2 questioned, he stated he began to feel ill about one week earlier, after inhaling a large amount of dust during his work as a tilesetter. He reported that he had spent a three-day period (8–10 days prior to presentation) sanding and dry- sweeping a ﬂoor patching compound used to ﬁll cracks in the cement ﬂoor. He had used this same material on many smaller jobs, but this job utilized a much larger amount of the patching material than he had used previously. He was exposed to clouds of visible dust during the mixing, sanding, and sweeping of the material. The compound contained 1% to 5% crystalline quartz silica. It was also noted that the product was highly alkaline (pH = 12). He experienced mucosal irritation while working, and had to go outside 3-4 additional times each workday to spit out dust and to “catch his breath.” He felt ill each night after work. After the third day of exposure he felt so poorly that he did not return to work. Over the following weekend, his symptoms progressed to chills and fever and he thought he had the ﬂu. He went to walk-in clinic and was given antibiotics and an inhaler. His pulmonary problems worsened that evening, prompting him to present to the emergency room from where he was admitted to the hospital. The patient reported a history of childhood asthma and a remote, one pack-year history of cigarette use. Physical exam at presentation was remarkable for diﬀuse crackles bilaterally and expiratory wheezes in all lung ﬁelds. After two treatments with nebulized albuterol and Atrovent the patient’s blood gas showed a pH of 7.45, PCO2 of 36, and PO2 of 56 on room air. Chemistry panel, CPK, and troponin levels were normal. White cell count was 17.7 thou/cu mm, hemoglobin 15 g/dL, and hematocrit 42%. A chest X-ray revealed abnormalities in the lung suggestive of a diﬀuse interstitial pattern. Serial AFB tests and sputum cultures were negative for mycobacterium, pneumocystis, and streptococcus pneumoniae. Two days after admission the patient became increasingly hypoxic and was intubated and put on a pressure ventilator. Fiberoptic bronchoscopy revealed bloody secretions, and BAL ﬂuid showed no particulate matter or evidence of bacterial infection. Transesophageal echocardiogram showed normal LV function, EF 65%, no signiﬁcant valvular abnormalities, and a trivial pericardial eﬀusion. He did not respond to oral antibiotics and made no progress in weaning oﬀ ventilation, but rather progressed to severe respiratory acidosis, with an arterial pH < 7.13 and pCO2 > 100 mmHg one week after presentation. He subsequently became unresponsive and developed oliguria and azotemia. Urinalysis one week after presentation showed hematuria and mild proteinuria consistent with glomerulonephritic disease, as well as muddy brown casts characteristic of acute tubular necrosis. At this time the patient tested positive for the anti-GBM (glomerular basement membrane) antibody and he was diagnosed with Goodpasture’s syndrome. This was conﬁrmed by renal biopsy, which demonstrated global glomerulosclerosis, focal hematuria, and linear immunoﬂu- orescence reactions (IgG, IgM, C3) on glomerular basement membranes. An open-lung biopsy revealed multifocal inter- stitial ﬁbrosis, diﬀuse interstitial PMNs (polymorphonuclear neutrophils), intravascular thrombi, and evidence of intra- Case Reports in Medicine alveolar damage; a constellation of symptoms consistent with Goodpasture’s syndrome. No polarizing particles were seen, but immunoﬂuorescence studies revealed linear alveolar septal IgG- and C3-immunoreactivity. Lung biopsy stains also conclusively ruled out fungi, bacteria, pneumocystis, and viral etiologies. The patient was then treated with continuous hemoﬁl- tration and dialysis, two weeks of plasmapheresis, and immunosuppressive drugs including Cytoxan and pred- nisone. Over the course of a three-month hospitalization the patient suﬀered complications including sepsis and cerebral hemorrhage, but renal function began to improve and he was gradually weaned oﬀ ventilation. Tests performed during the fourth week of his hospitalization were negative for anti- GBM antibody. At discharge, the patient was ambulatory and able to breathe on his own, but demonstrated permanent cognitive and motor impairment. Chest radiograph at this time revealed persistent bibasilar atelectasis and interstitial pulmonary edema. Subsequent outpatient pulmonary func- tion testing demonstrated FEV-1 and FEV-1 : FVC values signiﬁcantly below predicted, consistent with the patient’s reported symptoms and an obstructive picture. Quarterly follow-up has shown no recurrence of Goodpasture’s syn- drome, and the patient ceased immunosuppressive drugs several months after his initial hospitalization. However, the patient has required episodic treatment for recurrent dyspnea and hemoptysis in the three years following his initial disease onset and treatment due to lasting obstructive pulmonary damage. 3. Discussion Goodpasture’s Syndrome was ﬁrst described by Ernest Goodpasture in 1919 and later named after him in 1958 [2]. This disease is characterized by pulmonary hemorrhage and glomerulonephritis and is mediated by autoantibodies directed against the basement membrane in the renal glomerulus and the pulmonary alveolus. The etiology of Goodpasture’s Syndrome is still unknown; however, devel- opment of the disease following crystalline silica exposure has been reported in at least three case reports [3–5]. Other exposures have also been implicated as causal factors, including hydrocarbons [6, 7], cocaine use [8], hard metal dust [9], and D-penicillamine [10]. The circumstances of our case, a tilesetter with a minor history of tobacco use, suggest inhalation of silica as the salient factor, although some exposure to hydrocarbons is not uncommon amongst workers in construction related jobs. This patient started his 9-year career in ﬂooring work as a helper and was later promoted to ﬂoor mechanic. His job duties included mixing and applying compound, leveling and sanding the ﬂoor, sweeping up excess dust and debris, and physically laying tile or carpeting. No safety equipment was ever used, including respirators or gloves. He reports using the compound regularly in the seven years leading up to his hospitalization. Details of other chemical exposures during his career as a tilesetter are unknown. Prior to working in the ﬂooring industry, the