Ess ENTI A L

OIL SAF E T Y I
ROBERT T ISSERAND

The first of a three part series based on a presentation given at

I Aroma ‘95. The full transcript is published in the Conference

Proceedings. Part two will appear in the next issue.

T
he study of essential oil between the essential oil and the component. This is because the
safety raises issues human body. components of an essential oil can
fundamental to the practice affect each other’s biological action,
of aromatherapy, such as essential oil either by enhancing properties
integrity, chemical composition, (synergy) or by reducing them
metabolism, and the relevance of (antagonism). See table 1.
animal testing. New information on When discussing essential oil safety Synergy and antagonism can
phototoxicity, neurotoxicity, it is important to bear in mind that affect the toxicology of an essential
reproductive toxicity and different chemotypes of the same oil oil, just as they also influence
carcinogenesis will be presented in will frequently demonstrate great its therapeutic action. However, it
the context of these issues. differences in levels of toxicity. This is difficult to predict when
Unfortunately essential oil is because the major component in either synergy or antagonism will
safety is also an area where each rhemotype plays a significant in fact take place, and what form
confusion is rife. Sources of role in the toxicity of that essential it will take. For example, if
information given on safety in oil. It is also worth remembering we know that an essential
consumer books are frequently that, although many chemotypes oil contains a large percentage of
unknown or dubious, and yet exist for many essential oils, they are a toxic component, it would
pronouncements, frequently without not always commercially available. be unwise to assume that some
any supporting evidence, are treated Essential oils are chemically other component of the oil will
as established Pacts. complex, and typically contain over reduce the toxic effect of the
Essential oil safety is a big 100 components with one, two OI component. In theory, it is just as
subject, and one that my colleague sometimes three of these likely that the toxicity of the main
Tony Ralars and myself started dominating in terms of percentage. component will be enhanced, not
researching, in great depth, in 1991. while it is true that components can reduced, by other chemicals present
The aim of that project was to gather and do modify each others’ in the oil.
data for a definitive textbook, and biological action, it is also true that M’har this means in practice,
thus shed light on the confusion. In the major components tend to 1 believe, is that an essential
this article I will concentrate on just dominate both pharmacological oil containing a worrying quantit!
a few examples. As well as and toxicological effects. Less of a toxic component should
highlighting some areas of risk, 1 commonly, minor components have be assumed dangerous until
want to debunk one OI- Two myths, been found to play an important proven safe. A classic example of
and I also want to emphasise the biological role. this scenario can he found in
great importance of being educated It is sometimes said that safety the estl-agole (= methyl chavicol)
in the science of emential oils and, data on essential oil componenrs chemotype of hasil oil (table 2).
in particular, of. knowing the may not be relevant, since a whole Estragole is known to he
chemical composition of each oil wc essential oil ma\ have a different carcinogenic in rodents, and
use, and of the process ofinteracrion action to thar of its ma, j 0 L the likelihood is that it will
alSo be carcinogenic in humans, more rapidly oxidation will take principal sensitising agent is believed
if sufficient quantity enters place. One implication of chemical to be oxidised delta-3-carene [Pirili
the body. (I will discuss this point degradation is that it involves a & Siltanen, 1957; Pirila et al., 1964;
in more detail later on.) chemical change in the essential oil. Opdyke, 1973; Opdyke, 19761.
Because of this chemical change both In tests using various undiluted
the efficacy and the safety of an citrus oils on 1nouse skin, orange,
essential oil can be altered from the lime, lemon and grapefruit oils were
norm. all been found to produce tumours at
Another factor affecting the In one recent study where the site of application [Roe 8c Pierce,
composition of an essential oil, lemongrass oil was intentionally 1960; Roe, 1959; Pierce, 1961; Roe &
is what we could call its oxidised, it was found to have lost Field, 19651. It is important to bear
integrity. Integrity would include, for much of its antibacterial activity in mind that these turnout-s appear in
instance, the possibility of when compared to fresh, unoxidised mice who have been primed with a
contamination or adulteration, but lemongrass oil [Orafidiya, 19931. In cancer initiator, and that the
right now I want to focus on extensively oxidised samples essential oils do not give rise to
degradation. antibacterial activity was completely tumours on their own. Some of the
Chemical degradation is the lost. In bitter almond oil the major tumours produced were malignant,
process by which the quality of a component, benLaldehyde, tends to and some were benign.
chemical substance is reduced over oxidise to benzoic acid [Budavari, In searching for the component
time. In the case of essential oils for 19891. BenLoic acid is not dangerous, of citrus oils causing these tumours,
nromatherapy it is definitely in f&t it occurs widely in nature, and suspicion fell on d-limonene, and
undesirable, and tends to OCCIW on is used as a food preservative. these suspicions were eventually
prolonged storage, or unclct- poor However, it does not possess the conf.irmed. However, further
storage conditions. The three major therapeutic properties (immune research revealed that it was not tl-
factors responsible for essential oil stimulant and anticarcino~enic) limoncne itself which caused the
degradatioil are: associated with benzalclehyde. problem, but chemicals for1necl bv
A more serious implication of the oxidation of d-limonene, which is
0 atmospheric ox>grn degradation is that chemical change an unstable terpenc [Hornburger Xc
0 heat can render essential oils more Boger, 19681, The implication of this
0 light. hazardous. Terpene degradation in is that only old, oxidised citrus oils
certain oils leads to compounds would be capable of cauai11g an)
Atinosphri-ic osygcn call being formed \vhich make the oils prol~ltms.
rhange the chemical composition potential skin sensitisers, while fresh Paradoxically, more rccc11t

of’ an essential oil by combining oils are safe to use. Examples include research has demonstrated that cl-
with SOl,,C of its components. terebinth and all pine oils; the limonene itself is antitumoral, a11d
This process is called prevents malignant
oxidation and tends tumours in 1-odents
to OCCIII‘in essential primed with callce1
:)ils rich in terpene\, i n i t i a t 0 r s
SUCll ;ts 1e111011 and [Homburger et al.,
piile. I.imonene and 1971; Elegbede et
pinene, the relative al., 1984; Elegbede
major components, et al., 1986]. The
Ire both somewhat earl\ tests, it is
Irnstablc terpenes. assumed, must have
Oxidation ia all used oxidised
,peetled up bp both citrus oils 01

heat and light: this is oxidisrd limonrne.

,vhv it is important to Although cvt!,,

<to,-c essential oils in oxidiscd citrus oils

-lark bottlrs and are ye,-y u11likely to
Iway 1’1~oni \ourceh of present a hazai-d in
thral. The more ail- aromatherapy, this
there is in a bottlr of ,%3earct1 very 1nuct1

2srntial oil 1hC underlines the

importance of using relatively fresh highest dose which was non-fatal (24
essential oils, which have not ml) this gives us a human lethal dose
oxidised. The relevance of tests on animals is of between 0.23 g/kg and 0.37 g/kg,
It is recommended that, in frequently called into question, not assuming the individuals were of
general, essential oils should be used least by toxicologists themselves. average weight. This compares with
within I year of purchase, or 1 year of However, for those of us who an LD,,, of 1.2 g/kg for methyl
first opening the bottle. The best instinctively rebel against the whole salicylate in rodents; 4-8 ml of methyl
single way to maximise the useful notion of animal testing there is a salicylate is considered a lethal dose
lifespan of essential oils is to store tendency for emotion to cloud the for a child [Opdyke, 19781. If these
them in a cool place, such as a issue. figures do represent reality, this
refrigerator. Oils kept in this way will Most essential oil toxicity testing means that wintergreen oil is three to
keep for roughly twice as long, i.e. 2 is carried out using rats or mice, and five times more toxic in humans than
years following purchase. Essential there is one ma_jor problem with it is in rodents.
oils which readily degrade should using toxicity data obtained in Wintergreen is a useful oil to
ideally be used within 6 months of rodents. Both the skin and make comparisons with, because
purchase, or 12 months if kept cool. metabolism of rodents are different there are many recorded cases of
Note that some essential oils, poisoning to draw on

when refrigerated, become compared to other essential

BASILOILCHEMOTYPES
more viscous, and may be oils, and because chemical
difficult to pour. variation between different
Another useful way to wintergreen oils is minimal.
avoid degraded oils is never to The variation in toxicity seen
buy oils in clear glass bottles. between the cases cited above
Light rays can damage may be due to differences in
undiluted oils (especially citrus body weight and/or differences
oils again) by causing the in individual health status.
formation of free radicals. Four of the cases cited were
Coloured glass bottles give between 21 and 28 years old,
sufficient protection against one was 55, and one was adult,
light rays to prevent this age unknown.
happening.
I have heard Eucalyptus
aromatherapists say that oils of to those of humans. Therefore, the Eucalyptus oil seems to be fatal to
patchouli, sandalwood and results obtained by animal testing, humans in amounts between 30 ml
f1-ankincense are all best 11sed when while often having considerable and 60 ml [Gurr and Scroggie,
aged. In the case of patchouli, it is relevance, cannot be assu1ned to 19651. If true, this would make it
certainly true that aged oils are reliably indicate the results which some S-6 times 1nore toxic in humans
sometimes used in perfumery, and human testing would give. It is than in laboratory animals.
this is to make use of a particular type interesting to compare rodent
of fragrance note. However, 1 am not toxicity data with cases of poisoning Pennyroyal
aware of any reason whv this would in humans. Comparison indicates RIFM give the rat oral LD,,, for
be desirable in aromatherapy. that, in some instances, rodent pennyroyal oil as 0.4 g/kg [Opdyke,
Certainly, patchouli oil is terpene- toxicity data give a poor indication of 19741 equivalent to about 30 g (or 35
rich, and it seen1s likely that either human toxicity (table 3). ml) in an adult. In two cases one fluid
the cfficac) or the safety of the ounce (about 30 ml) of pennyroyal
essential oil might hc adverselv Wintergreen oil produced a fatal outcome when
affected through terpene oxidation Taking six cases of winter-green oil ingested hy an adult [Allen, 1897;
on aging. For frankincense oil, poisoning in adult humans, three Anon., 19781. In three cases half the
oxidation of pinene is very likely to people died from ingestion of 1.5 ml, amount of ingested pennyroyal oil
lead to safety problems, and this oil 30 ml and 80 ml respectively; three (15 ml) produced symptoms 01
should certainly bc rrsed as fresh as survived after ingesting 6 ml, 16 ml poisoning, but 11ot death
possible. \Vith sandalwood, aged oils and 24 ml [Stevenson, 19371. None [Braithwaite, 1906; Jones, 1913;
certainly do degrade, and fresh oils of these cases received anv medical Buechel et al., 19X3]. In the case of
would he highl! drsir-able for intervention. If we take the lowest pennyroyal the animal data seem to
therapeutic use. dos:e which was fatal (15 ml) and the correlate well with human toxicity.
Apiol higher levels in tonka bean products. damage in the liver [Gangoli et al.,
Apiol is an abortifacient, and is used Chronic oral administration of 19741. In another study, coumarin was
to procure illegal abortion in Italy. It coumarin has produced severe liver administered to baboons for between
is found as a major component of damage at a level of 2500 p.p.m. in the 16 and 24 months at 2.5, 7.5, 22.5 ot
parsley leaf (~18%) parsleyseed (21- diet of rats and 100 mg/kg per day 67.5 mg/kg/day [Evans et al., 19791.
80%) and Indian dill seed (20-30%) for dogs [Hazleton et al., 19561. This At the highest dose level only, an
oils. In animal studies, considerably hepatotoxicity was confirmed by increase in liver weight was noted, and
higher dosages of apiol appear to be subsequent research [Hagdn et al., ultrastructural examination of the
tolerated compared to humans. In 1967; Bar and Griepentrog, 19671 and liver revealed dilatation of the
pregnant guinea pigs, abortion one of these studies reported finding endoplasmic reticulum.
generally did not occur except at bile duct carcinomas in coumarin-fed In clinical trials using coumarin
lethal doses, around 2 g [D’Aprile, rats [BBr and Criepentrog, 19671. as an anti-cancer agent only 0.37% of
19281. In pregnant rabbits, abortion Coumarin shows a high toxicity in patients developed (reversible)
occurred at dosages of 5-14 g, with several animals; its acute oral L.D,,, is abnormal liver function. The majority
severe haemorrhage [Patoir et al., 0.2 g/kg in both guinea pigs and of 2,173 patients received 100
19361. In both types of animal, the mice [Opdykc, 19741 and 0.68 g/kg mg/day of coumarin for 1 month,
dosage is equivalent to in rats [lenner et al., 19641. Based on followed by 50 mg/day for 2 years.
approximatel! 100-200 g in a all the animal data, the FDA (The other patients received between
human. This is some 20-40 times prohibited the llse of comnarin in 25 mg/day and 2000 mg/day.) Of
higher than the amount of apiol food in 1954; hoth the UK and EC the total, only eight patients
carlsin,g ahortion in humanr. ‘standard permitted proportion’ of developed elevated live, enLvme
coumarin in food flarourings is 0.002 levels, which returned to normal on
Camphor g/kg [Anon., 1988; Anon., 19921. stopping the coumarin [Cox et al.,
Camphor (the chemical not the oil) It was noticed by several workers I9891 On this evidence, coumarin
is thought to he significant]) that there was a significant cannot be regarded as hepatotoxic in
(perhaps JO times) nicjre toxic in interspecies difference in the wan hllrnalls.
humans than in I-odents. The coumarin was metaholised [Booth et (The second baboon study
probable oral lethal dose in humans al., 1959; Shilling et al., 1969; Gangoli indicates a no-effect level of 22..5
is reckoned to be 0.005-0.5 g/kg, et al., 1974; Cohen, 19791. Fol mg/kg/day, which equates to around
compared to an animal oral lethal example, the percentage of orall) 1.5 g/day for an average (65 kg)
dose of 0.5-15 g/kg [Gleason et al, administered coumarin excreted in adult human. This dosage level is 30
19841. The f.atal dose of camphor for the urine as 7-hydroxycoumarin is 1% times higher- than the 50 mg/da)
children is reported iis being about 1 in the guinea pig, 3% in the dog, 19%, received by many of the cancc~‘
g [Rlthin ct al., 19493 in the cat, and 60% in the baboon patients for 2 years.)
[Gangoli et al., 19741. In the 1970s In comparison with rodent
Coumarin the relevance of. the animal data to toxicity, we have seen two examples of
Corimarin is a lactonr found in humans was being srrioush essential oils which appear to be more
quantity in several absolutes, and ill questioned. One *tuc1\, giving toxic in humaiis and one example of
very small amounts in a few essential coumarin to baboons at 50 p.p.m. similar toxicity. Looking at essential
oils. It is a major component (40%) and 100 p,p.m, (9 weeks at each oil con~ponents. we have seen two
of flouve oil and occur\ at c‘vci1 dosage level) did find histological instances of increased toxicity in
humans, and one of i-educed toxicity. sull’intossicazioIle da apiolo. Annali di 0 Opdyke, D. 1.. J. (1976)
It seems apparent that sometimes ostrtric1n P Ginrcologin 50: 1204-1227. Monographs on fragrance raw
animal toxicology data extrapolate 0 Elegbede, J .A. et al. (19X6) materials. Foot/ urln Cosmetics 7hxirology
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essential oils, very often they do not. It tumours following dietary d-limonene. 0 Opdyke, D. 1~. J. (1978)
is probably unwise to make sweeping Journal of the Nntioncrl Cancer Inrlitctte Monographs 011 fragrance raw
statements about how relevant or 76 (2): 323-325. materials. Food nnd Casmrtir.s 7‘oxicolo,qy
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