3.14.1) SUMMARY
A) Irritant contact dermatitis may be caused by numerous agents and can be worsened in the setting of wet work, low humidity, friction, or pressure. It is one of the most common causes of occupational skin disorders.
B) Allergic contact dermatitis can occur following sensitization to an agent; hyperpigmentation may follow. Pigmented allergic contact dermatitis is a more severe form of this type of skin disorder.
C) Photosensitivity dermatitis may appear similar to irritant or allergic contact dermatitis and develops following contact with numerous chemicals or plants. It usually causes an initial stinging or burning sensation on the skin after sunlight exposure followed by hyperpigmented, nonpruritic lesions.
D) Other potential skin lesions that can occur in the occupational setting include: contact urticaria, chloracne, pigment alterations, and malignant neoplasms following chronic exposure.
3.14.2) CLINICAL EFFECTS
A) IRRITANT CONTACT DERMATITIS 1) DESCRIPTION a) Dermatitis due to chronic exposure to mildly irritating substances usually begins with erythema and progresses to eczema with oozing vesicles and papules, usually limited to the area of direct contact (Adams, 1983; Raffle et al, 1987). Crusts and scales may later form (Adams, 1983; Rosenstock & Cullen, 1986). b) The rash usually resolves spontaneously over 1-3 weeks when the offending irritant is removed (Adams, 1983). With stronger irritants, itching, stinging, and burning sensations may be noted, but are generally not as severe as seen with allergic contact dermatitis (Adams, 1983; Raffle et al, 1987). c) After days to weeks of chronic irritant exposure, the skin may feel thickened; lichenification, hyperpigmentation, and painful fissures may also develop (Adams, 1983; Raffle et al, 1987). Spread to remote areas of the body is rare in this setting (Adams, 1983; Mathias, 1994). d) In addition, unprotected wet work for 2 hours or longer daily (i.e., hairdressers {shampooing}) was considered to be a significant risk factor for the development of irritant dermatitis (Uter et al, 1999). The dental and allied health professionals are also exposed to wet work and at risk for irritant contact dermatitis (Kanerva et al, 1999). e) "Hardening" may be seen with daily continued exposure to irritating substances (i.e., the skin becomes tough and resistant at the site(s) of contact, allows further exposure to the irritant without development of irritation) (Adams, 1983; Raffle et al, 1987; Dahl, 1988). This protective "hardening" adaptation is rapidly lost; however, without ongoing irritant exposure (Adams, 1983). 1) An observational study of metalworker trainees reported the decrease of new cases of irritant dermatitis over time and related this occurrence to the effects of "hardening" despite ongoing exposure (Berndt et al, 2000).
2) INCIDENCE - Irritant contact dermatitis is the most common occupational disease involving the skin; 80% of contact dermatitis cases are due to an irritant (Cohen, 1998). 3) COMMON ETIOLOGIES- a) Nearly all substances can be contact irritants (Mathias, 1988), although contact with some of these agents (e.g., some alcohols, oils, and glycols) results in irritant dermatitis in only a small portion of exposed individuals (Adams, 1983; Dahl, 1988). b) STRONG IRRITANTS, many of which are caustic substances (e.g., sulfuric acid, hydrofluoric acid, sodium or potassium hydroxide, etc), cause chemical burns or contact irritant dermatitis (potentially after only one exposure) in almost everyone exposed (Adams, 1983; Rosenstock & Cullen, 1986; Dahl, 1988). Exposure can result in immediate irreversible and potentially scarring dermatitis, often described as an "etching reaction" (Cohen, 1998). c) MILD-TO-MODERATE IRRITANTS also known as MARGINAL IRRITANTS (e.g., soaps, organic hydrocarbon solvents, etc) generally produce irritant dermatitis in only a small portion of exposed individuals following a single contact, but will cause a reaction in nearly everyone with prolonged or repeated exposure (Adams, 1983; Rosenstock & Cullen, 1986; Dahl, 1988; Cohen, 1998). d) Irritant contact dermatitis may also be due to continued cumulative exposure to more than one irritating substance (Mathias, 1994). This repeated exposure can result in either eczematous dermatitis with clinical and histopathologic changes (similar to contact dermatitis) or a fissured, thickened eruption without a substantial inflammatory component (Cohen, 1998). e) A number of ENVIRONMENTAL FACTORS such as low relative humidity, friction, occlusion, lacerations or other mechanical skin damage, and excessive ambient temperature with sweating (which can put solid form irritants into solution) are predisposing factors (Adams, 1983; Raffle et al, 1987; Lammintausta & Maibach, 1988; Dahl, 1988; Abel & Wood, 1986; Berndt et al, 2000). 1) In one observational study of metalworker trainees, multiple factors (i.e., the combination of various chemical substances, pressure, and friction) prompted the development of hand eczema by injuring the horny layer, which is more likely to occur in persons with an atopic skin diathesis (Berndt et al, 2000).
f) Thresholds for irritant reactions vary from person to person, and may be due to a genetic component (Cohen, 1998). 1) Individuals with ATOPIC DERMATITIS are at increased risk for the development of irritant contact dermatitis (Adams, 1983; Raffle et al, 1987; Lammintausta & Maibach, 1988). Previous episodes of ECZEMA and the normal drying of the skin with aging are other predisposing factors (Raffle et al, 1987; Lammintausta & Maibach, 1988).
4) DIFFERENTIAL DIAGNOSIS - Irritant contact dermatitis is quite difficult to differentiate from allergic contact dermatitis, as these two conditions have a similar clinical and histologic appearance (Adams, 1983). B) CONTACT DERMATITIS 1) DESCRIPTION- a) Once sensitization has occurred by an offending substance, further exposure will result in a relatively rapid development of local inflammation with erythema, papule formation, induration, and weeping vesiculation beginning at about 12 hours postexposure and peaking in intensity at about 24 to 96 hours (Adams, 1983; Mathias, 1994). Since this is a true allergy, only small amounts will produce an overt reaction (Cohen, 1998).
b) Spread of the rash, either locally around the margins of the original site or at distant sites not in contact with the allergen, may occur in allergic contact dermatitis. Theoretically, the entire skin surface could become involved (Adams, 1983; Mathias, 1988; Raffle et al, 1987; Rosenstock & Cullen, 1986; Abel & Wood, 1986). Mucous membranes are usually spared in allergic contact dermatitis; also the scalp, soles, and palms are NOT commonly involved (Adams, 1983).
c) Allergic contact dermatitis, with or without inflammation, can result in hyperpigmentation of the skin and is often referred to as a lichenoid reaction. Pigmented allergic contact dermatitis is considered a more severe form of this condition (Penagos et al, 1996). Conversely, allergic contact dermatitis has resulted in contact leukoderma (Kumar & Freeman, 1999).
d) ONSET - In contrast to irritant contact dermatitis, allergic contact dermatitis tends to require a longer induction period with more severe itching, less erythema and more vesiculation, and an explosive rather than insidious onset (Adams, 1983; Cohen, 1998).
2) POTENTIAL RISK FACTORS a) A VARIETY OF FACTORS involving the allergen itself, patient factors, and environmental conditions can affect the development of allergic contact dermatitis.
b) ALLERGEN FACTORS include the physiochemical nature of the substance, its concentration and the total dose that contacts the skin, the actual site of contact, the total number and frequency of exposures, the vehicle (if present), and whether or not occlusion under clothing, gloves, etc has occurred (Adams, 1983).
c) Such PATIENT FACTORS as a history of previous irritant contact dermatitis (most important), age, genetic predisposition, gender, and pregnancy may influence the development of allergic contact dermatitis (Adams, 1983; Abel & Wood, 1986). Individuals with ATOPIC DERMATITIS may actually be at LESS RISK for developing allergic contact dermatitis (Adams, 1983). In some individuals, there may be a genetic component, which resides in specific human leukocyte antigen (HLA) alleles, that is associated with allergies to certain agents (i.e. nickel, chromium and cobalt) (Cohen, 1998).
d) ENVIRONMENTAL FACTORS of relative humidity, ambient temperature, and season of the year may also play a role (Adams, 1983).
3) COMMON ETIOLOGIES a) It is estimated that over 3000 chemical agents may cause allergic contact dermatitis (Cohen, 1998). Generally, low molecular weight chemicals (haptens - most less than 1,000 daltons) are responsible for causing allergic contact dermatitis; haptens penetrate the stratum corneum and link to epidermal carrier proteins to form a complete allergen (Cohen, 1998). Strong inorganic alkalis and acids seldom cause allergic sensitization (Adams, 1983). In an observation study of the dental profession, plastic chemicals and materials, rubber chemicals, disinfectants, antimicrobials and mercury and mercury salts were the most common causes of allergic contact dermatitis (Kanerva et al, 1999). b) While it is not possible to determine a substance's sensitization potential from its chemical structure alone, aromatic compounds with polar or ionic substituents and aminobenzene compounds with -NH2, -CH3, or -OH groups have been shown to be more potent sensitizing agents (Adams, 1983). c) Substances that commonly cause allergic contact dermatitis can be grouped as plants (i.e., Rhus plants such as poison ivy, poison oak, and poison sumac), rubber products (accelerators, antioxidants), plastic resins (epoxy, phenolic, formaldehyde, and acrylic resins; colophony), organic dyes (paraphenylenediamine, many others), topical medications (benzocaine, neomycin, thimerosal), germicidal and biocidal preparations (formaldehyde and formaldehyde releasing compounds, parabens, quaternary ammonium compounds, derivatives of isothiozolin-3-one), and various common commercial and medication product ingredients (antioxidants, fragrances, ethylenediamine) (Mathias, 1988; ILO, 1983; Abel & Wood, 1986). d) LATEX ALLERGY - 1) SUMMARY - Increased exposure in recent years to personal protective equipment (i.e., rubber gloves) in health care workers has led to increased reactivity patterns and to sensitization in some individuals (Brown et al, 1998; Cohen, 1998). a) CASE SERIES - In a prevalence study (methods included a clinical questionnaire, serum levels, skin testing and a two-stage latex glove provocation procedure) of anesthesiologists and nurse anesthetists (n=168), the prevalence of latex allergy with clinical symptoms and latex sensitization without clinical symptoms was 2.4% and 10.1%, respectively; prevalence of irritant or contact dermatitis was 24% (Brown et al, 1998). 1) COMMON SYMPTOMS - Exposure to natural rubber latex can produce the following: mild rhinoconjunctivitis and hives to life-threatening asthma and anaphylaxis.
2) RISK FACTORS - Potential risk factors for developing sensitization were likely to be due to the presence of skin symptoms with the use of powdered gloves (common findings included hives, rash, swelling, itching, redness and irritation), a history of allergies to selected foods (i.e., bananas, avocados, or kiwis) and a history of atopy. NO correlation between duration of exposure (either by age or years of exposure), gender or ethnic differences were observed in this study (Brown et al, 1998).
e) Cross-reacting substances in individuals sensitized to Rhus plants may be exotic woods (e.g., mango tree, cashew nut tree, Japanese lacquer tree, Indian marking nut tree), lacquers or varnishes derived from the Japanese lacquer tree or objects coated with them, and a resinous oil derived from the cashew nut tree utilized in such applications as brake linings, plastic coatings and resins, and various lubricants (Mathias, 1988; ILO, 1983). f) By chemical classes, common allergens causing contact dermatitis can be classified as aromatic amines, caine-type local anesthetics, phenolic compounds, benzothiazoles, thiurams, the Streptomycin group of antibiotics, ethylenediamine compounds, halogenated germicides, hydroxyquinolines, and phenothiazines. All members of these chemical classes generally also have cross-sensitivity (Adams, 1983). g) Allergic contact dermatitis may also occur due to some airborne contaminants (i.e., dichromates in cement dust, rosins used in soldering operations, various epoxy resins and aliphatic amine catalysts, sawdust from exotic woods, and various allergenic plant pollens or Rhus-type plant oleoresins carried on pollen) (Adams, 1983). 4) DIFFERENTIAL DIAGNOSIS a) The major clinical entity commonly confused with allergic contact dermatitis is irritant contact dermatitis; NO absolute clinical features differentiate the two conditions (Adams, 1983; Rosenstock & Cullen, 1986). b) Depending on the severity and clinical presentation, other conditions that must be ruled out include: atopic dermatitis, pustular eruptions on the palms and soles, psoriasis, herpes rashes (simplex and zoster), insect bites, fungal infections of the feet with idiopathic vesicular reactions, nummular eczema, drug eruptions, and erythema multiforme (Adams, 1983; Raffle et al, 1987; Rosenstock & Cullen, 1986). c) DIAGNOSIS 1) NO absolute clinical features allow the differentiation between allergic or irritant contact dermatitis (Adams, 1983; Rosenstock & Cullen, 1986). Allergic contact dermatitis; however, usually causes more severe itching and burning sensations, less erythema but more vesiculation, and the onset tends to be explosive rather than the insidious onset common with irritant contact dermatitis (Adams, 1983). A further diagnostic clue is possible spread of the rash to areas remote from the site of actual contact (Adams, 1983).
C) PHOTODERMATITIS 1) DESCRIPTION a) SUMMARY - Ultraviolet light can produce two effects on the skin: phototoxic or a photoallergic response (Cohen, 1998). Photodermatitis requires activation of a chemical on the skin by ultraviolet radiation (290 to 400 nm wavelength); compounds that contain aromatic rings in their molecular structure and absorb ultraviolet radiation are capable of producing symptoms (Mathias, 1994). b) The skin lesions of photosensitivity dermatitis generally resemble those of irritant and/or allergic contact dermatitis, but they are mainly found on such sun-exposed areas as the face, upper anterior chest, posterior portion of the neck, extensor surfaces of the forearms, the dorsum of the hands and feet, and the anterior surfaces of the lower legs (Adams, 1983; Mathias, 1994). c) Skin areas normally covered by jewelry and clothing are spared, as are the submental areas, upper portions of the ears covered by hair, and eyelids (Adams, 1983; Mathias, 1994). d) Lesions have been described as: discrete or confluent, polymorphous linear streaks and/or patches which are macular, hyperpigmented, and nonpruritic (Gross et al, 1987). A stinging or burning sensation of the skin may be described beginning shortly after sunlight exposure (Mathias, 1994). 1) Lichenification and hyperpigmentation may occur, and the skin lesions may persist for months or years. In some cases, widespread skin involvement may later develop (Adams, 1983).
2) COMMON ETIOLOGIES a) Psoralens contained in the oil released by puncturing limes with scissors were responsible for an outbreak of photosensitivity dermatitis in children at a summer camp who handled the lime skins in a crafts class (Gross et al, 1987).
b) Musk ambrette in aftershave lotions; 6-methylcoumarin, homosalicylate, and PABA in sunscreens; and diphenhydramine have all been responsible for cases of photosensitivity dermatitis (Adams, 1983).
c) Germicidal agents in soaps and detergents and perfume ingredients may cause photosensitivity dermatitis (Adams, 1983).
d) A wide variety of plants can produce symptoms, especially in individuals who routinely handle or harvest them (Mathias, 1994). The photoactive ingredients in plants that are able to produce the reaction are likely to be psoralens or furocoumarins; some examples of photoallergens are celery, parsnip, dill, fennel, wild carrot, and wild parsnip and all members of the Umbelliferae family (Cohen, 1998).
e) A similar condition, photoallergic drug reaction, can be caused by a variety of systemically administered medications (e.g., griseofulvin, nalidixic acid, phenothiazines, psoralens, sulfonamides, sulfonylureas, tetracyclines, thiazide diuretics, and various phototoxic oils used in fragrances) (Adams, 1983; Cohen, 1998).
f) Phototoxic or photoallergic reactions may occur in pharmacists, nurses, and others who routinely have skin contact with these drugs (Mathias, 1994).
3) DIFFERENTIAL DIAGNOSIS - Photosensitivity dermatitis from direct dermal contact with the offending substance must be differentiated from allergic contact dermatitis due to airborne contaminants, photoallergic drug reaction, polymorphous light eruption, systemic lupus erythematosis, pellagra, dermatomyositis, and porphyria (Adams, 1983; Mathias, 1988; Lachapelle, 1987). D) CHLORINE ACNE 1) DESCRIPTION a) The skin lesions of chloracne consist of straw-colored cysts, numerous comedones and milia, and papules (Adams, 1983; Raffle et al, 1987).
b) Pruritus is common (Adams, 1983; Mathias, 1988). The lesions are located on the face (especially at "crow's feet" and below and lateral to the eyes), neck, earlobes, shoulders, abdomen, legs, and genitalia; the nose is often NOT included (Adams, 1983; Raffle et al, 1987; Mathias, 1994).
c) With severe chloracne, all the follicles in an area may be involved, resulting in a rather bizarre "pebbled" appearance. Inflammatory lesions with larger cysts and abscesses are later developments (Adams, 1983). Scarring may be seen. Intense itching occurs in about 50% of cases (Adams, 1983; Mathias, 1988).
d) Increased fragility of the skin, hypertrichosis, widespread follicular hyperkeratosis, or hyperpigmentation may develop. A brownish discoloration of the nails, swollen eyelids, and conjunctivitis or discharge may be present in some cases (Adams, 1983).
2) COMMON ETIOLOGIES- a) SUMMARY - Exposure to halogenated aromatic hydrocarbons (sometimes referred to as "halogen acne") can produce chloracne. Over time sebaceous glands are destroyed and hyperkeratosis can occur (Mathias, 1994; Cohen, 1998). Typically, chloracne is resistant to treatment, including systemic retinoids, and may persist decades after exposure (Cohen, 1998).
b) A variety of chlorinated organic compounds can cause chloracne, including chlorinated naphthalenes, polychlorinated biphenyls, dioxins, polychlorinated dibenzofurans, pentachlorophenol, azobenzenes, and azoxybenzenes (Adams, 1983; Raffle et al, 1987; Hryhorczuk et al, 1981; Mathias, 1994). It is considered a relatively rare skin disorder (Cohen, 1998).
3) DIFFERENTIAL DIAGNOSIS - Oil acne or folliculitis (from exposure to grease and oils), acne vulgaris, acne cosmetica (from heavy cosmetic use), acne mechanica (from local pressure and friction), acne medicamentosa (from a variety of medications including corticosteroids, hormonal preparations, phenytoin, iodides, and bromides), solar elastosis with comedones, and acne due to excessive intake of iodides in kelp tablets must be differentiated from chloracne (Adams, 1983; Mathias, 1988). E) SKIN PIGMENTATION 1) DESCRIPTION a) Lesions may be either hypo- or hyper-pigmented (Gian et al, 1985; Mathias, 1988; Raffle et al, 1987), and may be associated with the development of allergic contact dermatitis in some cases (Gian et al, 1985; Mathias, 1988; Penagos et al, 1996; Kumar & Freeman, 1999).
2) COMMON ETIOLOGIES a) HYPOPIGMENTATION is primarily caused by phenolic and catecholic compounds, such as hydroquinone and its monoethyl and monobenzyl ethers; paracresol; para-tertiary butylcatechol, butylphenol, and amylphenol; ortho-phenylphenol; ortho-benzyl-chlorophenol; epoxy resin; colophony; and 4-isopropylcatechol (Mathias, 1988; ILO, 1983; Raffle et al, 1987; Rosenstock & Cullen, 1986; Gellin, 1982; Kumar & Freeman, 1999). b) Production of a powder form of N,N'-methylene-bis-(2-amino-1,3,4-thiadiazole) was responsible for an outbreak of pigment-change skin lesions in production workers and children in a nearby school (Gian et al, 1985). 1) MECHANISM - The apparent mechanism is due to either destruction or inhibition of melanocytes by the offending substance or chemical. The appearance of contact leukoderma may be difficult to distinguish from idiopathic vitiligo. In two cases, the presence of leukoderma occurred in areas that corresponded to a preceding allergic contact dermatitis; allergy was confirmed by patch testing (Kumar & Freeman, 1999).
c) HYPERPIGMENTATION can follow dermal inflammation from any cause (e.g., inflammatory physical stimuli like heat, other radiations, trauma and friction), especially allergic contact dermatitis (Mathias, 1988; ILO, 1983; Paul et al, 1998). Allergic contact dermatitis, with or without inflammation, can result in hyperpigmentation of the skin and often referred to as a lichenoid reaction. Pigmented allergic contact dermatitis is considered a more severe form of this condition (Penagos et al, 1996). 1) CASE REPORT - A furnace worker that was exposed to an open furnace for 2-8 hours daily for over 22 years, developed hyperpigmentation (no erythema or telangiectasia) following long-term exposure to heat. Following a job change and the use of topical hydroquinone 4% and sunscreen, hyperpigmentation improved by 25% in 6 months and 50% by 14 months (Paul et al, 1998).
d) Coal tar pitch, creosote, and various aromatic chlorinated hydrocarbons can stimulate overproduction of melanin pigment (ILO, 1983; Raffle et al, 1987; Rosenstock & Cullen, 1986). 3) DIFFERENTIAL DIAGNOSIS a) HYPOPIGMENTATION due to occupational or environmental chemical exposure must be differentiated from idiopathic vitiligo and pigment loss due to tissue destruction from chemical or thermal burns (Mathias, 1988; Raffle et al, 1987).
b) HYPERPIGMENTATION should not be confused with direct skin staining or discoloration due to contact with such substances as heavy metals, nitrosylated compounds (nitric acid, dinitrophenol, etc), and coal dust (Mathias, 1988; Rosenstock & Cullen, 1986).
4) DIAGNOSIS - In most cases, the history and physical examination should be sufficient for diagnosis of pigment alterations. Loss of melanin in light-complexed individuals can be detected by failure of affected skin areas to fluoresce under a Wood's (UV) lamp (Raffle et al, 1987). F) CONTACT URTICARIA 1) DESCRIPTION a) The skin lesion of contact urticaria is a localized wheel-and-flare response (hive) which develops a few minutes to about one hour after direct dermal contact with certain rapidly absorbed substances (Adams, 1983; Cohen, 1998). b) A large number of patients afflicted with this disorder, however, present with complaints of a variety of skin sensations such as itching, burning, or tingling, recurrent bouts of dermatitis, or generalized urticarial reactions (Adams, 1983). 1) It is commonly referred to as CONTACT URTICARIA SYNDROME and may be accompanied by complaints of asthma, rhinitis, conjunctivitis, oropharyngeal symptoms (itching and tingling sensations or edema of the lips, tongue, and mouth; throat irritation), or gastrointestinal signs or symptoms (Adams, 1983).
2) Otherwise unexplained attacks of vascular collapse (anaphylactoid reactions) may occur in patients having this syndrome (Adams, 1983).
2) COMMON ETIOLOGIES - a) The NONIMMUNOLOGIC FORM has been provoked by contact with acids (acetic, benzoic, butyric, cinnamic, sorbic), alcohols (ethyl-, butyl-), balsam of Peru, benzocaine, cinnamic aldehyde, cobalt chloride, dimethylsulfoxide, formaldehyde, sodium benzoate, and thurfyl nicotinate (Adams, 1983; Raffle et al, 1987). b) IMMUNOLOGIC CONTACT URTICARIA has been caused by a wide variety of common chemicals (various alcohols, ammonia, parabens, polyethylene glycol, etc); medications (bacitracin, cephalosporins, chloramphenicol, gentamicin, lindane, neomycin, salicylic acid, etc); animal products (hair, dander, saliva, serum, placenta); foods (eggs, flour, meats, produce, milk, spices); textiles (silk, wood, rubber); food; cosmetics (hair spray, nail polish, perfumes); seminal fluid; and cold (Adams, 1983; Mathias, 1988; Raffle et al, 1987). 1) LATEX - The latex in rubber gloves has become an increasing source of contact urticaria in health-care workers; the reaction is caused by the inhalation of the latex protein (powder from gloves is frequently inhaled during removal of gloves) which can trigger a severe allergic reaction (Cohen, 1998).
c) UNCERTAIN MECHANISM-MEDIATED CONTACT URTICARIA has been related to exposure to ammonium persulfate, or can be solar (visible and/or ultraviolet light) related or aquagenic (caused by direct skin contact with water, saline, or the patient's own perspiration) (Adams, 1983; Raffle et al, 1987). 3) DIFFERENTIAL DIAGNOSIS - Contact urticaria must be differentiated from urticaria due to systemic exposure to allergens and erythema multiforme. G) INFECTION OF SKIN 1) SUMMARY - Workers exposed to animals or natural environments may be at increased risk for the development of primary or secondary infections due to biologic agents. Infections can be either cutaneous or result in systemic infections (due to possible trauma or "breaks" in the skin) (Cohen, 1998). The more common infectious agents that may develop during occupational exposure are discussed below.
2) BACTERIA - Staphylococcus and streptococcus are the most common bacteria for producing routine trauma-induced cutaneous infections, while Erysipelothrix rhusiopathiae inhabits the surface of fresh and saltwater fish, crustacea, and poultry which can infect fisherman and butchers (Cohen, 1998).
3) FUNGI - Can result in localized cutaneous disease. Yeast (Candida) infections are opportunistic, and can occur in workers continually exposed to wet work (e.g., bartenders, fruit processors). Gardeners and landscapers (individuals who frequently come in contact with the soil) can develop sporotrichosis via entry by trauma to the skin, and is generally treated with systemic imidazole antifungals (Cohen, 1998).
H) MALIGNANT NEOPLASM OF SKIN 1) DESCRIPTION a) Skin cancers induced by occupational or environmental substances or factors may include basal cell carcinoma, squamous cell carcinoma, malignant melanoma, keratoacanthoma, and Bowen's disease (intraepidermal squamous cell carcinoma) (Adams, 1983; Rosenstock & Cullen, 1986; Mathias, 1994). b) When a patient presents with any of these malignant lesions, the history of possible exposure to known carcinogenic agents should be explored. 1) Chronic exposure to compounds containing POLYCYCLIC AROMATIC HYDROCARBONS (PAHs) first results in a burning sensation and diffuse dermal erythema. Edema, skin thickening, and a yellowish-brown discoloration develop next, followed by folliculitis and comedones which itch intensely (Adams, 1983).
2) Poikilodermatous changes then occur (irregular areas of dermal atrophy, patchy areas of hypo- and hyper-pigmentation, diffuse telangiectasia) (Adams, 1983).
3) "Tar warts" (keratotic papillomas) develop in areas with poikilodermatous changes, and may rarely develop into squamous cell carcinomas (Adams, 1983; Cohen, 1998).
4) Patients exposed may also develop basal cell carcinomas or keratoacanthomas (Adams, 1983).
c) Exposure to INORGANIC ARSENICAL COMPOUNDS causes a variety of skin lesions, often beginning with mild erythema and hyperhidrosis of the palms and soles, followed by the development of slightly raised, firm, generally symmetrical punctate keratoses (Adams, 1983; Mathias, 1988; Peters et al, 1984). 1) White colored, nonraised hyperkeratoses may also develop on the ankles, shins, and dorsum of the hands. 2) A diffuse hyperpigmentation of the skin interspersed with white, somewhat atrophic macules ("raindrops on a dusty road" appearance) may also be seen (Mathias, 1988). 3) Basal cell and squamous cell carcinomas may then develop (Adams, 1983; Mathias, 1988) ILO, 1988). 4) BOWEN'S DISEASE may also be seen following chronic inorganic arsenical exposure (Adams, 1983; Mathias, 1988). a) Bowen's disease consists of randomly distributed, sharply demarcated, erythematous, scaling lesions that range in size from a few millimeters up to 1 to 2 centimeters in diameter and grow only slowly; it rarely metastasizes (Adams, 1983).
2) COMMON ETIOLOGIES a) Skin cancers caused by substances or factors that may be encountered in the workplace or general environment include those due to ultraviolet light (including sunlight).
b) Exposure to various polycyclic aromatic hydrocarbons (PAH's) found in a variety of products including soot, coal tar and coal tar products, pitch, creosote, oils (cutting oil, mineral oil, shale oil), and petroleum; ionizing radiation (beta rays, gamma rays, X-rays, gamma particles, protons, neutrons); inorganic arsenical compounds; and physical trauma may all potentially lead to the development of skin cancer (Adams, 1983; Mathias, 1994).
c) DIFFERENTIAL DIAGNOSIS - All potentially cancerous skin lesions must be differentiated from benign lesions.
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