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Acute Effects on Blood Pressure Following Controlled Exposure to Cookstove Air Pollution in the STOVES Study.

ABSTRACT: Background Exposure to air pollution from solid fuel used in residential cookstoves is considered a leading environmental risk factor for disease globally, but evidence for this relationship is largely extrapolated from literature on smoking, secondhand smoke, and ambient fine particulate matter ( PM 2.5). Methods and Results We conducted a controlled human-exposure study (STOVES [the Subclinical Tests on Volunteers Exposed to Smoke] Study) to investigate acute responses in blood pressure following exposure to air pollution emissions from cookstove technologies. Forty-eight healthy adults received 2-hour exposures to 5 cookstove treatments (three stone fire, rocket elbow, fan rocket elbow, gasifier, and liquefied petroleum gas), spanning PM 2.5 concentrations from 10 to 500 ?g/m3, and a filtered air control (0 ?g/m3). Thirty minutes after exposure, systolic pressure was lower for the three stone fire treatment (500 ?g/m3 PM 2.5) compared with the control (-2.3 mm Hg; 95% CI, -4.5 to -0.1) and suggestively lower for the gasifier (35 ?g/m3 PM 2.5; -1.8 mm Hg; 95% CI , -4.0 to 0.4). No differences were observed at 3 hours after exposure; however, at 24 hours after exposure, mean systolic pressure was 2 to 3 mm Hg higher for all treatments compared with control except for the rocket elbow stove. No differences were observed in diastolic pressure for any time point or treatment. Conclusions Short-term exposure to air pollution from cookstoves can elicit an increase in systolic pressure within 24 hours. This response occurred across a range of stove types and PM 2.5 concentrations, raising concern that even low-level exposures to cookstove air pollution may pose adverse cardiovascular effects.

SUBMITTER: Fedak KM

PROVIDER: S-EPMC6662148 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature

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Acute Effects on Blood Pressure Following Controlled Exposure to Cookstove Air Pollution in the STOVES Study.

Fedak Kristen M KM Good Nicholas N Walker Ethan S ES Balmes John J Brook Robert D RD Clark Maggie L ML Cole-Hunter Tom T Devlin Robert R L'Orange Christian C Luckasen Gary G Mehaffy John J Shelton Rhiannon R Wilson Ander A Volckens John J Peel Jennifer L JL

Journal of the American Heart Association 20190709 14

Background Exposure to air pollution from solid fuel used in residential cookstoves is considered a leading environmental risk factor for disease globally, but evidence for this relationship is largely extrapolated from literature on smoking, secondhand smoke, and ambient fine particulate matter ( PM <sub>2.5</sub>). Methods and Results We conducted a controlled human-exposure study (STOVES [the Subclinical Tests on Volunteers Exposed to Smoke] Study) to investigate acute responses in blood pres ...[more]

PMID: 31286826

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Project description:Household air pollution emitted from solid-fuel cookstoves used for domestic cooking is a leading risk factor for morbidity and premature mortality globally. There have been attempts to design and distribute lower emission cookstoves, yet it is unclear if they meaningfully improve health. Using a crossover design, we assessed differences in central aortic hemodynamics and arterial stiffness following controlled exposures to air pollution emitted from five different cookstove technologies compared to a filtered air control. Forty-eight young, healthy participants were assigned to six 2-h controlled treatments of pollution from five different cookstoves and a filtered air control. Each treatment had a target concentration for fine particulate matter: filtered air control = 0 μg/m3, liquefied petroleum gas = 10 μg/m3, gasifier = 35 μg/m3, fan rocket = 100 μg/m3, rocket elbow = 250 μg/m3, three stone fire = 500 μg/m3. Pulse wave velocity (PWV), central augmentation index (AIx), and central pulse pressure (CPP) were measured before and at three time points after each treatment (0, 3, and 24 h). Linear mixed models were used to assess differences in the outcomes for each cookstove treatment compared to control. PWV and CPP were marginally higher 24 h after all cookstove treatments compared to control. For example, PWV was 0.15 m/s higher (95% confidence interval: -0.02, 0.31) and CPP was 0.6 mmHg higher (95% confidence interval: -0.8, 2.1) 24 h after the three stone fire treatment compared to control. The magnitude of the differences compared to control was similar across all cookstove treatments. PWV and CPP had no consistent trends at the other post-treatment time points (0 and 3 h). No consistent trends were observed for AIx at any post-treatment time point. Our findings suggest higher levels of PWV and CPP within 24 h after 2-h controlled treatments of pollution from five different cookstove technologies. The similar magnitude of the differences following each cookstove treatment compared to control may indicate that acute exposures from even the cleanest cookstove technologies can adversely impact these subclinical markers of cardiovascular health, although differences were small and may not be clinically meaningful.

Project description:BackgroundChildhood exposure to air pollution contributes to cardiovascular disease in adulthood. Immune and oxidative stress disturbances might mediate the effects of air pollution on the cardiovascular system, but the underlying mechanisms are poorly understood in adolescents. Therefore, we aimed to identify immune biomarkers linking air pollution exposure and blood pressure levels in adolescents.MethodsWe randomly recruited 100 adolescents (mean age, 16 years) from Fresno, California. Using central-site data, spatial-temporal modeling, and distance weighting exposures to the participant's home, we estimated average pollutant levels [particulate matter (PM), polyaromatic hydrocarbons (PAH), ozone (O3), carbon monoxide (CO) and nitrogen oxides (NOx)]. We collected blood samples and vital signs on health visits. Using proteomic platforms, we quantitated markers of inflammation, oxidative stress, coagulation, and endothelial function. Immune cellular characterization was performed via mass cytometry (CyTOF). We investigated associations between pollutant levels, cytokines, immune cell types, and blood pressure (BP) using partial least squares (PLS) and linear regression, while adjusting for important confounders.ResultsUsing PLS, biomarkers explaining most of the variance in air pollution exposure included markers of oxidative stress (GDF-15 and myeloperoxidase), acute inflammation (C-reactive protein), hemostasis (ADAMTS, D-dimer) and immune cell types such as monocytes. Most of these biomarkers were independently associated with the air pollution levels in fully adjusted regression models. In CyTOF analyses, monocytes were enriched in participants with the highest versus the lowest PM2.5 exposure. In both PLS and linear regression, diastolic BP was independently associated with PM2.5, NO, NO2, CO and PAH456 pollution levels (P ≤ 0.009). Moreover, monocyte levels were independently related to both air pollution and diastolic BP levels (P ≤ 0.010). In in vitro cell assays, plasma of participants with high PM2.5 exposure induced endothelial dysfunction as evaluated by eNOS and ICAM-1 expression and tube formation.ConclusionsFor the first time in adolescents, we found that ambient air pollution levels were associated with oxidative stress, acute inflammation, altered hemostasis, endothelial dysfunction, monocyte enrichment and diastolic blood pressure. Our findings provide new insights on pollution-related immunological and cardiovascular disturbances and advocate preventative measures of air pollution exposure.

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Acute Effects on Blood Pressure Following Controlled Exposure to Cookstove Air Pollution in the STOVES Study.

Publications

Acute Effects on Blood Pressure Following Controlled Exposure to Cookstove Air Pollution in the STOVES Study.

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