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  • 1
    Online Resource
    Online Resource
    Multi‐organ carcinogenicity by inhalation exposure to 2‐Bromopropane in rats
    Wiley ; 2023
    In:  Journal of Occupational Health Vol. 65, No. 1 ( 2023-01)
    Details
    In: Journal of Occupational Health, Wiley, Vol. 65, No. 1 ( 2023-01)
    Abstract: The purpose of this study was to investigate the carcinogenicity of 2‐bromopropane (2‐BP) in rats. Methods Male and female F344 rats were exposed by whole body inhalation to 2‐BP vapor at concentrations of 0, 67, 200, and 600 ppm for 6 h/day, 5 days/week for 2 years. Results All rats of both sexes exposed to 600 ppm died or became moribund within 85 weeks. Death/moribundity was caused by 2‐BP induced tumors. In males, significantly increased tumors were malignant Zymbal's gland tumors; sebaceous adenoma and basal cell carcinoma of the skin/appendage; adenocarcinoma of the small/large intestine; follicular cell adenoma of the thyroid; fibroma of the subcutis, and malignant lymphoma of the lymph node. In addition, an increased trend in tumor incidence was found in the preputial gland, lung, forestomach, pancreas islet, brain, and spleen. In females, significantly increased tumors were adenocarcinoma and fibroadenoma of the mammary gland, squamous cell papilloma of the vagina, and large granular lymphocytic leukemia of the spleen. In addition, an increased trend in tumor incidence was found in Zymbal's gland, the clitoral gland, skin, large intestine, pancreas islet, uterus, and subcutis. Particularly, malignant Zymbal's gland tumors were induced even in males exposed to the lowest concentration, 67 ppm. Conclusion Two‐year inhalation exposure to 2‐BP resulted in multi‐organ carcinogenicity in rats. Based on sufficient evidence of carcinogenicity in this study, 2‐BP has the potential to be a human carcinogen.
    Type of Medium: Online Resource
    ISSN: 1341-9145 , 1348-9585
    URL: Article
    DOI: 10.1002/1348-9585.12388
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 1340985-2
    detail.hit.zdb_id: 2075956-3
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  • 2
    Online Resource
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    Dose–response relationship of pulmonary disorders by inhalation exposure to cross-linked water-soluble acrylic acid polymers in F344 rats
    Springer Science and Business Media LLC ; 2022
    In:  Particle and Fibre Toxicology Vol. 19, No. 1 ( 2022-12)
    Details
    In: Particle and Fibre Toxicology, Springer Science and Business Media LLC, Vol. 19, No. 1 ( 2022-12)
    Abstract: In Japan, six workers handling cross-linked water-soluble acrylic acid polymer (CWAAP) at a chemical plant suffered from lung diseases, including fibrosis, interstitial pneumonia, emphysema, and pneumothorax. We recently demonstrated that inhalation of CWAAP-A, one type of CWAAP, causes pulmonary disorders in rats. It is important to investigate dose–response relationships and recoverability from exposure to CWAAPs for establishing occupational health guidelines, such as setting threshold limit value for CWAAPs in the workplace. Methods Male and female F344 rats were exposed to 0.3, 1, 3, or 10 mg/m 3 CWAAP-A for 6 h/day, 5 days/week for 13 weeks using a whole-body inhalation exposure system. At 1 h, 4 weeks, and 13 weeks after the last exposure the rats were euthanized and blood, bronchoalveolar lavage fluid, and all tissues including lungs and mediastinal lymph nodes were collected and subjected to biological and histopathological analyses. In a second experiment, male rats were pre-treated with clodronate liposome or polymorphonuclear leukocyte-neutralizing antibody to deplete macrophages or neutrophils, respectively, and exposed to CWAAP-A for 6 h/day for 2 days. Results CWAAP-A exposure damaged only the alveoli. The lowest observed adverse effect concentration (LOAEC) was 1 mg/m 3 and the no observed adverse effect concentration (NOAEC) was 0.3 mg/m 3 . Rats of both sexes were able to recover from the tissue damage caused by 13 weeks exposure to 1 mg/m 3 CWAAP-A. In contrast, tissue damage caused by exposure to 3 and 10 mg/m 3 was irreversible due to the development of interstitial lung lesions. There was a gender difference in the recovery from CWAAP-A induced pulmonary disorders, with females recovering less than males. Finally, acute lung effects caused by CWAAP-A were significantly reduced by depletion of alveolar macrophages. Conclusions Pulmonary damage caused by inhalation exposure to CWAAP-A was dose-dependent, specific to the lung and lymph nodes, and acute lung damage was ameliorated by depleting macrophages in the lungs. CWAAP-A had both a LOAEC and a NOAEC, and tissue damage caused by exposure to 1 mg/m 3 CWAAP-A was reversible: recovery in female rats was less than for males. These findings indicate that concentration limits for CWAAPs in the workplace can be determined. Graphical Abstract
    Type of Medium: Online Resource
    ISSN: 1743-8977
    URL: Article
    DOI: 10.1186/s12989-022-00468-9
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2170936-1
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  • 3
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    Correction to: Dose–response relationship of pulmonary disorders by inhalation exposure to cross-linked water-soluble acrylic acid polymers in F344 rats
    Springer Science and Business Media LLC ; 2022
    In:  Particle and Fibre Toxicology Vol. 19, No. 1 ( 2022-12)
    Details
    In: Particle and Fibre Toxicology, Springer Science and Business Media LLC, Vol. 19, No. 1 ( 2022-12)
    Type of Medium: Online Resource
    ISSN: 1743-8977
    URL: Article
    DOI: 10.1186/s12989-022-00475-w
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2170936-1
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  • 4
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    Mechanisms of pulmonary disease in F344 rats after workplace-relevant inhalation exposure to cross-linked water-soluble acrylic acid polymers
    Springer Science and Business Media LLC ; 2023
    In:  Respiratory Research Vol. 24, No. 1 ( 2023-02-13)
    Details
    In: Respiratory Research, Springer Science and Business Media LLC, Vol. 24, No. 1 ( 2023-02-13)
    Abstract: Recently in Japan, six workers at a chemical plant that manufactures resins developed interstitial lung diseases after being involved in loading and packing cross-linked water-soluble acrylic acid polymers (CWAAPs). The present study focused on assessing lung damage in rats caused by workplace-relevant inhalation exposure to CWAAP and investigated the molecular and cellular mechanisms involved in lung lesion development. Methods Using a whole-body inhalation exposure system, male F344 rats were exposed once to 40 or 100 mg/m 3 of CWAAP-A for 4 h or to 15 or 40 mg/m 3 of CWAAP-A for 4 h per day once per week for 2 months (9 exposures). In a separate set of experiments, male F344 rats were administered 1 mg/kg CWAAP-A or CWAAP-B by intratracheal instillation once every 2 weeks for 2 months (5 doses). Lung tissues, mediastinal lymph nodes, and bronchoalveolar lavage fluid were collected and subjected to biological and histopathological analyses. Results A single 4-h exposure to CWAAP-A caused alveolar injury, and repeated exposures resulted in regenerative changes in the alveolar epithelium with activation of TGFβ signaling. During the recovery period after the last exposure, some alveolar lesions were partially healed, but other lesions developed into alveolitis with fibrous thickening of the alveolar septum. Rats administered CWAAP-A by intratracheal instillation developed qualitatively similar pulmonary pathology as rats exposed to CWAAP-A by inhalation. At 2 weeks after intratracheal instillation, rats administered CWAAP-B appeared to have a slightly higher degree of lung lesions compared to rats administered CWAAP-A, however, there was no difference in pulmonary lesions in the CWAAP-A and CWAAP-B exposed rats examined 18 weeks after administration of these materials. Conclusions The present study reports our findings on the cellular and molecular mechanisms of pulmonary disease in rats after workplace-relevant inhalation exposure to CWAAP-A. This study also demonstrates that the lung pathogenesis of rats exposed to CWAAP-A by systemic inhalation was qualitatively similar to that of rats administered CWAAP-A by intratracheal instillation. Graphical Abstract
    Type of Medium: Online Resource
    ISSN: 1465-993X
    URL: Article
    DOI: 10.1186/s12931-023-02355-z
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2041675-1
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  • 5
    Online Resource
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    No evidence for carcinogenicity of titanium dioxide nanoparticles in 26-week inhalation study in rasH2 mouse model
    Springer Science and Business Media LLC ; 2022
    In:  Scientific Reports Vol. 12, No. 1 ( 2022-09-02)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 12, No. 1 ( 2022-09-02)
    Abstract: With the rapid development of alternative methods based on the spirit of animal welfare, the publications of animal studies evaluating endpoints such as cancer have been extremely reduced. We performed a 26-week inhalation exposure studies of titanium dioxide nanoparticles (TiO 2 NPs) using CByB6F1-Tg(HRAS)2Jic (rasH2) mice model for detecting carcinogenicity. Male and female rasH2 mice were exposed to 2, 8 or 32 mg/m 3 of TiO 2 NPs for 6 h/day, 5 days/week for 26 weeks. All tissues and blood were collected and subjected to biological and histopathological analyses. TiO 2 NPs exposure induced deposition of particles in lungs in a dose-dependent manner in each exposure group. Exposure to TiO 2 NPs, as well as other organs, did not increase the incidence of lung tumors in any group, and pulmonary fibrosis and pre-neoplastic lesions were not observed in all groups. Finally, the cell proliferative activity of alveolar epithelial type 2 cells was examined, and it was not increased by exposure to TiO 2 NPs. This is the first report showing the lack of pulmonary fibrogenicity and carcinogenicity (no evidence of carcinogenic activity) of TiO 2 NPs in 26-week inhalation study in rasH2 mice exposed up to 32 mg/m 3 , which is considered to be a high concentration.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-022-19139-y
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2615211-3
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  • 6
    Online Resource
    Online Resource
    Pulmonary dust foci as rat pneumoconiosis lesion induced by titanium dioxide nanoparticles in 13-week inhalation study
    Springer Science and Business Media LLC ; 2022
    In:  Particle and Fibre Toxicology Vol. 19, No. 1 ( 2022-09-14)
    Details
    In: Particle and Fibre Toxicology, Springer Science and Business Media LLC, Vol. 19, No. 1 ( 2022-09-14)
    Abstract: Most toxicological studies on titanium dioxide (TiO 2 ) particles to date have concentrated on carcinogenicity and acute toxicity, with few studies focusing of pneumoconiosis, which is a variety of airspace and interstitial lung diseases caused by particle-laden macrophages. The present study examined rat pulmonary lesions associated with pneumoconiosis after inhalation exposure to TiO 2 nanoparticles (NPs). Methods Male and female F344 rats were exposed to 6.3, 12.5, 25, or 50 mg/m 3 anatase type TiO 2 NPs for 6 h/day, 5 days/week for 13 weeks using a whole-body inhalation exposure system. After the last exposure the rats were euthanized and blood, bronchoalveolar lavage fluid, and all tissues including lungs and mediastinal lymph nodes were collected and subjected to biological and histopathological analyses. Results Numerous milky white spots were present in the lungs after exposure to 25 and 50 mg/m 3 TiO 2 NPs. Histopathological analysis revealed that the spots were alveolar lesions, characterized predominantly by the agglomeration of particle-laden macrophages and the presence of reactive alveolar epithelial type 2 cell (AEC2) hyperplasia. We defined this characteristic lesion as pulmonary dust foci (PDF). The PDF is an inflammatory niche, with decreased vascular endothelial cells in the interstitium, and proliferating AEC2 transformed into alveolar epithelial progenitor cells. In the present study, the AEC2 in the PDF had acquired DNA damage. Based on PDF induction, the lowest observed adverse effect concentration for pulmonary disorders in male and female rats was 12.5 mg/m 3 and 6.3 mg/m 3 , respectively. The no observed adverse effect concentration for male rats was 6.3 mg/m 3 . There was a sex difference in lung lesion development, with females showing more pronounced lesion parameters than males. Conclusions Inhalation exposure to TiO 2 NPs caused PDF, an air-space lesion which is an alveolar inflammatory niche containing particle-laden macrophages and proliferating AEC2. These PDFs histopathologically resemble some pneumoconiosis lesions (pulmonary siderosis and hard metal pneumoconiosis) in workers and lung disease in smokers, suggesting that PDFs caused by exposure to TiO 2 NPs in rats are an early pneumoconiosis lesion and may be a common alveolar reaction in mammals. Graphical Abstract
    Type of Medium: Online Resource
    ISSN: 1743-8977
    URL: Article
    DOI: 10.1186/s12989-022-00498-3
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2170936-1
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