Question:

My friend is a breast cancer survivor. She had another friend, also a breast cancer survivor tell her she should not use any products containing essential oils because essential oils contain estrogen and it is a build up of estrogen in the body which causes cancer.

I would love a scientific response to this as I believe it to be a misconception that is spreading.

Thank-you

Kris

Answer:

Kris –

No essential oils contain estrogen. Some essential oils contain compounds that have very weak, estrogen-like effects in in vitro tests. However, in the case of tea tree oil, for example, the estrogen-like compounds do not penetrate human skin, and a hormonal effect from dermal application of the oil is therefore impossible.

The National Cancer Institute states that “Applying lavender and tea tree oils to the skin over a long period of time has been linked in one study to breast enlargement in boys who have not yet reached puberty.” This is incorrect on two counts: (1) neither lavender oil nor tea tree oil were applied to the skin in any of the three cases. Various unidentified products (such as hair gel) were used, that were alleged to contain either lavender oil or tea tree oil. However, no evidence was presented to show that the products used by the boys did actually contain either essential oil. Also, it is not known whether the personal care products used actually caused the gynecomastia, since (b) they were NOT used over a long period of time. This sheds considerable doubt on any causal connection, and the study has drawn criticism from the scientific community for its lack of rigor.

For a full account of the facts and critique, read below “Neither Lavender Oil nor Tea Tree Oil Can Be Linked to Breast Growth in Young Boys“.

Introduction
In 2007, a correlation was alleged between commercial products containing lavender and tea tree oils and breast growth in young boys. Three cases were seen in boys aged 4-7, who had all been using such products. In each case, the breast growth reduced to normal parameters within several months of ceasing to use the products. Subsequent laboratory testing showed that both essential oils had estrogen-like properties (Henley et al 2007). In the report, no information was given about any of the product ingredients, and there is scant information on product use. No analysis was carried out to confirm or rule out the presence of essential oil constituents.

Case One
In the first case, “The patient’s mother reported applying a “healing balm” containing lavender oil to his skin starting shortly before the initial presentation.” No further details of the product or its use are given, but a healing balm sounds like something that might only be applied to a small area of skin. If so, then it is unlikely that any ingredient couldhave entered the boy’s blood in sufficient concentration to cause gynecomastia within a short time period.

Case two
In the second case, a styling hair gel was applied to the hair and scalp every morning, along with regular use of a shampoo. Both tea tree oil and lavender oil are cited on the ingredient list of both products. In a subsequent website report, it is claimed that the two hair products used in this case were manufactured by Paul Mitchell®, and that these were analyzed by a competitor. The shampoo was said to contain “very low concentrations” of tea tree oil, and the
content in the hair gel was “virtually undetectable”. Lavender oil concentration was not checked (Neustaedter 2007).

Dermal absorption of fragrance from shampoo application has been estimated to be 80 times less than that from body lotion (Cadby et al 2002) and tea tree oil constituents are poorly absorbed by human skin. In one study, only 3% of the essential oil volume, applied as a 20% concentration in ethanol, was absorbed in a 24 hour period (Cross and Roberts 2006). If the website report is reliable, considering that shampoo is a wash-off product, and that there was only a negligible amount of tea tree oil in the hair gel, tea tree oil can be ruled out as a possible cause of this boy’s gynecomastia. However, liberal use of a hair gel rich in lavender oil could result in moderate dermal absorption of lavender oil constituents (Cal 2006).

Case Three
The third case involved “lavender-scented soap, and intermittent use of lavender-scented commercial skin lotions”. This sounds as if there may not be very much natural lavender oil present. Since soap is a wash-off product, and use of the skin lotions is described as “intermittent”, whether any meaningful absorption of lavender oil constituents took place at all seems doubtful.As dermal absorption of soap fragrance is some 266 times less than that from body lotion, it is virtually impossible that the fragrance in a soap could be absorbed in sufficient quantity to cause any physiological effect (Cadby et al 2002).

Of great interest is the statement that, in this third case, a fraternal twin used the same skin lotions, but not the soap, and did not develop gynecomastia. It would be reasonable to assume that, since the soap could not be responsible for the effect, and since the twin used the lotions without any problem, the gynecomastia in this third case must have been due to some cause other than essential oils.

The in vitro evidence shows weak but definite endocrine disrupting effects for both lavender and tea tree oils. The second case was the only one in which tea tree oil was involved. Tea tree oil was tested because it was deemed to be “chemically similar” to lavender oil. However, apart from the fact that both are essential oils, they have very little in common chemically. 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.

Discussion
It is unusual in such reports not to name the products suspected as being responsible for the effects in question. In the circumstances, it is also curious that the labeled ingredients were not cited. It is even more surprising that no attempt was made to ascertain, retrospectively, whether any constituents of lavender or tea tree oil were detectable, and if so at what concentrations. If the products are not named, no one else can test them either.

Subsequent research has confirmed that tea tree oil does show weak in vitro estrogenic action in MCF-7 cells (Nielsen 2008). However, none of the tea tree oil constituents that penetrate human skin (terpinen-4-ol, α-terpineol, 1,8-cineole) act as estrogens, either singly or in combination, in fact α-terpineol is anti-estrogenic (Cross et al 2008, Nielsen 2008, Reichling et al 2006). Tea tree oil is not a skin penetration enhancer, and in one study reduced the quantity of other substances (benzoic acid and methiocarb) crossing the dermal barrier (Nielsen and Nielsen 2006).

The two main lavender oil constituents, linalool and linalyl acetate, are absorbed by human skin (Jäger et al 1992). However, transcutaneous absorption from fragrances takes some time. The amount that could find its way into the blood from a wash-off product such as a shampoo or soap is negligible, because the time of skin contact is so short. Skin absorption from tea tree oil and lavender oil constituents is measured in hours rather than minutes, and in some instances even leave-on products result in minimal dermal penetration (Cal 2006, Reichling 2006).

No attempt was made to identify the constituent(s) responsible for the in vitro effect, but it is reasonable to expect that any hormonal action in an essential oil would be due to one or two constituents, or even contaminants. It is noteworthy that, while in vitro hormonal effects from essential oil constituents have been previously reported, these are generally very weak, and have been estimated as being at least 10,000 times less potent than 17β-estradiol (Howes et al 2002). Very weak activity is typical of estrogens from plant sources (Chadwick et al 2006).

There is no evidence that the effect seen in vitro would take place in vivo, and much more research would be needed before any such conclusion could be drawn. The report mentions that none of the boys had been exposed to any known endocrine disruptor, such as medications, oral contraceptives(!), marijuana or soy products. However, no mention is made of other known endocrine disruptors, including organochlorine pesticides, PCBs, polychlorinated dioxins, alkyl phenols, pthalates and parabens (Darbre 2006). Both pesticides and phthalates have been found in essential oils, and both phthalates and parabens are commonly found in cosmetic products.

Personal care products have been identified as contributing to phthalate body burden in adult men (Duty et al 2005); phthalates are commonly found in cosmetic products, and are potential hormone disruptors (Darbre 2006). DEHP, for example, has hormone disrupting effects in both male and female rats (Lovekamp-Swan and Davis 2003, Parks et al 2000), and high levels of several phthalates were found in the blood of 28 of 41 prepubertal girls (68%) with premature breast development compared to only 1 of 35 controls (3%) (Colón et al 2000).

It is, therefore, entirely possible that other ingredients or contaminants in the products caused the gynecomastia. Pesticides, PCBs and dioxins are found in the environment, often in food, and it is also possible that a local surge of environmental hormone disruptors caused these cases in Colorado.

Conclusions
As the report states, breast growth in pre-pubertal boys is extremely uncommon, yet three cases were reported within a short period of time, and all in the same clinic. Considering that some 200 tonnes per annum are produced of both lavender oil and tea tree oil, that most of this goes into personal care products, and that very little of the evidence presented for these three cases is convincing, the initial press reports of caution were premature, as are the cautions now found on many websites.

Even if one or more of these cases was linked to product use, any connection with either lavender or tea tree oil is unproven. Other endocrine disrupting ingredients in the products could have played a role. Furthermore, we do not know what other factors, such as dietary or environmental, may have played a part.

The in vitro work reported by Henley et al (2007) does indicate a hormonal effect. However, this cannot be extrapolated to estimate actual human risk, especially without knowing more about the essential oil constituents causing the in vitro effects seen, the amounts being applied to the body, and their bioavailability.

No connection was established between the in vitro work and the three cases, and the evidence for tea tree oil having an effect on prepubertal gynecomastia is non-existent. Phytoestrogens generally have a very weak hormonal activity, and it is implausible that the amounts of essential oil that enter the body from product use would have a significant effect.

References

Cadby PA, Troy WR, Vey MG 2002 Consumer exposure to fragrance ingredients: providing estimates for safety evaluation. Regulatory Toxicology & Pharmacology 36: 246-252

Cal K 2006 How does the type of vehicle influence the in vitro skin absorption and elimination kinetics of terpenes? Archives of Dermatological Research 297: 311-315

Chadwick LR, Pauli GF, Farnsworth NR 2006 The pharmacognosy of Humulus lupulus L. (hops) with an emphasis on estrogenic properties. Phytomedicine 13: 119-131

Colón I, Caro D, Bourdony CJ et al 2000 Identification of phthalate esters in the serum of young Puerto Rican girls with premature breast development. Environmental Health Perspectives 108:895-900

Cross S, Roberts M 2006 In-vitro human epidermal membrane penetration of tea tree oil components from pure oil and a 20% formulation. A report to RIRDC (Australian Rural Industry Research and Development Corporation)

Cross SE, Russell M, Southwell I et al 2008 Human skin penetration of the major components of Australian tea tree oil applied in its pure form and as a 20% solution in vitro. European Journal of Pharmaceutics & Biopharmaceutics 69:214-222

Darbre PD 2006 Environmental oestrogens, cosmetics and breast cancer. Best Practice & Research Clinical Endocrinology & Metabolism 20: 121-143

Duty SM, Ackerman RM, Calafat AM et al 2005 Personal care product use predicts urinary concentrations of some phthalate monoesters. Environmental Health Perspectives 113:1530-1535

FMA 2007 http://www.fmafragrance.org/sub_pages/020107henleyresponse.pdf

Henley DV, Lipson N, Korach KS, Bloch CA 2007 Prebubertal gynecomastia linked to lavender and tea tree oils. New England Journal of Medicine 365(5): 479-485

Howes M-JR, Houghton PJ, Barlow DJ et al 2002 Assessment of estrogenic activity in some common essential oil constituents. Journal of Pharmacy & Pharmacology 54:1521–1528

Jäger W, Buchbauer G, Jirovetz L et al 1992 Percutaneous absorption of lavender oil from a massage oil. Journal of the Society of Cosmetic Chemists 43:49-54

Lovekamp-Swan T, Davis BJ 2003 Mechanisms of phthalate ester toxicity in the female reproductive system. Environmental Health Perspectives 111:139-145

Neustaedter R 2007 http://www.cureguide.com/Natural_Health_Newsletter/Lavender_Dangers/lavender_dangers.html

Nielsen JB 2008 What you see may not always be what you get – bioavailability and extrapolation from in vitro tests. Toxicology in Vitro 22:1038-1042

Nielsen JB, Nielsen F 2006 Topical use of tea tree oil reduces the dermal absorption of benzoic acid and methiocarb. Archives of Dermatological Research 297:395-402

Parks LG, Ostby JS, Lambright CR et al 2000 The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Toxicological Sciences 58:339-349

Reichling J, Landvatter U, Wagner H et al 2006 In vitro studies on release and human skin permeation of Australian tea tree oil (TTO) from topical formulations. European Journal of Pharmaceutics & Biopharmaceutics 64: 222-228

Robert Tisserand

Author

Robert Tisserand has been instrumental in bringing widespread professional and public recognition to aromatherapy. During his 15 years as a massage therapist, he wrote one of the first books on aromatherapy in 1977. The Art of Aromatherapy is now published in twelve languages. In 1974 he established The Aromatic Oil Company (a predecessor of Tisserand Aromatherapy) and in 1988 he founded The Tisserand Institute, setting new standards for vocational aromatherapy education. Also in 1988, he launched The International Journal of Aromatherapy, which he published and edited for 12 years. In the 1990s, Robert orchestrated three international AROMA conferences at British Universities, each attracting some 300 attendees. Robert tracks all the published research relevant to essential oils and collaborates with doctors, herbalists and pharmacologists, integrating scientific data with traditional medicine and holistic principles. He is familiar with the foundations of oriental medicine, and Western herbal and naturopathic traditions, with their emphasis on cleansing, protecting, strengthening immune function and aiding natural healing processes. Robert also has 40 years of experience in essential oil blending and aromatherapy product development, and has an expert knowledge of essential oil safety. Robert is on the International Advisory Board of Complementary Therapies in Clinical Practice, and is a member of the Natural Perfumers Guild. In recognition of his pioneering work, he has been awarded Honorary Lifetime Membership of the International Federation of Aromatherapists, the International Federation of Professional Aromatherapists, and the Alliance of International Aromatherapists. He was privileged to receive a Lifetime Achievement Award from the AIA in Denver in 2007, and is the current chair of the AIA Research Committee. Books: The Art of Aromatherapy (1977), Aromatherapy for Everyone (1987), Essential Oil Safety (1995) co-author. Books chapters: “Essential Oils as Psychotherapeutic Agents”. In: Perfumery: The Psychology and Biology of Fragrance (1988). Books edited: Gattefossé’s Aromatherapy (1993), The Practice of Aromatherapy, Dr Jean Valnet (1982)

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