ArticleRespiratory research2023
Mechanisms of pulmonary disease in F344 rats after workplace-relevant inhalation exposure to cross-linked water-soluble acrylic acid polymers.
Article in Respiratory research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Pulmonary responses to polyacrylic acid with and without carboxyl groups following intratracheal instillation in rats.Archives of toxicology · 2026Article
- Protective Role of Octreotide in Acute and Chronic Lung Injuries.International journal of preventive medicine · 2026Article
- Mouse pulmonary pathological characteristics induced by Asian-mineral dust transported with Coniothyrium fuckelii at a high altitude of 2,000 meters.Scientific reports · 2025Article
- Fibrotic pulmonary dust foci is an advanced pneumoconiosis lesion in rats induced by titanium dioxide nanoparticles in a 2-year inhalation study.Particle and fibre toxicology · 2025Article
- Comparative anatomy of respiratory bronchioles and lobular structures in mammals.Journal of toxicologic pathology · 2025Review
- Chromium and formoterol therapy for obesity-induced asthma in rats.Frontiers in pharmacology · 2025Article
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecently 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.
methodsUsing a whole-body inhalation exposure system, male F344 rats were exposed once to 40 or 100 mg/m
resultsA 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.
conclusionsThe 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.
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