Methods: We calculated intake REPs and systemic REPs based on administered dose and liver, adipose, or plasma concentrations relative to TCDD. Hepatic cytochrome P450 1A1–associated ethoxyresorufin-O-deethylase (EROD) activity and gene expression of Cyp1a1, 1a2 and 1b1 in the liver and peripheral blood lymphocytes (PBLs) were used as biological end points.Results: We observed up to one order of magnitude difference between intake REPs and systemic REPs. Two different patterns were discerned. Compared with intake REPs, systemic REPs based on plasma or adipose levels were higher for PeCDD, 4-PeCDF, and PCB-126 but lower for the mono-ortho PCBs 118 and 156.Conclusions: Based on these mouse data, the comparison between intake REPs and systemic REPs reveals significant congener-specific differences that warrants the development of systemic TEFs to calculate toxic equivalents (TEQs) in blood and body tissues.     

Persistence of various polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDDs and PCDFs) in hepatic and adipose tissue of marmoset monkeys

A defined mixture of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDDs and PCDFs) was subcutaneously administered to marmoset monkeys (Callithrix jacchus). Tissue concentrations in hepatic and adipose tissue were measured at different times after treatment (1–28 weeks). One week after application high concentrations could be detected for the 2,3,7,8-substituted congeners only. The percent of the administered dose in whole liver differed for the various 2,3,7,8-substituted congeners, ranging from 24.5±4.5% for 2,3,7,8-TCDD to 74.1±4.9% for 2,3,4,6,7,8-H6CDF. Therefore, the concentration ratio (liver/adipose tissue) was also very different, ranging from about 1 (2,3,7,8-T4CDD or 2,3,7,8-T4CDF) to >10 in the case of some higher chlorinated PCDDs and PCDFs. Half-lives of PCDDs and PCDFs were very different for the various 2,3,7,8-substituted congeners. For the most toxic compound (2,3,7,8-T4CDD) a t/2 of about 8 weeks in hepatic tissue and about 11 weeks in adipose tissue was found when calculated from data obtained later than 6 weeks after injection. For 2,3,7,8-T4CDD and 1,2,3,7,8-P5CDD the decreases in hepatic concentrations were much faster during the first 6 weeks after administration (t/2 of 4 weeks). This was apparently due to redistribution phenomena. Half-life increased with increasing degrees of chlorination. In some cases (e.g. OCDD, OCDF) no significant decrease in tissue concentrations could be observed after 28 weeks. The shortest t/2 was determined for 2,3,7,8-T4CDF: shorter than 6 days in hepatic tissue and about 10 days in adipose tissue. Calculation of the body burden of thenon-2,3,7,8-substituted PCDDs/PCDFs 1 week after injection revealed that all groups of isomers were present at less than 5%. Consequences of these findings for the use of TCDD-toxic-equivalency factors are discussed and a change in strategy is suggested.Data presented in this paper are part of the doctoral thesis of Thomas Wiesmüller submitted to the Fakultät für Chemie und Pharmazie, Eberhard-Karls-Universität, Tübingen     

Genetically mediated induction of aryl hydrocarbon hydroxylase activity in human lymphoblastoid cells by polychlorinated dibenzofuran isomers and 2,3,7,8-tetrachlorodibenzo-p-dioxin

Aryl hydrocarbon hydroxylase(AHH)-inducing potency of toxic polychlorinated aromatic hydrocarbons such as polychlorinated dibenzofuran (PCDF) isomers, 3,4,5,3,4,5-hexachlorobiphenyl (HCB) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was investigated in human lymphoblastoid cell lines with different AHH inducibility for 3-methylcholanthrene (3-MC) obtained from healthy subjects. Each of the cell lines was treated with eitht individual PCDF isomers, TCDD, and HCB at doses of 1.9–15 ng/ml of culture medium, 1.9–7.5 ng/ml and 95 ng/ml, respectively. Lymphoblastoid cell lines were arbitrarily classified into three groups based on their AHH inducibilities with 3-MC (2.5 M); low (3-MC/ control=I<3), middle (3<=I<6) and high (I>=6). Degrees of the enzyme inducibilities of the organochlorine compounds proportionally increased with those for 3-MC. AHH inducibilities with 2,3,4,7,8-pentachlorodibenzofuran(2,3,4,7,8-PCDF), 1,2,3,4,6,7-hexachlorodibenzofuran(1,2,3.4,6,7-HCDF) and 1,2,3,4,7,8-hexachlorodibenzofuran(1,2,3,4,7,8-HCDF) were comparable to those of TCDD at doses of 7.5 ng/ ml, and about twice as high as those of 2,3,7,8-tetrachlorodibenzofuran (TCDF), at the same dose, HCB, at a dose of 95 ng/ ml, did not induce enzyme activity. The experimental evidence indicated that AHH inducibility by the organochlorine compounds reflected the genetic susceptibility of the cells to the phenomenon of induction, and PCDF isomers found at relatively high concentrations in tissues of mammals exerted the highest values of AHH induction.Part of this work was presented at the 53rd annual meeting of the Japanese Society for Hygiene, April 5–7, 1983, Osaka, Japan     

PCDDs, PCDFs, PCBs, OC pesticides and mercury in fish and osprey eggs from Willamette River, Oregon (1993, 2001 and 2006) with calculated biomagnification factors

The osprey (Pandion haliaetus) population nesting along the main stem Willamette River and lower Santiam River was first studied to evaluate contaminants and reproductive rates in 1993 when 78 occupied nests were present. By 2001, the population increased to 234 occupied nests, a 13.7% annual rate of population increase. A sample egg was collected from each of a series of nests along the Upper River (river mile 55–187) in 1993, 2001 and 2006 to evaluate trends of persistent contaminants (organochlorine [OC] pesticides, polychlorinated biphenyls [PCBs], polychlorinated dibenzo-p-dioxins [PCDDs], and polychlorinated dibenzofurans [PCDFs]). Nearly all OC pesticide residues decreased significantly, e.g., p, p′-DDE (DDE) from 2,350 to 1,353 to 210 μg/kg wet weight (ww). PCBs followed a similar pattern over time, e.g., ΣPCBs 688 to 245 to 182 μg/kg ww, while PCDDs and PCDFs showed a more precipitous decline (often 85–95%) between 1993 and 2001, with no egg analyses warranted in 2006. During 2001–2002, sample osprey eggs were also collected from nests at three Headwater Reservoirs and two lower reaches (Newberg Pool and Tidal Portland) of the Willamette River, as well as the lower portion of the Santiam River to evaluate spatial residue patterns. Significant differences were seldom detected among the different sampling areas for OC pesticides (probably due to small sample sizes), although higher concentrations were often seen in the lower reaches, e.g., DDE 901 μg/kg ww (Headwater Reservoirs), 1,353 (Upper River), 1,384 (Newberg Pool) and 2,676 (Tidal Portland). PCB congener concentrations in eggs were usually higher in the Tidal Portland reach than at other locations and often significantly higher than at the Headwater Reservoirs or Upper River. Mercury (first analyzed in eggs in 2001), PCDDs and PCDFs were extremely low in 2001/2002 with no significant spatial patterns. Whole fish composite samples of largescale sucker (Catastomus macrocheilus) and northern pikeminnow (Ptychocheilus oregonensis), which account for about 90% of the biomass in the diet of this osprey population, were also collected from the Willamette River in 1993 and 2001 and analyzed for the same contaminants as osprey eggs. Contaminant residues in fish from the Upper River decreased between 1993 and 2001, paralleling findings for osprey eggs. Likewise, spatial patterns for fish residues paralleled findings for osprey eggs from the different reaches in 2001. A second empirical estimate of biomagnification factors (BMFs) from fish to osprey eggs for OC pesticides, PCBs, PCDDs and PCDFs (ww and lipid weight [lw] basis) was calculated based on residue data collected in 2001. The two independent BMF estimates (1993 and 2001) for each contaminant from the Upper River provide a measure of consistency, e.g., DDE (ww) 87 and 79, (lw) 103 and 112; ΣPCBs (ww) 11 and 8.4, (lw) 13 and 12. Mercury did not biomagnify from fish to osprey eggs (BMF = 0.60). Legacy contaminants investigated had limited (perhaps only DDE), if any, effects on reproductive success of the increasing osprey population nesting along the Willamette River by 2001.     

Risk assessment of PCDD/PCDFs and indicator PCBs contamination in Spanish commercial baby food

Polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) as well as polychlorinated biphenyls (PCBs) are ubiquitous highly toxic environmental pollutants which exhibit a potential risk for human health. PCDD/Fs and PCBs contamination has been measured in samples of commercial baby food products: processed cereal and meat-and-fish-based baby food, which were made of individual samples collected from Spanish markets and pharmacies. They all presented a low dioxin content with a mean concentration ranging between 0.014 pg WHO-TEQ g⁻¹ product for fish-based baby food and 0.089 pg WHO PCDD/Fs-TEQ g⁻¹ product for processed cereal containing gluten. The mean concentration of the sum of the seven indicator PCBs was between 0.03 ng g⁻¹ product for fish-based baby food and 0.29 ng g⁻¹ product for gluten-free cereals. The estimated PCDD/Fs and indicator PCBs mean daily intake through the consumption of this kind of food has been calculated taking into account body weight and food consumption data for children aged 6–12 months. In order to assess the health risk derived from the exposure to these pollutants in children during the first year of life, data concerning infant formulae contamination has been also considered.