Was Paul Klee’s scleroderma an occupational disease? A series of historical and clinical vignettes, part III

Abstract

Paul Klee (1879–1940), one of the most influential artists of the 20th century, died at 60 years of age from complications of systemic sclerosis (scleroderma). The precipitating event(s) of Klee’s scleroderma, as in most cases, will never be known. Among various potential factors, exposure to heavy metals, crystalline silica, and organic solvents—acting alone or in combination—can now be considered potential factors in the onset of Klee’s disease. By altering and modulating epigenetic determinants in a genetically susceptible host, these and other environmental factors may have led to perturbations of self-tolerance and inflammation culminating in Klee’s scleroderma.

Paul Klee (1879–1940) was one of the most influential artists of the 20th century (Figure 1). Klee died at 60 years of age from complications of systemic sclerosis (SSc, scleroderma). In two earlier vignettes, I described what was perhaps the earliest manifestation of Klee’s scleroderma, that is, Raynaud phenomenon, ¹ and the musculoskeletal symptoms that followed. ² SSc is a rare autoimmune connective tissue disease that is far more frequent in women than men. The etiology is unknown but likely involves genetic susceptibility together with environmental factors.

Figure 1.

Klee’s studio in Munich, 1920. Photograph kindly provided by Zentrum Paul Klee.

A variety of different environmental triggers have been postulated to play a role in SSc, with silica and solvent exposures having the strongest epidemiologic support. ³ A recent report from Belgium of males with SSc found occupational exposure to silica or solvents to be highly prevalent: 73% had a history of occupational exposure to crystalline silica, solvents, or to both. ⁴ The occurrence of rheumatoid arthritis in several famous artists, for example, Rubens, Renoir, and Dufy, and of scleroderma in Klee, led some to speculate that exposure to heavy metals in paint pigments might in some way have triggered autoimmune rheumatic disease in these artists. ⁵ Given the relative rarity of scleroderma in males and the reported association with various environmental exposures, it is intriguing to consider the potential occupational exposures that may have played a role in Klee’s scleroderma.

In the course of their work, painters are exposed to a number of different agents that could potentially lead to disease, including exposure to heavy metals, silica, and solvents. Felix Klee, the artist’s son, speculated that exposure to toxic heavy metals in paint pigments played a role in the development of his father’s scleroderma. ⁶ In an analysis of various colors in randomly selected paintings, Pedersen and Permin concluded that the aforementioned artists with rheumatoid arthritis and Klee with scleroderma used significantly more bright and clear colors containing toxic heavy metals than did “control” contemporary painters without rheumatic disease. ⁵ Klee may have been exposed to mercury, cadmium, arsenic, lead, antimony, tin, cobalt, manganese, and chromium in the course of his art career. ⁵ There had been little scientific support for the hypothesis that heavy metal exposure may be associated with scleroderma until recently, when a case–control study of 100 scleroderma patients and 300 controls found significantly higher levels of antimony, cadmium, lead, mercury, molybdenum, palladium, and zinc in SSc hair samples. ⁷ Thus, the potential role for exposure to heavy metals cannot be discounted in Klee’s case, and should be included in the occupational history for all SSc patients. ⁸

Exposure to crystalline silica is perhaps the oldest known environmental risk factor for SSc. The earliest report of scleroderma and silica exposure appeared in 1914, when Bramwell described “diffuse” scleroderma in nine Scottish stone masons. ⁹ This was followed by Erasmus’ account of scleroderma and silicosis in gold miners on the Witwatersrand of South Africa. ¹⁰ Subsequent reports appeared from the United States and from the former German Democratic Republic of coal miners with scleroderma.^11,12 The association of scleroderma with silica exposure has now been confirmed worldwide and is recognized legally as an occupational disease in several countries. Klee’s range of artistic expression was enormous and included sculpture. Both systemic (SSc) and localized (morphea) scleroderma have been described in sculptors, including a case report of morphea in a sculptor and his wife. ¹³ Klee used stone in some of his art, but he did not sculpt stone (Eva Wiederkehr Sladeczek, Zentrum Paul Klee, Personal communication, 2020). Among his different teaching roles at the Bauhaus, Klee was director of free sculptural and artistic design from 1926–1927 to 1930. It is unknown if Klee had exposure to crystalline silica in concentrations high enough to be considered a factor in his disease.

In addition to heavy metals and crystalline silica, another factor in Klee’s scleroderma may have been exposure to organic solvents. A case–control study found a significant association of high cumulative occupational exposure to solvents among males with SSc (odds ratio (OR) = 2.9, 95% confidence interval [CI] = 1.1–7.6). ¹⁴ Such an association was not observed in women in this study, but another study found an association with exposure to paint thinners and removers in women with SSc. ¹⁵ A potential role for solvent exposure may have played out in two different contexts of Klee’s life— (1) during Klee’s military experience in World War I (WWI) and (2) during Klee’s lifelong career as an artist.

Klee was conscripted into the German army toward the end of WWI (Figure 2). Although Swiss-born, Klee’s father was German and the Swiss defined citizenship by patrilineal descent. In February 1916, Klee was graded as suitable for war service and the following month was conscripted as a Landsturmsoldat (soldier of the reserve forces in Prussia or Imperial Germany). Klee received his call-up orders on the same day he learned of the death of his friend and fellow artist, Franz Marc, who died in the Battle of Verdun. ¹⁶ Another friend and fellow Blaue Reiter artist, Auguste Macke, died in combat in September 1914. Following the deaths of Franz Marc, August Macke, and other Munich artists, the Bavarian king issued a decree that artists were to be spared combat duty, ¹⁶ thus Klee was spared from being sent to the front for combat.

Figure 2.

Klee was conscripted as a Landsturmsoldat (soldier of the reserve forces in Prussia or Imperial Germany) in March 1916. With permission, Zentrum Paul Klee, Bern.

Following basic training and time spent in the Second Reserve Infantry Regiment, Klee was transferred to the Airforce Replacement Unit in Oberschleissheim. He worked there from 9 November 1916 until 15 January 1917, executing skilled manual work restoring aircraft camouflage. The irony was not lost on Klee who wrote, “a factory worker; how adventurous!” ¹⁷ In his diaries, Klee speaks a lot about his military service, but more about his travels through Germany accompanying aircraft transports. He gives no detailed description of his work on airplanes (Eva Wiederkehr Sladeczek, Zentrum Paul Klee, Personal communication, 2020); however, it would seem likely that Klee was exposed to solvents in the course of his work in the airplane hangar at Oberschleissheim. In 1919, the year he was discharged from service in the army, one of Klee’s paintings clearly reflects his experience of working in the Airforce Replacement Unit in Oberschleissheim (Figure 3).

Figure 3.

Luftkampf (Air battle or aerial dogfight), 1919. With permission, Zentrum Paul Klee, Bern.

WWI was the first time airplanes were used in combat. Most were biplanes with wings covered in fabric. The most famous of all WWI German airplanes was the Fokker Doppeldecker, a single-seat fighter plane that first incorporated the synchronized machine gun and provided Germany with air superiority for a period of time during the war (Figure 4).

Figure 4.

A World War I Fokker DVII displayed at the Deutsches Museum Airfield Schleissheim—Oberschleissheim, where Klee was stationed and assigned to paint and repair aircraft.

During the early stages of the war, the Germans were looking for a way to effectively camouflage the aircraft of the Luftstreitkräfte to inhibit enemy observation of the aircraft while airborne and when on the ground. Large, irregular blotches with two or three colors were used on the upper surfaces of the wing made up of repeating patterns of irregularly shaped four-, five- or six-sided polygons, known as lozenge camouflage. ¹⁸ Because painting such a pattern was very time consuming and the paint added considerably to the weight of the aircraft, the patterns were printed on fabric and the fabric was then used to cover the aircraft (Figure 4). This printed fabric was used in various forms and colors from late 1916 until the end of the war. ¹⁸ Klee’s work to repair airplanes may have been accompanied by inhalational and dermal exposure to solvents in airplane “dope,” a plasticized lacquer applied to fabric-covered aircraft that tightens and stiffens fabric stretched over airframes rendering them airtight and weatherproof (Figure 5).

Figure 5.

For enforcement and weatherproofing, narrow strips of fabric were glued over the wing rips of the covered wing. Aviation Archive, Deutsches Museum, Munich.

A 1918 report issued by the Bureau of Labor Statistics, U.S. Department of Labor, described the various health hazards associated with the manufacture of airplanes, most notably the adverse health effects of applying dope, that is, “airplane doping.” ¹⁹ Cases of acute liver disease (“toxic jaundice”) and renal and neurological effects of airplane doping were first reported in the German medical literature. During the time that Klee was assigned to the Airforce Replacement Unit, airplane dope consisted of cellulose acetate dissolved in a mixture of solvents, that is, tetrachloroethane, acetone, alcohol, benzene, ketones, etc. ¹⁹ As previously noted, a number of these and similar organic solvents have been associated with an increased risk of systemic sclerosis.^14,15 There are also case reports of localized scleroderma associated with such solvents. ²⁰ We do not know if Klee encountered any of these solvents while stationed at Oberschleissheim; if so, any such exposure would have been limited in duration due to his brief stay of only 2.5 months before his transfer to another location where Klee worked as a clerk.

The risk of SSc with solvent exposure may relate not only to intensity of exposure, but also to cumulative exposure. ¹⁴ Klee likely had high cumulative exposure to white spirit, also known as mineral spirit, mineral turpentine, petroleum spirit or Stoddard solvent, used by artists to dilute paints and clean brushes (Figure 6).

Figure 6.

Close up of Figure 1 showing the artist’s table with a bottle likely containing white spirit.

White spirit would be used especially with oil painting. Klee turned to painting in oil in 1919 and continued in this medium, among others, up until the time of his death. All told, Klee produced 730 works in oil paint, 550 prior to 1935, when the first non-Raynaud symptoms of SSc developed (Eva Wiederkehr Sladeczek, Zentrum Paul Klee, Personal communication, 2020). During various periods of his life, Klee lived with his wife, Lily, and later their son, Felix, in small apartments where Lily would give music lessons in the living room and Klee would use the kitchen for his studio. Klee was known to be meticulous in his habits, ²¹ so it is likely that he kept his brushes and easels clean, all the while incurring exposure to white spirit over several decades. High cumulative exposure to white spirit, like other solvents, may confer an increased risk of developing SSc.^15,22

The precipitating event(s) of Klee’s scleroderma, as in most cases, will never be known. Among various potential factors, exposure to heavy metals, crystalline silica, and organic solvents—acting alone or in combination—can now be considered potential factors in the onset of Klee’s disease. By altering and modulating epigenetic determinants in a genetically susceptible host, these and other environmental factors may lead to perturbations of self-tolerance and inflammation culminating in the vasculopathy, autoimmunity, and fibrosis that characterizes SSc.