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Household Air Pollution and Children's Blood Pressure

Baumgartner, Jill; Zhang, Yuanxun; Schauer, James J.; Ezzati, Majid; Patz, Jonathan A.; Bautista, Leonelo E.

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doi: 10.1097/EDE.0b013e3182593fa9

To the Editor:

Childhood blood pressure (BP) is an important predictor of hypertension and cardiovascular risk later in life1; risk factors for elevated BP in children remain mostly unknown. Ambient air pollution is associated with impaired vascular health, oxidative stress, and systemic inflammation in children.2 Limited evidence suggests that household air pollution is associated with higher BP in adult women,35 but this relationship has not been studied in children. Half the world's population uses biomass and coal for energy6; thus, even a small effect of household air pollution on BP in childhood could have large cardiovascular implications. We investigated the association between exposure to household air pollution from biomass combustion and BP in Chinese children.

We recruited school-aged children from 180 rural households cooking with biomass in Yunnan, China. Detailed information on the study population, exposure assessment, and quality control is published elsewhere.7 Participants wore a small backpack containing equipment to measure personal exposure to particles <2.5 μg in aerodynamic diameter (particulate matter [PM]2.5) over a 24-hour period. PM2.5 samples were analyzed for mass and black carbon (BC) (eAppendix 1, We measured children's BP before and after pollution exposure measurement, using an automated device (Omron-705). We also collected household sociodemographic and health information, including caffeine intake, exposure to cigarette smoke, physical activity, and 24-hour salt and monosodium glutamate intake, and we measured each child's height and weight. Mother's BP was assessed in a 40% subsample (eAppendix 2,

We investigated the associations between personal PM2.5 and BC exposures and BP using one- and two-pollutant multivariate regression models. Pollution measures were transformed to the natural log scale to account for their skewedness toward high values (eAppendix 3,

We enrolled 240 children (47% girls). Mean age was 10.3 years (95% confidence interval: 10.0–10.6; range: 5–14 years), average body mass index was 15.3 kg/m2 (15.0–15.6), and 85% lived with a smoker (eTable 1, Personal 24-hour PM2.5 exposure ranged from 14 to 393 μg/m3 (geometric mean = 53 μg/m3 [46–61]). BC exposure ranged between 2.0 and 9.6 μg/m3 (geometric mean = 3.2 μg/m3 [3.1–3.3]). PM2.5 and BC exposures were moderately correlated (Pearson r = 0.41).

In the single-pollutant multivariate regression models, a 1-ln(μg/m3) increase in PM2.5 was associated with small decreases in systolic BC (−1.8 mmHg [95% confidence interval: −3.6, 0.1]) and diastolic BC (−0.5 mmHg [−2.1 to 1.2]). Similarly, a 1-ln(μg/m3) increase in BC was also associated with small decreases in systolic BC (−2.2 mmHg [−5.4 to 1.0]) and diastolic BC (−0.4 mmHg [−3.3 to 2.6]). In two-pollutant models, the effect of PM2.5 exposure on BP was largely unchanged; however, the effect of BC was greatly weakened (Table). Sensitivity analyses included adjustment for maternal BP, restricting the analysis to smaller age-groups, and transforming BP into quantiles; none of these affected the qualitative interpretation of our results (eAppendix 4,

Multivariate Adjusted Associations of Personal PM2.5 and Black Carbon Exposure With Blood Pressure Using One- and Two-pollutant Modelsa

We found that increased PM2.5 and BC exposures were not associated with higher BP among children in households cooking with biomass. Our findings do not support our previous study of older women in this setting, showing a positive relationship between PM exposure and BP. Possible explanations include the lower levels and shorter durations of PM exposure among children compared with adult women7 (eAppendix 5, Older women would be more likely than young children to experience a resetting of BP-regulating mechanisms to higher levels, as a result of repeated acute increases in BP after PM inhalation. We also cannot rule out the possibility of residual confounding by difficult-to-measure or unmeasured covariates in this cross-sectional study.

Future longitudinal studies could advance our understanding of the vascular effects of household air pollution in children and should incorporate measures of PM pollution exposure and BP over a span of years.

Jill Baumgartner

Institute on the Environment

College of Food, Agricultural and Natural Resource Sciences

University of Minnesota

St. Paul, MN

Yuanxun Zhang

College of Resources and Environment

Graduate University of the Chinese Academy of Sciences

Beijing, China

James J. Schauer

Department of Civil and Environmental Engineering

College of Engineering

University of Wisconsin

Madison, WI

Majid Ezzati

MRC-HPA Centre for Environment and Health

Department of Epidemiology and Biostatistics

School of Public Health, Imperial College

London, United Kingdom

Jonathan A. Patz

Global Health Institute

School of Medicine and Public Health

University of Wisconsin

Madison, WI

Leonelo E. Bautista

Department of Population Health Sciences

School of Medicine and Public Health

University of Wisconsin

Madison, WI


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We thank the children and parents who participated in our study and the field team for their assistance with data collection.

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