|
| Compound | TEF |
|---|---|
| Mono-, Di-, and Tri-CDD | 0 |
| 2,3,7,8 TetraCDD | 1 |
| Other TetraCDDs | 0 |
| 2,3,7,8 PentaCDD | 0.5 |
| Other PentaCDDs | 0 |
| 2,3,7,8 HexaCDD | 0.1 |
| Other HexaCDDs | 0 |
| 2,3,7,8 HeptaCDD | 0.01 |
| Other HeptaCDDs | 0 |
| OctaCDD | 0.001 |
A similar scheme is developed for furans, but with lower TEFs. Thus, as the number of chlorine atoms present on the molecule increases above four, the toxicity of the dioxin/furan decreases. Most of the information about dioxin toxicity is derived from studies of the 2,3,7,8-TCDD and simple screening tests for the others. Little work has been done to evaluate the toxicity of the other 74 dioxins and the validity of the TEF relationships.
An often repeated statement is that TCDD is "one of the most toxic man-made compounds known." This is based on the observed effect that very small doses of 2,3,7,8-TCDD are lethal to guinea pigs. However, other species, including humans, react differently. Humans appear to be markedly less sensitive, requiring very large doses of dioxin before any adverse health effect is noted (chloracne).
What are the Health Effects Associated with Dioxin?
Some scientist, including those in the EPA, have alleged a number of adverse health effects such as reproductive impairment, adverse effects on development of offspring, changes in some enzymes, onset of diabetes, endometriosis, and potential disruption of certain components of the immunological system. However, scientific evidence to support these allegations has not been found. The only adverse health effect directly associated with dioxin exposure for which there is conclusive evidence in humans is the appearance of chloracne. This effect occurs only following very large doses, generally resulting from occupational exposures or accidental releases (Seveso, Italy). When epidemiological studies of these types of exposures are evaluated, there is no conclusive evidence of any association with cancer.
There have been three major human exposures to dioxin in recent history. Some Vietnam veterans were exposed to 2,3,7,8-TCDD while handling Agent Orange (Operation Ranch Hand). A number of residents of Times Beach, Missouri, were exposed to dioxin when contaminated oil was sprayed on dirt surfaces to control dust. The third exposure was to the residents of Seveso, Italy, due to an accidental explosion and subsequent release of dioxins. Extensive studies of these three populations have failed to show any short-term (except chloracne) or long-term health effects in humans. However, it is clear that dioxins will have significant impacts on other animals (death in guinea pigs, endometriosis in Rhesus monkeys).
At What Levels of Dioxin Exposure will People Experience Health Problems?
Recently, allegations have been made that the current levels of exposure to dioxin in our air, water and food exceed levels that cause adverse health effects. Not all scientists agree with this assessment. Scientists at the Center for Disease Control have stated that if humans are likely to respond with a plethora of effects from exposure to dioxin and related compounds because of current body burdens, these non-cancer effects should have become apparent in our population during the past 16 years. If these levels cause adverse health effects, non-cancer effects should be apparent throughout our population. The fact that these effects have not emerged reinforces the results of human epidemiological studies. The only proven adverse effect associated with very high concentrations of dioxin is chloracne.
How are People Exposed to Dioxin?
Dioxin is present in air, soil, water, and the food chain. However, the amounts of dioxin detected in our environment are small. Most scientists agree that the most probable exposure route, other than accidental release, for the general population is through the food chain. Fortunately, the forms of dioxin detected in various food groups generally represent the least toxic forms (HeptaCDD and OctaCDD) of dioxin (Furst et al, 1990). EPA and the U. S. Department of Agriculture have done a number of "market basket" surveys and failed to find significant amounts of dioxins in our food. Thus, your food supply is safe.
EPA has recently begun the use of indirect risk assessment methodologies to estimate the levels of dioxin that may be found in particular food groups. This methodology incorporates several assumptions about the ability of plants to absorb dioxin from air, the ability of animals and humans eating these plants to accumulate dioxin in tissue, and the amount of contaminated plant and animal tissue that an individual might consume everyday for 70 years. These assumptions have not been tested or verified as being accurate. Until these models are tested against field data, their results should only be used as a part of an uncertainty analysis.
What is TEQ and how is it Calculated?
TEQ is toxic equivalents. It is a method developed by scientists and regulators to estimate the toxicity of all dioxins and furans relative to 2,3,7,8-TCDD. TEQs are calculated by multiplying the amount of a specific dioxin times its TEF. Thus, one gram of 2,3,7,8-TCDD is also one gram TEQ dioxin (because it has a TEF of 1). However, 1 gram of 2,3,5,7,8-PCDD has a TEQ of 0.5 (one gram times 0.5 TEF). The two could be combined into 2 grams of dioxin or 1.5 grams TEQ of dioxin. Both numbers are correct. The two grams accurately describes the total amount of dioxin present but does not give any information on the total toxicity of those two grams. The 1.5 grams accurately represents the toxicity but does not give any indication on the total amount of dioxin present.
What are the Major Sources of Dioxin?
Dioxin is not intentionally produced but is a by-product of many industrial activities and natural processes. Dioxin can be produced naturally during forest fires and volcanic eruptions, through chemical and photochemical reactions occurring in air and water and during enzymatic reactions in natural organisms. Anthropogenic sources comprise a broad range of industrial and residential activities, including motor vehicle use, industrial processes, incineration of waste material, and burning of wood and coal.
EPA initially developed a list of sources of dioxins in 1994 (EPA, 1994). The source list was updated in 1998 (EPA, 1998a) and the estimated dioxin emissions to the air for 1995 from these sources are summarized in the following table.
| Source | Annual dioxin emissions |
|---|---|
| |
g TEQ/year |
| Municipal solid waste incineration | 1100 |
| Secondary copper smelting | 541 |
| Medical waste incineration | 477 |
| Forest fires | 208 |
| Cement kilns burning hazardous waste | 153 |
| Utility/industrial coal combustion | 73 |
| Residential wood burning | 63 |
| On-road diesel fuel combustion | 34 |
| Industrial wood burning | 29 |
| Cement kilns not burning hazardous waste | 18 |
| Secondary aluminum smelting | 17 |
| Utility/industrial oil combustion | 9 |
| On-road unleaded gas fuel combustion | 6 |
| Sewage sludge incineration | 6 |
| Hazardous waste incineration | 6 |
| Kraft black liquor Boilers | 2 |
| Secondary lead smelting | 2 |
| Total | 2,745 |
As can be seen from this list, municipal waste incineration, secondary copper smelting, and medical waste incineration dominate the total emissions of dioxins to the air. Surprisingly, forest fires and residential wood burning produce a substantial amount of the estimated dioxin emissions. Hazard waste incineration contributes about 0.2% of the annual estimated dioxins emissions to the atmosphere. It should be noted that recent EPA rules limiting dioxin emissions from municipal and medical waste incinerators will substantially reduce the amount of dioxin emissions from these facilities over the next five years. Similar emission restrictions for hazardous waste incinerators are expected in early 1999.
How do Dioxins get into the Emissions from Waste Combustors?
There are only a few combustion devices in the United States that are allowed to burn dioxin-contaminated waste. To obtain a license to burn dioxin-contaminated waste, a facility must pass a series of rigid tests that show that 99.9999% of the dioxins are destroyed in the process. Since there are only a few facilities that have this license and the vast majority of the dioxin is destroyed, most of the dioxin found in the emissions of waste combustors is newly formed in the air pollution control devices.
A considerable amount of scientific research has gone into determining the conditions where new synthesis of dioxins occurs in combustor air pollution control devices. If the following conditions are met, dioxins can be formed: a) temperatures between 400 and 750 °F, b) residence time (time in the air pollution control device) greater than 2 seconds, c) presence of chlorine, d) the presence of carbon molecules, and e) the presence of a catalytic surface. Remove any one of these factors, and dioxin formation in the air pollution control device is much slower. Combustors that have dioxin formation problems can often change their air pollution control operating parameters and eliminate the problem. Combustors with waste heat boilers often have to add additional air pollution control equipment to reduce dioxin concentrations in the stack gas to levels below concern. There is a good discussion of the mechanisms of dioxin synthesis in EPA's trial burn guidance document (EPA, 1998b).
Furst, P., Furst, C. and Groebel, W. 1990. Levels of PCDDs and PCDFs in Food-Stuffs from the Federal Republic of Germany. Chemosphere 20, Nos. 7-9, (1990) 787-792.
Gough, M. 1993. Dioxin: Perception, Estimates, and Measures. Phantom Risk: Scientific Inference and the Law Eds. K.R. Foster. D.E. Bernstein and P W. Hubber. Cambridge, MA: MIT Press.
U. S. Environmental Protection Agency (EPA). 1994. Estimating Exposure to Dioxin-Like Compounds, Volume 1: Executive Summary. EPA/600/6-88/005Ca. June 1994.
EPA. 1998a. The Inventory of Sources of Dioxin in the United States. EPA/600/P-98/002Aa. April 1998.
EPA. 1998b. Guidance on Collection of Emissions Data to
Support Site-Specific Risk Assessments at Hazardous Waste Combustion
Facilities. EPA530-D-98-002. August 1998.
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