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Exposure to household air pollution from biomass cookstoves and biomarkers of systemic inflammation from dried blood spots among women in rural Honduras
Citation:
Benka-Coker, M., M. Clark, S. Rajkumar, B. Young, A. Bachand, D. Diaz-Sanchez, L. Neas, R. Brooke, T. Nelson, J. Volckens, S. Reynolds, A. Wilson, C. L'Orange, N. Good, C. Quinn, K. Koehler, S. Africano, A. Osorto-Pinel, AND J. Peel. Exposure to household air pollution from biomass cookstoves and biomarkers of systemic inflammation from dried blood spots among women in rural Honduras. International Society for Environmental Epidemiology (ISEE), Ottawa, Ontario, CANADA, August 26 - 30, 2018.
Impact/Purpose:
This abstract makes a modest contribution to the growing body of scientific knowledge concerning the role of cookstoves to indoor air quality and inflammatory markers.
Description:
Household air pollution from the burning of solid fuels for cooking and heating is estimated to cause 2.9 million deaths annually. Cardiovascular-related disease is a substantial contributor to the burden although evidence is limited. We evaluated the cross-sectional association of household air pollution with inflammatory markers, as indicators of cardiovascular health, among women in rural Honduras using traditional or cleaner-burning Justa stoves. We collected 24-hour exposure to gravimetric kitchen and personal fine particulate matter (PM2.5) and black carbon (BC) for 106 female primary cooks. The women provided a finger-stick dried blood spot sample from which markers of systemic inflammation (C-reactive protein [CRP], Serum Amyloid A [SAA], Interleukin 1-β [IL-1 β], IL-8, Tumor Necrosis Factor-α [TNF- α], Intercellular Adhesion Molecule 1 [ICAM-1], and Vascular Cell Adhesion Molecule [VCAM]) were measured. We used linear regression modeling, adjusting for age, body mass index, education, and number of assets. We observed that increased levels of 24-hour kitchen and personal PM2.5, and kitchen and personal BC were associated with increased levels of SAA (e.g. a 25% increase in personal PM2.5 was associated with a 10.5% increase in SAA levels [95% CI (confidence interval): 1.2-20.6]). Similar results were observed with CRP (e.g., a 25% increase in personal BC was associated with a 5.3% increase in CRP levels [95% CI: 2.2-8.5]). Results also demonstrated a positive association between kitchen BC and IL-8. No associations were observed between exposure and IL-1 β, TNF- α, ICAM-1, or VCAM. Results support the hypothesis that exposure to household air pollution is associated with markers of inflammation, such as CRP and SAA. Research should continue to assess the utility of dried blood in field studies as a means to measure indicators of future cardiovascular disease risk associated with household air pollution. This abstract does not necessarily reflect EPA policy.