J Occup Health 2005; 47: 346–349 Case Study Silicosis Caused by Sandblasting of Jeans in Turkey: A Report of Two Concomitant Cases Metin AKGUN 1 , Metin GORGUNER 1 , Mehmet MERAL 1 , Atila TURKYILMAZ 2 , Fazli ERDOGAN 3 , Leyla SAGLAM 1 and Arzu MIRICI 1 1 Chest Disease, 2 Chest Surgery and 3 Pathology Departments, School of Medicine, Atatürk University, Turkey Key words: Sandblasting, Jeans, Silicosis, Occupation Silicosis is a fibrotic disease of the lungs caused by inhalation, retention, and pulmonary reaction to crystalline silica. Crystalline silica exposure is widespread, and silica sand is an inexpensive and versatile component of many manufacturing processes 1) . Its use and the incidence of silicosis are increased in industrial operations by the mechanization and the use of sandblasting, drilling, pulverizing, cutting, grinding tools and other pneumatic equipment 2) . Sandblasting involves forcefully projecting a stream of abrasive particles onto a surface, usually with compressed air or steam. Mostly, silica sand is forced by compressed air onto the target surface. It has been commonly used in abrading metal or glass 3) . Recently, it has been widely and increasingly used in sandblasting of jeans in Turkey. In this report, we present two concomitant cases of silicosis occurring in the same workplace, located in Istanbul, and caused by sandblasting of jeans. To our knowledge, there is no previous description of silicosis in such an occupation. Case Reports Case 1 A 19-yr-old man was admitted to our hospital in August 2004 with a history of 3 months of malaise, dry cough, sweating and loss of weight. A month prior to the admission he had been admitted to the local government hospital with these complaints, and tuberculosis (TB) treatment had been given without any bacteriologic proof. On admission he was continuing to take anti-tuberculous medication. He also reported he did not have any benefit from the medication and had had dyspnea for a week. He had no smoking history. He initially stated he had worked in a textile factory between March 2000 and November 2003. When he was asked to detail his work, he explained that he had worked in a small-scale workplace producing sandblasted jeans. Physical examination showed a non-productive cough, fever (38°C), dyspnea, tachypnea, and bibasilar coarse crackles. His initial investigation revealed WBC of 11,300 × 10 6 cells per liter, an erythrocyte sedimentation rate (ESR) of 55 mm/h, an albumin level of 2.7 mg/dl (normal range: 3.5–5.5) a CRP level of 21.8 mg/dl (upper limit: 0.5), and a LDH level of 2,103 U/ml (normal range: 250–500). On hospital admission arterial blood gas values were pH=7.53, arterial oxygen tension (PaO 2 ) 49 mmHg (FIO 2 =0.21), arterial carbon dioxide tension (PaCO 2 ) 21.8 mmHg and percent of arterial oxygen saturation (SaO 2 ) 70.6%. Pulmonary function testing (PFT) was not performed because of TB or other infection suspicion. Sputum smears for TB and blood cultures were negative. Other laboratory tests were unremarkable. Chest radiography showed bilateral reticulonodular infiltrates (Fig. 1a). High resolution computer tomography (HRCT) revealed diffuse intralobular micronodules, which were prominent in the mid-to-lower lung zones (Fig. 2a, 2b and 2c). The patient underwent bronchoscopy with BAL and TBB, but no clue was identified. Anti-tuberculous treatment was stopped due to negative confirmation of the diagnosis and no substantial improvement of his symptoms, and antibiotic treatment with levofloxacin 500 mg once daily was initiated empirically due to clinical findings of infection. Although the findings of infection after the treatment were partially improved, the respiratory symptoms continued to worsen. An open lung biopsy specimen lead us to the diagnosis of silicosis (Fig. 3a). Case 2 An 18-yr-old non-smoking man was admitted to our hospital in September 2004 with a history of dyspnea for 4 yr. His symptoms had started a short time after beginning work in the same workplace as Case 1. He had worked in that place between March 2000 and December 2003 years. Later, non-productive coughing, malaise, and weight loss had developed. He was seen by a physician on two occasions, May 2004 and August 2004, and bronchodilator drugs were prescribed. However, the diagnosis was not proven nor was there any benefit from the medications. Physical examination showed a non- productive cough, dyspnea, and fine crackles at the end of inspiration. Chest radiography showed diffuse interstitial infiltrates (Fig. 1b). HRCT revealed diffuse intralobular micronodules in the upper zones and fibrotic changes, which were prominent in the mid-to-lower zones of the lung, with bilateral minimal pneumothorax (Fig. 2d, 2e and 2f). The laboratory tests revealed an ESR of 20 mm/h and increased LDH levels of 1,426 U/ml . Sputum smears for tuberculosis were negative. Other laboratory tests were unremarkable. On hospital Received Nov 15, 2004; Accepted May 2, 2005 Correspondence to: M. Akgun, Chest Disease, School of Medicine, Atatürk University, Aziziye Arastirma Hastanesi, Gogus Hastaliklari, 25240, Erzurum, Turkey (e-mail: makgun@atauni.edu.tr, akgunm@gmail.com)