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Simple silicosis is characterized radiographically by numerous small( ≤10 mm), predominantly rounded nodular opacities with a centrilobular and peripheral( perilymphatic) distribution, demonstrating a predilection for the posterior upper lung zones, likely attributable to reduced clearance efficiency in these regions. 2, 91 In some patients, small nodules enlarge and merge into mass-like fibrotic opacities predominantly in the upper lung zones(> 10 mm), a pattern known as PMF or complicated silicosis. 2 AS fabricators show substantially higher rates of PMF than other silica-exposed groups, with 30 – 40 % affected. 4, 8, 46, 92, 93 PMF is associated with mixed ventilatory defects, reduced total lung capacity( TLC) and DLCO, 72, and carries a poor prognosis with high risk of rapid progression to cardiopulmonary failure without transplantation.
18, 46, 94
Acute silicosis, also called silicoproteinosis, arises after higher intensity exposures over weeks to a few years, producing alveolar filling with proteinaceous material and rapid respiratory decline. It is a form of secondary pulmonary alveolar proteinosis, though histopathology will demonstrate birefringent particles under polarized light. 2, 95 Reflective of the high silica exposures that can occur with AS fabrication, multiple case series of AS silicosis have demonstrated the pathologic findings of silicoproteinosis on 7-9 % of lung biopsies or explants. 4, 96
Accelerated silicosis is a loosely defined term used to describe silicosis that develops within months to 10 years of intense exposure. However, pathologically and radiographically, it demonstrates overlapping features of simple, complicated, and acute silicosis, including silicotic nodules, interstitial fibrosis, and groundglass opacities. 74 Multiple studies globally have documented that patients with simple AS silicosis may progress rapidly to PMF even following cessation of silica exposure, conferring high morbidity and mortality. 4, 74 This combination of rapid onset, severe lung pathology, and poor outcomes reflects the high silica content, small particle size, concomitant exposure to toxic VOCs and metals, and short but intense exposure durations typical of AS fabrication, making AS silicosis especially aggressive and clinically challenging.
Diseases Associated with Respirable Crystalline Silica Exposure
RCS exposure confers risk for a broad spectrum of diseases beyond silicosis, 2 including dust-related diffuse fibrosis, chronic obstructive pulmonary disease, lung cancer, sarcoidosis, mycobacterial infections, autoimmune diseases, and chronic kidney disease. These associations and their manifestations in AS workers are summarized in Table 3. Of note, sarcoidosis is considered an idiopathic multisystem inflammatory disease; however, up to 30 % of cases diagnosed as sarcoidosis may be exposure-related. 95 Histopathologic findings of granulomas in patients with significant RCS exposure should prompt a diagnosis of silicosis rather than sarcoidosis. Silicosarcoidosis is another term proposed to describe granulomatous lung disease in patients with occupational exposure to silica dust. 97 In addition, asthma should be considered in AS-exposed workers, as volatile organic compounds released during fabrication( e. g., styrene, methyl methacrylate, phthalic anhydride) act as respiratory irritants. 48, 50 In Australia, 20 % of AS workers reported asthma symptoms 98; 11 % of exposed workers without radiographic silicosis still had obstructive / mixed PFT patterns. 8
Progressive Disease
Observations from other industries suggest that silicosis frequently progresses even after exposure to RCS ceases, with studies showing progression in one-third to two-thirds of cases and up to 100 % in some cohorts. 43, 99 – 102 Risk factors for progression include younger age at diagnosis, more advanced radiological severity, rapid initial worsening, and high cumulative or continued exposure. 99 100 Additionally, ongoing exposure is linked to a heightened risk of PMF among South African and Brazilian gold miners. 101, 103 Workers exposed to artificial stone appear to experience particularly rapid disease progression, with more than half demonstrating radiologic progression within four years of exposure cessation and over one-third developing PMF in one study. 77 In contrast, the prevalence of PMF among long-tenured U. S. coal miners has ranged between 1 %- 5 %. 104 This underscores the critical importance of early recognition and complete removal from
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