I am concerned how the media and some researchers have jumped on the bandwagon following a 2007 report by Henley et al. that was published in the New England Journal of Medicine suggesting that repeated topical exposure of lavender and tea tree essential oils in skin care preparations were identified as hormone disruptors – having oestrogenic and antiandrogenic activities.

The paper reported that gynaecomastia resolved in each patient shortly after the use of the products containing lavender and tea tree was discontinued.  Henley et al. also conducted an in vitro cell culture study that identified lavender and tea tree oils to be oestrogenic and antiandrogenic at 0.005% vol/vol for both oils.1

The media never reported all the studies that had disproved this claim and were critical of all the flaws in the original study. For example, Kemper et al. asked if the authors had contacted the manufacturers of the products to identify if there had been adulteration or contamination of the products.2

I would have asked – did anyone identify all the cosmetic ingredients in the products in question? There are other ingredients used in commercial cosmetics that have been identified as endocrine disrupters. The original report did not conduct a thorough pathological examination of the three boys’ gynaecomastia. It was also stated that an in vitro test alone is not adequate grounds for indicting traditionally used products and raising public fear.2

This is the very argument that is often used to criticise natural therapies – we need more than just in vitro studies!

Since this 2007 report, there have been many unsubstantiated warnings leading to all sorts of outrageous online claims such as this response made in regards to men using lavender:

An investigation of hormone activity found that both lavender and tea tree activate oestrogen receptors much as estradiol does. In addition, both oils block male hormones, suggesting that you are right; it probably makes sense for men to be cautious about utilizing products containing lavender or tea tree oil.3

However, Politano et al. investigated the oestrogenic potential of lavender oil and found that at dosages of 20 to 100 mg/kg lavender oil was not active in the rat uterotrophic assay* and had no evidence of oestrogenic activity.4

* The uterotrophic assay is an in vivo screen that evaluates the ability of a test chemical to elicit biological activities consistent with agonists of oestrogens. This bioassay for oestrogenicity is intended to be included in a battery of in vitro and in vivo tests to identify substances with the potential to interact with the endocrine system. Uterotrophic Assay – OCSPP Guidelines 890.1600. U.S. Environmental Protection Agency. Washington DC, 2011.

Let me remind you that both tea tree and lavender oils have been the most extensively pharmacologically researched essential oils and no previous studies have ever identified lavender or tea tree or any of their constituents as having oestrogenic activity and being endocrine disrupters. An extensive review of literature by Lawrence confirmed that lavender oil does not possess any oestrogenic activity.5,6

However, in this same report, Lawrence stated that when essential oils are stored in or exposed to plastic containers, it is common for the oil to leach out phthalates which are plasticisers (plastic softeners).  Lawrence also states that the geographic origins of the essential oils are important to know as some commercial oils may have agrochemical contamination.6

Many studies have also confirmed that phthalates commonly used in flexible plastics and consumer products have become ubiquitous contaminants, which also exhibit enhanced oestrogenic activity. A recent report states that:

Some phthalates were reported to have the potential to cause decreased testicular weight and seminiferous tubular atrophy, increased DNA damage to men’s sperm, premature breast development in girls, shortened pregnancy and decreased anogenital distance in newborn male babies. These reproductive defects most likely result from the estrogen disrupting activity of certain phthalates.7

At no time did Henley et al. investigate if the cosmetic products in question used parabens which have also been identified as endocrine disrupters.  Parabens can enter the systemic circulation via oral intake or by transdermal penetration. However, it has been reported that parabens are very rapidly metabolised in the liver and in the skin, followed by excretion via the urine.8

While parabens have been identified as having weak oestrogenic activity, studies have identified that subcutaneous application of high doses of butylparaben (600-1200 mg/kg/day) significantly increased uterotrophic response in rats. However, it was reported that this is approximately 100,000 times less potent than the positive control oestradiol l (0.4 mg/kg/day). Oral administration of butylparaben failed to increase uterotrophic response. The researchers stated that this observation may be explained by the highly abundant paraben-metabolising enzymes, located in the intestine and the liver. The researchers claimed that it is difficult to extrapolate in vivo data from mice and data from yeast-based assays to humans. It was suggested that due to the rapid metabolism of parabens it is unlikely that they have oestrogenic effects through direct oestrogen receptor activation that can cause harmful effects to humans.8

However, the researchers then investigated alternative mode of action for possible oestrogenic effects of parabens. They found that parabens may displace oestradiol from binding to its receptor, thereby blocking local oestrogen conjugation and inactivation. It was suggested that a chronic application together with a potent accumulation of parabens on the skin may lead to increasing local oestrogen concentrations due to the inhibition of sulfotransferases. Therefore, parabens may not have a direct oestrogenic effect after all. However, the subcutaneous accumulation of parabens due to extensive use of dermally applied cosmetic products might lead to endocrine disruption due to the interference with oestrogen sulfation by parabens.8

Henley et al. did not investigate or confirm the full ingredients listing of the products in question before rushing to the conclusion that lavender and tea tree cause gynaecomastia.

What I truly find unbelievable is that this 2007 study keeps being referenced. In 2014, a paper written by Fisher and Eugster in Reproductive Toxicology cited many studies which have been identified as endocrine disrupters at the time of puberty. Among naturally occurring endocrine disrupter, the authors list plant-derived phytoestrogens such isoflavones found in soy products. They state that studies show conflicting evidence regarding the exposure of soy in infancy and during puberty. They conclude that the true impact of soy ingestion at the time of puberty is far from clear.9

This paper then proceeds to reference Henley et al. to explain that lavender and other essential oils have been identified as endocrine disrupters but no mention is made of the study by Politano et al. which confirmed that lavender did not have an oestrogenic effect.9

To be fair to the authors, they did state that the relationship between natural endocrine disrupters and pubertal timing remains inconclusive and is in need of further studies.

Tisserand, Carson and Larkman have justifiably refuted these claims. They claim that both lavender and tea tree have a long history of safe use and that it was more than likely that phthalates may have contributed to the hormonal disruption.10

No compositional data was ever provided on the lavender and tea tree oils and the presence of xenoestrogenic contaminants such as plasticisers, herbicides and pesticides were never investigated.

Another very interesting hypothesis made by Tisserand, Carson and Larkman is that in vitro studies may provide false positive evidence. Commonly utilised disposable laboratory plasticware made from polystyrene plastic in which the tests for oestrogenic activity are often performed contain xenoestrogenic compounds such as phthalates and nonylphenols that may leach into the essential oils being tested.10

Therefore, while I do not refute that the cosmetic products that Henley et al. tested were responsible for the boys’ gynaecomastia, there is absolutely no sound clinical and scientific evidence that can link this to lavender and tea tree essential oils. It is very likely to have been triggered by contaminants or other ingredients that we have just examined.

A number of essential oil constituents have the capacity to mimic the female hormone oestrogen. These compounds are known as phytoestrogens. The most notable oils would be aniseed and fennel seed which contain anethole.

References

  1. Henley D et al. Prepubertal gynecomastia linked to lavender and tea tree oils. The New England Journal of Medicine. 2007, 356(5):479-485. Retrieved October 8, 2017 from www.nejm.org.
  2. Kemper K, Romm A, Gardiner P. To the editor – Prepubertal gynecomastia linked to lavender and tea tree oils. New England Journal of Medicine, 2007;356: 2541-2542.
  3. Lavender and tea tree oil block male hormones. Retrieved April 7, 2016 from http://www.peoplepharmacy.com/2015/02/02/lavender-and-tea-tree-oil-block-male-hormones/
  4. Politano V, Hoberman A, Api AM, Uterotrophic assay of percutaneous lavender oil in immature female rats. International Journal of Toxicology. Jan 2013. doi 10.1177/1091581812472209
  5. Lawrence BM. Estrogenic activity in lavender and tea tree oils, Part I. Perfumer & Flavorist, 2007;32:20-25.
  6. Lawrence BM. Estrogenic activity in lavender and tea tree oils, Part II. Perfumer & Flavorist, 2007;32:14-20.
  7. Chen X et al. Toxicity and estrogenic endocrine disrupting activity of phthalates and their mixtures. International Journal of Environmental Research and Public Health, 2014;11(3):3156-3168. doi:10.3390/ijerph110303156.
  8. Engeli R et al. Interference of paraben compounds with estrogen metabolism by inhibition of 17b-hydroxysteroid dehydrogenases. International Journal of Molecular Science, 2017;18(9):2007. doi:10.3390/ijms18092007.
  9. Fisher MM, Eugester EA. What is in our environment that effects puberty? Reproductive Toxicology, 2014;44:7-14. doi: 10.1016/j.reprotox.2013.03.012.
  10. Carson CF, Larkman T, Tisserand R. Lack of evidence that essential oils affect puberty. Reproductive Toxicology, 2014;44:50-51. doi:10.1016/j.reprotox.2013.09.010.