pulmonary toxicity induced by subacute inhalation of polyvinyl chloride microplastics: oxidative stress and nf-κb pathway activation in rat models

Background: polyvinyl chloride (pvc) microplastics (mps) are among the most hazardous types of mps due to their widespread use and environmental persistence. the increasing production and degradation of pvc mps pose significant concerns about their adverse effects on living organisms, particularly through inhalation exposure. methods: the present study investigated the pulmonary toxicity of pvc mps in rat models following 28 days of subacute inhalation exposure at a dose of 15 mg/m³. pulmonary inflammation and tissue morphology were evaluated using immunofluorescence staining for p65 nf-κb and hematoxylin and eosin (h&e) staining. oxidative stress was assessed by measuring malondialdehyde (mda) levels as a marker.results: the results demonstrated that subacute inhalation exposure to pvc mps significantly increased mda levels (p<0.05), indicating heightened oxidative stress. immunofluorescence analysis revealed elevated p65 nf-κb expression (p<0.05), confirming the activation of the inflammatory pathway. histopathological evaluation demonstrated severe pulmonary tissue damage, including widespread inflammation and structural disruption (p<0.05). conclusion: the present work highlights that subacute inhalation of pvc mps induces pulmonary toxicity through mechanisms involving oxidative stress and activation of the nf-κb signaling pathway.