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Stress, Environment, and Genetics in Urban Children With Asthma

This study has been completed.
National Heart, Lung, and Blood Institute (NHLBI)
Information provided by (Responsible Party):
Rosalind Jo Wright M.D.,M.P.H., Brigham and Women's Hospital Identifier:
First received: December 21, 2005
Last updated: February 2, 2016
Last verified: February 2016
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.

Lung Diseases

Study Type: Observational
Study Design: Observational Model: Cohort
Time Perspective: Prospective
Official Title: Stress, Environment, and Genetics in Urban Asthma

Further study details as provided by Brigham and Women's Hospital:

Biospecimen Retention:   Samples With DNA
Maternal DNA Child DNA

Enrollment: 959
Study Start Date: September 2005
Study Completion Date: March 2010
Primary Completion Date: March 2010 (Final data collection date for primary outcome measure)
Detailed Description:


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.


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.


Ages Eligible for Study:   18 Years to 50 Years   (Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Sampling Method:   Non-Probability Sample
Study Population
Pregnant women and their children followed over first 5 years.

Inclusion criteria:

Mothers aged 18 years or more at time of enrollment and speak English or Spanish.

Exclusion criteria: None

  Contacts and Locations
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Please refer to this study by its identifier: NCT00269256

United States, Massachusetts
Brigham & Women's Hospital
Boston, Massachusetts, United States, 02115
Sponsors and Collaborators
Brigham and Women's Hospital
National Heart, Lung, and Blood Institute (NHLBI)
Principal Investigator: Rosalind Wright Brigham and Women's Hospital
  More Information


Responsible Party: Rosalind Jo Wright M.D.,M.P.H., Assistant Professor, Brigham and Women's Hospital Identifier: NCT00269256     History of Changes
Other Study ID Numbers: 1322
R01HL080674 ( US NIH Grant/Contract Award Number )
Study First Received: December 21, 2005
Last Updated: February 2, 2016
Individual Participant Data  
Plan to Share IPD: Undecided

Additional relevant MeSH terms:
Lung Diseases
Bronchial Diseases
Respiratory Tract Diseases
Lung Diseases, Obstructive
Respiratory Hypersensitivity
Hypersensitivity, Immediate
Immune System Diseases processed this record on April 26, 2017