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.