Air pollution particles lodge deep in the lungs of infants and unborn children, and decades later those same people may develop asthma—but no one knows why. This project tackles that gap. Asthma affects over 300 million people worldwide, and early-life exposure to fine particulate matter (PM2.5) is a known risk factor for developing the disease later. Yet the biological mechanism remains unknown. The researchers suspect a form of "biological memory" in the two main cell types of the lung’s air sacs—epithelial cells and macrophages—caused by epigenetic modifications from early exposure. They will test this by exposing cells and animal models to different particulate aerosol components and tracking what changes occur in cell function. If the hypothesis holds, it would reveal a concrete biological pathway linking a common environmental exposure to a chronic disease that appears years later. That could shift how air quality regulations are designed—for example, by identifying which particulate components are most hazardous during pregnancy and infancy—and open the door to early interventions that prevent asthma before symptoms ever begin.
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Air pollution comprises a complex mix of gases and particulate matter (PM) that are both detrimental to health, increasing morbidity and mortality. Fine PM (PM2.5) is known for its capacity to infiltrate the alveolar region of the lungs. PM2.5 is strongly associated with respiratory diseases, including asthma. Asthma is a chronic respiratory disease that affects more than 300 million people worldwide. Environmental factors, including exposure to PMs, play a significant role in the development and exacerbation of asthma. Exposure to air pollution in early life, particularly during critical pre-natal developmental windows and in infancy, has been shown to increase potential to develop asthma vulnerability later in life. However, the cellular and biological reasoning of this susceptibility is still unknown, though a form of biological memory in the two main cell types of the alveoli, namely epithelial cells and macrophages, is suspected. This proposal aims to test the hypothesis that early life exposure to PM cause epigenetic modifications in those cells, and that these changes may contribute to asthma in later life. Three main objectives will be carried out to determine which particulate aerosol components may be more hazardous and the changes that happen to epithelial and macrophage function following particulate exposure using a combination of in vitro and in vivo models and their respective exposure systems.
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