THE CHEMICAL EDGE

MCS 101 – Appendix

1) Summary of research on genetics and MCS:

May 2007 MCS America News: Multiple Chemical Sensitivity (MCS) and Genetics

http://thetruthaboutmcs.blogspot.com/2007/05/may-2007-mcs-america-news-multiple.html

by Christiane Tourtet

Millions of people all over the world, including small children, have developed Multiple Chemical Sensitivity (MCS) upon exposure to toxic chemicals in the environment. Due to the incessantly growing number of the worldwide general population stricken by MCS upon exposure to toxic chemicals, MCS has become one of the most serious and overlooked public health problem in the world. But what causes this terrible hypersensitivity to chemicals and other substances in the environment for millions of people of any race, gender, age, and national origin? Why is it that millions of these people, who lived normal lives, until one day a chemical exposure, ranging anywhere from pesticides, insecticides, fumigants, building renovations, installation of new carpeting, fresh paint… the list could go on almost endlessly, started to develop reactions from mild to severe.

The wide variety of symptoms experienced by persons with MCS has puzzled everybody, including the medical profession, for decades and the medical profession is unprepared to deal with such occurrence of a worldwide epidemic of this environmentally induced disease. However, regardless of the large variety of symptoms experienced by persons suffering from MCS, there tends to be a definite pattern of neurological, respiratory and cardiac symptoms.1

Pesticides2, especially organophosphates pesticides and insecticides, among so many other neurotoxic chemicals, are playing a major role in triggering MCS. According to the environmental medicine publication, Environmental Health Perspectives, a survey in September 2003 showed indeed, that about one third of persons developed MCS after being exposed to pesticides and another third developed MCS after being exposed to solvents.3

 Many research studies have been done on MCS, among them the SPECT brain Scan, with sponsors including the US Department of Health and Human Services, which found that MCS patients exposed to neurotoxic chemicals indicated a random thinning of cortical gray matter (tissue in the cortex of the brain). The researchers made the very important conclusion that symptomatic MCS patients with an history of exposures to chemicals, had significantly diminished cerebral blood flow to the brain, and that significant impairment of brain function may last for years after exposure to neurotoxic chemicals has ceased.4,5

 Some other studies are indicative that persons with MCS have little or no brain barrier that protects them from damages from low-level chemical exposures due to an excess of peroxynitrite (Pall M. 2001) that breaks down the blood barrier, therefore allowing greater access to the brain of persons afflicted by MCS. The more there is an excess of peroxynitrite, the more there is an inhibition of cytochrome P450, which means that it slows down the body’s natural detoxification process. Nitric oxide inhibits cytochrome P450 activity, thus slowing degradation of hydrophobic organic chemicals (Pall, 2003).6, 7

 These findings can explain the reactivity of persons with MCS to even minute doses of chemical exposures to which the non-MCS population would not react to. The combination of reduced or non-existent blood brain barrier and impaired detoxifying process of persons with MCS may induce long term, and even permanent brain and central nervous system damage, which can include toxic encephalopathy.

 It also has been found that brain inflammation corresponds with symptoms of MCS. In 1999, Meggs came to the conclusion that Multiple Chemical Sensitivity (MCS) is potentially caused by low molecular weight chemicals, binding to chemoreceptors on sensory nerve C-fibers, thus leading to the release of inflammatory mediators.8

 Others studies also showed certain vitamins and minerals deficiencies, abnormal lipid and carbohydrate metabolism.9 In 2005. Gibson suggested limbic kindling, neural sensitization, and neurogenic inflammation upon exposures to various pesticides, volatile organic compounds, solvents and other toxic compounds.10

 However, all these very interesting findings are rather secondary effects of MCS in a vulnerable population, and do not really reveal the true cause of MCS. So what is the real cause of Multiple Chemical Sensitivity? The real cause of MCS may lie in the susceptibility of genes. This may be why, even though we are all exposed daily to toxic chemicals in the environment, millions of people have developed MCS, while millions of others not only did not develop MCS, but have been totally unaffected by exposures to toxic/neurotoxic chemicals in the environment.

 An individual with normal genes will be very resistant to exposures to toxic/neurotoxic chemicals in the environment, while an individual with gentic variants will have very little resistance to exposures to toxic/neurotoxic chemicals in the environment, which explains why millions of people all over the world have developed MCS versus millions of others who have not. This determines how the body responds to exposures to chemicals. Certain segments of the population are generally more sensitive including the very young, the old and people with compromised immune systems or livers. Men and women may respond differently to chemical exposures and are at risk for different adverse health effects.11

 Because of their genetic makeup some people are more susceptible to chemical exposures than others. The adverse health effect of chemicals depends on their toxicity and how people are exposed to the chemicals, as well as individual susceptibility. Exposures to toxic chemicals can lead to a very wide range of health effects which may take place immediately or may take very long time to develop, which include impairment of the immune system, genetic damage (mutagenicity) and inhibition of the body’s ability to breakdown chemicals.13, 14, 16

 Persons with MCS have a genetic susceptibility to toxic chemicals found in the environment. In other words they have gene variants that make them vulnerable to exposures to toxic chemicals in the environment. These abnormal genes impair the detoxifying process in the MCS population, which in turn has the consequence of bio-accumulation of toxic chemicals in the body (body burden). Once the body has reached its saturation point, any subsequent exposure to any chemicals will trigger the symptoms of Multiple Chemical Sensitivity. The accumulation of toxic/neurotoxic chemicals in the body of persons with MCS may explain the characteristics of the symptoms of neurotoxicity experienced by all persons afflicted by severe MCS.

 There lies an answer to the puzzle of Multiple Chemical Sensitivity. Now, let’s look scientifically into how genetics apply to Multiple Chemical Sensitivity. Genetic factors seem to contribute to virtually every human disease. The majority of diseases are influenced by multiples genes and environmental factors. Genetic variation plays a role in whether an individual has a higher or lower risk for getting a particular illness.12.

 The DNA sequence in every human being is 99.9 % percent identical to the one of every other human. The slight variation in our genes is known as single nucleotide polymorphisms or SNPS. It is estimated by scientists that there are about 1.4 million locations on the genome, where SNPS can possibly occur in humans. Small variations contribute to individual differences and can also be triggered by toxic substances in the environment. Some SNPS can cause or predispose a person to disease or influence the person’s response drugs.11

 Some human illnesses and defects are directly or indirectly caused by genetic abnormalities. Some other illnesses however are caused by complex interacting genetics and environmental factors that cannot be explained by inheritance patterns,11 We may inherit a specific condition, as well as the particular ability to respond to environmental stresses such as bacteria, viruses and environmental toxins.11,12 Understanding how DNA can influence every health aspect will hopefully and eventually lead to effective ways to prevent, treat, and cure thousands of diseases afflicting humankind.

 Genes are pieces of DNA that hold instructions for building a particular protein. Proteins are most essential for all aspects of life. Through these proteins, our genes dictate how we look, how we respond to infections, how well we process our foods, and detoxify poisons. Harmful DNA variations, called mutations, can cause or constitute many different disease and conditions. It depends on their size and location, and they can be devastating;11, 12

 An interesting scientific study done in Israel, “A transcription –activating polymorphism in the ACHE promoter associated with acute sensitivity to anti-acetylcholinesterases”, by Michael Shapira et. al, showed that chemical hypersensitivity to xenobiotics causes adverse responses to normally subacute levels of a specific chemical or a group of chemicals. Persons afflicted with this abnormality may suffer from an exaggerated immune response showing itself as inflammation of mucosal and epithelial tissues. They may also alternatively show abnormal capacity for scavenging, modifying or degrading relevant chemicals.17

 The aberrantly processed chemicals may in turn cause toxicological stress in target tissues with many symptoms of varying nature and timing according to the tissue, the type of exposure, and the actual permeability of the chemicals.

 The mutations that lead to such faulty chemical metabolism were identified largely within the coding regions and consequently affecting the detoxifying protein properties. However, the impaired transcriptional activation of genes responsible for detoxification, because of their regulatory sequences, may be an equally important cause of chemical hypersensitivity. For instance, the metal-chelating metallothioneins, and some of the members of the cytochrome P450 chemical-modifying enzyme family, respond to exposure to xenobiotics by transcriptional activation, which is responsible for increased protection. The most significant finding thus, is that impaired transcriptional activation due to promoter polymorphisms in these genes would be then the cause of chemical hypersensitivity.17

 In another extremely interesting scientific study, researchers at the University of California, Berkley and the University of Washington have found that some newborns can be 26 to 50 times more susceptible to certain organophosphates pesticides and 65 to 130 times more sensitive than adults.16 The study also revealed much greater variability in susceptibility to pesticides, than it was previously predicted. The researchers used the activity levels of paraoxonase 1 (PON1) measured in blood samples as a marker for pesticides susceptibility.16

 PON1 is an enzyme whose function is to break down the toxic metabolites of organophosphate pesticides. Research Professor, Clement Furlong in the Department of Medicine and Genome Sciences at the University of Washington and co-lead author of the paper, had found the significance of PON1 in prior animal studies.16 In these studies, mice that lacked the PON1 enzyme died when exposed to low levels of organophosphates pesticides, while the other mice with normal levels of the enzyme PON1 and given the same dose did not develop any symptoms at all. Both the quality and quantity of the PON1 enzyme is very important in determining the ability to detoxify pesticides.16

 What is extremely significant for the MCS population is that the ability of the PON1 enzyme to protect the body from the toxicity of pesticides is determined by genetics, more specifically, whether a person has the Q or R form of the PON1 gene at position 192 on the chromosome.16

 In addition to the factors that affect the type of PON1 enzyme, there are also additional genetic variants that affect the levels of enzyme available. People have remarkable differences in enzymes that defend their health from toxic pesticides exposures.16

 A very important, most recent, cross-sectional study19 of self-reported – related sensitivity, conducted by Eckart Schnakenberg, Institute for Pharmacogenenetic and Genetic Disposition, Langenhagen, Germany, Karl-Rainer Fabig, Nathalie Fabig, Clinical Practice for Toxicology and Environmental Medicine, Hamburg, Germany, Martin Stanulla, Children’s Hospital, Pediatric Hematology and Oncology, Hannover Medical School, Hannover, Germany, Nils Strobl, Michael Lustig, Werner Schloot, Center for Human Genetics and Genetic Counseling, University of Bremen, Bremen, Germany, analyzed genetic variants of the NAT2, GSTM1,GSTT1, and GSTP1 genes.

The result showed evidence of significant differences between individuals with and without self-reported chemical-sensitivity in regard to the distribution of NAT2, GSTM1, and GSTT1 gene variants. Cases with self-reported chemical-related sensitivity were quite significantly more frequently NAT2 slow acetylators. GSTM1 and GSTT1 genes were very significantly more often homozygously deleted in the individuals who were reporting sensitivity to chemicals in comparison to controls, and the effects for GSTP1 gene variants were observed in conjunction with GSTM1, GSTT1 and NAT2 gene.

 In conclusion, the results from this study population show that individuals who are slow acetylators and/or having a homozygous GSTM1 and/or GSTT1 deletion reported more frequently chemical-related hypersensitivity, thus providing the genetic evidence of MCS.

 Brenda Eskenazi of the University of California, Berkley, Professor of Epidemiology and Director of the Center for Children’s Environmental Health Research said “Our next step is to look at the relationship between pesticides exposure and neurodevelopment, specifically for young children and genetically susceptible populations”.

 On of the most significant scientific genetic findings for the MCS population is the Case-control study of genotypes in Multiple Chemical Sensitivity: CYP2D6, NAT2, PON1 and MTHFR, conducted by: Gail Mckeown-Eyssen,18 Department of Public Health Sciences, University of Toronto, Department of Nutritional Sciences, University of Toronto, Toronto, Canada, Cornelia Baines, Nicole Railey, Vartouhi Jazmaji, Department of Public Health Sciences, University of Toronto, Toronto, Canada, David E.C. Cole, Department of Laboratory Medicine and Pathology, University of Toronto, Department of Medicine, University of Toronto, Toronto, Department of Pediatrics (Genetics), University of Toronto, Toronto, Canada. Rachel F.Tyndale, Centre for Addiction and Mental Health, Toronto, Department of Pharmacology, University of Toronto, Toronto, Canada, Lynn Marshall, Environmental Health Clinic Unit, Women’s College Hospital Toronto, Canada, Ambulatory care Center, Sunnybrook and Women’s College Health Sciences Centre, Toronto, Canada.

 The research team collected the blood samples of the 203 cases and 162 controls participating in the research for genetic analysis. They isolated genomic DNA and identified specific polymorphisms in order to determine the frequency of occurrence of certain polymorphisms, in cases compared to controls, for several genes that play major roles in how the body responds to chemicals. In their testing for different allele frequencies in specific genes, they found quite significant differences for the CYP2D6 (Cytochrome P450 2D6) gene and a marginally significant difference for the NAT2 gene.18

 CYP2D6 is responsible for encoding enzymes that metabolize many toxic chemicals as well as therapeutic drugs. Cytochrome P450 enzymes are a large group of enzymes that include a quite important part of the body’s instruments to get rid of potentially harmful substances.18

 NATI and NAT2 (N-acetyltransferases) are responsible for encoding enzymes needed for metabolizing toxic chemicals, different drugs, aromatic amines. PON (paraoxonase) are genes code for the products of proteins that react with toxins such as pesticides and nerve agents.18

 MTHFR (methylenetetrahyrofolate reductase) is responsible for encoding a key enzyme involved in the metabolism of some B vitamins (including folate and B 12). MTHFR –C677T gene was studied because impaired vitamin B12 metabolism can contribute to neurological symptoms.18

 The distribution of genotypes between cases and controls were significantly different for both the CYP2D6 and NAT2. The women who were homozygous for the active form of the gene CYP2D6, had over three times the risk of getting MCS compared to the women who were homozygous for the inactive form of CYP2D6. The women who were heterozygous for the active form of the gene CYP2D6, also showed an increased risk of developing MCS.18

This suggest a “gene-dose effect”, with the risk of getting Multiple Chemical Sensitivity (MCS) increasing in respect to the number of active CYP2D6 alleles. The women who were homozygous for the fast form of the gene NAT2, (the 4 allele) called ” rapid acetylators” had over four times the risk of getting Multiple Chemical Sensitivity (MCS) in comparison to slow acetylators who have a lack of the 4 allele of the gene NAT2. As for the women who were heterozygous, intermediate and had only one 4 allele, they did not show an increased risk.18

The most striking finding was that the women with genes that encodes rapid metabolism by both enzymes CYP2D6 homozygous active and NAT2 “rapid acetylator” genotypes, were over 18 times more likely to get MCS in comparison to the women with the slow metabolic forms.18

 So in resume, in this epidemiology study, the researchers have reported an extremely important finding for the MCS population of several genetic differences between cases and controls in the genes involved in the detoxifying process of contaminants and that basically a genetic predisposition for MCS involves altered biotransformation of environmental chemicals.

 Not only did they discover that indeed differences do exist, but also these differences were found in genes that are crucial to detoxifying toxic compounds, and that MCS patients are more likely to have the type of genes that would impair their ability to detoxify toxics themselves. When they looked at two genes at the same times, they found that women with MCS were over 18 times more likely than controls to have a very specific combination of forms of two separate genes.

 Their data is the first of a kind to demonstrate such genetic differences in enzymes crucial for the detoxification of contaminants by comparing people with MCS to those who do not have MCS. It is thus providing strong genetic evidence for the physically- based occurrence of MCS.

 The studies of Haley20 and Furlong20, of the Gulf War Veterans, which implicated the gene PON1, of Shapira17et al, of Schnakenberg19 et al involving three genes, and of Mc Keown-Eyssen18 and colleagues implicating five genes, show that one or more genes controlling the metabolism of compounds previously implicated in Multiple Chemical Sensitivity, control the occurrence of chemical sensitivity, thus providing the physical evidence of the genetic origin of Multiple Chemical Sensitivity (MCS) upon exposures to chemicals.

 Due to the increasing magnitude of this pandemic environmentally induced disease affecting millions of people all over the world, further scientific genetic research must urgently be done in order to fully identify and understand all the genes variations and mechanisms that make the MCS population so susceptible to toxic chemicals and other substances in the environment.

Research into possible treatment, such as gene therapy, would hopefully be on its way to possibly prevent and even cure the millions of people from all over the world, suffering from the devastating health effects of MCS, and would be the scientific turning point for a better world for future generations.

 - Christiane Tourtet

 Copyright Christiane Tourtet © 2007

References

1. Joffres, MR, Sampalli ,T, & Fox, Roy (2005). Physiologic and symptomatic responses to low-level substances in individuals with and without chemical sensitivities, a randomized controlled blinded pilot booth study. Environmental Health Perspectives. 113: 9, 1178-1183.

2. Windham Bernard Ed- Health Effects of Pesticides, 6-1- 2001 Leon County Public Health Department. http://flcv.com/pesticid.html

3. Ferrie, H. (October 2003), Multiple Chemical Sensitivity: Government and Medical Science Finally Recognize Crippling effects of MCS, http://www.vitalitymagazine.com/node/112

4. Callender, TJ, et al (1995), Evaluation of chronic neurological sequelae after acute pesticide exposure using SPECT brain scan, Journal Toxicology & Environmental health.41:275-284.

5. Heuser, G, et. al. (1994), Neurospect findings in patients exposed to neurotoxic Chemicals, Toxicology & Industrial Health.10:561-57

6. Pall, M. (2001), Multiple Chemical Sensitivity-The End of the Controversy, Washington State University, School of Molecular Biosciences. http://molecular.biosciences.wsu.edu/faculty/pall/pall_mcs.htm

7. 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.

8. Meggs, WJ (1999), Mechanisms of allergy and chemical sensitivity, Toxicology and Industrial Health.15:3-4,331-338.

9. Rea, WJ, Johnson, AR, Ross et. al. (2006), Considerations for the Diagnosis of Chemical Sensitivity. http://www.aehf.com/articles/A55.htm

10. Gibson,P. (2005), Understanding & Accommodating People with multiple Chemical Sensitivity in Everyday Living. Houston TX: Independent Living Research Utilization.

11. JGI, Doe Joint Genome Institute- US Department of Energy- Office of Science. http://www.jgi.doe.gov/index.html

12. National Human Genome Research Institute, National Institute of Health. http://www.genome.gov/education

13. Gilbert, S.G. 2001, An introduction to toxicology, A lecture given at “A Small Dose of Toxicology: How chemicals Affect Your health”, a conference sponsored by the Northwest Center for Occupational Safety and Health, University of Washington, Oct.17

14. Dickey, P.2001, Toxicity of common household products. A lecture given at “A Small Dose of Toxicology: How Chemicals Affect Your Health”, a conference sponsored by the Northwest Center for Occupational safety and Health, University of Washington, Oct.17.

15. Ponce, R. 2001, How chemicals attack cells, A lecture given at “A small Dose of Toxicology: How Chemicals Affect Your Health” a conference sponsored by the Northwest Center for Occupational Safety and Health, University of Washington, Oct.17.

16. Medical News Today, 01/12/2007, Public Health News, Some Newborns May Be 26 to 50 Times More Susceptible To Exposure To Certain Organophosphate Pesticides Than Other Newborns. http://www.medicalnewstoday.com/medicalnews.php?newsid=38839

17. Shapira Michael, et. al., A transcription–activating polymorphism in the ACHE promoter associated with acute sensitivity to anti-acetylcholinesterases, Human Molecular Genetics, 2000, Vol.9, No.9 1273-1281.

18. McKeown-Eyssen, G, C Baines, DEC Cole, N Riley, RF Tyndale, L. Marshall, V.Jazmaji.2004, Case-control study of genotypes in multiple chemical sensitivity: CYP2D6, NAT1, PONI, PON2, and NTHFR . International Journal of Epidemiology 33 (5): 1-8.

19. Schnakenberg Eckart et al, A cross-sectional study of self-reported chemical-related sensitivity is associated with gene variants of drug metabolizing enzymes, Environmental Health 2007, 6:6 doi: 10.1186/1476-069X-6-6.

20. Furlong Clement E., PON1 Status and Neurologic Symptoms Complexes in Gulf War Veterans, Genome Res.2000 10: 153-155.Retrieved on February 12, 2007 from www.genome.org

Christiane Tourtet is a well-known free-lance, award-winning Medical, Sciences, and Environmental writer, photo-journalist, photographer, and devoted Multiple Chemical Sensitivity (MCS) activist for over 20 years. She is the Founder and President of International MCS Awareness, and USA and Florida State Coordinator for MCS-Global. Her biography has been included in numerous world-wide publications, notably in Who’s Who in America and Who’s Who in the World.

 

2) from Adventures with Multiple Chemical Sensitivities: Tales of The Masked Avenger: Chronicles of the life and musings of a woman with Multiple Chemical Sensitivities

http://multiplechemicalsensitivities.blogspot.com/2006/03/supergirls.html

(This brief summary is from a beautifully written blog that can give readers a very good idea of the daily struggles for MCS sufferers, VB)

Monday, February 12, 2007

More Evidence for Physical Causation of MCS

A German study relating particular genes to chemical sensitivity was published Saturday in the on-line, peer-reviewed journal Environmental Health. The genes code for enzymes that help break down and detoxify a wide variety of common chemicals, including both pharmaceuticals and known carcinogens. Eckart Schnakenberg and the other authors of the study are actually illuminating the important role of environmental exposures in causing chemical sensitivity by helping us understand the genetics. (No, folks, it’s really not an either/or situation and their work is not a disguised attempt to blame the victims or suggest that we are a tiny group of strange mutants who collapse under our own weight without provocation.) One of the studied enzymes, an N-acetyltransferase (NAT), is involved in the metabolism (break down) of substances “produced in industry, and found in cigarette smoke as well as the human diet.” Around half of all Caucasians carry a variation that’s slower rather than faster at its job. People who have it don’t clear low-dose carcinogens from the body as efficiently as the rest of the population. The Schnakenberg study showed that they are also likelier to report problems with chemical sensitivity.

Two other genes the researchers examined code for glutathione S-transferases (GST), which are also involved in detoxification. These genes are more frequently deleted on both chromosomes in the chemically sensitive. That is to say that neither mom or dad contributed a copy of one or both genes. And no gene, no enzyme.

I’m sure it’s still a long road to understanding the mechanisms for Multiple Chemical Sensitivities (MCS), but studies like Shnakenberg’s should silence the it’s-all-in-your-head crowd at some point along the way. As we know, that bunch is still annoyingly noisy, but you’ll notice its “experts” tend to ignore, rather than try to refute, this type of ground-breaking research. You are born with your genes and the ones that are being associated with chemical sensitivity are implicated not in mental illness, but in protecting the body from toxic chemicals.

My knowledge of biology is rusty, so if I have made any errors in my effort to summarize the Germans’ work please let me know. Also, for a better explanation of the relevant scientific concepts and terminology please see an excellent article on a pioneering and closely-related study published by Gail McKeown-Eyssen and her colleagues in 2004.

 

3) from the online THE AMERICAN CHRONICLE

http://www.americanchronicle.com/articles/viewArticle.asp?articleID=24334

Governors and Mayors Proclaim May as Multiple Chemical Sensitivity Awareness and Education Month

Lourdes Salvador

April 16, 2007

 

Governor Bill Ritter of Colorado, Governor Ted Strickland of Ohio, Mayor Josephus Eggelletion of Broward County Florida, Governor Jim Gibbons of Nevada, and Governor Christine Gregoire of Washington are among the first governors and mayors to proclaim the month of May 2007 as Multiple Chemical Sensitivity Awareness and Education Month.

Multiple Chemical Sensitivities (MCS) is also known as Environmental Illness (EI), Toxic Injury (TI), Toxicant Induced Loss of Tolerance (TILT), and several other names. Originally identified in a 1989 multidisciplinary survey of 89 clinicians and researchers, and modified in 1999, top consensus criteria (Nethercott et al, 1993) for MCS define the condition as:

1. A chronic condition.

2. Symptoms recur reproducibly.

3. Symptoms recur in response to low levels of chemical exposure.

4. Symptoms occur when exposed to multiple unrelated chemicals.

5. Symptoms improve or resolve when trigger chemicals are removed.

6. Multiple organ systems are affected.

Products that MCS patients react to include ANY quantity of exposures to pesticides, secondhand smoke, alcohol, fresh paint, scented products and perfumes, candles, fragrances, food preservatives, flavor enhancers, aerosols, tap water, cosmetics, personal care products, new carpets, petroleum products, formaldehyde, outdoor pollutants, newspaper ink, cleaning compounds, printing and office products, and other synthetically derived chemicals. Some also react to natural products that are highly concentrated such as natural orange cleaners due to high volatile organic compound and pesticide concentration. Symptoms can range from minor annoyances to life-threatening reactions.

Prevalence

The prevalence of MCS, based on self-reported symptoms by sample populations provides an estimate of 16% of the population who experience reactions to everyday chemicals (Gibson, 2005; Meggs et al, 1996). MCS affects more women than men. All education levels, income levels, and nationalities are affected equally.

Etiology (Causation)

There is no clear consensus as to what causes the symptoms of MCS.  One of the first studies on MCS focused on possible long term potentiation in the hippocampus and neural sensitization as a central mechanism (Pall, 2003). Later studies examined the role of the inflammatory process and found that brain inflammation was correlated with symptoms of MCS (Pall, 2003). 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 (Meggs, 1999). Many observable and empirical, scientific facts can help identify MCS including SPECT scans and chemical encephalopathy, vitamin deficiencies, mineral deficiencies, excess amino acid deficiency, and disturbed lipid and carbohydrate metabolism (Rea et al, 2006; Ziem, 2001; Callendar et al, 1995; Heuser et al, 1994).

McKeown-Eyssen et al (2004) studied 203 MCS sufferers and 162 controls and found that blood tests revealed that genetic differences relating to the body’s detoxification processes were present more often in those with MCS than those without. Data showed that five genetic polymorphisms have a statistically significant role in determining MCS prevalence (McKeown-Eyssen et al 2004). Each of these genes encode 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) ( McKeown-Eyssen et al 2004). People with a ”high” expression of two specific genes (CYP2D6 and NAT2) were 18 times more likely to have MCS than those without ( McKeown-Eyssen et al 2004). It was concluded that “a genetic predisposition for MCS may involve altered biotransformation of environmental chemicals” ( McKeown-Eyssen et al 2004). Haley found similar, confirmatory results with the PON1 gene in studies of the Gulf War syndrome veterans.

A new study by Schnakenberg et al (2007) 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 (Schnackenberg et al, 2007). 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 because “glutathione S-transferases play an important role in the detoxification of chemicals” (Schnackenberg et al, 2007). The deletion of another gene, the GSTP1 gene, leaves individuals more susceptible to developing these diseases, as lack of these genes means a loss of protection from oxidative stress (Schnackenberg, et al, 2007).

The NO/ONOO- cycle is implicated by Pall as being a plausible etiology for Multiple Chemical Sensitivities (MCS), Fibromyalgia (FM), Chronic Fatigue Syndrome (CFS), Post-Traumatic Stress Disorder (PTSD), and Gulf War Syndrome. Peroxynitrite (ONOO-) is oxidized from nitric oxide. Excess peroxynitrite depletes energy stores, which is perceived to cause extreme fatigue (Pall, ND). Of more interest to those who suffer from MCS is the fact that peroxynitrite breaks down the blood brain barrier and excess levels allow greater access to the brain (Pall, ND). This greatly increases the effects of chemicals on the brain. Essentially a non-MCS person has a barrier that protects the brain from damage from low-level chemical exposure, however a person who suffers from MCS has little or no barrier making the brain subject to increased damage and reactivity with minute exposures most people do not react to. The key effect of nitric oxide (NO) is that it inhibits cytochrome P-450 activity and slows degradation of hydrophobic organic chemicals (Pall, ND). This means that excess nitric oxide slows down the body’s natural detoxification processes leaving MCS patients subject to the effects of chemical exposure longer than non-sufferers. Between a reduced blood-brain barrier and increased time to naturally detoxify the body MCS patients are subject to permanent and long-term brain and nervous system damage which includes toxic encephalopathy.

“The only etiologic mechanism proposed for each of these is a vicious cycle mechanism involving elevated levels of nitric oxide and its oxidant product, peroxynitrite. This cycle may be initiated by a variety of diverse short-term stressors, including viral and bacterial infections, physical trauma, severe psychological stress, organic solvent exposure, and exposure to three classes of pesticides, organophosphorus / carbamate pesticides, organochlorine pesticides and pyrethroid pesticides). Each of these short-term stressors are known to be able to trigger responses that lead to increases in nitric oxide levels. Indeed, other initiating short-term stressors, including a protozoan infection, carbon monoxide exposure, thimerosal exposure and ciguatoxin exposure are also known or thought to act to increase nitric oxide levels, as well” (Pall, 2006).

Regardless of cause, victims of MCS suffer isolation and require the support of family, friends, and medical providers. The month of May is designated to raise awareness of the condition and foster better understanding of its cause and prevention. With reasonable accommodations, victims can experience increased ability to work, attend school, shop, dine, go to church, and socialize. Accommodations are often simple and involve things such as opening windows, increasing ventilation, and substituting safer products that increase the safety of both the patient and others the general population.

References

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.

Caress, S., & Steinemann, A. (2003). A Review of a Two-Phase Population Study of Multiple Chemical Sensitivity. Environmental Medicine. 111, 1490 - 1497.

Davidoff, L. (1989). Multiple Chemical Sensitivities (MCS). The Amicus Journal. Winter.

Ferrie, H. (October 2003). Multiple Chemical Sensitivity: Government and Medical Science Finally Recognize Crippling Effects of MCS. Vitality, Retrieved May 17, 2006, from http://www.vitalitymagazine.com/node/112

Gibson, P. (2005). Understanding & Accommodating People with Multiple Chemical Sensitivity in Everyday Living. Independent Living Research Utilization.

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.

Heuser, G, et al. (1994).  Neurospect findings in patients exposed to neurotoxic chemicals.  Toxicology & Industrial Health. 10:561-571.   McKeown-Eyssen, G, Baines, C, Cole, D, Riley, N, Tyndale, R, Marshall, L, &

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Disclaimer

This is for informational purposes and is not intended to replace the examination, diagnosis and treatment of a licensed physician and no such claims are inferred. The author and publisher will not be responsible for misuse of this information and recommend consulting with a doctor qualified to diagnose MCS if it is suspected.

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 www.mcs-america.org. She is a passionate advocate for the homeless, working with the local governor to open new shelters and provide services to the homeless based on a presentation of her ideas to the governor. 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: www.mcs-america.org, www.thetruthaboutmcs.blogspot.com, and www.cafepress.com/mcsamerica.

Copyrighted © 2007 Lourdes Salvador

 

APPEAL FOR SUPPORT FROM DR. WILLIAM REA

ENVIRONMENTAL HEALTH CENTER, DALLAS

September 14, 2007

Dear Patients:

This letter is being sent to you so that we may provide information about a potential serious threat to your choice of medical care. To put it bluntly, there is currently an organized nation-wide effort to destroy the specialty of Environmental Medicine and to eliminate from practice physicians who diagnose and treat patients suffering from chemical sensitivities.

Since October of 2005 the Texas Medical Board has been investigating me on charges of providing substandard care and “endangering public health”. An anonymous third party complaint was made to the board against me, citing five specific patients as being mistreated. You may ask “What is an anonymous third party complaint?” This type of complaint is made to the board without the knowledge or consent of the patient. The complaint against me was almost certainly made by United Health Care/Oxford. All five patients cited in the complaint had no knowledge that they or their information was being used in this way. Further, none of the patients are alleging mistreatment or malpractice against me and all five are still under my care. Additionally, these patients have all written to the Texas Medical Board and informed them that they are not part of this complaint and they are not making any allegations against me of any kind. Two of the patients have stated that I saved their lives.

The Texas Medical Board has dismissed the protests of these patients and continued to pursue charges against me. Further, the board refuses to officially reveal who made the complaint, what I am alleged to have done, or what evidence was presented against me. They continually maintain that this information is protected and does not have to be revealed.

However, we are almost certain that United Health Care/Oxford is behind the complaint. All five patients were from Manhattan (New York City), New York and all had the same insurance company – United Health Care/Oxford.  As you know, our clinic does not take insurance assignment, so all patients file claims directly with their respective insurance companies. We therefore do not have any direct connection with this insurance company. We deny that we have ever defrauded anyone, including this insurance carrier. Evidence showing these facts was supplied to the Texas Medical Board, but was apparently disregarded as they have decided to pursue the charges despite the evidence.

The board has conducted a so-called peer review of the five patient’s medical records and the treatment they received, again without the permission of these patients. A peer review of a physician’s action can be undertaken for a variety of

reasons but there is always one common factor in the process. That common factor is that the reviewer is required to be knowledgeable about and a practitioner of the specialty that is being reviewed. Thus, the reviewer is a “peer” of the physician being reviewed.

In my case the Texas Medical Board chose a reviewer who does not specialize in Environmental Medicine, and who is in fact an allergist. This reviewer, who was anonymous, gave a negative review of the treatment of the five patients, despite the fact that all have improved, several of them substantially so, while under my care. I had 17 actual peers, physicians who practice Environmental Medicine, review all five of these cases as well. To a person these 17 reviewers found that my treatment of these patients was not only adequate, but that it met or exceeded the standard of care for treatment in our specialty. Further, the reviewers also noted that the state board reviewer was uniformed about the specialty of Environmental Medicine, clearly did not understand the complex nature of the diagnosis and treatment of patients who suffer from chemical sensitivities, grossly misunderstood many of the facts in the medical records, was antagonistic and biased against the specialty of Environmental Medicine, and was clearly unqualified to conduct such a review due to lack of experience, knowledge, and expressed biases. The board has chosen to dismiss the review done by 17 actual peers and has chosen to support the conclusion of their one unqualified reviewer.

Based on secret evidence provided by an anonymous accuser and supported by and anonymous reviewer the board has recommended that my license to practice medicine be revoked. Currently, the Texas Medical Board is one of the most difficult for physicians to deal with in the entire country. It is particularly noted for not treating physicians fairly and denying their basic constitutional rights. Pleased be assured that I still have my license, that I am fighting the charges, that the Environmental Health Center is still open, and we are still seeing patients.

Unfortunately, my case is not unique. Recently across the United States there has been an organized attempt to deprive citizens of their choice in individual health care by attempting to have the licenses of doctors who are deemed to practice “alternative” medicine revoked. This campaign has been going on for at least 10 years now and is being led primarily by health insurance companies. These efforts are also being supported by a small group of individuals (and other groups) working for or associated with the National Council Against Health Fraud in Allentown, Pennsylvania. 

The typical pattern in these attacks is to single out physicians they do not like and file anonymous complaints against them with different state medical boards. For example, over the past 10 years the number of physicians who are willing to diagnose and treat Lyme Disease has dropped sharply, while cases of Lyme disease have skyrocketed. This is because several health insurance companies have systematically targeted the doctors who specialized in treating that illness. Many of these physicians have had complaints made against them in exactly the same manner that they have been made against me. These same types of complaints have been made against doctors who treat patients for chemical sensitivities, mold exposure, for Gulf War Syndrome, and now possibly against physicians who are treating patients who were injured in the 911 tragedy.

You may ask why this campaign is taking place. It appears that quite simply the health insurance companies want to be the sole arbiter of what types of treatments are available to patients, and thus what they will be required to pay for. They clearly do not want new diagnoses and treatments established because they will then have to pay for these. Finally, many of us who have been turned in to state medical boards do not take insurance assignment. We do this so that we can provide treatment to our patients without insurance company interference. In recent years the health insurance carriers have tried to automate their claims processing processes. When claims are denied, they then have to be handled by a human and this costs money. When physicians do not accept insurance assignment, the claims submitted by their patients often have a higher denial rate. This results in higher processing costs for the insurance companies. If these carriers can eliminate the independent physicians with higher denial rates they can potentially save a lot of money. Certain state medical boards appear to agree with this strategy and cooperate in the process.

Of course, these attempts are also being made in order to try and standardize treatments and make all patients fit into one “box”. Americans need more choices in health care, not less.  We would hope you, as an informed citizen, would want to be part of an effort to help preserve freedom of choice in health care. Insurance carriers and a small group of “Quack busters” should not be allowed to decide what type of health care is available in this country.

It is unconscionable that the Texas Medical Board would want to limit freedom of choice in health care, and allow insurance carriers to interfere with the doctor-patient relationship.  Please join our effort for freedom of choice in health care and write your protest to your members of the Texas Legislature. You can also copy your protest to members of the Texas Medical Board. If you do not know who your representatives are, go to the following website to find out:

http://www.fyi.legis.state.tx.us/

If you are out of state, you can contact Texas State Senator Jane Nelson and Representative Fred Brown, both of whom have taken an interest in recent activities of the Texas Medical Board. You can also send your letters of protest to the Executive Director of the Texas Medical Board, Donald Patrick, M.D., J.D., by e-mail, phone, or fax.  Please petition the elected officials to:

1.      Support the dismissal of the anonymous complaint made against Dr. Rea, or at the very least the revelation of who made the complaint and what evidence was presented against him.

2.      Prohibit the Texas Medical Board from conducting anonymous peer reviews by unqualified reviewers, or using reviewers with a bias or conflict of interest.

3.      Prohibit the Texas Medical Board from accepting and pursuing complaints in such a way that they deprive physicians of their constitutional rights and their ability to defend themselves.

4.      Strongly oppose the anonymity given to billion dollar insurance companies when making state board complaints against physicians.

5.      Urge the Texas Legislature to hold hearings on the Texas Medical Board and their seeming cooperation with health insurance companies’ attempts to de-license physicians in specialties that they do not like and the board’s denial of due process to accused physicians in direct contradiction to the due process that the board claims that it provides.

Thank you very much for your help. Together, we can stop the Texas Medical Board and other state medical boards from unfairly targeting physicians that outside interests do not like. We can also expose the despicable tactics of the insurance companies in their efforts to control all aspects of healthcare.

Sincerely,

William J. Rea, M.D.

President

Environmental Health Center-Dallas