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CHEMICAL ENVIRONMENT W.J.REA.

The rapidly accelerating rate of growth of modern technology has been

accompanied by a proliferation of a wide variety of new toxic chemicals such

as styrene, polyesters, polythene, etc. Recent studies1-3 show that nearly

50% of the global pollution isolated from natural products or synthesized

which enter the atmosphere are generated by man. The pervasiveness of toxic

chemical agents is well documented. In 1987, American industry poured 22

billion lb. of toxic chemicals into the air, food and water. Overall, Texas,

ranking first in air and land releases,4 dumped the most pollutants. Every

day several million gallons of chemicals are emptied into Lake Erie, which

is the source of drinking and bathing water for most cities from Toledo to

Cleveland, OH, to Buffalo, NY.

Inorganic pollutants include ozone, carbon monoxide, nitrous oxides, sulphur

dioxides, heavy metals,5-10 and other metals (e.g., Al, Cu, etc.).11,12

Organic pollutants include pesticides, formaldehyde,13 solvents (e.g.,

toluene and xylene), drugs,14 terpenes, cleaning chemicals, cigarette smoke,

combustion products, consumer products (e.g., clothing, building materials,

hygiene products, etc.),15-17 and biological compounds (mold toxins).18,19

The most toxic organic pollutants are those classified as halogenated

aromatic and aliphatic hydrocarbons.20

According to the EPA,21 more than four million chemical compounds are

currently recognised. Over 60,000 of these are produced commercially, and

about 3 new compounds are introduced each day. The rampant widespread

presence of hazardous chemicals in our environment has become critical.

Unfortunately, the link between chemical sensitivity and our individual

wellbeing described by Randolph22 over 35 years ago has been ignored until

now. While celebrated instances of gross contamination through industrial

waste have long been the object of professional attention, only recently

have literally thousands of synthetic chemical products, heretofore believed

innocuous, been incriminated as agents of homeostatic dysfunction.

Throughout this book, we will emphasize understanding and interpreting the

effects of this environmental load on individual malfunction.

In our opinion, the major stumbling block in recognising the etiology of

chemical sensitivity and many instances of resultant fixed-named diseases

has been the general failure of the medical profession to appreciate the

massive increase in and adverse effects of exposure to environmental

pollution. Nonetheless, ten environmental centres and thousands of

physicians and scientists on four continents acknowledge the effects of

environmental pollution on human health and have contributed to the

scientific and clinical evidence for the existence of chemical sensitivity.

CHEMICAL SENSITIVITY W.J.REA.

Definition:

Chemical sensitivity is one of the major manifestations of environmentally

triggered disease and is the main focus of this book. It is an adverse

reaction(s) to ambient levels of toxic chemical(s) contained in air, food,

and water. The nature of these adverse reactions depends upon the tissue(s)

or organ(s) involved, the chemical and pharmcologic nature of the

substance(s) involved (i.e., duration of time, concentration, and virulence

of exposure), the individual susceptibility of the exposed person (i.e.,

nutritional state, genetic makeup, and toxic load at the time of exposure),

and the length of time and amount and variety of other body stressors (i.e.,

total load), and synergism at the time of reaction(s).

ALLERGIC AND TOXIC RESPONSES W.J.REA.

Definition:

Chemical allergies are a small but significant part of the overall spectrum

of chemical sensitivity. They may involve both allergic (immunologically

mediated mechanisms including all of the four types of hypersensitivity

reactions) and toxic (nonimmune mechanisms) responses. They involve the

mechanisms of the 1gE class of immunoglobulins. An example of chemical

allergy is the 1gE-mediated toluene diisocyanate antigen/antibody reaction

which frequently manifests itself as asthma or some other form of

respiratory or vascular dysfunction. Other immune mechanisms such as 1gG,

cytotoxic response, immune complex (1gG + complement), or T and B cell

abnormalities are often involved in chemical sensitivity, although these

reactions are frequently secondary responses following an initial enzyme

detoxification response. Failure of enzyme detoxification appears to be the

prime mechanism in chemical sensitivity. Regardless of the mechanisms

involved, clinical manifestations of chemical sensitivity may be the same.

For example, rhinitis may occur either as an 1gE response to toluene

diisocyanate, or it may be an enzyme detoxification system response to

formaldehyde.

CAUSES OF CHEMICAL SENSITIVITY W.J.REA.

Chemical sensitivities may arise in several ways. Individuals who survive

near-fatal exposures to toxic substances often experience lowered resistance

to disease as a result of the depletion of their nutrient pool brought on by

exposure. They may then develop chronic symptoms of ill health. If these

people are later exposed to ambient doses of toxic chemicals, they may

experience additional and/or enhanced symptoms. " Spreading, " which can

involve both new organ systems and increased sensitivities to additional

substances, may occur. For example, an individual working in a chemical

plant may be exposed to high doses of xylene after an explosion. He

immediately develops headaches and flu-like symptoms that become chronic.

Weeks later, after ongoing ambient exposures in the workplace and at home,

this person develops asthma and sensitivity to ambient doses of various

toxic and nontoxic (e.g., perfume) substances. Of the chemically sensitive

patients seen at the EHC-Dallas, 13% relate the onset of their sensitivity

to a severe acute exposure.

Three major incidents have occurred in the 20th century which graphically

illustrate that chemical sensitivity may be caused by a significant, acute

exposure to toxic substances. The first occurred during World War 1 when

many of the troops were gassed with mustard gas.23,24 The clinical aftermath

for many of the survivors was the development of chemical sensitivity. The

second incident involved military personnel who were sprayed with defoliants

while serving in Vietnam. The " agent orange " syndrome, as symptoms from this

exposure where later dubbed, persisted for years after their initial

contact. The third incident occurred in Bhopol, India, where an accidental

atmospheric exposure to large quantities of cyanate left an estimated 86,000

people injured.25 Several months later, many remained afflicted with

recurrent symptoms that are today believed to be manifestations of chemical

sensitivity.

Chemical sensitivity can occur subsequent to severe bacterial, viral, or

parasitic infliction. Of the patients treated for chemical sensitivity at

the EHC-Dallas, 1% have traced the origin of their illness to such an event.

The onset of chemical sensitivity has also been attributed to exposure to

ambient doses of toxic chemicals following massive trauma, childbirth,

surgery, or immunizations. At the EHC-Dallas, 12% of our patients associated

massive trauma with the start of their illness; 9% identified childbirth as

the triggering event; 2% traced onset to surgery; and linked their illness

to other causes.

In contrast to those who develop chemical sensitivity as a result of acute

exposure to toxic substances, there exists another group for whom a specific

cause of illness is often difficult to discern. This group includes

individuals who have become chemically sensitive following accumulative

subacute toxic exposures over time. Of our patients at the EHC-Dallas, 60%

fit into this category.

Only 2% of our chemically sensitive patients are unable to account for the

specific events that precipitated onset of their illness. Because we can

link only 28% of our patients' illnesses to employment that involved

exposure to high levels of toxic chemicals, such as work in pesticide plants

or refineries or work involving pesticide spraying, we speculate that some

cases of chemical sensitivity may evolve as a result of a series of events

that occur with the passage of time. These events may include an

individual's long-term exposure to ever-present, subtle levels of pollutants

of which he is unaware. We believe that as these toxic, environmental

exposures occur, an insidious breakdown in resistance mechanisms takes

place. An individual's vulnerability increases and eventually chemical

sensitivity ensues.

Chapter 3. Principles, details how this phenomenon can occur. The

development of chemical sensitivity may be chronic and, therefore,

insidious. Individuals are often unaware of their developing sensitivity

until their chemical intolerance is such that only minuscule concentrations

of chemicals are needed to trigger symptoms of illness. At this point,

reactions to lower levels of toxic chemicals commonly occur. " Spreading, "

which involves both single-organ susceptibility to increasing numbers of

toxic chemicals and increasing susceptibility of new organ systems to one or

many toxic chemicals, may then follow. Fixed-named or end-stage disease may

occur, and eventually its course may proceed autonomously. For example, an

individual may develop arthralgia due to a sensitivity to formaldehyde.

Symptoms may fluctuate from many months to years. Then the individual may

develop sensitivities to more toxic chemicals, and arthritis may result.

Eventually, if left environmentally untreated, this individual may develop

fixed intractable arthritis that appears to be self-perpetuating.

" Low levels " of toxic chemicals have been implicated in the insidious onset

of some chemical sensitivities. Because of this connection, use of the term

" low level " itself needs to be reconsidered. We believe the term should not

be used because it implies that such levels are harmless when, in fact, many

chemicals are potentially lethal at low levels. The herbicide 2,4,5-T, for

example, has been found to be harmful in the parts-per-trillion or even

less. Furthermore, the levels of chemicals considered to be " low " by today's

standards are based on levels found in the average population or environment

and then termed " normal " and, hence, " low level. " Unless a toxic chemical

such as formaldehyde or pentane is generated by the body, the control levels

usually be nondetectable and not " low level. " For example, mathematical

calculations of a toxic substance reveal that the number of chlordane

molecules per cell is between 700 and 1500 when serum levels are measured at

one part per billion.

Too often, " safe " levels of toxic chemicals are assigned based on inferences

from an unhealthy control population who are assumed healthy because they

are able to function with a minimum of short-term illnesses such as flu or

symptom-masking medications. More commonly, levels are assigned from animal

studies. We believe the control population from which " safe " levels of toxic

chemicals ought to be derived should be those who are totally well and

medication free. This population in western society, however, is hard to

find. Until such a population can be isolated and appropriate " safe " levels

of toxic chemicals determined from their examination, we advocate a

reference point for blood and tissue levels of toxic chemicals that is

nondetectable.

Because modern medical practitioners accept occasional illness or medicated

wellness as part of general good health, we often fail to detect what may be

symptoms of the early stages of chemical sensitivity, and because we fail to

recognize these stages for what they are, we miss the opportunity to

intervene in time to reverse any ongoing damage or prevent the development

of serious, fixed-named illnesses. Instead, we misdiagnose and mistreat

symptoms, and as a result of our present attitudes and practices, we

probably grossly underestimate the incidence of chemical sensitivity.

MANIFESTATION OF CHEMICAL SENSITIVITY W.J.REA.

Symptoms of chemical sensitivity typically are multiple in nature. Usually,

one main organ is affected with secondary symptoms occurring in others.

End-organ responses are often in the smooth muscles of the cardiovascular,

gastrointestinal, urogenital, respiratory systems, or in the nervous system.

Also, common early responses may occur in the skin (such as nonjaundice

yellowing or edema) or other body organs. At their onset, symptoms of

chemical sensitivity are almost always reversible. As end-organ involvement

increases, however, responses are more difficult to decipher and reverse.

Pollutant damage can occur at the main site of pollutant entry or in the

detoxifying organ or it can be random, affecting any end-organ. Usually,

however, the weakest end-organ, that which has been genetically damaged or

previously harmed by trauma or exposure, is the first affected.

The sicker the patient with chemical sensitivity, the more diverse and

multiple are his responses to a large number of individual incitants,

suggesting primary and secondary organ involvement. For example, a patient

develops rhinitis on exposure to formaldehyde. Later in the course of his

illness, symptoms and signs of cystitis and colitis develop in addition to

the rhinitis. Although these various illnesses involve multiple systems and

organs, only one end-organ may ultimately be damaged as the result of

repeated insults to the same resistance mechanism. After this damage occurs,

however, end-organ failure follows and extreme fixed-named illness results.

For example, a mechanic constantly exposed to car exhaust could develop

general symptoms such as aches, pains, malaise, headaches, and fatigue.

These symptoms might then continue for several months until finally renal

failure or some other specific end-organ disease develops.

FACTORS INFLUENCING THE ONSET OF CHEMICAL SENSITIVITY W.J.REA.

Onset of chemical sensitivity is influenced by multiple factors including

total body load (burden), total toxic load, nutritional state, synergisms,

competition for storage, bioaccumulation, and biological half-life of the

chemicals themselves.

Total Toxic (Body) Load (Burden)

Total toxic (body) load is the sum of all pollutants in the body at one

time. When this accumulation overloads the system, chemical sensitivity can

occur.

Nutritional State

The nutritional state needed to maintain good health is depleted by toxic

exposure. Overload of pollutants can increasingly tax the detoxification

systems, eventually resulting in depletion of nutrients, system/organ

malfunctions, and susceptibility to illness.

Synergisms

Synergisms may be additive if the effects of the pollutants equal the sum of

the individual pollutants involved. For example, a patient whose sensitivity

to mold results in a runny nose and whose sensitivity to formaldehyde yields

burning eyes might react to exposure to both with runny nose and burning

eyes. Synergisms may also be potentiative where the effects of the

potentially harmful substances exceed the sum of the individual substances

involved. For example, mold toxin and formaldehyde combined may together

give swollen eyes along with a swollen face and extremities in addition to

or substituting for the burning eyes and runny nose. Occasionally,

individual pollutants may have antagonistic effects. If introduced

simultaneously,these substances may cancel each other's usual effects. For

example, salicylic acid and acetophenomen introduced simultaneously reduce

each others effects so that an individual exposed to these might exhibit

slight or no symptoms.

Competition for Storage and Removal

Some chemicals may be competitive for both storage and removal. DDT, for

example, increases and dieldrin decreases when they are introduced

simultaneously. Both compete for the same enzyme sites for detoxification

and metabolic function for detoxification, thus, one may circulate and even

be deposited in a lipid membrane while the other is metabolized and used or

cleared from the body. In our clearing studies, we have observed that

certain toxic chemicals cannot be removed until others are mobilized and

removed.

Bioaccumulation of Toxic Substances

The accumulation of a single agent in the body is dependent upon the dose

level, interval and duration of exposure, and half-life and lipophilic

nature of a chemical. Accumulation of a toxic substance also depends on an

individual's quantity and quality of immune and enzyme detoxication

responses along with his age and overall health. Accumulation may also occur

with constant exposures that allow no time for clearing.

The factors influencing chemical accumulation are solubility quotient, the

storage of chemicals in poorly perfused tissues, poor glomerular filtration,

intensive tubular reabsorption, and slow biotransformation. This

bioaccumulation may be likened to a layered sponge. Each layer fills due to

the excess pollutants that are absorbed yet unable to be immediately

metabolized.

With each new contact, more layers fill with excess pollutants until the

maximum load is exceeded and the disease process begun.

Biological Half-Life of Toxic Substances

The biological half-life of a chemical is one half the time a chemical takes

to disintegrate. It is usually calculated from animal exposures. It is also

based on inadvertent acute exposures of healthy people to toxic substances.

The half-life may have little relationship to the detoxification mechanisms

available. Metabolism may be high for initial high-dose exposures, but very

slow for low doses.26 This latter response will leave residue in blood and

tissues and may explain why low dose exposures can be a significant cause of

disease. (See Chapter 4. Nonimmune Mechanisms). Various investigators 27-29

have shown a relationship between the presence and the bioaccumulation of

foreign chemicals in human tissue and the incidence of cancer. This

correlation appears to exist for nonmalignant diseases as well. This finding

should cause even greater concern because apparently some environmentally

persistent halogenated hydrocarbons such as DDT or chlordane may have a

significant negative effect on the human immune system.30

REFERENCES

1. National Research Council, Safe Drinking Water Committee. " Drinking

Water and Health " (Washington. DC: National Academy of Sciences, 1977).

2. National research Council. " Indoor Pollutants " (Washington, DC: National

Academy Press, 1981), pp. 16-27.

3. Winslow, S.G. " The Effects of Environmental Chemicals on the Immune

System: A Selected Bibliography with Abstracts " (Oak Ridge, TN:

Toxicology Information Response Centre, Oak Ridge National Laboratory,

1981).

4. " Is Your Drinking Water Safe? " (Washington, DC: U.S. Environmental

Protection Agency, Office of Public Affairs, March 1977).

5. National Research Council, Safe Drinking Water Committee. " Drinking

Water and Health " Washington, DC: National Academy of Sciences, 1977).

6. Dooms-Goossens. A., A. Ceuterick, N. Vanmaete, and H. Degreef. " Follow-

up study of patients with contact dermatitis caused by chromates, nickel,

and cobalt, " Dermatologica 160(4): 249-260 (1980).

7. Freedman, B. J. " Sulphur dioxide in food and beverages: its use as a

preservative and its effect on asthma, " Br. J. Dis. Chest 74(2):128-134

(1980).

8. Mustafa. M. G., and D. F. Tierney. " Biochemical and metabolic changes

in the lung with oxygen, ozone, and nitrogen dioxide toxicity, " Am. Rev.

Respir. Dis. 118(6):1061-90 (1978).

9. Vermeiden. I., A. P. Oranje, V. D. Vuzevski, and E. Stolz. " Mercury

exanthum as occupational dermatitis. " Contact Dermatitis 6(2): 88-90

(1980).

10.Whittemore, A. S., and E. L. Korn. " Asthma and air pollution in the

L., A. area, " Am. J. Public Health 70(7): 687-696 (1980).

11.National Research Council, Safe Drinking Water Committee. " Drinking

Water and Health " (Washington DC: National Academy of Sciences, 1977).

12.Clemmenson, O., and H. E. Knudsen. " Contact sensitivity to aluminium

in a patient hyposensitized with aluminium precipitated grass pollen, "

Contact Dermatitis 6(2): 305-308 (1980).

13.Fisher, A. A. " Dermatitis due to the presence of formaldehyde in

certain sodium lauryl sulphate (SLS) solutions, " Cutis 27(4): 360-366

(1981).

14.Dahl, R. " Sodium salicylate and aspirin disease, " Allergy 35(2): 155-

156 (1980).

15.Frigas, E., W. V. Filley, and C. E. . " asthma induced by dust from

urea formaldehyde foam insulating material, " Chest 79(6): 706-707 (1981).

16.Imbeau, S. A., and C. E. . " Nylon stocking dermatitis. An unusual

case, " Contact Dermatitis 5(3): 163-164 (1979).

17.Larson, W. G. " Sanitary napkin dermatitis due to the perfume, " Arch.

Dermatol. 115(3): 363 (1979).

18.Olson, K. R., S. M. Pond, J. Seward, K. Healey, O. F. Woo, and C. E.

Becker, " Amanita phalloides-type mushroom poisoning, " West J. Med. 37:

282-289 (1982).

19., C. W. M. " Hypersensitivity to Maine tap water in children: Its

clinical features and treatment, " Nutr. Health 2: 51-63 (1983).

20.Laseter, J. L., I. R. DeLeon, W. J. Rea, and J. R. .

" Chlorinated hydrocarbon pesticides in enviromentally sensitive patients "

Arch. Clin. Ecol. 2(1):6 (1983). 21.Schnare, D. W., D. B. Katzin, and D.

E. Root, " Diagnosis and Treatment of Patients Presenting Subclinical

Signs and Symptoms of Exposure to Chemicals which Bioaccumulate in Human

Tissue, " P-150, Proceedings of the National Conference on Hazardous

Wastes and Environmental Emergencies. Cincinnati, OH. May 14-16, 1985.

22.Randolph, T. G. " Sensitivity to petroleum: Including its derivatives

and antecedents " J. Lab. Clin. Med. 40: 931-932 (1952).

23.Lefebure, V. The Riddle of the Rhine: Chemical Strategy in Peace and

War (New York: E. P. Dutton and Co., 1923).

24.Heller, C. E. " Chemical warfare in World War 1: The American

experience 1917-1918, " Leavenworth papers, No 10, Combat Studies

Institute, Library of Congress Cataloging in Publication Data, Forth

Leavenworth, KA(1984),pp. 24-25.

25.Shrivastava, P. Bhopal: Anatomy of a Crisis (Cambridge, MA: Ballinger

Publishing Company, 1987).

26.Balazs, T. " Hepatic reactions to chemicals, " in Toxicology: Principles

and Practices,Vol.1,A.L.Reeves, Ed.(New York: Wiley & Sons, Inc.,

1981), p,93.

27., G. M.,and J. H. Weisburger. " Chemical carcinogens, " in

Caserett and Doull's Toxicology: The Basic Science of Poisons,3rd ed., C.

D. Klassen, M. O. Amdur, and Doull, Eds. (New York: Macmillan

Publishing Co., Inc. 1986), pp. 124 and 153.

28.Unger, M., and V. Olsen, " Organochlorine compounds in the adipose

tissue of deceased people with and without cancer, " Environ. Res. 23: 257-

263 (1980).

29.Wasserman, N. M., D. P. Nogueira, S. Cucos, A. P. Mirra, H. Shibata,

g. Arie, H. and D. Wasserman. " Organochlorine compounds in

neoplastic and apparently normal gastric mucosa, " Bull. Environ. Contam.

toxicol. 20: 544-553 (1978).

30.Klotz, V. I., R. A. Bahayantz, V. G. Brysin, and A. Safarova, " Effects

of pesticides on the immunological reactivity of the body of animals and

man, " Gig. Sanit. 9: 35-36 (1978).

AN EXTRACT FROM:CHEMICAL SENSITIVITY VOLUME 1 BY PROFESSOR WILLIAM J. REA.

PUBLISHED 1992.

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