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Acute differences in blood lipids and inflammatory biomarkers following controlled exposures to cookstove air pollution in the STOVES study.

ABSTRACT: Household air pollution is a leading risk factor for morbidity and premature mortality. Numerous cookstoves have been developed to reduce household air pollution, but it is unclear whether such cookstoves meaningfully improve health. In a controlled exposure study with a crossover design, we assessed the effect of pollution emitted from multiple cookstoves on acute differences in blood lipids and inflammatory biomarkers. Participants (n = 48) were assigned to treatment sequences of exposure to air pollution emitted from five cookstoves and a filtered-air control. Blood lipids and inflammatory biomarkers were measured before and 0, 3, and 24 hours after treatments. Many of the measured outcomes had inconsistent results. However, compared to control, intercellular adhesion molecule-1 was higher 3 hours after all treatments, and C-reactive protein and serum amyloid-A were higher 24 hours after the highest treatment. Our results suggest that short-term exposure to cookstove air pollution can increase inflammatory biomarkers within 24 hours.

SUBMITTER: Walker ES

PROVIDER: S-EPMC7775880 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature

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Acute differences in blood lipids and inflammatory biomarkers following controlled exposures to cookstove air pollution in the STOVES study.

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

International journal of environmental health research 20200702 3

Household air pollution is a leading risk factor for morbidity and premature mortality. Numerous cookstoves have been developed to reduce household air pollution, but it is unclear whether such cookstoves meaningfully improve health. In a controlled exposure study with a crossover design, we assessed the effect of pollution emitted from multiple cookstoves on acute differences in blood lipids and inflammatory biomarkers. Participants (n = 48) were assigned to treatment sequences of exposure to a ...[more]

PMID: 32615777

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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:Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (PD).We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 ?m in diameter (PM10) and < 2.5 ?m in diameter (PM2.5) and nitrogen dioxide (NO2) in relation to PD risk.Our nested case-control analysis included 1,556 self-reported physician-diagnosed PD cases identified between 1995 and 2006 and 3,313 controls frequency-matched on age, sex, and race. We geocoded home addresses reported in 1995-1996 and estimated the average ambient concentrations of PM10, PM2.5, and NO2 using a national fine-scale geostatistical model incorporating roadway information and other geographic covariates. Air pollutant exposures were analyzed as both quintiles and continuous variables, adjusting for matching variables and potential confounders.We observed no statistically significant overall association between PM or NO2 exposures and PD risk. However, in preplanned subgroup analyses, a higher risk of PD was associated with higher exposure to PM10 (ORQ5 vs. Q1 = 1.65; 95% CI: 1.11, 2.45; p-trend = 0.02) among women, and with higher exposure to PM2.5 (ORQ5 vs. Q1 = 1.29; 95% CI: 0.94, 1.76; p-trend = 0.04) among never smokers. In post hoc analyses among female never smokers, both PM2.5 (ORQ5 vs. Q1 = 1.79; 95% CI: 1.01, 3.17; p-trend = 0.05) and PM10 (ORQ5 vs. Q1 = 2.34; 95% CI: 1.29, 4.26; p-trend = 0.01) showed positive associations with PD risk. Analyses based on continuous exposure variables generally showed similar but nonsignificant associations.Overall, we found limited evidence for an association between exposures to ambient PM10, PM2.5, or NO2 and PD risk. The suggestive evidence that exposures to PM2.5 and PM10 may increase PD risk among female never smokers warrants further investigation. Citation: Liu R, Young MT, Chen JC, Kaufman JD, Chen H. 2016. Ambient air pollution exposures and risk of Parkinson disease. Environ Health Perspect 124:1759-1765;?http://dx.doi.org/10.1289/EHP135.

Project description:BackgroundIndoor air pollution, including fine particulate matter (PM2.5) and carbon monoxide (CO), is a major risk factor for pneumonia and other respiratory diseases. Biomass-burning cookstoves are major contributors to PM2.5 and CO concentrations. However, high concentrations of PM2.5 (> 1000 μg/m3) have been observed in homes in Dhaka, Bangladesh that do not burn biomass. We described dispersion of PM2.5 and CO from biomass burning into nearby homes in a low-income urban area of Dhaka, Bangladesh.MethodsWe recruited 10 clusters of homes, each with one biomass-burning (index) home, and 3-4 neighboring homes that used cleaner fuels with no other major sources of PM2.5 or CO. We administered a questionnaire and recorded physical features of all homes. Over 24 h, we recorded PM2.5 and CO concentrations inside each home, near each stove, and outside one neighbor home per cluster. During 8 of these 24 h, we conducted observations for pollutant-generating activities such as cooking. For each monitor, we calculated geometric mean PM2.5 concentrations at 5-6 am (baseline), during biomass burning times, during non-cooking times, and over 24 h. We used linear regressions to describe associations between monitor location and PM2.5 and CO concentrations.ResultsWe recruited a total of 44 homes across the 10 clusters. Geometric mean PM2.5 and CO concentrations for all monitors were lowest at baseline and highest during biomass burning. During biomass burning, linear regression showed a decreasing trend of geometric mean PM2.5 and CO concentrations from the biomass stove (326.3 μg/m3, 12.3 ppm), to index home (322.7 μg/m3, 11.2 ppm), neighbor homes sharing a wall with the index home (278.4 μg/m3, 3.6 ppm), outdoors (154.2 μg/m3, 0.7 ppm), then neighbor homes that do not share a wall with the index home (83.1 μg/m3,0.2 ppm) (p = 0.03 for PM2.5, p = 0.006 for CO).ConclusionBiomass burning in one home can be a source of indoor air pollution for several homes. The impact of biomass burning on PM2.5 or CO is greatest in homes that share a wall with the biomass-burning home. Eliminating biomass burning in one home may improve air quality for several households in a community.

Project description:In experimental settings, replacing old wood stoves with new wood stoves results in reduced personal exposure to household air pollution. We tested this assumption by measuring PM2.5 and levoglucosan concentrations inside homes and correlated them with wood stove age.MethodsThirty homes in the Albuquerque, NM area were monitored over a seven-day period using in-home particulate monitors placed in a common living area during the winter months. Real-time aerosol monitoring was performed, and filter samples were analyzed gravimetrically to calculate PM2.5 concentrations and chemically to determine concentrations of levoglucosan. A linear regression model with backward stepwise elimination was performed to determine the factors that would predict household air pollution measures.ResultsIn this sample, 73.3% of the households used wood as their primary source of heating, and 60% burned daily or almost daily. The mean burn time over the test week was 50 ± 38 h, and only one household burned wood 24/day (168 h). The average PM2.5 concentration (standard deviation) for the 30 homes during the seven-day period was 34.6 µg/m3 (41.3 µg/m3), and median (min, max) values were 15.5 µg/m3 (7.3 µg/m3, 193 µg/m3). Average PM2.5 concentrations in 30 homes ranged from 0-15 μg/m3 to >100 μg/m3. Maximum PM2.5 concentrations ranged from 100-200 μg/m3 to >3000 μg/m3. The levoglucosan levels showed a linear correlation with the total PM2.5 collected by the filters (R2 = 0.92). However, neither mean nor peak PM2.5 nor levoglucosan levels were correlated with the age (10.85 ± 8.54 years) of the wood stove (R2 ≤ 0.07, p > 0.23). The final adjusted linear regression model showed that average PM2.5 was associated with reports of cleaning the flue with a beta estimate of 35.56 (3.47-67.65) and R2 = 0.16 (p = 0.04).DiscussionCleaning the flue and not the wood stove age was associated with household air pollution indices. Education on wood stove maintenance and safe burning practices may be more important in reducing household air pollution than the purchase of new stoves.

Dataset Information

Acute differences in blood lipids and inflammatory biomarkers following controlled exposures to cookstove air pollution in the STOVES study.

Publications

Acute differences in blood lipids and inflammatory biomarkers following controlled exposures to cookstove air pollution in the STOVES study.

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