Hypertension is the leading modifiable cardiovascular risk factor globally,1 with ≈25% of cardiovascular events attributed to hypertension. A large body of evidence supports that exposure to particulate matter air pollution, especially fine particulate matter (PM2.5), increases blood pressure (BP) and promotes hypertension. 2
Portable air cleaners (PACs) are an individual‐level intervention to decrease air pollution exposure. In our recent meta‐analysis, PACs reduced systolic BP by 4 mm Hg over a median of 6 (interquartile range, 2–14) days. 3 Studies to date did not use self‐measured home BP, a stronger predictor of cardiovascular risk and more accurate estimate of 24‐hour BP than office BP. 4 In addition, there is a dearth of evidence on the effects of PACs to reduce air pollution exposure and lower BP specifically in underresourced communities.
To address this gap and inform design of future trials, we conducted a randomized, double‐blind, sham‐controlled, pilot trial of PACs on self‐measured home blood pressure in adults with hypertension living in urban public housing. We hypothesized that continuous bedroom PAC use would reduce self‐measured morning (am) home systolic BP (H‐SBP) in an urban cohort of adults with hypertension. The data used in this study are available from the corresponding author on reasonable request. We enrolled 20 English‐ or Spanish‐speaking, nonsmoking adults with self‐reported hypertension from nonsmoking apartments in New York City public housing. Exclusion criteria included normal BP without antihypertensive medications or an enrollment visit BP >160/100 mm Hg. Participants were randomized in a 1:1 ratio to active versus sham PACs (without high efficiency particulate air filters). PACs were placed in participant bedrooms (or primary sleeping space, if studio apartments). Sham and active units were identical in appearance and sound. This study was approved by the NYU Grossman School of Medicine Institutional Review Board, and all subjects provided informed consent.
Participants measured home BP twice each morning, 1 minute apart, following American Heart Association guidelines. Deidentified measurements were transmitted to an online dashboard. A 3‐day run‐in phase was used to confirm eligibility. PACs were used continuously for 14 days. We used publicly available ambient outdoor PM2.5 concentration from New York State Department of Environmental Conservation monitoring stations within 1 km of home for background PM2.5. Indoor sources of PM2.5 were determined by self‐report. We analyzed outdoor mean (±SD) concentrations of PM2.5. We defined baseline am H‐SBP as the per‐person average in am H‐SBP measured during run‐in phase. Treatment phase am H‐SBP was the average per person of all am H‐SBP during treatment. Independent t‐tests compared (1) baseline am H‐SBP by arm, (2) treatment phase am H‐SBP by arm, and (3) difference in am H‐SBP between baseline and treatment phase by arm.
Study cohort included 20 non‐White adults (who self‐identified as non‐Hispanic Black, Hispanic or Latino, Asian, or American Indian or Alaska Native), 70% women, with mean (±SD) age of 55 (±14) years; the mean (±SD) body mass index was 33.7 (±6.2) kg/m2. Of the cohort, 65% had hypertension for >10 years; 85% reported antihypertensive medication use. Average ambient outdoor PM2.5 during run‐in phase was lower for active versus sham (5.1±0.1 versus 6.0±0.27 μg/m3; P<0.0001; Figure [A]), whereas during intervention, there was no difference in PM2.5 by arm (5.5±0.2 versus 5.75±0.1 μg/m3; P=0.24). All participants reported comparable exposures to known sources of indoor particulate matter.
Figure 1. Outdoor fine particulate matter (PM2.5) and home systolic blood pressure (BP) during run‐in and treatment phases.
A, Average outdoor PM2.5 by study arm during run‐in and treatment phases (representative time points shown; bars represent SD). B, Average systolic BP by study arm during run‐in and treatment phases (representative time points shown; bars represent SD).
During run‐in phase, baseline am H‐SBP was similar for participants randomized to active (133.6±1.99 mm Hg) versus sham (137.2±1.7 mm Hg) PACs (P=0.24). During treatment, there was a nonsignificant trend for a lower am H‐SBP for active (129.6±8.9 mm Hg) versus sham (134.6±9.6 mm Hg; P=0.25; Figure [B]). There was also a nonsignificant difference in am H‐SBP from baseline to treatment for participants randomized to active (5.67±10.08 mm Hg) versus sham (2.18±9.16 mm Hg) PACs (P=0.25).
In a cohort of nonsmoking adults with hypertension residing in public housing, there was a nonsignificant decrease in am H‐SBP over 14 days with PACs. The magnitude of BP reduction achieved with PACs among adults with hypertension could meaningfully reduce cardiovascular disease morbidity and mortality if sustained on a population level. 5 Limitations of this pilot study include cohort size and inability to source apportion and characterize PM2.5 composition. Also, because of cohort size, we were underpowered to investigate if the effects of PAC use on BP were mediated by reductions in PM2.5. Findings from this pilot study can be used to inform the design of future studies to establish use of PACs as a viable personal intervention to reduce the cardiovascular effects of air pollution.
Sources of Funding
Pilot funding for this study was provided by the NYU Grossman School of Medicine Cardiovascular Research Center.
Disclosures
None.
This work was presented in part at the Society for Epidemiologic Research Conference, June 14 to 17, 2022.
This article was sent to Kori S. Zachrison, MD, MSc, Associate Editor, for review by expert referees, editorial decision, and final disposition.
For Sources of Funding and Disclosures, see page 3.
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