In 1964, Dr Jean Valnet’s book Aromathérapie was published. It was a hugely important publication in the development of aromatherapy, and it had a tremendous impact on my own aromatherapy career. However, the quantity and quality of essential oil research available in the early 1960s was extremely poor. There simply wasn’t very much to go on.

In his book, Valnet lists the above four essential oils as “hypertenseur”, and for each one he gives two references: Caujolle, and Cazal. However, the 1944 Caujolle paper he cites is actually about essential oils of lavender, lavandin and spike lavender, all of which were reported to produce a brief reduction in blood pressure after intravenous injection into dogs. None of the other four oils are mentioned, so clearly, this reference was a mistake.

Caujolle and Franck published two other papers, both in 1945, that Valnet might have in fact be referring to. One was about hyssop oil. Injected iv into dogs, it caused an initial drop in blood pressure and then (since the dose was high enough to induce seizures) blood pressure suddenly increased as the seizures came on, and decreased again when they subsided. This spike in blood pressure was considered to be a consequence of the muscular contractions related to the seizures. Unless used in convulsant doses, hyssop oil is in fact hypotensive. The other paper was about clary sage oil, not sage oil. Injected iv into dogs, it caused a slight increase in blood pressure. This paper also noted that sage oil usually caused blood pressure to reduce. The other reference given by Valnet (Cazal) was a thesis from 1943, which I have not been able to find.

Dr Jean Valnet

Valnet’s contraindication in Aromathérapie is under “usage interne” – internal use – but he does not give a contraindication for “usage externe”. So, even according to Valnet, massage with any of these four oils would NOT be contraindicated in high blood pressure.

In spite of all of the above, Valnet’s advice has been (a) assumed to apply to all uses of these four oils, and (b) repeated in almost all aromatherapy texts since, at least the ones that give safety advice for hypertension. And other oils have been added to the list over time. However, if you look at the research the surprising conclusion is that there is no evidence that any of the contraindicated essential oils – whether listed by Valnet or anyone else – raises blood pressure. In fact most of them reduce it.

In: Essential Oils and Hypertension – is There a Problem? I explain why I believe that there is no case for contraindicating any essential oil in someone with high blood pressure. As well as closely examining the evidence above, I also refer to more recent research, which confirms that the four “Valnet oils” present no risk. The lack of compelling evidence is reason enough to let go of this chimera. There’s also the fact that aromatherapists have plenty of legal challenges to deal with already, and it makes no sense to add to this burden by coming up with restrictions that are scientifically unsound, and that are based on a mistake made in a book in 1964.

SCA 2010 is unscientific, unworkable, and if passed as is, would likely cause widespread job loss in the cosmetics industry. Far from being a step in the right direction, it would be a leap into regulatory chaos, as well as targeting small businesses and natural products.

Yes, cosmetics could and should be safer, and cosmetics labeling in the USA does need more transparency. Safety can always be improved in any field, especially in the light of new scientific data, but SCA 2010 over-reaches what is needed to such an extent that, with the possible exception of distilled water, I cannot think of any cosmetic ingredient that would be acceptable under its terms.

These require that there is “data demonstrating that exposure to all sources of the ingredient or cosmetic present not more than 1 in a million risk for any adverse effect in the population of concern”. Unfortunately, “population of concern” is not defined, but SCA 2010 further states that, in establishing a safety standard, “no harm will be caused by aggregate exposure for a member of a vulnerable population to that ingredient or cosmetic.” “Vulnerable populations” are defined, and include “pregnant women, infants, children, the elderly, and people with compromised immune systems.” Would “infants” include pre-term babies? Would “people with compromised immune systems” include those who do not get sufficient sleep, or who suffer from frequent colds? Much of the wording of the bill is vague and open to many possible interpretations.

“Ingredient” includes every substance present in an ingredient “at levels above technically feasible detection limits.” This last phrase is not defined, but it could be as low as one part per billion (ppb, 0.0000001%) or one part per trillion (ppt, 0.0000000001%). SCA 2010 specifically mentions contaminants, and in foods and beverages they are commonly measured at these levels.

Most essential oils contain about 100 constituents. The above data – for example no more than 1 in a million risk – must be demonstrable for each one of these constituents. Otherwise, the essential oil may not be acceptable in cosmetics, according to the terms of the bill. I can think of of no substance, natural or synthetic, that is known to cause no adverse reaction of any kind in less than 1 in a million people. In human tests for skin reactions, there are sometimes data covering tens of thousands of patch tests. But, that’s still a long way from a million, and there is no cosmetic ingredient that, if patch tested on one million people, would cause no more than one reaction. Except for distilled water perhaps.

“Any adverse effect” is not defined, but is not as simple as it might seem. Linalool, for example, has caused CNS depression when inhaled by animals. (Alcohol is the classic CNS depressant – in large enough amounts, it causes loss of muscular control, slurred speech, stupor and other effects.) Linalool is one of the most common constituents of fragrant herbs and flowers, inhalation of which could therefore be regarded as hazardous under the vague terms of SCA 2010. In reality, linalool has no more than a mild calming, anti-anxiety effect when inhaled by humans. It’s one of the main constituents of lavender oil.

The issue of dose and concentration is not given much consideration. “The Secretary shall presume that any ingredient or cosmetic that induces cancer or birth defects or has reproductive or developmental toxicity when ingested by, inhaled by, or dermally applied to a human or an animal has failed to meet the safety standard.” This is a complete reinvention of the science of toxicology, which up until now has been based on the principle of dose and of threshold levels. Above certain amounts toxicity may occur, below them it will not. This is why there are permissible levels for substances such as hydrocyanic acid (”cyanide”, restricted to 1 ppm) which naturally occurs in some foods.

There’s also the question of the interaction between the constituents of a natural substance. Basil herb, for example, contains two known carcinogens – estragole and methyleugenol. Pesto is a particularly concentrated form of basil, yet the WHO has determined that the amounts in basil/pesto are so small that they present no risk to humans. Since that ruling, research has been published demonstrating that basil herb contains anticarcinogenic substances that counter any potential toxicity of the two carcinogens, and is itself anticarcinogenic (Alhusainy et al 2010, Dasgupta et al 2004, Jeurissen et al 2008). Some basil essential oils have been shown to have anticarcinogenic effects (Aruna & Sivaramakrishnan 1996, Manosroi et al 2005).

Probable or known human carcinogens, such as acetaldehyde and benzo[a]pyrene (BaP) are ubiquitous in fruits, vegetables, dairy products, meat and fish at low ppb. I’m not saying this is a good thing, I’m just saying it’s a fact, and these foods are not regarded as dangerous, because the toxins are present in such minuscule amounts. BaP is one of the many carcinogens found in cigarette smoke, but it is also found in American drinking water at 0.2-2.0 ppb, and in olive oil at about 3 ppb. Olive oil is actually anticarcinogenic, because of its content of antioxidant polyphenols, squalene, β-sitosterol and linoleic acid (Sotiroudis & Kyrtopoulos 2008). It’s the same story with fruits and vegetables – they are generally anticarcinogenic due to a very much higher content of antitoxic substances.

Many essential oils, herb extracts and foods contain tiny amounts of single constituents that alone, and in substantial amounts, are known to be toxic, but the parent natural substance is not toxic. However, this scenario is not taken into consideration by the CFSC or EWG. These organizations are, wittingly or unwittingly, campaigning to have natural substances banned from use in cosmetics because of their “tunnel vision”  and “parts per billion” approach to safety.

The thinking behind the wording of SCA 2010 is naive because there is an assumption that substances are either “safe” or “toxic”, and that if we simply eliminate the toxic ones from personal care products, the world will be a better place. It may seem like an excellent idea, but once you start talking about parts per million or lower, it is unnecessary and unrealistic. Not even foods are regulated to that degree, and our exposure to foods is far greater than our exposure to cosmetics.

SCA 2010 requires that every constituent or trace contaminant of every ingredient be listed on the product label. This arguably discriminates against natural products, since their ingredient lists would have to include hundreds of substances, if they could be proved to be safe under the terms of the bill, and if there was some way of actually listing that many ingredients on a label. A product containing what would normally would be regarded as five ingredients – olive oil, blue chamomile extract, and essential oils of orange, rose and vetiver – would require an ingredient list looking something like this:

oleic acid, palmitic acid, stearic acid, linoleic acid, linolenic acid, squalene, hydroxytyrosol, tyrosol, oleuropein, ligstroside, elenolic acid, acetoxy-pinoresenol, oleocanthal, α-tocopherol, herniarin, hyperoside, umbelliferone, methylumbelliferone, caffeic acid, chlorogenic acid, quercetin, rutin, flavanone, isorhamnetin, quercimeritin, anthemic acid, choline, triacontane, patuletin, patulitrin, apigetrin, apigenin-7-glucoside, apigenin-7-apiosylglucoside, luteolin-7-glucoside, apigetrin-7-acetylglucoside, luteolin-4-glucoside, luteolin, patuletin, matricin, matricarin, galacturonic acid, d-limonene, citronellol, geraniol, myrcene, linalool, α-pinene, sabinene, β-phellandrene, geranial, neral, decanal, citronellal, (Z)-β-ocimene, β-pinene, valencene, β-elemene, terpinolene, dodecanal, γ-terpinene, β-sinensal, α-sinensal, δ-cadinene, α-copaene, γ-muurolene, nerol, δ-3-carene, (Z)-3-hexenol, perillaldehyde, octanol, cis-sabinene hydrate, undecanal, nonadecane, heneicosane, 1-nonadecene, 2-phenylethanol, (E)-β-ocimene, methyleugenol, eugenol, 1-heptadecene, eicosane, trans-linalool oxide, β-caryophyllene, 1-tricosene, α-terpineol, α-farnesene, farnesyl acetate, citronellyl formate, pentadecane, α-guiaiene, benzaldehyde, (Z)-β-farnesene, terpinen-4-ol, geranyl acetate, isogeranyl acetate, farnesyl propionate, methyl salicylate, citronellyl acetate, hexanol, α-humulene, methyl geranate, α-terpinene, cis-rose oxide, isogeraniol, β-bergamotene, δ-2-carene, cis-linalool oxide, octadecane, heptadecane, α-phellandrene, cis-rose oxide, β-maaliene, ethyl benzoate, geranyl acetone, 3-methylbutanol, docosane, 1-heneicosene, p-cymene, 1-eicosene, bourbonene, γ-cadinene, hexadecane, 1-tricosene, octanal, nerolidol, 2-undecanone, benzyl benzoate, α-muurolene, 2-phenylethyl phenylacetate, farnesol, geranyl formate, guaiol, heptanal, allo-ocimene, 1-octadecene, 2-phenylethyl-3-methyl valerate, hexadecanol, hexanal, 3-hexenyl formate, 2-phenylethyl benzoate, khusimol, vetiselinenol, cyclocopacamphan-12-ol (epimer A), α-cadinol, α-vetivone, β-vetivenene, β-eudesmol, β-vetivone, khusenic acid, β-vetispirene, γ-vetivenene, α-amorphene, (E)-eudesm-4(15),7-dien-12-ol, β-calacorene, (Z)-eudesm-6-en-11-ol, γ-amorphene ziza-5-en-12-ol, β-selinene, (Z)-eudesma-6,11-diene, salvial-4(14)-en-1-one, khusinol, cyclocopacamphan-12-ol (epimer B), selina-6-en-4-ol, khusian-ol, δ-amorphene, 1-epicubenol, khusimene, ziza-6(13)-en-3β-ol, ziza-6(13)-en-3-one, 2-epi-ziza-6(13)-en-3α-ol, 12-nor-ziza-6(13)-en-2β-ol, α-vetispirene, eremophila-1(10),7(11)-diene, dimethyl-6,7-bicyclo-[4.4.0]-deca-10-en-one, 10-epi-γ-eudesmol, α-calacorene, (E)-opposita-4(15),7(11)-dien12-ol, prekhusenic acid, 13-nor-eudesma-4,6-dien-11-one, isovalencenol, spirovetiva-1(10),7(11)-diene, 2-epi-ziza-6(13)-en-12-al, (E)-isovalencenal, preziza-7(15)-ene, (Z)-eudesma-6,11-dien-3β-ol, intermedeol, isoeugenol, isokhusenic acid, elemol, eremophila-1(10),6-dien-12-al, juniper camphor, khusimone, eremophila-1(10),4(15)-dien-2α-ol, eremophila-1(10),7(11)-dien-2β-ol, (Z)-isovalencenal, allo-khusiol, methyl-(E)-eremophila-1(10),7(11)-dien-12-ether, (E)-2-nor-zizaene, (Z)-eudesm-6-en-12-al, funebran-15-al

No contaminants have been shown here, only natural constituents of the five ingredients. Whether this list of 200 chemicals would be useful for consumers is debatable, and it would be one of the shorter lists, since most natural products contain much more than five ingredients. Even single synthetic chemicals are not really single chemicals at all – they also contain some minor and trace constituents. Most fragrance chemicals for example are about 95% pure, the other 5% consisting of “impurities” which of course would have to be listed. So synthetic chemicals are not exempt from this challenge.

This is one of the reasons that a naturally-occurring chemical is not the same as a synthetic one – the impurities present in the synthetic version. Synthetic coumarin, for example, causes skin allergies because of the impurities it contains (Vocanson 2006, 2007). But, SCA 2010 treats all chemicals of the same name as equal, which may be expedient if you are trying to pass legislation, but it’s not really scientific.

SCA 2010 proposes that hundreds of ingredients should be assessed for safety in unrealistically short amounts of time, with no proposal as to what form this assessment process will take, who will undertake the work, and exactly what criteria will be used. The wording of the bill shows very little understanding of either toxicology or cosmetics science. It also assumes that any existing legislation in other countries must be good legislation, when in fact nothing could be further from the truth.

I happen to believe that incremental legislation is generally a good thing. It at least allows for the possibility of public debate, and for finer points to be properly considered. Legislation as sweeping as SCA 2010 will cause chaos in the cosmetics industry, especially since States will be given the option to add further safety standards as they see fit. So, each State could have different standards – a manufacturer’s nightmare, and a pointless provision. Even without it, how any agency could enforce legislation involving hundreds of thousands of existing products, with hundreds of ingredients to consider for each one is mind-boggling.

SCA 2010 will cost unknown millions or billions of dollars which the consumer will ultimately pay for. It will probably have no more than a negligible effect on cosmetics safety, but it poses a serious threat to many businesses especially those making natural products, those supplying natural ingredients, and the farmers that grow the plants they come from.

SCA 2010 is especially onerous to small businesses (any corporation with a turnover of $7 million or less.) It requires each manufacturer to not only declare every constituent chemical of every ingredient on the label, but to also test each finished cosmetic to ensure that there is not even a trace amount of some toxic chemical that might have been formed during the making of the product. Most small personal care product businesses will not survive if SCA 2010 passes, a fact that may possibly be attractive to larger corporations.

However, the bill has been criticised by Lezlee Westine, President and CEO of the Personal Care Products Council, which represents the larger cosmetics companies. Her statement includes the following: “We are concerned that the Safe Cosmetics Act of 2010 as written is not based on credible and established scientific principles, would put an enormous if not impossible burden on FDA, and would create a mammoth new regulatory structure for cosmetics, parts of which would far exceed that of any other FDA-regulated product category including food or drugs. The measures the bill would mandate are likely unachievable even with the addition of hundreds of additional FDA scientists and millions more in funding and would not make a meaningful contribution to product safety.”

The Skin Deep database, mentioned in the first paragraph, gives an insight into the thinking of the CFSC and EWG. Skin Deep exaggerates toxicity by being selective in its reporting. For example, limonene, the major constituent of citrus essential oils, is flagged as being developmentally toxic in large doses. This is true, since when pregnant mice were fed 2,363 mg/kg limonene by stomach tube on days 7-12 of gestation, there was an increase in the number of fetuses with skeletal anomalies and delayed ossification (Kodama et al 1977).

However, what is not stated by Skin Deep is that in the same report, when pregnant mice were given a lower dose, 591 mg/kg/day, there was no developmental toxicity. The higher dose is equivalent to daily human ingestion of 5.7 oz of limonene, and the lower dose is equivalent to 1.4 oz. If ingestion of 1.4 oz per day for 6 days is known to be non-fetotoxic, then there is no reason to believe that the use of limonene in cosmetics is likely to be in any way hazardous during pregnancy; in fact, quite the opposite (especially since stomach tube feeding generally increases toxicity).

The Skin Deep page on limonene also mentions, under “cancer” that“one or more tests on mammalian cells show positive mutation results.” One reference is given. However, this ignores the fact that eleven other studies found no evidence of mutagenicity or genotoxicity for limonene (Anderson et al 1990, Connor et al 1985, Florin et al 1980, Haworth et al 1983, Myhr et al 1990, Pienta 1980, Sasaki et al 1989, Sekihashi et al 2002, Turner et al 2001, Watabe et al 1980, 1981), and two further studies reported antimutagenic effects (De Oliveira et al 1997, Kim et al 2001). This 13:1 “score” is part of the weight of evidence used to assess risk in toxicology.

Mutagenicity testing is used to identify substances that may be carcinogenic. However, 85% of substances that are not in fact carcinogenic test positive in a least one mutagenicity test (Kirkland et al 2005). These are “false positives”, and present no risk. The one study cited by Skin Deep for limonene is a false positive.

If you want to imply risk, it’s possible to do so simply by being selective about which facts you choose to report. Many small cosmetics manufacturers have become disenchanted with the manipulative ways of the CFSC and EWG. If they were sincere in caring about cosmetics safety they would welcome any pertinent opinions and facts, but they don’t. They either ignore or stridently oppose anything that does not accord with their fear-driven political agenda. It’s a shame, because a few of their concerns are genuine and well-founded, but their focus has become highly distorted.

I urge you to oppose the Safe Cosmetics Act 2010. Here are some steps you can take.

References

Alhusainy W, Paini A, Punt A et al 2010 Identification of nevadensin as an important herb-based constituent inhibiting estragole bioactivation and physiology-based biokinetic modeling of its possible in vivo effect. Toxicology & Applied Pharmacology 245:179-190

Anderson BE, Zeiger E, Shelby MD et al 1990 Chromosome aberration and sister chromatid exchange test results with 42 chemicals. Environmental & Molecular Mutagenesis 16(Suppl. 18):55-137

Aruna K, Sivaramakrishnan VM 1996 Anticarcinogenic effects of the essential oils from cumin, poppy and basil. Phytotherapy Research 10:577-580

Connor TH, Theiss JC, Hanna HA et al 1985 Genotoxicity of organic chemicals frequently found in the air of mobile homes. Toxicology Letters 25:33-40

Dasgupta T, Rao AR, Yadava PK 2004 Chemomodulatory efficacy of basil leaf (Ocimum basilicum) on drug metabolizing and antioxidant enzymes, and on carcinogen-induced skin and forestomach papillomagenesis. Phytomedicine 11:139-151

De Oliveira AC, Ribeiro-Pinto LF, Paumgartten FJ 1997 In vitro inhibition of CYP2B1 monooxygenase by b-myrcene and other monoterpenoid compounds. Toxicology Letters 92:39-46

Florin I, Rutberg L, Curvall M et al 1980 Screening of tobacco smoke constituents for mutagenicity using the Ames test. Toxicology 15:219-232

Haworth S, Lawlor T, Mortelmans K et al 1983 Salmonella mutagenicity test results for 250 chemicals. Environmental Mutagenesis 5:3-38

Jeurissen SM, Punt A, Delatour T et al 2008 Basil extract inhibits the sulfotransferase mediated formation of DNA adducts of the procarcinogen 1′-hydroxyestragole by rat and human liver S9 homogenates and in HepG2 human hepatoma cells. Food & Chemical Toxicology 46:2296-2302

Kim MH, Chung WT, Kim YK et al 2001 The effect of the oil of Agastache rugosa O. Kuntze and three of its components on human cancer cell lines. Journal of Essential Oil Research 13:214-218

Kirkland D, Aardema M, Henderson L et al 2005 Evaluation of the ability of a battery of three in vitro genotoxicity tests to discriminate rodent carcinogens and non-carcinogens I. Sensitivity, specificity and relative predictivity. Mutation Research 584:1-256

Kodama, R, Okubo A, Araki E et al 1977 Studies on d-limonene as a gallstone solubilizer (VII). Effects on development of mouse fetuses and offspring. Oyo Yakuri 13:863-873

Manosroi J, Dhumtanom P, Manosroi A 2005 Anti-proliferative activity of essential oil extracted from Thai medicinal plants on KB and P388 cell lines. Cancer Letters 235:114-120

Myhr B, McGregor D, Bowers L et al 1990 L5178Y Mouse lymphoma cell mutation assay results with 41 compounds. Environmental & Molecular Mutagenesis 16(Suppl 18):138-167

Pienta R J 1980 Evaluation and relevance of the Syrian hamster embryo cell system. Applied Methods in Oncology 3:149-169

Sasaki YF, Imanishi H, Ohta T et al 1989 Modifying effects of components of plant essence on the induction of sister-chromatid exchanges in cultured Chinese hamster ovary cells. Mutation Research 226:103-110

Sekihashi A, Yamamoto A, Matsumura Y et al 2002 Comparative investigation of multiple organs of mice and rats in the comet assay. Mutation Research 517:53-74

Sotiroudis TG, Kyrtopoulos SA 2008 Anticarcinogenic compounds of olive oil and related biomarkers. European Journal of Nutrition 47:69-72

Turner SD, Tinwell H, Piegorsch W et al 2001 The male rat carcinogens limonene and sodium saccharin are not mutagenic to male Big Blue rats. Mutagenesis 16:329-332

Vocanson M, Goujon C, Chabeau G et al 2006 The skin allergenic properties of chemicals may depend on contaminants – evidence from studies on coumarin. International Archives of Allergy & Immunology 140:231-238

Vocanson M, Valeyrie M, Rozières A et al 2007 Lack of evidence for allergenic properties of coumarin in a fragrance allergy mouse model. Contact Dermatitis 57:361-364

Watabe T, Hiratsuka A, Isobe M et al 1980 Metabolism of d-limonene by hepatic microsomes to non-mutagenic epoxides toward Salmonella typhimurium. Biochemical Pharmacology 29:1068-1071

Watabe T, Hiratsuka A, Ozawa N et al 1981 A comparative study on the metabolism of d-limonene and 4-vinylcyclohex-1-ene by hepatic microsomes. Xenobiotica 11(5):333-344

Some of the more common Internet comments about the hormonal effects of clary sage oil include:

* Clary sage essential oil contains sclareol, which mimics the effects of estrogen.

* Sclareol has an estrogen-like structure, contributing to clary sage’s effectiveness in treating amenorrhea, cramps, and menstrual pain.

* Sclareol, a compound in clary sage, is not an estrogen, although it can mimic estrogen if there is an estrogen deficiency. If there is not an estrogen deficiency, sclareol will not create more estrogen in the body.

* Certain essential oils have phytoestrogenic activity.  For example, sclareol, a constituent of clary sage, stimulates the body to produce its own estrogen.

* The high sclareol content gives clary sage essential oil its powerful action for relieving premenstrual tension in women as it has a balancing effect on hormones.

Note that four distinct claims are made in the above:

1) Clary sage/sclareol mimics the effects of natural estrogens.

2) Clary sage/sclareol mimics the effects of natural estrogens, but only if there is an estrogen deficiency.

3) Clary sage/sclareol stimulates the body to produce its own estrogen.

4) Clary sage/sclareol balances hormones.

Only the first of these is in line with the original statement made by Franchomme & Pénöel (1990). But is any of this supported by evidence? One of my first blogs was about parabens, and I made reference to the possibility that these chemicals might have estrogen-like effects. Many people avoid parabens for this very reason. Substances with such “hormone-disrupting” action are suspected of adversely affecting male fertility and breast cancer, among others.

So, let me pose an obvious question: if clary sage oil has an estrogen-like effect, and if you avoid parabens because you believe that they have estrogen-like effects, do you similarly avoid clary sage oil?

If you look at Dene Godfrey’s comment on The Paraben Parable you will see that butylparaben was indeed estrogen-like in an in vitro study, with an action 100,000 times weaker than estradiol. But one in vitro test tells us very little about in vivo effects. As for sclareol, I am aware of no research that has any bearing on a possible hormonal action. [Clary sage oil is sometimes contraindicated in pregnancy, though there is no supporting evidence for this. It was used in two childbirth studies in the UK, with no apparent adverse effects (Burns et al 2000, 2007)].

Both estradiol and butylparaben contain a phenol functional group: a hydroxyl group (OH) attached to a benzene ring. The phenolic structure is important for estrogenicity, as is the presence of a second ring (Anstead et al 1997, Blair et al 2000). However, sclareol does not contain a phenolic structure, it doesn’t even contain a benzene ring. Sclareol is a labdane diterpene, and this class of molecule does not incorporate estrogen-like structures, nor is it noted for estrogenic activity (Topçu and Gören 2007).

Therefore, on the basis of its structure, sclareol is unlikely to have any estrogenic action. Even if sclareol was estrogenic, at about 4% of clary sage oil, it would have to have a very high binding affinity for estrogen receptor sites for the essential oil to have any effect, and this is extremely unlikely.

This does not mean that clary sage oil is not effective. It may well be useful in relieving menstrual pain, pre-menstrual symptoms, menopausal symptoms and other problems, but none of this necessitates an estrogen-like action. And, I’m not saying that sclareol could not possibly be estrogen-like, I’m just saying there’s no evidence that it is, nor does its structure suggest such an effect. This also means that there’s no evidence to support clary sage oil “balancing hormones”, mimicking estrogens only if there is an estrogen deficiency, or stimulating the body to produce natural estrogens.

Sclareol does have an interesting anticancer activity, including in vitro action against human breast cancer MCF-7 cells (Dimas et al 2006). An isomer, 13-epi-sclareol, which is also present in clary sage oil, inhibits the growth of breast and uterine cancers in vitro, and was slightly more potent than Tamoxifen, but was not toxic to normal cells (Sashidhara et al 2007). This suggests the possibility that sclareol might actually inhibit estrogen, and might after all have some capacity to interact with estrogen receptor sites. What we do know is that sclareol will not give you breast cancer.

Thanks to Sherrie Bitts for raising the question of sclareol safety on the Aromatherapy Thymes blog, and to Lora Cantele for suggesting this to me as a subject.

References

Anstead GM, Carlson KE, Katzenellenbogen JA 1997 The estradiol pharmacophore: ligand structure-estrogen receptor binding affinity relationships and a model for the receptor binding site.

Blair RM, Fang H, Branham WS et al 2000 The estrogen receptor relative binding affinities of 188 natural and xenochemicals: structural diversity of ligands. Toxicological Sciences 54:138-153

Burns E E, Blamey C, Ersser S J et al 2000 An investigation into the use of aromatherapy in intrapartum midwifery practice. Journal of Alternative & Complementary Medicine 6:141-147

Burns E, Zobbi V, Panzeri D et al 2007 Aromatherapy in childbirth: a pilot randomised controlled trial. BJOG 114:838-844

Dimas K, Papadaki M, Tsimplouli C et al 2006 Labd-14-ene-8,13-diol (sclareol) induces cell cycle arrest and apoptosis in human breast cancer cells and enhances the activity of anticancer drugs. Biomedicine & Pharmacotherapy 60:127-133

Franchomme P, Pénöel D 1990 L’aromathérapie exactement. Jollois, Limoges

Sashidhara KV, Rosaiah JN, Kumar A 2007 Cell growth inhibitory action of an unusual labdane diterpene, 13-epi-sclareol in breast and uterine cancers in vitro. Phytotherapy Research 21:1105-1108

Topçu G, Gören AC 2007 Biological activity of diterpenoids isolated from Anatolian Lamiaceae plants. Records of Natural Products 1:1-16

One rainy autumn afternoon, while I was still working on the book, I took a train from London to Cambridge, because I knew that Trinity College Library had a copy of a book I wanted to look at. It had no apparent title, was hand-written in the 13th century, and was described in the catalogue as “A medical work in French apparently based on the Chirurgia of Roger of Salerno.” I don’t remember why I thought it would be useful.

By the time I got to Trinity College Library, filled out a book application, and waited about 30 minutes for the small, compact volume to be delivered to my seat, there wasn’t much time left before the library closed. Old manuscripts are written in a dense, gothic script. Even English manuscripts sometimes look at first like another language. You have to read each word with great care to decipher it. This was my first experience of Medieval French. Time was pressing hard, and I was looking for some words about essential oils! I settled on a passage about frankincense. Not quite the treasure I had hoped for but at least something aromatic, with a rare reference to energetic properties.

Handling old, hand-written books has always been an awesome experience for me, almost like going back in time and feeling what the person who wrote the book was feeling. Most times, I would imagine that I had written it myself, in a previous incarnation. But not this time. In spite of my French heritage (my father was French) the book seemed totally foreign.

As I made my way back home on the rattling train in the dark wet evening I was excited. I was re-discovering the ancient roots of aromatherapy. I was fulfilling a self-appointed mission. In the 1970s there was not much published scientific research on essential oils, and the past seemed an equally valid route to knowledge. So, I had plunged in. My father helped me translate my ten lines, but even so, two of the words resisted translation. Here is the result of my afternoon’s adventures:

Olibanum ceo est encens, il est chaud et Seche el secunde de grei; il ad verru de conforter et de afermer, de traire ensemble, et de rettreindre. Il est bon, en auttre, les fermer des oyls et la dolur de denz, et encontre le hunel et encontre la grossesse et la rouillor des nariles et encontre in digestiun et amer eruc tuations et pur les mameles en greder un podre confit ad eysil e enplastre sur un dray e nus sur le mameles. roine chaude et seche el secunde de grei. Ele advertu a de faire e a degant.

Olibanum is known as frankincense, it is hot and dry in the second degree; it has the capacity to comfort and to fortify, to bring together, and to bind. It is also good for the shutting of the eyes, toothache, and against le hunel [?], and against pregnancy and soreness of the nostrils, and also indigestion and sour eructations. For the breasts, make up a powder prepared with vinegar and plaster on a sheet, and place it on the naked breasts. An excellent remedy, hot and dry in the second degree, it has the property of forming and degant [?].

The last word “gant” here is a verb. As a noun, it means “glove”. Perhaps “de gant” was another way of saying to hold, to bind, to bring together.

P&G’s promise to reformulate its Herbal Essences line follows a notice of intent to file a lawsuit filed by the GPWG against P&G (as well as lawsuits filed by the California Attorney General’s office in June 2008 directed at other manufacturers) for dangerous levels of 1,4-dioxane as established by proposition 65. The OCA, CSC, and GPWG consider cooperation from industry leader P&G (with a 40% share of the hair care market in 2003) to be a significant step forward in the campaign for all brands to remove unnecessary 1,4-dioxane and other carcinogenic and harmful chemicals from consumer products.

1,4-dioxane is generated as a byproduct of ethoxylation, a cheap shortcut used by companies to provide mildness to harsh cleaning ingredients, which requires use of the cancer-causing petrochemical ethylene oxide. 1,4-dioxane is considered a chemical “known to the State of California to cause cancer” under proposition 65, and is also suspected as a kidney toxicant, neurotoxicant and respiratory toxicant, among others, according to the California EPA.

While previous press conferences on this topic have revealed the presence of 1,4-dioxane in personal care and household cleaning products (including products targeted at babies and children) and tracked improvement as certain “natural” and conventional brands reformulated, this year’s press conference will focus on the problem of groundwater and reclaimed water contamination resulting from the toxin’s presence in laundry detergents, and health risks from the chemical’s presence in drinking water. David Steinman is the author of Diet for a Poisoned Planet and formerly represented the public interest on a committee at the National Academy of Sciences.

There is an assumption that safety legislation passed in Europe is somehow intrinsically right, of a higher standard, and deserving of our close attention. Some of it may indeed be, but the general assumption is misplaced. The bill that has created the most anguish, controversy and chaos – in Europe – concerns allergens. It is regarded with skepticism by some dermatologists, and its scientific basis is seriously flawed, as I will explain momentarily. There is no evidence so far that it has done anything to reduce adverse reactions to cosmetics, but it has negatively affected essential oil production and availability. Many suspect that it has spurred the larger fragrance manufacturers to turn to alternative synthetic materials that have not been subject to such stringent safety testing. Even in Europe, fragrance ingredients do not have to be listed.

Linalool is one of the 26 fragrance materials listed as an allergen in the European Union. If present in a cosmetic product at over 100 ppm (0.01%) in a wash-off product or 10 ppm (0.001%) in a leave-on product, linalool must be declared on the ingredient list if sold in an EU member state. Doesn’t sound too bad, does it? The problem is, neither manufacturers nor retailers want to get sued, or branded as selling unsafe products, and most retailers will only carry cosmetics that have passed an independent safety assessment, which is almost entirely based on looking at the levels of “allergens”. So the de facto result is that very few manufacturers take the risk of having a “known allergen” in a product at over the declarable amount.

Linalool is a major constituent of ho wood, ho leaf, rosewood, coriander seed, neroli, lavender, lavandin, bergamot, ylang-ylang, clary sage and petitgrain, and is found in some 200 other essential oils. But the really strange part is, linalool is not a high-risk allergen. In fact, it’s superlatively safe on the skin. Between 1969 and 2007 (38 years), a total of thirteen dermatitis patients out of the 25,164 tested, (0.05%) were allergic to linalool when patch tested, and less than this actually had allergic reactions to products containing linalool. Yes, 0.05% is more than zero, but it’s pretty close to the 0.03% reaction rate for petrolatum, the least dermally allergenic substance known to mankind. One way of looking at this is that adding linalool to a product increases risk by about 0.02%. That’s probably less than almost any other known cosmetic ingredient.

So why did the EU list linalool as an allergen? Because – according to their own report – five dermatitis patients had allergic reactions to it over a five-year period on patch testing, and at the time, their criteria for listing a substance included two or more reports of allergic reaction. Incredible, but true. Considering that linalool is (or at least used to be) one of the most commonly-occurring fragrance materials, an average of one reported reaction per year, on planet earth, is about a negligible as it is possible to get.

So, I’m just saying… if you think European safety regulations are a shining example of how things should be done, I suggest you re-consider. This one, at least, has been a massively expensive and largely misdirected fiasco.