Occupational skin diseases

Occupational skin diseases are contracted from exposure in the workplace and are the second most common employer-reported occupational disorder. The most common manifestations include irritant contact dermatitis, occupational acne, and latex allergy. Other occupational diseases covered elsewhere include work-related musculoskeletal disorders (e.g., carpal tunnel syndrome, low back pain), asbestosis, mesothelioma, and silicosis.

• Second most common cause of occupational disorders (15–20% of all reported occupational diseases) ^[1]
• 75% of patients with occupational contact dermatitis develop chronic skin disease. ^[1]

General principles ^[2][3][4]

• Occupational contact dermatitis is a localized inflammatory skin reaction resulting from exposure to substances at work; manifestations include:
  • Irritant contact dermatitis (ICD)
  • Allergic contact dermatitis
• ICD is caused by a direct cytotoxic effect of a causal agent. ^[2]
  • Most common form of occupational skin disease
  • Can either be acute or chronic; most cases of ICD are chronic.
• For information on allergic contact dermatitis, and nonoccupational ICD (e.g., diaper dermatitis), see the respective articles.

Risk factors ^[2][5]

• Exposure to chemical irritants, e.g.:
  • Heavy metals
  • Strong acids and alkalis
  • Water, soaps and detergents
  • Solvents, synthetic oils
  • Topical medications
• Exposure to physical irritants e.g.:
  • Friction
  • Certain fabrics that prevent ventilation (e.g., synthetics) or are rough (e.g., wool)
  • Dust (e.g., coal, rock, sawdust)
• Environmental factors, e.g.:
  • Low humidity
  • Frequent exposure to moisture (e.g., frequent handwashing or hand disinfection, food preparation) ^[2]
  • Extreme temperatures (e.g., thermal burns, sunburn, cold injury)
• History of atopy

Clinical features ^[2]

• Skin lesions limited to the area of irritant exposure are characteristic of contact dermatitis.
• The dorsum of the hands are most commonly affected. ^[2][5]

Diagnostics ^[2][6]

• A presumptive diagnosis of occupational contact dermatitis can be made if symptoms improve with avoidance of the irritant.
  • History and examination may help differentiate irritant vs. allergic contact dermatitis.
  • Irritant contact dermatitis usually resolves within 6 weeks. ^[7]
• In case of diagnostic uncertainty, refer to a specialist (e.g., dermatologist, allergist) for further evaluation, which may include:
  • Dermoscopy
  • Patch test
  • Microscopy (e.g., KOH preparation, culture of exudate)

ICD disrupts the skin barrier, so patients may present with concurrent atopic dermatitis or allergic contact dermatitis. ^[2][3]

Differential diagnosis ^[2][6]

• Other types of dermatitis, e.g.:
  • Allergic contact dermatitis (see “Irritant vs. allergic contact dermatitis”)
  • Atopic dermatitis
  • Seborrheic dermatitis
  • Stasis dermatitis
• Psoriasis
• Eczema
• Phototoxicity and/or sunburn
• Scabies
• Tinea pedis
• Cutaneous T cell lymphoma

Differentiating irritant and allergic contact dermatitis

Management ^[2][3][6]

• All patients
  • Maintain the integrity of the skin barrier. ^[3]
  • Identify and avoid causative agents. ^[4]
    • If unable to avoid irritant, wear PPE (e.g., gloves, face shield, smock).
    • If symptoms persist despite the use of PPE, reassignment may be necessary. ^[2][6][7]
• Acute ICD ^[3][5][6]
  • Exposure to severe chemical irritants:
    • Immediately irrigate with water for up to 3 hours.
    • Remove contaminated clothing.
    • Consider inpatient management for patients with severe or extensive chemical burns.
  • Apply wet dressings soaked in cool water or diluted aluminum acetate solution (Burow solution). ^[5]
  • Apply calamine lotion or colloidal oatmeal as needed for symptom relief. ^[6]
  • Consider draining large vesicles. ^[7]
• Chronic ICD
  • Regular use of emollients or barrier creams ^[2]
  • Consider topical corticosteroids (e.g., clobetasol ) for patients with persistent inflammation. ^[2][6][8]
  • Severe or widespread disease: Refer to dermatology. ^[3][6]

Prognosis

• ICD usually resolves within 2–6 weeks of removing the irritant. ^[7]
• For patients with ongoing exposure:
  • Resolution after treatment occurs in only ∼30% of patients ^[7]
  • Spontaneous resolution can occur in patients exposed to mild-to-moderate irritants (hardening phenomenon). ^[5][9]

Oil acne ^[5]

• Acne caused by clogging of pilosebaceous units by lubricants (e.g., oils, greases) and/or solvents
• Most common form of occupational acne
• Seen frequently in mechanics
• Lubricant or solvent exposure → reactive follicular hyperkeratosis → open comedones (blackheads) → folliculitis and microcystic lesions
• Clinical features
  • Comedones, papules, and pustules affecting areas exposed to lubricants or solvents (e.g., hands, thighs)
  • Commonly complicated by folliculitis
• Treatment ^[5]
  • Avoid exposure to causative agents or use PPE.
  • Recommend frequent cleansing of skin and work clothes.
  • Persistent symptoms: Start pharmacotherapy for acne (e.g., topical benzoyl peroxide and retinoic acid).

Chloracne ^[10]

• Most serious form of occupational acne
• Caused by halogenated aromatic hydrocarbons penetrating the skin
• Clinical features
  • Closed comedones, yellowish cysts, and scarring
  • The nose is typically spared.
  • May be associated with systemic disease
• Treatment is the same as for oil acne.

Mask acne ^[11][12]

• Acne affecting areas covered by a mask
• Caused by increased temperature and humidity beneath the mask
• First-line treatment is prevention, e.g.:
  • Wash skin before and after mask use with a gentle noncomedogenic cleanser.
  • Avoid wearing makeup if a mask will be worn all day.
  • Take a 15-minute break from mask use every 2 hours.
  • Change masks daily.
• If acne persists, consider topical acne treatment during mask-free intervals.

A type I hypersensitivity or type IV hypersensitivity reaction to latex-based products (e.g., rubber gloves, condoms, balloons) ^[13]

Epidemiology

• Affects 1–2% of the general population ^[13]
• Increased risk of allergy in individuals who have:
  • Atopy, eczema, and hand dermatitis
  • Occupational exposure, e.g., healthcare workers, hairdressers
  • Multiple surgeries (e.g., patients with spina bifida) ^[13]

Pathophysiology

• Immediate hypersensitivity (type I HSR): preformed IgE antibodies coating mast cells and basophils are crosslinked by contact with antigen (usually latex allergens) → cell degranulation → release of histamine and other inflammatory mediators.(e.g., leukotrienes, prostaglandins) → vasodilatation, increased capillary permeability, smooth muscle contraction, and inflammatory cell chemotaxis ^[14]
• Delayed-type hypersensitivity (type IV HSR): contact of antigens (usually chemicals used during glove manufacturing such as benzothiazoles or amines) with presensitized T lymphocytes ^[15]
  • Presensitized CD4+ T cells recognize antigens on antigen-presenting cells → release of inflammatory cytokines → activation of macrophages
  • Presensitized CD8+ T cells recognize antigens on somatic cells → cell-mediated cytotoxicity

Clinical features

• Urticaria in the areas of contact
• Rhinitis, asthma ^[16]
• Anaphylactic shock (in sensitized individuals)

Diagnostics ^[13][17]

There is no standardized diagnostic algorithm to confirm latex allergy.

• Take a comprehensive history; consider screening questionnaires. ^[13]
• Confirm the diagnosis with laboratory studies or skin testing. ^[13][17]
  • Suspected immediate hypersensitivity reaction
    • Latex-specific serum Ig E testing
    • Skin prick testing
  • Suspected delayed-type hypersensitivity reaction : patch testing
• For patients with a suggestive history but negative skin and antibody tests, consider a provocation test. ^[13][17]

Treatment ^[13][17]

• Treat the allergic reaction (e.g., see “Anaphylaxis,” “Allergic contact dermatitis,” and “Allergic rhinitis” as needed).
• Educate patients on allergen avoidance in the community.
• For hospitalized patients: Ensure latex-allergy status is documented on admission and the patient's environment remains latex-free.

Prevention ^[13][17]

For individuals at the highest risk (e.g., patients with spina bifida), maintain a latex-free environment from birth.

• Bacterial infections
  • Folliculitis
  • Paronychia
• Fungal infections: tinea pedis
• Viral infections: milker's nodules ^[18]
  • Skin condition caused by the Cowpox virus from the family of Poxviridae that infects the teats of cows
  • Individuals with occupational exposure to cows are at increased risk of developing the disease.
  • Usually manifests on the fingers with raised, red spots that develop into red-blue, firm and slightly tender nodules.
  • Resolves spontaneously
  • Complications include lymphangitis and secondary bacterial infection.

Exposure to chemicals or UV radiation may lead to development of skin cancers, for more information see:

• Actinic keratosis
• Basal cell carcinoma
• Squamous cell carcinoma
• Melanoma
• Precancerous skin lesions

Environmental exposure may lead to the development of the following skin conditions:

• Sunburn
• Photoallergic dermatitis
• Burns
• Frostbite
• Miliaria