Coverage Policy Manual
Policy #: 1997035
Category: Alternative Medicine
Initiated: January 1993
Last Review: June 2022
  Chemical Ecology (Environmental Illness, Multiple Chemical Sensitivities, Environmental Hypersensitivity Disorder, Total Allergy Syndrome)

Description: Clinical ecology involves the diagnosis and treatment of environmental illness.  Environmental illness is defined as multiple complex allergies or toxicities alleged to cause symptomatic involvement of the gastrointestinal, musculoskeletal, respiratory, or central nervous system.  These symptoms result from continued exposure to atmospheric contamination or exposure to common foods that may have been treated with pesticides and herbicides.  The major objective of the treatment program is to help patients avoid as many potential environmental allergens, such as formaldehyde or intolerable foods that may have been treated with herbicides and pesticides, as possible.

In 1999 The American Academy of Allergy, Asthma and Immunology updated their original 1986 position statement on clinical ecology with the following: "IEI [idiopathic environmental illness]- also called environmental illness and multiple chemical sensitivities - has been postulated to be a disease unique to modern industrial society in which certain persons are said to acquire exquisite sensitivity to numerous chemically unrelated environmental substances.  The patient experiences wide-ranging symptoms, but evidence of pathology or physiologic dysfunction in such patients has been lacking in studies to date.  Because of the subjective nature or the illness, an objective case definition is not possible.  Allergic, immunotoxic, neurotoxic, cytotoxic, physiologic, sociologic, and iatrogenic theories have been postulated for both etiology and production of symptoms, but there is an absence of scientific evidence to establish any of these mechanism definitive.  Most studies to date, however, have found an excess of current and past psychopathology in patients with this diagnosis.  The relationship of these findings to the patient's symptoms is also not apparent.  Rigorously controlled studies to verify the patient's reported subjective sensitivity to specific environmental chemical have yet to be done.  Moreover, there is not evidence that these patients have any immunologic or neurologic abnormalities.  In addition, no form of therapy has yet been shown to alter the patient's illness in a favorable way.  A causal connection between environmental chemicals, foods, and/or drugs and the patient's symptoms continues to be speculative and cannot be based on the results of currently published scientific studies."

Policy/
Coverage:
Does Not Meet Primary Coverage Criteria Or Is Investigational For Contracts Without Primary Coverage Criteria
 
Treatment modalities, nutritional assessments and laboratory tests related to Multiple Chemical Sensitivities, Environmental Illness, Environmental Hypersensitivity Disorder, Total Allergy Syndrome, or Clinical Ecology do not meet  member benefit certificate primary coverage criteria that there be scientific evidence of effectiveness in improving health outcomes.
 
For contracts without primary coverage criteria, treatment modalities, nutritional assessments and laboratory tests related to Multiple Chemical Sensitivities, Environmental Illness, Environmental Hypersensitivity Disorder, Total Allergy Syndrome, or Clinical Ecology are considered investigational.  Investigational services are contract exclusions in most member benefit certificates of coverage.

Rationale:
2002 Update
The clinical entity of idiopathic environmental illness has been controversial for decades, in part due to a set of reproducible diagnostic criteria. Absent a clear definition of the disorder, basic science research into the etiology of the disorder, appropriate laboratory tests, and identifications of effective treatment are obviously problematic. A variety of organizations have presented position papers on idiopathic environmental illness, previously referred to as multiple chemical sensitivity or clinical ecology. Most recently, in 1999 the American Academy of Allergy, Asthma and Immunology updated their original 1986 position statement on clinical ecology.  This statement offered the following summary:
 
“IEI [idiopathic environmental illness]– also called environmental illness and multiple chemical sensitivities – has been postulated to be a disease unique to modern industrial society in which certain persons are said to acquire exquisite sensitivity to numerous chemically unrelated environmental substances. The patient experiences wide-ranging symptoms, but evidence of pathology or physiologic dysfunction in such patients has been lacking in studies to date. Because of the subjective nature of the illness, an objective case definition is not possible. Allergic, immunotoxic, neurotoxic, cytotoxic, psychologic, sociologic, and iatrogenic theories have been postulated for both etiology and production of symptoms, but there is an absence of scientific evidence to establish any of these mechanisms as definitive. Most studies to date, however, have found an excess of current and past psychopathology in patients with this diagnosis. The relationship of these findings to the patient’s symptoms is also not apparent. Rigorously controlled studies to verify the patient’s reported subjective sensitivity to specific environmental chemical have yet to be done. Moreover, there is no evidence that these patients have any immunologic or neurologic abnormalities. In addition, no form of therapy has yet been shown to alter the patient’s illness in a favorable way. A causal connection between environmental chemicals, foods, and/or drugs and the patient’s symptoms continues to be speculative and cannot be based on the results of currently published scientific studies.”
 
In 1999, the American College of Occupational and Environmental Medicine also published a position statement that concluded, in part:
 
“Although specific diagnostic test and treatment have not yet been demonstrated to be helpful, a generalized clinical approach useful in the management of other nonspecific medical syndromes can be adopted pending further scientific findings. This approach emphasizes
    • establishing a therapeutic alliance with a goal toward functional restoration;
    • performing a medical evaluation appropriate to the presenting complaints and physical findings;
    • avoiding ineffective, costly, and potentially hazardous, unproven diagnostic tests or remedies that may increase a patient’s distress or disease;
    • treating all diagnosable medical and psychologic problems;
    • individualizing medical and behavioral coping strategies useful in managing symptoms; and
    • educating the patients about the current sate of knowledge about MCS [multiple chemical sensitivity].”
 
In 1989, the American College of Physicians published a position paper on clinical ecology that recommended the following:
“The controversial nature of clinical ecology within the medical profession today requires that acceptance or rejection of its theories and practice be based on standards of evidence as rigorous as those currently being applied in other areas of medicine. Clinical ecologists who wish to carry out definitive study of provocation-neutralization testing and neutralizing therapy should established a precise definition of the condition to be diagnosed and treated, and they should document that study subjects fulfill these criteria. Each study should include control subjects whose symptoms and vital statistics match those of the patients as closely as possible.”
 
A literature search based on the MEDLINE database, performed for the period of 1999 (i.e., the date of position papers from AAAAI and ACOEM) to July 2002, did not identify any articles that would address the research limitations of the above policy statements. The published literature suggests ongoing controversy regarding the etiology of the condition, appropriate diagnostic criteria, and treatment strategies.
 
2005-2006 Update
A literature search of the MEDLINE database was performed for the period of 2003 through March 2006. No published studies were identified that would prompt reconsideration of the policy statement.
Since 1993, publications have described a relationship between deregulation of the 2,5A RNase L antiviral pathway and chronic fatigue syndrome. Deregulation suggests a suppressed ability to battle antigens and possibly results from a prolonged exposure to viral antigens. Recent studies have found a high ratio of low molecular weight, 37- to 83-kilodalton (37/83) RNase L isoforms on peripheral blood mononuclear cells might be used for the diagnosis of chronic fatigue syndrome.  At a clinical cutoff ratio of 0.4, sensitivities have been reported between 76% and 91% and specificities between 33.3% and 71%.  However, high variability and poor reproducibility in testing the 37/83 RNase L ratio have been reported along with finding a weak correlation between 37/83 RNase L ratios and the Multidimensional Fatigue Inventory score in patients with chronic fatigue syndrome.  Therefore, further studies are needed in larger populations to confirm these observations and correlations for use of the 37/83 RNase L ratio for the diagnosis of chronic fatigue syndrome, and the policy statement is unchanged.
 
2007–2008 Update
A literature search was conducted using the MEDLINE database in December 2007. No published studies were identified that would prompt reconsideration of the policy statement. Das-Munshi presented a systematic review of provocation studies in individuals with multiple chemical sensitivities (MCS) (Das Munshi, 2006).  After a review of 37 studies, including 784 persons reporting MCS, the authors concluded that persons with MCS react to chemical challenges but that responses occur when they can discern differences between active and sham substances, suggesting that the mechanism is not specific to the chemical itself. Another review studied behavioral and social factors as a potential cause of MCS.   While the authors note that behavioral or psychological causes may contribute to MCS, there is a paucity of treatment trials. In particular, treatment trials examining psychological approaches are needed.
 
2009 Update
The policy was updated with a literature search using MEDLINE through November 2008. One publication involving only 12 patients with well-characterized idiopathic environmental intolerance reported results of neuropsychological testing and PET scans (Bornschein, 2007).  The study noted no consistent pathological cognitive performance, and no functional imaging pattern was found. The authors concluded that it appears premature to claim specific neuropsychological or neuroimaging findings characteristic of idiopathic environmental intolerance and that therefore cerebral F-18 FDG PET should not be used to corroborate or rule out suspected idiopathic environmental intolerance. In reports from Europe, Bailer, Witthoft, and Rift noted that findings of trait anxiety, somatic attribution, and absorption (predisposition to get deeply immersed in sensory or mystical experiences) were related to the presence of idiopathic environmental intolerance.  No additional clinical studies relevant to this policy were identified in the literature search; the policy statements are unchanged.
 
2010 Update
Since the last update, one relevant, randomized, controlled trial was identified.  Bornschein and colleagues published the findings of a double-blind placebo-controlled provocation study, conducted in Germany, that included 20 patients with multiple chemical sensitivity and 17 healthy controls matched for age and gender (Bornschein, 2008). Patients with MCS met several sets of diagnostic criteria developed in the 1990s including criteria for Idiopathic Environmental Intolerances defined by the International Program for Chemical Safety. Specific eligibility criteria included reporting symptoms that usually arise and recede within a time span of 10 minutes after the beginning of exposure and MCS symptoms that can be provoked by organic solvents. Provocations took place in a “climate chamber” (room for climatological and chemical provocations). Participants underwent 6 consecutive 15-minute sessions, each followed by a 15-minute break. Three sessions were exposures to solvents and the other 3 were exposure to placebo (clean air), in random order; patients and staff were blinded. The solvents were a mixture of 6 hydrocarbons found in common household solvents; to avoid the need for olfactory masking, room air concentrations were set below a detectable odor threshold. Only one participant failed to complete the provocation sessions. A positive reaction to exposure was defined as 1) the individual believed they were exposed to an active agent; 2) there was an objective sign of a reaction, e.g., rash, increase in heart rate; or 3) symptom severity rose to 3 or 4 (on 4-point scale). Fifty percent of patients with MCS and 53% of matched controls showed a positive reaction in all 6 exposure sections. Eighty-two percent of controls and 50% of patients had 3 correct reactions. More patients, however, than controls (30% versus 12%) reacted correctly more than 3 times. Considering only the subjective perception of exposure, 40% of patients and 35% of controls voted correctly more than 3 times. Overall, study findings suggest that patients with multiple chemical sensitivity disorders cannot reliably distinguish between solvents and placebo.
 
No well-designed studies were identified in the literature searches that evaluated the ability of laboratory tests, nutritional assessments or other diagnostic tests to accurately diagnose idiopathic environmental intolerance (or multiple chemical sensitivity). In addition, no high-quality studies were identified that evaluated the impact of any treatment for idiopathic environmental intolerance on health outcomes.
 
There is a lack of clear diagnostic criteria for idiopathic environmental intolerance (also known as multiple chemical sensitivities). Overall, studies have not found that individuals diagnosed with the condition using existing criteria can reliability distinguish between chemical exposure and placebo. There is also a lack of evidence on any diagnostic tests that are useful for diagnosing idiopathic environmental intolerance and a lack of controlled studies evaluating treatments. The coverage statement is unchanged.
 
2012 Update
A literature search was conducted using the MEDLINE database through May 2012.  There were no studies identified that would prompt a change in the coverage statement.  In 2011, Rubin and colleagues published a systematic review of studies on the diagnosis of idiopathic environmental intolerance attributed to electromagnetic fields (EMF) (Rubin, 2011).  The investigators identified 29 studies which were single- or double-blind, exposed participants to EMF fields, and measured objective outcomes. Twenty of the 29 studies used outcomes related to the autonomic nervous system (e.g., heart rate or blood pressure). Two of 20 (10%) studies found a significant impact of EMF on function and the other 18 studies found no effect. The authors noted that findings of the 2 positive studies might have been influenced by the order of exposure e.g. including a sham exposure that was always first or second in a series of 3 or 4 consecutive exposures. None of the 4 studies measuring blood chemistry or 3 studies measuring brain physiology found a significant effect of EMF levels on outcomes. Seven studies tested cognitive function; 2 of 7 (29%) had at least one positive finding. The authors concluded that there is insufficient evidence suggesting that individuals with idiopathic environmental intolerance attributed to EMF experience their physiological reactions as a result of exposure to EMF.
 
2013 Update
A literature search was conducted using the MEDLINE database through May 2013. There was no new information identified that would prompt a change in the coverage statement. The following is a summary of the key identified literature.
 
In 2012, Baliatsas and colleagues reviewed 63 studies that included definitions or criteria for identifying individuals with idiopathic environmental intolerance related to EMF exposure (Baliatsas, 2012). The major criteria used in the studies were: 1) attribution of non-specific physical symptoms to either various or specific sources of EMF (n=13 studies); 2) self-reported idiopathic environmental intolerance attributed to EMF exposure (or similar terms) (n=14 studies); 3) experience of symptoms during or within 24 hours after perceived or actual EMF exposure (n=10 studies); and 4) high score on a symptom scale (n=6). The review found considerable variation among studies in terms of definitions and criteria; uniform diagnostic criteria have not yet been developed.
 
In 2012, Skovbjerg and colleagues in Denmark published a randomized non-blinded pilot study to evaluate mindfulness-based cognitive therapy to treat multiple chemical sensitivities (Skovbjerg, 2012). Thirty-seven individuals with self-reported symptoms attributed to exposure to common airborne chemicals, or with physician-diagnosed MCS were included. Participants were randomized to receive weekly group therapy for 8 weeks or usual care. At the 4-, 8- and 12-week follow-ups, no statistically significant differences were found between groups in the 2 main outcome measures, the Symptom Checklist-92 (SCL-92) and the Brief Illness Perception Questionnaire (Brief IPQ). For example, 8 weeks after the beginning of the intervention, mean scores on the somatization scale of the SCL-92 were 0.78 in the therapy group and 0.79 in the control group (p=0.59).
    
2014 Update
A literature search conducted through May 2014 did not reveal any new information that would prompt a change in the coverage statement.
 
2015 Update
A literature search conducted through May 2015 did not reveal any new information that would prompt a change in the coverage statement.
 
2018 Update
Annual policy review completed with a literature search using the MEDLINE database through May 2018. No new literature was identified that would prompt a change in the coverage statement.
2019 Update
Annual policy review completed with a literature search using the MEDLINE database through May 2019. No new literature was identified that would prompt a change in the coverage statement.
 
2020 Update
A literature search was conducted through May 2020.  There was no new information identified that would prompt a change in the coverage statement.  
 
2021 Update
Annual policy review completed with a literature search using the MEDLINE database through May 2021. No new literature was identified that would prompt a change in the coverage statement.
 
2022 Update
Annual policy review completed with a literature search using the MEDLINE database through May 2022. No new literature was identified that would prompt a change in the coverage statement.

References: Aaron LA, Buchwald D.(2001) A review of the evidence for overlap among unexplained clinical conditions. Ann Intern Med 2001; 134(9 pt 2):868-81.

Am Academy of Allergy, Asthma and Immunology Board of Directors. Position statement. Idiopathic environmental intolerances. J Allergy Clin Immunol 1999; 103:36-40.

Am College of Physicians Clinical Efficacy Assessment Project. Ann Int Med 1989; Ill:168-178.

Bailer J, Witthoft J, Rist F.(2008) Psychological predictors of short- and medium term outcome in individuals with idiopathic environmental intolerance (IEI) and individuals with somatoform disorders. J Toxicol Environ Health A 2008; 71(11-12):766-75.

Baliatsas C, Van Kamp I, Lebret E et al.(2012) Idiopathic environmental intolerance attributed to electromagnetic fields (IEI-EMF): a systematic review of identifying criteria. BMC Public Health 2012; 12:643.

Barsky AJ, Borus JF.(1999) Functional somatic syndromes. Ann Intern Med 1999; 130(11):910-21.

Bolt HM, Kiesswetter E.(2002) Is multiple chemical sensitivity a clinical defined entity? Toxicol Lett 2002; 128:99-106.

Bornschein S, Hausteiner C, Drzezga A et al.(2007) Neuropsychological and positron emission tomography correlates in idiopathic environmental intolerances. Scand J Work Environ Health 2007; 33(6):447-53.

Bornschein S, Hausteiner C, Rommelt H et al.(2008) Double-blind placebo-controlled provocation study in patients with subjective Multiple Chemical Sensitivity (MCS) and matched control subjects. Clin Toxicology 2008; 46(5):443-9.

Cullen MR.(1987) The worker with multiple chemical sensitivities: an overview. Occup Med 1987; 2(4):655-61

Das-Munshi J, Rubin GJ, Wessely S.(2006) Multiple chemical sensitivities: a systematic review of provocation studies. J Allergy Clin Immunol 2006; 118(6):1257-64.

Das-Munshi J, Rubin GJ, Wessely S.(2007) Multiple chemical sensitivities: review. Curr Opin Otolaryngol Head Neck Surg 2007; 15(4):274-80.

Fremont M, Vaeyens F, Herst CV et al.(2005) 37-Kilodalton/83-kilodalton RNase L isoform ratio in peripheral blood mononuclear cells: analytical performance and relevance for chronic fatigue syndrome. Clin Diagn Lab Immunol 2005; 12(10):1259-60.

Graveling RA, Pilkington A, George JP et al.(1999) A review of multiple chemical sensitivity. Occup Environ Med 1999; 56(2):73-85.

Lacour M, Zunder T, Huber R et al.(2002) The pathogenetic significance of intestinal Candida colonization--a systematic review from an interdisciplinary and environmental medical point of view. Int J Hyg Environ Health 2002; 205(4): 257-68.

Multiple chemical sensitivities. Idiopathic environmental intolerances. ACOEM Position Statement. J Occup Environ Med 1999; 41:940-1.

Rubin GJ, Hillert L, Nieto-Hernandez R et al.(2011) Do people with idiopathic environmental intolerance attributed to electromagnetic fields display physiological effects when exposed to electromagnetic fields? A systematic review of provocation studies. Bioelectromagnetics. 2011; 32(8):593-609.

Skovbjerg S, Hauge CR, Rasmussen A et al.(2012) Mindfulness-based cognitive therapy to treat multiple chemical sensitivities: a randomized pilot trial. Scand J Psychol 2012; 53(3):233-8.

Suhadolnik RJ, Reichenbach NL, Hitzges PM et al.(1993) RNA drug therapy acting via the 2-5A synthetase/RNase L pathway. Ann NY Acad Sci 1993; 685:756-7.

Tiev KP, Briant M, Ziani M et al.(2005) Variability of the RNase L isoform ratio (37 kiloDaltons/83 kiloDaltons) in diagnosis of chronic fatigue syndrome. Clin Diagn Lab Immunol 2005; 12(2):366.

Tiev KP, Demettre E, Ercolano P et al.(2003) RNase L levels in peripheral blood mononuclear cells: 37-kilodalton/83-kilodalton isoform ratio is a potential test for chronic fatigue syndrome. Clin Diagn Lab Immunol 2003; 10(2):315-6.

Winder C.(2002) Mechanisms of multiple chemical allergy. Toxicol Lett 2002; 128:85-97.

Witthoft M, Rist F, Bailer J.(2008) Evidence for a specific link between the personality trait of absorption and idiopathic environmental intolerance. J Toxicol Environ Health A 2008; 71(11-12):795-802.


Group specific policy will supersede this policy when applicable. This policy does not apply to the Wal-Mart Associates Group Health Plan participants or to the Tyson Group Health Plan participants.
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