Case Reports in Medicine patient brieﬂy worked as a driver for a feed store, at a printing company, and at a glass company. He also worked for a pest control company for seven years, where he reports wearing protective equipment, including gloves and respirator during job duties. Information reported by this case indicates an intense acute exposure to respirable silica prior to the onset of disease. There was not an industrial hygienist present to measure air levels during sanding and sweeping work at his ﬁnal job, however, the patient reports that there were consistently large dust clouds present on each of the three work days and that the quantity of the ﬂoor patching product was tremendously greater than he had ever used in any job prior. The exact amount of the patching compound used at this site is unknown; however, purchasing record invoices for the job totaled over 10,000 pounds. It is likely that the case applied, sanded, and swept most, if not all, of the product during his three days at the job. He used a small fan to dry each application, but no dust controls, engineering controls, or other ventilation controls were used. Given a crystalline silica content of 1% to 5%, these factors indicate a maximum potential for inhalation of a high quantity of silica-containing dust prior to the onset of symptoms, presumably far exceeding recommended occupational limits (Table 1). Crystalline silica is recognized as both a pneumotoxin and nephrotoxin, and has been reported to cause multiple autoimmune diseases [1]. As such, our case revealed severe target organ toxicity to the lungs, kidneys, and other target organ systems consistent with those reported in the literature. A multitude of epidemiological studies connect silica exposure to various known autoimmune diseases [13–20]. Frequently reported diseases include scleroderma, systemic lupus erythematosus, rheumatoid arthritis, autoimmune hemolytic anemia, and sarcoidosis [1]. Several studies of silica-exposed workers have shown increased rates of several common autoimmune diseases, indicating that studies that examine rates of only one disease may underestimate the risks posed by silica exposure [21, 22]. Consistent with its correlation to autoimmune eﬀects, epidemiological data has implicated silica as a cause of renal disease [18, 23, 24]. A cohort study of 4,626 silica-exposed workers showed comparatively high rates of mortality from acute renal disease, chronic renal disease, and arthritis. There was an excess in incidence of end-stage renal disease, which was highest for glomerulonephritis. They found increasing end-stage renal disease incidence with increasing cumulative exposure [25]. Another study examined rates of renal disease in a remote mining area in the United Kingdom, in comparison to the nonmining areas of a clinical practice. Statistical analysis conﬁrmed a signiﬁcant excess of renal dis- ease, especially glomerulonephritis, in the mining area. The authors propose that this excess is due to high silica exposure inherent to ﬂuorspar mining. Of the six workers with long- term silica exposure, ﬁve had glomerulonephritis proven by biopsy and the other had signs and symptoms compatible with chronic glomerulonephritis [26]. These ﬁndings are consistent with other studies that show an increased risk 3 between silica exposure and glomerulonephritis [14, 27, 28]. Case reports also describe the acute onset of pulmonary, renal, and autoimmune disease following silica exposure, detailing clinical manifestations similar to our case pre- sentation [29–33]. One case series presents four patients who all developed rapidly progressive renal failure following high-intensity silica dust exposure. Histological ﬁndings in each case showed glomerular hypercellularity and sclerosis, crescents, interstitial cellular inﬁltrates, and tubular necrosis. Circulating immune complexes were present in three of the patients, and electron microscopy showed electron- dense glomerular basement membrane deposits in all of the patients. Additionally, all four cases presented with respiratory disease [34]. Simultaneous presence of lung and kidney failure fol- lowing exposure to silica is not conﬁned to Goodpasture’s Syndrome. In a case-control study, the occupational histories of 16 cases with a clear diagnosis of Wegener’s granulomato- sis with renal involvement were compared with those of 32 matched controls. Wegener’s granulomatosis is a systemic vasculitis with autoimmune and renal manifestations similar to Goodpasture’s. Five cases reported exposure to silica dust resulting in an odds ratio of 5.0 (95% CI 1.4–11.6) for this autoimmune disease compared the nonexposed controls, and seven cases reporting exposure to any silicon-containing compounds yielded an odds ratio of 6.5 (95% CI 1.3– 13.5). Reported exposure to lead, cadmium, chromium, welding fumes, and hydrocarbon was not associated with a signiﬁcantly increased risk of Wegener’s granulomatosis [35]. Available to us in the literature are three case reports (four cases) linking chronic exposure to silica directly to the development of Goodpasture’s syndrome. Stratta et al., in a 2001 publication, proposed several reasons why there are few studies and examples of crystalline silica- related Goodpasture’s Syndrome present in the literature. Reasons stated include limited records on patients with acute symptoms leading to death, lack of renal clinical data from the exposed workers, lack of correct diagnosis from the hospitals and medical institutions carrying out the dialysis, and relatively low occurrence to cross-reference to occupational factors [36]. One report describes a 46-year-old foundry worker with a history of intense exposure to respirable crystalline silica that was admitted to the hospital with dyspnea, hematuria, proteinuria, severe restrictive pulmonary function disorder, and rapidly declining renal function. Immunological tests and biopsy were positive for anti-GBM antibody and pauci-immune crescentic glomerulonephritis, and he was diagnosed with Goodpasture’s syndrome and treated by hemodialysis and plasmapheresis. A workplace survey found that the exposure level of respirable crystalline silica exceeded the exposure limit, a TLV-TWA of 0.0106 mg/m3 which was calibrated for overtime. The authors conclude that based on his clinical presentation and industrial hygiene examination, his Goodpasture’s syndrome was caused by long-term silica exposure [3].