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Chloracne – the most common effect of dioxins, this is a skin disease which has an appearance similar to that of normal acne.
- Cancer
- Immune system suppression
- Liver and thymus damage
- Birth defects in infants
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Endometriosis – a painful disorder which involves the inflaming of membrane growing on the outside of uterus in female animals.
Dioxins and dioxin-related substances are extremely difficult for the body to get rid of, due to them being highly hydrophobic, therefore highly soluble in fats, and males have no way of expelling dioxins from their bodies except to let the dioxins biodegrade.
Dioxins have a half-life of ~12 years in the human body.
In females, the only way to rid the body of dioxins is either
- Passing it on to an unborn fetus, thus infecting the fetus with the dioxins; or
- Transmitted via breast milk into an infant.
It is due to this transmission of dioxins from the mother to the unborn infant, that birth defects and dioxins are correlated.
How dioxins work
In cells there are small masses, usually comprised of proteins, which are called receptors. These function to bind to specific molecules, which activates the receptor. This complex of receptor and its conjugate ligand can then be translocated into the cell’s nucleus and interact with the DNA within; thus controlling gene activity.
The dioxin-specific receptor, which is present in most living organisms, is called the Ah receptor, or aryl hydrocarbon receptor (AhR).
Most dioxins and their related compounds bind to this receptor with a high affinity, thus being able to be translocated into the cell’s nucleus and bind to the DNA.
The AhR receptor’s main function is to attach to natural toxicants, attach to the DNA and induce the production of a group of enzymes, which work to catalyse the breakdown of the toxicant, thus rendering it harmless.
Once the dioxin-receptor complex has entered the cell’s nucleus, it binds to certain elements within the DNA strands called Dioxin Responsive Elements (DRE’s), which are also named Xenobiotic Responsive Elements (XRE’s).
The main DRE interaction that occurs is the interaction between the dioxin-receptor complex and a gene CypIA1.
CypIA1 is responsible for the synthesis of the cytochromes P450IA1 and P450IA2, groups of enzymes, which are used for the metabolism of the toxicants, and ligands that bind to the AhR.
These enzymes attempt to break down dioxin, however, if that fails, the dioxin remains bound to the gene and the cytochromes are continuously produced.
This increase in enzymes present causes liver and thyroid damage, for example, an increase in the enzyme UDP-glucuronyltransferases leads to elimination of thyroxine, which can lead to damage to the thyroid.
There is also evidence to suggest that the gene expression is altered by dioxin exposure, which could explain the fact that dioxins are a factor in many health effects, including cancer. For example, dioxins influence growth factors in cells, which can be devastating in a growing fetus, causing birth defects and miscarriages.
Research into dioxins and related compounds
Dioxin research, which is specific to humans, is mainly data collection from populations accidentally exposed to dioxins.
Two of the most notable cases of accidental exposure to dioxin, in particular 2,3,7,8-TCDD, are:
- Industrial accident in Seveso, Italy, in 1976. A few kilograms of 2,3,7,8-TCDD were released into the environment and over the neighbourhood.
- Agent Orange, used in the Vietnam War, was contaminated with relatively large amounts of 2,3,7,8-TCDD.
Data was collected from people directly affected by these incidents, and trends were analysed.
The following data was collected ten years after the Seveso accident:
*n.d – not detectable
Source: Bertazzi, P.A et al. (1993); Cancer incidence in a population accidentally exposed to TCDD, Epidemiology 4 pp. 398-406.
As can be seen, the area around Seveso was divided up into 3 zones based on dioxin levels, dependant upon the dioxin levels in the soil.
The above results suggest that perhaps the carcinogenicity of dioxins has been overestimated slightly, due to the number of real cases being below the number of expected cases.
The results of a long-term study involving people directly affected by the disaster were presented at a symposium, 20 years after the accident, and they concluded that:
- Chloracne was positively correlated to 2,3,7,8-TCDD exposure.
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Miscarriages, perinatal mortality, and other birth defects rose slightly.
In research not directly related to humans, rats are a common subject to dioxin research.
As mentioned earlier, exposure to dioxins (2,3,7,8-TCDD in particular) can cause adverse effects to a number of organs, most notably the liver and thyroid.
This was observed in experiments carried out in rats and mice exposed to 2,3,7,8-TCDD.
Conclusion
There is evidence to suggest that perhaps dioxins are the causative agents for these diseases, however, the results do not conclusively prove that this is the case.
However, most of the results so far obtained by laboratory experiments have supported the hypothesis discussed earlier in this paper.
The dioxin debate will continue to rage for years, and only through extensive laboratory research can the true measure of what dioxins are capable of be fully realised.
Bibliography
Schechter, A. (1994) Dioxins and health. (New York : Plenum Press)
2
3 Buckley-Golder, D. Compilation of EU Dioxin Exposure and Health Report Data, October 1999
4 Creasey, W.A (1999), Review of the Literature on Herbicides, Including Phenoxy Herbicides and Associated Dioxins
5
6 EPA Dioxin Reassessment Health Assessment, Volume III: Risk Characterization (1994), section 9.7.6.3 Enzyme Induction.
7 Mocarelli, P. University Department of Clinical Pathology, at the October 21, 1996 meeting on "Chemistry, man and environment" in Milano
8 EPA Dioxin Reassessment Health Assessment, Volume III: Risk Characterization (1994), section 9.7.6.3 Enzyme Induction.
Schechter, A. (1994) Dioxins and health. (New York : Plenum Press)
http://www.ejnet.org/dioxin
Buckley-Golder, D. Compilation of EU Dioxin Exposure and Health Report Data, October 1999
Creasey, W.A (1999), Review of the Literature on Herbicides, Including Phenoxy Herbicides and Associated Dioxins
http://www.gascape.org/index%20/Health%20effects%20of%20Dioxins.html
EPA Dioxin Reassessment Health Assessment, Volume III: Risk Characterization (1994), section 9.7.6.3 Enzyme Induction.
Mocarelli, P. University Department of Clinical Pathology, at the October 21, 1996 meeting on "Chemistry, man and environment" in Milano
EPA Dioxin Reassessment Health Assessment, Volume III: Risk Characterization (1994), section 9.7.6.3 Enzyme Induction.
