Food and Chemical Susceptibility after Environmental Chemical Overexposure: Case Histories William J. Rea, M.D., Director of Brookhaven Environmental Unit, Clinical Assistant Professor of Thoracic and Cardiovascular Surgery, University of Texas Southwestern Medical School, Dallas, TX Iris R. Bell, PhD, medical student, Stanford University School of Medicine, Stanford, CA

Charles W. Suits, B.S., Research Assistant

Ralph E. Smiley, M.D.

This study was supported by the Human Ecology Research Foundation of the Southwest, Inc.

Source: Rpt from Annals of Allergy, 41(2):101-110, Aug. 1978.
 
 

Chemical agents are rarely considered as precipitators of common diseases. However, Randolph1 has developed a diagnostic methodology which facilitates demonstration of cause-effect relationships between exposures to environmental incitants, such as common foods and chemicals, and the symptomatology of certain inflammatory diseases of otherwise unknown etiology. The senior author has further been able to relate this principle to establish triggering agents in some cases of phlebitis and vasculitis.2,3 In any given patient overload of synthetic chemicals and foods may disturb homeostasis and thereby provoke illness. This report deals with the role of overexposure to common synthetic chemicals in producing and propagating illness.
 
 

PART ICCASE STUDIES

Case A In her job at a semiconductor plastic factory, Mrs. A, a 53-year-old white female, mixed a variety of dry chemicals (sodium hyposulfate, ammonium sulfate, ammonium chloride, and nickel) into solution. She had worked at this job for approximately three years without symptoms. During this period she was breathing the fumes of these chemicals as well as those of the plastics. Her symptoms began with one month of malaise after an accidental overexposure to the chemical powders and synthetic solutions. The malaise gradually worsened when she was at work but improved when she was away from the factory. Later, symptoms consisting of irritation in the nose, otitis, ringing in the ears and hoarseness developed in the upper respiratory tract. Symptoms progressed to disabling nasal and ear problems and aphonia, which was treated by an otolaryngologist. The doctor recommended that she stay away from work for a period of time. As soon as she felt improved, she returned to work but was unable to obtain better ventilation around the chemicals and again became ill with sinusitis. Again she stayed away from work and felt better. Then she was moved to another part of the factory but still perceived ambient chemicals in the air. This time she developed wheezing, spontaneous bruising, gastrointestinal upset, skin rashes, and an inability to concentrate. At this point Mrs. A entered the environmental unit for chemical incitant testing. Her symptoms cleared in four days, at which time food challenges with less chemically contaminated food produced no symptoms. With inhalation chemical challenges a transient exposure to polyester clothing gave immediate hoarseness, followed by watering eyes, which lasted 30 minutes. Wearing permanent pressed clothing for one hour caused a stuffy nose, closed eustachian tubes, and a dry cough which lasted for six hours. A 10-minute exposure to nylon caused facial flushing and itching that lasted 20 minutes. The odor of ordinary tap water when exposed while drawing for a bath caused headache, while ingestion of one glass produced a stomach ache and extreme bloating. Chlorine odor challenge derived from fumes coming from diluted Chlorox did the same. Additives in commercial foods triggered confusion, bloating, nausea, headache, spontaneous bruising, and depression. Inhalation of Raid insecticide at ordinary ambient concentrations (ambient concentrations=the amount of a chemical substance in the air accepted as safe by commercial and governmental agencies) produced nausea, confusion, loss of equilibrium, and a dry cough. Fumes from the flames of a well-functioning gas stove caused lightheadedness, swollen glands, earache, sore throat, and pressure in the head. After discharge the patient was placed on a rotary diversified diet of chemically less contaminated foods and instructed to drink only spring water and to avoid chemicals that would incite her problem. Although the patient is now avoiding petrochemically contaminated situations and is steadily improving, one year after withdrawal from this contaminated environment she still can not work in her previous job. Case B This 41-year-old white female had been living comfortably in her home for the previous four years. She experienced symptoms of excess salivation, tremors, diarrhea, nausea, swollen hands, slight fever, fatigue, sore throat, and coughing within 24 hours of exposure to heptachlor after pesticide treatment of her home. These symptoms have continued for approximately one year with lessening of the tremors, diarrhea, and fever.

Since the overexposure Mrs. B is unable to tolerate common chemicals found in the ordinary living situation. Examples are as follows:

(1) Gas utilities (hot water and heat) produce symptoms of facial flushing and impaired intellectual functioning. Continued exposure results in nausea and vomiting.

(2) Vapors resulting from filling a bathtub with city water cause coughing and sore throat. This gets worse if she gets in the tub.

(3) Contact with permanent pressed or synthetic fabrics results in itching on back and shoulders.

(4) Pesticide inhalation produces headache and malaise.

(5) The patient is no longer able to wear perfume or to tolerate the odor on others. Headache results.

(6) Dye in fabric or clothing produces nasal tightness.

(7) Vinyl wallpaper causes vice-like pressure headache.

(8) Alcoholic beverages cause nasal burning and nausea.

(9) The patient=s reading speed is greatly decreased.

(10) Loss of tolerance to some formerly nonreactive foods has also occurred.

Case C

This 31-year-old white male owned and operated an automobile body shop. Mr. C entered the environmental unit with a chief complaint of not being able to talk due to slurred speech because of muscle malfunction in the area of the tongue and mouth. It must be noted that Mr. C had been previously diagnosed by other physicians as having cerebral palsy, but speech was perfect until five years prior to admission, at which time he had also developed symptoms of fatigue, backache, and neck pain. He related these to the odors of his spray paint. Two years ago his speech declined to a Amush-mouth sound.@ The referring doctor felt the condition to be environmentally triggered.

Under environmental control the patient=s speech gradually improved over a three-week period and was quite understandable before discharge. Five foods produced such symptoms as mild nausea and anxiety. Fifteen-minute ambient concentration exposures to natural gas, alcohol, cigarette smoke, formaldehyde, chlorine, and an insecticide produced no reaction. When challenged with a single inhalation of acrylic enamel spray paint, Mr. C immediately developed headache, nausea, chest pains, nervousness, heartburn, drawing sensation of his face, and severe impairment of his speech which lasted for 48 hours.

Case D This 37-year-old white female=s job was mixing chemicals to make typing correction fluid containing trichloroethylene and trichloroethane. She entered the environmental unit with chief complaints of headache, disorientation, pressure in back of head, spontaneous bruising, and severe eructation. The patient noted that at work she experienced esophageal burning, shortness of breath, and headaches. These symptoms would occur on contact with various chemicals in her work. She related her problems to the company physician, and he strongly suggested that it was Aall in her head.@ The patient had surgery for a hiatal hernia, but the substernal burning recurred and persisted as soon as she returned to work. Symptoms cleared in our environmental unit. An ambient concentration blind challenge with the fumes of the correction fluid led to the following sequence: two minutes after inhalation, mild pressure in head; 10 minutes, tightness in chest and difficulty breathing, hoarseness; 30 minutes, sneezing and complaining of stabbing pain in arms, coughing up sputum. Twenty-four hours later she still had a cough. A five-minute inhaled exposure of phenol caused headache. A single inhalation of formaldehyde produced sleepiness. Alcohol produced red patches on the area swabbed. Exposure to gas heat for 30 minutes made her head feel tight and painful. On challenge 11 foods reproduced symptoms such as nausea, headache, spontaneous bruising, edema, and GI distress. Before her occupational exposure to the correction fluid Mrs. D recalled no difficulty with perfumes, gasoline, car exhaust, synthetic fabric, or ordinary commercial foods. Her symptoms to various odors after this overexposure at work were as follows: (1) Perfumes caused headache and confusion immediately upon exposure;

(2) GasolineCa single inhalation produced a headache;

(3) Car exhaustCexposure triggered headache, pressure in back of head and mental confusion;

(4) Cooking odorsCprecipitated mental confusion, irritability, anxiety, and desperation;

(5) North Dallas air pollutionCcaused irritability and nasal burning;

(6) Synthetic fabricsCproduced an intensely disagreeable odor in addition to itching, peripheral edema, and spontaneous bruising. The patient was discharged on a rotary diet using chemically less contaminated foods, drinking only spring water and avoiding chemicals which incite her problems. Case E This 37-year-old white female worked in the food division of a country club. The country club had installed pesticide (pyrethrum) aerosol that sprayed automatically every 15 minutes from 12 different vents. While working near the pesticides Miss E would develop a burning sensation in the esophagus, extreme nausea, numerous mental aberrations, shortness of breath, numbness in her legs, tachycardia, and spontaneous bruising over the extremities. On one occasion of direct contact with the spray she was taken to an Emergency Room where a diagnosis of hyperventilation was made. As her problems continued she was admitted to a Chicago hospital and was seen by a psychiatrist who suspected chemical susceptibility. He referred her for diagnosis and treatment.

The testing in a Chicago unit similar to ours showed the patient to have widespread food and chemical susceptibility. After leaving the Chicago environmental unit, the patient was unable to tolerate the polluted city air. She became paralyzed from the waist down and developed severe tachycardia, uncontrollable with drugs. She was sent to the Dallas environmental unit, where most symptoms gradually cleared. She had severe reactions to numerous test foods. A challenge ingestion of one drop of kerosene diluted 5-15 in saline produced spontaneous bruising and hemoptysis. One drop of sublingual phenol (0.4% concentrate diluted by factor of 5-15) produced hemoptysis and spontaneous bruising. The patient was put on a rotary diet of chemically less contaminated food and sent to live with a local patient in an environmentally controlled home that was electrically heated and free of petrochemicals, including plastics. Though her sensitivities have diminished over the last year, she still must live in a relatively natural environment and cannot tolerate exposure to any of the chemicals which produced symptoms during testing.

Case F This 51-year-old white female entered with a chief complaint of cardiac irregularities on exposure to nontolerated substances at work. She had worked eight years in the fuming etching room of a large factory. At work she developed arrhythmia, visual irregularities, recurrent bruising, and impaired intellectual functioning. She also gained a large amount of weight though consciously attempting to limit her intake of food. After fume overexposure at work Mrs. F noticed that chemicals in her home environment also caused symptoms. She was placed in the environmental unit and developed withdrawal symptoms of headache, abdominal pain, pallor, difficulty in breathing and bloating. After her symptoms subsided, she was challenged with chemically less contaminated food and experienced symptoms from 23 foods. Foods tolerated in the chemically less contaminated form were then retested in their ordinary commercial forms. While eating commercial foods she developed abdominal pains, bloating, swelling of the legs, insomnia, and palpitations. Transient exposure to perfume resulted in dizziness and difficulty in breathing. A one-minute exposure to phenol vapors produced a tight chest, nasal itching, and burning and earache. A one-hour challenge to a lighted gas stove produced no symptoms. Cigarette smoke, since the occupational overexposure, has proved to be her most severe susceptibility. The odor of smoke on the clothing of a smoker triggered her reaction of difficulty breathing and tachycardia of 120 to 160 bpm, blood pressure of 70/40 and pallor. This reaction lasted from eight to 24 hours. Transient exposure to formaldehyde produced tearing eyes, difficulty in breathing, weakness, and hoarseness for 24 hours. A five-minute ambient concentration of Raid insecticide triggered difficulty breathing and impaired intellectual functioning followed by insomnia. Exposure to sulphuric acid fumes, one of the substances at her work, gave her mild chest tightness, headache, and sneezing. A single inhalation of hydrochloric acid, with which she also worked, caused a severe shortness of breath, tearing, and bloating. This reaction continued for 24 hours. Transient exposure to hair spray resulted in dizziness and difficulty breathing. A one-minute exposure to a modern plastic telephone resulted in hoarseness, itching, choking, bloating, and weakness; however, she could talk at length an a black Bakelite telephone without any difficulty. The patient was discharged on a rotary diversified diet of chemically less contaminated foods which eliminated offending items. She was instructed in environmental control of her home, avoiding nonotolerated substances. She has been symptom-free while living in the country but still suffers acute reactions when she returns to the city.
 
 
PART II The six patients presented in Part I, plus six additional patients with similar histories and findings, were studied. All patients were nonsmokers. Each patient was placed in a relatively fume- and particle-free environment specially constructed after the method of Randolph4 and described by the first author in previous papers.5-7 Patients were withdrawn from all foods, medications, and as many ambient chemicals as possible. After three days in the controlled environment, double-blind studies were performed to determine an agreeable water. This was necessary because experience has shown that both chlorinated and nonchlorinated waters, consisting of numerous spring, charcoal-filtered and distilled waters, often elicit symptoms in chemically sensitive patients.

After an acceptable water which did not produce symptoms was determined, individual challenges with various (no more than four per day) chemically less contaminated source foods (source foods=distinct biological entities such as wheat, oats, rice, beef, pork, lettuce, and carrots) were made. Once acceptable foods were determined, oral challenge was repeated with the same foods but in a form grown, processed and stored according to conventional marketing methods. Finally, double-blind challenges with ambient concentrations of common types of inhaled chemicals were performed. Attempts were made to include the chemical which apparently had precipitated the patient=s problem.

The following laboratory tests were done to investigate possible mechanisms: complete blood count by the Coulter Model S Method; sodium, potassium, chloride, carbon dioxide, blood urea nitrogen, serum glutamic oxalo-acetic aminase, lactic dehydrogenase, and serum calcium by the SMA Method; protein electrophoresis by the Helena Cellulose Acetate Method; immunoglobulins (IgE, IgG, IgA, IgM) C3 and C4, alpha 1 antitrypsin and C-reactive protein by the Behring Radial Immuno Diffusion Method; total hemolytic serum complements CH100 and serum complement components by the Hemolysis Sheep Cells Method; prothrombin time, partial thromboplastin time, platelets, and Lee White clotting time by the Dade Reagents Method; phosphorus by the Hycel Metho, fibrinogen, and fibrinolysins, clot lysis by the Biuret Quantitative Method; fibrin split products by the Burroughs-Wellcome Method; C1 esterase inhibitor by the Behring IEP Method; B lymphocytes and T lymphocytes by the Sheep Cell Rosetting Method. All tests were performed when the patient entered the test room and at the beginning and end of the challenge period. C3 and C4 were measured daily during the period of fasting.

Results As shown in Table 1, there were varied food and chemical triggering agents in addition to the prime chemicals from the occupational exposure. Table II shows that immunoglobulins generally were within normal limits, except for two which were low. C-reactive proteins were positive in six reactors while the white blood count was depressed in three reactors. Table III shows alterations in total serum hemolytic complement in nine patients. Frequently this was due to abnormalities in several of the components. C3 assays were abnormally low in nine patients. C4 determinations were altered in only five patients, all being slightly elevated. Bleeding studies were all normal. Total eosinophil counts were often low on admission and returned to normal or increased with time in the controlled environment. However, two patients had initial elevation. T-cell decrease on or near admission was seen in all patients measured. Frequently, with time in environmental control, depressed T-lymphocytes would return to normal. At times when the chemical overload occurred the food handling mechanism would be distorted. Upon challenge with chemically less contaminated food, the total eosinophil count would be depressed paralleling symptoms. Rarely, this occurred with IgG depression as shown in patient 8 and patient 9. At times total complement would be depressed on admission and then come up with time in the controlled environment. Often total complement would be depressed upon challenge. One patient showed depression of the T-lymphocyte when challenged with pesticide.

Table I

Triggering Agents of Chronic Symptoms

 

Chemicals CDouble-blind

Food
 

Patient

+ Reactors
# Tested
+ Reactors
# Tested
Severe Symptoms due to:
53 F
10
12
0
16
1. Cigarette Smoke

2. Chlordane

37 F
8
10
4
29
Pesticide (heptachlor)
31 M
2
10
5
21
Paint (acrylic)
37 F
7
10
11
27
Trichloroethylene
51 F
11
13
23
39
1. Cigarette smoke 

2. Hydrochloric acid

27 F
1
10
41
57
Natural gas
37 F
3
10
25
46
Volatile plastic
41 F
13
15
12
28
Pesticide
41 F
6
10
10
26
Trichloroethylene
44 M
6
10
10
26
1. Pesticide (heptachlor)

2. Gasoline

21 F
2
10
11
27
Pesticide (chlordane)
32 F
10
10
34
48
Natural gas

Table II

Admitting Laboratory Values

Control Patient
800-1800 mg/dl

IgG

10-200 mg/dl

IgE

90-450 mg/dl

IgA

60-280 mg/dl

IgM

CRP
WBC
1
600
50
247
72
pos
7100
2
780
15
109
106
neg
5200
3
1020
73
160
84
neg
6300
4
960
25
180
244
pos
5100
5
1020
65
118
258
neg
3500
6
1195
40
141
240
pos
3000
7
830
90
207
114
pos
5000
8
1020
 

134

140
pos
10400
9
1100
68
159
94
neg
6400
10
1100
40
264
156
pos
6900
11
1530
925
203
180
neg
5000
12
1160
15
324
198
neg
4000

Table III

Admitting Laboratory Values

Control Patient
80-120 mg/dl C3
20-40 mg dl C4
90-98% CH100 Total Comp
50-200 mm3 EOS
60-80% Lymph T%
20-40% B%
1800 " 200 E. Rosettes Absolute L
3-4000 Total lymphocyte
1
64
44
98
67
 

 

 

 

2

79
40
80
33
 

 

 

 

3

75
40
80
300
41
45
834
1600
4
90
60
90
55
41
45
629
1500
5
98
44
80
77
 

 

 

 

6

76
52
80
230
32
30
404
1260
7
98
36
80
18
40
40
600
1500
8
70
37
94
156
 

 

 

 

9

77
32
80
89
 

 

 

 

10

62
41
80
66
 

 

 

 

11

60
30
80
176
54
68
810
1500
12
58
24
80
0
27
40
476
1763

 

Discussion

Massive chemical overexposure has been implicated in a variety of serious occupational diseases as well as certain malignancies.8-10 The present data suggest that some chemicals can also trigger and propagate certain nonmalignant inflammatory diseases of otherwise unknown etiology. In his studies of patients with food susceptibility Randolph11 noted many persons to be intolerant to inhaled and ingested chemicals at dose levels to which the general population is exposed daily. Through studies over the last 30 years, he developed the concept of chemical sensitivity in an individual as the causative and/or propagating factor of many chronic diseases of unknown etiology. Many of his patients developed susceptibilities to numerous synthetic chemicals after chronic ambient concentration exposures. However, some previously healthy patients suffered acute, massive chemical exposures which precipitated widespread and persistent susceptibilities to numerous ambient inhaled and ingested chemicals. This usually resulted in inflammatory diseases such as recurrent colitis, arthritis, bronchitis, sinusitis, asthma, or vascular-type headaches. Patients in this series showed what appeared to be sensitization of various smooth muscle systems which resulted in the aforementioned clinical entities. Follow-up in these patients showed an extremely slow recovery time from their multiple sensitizations. In fact, those patients who did not maintain strict avoidance of their incitants in all facets of life would rapidly lose their asymptomatic state and deteriorate into severe disabling symptomatology.

The findings in this series of patients confirm Randolph=s observations and re-emphasize the seriousness of exposures to levels of some chemicals in our environment which were previously considered safe. Since safety has only been determined in studies of acute exposure to uniform genetic animals, a high level of error exists as to what amount of chemicals are safe in the environment. Susceptible humans acting as monitors might help us to better determine safe levels of chemicals in our environment.

Once an individual is sensitized to a solitary chemical, it is apparent that continued exposures result in a spreading phenomenon. Once this spreading occurs, reactions then proceed upon minute exposures. Spreading was demonstrated clearly in the patients in this series. After a massive exposure to one type of chemical the individual then became intolerant to ambient concentrations of many others. The mechanism of this spreading phenomenon is unclear at the present time.

It is notable that those patients who developed food intolerance did not have it before they had massive chemical exposures. Most could eat any foods as much as often as desired. After the exposure, it was apparent to most of these patients that the ingestion of foods in general seemed to bother them. Until the unmasking process occurred in the environmental unit, it was not clear which specific foods were involved in triggering their symptoms. Many found that by using meticulous selection they could have a symptom-free meal for the first time in months. In order to remain symptom free, it was clear that these patients had to continue avoiding their symptom-producing foods for a period of at least six to twelve months. As their daily chemical exposure decreased their tolerance increased and they were then able to eat the foods previously not tolerated. In fact, many of the foods could be returned to the diet in rotation after a long period of avoidance. Furthermore, during visits to areas of significantly less air pollution, they could suddenly tolerate foods to which they were usually susceptible.

A working hypothesis that has evolved from the study of these patients with chemical overexposure is that of total body load. One might make the analogy of a person being a barrel. When the barrel fills and subsequently overflows, symptoms are produced. Once the overflow load is reached minute levels of inhaled or ingested chemicals cause symptoms. Each person in this series apparently reached and exceeded his total body chemical load, with the result of extreme sensitivity and chemical intolerance. Presumably at the total tolerated load, enzyme systems or mediators have been maximally interfered with so that any further interference leads to chemically expressed symptoms.

This body load is created by many factors. In addition to the daily exogenous load from the foods per se, the body=s adaptive mechanism must cope with the large amount of synthetic chemicals in food. It is estimated that the average individual ingests at least one gallon of synthetic additives, coloring agents, pesticides and preservatives in a year=s time. For all patients in this series it was necessary to acquire specially grown, chemically less contaminated foods.

Daily use of chemically contaminated water is still another major component of the total environmental load. In a recent analysis in which local city water was compared to various spring waters, city water was shown to have 1,000 to 10,000 times more synthetic compounds.12 Water intolerance was a problem in these patients and necessitated the use of spring water.

The additive effect continues with the air that is breathed. Outdoor air pollution is increasing in many areas. Studies by Whitby13 have shown that city air may be three to four thousand times more polluted than sea air. If one then adds an increase in indoor air pollution at the place of employment to his already burgeoning load, one can see how environmentally triggered disease could occur. For example, one place of work which was analyzed had 400 times greater concentrations of chemicals in the air when compared with outside air. Of course, each threshold limit was below the theoretically safe level for individual exposure to that particular chemical. However, in this instance, combined and accumulated effects of multiple chemicals had never been evaluated, and the patient became ill from the overexposure.

Together with the high ambient levels of chemicals in city and industrial air, the environment of the average home has been shown to be highly polluted.15,16 Fumes from gas heating and cooling appliances, from the outgassing of the soft plastics such as Nylon, polyester, polyurethane, and polyethylene and from routinely using pesticides all contribute to this domiciliary air contamination. Acute chemical exposures can add insults that persist after cessation of the exposure. Stewart,17 for instance, showed that people using furniture paint stripper would continue to have an adverse change in their carboxyhemoglobin for several hours after leaving the exposure. Isolated exposures of this nature might still be tolerated if a person had a chronic total load and was able to obtain fresh air at home. Our study suggests that patients become symptomatic on exposure to minute amounts of several chemicals as a result of cumulative acute and chronic exposures.

Radical changes were necessary in the home environments of patients in this series. These changes included replacement of their heating systems with electric heat and the removal of virtually all petrochemically derived synthetics from the home. This satisfactorily lowered the previous high total load of chemicals and was associated with marked clinical improvement.

The total load concept is related to Selye=s18 model of general adaptation. He observed that a general environmental stimulus causes an initial alarm reaction. If the stimulus continues, a stage of adaptation follows and lasts from minutes to years. Finally, adaptation fails and the stage of exhaustion develops, in which the organism enters a disease state and eventually expires. Adolph19 further expanded these ideas to include individual differences in response to specific stressors. Randolph20 later showed that individual susceptibility interacted with long-term and /or massive chemical exposure to produce clinical maladaptation or rapid exhaustion.

The bipolar nature of the chemically maladapted state has been described by Randolph..21 Frequently patients in the present series who developed chemical susceptibility reported stimulatory responses of central nervous system activation with such symptoms as increased motor activity, anxiety, insomnia, etc., when they initially came in contact with the chemical to which they eventually became susceptible. Some even experienced an unusually euphoric feeling of being in an intoxicated-like high. Of course, once their bodies reached the stage of exhaustion, they then perceived only the maladaptive withdrawal response with physical symptoms and central nervous system depression. Such bipolar responses are well-known in addictions to drugs such as opiates and alcohol and to other items such as cigarettes, coffee, candy, and soft drinks and suggest a common mechanism of homeostatic disruption. In food and chemical maladaptation, both the stimulatory and withdrawal phases can last from minutes to hours to years.

It was Rinkel22 who utilized the adaptation principle to evaluate food intolerance. He showed that temporary avoidance (4-5 days) of foods to which an individual was maladapted would unmask or return the patient to the stage of alarm reaction. Therefore, acute challenge with an offending food that has been unmasked would cause a definitive reaction. Similar tests with foods to which the individual was not susceptible would cause no reaction. Both unintentional and deliberate test exposures by Rinkel=s approach in the current series have confirmed the usefulness of his diagnostic technique.

The nature of the specific derangement(s) of the internal homeostatic mechanism is currently ambiguous but the altered laboratory tests suggest that different elements of the system were involved in individual patients. Unfortunately, laboratory work thus far has not defined the initial steps which trigger the subsequent ecologic and/or cellular abnormalities during adverse reactions to incitants. Involvement of the immune system, although not readily apparent, is possible. The chemicals may have acted as haptens. Reaginic IgG may have been active since IgE levels were not significantly elevated in most of the patients studied. Furthermore, IgG was changed on challenge by individual incitants in some patients in this series. This type of change has been reported with food challenge.23 Certainly activation of the complement system was present in some patients. When all nine components were measured in some select patients, C 1, 4, and 2 were near control values when C3 was depressed, suggesting alternate pathway involvement. Since total hemolytic complement depression occurred during challenge in some instances with resulting bruising or purpura, immune complexes may have been involved. Perhaps these were bound to cutaneous blood vessels, causing leaking of erythrocytes. Possibly this is similar to the C1 and IgG deposition reported by Papish24 in animals and Theorell25 in humans. Unfortunately, fluorescence studies were not available on the biopsies of our patients. However, light microscope section in patients who bruised showed a monocellular infiltrate in the precapillary arterioles. While no evidence of involvement of the fibrinolytic or clotting systems was seen, local levels could have been changed without being reflected in the patient=s peripheral blood. Also, clotting studies were not done during challenge reactions. Direct kinin activation also could have been involved but was not measured in this series. Since T-cell depression occurs in some patients and returns to higher levels when being away from the chemicals, it would appear that this system is significantly involved. Thus, derangements of different potential mediating mechanisms were apparent. Presumably they were secondary to some as yet unknown primary change in body physiology.
 
 

SUMMARY Twelve patients with over exposure to commonly used environmental chemicals were studied. After the overexposure all developed recurrent signs and symptoms of inflammatory type diseases that were the results of ambient chemical fumes in the air and home environments. A period of time in a relatively fume- and particle-free environment cleared the majority of symptoms and signs without the use of medication.

Double-blind rechallenge with ambient dose levels of synthetic chemicals reproduced most of the symptomatology. Laboratory findings included abnormalities in complement, T-lymphocytes, eosinophils, and IgG.
 
 

REFERENCES 1. Randolph, T.G. Ecologic orientation in medicine: Comprehensive environmental control in diagnosis and therapy. Ann Allerg 23:7, 1965. 2. Rea, W.J. Environmentally triggered phlebitis. Ann Allerg 37:101, 1976.

3. Rea, W.J. Environmentally triggered small vessel vasculitis. Ann Allerg 38:245, 1977.

4. Randolph, T.G. Ecological orientation in medicine: Comprehensive environmental control in diagnosis and therapy. Ann Allerg 23:7, 1965. 5. Rea, W.J. Environmentally triggered small vessel vasculitis. Ann Allerg 38:245, 1977.

6. Rea, W.J. Environmentally triggered phlebitis. Ann Allerg 37:101, 1976.

7. Rea, W.J. Environmentally triggered cardiac disease. Ann Allerg 40:243, 1978.

8. Randolph, T.G. Human Ecology and Susceptibility to the Chemical Environment. Springfield, IL: Charles C. Thomas, 1962.

9. Bernstein, I.L., et al. Occupational Bronchial Asthma. Allergology (Proceedings of the VIII International Congress of Allergology). New York: American Elsevier Publishing Co., Inc., 1973, p. 112.

10. Creech, J.L., Jr., et al. Liver Disease among polyvinyl chloride production workers. Ann Aca Sci 246:88, 1975.

11. Randolph, T.G. Food susceptibility (food allergy). In Current Therapy, Conn H (ed.). Philadelphia: Saunders, p. 418.

12. Glaze, W.E. North Texas State Univ Div Personnel communication. 13. Willeke, K., and K. Whitby. Atmospheric aerosols: Size distribution interpretation. Air Pollution Control Assoc 25:529, 196. 14. Dickey, L. Personal communication. 15. Randolph T.G. Human Ecology and Susceptibility to the Chemical Environment. Springfield, IL: Charles C. Thomas, 1962.

16. Wade W.A., W.A. Cote, and J.E. Yocom. A study of indoor air quality. J Air Pollution Control Assoc 25:923, 1975.

17. Stewart, R.D., and C.L. Hake. Paint remover hazard. JAMA 2??: 298, 1976.

18. Selye, H. The general adaptation syndrome and the disease of adaptation. J Allerg 17:231, 1946.

19. Adolph, E.F. General and Specific characteristics of physiological adaptations. Am J Physics 184:8, 1956.

20. Randolph, T.G. Human Ecology and Susceptibility to the Chemical Environment. Springfield, IL: Charles C. Thomas, 1962.

21. Randolph, T.G. Adaptation to specific environmental exposures by individual susceptibility. In Clinical Ecology by L.D. Dickey. Springfield, IL: Charles C Thomas, 1976.

22. Rinkel H.J., C.H. Lee, D.W. Brown, Jr., and J.R. Williams. The diagnosis of food allergy. AMA Acta Otolaryngology 79:71, 1964.

23. Sandberg, D.H., R.M. McIntosh, C.W. Burnstein, and R. Carr. Severe steroid response nephrosis associated with food hypersensitivity. Lancet 1:388, 1977.

24. Papish,W.E. Studies on vasculitis, immunoglobulins, BIC C-reactive steroid response nephrosis associated with food hypersensitivity. Lancet 1:388, 1977.

25. Theorell, H., M. Blomback, and C. Kockum. Demonstration of reactivity to airborne and food antigens in cutaneous vasculitis by variations in fibrino peptide A and others, blood coagulation, fibrinolysis and complement parameters. Thrombos Haemostos (Stuttg) 36:593, 1976. ACKNOWLEDGMENTS Thanks to Drs. A.A. Kahn for assisting in setting up our laboratory, B. Park and R.M. Stroud for evaluating data, and Louis Henderson for compiling data.