Idiopathic Environmental Intolerance is the name assigned to a condition of varying symptoms, typically involving several organ systems, that the patient believes are related to environmental exposures. This paper will argue that the condition does not exist, but is a cultural artefact, projected on psychiatric patients by unprofessional therapists.

The condition was first proposed by TG Randolf in the 1950s. In a series of books and articles, he described a new illness caused by the anthropogenic introduction of chemicals distinct from those in our evolutionary ancestry, which he believed could induce the assortment of symptoms observed among his patients, which had no apparent cause, and seemed to involve reactions to environmental substances. Randolf and others assigned various names to the syndrome: universal allergy, 20th Century disease, chemical hypersensitivity syndrome, total allergy syndrome, cerebral allergy, candidiasis hypersensitivity syndrome, and multiple chemical sensitivity (AAAI, 1986). Treatment focuses on the patient's environment, and the field of study and care is named clinical ecology.

Symptoms are not limited, but typically include: dizziness, lethargy, confusion, fatigue, irritability, poor concentration, migraine, bowel and respiratory problems. Patients entertain a narrative that implicates anthropogenic environmental contaminants as the single origin of the symptom cluster. Alleged triggers are also unlimited, but commonly include: clothing, furniture, construction materials, workplace solvents, food, water, detergents, and air properties.

The majority of toxicologists and physicians dispute the existence of this condition (AAAAI, 1999; AAAI, 1986; AMA, 1992), citing evidence of psychogenic disorder: the claim of injury by toxic elements does not precipitate many cases, no physical evidence exists to verify the organic nature of discomfort, symptoms resemble somatization (Leznoff, 1997), most have a history of overt psychiatric symptoms (Black, 1993; Salvaggio, 1994), there is a strong gender assymetry in favour of women, the patients are suspiciously diagnosed by a small network of clinical ecologists, and for most patients, identity revolves around diagnosis (Brodsky, 1983). Furthermore, the symptom cluster resembles hypothetical diagnoses previously proposed and withdrawn (Stewart, 1986). Consequently, organizational consensus statements assert that scientific support for this theory is lacking.

Nevertheless, patients continue to seek out and engage clinical ecologists. This is no doubt because conventional psychology lacks treatment modalities to relieve their discomfort, while clinical ecologists promote their treatments as promising (Brodsky, 1983). However, this practice by hypothesis is not successful by medical standards, and a proper treatment strategy remains forthcoming. Treatments proposed by clinical ecologists - such as sublingual desensitization or the avoidance of 'processed' foods - pivot on the organic etiology and the validity of the theories behind testing, both of which are questionable assumptions (Greico, 1982).

Delay in developing treatments results from the need to reject organic etiology as proposed by clinical ecologists, to divert those patients who may have organic or psychotic illnesses that resemble somatiforms, and finally to propose a psychogenic model and propose and compare the efficacy of alternative modalities.

Doubt was shed on the immunological hypothesis by a series of experiments wherein the patient was challenged, blinded, with an antigen demonstrated earlier to have induced reactions (Rea, 1989; Staudenmayer, 1993; Leznoff, 1997; Grieco, 1982; Stewart, 1986). Blinded exposures were no more likely to trigger symptoms than chance. However, debate ensued about the validity of these experiments. Criticisms included observing that not all patients could specify their triggers, some patients had shifting triggers, and that most triggers could not be effectively blinded, such as odours or tactile sensations (Lenzoff, 1997).

In addition, the central claim of immunological imbalances was thrown into question when the quantitative techniques so vital to substantiating it were pronounced dubious by immunological authorities. And finally, objective examination of the most common symptoms indicates many diagnoses take subjective exaggeration of symptom presentation indistinguishable from the general population at face value(Staudenmayer, 1993).

Despite these findings, most clinical continue to treat patients according to environmental toxin theory, dismissing criticisms as either ignorance or conspiracy. Current research in clinical toxicology does not question the objectivity of complaints (Miller, 2000). In addition, many naturopaths subscribe to the principles, and the theory is propagating outside the clinical environment.

A valuable finding of the investigations was that some patients genuinely demonstrated a sensitivity to a particular substance, such as TDI asthma (Gots et al, 1993; Gots, 1996; Brodsky, 1989; Salvaggio, 1994). These individuals can be diverted from psychiatric care. Additionally, development in assay tools improved the ability to distinguish between genuine pathogenic origins of Sick Building Syndrome, and the similar idiopathic group hysterias. In the former condition, propagation through the building is consistent with air flow, a pathogen is identified, and symptoms are consistent with the pathogen's nature. In the latter situation, none of these things are true (Terr, 1994; Montgomery, 1994).

Also, many mundane conditions had been overlooked by therapists: headaches from meningiomas, palpitations from myocardiopathy, fatigue from lyphomas, dizziness from middle ear infections, nausea from ulcers, abdominal pains from pancreatic tumours, and paralysis from spinal cord injuries (Gots, 1996).

Another was the observation that some patients presented ideation, such as considering food toxic because of a conspiracy to poison the subject, rather than simply due to its anthropogenic additives. This demonstrated that some patients were misdiagnosed psychotics, and ordinary diagnostic criteria could identify these individuals so they could receive appropriate treatment.

At this time, the profession has progressed to the final hurdle: a model of illness, and the developing of treatments. The name Multiple Chemical Sensitivity was deemed vernacular (Amundsen, 1996).Current debate involves the paradoxically contradictory nature of patient properties.The almost universal features of doctor-shopping (Brodsky, 1982; Stewart, 1987) and fear of health problems, make hypochondria a candidate; avoiding enclosures (claustrophobia) or outdoors (agorophobia), pathological fear of contacting toxins, and the influence of odour - which promotes strong conditioning - suggests a new phobia (Stewart, 1985; Salvaggio, 1994). But, studies find no elevated anxiety (Black, 1993).

The etiology shifted attention to somatiform disorder - also characterized by doctor-shopping, chronic symptoms, and a curious acceptance of the condition (AAAI, 1986). Clear-cut somatization disorder had been abundantly diagnosed (Stewart, 1985; Black, 1990), shifting symptoms recalled transference (Terr, in Gots, 1993), the gender demographics were 4:1 female as expected for somatiforms (Black, 1993; Stewart, 1987), and age tended to maturity, most patients were over 30, averaging about 52 (Bolla, 1996). But, overwhelming evidence of anxiety has emerged (Leznoff, 1997). Sodium lactate induces anxiety-like symptoms in the majority of one study's patients, demonstrating a biological predisposition particular to anxiety disorders (Binkley, 1997).

Histrionic personality disorder predominated in some clinics (Black, 1993), but was unseen in others. Many presented with classic features, becoming involved in the support groups and government lobbying for official recognition of their unique condition.

The perennial contradictory nature of symptoms should be sufficient proof that IEI does not represent a particular disorder. This paper asserts that IEI is an accidental reification of similarities in psychotic, anxiety, somatoform, and personality disorders, derived from instinctive mistrust of pollution. Iatrogenic introduction and perpetuation of this nomenclature systemically inspires the creation of new patients.

table 1 shows a proposed clustering of symptom sets within the IEI 'diagnosis': schizophrenia, phobias, somatization, and histrionic disorders, all bear striking superficial similarities when they avoid environmental toxins. Nevertheless, the apparent convergence is illusory, and the seperate etiologies dictate symptom manifestation, and these, in turn, demand particular treatments. The diagnostic criteria need not depart from DSM-IV, and special attention should be given to considerations of comorbidity. On the other hand, some treatment strategies should be adapted. In all cases, the therapist must emphasize that the symptoms are not in question, merely the explanation.

Those who demonstrate panic symptoms may respond to desensitization therapy, using the environment or chemical in question as the target of a phobia. SSRIs may assist (Stenn, 1998). The therapist should be mindful that traditionally the phobic would be able to recognize that a phobia, such as driving over bridges, is irrational for the reason that other people do these things every day. However, the IEI patient has a unique relationship with their target, in that they believe that it is specifically toxic to them. There is no external model who can demonstrate its neutral safety.

Somatization disorder has very low success at the best of times (Barsky, 1995), but IEI patients are very resistant to insight (Gots, 1996). Very few will accept psychogenic explanations. The dominant reason for this is because somatization suppresses conflicts, or resolves them in their favour. One patient reported that her life was "...like a vacation" (Brodsky, 1983).By becoming invalids, sexual, domestic, employment, and other antagonisms evaporate as they retire to a permanent state of convalescence. Nevertheless, most remain active, explaining that their triggers are associated with responsibilities they would coincidentally prefer to avoid, particularly social interactions. "It's very hard to socialize with people when you can't stand the soap they use" (Brodsky, 1983). Not surprisingly, many of the clinical ecologists and other practitioners diagnosing IEI claim to suffer from the condition (Terr, in Gots, 1993; Gothe, 1995). Comparisons with cults are exaggerated, but certainly there is a medical subculture and an iatrogenic explanation is tenable (Kahn, 1989).

Histrionic disorder also features resistance. IEI provides a platform on which the Histrionic patient can emphasize unique personality: many carry oxygen tanks or wear masks in public, require special work arrangements, wear protective suits, buy expensive and unnecessary elixers (see Appendix I). This subtype of IEI patients is probably overrepresented in the tireless lobbying and 'cause' pursuit that has strengthened populatity of environmental insensitivity, in the lay public, in medical literature (Green, 1985; Dudley, 1986), and in policymaking (Waddell, 1993; Tollefson, 1993; Gori, 1996; Gothe, 1995).

The therapeutic strategy is to relieve the symptoms of IEI without depriving the patient of the sick role (Staudenmayer, in Gots, 1993). Enable the patient to function in society, but not adopt the perception that they are well. This is a compromise intended to favour the patient's overall mental health.

Success does not follow from avoidance or other clinical ecologists' treatments: only 4% of patients improve after two years of treatment (Terr, in Gott, 1993), and a disturbing number get worse (Stewart, 1986; Stewart, 1987). Misdiagnosis appears to be worse than no treatment, and no only ventures perilously into litigious practice (Appendix I), but incurs greater financial cost on the individual (Brodsky, 1983), the sysem (Staudenmayer, 1996; Weaver, 1996), and most importantly, does not foster the long-term betterment of the patient (Stewart, 1986).

Since the diagnosis stems, in part, from popular beliefs about pollution and a systematic cultural prejudice against psychological illness (Gothe, 1995), it follows that harm reduction originates in a combined strategy of jettisonning the nomenclature in favour of existing DSM-IV or ICD-9 criteria (diverting patients to the conventional system), reducing the influx of sufferers who seek out these narratives (diverting patients self-diagnosis to the conventional system) by publicly demanding better research methods toward resolving the authenticity of the hypothesis (Stewart, 1986), and improving the appeal of the conventional therapies by adapting them to unconventional goals, such as the'functional, but uncured', fostering the subject's perception of empowerment and legitemacy as a psychological patient, while maintaining the convalescent identity.

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appendix I