" DISCLAIMER: The ILO does not take responsibility for content presented on this web portal that is presented in any language other than English, which is the language used for the initial production and peer-review of original content. Certain statistics have not been updated since the production of the 4th edition of the Encyclopaedia (1998)."

Monday, 07 March 2011 17:42

Occupational Contact Dermatitis

Written by
Rate this item
(1 Vote)

The terms dermatitis and eczema are interchangeable and refer to a particular type of inflammatory reaction of the skin which may be triggered by internal or external factors. Occupational contact dermatitis is an exogenous eczema caused by the interaction of the skin with chemical, biological or physical agents found in the work environment.

Contact dermatitis accounts for 90% of all occupational dermatoses and in 80% of the cases, it will impair a worker’s most important tool, the hands (Adams 1988). Direct contact with the offending agent is the usual mode of production of the dermatitis, but other mechanisms may be involved. Particulate matter such as dust or smoke, or vapours from volatile substances, may give rise to airborne contact dermatitis. Some substances will be transferred from the fingers to distant sites on the body to produce ectopic contact dermatitis. Finally, a photocontact dermatitis will be induced when a contactant has become activated by exposure to ultraviolet light.

Contact dermatitis is divided into two broad categories based on different mechanisms of production. Table 1 lists the salient features of irritant contact dermatitis and of allergic contact dermatitis.

Table 1. Types of contact dematitis

Features

Irritant contact dermatitis

Allergic contact dermatitis

Mechanism of production

Direct cytotoxic effect

Delayed–type cellular immunity
(Gell and Coombs type IV)

Potential victims

Everyone

A minority of individuals

Onset

Progressive, after repeated or prolonged exposure

Rapid, within 12–48 hours in sensitized individuals

Signs

Subacute to chronic eczema with erythema, desquamation and fissures

Acute to subacute eczema with erythema, oedema, bullae and vesicles

Symptoms

Pain and burning sensation

Pruritus

Concentration of contactant

High

Low

Investigation

History and examination

History and examination
Patch tests

 

Irritant Contact Dermatitis

Irritant contact dermatitis is caused by a direct cytotoxic action of the offending agent. Participation of the immune system is secondary to cutaneous damage and results in visible skin inflammation. It represents the most common type of contact dermatitis and accounts for 80% of all cases.

Irritants are mostly chemicals, which are classified as immediate or cumulative irritants. Corrosive substances, such as strong acids and alkalis are examples of the former in that they produce skin damage within minutes or hours of exposure. They are usually well identified, so that contact with them is most often accidental. By contrast, cumulative irritants are more insidious and often are not recognized by the worker as deleterious because damage occurs after days, weeks or months of repeated exposure. As shown in table 2 (overleaf) such irritants include solvents, petroleum distillates, dilute acids and alkalis, soaps and detergents, resins and plastics, disinfectants and even water (Gellin 1972).

 


Table 2. Common irritants

 

Acids and alkalis

Soaps and detergents

Solvents

Aliphatic:                               Petroleum distillates (kerosene, gasoline, naphta)
Aromatic:                              Benzene, toluene, xylene
Halogenated:                        Trichloroethylene, chloroform, methylene chloride
Miscellaneous:                     Turpentine, ketones, esters, alcohols, glycols, water

Plastics

Epoxy, phenolic, acrylic monomers
Amine catalysts
Styrene, benzoyl peroxide

Metals

Arsenic
Chrome

 


 

Irritant contact dermatitis, which appears after years of trouble-free handling of a substance, may be due to loss of tolerance, when the epidermal barrier ultimately fails after repeated subclinical insults. More rarely, thickening of the epidermis and other adaptive mechanisms can induce a greater tolerance to some irritants, a phenomenon called hardening.

In summary, irritant contact dermatitis will occur in a majority of individuals if they are exposed to adequate concentrations of the offending agent for a sufficient length of time.

Allergic Contact Dermatitis

A cell-mediated, delayed allergic reaction, similar to that seen in graft rejection, is responsible for 20% of all cases of contact dermatitis. This type of reaction, which occurs in a minority of subjects, requires active participation of the immune system and very low concentrations of the causative agent. Many allergens are also irritants, but the threshold for irritancy is usually much higher than that required for sensitization. The sequence of events which culminate in visible lesions is divided in two phases.

The sensitization (induction or afferent) phase

Allergens are heterogeneous, organic or non-organic chemicals, capable of penetrating the epidermal barrier because they are lipophilic (attracted to the fat in the skin) and of small molecular weight, usually less than 500 daltons (table 3). Allergens are incomplete antigens, or haptens; that is, they must bind to epidermal proteins to become complete antigens.

Langerhans cells are antigen-presenting dendritic cells which account for less than 5% of all epidermal cells. They trap cutaneous antigens, internalize and process them before re-expressing them on their outer surface, bound to proteins of the major histocompatibility complex. Within hours of contact, Langerhans cells leave the epidermis and migrate via the lymphatics towards draining lymph nodes. Lymphokines such as interleukin-1 (IL-1) and tumour necrosis factor alpha (TNF-α) secreted by keratinocytes are instrumental in the maturation and migration of Langerhans cells.

 


Table 3. Common skin allergens

 

Metals

Nickel
Chrome
Cobalt
Mercury

Rubber additives

Mercaptobenzothiazole
Thiurams
Carbamates
Thioureas

Dyes

Paraphenylene diamine
Photographic colour developers
Disperse textile dyes

Plants

Urushiol (Toxicodendron)
Sesquiterpene lactones (Compositae)
Primin (Primula obconica)
Tulipalin A (Tulipa, Alstroemeria)

Plastics

Epoxy monomer
Acrylic monomer
Phenolic resins
Amine catalysts

Biocides

Formaldehyde
Kathon CG
Thimerosal

 


 

In the paracortical area of regional lymph nodes, Langerhans cells make contact with naive CD4+ helper T cells and present them with their antigenic load. Interaction between Langerhans cells and helper T cells involve recognition of the antigen by T-cell receptors, as well as the interlocking of various adhesion molecules and other surface glycoproteins. Successful antigen recognition results in a clonal expansion of memory T cells, which spill into the bloodstream and the entire skin. This phase requires 5 to 21 days, during which no lesion occurs.

The elicitation (efferent) phase

Upon re-exposure to the allergen, sensitized T cells become activated and secrete potent lymphokines such as IL-1, IL-2 and interferon gamma (IFN-γ). These in turn induce blast transformation of T cells, generation of cytotoxic as well as suppressor T cells, recruitment and activation of macrophages and other effector cells and production of other mediators of inflammation such as TNF-α and adhesion molecules. Within 8 to 48 hours, this cascade of events results in vasodilatation and reddening (erythema), dermal and epidermal swelling (oedema), blister formation (vesiculation) and oozing. If left untreated, this reaction may last between two and six weeks.

Dampening of the immune response occurs with shedding or degradation of the antigen, destruction of Langerhans cells, increased production of CD8+ suppressor T cells and production by keratinocytes of IL-10 which inhibits the proliferation of helper/cytotoxic T cells.

Clinical Presentation

Morphology. Contact dermatitis may be acute, subacute or chronic. In the acute phase, lesions appear rapidly and present initially as erythematous, oedematous and pruritic urticarial plaques. The oedema may be considerable, especially where the skin is loose, such as the eyelids or the genital area. Within hours, these plaques become clustered with small vesicles which may enlarge or coalesce to form bullae. When they rupture, they ooze an amber- coloured, sticky fluid.

Oedema and blistering are less prominent in subacute dermatitis; which is characterized by erythema, vesiculation, peeling of skin (desquamation), moderate oozing and formation of yellowish crusts.

In the chronic stage, vesiculation and oozing are replaced by increased desquamation, thickening of the epidermis, which becomes greyish and furrowed (lichenification) and painful, deep fissures over areas of movement or trauma. Long-lasting lymphoedema may result after years of persistent dermatitis.

Distribution. The peculiar pattern and distribution of a dermatitis will often allow the clinician to suspect its exogenous origin and sometimes identify its causative agent. For example, linear or serpiginous streaks of erythema and vesicles on uncovered skin are virtually diagnostic of a plant contact dermatitis, while an allergic reaction due to rubber gloves will be worse on the back of the hands and around the wrists.

Repeated contact with water and cleansers is responsible for the classic “housewives’ dermatitis”, characterized by erythema, desquamation and fissures of the tips and backs of the fingers and involvement of the skin between the fingers (interdigital webs). By contrast, dermatitis caused by friction from tools, or by contact with solid objects tends to be localized on the palm and underside (volar) area of the fingers.

Irritant contact dermatitis due to fibreglass particles will involve the face, hands and forearms and will be accentuated in flexures, around the neck and waist, where movement and friction from clothes will force the spicules into the skin. Involvement of the face, upper eyelids, ears and submental area suggests an airborne dermatitis. A photocontact dermatitis will spare sun-protected areas such as the upper eyelids, the submental and retroauricular areas.

Extension to distant sites. Irritant dermatitis remains localized to the area of contact. Allergic contact dermatitis, especially if acute and severe, is notorious for its tendency to disseminate away from the site of initial exposure. Two mechanisms may explain this phenomenon. The first, autoeczematization, also known as id-reaction or the excited skin syndrome, refers to a state of hypersensitivity of the entire skin in response to a persistent or severe localized dermatitis. Systemic contact dermatitis occurs when a patient topically sensitized to an allergen is re-exposed to the same agent by oral or parenteral route. In both cases, a widespread dermatitis will ensue, which may easily be mistaken for an eczema of endogenous origin.

Predisposing factors

The occurrence of an occupational dermatitis is influenced by the nature of the contactant, its concentration and the duration of contact. The fact that under similar conditions of exposure only a minority of workers will develop a dermatitis is proof of the importance of other personal and environmental predisposing factors (table 4).

Table 4. Predisposing factors for occupational dermatitis

Age

Younger workers are often inexperienced or careless and are more likely to develop occupational dermatitis than older workers

Skin type

Orientals and Blacks are generally more resistant to irritation than Whites

Pre-existing disease

Atopy predisposes to irritant contact dermatitis

Psoriasis or lichen planus may worsen because of the Koebner phenomenon

Temperature and humidity

High humidity reduces the effectiveness of the epidermal barrier

Low humidity and cold cause chapping and desiccation of the epidermis

Working conditions

A dirty worksite is more often contaminated with toxic or allergenic chemicals

Obsolete equipment and lack of protective measures increase the risk of occupational dermatitis

Repetitive movements and friction may cause irritation and calluses

 

Age. Younger workers are more likely to develop occupational dermatitis. It may be that they are often less experienced than their older colleagues, or may have a more careless attitude about safety measures. Older workers may have become hardened to mild irritants, or they have learned how to avoid contact with hazardous substances, or older workers may be a self-selected group that did not experience problems while others who did may have left the job.

Skin type. Most Black or Oriental skin appears to be more resistant to the effects of contact irritants than the skin of most Caucasians.

Pre-existing disease. Allergy-prone workers (having a background of atopy manifested by eczema, asthma or allergic rhinitis) are more likely to develop irritant contact dermatitis. Psoriasis and lichen planus may be aggravated by friction or repetitive trauma, a phenomenon called koebnerization. When such lesions are limited to the palms, they may be difficult to distinguish from chronic irritant contact dermatitis.

Temperature and humidity. Under conditions of extreme heat, workers often neglect to wear gloves or other appropriate protective gear. High humidity reduces the effectiveness of the epidermal barrier, while dry and cold conditions promote chapping and fissures.

Working conditions. The incidence of contact dermatitis is higher in worksites which are dirty, contaminated with various chemicals, have obsolete equipment, or lack protective measures and hygiene facilities. Some workers are at higher risk because their tasks are manual and they are exposed to strong irritants or allergens (e.g., hairdressers, printers, dental technicians).

Diagnosis

A diagnosis of occupational contact dermatitis can usually be made after a careful history and a thorough physical examination.

History. A questionnaire that includes the name and address of the employer, the worker’s job title and a description of functions should be completed The worker should provide a list of all the chemicals handled and supply information about them, such as is found on the Material Safety Data Sheets. The date of onset and location of the dermatitis should be noted. It is important to document the effects of vacation, sick leave, sun exposure and treatment on the course of the disease. The examining physician should obtain information about the worker’s hobbies, personal habits, history of pre-existing skin disease, general medical background and current medication, as well.

Physical examination. The involved areas must be carefully examined. Note should be taken of the severity and stage of the dermatitis, of its precise distribution and of its degree of interference with function. A complete skin examination must be performed, looking for tell-tale stigmata of psoriasis, atopic dermatitis, lichen planus, tinea, etc., which may signify that the dermatitis is not of occupational origin.

Complementary investigation

The information obtained from history and physical examination is usually sufficient to suspect the occupational nature of a dermatitis. However, additional tests are required in most cases to confirm the diagnosis and to identify the offending agent.

Patch testing. Patch testing is the technique of choice for the identification of cutaneous allergens and it should be routinely performed in all cases of occupational dermatitis (Rietschel et al. 1995). More than 300 substances are now commercially available. The standard series, which regroup the most common allergens, can be supplemented with additional series aimed at specific categories of workers such as hairdressers, dental technicians, gardeners, printers, etc. Table 6 lists the various irritants and sensitizers encountered in some of these occupations.

Table 5. Examples of skin irritants and sensitizers with occupations where contact can occur

Occupation

Irritants

Sensitizers

Construction
workers

Turpentine, thinner,
fibreglass, glues

Chromates, epoxy and phenolic
resins, colophony, turpentine, woods

Dental
technicians

Detergents, disinfectants

Rubber, epoxy and acrylic monomer, amine catalysts, local anaesthetics, mercury, gold, nickel, eugenol, formaldehyde, glutaraldehyde

Farmers, florists,
gardeners

Fertilizers, disinfectants,
soaps and detergents

Plants, woods, fungicides, insecticides

Food handlers,
cooks, bakers

Soaps and detergents,
vinegar, fruits, vegetables

Vegetables, spices, garlic, rubber, benzoyl peroxide

Hairdressers,
beauticians

Shampoos, bleach, peroxide,
permanent wave, acetone

Paraphenylenediamine in hair dye, glycerylmonothioglycolate in permanents, ammonium persulphate in bleach, surfactants in shampoos, nickel, perfume, essential oils, preservatives in cosmetics

Medical
personnel

Disinfectants, alcohol, soaps
and detergents

Rubber, colophony, formal­dehyde, glutaraldehyde, disinfectants, antibiotics, local anaesthetics, pheno-thiazines, benzodiazepines

Metal workers,
machinists and
mechanics

Soaps and detergents, cutting
oils, petroleum distillates,
abrasives

Nickel, cobalt, chrome, biocides in cutting oils, hydrazine and colophony in welding flux, epoxy resins and amine catalysts, rubber

Printers and
photographers

Solvents, acetic acid, ink,
acrylic monomer

Nickel, cobalt, chrome, rubber,colophony, formaldehyde, paraphenylene diamine and azo dyes, hydroquinone, epoxy and acrylic monomer, amine catalysts, B&W and colour developers

Textile workers

Solvents, bleaches, natural
and synthetic fibres

Formaldehyde resins, azo- and anthraquinone dyes, rubber, biocides

 

The allergens are mixed in a suitable vehicle, usually petroleum jelly, at a concentration which was found by trial and error over the years to be non-irritant but high enough to reveal allergic sensitization. More recently, prepackaged, ready-to-apply allergens embedded in adhesive strips have been introduced, but so far only the 24 allergens of the standard series are available. Other substances must be bought in individual syringes.

At the time of testing, the patient must be in a quiescent phase of dermatitis and not be taking systemic corticosteroids. A small amount of each allergen is applied to shallow aluminium or plastic chambers mounted on porous, hypoallergenic adhesive tape. These rows of chambers are affixed to an area free of dermatitis on the patient’s back and left in place for 24 or more commonly 48 hours. A first reading is done when the strips are removed, followed by a second and sometimes a third reading after four and seven days respectively. Reactions are graded as follows:

Nul      no reaction

?          doubtful reaction, mild macular erythema

+          weak reaction, mild papular erythema

++       strong reaction, erythema, oedema, vesicles

+++     extreme reaction, bullous or ulcerative;

IR        irritant reaction, glazed erythema or erosion resemblinga burn.

When a photocontact dermatitis (one that requires exposure to ultraviolet light, UV-A) is suspected, a variant of patch testing, called photopatch testing, is performed. Allergens are applied in duplicate to the back. After 24 or 48 hours, one set of allergens is exposed to 5 joules of UV-A and the patches are put back in place for another 24 to 48 hours. Equal reactions on both sides signify allergic contact dermatitis, positive reactions on the UV-exposed side only is diagnostic of photocontact allergy, while reactions on both sides but stronger on the UV-exposed side mean contact and photocontact dermatitis combined.

The technique of patch testing is easy to perform. The tricky part is the interpretation of the results, which is best left to the experienced dermatologist. As a general rule, irritant reactions tend to be mild, they burn more than they itch, they are usually present when the patches are removed and they fade rapidly. By contrast, allergic reactions are pruritic, they reach a peak at four to seven days and may persist for weeks. Once a positive reaction has been identified, its relevance must be assessed: is it pertinent to the current dermatitis, or does it reveal past sensitization? Is the patient exposed to that particular substance, or is he allergic to a different but structurally-related compound with which it cross-reacts?

The number of potential allergens far exceeds the 300 or so commercially available substances for patch testing. It is therefore often necessary to test patients with the actual substances that they work with. While most plants can be tested “as is,” chemicals must be precisely identified and buffered if their acidity level (pH) falls outside the range of 4 to 8. They must be diluted to the appropriate concentration and mixed in a suitable vehicle according to current scientific practice (de Groot 1994). Testing a group of 10 to 20 control subjects will ensure that irritant concentrations are detected and rejected.

Patch testing is usually a safe procedure. Strong positive reactions may occasionally cause exacerbation of the dermatitis under investigation. On rare occasions, active sensitization may occur, especially when patients are tested with their own products. Severe reactions may leave hypo- or hyperpigmented marks, scars or keloids.

Skin biopsy. The histological hallmark of all types of eczema is epidermal intercellular oedema (spongiosis) which stretches the bridges between keratinocytes to the point of rupture, causing intraepidermal vesiculation. Spongiosis is present even in the most chronic dermatitis, when no macroscopic vesicle can be seen. An inflammatory infiltrate of lymphohistiocytic cells is present in the upper dermis and migrates into the epidermis (exocytosis). Because a skin biopsy cannot distinguish between the various types of dermatitis, this procedure is rarely performed, except in rare cases where the clinical diagnosis is unclear and in order to rule out other conditions such as psoriasis or lichen planus.

Other procedures. It may at times be necessary to perform bacterial, viral or fungal cultures, as well as potassium hydroxide microscopic preparations in search of fungi or ectoparasites. Where the equipment is available, irritant contact dermatitis can be assessed and quantified by various physical methods, such as colorimetry, evaporimetry, Laser-Doppler velocimetry, ultrason- ography and the measurement of electrical impedance, conductance and capacitance (Adams 1990).

Workplace. On occasion, the cause of an occupational dermatitis is uncovered only after a careful observation of a particular worksite. Such a visit allows the physician to see how a task is performed and how it might be modified to eliminate the risk of occupational dermatitis. Such visits should always be arranged with the health officer or supervisor of the plant. The information that it generates will be useful to both the worker and the employer. In many localities, workers have the right to request such visits and many work sites have active health and safety committees which do provide valuable information.

Treatment

Local treatment of an acute, vesicular dermatitis will consist of thin, wet dressings soaked in lukewarm saline, Burow’s solution or tap water, left in place for 15 to 30 minutes, three to four times a day. These compresses are followed by the application of a strong topical corticosteroid. As the dermatitis improves and dries up, the wet dressings are spaced and stopped and the strength of the corticosteroid is decreased according to the part of the body being treated.

If the dermatitis is severe or widespread, it is best treated with a course of oral prednisone, 0.5 to 1.0 mg/kg/day for two to three weeks. Systemic first-generation antihistamines are given as needed to provide sedation and relief from pruritus.

Subacute dermatitis usually responds to mid-strength corticosteroid creams applied two to three times a day, often combined with protective measures such as the use of cotton liners under vinyl or rubber gloves when contact with irritants or allergens cannot be avoided.

Chronic dermatitis will require the use of corticosteroid ointments, coupled with the frequent application of emollients, the greasier the better. Persistent dermatitis may need to be treated with psoralen and ultraviolet-A (PUVA) phototherapy, or with systemic immunosuppressors such as azathioprine (Guin 1995).

In all cases, strict avoidance of causative substances is a must. It is easier for the worker to stay away from offending agents if he or she is given written information which specifies their names, synonyms, sources of exposure and cross-reaction patterns. This printout should be clear, concise and written in terms that the patient can easily understand.

Worker’s compensation

It is often necessary to withdraw a patient from work. The physician should specify as precisely as possible the estimated length of the disability period, keeping in mind that full restoration of the epidermal barrier takes four to five weeks after the dermatitis is clinically cured. The legal forms that will allow the disabled worker to receive adequate compensation should be diligently filled out. Finally, the extent must be determined of permanent impairment or the presence of functional limitations, which may render a patient unfit to return to his former work and make him a candidate for rehabilitation.

 

Back

Read 10282 times Last modified on Tuesday, 11 October 2011 21:19

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

Click the Button below to view additional resources for this topic.

button

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.