Gestational exposure to micro and nanoplastics differentially impacts cardiac development and function in male and female rats throughout the lifespan

Abstract

Micro- and nanoplastics (MNPs) are a ubiquitous contaminant. Identification of MNPs in the human placenta suggests this toxicant poses a danger to developing offspring. Previously, we demonstrated that maternal pulmonary MNP exposure restricts fetal growth and disrupts fetoplacental cardiovascular function in rats. Herein, we investigated how repeated maternal inhalation of polyamide-12 MNP from gestational day 4-19 during pregnancy (10 mg/m³, geometric mean 175.8 ± 1.9 nm, mode particle size 19 nm, size range 6 nm-8 μm) in Sprague Dawley rats influences cardiovascular development and function in male and female offspring at gestational day 20, 2 weeks, 1 month and 3 months of age. Exposed neonates demonstrated decreased relative left ventricle wall thickness while dilation of the left ventricle was identified in MNP-exposed adolescents and adults. Analyses of offspring myocardial mRNA suggest that maternal MNP exposure disrupted mitochondrial function, calcium handling, and defense against oxidative species. MNP exposure increased blood flow velocity within the left ventricle, decreased fractional shortening, and increased relative cardiac output at the fetal, adolescent and adult stages, respectively. Although variable, select experimental outcomes were changed in a sexually dimorphic manner after gestational MNP.

Keywords: Cardiovascular; DOHaD; Fetal growth restriction; Microplastics; Nanoplastics; Particulate matter.