Hämeenkyrö MSWI risk assessment: Dioxin: Difference between revisions

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====Health effects caused by dioxin exposure====
==== Dioxin exposure-response function on population level====
Sanna
Sanna L./Anu T.
 


{{var  
{{var  
|Name        = Responses of dioxin exposure on human health at the population level
|Name        = Dioxin exposure-response function on population level
|Focus      = Determine health effects caused by dioxin exposure {{Disclink|Ambiguity with Health effects of dioxins and PM2.5}}
|Focus      = health effects caused by dioxin exposure {{Disclink|Ambiguity with Health effects of dioxins and PM2.5}}
|Scope      = General population average considered. Accidental local releases excluded  
|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.


''(Comment: This would rather go to the variable Dioxin emissions in Hämeenkyrö).''
In this specific case
|Description = Dioxins are persistent environmental contaminants which accumulate and their elimination half life in the body  
* 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).


is rather high (~7 years). In the exposure low doses and high doses cause totally indifferent effects. Most probable
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}})


exposures for humans from MSWI are low dioxin exposures for a long period of time, which may affect the population  
|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


"background exposure levels" by increasing them. The most susceptible subgroups among human population are children and young
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)''


females (women at the childbearing age and before) in addition to the subgroups in the occupational hazard or those who may
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) 


get high exposures via the food (fishermen).
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.


* In this specific case it is relevant to think about health effects of long-term exposure on human population. Also the risk
Crump et al. 2003. Meta-analysis of dioxin-cancer dose-response for three occupational cohorts. Environmental Health Perspectives 111 (5), 681-687.


of accidental exposure is low; only if the burning process is working improperly the amount of dioxin emissions will
Kiviranta et al. Chemosphere. 2005 Aug;60(7):854-69.


increase.  
Kogevinas 2001. Human health effects of dioxins: cancer, reproductive and endochrine system effects. Human Reproduction Update 7 (3), 331-339.
* Dioxins are classified as known human carcinogen by IARC; Evidence concerning cancer risk is mainly from animal studies,  


and dioxins are probably quite weak carcinogens in humans. Data exist which supports the hypothesis of hormesis type of
Miettinen HM et al. Toxicol Sci. 2005 Jun;85(2):1003-12.


dose-responses (Tuomisto et al., 2004) in cancer.
Tuomisto JT et al. Int J Cancer. 2004 Mar 1;108(6):893-900.
* Effects on development and endocrine functions are of more of concern than cancer. According to animal data, tolerable


daily intake (TDI) is set in a range of 1-4 pg TEQs/kg bodyweight/day.
Tuomisto et al. 1999. Synopsis on dioxins and PCBs. Publications of the National Public Health Institute B17/1999.  
* health effetcs of low doses should be modelled from animal data and existing human data. Eg. on tooth development exists a


study by Alaluusua et al. (1996). In a study by Miettinen et al. (2005) exposure to 0.5 μg TCDD/kg body weight on GD 15
van Leeuwen FX et.al. Chemosphere. 2000 May-Jun;40(9-11):1095-101.
 
resulted in maternal adipose tissue concentration 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 which is sufficient to induce developmental dental defects in rat offspring, 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).
|Inputs      = *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 developmental defects/ pg/kg body weight/ year,
increased cancer 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)''
|Result      =
|References  = 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.
Alaluusua et al. Eur J Oral Sci. 1996 Oct-Dec;104(5-6):493-7.
Miettinen HM et al. Toxicol Sci. 2005 Jun;85(2):1003-12.
Kiviranta et al. Chemosphere. 2005 Aug;60(7):854-69.
}}
}}

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

Baseline dioxin exposure in Hämeenkyrö

Marjo

Dioxin exposure due to MSWI in Hämeenkyrö

Martin


Dioxin exposure-response function on population level

Sanna L./Anu T.