We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
A systematic review of microplastics in the environment: Sources, ageing processes, toxicity mechanisms, human health impacts, and remediation strategies
Summary
This review pulls together years of research on microplastics and finds that as these tiny plastic particles break down in the environment (from sun, heat, and weathering), they actually become more harmful—triggering more inflammation, cell damage, and oxidative stress in the body. Some plastics, like polystyrene (found in food containers) and PVC, seem especially likely to cause harm, particularly once they've broken into smaller pieces. While most evidence so far comes from lab and animal studies rather than large human health studies, the findings suggest that "aged" microplastics circulating in our air, water, and food could pose a bigger health risk than previously assum
Microplastics are ubiquitous contaminants of the environment that are increasingly threatening to ecosystems and human health because of their persistence, widespread distribution and ability to interact biologically. Their toxicological properties depend on various factors such as polymer structure, particle size, surface properties, and environmental changes. Microplastics degrade by ageing (through photoaging, thermal degradation, mechanical weathering, chemical oxidation, and biological degradation), which collectively change their physicochemical properties and enhance their biological reactivity. Such changes usually lead to surface oxidation, increased pollutant adsorption, increased hydrophilicity, and increased bioavailability, thus modulating toxicity. The review is a critical synthesis of the existing evidence on the biological toxicity of microplastics, with a particular focus on how environmental ageing contributes to changes in toxicity profiles among the polymer types. The articles published in the period 2020-2025 were reviewed to assess the impact of polymer composition, particle size, and ageing on oxidative stress, inflammation, genotoxicity, and other biological outcomes related to exposure to microplastics. Oxidative stress and inflammatory signalling consistently appeared as central mediators of toxicity in a range of experimental systems, and they play a role in mitochondrial pathology, apoptosis, DNA damage and metabolic disturbance. Environmental ageing was also discovered to enhance the microplastic toxicity by increasing the generation of reactive oxygen species, promoting the adsorption of co-contaminants and altering the particle surface chemistry. Polymer-specific effects were also evident, with polyethylene terephthalate (PET) and polyvinyl chloride (PVC) commonly implicated in increased cytotoxicity, and polystyrene was significantly implicated in high genotoxic and inflammatory effects, especially after the ageing process had occurred, or the polymer had been reduced in size. Polyethylene tended to have lower acute toxicity and oxidative and endocrine-disrupting effects under environmentally transformed conditions. Microplastics were linked to oxidative, reproductive, developmental, and behavioural dysfunction in aquatic and terrestrial organisms at the ecological and organismal levels. There is evidence of possible multi-organ toxicity based on human-relevant models, but limited epidemiological evidence is present. In general, the toxicity of microplastics is a multifactorial process that is predetermined by the interaction of polymer properties, particle size, and environmental ageing. These findings justify the need to have standardised methodologies, environmentally relevant exposure models, and integrated risk assessment frameworks to gain a better understanding and mitigate the biological and ecological risks related to microplastic pollution.