Aetna considers chemical hair analysis experimental and investigational, except for diagnosis of suspected chronic arsenic poisoning.
Note: Microscopic evaluation of hair structure (trichogram) may be medically necessary as part of the work-up of members with alopecia or abnormal-appearing or abnormally growing hair.
Note: Although hair samples may be used for verifying abuse of illicit substances in persons who wish to evade detection, its use in this situation is not considered treatment of disease.
Hair analysis has been proposed as an aid in the diagnosis of disorders such as mineral or protein deficiency or mineral toxicity. Hair analysis has not been proven to be effective in ascertaining mineral or metabolic imbalances or IgE-mediated allergic diseases. Hair analysis has also not been proven to be of use in either the diagnosis or treatment of autism.
Because arsenic is taken up and bound in hair and fingernails, analysis of hair and nails have been used to detect chronic arsenic exposure (Goldman, 2008). However, in a setting in which air exposure is a consideration, as in an industrial environment, it is very difficult to remove exogenous arsenic from hair, and therefore to get a reliable reading. Also a lack of standardization of analysis contributes to the variability of results from hair and nail testing. Goldman (2008) explained that commercial laboratory hair analyses for multiple elements including arsenic are highly inaccurate. Determination of arsenic in hair and nails has been most useful in epidemiological studies performed to evaluate environmental exposures of populations to inorganic arsenic; it is less useful in the evaluation of an individual patient (Goldman, 2008).
Microscopic evaluation of hair structure (trichogram) may be indicated as part of the work-up of members with alopecia or abnormal-appearing or abnormally growing hair. Hair may be examined under the microscope to determine the number of hairs that are actively growing (anagen phase) versus the resting phase (telogen). In addition, microscopic examination of clipped hair can reveal structural abnormalities of the hair bulb or shaft.
Rahman et al (2009) determined the concentration of trace elements present in scalp hair sample of schizophrenic patients and examined the relationship between trace elements level and nutritional status or socioeconomic factors. The study was conducted among 30 schizophrenic male patients and 30 healthy male volunteers. Hair trace element concentrations were determined by flame atomic absorption spectroscopy and analyzed by independent t-test, Pearson's correlation analysis, regression analysis, and analysis of variance (ANOVA). Mn, Zn, Ca, Cu, and Cd concentrations of schizophrenic patients were 3.8 +/- 2.31 microg/gm, 171.6 +/- 59.04 microg/gm, 396.23 +/- 157.83 microg/gm, 15.40 +/- 5.68 microg/gm, and 1.14 +/- 0.89 microg/gm of hair sample, while those of control subjects were 4.4 +/- 2.32 microg/gm, 199.16 +/- 27.85 microg/gm, 620.9 +/- 181.55 microg/gm, 12.23 +/- 4.56 microg/gm, and 0.47 +/- 0.32 microg/gm of hair sample, respectively. The hair concentration of Zn and Ca decreased significantly (p = 0.024; p = 0.000, respectively) and the concentration of Cu and Cd increased significantly (p = 0.021; p = 0.000, respectively) in schizophrenic patients while the concentration of Mn (p = 0.321) remain unchanged. Socioeconomic data reveals that most of the patients were poor, middle-aged and divorced. Mean body mass indices (BMIs) of the control group (22.26 +/- 1.91 kg/m(2)) and the patient group (20.42 +/- 3.16 kg/m(2)) were within the normal range (18.5 to 25.0 kg/m(2)). Pearson's correlation analysis suggested that only Ca concentration of patients had a significant positive correlation with the BMI (r = 0.597; p = 0.000) which was further justified from the regression analysis (R (2) = 44 %; t = 3.59; p = 0.002) and 1-way ANOVA test (F = 3.62; p = 0.015). A significant decrease in the hair concentration of Zn and Ca as well as a significant increase in the hair concentration of Cu and Cd in schizophrenic patients than that of its control group was observed, which may provide prognostic tool for the diagnosis and treatment of this disease. However, further work with larger population is suggested to examine the exact correlation between trace element level and the degree of disorder.
Guidelines from the National Institute for Health and Clinical Excellence (2011) recommended against the use of hair analysis in the diagnosis of food allergy. An NIAID expert panel (Boyce et a., 2010) made similar recommendations against the use of hair analysis in food allergy. Guidelines from the American Academy of Asthma, Allergy and Immunology (Wallace et al, 2008) state that hair analysis has no diagnostic validity in rhinitis. Autism guidelines from the Singapore Ministry of Health (2010) recommend against the use of hair mineral analysis for autism.
Albar et al (2013) stated that recently, hair cortisol has become a topic of global interest as a biomarker of chronic stress. Different research groups have been using different methods for extraction and analysis, making it difficult to compare results across studies. A critical examination of the reported analytical methods is important to facilitate standardization and allow for a uniform interpretation. These researchers qualitatively compared 4 published procedures from laboratories in Germany, the Netherlands, the United States of America and Canada. Multiple aspects of their procedures were compared. A major difference among the laboratories was the enzyme-linked immunosorbent assay (ELISA) kit used: the Canadian laboratory used the kit from ALPCO Diagnostics (Salem, MA), the American laboratory used the kit from DRG International (Springfield, NJ), the German laboratory used the kit from DRG Instruments GmbH (Marburg, Germany), or IBL (Hamburg, Germany), and the Dutch used the kit from Salimetrics (Suffolk, UK). In addition, there were noted differences in hair mass used as well as washing and extraction procedures. The range of hair cortisol levels determined in healthy volunteers by the 4 groups was within 2.3-fold: Koren, 46.1 pg/mg; Van Rossum, 29.72 pg/mg; Kirschbaum, 20 pg/mg and Laudenslager ~ 27 pg/mg. The authors concluded that the relative similarities in hair cortisol values in volunteers among the 4 laboratories should facilitate a quality assurance exchange program, as a necessary step toward clinical use of this novel test.
Karlen and colleagues (2013) examined cortisol concentrations in hair as biomarker of prolonged stress in young children (n = 100) and their mothers and the relation to perinatal and socio-demographic factors. Prolonged stress levels were assessed through cortisol in hair. A questionnaire covered perinatal and socio-demographic factors during the child's first year of life. Maternal hair cortisol during the 2nd and 3rd trimester and child hair cortisol at year 1 and 3 correlated. Child cortisol in hair levels decreased over time and correlated to each succeeding age, between years 1 and 3 (r = 0.30, p = 0.002), 3 and 5 (r = 0.39, p < 0.001), and 5 and 8 (r = 0.44, p < 0.001). Repeated measures gave a significant linear association over time (p < 0.001). There was an association between high levels of hair cortisol and birth weight (β = 0.224, p = 0.020), non-appropriate size for gestational age (β = 0.231, p = 0.017), and living in an apartment compared with a house (β = 0.200, p = 0.049). In addition, these investigators found high levels of cortisol in hair related to other factors associated with psychosocial stress exposure. The authors concluded that correlation between hair cortisol levels in mothers and their children suggested a heritable trait or maternal calibration of the child's hypothalamic-pituitary-adrenocortical axis. Cortisol output gradually stabilizes and seems to have a stable trait. They stated that cortisol concentration in hair has the potential to become a biomarker of prolonged stress, especially applicable as a non-invasive method when studying how stress influences children's health.
Russell et al (2014) noted that cortisol is assumed to incorporate into hair via serum, sebum, and sweat sources; however, the extent to which sweat contributes to hair cortisol content is unknown. In this study, sweat and saliva samples were collected from 17 subjects after a period of intensive exercise and analyzed by salivary ELISA. Subsequently, an in-vitro test on exposure of hair to hydrocortisone was conducted. Residual hair samples were immersed in a 50-ng/ml hydrocortisone solution for periods lasting 15 mins to 24 hrs, followed by a wash or no-wash condition. Hair cortisol content was determined using the authors’ modified protocol for a salivary ELISA. Post-exercise control sweat cortisol concentrations ranged from 8.16 to 141.7 ng/ml and correlated significantly with the log-transformed time of day. Sweat cortisol levels significantly correlated with salivary cortisol concentrations. In-vitro hair exposure to a 50-ng/ml hydrocortisone solution (mimicking sweat) for 60 mins or more resulted in significantly increased hair cortisol concentrations. Washing with isopropanol did not affect immersion-increased hair cortisol concentrations. The authors concluded that human sweat contains cortisol in concentrations comparable with salivary cortisol levels. The findings of this study suggested that perfuse sweating after intense exercise may increase cortisol concentrations detected in hair. This increase likely cannot be effectively decreased with conventional washing procedures and should be considered carefully in studies using hair cortisol as a biomarker of chronic stress.
CPT Codes / HCPCS Codes / ICD-9 Codes
Chemical hair analysis:
CPT codes covered if selection criteria are met:
HCPCS codes not covered for indications listed in the CPB:
Hair analysis (excluding arsenic)
ICD-9 codes covered if selection criteria are met:
Poisoning by arsenical anti-infectives
Toxic effect of arsenic and its compounds
Accidental poisoning by arsenic and its compounds and fumes
Special screening for chemical poisoning and other contamination [suspected chronic arsenic poisoning]
ICD-9 codes not covered for indications listed in the CPB (not all-inclusive):
Mineral deficiency, not elsewhere classified
270.0 - 277.9
Other metabolic disorders
477.0 - 477.9
493.00 - 493.92
Other atopic dermatitis and related conditions
Dermatitis due to food taken internally
708.0 - 708.9
Nonspecific abnormal toxicological findings
Toxic effect of venom
Other anaphylactic shock
995.20 - 995.29
Other and unspecified adverse effect of drug, medicinal and biological substance
995.60 - 995.69
Anaphylactic shock due to adverse food reaction
Other adverse food reactions, not elsewhere classified
V15.0 - V15.09
Allergy, other than medicinal agents
Special screening for other and unspecified endocrine, nutritional, metabolic, and immunity disorders
Microscopic evaluation of hair structure (trichogram):
CPT codes covered if selection criteria are met:
ICD-9 codes covered if selection criteria are met:
Alopecia, other [abnormal alopecia]
Abnormalities of hair
704.8 - 704.9
Other and unspecified diseases of hair and hair follicles
The above policy is based on the following references:
U.S. Department of Health and Human Services, Health Care Financing Administration (HCFA). Hair analysis -- not covered. Medicare Coverage Issues Manual §50-24. Baltimore, MD: HCFA; 2000.
Lazar P. Hair analysis: What does it tell us? JAMA. 1974;229:1908-1909.
Hambidge KM. Hair analyses: Worthless for vitamins, limited for minerals. Am J Clin Nutr. 1983;36:943-949.
Klevay LM, Bistrian BR, Fleming CR, Neumann CG. Hair analysis in clinical and experimental medicine. Am J Clin Nutr. 1987;46(2):233-236.
Barrett S. Commercial hair analysis: Science or scam? JAMA. 1985;254:1041-1045.
Filipek PA, Accardo PJ, Ashwal S, et al. Practice parameter: Screening and diagnosis of autism. Report of the Quality Standards Subcommittee of the American Academy of Neurology and the Child Neurology Society. Neurology. 2000;55(4):468-479.
Kruse-Jarres JD. Limited usefulness of essential trace element analyses in hair. Am Clin Lab. 2000;19(5):8-10.
Hu H. Exposure to metals. Prim Care. 2000;27(4):983-996.
Hindmarsh JT. Caveats in hair analysis in chronic arsenic poisoning. Clin Biochem. 2002;35(1):1-11.
Niggemann B, Gruber C. Unproven diagnostic procedures in IgE-mediated allergic diseases. Allergy. 2004;59(8):806-808.
Tsatsakis A, Tutudaki M. Progress in pesticide and POPs hair analysis for the assessment of exposure. Forensic Sci Int. 2004;145(2-3):195-199.
Dolan K, Rouen D, Kimber J. An overview of the use of urine, hair, sweat and saliva to detect drug use. Drug Alcohol Rev. 2004;23(2):213-217.
Passalacqua G, Compalati E, Schiappoli M, Senna G. Complementary and alternative medicine for the treatment and diagnosis of asthma and allergic diseases. Monaldi Arch Chest Dis. 2005;63(1):47-54.
Savvopoulos MA, Pallis E, Tzatzarakis MN, et al. Legal issues of addiction assessment: The experience with hair testing in Greece. J Appl Toxicol. 2005;25(2):143-152.
Gambelunghe C, Rossi R, Ferranti C, et al. Hair analysis by GC/MS/MS to verify abuse of drugs. J Appl Toxicol. 2005;25(3):205-211.
Kapaj S, Peterson H, Liber K, Bhattacharya P. Human health effects from chronic arsenic poisoning -- a review. J Environ Sci Health A Tox Hazard Subst Environ Eng. 2006;41(10):2399-2428.
Caprara DL, Klein J, Koren G. Diagnosis of fetal alcohol spectrum disorder (FASD): Fatty acid ethyl esters and neonatal hair analysis. Ann Ist Super Sanita. 2006;42(1):39-45.
Ng DK, Chan CH, Soo MT, Lee RS. Low-level chronic mercury exposure in children and adolescents: Meta-analysis. Pediatr Int. 2007;49(1):80-87.
Wallace DV, Dykewicz MS, Bernstein DI, et al.; Joint Task Force on Practice, American Academy of Allergy, Asthma & Immunology, American College of Allergy, Asthma and Immunology, Joint Council of Allergy, Asthma and Immunology. The diagnosis and management of rhinitis: An updated practice parameter. J Allergy Clin Immunol. 2008;122(2 Suppl):S1-S8.
Rahman A, Azad MA, Hossain I, et al. Zinc, manganese, calcium, copper, and cadmium level in scalp hair samples of schizophrenic patients. Biol Trace Elem Res. 2009;127(2):102-108.
Gow R, Thomson S, Rieder M, et al. An assessment of cortisol analysis in hair and its clinical applications. Forensic Sci Int. 2010;196(1-3):32-37.
Boyce JA, Assa'ad A, Burks AW, et al.; NIAID-Sponsored Expert Panel. Guidelines for the diagnosis and management of food allergy in the United States: Report of the NIAID-sponsored expert panel. J Allergy Clin Immunol. 2010;126(6 Suppl):S1-S58.
Singapore Ministry of Health (MOH). Autism spectrum disorders in preschool children. Singapore: MOH; March 2010.
National Institute for Health and Clinical Excellence (NICE). Food allergy in children and young people. Clinical Guideline 116. London, UK: NICE; February 2011.
Aleksa K, Liesivuori J, Koren G. Hair as a biomarker of polybrominated diethyl ethers' exposure in infants, children and adults. Toxicol Lett. 2012;210(2):198-202.
Appenzeller BM, Tsatsakis AM. Hair analysis for biomonitoring of environmental and occupational exposure to organic pollutants: State of the art, critical review and future needs. Toxicol Lett. 2012;210(2):119-140.
Staufenbiel SM, Penninx BW, Spijker AT, et al. Hair cortisol, stress exposure, and mental health in humans: A systematic review. Psychoneuroendocrinology. 2013;38(8):1220-1235.
Wolowiec P, Michalak I, Chojnacka K, Mikulewicz M. Hair analysis in health assessment. Clin Chim Acta. 2013;419:139-171.
Albar WF, Russell EW, Koren G, et al. Human hair cortisol analysis: Comparison of the internationally-reported ELISA methods. Clin Invest Med. 2013;36(6):E312-E316.
Karlen J, Frostell A, Theodorsson E, et al. Maternal influence on child HPA axis: A prospective study of cortisol levels in hair. Pediatrics. 2013;132(5):e1333-e1340.
Russell E, Koren G, Rieder M, Van Uum SH. The detection of cortisol in human sweat: Implications for measurement of cortisol in hair. Ther Drug Monit. 2014;36(1):30-34.
Copyright Aetna Inc. All rights reserved. Clinical Policy Bulletins are developed by Aetna to assist in administering plan benefits and constitute neither offers of coverage nor medical advice. This Clinical Policy Bulletin contains only a partial, general description of plan or program benefits and does not constitute a contract. Aetna does not provide health care services and, therefore, cannot guarantee any results or outcomes. Participating providers are independent contractors in private practice and are neither employees nor agents of Aetna or its affiliates. Treating providers are solely responsible for medical advice and treatment of members. This Clinical Policy Bulletin may be updated and therefore is subject to change.