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Acute Pulmonary Response and Lung Burden Following Solid Surface Composite Dust Inhalation

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  • Description:
    Pulmonary exposure to emissions from manipulating solid surface composite (SSC) materials with power tools has been associated with adverse health effects in humans and laboratory animals. Previous in vitro and in vivo investigations of SSC toxicity have been limited by particle delivery methods that do not fully recapitulate the workplace environment. To represent a real-world particle exposure more accurately, our group constructed a chamber for simultaneous particle generation, characterization, and animal exposure. In order to determine lung deposition and clearance, 6-week-old male C57BL/6 mice were exposed to SSC particles for 4 hours (n = 9) or filtered air control in the exposure chamber. The mice were sacrificed immediately after the exposure as well as 24 hours post-exposure and divided into two subsets. In one subset, (n = 6), whole lungs were collected and analyzed for aluminum content using inductively coupled plasma atomic emission spectroscopy. In the other subset, (n = 3), in the right lobe was neutral buffered formalin for histopathology, while the left lobe was or snap frozen and kept at -80 deg C for later molecular analyses. The exposure apparatus was successfully able to generate and aerosolize particles and maintain them at the target concentration of 20 +/- 1.7 mg/m3) for the full exposure period. The aerosol count median aerodynamic diameter was 820 nm, while the geometric standard deviation was 2.884. Inductively coupled plasma-atomic emission spectroscopy analyses determined the lung deposition of 19.13+/-5.03 µg/g elemental aluminum, or approximately 60 µg/g SSC dust, based on the relative proportion of Al in SSC bulk material. No significant clearance after 24 hours was observed. No acute pulmonary inflammation or toxicity was observed in any histology section. Lung 4-hydroxynonenal was elevated at the 0-hour timepoint, while superoxide dismutase was depressed at the 24-hour timepoint, compared to control, suggesting an oxidative stress response. Lung tissue IL-6 was significantly increased at 0 hours compared to control and returned to baseline at 24 hours. IL1-β, IL-2, IL-5, TNFa, and IFNy were all decreased at 0 hour post-exposure and all except for TNFa remained decreased at the 24-hour time point. In conclusion, our system was able to reliably generate a consistent and reproducible real time SSC aerosol with a portion of that aerosol inhaled by the mice. A single 4-hour exposure to 20 mg/m3 SSC dust elicited changes in inflammatory markers in lung tissue, likely driven by an increase in oxidative stress. [Description provided by NIOSH]
  • Subjects:
  • Keywords:
  • ISSN:
    1096-6080
  • Document Type:
  • Genre:
  • Place as Subject:
  • CIO:
  • Division:
  • Topic:
  • Location:
  • Pages in Document:
    3 pdf pages
  • Volume:
    192
  • NIOSHTIC Number:
    nn:20067230
  • Citation:
    Toxicologist 2023 Mar; 192(S1):469-470
  • Federal Fiscal Year:
    2023
  • NORA Priority Area:
  • Peer Reviewed:
    False
  • Source Full Name:
    The Toxicologist. Society of Toxicology 62nd Annual Meeting & ToxExpo, March 19-23, 2023, Nashville, Tennessee
  • Collection(s):
  • Main Document Checksum:
    urn:sha-512:5dd441080d664cc262677262986a8771ba7fb6f652d55b6d8d15c02d43a681d0880551d471215c9f92d3a0da5f6fbc875e1e7014648e9a919a41938daaaeebd7
  • Download URL:
  • File Type:
    Filetype[PDF - 1.13 MB ]
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