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

项目摘要 空气污染每年在美国造成超过213，000人死亡，在全球范围内仍然是第四位 死亡的主要原因。此外，大多数与空气污染相关的死亡是由于心血管（CV）疾病。 我们和其他人发现，短期空气污染暴露使收缩压（SBP）增加2- 10毫米汞柱，而长期暴露促进高血压（HTN）的发病-这是一个关键 从空气污染暴露到CV疾病风险的途径。然而，在支持以下观点的证据方面存在差距： 减少空气污染对CV不利影响的个人策略，以及改变公众环境所需的共识。 有关空气污染的政策仍然难以捉摸。在这一证据缺口得到解决之前，空气污染暴露仍将是一个问题。 HTN和后续CV疾病的潜在可改变但未治疗的风险因素。在这方面， 我们建议的目的是进行一项关键的临床试验，以测试室内个人空气净化器（PAC） 减少<2.5 µM（PM2.5）的细颗粒空气污染的设置-空气中最具血管毒性的成分 污染和较低的收缩压之间的一个队列的成人治疗和未治疗的HTN。数据来自我们的团队， 其他研究表明，PAC在3-10天内使SBP降低3-5 mmHg， 在肥胖的成年人中，这些益处可能是由炎性细胞因子的减少驱动的。在- 资源丰富的社区--如城市公共住房居民--同时体验室内和室外空气 污染不公平，肥胖和HTN的过度负担，以及持续不良健康的高风险 PM2.5暴露的影响。我们假设PAC以持续的方式降低PM2.5和降低SBP 在纽约市公共住房中治疗和未治疗的HTN成人中。为了验证这个假设，我们将 评估PAC是否在更长的临床相关时间范围内降低PM2.5和SBP， 比其他研究者迄今为止研究的队列。此外，我们将评估炎性细胞因子， 对PAC反应的SBP预测因子。在强有力的初步数据的指导下，本提案将追求三个具体目标， 目的：1）确定PAC是否在30、90和180天内降低早晨（AM）自测的家庭SBP（H-SBP） 在纽约市公共住房的440名接受治疗和未接受治疗的HTN成年人中; 2）测试是否有 高血压和肥胖增加与PAC相比， 3）确定较高的基线炎症细胞因子是否预示着较高的收缩压反应， PAC。这项建议是创新的，它使用自我测量家庭血压，空气污染监测， 肥胖和HTN负担过重的城市公共住房社区的细胞因子测量 而且意义重大，因为它将推进PAC是否可以用于减少PM2.5暴露的知识- 在个体水平上，血压降低，这是一个与CV疾病有因果关系的有意义的健康终点。 最终，这些知识可能会为数百万美国人和世界各地的人口提供一个获得 个人策略，以减少空气污染暴露对CV的不利影响。

PROJECT ABSTRACT 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 risk of 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. Under- resourced communities—such as urban public housing residents—experience both indoor and outdoor air pollution inequities, excess burdens of 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. Further, we will 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 may provide millions of Americans and populations worldwide with access to a personal strategy to reduce the adverse CV effects of air pollution exposure.