Particular Air Pollution Accelerates Aging, Cellular Senescence is a Mechanism
Epidemiological data clearly indicates that particulate air pollution accelerates late-life mortality and the incidence of age-related diseases. This is primarily attributed to the chronic inflammation of aging triggered by the interaction between inhaled particulates and lung tissue. Researchers are now exploring how cellular senescence plays a role in mediating the harmful effects of these particulates. The emergence of senolytic drugs, capable of selectively removing senescent cells from tissues, presents an opportunity to mitigate some of the consequences of particulate air pollution.
Exposure to particulate matter 2.5 (PM2.5) is known to accelerate aging, leading to a decline in tissue and organ function and increasing the risk of diseases like cardiovascular, neurodegenerative, and musculoskeletal disorders. PM2.5, a prevalent environmental pollutant, is now recognized as a catalyst for human aging and a predisposing factor for various age-related ailments.
With approximately 85% of the global population exposed to unsafe levels of air pollution, long-term exposure to pollutants is linked to adverse health outcomes such as dementia, type 2 diabetes, cardiovascular diseases, and lung cancer. Air pollution has become the fourth largest global burden of disease, emphasizing the need to investigate its impact on aging and age-related diseases.
This study aims to unravel the mechanisms through which PM2.5 induces cellular senescence, including genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, and mitochondrial dysfunction, all of which contribute to age-related diseases. By raising awareness among researchers about the toxicity of environmental pollutants, advocating for measures to reduce their production, and promoting personal and public health initiatives, we strive to enhance population protection and longevity in older adults.
