Peanut oil, with the Inci name Arachis hypogaea oil, and its derivatives have a widespread
use in cosmetic products. The use of peanut oil in cosmetic products is not currently
regulated in the Cosmetics Directive. Several Member States have recently indicated safety
problems in relation to the use of this substance as an ingredient in cosmetic products.
Concerns were raised over the fact that an unexpected risk of food allergy to peanuts was
reported in particular at young children (0-3 years), where it was suspected that the
induction of the sensitisation might have appeared through the use of cosmetic products
containing peanut oil in the first six months of life.
A public call for scientific data on the use of peanut oil in cosmetic products was made by
the Commission Service during autumn/winter 2009-10.
1. Does the SCCS consider the use of peanut oil and/or its derivatives to be safe for
consumers in cosmetic products on the basis of the provided scientific data?
2. And/or does the SCCS has any scientific concerns with regard to the use of peanut oil
and/or its derivatives in cosmetic products?
Peanut (Arachis hypogaea) kernels contain approximately 45.5-50% fat, 25-30% protein, 8-
12% carbohydrate, 5% water, 3% fiber and 2.5% ash (CIR 2001, Koppelman 2001). The
protein content of refined oils, including peanut oil, was shown to be about 100 fold lower
than that in cold pressed oil (Crevel et al. 2000). The protein content of refined oils was
found to be 0.2-60 mg/L. However, in one study protein content of refined peanut oil was
reported to be < 0.3µg/L (Peeters et al. 2004). The refining process, which also included
heat treatment, did not destroy the allergenicity of the peanut allergens (Olszewski et al.
1998, Koppelman et al. 1999). This indicates that the major peanut allergens are heat
stable even when present in trace amounts in refined peanut oil.
Thirteen peanut allergens (Ara h 1 to Ara h 13) have been identified (Table 1, WHO-IUIS.
For detailed description of these allergens see also the review by de Leon et al. (2007).
The allergens Ara h1 and Ara h 2 have been shown to be the major allergens of peanut oil
(Burks et al. 1991, 1995, Koppelman et al. 2001, Maleki et al. 2000). It has been shown
that Ara h 2 and Ara h 6 are moderately homologous allergens and can act either
synergistically or in a redundant fashion, and partial similarity between these two allergens
has been demonstrated (Porterfield et al 2009, Chen et al. 2013, Koid et al. 2014).
Koppelman et al. (2010) have recently shown that Ara h 2 and Ara h 6 are considerably
more stable towards digestion than Ara h 1 and Ara h 3.
Cosmetic grade peanut oil is the refined (or hot pressed oil) fixed oil of one or more of the
cultivated varieties of Arachis Hypogaea. Functions and uses of peanut oil according to the
COSING Database is described in Table 2.
According to information supplied by Industry, peanut oil can be refined to protein levels
below 1 ppm, and for some products to a level below the 0.5 ppm detection limit by ELISA
The skin irritating potential of peanut oil has been evaluated in 4 different animal species
(Motoyoshi et al., 1979).
Undiluted technical grade arachis oil (0.1 g) was applied to the dorsal surface of groups of 6
albino angora rabbits, male Hartley guinea pigs and male Wistar rats (arachis oil was one of
19 oils or 20 synthetic perfumes tested). Three test compounds and one control (nhexadecane)
were applied to the rabbits, whereas only one test substance and one control
(n-hexadecane) were applied to the guinea pigs and rats. Sites were evaluated after 24
hours exposure and the test substances were re-applied 30 minutes after the reading. A
second set of reading and application was made 48 hours later. After the 72-hour
evaluation, the animals were injected with Evan’s blue, killed and a sample of dorsal skin
was taken for histopathological examination. The dilating rate of blood vessels, the swelling
rate (oedema), the bluing rate (as a result of increased capillary permeability), and the
bleeding rate on the test sites were read using transmitting light. The total score of the
averages of the reddening rate (erythema, 72-hour reading), the dilating rate, the swelling
rate and the bluing rate for 6 animals in a group was referred to as the primary irritation
index and was used for placing a compound in general groups with reference to irritant
properties. The bleeding rate was used as a reference. Compounds producing the total score
(primary irritation index) of 4 or less were mildly irritating whereas those with indexes from
4 to 8 were moderate irritants and those with scores above 8 were considered severe
irritants. Arachis oil was moderately irritating to the rabbit and guinea pig and mildly
irritating to the rat (Motoyoshi et al. 1979).
Arachis oil (technical grade, 0.05 g) was applied under occlusion for 48 hours to the dorsal
surface clipped free of hair, of 6 miniature swine. Sites were evaluated at the time of patch
removal and the animals were injected with Evan’s blue, killed and dorsal skin samples were
taken for histopathological examination. Reactions were evaluated as described above.
Arachis oil was not irritating to the miniature swine (Motoyoshi et al. 1979).
The specific number and grade of reactions were not reported in the original article by
Motoyoshi et al. (1979).
The ocular toxicity of ketoconazole has been tested in rabbits. One eye of each rabbit (18
animals) was treated with ketoconazole in an arachis oil vehicle (test eyes) and the other
eye (control eyes) was treated with undiluted arachis oil. Drops were applied hourly for 6
consecutive hours daily for 3 weeks. Eyes were examined by slit-lamp biomicroscopy before
the first instillation and twice weekly for the 3-week experimental period. A 4-point scoring
system was used for various sites in the eye and for various parameters (discharge,
oedema and hyperaemia). Six of the 18 control eyes that received arachis oil showed ‘a
small degree of hyperaemia’ (grade 1 out of 4) involving the bulbar conjunctiva in 4 eyes
and the eyelid in 2 eyes (Oji, 1982).
The author’s conclusion was that arachis oil ‘showed no ocular toxicity’.
The finding of slight hyperaemia in 6 of 18 eyes to which arachis oil was applied seems to
indicate that arachis oil can cause slight conjunctival irritation.
Local Lymph Node Assay (LLNA)
No LLNA study was supplied or referenced for peanut oil, but some other studies are
Using peanut flour, Strid et al. (2005) demonstrated in female BALB/c mice that
epicutaneous exposure to peanut protein induced potent Th2-type immunity with high levels
of IL-4 and serum IgE. This was able to prevent the induction of oral tolerance.
Hsieh et al. (2003) showed that allergen exposure through the skin in BALB/c mice could
serve as a pathway for sensitization for food allergy, but that 100 µg of ovalbumin applied
to a 1 cm square patch for 1 week was required to induce a positive challenge. This is more
than a million times higher than the detection limit of the ELISA described by Peeters et al.
No data provided.
No data available.
Background to consideration of the role of percutaneous sensitization
Nipple creams often contain arachis oil, as do topical preparations for eczema (Lever,
1996). Out of 406 patients reporting symptoms on first contact with peanuts, only 121
(19%) had been knowingly exposed to peanuts before the first documented reaction
(Hourihane et al., 1997). Peanut allergy was much more common in the group of children
fed vitamin D preparation containing peanut oil than those who took the vitamin D product
free from peanut oil (De Montis et al. 1993). Lack et al. (2003) found a significant
association between consumption of soya milk in the first 2 years of life and the
development of peanut allergy. About 90% of individuals with peanut allergy were exposed
to skin creams containing peanut oil in the first 6 months of life. Almost 91% of children
with peanut allergy (in a study of 49 children with symptoms of peanut allergy) had been
exposed to arachis oil in the first 6 months of life. In addition they were exposed to more
preparations containing arachis oil. Eczema was a risk factor as was intake of soya milk.
Filaggrin gene mutations, with and without concomitant clinically manifest atopic dermatitis,
have been shown to be associated with peanut allergy (Brown et al. 2011).
Consideration of maternal factors
According to Vadas et al. (2001), more than 70% of children with peanut allergy show
reactions already at the first known time of ingestion, possibly sensitized via breast feeding
since peanut protein is present in breast milk. In a questionnaire study on children with
peanut allergy and egg-allergic controls conducted before the subjects were diagnosed as
being peanut allergic, conducted by Fox et al. (2009), the mean household weekly peanut
consumption was significantly elevated in the 133 peanut allergic group compared to 150
controls. Peanut butter posed the greatest risk.
The mothers of infants with peanut allergy reported a statistically significantly higher intake
of peanuts during pregnancy and breast-feeding than controls (DesRoches et al., 2010). The
peanut allergic infants did not have a higher environmental exposure to peanut than did
controls. However, a systematic review has shown that several studies have confounding
variables. So much so that there is no clear evidence that maternal exposure or
early/delayed exposure to peanuts has an influence on the subsequent development of
peanut allergy (Thompson et al., 2010). Therefore conclusions regarding maternal
exposures are not possible at this stage. Notwithstanding, in a study of 140 infants with
peanut allergy (as judged by specific IgE to peanut of >5 KU/mL), multivariate analysis
showed an association with peanut consumption by the mother during pregnancy (odds
ratio 2.9, 95% CI 1.7-4.9; P< 0.001) (Sicherer et al., 2010). A yet further analysis has
concluded that the risk of childhood peanut allergy was not modified by maternal exposure
to peanut-containing food (Binkley et al., 2011).
There is some evidence that infant exposure via breast milk, nipple cream or vitamin D
supplements may sensitise infants to peanut proteins. However, it has been pointed out
that several studies have confounding factors which make a definite conclusion difficult.
Symptomatology of peanut allergy
Out of a series of 122 children with peanut and tree nut allergy, 89% had skin reactions,
52% had respiratory symptoms and 32% had symptoms related to the gastro-intestinal
tract (Sicherer et al., 1998).
A double-blind cross-over trial in 10 peanut-allergic patients as judged clinically and by
specific IgE was performed of the allergic potential of peanut oil. All subjects were negative
to intradermal injection of peanut oil (and to olive oil as a control). Each was tested with
each of 1, 2, and 5 mL capsules of peanut oil and olive oil as a control at 30 minute
intervals without adverse reaction. Re-testing 2 weeks later was again negative. Ten
patients who experienced systemic symptoms after peanut ingestion did not react to skin
prick tests or on oral provocation to peanut oil (Taylor et al, 1981).
A randomized double-blind crossover challenge study using 62 patients who were skin test
positive for peanut allergy, in whom crude or refined peanut oil was administered orally,
was negative in all those tested for the refined peanut oil (O’Hourihane et al, 1997).
In 41 children with positive tests for peanut allergy, none reacted to orally-administered
refined peanut oil but 15 reacted to unrefined oil (Kull et al, 1999).
Combining the data from various published and unpublished data on clinical oral challenge
studies in peanut-sensitised individuals, a New Zealand – Australian Expert Panel
established a minimal oral reference dose of 0.2 mg peanut protein (Taylor et al., 2014).
Undiluted arachis oil (technical grade, 0.05 g) was applied to the back of 50 male volunteers
for 48 hours (arachis oil was one of 19 oils or 20 synthetic perfumes tested). The patches
were then removed and inspected after 30 minutes (and at 72, 96 and 120 hours if
necessary). Compounds were classified in general groups according to their irritation
potential. Compounds producing the percentages of positive reactions of 10% or less were
considered almost non-irritating; those with percentages of 10-40% were considered as
mildly irritating; those with percentages of 40-70% were considered as moderately
irritating; and those with percentages above 70% were considered as severely irritating.
The exact results are not shown in this paper. Arachis oil was regarded as not being a skin
irritant in humans according to these authors (Motoyoshi et al. 1979).
CIR (2001) quotes a study by Frosch and Kligman (1976) in which 5 Caucasian volunteers
participated in a chamber-scarification test using USP-grade peanut oil, applied in 100 µL
quantities using aluminum chambers, daily for 3 days (length of exposure not stated). The
72-hour reading, done 30 minutes after last patch removal, was used for scoring, producing
mean scores of 0- 0.4, and assessed by the authors as non-irritating.
Peanut oil is not irritant to the skin.
Peanut proteins are known to cause severe potentially life-threatening type-I allergic
reactions. However, refined peanut oils contain very low levels of the peanut proteins which
are the moiety that has the allergenic potential (see below). Nonetheless, apparent allergy
to peanut oil has been recorded, the first suspected case being that of a 32-year-old woman
with asthma, who developed generalized urticaria related to IM injections of adrenaline in
peanut oil in whom subcutaneous tests seemed to confirm allergy to peanut oil (Chafee FH
The Working Party on Herbal Medicinal Products of the European Medicines Agency (EMEA,
2004) states the view that ‘Since no safe threshold for the exposure to topical oil
preparations can be defined and data point to the possibility of allergy induction due to the
use of oil containing ointments in infants, all medications for topical use containing soya or
peanut products should be treated as allergenic’. The report proceeds to state ‘It must be
kept in mind that with chronic oral consumption of oil-based formulas e.g. vitamin D
preparations in infants, containing only traces of protein the induction of new allergies
cannot be excluded.’ Exposure to peanut allergen may not necessarily occur through
exposure to peanut oil; it might occur through exposure to peanut butter (EMEA 2004).
Regarding the allergenicity of peanut proteins, Nordlee et al. (1981) performed a
radioallergosorbent test to assess the allergenic potential of various moieties of peanut
against the combined sera of 5 peanut allergic patients, as judged by the inhibition of
binding of serum IgE to solid-phase peanut allergen. Defatted peanut flour, peanut butter,
and raw and roasted peanuts were all allergenic but peanut oil was not as judged by this
test. Teuber et al. (1997) tested IgE-binding capacity of nut extracts, using pooled serum
from peanut allergic patients. Two minimally-processed peanut oils, with protein
concentrations of 11 microgram/ mL, were positive in this study but the refined bleached
peanut oils (protein levels 6 and 3 microgram/ mL) were respectively negative and showed
‘a very light band of binding’.
Data to derive a safe level of exposure to food in sensitised individuals exist, however to
derive a safe level of exposure of the skin (especially regarding induction) is problematic.
There is mounting evidence of access of proteins to the immune system via the (even
intact) skin (Kimber et al., 2014). This has implications for sensitisation to food proteins. A
compromised skin barrier function, promoting this immunological access, is not uncommon
in the general population; filaggrin loss-of-function mutations with or without clinically
manifest atopic dermatitis have been shown to be a significant risk factor for peanut allergy
(Brown et al., 2011). Evidence of enhanced epicutaneous sensitisation to protein (albeit not
peanut) in filaggrin deficiency is supported by a study in mice (Oyoshi et al., 2009).
A one-time application of body lotion on the entire skin is approximately 8 ml and a onetime
whole body cream application in dermatology patients is advised to be 20 gram
(SCCS/1501/12 2012, Long 1991). Thus, a one-time skin application with refined peanut oil
with 0.5 ppm would result in a total dose of max 10 microgram peanut protein, which is well
below the ED1 level of 200 microgram for ‘safe’ elicitation/challenge studies in sensitised
There is no known safe threshold currently defined at which the skin of peanut allergic subjects can safely be exposed to peanut proteins, although such thresholds are available for oral intake. The SCCS has followed the scientific debate about the importance of skin exposure as a route for induction of sensitisation to type I allergens such as peanut. The SCCS acknowledges that this is of concern, but that there are insufficient data to define a safe level of skin exposure in the non-sensitised population. However, in view of the documented safe levels of oral intake of peanut protein in sensitised individuals and in view of the industry’s capability to refine peanut oil below a protein level of 0.5 ppm, the SCCS can accept this value as maximum allowable concentration in (refined) peanut oil for cosmetic use.