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00000000000000.0 |
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240412 ||| eng |
| 100 |
1 |
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|a Halappanavar, Sabina
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| 245 |
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|a Substance interaction with the pulmonary resident cell membrane components leading to pulmonary fibrosis
|h Elektronische Ressource
|c Sabina, Halappanavar ... [et al]
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| 260 |
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|a Paris
|b OECD Publishing
|c 2023
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| 300 |
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|a 155 p.
|c 21 x 28cm
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| 653 |
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|a Environment
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| 700 |
1 |
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|a Sharma, Monita
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| 700 |
1 |
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|a Solorio-Rodriguez, Silvia
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| 700 |
1 |
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|a Wallin, Hakan
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| 041 |
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7 |
|a eng
|2 ISO 639-2
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| 989 |
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|b OECD
|a OECD Books and Papers
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| 490 |
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|a OECD Series on Adverse Outcome Pathways
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| 028 |
5 |
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|a 10.1787/10372cb8-en
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| 856 |
4 |
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|a oecd-ilibrary.org
|u https://doi.org/10.1787/10372cb8-en
|x Verlag
|3 Volltext
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| 082 |
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|a 363
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| 520 |
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|a Lung fibrosis is a dysregulated or exaggerated tissue repair process resulting in the thickening or scarring of lung tissue. It involves the presence of sustained or repeated exposure to a stressor and intricate dynamics between several inflammatory and immune response cells, and the microenvironment of the alveolar-capillary region consisting of both immune and non-immune cells, and the lung interstitium. This AOP is applicable to a broad group of stressors of diverse properties e.g. metal dusts, pharmacological products, fibres, microorganisms, chemicals, including novel technology-enabled stressors such as nanomaterials. This AOP is referred to as AOP 173 in the Collaborative Adverse Outcome Pathway Wiki (AOP-Wiki)
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