Cardiovascular diseases (CVD) are the primary disease burden in the US. Extensive research has established exposure to air pollutants such as PM2.5 and ozone as cause or likely cause of increased CVD mortality and morbidity. While the US has made steady progress in reducing air pollution from industrial and vehicle emissions, recent increase in wildfires has slowed or even reversed this progress particularly in the Western US. Massive quantities of air pollutants in fire smoke can travel hundreds of kilometers affecting highly populated areas in states far from the original fire. As climate change is projected to substantially increase the already high wildfire risk in this region, there is an important public health need to establish the effects of smoke exposure, which has a distinctly different chemical composition from ambient air pollution, on CVD risks. Understanding the key distinctions between the cardiotoxic effects of smoke constituents is important to design effective emergency response measures to fire smoke, and to assess the long-term health care needs in the Western US. In this study, we will investigate the relationship between CVD risks and acute or chronic exposure to major air pollutants in smoke, including major PM2.5 constituents (i.e., sulfate, nitrate, organic carbon, elemental carbon), and gas pollutants such as ozone and formaldehyde (HCHO).
PUBLICATIONS (* = student author)
Project Publications
- In progress
Study locations: Arizona, California, Nevada, Utah, and Oregon
Investigators: Yang Liu (PI), Howard Chang
Funding Sources: National Institutes of Health
Category: Climate and Health