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Occupational dermatoses
Occupational dermatoses Vincent S Beltrani, MD*
INTRODUCTION Shortly following the passage of the Occupational Safety and Health Act (OSHA) of 1970, 45% of the annually recorded occupational illnesses were dermatologic. That act has instigated workers’ compensation data to identify known and emerging workplace cutaneous hazards which has been applied for targeting prevention efforts.1 Nonetheless, skin disorders still rank second when viewed as a proportion of all work-related illness by organ system. The dermatologist’s definition of an occupational skin disease is “a cutaneous disorder caused by or otherwise expressed as the result of factors primarily associated with the workplace.” The three operational criteria useful to identify a skin disorder as occupational are as follows2: • The skin disorder should have developed for the first time while the patient was on a job presumably associated with that skin disorder. • The skin disorder should clearly improve when the patient is away from the work environment and flare while on the job. • There should be a plausible etiologic agent in the workplace that can be linked to the expression of the skin disorder. The importance of temporal factors notwithstanding, cause is the most important element of this definition. It is conceivable with job-related disorders that anxiety concerning job security, as well as other factors of a demanding nature, may cause a delay of diagnosis and treatment. (The average delay was reported to be 8.6 months by Rusca et * Associate Clinical Professor, Department of Dermatology, College of Physicians & Surgeons, Columbia University, New York, New York; and Associate Clinical Professor, Division of Allergy, Immunology & Rheumatology, University of Medicine and Dentistry of New Jersey, New Jersey Medical School.
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al3). Only when causality is traced to the workplace can an otherwise conventional skin condition be acknowledged as an occupational dermatosis. In order of frequency, the direct causes of occupational dermatoses are classified as chemical, mechanical, physical, and biologic in nature. Of work-related cases involving the skin, 90% to 95% will be a contact dermatitis. In fact, most cases of contact dermatitis treated by physicians, in some way, are work related. The laws of most states require that in those cases in which there is any (possible) work relationship, it must be reported. It is essential that the correct diagnosis be made, and both the cause and all secondary factors be specified. An addendum to the medical criteria for establishing a dermatosis as work-related, the Workers’ Compensation Laws state, “As long as the dermatitis has a definite work relationship, even though there may be other non-work related factors, the case is compensable under the laws of all the states.” The essential statutory criterion is whether or not the work constitutes a substantial contributing factor in the development or aggravation of the skin condition. Predisposing Host Factors As with all disease processes, host factors must be considered essential as a predisposing contingency. The important host factors considered to influence occupational skin problems are listed below: • Intellectual ability of worker • Anatomic site • Atopic diathesis • Pigmented skin • Aged skin • Immunosuppressed individuals These factors will be described with specific examples later in this paper.
Predisposing Environmental Factors Environmental factors, each of which can increase the vulnerability for injury, such as low ambient humidity and cold decrease the water content of the stratum corneum.4 Cold temperatures also reduce the plasticity of the horny layer causing cracking and fissuring of the stratum corneum. Occlusion increases the water content of the stratum corneum (by preventing evaporation), with consequent enhanced percutaneous absorption of water-soluble substances. Exposure to irritants is the cause of 80% of all occupational dermatoses. Many agents may act as both an irritant and an allergen. Infections are most likely to occur in health care workers, farm workers, and meat handlers. CONTACT DERMATITIS “Contact dermatitis” is defined as “any” change of the skin and/or its appendages (hair, nails, and mucus membranes) resulting from contact or “exposure” to an exogenous (chemical and/or physical) agent. While most of the skin changes of contact dermatitis manifest a spectrum of cutaneous inflammation, the clinical picture is often “suggestive” but rarely “pathognomonic.”5 To complicate matters there is a subclass of contact-induced disorders that result from, and present in different situations, ie, require the presence of ultraviolet light to produce a reaction (ie, tar and sunlight for road construction workers and roofers), other contact-induced reactions affect pigment cells producing hyperpigmentation (arsenic, halogenated hydrocarbons, and phototoxins cause a brown discoloration), hypopigmentation, or depigmentation (catechol and phenolic derivatives found in germicides, disinfectants, etc, have been associated with occupational vitiligo).
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Most common is irritant contact dermatitis, identified when the contact-induced inflammatory change is non-immunologic, and the clinical picture is the result of cellular damage by the irritating agent. Only when the contact-induced inflammatory skin changes are compatible with a recognized immunologic response to a putative hapten, is the contact dermatitis labeled allergic contact dermatitis. Irritant Contact Dermatitis The lack of a standard case definition for irritant contact dermatitis (ICD), and the precise expertise required for making the diagnosis of the varied types of ICD, results in the common misclassification of ICD, which results in either an overestimation or underestimation of disease frequency.6 The most frequent causes of ICD are water, soaps/detergents, fiberglass and particulate dusts, food products, cleaning agents, solvents, plastics and resins, petrolatum products and lubricants, metals, and machine oils and coolants.7 In contrast to allergic contact dermatitis, ICD is not a distinct clinical entity, but rather a spectrum of abnormal skin changes. The clinical aspect of ICD is dependent on a dose and timeeffect relationship.8 A severe, acutely inflammatory reaction caused by “strong,” primary irritants may include necrosis and ulcerations. While chronic lesions present with lichenification, excoriations, scaling, and hyperkeratosis. The hands are most frequently affected by ICD, since they interact most with the environment and have frequent contact with many irritants. The spectrum of ICD is described as9: • Acute • Acute delayed • Irritant reaction • Cumulative • Traumatic • Exsiccation eczematid • Pustular and acneiform • Subjective Acute ICD occurs when the skin is exposed to a potent irritant (eg, acids and alkaline solutions). Usually this
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results from an accident at work. With appropriate, symptomatic management, the prognosis for this type of ICD is usually good, and unless the dermis is damaged there should be no permanent scaring. Most often a (medical) assignment of “temporary partial disability” is given to these “accidents” at work. Precautions regarding avoidance of a recurrent accident should be reviewed prior to returning to the same job. Acute delayed ICD is characteristic for certain irritants, such as benzalkonium chloride (eg, Zephiran—an extensively used preservative and disinfectant), that elicits a retarded (8 to 24 hours after exposure) inflammatory reaction. Except when these chemicals are applied to compromised skin, ie, atopics, or xerotics, adverse reaction on “normal” skin must be considered “idiosyncratic.” The inflammatory reaction rarely needs treatment, and resolves with cessation of exposure. These reactions are rarely awarded more than a “temporary partial disability” assignment. Irritant reaction ICD is a subclinical form of contact dermatitis, seen in workers whose hands are excessively wet, such as hairdressers, bartenders, or caterers. Often times scaling and erythema is first noted under rings and then spreads over the fingers to the hands and the forearms. It usually effects the dorsum of the hands, where the skin is “thinner,” but irritants can also cause some vesiculation resembling dyshidrotic eczema. Frequently, irritant reaction ICD resolves spontaneously, but more often it progresses to cumulative irritant dermatitis. Patients with a history of atopic dermatitis should be dissuaded to choose an occupation requiring “wet work.” Anyone whose hands are immersed in water several hours a day will become “irritated.” While the skin of “normals” will heal spontaneously when removed from the irritating agent, the abnormal skin of atopics and xerotic individuals lacks that resiliency. This can be an example of the “permanent partial disability.” The patient can no
longer do “wet work,” but can certainly be assigned other type work. Cumulative ICD is a consequence of multiple subthreshold damages to the skin with the time between exposures being too short for resolution of skin barrier function. Patients with “sensitive skin” (ie, atopics) have a decreased irritant threshold or a prolonged restoration time making them more vulnerable to clinical ICD. Cumulative ICD is not dependent on exposure to a potent irritant, but exposure to weak irritants prompts the reaction. Often, the exposure (ie, water) is not only at work but also at home. These patients complain both of itching and pain due to fissuring of the hyperkeratotoic skin (“chapping”). Exsiccation eczematid is the ICD seen mainly in elderly individuals who wash, shower, or bathe too often without remoisturizing their skin. These patients present with very itchy, dry, scaling hands. It is more common during the winter months, when humidity is low. Traumatic ICD may develop after acute skin trauma, such as burns, lacerations, and acute ICD. The latter is seen most often after the use of “harsh” cleansers used at work. The continued use of the “irritant” causes this condition to persist and may require months after discontinuing the irritant before it resolves. Harsh soaps should be replaced by an appropriate soap. Soap is used to emulsify an unwanted material on the skin. Most often a specific cleanser, for the substance that is to be removed can be found, and it should be “harmless,” yet effective. This should definitely be the responsibility of the employer, and a “temporary partial disability” can be resolved. Pustular and acneiform ICD is a result of exposure to certain irritants, such as croton oil, mineral oil, tars, greases, and naphthalenes. This diagnosis should always be considered when acneiform lesions appear in postadolescent patients who never had teen-age acne. Subjective ICD or sensory ICD is characterized by the lack of objective
ANNALS OF ALLERGY, ASTHMA, & IMMUNOLOGY
clinical signs. Some acids (ie, lactic) may cause stinging and burning with no visible cutaneous irritation. These reactions are usually dose-related, and are likely to occur in all individuals exposed. The best example of these type reactions is the typical stinging reaction that occurs after applying “after-shave” lotion! More often patients complaining of subjective symptoms without objective finding present themselves as having the “20th Century disease” or multiple chemical hypersensitivities, recently renamed idiopathic environmental intolerances (IEI). Their litany of varied and subjective complaints, for which they have been told by a “clinical ecologist,” are the result of exposure to minute amounts of “toxic” substances. The self-serving symptomotology progressively associates the subjective complaints to virtually ubiquitous environmental exposures. The Academy of Allergy has exhaustively reviewed the available literature regarding this entity, and have issued a definitive position paper concluding “There is no evidence that these patients have any immunologic or neurologic abnormalities. . . A casual connection between environmental chemicals, foods, and/or drugs and the patient’s symptoms is speculative and not based on the results of published scientific studies!”10 The hearings officer (compensation judge) must listen to both sides, recognizing that those who proselytize the diagnosis can be teleologically convincing. Presenting the position paper of the Academy (which I always equate to a policy issued by the American Bar Association)—at the hearing is frequently most helpful. Allergic Contact Dermatitis (ACD) Few terms are more misused both by the layman and physician, than the term “allergic” when describing an adverse medical event. The hallmark of the allergic phenomenon is its specificity, recognized as a predictable clinical and histologic immunologic inflammatory reaction, which occurs exclusively in susceptible individuals who have the ability to elicit that specific response,
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only when exposed to a specific allergenic agent. In the workplace, the factors for allergic reactions to be considered are (1) the host or employee, (2) environmental factors, (3) a putative agent, and (4) the type of immunologic reaction [eg, type I–IV as describe by Gell & Coombs]. Host factors. Recognizing the risk factors which predict susceptibility to allergic reactions in worker populations through prescreening of prospective employees could prevent many potential cases of allergic dermatoses; however, the Americans With Disabilities Act (enacted in 1991) prohibit such pre-employment screening.11 Nevertheless, the genetic predisposition for atopy, which is estimated to be present in 20% of the general population identifies these individuals who are at constant risk to develop immediate (type I) reactions to common aeroallergen resulting in allergic rhinitis, asthma, and contact urticaria. The prevalence of dermatologic occupational allergies is greater among atopic than nonatopic workers, including health care workers exposed to natural rubber latex gloves, detergent workers sensitized to microbial enzymes, and laboratory animal workers exposed to epidermal and/or urinary proteins.12 While is was suspected that their suppressed cell-mediated immunity decreased the atopics susceptability to develop ACD (type IV reactions), it was later observed that the reduced rate of sensitization (to DNCB) was only present in patients with severe dermatitis (⬎70% body surface area involvement).13 Subsequent testing when the dermatitis was well controlled noted an increased rate of pos-
itive reactions, suggesting that reduced sensitization is a reversible epiphenomenon of severe atopic dermatitis activity. As already noted above, regarding the atopics increased susceptibility for ICD, pre-existing irritant dermatitis in atopics may also predispose him to allergic contact dermatitis via greater antigen exposure.14 Based on findings from several large studies which examined the incidence of ACD in atopics, it is reasonable to recommend patch testing be done in atopics in the same way, and for the same reasons (see below), as for nonatopics (same as Ref 8). Environmental factors such as the application of pressure, friction, exposure to heat, immersion, humidity, temperature, and season, all play a role in the development of ACD.15 Putative agents. Exposures to organic and inorganic chemicals in industry constitute a never-ending list of hazards. New chemicals are introduced every year, many without a full range of knowledge about their toxic or allergenic effects. The US Department of Health has tabulated potential causes of ACD and Human Services in a report dated 1983 (Table 1). They have omitted poison ivy and oak, which is the major cause of occupational contact dermatitis among the diverse groups of outdoor and environmental workers.16 Some of the most common allergens found in the workplace are among the most common allergens found in the ambient environment. While nickel and chromate are on the top 10 list of chemical sensitizers in patch testing results for the general population, paraphenylenediamine, epoxy derivatives, and rubber accelerators take precedence in the
Table 1. Potential Causes of ACD and Human Services Chemical Substances
Metals
3,350 pesticides
Chromium
3,410 cosmetics 1,815 drugs 8,627 food additives 48,523 commercial chemicals
Nickel Mercury Other metals
Comments Fewer than 30 allergens responsible for up to 80% of ACD
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workplace.17 Patch testing is the gold standard for identification of a contact allergen. It is recommended that any patient with a persistent, poorly responsive, eczematous rash be patchtested. Unfortunately, the deceptive simplicity of applying patch test materials and the required expertise for interpretation and recognition of clinical significance creates a major medical paradox!18 The basic 20 to 25 “standard” antigens included in the commercially available patch test panels (eg, TRUE test) may identify no more than 80% of workplace allergens. The standard-tray should be the starting point for patch testing all patients suspected of having ACD.19 Additionally, hundreds of “non-standardized” allergens for testing are available (from Dormer Laboratories, Inc or Omniderm Inc, both in Canada). Direct testing with industrial products should be done only by individuals with expertise in “open” patch testing, and all non-standardized materials must be tested on controls. Product labels must be carefully read, and further data may be required from Cosmetics, Toiletry, and Fragrance Association (CFTA); Cosmetic Ingredient Handbook (Washington DC, 1988); and the Material Safety Data Sheet (MSDS), the latter should be included with each industrial product used industrially. Establishing the relevance of all positive results is as important as the documentation of “pertinent negative” patchtest results. Incriminating an agent as the cause of ACD in the workplace can only be established with a properly interpreted patch test with the putative agent. Type of allergic reaction (Gell & Coombs Classification—as a Guideline). The “allergic” reaction pattern expressed by the skin when it reacts to an allergenic substance is an eczematous dermatitis (type IV or “delayed” hypersensitivity), and less frequently it may be urticarial (type I or “immediate” hypersensitivity). Allergic contact dermatitis is regarded as the prototypic example of delayed-type hypersensitivity, mediated primarily by sensitized Th1 cells. Clinically, it presents as an
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eczematous eruption—which when “acute” is very pruritic, erythematous, oozing and vesicular, when “chronic” it is mildly to moderately pruritic, thickened, scaly, less erythematous, and often fissured; subacute cases may present with some features of both acute and chronic “eczema.” All allergic reactions are allergen specific, and not dose dependent. While an intact skin surface deters penetrability of an antigen, maceration by sweating, occlusion, or water immersion, increases the accessibility of antigens (and irritants). Xerotic and/or dermatitic skin, which disrupts the barrier function of skin, increases vulnerability. The natural history of ACD must be appreciated to diagnose and manage the disorder. A period of “latency”, which may vary from 12 to 48 hours after contact with the allergen is required—pathogenically it is the travel time for the Langerhans cells (the “antigen-presenting-cells”) to deliver the hapten (allergen) to the area lymph nodes, where a small number (1 in 500) ThO cells become cloned, and then exit as sensitized Th1 cells which can “home” to the site of contact.20 Upon activation by residual hapten, they release their inflammatory mediators, which produce the clinical eczematous picture. When the antigen exposure is an episodic single encounter, the inflammatory reaction resolves within 7 to 21 days (but may rarely persist for 40 days!) after onset. Both genetic and environmental factors determine the individual course. With continued or persistent exposure to the allergen, the eczema evolves into the “chronic” phase and may persist for weeks, despite removal of the antigen. Spontaneous resolution occurs after the antigen is no longer present and the inflammatory T-cell mediators have dissipated. Potent topical and/or systemic corticosteroids inhibits the “homing” of T-cells and the release of inflammatory mediators, but does not alter the natural history of the episode. Comparison of ACD and ICD indicates that although the clinical definition of the two types of contact derma-
titis seem to be separate and distinct, comparative studies suggest that these two entities are more alike than they are not (ie, there is considerable overlap in the features of these types of dermatitis) (Table 2). Contact urticaria is a transient, wheal-and-flare response at the site of cutaneous contact to a topically applied agent. Both immunologic (IgEtype I) and non-immunologic mechanisms can produce contact urticaria. Like all immediate (type I) reactions, the lesions occur within minutes to an hour after contact, resolve within a few hours, and resolve leaving normal skin. While 15% of patients with contact urticaria also had a history suggesting extracutaneous symptoms involving the respiratory and gastrointestinal system, except for natural rubber (latex) hypersensitivity in atopic individuals, anaphylactic reactions were uncommon.1 Substances capable of causing immunologic and nonimmunologic contact urticaria are listed in an excellent reference: The contact urticaria syndrome, AE Burdick MD, MPH, CGT Mathias MD. Dermatologic Clin 1985;3.1:71– 84. Some individuals employed as food handlers have been known to develop a prototypical immediate exacerbation of affected eczematous skin. Since this occurs only after they have had contact with proteinaceous food substance it has been labeled protein contact dermatitis. Immediate swelling, itching, and vesiculation of the affected skin, rather than a classic wheal-and-flare reaction clinically characterize it. Diverse symptoms such as stinging or burning may be included in the contact urticaria syndrome spectrum. The putative agent causing immunologic contact urticaria can be confirmed by prick test and not by patch testing. Since foods (especially shellfish) are a common cause of this entity, prick testing with the (raw) foodstuff itself may be more helpful. The nonimmunologic agents can be applied to the skin, and when positive, a reaction is noted within minutes! Contact urticaria can be reduced (and at times in-
ANNALS OF ALLERGY, ASTHMA, & IMMUNOLOGY
Table 2. Comparison of Allergic and Irritant Contact Dermatitis Irritant Clinical morphology Reaction delay after contact Sharp demarcation Time for clinical resolution Common causes
Allergic
Dermatitis can be similar to ACD Dermatitis (spongiotic) From minutes to 48 hours. From 24 hours to 5 to 6 days Often typical Diminished by 96 hours
May occur 14 to 28 days
Water
Cosmetics (fragrances and preservative ingredients) Metallic salts (eg, nickel, chromium, cobalt) Germicides (eg, formaldehyde and releasers) Plants Rubber additives (eg, latex) Plastic resins (eg, Epoxy, acrylics) Rosin (eg, Colophony) Topical medications
Soaps Detergents “Wet work” Greases Solvents
Concentration of the agent Mechanism/trigger
Atopic predisposition Diagnostic test
Acids and alkalis Fiberglass Particulate dust More critical
Less critical
Non-immune, sensitization not required; damage to keratinocytes. Increased None
Immune; sensitization required; antigen activated primed T-cells. Decreased (initially) Patch test
Modified from Dermatology Nursing 1995; February Supplement page 6.
hibited) by taking an antihistamine prior to contact. Non-allegic, chemically-induced occupational dermatoses While fairly reliable physiologic and/or genetic risk factors have been associated with the contact dermatoses, risk factor for the other occupational dermatoses are more subtle. At best, the latter occurrences are medical mishaps. Since the oocupational hazard for these reactions is seen only in some individuals, they are considered idiosyncratic, or an individual peculiarity. The operational criteria to establish causality are virtually the same as for the contact dermatoses, however, since the skin changes may not be inflammatory (ie, changes in pigmentation, carcinogenic, infectious), resolution may not be dependent on removing the worker from the workplace. The scope of disability may vary from “cosmetic” (ie, acne, depigmentation) to ominous (ie, anthrax, tularemia, etc). A brief description of noncontact dermatoses follows.
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Acneiform reactions. Occupational acne and folliculitis may be precipitated by exogenous factors, ie, solvents, or wearing oil-impregnated clothing for prolonged intervals, inhalation of halogenated hydrocarbons (called chloracne). Their disability is cosmetic, but can be permanent in some cases. Yet, these workers will improve when removed from the putative exogenous agents. Chemicals that affect pigment cells. Industrial toxins that affect pigment cell biology have been identified. These “toxins” can result in hyperpigmentation, hypopigmentation or depigmentation. Hyperpigmentation can result from systemic toxicity caused by a variety of chemical agents, ie, arsenic, halogenated hydrocarbons, and silver. These pigmentary changes result from long term, chronic exposure. Hypopigmentation (occupational “vitiligo”) is noted in workers wearing inadequately cured synthetic rubber products (containing monobenzylether of hydroquinone). Catecholes and phenolic deriva-
tives found in germicides, disinfectants, metalworking fluids, and various rubber products have been associated with occupational vitiligo. While the disability is “cosmetic” it is permanent, unlike idiopathic vitiligo the depigmentation is not progressive, and occasionally may re-pigment when contact with the offending agent ceases. Carcinogens. Workers exposed to carbon black (soot), coal tar, pitch, tarry products, creosote oil, anthracene, or oil fractionation and distillation products are at risk for the development of keratotic papillomas (pitch/ tar warts), squamous cell carcinomas, basal cell carcinomas, and keratoacanthomas. Another well-recognized carcinogen in occupational settings is arensic. The most characteristic clinical feature of arsenic intoxication is symmetrical, flesh colored, punctate keratotic papules on the palms and soles. Despite the ominous connotation associated with the diagnosis of carcinoma, these malignancies rarely metastasize, thus are rarely fatal. These tumors are most amenable to appropriate therapy. While the disability is temporary, the propensity to develop other carcinomas is definitely permanent. Mechanically-induced Occupational Dermatoses Many of today’s jobs entail repetitive tasks. The wide range of mechanical assault upon the skin results in several response patterns, including callus formation, hemorrhage, blisters, fissures, vascular spasm, granulomas, and tattoos. Mechanical trauma associated with a particular occupation often gives rise to characteristic stigmata, also known as a “badge of the trade.” The median nail dystrophy in the house painter is an example. The pruritus associated with fiberglass exposure is typically sudden and intense. Vibration-induced injury now accounts for 60% of all reported occupational illness. The vibration syndrome is caused by exposure to vibrating tools. The clinical changes can present as Raynaud’s phenomenon, numbness,
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pain, and cold sensitivity of the fingers and/or arms. The disability resulting from mechanically induced dermatoses is temporary, with a predictable resolution when the mechanical stimulus is removed.
layed, the prognosis may be grave. Recurrent superficial fungal infections may be a sign of a Th1 suppression, which may occur more often in diabetics, and/or atopics. The disability is usually temporary and partial, but may be permanent and lethal.
Physical Causes of Occupational Dermatoses Injuries associated with chronic exposure to heat, cold, and nonionizing and ionizing radiation is common in various occupations. Heat may cause miliaria, intertrigo, or burns. Chilblains may occur in individuals who work in a persistently cold, damp environment. Work in cold temperatures can also provoke painful vasospastic reactions in digital vessels, resulting in another variant of occupational Raynaud’s phenomenon. The heat-induced problems are usually reversible when the workers environment is changed. Workers with the cold-induced vasospastic reactions may have uncovered an underlying vascular problem. In these individuals the cold exposure may be regarded as a provocative test for possible vascular insufficiency.
CONCLUSION A working knowledge of the epidemiology of occupational allergic dermatoses should allow the clinician to interact with industry, government, and academic medicine, to utilize the data, to identify defined populations, and to reduce the risk factors for occupational disabilities.21 The health provider’s obligation to society regarding workers’ compensation is to make a definite diagnosis, to clarify both the cause and all secondary factors, to prescribe the appropriate therapy, thereby preventing a recurrence of the work-related disability. As long as the skin problem has a definite work relationship, despite other possible significant nonwork-related factors, the case is compensable under the laws of all states. This remains a sore point for most physicians. The conflict is between the physicians, as advocates of the scientific method (which studies a disease confirming causality, and recommends a proven cause of therapy), and a legal system that advocates “individual’s rights,” irrespective of science! In these times of medical accountability and cost-effectiveness, the medical common sense of health care providers is more sensitive to the enormous burden of care imposed by the workers’ compensation laws. The essence of workers’ compensation laws are to entitle the employee medical treatment and compensation without regard to any fault, and to hold the employer accountable for the cost of any occupational disability. One of the effects of these laws is to encourage employer interest in safety and rehabilitation of the worker. Part of the physician’s role in workers’ compensation is to provide advice to the worker and industry about rehabilitation and prevention. Yet, not hiring a potential employee because they are
Biological Agents that cause Occupational Dermatoses Several occupations are characterized by an increased incidence of bacterial, fungal, and viral infections. Anthrax, brucellosis, erysipeloid, leptospirosis, and tularemia are still encountered where workers come in contact with animal hairs and hides. Superficial fungal infections due to Trichophyton and Microsporum species are seen almost entirely among farmers and other animal handlers. Sporotrichosis occurs in florists, forestry workers, miners, nursery workers, and farmers. Herpes simplex virus infections are often seen among health care workers. Arthropod infestations occur in gardeners and foresters. These workers are also subject to tick bites and their consequent Lyme disease. While many of these infections are very responsive to appropriate antibiotic therapy, when the diagnosis is de-
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identified as being at a high risk to develop a disability is disallowed by the Americans with Disabilities Act! This negates the value of epidemiology in occupational diseases. Allergic and non-allergic reactions cannot be all attributed to employee negligence anymore than an injury occurring to the employee while in transit to the workplace. But worker’s compensation laws ignore employee’s assumption of risk, be it genetic or otherwise. REFERENCES 1. Kaufman JD, Cophen MA, Saama SR, et al. Occupational skin diseases in Washington State 1989 –1993: using workers compensation to identify cutaneous hazards. Am J Public Health 1998;88:1947–1951. 2. VonKrogh GV, Maibach HI. The contact urticaria syndrome–and updated review. J Am Acad Dermatol 1981;5: 328 –342. 3. Rusca C, Hinnen U, Elsner P. “Patient’s delay”–analysis of the preclinical phase of occupational dermatoses. Dermatology 1997;194:50 –52. 4. Mozzanica N. Pathogenic aspects of allergic and irritant contact dermatitis. Clin Dermatol 1992;2:115–121. 5. Sheretz EF. Controversies in contact dermatitis. Am J Contact Dermatitis 1994;5:130 –135. 6. Lushniak BD. The public health impact of irritant contact dermatitis. Immunol Allergy Clin 1997;17:3: 345–355. 7. Mathias CGT. Occupational dermatoses. J Am Acad Dermatol 1988;6: 1107–1114. 8. Patil S, Maibach HI. Effect of age and sex on the elicitation of irritant contact dermatitis. Contact Dermatitis 1994;5: 257–264. 9. Iliev D, Elsner P. Clinical irritant contact dermatitis syndromes. Immunol Allergy Clin 1997;17:3:365–375. 10. Terr AI, Bardana EJ, Altman LC. Idiopathic environmental intolerances (IEI). J Allergy Clin Immunol 1997;. 11. Bernstein DI. Allergic reactions to workplace allergens. JAMA 1997;278: 1907–1913. 12. Yassin MS, Lierl MB, Fischer TJ, et al. Latex allergy in hospital employees. Ann Allergy 1994;72:245–249. 13. Uehara M, Sawai T. A longitudinal study of contact sensitivity in patients
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14. 15.
16. 17.
with atopic dermatitis. Arch Dermatol 1989;125:366 –368. Whitmore SE. Should atopic individuals be patch tested? Dermatol Clin 1994;12:491– 499. Gaspari AA. The role of keratinocytes in the pathophysiology of contact dermatitis. Immunol Allergy Clin 1997; 17:377–399. Epstein WL. Occupational poison ivy and oak dermatitis. Dermatol Clin 1994;12:511–516. Cohen SSR. Dermatitis and drudgery:
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skin disease in the workplace. Yale University/Glaxo Dermatology Lectureship Series in Dermatology. Lecture 14; page 4. 18. Beltrani VS, Beltrani VP. Contact dermatitis. Ann Allergy Asthma Immunol 1997;78:160 –175. 19. Marks JG, DeLeo VA. Standard allergens. In: Marks JG, DeLeo VA, eds. Contact and occupational dermatology. St Louis: Mosby Year Book, 1992. 20. Kalish RS. Recent developments in the
pathogenesis of allergic contact dermatitis. Arch Dermatol 1991;127: 1558 –1563. 21. Mostow EN. Role of epidemiology in occupational dermatology. Dermatol Clin 1994:577–582.
Request for reprints should be addressed to: Vincent S Beltrani, MD 29 Fox St Poughkeepsie, NY 12601
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INTRODUCTION Shortly following the passage of the Occupational Safety and Health Act (OSHA) of 1970, 45% of the annually recorded occupational illnesses were dermatologic. That act has instigated workers’ compensation data to identify known and emerging workplace cutaneous hazards which has been applied for targeting prevention efforts.1 Nonetheless, skin disorders still rank second when viewed as a proportion of all work-related illness by organ system. The dermatologist’s definition of an occupational skin disease is “a cutaneous disorder caused by or otherwise expressed as the result of factors primarily associated with the workplace.” The three operational criteria useful to identify a skin disorder as occupational are as follows2: • The skin disorder should have developed for the first time while the patient was on a job presumably associated with that skin disorder. • The skin disorder should clearly improve when the patient is away from the work environment and flare while on the job. • There should be a plausible etiologic agent in the workplace that can be linked to the expression of the skin disorder. The importance of temporal factors notwithstanding, cause is the most important element of this definition. It is conceivable with job-related disorders that anxiety concerning job security, as well as other factors of a demanding nature, may cause a delay of diagnosis and treatment. (The average delay was reported to be 8.6 months by Rusca et * Associate Clinical Professor, Department of Dermatology, College of Physicians & Surgeons, Columbia University, New York, New York; and Associate Clinical Professor, Division of Allergy, Immunology & Rheumatology, University of Medicine and Dentistry of New Jersey, New Jersey Medical School.
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al3). Only when causality is traced to the workplace can an otherwise conventional skin condition be acknowledged as an occupational dermatosis. In order of frequency, the direct causes of occupational dermatoses are classified as chemical, mechanical, physical, and biologic in nature. Of work-related cases involving the skin, 90% to 95% will be a contact dermatitis. In fact, most cases of contact dermatitis treated by physicians, in some way, are work related. The laws of most states require that in those cases in which there is any (possible) work relationship, it must be reported. It is essential that the correct diagnosis be made, and both the cause and all secondary factors be specified. An addendum to the medical criteria for establishing a dermatosis as work-related, the Workers’ Compensation Laws state, “As long as the dermatitis has a definite work relationship, even though there may be other non-work related factors, the case is compensable under the laws of all the states.” The essential statutory criterion is whether or not the work constitutes a substantial contributing factor in the development or aggravation of the skin condition. Predisposing Host Factors As with all disease processes, host factors must be considered essential as a predisposing contingency. The important host factors considered to influence occupational skin problems are listed below: • Intellectual ability of worker • Anatomic site • Atopic diathesis • Pigmented skin • Aged skin • Immunosuppressed individuals These factors will be described with specific examples later in this paper.
Predisposing Environmental Factors Environmental factors, each of which can increase the vulnerability for injury, such as low ambient humidity and cold decrease the water content of the stratum corneum.4 Cold temperatures also reduce the plasticity of the horny layer causing cracking and fissuring of the stratum corneum. Occlusion increases the water content of the stratum corneum (by preventing evaporation), with consequent enhanced percutaneous absorption of water-soluble substances. Exposure to irritants is the cause of 80% of all occupational dermatoses. Many agents may act as both an irritant and an allergen. Infections are most likely to occur in health care workers, farm workers, and meat handlers. CONTACT DERMATITIS “Contact dermatitis” is defined as “any” change of the skin and/or its appendages (hair, nails, and mucus membranes) resulting from contact or “exposure” to an exogenous (chemical and/or physical) agent. While most of the skin changes of contact dermatitis manifest a spectrum of cutaneous inflammation, the clinical picture is often “suggestive” but rarely “pathognomonic.”5 To complicate matters there is a subclass of contact-induced disorders that result from, and present in different situations, ie, require the presence of ultraviolet light to produce a reaction (ie, tar and sunlight for road construction workers and roofers), other contact-induced reactions affect pigment cells producing hyperpigmentation (arsenic, halogenated hydrocarbons, and phototoxins cause a brown discoloration), hypopigmentation, or depigmentation (catechol and phenolic derivatives found in germicides, disinfectants, etc, have been associated with occupational vitiligo).
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Most common is irritant contact dermatitis, identified when the contact-induced inflammatory change is non-immunologic, and the clinical picture is the result of cellular damage by the irritating agent. Only when the contact-induced inflammatory skin changes are compatible with a recognized immunologic response to a putative hapten, is the contact dermatitis labeled allergic contact dermatitis. Irritant Contact Dermatitis The lack of a standard case definition for irritant contact dermatitis (ICD), and the precise expertise required for making the diagnosis of the varied types of ICD, results in the common misclassification of ICD, which results in either an overestimation or underestimation of disease frequency.6 The most frequent causes of ICD are water, soaps/detergents, fiberglass and particulate dusts, food products, cleaning agents, solvents, plastics and resins, petrolatum products and lubricants, metals, and machine oils and coolants.7 In contrast to allergic contact dermatitis, ICD is not a distinct clinical entity, but rather a spectrum of abnormal skin changes. The clinical aspect of ICD is dependent on a dose and timeeffect relationship.8 A severe, acutely inflammatory reaction caused by “strong,” primary irritants may include necrosis and ulcerations. While chronic lesions present with lichenification, excoriations, scaling, and hyperkeratosis. The hands are most frequently affected by ICD, since they interact most with the environment and have frequent contact with many irritants. The spectrum of ICD is described as9: • Acute • Acute delayed • Irritant reaction • Cumulative • Traumatic • Exsiccation eczematid • Pustular and acneiform • Subjective Acute ICD occurs when the skin is exposed to a potent irritant (eg, acids and alkaline solutions). Usually this
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results from an accident at work. With appropriate, symptomatic management, the prognosis for this type of ICD is usually good, and unless the dermis is damaged there should be no permanent scaring. Most often a (medical) assignment of “temporary partial disability” is given to these “accidents” at work. Precautions regarding avoidance of a recurrent accident should be reviewed prior to returning to the same job. Acute delayed ICD is characteristic for certain irritants, such as benzalkonium chloride (eg, Zephiran—an extensively used preservative and disinfectant), that elicits a retarded (8 to 24 hours after exposure) inflammatory reaction. Except when these chemicals are applied to compromised skin, ie, atopics, or xerotics, adverse reaction on “normal” skin must be considered “idiosyncratic.” The inflammatory reaction rarely needs treatment, and resolves with cessation of exposure. These reactions are rarely awarded more than a “temporary partial disability” assignment. Irritant reaction ICD is a subclinical form of contact dermatitis, seen in workers whose hands are excessively wet, such as hairdressers, bartenders, or caterers. Often times scaling and erythema is first noted under rings and then spreads over the fingers to the hands and the forearms. It usually effects the dorsum of the hands, where the skin is “thinner,” but irritants can also cause some vesiculation resembling dyshidrotic eczema. Frequently, irritant reaction ICD resolves spontaneously, but more often it progresses to cumulative irritant dermatitis. Patients with a history of atopic dermatitis should be dissuaded to choose an occupation requiring “wet work.” Anyone whose hands are immersed in water several hours a day will become “irritated.” While the skin of “normals” will heal spontaneously when removed from the irritating agent, the abnormal skin of atopics and xerotic individuals lacks that resiliency. This can be an example of the “permanent partial disability.” The patient can no
longer do “wet work,” but can certainly be assigned other type work. Cumulative ICD is a consequence of multiple subthreshold damages to the skin with the time between exposures being too short for resolution of skin barrier function. Patients with “sensitive skin” (ie, atopics) have a decreased irritant threshold or a prolonged restoration time making them more vulnerable to clinical ICD. Cumulative ICD is not dependent on exposure to a potent irritant, but exposure to weak irritants prompts the reaction. Often, the exposure (ie, water) is not only at work but also at home. These patients complain both of itching and pain due to fissuring of the hyperkeratotoic skin (“chapping”). Exsiccation eczematid is the ICD seen mainly in elderly individuals who wash, shower, or bathe too often without remoisturizing their skin. These patients present with very itchy, dry, scaling hands. It is more common during the winter months, when humidity is low. Traumatic ICD may develop after acute skin trauma, such as burns, lacerations, and acute ICD. The latter is seen most often after the use of “harsh” cleansers used at work. The continued use of the “irritant” causes this condition to persist and may require months after discontinuing the irritant before it resolves. Harsh soaps should be replaced by an appropriate soap. Soap is used to emulsify an unwanted material on the skin. Most often a specific cleanser, for the substance that is to be removed can be found, and it should be “harmless,” yet effective. This should definitely be the responsibility of the employer, and a “temporary partial disability” can be resolved. Pustular and acneiform ICD is a result of exposure to certain irritants, such as croton oil, mineral oil, tars, greases, and naphthalenes. This diagnosis should always be considered when acneiform lesions appear in postadolescent patients who never had teen-age acne. Subjective ICD or sensory ICD is characterized by the lack of objective
ANNALS OF ALLERGY, ASTHMA, & IMMUNOLOGY
clinical signs. Some acids (ie, lactic) may cause stinging and burning with no visible cutaneous irritation. These reactions are usually dose-related, and are likely to occur in all individuals exposed. The best example of these type reactions is the typical stinging reaction that occurs after applying “after-shave” lotion! More often patients complaining of subjective symptoms without objective finding present themselves as having the “20th Century disease” or multiple chemical hypersensitivities, recently renamed idiopathic environmental intolerances (IEI). Their litany of varied and subjective complaints, for which they have been told by a “clinical ecologist,” are the result of exposure to minute amounts of “toxic” substances. The self-serving symptomotology progressively associates the subjective complaints to virtually ubiquitous environmental exposures. The Academy of Allergy has exhaustively reviewed the available literature regarding this entity, and have issued a definitive position paper concluding “There is no evidence that these patients have any immunologic or neurologic abnormalities. . . A casual connection between environmental chemicals, foods, and/or drugs and the patient’s symptoms is speculative and not based on the results of published scientific studies!”10 The hearings officer (compensation judge) must listen to both sides, recognizing that those who proselytize the diagnosis can be teleologically convincing. Presenting the position paper of the Academy (which I always equate to a policy issued by the American Bar Association)—at the hearing is frequently most helpful. Allergic Contact Dermatitis (ACD) Few terms are more misused both by the layman and physician, than the term “allergic” when describing an adverse medical event. The hallmark of the allergic phenomenon is its specificity, recognized as a predictable clinical and histologic immunologic inflammatory reaction, which occurs exclusively in susceptible individuals who have the ability to elicit that specific response,
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only when exposed to a specific allergenic agent. In the workplace, the factors for allergic reactions to be considered are (1) the host or employee, (2) environmental factors, (3) a putative agent, and (4) the type of immunologic reaction [eg, type I–IV as describe by Gell & Coombs]. Host factors. Recognizing the risk factors which predict susceptibility to allergic reactions in worker populations through prescreening of prospective employees could prevent many potential cases of allergic dermatoses; however, the Americans With Disabilities Act (enacted in 1991) prohibit such pre-employment screening.11 Nevertheless, the genetic predisposition for atopy, which is estimated to be present in 20% of the general population identifies these individuals who are at constant risk to develop immediate (type I) reactions to common aeroallergen resulting in allergic rhinitis, asthma, and contact urticaria. The prevalence of dermatologic occupational allergies is greater among atopic than nonatopic workers, including health care workers exposed to natural rubber latex gloves, detergent workers sensitized to microbial enzymes, and laboratory animal workers exposed to epidermal and/or urinary proteins.12 While is was suspected that their suppressed cell-mediated immunity decreased the atopics susceptability to develop ACD (type IV reactions), it was later observed that the reduced rate of sensitization (to DNCB) was only present in patients with severe dermatitis (⬎70% body surface area involvement).13 Subsequent testing when the dermatitis was well controlled noted an increased rate of pos-
itive reactions, suggesting that reduced sensitization is a reversible epiphenomenon of severe atopic dermatitis activity. As already noted above, regarding the atopics increased susceptibility for ICD, pre-existing irritant dermatitis in atopics may also predispose him to allergic contact dermatitis via greater antigen exposure.14 Based on findings from several large studies which examined the incidence of ACD in atopics, it is reasonable to recommend patch testing be done in atopics in the same way, and for the same reasons (see below), as for nonatopics (same as Ref 8). Environmental factors such as the application of pressure, friction, exposure to heat, immersion, humidity, temperature, and season, all play a role in the development of ACD.15 Putative agents. Exposures to organic and inorganic chemicals in industry constitute a never-ending list of hazards. New chemicals are introduced every year, many without a full range of knowledge about their toxic or allergenic effects. The US Department of Health has tabulated potential causes of ACD and Human Services in a report dated 1983 (Table 1). They have omitted poison ivy and oak, which is the major cause of occupational contact dermatitis among the diverse groups of outdoor and environmental workers.16 Some of the most common allergens found in the workplace are among the most common allergens found in the ambient environment. While nickel and chromate are on the top 10 list of chemical sensitizers in patch testing results for the general population, paraphenylenediamine, epoxy derivatives, and rubber accelerators take precedence in the
Table 1. Potential Causes of ACD and Human Services Chemical Substances
Metals
3,350 pesticides
Chromium
3,410 cosmetics 1,815 drugs 8,627 food additives 48,523 commercial chemicals
Nickel Mercury Other metals
Comments Fewer than 30 allergens responsible for up to 80% of ACD
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workplace.17 Patch testing is the gold standard for identification of a contact allergen. It is recommended that any patient with a persistent, poorly responsive, eczematous rash be patchtested. Unfortunately, the deceptive simplicity of applying patch test materials and the required expertise for interpretation and recognition of clinical significance creates a major medical paradox!18 The basic 20 to 25 “standard” antigens included in the commercially available patch test panels (eg, TRUE test) may identify no more than 80% of workplace allergens. The standard-tray should be the starting point for patch testing all patients suspected of having ACD.19 Additionally, hundreds of “non-standardized” allergens for testing are available (from Dormer Laboratories, Inc or Omniderm Inc, both in Canada). Direct testing with industrial products should be done only by individuals with expertise in “open” patch testing, and all non-standardized materials must be tested on controls. Product labels must be carefully read, and further data may be required from Cosmetics, Toiletry, and Fragrance Association (CFTA); Cosmetic Ingredient Handbook (Washington DC, 1988); and the Material Safety Data Sheet (MSDS), the latter should be included with each industrial product used industrially. Establishing the relevance of all positive results is as important as the documentation of “pertinent negative” patchtest results. Incriminating an agent as the cause of ACD in the workplace can only be established with a properly interpreted patch test with the putative agent. Type of allergic reaction (Gell & Coombs Classification—as a Guideline). The “allergic” reaction pattern expressed by the skin when it reacts to an allergenic substance is an eczematous dermatitis (type IV or “delayed” hypersensitivity), and less frequently it may be urticarial (type I or “immediate” hypersensitivity). Allergic contact dermatitis is regarded as the prototypic example of delayed-type hypersensitivity, mediated primarily by sensitized Th1 cells. Clinically, it presents as an
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eczematous eruption—which when “acute” is very pruritic, erythematous, oozing and vesicular, when “chronic” it is mildly to moderately pruritic, thickened, scaly, less erythematous, and often fissured; subacute cases may present with some features of both acute and chronic “eczema.” All allergic reactions are allergen specific, and not dose dependent. While an intact skin surface deters penetrability of an antigen, maceration by sweating, occlusion, or water immersion, increases the accessibility of antigens (and irritants). Xerotic and/or dermatitic skin, which disrupts the barrier function of skin, increases vulnerability. The natural history of ACD must be appreciated to diagnose and manage the disorder. A period of “latency”, which may vary from 12 to 48 hours after contact with the allergen is required—pathogenically it is the travel time for the Langerhans cells (the “antigen-presenting-cells”) to deliver the hapten (allergen) to the area lymph nodes, where a small number (1 in 500) ThO cells become cloned, and then exit as sensitized Th1 cells which can “home” to the site of contact.20 Upon activation by residual hapten, they release their inflammatory mediators, which produce the clinical eczematous picture. When the antigen exposure is an episodic single encounter, the inflammatory reaction resolves within 7 to 21 days (but may rarely persist for 40 days!) after onset. Both genetic and environmental factors determine the individual course. With continued or persistent exposure to the allergen, the eczema evolves into the “chronic” phase and may persist for weeks, despite removal of the antigen. Spontaneous resolution occurs after the antigen is no longer present and the inflammatory T-cell mediators have dissipated. Potent topical and/or systemic corticosteroids inhibits the “homing” of T-cells and the release of inflammatory mediators, but does not alter the natural history of the episode. Comparison of ACD and ICD indicates that although the clinical definition of the two types of contact derma-
titis seem to be separate and distinct, comparative studies suggest that these two entities are more alike than they are not (ie, there is considerable overlap in the features of these types of dermatitis) (Table 2). Contact urticaria is a transient, wheal-and-flare response at the site of cutaneous contact to a topically applied agent. Both immunologic (IgEtype I) and non-immunologic mechanisms can produce contact urticaria. Like all immediate (type I) reactions, the lesions occur within minutes to an hour after contact, resolve within a few hours, and resolve leaving normal skin. While 15% of patients with contact urticaria also had a history suggesting extracutaneous symptoms involving the respiratory and gastrointestinal system, except for natural rubber (latex) hypersensitivity in atopic individuals, anaphylactic reactions were uncommon.1 Substances capable of causing immunologic and nonimmunologic contact urticaria are listed in an excellent reference: The contact urticaria syndrome, AE Burdick MD, MPH, CGT Mathias MD. Dermatologic Clin 1985;3.1:71– 84. Some individuals employed as food handlers have been known to develop a prototypical immediate exacerbation of affected eczematous skin. Since this occurs only after they have had contact with proteinaceous food substance it has been labeled protein contact dermatitis. Immediate swelling, itching, and vesiculation of the affected skin, rather than a classic wheal-and-flare reaction clinically characterize it. Diverse symptoms such as stinging or burning may be included in the contact urticaria syndrome spectrum. The putative agent causing immunologic contact urticaria can be confirmed by prick test and not by patch testing. Since foods (especially shellfish) are a common cause of this entity, prick testing with the (raw) foodstuff itself may be more helpful. The nonimmunologic agents can be applied to the skin, and when positive, a reaction is noted within minutes! Contact urticaria can be reduced (and at times in-
ANNALS OF ALLERGY, ASTHMA, & IMMUNOLOGY
Table 2. Comparison of Allergic and Irritant Contact Dermatitis Irritant Clinical morphology Reaction delay after contact Sharp demarcation Time for clinical resolution Common causes
Allergic
Dermatitis can be similar to ACD Dermatitis (spongiotic) From minutes to 48 hours. From 24 hours to 5 to 6 days Often typical Diminished by 96 hours
May occur 14 to 28 days
Water
Cosmetics (fragrances and preservative ingredients) Metallic salts (eg, nickel, chromium, cobalt) Germicides (eg, formaldehyde and releasers) Plants Rubber additives (eg, latex) Plastic resins (eg, Epoxy, acrylics) Rosin (eg, Colophony) Topical medications
Soaps Detergents “Wet work” Greases Solvents
Concentration of the agent Mechanism/trigger
Atopic predisposition Diagnostic test
Acids and alkalis Fiberglass Particulate dust More critical
Less critical
Non-immune, sensitization not required; damage to keratinocytes. Increased None
Immune; sensitization required; antigen activated primed T-cells. Decreased (initially) Patch test
Modified from Dermatology Nursing 1995; February Supplement page 6.
hibited) by taking an antihistamine prior to contact. Non-allegic, chemically-induced occupational dermatoses While fairly reliable physiologic and/or genetic risk factors have been associated with the contact dermatoses, risk factor for the other occupational dermatoses are more subtle. At best, the latter occurrences are medical mishaps. Since the oocupational hazard for these reactions is seen only in some individuals, they are considered idiosyncratic, or an individual peculiarity. The operational criteria to establish causality are virtually the same as for the contact dermatoses, however, since the skin changes may not be inflammatory (ie, changes in pigmentation, carcinogenic, infectious), resolution may not be dependent on removing the worker from the workplace. The scope of disability may vary from “cosmetic” (ie, acne, depigmentation) to ominous (ie, anthrax, tularemia, etc). A brief description of noncontact dermatoses follows.
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Acneiform reactions. Occupational acne and folliculitis may be precipitated by exogenous factors, ie, solvents, or wearing oil-impregnated clothing for prolonged intervals, inhalation of halogenated hydrocarbons (called chloracne). Their disability is cosmetic, but can be permanent in some cases. Yet, these workers will improve when removed from the putative exogenous agents. Chemicals that affect pigment cells. Industrial toxins that affect pigment cell biology have been identified. These “toxins” can result in hyperpigmentation, hypopigmentation or depigmentation. Hyperpigmentation can result from systemic toxicity caused by a variety of chemical agents, ie, arsenic, halogenated hydrocarbons, and silver. These pigmentary changes result from long term, chronic exposure. Hypopigmentation (occupational “vitiligo”) is noted in workers wearing inadequately cured synthetic rubber products (containing monobenzylether of hydroquinone). Catecholes and phenolic deriva-
tives found in germicides, disinfectants, metalworking fluids, and various rubber products have been associated with occupational vitiligo. While the disability is “cosmetic” it is permanent, unlike idiopathic vitiligo the depigmentation is not progressive, and occasionally may re-pigment when contact with the offending agent ceases. Carcinogens. Workers exposed to carbon black (soot), coal tar, pitch, tarry products, creosote oil, anthracene, or oil fractionation and distillation products are at risk for the development of keratotic papillomas (pitch/ tar warts), squamous cell carcinomas, basal cell carcinomas, and keratoacanthomas. Another well-recognized carcinogen in occupational settings is arensic. The most characteristic clinical feature of arsenic intoxication is symmetrical, flesh colored, punctate keratotic papules on the palms and soles. Despite the ominous connotation associated with the diagnosis of carcinoma, these malignancies rarely metastasize, thus are rarely fatal. These tumors are most amenable to appropriate therapy. While the disability is temporary, the propensity to develop other carcinomas is definitely permanent. Mechanically-induced Occupational Dermatoses Many of today’s jobs entail repetitive tasks. The wide range of mechanical assault upon the skin results in several response patterns, including callus formation, hemorrhage, blisters, fissures, vascular spasm, granulomas, and tattoos. Mechanical trauma associated with a particular occupation often gives rise to characteristic stigmata, also known as a “badge of the trade.” The median nail dystrophy in the house painter is an example. The pruritus associated with fiberglass exposure is typically sudden and intense. Vibration-induced injury now accounts for 60% of all reported occupational illness. The vibration syndrome is caused by exposure to vibrating tools. The clinical changes can present as Raynaud’s phenomenon, numbness,
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pain, and cold sensitivity of the fingers and/or arms. The disability resulting from mechanically induced dermatoses is temporary, with a predictable resolution when the mechanical stimulus is removed.
layed, the prognosis may be grave. Recurrent superficial fungal infections may be a sign of a Th1 suppression, which may occur more often in diabetics, and/or atopics. The disability is usually temporary and partial, but may be permanent and lethal.
Physical Causes of Occupational Dermatoses Injuries associated with chronic exposure to heat, cold, and nonionizing and ionizing radiation is common in various occupations. Heat may cause miliaria, intertrigo, or burns. Chilblains may occur in individuals who work in a persistently cold, damp environment. Work in cold temperatures can also provoke painful vasospastic reactions in digital vessels, resulting in another variant of occupational Raynaud’s phenomenon. The heat-induced problems are usually reversible when the workers environment is changed. Workers with the cold-induced vasospastic reactions may have uncovered an underlying vascular problem. In these individuals the cold exposure may be regarded as a provocative test for possible vascular insufficiency.
CONCLUSION A working knowledge of the epidemiology of occupational allergic dermatoses should allow the clinician to interact with industry, government, and academic medicine, to utilize the data, to identify defined populations, and to reduce the risk factors for occupational disabilities.21 The health provider’s obligation to society regarding workers’ compensation is to make a definite diagnosis, to clarify both the cause and all secondary factors, to prescribe the appropriate therapy, thereby preventing a recurrence of the work-related disability. As long as the skin problem has a definite work relationship, despite other possible significant nonwork-related factors, the case is compensable under the laws of all states. This remains a sore point for most physicians. The conflict is between the physicians, as advocates of the scientific method (which studies a disease confirming causality, and recommends a proven cause of therapy), and a legal system that advocates “individual’s rights,” irrespective of science! In these times of medical accountability and cost-effectiveness, the medical common sense of health care providers is more sensitive to the enormous burden of care imposed by the workers’ compensation laws. The essence of workers’ compensation laws are to entitle the employee medical treatment and compensation without regard to any fault, and to hold the employer accountable for the cost of any occupational disability. One of the effects of these laws is to encourage employer interest in safety and rehabilitation of the worker. Part of the physician’s role in workers’ compensation is to provide advice to the worker and industry about rehabilitation and prevention. Yet, not hiring a potential employee because they are
Biological Agents that cause Occupational Dermatoses Several occupations are characterized by an increased incidence of bacterial, fungal, and viral infections. Anthrax, brucellosis, erysipeloid, leptospirosis, and tularemia are still encountered where workers come in contact with animal hairs and hides. Superficial fungal infections due to Trichophyton and Microsporum species are seen almost entirely among farmers and other animal handlers. Sporotrichosis occurs in florists, forestry workers, miners, nursery workers, and farmers. Herpes simplex virus infections are often seen among health care workers. Arthropod infestations occur in gardeners and foresters. These workers are also subject to tick bites and their consequent Lyme disease. While many of these infections are very responsive to appropriate antibiotic therapy, when the diagnosis is de-
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identified as being at a high risk to develop a disability is disallowed by the Americans with Disabilities Act! This negates the value of epidemiology in occupational diseases. Allergic and non-allergic reactions cannot be all attributed to employee negligence anymore than an injury occurring to the employee while in transit to the workplace. But worker’s compensation laws ignore employee’s assumption of risk, be it genetic or otherwise. REFERENCES 1. Kaufman JD, Cophen MA, Saama SR, et al. Occupational skin diseases in Washington State 1989 –1993: using workers compensation to identify cutaneous hazards. Am J Public Health 1998;88:1947–1951. 2. VonKrogh GV, Maibach HI. The contact urticaria syndrome–and updated review. J Am Acad Dermatol 1981;5: 328 –342. 3. Rusca C, Hinnen U, Elsner P. “Patient’s delay”–analysis of the preclinical phase of occupational dermatoses. Dermatology 1997;194:50 –52. 4. Mozzanica N. Pathogenic aspects of allergic and irritant contact dermatitis. Clin Dermatol 1992;2:115–121. 5. Sheretz EF. Controversies in contact dermatitis. Am J Contact Dermatitis 1994;5:130 –135. 6. Lushniak BD. The public health impact of irritant contact dermatitis. Immunol Allergy Clin 1997;17:3: 345–355. 7. Mathias CGT. Occupational dermatoses. J Am Acad Dermatol 1988;6: 1107–1114. 8. Patil S, Maibach HI. Effect of age and sex on the elicitation of irritant contact dermatitis. Contact Dermatitis 1994;5: 257–264. 9. Iliev D, Elsner P. Clinical irritant contact dermatitis syndromes. Immunol Allergy Clin 1997;17:3:365–375. 10. Terr AI, Bardana EJ, Altman LC. Idiopathic environmental intolerances (IEI). J Allergy Clin Immunol 1997;. 11. Bernstein DI. Allergic reactions to workplace allergens. JAMA 1997;278: 1907–1913. 12. Yassin MS, Lierl MB, Fischer TJ, et al. Latex allergy in hospital employees. Ann Allergy 1994;72:245–249. 13. Uehara M, Sawai T. A longitudinal study of contact sensitivity in patients
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14. 15.
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with atopic dermatitis. Arch Dermatol 1989;125:366 –368. Whitmore SE. Should atopic individuals be patch tested? Dermatol Clin 1994;12:491– 499. Gaspari AA. The role of keratinocytes in the pathophysiology of contact dermatitis. Immunol Allergy Clin 1997; 17:377–399. Epstein WL. Occupational poison ivy and oak dermatitis. Dermatol Clin 1994;12:511–516. Cohen SSR. Dermatitis and drudgery:
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skin disease in the workplace. Yale University/Glaxo Dermatology Lectureship Series in Dermatology. Lecture 14; page 4. 18. Beltrani VS, Beltrani VP. Contact dermatitis. Ann Allergy Asthma Immunol 1997;78:160 –175. 19. Marks JG, DeLeo VA. Standard allergens. In: Marks JG, DeLeo VA, eds. Contact and occupational dermatology. St Louis: Mosby Year Book, 1992. 20. Kalish RS. Recent developments in the
pathogenesis of allergic contact dermatitis. Arch Dermatol 1991;127: 1558 –1563. 21. Mostow EN. Role of epidemiology in occupational dermatology. Dermatol Clin 1994:577–582.
Request for reprints should be addressed to: Vincent S Beltrani, MD 29 Fox St Poughkeepsie, NY 12601
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