Multiple Chemical Sensitivity (MCS) is estimated to affect up to 15% of the population in the US and other industrialised nations (1), yet research into why people develop this hypersensitivity to chemicals is sorely lacking. Currently we have mainly animal testing and studies involving small numbers of participants diagnosed with MCS to go on.

One leading theory suggests the development of a hypersensitivity to chemical stimuli in an area of the brain known as the limbic system which controls a variety of functions including emotion, behaviour, long term memory, and olfaction (our sense of smell). Animals studies have shown that both large acute exposures and low-level chronic exposures to certain organic chemicals can result in hypersensitivity of the limbic system to subsequent minute exposures to the same, or similar chemicals (2). Perhaps the most complete theory of the pathophysiology of MCS thus far has been proposed by Martin Pall, Professor Emeritus of Biochemistry and Basic Medical Sciences at Washington State University. Pall believes the symptoms are the result of a trigger (primarily chemical exposures) that results in the body getting locked into a cycle involving elevated levels of nitric oxide, increased free radical production (oxidative stress), chronic inflammation, and again, excessive sensitivity of the brain and central nervous system to "normal" stimuli (mediated by the NMDA receptor) (3).

What all current biomedical research points to is that excessive exposures to chemicals that exceed the the body's detoxification capacity, may result in the development of MCS in susceptible individuals. This is true whether the exposure is acute and obvious or is more insidious, occuring at a low-level over a prolonged period of time.

For some who develop MCS it is obvious what initially caused their illness. Acute exposure to such things as organophosphate/organochlorine pesticides, formaldehyde, or various powerful industrial solvents are obvious examples.

There is much overlap between MCS and Gulf War Syndrome and this is little surprise since military personnel were exposed to a highly toxic environment during Operation Desert Storm in 1991.

In many cases however, the initial trigger for the development of MCS remains a mystery. For this reason I have decided to point out a few sources of chemical exposure you may not have considered that could potentially trigger MCS:

1. Mold -  For people living or working in water damaged buildings, mold could be a prime suspect if MCS subsequently develops. Dr. Lisa Nagy M.D., a leading environmental medicine physician, has attributed her own illness to mould exposure following water damage to her home. Mold and mycotoxins (mold/fungal toxins) in water-damaged buildings and their biological effects have been well studied. They have been found to trigger the production of autoantibodies that attack the brain and central nervous system, cause peripheral neuropathy, and result in various neuropathological effects including altered blood flow and electrical activity in the brain (4). EiR recommends scientifcally-proven natural mold removal products for body, home and laundry from Micro Balance Health Products.

2. Carbon Monoxide - Since it is a colourless and odourless gas, exposure to carbon monoxide (CO) can go undetected for long periods of time. For this reason it is important to install CO detectors in your home and have appliances such as gas-fired boilers serviced regularly. Pall suggests CO exposure as a likely trigger for the cascade of pathophysiological changes that can lead to MCS and points out that the symptoms of CO poisoning share many many similarities with those of MCS (5).   

3. Candida/Yeast Overgrowth - On the face of it perhaps the least obvious source of toxic chemical exposure that might lead to MCS would be an intestinal overgrowth of Candida/yeast. Yet, many MCS sufferers have good reason to believe they also suffer from an imbalance in their gut microflora that has allowed yeast to expand their presence. When we consider the chemical toxins that yeast such as Candida sp. produce as they ferment the carbohydrates in the food we consume, it in fact becomes obvious that when these are absorbed into the systemic circulation from the gut they are able to poison the brain and may ultimately contribute to the development of MCS. These micro-organisms produce ethanol (drinking alcohol), acetaldehyde (a chemical cousin of formaldehyde), and a host of other mycotoxins, which we have already established are neurotoxic.

4. Dental Work - Many MCS sufferers cite dental procedures as the trigger for their illness. Amalgam fillings contain mercury which is a known neurotoxin and increasingly people are complaining of the development of chemical sensitivities after they started using newer techniques for teeth alignment, such as Invisalign (see this blog). 

There are no doubt many other hidden sources of toxic chemicals that may trigger the development of MCS in those who are susceptible due to genetic characteristics and other factors. After all, our environment in the 21st century is saturated with such chemicals.

If you have any other suggestions please let us know using the comment form below. It was also be great to hear what you believe caused your own MCS.


References:

1. Caress SM and Steinemann AC (2004) Prevalence of Multiple Chemical Sensitivities: A Population-Based Study in the Southeastern United States American Journal of Public Health 94(5): 746–7
2. Gilbert ME (2001) Does the kindling model of epilepsy contribute to our understanding of multiple chemical sensitivity? Annals of the New York Academy of Sciences 933:68-9
3. http://www.ei-resource.org/articles/chronic-fatigue-syndrome-articles/the-no!-oh-noo!-theory-and-suggestions-for-treatment/
4. http://www.ei-resource.org/expert-columns/dr.-lisa-nagys-column/neurological-and-immunological-problems-associated-with-mold-and-mycotoxin-exposure/
5. Pall ML (2002) NMDA sensitization and stimulation by peroxynitrite, nitric oxide, and organic solvents as the mechanism of chemical sensitivity in multiple chemical sensitivity FASEB Journal 16(11):1407-17