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Indoor Air. 2016 Oct;26(5):768-75. doi: 10.1111/ina.12259. Epub 2015 Nov 26.

Chronic exposure to biomass fuel smoke and markers of endothelial inflammation.

Author information

1
Division of Pulmonary and Critical Care, School of Medicine, Johns Hopkins University, Baltimore, MD, USA.
2
Cardiovascular Division, Cardiovascular Imaging and Clinical Research Core Laboratory, Washington University School of Medicine, St. Louis, MO, USA.
3
Program in Global Disease Epidemiology and Control, Department of International Health, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
4
CRONICAS Center of Excellence for Chronic Diseases, Universidad Peruana Cayetano Heredia, Lima, Peru.
5
Department of Medicine, School of Medicine, Universidad Peruana Cayetano Heredia, Lima, Peru.
6
Division of Pulmonary and Critical Care, School of Medicine, Johns Hopkins University, Baltimore, MD, USA. wcheckl1@jhmi.edu.
7
Program in Global Disease Epidemiology and Control, Department of International Health, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA. wcheckl1@jhmi.edu.
8
CRONICAS Center of Excellence for Chronic Diseases, Universidad Peruana Cayetano Heredia, Lima, Peru. wcheckl1@jhmi.edu.

Abstract

Indoor smoke exposure may affect cardiovascular disease (CVD) risk via lung-mediated inflammation, oxidative stress, and endothelial inflammation. We sought to explore the association between indoor smoke exposure from burning biomass fuels and a selected group of markers for endothelial inflammation. We compared serum concentrations of amyloid A protein, E-selectin, soluble intercellular adhesion molecule 1 (ICAM-1) and VCAM-1, von Willebrand factor (vWF), and high-sensitivity C-reactive protein (hs-CRP) in 228 biomass-exposed vs. 228 non-exposed participants living in Puno, Peru. Average age was 56 years (s.d. = 13), average BMI was 26.5 kg/m(2) (s.d. = 4.4), 48% were male, 59.4% completed high school, and 2% reported a physician diagnosis of CVD. In unadjusted analysis, serum levels of soluble ICAM-1 (330 vs. 302 ng/ml; P < 0.001), soluble VCAM-1 (403 vs. 362 ng/ml; P < 0.001), and E-selectin (54.2 vs. 52.7 ng/ml; P = 0.05) were increased in biomass-exposed vs. non-exposed participants, respectively, whereas serum levels of vWF (1148 vs. 1311 mU/ml; P < 0.001) and hs-CRP (2.56 vs. 3.12 mg/l; P < 0.001) were decreased, respectively. In adjusted analyses, chronic exposure to biomass fuels remained positively associated with serum levels of soluble ICAM-1 (P = 0.03) and VCAM-1 (P = 0.05) and E-selectin (P = 0.05), and remained negatively associated with serum levels of vWF (P = 0.02) and hs-CRP (P < 0.001). Daily exposure to biomass fuel smoke was associated with important differences in specific biomarkers of endothelial inflammation and may help explain accelerated atherosclerosis among those who are chronically exposed.

KEYWORDS:

Biomass fuel exposure; Cardiovascular disease; Endothelial inflammation biomarkers; Epidemiology; Household air pollution; Rural communities

PMID:
26476302
PMCID:
PMC4935667
DOI:
10.1111/ina.12259
[Indexed for MEDLINE]
Free PMC Article

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