Salem, NY -- To date, 26 governors around the nation have proclaimed May 2007 as Multiple Chemical Sensitivity (MCS) and/or Toxic Injury (TI) Awareness and Education Month. A list of these states along with copies of the proclamations may be viewed at MCS and TI Proclamations
Many of the illnesses in our society today may result from exposure to toxicants in the environment. Numerous empirical studies have shown correlations between neurotoxicity and neurodevelopmental disorders such as autism, attention deficit hyperactivity disorder, environmental illness/multiple chemical sensitivities, encephalopathy, and possibly sudden infant death syndrome. Increasing numbers of Americans are developing multiple chemical sensitivity (MCS), chemical injury (CI), environmental illness (EI), asthma, reactive airway disease, autism, attention deficit hyperactivity disorder, fibromyalgia, chronic fatigue syndrome (CFS), and other disorders.
In the United States autism, once a rare condition, has increased from 4 – 5 per 10,000 children in the 1980’s to 30 – 60 per 10,000 children in the 1990’s, a greater than ten-fold increase. The prevalence of attention deficit hyperactivity disorder (ADHD) is currently estimated at 8% of the population. Gliniania suggests an etiological link between metals in particulate air pollution and some forms of sudden infant death syndrome (SIDS). The prevalence of MCS ranges from 16% to 33% of the population. When compared to the prevalence of diabetes, which is well publicized at 7% of the population, less than half the prevalence of MCS and other environmental illnesses.
Multiple chemical sensitivity is an environmental illness which causes negative health effects in multiple organ systems. Respiratory distress, seizures, cognitive dysfunction, heart arrhythmia, nausea, headache, and fatigue result from exposure to levels of common chemicals such as perfumes, fragrances, cleaners, and pesticides that are normally deemed as safe. In 1999 consensus criteria were established for the diagnoses and definition of MCS. The criteria define MCS as symptoms that are reproducible with repeated chemical exposure, are chronic, appear at levels of exposure lower than previously tolerated, improve or resolve when incitants are removed, appear in response to multiple chemically unrelated substances, and which involve multiple organ systems that commonly include the cardiac, pulmonary, and neurological systems.
History of MCS in Science
One of the first studies on MCS focused on possible long term potentiation in the hippocampus and neural sensitization as a central mechanism. Later studies examined the role of the inflammatory process and found that brain inflammation was correlated with symptoms of MCS. In 1999 Meggs proposed that MCS is caused by low molecular weight chemicals that bind to chemoreceptors on sensory nerve C-fibers leading to the release of inflammatory mediators. McKeown-Eyssen showed that polymorphisms in the CYP2D6 allele may be responsible for variation in toxicant metabolism pathways that may cause differences in susceptibility to MCS. Pall identified evidence suggesting elevated nitric oxide and peroxynitrite (NO/ONOO-) as the etiology for MCS and several related conditions including fibromyalgia, post traumatic stress disorder, gulf war syndrome, and chronic fatigue syndrome. Pall has identified organic solvents and related compounds, organophosphorus/carbamate pesticides, organochlorine (chlordane, lindane) pesticides, and the pyrethroid pesticides as initiating the NO/ONOO- cycle of biochemistry leading to MCS. With such a large percentage of the population suffering from MCS and a large number of toxicants capable of initiating the NO/ONOO- cycle it is conceivable that a common exposure may initiate or exacerbate MCS. It is also plausible that a combination of toxicants may be linked to the etiology of MCS.
Genetic Variants
There is a variety of physiological, biochemical, and genetic studies on MCS including objective biomarker tests for MCS that have been published by Kimata, Millqvist, Bell and Fox and their respective colleagues, each of which is based on measurable physiological changes in response to low level chemical exposures of MCS patients. Genetic data of McKeown-Eyssen and her colleagues and the earlier work of Haley and his colleagues shows that the chemicals initiating MCS act as toxicants, not as odors generating some strictly olfactory response. McKeown-Eyssen published data showing that five genetic polymorphisms each have a statistically significant role in determining MCS prevalence. Each of these genes encodes proteins that metabolize chemicals previously implicated in MCS, notably the organophosphorus pesticides (PON1 and PON2 genes) and the organic solvents (CYP2D, NAT1 and NAT2 genes). These data show that chemicals shown to initiate MCS must be in a specific chemical form to be active; therefore individuals who metabolize them at different rates vary in their susceptibility to MCS. Haley found similar, confirmatory results with the PON1 gene in studies of the Gulf War syndrome veterans. Genetic studies coupled with known biochemical functions of the genes involved are the recognized approach to determining biological mechanism. Therefore, these specific studies provided significant confirmation of the toxicogenic roles of chemicals previously implicated in MCS.
In simple terms, three recent studies show that a genetic variant makes sufferers of multiple chemical sensitivity (MCS) more likely to develop the condition. In 2004, McKeown-Eyssen studied 203 MCS sufferers and 162 controls and found that genetic differences relating to detoxification processes were present more often in those with MCS than those without. The study concluded that "a genetic predisposition for MCS may involve altered biotransformation of environmental chemicals. Haley found similar, confirmatory results in a 1999 study with the PON1 gene in Gulf War syndrome veterans.
A new study by Schnakenberg et al (2006) confirmed the genetic variation previously found by McKeown-Eyssen and Haley. A total of 521 unrelated individuals participated in the study. Genetic variants of four genes were analyzed: NAT2, GSTM1, GSTT1, and GSTP1. The researchers concluded that individuals who are NAT2 slow acetylators and those with homozygously deleted GSTM1 and GSTT1 genes are significantly more likely to develop chemical sensitivity.
According to the study the glutathione S-transferases act to inactivate chemicals so people without these GSTM1 and GSTT1 genes are less able to metabolize environmental chemicals. If a person cannot metabolize chemicals they build up in the body and cause disturbances in normal body function. Schnakenberg and fellow researchers explain that "glutathione S-transferases play an important role in the detoxification of chemicals... the deletion of this gene may be an important step in the early onset of diseases" which is a critical discovery that provides a biological basis behind the etiology of multiple chemical sensitivity. The researchers also noted that diseases such as non-Hodgkin's lymphoma, hepatocellular and prostate carcinoma, and Alzheimer's disease have been associated with the common chemicals metabolized by GSTP1. The deletion of the GSTP1 gene leaves individuals more susceptible to developing these diseases, as lack of these genes means a loss of protection from oxidative stress.
Economic Impact
The effect of these neurodevelopmental disorders reaches beyond the individual to the parent, the social system, the work force, school curriculum, medical providers, care providers, the welfare system, and therefore affects the pocketbooks of every taxpaying citizen. Cumulative social and economic costs identified in four case studies of illnesses that are candidates for environmental causation totaled between $568 billion and $793 billion dollars per year in Canada and the United States. Neurodevelopmental disorders cost the United States $81.5 to $167 billion annually and Methylmercury induced toxicity alone is estimated to cost $8.7 billion dollars in lost productivity in the United States. Sixty-seven percent of chemicals imported into the United States have not been examined for neurotoxicity and could be a further contributing factor. Individuals affected by neurodevelopmental disorders will increasingly become a burden to society for care as they age, giving rise to the essentiality that scientists discover the etiology behind this alarming increase. The costs of reduced IQ in the United States alone in 1987 may have reached $327 billion.
Impact on Victims
The sufferers of these conditions are often unable to obtain qualified medical care or rehabilitation services. These patients are often misdiagnosed with psychiatric disorders due to the outward symptoms of physiological neurotoxicity. While they may be treated with detoxification protocols and/or exposure education, they are too often referred for useless, and in some cases harmful, psychiatric therapy and medications that exacerbate their symptoms. Indeed 80% report no benefit from psychotherapy to treat MCS and 15% reported harm from psychotherapy. Though 65% find psychotherapy helpful to cope with the dramatic life changes the condition imposes upon them, psychotherapy is obviously not a cure because MCS is not a psychologically mediated disease. Not a single empirical study shows any significant remission rate in the symptoms of environmental illness from counseling.
The most effective treatments to date involve avoiding all chemicals, creating a chemical-free living space, and various methods employing detoxification to reduce body burden of toxicants. Most insurance in our medical system will not cover tests to determine body burden of chemicals or necessary detoxification. Of special note is that the Medicaid and Medicare that these patients must rely on once they become disabled does not cover the treatments that could very well return the patient to full productivity, thus removing them from the reliance on the disability and social systems. This is penny wise and pound foolish and amounts to draconian torture of innocent patients who truly desire qualified medical care and the opportunity to return to full lives and careers. Many report they had successful, professional careers prior to becoming ill and reported that they would happily resume their old lives if they could find relief from their MCS. Part of this relief would include proper accommodations for MCS in the workplace and school system so that patients. The solutions are really very simple and chemical avoidance should be practice by all people, regardless of health. To create a workplace and school without toxicants would benefit all who occupy it and prevent toxic injury to healthy occupants. No one is safe from this mass pandemic. These illnesses pose a clear threat to our welfare, social security, and disability systems and are completely avoidable!
Harmful to Everyone!
Regardless of MCS, a study by Anderson has shown toxicants like fragrances are harmful to everyone, not just those who develop MCS. This is conclusive scientific evidence that fragrances are harmful toxicants! The fragrance industry has made unsubstantiated claims to the safety of fragrances that are not backed by science and are insufficient protection for Americans. Just because a product is on the market does not mean it is safe. Consider pesticides which have been scientifically shown over and over again to be endocrine disruptors and are currently blamed for the huge increase in hypothyroidism, cancer, MCS, and many other illnesses. The trade secret laws of the fragrance industry block individuals from being able to determine what ingredients are in fragrances, furthering damage to innocent people. Second hand fragrance is equivalent to second hand smoke!
A perfect example of this dilemma is the toxic effects of commonly used fragranced items such as air fresheners. Many well-established toxicants are emitted during air freshener use including "d-limonene, dihydromyrcenol, linalool, linalyl acetate, and beta-citronellol which were emitted at 35-180 mg/day over 3 days while air concentrations averaged 30-160 microg/m3" as shown in a recent study. Maternal depression is also significantly associated with air fresheners. Glade, which contains short chain aliphatic hydrocarbons, is shown to cause ventricular fibrillation and is potentially fatal if inhaled. In a 1997 study, emissions of "air freshener at several concentrations (including concentrations to which many individuals are actually exposed) caused increases in sensory and pulmonary irritation, decreases in airflow velocity, and abnormalities of behavior measured by the functional observational battery score". A 2006 study at the University of Colorado and Baylor College of Medicine in Houston concluded that air-freshening chemicals may lead to the formation of cancerous cells by suppression of the enzymes that are essential for regulating normal cell death. There are many acute toxic effects of fragranced products including but not limited to neurotoxicity, sensory irritation, pulmonary irritation, decreasing expiratory airflow velocity, and alterations of functional observational battery. What is absolutely clear is the evidence that pollution and toxicants affect the brain and central nervous system in a negative way and cost taxpayers billions of dollars. MCS is not new; it is simply unacknowledged mainly because a clear etiology has yet to be replicated. Many currently recognized conditions including chronic fatigue syndrome (CFS), asthma, sudden infant death syndrome (SIDS), attention deficit hyperactivity disorder (ADHD), autism, diabetes, multiple sclerosis, Parkinson’s and cancer have no clear etiology either. Yet they are recognized and their victims supported by social and medical services and research funding. MCS, which affects more of the population than any of the above, needs similar recognition, investigation, and support.
A New Paradigm
Members of the work force needed to support a healthy economy are being lost to the productive sector. It is critical to global economies and global well-being in the upcoming century to have practitioners, health care service administrators, and public health officials well-educated in the new chemical paradigm of illness, toxicology, and environmental medicine so that patients are treated and returned to the workforce. Indeed, while infectious disease was formerly the main threat to health, it has now been over compensated for in our zeal to kill germs with potentially toxic chemical disinfectants and pesticides. This has generated a new disease paradigm in which anthropogenic chemicals are becoming an increasingly ominous threat to heath as even more diseases are revealed to be of chemical origin or are chemically aggravated.
Dr. Martin Pall, PhD of Washington State University Department of Molecular Biosciences, regards MCS as being related to other multi-system diseases including chronic fatigue syndrome (CFS), which was recently recognized by the Centers for Disease Control and Prevention, who cites chemical sensitivities as a symptom of CFS. MCS substantially limits the ability of it's victims to live normal lives, work, attend school, shop, and socialize as a myriad of common items generally recognized as safe cause dangerous reactions. These items include fragrances found in perfumes, lotions, soaps, and laundry products as well as cleaners, pesticides, diesel, news print, new carpets, and many other items encountered in day to day living.
Patients need more qualified medical care, increased access to public facilities under the Americans with Disabilities Act, and support from family and friends once afflicted while doctors need additional training and scientists need more funding for additional research into the etiology of MCS. This is truly a crisis situation! MCS affects a person’s ability to earn a living, travel, socialize, and function in our modern world in which chemicals and fragrances are impossible to avoid. Learn all you can. You could be next!
For additional information e-mail MCS America, admin@mcs-america.org or visit www.mcs-america.org.
About the Author
Lourdes Salvador is a writer and social advocate based in Hawaii. She is the president of MCS America and a featured monthly writer for MCS America News at http://www.mcs-america.org/. She is a passionate advocate for the homeless, having worked with her local governor to open new shelters and provide services to the homeless based on a presentation of her ideas. That passion soon turned to advocacy and activism for victims of multiple chemical sensitivity. For more information about Lourdes and her advocacy work, please visit: http://www.mcs-america.org/, http://www.thetruthaboutmcs.blogspot.com/, and www.cafepress.com/mcsamerica.
Copyrighted © 2007 Lourdes Salvador
References
Ader, R, (1987). Behavioral Influences of Immunity. Proceedings of American Academy of Environmental Medicine. Annual Meeting. Nashville, TN.
Air-freshening chemicals may lead to cancerous cells (2006) Denver Post. Nation: World News. Retrieved May 15, 2006 from: http://www.denverpost.com/search/ci_3823832
American Diabetes Association (2006). Diabetes Statistics. Retrieved January 1, 2007, Web site: http://www.diabetes.org/diabetes-statistics.jsp
Anderson, RC, & Anderson, JH (1998) Toxic effects of air freshener emissions. Archives of Environmental Health. 52(6):433-41.
Bell IR, Baldwin CM, Schwartz GE. (1998). Illness from low levels of environmental chemicals: relevance to chronic fatigue syndrome and fibromyalgia. Am J Med 105:74S-82S.
Binkley, K, King, N, Poonai, N, Seeman, P, Ulpian, C, Kennedy, J (2001). Increased prevalence of panic disorder-associated cholecystokinin B receptor allele 7. Journal of Allergy and Clinical Immunology. 107:887-890.
Binns JH, Cherry N, Golomb BA, et al (2004). [Research Advisory Committee on Gulf War Veterans’ Illnesses]. Report and Recommendations.
Body burden: the pollution in people, (2007). Retrieved January 2, 2007, from Environmental Working Group Web site: http://www.ewg.org/reports/bodyburden/
Bokina, AI, et al. (1976). Investigation of the mechanism of action of atmospheric pollutants on the central nervous system and comparative evaluation of methods of study. Environmental Health Perspectives. 13: 37-42.
Bonham, AC, Chen, CY, Mutoh, T, Joad, JP (2001). Lung c-fiber CNS reflex: role in the respiratory consequences of extended environmental tobacco smoke exposure in young guinea pigs. Environmental Health Perspectives. 109:4, 573-578.
Booker, S (2001). NIEHS investigates links between children, the environment, and neurotoxicity. Environmental Health Perspectives. 109:6, A258-A261.
Braun, JM, Robert SK, Froehlich, T, Auinger, P, & Lanphear, BP (2006). Exposures to environmental toxicants and attention deficit hyperactivity disorder in U.S. children. Environmental Health Perspectives. 114:12, 1904-1909.
Brostoff, J, & Challacombe, S (1987). Food Allergy and Intolerance. London: Bailliere Tindall/W.B. Saunders.
Bruhn, P, et al. (1981). Prognosis in chronic toxic encephalopathy: A two year follow-up study in 26 house painters with occupational encephalopathy. Acta Neurology Scandinavia. 64: 259-272.
Burbacher, TM, Shen, DD, Liberto, N, Grant, KS, Cernichiari, E, & Clarkson, T (2005). Comparison of blood and brain mercury levels in infant monkeys exposed to methylmercury or vaccines containing thimerosal. Environmental Health Perspectives. 113:8, 1015-1021.
Calabrese, EJ (1977). Pollutants and high risk groups. The Biological Basis of Increased Human Susceptibility to Environmental and Occupational Pollutants. New York: Wiley Interscience.
Callender, TJ, et al. (1993). Three-dimensional brain and metabolic imaging in patients with toxic encephalopathy. Environmental Res. 60: 295-319.
Callender, TJ, et al. (1995). Evaluation of chronic neurological sequelae after acute pesticide exposure using SPECT brain scans. Journal Toxicology & Environmental Health. 41:275-284.
Chronic Fatigue Syndrome, (2006). Symptoms. Retrieved January 2, 2007, from Centers for Disease Control Web site: http://www.cdc.gov/cfs/cfssymptomsHCP.htm
Clarkson, TW (2002). The Three Modern Faces of Mercury. Environmental Health Perspectives. 110:1, 11-23.
Clayson, CD, Amdur, MO, Doull, J. Casarett and Doull's Toxicology: The Basic Science of Poisons, MacMillan Publishing Co., New York, NY.
Colborn, T (2004).Neurodevelopment and endocrine disruption. Environmental Health Perspectives. 112:9, 944-949.
Davidson, M, & Fienleib. M (1972). Disulfide poisoning: A review. American Heart H 83:100.
Davis, TH, Jason, LA, & Banghart, MA (1995). The effect of housing on individuals with multiple chemical sensitivities. Archives of Environmental Health, 50:425-431.
DeRosa, CT, Hicks, HE, Ashizawa, AE, Pohl, HR, Mumtaz, MM (2006). A regional approach to assess the impact of living in a chemical world. Annals of the New York Academy of Sciences. 1076:829-38.
Dickey, LD (1976). Clinical Ecology. Springfield, IL: Charles C. Thomas.
Dodson, RF, Atkinson, MA (2006). Measurements of asbestos burden in tissues. Annals of the New York Academy of Sciences. 1076:281-91.
Edling, C, et al. (1990). Long-term follow-up of workers exposed to solvents. British Journal of Industrial Medicine 47:75-82.
Farrow, A, Taylor, H, Northstone, K, Golding, J (2003). Symptoms of mothers and infants related to total volatile organic compounds in household products. Archives of Environmental Health. 58(10):633-41.
Foo, SC, et al. (1990). Chronic neurobehavioral effects of toluene. Journal of Industrial Medicine. 47:480-44.
Freedman, BJ (1980). Sulphur dioxide in foods and beverages: Its use as a preservative and its effect on asthma. Br Journal Dis Chest 74(2):128-134.
Furst, P (2006). Dioxins, polychlorinated biphenyls and other organohalogen compounds in human milk. Levels, correlations, trends and exposure through breastfeeding. Molecular Nutrition & Food Research. 50(10):922-33.
Gibson, P (2003). Perceived treatment efficacy for conventional and alternative therapies reported by persons with multiple chemical sensitivity. Environmental Health Perspectives. 111:12, 1498 – 1504.
Gibson, P (2005). Understanding & accommodating people with multiple chemical sensitivity in everyday living. Houston, TX: Independent Living Research Utilization.
Gibson, PR, Cheavens, J, & Warren, ML Chemical injury chemical sensitivity and life disruption. James Madison University.
Gibson, PR, Elms, AN, Ruding, LA (2003). Perceived treatment efficacy for conventional and alternative therapies reported by persons with multiple chemical sensitivity. Environmental Health Perspectives. 111(12), 1498-1504.
Gibson, PR, Placek, E, Lane, J, Brohimer, SO, & Earehart Lovelace, AC (2005). Disability induced identity changes in persons with multiple chemical sensitivity. Qualitative Health Research. 15:4, 1-23.
Gilpin, A (1978). Air Pollution, 2nd edition. St. Lucia, Queensland: University of Queensland Press.
Glinianaia, SV, Rankin, J, Bell, R, Pless-Mulloli, T, & Howel, D (2004). Does particulate air pollution contribute to infant death? A systemic review. Environmental Health Perspectives. 112:14, 1365-1370.
Goodman, LR, & Koduru, S (2000). Chemicals in the environment and developmental toxicity to children: A public health and policy perspective. Environmental Health Perspectives. 108:S3, A412-A413.
Goth, SR, Chu, RA, Gregg, JP, Cherednichenko, G, & Pessah, IN (2006). Uncoupling of ATP-mediated calcium signaling and dysregulated interleukin-6 secretion in dendritic cells by nanomolar thimerosal. Environmental Health Perspectives. 114:7, 1083-1091.
Gregersen, P, et al.(1987). Chronic toxic encephalopathy in solvent-exposed painters in Denmark 1976-1980: Clinical cases and social consequences after a 5-year follow-up. American Journal of Industrial Medicine. 11: 399-417.
Haley, RW Billecke, S, & La Du, BN (1999). Association of low PON1 type Q (type A) arylesterase activity with neurologic symptom complexes in Gulf War veterans. Toxicology and Applied Pharmacology 157(3):227-33.
Hertz-Picciotto, I, Croen, L, Hansen, R, Jones, C, Van De Water, J, & Pessah, I (2006). The CHARGE study: an epidemiologic investigation of genetic and environmental factors contributing to autism. Environmental Health Perspectives. 114:7, 1119-1125.
Heuser, G, et al. (1994). Neurospect findings in patients exposed to neurotoxic chemicals. Toxicology & Industrial Health. 10:561-571.
Hill, J (1987). Peptides and their receptors as the biochemicals of emotion. Proceedings of the American Academy of Environmental Medicine. Annual Meeting. Nashville, TN.
Hodgson, MB, et al. (1989) Encephalopathy and vestibulopathy following short-term hydrocarbon exposure. Journal Occupational Medicine. 31: 51-54.
Innami, S, Tojo, H, Utsuja, S, Nakamura, A, & Nagazama, S (1974). PCB toxicity and nutrition. PCB Toxicity and Vitamin A. Japanese Journal of Nutrition 32:58-666.
Joffres MR, Sampalli T, Fox RA. (2005). Physiologic and symptomatic responses to low-level substances in individuals with and without chemical sensitivities: a randomized controlled blinded pilot booth study. Environ Health Perspect 113:1178-1183.
Jollow, DJ, et al. (1977). Biological reactive intermediates: Formation, toxicity, and innetivation. New York.
Jonkman, EJ, et al. (1992). Electroencephalographic studies in workers exposed to solvents or pesticides. Electro Clinical Neurophysiology. 82: 439-444.
Kerger, BD, Leung HW, Scott, P, Paustenbach, DJ, Needham, LL, Patterson, DG Jr., Gerthoux, PM, Mocarelli, P (2006). Age- and concentration-dependent elimination half-life of 2,3,7,8-tetrachlorodibenzo-p-dioxin in Seveso children. Environmental Health Perspectives. 114(10):1596-602.
Kilburn, KH (1998). Chemical Brain Injury. Van Nostrand Reinhold.
Kimata H. (2004). Effect of exposure to volatile organic compounds on plasma levels of neuropeptides, nerve growth factor and histamine in patients with self-reported multiple chemical sensitivity. In J Hyg Environ Health 207:159-163.
King, DS (1981). Can allergic exposure provoke psychological symptoms? A double-blind test. Biological Psychiatry 16:3-10.
Koch, L (2004).Multiple chemical sensitivity and rehabilitation planning implications. Kent State University Center for Disability Studies.
Larsen, JC (2006). Risk assessments of polychlorinated dibenzo- p-dioxins, polychlorinated dibenzofurans, and dioxin-like polychlorinated biphenyls in food.. Molecular Nutrition & Food Research. 50(10):885-96.
Laseter, JL, DeLeon, IR, Rea, WJ, & Butler, JR (1983). Chlorinated hydrocarbon pesticides in environmentally sensitive patients. Clinical Ecology. 2(1):3-12.
Li, QQ, Loganath, A, Chong, YS, Tan, J, Obbard, JP (2006). Levels of persistent organic pollutant residues in human adipose and muscle tissues in Singapore. Journal Toxicology & Environmental Health A. 69(21):1927-37.
Losiniecki, A, & Prahlow, JA (2006). Sudden Infant Death Due to Neurofibromatosis Type 1. American Journal of Medical Pathology. 27:4, 317-319.
Lovechio, F, & Fullton, SE (2001). Ventricular fibrillation following inhalation of Glade Air Freshener. European Journal of Emergency Medicine. 8(2):153-4.
McKeown-Eyssen, G, Baines, C, Cole, D, Riley, N, Tyndale, R, Marshall, L, & Jazmaji, V (2004). Case-control studies of genotypes in multiple chemical sensitivity: CYP2D, NAT1, NAT2, PON1, PON2 and MTHFR. International Journal of Epidemiology 33, 1-8.
Meggs, WJ (1999). Mechanisms of allergy and chemical sensitivity. Toxicology and Industrial Health. 15:3-4, 331-338.
Meggs, WJ, Dunn, KA, Bloch, RM, Goodman, PE, & Davidoff, AL (1996). Prevalence and nature of allergy and chemical sensitivity in the general population. Archives of Environmental Health. 51(4):275-82.
Miller, CS (1995). Multiple chemical sensitivity syndrome. Journal of Occupational and Environmental Medicine. 37:13-23.
Millqvist E, Bengtsson U, Lowhagen O. (1999). Provocations with perfume in the eyes induce airway symptoms in patients with sensory hyperreactivity. Allergy 54:495-499.
Morrow, LA, et al. (1990) Alternations in cognitive and psychological functioning after organic solvent exposure. Journal of Occupational Medicine. 32:444-450.
Muir, T, & Zegarac, M (2001). Societal costs of exposure to toxic substances: Economic and health costs of four case studies that are candidates for environmental causation. Environmental Health Perspectives. 109:6, 885-903.
National Research Council. Indoor Pollutants. Washington, D.C.: National Academy Press, 1981.
Orbaek, P, Lindgren, M (1988). Prospective clinical and psychometric investigation of patients with chronic toxic encephalopathy induced by solvents. Scandinavian Journal of Work & Environmental Health, 14:37-44.
Pall, M (2003). Elevated nitric oxide/peroxynitrite theory of multiple chemical sensitivity: central role of N-methyl-D-aspartate receptors in the sensitivity mechanism. Environmental Health Perspectives. 111:12, 1461-1464.
Pall, M (2006). Novel disease paradigm produces explanations for a whole group of illnesses. Washington State University, Department of Biochemistry and Basic Medical Sciences, Retrieved December 3, 2006, from: http://molecular.biosciences.wsu.edu/Faculty/pall/pall_main.htm
Pan, Y, Johnson, AR, & Rea, WJ (1987-88). Aliphatic hydrocarbon solvents in chemically sensitive patients. Clinical Ecology. 5(3):126-131.
Randolph, T.G. Human Ecology and Susceptibility to the Chemical Environment. Springfield, IL: Charles C. Thomas, 1962 (sixth printing 1978).
Rasmussen, H, et al. (1985). Risk of encephalopathia amongst retired solvent-exposed workers. Journal of Occupational Medicine. 27:581-565.
Rea, WJ, & Mitchell, MJ *(1982). Chemical sensitivity and the environment. Immunology Allergy & Practice Sept/Oct:21-31.
Rea, WJ, et al. (1987). Toxic volatile organic hydrocarbons in chemically sensitive patients. Clinical Ecology 5(2):70-74.
Rea, WJ, Johnson, AR, Ross, GH, Butler, JR, Fenyves, EJ, Griffiths, B,& Laseter, J (2006). Considerations for the Diagnosis of Chemical Sensitivity. Retrieved January 1, 2007 from http://www.aehf.com/articles/A55.htm
Rea, WJ, Peters, DW, Smiley, RE, et al. (1981). Recurrent environmentally triggered thrombophlebitis. Ann Allergy 47:338-344.
Schettler, T (2001).Toxic threats to neurologic development of children. Environmental Health Perspectives. 109:6, 813-816.
Schnare, D, & Shields, M (1954). Body burden reduction of PBS’s, PBB’s and chlorinated pesticides in human subjects. Ambio. 13:378-80.
Seppalainen, AM, et al. (1978). Neurophysiological effects of long-term exposure to a mixture of organic solvents. Scandinavian Journal of Work & Environmental Health. 4: 304-314.
Singer, BC, Destaillats, H, Hodgson, AT, Nazaroff, WW (2006). Cleaning products and air fresheners: emissions and resulting concentrations of glycol ethers and terpenoids. Indoor Air. 16(3):179-91.
Stokinger, HE (1965). Ozone toxicology: A review of research and industrial experience, 1954-1962. Archives of Environmental Health 110:719.
Stollery, BP, Flindt, MLH (1988). Memory sequelae of solvent intoxication. Scandinavian Journal of Work & Environmental Health. 14:45-48.
Szpir, M (2006). New thinking on neurodevelopment. Environmental Health Perspectives. 114:2, A100-A107.
Treatment efficacy, a survey of 305 MCS patients. The CFIDS Chronicle, Winter 1996, 52-53.
Tretjak, Z, et al. (1990). PCB reduction and clinical improvement by detoxification, Human Experiment Toxicology, 9:235-44.
Villeneune, DC, Grant, DL, Phillipos, WEJ, Clark, ML, & Clegg, DJ (1971). Effects of PCB administration on microsomal enzyme activity in pregnant rabbits. Bull Environmental Contamination & Toxicology. l6:120.
Walker, SJ, Segal, J, & Aschner, M (2006). Cultured lymphocytes from autistic children and non-autistic siblings up-regulate heat shock protein RNA in response to thimerosal challenge. Neurotoxicology. 27:5, 685-692.
Wasley, A, Lepine, L, Jenkins, R, Rubin, C (2002). An investigation of unexplained infant deaths in houses contaminated with methyl parathion. Environmental Health Perspectives. 110:6, 1053-1056.
Windham, GC, Zhang, L, Gunier, R, Croen, LA, & Grether, JK (2006). Autism spectrum disorder in relation to distribution of hazardous air pollutants in the San Francisco bay area. Environmental Health Perspectives. 114:9, 1438-1444.
Winslow, SG (1981). The effects of environmental chemicals on the immune system: Selected Bibliography with Abstracts. Oak Ridge, TN: Toxicology Information Response Center, Oak Ridge National Laboratory.
Yaktine, AL, Harrison, GG, Lawrence, RS (2006). Reducing exposure to dioxins and related compounds through foods in the next generation. Nutrition Reviews. 64(9):403-9.
Ziem, G (2001). Medical Evaluation and Treatment of Patients with Chemical Injury and Sensitivity. National Institute of Environmental Health Sciences.