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Images Of Poliomyelitis

The Environmental Aspects
Of The Post Polio Syndrome

W.J. Rea, M. D., F.A.C.S., A.R. Johnson, D. O. ;
Environmental Health Center, Dallas; Human Ecology Research Foundation Of The Southwest, Inc.

E. Fenyves, Ph. D.; University In Texas, Dallas, Professor In Physics & Environmental

J. Butler, Ph. D.; North Texas University, Professor of Behavioral Medicine

Introduction

The environmental aspects of health and disease are becoming much more clearly defined. The adverse influences of environmental incitants on wounded target organs have often been seen by people working in the area of environmental medicine. Because of these observations a preliminary survey of environmental influences on post polio patients who exhibited the post polio syndrome was done.

Materials and Methods

Seventeen post polio patients who had developed "post polio syndrome" (mean = 49 years, ages 31 to 63) (M 5, F 12) were evaluated initially. Polio history, with symptom and sign scores was done on each patient. Each patient was evaluated for the effects of pollutants upon their signs and symptoms searching for triggering agents. The effects of these pollutants and environmental antigens were studied using the controlled environmental unit and program as a scientific basis for the study. Testing on most patients was performed in an environmentally controlled outpatient area using cutaneous, oral, and inhaled challenges of incitants in air, food, and water. However, two patients were studied in the inpatient area. Signs and symptom scores were done periodically, and this was followed through at home with further observations. The patients were done periodically, and this was followed through at home with further observations. The patients were followed over a year after initial challenge to further define and confirm triggering agents and degrees of improvement. All had informed consent and were not charged for their evaluation or vaccine treatment.

The scientific basis for our studies is in the development of the controlled less polluted environment for testing and treating. This environmental wing is in an isolated area in the hospital designed specifically to be less polluted. All construction is done to minimize outgassing of fumes and particulates. Usually porcelain steel and ceramic tile are used for the walls and floors. No smoking, perfumes, or synthetics are allowed in the wing. All bedding materials are of natural fibers. Incandescent lights are used. The air is filtered by a series of especially designed depollution devices.(1) Nontoxic cleaning substances are generally used. Air analysis is monitored by particulate counts, gas chromatography, and mass spectrometry to assume continuous depollution. Available less contaminated drinking water is by charcoal filtration, distillation or use of natural spring water in glass containers. Food is raised, transported, stored, and prepared in the relative absence of petrochemicals, aluminum, copper, gas, and synthetics. Food, mold, pollen, dust and dust mite antigens for challenge are specifically prepared using only(2) NaHCO3 and NaCl as extracting agents and frozen. Chemical challenge incitants are made in a similar manner.(3) Intradermal skin challenges were done using 1/5 serial dilution. Inhaled challenges were done in a controlled booth within the controlled environment. Doses of chemicals used for the inhaled challenge were phenol <.0024ppm, formaldehyde <.20ppm, petroleum ethanol <.50ppm, chlorine <.33ppm, and pesticide 2,4,DNP <.0134ppm.

Dietary and lifestyle modifications including avoidance of harmful foods and ingested or inhaled chemicals (phenols, petroleum alcohol, insecticides, chlorine) were carried out on each individual. Injection therapy of inhalants, foods and, some chemicals were performed on all, but one patient. Often home environments were modified to eliminate smoke, mold, gas heat, routine pesticiding, and other synthetics. This was done in order to decrease total body ambient pollutant load.

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Results

All patients but two could walk with either crutches, braces, or post polio orthopedic prosthesis while the remaining two were confined to wheel chairs. All 17 patients had experienced lower extremity weakness as their chief complaint. In addition two had upper extremity weakness. Nine patients also complained of pain as being as disabling as the weakness. Fourteen patients developed marked improvement of their weakness while eight patients became pain free. One patient was improved intermittently for weeks, then lapsed back to his old symptoms for two to three week periods. Two patients showed no improvement. The types of incitants involved inhalants to which 15 patients were sensitive. These were predominantly molds that reproduced the symptoms. All 17 patients were food sensitive and 15 of these were sensitive to seven or more foods. Though all 16 patients that were tested to chemicals had multifactoral triggering agents, all 16 were sensitive to formaldehyde closely followed by the onset of signs and symptoms due to cigarette smoke in 14. Twelve of the 12 tested had a positive skin test to polio vaccines. The other five refused testing of the vaccine. Two patients got dramatic relief of pain and weakness with .05 ccs. of 1/25 dilution of the polio vaccine on numerous occasions. The other three who allowed treatment with the vaccine noted no relief. Seven patients were extremely sensitive to chlorine and had to give up their swimming pool therapy because they realized the adverse effects that occurred after such therapy were the very ones they were trying to eliminate. Two patients had inhaled double blind challenges in the hospital unit with reproducible results. (Table III) Also these were correlated well with the skin provocation. There were a minimum of 34 associated symptoms and signs in these 17 patients. (Table IV) These included ENT signs of headaches, dizziness, recurrent rhinosinusitis in nine; GI upset in four; overweight, edema, respiratory difficulties including one very severe case of asthma, and many other symptoms. These were brought under control with environmental manipulation in 14 of the 17 patients. Long term follow-up of the 14 improved patients showed general return of well being and renewed vigor. Two patients who had not been able to work returned. Several others who had feared loss of jobs because of decreasing function were able to perform better.

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Discussion

In 1970, Dickey(4) reported a case of a post polio patient who had been clearly made worse by exposure to environmental pollutants and improved by avoidance. Mandell(5) further built upon this observation in presenting a paper on several post polio patients who had environmental triggers, and Bailey(6) reported on oral antigen therapy at the first world conference in 1984 suggesting environmental triggering. Our work using the Environmental Control Unit as a scientific basis for studies of chronic diseases suggested that perhaps some of the late polio problems might be due to an overload of environmental pollutants on wounded target organs.(7,8,9,10,11,12) Upon viewing the previously mentioned studies it was suggested that further observations on post polio patients should be done. It has been well shown previously that many chronically recurring inflammations and post inflammatory diseases were significantly influenced by definition and elimination of environmental pollutants. Techniques are well developed for the precise definition of triggering agents using particle counters, gas chromatography and mass spectroscopy in controlled environments.(13) Studies of patients evaluated under environmentally controlled conditions can also be carried out correlating improvement with serial analysis of blood organic chemicals and pesticides.(14,15) Also challenge tests verifying deterioration of the clinical condition can be performed.(16) These principles and techniques were used on the post polio patients in this series with successful demonstration of triggering agents in all the cases that might suggest an adverse environmental aspect. Several subtle ancillary signs, such as rhinosinusitis were elicited in the post polio syndrome patients.

Also many signs and symptoms elicited were cyclic subtle periorbital, digital, and pedal edema, suggesting increased vascular disturbance. Often cold sensitivity, petechiae, purpura, spontaneous bruising and adult acne were seen. Heightened odor sensitivity to perfumes, pesticides, newsprint, etc. was observed in many patients. The vascular dysfunction and the odor sensitivity seemed to be clues to the presence of environmental influences in the post polio syndrome patient. The rapidity with which an incitant could bring on the symptoms of the post polio syndrome after de-adaptation was impressive. We frequently observed individuals who were doing well revert suddenly and completely to the post polio syndrome with symptoms of weakness or pain within a few minutes after a small exposure. They would then clear in a day or two being completely returned to their base line state. This observation apparently tended to reinforce the patient and physicians initial testing with provocation of symptoms. Following these post polio patients for a minimum of one year allowed us to see that their improvement was in fact real and that they were allowed to live a much more vigorous and pain free life. It further confirmed that our initial impressions from the challenge tests were valid. All successful patients not only received inhalant, food, and chemical injections, but also changed their life style and living environments. Some interesting observations were reported by these patients and correlated well with observations of environmentally sensitive non-polio patients. The most glaring fact was that the chlorine and other chemical odors eminating from the patients' therapeutic swimming pools often reproduced their symptoms including pain, aching, weakness, etc. Also that exposure to gas heat would often render them nonfunctional. It appeared that not only did certain foods trigger these patient's syndrome but often chemical odors in the work environment often triggered symptoms. At least half of the patients credited the program to saving their jobs.

Two other patients actually became employable when they had not been previously. One patient who had been confined to a wheel chair was again able to walk with crutches. Mechanisms of environmental triggering were not part of this study. However, the post polio syndrome patient appears not too different from other environmentally influenced patients. So far dysfunction appears to be the result of inappropriate vascular regulation via the involuntary nervous system.

Analysis done on a few post polio environmentally sensitive patients suggest involvement of certain enzyme detoxification systems such as superoxide dismustase, glutathione peroxidase, lipid peroxidase, aryl hydrocarbon hydrolase, chromium P-450 systems; as well as, changes in the suppressor and helper T-lymphocytes. The concept of reducing environmental pollutants in post polio patients with wounded target organs clearly is sound scientifically. Though results in this preliminary study were encouraging, further study should be carried out when funding is available. It should be pointed out that probably not all post polio syndrome patients are environmentally influenced to the study were, 15 patients who initially wanted to enter the study dropped out after initial contact before any testing could be done. They may have felt that defining the environmental aspects of their candidates didn't apply to them. Only a bigger number of patients could answer this question.

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Summary

Seventeen post polio syndrome patients were studied with the environmental control unit as the scientific basis for defining environmental triggering agents. Fourteen patients improved after definition and elimination of such triggering agents as molds, foods, formaldehyde, natural gas, etc. Preliminary results suggest pain and weakness can be positively influenced in these patients.

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Table I - Results
Ages: 31-63, Average Age: 49, Gender: M-5, F-12
 
Before Treatment
Patient Symptoms
17 Lower extremity weakness
(2) and upper extremity weakness
(9) Pain: Muscle and bone
   
After Treatment
Patient Symptoms
14 Gone
1 Recurrent
2 No Change
   

Treatment consisted of finding triggering agents of symptoms then 1) eliminating them; 2) neutralizing symptoms with intradermal injections.

 

Table II - Incitants
Patients Incitants
15 Inhalants (pred. molds)
17 Chemicals
16 Formaldehyde
14 Cigarette Smoke
12 Polio Vaccine
9 Terpenes
8 Perfume
8 Petroleum ethanol
7 Chlorine
5 Diesel
4 Phenol
4 Newsprint
17 17 Foods (is sensitive to 7 or more, i.e., coffee, tea, cane sugar, wheat, corn, milk, beef, chicken, eggs, etc.)
   

Triggering agents defined by inhaled, oral and intradermal challenge under environmentally controlled conditions.

 

Table III - Ambient Dose-Inhaled Toxic Chemical Challenge - Double Blind
Weakness, Asthma
Pt. #1 - 55 WF - SX - asthma, weakness
Pt. #2 - 45 WM - SX - arrhythmia, weakness, pain
  Dose ppm Pulse Change Flow Meter Change Symptom Change EKG Reproducible TX3
Booth Pt. 1 Pt. 2 Pt. 1 Pt. 2 Pt. 1 Pt. 2 Pt. 1 Pt. 2 Pt. 1 Pt. 2 Pt. 1 Pt. 2
Placebo #1, Spring Water 5cc 5cc 0 0 0 0 0 0 0 0 + +
Placebo #2, Filtered Water 5cc 5cc 0 0 0 0 0 0 0 0 + +
Placebo #3 5cc 5cc 0 0 0 0 0 0 0 0 + +
Petroleum Ethanol <0.5 <0.5 0 3SD 0 0 0 + 0 0 + +
Formaldehyde <0.2 <0.2 3SD 2SD 3SD 0 + + 0 + + +
Phenol <0.5 <0.5 0 2SD 0 0 0 + + 0 + +
Chlorine <0.33 <0.33 0 2SD 0 0 0 + + 0 + +
Pesticide (2,4,DNP) <0.0134 <0.0134 2SD 2SD 0 0 + + 0 0 + +
                         
Done in hospital environmental wing, under strictly controlled environmental conditions, having been deadptated for at least 4 days.

 

Table IV - Accessory Symptoms
Ear, Nose, Throat (headache, dizziness, recurrent rhinosinusitis) 9
Gastrointestinal Upset (bloating, abdominal cramps) 4
Weight Gain (non-edematous) 3
Edema 10
Respiratory Difficulties  
  severe asthma 1
  breathless 4
  short of breath 3
Hypertension 2
     
These were complaints that were reproduced by challenge under environmetally controlled conditions and then subsequently cleared with long-term treatment.

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References

1. Rea, W.J.: The Environmental Aspects of Ear, Nose, and Throat Disease: Part I. J.C.E.O.R.L. & Allergy, July, 1979.
2. Rea, W.J.: The Environmental Aspects of Ear, Nose, and Throat Disease: Part II. J.C.E.O.R.L. & Allergy, September, 1979.
3. Rea, W.J., Elimination of Oral Food Challenge Reaction by Injection of Food Extracts: A Double-Blind Evaluation, Archives of Otolaryngology, American Medical Association, April 1984, Volume 110, pp. 248-252.
4. Dickey, L.: Ecologic Illness, Rocky Mountain Medical Journal, Volume 68, pp. 23-28, 1971.
5. Mandell, M.: Personal Communication, August, 1985.
6. Bailey, A.: International Polio Conference, May, 1984.
7. Rea, W.J.: Environmentally Triggered Thrombophlebitis. Annals of Allergy, Volume 37, pp. 101-109; July, 1976.
8. Rea, W.J.: Environmentally Triggered Small Vessel Vasculitis. Annals of Allergy, Volume 38: pp. 245-251; April, 1977.
9. Rea, W.J., Bell, I.R., Suits, C.W., and Smiley, R.E.: Food and Chemical Susceptibility after Environmental Chemical overexposures: Case Histories. Annals of Allergy, August, 1978.
10. Rea, W.J., Peters, D.W., Smiley, R.E., Edgar, R., Greenberg, M. and Fenyves, E.J.: Recurrent Environmentally Triggered Thrombophlebitis (A 5-Year Follow-Up). Annals of Allergy; December, 1981.
11. Rea, W.J., Bell, I.R., and Smiley, R.E.: Environmentally Triggered Large-Vessel Vasculitis, Annals of Allergy, pp. 185-199; 1977.
12. Rea, W.J., Chemical Sensitivity in Environment, Allergy and Immunology Practice, September/October, 1982.
13. Edgar, R.T., Fenyves, E.J., and Rea, W.J.: Air Pollution Analysis Used In Operating An Environmental Control Unit. Annals of Allergy, March, 1979.
14. Laseter, J.L., Ildefonso, R.D., Rea, W.J. and Butler, J.R.: Chlorinated Hydrocarbon Pesticides in Environmentally Sensitive Patients. Clinical Ecology, Volume II Number 1, pp. 3-12; Fall 1983.
15. Rear W.J., Butler, J.R., Laseter, J.L., and Ildefonso, R.D.: Pesticides & Brain-Function Changes In A Controlled Environment. Clinical Ecology, Volume II, pp. 145-150, No.3/Summer, 1984.
16. Kroker, G.F., Stroud, R.M., Marshall, R., Bullock, T., Carroll, F.M., Greenberg, M., Randolph, T.G., Rea, W.J., and Smiley, R.E.: Fasting & Rheumatoid Arthritis: A Multicenter Study. Clinical Ecology, Volume II, pp. 137-144, No.3/Summer, 1984.

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