observations; no direct experiments have been done to test its validity in humans; however, animal models do exist. The concept aligns with Selye's work on the general adaptation syndrome (Selye, 1946).

Items 2 and 3 above confound epidemiological investigation of this problem.

Items 3 and 4 suggest a two step process-(1) induction or sensitization resulting from an initial "major" exposure and (2) triggering of symptoms by subsequent lower level exposures to many different incitants.

Although knowledge of the mechanism of a disease may be useful for developing better therapies, such knowledge is not a prerequisite for intervention. Preventing the development of multiple chemical sensitivities in those not yet afflicted may be possible by controlling environmental exposures that cause the initial sensitization.

The most frequently cited physiological theories to explain chemical sensitivity involve the nervous system, the immune system, or the interaction between them because these two systems most dearly link the external environment and the internal milieu.2 The rapid responsiveness of these systems also makes them attractive candidates because symptoms of food or chemical sensitivity have been reported to develop within seconds of exposure. Many chemicals, such as polybrominated biphenyls (PBBs) and trichloroethylene, affect both the nervous system and the immune system. Until 1980, the idea of a possible direct communication between the nervous and immune systems was widely debated. Subsequently, the existence of a neuroimmunoendocrine axis has been increasingly realized. Several discoveries have helped to confirm the presence of two-way communication between the nervous and immune systems (Payan et at., 1986).

Kilburn proposes that the human nervous system, because it is so highly evolved, may be most susceptible to environmental agents (Kilburn, 1989):

"Sensitivity may be its undoing. The intuitive hypothesis is advanced that the nervous system is the most liable of the body's systems to damage from environmental toxins. Appreciation of damage may be masked because subtle dysfunction is concealed by the nervous system's remarkable redundancy and substitution of functions, or it is overlooked in clinical evaluations which are usually only qualitative."


The hypothalamus (part of the limbic system) has attracted considerable attention because it is the focal point in the brain where the immune, nervous, and endocrine systems interact (Bell, 1982). Bell notes that assuming a direct cause-and-effect relationship would be premature, but that the hypothalamus could mediate food and chemical addictions in patients with multiple chemical sensitivities. The olfactory system has known links to the hypothalamus and other parts of the limbic system, which has led Bell to speculate that "the olfactory system, hypothalamus and limbic system pathways would provide the neural circuitry by which adverse food and chemical reactions could trigger certain neural, psychological and psychiatric abnormalities." Patients with chemical sensitivities have


 Discussions of possible immune system mechanisms and psychological hypotheses for chemical sensitivity appear in Ashford and Miller, 1991.

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