Stress, Environment, and Genetics in Urban Children With Asthma

The recruitment status of this study is unknown because the information has not been verified recently.
Verified November 2006 by National Heart, Lung, and Blood Institute (NHLBI).
Recruitment status was  Active, not recruiting
Sponsor:
Information provided by:
National Heart, Lung, and Blood Institute (NHLBI)
ClinicalTrials.gov Identifier:
NCT00269256
First received: December 21, 2005
Last updated: March 4, 2010
Last verified: November 2006

December 21, 2005
March 4, 2010
September 2005
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Complete list of historical versions of study NCT00269256 on ClinicalTrials.gov Archive Site
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Stress, Environment, and Genetics in Urban Children With Asthma
Stress, Environment, and Genetics in Urban Asthma

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.

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
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  • Asthma
  • Lung Diseases
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*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Active, not recruiting
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No eligibility criteria

Both
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No
Contact information is only displayed when the study is recruiting subjects
United States
 
NCT00269256
1322, R01 HL80674
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National Heart, Lung, and Blood Institute (NHLBI)
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Principal Investigator: Rosalind Wright Brigham and Women's Hospital
National Heart, Lung, and Blood Institute (NHLBI)
November 2006

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP