Body Malodours and Their Topical Treatment Agents

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Review Article

Body malodours and their topical treatment agents

M. Kanlayavattanakul and N. Lourith

School of Cosmetic Science, Mae Fah Luang University, Chiang Rai, Thailand

Received 4 October 2010, Accepted 3 February 2011

Keywords:anti-perspirant, body odour, deodourant, foot odour, treatment

Synopsis

Body malodour, including foot odour, suppresses social interaction

by diminishing self-confidence and accelerating damage to the

wearers clothes and shoes. Most treatment agents, including alu-

minium anti-perspirant salts, inhibit the growth of malodourousbacteria. These metallic salts also reduce sweat by blocking the

excretory ducts of sweat glands, minimizing the water source that

supports bacterial growth. However, there are some drawback

effects that limit the use of aluminium anti-perspirant salts. In

addition, over-the-counter anti-perspirant and deodourant products

may not be sufficiently effective for heavy sweaters, and strong

malodour producers. Body odour treatment agents are rarely men-

tioned in the literature compared with other cosmetic ingredients.

This review briefly summarizes the relationship among sweat, skin

bacteria, and body odour; describes how odourous acids, thiols,

and steroids are formed; and discusses the active ingredients,

including metallic salts and herbs, that are used to treat body

odour. A new class of ingredients that function by regulating the

release of malodourants will also be described. These ingredients do

not alter the balance of the skin flora.

Resume

Les mauvaises odeurs corporelles, y compris celles des pieds, atte-

nue linteraction sociale en diminuant la confiance en soi et favori-

sant des dommages aux vetements et aux chaussures portes. La

plupart des agents inclus dans les traitements, y compris les sels

daluminium antiperspirants, inhibent la croissance de bacteries

malodorantes. Ces sels metalliques reduisent aussi la sueur en blo-

quant les canaux excreteurs des glandes sudoripares, reduisant ainsi

au minimum leau, source de la croissance bacterienne. Cependant,

il y a quelques inconvenients qui limitent lutilisation de sels dalu-

minium anti-transpirants. De plus, les produits antiperspirants et

deodorants OTC peuvent ne pas etre suffisamment efficaces pour des

personnes produisant une grande quantite de sueur et producteursde fortes odeurs. Les agents actifs sur les Odeurs corporelles sont rar-

ement mentionnes dans la litterature comparativement a dautres

Ingredients cosmetiques. Cette revue recapitule brievement la rela-

tion entre la Sueur, les bacteries cutanees et lodeur corporelle; elle

decrit comment des acides odorants, des thiols, et des ste rodes sont

formes; et examine les principes actifs, y compris les sels metalliques

et les vegetaux utilises pour traiter lodeur corporelle. Une nouvelle

classe dingredients dont la fonction est de reguler la liberation de

mauvaises odeurs est egalement decrite. Ces ingredients ne modifient

pas lequilibre de la flore cutanee.

Introduction

Body odour, which encompasses axillary and foot odour, can com-

municate a strong non-verbal signal [1, 2]. These odours are often

unnoticed by the offender because that person has specific anosmia

[3]. As a result, the individual is embarrassed when alerted, and

his or her self-confidence is compromised. The offensive body odour

also has economical consequences stemming from the need to

replace damaged/stained clothes and shoes [4, 5].

In contrast to clear findings in animals, the presence of human

vomeronasal organs is still being debated. Clearly, the ability to

appreciate underarm and foot odours depends solely on an individ-

uals evolutionary culture and perceptual development. However,

the emission of odourless human pheromones has been reviewed

and is becoming a popular discussion topic [6].

The human scent is genetically controlled and systemically influ-enced by dietary and medicinal intake, as well as the application of

fragrance products [68]. Heavy sweating or hyperhidrosis, partic-

ularly at axillary sites, leads to unpleasant odours that cause social

embarrassment and reduce self-confidence, especially among

women. Hyperhidrosis results from the oversecretion of sweat.

Because there is an excessive amount of water in which bacteria

can grow, hyperhidrosis is often accompanied by bromhidrosis or

osmidrosis or offensive body odour. Both conditions can be treated

by topically applying anti-perspirant and deodourant products.

Body odour treatment products are part of a multibillion dollar

industry [9]. High levels of fragrance are often used in these prod-

ucts to mask malodour [10]. Surprisingly, there is little discussion

of odour treatment products in the literature [6], in contrast to

other personal care products [11, 12].

This review will summarize the chemical composition andformation of body odour, the use of anti-perspirant, deodourant

and herbal products to treat body odour, and a new class of treat-

ment agents that do not change the balance of the skins bacterial

population.

Sweat glands and body odour

Sweat is necessary for thermoregulation control, enabling humans

to live in different climate zones. There are three types of sweat

glands: eccrine, apocrine and apoeccrine. The eccrine glands are

Correspondence: Nattaya Lourith, School of Cosmetic Science, Mae Fah

Luang University, Chiang Rai, 57100, Thailand. Tel.: +66 53 916834;

fax: +66 53 916831; e-mail: [email protected]

International Journal of Cosmetic Science, 2011, 33, 298311 doi: 10.1111/j.1468-2494.2011.00649.x

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distributed throughout the human body, particularly in the palms,

soles and armpits. Sweat glands vary in density and size depending

on race, sex, body site and determination techniques [1315]. Apo-

crine gland secretions, which are initially odourless, are metabo-

lized by normal skin flora, producing malodour.

Eccrine glands exist and function at birth. Apocrine glands exist

at birth, but they do not begin to function until the onset of pub-erty. Within the axilla, apocrine glands outnumber eccrine glands

by 101 [16]. Apoeccrine glands develop from the eccrine gland

during adolescence, as the number of eccrine glands is observed to

decrease with age. Although the eccrine glands are mainly respon-

sible for thermoregulation, emotional stimuli also initiate a

response, particularly from those glands found in the palms, soles

and forehead. Emotional stimuli also initiate responses from the

apoeccrine and apocrine glands within the axilla [17].

Apocrine glands open into hair follicles and secrete malodour

precursors and microbial nutrients that provide an excellent envi-

ronment for the growth of cutaneous microorganisms [18]. Some

examples of apocrine gland secretions include: proteins, lipids, sul-

phur-containing amino acids, volatile short-chain fatty acids and

steroids such as dehydroepiandrosterone (DHEA), DHEA sulphates

(DHEAS), androsterone and testosterone [1921]. In adolescents, ahigh amount of 5a-reductase type I has been identified that con-

verts testosterone to dihydrotestosterone (DHT), another androgen

that contributes to malodour [22]. Such cutaneous microorganisms

include aerobic cocci of the Micrococcaceae family, aerobic diph-

theroids (mainly Corynebacterium), anaerobic diphtheroids (Propio-

nibacterium) and yeast (Pityrosporum) [23]. Some of the resulting

malodourous species include: (E)-3-methyl-2-hexenoic acid or

3M2H and 3-hydroxy-3-methyl hexanoic acid (HMHA) [24], 3-sul-

phanylalkanol (particularly 3-methyl-3-sulphanyl hexanol;

3M3SH) [2527], androstenone (5a-androst-16-en-3-one) and

androstenol (5a-androst-16-en-3a-ol).Trans-3M2H is detected more

frequently than its cis-isomer. The E/Z ratio is 10 : 1 in men and

16 : 1 in women [18, 28, 29], of which detection thresholds of

these characteristic malodourants were shown in Table I. It is the

presence of those bacteria population that metabolizes apocrinegland secretions producing axillary odour.

Hypersweating by eccrine glands, commonly known as hyper-

hidrosis, produces a water-rich environment that supports the

bacteria population (i.e. Corynebacteria, Stapphylococci and Propioni-

bacteria) that causes extreme body malodour known as osmidrosis

or bromhidrosis. Hypersweating does not occur before the onset of

puberty, similar to emotional sweating in the axillary region. Axil-

lary hyperhidrosis is defined as a sweat rate >20 in men and

10 mg min)1 in women. However, palmar hyperhidrosis in both

sexes is defined as a rate of sweat secretion >3040 mg min)1

[30]. The axillary odour is stronger given differences in the bacte-

rial populations at the different sites. Young females are often

hypersensitive to the resulting axillary malodour, perhaps because

male body odour from this site acts as a human pheromone [6].

Sweat from the eccrine gland mainly consists of water (99%)and amino acids, ions, lactic acid, glycerol, urea, peptides and

proteins (particularly cysteine containing) [31, 32]. Propionibacteria,

Staphylococcus and Corynebacteria that are apart of the normal skin

flora catabolize glycerol, and lactic acid to short-chain (C2C3)

volatile fatty acids (VFAs) such as acetic, and propionic acids.

These bacteria also degrade amino acids into C4C5 methyl-

branched VFAs such as isovaleric acid, a common foot odourant

[25, 33, 34]. Valine is transformed into isobutyric acid, leucine is

converted to isovaleric acid, and isoleucine is degraded to 2-methyl

butyric acid through aerobic metabolism [35]. The apoeccrine

glands secrete some of the same compounds that are found in

eccrine sweat [36] because these glands are believed to develop

from eccrine glands. Sweat collected from the skin surface contains

a diverse range of metabolites, depending on the physiology status

of the donor as well as the functional, and developmental states of

the sweat glands.

Sebaceous glands also secrete odourless compounds that includewax esters, cholesteryl esters, cholesterol and other sterols, squa-

lenes, hydrocarbons and triglycerides. These compounds are further

metabolized into malodourants by means of cutaneous bacteria

lipase. Triglycerides are hydrolysed yielding glycerol and subse-

quently VFAs.

Odourous acids

Staphylococci metabolize amino acids to generate short-chain

methyl-branched VFAs that contribute to malodour. Corynebacteria

metabolize skin lipids to generate medium-chain VFA (C6C11).

These bacteria transform, for example isopalmitic acid to isobutyric

acid [35]. Corynebacteria, previously called lipophilic diphtheroids,

populate the axillary region and are believed to be the main bacte-

rial contributor to axillary odour [37, 38]. The metabolic efficiencyof odourant generation by means of Coryneform lipase activity was

found to be superior to that mediated by Staphylococci and Propioni-

bacterium. Propionibacterium was found to be the least efficient

bacteria with regard to the generation of malodourants [37].

3-Hydroxy-3-methyl hexanoic acid, a very pungent axillary

odour, was the most abundant odourant identified in axillary secre-

tions [39] quantified by means of LC-MS/MS [12] and confirmed by

GC-MS [24] and GC techniques [25]. This odourant acid was

detected in a larger amount than its dehydroxylated analogue

(3M2H) [12]. HMHA might be a precursor of 3M2H, resulting from

an acid-catalysed dehydrolysis reaction [40]. HMHA, 3M2H and

28 other acids were determined to be degradation products of leu-

cine, isoleucine and tyrosine [39]. The bacterial exoenzyme, amino-

acylase, was shown to cleave these odourants from water-soluble

proteins, namely apocrine secretion odour-binding proteins 1 and 2(ASOB1 and ASOB2). ASOB2, a stable protein [41], was identified

as apolipoprotein D (apoD), which is an a2l-microglobulin in the

lipocalins family [42]. The mechanism of VFA transportation to the

skin involves the covalent binding of 3M2H (3M2H : apoD = 2 : 1)

and its hydroxylated derivative, HMHA, a spicy note characteristic

of axillary odour to a glutamine (Gln) residue of the ASOB proteins,

Na-3-methyl-2-hexenoyl-l-glutamine and Na-3-hydroxy-3-methyl-

hexanoyl-l-glutamine [30]. These odourants are released by a

Zn2+-containing Na-acyl-Gln-aminoacylase specifically from Coryne-

bacterium striatum strain Ax20, as shown in Fig. 1. This dipeptidase

has a certain affinity towards Na-acyl-Gln conjugates [12] and

Na-acyl-Gln-aminoacylase. This affinity is specific to cleaving at the

Gln residue and low for cleaving the Na-acyl bond [12, 24, 25].

Subsequently, the odourant acids cleaved from Na-acyl-Gln conju-

gates [43] are volatilized off of the skin surface [12]. Odourantacids are covalently bound to apoD at their carbonyl terminal ends.

The ASOB2 concentration was found to vary with race [20], con-

firming the race-related differential intensity of body odour [13,

15]. Nonetheless, the concentration of axillary bacteria did not

vary [20]. Therefore, an understanding of the molecular mecha-

nism underlying metallopeptidase enzyme activity will facilitate

the design of inhibitors to terminate the release of malodourous

compounds [12].

In addition to ASOB2, the ABCC11 gene, whose protein is

expressed and localized in apocrine glands, has recently been found

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to be associated with the presence of axillary malodour. This

protein is essential for Na-acyl-Gln conjugates in odourous acids

[44]. The enzymatic release of these conjugates results in long-last-ing malodour. Using HMHA with a detection threshold of 4 ppt,

the enantiomeric excess (ee) of the (+)-(S)-isomer (>97%) was

observed at a S: R ratio of 72 : 28. The S-isomer exhibited a

strong spicy odour, whereas its optical isomer exhibited a weak

animal-like odour [25]. However, the ABCC11 protein was less

associated with the production of straight-chain acids. The

straight-chain acids might derive from b-oxidation or bacterial deg-

radation of skin or sebum lipids [44]. Transportation and formation

of odourous acids are prospectively illustrated, as shown in Fig. 2.

The above learning suggests that controlling ABCC11 will control

the secretion and formation of amino acid precursors and axillary

odourants.

ABCC11 protein was also associated with a dry white earwax

phenotype among Asian individuals. Asians having this particular

phenotype had less body odour and lower levels of apoD than

Caucasians [20, 45]. Therefore, determination of whether the

ABCC11 gene is present, and whether this gene expresses a dryvs. wet earwax phenotype, represents a good way to screen for

osmidrosis.

In contrast to body odour, foot odour is mostly due to short-chain

fatty acids catabolized from components found in eccrine sweat.

Acetic, butyric and isobutyric acids, and particularly isovaleric acid,

are the main components in eccrine sweat, with traces of propionic,

valeric and isocaproic acids [34]. Isovaleric acid is an odourant

derived from leucine; acetic and propionic acids are produced via

the fermentation of glycerol and lactic acid; isobutyric acid is

derived from valine, 2-methyl butyric acid from isoleucine and

short-chain, branched fatty acids are formed by incomplete degrada-

tion of skin lipids. ABCC11 not only contributes to axillary odour

but also is associated with foot odour and strongly involved in isova-

leric acid formation and leucine/isoleucine degradation [44].

Odourous thiols

Odouriferous sulphanylalkanols include 3-sulphanylhexanol (3SH),

2-methyl-3-sulphanylbutanol (2M3SB), 3-sulphanylpentanol (3SP)

and 3M3SH. These compounds were found in low amounts in

human axillary sweat (110 ppt) [26], but human sensitivity to

them is high. Cystathione-b-lyase is the enzyme involved in cataly-

sing the release of sulphur-containing malodourous compounds.

The strong meaty, fruity odour of 3M3SH is contributed by the

97% stereometric excess of ())-(S)-isomer, which possesses a char-

acteristic sulphuric odour, whereas its (+)-(R)-isomer (>97% enan-

tiomeric excess) has a fruity odour. The odour of 3SP is described

as onion-like, sulphuric and weakly reminiscent of grapefruit. The

threshold for this compound is 2 ppt, whereas 3M3SH, the major

odourous sulphanylalkanol, has a lower threshold of 1 ppt. Anisomeric mixture of 2M3SB has a threshold of 8 ppt (Table I). Such

a mixture has an onion- and sweat-like odour. Although these

compounds are found at very low concentrations, they strongly

contribute to body odour [25]. These compounds are secreted from

apocrine glands [26] as Cys-(S) or Cys-Gly-(S) conjugates [43, 46,

47]. A metal-dependent dipeptidase hydrolyses the Cys-Gly bond.

Corynebacterium C-S lyase then releases the powerful odourant thiol

(Fig. 3). Na-acyl-Gln-aminoacylase was also found to cleave

Cys-Gly-(S) conjugates [43]. Corynebacterium b-lyase doses release

the sulphuric notes from fresh sweat. Similar to HMHA formation,

HN

HOO

OH

O

NH2O

HN

O

OH

O

NH2O

HO

HOO

HO

O

Corynebacteriumaminoacylase

Figure 1 Corynebacterium sp. function in 3-hydroxy-3-

methyl hexanoic acid and 3-methyl-2-hexenoic acid

formations.

HMHA-Gln-ABCC11

HMHA-Gln

HMHA-apoD-HMHA

HMHA

Figure 2 Odourous 3-hydroxy-3-methyl hexanoic acid transporta-

tion and cleavage.

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odourous acids and thiol formations are linked. Furthermore, the

1,4-addition of Cys to the a,b-unsaturated acids including an ester,

and aldehyde appears necessary for biosynthesis of the 3M3SH pre-cursor [26]. Therefore, the cross-specificity of these two metallopep-

tidases plays an important role in axillary odour formation. Thus,

dual metallopeptidase inhibitors blocking Na-acyl-Gln conjugates

associated with odourant acids and thiols should be designed as

treatment for body odour [43].

ABCC11 regulates the Cys-Gly-(S) conjugate of 3M3SH, which is

further catabolized into 3M3SH by b-lyase [44]. Direct hydrolysis

of 3-sulphanyl-3-methylhexanol (3M3SH), which was isolated from

human sweat, was proposed as the mechanism. The (S)-isomer of

this precursor was 7578% more prevalent than the (R)-isomer in

sweat and had an onion-like odour. In contrast, the (R)-enantiomer

exhibited a fruity, grapefruit-like odour [25, 27]. The transporta-

tion and cleavage of odourous thiols are graphically summarized in

Fig. 4.

Odourous steroids

Axillary sweat and hair contain androsterone (5a-androst-16-en-3a-ol), 17-oxo-5a-androstan-3a-yl sulphate (androsterone

sulphate; AS), 17-oxo-5a-androsten-3b-yl sulphate (DHEAS),

DHEA, 3b-androstadienol and androstadienone (androst-4,

16-dien-3-one), which are secreted by apocrine glands [19]. These

precursors are converted to 4,16-dienone, and 5a-androstenone

by Corynebacteria producing a characteristic urine-like odour. 5a-

Androstenone is catabolized to 3a- a n d 3b-androstenols, which

have musk, and urine scents, particularly the a-isomer. Coryne-

form and Staphylococcus epidermidis cleave DHEAS, which is trans-

ported by the ABCC11 protein [48], and androsterone sulphate

by means of sulphatases delivering their unconjugated corre-

sponding steroids (e.g. 5a-androst-2-en-17-one). In addition,

3b-androstenyl sulphate is converted to 3b-androstenol. Coryne-

bacteria is the most efficient in transforming 5a-androst-5,16-

diene-3a-ol to androst-4,16-diene-3-one, the malodourous steroid[49, 50]. The transformation is significantly associated with the

presence of oxygen, confirming the aerobic nature of Coryneform.

Thus, 5,6-dehydrostenols created by Coryneform 5a-reductase play

an important role in malodour steroid production. 4,5-Isomerase

is associated with odourous steroid formation through isomeriza-

tion of androst-5,16-dien-3-one into androst-4,16-diene-3-one

following the oxidation of androst-5,16-diene-3a-ol [49]. The con-

figuration of 3-hydroxy contributes to the odour of the steroids

produced. An equatorial arrangement of hydroxyl (3b-ol) showed

less odour, whereas axial configurations (3a-ol) increased the

malodour. Notably, androst-16-en-3a-ol creates the characteristic

male body odour. The enzymatic activity was stereospecific

towards b-isomer, as 3b-sterol dehydrogenase activity was much

greater than 3a-sterol dehydrogenase activity [48]. Thus, transfor-

mation of androst-5,16-diene-3-ol, androst-16-en-3-ol and and-rost-4,16-diene-3-ol are key components in the biosynthesis of

malodourous androst-16-en-3a-ol (in male body odour), androst-

4,16-dien-3-one and 5a- androst-16-en-3-one, which contribute

to the characteristic underarmpit odour, as proposed in Fig. 5.

These 3-oxo-steroids have very low thresholds (Table I), particu-

larly 5a-androst-16-en-3-one (0.2 ppb), which is a powerful urin-

ous odour. However, androstenone is perceived by only 50% of

the human population. Furthermore, testosterone is not a precur-

sor of 3-oxo-steroid (androst-4,16-dien-3-one) [50]. Therefore, the

action of axillary odour treatment agents should be reviewed to

S

O

HN

NH2

HO

O

OH S

O

HO

NH2

OH

HS OH

Corynebacterium

Dipeptidase

Corynebacterium

cystathionine-beta-lysase

Figure 3 Corynebacterium sp. function in 3-sulphanyl-3-methylhexanol formation.

ABCC11-Cys-Gly-3M3SH

Cys-Gly-3M3SH

3M3SH

Gly-3M3SH

Figure 4 Odourous 3-sulphanyl-3-methylhexanol transportation

and cleavage.

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effectively combat body malodour which do not affect skin

homeostatis by novel ways of action [24].

Thus, the remaining sections of this review article aim to

describe the topical treatment agents that are currently used, as

well as the newest generation of active ingredients in body odour

treatments. In addition, laundry products with active agents pre-

venting malodour are included, as typical axillary odour appears

on the cloth within approximately 2 h of wearing and stays

until washing. Indeed, skin microorganisms, particularly S. epide-rmidis and other malodour-producing bacteria, were found to

survive, low temperature washing and slow drying conditions

[51].

Active ingredients for body odour treatment

Topical anti-perspirants are the first line of body odour improve-

ment because they are inexpensive, with minimal side effects

[52]. Anti-perspirants are used to diminish sweat secretion by

blocking the excretory ducts of sweat glands. Most types of anti-

perspirants contain metallic salts, particularly aluminium. The

types of aluminium salts include: aluminium chlorohydrate

(ACH), aluminium bromohydrate, aluminium chloride, aluminiumsulphate, potassium alum and sodium aluminium chlorohydroxy

lactate. Aluminium salts are anti-bacterial. Aluminium anti-

perspirant salts (most notably ACH, aluminium sulphate, ACH

lactate and aluminium chloride) polymerize with increasing pH,

forming aluminium hydroxide gel plugs in the sweat tubule

[23]. These plugs prevent new sweat movement towards the skin

surface. However, they are not permanent, and the acidic nature

of these salts can be irritating to the skin which limits their use.

In an attempt to reduce skin irritation, salicylic acid was used

in combination with ACH [5]. The formulation, consisting of alu-

minium salts and salicylic acid, had a reduced incidence of skin

irritation and had good anti-bacterial and anti-fungal properties

[53].

Zinc salts

The anti-DHT activity of zinc gluconate, zinc glycerinate, zinc

acetate, zinc sulphate, zinc oxide, zinc citrate and zinc chloride was

used in combination with other anti-perspirants, natural androgen

receptor expression inhibitors and malodour carrier proteins inhibi-

tors in the formulations for body odour control [54]. Water-soluble

zinc salts (zinc pidolate or zinc pyrrolidonecarboxylate, zinc chlo-

ride, zinc gluconate, zinc lactate, zinc phenolsulphate and zinc

sulphate) were used to absorb human axillary smells [55]. This

function is an additional benefit of Zn salts, highlighting their

HO

H

H

H

Androstadienol

HO4SO

O

H

HH

H

Androsterone sulfate

HO

O

H

HH

H

HO

OH

H

HH

H

HOH

HH

H

Androst-16-ene-3-ol

Androsterone

3,17-androstadiol

HO

HH

H

HO

HH

H

O

HH

H

O

HH

H

OH

HH

H

Androst-16-ene-3-one

Androst-4,16-ene-3-ol Androst-5,16-ene-3-ol Androst-4,16-ene-3-one Androst-5,16-ene-3-one

Figure 5 Odourous steroids formation.

Table I Characteristic body odours and their detection thresholds

[23, 25]

Odourant

Organoleptic

property

Detection

threshold

HMHA Spicy 4 ppt

3M2H Sweaty 14 ppb

Isovaleric acid Sweaty 1 ppm

3M3SH Sweaty 1 ppt

2M3SB Sweaty 8 ppt

3SP Sulfuric 2 ppt

Androstenone Urinous 0.2 ppb

Androstenol Musky 6.2 ppb

HMHA, 3-hydroxy-3-methyl hexanoic acid; 3M2H, 3-methyl-2-hexenoic

acid; 3M3SH, 3-methyl-3-sulphanyl hexanol; 2M3SB, 2-methyl-3-sulphanyl

butanol; 3SP, 3-sulphanyl pentanol.

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efficacy in malodour treatment. Furthermore, zinc pyrithione and

zinc phenolsulphonate were formulated with a 1,3-diketone in a

laundry product [56] designed to suppress undesirable odour.

Similar to the case with micronized ACH, zinc oxide powder with

a particle size of 0.02200lm was compounded with sesquiter-

pene alcohols and volatile silicone, producing a dry-texture deodou-

rant [56] characterized by control-release enhancement andmoisture absorption, which eliminated microbial growth.

Mn salts

In addition to zinc and aluminium, porous manganese was used as

a deodourant carrier that exerted anti-bacterial activity [57]. Fur-

thermore, divalent manganese salts (manganese chloride, manga-

nese acetate and manganese sulphate) were found to reduce

axillary, foot and scalp odours in aerosol, spray, roll-on, cream,

stick and laundry detergents suitable for woven or non-woven

fibres [58].

Anti-microbial agent

A good anti-bacterial deodourant should work specifically againstaxillary bacteria within an effective time period as well as exhibit

good stability and compatibility with other ingredients in the for-

mulation. Furthermore, such formulations should be non-toxic and

non-irritating and safe. Thus, anti-microbial metal ions known as

anti-microbial ceramics (ACs) have become increasingly important

in peoples day-to-day lives because of their wide range of appli-

cations in personal and home care products (i.e. fabrics and

cosmetics). Formulations of ACs, for instance, zeolite AC, calcium

phosphate AC and amorphous silica AC, are used as anti-microbial

agents in household and personal care products because of their

good biocompatibility. ACs based on hydroxyapatile and nitrate-

apatile complexed to Ag+ demonstrated an obvious anti-microbial

effect [59] that allowed for controlled release, which was superior

in terms of safety and durability to the casual anti-bacterial vehi-

cles [60]. The bactericidal action of silver zeolite ACs resulted fromthe transfer of silver ion to the bactericidal cell and the formation

reactive oxygen species. This action mode was proved in the bacte-

ria treated, and untreated with Ag-zeolite, and in anaerobiosis

condition as well [61]. Furthermore, Ag-zeolite concentrated to

540% ww)1 was found to act as an anti-microbial against skin-

resident bacteria. Its activity was superior to that of triclosan. It

was long-lasting and had no adverse effects. It was promoted as an

excellent agent for anti-axillary odour preparations [62]. Ag salts

of fusidic acid were also found to be effective against S. epidermidis

growth, particularly silver fusidate (minimum inhibitory concentra-

tion; MIC = 608000 ppm), which was more effective than silver

sulphadiazine (MIC = 800016 000 ppm). These Ag salts were

additional candidate topical agents for use as body odour treatment

products [63].

Triclosan was used as a broad-spectrum anti-microbial agent formore than 40 years. Body odour control preparations were first

launched in 1967, because of the compounds efficacy and stabil-

ity, as well as the lack of resistance among malodour-forming

bacteria [64]. Corynebacterium sp. inhibition was found to be effec-

tive at an MIC of 3 ppm; activity against Staphylococcus sp., and

Propionibacterium acnes was also observed [65]. Triclosan and triclo-

carban were included as anti-microbial agents in combination with

sodium hydroxymethyl glycinate (used as a preservative) and aro-

matic compounds such as eucalyptol, menthol, methylsalicylate

and thymol [66].

Anti-microbial agents that could be used in deodourants include

cetyl trimethyl ammonium bromide; cetyl pyridinium chloride;

benzethonium chloride; diisobutyl phenoxy ethoxy ethyl dimethyl

benzyl ammonium chloride; sodium N-lauryl sarcosine, sodium

N-polymethyl sarcosine; N-myristoyl glycine, potassium N-lauroyl

sarcosine; stearyl trimethyl ammonium chloride; 2,4,4-trichloro-

2-hydroxydiphenyl ether; zinc pyrithione; sodium bicarbonate;2,2-methylene-bis-(3,4,6-trichlorophenol); zinc phenolsulphonate;

2,2-thio-bis-(4,6-dichorphenol); p-chloro-m-xylenol; dichloro-m-xy-

lenol; and diaminoalkyl amide. These agents were formulated with

a 1,3-diketone to obtain deodourant effects. Notably, 5-chloro-2-

(2,4-dichlorophenoxy)-phenol and 2,2-dimethyl-1,3-dioxane,4,6-di-

one were deodourant agents that were suitable at concentrations

of 0.0120% for topical application and in cloth worn in contact

with skin. In addition, these diketones were found to be compatible

with anti-microbial agents that were used in the conventional

formulations such as sticks, roll-on, cleansing and laundry products

[67]. The diketones were entrapped in cyclodextrin for controlled

release of active components, and for the absorption of malodou-

rous perspiration, with no associated irritation [68]. In addition,

benzalkonium chloride was used as an anti-microbial agent in a

deodourizing emulsion containing isopropyl myristate or isopropylsterate [69].

In addition to the use of the above agents, stick, spray and lotion

anti-microbial piroctone [70] (0.11.0%, w w)1), formulations were

used to control body odour [71]. Coryneform growth inhibition was

also exerted by b-chloro-d-alanine, and d-cycloserine at an MIC of

0.001 and 0.005% wv)1, respectively, similar to that of triclosan

which was 0.001% wv)1 [72]. Propylene glycol can also function in

deodourant formulations as a bacteria growth inhibition agent.

Aryl 2-acetoxyethanoic acids (phenyl 2-acetoxyethanoic acid,

diphenyl 2-acetoxyethanoic acid (4-chlorophenyl) 2-acetoxyetha-

noic acid, (2-chlorophenyl) 2-acetoxyethanoic acid, (4-chlorophe-

nyl)-(2-chlorophenyl) 2-acetoxyethanoic acid) were also applicable

to the development of deodourant products as they inhibited the

bacterial growth [73]. A formulation consisting of hexamethylene

biguanide hydrochloride inhibited body odour more effectively thantriclosan and was used in the production of solutions, lotions,

creams, ointments, powders, suspensions, soaps, gel sticks and

aerosols [74].

Azole anti-fungal agents include clotrimazole, miconazole, tioco-

nazole, butoconazole, econazole, terconazole, ketoconazole and

fenticonazole, as well as terbinafine and tolnaftate. These compounds

were used in creams for axillary odour treatment, in combination

with undecylenic and salicylic acids, and benzoyl and hydrogen per-

oxides [75]. x-Cyclohexylalkan-1-oles with anti-microbial activity

were formulated into body odour treatment products [76]. Androste-

none odour was found to decrease following application of povidone,

which is an anti-bacterial agent [77].

Odour-neutralizing agent

Axillary malodour neutralizing agents can act via a sulphydryl

reactant, yielding N-ethylmaleimide and N-coumarylmaleimide.

This technology was patented [78] in addition to the neutralization

effect of NaHCO3 towards odourous acids for instance 3M2H [23].

Metal oxide silicates in particular calcium silicate act as odour

absorbents and neutralizers to absorb and neutralize body malo-

dours accordingly. The silicate particles allow for the volatilized

malodourants, and fatty acids to be easily adsorbed onto the

surfaces. Therefore, less fatty acids evaporate, and less odour is

perceived [79, 80].

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Odour absorbers

Cyclodextrins are used to entrap active ingredients and thereby

control the release of polyols, anti-microbials, zinc salts, polymers,

bicarbonate salts, chelating agents, zeolites and activated carbon.

Cyclodextrin formulations can be sprayed or wiped onto the skin

[66]. Cyclodextrins absorb moisture and odour-causing molecules.In addition, silicates, silicas and carbonates absorb moisture [79

81] which indirectly reduces malodour formation by eliminating

cutaneous flora that cause the odour. Bacteria prefer cool and dry

to hot and humid environments. Polyamines hybridized with inor-

ganic oxide materials [e.g. SiO2, TiO2, ZnO, Al2O3 or Mg(OH)2]

have also been shown to absorb odour [82].

Novel ingredients for the treatment of body malodour

Inhibition of androgen receptor expression

Resveratrol, epigallocatechin-3-gallate and flufenamic acids were

used to prevent body odour by inhibiting the expression of andro-

gen receptors [68]. Androgen receptor blocking of DHT binding

was employed by a C-19 steroid with an androsten-17(OR)-3-onestructure, with R representing a hydrogen, or an alkyl, aryl or acyl

group [83]. Competitive inhibition of the malodour-producing

enzymes, aminoacylase and cystathionine b-lyase [12, 24, 26]

resulted in a neutral or pleasant odour. This result was achieved

through the use of O-acyl serine and threonine compounds at a

concentration of 0.0110% ww)1, in both stick and roll-on formu-

lations [84, 85].

ASOB2 inhibitor

Monesin, tunicamycin, amphomycin, diumycin, showdomycin,

tsushimycin, amphortericine, mycospocidin, streptovirudin and

d-glucosamine [86] are thought to be involved in apoD suppression

through the inhibition ofN-linked oligosaccharide-processing glyco-

protein synthesis. Therefore, terminal glycosylation was prevented,and body malodour was limited. Accordingly, a screening method

for enzymes mediating malodour involving incubation of Na-acyl-

Gln-aminoacylase with precursors, and measurement of the release

of HMHA or MHA and free l-Gln [87] was shown to be effective in

identifying agents that inhibited the aminoacylase-catalysed mal-

odour-generating reaction.

Ethylendiaminedisuccinic acid (EDDS) and pentetic acid, for

example, significantly reduced the enzyme activity, and subsequent

malodour production by chelating Zn2+ [25] rather than by acting

as bacteriostatic agents. Indeed, there could be other chelating

agents that could provide sequestration of the active-Zn2+-site in a

similar way.

Alternatively, deodourants have been designed using fragrance

precursors that bind with Gln residues. Corynebacteria enzymes use

these residues as substrates, providing a way to engineer enzymespecificity towards Gln but not acyl groups [24]. Thus, cutaneous

bacterial degradation of amino acid conjugates could one day

provide pleasant odourant precursors. Homeostasis of the skin

would be retained, as none of the skins normal flora would be

eliminated through the use of this novel deodourant system.

Nutrient deprivation

A combination system consisting of diethylenetriamine pentaacetic

acid (DTPA), and butylated hydroxytoluene (BHT) might exert

deodourant activity because of synergistic effects. The axillary mal-

odour could be controlled by sequestering iron depriving the bacte-

ria of a needed food source [88]. The use of DTPA and BHT were

found to significantly reduce body odour [89].

Exoenzyme inhibition

Steroidal axillary malodour production was inhibited by exoenzyme

inhibition. The exoenzymes involved were arylsulphatase and

b-glucuronidase. The inhibitors with deodourant effects were Cu2+,

hexametaphosphate, d-glucaro-D-lactone, ethylenediaminetetraace-

tic acid (EDTA), nitrilotriacetic acid, O-phenanthroline and sodium

sulphate or other phosphates [90].

Control of malodour with fabrics

Fe(III)-4,4,4,4-tetracarboxylic acid phthalocyanine, a deodouriz-

ing complex, was grafted onto the surface of polypropylene non-

woven fabric. This fabricated fabric showed high deodourizing

performance for 2-mecaptoethanol [91].

The production of odour-controlling textiles also incorporated

the use of a polymeric amine coating [92] of hydroxyl-containingamines, particularly trialkanol amines on cellulose fibres. The use

of trialkanol amines conferred anti-microbial properties to the fab-

ric. The soft resinous coating was durable to cleaning procedures.

The anti-microbial activity was regenerated at pH 10 or above.

This process controlled certain odours and diminished the offensive

body odour [93].

A laundry cleansing product containing lysostaphin (Gly-Gly

endopeptidase), which hydrolyses the Gly-Gly bond in the polygly-

cine interpeptide link joining staphylococcal cell wall peptidogly-

cans, was also patented as a component of a detergent

composition, suitable for all types of textiles, and fabrics. The deter-

gent system consisted of amylase, arabinase, galactanase, lipase,

mannanase, pectinase, protease and xylanase [94].

Herbs to treat body odour

Herbs and naturally derived compounds are alternatively available

for applications in body odour treatment. Natural flavonoids exert

deodourizing effects [95] because of 3,4-hydroxyl units. The addi-

tional 5,7-dihydroxyl groups enhance anti-microbial activity [96,

97] in addition to their efficiency in androgen receptor inhibition

[64]. The toxicity of flavonoids is minimal [98]. Traditional reme-

dies can also be used to control body odour; i.e. the Kampo formu-

lation. This traditional medicine contains Rehmanniae radix, Cnidii

rhizoma, Angelicae radix, Scutellariae radix (17%, each) and Phello-

dendri cortex, Coptidis rhizoma and Gardenae fructus (8%, each). The

mixture was found to suppress lipase activity of P. avidum, which

significantly reduced the production of butyric acid (P = 0.047)

[59]. Therefore, herbal extracts with high amounts of these natural

compounds and bactericidal activity towards malodour-generatingmicroorganisms are applicable in herbal deodourant product devel-

opment and the development of bactericidal essential oils.

Herbal extracts

Anti-microbial activity towards nine pathogenicArctopus species has

been studied in A. dregei, A. echinatus and A. monacanthus. The root

of each plant was extracted using 20% aqueous methanol.Arctopus

spp. showed the strongest activity against S. epidermidis;A. monacan-

thus was found to be the most potent (MIC = 2050 ppm), followed

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by A. echinatus (MIC = 50200 ppm) and A. dregei, respectively

(MIC = 100900 ppm), whereas the MIC of ciprofloxacin was

600 ppm [99].

Caesalpinia minosoides, which is freshly consumed as a vegetable

in Thailand, is a calming agent with carminative effects that

reduce dizziness. The anti-microbial activity of this compound was

investigated. To do so, the plant was macerated with several sol-vents at different polarities to yield crude acetone, aqueous, chloro-

form and ethanolic extracts. All parts of the extract were able to

inhibit S. epidermidis, particularly the aqueous extract, which

potently inhibited S. epidermidis at an MIC of 3130 ppm; streptomy-

cin (MIC = 63 ppm) was used as a positive control [100].

Tea or Camellia sinensis has remarkable biological activity with

respect to catechins and is widely used for its health benefits. Tea

components, mainly catechins, and other polyphenolic compounds

are used in pharmaceutical and cosmetic applications. Certain com-

ponents of tea are anti-oxidants as well as bacterial growth inhibi-

tors. Susceptibility of tea towards S. epidermidis was evaluated. Tea

showed bactericidal and inhibitory effects at an minimum bacterici-

dal concentration (MBC) and MIC of 550 and 410 ppm, respec-

tively. Gallocatechins and their gallates were claimed as the main

constituents responsible for anti-bacterial activity [101], with anadditional effect on androgen receptors [64] that synergistically

prevented and reduced body malodour. Furthermore, tea anti-bac-

terial activity was enhanced (1117%) by irradiation at 40 kGy

that resulted in the reduction in tea dark colour, enabling more

applications in cosmetics [102].

Furthermore, a mixture ofC. sinensis,Hibicus sabdariffa,Malva syl-

vestris, Vitis viticola, Daucus carota, Commiphora myrrh, Simmondsia

chinensis and Calendula officinalis was used to examine probiotic

effects that inhibited the growth of odour-producing microbes. Mix-

tures of these herbs were then incorporated into deodourant aerosols,

gels, emulsions, sticks, creams, powders, soaps and lotions [103].

Cassia alata (Senna alata) is also used as a traditional medicine to

treat body odour [104, 105]. Its S. epidermidis inhibitory effect was

compared with that of other medicinal plants used in Thailand.

Cassia alata showed a moderate MIC and MBC (2500 and>5000 ppm), similar to Barleria lupulina, Lawsonia inermis and Psid-

ium guajava. In the same study, Garcinia mangostana was found to

be the most potent S. epidermidis inhibitor (MIC = 39 ppm), fol-

lowed by H. sabdariffa and Eupatorium odoratum (MIC = 625 ppm,

each) [106]. Hibicus sabdariffa was formulated into deodourant

products [103].

Chaenomeles speciosa is used in China because of its hepatoprotec-

tive effect, anti-microbial, anti-inflammatory and anti-tumour activ-

ities. The essential oil of this species contains b-caryophyllene as a

major constituent (12.52%) and a moderate amount of linalool

(1.33%). The compound was effective against several microorgan-

isms including S. epidermidis ( MIC and MBC of 1570 and

3130 ppm) when compared with standard treatments (e.g. levo-

floxacin; MIC = 610, MBC = 1220 ppm) [107].

Garlic is used for a number of infectious diseases and for its anti-bacterial activity, including inhibition of S. epidermidis. It was found

that S. epidermidis was sensitive to garlic extract, particularly crude

aqueous. The majority of S. epidermidis was killed by garlic (90

93%) in 1 h, although resistance was found following 34 h of

incubation [108]. Furthermore, the MIC and MBC of garlic juice

were evaluated: the concentration was low, and the active

compound was found to be equally active at a dilution factor of

128. In addition to garlic, some vegetables and fruits play a role in

S. epidermidis inhibition. For example, the MIC of pomegranate was

found to be effective at a dilution factor of 16, whereas that of

rhubarb was effective at a dilution factor of 4. In addition, beet,

cherry, cranberry, red onion, red cabbage, raspberry and straw-

berry inhibited S. epidermidis with a dilution factor of 2 [109].

Ginkgo biloba leaf and Phellodendron amurens bark extracts were

used as deodourants because of their inhibition of the degradation

of the apoD-chelating odourant. The extracts could be effectively

used at 0.120% ww)1

, although the most commonly usedamount was 0.510% ww)1 [95].

Gunnera perpensa, an herb traditionally used for psoriasis

treatment, was purified, and benzoquinone, benzopyran (2-methyl-

6-(3-methyl-2-butenyl)benzo-1,4-quinone and 6-hydroxy-8-methyl-

2,2-dimethyl-2H-benzopyran) were isolated from leaves and stems.

The isolated benzoquinone significantly inhibited the growth of

microorganisms, particularly S. epidermidis, at an MIC of 9.8 ppm.

Additionally, benzopyran showed moderate activity towards this

microbe with an MIC of 187 ppm, whereas that of ciproflaxin was

1.25 ppm [110].

Resinous exudates from twigs and leaves of Haplopappus spp.

were shown to inhibit S. epidermidis, with an inhibition zone of

910 mm. Terpenoids in H. diplopappus, H. anthylloides, H. schuman-

nii, H. cuneifolius, H. velutinus, H. uncinatus and H. foliosus were

found to be effective, in combination with flavonoids in H. velutinusand H. foliosus [111].

Harungana madagascariensis is well known for its topical anti-bac-

terial properties and has been used to treat cutaneous mycoses

because of its high levels of biologically active flavonoids, alkaloids,

saponins, glycosides and tannins [112, 113]. Its in vitro inhibition

of skin microflora was evaluated. Crude leaf extract, particularly

the ethyl acetate fraction, was found to inhibit armpit- and foot

odour-producing bacteria with MIC and MBC ranges of 25250

and 100750 ppm, respectively. Furthermore, Corynebacterium

xerosis was killed at 200 ppm, whereas the growth of S. epidermidis

was inhibited at 250 ppm. This effect was mediated by flavanones

(i.e. astilbin or 3-O-a-l-rhamnoside-5,7,3,4-tetrahydroxydihydrofl-

avonol) [114].

Furthermore, hop (Humulus lupulus L.) supercritical fluid extrac-

tion was used to test related anti-microbial activity against odou-rant-producing bacteria. MIC and MBC of hop extract were found

to be 6.25 and 25 ppm, respectively, against C. xerosis and 25 and

>25 ppm, respectively, towards S. epidermidis. Deodourant-contain-

ing hop extract (0.2%) was formulated and compared with the deo-

dourant base. It was found that 0.2% hop deodourant inhibited

C. xerosis four times more stronger than S. epidermidis (inhibition

zone of 8, and 2 mm, respectively). In addition, axillary malodour

decreased from 6.28 0.70 to 1.80 0.71, 1.82 0.74 and

2.24 0.77 following 8, 12 and 24 h of application, respectively

[115].

Anti-bacterial activity of methanolic extract of Hypercicum perfo-

ratum or St. Johns Wort against S. epidermidis had been reported at

1000 ppm. Isolated hyperforin inhibited Corynebacterium diptheriae

at 100 ppm [116].

Anti-bacterial activity of lichen ethanol extract was evaluated. Itwas found that Cetrelia olivetorum (10 ppm), Lecanora muralis

(10 ppm), Ramalina farinacea (10 ppm) and Rhizoplaca melanophth-

alma (50 ppm) inhibited S. epidermidis with inhibition zones of 11,

13, 10 and 16 mm, respectively, whereas those of tobramycin and

cephalothin, standard antibiotics, were 18, and 20 mm, respec-

tively [117]. In addition, lichen extract-containing usnic acid was

found to inhibit body malodour microorganisms at an MIC of

0.002% [118].

Licorice root extract was used to formulate aerosol, roll-on,

powder, cream, lotion, stick and detergent deodourants to control

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axillary odour. The active ingredient, glycyrrhetic acid, was effec-

tive at a concentration of 0.015% ww)1. The preparation

comprised tannic acid, resorcin, phenol, sorbic acid and salicylic

acid with odour-masking agents: musk, skatole, lemon oil, laven-

der oil, absolute jasmine, vanillin, benzoin, benzyl acetate and

menthol [119].

Androstenone generation was inhibited >95% by incubation ofandrosterone sulphate with C. xerosis in the presence of 500 ppm

of plant extracts. The suppressive effect of androstenone was fur-

ther evaluated with lower concentrations of plant extracts (125

and 62.5 ppm). Apricot (Prunus armeniaca) kernel extract was more

effective than gentian, prune and triclosan, which was used as a

positive control [120].

Inhibition of isovaleric acid generation was screened by means

of anti-microbial activity. Sophora flavescens significantly inhibited

the growth of C. xerosis, eliminating malodour. Furthermore,

S. flavescens showed broad-spectrum inhibition of resident skin

microbes, mediated by flavonoids [121].

Madder, or Rubia tinctorium, which is widely used as a natural

dye and folkloric anti-bacterial in Turkey, was Soxhlet-extracted by

ethanol and water, individually. The crude extracts (483 lg disc)1)

were susceptibility tested against several bacteria including C. xero-sis. The aqueous extract exerted stronger activity against C. xerosis

than the ethanolic fraction (inhibition zones were 12 and 7 mm,

respectively), whereas the inhibition zone of ampicillin (10 mg), a

standard, was 15 mm [122].

Traditional astringent, and tonic Tamarix ramosissima or salt

cedar rich in tannins, and phenolics potently inhibitedC. diphthe-

riae. The ethyl acetate extract in particular displayed an MIC of

25 ppm, whereas the butanoic extract isolated from tamarixetin

showed lower activity at an MIC of 1000 ppm [123].

Usnea barbata, Salvia officinalis, Rosmarinus officinalis, Boswellia

serrata, Harpagophytum procumbens and Menyanthes trifoliata were

screened against S. epidermidis and Corynebacterium spp. for anti-

microbial activity. Usnea barbata was the strongest inhibitor with

an MIC of 1 ppm, followed by R. officinalis with an MIC of 10

and 2 ppm, respectively. Although B. serrata showed strongeractivity against Corynebacterium spp. (MIC = 110 ppm), its effect

on S. epidermidis was reduced (MIC = 100 ppm). Harpagophytum

procumbens had similar activity on the test microorganisms

(MIC = 10 ppm; S. epidermidis, and 1020 ppm; Corynebacterium

spp.). However, S. officinalis was the least effective anti-bacterial

agent (MIC = 20 ppm; S. epidermidis, and 1020 ppm; Corynebacte-

rium spp.). Isolated (+)-usnic and carnosic acid exhibited stronger

activity than the crude extract. (+)-Usnic acid inhibited S. epidermi-

dis at an MIC of 4 ppm, and Corynebacterium spp. at 48 ppm,

whereas values for carnosic acid were 64 and 3264 ppm, respec-

tively [124].

Essential oils

Abies cilicica, Cilician fir, is native to the Mediterranean region, andaffords resin traditionally used for antiseptic, anti-inflammatory,

anti-pyretic and anti-bacterial applications in Turkey. Essential oil

extracted from the cones was investigated on Gram-positive bacte-

ria including C. xerosis; the oil showed a potent inhibitory effect

with an MIC of 1.5 ppm. Aroma compounds in the oil were

extracted; limonene was the most potent inhibitor ofC. xerosis with

an MIC of 3 ppm. a-, and b-pinene as well as myrcene had an MIC

of >8 ppm [125].

Anethum graveolens oil inhibited Corynebacterium growth at 4.5,

0.09, 0.04 and 0.02 lg filter paper disc)1 [126]. Staphylococcus

epidermidis was inhibited by essential oil extracted from Anthemis

aciphylla [127, 128]. Grammosciadium platycarpum oil was found to

inhibit malodour-producing microorganisms: limonene inhibited

S. epidermidis at an MIC of 6005000 ppm [129]. In addition,

essential oils that inhibit Gram-positive bacteria may be applicable

to control malodour [130].

Hydrodistillation of essential oil from Inula helenium wasconducted. S. epidermidis was found to be inhibited by the oil

(MIC = 3700 ppm, MIC of streptomycin = 60 ppm); alantolactone

and isoalantolactone were reported as the main constituents [131].

Melaleuca alternifolia or tea tree oil was also applicable in

deodourants because it contains terpinen-4-ol, the active anti-

microbial agent. The MIC and MBC against Corynebacterium spp.

were found to be 0.5% and 2% (vv)1), respectively. In addition,

it inhibited Staphylococcus spp. at an MIC and MBC of 0.5% and

12% (vv)1), respectively, in particular S. epidermidis (MIC = 0.5%

and MBC = 2% vv)1) [132].

Coriander (Corriandrum sativum) oil inhibited micrococci and

diphtheroids at an MIC of 0.1% because of its oxygenated terpe-

noids. The lichen extracts and coriander oil could be incorporated

into a stick deodourant at 0.13% and 1.06.0% ww)1, respec-

tively, although the preferred amounts were 0.0380.42% and1.82.2% ww)1, respectively. In the same deodourant formulation,

witch hazel, Aloe vera and chamomile extracts were additionally

incorporated. This formulation absorbed moisture [118] and

thereby inhibited microbial metabolism.

Essential oils from commercialized spices such as oregano (Origa-

num minutiflorum and O. onites), black thyme (Thymbra spicata) and

savoury (Satureja cuneifolia), which contains cavracrol, were tested

against C. xerosis. Inhibition was observed at the dilution range of

1 : 501 : 200 [133]. Furthermore, Satureja species were distilled

to obtain essential oils and evaluated with regard to their anti-

microbial activities and chemical composition. Staphylococcus masu-

kensis potently inhibited S. epidermidis, followed by Staphylococcus

pseudosimensis and Staphylococcus biflora (MIC = 370, 750 and

980 ppm, respectively). Linalool levels were highest in S. masuken-

sis oil (4.44%); this compound was found to be the strongestinhibitor against S. epidermidis (MIC = 250 ppm), compared to

caryophyllene oxide and pulegone (MIC = 900 and 950 ppm,

respectively). The antibiotics amoxicillin with clavulanic acid and

netilmicin had an MIC of 3 and 4 ppm, respectively [134]. There-

fore, it could be concluded from this study that essential oils

containing linalool, caryophyllene oxide and/or pulegone should be

considered S. epidermidis growth inhibitors.

In addition, essential oils from cumin (Cuminum cyminum), sweet

fennel (Foeniculum vulgare), laurel (Laurus nobilis), mint (Mentha

spicata), marjoram (O. majorana), pickling herb (Echinophoria tenuifoli),

sage (Salvia aucheri) and thyme (T. sintenesi) were found to inhibit

C. xerosis at the oil concentration of 0.22% [135]. Anti-oxidant and

anti-bacterial activities of Salvia eremophila extracts were analysed by

means of hydrodistillation and Soxhlet extraction in methanol to

obtain essential oil and crude methanol extract, respectively. Freeradical scavenging and lipid peroxidation inhibitory activities of crude

methanol were more potent than those of the essential oil. However,

the inhibitory effect of essential oil that contained linalool was greater

than methanol extract against S. epidermidis (MIC = 125, and

250 ppm, respectively); activity towards P. vulgaris was relatively low

(MIC = 500, and 125 ppm, respectively) [136]. The anti-bacterial

activity of thyme oil prepared at different developmental stages

was compared. Essential oil prepared from thyme (Thymus caramani-

cus) at floral budding, and flowering states showed two-fold greater

S. epidermidisinhibition (MIC = 900 ppm) than essential oil from seed

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and vegetative stages (MIC = 1800 ppm). Cavacrol inhibited S. epide-

rmidis at an MIC of 0.22 lL (of 70% carvacrol solution in methanol).

The flowering stage of T. caramanicus development yielded compounds

that were the most potent (68.9%), followed by floral budding

(66.9%), seed (60.2%) and vegetative (58.9%) stages [137].

The essential oil of Semenovia tragioides, which is an endemic

plant with highly flavoured leaves that are frequently used in jam,and pickles in Iran, was prepared and tested against S. epidermis.

Its MIC was found to be 2000 ppm compared with an MIC of

500 ppm for rifampin and gentamicin, which were used as positive

controls. A lipid peroxidation inhibitory effect was also observed (%

inhibition = 9.1 0.3; 0.7 mg of test sample), although it was less

potent than that of the positive control (BHT = 95.6 1.3%).

Chemical composition analysis revealed anti-bacterial effects of

linalool 5.7 1% together with lavandulyl acetate and geranyl

acetate [138]. In addition to S. tragioides oil, essential oils from two

cultivars of Sideritis erythrantha (erythrantha, and cedretorum culti-

vars) were evaluated on S. epidermidis. The cedretorum cultivar,

which elicited greater anti-oxidant effects by means of 1,1-diphe-

nyl-2-picrylhydrazyl radicals (DPPH), b-carotene bleaching and

reducing power assays, showed stronger S. epidermidis inhibition

than the other cultivar. However, the cedretorum cultivar showedgood anti-bacterial activity (10.00 0.24 mm at 10lL) compared

to vancomycin (10.00 0.24 mm at 30 lg). In addition, the more

potent cultivar contained higher amounts of pulegone. However,

linalool content was similar [139]. Therefore, anti-bacterial activity

was consistent with the description of linalool and pulegone

reported previously [140].

Smyrniopsis aucheri oil containing a-bisabolol (19.91%), widely

used in cosmetics including underarm deodourants, as well as

a- and b-pinene (15.10% and 6.58%), was found to potently inhi-

bit S. epidermidis [141].

Staphylococcus epidermidis was inhibited by essential oil extracted

fromZiziphora clinopodioidesat 10-lL filter paper disc)1 [127] with an

MIC of 601000 ppm [128]. Ziziphora clinopodioides oil (10 lg)

contained (+)-pulegone (31.86%) 1,8-cineole (12.21%) and limonene

(10.48%) as the major aroma compounds and inhibited Corynebacte-rium spp. at an MIC of 15.6031.25 ppm, whereas its methanolic

extract showed less activity (MIC = 250 ppm) [142]. In addition,

Ziziphora persica oil containing high levels of (+)-pulegone (79.33%)

but low levels of limonene (6.78%), and no 1,8-cineole exhibited

a wide range of Corynebacterium spp. inhibition (MIC = 250

7.81 ppm); its methanolic extract showed the same activity [143].

Essential oils and the aromatic compounds contained therein

should be incorporated into anti-perspirant and deodourant prod-

ucts. Linalool and dihydromyrcenol were combined at a ratio of

4 : 11 : 4 in body odour-controlling products. The concentration

of aroma compounds ranged from 0.2% to 1% (ww)1). Further-

more, avocado and vegetable oils as well as lichen extract were

added, for their soothing effects [144]. Essential oils also mask

unexpected odours and exert bactericidal effects.

Vegetable and animal oils incorporated in a deodourizingemulsion were as follows: sweet almond, groundnut, wheatgerm,

linseed, jojoba, apricot stone, walnut, palm, pistachio, sesame, rape-

seed, cade, maize germ, peach stone, poppy seed, pine, castor, soya,

avocado, safflower seed, coconut, hazelnut, olive, grapeseed, sun-

flower, whale lard, horsehoof, tuna, caballine, otter, egg, sheep,

seal, turtle, halibut liver, marmot, cod liver, neat-foot and carbon

oils. The combination of these oils in the emulsion was stable and

washable with conventional detergents [145].In addition to the above herbs, those with astringency, and folk-

loric use as tonics should be applicable for body odour control.

Adiantum capillus, Bergenia ciliate, Bombax ceiba, Cannabis sativa,

Cynodon dactylon, Cyperus rotundus, Dalbergia sissoo, Dodonaea

viscose, Fumaria indica, Juglans regia, Olea ferruginea, Phyla nodiflora,

Punica granatum, Pyrus pashia, Rumex chalepensis, Sapindus mukoros-

si, Solanum miniatum and Woodfordia fruticosa were recently investi-

gated because of their ethnopharmacological uses in folk cosmetics

in Pakistan [146]. In particular, Pinus roxburghii was used as a

traditional deodourant [147]. Furthermore, Cassia occidentalis, an

Ayurvedic plant, contains flavonoids (particularly apigenin, flav-

ones, alkaloids, tannins and saponins) with biological activity

including C. diphtheriae inhibition that is applicable to deodourant

development [106].

In addition, some of the traditionally used herbs might be appli-cable for body malodour treatment product development because of

their S. epidermidis inhibitory effect. For instance, Bersama abyssini-

ca, Erlangea cordifolia, Hoslundia opposite, Lantana trifolia, Phyllanthus

guineense, Physalis peruviana, Podocarpus milanjianus, Rubus apetalus,

Steganotaenia araliacea and Vernonia auriculifera that are traditionally

used for their anti-microbial activity in Africa [147].

Conclusions

Body or axillary odour is offensive chemical communication that

strongly adheres to clothes and shoe fibres (remaining even after

laundering), negatively impacting ones self-confidence. Topical com-

pounds that inhibit microorganisms growth or bacteria enzyme reac-

tions, absorb sweat and malodour, neutralize odours, and/or limit

sweat secretion have been discussed in this review in terms of theirability to reduce malodour. These ingredients are natural, naturally

derived and synthetic in nature. Research involving the use of fra-

grance precursors as alternative substrates to bacteria enzymes has

also been discussed. Using this approach, bacteria enzymes catalyse

the release of pleasant, aromatic scents vs. unpleasant malodour-

leaving the natural skin flora unaltered. Although some deodourant

products can irritate the skin with long-term use, the many options

described in this review present a plethora of choices that have mini-

mal safety or skin irritation concerns.

Acknowledgements

The authors acknowledge Mae Fah Luang University on facility

support for this manuscript preparation and the reviewers on their

valuable suggestions that make the article more comprehensive.

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Body Malodours and Their Topical Treatment Agents