Effects of air pollution on the skin: A review

Abstract

The increase in air pollution over the years has had major effects on the human skin. Various air pollutants such
as ultraviolet radiation, polycyclic aromatic hydrocarbons, volatile organic compounds, oxides, particulate matter,ozone and cigarette smoke affect the skin as it is the outermost barrier. Air pollutants damage the skin by inducing oxidative stress. Although human skin acts as a biological shield against pro‑oxidative chemicals and physical air pollutants, prolonged or repetitive exposure to high levels of these pollutants may have profound negative effects on the skin. Exposure to ultraviolet radiation has been associated with extrinsic skin aging and skin cancers. Cigarette smoke contributes to premature aging and an increase in the incidence of psoriasis, acne and skin cancers. It is also implicated in allergic skin conditions such as atopic dermatitis and eczema. Polyaromatic hydrocarbons are associated with extrinsic skin aging, pigmentation, cancers and acneiform eruptions. Volatile organic compounds have been associated with atopic dermatitis. Given the increasing levels of air pollution and its detrimental effects on the skin, it is advisable to use strategies to decrease air pollution.
Key words: Ozone, particulate matter, pollution, polycyclic aromatic hydrocarbons, skin, ultraviolet radiation,
volatile organic compounds

Full text

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© 2017 Indian Journal of Dermatology, Venereology, and Leprology | Published by Wolters Kluwer - Medknow
Effects of air pollution on the skin: A
review
Poonam Puri, Shashi Kumar Nandar1, Sushruta Kathuria, V. Ramesh
Department of Skin and STD, Vardhman Mahavir Medical College, Safdarjung Hospital, 1Department of
Environmental Toxicology Laboratory, National Institute of Pathology‑ICMR, Safdarjung Hospital Campus,
New Delhi, India
Review Arcle
Abstract
The increase in air pollution over the years has had major effects on the human skin. Various air pollutants such
as ultraviolet radiation, polycyclic aromatic hydrocarbons, volatile organic compounds, oxides, particulate matter,
ozone and cigarette smoke affect the skin as it is the outermost barrier. Air pollutants damage the skin by inducing
oxidative stress. Although human skin acts as a biological shield against pro‑oxidative chemicals and physical air
pollutants, prolonged or repetitive exposure to high levels of these pollutants may have profound negative effects on
the skin. Exposure to ultraviolet radiation has been associated with extrinsic skin aging and skin cancers. Cigarette
smoke contributes to premature aging and an increase in the incidence of psoriasis, acne and skin cancers. It is also
implicated in allergic skin conditions such as atopic dermatitis and eczema. Polyaromatic hydrocarbons are associated
with extrinsic skin aging, pigmentation, cancers and acneiform eruptions. Volatile organic compounds have been
associated with atopic dermatitis. Given the increasing levels of air pollution and its detrimental effects on the skin, it
is advisable to use strategies to decrease air pollution.
Key words: Ozone, particulate matter, pollution, polycyclic aromatic hydrocarbons, skin, ultraviolet radiation,
volatile organic compounds
Correspondence:
Dr. Sushruta Kathuria,
Department of Skin and STD,
Vardhman Mahavir Medical
College, Safdarjung Hospital,
New Delhi ‑ 110 029, India.
E‑mail: drsushruta@gmail.com
Introducon
Pollution is dened as contamination of the earth’s environment
with materials which interfere with human health, quality of life,
or the natural functioning of the ecosystem. The major types of
pollution are water pollution, air pollution, noise pollution and soil
pollution. The World Health Organization denes air pollution
as contamination of the indoor or outdoor environment by any
chemical, physical, or biological agent that modies the natural
characteristics of the atmosphere.1 The sources of air pollution
could be natural sources such as volcanic eruptions, forest
res, biological decay, pollen grains, marshes and radioactive
materials or human‑made sources such as thermal power plants,
industries, vehicular emissions, household combustion devices,
fossil fuel burning and agricultural activities. Pollutants of the
major public health concern include particulate matter, carbon
monoxide, ozone, nitrogen dioxide and sulfur dioxide.1 Air
pollution is responsible for a large proportion of health‑related
problems.2
Mechanism of Skin Damage by Air Pollutants
Living organisms are exposed to air pollutants which have major
effects on the human skin. Air pollutants can exist as solids,
liquids, gases and particulate matter. These are absorbed directly
through the skin into the subcutaneous tissue or via hair follicles
and sweat/sebaceous glands. Rapid urbanization and increased
energy consumption worldwide have exposed the human body to
increased quantities of ambient air pollution. The skin, being the
largest and outermost body organ, acts as a physical, chemical and
an immunological barrier against the environmental factors. Human
skin is exposed not only to natural environmental factors but also
to pollutants of anthropic origin.3 Whenever a prolonged and
repetitive exposure to environmental stressors exceeds the skin’s
normal defensive potential, there is a disturbance in the skin barrier
function leading to the development of various skin diseases.3 Major
air pollutants which affect the skin are solar ultraviolet radiation,
polycyclic aromatic hydrocarbons, volatile organic compounds,
How to cite this article: Puri P, Nandar SK, Kathuria S, Ramesh V.
Effects of air pollution on the skin: A review. Indian J Dermatol
Venereol Leprol 0;0:0.
Received: January, 2016. Accepted: June, 2016.
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Puri, et al. Air pollution and the skin
Indian Journal of Dermatology, Venereology, and Leprology | Volume XX | Issue X | Month XXXX 2
nitrogen oxides, particulate matter, cigarette smoke, heavy metals
and arsenic.
Air pollutants exert a harmful effect on the skin by increasing
oxidative stress which counters the skin’s antioxidant defenses.
There is a depletion of enzymatic (glutathione peroxidase,
glutathione reductase, superoxide dismutase and catalase) and
non‑enzymatic (Vitamin E, Vitamin C and glutathione) antioxidant
capacity. Free radicals and reactive oxygen species are generated
that interact with the lipid‑rich plasma membrane to initiate the
lipid peroxidation reaction cascade. Reactive oxygen species also
stimulate the release of pro‑inammatory mediators which results
in the accumulation of neutrophils and other phagocytic cells that
further generate free radicals, thereby resulting in a vicious cycle.
Oxidative stress initiates complex biological processes resulting in
genetic damage, activation of transcription factors such as activator
protein 1 and nuclear factor kappa B, and signalling pathways such
as extracellular signal‑regulated kinases, c‑Jun N‑terminal kinases
and p38 mitogen‑activated protein kinases, involved in cell growth
and differentiation and in the degradation of the connective tissue
of the dermis. Air pollutants induce severe alterations of the normal
functions of lipids, deoxyribonucleic acid and/or proteins in the
human skin via oxidative damage, leading to extrinsic skin aging,
inammatory or allergic conditions such as contact dermatitis,
atopic dermatitis, psoriasis, acne and skin cancer.4,6‑8
Air Quality Guidelines
The World Health Organization air quality guidelines are based on
four major air pollutants, namely particulate matter, ground‑level
ozone, nitrogen dioxide and sulfur dioxide.1 The World Health
Organization guidelines for the various air pollutants are shown in
Table 1. The Revised National Ambient Air Quality Standards, 2009,
are also shown in Table 1.9 Another measure for air pollution is air
quality index based on ve major air pollutants regulated by the Clean
Air Act:‑ ground‑level ozone, particulate matter, carbon monoxide,
sulfur dioxide and nitrogen dioxide. Its value lies between 1 and 500,
with higher values indicating more air pollution. Air quality index
value of 50 represents a good air quality with some potential to affect
public health, while an air quality index value over 300 represents
hazardous air quality. Real‑time records of air quality index in
New Delhi show that it is between 150 and 170, which is categorized
as unhealthy.10 This article focuses on the detrimental effects of air
pollutants on various skin disorders.
Air Pollutants and their Role in Skin Diseases
Ultraviolet radiation
Ultraviolet radiation is a physical pollutant. The solar spectrum
consists of ultraviolet A (320–400 nm), ultraviolet B (290–320 nm)
and ultraviolet C (200–290 nm). More than 95% of ultraviolet
A and 1–5% of ultraviolet B reach the Earth’s surface, whereas
most ultraviolet C is absorbed by the ozone layer and oxygen
in the atmosphere.11 The depletion of stratospheric ozone by
environmental pollutants such as photochemical smog, supersonic
aircraft ights and refrigerant gases increases the penetration
of the shorter ultraviolet wavelengths to the ground level. The
effects of ultraviolet radiation on human skin differ depending on
the wavelength. Ultraviolet A exposure results in extrinsic skin
aging (photoaging) characterized by coarse wrinkles, solar elastosis
and pigment irregularities. Aging results from the combined action
of intrinsic and extrinsic factors. The general aging process which
is genetically determined and occurs in all skin by passing time is
called intrinsic aging [Figures 1 and 2] whereas skin aging induced
by environmental factors is termed as extrinsic aging. Clinical
signs of extrinsic aging include solar elastosis [Figure 3], pigment
spots [Figure 4], coarse wrinkles and telangiectasias. The differences
between intrinsic and extrinsic aging are tabulated in Table 2.12‑15
Photoaging is mainly caused by ultraviolet A. In an in vitro study,
it was seen that ultraviolet B may also contribute to photoaging
by increasing stratin. Stratin is a member of the 14‑3‑3 protein
family, secreted by keratinocytes and its expression was more in
skin exposed to ultraviolet B than in skin protected by ultraviolet
B.16 The mechanism of premature/extrinsic skin aging induced by
ultraviolet rays is a complex process, which is triggered by various
pathways, namely activation of receptors, mitochondrial damage,
protein oxidation, alteration of Ca2+ levels, telomere damage and
arylhydrocarbon receptor activation. The stimulation of receptor
pathway is induced by the generation of reactive oxygen species
on exposure to ultraviolet radiation, smoking and air pollutants. As
a result, the cell surface receptors of cytokines and growth factors
in keratinocytes as well as broblasts are activated which leads to
the intracellular stimulation of intracellular kinases, inducing the
transcription of nuclear transcription factor activator protein 1 and
nuclear factor kappa B. Increased activator protein 1 transcription
decreases the gene expression of the major dermal collagens I and III
in broblasts leading to a reduction in collagen synthesis. Activator
protein 1 also increases the synthesis of matrix metalloproteinases in
keratinocytes and broblasts resulting in the increased degradation
of mature dermal collagen. On the other hand, nuclear factor kappa
B stimulates the transcription of inammatory cytokines resulting
in the accumulation of neutrophils. The collagenases in neutrophils
help in collagen degradation.
Ultraviolet B alone is responsible for sunburn. Ultraviolet A and B
both have been implicated in cutaneous immunosuppression and
skin cancers (photocarcinogenesis) such as malignant melanoma,
basal cell carcinoma and squamous cell carcinoma.3,7,17 There is
a growing concern worldwide regarding the increased incidence
of skin cancer. Excessive exposure to sunlight and tanning
Table 1: Guidelines for limit of air pollutants1
Air pollutant Maximum limit (WHO,2006) Revised National Ambient air quality
standards (2009)
Particulate matter having size
between 2.5 and 10 μm
Mean value of 20 μg/m3 over a year or 50 μg/m3
over 24 h
Mean value of 60 μg/m3 over a year or 100 μg/m3
over 24 h
Ozone at ground level Mean value of 100 μg/m3 over 8 h Mean value of 100 μg/m3 over 8 h
Nitrogen dioxide Mean value of 0 μg/m3 over a year or 200 μg/m3
over 1 h
Mean value of 40 μg/m3 over a year or 80 μg/m3
over 24 h
Sulfur dioxide Mean value of 20 μg/m3 over 24 h or 500 μg/m3
over 10 min
Mean value of 50 μg/m3 over a year or 80 μg/m3
over 24 h
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Puri, et al. Air pollution and the skin
3Indian Journal of Dermatology, Venereology, and Leprology | Volume XX | Issue X | Month XXXX
lamps is responsible for cumulative damage, which induces
immunosuppression responsible for skin cancer.18 Fair‑skinned
people are more susceptible than dark‑skinned individuals.
Australia has the world’s highest rate of skin cancer which is due to
high sunshine levels. Depletion of ozone increases the penetration
of ultraviolet rays to the earth’s surface, leading to an increase in
incidence of skin cancers, and a decrease in their age of onset.19,20
Ultraviolet A and B damage deoxyribonucleic acid through
different mechanisms. Melanocytes in the basal layer of epidermis
produce the pigment melanin, which protects the neighbouring
keratinocytes from ultraviolet radiation. However, prolonged
exposure to sunlight can induce carcinogenesis. Ultraviolet A
and B are absorbed by proteins, lipids, nuclear and mitochondrial
deoxyribonucleic acid, causing a cascade of oxidative events
Figure 1: Intrinsic aging. Sagging and lax skin with deep wrinkles in a
63‑year‑old woman
Figure 2: Intrinsic aging. Fine wrinkles in a 45‑year‑old woman
Figure 3: Extrinsic aging. Solar elastosis in a 40‑year‑old woman living in
hilly region
Figure 4: Extrinsic aging. Freckles in a 55‑year‑old woman
Table 2: Differences between intrinsic and extrinsic (photoaging)12-15
Intrinsic aging Extrinsic (photoaging)
Texture of skin Dry, pale with certain degree of laxity Very dry, atrophic, sallow, very lax
Sagging of skin More prominent Less prominent14
Wrinkles Fine wrinkles In addition, coarse wrinkles forming deep
furrows (pathognomic)
Hyperpigmentation Some freckles Lot of irregularly pigmented freckles, heterogeneity of
pigmentation (specic for photoaging)
Other features Benign neoplasms Premalignant lesions, actinic keratoses, telangiectasias
Histology (epidermis) Flattening of the dermal‑epidermal junction, decrease in
melanocyte and Langerhans cell density
Variable epidermal thickness, some cytologic atypia,
uneven distribution of melanocytes, signicant decrease in
Langerhans cells
Histology (dermis) Loss of extracellular matrix, increased levels of
collagen‑degrading metalloproteinases, loss of broblasts and
vascular network, and, in particular, loss of the capillary loops
that occupy the dermal papillae
Dermal elastosis (deposition of abnormal amorphous elastic
material in the papillary dermis), abundant inammatory
cells in the dermis, and degenerative changes in collagen
and elastic bers
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Puri, et al. Air pollution and the skin
Indian Journal of Dermatology, Venereology, and Leprology | Volume XX | Issue X | Month XXXX 4
which results in the deterioration of structure and function of cells.
Ultraviolet A causes mutation of tumor suppressor p53 gene in the
basal layer which has stem cells, and thus leads to carcinogenesis,
which is due to deoxyribonucleic acid damage, gene mutation and
immune suppression.
Ultraviolet A in combination with common environmental
pollutants, such as polycyclic aromatic hydrocarbons, signicantly
increases visible photodamage in the skin.21 Ultraviolet A in
combination with ozone causes synergistic oxidative stress in
human skin.22 Some air pollutants (ozone, nitrogen dioxide and
sulfur dioxide) and scattering particulates (clouds and soot) in the
troposphere reduce the effects of shorter wavelength ultraviolet
radiation, mainly ultraviolet B, and cause signicant reduction in
ultraviolet B irradiance in polluted urban areas. There is a reduction
of more than 50% in ultraviolet radiation (mainly ultraviolet B)
on days with high levels of air pollution. An inverse relationship
exists between the total ozone content and ground levels of
ultraviolet B radiation. Ultraviolet A, however, is not affected
much in the presence of air pollutants and ozone. Therefore, the
ratio of ultraviolet B/ultraviolet A is highly dependent on factors
such as thickness of ozone layer and air pollution.23
Cigarette smoke
Cigarette smoke is a highly complex aerosol composed of
thousands of chemical substances, including reactive oxygen
species, carbon monoxide, reactive nitrogen species and
electrophilic aldehydes.3 Reactive oxidants and free radicals from
cigarette smoke cause oxidative stress or secondary oxidative
events and inhibition of antioxidant mechanisms.24‑26 Chemical
substances from cigarette smoke increase transepidermal water
loss, degeneration of connective tissue in the skin and upregulation
of matrix metalloproteinases‑1 and 3 which degrade collagen and
elastic bers.3,27,28
Smoking causes premature aging which clinically manifests as
deeper periorbital wrinkling.29‑31 Premature facial skin aging in
smokers, with a characteristic pattern of wrinkling and orange‑purple
skin discoloration, was dened as smoker ’s face.32 Smoker’s face
typically has lines or wrinkles radiating at the right angles from the
upper and lower lips or corners of the eyes, deep lines on the cheeks,
or numerous shallow lines on the cheeks and lower jaw. The bony
contours become prominent, and the skin is slightly pigmented gray
with orange, purple and red complexion. Heavy cigarette smokers
were 4.7 times more likely to have facial wrinkles than nonsmokers,
independent of sun exposure, although the combination of smoking
and sun exposure may have a synergistic effect.31‑33 It has been
observed that wrinkling in a 40‑year‑old smoker resembles that
of a 70‑year‑old nonsmoker.34 Sometimes, large open and closed
comedones with furrows (smoker’s comedones) [Figure 5] are seen
in the periorbital area, similar to those seen in Favre–Racouchot
syndrome. There is yellow discoloration of nails, and in persons
who have stopped smoking, a sharp demarcation line may be seen
between the yellow nail plate and the newly formed pink nail
plate (known as Harlequin nail or quitter’s nail). Other changes
noticed in smokers include yellowish discoloration of the hair and
beard (e.g. smoker’s moustache), premature graying and loss of
hair, gingival pigmentation (smoker’s melanosis), leukoplakia of
the tongue (smoker’s tongue), oral leukoplakia [Figure 6] and a
gray‑white keratinized palate with multiple red umbilicated papules
that represent inamed salivary glands (smoker’s palate/nicotine
stomatitis).35 Various mechanisms have been postulated for
premature aging caused by cigarette smoke. In mice models,
second‑hand smoke, also known as environmental tobacco smoke,
involuntary smoke and passive smoke caused premature aging
by increased cytoplasmic translocation of high‑mobility group
box 1 protein, and hence, the loss of collagen.36 Transcription of
p16INK4a has been associated with aging, and p16INK4a is a known
gerontogen. In murine models, cigarette smoke and ultraviolet light
have augmented the transcription of p16INK4a.37 Cigarette smoke
extract caused senescence of broblasts, possibly by oxidative
stress injury and inhibition of antioxidant defense activity in in vitro
studies.38 Cigarette smoke‑induced early growth response‑1 induces
the expression of cysteine‑rich 61 in human skin dermal broblasts
which may be the cause of premature aging.39
An association between cigarette smoke and psoriasis has been
reported in several epidemiologic studies. In a Norwegian
cross‑sectional study, male smokers had a signicantly increased
risk of developing psoriasis.40 A meta‑analysis suggested that there
is a signicant association between smoking and psoriasis with a
relative risk of 1.88 for smoking in patients with psoriasis versus
patients without psoriasis.41 In addition, there is a dose‑dependent
relationship between the development of psoriasis and the number
of cigarettes smoked. A population‑based twin study showed
that childhood exposure to environmental tobacco smoke was
signicantly associated with psoriasis in the whole population, with
an odds ratio of 1.28. Smokers with a history of >5 pack‑years of
cigarette had an increased risk of psoriasis with an odds ratio of
2.18. The same study showed that genetic factors could explain only
20% of the correlation between psoriasis and smoking, whereas
non‑shared environmental factors explained even less at 8 percent.42
Several single nucleotide polymorphisms located in the CHRNA5/
A3/B4 gene cluster have been linked to smoking behaviour
and nicotine dependence, but these known single nucleotide
polymorphisms were not found to be linked with psoriasis incidence
or severity in the Chinese population.43 The effect of smoking could
be mediated by the reactive oxygen species and by the imbalance
between oxidants and antioxidants indicated by low levels of
Figure 5: Smokers comedones. Comedones in periorbital area and ne
wrinkles in a 35‑year‑old man
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Puri, et al. Air pollution and the skin
5Indian Journal of Dermatology, Venereology, and Leprology | Volume XX | Issue X | Month XXXX
vitamin C and glutathione, and high levels of superoxide dismutase
and malonaldehyde.3,44
Schäfer et al. reported a high prevalence of acne among smokers and
described a correlation between the acne severity and the number of
smoked cigarettes in post adolescent women, where predominantly
comedonal acne was seen compared to the papulopustular form.45
The authors reported that although the correlation between acne and
smoking is still controversial, there is a hyperkeratinizing effect of
cigarette smoke compounds, and in particular, of nicotine. Nicotine,
an agonist of acetylcholine present in the cigarette, induces
comedogenesis via the stimulation of acetylcholine‑nicotinic
receptor on epidermal keratinocytes.46
A meta‑analysis done in 2010 shows that tobacco smoking is associated
with cutaneous squamous cell carcinoma with an odds ratio of 1.52
while the association between smoking and basal cell carcinoma
and other nonmelanoma skin cancers is controversial.3,25,47‑50 In mice
models, 4‑(methylnitrosoamino)‑1‑(3‑pyridyl)‑1‑butanone acted as
tumor initiator causing skin cancer and lung adenomas.19
Interestingly, many case series and case‑control studies report
that smoking is associated with a lower prevalence of aphthous
ulcers, Behcet’s disease, herpes labialis, Kaposi’s sarcoma (in
acquired immune deciency syndrome) and pemphigus vulgaris.49
The various skin diseases aggravated by smoking are tabulated in
Table 3.
Polycyclic aromatic hydrocarbons
Polycyclic aromatic hydrocarbons are among the most widespread
and dangerous organic pollutants.20 Polycyclic aromatic
hydrocarbons are absorbed on the surface of suspended particulate
matter in the air in urban areas.51 They are converted into quinines,
redox‑cycling chemicals that produce reactive oxygen species.52
Irrespective of the route of entry in the human body, they are
found in almost all the internal organs, especially in the lungs and
digestive tract. The main source of atmospheric polycyclic aromatic
hydrocarbon benzo(a) pyrene is residual wood burning, the other
sources being automobile exhaust, diesel fumes, metallurgical
industry, production of plastics, pesticides, dyes, cigarette smoke
and smoke resulting from the combustion of organic material.21
Polycyclic aromatic hydrocarbons are associated with extrinsic skin
aging, pigmentation, cancers and acneiform eruption. Melanocyte
proliferation and skin pigmentation have been observed in mice.53
Scrotal cell carcinoma due to coal soot in British chimney sweeps
was reported in 1775, and polycyclic aromatic hydrocarbon was the
carcinogen responsible for it. Coal soot is more carcinogenic than
wood soot as it contains a higher amount of polycyclic aromatic
hydrocarbons. Among polycyclic aromatic hydrocarbons, benzo(a)
pyrene has been shown to cause nonmelanoma cancers whereas
7,12‑dimethylbenz(a) anthracene is capable of inducing lymphoma
in hamsters. Ultraviolet A enhances the carcinogenic action of
benzo(a) pyrene.54 However, Sowada et al. have demonstrated that
resident skin ora, predominantly micrococci, can degrade benzo(a)
pyrene, thus forming an innate mechanism of defense against
polycyclic aromatic hydrocarbons.55,56
Epoxides and diols produced by activated polycyclic
aromatic hydrocarbons bind to deoxyribonucleic acid, leading
to carcinogenesis.7,54 Polycyclic aromatic hydrocarbons
can lead to acneiform eruptions due to the presence of
2,3,7,8‑tetrachlorodibenzo‑p‑dioxin which is a polyhalogenated
aromatic hydrocarbon.7 It is formed in any burning, waste
incineration, metal production and fossil‑fuel and wood combustion.
Sorg et al. described chloracne in Viktor Yushchenko’s poisoning
with 2,3,7,8‑tetrachlorodibenzo‑p‑dioxin in 2005.57 Chloracne is
Figure 6: Oral leukokeratosis in a smoker
Table 3: Skin diseases aggravated by cigarette smoke
Commonly associated skin changes
Premature skin aging
Hyperpigmentation of oral mucosa
Submucous brosis
Yellowish discoloration of nails
Smokers comedones
Skin diseases with denite evidence of aggravation with smoking
Cutaneous squamous cell carcinoma
Hidradenitis suppurativa
Systemic lupus erythematosus
Oral cancers
Palmoplantar pustulosis
Psoriasis
Skin diseases with conicting evidence of aggravation with smoking
Basal cell carcinoma
Discoid lupus erythematosus
Acne
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Puri, et al. Air pollution and the skin
Indian Journal of Dermatology, Venereology, and Leprology | Volume XX | Issue X | Month XXXX 6
a systemic toxic disease caused by the exposure to halogenated
aromatic hydrocarbons. It is characterized by comedones and cysts
mainly on the face (outer sides of the eye and behind the ears)
and neck. Other manifestations of chloracne include fatigue, liver
dysfunction, neuropathy and arthritis.58
Ground‑level ozone
Ozone is a ubiquitous pollutant in the urban environment. Its
concentrations in urban environment can range from 0.2 to 1.2 ppm.59
Mexico City has the highest ozone levels in the world. It is a gaseous
oxidant that exists in the stratosphere and troposphere.70,50 Normally,
the concentrations of ozone at ground‑level are low. Ozone, after
interaction with sunlight (ultraviolet radiation), hydrocarbons,
volatile organic compounds and nitrogen oxides, forms a major
active component of the photochemical smog.7,50
The effect of ozone is mediated by its ability to induce oxidative
stress. It leads to the formation of peroxides, aldehydes and lipid
ozonation products, as a result of unsaturated fatty acid oxidation
and damages the barrier function of epidermis. Thiele et al.
reported that ozone causes a reduction in the level of antioxidants
such as tocopherol (vitamin E) and ascorbic acid (vitamin C) and
increases malondialdehyde, a lipid peroxidation product in murine
skin causing impairment of barrier function and inammation.22,60
In human skin, exposure to ozone caused a 70% decrease in
vitamin E concentration in stratum corneum, and 50% reduction
in skin microora.61 Ozone causes disturbed activity of matrix
metalloproteinases. Ozone‑induced inammation is mainly
mediated through redox‑sensitive transcription factor, nuclear factor
kappa B. In an in vitro study, cells exposed to ozone demonstrated
a dose‑dependent increase in p65 subunit nuclear expression as a
marker of nuclear factor kappa B activation, while pretreatment with
vitamin C mixtures which acted as antioxidants abolished nuclear
factor kappa B nuclear translocation. In addition, a signicant
activation of Nrf2 was observed in keratinocytes treated with the
mixtures.62 Nrf2 is a basic leucine zipper protein that regulates the
expression of antioxidant proteins that protect against oxidative
damage triggered by injury and inammation.
Ozone along with ultraviolet A rays and cigarette smoke is a powerful
oxidizing agent of squalene. Oxidation of squalene produces
squalene by‑products, mostly peroxidized forms, which lead to
comedogenesis, thus aggravating inammatory acne. Oxidation of
epidermal lipids and disturbed activity of matrix metalloproteinases
contribute to wrinkling and extrinsic skin aging.63 Tropospheric
ozone exposure has been associated with urticaria, eczema, contact
dermatitis, rashes and infected skin disease.64
Particulate matter
Particulate matter in the air consists of complex and varying
mixtures of different size and composition. Factories, power plants,
refuse incinerators, automobile, construction activities, res and
natural windblown dust are some of the main sources of particulate
matter.65,66
Particulate matter penetrates skin either through hair follicles
or transdermally, and exerts its detrimental effects through the
generation of oxidative stress, which contributes to extrinsic skin
aging, characterized particularly by pigment spots on the face and
nasolabial folds, and less so by coarse wrinkles, solar elastosis
and telangiectasia.67‑69 The most harmful components of ambient
particulate matter are nanosize particles from trafc sources; these
particles can serve as carriers for organic chemicals and metals that
are capable of localizing in mitochondria and generating reactive
oxygen species. It has been noted that an increase in soot (per
0.5 × 10−5/m) and particles from trafc (per 475 kg per year and
square km) was associated with 20% more pigment spots on the
forehead and cheeks. Polycyclic aromatic hydrocarbons are adsorbed
on the surface of suspended particulate matter in air of urban
areas.68 Polycyclic aromatic hydrocarbons can activate xenobiotic
metabolism which converts polycyclic aromatic hydrocarbons to
quinones. Quinones are redox‑cycling chemicals which produce
reactive oxygen species responsible for particulate matter toxicity.52
Although many cohort studies report that there is no association
between air pollutants and incidence and prevalence of atopic
dermatitis, the severity of symptoms of atopic dermatitis may have
a direct association with increased particulate matter.70 Kim et al.
also report that with indoor air quality improvement program, the
level of particulate matter decreased and there was a signicant
decrease in the prevalence and severity of atopic dermatitis.71 The
exact mechanism is unclear, but it is proposed that particulate matter
may induce inammation in the skin in a similar fashion as that in
the respiratory system.70
Volatile organic compounds
Emission of volatile organic compounds occurs from the use of
organic solvents in paints, varnishes (aliphatic hydrocarbons, ethyl
acetate, glycol ethers, methylene chloride and acetone) vehicle
renishing products in repairing car paint, environmental tobacco
smoke, stored fuels, exhaust from cars (benzene) and from emissions
from industrial facilities (tetrachloroethylene).6,72,73 It is an important
indoor source of air pollutants. A longitudinal study has shown
that symptoms of atopic dermatitis increase in children shifted to
a new building due to an increase in exposure to volatile organic
compounds.74 Volatile organic compounds along with sunlight and
nitrogen oxides form photochemical oxidant products such as ozone
at ground level which is the summer photochemical smog. Volatile
organic compounds (ingestion of hexachlorobenzene) may induce
precancerous skin lesions in rats.75 Exposure to volatile organic
compounds increases cytokines (interleukin‑8 and interleukin‑1B)
in cultured keratinocytes which cause atopic dermatitis or eczema.
Oxides
Nitrogen oxides are emitted mainly from mobile and stationary
combustion sources. They react with ozone‑forming nitrogen
dioxide. Among nitrogen oxides, nitrogen dioxide causes oxidative
damage leading to the formation of free radicals that oxidize
amino acids in tissue proteins and initiate lipid peroxidation of
polyunsaturated fatty acids.76
Atmospheric sulfur dioxide is formed from fuel combustion from
industrial processes, volcanic activity and forest res. Carbon
monoxide, a product of incomplete combustion from mobile
sources, acts on cell metabolism which binds to heme and alters
its function.6 Flexural eczema was associated with trafc‑related
air pollutants, including nitrogen oxides and carbon monoxide in
Taiwan in middle‑school children. A study comparing atopic eczema
in East and West Germany showed that the prevalence was higher
in East Germany (sulfurous type pollution) and also exhibited a
stronger association with nitrogen oxides and close proximity to
heavy trafc.77
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Puri, et al. Air pollution and the skin
7Indian Journal of Dermatology, Venereology, and Leprology | Volume XX | Issue X | Month XXXX
Heavy metals
Cadmium, lead and mercury are common air pollutants that pose
health hazards. The main sources are volcanoes, waste incineration,
cement, iron and steel production and leaded gasoline.56
Prevenon Strategies
Control of air pollution is necessary to improve the health conditions.
There are two steps in the prevention of dermatological diseases due
to air pollution: the rst is to reduce air pollution and the second
is to use strategies to protect oneself from pollutants. In Korea,
indoor air quality improvement program was conducted in nine
kindergarten classes, following which mean particulate matter 10
levels decreased signicantly from 182.7 to 73.4 µg/m3. Along with
that, the prevalence, severity of atopic dermatitis in children and
the number of hospital visits per month also decreased signicantly,
thus showing the benet of improvement of air quality.71 The Health
Event project in Europe for the improvement of indoor air quality
is based on three components, namely optimizing ventilation rates,
ltration of outdoor air and indoor source control.78 This project has
shown an improvement in different cardiovascular and respiratory
diseases. Such strategies should be studied for dermatological
diseases too.
Control of air pollution
The natural sources of pollution are difcult to predict and prevent
such as volcano eruptions or forest res. However, human‑made
sources can be controlled. Some strategies include less use of
personal vehicles, increase in the use of car pools and public modes
of transport, supply of low‑sulphur petrol, shifting of industries to
areas away from the cities, development and usage of industrial
machines and methods which are eco‑friendly, avoiding burning
of garbage in the open, avoidance of smoking and no use of wood
and crop residues as fuel for the purpose of household cooking and
heating. Various methods have been tried to reduce trafc induced
pollution. For example, in New Delhi, biofriendly fuels such as
compressed natural gas is used by all public transport vehicles,
odd‑even formula for private vehicles has been implemented and
old diesel vehicles are gradually being phased out.
Personal protection
Strategies for personal protection include physical photoprotection;
use of sunscreens; avoidance of areas with public smoking, and
around industries; usage of topical antioxidants such as vitamin
C and E in formulations along with sunscreen; and of indoor air
puriers and ventilators. People with high occupational risk, such as
trafc police and sweepers, should use masks while at work.
Conclusions
Skin is the largest organ of human body, and any factor affecting skin
health will impact the body as a whole. Major air pollutants having
detrimental effects on the skin include solar ultraviolet radiation,
polycyclic aromatic hydrocarbons, volatile organic compounds,
nitrogen oxides, particulate matter, ozone and cigarette smoke.
Sunlight, cigarette smoke and ambient particulate matter have a role
to play in extrinsic skin aging. Smoking has also been associated
with skin cancer, psoriasis, acne and skin malignancy. Exposure to
ozone has been associated with urticaria, eczema, contact dermatitis
and other nonspecic eruptions. Polyaromatic hydrocarbons cause
skin cancer, extrinsic skin aging, pigmentation and acneiform
eruptions. Oxides have been associated with increased prevalence,
as well as exacerbations of atopic dermatitis in children.
Financial support and sponsorship
Nil.
Conicts of interest
There are no conicts of interest.
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