MCS - A Medical Perspective
Multiple Chemical Sensitivities (MCS) is an acquired condition in which the sufferer becomes sensitised or abnormally reactive to volatile chemicals following prolonged, recurrent or high dose exposure to volatile chemicals. The most distinctive symptom is "cacosmia", or a heightened sensitivity and lowered threshold to odours that most of the population find inoffensive or would not notice.
Multiple chemical sensitivities is a condition that primarily affects the nervous system, particularly the brain, and most often has characteristic symptoms, including:
Recent published studies demonstrate alterations of SPECT brain scans, central evoked responses (especially visual and auditory), and altered autonomic nervous system function. The mechanisms of such damage remain unclear at present, but direct neurotoxicity is regarded as the most likely cause. There is no current evidence that the condition is reversible, and MCS appears to represent a form of subtle toxic brain damage with the potential for lifelong disability.
The sufferer's history and clinical state should meet the criteria laid down by Cullen et al, that multiple chemical sensitivities is "... an acquired disorder characterised by recurrent symptoms, referable to multiple organ systems, occurring if response to demonstrable exposure to many chemically unrelated compounds at doses far below those established in the general population to cause harmful effects. No single widely accepted test of physiologic function can be shown to correlate with the symptoms." (Cullen M. R. The worker with multiple chemical sensitivities: An overview. Occup Med 1987;2: 655-661).
This and subsequent publications suggest that the critical defining features of multiple chemical sensitivities are that:
Specific tests such as Auditory Evoked Response Potential (AERP) testing and SPECT brain scans have shown significant changes in people suffering Multiple chemical sensitivities, and these changes are consistent with neurotoxic brain damage. Minimising of exposure is the only proven way of reducing the disability experienced, as there is no form of treatment proven to be effective.
The degree of disability suffered by those suffering is very high, and there is currently no clear evidence as to whether the damage to the nervous system is permanent or temporary. My personal impression, based on my clinical experience with over 500 sufferers in the past nine years, is that recovery is rare, and that the condition is associated with permanent neurotoxicity, or brain damage, in adults.
I have insufficient data regarding recovery in children to make an informed judgement. From first principles, however, recovery would be more likely in pre-pubertal children, assuming that they have minimal ongoing exposure, because of the ability of neurons (brain cells) to regenerate and form new links during those years. Whether this does happen is an entirely different, and at present unanswered, question.
Although described and defined by Cullen in 1987, acceptance of Multiple chemical sensitivities as a distinct clinical entity (disease) has been slow in occurring. The fact that the dosage for such damage is so low, and apparently 'neurotic' symptoms are maintained many years after exposure, has led many people to dismiss it as a psychological complaint, or a psychiatric disease. As increasing evidence of neuro-biochemical and neuro-pathological changes accrue, this view is currently changing among serious researchers.
Of the 84 articles and letters in the peer reviewed literature from 1993 to 1996, the majority now support the view of Multiple chemical sensitivities as a distinct clinical entity deserving of further research. Of the original articles (as opposed to letters, opinions and editorials), 51 identify non-psychiatric causes and contributions as being of major importance in the development of Multiple chemical sensitivities, while 14 attribute the disorder to psychiatric or psychological causes. All note the neuropsychological abnormalities in sufferers. Thus is a significant reversal of the weight of medical opinion presented in the peer reviewed medical literature in the five years prior to 1993.
In my opinion, it would now be correct to say that the majority of the medical literature on the subject supports the existence of the disease, the organ specific pathology, and the low level exposure as a significant factor in causation and symptom generation. In Australia, the majority of physicians appear to be relatively unaware of the change in scientific perspective on this condition, while others who have previously publicly stated their incredulity about the existence of the syndrome appear to have understandable difficulties in changing their viewpoint based on the recent available data.
While the disease is now generally well accepted as a clinical entity, however, the mechanisms of damage and therapeutic approaches which may be of benefit to sufferers are far from elucidated. This is true for many diseases, however, including Multiple Sclerosis, most cancers, and sudden infant death, to name only a few.
Dr Mark Donohoe has asked that contact details are provided for himself as well as other useful contacts and resources.
Australian representative, FIT Investments, for US diagnostic testing of detoxification pathways, UltraClear products, Toxicity '96 Conference.
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Measurement of blood organochlorines, urinary and lipid metabolic profiling.
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or WWW Home page: http://www.newcastle.edu.au/department/bi/birjt/cpruis/
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