Toxicity Myths the Actual Risks of Essential Oil Use
by Ron Guba Part 3
Essential Oils and Medical Conditions:
There are other, oft-repeated statements about the use of essential oils in certain medical conditions (it does seem that many Aromatherapy statements are copied from author to author to author…):
“Essential oils not to be used with high blood pressure”
The essential oils of Hyssop, Rosemary, Sage and Thyme are most often listed as oils “not to be used in high blood pressure” (51, 52). I am not certain where these statements originated from, but there is no
support to be found anywhere in available literature. No such contraindications appear in herbal texts (53, 54), in more scientifically based phytotherapy texts (55, 56) nor in French Aromatherapy texts. (57, 58)
Some essential oils have been shown to have hypotensive effects in laboratory animals, such as Garlic, Tagetes, Geranium and True Lavender. (59) Only one essential oil, Clary Sage, was shown to produce a slight increase in both systolic and diastolic blood pressure. (60) However, these effects generally take huge dosages, Clary Sage required a dose of 1.0 gram per kg about 70 grams for an average adult!
In summary, neither evidence nor experience supports the above statements. Such essential oils will not create negative effects in either low or high blood pressure conditions.
“Essential oils not to be used in epilepsy”
The essential oils of Sweet Fennel, Hyssop, Sage and Wormwood are often listed as contraindicated in the case of epilepsy. (61) In this case, such contraindications do have a basis in fact. Large doses of
monoterpenic ketones, notably pinocamphone. thujone, camphor and pulegone, have been found to create epileptiform seizures in both animals and humans.(62) This would include, then, the more common essential oils of Wormwood, Mugwort, Buchu, Hyssop, Pennyroyal, Sage and Thuja. Hence, those with epilepsy (as well as people with high fevers) have a lower threshold to CNS (central nervous system) stimulant effects of oils containing large amounts of these ketonic compounds.
How Sweet Fennel entered the picture, I am not sure. Dr. Jean Valnet mentions in his book, The Practice of Aromatherapy, “In high doses, fennel causes convulsions (in direct contrast to aniseed). (I assume in animals italics mine) The essence makes animals timid.”
To comment, firstly no dosages are mentioned (I would assume a large dose). Interestingly, both Sweet Fennel and Anise Seed oils contain high amounts of trans-anethole (up to 70% and 96%, respectively). If anethole were the responsible agent, similar actions would be seen.
I theorise that a “Bitter” Fennel (Foeniculum vulare var. vulgare) may have been used. The ketone, fenchone, with potential epileptic effects at high doses, is present at up to 18% in the essential oil,
whereas Sweet Fennel (Foeniculum vulgare var. dulce) contains generally less than 3%. (63)
No other study suggests this potential effect of either Sweet or Bitter Fennel oil. Given the available information, there is no reason to not use Sweet Fennel, certainly, even in those with epilepsy.
Lastly, people whose epileptic seizures are under full control by medication, do not then appear to any more sensitive to such essential oils then those without epilepsy. Low-dose topical uses of such essential oils should be without incident. (64) Such contraindications (even for low-dose topical use) would most
specifically be true for those with uncontrolled epilepsy, or those with high fevers.
“Essential oils as kidney irritants”
Juniper “Berries” (Juniperus communis ssp. communis) and the essential oil derived from them, have long been indicated as a useful diuretic. (65)
However, since the late 1800’s onwards, Juniper essential oil (and other high-terpene hydrocarbon containing essential oils, such as in various Pinus species) has been suggested to be a kidney irritant, that
should not be used on a long-term basis nor during acute kidney disease. Such statements are still mentioned in a number of Aromatherapy texts. It appears that the origin of these statements came from the use of large, fatal doses of Juniper oil being given to dogs. Such high doses cause clouding of the urine, which was then assumed to be due to kidney damage. It appears, though, that such cloudiness was simply due to the presence of large quantities of Juniper oil metabolites.
More recent studies using laboratory rats have found no kidney damage, even when high oral doses of Juniper oil were given.
The authors hypothesised that the reputation of Juniper oil as a kidney irritant may have come from the use of essential oils containing high levels of the monoterpene hydrocarbons, a- & ß-pinene. The Juniper
oil used in the study was said to have low levels of pinenes. (66) This study does highlight the non-irritancy of Juniper Berry oil. But the further hypothesis regarding the irritancy of pinenes does appear to be unfounded.
Both Juniper Berry and Juniper branches/berries essential oil contain significant amounts of a- & ß-pinene, as well as other terpene hydrocarbons (Juniper Berry a-pinene up to 46%, sabinene up to 28%,
myrcene up to 8% and Juniper branches/berries a-pinene from 40 to 90%, sabinene from 10 to 40%). (67) Given such similarities in terpene hydrocarbon content, such a hypothesis is not supported.
Further, a number of reports concerning the ingestion of massive amounts (up to 500mL) of Pine essential oil (from Pinus pinaster and related species), which generally consists of up to 90% of a- &
ß-pinene, do not show any kidney dysfunction nor damage. Arguably, both gastric lavage and hemoperfusion are generally employed to reduce the quantity of essential oil compounds from both the stomach and the blood circulation (a lethal dose of “Pine” oil is approximately from 60 to 120mL). Nevertheless large quantities of metabolites, such as bornyl acetate are still excreted via the kidneys over a number of days. (68)
Of all the essential oil compounds, only apiol (as in Parsley Seed oil) has been shown to create kidney damage, as observed in post-mortem studies. Obviously, these represented large, fatal doses of apiol; the
lowest acute fatal dose was 6.3 grams, while up to a dose of 19 grams has been survived. (69)
Given the comparatively tiny doses that would be used in Aromatherapy treatments, even orally, we can see that such dosages do not pose any threat to the kidneys, even with extended use. Of course,
acute (such as glomerulonephritis) or advanced kidney disease (such as requiring dialysis) is where caution must be taken, not just for such essential oils, but for a wide variety of drugs.
Essential oils and other medical conditions:
There are both known and potential contraindications for the use of essential oils in certain medical conditions (such as high-menthol containing essential oils in heart disease with cardiac fibrillation)
and combined with other drugs (such as using high-methyl salicylate containing oils in conjunction with warfarin anti-coagulant therapy).
With the exception of the two above examples, such contraindications are for the oral ingestion of essential oils, not topical applications. (70)
Essential Oil “First Aid”
As with most medicinal drugs, whether of a “synthetic” or a “natural” origin, the compounds present in essential oils have the potential to create serious, even fatal toxic effects, if ingested in overly large quantities.
There are numerous cases reported in toxicological literature regarding both serious (non-fatal) and fatal outcomes of essential oil ingestion in both children and adults. These cases are generally due to accidental ingestion by young children, attempts at creating abortions in past years and the use of
essential oils for suicide attempts. There are more rare cases of toxic effects due to overly large doses of specific essential oils being “self-prescribed”, “prescribed” to children by parents or prescribed to
clients by ill-informed therapists.
Most essential oil compounds have a “non-specific” toxic effect, whereby the absorption of these lipophilic compounds into cellular membranes can eventually lead to disruption of membrane permeability.
The primary toxic outcome is that of the disruption of ion channel function in nerve cells, first affecting the heart and central nervous system, leading to cardiac and respiratory depression. (71) To create such effects, however, require huge dosages, in the order of 300mL and beyond.
Certain aromatic compounds, most notably 1,8 cineole (as in many Eucalyptus species), camphor (borneone) (as an isolated compound or as in Rosmarinus officinalis CT camphor and Lavandula latifolia) and methyl salicylate (as a synthetically derived compound or as in Gaultheria procumbens) have specific toxic effects at much lower doses. These compounds make up the bulk of both serious and fatal poisonings in children and adults, due not just to their toxicity, but to the common availability of products containing these compounds and their reputed beneficial properties. (72)
Given the rapid and almost complete absorption of essential oils ingested orally, this route of administration has the highest potential for toxic effects.
First aid measures for ingestion of significant amounts of particularly toxic essential oils (such as more than 2mL of high-cineole Eucalyptus oils in young children) is straightforward: take the child to
the nearest hospital emergency room or at least call or a Poisons Information Centre for instructions. The vast majority of accidental essential oil ingestion in children result in few, if any symptoms and resolve safely with no medical intervention. (73)
It is often difficult to determine just how much of an essential oil (or any product) a young child has ingested. If toxic symptoms do begin to develop, gastric lavage, hemodialysis and other supportive
medical measures may well be necessary. To attempt to either dilute the stomach contents by giving burnt toast (or activated charcoal), milk or other foods or to try to induce vomiting is not recommended. Either
approach, if vomiting occurs, has the potential to allow these volatile compounds to enter the lungs, potentially creating aspiration pneumonia. (74)
“Aromatic Medicine”, or the use of essential oils as ingested herbal medicines by trained physicians and complementary therapists, has not been responsible for any severe cases of toxicity. As with any
“drug”, if an appropriate dose is used (with essential oils, this is often in the range of only 100 to 300 mg per day), toxicity is not an issue.
In the case of the more common practices in Aromatherapy, we are speaking of topical applications in the form of essential oil preparations used in massage treatments, in baths, etc. or in the form of “low dose” inhalations.
Such applications do not create any acute or chronic systemic toxicity the amounts absorbed into the body and the dosages used are far too low.
However, such applications do have the potential to create problems, which include phototoxicity, sensitization and irritant reactions.
Phototoxicity is due to the capacity of various furanocoumarin compounds found in small amounts in some essential oils (most notably, expressed Bergamot and Lime oils, Tagetes, Cumin and Angelica Root; to a lesser degree, the expressed oils of Bitter Orange, Lemon and Grapefruit) to absorb and store ultraviolet wavelengths. This UV radiation is then released in a short, concentrated burst.
When essential oils such as expressed Bergamot are topically applied and the skin exposed to significant amounts of UV radiation in the form of sunlight or tanning beds, a bad “sunburn” is the common
result. In more serious cases this can lead to quite extensive 2nd degree burns.
Another common outcome is that of berloque dermatitis, where patches of overly-pigmented skin develop, which can last for many years.
Lastly, there is evidence to support the promotion of skin cancer, caused by repeated exposure to UV light of mouse skin treated with Bergamot oil (with bergapten as the responsible agent). However, such
results required extensive repeated exposures (5 days per week for 75 weeks), with mice thought to be less capable of repairing DNA damage as compared to humans. Hence, given common uses of such essential oils, carcinogenesis is not an area for concern. (75)
On a more positive note, evidence suggests that the use of photosensitizing essential oils such as Bergamot, along with the use of a sunscreen preparation, provides better protection against UV-induced
skin damage than the use of a sunscreen alone. (76)
First Aid measures - first and foremost should be the provision of appropriate label warnings on packages of any photosensitizing essential oil available for public sale. This is presently far too often not the
case.
In the case of a phototoxic “sunburn” developing, it should be treated as any other burn. If applied soon after exposure, both Vitamin E acetate (up to a 25% concentration) and panthenol (up to a 5% concentration) are excellent at quenching the “free radicals” produced by UV exposure, significantly reducing erythmea and burning. (77)
In terms of treating a burn, there is a good body of both clinical and anecdotal evidence for the wound healing effects of various essential oils (notably True Lavender Lavandula angustifolia, Everlasting Helichrysm italicum and the carbon dioxide extract of Calendula flowers Calendula officinalis), polyunsaturated vegetable oils (such as Rose Hip Rosa rubiginosa) and a variety of herbal extracts (such as the infused oil of Gotu Kola Centella asiatica). (78)
Sensitization refers to the development of an allergic skin reaction to certain aromatic compounds present in some essential oils. Responsible compounds penetrate the epidermis, bind to skin proteins and
provoke an immune reaction that leads to the production of histamine and other irritant compounds by basophils and mast cells. A skin rash or eczema is the usual outcome and subsequent exposure to even tiny amounts of the sensitizing compound can elicit the same response, as well as creating cross-sensitivities to other compounds. (79)
In sensitive individuals, the skin reaction can create quite extensive skin damage, as I have personally witnessed in the case of a friend applying undiluted Tea Tree oil to a small foot wound both feet
developed extensive lesions and required up to six weeks to fully heal.
The compounds most often responsible for sensitization include sesquiterpene lactones (such as costuslactone in Costus and alantolactone in Elecampane), cinnamic aldehyde (as in Cinnamon bark
C. zeylanicum and C. cassia) and oxidized hydrocarbons (such as d-limonene in citrus oils; delta-3-carene, a- & b-pinene as in various Pinus ssp.).
Of potentially sensitizing essential oils, it is Cinnamon oil, old citrus and old pine oils that are commonly available to the public and present the highest risk. The commonly available oils of Tea Tree, Star
Anise, Ylang Ylang and the citral-containing oils of Lemongrass and May Chang pose a slighter risk. (80)
Sensitization reactions (which are relatively rare) can develop in any healthy individual. However, it is clear that individuals already with “hypersensitive” skin and/or present allergies (including those
suffering from eczema, psoriasis and asthma) are more prone to allergic reactions with essential oils.
The most prudent approach, especially for those with present allergic conditions, is to do a simple “patch test” with potentially sensitizing essential oils first. This can be done by preparing a 5% to 10% dilution of the essential oil in question in vegetable oil and applying a few drops to the inner forearm, covering with a “band aid”.
Generally, any sensitization reaction will occur within 24 to 48 hours. Repeat the application twice to be the most certain. If a sensitization reaction does occur to any essential oil, obviously it’s use should be discontinued immediately. Other “risky” essential oils or potential cross-sensitizers should only be used with
caution. The allergic reaction to an individual compound can disappear over time but a patch test before using would be highly advised.
The common treatment for an allergic reaction would be the use of either prescribed or OTC corticosteroid preparations.
Alternatively, some practitioners, including myself, have had anecdotal success with the application of essential oils and herbal extracts with anti-inflammatory properties.
I have personally found the application of a 5% dilution of the carbon dioxide extracts of German Chamomile (Matricaria recutita) and Calendula (Calendula officinalis) in a “hypo-allergenic”, vegetable
oil-based cream to be useful in quenching allergic reactions.
Irritation reactions are not allergic in nature, but represent a level of direct skin damage, followed by an inflammatory response. Irritation reactions arise quickly and are dependent on the amount of the compound applied.
Of essential oils that are commonly available to the public, those containing large amounts of phenols, aromatic aldehydes and oxidized hydrocarbons pose the most risk. This includes the commonly available
essential oils of Cinnamon (bark and leaf), Clove (bud and leaf), Thyme, Oregano, Savoury, Pimento and old, oxidized citrus and pine oils.
As volatile, lipophilic compounds, any essential oil can be irritating if applied to sensitive mucous membranes or skin eyes, genitals, etc. The common Aromatherapy application of using essential
oils in baths (by “floating” them on the surface of the bath water) also increases the potential irritancy of essential oils.
This is another area where the inclusion of appropriate caution statements, use instructions and realistic expiry dates on essential oil packages for public sale would be highly recommended.
The first aid for irritancy reactions is to remove the essential oil as quickly as possible from the skin and/or mucous membranes.
The common method suggested is to wash the affected skin with soap and water and then rinse with water liberally. It has been found with essential oils, however, that the use of water can often increase the
skin irritation initially.
I have found a more effective method is to use a vegetable oil. In this method, apply any vegetable oil to the affected area. Remove with an absorbent towel or cloth. Apply the vegetable oil again and remove,
from three to six times. The vegetable oil removes the essential oil with no irritation.
This method also is excellent for mucous membrane irritation, such as in irritation of the eyes. A bland vegetable oil is used as an eyebath, instead of water or saline solution. I have had the occasion to
use this method myself, accidentally having a large amount of Red Thyme oil splashed into my eyes. The vegetable oil method was very effective, with any eye irritation abating without ten minutes of use.
Summary
In this presentation, I have attempted to cover the fundamental “toxicity myths” that appear in Aromatherapy literature and training courses. There are other topics that can be considered further, such as
the appropriate use of essential oils with children and issues concerning carcinogenic potential.
I personally see no problem in authors and trainers suggesting cautious levels of use. However, I would hope to see such statements given be based on the actual known facts of potential toxicity.
Such statements and recommendations would then be given, not as an “absolute” or as a “forbidden”, but based on personal preference and philosophy.
The present Aromatherapy recommendations commonly given are more than cautious. I sense they are creating more a mood of fear amongst both practitioners and public.
The results in public perception are more prone to the attraction of lawsuits (what do you do if a pregnant client wants to sue you after having received a massage with True Lavender oil and then had a
miscarriage?).
There is also then, a level of suppression of the free and discriminative exploration of the therapeutic possibilities of essential oils, which, we must be clear, are not going to be studied by large pharmaceutical corporations anytime in the foreseeable future. Essential oil compounds are too “simple” and cannot be patented. Hence, there is no present incentive for serious research money to be expended on
“Aromatic Medicine”.
In contrast, there are certainly negative, toxic aspects to the misuse and overdosing of essential oils.
For products available to the public, clear instructions and appropriate cautions should be given. As well, the inclusion of “dropper inserts”, so that liquids are only dispensed slowly as measured drops, should be the requirement for all undiluted essential oils and “fragrance” oils (“perfume” oils mixtures of essential oil isolates, synthetic fragrance compounds, etc.).
Experience strongly suggests that these types of “restrictive flow” inserts would do more to prevent accidental childhood poisonings than child-resistant closures alone.
For those who would use essential oils as a form of complementary therapy, I suggest that training should take into account all aspects of the safe use of essential oils. The common “myths” should be excluded and the real potential for negative effects should be fully understood.
References
1. Pénöel, D. 1998 Natural Home Health Care Using Essential Oils Editions Osmobiose La
Drôme
2. Maury, M. 1992 Giude to Aromatherapy C.W. Daniel Co. Essex
3. Ibid.
4. Schnaubelt, K. 1986 Aromatherapy Course 2nd edition pg. 116 Kurt Schnaubelt Ph.D. San Rafael
5. National Drugs and Poisons Scheduling Committee Working Party on Essential Oils 1998 Essential Oil Monographs Australian Therapeutic Goods Administration Canberra
6. Davis, P. 1988 Aromatherapy: An A Z C.W. Daniel Co. Essex
7. LeBourhis, B. and Soenen, A.M. 1973 Recherces sur l’action psychotrope de quelques substances aromatiques utilisées en alimentation Foods and Cosmetics Toxicology 11: 1-9, cited in Tisserand, R. and
Balacs, T. 1995 Essential Oil Safety pg. 195 Churchill Livingstone Edinburgh
8. Franchomme, P. and Pénöel, D. 1990 L’Aromathérapie Exactement pg. 197 Roger Jollois, Editeur Limoges
9. Bronaugh et al 1990 In vivo percutaneous absorption of fragrance materials in rhesus monkeys and humans Fd Chem. Toxic 28(5) 369-373
10. Hotchkiss, S. 1997 Percutaneous absorption of fragrance materials through human tissue samples Presentation at Aroma ’97 Conference Warwick University
11. Jäger et al 1992 Percutaneous absorption of lavender oil from
a massage oil Journal of the Society of Cosmetic Chemists 43: 49-54
12. Bronaugh et al 1990 op. cit.
13. Bowman and Reed 1980 Textbook of Pharmacology Section 32-35,
cited in Balacs, T. 1992 International Journal of Aromatherapy 4: 2 pg. 23
14. Battaglia, S. 1995 The Complete Guide to Aromatherapy pg. 136 The Perfect Potion
Virginia
15. Grace, U. M. 1996 Aromatherapy for Practitioners pg. 19 C. W. Daniel Co. Essex
16. Tisserand, R. and Balacs, T. 1995 Essential Oil Safety pgs. 108-110 Churchill Livingstone
Edinburgh
17. Gunn, J.W.C. 1921 The action of the “emmenagouge” oils on the human uterus.
The Journal of Pharmacology and Experimental Therapeutics 16: 485-489, cited
by Tisserand, R. and Balacs, T. 1995 Op. cit. pg. 108
18. Tisserand, R. and Balacs, T. Op. cit. pg. 108
19. Ibid. pg 108
20. Ibid pg. 108
21. Ibid. pg 109
22. Young, J. 1998 Complementary Therapies in Nursing Care Presentation at Australian
Holistic Nurses Association Conference Sydney
23. Tisserand, R. and Balacs, T. 1995 Op. cit. pg 108
24. Vesselinovitch, S.D. et al 1979 Transplacental and lactational carcinogenesis by safrole
Cancer Research 39: 4378-4380
25. Heinerman, J. 1980 Science of Herbal Medicine pgs. xx-xxi Bi World Publishers Orem
26. Franchomme, P. and Penoel, D. 1990 Op. cit. pg. 178
27. Holmes, P. 1993 The Energetics of Western Herbs Vol. 1 pg. 254 NatTrop Berkeley
28. Tisserand, R. and Balacs, T. 1995 Op cit pg. 142
29. Ibid. pg. 142
30. Holmes, P. 1993 Op. cit. Vol. 2 763-764
31. Wichtl, M. 1994 Herbal Drugs and Phytopharmaceuticals Medpharm Publishers Stuttgart
32. Weiss, R.F. 1985 Herbal Medicine Hippokrates Verlag GmbH Stuttgart
33. Wichtl, M. 1994 Op. cit. pg. 495
34. Druda, A. TCM practitioner Personal communication
35. Holmes, P. 1993 Op. cit. pg. 495
36. Battaglia, S. 1995 Op. cit. pg. 136
37. Fawcett, M. 1993 Aromatherapy for Pregnancy and Childbirth pgs.
23-24 Element Books Ltd. Dorset
38. Weiss, R.F. 1985 Op. cit. pgs. 317-319
39. Franchomme, P. and Penoel, D. 1990 Op. cit. pg. 175
40. Guba, R. 1996 Aromatic Medicine Course Notes pgs. 20-21 The Centre for Aromatic
Medicine Melbourne
41. Motluck, A. 1998 Snort it how the nose could transform the treatment of brain diseases
pg. 24 New Scientist 5 Sept. 1998
42. Battaglia, S. 1995 Op. cit. pg. 136
43. Pénöel, D. 1998 Op. cit.
44. Valnet, J. 1985 The Practice of Aromatherapy C. W. Daniel Co. Essex
45. Allenby, C.F. et al 1984 Diminution of immediate reactions to cinnamic aldehyde by
eugenol Contact Dermatitis 11: 322-323
46. Schnaubelt, K. 1986 Op. cit. pgs. 16-17
47. Mark, H. 1993 Clove oil anti-inflammatory for skin, cited in Medi Herb Monitor pg. 3 No.
7 Dec. 1993 Brisbane
48. Sheppard Hanger, S. 1994 The Aromatherapy Practitioner Reference Manual Aquarius
Publishing Willeton
49. Watt, M. 1995 A Data and Reference Manual on Essential Oils and Aromatic Plant
Extracts pg. 47 The Atlantic Institute of Aromatherapy Tampa
50. Sheppard Hanger, S. 1994 Op. cit.
51. Battaglia, S. 1995 Op. cit. pg. 136
52. Davis, P. 1988 Op. cit. pg. 363
53. Holmes, P. 1993 Op. cit.
54. Weiss, R.F. 1985 Op. cit.
55. Wichtl, M. 1994 Op. cit.
56. Willard, T. 1990 Scientific Herbology Wild Rose College of Natural Healing Calgary
57. Franchomme, P. and Penoel, D. 1990 Op. cit.
58. Belaiche, P. 1988 Phytothérapie et Aromathérapie Edtions Maloine Paris
59. Tisserand, R. and Balacs, T. 1995 Op. cit. pg. 65
60. Ibid. pg. 65
61. Davis, P. 1988 Op. cit. pg. 363
62. National Drugs and Poisons Scheduling Committee Working Party on Essential Oils 1998
Essential Oil Monographs Op. cit.
63. Progress in Essential Oils 1981-1987 pg. 214 Allured Publishing Wheaton
64. Tisserand, R. and Balacs, T. 1995 Op. cit. pg. 68
65. Weiss, R.F. 1985 Op. cit. pg. 235
66. Heil, B.M. and Schilcher, H. 1993 Juniperberry is not a kidney irritant, cited in Medi Herb
Monitor Op. cit. pg. 1
67. Progress in Essential Oils 1981-1987 Op. cit. pg. 110-111
68. Koppel, c. et al 1981 Acute poisoning with Pine oil Arch Toxicol
49: 73-78
69. Tisserand, R. and Balacs, T. 1995 Op. cit. pgs. 52-53
70. Ibid. pgs. 41- 44
71. Henry, J. A. and Cassidy, S. L. Acute Non-Specific Toxicity 1998 NDPSC Working Party
on Essential Oils Toxicity monographs
72. Compilation of Poisons Information Centre reports 1998 NDPSC Working Party on
Essential Oils Toxicity monographs
73. Webb, N. J. and Pitt, W. R. 1993 Eucalyptus oil poisoning in childhood: 41 cases in SE
Queensland J. Paediatr. Child Health, 368-371
74. Thorn, G. W. et al, editors 1986, Harrison’s Principles of Internal Medicine 8th edition
pgs 701-702 McGraw Hill
75. Young, A. R. et al 1990 Phototumorigenesis studies of 5-methoxypsoralen in Bergamot oil
Journal of Phytochemistry and Photobiology 7: 231-250
76. Sambuco, C. P. et al 1987 Protective value of skin tanning induced by ultraviolet radiation
plus a sunscreen containing bergamot oil Journal of the Society of Cosmetic Chemists
38: 11-19
77. Guba, R. 1995 Aromatherapy and Regenerative Skin Care Course Notes pgs 107-115
The Centre for Aromatic Medicine Melbourne
78. Tisserand, R. and Balacs, T. Op. cit. pgs 77-83
79. Ibid.