Non-carcinogenic effects of TCDD in animals

  title={Non-carcinogenic effects of TCDD in animals},
  author={Linda S. Birnbaum and Jouko Tuomisto},
  journal={Food Additives \& Contaminants},
  pages={275 - 288}
Exposure to TCDD and related chemicals leads to a plethora of effects in multiple species, tissues, and stages of development. Responses range from relatively simple biochemical alterations through overtly toxic responses, including lethality. The spectrum of effects shows some species variability, but many effects are seen in multiple wildlife, domestic, and laboratory species, ranging from fish through birds and mammals. The same responses can be generated regardless of the route of exposure… 

Toxicogenomic analysis of exposure to TCDD, PCB126 and PCB153: identification of genomic biomarkers of exposure to AhR ligands

Time independent gene expression signature of the AhR ligands may assist in identifying other agents with the potential to elicit dioxin-like hepatotoxic responses and will help to isolate those genomic responses which are contributing to the hepatotoxicity observed with exposure to DLCs.

Hormones and endocrine-disrupting chemicals: low-dose effects and nonmonotonic dose responses.

It is concluded that when nonmonotonic dose-response curves occur, the effects of low doses cannot be predicted by the effects observed at high doses, and fundamental changes in chemical testing and safety determination are needed to protect human health.

The Comparative Immunotoxicity of Five Selected Compounds Following Developmental or Adult Exposure

It is demonstrated that functional immaturity alone predisposes the young to infection, and the developing immune system was found to be at greater risk than that of the adult, either because lower doses produced immunotoxicity, adverse effects were more persistent, or both.

Bone as a target for persistent organic pollutants

Investigation of the adverse effects of three common POPs on the skeletal system shows disruption of bone development, bone cell differentiation, and PFAS accumulation in bone, traceable even 17 months after exposure.

An Overview of the Effects of Dioxins and Dioxin-Like Compounds on Vertebrates, as Documented in Human and Ecological Epidemiology

  • S. WhiteL. Birnbaum
  • Biology
    Journal of environmental science and health. Part C, Environmental carcinogenesis & ecotoxicology reviews
  • 2009
P prudent public health policy should include the continued reduction of exposures to dioxins, as humans appear to be susceptible to these effects in a manner similar to that of the laboratory and wildlife species, which have demonstrated such outcomes.

Toxicological implications of polymorphisms in receptors for xenobiotic chemicals: the case of the aryl hydrocarbon receptor.


The development of the third molar in bank vole was found to be a sensitive biomarker for dioxin exposure, confirming the fact that dioxins are ubiquitous in the environment, also in areas far from contaminant sources and human activity.

Cancer and developmental exposure to endocrine disruptors.

Findings suggest that causes of endocrine-related cancers or susceptibility to cancer may be a result of developmental exposures rather than exposures existing at or near the time of tumor detection.

Receptor- and reactive intermediate-mediated mechanisms of teratogenesis.

The teratogenicity of reactive intermediates is determined to a large extent by the balance among embryonic and fetal pathways of xenobiotics bioactivation, detoxification of the xenobiotic reactive intermediate, detoxifying of ROS, and repair of oxidative macromolecular damage.

Hepatic transcriptomic responses to TCDD in dioxin-sensitive and dioxin-resistant rats during the onset of toxicity.




Effects of Small Doses of Dioxins on the Immune System of Marmosets and Rats

Some of the effects observed (such as the changes in the pattern of lymphocyte subpopulations) must certainly be considered as biological effects induced by TCDD, and the situation is similar to the induction of hepatic monooxygenases, which are also observable in this dose range.

Toxic equivalency factors for dioxin-like PCBs

  • U. AhlborgA. Hanberg
  • Chemistry, Biology
    Environmental science and pollution research international
  • 1994
Several PCDDs and PCDFs, as well as a few (dioxin-like) PCBs have been shown to exert a number of common toxic responses similar to those observed for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

Developmental exposure to polychlorinated biphenyls (Aroclor 1254) reduces circulating thyroid hormone concentrations and causes hearing deficits in rats.

Data indicate that while some effects of Aroclor 1254 exposure are dissimilar to drug-induced hypothyroidism, effects on hormone levels and body weight are comparable and may reflect the effects of thyroid hormone disruption on the development of the cochlea.

The mechanism of dioxin toxicity: relationship to risk assessment.

  • L. Birnbaum
  • Biology
    Environmental health perspectives
  • 1994
Increased understanding of the mechanism of dioxin's effects as well as elucidation of exposure-dose relationships is leading to the development of a biologically based dose-response model in the ongoing process of incorporating the best science into the risk assessment of TCDD and related compounds.

Biochemical effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds on the central nervous system.

In utero 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alters reproductive morphology and function in female rat offspring.

In the LE rat, vaginal and behavioral estrous cyclicity, estrous cycle-mediated running wheel activity, and female sexual behaviors at proestrus were not affected by gestational GD 15 TCDD treatment, but untreated stud males had difficulty attaining intromission and took longer to ejaculate.

Aryl-hydrocarbon receptor-deficient mice are resistant to 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced toxicity.

Results suggest that the pathological changes induced by TCDD in the liver and thymus are mediated entirely by the AHR, however, it is important to note that at high doses of T CDD, AHR-deficient mice displayed limited vasculitis and scattered single cell necrosis in their lungs and livers, respectively.

Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on influenza virus host resistance in mice.

Enhanced mortality to influenza virus in mice following a single dose of 10 ng TCDD/kg represents the most sensitive adverse effect yet reported for T CDD.