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What is Multiple Chemical Sensitivity (MCS)? |
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General Information
Multiple Chemical Sensitivities (MCS) was identified in a 1989 multidisciplinary survey of 89 clinicians and researchers, and modified in 1999. Top consensus criteria (Multiple chemical sensitivity: a 1999 consensus, 1999) 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. |
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Etiology (Causation) |
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MCS is often misconstrued as an allergy, though IgE (immunoglobulin E) is generally not a factor. Allergies may co-occur with MCS as with any population, however MCS is not an allergy itself.
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 bodys 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 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). |
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Prevalence |
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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, & Jazmaji, V (2004). Case-control study of genotypes in multiple chemical sensitivity: CYP2D6, NAT1, NAT2, PON1, PON2 and MTHFR]. International Journal of Epidemiology 33, 1-8.
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. Jul-Aug;51(4):275-82.
Meggs, WJ (1999). Mechanisms of allergy and chemical sensitivity. Toxicology and Industrial Health. 15:3-4, 331-338.
Multiple chemical sensitivity: a 1999 consensus. Arch Environ Health. 1999 May-Jun;54(3):147-9.
Pall, M. (ND). Multiple Chemical Sensitivity: The End of Controversy. Washington State University School of Molecular Biosciences, Retrieved May 18, 2006, from: http://molecular.biosciences.wsu.edu/faculty/pall/pall_mcs.htm
Pall, M (2006). The NO/ONOO- Cycle as the Cause of Fibromyalgia and Related Illnesses: Etiology, Explanation and Effective Therapy. Washington State University School of Molecular Biosciences.
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. (2001). Multiple Chemical Sensitivity - The End of Controversy. Washington State University, School of Molecular Biosciences, Retrieved May 17, 2006, from http://molecular.biosciences.wsu.edu/faculty/pall/pall_mcs.htm
Schnackenberg,E. et al (2007). A cross-sectional study of self-reported chemical-related sensitivity is association with gene variations of drug-metabolizing enzymes. Environmental Health.
Ziem, G (2001). Medical Evaluation and Treatment of Patients with Chemical Injury and Sensitivity. National Institute of Environmental Health Sciences.
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The prevalence of MCS, based on sample populations, provides an estimate of 16% of the population and 33% of Gulf War Veterans who experience chemical hypersensitivity (Gibson, 2005; Meggs et al, 1996).
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Treatment |
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Most doctors recommend two primary treatments for MCS: 1. Strict avoidance of contact with all chemicals, even those one is not sensitized too, as sensitization is more likely to occur with repeated exposure. 2. Proper nutrition to increase nutrients needed for normal detoxification when exposures do occur.
Some also use diet, desensitization drops, NAET, and other forms of treatments. The following agents have been predicted to be useful by Dr. Pall and Dr. Ziem (Pall, 2006) in the Pall/Ziem protocol to down-regulate the NO/ONOO- cycle biochemistry:
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References |
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Age of Onset (Caress et al, 2003) < 20 ..32.4% 21 35 .35.2% 36 50 .14.8% > 50 ...7.9% Dont Know. ..9.7%
Gender (Caress et al, 2003) Males 40% Females .60%
Education Level (Caress et al, 2003) Did not Complete High School .10.1% High School Graduate ...24.7% Some College .25.7% College Graduate ...31.5% Professional/Graduate School .7.9% |
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Nebulized Inhaled Reduced Glutathione (RX Only) Nebulized Inhaled Hyroxocobalamin (RX Only) Mixed Natural Tocopherols Buffered Vitamin C Magnesium as Malate Four Different Flavonoid Sources: Ginkgo Biloba Extract, Cranberry Extract, Silymarin, & Bilberry Extract Selenium as Selenium-Grown Yeast Coenzyme Q10 Folic Acid Carotenoids Including Lycopene, Lutein and Alpha-carotene Alpha-Lipoic acid Zinc (modest dose) Manganese (low dose) Copper (low dose) Vitamin B6 in the Form of Pyridoxal Phosphate Riboflavin 5-Phosphate (FMN) Betaine (Trimethylglycine) Green Tea Extract Acetyl L-Carnitine
For more information on treatments for MCS, see Medical Treatment. |
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