AirPressureNYC: Reducing AIR pollution to lower blood PRESSURE among New York City public housing residents

Air pollution is responsible for >213,000 excess deaths in the U.S. annually, and globally remains the 4th leading cause of mortality. Further, most air pollution-related mortality is due to cardiovascular (CV) disease. We and others have found that short term air pollution exposure increases systolic blood pressure (SBP) by 2-10 mmHg, while longer term exposure promotes the onset of hypertension (HTN)—which represents a key pathway from air pollution exposure to CV disease. However, there is a gap in evidence in support of personal strategies to reduce the adverse CV effects of air pollution, and consensus required to change public policy on air pollution remains elusive. Until this evidence gap is addressed, air pollution exposure will remain a potentially modifiable yet untreated risk factor for HTN and subsequent CV disease. In this context, the overall objective of our proposal is to perform a pivotal clinical trial to test personal air cleaners (PACs) in indoor settings to reduce fine particulate air pollution <2.5 µM (PM2.5)—the most vasculotoxic component of air pollution—and lower SBP among a cohort of adults with treated and untreated HTN. Data from our group and others show that PACs lower SBP by 3-5 mmHg over 3-10 days, have larger (≈8mmHg) reductions in SBP among obese adults, and that these benefits may be driven by reductions in inflammatory cytokines. Many Americans—including urban public housing residents—experience both indoor and outdoor air pollution, in addition to obesity and HTN, and are at high risk for the persistent adverse health effects from PM2.5 exposure. We hypothesize that PACs reduce PM2.5 and lower SBP in a sustained fashion among adults with treated and untreated HTN in New York City public housing. To test this hypothesis, we will evaluate whether PACs reduce PM2.5 and SBP over longer, clinically relevant time horizons, and in a larger cohort than studied by other investigators to date. We will also evaluate inflammatory cytokines as predictors of SBP response to PACs. Guided by strong preliminary data, this proposal will pursue three specific aims: 1) Determine if PACs lower morning (AM) self-measured home SBP (H-SBP) over 30, 90 and 180 days among 440 adults with treated and untreated HTN living in New York City public housing; 2) Test if adults with HTN and increased adiposity have larger decreases in morning H-SBP with PACs compared to adults with less adiposity; and 3) Determine whether higher baseline inflammatory cytokines predict a greater SBP response to PACs. This proposal is innovative in its use of self-measured home blood pressure, air pollution monitoring, and cytokine measurements in an urban public housing community with excess burdens of obesity and HTN and is significant because it will advance knowledge of whether PACs can be used to reduce PM2.5 exposure on an individual level and lower blood pressure, a meaningful health endpoint causally linked to CV disease. Ultimately, such knowledge could provide millions of Americans and populations worldwide with access to a personal strategy to reduce the adverse CV effects of air pollution exposure.