Air pollution may increase children’s risk of heart disease in adulthood

A new Stanford study shows that children exposed to air pollution through wildfire smoke, car exhaust, etc. can lead to adult heart disease.

These new findings confirm previous research on air pollution altering gene regulation, which will reframe the way health experts think about the air that their children breathe.

“It looks like even brief air pollution exposure can actually change the regulation and expression of children’s genes and perhaps alter blood pressure, potentially laying the foundation for increased risk of disease later in life”, says study lead author Mary Prunicki, director of air pollution and health research at Stanford’s Sean N. Parker Center for Allergy & Asthma Research.

The study focused on a group of Hispanic children ages 6-8 in Fresno, California, where the nation’s highest air pollution levels stem from wildfires and industrial agriculture.

The researchers used a combination of continuous daily pollutant concentrations measured at central air monitoring stations in Fresno. The study team estimated average air pollution exposures for 1 day, 1 week, and 1, 3, 6, and 12 months before visiting each child. When combined with health and demographics questionnaires, blood pressure readings, and blood samples, the data reinforced the preconceptions that the team had in mind.

Exposure to a fine particulate known as PM2.5, carbon monoxide, and ozone over time is linked to increased methylation, a phenomenon of DNA molecules that alter their activity without changing their genetic sequence. This alteration may be passed down to future generations.

The researchers also found that air pollution exposure correlates with an increase in white blood cells, which participate in the buildup of plaques in arteries, potentially predisposing children to heart disease in adulthood. Future studies must be conducted to verify the long-term implications.