Toxic Equivalency Factors (TEFs) for PCBs, PCDDs, PCDFs for Humans and Wildlife

Berg, Martin van den; Birnbaum, Linda S.; Bosveld, A.T.C.; Brunström, Björn; Cook, Philip M.; Feeley, Mark; Giesy, John P.; Hanberg, Annika; Hasegawa, Ryuichi; Kennedy, Sean W.; Kubiak, Timothy J.; Larsen, John Christian; Leeuwen, F.X.R. van; Liem, A.K.D.; Nolt, Cynthia; Peterson, R.E.; Poellinger, Lorenz; Safe, Stephen; Schrenk, Dieter; Tillitt, Donald E.; Tysklind, Mats; Younes, Maged; Wærn, Fredrik; Zacharewski, Tim

doi:10.2307/3434121

Cited by 567 publications

(874 citation statements)

References 57 publications

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“…Top: Control rats(1-4). Middle: Administered rats in the PCB 126 group (5)(6)(7)(8). Bottom: Administered rats in the PCB 169 group (9)(10)(11)(12).…”

Section: Resultsmentioning

confidence: 99%

Micro two-dimensional electrophoretic analysis of changes in plasma proteins of next-generation rat of the pregnant rats administered to coplanar PCBs

et al. 2006

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SUMMARYPolychlorinated biphenyl (PCB) 126 or PCB 169 was administered to pregnant rats and kinetic changes in plasma protein spots of their next generation (F2 rats) ages 1, 3, 6, and 15 weeks were observed by micro two-dimensional polyacrylamide gel electrophoresis (M2D-PAGE).In the control group in which age-related changes were observable, changes in the form of the albumin (Alb) spot were recognized at ages 1-3 weeks. Only the Alb spot on the acid side, i.e., non-mercaptoalbumin, was recognized at age 1 week. At age 3 weeks, the Alb spot on the alkaline side, i.e., mercaptoalbumin, also became observable. On the other hand, qualitative changes in the form of Alb, i.e., manifestations of mercaptoalbumin, were recognized at age 1 week by administration of PCB 126. This result suggested that the influence of PCB 126 on the living body is greater than that of PCB 169. In spite of the treatment for toxicity by equivalence of dose control on the basis of toxicity equivalency factor (TEF) 0.1 for PCB 126 (PeCB) and 0.01 for PCB 169 (HxCB), the influence of PCB 126 on the living body was greater than that of PCB 169.The C3 spot was increased at age 3 weeks in the PCB 126 and the PCB 169. The spot showed a tendency toward increase at age 6 weeks in the PCB 126. The TEF compared PCB169 with PCB126, and distinctly increase of the C3 spot was observed for 15 weeks though the TEF was low. From these, as for the PCB 169, it was suggested appearing remarkably in aging influence of the immunity toxicity.The observations of the changes in these spots led to the conclusion that the changes in these spots resulted from transfer of the drugs accumulating in the maternal body to the F2 rats of the maternal rats administered PCB 126 and those administered PCB 169 via the breast milk and that these changes are involved with inflammatory proteins, including the target genes influenced by the toxicity of coplanar PCBs.

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“…Top: Control rats(1-4). Middle: Administered rats in the PCB 126 group (5)(6)(7)(8). Bottom: Administered rats in the PCB 169 group (9)(10)(11)(12).…”

Section: Resultsmentioning

confidence: 99%

Micro two-dimensional electrophoretic analysis of changes in plasma proteins of next-generation rat of the pregnant rats administered to coplanar PCBs

et al. 2006

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“…In addition, the amount of these PCBs in the mixture was slightly increased by the presence of eight times more PCB #77 than what we expected (Table 1). This difference might not have biologic consequences given that the TCDD-TEF for PCB #77 is 0.0001 (92), and it modifies the total TCDD-TEF exposure dose for the complete mixture from 31.42 to 31.44 ng. Nevertheless, a lack of information on the effects of more complete mixtures and on the effects occuring in utero, and a lack of understanding of the relations between toxicologic and carcinogenic processes, prevent us from ruling out the possibility of a link between TCDD, PCB, DDT, and DDE exposure and the risk of developing some types of breast cancer.…”

Section: Discussionmentioning

confidence: 99%

Modulatory effects of neonatal exposure to TCDD, or a mixture of PCBs, p,p'-DDT, and p-p'-DDE, on methylnitrosourea-induced mammary tumor development in the rat.

Desaulniers

Leingartner

Russo

et al. 2001

Environ Health Perspect

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The role of organochlorine (OC) exposure in the etiology of breast cancer remains controversial. Thus, our objective was to determine whether the most abundant and toxic OCs found in human milk could, when ingested during the neonatal period, modulate the development of mammary tumors in the rat. We prepared a mixture composed of p,p'-dichlorodiphenyltrichloroethane (DDT), its major metabolite, p,p'-dichlorodiphenyldichloroethene (DDE), and 19 polychlorinated biphenyls (PCB) based on their concentrations found in the milk of Canadian women. Neonate rats at 1, 5, 10, 15, and 20 days of age were gavaged with this mixture, at 10, 100, and 1,000 times the amount that a human baby would consume. An additional group received 2.5 microg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)/kg body weight (bw) by gavage at 18 days of age, instead of the mixture. On day 21, all treatment groups, except for a control group and a 1,000-mix group, received a single intraperitoneal injection of methylnitrosourea (MNU, 30 mg/kg bw), the initiator of the carcinogenic process. The average number of rats per treatment group was 33. Rats were sacrificed when their tumors reached 1 cm in size, or at 308 days of age. We prepared mammary tumors and mammary gland whole mounts for histologic analysis. There were no significant effects when only the malignant or only the benign tumors were considered. After all benign and malignant lesions were pooled, the number of mammary tumors differed among all MNU-treated groups (p = 0.02) with more lesions developing in the MNU-1,000[times] (median = 4.5; p = 0.05) and MNU-TCDD (median = 5.5; p = 0.07) compared to the MNU-0 rats (median = 2). Compared to the MNU-0 group, the percentage of rats that developed palpable tumors (benign plus malignant) was slightly higher (p = 0.06) in the MNU-TCDD group, but not in the MNU-1,000[times] group. The percentage of palpable tumors that were malignant was higher (p = 0.02) in the MNU-100[times] group (15/16, 94%) than in the MNU-0 group (10/18, 56%). The highest dose of the mixture delayed (p = 0.03) the development of tumors, but this was not observed with the MNU-TCDD treatment. These results suggest that neonatal exposure to high doses of organochlorines could favor the development of MNU-induced mammary lesions, but also delays the development of palpable tumors in the rat.

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“…Most toxicologic work has been carried out with TCDD, and the toxicologic behavior of other DLCs is usually assumed to be similar. The total dioxin concentration is estimated as its toxic equivalence (TEQ), where TEQ = Σ(DLC) i × (TEF) i and the TEFs are toxic equivalency factors that normalize the toxic potencies of the various DLCs to that of the reference toxicant TCDD, with TEF = 1 (1).…”

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confidence: 99%

Linking dioxins to diabetes: epidemiology and biologic plausibility.

Remillard

Bunce

2002

Environ Health Perspect

180

115

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Recent epidemiologic studies suggest a possible association between dioxin-like compounds (DLCs) and diabetes in human populations, although experimental links between DLCs and diabetes are lacking. The public health significance of such an association is that all populations are exposed to small but measurable levels of DLCs, chronic low-dose exposure to which may hasten the onset of adult-onset diabetes in susceptible individuals. In this article, we review the epidemiologic studies and propose biologically plausible connections between dioxins and diabetes. Specifically, we suggest that aryl hydrocarbon (Ah) receptor functions may antagonize peroxisome proliferator-activated receptor (PPAR) functions, and hence that the Ah receptor may promote diabetogenesis through a mechanism of PPAR antagonism.

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Toxic Equivalency Factors (TEFs) for PCBs, PCDDs, PCDFs for Humans and Wildlife

Cited by 567 publications

References 57 publications

Micro two-dimensional electrophoretic analysis of changes in plasma proteins of next-generation rat of the pregnant rats administered to coplanar PCBs

Micro two-dimensional electrophoretic analysis of changes in plasma proteins of next-generation rat of the pregnant rats administered to coplanar PCBs

Modulatory effects of neonatal exposure to TCDD, or a mixture of PCBs, p,p'-DDT, and p-p'-DDE, on methylnitrosourea-induced mammary tumor development in the rat.

Linking dioxins to diabetes: epidemiology and biologic plausibility.

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