Idiopathic environmental intolerance is characterized by recurrent, nonspecific symptoms attributed to low-level exposure to chemically unrelated substances commonly occurring in the environment. Symptoms are numerous, often involving multiple organ systems, but physical findings are unremarkable. Diagnosis is by exclusion. Treatment is psychologic support and avoidance of perceived triggers, although triggers rarely can be defined.
No universally accepted definition exists, but idiopathic environmental intolerance is generally defined as the development of multiple symptoms attributed to exposure to any number of identifiable or unidentifiable chemical substances (inhaled, touched, or ingested) in the absence of clinically detectable organ dysfunction or related physical signs.
Reported triggers for idiopathic environmental intolerance include
Immunologic and nonimmunologic theories have been proposed. They are hampered by lack of a consistent dose response to proposed causative substances; ie, symptoms may not be replicated after exposure to high levels of a substance that previously, at much lower levels, seemed to provoke a reaction. Similarly, consistent objective evidence of systemic inflammation, cytokine excess, or immune system activation in relation to symptoms is lacking. Many physicians consider the etiology to be psychologic, probably a form of somatic symptom disorder (see Somatic Symptom Disorder). Others suggest that the syndrome is a type of panic attack (see Panic Attacks and Panic Disorder) or agoraphobia (see Somatic Symptom Disorder).
Idiopathic environmental intolerance occurs in 40% of people with chronic fatigue syndrome (see Chronic Fatigue Syndrome) and in 16% of people with fibromyalgia (see Fibromyalgia). Idiopathic environmental intolerance is more prevalent in women.
Although measurable biologic abnormalities (eg, decreased levels of B cells, elevated levels of IgE) are rare, some patients have such abnormalities. However, these abnormalities appear without a consistent pattern, their significance is uncertain, and testing for these abnormalities to establish an immunologic basis for the disorder should be discouraged.
Symptoms and Signs
Symptoms (eg, palpitations, chest pain, sweating, shortness of breath, fatigue, flushing, dizziness, nausea, choking, trembling, numbness, coughing, hoarseness, difficulty concentrating) are numerous and usually involve more than one organ system. Most patients present with a long list of suspected agents, self-identified or identified by a physician during previous testing. Such patients often go to great lengths to avoid these agents by changing residence and employment, avoiding foods containing “chemicals,” sometimes wearing masks in public, or avoiding public settings altogether. Physical examination is characteristically unremarkable.
Diagnosis initially involves exclusion of known disorders with similar manifestations:
Atopic disorders are excluded based on a typical clinical history, skin-prick testing, serum assays of specific IgE, or all 3. Consultation with an allergy specialist may be helpful. Building-related illnesses, including sick building syndrome, in which many people who spend time in the same building develop symptoms (see Specific BRIs), should be considered.
If symptoms and signs are not strongly suggestive of a connective tissue or autoimmune rheumatologic disorder (eg, joint, skin and/or mucous membrane manifestations), testing for a wide range of autoantibodies (eg, antinuclear antibodies [ANA], rheumatoid factor, extractable nuclear antigens [ENA]) should be avoided. In such cases, pretest probability is low and false-positive results are far more likely than true-positive results; a weakly positive ANA is present in about 20% of the population.
Despite an uncertain cause-and-effect relationship, treatment is sometimes aimed at avoiding the suspected precipitating agents, which may be difficult because many are ubiquitous. However, social isolation and costly and highly disruptive avoidance behaviors should be discouraged. A supportive relationship with a primary care physician who offers reassurance and protects patients from unnecessary tests and procedures is helpful.
Psychologic evaluation and intervention may help, but characteristically many patients resist this approach. However, the point of this approach is not to convince patients that the cause is psychologic but rather to help them cope with their symptoms and improve quality of life. Useful techniques include psychologic desensitization (often as part of cognitive-behavioral therapy) and graded exposure—see Treatment). Psychotropic drugs can be helpful if targeted toward coexisting psychiatric disorders (eg, major depression, panic disorder).
Last full review/revision May 2014 by Donald W. Black, MD
Content last modified May 2014