Prenatal Household Air Pollution Exposure Research Articles

Prenatal and Postnatal Household Air Pollution Exposures and Pneumonia Risk: Evidence From the Ghana Randomized Air Pollution and Health Study

Nearly 40%of the world's population is exposed daily to household air pollution. The relative impact of prenatal and postnatal household air pollution exposure on early childhood pneumonia, a leading cause of mortality, is unknown. Are prenatal or postnatal household air pollution, or both, associated with pneumonia risk in the first year of life? The Ghana Randomized Air Pollution and Health Study enrolled 1,414 nonsmoking, pregnant women before 24weeks' gestation with prospective follow-up to the child's age of 1 year. We measured 72-h personal household air pollution exposures, indexed by carbon monoxide (CO), four times prenatally and three times postnatally. Weekly fieldworker surveillance identified ill-appearing children for physician pneumonia assessment. We used quasi-Poisson models to examine associations between prenatal and postnatal CO and physician-diagnosed pneumonia and severe pneumonia. Sex-specific effects were examined. Of the 1,306 live births, 1,141 infants were followed up with 55,605 child-weeks of fieldworker surveillance. The estimated risk for pneumonia and severe pneumonia in the first year of life increased by 10%(relative risk [RR], 1.10; 95%CI, 1.04-1.16) and 15%(RR, 1.15; 95%CI, 1.03-1.28), respectively, per 1-part per million (ppm) increase in average prenatal CO exposure and by 6%(RR, 1.06; 95%CI, 0.99-1.13) per 1-ppm increase in average postnatal CO exposure. Sex-stratified analyses suggest that in girls, higher prenatal CO exposure was associated with pneumonia risk, while no association was seen in boys. Prenatal household air pollution exposure increased risk of pneumonia and severe pneumonia in the first year of life. Clean-burning interventions may be most effective when begun prenatally. ClinicalTrials.gov; No.: NCT01335490; URL: www.clinicaltrials.gov.

Prenatal Household Air Pollution Exposure, Cord Blood Mononuclear Cell Telomere Length and Age Four Blood Pressure: Evidence from a Ghanaian Pregnancy Cohort.

Associations between prenatal household air pollution exposure (HAP), newborn telomere length and early childhood blood pressure are unknown. Methods: Pregnant women were randomized to liquefied petroleum gas (LPG) stove, improved biomass stove or control (traditional, open fire cook stove). HAP was measured by personal carbon monoxide (CO) (n = 97) and fine particulate matter (PM2.5) (n = 60). At birth, cord blood mononuclear cells (CBMCs) were collected for telomere length (TL) analyses. At child age four years, we measured resting blood pressure (BP) (n = 97). We employed multivariable linear regression to determine associations between prenatal HAP and cookstove arm and assessed CBMC relative to TL separately. We then examined associations between CBMC TL and resting BP. Results: Higher prenatal PM2.5 exposure was associated with reduced TL (β = −4.9% (95% CI −8.6, −0.4), p = 0.03, per 10 ug/m3 increase in PM2.5). Infants born to mothers randomized to the LPG cookstove had longer TL (β = 55.3% (95% CI 16.2, 109.6), p < 0.01)) compared with control. In all children, shorter TL was associated with higher systolic BP (SBP) (β = 0.35 mmHg (95% CI 0.001, 0.71), p = 0.05, per 10% decrease in TL). Increased prenatal HAP exposure is associated with shorter TL at birth. Shorter TL at birth is associated with higher age four BP, suggesting that TL at birth may be a biomarker of HAP-associated disease risk.

284: Prenatal household air pollution exposure associated with lower birth weight and length in rural Ghana

Approximately 3 billion people rely on biomass fuels to meet their daily cooking needs and are exposed to household air pollution. The effects of such exposure among pregnant women cooking with these fuels on birth outcomes have not been rigorously characterized. Between 2013 and 2016, 1414 pregnant women were recruited from 35 communities in central Ghana into the Ghana Randomized Air Pollution and Health Study. Gestational age was established by ultrasound at enrolment. Personal exposure to carbon monoxide (CO) was measured at repeated intervals across gestation to estimate air pollution exposure. Newborn weight was measured with digital scales. We conducted planned exposure-response analyses among 1303 live-born infants using generalized linear regression models to investigate the association between prenatal exposure to household air pollution and birth anthropometrics and pregnancy outcomes. Mean maternal exposure to CO was 1.3 ppm (IQR:1.0 ppm). Each doubling in CO exposure was associated with a 49.2g reduction in birth weight (95%CI: -69.1, -29.3g) and a 0.3 cm reduction in birth length (95%CI -0.5, -0.1cm) adjusting for maternal age, parity, infant sex, antenatal visits, placental malaria, ethnicity, and asset index (Table). Odds were also elevated for delivering an SGA infant (OR 1.3, 95%CI 1.1, 1.5) or LBW infant (OR 1.3, 95%CI 1.1, 15) per doubling of exposure. Associations were not modified by infant sex. Results suggest that associations were stronger among infants born to mothers without evidence of placental malaria. No significant associations were observed between CO exposure and head circumference, gestational length, or preterm birth. Exposure-response analyses conducted among 1,303 Ghanaian mother-infant pairs demonstrate an association between prenatal exposure to household air pollution and adverse effects on infant size at birth. Notably, exposure-response curves were steepest at the lower end of the exposure range, at exposures relevant to US cities. Reducing exposure to air pollution could yield important global public health benefits.

Prenatal Household Air Pollution Exposure and Cord Blood Mononuclear Cell Telomere Length

Prenatal Household Air Pollution Exposure and Cord Blood Mononuclear Cell Telomere Length

Prenatal Household Air Pollution Is Associated with Impaired Infant Lung Function with Sex-Specific Effects. Evidence from GRAPHS, a Cluster Randomized Cookstove Intervention Trial.

Approximately 2.8 billion people are exposed daily to household air pollution from polluting cookstoves. The effects of prenatal household air pollution on lung development are unknown. To prospectively examine associations between prenatal household air pollution and infant lung function and pneumonia in rural Ghana. Prenatal household air pollution exposure was indexed by serial maternal carbon monoxide personal exposure measurements. Using linear regression, we examined associations between average prenatal carbon monoxide and infant lung function at age 30 days, first in the entire cohort (n = 384) and then stratified by sex. Quasi-Poisson generalized additive models explored associations between infant lung function and pneumonia. Multivariable linear regression models showed that average prenatal carbon monoxide exposure was associated with reduced time to peak tidal expiratory flow to expiratory time (β = -0.004; P = 0.01), increased respiratory rate (β = 0.28; P = 0.01), and increased minute ventilation (β = 7.21; P = 0.05), considered separately, per 1 ppm increase in average prenatal carbon monoxide. Sex-stratified analyses suggested that girls were particularly vulnerable (time to peak tidal expiratory flow to expiratory time: β = -0.003, P = 0.05; respiratory rate: β = 0.36, P = 0.01; minute ventilation: β = 11.25, P = 0.01; passive respiratory compliance normalized for body weight: β = 0.005, P = 0.01). Increased respiratory rate at age 30 days was associated with increased risk for physician-assessed pneumonia (relative risk, 1.02; 95% confidence interval, 1.00-1.04) and severe pneumonia (relative risk, 1.04; 95% confidence interval, 1.00-1.08) in the first year of life. Increased prenatal household air pollution exposure is associated with impaired infant lung function. Altered infant lung function may increase risk for pneumonia in the first year of life. These findings have implications for future respiratory health. Clinical trial registered with www.clinicaltrials.gov (NCT 01335490).