Date on Master's Thesis/Doctoral Dissertation

12-2023

Document Type

Master's Thesis

Degree Name

M.S.

Department

Pharmacology and Toxicology

Degree Program

Pharmacology and Toxicology, MS

Committee Chair

O'Toole, Timothy

Committee Co-Chair (if applicable)

Haberzetti, Petra

Committee Member

Haberzetti, Petra

Committee Member

Moore IV, Joseph

Committee Member

Hein, David

Committee Member

Srivastava, Sanjay

Author's Keywords

particulate matter 2.5; telomeres; aging; epigenetics; cellular senescence; environmental exposure; air pollution

Abstract

In recent years, research into air pollution has shown that exposure to certain components in air pollution, primarily PM2.5 can accelerate biological aging and thereby lead to increased susceptibility to multiple diseases. We hypothesize that prolonged exposure to air pollutants can result in premature aging leading to extensive tissue dysfunction and susceptibility to diseases. To examine this, we exposed mice to PM2.5 for 9, 15, and 21 days, then measured the telomere lengths, cellular senescence, and histone methylation patterns of multiple cell types. We found consistently increased telomere attrition, cellular senescence and advanced age-consistent histone methylation patterns in groups exposed to PM2.5 across all examined cell types. Our investigation provides ample evidence that exposure to PM2.5 can cause premature aging and has the potential to lead to diseases such as cardiovascular disorders, type II diabetes, immune system dysfunction, and neurodegenerative disorders.

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