Toxicity of long term exposure to low dose polystyrene microplastics and nanoplastics in human iPSC-derived cardiomyocytes

Abstract

Microplastics and nanoplastics (MNPs) are widespread environmental pollutants with potential risks to human health including cardiovascular effects. However, the impact of MNPs on the heart, particularly in human-relevant cardiac models, remains poorly understood. In this study, we investigated the long term effects of polystyrene (PS) MNPs-1 μm (PS-1) and 0.05 μm (PS-0.05) in human iPSC-derived cardiomyocytes (hiPSC-CMs). PS MNPs exposure reduced myocyte viability in a time- and dose-dependent manner. At a low dose of 0.1 μg/L, both PS-0.05 and PS-1 suppressed myocyte contractility, reduced Ca²⁺ transient amplitude, and altered contraction and Ca²⁺ transient dynamics. In hypertrophic hiPSC-CMs, PS-0.05 exposure exacerbated hypertrophy, increasing cell size and proBNP expression, a marker of myocyte hypertrophy. The mechanism of PS MNPs-induced cardiotoxicity likely involved mitochondrial dysfunction, as indicated by decreased mitochondrial membrane potential, increased mitochondrial ROS, and elevated intracellular ROS levels. This is the first study to assess the long term impact of low dose MNPs in human cardiomyocytes, providing crucial insight into the potential cardiac toxicity of MNPs and their implications for human heart health.

Keywords: Cardiomyocytes; Heart; Hypertrophy; Microplastics; Nanoplastics; Toxicity.