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The syndrome of multiple chemical sensitivities has many manifestations and undoubtedly many causes. Treatment must be individualized based on a thorough psychosocial and biological diagnostic evaluation. Careful listening, as is usually the case, not only results in a more complete history but also serves a critical therapeutic purpose in cementing a trusting, working partnership. Family dynamics, and larger social concerns, such as litigation, may figure importantly as obstacles to rehabilitation if they are ignored in treatment planning. In chronically disabled patients, the importance of psychosocial interventions is even greater but should not eclipse attention to relevant medical interventions. The most basic physiologic manipulation involves a program of environmental avoidance. Such a program should be applied with caution since it is not without risks of inadvertent exacerbation of medical and psychologic disabilities. Therefore, from a medical perspective, interventions should focus on improving chemical tolerance by the appropriate application of first aid, chronohygiene, nutrition, psychophysiology, and correction of microbiological disruptions. Thorough investigation for intercurrent disease and its appropriate management is paramount. Attempts to treat the entire problem by isolating attention to one area or based on a single theory are likely to fail.
The phenomenon of multiple chemical sensitivities is a peculiar manifestation of our technophobic and chemophobic society. It has been rejected as an established organic disease by the American Academy of Allergy and Immunology, the American Medical Association, the California Medical Association, the American College of Physicians, and the International Society of Regulatory Toxicology and Pharmacology. It may be the only ailment in existence in which the patient defines both the cause and the manifestations of his own condition. Despite this, it has achieved credibility in workmen's compensation claims, tort liability, and regulatory actions, all of which are briefly reviewed.
After describing two patients seen by the author, we define multiple chemical sensitivities and discuss the scope of the problem and the epidemiology. Although the incidence of multiple chemical sensitivities is not known, the demographics are similar to that of agoraphobia. The classical conditioning model is proposed as a useful description of multiple chemical sensitivities. The desensitization approach to the diagnosis and treatment is proposed. Results with three patients were encouraging and the approach seems worthy of further evaluation and refinement.
A frequent, if not predominant, complaint of persons reporting symptoms of multiple chemical sensitivities (MCS) is that of heightened sensitivity to smells. In this study odor detection thresholds for phenyl ethyl alcohol (a major component of rose oil) and methyl ethyl ketone (a common solvent) were measured in 18 persons exhibiting symptoms of MCS and in 18 matched normal controls. In addition, nasal resistance, blood pressure, heart rate, and respiration rate were determined before and after the olfactory tests. Scores on the Beck Depression Inventory were obtained prior to testing. Although olfactory thresholds were equivalent in the two study groups, the MCS group evidenced significantly higher nasal resistances, respiration rates and Beck Depression Inventory scores. Decreases in systolic blood pressure and pulse were noted in both groups across the test sessions. These results do not support the hypothesis that MCS is associated with greater olfactory threshold sensitivity (at least to the two target chemicals), but do suggest that MCS is associated with depression, increased respiration rate, and decreased nasal airway patency.
The term multiple chemical sensitivity confuses etiology with diagnosis. Chemical sensitivity is a symptom expressed by patients. The symptoms complex is also expressed by the majority of patients with asthma reactive airway dysfunction syndrome or rhinitis following a single acute exposure, called reactive upper airway dysfunction syndrome. The chemically sensitivity patient merits evaluation for upper airway and bronchial reactivity that may cause extra-airway symptomatology.
The history of and nomenclature of the multiple chemical sensitivities are reviewed. The author's definition of multiple chemical sensitivity is a symptom complex 1) triggered by odor or a perceived exposure; 2) occurring at exposure levels below those of allergic sensitivity or irritation; 3) analogous to the symptoms of panic disorder as defined by DSM-IV-R; 4) lacking objective clinic pathologic criteria; and 5) responsive to panic disorder management.
Multiple chemical sensitivity is an environmental illness that demands exacting methods of diagnosis. Proposed associations between symptoms and specific substances, whether to one substance or to multiple chemicals, need to be critically examined through adequately designed scientific studies. Appropriate methods for controlled scientific study of adverse reactions to chemicals are discussed as well as the Food and Drug Administration's (FDA's) experience with aspartame as an example of the need for controlled scientific studies to refute or confirm anecdotal evidence. Since 1986 the FDA has received reports of 265 cases of epileptic seizures temporally associated with the ingestion of aspartame. Information obtained from the complainants' medical records as well as data on consumption patterns, temporal relationships, and challenge tests do not support the claim that the occurrences of the seizures are linked to consumption of aspartame. In addition, two double-blind, placebo-controlled crossover studies failed to demonstrate an association between epileptic seizures in children and adults and the ingestion of aspartame.
The clinical ecology model of environmental illness, or multiple chemical sensitivity (MCS), and particularly the theoretical assumptions, diagnostic procedures, and therapeutic recommendations promulgated by clinical ecologists are reviewed. No scientific evidence is found for their claims. MCS is conceptualized, instead, as a phobic disorder explicable in terms of the two-factor model of avoidance. Three cases of MCS are discussed in light of this model, and a comprehensive behavioral treatment package that includes biofeedback-assisted in vivo desensitization and cognitive restructuring is proposed.
The purpose of this review was to critically evaluate research on the psychogenic origins of multiple chemical sensitivities (MCS) syndrome. Using as keywords environmental illness, multiple chemical sensitivities, and clinical ecology, two databases--PsychLit and Medline--were searched by computer; reference lists of all articles located were also searched manually. Ten articles meeting three criteria were selected for review. Five sample selection problems, seven measurement problems, and three study design problems were common in all but one of the articles reviewed. Current studies investigating psychogenic hypotheses of MCS syndrome are methodologically problematic and their conclusions questionable. Studies of psychiatric profiles observed in MCS syndrome need to be designed to differentiate between competing psychogenic and biogenic hypotheses.
Multiple chemical sensitivities (MCS) defies diagnostic categorization because of its pansystemic manifestations, its lack of consistent symptomatology, and its absence of specific, measurable endpoints, either physical stigmata or laboratory findings. Controlled studies have been few and difficult to perform. Moreover, the phenomenon resists systematic investigation for two reasons. First, it has coalesced into a movement championed by zealous proponents and organized adherents. Second, it has gained support in the courts, the legislatures, and the regulatory agencies which have provided special protection and monetary awards to this phenomenon before science and medicine have defined it as a medical disorder. One hotly contested issue in the MCS debate is the relative role of organic versus psychological contribution to the symptoms of MCS patients. This is a critical issue most importantly because it determines approaches to treatment, secondarily because it affects regulatory action, disability determination, and compensability. The interest of the ISRTP in this phenomenon derives from the significant regulatory impact of this diagnosis on OSHA standards, EPA regulations, and FDA standards. The symposium was convened to explore the quality of the science underlying MCS with respect to diagnosis, and, particularly, to cause. The general objective of the symposium was to discuss the state of the science regarding MCS and its implications in regulatory toxicology and public health. The panel of speakers represented a variety of disciplines including toxicology, immunology, occupational medicine, psychiatry, psychology, epidemiology, and public health. The symposium was attended by a diverse audience representing the medical, scientific, business, legal, and regulatory communities. The majority of speakers critically questioned the characterization of MCS as a clinical entity, in light of historical comparisons to earlier false diagnoses, toxicological implausibility, and clinical inconsistencies.
BACKGROUND: Chronic fatigue syndrome (CFS), fibromyalgia (FM), and multiple chemical sensitivities (MCS) are conditions associated with fatigue and a variety of other symptoms that appear to share many clinical and demographic features. Our objectives were to describe the similarities and differences among patients with CFS, FM, and MCS. Additional objectives were to determine how frequently patients with MCS and FM met the criteria for CFS and if they differed in their health locus of control. METHODS: Demographic, clinical, and psychosocial measures were prospectively collected in 90 patients, 30 each with CFS, FM, and MCS. Patients were recruited from a university-based referral clinic devoted to the evaluation and treatment of chronic fatigue and three private practices. Variables included demographic features, symptoms characteristic of each condition, psychological complaints, a measure of health locus of control, and information on health care use. RESULTS: Overall, the three patient groups were remarkably similar in demographic characteristics and the presence of specific symptoms. Patients with CFS and FM frequently reported symptoms compatible with MCS. Likewise, 70% of patients with FM and 30% of those with MCS met the criteria for CFS. Health care use was substantial among patients with CFS, FM, and MCS, with an average of 22.1, 39.7, and 23.3 visits, respectively, to a medical provider during the prior year. Health locus of control did not differ among the three populations. CONCLUSIONS: In general, demographic and clinical factors and health locus of control do not clearly distinguish patients with CFS, FM, and MCS. Symptoms typical of each disorder are prevalent in the other two conditions.
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OBJECTIVE: To examine the role of immunologic, psychological, and neuropsychological factors in multiple chemical sensitivity. DESIGN: Case-control comparison. SETTING: Community allergy practice (cases), university-based clinics for musculoskeletal injuries (controls). PARTICIPANTS: Forty-one patients with chemical sensitivity and 34 control patients with chronic musculoskeletal injuries. MAIN OUTCOME MEASURES: Immunologic measures included autoantibody titers, lymphocyte surface markers, and interleukin-1 generation by monocytes. Psychological evaluation included standardized measures of anxiety, depression, and somatization. RESULTS: Immunologic testing did not differentiate patients with chemical sensitivity from controls. The only difference noted (lower interleukin-1 generation among cases) appeared attributable to laboratory methods. Patients with chemical sensitivity reported greater prevalence of current anxiety or depressive disorder (44% versus 15%, P = 0.006). This difference, however, did not appear to precede the onset of chemical sensitivity, and 25% of chemically sensitive patients showed no significant current psychological disturbance. Cases reported significantly more "medically unexplained" physical symptoms before and after the onset of chemical sensitivity. When considering only symptoms that preceded chemical sensitivity, 25% of cases (and no controls) satisfied criteria for somatization disorder. Neuropsychological testing revealed no significant case-control differences. CONCLUSIONS: Immunologic testing failed to confirm findings from earlier uncontrolled studies, militating against proposed immunologic mechanisms. The decreased memory and concentration frequently described in multiple chemical sensitivity were not confirmed by brief neuropsychological testing. Psychological symptoms, although not necessarily etiologic, are a central component of chemical sensitivity.
Neurological sensitization has been proposed as a model for post-traumatic stress disorder (PTSD) (Lipper et al., 1986; van der Kolk, 1987; Friedman, 1988; Post et al., 1988, 1994; Charney et al., 1993). Laboratory paradigms in which repeated exposure to a discrete stimulus is associated with progressive intensification of a neurophysiologic, behavioral, or pharmacologic response has many parallels with the sequence of events that precipitates PTSD. Investigators with other clinical interests have also been attracted to sensitization models. Specifically, Bell and associates (1992) have proposed that olfactory-limbic kindling is a very good model for understanding the etiology of multiple chemical sensitivity (MCS) syndrome. A number of articles in this volume have addressed the goodness-of-fit between this model and MCS. My major assignment is to review laboratory data and clinical observations pertinent to sensitization models of PTSD. I will show that although there are intriguing parallels between the two phenomena, one must have great respect for the complexity and polymorphism of both sensitization and PTSD before grasping for simplistic theoretical conclusions. Secondly, I will address the following question; if both PTSD and MCS can be understood as sensitization phenomena, are PTSD patients at greater risk to develop MCS and vice versa? This article is divided into four sections: a) a description of three distinct sensitization phenomena; b) a description of the symptoms of PTSD; c) a review of the applicability of sensitization models to the clinical phenomenology of PTSD; and d) a review of the hypothesis that PTSD patients might be more vulnerable to MCS.
Multiple chemical sensitivity syndrome (MCS) does not appear to fit established principles of toxicology. Social, political, and economic forces are demanding that MCS be defined medically, even though scientific studies have failed as yet to identify pathogenic mechanisms for the condition or any objective diagnostic criteria. Consequently, a working definition of MCS can only rely on a person's subjective symptoms of distress and attribution to environmental exposures rather than currently measurable objective evidence of disease. Nevertheless, patients labeled with MCS are clearly distressed and many are functionally disabled. Without reconciling the different theories of etiology of MCS discussed in Part I of this report, and recognizing that the cause of the syndrome may be multifactorial, strategies are proposed for clinical evaluation and management of patients with MCS using a biopsychosocial model of illness. The social implications of this illness are also discussed.
Multiple chemical sensitivity syndrome (MCS) does not appear to fit established principles of toxicology. Yet social, political, and economic forces are demanding that MCS be defined medically, even though to date scientific studies have not identified pathogenic mechanisms for the condition or any objective diagnostic criteria. Consequently, a working definition of MCS can rely only on an individual's subjective symptoms of distress and attribution to environmental exposures rather than currently measurable objective evidence of disease. Nevertheless, patients labeled with MCS are clearly distressed and many are functionally disabled. In this review, four theories of causation are explored: (1) MCS is a purely biologic/physical or psychophysiologic reaction to low-level chemical exposures. (2) MCS symptoms may be elicited by low-level environmental chemical exposures, but the sensitivity is initiated by psychologic stress. (3) MCS is a misdiagnosis and chemical exposure is not the cause. The symptoms may be due to misdiagnosed physical or psychologic illness. (4) MCS is an illness belief system manifest by culturally shaped illness behavior. Areas for further research regarding the etiologies of MCS are suggested. Recognizing that the cause of the syndrome may be multifactorial, strategies are proposed for clinical evaluation and management in Part II of this manuscript using a biopsychosocial model of illness.
It often happens in science that clues to the nature of a problem under study come from a completely different, seemingly unrelated, line of investigation. This may be the case with MCS and Time-Dependent Sensitization (TDS), a phenomenon we discovered in rats in the late 1970s and later named. TDS refers to the ability of mild stressors--whether pharmacological or environmental--to induce physiological and behavioral effects which then progress, i.e., get stronger, entirely as a function of the passage of time since stressor presentation. This strengthening is revealed when the organism is later exposed to either the original or another stressor. The characteristics of TDS bear a remarkable resemblance to the features of MCS and that similarity is the subject of this manuscript.