Inflammogenic effect of polyacrylic acid in rat lung following intratracheal instillation

Background Some organic chemicals are known to cause allergic disorders such as bronchial asthma and hypersensitivity pneumonitis, and it has been considered that they do not cause irreversible pulmonary fibrosis. It has recently been reported, however, that cross-linked acrylic acid-based polymer,...

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Published inParticle and fibre toxicology Vol. 19; no. 1; pp. 8 - 17
Main Authors Nishida, Chinatsu, Tomonaga, Taisuke, Izumi, Hiroto, Wang, Ke-Yong, Higashi, Hidenori, Ishidao, Toru, Takeshita, Jun-ichi, Ono, Ryohei, Sumiya, Kazuki, Fujii, Shota, Mochizuki, Shinichi, Sakurai, Kazuo, Yamasaki, Kei, Yatera, Kazuhiro, Morimoto, Yasuo
Format Journal Article
LanguageEnglish
Published London BioMed Central 21.01.2022
BioMed Central Ltd
BMC
Subjects
Acids
Acrylic acid
Acrylic Resins
Aerosols
Alveolitis
Animals
Asbestos
Asthma
Biomedical and Life Sciences
Biomedicine
Bronchoalveolar Lavage Fluid
Bronchus
Cerium oxides
Chemokines
Chrysotile
Comparators
Cross-linked polyacrylic acid (CL-PAA)
Crosslinking
Cytokines
Development and progression
Dust
Environmental Health
Exposure
Fibrosis
Gene expression
Health aspects
Heme
Heme oxygenase (decyclizing)
Hypersensitivity
Inflammation
Leukocytes (neutrophilic)
Lung
Lung diseases
Lungs
Male
Medical prognosis
Nanoparticles
Nanotechnology
Neutrophils
Nickel oxides
Organic chemicals
Organic chemistry
Oxidative stress
Oxygenase
Pharmacology/Toxicology
Pneumology/Respiratory System
Pneumonitis
Polyacrylic acid
Polymers
Public Health
Pulmonary fibrosis
Pulmonary toxicity
Rats
Rats, Inbred F344
Risk factors
Silica
Silicon dioxide
Trachea
Working groups
Japan
Cross-linked polyacrylic acid (CL-PAA)
Pulmonary toxicity
Organic chemicals
Online AccessGet full text
ISSN1743-8977
1743-8977
DOI10.1186/s12989-022-00448-z

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Abstract Background Some organic chemicals are known to cause allergic disorders such as bronchial asthma and hypersensitivity pneumonitis, and it has been considered that they do not cause irreversible pulmonary fibrosis. It has recently been reported, however, that cross-linked acrylic acid-based polymer, an organic chemical, might cause serious interstitial lung diseases, including pulmonary fibrosis. We investigated whether or not intratracheal instillation exposure to cross-linked polyacrylic acid (CL-PAA) can cause lung disorder in rats. Methods Male F344 rats were intratracheally instilled with dispersed CL-PAA at low (0.2 mg/rat) and high (1.0 mg/rat) doses, and were sacrificed at 3 days, 1 week, 1 month, 3 months and 6 months after exposure to examine inflammatory and fibrotic responses and related gene expressions in the lungs. Rat lungs exposed to crystalline silica, asbestos (chrysotile), and NiO and CeO 2 nanoparticles were used as comparators. Results Persistent increases in total cell count, neutrophil count and neutrophil percentage, and in the concentration of the cytokine-induced neutrophil chemoattractant (CINC)-1, CINC-2 and C-X-C motif chemokine 5 (CXCL5), which correlated with lung tissue gene expression, were observed in bronchoalveolar lavage fluid (BALF) from 3 days until at least 1 month following CL-PAA intratracheal instillation. Persistent increases in heme oxygenase-1 (HO-1) in the lung tissue were also observed from 3 days to 6 months after exposure. Histopathological findings of the lungs demonstrated that extensive inflammation at 3 days was greater than that in exposure to silica, NiO nanoparticles and CeO 2 nanoparticles, and equal to or greater than that in asbestos (chrysotile) exposure, and the inflammation continued until 1 month. Fibrotic changes also progressed after 1 month postexposure. Conclusion Our results suggested that CL-PAA potentially causes strong neutrophil inflammation in the rat and human lung.
AbstractList Abstract Background Some organic chemicals are known to cause allergic disorders such as bronchial asthma and hypersensitivity pneumonitis, and it has been considered that they do not cause irreversible pulmonary fibrosis. It has recently been reported, however, that cross-linked acrylic acid-based polymer, an organic chemical, might cause serious interstitial lung diseases, including pulmonary fibrosis. We investigated whether or not intratracheal instillation exposure to cross-linked polyacrylic acid (CL-PAA) can cause lung disorder in rats. Methods Male F344 rats were intratracheally instilled with dispersed CL-PAA at low (0.2 mg/rat) and high (1.0 mg/rat) doses, and were sacrificed at 3 days, 1 week, 1 month, 3 months and 6 months after exposure to examine inflammatory and fibrotic responses and related gene expressions in the lungs. Rat lungs exposed to crystalline silica, asbestos (chrysotile), and NiO and CeO2 nanoparticles were used as comparators. Results Persistent increases in total cell count, neutrophil count and neutrophil percentage, and in the concentration of the cytokine-induced neutrophil chemoattractant (CINC)-1, CINC-2 and C-X-C motif chemokine 5 (CXCL5), which correlated with lung tissue gene expression, were observed in bronchoalveolar lavage fluid (BALF) from 3 days until at least 1 month following CL-PAA intratracheal instillation. Persistent increases in heme oxygenase-1 (HO-1) in the lung tissue were also observed from 3 days to 6 months after exposure. Histopathological findings of the lungs demonstrated that extensive inflammation at 3 days was greater than that in exposure to silica, NiO nanoparticles and CeO2 nanoparticles, and equal to or greater than that in asbestos (chrysotile) exposure, and the inflammation continued until 1 month. Fibrotic changes also progressed after 1 month postexposure. Conclusion Our results suggested that CL-PAA potentially causes strong neutrophil inflammation in the rat and human lung.
Some organic chemicals are known to cause allergic disorders such as bronchial asthma and hypersensitivity pneumonitis, and it has been considered that they do not cause irreversible pulmonary fibrosis. It has recently been reported, however, that cross-linked acrylic acid-based polymer, an organic chemical, might cause serious interstitial lung diseases, including pulmonary fibrosis. We investigated whether or not intratracheal instillation exposure to cross-linked polyacrylic acid (CL-PAA) can cause lung disorder in rats. Male F344 rats were intratracheally instilled with dispersed CL-PAA at low (0.2 mg/rat) and high (1.0 mg/rat) doses, and were sacrificed at 3 days, 1 week, 1 month, 3 months and 6 months after exposure to examine inflammatory and fibrotic responses and related gene expressions in the lungs. Rat lungs exposed to crystalline silica, asbestos (chrysotile), and NiO and CeO.sub.2 nanoparticles were used as comparators. Persistent increases in total cell count, neutrophil count and neutrophil percentage, and in the concentration of the cytokine-induced neutrophil chemoattractant (CINC)-1, CINC-2 and C-X-C motif chemokine 5 (CXCL5), which correlated with lung tissue gene expression, were observed in bronchoalveolar lavage fluid (BALF) from 3 days until at least 1 month following CL-PAA intratracheal instillation. Persistent increases in heme oxygenase-1 (HO-1) in the lung tissue were also observed from 3 days to 6 months after exposure. Histopathological findings of the lungs demonstrated that extensive inflammation at 3 days was greater than that in exposure to silica, NiO nanoparticles and CeO.sub.2 nanoparticles, and equal to or greater than that in asbestos (chrysotile) exposure, and the inflammation continued until 1 month. Fibrotic changes also progressed after 1 month postexposure. Our results suggested that CL-PAA potentially causes strong neutrophil inflammation in the rat and human lung.
Some organic chemicals are known to cause allergic disorders such as bronchial asthma and hypersensitivity pneumonitis, and it has been considered that they do not cause irreversible pulmonary fibrosis. It has recently been reported, however, that cross-linked acrylic acid-based polymer, an organic chemical, might cause serious interstitial lung diseases, including pulmonary fibrosis. We investigated whether or not intratracheal instillation exposure to cross-linked polyacrylic acid (CL-PAA) can cause lung disorder in rats.BACKGROUNDSome organic chemicals are known to cause allergic disorders such as bronchial asthma and hypersensitivity pneumonitis, and it has been considered that they do not cause irreversible pulmonary fibrosis. It has recently been reported, however, that cross-linked acrylic acid-based polymer, an organic chemical, might cause serious interstitial lung diseases, including pulmonary fibrosis. We investigated whether or not intratracheal instillation exposure to cross-linked polyacrylic acid (CL-PAA) can cause lung disorder in rats.Male F344 rats were intratracheally instilled with dispersed CL-PAA at low (0.2 mg/rat) and high (1.0 mg/rat) doses, and were sacrificed at 3 days, 1 week, 1 month, 3 months and 6 months after exposure to examine inflammatory and fibrotic responses and related gene expressions in the lungs. Rat lungs exposed to crystalline silica, asbestos (chrysotile), and NiO and CeO2 nanoparticles were used as comparators.METHODSMale F344 rats were intratracheally instilled with dispersed CL-PAA at low (0.2 mg/rat) and high (1.0 mg/rat) doses, and were sacrificed at 3 days, 1 week, 1 month, 3 months and 6 months after exposure to examine inflammatory and fibrotic responses and related gene expressions in the lungs. Rat lungs exposed to crystalline silica, asbestos (chrysotile), and NiO and CeO2 nanoparticles were used as comparators.Persistent increases in total cell count, neutrophil count and neutrophil percentage, and in the concentration of the cytokine-induced neutrophil chemoattractant (CINC)-1, CINC-2 and C-X-C motif chemokine 5 (CXCL5), which correlated with lung tissue gene expression, were observed in bronchoalveolar lavage fluid (BALF) from 3 days until at least 1 month following CL-PAA intratracheal instillation. Persistent increases in heme oxygenase-1 (HO-1) in the lung tissue were also observed from 3 days to 6 months after exposure. Histopathological findings of the lungs demonstrated that extensive inflammation at 3 days was greater than that in exposure to silica, NiO nanoparticles and CeO2 nanoparticles, and equal to or greater than that in asbestos (chrysotile) exposure, and the inflammation continued until 1 month. Fibrotic changes also progressed after 1 month postexposure.RESULTSPersistent increases in total cell count, neutrophil count and neutrophil percentage, and in the concentration of the cytokine-induced neutrophil chemoattractant (CINC)-1, CINC-2 and C-X-C motif chemokine 5 (CXCL5), which correlated with lung tissue gene expression, were observed in bronchoalveolar lavage fluid (BALF) from 3 days until at least 1 month following CL-PAA intratracheal instillation. Persistent increases in heme oxygenase-1 (HO-1) in the lung tissue were also observed from 3 days to 6 months after exposure. Histopathological findings of the lungs demonstrated that extensive inflammation at 3 days was greater than that in exposure to silica, NiO nanoparticles and CeO2 nanoparticles, and equal to or greater than that in asbestos (chrysotile) exposure, and the inflammation continued until 1 month. Fibrotic changes also progressed after 1 month postexposure.Our results suggested that CL-PAA potentially causes strong neutrophil inflammation in the rat and human lung.CONCLUSIONOur results suggested that CL-PAA potentially causes strong neutrophil inflammation in the rat and human lung.
Background Some organic chemicals are known to cause allergic disorders such as bronchial asthma and hypersensitivity pneumonitis, and it has been considered that they do not cause irreversible pulmonary fibrosis. It has recently been reported, however, that cross-linked acrylic acid-based polymer, an organic chemical, might cause serious interstitial lung diseases, including pulmonary fibrosis. We investigated whether or not intratracheal instillation exposure to cross-linked polyacrylic acid (CL-PAA) can cause lung disorder in rats. Methods Male F344 rats were intratracheally instilled with dispersed CL-PAA at low (0.2 mg/rat) and high (1.0 mg/rat) doses, and were sacrificed at 3 days, 1 week, 1 month, 3 months and 6 months after exposure to examine inflammatory and fibrotic responses and related gene expressions in the lungs. Rat lungs exposed to crystalline silica, asbestos (chrysotile), and NiO and CeO 2 nanoparticles were used as comparators. Results Persistent increases in total cell count, neutrophil count and neutrophil percentage, and in the concentration of the cytokine-induced neutrophil chemoattractant (CINC)-1, CINC-2 and C-X-C motif chemokine 5 (CXCL5), which correlated with lung tissue gene expression, were observed in bronchoalveolar lavage fluid (BALF) from 3 days until at least 1 month following CL-PAA intratracheal instillation. Persistent increases in heme oxygenase-1 (HO-1) in the lung tissue were also observed from 3 days to 6 months after exposure. Histopathological findings of the lungs demonstrated that extensive inflammation at 3 days was greater than that in exposure to silica, NiO nanoparticles and CeO 2 nanoparticles, and equal to or greater than that in asbestos (chrysotile) exposure, and the inflammation continued until 1 month. Fibrotic changes also progressed after 1 month postexposure. Conclusion Our results suggested that CL-PAA potentially causes strong neutrophil inflammation in the rat and human lung.
Background Some organic chemicals are known to cause allergic disorders such as bronchial asthma and hypersensitivity pneumonitis, and it has been considered that they do not cause irreversible pulmonary fibrosis. It has recently been reported, however, that cross-linked acrylic acid-based polymer, an organic chemical, might cause serious interstitial lung diseases, including pulmonary fibrosis. We investigated whether or not intratracheal instillation exposure to cross-linked polyacrylic acid (CL-PAA) can cause lung disorder in rats. Methods Male F344 rats were intratracheally instilled with dispersed CL-PAA at low (0.2 mg/rat) and high (1.0 mg/rat) doses, and were sacrificed at 3 days, 1 week, 1 month, 3 months and 6 months after exposure to examine inflammatory and fibrotic responses and related gene expressions in the lungs. Rat lungs exposed to crystalline silica, asbestos (chrysotile), and NiO and CeO.sub.2 nanoparticles were used as comparators. Results Persistent increases in total cell count, neutrophil count and neutrophil percentage, and in the concentration of the cytokine-induced neutrophil chemoattractant (CINC)-1, CINC-2 and C-X-C motif chemokine 5 (CXCL5), which correlated with lung tissue gene expression, were observed in bronchoalveolar lavage fluid (BALF) from 3 days until at least 1 month following CL-PAA intratracheal instillation. Persistent increases in heme oxygenase-1 (HO-1) in the lung tissue were also observed from 3 days to 6 months after exposure. Histopathological findings of the lungs demonstrated that extensive inflammation at 3 days was greater than that in exposure to silica, NiO nanoparticles and CeO.sub.2 nanoparticles, and equal to or greater than that in asbestos (chrysotile) exposure, and the inflammation continued until 1 month. Fibrotic changes also progressed after 1 month postexposure. Conclusion Our results suggested that CL-PAA potentially causes strong neutrophil inflammation in the rat and human lung. Keywords: Cross-linked polyacrylic acid (CL-PAA), Organic chemicals, Pulmonary toxicity
Background Some organic chemicals are known to cause allergic disorders such as bronchial asthma and hypersensitivity pneumonitis, and it has been considered that they do not cause irreversible pulmonary fibrosis. It has recently been reported, however, that cross-linked acrylic acid-based polymer, an organic chemical, might cause serious interstitial lung diseases, including pulmonary fibrosis. We investigated whether or not intratracheal instillation exposure to cross-linked polyacrylic acid (CL-PAA) can cause lung disorder in rats. Methods Male F344 rats were intratracheally instilled with dispersed CL-PAA at low (0.2 mg/rat) and high (1.0 mg/rat) doses, and were sacrificed at 3 days, 1 week, 1 month, 3 months and 6 months after exposure to examine inflammatory and fibrotic responses and related gene expressions in the lungs. Rat lungs exposed to crystalline silica, asbestos (chrysotile), and NiO and CeO2 nanoparticles were used as comparators. Results Persistent increases in total cell count, neutrophil count and neutrophil percentage, and in the concentration of the cytokine-induced neutrophil chemoattractant (CINC)-1, CINC-2 and C-X-C motif chemokine 5 (CXCL5), which correlated with lung tissue gene expression, were observed in bronchoalveolar lavage fluid (BALF) from 3 days until at least 1 month following CL-PAA intratracheal instillation. Persistent increases in heme oxygenase-1 (HO-1) in the lung tissue were also observed from 3 days to 6 months after exposure. Histopathological findings of the lungs demonstrated that extensive inflammation at 3 days was greater than that in exposure to silica, NiO nanoparticles and CeO2 nanoparticles, and equal to or greater than that in asbestos (chrysotile) exposure, and the inflammation continued until 1 month. Fibrotic changes also progressed after 1 month postexposure. Conclusion Our results suggested that CL-PAA potentially causes strong neutrophil inflammation in the rat and human lung.
Some organic chemicals are known to cause allergic disorders such as bronchial asthma and hypersensitivity pneumonitis, and it has been considered that they do not cause irreversible pulmonary fibrosis. It has recently been reported, however, that cross-linked acrylic acid-based polymer, an organic chemical, might cause serious interstitial lung diseases, including pulmonary fibrosis. We investigated whether or not intratracheal instillation exposure to cross-linked polyacrylic acid (CL-PAA) can cause lung disorder in rats. Male F344 rats were intratracheally instilled with dispersed CL-PAA at low (0.2 mg/rat) and high (1.0 mg/rat) doses, and were sacrificed at 3 days, 1 week, 1 month, 3 months and 6 months after exposure to examine inflammatory and fibrotic responses and related gene expressions in the lungs. Rat lungs exposed to crystalline silica, asbestos (chrysotile), and NiO and CeO nanoparticles were used as comparators. Persistent increases in total cell count, neutrophil count and neutrophil percentage, and in the concentration of the cytokine-induced neutrophil chemoattractant (CINC)-1, CINC-2 and C-X-C motif chemokine 5 (CXCL5), which correlated with lung tissue gene expression, were observed in bronchoalveolar lavage fluid (BALF) from 3 days until at least 1 month following CL-PAA intratracheal instillation. Persistent increases in heme oxygenase-1 (HO-1) in the lung tissue were also observed from 3 days to 6 months after exposure. Histopathological findings of the lungs demonstrated that extensive inflammation at 3 days was greater than that in exposure to silica, NiO nanoparticles and CeO nanoparticles, and equal to or greater than that in asbestos (chrysotile) exposure, and the inflammation continued until 1 month. Fibrotic changes also progressed after 1 month postexposure. Our results suggested that CL-PAA potentially causes strong neutrophil inflammation in the rat and human lung.
ArticleNumber 8
Audience Academic
Author Tomonaga, Taisuke
Sakurai, Kazuo
Fujii, Shota
Morimoto, Yasuo
Wang, Ke-Yong
Ishidao, Toru
Yatera, Kazuhiro
Sumiya, Kazuki
Higashi, Hidenori
Mochizuki, Shinichi
Takeshita, Jun-ichi
Yamasaki, Kei
Izumi, Hiroto
Ono, Ryohei
Nishida, Chinatsu
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  givenname: Chinatsu
  surname: Nishida
  fullname: Nishida, Chinatsu
  organization: Department of Respiratory Medicine, University of Occupational and Environmental Health
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  givenname: Taisuke
  surname: Tomonaga
  fullname: Tomonaga, Taisuke
  organization: Department of Occupational Pneumology, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health
– sequence: 3
  givenname: Hiroto
  surname: Izumi
  fullname: Izumi, Hiroto
  organization: Department of Occupational Pneumology, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health
– sequence: 4
  givenname: Ke-Yong
  surname: Wang
  fullname: Wang, Ke-Yong
  organization: Shared-Use Research Center, School of Medicine, University of Occupational and Environmental Health, Japan
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  givenname: Hidenori
  surname: Higashi
  fullname: Higashi, Hidenori
  organization: Department of Environmental Health Engineering, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Japan
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  givenname: Toru
  surname: Ishidao
  fullname: Ishidao, Toru
  organization: Department of Environmental Management, School of Health Sciences, University of Occupational and Environmental Health, Japan
– sequence: 7
  givenname: Jun-ichi
  surname: Takeshita
  fullname: Takeshita, Jun-ichi
  organization: Research Institute of Science for Safety and Sustainability, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba
– sequence: 8
  givenname: Ryohei
  surname: Ono
  fullname: Ono, Ryohei
  organization: Department of Chemistry and Biochemistry, The University of Kitakyushu
– sequence: 9
  givenname: Kazuki
  surname: Sumiya
  fullname: Sumiya, Kazuki
  organization: Department of Chemistry and Biochemistry, The University of Kitakyushu
– sequence: 10
  givenname: Shota
  surname: Fujii
  fullname: Fujii, Shota
  organization: Department of Chemistry and Biochemistry, The University of Kitakyushu
– sequence: 11
  givenname: Shinichi
  surname: Mochizuki
  fullname: Mochizuki, Shinichi
  organization: Department of Chemistry and Biochemistry, The University of Kitakyushu
– sequence: 12
  givenname: Kazuo
  surname: Sakurai
  fullname: Sakurai, Kazuo
  organization: Department of Chemistry and Biochemistry, The University of Kitakyushu
– sequence: 13
  givenname: Kei
  surname: Yamasaki
  fullname: Yamasaki, Kei
  organization: Department of Respiratory Medicine, University of Occupational and Environmental Health
– sequence: 14
  givenname: Kazuhiro
  surname: Yatera
  fullname: Yatera, Kazuhiro
  organization: Department of Respiratory Medicine, University of Occupational and Environmental Health
– sequence: 15
  givenname: Yasuo
  orcidid: 0000-0002-5339-6905
  surname: Morimoto
  fullname: Morimoto, Yasuo
  email: yasuom@med.uoeh-u.ac.jp
  organization: Department of Occupational Pneumology, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35062982$$D View this record in MEDLINE/PubMed
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Keywords Cross-linked polyacrylic acid (CL-PAA)
Pulmonary toxicity
Organic chemicals
Language English
License 2022. The Author(s).
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PublicationTitle Particle and fibre toxicology
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Snippet Background Some organic chemicals are known to cause allergic disorders such as bronchial asthma and hypersensitivity pneumonitis, and it has been considered...
Some organic chemicals are known to cause allergic disorders such as bronchial asthma and hypersensitivity pneumonitis, and it has been considered that they do...
Background Some organic chemicals are known to cause allergic disorders such as bronchial asthma and hypersensitivity pneumonitis, and it has been considered...
Abstract Background Some organic chemicals are known to cause allergic disorders such as bronchial asthma and hypersensitivity pneumonitis, and it has been...
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StartPage 8
SubjectTerms Acids
Acrylic acid
Acrylic Resins
Aerosols
Alveolitis
Animals
Asbestos
Asthma
Biomedical and Life Sciences
Biomedicine
Bronchoalveolar Lavage Fluid
Bronchus
Cerium oxides
Chemokines
Chrysotile
Comparators
Cross-linked polyacrylic acid (CL-PAA)
Crosslinking
Cytokines
Development and progression
Dust
Environmental Health
Exposure
Fibrosis
Gene expression
Health aspects
Heme
Heme oxygenase (decyclizing)
Hypersensitivity
Inflammation
Leukocytes (neutrophilic)
Lung
Lung diseases
Lungs
Male
Medical prognosis
Nanoparticles
Nanotechnology
Neutrophils
Nickel oxides
Organic chemicals
Organic chemistry
Oxidative stress
Oxygenase
Pharmacology/Toxicology
Pneumology/Respiratory System
Pneumonitis
Polyacrylic acid
Polymers
Public Health
Pulmonary fibrosis
Pulmonary toxicity
Rats
Rats, Inbred F344
Risk factors
Silica
Silicon dioxide
Trachea
Working groups
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Title Inflammogenic effect of polyacrylic acid in rat lung following intratracheal instillation
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