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Eucalyptol: Safety and Pharmacological Profile

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DOI: 10.5530/rjps.2015.4.2

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 Review Article

Eucalyptol: Safety and Pharmacological Profile

Mridul Bhowal and Murugananthan Gopal*
Department of Pharmacognosy, PES College of Pharmacy, 50 feet road, Hanumanthanagar, Bangalore-560050, Karnataka, INDIA.

ABSTRACT
Purpose: Eucalyptol is a colourless liquid and occurs as natural organic compound being used in food preparations.
This study aims to summarize the literature reporting on the pharmacokinetic studies, pharmacological activities,
its safety profile and limits of eucalyptol to be used in the food preparations. Methods: A systematic search was
conducted using PubMed, Google Scholar, and EMBASE to identify relevant literature published. Methodologies used
in pharmacological and toxicological studies of Eucalyptol are being reviewed comprehensively. The pharmacokinetics,
safety profile and pharmacological profile are being summarised. Conclusion: Eucalyptol is approved by the US Food
and Drug Administration (FDA) for adding in food preparation to enhance the odour and taste. Many nutraceuticals,
cakes, creams and other eatables are flavoured with eucalyptol in most countries of the world. Developing and under
developed countries have to take the measures to ensure the level of eucalyptol being used in the food preparations as
it has toxic effect too.
Key words: 1, 8-cineole, Eucalyptol, Pharmacological activity, Safety, Toxicity.

INTRODUCTION
1, 8-cineole is a naturally occurring monocy- Manufacturer’s Association (FEMA) in
clic monoterpene ether (oxide) (1, 3, 3-trim­ the year 1965 and also by US Food and
ethyl-2-oxabicyclo[2, 2, 2]octane) (Figure 1) Drug Administration (FDA), Eucalyptol is
with an aromatic and camphor like odour safe and can be used for addition in food
found in essential oils of various plant products.10 The typical concentrations of
species like Eucalyptus globulus, Eucalyptus eucalyptol in cosmetic products have been Received Date : 23/09/2015
Revised Date : 28/11/2015
polybractea (95% of 1, 8-cineole),1 Helichry- reported to be 1.6% in perfume, 0.4% in Accepted Date : 05/12/2015
sum gymnocephalum (47.4% of 1,8-cineole),2 soap, 0.1% in creams and lotions and 0.04%
DOI: 10.5530/rjps.2015.4.2
Zingiber chrysanthum (42% of 1, 8-cineole),3 in detergents.10 Committee of Experts on
Address for
Rosmarinus officinalis (43.7% of 1, 8-cineole)4 Flavouring Substances of the Council of correspondence
and many more, with the important natural Europe (CEFS) proposed upper levels Dr. Murugananthan Gopal,
source being eucalyptus essential oil.5 Due of 0.1 mg/kg in beverages and 5 mg/kg Assistant Professor,
Department of
to its natural abundance in Eucalyptus, in food with the exception of 15 mg/kg in Pharmacognosy,
1, 8-cineole is also called eucalyptol. candy and confectionery and 50 mg/kg in PES College of Pharmacy,
50 feet road,
It should not be confused with Eucalyptus alcoholic beverages.10 The typical concen- Hanumanthanagar,
oil, which is a mixture of other constituents.6,7 tration of eucalyptol in mouthwashes was Bangalore-560050,
Karnataka, INDIA.
1, 8-cineole or eucalyptol can also be synthe­ observed to be 0.092%.11 Phone : +919886444405,
sized by isomerization of α-terpineol.8 The estimated daily per capita intake of E-mail : murugan13@gmail.
com
Because of its pleasant spicy aroma and eucalyptol in Europe and the USA is 1439 µg
taste, eucalyptol is used as a flavouring agent, and 1954 µg, respectively.12 A mean daily
fragrances, and in cosmetics. Eucalyptol intake of eucalyptol from flavoured food-
is listed in Code of Federal Regulation as stuffs in France has been estimated to be
Flavouring Agents and Related Substances.9 4.5 mg/person, equivalent to 0.075 mg/kg.
As per the report of Flavor and Extract This exercise was based on use levels of www.rjps.in

RGUHS J Pharm Sci | Vol 5 | Issue 4 | Oct–Dec, 2015 125

 Mridul Bhowal and Murugananthan Gopal.: Eucalyptol: Safety and Pharmacological Profile

over the next 90 min, while at 520 mg/kg, the peak

blood concentration dropped to 60% of the maximum
value and remained in that range for the following
80 min.23 These results indicate that at doses of up to
200 mg/kg, eucalyptol goes through a rapid absorption
into the blood, metabolism and conjugation to polar
metabolites. At higher or inflated doses, however,
metabolism appears to be slow, probably due to saturation
of the metabolic pathway.

SAFETY
Figure 1: Structure of eucalyptol (1, 3, 3-Trimethyl-2-oxabicyclo Eucalyptol doesn’t have negative effects from animal
[2, 2, 2]octane)
experiments which have been reported so far, but data
are rather insufficient. No mutagenicity, or reproductive
eucalyptol provided by industry and took into account or developmental toxicity or carcinogenicity has been
the market share of all food categories possibly flavoured reported until now and subacute hepatotoxic and neph-
by plants, extracts of plants or eucalyptus oil.10 rotoxic effects in animal experiments appeared only
after the application of high doses, in accordance with a
PHARMACOKINETICS rather high acute oral LD50 in rats of 2.5 g/kg.5
Eucalyptol is quickly absorbed from the gastrointestinal Acute toxicity study
tract. It’s lipid soluble and absorption is enhanced in The LD50 of orally administered eucalyptol in rats has
the presence of milk. Inhalation of the liquid is directly been reported as 1560 mg/kg24 and 2480 mg/kg.25 Toxic
toxic to the lungs; however there is no data suggesting effects at the 1560 mg/kg reported to produce rapid
systemic absorption by lungs.13 cyanosis, stupor, irregular breathing, and utmost sen-
Eucalyptol undergoes oxidation in vivo with the formation sitivity to noise, convulsions, and death from respira-
of hydroxycineole which excretes as glucuronide.14 The tory failure.24 The estimated lethal dose of Eucalyptol in
metabolism of eucalyptol was studied previously in humans ranged from 0.05 to 0.5 ml/kg.26
rats and rabbits. The results revealed that two alcohols,
namely 2-hydroxy-eucalyptol and 3-hydroxy-eucalyptol, Short-term toxicity study
were excreted in the urine.15,16 It was also reported that In rats eucalyptol administered orally through stomach
eucalyptol is metabolized to several dihydroxycineoles, tube at doses up to 1200 mg/kg 5 days per week or
cineolic acids and hydroxycineolic acids after feeding encapsulated and added to feed at doses up to 3342 mg/kg
brushtail possums and male koalas.16-20 Report revealed daily for 28 days, a dose-related decrease in weight gain
that eucalyptol gets metabolized by rat and human liver and a normal degree of hepatic centrilobular cytoplasmic
microsomes as well as by several recombinant cyto- vacuolization was found to be absent in male rats. Dose
chrome oxidases to solely 2- hydroxy-eucalyptol.21,22 related lesions in the kidneys, liver and parotid salivary
Administration of 200 mg/kg of eucalyptol p.o. to rabbits glands were found at all dose levels in male rats fed
showed peak plasma concentrations of the alicyclic sub- encapsulated eucalyptol.27
stance, eucalyptol and its major unconjugated metabolites In male rats administered 0, 500, or 1000 mg/kg of
occurred within 30 min and 1 hour. The Parent ether the compound eucalyptol daily for 28 days, statistically
reached Cmax of 840 µg/dl within 30 min, while the significant decreases in terminal and increases in relative
plasma concentration of the chief unconjugated metabo- liver and kidney were found in both dose groups,
lite, (+)-2-exo-hydroxy-1, 8-cineole, peaked at 2400 µg/dl whereas relative brain weight was increased only in highest
within 1 h and then decreased slowly between 2 hour dose group. Minor focal infiltration of mono nuclear
and 6 hour. Peak plasma concentration (1250 µg/dl) of cells in the liver was observed in all groups. In kidneys,
the major conjugated metabolite, (+)-2-exo-hydroxy- a dose-related accumulation of eosinophilic protein
1,8-cineole, occurred 1.5–2 h after dosing.22 In mice, 4 µl, droplets containing α2μ-globulin in the cytoplasm of
20 µl or 40 µl of rosemary oil containing 39% of eucalyp- proximal tubular epithelial cells were observed.28
tol (approximately equivalent to 52, 260 and 520 mg/kg Doses of 150, 300, 600 and 1200 mg/kg of eucalyptol
of eucalyptol, respectively) is given by oral route shows was fed to groups of 6 male and 6 female B6C3F1
blood concentrations of eucalyptol reached a peak 5 min. mice for 28 days either by stomach tube on 5 days/week
At 260 mg/kg, blood concentrations remained constant at doses or in encapsulated form at concentrations of
126 RGUHS J Pharm Sci | Vol 5 | Issue 4 | Oct–Dec, 2015
 Mridul Bhowal and Murugananthan Gopal.: Eucalyptol: Safety and Pharmacological Profile

3750, 7500, 15000 and 30000 mg/kg, equal to 705-6777 assay with Chinese Hamster Ovary (CHO) cells (except
mg/kg /day for female mice and 600–5607 mg/kg/day for at doses inducing cell cycle delay when administered
male mice. The liver weight/ratio in males was increased without metabolic activation).34,35 It did not cause DNA
at all but the lowest dose given in encapsulated form as damage in bacteria. Damage in chromosome was not
the brain weight/ratio in females at the top dose level. induced in mammalian cells treated in culture, but there
Microscopic examination divulged a minimal hypertro- were some indications of other chromosomal effects.
phy of centrilobular hepatocytes in animals of both
sexes fed the encapsulated compound, especially at the Human data and Safety considerations
two highest dose levels.29 Accidental toxicity has been reported after ingestion
of eucalyptus oil. The lowest lethal doses reported are
Long-term studies of toxicity and carcinogenicity 1.9 g eucalyptus oil in a 10 year old boy36 and 4-5 ml
In a study of the carcinogenic effects of toothpaste in adults.37 In other cases, asymptomatic or less severe
constituents including chloroform, eucalyptol, and pep- effects were observed after ingestion of higher doses.38
permint oil, eucalyptol was given to groups of 52 male Two people died after accidently ingesting 3.5-5 ml
specific pathogen-free CFLP mice at a dose of 8 of eucalyptus oil; however recovery after much higher
or 32 mg/kg per day by gavage, 6 days per week for doses has also been reported.39 Dose recommended for
80 weeks. Control groups of 52 mice were either adults 0.05-0.2 ml and it is as a rubifacient 0.5%-3%.
untreated or received a toothpaste base which lacked Fatal dose is 4-5 ml. Death is definite at 30ml. In children
chloroform, peppermint, or eucalyptol (vehicle control). 3-5 ml of 100% eucalyptus oil is sufficient to cause fatal
Animals were housed four per cage and given food and complications.13
water at libitum. Mice were weighed weekly for the first
The use of eucalyptol containing products in children
6 months and then every 2 weeks during the last 6 months
below 30 months old should be avoided. Children
of the study. The consumption of food was noted on
younger than 7 years, the eucalyptol content of the fini­
a cage-by-cage basis. Animals were observed twice daily
shed product should not exceed 1.12% and its presence
and those found dead or in a moribund condition during
should be mentioned in the product labelling.39
the study were gross inspected. At week 80, animals
were killed and organ weights for the kidneys, adrenals, Risk assessment
lungs, liver, and spleen were noted. All macroscopically
The toxicological studies which were available are limited
identified tumours were examined histopathologically,
and inadequate to derive an acceptable daily intake.
along with tissues from the kidneys, liver, lungs and
However, the animal data which were available does not
brain. No treatment-related changes were reported for
indicate a cause of concern associated with the daily
the following parameters: food consumed, body weight,
intake from food. The case reports on acute toxicity in
organ weights, and clinical signs of toxicity. Necropsy
humans refer to the ingestion of eucalyptus oil and not
and organ weight measurements showed no treatment-
to eucalyptol as such.10 They do not provide information
related differences between control and test groups.
for ample estimates of toxic dose levels for eucalyptol.
Histopathological examination revealed no notable
Even if eucalyptol were responsible for the acute toxicity
differences between control, test, or vehicle control
of eucalyptus oil, the estimated daily intake of eucalyptol
groups in the incidence or severity of tumours of the
from food would be much lower than the amount
kidney, liver, lung, or malignant lymphoma.30
tentatively assumed to be present in the lowest lethal
Studies using the Substrain of A mouse strain originating doses of eucalyptus oil reported.10 For a more precise
from Walter Heston [A/HE] primary lung tumor model risk assessment, further data on exposure and toxicity
was carried out for carcinogenicity of eucalyptol (12 g/Kg/ would be needed.
8 wk intermittent; Max tolerated dose) but it was
observed to be not positive for tumor induction. None
of the other components of this product are listed as PHARMACOLOGICAL ACTIONS OF EUCALYPTOL
carcinogens by Occupational Safety and Health Admin- Effects on Central Nervous System (CNS)
istration (OSHA), International Agency for Research on
Cancer (IARC), American Conference of Govermental Eucalyptol exhibit antinociceptive properties and
Industrial Hygienists (ACGIH), National Toxicology thereby, indicating a potential calmative and depressant
Program (NTP) or European Union (EU) Directives.31 action on the central nervous system.
A study carried out by Santos et. al.,40 using Male Swiss
Mutagenicity study mice and Wistar rats showed potential antinociceptive
Eucalyptol was not found to be mutagenic in Ames bac- property. They induced chemical nociception by intra-
terial tests32,33 or in a sister chromatid exchange (SCE) plantar formalin and intraperitoneal acetic acid. Activity
RGUHS J Pharm Sci | Vol 5 | Issue 4 | Oct–Dec, 2015 127
 Mridul Bhowal and Murugananthan Gopal.: Eucalyptol: Safety and Pharmacological Profile

was present in these tests, at an oral dose range of tolerated dose reduction during eucalyptol was four
100–400 mg/kg. In the formalin test, the antinociceptive times than that in the placebo group with a four times
effect of cineole was not reversed by pretreatment of greater reduction of cumulative steroid doses in the
mice with naloxone (1 mg/kg, s.c.), a µ-opioid receptor verum group. Therefore, this was the first report to be
antagonist, suggesting the involvement of a non-opioid proposed for the clinically pertinent anti-infammatory
mechanism. Eucalyptol also demonstrated a significant activity of eucalyptol in bronchial asthma.43
inhibitory effect on locomotion and also potentiated the Relatively high concentrations of systemic eucalyptol
pentobarbital sleeping time in mice, indicating a prob- were also reported to display an inhibitory effect on the
able depressant effect on the central nervous system.40 classic types of experimental inflammation in rats, i.e.
Effects on Cardio Vascular System (CVS) paw oedema by carrageenan and cotton pellet-induced
granuloma.40
In normotensive rats, a study was carried out to inspect
Another study on the anti-inflammatory activity of euca-
whether Autonomic Nervous System (ANS) is involved
lyptol was carried out by using the trinitrobenzenesul-
in the mediation of eucalyptol induced changes in mean
aortic pressure (MAP) and heart rate (HR). In both fonic acid (TNBS)-induced colitis model in rats, which
pento­barbital-anesthetized and conscious, freely moving was considered as one of the most common experi-
rats, bolus injections of eucalyptol (0.3-10 mg/kg, i.v.) mental models used in screening drugs active against
elicited similar and dose-dependent decreases in MAP. human inflammatory bowel disease.44 Male Wistar rats
Concomitantly, eucalyptol significantly decreased HR received eucalyptol (200 and 400 mg/kg) rectally,
only at the highest dose (10 mg/kg). Pretreatment of 24 and two hours before (pre-treatment) or two and
anesthetized rats with bilateral vagotomy significantly 24 h after (post-treatment) the induction of colitis via
reduced the bradycardic responses to eucalyptol (10 mg/kg) intracolonic administration of TNBS. The administration
without affecting hypotension. In conscious rats, i.v. of TNBS induced an extensive inflammation and ulcer-
pretreatment with methylatropine (1 mg/kg), atenolol ation in the colon associated with an increase in myeloper­
(1.5 mg/kg), or hexamethonium (30 mg/kg) had no oxidase (MPO) activity, an indicator of neutro­philic
significant effects on the eucalyptol induced hypotension, infiltration.45 Animals pre-treated but not post-treated
while bradycardic responses to eucalyptol (10 mg/kg) with eucalyptol showed a significant reduction in gross
were significantly reduced by methylatropine. In rat isolated damage scores and wet weights of the inflamed colonic
thoracic aorta preparations, eucalyptol (0.006-2.6 mM) tissue, a parameter considered a reliable and sensitive
induced a concentration-dependent reduction of the indicator of the severity and extent of the inflammatory
contraction induced by potassium (60 mM). However, response.46 In addition, it also significantly reduced
direct actions of eucalyptol on the cardiac muscle or MPO activity, thus indicating anti-inflammatory effect
contractile proteins were not described yet.41 of eucalyptol with a possible preventive action for gastro­
intestinal inflammation and ulceration.47
Eucalyptol enhances blood circulation, leading to skin
hyperemia after local application.23 Other reports have Investigations of anti-inflammatory efficacy of eucalyptol
shown that prolonged exposure to eucalyptol (inhalation) in inhibiting polyclonal stimulated cytokine production
increases cerebral blood flow correlated with eucalyptol by human unselected lymphocytes and lipopolysaccharide
concentration in blood suggesting a vasodilator action.42 (LPS)-stimulated monocytes was carried out.48 At
1.5 μg/mL, eucalyptol significantly inhibited cytokine
Anti-inflammatory effects production in lymphocytes of TNF-α (92%), IL-1β
Anti-inflammatory efficacy of eucalyptol was evaluated (84%), IL-4 (70%) and IL-5 (65%), and monocytes of
by determining its equivalent potency of prednisolone TNF-α (99%), IL-1β (84%), IL-6 (76%) and IL-8 (65%),
in patients with severe asthma. 32 patients aged and at 0.15 μg/mL, it significantly suppressed production
32-75 years who met NHLBI (National Heart, Lung, of TNF-α and IL-1β by monocytes (77% and 61%,
and Blood Institute) criteria for the diagnosis of bron- respectively) and of IL-1β and TNF-α by lymphocytes
chial asthma were recruited in the double-blind placebo (36% and 16%, respectively). The results obtained in
controlled trial, the majority of patients with chronic this study show that eucalyptol acts as a strong inhibitor
asthma receiving oral eucalyptol 200 mg t.i.d. remained of TNF-α and IL-1β and strengths its use as an agent
clinically stable despite a mean reduction of oral steroid to control airway mucus hyper secretion by cytokine
dosage of 36% equivalent to 3.8 mg/day. This was in inhibition, suggesting long-term treatment to reduce
sharp contrast to the placebo group (7% equivalent to the severity of asthma, sinusitis and chronic obstructive
0.9 mg/day); in which 12 of 16 patients were noted pulmonary disease (COPD).
to tolerate any decrease of oral steroids according to Eucalyptol, for its potential beneficial use in therapy as
pre-defined stability criteria. The mean duration of the an anti-inflammatory agent it can be efficient in treating
128 RGUHS J Pharm Sci | Vol 5 | Issue 4 | Oct–Dec, 2015
 Mridul Bhowal and Murugananthan Gopal.: Eucalyptol: Safety and Pharmacological Profile

asthma, gastric inflammation, sinusitis, COPD and also increased GPx, CAT, GSH levels, while reducing MDA
in neurodegenerative disease like Alzheimer’s disease.49 concentration close to the level of the control group,
suggesting activation of antioxidant defence systems as
Effects on Smooth Muscle one of the mechanisms of hepatoprotection induced
Controlled study was carried out in patients with by eucalyptol.54
asthma following oral therapy with eucalyptol for 7 days
reported on surprisingly strong bronchodilators effects.50 Antitumorogenic effect
It relaxes bronchial and vascular smooth muscle due to Anti-proliferative action of eucalyptol was studied on
its secretolytic properties and in addition to its myor- human colon cancer cell lines HCT116 and RKO by
elaxant effects.51 WST-8 (Water-soluble tetrazolium salt-8) and Bromo-
deoxyuridine (BrdU) assays. The cytotoxicity of euca-
Gastroprotective effect52 lyptol was investigated by lactate dehydrogenase activity
Study carried out in rats for the investigation of the gastro­ and TUNEL (Terminal deoxynucleotidyl transferase
ptrotective effect of eucalyptol on ethanol-induced dUTP nick end labelling ) staining. The mechanism of
gastric mucosal damage and the possible mechanisms apoptosis by eucalyptol was determined by western blot
involved. Eucalyptol (50-200 mg/kg) was given orally analyses. In the in vivo study, injections of RKO cells into
1 hr before administration of 1 ml of absolute ethanol the Severe combined Immunodeficiency (SCID) mice
significantly attenuated the ethanol-induced gastric and the effect of eucalyptol were investigated. Specific
injury in a manner similar to nordihydroguairetic acid, induction of apoptosis, not necrosis, was observed in
a known lipoxygenase inhibitor. Eucalyptol showed a human colon cancer cell lines HCT116 and RKO by
tendency to restore the ethanol-associated decreases eucalyptol. The treatment with eucalyptol was associ-
in nonprotein sulfhydryls, suggesting a possible anti- ated with inactivation of survivin and Akt and activa-
oxidant effect. In gastric secretion studies, eucalyptol, tion of p38. These molecules induced cleaved Poly ADP
similar to cimetidine, a known histamine-2 receptor ribose polymerase (PARP) and caspase-3, which finally
antagonist, demonstrated significant inhibitions of both causes apoptosis. In xenotransplanted SCID mice, the
gastric juice volume as well as total acid output. The eucalyptol group showed significantly inhibited tumour
protection offered by eucalyptol was found to be unal- progression compared to the control group. Based on
tered by 8-phenyltheophylline or L-NAME, indicating these studies eucalyptol would be an effective strategy
that its effect is not mediated by endogenous adenosine to treat colorectal cancer.55
or nitric oxide. These results, suggest that the antioxidant
Antimycotic activity
and lipoxygenase inhibitory actions of eucalyptol are of
prime importance in affording gastroprotection against Antifungal activity of eucalyptol was evaluated by contact
ethanol injury in the rat. assay on Czapek’s dox agar. Eucalyptol (0.918 mg/mL)
showed remarkable antifungal effect against all the
Hepatoprotective effect fungi isolates of chickpea. Its minimal inhibitory (MIC)
The hepatoprotective mechanism of eucalyptol was and fungicidal (MFC) concentrations for Aspergillus
investigated in an in vivo murine model of septic shock flavus were lower than those of the prevalent systemic
syndrome in mice which was induced by D-galactos- fungicide Nystatin. Aflatoxin B1  (AFB1) production
amine/lipopolysaccharide and that is characterized by by NKD-208 isolates of   Aspergillus flavus was strongly
early apoptosis and subsequent lysis of hepatocytes. inhibited even at the lower fungistatic concentration of
Eucayptol suppresses the increase in liver weight along eucalyptol.56
with suppression of the elevation in serum transaminase In another study, eucalyptol was evaluated for antifungal
activity, it also prevented the necrosis and haemorrhage activity against Aspergillus flavus and Aspergillus parasiticus.
to a greater extent than dexamethasone. Hepato­ The evaluation was performed by compound dissolution
protection was suggested to be associated with a in yeast extract sucrose (YES) medium and by head-
reduction in Tumor Necrosis Factor-α (TNF-α) serum space volatile exposure assays. The antifungal activity
concentration.53 In rats treated with the environmental offered by eucalyptol was incomplete and only showed
contaminant 2, 3, 7, 8-tetracholorodibenzo-p-dioxin effects at the highest concentration tested (1.3492 µl).57
(TCDD) for 30 days, activities of antioxidant enzymes
Glutathione Peroxidase (GPx) and Catalase (CAT), and Antibacterial activity58
Glutathione (GSH) levels in liver were significantly Standard species of bacteria Staphylococcus aureus (ATCC
decreased, whereas Malondialdehyde (MDA) levels were 29213) and Enterococcus faecalis (ATCC 29212), and blood
significantly increased compared to the non-treated agar were used for the study. Chloroform was used as
group. When given together with TCDD, eucalyptol the positive control and 0.9% saline was used as the
RGUHS J Pharm Sci | Vol 5 | Issue 4 | Oct–Dec, 2015 129
 Mridul Bhowal and Murugananthan Gopal.: Eucalyptol: Safety and Pharmacological Profile

negative control. The study was carried out on in vitro sinusitis and even several neurodegenerative disorders
on Staphylococcus aureus (ATCC 29213) and Enterococcus like Alzheimer’s because of its anti-inflammatory activity.
faecalis (ATCC 29212) species for the antibacterial activity It is hepatoprotective as well as gastroprotective and
of eucalyptol. Eucalyptol showed antibacterial effect also posse’s antibacterial, antimycotic and antitumoro-
for Staphylococcus aureus in both time period, but not for genic activities. Studies done under its antitumorogenic
Enterococcus faecalis, which grew colonies after both time property shows that eucalyptol would be an effective
periods, in the dilution of the standard inoculum, and strategy to treat colorectal cancer. The pharmacological
also in the negative control. investigations carried out on eucalyptol validate the
immense potential of this constituent in the treatment
CONCLUSION of numerous diseases. The use of eucalyptol in food
preparation needs to be monitored. Additional research
Extensive studies revealed that Eucalyptol is considered and clinical trials are needed for the product develop-
to be a chemical which is safe when taken in normal ment to strengthen the use of  eucalyptol for the future
doses. In higher doses, eucalyptol is hazardous via inges- generations. The uses of eucalyptol in food preparation
tion, skin contact or inhalation. Eucalyptol doesn’t show need to be monitored by the regulatory bodies.
genotoxicity or carcinogenicity, but the substance may
be toxic to the reproductive system. Repeated or pro-
longed exposure to the substance can produce damage ACKNOWLEDGEMENT
to target organs.59 Detailed research is required to fix the Authors are thankful to Prof Dr. J. Saravanan, Principal,
recommended dose level at universal level. Complete PES College of Pharmacy for the needful support.
toxicity studies also need to be carried out. Eucalyptol
depresses CNS and shows antinociceptive property, it
enhances blood circulation, causes vasodilation and also CONFLICT OF INTEREST
bronchodilation. Eucalyptol has therapeutic potency The authors declare that there are no conflict of
against bronchial asthma, COPD, gastric inflammation, interest.

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