The Twelfth Annual International Symposium on Man and His Environment in Health and Disease

Special Focus: Psychological Mechanisms Involved in the Development and Progression of Chemical Sensitivities and the Environmental Aspects of Biological Cycles

February 24-27, 1994

                Specific Densitization to Chemicals: Pilot Study of 100 Patients

                    Miklos Boczko, MD
                    Lawrence J Caprio, MD
                    Westport, CT

We are not aware of any attempt at a systematic investigation of specific desensitization to common chemicals in the environment. Our experience over the past 7 years using a modified Rinkel method of neutralization in the treatment of chemically sensitive individuals is reviewed. We have randomly selected 100 cases from a patient population of nearly 6,000. Additional supportive measures in line with accepted guidelines by the AAEM were employed. The specific treatment is carried out by self-administered sublingual neutralizing doses of the offending substances on a t.i.d. basis. We were interested in validation of our anecdotally gained impression that such treatment is not only feasible and safe but also an effective and practical method for the long-term. Our pilot study shows that recovery is achievable in almost one-fifth of cases, irrespective of age, but not sex. The median time interval needed for recovery was between one to two years. An overall favorable response was seen in 90% of the patients treated for a median period of over three years. In conclusion, we have shown that full recovery from specific chemical sensitivities is feasible for extended periods of time.


Goals and Objectives:
1. To determine the feasibility of specific chemical desensitization.
2. To determine the safety, effectiveness, and practicality of the method.
3. To determine the feasibility of complete desensitization without the need for ongoing treatment.
4. To establish parameters of treatment time intervals needed to achieve desired therapeutic objectives.

1. We have substntiated our clinical impressions.
2. We have shown that full recovery from specific chemical sensitivities is feasible for extended periods of time.
3. We have also shown that with consistent application of this method, prognosis for a satisfactory outcome appears to be feasible for the substances investigated.

1. Hunter, L.M. 1989. The healthy home: An attic to basement guide to toxin free living, 4-6. New York: Pocket Books (Simon and Schuster).
2. Upton, A. C., ed. 1993. Staying healthy in a risky environment. The New York University Health Center Family Guide, 607-717. New York: Simon and Schuster.3. Randolph, T.G. 1952. Sensitivity to petroleum: Including its derivitives and antecedents. J Lab Clin Med 40:931-932. (Abstract)
4.. Upton, A.C., op cit, p. 160.
5. Crop, Jozef. Personal communication.
6. Maclennan, John G. Personal communication.
7. Rea, William J. Personal communication.
8. Zazula, Marian. Personal communication.
9. Voll, Reinhold. 1980. The phenomenon of medicine testing in electroacupuncture according to voll. American Journal of Acupuncture 8:2.
10. Dickey, L.D., ed. 1976. Clinical Ecology, 459-465. Springfield, IL: Charles C. Thomas.
11. Tsuei, J.J., C.W. Lehman, F.M. Lam, and D.A. Zhu. 1984. A food allergy study utilizing the EAV acupuncture technique. American Journal of Acupuncture 12(2):105-116.
12. Dickey, L.D., op cit, pp. 544-553.
13. Pfeiffer, C.C. 1975. Mental and elemental nutrients, New Canaan, CT: Keats Publishing.
14. Bionostics, Inc. 1986. Technical Memorandum, No. 2. Function of Amino Acids. Lisle, IL.
15. Randolph, T.G. Personal communication.

Differentiating between Environmental and Psychiatric Patients by Configuration of Symptoms and Severity Ratios: A Practical Guide for Physician's/Clinician's Use

Joel R. Butler, PhD
Dewey Oklahoma

Susan Franks, PhD
Fort Worth, TX

The Ecological Differential Configuration (EDC) is a test designed to provide the Environmental Illness practitioner with statistically significant information about the psychiatric and ecological status of a given patient. The EDC presents reliable and valid data to determine the probability of environmental or psychiatric involvement as well as accurately indicating the diagnostic classification (environmental illness or psychiatric) and cological status of a given patient, which Abest fits@ the patient. The classifications will also meet diagnostic criteria established by other sources.

The EDC can be adminstered by office staff. Scoring, statistical data measurements (percent ratios, probability statement, significance levels, etc.) and narrative interpretation will be provided in a timely and highly cost-effective manner.


Goals and Objectives:
The purpose of this study was to determine if a research-based instrument could be developed that would identify and differentiate the environmentally ill patient from psychiatric patients and from other patient groups or normals. The goal was to generate a statistically proven standardized test that would serve as a screen for environmentally ill patients as contrasted to psychiatric for other groups. The objectives were to produce such a test that could be administered by staff personnel in a speedy and econmical manner.

Conclusions of what is to be learned:
The results indicate that this logic and research-based instrument utilizing a criterion group methodology has been empirically tested and found to be a reliable and valid procedure as a screen for differentiating between environmental and psychiatric and other medical classifications.

Anderson, A. 1982. Neurotoxic follies. Psychology Today July:30-42
Flanagan, W.J. 1990. Symptom-based classification of environmentlly ill patients: An exploratory study. Unpublished master's thesis, University of North Texas, Denton, TX.

Rea, W.J. , J.R. Butler, J.L. Laseter, and I.R. DeLeon. (1984). Pesticides and brain function changes in a controlled environment. Clinical Ecology 2(3):144-155.

Singer, R.M. 1990. Neurotoxic Guide Book. New York: Van Nostrand Reinhold.

The Role of Tissue Repair as an Adaptive Strategy: Why Low Doses Are Often Nontoxic and Why High Doses Can Be Fatal

EJ Calabrese, PhD
University of Massachusetts
Amherst, MA

The role of tissue repair as an adaptive strategy by species is an important one to consider in both evolutionary and toxicological perspectives. This paper assesses the distinct and integrative roles of early phase regeneration (EPR) (i.e., arrested G2 hepatocytes chemically activated to proceed through mitosis) and secondary phase regeneration (SPR) (i.e., hepatocytes mobilized principally from G0/G1 to proceed through mitosis) in the repair of CCl4-induced liver damage. The induction and function of EPR as a triage system repairing minor toxic insults as well as providing an essential role in autoprotection as an initial step to augment and sustain tissue repair is proposed. The function EPR is then compared to that of SPR in tissue recovery following more massive injury. The interrelationships of these two repair processes with the EPR invoking an accelerate SPR following low-to-modest degrees of toxicant-induced hepatotoxicity as well as in auto- or heteroprotection supports the theory that the two responses are coordinated in time and functionality.

A Single Exposure to Certain Chemical Carcinogens Can Cause Cancer: Documentation, Limitation, and Implications for Risk Assessment

EJ Calabrese, PhD
University of Massachusetts
Amherst, MA

A sinlge exposure to over 250 chemical carcinogens representing more than 30 chemical classes have been found to cause cancer in 36 mouse strains, 24 rat strains as well as in other less frequently used models such as hamsters, gerbils, guinea pigs, rabbits, and fish. Similarly, this phenomeon is not restricted to a given tumor type, a specific age, or sex nor is it limited to extremely high doses as judged by percentage of the LD50. Epdiemiologic evidence indicating that brief exposures (e.g., <1 year) to some chemical carcinogens (e.g., benzene, beryllium, DES) are associated with enhanced cancer risk add weight-of-evidence support to the animal model findings. The implications of these findings for carcinogen testing and risk assessment procedures, especially those concerning less than lifetime exposures, are addressed in light of potential mechanistic interpretations by which single dose carcinogens act.

How to Interpret Soil Ingestion Studies: Why Soil Tracers Have Provided Widely Varying Soil Ingestion Estimates, How to Correct It and Derive Improved Soil Ingestion Estimates

EJ Calabrese, PhD
University of Massachusetts
Amherst, MA

The principal sources and magnitude of positive and negative error in soil ingestion estimates of Calabrese et al. (1989) on a subject-seek and tracer basis are documented, thereby leading to vastly greater intertracer consistency in subject-week soil ingestion estimates for children and adults. Highly variable susceptibility to different types of possible positive and negative error exists amongst the tracers. Tracers such as Y and Zr displayed a predominantly negative error for children while tracers such as Ti and V displayed an enhanced susceptibility to positive error for children and adults. These factors lead to underestimation of soil ingestion estimates by Y and Zr and overestimation by Ti and V in the Calabrese et al. (1989) children study. The most reliable tracer for soil ingestion estimates in general was A1 since this tracer was least affected by positive and negative error. However, the most reliable tracer for a specific subject-week would be that tracer with the least error.

How Environmental Chemicals May Contribute to Total Body Load. CA Study of the Effect of Four Compounds on the Liver-Thyroid Axis

B. Chen, Graduate Student
SC Price, PhD
WJ Rea, MD
JW Bridges, PhD
Robens Institute of Health and Safety
University of Surrey
Guildford, Eng

The aim of this investigation was to study the combined effects of environmental chemicals on the liver-thyroid axis and their contributions to total body burden (Rea 1992) using the rate as an animal model.

First, groups of male Wistar Albino rats were given di(2-ethylhexyl)phthalate (DEHP) at 10 and 1000 mg/kg body weight, butylated hydroxytoluene (BHT) at 25 and 500 mg/kg body weight, hexachlorobenzene (HCB) at 10 and 200 mg/kg body weight, erythrosine (ERY) at 50 and 500 mg/kg body weight solely or in combination for 14 days. Treatment at the higher doses produced a significant induction of UDP-glucuronyl transferase (UDP-GT) by HCB and BHT whereas DEHP induced %-glycerophosphate dehydrogenase (%-GPDH). Total serum thyroxine levels (T4) induced by ERY, but decreasd following DEHP and HCB treatment at the higher doses. Serum TSH was induced following tretment. At the lower doses of these compounds was induction of UDP-GT with HCB. A combined treatment with DEHP and BHT at the lower dose showed an induction of%-GPDH.

In a second experiment, groups of rats were given BHT for 14 days, and treatment was withdrawn for 14 days. The rats were then rechallenged with either BHT or HCB. The results showed that all biochemical effects tended to return to control values on cessation of treatment. Following rechallenge with BHT %-GPDH was significantly depressed in the low-dose BHT-pretreated group. When rechallenged with HCB, a similar depression was seen in both high-dose and low-dose BHT-pretreated groups. HCB caused a fall in serum T4 following a two-day challenge.

These results indicate that these four compounds can cause changes in hepatic drug metabolizing enzymes and serum T4 or TSH, which may result in disturbance of homeostasis. Even though few changes were seen after treatment at the lower doses, trends were still seen. Furthermore, these results address the question as to whether initial change seen with some classes of compounds is a direct effect on certain thyroid parameters or an indirect effect via metabolism by hepatic enzymes.


Goals and Objectives:

How environmental chemicals may contribute to ATotal Body Load@CA study of the effect of four compounds on the liver-thyroid axis.

The aim of this investigation is to study the combined effects of environmental chemicals on the liver-thyroid axis and their contributions to total body burden using the rat as an animal model.

Conclusions of what is to be learned:

The results obtained will be used to elucidate the possible effects due to body overload seen in man.


Rea, WJ. (1992). Chapters 1-3. Chemical Sensitivity, Vol. 1, 1-40. Boca Raton, FL: Lewis Publishers.

The Biological Rhythms of Biosphere 2:

John B. Corliss, PhD
Biosphere 2
Oracle, AZ

Biosphere 2 is a closed ecological system in which technological and biological systems must be designed and operated to work together to provide a healthy life-support environment for the people living inside. Because the Biosphere is closed and intensely monitored, it serves as a powerful laboratory for the study of questions of environmental health.

The first mission achieved extremely tight closure and success with food production, waste recycling, atmospheric management, and basic environmental controls. In the short term, achieving an atmospheric balance of the oxygen-carbon dioxide cycle was, as expected, a learning experience. Our monitoring of some 100 technogenic and biogenic trace gases revealed short-term success and provides a basis for research into long-term maintenance of atmospheric health. Creating the agricultural system required the substitution of integrated pest management for use of toxic chemicals. Recycling waste water required operation of a nonpolluting wastewater recycling system.

With the success of the shakedown, Biosphere 2 now provides opportunities for guest investigators to enter and live inside for a week to months at a time to observe and sample. This capability enhances the potential of the facility as an experimental system for research into the interactions of humans and their environment.

Endocrine Tumors of the Stomach

Yogeshwar Dayal, MD
Tufts University School of Medicine and The New England Medical Center Hospitals
Boston, MA

Gastrointestinal (GI) carcinoids are slow growing, potentially malignant neoplasms of endocrine cells or their precursors that are normally dispersed throughout the GI mucosa. In the stomach, carcinoids arise either from pluripotent stem cells in the foveolar epithelium, from fully differentiated endocrine cells dispersed in glandular epithelium, or from the neuroendocrine complexes of the lamina propria. These tumors are conventionally classified into (1) ECL cell carcinoids, (2) non-ECL carcinoids, and (3) mixed-cell carcinoids. ECL cell tumors represent the neoplastic endpoint in the hyperplasia-neoplasia sequence of ECL cell proliferations and are therefore most commonly seen in chronic hypergastrinemic states. The non-ECL cell carcinoids include those exclusively or predominantly composed of a gastric non-ECL type endocrine cell. The mixed-cell type arise from foci of intestinal metaplasia in the stomach and contain both gastric and intestinal type of endocrine cells. Hypergastrinemia-associated ECL cell carcinoids differ significantly from the non-ECL cell and mixed cell carcinoids that arise sporadically in normogastrinemic patients. While ECL cell carcinoids are usually multiple, the sporadic ones are invariably solitary. Whereas ECL cell carcinoids arise in a background of ECL cell hyperplasia, the non-ECL cell and mixed-cell carcinoids do not. However, all gastric carcinoids are diffusely argyrophilic by the Grimelius technique. Although the vast majority of ECL cell carcinoids are functionally inert, some of them may produce an atypical carcinoid syndrome due to overproduction of histamine by the tumor cells. The atypical carcinoid syndrome in sporadic gastric carcinoids, on the other hand, is due to overproduction of 5-HTP. Biologically, too, the sporadic tumors have a much more aggressive clinical course. Because of differences in their clinical management and biological outcome, the hypergastrinemia-associated ECL cell carcinoids need to be differentiated from the non-ECL cell and mixed-cell carcinoids occurring sporadically in normogastrinemic patients.

Hyperplasias of Gastric Endocrine Cells

Yogeshwar Dayal, MD
Tufts University School of Medicine and The New England Medical Center Hospitals
Boston, MA

The human gastric mucosa is populated by at least seven distinct endocrine cell types, of which the histamine-producing Enterochromaffin-like (ECL) cells are the most numerous. These cells are exquisitely sensitive to the trophic action of gastrin and therefore undergo hyperplasia in a variety of hypergastrinemic conditions. Increasing scientific attention is currently being focused on ECL cell hyperplasia because of its relevance in a variety of clinical situations. A hyperplasia-neoplasia sequence has recently been proposed following the realization that (1) ECL cell hyperplasias occur in up to 10% of patients undergoing UGI endoscopy and (2) increasingly severe degrees of ECL cell hyperplasias can eventually progress to ECL cell carcinoids. Because of their neoplastic potential, ECL cell hyperplasias were initially regarded as preneoplastic lesions. However, since the clinical risk lies not in the presence of ECL cell hyperplasia but in whether these lesions will progess to carcinoids, it is important to bear in mind that not all such hyperplasias progress to carcinoids, and even the few that do take ten or more years to do so. We now know that this risk, while negligible in the earlier stages of hyperplasia, becomes significant only when dysplastic lesions develop. Although the exact magnitude of this risk or the factors that influence it are not known, we do know that while chronic hypergastrinemia in man does lead to ECL cell hyperplasia, hypergastrinemia alone is insufficient for its progression to carcinoidogenesis and several additional factors also have a role to play. Thus, patients being evaluated for ECL cell hyperplasia should undergo a careful baseline endocscopy to look for clinically occult carcinoid tumors. If none are found, they sould be managed conservatively with periodic serum gastrin determinations and endocscopy with multiple full-thickness biopsies to monitor the progression of their hyperplasia. If a dysplastic lesion or a carcinoid tumor is identified, an antrectomy should be seriously considered.

Environmental Factors in Renal Disease

Ronald Finn, MD
Royal Liverpool University Hospital
Liverpool, England

The kidney is a prime target for Environmental Disease as it is the principal excretory organ, and many environmental chemicals or their metabolites are excreted in concentrated form through the kidneys.

Examples include heavy metal poisoning, analgesic nephropathy, certain antibiotics, high purine diets and hypertensive damage due to excessive salt consumption. This presentation will concentrate on solvent-induced renal disease.

Epidemiological data shows that patients with glomerulonephritis have a much higher exposure to solvents than age and sex-matched controls.

Subsequent studies have compared industrial workers with high and low solvent exposures, but no obvious renal or other disease. These apparently healthy workers in contact with solvents have evidence of renal damage as shown by albumen excretion, urinary enzyme excretion, and minor changes in renal function.

The data also suggests that the disease progresses more rapidly if the subjects remain exposed to solvents. Conversely, avoidance of further solvent exposure significantly slows the progression of glomerulonephritis.

Prospective Substitution of Transfer Factor with In Vitro Stimulated T Lymphocytes

Bertie Griffiths, PhD
Environmental Health Center-Dallas
Dallas, TX

From peripheral blood of environmentally ill patients, lymphocytes were harvested. A set of these lymphocytes from each patient was stained with propidium iodide and fluorescein isothiocyanate (FITC). These were analyzed by flow cytometry for DNA content, which is presented as a histogram. This histogram reflects the percentage distribution of lymphocytes in each growth phase of the cell cycle. Comparison of the profile thus obtained with controls provides a Asnapshot@ of the patient=s cell growth cycle profile and, consequently, a guideline for therapy.

If a patient has an irregular cell cycle profile, the other set of lymphocytes is cultured, stimulated to blast, harvested, lysed, and administered parenterally.

Results showed that the lymphocyte extract of each patient acts as an excellent biological response modifier, which regulates the cell growth cycle to reflect a normal profile.

These findings project the possiblity of a more efficient treatment and management of environmentally ill patients on an individual basis.


Goals and Objectives:

1. To compare the cell growth cycle profiles of environmentally ill patients with normal individuals.
2. To prepare a biological response immune regulator from the T lymphocytes of the perpheral blood of each patient.
3. To observe the immunological regulatory effect of this autoimmune regulator on the lymphocyte growth cycle.

Outline of Talk/Abstract:

This investigation provides the following:
1. A rapid and highly reproducible method for assessing the state-of-affairs of the T lymphocyte function of environmentally ill patients (and probably immunodeficient patients in general).
2. By pinpointing the deficiency(cies), an individual therapeutic program can be set.
3. The use of the individual=s own T lymphocytes to prepare an immune regulator offers the individual peace of mind as to the possibility of contracting AIDS and other bloodborne illnesses from biological response modifiers from external sources.

Conclusion of What Is to Be Learned:
1. Flow cytometric analysis of the DNA of T lymphocytes gives a histogram that reflects the cell growth cycle profile of each individual.
2. From the growth cycle profile, a program of treatment and management can now be initiated on an individual basis.
3. Lysate from the stimulated peripheral T lymphocytes of an environmentally ill individual is effective as an immune regulator.
4. T lymphocyte function and enumeration can now be assessed, as compared with the popular method of assessing, predominantly, only enumeration of T lymphocytes in immune deficiency illnesses.

Given, A. L. 1992. Flow cytometry, first principles. New York: Wiley-Loss.

Abnormalities of the Autonomic Nervous System Seen in Patients Who Have Silicone Breast Implants

Hirohiko Higuchi, MD
Kitasato University
Kanagawa, Japan

Approximately one to two million women in the United States have had silicone breast implants inserted for reconstruction or augmentation mammoplasty. And recently it is well known that patients who have silicone breast implants can develop a variety of immune disorders such as progressive systemic sclerosis. But to the best of our knowledge, the condition of the autonomic nervous system in patients who have silicone breast implants hasn''t been defined.

In this study, we have evaluated the function of the autonomic nervous system seen in patients who have silicone breast implants using pupillography (Iriscorder). Ninety-three percent of all patients had abnormalities on their pupillogram. This result suggests that a high frequency of change occurs in the autonomic nervous system in patients who have silicone breast implants.

Rads, Ruds, and Rids, the Third R

Allan D. Lieberman, MD
Center for Environmental Medicine
N. Charleston, SC

To the previously described clinical syndromes Reactive Airway Dysfunction Syndrome (RADS) and Reactive Upper Airway Dysfunction Syndrome (RUDS) is added a third RCReactive Intestinal Dysfunction Syndrome (RIDS).

These syndromes all sem to have the following in common:

1. An initial high level of, or significant environmental or occupational exposure to, a chemical or irritant, resulting in an acute clinical illness.
2. Development of a persistent or chronic hyper-responsiveness to multiple chemicals and irritants.
3. An apparent mechanism of inflammatory mediators and local tissue hyper-responsiveness.
4. Their importance in producing disability because of the multiple chemical or irritant triggers found in most industrial and occupational settings.

Seven cases are presented.

Goals and Objectives:

To introduce a new clinical syndrome describing the recognizing signs and symptoms in seven cases.


Brooks, S.M., M. Weiss, and I.L. Bernstein. 1985. RADS: Case reports of persistent airways hyperreactivity following high level irritant exposure. Journal of Occupational Medicine 27:473-475.

Gilman, A.G., L.S. Goodman, T.W. Rall, and F. Murad, eds. 1985. The Pharmacological basis of therapeutics. New York: Macmillan.

Meggs, W. 1993. Rhinolaryngoscopic examination of patients with the multiple chemical sensitivity syndrome. Archives of Environmental Health 48(1):14-18.

Lee, T.D.G., M. Swieter, and D. Befus. Dec. 1988. Mast cells, eosinophils, and gastrointestinal hypersensitivity. Gut and Intestinal Immunology/Immunology and Allergy Clinics of North America 8:468-483.

Stead, R.H., J. Bienenstock, and A.M. Stanisz. 1987. Neuropeptide regulation of mucosal immunity. Immunology Review 100:333.

Wyngaarden, J.B., and L.H. Smith, eds. 1982. Cecil textbook of medicine. Philadelphia: WB Saunders.

Early Man's Diet

Katharine Milton, PhD
University of California
Berkeley, CA

In the past, people tended to grow up and remain in the same culture and geographic region in which they were born. Thus, they ate time-tested diets developed over many generations by their ancestors in these same locales. In contrast, today most individuals are faced with a tremendous variety of food choices, and traditional dietary wisdom is largely a thing of the past. Ironically, it is also the case today that many chronic health problems are linked to diet including high blood pressure, atherosclerosis, heart disease, osteoporosis, several leading cancers, obesity, and others. This suggests that modern humans have somehow gotten out of step with their evolutionary biology in terms of diet. The ancestral line leading to our genus is generally agreed to have been strongly herbivorous. Indeed, as an order, most primates take the bulk of the diet from plant foods, particularly the leaves, fruits, and flowers of the dicotyledonous trees and vines composing the tropical forest conopy. If present-day primates are any indication, the primate gut was initially adapted for both the nutritive and defensive components of dicotyledonous C3 rather than mo C4 plantsCthe major food source of most modern human populations. Chemical analyses of wild plant foods eaten by nonhuman primates suggest that the past diet of human ancestors is likely to be different in many important respects from the diets humans consume today.


Goals and objectives:

To enhance our understanding of the possible causes of some current health problems associated with dietary factors, particularly to look at the nutrient content of some of the wild plant foods eaten by nonhuman primates today and human ancestors in the past and see in what ways they are similar to and different from the foods we currently rely on.


Sih, A., and K. Milton. 1985. Optimal diet theory: Should the Kung eat mongongos? American Anthropologist 87:395-401.

Milton, K., and R. Jenness. 1987. Ascorbic acid content of neotropical plant parts available to wild monkeys and bats. Experientia 43:339-342.

Milton, K. 1991. Pectin content of neotropical plant parts. Biotropica 23:20-92.

Milton, K. 1993. Diet and primate evolution. Scientific American 269:86-93.

Chamberlain, J.C., G.J. Nelson, and K. Milton. 1993. Fatty acid profiles of major food sources of howler monkeys (alouatta palliata) in the neotropics. Experientia 49(9):820-824.

Diet and Primates

Katharine Milton, PhD
University of California
Berkely, CA

As an order, primates are generally described as monivores, a term too general to convey any real idea of what primates actually eat. Is there a specific pattern of omnivory that characterizes the primate order? Numerous field studies show that primates are omnivores of a particular type in that the greatest percentage of their diet comes from plant foods, generally the leaves, fruits, and flowers of tropical forest trees and vines. This particular dietary focus poses some challenging problems to a nascent plant eater and the particular response to these problems in essence is what has made primates primatesCthus, the old adage, you are what you eat. Primates generally rely heavily on behavioral rather than morphological adaptations to solve many of their dietary problems. Indeed, the fossil record shows that primates have been characterized by a large brain-to-body ratio since the inception of the order. Certain types of plant-based diets appear to call for greater mental abilities than others and these are the primate lineages generally showing the largest brain-to-body ratios. When we examine the probably evolutionary trajectory of our own genus, Homo, we find evidence for the same basic primate trend of using brain power and behavior to solve dietary problems. In particular, the development of a division of labor and food sharing appears to be a unique trait of the human foraging strategy and one which has conferred obvious evolutionary benefits.


Goals and Objectives:

To clarify dietary niche of primates and use this information to examine current food habits and nutritional content of foods eaten by individuals in western nations.

Conclusions of what is to be learned:

Primates are plant-eaters that traditionally have focused feeding on the highest quality plant foods available in the forest canopy and have lowered the costs associated with the procurement of these foods largely through behavioral adaptations conferred by an unusually large brain.


Silton, K., and R. McBee. 1982. Structural carbohydrate digestion in a New World Primate, Alouatta palliata Gray. Comparative Biochemistry and Physiology 74:29-31.

Milton, K. 1984. The role of food processing factors in primate choice. In Adaptations for foraging in nonhuman primates, ed. P. Rodman and J. Cant, 249-279. Columbia University Press.

Milton, K. 1987. Primate diets and gut morphology: Implications for human evolution. In Food and evolution: Toward a theory of human food habits, ed. M. Harris and E.B. Ross, 93-116. Philadelphia, PA: Temple University Press.

Milton, K. 1988. Foraging behavior and the evolution of primate cognition. In Machiavellian Intelligence: Social expertise and the evolution of intellect in monkeys, apes and humans, ed. A. Whitten and R. Byrne, 285-305. Oxford: Oxford University Press.

Milton, K. 1993. Diet and primate evolution. Scientific American 269:86-93.

Environmental Factors and Experimental Allergic Conjunctivitis

M. Miyata, MD
T. Namba, MD
H. Nishimoto, MD
H. Kashiwagi, MD
T. Nakayama, MD
S. Ishikawa, MD
Kitasato University
Kanagawa, Japan

We have reported that experimental allergic conjunctivitis in guinea pigs was aggravated by extremely low dosage of organophosphorus pesticides and organochlorine herbicide as well as electromagnetic waves from cathode ray tube. Our next concern was other environmental factors besides the above that aggravate experimental allergic conjunctivitis.

The chemical factors in the environment examined were p-dichlorobenzene as air pollutant, trihalomethane was water pollutant, and some food additives such as food colorings (amaranth, tartradin), food preservative (BHA), and artificial sweetening. Those environmental chemicals were proven to have immunotoxicity at extremely low levels, and the dose response curve showed a bell-shaped curve similar to that of organophosphorus pesticides and organochlorine herbicide reported previously. They also revealed to have residual effects more than two weeks. Food colorings showed accumulative effects, moreover.

The physiological factor that seemed to have to be examined was ultraviolet (UV) light, because it becomes a big problem by ozone hall. Like electromagnetic waves, UV light at ordinal energy level aggravates the allergic conjunctivitis.

Much attention should be paid to the immunotoxicity of environmental factors even at extremely low levels.

Illness and Wood Preservatives The German Courts Make a Ruling

Jean Monro, MD
Breakspur Hospital
Hertfordshire, England

A German lawsuit known as the Wood Preservative Trial has been proceeding for some years.

The German legal system is one in which a judge can call expert witnesses and is not an adversarial system. The judge concerned, Dr. Thomas M. Seibert, Presiding Judge of the Regional Court, 26th Criminal Division in Frankfurt, called physicians to give reports on chemical sensitivity, toxicology, and neurology.

In May 1993 Athe court held two accused managers of the producer=s firm to be guilty of bodily harm and poisoning because of negligence. They were condemned to a year of imprisonment, which is set under probation and a fine of fifty thousand pounds each (120.000 DM).

Appeals are under way.

A review of this case and of wood preservatives and their effects will be discussed.


Goals and Objectives:

To present the findings of a German Court in relation to toxicity of wood preservative experienced by families in Germany and to provide an understanding of the historical context and future implications of the ruling.

Conclusion of what is to be learned:

Knowledge of a historical court ruling in Europe and understanding of the personal/industrial and political factors leading to wood preservative toxicity.


The case of: The State vs. Desowag in the Landgericht (5/26 KLS 65 Js 8793/84). Frankfurt am Main, Germany. 1 June 1992.

Wood Preservatives Their Use and Toxicity

Jean Monro, MD
Christopher Heard, MD
Breakspear Hospital
Hertfordshire, Eng.

Timber in use can be damaged by the destructive agents of fungi, insects, marine borers and fire, making it unsuitable for normal purposes.

Both fungus and insect treatments are widely used to preserve wood; it is these that the presentation will be particularly addressing. Preservatives can be widely classified into the following:

1. Creosote and heavy tar oil preservatives;
2.. Water-borne preservatives; and
3. Organic solvent preservatives.

It is the third of these, organic solvent preservatives, which gives the greatest cause for concern. They include pentachlorophenol, tributyl tin oxide and the metallic naphthenates and these may contain dieldrin and gamm-hexochlorohexane (Lindane). The toxicity of the more commonly used preservatives will be presented.


Goals and Objectives:

Provision of an overview of the use and toxicity of chemicals used in the preservation of timber with detailed toxicological information relating to Lindane and Pentachlorophenol.

To provide an understanding of the historical and potential effects of wood preservative in human health.

Conclusion of what is to be learned:

An overview of wood preservatives and their use and toxicity; detailed appreciation of the absorption, storage, distribution and toxicity of Lindane and Pentachlorophenol.

Urinary Sulphite in the Chemically SensitiveCAn Index of Detoxification Capacity

Jean Monro, MD
Christopher Heard, MD
Breakspear Hospital
Hertfordshire, Eng

Some asthmatic children are sensitive to sulphite (Towns et al. 1994), and conversion of sulphite to sulphate may be defective, which in turn may lead to a deficiency of sulphate for conjugation reactions (Wright and Kirk 1989). The conversion of sulphite to sulphate occurs via the enzyme sulphite oxidase. If this enzyme is underactive, then inorganic sulphite can appear, inappropriately, in the urine. There have been reports of allergic symptoms improving with intensive supplementation of the molybdenum upon which sulphite oxidase is dependent. This indirect measure of molybdenum status (urinary sulphite) may be important in other detoxification enzymes, as molybdenum is essential for the function of other enzymes including xanthine oxidase and aldehyde dehydrogenase.

Measurements of urinary sulphite in chemically sensitive patients have been undertaken at Breakspear Hospital, and the results will be presented.


Goals and Objectives:

1. To provide understanding of enzyme detoxification by oxidation of sulphite to sulphate oxidase.
2. To provide appreciation of Molybdenum dependence of sulphite oxidase.
3. To provide awareness of measurement of urinary sulphite as an index of sulphite oxidase activity, and, indirectly, of Molybdenum status.
4. To present findings of urinary sulphite estimations in a group of chemically sensitive patients attending Breakspear Hospital.

Conclusions of what is to be learned:
Sulphite oxidase is an essential detoxification enzyme whose activity can be simply estimated by measurement of inorganic sulphite in urine. It is a Molybdeum-dependent enzyme, in common with Xanthine oxidase and Aldehyde dehydrogenase.

Allergic and chemically sensitive patients have a greater than expected underactivity of this enzyme and hence raised urinary sulphite.

Towns, S.J., and C.M. Mellis. 1984. The role of acetyl salicylic acid and sodium metabisulphite in chronic childhood asthma. Pediatrics 73:631-37.

Wright, J., and K. Littleton. July 1989. Defects in Sulfur Metabolism. International Clinical Nutrition Review 9(1): pages?

Wright, J., and F.R. Kirk. Oct. 1989. Defects in Sulphur Metabolism II, Apparent Failure of Sulphate Conjugation. International Clinical Nutrition Review 9(4): pages?

Sick Schools What Do You do?

Doris J. Rapp, MD
Environmental Allergy Center
Buffalo, NY

In 1992, a new carpet was placed in an upper New York state school. About 30% of the teachers had symptoms by October. Because of their union, they received medical help at that time. The students' diagnosis was recurrent flu, and they were not seen for an EI evaluation until about December.

This presentation will answer the following questions: Who developed which signs and symptoms and why? What clues indicated veracity of history? How do you confirm your suspicions and prove the probable cause? How and when do you treat the children and teachers? What=s the response to treatment thus far? Political, economic, social and governmental agency aspects of this problem will also be addressed.

Supplementary sheets for essential addresses and phone numbers will be supplied at time of presentation.


Goals and Objectives:

To summarize the results concerning these patients who are representative of many others seen in daily clinical practice.

Conclusions of what is to be learned:

We are all faced with a similar challenge. Is the patient sensitive to something inside the school? Are the waters muddied by other exposures at home or elsewhere? Does the patient have some other medical problem that is totally unrelated to the school or unrelated to the environment? One cannot ideally seaparate the many variables, but it is often surprisingly simple to detect if a school is a major factor because the child or teacher will repeatedly become ill shortly after arriving in school and improve shortly after returning home.

Biological Mechanisms of Chemical Sensitivity

W.J. Rea, MD
Environmental Health Center-Dallas
Dallas, TX

The biological mechanisms of chemical sensitivity are becoming much more clearly defined. Defects may be found in surface barriers, in neurovascular triggering, and in the end organs that are involved. However, there is a nondefined switch mechanism that exists that moves the patient from sensitive to nonsensitive. Observations on some patients who were well before exposure and then developed sensitivity and then reverted back to wellness have been observed. Mechanistic features of the sensitivity are related to microvascular hypoxia, immune changes, nonimmune changes, and deficiency and excess in vitamins, minerals, amino acids, and fatty acids.

Cyclic Phenomena Observed in the Environmental Unit

W.J. Rea, MD
Environmental Health Center-Dallas
Dallas, TX

Studies over the last 20 years at the Environmental Health Center-Dallas using controlled environments have defined numerous cycles in the spectrum of chemical sensitivity. There are yearly cycles of the individual and the weather. There are monthly cycles, bimonthly cycles, and 24-hr cycles. There are both 24-hr human cycles and 24-hr weather cycles that can adversely or positively influence the chemically sensitive patient's health. Knowledge of the existence of these cycles, perception of their actions and how the individual chemically sensitive patient responds is necessary for the environmental patient to respond.

Melatonin: Antioxidant Par Excellence

Russel J. Reiter, PhD
University of Texas Health Science Center
San Antonio, TX

The pineal hormone melatonin was recently demonstrated to be a potent scavenger of the highly toxic oxygen free radical, the dydroxyl radical (COH). Molecules that scavenger or neutralize oxygen-based radicals are referred to as antioxidants. The previously best-known antioxidant was glutathione, a compound synthesized in the body where it exists in high concentrations. However, when glutathione was compared with melatonin in terms of its ability to quench the COH, melatonin proved to be 5X more effective than did glutathione. Thus, the concentration of scavenger required to quench 50% (the IC50) of the COH produced in an in vitro system was 21FM for melatonin and 123 FM for glutathione. Compared to mannitol, a well-known exogenous scavenger found in some foods, melatonin was roughly 15X more effective. Melatonin=s protection against oxidative damage may be somewhat specific for nuclear DNA. The highest concentrations of melatonin seem to be found in the nuclei of cells, and it appears that melatonin is retained in the nucleus by virtue of its ability to bind to DNA. Melatonin likely forms hydrogen bonds with the adenine-thymine base pairs in the DNA molecule. In so doing, melatonin stabilizes and thereby prevents denaturation of double-stranded DNA thereby increasing its melting temperature (Tm). Likewise, when double stranded DNA is denatured by the addition of Cu++ and melatonin prevents the denaturing action of the copper ions. The binding of melatonin to DNA puts melatonin in a unique position to scavenge COH produced in the vicinity of DNA. Because of their very high reactivity, COH travel less than 15A before they interact with macromolecules. Therefore, to afford protection to DNA, melatonin must be in the vicinity of the nucleotide.


Goals and Objectives:

To provide experimental proof of the potent free radical scavenging ability of the pineal hormone melatonin and to illustrate how melatonin protects the genetic material, DNA.

Conclusion of what is to be learned:

Melatonin, an endogenously produced hormone in the pineal gland is the most potent free radical scavenger in the body.


Tan, et al. 1993. Endocrine J 1:57-60.
Reiter, et al. 1993. [Letter] Neuroendocrinol 15:103-116.
Poeggeler, et al. 1993. J Pineal Res 14:151-158.

Melatonin, Free Radicals, and Cancer Initiation

Russel J. Reiter, PhD
University of Texas Health Science Center
San Antonio, TX

Free radicals are molecules, or portions thereof, which contain one or more unpaired electrons in their outermost orbital. As such, free radicals are highly toxic to cellular macromolecules, including DNA. Oxygen is a major source of free radicals (the oxygen-based radicals) that are formed in the body. The most toxic, i.e., damaging, of the oxygen-based radicals is the hydroxyl radical (COH). COH are specifically scavenged (quenched) by the pineal hormone melatonin. Because of this, melatonin may be a very effective agent in the prevention of cancer initiation. When animals are injected with the indirect carcinogen, safrole, massive DNA damage occurs in the nuclei of liver cells. Safrole produces this damage because it induces the formation of free radicals which, in turn, damage DNA. If animals are given pharmacological amounts of melatonin just prior to their treatment with the carcinogen, up to 99% of the damage to hepatic DNA is prevented. Any substance that reduces damage to DNA can be regarded as an anticancer agent, since altered DNA, if it goes unrepaired, can mutate and a tumor may result. Physiological levels of melatoninn, likewise, are effective in reducing DNA damage that is a consequence of the administration of safrole. For example, the nighttime rise in circulating melatonin inhibits 20% of the DNA damage produced by the administration of massive quantities (100 mg/kg) of safrole. This finding suggests that at levels of carcinogens to which humans are normally exposed, melatonin would be very highly protective of DNA against carcinogen-induced damage. Thus, melatonin, a hormone normally produced in the body, is a potent agent against cancer initiation by virtue of its ability to scavenge free radicals. Melatonin may specifically protect DNA because it binds to the adenine-thymine base pairs in the DNA molecule.


Goals and Objectives:

To define the mechanisms whereby the pineal hormone, melatonin, protect nuclear DNA from damage by toxic oxygen-based radicals. Damaged DNA, if it goes unrepaired, can lead to cancer.

Conclusions of what is to be learned:

Since melatonin, which is normally produced in the body, is such a potent free radical scavenger, it also provides important protection against cancer initiation. Thus, any environmental factor (e.g., light at night or magnetic field exposure) that reduces nighttime melatonin production could lead to an increased cancer risk.


Tan, et al. (1993). Cancer Lett 70:65-71.

Reiter, et al. (1993). Adv Pineal Res 7:130-144.

Allergy and Cereals

Saida Robbana-Barnat, MD
Jacques Fradin, MD
Institut de Medicine Environnementale
Paris, France

In this paper, we have studied the link between cereals and diseases as its clinical consequences are often underestimated. The cereal most commonly incriminated is wheat both when it is ingested and when it is inhaled.

The best known disease caused by cereals is celiac disease (CD). Because many of its clinical features are atypical and nonstandard, long delays still exist in the diagnosis of CD, which may have serious consequences.

Several diseases have been described as being associated with CD. Thus, CD may be suspected in patients suffering from these diseases.

Among other long-term problems, an increased risk of malignancy and mortality has been reported in patients on a normal or even gluten-poor diet. Thus, for the sake of patients, a lifelong strict gluten-free diet is mandatory.

It has become necessary to make physicians more aware of the problem and to label gluten additives in foodstuffs for sale. Health care professionals, the food industry, and the public should be educated about CD and gluten-free diets.


Goals and Objectives:

Our objective has been to investigate atypical forms of diseases related to cereals and more particularly celiac disease, which is associated with several other diseases, making long-term risks very harmful.

Unlike classical and true allergies, where the aim is the disappearance of symptoms, with celiac disease the objective is to prevent long-term occult risks that may exist without any clinical symptoms.

Thus, increased awareness of the disease may lead to a lesser risk of developing other diseases.

Conclusions of what is to be learned:

Much more support and research are needed in the treatment of celiac disease. There is a real need for better training of health care professionals, the food industry, the public, and the authorities. The latter is concerned because of a lack of labels for gluten additives on foodstuffs for sale.

Celiac patients have problems in adopting a gluten-free diet, more particularly when they eat out, as it seriously interferes with a normal lifestyle.

In most cases, this disease can be treated through a global environmental approach that goes beyond the classical medical field application.


More than 150 references. You can find some of them below.

Davidson, A.G., and J.A. Campbell. 1992. Celiac disease and dermatitis herpetiformis: National survey indicates delays in diagnosis. Canadian Family Physician 38:2604-2607.

Sigurs, N., et al. 1993. Prevalence of celiac disease in diabetic children and adolescents in Sweden. Acta Pediatr 82:748-751.

Collin, P., et al. 1989. Atypical celiac disease found with serologic screening.

Ascher, H., et al. 1991. Increasing incidence of CD in Sweden. Archives of Disease in Childhood 66:608-11.

Pare, P., et al. 1988. Adult celiac sprue: Changes in the pattern of clinical recognition. J Clin Gastroenterol 10:395-400.

Troncone, R., and S. Auricchio. 1991. Gluten-sensitive enteropathy. Food Reviews International 7:205-231.

Bergman, TJ, et al. (1991). In Handbook of natural toxins, Vol. 3, ed. Anthony T. Tu. New York: Marcel Dekker, Inc.

A Unique Method to Accelerate Xenobiotic Detoxication

Sherry A. Rogers, MD
Northeast Center for Environmental Medicine
Syracuse, NY

Researchers have shown that active diterpene esters, kahweol palmitate and cafestol palmitate trigger the hepatic production of glutathione-S-transferase in the small intestine and liver. Others have demonstrated that when these reach the liver through the enterohepatic circulation, they cause the bile ducts to dump their accumulated xenobiotic products of conjugation into the colon. This, in turn, unblocks the backlog of other xenobiotics awaiting futher hepatic processing. Application of this inexpensive and easily performed at home technique takes only 20 minutes, costs less than $1.00, and within minutes can clear chemically induced reactions that formerly took hours or days to clear, as case examples will demonstrate. The applications of this acceleration of xenobiotic detoxication extend much further than for chemical sensitivity, for it is even more important in preventing deaths of patients on chemotherapy for cancer.


Goals and Objectives:

Many chemically sensitive patients can have their progress set back days and weeks by one inadvertent exposure that would be considered harmless to others. Many are incapacitated and even bedridden during this setback. We were searching for a way to reduce the recovery time.

Researchers have shown that the acive diterpene esters, kahweol palmitate and cafestol palmitate, trigger the hepatic production of glutathione-S-transferase in the small intestine and liver. Others have demonstrated that when these reach the liver through the enterohepatic circulation, they cause the bile ducts to dump their accumulated xenobiotic products of conjugation into the colon. This, in turn, unblocks the backlog of other xenobiotics awaiting further hepatic processing.

Application of this inexpensive and easily performed at home technique takes only twenty minutes, costs less than $1.00, and within minutes or hours can clear chemically induced reactions that formerly took hours or days to clear, as case examples will demonstrate. As an example, in one patient, chemical exposures that would leave this patient incapacitated for four days now only requires 1c hrs for recovery.

In a survey of thirty patients who used this method to accelerate detoxication after chemical exposure or dietary indiscretions, 27 (90%) felt it enabled them to clear faster. The application for this acceleration of xenobiotic detoxication extends much further than for chemical sensitivity, for it is even more important in preventing deaths of patients on chemotherapy for cancer, the lethal retinoic acid syndrome and much more.


Lam, L.K., et al. 1987. Effects of derivatives of kahweol and cafestol on the activity of glutathione-S-transferase in mice. J Med Chem 30:1399-1403.

Lam, L.K.T., V.L. Sparinus, and L.W. Walterbery. 1982. Isolation and identification of Kahweol palmitate and cafestol palmitate as active constituents of green coffee beans that enhance glutathione-S-transferase activity in the mouse. Cancer Res 42:1193-1198.

Rogers, S.A. 1994. Wellness Against All Odds. (For additional references and information) Syracuse, NY: Prestige Publishers. (Box 3161, Syracuse, NY 13220).

Experience with Detoxification at the Environmental Health Center-Dallas

Gerald H. Ross, MD
Environmental Health Center-Dallas
Dallas, TX

The history and experience with detoxification at the Environmental Health Center-Dallas (EHC-D) will be reviewed and discussed, with reference to historical perspectives, modern chemical environmental contamination, and resulting human pollution.

Factors that influence adipose tissue, metabolism, and common detoxification pathways will be reviewed, along with the physiological goals of sauna/detox therapy. The variable response to stored toxic xenobiotics will be presened as well as the percentage of clearance of a spectrum of xenobiotics from the blood after a detox program.

Data on patient outcomes will be presented along with illustration and case histories of detoxification in patients with chemical contamination and chemical sensitivity.


Goals and Objectives:

To review the mechanisms of detoxification and the major enzyme pathways in the body and to educate the participant on the methods used at the EHC-D for detoxification. Review of extent of clearance of certain xenobiotics and the outcomes of treatment in a group of patients, to present options to the practitioner who treats environmentally-triggered illness including chemical sensitivity.

Conclusion of what is to be learned:

Detoxification involving exercise, sauna, nutrient therapy, and massage can be very helpful in the treatment of chemical contamination and chemical sensitivity.


Rea, W.J., Y. Pan, and A.R. Johnson. 1987. Clearing of toxic volatile hydrocarbons from humans. Clinical Ecology 5(4):166-170.

Schnare, D.W., G. Denk, M. Shields, and S. Brenton. 1982. Evaluation of a detoxification regimen for fat- stored xenobiotics. Medical Hypotheses 9:265-282.

Schnare, D.W., M. Ben, and M. Shields. 1984. Body burden reductions PCBs, PBBs, and chlorinated pesticides in human subjects. Ambio 13(5-6):378-380.

Case Presentations (When Pried Open Reveal Valuable Clinical Pearls)

Gerald H. Ross, MD
Environmental Health Center-Dallas
Dallas, TX

To illustrate practical clinical pearls, a series of case presentations will be used, where a specific insight or intervention might help our understanding of disease processes and improve our investigation and treatment, within the framework of an Environmental Medicine approach.


Goals and Objectives:

To illustrate important features of the etiology, presentation, investigation, and treatment of environmentally triggered illnesses by means of case presentations.

Outline of Talk:

A series of short case presentations will be delivered and discussed.

Conclusions of what is to be learned:

Practical insight that will help the participant be more effective in helping patients with environmentally-triggered illness.


Rea, W.J. 1993. Chemical sensitivity. Boca Raton, FL: Lewis Publishers.

Ross, GH. 1992. The history and clinical presentation of the chemically sensitive patient. Toxicology and Industrial Health 8(4):21-28.

Ross, GH. 1992. Treatment pptions in multiple chemical sensitivity. Toxicology and Industrial Health

Use of the ALCAT Blood Test in Treatment of Patients with Food and Chemical Sensitivity

Douglas H. Sandberg, MD
University of Miami
Miami, FL

We have had the opportunity of using the ALCAT screen blood test for the past nine years to evaluate patients with food sensitivity. It is based on reactivity of whole blood to specific extracts or substances with reactions producing alterations in size of WBCs as well as changes in platelets. In the past two years, the test has been expanded to include testing for some chemical compounds as well. Over this time the test has matured and is performed now with automated equipment. We have results on tests for 790 individuals including both children and adults. As dictated by the nature of our practice, we have evaluated small numbers of patients with a range of different medical problems, including gastrointestinal disorders, migraine, chronic urticaria, atopic dermatitis, asthma, allergic rhinitis, AD(H)D, and chronic fatigue syndrome. We will describe results of these tests, including correlation with open oral challenges after a period of 4-5 days avoidance and ID skin testing as well as response to treatment. Treatment consisted of avoidance when possible as well as allergy extract therapy by injection of SL route. These results have shown good correlation with both challenges and provocation of symptoms by ID tests, and we have concluded that this test is the best tool presently available for initial screening for possible food and/or chemical sensitivity (non-IgE mediated), with confirmation of results by one or both of the other methods.


Goals and Objectives:

We will describe results of these tests, including correlation with open oral challenges after a period of 4-5 days avoidance and ID skin testing as well as response to treatment. Treatment consisted of avoidance when possible as well as allergy extract therapy by injection or SL route.

Conclusions of what is to be learned:

These results have shown good correlation with both challenges and provocation of symptoms by ID tests, and we have concluded that this test is the best tool presently available for initial screening for possible food and/or chemical sensitivity (non-IgE mediated), with confirmation of results by one or both of the other methods.


Sandberg, D.H. 1990. Gastrointestinal complaints related to diet. International Pediatr 5:23-29.

Fell, P.J., S. Soulsby, and J. Brostoff. 1991. Cellular responses to food in IBSCAn investigation of the ALCAT test. J Nutr Med 2:143-149.

Abnormalities in Scintigraphic Examinations of the Brains of Desert Storm/Desert Shield Veterans

T.R. Simon, MD
D.C. Hickey, MD
Nuclear Medicine Consultants
Dallas, TX

R. Harrell, PhD
University of North Texas
Denton, TX

A. Johnson, DO
G. Ross, MD
W. Rea, MD
Environmental Health Center-Dallas
Dallas, TX

This study addressed the question of whether Desert Shield/Desert Storm veterans who present with abnormal neurological and psychological symptoms, exhibit abnormalities by brain scintigraphy that are typical of those seen in patients with documented exposure to neurotoxic compounds.

Exposure to cocaine, alcohol, and other substances of abuse can result in abnormal scintigrams of the brain using tracers such as Tc-99m HMPaO. This study used techniques described by others and added an earlier image set obtained nearly concurrently with the injection. This earlier data set depends upon a fast gamma camera system and a controlled injection procedure to image the blood flow distribution as the tracer enters the brain. This two-phase examination thus combines regional cerebral blood flow information with images of the tracer distribution after the tracer has undergone a chemical change through which the fat soluble tracer that enters the neurons is trapped within the cell.

In addition to the well-described functional image abnormalities, we noted a mismatch in regional activity between the image sets of the veterans. This degree of mismatch was not seen in control subjects who have not had known exposure to neurotoxic chemicals. Patterns identified from examinations performed on patients with known exposure to petroleum distillates, pesticides, and other materials linked with neurotoxicity were identified in some veterans of the Desert Shield/Desert Storm operation.

Moreover, we have seen a reversion of these patterns toward normal after therapy. Such reversion has followed independent assessments of clinical improvement.

The Electromagnetic Aspects of Biological Cycles

Cyril W. Smith, PhD
Salford University Business Services, Ltd.
Salford, England

The literature concerning electromagnetic influences on biological cycles is surveyed. Experimental work on the frequencies of a single cell of Acetabularia, T4 lymphocytes in culture and the human subject show that there are both simulating and depressive frequencies which occur alternately as frequency is increased. These both exhibit a cyclic variation in frequency occurring as discrete humps every few minutes. Exposure to weak fields of a stimulating frequency increases the rate at which the frequency jumping occurs. Exposure to weak fields of a depressive frequency completely halts the humping at this frequency. The clinically therapeutic frequencies are the stimulating ones, the depressive frequencies create stress by suppressing frequency fluctuations, which in hypersensitive persons lead to the observed patient specific reactions.

Exposure as a Cause of Phasic Muscle Weakness

RC Sweeting, MD
Fraser Valley Orthopaedic and Sports Medicine Clinic
Abbotsford, British Columbia, Canada

Musculoskeletal pain syndromes have become epidemic in the western world and are extremely resistant to treatment.

Such patients generally exhibit a particular type and pattern of weakness of the phasic musculature and shortening of the postural musculature. They also frequently have numbness in a nonanatomical distribution, with postural decompensation and dysfunction in several other bodily systems.

Rectified electromyography shows a specific deficit of the load compensation reflex of these phasic muscles, indicating a failure of centrally mediated control. The cause may likely be due to xenobiotic exposure, such as volatile organic solvents and/or organochlorine pesticides, which can be frequently detected in such patients.

Treatment by environmental control, a nutritional program and detoxification methods, along with a specific exercise program, can restore the load compensation reflex, muscle power and extensibility, with a subsequent resolution of the pain syndrome in certain patients.


Goals and Objectives:

To discuss the probable relevance of xenobiotic exposure in the etiology of chronic musculoskeletal pain associated with a dysfunctional load compensation reflex.


Chronic musculoskeletal pain syndromes and repetitive strain injury have become epidemic in the western world and are quite recalcitrant to currently available treatment methods.

These complaints are generally named by the site of the origin of painCfor example, patellar tendonitis, tennis elbow, low back pain, etc. However, such diagnoses say nothing about any likely etiology.

Such patients generally exhibit a particular type and pattern of weakness of the phasic musculature and a shortening of the postural muscles. They also frequently have numbness in a nonanatomical distribution and postural decompensation. They may have dysfunction in several other body systems concurrently.

Standard electromyography does not reveal any abnormality. However, rectified EMG shows a specific absence of the load compensation reflex, indicating a possible failure of centrally mediated control.

Without this protective reflex, tendons, ligaments, and bones are subjected to progressive and repetitive overload, with subsequent tissue failure.

Several patients tested for xenobiotic load have shown elevated levels particularly of trichloromethane and/or organochlorine pesticides. Although they may well not be the causative agents, they do confirm ongoing exposure of such patients to xenobiotics. Also, certain individual patients do recall multiple contacts with organophosphate pesticides such as Chlorpyrifos.

Treatment by environmental controls, nutritional and detoxification methods, along with a specific exercise program, can restore the load compensation reflex, muscle power, and extensibility, with a subsequent resolution of the pain syndrome.

Conclusion of what is to be learned:

It is very likely that many chronic musculoskeletal pain syndromes are a further manifestation of an environmentally triggered illness.

Treatment of Mycotoxicoses with Protective Foods and Hydrogen Peroxide
Major A. Ramsay Tainsh, MBE
Industrial Consultant
Stockholm, Sweden

I first hear the work mycotoxin in Stockholm in September 1963. The word Mycotoxicoses has not been listed in the Oxford English Dictionary. However, I learned about Athe mouldy grain and the bloody mindedness diseases@ shrotly after my fourth birthday, when my mother went to live on a former indigo estate at Hasuli, North Bihar, India.

On the very first morning the head gardener arrived at dawn with a large basket of fruit, roots, and vegetables. I was fascinated by their sight and smell. The head gardener observed my interest and told me something I have never forgotten. AVery fresh fruits, roots and vegetables, spices, herbs, onions, and garlic contain an invisible substance that prevents and cures the diseases of the monsoon season. This invisible substance withstands cooking, but is lost forever when wilting sets in. The cook, who was standing by, added "the same applies to fresh fish".

My training in domestic gardening began that day along with the gardener's son. Later in the season I was taught how to harvest grains and thoroughly dry them before airtight storage in a windowless room. While the grain was turned to ensure even sun drying, the children were taught the Bihari sayings. We were also taught that spoilt grain remained unwholesome. It is impossible to raise healthy, happy children or livestock on spoilt grain. We were also taught how to treat the mouldy grain and the bloody mindedness diseases by avoiding alcohol and all allopathic drugs. All that was needed was fresh foods, grown with compost, and fresh fish.

Later on I learned that fresh fish and garden produce were called by the Indian Medical Service "protective foods". They are protective because they contain a trace of natural hydrogen peroxide and cure all forms of mycotoxicoses.