Review article

Occupational skin cancer and precancerous lesions

Fifinela Raissa, Githa Rahmayunita, Sri Linuwih Menaldi, Dewi Soemarko*

Department of Dermatology and Venereology

*Department of Occupational Medicine
Faculty of Medicine, Universitas Indonesia, dr. Cipto Mangunkusumo General Hospital,
Jakarta, Indonesia

Email: dr.fifinelaraissa@gmail.com

Abstract

Occupational skin cancer and precancerous lesions are skin disorders caused by exposure to chemical
carcinogens such as polycyclic hydrocarbons and arsenic, or radiation, such as ultraviolet light and ionizing
light in the workplace. Annual increase in skin cancer incidence is believed to be related to various factors
such as frequent intense sunlight exposure (i.e. at work, recreational activities, and sun-tanning habit), ozone
depletion, an increase in number of geriatric population, and an increase of public awareness in skin cancer.
The most common occupational skin cancers are basal cell carcinoma, squamous cell carcinoma, and
melanoma. Examples of occupational precancerous lesion of the skin are actinic keratosis and Bowen’s
disease. Particular diagnostic criteria to diagnose occupational diseases has been developed. Early
detection of occupational skin cancer and precancerous lesion is necessary. An effective prevention program
consists of primary prevention such as prevention of hazardous material exposure, secondary prevention
such as early detection of disease for early intervention, and tertiary prevention such as minimizing long-term
impact of the disease.

Keywords: Occupational, skin cancer, precancerous lesion, radiation, carcinogen

Abstrak

Kanker dan prakanker kulit akibat kerja ialah kanker dan prakanker kulit yang disebabkan oleh pajanan
terhadap karsinogen kimia, misalnya hidrokarbon polisiklik dan arsenik, atau radiasi, misalnya sinar
ultraviolet dan sinar pengion,di tempat kerja. Peningkatan insidens kanker kulit setiap tahun dapat
disebabkan oleh berbagai faktor, antara lain peningkatan pajanan terhadap sinar matahari saat bekerja
maupun rekreasi, kebiasaan berjemur, deplesi ozon, bertambahnya populasi usia tua, dan peningkatan
kewaspadaan masyarakat. Jenis kanker kulit akibat kerja tersering ialah karsinoma sel basal, karsinoma sel
skuamosa, dan melanoma. Contoh lesi prakanker yang berhubungan dengan pekerjaan adalah keratosis
aktinik dan penyakit Bowen. Kriteria diagnosis tertentu dapat digunakan untuk mendiagnosis penyakit akibat
kerja. Deteksi dini diperlukan untuk tatalaksana dini kanker dan prakanker kulit akibat kerja. Program
pencegahan yang efektif meliputi pencegahan primer yakni pencegahan terhadap pajanan bahan berbahaya,
pencegahan sekunder yakni deteksi dini penyakit agar dapat dilakukan tatalaksana penyakit, serta
pencegahan tersier yaitu meminimalisasi dampak penyakit secara jangka panjang.

Kata kunci: kanker kulit, akibat kerja, lesi prakanker, radiasi, karsinogen

J Gen Pro DVI. 2016;1(3):77-85 77

Introduction
Occupational skin cancer and precancerous
lesions are skin disorders caused by chemical
carcinogenic exposure or radiation in the
workplace.1,4 The most prevalent skin cancer is
melanoma and non-melanoma skin cancer such
as basal cell carcinoma (BCC) and squamous cell
carcinoma (SCC). The incidence of non-melanoma
skin cancer is approximately 2-3 million cases per
year worldwide, whereas melanoma incidence is
132,000 cases per year.5 New cases of BCC and
SCC in Surgery and Oncology Division,
Dermatology and Venereology Department Faculty
of Medicine Universitas Indonesia/ dr. Cipto
Mangunkusumo National Hospital (RSCM) in 2014
are 24 and 2 cases, respectively; however to
determine the correlation between these cases
with occupation requires further observation.6
Occupational skin cancer in England is estimated
to be less than one percent of all skin cancer
cases.7 Precancerous skin lesion refers to a skin
lesion that is likely to become malignant. Examples
of precancerous skin lesion are actinic keratosis
and Bowen’s disease.8 Four cases were
considered as premalignant from 32 cases of both
cancerous and precancerous occupational skin
disease in Denmark from 2000-2009.9 There were
two cases of actinic keratosis and Bowen’s
disease in RSCM in 2014, but the occupational
relationship in these cases remains unknown.6 An
annual increase in skin cancer incidence is
believed to be related to various factors such as
increased incidence of sun exposure (during
working hours or recreation, and sun-tanning
habit), ozone depletion, increase number of
geriatric population, and increased public
awareness of skin cancer.2,10 In developing
countries with developing industries, Hashim and
Boffeta suspect that the incidence of skin cancer
and precancerous lesion is related to increased
exposure to carcinogenic chemicals.11 This
literature review will discuss occupational cancer
and precancerous skin lesions, their clinical
manifestations, diagnosis, and prevention.
Etiopathogenesis
There are several carcinogens at the workplace
that may induce skin cancer, such as:
Arsenic
Arsenic is found naturally in ores together with zinc,
lead, copper, and iron. In the past, arsenic was
used for paint, pesticides, and as medicine. 1
Currently, arsenic is widely used in the microchip,
semiconductor, and glass industries. Arsenic and
inorganic arsenic compounds mainly enter the
human body through inhalation and ingestion.1,11
Arsenic and its compounds are carcinogenic.
J Gen Pro DVI. 2016;1(3):77-85
Arsenic is known as a strong mutagen due to its
ability to induce chromosome mutation and work
as co-carcinogen with ultra violet (UV) radiation.3,12
Target organs of these carcinogenic effects are the
lungs, bladder, kidneys, and skin.1,13
The pathogenesis of arsenic-induced skin cancer
remains to be elucidated. There are three
mechanisms suspected to be responsible in
cancer development (Figure 1):
1. Biotransformation process
Pentavalent arsenical species (AsV) are reduced
by nucleoside phosphorylase into trivalent species
(AsIII) through oxidative methylation process.14,15
AsIII is methylated via AsIII methyltransferase with
S-adenosylmethionine (SAM) as a methyl donor,
forming trivalent mono- and dimethylated species,
such as monomethylarsonic acid (MMAIII),
dimethylarsinic acid (DMAIII), monomethylarsonic
acid (MMAV), as well as pentavalent mono- and
dimethylated species, which is dimethylarsinic acid
(DMAV).14-16 In vitro studies show that
keratinocytes display very slow rates of arsenic
methylation, and only mono-methylated species
are produced. Individuals with arsenic-related skin
lesion or skin cancer exhibit low level of
dimethylated species. It shows that low
methylation activity could predispose individuals to
arsenic-related skin malignancies.14,15 This
process also influences gene transcription,
enzyme inhibition, cytotoxin, and results in
changes in epigenetic mechanism.14-16
2. Oxidative stress
Oxidative stress produces reactive oxygen species
(ROS), which affects gene transcription through
Wnt/ β-catenin pathway and calcium signal. ROS
metabolites can induce single or double strand
DNA breaks.14-16
3. Epigenetic changes
Biotransformation process using SAM inside the
cell results in depletion of methyl chain.13,14 This
process can disrupt the ability of epigenetic
arrangement through a disturbance in DNA
methylation, histone modification, and microRNA
expression.14,15 Epigenetic modification does not
change DNA sequence, but results in DNA
chemical modification.14-16
Some experts believe that arsenic absorption
through skin at the workplace does not correlate
with SCC and BCC,1 however, most experts stand
on the opposing side.3,11 Arsenic is accumulated in
the epidermis and dermis. Keratinocytes and
epidermal stem cells are believed to be the target
of carcinogenic effects. Long-term exposure to
arsenic can cause fever, sleep disturbance, weight
loss, liver enlargement, skin discoloration, sensor
78
and motorneuropathy, as well as
encephalopathy.1,13
*As: arsenic
DMA: dimethylarsinic acid
DNA: deoxyribonucleic acid
GSH: gluthathione
MiRNA: micro-ribonucleic acid
MMA: monomethylarsonic acid
ROS: reactive oxygen species
SAM: S-adenosylmethionine
UV: ultraviolet
Figure 1. The pathogenesis of arsenic-induced
skin malignancy.12
Polycyclic Aromatic Hydrocarbons
Polycyclic aromatic hydrocarbons (PAH) exist in
coal tar products and oil such as brown coal tars
(soft coal tars), coal tars (black coal tars), coal tar
pitches, coal tar oils, coke oven emissions, carbon
black (soot), creosote, anthracene, fuel and diesel
oils, crude paraffin, asphalt, and tars from
distillation products of shale oil. Inside the body,
PAH will be converted into carcinogenic
metabolites by monooxygenase enzyme (CYP 1A1,
1A2, 1B1) and can be found in hair follicles. PAH
is known to influence p53 tumor suppressor gene
in lung cancer, but the mechanism of PAH in the
development of skin cancer is unknown.3 Direct
skin contact with PAH can induce BCC and SCC. 3
Latent phase can take several years to decades
from initial exposure to the onset of skin cancer.
Skin cancer can develop even after the exposure
has been discontinued.1
Ultraviolet Light
The spectrum of ultraviolet (UV) light comprises of
wavelengths of 100–400 nm, shorter than visible
light (400–780 nm). Depending on its wavelength,
UV radiation is divided into UVA (315–400 nm),
UVB (280–315 nm), and UVC (100–280 nm).17
Based on the source of light, UV light can be
differentiated into natural and artificial light. Source
of natural UV light are sunlight, and artificial lights
can be linked to the exposure at the work place,
J Gen Pro DVI. 2016;1(3):77-85
such as welding process, food industry, health
industry, etc.18,19 UV radiation is carcinogenic,
whether directly by inducing cell damage (DNA
mutation), or indirectly by inducing
immunosuppression (T lymphocyte suppression).
UVB radiation works specifically at oncogene and
p53 tumor suppressor gene that initiate and
progress to skin malignancy. UV radiation,
especially UVB, forms pyrimidine dimer on
deoxyribonucleic acid (DNA) and ribonucleic acid
(RNA). This event causes keratinocytes mutation
and transformation into neoplasm. UVA is less
mutagenic when compared to UVB. UVA light can
induce indirect DNA damage through a
mechanism mediated by photooxidative stress.
This incident results inthe formation of reactive
oxygen species (ROS). ROS is able to interact
with lipid and protein to produce intermediate
product that can coalesce with DNA to form an
adduct (a carcinogenic material which forms
covalent bond with DNA).1,17,20,21
UVA radiation can penetrate to reach deep skin
layers. This radiation enhances the carcinogenic
effect of UVB, which in turn will result in aging and
immunosuppression. Therefore, UVB and UVA
lights are involved in the development of skin
malignancy. Risk factors for skin cancers are fair
skin (type I-II in particular), freckles, and easily
burned skin.1,17,20
Ionizing Radiation
Ionizing radiation consists of alpha particles, beta
particles, neutron, and electromagnetic wave (X-
and Y-ray). Alpha particles are absorbed as it is by
the stratum corneum and do not cause skin
damage. Ionizing radiation may cause DNA
damage. The damage can induce carcinogenesis
such as mutation, chromosome aberration, and
genomic instability. Ionizing radiation can induce
skin malignancy, especially SCC, BCC, and
melanoma. Actinic keratosis, induced by X-ray is
carcinoma in situ and in the old days, used to be
discovered in the hands of surgeons and
radiologists. Nowadays, there is no increased
incidence of radiation-induced disease in workers
exposed with ionizing radiation. The risk of
melanoma is increased in radiology technician who
started working before 1950; a time where
personal protective equipment (PPE) was not
regularly used.1,2,22 Table 1 summarized skin
malignancies linked with occupation/exposure, and
the type of cancer or precancerous lesion.
Types of occupational skin cancer and
precancerous lesion
The followings are types of occupational skin
cancer and precancerous lesion:
79
Cancerous lesions:
Basal cell carcinoma
BCC is the most prevalent skin carcinoma. BCC
lesion is usually found on sun-exposed areas.
Clinically, there are 5 types of BCC, namely
nodular, superficial, morphea, pigmented BCC,
and fibroepithelioma of Pinkus (FEP). Nodular type
lesion consists of translucent papules or nodules
with telangiectasia and high borders. The clinical
presentation of pigmented BCC consists of
translucent papules, hyper-pigmentation, and may
be accompanied by erosion. Erythematous plaque
mimicking dermatitis can be found in the
superficial type of BCC. The morphea type is
characterized by scar-like lesion or ivory-colored
morphea. The FEP type usually comprises of pink
papules, usually found on the lower back. The
most siginificant risk factor to develop BCC is
intermittent exposure to sunlight and genetic factor.
Other risk factors include exposure to ionizing
radiation, tar, DNA repair disturbance (for example
in xeroderma pigmentosum) and
immunosuppression.23

Table 1. Etiology of occupational skin cancer and precancerous lesion and associated industries/
exposures1.3-4,16

Etiology Industry/ exposure Cancer/precancerous lesion

Arsenic Insecticide, herbicide, and pesticide factory; Lead, Arsenic keratosis, Bowen’s
copper, and zinc smelter; Arsenic mining disease, SCC, BCC
Hydrocarbon Coal tar distillation; coal gas factory; exposure to Tar keratosis,
aromatic shale oil, creosote, asphalt, and soot keratoacanthoma, SCC, BCC
polycyclic
Ultraviolet light Outdoor workers (farmer, driver, fisher, SCC, BCC, melanoma,
construction worker), welding, laser exposure, actinic keratosis,
and printing industry worker keratoacanthoma, Bowen’s
disease
Ionizing radiation Nuclear power plant, uranium mine worker, Bowen’s disease, SCC,
diagnostic radiology worker, pilot and cabin crew BCC, melanoma
*BCC: basal cell carcinoma, SCC: squamous cell carcinoma

Squamous cell carcinoma exposure are superficial spreading melanoma

SCC is a suprabasal epidermal keratinocyte
neoplasm. SCC mostly originates as a
precancerous lesion such as actinic keratosis and
Bowen’s disease. SCC is usually found in patients
over 55 years old. Occupational SCC cases are
seldom reported.
The predilection sites for SCC are usually on sun-
exposed areas. Fixated, keratotic, erythematous
or skin-colored plaque or papules are common
clinical findings in SCC. Other findings may
include ulcer, shiny nodules, verrucous lesion,
cornu cutaneum, and abscess.24
Predisposing factors of SCC are chronic sun
exposure or occupational exposure to
carcinogens (arsenic and PAH), scars,
immunosuppression, burns, long-term heat
exposures, HPV infection, and genodermatosis
(albinism, xeroderma pigmentosum, porokeratosis,
bullous epidermolysis).25,26
Melanoma
Melanoma is found in every race and ethnicity.
The incidence of melanoma is lower than non-
melanoma skin cancer, but in fair-skinned
population the incidence of melanoma has
surpassed the non melanoma within the last
decade. Types of melanoma related to sun
(SSM), lentigo maligna (LM), and lentigo maligna
melanoma (LMM). SSM is mostly found on areas
exposed intermittently to sunlight such as the
back and lower extremities.1,27 LM and LMM are
found on areas chronically exposed to UV such as
the cheeks, nose, neck, skin of the head, and
ears.27,28
Risk factors for melanoma are fair skin (skin type I
and II), familial history of melanoma, typical nevus
and/or >1 atypical nevi, gene mutation (p16,
BRAF, MC1R), sun exposure whether intermittent
or chronic, sun burns during childhood and
adolescence, certain medical condition (such as
xeroderma pigmentosum), immunosuppression,
other malignancies, as well as history of previous
melanoma.27
Precancerous lesions:
Actinic keratosis
Actinic keratosis is a skin neoplasm induced by
continuous exposure to UV light, characterized by
abnormal proliferation of keratinocytes. This lesion
is a predictor of skin cancer, both melanoma and
non-melanoma. Risk factors for actinic keratosis
include individual susceptibility, cumulative UV
light radiation, immunosuppression, previous skin
cancer history, and genetic syndrome. Sites of

J Gen Pro DVI. 2016;1(3):77-85 80

predilection are sun-exposed areas such as the
dorsal side of the hand, lower arm, head, and
neck.8 Erythematous, flat-topped, coarse,
squamous papules are characteristic for this
disease, which are commonly found on the skin
area that have multiple UV-induced skin damage,
such as telangiectasia, yellowish discoloration,
solar elastosis, sagging skin, freckles, and
lentigo.3,8
Tar keratosis
The clinical presentations of tar keratosis are
small, brownish, round- or oval-shaped plaque
with flat surface (smooth or verrucous), likely
appear in groups. This lesion commonly appears
on the dorsal side of the hand, lower arms, and
face. This lesion usually appears concurrently with
other skin lesions such as folliculitis, acne, and
diffuse brownish macules. The lesion correlates
with the exposure to coal tar, shale oil, and coal
distillation products. Lesions can appear 2.5-45
years after exposure.1,3,8
Arsenic keratosis
Arsenic keratosis refers to a precancerous lesion
associated with chronic arsenicosis. This lesion is
potentially developed into malignancy, such as
SCC and can be related to intra-epidermal
carcinoma or multiple BCC. This lesion is usually
numerous with typical multiple yellowish punctate
papules on the palms and soles of patient with
arsenic exposure.3,8 Other skin lesion that can be
found include hyperpigmented macules on the
trunk or extremities, generalized
hyperpigmentation, mucosal pigmentation, hypo-
/depigmented macules with underlying normal
skin or hyperpigmented skin (leukomelanosis). 5
Bowen’s disease (intra-epidermal carcinoma)
Bowen’s disease is an insitu SCC with a potential
to become SCC. Lesions appear as thin
erythematous plaques, may be solitary or multiple,
irregular, well-defined, and topped with scales or
crust. The surface of the lesion may appear
hyperkeratotic or verrucous. The predilection sites
are on sun-exposed areas such as the head, neck,
lower leg, and arms. There are several variants of
this disease, including intertriginous, periungual,
and mucosal types. This lesion is usually induced
by chronic arsenism, exposure to UV and ionizing
radiation, immunosuppression, HPV infection,
history of psoralen therapy, and UVA (PUVA).1,3,8
Keratoacanthoma
Keratoacanthoma refers to an epithelial tumor
with rapid growth, histopathologically similar with
SCC, with a tendency to undergo spontaneous
regression. Some experts believe that
J Gen Pro DVI. 2016;1(3):77-85
keratoacanthoma is a benign skin tumor or
pseudomalignant tumor, while others believe that
keratoacanthoma is a variant of SCC and
therefore, malignant in nature. The etiology
consists of chronic exposure to UV and chemical
carcinogens such as mineral oil and tar (pitch).
Chemical carcinogens along with UV light can
induce the onset of keratoacanthoma. Other risk
factors include immunosuppression, xeroderma
pigmentosum, long-term PUVA therapy, and
smoking. The predilection site is usually sun-
exposed areas, such as the face, lower arms, and
dorsal side of the hands.24
There are three clinical phases of the disease
namely proliferation, maturation, and resolution
phases. The proliferation phase is characterized
by rapid growing erythematous papules, 1-2 cm in
size or larger, firm in consistency, with smooth
surface. The maturation phase is characterized by
erythematous or skin-colored nodules, firm in
consistency, with a keratotic center. The
resolution stadium is characterized by keratotic
nodules, some are necrotic, and would eventually
become flattened, forming hypopigmented scar.24
Diagnostic criteria for occupational
diseases
Diagnosis of occupational disease is important.
Not only it impacts the management of the
disease, but also plays some roles in:29
1. High risk exposure control at the root of the
problem
2. Early identification of new material exposure
3. Medical care and rehabilitation for
workers/patients
4. Preventing recurrence or worsening of the
disease or accident
5. Protecting other workers
6. Fulfillment of employee’s right
7. Identification of new relationship between
exposure and disease
Based on the 2011 Indonesian Occupational
Medicine Specialty Consensus in diagnosing
occupational disease, the 7 steps required to
establish occupational diagnosis are
determining:29
1. Establishing clinical diagnosis
Clinical diagnosis is established by history
taking, physical examination, and supporting
examinations.
81
2. The exposure in a worker’s workplace.
An occupational medicine specialist takes all
medical history which consists of
chronological job descriptions, working
period/duration, produced materials, used
materials, and working methods.
3. Relationship between exposure and the
disease.
This relationship should be based on research,
including thorough review of the literature
4. Sufficient exposure.
The magnitude of the exposure can be
measured qualitatively by assessing working
methods, working process, and working
environment. It is also important to perform
observation of the workplace and to take
workers’ working hours into account. The
qualitative measurement can be done by
measuring exposure in the working
environment and evaluating whether the value
passed the threshold. Protection levels and
compliance of PPE use also needs to be
evaluated.
5. Individual host factors.
Host factors such as history of atopy, allergy,
and personal hygiene also play some role.
This assessment is needed to identify roles of
host factors.
6. Other non-occupational factors.
Other non-occupational factors such as hobby,
habit, activities at home and during vacations
that may cause similar disease should be
explored.
7. The occupational diagnosis.
Analysis through collected information to
determine the causality between the exposure
in the workplace and the disease is performed.
If the relationship is significant, the
occupational disease diagnosis can be
established. If the third and the fourth steps
are completed, the occupational disease
diagnosis also can be established. If the 3rd,
4th, 5th, and 6th steps are completed, it
indicates that the disease is exaggerated by
occupation. If only the 5th and 6th steps are
completed, the disease is not occupational.
In addition to the consensus, there are several
items that can help doctors in identifying the
involvement of working environment in the
development of skin cancer:30
 History of exposure with caustic materials in
the workplace which caused similar skin
disease in other people
 The appearance of similar skin cancer in fellow
workers with the same occupation.
 Younger age of onset compared to the usual
J Gen Pro DVI. 2016;1(3):77-85
onset of disease
 Timeliness between the exposure of the
caustic agents and skin cancer
 The type and location of lesion is consistent
with the occupational exposure
Prevention
Types of prevention can be categorized into
primary prevention, secondary prevention, and
tertiary prevention. Primary prevention is
preventing exposure to hazardous material, e.g.
by using PPE, hazardous material risk
assessment, and labeling hazardous material
specifically.1,31 Secondary prevention is early
detection of disease for early treatment; and
tertiary prevention is minimizing the long-term
impact of the disease.31
In particular, the primary and secondary
prevention of skin cancer due to PAH consist of:30
1. Replace PAH containing ingredients with non-
toxic ingredients
2. Good personal hygiene can limit the duration
of exposure and therefore will decrease the
incidence of cancer
3. Industrial hygiene to eliminate or limit the
exposure
4. Avoid simultaneous exposure to sunlight
5. Periodic examination for exposed workers for
early detection and management
Regular worker checkup for specific toxic material
exposure is known as biological monitoring
(biomonitoring). Biomonitoring of PAH could be
performed by measuring 1-hydroxypyrene (1-
OHP) in the urine. The normal range of 1-OHP in
urine is 0.24-0.7 µmol mol-1creatinine.32 Arsenic
biomonitoring can use hair, nail, or urine as a
sample. Arsenic level in the hair and nail is used
as an indicator of previous exposure, whereas
arsenic and its metabolites level in the blood or
urine can be used as an indicator of recent
exposure. The World Health Organization
recommends the level of >50 µg/L in the urine
with a period of not consuming seafood for 4 days.
Arsenic level of >1mg/kg in dry hair and of >1.5
mg/kg in nails are indicative of arsenic exposure
exceeding the safe limit during the last 11
months.13,33
The primary prevention of skin cancer in outdoor
workers comprises of three aspects:34
1. Change of attitude towards health awareness
and diseases caused by UV radiation exposure.
Change of attitude such as avoiding direct UV
82
 light from 11:00 to 15:00, using proper clothing
in outdoor places, applying sunscreen regularly,
and staying in areas that provide shade. Those
advices apply not only for exposures during
recreational activities in the weekends or
vacations, but for occupational exposures as
well.
2. Direct UV radiation protection using
appropriate clothing.
Proper clothing has to protect both arms and
legs, and should not have a low cut neck and
back. Wide hat is used to protect the head,
face, ears, and the back of the neck. The
material used should be thick, dark colored,
and not tight. The material should have UV
protection factor of >40 (UPF 40+), UVA
transmission of <5%, and standardized design.
3. Proper and regular use of sunscreen.
The use of broad-spectrum sunscreen with
SPF shows protection to UV-induced
immunosuppression. Several clinical trials in
Australia showed that regular use of sunscreen
can limit the incidence of actinic keratosis and
skin lesion regression.
Prevention strategies to skin cancer induced by
UV light that can be applied in working
environment are as follows:35
 Company and organization policy consisting
of basic rules and risk management
intervention to sunlight exposure at the
workplace
 Education and training:
o Special programs on particular seasons,
for example in early summer
o Integrated occupational health and safety
training
 Sun protection steps:
o Technical control: natural or artificial
shelter
o Administrative control: arrangement of
outdoor working schedule
o Clothing and PPE for sunlight including
hat, long sleeved shirts, long pants (UV
protective clothing), goggles, and
sunscreen.
 Periodic risk assessment of UV light exposure
for all workers. Monitoring and re-evaluating
the effectiveness of the programs in certain
periods of time.
In Australia, there are no screening programs for
melanoma and non-melanoma skin cancer;
sunlight-exposed workers are educated to perform
self-inspection of their skin regularly as follows:35
J Gen Pro DVI. 2016;1(3):77-85
 Check the whole body including the soles, in
between fingers, armpits, ears, eyelids, nail
beds, and the scalp.
 Use a mirror or ask others to check some
parts of the body that cannot be seen by
him/herself, such as the back, nape, and both
legs.
 Check for new spots or spots which are
different from the surrounding skin, poor
wound healing, and spots or moles changing
in size, shape, or color.
Exposure to ionizing radiation can be prevented
by eliminating or limiting radiation through the use
of PPE, shutting the radiation source, correcting
radiation waste management, and by periodic
monitoring.36
Primary prevention to arsenic is by eliminating
arsenic exposure from drinking water source.
Steps needed to be done including changing the
drinking water source and the technology to
eliminate arsenic from the water source. These
also include education concerning health risk to
the population exposed to arsenic from drinking
water, periodic test of arsenic levels in the urine,
and by building common wells.37
Conclusion
Occupational skin cancer seldom gets attention,
especially in terms of prevention. Precancerous
lesion can be used as one of the clinical clues for
suspected occupational skin cancer.
Comprehensive management, especially in the
working environment, can be integrated with the
company/institution’s occupational health and
safety program.
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