Occupational Skin Cancer

  • Thomas L. DiepgenEmail author
  • Hans Drexler
Living reference work entry


Occupational skin cancer can be induced due to industrial exposure to chemical carcinogens but nowadays more important due to occupational exposure to UV radiation (UVR).

Occupational skin cancer is characterized by long induction periods (years or decades), and its first manifestation is often seen many years after the occupational exposure or even when the affected individuals are not more occupationally exposed.

Important industrial chemicals are arsenic and inorganic arsenic compounds, polycyclic aromatic hydrocarbons (PAHs) with particularly high levels in brown coal tars (soft coal tars), coal tars (black coal tars), coal tar pitches, coal tar oils, and coke oven emissions and can cause basal cell carcinomas and squamous cell carcinomas.

A published systematic appraisal of the epidemiologic literature and meta-analysis clearly indicates that occupational UV-light exposure is a substantial and robust risk factor for the development of cutaneous squamous cell carcinoma (SCC).

The actually available evidence of the epidemiologic literature could also clearly show a significant risk increase for occupationally UV-exposed workers to develop basal cell carcinoma (BCC) compared to nonexposed workers.

There is enough scientific evidence that outdoor workers have an increased risk to develop work-related occupational skin cancer due to natural UVR exposure, and adequate prevention strategies have to be implemented.

The three measures that are successful and of particular importance in the prevention of nonmelanoma skin cancer in outdoor workers are the following:
  1. 1.

    Changes in behavior regarding awareness of health and disease resulting from exposure to natural UV radiation

  2. 2.

    Protection from direct UV radiation by wearing suitable clothing

  3. 3.

    Regular and correct use of appropriate sunscreens



Actinic (solar) keratoses Bowen’s disease Keratoacanthoma Malignant melanoma Nonmelanoma skin cancer Pitch skin disease Tar keratoses 

1 Core Messages

  • Occupational skin cancer can be induced due to industrial exposure to chemical carcinogens but nowadays more important due to occupational exposure to UV radiation (UVR).

  • Occupational skin cancer is characterized by long induction periods (years or decades), and its first manifestation is often seen many years after the occupational exposure or even when the affected individuals are not more occupationally exposed.

  • Important industrial chemicals are arsenic and inorganic arsenic compounds, polycyclic aromatic hydrocarbons (PAHs) with particularly high levels in brown coal tars (soft coal tars), coal tars (black coal tars), coal tar pitches, coal tar oils, and coke oven emissions and can cause basal cell carcinomas and squamous cell carcinomas.

  • A published systematic appraisal of the epidemiologic literature and meta-analysis clearly indicates that occupational UV-light exposure is a substantial and robust risk factor for the development of cutaneous squamous cell carcinoma (SCC).

  • The actually available evidence of the epidemiologic literature could also clearly show a significant risk increase for occupationally UV-exposed workers to develop basal cell carcinoma (BCC) compared to nonexposed workers.

  • There is enough scientific evidence that outdoor workers have an increased risk to develop work-related occupational skin cancer due to natural UVR exposure, and adequate prevention strategies have to be implemented.

  • The three measures that are successful and of particular importance in the prevention of nonmelanoma skin cancer in outdoor workers are the following:
    1. 1.

      Changes in behavior regarding awareness of health and disease resulting from exposure to natural UV radiation

    2. 2.

      Protection from direct UV radiation by wearing suitable clothing

    3. 3.

      Regular and correct use of appropriate sunscreens


2 Introduction

Occupational skin cancer is, especially in the historical sense due to industrial exposure to chemical carcinogens, important, but nowadays, the relation of skin cancer to occupation is often confounded by concurrent sun exposure from leisure pursuits. The term “skin cancer” is nonspecific. Under such a heading come different clinicopathological entities with different etiologic factors, presentation, clinical course, and prognosis (Naldi and Diepgen 2007). A distinction is usually made between “cutaneous melanoma” and “nonmelanoma skin cancer.” The term “nonmelanoma skin cancer” includes a large number of different disorders, especially basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). Nonetheless, it is common practice to use it with reference to only two entities, which, by far, are the most frequent ones, namely, basal cell carcinoma and squamous cell carcinoma, also collectively labeled as “keratinocyte carcinomas” or “epidermal skin cancer.” Besides the abovementioned disorders, a large number of clinicopathological entities may be listed as representing “skin cancer” (Table 1).
Table 1

Classification of skin cancer (According to Naldi and Diepgen 2007)



Epidermal skin tumors

Basal cell carcinoma

Squamous cell carcinoma

Paget’s disease


Tumors of skin appendages

Hair follicle tumors

Pilary complex carcinoma

Sebaceous glands

Sebaceous carcinoma

Apocrine gland tumors

Apocrine carcinoma

Eccrine gland tumors

Sweat gland carcinoma

Microcystic adnexal carcinoma

Eccrine epithelioma

Mucinous eccrine epithelioma

Adenoid cystic carcinoma

Lymphoepithelioma-like carcinoma

Melanocytic tumors


Malignant blue nevus

Langerhans cell tumors

Histiocytosis X

Mast cell tumors

Lymphadenopathic mastocytosis and eosinophilia

Subcutaneous tissue tumors


Fibrohistiocytic tumors

Dermatofibrosarcoma protuberans

Atypical fibroxanthoma

Malignant fibrous histiocytoma

Neoplasms of the vessel wall


Kaposi’s sarcoma

Smooth muscle tumors

Superficial leiomyosarcoma

Neural and neuroendocrine tumors

Granular cell tumor

Neuroendocrine and Merkel cell carcinoma

Cutaneous lymphoproliferative disease

T cell

Mycosis fungoides

Sézary syndrome

Adult T-cell leukemia/lymphoma

Primary cutaneous CD30+ lymphoproliferative disorders

B cell

Primary cutaneous marginal zone B-cell lymphoma

Primary cutaneous diffuse large B-cell lymphoma, leg type

Precursor hematologic neoplasms

In contrast to most inflammatory occupational skin diseases, especially allergic and irritant contact dermatitis and contact urticaria, occupational skin cancer is characterized by long induction periods (years or decades), and its first manifestation is often seen many years after the occupational exposure or even when the affected individual is not more occupationally exposed.

An additional problem related to occupational skin cancer is the fact that skin cancer nowadays is a widespread disease, especially in Caucasians, and is comparable rarely induced by occupational carcinogens but by constitutional (skin type) and lifestyle factors (sun exposure).

This chapter introduces different types of occupational skin cancer and discusses its occupational hazards. In the last paragraph, measures for the prevention of occupational skin cancer are presented.

3 Epidemiology of Melanoma and Nonmelanoma Skin Cancer

Melanoma and nonmelanoma (basal and squamous cell carcinomas) skin cancer (NMSC) are now the most common types of cancer in the white populations, and the incidence of skin cancer has reached epidemic proportions (Diepgen and Mahler 2002; Madan et al. 2010). According to population-based studies from Australia, the incidence rate is over 2% for basal cell carcinoma (BCC) in males and 1% for squamous cell carcinoma (SCC), and there are over 50 new cases of melanoma per 100,000 (Buettner and Raasch 1998). According to a recently published study (Pandeya et al. 2017), the person-based incidence of keratinocyte cancer excisions in Australia was 1,531 per 100,000 person-years; incidence increased with age and was higher for men than women (SIR, 1.43; 95% CI, 1.42–1.45). Lesion-based incidence was 3,154 per 100,000 person-years. The estimated age-standardized incidence rates (ASRs) for BCC and SCC were 770 per 100,000 and 270 per 100,000 person-years, respectively. In a population-based study in Olmsted County, Minnesota (USA), the age-adjusted BCC incidence (cases per 100,000 person-years) was 360.0 (95% CI, 342.5–377.4) in men and 292.9 (95% CI, 278.6–307.1) in women. The age-adjusted cSCC incidence (cases per 100,000 person-years) was 207.5 (95% CI, 193.9–221.1) in men and 128.8 (95% CI, 119.4–138.2) in women (Muzic et al. 2017). Without doubt, skin cancer is by far the most common kind of cancer diagnosed in many western countries. The chance of developing a skin cancer in British Columbia, Canada, is approximately 1 in 7, over lifetime (Demers et al. 2005). The most common skin cancer is basal cell carcinoma, followed by squamous cell carcinoma and melanoma.

4 Types of Occupational Skin Cancer

4.1 Nonmelanoma Skin Cancer

The term “nonmelanoma skin cancer” (NMSC) covers those cancers of the skin (epidermis) which are not malignant melanomas. The two commonest NMSCs are basal cell carcinoma and squamous cell carcinoma of the skin. Both of these types of malignant tumor arise from the epidermal tissues: squamous cell carcinomas from the epidermal keratinocytes and basal cell carcinomas from the basal cells of the epidermis. Basal cell carcinoma is the commonest malignant tumor in fair-skinned people: it is extremely locally invasive and destructive but only rarely metastasizes.

Different types of basal cell carcinoma can be distinguished clinically: nodular, cystic, pigmented, superficial (multicentric), morphoea-like, and ulcerative. The nodular and cystic variants are usually found on the face and are up to 10 mm or more in diameter. The morphoeic type shows scarring and a diffuse edge and is often found on the face too, whereas the multicentric superficial tumors, which can extend to several centimeters in diameter, typically occur on the trunk. Exposure to the sun, to ionizing radiation, and to chemical carcinogens including tar products can be involved in the causation of basal cell carcinoma.

Like squamous cell carcinoma, it is more commonly found in men than in women. Basal cell carcinoma occurs about four times more frequently than squamous cell carcinoma, which is the second most common form of skin cancer.

Squamous cell carcinoma has a destructive pattern of growth and it metastasizes. It nearly always arises from characteristic precancerous lesions; actinic keratoses (AKs) are preinvasive squamous cell carcinomas and can therefore be regarded as carcinoma in situ. Basal cell carcinomas and squamous cell carcinomas exhibit both epidemiological and biological differences.

Squamous cell carcinomas and basal cell carcinomas are the commonest skin cancers in spi1;fair-skinned people all over the world (Wang and Diepgen 2006). In the USA, it has even been estimated that the incidence rate of NMSCs (basal cell and squamous cell carcinomas combined) is about as high as all other types of cancer put together (American Cancer Society 2006). In the year 2002, some one million Americans were diagnosed with NMSC. Because of the high morbidity and associated treatment costs, NMSCs represent a heavy burden on the health-care system, even though they are not usually associated with very high mortality. NMSC has therefore been included in the top 10 health-care priorities in the USA for this decade, currently occupying place eight.

Since the 1960s, the annual incidence of NMSC has increased by 3–8% (Glass and Hoover 1989; Green 1992).

Sex-related differences in exposure to the sun during occupational and leisure activities, the use of sun protection, and scalp hair are probably reasons for the higher prevalence of nonmelanoma skin cancer in men (Oberyszyn 2008; Hall et al. 1997).

Basal cell and squamous cell carcinomas are usually considered together under the heading “nonmelanoma skin cancer,” but they present rather different distribution and etiologic factors. The two tumors share the difficulties of obtaining reliable incidence data and the limited contribution of mortality to understand their distribution and burden. Incidence estimates for “cancer of the skin other than melanoma” based on registry data, range from around 0.5/100,000 in Hispanics, Blacks, and Asians to more than 100/100,000 in white people in Switzerland and Ireland (Parkin et al. 2005). However, few cancer registries provide reliable data on nonmelanoma skin cancer, and ad hoc studies should be better conducted.

Within populations of European descent, the incidence of squamous cell carcinoma is lower in those with darker skins (Mediterranean skin type). In Australia and the USA, the incidence of squamous cell carcinoma increases with proximity to the equator. Squamous cell carcinoma of the skin shows clear associations with geographical latitude of the domicile and measured UVB radiation. Lifetime cumulative exposure is decisive for risk. In contrast to malignant melanomas and basal cell carcinomas, the incidence of squamous cell carcinoma shows an exposure-response curve without any plateau phase. Benign UV-light-induced skin changes (lentigo, telangiectasia, and elastosis) also show a strong association with the incidence of squamous cell carcinoma.

4.1.1 Risk Factors for NMSC

Table 2 shows the similarities and differences in the risk factors for basal cell carcinoma and squamous cell carcinoma. Whereas squamous cell carcinomas are clearly associated with chronic exposure to UV light, occur on areas of the skin exposed to light, and, in Caucasian populations, show clear associations with the geographical latitude of domicile and measured UVB radiation, important risk factors for basal cell carcinomas also include intermittent exposure to sunlight and a genetic predisposition. A decisive factor for the development of squamous cell carcinoma is the cumulative lifetime UV exposure. In contrast to malignant melanomas and basal cell carcinomas, the incidence of squamous cell carcinoma shows an exposure-response curve without a plateau phase.
Table 2

Risk factors for nonmelanoma skin cancer (NMSC): basal cell carcinomas and squamous cell carcinomas – similarities and differences

Risk factor

NMSC: squamous cell carcinomas and basal cell carcinomas


Clear increase with age


More common in men


Increased risk with a positive family history of basal cell carcinoma, but not of squamous cell carcinoma


Higher incidence in fair-skin types – people who do not tan easily, have many freckles, get sunburn easily, and have red or blonde hair

Past history of skin cancer

36–52% probability of the occurrence of a new skin cancer within the next 5 years

Ethnic group

More common in people of Caucasian origin

Geographical location

The incidence increases in Caucasian people with proximity to the equator

Medical causes

Chronic ulceration, burn scars, xeroderma pigmentosum, immunosuppression (organ transplantation), and HPVa infections are associated with increased risk


Higher incidence of squamous cell carcinoma but also of basal cell carcinoma, in outdoor workers

Exposure to chemicals and other substances

Ionizing radiation, PUVA therapy, and exposure to tar increase the risk. Smoking is a risk factor for squamous cell carcinoma; arsenic exposure is a more important risk factor for basal cell carcinoma

Exposure to sunlight


The highest individual risk factor for squamous cell carcinoma, less important (together with other risk factors) for basal cell carcinoma


Intensive, intermittent exposure with sunburn and blistering especially in childhood/adolescence is associated with an increased risk of basal cell carcinoma but not of squamous cell carcinoma

aHuman papilloma virus

Besides UV radiation, other influences such as ionizing radiation, exposure to tar and other carcinogens, smoking, DNA repair defects (such as xeroderma pigmentosum), and/or immunosuppression may induce nonmelanoma skin cancer. Smoking and other types of tobacco use are clearly associated with squamous cell carcinoma of the lip. Malignant tumors of the skin may form in scars. Burns and other firm scar tissue are predisposed to skin cancer. Most of them are squamous cell carcinomas or basal cell carcinomas, although the former are more common (Kowal-Verna and Criswell 2005). Simultaneous exposure to UV light and benzopyrenes considerably intensifies the development of cancer.

In white transplant recipients, risk of squamous cell carcinoma increases 65–250-fold and risk of basal cell carcinoma 10–16-fold compared with the nontransplanted population (Lindelof et al. 2000; Moloney et al. 2006). The risk of developing actinic keratosis (AK) is about 250 times greater in organ transplant recipients (Stockfleth et al. 2002; Stoff et al. 2010). The ratio of squamous cell to basal cell carcinoma also reverses in iatrogenic immunosuppression, because squamous cell carcinomas and actinic keratosis occur more frequently in transplant recipients than do basal cell carcinomas.

Although basal cell carcinomas usually occur in light-exposed areas, unlike squamous cell carcinomas, they may also occur in areas hardly exposed to sunlight at all and without any significant actinic damage, such as the trunk. UV light is also the most potent causative factor for basal cell carcinoma, but its effects are less evident than in squamous cell carcinoma.

A carcinogen typically associated with basal cell carcinomas is arsenic. An increased incidence of basal cell carcinomas has been reported with a hereditary syndrome of congenital defects (basal cell nevus syndrome). A sebaceous nevus may enhance the development of basal cell carcinomas. Apart from the genetic predisposition, intermittent intense exposure to UV light with sunburn is a key risk factor.

People who already have one squamous cell carcinoma of the skin have an approximately 50% risk of developing a second malignant skin lesion (nonmelanoma skin cancer) in the following 3–5 years (Hemminki and Dong 2000).

4.2 Malignant Melanoma

Malignant melanoma (MM) occurs among all adequately studied racial and ethnic groups. Its incidence is much lower compared to NMSCs but has been rising in fair-skinned populations throughout the world for several decades (Armstrong and Kricker 1994). The incidence of malignant melanoma varies over 100-fold around the world (Naldi and Diepgen 2007). According to data provided in Cancer Incidence in Five Continents, the lowest rates reported around 1993–1997 were 0.3–0.5/100,000 person-years, in parts of Asia and in Asian and black people in the USA, while the highest were up to 50/100,000 in Queensland, Australia (Parkin et al. 2005). Incidence rates have risen significantly over the last 30–40 years and continue to increase in the USA, Canada, Australia, and Europe, being perceived as a major public health concern. Geographic variations with incidence of cutaneous melanoma appear to reflect the combined effect of constitutional characteristics and latitude. Epidemiological data from the USA and Australia show that melanoma incidence in white people increases the closer to the equator people live.

In contrast to nonmelanoma skin cancer, the greatest numbers of melanomas are found on the intermittently sun-exposed areas of the back and legs. Increases in incidence in populations of European origin have been most pronounced on the trunk and other intermittently exposed areas, particularly in men, while the incidence of melanoma of the face has remained reasonably stable over time (Bulliard and Cox 2000; Thorn et al. 1990). The anatomical distribution in black people and people of Asian origin is quite different with most melanomas occurring on the soles of the feet (Cress and Holly 1997).

There are important clinical and epidemiological differences in risk factors for the different subtypes of cutaneous malignant melanoma (superficial spreading melanoma, nodular melanoma, lentigo maligna melanoma, and acrolentigo melanoma). The following are the most important risk factors for malignant melanoma:
  • Skin type/ethnicity: Increased incidence in those with fair complexions; those who burn easily, tan poorly, and freckle; those who have red, blonde, or light brown hair; and those of Celtic ancestry.

  • Family history: Occurrence of melanoma in a first- or second-degree relative confers increased risk. Familial atypical mole melanoma syndrome (FAMMS) confers even higher risk.

  • Nevi: A large number of melanocytic nevi and giant pigmented congenital nevi confer increased risk. Melanocytic nevi are markers for risk, not precursor lesions.

  • Geographic location: Higher incidence in whites living near the equator.

  • Sun exposure: Cumulative sun exposure probably does not influence risk, but intense, intermittent exposure and blistering sunburns in childhood and adolescence are associated with increased risk. However, lentigo maligna melanoma (LMM) occurs in sun-exposed sites, typically on the face, and is typically associated with prolonged cumulative exposure to sunlight, usually over a period of many years, in somebody employed in outdoor work. LMM might be considered as an occupational skin cancer because there is a “general suitability,” given that LMM may be caused by prolonged occupational exposure to natural UV light (Elsner et al. 2014).

  • Occupation: Higher incidence in indoor workers, as well as those with higher education and income.

  • Medical conditions: Xeroderma pigmentosum, immunosuppression, other malignancies, and previous nonmelanoma skin cancer all increase risk. Previous melanoma is associated with increased risk.

The single greatest predictor of risk for developing melanoma is the total number of nevi (Gandini et al. 2005b). Studies over the last decades have revealed a great deal about the way nevi develop and the relationship between nevi and melanoma. Interestingly, red-haired children have a reduced count of nevi as compared to other skin phenotypes but a higher melanoma risk, suggesting different pathways to melanoma development.

Intermittent sun exposure and sunburn history were shown to play considerable roles as risk factors for melanoma, whereas a high occupational sun exposure seemed to be inversely associated to melanoma (Gandini et al. 2005a). Overall, high occupational exposure is inversely associated with melanoma and directly related to the risk of squamous cell carcinoma.

5 Other Occupational Skin Cancers

Actinic (solar) keratoses clinically are brownish or reddish scaly areas, sometimes with a popular component or with inflammation, a few millimeters in diameter, and a rough surface. They are located on sun-exposed sites, typically the dorsal aspects of the hands, the forearms, the face, and the scalp. They may be associated with other stigmata of sun-damaged skin, such as telangiectasia, irregular pigmentation, solar elastosis, or skin atrophy. Actinic keratoses are nowadays considered as a squamous cell carcinoma in situ and belong therefore to NMSC (Röwert-Huber et al. 2007).

Tar keratoses are related to exposure to coal tar, pitch, shale oil, and products of the distillation of coal (Gawkrodger 2004). They may appear some years after the period of exposure. Clinically, they are brown-colored, flat-topped, round, or oval small plaques a few millimeters in diameter, with a tendency to be clustered. Their surface may be smooth or warty. They tend to be seen on the dorsal aspects of the hands, the forearms, and around the face.

Arsenical keratoses are typically seen as punctate keratoses on the palms of the hands and soles of the feet in subjects exposed to arsenic and are not seen with any other condition. They are usually multiple and may progress to squamous cell carcinoma. Intraepidermal carcinoma or multiple basal cell carcinomas may be associated (Gawkrodger 2004).

Keratoacanthoma is a rapidly growing dome-shaped nodule up to 2 cm in diameter, with a central keratinous plug, that is usually found in sun-exposed areas such as the face, dorsa of hands, and the forearms (Gawkrodger 2004). Histologically, they resemble squamous cell carcinomas, but spontaneous resolution may occur. It is associated with sunlight and tar exposure (Letzel and Drexler 1998).

Intraepidermal carcinoma (Bowen’s disease) is in situ squamous cell carcinoma. It occurs as scaly red plaques up to several centimeters in size, located on the sun-exposed sites of the lower legs, face, or arms (Gawkrodger 2004). Progression to invasive carcinoma may occur. It is typically associated with arsenic ingestion.

6 Occupational Hazards

6.1 Arsenic

Arsenic occurs naturally in ores together with zinc, lead, copper, and iron. In the past, it was used for paints, pesticides, and as a medicine. Today, arsenic is only used in the semiconductor and microchip industry. Arsenic and inorganic arsenic compounds are mainly absorbed via inhalation and ingestion. Several studies show that the internal exposure to arsenic correlates well with the external exposure. Therefore, dermal absorption under workplace conditions does not seem to be relevant. Arsenic and inorganic arsenic compounds are distributed rapidly in all organs. Accumulation is observed particularly in the liver, kidneys, and lungs. Long-term exposure to arsenic in humans causes fever, sleep disorders, weight loss, swelling of the liver, dark discoloration of the skin, sensory and motor neuropathy, and encephalopathy with symptoms such as headaches, poor concentration, deficits in the learning of new information, difficulties in remembering, mental confusion, anxiety, and depression. Long-term exposure to arsenic can also cause peripheral vascular effects such as acrocyanosis, Raynaud’s disease, and tissue necrosis on the extremities (blackfoot disease) . Long-term exposure to dust containing arsenic causes irritation of the conjunctiva and mucous membranes of the nose and throat. The pustular or follicular skin reactions observed after contact with inorganic arsenic compounds are usually attributed to irritative effects and not to sensitizing effects of the arsenic compounds.

Arsenic and inorganic arsenic compounds are carcinogenic in humans. The target organs of the carcinogenic effects after inhalation are the lungs and after ingestion the bladder, kidneys, lungs, and skin (Greim 2005).

The premalignat skin tumors are punctuate keratoses on the palms of the hand and soles of the feet in subjects exposed to arsenic. They cannot be observed under other conditions and are therefore pathognomonic for chronic arsenic exposure. They are usually multiple and may progress to squamous cell carcinoma (Gawkrodger 2004). Besides the squamous cell carcinomas which can also occur on each position on the skin besides palms and soles, superficial basaliomas are often associated with a chronic arsenic exposure.

6.2 Polycyclic Aromatic Hydrocarbons (PAHs)

In 1773, Sir Percivall Pott was the first to describe the occurrence of occupational causes of cancers. He observed the frequent occurrence of squamous cell carcinomas of the scrotum in young chimney sweeps and identified soot as the causal agent. Soot is a pyrolysis product of organic materials which contain, among numerous other substances, polycyclic aromatic hydrocarbons (PAHs). The extremely complex mixtures which have been examined to date contain, simultaneously and in widely differing proportions, carcinogenic components and substances which promote cancer development. Many of the PAHs, which occur regularly in pyrolysis products, are carcinogenic in animal studies. They exist at particularly high levels in brown coal tars (soft coal tars), coal tars (black coal tars), coal tar pitches, coal tar oils, and coke oven emissions (DFG 2010).

The carcinogenic effect after occupational exposure to these mixtures of aromatic compounds has been demonstrated in epidemiological studies. Therefore, they are classified into the category of the human cancerogens.

In the organism, PAHs are enzymatically converted into carcinogenic metabolites. The enzymes required for this activation are monooxygenases (CYP 1A1, 1A2, 1B1) and are found in the hair follicles of the skin. Therefore, the initial cancers (“tar warts”) develop – in contrast to solar keratosis – in the deeper layers of the epidermis.

PAHs can cause basal cell carcinomas and squamous cell carcinomas. Direct skin contact seems to be a prerequisite. The latency of the initial exposure to PAHs to an onset of skin tumors may be relevant for years to decades. Skin cancer can occur even after termination of exposure. Often, there are other signs of a so-called tar or pitch skin disease (e.g., folliculitis, acne, diffuse brownish pigmentation, and hyperkeratosis). The tumors can also occur without these signs. The skin tumors are localized, in particular, in the exposed areas including the nose, periorbital region, and ears and on the backs of the hands and forearms. The location seems to deviate from that of the light-induced tumors (more often lower lip than upper lip, more often nasal vestibule than bridge) (Letzel and Drexler 1998).

6.3 Ionizing Radiation

Ionizing radiation consists of particles (alpha particles, beta particles, neutrons) or electromagnetic waves (gamma rays with wavelengths less than 0.01 nm, which are less than the diameter of an atom, and X-rays with wavelengths from 0.01 to 10 nm). Alpha particles are absorbed completely in the stratum corneum and do not cause a damage in the skin. Under high acute radiation exposure (1 Sv and above), the development of acute radiation dermatitis is expected with redness, itching, and infiltration of the skin. Higher doses may cause bleeding into the skin, blisters, and necrosis. The final stage can be a chronic dermatitis with radio atrophy of the skin, increasing sclerosis, keratinization disorders, pigmentary changes, and dryness developing due to loss of sebaceous glands, hair loss, and telangiectasia.

Ionizing radiation can cause malignant diseases of the skin, especially squamous cell and basal cell carcinomas and less often sarcomas. Actinic keratoses caused by X-rays are carcinomas in situ and were often observed in the past at the hands of surgeons and radiologists. Today, in compliance with the radiation limits, however, no higher incidence of radiation-induced diseases is observed in occupationally to ionizing radiation-exposed persons. The radiation exposure from accidents such as Chernobyl or Fukushima, in contrast, is much higher and suitable to cause both stochastic damages (cancer) and deterministic damages (inflammation to necrosis) on the skin.

6.4 UV Radiation

The spectrum of ultraviolet (UV) light comprises wavelengths of 100–400 nm and is therefore below the range of 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), although on the Earth, human beings are exposed only to UVA and UVB. Natural solar UV radiation on this planet consists of ≥95% UVA and ≤5% UVB.

UV radiation is the most important cause of skin aging and skin cancer. It causes chronic cutaneous photodamage (Saladi and Persaud 2005). The carcinogenic effects of UV radiation on the skin and eyes are well documented both experimentally and epidemiologically (Saladi and Persaud 2005). UV radiation acts as a carcinogen both directly, by inducing cell damage (DNA mutations), and indirectly, by inducing immunosuppression (suppression of T lymphocytes).

There is good evidence that UVB radiation acts directly through specific changes in oncogenes and p53 tumor suppressor genes, which are responsible for the initiation and progression of skin cancer. UV radiation, and in particular UVB, leads to the formation of pyrimidine dimers in deoxyribonucleic acid (DNA) and ribonucleic acid (RNA). This gives rise to mutations in keratinocytes and hence to neoplastic transformation. Particularly, significant mutations affect the telomerase gene and the p53 tumor suppressor gene. These mutations are important steps toward neoplastic transformation.

UVB radiation causes direct damage to DNA and RNA by inducing covalent bond formation between adjacent pyrimidines, leading to generation of mutagenic photoproducts such as cyclopyrimidine dimers (TT) and pyrimidine-pyrimidine (6–4) adducts (Rünger 2007). UVA is less mutagenic than is UVB and causes indirect DNA damage via a photooxidative stress-mediated mechanism, resulting in formation of reactive oxygen species, which interact with lipids, proteins, and DNA to generate intermediates that combine with DNA to form adducts (Ridley et al. 2009). Several complex DNA repair systems are needed to prevent the harmful effects of these premutagenic adducts (Lear et al. 2000).

UVA radiation, which penetrates deeper into the skin, reinforces the carcinogenic effects of UVB rays and causes aging and immunosuppression. In this way, both UVB and UVA are involved in the development of skin cancer.

The relationship between UV radiation and skin cancer has been well demonstrated at various levels by epidemiology, clinical distribution of the tumors, molecular biology, and plausible mechanisms. However, some aspects in the development of the disease and in the counter-regulatory mechanisms, the interaction of various photobiological processes, and the secondary biochemical effects after irradiation are still unclear.

Light skin complexion (especially light skin and blond-red hair), freckling, and tendency to burn, not tan, after sun exposure, are constitutional variables which affect the risk of skin cancer. People from Southern European ethnic origin are at a significantly lower risk than those from English, Celtic, and Scandinavian origin. Those who migrate early in their life from such regions to lower latitudes increase their exposure levels to sunlight and show a higher risk of developing skin cancer. It can be further stated that the timing and character of sun exposure may affect differently the risk of different skin cancers. Cutaneous melanoma and basal cell carcinoma are most significantly linked to early exposure to ultraviolet light. Intermittent sun exposure and sunburn history are more important than cumulative dose in predicting adult risk for these tumors. Basal cell carcinoma and melanoma tumors appear to have a rapidly accelerating relative risk with relatively low exposures, followed by a broad plateau. Among sensitive individuals, sun avoidance behavior in adulthood may not markedly reduce risk for these tumors. On the contrary, squamous cell carcinoma is associated with total lifetime sun exposure. It has also been demonstrated that intermittent and chronic sun exposure is a risk factor for basal cell carcinoma (Walther et al. 2004).

Outdoor workers such as farmers, welders, watermen, police officers, physical education teachers, pilots, and cabin attendants have an increased risk of skin cancer (Ramirez et al. 2005). There is scientific and epidemiological evidence to recognize squamous cell carcinoma induced by occupational UV-light exposure as an occupational disease since a doubling of risk due to occupational UV radiation can be demonstrated (Diepgen and Drexler 2004). Two published systematic reviews demonstrate the increased risk of nonmelanoma skin cancer in outdoor workers (Schmitt et al. 2011; Bauer et al. 2011).

Schmitt et al. 2011 demonstrated in a systematic review and meta-analysis that occupational UV-light exposure increases the risk for the development of cutaneous squamous cell carcinoma. The authors performed a systematic electronic literature search in PubMed (until May 2010) supplemented by handsearch identified 18 relevant studies that were included in the review. Eighteen studies (6 cohort studies, 12 case-control studies) met the eligibility criteria and were included in the systematic review. Sixteen studies (89%) found an increased risk of SCC in individuals with occupational UV-light exposure compared to individuals without occupational UV-light exposure, reaching statistical significance in 12 studies. Two studies found no association between occupational UV-light exposure and SCC occurrence. The pooled OR (95% CI) was 1.77 (1.40–2.22) and did not differ significantly between cohort studies (OR; 95% CI: 1.68; 1.08–2.63) and case-control studies (OR; 95% CI: 1.77; 1.37–2.30). Meta-regression analyses suggested an increasing strength of the association between occupational UV-light exposure and SCC risk with decreasing latitude. In addition, the authors identified several reasons why the observed increase in the risk for cutaneous SCC among individuals with work-related UV-light exposure compared to indoor workers is an underestimation of the true association. This systematic appraisal of the epidemiologic literature and meta-analysis clearly indicates that occupational UV-light exposure is a substantial and robust risk factor for the development of cutaneous SCC. These findings are of significant public health impact as they highlight the need for preventive measures for individuals with high levels of work-related UV-light exposure.

It is reasonable to assume that outdoor workers with a long history of work-related UV exposure are at increased risk of developing BCC; however, it has not yet been demonstrated epidemiologically as clearly as for cutaneous SCC. Bauer et al. (2011) summarized the actually available evidence of the epidemiologic literature and could also clearly show a significant risk increase for occupationally UV-exposed workers to develop BCCs compared to non-exposed workers. In this systematic review and meta-analysis, 24 relevant epidemiologic studies (5 cohort studies, 19 case-control studies) were identified. Twenty-three studies reported sufficient data to be included in the meta-analysis. The pooled OR for the association between outdoor work and BCC risk was 1.43 (95% CI: 1.23–1.66; p = 0.0001). Studies adjusting for sex (p < 0.0001) and individual nonoccupational UV exposure (p = 0.014) showed a significant stronger association of occupational UV exposure and BCC risk. Taking into account that the majority of the studies published to date lack precision in the assignment of workers to indoor and outdoor tasks as well as concerning UV-exposure measurements and adjustment for major confounders, it is most likely that the real risk is largely underestimated. In addition, meta-regression revealed a significant inverse relationship between occupational UV-light exposure and BCC risk with latitude (p = 0.015). This systematic review indicates that outdoor workers are at significantly increased risk for BCC. This study is important to inform occupational safety representatives, stimulate the implementation of prevention strategies, and encourage further research in this important field.

It has been estimated by the IARC that outdoor workers had the two to three times higher UV radiation dose than indoor workers (IARC 1992). In subjects older than 20 years, the UV radiation (UVR) exposure is not related to age but to occupation, outdoor sports activities, or being a sun worshipper (Thieden et al. 2004). Thieden et al. (2004) developed a personal electronic UVR dosimeter in a wristwatch and measured continuously time-related UVR doses in standard erythemal dose (SED). They demonstrated that the median estimated yearly UVR dose was 132 SEDs for indoor workers but 224 SEDs for gardeners. Knuschke et al. (2007) also found significantly increased UVR doses in different outdoor workers compared to indoor workers. It was estimated that the average annual UVR exposure of the general population is 130 SED per year in Germany (Knuschke et al. 2008). In a recent study from Denmark, the solar ultraviolet radiation exposure of 457 workers in the Danish summer season was measured (Grandahl et al. 2018): presented as semiannual standard erythemal dose (SED) on working days, respectively, at leisure, the results are for mainly outdoor workers 214.2 SED and 64.8 SED, equal-parts-outdoor-and-indoor workers 131.4 SED and 64.8 SED, and indoor workers 55.8 SED and 57.6 SED.

In Canada, an estimated 2,846 (5.3%) of the 53,696 newly diagnosed cases of basal cell carcinoma (BCC) and 1,710 (9.2%) of the 18,549 newly diagnosed cases of squamous cell carcinoma (SCC) in 2011 were attributable to occupational solar radiation exposure (Mofidi et al. 2018).

In conclusion, there is enough scientific evidence that outdoor workers have an increased risk to develop a work-related occupational nonmelanoma skin cancer due to natural UVR exposure during working hours. In contrast to natural UVR exposure, epidemiological studies are still missing to demonstrate an increased risk of occupational skin cancer due to occupational exposure to artificial UVR.

6.5 Malignant Skin Tumors in Scars

Malignant skin tumors can develop within scars. Thus, they can be caused indirectly by an industrial accident. Only burn scars and other tight scars are premalignant conditions for squamous cell carcinomas and basal cell carcinomas. Squamous cell carcinomas occur more frequently (Kowal-Verna and Criswell 2005; Dix 1960). In order to postulate a causal context between the tumor and accidental scar, according to Ewing (cited in Kowal-Verna and Criswell 2005), the following conditions must be met:
  1. 1.

    The presence of a scar.

  2. 2.

    The tumor has developed within the boundaries of the scar.

  3. 3.

    The absence of a preexisting tumor of the same type.

  4. 4.

    Any tumor cells must correspond to the cells of the primary tumor in the scar (this item is only relevant for metastasis).

  5. 5.

    An adequate time interval between the scar and the development of the neoplasm.


7 Occupational Skin Cancer According to German Low

In Germany, occupational skin cancer may be caused by occupational exposure to certain carcinogens, and currently, the following occupational disease numbers (BK numbers) may be applied (Diepgen JDDG 2016).

7.1 BK No. 1108: Diseases Caused by Arsenic or Its Compounds

According to Diepgen et al. (2016), it is noted: “Arsenic and its compounds may cause basal cell carcinoma and squamous cell carcinoma, including Bowen’s disease and Bowen’s carcinoma. Pathognomonic manifestations include palmoplantar keratoses, which, however, are not necessarily present in all cases. Exposure mainly occurs through the respiratory tract, but may also take place via the gastrointestinal tract and, under special conditions, through the skin. Typically, arsenic-induced lesions include multiple superficial basal cell carcinomas that also occur at non-UV-exposed sites. Squamous cell carcinomas develop from precursors or on healthy skin.”

7.2 BK No. 2402: Diseases Caused by Ionizing Radiation

In the newly revised Bamberg recommendations (Diepgen et al. 2016), it is noted: “Depending on the dose (see scientific argumentation for BK No. 2402), exposure to ionizing radiation may induce malignant skin diseases, primarily squamous cell carcinoma, less commonly basal cell carcinoma, and rarely fibrosarcoma and angiosarcoma.”

7.3 BK No. 5102: Skin Cancer or Skin Alterations Showing a Cancerous Tendency Caused by Soot, Raw Paraffin, Tar, Anthracene, Pitch, or Similar Substances

One of the oldest occupational diseases in Germany, it was included in the ordinance on occupational diseases in 1925. In the newly revised Bamberg recommendations (Diepgen et al. 2016), it is noted: “According to current knowledge, substances in the context of BK No. 5102 may cause squamous cell carcinoma, carcinoma in situ, as well as basal cell carcinoma. Direct skin contact plays a crucial role. The latency period from initial exposure to the occurrence of skin tumors may be years or even decades long. At the onset of skin cancer, there are frequently also other signs of what is referred to as “tar- or pitch-induced skin disease” (e.g., folliculitis, acne, diffuse brownish pigmentation, hyperkeratosis). However, cancer lesions may also occur without these symptoms. Tar warts represent carcinomas in situ. Tumors are primarily located in the head region (e.g., nose, periorbital region, ears) as well as on the back of the hands and forearms.

7.4 BK No. 5103: Squamous Cell Carcinoma or Multiple Actinic Keratoses of the Skin Caused by Natural UV Irradiation

This occupational disease was newly added to the occupational disease list on January 1, 2015. In 2016, out of 75,491 notified occupational diseases (BK notification) of the commercial occupational insurance associations (BGs) and of the accident insurance institutions of the public sector, 6,101 cases have been notified according to BK 5103 plus another 2,453 cases of the agricultural BG. Occupational skin cancer due to BK 5103 ranks number 3 of all notified occupational diseases (after noise).

Based on current scientific knowledge, it is safe to assume that additional occupational UV exposure of 40% at the site of tumor development results in at least a twofold risk for cutaneous squamous cell carcinoma and therefore suggests predominantly occupational causation (Drexler et al. 2012; Diepgen et al. 2014). With respect to the notification and recognition of skin cancer as BK 5103, it is crucial that the clinical criteria of this new occupational disease are met (Table 3).
Table 3

Criteria for occupational skin cancer pursuant to BK 5103 (squamous cell carcinoma or multiple actinic keratoses of the skin caused by natural UV irradiation) according to Diepgen 2016



Location of skin tumors

Has to be in areas of the body occupationally exposed to UV radiation (note protective measures such as wearing a hard hat in the case of scalp tumors)

Clinical diagnosis confirmed

Squamous cell carcinoma (histologically confirmed) or at least six individual actinic keratoses diagnosed on clinical grounds within 12 months (histological confirmation of one AK is recommended) or field cancerization of at least 4 cm2.

Non-genital Bowen’s disease is equivalent to AK; Bowen’s carcinoma is equivalent to squamous cell carcinoma

Signs of chronic UV damage of the skin at which locations

Chronic UV damage of the skin is not necessarily a prerequisite for the recognition as BK

However, the intensity and distribution of UV damage in terms of occupationally and recreationally exposed skin areas are important clues as regards causation

Skin phototype according to Fitzpatrick

Plays no essential role with respect to the recognition as BK but should always be provided as part of the BK notification.

Equally modified by nonoccupational and occupational UV exposure, the skin phototype is a major risk factor for skin cancer. It may also affect the age of initial disease onset

Nonoccupational risk factors

Other nonoccupational risk factors, if any, should be taken into account, including immunosuppression, drugs that may affect light sensitivity, phototherapy, defects in pigmentation, impaired DNA repair mechanisms, and others

Additional occupational UV exposure of at least 40%

An estimate is sufficient to file a BK report. Quantitative determination of occupational UV exposure is carried out (by specific calculation) by the Prevention Services Division of the competent accident insurance

Information on differences from the general population with respect to vacations and leisure activities

Calculations done by the Prevention Services Division are based on the average recreational UV exposure of the general population (130 SEDs (standard erythemal dose) annually). Marked deviations caused by vacations spent in unusual places or unusual leisure activities should be documented

Note: In order for the causal relation to be recognized, particularly with regard to “exposure” and “disease” (causation in terms of liability), “sufficient probability” is required. This means that – considering all circumstances – there is a preponderance of circumstances that corroborate the causal relation, on which the medical expert/accident insurance/court may then base their judgment (Diepgen et al. 2016)

Recent measurements of the Institute for Occupational Safety and Health (IFA) of the German Statutory Accident Insurance (DGUV) have in some cases yielded significantly higher UV exposures. A so-called job-exposure matrix for UV exposure is therefore currently being developed (Wittlich et al. 2016).

8 Prevention

8.1 Primary Prevention

Risk assessment is the systematic identification and evaluation of relevant risks of workers with the aim of necessary measures for safety and health at work. It is based on an assessment of the hazard. Hazardous substances are labeled by many organizations regarding their potential effects (carcinogen, absorbed through the skin, sensitizing, irritating, etc.). To remove differences in the existing international systems of classification and labeling, a Globally Harmonized System of Classification and Labeling of Chemicals (GHS) was developed. The exposure is important too, which makes an assessment of the activities associated with the inhalation (breathing), the dermal uptake (through skin contact), and the physical-chemical hazards necessary. If occupational exposure limits (OELs) are available, it must be ensured that these values are not exceeded. In many situations (skin absorption, long half-life time of the hazards, etc.), the concentration of a hazardous substance in workplace air is less significant. A biological monitoring is more suitable to assess the individual risk of an exposed subject (Drexler et al. 2008).

8.2 Occupational Skin Cancer Prevention Strategies for Outdoor Workers

Experts believe that 90% of nonmelanoma skin cancer and two-thirds of melanomas may be attributed to excessive exposure to the sun. The aim of primary skin cancer prevention is therefore to limit UVR exposure. Campaigns to prevent skin cancer have incorporated numerous messages including the need to avoid sunburn and generally reduce exposure to ultraviolet radiation by staying out of the midday sun (between 11 a.m. and 3 p.m.), wearing protective clothing, seeking shade, and applying sunscreen. These campaigns are also needed for outdoor workers and subjects with an increased occupational UVR exposure.

There are three measures which are successful and of particular importance in the prevention of nonmelanoma skin cancer in outdoor workers:
  1. 1.

    Changes in behavior regarding awareness of health and disease resulting from exposure to natural UV radiation

  2. 2.

    Protection from direct UV radiation by wearing suitable clothing

  3. 3.

    Regular and correct use of appropriate sunscreens


In the first place, changes in behavior have to be aimed at avoiding direct exposure to natural UV light between 11 o’clock in the morning and 3 o’clock in the afternoon, wearing suitable clothing when outdoors, applying sunscreen regularly, and keeping in the shade (Fry and Verne 2003). This applies not only to exposure during leisure activities, at weekends, or on holiday but also to occupational exposure to natural UV radiation.

Suitable clothing must cover the arms and legs and should not have low-cut backs or necklines. Broad-brimmed hats should not only cover the head and face but also protect the ears and back of the neck. Materials used should be sufficiently thick in weave and in dark colors; clothing should not be too tight-fitting. Materials that are to be worn in the sun for any length of time should have an UV protection factor (UPF) greater than 40 (Gambichler et al. 2006). The European Committee for Standardization (CEN) has developed a new standard on requirements for test methods and labeling of sun-protective garments. This document has now been completed and is published. The first part of the standard (EN 13758-1) deals with all details of test methods (e.g., spectrophotometric measurements) for textile materials and part 2 (EN 13758-2) covers classification and marking of apparel textiles. UV-protective cloths for which compliance with this standard is claimed must fulfill all stringent instructions of testing, classification, and marking, including a UV protection factor (UPF) larger than 40 (UPF 40+), average UVA transmission lower than 5%, and design requirements as specified in part 2 of the standard. A pictogram, which is marked with the number of the standard EN 13758-2 and the UPF of 40+, shall be attached to the garment if it is in compliance with the standard. Garment manufacturers and retailers may now follow these official guidelines for testing and labeling of UV-protective summer clothes, and the sun-aware consumer can easily recognize garments that definitely provide sufficient UV protection.

In the year 2001, a study carried out by Gambichler et al. (2001) had demonstrated that one-third of European textiles are unsuitable and have a UPF of less than 15. Wet or damp clothing reduces the protective effects by one-third.

The regular use of appropriate photoprotective agents has been shown to protect against the development of UV-induced skin cancers in experimental, clinical, and epidemiological studies. Using a broad-spectrum sunscreen with a high sun protection factor (SPF) has been clearly shown to protect against UV-induced immunosuppression (Roberts et al. 1995).

Several randomized clinical trials carried out in Australia have shown that consistent use of sunscreens not only reduces the occurrence of new actinic keratoses (AKs) but also causes existing lesions to regress (Thompson et al. 1993; Darlington et al. 2003). Also in Texas, USA, a prospective 2-year study showed a reduction in actinic keratosis by the regular use of sun protection agents (Naylor et al. 2004). Likewise, over an observation period of 4.5 years, a prospective epidemiological study in Queensland showed that the incidence of squamous cell carcinoma is significantly reduced by the daily use of sunscreens (Green et al. 1999).

Regular use of a sunscreen is therefore part of the treatment of chronically photodamaged skin. Particularly, in high-risk patients, the regular use of an appropriate sunscreen of SPF 50+ has to be strongly recommended. In an open interventional study, it was shown that daily use of a liposomal sunscreen with photostable broad-spectrum filters (Daylong actinica) significantly reduced the occurrence of new actinic keratoses and squamous cell carcinomas in organ recipients over a follow-up period of 24 months (Ulrich et al. 2009). While nine invasive squamous cell carcinomas were diagnosed in the control group of 60 transplant patients using freely selected sunscreens, not a single new squamous cell carcinoma appeared in the interventional group using a sunscreen of SPF 50+ every day. During the 24-month study, 42 of the 120 patients developed 82 new actinic keratoses (all in the control group). In the sunscreen group, 102 actinic keratoses healed spontaneously.

It is also important to use a photoprotective agent with a high SPF, as sunscreens are often applied too thinly. This means that the actual protective effect is very much lower than that stated on the packaging. The SPF is based on the application of 2 mg sunscreen per cm2 skin. In fact, on average, only 0.5 mg/cm2 (range: 0.39–0.79 mg/cm2) is applied (Neale et al. 2002; Autier et al. 2001). The sun protection factor does not show a linear correlation with the insufficient amount of sunscreen applied but rather an exponential one, so that a sunscreen of SPF 16 is reduced to SPF 2 if only 0.5 mg/cm2 is applied (Wulf et al. 1997). This has also been demonstrated recently for sunscreens with high SPFs (Kim et al. 2010). The sufficient dosing of a sunscreen can be visualized under a Wood’s lamp by adding to sunscreens fluorescent substances (Antonov et al. 2017).

A change in health awareness regarding exposure to UV radiation, knowledge of the previously mentioned preventative measures, and observing and regularly applying them are all important for the high-risk group in particular. Appropriate preventative health-care concepts need to be developed. Halpern and Kopp (2005) found significant differences in awareness of skin cancer and sun protection habits between normal people in Australia, the USA, and Europe. In Australia, where the incidence of skin cancer is very high, more than 80% of survey responders expressed concerns about the dangers of sun exposure and skin cancer, while the figures were only 30% in Germany and 34% in France.

Another important public health message is that patients should promptly seek medical (dermatological) attention when they notice a suspicious or changing skin lesion. The detection of skin cancer at an early stage when it is most likely to be cured by simple outpatient excision is classified as secondary prevention. UVR-induced skin cancerogenesis is a multistep process that provides an excellent chance for effective prevention strategies to reduce the incidence, morbidity, and mortality of skin cancer and its precursor lesions. Therefore, outdoor workers should be screened for skin cancer regularly.

In Australia, where skin cancer is of epidemic proportions, aggressive public health campaigns have been underway since the 1980s. In addition to identifying tumors at an early stage, Australia managed an exciting educational program on photodamage prevention and sets standards for a wide variety of sun-protective products to include sunscreens, photoprotective apparel, sunglasses, and occupational standards for sun exposure. There, attitudes have already shifted positively toward avoiding exposure to the sun and away from desire for a tan.

The mainstay of sun protection is through avoidance of deliberate sun tanning; use of adequate protection measures such as wearing wide-brimmed hats, sunglasses, and protective clothing; and avoidance of peak hours for UV light. Sunscreens cannot be a substitute for other protective means. However, sunscreen use is the most popular form of sun protection and can significantly reduce the risk of developing skin cancer (Green et al. 1999). However, the results of a study from the UK, France, Italy, Germany, and Spain showed that both the general public and the majority of outdoor workers do not regularly apply sunscreens (MacKie 2004). Concern has also been raised that they may directly or indirectly increase the risk of malignancy, primarily because of poor application and increased exposure to the sun. The thickness of application has been shown to be less than half that officially tested, and key-exposed sites are often missed completely (Johnson et al. 2001).

For future public health policy, it is important to increase skin cancer awareness among outdoor workers, together with safe sun practices, such as application of sunscreen, wearing protective clothing, and avoiding the sun during times of peak solar intensity. In Germany, more than 40% of apprentices in outdoor occupations (n = 245) did not receive any sun protection measures by their employer, and 34.5% of the students got sunburned during work (Ruppert et al. 2016). Working in the shade was a protective factor for occupational sunburn but was merely available for 23.7% of the outdoor workers (Ruppert et al. 2016).


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Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  1. 1.Department of Clinical Social Medicine, Occupational and Environmental DermatologyUniversity of HeidelbergHeidelbergGermany
  2. 2.Institute and Outpatient Clinic of Occupational, Social and Environmental MedicineFriedrich-Alexander-University Erlangen-Nürnberg (FAU)ErlangenGermany

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