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Subchronic Effects of Different Nickel-Based Thermal Spray Coating Aerosols on Lung Toxicity Using an Animal Inhalation Model

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English


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  • Description:
    Background and Purpose: Thermal spray coating is an emerging industrial process that applies molten metal under pressure onto a surface as a protective coating. The aerosols that are formed during this process may contain metals, such as nickel (Ni), chromium (Cr), manganese (Mn), and iron (Fe). Exposure to these potentially toxic metals may pose an adverse health risk to the manual operator, who often performs the process without proper respiratory protection, as well as to other workers in the vicinity of the operation who commonly are not using any respiratory protection at all. Information about the possible health effects and the physical and chemical properties for nickel-based thermal spray coating aerosols is lacking. Methods: A thermal spray coating aerosol generator and inhalation exposure system was developed to perform animal studies to simulate workplace exposures. Male Sprague- Dawley rats were exposed by whole body inhalation to 10 mg/m3 x 4 hr/d x 4 d with aerosols generated from electric arc wire- thermal spray coating using two different nickel (Ni)-based consumable wires-PMET885 and PMET876. Control animals were exposed to filtered air. At 45 and 90 d after the last exposure, bronchoalveolar lavage (BAL) was performed on the right lung and a histopathological analysis was performed on the left lung to assess lung toxicity. Animal body weights were measured throughout the 90-d post-exposure period to assess general health status of the exposed animals. Results: The metal composition of each aerosol was determined by inductively coupled plasma- atomic emission spectroscopy (ICP-AES): PMET885 (97% Ni, 2% Al) and PMET876 (56% Ni, 17% Cr, 17% Mo, 5% Fe, 3% Mn). The generated particles were complex metal oxides arranged as chain-like agglomerates with similar mass median diameters (MMADs) of 316 (PMET885) and 367 nm (PMET876). At 45-d post-exposure, BAL fluid lactate dehydrogenase (LDH; lung cell injury marker) and the number of total BAL cells recovered (index of inflammation) were significantly elevated for the PMET885 group compared to air control. This increase in lung toxicity persisted for 90 d and was still significantly different from air control, however, LDH and total number of BAL cells recovered were significantly less than both values for the PMET885 group at 45-d post-exposure. Histopathologic pulmonary changes observed at 45-d and 90-d postexposure for the PMET885 group included bronchiolo-alveolar chronic inflammation and associated alveolar fibrin and alveolar epithelial hyperplasia. Chronic inflammation and the associated pulmonary changes were similar at both timepoints, although the chronic inflammation was more focused on terminal bronchioles and slightly increased in severity in the 90-d post-exposure group. In contrast, LDH and the number of BAL cells recovered for the PMET876 group were slightly but significantly elevated at 45-d post-exposure but not at 90-d post-exposure when compared to air control. Both parameters of toxicity were significantly elevated in the PMET885 group when compared to the PMET876 group at both 45- and 90-d post-exposure timepoints. Similar histopathologic changes were observed in the lungs of some rats exposed to the PMET876 aerosol compared with the PMET885 aerosol at 45-d post-exposure, but they were less prevalent and severe. There were some animals in the PMET876 group that were similar in histopathologic response to air controls at 45-d and 90-d post-exposure. This may suggest no lung response to the PMET876 aerosol and/or resolution of associated lung toxicity at the timepoints examined in the study. In the assessment of general health status, animal body weights were significantly less at each timepoint measured throughout the 90-d post-exposure regimen for the PMET885 aerosol compared to air control beginning after the second day of exposure. There was no significant difference in body weight at any timepoint during or after exposure to the PMET876 aerosol compared to air control. Conclusions: The PMET885 aerosol was more pneumotoxic at both timepoints compared to the PMET876 aerosol. In addition, lung toxicity persisted for 90-d after exposure to the PMET885 aerosol, although the lungs appeared to be recovering as injury and inflammation were both subsiding compared to the response at 45-d post-exposure. Results of this inhalation toxicology study indicated that different Ni-based thermal spray coating aerosols were toxic to the lungs, and the degree of pulmonary injury, inflammation and pathological alteration appeared to be associated with the Ni content in the thermal spray consumable. Description provided by NIOSH
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  • Source:
    Toxicologist 2025 Mar; 204(S1):251
  • ISSN:
    1096-6080
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  • Pages in Document:
    2 pdf pages
  • Volume:
    204
  • NIOSHTIC Number:
    nn:20071576
  • CAS Registry Number:
  • Federal Fiscal Year:
    2025
  • NORA Priority Area:
  • Peer Reviewed:
    False
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  • File Type:
    Filetype[PDF - 260.11 KB]
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  • Main Document Checksum:
    urn:sha-512:e576eebd921f72bd6fd37ddb0d47297903bca880556879b5bc54002958b2ee35b95887bb4acaf3f7bdbbb6d3bc2ae0b45fc6b1a8a031078dd7974ca399d7a559
File Language:
English
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