Correspondence
Prepubertal Gynecomastia Linked to Lavender and Tea Tree Oils
N Engl J Med 2007; 356:2541-2544June 14, 2007DOI: 10.1056/NEJMc070572
- Article
To the Editor:
The study by Henley et al. (Feb. 1 issue)1 raises many questions. Product names were not provided. Did the authors contact manufacturers to report concerns or ask about constituents? The variability, adulteration, and contamination of herbal products have been widely reported,2,3 as have discrepancies between labels and contents.4 Plastic containers may contain phthalates, known endocrine disrupters.5 What was actually in the products cited in this report?
None of the hormonal testing showed abnormal results, except in Patient 2, who had elevated levels of testosterone (not estrogen). There was no report on ultrasound examination or needle biopsy, nor were subsequent weight changes reported. Might the patients' gynecomastia have reflected another pathophysiological process that resolved spontaneously?
Traditional use and clinical trials have not suggested estrogenic effects of tea tree or lavender oil, though estrogenic effects have been reported for other essential oils and plants. Are occupational exposures to lavender and tea tree associated with estrogenic symptoms? In vitro testing alone is not adequate grounds for indicting traditionally used products and may raise public fear.
5 ReferencesKathi J. Kemper, M.D., M.P.H.
Wake Forest University School of Medicine, Winston-Salem, NC 27157Aviva J. Romm
Yale University School of Medicine, New Haven, CT 06510Paula Gardiner, M.D., M.P.H.
Harvard Medical School, Boston, MA 022151
Henley DV Lipson N Korach KS Bloch CA
Free Full Text | Web of Science | Medline2
Homer LE Leach DN Lea D Slade Lee L Henry RJ Baverstock PR
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Keane FM Munn SE du Vivier AW Taylor NF Higgins EM
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Garrard J Harms S Eberly LE Matiak A
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Schettler T
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To the Editor:
Henley et al. do a commendable job of sleuthing out the likely cause of prepubertal gynecomastia in the young boys exposed to either lavender or tea tree oil. However, given that estrogenic compounds have yet to be detected in either oil, it is important that we carefully interpret these important findings. A growing number of endocrine disrupters in our environment have been shown to accumulate in adipose tissue.1,2 A number of such industrial by-products have also been implicated in early thelarche.3 Since these molecules with hormone-modulating activity are fat soluble, topically applied oils may serve as very efficient delivery agents for environmental endocrine disrupters by concentrating them and delivering them into cells. Although Henley et al. attempt to show that these oils have estrogenic activity, the results of their reported assays indicate a very weak effect. It would be bewildering if such relatively low hormonal activity alone could instigate prepubertal gynecomastia.
3 ReferencesShirin Kalyan, Ph.D.
University of British Columbia, Vancouver, BC V5Z 1M9, Canada1
Paris F Jeandel C Servant N Sultan C
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Brevini TA Zanetto SB Cillo F
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Colon I Caro D Bourdony CJ Rosario O
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To the Editor:
The evidence in the three case studies by Henley et al. does not support their conclusion. Only one of three boys (Patient 2) was exposed to any amount of tea tree oil, and that subject was also exposed to lavender oil. Patients 1 and 3 used cosmetic products containing lavender oil alone. There is no rational process that could allow the authors to conclude that tea tree oil caused the gynecomastia in Patients 1 and 3 or separate the effects of lavender oil from those of tea tree oil in Patient 2. Thus, how can one reach the conclusion that tea tree oil has any causative role in the observed gynecomastia?
Moreover, the authors make no attempt to correlate the three case studies and the cell-culture assays scientifically. The estrogenic activity expressed in the cell-culture assays was dose dependent. The response was negative at low levels and became positive at levels that corresponded to 600,000 to 1.4 million times the 1 nM level of the positive control, estradiol. It is beyond reason to conclude that the one boy who used a shampoo and hair gel containing a minimal amount of tea tree oil could have been exposed at this high a dose.
Of equal significance is the fact that the testing conducted in this preliminary study was far from comprehensive. The researchers themselves acknowledge that there were other compounds, including other essential oils, in the personal care products used by the boys that the researchers did not test.
If casual exposure to products containing tea tree oil could indeed induce gynecomastia in otherwise normal young males, this effect would have been manifested long ago in the population, given the number of products on the market containing this ingredient. My employer has sold 123 million bottles of cosmetic and household products containing tea tree oil during the past two decades, and it has never received a report of gynecomastia before this study. Although those who have worked with tea tree oil for many years are convinced it does not cause gynecomastia, we do not want to be blind to that remote possibility. If anyone in the medical community becomes aware of any cases involving tea tree oil and gynecomastia, please contact me.
James L. Kurtz, Ph.D.
Melaleuca, Idaho Falls, ID 83402
jkurtz@melaleuca.com Dr. Kurtz is an employee of Melaleuca, a company that manufactures and markets personal-care, pharmaceutical, household, and nutritional products, including many products incorporating tea tree oil. No other potential conflict of interest relevant to this letter was reported.
To the Editor:
The study by Henley et al. does not support a causative link between the use of products containing minimal amounts of lavender and tea tree oils and gynecomastia in three boys. The study was uncontrolled, with hundreds of other suspect agents — such as soy, licorice, hops, garbanzo beans, lentils, flaxseed, and sunflower seed — possibly having a role. Henley and colleagues' data suggesting that tea tree oil penetrated skin are misleading. Various studies1 have shown that only 3 of more than 100 compounds enter the skin from 100% pure tea tree oil. In a wash-off product containing less than 1% tea tree oil, the amount would be almost undetectable.
If the study by Henley et al. shows any estrogenic activity of these oils, it is at a level up to 1 millionth that of estradiol, the positive control. Thus, an average 20-kg child would have had to use approximately 40 bottles of shampoo for each application. The claim of a causative link between the use of tea tree oil products and prepubertal gynecomastia appears to be misleading and unwarranted.
Christopher J. Dean, B.A.
Australian Tea Tree Oil Industry Association, Byron Bay, NSW 2481, Australia
cdean@bigpond.net. au Mr. Dean founded, worked for, and is currently consulting for TP Health, a company that produces a range of tea tree oil products, and is chair of the Technical and Safety Committee of the Australian Tea Tree Oil Industry Association. No other potential conflict of interest relevant to this letter was reported.
1 ReferenceThe authors reply: With regard to the comments of Kemper et al.: we were deliberate in not naming commercial products. We did not contact the manufacturers but, rather, found the listed ingredients on the product labels or in the product information on the manufacturers' Web sites. Since these products are available to consumers and fall under federal regulation, it would be illegal for the manufacturers to list the ingredients inaccurately. We are not aware of any systematic study examining estrogenic symptoms from occupational exposure to lavender or tea tree oil. Our study involved boys, not adults. Furthermore, we are not aware of any randomized, controlled clinical trials examining the estrogenic effects of exposure to lavender or tea tree oil in children. We are open to the idea, however, that there may be other essential oils that could have contributed to the clinical findings in our subjects.
We agree with Kalyan that our findings should be interpreted carefully. Again, we are open to the possibility that the estrogenic effects could be modified by other disrupters and encourage further research in this regard. We would remind readers that we observed an unusual clinical phenomenon in prepubertal boys that resolved on discontinuation of the topically applied products.
Kurtz and Dean question our findings, apparently in an effort to defend their commercial interest — namely, the marketing of tea tree oil. Of course our study was uncontrolled. It is highly unlikely that “hundreds of other suspect agents” might have caused the gynecomastia or that the condition would have developed earlier and would not have resolved by discontinuation of the suspected products. We agree that Patient 2 was exposed to lavender oil as well as to tea tree oil. There may be a valid argument that it was the lavender oil that caused the gynecomastia. However, the tea tree oil had activity similar to that of lavender oil with respect to in vitro estrogenic and antiandrogenic effects. Thus, one could just as easily make the case that the effects of two essential oils were additive in causing the in vivo gynecomastia. We would argue that the hair gel may not have been simply a “wash-off product,” as Dean claims, but may instead have remained on the scalp and palms, resulting in prolonged exposure, particularly if washing was incomplete.
We agree that further scientific studies are necessary to answer the questions that the correspondents have posed. Since exact components of the oils have not been identified, any comparison regarding relevant activity cannot be made. Furthermore, we hope that epidemiologic studies will follow and other potential endocrine disrupters will be sought by direct analysis of the essential oils and over-the-counter commercial products.
Clifford A. Bloch, M.D.
Pediatric Endocrine Associates, Greenwood Village, CO 80111Kenneth S. Korach, Ph.D.
National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709
korach@niehs.nih. gov - Citing Articles (1)
Citing Articles
1
Christine F.Carson, RobertTisserand, TonyLarkman. (2014) Lack of evidence that essential oils affect puberty. Reproductive Toxicology 44, 50-51
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