Volume 3, Number 5
Some Credible Information on Dioxin
In the October issue of this newsletter, in the article entitled
"The Shortage of Credible information on Dioxin," there was a
two-paragraph description of a literature review prepared for a
March 1990 seminar of the Chlorine Institute, presented by George L.
Carlo, Health & Environmental Sciences Corporation. The title
of that review is "Scientific Research on the Health Effects of
Dioxins in the Environment," and it is available as part of the
proceedings from that seminar for $15 from the Chlorine Institute,
2001 L St., NW, Suite 506, Washington, DC 20036. The excerpts that
follow were taken from p. 4, 6-8 and 11-12.
Dioxins have been with us since cavemen first harnessed fire.
The main source of trace levels of these chemicals in the
environment is low temperature combustion (Bumb, R. C., et al.,
1980). Dioxins, including TCDD
[2,3,7,8-tetrachlorodibenzo-p-dioxin, the most toxic form], are
produced during such everyday sources of combustion as refuse
incinerators or open air burning facilities, wood-burning stoves,
automobiles and trucks, fireplaces, charcoal grills, cigarettes,
some chemical manufacturing processes and even lightning strikes.
In the United States, the major source of these chemicals is
municipal incinerators. As a result of these various sources of low
temperature combustion, background levels of dioxins can be expected
in the parts per trillion range everywhere....
As the epidemiological database on dioxins has evolved over the
last decade, the human health risks which are predicted based m the
animal studies are not being seen in humans. Humans appear to be
less sensitive to TCDD than laboratory animals. The weight of the
scientific evidence suggests that:
- Parts per million levels of exposure in humans produce
chloracne, a rash-like condition considered the clinical marker for
- Parts per million levels also can produce adverse liver and
- Chloracne and other acute toxic effects, caused by high doses of
TCDD, are not progressive and disappear with time. In addition, in
the absence of chloracne, other toxic effects are unlikely.
- At background levels of exposure (parts per trillion ranges), m
human health effects have been documented. The PPT range is
actually a million times lower than the levels at which scientists
have seen health effects in humans.
Many scientists now believe that low level exposure to dioxins
does not represent a serious public health hazard.
While some studies purport to show an association between
exposure to dioxins and cancer in human, those studies are widely
criticized and not widely accepted by the scientific community.
Several international organizations have reviewed the extensive
scientific databases on health effects of dioxins, including the
American Medical Association; Universities Associated for Research
mid Education in Pathology, Inc.; the United Nations Food and
Agricultural Organization; the United Kingdom Ministry of
Agriculture, Fisheries and Food; the Commission of European
Communities; the American Council on Science and Health; the Council
for Agricultural Science and Technology (CAST); the Scientific
Advisory Panel for the U.S. Federal Insecticide, Fungicide and
Rodenticide Act; the U.S. National Institute for Occupational Safety
and Health; the U.S. Veterans Administration; and the U.S. Centers
for Disease Control.
These scientific reviews point in the same direction:
Epidemiological data evaluating chronic effects of TCDD exposure
indicate that human are far less susceptible to TCDD than laboratory
animals. The weight of the scientific evidence does not suggest an
association between exposure to TCDD and cancer in human -nor does
the weight of the evidence suggest an association between TCDD and
reproductive effects in humans . At low levels in the parts per
billion and parts per trillion ranges, there are m known adverse
effects of TCDD exposure in human....
Characteristics of Dioxin
Extensive research on the environmental fate of dioxins indicates
- Dioxins are not translocated into plants --
- They do not move from the soil into plants. Therefore, dioxins
do not move into the food chain through plants by simply being
present in the soil. Dioxins can, however, be present in plants as
a result of airborne deposition.
- Dioxins have low water solubility --
- If they get into water, the dioxins stick to the solid material
and settle out. This is why dioxins are found in sludge
- Dioxins have low volatility --
- They do not vaporize, but remain bound to particulate matter
- Dioxins bind strongly to the soil --
This soil binding reduces the amount that can be absorbed through
the skin or ingested. Animal studies show that only a small amount
of TCDD is absorbed from contaminated soil. For example, in one
animal study, only about 1/1,000 of the TCDD in the soil was
absorbed when soil contaminated with about 500 parts per billion
TCDD was held in contact with skin for 24 hours (covered with
Estimates of TCDD absorption from an industrial accident in Seveso,
Italy (exposing approximately 30,000 people to high levels of TCDD)
suggest that people are expected to absorb about 1/2,000 of the
average amount of material present in one square meter
(approximately 1.2 square yards) of their environment each day. By
using the laboratory or data collected after Seveso, researchers
estimate that 100-1,000 parts per billion of TCDD in soil could
result in human absorption of as much as a dose equivalent to that
which produced no effect when fed to laboratory rats for a lifetime.
If one assumes that soil is eaten in significant amounts by
children, the permissible level is less, perhaps 10 parts per
Based m these assumptions (particularly those based on the work of
Dr. Kingsley Stevens, 1981), it appears that general environmental
soil contamination in the range of low parts per billion does not
pose a health hazard to the general population, including the
unborn, children, pregnant women, the elderly or the infirm. For
the general population, excluding children with intimate soil
contact or those who ingest soil, a level of 100 parts per billion
would still pose m hazard. In occupational settings, where workers
are protected by standard industrial hygiene practices, higher
levels of contamination are not accompanied by greater exposure or
- Dioxins are lipophilic --
While they accumulate in certain tissues, dioxins metabolize or
break down. The half life of dioxins in the human body, m average,
is seven years. Human data suggest that they do not bioaccumulate
or biomagnify over time in the system. For instance, studies
indicate that if a person lives in a parts per trillion environment,
blood levels of dioxins will be in the parts per trillion range. It
appears that these levels will not magnify into parts per
- Dioxins do not appear to cause genotoxic or mutagenic effects
While dioxins freely cross the cell membrane in both directions,
they do not penetrate the nucleus on their own. This binding to the
carrier protein also is reversible. Dioxins have to bind to another
protein that will carry them into the nucleus. Even when TCDD does
make it into the nucleus of the cell, it does not bind directly to
the DNA. This is why dioxins do not appear to cause genotoxic or
mutagenic problems in the cell.
- Dioxins are not cancer initiators --
Scientists know from both animal and human studies that cancer is a
disease that generally has two steps-initiation and promotion.
Initiation is the genetic alteration. Promotion is the non-genetic
alteration. Because TCDD doesn't bind to the DNA., it does not
appear to be a carcinogenic initiator. In animal studies, TCDD
alone does not cause cancer; its mechanism of carcinogenesis appears
to be promotion. Studies indicate that the cell must undergo some
other sort of genetic change before TCDD can promote cancer in
animals. It is important to note that with carcinogenic promoters,
such as TCDD, there appears to be a threshold or level below which
no toxic effects occur.
Bumb, R. R., Crumett, W. B., et al. (1980): "Trace Chemistries of
Fire: A Source of Chlorinated Dioxins." Science,
210:385-390. Oct. 24, 1980.
Stevens, K. M. (1981): "Agent Orange Toxicity: The Quantitative
Perspective." Human Toxicology, 1:31-39.