Clinically relevant EEG studies and psychophysiological findings: possible neural mechanisms for multiple chemical sensitivity.

This paper addresses the evidence for the face, construct, and criterion-related validity of the olfactory-limbic/neural sensitization model for multiple chemical sensitivity (MCS). MCS is a poorly-understood, controversial condition in which low levels of environmental chemicals are reported to trigger disabling levels of illness in certain individuals. Neural sensitization processes could generate an endogenous amplification of responsivity to exogenous substances, thereby providing a plausible explanation for the apparent lack of a classical toxicological dose-response relationship in MCS. Convergent data from both survey and psychophysiological studies of MCS patients and of persons from the community without MCS, but who report elevated frequency of illness from chemical odors (cacosmics), support the involvement of the limbic system and the sensitizability of cacosmics, as predicted by the model. Recent studies show that cacosmics do sensitize their heart rate, blood pressure, and plasma beta-endorphin responses to repeated exposures to a novel laboratory procedure involving dietary manipulations over time. Cacosmia may represent a pathological form of neural plasticity. Taken together, the model and the available evidence suggest the need for more intensive investigation of MCS from the standpoint of possible neurobiological mechanisms affecting cognitive, emotional, and somatic functions.