Chemical sensitivity is the adverse reaction to ambient doses [parts per million (ppm) and parts per billion (ppb)] of toxic and non-toxic chemicals contained in air, food, and water. Electromagnetic sensitivity is an adverse reaction to the specific ambient electromagnetic field (EMF) frequencies below the heating level. This quantum field involves fewer particles and has an uncertainty described by the Heisenberg relation.
History of the development of chemical sensitivity
The history of food and chemical sensitivity stretches back over 2000 years to when Hippocrates described people who were made ill by certain food and drink after they fasted or just could not tolerate a food that others could (1).
Hippocrates showed that some people can eat cheese and do well; others, it makes them sick. Also, he showed that if a person fasts for 3 days and takes the wrong food on the 4th or 5th day, he will be sick. Text from Gray’s Anatomy showed intricate anatomical parts that got inflamed and made people ill (2). Guyton’s Physiology showed multiple principles and physiology and absorption that involved food and chemical changes (3). Heine’s book on the ground regulation system laid out the physiology for chemical sensitivity (4).
Rowe also showed the food factor in disease in 1931 (9), while Rinkle described masking in 1936 (10). Hansel [ear, nose, and throat (ENT)] showed there was an optimal dosage concept in 1941 for intradermal treatment (11).
Rinkle described cyclic food allergy and serial dilution (1:5) and titration in 1949 (10). Randolph showed triggering by chemicals and foods and the adaptation syndrome in the specific foods and chemicals in the 1950s (12).
He (in Chicago, IL, USA) wrote Human Ecology and Susceptibility to the Chemical Environment, 1962 (first printing) (13). This was the first description of chemical sensitivity performed in a controlled environment.
Willoughby in Kansas City, KS, USA, emphasized the intradermal serial dilution and titration of molds in 1963 (14). Binkley described intradermal food neutralization that demonstrated the same for chemicals in 1964 (15). Lee did serial dilution provocation and neutralization tests for the diagnosis of food, pollens, and mold incompatibilities in 1961 (16). Miller confirmed Lee’s findings (17).
MacLennan, in Hamilton, Ontario, Canada, in 1974 also played a role in elaborating the intradermal diagnosis and treatment for foods and chemicals (18).
History of the EMF spectrum
For most of history, light was the only known part of the EM spectrum. The ancient Greeks studied light and its properties. It was not until scientific experiments almost 2000 years later discovered new findings about the EMF spectrum (19).
In 1800, Herschel discovered infrared light (20); the next year, Ritter described invisible light rays that induced chemical variations (21). In 1845, Faraday linked EMF to the polarization of light traveling through a transparent material that responded to an EMF (22).
This observation lead to the inference that light itself was an EM wave. This equation predicted an infinite number of frequencies of EM waves all traveling at the speed of light. He also produced and measured the properties of the microwave.
The knowledge of these new types of waves paved the way for the telegraph and the radio. Edison (23) and Telsa (24) each developed certain aspects of electricity making it practical. Many scientists showed problems with wired telephones, and especially with wireless apparatuses, Wi-Fi, smart meters, etc (25), (26).
Roentgen noticed X-rays when experimenting with high voltage radiation in a vacated tube (27). Villard studied the radioactive emission of radiation and identified x and b particles with the power being greater than either (gamma rays) (28). Audrode measured the length of gamma rays and found they were shorter and with higher frequencies than X-rays. Of course, today we have myriads of aberrations and technical changes in this field (29). Schliephake in 1932 showed that radar operators developed microwave illness (30). Johansen is a pioneer in EMF with his mast cell studies in 1980 (31). Rea et al. did a double-blind study on the presence of EMF sensitivity in some people (32). Belpomme in 2015 presented 1500 electromagnetically sensitive patients (33). Carpenter and Sage showed the effects of EMF on health in 2007 and 2012 (34). Hardell showed tissue changes in EMF-sensitive patients (35).
This was described by Smith and Monro in 1980–1982 (36), derived from Frolich’s (37) approach to cellular communication systems, which demonstrated the coherence phenomenon where EMF frequencies were common markers in molds, pollens, foods, and chemicals, as well as the physical and human electromagnetic phenomena. This commonality allowed communication between these entities for diagnosis and treatment. It is one of the most important concepts in the diagnosis and treatment of chemical and electrical sensitivity.
Diagnosis under less polluted, controlled conditions
The first diagnostic tool under controlled conditions was developed by Randolph (38) and Dickey (39), a general surgeon and urologist. Dickey developed the first environmental control unit (ECU, 20%–40% less polluted, and pesticide and natural gas free) with longevity in Fort Collins, CO, USA, and also wrote the first book on Clinical Ecology in 1976. Randolph had developed the first ECU but it was closed before it opened due to hospital politics. Lee introduced intradermal provocative neutralization in 1987 (16). Miller in Mobile, Alabama also emphasized provocation intradermal neutralization (17), confirming Lee’s observation. This procedure allowed mold, dust, pollen, food, and chemicals to be provoked and neutralized so the clinician and patient could observe the provocation of symptoms and signs under controlled conditions. The provocation allows reproduction under controlled environmental conditions. The lesser neutralization dose allows for the clearing of symptoms and signs.
Principles used in defining and treating chemical sensitivity were outlined by many physicians and scientists who have studied chemical and EMF sensitivity. These eight principles have evolved
Total body pollutant load (sum total of pollutants in the body) (13), (36), (40), where these substances are minimized when the total environmental pollutant load decreases the total load in the environment – in air, food, and water. However, when the body’s pollutant load stays too high, it can trigger or exacerbate chemical sensitivity (41).
According to Selye’s, Randolph’s, and our observations, adaptation or masking occurs when the individual rapidly gets used to an incitant and does not perceive the entry or reaction as causing and aggravating chemical sensitivity (42). The patient has to decrease the total body pollutant load with the removal of all possible incitants so triggering agents can be found (43) with challenge at the ambient doses in ppm or ppb. The idea of doing studies in less-polluted environments has been observed to allow the patient to depurate the toxics, which allows the adaptation or masking to be eliminated. This procedure allows cause and effect to be proven with individual ambient dose challenge in ppm or ppb. Each chemical has its own detoxification pathway; therefore, some are easy to detoxify while others are difficult – causing or exacerbating chemical sensitivity.
Biochemical individuality occurs where each individual has his own specific individual reaction and threshold for triggering chemical sensitivity (42), (44), some of which can be fended off while others cause chemical sensitivity.
The switch phenomenon is where the individual can change the reaction individually, i.e. stimulatory to depressed phase; or the ENT reaction is overtaken by asthma or arrhythmias (45).
Bipolarity of the response, where there is a stimulating phase and a depressive phase from the same exposure, which often can confuse the clinician as to the cause of the original disease (13). Often, the clinician misinterprets this problem to be a psychosomatic disease without any proof. They use failure to trigger under uncontrolled conditions, therefore, calling something psychosomatic without proof.
Spreading phase, where the reaction spreads to different organs, which often involves numerous specialists who have different interpretations as to the rightful cause of the disease and often suggest that the cause is unknown (46). In fact, if studied under controlled, less-polluted conditions, individual causes can be found, i.e. pulmonary dysfunction, fibromyalgia, arthritis, and arrhythmia (40), (47), (48), (49), (50). Also, the spreading of incitants can be large with many molds, foods, and chemicals as triggers, until the individual has no safe food.
The law of nerve injury: when the injury heals, it results in hypersensitivity to subsequent incitants, i.e. scar sensitivities. The clinician often is confused about the origin of the problem. Diseases like polio or other bacteriological or virus problems can predispose to chemical sensitivity with a subsequent lighter exposure of the chemicals or mycotoxins years later (51).
Subtle or large head injury results in memory loss; usually, short-term memory loss or episodes of confusion and imbalance may occur (52). Like the bacterial or viral disease, these injuries can predispose a subject to chemical sensitivity when another exposure occurs later in life.
Technology was developed not only at the Environmental Health Center – Dallas (EHC-D) but also by members of the American Academy of Environmental Medicine (AAEM) to verify and quantify chemical and electrical sensitivity in a less-polluted environment.
Materials for cleanliness (less-polluted environment for decreased air pollution, pesticides, specific herbicides and formaldehyde reduction), tissue oxygenation, nutrition, and less-polluted food and water were emphasized from our background in cardiovascular surgery at the University of Texas SW Medical School, Parkland Trauma Hospital, and at the Veterans’ Hospital. Randolph’s principle of low to no outgassing of construction materials in the rooms were followed and improved by particulate counts, gas chromatography, and mass spectrometry. These materials had no formaldehyde, phenol, pesticide, natural gas, or other chemicals and the construction principles outlined were followed (53). High-efficiency filters of non-toxic metal, ceramic, and charcoal for gases and particulates were used. However, low outgassing is paramount in constructing less-polluted rooms (54) made of stone, ceramic, hardwood, porcelain, glass, etc. This technology is the principle for accurate diagnosis and treatment. Clean living accounts for 60%–75% of the treatment (55). Less-polluted rooms for better diagnosis and treatment were constructed (53), (56), (57), (58).
Fenyves and Edgar did quantitative air analysis studies of indoor and outdoor air. Their Department of Physics, University of Texas at Dallas did building analyses and inspections. Evaluations were eventually performed in 500 buildings (57). However, they helped develop less-polluted areas and buildings consisting of 5× less particle counts which were also analyzed by gas chromatography and mass spectrometry for lower gaseous pollutants.
Matrix Laboratories (Gary Cude) now performs air analysis by commercial means and have performed 500–1000 air analyses in buildings. Also, Matrix Laboratories does portable air analysis that can be shipped from remote areas (59), (60). Formaldehyde, benzene, methane, ethane, propane, butane, toluene, and xylene, as well as pesticides and many other chemicals are found. A typical air analysis is shown in Table 1A and 1B. This analysis can be done for hundreds of chemicals.
|B. Microscopic examination of particulates on Air-O-Cell Filters of a home:|
|sample volume: 0/2 m3|
|Method: transmitted and polarized light microscopy, 100–1000×|
|Particulates>1 μ dia.||4555-1 Bedroom|
|4555-3 Living Room|
|Natural fibers (cellulose)||600||250||540|
Laboratory tests and their results: blood, urine, inhaled, total body
Rea presented papers on environmentally triggered cardiovascular disease, vasculitis, phlebitis, including biopsies, incitant tests and immune parameters, and implants, showing toxic substances could cause internal problems like gastrointestinal (GI) and genitourinary (GU) malfunction, kidney disease, and cardiovascular and brain dysfunction, in addition to fatigue, fibromyalgia, and ENT disease (60), (61), (62).
Wing, an Australian ENT surgeon, researched 100 nasal biopsies in the 1990s for molds and foods which triggered chemical sensitivity (63), showing the ground regulation system of the connective tissue matrix being congealed and destroyed.
Blood and urine analysis
Laseter quantitatively analyzed blood, air, and chemicals before and after chemically sensitive patients were placed in the controlled environment (64).
He also analyzed blood in 13,000 patients. Urine was measured in 5000 patients; solvents in 3000 patients; toxics, i.e. formaldehyde, phenol, petrochemicals, etc. and organophosphates and chlorinated pesticides were measured in 5000 patients (64).
Butler and Didriksen at the University of North Texas developed psychological profiles objectively showing brain injury, not psychological conditions. Over the years, approximately 2000–3000 profiles were done; approximately 2000 showed brain injury, not psychological conditions. Other abnormal laboratory analyses were found in the chemically sensitive (65), (66).
Brain SPECT scan
Simon and Hickey developed a triple-camera SPECT brain analysis technique for diagnosing brain toxicity patterns at Dallas Radiological Associates. Six hundred and eighty-two SPECT brain scans were taken between 2000 and 2015 (67) (Figure 1).
Autonomic nervous system disturbance in chemical sensitivity has been demonstrated objectively by two types of technologies:
Heart Rate Variability (68) – 1500 cases have been performed at the Environmental Health Center-Dallas. Pupillography for measuring the chemically sensitive were found by Ishikawa, S. and Miyata, M., Kitasato University Medical School, Kitasato, Japan.
These were found to be abnormal in the chemically sensitive with the following results: sympathetic increase alone, sympathetic increase and parasympathetic decrease, and parasympathetic decrease alone.
Thermography has been performed on 3000 chemically sensitive patients showing aberrations at the EHC-D (69).
Pangborn, Bland, and Pall first developed ways to define nutrient mechanisms for detoxification which have been used at the EHC-D in 10,000 patients (70), (71), (72). Many parameters were abnormal, including the detoxification mechanisms of methylation, sulfonation, gluconization, peptides, glutathione conjugation, and abnormal levels of peptides, individual vitamins, amino acids, carbohydrates, lipids, and minerals.
Nutrition has been measured subsequently and practically by Overberg for oral nutrition in 2000 patients (73) at the EHC-D.
Rea et al. has measured nutrient levels in 5000 patients treated them with intravenous nutrition (74) at the EHC-D.
Immune modulation is now measured objectively for chemical sensitivity by:
IgG subsets: IgG subsets in 200 patients (75) started at the EHC-D for immune evaluation were found to be abnormal.
T-cell deficiency or malfunction: T-cell deficiency or malfunction was analyzed in 5000 patients (76) finding 90% to be abnormal.
Body fluid analysis: Griffiths analyzed body fluids for the presence of molds and mycotoxins at EHC-D (77) in 500 patients and found 90% to be abnormal.
Urine mycotoxin analysis: Hooper analyzed urine mycotoxins which were first developed at the EHC-D for 200 patients (78). Now, he has measured several thousands in his facility, Real Time Laboratories (78), with 87% cases being found to be abnormal.
Serum complement: serum complement was found to be abnormal in 95% of the chemically sensitive patients.
Challenge tests are a way to quantify and verify chemical and electrical sensitivity
Challenge tests can involve oral (79), inhaled (80), and intradermal (81) tests; both oral and inhaled challenges with organic and commercial food can be used. Intradermal challenge, shown in a less-polluted room with preservative-free antigens, can be performed to confirm the diagnosis. Intradermal challenge was done with antigens for molds, pollens, foods, chemicals, and implant materials. These have been performed on 20,000 patients. Inhaled chemicals in the ECU room inside a less-polluted booth can be done and have been done in 1000 patients.
Provocation EMF challenge is done in a copper and porcelain steel room with various frequencies from a frequency generator.
EMF modulation was performed by:
Grounding – leather shoes
Shielding – copper, aluminum, silver – total body
Gowns – copper, silver, cotton
Metallic and magnetic impregnated blankets – vests, pads, energy balancing
1,3-Butadiene was the most commonly found chemical. This can be produced by natural isoprene in the body. It can also be a byproduct of the production of synthetic rubber found in automobile tires, nylon, styrene, or acrylonitrile, which is used in the production of rubber tires. Factories that produce butadiene are involved in the industrial production of 4-vinylcyclohexene.
|Examples of sources:|
|Butane (2-methyl propane) –||Cyclopropane, ethylidene –|
|Natural gas, refining petroleum, oil||Anesthetic, pyrethrum pesticides, chrysanthemums|
Exposure symptoms include blurred vision, vertigo, fatigue, low and high blood pressure, headaches, nausea, fainting, and decreased pulse for up to 2 years of exposure. Using breath analysis can broaden the clinician’s outlook on what toxics are present in patients and where they might be found in their environment so that avoidance can take place.
These different tests can be performed under less- polluted, environmentally controlled conditions to diagnose chemical and electrical sensitivity precisely. They take the guess work out of the diagnosis as they have now been performed in 30,000 patients seen at the EHC-D in the last 35 years. They should be spread out universally to aid in diagnosis. The pitfalls of ignoring the principles and facts developed, as well as the less-polluted controlled environment, over the last 30 years are obvious, and if not followed, can lead to errors in diagnosis and treatment.
Diagnostic tools are now available in the practicing physician’s office when construction and maintenance is performed on a routine basis, with attention to using less-polluted materials. The history and techniques have evolved over the last 30 years, taking the guess work out of chemically and electrically sensitive patient diagnosis and using the term psychological in the solid diagnosis of chemical and electrical sensitivity.
Lundy L. A brief history of food allergies. Hippocrates. 2007. Available at http://www.thesuperallergycookbook.com/pdf/foodallergypaper.pdf.
Gray’s Anatomy 2005. Greenwich Editions. London W10 6SP.
Guyton A. The Textbook of Modern Physiology. Philadelphia, PA: Saunders, 2010.
Heine H. Extracellular Matrix and Ground Regulation. Berkeley, CA: North Atlantic Books, 2007.
Corwin A. The crucial role of calcium plays in the body’s metabolism. Clin Ecol 1981;1(1):31–6.
Bland J, Barrager E, Reedy R, Bland K. A medical food-supplemented detoxification program in the management of health problems. Alt Ther 1995;1:62–71.
Selye, H. The general adaptation syndrome and the diseases of adaptation. J Allergy 1946;17:231–47.
Hare F. The food factor in disease. Vol. I, II. London: Longmans, 1905.
Rowe AH. Food allergy: its manifestation, diagnosis and treatment. Philadelphia, PA: Lea & Febiger, 1931.
Rinkel HJ. The role of food allergy in internal medicine. Ann Allergy 1944;2:115.
Hansel F. Coseasonal intracutaneous treatment of hay fever. J Allergy. 1941;12:457–69.
Randolph TG. The specific adaptation syndrome. J Lab Clin Med 1956;48:934.
Randolph TG. Human ecology and susceptibility to the chemical environment. Springfield, IL: Charles C. Thomas, 1962.
Willoughby JW. Serial dilution titration skin tests in inhalant allergy. Otolaryngol Clin North Am 1974;7:579–615.
Binkley E. Provocative testing and treatment for foods. Arch Otolaryngol 1969;90:113.
Lee CH. A new test for detection of food allergies, pollen and mold incompatibilities. Buchanan Co Med Bull 1961;25:9.
Miller JB. Food allergy, provocative testing and injection. Springfield, IL: Charles C. Thomas, 1972.
Maclennan J. Clinical titration principles & techniques Part 1. Clin Ecol 1974;II(3):151–8. Part II. II(4):207–13.
Herschel Discovers Infrared Light. Cool Cosmos Classroom activities. Retrieved 4 March 2013. He directed sunlight through a glass prism to create a spectrum […] and then measured the temperature of each colour. […].
Herschel W. Observations tending to investigate the nature of the Sun, in order to find the causes or symptoms of its variable emission of light and heat; With remarks on the use that may possibly be drawn from solar observations. Philos Trans R Soc Lond 1801;91:26–318.
Ritter J. Reception and discovery: the nature of Johann Wilhelm Ritter’s invisible rays. Stud Hist Philos Sci 1801;40(2);143–56.
Faraday M. Faraday’s chemical history of a candle: twenty two experiments and six classic lectures. Chicago, IL: Chicago Review Press, 1988.
Edison TA. Edison’s electric light and power system. Engineering and Technology History. Wikipedia. Available at: http://ethw.org/Edison’s_Electric_Light_and_Power_System.
Telsa N. Power and resonance. J Int Telsa Soc 6(4).
O’Sullivan JD. The CSIRO WiFi technology invention. Australian Academy of Science, 1977.
Mr. Paraskevakos was awarded U.S. Patent 3,842,208 (Sensor Monitoring Device) 1974.
Roentgen W. The discovery of x-ray beams; 1895. Available at: https://explorable.com/wilhelm-conrad-roentgen.
Villard P. Sur la réflexion et la réfraction des rayons cathodiques et des rayons déviables du radium. Compt Ren 1900;130:1010–2. See also: Villard P. Sur le rayonnement du radium. Compt Ren 1900;130:1178–9.
Audrode E. “Rays and Particles.” Galileo.phys.virginia.edu. Retrieved 2013-08-27.
E. Schliephake’s magnum opus on his new therapeutic techniques: Kurzwellentherapie (1932), translated by King Brown, short wave therapy (1935 London) and William Bierman and Myron M. Schwarzchild, The medical applications of the short wave current (1938 Baltimore).
Johannsen O. Cutaneous mast cells are altered in normal health Volunteers sitting in front of ordinary TVS/PCS – results from open-Field provation experiements; 2001. Available at: http://www.foodsmatter.com/es/computers_wifi_bluetooth/articles/johansson_tv_healthy_volunteers.pdf.
Real WJ, Pan Y, Fenyves EJ, Sujisawa I, Nasrola S, et al. Electromagnetic field sensitivity. J Bioelectricity 1991;10(1 & 2):241–56.
Belpomme D, Irigaray P, Hardell L. Electromagnetic fields as cancer-causing agents. Environ Res 2008;107:289–90.
Carpenter D, Sage C, editors. BioInitiative Working Group BioInitiative Report: A Rationale for a Biologically-based Public Exposure Standard for Electromagnetic Fields (ELF and RF); 2007. Available at: http://www.bioinitiative.org.
Hardell L, Carlberg M, Söderqvist F, Hardell K, Björnfoth H, et al. Increased concentrations of certain persistent organic pollutants in subjects with self-reported electromagnetic hypersensitivity–a pilot study. Electromagn Biol Med 2008;27(2):197–203.
Smith C, Monro J. Electrical sensitivities in allergy patients. Clin Ecol 1980-1982;4(3):93–102.
Frohlich H. The extraordinary dielectric properties of biological molecules and the actions of enzymes’. Proc Natl Acad Sci USA 1975;72:4211–15.
Randolph TG. The ecologic unit. Part I. Hosp Manage 1964;97:45–7.
Dickey LD, editor. Clinical ecology. v. 86. Springfield, IL: Thomas, 1976.
Mustafa MG, Tierney DF. Biochemical and metabolic changes in the lung with oxygen, ozone, and nitrogen dioxide toxicity. Am Rev Respir Dis 1978;118:6.
Rea WJ. Chemical sensitivity. Vol. I. Mechanisms of Chemical Sensitivity. Boca Raton, FL: Lewis Publishers, 1992;1:19–21.
Stokinger HE, Coffin DL. “Biological effects of air pollution,” in air pollution. v. 1, 2nd ed., Stern AC, editor. New York: Academic Press, 1968:445.
Stokinger HE. Ozone toxicology: a review of research and industrial experience (1954-1964). Arch Environ Health 1965;10:719.
Bennett G. Ozone contamination of high altitude aircraft cabins. Aerosp Med 1962;33:969.
National Research Council. Toxicity testing: strategies to determine needs and priorities. Washington, DC: National Academy of Sciences, 1984.
Evans MJ, Cabral LJ, Stephens RJ, Freeman G. Renewal of alveolar epithelium in the rat following exposure to nitrogen dioxide. Am J Pathol 1973;70:175.
Adolph EF. General and specific characteristics of physiological adaptations. Am J Physiol 1956;184:18.
Adamson IYR, Bowden DH. The type II cell as a progenitor of alveolar epithelial regeneration: A cytodynamic study on mice after exposure to oxygen. Lab Invest 1974;30:35.
Evans MJ, Cabral LJ, Stephens RJ, Freeman G. Transformation of alveolar type II cells to type I cells following exposure to nitrogen dioxide. Exp Mol Pathol 1975;22:142.
Rea WJ. Chemical sensitivity. Boca Raton, FL: Lewis Publishers, 1992;1:12–4.
Rea WJ. Personal Communications – Nerve Injury, 1992.
Rea WJ. Personal Communications – Head Injury, 1992.
Randolph TG. Hospital comprehensive environmental control program. Clinical Ecology. Dickey LD, editor. Springfield, IL: Thomas, 1976;70.
Randolph TG, editor. Human ecology and susceptibility to the chemical environment. Springfield IL: Thomas, 1962.
Rea WJ. Chemical sensitivity. Volume I. Clean living makes up 60–75% of treatment. Boca Raton, FL: Lewis Publishers, 1992.
Cull I. Interpreting Mold Spore Counts from EAA, Inc.; 2010. Available at: http://indoorairnerd.com/mold/interpreting-mold-spore-counts-from-eaa-inc.
Rousseau D, Rea WJ, Enwright J. Your home, your health, and well-being. Vancouver, B.C.: Hartley and Marks, 1988.
Edgar RT, Fenyves EJ, Rea WJ. Air pollution analysis used in operating an environmental control unit. Ann Allergy 1979;42(3):166–73.
Matrix Laboratories (Gary Cude), 1206 Industrial Drive, Royce City, TX 75189.
Rea WJ, Suits CW, Gerrard JW, D.M. editors. Cardiovascular disease triggered by Foods and Chemicals. Food allergy: new perspectives. Charles C. Thomas, 1980:99–143.
Rea WJ. Review of Cardiovascular Disease in Allergy. Bi-Annual Review of Allergy. Frazier C, editor, 1979–80:282–347.
Rea WJ. Environmental Aspects of Ear, Nose and Throat Disease. Otolaryngologic Allergy, King HC, editor, Symposia Specialists, Inc., Miami, FL, 1981.
Wing L. Australian ENT surgeon. Personal communication.
Laseter JL, Ildefonso RD, Rea WJ, Butler JR. Pesticides and brain-function changes in a controlled environment. Clin Ecol 1984;II(3):145–50.
Butler JR, Didriksen NA. Environmental Symptom Checklist Psychological. Unpublished assessment instrument. Environmental Health Psychologists. P.O. Box 399, Dewey, OK, 74029, 1981.
Rea WJ, Didriksen N, Simon TR, Pan Y, Fenyves EJ, et al. Effects of toxic exposure associated with neurobehavioral and pulmonary impairment: a preliminary report. Archives of Environmental Health, Heldref Publications, 2003.
Fincher CE, Chang T-S, Harrell EH, Kettelhut MC, Rea WJ, et al. Comparison of single photon emission computed tomography findings in cases of healthy adults and solvent-exposed adults. Am J Indus Med 1997;31:4–14.
Shirakawa S, Rea WJ, Ishikawa S, Johnson A. Evaluation of the autonomic nervous system response by pupillographical study in the chemically sensitive patient. Environ Med 1991;8(4):121–7.
Isikawa S, Naito M, Inabe K. A new videopupillography. Opthalmologica 1970;160:248.
Medical Digital Infrared Thermal Imaging-Environmental Health Center, Dallas, TX; 1998. Available at: https://www.ehcd.com/medical-digital-infrared-thermal-imaging-thermography/.
Pangborn J. Nutritional and anti-inflammatory aspects of amino acids. In 1984-85 yearbook for nutritional medicine. 1st ed., Bland J, editor. New Canaan, CT: Keats Publishing Inc., 1985:153–78.
Bland J. Nutritional and anti-inflammatory aspects of amino acids. In 1984-85 yearbook for nutritional medicine. 1st ed., Bland J, editor. New Canaan, CT: Keats Publishing Inc., 1985:153–78.
Rea WJ. Environmental Health Center-Dallas. Personal Communication, 2011.
Pall ML, Anderson JH. The vanilloid receptor as a putative target of diverse chemicals in multiple chemical sensitivity. Arch Environ Health 2004;59(7):363–75.
Overberg R. Environmental Health Center-Dallas. Personal Communication.
Rea WJ. Environmental Health Center-Dallas. Personal Communication – Gamma Globulin, 2011.
Rea WJ, Johnson AR, Youdim S, Fenyves IJ, Samadi Na. T and B lymphocyte parameters measures in chemically sensitive patients and controls. Clin Ecol 1986;4(1):11–4.
Rea WJ, Pan Y, Griffiths B. The treatment of patients with mycotoxin-induced disease. Toxicol Indus Health 2009; 25(9–10):711–4.
Hooper D. Real Time Laboratories, Carrollton, TX 75010; 2001. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3920250/, Chronic Illness Associated with Mold and Mycotoxins.
Rea WJ. Chemical sensitivity. Vol. IV. Tools of diagnosis and methods of treatment. Boca Raton, FL: Lewis Publishers, 1986:2275–80.
Rea WJ. Chemical sensitivity. Vol. IV. Tools of diagnosis and methods of treatment. Boca Raton, FL: Lewis Publishers, 1986:2261–71.
Published Online: 2016-07-06
Published in Print: 2016-09-01
Citation Information: Reviews on Environmental Health. Volume 31, Issue 3, Pages 353–361, ISSN (Online) 2191-0308, ISSN (Print) 0048-7554, DOI: https://doi.org/10.1515/reveh-2015-0021, July 2016