Inhaled polycarbonate feedstock 3-D printer emissions initiate a bisphenol A-like phenotype in rat liver.

Concerns with 3D filament fused fabrication (FFF) printer emissions have increased due to release of nanoplastic particles, plasticizers, and volatile mixtures. At present, few data exist examining polycarbonate emissions from 3D FFF printers and potential adverse health effects on liver following inhalation exposure. This study aimed to investigate hepatic toxicity following inhalation exposure to 3D FFF polycarbonate (PC) emissions in rats. It was postulated that increasing levels of inhaled 3D printer PC emissions initiate adverse liver histopathologic alterations associated with oxidative stress, inflammation, lipid and sterol metabolism markers. Sprague-Dawley rats were whole-body exposed to 3D FFF PC emissions (2.42 mg particulate/m3) for 4 hr/day, 4 days/week for 1, 4, 8, 15, or 30 days. Liver tissue was assessed for changes in inflammation, oxidative stress, fatty acid, lipid, sterol metabolism, and adverse liver pathology. One day exposure resulted in altered inflammation, glucose, fatty acid, and sterol metabolism gene biomarkers in 3D FFF PC-exposed animals compared to HEPA filter controls. Following 8-day treatment, 3D FFF PC animals exhibited decreased glutathione S-transferase activity. After 30 days exposure, liver pathology characterized by dilated sinusoids, clear hepatocyte cytoplasm, and focal leukocyte infiltrate were detected in 3D FFF PC-exposed animals which were markedly similar to bisphenol A-induced liver alterations. Data suggest that bisphenol A levels in 3D FFF PC emissions may partially be responsible for observed adverse liver phenotype. This study informs future hazard characterization for 3D FFF PC- induced liver toxicity and implementing intervention practices for thermoplastic emissions in additive manufacturing applications.