A Report on Multiple Chemical Sensitivity (MCS)

The Interagency Workgroup on
Multiple Chemical Sensitivity

August 24, 1998

Predecisional Draft


Immune Mechanisms


Neurologic Mechanisms Including Altered Sense of Smell

Psychological Mechanisms

Other Syndromes

Clinical Ecology Approach

Summary of Mechanisms

Table of Contents

III. Theories of Causation and Mechanisms


The proposed theories of causation of MCS can only be summarized in this report. Although these theories can be grouped into three broad categories (immunologic, neurologic, and psychological), there are many variations. Some theories are interrelated, and each theory is still being considered and debated within the scientific community. For example, Miller et al. (1997) proposed a theory of "toxicant-induced loss of tolerance" (TILT), which suggests that acute or chronic chemical exposures might cause certain susceptible persons to lose their tolerance for previously tolerated chemicals, drugs, and foods. Subsequently, even minute quantities of these and other substances may trigger symptoms. They argue that TILT may prove to be a new theory of disease causation parallel to the germ, immune, and cancer theories.

Discussions regarding the mechanisms of MCS can be divided into two distinct categories. Some persons assert that MCS symptoms are psychologically based or have strong psychological components. Others who accept a physiological basis for MCS may concur that psychological factors are present, but contend that they are only a component of the condition or are the natural result of coping with an intractable chronic condition.

The following sections summarize key literature on immune system, neurologic, and psychological mechanisms postulated to be associated with MCS.

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Immune Mechanisms

Disorders of the immune system have been suggested as causing or contributing to MCS (Rea et al., 1992; Levin and Byers, 1987; Thrasher et al., 1990; Heuser et al., 1992; Ross, 1992; Levin and Byers, 1992). Some practitioners employ tests for immune sensitization and/or laboratory determinations of immune parameters in diagnosing MCS, and some use therapeutic regimens directed at correcting putative immune deficiencies (Rea et al., 1992; Heuser et al., 1992; Ross 1992; Levin and Byers, 1992). However, these investigators generally agree that MCS differs from disorders known to be associated with overt immunopathology (i.e., allergies, immune deficiencies, and autoimmune diseases) and suggest that MCS is not mediated solely by known immune mechanisms (Ziem, 1992). Instead, MCS is argued to be associated with a more general form of "immune dysregulation" which leads to the MCS symptom complex, perhaps through interaction of immune mediators with the neuroendocrine systems (Meggs, 1992; Levin and Byers, 1992).

The theories and reports of immune involvement in MCS presented by some environmental medicine practitioners have not been accepted by most physicians and researchers (Terr, 1987; Albright and Goldstein, 1992), but some do acknowledge that allergic or immunotoxicologic reactions could be contributing factors in at least a subset of MCS patients (Selner and Staudenmayer, 1992; Albright and Goldstein, 1992; Meggs, 1992). Because immune responsiveness and inflammation are closely related, hypotheses relating inflammation to MCS (which are discussed in the next section) are likely to overlap with immunologic considerations (Meggs, 1992).

Evidence for or against immune involvement in MCS depends to some extent on laboratory measurements of certain immune biomarkers (defined by the National Research Council [NRC] [1987] as "[i]ndicators of events in biological systems or samples"). Some studies have reported that results of immune biomarkers lie outside "normal" ranges in many MCS patients (Heuser et al., 1992; reviewed in Meggs, 1992). Immune abnormalities reported to be associated with MCS include alterations in the distribution of peripheral blood lymphocyte subsets, increases in the proportion of activated T-cells in circulation, and abnormal serum antibodies to tissue antigens and chemical-protein conjugates (Rea et al., 1992; Thrasher et al., 1990; Heuser et al., 1992; Levin and Byers, 1992). In contrast, studies conducted by other researchers have not detected abnormal immune test results in MCS patients (Terr 1986; Simon et al., 1993).

The role of the immune system in MCS is difficult to assess from many of the published reports because the laboratory methods are inadequately documented or, in some cases, clearly deficient. Results reported for lymphocyte phenotypes illustrate these methodologic concerns. For example, Levin and Byers (1987) cited results originally reported in court records but gave no methodologic information. Similarly, an article by Terr (1986), provides no description of laboratory methods. Another example is the use of an inadequate method, peripheral blood lymphocyte phenotypes determined by manual fluorescent microscopy on separated cells, to assess the role of the immune system in MCS (Thrasher et al., 1990; Simon et al., 1993). This technique is considered to be unacceptable for clinical use (Kidd and Vogt, 1989; CDC, 1992). Comparable methodologic uncertainties attend reports on immune tests for autoantibodies, antibodies to chemical-protein conjugates, and cellular function assays in MCS patients (Vogt 1991; Vogt and Margolick , 1994). Fully controlled studies with appropriate quality assurance are needed to verify the suggested changes in immune system markers postulated to be associated with MCS.

In addition to limitations in laboratory analyses, another major difficulty with interpreting data on immune functions and MCS is the lack of sound epidemiologic methods in most of the published reports, which are limited to individual cases or small numbers of individuals identified in clinical settings. While such reports have value in suggesting directions for rigorous investigations with sound study design, they must be interpreted cautiously because they do not account for the numerous confounding variables (including age, sex, smoking, diurnal and seasonal variation, and stress) that can influence immune parameters (Vineis et al., 1993).

The importance of both laboratory methods and epidemiologic design has been underscored by one particular study of MCS and immunologic tests (Simon et al., 1993). The study used careful epidemiologic design to determine the usefulness of certain immunologic tests in discriminating MCS patients from matched controls. The results showed clearly that the immunologic tests, as selected and performed by a laboratory specializing in tests for MCS, were of no use for identifying MCS patients. Subsequent to the publication of this study, one of its investigators, Simon, released unpublished results from 10 sets of split (i.e., duplicate) samples (20 specimens), to which the specialty laboratory had been blinded, showing that results across samples had not been replicated (Friedman et al., 1994).

The sound epidemiologic design of this study was important for raising questions about the reliability of results from the specialty laboratory and reports previously published by the laboratory (Thrasher et al., 1990). Moreover, because the same laboratory was used by at least one physician who claimed to have found immunologic tests useful for diagnosing MCS (Friedman et al., 1994), the results of the Simon et al. (1993) study cast doubt on some accounts that suggest immune system involvement in MCS. However, because of the laboratory deficiency, the study provides inadequate information about immune effects in MCS patients.

Clarification of the role of the immune system in MCS may be forthcoming from an ongoing multicenter study that is comparing results on a comprehensive panel of immunologic biomarkers between MCS patients and matched controls using rigorous inter-laboratory quality assurance (personal communication, Joseph B. Margolick, Johns Hopkins University).

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Inflammation has been suggested as being causally related to MCS as a result of the initiation of mediators released from cell membranes by the action of free radicals produced from toxic chemical exposures (Sparks et al., 1994). Bascom (1992) has suggested that exposure to low-level irritants may result in chronic respiratory health effects and that "[d]ifferential susceptibility exists to illnesses resulting from chronic exposure to irritant mixtures." She suggests this occurs through several mechanisms, primarily induction of inflammation through irritation of the upper airway epithelium.

The role of respiratory tract inflammation in MCS has also been hypothesized to resemble the changes seen in other conditions that include hyperreactivity of the airways. It has been suggested that a single acute, high-dose induction exposure to a chemical is followed by a chronic intolerance to low levels of chemicals. This two-stage process has been observed in reactive airways dysfunction syndrome, in which a high-dose exposure to airway irritants is followed by chronic asthma with bronchial hyperactivity (Brooks et al., 1985). Meggs has theorized that patients who develop rhinitis after a single high-dose exposure can be said to have reactive upper-airways dysfunction syndrome (Meggs, 1995). He suggests that chemical sensitivity may be a symptom of airway inflammation. In support of this hypothesis, Meggs gives several examples of studies where chemical sensitivity was associated with upper airway disease for which the examined health outcomes did not require rhinolaryngoscopic examinations (e.g., Doty et al., 1988; Chester, 1991). Fiber-optic rhinoscopy has been used to detect nasal inflammation in a chemically sensitive population, and nasal biopsies have indicated chronic inflammation and a cobblestone appearance of the pharynx and tongue accompanied by mucosal injection (Meggs and Cleveland, 1993).

Meggs (1995) reported airway inflammation that he noted on rhinolaryngoscopic examinations; he hypothesized that inflammation in the airways can produce many of the extra-airway symptoms seen in MCS. He argued that patients with allergies have extra-airway symptoms such as nausea, fatigue, mental confusion, and myalgia at sites other than the site of inoculation with antigen. He speculated that the mechanism by which chemicals cause airway inflammation is a chemical interaction with chemoreceptors on sensory nerves, leading to release of substance P and other mediators of neurogenic inflammation. Leznoff, however, reported that five patients he examined who complained of throat-related symptoms (choking, cough, dysphonia, and "swollen glands") following challenge with a chemical showed no visible changes in the throat or larynx using fiber-optic laryngoscopy and no change in recorded phonograms (Leznoff, 1992). It should be noted that in neither of the two previous studies where the investigators were blinded (i.e., unaware) to the MCS status of the patients.

In studies that have been useful in elucidating inflammogenic pathways, inflammatory mediators (including cytokines and neuropeptides) have been quantified in serum and in nasal biopsies, scrapings, and washings of persons with well-defined allergic and nonallergic inflammatory reactions (Straight and Vogt, 1997). There is no convincing evidence that such mediators are involved with MCS (Salvaggio, 1992), although the hypothesis has not been adequately tested. The analytical methods for measuring these mediators require close attention, because many of the assays yield highly variable results between different sources and even between different reagent lots from the same source.

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Neurologic Mechanisms Including Altered Sense of Smell

Of the neurophysiologic models that have been advanced to explain MCS-related clinical phenomena and to provide possible mechanisms for the condition, the olfactory-limbic and neural sensitization model developed and refined by Bell and colleagues is the one most completely explicated (Bell et al., 1992; Sparks et al., 1994). In a description of this model, Bell et al. (1997b) proposed that neural stimulation is the underlying mechanism for the disorder. Neural stimulation is defined as the "[p]rogressive amplification of responsivity by the passage of time and repeated, intermittent exposures" and can be initiated by a single exposure to a chemical or by multiple low-level exposures. Several forms of sensitization are proposed, including "limbic kindling," a phenomenon described in animal research in which exposures to excitants, such as electricity or chemicals, result in abnormal electrical activity in the brain and seizures or seizure-like phenomena. Other forms of sensitization include time-dependent sensitization of neurochemical, immunologic, endocrinologic, and behavioral responses. According to Bell's model, these forms of sensitization directly involve limbic and mesolimbic systems in the brain. Because these brain systems include structures that are known to be associated with emotion and cognition, Bell concludes that the cognitive and mood symptoms associated with MCS are related to the involvement of these brain regions through sensitization. She feels that sensitization is distinct from other possible mechanisms associated with MCS symptomatology (e.g., conditioning and habituation), but suggests that these distinct mechanisms might be integrated to better explain MCS.

To test their model of MCS, Bell and colleagues have conducted a number of studies comparing persons who are chemically intolerant and chemically tolerant (based on the cacosmia screening index). In studies of college students, Bell has tied the phenomenon of chemical intolerance to limbic system function through demonstration of associations between higher reports of psychological distress and drug use (Bell et al., 1996a) and higher rates of personal histories of anxiety and depression and family histories of substance abuse (Bell et al., 1995b) among students who report chemical intolerance in comparison with those without such intolerance. In the latter study, she also reported that the chemically intolerant students scored higher on a measure of "limbic system symptoms" than did the chemically tolerant students. As support of the limbic system hypothesis, Bell and colleagues have also reported lower scores on a memory test among chemically intolerant persons in a sample of Veterans Administration patients (Bell et al., 1997a) and slowed reaction times on a divided attention task performed by chemically intolerant retired adults (Bell et al., 1996b). In a series of studies, Bell et al. (1996c, 1996d, 1997d) reported changes in endorphin levels, blood pressure, and wakefulness in chemically intolerant persons relative to controls. All of these studies represent attempts to explore the hypothesized model. It should be noted that the experiments have been carried out primarily among persons who had not received a diagnosis of MCS.

Animal models of sensitization have been proposed and initiated (Sorg et al., 1994; Sorg, 1995; Bell et al., 1997c). Gilbert (1995) reported that rats with chronic, low-dose exposure to lindane developed electrical changes in the brain and seizure-like symptoms, while those with a single-dose exposure did not. He tied these results to the concept of chemical kindling. Animal models have also been used to test hypotheses that responsivity to chemicals might have a genetic component (Wang et al., 1993). In addition, the use of a specific breed of rats (Flinders Sensitive Line rats) that are highly sensitive to the organophosphate diisopropylfluorophosphate and which have increased cholinergic receptors and behavioral changes resembling those seen in human depression has been suggested for studies in animal models of MCS (Overstreet et al., 1996).

In a study of odor responsivity among persons diagnosed with MCS, Fiedler et al. (1995) tested 31 subjects to assess odor detection thresholds to rose-scented alcohol and an unpleasant-smelling pyradine; no differences were found between the MCS subjects, controls, and asthma patients.

Quantitative electroencephalography (EEG), brain electrical activity mapping (BEAM), positron emission tomography (PET), and single photon emission computed tomography (SPECT) have been used as neurologic correlates of MCS. Mayberg (1994) reviewed the studies that used these methods and concluded that, although patterns seen in some studies have shown abnormalities that might be related to MCS (particularly with SPECT), these studies are deficient in standardization of techniques, replication of results using testable hypotheses, and use of appropriate control groups.

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Psychological Mechanisms

Psychiatric factors have been seen as the cause of MCS, an effect of having MCS, a predisposing factor in the development of MCS, and a co-morbid occurrence with MCS. Some investigators believe that MCS is a somatoform reaction (i.e., physical symptoms not explained by objective clinical findings), if not a frank psychiatric condition. For example, one investigator believes the symptom complex of MCS resembles the DSM-III-R description for panic disorder (Kurt, 1995), and others have suggested that MCS is an "odor-triggered panic attack" (Shusterman and Dager, 1991).

Black et al. (1990) conducted a study on the emotional profile of persons identified as having "environmental illness." Persons who were included had illnesses diagnosed as chronic yeast disease, environmental allergy syndrome, 20th century disease, and the multiple chemical hypersensitivity syndrome. No physical or laboratory examinations were included. Significantly more study subjects than controls met lifetime criteria for a major mental disorder, suggesting that patients with a diagnosis of environmental illness may have one or more commonly recognized psychiatric disorders that could explain some or all of their symptoms. Psychiatric diagnoses were recommended for consideration as an explanation for patients with multiple ill-defined symptoms in the absence of clinical or laboratory findings. This suggestion was supported by an earlier study (Stewart and Raskin, 1985) of patients with "20th century disease." Another study (Simon et al., 1993) compared 41 patients who had chemical sensitivity with 34 control patients who had chronic musculoskeletal injuries to examine the role of psychological and other factors in MCS. Psychological evaluation included standardized measures of anxiety, depression, and somatization. Patients with chemical sensitivity reported a greater prevalence of current anxiety or depressive disorder, but this difference did not appear to precede the onset of chemical sensitivity. The investigators concluded that psychological symptoms, while not necessarily a cause, are a central component of chemical sensitivity. Davidoff and Fogarty (1994) have pointed out methodologic problems, such as patient selection, in these and other reports.

Fiedler and colleagues have examined neuropsychological test performance as a marker of central nervous system (CNS) dysfunction in patients in whom MCS has been diagnosed or who have related problems. In 1992, Fiedler et al. summarized data on 11 patients who met Cullen's criteria for diagnosis of MCS. On the basis of these data, the investigators concluded that there were neuropsychological findings suggestive of CNS involvement in MCS. This conclusion was questioned in a later study (Fiedler et al., 1996). In this study, Fiedler and colleagues compared neuropsychological and psychiatric function among MCS patients who met and those who did not meet Cullen's criteria of MCS (labeled MCS and CS, respectively), patients who had chronic fatigue syndrome (CFS), and healthy controls. Standardized measures of psychiatric and neuropsychological function did not distinguish the MCS and CS groups from the CFS group. The prevalence of current Axis I Psychiatric Diagnosis was higher in the MCS, CS, and CFS groups than in controls. Seventy-four percent of MCS, 38 percent of CS, and 61 percent of CFS patients did not meet criteria for any current Axis I Psychiatric Diagnosis. Neuropsychological test results did not account for the level of impairment implied by the patients' symptom reports.

It has been suggested that MCS is an example of a conditioned response (Siegel and Kreutzer, 1997). In classical conditioning, a neutral conditioned stimulus is paired with an unconditioned stimulus. The unconditioned stimulus reflexively elicits some response, termed the unconditioned response. Initially, the conditioned stimulus does not evoke a response. However, as a result of conditioned stimulus-unconditioned stimulus pairings, the conditioned stimulus becomes associated with the unconditioned stimulus. As a result, the previously neutral stimulus elicits a new response, termed the conditioned response. Once established, generalization may occur during which the conditioned response is elicited by stimuli other than the conditioned stimulus. Typically, the greater the similarity between the novel stimulus and the conditioned stimulus used during acquisition, the greater the strength of the generalized conditioned response. Davidoff (1992) examined three models of MCS, including the classical conditioning model. She listed predictions derived from this model, including those that incitants will have somewhat similar odors and that responses will be "stereotyped and reflex-like" and will occur predictably with certain odors. This model also does not require prior psychopathology, because emotional responses can be reflexively induced. Davidoff listed data consistent with the classical conditioning model, including reports of the absence of a psychiatric history predating the condition and reports that odor awareness is often salient in MCS. She also listed data inconsistent with the classical conditioning model, including MCS patients' reporting that odors and response patterns to incitants vary (Davidoff, 1992).

A 1993 exposure chamber study that was designed to investigate odor thresholds and the ability of MCS patients to determine the presence of chemicals included double-blind provocation challenges to 20 patients (Staudenmayer et al., 1993). The investigators used an olfactory masker and a variety of chemicals (i.e., one chemical per patient); each patient received five–10 challenges. All patients believed that they were reactive or hypersensitive to low-level exposure to multiple chemicals. Clean air challenges that contained the olfactory masker were used as placebo controls. As a group, the patients did not show a "reliable response pattern across a series of challenges." The patients as a group showed 33.3 percent sensitivity, 64.7 percent specificity, and 52.4 percent efficiency in responding to stressors. The investigators concluded that such testing helps differentiate toxicologic mechanisms from psychological mechanisms such as stress psychophysiology and learned sensitivity. However, the results of this study may have been influenced by the choice of placebos used in the experiment, the use of masking, and the outcome measures that were used. In an earlier report, the same investigators suggested that, in any environmentally related case, an evaluation should be made of psychological motivation and evidence of psychological symptoms, including repressed childhood trauma (Selner and Staudenmayer, 1992).

In summary, the suggestion that psychiatric disorders are the basis of MCS has complicated communication between those who believe that, if present, psychiatric symptoms are a secondary accompaniment to a chronic disease process and those who believe that MCS is primarily the symptomatic manifestation of a psychiatric disorder. The thread of this debate runs throughout the discussion of MCS. It continues despite recent evidence that many disorders and syndromes that are considered to be psychiatric (e.g., panic disorder and post-traumatic stress disorder) are accompanied by measurable changes in brain function as assessed by techniques such as functional magnetic resonance imaging and single photon emission computed tomography (Dager and Steen, 1992).

Although causal psychological mechanisms in MCS remain uncertain, the data suggest that psychological factors should be carefully evaluated in the diagnosis and treatment of patients who have MCS. The workgroup finds the need for carefully designed studies to evaluate both the primary and secondary psychological factors in MCS.

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Other Syndromes

Sick Building Syndrome

Although not discussed in detail in this report, the syndrome known as Sick Building Syndrome (SBS) has been linked to MCS as an initiating factor. Persons with SBS experience symptoms that include eye, nose, and throat irritation; headaches; cough; difficult breathing; fatigue; dizziness; and difficulty in concentrating. These symptoms are temporally related to being in a particular building. The cause of SBS is unknown, but it is often thought to result from poor building ventilation causing a buildup of vapors from sources that include building materials, furnishings, and office equipment. SBS has also been linked to contamination of indoor spaces or ventilation systems by biologic organisms. Occasionally, some persons with SBS report that they later develop MCS. One published study describes the clinical follow-up of 20 persons whose work-related illnesses were considered related to a "sick building" (Welch and Sokas, 1992). Over time, three of the 20 persons had ongoing symptoms consistent with Cullen's definition of MCS.


Several MCS patients have been reported with neurologic and/or cutaneous symptoms suggestive of porphyrin disorders (Ziem and McTamney, 1995). These patients reported symptoms such as "dark brown or red urine," skin sensitivity to sunlight exposure, and sharp abdominal pain. Porphyrin disturbances were reported in a substantial percentage of the patients. Others have pointed out that derangements of porphyria metabolism do not result in symptoms reported by MCS patients, and that laboratory evaluations of confirmed porphyria-related conditions generally do not resemble those seen in MCS patients (Hahn and Bonkovsky, 1997; Washington State, 1995, 1996b; Gots, 1996).

Other Conditions

Other conditions putatively linked to MCS include systemic lupus erythematosus, chronic fatigue syndrome, fibromyalgia, scleroderma, and multiple sclerosis (NRC, 1992c).

Buchwald and Garrity (1994) compared 30 adults with CFS, 30 with fibromyalgia, and 30 with MCS to evaluate the similarities between these three conditions. The majority of the persons in each group were female. The mean age (40.8–44.0 years) and mean educational level (14.7–14.9 years) of the three groups were similar. Approximately 80 percent of both the fibromyalgia and MCS groups met the major criteria of the Centers for Disease Control and Prevention's (CDC) CFS criteria (Holmes et al., 1988), and both groups also frequently reported the minor CFS symptom criteria. Persons with MCS most frequently reported adverse effects after exposure to pollution; perfume; and gas, paint, and solvent fumes. However, 53–67 percent of the CFS group and 47–67 percent of the fibromyalgia group also reported adverse effects with exposure to these substances. Persons in all three groups were infrequently employed full time (13–23 percent) and often were receiving disability (30–57 percent). The mean number of visits per person to medical providers during the preceding year was 22.1 for persons with CFS, 39.7 with fibromyalgia, and 23.3 with MCS. The investigators concluded that the data, though limited, suggest that these illnesses may be similar, if not identical, conditions. They noted that the diagnosis assigned to an individual with one of these conditions may depend more on the chief complaint and the medical specialty of physicians making the diagnosis than on the actual illness process.

Fiedler et al. (1996) compared 23 persons who had MCS, 13 who had chemical sensitivity (CS), 18 who had CFS, and 18 healthy controls. Individuals with MCS met the full criteria for MCS proposed by Cullen, including an initial identifiable environmental exposure. The individuals with CS met the same criteria for MCS with the exception of a clear onset. Psychiatric and neuropsychological evaluation demonstrated more similarities than differences between the CFS group and MCS and CS groups. In comparison with the control group, the CFS group reported twice as many substances, on average, caused symptoms. However, 30 percent of the CFS group reported that no substance causing illness, and 39 percent reported more than 20 substances. The investigators suggested that investigators may want to consider stratifying individuals with CFS by chemical sensitivities in future studies that evaluate differences between CFS and chemical sensitivities.

In 1994, a conceptual framework and guidelines were proposed for a comprehensive, systematic, and integrated approach to the evaluation, classification, and study of persons with CFS and other fatiguing illnesses (Fukuda et al., 1994). The guidelines specifically stated that MCS and other conditions, including fibromyalgia, that are defined primarily by symptoms that cannot be confirmed by diagnostic laboratory tests, do not exclude an individual from the diagnosis of CFS.

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Clinical Ecology Approach

Members of the American Academy of Environmental Medicine (AAEM) support the application of a comprehensive model of environmental medicine (see Section I). A number of definitions and descriptive terms have been developed from this model that are not well known or understood by other clinicians or scientists. The terms were developed in part because physicians practicing clinical ecology believe that these terms and descriptors better define their patients' conditions than do other terms. A basic understanding of these terms gives perspective to the clinical ecology approach to MCS and attendant theories of causation and mechanisms.

The following definitions are taken verbatim from An Overview of the Philosophy of the American Academy of Environmental Medicine (AAEM, 1992):

Total load is the sum total at any one time of all an individual's exposures to specific environmental stressors to which he is individually susceptible.

Adaptation is the process by which the body attempts to maintain homeostasis in the face of exposures to stressors.

Maladaptation is when one or more of the body's biologic mechanisms or systems has been overwhelmed or weakened for various reasons (either acquired and/or genetic), and is not able to maintain homeostasis in the face of the current total load of stressors. Symptoms of illness then occur.

Deadaptation allows the body's biologic mechanisms that deal with a particular substance to metabolize, compartmentalize, or excrete it and when this is accomplished, to then reset to a lower set point of nonadaptation, where an acute challenge may then result in an acute measurable reaction.

Bipolarity of response refers to the changing manifestations of an ongoing case of Environmentally Triggered Illness being the result of a dynamic continuum of alternating stimulatory and withdrawal states, rather than being a static block of symptoms over time. The phenomenon of bipolarity occurs in all three Stages of Adaptation and consists of a biphasic response: a stimulatory phase upon exposure to a stressor(s) and a withdrawal phase upon withdrawal of a stressor(s).

Spreading phenomenon—there are two types. One type refers to the acute or chronic spreading of susceptibility to previously tolerated substances. The second type refers to the acute or chronic spreading of susceptibility to new target organs. Both types of the spreading phenomenon generally occur while maladapting to a total body overload.

Switch phenomenon manifests clinically as the patient's symptoms switching back and forth over time from one target organ to another, either acutely or more slowly over time. The clinical presentation is further modified by the stage of adaptation that the patient is in at the time.

Individual susceptibility (biochemical individuality) If a group of patients are all susceptible to a particular stressor, each will have a unique individual response to that particular stressor. On the other hand, if a group of patients all share the same clinical symptom due to susceptibilities, each will have his own unique list of stressors that set off that symptom in his case.

Other descriptors used by clinical ecologists include incitant, which is a triggering or causative agent (one that induces an allergic or hypersensitive reaction), and environmental stressor, which is any substance or situation that has the potential capacity to destabilize homeostasis in a susceptible person (AAEM, 1992).

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Summary of Mechanisms

A review of the postulated mechanisms of MCS shows several theories of causation and a considerable body of literature, though not all literature meets current standards of independent peer review. However, definitive data that would confirm or refute hypothesized mechanisms for MCS are generally lacking and those available are confined to a few models of the condition. Because investigators have used different definitions of MCS and because MCS classification in studies is based on self-report, it is difficult to compare patient groups used in various studies to each other or to evaluate the application of theories to the patient groups. Many of the studies are based on an investigator's concept of an etiology for MCS, which may not be compatible with concepts held by others.

Papers written by clinicians and investigators on mechanisms of chemical sensitivity need to be based on sound science and to be capable of passing review for publication in mainstream biomedical journals. Only in this way will they receive review and comment by the entire medical and scientific communities and achieve wider critical review and discussion. Similarly, traditional medical journals need to be open to review and publication of rigorous scientific papers concerning the mechanisms of chemical sensitivity.

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