Occupational skin disease

Postgraduate Occupational Edward A. Emmett,

course skin disease M.D. Baltimore, Md.

Occupational skin diseases ure the most frequent occupational diseases. Certain industries are at a particularly high risk. Important factors to consider include percutaneous absorption and ulterutions in resistance to microbial agents. The most common condition is contact dermatitis, usuully irritant but frequently causing allergy. Other selected conditions include photosensitization, acne and chloracne, fiberglass dermatitis, pigmentaty changes, and skin tumor. The approach to the patient and diagnostic criteria for occupational skin disease are described. (.I ALLERGYCUN

IMMUNOL72.649-656, 1983.)

Occupational skin disease has been the subject of at least three recent books1-3 and a report to the Occupational Safety and Health Administration.4 This brief survey will concentrate on information about the occurrence of occupational skin disease, considerations regarding the normal relevant functions of the skin, a survey of some of the more important occupational skin diseases, and the approach to the patient with possible occupational skin disese. OCCURRENCE OF OCCUPATIONAL SKIN DISEASE Although no entirely satisfactory source exists, the best data regarding the relative incidence of occupational diseases of different types come from the state of California, where a report is bled by the physician attending any injured or ill employee when either the disability lasts beyond the day of injury or the condition requires medical service other than ordinary tirst aid attention. Table I indicates the types of occupational diseases reported in California in 19735; the relative distribution has not changed greatly in recent years. In California, occupational skin diseases are the most frequent occupational diseases in all major categories of industry and are due to a very wide range of agents-chemical, biologic, and physical. It is also important to note that approximately 80% of From the Division of Occupational Medicine, ical Institutions, Baltimore, Md. Received for publication July 19, 1983. Accepted for publication July 19, 1983. Reprint requests: Edward A. Emmett, M.D., cal Institutions, Center for Occupational Health, Building 6, 3100 Wyman Park 21211.

Johns Hopkins

Med-

Johns Hopkins Mediand Environmental Dr., Baltimore, MD

the reported illness is in the categories of occupational skin disease and chemical bums to the skin and eyes. All of these are due primarily to direct contact with chemical agents and in many cases to contact with contaminated work surfaces. A great deal of attention has been given in recent years to reducing the level of contaminants in the air of the occupational environment; however, contamination of surfaces and of skin is often overlooked, and control measures are often rudimentary at best. In California in 1977, 92.5% of all cases of occupational skin disease were due to contact dermatitis, either irritant or allergic, 5.4% were due to primary or secondary infections, and 2.4% were due to other skin disorders,fi As might be expected, the incidence of occupational skin diseases is not evenly distributed among industries but is highest in manufacturing and agriculture and lowest in finance, insurance, and real estate4 as shown in Table II, which summarizes data from workmen’s compensation insurance reports collected by the United States Bureau of Labor Statistics. Industries with the highest risk of occupational skin disease in terms of lost work days as based on statistics from the United States Bureau of Labor Statistics are: (1) poultry dressing, (2) meat packing, (3) rubber fabrication, (4) leather tanning and finishing, (5) ophthalmic goods, and (6) plating and polishing. The industries with the highest incidence of cases of dermatitis per 1000 workers are: (1) leather tanning and finishing, (2) poultry dressing, (3) adhesives and sealants, (4) boat building and repairing, (5) fresh or frozen fish packaging, (6) poultry and egg processing, (7) abrasive products, (8) landscape and horticultural services, (9) beet sugar, and (10) farm labor and management services. Interestingly, authorities in occupational dermatology would develop a list with a 649

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Emmett

Ahhre\~itlrion

UV:

med

Ultraviolet

times. From the public health viewpoint, this tendency is most unfortunate, and underreporting does hinder our ability to take action to reduce the burden of occupational disease. CONSIDERATIONS

somewhat different order based on their own experiences. ’ There are many good reasons why each of these industries is an important cause of dermatitis. For example, in leather tanning, after being sorted and trimmed, hides are soaked and limed to remove hair with the use of hydrated lime or certain sulfides, amines, or cyanide. After the skin is cleaned of hair and subcutaneous tissue, it is bated with buffering salts and proteolytic enzymes and pickled. The hide is tanned with one or more vegetable extracts, basic chromium salts, formaldehyde, glutaraldehyde, or other chemicals. The hide is now soft and porous. It is dried and split to desired thickness and may be dyed, lubricated, bleached, oiled, and made water repellent with waxes, oils, and greases. Synthetic resins, shellac, albumin, or other materials may be used for the final finish. Obviously there are many irritants and allergens to which the worker is exposed and varying types of liquids with which the hands make contact. Useful sources of brief descriptions of the type of work performed in high-risk industries are avilable.l. :3.i. X Although some useful information is available to pinpoint high-risk situations, clearly our data base is incomplete as a result of substantial underreporting. This is true not only of occupational skin disease but of other occupational diseases as well. For example, a recent pilot study in Oregon and Washington with environmental surveys, medical questionnaire, and medical examination found that of 1116 cases of physician-determined occupational disease, only 2% were recorded in the Bureau of Labor Statistics criteria.“ A number of reasons for this underreporting exist; three will be mentioned here. First, occupational skin diseases are often undiagnosed. Second, most cases represent irritant dermatitis for which no definitive diagnostic test exists. Third, dermatitis is frequently multifactorial, and there is often room for dispute as to the relative roles of intrinsic and extrinsic and/or occupational and nonoccupational exposures in disease causation and aggravation. Fourth, in times of substantial unemployment in the manufacturing and agricultural sectors, the patient’s fear of losing employment may be substantial and may lead physician and patient to consider workmen’s compensation insurance and case reporting more warily than at other

OF SKIN FUNCTION

Important functions of the skin include a barrier against physical and chemical agents, antibacterial and antifungal properties, temperature regulation, sensation, vitamin D production, emotional expression, and sexual attraction. The first two will be discussed in connection with occupational dermatoses. Resistance to bacterial and fungal infection depends in large part on desiccation, which is lethal to many organisms on the skin surface. In occupations in which the worker is subjected to wet work or work under hot, sweat-inducing conditions and, particularly, to poor posture so that intertrigonous areas and other areas do not dry out, desiccation does not occur. and there is predisposition to a variety of cutaneous infections, including candidiasis and others. Percutaneous absorption is a major determinant of the development of occupational skin disease. The outer stratum comeum layers of the skin are essentially dead, but this dead layer constitutes the major barrier layer to foreign substances. Damage to the organ occcurs as a result of passage of substances to the subjacent living layers or to the systemic circulation. Percutaneous absorption occurs by a process of passive transfer by diffusion; the driving force is the concentration difference between the outer and inner surfaces of the skin.Y The process. however, is affected by a large number of factors”, I0 that may be broadly classified as pertaining to the substance, vehicle, or skin. Important properties of the substance include lipid and water solubility characteristics with lipid solubility favoring penetration. Organic solvents that damage the skin greatly enhance the penetration of all materials. Electrolytes do not penetrate well when dissociated crystalline material, and large molecules penetrate poorly. The vehicle plays an important role; absorption from a solution is normally dependent on the vehicle/stratum comeum partition coefficient. This may clearly be altered by changing the nature of the vehicle, which is done in designing many topical medications. Surface-active agents greatly increase the penetration of water-soluble materials; vehicle pH may alter absorption by changing the ionization state of weak acids and bases. The state of the skin is also important. Damaged or disease skin may have impaired barrier properties; furthermore the barrier must regenerate after injury. This may be one of the reasons why skin that has

Occupational

VOLUME 72 NUMBER 6

apparently healed to visible inspection may remain more susceptible to further insult. There is marked regional variation in barrier capacity and absorption. Data for the absorption of topically applied hydrocortisone from different sites are given in Table III.” These regional differences in the skin are major factors in determining the distribution of contact dermatitis. The physical state of the skin is relevant; increasing hydration and temperature increase absorption. As an example, occlusion, which has both of these effects, greatly accelerates the absorption of hydrocortisone. All these factors affect absorption and thereby the development of contact dermatitis. Experimentally important differences in species are also noted in percutaneous absorption. ” It must not be assumed that artificial barriers such as gloves are always effective; these can be very pervious to industrial materials. In general, relatively little data are conveniently available regarding glove effectiveness, although test procedures have been developed recently. ‘zi

TABLE I. Percentage distribution occupational diseases reported 1973” Diseases

*Modified

TABLE

diseases 1976”

from

% Distribution

40.6 29.2 IO. I 5.4 4.4 2.9 1.8 1.4 1.1 1.1 1.9

Baginsky.”

II. Relative risk of occupational skin or disorders by major industry division,

Industry

-

651

of types of in California for

Skin conditions Eye conditions Chemical bums Respiratory conditions Symptoms due to toxic materials Ear conditions Systemic effects of toxic materials Cardiovascular conditions Effects of environmental conditions Infective and parasitic diseases Other and unspecified

SURVEY OF SELECTED OCCUPATIONAL SKIN DISEASES Selected occupational skin diseases of interest will be surveyed briefly; there is no attempt to be exhaustive. As indicated, contact dermatitis is the most common occupational disease; major forms are irritant dermatitis, allergic contact dermatitis, and photosensitivity dermatitis. Irritant dermatitis may be divided into direct toxic dermatitis and cumulative insult dermatitis. Direct toxic dermatitis results from contact with a strongly irritating substance. The diagnosis is generally straightforward, and a good history of contact with the injurious substance can generally be obtained. Cumulative insult dermatitis is more difficult both to diagnose and to treat. It can be shown both in experimental animals and in humans that many weak irritants produce dermatitic responses only after a number of days of repeated application,14 although once dermatitis is present, it may progress quite rapidly. A cumulative-insult patch test performed in rabbits or humans appears to be the best predictive test to identify weak or marginal irritants. I’* I5 Clinically, cumulative-insult dermatitis is frequently multifactorial with many different weak irritants such as soaps, detergents, industrial chemicals as well as physical conditions and other factors, such as those that affect percutaneous absorption, playing a role. 16. Ii The effects of repeated contact are not always straightforward; under some circumstances, tolerance of the effects of subsequent exposure (“hardening of the skin”) occurs.1s In the evaluation of occupational contact der-

skin disease

Risk other

division

relative to industries

Agriculture, forestry, and fishing

4.1

Manufacturing

Construction

4.1 0.8

Transportation and public utilities Services Wholesale trade

0.6 0.5 0.4

Mining Retail trade

0.3 0.2 0. I

Finance, insurance, and real estate

*United States Bureau report4

of Labor

Statistics;

modified

from

OSHA

matitis, the distribution of the dermatitis is of great importance. Approximately 90% of occupational dermatitis involves the hands,‘* generally the backs and palmar surface of the wrist; occupational dermatitis commonly commences under rings and watchbands if these are worn at work. Although there are exceptions (dermatitis in bank tellers, dermatitis resulting from contact with a steering wheel, etc.), dermatitis confined to the palms is less commonly occupational. Whenever contact dermatitis is suspected, matching the location of the dermatitis and the exposure source is of paramount importance; indeed, simulated demonstration of work practices or actual observation of the work tasks may be necessary. The extent to which the exposure will be modified by regional variations in percutaneous absorption must also be borne in mind.

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TABLE III. Effect of anatomic region on absorption of topical ‘T hydrocortisone over 5 days compared with absorption from plantar foot arch skin* Anatomic

region

Relative absorption

Plantar foot arch Lateral ankle Palm Ventral forearm Dorsal forearm Back Scalp Axilla Forehead Jaw angle Scrotum

6 8 12 25 26 43 93 300

*Data modified from Feldmann and Maibach.”

Allergic contact dermatitis, a type IV reaction, is accepted as responsible for 20% to 30% of cases of occupational contact dermatitis overall, although this figure varies greatly with the industrial setting. A large number of new organic chemicals that have been introduced in recent years have contributed significantly to our burden of potent allergens. However, the most frequent causes of allergic contact dermatitis remain as the poison ivy/oak group, rubber additives, paraphenylenediamine derivatives, nickel, and chromium. A subject of recent interest has been the role of the Langerhans cells in allergic contact dermatitis. These cells, which constitute about 5% to 10% of epidermal cells, are epidermal macrophages that form an intraepidermal network and have distinctive properties. Their role appears to be to process antigens absorbed through the skin. It seems that these cells are intimately involved in the sensitization-tolerance dichotomy that determines reaction or nonreaction to materials applied topically. ~3 20 Any chemical in the skin that can absorb UV radiation from sunlight is a candidate for photochemical reactions in the skin, possibly leading to photosensitivity or to other changes such as photocarcinogenesis. Photocontact dermatitis may be phototoxic, i.e., immunologic mechanisms are not primarily involved, or photoallergic. A relatively well-studied type of phototoxic reaction is that caused by psoralens, which are present in a variety of plants and used therapeutically in psoralen ultraviolet A. A number of photochemical reactions occur between psoralens and tissue components in the presence of UV radiation of long

wavelength but do not occur in the dark. These include psoralen binding to the pyrimidine bases of DNA and the formation of cross-linkages between DNA strands. A number of new phototoxic agents have been introduced into commercial use in recent years.“’ Photoallergic reactions are less common; they appear to result from the photochemical conversion of a hapten. “:! Photosensitivity reactions must be distinguished clinically from a number of other conditions, including airborne contact dermatitis. Particularly useful is the sparing of shaded, fold areas in photosensitivity, whereas these are prime sites for the deposition of airborne allergens and for airborne allergic contact dermatitis. A number of other occupational dermatoses are seen. Here we will briefly deal with fiberglass dermatitis, acne including chloracne, pigmentary changes, and skin tumors. Fiberglass dermatitis”‘-‘” often produces marked itching and pinpoint-sized papules, which are often excoriated or petechial. Pruritus may occur in the absence of visible lesions. Urticaria and linear erosions may occur often, seconday to scratching. Lesions are more common in skin folds where clothing is in tight contact with the skin, or on bared surfaces. Fiberglass, like lead, dust, asbestos, and other substances, has been shown to produce problems in the family when brought home from work on clothes. The likelihood that fiberglass will produce dermatitis is directly related to its diameter (>4.5 p in diameter) and inversely to fiber length. Most fiberglass used in the United States today is capable of producing this dermatitis. A high index of suspicion is necessary; microscopic examination of cellophane tape strippings of the skin or a potassium hydroxide preparation of a skin scraping will disclose the very uniform rodlike fibers. A number of oily substances may aggravate juvenile acne or produce “oil” acne on exposed skin; these include oil-based metal working fluids used in machine shops and other machine operations, certain cosmetics, and oils and greases contacted from work as fast-order chefs and in other food processing operations. Of particular interest is chloracne, a refractory, follicular dermatosis resulting from envimomental exposure to halogenated aromatic compounds that have a specific molecular shape.2”, 2i These include certain polyhalogenated napthalenes, biphenyls, dibenzofurans, dioxins, chlorophenols, and azoxybenzenes. Straw-colored cysts are characteristic, comedones are often frequent, and other acute lesions may occur. The crow ‘s-foot area of the face is preferentially involved, although widespread involvement

VOLUME 72 NUMBER 6

may occur. Photosensitivity and porphyria cutanea tarda may occur. The causal agents are potent enzyme inducers; this may be the mechanism of action.” Systemic effects may occur, including hepatotoxicity and neuromuscular complaints. Experimentally these agents also produce complex effects on the immune system with some immunosuppression.2s Some immunologic changes have recently been described in Taiwanese who ingested rice oil contamined with polychlorinated biphenyls, polychlorinated dibenzofurans, and other related substances .‘r” Various pigmentary changes may be induced by occupational exposures, including hyperpigmentation, hypopigmentation, and, in the case of agents like arsenic, a variety of bizarre pigmentary changes .s’ Hyperpigmentation can result from heat, cold, UV radiation, and as a nonspecific effect of inflammation. Photosensitivity reactions such as to coal tar pitch or to psoralens commonly result in hyperpigmentation. Depigmentation may also occur; chemically induced leukoderma is of particular interest. This condition is quite obvious in the deeply pigmented skin but much less obvious in lighter pigmented skin. It must be distinguished from vitiligo, principally by the different distribution of lesions. Causes include various structurally related alkyl phenols that resemble tyrosine and appear to have selective melanocytotoxicity, Y-N including hydroquinone, monobenzyl ether of hydroquinone, and a variety of phenols used as germicides, antioxidants, rust inhibitors, and the like .:(5.:l(i Occupational skin cancers from sunlight and UV exposure occur most commonly in persons with light pigmented skin. Other significant causes include tars, pitches, creosote, soot and similar sources of polycyclic aromatic hydrocarbon carcinogens, inorganic arsenic, and ionizing radiation .37 Immunologic factors appear to play a significant role, especially in photocarcinogenesis. UV light- induced tumors are highly antigenic with characteristic tumor-specific antigens.:” Of particular interest are the experimental studies of Kripke:‘s indicating that, whereas UV induced- tumors are rejected when transplanted into normal mice, pretreatment of the recipient mouse with subcarcinogenic doses of UV light results in failure of rejection and tumor growth. This effect appears to be mediated by suppressor T-lymphocytes.40

APPROACH TO THE PATIENT The objectives of the investigation of potential occupational skin disease are appropriate management and rehabilitation of the individual patient, prevention of further dermatoses by the elimination or control of causal agents at the work place, and the satisfying of

Occupational

skin disease

TA‘BLE IV. Components of effective occupational skin disease

history

653

in

Eruption Onset and cause Localization and time of onset Work activities at the time Appearance of initial lesions Nature of progression Recurrence and remissions Relationship to work, weekends, vacation, sick leave

Responseto therapy Prescribed Over the counter, folk remedies Systemic manifestations Work hisrory

Pastand present occupational history Description

of actual duties

Material and processexposure Ambient conditions Habits, use of protective equipment Skin cleaning techniques Experience

of other employees

Past history

Skin disease, including atopy Allergic contact dermatitis (jewelry, cement, etc.) Systemic illness and medication Other exposures and inJluencing factors

Home Hobbies Cosmetics Medications

Clothing Food Emotional

factors

workmen’s compensation insurance and other legal and regulatory matters. All of these functions require a precise etiologic diagnosis so that the various causal agents can be delineated. In approaching the patient, the psychologic importance of the skin must be borne in mind. The worker’s anger is often marked, more so than in many systemic occupational diseases, and in my experience is frequently exacerbated by remarks belittling the seriousness of the condition by those forgetting the importance of the skin for comfort and for self-image. Often good rapport may be aided by physically touching the patient at an early stage. One should bear in mind that whether verbalized or not, the patient is probably questioning whether the condition is contagious and whether carcinogenic, reproductive, or other effects ate occurring on the “inside” to match the changes on the “outside. ” The physician will have to be

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mindful of the possibility of upset worker-management relationships that may be complicating the situation and should therefore be careful to avoid premature conclusions or offhand prejudicial remarks. The occupational history plays a critical role in diagnosis. Important questions are indicated in Table IV. It is most important to have the patient describe his or her job in detail; this is usually best done by having the activities described from the start to the end of the day. The importance of the history can be exemplified by irritant dermatitis for which there is no reliable confirmatory test; the diagnosis must be made on the history and circumstances of exposure, an assessment of irritancy of the various materials contacting the skin, and the state of predisposition, if any, of the individual’s skin, all leading to a judgment as to whether irritant dermatitis was a likely result of the exposure. The accuracy of such a diagnosis is obviously highly dependent on the skill with which the history is elicited. If the actual identity of the work place materials is unknown to the patient, this information must be obtained from other sources. A complete examination of the skin should be performed. Primary lesions that have recently developed and have not been traumatized by rubbing or scratching should be sought. As occupational dermatitis occurs so frequently on the hands, examination of the feet to exclude dermatophytosis with a secondary id reaction is critical. In contact dermatitis much attention must be given to the relationship between the distribution of the dermatitis and potential causal exposures. The most important diagnostic procedure in occupational skin disease is frequently the diagnostic patch test, useful only in the diagnosis of allergic contact dermatitis. The principle of this test is simple: A concentration of the test substance, usually in a petrolatum vehicle, which is demonstrably nonirritating to the skin of nonsensitized individuals but which is capable of eliciting a response in the sensitized individual, is left on the skin for 48 hr. A delayed reaction, morphologically consistent with an eczematous response, presupposes sensitization. The technique has been fully standardized for only a limited number of allergens. Recently the North American Contact Dermatitis Group (a task force of the American Academy of Dermatology) and the International Contact Dermatitis Group have taken a major role in this standardization. A major problem with many allergens is the lack of well-validated test concentrations and vehicles; establishing these details of a test requires a large number of control observations, which unfortunately are commonly omitted. Testing an individual patient with industrial-grade products of unknown composition is problematic and may lead to sensitiza-

J. ALLERGY CLIN. IMMUNOL. DECEMBER 1983

tion and/or extreme bullous or ulcerative reactions. as well as results that are difficult to interpret. False positive reactions include those from the use of incorrect irritant concentrations, pustular reactions from metallic salts, seen especially in atopic individuals,41 edematous reactions from presssure of solid substances, contact urticaria, and the so-called “angry back” or “excited skin” syndrome,“” a regional phenomenon in which a strongly positive reaction causes hyperreactivity in other skin sites. As a result of this phenomenon, the existence of many positive responses in the same individual is always suspect. Much of our old information on cross-sensitization based on reactions of multiple patch tests will need reevaluation in the future to exclude this effect. False negative reactions can occur through poor application, use of too low a concentration, failure to perform delayed readings (especially at 72 and 96 hr), and the effects of local or systemic steroids.lZS A positive patch test is evidence of sensitization but does not prove that the dermatitis is due to that cause. They may be established for nonirritating substances by a provocative-usage test. The suspected agent is rubbed directly into the skin above the anticubital fossa twice in a period of 1 week. It is difficult to underestimate the importance of plant visits in occupational medicine. By giving a physician the opportunity to observe the work and working conditions of a patient firsthand, he or she may be able to make a better etiologic diagnosis. Plant visits should enable the physician to develop a better rapport with both workers and management. The visit gives an opportunity to obtain further information on substances used at the plant, on physical conditions, hygienic practices, etc., to perform a survey of workers, and review medical records as appropriate. Having observed a job, the physician is better able to make recommendations to prevent further occurrences of dermatitis that are sufficiently practical as likely to be successfully implemented.“’ By making a variety of plant visits, the physician is able to develop a firsthand knowledge of various occupations. On a “walk-through” survey of the work place in the case of possible occupational skin disease, attention should be given to processes and job functions, especially with regard to opportunities presented for skin contact; the existence or potential for engineering control measures; the use or potential for protective clothing such as gloves, aprons, suits, totes, and overshoes; general cleanliness and housekeeping; and the ambient physical environment. Inquire as to how the physical conditions, ventilation, etc. may vary with seasons. Are there significant alterations in the process from time to time? Hygienic and washing

VOLUME 72 NUMBER 6

facilities and locker rooms should be inspected, and the types and usage of soaps, towels, etc. determined. Remember that contact dermatitis caused by airborne materials is rare and that most instances are due to contact with surfaces, dusts, or liquids. Further data may be necesary to complete the evaluation. This may include an evaluation of possible contactants for their actual identity, previously observed or unexpected effects, and relevant toxicologic studies. An industrial hygiene evaluation of the work place may be helpful to identify materials and help quantitate exposures. In such an evaluation, it is necessary that attention be given to materials that will contact the skin, such as in the measurement of substances in wipe samples from surfaces. Measurements of air levels of substances often tend to be performed in such circumstances but are of virtually no value in occupational dermatitis. In more complex cases in which a relationship with work cannot be proved in an individual instance and a number of workers appear to be involved, simple epidemiologic techniques may be appropriate, such as determining attack rates by department or area of the plant, an evaluation of temporal relationships to the use of certain materials or processes or to areas where affected employees worked at the onset of sensitization, etc. Diagnostic criteria to determine whether a dermatitis is occupational can be grouped in six categories: 1. Physical appearance of lesions, patterns of clinical reaction, and regional distribution are consistent with disease caused by the suspected chemical, physical, or biologic agents. 2. Appropriate history to determine whether there has been exposure to agents capable of producing the skin disease under evaluation. Remember multiple causal agents may be involved. 3. A logical time relationship between exposure(s) and skin disease must be determined. 4. Removal from the suspected causal exposure(s) leads to improvement or remission in an appropriate time period. Although clear-cut improvement may occur, studies have shown that long-standing dermatitis is often very slow to improve, even after causal factors have been removed, and that occupational contact dermatitis in any case carries a suprisingly poor prognosis. 45-47In addition, other aggravating exposures may be continuing. 5. Possible nonoccupational provoking agents appear to be ruled out or are less likely as causes. 6. In certain types of disorders, investigation may show a specific possible causal reaction (e.g., patch testing in allergic contact dermatitis). Based on the above considerations, the diagnosis can be made as to whether the dermatosis is caused or

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aggravated by the work situation. The skin disease may be unrelated to employment, in which case the physician should be satisfied that the skin disorder would exist in its present state and extent even if the individual had never had this particular occupation. REFERENCES 1. Adams RM: Occupational skin disease. New York. 1983, Grune & Stratton Inc 2. Foussereau J, Benezra C, Maibach HI: Occupational contact dermatitis. Philadelphia, 1982, WB Saunders Co 3. Maibach HI, Gellin GA: Occupational and industrial dermatology. Chicago, 1982, Year Book Medical Publishers Inc 4. Report of the OSHA Advisory Committee on Cutaneous Hazards. Washington, 1979, Office of Consumer Affairs. US Department of Labor E: Occupational diseases in California. State of 5. Baginsky California, 1973, Department of Public Health, Occupational Health Section and Center for Disease Statistics 6. Baginsky E: Occupational skin disease in California. Division of Labor Statistics and Research, California Department of Industrial Relations, 1982 7 Schwartz L, Tulipan L, Birmingham DJ: Occupational disease of the skin. Philadelphia, 1957, Lea & Febiger 8 Encyclopaedia Britannica, ed 15. Chicago. 1977, Encyclopaedia Britannica, International RJ, Blank IH: Permeability of the skin. Physiol 9 Schevplein Rev 51:702, 1981 10 Bronaugh RL, Maibach HI: In vitro percutaneous. In Marzulli FN, Maibach HI, editors: Dermatotoxicology, ed 2. Washington, 1983, Hemisphere Publishing Corp RJ, Maibach HI: Regional variation in penetration 11 Feldmann of “C cortisone in man. J Invest Dermatol 48:181, 1967 12 Wester RC, Maibach HI: In vivo percutaneous absorption. In Marzulli FN, Maibach HI, editors: Dermatotoxicology, ed 2. Washington, 1983, Hemisphere Publishing Corp 13 Figard WH: Permeation: An important factor in hand protection selection. Occup Health Saf 51:32, 1982 14 Philips L, Steinberg M, Maibach HI, Akers WA: A comparison of rabbit and human skin response to certain irritants. Toxic01 Appl Pharmacol 21:369, 1972 15 Steinberg M, Akers WA. Weeks MH, McCreesh AH, Maibath HI: A comparison of test techniques based on rabbit and human skin responses to irritants. In Maibach HI, editor: Animal models in dermatology. Edinburgh, 1975, Churchill Livingstone Inc, pp 1- 11 16 Mathias CGT: Clinical and experimental aspects of cutaneous irritation. In Marzulli FN, Maibach HI, editors: Dermatotoxicology, ed 2. Washington, 1983. Hemisphere Publishing Carp, pp 167-84 17 Rothenborg HW, Meme T, Sjolin KE: Temperature dependent primary irritant dermatitis from lemon perfume. Contact Dermatitis 3:37, 1977 18 Fregert S: Manual of contact dermatitis. Copenhagen, 1981, Munksgaard 19 Sting1 G, Katz SI, Green I, Shevach EM: The functional role of Langerhans cells. J Invest Dermatol 74:315, 1980 20 Baer RL, Berman B: Langerhans cells. In Safai B, Good RA, editors: Immunodermatology: Comprehensive immunology, vol 7. New York, 1981, Plenum Publishing Corp 21 Emmett EA: Phototoxicity from endogenous agents. Photochem Photobiol 30:429, 1979 22. Emmett EA: Drug photoallergy. Int J Dermatol 17:370, 1978 23. Konzen JK: Fiberglass and the skin. In Maibach HI. Gellin

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3 1.

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33. 34.

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GA, editors: Occupational and industrial dermatology. Chicago, 1982, Year Book Medical Publishers Inc Possick PA, Gellin GA, Key MD: Fibrous glass dermatitis. Am Ind Hyg Assoc J 31:12, 1970 Heisel EB, Junt FE: Further studies in cutaneous reactions to glass fibers. Arch Environ Health 17:705, 1978 Taylor JS: Chloracne-Update and overview. Ann NY Acad Sci 320:295. 1979 Taylor JS: Chloracne from 3,3’ ,4,4’-tetrachloroazoxybenzene and 3,3’,4,4’tetrachloroazonxybenzene-Update and review. In Hutziner 0, et al, editors: Chlorinated dioxins and related compounds: Impact on the environment. Oxford, 1982, Pergamon Press Poland A, Knutson JC: 2,3.7,8-Tetrachlorodibenzep-dioxin and related halogenated aromatic hydrocarbons: Examination of the mechanism of toxicity. Annu Rev Pharmacol Toxic01 22:517, 1982 Vos JG, Faith RE, Luster MI: Immune alterations. In Kimbrough R, editor: Halogenated biphenyls, terphenyls, naphthlenes, dibenzodioxins and related products. New York, 1980, Elsevier/North Holland, Biomedical Press Chang KY, Hsieh KH, Lee TP, Tang SY, Tung TC: Immunologic evaluation of patients with polychlorinated biphenyl poisoning: Determination of lymphocyte subpopulations. Toxic01 Appl Pharmacol 61:58, 1981 Gellin GA: Pigment responses: Occupational disorders of pigmentation. In Maibach HI, Gellin GA, editors: Occupational and industrial dermatology. Chicago, 1982, Year Book Medical Publishers Inc Bleeker SS. Pathak MA, Hori Y, et al: Depigmentation of skin with 4 isopropyl catechol, mercaptoamines and other compounds. J Invest Dermatol 50:103, 1968 Jimbow K. Obata H, Pathak MA, et al: Mechanism of depigmentation by hydroquinone. J Invest Dermatol 62:436, 1974 McGuire J, Hendee J: Biochemical basis for depigmentation of

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