Microplastic and Nanoplastic Exposure in the Context of Aging
Animal studies show that ascending doses of nanoplastic particle infiltration into tissues eventually rise to the level of inducing dysfunction. Evidently harmful nanoplastic exposure doses are considerably higher than what are thought to be environmental exposure doses in the wild at the present time, but equally it is challenging, costly, and takes a long time to build a body of literature focused on subtle effects that may only emerge over the long term to affect the pace of aging. This is a work in progress.
The difference between nanoplastics and particulate air pollution is that there is a very large body of evidence to quantify the harms done by exposure to air pollution in human populations, alongside convincing mechanistic studies to show how long-term health and pace of aging can be negatively impacted. That body of evidence has yet to be constructed for nanoplastic exposure in human populations, so while there is a great deal of concern around this topic, it is unclear as to how much of that concern is justified. The level of interest in the topic means that the necessary epidemiological and supporting mechanistic data, analogous to the existing body of work covering air pollution, will almost certainly be produced in the years ahead, however.
Microplastics and nanoplastics (MNPs) are pervasive environmental contaminants with growing relevance for human health across the lifespan. Older adults may be especially vulnerable to their effects due to cumulative lifetime exposure, age-related physiological changes, and a higher burden of chronic disease. Adopting a One Health perspective, this review synthesizes current evidence on the sources, exposure pathways, and biological effects of MNPs, integrating findings from environmental, animal, and human studies with a specific focus on aging populations.
Experimental studies consistently show that MNP exposure triggers oxidative stress, inflammation, mitochondrial dysfunction, and cellular senescence, mechanisms central to biological aging. These processes are linked to dysfunction of the cardiovascular, nervous, gastrointestinal, and immune systems, suggesting that MNPs may contribute to the development or progression of age-related diseases. Within the One Health framework, MNPs also act as carriers of chemical additives and environmental pollutants, potentially amplifying health risks through combined and cumulative exposures along food chains and ecosystems.
Despite increasing mechanistic evidence, direct epidemiological data in older adults remain limited. This review highlights key knowledge gaps and emphasizes the need for integrative, longitudinal research to clarify the role of MNPs in aging and to inform public health and environmental policy.