Multiple Chemical Sensitivities
By Iris R. Bell, M.D., Ph.D.
January 1, 2003
Dr. Bell is professor of psychiatry, psychology, medicine, surgery and public health, and director of research for the Program in Integrative Medicine at the University of Arizona College of Medicine in Tucson. Her major research interest is neural sensitization as a model for multiple chemical sensitivity.
The symptom profile of MCS reveals that almost all patients have subjective dysfunction in the central nervous system (McKeown-Eyssen et al., 2001), with the majority also reporting respiratory and gastrointestinal (GI) disturbances (Fiedler and Kipen, 1997). Cardiovascular symptoms, endocrine dysfunction and musculoskeletal complaints vary from study to study (Miller and Prihoda, 1999). Some clinicians indicate that a subset of patients exhibit an atypical form of porphyria as a mechanism for their symptoms (Ziem and McTamney, 1997). Porphyria is a disorder of heme metabolism that can manifest with neuropsychiatric and GI symptoms. Only certain highly sensitive tests can detect this postulated abnormality in MCS patients. To date, no controlled studies are available to confirm or disprove the porphyria hypothesis for MCS.
A better-studied mechanism in MCS for which there are replicated findings in controlled human and animal studies is that of time-dependent or neural sensitization (Antelman, 1994; Bell et al., 1999a; Pall, 2002). Sensitization is the progressive amplification over time of host responses to repeated, intermittent exposures to an exogenous stimulus. Drugs, volatile organic chemicals and stress can all initiate sensitization and cross-sensitize with each other. Some sensitization involves the mesolimbic system, including the well-studied nucleus accumbens, a key structure in CNS responses to drugs of abuse. A special case of neural sensitization is limbic kindling, which is an animal model for temporal lobe epilepsy. On a scale assessing limbic system symptomatology, those with CI score higher than do normals on derealization, "spaciness" and memory problems (Bell et al., 1995). Individual difference factors that favor sensitization include characteristics that overlap markedly with MCS and CI, e.g., female gender, sucrose preference, behavioral hyper-reactivity to novelty, early life stress and genetic traits (e.g., parental vulnerability to drug self-administration) (Bell et al., 1999a).
Patients with CI have exhibited sensitization of heart rate, blood pressure, resting EEG α activity and EEG ∆ activity after chemical exposures (Bell et al., 1999a, 1999c, 1998b; Fernandez et al., 1999). Animal researchers have also found evidence for behavioral sensitization to environmental chemicals such as toluene (von Euler et al., 1994) and formaldehyde(Drug information on formaldehyde) (Sorg et al., 1998). In other words, people who become ill from low levels of environmental chemicals may be unusually sensitizable individuals to a wide range of exogenous influences such as chemicals, drugs, foods, noise and stress (Bell et al., 1999a). Their addictive-like features may fall in the arena of food cravings, rather than drug cravings (Miller, 2001). As in animals, such sensitizability may manifest as amplification in numerous psychological, behavioral and physiological parameters in the clinical situation (Bell et al., 2001).
Another potentially interactive model for the somatic symptoms of MCS is that of neurogenic inflammation (NI) (Bascom et al., 1997). Neurogenic inflammation is a form of nonimmunological inflammation initiated by stimulation of peripheral c-fiber sensory neurons. The inflammation results from neuropeptide release as part of a peripheral axon reflex response, e.g., via actions of substance P, calcitonin gene-related peptide, neurokinin A and other mediators. The CNS receives the signal that such inflammation and related pain have developed. In turn, areas of the spinal cord and limbic system are required for the initiation of chronic susceptibility to subsequently amplified pain, experienced at the peripheral site originally injured. Neurogenic inflammation plays a role not only in chronic pain, but also in irritant rhinitis, asthma and arthritis. Consistent with an inflammatory model, Bell et al. (1998c, 1998d) observed a significant correlation between serum neopterin, a general marker of inflammation, and scores on standardized scales of somatization in women with CI, but not in depressives without CI or normals. Taken together, neural sensitization and neurogenic inflammation provide models for mechanisms that could account for much of the phenomenology in MCS and CI.
Even when patients accept psychiatric treatment with psychotherapy and psychiatric medications for a comorbid depression or anxiety disorder, they often report that their sensitivities to chemicals and foods are at best dampened, but not resolved (LeRoy et al., 1996). Theoretically, inhibitors of substance P and blockers of other mediators of neurogenic inflammation could also be beneficial (Di Sebastiano et al., 1999). Many patients with MCS report intolerance to most medications, however.
Psychiatric interventions for somatization per se emphasize improving case management more than providing definitive treatment (Bass et al., 2001; Sharpe and Carson, 2001). Notably, one of the few treatment outcome studies in this area recently showed significant improvement in a small sample of patients with MCS and CFS on the SF-36 measure of health-related functional quality of life (Lacour et al., 2002). The treatment involved an eight-week interdisciplinary intervention that included a self-help program, acupuncture and a psychosomatic supportive therapy group. In addition, other patient-centered interventions that support the patient's efforts to regain a sense of control over their health and their world may be beneficial, e.g., with journal writing, guided imagery and/or biofeedback.
Patients with multiple chemical sensitivity report an average of 23 health care provider visits per year (Buchwald and Garrity, 1994). Lost U.S. worker productivity associated with related conditions such as sick building syndrome (workplace-specific illness, elicited in part by indoor pollutants at low levels) has been estimated at $10 billion/year. Society is puzzled over how to address the growing number of workers' compensation claims, disability cases and personal injury lawsuits associated with alleged chemical injury at work and at home. Given the high stakes, neuropsychiatric researchers have many promising leads that demand exploration. In the meantime, clinicians have tools to provide compassionate and supportive care for people with MCS and CI.
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