Abstract
BackgroundSingle birth cohort studies have been the basis for many discoveries about early life risk factors for childhood asthma but are limited in scope by sample size and characteristics of the local environment and population. The Children’s Respiratory and Environmental Workgroup (CREW) was established to integrate multiple established asthma birth cohorts and to investigate asthma phenotypes and associated causal pathways (endotypes), focusing on how they are influenced by interactions between genetics, lifestyle, and environmental exposures during the prenatal period and early childhood.Methods and resultsCREW is funded by the NIH Environmental influences on Child Health Outcomes (ECHO) program, and consists of 12 individual cohorts and three additional scientific centers. The CREW study population is diverse in terms of race, ethnicity, geographical distribution, and year of recruitment. We hypothesize that there are phenotypes in childhood asthma that differ based on clinical characteristics and underlying molecular mechanisms. Furthermore, we propose that asthma endotypes and their defining biomarkers can be identified based on personal and early life environmental risk factors. CREW has three phases: 1) to pool and harmonize existing data from each cohort, 2) to collect new data using standardized procedures, and 3) to enroll new families during the prenatal period to supplement and enrich extant data and enable unified systems approaches for identifying asthma phenotypes and endotypes.ConclusionsThe overall goal of CREW program is to develop a better understanding of how early life environmental exposures and host factors interact to promote the development of specific asthma endotypes.
Highlights
Single birth cohort studies have been the basis for many discoveries about early life risk factors for childhood asthma but are limited in scope by sample size and characteristics of the local environment and population
The overall goal of Children’s Respiratory and Environmental Workgroup (CREW) program is to develop a better understanding of how early life environmental exposures and host factors interact to promote the development of specific asthma endotypes
We further propose that these phenotypes will have closer associations with etiologic factors, compared to a general yes/no definition of childhood asthma due to reduction in misclassification
Summary
Single birth cohort studies have been the basis for many discoveries about early life risk factors for childhood asthma but are limited in scope by sample size and characteristics of the local environment and population. Birth cohort studies from single research centers have identified individual factors that affect the risk for developing childhood asthma, including exposure to allergens, pollutants, bacteria, psychosocial stress, viral respiratory illnesses and patterns of microbial colonization Despite such advances, further progress in understanding the root causes of asthma have been hampered by the relatively small size of previous studies that typically lack diverse population and broad assessments of early life exposures. Broad and diverse populations and environmental assessments are needed to determine and compare interactions with genetics, effect sizes, mediation and additive effects and dose response relationships, and to identify geographical and temporal differences in exposures and how they impact asthma development across the US Another notable limitation of individual cohorts with modest sample size is the inability to define prenatal and early life risk factors for infrequent outcomes that are of special clinical significance, such as severe asthma and susceptibility to acute exacerbations. Differences in data collection and sample analyses make it challenging to pool, harmonize and integrate findings from different cohorts
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