Martin Pall releases a paper on the causes of Multiple Chemical Sensitivity, his research shows chemicals acting as toxicants initiate cases of MCS.
Martin Pall, PhD, professor emeritus of biochemistry and basic medical sciences at Washington State University, has released a paper on his research into the causes of Multiple Chemical Sensitivity. In the paper entitled Multiple Chemical Sensitivity: Toxicological and Sensitivity Mechanisms, Pall’s research shows the role of chemicals acting as toxicants in initiating cases of MCS has been confirmed by genetic evidence.
Professor Pall started looking into Chronic Fatigue Syndrome/Myalgic Encephalomyelitis after he was diagnosed with it. His groundbreaking research into a common cause for CFS/ME, MCS, Fibromyalgia and Post-Traumatic Stress Disorder led to his theory that short-term stressors cause a build up of naturally occurring nitric oxide, which starts a vicious cycle and leads to long-term illness. He calls this the NO/ONOO cycle.
Click here to download the pdf of the complete paper entitled Multiple Chemical Sensitivity: Toxicological and Sensitivity Mechanisms. This paper will be the “Multiple Chemical Sensitivity” page on Professor Pall’s website, but he’s released it early and kindly given The Canary Report permission to post.
Here’s the abstract:
Multiple Chemical Sensitivity: Toxicological and Sensitivity Mechanisms
Martin L. Pall
Professor Emeritus of Biochemistry and Basic Medical Sciences, Washington State University and Research Director, The Tenth Paradigm Research GroupAbstract:
Cases of multiple chemical sensitivity (MCS) are reported to be initiated by seven classes of chemicals. Each of the seven acts along a specific pathway, indirectly producing increases in NMDA activity in the mammalian body. Members of each of these seven classes have their toxicant responses lowered by NMDA antagonists, showing that the NMDA response is important for the toxic actions of these chemicals. The role of these chemicals acting as toxicants, in initiating cases of MCS has been confirmed by genetic evidence showing that six genes that influence the metabolism of these chemicals, all influence susceptibility to MCS. It is likely that chemicals act along these same pathways, leading to increased NMDA activity when they trigger sensitivity responses in MCS patients.
The chronic nature of MCS and also related multisystem illnesses is thought to be produced by a biochemical vicious cycle mechanism, the NO/ONOO- cycle, which is initiated by various stressors that increase nitric oxide and peroxynitrite levels (with some but not others acting via NMDA stimulation). The NO/ONOO- cycle is based on well documented individual mechanisms. The interaction of this cycle with previously documented MCS mechanisms, notably neural sensitization and neurogenic inflammation, explains many of the previously unexplained properties of MCS. This overall mechanism is also supported by physiological correlates found in MCS and related multisystem illnesses, objectively measurable responses to low level chemical exposure in MCS patients, many studies of apparent animal models of MCS and also evidence from therapeutic trials of MCS-related illnesses.
Some have argued that MCS is a psychogenic illness, but this view is completely inconsistent with this diverse data on MCS and related illnesses and the literature claiming psychogenesis of MCS is deeply flawed. In addition, two rare predictions that can be used to test psychogenesis both lead to rejection of the psychogenic hypothesis.
While the NO/ONOO- cycle mechanism for MCS is supported by many different observations, there are also multiple areas where further study is needed.
Another version of this paper is scheduled to be published as a chapter on Multiple Chemical Sensitivity in the prestigious General and Applied Toxicology, 3rd Edition due out in December.
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