Stress, Environment, and Genetics in Urban Children With Asthma
Status: | Completed |
---|---|
Conditions: | Asthma, Pulmonary |
Therapuetic Areas: | Pulmonary / Respiratory Diseases |
Healthy: | No |
Age Range: | 18 - 50 |
Updated: | 4/21/2016 |
Start Date: | September 2005 |
End Date: | March 2010 |
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.
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.
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.
Inclusion criteria:
Mothers aged 18 years or more at time of enrollment and speak English or Spanish.
Exclusion criteria: None
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