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Bacterial resistance: It has been proposed that the habitual use of tea tree oil in products applied to the skin at sub-bactericidal concentrations might encourage resistant strains to develop (McMahon et al 2007, 2008). However, studies in bacteria and yeasts suggest that any resistance to tea tree oil is transient and/or negligible (Mondello et al 2006; Ferrini et al 2006). This holds true even in bacteria subcultured up to 22 times (Hammer et al 2008, 2012). In cases where they have an effect on resistance, essential oils in general tend to reduce or eliminate it, rather than increasing it. The effect of personal care products containing essential oil mixtures, with or without tea tree oil, is unknowable, since there are thousands of such products. However, the great variety of these mixtures will make it very difficult for resistance to develop.

Ingestion: There are insufficient data to establish a safe maximum oral human dose, which has led some to suggest that the oil is not safe to ingest at all. When taken orally in doses of 0.8 mL/kg or more, equivalent to over 50 mL in an adult, tea tree oil has notable CNS effects, as cited above under Acute toxicity, human. However, an oral dose of ~ 2.5 mL elicited no CNS toxicity in an adult male (Elliott 1993) and this is above the normal oral dose range of 0.3–1.3 mL for essential oils (Table 4.7). No neurotoxicity has been reported following the dermal application of tea tree oil in humans, even when used undiluted. Severe neurotoxic effects have occurred in cats following dermal administration, in amounts equivalent to 280 – 462 mL being applied to an adult human. Since a dermal dose of 2 g/kg elicited no apparent toxicity in rabbits, cats are probably more susceptible to tea tree toxicity than other species. In our opinion, the human toxicity data are more or less consistent with the rat oral LD 50 of 1.9 g/kg, which is within the ‘slightly toxic’ range of 1–5 g/kg, since doses about half of this amount elicited clear signs of neurotoxicity.

Dermal application: Undiluted tea tree oil was irritating to rabbits and mice, but its irritancy to healthy human skin is negligible. In six clinical trials using tea tree oil at either 5% or 10%, there were no allergic reactions among 295 patients, 67 of them with an inflammatory skin condition (Table 13.4B). Mild reactions were not significantly greater than in placebo groups, and in some cases were less. In skin sensitization, both the concentration and the degree of oxidation need to be considered (Table 13.4A). For example, unoxidized tea tree oil at 5% produced one positive reaction in 725 dermatitis patients (Lisi et al 2000), while oxidized tea tree oil at 5% produced a seven times greater response: 36 reactions in 3,375 patients (Pirker et al 2003). Using the same patient group of 725, when 100% unoxidized tea tree oil was used, there were five reactions, an increase of five times over the 5% dilution (Lisi et al 2000). However, 100% oxidized tea tree oil produced 13/550 reactions, an increase of 3.5 times compared to the 100% unoxidized oil (Coutts et al 2002).

The oil used in the Coutts et al (2002) report was allowed to photo-oxidize in a clear glass bottle over 12 months, during which time 550 dermatitis patients were patch tested. No increase in sensitization rate was noted as the oil aged, but no assessement of peroxide value was made at any point. Of the 13 patients who reacted to 100% tea tree oil, nine were later re-tested with 5% tea tree oil. Four of these reacted, the other five did not (Clayton & Orton 2005). It is important to note that the way tea tree oil was oxidized for these tests does not reflect the quality of tea tree oil found in the marketplace, so these data do not represent real world risk. There were 614 reported adverse events from the sale of 37,135,48 products containing tea tree oil over a 10 year period in four countries, 0.0016% of products sold (Wabner et al 2006).

Unoxidized tea tree oil presents a very low risk, even in patients with compromised skin, when used at concentrations up to 10%. Undiluted tea tree oil naturally presents a greater risk than diluted oil, but there is little information on the use of concentrations between 10% and 100%. Satchell et al (2002a) reported 3.8% of tinea pedis patients with adverse reactions to 25% or 50% tea tree oil. As an experimental treatment for contact dermatitis, 50% unoxidized tea tree oil was applied to 15 patients with nickel allergy. Since this concentration produced “some redness” in several patients, a 20% dilution was used on the remaining six patients, and there were no adverse reactions (Wallengren 2011).

According to the SCCP: “The sparse data available suggest that the use of undiluted tea tree oil as a commercial product is not safe” (SCCP 2004a). However, there is no definition of what constitutes safe or unsafe. According to Wabner et al (2006) there were 16 reported adverse events from the sale of 12,205,539 bottles of undiluted tea tree oil by an Australian company. This represents 0.00013% of bottles sold.

Misinformation: Much nonsense has been written about tea tree oil safety. About.com, for example, states that the three reported cases of breast enlargement in boys caused by tea tree oil (there was only one, with no causal link) demonstrate that the oil ‘may alter hormone levels’ and that therefore ‘people with hormone-sensitive cancers or pregnant or nursing women should avoid tea tree oil.’ The same website goes on to warn that tea tree oil ‘can cause impaired immune function.’ No literature is cited, but this may be in reference to research showing that the anti-inflammatory action of inhaled tea tree oil acts by inhibiting the (inflammatory) immune response in mice following induced inflammation, while having no effect on mice with no inflammation (Golab et al 2005; Golab & Skwarlo-Sonta 2007). Either that, or it is a very odd way to describe allergic reactions. To refer to either as ‘impaired immune function’ makes no sense.

The Consultant360 site carries a report published on July 1 2007, by Stonehouse and Studdiford, who make the claim that ‘allergic contact dermatitis has been reported in about 5% of those who use tea tree oil’ (http://consultant360.com/content/allergic-contact-dermatitis-tea-tree-oil, accessed August 8th 2011). However no substantive evidence is, nor could be, given to support this misleading statement.

Species: The ISO standard allows that tea tree oil may be obtained from Melaleuca species other than M. alternifolia, “provided that the oil obtained conforms to the requirements given in this International Standard”. The composition of M. dissitiflora and M. linariifolia may be very similar to that of M. alternifolia (Cornwell et al 1999). However, the Australian Tea Tree Industry Association is not aware of any commercial oil production from these species, and there is no safety information on these oils, such as methyleugenol content. We therefore do not consider them viable sources of tea tree oil. Six chemotypes exist for M. alternifolia, although only the terpinen-4-ol chemotype is cultivated on a commercial scale. Of the other five, one is dominated by terpinolene, and the others are all cineole-rich, with varying concentrations of other constituents (Homer et al 2000).