Critical Reviews in: Carcinogenicity of Polyhalogenated Biphenyls: PCBs and PBBs

Silberhorn, Eric M.; Glauert, Howard P.; Robertson, Larry W.

doi:10.3109/10408449009029331

Cited by 322 publications

(215 citation statements)

References 196 publications

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“…The relative risks in these four studies are in the same range as those estimated from the animal data (16,17). The potential association with ER status is of some interest, given the estrogenic activity of DDT and the rising rates of ER-positive cancer among older women (18).…”

supporting

confidence: 59%

Pesticides--how research has succeeded and failed in informing policy: DDT and the link with breast cancer.

Wolff

1995

Environ Health Perspect

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Investigation of chemical exposures as possible etiologic factors for breast cancer has not been a research priority in the United States, which is surprising given the evidence from animal studies that environmental chemicals cause cancer and reproductive dysfunction. Study of environmental chemicals has also been indicated by the failure of traditional epidemiologic methods to account for significant proportions of breast cancer incidence with other risk factors. The fact that breast cancer risk is strongly associated with reproductive hormones is a further clue that environmental chemicals should be investigated. In addition to cancer, specific outcomes that need to be explored are reproductive dysfunction, immunotoxicity and neurotoxicity. Policy guiding our research should encourage toxicologic investigations of exposures to environmental chemicals that use stateof-the-art methods to determine exposure and human health effects. Using the approach suggested by John McLachlan, functional toxicology should be used to assess the activity of chemicals with regard to these outcomes. Just as dioxin toxicity can be expressed as toxic equivalents, estrogenic activity, for example, can be characterized in terms of estrogenic equivalents. In addition to the need to undertake this kind of research, needs for methods development and creative research funding mechanisms are discussed. Prevention of breast cancer may require intervention at an early age. Better understanding of breast cancer etiology, and especially its environmental components, may lead us toward that goal. -Environ Health Perspect 1 03(Suppl 6): 87-91 (1995)

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supporting

confidence: 59%

Pesticides--how research has succeeded and failed in informing policy: DDT and the link with breast cancer.

Wolff

1995

Environ Health Perspect

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“…A number of carcinogenic mechanisms [127], including formation of reactive oxygen species [69,145,157], endocrine disruption [80,180,204], and immune compromise [50,147,162,173,174,209,219], are known to be activated by PCBs. The evidence that PCBs can cause immune suppression is of particular interest because melanoma risk is known to increase between threefold and fourfold in individuals who are immunosuppressed due to agents given for organ transplantation [104,117,138].…”

Section: Pcbsmentioning

confidence: 99%

Melanoma Epidemiology and Prevention

Berwick

Buller

Cust

et al. 2015

Cancer Treatment and Research

122

121

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The epidemiology of melanoma is complex, and individual risk depends on sun exposure, host factors, and genetic factors, and in their interactions as well. Sun exposure can be classified as intermittent, chronic, or cumulative (overall) exposure, and each appears to have a different effect on type of melanoma. Other environmental factors, such as chemical exposures-either through occupation, atmosphere, or food-may increase risk for melanoma, and this area warrants further study. Host factors that are well known to be important are the numbers and types of nevi and the skin phenotype. Genetic factors are classified as

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“…They activate specific receptors, such as the Ah receptor and the constitutive androstane receptor (CAR), and induce the specific cytochrome P-450s that are activated by these receptors (Robertson and Hansen 2001). PCB mixtures have been shown to be carcinogenic in the liver (Silberhorn et al 1990). In addition, many PCB congeners have been demonstrated to have promoting activity; studies have found them to increase the formation of both tumors and altered hepatic foci (Glauert et al 2001).…”

Section: Introductionmentioning

confidence: 99%

Role of oxidative stress in the promoting activities of PCBs

Glauert

Tharappel

et al. 2008

Environmental Toxicology and Pharmacology

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PCBs are organic pollutants that persist and bioaccumulate in the environment. These chemicals induce and promote liver tumors in rodents. Previous studies have shown that they increase oxidative stress in the liver, including lipid peroxidation, oxidative DNA damage, and NF-κB activation. The objective of these studies was to determine if the promoting activities of PCBs could be inhibited by dietary antioxidants (vitamin E, selenium, or phytochemicals) or by knocking out the p50 subunit of NF-κB. In the antioxidant studies, female rats were first injected with DEN (150 mg/kg) and then administered 4 biweekly i.p. injections (300 μmol/kg/injection) of PCB-77, PCB-153, or vehicle; the number and volume of placental glutathione S-transferase (PGST)-positive foci were then quantified. Vitamin E did not influence the promoting activities of PCBs. Increasing dietary selenium above the recommended intake increased the number of foci induced but decreased their volume. Most of the phytochemicals examined (N-acetyl cysteine, β-carotene, resveratrol, EGCG) had no significant effect on the promoting activity of PCB-77. Ellagic acid increased and lycopene decreased the number of foci; ellagic acid, CoQ 10 , and curcumin decreased the volume of foci. In the NF-κB knockout study, male mice were first injected with DEN (90 mg/kg); controls not receiving DEN were also studied. Both p50 −/− and wild-type mice were then injected biweekly 20 times with PCB-153 (300 (μmol/kg). In DEN-treated and DEN + PCB-treated mice, the incidence of tumors was lower in the p50 −/− mice than in wild-type mice. In mice receiving PCB-153, the tumor incidence and tumor volume were higher. The volume of tumors that were positive for glutamine synthetase was increased in mice administered PCB-153. This study shows that the promotion of hepatocarcinogenesis by PCBs is largely unaffected by dietary antioxidants but is diminished when NF-κB activation is impaired by the absence of the p50 subunit.

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Critical Reviews in: Carcinogenicity of Polyhalogenated Biphenyls: PCBs and PBBs

Cited by 322 publications

References 196 publications

Pesticides--how research has succeeded and failed in informing policy: DDT and the link with breast cancer.

Pesticides--how research has succeeded and failed in informing policy: DDT and the link with breast cancer.

Melanoma Epidemiology and Prevention

Role of oxidative stress in the promoting activities of PCBs

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