The concept of multiple food or chemical sensitivities manifested by numerous symptoms in the absence of objective physical findings lacks a scientific foundation. There is no evidence that such patients suffer from an immunologic abnormality. The existence of such an illness is based on anecdotal reports with no verification using properly controlled blinded challenges. The diagnosis is made on the basis of the subjective history alone or in combination with provocation-neutralization testing, which has been shown to be unreliable. The treatment and theories underlying this presumed illness are not consistent with current immunologic knowledge and theory. Medical and psychiatric evaluations of these patients indicate instead that most may suffer from psychiatric illness that they cannot accept, preferring instead to interpret their symptoms as environmental sensitivities. Treatment by environmental chemical and food avoidance in combination with administration of neutralizing injections or sublingual drops is ineffective and likely to lead to harmful social isolation. In many cases, the diagnosis of IEI obscures a treatable psychiatric or physical disease.
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The American Academy of Allergy and Immunology issued a position statement as follows: “An objective evaluation of the diagnostic and therapeutic principles used to support the concept of clinical ecology indicates that it is an unproven and experimental methodology. It is time-consuming and places severe restrictions on the individual’s lifestyle. Individuals who are being treated in this manner should be fully informed of its experimental nature.”
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The American College of Physicians position statement concludes: “Review of the clinical ecology literature provides inadequate support for the beliefs and practices of clinical ecology. The existence of an environmental illness as presented in clinical ecology theory must be questioned because of the lack of a clinical definition. Diagnoses and treatments involve procedures of no proven efficacy.” The American College of Occupational Medicine has adopted the position on clinical ecology of the American College of Physicians.

Two studies up to now have reviewed the clinical and laboratory evidence for immunologic illness in patients with multiple food and chemical sensitivities. In 50 cases studied by Terr, levels of circulating immunoglobulins, complement components, and lymphocyte subsets fell mostly within the normal expected range and did not correlate with severity of reported illness or length of reported exposure to the foods or chemicals believed to cause the illness. None of the patients had clinical evidence of immunodeficiency or autoimmune disease, and the prevalence of allergic disease was similar to that found in the general population.

Sparks et al studied the 53 aircraft workers exposed to phenol-formaldehyde. Blood tests performed by a commercial laboratory reportedly showed abnormal numbers of TA-1 receptor-positive lymphocytes, various autoantibodies, and low-level antibodies to formaldehyde, trimellitic anhydrides, and isocyanates. Serum from 33 of these subjects were reexamined for the presence of formaldehyde antibodies by Sparks et al and were found to have test results no different from those of controls.

A review of the clinical ecology literature citing results of a variety of immunologic tests in patients with environmental illness fails to reveal a significant common pattern of abnormalities.

In recent years, results of several critical evaluations of patients claiming IEI have been published. Collectively these studies do not support a role for food and chemical sensitivities as a cause of the patient’s symptoms nor do they indicate immunologic dysfunction. Instead, they do provide evidence for a significant role for underlying psychiatric illness.
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Patients with IEI are predominantly female. Typically they had consulted numerous physicians for their symptoms before their diagnosis of IEI. In the absence of objective findings “case definition” is necessarily by self-report. Histories of the patients are extremely heterogeneous, with a majority reporting having multiple symptoms, although some are asymptomatic and a few have a clearly defined physical illness that had been undiagnosed and therefore not treated. There are no consistent physical findings or laboratory abnormalities. A series of 90 patients evaluated for work-related IEI showed that illness was attributed to an extremely heterogeneous group of environmental substances of different chemical compositions from an extremely diverse group of occupations. Their prior medical records revealed that two thirds of them had been treated for the same symptoms for many years before their occupational exposure, and three fourths had developed a new set of symptoms after provocation-neutralization testing. Furthermore, the most common alternative diagnoses made by nonclinical ecologists were somatoform illness, anxiety disorder, depression, hyperventilation, and iatrogenic disease.
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Several published series of psychiatric evaluations of IEI patients confirm the general impression that their perceived reactions to environmental chemicals and foods are best explained as a manifestation of underlying psychiatric disease. These reports are summarized in, which shows that many patients with environmental illness fit the DSM-IV criteria for several psychiatric illnesses. The predominance of women and the multisystemic polysomatic nature of the illness are suggestive of somatoform disorder, though not all patients meet the strict descriptive criteria. By including normal controls in their study, Black et al showed that the number of reported symptoms and the prevalence of mood disorder, anxiety disorder, and somatoform illness were all significantly higher in patients than in a normal population. Stewart et al pointed out that although somatoform illness is notoriously difficult to treat effectively the majority of patients in her study had psychotic, affective, or anxiety disorders all of which can be effectively treated with appropriate medications or psychotherapy or both. Unfortunately, most IEI patients are reluctant to accept a psychiatric diagnosis or treatment, opting instead for the extreme lifestyle changes that are recommended as treatment for that condition. Terr showed that clinical ecology treatment is almost always ineffective or counterproductive. Brodsky has studied the social consequences of extreme environmental chemical avoidance that leads to a lifestyle of social isolation centered around the illness.

The importance of preexisting psychiatric illness is made particularly clear by the study of Simon et al. They evaluated 37 aircraft workers who were exposed to phenol-formaldehyde and developed transient mucosal irritation that resolved on cessation of exposure. However, 13 of them reported chronic disabling symptoms provoked by common environmental agents diagnosed as IEI by a clinical ecologist. These patients had a significantly higher prevalence of preexisting psychiatric morbidity caused by anxiety, depression, somatization, and medically unexplained symptoms compared with the 24 with transient symptoms only.
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Patients who accept the concept of IEI as the explanation for their somatic symptoms are psychologically diverse, though limited or full-blown somatoform illness is the most common pattern. Other patients have been noted to display features of post-traumatic stress disorder, agoraphobia caused by conditioning, and panic disorder, and as an adult manifestation of childhood abuse. The phenomenon has also been called a “belief system” and “illness and disability as lifestyle.”

Treatment of environmental illness is accomplished according to primarily three modalities: a program of avoidance of environmental chemical exposure, special elimination diets, and neutralization therapy. Drugs are regarded as harmful synthetic chemicals that cause environmental illness. Nevertheless, patients are often instructed to take vitamin and mineral supplements, and some are treated with certain salts, such as sodium bicarbonate, to “neutralize” allergic reactions and with amino acids, intravenously administered gamma-globulin, or oxygen inhalation to relieve symptoms. Patients with a diagnosis of Candida hypersensitivity are usually treated with several drugs to eliminate Candida albicans.

The rationale for the treatment program is twofold: (1) to eliminate or reduce symptoms and (2) to “strengthen” the immune system. Avoidance of multiple environmental chemicals is universally recommended, often requiring a significant change in lifestyle. Many patients remodel their homes to create an “oasis” where they can feel “safe” from exposure to toxic chemicals. Some patients are advised to leave their homes, particularly if they are located in urban environments. Several isolated communities have been established in rural areas or trailer parks for patients with this illness. Many patients wear masks in public or even within their own homes.The elimination diet usually consists in avoidance of all food additives by the purchasing of foods in special health food stores. Patients are frequently prescribed a rotary diversified diet in which foods are rotated on a 4- to 5-day cycle.

Neutralization therapy, also called relieving therapy, is discussed in more detail later in this chapter.

There have been no prospective controlled clinical trials to evaluate the effectiveness of the combination of food and chemical avoidance with neutralization therapy. Finn et al attempted an unblinded evaluation of 21 patients who were treated by avoidance of foods and chemicals “when indicated” and by neutralizing injections for food sensitivity. The patients had a variety of illnesses that included asthma, eczema, irritable bowel, joint complaints, and psychologic problems. Eight patients given specific antigen neutralization reported improvement, but so did five patients taking benzyl alcohol injections used as a control. A retrospective review of 50 cases of environmental illness showed that after an average of 2 years of treatment only 4%improved, whereas 44% were unchanged and 52% worsened.

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The diagnosis of IEI is most often made by the combination of an extensive environmental history and a battery of provocation-neutralization tests. The patient’s self-report of symptoms occurring after presumed exposure to environmental odors and fumes or after ingestion of particular foods usually suffices to make the diagnosis. The provocation-neutralization test, described below, consists of exposing the patient to a particular test substance to elicit symptoms, followed by exposure at a lower or higher dose to cause disappearance of those symptoms. Testing is done without controls, and specific sensitivities are diagnosed by the appearance or disappearance of subjective symptoms.

Many clinical ecologists supplement the provocation-neutralization testing with various laboratory tests. These include quantitation of serum immunoglobulins and complement components; detection of circulating autoantibodies and immune complexes; quantitative counts of lymphocyte subsets; quantitative measurement of a variety of environmental chemicals in blood, urine, fat, and hair samples; and assays for levels of circulating hormones, amino acids, and mediators.

Data from the clinical ecology literature and from independent review of series of patients with IEI lend no support to the diagnostic usefulness of any of these tests. Levels of serum immunoglobulins and complement components; blood levels of total lymphocytes and various subsets; circulating hormones or other natural body constituents; and quantities of xenobiotics in various body fluids are not consistently abnormal.

The clinical ecology literature discusses a variety of theories and concepts to explain both the etiology and pathogenesis of environmental illness. Initially Randolphproposed a theory that failure of the human body to adapt to industrial synthetic chemicals produces a condition of hypersensitivity to these chemicals. This theory does not explain the mechanism of the hypersensitivity, and there has been no evidence up to now to support it.
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A variety of immunologic mechanisms has been proposed to explain IEI. In general, these theories are made under the presumption that environmental chemicals function as haptens to induce formation of IgG antibodies, IgE antibodies, or specifically sensitized T cells. However, the pattern of illness and the absence of any objective evidence of inflammation or organ dysfunction do not support immunologic hypersensitivity in IEI. Furthermore, there has been no evidence of a quantitative or qualitative abnormality of either specific antibodies or a cellular immune response to any of the numerous environmental agents that these patients identify as a cause of their illness. There is an autoimmune theory derived from an unconfirmed report of circulating immune complexes or autoantibodies in some patients with IEI. Disturbance of the normal intrinsic regulation of the immune response is another theory of disease causation, but there is no evidence to support this theory, nor is there evidence of abnormal immune function or immune deficiency.
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These theories subsume additional concepts that are unique to the field of clinical ecology: total body load, chemical overload, masked food sensitivity, and spreading phenomenon. They are employed to explain the lack of a consistent dose-response relationship between the perceived chemical exposure and the symptoms but are inconsistent with modern concepts of immunology. The concepts of total body load and chemical overload are made under the assumption that the immune system has a fixed capacity to handle a limited quantity of environmental antigen and that exceeding it provokes symptoms. Masked food sensitivity is a term used to explain the fact that sometimes a patient may react adversely to a food when it is eaten after several days of abstention, whereas frequent ingestion of the same food causes these symptoms to disappear. These concepts are sometimes referred to collectively as “adaptation-deadaptation,” but they have never been explained physiologically or even been documented as a valid observation. Spreading phenomenon is a concept that exposure to one environmental substance induces or predisposes to immune responses to other unrelated environmental substances and is used to explain periods of an increasing number of symptoms in the absence of environmental changes.
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Several nonimmunologic theories have been proposed. These include (1) deficiency of antioxidants induced by the generation of free radicals by environmental chemicals, drugs, and foods; (2) neurotoxicity caused by endogenous beta-endorphin “sensitization” induced by environmental stimuli, odor-induced “kindling” of olfactory-limbic neural pathways, immunologic-to-neurogenic inflammation “switching” mediated by neuropeptides; (3) end-organ dysesthesia involving the nasal mucosa, lung, the entire respiratory tree, or multiple organs; and (4) hereditary coproporphyria. None of these theories are supported by experimental or controlled clinical studies.

The most common complaints–fatigue, headache, nausea, malaise, pain, mucosal irritation, disorientation, and dizziness–are nonspecific. All these symptoms can occur in diseases with specified pathologic characteristics, but they also occur commonly in the absence of physical illness.

No gross or microscopic evidence of inflammation or other objective signs of a disorder have been associated with IEI.

The list of the specific items believed to cause this condition is virtually unlimited. It includes any naturally occurring food, including drinking water; artificial food additives of all types; almost any synthetic product; specific chemicals such as formaldehyde, phenol, ethanol, ammonia, “hydrocarbons,” and “petrochemicals”; and sources of environmental chemicals, particularly cleaning solvents, paints, smoke, gasoline, vehicle exhaust fumes, fumes from office machines, perfumes, synthetic clothing, pesticides, structural plastics, building construction materials, and new carpeting. In many cases, patients complain of difficulty in stores, shopping malls, and public buildings. Although the emphasis is on synthetic chemicals, causes of illness have also included natural gas, electromagnetic radiation, viruses, fungi, yeast, and wood dust. In certain cases, the causative chemical is an endogenous hormone, especially progesterone. Patients with the diagnosis of environmental illness almost always attribute their illness to many of these substances and usually to a combination of foods, environmental chemicals, and drugs.

The items listed here as “causes” are believed to act in a dual role, both in the induction of the disease and in provoking symptoms once disease occurs. A unique feature of environmental illness is the absence of a consistent dose-response relationship in provocation of symptoms. The length of exposure to environmental agents required to induce the disease has varied from seconds to years with no correlation of presumed dose and length of exposure to the severity of illness.

The diagnostic procedure most commonly used by clinical ecologists is provocation-neutralization, discussed later in this chapter. After provocation-neutralization testing, many of these patients develop a new list of “causes” corresponding to the items used in the test.

The concept that certain individuals suffer a specific illness caused by multiple food and chemical sensitivities is the basis of a medical practice known as “clinical ecology.” This concept evolved from the earlier theory of allergic toxemia caused by multiple food sensitivities, described above. In the early 1950s Randolph broadened the idea of allergic toxemia to include sensitivity to environmental chemicals, in addition to foods, as causative agents of this disease, which he called “environmental illness.” Later, hypersensitivity to microorganisms, especially Candida albicans, was added to the list of causes.
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The term “environmental illness” was used for many years, along with other names such as environmentally induced disease, chemical hypersensitivity syndrome, multiple chemical sensitivities, cerebral allergy, chemically induced immune dysregulation, twentieth century disease, total allergy syndrome, ecologic illness, and food and chemical sensitivities. In recent years, “multiple chemical sensitivities” has been the preferred term.

Cullen introduced the term “multiple chemical sensitivities” to apply to a subgroup of such patients who have attributed their illness to their workplace, using the following definition:
An acquired disorder characterized by recurrent symptoms, referable to
multiple organ systems, occurring in response to demonstrable exposure to
many chemically unrelated compounds at doses far below those established
in the general population to cause harmful effects. No single widely
accepted test of physiologic function can be shown to correlate with
symptoms.

In February 2006, a workshop organized by the International Programme on Chemical Safety of the World health Organization recommended a new name, “idiopathic environmental intolerances,” because the term multiple chemical sensitivities “makes an unsupported judgment on causation” (i.e., environmental chemicals), does not refer to “a clinically defined disease,” and is not based on “accepted theories of underlying mechanisms nor validated clinical criteria for diagnosis.” Furthermore, the “relationship between exposures and symptoms is unproven.” 53 For these reasons, the term “idiopathic environmental intolerances” (IEI) is to be used here.
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IEI is described by clinical ecologists as a condition of multiple symptoms involving numerous areas and systems of the body without accompanying abnormal physical findings or laboratory test results. Many complaints are nonspecific. Additionally, certain defined illnesses such as rheumatoid arthritis, multiple sclerosis, and inflammatory bowel disease, as well as defined psychiatric disorders, have been attributed to multiple food and chemical sensitivities. The methods used for diagnosing and treating multiple food and chemical sensitivities encompass many of the unproved and inappropriate procedures described in more detail later in this chapter. The clinical findings and theories of IEI and the phenomenon of the clinical ecology movement have been critically scrutinized in recent years.
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