Epidemiological data clearly shows that particulate air pollution increases late life mortality and incidence of age-related disease. The primary mechanism is thought to be an increase in the chronic inflammation of aging induced by the interaction between inhaled particulates and lung tissue. Here, researchers focus on the degree to which cellular senescence mediates the harms caused by particulates. The advent of senolytic drugs capable of selectively clearing senescent cells from tissues offer a change to reduce some of the consequences of particulate air pollution.
Exposure to particulate matter 2.5 (PM2.5) accelerates aging, causing declines in tissue and organ function, and leading to diseases such as cardiovascular, neurodegenerative, and musculoskeletal disorders. PM2.5 is a major environmental pollutant and an exogenous pathogen in air pollution that is now recognized as an accelerator of human aging and a predisposing factor for several age-related diseases.
Approximately 85% of the global population is exposed to air pollution levels above safe limits. Long-term exposure to air pollutants is associated with an increased risk of adverse health outcomes such as dementia, type 2 diabetes, cardiovascular diseases, and lung cancer. Air pollution is now the fourth largest global burden of disease. Therefore, it is imperative to scrutinize the role of air pollution in aging and age-related diseases.
In this paper, we seek to elucidate the mechanisms by which PM2.5 induces cellular senescence, such as genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, and mitochondrial dysfunction, and age-related diseases. Our goal is to increase awareness among researchers within the field of the toxicity of environmental pollutants and to advocate for personal and public health initiatives to curb their production and enhance population protection. Through these endeavors, we aim to promote longevity and health in older adults.
Link: https://doi.org/10.1016/j.ecoenv.2024.116920
View the full article at FightAging
