Overview: Chronic Respiratory Effects of Early Childhood Exposure to Respirable Particulate Matter (CRECER)
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CRECER Study Details
Our primary goal is to follow the cohort of children who participated in the Randomized Exposure Study of Pollution Indoors and Respiratory Effects (RESPIRE) – Guatemala, longitudinally for a 5-year period to elicit the chronic effects of inhaled PM during the critical time window of infant lung development on respiratory health.
This recently concluded intervention trial randomized 500 rural Guatemalan households to improved plancha stoves (intervention) or traditional open wood stoves (control) and measured as the main study outcome, the incidence of acute lower respiratory infections (ALRI) in children from birth to 18 months. In addition, extensive exposure assessment was performed and preliminary data suggests that the plancha stove has significantly decreased the levels of biomass smoke exposure inside the intervention homes. At the end of the trial, which concluded in December 2004, all control households were offered an improved plancha stove.
This randomized trial has created a unique opportunity to follow this cohort of children who had variable exposures to biomass smoke from birth to 18 months (critical time window for lung development) and observe the effects of these exposures on future respiratory health.
Our primary hypothesis is that inhaled biomass smoke that contains high levels of PM during the critical time window of the first 18 months of life will negatively affect respiratory health later in childhood by causing increased symptoms of cough, phlegm production, and wheeze; decreased rate of growth of lung function; increased risk of sensitization to aeroallergens; and decreased somatic growth.
Our secondary hypothesis is that the combustion-generated organic compounds present on fine particles in biomass smoke induce oxidative stress, upregulation of inflammatory cytokine production, and subsequent inflammation in the airways of children who inhale such smoke.
Based on these hypotheses, we posit that (i) PM inhalation will generate oxidative stress in the developing airways of infant children exposed to high levels of biomass smoke, (ii) chronic exposure to PM-induced oxidative stress will result in increased respiratory symptoms, decreased somatic growth, and abnormal structural development of the respiratory tract leading to a reduced rate of lung function growth. Additionally, we would like to obtain more detailed exposure assessments to create and validate a model of measured and observed household parameters that reasonably estimate the overall exposure level of every child for use in the final longitudinal analyses.