Hämeenkyrö MSWI risk assessment: Dioxin: Difference between revisions
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==== | ==== Dioxin exposure-response function on population level==== | ||
Sanna | Sanna L./Anu T. | ||
{{var | {{var | ||
|Name = | |Name = Dioxin exposure-response function on population level | ||
|Focus = | |Focus = health effects caused by dioxin exposure {{Disclink|Ambiguity with Health effects of dioxins and PM2.5}} | ||
|Scope = | |Scope = general population average, accidental local releases excluded | ||
|Description = '''Dioxins''' are a group of polychlorinated dibenzo-''p''-dioxins (PCDDs) and dibenzofurans (PCDFs). They are persistent environmental contaminants that accumulate in the human body. Their elimination half-life is quite high (~7 years). 2,3,7,8-tetrachlorodibenzo-''p''-dioxin (TCDD) is the most toxic PCDD/Fs congener, and it is classified as a known human carcinogen by the International Agency for Research on Cancer (IARC). | |||
*Health effects related to '''long-term exposure''' | |||
**impairment of the immune system | |||
**impairment of the developing nervous system | |||
**impairment of the endocrine system | |||
**impairment of reproductive functions | |||
**increased cancer risk | |||
Evidence concerning cancer risk is mainly from animal studies, and dioxins are probably quite weak carcinogens in humans. Hormesis type of dose-response is suspected. Evidence concerning other health effects is inconsistent. | |||
In this specific case | |||
* MSWI is likely to increase background dioxin exposure (additional low exposure) | |||
*the risk of accidental exposure is low (dioxin emissions will increase only if burning process is working improperly) | |||
*health effects of long-term exposure are relevant | |||
*effects on development and endocrine functions are more relevant than the risk of cancer | |||
* The health effects of low doses should be modelled from animal and human data. Eg. Alaluusua et al. (1996) have studied tooth development. In a study by Miettinen et al. (2005), exposure to 0.5 μg TCDD/kg body weight on GD 15 resulted in maternal adipose tissue concentration of 2185 pg/g fat. In that study, linear extrapolation of the data predicts a maternal adipose tissue concentration of 100-120 pg/g fat after exposure to 0.03 μg TCDD/kg body weight. This estimated maternal adipose tissue concentration is sufficient to induce developmental dental defects in rat offspring, and is similar to the highest values measured in the Finnish average population (PCDD/F 145.5 pg WHO-TEQ/g fat (Kiviranta et al. 2005). | |||
Sensitive subgroups: foetuses, newborns, young females (women below or at childbearing age), individuals with high fish consumption (e.g. fishermen), individuals working in incineration plants etc. (For health effects related to '''short-term exposure''' {{Reslink|Discussion on short term effects of dioxins}}) | |||
|Inputs = Dioxins | |||
*Dioxin emissions and in Hämeenkyrö ''(Comment: This is not actually an input, but [[#Dioxin exposure due to MSWI in Hämeenkyrö]] | |||
*[[#Background incidence rates for selected diseases and causes of death in Hämeenkyrö]] population; susceptible groups, demographic data ''(Comment: This background variable is actually missing: Anne knows about the population size, but does someone know about the background disease rates?)'' | |||
*[[#Population size in Hämeenkyrö]] | |||
*[[#Baseline dioxin exposure in Hämeenkyrö]] | |||
|Index = | |||
|Definition = | |||
|Unit = increased incidence of developmental defects/ pg/kg body weight/ year | |||
increased cancer incidence per pg/kg body weight OR per adipose tissue concentration ''(Comment: units are good for exposure-response function (as this variable used to be) but not for health effect (as it currently seems to be)'' | |||
increase in lifetime risk per pg/kg body weight | |||
|Result = effective dose resulting in a 0.01 increase in lifetime risk of cancer mortality (ED<sub>01</sub>): 45 pg/kg body weight (95% CI 21-324 pg/kg body weight) | |||
tolerable daily intake (TDI): 1-4 pg/kg body weight | |||
|References = Alaluusua et al. Eur J Oral Sci. 1996 Oct-Dec;104(5-6):493-7. | |||
Crump et al. 2003. Meta-analysis of dioxin-cancer dose-response for three occupational cohorts. Environmental Health Perspectives 111 (5), 681-687. | |||
Kiviranta et al. Chemosphere. 2005 Aug;60(7):854-69. | |||
Kogevinas 2001. Human health effects of dioxins: cancer, reproductive and endochrine system effects. Human Reproduction Update 7 (3), 331-339. | |||
Miettinen HM et al. Toxicol Sci. 2005 Jun;85(2):1003-12. | |||
Tuomisto JT et al. Int J Cancer. 2004 Mar 1;108(6):893-900. | |||
Tuomisto et al. 1999. Synopsis on dioxins and PCBs. Publications of the National Public Health Institute B17/1999. | |||
van Leeuwen FX et.al. Chemosphere. 2000 May-Jun;40(9-11):1095-101. | |||
}} | }} |
Revision as of 17:56, 25 September 2006
See the main page of this assessment: Hämeenkyrö MSWI risk assessment: General
Dioxin emissions in Hämeenkyrö
Virpi
Intake fraction for dioxin emissions from Hämeenkyrö
Intake fraction for dioxin emissions from Hämeenkyrö
Baseline dioxin exposure in Hämeenkyrö
Marjo
Baseline dioxin exposure in Hämeenkyrö
Dioxin exposure due to MSWI in Hämeenkyrö
Martin
Dioxin exposure-response function on population level
Sanna L./Anu T.
Dioxin exposure-response function on population level