Volume 3, Number 5
Nov 1990

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 TCDD over-exposure.
• Parts per million levels also can produce adverse liver and nerve effects.
• 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.

Independent Reviews

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 the following:

• 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 aluminum foil).
  
  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 billion.
  
  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 hazard.
• 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 billion.
• 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.

References

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.