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Description
Dioxins are a family of chemicals comprising 75 different types of dioxin compounds and 135 related
compounds called furans. For the purposes of this web site, the term “dioxin” includes both dioxins and
furans. They are unwanted by-products of industrial and natural processes, usually involving combustion.
Dioxins are also produced by non-industrial sources such as backyard burning of household trash and
forest/brush fires.
According to the U.S. Environmental Protection Agency, dioxin and furan emissions to the environment in
the U.S. have been reduced by 89 percent between 1987 and 2000, and reductions are expected to reach
92 percent by 2005. Additionally, global emissions continue to decline. Today, the uncontrolled burning of
residential waste and accidental fires at landfills are believed to be among the largest sources of dioxin
emissions, globally. The primary way people are exposed to dioxins today is through diet. While dioxin
effects have been reported in some studies, there is no consensus within the scientific community on
whether today’s low-level exposures pose a risk of human health effects and we believe that there is a lack
of evidence of humans having experienced health effects from low-level exposures.
Dioxin from historical emissions also has been part of ongoing discussions with local communities in Mid-
Michigan and New Zealand.
Dow's Position
Dow has undertaken considerable efforts to reduce dioxin emissions and actively promotes improvements
and solutions across industry. Dow believes any action toward resolving dioxin-related issues should be
based on science. We seek science-based solutions that protect human health and the environment, while
also contributing to the well-being of the local community. Dow supports corrective action that is specific to a
particular site and decisions based on the realistic probability for exposure.
Dow's Actions:
• In 1995, Dow committed to reduce its worldwide dioxin emissions to air and water by more than
90% by the year 2005. As of 2004, our emissions have been reduced by more than 80%.
• Since 1967, Dow has conducted extensive studies of its employees who have been exposed to
dioxins. After almost 40 years of studying employees with high exposures in the workplace, results
continue to show no increased risk of disease with the exception of chloracne, a temporary skin
condition resembling acne. We seek to publish the results of all our health studies in peer-reviewed
scientific journals and more than 150 have been published to date.
• Dow also is funding or supports additional studies that will provide answers to dioxin-related issues.
For example, in Mid-Michigan Dow has commissioned a broad array of human health exposure and
environmental studies to evaluate the potential impact of dioxins and furans.
"Dioxins and furans" refer to a group of chemical compounds that share certain similar chemical structures
and biological characteristics. Dioxins and furans are an unwanted byproduct of combustion, both from
natural sources like forest fires and from man-made sources like power plants, backyard burn barrels and
industrial processes.
According to the EPA, dioxins and furans released into the air during combustion can be carried long
distances before settling to the earth's surface. As a result, they are found almost everywhere at low levels.
Dioxins and furans are produced by both natural and man-made processes and have therefore existed for
centuries. The term "current background" is used to refer to the levels of dioxins and furans in the
environment today.
Dioxins and furans falling to land from air emissions tend to bind tightly to vegetation and soil. When dioxins
and furans are released into water, they tend to settle into sediments where they can become trapped and
stationary, or be ingested by fish and other aquatic organisms. Dioxins and furans trapped in sediment can
be further transported during activities that dislodge sediment, such as flooding or dredging.
In the United States, the primary way people are exposed to dioxins and furans is through eating meat and
dairy products. The animals we eat are exposed to background levels of dioxins and furans in the soil, on
vegetation and in some commercial animal feeds. Eating meat or dairy products exposes us to these low
levels of dioxins and furans. Over time, we accumulate dioxins and furans in the fatty tissues of our own
bodies.
Possible significance of the study- look at the dioxin/furan situation "off-site" and to manage the situation to
reduce or eliminate exposure, if possible. This is known as remediation.
The Problem:
u Localized dioxin contamination at numerous
sites around the world
u Persistence and bioaccumulation pose human
and environmental health threat
Alexander Clark
An essential prerequisite for determining the human health risk from dioxin in the
environment is accurately characterizing the toxicities of individual dioxin and dioxin-
like compounds. Measuring the toxicities of these compounds, however, is neither
straightforward nor simple.
Contrary to popular usage, "dioxin" is not one compound of a single, defined toxicity,
but a family of compounds consisting of 17 dioxins and furans and 13 PCB1 members
of widely ranging toxicity. Whether it is formed as an unwanted byproduct of
industrial processes, in a barrel of burning trash, or in a forest fire or volcanic
eruption, what we call dioxin is really a complex, variable mixture of dioxin, furan
and PCB components.
The ability to arrive at the best possible estimates of the toxicities of individual dioxin
compounds and to combine them appropriately, with full disclosure of levels of
uncertainty and variability, is critical to protecting public health. After all, these
estimates help regulators set dioxin health standards and permissible environmental
levels. Scientists and regulators, therefore, have a responsibility to
ensure that the best science has been employed in the development of
dioxin toxicity estimates.
Toxic Equivalency Factors (TEFs) are toxicity potency factors that are used by the
World Health Organization (WHO) and by scientists and regulators globally as a
consistent method to evaluate the toxicities of highly variable mixtures of dioxin
compounds. In the dioxin family, 2,3,7,8-TCDD is the "habanero" of the bunch, the
most studied and the most toxic member, and it is assigned a TEF of one. (One other
dioxin-like compound, 1,2,3,7,8-PnCDD, also has a TEF of one.) The other family
members are less toxic than 2,3,7,8-TCDD, and are also much less studied on an
individual basis.
As an interim measure, the use of TEFs is seen as the only practical approach for
addressing exposure and risks from mixtures of dioxin compounds. The values of
individual TEFs indicate how closely family member compounds resemble the mouth-
burning "habanero", 2,3,7,8-TCDD. For example, using the chart below of dioxin and
furan TEFs, OCDD and OCDF, both of TEF value 0.0001, are the sweet red peppers of
the mix-adding only slightly to the total toxicity of most mixtures.
Reference: Van den Berg, M., Birnbaum, L., Bosveld, B.T.C., Brunstrom, B., Cook, P.,
Feeley, M., Giesy, J.P., Hanberg, A., Hasegawa, R., Kennedy, S.W., Kubiak, T., Larsen,
J.C., van Leeuwen, F.X.R., Liem, A.K.D., Nolt, C., Peterson, R.E., Poellinger, L., Safe,
S., Schrenck, D., Tillitt, D., Tysklind, M., Younes, M., Waern, F., and Zacharewski, T.
(1998). Toxic Equivalency Factors (TEFs) for PCBs, PCDDs, PCDFs for Humans and
for Wildlife. Environmental Health Perspectives 106, 775.
WHO is currently re-evaluating dioxin TEFs to ensure they are grounded as firmly in
science as possible. Many scientists see significant room for improvement in the
process of setting TEFs.
A large body of relevant, peer-reviewed research, conducted since TEF values were
last set in 1998, must be used to refine and update TEF values. A recent Toxicology
Forum was convened in Washington, D.C. to address dioxin toxicity issues. Speakers,
including experts from the Environmental Protection Agency (EPA), the National
Institutes of Health, the National Cancer Institute, the National Academy of Sciences
and academia, explored the underpinnings of TEFs currently in use and provided a
critical analysis of their validity and limitations. They also presented
recommendations for improved approaches to estimating dioxin toxicities.
Participants in the forum identified the need to incorporate uncertainty factors into
the estimation of TEFs. Simply put, researchers are not equally confident of all TEFs
in use. Some are based on a shakier foundation than others, to the point where the
confidence interval of some TEFs spans over several orders of magnitude, or factors
of ten. Missing from the current system is a way to express this startling variability.
Confidence statements, such as "high," "medium" and "low" are needed to attach to
TEFs to provide risk managers with information regarding both the quality and
quantity of information supporting the toxicity estimate.
At the forum, Dr. Laurie Haws of Exponent, Inc. presented the results of a
comprehensive and critical review of the WHO TEF database. She assigned weighting
factors to TEFs based on the quality and relevance of individual studies that
contributed to their derivation. This exercise serves to refine the existing database
that supports the TEFs currently in use and provides a helpful statistical spread of
potency estimates.
Current TEFs are based on health effects assessed in laboratory animals exposed to
dioxin by an intake route, such as ingestion through the diet. The measure of
exposure used in such studies is the quantity of dioxin taken into the body. But more
realistic assessments consider not the amount of dioxin taken into the body, but the
internal dose of dioxin, a blood level, for example, that could reflect large differences
in the distribution of individual dioxin compounds within the body and their variable
rates of elimination from the body. It is not logical to expect TEFs, derived using
intake as measure of exposure to be compatible with risk assessments conducted
using internal exposure.
Toxic Equivalents
With the ability to assign TEFs to individual dioxin family member compounds, it is
possible to arrive at a number that represents the total toxicity of any given sample
of dioxin. To do that, the mass of each family member compound must be measured
and multiplied by the appropriate potency factor, or TEF. When this is done for each
of the compounds in a mixture, the products are summed to obtain a toxicity-
weighted mass quantity, known as dioxin-Toxic Equivalents (dioxin-TEQ) (see the
blue box below). If component compound masses have been measured in grams, the
toxicity-weighted sum is reported in "grams-TEQ."
Fans of hot and spicy peppers owe much of their culinary delight to chemical
compounds known as capsaicinoids. Capsaicinoids are responsible for the pungent
flavor of peppers, and the hotter the pepper, the more capsaicinoids present.
Theoretically then, any assortment of peppers could be finely ground, mixed and
chemically analyzed for its capsaicinoid level. The resulting numerical concentration
level would be directly representative of the degree of hotness of the pepper medley.
Dioxin "medleys" are not as easy to characterize because there is not one single
toxic ingredient to measure. What can be measured are less direct: health effects in
laboratory animals with increasing exposure to individual dioxin compounds, or a
complex biochemical reaction in which the dioxin compound binds to and activates a
component of cells known as the "Ah receptor."
The ultimate goal of setting TEFs is to obtain a clear measure of dioxin toxicity for
any mixture of dioxins-a dioxin-TEQ. But because not all individual dioxin compounds
have been investigated systematically to the same extent, the scientific literature
lacks a uniformly derived, similarly reliable database of TEFs.
Thus, TEFs have been set, for better or for worse, using the available research, but
without noting associated uncertainties.
Given the variable uncertainties associated with TEFs derived from a heterogeneous
body of data, is it legitimate to add TEFs in the calculation of dioxin-TEQ? For such an
important outcome as the calculation of dioxin toxicity, which will inform public
health policy, it is important to ask this question.
The measurement of the Ah receptor response to dioxin compounds may hold more
promise for being an objective metric of dioxin toxicity than might dose-response
data on laboratory animals. However, at the Toxicology Forum, Dr. Stephen Safe of
Texas A&M University showed that interaction between various dioxin compounds
(dioxins, furans and PCBs) and the Ah receptor varied substantially. This finding
represents an obstacle to adding TEFs.
In reality, dioxin compounds are only one family of chemical compounds that
interact with the Ah receptor. Many other components of foods interact with the
Ah receptor, some activating it and some inhibiting it. Thus, it is important to
consider the contributions of naturally-occurring Ah receptor-binding
components when evaluating TEFs this way.
Conclusions
The scientific basis for estimating TEFs of dissimilar compounds is tenuous, and
caution should be exercised in arbitrarily including new compounds into TEQ
calculations. TEQ calculations are further complicated by the fact that some natural
dietary components activate the Ah receptor, but are not accounted for in TEQ
exposure estimates.
Finally, it would be prudent to plan an "exit strategy" from the present approach of
estimating toxicities of dioxin compounds using TEFs. As toxicity data are collected
for individual family member dioxin compounds, these data would be most
appropriately used to derive the more rigorous toxicity parameters that have already
been investigated extensively for 2,3,7,8-TCDD. A logical approach would be a tiered
system that focuses first on those compounds with the greatest impact on public
health.
Notes
1
Polychlorinated biphenyls
Reference
Van den Berg, M., Birnbaum, L., Bosveld, B.T.C., Brunstrom, B., Cook, P., Feeley, M.,
Giesy, J.P., Hanberg, A., Hasegawa, R., Kennedy, S.W., Kubiak, T., Larsen, J.C., van
Leeuwen, F.X.R., Liem, A.K.D., Nolt, C., Peterson, R.E., Poellinger, L., Safe, S.,
Schrenck, D., Tillitt, D., Tysklind, M., Younes, M., Waern, F., and Zacharewski, T.
(1998). Toxic Equivalency Factors (TEFs) for PCBs, PCDDs, PCDFs for Humans and
for Wildlife. Environmental Health Perspectives 106, 775.
The 3-T Rule: Total environmental releases of dioxins from all quantified
Combustion sources decreased by 90% between 1987 and 2000 (see Figure
temperature, time 1). This significant decrease in dioxin emissions can be
and turbulence
conditions are
adjusted to minimize
dioxin formation.
attributed to successful US government regulation as well as to the voluntary
application of control technologies by industry. Emissions from the major historic
source of dioxin for the past 30 years, incineration (especially of municipal solid
waste and medical waste), have been continually declining since at least 1987.
According to EPA data, backyard burning of rubbish2, currently a largely unregulated
source, is the largest identifiable source of dioxin emissions. ("Regulated sources"
refers to those sources which have controlled emissions of dioxins, either by virtue of
regulations designed specifically for that purpose or by virtue of regulations targeting
other pollutants, which have also reduced dioxin emissions.)
**Other category includes: leaded and unleaded gasoline, land applied 2,4-D, iron
ore sintering, oil-fired utilities, EDC/vinyl chloride, lightweight aggregate kilns that
combust hazardous waste, petroleum refinery, catalyst regeneration, cigarette
smoke, boilers/industrial furnaces, crematoria and drum reclamation.
1
"Dioxin" here is defined as the totality of 7 dioxins and 10 furans. "TEQ" denotes
"toxic equivalent," a quantitative measure of the combined toxicity of a mixture of
dioxin-like chemicals.
2
U.S. EPA (Environmental Protection Agency). 2006. An inventory of sources and
environmental releases of dioxin-like compounds in the United States for the years
1987, 1995, and 2000. National Center for Environmental Assessment, Washington,
DC; EPA/600/P-03/002F.
(http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=159286)
*
"Dioxin" here is defined as the totality of 7 dioxins and 10 furans. "TEQ" denotes
"toxic equivalent," a quantitative measure of the combined toxicity of a mixture of
dioxin-like chemicals.
Source: U.S. EPA (Environmental Protection Agency). 2006. An inventory of sources
and environmental releases of dioxin-like compounds in the United States for the
years 1987, 1995, and 2000. National Center for Environmental Assessment,
Washington, DC; EPA/600/P-03/002F.
(http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=159286)
Based on the EPA's inventory of dioxin sources, more stringent restrictions on the
regulated community will not significantly reduce dioxin emissions. Instead, the
mostly unregulated practice of backyard barrel burning of rubbish is a likely
candidate for effecting further emissions reductions. In fact, Maine, New Hampshire,
California, and other states have recently enacted legislation to control dioxin
emissions from burn barrels.
Overall environmental levels of dioxin have fallen over the past 30 years. In addition,
the relative proportions of dioxin congeners emitted to the environment have
changed such that greater proportions of dioxin congeners of lower toxicity are
emitted. This pattern of decline has resulted in significant reductions in average
human exposure to 2,3,7,8-TCDD, the dioxin congener of greatest toxicity and
concern, and current exposures to dioxin are typically composed of smaller amounts
of lower toxicity congeners.
Hays and Aylward (2001) examined mean serum lipid levels of 2,3,7,8-TCDD in
1,419 US Air Force Vietnam era veterans not occupationally exposed to Agent
Orange. These researchers back-calculated the amount of 2,3,7,8-TCDD the veterans
would have had to be exposed to in order to produce the measured serum lipid levels
of this compound. Their model predicts that 2,3,7,8-TCDD intake must have declined
to very low levels by 1992 in order to produce the mean measured serum lipid
2,3,7,8-TCDD decrease seen over the decade 1986-1996.
Thus, not only are overall environmental levels of dioxin declining through decreased
emissions, but also, the total toxicity of the congeners to which humans are exposed
are decreasing. As environmental levels of 2,3,7,8-TCDD have dropped, average
body levels of this chemical also have decreased substantially. Indeed, Petreas et al.
(2001) in a study of persistent halogenated contaminants, recently documented a
decrease in Californians' dioxin body burdens which demonstrated statistically
significant decreases in all but one major congener (2,3,4,7,8-PeCDF). The authors
claim the decline is ".consistent with decreases observed worldwide and probably
reflects successful measures of pollution control" (p. 878).
Summary
References
Hays, S.M. and Aylward, L.L. (2001). Temporal trends in body-burden suggest that
dioxin exposure in the general population have declined significantly. Organohalogen
Compounds, 52, 214.
Petreas, M., She, J., Visita, P., Winkler, J., McKinney, M., Brown, F.R., Dhaliwal, J.,
Denison, G., and Mok, M. (2201). Trends in persistent contaminants in California
biota, Symposia Papers Presented Before the Division of Environmental Chemistry,
American Chemical Society, Sand Diego, CA, April 1-5, 2001.
U.S. EPA (September, 2000 Draft). Exposure and Human Health Reassessment of
2.3.7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds. Part III:
Integrated Summary and Risk Characterization for 2.3.7,8-Tetrachlorodibenzo-p-
dioxin (TCDD) and Related Compounds.
World Health Organization, (June, 1999). "Dioxins and their effects on human
health". [On-Line]. Available: http://www.who.int/inf-fs/en/fact225.html.
Notes
1
"Dioxin" here is defined as the totality of 7 dioxins and 10 furans (of a much larger
family of similar but less toxic compounds) of environmental concern.
2
"Backyard barrel burning of rubbish" is the mostly rural practice of burning domestic
household and garden refuse in open air, often in steel barrels.
What is dioxin?
The World Health Organization sets its Tolerable Daily Intake (TDI) at a
range of 1 to 4 pg/kg/bw/day (picograms per kilogram of body weight
per day) for adults. A picogram is one-trillionth of a gram. EPA
estimates that the average U.S. adult intake is 0.5 to 1 pg/kg/bw/day,
clearly within, or below, that range.
People today are exposed to less dioxin than at any time in the recent
past. According to EPA, the amount of dioxin in the average person’s
body has declined by more than 50% since the late 1980s. [5] Studies
of levels of dioxin in human breast milk, blood and fat tissue all show
significant declines -- with decreases ranging from 50 to 70 percent
between 1980 and 1996. [6]
[7]
Average Body Levels of TCDD Are Down Dramatically
What are the possible health effects of exposure to dioxin?
The EPA, FDA and other agencies note that since dioxin accumulates in
animal fats, following normal dietary recommendations for a healthy,
low-fat diet is the best way to reduce the potential for dioxin
exposure.
"The best strategy for lowering the risk of dioxins while maintaining
the benefits of a good diet, according to the agencies," is to follow the
recommendations in the Dietary Guidelines to choose fish, lean meat,
poultry, and low or fat-free (skim) dairy products and to increase
consumption of fruits, vegetables and grain products..[12]
[1]
Questions and Answers About Dioxins, Interagency Working Group
on Dioxin (representatives from the U.S. Environmental Protection
Agency, Department of Health and Human Services, Department of
Agriculture, Department of Veterans Affairs, Department of Commerce,
Department of State, and the White House Office of Science and
Technology Policy), October 2004.
[2]
Draft Dioxin Reassessment, Part I: Estimating Exposure to Dioxin-
Like Compounds, Volume 2: Sources of Dioxin-Like Compounds in the
United States , Chapter 1, U.S. Environmental Protection Agency,
September 2000.
[3]
Assessment of the Health Risk of Dioxins: Re-Evaluation of the
Tolerable Daily Intake (TDI), Executive Summary, World Health
Organization, 1998.
[4]
Questions and Answers About Dioxins (see citation #1)
[5]
Draft Dioxin Reassessment, Environmental Protection Agency,
September 2000.
[6]
Päpke, O., "PCDD/PCDF: Human Background Data for Germany, a
10-Year Experience," Environmental Health Perspectives 106: 723-
731, 1998. Stanley, J.S., Ayling, R.E., Cramer, P.H., Thornburg, K.R.,
Remmers, J.C., Breen, J.J., Schwemburger, J., Kang, H.K., and
Watanabe, K., "Polychlorinated Dibenzo-p-Dioxin And Dibenzofuran
Concentration Levels in Human Adipose Tissue Samples From The
Continental United States Collected From 1971 Through 1987,"
Chemosphere 20: 895-901, 1998.
[7]
Pinsky, P. & Lorber, M.N., "A model to evaluate past exposure to
2,3,7,8-TCDD," Journal of Exposure Analysis and Environmental
Epidemiology, 8, (2), 187-206, 1998.
[8]
Dioxin: Summary of the Dioxin Reassessment, Information Sheet 1,
U.S. Environmental Protection Agency, Office of Research and
Development, June 12, 2000.
[9]
Steenland, K., Piacitelli, L., Deddens, J., Fingerhut, M. and Chang,
L.I., "Cancer, Heart Disease and Diabetes in Workers Exposed to
2,3,7,8-Tetrachlorodibenzo-p- dioxin," Journal of the National Cancer
Institute 91:779-86, 1999.
[10]
Questions and Answers About Dioxins (see citation #1)
[11]
Hagenmeier, H. and Walczok, M., "Time Trends in Levels, Patterns
and Profiles for PCDD/PCDF in Sediment Cores of Lake Constance,"
Organohalogen Compounds 28: 101-104, 1996 (sediment). Ferrario,
J., Byrne, C., Dupuy, A.E., Winters, D.L., Lorber, M., and Anderson, S.,
"Analytical Method and Results from the Analyses of USEPA Historical
Food Samples for Dibenzo-p-Dioxins/-Furans/Coplanar PCBs,"
Organohalogen Compounds 35: 29-32, 1998 [food]. Winters, D.L.,
Anderson, S., Lorber, M., Ferrario, J., and Byrne, C., "Trends in Dioxin
and PCB Concentrations in Meat Samples from Several Decades of the
20th Century," Organohalogen Compounds 38: 75-78, 1998 [food].
[12]
Questions and Answers About Dioxins (see citation #1)