Particulate Air Pollution and Its Effects on the Mechanisms of Degenerative Aging

There is a great deal of data on air quality for researchers to peruse and link to the even larger set of data on human health and mortality. This has resulted in studies demonstrating strong correlations between higher levels of particulate air pollution and raised mortality, both in the context of exposure differences between large regions, and in the variations across a single metropolitan area. A large part of the problem is smoke, with industry, wildfires, and cooking fires all contributing to this issue to different degrees in different regions. Mechanistically, these particles lead to increased chronic inflammation through their interactions with lung tissue, and raised chronic inflammation contributes to the onset and progression of all of the common fatal age-related conditions.

Aging is a complex biological process involving multiple interacting mechanisms and is being increasingly linked to environmental exposures such as wildfire smoke. In this review, we detail the hallmarks of aging, emphasizing the role of telomere attrition, cellular senescence, epigenetic alterations, proteostasis, genomic instability, and mitochondrial dysfunction, while also exploring integrative hallmarks - altered intercellular communication and stem cell exhaustion. Within each hallmark of aging, our review explores how environmental disasters like wildfires, and their resultant inhaled toxicants, interact with these aging mechanisms. The intersection between aging and environmental exposures, especially high-concentration insults from wildfires, remains under-studied.

Preliminary evidence, from our group and others, suggests that inhaled wildfire smoke can accelerate markers of neurological aging and reduce learning capabilities. This is likely mediated by the augmentation of circulatory factors that compromise vascular and blood-brain barrier integrity, induce chronic neuroinflammation, and promote age-associated proteinopathy-related outcomes. Moreover, wildfire smoke may induce a reduced metabolic, senescent cellular phenotype. Future interventions could potentially leverage combined anti-inflammatory and NAD+ boosting compounds to counter these effects. This review underscores the critical need to study the intricate interplay between environmental factors and the biological mechanisms of aging to pave the way for effective interventions.


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