Endocrine and metabolic effects of microplastic exposure – current evidence and biological mechanisms

Abstract

Introduction and Objective. Microplastics are widespread environmental contaminants, and their potential impact on human health has attracted increasing scientific attention. Due to their small size and physicochemical properties, they may enter the human body mainly through ingestion and inhalation, and have been detected in several biological matrices, including placenta, blood and lung tissue. The aim of this review is to summarise current knowledge on the endocrine-disrupting effects of microplastics and their potential metabolic consequences. Brief description of the state of knowledge. Available evidence suggests that microplastics may interfere with endocrine function through oxidative stress, inflammatory signalling, interactions with endocrine-disrupting chemicals, and disruption of intracellular pathways involved in hormone synthesis. Human bio-monitoring studies confirm internal exposure, whereas experimental studies provide mechanistic data on activation of inflammatory pathways, impairment of steroidogenesis, altered insulin signalling, gut microbiota dysbiosis, and adipose tissue dysfunction. These mechanisms may affect major hormonal axes, including the HPA, HPT, and HPG axes, and contribute to disturbances in glucose and lipid metabolism, insulin resistance, and obesity-related processes. Summary. Current data suggest that microplastics may act as potential modulators of endocrine and metabolic processes. However, most mechanistic evidence comes from in vitro and animal studies, and direct causal relationships between microplastic exposure and endocrine or metabolic diseases in humans remain unconfirmed. Further studies using standardized analytical methods, reliable contamination control, and clinically relevant endocrine and metabolic endpoints are needed.