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Household air pollution is a leading risk factor for morbidity and premature mortality. Numerous cookstoves have been developed to reduce household air pollution, but it is unclear whether such cookstoves meaningfully improve health. In a controlled exposure study with a crossover design, we assessed the effect of pollution emitted from multiple cookstoves on acute differences in blood lipids and inflammatory biomarkers. Participants (n = 48) were assigned to treatment sequences of exposure to air pollution emitted from five cookstoves and a filtered-air control. Blood lipids and inflammatory biomarkers were measured before and 0, 3, and 24 hours after treatments. Many of the measured outcomes had inconsistent results. However, compared to control, intercellular adhesion molecule-1 was higher 3 hours after all treatments, and C-reactive protein and serum amyloid-A were higher 24 hours after the highest treatment. Our results suggest that short-term exposure to cookstove air pollution can increase inflammatory biomarkers within 24 hours.

BACKGROUND Lower socioeconomic status (SES) has been associated with hypertension; however, the mediators and moderators of this association remain understudied. We examined the mediation effect of psychological distress on the link between lower SES and self-reported hypertension and the racial and sex moderation effects. METHODS We analyzed the data collected from 2009 to 2019 among adults from the Panel Study of Income Dynamics (PSID). Lower SES was defined as one of 3 indicators: education ≤12 years, unemployed, or individual annual income <$27,800. Psychological distress was assessed using the Kessler K6 scale. Cox proportional hazard regression was conducted. Mediation analyses were performed using the PROCESS macro. RESULTS In the sample of heads of family who did not have self-reported hypertension in 2009 (N  = 6,214), the mean age was 41 years, 30.6% were female, 32.9% were African American. The cumulative incidence of self-reported hypertension was 29.8% between 2009 and 2019. Cox proportional hazard regression analysis showed that after controlling for covariates, lower SES (score > 0 vs. score = 0) was associated with self-reported hypertension (hazard ratio = 1.27, 95% confidence interval = 1.14–1.42). SES had indirect effect on self-reported hypertension through psychological distress and the indirect effect (0.02 in females, 0.01 in males, P  < 0.05) was moderated by sex but not by race. CONCLUSIONS The association of SES and self-reported hypertension was mediated by psychological distress and sex moderated the mediation effect. Interventions focused on reducing contributors to SES and psychological stress should be considered to reduce hypertension risk. [ABSTRACT FROM AUTHOR]

Background: The Reducing Air Pollution in Detroit Intervention Study (RAPIDS) was designed to evaluate cardiovascular health benefits and personal fine particulate matter (particulate matter < 2.5 μm in diameter, PM2.5) exposure reductions via portable air filtration units (PAFs) among older adults in Detroit, Michigan. This double-blind randomized crossover intervention study has shown that, compared to sham, air filtration for 3 days decreased 3-day average brachial systolic blood pressure by 3.2 mmHg. The results also showed that commercially available HEPA-type and true HEPA PAFs mitigated median indoor PM2.5 concentrations by 58% and 65%, respectively. However, to our knowledge, no health intervention study in which a significant positive health effect was observed has also evaluated how outdoor and indoor PM2.5 sources impacted the subjects. With that in mind, detailed characterization of outdoor and indoor PM2.5 samples collected during this study and a source apportionment analysis of those samples using a positive matrix factorization model were completed. The aims of this most recent work were to characterize the indoor and outdoor sources of the PM2.5 this community was exposed to and to assess how effectively commercially available HEPA-type and true HEPA PAFs were able to reduce indoor and outdoor PM2.5 source contributions. Methods: Approximately 24 h daily indoor and outdoor PM2.5 samples were collected on Teflon and Quartz filters from the apartments of 40 study subjects during each 3-day intervention period. These filters were analyzed for mass, carbon, and trace elements. Environmental Protection Agency Positive Matrix Factorization (PMF) 5.0 was utilized to determine major emission sources that contributed to the outdoor and indoor PM2.5 levels during this study. Results: The major sources of outdoor PM2.5 were secondary aerosols (28%), traffic/urban dust (24%), iron/steel industries (15%), sewage/municipal incineration (10%), and oil combustion/refinery (6%). The major sources of indoor PM2.5 were organic compounds (45%), traffic + sewage/municipal incineration (14%), secondary aerosols (13%), smoking (7%), and urban dust (2%). Infiltration of outdoor PM2.5 for sham, HEPA-type, and true HEPA air filtration was 79 ± 24%, 61 ± 32%, and 51 ± 34%, respectively. Conclusions: The results from our study showed that intervention with PAFs was able to significantly decrease indoor PM2.5 derived from outdoor and indoor PM2.5 sources. The PAFs were also able to significantly reduce the infiltration of outdoor PM2.5. The results of this study provide insights into what types of major PM2.5 sources this community is exposed to and what degree of air quality and systolic blood pressure improvements are possible through the use of commercially available PAFs in a real-world setting. [ABSTRACT FROM AUTHOR]

Background Serious cardiovascular health disparities persist across the United States, disproportionately affecting Black communities. Mounting evidence supports negative social determinants of health (SDoH) as contributing factors to a higher prevalence of hypertension along with lower control rates. Here, we describe a first-of-a-kind approach to reducing health disparities by focusing on preventing hypertension in Black adults with elevated blood pressure (BP) living in socially vulnerable communities. Methods and Results Linkage, Empowerment, and Access to Prevent Hypertension (LEAP-HTN) is part of the RESTORE (Addressing Social Determinants to Prevent Hypertension) health equity research network. The trial will test if a novel intervention reduces systolic BP (primary outcome) and prevents the onset of hypertension over 1 year versus usual care in 500 Black adults with elevated BP (systolic BP 120–129 mm Hg; diastolic BP <80 mm Hg) in Detroit, Michigan. LEAP-HTN leverages our groundbreaking platform using geospatial health and social vulnerability data to direct the deployment of mobile health units (MHUs) to communities of greatest need. All patients are referred to primary care providers. Trial participants in the active limb will receive additional collaborative care delivered remotely by community health workers using an innovative strategy termed pragmatic, personalized, adaptable approaches to lifestyle, and life circumstances (PAL2) which mitigates the impact of negative SDoH. Conclusions LEAP-HTN aims to prevent hypertension by improving access and linkage to care while mitigating negative SDoH. This novel approach could represent a sustainable and scalable strategy to overcoming health disparities in socially vulnerable communities across the United States. [ABSTRACT FROM AUTHOR]

Patients with chronic obstructive pulmonary disease (COPD) may suffer from acute episodes of worsening dyspnea, often associated with increased cough, sputum, and/or sputum purulence. These exacerbations of COPD (ECOPDs) impact health status, accelerate lung function decline, and increase the risk of hospitalization. Importantly, close to 20% of patients are readmitted within 30 days after hospital discharge, with great cost to the person and society. Approximately 25% and 65% of patients hospitalized for an ECOPD die within 1 and 5 years, respectively. Patients with COPD are usually older and frequently have concomitant chronic diseases, including heart failure, coronary artery disease, arrhythmias, interstitial lung diseases, bronchiectasis, asthma, anxiety, and depression, and are also at increased risk of developing pneumonia, pulmonary embolism, and pneumothorax. All of these morbidities not only increase the risk of subsequent ECOPDs but can also mimic or aggravate them. Importantly, close to 70% of readmissions after an ECOPD hospitalization result from decompensation of other morbidities. These observations suggest that in patients with COPD with worsening dyspnea but without the other classic characteristics of ECOPD, a careful search for these morbidities can help detect them and allow appropriate treatment. For most morbidities, a thorough clinical evaluation supplemented by appropriate clinical investigations can guide the healthcare provider to make a precise diagnosis. This perspective integrates the currently dispersed information available and provides a practical approach to patients with COPD complaining of worsening respiratory symptoms, particularly dyspnea. A systematic approach should help improve outcomes and the personal and societal cost of ECOPDs. [ABSTRACT FROM AUTHOR]