Art hazards

Art Hazards STEVEN H. LESSER, MD, STEVEN J. WEISS, MD The awareness of art hazards spans centuries. "De Morbis Artifacum" ("Diseases of Workers") by Bernardini Ramazzini, published in 1713, reported silicosis in stone workers and plumbism ("lead poisoning") in potters. It is postulated that numerous artists have had diseases related to art hazards. For instance, the Spanish painter Goya may have had disease related to the lead in white paint, and Vincent Van Gogh may have developed insanity and optic neuritis from lead exposure. A sentinel warning to artists appeared in Art News in 1963 describing a flulike illness followed by kidney and liver damage. The illness was associated with a 15-year exposure to paint sprays containing polyester and epoxy resins. Other case reports began to appear. Mercury poisoning was described in a mural painter, lead poisoning in a stained glass worker, aplastic anemia secondary to benzene in lithographers, respiratory allergies from dyes, and chlorine poisonings with etching acids. There was even a case of anthrax in a weaver in California.1 As a result of these many cases, the general awareness of this problem has been increasing. Artists are particularly at risk for toxicity because of their exposures to toxic materials and their lifestyles. A significant number of artists work in home studios. Working in the living areas exposes children and other family members to risk. Artists are sometimes in other high-risk groups, such as operators of dangerous machinery, pregnant females, or people with heart disease, allergies or kidney problems. The degree of exposure may be much greater than that considered safe by the Occupational Safety and Health Administration (OSHA). Standard industrial tolerances for chemical exposures are predicated on an eight-hour work day with 16 hours to detoxify. Artists, when faced with deadlines, frequently work long hours, sleep in their workplaces and continue work after waking, all of which exaggerates the potential for chemical toxicity by increasing the duration of the artist's exposure. The cumulative effect of exposures may produce disease. One example is the sculptor who smokes a cigarette, turns on a gas kiln, then uses an oxyacetylene torch in a poorly ventilated studio, thereby increasing his or her risk of carbon monoxide poisoning. Another example is the painter who uses turpentine to thin paints, then uses strong soaps to clean the skin, consequently increasing dramatically the risk of developing contact dermatitis. From the Department of Emergency Medicine, Louisiana State University Medical School, New Orleans, LA. Manuscript received July 21, 1994; revision accepted September 21, 1994. Presented at the New Orleans Emergency Medicine Seminar, May, 1993. Address reprint requests to Dr Lesser, Department of Emergency Medicine, Medical Center of Louisiana, 1532 Tulane Ave, New Orleans, LA. Key Words: Medicine in art, occupational hazards, art hazards. Copyright © 1995 by W.B. Saunders Company 0735-6757/95/1304-002055.00/0

The purpose of this article is to familiarize emergency personnel with toxicity and physical trauma that may be associated with various fine art media and to promote the health care worker's understanding of the reasons artists are specifically at risk for toxicity and injury. To this end there are five sections to this article. First, an illustrative case report is presented and discussed. Art hazards then are discussed both in relation to the diseases associated with specific art processes and in relation to the organ system involved. The fourth section addresses the role of governmental agencies in protection of the artist, and finally, children's art products are discussed. The physician guided by an increased awareness of the various art processes and knowledge of the attendant toxic exposures will be able to obtain a better industrial history, diagnose art-related maladies more effectively, and provide guidance to patients involved in these processes.

CASEREPORT A 22-year-old painter presented with gradual onset of fatigue and weight loss over several months. History was negative for any significant medical or psychiatric disease. He denied allergies or medication use. The patient was a heterosexual who occasionally smoked tobacco and marijuana. He denied intravenous drug abuse or any other substance abuse. On review of systems, he described nervousness, irritability, malaise, and easy fatiguability. Physical examination showed a slender white man appearing his stated age in no apparent distress. His vital signs were normal and there were no abnormal physical findings. Lab work consisting of an SMA-7, complete blood count, urinalysis, and thyroid functions was all normal. His VDRL and human immunodeficiency virus tests were negative. He was discharged with a diagnosis of viral syndrome. Because of the persistence of his vague symptoms, he returned for a repeat examination but no changes were found. At this time an expanded history included an occupational contact with oil paints, which he often mixed from dry pigments, particularly blue and purple. The painter was asked to bring in a sample of the powdered pigments that he used. The primary pigment he used contained manganese. A heavy metal screen was obtained and initially reported as negative. A repeat screen, with a specific request for manganese level, was positive. The patient was diagnosed with Locura Manganica or manganism. He gradually became symptom-free after cessation of exposure following education on exposure risk and routes of contamination. Follow-up of three years showed no evidence of recurrence of disease. There was neither monitoring nor evaluation of the environment available because no laws cover this type of occupational exposure in a private studio. Discussion Manganism is a disease that has respiratory, hepatic, psychiatric and neurological symptoms. 2-5 The most prominent manifestations are the psychiatric and neurological. "Locura manganica" or "manganese madness" is the insidious onset of psychiatric symptoms including apathy, insomnia, confusion, bizarre behavior, visual hallucinations, emotional 451

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lability, decreased libido, impotence, and anxiety. Neurological manifestations include nystagmus, disequilibrium, paresthesia, memory impairment, a vocal pattern described as "whispering speech," problems with fine motor movement, lumbosacral pain, urgency, and incontinence. The neurological syndrome is similar to Parkinson's Disease with tremor, ataxia, loss of memory, flat affect, muscle rigidity, and gait disturbances. Unlike Parkinson's, however, pathological lesions are found in the globus pallidus and the striatum rather than the globus paUidus and the substantia nigra. 6 The most common respiratory symptom is dyspnea. 5 Because of its low solubility in water, airborne manganese does not cause oral or dermal problems. Instead, it penetrates the lower respiratory tract toward the alveolar membrane leading to the development of manifestations of pneumonitis, pneumonia, and bronchitis. This is true of most lowsolubility airborne toxins. Patients with manganism have pathological hepatic changes (increased golgi bodies and dilated biliary canaliculi) but rarely develop clinical hepatitis. Diagnosis of manganism relies heavily on the history and physical examination. Urine and serum manganese levels, assays of head hairs, assays of the slow growing chest hairs, and an elevation of serum calcium can suggest the diagnosis. Response to calcium edetic acid (EDTA) chelation therapy helps to confirm the diagnosis. Treatment is withdrawal from exposure, which is the treatment for most nonsevere heavy metal exposures. There is a good response to L-dopa in doses of 3.5 g daily and, interestingly, these patients can tolerate greater doses of L-Dopa than can unaffected patients. The anti-parkinsonian drug trihexyphenidyl (Artane; Lederle Laboratories, American Cyanamid Co, Pearl River, NY) may ameliorate the psychiatric manifestations, but does not improve neurological symptoms. 6 The differential diagnosis for "Locura Manganica" includes Wilson's disease, Parkinson's Disease, myxedema, psychiatric disease, and other heavy metal exposures. There are four important points illustrated in this case. First, if the physician does not ask for an occupational history, the patient may not volunteer one. Second, even armed with the occupational history, a physician may not be able to figure out the problem without an awareness of the materials, processes, and hazards associated with that particular occupation. Third, this case illustrates the point that standard heavy metal screens only detect mercury, arsenic, bismuth, and antimony. If the physician suspects another heavy metal, it must be specifically requested. Finally, most artists work in private studios not covered by occupational laws governing exposures. The risk of disease is variable and relates to each artist's awareness of the toxicity of his or her materials and the level of avoidance that he or she can afford.

SPECIFICART PROCESSES This section discusses each of the six major art processes: sculpture, printmaking, painting, photography, glassmaking, and ceramics. For each process the major toxic problems are discussed. Only the hazards are described. Information relating to actual risks for developing clinical syndromes from

toxic exposures is from industrial hygiene journals. These are translated into OSHA guidelines for safe industrial practices. Ai-tists' risks are nearly impossible to predict because of the variable level of awareness and the variable level of compliance.

Sculpture There are two types of sculptural techniques, constructive and subtractive. Constructive techniques involve fabrication of forms from preformed ferrous and nonferrous materials (eg, metal sculpture). Subtractive sculpture involves carving stone, plaster, or wood, thereby reducing its mass to form the object. Constructive and subtractive techniques each have a distinct set of toxicities and physical perils.

Metal Sculpture Metal sculpture is a constructive sculptural technique that includes foundry casting, metal fabrication, and blacksmithing. Foundry casting. This is the art of producing constructive sculpture with cast iron, bronze, and brass. The process of cast-iron sculpture begins with the melting of scraps of iron. The metal is melted in between layers of coke, a specially prepared form of coal, in a large pot called a cupola. To produce the heat necessary to burn the coke and smelt the iron, the gas-fired cupola is fanned by an electric blower. After the iron melts, a clay plug on the bottom of the cupola is removed, allowing the hot iron to pour into the crucible, a ceramic pot made to withstand temperatures of about 5,000°F. Molten iron from the crucible is then poured into molds. The composition of molds ranges from sand with an epoxy resin binder to modern thin-walled, ceramic-shelled molds developed by the aerospace industry. Molds are either hollow or have a combustible solid core that is destroyed by the molten metal. When the metal cools, the mold is fractured with hammers and pried from the metal. The surface of the newly created sculpture is cleaned or chased using grinders, chisels, and files. The sculpture is then treated with chemicals to form a patina, the coloration on the surface producing the characteristic aged look of the sculpture. Among the specific hazards of cast-iron sculpture are those associated with the lack of appropriate protective equipment, the metal itself, and impurities in the materials. Additionally, the physical fatigue associated with the high ambient temperatures and heavy materials, especially in primitive foundries, increases the likelihood of accidents. Artists wear face shields constructed from metal window screen to prevent droplets of splashed molten iron at 6,300°F (termed "bees") from hitting their faces. Kevlar gloves, aprons, and foot covers are worn to protect the torso and extremities from the intense radiant heat. Respirators used to protect the airway from contaminants such as the sooty black smoke diffused by the blowers are only effective if the correct cartridges specific for dusts, fumes, or solvents are used. The metal itself is extremely dangerous. It"there is any fatigue in the crucible or the mold, or if either is dropped, it will fracture, releasing molten iron hot enough to shatter concrete floors, producing shards of concrete shrapnel. Contact of the hot metal with oxyacetylene tanks near an accidental spill can cause the tanks to explode, producing metal shrapnel. Protective equipment that is designed for radiant

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heat reflection is minimally effective against flying debris. Impurities are present in both hollow and solid core molds. Hollow molds may contain residual impurities (ie, lime dusts and soda ash) that are released into the atmosphere when the hot metal is poured. Solid core molds contain wax, plastics (such as styrofoam), or other organic materials that release toxic fumes when they are "burnt out" (the term used for the destruction of the core material by the molten metal). "Burnt out" styrofoam, for example, produces cyanide gas. Other respiratory toxins include ammonia, benzene, carbon monoxide, hydrogen sulfide, and sulfur oxide. Unlike iron casting, brass and bronze casting does not employ a cupola because lower temperatures are used (2,000°F to 3,000°F). At these temperatures, gas heat is required but coke is not. Lead, copper, or glass may be added to the brass or bronze as a lux to make it more workable and less brittle. Fumes produced in this process may cause a metal fume fever (see below) or plumbism (lead poisoning), which would not necessarily occur in cast-iron foundries. Metal fabrication. This is another type of constructive sculpture. Pieces of metal are joined together using the welding techniques such as arc welding, MIG (metal inert gas) welding, oxyacetylene welding, or TIG (tungsten inert gas) welding. Steel is the most commonly used metal because it is easy to work and economical. After the materials are welded, surface preparations such as grinding, polishing, and finishing are performed. An arc welder uses a high-voltage electrical arc to produce heat that melts a metal rod, fusing two pieces of metal together. The metal rods are coated with a flux that stabilizes the weld when combusted. Fluxes used in the steel welding rods include cadmium, manganese, chromates, phosphorus, zinc, and hydrofluoric acid. The toxic fumes produced when the flux burns causes respiratory tract irritation and metal fume fever. 7 Metal fume fever is also known as Foundry Augue, Zinc Shakes, Monday Morning Fever, Welder's Fever, and Solderer's Fever. It is called Monday Morning Fever because workers develop a tolerance to the effects of the fumes during repeated exposures. They lose their tolerance over the weekend, and get sick on Monday night after a full day back at work. The presentation is as a flulike illness with a four- to six-hour onset of symptoms, generally manifesting the evening after exposure to noxious fumes. 6 The patient complains of fever, chills, fatigue, myalgias, cough, dyspnea, thirst, a metallic taste in the mouth, salivation, rhinitis, and conjunctivitis. The chest X-ray may show nondescript increased interstitial markings and there is a nonspecific leukocytosis. Resolution occurs within 36 hours after cessation of exposure. The substances associated with metal fume fever are copper, magnesium, aluminum, antimony, iron, manganese, nickel, and zinc. 6'8"9 The fumes from molybdenum, an additive in some welding rods or in the steel itself, produce a unique clinical picture. The symptoms of molybdenum exposure are decreased appetite, listlessness, weakness, fatigue, anorexia, headache, arthralgias, myalgias, chest pain, nonproductive cough, and diarrhea. Molybdenum increases production of xanthine oxidase and is a cofacter required for transferases to bind iron. Therefore, patients with high molybdenum levels develop gouty attacks and a hypochromic microcytic anemia. The

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patient may develop an X-ray pattern that looks like a pneumoconiosis. Chronic molybdenism causes testicular atrophy. The release of toxic metal fumes is avoided by the use of a MIG (metal inert gas) welder. This type of welding uses inert gases or carbon dioxide to create a stable environment for the arc, avoiding the need for fluxes like those on the welding rods used in arc welding. A MIG welder supplies the welding material as a wire spool rather than a flux-coated rod. MIG and Arc welders both emit ozone (03) because of the high-voltage arc that is produced. Ozone produced by a MIG or an arc welder has a very pungent odor, is water soluble, and is primarily an upper respiratory tract irritant. Low-grade exposures to this strong irritant cause burning of the eyes and throat, nonproductive cough, substernal pain, and bronchial irritation. The more serious syndrome of acute ozonism presents with respiratory distress, dyspnea, cyanosis, and pulmonary edema. X-rays show increased interstitial markings. Other symptoms include alteration of visual responses, increased red blood cell fragility, an increase in glucose-phosphate dehydrygenase and lactic dehydrogenase, and a decrease in RBC acetylcholinesterase. The symptoms will usually resolve in about one or two weeks, although there may be long-lasting, persistent headache, fatigue and dyspnea. 6,a°-12 Oxyacetylene welding is the combustion of a mixture of oxygen and acetylene producing heat to melt metal rods without flux. Oxygen is stored in steel bottles under 2,000 pounds of pressure, lfthe oxygen tank is tipped over and the regulator is knocked off, the tank can become a missile that can penetrate walls. Acetylene is also stored in steel bottles at 200 pounds of pressure. To prevent the acetylene from exploding under pressure, it is stabilized by an equilibrium reaction with acetone (contained in an inner ceramic core of the tank). If the acetylene in the tubes to the welding torch develops pressures >35 psi, it can explode spontaneously. Oxyacetylene, MIG and Arc welding processes all may produce airborne molten metal droplets. Welders seen in the emergency department (ED) often have innumerable holes in their clothing caused by these bits of metal or "bees." If the clothing is penetrated, third-degree burns may be sustained from the "bees" trapped within the clothing. TIG welding is the best welding process for stainless steel and nonferrous metals. In addition to producing flux fumes, like the arc welder, and ozone, like both the arc and MIG welders, it produces intense ultraviolet radiation. The light may produce first- and second-degree burns on unprotected areas of the artist's skin and a punctate keratopathy on the cornea known as "welder's burn." TIG welding is the most likely welding process to cause damage to the retina because the torch (approximate temperature, 6,300°F) produces visible, ultraviolet, and infrared light. Welding masks come in dark shades of green glass to protect the eyes from the intense ultraviolet invisible light produced by welding. The artist needs to know which of the shades (3 through 12) is appropriate for the work they are doing. Different eye colors and welding processes require different shades. Surface preparation is the next stage in metal fabrication. After metals are welded they are ground, polished, and then finished. Grinding is done with 3- to 4-horsepower hand-held grinders, weighing 20 to 30 pounds, with abrasive wheels

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spinning at up to 9,000 rpm. Fiberglass and polymer resin are used as a matrix for support of the abrasive silicon dioxide and carborundum in the grinding wheels. The sculpture is polished using a wire wheel composed of hundreds of stiff wires formed into a cup or disk, also rotating at speeds up to 9,000 rpm. Finishing includes surface preparation with acids and cleansers, or by anodizing (electromagnetic pigment binding), galvanizing (electromagnetically binding a layer of zinc to the surface), or painting with a variety of paints, polymers, or resins. The grinding and polishing wheels can fatigue and shatter, producing shrapnel flying at speeds sufficient to go through clothes, skin, and eyes. As grinding wheels wear down, they produce fiberglass and resin dusts that are respiratory irritants. Although masks will protect an artist from chips and dust produced by the wire wheels, they will not always protect the artist from a wire thrown from a polishing wheel turning at 9000 rpm. This is fast enough to propel an unfortunately directed wire through the mask to become an intraocular or even intracranial foreign body. Blacksmithing. This is another form of metal sculpture. Iron heated in a forge is given form by being struck by a hammer on an anvil. The forge generates heat by using a forced stream of air to maintain the combustion of coke. The hammer and anvil are both made of hot iron that is frozen into shape (forged). This process creates brittle tools, which when struck together may shatter, producing shrapnel-like shards of iron. Blacksmiths are exposed to fumes from the forge that contain carbon monoxide, carbon dioxide, various cyanogenic compounds, and lead. Burns and respiratory irritation (chronic or acute) are sources of morbidity to blacksmithing artists.

Stone, Wood, and Fiberglass Sculpture Stonecarving. This type of subtractive sculpture is formed by chipping, slicing, grinding, and polishing. Two major problems encountered by stone sculptors are dust inhalation and vibration-induced peripheral neuropathy. Dust exposure occurs each time a sculptor strikes a stone with chisel, grinder, or polishing device. White marble is relatively pure calcium carbonate; however, common stones such as field stone may contain harmful or irritating minerals including asbestos. Exposure to dusts can cause or exacerbate sinus, bronchus, and small airway diseases) Stone dust-related pneumoconiosis (including silicosis and silicotuberculosis) based on characteristic gross pathological changes has been noted in the lungs of stoneworking artisans for centuries. The vibration-induced peripheral neuropathy is produced by pneumatic or electromotive hammers or grinders frequently used to form the stone. "Vibration syndrome" is a neuropathy in the hands after prolonged exposure to vibration. Stonecutters may present with complaints of bilateral parasthesias in their upper extremities. Occupational stone cutters in Italy who worked with pneumatic tools throughout their lifetimes developed edematous clawlike hands. Foam placed around the tools or specialized gloves may be used to decrease vibrational exposures. Woodcarving. Respiratory and dermatologic irritants are produced from woodcarving. The dust produced from sanding can cause bronchial irritation, exacerbating asthma, and can produce hypersensitivity pneumonitis or induce a pneumoconiosis. Certain exotic woods (eg, Western Red Cedar)

contain caustic oils that may cause contact dermatitis and are particularly irritating to the respiratory tract. Exposure to glues (including epoxies) and solvents (eg, toluene) can potentiate the irritative respiratory effects of wood dusts. Rhus sensitivity (poison ivy, poison oak, etc) has been described as cross-sensitizing some individuals to the dermatologlc effects of substances in exotic trees and their derivatives (lacquers, varnishes, and oils). Fiberglass. Reinforced fiberglass is used to form hollow sculptures. The production of fiberglass sculptures requires a fiberglass fiber mat or fibers, a liquid resin, and a catalyst. The fiberglass fiber mat or fibers are used to reinforce the resin. The liquid synthetic resin is poured, sprayed, or painted onto the reinforcing fiberglass mesh or fiberglass fibers. The catalyst that is used to harden the liquid resin is a concentrated peroxide. The hardened resin, reinforced by the fibers, becomes a strong structural material. Silica gel, a finely divided silica dust, is sometimes added to the liquid resin as additional reinforcement. The elements are occasionally combined using a "chop gun," a pneumatic device that chops long ribbons of fiberglass into small slivers. The chop gun combines the fiberglass slivers with a resin catalyst and sprays them on the surface of a mold to build up the reinforced fiberglass mass. When finished, reinforced fiberglass is ground or sanded to produce the final product. Fibers from the mat can produce a localized pruritic dermatitis caused by fibrils entering the skin. The resin contains organic solvents that are irritating to the skin and mucus membranes, hepatotoxic, and neurotoxic. The catalyst can be intensely irritating to the skin. During sanding or grinding, fragments are released into the air. These fragments can cause a pruritic dermatitis or a pneumoconiosis. The aerosolized solvents, fibers, resins, and catalysts are respiratory irritants. Pneumatic chop guns are notorious for producing particularly large amounts of noxious fumes.

Printmaking Printmaking processes share in common the application of liquid or semiliquid pigment-bearing media to a prepared surface, which is then transferred to paper in a pressing device. Intaglio. This very old form of printmaking utilizes the surface of copper, aluminum, or zinc plates, which are etched by exposure to inorganic acids. Ink, a complex medium consisting of pigment, oil, and modifiers in an organic solvent, is applied to the plates and rubbed into the recesses formed in the etching process. The excess ink is removed, and the prepared plate is then passed through a printing press where the image is produced by transferring the remaining ink to paper. The intaglio press is a machine consisting of a roller and a flat bed. The paper is run between the roller and bed at enormous pressures, typically 24,000 pounds per linear foot. Excess ink is then cleaned from the plate with organic solvents. Because these machines frequently lack guards, fingers may be entrapped between the roller and the press bed. Lithography. This is a related process classically using a fine-grained limestone instead of metal plates. The first step in lithography is applying the image to the surface of a clean flat limestone using an oily crayon called "tuche," producing hydrophobic areas. A negative image is then bitten into the stone using organic acids that dissolve a tiny layer of the

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stone face not protected by the tuche. Finally, ink, a hydrophobic oily substance, is applied to the face of the stone, adhering specifically to the areas that were covered with tuche and now are slightly raised. The ink is rolled on, and the image is transferred to paper by scraping the back surface of the paper with a bar. Photoetching. In this process, a copper or zinc plate is coated with light-sensitive emulsion and a photographic transparency is placed on top of it. The plate is exposed with a carbon arc lamp, a source of intense ultraviolet emissions, which hardens the areas that are exposed to the ultraviolet light as it passes through the transparency. These hardened areas create an acid resistance. The plate is bitten with acid after organic solvent (eg, toluene) is used to remove the nonhardened sections. Prolonged contact with toluene (similar to "glue sniffing") causes dermatitis, sinusitis, hepatitis, and damage. The lamps can cause retinal and corneal damage. 6 Printmakers may be exposed to organic or inorganic etching acids, alkali, hydrofluoric acid, nitric acid, and hydrochloric acid. These agents are chiefly upper respiratory and mucous membrane irritants. Acids release water and heat on contact with mucous membranes. The printing inks, in addition to pigment and oil, are complex mixtures containing stabilizers, surface agents, various organic solvents, antiskinning agents, reducers, thinners, tack reducers, stiffeners, and dryers. As an example, eugenol, an ingredient of the antiskinning agent, is a strong upper respiratory and dermatologic irritant. Some of the dryers contain lead or magnesium. Central nervous system toxicity caused by organic solvent exposure is important in lithography and photoengraving, particularly when the solvents are volatilized in sprays. Toxicity may not be suspected until the physician determines the composition of the ink.

Painting The cutaneous exposure of painters to their paints dates back to the Cro-Magnon man as evidenced by the handprints found on the walls of the Cave of Lasceux on the European continent. Modern painters are exposed to heavy metal pigments when mixing their own paints. There is a long list of toxic exposures associated with painting (Table 1), most of which are from the solvents and the pigment agents that constitute the paints. The powdered pigments are added to an organic medium such as linseed oil to make paint, then thinned with solvents such as acetone, benzene, turpentine, methanol, or methylene chloride. Acrylic paints are waterbased instead of oil-based but have similar pigments and release ammonia fumes as they dry. Mucous membrane absorption can occur from pointing the brush (the process of sharpening the tip of a paintbrush by placing it between the pursed lips of the painter) or from other fomites such as food or cups used in the studio. Heavy metals, used as coloring agents in paints, have a wide range of site-specific toxicities. These include metals used to produce whites (barium, magnesium, titanium, and lead), ultramarine blue (cobalt), 13'14 blues, purples, and greens (manganese), 2-5 and the reds and yellows (zinc and cadmium). ~L ~2.15-~9 Barium and cobalt, for example, are direct cardiac toxins, causing cardiomyopathy. Other specific sites of disease caused by pigments and solvents include the

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renal bed, the central nervous system, and the reproductive systems. Cadmium, the coloring agent in some vivid yellow, red, and orange paints, provides a typical example of pigmentrelated heavy metal poisoning. 11 The clinical problems associated with exposure illustrate the complexity of disease processes that are encountered with the heavy metals. Normally, in the nonexposed individual, the total life body burden of cadmium is 30 ng. The elimination half-life of the element is between 16 and 33 years. 6 Distinct acute and chronic exposure syndromes exist for cadmium toxicity. Acute exposure is rare but massive ingestions have been described in industrial settings and are associated with a 15% mortality. 1~ Symptoms can be respiratory, dermatologic, or gastrointestinal. In small quantities, inhalation exposures are more toxic than ingestions. Acute respiratory exposure begins with a metal fume feverlike flu syndrome further characterized by decreased sense of smell, edema of the face and larynx, yellow discoloration of the teeth (yellow rings), cough, and dyspnea developing 12 hours after the exposure. Acute ingestion was described in a painter who developed a severe stomatitis. 6 Acute massive ingestions are described with acute pulmonary edema developing over 1 to 4 days and persisting for months. Systems involved in chronic cases include respiratory (bronchitis, emphysema and pneumonitis), gastrointestinal (nausea, vomiting, diarrhea), genitourinary (decreased spermatid and spermatocyte counts, testicular necrosis, increase calciuria resulting in renal stone formation, and [32-microglobulin proteinuria), 17,18 hematologic (hypochromic anemia), musculoskeletal (osteoporosis associated with calcium loss), and neurological (vertigo, headache, and shivering) symptoms. 16 It causes an increased risk of lung and prostate cancer. "Itai itai" ("ouch ouch") disease has been described in middle-aged Japanese women with low calcium intake who are exposed to cadmium. 19 They develop lumbar pain, lower extremity myalgias, and osteomalacia. Treatment, as with any other metal exposure, is cessation of contact and chelation therapy. The most important component of management is the high index of suspicion that leads to the diagnosis.

Photography Photography is another chemical playground (Table 1). Industrial and amateur photographers use three sequential chemical baths to produce prints: a developer, a stop bath, and a fixer. Photographic developers are the most toxic chemical used in the process, especially after accidental ingestion. Nervous system (tinnitus, headache, vertigo, diploplia, and weakness), respiratory (asthma), gastrointestinal (nausea, vomiting, spleen and liver disease), and dermatologic symptoms (allergic reactions) occur secondary to these complex hydrocarbons. Stop baths are usually weak solutions of acetic acid, and fixing baths contain sodium thiosulfate, acetic acid, and preservatives, none of which produce serious disease from short-term small-dose contact. Unlike industrial and amateur photography, fine arts photography encompasses a wider range of printmaking processes that use exotic pigmenting and developing systems with unique hazards that must be considered. A good example of this is salt printing, a primitive process used by civil war photographers (eg, Mathew Brady) using salt and silver

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TABLE1. Hazards to Photographers and Painters Photographers

Painters

Metals

Borate Bromides Chromates Iodine Lead Mercury Silver Tellurium Uranium Vanadium

Arsenic Barium Chromates Cadmium Lead Manganese Mercury Magnesium Titanium Zinc

Solvents

Aminophenols Amylacetate Benzene Ethylene Glycol Formaldehyde Methanol Trichloroethylene

Acetone Benzene Carbon Tetrachloride Methanol Turpentine

Others

Acids and Alkalis Cyanide Hydroquinone Oxylate Sodium Bisulfate Sodium Hypochrome Sodium Sulfide Sodium Thiosulfite

Acids and Alkalis Carbon Disulfide Methylene Chloride Nitrogen Oxides

nitrate to produce a yellowish image. The photograph is then given a rich brown hue by the addition of potassium bichromate. Today, many photographers continue to utilize the subtle gradations of tone that can be achieved by the process. Bichromate, a powder that must be mixed with water, causes severe upper respiratory disease, including nasal septal perforations, allergies, and annoying skin irritation. 2°-2z

Glassworking Glassworking includes hot glass (blown and casted), neon art (manipulation of glass tubes evacuated and filled with neon), and stained glass (cutting and joining of pigmented glass). Hot glass art is produced from bags of pure silica in a fine powdered form known as "batch." Gas fire tanks are charged (filled) with batch, which is heated until molten. Minerals may be added to the hot glass as colorants. The white-hot glass has a honeylike consistency. It is removed from the tank either on the end of a blowpipe (to be blown) or with a steel ladle (to be poured into a mold). After the glass is formed by either technique, it is placed in an annealing oven to cool slowly, which relieves internal stresses in the hardening glass. Hot glass sculptors can develop disease related to exposure to heat, silica, and the minerals used as colorants. Prolonged thermal exposure of the lenses of the eyes can result in cataracts. The potential for physical trauma from hot materials, the hot working environment, and the stress to work the glass quickly before it cools, is high. Pieces of hot glass that are rejected are not placed in an annealing oven and may shatter spontaneously when cooling in the working environment. Silica exposure occurs during the charging process or

from the production of silica dusts when the cooled glass is cut or ground. Cobalt, a mineral used as coloring agent in glass, causes cardiac disease. Neon art is a form of glassworking that begins with the manipulation of glass tubes into a desired shape or form. The hot tubes are washed by flushing them with a bolus of liquid mercury to remove particulate contaminants. The glass tube is sealed by heating one end and applying oral suction on a rubber tube connected to the other end of the glass tube, causing the soft treated glass walls to collapse into a point. The tube is then completely evacuated using a vacuum pump, and filled from flasks containing noble gasses (helium, neon, argon, and krypton). The contents are finally purged of impurities by the application of 24,000 volts across the tube. Toxicity can be caused by inhalation of either mercury vapors or electrical arc-produced ozone, thermal trauma from hot glass, and electrical injuries from high-voltage transformers. Elemental mercury, although poorly absorbed through the gastrointestinal tract, may become volitalized when passed over hot glass, and subsequently may be inhaled. Symptoms of mercury poisoning (erethism) include the insidious onset of behavioral changes (the "mad hatters" of England), anorexia, peripheral neuritis, tremor known as "hatter's shakes," weakness, and renal impairment. ]8'23-26 The arc associated with tremendous voltages may cause ozone release leading to ozonism (as discussed previously in relation to welding). Stained glass is produced by cutting pieces of colored glass and joining them with lead strips called "caming." Ingestion of the lead from fomites leads to plumbism ("saturnine gout").

Ceramics Ceramic art is produced by forming and baking (bisquefiring) selected clays into sculptures and pottery. Pigment agents are applied to the surface to produce textures and colors (glazes), then the ceramic is fired again at higher temperatures to fuse the glazes to the clay. Exposures are from the glazes and sulfur dioxide produced in firing. Although lead is no longer used in pottery glazes in the United States, pottery in Third World countries still commonly contains lead glazes. Oral absorption can occur when drinking or eating acid foods (eg, grapefruit juice) which solubilize the lead from the glaze. Heavy metals used in glazes in the US include arsenic, antimony, and cadmium. Sulfur dioxide, emitted during the initial firing of clay, can produce pulmonary disease and may act synergistically with particulate matter. 27

SITE-SPECIFICEXPOSURES Some hazards span numerous different artistic endeavors and are better discussed in relation to the organ system involved. Nervous system problems are split into four groups: those that affect the entire system, those that cause isolated peripheral or central nervous system diseases, and those causing neurotrauma. Generalized neurotoxins include mercury, manganese, carbon disulfate, and organophosphate plasticizers. Plasticizers are substances used to improve the working properties of resins in fiberglass sculpture. Isolated pe-

LESSER AND WEISS • ART HAZARDS

ripheral neuropathies are produced by methylberyl ketone, aerosols, polyester resins, and lead. Central nervous system problems are caused by organic solvent intoxication (eg, toluene and xylol). Printmakers and silk screen printers volatilize these solvents as sprays, potentiating their toxicity. 28-3~ Neurotrauma from the use of hammers and chisels can cause vibration syndrome and carpal tunnel syndrome. The eyes are a site of trauma and toxicity from almost all art forms. Chips of flying materials used by sculptors and blacksmiths can penetrate the globe and even enter the cranial cavity. Ultraviolet light and heat exposure can cause cataracts, retinal damage, and a superficial punctate keratopathy ("welder's conjunctivitis"). Cardiotoxic heavy metals are contained in paints. Barium, cobalt 24"z5 and many of the organic solvents (toluol, methyl chloroform, and methylene chloride) 32'33 are direct cardiac toxins. Stewart and Hake 3~ described a methylene chloride induced heart attack. Respiratory tract irritants affect different sites based on particle size and solubility. 34 Highly lipid-soluble dusts and fumes cause more systemic injury and minimally lipidsoluble substances produce more local effects. Those substances that are more water-soluble will remain in the upper tract and the skin, whereas the less water-soluble substances will affect the lower respiratory tract. Among the direct irritants are nitrogen dioxide (welding gas, carbon arc, etching, and enameling), chromium gas (from etching acid), hydrogen chromide (heating, plastics, and polyvinyl chloride), caustic dusts (lime, dichromate, soda ash, and potassium), and antiskinning agents (eugenol and clove oil). Certain substances have been associated with specific respiratory diseases. Pneumoconiosis is caused by iron oxides, aluminum, and barium sulfate. Pulmonary fibrosis is caused by silica, coal, talc, scrap stone, and asbestos. Asthma is exacerbated by wood and bone dust, fibers, reactive dyes, formaldehyde, turpentine, polyurethane, isocyanate, and freshly formed aluminum oxide. ("pot-room asthma") Hypersensitivity pneumonitis is caused by wood dusts and heavy metals. Anthracosis is caused by smoke elaborated when coke is cornbusted. Clinical hepatitis is caused by chlorinated hydrocarbons, phenol, ethyl alcohol nitrobenzene, cadmium, styrene, arsenic, toluene, lead, and xylene. Manganese causes pathological hepatic changes; however, clinical hepatitis has never been reported. Direct renal toxins include oxalic acid, turpentine, ethylene glycol, and mercury. Chronic renal disease caused by cadmium is characterized by a 132-microglobunemia and proteinuria. Lead poisoning causes menstrual disorders in females and testicular atrophy in males. 35 Severe dermatitis is caused by various compounds. The grinding of fiberglass-reinforced sculptures produces particles that can cause an intensely pruritic rash. Plaster and cement contain lime, which can produce a severe dermatitis. Other causes of dermatitis include photographic developers, exotic woods, soaps, drying agents, and solvents. Numerous hematologic effects can be seen. Cyanosis is caused by hydroxyamine (a color developer), polyvinyl chloride, nitrates, cobalt, and other photographic developers. Lead, cadmium, benzene, and naphthalene can cause a hemolytic anemia. Other hemaglobinopathic disease include

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carboxyhemobglobinemia, methemoglobinemia, sulfhemoglobinemia, and cyanohemoglobinemia. Teratogens and carcinogens include chromium, zinc, and arsenic. Chromium, a documented carcinogen, may be inhaled when metal sculptors grind through or weld scraps of chromium-plated steel (used in car manufacturing). Cadmium, a chronic renal toxin (see painting), is also a carcinogen. Driscoll et a136 described a mesothelioma in jewelers.

GOVERNMENTALPROTECTION No governmental agencies protect the self-employed artist from injury. OSHA started in 1970 to "improve the health conditions of working men and women." However, it does not protect either government employees or the selfemployed. Most people who work in the fine arts are selfemployed. The National Institute of Occupational Safety and Health (NIOSH), a research arm of OSHA and a branch of the Department of Health, makes recommendations for industrial hygiene and product usage but does not protect the self-employed. 1 The Consumer Product Safety Agency requires labeling but cannot regulate how a product is used. They only intervene if"there is a reasonable risk of injury," such as in 1978 when they banned benzene in paint remover because it was linked to leukemia. The Toxic Substance Control Act from 1976 allows the Environmental Protection Agency to test things before release rather than waiting for illnesses to manifest themselves. The Federal Hazardous Substances Act requires safe and adequate labels. The rules do not apply if the product is repackaged. For example, McCann I describes the fact that the label on a 55-gallon drum of bulk-reactive dye would read, "Dust may cause allergic respiratory reactions. Avoid breathing dust. Keep container closed. Use forced ventilation. Use respirators or dust masks approved by the Bureau of Mines." The same item sold in a jar, however, may read, "Ecologically safe." Glazes are often poorly labeled, or toxic ingredients may be trade secrets and not included on lists of ingredients. The Center for Safety in the Arts was established in New York City in 1972 as a national clearinghouse. They provide information, education, and a newsletter to interested parties (1-212-227-6220).

CHILDREN AND ART SUPPLIES Children are particularly at risk for the effects of toxic exposures. 34 They have a faster metabolic rate, higher surface area, developing brain and nervous system, faster absorption through their intestines, and (particularly those younger than the age of five years) tend to put everything in their mouth. "Nontoxic" on children's products refers to a definition in the Federal Hazardous Substance Act. It defines nontoxic as "any substance that has capacity to cause personal injury through ingestion, inhalation or absorption." These laws only relate to immediate toxicity, not long-term poisoning. The Crayon, Watercolor and Craft Institute puts a CP or AP on the product, meaning "certified product" or "approved product." These are tested by toxicologists for immediate toxicity but not for long-term toxicity. 6

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AMERICAN JOURNAL OF EMERGENCY MEDICINE [] Volume 13, Number 4 [] July 1995

The common misconception that all children's products that are water-soluble are safe is not necessarily true because of the presence of preservatives. For example, watersoluble paints might be preserved with ammonia or formaldehyde. Fluorescent paints are toxic. Felt-tip markers have aromatic hydrocarbons. Modeling clay may contain toxic preservatives. Paper mach6 is just flour and water, but if fresh newspaper is used, the color-illustrated sections may have toxic materials in the inks. There are several types of glue. Water-based glues have polyvinyl acetate emulsions. Many organic glues have solvents and super glues have cyanoacrylate, which can cause adhesions of the conjunctiva if it gets in the eyes.

SUMMARY The diseases associated with art forms range from trauma (vibration syndrome, flying objects, etc) and heat exposure, to heavy metal and solvent exposure. Specific substances such as ozone, cadmium, and molybdenum have unique diseases associated with them. Sadly, artists may not have the medical knowledge to know how to deal with or avoid hazards. They and their immediate families often may be at risk. Many artists are not educated in what protective gear to use and do not have the money to purchase the specialized equipment for their particular work, or they refuse to wear protective gear because they are uncomfortable in the conditions encountered in the workplace. Education is often required for the use of the protective gear (respiratory, eyewear, contact protection). To make matters worse, artists are poorly protected from toxins. Government regulations are not adequate to protect self-employed artists. Laws regulating children's exposure do not address long-term toxicity. Most artists with acute problems present to the ED first. An awareness of the occupational hazards to which selfemployed artists are exposed will prevent the treating physician from overlooking important clues. When an artist presents with unusual symptoms, the physician must get a complete occupational history and must have the patient bring a list or samples of any substances to which he or she has been exposed. In essence, artists are a group of enthusiastic, hardworking people that can be protected by a keen awareness of these basic principles by the treating physician.

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8. Dula D: Metal fume fever. J Am Coil Emerg Phys 1978;7: 448-450 9. Mueller EJ, Seger DC: Metal fume fever. A review. J Emerg Med 1985;2:271-274 10. Nasr ANH: Ozone poisoning in man: Clinical manifestations and differential diagnosis. A review. Clin Toxicol 1971;4: 461-466 11. Lucas PA, Jariwalla AG, Jones JH, et al: Fatal cadmium fume inhalation. Lancet 1980;2:205 12. Elinder CG, Edling C, Lindberg E, et al: B2-Microglobulinemia among workers previously exposed to cadmium. Followup and dose response analyses. Am J Ind Med 1985;8:553-564 13. Lahaye D, Demedts M, Vanden Oever R, et al: Lung diseases among diamond polishers due to cobalt? Lancet 1984;1 : 156-157 14. Kennedy A, Dornan JD, King R: Fatal myocardial disease associated with industrial exposure to cobalt. Lancet 1981 ;1: 412-414. 15. Roels H, Djubgang J, Buchet JP, et al: Evolution of cadmium-induced renal dysfunction in workers removed from exposure. Scand J Work Health Environ 1982;8:191-200 16. De Silva PE, Donnan MB: Chronic cadmium poisoning in a pigment manufacturing plant. Br J Ind Med 1981;38:76-86 17. Armstrong DG, Kazantzis G: The mortality of cadmium workers. Lancet 1983;1:1425-1427 18. Landrigan PJ: Occupational and community exposures to toxic metals: Lead, cadmium, mercury and arsenic. West J Med 1982;137:531-539 19. Emmerson BT: "Ouch-ouch" disease: The osteomalacia of cadmium nephropathy. Ann Intern Med 1970;73:854-855 20. Langard S, Vigander T: Occurrence of lung cancer in workers producing chromium pigments. Br J Ind Med 1983;40:71-74 21. Fisher AA: "Blackjack diseases" and other chromate puzzles. Cutis 1976;18:21-36 22. Walsh EN: Chromate hazards in industry. JAMA 1953;153: 1305-1308 23. Waldren HA: Did the Mad Hatter have mercury poisoning? BMJ 1983;287:1961 24. Joselow MM, Louria DB, Browder AA: Mercuralism: Environmental and occupational aspects. Ann intern Med 1972;76: 119-130 25. Jaffe KM, Shurtleff DB, Robertson WO: Survival after acute mercury vapor poisoning. Role of supportive care. Am J Dis Child 1983;137:749-751 26. Hallee TJ: Diffuse lung disease caused by inhalation of mercury vapors. Am Rev Resp Dis 1969;99:430-436 27. Fischbein A, Wallace J, Sassa S, et al: Lead poisoning from art restoration and pottery work: Unusual exposure source and household risk. J Environ Path Tox Onc 1992;11:7-11 28. Lindstrom K: Psychological performances of workers exposed to various solvents. Work Envir Health 1973;10:151-155 29. Hanninen H, Eskelinen L, Husman K, et al: Behavioral effects of long term exposure to a mixture of organic solvents. Scand J Work Environ Health 1976;2:240-255 30. Elofsson SA, Gamberale F, Hindmarsh T, et al: Exposure to organic solvents. A cross-sectional epidemiologic investigation on occupationally exposed car and industrial spray painters with special reference to the nervous system. Scand J Work Environ Health 1980;6:239-273 31. Maizlish NA, Langolf GD, Whitehead LW, et al: Behavioral evaluation of workers exposed to mixtures of organic solvents. Br J Ind Med 1985;42:579-590 32. Stewart RD, Hake CC: Paint remover hazard. JAMA 1976; 235:398-401 33. Roberts CJC, Marshall FPF: Recovery after "lethal" quantity of paint remover. BMJ 1976;1:20-21 34. Brooks SM: The evaluation of occupational airways disease in the laboratory and workplace. J Allegy Clin Immunol 1982 ;70:56-66 35. Barach AL: Treatment of sulfur dioxide poisoning. JAMA 1971 ;215:485 36. Driscoll RJ, Mulligan WJ, Schultz D, et al: Malignant mesothelioma. A cluster in a native American pueblo. New Engl J Med 1988;318:1437-1438