Polychlorinated dibenzo-p-dioxin: Difference between revisions

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'''Polychlorinated dibenzo-p-dioxins''' (PCDDs): a group of related
chemicals which are usually present in mixtures and usually as minor
impurities among other chemicals such as PCBs, chlorophenols,
phenoxy acid herbicides, hexachlorophene antiseptic etc. They are
poorly water soluble and lipophilic (see ''[[PCDD/F]] – physicochemical
properties''), and therefore accumulate in lipids (fats) of living organisms
(see ''[[PCDD/F]] – environmental persistence''), and bioaccumulate
in trophic levels (see ''[[PCDD/F]] – biomagnification'').<ref>Jouko Tuomisto, Terttu Vartiainen and Jouni T. Tuomisto: Dioxin synopsis. Report. National Institute for Health and Welfare (THL), ISSN 1798-0089 ; 14/2011 [http://www.thl.fi/thl-client/pdfs/81322e2c-e9b6-4003-bb13-995dcd1b68cb]</ref> (For detailed
information, see ''IARC Monographs on the Evaluation of Carcinogenic
Risks to Humans, Volume 69, pp. 33-343, Lyon, 1997'')<ref>IARC Monographs on the Evaluation of Carcinogenic
Risks to Humans, Volume 69, pp. 33-343, Lyon, 1997 [http://monographs.iarc.fr/ENG/Monographs/vol69/volume69.pdf]</ref>


== Carcinogenicity ==
== Carcinogenicity ==


capacity of dioxins to cause cancer. TCDD has been shown to be carcinogenic (causing cancer) in several species of experimental animals. TCDD is not mutagenic, i.e. it does not cause mutations which may initiate a cancer cell by changing the genetic information of the cell. Rather TCDD is a promoting agent: it promotes the growth and transformation of already initiated cancer cells. It has also been proposed that TCDD will induce active oxygen radicals, which may secondarily cause genetic damage. These mechanisms may mean that there is a practical threshold level or dose, below which TCDD will not cause cancer. In human beings cancer assessment has proved difficult, because, with the possible exception of Seveso accident (see this), the groups investigated have always been exposed to many chemicals simultaneously. Some of these (such as chlorophenols and several solvents) may be carcinogenic in their own right, and it is hard to know which chemical is responsible for the effect. In short, human carcinogenicity is likely, but very high exposures to TCDD and other dioxins are needed to cause a modest increase in cancer incidence. The maximum TCDD concentrations in Seveso were 56,000 ng/kg (TCDD in fat), in occupational studies max. 32,000 ng/kg (TEq in fat) and average 2,000 ng/kg (while the average concentrations in the population are 30 to 50 ng/kg, as I-TEq in fat). Regardless of the high concentrations, the increases in cancer rates were barely detectable (e.g. in the latest occupational study 13&nbsp;% increase in total cancer). This means that dioxins are relatively weak carcinogens in humans (More information on this topic in IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 69, Lyon, 1997; Bertazzi et al., Epidemiology 1997:8:646-652; Steenland et al., J. Natl. Cancer Inst. 1999:91:779-786).  
capacity of dioxins to cause cancer. TCDD has been shown to be carcinogenic (causing cancer) in several species of experimental animals. TCDD is not mutagenic, i.e. it does not cause mutations which may initiate a cancer cell by changing the genetic information of the cell. Rather TCDD is a promoting agent: it promotes the growth and transformation of already initiated cancer cells. It has also been proposed that TCDD will induce active oxygen radicals, which may secondarily cause genetic damage. These mechanisms may mean that there is a practical threshold level or dose, below which TCDD will not cause cancer. In human beings cancer assessment has proved difficult, because, with the possible exception of Seveso accident (see this), the groups investigated have always been exposed to many chemicals simultaneously. Some of these (such as chlorophenols and several solvents) may be carcinogenic in their own right, and it is hard to know which chemical is responsible for the effect. In short, human carcinogenicity is likely, but very high exposures to TCDD and other dioxins are needed to cause a modest increase in cancer incidence. The maximum TCDD concentrations in Seveso were 56,000 ng/kg (TCDD in fat), in occupational studies max. 32,000 ng/kg (TEq in fat) and average 2,000 ng/kg (while the average concentrations in the population are 30 to 50 ng/kg, as I-TEq in fat). Regardless of the high concentrations, the increases in cancer rates were barely detectable (e.g. in the latest occupational study 13&nbsp;% increase in total cancer). This means that dioxins are relatively weak carcinogens in humans (More information on this topic in IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 69, Lyon, 1997; Bertazzi et al., Epidemiology 1997:8:646-652; Steenland et al., J. Natl. Cancer Inst. 1999:91:779-786).<ref>Jouko Tuomisto, Terttu Vartiainen and Jouni T. Tuomisto: Dioxin synopsis. Report. National Institute for Health and Welfare (THL), ISSN 1798-0089 ; 14/2011 [http://www.thl.fi/thl-client/pdfs/81322e2c-e9b6-4003-bb13-995dcd1b68cb]</ref>
 


== Chemical structure ==
== Chemical structure ==


See chemical structures.
See chemical structures.
==References==
<references/>
[[category:Dioxin synopsis]]
[[category:Dioxin synopsis]]
[[op_fi:PCDD]]

Latest revision as of 11:20, 1 June 2011


Polychlorinated dibenzo-p-dioxins (PCDDs): a group of related chemicals which are usually present in mixtures and usually as minor impurities among other chemicals such as PCBs, chlorophenols, phenoxy acid herbicides, hexachlorophene antiseptic etc. They are poorly water soluble and lipophilic (see PCDD/F – physicochemical properties), and therefore accumulate in lipids (fats) of living organisms (see PCDD/F – environmental persistence), and bioaccumulate in trophic levels (see PCDD/F – biomagnification).[1] (For detailed information, see IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 69, pp. 33-343, Lyon, 1997)[2]


Carcinogenicity

capacity of dioxins to cause cancer. TCDD has been shown to be carcinogenic (causing cancer) in several species of experimental animals. TCDD is not mutagenic, i.e. it does not cause mutations which may initiate a cancer cell by changing the genetic information of the cell. Rather TCDD is a promoting agent: it promotes the growth and transformation of already initiated cancer cells. It has also been proposed that TCDD will induce active oxygen radicals, which may secondarily cause genetic damage. These mechanisms may mean that there is a practical threshold level or dose, below which TCDD will not cause cancer. In human beings cancer assessment has proved difficult, because, with the possible exception of Seveso accident (see this), the groups investigated have always been exposed to many chemicals simultaneously. Some of these (such as chlorophenols and several solvents) may be carcinogenic in their own right, and it is hard to know which chemical is responsible for the effect. In short, human carcinogenicity is likely, but very high exposures to TCDD and other dioxins are needed to cause a modest increase in cancer incidence. The maximum TCDD concentrations in Seveso were 56,000 ng/kg (TCDD in fat), in occupational studies max. 32,000 ng/kg (TEq in fat) and average 2,000 ng/kg (while the average concentrations in the population are 30 to 50 ng/kg, as I-TEq in fat). Regardless of the high concentrations, the increases in cancer rates were barely detectable (e.g. in the latest occupational study 13 % increase in total cancer). This means that dioxins are relatively weak carcinogens in humans (More information on this topic in IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 69, Lyon, 1997; Bertazzi et al., Epidemiology 1997:8:646-652; Steenland et al., J. Natl. Cancer Inst. 1999:91:779-786).[3]


Chemical structure

See chemical structures.


References

  1. Jouko Tuomisto, Terttu Vartiainen and Jouni T. Tuomisto: Dioxin synopsis. Report. National Institute for Health and Welfare (THL), ISSN 1798-0089 ; 14/2011 [1]
  2. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 69, pp. 33-343, Lyon, 1997 [2]
  3. Jouko Tuomisto, Terttu Vartiainen and Jouni T. Tuomisto: Dioxin synopsis. Report. National Institute for Health and Welfare (THL), ISSN 1798-0089 ; 14/2011 [3]