Malignant melanoma is rarer than non-melanocytic skin cancer. Apart from exposure to solar radiation, no other environmental factors show a consistent association with malignant melanoma of the skin. Associations with occupation, diet and hormonal factors are not firmly established (Koh et al. 1993).

Malignant melanoma is an aggressive skin cancer (ICD-9 172.0 to 173.9; ICD-10: C43). It arises from pigment-producing cells of the skin, usually in an existing naevus. The tumour is usually a few millimetres to several centimetres thick, brown or black in colour, that has grown in size, changed colour and may bleed or ulcerate (Balch et al. 1993).

Indicators of poor prognosis of malignant melanoma of the skin include nodular subtype, tumour thickness, multiple primary tumours, metastases, ulceration, bleeding, long tumour duration, body site and, for some tumour sites, male sex. A history of malignant melanoma of the skin increases the risk for a secondary melanoma. Five-year post-diagnosis survival rates in high incidence areas are 80 to 85%, but in low incidence areas the survival is poorer (Ellwood and Koh 1994; Stidham et al. 1994).

There are four histologic types of malignant melanoma of the skin. Superficial spreading melanomas (SSM) represent 60 to 70% of all melanomas in Whites and less in non-Whites. SSMs tend to progress slowly and are more common in women than in men. Nodular melanomas (NM) account for 15 to 30% of malignant melanomas of the skin. They are invasive, grow rapidly and are more frequent in men. Four to 10% of malignant melanomas of the skin are lentigo malignant melanomas (LMM) or Hutchinson’s melanotic freckles. LMMs grow slowly, occur frequently in the face of old persons and rarely metastasize. Acral lentiginous melanomas (ALM) represent 35 to 60% of all malignant melanomas of the skin in non-Whites and 2 to 8% in Whites. They occur frequently on the sole of the foot (Bijan 1993).

For the treatment of malignant melanomas of the skin, surgery, radiation therapy, chemotherapy and biologic therapy (interferon alpha or interleukin-2) may be applied singly or in combination.

During the 1980s, the reported age-standardized annual incidence rates of malignant melanoma of the skin varied per 100,000 from 0.1 in males in Khon Kaen, Thailand to around 30.9 in males and 28.5 in females in Queensland, Australia (IARC 1992b). Malignant melanomas of the skin represent less than 1% of all cancers in most populations. An annual increase of about 5% in melanoma incidence has been observed in most white populations from the early 1960s to about 1972. Melanoma mortality has increased in the last decades in most populations, but less rapidly than incidence, probably due to early diagnoses and awareness of the disease (IARC 1985b, 1992b). More recent data show different rates of change, some of them suggesting even downward trends.

Malignant melanomas of the skin are among the ten most frequent cancers in incidence statistics in Australia, Europe and North America, representing a lifetime risk of 1 to 5%. White-skinned populations are more susceptible than non-White populations. Melanoma risk in white-skinned populations increases with proximity to the equator.

The gender distribution of melanomas of the skin varies widely between populations (IARC 1992a). Women have lower incidence rates than men in most populations. There are gender differences in patterns of body distribution of the lesions: trunk and face dominate in men, extremities in women.

Malignant melanomas of the skin are more common in higher than in lower socio-economic groups (IARC 1992b).

Familial melanomas are uncommon, but have been well documented. with between 4% and 10% of patients describing a history of melanoma among their first degree relatives.

Solar UV-B irradiation is probably the major cause for the widespread increase in the incidence of melanomas of the skin (IARC 1993). It is not clear whether depletion of the stratospheric ozone layer and the consequent increase in UV irradiance has caused the increase in the incidence of malignant melanoma (IARC 1993, Kricker et al. 1993). The effect of UV irradiation depends on some characteristics, such as I or II phenotype and blue eyes. A role for UV radiation emanating from fluorescent lamps is suspected, but not conclusively established (Beral et al. 1982).

It has been estimated that reduction in recreational sun exposure and use of sun-screens could reduce the incidence of malignant melanomas in high risk populations by 40% (IARC 1990). Among outdoor workers, the application of sunscreens having a protective UV-B factor rating of at least 15 and UV-A sunscreen and the use of appropriate clothing are practical protective measures. Although a risk from outdoor occupations is plausible, given the increased exposure to solar radiation, results of studies on regular outdoor occupational exposure are inconsistent. This is probably explained by the epidemiological findings suggesting that it is not regular exposures but rather intermittent high doses of solar radiation that are associated with excess melanoma risk (IARC 1992b).

Therapeutic immunosuppression may result in increased risk of malignant melanoma of the skin. An increased risk with the use of oral contraceptives has been reported, but it seems unlikely to increase the risk of malignant melanoma of the skin (Hannaford et al. 1991). Melanomas can be produced by oestrogen in hamsters. There is no evidence of such an effect in humans.

In White adults, the majority of primary intraocular malignant tumours are melanomas, usually arising from uveal melanocytes. The estimated rates for these cancers do not show the geographic variations and increasing time trends observed for melanomas of the skin. The incidence and mortality of ocular melanomas are very low in Black and Asiatic populations (IARC 1990, Sahel et al. 1993) The causes of ocular melanoma are unknown (Higginson et al. 1992).

In epidemiological studies, excess risk for malignant melanoma has been observed in administrators and managers, airline pilots, chemical processing workers, clerks, electrical power workers, miners, physical scientists, policemen and guards, refinery workers and gasoline exposed workers, salesmen and warehouse clerks. Excess melanoma risks have been reported in industries such as cellulose fibre production, chemical products, clothing industry, electrical and electronics products, metal industry, non-metallic mineral products, petrochemical industry, printing industry and telecommunications. Many of these findings are, however, solitary and have not been replicated in other studies. A series of meta-analyses of cancer risks in farmers (Blair et al. 1992; Nelemans et al. 1993) indicated a slight, but significant excess (aggregated risk ratio of 1.15) of malignant melanoma of the skin in 11 epidemi-ological studies.

In a multi-site case-control study of occupational cancer in Montreal, Canada (Siemiatycki et al. 1991), the following occupational exposures were associated with a significant excess of malignant melanoma of the skin: chlorine, propane engine emissions, plastics pyrolysis products, fabric dust, wool fibres, acrylic fibres, synthetic adhesives, “other” paints, varnishes, chlorinated alkenes, trichloroethylene and bleaches. It was estimated that the population attributable risk due to occupational exposures based on the significant associations in the data of the same study was 11.1%.

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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

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 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

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

The goal of occupational health programmes is to allow workers to maintain their job and their health over several years. The development of effective programmes requires the identification of sectoral, population-based, and workplace-specific risk factors. This information can then be used to develop prevention policies both for groups and individuals.

The Québec Occupational Health and Safety Commission (Commission de la santé et de la sécurité au travail du Québec) has characterized work activities in 30 industrial, commercial, and service sectors (Commission de la santé et de la sécurité au travail 1993). Its surveys reveal that occupational dermatoses are most prevalent in the food and beverage industries, medical and social services, miscellaneous commercial and personal services and construction (including public works). Affected workers are typically engaged in service, manufacturing, assembly, repair, materials handling, food-processing, or health-care activities.

Occupational dermatoses are particularly prevalent in two age groups: young and inexperienced workers who may be unaware of the sometimes insidious risks associated with their work, and those workers approaching retirement age who may not have noticed the progressive drying of their skin over the years, which increases over several consecutive workdays. Because of such dehydration, repeated exposure to previously well-tolerated irritant or astringent substances may cause irritative dermatitis in these workers.

As table 1 indicates, even though most cases of occupational dermatoses do not involve compensation exceeding two weeks, a significant number of cases may persist for over two months (Durocher and Paquette 1985). This table clearly illustrates the importance of preventing chronic dermatoses requiring prolonged work absences.

Table 1. Occupational dermatoses in Quebec in 1989: Distribution by length of compensation

Source: Commission de la santé et de la sécurité au travail, 1993.

Risk Factors

Many substances used in industry are capable of causing dermatoses, the risk of which depends on the concentration of the substance and the frequency and duration of skin contact. The general classification scheme presented in table 2 (overleaf) based on the classification of risk factors as mechanical, physical, chemical or biological, is a useful tool for the identification of risk factors during site visits. During workplace evaluation, the presence of risk factors may be either directly observed or suspected on the basis of observed skin lesions. Particular attention is paid to this in the classification scheme presented in table 2. In some cases effects specific to a given risk factor may be present, while in others, the skin disorders may be associated with several factors in a given category. Disorders of this last type are known as group effects. The specific cutaneous effects of physical factors are listed in table 2 and described in other sections of this chapter.

Table 2. Risk factors and their effects on the skin

Mechanical factors

Trauma
Friction
Pressure
Dusts

Physical factors

Radiation
Humidity
Heat
Cold

Chemical factors

Acids, bases
Detergents, solvents
Metals, resins
Cutting oils
Dyes, tar
Rubber, etc.

Biological factors

Bacteria
Viruses
Dermatophytes
Parasites
Plants
Insects

Risk co-factors

Eczema (atopic, dyshidrotic, seborrhoeic, nummular)
Psoriasis
Xeroderma
Acne

Group effects

Cuts, punctures, blisters
Abrasions, isomorphism
Lichenification
Calluses

Specific effects

Photodermatitis, radiodermatitis, cancer
Maceration, irritation
Heat rash, burns, erythema
Frostbite, xeroderma, urticaria, panniculitis, Raynaud’s phenomenon

Group effects

Dehydration
Inflammation
Necrosis
Allergy
Photodermatitis
Dyschromia

Specific effects

Pyodermatitis
Multiple warts
Dermatomycosis
Parasitosis
Phytodermatitis
Urticaria

Mechanical factors include repeated friction, excessive and prolonged pressure, and the physical action of some industrial dusts, whose effects are a function of the shape and size of the dust particles and the extent of their friction with the skin. The injuries themselves may be mechanical (especially in workers exposed to repeated vibrations), chemical, or thermal, and include physical lesions (ulcers, blisters), secondary infection, and isomorphism (Koebner phenomenon). Chronic changes, such as scars, keloid, dyschromia, and Raynaud’s phenomenon, which is a peripheral neurovascular alteration caused by prolonged use of vibrating tools, may also develop.

Chemical factors are by far the most common cause of occupational dermatoses. To establish an exhaustive list of the many chemicals is not practical. They may cause allergic, irritant or photodermatotic reactions, and may leave dyschromic sequelae. The effects of chemical irritation vary from simple drying to inflammation to complete cell necrosis. More information on this subject is provided in the article on contact dermatitis. Material Safety Data Sheets, which provide toxicological and other information are indispensable tools for developing effective preventive measures against chemicals. Several countries, in fact, require chemical manufacturers to provide every workplace using their products with information on the occupational health hazards posed by their products.

Bacterial, viral and fungal infections contracted in the workplace arise from contact with contaminated materials, animals, or people. Infections include pyodermatitis, folliculitis, panaris, dermatomycosis, anthrax, and brucellosis. Workers in the food-processing sector may develop multiple warts on their hands, but only if they have already suffered microtraumas and are exposed to excessive levels of humidity for prolonged periods (Durocher and Paquette 1985). Both animals and humans such as day-care and health-care workers, may act as vectors for parasitic contamination like mites, scabies and head lice. Phytodermatitis may be caused by plants (Rhus sp.) or flowers (alstromeria, chrysanthemums, tulips). Finally, some wood extracts may cause contact dermatitis.

Risk Co-factors

Some non-occupational cutaneous pathologies may exacerbate the effects of environmental factors on workers’ skin. For example, it has long been recognized that the risk of irritant contact dermatitis is greatly increased in individuals with a medical history of atopy, even in the absence of an atopic dermatitis. In a study of 47 cases of irritant contact dermatitis of the hands of food-processing workers, 64% had a history of atopy (Cronin 1987). Individuals with atopic dermatitis have been shown to develop more severe irritation when exposed to sodium lauryl sulphate, commonly found in soaps (Agner 1991). Predisposition to allergies (Type I) (atopic diathesis) does not however increase the risk of delayed allergic (Type IV) contact dermatitis, even to nickel (Schubert et al. 1987), the allergen most commonly screened for. On the other hand, atopy has recently been shown to favour the development of contact urticaria (Type I allergy) to rubber latex among health-care workers (Turjanmaa 1987; Durocher 1995) and to fish among caterers (Cronin 1987).

In psoriasis, the outmost layer of the skin (stratum corneum) is thickened but not calloused (parakeratotic) and less resistant to skin irritants and mechanical traction. Frequent skin injury may worsen pre-existing psoriasis, and new isomorphic psoriatic lesions may develop on scar tissue.

Repeated contact with detergents, solvents, or astringent dusts may lead to secondary irritant contact dermatitis in individuals suffering from xeroderma. Similarly, exposure to frying oils may exacerbate acne.

Prevention

A thorough understanding of relevant risk factors is a prerequisite to establishing prevention programmes, which may be either institutional or personal ones such as relying on personal protective equipment. The efficacy of prevention programmes depends on the close collaboration of workers and employers during their development. Table 3 provides some information on prevention.

Table 3. Collective measures (group approach) to prevention

Collective measures

• Substitution

• Environmental control:

Use of tools for handling materials
Ventilation
Closed systems
Automation

• Information and training

• Careful work habits

• Follow-up

Personal protection

• Skin hygiene

• Protective agents

• Gloves

Workplace Prevention

The primary goal of workplace preventive measures is the elimination of hazards at their source. When feasible, substitution of a toxic substance by a non-toxic one is the ideal solution. For example, the toxic effects of a solvent being incorrectly used to clean the skin can be eliminated by substituting a synthetic detergent that presents no systemic hazard and that is less irritating. Several non-allergenic cement powders which substitute ferrous sulphate for hexavalent chromium, a well-known allergen, are now available. In water-based cooling systems, chromate-based anti-corrosion agents can be replaced by zinc borate, a weaker allergen (Mathias 1990). Allergenic biocides in cutting oils can be replaced by other preservatives. The use of gloves made of synthetic rubber or PVC can eliminate the development of latex allergies among health-care workers. Replacement of aminoethanolamine by triethanolamine in welding fluxes used to weld aluminium cables has led to a reduction in allergies (Lachapelle et al. 1992).

Modification of production processes to avoid skin contact with hazardous substances may be an acceptable alternative when substitution is impossible or the risk is low. Simple modifications include using screens or flexible tubes to eliminate splashing during the transfer of liquids, or filters that retain residues and reduce the need for manual cleaning. More natural grasp points on tools and equipment that avoid exerting excessive pressure and friction on the hands and that prevent skin contact with irritants may also work. Local capture ventilation with capture inlets that limit nebulisation or reduce the concentration of airborne dusts are useful. Where processes have been completely automated in order to avoid environmental hazards, particular attention should be paid to training workers responsible for repairing and cleaning the equipment and specific preventive measures may be required to limit their exposure (Lachapelle et al. 1992).

All personnel must be aware of the hazards present in their workplace, and collective measures can only be effective when implemented in conjunction with a comprehensive information programme. Material Safety Data Sheets can be used to identify hazardous and potentially hazardous substances. Hazard warning signs can be used to rapidly identify these substances. A simple colour code allows visual coding of the risk level. For example, a red sticker could signal the presence of a hazard and the necessity of avoiding direct skin contact. This code would be appropriate for a corrosive substance that rapidly attacks the skin. Similarly, a yellow sticker could indicate the need for prudence, for example when dealing with a substance capable of damaging the skin following repeated or prolonged contact (Durocher 1984). Periodic display of posters and the occasional use of audio-visual aids reinforce the information delivered and stimulate interest in occupational dermatosis prevention programmes.

Complete information on the hazards associated with work activities should be provided to workers prior to starting work. In several countries, workers are given special occupational training by professional instructors.

Workplace training must be repeated each time a process or task is changed with resulting change in risk factors. Neither an alarmist nor paternalistic attitude favours good working relationships. Employers and workers are partners who both desire work to be executed safely, and the information delivered will only be credible if it is realistic.

Given the absence of safety standards for dermatotoxic substances (Mathias 1990), preventive measures must be supported by vigilant observation of the state of workers’ skin. Fortunately this is easily implemented, since the skin, particularly that on the hands and face, can be directly observed by everyone. The goal of this type of observation is the identification of early signs of cutaneous modifications indicating an overwhelming of the body’s natural equilibrium. Workers and health and safety specialists should therefore be on the lookout for the following early warning signs:

• progressive drying
• maceration
• localized thickening
• frequent trauma
• redness, particularly around hairs.

Prompt identification and treatment of cutaneous pathologies is essential, and their underlying causal factors must be identified, to prevent them from becoming chronic.

When workplace controls are unable to protect the skin from contact with hazardous substances, the duration of skin contact should be minimized. For this purpose, workers should have ready access to appropriate hygienic equipment. Contamination of cleaning agents can be avoided by using closed containers equipped with a pump that dispenses an adequate amount of the cleanser with a single press. Selecting cleansers requires compromising between cleaning power and the potential for irritation. For example, so-called high-performance cleansers often contain solvents or abrasives which increase irritation. The cleanser selected should take into account the specific characteristics of the workplace, since workers will often simply use a solvent if available cleansers are ineffective. Cleansers may take the form of soaps, synthetic detergents, waterless pastes or creams, abrasive preparations and antimicrobial agents (Durocher 1984).

In several occupations, the application of a protective cream before work facilitates skin cleaning, regardless of the cleaner used. In all cases, the skin must be thoroughly rinsed and dried after each washing. Failure to do so may increase irritation, for example by re-emulsification of the soap residues caused by the humidity inside impermeable gloves.

Industrial soaps are usually provided as liquids dispensed by hand pressure. They are composed of fatty acids of animal (lard) or vegetable (oil) origin, buffered with a base (e.g., sodium hydroxide). Buffering may be incomplete and may leave residual free radicals that are capable of irritating the skin. To avoid this, a near-neutral pH (4 to 10) is desirable. These liquid soaps are adequate for many tasks.

Synthetic detergents, available in both liquid and powder form, emulsify greases. Thus they usually remove the human skin’s sebum, which is a substance that protects the skin against drying. Skin emulsification is generally less marked with soaps than with synthetic detergents and is proportional to detergent concentration. Emollients such as glycerine, lanolin, and lecithin are often added to detergents to counteract this effect.

Pastes and creams, also known as “waterless soaps” are emulsions of oil-based substances in water. Their primary cleaning agent is a solvent, generally a petroleum derivative. They are called “waterless” because they are effective in the absence of tap water, and are typically used to remove stubborn soils or to wash hands when water is unavailable. Because of their harshness, they are not considered cleansers of choice. Recently, “waterless soaps” containing synthetic detergents that are less irritating to the skin than solvents have become available. The American Association of Soap and Detergent Manufacturers recommends washing with a mild soap after using solvent-based “waterless soaps.” Workers who use “waterless soaps” three or four times per day should apply a moisturizing lotion or cream at the end of the work day, in order to prevent drying.

Abrasive particles, which are often added to one of the cleaners described above to increase their cleaning power are irritants. They may be soluble (e.g., borax) or insoluble. Insoluble abrasives may be mineral (e.g., pumice), vegetal (e.g., nut shells) or synthethic (e.g., polystyrene).

Antimicrobial cleaners should only be used in workplaces where there is a real risk of infection, since several of them are potential allergens and workers should not be exposed needlessly.

Under the influence of certain substances or repeated washings, workers’ hands may tend to dry out. Long-term maintenance of good skin hygiene under these conditions requires daily moisturizing, the frequency of which will depend on the individual and the type of work. In many cases, moisturizing lotions or creams, also known as hand creams, are adequate. In cases of severe drying or when the hands are immersed for prolonged periods, hydrophilic vaselines are more appropriate. So-called protective or barrier creams are usually moisturizing creams; they may contain silicones or zinc or titanium oxides. Exposure-specific protective creams are rare, with the exception of those which protect against ultraviolet radiation. These have been greatly improved over the last few years and now provide effective protection against both UV-A and UV-B. A minimum protection factor of 15 (North American scale) is recommended. StokogarÔ cream appears to be effective against contact dermatitis caused by poison ivy. Protective or barrier creams should never be seen as equivalent to some form of invisible impermeable glove (Sasseville 1995). Furthermore, protective creams are only effective on healthy skin.

While few people like wearing protective equipment, there may be no choice when the measures described above are inadequate. Protective equipment includes: boots, aprons, visors, sleeves, overalls, shoes, and gloves. These are discussed elsewhere in the Encyclopaedia.

Many workers complain that protective gloves reduce their dexterity, but their use is nevertheless inevitable in some situations. Special efforts are required to minimize their inconvenience. Many types are available, both permeable (cotton, leather, metal mesh, KevlaÔasbestos) and impermeable (rubber latex, neoprene, nitrile, polyvinyl chloride, VitoÔ, polyvinyl alcohol, polyethylene) to water. The type selected should take into account the specific needs of each situation. Cotton offers minimal protection but good ventilation. Leather is effective against friction, pressure, traction, and some types of injury. Metal mesh protects against cuts. KevlaÔis fire-resistant. Asbestos is fire- and heat-resistant. The solvent resistance of water-impermeable gloves is highly variable and depends on their composition and thickness. To increase solvent resistance, some researchers have developed gloves incorporating multiple polymer layers.

Several characteristics have to be taken into account when selecting gloves. These include thickness, flexibility, length, roughness, wrist and finger adjustment, and chemical, mechanical, and thermal resistance. Several laboratories have developed techniques, based on the measurement of break-through times and permeability constants, with which to estimate the resistance of gloves to specific chemicals. Lists to help guide glove selection are also available (Lachapelle et al. 1992; Berardinelli 1988).

In some cases, the prolonged wear of protective gloves may cause allergic contact dermatitis due to glove components or to allergens that penetrate the gloves. Wearing protective gloves is also associated with an increased risk of skin irritation, due to prolonged exposure to high levels of humidity within the glove or penetration of irritants through perforations. To avoid deterioration of their condition, all workers suffering from hand dermatitis, regardless of its origin, should avoid wearing gloves that increase the heat and humidity around their lesions.

Establishing a comprehensive occupational dermatosis prevention programme depends on careful adaptation of standards and principles to the unique characteristics of each workplace. To ensure their effectiveness, prevention programmes should be revised periodically to take into account changes in the workplace, experience with the programme and technological advances.

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The function of the epithelium of the epidermis is to form the surface or horny layer of the skin, of which the major component is the fibrous protein, keratin. In certain areas the epithelium is specially developed to produce a particular type of keratin structure. One of these is hair, and another is nail. The nail plate is formed partly by the epithelium of the matrix and partly by that of the nail bed. The nail grows in the same way as the hair and the horny layer and is affected by similar pathogenic mechanisms to those responsible for diseases of the hair and epidermis. Some elements such as arsenic and mercury accumulate in the nail as in the hair.

Figure 1 shows that the nail matrix is an invagination of the epithelium and it is covered by the nail fold at its base. A thin film of horny layer called the cuticle serves to seal the paronychial space by stretching from the nail fold to the nail plate.

Figure 1. The structure of the nail.

The most vulnerable parts of the nail are the nail fold and the area beneath the tip of the nail plate, although the nail plate itself may suffer direct physical or chemical traumata. Chemical substances or infective agents may penetrate under the nail plate at its free margin. Moisture and alkali may destroy the cuticle and allow the entry of bacteria and fungi which will cause inflammation of the paronychial tissue and produce secondary growth disturbance of the nail plate.

The most frequent causes of nail disease are chronic paronychia, ringworm, trauma, psoriasis, impaired circulation and eczema or other dermatitis. Paronychia is an inflammation of the nail fold. Acute paronychia is a painful suppurative condition requiring antibiotic and sometimes surgical treatment. Chronic paronychia follows loss of the cuticle which allows water, bacteria and Candida albicans to penetrate into the paronychial space. It is common among persons with intense exposure to water, alkaline substances and detergents, such as kitchen staff, cleaners, fruit and vegetable preparers and canners and housewives. Full recovery cannot be achieved until the integrity of the cuticle and eponychium sealing the paronychial space has been restored.

Exposure to cement, lime and organic solvents, and work such as that of a butcher or poulterer may also cause trauma of the cuticle and nail folds.

Any inflammation or disease of the nail matrix may result in dystrophy (distortion) of the nail plate, which is usually the symptom which has brought the condition to medical attention. Exposure to chilling cold, or the arterial spasm of Raynaud’s phenomenon, can also damage the matrix and produce nail dystrophy. Sometimes the damage is temporary and the nail dystrophy will disappear after removal of the cause and treatment of the inflammatory condition. (An example is shown in figure 2.)

Figure 2. Onychodystrophy secondary to contact dermatitis resulting from chronic irritation.

One cause of nail damage is the direct application of certain cosmetic preparations, such as base coats under nail polish, nail hardeners and synthetic nail dressings to the nail.

Some special occupations may cause nail damage. There has been a report of dystrophy due to handling the concentrated dipyridylium pesticide compounds paraquat and diquat. During the manufacture of selenium dioxide, a fine powder of this substance may get under the fringe of the nail plate and cause intense irritation and necrosis of the finger tip and damage to the nail plate. Care should be taken to warn workers of this hazard and advise them always to clean the subungual areas of their fingers each day.

Certain types of allergic contact dermatitis of the finger tips frequently result in secondary nail dystrophy. Six common sensitizers which will do this are:

1. amethocaine and chemically related local anaesthetics used by dental surgeons
2. formalin used by mortuary attendants, anatomy, museum and laboratory assistants
3. garlic and onion used by cooks
4. tulip bulbs and flowers handled by horticulturists and florists
5. p-tert-butylphenol formaldehyde resin used by shoe manufacturers and repairers
6. aminoethylethanolamine used in some aluminium fluxes.

The diagnosis can be confirmed by a positive patch test. The condition of the skin and nails will recover when contact ceases.

Protective measures

In many cases nails can be safeguarded by the use of suitable hand protection. However, where hand exposure exists, nails should receive adequate care, consisting essentially of preserving the cuticle and protecting the subungual area. The skin under the free margin of the nails should be cleaned daily in order to remove foreign debris or chemical irritants. Where barrier creams or lotions are employed, care should be taken to ensure that the cuticle and the area under the free margin are coated.

To preserve the intact cuticle it is necessary to avoid excessive manicure or trauma, maceration by prolonged exposure to water, and dissolution by repeated exposure to alkali, solvent and detergent solutions.

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