HOUSEHOLD AIR POLLUTION AND CARDIOMETABOLIC HEALTH AMONG ADULTS AND CHILDREN IN LOW-RESOURCE SETTINGS

Abstract

BackgroundHousehold air pollution (HAP) from the combustion of biomass fuels for domestic energy needs is a key driver of morbidity and mortality globally. The burden is highest in low and middle-income countries (LMICs), where solid fuel use is the primary source of energy for meeting cooking and heating needs. To address the burden of HAP, cleaner cooking solutions have been promoted; however, despite the reported reductions in HAP levels in some intervention studies, it is unclear whether these reductions translate into improved health outcomes. HAP, which is associated with various adverse health outcomes, including cardiovascular and metabolic health outcomes, primarily exerts its effects through mechanisms such as oxidative stress, systemic inflammation, and autonomic dysregulation. In LMIC regions like Africa and Latin America, where HAP exposure is high and cardiometabolic disease rates are rising across all demographic profiles, limited research has examined the impact of HAP on cardiometabolic disease risk. Against this background, this dissertation aims to provide evidence that contributes to our current understanding of how HAP-related interventions and exposures impact cardiometabolic disease burden across demographic profiles in low-resource settings. Methods and Results The first two chapters of this dissertation provide a detailed description of the scope and nature of the problem of HAP, including its exposures, solutions, and relationship with cardiometabolic outcomes. The first chapter provides a broad summary of the problem and outlines the aims of this dissertation, whereas the second chapter offers a comprehensive review of the literature on the relationship between HAP-related interventions and exposures and cardiometabolic outcomes. The third chapter of the dissertation provides detailed information on aims 1 and 2. Both aims leveraged data from a randomized stepped-wedge cookstove intervention conducted via a community-engaged lens among 230 female primary cooks in rural Honduras over three years, with six repeated measures of exposure and health endpoints about every six months. The first aim explores the impact of the intervention, an engineered biomass stove which was designed via a community-engaged process, the Justa, on inflammatory marker levels (C-reactive protein [CRP], interleukins 1ꞵ,6, and 8 [IL-1ꞵ, IL-6, and IL-8], and tumor necrosis factor-alpha [TNF-α]) via intent-to-treat (ITT) and per-protocol (self-reported stove-use) analyses using a linear mixed model. The second aim explores the exposure-response relationship between 24-hour averaged and long-term personal and kitchen levels of fine particulate matter (PM2.5 - particulate matter less than 2.5 microns in diameter) and black carbon (BC) exposures on the inflammatory marker levels (CRP, IL-1ꞵ, IL-6, IL-8, and TNF-α) via a linear mixed model. In brief, we did not observe an association between assigned use of the Justa intervention compared to traditional stove use and the inflammatory marker levels (e.g., CRP: -7.32%, 95% Confidence Interval [CI]: -18.54, 5.44; IL-8: 4.50%, 95% CI: -2.27, 11.74) or for the effect of self-reported cookstove use on the inflammatory marker levels. In the exposure-response analyses, we observed that higher HAP exposures were associated with higher levels of IL-8, TNF-, and IL-1ꞵ, but not with CRP or IL-6. The third aim which is divided in two chapters, Chapters 4 and 5 relied on data from a randomized controlled trial (the Sustainable Household Energy Adoption in Rwanda [SHEAR]) conducted among 626 households in rural Rwanda, which seeks to investigate the health impact of substituting traditional forms of household energy (biomass for cooking and kerosene for lighting) with solar power (for lighting) and liquefied petroleum gas stoves (for cooking). This aim explores the cross-sectional associations between 48-hour averaged personal PM2.5 and child (8-15 years) and adult blood pressure (BP) levels assessed at baseline; the children’s analysis is presented in Chapter 3, and the adult analysis is presented in Chapter 4. In the analysis among children, we did not observe evidence of an association between PM2.5 (per interquartile range [IQR] increase for all estimates) and BP levels (systolic BP [SBP]= 0.40mmHg, 95% confidence interval [CI]: -0.60, 1.40; diastolic BP [DBP]= -0.69mmHg, 95% CI: -1.50, 0.13). In the two-way (involving PM2.5 and sex) (SBP p-for-interaction= 0.06, DBP p-for-interaction=0.26 ) and three-way (involving PM2.5, sex, and age group) interaction analyses (SBP p-for-interaction = 0.43; DBP p-for-interaction = 0.19), we observed an inconsistent pattern of effect modification. For instance, in the former, we observed a positive association between PM2.5 exposure and SBP (1.16 mmHg, 95% CI: -0.12, 2.44) among male children. We did not observe associations among female children and across all DBP analyses. In the latter (the three-way interaction), we observed a negative association between PM2.5 exposure and DBP (-1.98 mmHg, 95% CI: -3.51, -0.46) among younger females (<13 years old). We did not observe associations across the other age and sex groups and across all SBP analyses. Among the adults, we also did not observe main effects evidence of a cross-sectional association between PM2.5 (per IQR increase) and BP (SBP= -0.41mmHg, 95% CI: -1.52, 0.71; DBP= -0.60mmHg, 95% CI: -1.30, 0.10). In the two-way interaction analysis (involving PM2.5 and sex), we did not observe evidence of effect modification (SBP p-for interaction= 0.95, DBP p-for interaction= 0.79). We did not observe an association across all sex-specific analyses. However, in the three-way interaction (involving PM2.5, sex, and age group), there was consistent evidence of effect modification, albeit with inconsistent patterns of association (SBP p-for-interaction= 0.002, DBP p-for-interaction= 0.32). For instance, among adult women, 41-50 years, an IQR higher PM2.5 was associated with 3.25 mmHg (95% CI: -6.08, -0.43) and 2.18 mmHg (95% CI: -3.93, -0.39) lower SBP and DBP, respectively. There was no evidence of associations in the other age-sex analyses. In summary, in these aims, we did not find evidence of an association between Justa stove assignment and inflammation, but found HAP exposures associated with inflammation and BP. However, the association with BP was weak and inconsistent across different demographic profiles. Overall, this dissertation offers a nuanced understanding of how HAP interventions and related exposures affect cardiometabolic outcomes in low-resource settings.