Structure Function Occupational disorder
Stratum corneum Barrier against chemicals,
microorganisms, and some radiationChapping from low humidity, chemical stains
Squamous cells/basal cells Cell regeneration, synthesis of
stratum corneum, wound repair Infection, contact dermatitis, neoplasms
Connective tissue Mechanical protection against trauma, wound repair, development of scar tissue
Infection, granulomatous reactions, scleroderma, solar elastosis, scarring
Hair follicles Insulation and protection, secondary sensory organs
Folliculitis, traumatic or toxic alopecia
Melanocytes Absorption of UV radiation Toxic vitiligo, melanoma, hyperpigmentation Eccrine sweat glands Thermoregulation, buffering of skin
surface Miliaria, ‘rusting’
Sebaceous glands Synthesis of skin lipids, chemical
barrier against microorganisms Oil acne, chloracne Nerve tissue elements,
Merkel cells, other sensory receptors
Perception, sensation Toxic neuropathies
Blood vessels, mast cells Thermoregulation, nutrition of tissue Heat stroke, urticaria, flushing reactions, vibration white finger Langerhans cells, dermal
macrophages
Immune regulation and surveillance Delayed hypersensitivity reactions
■ a description of the skin lesions and their initial anatomical locations and (if any) spread to other body sites
■ disability caused by the skin condition
■ identification of all relevant skin exposures
■ identification of skin protection controls
■ identification of personal hygiene and skin cleansing methods
■ presence of skin disease in coworkers exposed to similar risks
■ response to previous medical treatment
■ whether the skin problem improves while away from work
■ any factors which exacerbate the symptoms
■ identification of other risk factors, such as personal or family history of atopic allergies, previous skin problems, medications, potential causative factors in the domestic environment (second job, hobbies, outside activities, and so forth).
These may need to be followed up by contact with the employer, and possibly a workplace assessment.
Physical examination
The physical examination must assist in the differentiation of occupational from nonoccupational skin disorders. For example, some patterns of dermatitis are suggestive of endogenous dermatitis—localised dermatitis spreading towards the heel of the palm is probably always endogenous, as is involvement of elbow and knee creases. Therefore, the entire skin should be examined for the presence of skin lesions.
The patch test
Although virtually any diagnostic procedure can be used to evaluate suspected occupational dermatitis, the patch test is the most frequently employed. This is a simple but useful diagnostic tool.
Firstly, a small amount of the suspect substance is placed on a metal disc or filter paper backed with aluminium foil. This disc (the patch) is placed on adhesive tape with a number of other patches (normally 10–20) containing a range of routine ‘screens’
(compounds known to cause positive reactions). The adhesive tape is then placed on the upper back or (rarely) the upper, outer arm. Both the patch and the tape are impermeable to water, thus providing total occlusion of the test (and screen) substances against the skin (Freeman 1991).
Test strips are removed about 2 days later, and the sites evaluated. A positive reaction is scored in the presence of numerous papules or vesicles. Weaker reactions (skin redness or swelling without papules or vesicles) cannot be reliably distinguished from false-positive marginal reactions alone. Test sites should be re-evaluated 72–96 hours following initial application, since 30–40% of all positive readings will be equivocal or negative at the 48 hour reading.
The patch test should not be used to diagnose irritant contact dermatitis since the conditions of the test seldom approximate the actual conditions under which exposure occurs.
Common occupational skin disorders
Contact dermatitis
Contact dermatitis (also called contact eczema) is by far the commonest occupational dermatosis (Shama 1988; Stevenson 1989; Adams 1990; Nethercott 1994; Halkier-Sorensen 1996; ATSDR 1996; Rycroft et al. 2001). The term refers to changes in the skin, usually accompanied by inflammation, from direct skin exposure to exogenous physical or chemical agents (Linn Holness 1994). Inflammation is provoked by two mechanisms: irritation or allergy (Lachapelle 1986). A key diagnostic feature is itching.
The resulting skin lesions are difficult to differentiate clinically, since each can appear as acute or chronic forms.
The acute form is erythmatous (increased skin redness), may be vesicular (small blisters), bulbous (large blisters), oedematous (swollen) or oozing. This form is usually of short duration, lasting days or weeks.
The chronic form has some of these features, although it is more likely to be lichenified (thickened), scaly, and fissured, which can last for years.
One important clinical feature of occupational contact dermatitis is the distribution of the dermatitic lesions. These generally occur on those areas of the skin which have come into contact with the irritating or allergenic agent (Burry 1982). At work, the most common areas for skin lesions are the hands, wrists and forearms, where they come into contact with materials by dipping or washing. Dusts and mists may affect other areas, such as the forehead, eyelids, face, ears and neck. Areas can be affected where agents accumulate, such as beneath watch straps, collars or waistbands, and in creases and folds of skin (Coenraads et al. 1985).
Physical damage, such as abrasion or erosion, may also predispose a person into developing a contact dermatitis reaction.
Other, less indirect factors include:
■ skin thickness
■ sweating
■ personal or environmental hygiene
■ medications
■ alcohol, smoking and other social drug use
■ season of the year or climatic conditions
■ pigmentation.
Finally, individuals may have an innate genetic susceptibility to developing dermatitis.
This predisposition is called atopy.
Irritant contact dermatitis
Primary irritants damage the skin because they are irritating. Almost any substance can be a contact irritant.
Irritants are generally divided into strong and mild types. Strong irritants include strong acids, alkalis, aromatic amines, and many metallic salts. They produce an irritating effect within minutes after contact. A feature of many strong irritants is their ability to damage the skin irreparably, causing eschar formation (scarring). An irritant that causes permanent skin damage is also called a corrosive.
On the other hand, mild irritants, such as detergents, solvents, oils, soap and water, can require repeated and prolonged exposures for many days before clinical changes occur in skin. Mild skin irritants cause many cases of occupational irritant dermatitis and are a major problem in the workplace. One reason for this is that the systems for dealing with mild irritants are unlikely to be present in the work-place—while people know to be careful about acids, taking basic preventive measures is not so obvious when, for example, using shampoo in a hairdressing establishment.
Common skin irritants, either in the domestic or occupational environment, are shown in Table 5.4.
Important hazard properties of a primary skin irritant are:
■ pH
■ solubility
■ molecular size (large molecules of molecular weight >1000 are poor penetrants in general)
■ ionisation and polarity
■ physical state
■ concentration of the irritant within the material Important risk properties of a primary skin irritant are:
■ duration of contact
■ intensity of contact
■ occlusion.