Occupational Dermatoses

Introduction

Contact dermatitis accounts for the majority of occupational skin disease that predominantly affects the hands. The prevalence of hand dermatitis in the population has been estimated at approximately 0.5%, rising in some studies to 10% when an industrial workforce has been examined. While most individuals will remain at work, over half will change jobs and a large proportion will be absent from work for a month or more.

History

In the first century AD, Pliny the Younger recorded dermatitis in individuals after they cut down pine trees, presumably representing allergic contact dermatitis to colophony in pine resin. Ramazzini in his 1700 treatise described irritant contact dermatitis of the hands and forearms in soap and laundry workers.

Epidemiology

An age-related increase in rates of occupational dermatitis is seen in men, but in women the peak age of incidence is 16–29 years with a decline thereafter. However, a comparison of rates by age within specific occupational groups suggests that the sexes follow a similar pattern. Among chefs and cleaners of either sex, higher rates are seen in young workers, whereas rates among machine tool operators increase with age, reflecting the type of occupational exposure. Materials giving rise to contact dermatitis in the UK are shown in Figure 16.2 , and the highest risk UK occupations in Figure 16.3 . In contrast to the UK, in Finland and the US, the highest rate of skin disease is among agricultural workers.

Pathogenesis

The initial events of both irritant and allergic contact dermatitis (see Chs 14 & 15 ) are similar. Depending upon the severity of the insult, the tissue response can reach a level at which it becomes clinically apparent as cutaneous inflammation ( Fig. 16.4 ). If tissue perturbation is maintained via repeated insults, then chronic dermatitis ensues, while an early withdrawal of the insult may result in healing.

Clinical features

Contact dermatitis, both allergic and irritant, is morphologically indistinguishable from endogenous eczema ( Fig. 16.5 ). Although most cases of dermatitis will result from direct exposure that leads to localized dermatitis, there are other routes of absorption that can lead to dermatitis. In the case of solvents, inhalation may result in widespread dermatitis, often with systemic involvement.

Diagnosis of an occupational cause is dependent on a thorough dermatologic and occupational history ( Table 16.2 ), combined with examination of the entire skin. Material safety data sheets (MSDS) provide a guide to the nature of materials handled at work. They list the chemical composition and the hazards associated with the product, e.g. irritant, corrosive, contains a sensitizer. However, total reliance should not be placed on the MSDS as they may not list all ingredients of relevance, and communication with the manufacturer may prove helpful. When occupational dermatitis is suspected but a cause cannot be established from the history, a workplace visit may prove invaluable and may also elucidate the source of an allergen previously detected via patch testing.

Although the primary site is usually the hands, spread to adjacent areas of skin (even without primary contact) is relatively common. Spread to distant sites, such as the face and feet, is more frequently seen in allergic contact dermatitis than in irritant contact dermatitis. Notably, airborne allergens, e.g. from paint sprayers, can lead to a pattern of dermatitis that suggests this type of exposure. Covered areas such as the trunk and feet are unusual sites of onset of disease. Improvement of the dermatitis during periods away from work is an important clue to an occupational cause, but it should be remembered that endogenous eczema may also be exacerbated by workplace exposures. As the dermatitis becomes chronic, the relationship between work and exacer­bations becomes less clear-cut.

Fiberglass dermatitis

Glass fibers are subdivided into various types, depending on fiber diameter, and are used for their insulating (thermal, acoustic, and electrical), strengthening, and filtering abilities. They are chemically inert and the mechanism of skin injury is via direct penetration, which is directly proportional to the diameter (>3.5 microns) of the fiber and inversely proportional to its length. Histologically, eczematous changes including spongiosis are seen.

Pruritus and tingling are the usual initial symptoms of fiberglass dermatitis. Subsequently, erythematous papules develop (often with follicular accentuation), either on exposed areas when there is airborne exposure or on the forearms when there is contamination of a work surface ( Fig. 16.7 ) . Contamination of clothing leads to involvement of sites where there is close contact with the skin, particularly flexural areas. Paronychia is common, and airborne exposure may also cause burning eyes, sore throat, and cough.

The diagnosis is often based on clinical findings, but can be confirmed by detecting the glass fibers either by tape stripping affected skin or by examining skin scrapings in 20% potassium hydroxide. The dermatitis resolves rapidly after cessation of exposure. In most individuals, hardening occurs and symptoms resolve over a few weeks despite continued exposure; of note, the use of resins to bind glass fibers can result in an allergic contact dermatitis.

Mechanical

Occupational marks are usually areas of lichenification or calluses and corns that develop at sites of friction and are specific to a particular job ( Fig. 16.8 ). Mechanical injury to the skin is also thought to cause dermatitis analogous to irritant chemical damage. It may result in a keratotic hand dermatitis or post-traumatic eczema (Koebner phenomenon).

Pathology

The histologic features of allergic contact dermatitis and irritant contact dermatitis are discussed in Chapters 14 and 15 , respectively.

Differential diagnosis

The etiology of occupational dermatitis is frequently multifactorial and coexisting endogenous eczema may contribute to the clinical appearance. Tinea manuum may resemble hand dermatitis, especially following treatment with topical corticosteroids, and scabies infestation of the interdigital spaces can simulate irritant dermatitis. Rarely, blistering of the dorsal hands due to porphyria cutanea tarda is misconstrued as contact dermatitis.

Psoriasis frequently affects the palms, resulting in keratotic plaques, sometimes with fissures. This can be difficult to distinguish from dermatitis when there are no lesions elsewhere. Furthermore, psoriasis may be exacerbated by repeated, work-related trauma leading to Koebner phenomena. Nail involvement and plaques over the interphalangeal joints are helpful clues.

Treatment

Occupational disease prevention is divided into primary, secondary, and tertiary measures ( Table 16.4 ) . During pre-employment screening, a history of severe childhood atopic dermatitis, particularly with hand involvement, indicates an individual at risk of developing dermatitis from exposure to irritants. Employment in a “dry” job should be recommended. In the workplace, the use of protective equipment and skin care preparations should be encouraged ( Table 16.5 ). Use of protective creams prior to exposure may aid in the subsequent removal of irritants and application of emollients throughout the day may prevent the development of dermatitis. Education of the workforce in skin care has been shown to reduce the development of skin disease .

Treatment is discussed in Chapters 14 and 15 . The most important aspect, however, is avoidance of the cause. Ideally, a change in the production process may avoid the need for exposure, but this may not be feasible. A practical compromise is the use of personal protective equipment and/or substitution of a particular chemical. Advice on appropriate glove type may be found on the MSDS or from glove manufacturers (e.g. www.ansellpro.com ). Gloves need to be replaced regularly and each particular type of glove will have a penetration time for any given chemical. For example, acrylate glues (orthopedic surgeons, dentists), the hair dye para-phenylenediamine (hairdressers), and “acid perm” solutions containing glycerol monothioglycolate (hairdressers) rapidly penetrate latex gloves.

Initial treatment of chemical burns requires irrigation with large volumes of water. When the chemical is insoluble in water, a soap solution may be used instead. High pressures should not be used, in order to avoid splashing other areas of the body or bystanders with the corrosive material. For some chemicals, specific antidotes can then be used, e.g. 2.5% calcium gluconate gel for hydrofluoric acid; reduction of pain is a sign of successful treatment. When there is a risk of toxicity from systemic absorption, as with chromic acid, early debridement of necrotic areas reduces blood levels.

Several chemicals (e.g. hydrofluoric acid, phenolic compounds, chromic acid, gasoline) carry a significant risk of systemic toxicity even when the area of skin involved is small (approximately 1% of body surface area). In these instances, regular monitoring of blood, liver and kidney function plus appropriate supportive treatment (e.g. dialysis) is required. When the chemical is also a sensitizer, allergic contact dermatitis may subsequently appear on re-exposure to non-irritant concentrations, as burns and irritant dermatitis promote sensitization.

Once it has developed, the outlook for occupational contact dermatitis is poor , and patients frequently have persistent disease despite interventions. While a change of occupation is associated with a better prognosis, the possibility exists that the new workplace will have the same or similar chemical exposures. Prognosis is also worse when there is a contact allergy (delayed or immediate) to a chemical that is present in the domestic as well as the industrial environment. Some individuals (~10%) have persistent disease in the absence of any obvious cause, for which the term “persistent post-occupational dermatitis” has been coined.