Polyvinyl Chloride and Polyethylene Microplastics Promote Cardiac Oxidative Stress and Histopathological Remodeling in Wistar Rats

Abstract

Microplastic pollution is an emerging environmental concern with accumulating evidence of systemic toxicity. Polyethylene (PE) and polyvinyl chloride (PVC) are persistent polymers that may promote oxidative stress and influence redox-sensitive signaling pathways such as nuclear factor kappa-B (NF-κB). This study investigated the cardiac effects of subacute inhalation of PE and PVC microplastics (MPs) in Wistar rats, focusing on oxidative stress, structural alterations, and NF-κB-related responses. Eighteen female Wistar rats were randomly assigned to control, PE, or PVC groups. Exposure groups underwent whole-body inhalation of 15 mg/m³ PE or PVC MPs for 4 h/day, 5 days/week, for 28 days. Cardiac tissue was examined histologically and assessed for malondialdehyde (MDA) levels and p65 NF-κB expression {a marker of NF-κB pathway activity} using immunofluorescence. Microplastic exposure resulted in significant cardiac structural alterations. Mean ventricular wall diameter increased by approximately 48% in the PE group and 75% in the PVC group compared with controls {p < 0.05}, indicating more pronounced histopathological remodeling in PVC-exposed animals. Cardiac MDA concentrations increased markedly {control: 0.0189 µmol/g; PVC: 0.272 µmol/g; PE: 0.554 µmol/g}, corresponding to roughly 14-fold (PVC) and 29-fold (PE) increases relative to controls {p < 0.001}. In contrast, p65 NF-κB expression did not differ significantly among groups {p > 0.05}, suggesting that any potential inflammatory pathway involvement remains exploratory and was not statistically demonstrated under subacute exposure conditions. Subacute inhalation of PE and PVC MPs induces oxidative stress and early cardiac remodeling in Wistar rats. Notably, PVC produced greater structural alterations, whereas PE generated higher oxidative stress, indicating distinct cardiotoxic profiles. These findings reflect early cardiac responses, and long-term studies are needed to determine whether sustained exposure leads to persistent inflammation and definitive NF-κB pathway activation.

HIGHLIGHTS

• Subacute whole-body inhalation of polyethylene (PE) and polyvinyl chloride (PVC) microplastics for 28 days resulted in measurable cardiac effects in female Wistar rats.
• Microplastic exposure significantly elevated cardiac oxidative stress, with MDA levels increasing from 0.0189 ng/mL in controls to 0.272 ng/mL in PVC and 0.554 ng/mL in PE groups (p < 0.001), indicating stronger oxidative induction by PE.
• These oxidative changes were accompanied by marked structural remodelling, as mean ventricular wall diameter increased from 37 mm (control) to 2.03 mm (PE) and 2.40 mm (PVC) (p < 0.001), confirming hypertrophic alterations after microplastic exposure.
• Despite oxidative and structural changes, cardiac NF-κB p65 expression did not differ significantly among groups (p = 0.650), suggesting that early tissue injury may occur prior to detectable NF-κB activation under subacute conditions.
• Collectively, these findings support airborne microplastics as a potential cardiovascular risk factor and underscore the importance of long-term exposure studies to clarify downstream signalling progression.

GRAPHICAL ABSTRACT