Transcript Occupational Skin Diseases

Occupational Skin Diseases
Dr. Alireza Safaiyan
Occupational Medicine Specialist
Introduction
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The second cause of occupational
diseases ( 23-25% of all occ.diseases )
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A skin disease that is caused by physical,
biological or chemical factor in work
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Also a worsening of pre-existing skin
disease can be termed as occupational
skin disease
Classifications of work-induced skin
diseases
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Occupational dermatitis
Occupational photosensitivity reactions
Occupational phototoxicity reaction
Occupational skin cancers
Occupational contact urticaria
Occupational acne
Occupational skin infections
Occupational pigmentary disorders
Miscellaneous
Work-aggravated Skin Diseases
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Psoriasis
Acne
Diagnosis Of Occupational Skin
Diseases
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Patient history: Does skin
disease relate to work?
Exposure: Are there causative
agents (allergens, irritants) in
the work-place?
Clinical symptoms: Are they in
accordance to clinical disease?
Questions
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When did disease start?
In which skin area was the first
symptom?
What is work technique?
Free time, other works
Cleaning measures
Protection
Vacation, holidays
Contact Dermatitis
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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:
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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).
What Types?
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
What Causes it?
Irritants
 Detergents
 Solvents
 Engine oils
 Cutting fluid
 Lubricants
 Fibreglass
Allergens
 Salts
 Nickel
 Epoxy resins
 Dyes
 Rubber
Common site of involvement
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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.
Prognosis Of Occupational
Dermatitis After Treatment
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25% complete recovery
25% refractory
50% remitting / relapsing
Irritant Contact Dermatitis
ICD
Classification of ICD
 Acute
 Chronic
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
Clinical Presentation
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Stinging, burning, painful, erythematous
eruption occur after brief contact with
strong irritant chemicals.
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Erosion and skin ulceration may occur.
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May result in permanent scar.
Chronic (cumulative) ICD
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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
Predisposing Factors
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Endogenous factors:
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Dryness vs wetness
Sweating
Age
Atopic predisposition
Hx of skin diseases
Causes of Chronic ICD
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Water/wet work
Detergents
Antiseptics
Disinfectants
Soap/cleansing agents
Weak Acids & alkali
Wet cement
Solvents
Low humidity
friction
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Fiberglass fibers
Cutting oil
Food
Pesticides
Plants & vegetation
Rubber products
Acrylic resins
Soldering flux
Dusts
Degreasing agents
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35% Washing
10% Solvents
6% Plastics and
adhesives
6% Foodstuff
5% Dirty, wet work
5% Mineral oils
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At risk occupations:
Bartenders
Caterers
Cleaners
Hairdressers
Metalworkers
Nurses
Solderers
Fisherman
construction
workers.
Clinical Presentations
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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
Management
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Removal from exposure in active lesion
Treating the active case
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Second line (for steroid resistant cases):
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• Topical corticosteroids
• Soap substitutes
• Emollients
• Topical PUVA
• Azathioprine
• Cyclosporin
Allergic Contact Dermatitis
ACD
Allergic Contact Dermatitis
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Caused by low-molecular weight
haptens
Hapten is “incomplete allergen”
Binds to carrier protein for
immunogenicity
Low molecule weight enables
penetration of hapten
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Hapten penetrates through
stratum corneum of a sensitized
individual
A classical Type IV reaction
Occupational Skin Allergens
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Poison oak/ivy
Metals:
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Chromium
Nickel
Gold
Mercury
Cobalt
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Accelerators
Antioxidants
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Epoxy resins
PU resins
Phenolic resins
Formaldehyde resins
Acrylic resins
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Soft soldering
Rubber industry
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Plastic resins
Rosin ( colophony )
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Organic dyes ( azo dyes )
Methyl metacrylate
Plants
Latex and its powder
Germicides and biocides
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e.g. lanolin
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Formaldehyde
Turpentine
Aliphatic amines
Some pesticides
Some solvents
Nitrates
Ethylene oxide
Classification of ACD
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Acute
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chronic
Clinical Features ( Acute Form )
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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.
Clinical Features ( Chronic Form )
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Thickened , fissured, lichenified
skin with scaling
The most common sites:
• Dorsal aspect of hands
• Eyelids
• periorbital
Diagnosis
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Complete history
• Occupational
• Non-occupational
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Physical examination
Patch test
Patch Test
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Confirm delayed hypersensitivity
Material& technique:
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Medium
Adhesive
Marking of the test
Occlusion for 48 h
Read in after 72-96 h
Angry back
Interpretation of patch test result
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Nothing: negative reaction
Erythema, papules, infiltration, no vesicle:
weak reaction
Erythema, vesicular eruption, edema:
strong reaction
Bulla, ulceration: extreme reaction
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Erythema to eczematous: irritant reaction
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Doubtful reaction •
(?)
Faint macular or
homogeneous
Erythema, no infiltration
Weak positive reaction
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Erythema , Infiltration
Discrete papules
Strong positive reaction •
(++)
Erythema
Infiltration
Papules
Discrete vesicles
Extreme positive reaction •
(+++ )
Coalescing vesicles/bullous
reaction
Interpretation codes (Ladou 2004)
Management & Prevention
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Removal from exposure
Drug treatment
• Topical steroid
• Emollients
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Prevention
• Like ICDs
( lifelong)
Irritant versus Allergic dermatitis
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ICD
• Hx. Of contact with
known irritant
• Acute onset
• Stinging, Burning
• Neg. patch test
• Localized
• Many people
• Improved with long
vacation (3 weeks)
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ACD
• Hx. Of contact with
known allergen
• Delay onset (1-3d)
• Itching, Vesicle
• Positive patch test
• Spreads
• Few people
• May improved even on
weekends
Mathias criteria for occupational
contact dermatitis (4 of 7)
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Clinical appearance
Workplace exposures
Anatomic distribution
Temporal relationship
Non-occupational exposure
Improvement
Patch test
Contact photodermatitis
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Some chemicals may cause CD only
in the presence of light
Sunlight or artificial light sources
that emit specific wavelengths
2 categories:
-phototoxic
-photoallergic
Phototoxic
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Coal-tar derivative
Dyes (Eosin)
Drug
-phenothiazines
-sulfonamides
Plants&derivative
-psoralen
-lemon
Photoallergic
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Antifungal agents
Fragrances
Halogenated
salicylanilide
Phenothiazines
Sunscreens
Whiteners
Agricultural
Clinical course
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Phototoxcic:
- painful , exaggerated sunburn that may
develop bullae and pigmentation
-by avoiding the agent, dermatitis usually
disappears promptly
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Photo-ACD:
- many of the features of ACD ( itching ,
vesiculation)
Where involved ?
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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
DX
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Distribution (on sun-exposed
surfaces) of the reaction
Photopatch test
treatment
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Avoidance of contact
Other are the same as CD
Contact Urticaria
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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
Contact Urticaria
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Nonimmunologic:
• Caused by chemicals
• Direct pharmacologic action on
skin cells
• No sensitization necessary
• More common than suspected
Occupational Causes
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Latex allergy ( m/c )
Formaldehyde
Food industry
• Plants
• Vegetables
• Animal products
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Pharmaceutical industry
• Streptomycin
Clinical Features Of Contact Urticaria
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Hives (edema) appear on sites
of contact within minutes
The hives disappear within 1-4
hours
Mild: Only itching
Severe: Systemic symptoms
(anaphylaxis)
Contact Urticaria
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Nonimmunologic:
• Caused by chemicals
• Direct pharmacologic action on
skin cells
• No sensitization necessary
• More common than suspected
Management & Prevention
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Removal from exposure
Treatment of active disease
Preventive measures
Occupational Skin Cancers
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The second m/c form of
occupational skin diseases
About 17% of all cases of
occupational skin diseases
What Cancers?
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Malignant
lesions:
• Basal cell
carcinoma
• Squamous cell
carcinoma
• Malignant
melanoma
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Pre-malignant
lesions:
• Actinic (solar)
keratoses
• Tar keratoses
(‘warts’)
• Arsenical keratoses
• Keratoacanthoma
• Intra-epidermal
carcinoma (Bowen’s
disease)
• Lentigo maligna
‫زالل باش ‪، ....‬‬
‫زالل باش ‪، ....‬‬
‫فرقی نمی كند كه‬
‫گودال كوچك آبی‬
‫باشی ‪ ،‬یا دریای‬
‫بیكران ‪،‬‬
‫زالل كه باشی ‪،‬‬
‫آسمان در توست‬