Worldwide, inhaled environmental exposures result in more than 12 million fatalities annually. Air pollution and tobacco use continue to be the major public health issues causing the rising incidence of respiratory illnesses, even in the face of regional initiatives to limit environmental exposures. This review describes how environmental exposures accelerate lung aging and cause lung illness. Silica and coal mining, tobacco, and fossil fuel usage induce lung inflammation and oxidative stress. DNA damage, epigenetic instability, mitochondrial malfunction, and cell cycle arrest in lung progenitor cells, which are crucial for lung expansion, can result from long-term oxidative stress. Consequently, vital healing processes are compromised, causing the lung parenchyma to prematurely degrade. By harming the lungs and the cells that repair wounds, inhaled environmental exposures hasten the aging process of the lungs. Taking steps to lower exposure to harmful antigens is important for improving lung health, and more research is needed to learn more about treatments that might slow down or stop lung aging before it starts.
Keywords: Lung inflammation, Oxidative stress, DNA damage, Mitochondrial dysfunction, Respiratory illnesses