Key result
Personal household PM2.5 exposure is not associated with blood pressure changes in rural Rwandan children.
Why the study?
Evidence of household air pollution's impact on blood pressure among children in low-resource settings is limited.
Does exposure to household air pollution (PM2.5 and black carbon) increase blood pressure in children living in rural Rwanda?
Cross-Sectional (n=622)
No
Does exposure to household air pollution (PM2.5 and black carbon) increase blood pressure in children living in rural Rwanda?
Mean Difference: 0.51 (95% CI -0.46–1.49)
Despite the lack of clear associations between household air pollution and blood pressure, the study reveals a highly elevated burden of undiagnosed hypertension among children in rural Rwanda compared to US references, indicating a critical need for localized pediatric cardiovascular screening.
Suggests acute household air pollution may not drive pediatric hypertension in this setting; leaves open the need for.
Household air pollution (HAP) contributes to the global cardiovascular disease burden. Early life exposures may impact future disease risk; however, evidence of HAP’s impact on blood pressure (BP) among children in low-resource settings is limited. We assessed baseline cross-sectional associations between personal exposure to fine particulate matter (PM 2.5 ) and black carbon (BC) and children’s (8–15 years) systolic and diastolic BP (SBP, DBP) from the Sustainable Household Energy Adoption in Rwanda study. We enrolled 626 households in rural Eastern Rwanda that used traditional biomass fuels for cooking. Children wore Ultrasonic Personal Aerosol Samplers for 48 h monitoring of personal exposure, followed by BP measurement using standard protocols. Multiple linear regression was used to characterize associations between PM 2.5 and BC exposure and BP in separate models; effect modification by age and sex was evaluated. Among 622 children (mean age = 11.8 years, standard deviation [SD] = 2.1; males = 303, females = 319), the average SBP and DBP were 105.8 mmHg (SD = 10.0) and 68.3 mmHg (SD = 7.6), respectively. BP percentiles were higher than those in a US reference population (e.g. 59.0% and 85.5% had SBP and DBP percentiles >50th, respectively; 24% were classified as having elevated BP and/or were hypertensive, defined as ⩾90th percentile). The median 48 h PM 2.5 and BC concentrations were 192.9 µ g m −3 (25th percentile [ Q 1] = 119.7, 75th percentile [ Q 3] = 336.0) and 9.85 µ g m −3 ( Q 1 = 6.56, Q 3 = 13.23), respectively. We did not observe evidence of associations between HAP and BP levels (e.g. PM 2.5 –SBP = 0.51 mmHg per interquartile range [IQR, 211.7 μ g m −3 ] increase, 95% confidence interval: −0.46, 1.49). We did not observe clear evidence of effect modification. Exposures well above international health-based guidelines may have limited our ability to observe associations if the true exposure–response is flat in that part of the global exposure continuum. Importantly, our BP data suggest an elevated cardiovascular disease burden among children in this low-resource setting compared to in the US, demonstrating a need for more research and the development of more appropriate reference data in these settings. ClinicalTrials.gov Identifier: NCT05668624.
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Sewor et al. (2026) conducted a cross-sectional in Household air pollution exposure and blood pressure (n=622). Household air pollution (PM2.5 and black carbon) vs. Lower exposure levels (per interquartile range increase) was evaluated on Systolic blood pressure (0.51 mmHg per IQR increase, 95% CI -0.46, 1.49). Personal exposure to household PM2.5 was not significantly associated with systolic blood pressure (0.51 mmHg per IQR increase) or diastolic blood pressure among children in rural Rwanda.
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