Dioxin

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Reports and Studies

  • Entine J, Scare to Death: How Chemophobia Threatens Public Health, American Council on Science and Health, January 18, 2011.
  • Goodman J et al., Weight-of-evidence analysis of human exposures to dioxins and dioxin-like compounds and associations with thyroid hormone levels during early development, Regulatory Toxicology and Pharmacology (58:1;79-99), October 2010.
    • Abstract. "Thyroid hormones play a critical role in the proper development of brain function and cell growth. Several epidemiological studies have been conducted to assess potential associations between pre- and post-natal exposure to dioxins or dioxin-like compounds (DLCs) and the levels of circulating thyroid hormones during early development. Dioxins and DLCs include chlorinated dibenzo-p-dioxins, chlorinated dibenzofurans, and mono- and non-ortho polychlorinated biphenyls (PCBs). We identified a total of 23 relevant epidemiological studies (21 cohort studies and 1 case–control study) that measured exposures to various types of dioxins and DLCs as well as markers of thyroid function, such as thyroid stimulating hormone (TSH), total thyroxine (T4), free T4, total triiodothyroxine (T3), free T3, and thyroid-binding globulin concentrations in cord blood or circulation. While some of the studies reported associations between concentrations of dioxins and/or DLCs and some biomarkers of thyroid function, the majority of the observed associations were not statistically significant. Moreover, there were no clear and consistent effects across studies for any of the hormone levels examined, and while a number of studies showed a statistically significant association with exposure for a given marker of thyroid function, other studies showed either no change or changes in the opposite direction for the same thyroid function marker. Similarly, when the results were analyzed considering developmental stage, there generally were no clear and consistent effects at any age from birth through 12 years of age. The absence of a clear correlation between background exposures to dioxins and DLCs and thyroid function biomarkers during development is not consistent with the hypothesis that background exposures to these chemicals cause effects on thyroid function during development." (Emphasis added)
  • Burns C et al., Mortality in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin at a trichlorophenol plant in New Zealand, J Occup Environ Med. 2009 Sep;51(9):1049-56.
    • Conclusions. "Although this study is small, we found no increasing trend of cancer or disease risk with increasing 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure with the possible exception of all cancers combined."
  • Cole P et al., Dioxin and cancer: a critical review, Regul Toxicol Pharmacol. 2003 Dec;38(3):378-88.
    • Abstract. "2,3,7,8-tetrachlordibenzo-p-doxin (TCDD) would not have been designated as a Group 1 carcinogen by IARC had there not been a change in the criteria used for inclusion in this category. Furthermore, there is no precedent for indicating, as did IARC, that a single chemical acts as a pluripotential carcinogen by modestly increasing human risk for all cancer while not increasing the risk for any single cancer at least moderately. IARC moved TCDD to Group 1 based on mechanistic considerations focusing on the Ah receptor. However, while occupancy of the Ah receptor by TCDD may be necessary for its toxicity, it is not sufficient for toxicity or for potential carcinogenicity. Animal evidence relating TCDD exposure to cancer is much stronger than that for humans. However, the large inter-species variation in the relevant dose-response slopes severely limits generalizations from animals to humans. The epidemiologic studies of occupational exposures, pesticide applicators, and community exposures following industrial accidents, notably Seveso, have generated overall relative risks of all cancer of about 1.0. Only case-control studies of soft-tissue sarcoma and non-Hodgkin's lymphoma, all by the same investigator, reported elevated risk from TCDD exposure. However, these results have not been replicated. The representation that a chemical compound (TCDD) would be a late-stage carcinogen for all types of cancer has no precedent and lacks biological foundation. Virtually all late-stage or promoting carcinogens (e.g., hepatitis-C virus, asbestos, and estrogens) cause a very limited number of forms of cancer. The exposure-response meta-analysis of TCDD and cancer developed by the United States Environmental Protection Agency (USEPA) is seriously compromised by its failure to adequately fit the data. The studies used by the USEPA also likely underestimate TCDD body burdens and may be confounded by smoking and other occupational exposures. Furthermore, the use of a linear dose-response model by the USEPA is scientifically unjustified since the underlying model of TCDD as a human carcinogen is based primarily on its supposed receptor-mediated, non-genotoxic (or promotional) mode of action. There are few examples of an agent being suspected as a human carcinogen for decades and then eventually moving into the category of "known" human carcinogens. In contrast, there are hundreds of compounds that remain for decades on lists of "suspected" human carcinogens despite the lack of confirming evidence. The long-term accumulation of negative, weak, and inconsistent findings suggests that TCDD eventually will be recognized as not carcinogenic for humans."
  • Hayes S and Aylward L, Dioxin risks in perspective: past, present, and future, Regulatory Toxicology and Pharmacology (37:2;202-217), April 2003.
    • Abstract. "The United States Environmental Protection Agency (USEPA) and other U.S. and international agencies have focused extensive efforts on the evaluation of the potential health risks of exposures to chlorinated dioxins (PCDDs), furans (PCDFs), and related dioxin-like polychlorinated biphenyls (PCBs). Extensive regulatory efforts over the past 20 years have also been made to control emissions of these compounds and thus to reduce exposures in the general population. This paper reviews the available information on temporal trends in emissions, environmental levels, intake levels through foods, and human body burdens of dioxins. This paper also provides an overview and comparison of recent hazard assessments for dioxins from U.S. and international agencies. Available data on emissions, environmental and food levels, and human body burdens of dioxins in the general population indicate a several-fold reduction in exposures and body burdens in the general population over the three decades from 1970 to 2000. U.S. and international hazard assessments concur on certain aspects, but disagree on fundamental issues including the likelihood of a threshold for carcinogenic dose–response and the degree of safety factors needed in deriving a protective exposure limit. These disagreements have significant consequences for interpreting the potential health risks of current background dioxin exposure levels. However, whatever the degree of health risk that may be associated with current background exposures, the general population is experiencing several-fold lower exposures, and, therefore, lower health risks, currently compared to 30 years ago. In light of the dramatic declines in exposure already observed, further efforts to reduce exposures through attempts to control emissions or food levels should be carefully evaluated to understand the likely efficacy of the efforts and the relative costs and benefits.'
  • Schnorr T et al., Spontaneous abortion, sex ratio, and paternal occupational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin, Environ Health Perspect. 2001 Nov;109(11):1127-32.
    • Abstract. "There is conflicting research regarding an association between fetal death and paternal exposure to Agent Orange, a phenoxy herbicide widely used in Vietnam that was contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Men who worked in the U.S. factories that produced Agent Orange were exposed to TCDD at levels hundreds of times higher than TCDD levels in the general population. Wives of TCDD-exposed chemical workers and wives of nonexposed neighborhood referents were interviewed to determine reproductive history. Paternal serum TCDD level at time of conception was estimated for each pregnancy using serum samples taken in 1987. Estimated TCDD levels of workers during or after exposure were high (median, 254 ppt; range, 3-16,340 ppt) compared to referent levels (median, 6 ppt; range, 2-19 ppt). No association between paternal TCDD level at the time of conception and spontaneous abortion was observed among pregnancies fathered by workers with TCDD levels of < 20 ppt [odds ratio (OR) = 0.77; 95% confidence interval (CI), 0.48-1.22], 20 to < 255 ppt (OR = 0.81; 95% CI, 0.40-1.63), 255 to < 1,120, (OR = 0.69; 95% CI, 0.30-1.58), and >or= 1,120 ppt (OR = 0.95; 95% CI, 0.42-2.17) compared to pregnancies fathered by referents. The sex ratio [males/(males + females)] of offspring also did not differ by TCDD exposure (0.53 and 0.54 among workers and referents, respectively). We did not find an association between paternal serum TCDD level and spontaneous abortion or sex ratio of offspring in this population. The estimated TCDD levels in this exposed worker population were much higher than in other studies, providing additional evidence that paternal TCDD exposure does not increase the risk of spontaneous abortion at levels above those observed in the general population. The study could not evaluate the effect of father's childhood or prenatal TCDD exposure on subsequent sex ratio.


  • Hays S et al., The relative susceptibility of animals and humans to the carcinogenic hazard posed by exposure to 2,3,7,8-TCDD: an analysis using standard and internal measures of dose, Chemosphere. 34(5-7):1507-22, March-April 1997.
    • Abstract. "An analysis of the carcinogenic dose-response for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in humans and animals was performed based on measured tissue and serum concentrations and using alternatives to administered dose as the dosimetric. The TCDD-related carcinogenic response in rats (female rat liver tumors from Kociba et al., using revised pathology from Goodman and Sauer, was compared to that in humans (lung cancer rates in Fingerhut et al.,). Three dosimetries were used: serum lipid TCDD area-under-the-curve (AUC), peak serum lipid concentration (Cpeak) and average serum lipid concentration (Cavg). Rat serum concentration-time profiles were estimated based on measured adipose lipid TCDD concentrations at the end of the Kociba et al. bioassay, assuming first-order elimination and a half-life of 25 days. Human concentration-time profiles were estimated based on measured serum lipid TCDD concentrations and known dates of first and last exposure, with an assumed 7.5 year half-life and first-order elimination. Comparison of rat and human responses indicated that, using all three of these dosimetries, humans are much less sensitive than rats to the carcinogenic effects of TCDD. Regardless of the dosimetric chosen, the cancer mortality in humans in the NIOSH cohort, if due to TCDD, is relatively insensitive to dose as defined in Fingerhut et al., [3]. Our analysis indicates that human exposure to background levels of TCDD (about 5 ppt serum lipid concentration) is not likely to produce an incremental cancer risk."
  • Gough M, Human health effects: what the data indicate, Sci Total Environ. 1;104(1-2):129-58, May 1991.
    • Abstract. "Information about the possible human health effects of dioxin is available from studies of chemical plant workers, sprayers of dioxin-contaminated herbicides, and other exposed people. No human illness, other than the skin disease chloracne, which has occurred only in highly exposed people, has been convincingly associated with dioxin. Some epidemiologic studies have suggested associations between dioxin and stomach cancer, soft tissue sarcomas, and lymphomas, but other studies, powerful enough to detect excesses of those diseases, if they exist, have not done so. With the exception of one study of chemical plant workers that reported an excess of stomach cancer, all the suggested associations of increased cancer risks and dioxin exposures are from studies of herbicide applicators. Both direct measurements of the concentrations of dioxin in the body fat of chemical plant workers and the occurrence of chloracne in those men support the conclusion that they were exposed to far greater amounts of dioxin than herbicide applicators. Therefore, if the cancers found in herbicide users were associated with dioxin, even more of those cancers would be expected among the chemical plant workers; the expected increases are not found. In short, epidemiologic studies in which dioxin exposures are known to have been high, either because of the appearance of chloracne or from measurements of dioxin in exposed people, have failed to reveal any consistent excess of cancer. In those studies that have reported associations between exposure and disease, no chloracne was reported, and there are no measurements of higher-than-background levels of dioxin in the people who are classified as exposed."

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