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Non-Melanocytic Skin Cancer

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There are three histological types of non-melanocytic skin cancers (NMSC) (ICD-9: 173; ICD-10: C44): basal cell carcinoma, squamous cell carcinoma and rare soft tissue sarcomas involving the skin, subcutaneous tissue, sweat glands, sebaceous glands and hair follicles.

Basal cell carcinoma is the most common NMSC in white populations, representing 75 to 80% of them. It develops usually on the face, grows slowly and has little tendency to metastasize.

Squamous cell cancers account for 20 to 25% of reported NMSCs. They can occur on any part of the body, but especially on the hands and legs and can metastasize. In darkly pigmented populations squamous cell cancers are the most common NMSC.

Multiple primary NMSCs are common. The bulk of the NMSCs occur on the head and neck, in contrast with most of the melanomas which occur on the trunk and limbs. The localization of NMSCs reflects clothing patterns.

NMSCs are treated by various methods of excision, radiation and topical chemotherapy. They respond well to treatment and over 95% are cured by excision (IARC 1990).

The incidence of NMSCs is hard to estimate because of gross underreporting and since many cancer registries do not record these tumours. The number of new cases in the US was estimated at 900,000 to 1,200,000 in 1994, a frequency comparable to the total number of all non-cutaneous cancers (Miller & Weinstock 1994). The reported incidences vary widely and are increasing in a number of populations, e.g., in Switzerland and the US. The highest annual rates have been reported for Tasmania (167/100,000 in men and 89/100,000 in women) and the lowest for Asia and Africa (overall 1/100,000 in men and 5/100,000 in women). NMSC is the most common cancer in Caucasians. NMSC is about ten times as common in White as in non-White populations. The lethality is very low (Higginson et al. 1992).

Susceptibility to skin cancer is inversely related to the degree of melanin pigmentation, which is thought to protect by buffering against the carcinogenic action of solar ultraviolet (UV) radiation. Non-melanoma risk in white-skinned populations increases with the proximity to the equator.

In 1992, the International Agency for Research on Cancer (IARC 1992b) evaluated the carcinogenicity of solar radiation and concluded that there is sufficient evidence in humans for the carcinogenicity of solar radiation and that solar radiation causes cutaneous malignant melanoma and NMSC.

Reduction of exposure to sunlight would probably reduce the incidence of NMSCs. In Whites, 90 to 95% of NMSCs are attributable to solar radiation (IARC 1990).

NMSCs may develop in areas of chronic inflammation, irritation and scars from burns. Traumas and chronic ulcers of the skin are important risk factors for squamous cell skin cancers, particularly in Africa.

Radiation therapy, chemotherapy with nitrogen mustard, immunosuppressive therapy, psoralen treatment combined with UV-A radiation and coal tar preparations applied on skin lesions have been associated with an increased risk of NMSC. Environmental exposure to arsenic trivalent and arsenical compounds have been confirmed to be associated with skin cancer excess in humans (IARC 1987). Arsenicism can give rise to palmar or plantar arsenical keratoses, epidermoid carcinoma and superficial basal cell carcinoma.

Hereditary conditions such as lack of enzymes required to repair the DNA damaged by UV radiation may increase the risk of NMSC. Xeroderma pigmentosum represents such a hereditary condition.

A historical example of an occupational skin cancer is scrotal cancer that Sir Percival Pott described in chimney sweeps in 1775. The cause of these cancers was soot. In the early 1900s, scrotal cancers were observed in mulespinners in cotton textile factories where they were exposed to shale oil, which was used as a lubricant for cotton spindles. The scrotal cancers in both chimney sweeps and mulespinners were later associated with polycyclic aromatic hydrocarbons (PAHs), many of which are animal carcinogens, particularly some 3-, 4- and 5-ring PAHs such as benz(a)pyrene and dibenz(a,h)anthracene (IARC 1983, 1984a, 1984b, 1985a). In addition to mixtures that readily contain carcinogenic PAHs, carcinogenic compounds may be formed by cracking when organic compounds are heated.

Further occupations with which PAH-related excesses of NMSC have been associated include: aluminium reduction workers, coal gasification workers, coke oven workers, glass blowers, locomotive engineers, road pavers and highway maintenance workers, shale oil workers, tool fitters and tool setters (see table 1). Coal tars, coal-based pitches, other coal-derived products, anthracene oil, creosote oil, cutting oils and lubricating oils are some of the materials and mixtures that contain carcinogenic PAHs.

Table 1. Occupations at risk

Carcinogenic
material or agent

Industry or hazard

Process or group at risk

Pitch, tar or
tarry product

Aluminium reduction


Coal, gas and coke industries


Patent fuel manufacture

Asphalt industry

Creosote users

Pot room worker


Coke ovens, tar distillation, coal
gas manufacture, pitch loading

Briquette making

Road construction

Brick and tile workers, timber
proofers

Soot

Chimney sweeps

Rubber industry



Mixers of carbon black
(commercial soot) and oil

Lubricating and
cutting oils

Glass blowing

Shale oil refining

Cotton industry

Paraffin wax workers

Engineering





Mulespinners



Toolsetters and setter operators
in automatic machine shops
(cutting oils)

Arsenic

Oil refinery

Sheep dip factories

Arsenical insecticides



Arsenic mining

Still cleaners



Manufacturing workers and users
(gardeners, fruit farmers and
vintagers)

Ionizing radiation

Radiologists

Other radiation workers

 

Ultraviolet radiation

Outdoor workers


Industrial UV

Farmers, fishermen, vineyard and
other outdoor construction workers

Welding arc: germicidal lamps;
cutting and printing processes

 

Additional job titles that have been associated with increased NMSC risk include jute processors, outdoor workers, pharmacy technicians, sawmill workers, shale oil workers, sheep-dip workers, fishermen, tool setters, vineyard workers and watermen. The excess for watermen (who are primarily involved in traditional fishing tasks) was noticed in Maryland, USA and was confined to squamous cell cancers. Solar radiation probably explains fishermen’s, outdoor workers’, vineyard workers’ and watermen’s excess risks. Fishermen also may be exposed to oils and tar and inorganic arsenic from the consumed fish, which may contribute to the observed excess, which was threefold in a Swedish study, as compared with the county-specific rates (Hagmar et al. 1992). The excess in sheep dip workers may be explained by arsenical compounds, which induce skin cancers through ingestion rather than through skin contact. While farmers have slightly increased risk of melanoma, they do not appear to have increased risk of NMSC, based on epidemiological observations in Denmark, Sweden and the USA (Blair et al. 1992).

Ionizing radiation has caused skin cancer in early radiologists and workers who handled radium. In both situations, the exposures were long-lasting and massive. Occupational accidents involving skin lesions or long-term cutaneous irritation may increase the risk on NMSC.

Prevention (of Non-Melanocytic OccupationalSkin Cancer)

The use of appropriate clothing and a sunscreen having a protective UV-B factor of 15 or greater will help protect outdoor workers exposed to ultraviolet radiation. Further, the replacement of carcinogenic materials (such as feed stocks) by non-carcinogenic alternatives is another obvious protective measure which may, however, not always be possible. The degree of exposure to carcinogenic materials can be reduced by the use of protective shields on equipment, protective clothing and hygienic measures.

Of overriding importance is the education of the workforce about the nature of the hazard and the reasons for and value of the protective measures.

Finally, skin cancers usually take many years to develop and many of them pass through several premalignant stages before achieving their full malignant potential such as arsenic keratoses and actinic keratoses. These early stages are readily detectable by visual inspection. For this reason, skin cancers offer the real possibility that regular screening could reduce mortality among those known to have been exposed to any skin carcinogen.

 

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Contents

Preface
Part I. The Body
Blood
Cancer
Cardiovascular System
Digestive System
Mental Health
Musculoskeletal System
Nervous System
Renal-Urinary System
Reproductive System
Respiratory System
Sensory Systems
Skin Diseases
Resources
Systematic Conditions
Part II. Health Care
Part III. Management & Policy
Part IV. Tools and Approaches
Part V. Psychosocial and Organizational Factors
Part VI. General Hazards
Part VII. The Environment
Part VIII. Accidents and Safety Management
Part IX. Chemicals
Part X. Industries Based on Biological Resources
Part XI. Industries Based on Natural Resources
Part XII. Chemical Industries
Part XIII. Manufacturing Industries
Part XIV. Textile and Apparel Industries
Part XV. Transport Industries
Part XVI. Construction
Part XVII. Services and Trade
Part XVIII. Guides

Skin Diseases Additional Resources

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Skin Diseases References

Adams, RM. 1988. Medicolegal aspects of occupational skin diseases. Dermatol Clin 6:121.

—. 1990. Occupational Skin Disease. 2nd edn. Philadelphia: Saunders.

Agner, T. 1991. Susceptibility of atopic dermatitis patients to irritant dermatitis caused by sodium lauryl sulfate. A Derm-Ven 71:296-300.

Balch, CM, AN Houghton, and L Peters. 1993. Cutaneous melanoma. In Cancer: Principles and Practice of Oncology, edited by VTJ DeVita, S Hellman, and SA Rosenberg. Philadelphia: JB Lippincott.

Beral, V, H Evans, H Shaw, and G Milton. 1982. Malignant melanoma and exposure to fluorescent lighting at work. Lancet II:290-293.

Berardinelli, SP. 1988. Prevention of occupational skin disease through use of chemical protective gloves. Dermatol Clin 6:115-119.

Bijan, S. 1993. Cancers of the skin. In Cancer: Principles & Practice of Oncology, edited by VTJ DeVita, S Hellman, and SA Rosenberg. Philadelphia: JB Lippincott.

Blair, A, S Hoar Zahm, NE Pearce, EF Heinerman, and J Fraumeni. 1992. Clues to cancer etiology from studies of farmers. Scand J Work Environ Health 18:209-215.

Commission de la santé et de la sécurité du travail. 1993. Statistiques sur les lesions professionnelles de 1989. Québec: CSST.

Cronin, E. 1987. Dermatitis of the hands in caterers. Contact Dermatitis 17: 265-269.

De Groot, AC. 1994. Patch Testing: Test Concentrations and Vehicles for 3,700 Allergens. 2nd ed. Amsterdam: Elsevier.

Durocher, LP. 1984. La protection de la peau en milieu de travail. Le Médecin du Québec 19:103-105.

—. 1995. Les gants de latex sont-ils sans risque? Le Médecin du Travail 30:25-27.

Durocher, LP and N Paquette. 1985. Les verrues multiples chez les travailleurs de l’alimentation. L’Union Médicale du Canada 115:642-646.

Ellwood, JM and HK Koh. 1994. Etiology, epidemiology, risk factors, and public health issues of melanoma. Curr Opin Oncol 6:179-187.

Gellin, GA. 1972. Occupational Dermatoses. Chicago: American Medical Assoc.

Guin, JD. 1995. Practical Contact Dermatitis. New York: McGraw-Hill.

Hagmar, L, K Linden, A Nilsson, B Norrving, B Akesson, A Schutz, and T Moller. 1992. Cancer incidence and mortality among Swedish Baltic Sea fisherman. Scand J Work Environ Health 18:217-224.

Hannaford, PC, L Villard Mackintosh, MP Vessey, and CR Kay. 1991. Oral contraceptives and malignant melanoma. Br J Cancer 63:430-433.

Higginson, J, CS Muir, and M Munoz. 1992. Human Cancer: Epidemiology and Environmental
Causes. Cambridge Monographs on Cancer Research. Cambridge, UK: CUP.

International Agency for Research on Cancer (IARC). 1983. Polynuclear aromatic compounds, Part I, Chemical, environmental and experimental data. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans, No. 32. Lyon: IARC.

—. 1984a. Polynuclear aromatic compounds, Part 2, Carbon blacks, mineral oils and some Nitroarenes. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans, No. 33. Lyon: IARC.

—. 1984b. Polynuclear aromatic compounds, Part 3, Industrial exposures in aluminium production, coal gasification, coke production, and iron and steel founding. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans, No. 34. Lyon: IARC.

—. 1985a. Polynuclear aromatic compounds, Part 4, Bitumens, coal tars and derived products, shale-oils and soots. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans, No. 35. Lyon: IARC.

—. 1985b. Solar and ultraviolet radiation. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans, No. 55. Lyon: IARC.

—. 1987. Overall Evaluations of Carcinogenecity: An updating of IARC Monographs Volumes 1 to 42. Monographs on the Carcinogenic Risks to Humans. Suppl. 7. Lyon: IARC

—. 1990. Cancer: Causes, occurrence and control. IARC Scientific Publications, No. 100. Lyon: IARC.

—. 1992a. Cancer incidence in five continents. Vol. VI. IARC Scientific Publications, No. 120. Lyon: IARC.

—. 1992b. Solar and ultraviolet radiation. Monographs On the Evaluation of Carcinogenic Risks to Humans, No. 55. Lyon: IARC.

—. 1993. Trends in cancer incidence and mortality. IARC Scientific Publications, No. 121. Lyon: IARC.

Koh, HK, TH Sinks, AC Geller, DR Miller, and RA Lew. 1993. Etiology of melanoma. Cancer Treat Res 65:1-28.

Kricker, A, BK Armstrong, ME Jones, and RC Burton. 1993. Health, solar UV radiation and environmental change. IARC Technical Report, No. 13. Lyon: IARC.

Lachapelle, JM, P Frimat, D Tennstedt, and G Ducombs. 1992. Dermatologie professionnelle et de l’environnement. Paris: Masson.

Mathias, T. 1987. Prevention of occupational contact dermatitis. J Am Acad Dermatol 23:742-748.

Miller, D and MA Weinstock. 1994. Nonmelanoma skin cancer in the United States: Incidence. J Am Acad Dermatol 30:774-778.

Nelemans, PJ, R Scholte, H Groenendal, LA Kiemeney, FH Rampen, DJ Ruiter, and AL Verbeek. 1993. Melanoma and occupation: results of a case-control study in The Netherlands. Brit J Ind Med 50:642-646.

Rietschel, RI, and JF Fowler Jr. 1995. Fisher’s Contact Dermatitis. 4th ed. Baltimore: Williams & Wilkins.

Sahel, JA, JD Earl, and DM Albert. 1993. Intraocular melanomas. In Cancer: Principles & Practice of Oncology, edited by VTJ DeVita, S Hellman, and SA Rosenberg. Philadelphia: JB Lippincott.

Sasseville, D. 1995. Occupational dermatoses: Employing good diagnostic skills. Allergy 8:16-24.

Schubert, H, N Berova, A Czernielewski, E Hegyi and L Jirasek. 1987. Epidemiology of nickel allergy. Contact Dermatitis 16:122-128.

Siemiatycki J, M Gerin, R Dewar, L Nadon, R Lakhani, D Begin, and L Richardson. 1991. Associations between occupational circumstances and cancer. In Risk Factors for Cancer in the Workplace, edited by J Siematycki. London, Boca Raton: CRC Press.

Stidham, KR, JL Johnson, and HF Seigler. 1994. Survival superiority of females with melanoma. A multivariate analysis of 6383 patients exploring the significance of gender in prognostic outcome. Archives of Surgery 129:316-324.

Turjanmaa, K. 1987. Incidence of immediate allergy to latex gloves in hospital personnel. Contact Dermatitis 17:270-275.