Turk Toraks Derg 2014; 15: 1-8 REVIEW Expanding the Spectrum of Particle-and Fiber-Associated Interstitial Lung Diseases While interstitial lung disease (ILD) is common, less than fve percent of diagnoses appear to be related to occupational and environmental exposures to particles and fbers; these injuries are most frequently recognized as pneumoconioses and hypersensitivity pneumonitides. As a result of this small contribution to recognized ILD, the association of particles and fbers with this group of diseases is frequently deemed of little consequence. However, it has been proposed that some portion of ILD without a recognized cause (i.e. idiopathic disease) can also be related to exposures to particles and fbers. Many of these diagnoses are determined without beneft of microscopic examination of lung tissue. Even when tissue is available, the conventional examination for the presence of particles and fbers is used. This approach employ- ing optical microscopy is insensitive and leads to misdiagnosis. A review of previous investigation demonstrates associations of idiopathic pulmonary fbrosis, desquamative interstitial pneumonia, pulmonary alveolar proteinosis, sarcoidosis, and eosinophilic granuloma with particle and fber exposures. It is recommended that scanning electron microscopy in combination with the use of electron dispersive X-ray analysis be employed whenever the question of a possible relationship between ILD and particle and fber exposure arises. Key words: Pulmonary fbrosis, pulmonary alveolar proteinosis, sarcoidosis, eosinophilic granuloma INTrodUCTIoN Interstitial lung diseases (ILDs), a group also described as diffuse parenchymal lung diseases (DPLDs), includes over 200 distinct diseases in which the interstitium is altered by inflammation and/or fibrosis [1]. The interstitium of the lung is comprised of the alveolar wall (and the lumen), vasculature, interstitial macrophages, fibroblasts, myofibroblasts, and matrix components; the inflammatory and fibrotic disorders encompassed by ILD may affect any of these components. The resulting infiltration by cellular and extracellular elements either causes distortion and destruction of the alveolar and bronchiolar architecture or has little associated damage. Interstitial lung disease is a diverse group of both acute and chronic disorders. Common clinical, radiographic, and pathophysiologic features form the basis for collectively referring to this massive group of injuries as a single entity. Frequently, the patient with ILD presents with the symptoms of dyspnea and nonproductive cough and crackles particu- larly “Velcro rales” on physical examination. A chest radiograph shows reticular, nodular or mixed pattern markings and lung function tests demonstrate some loss including decreased volumes and reduced diffusing capacity. Interstitial lung disease is common and the diagnosis is established in about 70 out of every 100.000 individuals in the United States [2]. About 10.000 Americans die every year from ILD [2]. This group of lung disorders includes disease with both known and unknown causes. Less than five percent of ILD appears to be related to occupational and environ- mental exposures to particles and fibers [3]. These injuries are most frequently recognized as pneumoconioses and hypersensitivity pneumonitides and are almost always related to occupational exposures to particles and fibers. A diag- nosis of work-related ILD is most frequently established on the basis of an occupational history, revealing a pertinent exposure, and an abnormal chest x-ray. As a result of the small contribution to recognized lung injury, the association of particles and fibers with ILD is fre- quently deemed of little consequence. In the clinical setting or in the conduct of observational studies, a number of factors may limit recognition of an association between a patient with idiopathic pulmonary fibrosis (IPF) and his or her environmental and occupational exposures. These factors may include diagnostic misclassification, infrequent occur - rence of IPF, exposure misclassification, and variation in susceptibility to exposures. However, it has been speculated that some portion of that ILD without a recognized cause (i.e. idiopathic disease, which includes the majority of diagnoses DOI: 10.5152/ttd.2014.3950 Andrew Ghio 1 , Rahul Sangani 1 , Victor Roggli 2 1 United States Environmental Protection Agency, NHEERL, Human Studies Facility, Chapel Hill/North Carolina, USA 2 Duke University, Duke University Medical Center, Department of Pathology, Durham/North Carolina, USA Address for Correspondence: Andrew Ghio, United States Environmental Protection Agency, NHEERL, Human Studies Facility, Chapel Hill/North Carolina, USA Phone: +1 919 9660670 E-mail: ghio.andy@epa.gov ©Copyright 2014 by Turkish Thoracic Society - Available online at www.toraks.dergisi.org Abstract Received: 05.09.2013 Accepted: 17.10.2013