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Environmental Medicine: Integrating a Missing Element into Medical Education 28 Skin Lesions and Environmental Exposures Rash Decisions Environmental ALERT… Dermatitis accounts for about 30% of all illnesses in the workplace; the prevalence of skin diseases caused by chemicals in the environment is unknown. A thorough exposure history is the most important element in accurate diagnosis of skin lesions. In some cases, skin lesions are a diagnostic clue to the presence of systemic toxicity. This monograph is one in a series of self-instructional publications designed to increase the primary care provider’s knowledge of hazardous substances in the environment and to aid in the evaluation of potentially exposed patients. See page 45 for more information about continuing medical education credits and continuing education units. Guest Contributor: Alan H.Hall, MD Guest Editor: Daniel J.Hogan, MD Peer Reviewers: John Ambre, MD, PhD; Charles Becker, MD; Jonathan Borak, MD; Joseph Cannella, MD; Howard Kipen, MD, MPH; Richard J.Jackson, MD, MPH; Jonathan Rodnick, MD; Brian A.Wummer, MD Reviewed by the American Academy of Dermatology U.S. DEPARTMENT OF HEALTH & HUMAN SERVICES Public Health Service Agency for Toxic Substances and Disease Registry
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Environmental Medicine: Integrating a Missing Element into Medical Education Introduction Unlike most organs, the skin is in constant contact with the external environment. The skin ensures the body’s integrity by preserving internal fluids and electrolytes, maintaining thermoregulation, and protecting against physical injury and entry of harmful agents. Because the skin has such a prominent and protective role, many factors affect it adversely, including mechanical agents (friction, vibration, pressure, and trauma); physical agents (heat, cold, and radiation); biologic agents (plants, insects, animals, and microbes); and a variety of chemical agents. The large number of chemicals in the home and workplace and the accidental and intentional releases to air, water, and soil potentially allow ever-increasing contact with chemicals in the environment. Dermatitis from chemical exposures in the workplace accounts for about 30% of all reported occupational illness; the prevalence of skin lesions due to chemicals encountered outside the workplace (i.e., environmental exposures) may never be known. Seven common skin conditions that can have environmental etiologies are presented in this monograph. Accurate diagnoses and identification of etiologies are necessary, not only to properly treat skin diseases, but also to prevent future occurrence of disease or exposure. Familiarity with the vocabulary of dermatology is helpful in understanding this specialized topic. A glossary of terms begins on page 42. (a) What are the most likely nonoccupational etiologies for four of the more common skin conditions: irritant and allergic contact dermatitis, urticaria, and photosensitivity? _________________________________________________________________ _________________________________________________________________ (b) What are the most effective treatments and preventive measures for each of these skin conditions? _________________________________________________________________ _________________________________________________________________ _________________________________________________________________ Answers begin on page 39.
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Environmental Medicine: Integrating a Missing Element into Medical Education
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Environmental Medicine: Integrating a Missing Element into Medical Education Case 1—Irritant Contact Dermatitis A husband and wife consult you because of skin rashes that have developed since they began renovating a recently purchased older home. They have no history of skin problems. The man complains of severe itching of the hands and an erythematous rash with papules and excoriations on the arms and lower legs. This rash began during the time he was placing new insulation in the attic. The woman complains of a rash with redness and a small amount of blistering on the hands and wrists. There is mild itching, and some painful fissures have formed on the fingertips. The rash developed over a period of several days, beginning with only erythema while she was using a commercial paint-stripping product to remove old paint from interior trim. Although she wore rubber gloves, some of the stripping compound came in contact with her skin by running down into the gloves from the wrist area and through small holes in the fingers. (1a) What is the most likely cause of the husband’s rash? How could this be confirmed? _________________________________________________________________ _________________________________________________________________ (1b) What are the most likely causes of the woman’s rash? _________________________________________________________________ _________________________________________________________________ (1c) How would you treat the skin lesions experienced by these patients? _________________________________________________________________ _________________________________________________________________
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Environmental Medicine: Integrating a Missing Element into Medical Education Description ❑ More than 90% of skin lesions caused in the workplace are contact dermatitis. ❑ Lesions of irritant contact dermatitis are localized and the symptoms are generally less severe than those of allergic contact dermatitis. In the occupational exposure setting, the most common skin lesions (greater than 90%) are dermatitis due to either contact irritation or contact allergy, with irritant contact dermatitis being reported more frequently. Irritant contact dermatitis caused by chronic exposure to mild irritants typically begins with erythema and progresses to eczema with exudative vesicles and papules, most often limited to the area of direct contact. Itching, stinging, and burning sensations may be noted—especially with stronger irritants—but are generally not as severe as symptoms of patients who have allergic contact dermatitis. (For a discussion of allergic contact dermatitis, see page 9.) After days to weeks of chronic irritant exposure, the skin may become lichenified. Painful fissures may develop, along with hyperpigmentation, crusts, and scales. When contact with the offending irritant is discontinued, the rash usually resolves spontaneously in 1 to 3 weeks. Irritant contact dermatitis rarely spreads to areas of the body remote from the site(s) of direct contact. Cutaneous hardening can develop when patients with irritant contact dermatitis have daily exposure to irritating substances. The skin becomes tough and resistant at the sites of contact, allowing further exposure to the irritant but without reaction. If exposure ceases, however, this protective adaptation is lost rapidly. Pathophysiology ❑ Irritant contact dermatitis is caused by direct action of irritants on the skin. Irritant substances cause dermatitis by direct chemical action (i.e., nonimmune-mediated) on contacted components of the skin. Irritants may be acidic substances, which coagulate skin proteins, or alkaline substances, which remove surface lipids. Both types of substances may cause drying and cracking of the skin. Epidermal necrosis with separation of the epidermis from the underlying dermis results in formation of vesicles that contain mainly polymorphonuclear (PMN) leukocytes. Vesicles and bullae with both PMN leukocytes and lymphocytes occur in the upper portion of the dermis.
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Environmental Medicine: Integrating a Missing Element into Medical Education Common Etiologies Almost any substance can be a contact irritant (Table 1), although some substances, such as some alcohols, oils, and glycols cause irritant contact dermatitis in only a small percentage of exposed persons. In contrast, strong irritants, such as concentrated mineral acids, alkalies, and amines, cause chemical burns or irritant contact dermatitis in almost everyone exposed. Mild to moderate irritants (e.g., dilute acids, organic hydrocarbon solvents, and some detergents) generally produce irritant dermatitis in only a small percentage of persons after a single contact but will cause a reaction in nearly everyone after prolonged or repeated exposure. Table 1. Common irritants in the home and workplace* Home Bleaches Copper and metal brighteners Detergents Drain cleaners Fertilizers Furniture polishes and waxes Oven cleaners Pesticides Pet shampoos Rug shampoos Scouring pads and powders Soaps Toilet bowl cleaners Window cleaners Workplace Acids and alkalies Cleaning products Epoxy resins Foams (e.g., insulation foams) Noncarbon-required (NCR) paper Powders Aluminum Calcium silicate Cement Cleaning agents Metallic oxides Particles Ore particles in mining Plant particles Plastics, dry Sawdust Wool Volatile substances Ammonia Formaldehyde Organic solvents *Adapted from Robert M.Adams, Occupational skin disease, 2nd edition. Philadelphia: W.B.Saunders Co., 1990.
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Environmental Medicine: Integrating a Missing Element into Medical Education The young are generally more susceptible to irritant contact dermatitis than adults are because the threshold for skin irritation is low in children, particularly infants. Irritation reactivity gradually lessens after about 8 years of age. During play, children are likely to have skin contact with soils containing hazardous substances or with wooden playground structures that may have been treated with irritating chemicals such as arsenate and pentachlorophenol. The occurrence of skin problems is also common in the elderly. Besides age, personal factors that predispose persons to irritant contact dermatitis include genetic constitution and previous episodes of eczema. Environmental and physical factors influence the skin’s susceptibility to irritant contact dermatitis. Susceptibility is often enhanced by wet work and conditions such as cold and windy weather, low relative humidity, and high temperatures that cause sweating. Some anatomic regions are more sensitive than others. Friction and lacerations or other mechanical skin injury may facilitate the development of irritant contact dermatitis. Occlusion by protective equipment such as gloves provides a humid environment, minimizing evaporation and making the stratum corneum more permeable to chemical substances that come in contact with the skin. Diagnosis ❑ Onset of irritant contact dermatitis tends to be insidious. Irritant contact dermatitis is often difficult to differentiate from allergic contact dermatitis. Routine skin biopsy generally is not helpful because the histologic appearance of irritant and allergic contact dermatitis is similar. However, unlike allergic contact dermatitis, irritant contact dermatitis tends to localize at the exposed area and to cause mild itching and more erythema than vesiculation. The onset of irritant contact dermatitis is insidious rather than explosive. Patch testing by, or in consultation with, a dermatologist may be necessary to reach a diagnosis or to exclude allergic contact dermatitis. If fibrous glass is the suspected irritant, skin scrapings suspended in a few drops of 10% potassium hydroxide and examined under a light microscope at low power may reveal glass fibers. Treatment ❑ Removal from exposure is the most important step in treating irritant contact dermatitis. The most important step in treatment is to remove the patient, at least temporarily, from further exposure to the offending agent. Substituting less irritating chemicals for the offending substance and correctly using protective materials, such as gloves and barrier creams, may help reduce exposure. During healing, the skin should be protected from other insults such as frequent washing, trauma, wind, and rapid changes in temperature.
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Environmental Medicine: Integrating a Missing Element into Medical Education ❑ Topical corticosteroids may be useful in cases of irritant contact dermatitis. Treatment for acute vesicular irritant contact dermatitis includes topical application of wet dressings for 15 to 20 minutes, 3 to 6 times daily. Domeboro’s solution (diluted 1:40) or Burow’s solution may be used to soak the dressings. Dressings should be discontinued after 2 to 3 days to avoid drying the skin. Topical application of corticosteroid preparations may be efficacious. A low-potency corticosteroid should be used for mild to moderate skin conditions, with progression to more potent corticosteroids as required (Table 2). Some over-the-counter and prescription topical medications or their excipients can further irritate the skin or provoke allergic contact dermatitis. Administering mild sedatives and antihistamines to relieve itching may also be beneficial. Clinical signs of secondary bacterial infection include increased erythema and tenderness; development of a yellow, crusting, or purulent exudate; and occasionally, formation of small pustules around the edges of the dermatitis. Infection with monilia has an appearance similar to bacterial infection, except that the exudate is usually white. Infection may be difficult to recognize initially because the serous exudate and erythema of the dermatitis can obscure the signs. Obtaining samples of the exudate for culture and sensitivity before initiating topical or systemic antibiotic therapy is generally advisable.
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Environmental Medicine: Integrating a Missing Element into Medical Education Table 2. Groups of topical corticosteroid products, in order of decreasing potency* Drug Trade Name† % Concentration Group 1 Betamethasone dipropionate Diprolene 0.05 Halbertasol propionate Ultravate 0.05 Clobetasol propionate Temovate 0.05 Diflorasone diacetate Psorcon 0.05 Group II Amcinonide Cyclocort 0.1 Betamethasone dipropionate Diprosone 0.05 Desoximetasone Topicort 0.25 Diflorasone diacetate Florone, Maxiflor 0.05 Fluocinolone acetonide Synalar-HP 0.2 Fluocinonide Lidex 0.05 Halcinonide Halog 0.1 Triamcinolone acetonide Aristocort, Kenalog, etc. 0.5 Group III Betamethasone benzoate Benisone, Uticort 0.025 Betamethasone valerate Betatrex, Beta-Val 0.1 Desoximetasone Topicort LP 0.05 Flurandrenolide Cordran 0.025 Hydrocortisone valerate Westcort 0.2 Triamcinolone acetonide Aristocort, Kenalog, etc. 0.1 Group IV Betamethasone valerate Valisone, Reduced Strength 0.01 Clocortolone pivalate Cloderm 0.1 Fluocinolone acetonide Fluonid, Flurosyn, Synalar, etc. 0.025 Flurandrenolide Cordran SP 0.025 Triamcinolone acetonide Aristocort, Kenalog, Triacet 0.025 Group V Alclometasone dipropionate Aclovate 0.05 Desonide DesOwen, Tridesilon 0.05 Fluocinolone acetonide Fluonid, Synalar 0.01 Group VI Dexamethasone Aeroseb-Dex, Decaderm 0.01–0.1 Hydrocortisone (generic, over-the-counter) 0.25–2.5 Methylprednisolone acetate Medrol 0.25–1.0 Adapted from RC Cornell and RB Stoughton. The use of topical steroids in psoriasis. Dermatol Clin 1984;2:397–409. *No significant difference exists among agents in a group. These products come in various forms (i.e., creams, gels, lotions, solutions, and ointments), although some products are not available in all forms. †Use of trade names is for identification only and does not imply endorsement by the Public Health Service or the U.S. Department of Health and Human Services.
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Environmental Medicine: Integrating a Missing Element into Medical Education Case 2—Allergic Contact Dermatitis You are consulted by a 44-year-old male office worker who has a chief complaint of a rash on his hands and wrists. His company recently relocated from a building where each employee had a private office to an older, renovated building with large bay areas. New wallboard was placed, the area was painted, and new carpet was laid just before the move. Employees now work in cubicles; the patient’s cubicle is located in an interior area with no windows. A copying machine is adjacent to his work area. Since the move, many of the patient’s coworkers have been complaining of unpleasant odors, a feeling of fatigue or excessive tiredness, and mild irritation of the eyes, nose, and throat. They associate these symptoms with working in the new area. Although the patient has not noted such symptoms, he does complain of the increased noise and distraction in the new work area; he feels that his rash is somehow related to the new location. The rash began 5 days ago with itching and redness. It then developed weeping and raised, vesicular lesions that spread from the initial location on the hands to the volar surfaces of the wrists. The patient states that he has a history of reaction to poison ivy, which produces a similar rash, but he has not been in an infested area for the past 2 months. He has no direct contact with industrial cleaning agents or carbonless copy paper in his work. He does have contact with chemicals through his woodworking hobby. He recently built an end table from exotic Japanese woods and has been applying a varnish that a friend brought from Japan. (2a) Could the patient’s rash be due to airborne allergens or irritants in the new office location? _________________________________________________________________ _________________________________________________________________ (2b) Could the rash be related to his woodworking hobby? _________________________________________________________________ _________________________________________________________________ (2c) What is the most effective treatment for this patient? _________________________________________________________________ _________________________________________________________________
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Environmental Medicine: Integrating a Missing Element into Medical Education Description ❑ About 30% of occupational skin disorders are allergic contact dermatitis. ❑ In sensitized persons, inflammation begins about 12 hours after exposure to an allergen. Although contact allergens produce sensitization in only a small percentage of exposed persons, allergic contact dermatitis constitutes about 30% of the skin disorders found in the workplace. Once a person has been sensitized to an offending substance, further exposure may result in relatively rapid development of local inflammation with erythema, papule formation, induration, and weeping vesiculation. Inflammation usually begins about 12 hours after exposure; intensity peaks in 50 hours or more. The rash may spread locally around the margins of the original site or to distant sites that did not have contact with the allergen. Potentially, the entire skin surface could become involved (a condition known as erythroderma or exfoliative dermatitis). Pathophysiology ❑ Cross-reactivity with antigenically similar substances can occur with allergic contact dermatitis. ❑ The clinical and histologic appearances of allergic and irritant contact dermatitis are similar. Allergic contact dermatitis results from a true allergic (i.e., cell-mediated) sensitization to the offending substance. Cross-reactivity with antigenically similar substances may occur. Initially, during the refractory period, the patient may be exposed without developing a reaction. During the induction phase, which may last from 4 days to several weeks (usually about 14 to 21 days), the development of complete allergic sensitization occurs as the allergen comes in contact with the skin. After the skin is fully sensitized, further contact with the allergen may result in rapid and severe dermal manifestations. When no further contact with the allergen occurs, the patient is in the period of persistence of sensitivity. The level of sensitivity can decrease over time, but sensitization may be lifelong. Most allergens that cause allergic contact dermatitis have molecular weights of less than 500 daltons. The allergens are haptens rather than complete antigens; they must penetrate the skin and combine with endogenous proteins to form full antigens. Langerhans cells play a key role in then presenting the antigen to T lymphocytes, thereby activating the T cells. The sensitized T cells proliferate in the paracortical regions of the lymph nodes and produce effector and memory lymphocytes that remain in the general circulation. On subsequent contact with the complete antigen, the effector cells release lymphokines that may result in rapid and severe, local inflammation. Many factors can affect the development of allergic contact dermatitis, including characteristics of the allergen itself, patient factors, and environmental conditions. Allergen factors include the physiochemical nature of the allergen (e.g., lipophilicity, solubility, and inherent sensitizing potency), concentration, total dose that comes in contact with the skin, anatomic site of contact, number and frequency of exposures, and occlusion by clothing or gloves.
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Environmental Medicine: Integrating a Missing Element into Medical Education Treatment ❑ Treatment of skin cancer depends on whether the cancer is localized or is metastasizing. Prevention is the first line of defense for skin cancer. Avoiding overexposure to sunlight is most important. Protection from UV radiation can be accomplished by wearing tightly woven clothing and wide-brimmed hats and by applying sunscreens as absorbers. Sunscreens, which contain p-aminobenzoic acid (PABA) derivatives to absorb UV rays, can provide sun-protective factors (SPFs) ranging from 2 to 50 or more. An SPF of 15 allows most persons to remain out of doors for 5 hours before developing minimal erythema. Light-complexioned persons, persons of Celtic origin (i.e., Scotch, Irish, Welsh), and those with certain conditions (e.g., albinism, xeroderma pigmentosum, and erythropoietic protoporphyria) appear to be at increased risk for developing skin cancer. These sensitive populations may require more potent sunscreens. Surgical excision and radiation are the most common treatment modalities for localized malignant skin lesions. All excised tissue should be sent for histologic examination to confirm the diagnosis and to be certain that an adequate margin of normal skin was removed. Surveillance for the development of further skin cancers should be continued. The treatment of metastasizing skin cancers or lesions with extensive local infiltration is beyond the scope of this review. Patients who have malignant tumors should be referred to, or treated in consultation with, a physician knowledgeable in cancer therapy.
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Environmental Medicine: Integrating a Missing Element into Medical Education Diagnostic Procedures Obtaining and recording a detailed history of exposures (workplace, home, and environment) is essential in diagnosing skin disease. Besides physical examination, several special techniques may aid in the diagnosis of skin lesions. These include patch tests to detect contact allergy, skin biopsy, cultures, and microscopic scrapings of skin to detect yeasts, fungi, parasites, and fibrous glass. Referring patients to, or consulting with, a dermatologist who can perform or interpret dermatologic diagnostic testing, may be advisable. Patch Testing ❑ Patch testing can help differentiate allergic from other forms of dermatitis. Patch testing is frequently used to differentiate between allergic contact dermatitis and other forms of dermatitis. The presence of a delayed hypersensitivity reaction to an offending substance can be determined by placing a suitably prepared, nonirritating amount of a sample on the skin (usually on the back) under a chamber or impervious bandage (patch). If an eczematous dermatitis lesion develops under the patch during the 48 hours after application, allergy to the test substance or to an antigenically similar cross-reacting substance can be inferred. If no reaction is evident, the patches are removed, and the sites are reexamined for delayed reaction at 72 and 96 hours after application. Interpretation of patch testing is often difficult, and it is usually recommended that the testing be carried out in specialized centers or by consultants who routinely do patch testing. If no response is provoked, it does not mean unequivocally that the patient is not allergic. For example, if an offending or cross-reacting substance was not included, or was not applied in proper concentration, a false-negative result will occur. Complications of patch testing include the “angry back syndrome,” in which the patient’s entire back becomes edematous and erythematous. Flare-up of previously existing eczema can also occur, especially when testing materials are not obtained from standard commercial sources. Even local response to the test substance may be extensive, causing patient discomfort. Patch testing itself can result in allergic sensitization to a substance to which the patient was not allergic previously, although this is a rare occurrence. Infections, scarring, and pigment alterations may also be complications of patch testing. Photopatch Testing ❑ Photopatch testing may help reveal the cause of photosensitivity dermatitis. When photosensitivity dermatitis is suspected, a combination of chemical patch testing and special light exposure may reveal the cause. Duplicate patches are used; one set is covered, and the other
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Environmental Medicine: Integrating a Missing Element into Medical Education set is exposed to a measured amount of UV radiation. There are several difficulties in the performance and interpretation of photopatch testing, and it should be performed by practitioners who have experience and the requisite special equipment. Skin Biopsy ❑ Skin biopsy is not helpful in differentiating allergic contact dermatitis and irritant contact dermatitis. The appropriate skin biopsy (punch biopsy or excision of the lesion) usually can be performed under local anesthesia by experienced practitioners in an outpatient setting. Microscopic examination of the specimens obtained can allow differentiation between benign and malignant skin conditions. Irritant and allergic contact dermatitis cannot be readily differentiated on routine skin biopsy. Other Diagnostic Procedures ❑ Skin scrapings, UV-light examinations, cultures, and serologic testing are diagnostic tools used for various skin lesions. Other procedures include skin scrapings, UV-light examinations, cultures, and serologic testing. Skin scrapings can be used to look for fungal hyphae, for strands of fiberglass in suspected fibrous glass dermatitis, or for scabies mites and eggs. A Wood’s lamp, which produces UV radiation, can be used to examine suspected areas of hypopigmentation in light-complexioned persons. Areas deficient in melanin will not fluoresce under UV light, whereas areas of skin with normal melanin content will fluoresce. Bacterial, viral, or fungal cultures may be indicated if dermal infections are considered in the differential diagnosis. Crusts, when present, should be lifted with a scalpel blade before swabbing the lesion with a sterile cotton-tipped applicator to obtain material for bacterial cultures. Fungi may be collected for culture media by gently scraping the skin with a sterile scalpel blade. Viral cultures from skin lesions require specialized laboratory facilities. Viruses can be collected for special media by unroofing lesions and swabbing with a sterile cotton-tipped applicator. Patients who have immunologic-mediated contact urticaria may be evaluated by serologic testing. Protein electrophoresis and measurement of circulating IgE may be useful.
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Environmental Medicine: Integrating a Missing Element into Medical Education Suggested Reading List General Adams RM. Occupational skin disease. 2nd ed. Philadelphia: W.B.Saunders Co., 1990. Maibach HI, ed. Occupational and industrial dermatology. 2nd ed. Chicago: Year Book Medical Publishers, Inc., 1987. Mathias CGT. Occupational dermatoses. In: Zenz C, ed. Occupational medicine: principles and practical applications. 2nd ed. Chicago: Yearbook Medical Publishers, Inc., 1988:132–65. Raffle PAB, Lee WR, McCallum RI, Murray R, eds. Occupational diseases of the skin. In: Hunter’s diseases of occupations. Boston: Little, Brown & Company, 1987:917–48. Rosenstock L, Cullen MR. Skin disease. In: Clinical occupational medicine. Philadelphia: W.B.Saunders Co., 1986:147–73. Rycroft RJG. Occupational dermatoses among office personnel. Occup Med 1986;1:323–8. Seidenari S, Manzini BM, Danese P, Motolese A. Patch and prick test study of 593 healthy subjects. Contact Dermatitis 1990;23:162–7. Shama SK. Occupational skin disorders, In: McCunney RJ, ed. Handbook of occupational medicine. Boston: Little, Brown & Company, 1988:216–35. Suskind RR. Environment and the skin. Med Clin North Am 1990;74:307–24. Irritant and Allergic Contact Dermatitis Abel EA, Wood GS. Mechanisms in contact dermatitis. Clin Rev Allergy 1986;4:339–52. Dahl MV. Chronic irritant contact dermatitis: mechanisms, variables, and differentiation from other forms of contact dermatitis. Adv Dermatol 1988;3:261–75. Lammintausta K, Maibach HI. Exogenous and endogenous factors in skin irritation. Int J Dermatol 1988;27:213– 22. Photosensitivity Dermatitis Emmett EA. Drug photoallergy. Int J Dermatol 1978;17:370–9. Emmet EA. Evaluation of the photosensitive patient. Dermatol Clin 1986;4:195–202. Gross TP, Ratner L, de Rodriquez O, et al. An outbreak of phototoxic dermatitis due to limes. Am J Epidemiol 1987;125:509–14. Harber LC, Bickers DR. Photosensitivity diseases. Philadelphia: W.B.Saunders Co., 1981.
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Environmental Medicine: Integrating a Missing Element into Medical Education Chloracne American Medical Association. The Health effects of “Agent Orange” and polychlorinated dioxin contaminants: an update, 1984. Chicago: American Medical Association, 1984. Taylor JS. Environmental chloracne: update and overview. Ann NY Acad Sci 1979;320:295–307. Tindall JP. Chloracne and chloracnegens. J Am Acad Derm 1985;13:539–88. Zugerman C. Chloracne. Clinical manifestations and etiology. Dermatol Clin 1990;8:209–13. Pigment Abnormalities Gellin GA, Maibach HI, Misiaszek MH, Ring M. Detection of environmental depigmenting substances. Contact Dermatitis 1979;5:201–13. Gian C, Lu MY, Wang XS, et al. Epidemiologic study on the skin lesions of workers exposed to N,N’-methylenebis-(2-amino-1,3,4-thiadiazole) and of children in the neighborhood of the factory. Scand J Work Environ Health 1985;11 Suppl 4:55–9. Ortonne J-P, Mosher DB, FitzpatrickTB. Chemical hypomelanosis. In: Ortonne J-P, Mosher DB (eds). Vitiligo and other hypomelanoses of hair and skin. New York: Plenum Medical Book Co., 1983:479–508. Carcinogenesis Austin DF, Reynolds P. Occupation and malignant melanoma of the skin. In Gallagher RP (ed). Epidemiology of malignant melanoma. Recent results in cancer research. Vol 102. Berlin: Springer-Verlag, 1986:98–107. Callen J, Headington J. Bowen’s and non-Bowen’s squamous intraepidermal neoplasia of the skin. Arch Dermatol 1980;116:422–6. Emmett EA. Occupational skin cancers. Occup Med: State Art Rev 1987;2:165–77. Epstein JH. Photocarcinogenesis: A review. Natl Cancer Inst Monogr 1977;50:13. Shannon RL, Strayer DS. Arsenic-induced skin toxicity. Hum Toxicol 1989;8:99–104. Van der Leun JC. UV carcinogenesis. Photochem Photobiol 1984;39:861–8. Sources of Information More information on skin lesions and treating and managing cases involving skin lesions due to environmental exposure can be obtained from ATSDR, your state and local health departments, and university medical centers. Case Studies in Environmental Medicine: Skin Lesions and Environmental Exposures—Rash Decisions is one of a series. To obtain other publications in this series, please use the order form on the inside back cover. For clinical inquiries, contact ATSDR, Division of Health Education, Office of the Director, at (404) 639–6204.
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Environmental Medicine: Integrating a Missing Element into Medical Education Answers to Pretest and Challenge Questions Pretest questions are on page 1. Challenge questions begin on page 3. Pretest The Pretest questions (a) and (b) are answered in Challenge answers 1, 2, 3, and 6 below. Challenge (1a) The man in Case No. 1 has most likely developed an irritant contact dermatitis from the insulating material (e.g., fiberglass, rock wool). This possibility could be investigated by placing skin scrapings on a microscope slide with 1 to 3 drops of 10% potassium hydroxide (KOH) and examining the specimen under a light microscope using low power. The presence of fibrous strands would confirm the diagnosis. Dermatitis elicited by fibrous glass is variable and depends on individual characteristics and extent of exposure. (1b) The woman probably has either irritant or allergic contact dermatitis. The basic histopathologic appearance of these two conditions is essentially the same, and differentiating between them by appearance or routine skin biopsy is difficult. However, most paint-stripping products contain one or more of the following compounds: isopropyl alcohol, cresylic acid, methylene chloride, glacial acetic acid, aliphatic hydrocarbons, and aqueous ammonia, all of which tend to be irritants rather than allergens. The presence of mild rather than severe itching, more erythema than vesiculation, localized lesions, and insidious rather than explosive onset are more consistent with irritant contact dermatitis than with allergic contact dermatitis. (1c) Both the man and the woman should be advised to avoid exposure to the offending substances, at least temporarily. Applying and rapidly removing adhesive or Scotch tape from the man’s affected skin may remove the fibers and help relieve the itching. The contact dermatitis of both patients may be treated using Domeboro’s solution (1:40 dilution) or Burow’s solution. Dressings soaked with one of these solutions should be applied topically for 15 to 20 minutes, 6 times daily. Topical corticosteroids may be applied, starting with a steroid of low potency and progressing to more potent corticosteroids as needed. Mild sedatives and antihistamines may be administered to relieve itching. Topical or systemic antibiotic therapy may be used to combat secondary bacterial infection. Repeated exposure to UV radiation may be therapeutic in some cases, causing hardening or increased resistance to further irritation. (2a) The rash of the patient in Case No. 2 is not likely to be due to airborne allergens or irritants in the new office location. Although some cases of allergic or irritant contact dermatitis can develop from exposure to airborne allergens or irritants, the patient’s occupational history and the location of the rash do not suggest this etiology. Eyelids, cheeks, nasal folds, and the neck most probably would be involved if an airborne agent in the workplace were responsible. The hand and wrist location suggests contact with an allergen that is handled. (2b) Yes, the patient’s woodworking hobby, with recent introduction of various exotic woods and Japanese varnish (possibly derived from the Japanese lacquer tree), suggests a cross-sensitivity reaction to agents related to Rhus plants, to which he is known to be sensitized. (2c) The patient probably has allergic contact dermatitis. Therapy would be identical to the regimen for irritant contact dermatitis described in (1c) above. Attempts to desensitize sensitive persons have been unsuccessful in most cases.
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Environmental Medicine: Integrating a Missing Element into Medical Education (3a) Given the rural location and outdoor activities in which the children in Case No. 3 were involved, airborne allergic contact dermatitis to Rhus-type plant oleoresins (e.g., poison ivy, poison oak, poison sumac) or pollen could be the cause. However, vesiculation would be expected with allergic contact dermatitis. Patch testing could rule out this diagnosis. Puncturing lime skins while making sachets during craft class could have exposed the children to psoralens, which are known photoirritants. Immediately after the craft class, the children engaged in outdoor sports. This combination of activities could lead to photosensitivity dermatitis. Because the counselors were involved in a staff meeting during the craft class and did not puncture the limes, only the children were affected. (3b) One of the most important components in therapy for photoreactions is identification and avoidance of the photoactive agent. When exposure to the offending agent cannot be avoided, sunlight exposure should be minimized. Light exposure can be reduced by wearing protective clothing such as broad-brimmed hats, long sleeves, and tightly woven fabrics, or by using sunblocking agents. Symptomatic topical treatments may also be used. (4a) The rash of the patient in Case No. 4 is more consistent with chloracne than with acne vulgaris. Acne vulgaris has a different appearance, and its distribution is typically the central face, back, and chest; it seldom affects the buttocks. The sebaceous glands are usually active in acne vulgaris, but chloracne gives the skin a “dry” appearance. Comedones are small in size and number in cases of acne vulgaris, whereas typical straw-colored cysts are almost pathognomonic for chloracne. The patient’s occupation is a potentially relevant factor. A telephone call to a manager at the utility company reveals that old heat exchanger fluids contain PCBs, and in the process of replacing these fluids with less hazardous materials, the workers could have accidental contact with the material. The finding that PCBs are the most probable cause of the patient’s chloracne should prompt a health hazard evaluation by the appropriate regulatory authorities and should encourage action to prevent further exposure. (4b) The chloracnegenic agent should be identified and exposure stopped. Chloracne is resistant to treatment in many cases. Medications used for acne vulgaris are ineffective for chloracne, but oral and topical antibiotics, acne surgery, injection of inflammed cysts with triamcinolone, and dermabrasion of scars may be efficacious. Topical application of retinoic acid (Vitamin A) or 13-cis-isoretinoic acid (Accutane) has been used on carefully selected patients with some success. In addition to treating the skin lesions, examination and testing should be performed to rule out hepatotoxicity, porphyria cutanea tarda, and peripheral neuropathy—all possible systemic effects of PCB exposure. (For further information, see Case Studies in Environmental Medicine: Polychlorinated Biphenyl [PCB] Toxicity.) (5a) Yes, the manufacturing plant could be associated with the children’s skin lesions in Case No. 5. A similar outbreak among workers at a manufacturing facility and children in a neighboring school was reported in 1985; a powdered thiadiazole was responsible in that case. Because an etiologic agent for the pigment changes in the children has not been found in routine testing of the water and food at the school, it would be advisable to consider other common sources in the neighborhood, such as the school playground. The nearby chemical manufacturing facility should also be investigated as a possible source, especially because the parents of the two children with more severe manifestations are employed at this plant. The parents could be carrying contamination home on their skin, clothing, and shoes. In addition, the children may be playing in an area with contaminated soil. (5b) You could begin your investigation by contacting the nurse or health and safety manager at the parent’s workplace to determine whether a workplace agent or process is associated with the rashes of some workers. You could request from the manufacturer Material Safety Data Sheets (MSDSs) or other information about the raw materials, byproducts, chemical intermediates, and finished products used or produced at the plant.
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Environmental Medicine: Integrating a Missing Element into Medical Education The Toxic Chemical Release Inventory (TRI), which is maintained by the U.S. Environmental Protection Agency (EPA) and is available to the public either online through the National Library of Medicine or on CD-ROM, could be used to determine the normal releases from the plant. Plant management, the local EPA, or the local fire department could be consulted to determine whether any accidental chemical releases have occurred recently at this facility. If soil contamination is suspected, soil samples from nearby playgrounds, school yards, or other play areas should be tested. Local or state health officials may be contacted for assistance. (5c) If the lesions are persistent, large, and cosmetically displeasing, you could refer the children to a dermatologist for consideration of PUVA treatment. Sunscreens and protective clothing can protect areas with depigmented skin and prevent hypopigmentation from worsening. (6a) The constellation of complaints of the patient in Case No. 6 is consistent with contact urticaria syndrome. Balsam of Peru and various alcohols (especially propyl alcohol and ethyl alcohol) in numerous consumer cosmetic products and benzocaine in many over-the-counter topical analgesic preparations could be causative agents. (6b) Evaluation might include correlating the history of the illness with probable exposures, serologic studies of circulating IgE, and patch or scratch testing (performed by, or in consultation with, a dermatologist in a setting with resuscitation equipment in case of anaphylactoid reaction). (6c) Usual treatment for contact urticaria includes advice to avoid suspected or known causative substances and administration of antihistamines. In certain patients, nonsteroidal anti-inflammatory medications have shown some efficacy. (7a) The constellation of complaints of the couple in Case No. 7 suggests chronic arsenic poisoning. Arsenic toxicity from criminal activity, intentional surreptitious self-injury, occupational exposure, and environmental exposure should be investigated. On questioning, the couple reveals that they have obtained drinking water from a private well for the past 40 years and that they heat their home with a wood stove fueled with scrap wood. Analysis of the well water reveals arsenic at 0.62 milligrams per liter (mg/L), a concentration significantly above the EPA maximum contaminant level (MCL) of 0.05 mg/L. Ashes collected from the wood stove and soot from the chimney also contain arsenic in concentrations of several hundred parts per million; the most likely source of this contamination is arsenic-containing preservatives in the scrap wood. (7b) Initial action should be taken to terminate further arsenic exposure; it will be futile to treat the skin lesions (or provide chelation therapy to reduce body burden) if exposure continues. An alternative source of drinking water should be substituted immediately, contaminated lumber should not be burned, and the home should be decontaminated. Advice on abatement and remediation and aid in investigating any other possible sources of arsenic may be obtained from the state or local health department. (For further information on arsenic and arsenic poisoning, see Case Studies in Environmental Medicine: Arsenic Toxicity.) Treatment of the man’s basal cell carcinoma may involve radiation therapy or excisional biopsy, including a suitable margin of normal-appearing skin. All tissue removed should be submitted for histologic confirmation of diagnosis and to be certain the tissue borders are free of cancerous cells. The patient should be counseled to avoid prolonged exposure to sunlight and to use sunscreens or protective clothing whenever exposure to sunlight is anticipated.
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Environmental Medicine: Integrating a Missing Element into Medical Education Glossary* anaphylaxis. Commonly used to denote the immediate, transient kind of immunologic (allergic) reaction characterized by contraction of smooth muscle and dilation of capillaries due to release of pharmacologically active substances (histamine, bradykinin, serotonin, and slow-reacting substances), classically initiated by the combination of antigen (allergen) with mast cell-fixed, cytophilic antibody (chiefly IgE). acne mechanica. Acne caused or exacerbated by friction. acne medicamentosa. Acne caused or exacerbated by several classes of drugs including antiepileptics, halogens, and steroids. acne venenata. Acne produced by external irritants or drugs internally administered. acne vulgaris. Simple acne, probably caused by hormonal fluctuations. bullae (singular bulla). Large bubble-like structures (vesicles) appearing as a circumscribed area of separation of the epidermis from the subepidermal structure, typically filled with serum. chloracne. Acne-like eruptions due to prolonged contact with certain chlorinated aromatic hydrocarbon compounds. chloracnegenic agents. Substances that cause chloracne. comedones. A plug of sebaceous matter, capped with a blackened mass of epithelial debris, filling the pilosebaceous orifice. dermatitis. Inflammation of the skin. atopic d. Characterized by the distinctive phenomena of atopy, a Type I allergic reaction, specifically one with strong familial tendencies, caused by allergens such as pollens, foods, dander, and insect venoms, and associated with the Prausnitz-Küstner (IgE class) antibody. allergic contact d. A delayed type of induced sensitivity (allergy) of the skin with varying degrees of erythema, edema, and vesiculation, resulting from cutaneous contact with a specific allergen. irritant contact d. Irritation of skin caused by contact with substances that are toxic to epidermal or connective tissue cells; lesions are usually erythematous and papular, but can be purulent or necrotic, depending on the nature of the toxic material applied. dermatomyositis. A progressive syndrome characterized by muscular weakness with a purplish erythematous skin rash on the face. eczema. Generic term for acute or chronic inflammatory conditions of the skin, typically erythematous, edematous, papular, vesicular, and crusting; often followed by lichenification and scaling and occasionally by duskiness of the erythema; often accompanied by sensations of itching and burning. erythema. Inflammatory redness of the skin. * Adapted from Stedman’s Medical Dictionary, 25th edition, Baltimore: Williams and Wilkins, 1990. Modified with permission from Williams and Wilkins.
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Environmental Medicine: Integrating a Missing Element into Medical Education erythema multiforme. An acute eruption of macules, papules, or subdermal vesicles presenting a multiform appearance, the characteristic lesion is typically over the dorsal aspect of the hands and forearms; its origin may be allergic, seasonal, or from drug sensitivity, and the eruption may be recurrent or may run a severe course (Stevens-Johnson syndrome), possibly ending in death. excipient. An inert substance such as gum arabic, syrup, lanolin, or starch, that acts as a diluent or forms a vehicle for drug delivery. folliculitis. An inflammatory reaction in hair follicles; the lesions may be papules or pustules. exfoliative dermatitis. General scaling of the skin, usually with erythema. hapten. Incomplete or partial antigen; an antigen that is incapable, alone, of causing the production of antibodies. hives. See urticaria. hyperkeratosis. Hyperkeratinization; hypertrophy of the horny layer of the epidermis. hyperpigmentation. Increased pigmentation of the skin. hypertrichosis. Growth of hair in excess of normal. hypopigmentation. Decreased pigmentation of the skin. keratosis. Any lesion on the epidermis marked by the presence of circumscribed overgrowths of the horny layer. lichenification. Leathery induration and thickening of the skin with hyperkeratosis, due to a chronic inflammation caused by scratching or long-continued irritation. leukoderma. An absence of pigment, partial or total, in the skin. macular. Relating to or marked by a small, discolored patch or spot on the skin, neither elevated nor depressed below the skin’s surface. malar crescent. Around the cheek or cheekbones. melanin. Pigment that occurs in the hair, skin, or retinas. melanocytes. Pigment cells of the skin. melanoderma. An abnormal darkening of the skin by deposition of excess melanin, or of metallic substances such as silver and iron. melanoma. A malignant neoplasm derived from cells that are capable of forming melanin, which may occur in the skin of any part of the body; in the early phases, the lesion is characterized by proliferation of cells at the dermal-epidermal junction, and the neoplastic cells soon invade adjacent tissue extensively. Melanomas frequently metastasize widely; most examples of this neoplasm occur in adults and may originate de novo or from a pigmented nevus or malignant lentigo.
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Environmental Medicine: Integrating a Missing Element into Medical Education milia (singular milium). Sebaceous tubercle; whitehead; a small subepidermal keratin cyst, usually multiple, therefore commonly referred to in the plural. miliaria. An eruption of minute vesicles and papules due to retention of fluid at the mouths of the sweat follicles. nummular. Marked by circular or oval lesions. papules. Small, solid elevations on the skin. photoallergy. Sensitization of the skin to light. phototoxicity. The condition arising from overexposure to ultraviolet light. pruritis. Itching. psoralens. Furo[3, 2-g]coumarin; a phototoxic chemical derived from fruits of the citrus family (e.g., limes). psoriasis. A condition characterized by the eruption of circumscribed, discrete and confluent, reddish, silvery scaled macropapules. Rhus. A genus of trees and shrubs (family Anacardiaceae) containing various species that are used for their ornamental foliage; poison ivy, poison oak, and poison sumac belong to this genus. solar elastosis. Degenerative change in elastic tissue of the dermis due to repeated or constant exposure to sunlight over a period of years. urticaria. Hives; an immediate eruption of itching wheals, which may be due to physical and chemical agents, foods or drugs, foci of infection, or psychic stimuli. urticaria syndrome. Consists of the typical urticarial rash with systemic involvement. vesiculation. Blistering. vitiligo. The appearance on the otherwise normal skin of loss of melanin pigment with white patches of varied sizes, often symmetrically distributed; the skin bordering the affected sites is usually hyperpigmented, and hair in the affected areas is usually white.
Representative terms from entire chapter: