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Public Health and
Chemical Weapons Incineration
(This publication was made possible by a grant from the Educational Foundation of America.)
Should we expose children, our most vulnerable population, to toxic chemicals if the exposure can be avoided? Should we build hazardous waste incinerators if alternative technologies with no toxic emissions are available?
This collection of papers, authored by scientists experienced in toxic chemical research, argues against the use of incineration to destroy the United States arsenal of deadly chemical weapons stockpiled at nine sites. The decision to incinerate mustard agent and the organophosphate nerve agents GB and VX was made by the Army in 1982. Since that decision, chemical weapons incinerators have been built and are in operation at two of the sites--Johnston Atoll in the Pacific and Tooele, Utah. Analyses of the stack releases from the Johnston Atoll incinerator have shown that the products of incomplete combustion emitted into the atmosphere include PCBs, heavy metals, dioxin, dioxin-like compounds and nerve agent from the chemical weapons, plus many other substances, known and unknown, analyzed and not analyzed. The authors of the following papers have researched effects of these emissions that were not addressed in the risk assessments for chemical weapons incineration. Federal agencies, including the Army, do not know enough about the long-term effects of chronic exposure to chemical weapons incinerators' emissions, singly and in combination, to assume that the risk of this disposal process is acceptable.
Regulatory agencies in the US presume that toxic chemicals are innocent until proven guilty. Of the 1000 new chemicals that yearly enter commercial markets in the United States, federal agencies have the capability to study only about a dozen. Neither the US government nor anyone else will ever have the capacity to fully evaluate the dangers of the chemicals singly, much less in synergy with each other and the other 80,000 synthetic chemicals already produced. In the past 20 years, regulations have been issued to control only nine new chemicals. Synthetic chemicals are not regulated by federal agencies until they are proven injurious to humans and by then the harm is done. Such was the case with DDT (an organochlorine pesticide) and polychlorinated biphenyls (PCBs), two of the handful of these thousands of chemicals that have been studied in any depth. Due to possible cancer risks, the US restricted most uses of DDT in 1972 and in 1976, banned PCBs' production. The regulations came too late--both are persistent in the environment and in human body fat. These toxic chemicals are everywhere and cannot be escaped. They cross placental barriers into women's' wombs. They are in mother's milk, which is rich in fat.
Another persistent chemical compound that has emerged in the past decade as one of the most dangerous chemicals ever tested is dioxin. Unlike DDT and PCBs, dioxin was not intentionally created, but is a by-product of the manufacture of certain chlorine-containing chemicals, the bleaching of paper with chlorine and incineration. Like PCBs and DDT, dioxin is carcinogenic, persistent and transgenerational and can be found almost everywhere. The US Environmental Protection Agency (EPA), in its 1994 Dioxin Health Assessment, reported that adverse health effects may be caused at or near the current background levels of dioxin which are 1-2 orders of magnitude higher than any virtually safe dose that might be calculated. In the first paper of this collection, Dr. Richard Clapp, a scientist with the Center for Environmental Studies of the John P. Snow Institute in Boston, Massachusetts, in his review of the EPA's dioxin report, contends that because of existing dioxin levels, our ultimate goal should be zero intake of dioxin, thus the Army's decision to incinerate chemical weapons, which will create more dioxin, is unjustifiable.
Dioxin and PCBs, both emitted from chemical weapons incinerators, in addition to being carcinogens, are known to be hormone disruptors. Hormones are the chemical messengers of the endocrine system that travel through the blood stream, turning on and off bodily processes. When they are disrupted in their functions, damage can be done to almost any system in our bodies. The results of research on the effects of exposure to hormone- disrupting chemicals have shown that such exposures have the most damaging effects on populations at times in their development when their reproductive, immune and central nervous systems are the most vulnerable. For example, the sons and daughters of many of the millions of mothers who took the synthetic hormone DES (diethylstilbestrol) in the 1940s, 50s and 60s have been diagnosed with reproductive cancers. DES' purpose was to prevent miscarriage; its unintended effect was to alter the reproductive systems of the unborn of the women who took it. The reproductive system of the developing fetus is particularly sensitive to hormonal disruption. Like PCBs and dioxin, DES is a synthetic chemical that can cause disruption of the fetal endocrine system and the long-term effects of this disruption can take many forms besides cancer, including high-risk pregnancies, miscarriages, reduction of the quantity and quality of sperm, urethral abnormalities and undescended testicles.
In addition to causing reproductive problems, hormone disruption can impair our immune systems. If the immune system is damaged in certain ways, it can allow pathogens to overwhelm our defenses and make us sick. Under other circumstances, the immune system goes haywire and attacks its host, causing major damage of a different kind, known as "autoimmune" diseases. A third class of immune disorders is allergic reactions, such as asthma, hay fever and food allergies. At least 45% of Americans are living with one or more chronic conditions due to impaired immune systems and recent research has shown that the impairment is caused by low doses of toxic chemicals acting singly or synergistically with other chemicals. Dr. Peter deFur, Affiliate Associate Professor of Environmental Studies at the Virginia Commonwealth University in Richmond, Virginia, and Carol Raffensperger, Director of the Science and Environmental Health Network in Windsor, North Dakota, argue that "in order to act responsibly and with precaution in light of the known effects of endocrine disruption in animals and humans...the Army must shut down the existing incinerators and choose alternative technologies with no toxic emissions."
Despite evidence in the EPA's 1994 dioxin report that human reproductive and immune systems, among others, are harmed by low-level exposure to dioxin, the risk assessment for the Tooele chemical weapons incinerator, prepared for the permit process of Utah's Department of Environmental Quality (DEQ), totally ignored non-cancer health effects from the known levels of dioxin and dioxin-like compounds emitted into the atmosphere through the incinerator's stacks. Ignored also were potential effects of chronic low-level exposure to uncombusted nerve agent that would be emitted through the stacks, especially during upset conditions.
Although evaluation of the potential effects from low-level exposure to chemical warfare agents is complicated because of the agents' high acute toxicity, long-term consequences from low-level exposure have been demonstrated, according to Dr. Robert Ginsburg, Research Director of the Midwest Center for Labor Research in Chicago, Illinois. He cites a study of children in communities near agricultural areas using organophosphate pesticides (close relatives to the organophospate nerve agents) that revealed a pattern of chronic eye problems ranging from reduction of vision to inability to fixate. In researching exposure to low levels of the organophosphate warfare agent VX, Dr. Jerry Buccafusco, Director of the Neuropharmacology Laboratory of the Department of Veterans Affairs Medical Center in Augusta, Georgia, found that after low-level exposure, rats exhibit long-term memory impairment.
Traditionally, animal research on toxic chemicals was done using large doses of a single chemical to determine whether or not the chemical is carcinogenic. However, in recent years, research has gone beyond the cancer paradigm in order to determine the relationship of low doses of toxic chemicals to the development of chronic diseases and the effects of chemicals interacting synergistically. Combinations of two and three pesticides have been found to be anywhere from 160 to 1600 times as powerful as any of the individual pesticides. Moreover, it has been found that one chemical by itself (chlordane) shows no hormone-disrupting effects, yet it magnifies the hormone-disrupting power of other chemicals when combined with them.
In the Tooele risk assessment, the possible synergistic effects of the incinerator's stack emissions in combination with each other and in combination with the 25 tons of chlorine and the two tons of hydrochloric acid released into the air of Tooele County by Magnesium Corporation, the number one toxic polluter in the US, were not taken into consideration.
The interaction of a combination of toxic agents is the probable cause for the chronic illnesses diagnosed in more than 100,000 Gulf War veterans who were exposed to low levels of nerve agent when bunkers of stored chemical warfare agents were blown up in Iraq. Dr. Howard Urnovitz, Scientific Director of the Chronic Illness Research Foundation in Berkeley, California, has found that the veterans' chronic diseases are multi-factorial and multi-step; that they result from synergistic combinations of chemical agents and can take decades to develop. Veterans of the Gulf War were given live virus vaccines and doses of pyridostigmine bromide before they were deployed. Urnovitz argues that military personnel were at risk before they went to the Gulf because of the toxic chemicals and viruses already present in their bodies. Scientists do not know the exact synergistic interaction that has caused Gulf War veterans to become ill, just as scientists do not know what long-term effects could occur from the combination of emissions from chemical weapons incinerators and the 250 or more synthetic chemicals that have accumulated and are carried in our bodies.
Toxic chemicals like dioxin, PCBs and DDT bioaccumulate. Animals eating plants contaminated with synthetic chemicals store the chemicals in their fatty tissue. Bigger animals eat smaller animals and store even more of the chemicals. At the top of the food chain, humans get the biggest dose, inheriting all the toxic chemicals down the line. Children get the biggest dose of all. Especially prior to, or shortly after, birth, children have poorly developed systems for detoxifying chemicals. Children absorb chemicals more efficiently than adults, through their skin, their gastrointestinal tract and their lungs. They take in more calories per pound of body weight compared to adults. The EPA estimates that breast-feeding infants receive up to 12% of their lifetime exposure to dioxin from their mother's breast milk. These factors and others add up to many more toxic exposures for children than for adults.
In spite of these greater risks, Utah's DEQ regulators admitted in court to having intentionally removed breast-feeding infants from the Tooele incinerator risk assessment after they had calculated the dioxin dose for the infant as being 50 times greater than the dose considered safe by the US Agency for Toxic Substances and Disease Registry. Since non-cancer effects from dioxin for all populations were totally ignored in the assessment, non-cancer effects for fetuses, breast-feeding infants and young children were, of course, also ignored. DeFur criticizes the assessment and calls it incomplete for not adding the non-cancer risks for all populations, particularly the most vulnerable. DeFur contends that since the fetus is especially sensitive, fetal exposures should have been specifically assessed, just as exposures to breast-feeding infants should have been specifically assessed because of their dioxin intake through mother's milk.
Children are paying a heavy price for our toxic legacy. One out of every four children in the United States now lives with a chronic illness. Childhood cancer has risen 10.8% in the past decade. Asthma deaths among children and young people increased by 118% between 1980 and 1993. Children exposed to PCBs, passed to them by their mothers before birth, exhibit poor reading comprehension, difficulty paying attention and memory problems. We have already impaired the future of our children through the unbridled release of synthetic chemical agents. We must now act to eliminate further exposure both before and after birth. Since the Army's 1982 decision to incinerate, several non-toxins- emitting alternative technologies have been developed and successfully demonstrated to be effective in chemical weapons destruction. The Tooele incinerator risk assessment failed to assess whether the risks of toxic emissions could be avoided and failed to compare the risks of incineration to the risks of other disposal technologies.
Despite the evidence that the assessment inadequately addressed the serious health risks of chemical weapons incineration to children, born and unborn, the Army defended the DEQ incinerator risk assessment in two federal hearings and continued operations at the Tooele facility. The Army has failed to act protectively. To prevent further harm to vulnerable populations, the Army must look to safe alternative technologies, stop the incinerators that are in operation and reverse its plan to incinerate at other sites. In the case of emissions from incineration, as in the case with the release of all toxic chemicals, what we don't know can hurt us. What we didn't know in the past has hurt our children and the cycle must be stopped. No risk is acceptable if it is avoidable.
Public Health Effects of Chemical Weapons Incineration
Richard Clapp PhD.
Center for Environmental Studies
John P. Snow Institute
Boston, Massachusetts
The toxicity and health effects of dioxin and dioxin-like compounds (such as dibenzofurans) which are emitted from incinerators are of substantial public health concern. The health effects of these compounds have been reviewed recently by the Environmental Protection Agency (EPA) in its "Health Assessment Document for 2,3,7,8 Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds" (EPA/600/BP-92/001a-c). This review is the most comprehensive done to date and it includes consideration of non- cancer health effects that had not previously been the focus of concern. As a result of this review, as well as additional scientific information that has been published since the June, 1994 External Review Draft of the EPA document, it is now possible to describe a wide range of potential health and environmental impacts of facilities which emit dioxins and furans. In the following, we will use the term dioxin to include TCDD and other highly chlorinated dioxins and furans which have equivalent dioxin-like toxic effects.
The most serious health effects of dioxin have been cancer and birth defects in exposed humans and their offspring. The basis for concern about these effects was animal experiments and human epidemiologic studies of workers exposed to dioxin-containing pesticides, Vietnam veterans and people living downwind from chemical plant explosions such as the one in Seveso, Italy in 1986. These studies indicated that dioxin causes a variety of cancers in humans, including soft tissue sarcomas, lung cancers, lymphomas and others. The animal studies, in particular, show that dioxin causes birth defects even at relatively low doses to the parents. Recently, a new study of Vietnam veterans has been published suggesting that a defect of the spinal cord, called spina bifida, is also higher than expected. New scientific information, some of it carried out as part of the EPA Reassessment, now shows that there are other non-cancer health effects, such as damage to the immune system, the endocrine system and disruption of reproductive hormone systems that are more serious than previously thought. A number of studies of experimental animals have shown that the immune system can be harmed by exposure to dioxin. Since this system protects against other diseases caused by bacteria or viruses, it is possible that persons exposed to dioxin will be more susceptible to other diseases as well. A disease of the endocrine system, diabetes, has been shown to be elevated in Air Force Ranch Hand personnel who sprayed Agent Orange in Vietnam. And finally, the reproductive hormone levels of men exposed to dioxin at work have been shown to be lower than expected in studies conducted by the National Institute for Occupational Safety and Health (NIOSH).
Perhaps one of the most disturbing conclusions of the EPA Reassessment is the finding that some of the non-cancer health effects may be caused by exposure at or near current background dioxin levels in the US. For example, the EPA estimates that the average amount of dioxin in US residents is currently about nine nanograms (billionths of a gram) per kilogram of body weight. The effect of dioxin on male reproductive hormones appears at levels as low as 13 nanograms per kilogram of body weight and altered glucose tolerance (a symptom of diabetes) begins at levels as low as 14 nanograms per kilogram of body weight. Furthermore, the most sensitive humans may be nursing infants and developing fetuses since dioxin is concentrated in breast milk and also can pass through the placenta. Because of this potential for sensitive sub-populations and the variety of serious health effects caused by dioxin, one Federal agency, the Agency for Toxic Substances and Disease Registry, has suggested in its 1989 Toxicological Profile that daily intake of dioxin be no more than one picogram (trillionth of a gram) per kilogram of body weight per day. Until the EPA Reassessment is finalized, there is no better risk assessment guidance for public agencies and decision makers than this recommended daily intake level, recognizing that our ultimate goal should be zero intake of dioxin.
The leading sources of dioxin exposure in the US at the present time are incinerators, both municipal solid waste incinerators and hazardous waste incinerators. The way that dioxins form may include direct chemical reactions with the chlorinated materials being burned, as well as combinations of materials in the gases emitted from the incinerator that result in dioxin formation as the gases cool. In any case, dioxins can then be blown downwind from the incinerator and land on pasture land or water where they can enter the food chain. Most people will get their exposure to dioxin through what they eat, such as milk or meat from cattle that graze on dioxin-contaminated pasture land, or from fish that have consumed sediments that contain dioxin.
Once inside the body, dioxin can cause the variety of health effects through several mechanisms. All the details of the mechanisms are not yet understood, yet it seems clear from existing scientific evidence that a key step is when dioxin enters a cell and attaches to a receptor called the Ah receptor. This allows a series of steps to proceed, some of which lead to damage to the genetic material of the cell, and some of which change the way certain enzymes act inside the cell. There has been a debate about how much dioxin is necessary for these various steps to proceed, but at this time the most defensible assumption is that any increase in exposure to dioxin can increase the risk of adverse health effects. In other words, there is no "threshold" or "safe level" of dioxin exposure. It is also clear that there is a wide range of susceptibility to the harmful effects of dioxin among exposed humans. Some individuals may be much more susceptible than others for reasons that are not yet fully understood. In such a situation, the prudent public health approach must be to minimize exposure to all people. The Final Protocol for the Anniston Chemical Demilitarization Facility (dated February 6, 1996) and the Protocol for the Blue Grass Chemical Agent Disposal Facility indicate that there are many potential toxic exposures to persons living near or downwind from the proposed incineration sites. In particular, the documents list many substances of potential concern which may be emitted from the proposed facilities in some amount. These substances include numerous dioxin and furan congeners (types), other chemical agents or products of incomplete combustion such as arsenic, cadmium, chromium, nickel, various phthalates, PCBs, dintrotoluene and, inevitably, mixtures of these substances. Some of these compounds are well-known hazardous or carcinogenic materials, including the dioxins and furans, various heavy metals and PCBs. Others, such as the phthalates, are currently the subject of intensive scientific investigation because of their potential to mimic estrogens (female hormones) in laboratory experimental systems. Furthermore, some of the by-products of combustion are substances with incomplete toxicological information available at the present time.
Because of the inadequate and incomplete nature of the Department of Defense screening risk assessments and the likelihood of actual risks to humans, especially new-born infants, from dioxin and dioxin-like compounds released from chemical weapons incinerators, there is no sufficient justification for undertaking the program. Even small quantities of dioxin, added to the already existing burden in the bodies of Americans, have the potential to cause harm to the reproductive, endocrine, immune and various enzyme systems of those further exposed. There are alternatives to incineration that do not involve production of dioxin and other products of incomplete combustion. Therefore, in my opinion as a public health professional, the risks posed by emissions from the chemical weapons incineration program are not justified.
Howard Urnovitz PhD.
Scientific Director
Chronic Illness Research Foundation
Berkeley, California
There are 100 million Americans diagnosed with chronic illnesses, including asthma, diabetes, arthritis, motor neuron disease, multiple sclerosis, neuralpsychiatric disorders (which includes Gulf War Illness and chronic fatigue syndrome), AIDS, heart disease and cancer. The direct cost of these illnesses to our country is estimated at $452 billion.
One of the main reasons there have been no major breakthroughs in these diseases is because we are still working on the century-old dogma that one microbe causes one disease. Although successful for many bacterial diseases, this approach is limited if a disease process requires more than one agent, as is the case with chronic ilnesses. Unlike acute disorders which take days to weeks to develop, chronic diseases are now viewed as multifactorial and multistep (MFMS) processes often taking decades to develop. The MFMS model suggests that toxic exposures are dynamic and recent scientific articles suggest that their effects may also be synergistic. The need to change our conceptual approach for developing effective diagnostic and therapeutic modalities is evident and has become critical.
The challenges to model building are to clearly identify the role of low-level exposure to toxic factors (biologic, chemical and radiologic) and how the toxic factors or their derivatives synergistically contribute to disease progression. Obviously the identification of all cofactors relevant to the disease process may be a monumental undertaking, but the possible benefits could be significant. A conceptual approach to model building is to begin with examples that provide important insights. The clues to the origins of emerging chronic diseases come from two human studies and several animal studies
The first example of emerging human chronic disease is known as "post polio syndrome" (PPS). There are 1.63 million Americans alive today who lived through polio in the 40s and 50s. About 70% of these people suffer from persistent, chronic diseases which may have taken 20 to 40 years to develop. The problems they are having are central nervous system disorders, concentration problems, trouble finding words, fatigue and sleep disorders. These are consistent problems associated with a variety of different syndromes such as myalgic encephalomyelitis, chronic fatigue syndrome, Islandic Disease and post viral fatigue syndrome.
The one important clue about PPS as compared to the other ailments is that wild-type polio virus material can still be isolated from many of the PPS subjects. Viral expression decades after an infection is counterintuitive to conventional virologic wisdom. While some viruses stay in your body for years, polio-type viruses are thought to be rid from the body after acute exposures. This new clue suggests that even polio-type viruses, which represent a family of viruses which infect 10 to 30 million Americans per year, can remain in the human body for decades.
If polio-type viruses are indeed "archived" in the body, then there would be concern whether vaccination with live tenuated polio viruses can lead to these same persistent infections. We are now questioning whether and how the expression or re-expression of polio viral fragments (not the whole virus but fragments) is triggered by toxic exposure. Presently new evidence on the role of toxic exposures is coming from the field of cytogenetics. It appears that toxic exposures that damage DNA-containing chromosomes (genotoxicity) may play a significant role in initiation and progression of chronic diseases. There appears to be "fragile sites" or "hot spots" on the chromosome where viruses, biotoxins, chemicals and radiation prefer to target.
One important area to study for the source of genotoxic viruses is polio vaccines of the 1950s. Polio epidemics were never seen before the turn of the century, but by the 1940s, there were 5,000 to 20,000 cases of polio per year in the United States. When President Roosevelt contracted the disease and died from its complications, there was a surge in funding for polio research and in 1949 polio virus was grown for the first time in tissue culture. Between 1955 and 1961, 98 million Americans were given polio vaccine grown in monkey kidney cells, used because they were cheap and available. In 1958, it was found that the vaccine was contaminated with over 26 monkey viruses. As in the case of the public health services' Tuskegee human syphilis experiments, little public disclosure occured, most probably because of the "fear of public panic" policy.
In 1960, Monkey Tumor Virus SV40 (a significant cancer virus) was identified in vaccine preps. Suppliers moved to change the manufacturing process so that SV40 positive monkeys would not be involved. However, the damage had been done. 98 million Americans were given varying levels of SV40, depending on where they lived. We are finding now that these polio vaccine-associated viruses are archived in human cells and viral fragments can be reactivated as people are exposed to toxic agents. This synergistic interaction results in persistent chronic diseases.
Another human study that we are very interested in is Gulf War Illness. There are over 80,000 Gulf War veterans with chronic ailments. They have central nervous system disorders, concentration problems, trouble finding words, fatigue, sleep disorders--the same symptoms we have found in people who have PPS. In a 1996 study we collected serum from 22 randomly selected non-military civilians, 36 subjects deployed to the Persian Gulf (23 from California, 13 from Arkansas) and eight soldiers from Arkansas who were not deployed.
Using powerful gene amplification technologies, an unusual 750 gene band was found in 83% of the deployed from California, 77% of the deployed from Arkansas and 100% of the undeployed from Arkansas. These results really get to the point that this is a multifactorial disease. Military personnel who didn't go to the Gulf have the viral band, but they are healthy. In the random civilians we found one person who had an unusual band, but no one had the 750 band. Such bands can be found in serum of subjects with cancer. They appear to be fragments of chromosomes that should not be found in the serum of healthy individuals.
A multifactorial process appears to be at work in Gulf War Illness subjects--Gulf War-era military personnel may have been at risk before they even went over there. Military personnel were given up to 17 vaccines including live viral vaccines. They were given Pyridostygmine Bromide tablets (nerve gas protectants). In the Gulf they were exposed to low levels of nerve agent from the fallout from chemical munition plant bombings. Gulf War Illness is multifactorial: the genotoxic exposures; the archived viral fragments; the immune dysregulation. There may be other factors too, but these are the hierarchical ones.
The implications of this research on the siting of hazardous waste incinerators is profound. For example, the Health Risk Assessment being used to permit the Anniston, Alabama chemical weapons incinerator, disregards the additive effects of the emissions from the stack. The assessment lists more than 100 chemicals and heavy metals to be released into the environment during the incineration process and, although the precise health effects of exposure to this combination of chemicals is unknown, current scientific studies suggest there may be synergistic effects. Add to this possibly synergistic combination of toxins the viral fragments that many Americans have archived in their genes and you have a recipe for the emergence of chronic diseases in the population downwind of the incinerator. Americans born between the years of 1941 and 1961 have a very high risk of having contaminating polio vaccine-associated viral fragments archived in their genes and would be particularly vulnerable.
That's the bad news. The good news is that there are several closed-loop disposal technologies available that have no toxic emissions and have proven out effective. Based on what we are learning with regards to Gulf War Illness and chronic illnesses in general, I would urge caution with regards to the disposal of these lethal chemical weapons. A safe method of disposal with no toxic emissions must be chosen.
Critique of Chemical Weapons Incineration Risk Assessment
Peter L. deFur PhD.
Affiliate Associate Professor of Environmental Studies
Center for Environmental Studies
Virginia Commonwealth University
Richmond, Virginia
Adjunct Senior Scientist
Environmental Defense Fund
Washington, D.C.
The chemical known commonly as dioxin is actually a family or group of chemicals with a common basic structure. The differences among the individual "forms" (often called congeners) are based on the addition of chlorine atoms to the basic structure. Chlorine atoms may be added at one or more of eight positions on the basic chemical structure. Each one of the combinations of number and position of chlorine addition creates a different specific form of chlorinated dioxin. There are a total of 75 different such chlorinated "dioxin" forms. In addition, the basic structure to which chlorine is added may vary by the removal of an oxygen atom, to create a compound called a "furan." Furans are highly similar to dioxins in the ability to have chlorine additions. The resulting chlorinated furans are chemically and toxicologically similar (but not identical) to the dioxins. There are 135 possible chlorinated furans. The dioxins and furans together make up a group of chemicals formed from high temperature combustion, paper bleaching and certain high temperature industrial processes using chlorine and chlorinated materials.
A number of the dioxins and furans (at least 17) act in a common fashion, described and known largely by the way in which the most toxic form, 2,3,7,8 Tetrachlorodibenzo-p- Dioxin (TCDD), acts on biological systems. The biological action is based on the ability of dioxin to passively enter cells (because all cells have a fat-based cell membrane and dioxins dissolve in fat) and then bind to a specific protein (forming a two-part complex) within the cell. Once dioxin and protein bind, two other events take place in the cell: the dioxin- protein complex moves into the nucleus and the complex acts on (or interacts with) the DNA (deoxyribonucleic acid). Once the dioxin acts on the DNA, an entire array of effects may be stimulated. The most common one of which is increasing the number and activity of specific enzymes and chemical processes in the cell.
The different dioxins and furans that can act in this way are described and measured based on the ability to act at the first step--binding to the specific protein, called the Ah receptor. Chemicals that bind to this protein receptor have dioxin-like toxicological properties because of the similarity in stimulating the subsequent actions and processes.
The polychlorinated biphenyls (PCBs) are a group of chemicals that are chemically similar to the dioxins and related compounds. The PCBs are also formed from high temperature processes such as incineration and other combustion processes. There are 209 different PCBs. Some of the PCBs act in a toxicological mode similar to the dioxins; e.g., those PCBs that bind to the Ah receptor also have dioxin-like properties.
The dioxins and the dioxin-like furans and PCBs are often evaluated together as a group and the total effects of the entire group are determined on the basis of the effectiveness in binding to the Ah receptor. This approach has been endorsed by the Environmental Protection Agency (EPA) and the World Health Organization.
Dioxin-like compounds are responsible for a great number and variety of toxic effects in animals. These effects include cancer, reproductive toxicity, developmental toxicity, immune impairment, neuronal developmental abnormalities, liver toxicity, testicular atrophy, wasting syndrome, hormonal disturbance, chloracne (a skin disfigurement) and endometriosis. Dioxin can be lethal when animals are exposed to doses greater than 0.5 micrograms per kilogram of body weight per day (µg/kg-bw/day) and extremely low doses (0.00001 µg/kg-bw/day) can cause cellular enzymes to increase in level and activity. (A microgram is a millionth of a gram.) The species studied include humans, rats, mice, minks, guinea pigs, hamsters, cows, rabbits, chickens, more than one fish species and monkeys. Not all of the effects have been studied and observed in all the animals listed, nor are all animals equally sensitive to dioxin or related chemicals. Most of the effects caused by dioxin and related compounds are non-carcinogenic.
Two approaches have been used to determine dioxin toxicity, one for cancer and one for non-cancer effects. Carcinogenic effects have been regulated on the basis of a no- threshold, linear response of biological systems to dioxin exposure. All evidence and analysis support this conclusion and in the most recent draft of the dioxin risk assessment, EPA continues to use a linear response without a threshold for effects.
EPA originally determined the cancer potency of 2,3,7,8 TCDD to be 0.156 nanograms (ng)/kg-bw/day, based on rat assays, accounting for the differences between rats and humans and uncertainties. (A nanogram is a billionth of a gram.) EPA originally estimated that lifetime exposure to 1 ng/kg-bw/day would result in 156,000 additional cancer cases in a population of one million people, and 1560 additional cases in 10,000 people, and so on. The cancer potency is now under review, as are the assumptions that are used to estimate cancer potency for dioxin. The draft review suggests that the potency should be lowered from 0.156 to 0.100, based on re-evaluation of old data and consideration of new cancer data. The dioxin reassessment continues to find that dioxin is carcinogenic in all animals tested, including in humans, based on limited epidemiological data. The most recent Science Advisory Board review of the draft reassessment concurred. The same report also concludes that human data reveal a cancer potency value some 30 fold higher, 3.0 ng/kg- bw/day. The reconciliation of these two values has been left to the final report. In the draft report, EPA explained the use of the 0.10 ng/kg-bw/day value because of the strength of the experimental animal data. It is important to note, as I have before EPA and the Food and Drug Administration, that human data will always be limiting and seldom of the same high quality as data for experimental animals. We do not conduct experiments on humans and only obtain data from accidental and occupational exposures (often accidental as well, but classified differently), usually after the fact.
EPA has used a different approach for non-cancer effects--one that assumes that there is a threshold--a dose below which no biological effects will take place. Using this approach, EPA determines the dose above which effects may be expected. To determine the "safe" dose, EPA then divides the "effect" dose by safety factors in order to provide protection for human health. Safety factors account for differences among animals and between species and for the unknown aspects of the experiments and the real exposures. The safety factors are often 10, and each safety factor reduces the "effect" dose by 10. For many chemicals, the effect dose is divided by 10 to extrapolate to humans, by 10 to account for differences among humans, and by 10 to account for not knowing the precise dose at which "no effect" occurs; the total safety factor is 1000. The "effect" dose would be divided by 1000 to determine a "safe" dose.
Two recent developments have affected the way in which EPA or any other regulatory agency deals with non-cancer effects of dioxin and related compounds. First, EPA and independent researchers estimate that the existing exposures may be close to the level at which biological systems respond to dioxin. In the recent version of the dioxin reassessment, EPA estimated that the average US exposure from all sources is about 3-6 picograms (pg)/kg-bw/day (A picogram is a trillionth of a gram.) for all chemicals that act like dioxins, and that the average citizen carries about 9 ng/kg-bw in their body. This body burden is compared with estimated effects levels of 14-110 ng/kg-bw levels in humans for lowered testosterone, altered glucose tolerance and reduced testis size. On the basis of these and other data, EPA concluded that no safety margin of exposure remained. This report was reviewed by the Science Advisory Board of EPA and is in final revision. According to this line of evidence, the US population is already over-exposed to dioxin and additional exposures may substantially increase the probability of adverse non-cancer health effects.
The other recent development is based on data showing responses of developmental and reproductive systems at lower doses than previously used or considered in regulatory actions. The concept is that low-level exposures may have no threshold for action if the exposures occur at a time when the animal exhibits a heightened sensitivity to the effects of dioxin (or similar-acting compounds). Originally, pregnant rats were given a single small dose of dioxin and the male offspring displayed altered sexual development, part of which was not apparent until the rats' sexual maturity. These results, from the research laboratory of Dr. Richard Petersen of the University of Wisconsin at Madison, originally presented at the Banbury Conference in 1990, have been confirmed in other species. These results provide new data to determine a dose-response curve from which EPA can determine "safe" doses or thresholds in the absence of complete data for low-level exposures and effects not previously tested. Data analysis in the revised dioxin risk assessment indicates that some non-cancer effects do not show a threshold for response.
I have read the Screening Risk Assessment for the Tooele Chemical Demilitarization Facility, Tooele Army Depot South, EPA I.D. no. UT210090002, dated February 1996. I did not find in the assessment any consideration of the non-cancer effects of dioxin. The tables and text show 0 risk from 2,3,7,8 TCDD, a value that was only reached under the assumption that the agent, in this case dioxin, had no effect on the target or end point. This assumption of no risk from dioxin is not warranted nor supported by the current evidence, nor from existing documents. There is an extensive literature on the reproductive and developmental effects of 2,3,7,8 TCDD at low doses and in single doses. The assessment needs to evaluate these risks as well as the cancer risks from 2,3,7,8 TCDD. Guidance is available from several sources on protecting against health effects from dioxin exposure for non-cancer end points. First, EPA assessed the risks of dioxin exposure in the Times Beach Site Multimedia Risk Assessment for Production Burn (Feb. 26, 1996; contract no. 68-w8-0112) and used a reference dose of 1 pg/kg-bw/day for protecting against reproductive effects of dioxin. Second, the Agency for Toxic Substances and Disease Registry (ATSDR), in the June 1989 Toxicological Profile for 2,3,7,8 TCDD (contract no. 68-C8-004), the same value of 1 pg/kg-bw/day was given for reproductive effects. Finally, even a decade ago this was recognized by EPA as a serious toxic end-point in the EPA Ambient Water Quality Criteria (AWQC) Document for 2,3,7,8 TCDD of 1984 (EPA 440/5-84-007). The AWQC used experimental data for monkeys as the basis and the resulting reference dose was nearly the same (1.5 pg/kg-bw/day) as the one recommended in 1996 (1.0 pg/kg-bw/day).
The reference dose determined above is the basis for making decisions to control or further control exposures. The method used is a simple ratio of the exposure dose divided by the reference dose, yielding a fraction termed the Hazard Index (HI).
Hazard Index = Exposure dose / Reference dose
If the index is greater than one, exposure is greater than deemed "safe" and further action is warranted. For this screening assessment EPA uses a ratio of 0.25 to provide conservatism. In the present case, the exposure dose is the national exposure estimated from the dioxin reassessment, plus the dose from the incinerator emissions. The reference for non-cancer effects is given in ATSDR. The result
3-6 pg/kg-bw/day + Tooele Incinerator emissions / 1.0 pg/kg-bw/day
exceeds 1.0 and exceeds the value of 0.25 that EPA uses in the Tooele Risk Assessment as a protective screening level. Any emission of dioxin from the Tooele incinerator that enters into the human exposure pathway will pose an unacceptable risk of reproductive effects, based on EPA's own methods and practices.
In my professional opinion, any risk assessment for dioxin exposure must account for the effects of all dioxin-like compounds acting on non-cancer end points for human health. The assessment must particularly note the effects on reproduction, development and the immune system. Because development of the fetus is especially sensitive, fetal exposures must be specifically assessed. In addition, the exposure during breast feeding must be specifically addressed. Estimates of lactational exposure suggest that 12% of an individual's lifetime dioxin exposure may come during breast feeding. Several recent studies of breast milk in Inuit peoples by Eric Dewailly, of the Environmental Health Service in Quebec, Canada, show that breast feeding is a highly effective exposure pathway for infants. Furthermore, the laboratory work from Petersen's lab on rats and the human exposure research from the Great Lakes by Jacobson and co-workers indicate that low-level exposure at early life stages has the most profound and permanent effects.
The Tooele incinerator risk assessment is not complete without adding the non-cancer risks from dioxin exposure to all target groups or individuals, and especially to fetuses, infants and young children that are not included in the present assessment. The assessment needs to determine effects on immune function, reproduction, development and the central nervous system. In the assessment, the exposure paths need to be re-evaluated as discussed below.
The exposure assessment for the Tooele incinerator assumes that the population living in the affected area is within the US average for consumption of beef, dairy, vegetables, game, and that only 25% of vegetables are grown within the affected area. These assumptions do not seem warranted, based on my experience in reviewing risk assessments and considering that the area is a rural farm area. The assessment should use some more direct measure of produce consumption from local sources, and, if not available, attempt to find data from a comparable area in the state, or region of the US. The default should not use the US average for consumption. This assumption is, in my estimation, neither conservative nor substantiated.
The ecological effects of the operation of the Tooele incinerator have not been adequately characterized or assessed in the assessment. The assessment relies on satisfying US EPA AWQC that attempt to protect against known chronic and acute effects from identified chemicals. The exposure pathways are into water and then directly into the animals, or from particulate matter into the animals. The AWQC do not protect against sediment accumulation and subsequent release and exposure of wildlife (or humans, for that matter), nor do the AWQC protect against food chain exposure. In both exposure cases, animals concentrate dioxins, PCBs and related chemicals to levels sometimes thousands of fold higher than in the original waters or sediments. These food chain exposures have been associated with developmental toxicity in wildlife, including bald eagles, cormorants, gulls, mink and piscivorous animals. The chemicals released from the Tooele incinerator, especially dioxin, act in this way and can and will exhibit profound and long-term effects on wildlife at low doses.
Based on my participation in the scientific review of the Waste Technologies, Inc. (WTI) hazardous waste incinerator in East Liverpool, Ohio, one of the greatest possible risks may be the risk of uncontrolled releases from accidents. The accident analysis for the WTI incinerator was lacking entirely in the original assessment. Yet, the review panel agreed that accidents and uncontrolled releases of an accidental nature could account for a substantial fraction of the total releases. The same point is relevant to this or other incinerators, especially ones that burn hazardous and toxic material. This assessment needs to account for the releases and effects of accidental and upset releases.
Robert Ginsburg PhD.
Reseach Director
Midwest Center for Labor Research
Chicago, Illinois
In reviewing the literature on the toxicity of the Organophosphate Chemical Warfare Agents GB and VX through early 1995, I have found that evaluation of the potential effects from exposure to low levels of these chemicals is difficult because of complications arising from the chemicals' extremely high acute toxicity. For example, while the oral LD 50 (lethal dose for 50% of the population) for parathion, one of the more acutely toxic commercial organophosphate pesticides, is 13 milligrams per kilogram of body weight (mg/kg-bw), the LD 50 values for GB and VX are 1.1 and 0.1 mg/kg-bw, and the production of acute effects from exposure to these agents occurs in many species well below the LD 50 level. Various studies on GB have shown a variety of effects at levels below 1% of the LD 50.
The dramatically low dosage at which acute toxicity is produced by warfare agents has limited the ability to reliably measure the effects of sub-acute exposure. This is especially true for studies employing a limited number of animals (including bioassays for carcinogenicity, teratogenicity, reproductive effects and subchronic toxicity). A widely quoted teratogenicity study used only six sheep that were administered levels of VX below 0.004 mg/kg-bw. At these levels, which are typical of most of the reported studies on GB and VX, the sensitivity of the tests may not be sufficient to detect any significant increase in chronic effects. In tests where higher levels are used, significant depression of cholinesterase and other acute effects dominate which may mask the less severe chronic effects to be studied. The studies which looked at genotoxicity (mutagenicity) also noted a concern about the extreme acute toxicity of the chemicals. It is not surprising that the tests reviewed by researchers at the Aberdeen Proving Ground for the 1988 Programmatic Environmental Impact Statement were either not positive for chronic effects or were difficult to interpret.
Despite the limitations in testing, long-term consequences from low-level exposure to nerve agents as well as commercial organophosphate pesticides have been demonstrated. Effects of lower doses on larger populations should be considered likely, whether or not studies can be designed to demonstrate such effects.
EEG and behavioral changes are examples of more subtle but long-term effects that would be of particular concern in exposed populations and should be a focus for any potential studies. The interaction of GB and VX with multiple components of the body's systems is quite complex and the mechanism of the effects of this interaction is not known at this time. However, it clearly goes beyond cholinesterase inhibition. A number of studies have shown psychological and neurologic or neuromuscular changes (other than delayed neuropathy) which persist long after exposure has ceased. Data initially collected on industrial workers accidentally exposed to the agent GB demonstrated changes in EEG and sleep patterns a year after exposure had ceased. Those results were reproduced in monkeys given either a single large (non-lethal) dose or a series of smaller doses which did not produce any overt signs of toxicity. The existing studies suggest that the total amount of exposure (cumulative dose) is the critical factor for determining EEG changes.
Another effect of concern in populations exposed to low levels is the incidence of eye lesions. Studies on students and children in communities near agricultural areas using organophosphate pesticides reveal a pattern of eye problems ascribed to chronic exposure to the pesticides. The effects ranged from reduction of vision to inability to fixate. These effects were reproduced in dogs to support the connection to pesticide exposure. These results are also consistent with the use of miosis (constriction of the pupils) as the most sensitive indicator of nerve agent exposure. Doses of 0.003 mg of GB applied to the eye sacs produced significant miosis without any depression of cholinesterase levels in the eye.
The impact of low-level chemical agent exposure on a large population with "normal" other exposures cannot be thoroughly evaluated given the limited investigations of chronic, more subtle effects that have been done to date.
The persistence and reactivity of these nerve agents need to be studied in the context of low-level exposure over an extended period of time. In particular, VX is quite stable and can persist unchanged in the environment for months. Total exposure to the parent compounds through accidents and uncombusted materials could reach levels of concern if the incinerator and material handling operations did not continually operate at peak efficiency.
Jerry J. Buccafusco PhD.
Professor of Pharmacology and Toxicology
Medical College of Georgia
Director
Neuropharmacology Laboratory
Department of Veterans Affairs Medical Center
Augusta, Georgia
Organophosphorus agents have a wide use in medicine, agriculture and unfortunately in the arsenal of chemical weapons. However, it is the latter two uses that have been associated with significant toxicity and lethality to humans. With the demise of the chlorohydrocarbon insecticides such as DDT, the use of the organophosphorus insecticides, which are chemically related to chemical warfare agents, has become prevalent. Along with the manufacture and deployment of the more lethal nerve agents, this class of drug has prompted concern regarding not only their acute toxicity, but also the possibility that low- level, chronic exposure to these compounds is associated with subtle forms of chronic illness. The most recent event to bring such concern to the forefront was the Persian Gulf conflict wherein significant numbers of returning veterans continue to complain of the cluster of symptoms termed the Gulf War Illness.
Gulf War personnel had ample opportunities to undergo repeated exposure to drugs related to the organophosphate cholinesterase inhibitors. These included the liberal use of personal insecticides, the use and over-use of pyridostigmine bromide--a potential nerve agent protectant and the direct exposure to Iraqi chemical nerve agents. But it is the agricultural setting that has provided the little that is known regarding the consequences of chronic sub- toxic exposure to the organophosphorus pesticides. In fact, many of the symptoms reported by agricultural workers who had been subjected to repeated low-level intoxication are similar to those reported by Gulf War veterans.
One of the more prevalent and troubling of the symptoms reported by both groups is the subtle cognitive impairment characterized by forgetfulness and difficulty concentrating. Our research at the Medical College of Georgia has focused on human disorders of cognition and memory and it was the memory loss attributed to Gulf War Illness that we initially chose to address. Funded by a grant from the US Army over the past two years, we have developed a rat model in which chronic low-level exposure to an organophosphorus agent produced a subtle but reproducible memory impairment for as long as three weeks after termination of the exposure. Moreover, this protracted memory impairment was accompanied by a delayed recovery of the enzyme acetylcholinesterase, which is targeted by chemical warfare agents.
These changes were shown to occur specifically in the hippocamus, a portion of the brain that is critical for new memory formation. Additionally, there was a loss of a specific class of neurotransmitter receptors for acetylcholine--a brain substance that helps solidify new memories. The number of acetylcholine receptors had declined by over 50% and even after three weeks, the level had only slightly returned toward normal. The relevance of these findings is based on the facts that:
(1) the dementia and memory loss associated with Alzheimer's disease is acompanied by loss of acetylcholinesterase and acetylcholine receptors in the hippocamus;
(2) that the hippocamus is a brain structure that is intimately involved in normal memory processes; and
(3) that the neurochemical changes that took place after chronic low-level organophosphorus exposure appeared to parallel the memory loss in the animals.
Our data go on to show that only a particular form of memory--working memory (but not reference memory)--is affected by organophosphorus agents.
Our continuing studies are directed at more fully characterizing the behavioral and neurochemical, and perhaps the neuropathological, change associated with chronic organophosphorus exposure. With this knowledge, we anticipate the development of novel approaches to the treatment of the cognitive symptoms related to organophosphorus exposure whether it occurs on the peanut field or the battle field.
Peter L. deFur PhD.
Affiliate Associate Professor of Environmental Studies
Center for Environmental Studies
Virginia Commonwealth University
Richmond, Virginia
Adjunct Senior Scientist
Environmental Defense Fund
Washington, DC
Carolyn Raffensperger M.A., J.D.
Director
Science and Environmental Health Network
Windsor, North Dakota
Washington, DC
Scientists are certain that a number of synthetic chemicals act like hormones (especially estrogens) and interact with hormone systems. It has been known for years that some of these chemicals are able to affect animals in subtle ways. However, the magnitude of the problem, including human exposure, is uncertain: the puzzle is still being pieced together.
An endocrine system is a hormonal pathway characterized by the production of a biologically active substance by a ductless gland. The substance is carried through the bloodstream to initiate a cellular response in a target cell or tissue. The biologically active substances are hormones that serve as chemical messengers. Hormones are active at very low concentrations and most are specific in what responses they cause in the body. Endocrine systems generally control body growth, organ development, metabolism and regular body processes such as kidney function, body temperature and calcium regulation.
Endocrine systems are complex, looping cascades that can be disrupted or modulated at many points. Hormones circulate in the body and, even at low levels, are responsible for maintaining balanced conditions, such as blood pressure and reproductive cycling. Different hormones act in complementary ways on the same organs to regulate function. Hormones can also act on each other's synthesis and distribution to affect organ function. Just about all animals have endocrine systems and certainly all animals more complicated than a sponge rely on endocrine systems for normal life functions. In wildlife, hormones regulate mating behaviors, migration, fat deposition, hibernation, insect metamorphosis and the shedding of shells by shrimp, crabs and lobster.
Endocrine disruptors are chemicals that interfere with the normal function of hormones and the way hormones control growth, metabolism and body functions. There are different WAYS that chemicals can interfere with or disrupt hormones, and there are different KINDS of chemicals that disrupt. There are more than 80,000 chemicals in commerce, few of which have been tested for carcinogenicity, much less their capacity to disrupt endocrine systems.
Based on what we do know about the effects of chemicals on endocrine systems, three classes or types of disruptors have been identified.
The sources of endocrine-disrupting chemicals are twofold:
Most of these chemicals are synthetic, fat-soluble compounds that are persistent, remaining in the environment or animals for very long periods. As a result, the DDT, PCBs and dioxins that were released decades ago still contaminate soils, waters, animals and humans. All of us carry a certain body burden of these chemicals from past exposures and on-going intake. We get most of these chemicals from animal-based foods, primarily animal fats that have low levels of these chemicals contained in them. Fish from contaminated areas carry higher concentrations in their fat, as do cattle, pigs and chickens.
A certain amount also comes from drinking water if the water system does not remove pesticides that have endocrine-disrupting properties. Pesticides used at any point in food production can almost always be accumulated and passed on to the eventual consumers-- humans and animals.
Scientists are not certain of the extent to which humans have been and are being exposed to endocrine-disrupting chemicals. Just in the past six years, a number of chemicals with estrogenic properties have been identified in waste waters, in the leachate from plastic material and in the material used to coat tin cans. Researchers have identified several products found in plastics as estrogenic and at least some of these can leach out of the plastics into liquids. There is a potentially large exposure pathway here in the form of all the plastics used in food preparation and storage. It is not clear what the long-term effects of that exposure could be. The uncertainty is partly due to the fact that we have learned much about the sources and exposures of the endocrine disruptors from studying wildlife but lack extensive data from human populations.
Research on wildlife populations, especially in the Great Lakes, has demonstrated that endocrine-disrupting chemicals profoundly impair animal reproduction and development. Birds with deformed beaks, female birds that nest with females and male alligators with underdeveloped penises all have high levels of endocrine disruptors: PCBs, dioxins and DDEs, respectively. Laboratory research reveals that fish eggs do not develop when exposed to even low levels of PCBs and dioxin. Pregnant rats given a single low dose of dioxin at a specific time give birth to male rats with a range of reproductive problems.
Dioxin and PCBs are known to impair liver function and cause cancer in workers and veterans who were exposed years ago. Children whose mothers used cooking oil contaminated with PCBs and dioxin-like chemicals show a range of developmental problems. Scientists are now investigating possible links between endocrine disruptors and other developmental and reproductive disorders in people.
In both humans and wildlife, these effects are not obvious at the time of exposure, but show up later, or even in the next generation. Children of DES-exposed women demonstrate this transgenerational aspect of endocrine-disrupting chemicals.
Individuals and families can take steps to reduce their exposure to endocrine-disrupting chemicals. They can: reduce intake of fats and oils that potentially contain these toxic chemicals; avoid microwaving and storing food in plastics; eat pesticide-free organic food whenever possible; eliminate use of pesticides at home.
It is important that individuals take whatever measures they can to reduce exposure to themselves and their families. However, it is more important that the US government and its agencies take action to prevent toxic pollution at the source. Presently the US Army has two chemical weapons incinerators in operation with atmospheric emissions known to include the endocrine disruptors dioxin and PCBs. Both of these toxic chemicals are persistent in the environment, are transgenerational and have known disruptive effects at low doses. To act responsibly and with precaution in light of the known effects of endocrine disruption in animals and humans and the uncertainty of the extent of human exposure, the Army must shut down the existing incinerators and choose alternative technologies with no toxic emissions. It is the only ethical option. The Army should not make war on the health of US citizens.
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