4 Case Reports in Medicine Table 1: Recommended exposure limits for respirable crystalline silica in occupational settings. Description Threshold Limit Value (TLV) Time Weighted Average (TWA) Recommended Exposure Limit (REL) Level 0.025 mg/m3 0.050 mg/m3 Agency American Conference of Governmental Industrial Hygienists (AGCIH) [11] National Institute for Occupational Safety and Health (NIOSH) [12] Another case report discusses a 48-year-old male with a history exposure to silica and lead while employed a minimum of four years as a glazed-tile painter at a ceramic tile factory. Characterization of silica is absent from the report. This particular case was complicated by extensive lead exposure and a history of acute lead poisoning [4]. One other case report implicated crystalline silica in the development of Goodpasture’s Syndrome in two mine workers with pneumoconiosis [5]. Levels of exposure are not described in either report, although job histories reveal chronic exposure over a number of years. While studies suggest a causal relationship between silica and autoimmune disease, the cellular mechanism is not known. One theory is that when respirable silica particles are encapsulated by macrophages, ﬁbrogenic proteins and growth factors are generated, and ultimately the immune system is activated [37–39]. Inhalation of large doses of silica has been reported to increase mobilization from the lungs into other organs including the kidney [40]. One can therefore hypothesize that once silica has mobilized into other organs, the immune system erroneously damages normal tissues these organs. Some reports propose that silica can induce multisystem disease through both activation of the immune system and a direct tissue toxic eﬀect [34]. Furthermore, recent literature surveys suggest that silica has an adjuvant eﬀect and nonspeciﬁcally enhances the immune response, therefore, precipitating a variety of systematic autoimmune diseases [15, 17]. A 2005 report by Brown et al. focuses on potential mechanisms by which silica can lead to the development and progression of autoimmune disease [13]. Similarly, the pathogenesis of glomerulonephritis and other renal eﬀects in silica-exposed workers is not estab- lished. While some case reports provide evidence of an immunologic injury by immune complex formation, others point to a direct toxic eﬀect of silica [23, 41–43]. It has also been postulated that since lung damage is found in several kidney diseases, such as Goodpasture’s syndrome and Wegener’s granulomatosis, then pulmonary insults may have a role in the development of some chronic renal diseases [44]. We speculate that the highly alkaline nature of the product resulted in an irritating and corrosive eﬀect on the mucous membranes of the upper respiratory tract when inhaled. As a consequence of a mucous membrane injury, our case would have likely ampliﬁed vulnerability to the silica, increasing its absorption into the lung or submucousal tissue. Given the well-established health risks of silica dust and the temporality of disease progression, we conclude that our case of Goodpasture’s Syndrome was caused by intense exposure to alkaline silica dust. This patient was in good health prior to his acute exposure and had no prior history of pulmonary, renal, or autoimmune disease. It is likely that the high dose of respirable silica dust caused his acute respiratory failure and initiated the progression of autoimmune disease, which ultimately led to renal failure. Following his recovery from the event, he never had any recurrence of the illness, suggesting that the inciting event was resolved. Multiple subsequent blood tests for anti- glomerular basement membrane antibody came up negative. Previous studies have focused on chronic rather than acute occupational exposure to silica; however, evidence suggests that the intensity of exposure rather than duration seems to be important in selectively causing autoimmune disorders [45]. Characterization of exposures during his career is poor, however, this patient reports sanding and sweeping the ﬂooring compound on many occasions during a seven-year period leading up to his ﬁnal job. Whether adequate exposure controls were in place during prior jobs is unknown. We do know, however, that safety equipment, such as respirators, were not used, and we can expect that chronic exposure to respirable silica took place. However, our case’s experience may be somewhat unique, as we believe this to be the ﬁrst reported case in which there was an acute, high-intensity exposure immediately preceding the onset of development of Goodpasture’s Syndrome. Construction workers face an increased risk of silica- related disease due to their exposure while using, mixing, cutting, grinding, and sanding concrete and/or silica-based compounds. Over the past decades, techniques like dust sup- pression and increased use of respirators have lessened health risks to construction workers somewhat; yet, as our case demonstrates, silica exposure remains a pervasive hazard and important cause of disease in exposed persons. This report adds to the body of evidence supporting silica exposure as a causal factor in cases of Goodpasture’s Syndrome. Competing Interests Original funding of this clinical assessment was provided by a law ﬁrm representing the patient. The law ﬁrm was not involved with data analysis, data interpretation, or writing of the report. The corresponding author had full access to all the data in study and had ﬁnal responsibility for the decision to submit the manuscript for publication. Author’s Contributions J. Dahlgren interviewed the patient, with the assistance of T. Peckham. J. Dahlgren, T. Peckham, and M. Wardenburg