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Multiple Chemical Sensitivities

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Introduction

Since the 1980s, a new clinical syndrome has been described in occupational and environmental health practice characterized by the occurrence of diverse symptoms after exposure to low levels of artificial chemicals, although as yet it lacks a widely accepted definition. The disorder may develop in individuals who have experienced a single episode, or recurring episodes of a chemical injury such as solvent or pesticide poisoning. Subsequently, many types of environmental contaminant in air, food or water may elicit a wide range of symptoms at doses below those which produce toxic reactions in others.

Although there may not be measurable impairment of specific organs, the complaints are associated with dysfunction and disability. Although idiosyncratic reactions to chemicals are probably not a new phenomenon, it is believed that multiple chemical sensitivities (MCSs), as the syndrome is now most frequently called, is being brought by patients to the attention of medical practitioners far more commonly than in the past. This syndrome is prevalent enough to have generated substantial public controversy as to who should treat patients suffering with the disorder and who should pay for the treatment, but research has yet to elucidate many scientific issues relevant to the problem, such as its cause, pathogenesis, treatment and prevention. Despite this, MCS clearly does occur and causes significant morbidity in the workforce and general population. It is the purpose of this article to elucidate what is known about it at this time in the hope of enhancing its recognition and management in the face of uncertainty.

Definition and Diagnosis

Although there is no general consensus on a definition for MCS, certain features allow it to be differentiated from other well-characterized entities. These include the following:

  • Symptoms typically occur after a definitely characterizable occupational or environmental incident, such as an inhalation of noxious gases or vapours or other toxic exposure. This “initiating” event may be a single episode, such as an exposure to a pesticide spray, or a recurrent one, such as frequent solvent overexposure. Often the effects of the apparently precipitating event, or events, are mild and may merge without clear demarcation into the syndrome which follows.
  • Acute symptoms similar to those of the preceding exposure begin to occur after re-exposures to lower levels of various materials, such as petroleum derivatives, perfumes and other common work and household products.
  • Symptoms are referrable to multiple organ systems. Central nervous system complaints, such as fatigue, confusion and headache, occur in almost every case. Upper and lower respiratory, cardiac, dermal, gastrointestinal and musculoskeletal symptoms are common.
  • It is generally the case that very diverse agents may elicit the symptoms at levels of exposure orders of magnitude below accepted TLVs or guidelines.
  • Complaints of chronic symptomatology, such as fatigue, cognitive difficulties, gastrointestinal and musculoskeletal disturbances are common. Such persistent symptoms may predominate over reactions to chemicals in some cases.
  • Objective impairment of the organs which would explain the pattern or intensity of complaints is typically absent. Patients examined during acute reactions may hyperventilate or demonstrate other manifestations of excess sympathetic nervous system activity.
  • No better established diagnosis easily explains the range of responses or symptoms.

 

While not every patient precisely meets the criteria, each point should be considered in the diagnosis of MCS. Each serves to rule out other clinical disorders which MCS may resemble, such as somatization disorder, sensitization to environmental antigens (as with occupational asthma), late sequelae of organ system damage (e.g., reactive airways dysfunction syndrome after a toxic inhalation) or a systemic disease (e.g., cancer). On the other hand, MCS is not a diagnosis of exclusion and exhaustive testing is not required in most cases. While many variations occur, MCS is said to have a recognizable character which facilitates diagnosis as much or more than the specific criteria themselves.

In practice, diagnostic problems with MCS occur in two situations. The first is with a patient early in the course of the condition in whom it is often difficult to distinguish MCS from the more proximate occupational or environmental health problem which precedes it. For example, patients who have experienced symptomatic reactions to pesticide spraying indoors may find that their reactions are persisting, even when they avoid direct contact with the materials or spraying activities. In this situation a clinician might assume that significant exposures are still occurring and direct unwarranted effort to altering the environment further, which generally does not relieve the recurrent symptoms. This is especially troublesome in an office setting where MCS may develop as a complication of sick building syndrome. Whereas most office workers will improve after steps are taken to improve air quality, the patient who has acquired MCS continues to experience symptoms, despite the lower exposures involved. Efforts to improve the air quality further typically frustrate patient and employer.

Later in the course of MCS, diagnostic difficulty occurs because of the chronic aspects of the illness. After many months, the MCS patient is often depressed and anxious, as are other medical patients with new chronic diseases. This may lead to an exaggeration of psychiatric manifestations, which may predominate over chemically stimulated symptoms. Without diminishing the importance of recognizing and treating these complications of MCS, nor even the possibility that MCS itself is psychological in origin (see below), the underlying MCS must be recognized in order to develop an effective mode of management which is acceptable to the patient.

Pathogenesis

The pathogenic sequence which leads in certain people from a self-limited episode or episodes of an environmental exposure to the development of MCS is not known. There are several current theories. Clinical ecologists and their adherents have published extensively to the effect that MCS represents immune dysfunction caused by accumulation in the body of exogenous chemicals (Bell 1982; Levin and Byers 1987). At least one controlled study did not confirm immune abnormalities (Simon, Daniel and Stockbridge 1993). Susceptibility factors under this hypothesis may include nutritional deficiencies (e.g., lack of vitamins or antioxidants) or the presence of subclinical infections such as candidiasis. In this theory, the “initiating” illness is important because of its contribution to lifelong chemical overload.

Less well developed, but still very biologically oriented, are the views that MCS represents unusual biological sequelae of chemical injury. As such, the disorder may represent a new form of neurotoxicity due to solvents or pesticides, injury to the respiratory mucosae after an acute inhalational episode or similar phenomena. In this view, MCS is seen as a final common pathway of different primary disease mechanisms (Cullen 1994; Bascom 1992).

A more recent biological perspective has focused on the relationship between the mucosae of the upper respiratory tract and the limbic system, especially with respect to the linkage in the nose (Miller 1992). Under this perspective, relatively small stimulants to the nasal epithelium could produce an amplified limbic response, explaining the dramatic, and often stereotypic, responses to low-dose exposures. This theory also may explain the prominent role of highly odoriferous materials, such as perfumes, in triggering responses in many patients.

Conversely, however, many experienced investigators and clinicians have invoked psychological mechanisms to explain MCS, linking it to other somatoform disorders (Brodsky 1983; Black, Ruth and Goldstein 1990). Variations include the theory that MCS is a variant of post-traumatic stress disorder (Schottenfeld and Cullen 1985) or a conditioned response to an initial toxic experience (Bolle-Wilson, Wilson and Blecker 1988). One group has hypothesized MCS as a late-life response to early childhood traumas such as sexual abuse (Selner and Strudenmayer 1992). In each of these theories, the precipitating illness plays a more symbolic than biological role in the pathogenesis of MCS. Host factors are seen as very important, especially the predisposition to somaticize psychological distress.

Although there is much published literature on the subject, few clinical or experimental studies have appeared to support strongly any of these views. Investigators have not generally defined their study populations nor compared them with appropriately matched groups of control subjects. Observers have not been blinded to subject status or research hypotheses. As a result, most available data are effectively descriptive. Furthermore, the legitimate debate over the aetiology of MCS has been distorted by dogma. Since major economic decisions (e.g., patient benefit entitlements and physician reimbursement acceptance) may hinge upon the way in which cases are viewed, many physicians have very strong opinions about the illness, which limit the scientific value of their observations. Caring for MCS patients requires a recognition of the fact that these theories are often well known to patients, who may also have very strong views on the matter.

Epidemiology

Detailed knowledge of the epidemiology of MCS is not available. Estimates of its prevalence in the US population (from where most reports continue to come) range as high as several percentage points, but the scientific basis for these is obscure, and other evidence exists to suggest that MCS in its clinically apparent form is rare (Cullen, Pace and Redlich 1992). Most available data derive from case series by practitioners who treat MCS patients. These shortcomings notwithstanding, some general observations can be made. Although patients of virtually all ages have been described, MCS occurs most commonly among mid-life subjects. Workers in jobs of higher socio-economic status seem disproportionately affected, while the economically disadvantaged and non-White population seems underrepresented; this may be an artefact of differential access or of clinician bias. Women are more frequently affected than men. Epidemiological evidence strongly implicates some host idiosyncrasy as a risk factor, since mass outbreaks have been uncommon and only a small fraction of victims of chemical accidents or overexposures appear to develop MCS as a sequela (Welch and Sokas 1992; Simon 1992). Perhaps surprising in this regard is the fact that common atopic allergic disorders do not appear to be a strong risk factor for MCS among most groups.

Several groups of chemicals have been implicated in the majority of initiating episodes, specifically organic solvents, pesticides and respiratory irritants. This may be a function of the widespread usage of these materials in the workplace. The other commonplace setting in which many cases occur is in the sick building syndrome, some patients evolving from typical SBS-type complaints into MCS. Although the two illnesses have much in common, their epidemiological features should distinguish them. Sick building syndrome typically affects most individuals sharing a common environment, who improve in response to environmental remediation; MCS occurs sporadically and does not respond predictably to modifications of the office environment.

Finally, there is great interest in whether MCS is a new disorder or a new presentation or perception of an old one. Views are divided according to the proposed pathogenesis of MCS. Those favouring a biological role for environmental agents, including the clinical ecologists, postulate that MCS is a twentieth century disease with rising incidence related to increased chemical usage (Ashford and Miller 1991). Those who support the role of psychological mechanisms see MCS as an old somatoform illness with a new societal metaphor (Brodsky 1983; Shorter 1992). According to this view, the social perception of chemicals as agents of harm has resulted in the evolution of new symbolic content to the historic problem of psychosomatic disease.

Natural History

MCS has not yet been studied sufficiently to define its course or outcome. Reports of large numbers of patients have provided some clues. First, the general pattern of illness appears to be one of early progression as the process of generalization develops, followed by less predictable periods of incremental improvements and exacerbations. While these cycles may be perceived by the patient to be due to environmental factors or treatment, no scientific evidence for such relationships has been established.

Two important inferences follow. First, there is little evidence to suggest that MCS is progressive. Patients do not deteriorate from year to year in any measurable physical way, nor have complications such as infections or organ system failure resulted in the absence of intercurrent illness. There is no evidence that MCS is potentially lethal, despite the perceptions of the patients. While this may be the basis of a hopeful prognosis and reassurance, it has been equally clear from clinical descriptions that complete remissions are rare. While significant improvement occurs, this is generally based on enhanced patient function and sense of well-being. The underlying tendency to react to chemical exposures tends to persist, although symptoms may become sufficiently bearable to allow the victim to return to a normal lifestyle.

Clinical Management

Very little is known about the treatment of MCS. Many traditional and non-traditional methods have been tried, though none has been subjected to the usual scientific standards to confirm their efficacy. As with other conditions, approaches to treatment have paralleled theories of pathogenesis. Clinical ecologists and others, who believe that MCS is caused by immune dysfunction due to high burdens of exogenous chemicals, have focused attention on avoidance of artificial chemicals. This view has been accompanied by use of diagnostic strategies to determine “specific” sensitivities by various invalidated tests to “desensitize” patients. Coupled with this have been strategies to enhance underlying immunity with dietary supplements, such as vitamins and antioxidants, and efforts to eradicate yeasts or other commensal organisms. A most radical approach involves efforts to eliminate toxins from the body by chelation or accelerated turnover of fat where lipid-soluble pesticides, solvents and other organic chemicals are stored.

Those inclined to a psychological view of MCS have tried appropriately alternative approaches. Supportive individual or group therapies and more classic behavioural modification techniques have been described, though the efficacy of these approaches remains conjectural. Most observers have been struck by the intolerance of the patients to pharmacological agents typically employed for affective and anxiety disorders, an impression supported by a small placebo-controlled double-blind trial with fluvoxamine that was conducted by the author and aborted due to side effects in five of the first eight enrolees.

The limitations of present knowledge notwithstanding, certain treatment principles can be enunciated.

First, to the extent possible, the search for a specific “cause” of MCS in the individual case should be minimized—it is fruitless and counterproductive. Many patients have had considerable medical evaluation by the time MCS is considered and equate testing with evidence of pathology and the potential for a specific cure. Whatever the theoretical beliefs of the clinician, it is vital that the existing knowledge and uncertainty about MCS be explained to the patient, including specifically that its cause is unknown. The patient should be reassured that consideration of psychological issues does not make the illness less real, less serious or less worthy of treatment. Patients can also be reassured that MCS is not likely to be progressive or fatal, and they should be made to understand that total cures are not likely with present modalities.

Uncertainty about pathogenesis aside, it is most often necessary to remove the patient from components of their work environment which trigger symptoms. Although radical avoidance is of course counterproductive to the goal of enhancing the worker’s functioning, regular and severe symptomatic reactions should be controlled as far as possible as the basis for a strong therapeutic relationship with the patient. Often this requires a job change. Workers’ compensation may be available; even in the absence of detailed understanding of disease pathogenesis, MCS may correctly be characterized as a complication of a work exposure which is more readily identified (Cullen 1994).

The goal of all subsequent therapy is improvement of function. Psychological problems, such as adjustment difficulties, anxiety and depression should be treated, as should coexistent problems like typical atopic allergies. Since MCS patients do not tolerate chemicals in general, non-pharmacological approaches may be necessary. Most patients need direction, counselling and reassurance to adjust to an illness without an established treatment (Lewis 1987). To the extent possible, patients should be encouraged to expand their activities and should be discouraged from passivity and dependence, which are common responses to the disorder.

Prevention and Control

Obviously, primary prevention strategies cannot be developed given present knowledge of the pathogenesis of the disorder or of its predisposing host risk factors. On the other hand, reduction of opportunities in the workplace for the uncontrolled acute exposures which precipitate MCS in some hosts, such as those involving respiratory irritants, solvents and pesticides, will likely reduce the occurrence of MCS. Proactive measures to improve the air quality of poorly ventilated offices would also probably help.

Secondary prevention would appear to offer a greater opportunity for control, although no specific interventions have been studied. Since psychological factors may play a role in victims of occupational overexposures, careful and early management of exposed persons is advisable even when the prognosis from the point of view of the exposure itself is good. Patients seen in clinics or emergency rooms immediately after acute exposures should be assessed for their reactions to the events and should probably receive very close follow-up where undue concerns of long-term effects or persistent symptoms are noted. Obviously, efforts should be made for such patients to ensure that preventable reoccurrences do not come about, since this kind of exposure may be an important risk factor for MCS regardless of the causal mechanism.

 

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More in this category: « Sick Building Syndrome

Contents

Preface
Part I. The Body
Blood
Cancer
Cardiovascular System
Digestive System
Mental Health
Musculoskeletal System
Nervous System
Renal-Urinary System
Reproductive System
Respiratory System
Sensory Systems
Skin Diseases
Systematic Conditions
Resources
Part II. Health Care
Part III. Management & Policy
Part IV. Tools and Approaches
Part V. Psychosocial and Organizational Factors
Part VI. General Hazards
Part VII. The Environment
Part VIII. Accidents and Safety Management
Part IX. Chemicals
Part X. Industries Based on Biological Resources
Part XI. Industries Based on Natural Resources
Part XII. Chemical Industries
Part XIII. Manufacturing Industries
Part XIV. Textile and Apparel Industries
Part XV. Transport Industries
Part XVI. Construction
Part XVII. Services and Trade
Part XVIII. Guides

Systemic Conditions Additional Resources

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Systemic Conditions References

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Anon. 1990. Environmental controls and lung disease. (Erratum in Am Rev Respir Dis 143(3):688, 1991 Am Rev Respir Dis 142:915-939.

Ashford, NA and CS Miller. 1991. Chemical Exposures: Low Levels and High Stakes. New York: Van Nostrand Reinhold.
Bascom, R. 1992. Multiple chemical sensitivity: A respiratory disorder? Toxicol Ind Health 8:221-228.

Bell, I. 1982. Clinical Ecology. Colinas, Calif.: Common Knowledge Press.

Black, DW, A Ruth, and RB Goldstein. 1990. Environmental illness: A controlled study of 26 subjects with 20th century disease. J Am Med Assoc 264:3166-3170.

Bolle-Wilson, K, RJ Wilson, and ML Bleecker. 1988. Conditioning of physical symptoms after neurotoxic exposure. J Occup Med 30:684-686.

Brodsky, CM. 1983. Psychological factors contributing to somatoform diseases attributed to the workplace. The case of intoxication. J Occup Med 25:459-464.

Brown, SK, MR Sim, MJ Abramson, and CN Gray. 1994. Concentrations of VOC in indoor air. Indoor Air 2:123-134.

Buchwald, D and D Garrity. 1994. Comparison of patients with chronic fatigue syndrome, fibromyalgia, and multiple chemical sensitivities. Arch Int Med 154:2049-2053.

Cullen, MR. 1987. The worker with multiple chemical sensitivities: An overview. In Workers with Multiple Chemical Sensitivities, edited by M Cullen. Philadelphia: Hanley & Belfus.

—. 1994. Multiple chemical sensitivities: Is there evidence of extreme vulnerability of the brain to environmental chemicals? In The Vulnerable Brain and Environmental Risks, Vol. 3, edited by RL Isaacson and KIF Jensen. New York: Plenum.

Cullen, MR, PE Pace, and CA Redlich. 1992. The experience of the Yale Occupational and Environmental Medicine Clinics with MCS, 1986-1989. Toxicol Ind Health 8:15-19.

Fiedler, NL, H Kipen, J De Luca, K Kelly-McNeil, and B Natelson. 1996. A controlled comparison of multiple chemical sensitivities and chronic fatigue syndrome. Psychosom Med 58:38-49.

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Kipen, HM, K Hallman, N Kelly-McNeil, and N Fiedler. 1995. Measuring chemical sensitivity prevalence. Am J Public Health 85(4):574-577.

Levin, AS and VS Byers. 1987. Environmental illness: A disorder of immune regulation. State Art Rev Occup Med 2:669-682.

Lewis, BM. 1987. Workers with multiple chemical sensitivities: Psychosocial interventions. State Art Rev Occup Med 2:791-800.

Mendell, MJ. 1993. Non-specific symptoms in office workers: A review and summary of the literature. Indoor Air 4:227-236.

Middaugh, DA, SM Pinney, and DH Linz. 1992. Sick building syndrome: Medical evaluation of two work forces. J Occup Med 34:1197-1204.

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Shorter, E. 1992. From Paralysis to Fatigue. New York: The Free Press.

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