25410033 2009 safety assessment of coriander coriandrum sativum l essential oil

Food and Chemical Toxicology 47 (2009) 22–34

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Food and Chemical Toxicology

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Review

Safety assessment of coriander (Coriandrum sativum L.) essential oilas a food ingredient

George A. Burdock a,*, Ioana G. Carabin b

a Burdock Group, 801 N Orange Ave, Suite 710, Orlando, FL 32801, United Statesb Women in Science, 3785 7th Lane, Vero Beach, FL 32968, United States

a r t i c l e i n f o

Article history:Received 26 August 2008Accepted 4 November 2008

Keywords:CorianderToxicitySpiceEssential oilGRAS

0278-6915/$ - see front matter � 2008 Elsevier Ltd. Adoi:10.1016/j.fct.2008.11.006

Abbreviations: CAS, chemical abstracts service; Cchemicals codex; FEMA, flavor and extract manufacturof Flavor Industries; JECFA, joint FAO/WHO expertAssociation of Chewing Gum Manufacturers; NAS, Nmaximum daily intake; PPM, parts per million; TAMD

* Corresponding author. Tel.: +1 407 802 1400.E-mail address: [email protected] (G.A

a b s t r a c t

Coriander essential oil is used as a flavor ingredient, but it also has a long history as a traditional medi-cine. It is obtained by steam distillation of the dried fully ripe fruits (seeds) of Coriandrum sativum L. Theoil is a colorless or pale yellow liquid with a characteristic odor and mild, sweet, warm and aromatic fla-vor; linalool is the major constituent (�70%). Based on the results of a 28 day oral gavage study in rats, aNOEL for coriander oil is approximately 160 mg/kg/day. In a developmental toxicity study, the maternalNOAEL of coriander oil was 250 mg/kg/day and the developmental NOAEL was 500 mg/kg/day. Corianderoil is not clastogenic, but results of mutagenicity studies for the spice and some extracts are mixed; lin-alool is non-mutagenic. Coriander oil has broad-spectrum, antimicrobial activity. Coriander oil is irritat-ing to rabbits, but not humans; it is not a sensitizer, although the whole spice may be. Based on thehistory of consumption of coriander oil without reported adverse effects, lack of its toxicity in limitedstudies and lack of toxicity of its major constituent, linalool, the use of coriander oil as an added foodingredient is considered safe at present levels of use.

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Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23
1.1. Historical perspective . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23
1.1.1. Description, natural occurrence and sources . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231.1.2. Specifications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241.1.3. Composition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241.1.4. Contamination of coriander . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 251.1.5. Commercial uses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 251.1.6. Regulatory history . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

1.2. Consumption . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25
1.2.1. Estimation methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 251.2.2. Consumption summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
2. Biological data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
2.1. Absorption, metabolism and excretion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
2.1.1. Biochemical/pharmacological effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
2.2. Toxicological studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28
2.2.1. Acute toxicity studies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 282.2.2. Irritation studies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 282.2.3. Short-term and subchronic toxicity studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28

ll rights reserved.

FR, code of federal regulations; CoE, council of Europe; DINFO, daily intake via natural food occurrence; FCC, fooders association; FDA, food and drug administration; GRAS, generally recognized as safe; IOFI, International Organisationcommittee on food additives and contaminants; MSDI, maximum survery-derived daily intake; NACGM, Nationalational Academy of Sciences; NOEL, no-observed-effect-level; PADI, possible average daily intake; PMDI, possibleI, theoretical added maximal daily intake.

. Burdock).

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G.A. Burdock, I.G. Carabin / Food and Chemical Toxicology 47 (2009) 22–34 23

2.2.4. Developmental and reproductive toxicity. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 282.2.5. Immunotoxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 292.2.6. Genotoxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 292.2.7. Cytotoxicity studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 292.2.8. Sensitization studies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

2.3. Observations in humans . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31
3. Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 314. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31
Conflict of interest statement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31Acknowledegement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

Table 1General description of coriander oil.

Botanical source Coriandrum sativum L.

Botanical family Apiaceae (Umbelliferae)Synonyms Coriander oil; coriander, oil (Coriandrum

sativum L.); coriander fruit oil; oil ofcoriander; oils, coriander

Functionality in food Flavor ingredientCAS No. 8008-52-4NAS No. 2334FEMA No. 2334Packaging and storage Store in full, tight containers protected

from light. Avoid exposure to excessive heat

CAS = chemical abstracts service; FEMA = flavor and extract manufacturers’ asso-ciation; NAS = national academy of sciences.

1. Introduction

Coriander essential oil (CAS No. 8008-52-4) (hereinafter re-ferred to as ‘‘coriander oil”) is obtained by steam distillation ofthe dried fully ripe fruits (seeds) of Coriandrum sativum L. of thefamily Apiaceae (synonymous with Umbelliferae). The oil has acharacteristic odor of linalool and a mild, sweet, warm, aromaticflavor. In the food industry, coriander oil is used as a flavoringagent and adjuvant. Coriander oil is approved for food uses byFDA, FEMA and the Council of Europe (CoE). This review evaluatesthe safety-in-use of coriander oil as a food ingredient.

1.1. Historical perspective

Coriander has a long history of use. It is mentioned in Sanskritliterature as far back as 5000 B.C. and in the Greek Eber Papyrusas early as 1550 B.C. (Uhl, 2000). Coriander was used in traditionalGreek medicine by Hippocrates (ca. 460–377 B.C.). The seeds ofcoriander were found in the ancient Egyptian tomb of Ramsesthe Second. The Egyptians called this herb the ‘‘spice of happiness”,probably because it was considered to be an aphrodisiac. It wasused for cooking and for children’s digestive upset and diarrhea.The Greeks and Romans also used coriander to flavor wine andas a medicine (Grieve, 1971). Demand by the Romans for corianderwas so great, it was imported from as far away as Egypt. Subse-quently, it was introduced into Great Britain by the Romans (Livar-da and van der Veen, 2008). The use of coriander to acceleratechildbirth has been cited in manuscript illustrations (from theearly 13th Century) on medieval midwifery (Reus, 1996). Thus,the seeds (dried) have been in use for almost 7000 years (Kipleand Ornelas, 2000). The oil has been used as a food and fragranceingredient since the 1900s (Opdyke, 1973).

Coriander is a native to the Mediterranean and Middle Easternregion. The etymology of coriander starts with the Greek wordkorannon, a combination of koris and annon (a fragrant anise) andreferred to the ripe fruit (Uchibayashi, 2001). The Roman natural-ist, Pliny the Elder, first used the genus name Coriandrum, derivedfrom koris (a stinking bug), in reference to the fetid smell of theleaves and unripe fruit (Blumenthal, 2000; Grieve, 2003).

1.1.1. Description, natural occurrence and sourcesCoriander oil, essential or volatile, is obtained by steam distilla-

tion of the dried, fully ripe fruits (seeds) of C. sativum L. The seedsare comminuted just before distilling the oil. The volatile oil yieldranges between 0.3% and 1.1%. Coriander extract from the fruits ofC. sativum is very rich in fat and poor in essential oil (Salzer, 1977).The seeds contain on average 18% oil (fatty acids/triglycerides);however, the essential oil content of seeds is approximately0.84%. The essential oil (steam distilled) is produced mainly inEastern Europe, with Russia one of the leading producers (Floreno,1997). The inclusion of unripe fruits or other parts of the plant

during distillation of the dried seeds imparts an obnoxious odorto the oil. General descriptive characteristics of coriander oil aresummarized in Table 1.

The oil is a colorless or pale yellow liquid with a characteristicodor and taste of coriander. The oil has a mild, sweet, warm andaromatic flavor (Burdock, 2002a). The floral-balsamic undertoneand peppery-woody, suave top note of the oil are characteristicfeatures of this fragrance (Arctander, 1960). The aroma detectionthreshold value of coriander oil is reported as 37 ppm. Taste char-acteristics of coriander oil at 50 ppm are reported as sweet, fresh,herbal, spicy, terpy and cilantro-like. Nitz et al. (1992) reportedno obvious sensory differences in flavors of coriander extracts pre-pared by distillation or by supercritical carbon dioxide extraction.The organoleptic characteristics of the distilled oil tend to deterio-rate during prolonged storage especially if left exposed to light andair. However, storage of the oil for one year in the dark, did not af-fect the organoleptic characteristics of the oil (Misharina, 2001).

C. sativum is an annual, herbaceous plant originally from theMediterranean and Middle Eastern regions. It grows 25–60 cm(9–24 in.) in height. It has thin, spindle-shaped roots, erect stalk,alternate leaves and small, pinkish-white flowers. The plant flow-ers from June to July and yields round fruits consisting of two peri-carps. The plant is cultivated for its aromatic leaves and seeds. Thephylogenetic classification of C. sativum is provided in Table 2.There are two varieties of C. sativum: vulgare Alef. and microcarpumDC. These varieties differ in the fruit size and oil yield: vulgare hasfruits of 3–5 mm diameter and yields 0.1–0.35% essential oil, whilemicrocarpum fruits are 1.5–3 mm and yield 0.8–1.8% essential oil(Small, 1997). For the highest yield of quality essential oil, harvest-ing should be completed when the fruits have attained ripeness(Tsvetkov, 1970), as evidenced by a rust red color, then dried byplacing in drying lofts. The seeds are ground and used as a spice,particularly in Eastern Europe. The essential oil distilled from theseeds is used in condiments and liqueurs. The leaves, referred toin the US as cilantro, are extensively used in Eastern cooking,

Table 2Classification of the coriander plant (http://plants.usda.gov/java/profile?sym-bol=COSA, site accessed 09.08.08).

Kingdom Plantae (plants)

Subkingdom Tracheobionta (vascular plantsSuperdivision Spermatophyta (seed plants)Division Magnoliophyta (flowering plants)Class Magnoliopsida (dicotyledons)Subclass RosidaeOrder ApialesFamily Apiaceae (the carrot family)Genus Coriandrum L.Species Coriandrum sativum L.

24 G.A. Burdock, I.G. Carabin / Food and Chemical Toxicology 47 (2009) 22–34

Indian foods and in certain Mexican dishes. The roots are oftenused in Thai cooking.

The fresh herbs and unripe fruit have a ‘‘bug-like” smell, whileripe fruits exhibit a pleasant tangy odor and taste (PDR, 1998). Theseeds are used to prepare an infusion (3%), tincture and fluid ex-tract (Burdock, 2002a). Additionally, a brownish-yellow liquidoleoresin (a naturally occurring mixture of a resin and an essentialoil) is produced from selected quality seed (Arctander, 1960). Sub-bulakshmi et al. (1991) reported that c-irradiation and storage for3 months did not affect the sensory qualities of powdered corian-der spice. In another study, c-irradiation of coriander to reduce themicrobial content may result in decreased linalool content (Sjovallet al., 1990).

1.1.2. SpecificationsSpecifications of coriander oil from the (Food Chemicals Codex)

FCC (2003) are summarized in Table 3.

1.1.3. CompositionThe predominant constituent of essential oil of coriander is lin-

alool (Fig. 1), which forms approximately two thirds of the oil (Sal-zer, 1977; Lawrence, 1980a,b; Budavari et al., 1999; Gil et al., 2002;Grosso et al., 2008). Typical compositional analysis of coriander oilis as follows: alcohols: linalool (60–80%), geraniol (1.2–4.6%), terpi-nen-4-ol (trace-3%), a-terpineol (<0.5%); hydrocarbons: c-terpin-

Table 3Coriander oil specifications (FCC, 2003).

Characteristics Metrics

Angular rotation Between +8� and +15�Appearance Colorless or pale yellow liquidHeavy metals (as Pb) Passes testIdentification Infrared absorption spectrumOdor Characteristic of corianderSolubility in alcohol Passes test. One milliliter dissolves

in 3 ml of 70% alcoholSpecific gravity Between 0.863 and 0.875Refractive index Between 1.462 and 1.472 at 20 �C

FCC = food chemicals codex.

Fig. 1. Chemical structure of linalool, an important constituent of coriander oil.

ene (1–8%), r-cymene (trace-3.5%), limonene (0.5–4%), a-pinene(0.2–8.5%), camphene (trace-1.4%), myrcene (0.2–2%); Ketones(7–9%): camphor (0.9–4.9%); esters: geranyl acetate (0.1–4.7%),linalyl acetate (0–2.7%); coumarins/furanocoumarins: umbellifer-one, bergapten. Coriander oil was reported to contain approxi-mately 30% terpene hydrocarbons and 70% oxygenatedcompounds (Karlsen et al., 1971).

The BACIS (1999) reports the presence of 122 constituents incoriander seed (BACIS, 1999), although the final number may be>200. The 18 main components constitute approximately 97% ofthe total oil. When reconstituted in the concentrations found inthe natural sample, the reconstituted oil did not give the odorimpression of coriander oil (Smallfield, 2003). Hence, a major sen-sory effect of the oil apparently comes from the remaining traceconstituents that occur, on average, in concentrations of about0.01% or less. Although, mono and polyunsaturated fatty acidsare minor constituents of the oil, they contribute to the character-istic aroma of the oil (Bauer et al., 1997). Ishikawa et al. (2003) re-ported identification of 33 compounds from the water-solubleportion of the methanol extract of coriander fruit. Two photosensi-tizing furanocoumarins have been isolated and characterized fromthe plant, coriander (Ashwood-Smith et al., 1989).

Gil et al. (2002) compared the essential oil composition of cori-ander fruits from plants growing in Argentina and Europe. The var-iation in the oil composition was related to the relative proportionof the constituents and not to the presence or absence of a partic-ular component. Geographic location, fertilization and weediness(weed competition) also affected the chemical profile. The Euro-pean samples showed more stable concentration of the major com-ponents compared to samples from Argentina. Better conditionsfor fruit production favored linalool and camphor production insamples from both places. In a study of 15 samples of corianderseeds for volatile contents, the oil distilled from the Polish varietyof coriander (C. sativum var. microcarpum) met the requirements ofthe British Pharmacopoeia (Shellard, 1967).

The composition of coriander fruits was shown to changeaccording to the degree of maturity (Msaada et al., 2007). Corian-der fruits were gathered from northeastern Tunisia over a twomonth period, at initial maturity (full green fruits), for middlestage maturity (green–brown fruits) and, brown fruits representingthe final stage of maturity. During the initial stage, the quantita-tively predominant substance was geranyl acetate, but which rep-resented less than 1.0% of the total constituents at the maturestage. Linalool, the second most quantitatively predominant sub-stance (10.96 of 66.29%), became the most predominant substancein the mature fruit, representing 87.54% of a 95.39% of volumeidentified (Table 4).

Table 4Essential oil composition of coriander at various stages of maturity (adapted fromMsaada et al., 2007).

Constituents Percent of total identified for particular stage

Initial Mid-stage Mature

Geranyl acetate 46.72 2.85 <1.0Linalool 10.96 76.33 87.54p-Cymene-8-ol 1.36 Trace TraceNerol 1.53 Trace TraceNeral 1.42 <1.0 <1.0Carvacrol 1.04 <1.0 <1.0cis-Dihydrocarvone <1.0 3.21 2.36Anethole <1.0 1.41 <1.0Thymol <1.0 <1.0 1.85Other substances (32) <1.0 <1.0 <1.0Total quantity identified 66.29 86.91 95.39

http://plants.usda.gov/java/profile?symbol=COSA

http://plants.usda.gov/java/profile?symbol=COSA

Table 5Use levels of coriander oil in fragrance products (Opdyke, 1973).

Product Usual level (%) Maximum level (%)

Soap 0.02 0.05Creams, lotion 0.02 0.06Perfumes 0.04 0.6


1.1.4. Contamination of corianderSeveral investigators reported contamination of coriander and

its products with mycotoxins, pesticides and other materials. Azizand Youssef (1991) reported detection of aflatoxin B1 (8 lg/kg) andG1 (2 lg/kg) in two samples of coriander. In another study, El-Kadyet al. (1995) reported detection of aflatoxins B1 and G1 in one sam-ple of coriander seeds. In a screening of nine samples of corianderspice, Saxena and Mehrotra (1989) reported presence of mycotox-ins in six samples (5, aflatoxin; 1, ochratoxin; 2, zearalenone; and1, citrinin). In a screening of 126 spice samples for the presencemycotoxin, 20 out of 50 coriander samples showed the presenceof 10–51 lg/kg ochratoxin A (Thirumala-Devi et al., 2001). Severalother reports attempting to investigate the contamination of cori-ander could not detect presence of aflatoxin (Llewellyn et al., 1992;Jaffar et al., 1993; MacDonald and Castle, 1996). In a microbiolog-ical survey of four selected spices, including coriander, aerobic bac-teria plate count values for coriander ranged from 103 to 105colony forming units (CFU)/g of spice (Satchell et al., 1989).

Kaphalia et al. (1990) reported detection of hexachlorohexane(0.4 ppm) and DDT (0.36 ppm) in four samples of coriander spice.Briggs and McLaughlin (1975) reported a low-temperature, thin-layer chromatography method for the detection of polybutene con-tamination in volatile oils. Chaigneau and Muraz (1993) reportedthat the use of ethylene oxide as a disinfectant prior to storage ofcoriander resulted in detection of 2-chloroethanol (10 ppm) even6 months after treatment. Dent (1977) reported a rapid method,utilizing a cold isopropanol defatting system, for the extractionof filth from coriander.

1.1.5. Commercial uses1.1.5.1. Uses as a food ingredient. In flavor compositions, corianderoil blends well with cardamom, anise, bergamot, clary, nutmeg,clove and sage. The oil is extensively used as a flavoring agent inall types of food products, including alcoholic beverages, tobacco,candy, pickles, meat sauce and seasonings. The average use levelsrange from 0.1 to 100 ppm. Coriander oil is reported to possessantimicrobial properties against selected pathogenic and sapro-phytic microorganisms, indicating that it may be useful as a disin-fectant (Deans and Ritchie, 1987; Meena and Sethi, 1994; Elgayyaret al., 2001).

Coriander is recognized as one of the most important spices inthe world and is of great significance in international trade (Small,1997). It has been estimated that the annual world production ofcoriander oil has a value of about 50 million dollars, making itthe world’s second most important essential oil after orange oil(Lawrence, 1993). A large amount of coriander seeds are used incertain classic spice blends particularly those of ‘Indian Curry’. Thisspice blend has not been replaced by a liquid essential oil mixture.The seeds are widely used to season curries, puddings, breads, sau-sages, liqueurs, cakes, gin essences and spicy sauces (Facciola,1990).

Coriander oil may have future use as a free radical scavenger,preventing oxidative deterioration in foods. In a report by Rama-dan and Moersel (2006), coriander oil was shown to have greateractivity against the radical generating activity of 1,1-diphenyl-2-picrylhydrazyl in several oils. The order of effectiveness amongvarious oils in inhibiting free radicals was coriander> blackcumin>cottonseed> peanut> sunflower> walnut> hemp seed> linseed>olive> niger seed.

1.1.5.2. Non-food uses. In perfumery, the warm and sweet notes ofcoriander oil blend well with bergamot and sage colognes, with flo-ral notes in jasmine, lilac, honeysuckle and apple-blossom. In per-fumes of an ‘Oriental type’, coriander oil produces interestingeffects with Ceylon cinnamon and olibanum (olibanum is alsoknown as frankincense, an aromatic resin obtained from trees of

the genus Boswellia, particularly Boswellia sacra (syn. B. carteri, B.thurifera)). Coriander oil is also used in consumer products suchas soap, creams, lotions and perfumes (Opdyke, 1973). The re-ported use levels in these consumer products are summarized inTable 5. The fruits and oil of coriander are used to cover the tasteor correct the nauseating or griping qualities of other medicines.Coriander is also used in aromatherapy (Cooksley, 2003).

Coriander’s popularity comes not only from its use for oil, butalso from its use for decoration (e.g., for pastries) and as a domesticspice. The oil is mainly used as a flavoring agent in pharmaceuticalpreparations (Leung and Foster, 1996), however, because corianderoil has bactericidal and fungicidal properties, it is used as a sto-machic, spasmolytic and carminative. It is also used for sub-acidgastritis, diarrhea and dyspepsia of various origins as well as forits digestive stimulation, stomachic and antibilious properties (Pla-tel and Srinivasan, 2004). In folk medicine, coriander finds useagainst intestinal parasites and as a component of embrocationsfor rheumatism and joint pain (Wichtl, 1994). Coriander has beenreported to possess strong lipolytic activity (Leung and Foster,1996), and, as a member of carrot family, its use has been sug-gested with caution, because of potential allergic reactions fromfuranocoumarins (Brinker, 1998; NMCD, 2003).

1.1.6. Regulatory historyCoriander oil has been approved for use in food by FDA, FEMA

and the Council of Europe (Table 6). FDA has approved corianderoil as generally recognized as safe (GRAS) with no limitations citedfor the use of coriander oil as a flavoring agent and adjuvant. TheFlavor and Extract Manufacturers’ Association has approved cori-ander oil (FEMA No. 2334) as GRAS for use in foods as a flavoringingredient (Hall and Oser, 1965). The CoE (1970) included corian-der oil in its recommendation of substances, spices and seasoningswhose use is ‘‘deemed admissible with a possible limitation of theactive principle in the final products” (Opdyke, 1973). The Councilof Europe is currently evaluating 600 natural flavoring sourcematerials and has published its first report, which does not includecoriander oil.

The International Organisation of Flavor Industries (IOFI) hascategorized coriander oil as nature identical. Coriander is also re-ported in the Herbs of Commerce (Foster, 1992). Use of corianderis approved by Commission E for dyspeptic complaints and lossof appetite (Blumenthal, 1998). Coriander oil is included in thechemical inventory of the EPA Toxic Substances Control Act. Cori-ander oil is included in the FDA report of inactive ingredients forcurrently marketed drug products for oral solution and elixir(FDA, 1996). The American Herbal Products Association (McGuffinet al., 1997) has categorized coriander fruit as Class 1 (herbs thatcan be safely consumed when used appropriately).

The minimum and maximum use levels of coriander oil ap-proved by FEMA (Burdock, 2002a) and the (National Associationof Chewing Gum Manufacturers) NACGM (1977) for various foodcategories are presented in Table 7.

1.2. Consumption

1.2.1. Estimation methodsSeveral methods can be applied to estimate the consumption of

a substance in the diet. First, the per capita estimate of intake, also

Table 7Approved food uses of coriander oil by FEMA Burdock (2002a) and NACGM (1977).

Food category Use level (ppm) Food category Use level (ppm)

Usual Max Usual Max

Alcoholic beverage 105.70 121.20 Gelatin, pudding 26.18 32.86Baked goods 53.60 62.06 Hard candy 7.51 7.51Chewing gum 0.09 6.62 Hard candya 160.25 181.11Chewing guma 0.06 0.08 Meat products 43.00 68.47Confection frosting 8.90 13.80 Nonalcoholic beverages 2.77 8.94Frozen dairy 39.15 47.35 Soft candy 42.14 46.91

FEMA = flavor and extract manufacturers’ association.a NACGM = national association of chewing gum manufacturers; ppm = parts per million.

Table 6Regulatory status of coriander oil.

Agency Citation/comments Food category Permitted functionality Use limits

FDA 21 CFR 182.2 substances generallyrecognized as safe –essential oil, oleoresin (solvent-free),and natural extractives (including distillates)

Norestrictions

(12) Flavoring agents and adjuvants cGMP

FEMA 2334, GRAS III Flavor ingredientCoE Natural and artificial flavoring substances. partial

agreement in the social and public health field‘‘Deemed admissible with a possible limitationof the active principle in the final product”

IOFI Nature Identical

cGMP = current good manufacturing practices; CFR = code of federal regulations; CoE = council of Europe; FDA = US food and drug administration; FEMA = flavor and extractmanufacturers’ association; GRAS = generally recognized as safe; IOFI = international organisation of flavor industries.


called Maximum Survey-derived Daily Intake (MSDI), is based on‘‘disappearance data” of the amounts added to food as an ingredi-ent. The second, Daily Intake via Natural Food Occurrence (DINFO),is intake as the result of the presence of a substance as an intrinsicor natural part of food (Burdock, 2002b). In contrast to these meth-ods, which are based on the actual intake of the food ingredient,the Theoretical Added Maximal Daily Intake (TAMDI) values suchas FEMA Possible Average Daily Intake (PADI) and Possible Maxi-mum Daily Intake (PMDI) are calculated based on theoretical con-sumption of food to which the ingredient has been added. DINFO iscalculated based on the concentration of substance in food and theconsumption of the food(s). A brief description of each of thesemethods is provided below along with the calculated values.

1.2.1.1. Per capita consumption. Per capita estimate of intake, MSDI,is based on ‘‘disappearance data” from periodic surveys of ingredi-ent manufacturers of the volume of ingredients produced duringthe survey year. The method is easy to use because it divides thetotal annual production by the population in the survey year andthe number of days per year. The assumption is that there is a finiteamount of substance available and the general population ingestsit as an added food ingredient regardless of source at the retaillevel.

The primary sources of data for per capita estimates are the sur-veys conducted by the National Academy of Sciences (NAS) undercontract to FDA and published by Clydesdale (1997). The last sur-vey, conducted in 1987, was based on voluntary reporting by man-ufacturers. Because the NAS has not conducted a survey since1987, Lucas et al. (1999) conducted the FEMA 1995 Poundageand Technical Effects Update Survey. Lucas et al. (1999) claimeda response rate of 87% of total annual sales volume of FEMA-affil-iated flavor manufacturers and users with regard to the total an-nual sales volume.

Some considerations are necessary in the use of these surveydata: (1) because not all producers participate, it is generally heldthat the amount reported is a fraction of the actual volume and; (2)because not all persons eat all foods each day in each category inwhich the substance may be added and conversely, some consum-

ers may seek out the substance, therefore, distribution of con-sumption may be uneven. In order to compensate for thesevariables, FDA assumes (1) only 60% of the actual value was re-ported and (2) only 10% of the US population (243.9 million in1987) consumes 100% of the calculated amount (Clydesdale,1997). Based on these variables and the annual poundage ‘‘disap-pearance” reported by the producers to NAS of 34,800 lb for theyears 1987 (NAS, 1989), the calculated individual consumption ofcoriander oil is 2.95 mg/day or 0.0487 mg/kg/day (for an averageindividual weighing 60 kg).

For consumption estimates based on the Lucas et al. (1999) re-ported disappearance value, the following assumptions are made:(1) 10% of the population consumes the entire flavoring, (2) a cor-rection factor of 80% is used and (3) a 1995 US population of261.1 million. Based on these factors and the Lucas et al. (1999)reported disappearance value of 6090 lb, the calculated individualconsumption of coriander oil is 0.362 mg/day or 0.00604 mg/kg/day.

Several reports suggest that coriander is mainly consumed as aflavor ingredient and the annual consumption of coriander alone inUS during the year 1987 was 901,000 lbs, while the annual con-sumption of coriander oil during the same year was 34,800 lbs.As coriander contains approximately 1% oil, the oil consumptionfrom coriander will be 901 lbs. Thus the consumption ratio of cori-ander oil is 0.023, indicating negative food predominance. Based on‘‘disappearance” data of the coriander of 1501666.67 lb for theyears 1987 (Clydesdale, 1997), the calculated individual consump-tion of coriander oil from the intake of coriander seeds as a spice isestimated to be 0.0127 mg/kg/day.

1.2.1.2. Theoretical added maximum daily intake (TAMDI). The TAM-DI is calculated based on upper use levels and the estimated dailyintakes of foods. For example, FEMA GRAS is for two levels of use,the ‘‘average usual” and ‘‘average maximum” (Burdock, 2002a).The TAMDI is determined using the ‘‘average maximum” leveltimes the estimated daily intake of the food to which the substanceis added. The estimated daily intake would presumably be maxi-mized as well, using the 90th percentile consumption.


The FEMA PADI is similar to the TAMDI concept, using ‘‘usual”use level values and mean consumption estimates of designatedfood categories (based on Market Research Corporation of Americamean frequency of eating and USDA mean portion size of 34 gen-eral food categories) (MRCA, 1965). Therefore, the FEMA PADI of16.6413 mg/day or 0.2774 mg/kg/day is the mean consumptionof coriander oil that is based on an approved ‘‘usual” level of useby FEMA. The conservatism of the PADI method assumes that theusual amount of substance is added to the entire food category,not just the substance within that category. For example, the con-sumption of a substance added only to marshmallow cream cook-ies (a relatively rarely eaten food) would account for very littleconsumption, but the FEMA assumption is that the substance isadded to all baked goods, not just the small portion of baked goodsrepresented by an exotic cookie.

The PMDI can be calculated using the mean consumption offood as above and the maximum levels approved by FEMA (Table7). The PMDI calculated theoretical value for coriander oil was21.8813 mg/day or 0.3647 mg/kg/day.

1.2.2. Consumption summaryThe total lower-intake consumption value for coriander oil was

estimated by the FEMA disappearance per capita consumption, andequal to 0.3624 mg/day 0.00604 mg/kg/day. The total higher-in-take consumption value for coriander oil was estimated by theNAS disappearance per capita consumption and equal to or2.9476 mg/day or 0.0487 mg/kg/day (Table 8). As coriander seeds,which contains approximately 1% oil, is commonly consumed as aspice, intake of the oil from consumption of coriander seeds is esti-mated as 0.0127 mg/kg/day. Thus, the total consumption of corian-der oil from its presence in coriander seed (0.0127) and itsconsumption as an oil (0.0487; NAS determination) is estimatedas 0.0714 mg/kg/day.

2. Biological data

As coriander oil has been used for a long time without any re-ported serious toxic effects, very few studies on the toxicity ofthe oil have appeared in the published literature. Some studieshave appeared on coriander seed, powder and extract and, thesestudies are included in the following section to gain a better per-spective on the possible toxicity, if any, of the oil. It is also impor-tant to distinguish studies between the essential oil and the fattyacid oil of coriander. Fatty acid oil is different (contains oleic, pet-roselinic and linolenic fatty acids and not linalool) and thereforeshould not be confused with essential oil of coriander. Some ofthe studies in the published literature on the fatty acid oil of cori-ander mistakenly designate it as ‘‘coriander oil.”

The single greatest constituent of coriander oil, linalool (�70%of the oil), has been investigated for its safety. The available dataon coriander oil, along with relevant summary information onthe biological effects and toxicity of linalool is described below.Other substances are present at fairly low levels, at or below theiruse in food (Burdock, 2002a) and would therefore not make a sub-stantive contribution to the potential effect(s) of coriander oil.

Table 8Consumption of coriander oil.

FEMA per capita NAS per capita

Low-intake value High-intake value

(mg/day) (mg/kg/day) (mg/day) (mg/kg/day)

Added ingredient 0.3624 0.00604 2.9476 0.0487

FEMA = flavor and extract manufacturers’ association; NAS = national academy ofsciences.

2.1. Absorption, metabolism and excretion

No studies on absorption, metabolism and excretion of corian-der oil were found in the published literature, but several investi-gators have studied the absorption, metabolism and excretion oflinalool in both in vivo and in vitro experiments (Hildebrandt,1901; Parke et al., 1974; Chadha and Madhyastha, 1984; Boutinet al., 1985; Scheline, 1991). These studies suggest that glucuronicacid conjugation and excretion are the primary routes of metabo-lism of linalool, while repeated administration results in allylic oxi-dation. The majority of linalool and its metabolites are excreted inthe urine and, smaller amounts excreted in expired air and feces. Inaddition to conjugation with glucuronide, linalool is hydroxylatedand sulfated. These studies, therefore, also suggest that the pri-mary constituent of coriander oil, linalool, is rapidly absorbed,metabolized and excreted from the body.

2.1.1. Biochemical/pharmacological effectsThe effects of coriander oil on pentobarbital-induced sleeping

time in mice were investigated by Marcus and Lichtenstein(1982). Groups of six ‘‘Sprague–Dawley male white mice”(although, no such strain has been reported) were injected intra-peritoneally with 50 mg/kg pentobarbital plus 50 mg/kg of corian-der oil. Simultaneous administration of coriander oil andpentobarbital to mice did not significantly increase pentobarbi-tal-induced sleeping time. However, administration of corianderoil 30 min prior to the administration of pentobarbital resulted ina prolongation of pentobarbital-induced sleeping time (146% ofcontrol) (Marcus and Lichtenstein, 1982).

Coriander has been advocated as an anti-diabetic remedy.Recent experimental studies have suggested antihyperglycemic ef-fects of coriander seeds in streptozotocin-diabetic mice (Swanston-Flatt et al., 1990; Gray and Flatt, 1999). Gray and Flatt (1999) re-ported that incorporation of coriander into the diet (62.5 g/kg) orin drinking water (2.5 g/L, prepared by 15 min decoction) reducedhyperglycemia of streptozotocin-diabetic mice.

Medhin et al. (1986a) demonstrated that aqueous extracts ofcoriander seeds inhibit the electrically-evoked contractions ofspiral strips and tubular segments of isolated central ear arteryfrom rabbit. In another study, Medhin et al. (1986b) reported thatthe water extract of coriander seed had hypotensive effects inrats.

Chithra and Leelamma (1997) investigated changes in lipidmetabolism in Sprague–Dawley female rats (n = 6) fed a high fatdiet containing coriander seed powder (10%) for 75 days. The levelsof total cholesterol and triglycerides were decreased significantlyin serum, liver and heart. The serum levels of very low and low-density lipoprotein cholesterol were decreased, while high-densitylipoprotein cholesterol increased. The investigators concluded thatcoriander seeds had hypolipidemic effects. In another study, Chi-thra and Leelamma (1999) studied the changes in levels of lipidperoxides and activity of antioxidant enzymes in Sprague–Dawleyfemale rats (n = 6) maintained on a high fat diet containing 10%coriander seed powder for 90 days. Feeding a diet containing cori-ander seed powder resulted in a significant decrease in the levels oflipid peroxides as determined by malondialdehyde, hydroperox-ides and conjugated dienes in liver and heart. The levels of freefatty acids in serum, liver and heart of the treated animals weresignificantly decreased. Antioxidant-related enzymes, such assuperoxide dismutase, catalase, glutathione peroxidase, glutathi-one-S-transferase, glucose 6-phosphate dehydrogenase and gluta-thione reductase were significantly increased in the liver andheart of the treated animals. The results of this study suggest thatcoriander seed may protect various tissues by preventing the for-mation of free radicals. In yet another study, Chithra and Leelamma(2000) reported that feeding coriander seed (10%) protected


against the 1,2-dimethylhydrazine-induced colon and intestine tu-mors in male Sprague–Dawley rats.

As a major constituent of a spice mix added to a diet (2%), ‘‘cori-ander”, at a level of 40% in the mix (80 ppm), when fed to femaleWistar rats for 8 weeks, ‘‘favorably enhanced” the activities of pan-creatic lipase, chymotrypsin and amylase. Additionally, feeding thediet containing the spice mix significantly stimulated the bile flowand bile acid secretion (Platel et al., 2002). In a series of experi-ments on spice principles as antioxidants in the inhibition of lipidperoxidation of rat liver microsomes, Reddy and Lokesh, 1992 re-ported that linalool, the principle component of coriander oil, atconcentrations up to 600 lM had no significant effects on ascor-bate/Fe2+-induced lipid peroxidation of rat liver microsomes.

In a series of studies, Weber and colleagues studied the effectsof fatty acids (oil) from the seeds of coriander on lipid metabolism(Weber et al., 1995, 1999, 2003; Richter et al., 1996). Feeding of‘‘coriander oil” containing high proportions (72%) of a positionalisomer of oleic acid, i.e. petroselinic (cis-6-octadecenoic) acid torats (12% in diet) for 10 weeks resulted in a significant decreasein proportions of arachidonic acid in the cellular lipids of rats. Amarked- to severe-fat infiltration, as well as fatty cysts in liversof rats fed ‘‘coriander oil” were noted. It should be indicated thatin all these studies the ‘‘coriander oil” used was not the essentialoil.

2.2. Toxicological studies

2.2.1. Acute toxicity studiesThe acute oral toxicity (LD50) of coriander oil in rats was re-

ported as 4.13 g/kg (2.48–6.14 g/kg). The acute dermal toxicity(LD50) of coriander oil in rabbits was reported as >5 g/kg of bodyweight (Hart, 1971). Details of both of these acute toxicity studieswere not available. The acute oral LD50 of the major constituent ofcoriander oil, linalool, in Osborne–Mendel rats was reported to begreater than 2.79 g/kg. The authors noted ataxia ‘‘soon” after treat-ment and, time of death to be 4–18 h (Jenner et al., 1964).Although, the study was performed before the institution of goodlaboratory practices, the study meets the FDA Redbook core stan-dards (FDA, 1982). Collectively, these studies indicate that corian-der oil and its major constituent, linalool (60–80%), are of slightacute toxic potential (Hodge and Sterner, 1949; Derelanko andHollinger, 1995). As coriander oil contains approximately 70% lin-alool, the oral LD50 studies suggest that the lethality caused by theoil is from its constituent, linalool.

2.2.2. Irritation studiesApplication of full strength coriander oil to intact or abraded

rabbit skin for 24 h under occlusion was irritating (Hart, 1971).In another report, coriander oil was classified as very mildly irritat-ing to the skin (Tisserand and Balacs, 1995).

In a 48 h closed-patch test, coriander oil at a concentration of 6%in petrolatum, produced no irritation in 25 human subjects (Klig-man, 1971). Kligman (1970) reported that a 20% solution of linalool(major component of coriander oil) in petrolatum was non-irritat-ing in a 48 h patch test in humans. In another study of linalool, Fujiet al. (1972) reported that in a closed-patch test, linalool did notproduce primary irritation in 28 ‘‘normal” human subjects at 20%in Vaseline� or ointment, in 30 subjects when applied at 2%, orin 84 subjects with dermatoses, when tested at 0.4% in ethanolor cream base.

2.2.3. Short-term and subchronic toxicity studiesIn an unpublished study submitted to the Research Institute for

Fragrance Materials (RIFM) (proprietary data, published assummary report in peer-reviewed journal), coriander oil wastested in a 28 day study in rats (RIFM, 1990; Letizia et al., 2003).

The oil at a dose level of 160, 400 and 1000 mg/kg/day in 1% meth-ylcellulose was administered by gavage to Sprague–Dawley rats(10/sex/group). Control animals received vehicle alone. No treat-ment related effects on survival, clinical observations, bodyweights or food consumption were noted. In the high-dose(1000 mg/kg/day) males and females and, in the mid-dose(400 mg/kg/day) males, increases in absolute and relative kidneyweights were noted. Both absolute and relative liver weights wereincreased in the mid- and high-dose males and females. Although asignificant increase in absolute liver weight was noted in low-dose(160 mg/kg/day) females, the corresponding relative liver weightwas not significant. Increases in total protein and serum albuminwere observed in the mid- and high-dose males and the high-dosefemales. Serum calcium was also increased in male rats receivingthe high-dose of coriander oil. Histological observations revealeda high incidence of degenerative lesions in the renal cortex of thehigh-dose males, a low incidence of lesions in the non-glandularregion of the stomach in the mid- and high-dose females and ahigh incidence of slight peritoneal hepatocellular cytoplasmic vac-uolization in the liver of high-dose females. Similar hepatic lesionswith lower incidence were also noted in the low- and mid-dose fe-males. No macroscopic or microscopic changes in reproductive or-gans were noted. Based on the results of this study, a no-observed-effect-level (NOEL) was determined as 160 mg/kg/day for malerats, while for females the NOEL was less than 160 mg/kg/day (Let-izia et al., 2003). The details of the study were not available forindependent evaluation.

No subchronic studies on coriander oil were found in the pub-lished literature. In an unpublished report cited in JECFA (2003)and Oser (1968) evaluated the subchronic toxicity of linalool inmale and female rats. The details of the study were not reported,but the no-observed-effect-level (NOEL) of linalool was reportedas 50 mg/kg/day (Oser, 1968).

2.2.4. Developmental and reproductive toxicityIn an in vivo reproductive and developmental toxicity screening

test, virgin Crl CD rats (10/group) were administered (by gavage) 0,250, 500 or 1000 mg coriander oil/kg body weight daily, 7 daysprior to cohabitation, through cohabitation (maximum of 7 days),gestation, delivery and a 4 day post-parturition period. The totalduration of the exposure to coriander oil was 39 days. In this study,the maternal indices studied were twice daily observation, mea-surement of body weights, food consumption, duration of gesta-tion and fertility parameters (mating and fertility index,gestation index, number of offspring per litter). Offspring were ob-served daily for clinical signs, examination for gross external mal-formations and measurement of body weight. An increase in bodyweight and food consumption was noted at 250 mg/kg/day of cori-ander oil treatment. A non-statistically significant decrease in bodyweight and food consumption and decreased gestation index anddecreased length of gestation were noted at 500 mg/kg/day. Atthe highest dose (1000 mg/kg/day) a statistically significant de-crease in body weight and food consumption, decrease in gestationindex, length of gestation and litter size were noted. The only effecton offspring was a decrease in viability of pups at 1000 mg/kg/day.The investigators concluded that there were no effects observed inthe dams at the low-dose of 250 mg/kg/day or in the offspring atthe 250 and 500 mg/kg/day levels. The maternal no-observed-ad-verse-effect-level (NOAEL) was determined as 250 mg/kg/day andthe developmental NOAEL was established as 500 mg/kg/day(RIFM, 1989; Vollmuth et al., 1990; FFHPVC, 2002).

Al-Said et al. (1987) studied the effect of the aqueous extract offresh coriander seeds on fertility in Wistar female rats. The extractwas prepared by boiling coriander seeds in water and lyophilizingthe filtrate (1 kg seeds yielded about 6 g of the dried extract). Ratswere treated orally (not further defined, but presumably via


gavage) with 0, 250 and 500 mg/kg coriander extract and weremonitored for effects on estrus cycle, implantation, fetal loss, abor-tion, teratogenicity and serum progesterone levels on days 5, 12and 20 of pregnancy. At both dose levels (250 and 500 mg/kg), cori-ander extract produced a dose-dependent, significant anti-implan-tation effect, but failed to produce complete infertility. Nosignificant changes in the weight and length of the fetuses and noabnormalities in the organs of the offspring were noted. On day 5of the extract treatment, a significant decrease in the serum proges-terone level was noted. The investigators suggested that decrease inprogesterone may be responsible for the anti-implantation effectsof the extract. In another study, Matsui et al. (1967) evaluated theeffects of 112 natural products on fertility in mice. The investigatorsconcluded that aqueous extract of ‘‘coriander” did not affect fertilityin the female mouse. As both these studies were conducted with anaqueous extract of the coriander, the observed effects may not berelevant to the effects of coriander essential oil.

2.2.5. ImmunotoxicityGaworski et al. (1994) investigated the immunotoxicity of sev-

eral food flavoring ingredients, including coriander oil, in mice. Fe-male CD1 mice (6–8 weeks of age; n = 30) were administered(gavage) coriander oil at concentrations of 313, 625 or 1250 mg/kg/day for 5 days. Based on acute toxicity studies, the highest dosewas expected to produce minimal toxicity. Immunotoxicity wasevaluated using the plaque-forming cell (PFC) and host-resistanceassays. Coriander oil did not show any effect on immune functionin this study. Similarly, in a screening test in female B6C3F1 micefor humoral and cell-mediated immune responses, no adverse ef-fects of linalool were reported (Gaworski et al., 1994).

2.2.6. GenotoxicityHigashimoto et al. (1993) studied the mutagenicity of coriander

extracts (hot water, methanol and hexane) in Salmonella typhimu-rium strains TA98 and TA100 by the Ames assay. The extracts werenot mutagenic in either of the strains, with and without S9 meta-bolic activation. Similarly, Bersani et al. (1981) and Chughtai et al.(1998) reported that coriander spice was negative in Ames Salmo-nella microsome test. Contrary to these observations, corianderfruit extract has been reported to be mutagenic in the Ames assaywith S. typhimurium strains TA98 and TA100 (Mahmoud et al.,1992). In this study, the extract was prepared from fine powderwith 95% ethanol and concentrating the extract under vacuum.The test was performed by adding 10 mg of the extract. In anotherstudy on the screening of streptomycin-dependent strains of S.typhimurium TA98 for in vitro detection of spice-induced mutage-nicity, the alcoholic extract of coriander spice was mutagenic tothe streptomycin-dependent TA98 strain. With a streptomycin-independent TA98 strain, the spice extract was not mutagenic inthe absence of S9, but was ‘‘somewhat” (statistical analysis not re-ported by authors) mutagenic in the presence of S9 (Shashikanthand Hosono, 1987).

Heibatullah et al. (2008), examined the genotoxicity in culturedrat embryo fibroblast cells in the comet assay, of coriander drop(not further defined) and an alcoholic extract of coriander at con-centrations of up to 1019 and 1020 mg, respectively. The freshlyprepared fibroblasts were incubated with test substances for20 min at 37 �C according to the laboratory’s modified McKel-vey–Martin procedure. Hydrogen peroxide was used as a positivecontrol. The authors concluded that neither coriander preparationwas genotoxic in this assay.

Ishidate et al. (1984) investigated the primary mutagenicityscreening of food additives, including coriander fruit oil, in thechromosomal aberration test in vitro using a Chinese hamsterfibroblast cell line CHL. The cells were exposed to three differentdoses of coriander oil (maximum dose, 0.125 mg/ml) for 24 and

48 h and the incidence of polyploid cells, as well as of cells withstructural aberrations, such as chromatid or chromosome gaps,breaks, exchanges, ring formations, fragmentations, etc., was mea-sured. Treatment with coriander oil resulted in a 2% formation ofpolyploid cells; the incidence of cells with structural aberrationswas 0%. These results suggest that coriander oil was notclastogenic.

In an antimutagenic/anticarcinogenic activity testing of 62Egyptian food and medicinal preparations, Badria (1994) reportedthat coriander seed extract did not show antimutagenicity activityagainst 2-aminoanthracene-induced mutagenesis in S. typhimuri-um strain TA98 in the presence of metabolic activation (S9). Kanaz-awa (1995) reported that a 90% methanol extract from 50 mg of‘‘coriander” suppressed Trp-P-2 [3-amino-1-methyl-5H-pyr-ido(4,3-b)indole]-induced mutagenicity in an S. typhimuriumTA98 strain in the presence of S9. Similarly, in another report, Na-take et al. (1989) also reported that coriander herb extract mark-edly suppressed the mutagenic action of Trp-P-2 in the Amesassay.

Several investigators have studied the genotoxicity of linalool indifferent assays (Rockwell and Raw, 1979; Florin et al., 1980; Ishi-date et al., 1984; Heck et al., 1989). Linalool was negative in S.typhimurium strains TA92, TA94, TA98, TA100, TA1535, TA1537and TA1538 in the presence or absence of S9 metabolic activation.Similarly, in the Chinese hamster fibroblast cell assay, at a maxi-mum concentration of 0.25 mg/ml, linalool did not induce chromo-somal aberrations (Ishidate et al., 1984). When tested in rathepatocytes at concentrations up to 50 nl/ml, linalool did not in-duce unscheduled DNA synthesis (UDS) (Heck et al., 1989). Incuba-tion of linalool (125–1000 mg/plate) with Escherichia coli WP2 uvrAdid not induce mutations (Yoo, 1986). Similarly, incubation of lin-alool at a concentration 17 pg with Bacillus subtilis H17 (ret+) andM45 (ret�) was negative (Oda et al., 1979). However, in anotherstudy, linalool was found to be mutagenic at 10 ll/disk (Yoo,1986). The positive responses are contradicted by the results ofthe same assay by other investigators (Oda et al., 1979). In a mouselymphoma assay in L5 178Y TK± cells with S9 metabolic activation,linalool (at a concentration of 200 nl/ml) was negative, but wasweakly positive (details of statistical significance not available; re-port in abstract form) without S9 activation at 150 nl/ml (Hecket al., 1989). In an in vivo study employing the standard mousemicronucleus assay, there was no evidence of an increased inci-dence of micronucleated polychromatic erythrocytes at any ofthe dose levels of linalool studied (Putman, 1987).

In summary, results of a chromosomal aberration test usingChinese hamster fibroblasts demonstrate that coriander oil wasnot clastogenic. No genotoxicity studies with coriander oil werefound in the published literature, however, studies on the mutage-nicity of coriander spice or extracts ranged from equivocal to posi-tive in the S. typhimurium Ames assay. Linalool, the majorconstituent of coriander oil, was found to be non-mutagenic in sev-eral different genotoxicity assays.

2.2.7. Cytotoxicity studiesCoriander oil has been reported to inhibit a broad-spectrum of

microorganisms (Dwivedi and Dwivedi, 1972; Deans and Ritchie,1987; Baratta et al., 1998; Cantore et al., 2004). Basilico and Basil-ico (1999) investigated the inhibitory effects of coriander essentialoil on the mycelial growth and ochratoxin A production by Asper-gillus ochraceus NRRL 3174. Treatment of the fungus with corianderoil at concentrations of 0, 500, 750 and 1000 ppm for 7, 14 or 21days at 25 �C was not effective in inhibiting the growth or produc-tion of ochratoxin A. In another study, coriander oil, at a concentra-tion of 0.2% and greater, completely inhibited the growth ofAspergillus parasiticus NRRL 2999 (Tantaoui-Elaraki and Beraoud,1994). In, contrast, the essential oil of coriander was found not to


inhibit the growth of A. parasiticus CFR 223 or aflatoxin productionon palm kernel broth inoculated at 106 spores/ml, in contrast to theessential oil of sweet basil (Ocimum basilicum) (Atanda et al., 2007).

The coriander essential oil was tested for its antibacterial activ-ity against eight human pathogenic gram-positive and gram-nega-tive bacteria by the filter paper disc agar method. Except for theCorynebacterium diphtheriae, coriander oil was effective againstStaphylococcus aureus, Streptococcus haemolyticus, B. subtilis(gram-positive), Pseudomonas aeruginosa, E. coli, Klebsiella speciesand Proteus vulgaris (gram-negative) (Singh et al., 2002).

Lis-Balchin et al. (1998) compared the antimicrobial activity ofcoriander oil with Pelargonium spp. essential oils at concentrationsof 500 ppm against Saccharomyces ludwigii, Zygosaccharomycesbailii, Salmonella enteriditis and Listeria innocua. Coriander oil, atconcentrations of 500 ppm, was effective against all four bacterialspecies.

Delaquis et al. (2002) determined the minimum inhibitory con-centration (MIC) of coriander oil against gram-positive bacteria,gram-negative bacteria and Saccharomyces cerevisiae. The MIC forcoriander oil were as follows: E. coli O157:H7, 0.23%; Listeria mon-ocytogenes, 0.47%; S. aureus, 0.4% and; S. cerevisiae 0.13%. These re-sults demonstrate that coriander oil was effective atconcentrations less than 0.5% (vol/vol).

2.2.8. Sensitization studiesIn an attempt to induce sensitization in a maximization test,

coriander oil was tested on 25 volunteers at a concentration of4% in petrolatum. The oil did not produce a sensitization reactionin any of the subjects tested (Kligman, 1966, 1971).

Several studies have shown that commonly used spices produceallergic symptoms in a small percentage of individuals with atopicdermatitis. In these individuals, symptoms may vary from itchingand stinging of the lips and mouth, to anaphylatic shock. Skin test-ing has been recommended to identify individuals who may beallergic to spices. In a study of 50 patients with known allergiesto spices with 2+ or stronger skin prick test reactions, 42 were skinprick tested with an extract of coriander spice (5%). The reactionswere graded from 1+ to 4+ according to the recommendations ofthe Northern Society of Allergology. Of the 42 tested, 29 showedreaction to coriander. The distributions of graded reactions wereas follows: seven showed 4+; 13 showed 3+; eight showed 2+and one showed 1+ reaction (Ono et al., 1998). In another studyby the same group of investigators, from a group of 46 patientswith positive prick test reaction to spices, 20 were (containing pro-tein; molecular weight >1 kD), 3, 5 and 12 showed positive reac-tions, tested with 1%, 5% and 10% coriander extract. Of the 20tested at 1%, 5% and 10% coriander spice extract, respectively(Niinimaki et al., 1995). In a study of 71 patients with a skin testpositive to curry, 59% showed positive reaction to coriander in ascratch method test (Niinimaki and Hannuksela, 1981). In a scratchtest with powdered ‘‘coriander spice” in 70 patients with positiveskin test to birch and/or mugwort pollens and celery, 26 showedpositive reactions to coriander (Stager et al., 1991).

Bock (1993) reported a case of a 14-year-old girl with a severeallergic reaction (anaphylaxis) after consuming a food containingcoriander. A skin prick test with ‘‘coriander” produced a positivereaction. A double-blind, placebo-controlled, food challenge testwas performed with ‘‘coriander” in this subject. The challenge elic-ited mild symptoms, but a reaction sufficient to suggest that cori-ander was responsible for the symptoms seen in this patient. Inanother report, Moneret-Vautrin et al. (2002) presented a case ofa 26-year-old woman with multiple systemic reactions (urticariaand laryngeal angioedema) after consumption of food containingdifferent spices. Skin prick tests confirmed polysensitization to pol-lens from artemisia, sunflower, grass and paritory (Anacycluspyrethrum). Tests with food allergens were highly positive to

Compositae (sunflower flour) and Apiaceae (coriander). The dou-ble-blind, placebo-controlled, oral challenge to coriander was posi-tive at 265 mg, resulting in sneezing and rhinorrhea. At 1.5 h afterthe challenge, the quantitative score for nasal dysfunction in-creased from 0/15 to 10/15. The results of the study suggest thatthe patient was allergic to sunflower flour and ‘‘coriander” spicewith associated sensitization to pollens from mugwort, birch,Gramineaceae and Parientaria. These investigators also reported re-sults of skin prick tests in 15 children (<15 years) and 50 adultswith food allergies. Of the 15 children tested, four developed posi-tive prick tests to coriander, while 9 of the 50 adults showed a po-sitive reaction (Moneret-Vautrin et al., 2002).

Garcia-Gonzalez et al. (2002) reported a case of a 43-year-oldwoman (baker, confectioner) with work related rhinoconjunctivi-tis. On skin prick testing, the woman showed an immediate posi-tive response with ‘‘coriander” protein extract. Enzymeimmunoassay inhibition studies with the patient’s serum revealedcross-reactivity among the IgE components from coriander, ani-seed, caraway, fennel and dill extract. Suhonen et al. (1979) re-ported a case of a 51-year-old woman, who after 3 years ofoccupational exposure to coriander (spice) developed respiratorysymptoms of immediate hypersensitivity. Skin prick tests, nasaland bronchial challenge tests and the RAST assay were positiveto coriander. Additional studies on the spice were performed bysubjecting the spice to column chromatography, enzymatic diges-tion of the fractions and skin testing. These studies suggested thatthe allergen was a protein. A 27-year-old male butcher with symp-toms of rhinitis and asthma, showed a positive reaction whentested with coriander extract by skin prick test; ELISA results con-firmed the presence of IgE-mediated hypersensitivity (Sastre et al.,1994, 1996).

In a study on the characterization of allergens in Apiaceaespices, including coriander, Jensen-Jarolim et al. (1997) tested seraof 15 patients who experienced adverse reactions to spiced foodsand characterized their IgE binding patterns on coriander extractsthrough immunoblot and inhibition experiments. Of the 15 pa-tients tested, five showed a positive IgE immunoblot to corianderprotein extract. The investigators concluded that Bet v 1 (mainallergen of birch pollen, a 17 kDa glycoprotein) and profiling-re-lated allergens may, besides higher molecular weight allergenicmolecules, be responsible for Type I allergy to coriander, a memberof the Apiaceae family. Kanny et al. (1995) reported a 38-year-oldwoman pharmacist with severe anaphylactic reaction to mustardmasked in ‘‘chicken dips”. Although coriander was not reportedto be present in the ‘‘chicken dip”, on skin prick test, the womandeveloped a positive reaction with mustard, curry and coriander.

In a spice allergy evaluation study, 55 patients with localizedand generalized suspected contact dermatitis were patch testedwith several spice preparations, including coriander, at concentra-tions of 10% and 25% in white petrolatum. Using the Finn chamber,the spice preparations were applied to the upper back. The samplewas applied for 48 h and the application site was scored at 48 and96 h. No patient showed any reaction at a concentration of 10%,however two patients showed positive reaction at 25% spice prep-aration (Futrell and Rietschel, 1993).

In summary, the above-described studies show that spices,including coriander, produce allergic symptoms in a small percent-age of individuals. The symptoms of allergy to coriander may varyfrom itching and stinging of the lips and mouth to anaphylacticshock. Some investigators have reported positive skin prick testsand specific IgE production to coriander. In a few individuals, fol-lowing consumption of coriander, severe allergic reactions havebeen reported. The majority of these reports are from the use ofcoriander as a spice and not as an essential oil. In one study, theallergen has been shown to be heat-resistant and probably a pro-tein with a specific IgE in the serum. The essential oil is unlikely


to contain the protein component that has been suggested to beresponsible for the allergic reaction. Considering the high con-sumption of coriander, the reported incidence of anaphylaxis isvery low.

2.3. Observations in humans

In a case-control study in Tunisia of nasopharyngeal carcinoma(n = 80), Jeannel et al. (1990) reported that after adjustment for‘‘empirical living” condition score, the spices included in the basicstewing preparation (mixture of red and black pepper, garlic oil,caraway, and coriander) in home-cooked foods was one of the foodfactors associated with an increased incidence of nasopharyngealcancer. As other factors were also associated with the nasopharyn-geal carcinoma and coriander was a constituent of one of the prep-arations, it is unlikely that coriander was associated withnasopharyngeal carcinoma. Other studies of coriander, includinggenotoxicity studies, suggest that coriander oil may not becarcinogenic.

3. Discussion

Coriander oil is used in the food industry as a flavor ingredient.It is obtained by steam distillation of the dried fully ripe fruits(seeds) of C. sativum L. The oil is a colorless or pale yellow liquidwith a characteristic odor and mild, sweet, warm and aromatic fla-vor. Coriander oil has been recognized as GRAS for use in food byFDA and FEMA and is approved for use by the Council of Europe.The oil is used as a flavor ingredient in the majority of the food cat-egories, including alcoholic beverages, candy, pickles, meat sauceand seasonings. The average use levels range from 0.1 to100 ppm. The oil is also used in consumer products such as soap,creams, lotion and perfumes. The major constituent of the volatileoil is the monoterpene alcohol, linalool (�70%).

Coriander has a long history of use as a traditional medicine andflavoring agent; however, few studies evaluating its toxic effectswere found in the scientific literature. The main constituent of cori-ander oil, linalool, has been studied to some extent for its safety.

No studies on the biological fate of coriander oil per se in thehuman body have appeared, but in animal studies one of the majorconstituents of the oil, linalool, is rapidly absorbed, metabolizedand excreted from the body. Coriander oil and its major constitu-ent, linalool, have low acute oral and dermal toxicity in laboratoryanimals. The acute lethality studies suggest that the toxicity of theoil is from its constituent, linalool. Based on the results of a 28 dayoral gavage study in rats, a NOEL for coriander oil was determinedas 160 mg/kg/day for male rats, while in females the NOEL for cori-ander oil was less than 160 mg/kg/day. The details of the studywere not available for independent review as the original dataare proprietary.

In animal skin testing, coriander oil was irritating to rabbits.However, in human skin testing, both coriander oil and its majorconstituent, linalool, produced no irritation. In a sensitizationstudy in humans, coriander oil did not produce sensitization reac-tion. Published studies in the literature have shown that spices,including coriander, produce allergic symptoms in a small percent-age of individuals. In these individuals, symptoms may vary fromitching and stinging of the lips and mouth, to anaphylactic shock.Skin testing has been recommended to identify individuals whomay be allergic to spices. Some investigators have reported posi-tive skin prick tests and specific IgE to coriander. Severe allergicreactions have been reported in few individuals following con-sumption of coriander. The allergen in coriander has been shownto be heat-resistant and probably a protein with a specific IgE anti-body in the serum. The essential oil is unlikely to contain the pro-tein component, which is suggested to be responsible for the

allergic reaction. Considering the high consumption of coriander,the reported incidence of anaphylaxis is rare.

No subchronic studies on coriander oil were found in the pub-lished literature, but its major constituent, linalool, was evaluatedin a subchronic toxicity in male and female rats. The details of thestudy were not available, however, the NOEL of linalool was re-ported as 50 mg/kg/day. In a developmental toxicity study, thematernal NOAEL of coriander oil was determined as 250 mg/kg/day and the developmental NOAEL was established as 500 mg/kg/day. In a chromosomal aberration test using Chinese hamsterfibroblasts, coriander oil was found to be non-clastogenic. Somestudies have appeared on the mutagenicity of coriander spice orextracts. These studies reported equivocal to positive results inthe S. typhimurium Ames assay. The major constituent of corianderoil, linalool, has been studied for mutagenicity in several differentassays and was found to be non-mutagenic. Coriander oil has beenreported to possess broad-spectrum, antimicrobial activity.

4. Conclusion

The data available on the toxicity of coriander oil are limited.However, coriander and its oil have a long history of dietary use,with no record of harm caused by consumption of these ingredi-ents. Moreover, coriander oil has been in commercial use in the fra-grance industry for at least 100 years, without any record of havingcaused adverse effects. In summary, based on the history of con-sumption of coriander oil without reported adverse effects, lackof its toxicity in limited studies and lack of toxicity of its majorconstituent, linalool, the use of coriander oil as an added foodingredient is considered safe at present levels of use.

Conflict of interest statement

The authors declare that there are no conflicts of interest.

Acknowledgement

The descriptions, compilations, analysis and reviews of researchcontained in this article were funded by Philip Morris USA Inc.

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25410033 2009 safety assessment of coriander coriandrum sativum l essential oil

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