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Assessment of pulmonary toxicity of inhaled polycarbonate 3D printer emissions in rats.
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Rats exposed to polycarbonate 3D printer emissions at 2.5 mg/m3 for up to 30 days showed no significant pulmonary inflammation or toxicity, with only mildly elevated protein and TIMP-1 levels in the 30-day group. Estimated alveolar deposition was 0.28 micrograms per day with limited evidence of macrophage uptake of deposited particles.
This study investigated the potential pulmonary toxicity of polycarbonate (PC) emissions from fused filament fabrication (FFF) three-dimensional printing (3DP) via inhalation in Sprague Dawley rats. Previously, our results demonstrated no significant pulmonary effects following exposure to a 0.5 mg/m PC. A new exposure apparatus was developed that exposed animals at a concentration of 2.5 mg/m. Sixty rats were randomized into control (filtered air) and exposure groups ( = 30/group). Each group was further divided into five subgroups ( = 6/subgroup) with exposure durations of 1, 4, 8, 15, or 30 days (4 hr/day, 4 days/week). Following a 24-hr post-exposure period, body weight was measured, and blood samples were collected for hematological and biochemical analysis. Bronchoalveolar lavage fluid (BALF) was obtained from the right lung for cytology. The left lung and head/nasal tissues were preserved for histopathological evaluation. Lung deposition was estimated using the Multiple-Path Particle Dosimetry model, electron microscopy, and enhanced darkfield microscopy. In addition, filter samples were collected to measure bisphenol A. Exposure resulted in an estimated deposition of 0.28 µg/day within the alveoli and small airways. Microscopy indicated limited evidence of macrophage uptake. No significant changes were observed in BALF cell counts, lactate dehydrogenase activity, or hematological parameters. BALF levels of tissue inhibitor of metalloproteinases-1 and protein were elevated in the 30-day exposure group, although histopathology revealed no exposure-related changes in the lungs. In conclusion, this study found no marked pulmonary inflammation or toxicity in rats exposed to 2.5 mg/m of PC 3D printing emissions for up to 30 days (4 hr/day).
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Scientists found that when rats breathed in fumes from 3D printers using polycarbonate plastic, their livers developed damage strikingly similar to the effects of bisphenol A (BPA), a chemical linked to hormone disruption and liver problems. This suggests that people who regularly use these 3D printers, especially in poorly ventilated spaces, may be inhaling BPA-related compounds that could harm liver health over time, highlighting a need for better ventilation and safety practices around 3D printing.
Inhaled polycarbonate feedstock 3-D printer emissions initiate a bisphenol A-like phenotype in rat liver
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Rats that breathed in fumes from 3D printers using polycarbonate plastic developed liver damage that looked strikingly similar to injuries caused by BPA, a chemical linked to hormone disruption and other health problems. The effects showed up quickly (within a day) and worsened over a month of exposure, suggesting that these printers may release BPA-like substances into the air that could pose real risks to people who use them regularly, especially in poorly ventilated spaces like homes or classrooms.
Inhaled polycarbonate feedstock 3-D printer emissions initiate a bisphenol A-like phenotype in rat liver
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When rats breathed in fumes from 3D printers using polycarbonate plastic, their livers developed damage, including inflammation and altered fat metabolism, that closely resembled the harmful effects seen with bisphenol A (BPA), a chemical linked to hormone disruption. This suggests that 3D printer emissions may release BPA-like compounds that can harm your liver if inhaled, which is worth knowing if you use or work near these printers regularly, especially without proper ventilation.
Tracing 3D printing emissions: Micro- and nanoplastic formation and the trade-off of mass-based mitigation.
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Testing five 3D printer filaments found that ASA and ABS types released micro- and nanoplastic particles, made of polyethylene and PVC rather than the original plastic. Standard printer enclosures blocked most particle mass but let smaller particles escape, which modeling estimated could increase lung deposition of inhaled particles, especially in children.
Inhalation of polycarbonate emissions generated during 3D printing processes affects neuroendocrine function in male rats
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Researchers exposed male rats to emissions from polycarbonate 3D printing for up to 30 days and found significant neuroendocrine disruption, including reduced thyroid-stimulating hormone, FSH, and prolactin, along with olfactory bulb cell injury and decreased sperm precursor cells — effects similar to known bisphenol A exposure.
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