Multiple Chemical Sensitivity: Toxicological and Sensitivity Mechanisms

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/ONOOcycle, which is initiated by various stressors that increase nitric oxide and peroxynitrite levels (with some but not others acting via NMDA stimulation). The NO/ONOOcycle 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 MCSrelated 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