Stress, Environment, and Genetics in Urban Children With Asthma
Condition: Asthma; Lung Diseases
MeSH terms: Asthma; Lung Diseases
Study type: Observational

Summary: 
      The purpose of this study is to evaluate the multiple mechanisms through which stress,
      physical environment, and genetic predisposition contribute to asthma in urban children.
    

Detailed description: 
      BACKGROUND:

      The study design builds on the ACCESS Study, a prospective pregnancy cohort study begun in
      2003 of a cohort from birth to age four. The present study includes two new aims regarding
      the interaction of stress and genetic or environmental variables, reflecting a more
      comprehensive conceptualization of the multiple mechanisms by which stress can contribute to
      asthma. In addition, the current study proposes to follow the cohort until the age of three.

      DESIGN NARRATIVE:

      The study examines the role of psychosocial stressors in a systems biology framework
      considering multiple biologic pathways by which stress can contribute to asthma. The
      investigators will not only study the independent effect of stress on asthma/wheeze
      phenotypes in early childhood but also will consider stress as a modifier of physical
      environmental factors (allergens, cigarette smoking, and diesel-related air pollutants) and
      genetic predisposition on asthma risk. They will determine the independent effect of maternal
      stress (both prenatal and postnatal) on early childhood asthma phenotypes. They further
      hypothesize that multi-life stressors prevalent in disadvantaged populations can cumulatively
      influence immune system development and airway inflammation in early life, thus making the
      populations more susceptible to other environmental factors and genetic risk factors
      explaining, in part, observed asthma disparities associated with SES and race/ethnicity. They
      will take a multi-level approach, measuring both individual-level stress (negative life
      events, perceived stress, pregnancy anxiety) and community-level stress [neighborhood
      disadvantage (e.g., percent of subjects living in poverty, percent unemployed), diminished
      social capital, and high crime/violence rates]. They will also assess the influence of stress
      on the infant hormonal stress response and on T-helper cell differentiation as reflected in
      cytokine profiles and IgE expression (a topic or pro inflammatory phenotype). Additional
      physical environmental (indoor allergens, diesel-related air pollutants, tobacco smoke) and
      genetic factors will be assessed given their influence on the immune response and expression
      of early childhood asthma/wheeze. This interdisciplinary approach is unique because
      researchers are considering the context in which physical exposures and host susceptibility
      occur, analyzing their multiplicative joint effects and considering multiple biologic
      pathways, as such it is consistent with the NIH roadmap objectives.
    

Observational model: Cohort
Time perspective: Prospective
Sampling method: Non-Probability Sample
Study population: 
        Pregnant women and their children followed over first 5 years.
      
Biospecimen description: 
      Maternal DNA Child DNA