Pulmonary disorder induced by cross‐linked polyacrylic acid

• Published in: Journal of occupational health Vol. 64; no. 1; pp. e12369 - n/a
• Main Authors: Higashi, Yasuyuki, Morimoto, Yasuo, Nishida, Chinatsu, Tomonaga, Taisuke, Izumi, Hiroto, Wang, Ke‐Yong, Higashi, Hidenori, Ono, Ryohei, Sumiya, Kazuki, Sakurai, Kazuo, Yamasaki, Kei, Yatera, Kazuhiro
• Format: Journal Article
• Language: English
• Published: Australia Oxford University Press 01.01.2022; John Wiley and Sons Inc
• Subjects: Acids; Acrylic Resins - toxicity; Aerosols; Alkaline phosphatase; Animals; Bronchoalveolar Lavage Fluid; Bronchus; cross‐linked polyacrylic acid; Environmental health; Exposure; Fibrosis; Heme; Inflammation; L-Lactate dehydrogenase; Laboratory animals; Lactate dehydrogenase; Lactic acid; Lavage; Leukocytes (neutrophilic); Lung Diseases; Lungs; Male; Molecular weight; Neutrophils; Occupational health; organic polymers; Original; Oxygenase; Pneumonia; Polyacrylic acid; Polymers; Protein D; Proteins; pulmonary toxicity; Rats; Rats, Inbred F344; Surfactant protein D; Trachea; Viscosity; St Louis Missouri; United States > US; Japan; Germany; pulmonary toxicity; organic polymers; cross-linked polyacrylic acid
• ISSN: 1348-9585; 1341-9145; 1348-9585
• DOI: 10.1002/1348-9585.12369

Objectives Organic polymers are materials widely used in our daily lives, such as daily necessities, foods, and medicines. There have been reports recently that cross‐linked polyacrylic acid (CL‐PAA) can possibly cause serious lung disease. We investigated whether intratracheal instillation of CL‐PAA causes pulmonary disorder in rats. Methods Male F344 rats were administered low (0.2 mg/rat) and high (1.0 mg/rat) doses of CL‐PAA intratracheally and were dissected 3 days, 1 week, 1 month, 3 months, and 6 months after exposure to examine inflammatory and fibrotic responses in the lungs. Only the high‐dose specimens were subjected to ultrasonic dispersion treatment of the administered material. Results There was a dose‐dependent increase in the total cell count, neutrophil count, neutrophil percentage, lactate dehydrogenase (LDH), surfactant protein D (SP‐D), cytokine‐induced neutrophil chemoattractant (CINC)‐1 and CINC‐2 values in bronchoalveolar lavage fluid (BALF) from 3 days to at least 3 months after intratracheal administration of CL‐PAA. Heme oxygenase‐1 (HO‐1) in lung tissue was also persistently elevated from 3 days to 6 months after exposure. Alkaline phosphatase (ALP) in BALF was elevated at 3 days and 1 month after exposure only in the high‐dose group. Histopathological findings in lung tissue showed inflammatory and fibrotic changes from 3 days after administration, and we observed obvious inflammatory changes for up to 3 months and fibrotic changes for up to 6 months. Conclusion Intratracheal administration of CL‐PAA induced persistent neutrophilic inflammation and fibrosis in the rats' lungs, suggesting that CL‐PAA may have inflammogenic and fibrogenic effects.