Difference between revisions of "Hämeenkyrö MSWI risk assessment: Dioxin"

Dioxins are produced unintentionally as by-products of many chemical industrial processes and of all combustion processes. Sources include metal industry, power plants, industrial combustion plants, small combustion units (mostly domestic), waste incineration, road transport and mineral products production.

Total dioxin emissions are usually reported in toxic equivalency values (TEQ), which enables comparison of the toxicity of different combinations of dioxins and dioxin-like compounds. A TEQ is calculated by multiplying the actual grams weight of each dioxin and dioxin-like compound by its corresponding toxic equivalency factor (TEF) and then summing the results. The number that results from this calculation is referred to as grams TEQ.

(Comment: The emissions sources of dioxin are known pretty well. Although it is unlikely that these factories have direct dioxin measurements, emission estimates for the sources of this size should be available. You should ask Juhani Ruuskanen (KuY) or Päivi Ruokojärvi (KTL)).

Possible dioxin sources in Hämeenkyrö:

Currently: the local gas power plant, traffic, domestic combustion (cardboard factory, sawmill) D↷

Future: Municipal solid waste incinerator, biofuel power plant

Emission factors for different processes

Municipal solid waste incineration (µg TEQ/t MSW burned)

Low technology combustion, no APC system: air 3500, fly ash 0, bottom ash 75

Controlled combustion, minimal APC: air 350, fly ash 500, bottom ash 75

Controlled combustion, good APC: air 30, fly ash 200, bottom ash 7

High technology combustion, sophisticated APC system: air 0.5, fly ash 15, bottom ash 1.5

Energy production (µg TEQ/TJ)

Natural gas fired power boiler: 0.5

Mixed biomass fired power boiler: air 500, residue 0

Clean wood fired power boiler: air 50, residue 15

Household heating and cooking (biomass):

More accurate information to be added later..

http://www.epa.gov/ncea/pdfs/dioxin/2k-update/

http://www.oztoxics.org/ipepweb/library/DioxinInventory.pdf#search=%22dioxine%20emissions%20from%20traffic%22

SYKE 2004. Finnish Environment Institute. Air pollutant emissions in Finland 1990-2002. National inventory report. http://www.ymparisto.fi/download.asp?contentid=13512#search=%22dioxine%20emissions%20from%20traffic%22

Margni and coworkers have estimated an iF for Western European sources. The iF is approximately 3.5.10(-3) for emissions of dioxin in Western Europe. This iF compares well to the traditional non-spatial multi-media/-pathway model predictions of 3.9.10(-3) for the same region and to 2.10(-3) for the USA. Approximately 95% of the intake from Western European emissions occurs within the same region, 5% being transferred out of the region in terms of food contaminants and atmospheric advective transport. (Margni et al., 2004) However, when the emission source is in the North-Eastern corner of Europe like Hämeenkyrö is, the population exposed is likely smaller than on average, especially because the predominant wind direction is from southwest and away from densely populated areas. Therefore, the published value is likely an overestimate.

Bennett DH, Margni MD, McKone TE, Jolliet O. Intake fraction for multimedia pollutants: a tool for life cycle analysis and comparative risk assessment. Risk Anal. 2002 Oct;22(5):905-18.

Here we will use the daily PCDD/F intake estimated for the Finnish population in average as a starting point. In addition, the other variable in this model, "Dioxin emissions in Hämeenkyrö", may affect the estimate of baseline dioxin exposure in Hämeenkyrö.

For the adipose tissue PCDD/F concentration the value estimated for the general population living in Finnish inland is used.

It is noteworthy, that some subgroups within society, such as nursing babies and people consuming lot of fish may be more highly exposed to dioxins than the average people.

PCBs, another group of persistent environmental contaminants, were included as they behave similarly in the food chain and have partly similar health effects as dioxins.D↷

Intake fraction for dioxin emissions from Hämeenkyrö

2) Adipose tissue concentration: WHO-TEQ pg/g fat

Average daily intake of PCBs 0.74 pg/kg bw

Average adipose tissue PCDD/F concentration 26.4 pg/g

Average adipose tissue PCB concentration 18.1 pg/g

Note: During the nursing period, the PCDD/F intake of a child can be 1-2 orders of magnitude higher than that of an adult.

Kiviranta H, Ovaskainen ML, Vartiainen T. Market basket study on dietary intake of PCDD/Fs, PCBs, and PBDEs in Finland. Environ Int. 2004 Sep;30(7):923-32.

Kiviranta H, Tuomisto JT, Tuomisto J, Tukiainen E, Vartiainen T. Polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls in the general population in Finland. Chemosphere. 2005 Aug;60(7):854-69.

Tuomisto et al. 1999. Synopsis on dioxins and PCBs. Publications of the National Public Health Institute B17/1999.

(Comment: This would rather go to the variable Dioxin emissions in Hämeenkyrö).

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

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

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

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

get high exposures via the food (fishermen).

• 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

Evindence concerning other health effects is inconsistent.

• In this specific case it is relevant to think about health effects of long-term exposure on human population. Also the risk

of accidental exposure is low; only if the burning process is working improperly the amount of dioxin emissions will

increase.

• 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

dose-responses (Tuomisto et al., 2004) in cancer.

• 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.

• 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

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).

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

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)

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.