Occupational Dermatitis f ram Physical Causes PAOLO DANIELE PIGATTO, MD, AGOSTINA LEGORI, MD, ANDREA STEFANO BIGARDI, MD

T

his article concerns a wide range of skin diseases characterized by a number of clinical pictures that are related to several etiologic varieties. A single pathogenic agent may give rise to various pathologic phenomena, depending on the duration and intensity of exposure and on whether other physical, chemical, or biotic agents involved. Physical agents may be concomitant or aggravating factors in skin diseases: some environmental factors (including variations in skin humidity, friction, occlusion, or an excessively cold or hot environment) are very important in the pathogenesis of irritative contact dermatitis. Little is known about the real incidence of physically induced occupational diseases, although they seem to be less frequent than those caused by chemical agents. Epidemiologic data from different countries are contradictory, because of differences in the national regulations for occupational medicine. In the final analysis, the physician has to establish the cause and the extent to which this affects the onset, persistence, or worsening of a disease; in fact nonoccupational activities and/or environmental stimuli may become aggravating factors. Other factors, such as genetics, race, age, nutrition, and systemic diseases, may make certain individuals particularly susceptible to cutaneous pathologies because they affect the sensitivity and reactivity of the skin (Table l).Q From a medicolegal point of view, it is important that the patient’s dermatologic and occupational history is thoroughly investigated and that a complete clinical and environmental study is carried out, to establish any direct relationship between the clinical picture and a suspected causative factor. Suspect factors are those to which the patient has only (or prevalently) been exposed during From

the Department

of Dermatology

IZ, University

of Milan,

Milan,

Italy. Address correspondence to Paolo Daniele Pigatto, Department tology 11, University of Milan, Via Pace, 9, 20122, Milan, Italy.

0 1992 by Elsevier Science Publishing

Co., Inc.

l

of Derma-

0738-081x/92/$5.00

working activities that lead to an exacerbation or worsening of the condition on return to work, or, on the other hand (providing the condition is not irreversible), there must be a partial or total regression during interruptions in occupational exposure. Some clinical pictures are called occupational stigmata because of their frequency and particular characteristics such as hyperkeratotic lesions provoked by mechanical stimuli; these were more frequently observed in the past.

Skin Diseases Caused by Occupational Mechanical Factors The mechanical factors that can cause occupational dermatitis are acute traumas, friction and chronic repeated microtraumas, pressure, and vibration. Tolerance to traumatic events is affected by genetic, racial, and individual (age, sex, etc) factors. The skin responds to mechanical stimuli by means of various defensive mechanisms; but once these are overcome, the mechanical stimuli may lead to a number of different types of pathologic manifestations. Some mechanical factors are often concomitant causes of occupational pathologies because they alter the integrity of the skin barrier and facilitate the action of chemical or infective agents. The role of microtraumas can be important in the development and persistence of both allergic and irritative contact dermatitis.

Acute Traumas Here we consider cutaneous lesions of surgical interest that, from the medicolegal point of view, can be considered as working accidents. Traumas from sharp or blunt objects may lead to lesions of the dermis thorium in the case of superficial wounds, but also of the subcutaneous layers if the wound is deep. In the case of dragging or stretching forces (from gears, transmission belts, wheels, etc),3 there are laceration and contusion.

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Table 7. Individual Factors Predisposingto Occupational Skin Diseases

Violinists’ neck. Violin and viola players present with a dermatitis at the part of the neck supporting the instrument that is characterized by folliculitis, erythema, dyschromatosis, papules, pustules, and, in severe cases, the formation of follicular cysts (mechanical acne); in some cases, there may be hyperkeratotic lesions. Analogous cases are described among American football players and are due to the chinstraps of their helmets.6-9 Black heel (hemorrhagic hyperkeratosis and calcaneal petechiae). This condition is caused by repeated traumas of an intensity sufficient to provoke lesions in the capillaries of the superficial derma that may also involve the sole of the foot and the big toe.‘O Clinical manifestations are groups or lines of bluish-black punctiform lesions a few millimeters in diameter (1 to 4 mm or more), sometimes surrounded by punctiform hemorrhages and hyperkeratosis, which can make it difficult to differentiate from warts or pigmentary lesions.5 This picture is typical in professional sportsmen, particularly basketball, volleyball, and tennis players, and weight lifters (in which case, of course, it is localized to the palms of the hands).’ Rower’s hands. Microtraumas, low temperatures, wind, and dampness act in synergy in the creation of erythematous blotches on the fingers and backs of the hands, sometimes associated with blisters.lOJ1 Subjectively, there is a sensation of pain.

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Hereditary Hereditary palmoplantar keratodermatitis Albinism Phenylketonuria Epidermolysis bullosa Mild recessive articular atrophic epidennolysis Ichthyosis vulgare Constitutional Palmoplantar hyperhidrosis Acrocyanosis Allergic diathesis Seborrheic dermatitis Acquired Cutaneous Irritative dermatitis lack of vitamins A, pellagra preventing factor, Photodermatitis Extracutaneous Porphyria cutanea tarda Digestive dyspepsia Systemic neoplasias Nervous svstem diseases

bullosa

and 8,

From a dermatologic point of view we consider only alterations in the healing process resulting from the formation of hypertrophic or keloid scarring. In the first case, there is an excessive production of collagenous tissue with a high degree of angioblastic involvement and the persistence of granulation tissue; in the second, macro- or microtraumas lead to an abnormal fibrosclerotic skin reaction affecting mainly the shoulders and the presternal region. This latter reaction may also occur spontaneously in predisposed subjects (eg, blacks, diabetics, or patients with Touraine - Rue1 polyfibromatosis).4

Friction

and Chronic Repeated Microtraumas

If the intensity of this type of mechanical stimulus is low, it leads to an increase in the cell turnover of the basal layer and the formation of hyperkeratosis; if it is high, it leads to an intraepidermic bullous formation (such as that found on the palm of the hands after using tools).5 During some working activities, specific areas of the skin are inevitably exposed to this type of stimulus. This gives rise to the so-called occupational stigmata (characteristic lesions in terms of morphology, location, and frequency), the pathogenesis of which also involves constitutional, local (circulation, temperature, chemical substances, and infections), and physical (radiation and humidity) factors. These may manifest as hyperkeratosis, tylomas, scarring, or dyschromatosis. Particular examples follow:

Small wounds and abrasions can be found in butchers, poulterers, and fishmongers as a result of contact with bone fragments, as well as in all occupations involving direct contact with sharp material (glass- and metalworkers); for example, erosion and scarring are typically found on the anterior parts of the legs of shovelers.5 Continuous exposure to the causative agent and the concomitance of other factors (eg, contact with chemical substances such as soluble oils) may lead to infections, making healing difficult. Tylomas, mainly on the palms of the hands and the flexing part of the fingers, are frequent in many occupational activities. If they become extremely marked or complicated by rhagades or cracks, the pain they cause may limit working activities. Certain locations are particular to specific types of work or the tools used. In musicians, these are the tips of the fingers in the players of stringed or wind instruments (with typical pictures for the different instruments); in trumpet players, the lips are aff ected.5*12 Hairdressers are affected on the fingers of the right hand as a result of friction from their use of scissors; in

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shoe repairers, it is the flexor region of the right thumb. Sometimes, such calluses are associated with bullous reactions. Large hyperkeratotic patches are typical on the knees of floor layers and on the little fingers of spinners, possibly associated with chronic tenosynovitis of the hand and considerable functional damage.‘O Onycholysis is typical in furriers and is caused by the act of separating the chorion from the fur. Microtraumas may also affect the appearance and persistence of other skin diseases (eg, eczema on the hands of housewives), or be a concomitant cause of particular reactions in patients suffering from particular forms of dermatitis. Friction or rubbing can lead to a dermatographic urticaria of unknown pathogenesis (2 to 5% of the population), in which linear pruritic wheals appear for a few hours. More severe cases may hide a clinical picture of hereditary angioedema.5 Typical, for example, is Koebner’s sign (Table 2) (or reactive isomorphism) in which an isomorphic lesion to the primary dermopathy appears at the site of the trauma after a certain period (14 to 21 days in the case of activephase psoriasis). Psoriasis is not always easy to diagnose, particular when there are slightly erythematous scaling lesions or rhagadiform and keratotic manifestations on the hands which make it difficult to differentiate from contact dermatitis. Plumbers, carpenters, and other hand-tool users who may come into contact with caustic substances are more susceptible. Psoriasis may be generalized to all of the body after important traumatic events, or after an emotional shock following an accident. The use of heavy-duty working boots may lead to psoriasis appearing on the soles of the feet4 Even the nails may be involved (psoriatic onychopathy). Occupational psoriasis accounts for about 1.2% of all technopathies; 90% of these patients suffer from psoriasis minima (plumbers, carpenters, etc).13 In such subjects, an appropriate choice of work may be a useful preventive measure. Koebner’s sign may be expressed in other occu-

Table 2. Koebner’s Sign Lichen ruber planus Lichen nitidus Lichen simplex chronicus Follicular keratosis Pemphigoids Flat warts Molluscum contagiosum Psoriasis Eczemas

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pational diseases or diseases that are aggravated by working conditions. Some cases may also involve stimuli from pressors, heat, cold, or chemical irritation.14 The reaction to mechanical trauma is anomalous in some skin diseases, leading to excessive cutaneous fragility and the formation of bruises and bullous eruptions, for example, mild bullous epidermolysis and porphyria cutanea tarda, in which bullae form after minimal traumas. In keratoderma palmaris et plantaris, hyperkeratotic patches are easily formed. Rare reports concern, for example, the appearance of Buschke’s scleroedema at the site of a trauma after a latency period lasting as long as 3 years.15 Finally, it is necessary to remember the possibility of the appearance of skin tumors (particularly basal cell carcinoma) following acute and chronic repeated traumas.i6 Virchow noted this correlation in 1863, but it is still a subject of controversy.” The mean period of latency for acute traumas is about 21 months (3 to 57 months), whereas it is 36 months in the case of chronic repeated microtraumas. It is thought that the trauma is capable of accelerating or encouraging an already-present cancerogenic potential, or rather that it may alter the delicate proliferation-regulating mechanisms by reducing tissue control. There is a frequent association with other favoring factors, particularly solar exposure or heat (welders and engine room workers).‘a

Pressure Some workers exposed to heavy localized pressure on a particular skin area may be affected by pressure urticaria; after a 6- to B-hour latency period, there is a profound and painful wheallike reaction that can last as long as 8 to 24 hours5 It may be associated with delayed dermatographism 8 to 18 hours after the stimulus or with a picture of generalized urticaria. In the case of a long-lasting pressure stimulus, manifestations are localized to the hands (as a result of using a screwdriver or similar tool) or to the soles of the feet after a race or standing.4 Prolonged pressure and an erect position may lead to the appearance of painful or nonpainful papules, particularly on the heel, as a result of the hemiation of the subcutaneous layers of the dermis (piezogenic pedal papules).‘O Excessive pressure from a tool or a shoe leads to erythema, blebs, and sometimes necrosis, particularly if the skin is damp or in contact with caustic substances, such as cement.lg

Vibration After varying lengths of time, the use of vibrating or shaking tools (eg, pneumatic hammers, chainsaws, or chipping tools) or actions that transmit vibrations of 8 to

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150 Hz to the hands (as with pianists, typographers, typists, and seamstresses) may lead to the development of Raynaud’s phenomenon. lo These vibratory stimuli cause lesions in vessel walls, in phalangeal bone, nerves, and muscles, and in the central and autonomic nervous systems (alterations in sympathetic tone). Useful preventive measures include the use of vibration-absorbing equipment, such as special air-filled gloves, and a reduction in the amount of time spent on such activities. An important concomitant causal factor is the cold, which may trigger an angioblastic crisis. In fact, a number of studies have shown that the frequency of the pathology is less when the same work is performed at higher environmental temperatures.20 Symptoms are initially fleeting and slight: tingling and hypoesthesia in the fingers. A more fastidious symptom is the polyhidrosis of the palms, which affects 50% of cases. With time, sometimes even years, there are episodes of waxy pallor of the ungual phalanges (white finger) that conclude with a burning sensation and phalangeal hyperemia. These vasoconstrictive crises usually last between 15 and 40 minutes, but may continue for as long as 1 to 2 hours.21,22 Trophic disturbances are rare; they include an alteration in tactile and thermal sensitivity with functional impairment of the hand and the loss of the ability to carry out manual precision work.5 Providing the disease is in its initial stages and no irreversible damage has been caused, the symptoms regress when the stimulus is interrupted; more severe cases may lead to cutaneous necrosis of the fingertips.23 There are reports of cases of hereditary angioedema and forms of familial vibratory urticaria associated with these types of work.24

Skin Disease Caused by Radiation in the Workplace Working activities may lead to exposure to various types of radiation (Tables 3 and 4); consequently, it is important to understand the effects these might have on living beings. Protective measures and careful plant design are indispensable in the prevention of all skin diseases caused by ionizing radiations. Table 3. Workers Exposed to lonizinx

Radiation

Workers in the production of plastics Workers in food and drug sterilization Radiologists and technicians in diagnostic and therapeutic Television operators Workers with radium and radioactive substances

services

Table 4. Workers Exposed to Ultraviolet Sun rays

Arc welding

Sterilizing sources (antibacterial UV lamps)

A laser’s UV rays Lamps used in type processing:

Stage lamps (xenon lamps and gasdischarge lamps)

Radiation

Farmers Gardeners Masons Bathing attendants Fishermen Dockers Miners Oil field workers Oil pipeline workers Railway line workers Asphalt workers Building Road menders Skiers and tennis players Open-air workers Welders Smelting furnace workers Chief foremen Welder maintenance workers Oil pipeline maintenance workers Physicians Laboratory workers Nurses Barbers Food preservations workers Spectrophotometric workers Phototherapists Surgeons Lithographers Printers Inking workers Photoengravers Television operators Comedy and screen actors

In the case of nonionizing radiation, particularly sensitive subjects must totally avoid any kind of exposure. Given the considerable variations in individual susceptibility (as a result of genetic and constitutional factors, sex, age, and other physiologic or pathologic conditions) and local skin sensitivity (eg, the volar surfaces are more radiosensitive), an initial preventive and subsequent periodic medical examinations are essential. Preexistent skin diseases that alter the cutaneous barrier may increase the effects of radioactive contamination or limit the effects of decontamination treatments. These diseases include eczema, psoriasis, ichthyosis, severe hand dyshidrosis, and, in general, all chronic and recurring exudative and hyperkeratotic dermopathologies.25 Precancerous lesions, radiodermatitis, benign tumors, and keloid scarring also represent conditions of increased susceptibility to ionizing radiation, but it is the nonionizing radiation (ultraviolet, infrared, and invisible radiation) that is more frequently found in working environ-

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PIGATTO, LEGORI, AND BIGARDI PHYSICAL CAUSES OF OCCUPATIONAL DERMATITIS

ments and to which the largest number of workers is exposed (Table 3). Exposure to ionizing radiation occurs much less than it did 20 or 30 years ago. Greater understanding of its acute and chronic effects has led to the development of a number of more effective protective measures, such as screens and the like, and the risk is now mainly accidental; however, the increased use of ionizing radiation in processes such as the curing of plastics, the sterilization of food and drugs, the analysis of metals, and the manufacture of color televisions has led to an increase in the number of exposed workers.

Occupational Skin Dermatitis Ionizing Radiation

Caused by

Acute Radiodermatitis The epidermis is very sensitive to ionizing radiation because of the presence of continuously replicating cells in its germinal layer. Acute radiodermatitis is the result of accidental exposure to ionizing radiation or radioactive substances. The more limited the irradiated area, the greater the dose tolerated by the exposed tissue; depending on the dose, there may be various degrees of lesion. After a latency period varying from 24 hours to 2 to 3 days, transitory erythema develops in the affected area as a result of the release of histamine and/or serotonin. Erythemogenic doses are around 3 to 8 Gy (if the dose is less, there must be a longer exposure time); the total dose needs to be greater if it is divided over a period (eg, 30 daily doses leading to a total of more than 25 Gy). The level of erythemogenic doses is conditioned by constitutional factors, skin localization, sex, race, age, and the type of ionizing radiation.26*27 After a period varying from 3 days to 3 weeks, this “initial” phase (which resolves itself in 24 to 48 hours) is followed by a “delayed’ erythema probably connected with the release of proteolytic enzymes from radiated epidermic cells that have undergone replicative, degenerative, or necrotic modifications. Occasionally, after 3 to 4 weeks, a third phase of erythema may develop involving hyperpigmentation, which may persist indefinitely as a result of tyrosinase activation. If the dose is higher (30 to 40 Gy), the time to onset of these manifestations is shorter, and they are accompanied by edema, purpuric bruising, dermo-epidermic blebs, erosion and ulceration. The symptoms are very painful. Reepithelialization of the necrotic area takes place in 1 to 3 months, leaving it with an atrophic appearance and the temporary or permanent loss of the sudoriparous sebaceous glands and pilar apparatus, and, if the lesion affects the extremities, also loss of the nails. If the dose is very high, the area becomes

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hypopigmented as a result of the destruction of melanocytes. At the dermal level, there is vascular damage and damage to the collagen and elastic fibers. This epithelium is particularly sensitive to further radiation, or any other kind of chemicophysical or biotic insult. Total-body exposure to 30 Gy or more is fata1.28 Exposure to between 10 and 30 Gy is associated with systemic symptoms; initial nausea, asthenia, vomiting, diarrhea, fever, and shock are followed, after 10 to 14 days, by hemopoietic alterations and the appearance of bruising and diffuse petechiae, alopecia, fever, hematic diarrhea and asthenia, and infections leading to death as a result of the suppression of bone marrow function. Exposure to extremely low levels of radiation may lead to subclinical damage, with no associated symptoms except for a slight cutaneous atrophy similar to senile atrophy. Over time, the clinical picture may evolve into chronic radiodermatitis, a development that is also possible in the case of acute radiodermatitis.

Chronic Radiodermatitis Chronic radiodermatitis develops as a result of chronic exposure to small suberythemogenic doses repeated over time or on an area with acute radiodermatitis after a long latency (weeks, months, or even years after the last exposure). Its appearance may also be triggered by a trauma or skin infection, Clinically, the skin appears atrophic (for the reasons described earlier), necrotic, and dyschromic. There may also be associated fissurations, chronic evolutive ulcerations that may become cancerous; these are very painful and resistant to treatment. Localized hyperkeratosis, telangiectasia, and punctiform hemorrhages can also be observed. Because of the temporary or permanent loss of cutaneous appendages, the skin appears glabrous. The nails become thin and brittle with longitudinal melanotic streaks, and there are small periungual hemorrhages and chronic inflammation of the paronychia.26*27 Sometimes, there may be sclerosis of the dermis and hypodermis, which gives the skin a hard and pasty consistency and, in more severe cases, may lead to considerable functional impairment. The dermoepidermic ridges on the fingertips may become smooth to the point that fingerprints disappear. The skin is extremely vulnerable, and this may limit occupational activities, particularly in the case of manual work. Rhagades may form on the backs of the hands and are very painful. After a latency period varying from 4 to 10 years, these lesions may become cancerous and give rise to a number of different types of skin tumors. These are prevalently squamous and basal cell carcinomas, Bowen’s disease, and, less frequently, fibrosarcomas,30 all of which may

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also appear in apparently healthy skin. Squamocellular carcinomas make up almost all of the radio-induced carcinomas and have greater metastasizing properties than photo-induced carcinomas. Fused cell mesenchymal tumors, sudoriparous sebaceous gland tumors, and melanomas are rarely observed. In occupational environments, the most frequently affected sites are the hands, particularly the index and middle fingers; the face and forearms are rarely affected. In part, the speed of onset is directly proportional to the absorbed dose and the time of exposure.

Occupational Skin Disease Caused by Nonionizing Radiation Nonionizing radiation includes radiation of different wavelengths, classified as UV-A (400 to 320 nm), UV-B (320 to 290 nm), and UV-C (290 to 200 nm). The visible solar spectrum (also called visible radiation) includes wavelengths between 400 and 740 nm. The subdivision of infrared radiation is more complex and includes type A (740 to 1400 nm), type B (1400 to 3000 nm), and type C (3000 to 3500 nm). The biologic effects of all of these types of radiation depend on their wavelengths. Like ultraviolet radiation, visible radiation causes certain kinds of photodermatosis. The effect of infrared radiation (particularly in the type B and C bands) is essentially thermic; however, some sources of these types of radiation are sufficiently intense to provoke skin burns and vasodilation, for example, laser beams.26 The mechanisms by which the skin defends itself from both visible and invisible radiation can be summarized as follows: a thickening of the corneum, which occurs promptly after a few days’ exposure and is the main mechanism of photoprotection; increased production of melanin, which is capable of absorbing the majority of wavelengths, particularly ultraviolet radiation. The skin is also capable of activating itself metabolically by forming stable free radicals. A few hours after photoirradiation, there is a so-called “immediate” pigmentation, which is caused, above all, by U-VA and visible radiation and is due to the oxidation of the melanin already present in the epidermis. This pigmentation disappears after a few hours at most, and has no protective effect, unlike the “delayed” pigmentation caused by UV-B radiation, which usually appears about 72 hours after exposure as a result of the formation of new melanin pigment. Exposure to the sun is, however, necessary to humans because it is solar radiation that leads to the production of vitamin D, particularly radiation of the infrared type B band (with peak wavelengths of up to 125 nm) which has greater skin penetration; but such radiation can also give rise to certain skin pathologies.31-33

Clinics in Dermatology 1992;10:231-243 Acute Actinic Dermatitis or Solar Eythema Ultraviolet, infrared, and visible radiation act synergically in causing solar erythema when exposure is sufficiently intense. Solar erythema is due mainly to the action of highly phlogogenic UV-B radiations from 15 to 80 mJ/ cm2; in the case of UV-A, however, irradiation must be more than a good 10 to 40 J/cm2. Solar erythema may be accompanied by other primitive lesions as a result of intense photoexposure (such as blisters and blebs), as well as by inflammatory signs such as spontaneous pain, edema, and functio laesa. Erythema is present about 6 hours after exposure, reaches its acme after 12 to 24 hours, and then resolves within about 36 hours. Doses of more than four times the minimal erythema dose lead to a more rapid and intense response, which tends to persist for a number of days (sunburn) and is followed by scaling, desquamation, and pigmentation. Sunburn is always accompanied by general symptoms (eg, nausea, hyperpyrexia, headache, and lassitude) associated with the release of interleukin-1 and interleukin-4 from the keratinocytes in necrosis (sunburn cells).34,35

Chronic Actinic Dermatitis Chronic actinic dermatitis includes a series of histologic and skin alterations similar to those present in senile cutaneous involution.5,31,35 Clinical signs include the appearance of wrinkles in subjects over 40 years old and a yellowish skin with atrophy, xerosis, lentiginosis, solar keratosis, telangiectasis, petechiae, and a loss of elasticity. The skin seems to be particularly vulnerable to even the slightest physical trauma, with epidermal detachment and purpuric manifestations. Constitutional and individual factors such as pale skin, xerosis, seborrhea, and differences in the capacity to repair photo-induced damage, or metabolic factors (eg, liver disease) and a state of chronic physical fatigue36 may all affect the early onset of this clinical picture. The main histopathologic lesion is elastosis of the derma (particularly its papillary portion) with an irreversible degeneration of collagen fibers, whereas the epidermis presents irregular thickening.26*37 The sites most affected are typically those most exposed to the light: the face (cheeks, temples, and ears), the backs of the hands, and the forearms. Clinical pictures such as these include the cystic and comedonic dermatitis of Favre - Racouchot syndrome, Milian’s citrin skin, cutis rhomboidalis nuchae (frequent in sailors, stokers, salt workers, sportsmen, and country people), and Pellizzari’s colloid pseudomilium.35 Photodermatitis Photodermatitis covers a wide range of dermopathies characterized by an altered cutaneous response to non-

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PHYSICAL

Table 5. Skin DiseasesInduced by Sun Exposure Direct photodermatitides Acute solar dermatitis Chronic solar dermatitis Mediated photodermatitides Contact Phototoxic Immediate (drug) Delayed (drug/phytodermatitis) Photoallergic Drug/other chemical substance Systemic Exogenous phototoxicity (drugs) Immediate Delayed Endogenous phototoxicity Porphyria Idiopathic photodermatoses Solar urticaria Polymorphous photodermatitis Hutchinson’s freckle Hydroa vaccinifonne Actinic reticuloid dermatitis Photosensitive eczema Actinic lichenoid dermatitis Actinic porokeratosis Photoconditioned dermatoses Altered tryptophan metabolism DNA repair deficiency (xeroderma pigmentosum) Telangiectatic diseases Albinism Photoaggravated dermatoses Lupus erythematosus systemic/lupus erythematosus Dermatomyositis Lymphocytoma and lymphocytic skin infiltration Rosacea Pemphigus erythematosus and pemphigus foliaceus Pityriasis rubra pilaris Darrier-Ferrand disease Hailey - Hailey disease Grover’s disease Polymorphous erythema Herpes and viral exanthemas Psoriasis Atopic dermatitis Stucco keratosis Solar granuloma

disseminatus

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sures to be taken. The most frequent forms of occupational photodermatitis are mediated by exogenous factors, by which is meant that there is an abnormal reaction between ultraviolet or visible radiation and substances present on or in the skin (light-sensitizing drugs or natural or synthetic chemical substances) (Tables 6 and 7). These substances may come to the skin either topically or systemically. It is recognized that there are two distinct physiopathologic mechanisms in reaction to light, phototoxicity and photoallergy, although it is admitted that there may also be other mechanisms that are pathogenetically less known and certainly less frequent.35,38 The origin of the light-sensitizing substances found in occupational environments may be natural (eg, the psoralens contained in plants or in the Bryozoa, a class of small marine invertebrates) or industrial (chemical synthesis), but they generally lead to phototoxic reactions. A phototoxic reaction is the nonimmunologically based skin response of the majority of subjects to the simultaneous presence of an appropriate level of radiation and an appropriate quantity of chemical substance on the skin. In the case of photoallergy, on the other hand, there is a cell-mediated immunologic response and even small quantities of radiation and chemical substances may be sufficient to induce a reaction. Some photosensitizing reactions may require various exposures over a period. Other mechanisms include the induction of delayed cutaneous porphyria by compounds such as hexachlorobenzene, chloroquinine, ethanol, the di- and trichlorophenols, ethylstilbestrol, and polycyclic aromatic hydrocarbons.32,33 In the majority of cases, the phototoxic reaction manifests as a first- or second-degree sunburn, with a prickling and burning sensation, erythema, and edema. Typically affected areas are those that are exposed to the sun (face, lower neck, nape of the neck, forearms, and backs of the

Table 6. SubstancesThat Frequently Cause Photoallergic Reactions

ionizing radiation (ultraviolet, visible, and, more rarely, infrared) or to photoexposure in association with other endogenous or exogenous factors. There are five classes of photodermatitis as shown in Table 5. Detailed anamnestic investigation and a thorough clinical examination using laboratory and instrumental diagnostic tests allow subjects with photodermatitis to be identified and kept away from worksites where they would be exposed to artificial sources of ultraviolet radiation or, where this is not possible, permit preventive mea-

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DERMATITIS

Psoralens Anthracene Benzopyrene Musk ambrette Phenothiazine Sulfamide p-Aminobenzoic Hexachlorophene Trichlorocarbanilide Tribromosalicylanilide Benzocaine Cinnamate Chlorhexidine

acid

Diphenhydramine Hydrocortisone p-Phenylendiamine Epoxy resins Zinc pyrithione Thiazide Sulfanilamide Phenofibrate Quinidine Furosemide Amitriptyline o-Penicillamine Ketoprofen

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Table 7. Substances That Cause Occupational Photoallergic Reactions Olaquindox Mineral oil CRT 20 Coal tar Salicylanilides alogenate Bryozoa Alcynodium gelatinosum Alcynodium hirsutum Electra pilosa

Algae Sargassum Laminaria Porphyra

muticum

(Japanese sargassum)

Thiourea and derivatives Celery Parthenium Heradeum

hysterophorus spondylium

Ethylene glyconitrate Ammonium nitrate Dinitrotoluene Sodium nitrate Quinine sulfate Fig latex Diaminodiphenylmethane Potassium dichromate Anthraquinone Fenticlor Hatacide LP5 Carbimazole Epoxy resins Cadmium Cobalt Epidian 3 and 5 Aromatic hydrocarbons Anthracene Carbonic washing fluid

whereas those areas that are relatively protected (such as the upper eyelids and the submental area of the neck) are spared. The condition resolves itself in 2 to 3 days with desquamation and, sometimes, pigment alterations (hyperpigmentation in the case of psoralens). There is sometimes a biphase or delayed phototoxic reaction that is clinically similar to that of chronic actinic dermatitis, and it is worth noting that phototoxic reactions are more intense in warm and damp environments.39 The most common phototoxic substances are coal tar and aromatic anthracene derivatives (which are also capable of inducing photoallergic reactions), such as acridine, pyrene, butyl-anthracene, fenanthrene, benzopyrene, fluoranthracene, and the psoralens (coumarins).40 The psoralens are present in some of the fruits and vegetables (carrots, figs, lemons, and celery) handled by workers in hands),

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the food industry, who are exposed to large quantities of psoralen derivatives when cutting or mincing them.41,42 The lesions may be linear as a result of contact with grass filaments (gardeners’ striped meadow-grass dermatitis) or may present the picture of Berloque dermatitis, with hyperpigmentation of sites of application of perfumes or after-shave lotions (face, neck, behind the ears, shoulders, breasts, and hands) as a result of the presence of 5-methoxypsoralen (bergapten) and other coumarins in perfumes. 43Photodermatitides from benzene derivatives can be observed in open-air workers in contact with asphalt or roofing pitch.32 Photoallergic dermatitis is less common than phototoxic dermatitis. Clinically, it looks like an eczema (although it may sometimes present with lichenoid papules); pruritis is an ever-present subjective symptom. This type of dermatitis affects mainly photo-exposed areas but, in particularly severe cases, it may involve regions not exposed to the light, and thus may be difficult to differentiate from airborne contact dermatitis or allergic contact dermatitis (Fig 1). Unlike cases of phototoxic reaction, dark skin is not a protective factor. It seems that the light converts haptens into full-blown allergens by various mechanisms. Occupational photohaptens are no different from those found in the population at large and,

Figure 1. Typical photoallergic contact dermatitis Guipositae in a cemete y worker.

due to

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in some cases, they are substances capable of causing phototoxic lesions. The substances that cause almost exclusively occupational allergic photodermatitis include, for example, thioureas and their derivatives,44,45 which are used in the vulcanization of rubber, but also in many other materials (such as plastic, plants, and clothes). Among the biologic substances involved in photoallergies, we have to remember the already-mentioned Bryozoaa (small marine invertebrates of the genus Alcynodium gelatinosum present in the North Sea and the Bay of the Seine), which cause occupational photodermatitis in fishermen during the summer.46-48 A possible complication in contact photoallergies is the development of a persistent reaction to the light (in particular, in those exposed to halogenated salicylanilide drugs, promethazine, chlorpromazine) with an abnormal reaction to radiation that may last months, even after removal of the suspected substance.

Prevention As in other technopathies, ber of specific points:

prevention

is based on a num-

1. Identification

2. 3.

4. 5.

of the phototoxic or photoallergic substances and their substitution with nonreactogenic molecules or, if this is impossible, avoidance of contact by means of careful engineering design or the use of protective clothing (dark clothes, glasses, gloves, etc) designed to reduce irradiation49*50 Use of barrier creams (solar screens) when exposure is unavoidable (open-air working activities) Periodic measurement and monitoring of the artificial sources of ultraviolet radiation and the use of protective screens Measurement of ultraviolet radiation exposure by means of polysulfone film badges Appropriate environmental hygiene, avoiding unnecessary exposure

In addition, workers should be adequately informed about the risks connected with excessive exposure to radiation. Finally, skin sensitivity to ultraviolet radiation associated with skin phototype must also be taken into serious consideration, and every effort must be made not to employ particularly sensitive subjects in jobs involving exposure to intense irradiation. It needs to be remembered that the incidence of photosensitivity in photodermatitis as a whole is very low. More important from the clinicodevelopmental point of view is the possibility that an occupation involving a high degree of exposure to UV-A radiation leads to photoaging, inducing neoplastic cell clones and the subsequent development of skin tumors.

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lnfrared Radiation Infrared radiation comprises the band 750 to 3,000,OOO nm in the electromagnetic spectrum, but biologically active infrared radiation ranges from 750 to 200 nm.10,2* Its main effect is thermic, and only in cases of highly intense sources (such as lasers) does skin burning occur; in cases of chronic exposure, there may be dyschromic alterations (particularly hyperpigmentation), telangiectasia, and clinical manifestations similar to those of erythema ab igne, the latency period of which may even be longer than 10 years. Workers exposed to infrared radiation include, among others, those working in metal foundries, furnace workers and glassworkers.

Visible Radiations Visible radiation comprises the wavelengths between 380 and 770 nm. Only in the case of stimulation with highpowered lamps do some forms of photodermatitis (usually in association with ultraviolet rays) or urticaria occur. Intense light sources include cinema studio and theater stage lights, the lights used in photographic studios, and electric or oxyacetylene gas arc welding lamps. Obviously, all open-air workers run the risk of developing reactions to visible radiation.

Video Display Terminal Dermatosis As early as 1981, Berg and Lidien in Norway described the appearance of a cutaneous face rash (particularly localized around the cheek bones and the mouth) after 2 to 3 days of exposure to a video display terminal.51 Other cases have since been described with clinical pictures characterized by erythema, telangiectasia, papules, and rosacea-like lesions, which are sometimes also found on the backs of the hands. Discussion still continues as to whether there is a real correlation between video display terminal exposure and the development of dermatosis. There is another possible correlation with the worsening of preexisting pathologies, such as acne, seborrheic dermatitis, rosacea, and Civatte’s poikiloderma; but once again, no cause-effect relationship has been clearly demonstrated. Video display terminals emit various types of electromagnetic radiation, including minimal quantities of UVA radiation, and may give rise to electrostatic fields that lead to the deposit of irritative volatile particles on the skin; but it is more likely that the stress of office work aggravates preexisting skin diseases.52*53

Occupational

Thermodermatitis

Cold Dermafosis Environmental temperatures can affect skin condition considerably, particularly after the long periods of expo-

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sure frequently occurring in working environments5 Cold (that is, a temperature of about O’C) may have a direct effect on the skin and can induce frostbite and cold urticaria (see the article by Fumagalli and Gibelli), although of course with different frequency. The pathogenetic mechanism by which near-zero temperatures act on skin tissue is the same for all cold-induced dermatoses, and is due to the crystallization of the water in intercellular space. 54 This leads to osmotic shock; the cells lyse on account of the low temperature and cause tissue necrosis. Cold can also have an inductive action in subjects affected by other pathologies (eg, vascular diseases),55 who may be more prone to develop dermatoses such as dry skin, eczema hiemalis, acrocyanosis, livedo reticularis, or Raynaud’s syndrome. Simple acrocyanosis, which is much more frequent in both occupational and nonoccupational dermatology, needs to be distinguished from its chronic hypertrophic form which is associated with acute organic wasting and chronic diseases. Although its etiopathogenesis is still unknown, there is often a positive family history.54 Frostbite is another cold dermatosis that can cutaneously manifest itself by various lesions, according to its severity. There is an initial phase when the skin is pale and hypoesthetic, which, with the persistence of low temperature, quickly leads to erythema caused by venous vasodilation as a result of active hyperemia.56 The second phase is characterized by the presence of dermoepidermic blebs (phlyctenae), accompanied by a worsening in symptomatology until it becomes painful; in peripheral regions, impressive edemas are often observed.57 Up to this stage, the lesions are reversible by means of restitutio ad integrum, but the development of the gangrenous and necrotic lesions that characterize the third stage is very serious. Symptoms are generally marked and, in severe cases and with the persistence of temperatures considerably below freezing, may lead to mutilation. This condition develops very slowly and requires the persistence of environmental stimulation. A much more frequently encountered occupational dermatosis is erythema pernio (or chilblains), which occurs in unprotected sites such as the fingers, forearms, lower legs, and nose. 28At onset, it presents an erythematous cyanotic picture with hypothermic skin, and may be accompanied by symptoms of pruritis or tenderness to finger pressure. It has a characteristic tendency to recur at every new exposure to the cold. Xerotic skin is frequently found in occupational environments and electively affects people working in refrigerated chambers (eg, butchers, warehousemen in the food conservation industry, laboratory storemen). Its clinical presentation is hyperkeratotic skin, which may evolve into a painful rhagadiform dermatitis58 that is dif-

Clinics in Dermatology 2992;10:231-243 ficult to cure unless provisions such as moving the subject from the place of work are taken, at least in the more obstinate cases. Eczema hiemalis, or asteatotic eczema, is comparatively rare in occupational environments. This is a xerotic and sometimes pruritic dermatitis that affects the lower limbs of elderly subjects58 and develops along the lines of the paraphysiologic condition of epidermic asteatosis present in old age. Among the vascular-based diseases triggered by the cold (although it can also be caused by vibrations in the working environment), Raynaud’s syndrome is worthy of mention5’ Pathogenetically, it is characterized by vessel hyperreactivity; consequently, on exposure to low temperatures, it presents with pallor of the distal phalanges of the fingers, which are also painful. Livedo reticular-is, which gives the skin a bluish color, may be idiopathic, secondary to a number of other diseases (vascular or not), or subsequent, for example, to intravenous bismuth tartrate therapies (used in the past for treating syphilis). This condition is more frequently associated with cryoglobulinemia or (even transient) thrombocytopenia, and it may also manifest after erythema ab igne. It is not rare to find it in association with other systemic diseases, such as pancreatitis, systemic lupus erythematosus, and rheumatoid arthritis.57 Occupational Skin Lesions Caused by Electricity Electricity is used in a large number of industrial working activities, but exposure to the risk of accident is greatest in places where electricity is produced (eg, hydroelectric power stations) and very high in companies involved in the distribution of electricity and the maintenance of the related plant and equipment.59 Statistically, however, the industrial sector most affected by accidents is the construction industry, followed by the producers of electrical energy, and then by the engineering and metallurgic industries. Lesions caused by electricity represent one of the most common industrial accidents2* Intuitively, the effects of an electric current passing through living beings depends on differences in potential, the resistance offered by the human body, and the duration of exposure. Any evaluation of the damage inflicted by an electrical current must be based on a knowledge of its intensity, because this is the parameter that best correlates with lesions that may be virtually invisible from a clinical point of view. A current of approximately 20 mA is capable of maintaining human skeletal muscles in their contracted state; in this case, continuation of the current leads to asphyxiation as a result of the contraction of the respiratory muscles. When an electrical current passes through skin tissue, its energy is converted into heat. Given that the human

Clinics in Dermatology 1992;10:231-243 body represents a resistance, the electricity passes from its point of entry (or contact) to its point of discharge (called “earth”) along the lines of least electrical resistance. It is at the latter point that the more profound and generally necrotic lesions corresponding to third-degree burns occur. It should be underlined that the alternating current (AC) more generally used in industry and homes causes much greater tissue damage than the direct current (DC) used, for example, in accumulators. As mentioned before, the skin lesions are similar to those induced by heats7 and they can therefore be graded according to the degree of insult, It is therefore possible to observe a phlyctena or an eschar, according to the profundity and severity of the lesion; however, unlike heat lesions, electric shocks cause little pain because of the destruction of cutaneous nerve endings. High-tension electricity has a fundamentally coagulative effect on tissue. * It is difficult to evaluate the general condition of the patient by inspection because, even though there may be only a few superficial skin lesions, the internal organs may have been severely damaged by the passage of the current.59 Treatment is similar to that used in cases of severe burns: escharectomy must be performed as soon as possible (ie, immediately after the hypovolemic shock has been corrected), to prevent the toxic substances released from the necrotic zone from entering into circulation. As in the case of severe burns, management of the patient during the days following the accident should be directed toward avoiding septic complications and encouraging tissue repair.60 Skin Lesions induced by Heat SKIN DISEASES. Exposure to heat sources in occupational environments is quite common and the use of heat is unavoidable in many working processes (eg, foundries). In some industries, the risk of acute and chronic heat skin diseases is closely connected with production activities, although, as can be seen in the case of the metallurgic industry, the current norms governing occupational medicine have made them much rarer than they were. It is certain that, in both occupational and nonoccupational environments, the most widespread form of heat dermatosis is burning. Burns are classified as superficial or deep according to the depth of the thermic insult, although it would be more correct to adopt the modern classification now used in many large burn centers and plastic surgery departments.’ This classification is based on tegument mortification criteria beginning from the external surface. First-degree burns are erythematous thermal injury lesions that resolve themselves in a few days, exclusively involve the epidermis, and show a burning sensation; HEAT

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these are superficial lesions whose outcome is resfifufio ad infegrum. A second-degree bum is characterized by the appearance of a phlyctena, a dermoepidermic blistering that is a much more painful lesion than the erythema of first-degree burns. The presence of the blister bears witness to transudation and consequent edema with cellular necrosis. The burn heals with temporary atrophy but without scarring. Evidently more serious, third-degree burns are characterized by necrotic tissue resulting from exposure to very intense or prolonged heat. There is present a blackish crust known as eschar, which represents the considerable mortification of the tegument in toto, extending to the subcutaneous layer and, in very severe cases, threatening life, even including muscle and bone layers. Some authors use other classifications: Artz and MoncriefZ distinguish bums of partial dermoepidermic depth, which include both first- and second-degree bums, and those of full depth, which correspond to third-degree bums. A fourth degree is contemplated for thermal lesions involving deeper muscle layers. Another general criterion is the extent of the bums according to Wallace’s classic schema (also known as the rule of nines), which allocates various points to different parts of the body: 9 points each to the head, left arm, and right arm; 18 points each to the trunk, back, left leg, and right leg; and 1 point to the perineal area.3 It needs to be borne in mind that the intensity of the thermal insult causing the bum is frequently not the same at all points of the involved parts, and it is therefore possible to find bums of different degree in sites that are physically very near each other. For this reason it is often difficult to say whether a second-degree bum will heal with or without leaving a scar, because it may involve bordering areas with deep second-degree lesions or even third-degree necrosis.57 Obviously, the seriousness of a patient’s condition depends on the type of bum, defined in terms of the depth and extent of the lesion. Treatment is oriented toward preventing infection as much as possible and assisting the cicatrization of the lesions. Severe bums involving more than 30% of the skin area give rise to problems more directly concerning internal medicine, particularly as far as volemia and the limitation of heat shock are concemed.60 Autologous skin transplantation using modem expanders should be considered in all cases of third-degree bums and in selected cases of deep second-degree bums. SKIN DISEASES CAUSED BY HEAT. These include skin diseases already described in this article, because they are due mainly to infrared and ultraviolet irradiation. Brief reference is made to those dermatoses the ex-

OTHER

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pression of which is due principally to prolonged exposure. Hand-warmer erythema (or erythema ab igne), which occurs much less frequently than in the past, affects primarily women. 54 It can be observed during the winter or after a stay in the high mountains, and is due to the action of infrared radiation, giving rise first to erythematous, then pigmentary, and finally (if the exposure continues) telangiectactic lesions. In occupational environments, furnace workers, glassmakers, firemen, boiler maintenance workers, and others are exposed to this skin disease.28 Heat urticaria, which is described in the article on occupational contact urticaria, should also be mentioned (see article by Fumagalli and Gibelli).

References 1. Wilkinson

2. 3. 4.

5. 6. 7. 8. 9.

10. 11.

12. 13. 14. 15.

DS. Cutaneous reaction to mechanical and thermal injury. In: Rook A, Wilkinson DS, Ebling FJG, et al, editors. Textbook of dermatology. 4th ed. Oxford: Blackwell Scientific, Publications 1986:587-622. Shmunes E. Predisposing factors in occupational skin diseases. Dermatol Clin 1988;6:7-13. Gallone L. Patologia chirurgica. 5th ed. Milan: Casa editrice Ambrosiana, 1986:46-55. Palminteri G, Allegri F, La Paglia G. Dermopatie professionali in rapport0 a fattori traumatici. In: Palminteri G, editor. Dermatologia professionale-patologia cutanea e medicina generale. Palermo: Medical Books 1990:131-9. Lachapelle JM. Dermatologia professionale. Milan: Masson, 1986:chap 3, pp 11-34. Zina AM, Annunziata M. I1 “callo” de1 violinista. G Ital Dermatol Venereol 1981;116:31-3. Peachey RDG, Mattheus CNA. “Fiddler’s neck.” Br J Dermatol 1978;98:669-75. Mills OH Jr, Kligman AM. Acne mechanica. Arch Dermatol 1975;111:481-3. Bnm I’, Baran R. Une acne mecanique meconnue: La dermatite du cou des violonistes. Ann Dermatol Venereol 1984;111:241-5. Sertoli A. Dermatologia allergologica professionale ed ambientale. Milan: 11 Pensiero scientifico, 1991:17-41. Toback AC, Korson R, Krusinski PA. Pulling boat hands: A unique dermatosis from coastal New England. J Am Acad Dermatol 1985;12:649-52. Rimmer S, Spielvogel RL. Dermatologic problems of musicians. J Am Acad Dermatol 1990;22:657-63. Moroni P, Cazzaniga R, Pierini F, et al. Occupational contact psoriasis. Dermatosen 1988;36:163-4. Ancona A, Fernandez-Diez J, Bellamy C. Occupationally induced psoriasis. Dermatosen 1989;34:176 - 8. Von Th. Bergner, Przybilla B. Posttraumatishes Scleroedema adultorum (Buschke). Dermatosen 1989;37:176-8.

Clinics in Dermatology 1992;10:231-243 16. De Paoli M, Grass0 R. Ruolo dei microtraumi nella genesi degli epiteliomi cutanei. G Ital Dermatol Venereol 1982; 117:213-7. 17. Epstein JH, Ormsby A, Adams RM. Occupational skin cancer. In: Adams RM, editor. Occupational skin disease. 2nd ed. Philadelphia: WB Saunders, 1990:136-59. cutanei 18. Alessi M, Caccialanza M, Contini D. Epiteliomi posttraumatici. G Ital Dermatol Venereol 1986;121:405-9. 19. Gellin GA. Physical and mechanical causes of occupational dermatoses. In: Maibach HI, Gellin GA, editors. Occupational and industrial dermatology. Chicago: Year Book Medical, 1982:109-14. 20. Hellstrom B, Andersen KL. Vibration injuries in Norwegian forest workers. Br J Ind Med 1972;29:255-63. 21. Yu Hsin-Su, Yao Tsing-Hua, Tseng Ho-Hing, et al. Vibration syndrome. J Dermatol 1988;15:466-72. 22. Futatsuka M, Veno T. Vibration exposure and induced white finger due to chain saw operation. J Occup Med 1985;27:257-64. 23. Taylor W, Pelmear PL. Vibration white finger in industry. New York: Academic Press, 1975;1:166-9. 24. Brai M, Clemanza L, Giglio MA. L’angioedema ereditario. In: Palminteri G, editor. Dermatologia professionale-patologia cutanea e medicina generale. Palermo: Medical Books, 1990:275 - 7. 25. Righi E, Strambi E. Problemi dermatologici dell’idoneith al lavoro con rischio da radiazioni ionizzanti. Securitas 1952;7/8:101-8. 26. Palminteri G, editor. Dermatologia professionale-patologia

cutanea e medicina generale. Palermo: Medical Books, 1990:163-9, 171-7, 191-9. 27. Malkinson DM, Wiskemann A. Some principles of radiobiology and the effects of ionizing radiation on skin. In: Fitzpatrick TB, Eisen AZ, Wolft K, Freedberg IM, Austen KF, editors. Dermatology in general medicine. 3rd ed. New York: McGraw-Hill, 1979:1431-9. 28. Kanerva L. Physical causes of occupational skin disease. In: Adams RM, editor. Occupational skin disease. 2nd ed. Philadelphia: WB Saunders, 1990:41-72. 29. Galasso F. Le radiodermiti professionali. Riv Infortuni Ma1 Prof Parte I, 1974:620-32. 30. Paris B, Zultak M, Drobacheff Ch, et al. Maladie de Bowen disseminee vingt ans apres la manipulation de produits radioactifs dans l’horlogerie. Ann Dermatol Venereol 1988;115:43-46. 31 Ramsey CA. Cutaneous reactions to actinic and ionizing radiation. In: Rook A, Wilkinson DS, Ebling FJG, et al, editors. Textbook of dermatology. 4th ed. Oxford: Blackwell Scientific, 1986:637-56. 32. Edward AM. Photobiologic effects. In: Maibach HI, Gellin GA, editors. Occupational and industrial dermatology. Chicago: Year Book Medical, 1982:115 -24. 33. Schmidt R. Cutaneous 1960;263:397-8.

porhyria

in Turkey.

N Engl J Med

Clinics in Dermatology 1992;10:231-243

PHYSICAL

34. Kochevar IE, Pathak MA, Parrish JA. Photophysics, photochemistry and photobiology. In: Fitzpatrick TB, Eisen AZ, Wolf K, et al, editors. Dermatology in general medicine. 3rd ed. Oxford: Blackwell Scientific, 1987;1441-51. 35. Pigatto PD, Bigardi A. Inquadramento della patologia cutanea fotoindotta. Doctor Dermatol 1990;4:39-51. 36. Epstein JH. Adverse cutaneous reactions to the sun. In: Malkinson FD, Pearson RW, editors. The year book of dermatology. Chicago: Year Book Medical, 1971:5-43. 37. Palminteri G, Caramanna V. Rilievi igienico-sanitari nei lavoratori delle saline. Folia Med 1961;54:836-9. 38. Skreb Y, Saric M. The effects of ultraviolet radiation on occupationally exposed workers. Arh Hig Rada Toksikol 1983;34:275 -86. 39. Levine GM, Harber LC. The effect of humidity on the phototoxic response to B-methoxypsoralen in guinea pig. Acta Derm Venereol (Stockh) 1969;49:82-4. contact 40. Sakakibara S, Kawabe Y, Mizuno N. Photoallergic dermatitis due to mineral oil. Contact Dermatitis 1989; 20:291-4. 41. Seligman PJ, Mathias CGT, O’Malley MA, et al. Phytophotodermatitis from celery among grocery store workers. Arch Dermatol 1987;123:1478-82. 42. Wu CM, Koehler PE, Ayres JC. Isolation and identification of xanthotoxin (B-methoxypsoralen) and bergapten (5-methoxypsoralen) from celery infected with Sclerotinia sclerotiorum. Appl Microbial 1972;23:852-6. 43. Oakley AMM, Ive FA, Harrison MA. String trimmer’s matitis. J Sot Occup Med 1986;36:143-4.

der-

44. Dooms-Goossens A, Chrispeels MT, De Veylder H, et al. Contact and photocontact sensitivity problems associated with thiourea and its derivatives: A review of the literature and case reports. Br J Dermatol 1987;116:573-9. 45. Goh CL, Ng SK. Photoallergic contact dermatitis mazole. Contact Dermatitis 1985;12:58-9.

to carbi-

46. Leroy D, Dompmartin A, Lauret P, et al. Allergic contact dermatitis to Bryozoa and photosensitivity. Photodermatology 1988;5:227-9.

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47. Jeanmougin M, Janier F, Prigent F, et al. Eczema de contact avec photosesibilite a Alcyonidium Gelatinosum. Ann Dermatol Venereol 1983;110:725-6. 48. Jeanmougin M, Lemarchand-Venencie F, Hoang XD, et al. Eczema professionel avec photosensibilite’ par contact de Bryozoaires. Ann Dermatol Venereol 1987;114:353 -7. 49. Mathias CGT. Occupational dermatoses. J Am Acad Dermatol 1988;19:1107-14. and the skin. Med Clin North 50. Suskind RR. Environment Am 1990;74:307-24. 51. Berg M, Lidien S. Skin problems in video display terminal users. J Am Acad Dermatol 1987;17:682-4. 52. Berg M. Skin problems in workers using visual display terminals. A study of 201 patients. Contact Dermatitis 1988;19:335-41. 53. Swanbeck G, Bleeker T. Skin problems from visual display units. Acta Derm Venereol (Stockh) 1989;69:46-51. RH. Cutaneous reaction to cold. In: Rook A, 54. Champion Wilkinson DS, Ebling FJG, et al, editors. Textbook of dermatology. 4th ed. Oxford: Blackwell Scientific, 1986;1:623632. 55. Palminteri G, Picciotto D. Dermopatie in rapport0 al freddo. In: Palminteri G, editor. Dermatologia professionale-pathologia cutanea e medicina generale. Palermo: Medical Books, 1990:157, 160. 56. Pelfini C. Dermatosi da freddo. In Serri F, editor. Trattato di dermatologia. Padova: Piccin, 1987;2:chap 46, p 37. 57. Monacelli M, Nazzaro P. Dermatologia e venereologia. Milano: Vallardi, 1967;1:148, 153. 58. Meneghini CL, Angelini G. Eczema. In: Serri F, editor. Trattato di dermatologia. Milano: Piccin, 1987;2:chap 51, pp 6-7. 59. Masellis M, Ferrara MM, Tranchina G. Patologia da elettricita. In: G. Palminteri. Dermatologia professionale-patologia cutanea e medicina generale. Palermo: Medical Books, 1990:153, 155. 60. Micali G, Romeo L, et al. Malattie cutanee da cause termiche. In: Serri F, editor. Trattato di dermatologia. Padova: Piccin, 1987;2:chap 46, p 18.