Christine F Carson

Robert Tisserand

Tony Larkman

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Accepted Manuscript
Title: Lack of evidence that essential oils affect puberty
Author: Christine F. Carson Robert Tisserand Tony Larkman
PII: S0890-6238(14)00023-9
DOI: http://dx.doi.org/doi:10.1016/j.reprotox.2013.09.010
Reference: RTX 6923
To appear in: Reproductive Toxicology
Received date: 28-6-2013
Revised date: 23-9-2013
Accepted date: 24-9-2013
Please cite this article as: Christine F. CarsonRobert TisserandTony
Larkman Lack of evidence that essential oils affect puberty (2014),
http://dx.doi.org/10.1016/j.reprotox.2013.09.010
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Title: Lack of evidence that essential oils affect puberty 
 
Christine F. Carson a, Robert Tisserand b, Tony Larkman c,* 
 
a School of Pathology & Laboratory Medicine (M504) 
The University of Western Australia 
35 Stirling Hwy 
Crawley WA 6009, Australia 
christine.carson@uwa.edu.au 
 
b 407 Park Road 
Ojai CA 93023, USA 
robert@roberttisserand.com 
 
c Australian Tea Tree Industry Association Ltd. 
PO Box 903, Casino NSW 2470, Australia 
 
*Corresponding author at: Australian Tea Tree Industry Association Ltd., 
PO Box 903, Casino NSW 2470, Australia  
Tel: +61 2 6674 2925 
Fax: +61 7 5604 1629 
E-mail address: tlarkman@attia.org.au (Tony Larkman) 
*Manuscript
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Dear Sir,  
The review by Fisher and Eugster [1] due to be published in Reproductive 
Toxicology repeats the putative link between the essential oils of lavender and tea 
tree and breast development stating: 
“Other examples of naturally occurring endocrine disruptors include lavender 
oil, tea tree oil and fennel, all of which have been linked to breast 
development in prepubertal children presumably due to estrogenic effects.” 
Here the authors have referred to the 2007 paper by Henley et al. [2]. They have 
linked essential oils to endocrine disruption by referring to gynecomastia and/or to in 
vitro estrogenic activity, without also referring to other studies that suggest 
otherwise.  
 
The review “summarizes the current understanding of the major environmental 
influences on pubertal timing, focusing on factors for which the most scientific 
evidence exists” [1]. Knowledge in the field is growing steadily and recently 
published data on lavender oil provide compelling evidence that lavender oil is not 
estrogenic [3]. In this study, lavender oil at dosages of 20 or 100 mg/kg was not 
active in a rat uterotrophic assay, the gold-standard in vivo assay, with no evidence 
of estrogenic activity shown. 
 
While tea tree oil has not yet been tested in vivo, in a report on the oil by the 
European Commission’s Scientific Committee on Consumer Products (now the 
Scientific Committee on Consumer Safety) [4], the committee commented: 
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“Since the hormonal active ingredients of Tea Tree Oil were shown not to 
penetrate the skin, the hypothesized correlation of the finding of 3 cases of 
gynecomastia to the topical use of Tea Tree Oil is considered implausible.” 
The implausibility of tea tree oil having any estrogenic effect is further supported by 
Tisserand’s review [5] of the estrogenic activity of clary sage in which he notes that 
according to Anstead et al. [6] and Blair et al. [7] phenolic structure is important for 
estrogenicity, as is the presence of a second ring. This does not rule out other 
mechanisms of xenoestrogenic action such as metabolic activation [8-10] or 
epimutations after developmental exposure [11, 12]. However, none of this negates 
the fact that a putative link [2] has been made and is being overstated and 
perpetuated. Since the Henley et al. article was published, it has been cited more 
than 170 times (Google Scholar, accessed 16 Sep 2013) to reference the estrogenic 
or endocrine disrupting activity of lavender and/or tea tree oils without the benefit of 
additional data. 
 
Case reports are a very useful means of identifying possible links between product 
exposure and detrimental biological effects. However, they are not definitive in their 
own right. The co-incidence of oil exposure and endocrine disruption, manifested as 
breast development, has not been demonstrated to be causal. The cause of the pre-
pubertal gynecomastia has not been identified and tea tree and lavender oils have 
not been definitively identified as endocrine disrupting compounds. Both tea tree 
(Melaleuca alternifolia) and lavender (Lavandula angustifolia) oils have a long history 
of apparently safe use [13, 14]. 
 
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Tisserand has previously postulated [15] that phthalates may have contributed to the 
endocrine effect noted by Henley et al. [2]. Tisserand [15] also noted: 
“The composition of the essential oils tested is not given, nor is any other 
information about them, apart from the supplier. Since they do not appear to 
be organically grown, biocide content is a possibility.” 
Since no compositional data on the lavender or tea tree oils was provided in the 
original paper [2], the presence or absence of xenoestrogenic contaminants such as 
plasticisers, pesticides or herbicides is unknown. Conclusions about the estrogenic 
activity of the oils are not possible without these data. The absence of tea tree oil 
exposure by two of the three reported cases [2] also argues against a causative role 
for tea tree oil and a number of publications questioned the purported link between 
gynecomastia and the two essential oils at the time [16-20]. 
 
Any link, casual or causal, between lavender or tea tree oil product use and the 
development of pre-pubertal gynecomastia has public health, regulatory, 
ecotoxicological and/or commercial consequences. It is worth considering that the 
chemical constituents of lavender and tea tree essential oils are not unique to those 
oils [21-23]. They are found in hundreds of other essential oils. If these two oils did 
possess estrogenic activity, then it is likely that other essential oils would also have 
estrogenic activity by virtue of the constituents they share with lavender and tea tree 
oil. Each year thousands of tonnes of essential oils are ubiquitously ingested by and 
applied to humans and other animals in products such as foods [24], beverages [25, 
26], personal care products and pharmaceutical agents. Consequently, it is important 
that the nature of any link between essential oils and endocrine disruption be 
clarified. This may be achieved by continued research into the safety and efficacy of 
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the oils funded by industry and independent sources combined with ongoing 
surveillance of reports of adverse effects by industry and regulatory authorities. 
 
Finally, a recent revisiting of the existing literature on the in vitro and in vivo 
estrogenic activity of essential oils has led one of the authors (CFC) to suggest an 
alternative hypothesis. It may be that a large proportion of the in vitro results 
suggesting that essential oils and/or their components are estrogenic, are false 
positive results. Commonly utilised disposable laboratory plasticware, such as the 
96-well polystyrene plastic trays in which the tests for estrogenic activity are often 
performed, contains many xenoestrogenic compounds including phthalates and 
nonylphenols that may leach into the test system, especially in the presence of 
essential oils which have solvent properties. The use of disposable laboratory 
plasticware may be confounding the results, a phenomenon that has been reported 
in the past [27, 28]. This needs testing and it is worth noting that Henley et al. used 
polystyrene plates (Korach, K, Personal Communication). 
 
Closing remarks go to Fisher and Eugster [1] who rightly point out that more 
research is “needed to address the question of what environmental factors affect 
puberty and how we can best eliminate relevant exposures with the goal of 
maximizing the health and well-being of today’s children and future generations to 
come.” 
 
Disclosure Statement 
In the past, CF Carson has received research grants and/or consulting fees from the 
Australian Government and/or from industry for research about essential oils. R 
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Tisserand is a shareholder of First Natural Brands, which owns Tisserand 
Aromatherapy. T Larkman is CEO of the Australian Tea Tree Industry Association 
(ATTIA Ltd), an Australian based not-for-profit organisation formed in 1986 as the 
peak body to promote and represent the interests of the Australian tea tree industry.  
 
  
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References 
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2013;http://dx.doi.org/doi:10.1016/j.reprotox.2013.03.012. 
[2] Henley DV, Lipson N, Korach KS, Bloch CA. Prepubertal gynecomastia linked to lavender and tea 
tree oils. N Engl J Med 2007;356(5):479-85. 
[3] Politano VT, McGinty D, Lewis EM, Hoberman AM, Christian MS, Diener RM, et al. Uterotrophic 
assay of percutaneous lavender oil in immature female rats. Int J Toxicol 2013;32(2):123-9. 
[4] Scientific Committee on Consumer Products. Opinion on tea tree oil. Report No. SCCP/1155/08. 
2008. Available from: 
http://ec.europa.eu/health/archive/ph_risk/committees/04_sccp/docs/sccp_o_160.pdf. 
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http://roberttisserand.com/2010/04/is-clary-sage-oil-estrogenic/. 
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Title: Lack of evidence that essential oils affect puberty

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Title: Lack of evidence that essential oils affect puberty

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