1. Occupational Skin Diseases
Dr. Alireza Safaiean
Occupationala Medicine Specialist

2. Introduction
The second cause of occupational diseases ( 23-25% of all occ.diseases )
A skin disease that is caused by physical, biological or chemical factor in work
Also a worsening of pre-existing skin disease can be termed as occupational skin disease

3. CAUSES OF SKIN DISORDERS
CONTACT
DERMATITIS
FOLLICULITIS
AND ACNE
PIGMENTARY
DISTURBANCE
NEOPLASMS,
ULCERATION
GRANULOMA
CHEMICAL X
MECHANICAL
PHYSICAL
BIOLOGICAL

4. Classifications of skin diseases
Occupational dermatitis
Occupational photosensitivity reactions
Occupational phototoxicity reaction
Occupational skin cancers
Occupational contact urticaria
Occupational acne
Occupational skin infections
Occupational pigmentary disorders
Miscellaneous

5. Work-aggravated Skin Diseases
Psoriasis
Acne

6. APPROACH TO THE WORKER WITH SKIN DISEASE
History
Physical examination
Diagnostic techniques
Supplemental information

7. History A. Present illness Date of onset Body site at onset
Patient description
Onset – abrupt or gradual
Appearance, spread
Frequency
Effect of treatment
Course of disease
Effect of weekend, vacation
Work procedure change
Treatment and effect on dermatitis

8. History B. Occupational information Current employer Employment dates
Job title (At time of onset, Description of job tasks, Materials contacted, Protection, Water exposure, Hand washing)
Clothing/equipment: (Protective creams/cleansers, Skin cleaning, Method and frequency)
Other workers affected
Job since dermatitis
Previous job tasks or jobs
Episodes of dermatitis
Second job
Dates of disability
Date of job changes

9. History C. Personal history
Other exposures (Animals, Foods, Plants, Clothing, Personal care products, Hobbies)
Past history of skin disease (Plant dermatitis, Hand dermatitis, Psoriasis, Athlete’s foot)
History of atopy
Personal/family (Atopic dermatitis, Hay fever, Asthma)
Medical problems
Medications

10. Physical examination Lesion type Secondary changes Distribution
Other skin disease
Photographic documentation

11. Diagnostic techniques
Skin scrapings
Fungus
Fibers
Culture
Skin biopsy
Patch test
Contact urticaria test
Photopatch test

13. Supplemental information
Material safety data sheets
Medical records
Workplace
Other physician

14. Diagnosis Of Occupational Skin Diseases
Clinical symptoms: Are they in accordance to clinical disease?
Patient history: Does skin disease relate to work?
Exposure: Are there causative agents (allergens, irritants) in the work-place?

15. CAUSES OF OCCUPATIONAL SKIN DISEASE

16. Chemical agents
The main cause of occupational skin diseases and disorders.
These agents are divided into two types:
Primary irritants: Primary or direct irritants act directly on the skin though chemical reactions.
Sensitizers: may not cause immediate skin reactions, but repeated exposure can result in allergic reactions.
A worker’s skin may be exposed to hazardous chemicals through:
direct contact with contaminated surfaces,
deposition of aerosols,
immersion,
splashes

17. Other Causes
Physical agents such as extreme temperatures (hot or cold) and radiation (UV/solar radiation).
Mechanical trauma includes friction, pressure, abrasions, lacerations and contusions (scrapes, cuts and bruises).
Biological agents include parasites, microorganisms, plants and other animal materials. (Animal breeders, vets, horticulturists, bakers, tanners, bricklayers, etc. are all possible victims of biological)

18. CAUSES OF OCCUPATIONAL SKIN DISEASE
Predisposing Factors
Age & experience
Skin type
Sweating
Gender
Seasons and humidity
Hereditary allergy
Personal hygiene
Preexisting skin disease
Atopy A type of inherited allergic response involving elevated immunoglobulin E . Sometimes called a reagin response, it means that you have hay fever , bronchial asthma , or skin problems like urticaria or eczema . It can also be acquired, sometimes following hepatitis or extended contact with solvents or alcohol.
Atopic dermatitis Signs and symptoms of this type include itchy, thickened, scaly skin, most often in the folds of your elbows or backs of your knees. It's also common on the face, hands and feet. When this type occurs in babies, it's called infantile eczema. About 15 million Americans have atopic dermatitis.

19. Contact Dermatitis
Occupational dermatitis is an inflammation of the skin causing itching, pain, redness, swelling and small blisters.
Contact dermatitis is an eczematous eruption caused by external agents, which can be broadly divided into:
Irritant substances that have a direct toxic effect on the skin (irritant contact dermatitis, ICD)
Allergic chemicals where immune delayed hypersensitivity reactions occur (allergic contact dermatitis, ACD).

20. Types of contact dermatitis
Irritant Contact 80% of all dermatitis is caused by direct contact with a substance It may occur randomly
Allergic Contact Once sensitised, the problem is life long and any exposure to the substance will result in an attack

21. The Causes Irritants Detergents Solvents Engine oils Cutting fluid
Lubricants
Fibreglass
Allergens
Salts
Nickel
Epoxy resins
Dyes
Rubber

22. Common site of involvement
Skin disease starts on the area of contact.
Dorsal aspects of hands and fingers, volar aspects of arms, interdigital webs, medial aspect of thighs, dorsal aspects of feet.

23. Prognosis Of Occupational Dermatitis After Treatment
25% complete recovery
25% refractory
50% remitting / relapsing

24. Irritant Contact Dermatitis ICD

25. Classification of ICD
Acute
Chronic

26. Acute ICD
This is often the result of a single overwhelming exposure or a few brief exposures to strong irritants or caustic agents.
Common work chemicals:
– Concentrated acids (sulfuric, nitric, chromic, hydrochloric, hydrofluoric acids)
– Strong alkali(CaOH,NaOH,KOH),wet concrete, sodium and potassium cyanide
– Organic and inorganic salts, e.g. dichromates, arsenic salts
– Solvents/gases, e.g. acrylonitrile, ethylene oxide, CS2

27. Clinical Presentation
Stinging, burning, painful, erythematous eruption occur after brief contact with strong irritant chemicals.
Erosion and skin ulceration may occur.
May result in permanent scar.

32. Chronic (cumulative) ICD
Repetitive exposure to weaker irritants
-Wet : detergents, organic solvents, soaps, weak acids, and alkalis
-Dry : low humidity air, heat ,dusts , and powders
Disease of the stratum corneum
Is due to a stepwise progression of damage to the barrier function of the skin

33. Predisposing Factors Endogenous factors: Dryness vs. wetness Sweating
Age
Atopic predisposition
Hx of skin diseases

34. Causes of Chronic ICD Water/wet work Fiberglass fibers Detergents
Antiseptics
Disinfectants
Soap/cleansing agents
Weak Acids & alkali
Wet cement
Solvents
Low humidity
friction
Fiberglass fibers
Cutting oil
Food
Pesticides
Plants & vegetation
Rubber products
Acrylic resins
Soldering flux
Dusts
Degreasing agents

35. At risk occupations:
Bartenders
Caterers
Cleaners
Hairdressers
Metalworkers
Nurses
Solderers
Fisherman
construction workers.
35% Washing
10% Solvents
6% Plastics and adhesives
6% Foodstuff
5% Dirty, wet work
5% Mineral oils

36. Clinical Presentations
Usually presents with dry, scaly fissuring, lichenified and eczematous lesions on the fingers and hands.
Vesicular lesions do occur but are less common than in ACD.
May in face ( forehead, eyelids, ears, neck) and arms due to airborne irritant dusts and volatile irritant chemicals

40. Management In workplace Treating the active case
Removal from exposure in active lesion
Skin cleansing (water rinse without soap if possible)
Barrier cream
Gloves
Treating the active case
Topical corticosteroids
Soap substitutes
Emollients (either water- or oil-based)
Second line (for steroid resistant cases):
Topical PUVA
Azathioprine
Cyclosporin

42. Allergic Contact Dermatitis ACD

43. Allergic Contact Dermatitis
Caused by low-molecular weight haptens
Hapten is “incomplete allergen”
Binds to carrier protein for immunogenicity
Low molecule weight enables penetration of hapten
Hapten penetrates through stratum corneum of a sensitized individual
A classical Type IV reaction

44. Occupational Skin Allergens
Poison oak/ivy
Metals:
Chromium
Nickel
Gold
Mercury
Cobalt
Rubber industry
Accelerators
Antioxidants
Plastic resins
Epoxy resins
PU resins
Phenolic resins
Formaldehyde resins
Acrylic resins
Rosin ( colophony )
Soft soldering
Organic dyes ( azo dyes )
Methyl metacrylate
Plants
Latex and its powder
Germicides and biocides
e.g. lanolin
Some pesticides
Some solvents
Formaldehyde
Turpentine
Aliphatic amines
Nitrates
Ethylene oxide

45. Classification of ACD
Acute
chronic

46. Clinical Features ( Acute Form )
Rash appears in areas exposed to the sensitizing agent, usually asymmetric or unilat.
Sensitizing agent on the hands or clothes is often transferred to other body parts.
The rash is characterized by erythema, vesicles and sever edema.
Pruritus is the overriding symp.

47. Acute Allergic Contact Dermatitis
Showing Erythema, Edema, and Vesiculobullae

54. Clinical Features ( Chronic Form )
Thickened , fissured, lichenified skin with scaling
The most common sites:
Dorsal aspect of hands
Eyelids
periorbital

55. Subacute Eczema Showing Erythema, Oozing, Crusting, Lichenification, and Scale

56. Chronic Eczema: Showing Lichenification, Fissuring, and Scale

63. Diagnosis Complete history Physical examination Patch test
Occupational
Non-occupational
Physical examination
Patch test

65. Patch Test Confirm delayed hypersensitivity Material& technique:
Medium
Adhesive
Marking of the test
Occlusion for 48 h
Read in after h

66. Angry back

67. Interpretation of patch test result
Nothing: negative reaction
Erythema, papules, infiltration, no vesicle: weak reaction
Erythema, vesicular eruption, edema: strong reaction
Bulla, ulceration: extreme reaction
Erythema to eczematous: irritant reaction

68. Weak positive reaction (+)
Doubtful reaction
(?)
Faint macular or homogeneous Erythema, no infiltration
Weak positive reaction
(+)
Erythema , Infiltration Discrete papules

69. Strong positive reaction
(++)
Erythema Infiltration Papules Discrete vesicles
Extreme positive reaction
(+++ )
Coalescing vesicles/bullous reaction

70. Interpretation codes (Ladou 2004)

73. Management & Prevention
Removal from exposure ( lifelong)
Drug treatment
Topical steroid
Emollients
Prevention
Like ICDs

75. Irritant versus Allergic dermatitis
Hx. Of contact with known irritant
Acute onset
Stinging, Burning
Neg. patch test
Localized
Many people
Improved with long vacation (3 weeks)
ACD
Hx. Of contact with known allergen
Delay onset (1-3d)
Itching, Vesicle
Positive patch test
Spreads
Few people
May improved even on weekends

76. Criteria to Determine Occupational Causation
1. The clinical appearance is consistent with contact dermatitis.
2. There are workplace exposures to potential cutaneous irritants or allergens.
3. The anatomic distribution of dermatitis is consistent with cutaneous exposure in relation to the job task.
4. The temporal relationship between exposure and onset is consistent with contact dermatitis.
5. Non-occupational exposures are excluded as probable causes.
6. The dermatitis improves if work exposure to the suspected irritant or allergen ceases.
7. Patch or provocation tests identify a probable causal agent.
If four of the seven statements in Table are true, the eczema is probably occupational in origin.

77. Contact photodermatitis
Some chemicals may cause CD only in the presence of light
Sunlight or artificial light sources that emit specific wavelengths
2 categories:
-phototoxic
-photoallergic

78. Phototoxic Photoallergic Antifungal agents Fragrances
Halogenated salicylanilide
Phenothiazines
Sunscreens
Whiteners
Agricultural
Coal-tar derivative
Dyes (Eosin)
Drug
-phenothiazines
-sulfonamides
Plants&derivative
-psoralen
-lemon

79. Clinical course Phototoxcic:
- painful , exaggerated sunburn that may develop bullae and pigmentation
-by avoiding the agent, dermatitis usually disappears promptly
Photoallergic:
- many of the features of ACD ( itching , vesiculation)

80. Where involved ?
Exposed areas: face, ant. V of the neck, back of the hand, uncovered sites on the arm&leg
Hairy areas, upper eyelids, and below the chin may be spared

81. Diagnoses Distribution (on sun-exposed surfaces) of the reaction
Photopatch test

82. treatment
Avoidance of contact
Other are the same as CD

83. Contact Urticaria Immunologic :
Caused by proteins that act as allergens
Proteins penetrate through skin⇝bind to IgE on the surface of mast cell⇝ release
of histamine and other mediators
(type-1 reaction)
Sometimes generalized reactions occur
Latex allergy

84. Contact Urticaria Nonimmunologic: Caused by chemicals
Direct pharmacologic action on skin cells
No sensitization necessary
More common than suspected

85. Occupational Causes Latex allergy ( m/c ) Formaldehyde Food industry
Plants
Vegetables
Animal products
Pharmaceutical industry
Streptomycin

86. Clinical Features Of Contact Urticaria
Hives (edema) appear on sites of contact within minutes
The hives disappear within 1-4 hours
Mild: Only itching
Severe: Systemic symptoms (anaphylaxis)

88. Management & Prevention
Removal from exposure
Treatment of active disease
Preventive measures

89. Occupational Skin Cancers
The second m/c form of occupational skin diseases
About 17% of all cases of occupational skin diseases

90. What Cancers? Actinic (solar) keratoses Basal cell carcinoma
Malignant lesions:
Basal cell carcinoma
Squamous cell carcinoma
Malignant melanoma
Pre-malignant lesions:
Actinic (solar) keratoses
Tar keratoses (‘warts’)
Arsenical keratoses
Keratoacanthoma
Intra-epidermal carcinoma (Bowen’s disease)
Lentigo maligna

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