Airborne Contact Dermatitis GIANNI ANGELINI, MD GINO A. VENA, MD
A
irborne dermatitides are induced by off ending agents in the external environment transported by air. l-3 They can be divided into two groups: (1) dermatitis brought on by inhaling substances that are then absorbed into the system, for example, inhalation urticaria, a very rare clinical picture that may occur in atopic subjects; (2) dermatitis resulting from direct contact of the skin with various airborne agents. This article considers mainly the second group of airborne dermatitis, which may well have a much higher incidence than has been reported in the literature to date. Mixed forms may also develop, brought on by both inhalation of and skin contact with the airborne agents in question (mercury exanthem, acne from airborne chlorinated compounds).
Nature of Airborne Contactants There is considerable variation in the nature of airborne contactants, especially at work but also in nonprofessional environments, and in the form in which they are present.
Vapors, Gases,and Smoke Chemical substances that come into contact with the skin are in the form of gases (mustard gas) and vapors (formaldehyde) or smoke (burning plants, the obvious example being poison ivy). One may be alerted to the presence of these substances by a typical odor.
Droplets The offending agent can sometimes be disseminated in the form of droplets, as in sprays such as insecticides, From the Department of Dermatology, University of Bnri, Bari, Italy. Address correspondence to Gianni Angelini, Department of Dermatology, University of Bari, 70124 Bari, Italy.
0 1992 by Elsevier Science Publishing
Co., Inc.
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perfumes, and hairsprays; in pesticides sprayed on plants; or in epoxy resins used in the metal-mechanical industry.
Solid Nonbiologic Particles In most cases, the agents responsible are in the form of “dust” of various chemical origins. These may be substances in a pure state or else particles with a complex chemical composition (compounded with numerous constituents). Some examples of solid nonbiologic particles are glass fibers, industrial powders, cement, and anhydrite.
Solid Biologic Particles In some cases, airborne agents can be solid biologic particles of vegetable origin (pollen, dust from exotic wood) or animal origin (caterpillar hairs).
Predisposing Physical Factors Particular physical conditions can often predispose to the development of airborne dermatitis. An increase in temperature, for example, can volatilize some substances (dimethylthiourea) .’ Low environmental humidity, less than 35%, favors the dispersion of various substances in the air5 In this context, airborne contact dermatitis from plants is reported mainly in hot countries, as under dry environmental conditions, plants wither easily and their dry particles become volatile;- this form of dermatitis is uncommon in Europe and generally more humid countries.6-8 Finally, a facial eruption has been reported in visual display operators, which favors the onset of airborne contact dermatitis from particles present in the workplace.9
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Table 2. Airborne
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Confacf Dermatitis
Irritant contact dermatitis Allergic contact dermatitis Phototoxic contact dermatitis Contact urticaria Atopic dermatitis (in some cases) Chloracne (chlorinated compounds) Purpura (epoxy resin) Paresthesia (pyrethroids) Subcomeal pustular eruptions (trichloroethylene) Erythema multiforme-like eruptions (tropical
Table 2. Differential the Face and Neck
wood
dust)
Diagnoses of Airborne
Contact Dermatitis
of
Irritant contact dermatitis from directly applied agents Allergic contact dermatitis from directly applied agents Phototoxic contact dermatitis from directly applied agents Photoallergic contact dermatitis from directly applied agents Connubial (consort) dermatitis Ectopic contact dermatitis Systemic contact dermatitis Id-like spread of contact dermatitis elsewhere on the body Atopic dermatitis Seborrheic dermatitis Polymorphic light eruptions
Classification of Airborne Dermatitis Skin reactions to airborne agents manifest with different clinical pictures, according to whether they are mediated by direct pathogenetic mechanisms of the irritant type or by indirect immunologic mechanisms (Table 1). The same agent can induce different clinical pictures. Thus, airborne formaldehyde can cause contact urticaria,‘O irritant reactions, and allergic contact dermatitis.” Airborne particles from Parthenium hysterophorus can cause both allergic contact dermatitis and photocontact dermatitis.*2 Finally, airborne phosphoric sesquisulfide can cause contact urticaria13J4 and allergic contact dermatitis.15 In the south of Italy, we continually observe cases of common allergic contact dermatitis from phosphorus sesquisulfide, often associated with a simultaneous airborne contact allergy.3J6 The first, more common form involves the anterolateral area of the thighs and/or the anterior area of the trunk and is associated with contact with so-called zolfanel2i (sulfur) matches carried in trouser, vest, or shirt pockets, respectively. It presents exclusively in men, generally farm or manual workers, who usually use these matches (similar to “strike anywhere” matches). Airborne contact dermatitis, on the other hand, affects the face and neck and occurs in both men and women, as a result of use of zolfunelli or “strike anywhere” matches (the latter are similar to zolfunelli matches, used for pipes). In this form, the erythema is recurrent and is sometimes intense and accompanied by edema; it may be asymmetric, involving one side of the face only, and can affect the palms of the hands, again asymmetrically. Airborne contact allergy from phosphorus sesquisulfide can also present in nonsmokers, of course, in environments saturated with the smoke from the said matchesI In this article we are concerned primarily with irritant and allergic reactions to occupational airborne agents.
Skin Symptoms of Airborne Contact Dermatitis The symptoms of airborne contact dermatitis do not generally have any special characteristics and can thus often
be confused with those of common contact dermatitis of the corresponding category. The clinician bases his or her diagnosis of the airborne origin of the dermatitis mainly on the case history and the sites of the lesions. The areas most commonly affected are exposed to the air: face, neck, upper part of the chest, hands, wrists, forearms, and, in women, sometimes the legs. A differential diagnosis must be made in these cases, sometimes with some difficulty, with various dermatitis forms (Table 2) and particularly with photodermatitis. In the latter case, however, “shadowed’ anatomic areas such as the upper eyelids, behind the ears, and under the chin and hair (scalp and nape of the neck) are not affected. The nature of the allergen and the results of the photopatch tests on the other hand will guide differential diagnosis with classical contact photodermatitis. The upper eyelid is particularly susceptible to airborne allergens or irritants, which can easily accumulate in this area. It is sometimes the only area affected and, on occasion, is associated with acute conjunctivitis. In cases of nickel allergy, too, skin lesions around the eyes only can be observed. These lesions are sometimes so symmetric that it is difficult to believe the allergen is simply carried on the hands, as is usually postulated. Apart from the possibility that they may be an id-like manifestation from hematogenic spread of the allergen, it is likely that the nickel present in the air as dust may contribute to the onset of these clinical pictures.2~17-20 In fact, in working environments, the monitoring of nickel and chrome in the air in plating areas with these metals has revealed levels well beyond those recommended.*l In cases pointing to solid particles suspended in the air, the skin symptoms can include occluded areas. Dust easily accumulates in the genital area and, in particular, in flexures (axillae, groin, popliteal fossae). These cases require differential diagnosis with other afflictions of the flexures, like atopic dermatitis, clothing dermatitis, and id-like spread of contact dermatitis from other areas. In some exceptional cases, the clinical lesions can even be generalized, resembling erythrodermia, as a result of
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Table 3. Airborne lrritants Glass fibers Formaldehyde Cement Acids and alkalis Tropical wood dusts Aluminum powder Anhydrite Arsenical dusts Dyes Food additives Sewage sludge Slag Trona
Urea-formaldehyde foam Epoxy resins Calcium silicate Domestic cleaning Industrial solvents Phenol-formaldehyde Silver Caterpillar hairs Rock wool fibers Perchloroethylene Mica dust Mustard gas
insulating
products resins
the high concentration of the allergen in the air, for example, expression of a Compositae dermatitis,22 or as a result of particularly contaminated articles of clothingz3
Airborne Irritant Contact Dermatitis A great number of airborne contact agents have been identified up to now, nearly all in occupational environments (Table 3). In most cases, they are highly alkaline substances (pH > lo), in which the irritant effect is both chemical and mechanical. Some examples of airborne contact irritation are reported next.
FiberglassDermatitis Fiberglass dermatitis is the most common, classic example of an airborne irritant contact dermatitis. Today, fiberglass is used in many different fields.24 It is obtained from the fusion and subsequent spinning of glassable prime materials like silicone sand, kaolin, calcium carbonate, dolomite, and feldspar. Fibers causing skin irritation are those exceeding 4.5 pm. 25-28 The professional epidemics observed have been triggered by fibers between 15 and 20 pm in diameter, released into the air when the air conditioners stopped working.29 Clinical symptoms (pruritis, a pricking feeling, papules of 0.1 to 0.5 mm, lesions from scratching, and sometimes pustules) manifest 2 to 3 hours after exposure. The lesions are present in uncovered but primarily covered areas. The fibers penetrate under clothing and accumulate mainly in flexures (axillae, popliteal fossae) and on the extensor plane of the thighs. Sweat helps the fibers agglutinate. The histopathologic findings are varied. Cuypers et aP“ found changes typical of dermatitis, similar to those in allergic contact dermatitis (ie, spongiosis, spongiotic vesicles, exocytosis of lymphoid cells into the epidermis, and presence of a perivascular mononuclear cell infiltrate in the upper and middermis). Lachapelle25 was unable to find similar changes: the histologic picture was nonspe-
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cific. The epidermis showed superficial erosions with coagulated material, and glass fibers were found in the horny layer (more easily under polarized light). In selected fields of serial sections, fibers were found to have penetrated into the stratum Malpighi.25 These fibers can be observed in the horny layer under polarized light even using simple chemical stripping methods: a drop of cyanoacrylate glue is placed on the skin and a clean glass slide is gently pressed down on the drop for 30 seconds. A layer of horn is removed with the adhesive, which sticks to the glass slide. In a slight modification of this method polyester tape is used instead of glass as the holder. 25 It should be noted that some fibers are coated with epoxy or phenol-formaldehyde resins, a potential cause of allergic contact dermatitis. Rock wool fibers come from fibrous glass wool made out of minerals, coke, and limestone, compounded with a mineral oil, a silicone compound, and a phenolformaldehyde resin. These fibers provoke an airborne irritant contact dermatitis with symptoms similar to those described for glass fibers. Cases of airborne irritant contact dermatitis caused by sewage sludge were described by NethercotP among incinerator workers employed in a sewage treatment plant. The problem was found to be caused by contamination of the workplace and workers’ clothing with sludge from the interstices of an incinerator exhaust fan. The irritant nature of the sludge was determined by tests in rabbits.
Trona Dermatitis Trona dermatitis was described by Rom et aP2 in trona miners and millers. Trona (sodium sesquicarbonate) is mined in an underground deposit in Wyoming in the United States and is processed for use in the manufacture of glass, paper, and detergents and in chemical applications. Trona dust is alkaline (pH 10.5) and can have an irritant effect on the respiratory tract, the mucous membranes, and the skin. Trona dermatitis consists of itchy, erythematous, and dry lesions affecting the hands (direct contact) and face and limbs (airborne contact).
Anhydrite Dermatitis Anhydrite is an anhydrous calcium sulfate powder that contains traces of calcium fluoride and hydrofluoric acid. Highly alkaline (pH 11.2), it is used to fill gaps between the rock and the beams in tunnels in coal mines. Complaints of skin irritation were made by coal miners engaged in this procedure,33 with symptoms of itching or burning sensations on the face, neck, forearms and thighs. No erythema or eczematous reactions were observed. Skin irritation from the alkaline anhydrite paste was assessed by laser Doppler flowmetry: the iterative
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application of anhydrite on the flexor plane on volunteers’ forearms induced an increase in blood flow to the top layer of the derma. This dermatitis is a classic example of purely subjective airborne irritant contact dermatitis (ie, with no objective clinical manifestations). Replacing the anhydrite paste with a less alkaline paste (hemihydrate) was successful in preventing further cases of skin irritation.33
Slag Dermatitis Slag dermatitis occurs in metallurgic plants where permanent mold casting techniques have been introduced.34 During one stage of production, workers pour slag (a mixture of silicium oxide and calcium oxide powders) into the ingot molds. Workers wear asbestos coveralls but dust, penetrating the protective clothes or between the sleeves and the gloves, accumulates in the flexures and on the extensor planes of the thighs and arms. The subjective and objective symptoms are similar to those in fiberglass dermatitis. Microscopic examination of the powder particles revealed that some were oblong and sharp-edged (length: + 10 to 80 pm). Dermatitis was considered to follow mechanical injury to the skin by the sharp-edged particles.34
Dermatitis
From Miscellaneous
Agents
Other examples of airborne irritant contact dermatitis include indigenous or exotic wood particles, cement,35 cellulose fibers, mica dust, food additives,36 dust from urea formaldehyde insulating foam, and perchloroethylene. Alkaline vapors (such as ammonia) are often implicated in the provocation of skin irritation among laboratory technicians. Finally, it is worth mentioning that formaldehyde may be released from many industrial or domestic sources, such as urea-formaldehyde insulating foam3’ and formaldehyde-releasing preservatives in soluble oils. An exceptional and curious form of airborne irritant contact dermatitis came to our notice in five fishermen.38 It was due to mustard gas contained in bombs thrown into the sea as war relics after the World War II. The bombs were caught in the nets full of fish. The fishermen freed them from the nets and threw them back into the sea. The nets, however, which were contaminated by the liquid gas contained in the generally corroded bombs, were handled by the fishermen, who after some hours developed the symptoms of erythema, edema, vesicles, bullae, and a burning sensation. These symptoms involved mainly the hands and forearms, as a result of direct contact with the liquid gas. In addition, there were erythema and swelling of the face and particularly eyelids, with acute conjunctivitis, signs of an airborne contact dermatitis from mustard gas vapors. In fact, although the gas has
Table 4. Airborne
Allergens
Metals Chromates in cement welding fumes Cobalt Nickel Silver Mercury Solvents Formaldehyde Turpentine Insecticides Carbamates Pyrethrum Pesticides Vegetables Lichens Compositae spp Frullania spp Tulip bulbs Poison ivy Poison oak
and
Parthenium Tropical wood dusts Plastics and rubbers Cyanoacrylate Epoxy resins Phenol-formaldehyde resins Polyacrylates Polyurethane Resin additives Rubber additives (thiuram)
Medicaments Chloroquine sulfate Chlorpromazine Streptomycin Spiromycin Viiginiamycin Quinoline compounds b-Methoxypsoralen Miscellaneous Halogenated compounds Colophony Fragrances Bryozoans (Dogger Bank Animal feed additives Pyritinol HCl NCR paper Deodorants Hair sprays Dimethylthiourea Persulfates Phosphorus sesquisulfide Chloracetamide Propolis Chloroacetophenone
itch)
a low heat of evaporation, it evaporates slowly because of the low vapor tension, which, however, increases considerably with an increase in temperature. The mustard gas is toxic in both the liquid and the vapor state: in the former it can damage the skin directly, whereas in the latter, apart from the skin and the conjunctiva, it can also affect the mucosa of the respiratory and digestive tracts. Besides the five cases we observed, all in the summer months, the port authorities of Molfetta (a town near Bari in southern Italy) received 94 complaints, over a period of 10 years, from fishermen with irritant contact dermatitis of varying degrees from mustard gas, all of whom had clinical manifestations on the hands, forearms, face, and conjunctiva.38
Airborne Allergic Contact Dermatitis Airborne contact allergy seems to be a frequent complaint. Volatile contactants with allergic potential or allergens present in dust particles are mainly diffuse in professional environments (Table 4).2,3,25Clinical symptoms are typical of common allergic contact dermatitis
Clinics in Dermafokyy 2992;20:223-131 with no specific signs of its airborne nature. The lesions are usually symmetric and evolution can be acute or chronic, according to the nature and/or concentration of the allergen and the frequency of the airborne contact. The sites involved are those exposed to the air (face and neck) and often covered areas (flexures), as a result of the accumulation of solid particles under clothing. The simultaneous involvement of face and hands may suggest the possibility of associated airborne and direct contact, respectively. Differential diagnosis of facial allergic airborne contact dermatitis must be made with direct (or “true”) allergic contact dermatitis, with a flareup of the so-called “id’ type, with atopic dermatitis confined to the face, and with photoallergic contact dermatitis. Unlike allergic airborne contact dermatitis, in nonairborne photoallergic reactions some parts of the face, like the eyelids, the area under the chin, and the folds behind the ears, are not affected. Allergic airborne contact dermatitis lesions are symmetric, whereas asymmetric facial lesions suggest a direct contact allergy. Typical examples of professional airborne contact allergy often observed are those from epoxy resins, present in the form of dust or droplets in the metal/mechanical industry, from turpentine, from dust of exotic wood, from chrome in cement, and from pesticides in agriculture. With respect to the last, it must be remembered that thiurams may cause airborne reactions not only when used as fungicides in professional agricultural environments but also when used in medicaments. Nobecutan spray (which contains tetramethylthiuram disulfide), a bactericide and fungicide aerosol indicated for disinfecting the skin and protecting wounds and abrased dermatitis, can induce airborne reactions on the faces of subjects who are sensitive to the thiurams present in professional and nonprofessional rubber products. Allergic contact dermatitis from bryozoans (“Dagger Bank itch”), which affects fishermen during the summer, is mediated by two different pathogenic mechanisms: direct contact with the bryozoans, which is responsible for the dermatitis in the hands, and airborne contact from drops of seawater containing allergic material, which is responsible for dermatitis of the face and neck. The causative agent is generally Alcyonidium gelutinosum.39~40 As examples of nonprofessional forms, we report two recent observations. Two young women with contact dermatitis of the axillae and intense sensitivity to perfume (cinnamic aldehyde in fragrance mix) developed erythemato-edematous eruptions on the face and particularly the eyelids after a visit to a perfumery where they were sprayed with perfume samples. In one of the cases, a specific test made with a perfume sprayed in the allergy outpatient clinic was followed after some hours by ery-
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thema and edema of the eyelids. A similar case was observed by Dooms-Goossens et a1.2
Airborne Phototoxic Contact Dermatitis Airborne phototoxic contact dermatitis has no peculiar characteristics. Lachapelle’ observed a small epidemic of phototoxic reactions to Smethoxypsoralen in three female workers who were concerned with the confecting of tablets at a pharmaceutical company. After prolonged sunbathing at the end of a day’s work, phototoxic lesions developed in the skin areas that were uncovered during work. The reaction was of mixed type, involving the hands (as a result of direct contact) and the face, decollete, and arms (as a result of airborne contact). The airborne spread can be explained by the powdery nature of Bmethoxysporalen tablets.
Airborne Photoallergic Contact Dermatitis Airborne photoallergic contact reactions are very rare. The limits of clinical lesions are generally imprecise in these cases. Reactions to halogenated salicylanilides, phenothiazines, and musk ambrette (contained in cosmetics) under suitable conditions have been observed.’
Airborne Contact Urticaria The classic example of airborne contact urticaria is induced by the processional pine caterpillar.” The pine caterpillar, Thaumetopoea pityocampa Schif, is an herbivorous lepidopteran, responsible for a delay in the growth of maritime pines. Apart from the damage to nature and silvicultivators, the lepidopteran causes urticarious reactions of the strophulus type, as a result of the urticant hairs, in humans and domestic animals (dogs, sheep). The caterpillars causing urticaria are those in the last three larval stages (L3, L4, L5). The density of the urticant hairs on the caterpillar is approximately 60,000/ mm2; thus there are at least 1 million hairs on its back. The urticant hair, hollow on the inside, carries pointed spikes directed toward its distal end. It has no hole or pores, and as the bristles must be ground to extract the urticant substance, we are led to believe that the hair is really a bulb that must be broken, in the skin for example, to release its urticant (histamine-liberating) substance. Up to the age of 21, men seem to be more affected, owing perhaps to a predilection for games among the pines and attacks on nests with sticks. Although the dermatitis occurs among professionals (in nursery gardeners and foresters) it is primarily extraprofessional. Contamination generally occurs in pinewoods, rarely in cities, although infested pines may even be found in cities. There
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are various means of contamination: direct contact with the nest, direct contact with the processional caterpillar, indirect contact with the hairs suspended in the air or present on objects and clothes. This airborne contact urticaria can be observed from February to June, and during the summer months there are many cases along the coast among campers and picnic lovers (camping sites are usually situated under pines). The pathology induced by T. pityocampa involves the skin, eyes, and, in rare cases, the airways. The skin sites affected can be exposed (particularly by direct contact) and occluded, as the hairs can penetrate clothing. In most cases, the lesions spread over all the skin area; in 15% of cases they are isolated. Airborne contact urticaria from urticant hairs blown on the wind is favored by sweat, has its onset 2 to 12 hours after contact with the hairs, and presents subjectively with intense and continuous pruritis. The eruption consists of papulous, excoriated, and pinkish lesions on an edematous base. Exceptionally, the lesions can be bullous. Each lesion evolves over 3 to 4 days and leaves a hyperchromic outcome that lasts about 2 weeks. Diagnosis is aided by the onset of the same eruption in other members of the patient’s party, by the sites affected, and mainly by a case history describing a recent stay or walk in or near pinewoods. Epicutaneous tests with minced hairs (to release the urticant histamine-liberating) substance must be done on scarified skin. The clinical nature of the urticant substance contained inside the hair is unknown. Lesions to the eyes can be associated with those on the skin or not and can be early or late. The former manifest with a very intense burning sensation, hyperemia, and edema of the conjunctiva and eyelids. This is followed by photophobia, abundant secretion, and conjunctival nodules the size of peppercorns, as a reaction to the hair (ophthalmitis nodosa). Late lesions, on the other hand, are secondary to the penetration of the hair inside the eye; the clinical pictures include cheratitis, iritis, uveitis, cataract, nodules of the iris, and finally glaucoma. The clinical picture and pathogenetic mechanism of papillonite de Guyane Francaise (an airborne contact urticaria provoked by the urticant apparatus of the Hylesia urticans butterfly)42 and of other forms of airborne contact urticaria from Lepidoptera are similar.43,44 All these examples belong to the nonimmunologic contact urticaria group, according to Von Krogh and Maibach.45
Airborne Atopic Dermatitis In our opinion, there exist data in a certain percentage of cases suggesting the airborne nature of atopic dermatitis.46-50
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1, Atopic dermatitis is characterized by apparent clinical lesions of the eczematous type, which are histologically and immunotypically the same as those of contact allergy. 2. In varying percentages of subjects with atopic dermatitis, many recent studies using patch tests on healthy skin have shown positive delayed responses to aeroallergens like mites, pollens, and epidermic derivatives. 3. Patch tests with the same aeroallergens were negative in subjects with respiratory allergy but not dermatitis. 4. The aeroallergens that induce positive delayed responses are always those that determine recurrences of dermatitis. 5. Finally, it is known that acari, which are the allergens that most often cause delayed contact allergy, are present in greater quantities in damp climates, where atopic dermatitis is also more prevalent. On the basis of these data, it seems reasonable to suppose that the patch test can be considered as a direct skin test to elicit atopic dermatitis, and that both the immunoglobulin E and factors inherent to cell-mediated immunity contribute to the pathogenetic mechanism underlying this pathology.
Other Airborne Contact Dermatitis Chloracne has recently been defined by CroW5l as the production in the human of a type of acne with characteristic clinical features that have so far been induced only by aromatic chlorinated hydrocarbons with varying structure (polyhalogenated naphthalenes, polyhalogenated biphenyl, polychlorinated dibenzofurans, dioxins, azo- and azoxybenzenes). Skin contact with these substances can be direct or airborne and the same substances can also be inhaled or ingested. Chloracne lesions have a peculiar distribution. The most sensitive areas are below and to the outer side of the eye (the so-called malar crescent) and behind the ear. The nose is highly resistant. The genitalia, both penis and scrotum but particularly the latter, are also sensitive regions. If a sufficient exposure and toxic reaction have occurred, lesions may appear on the shoulders, chest, back, and, in some cases, buttocks and abdomen. The primary lesion of chloracne is the comedone. Other possible lesions are small, pale yellow cysts, cold abscesses, and follicular hyperkeratosis.52 Other dermatitides described are paresthesias caused by airborne pyrethroids, purpura from airborne epoxy resin, subcorneal pustular eruptions from airborne trichloroethylene, and erythema multiforme-like eruptions from tropical wood dust.*
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Mixed Forms Some particular clinical forms have been reported in the literature featuring a generalized dermatitis that can be explained by a mixed mechanism; in addition to the airborne skin contact, inhalation of the airborne factor could play a role. This is the case in the mercury exanthem described by Nakayama et a1.53These authors observed 15 patients with erythematous or erythematopapulous rashes that manifested 1 to 2 days after breaking a clinical thermometer or during dental treatment. The exanthem was diffuse and symmetric and involved particularly the flexures, axillae, popliteal fossae, and antecubital and internal planes of the thighs. In the more severe cases, pustular lesions, petechiae, and swelling of the legs occurred. The eruption subsided after 10 to 12 days, leaving no trace, and was accompanied by itching, fever, and a feeling of illness. Eleven of the fifteen patients had a history of contact allergy to mercurochrome. As mercury evaporates at room temperature, and the rash was diffuse and symmetric, it seems possible that in these cases the airborne skin contact was exacerbated by the systemic absorption of the substance through inhalation. We have observed another example of airborne dermatitis with a mixed underlying mechanism has been observed several times in patients with allergy to mercury following treatment with MOM in powder form (with an ammoniated mercury and metallic mercury base) for pubic phthyriasis (data not published). Intense erythematoexudative lesions of the genitalia, pubic region, and internal plane of the thighs were associated with involvement of the face, neck, folds, and trunk. In these cases, the types of contact were probably multiple: (1) direct skin contact during application of the mercury-based powder; (2) airborne contact resulting from airborne spread of the powder, producing the lesions of the face and trunk; (3) inhalation of the powder, inducing the clinical signs of “systemic contact dermatitis.” In seven of the nine cases observed, in fact, the skin lesions were associated with a feeling of illness, high temperature, and leukocytosis.
Diagnosis In cases of suspected airborne contact dermatitis, the common skin tests, like the open test, the scratch test (for airborne contact urticaria), and the patch test, can be performed. With due precautions, the exposure test (spray products) may be useful. Laser Doppler flowmetry may also be valuable in subjective symptomatic forms, with no objective clinical signs. In cases of reactions to solid particles in the professional environment, it is necessary to carry out a microscopic examination of the particles, collected in the work-
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place, under polarized light, and to determine the presence of any particles on the skin surface. This can be determined by stripping (with cyanoacrylate glue and polyester tape) the horny surface. Other important pathogenetic and diagnostic data are the pH of the particles, the relative humidity of the air in the workplace, and the relationship between the clinical symptoms and the working periods.26
Therapy and Prevention Treatment is symptomatic. The problem may be solved simply by taking protective prevention measures. In professional environments, silicone barrier creams are ineffective. The preventive methods suitable for each situation are both general and individual. The former consist of aspirating the particles in the workplace, monitoring the relative humidity, and, where possible, automating the whole working cycle. Individual prevention, on the other hand, requires the use of the most functional protective clothing.
Conclusions As airborne allergens and irritants are numerous and widely present in the environment, skin pathologies induced by them are undoubtedly more frequent than would appear from the literature. Reactions to irritants, generally in the workplace, are more common than allergic reactions, but often more difficult to demonstrate. On the whole, airborne contact dermatitis must be suspected when symmetric lesions are present in exposed areas, particularly the face and eyelids, when the patient denies having applied topical agents, and when the symptoms subside with a change in the environment.
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7. Pecegueiro M, Brandgo FM. Airborne contact dermatitis plants. Contact Dermatitis 1985;13:277-9.
to
8. Sharma SC, Kaur S. Airborne contact dermatitis from Compositae plants in northern India. Contact Dermatitis 1989;21:1-5. 9. Nilsen A. Facial rash in visual display unit operators. Contact Dermatitis 1982;8:25-8. 10. Lindskov R. Contact urticaria Dermatitis 1982;8:333-4.
to formaldehyde.
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11. Fisher AA. Contact dermatitis in medical and surgical personnel. In: Maibach HI, Gellin GA, editors. Occupational and industrial dermatology. Chicago: Year Book Medical, 1982:223-4. 12. Bhutani LK, Rao DS. Photocontact dermatitis caused by Parthenium hysterophorus. Dermatologica 1978;157:206-9. 13. Burge SM, Powell SM. Contact urticaria to phosphorus quisulfide. Contact Dermatitis 1983;9:424.
ses-
14. White IR, Rycroft RJG. Contact urticaria from phosphorus sesquisulfide. Contact Dermatitis 1983;9:162. 15. Steele MC, Ive FA. Recurrent facial eczema in females due to “strike anywhere” matches. Br J Dermatol 1982; 106:477-80. 16. Meneghini CL, Angelini G. Le dermatiti da contatto. Rome: Lombard0 Editore, 1982:69-71. 17. Clemmensen OJ, Men& T, Kaaber K, et al. Exposure of nickel and the relevance of nickel sensitivity among hospital cleaners. Contact Dermatitis 1981;7:14-8. 18. Clemmensen OJ, Jorgensen J, Jons 0, et al. Exposure to chromium from hospital cleaning. Derm Beruf Umwelt 1983;31:54-7. 19. Pirill V, Noro L, Laamanen Acta Allerg 1963;18:113-30.
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20. Angelini G, Vena GA. Allergia da contatto al nichel. Considerazioni su vecchie e nuove acquisizioni. Boll Dermatol Allerg Prof 1989;4:5 -29. 21. Handfield-Jones S, Boyle J, Harmann RRM. Contact allergy caused by metal sprays. Contact Dermatitis 1987;16:44-5. 22. Mensing H, Kimming W, Hausen BM. Airborne dermatitis. Hautarzt 1985;36:398-402.
contact
23. Arlette J, Mitchell JC. Compositae dermatitis: aspects. Contact Dermatitis 1981;7:129-36.
Current
24. Konzen JL. Fibreglass and the skin. In: Maibach HI, Gellin GA, editors. Occupational and industrial dermatology. Chicago: Year Book Medical, 1982:229-32. 25. Lachapelle JM. Industrial airborne irritant or allergic contact dermatitis. Contact Dermatitis 1986;14:137-45.
28. Sertoli A, Spallanzani I’, Cappelli U, et al. Patologia dermatologica da fibre di vetro in una officina delle Ferrovie dello Stato. Boll Co11 Med Ital Trasporti 1982;2:31-41. 29. Meneghmi CL. Fibreglass 1977;3’:218.
dermatitis.
Contact
Dermatitis
30. Cuypers JMC, Hoedemaeker PhJ, Nater JP, et al. The histopathology of fibreglass dermatitis in relation to von Hebra’s concept of eczema. Contact Dermatitis 1975;1:88-95. 31. Nethercott JR. Airborne irritant contact dermatitis sewage sludge. J Occup Med 1981;23:771-4.
due to
32. Rom WN, Moshell A, Greaves W, et al. A study of dermatitis in trona miners and millers. J Occup Med 1983;25: 295-9. 33. Lachapelle JM, Mahmoud G, Vanherle R. Anhydrite dermatitis in coal miners. An airborne irritant reaction assessed by laser Doppler flowmetry. Contact Dermatitis 1984; 11:188-9. 34. Lachapelle JM. Occupational airborne irritant contact dermatitis to slag. Contact Dermatitis 1984;10:315-6. 35. Lachapelle JM, Minne GJ. Btilures lie& a l’emploi ment. Apropos de 4 observations. Ann Fr Dermatol ligr 1985;112:123-9.
du ciSyphi-
36. Lachapelle JM. Occupational airborne irritant reaction to the dust of a food additive. Contact Dermatitis 1984; 10:250-l. 37. Williams DT, Otson R, Bothwell PD. Formaldehyde in the air of houses containing urea formaldehyde insulation. Can J Public Health 1981;72:331-4.
levels foam
38. Angelini G, Vena GA, Foti C, et al. Dermatite da contatto con gas iprite. Boll Dermatol Allerg Prof 1990;5:71-4. 39. Martin I’, Fontaine T, Dalle E, et al. Dermatoses due to bryozoans. In: Kukita A, Seiji M, editors. Proceedings of the XVIth international congress of dermatology. Tokyo: University of Tokyo Press, 1983:503-8. 40. Angelini G, Vena GA, editors. Dermatologia Milan: Gruppo Lepetit, 1991:59-60.
acquatica.
41. Ducombs G, Lamy M, Bergaud JJ, et al. La Chenille processionnaire (Thaumetopoea pityocampa Schiff. Lepidopteres) et l’homme. Etude morphologique de l’appareil urticant. EnquPte epidemiologique. Ann Dermatol Venereol 1979; 106:769-78. 42. Ducombs G, Lamy M, Michel M, et al. La papillonite de Guyane francaise. Etude clinique et epidemiologique. Ann Dermatol Venereol 1983;110:809-16.
26. Lachapelle JM. Industrial airborne irritant contact dermatitis due to dust particles. Boll Dermatol Allerg Profes 1987;2:83-9.
43. Dinehart SM, Archer ME, Wolf JE, et al. Caripito itch: Dermatitis from contact with Hylesia moths. J Am Acad Dermat01 1985;13:743-7.
27. Cronin E, editor. Contact dermatitis. Livingstone, 1980:78-80.
44. Burnett JW, Calton GJ, Morgan dermatitis. Cutis 1986;37:320.
Edinburgh:
Churchill
RJ. Caterpillar
and moth
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45. Von Krogh G, Maibach HI. The contact urticaria syndrome. In: Marzulli FN, Maibach HJ, editors. Dermatotoxicology. Washington, DC: Hemisphere, 1983:301-22. 46. Mitchell EB, Crow J, Chapman MD, et al. Basophils in allergen-induced patch test sites in atopic dermatitis. Lancet 1982;1:127-30. 47. Platts-Mills TAE, Mitchell EB, Rowntree S, et al. The role of dust mite allergens in atopic dermatitis. Clin Exp Dermatol 1983;8:233-47. 48. Reitamo S, Visa K, Klhonen K, et al. Eczematous reactions in atopic patients caused by epicutaneous testing with inhalant allergens. Br J Dermatol 1986;114:303-9.
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49. Platts-Mills TA, de Week AL. Mite allergy: A worldwide problem. Allergy Clin Immunol News 1989;1:21-25. 50. Adinoff AD, Tellez P, Clark RAF. Atopic dermatitis and aeroallergen contact sensitivity. J Allergy Clin Immunol 1988;81:736-42. 5 1. Crow KD. Chloracne: A critical review, including a comparison of two series of acne from chloronaphthalene and pitch fumes. Trans St Johns Hosp Dermatol Sot 1970;56:79-99. 52. Tindall JP. Chloracne and chloracnegens. J Am Acad Dermat01 1985;13:539-58. 53. Nakayama H, Niki F, Shono M, Hada S. Mercury exanthem. Contact Dermatitis 1983;9:4117.
’
A
irborne dermatitides are induced by off ending agents in the external environment transported by air. l-3 They can be divided into two groups: (1) dermatitis brought on by inhaling substances that are then absorbed into the system, for example, inhalation urticaria, a very rare clinical picture that may occur in atopic subjects; (2) dermatitis resulting from direct contact of the skin with various airborne agents. This article considers mainly the second group of airborne dermatitis, which may well have a much higher incidence than has been reported in the literature to date. Mixed forms may also develop, brought on by both inhalation of and skin contact with the airborne agents in question (mercury exanthem, acne from airborne chlorinated compounds).
Nature of Airborne Contactants There is considerable variation in the nature of airborne contactants, especially at work but also in nonprofessional environments, and in the form in which they are present.
Vapors, Gases,and Smoke Chemical substances that come into contact with the skin are in the form of gases (mustard gas) and vapors (formaldehyde) or smoke (burning plants, the obvious example being poison ivy). One may be alerted to the presence of these substances by a typical odor.
Droplets The offending agent can sometimes be disseminated in the form of droplets, as in sprays such as insecticides, From the Department of Dermatology, University of Bnri, Bari, Italy. Address correspondence to Gianni Angelini, Department of Dermatology, University of Bari, 70124 Bari, Italy.
0 1992 by Elsevier Science Publishing
Co., Inc.
l
0738-081x/92/$5.00
perfumes, and hairsprays; in pesticides sprayed on plants; or in epoxy resins used in the metal-mechanical industry.
Solid Nonbiologic Particles In most cases, the agents responsible are in the form of “dust” of various chemical origins. These may be substances in a pure state or else particles with a complex chemical composition (compounded with numerous constituents). Some examples of solid nonbiologic particles are glass fibers, industrial powders, cement, and anhydrite.
Solid Biologic Particles In some cases, airborne agents can be solid biologic particles of vegetable origin (pollen, dust from exotic wood) or animal origin (caterpillar hairs).
Predisposing Physical Factors Particular physical conditions can often predispose to the development of airborne dermatitis. An increase in temperature, for example, can volatilize some substances (dimethylthiourea) .’ Low environmental humidity, less than 35%, favors the dispersion of various substances in the air5 In this context, airborne contact dermatitis from plants is reported mainly in hot countries, as under dry environmental conditions, plants wither easily and their dry particles become volatile;- this form of dermatitis is uncommon in Europe and generally more humid countries.6-8 Finally, a facial eruption has been reported in visual display operators, which favors the onset of airborne contact dermatitis from particles present in the workplace.9
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Table 2. Airborne
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Confacf Dermatitis
Irritant contact dermatitis Allergic contact dermatitis Phototoxic contact dermatitis Contact urticaria Atopic dermatitis (in some cases) Chloracne (chlorinated compounds) Purpura (epoxy resin) Paresthesia (pyrethroids) Subcomeal pustular eruptions (trichloroethylene) Erythema multiforme-like eruptions (tropical
Table 2. Differential the Face and Neck
wood
dust)
Diagnoses of Airborne
Contact Dermatitis
of
Irritant contact dermatitis from directly applied agents Allergic contact dermatitis from directly applied agents Phototoxic contact dermatitis from directly applied agents Photoallergic contact dermatitis from directly applied agents Connubial (consort) dermatitis Ectopic contact dermatitis Systemic contact dermatitis Id-like spread of contact dermatitis elsewhere on the body Atopic dermatitis Seborrheic dermatitis Polymorphic light eruptions
Classification of Airborne Dermatitis Skin reactions to airborne agents manifest with different clinical pictures, according to whether they are mediated by direct pathogenetic mechanisms of the irritant type or by indirect immunologic mechanisms (Table 1). The same agent can induce different clinical pictures. Thus, airborne formaldehyde can cause contact urticaria,‘O irritant reactions, and allergic contact dermatitis.” Airborne particles from Parthenium hysterophorus can cause both allergic contact dermatitis and photocontact dermatitis.*2 Finally, airborne phosphoric sesquisulfide can cause contact urticaria13J4 and allergic contact dermatitis.15 In the south of Italy, we continually observe cases of common allergic contact dermatitis from phosphorus sesquisulfide, often associated with a simultaneous airborne contact allergy.3J6 The first, more common form involves the anterolateral area of the thighs and/or the anterior area of the trunk and is associated with contact with so-called zolfanel2i (sulfur) matches carried in trouser, vest, or shirt pockets, respectively. It presents exclusively in men, generally farm or manual workers, who usually use these matches (similar to “strike anywhere” matches). Airborne contact dermatitis, on the other hand, affects the face and neck and occurs in both men and women, as a result of use of zolfunelli or “strike anywhere” matches (the latter are similar to zolfunelli matches, used for pipes). In this form, the erythema is recurrent and is sometimes intense and accompanied by edema; it may be asymmetric, involving one side of the face only, and can affect the palms of the hands, again asymmetrically. Airborne contact allergy from phosphorus sesquisulfide can also present in nonsmokers, of course, in environments saturated with the smoke from the said matchesI In this article we are concerned primarily with irritant and allergic reactions to occupational airborne agents.
Skin Symptoms of Airborne Contact Dermatitis The symptoms of airborne contact dermatitis do not generally have any special characteristics and can thus often
be confused with those of common contact dermatitis of the corresponding category. The clinician bases his or her diagnosis of the airborne origin of the dermatitis mainly on the case history and the sites of the lesions. The areas most commonly affected are exposed to the air: face, neck, upper part of the chest, hands, wrists, forearms, and, in women, sometimes the legs. A differential diagnosis must be made in these cases, sometimes with some difficulty, with various dermatitis forms (Table 2) and particularly with photodermatitis. In the latter case, however, “shadowed’ anatomic areas such as the upper eyelids, behind the ears, and under the chin and hair (scalp and nape of the neck) are not affected. The nature of the allergen and the results of the photopatch tests on the other hand will guide differential diagnosis with classical contact photodermatitis. The upper eyelid is particularly susceptible to airborne allergens or irritants, which can easily accumulate in this area. It is sometimes the only area affected and, on occasion, is associated with acute conjunctivitis. In cases of nickel allergy, too, skin lesions around the eyes only can be observed. These lesions are sometimes so symmetric that it is difficult to believe the allergen is simply carried on the hands, as is usually postulated. Apart from the possibility that they may be an id-like manifestation from hematogenic spread of the allergen, it is likely that the nickel present in the air as dust may contribute to the onset of these clinical pictures.2~17-20 In fact, in working environments, the monitoring of nickel and chrome in the air in plating areas with these metals has revealed levels well beyond those recommended.*l In cases pointing to solid particles suspended in the air, the skin symptoms can include occluded areas. Dust easily accumulates in the genital area and, in particular, in flexures (axillae, groin, popliteal fossae). These cases require differential diagnosis with other afflictions of the flexures, like atopic dermatitis, clothing dermatitis, and id-like spread of contact dermatitis from other areas. In some exceptional cases, the clinical lesions can even be generalized, resembling erythrodermia, as a result of
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Table 3. Airborne lrritants Glass fibers Formaldehyde Cement Acids and alkalis Tropical wood dusts Aluminum powder Anhydrite Arsenical dusts Dyes Food additives Sewage sludge Slag Trona
Urea-formaldehyde foam Epoxy resins Calcium silicate Domestic cleaning Industrial solvents Phenol-formaldehyde Silver Caterpillar hairs Rock wool fibers Perchloroethylene Mica dust Mustard gas
insulating
products resins
the high concentration of the allergen in the air, for example, expression of a Compositae dermatitis,22 or as a result of particularly contaminated articles of clothingz3
Airborne Irritant Contact Dermatitis A great number of airborne contact agents have been identified up to now, nearly all in occupational environments (Table 3). In most cases, they are highly alkaline substances (pH > lo), in which the irritant effect is both chemical and mechanical. Some examples of airborne contact irritation are reported next.
FiberglassDermatitis Fiberglass dermatitis is the most common, classic example of an airborne irritant contact dermatitis. Today, fiberglass is used in many different fields.24 It is obtained from the fusion and subsequent spinning of glassable prime materials like silicone sand, kaolin, calcium carbonate, dolomite, and feldspar. Fibers causing skin irritation are those exceeding 4.5 pm. 25-28 The professional epidemics observed have been triggered by fibers between 15 and 20 pm in diameter, released into the air when the air conditioners stopped working.29 Clinical symptoms (pruritis, a pricking feeling, papules of 0.1 to 0.5 mm, lesions from scratching, and sometimes pustules) manifest 2 to 3 hours after exposure. The lesions are present in uncovered but primarily covered areas. The fibers penetrate under clothing and accumulate mainly in flexures (axillae, popliteal fossae) and on the extensor plane of the thighs. Sweat helps the fibers agglutinate. The histopathologic findings are varied. Cuypers et aP“ found changes typical of dermatitis, similar to those in allergic contact dermatitis (ie, spongiosis, spongiotic vesicles, exocytosis of lymphoid cells into the epidermis, and presence of a perivascular mononuclear cell infiltrate in the upper and middermis). Lachapelle25 was unable to find similar changes: the histologic picture was nonspe-
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cific. The epidermis showed superficial erosions with coagulated material, and glass fibers were found in the horny layer (more easily under polarized light). In selected fields of serial sections, fibers were found to have penetrated into the stratum Malpighi.25 These fibers can be observed in the horny layer under polarized light even using simple chemical stripping methods: a drop of cyanoacrylate glue is placed on the skin and a clean glass slide is gently pressed down on the drop for 30 seconds. A layer of horn is removed with the adhesive, which sticks to the glass slide. In a slight modification of this method polyester tape is used instead of glass as the holder. 25 It should be noted that some fibers are coated with epoxy or phenol-formaldehyde resins, a potential cause of allergic contact dermatitis. Rock wool fibers come from fibrous glass wool made out of minerals, coke, and limestone, compounded with a mineral oil, a silicone compound, and a phenolformaldehyde resin. These fibers provoke an airborne irritant contact dermatitis with symptoms similar to those described for glass fibers. Cases of airborne irritant contact dermatitis caused by sewage sludge were described by NethercotP among incinerator workers employed in a sewage treatment plant. The problem was found to be caused by contamination of the workplace and workers’ clothing with sludge from the interstices of an incinerator exhaust fan. The irritant nature of the sludge was determined by tests in rabbits.
Trona Dermatitis Trona dermatitis was described by Rom et aP2 in trona miners and millers. Trona (sodium sesquicarbonate) is mined in an underground deposit in Wyoming in the United States and is processed for use in the manufacture of glass, paper, and detergents and in chemical applications. Trona dust is alkaline (pH 10.5) and can have an irritant effect on the respiratory tract, the mucous membranes, and the skin. Trona dermatitis consists of itchy, erythematous, and dry lesions affecting the hands (direct contact) and face and limbs (airborne contact).
Anhydrite Dermatitis Anhydrite is an anhydrous calcium sulfate powder that contains traces of calcium fluoride and hydrofluoric acid. Highly alkaline (pH 11.2), it is used to fill gaps between the rock and the beams in tunnels in coal mines. Complaints of skin irritation were made by coal miners engaged in this procedure,33 with symptoms of itching or burning sensations on the face, neck, forearms and thighs. No erythema or eczematous reactions were observed. Skin irritation from the alkaline anhydrite paste was assessed by laser Doppler flowmetry: the iterative
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application of anhydrite on the flexor plane on volunteers’ forearms induced an increase in blood flow to the top layer of the derma. This dermatitis is a classic example of purely subjective airborne irritant contact dermatitis (ie, with no objective clinical manifestations). Replacing the anhydrite paste with a less alkaline paste (hemihydrate) was successful in preventing further cases of skin irritation.33
Slag Dermatitis Slag dermatitis occurs in metallurgic plants where permanent mold casting techniques have been introduced.34 During one stage of production, workers pour slag (a mixture of silicium oxide and calcium oxide powders) into the ingot molds. Workers wear asbestos coveralls but dust, penetrating the protective clothes or between the sleeves and the gloves, accumulates in the flexures and on the extensor planes of the thighs and arms. The subjective and objective symptoms are similar to those in fiberglass dermatitis. Microscopic examination of the powder particles revealed that some were oblong and sharp-edged (length: + 10 to 80 pm). Dermatitis was considered to follow mechanical injury to the skin by the sharp-edged particles.34
Dermatitis
From Miscellaneous
Agents
Other examples of airborne irritant contact dermatitis include indigenous or exotic wood particles, cement,35 cellulose fibers, mica dust, food additives,36 dust from urea formaldehyde insulating foam, and perchloroethylene. Alkaline vapors (such as ammonia) are often implicated in the provocation of skin irritation among laboratory technicians. Finally, it is worth mentioning that formaldehyde may be released from many industrial or domestic sources, such as urea-formaldehyde insulating foam3’ and formaldehyde-releasing preservatives in soluble oils. An exceptional and curious form of airborne irritant contact dermatitis came to our notice in five fishermen.38 It was due to mustard gas contained in bombs thrown into the sea as war relics after the World War II. The bombs were caught in the nets full of fish. The fishermen freed them from the nets and threw them back into the sea. The nets, however, which were contaminated by the liquid gas contained in the generally corroded bombs, were handled by the fishermen, who after some hours developed the symptoms of erythema, edema, vesicles, bullae, and a burning sensation. These symptoms involved mainly the hands and forearms, as a result of direct contact with the liquid gas. In addition, there were erythema and swelling of the face and particularly eyelids, with acute conjunctivitis, signs of an airborne contact dermatitis from mustard gas vapors. In fact, although the gas has
Table 4. Airborne
Allergens
Metals Chromates in cement welding fumes Cobalt Nickel Silver Mercury Solvents Formaldehyde Turpentine Insecticides Carbamates Pyrethrum Pesticides Vegetables Lichens Compositae spp Frullania spp Tulip bulbs Poison ivy Poison oak
and
Parthenium Tropical wood dusts Plastics and rubbers Cyanoacrylate Epoxy resins Phenol-formaldehyde resins Polyacrylates Polyurethane Resin additives Rubber additives (thiuram)
Medicaments Chloroquine sulfate Chlorpromazine Streptomycin Spiromycin Viiginiamycin Quinoline compounds b-Methoxypsoralen Miscellaneous Halogenated compounds Colophony Fragrances Bryozoans (Dogger Bank Animal feed additives Pyritinol HCl NCR paper Deodorants Hair sprays Dimethylthiourea Persulfates Phosphorus sesquisulfide Chloracetamide Propolis Chloroacetophenone
itch)
a low heat of evaporation, it evaporates slowly because of the low vapor tension, which, however, increases considerably with an increase in temperature. The mustard gas is toxic in both the liquid and the vapor state: in the former it can damage the skin directly, whereas in the latter, apart from the skin and the conjunctiva, it can also affect the mucosa of the respiratory and digestive tracts. Besides the five cases we observed, all in the summer months, the port authorities of Molfetta (a town near Bari in southern Italy) received 94 complaints, over a period of 10 years, from fishermen with irritant contact dermatitis of varying degrees from mustard gas, all of whom had clinical manifestations on the hands, forearms, face, and conjunctiva.38
Airborne Allergic Contact Dermatitis Airborne contact allergy seems to be a frequent complaint. Volatile contactants with allergic potential or allergens present in dust particles are mainly diffuse in professional environments (Table 4).2,3,25Clinical symptoms are typical of common allergic contact dermatitis
Clinics in Dermafokyy 2992;20:223-131 with no specific signs of its airborne nature. The lesions are usually symmetric and evolution can be acute or chronic, according to the nature and/or concentration of the allergen and the frequency of the airborne contact. The sites involved are those exposed to the air (face and neck) and often covered areas (flexures), as a result of the accumulation of solid particles under clothing. The simultaneous involvement of face and hands may suggest the possibility of associated airborne and direct contact, respectively. Differential diagnosis of facial allergic airborne contact dermatitis must be made with direct (or “true”) allergic contact dermatitis, with a flareup of the so-called “id’ type, with atopic dermatitis confined to the face, and with photoallergic contact dermatitis. Unlike allergic airborne contact dermatitis, in nonairborne photoallergic reactions some parts of the face, like the eyelids, the area under the chin, and the folds behind the ears, are not affected. Allergic airborne contact dermatitis lesions are symmetric, whereas asymmetric facial lesions suggest a direct contact allergy. Typical examples of professional airborne contact allergy often observed are those from epoxy resins, present in the form of dust or droplets in the metal/mechanical industry, from turpentine, from dust of exotic wood, from chrome in cement, and from pesticides in agriculture. With respect to the last, it must be remembered that thiurams may cause airborne reactions not only when used as fungicides in professional agricultural environments but also when used in medicaments. Nobecutan spray (which contains tetramethylthiuram disulfide), a bactericide and fungicide aerosol indicated for disinfecting the skin and protecting wounds and abrased dermatitis, can induce airborne reactions on the faces of subjects who are sensitive to the thiurams present in professional and nonprofessional rubber products. Allergic contact dermatitis from bryozoans (“Dagger Bank itch”), which affects fishermen during the summer, is mediated by two different pathogenic mechanisms: direct contact with the bryozoans, which is responsible for the dermatitis in the hands, and airborne contact from drops of seawater containing allergic material, which is responsible for dermatitis of the face and neck. The causative agent is generally Alcyonidium gelutinosum.39~40 As examples of nonprofessional forms, we report two recent observations. Two young women with contact dermatitis of the axillae and intense sensitivity to perfume (cinnamic aldehyde in fragrance mix) developed erythemato-edematous eruptions on the face and particularly the eyelids after a visit to a perfumery where they were sprayed with perfume samples. In one of the cases, a specific test made with a perfume sprayed in the allergy outpatient clinic was followed after some hours by ery-
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thema and edema of the eyelids. A similar case was observed by Dooms-Goossens et a1.2
Airborne Phototoxic Contact Dermatitis Airborne phototoxic contact dermatitis has no peculiar characteristics. Lachapelle’ observed a small epidemic of phototoxic reactions to Smethoxypsoralen in three female workers who were concerned with the confecting of tablets at a pharmaceutical company. After prolonged sunbathing at the end of a day’s work, phototoxic lesions developed in the skin areas that were uncovered during work. The reaction was of mixed type, involving the hands (as a result of direct contact) and the face, decollete, and arms (as a result of airborne contact). The airborne spread can be explained by the powdery nature of Bmethoxysporalen tablets.
Airborne Photoallergic Contact Dermatitis Airborne photoallergic contact reactions are very rare. The limits of clinical lesions are generally imprecise in these cases. Reactions to halogenated salicylanilides, phenothiazines, and musk ambrette (contained in cosmetics) under suitable conditions have been observed.’
Airborne Contact Urticaria The classic example of airborne contact urticaria is induced by the processional pine caterpillar.” The pine caterpillar, Thaumetopoea pityocampa Schif, is an herbivorous lepidopteran, responsible for a delay in the growth of maritime pines. Apart from the damage to nature and silvicultivators, the lepidopteran causes urticarious reactions of the strophulus type, as a result of the urticant hairs, in humans and domestic animals (dogs, sheep). The caterpillars causing urticaria are those in the last three larval stages (L3, L4, L5). The density of the urticant hairs on the caterpillar is approximately 60,000/ mm2; thus there are at least 1 million hairs on its back. The urticant hair, hollow on the inside, carries pointed spikes directed toward its distal end. It has no hole or pores, and as the bristles must be ground to extract the urticant substance, we are led to believe that the hair is really a bulb that must be broken, in the skin for example, to release its urticant (histamine-liberating) substance. Up to the age of 21, men seem to be more affected, owing perhaps to a predilection for games among the pines and attacks on nests with sticks. Although the dermatitis occurs among professionals (in nursery gardeners and foresters) it is primarily extraprofessional. Contamination generally occurs in pinewoods, rarely in cities, although infested pines may even be found in cities. There
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are various means of contamination: direct contact with the nest, direct contact with the processional caterpillar, indirect contact with the hairs suspended in the air or present on objects and clothes. This airborne contact urticaria can be observed from February to June, and during the summer months there are many cases along the coast among campers and picnic lovers (camping sites are usually situated under pines). The pathology induced by T. pityocampa involves the skin, eyes, and, in rare cases, the airways. The skin sites affected can be exposed (particularly by direct contact) and occluded, as the hairs can penetrate clothing. In most cases, the lesions spread over all the skin area; in 15% of cases they are isolated. Airborne contact urticaria from urticant hairs blown on the wind is favored by sweat, has its onset 2 to 12 hours after contact with the hairs, and presents subjectively with intense and continuous pruritis. The eruption consists of papulous, excoriated, and pinkish lesions on an edematous base. Exceptionally, the lesions can be bullous. Each lesion evolves over 3 to 4 days and leaves a hyperchromic outcome that lasts about 2 weeks. Diagnosis is aided by the onset of the same eruption in other members of the patient’s party, by the sites affected, and mainly by a case history describing a recent stay or walk in or near pinewoods. Epicutaneous tests with minced hairs (to release the urticant histamine-liberating) substance must be done on scarified skin. The clinical nature of the urticant substance contained inside the hair is unknown. Lesions to the eyes can be associated with those on the skin or not and can be early or late. The former manifest with a very intense burning sensation, hyperemia, and edema of the conjunctiva and eyelids. This is followed by photophobia, abundant secretion, and conjunctival nodules the size of peppercorns, as a reaction to the hair (ophthalmitis nodosa). Late lesions, on the other hand, are secondary to the penetration of the hair inside the eye; the clinical pictures include cheratitis, iritis, uveitis, cataract, nodules of the iris, and finally glaucoma. The clinical picture and pathogenetic mechanism of papillonite de Guyane Francaise (an airborne contact urticaria provoked by the urticant apparatus of the Hylesia urticans butterfly)42 and of other forms of airborne contact urticaria from Lepidoptera are similar.43,44 All these examples belong to the nonimmunologic contact urticaria group, according to Von Krogh and Maibach.45
Airborne Atopic Dermatitis In our opinion, there exist data in a certain percentage of cases suggesting the airborne nature of atopic dermatitis.46-50
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1, Atopic dermatitis is characterized by apparent clinical lesions of the eczematous type, which are histologically and immunotypically the same as those of contact allergy. 2. In varying percentages of subjects with atopic dermatitis, many recent studies using patch tests on healthy skin have shown positive delayed responses to aeroallergens like mites, pollens, and epidermic derivatives. 3. Patch tests with the same aeroallergens were negative in subjects with respiratory allergy but not dermatitis. 4. The aeroallergens that induce positive delayed responses are always those that determine recurrences of dermatitis. 5. Finally, it is known that acari, which are the allergens that most often cause delayed contact allergy, are present in greater quantities in damp climates, where atopic dermatitis is also more prevalent. On the basis of these data, it seems reasonable to suppose that the patch test can be considered as a direct skin test to elicit atopic dermatitis, and that both the immunoglobulin E and factors inherent to cell-mediated immunity contribute to the pathogenetic mechanism underlying this pathology.
Other Airborne Contact Dermatitis Chloracne has recently been defined by CroW5l as the production in the human of a type of acne with characteristic clinical features that have so far been induced only by aromatic chlorinated hydrocarbons with varying structure (polyhalogenated naphthalenes, polyhalogenated biphenyl, polychlorinated dibenzofurans, dioxins, azo- and azoxybenzenes). Skin contact with these substances can be direct or airborne and the same substances can also be inhaled or ingested. Chloracne lesions have a peculiar distribution. The most sensitive areas are below and to the outer side of the eye (the so-called malar crescent) and behind the ear. The nose is highly resistant. The genitalia, both penis and scrotum but particularly the latter, are also sensitive regions. If a sufficient exposure and toxic reaction have occurred, lesions may appear on the shoulders, chest, back, and, in some cases, buttocks and abdomen. The primary lesion of chloracne is the comedone. Other possible lesions are small, pale yellow cysts, cold abscesses, and follicular hyperkeratosis.52 Other dermatitides described are paresthesias caused by airborne pyrethroids, purpura from airborne epoxy resin, subcorneal pustular eruptions from airborne trichloroethylene, and erythema multiforme-like eruptions from tropical wood dust.*
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Mixed Forms Some particular clinical forms have been reported in the literature featuring a generalized dermatitis that can be explained by a mixed mechanism; in addition to the airborne skin contact, inhalation of the airborne factor could play a role. This is the case in the mercury exanthem described by Nakayama et a1.53These authors observed 15 patients with erythematous or erythematopapulous rashes that manifested 1 to 2 days after breaking a clinical thermometer or during dental treatment. The exanthem was diffuse and symmetric and involved particularly the flexures, axillae, popliteal fossae, and antecubital and internal planes of the thighs. In the more severe cases, pustular lesions, petechiae, and swelling of the legs occurred. The eruption subsided after 10 to 12 days, leaving no trace, and was accompanied by itching, fever, and a feeling of illness. Eleven of the fifteen patients had a history of contact allergy to mercurochrome. As mercury evaporates at room temperature, and the rash was diffuse and symmetric, it seems possible that in these cases the airborne skin contact was exacerbated by the systemic absorption of the substance through inhalation. We have observed another example of airborne dermatitis with a mixed underlying mechanism has been observed several times in patients with allergy to mercury following treatment with MOM in powder form (with an ammoniated mercury and metallic mercury base) for pubic phthyriasis (data not published). Intense erythematoexudative lesions of the genitalia, pubic region, and internal plane of the thighs were associated with involvement of the face, neck, folds, and trunk. In these cases, the types of contact were probably multiple: (1) direct skin contact during application of the mercury-based powder; (2) airborne contact resulting from airborne spread of the powder, producing the lesions of the face and trunk; (3) inhalation of the powder, inducing the clinical signs of “systemic contact dermatitis.” In seven of the nine cases observed, in fact, the skin lesions were associated with a feeling of illness, high temperature, and leukocytosis.
Diagnosis In cases of suspected airborne contact dermatitis, the common skin tests, like the open test, the scratch test (for airborne contact urticaria), and the patch test, can be performed. With due precautions, the exposure test (spray products) may be useful. Laser Doppler flowmetry may also be valuable in subjective symptomatic forms, with no objective clinical signs. In cases of reactions to solid particles in the professional environment, it is necessary to carry out a microscopic examination of the particles, collected in the work-
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place, under polarized light, and to determine the presence of any particles on the skin surface. This can be determined by stripping (with cyanoacrylate glue and polyester tape) the horny surface. Other important pathogenetic and diagnostic data are the pH of the particles, the relative humidity of the air in the workplace, and the relationship between the clinical symptoms and the working periods.26
Therapy and Prevention Treatment is symptomatic. The problem may be solved simply by taking protective prevention measures. In professional environments, silicone barrier creams are ineffective. The preventive methods suitable for each situation are both general and individual. The former consist of aspirating the particles in the workplace, monitoring the relative humidity, and, where possible, automating the whole working cycle. Individual prevention, on the other hand, requires the use of the most functional protective clothing.
Conclusions As airborne allergens and irritants are numerous and widely present in the environment, skin pathologies induced by them are undoubtedly more frequent than would appear from the literature. Reactions to irritants, generally in the workplace, are more common than allergic reactions, but often more difficult to demonstrate. On the whole, airborne contact dermatitis must be suspected when symmetric lesions are present in exposed areas, particularly the face and eyelids, when the patient denies having applied topical agents, and when the symptoms subside with a change in the environment.
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