| Literature DB >> 33749948 |
Magdalena Fandiño-Del-Rio1,2, Josiah L Kephart1,2, Kendra N Williams2,3, Gary Malpartida4,5, Dana Boyd Barr6, Kyle Steenland6, Kirsten Koehler1, William Checkley2,3.
Abstract
Household air pollution (HAP) from biomass stoves is a leading risk factor for cardiopulmonary outcomes; however, its toxicity pathways and relationship with inflammation markers are poorly understood. Among 180 adult women in rural Peru, we examined the cross-sectional exposure-response relationship between biomass HAP and markers of inflammation in blood using baseline measurements from a randomized trial. We measured markers of inflammation (CRP, IL-6, IL-10, IL-1β, and TNF-α) with dried blood spots, 48-h kitchen area concentrations and personal exposures to fine particulate matter (PM2.5 ), black carbon (BC), and carbon monoxide (CO), and 48-h kitchen concentrations of nitrogen dioxide (NO2 ) in a subset of 97 participants. We conducted an exposure-response analysis between quintiles of HAP levels and markers of inflammation. Markers of inflammation were more strongly associated with kitchen area concentrations of BC than PM2.5 . As expected, kitchen area BC concentrations were positively associated with TNF-α (pro-inflammatory) concentrations and negatively associated with IL-10, an anti-inflammatory marker, controlling for confounders in single- and multi-pollutant models. However, contrary to expectations, kitchen area BC and NO2 concentrations were negatively associated with IL-1β, a pro-inflammatory marker. No associations were identified for IL-6 or CRP, or for any marker in relation to personal exposures.Entities:
Keywords: biomass stoves; black carbon; exposure-response; fine particulate matter; household air pollution; markers of inflammation
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Year: 2021 PMID: 33749948 PMCID: PMC8380676 DOI: 10.1111/ina.12814
Source DB: PubMed Journal: Indoor Air ISSN: 0905-6947 Impact factor: 6.554