Abstract 19288: Acute and Chronic Affects of Indoor Air Pollution on Endothelial Function
Objective: Pollution exposure has been linked to accelerated atherosclerosis. Endothelial dysfunction is a reversible indicator for early atherosclerosis, but it is unknown if indoor air pollution from biomass fuel cookstoves is associated with acute and chronic endothelial dysfunction.
Methods: We enrolled 76 adults in Puno, Peru (3825 m above sea level); 56 from a rural community that almost exclusively use biomass fuels for cooking (biomass fuel users) and 20 from urban communities that use clean fuels for cooking (clean fuel users). We measured flow-mediated dilatation (FMD) of the brachial artery before and after cooking. We compared baseline FMD in biomass vs. clean fuel users and evaluated for acute effects of cooking by looking and changes in FMD before and after cooking with biomass vs. clean fuels
Results: Mean age was 53 ± 9.1 years with 54% male. Biomass fuel users had similar age, blood pressure, and BMI but had lower LDL-cholesterol compared to clean fuel users (p<0.05). Mean baseline FMD was 5.2 ± 2.3% vs. 6.3 ± 3.2% in clean vs. biomass fuel users respectively (p=0.22). Adjusting for age, sex, blood pressure, BMI, and LDL-cholesterol demonstrated no difference in baseline FMD between biomass and clean fuel users (p=0.92). Among biomass fuel users, mean FMD dropped to 3.8 ± 3.0% after one hour of biomass fuel smoke exposure from cooking (p<0.001). This did not occur when FMD was repeated in clean fuel users one hour after baseline exam (FMD: 4.9 ± 2.9%, p=0.29).
Conclusion: Biomass fuel smoke exposure causes acute decrease in endothelial function in this population with already abnormal function. However, we found no differences in baseline endothelial function in these two heterogeneous populations. Larger studies are needed to determine if biomass fuel exposure is associated with chronic endothelial dysfunction and if interventions aimed to decrease biomass fuel smoke exposure can improve endothelial function and thus cardiovascular mortality.
Author Disclosures: C.H. Miele: None. M. Iantorno: None. R.G. Weiss: None. R.H. Gilman: None. G. Valdivia: None. R.A. Wise: None. V.G. Davila-Roman: None. W. Checkley: None.
- © 2015 by American Heart Association, Inc.