Impacts of residential indoor air quality and environmental risk factors on adult asthma-related health outcomes in Chicago, IL.

BACKGROUND: Residential environments are known to contribute to asthma. OBJECTIVE: To examine the joint impacts of exposures to residential indoor and outdoor air pollutants and housing risk factors on adult asthma-related health outcomes. METHODS: We analyzed >1-year of data from 53 participants from 41 homes in the pre-intervention period of the Breathe Easy Project prior to ventilation and filtration retrofits. Health outcomes included surveys of asthma control, health-related quality of life, stress, and healthcare utilizations. Environmental assessments included quarterly measurements of indoor and outdoor pollutants (e.g., HCHO, CO, CO2, NO2, O3, and PM), home walk-throughs, and surveys of environmental risk factors. Indoor pollutant concentrations were also matched with surveys of time spent at home to estimate indoor pollutant exposures. RESULTS: Cross-sectional analyses using mixed-effects models indicated that lower annual average asthma control test (ACT) scores were associated (p < 0.05) with higher indoor NO2 (concentration/exposure: ß = -2.42/-1.57), indoor temperature (ß = -1.03 to -0.94), and mold/dampness (ß = -3.09 to -2.41). In longitudinal analysis, lower ACT scores were also associated (p < 0.05) with higher indoor NO2 concentrations (ß = -0.29), PM1 (concentration/exposure: ß = -0.12/-0.24), PM2.5 (concentration/exposure: ß = -0.12/-0.26), and PM10 (concentration/exposure: ß = 10.14/-0.28). Emergency department visits were associated with poorer asthma control [incidence rate ratio (IRR) = 0.84; p < 0.001], physical health (IRR = 0.95; p < 0.05), mental health (IRR = 0.95; p < 0.05), higher I/O NO2 ratios (IRR = 1.30; p < 0.05), and higher indoor temperatures (IRR = 1.41; p < 0.05). SIGNIFICANCE: Findings suggest that residential risk factors, including indoor air pollution (especially NO2 and particulate matter), higher indoor temperature, and mold/dampness, may contribute to poorer asthma control. IMPACT: This study highlights the importance of residential indoor air quality and environmental risk factors for asthma control, health-related quality of life, and emergency department visits for asthma. Two timescales of mixed models suggest that exposure to indoor NO2 and particulate matter, higher indoor temperature, and mold/dampness was associated with poorer asthma control. Additionally, emergency department visits were associated with poorer asthma control and health-related quality of life, as well as higher I/O NO2 ratios and indoor temperatures. These findings deepen our understanding of the interrelationships between housing, air quality, and health, and have important implications for programs and policy.

Characterization of the Cardiac Overexpression of HSPB2 Reveals Mitochondrial and Myogenic Roles Supported by a Cardiac HspB2 Interactome.

Small Heat Shock Proteins (sHSPs) are molecular chaperones that transiently interact with other proteins, thereby assisting with quality control of proper protein folding and/or degradation. They are also recruited to protect cells from a variety of stresses in response to extreme heat, heavy metals, and oxidative-reductive stress. Although ten human sHSPs have been identified, their likely diverse biological functions remain an enigma in health and disease, and much less is known about non-redundant roles in selective cells and tissues. Herein, we set out to comprehensively characterize the cardiac-restricted Heat Shock Protein B-2 (HspB2), which exhibited ischemic cardioprotection in transgenic overexpressing mice including reduced infarct size and maintenance of ATP levels. Global yeast two-hybrid analysis using HspB2 (bait) and a human cardiac library (prey) coupled with co-immunoprecipitation studies for mitochondrial target validation revealed the first HspB2 "cardiac interactome" to contain many myofibril and mitochondrial-binding partners consistent with the overexpression phenotype. This interactome has been submitted to the Biological General Repository for Interaction Datasets (BioGRID). A related sHSP chaperone HspB5 had only partially overlapping binding partners, supporting specificity of the interactome as well as non-redundant roles reported for these sHSPs. Evidence that the cardiac yeast two-hybrid HspB2 interactome targets resident mitochondrial client proteins is consistent with the role of HspB2 in maintaining ATP levels and suggests new chaperone-dependent functions for metabolic homeostasis. One of the HspB2 targets, glyceraldehyde 3-phosphate dehydrogenase (GAPDH), has reported roles in HspB2 associated phenotypes including cardiac ATP production, mitochondrial function, and apoptosis, and was validated as a potential client protein of HspB2 through chaperone assays. From the clientele and phenotypes identified herein, it is tempting to speculate that small molecule activators of HspB2 might be deployed to mitigate mitochondrial related diseases such as cardiomyopathy and neurodegenerative disease.