Environmental Determinants of Early Host Response to RSVEPA Grant Number: RD834515C002
Subproject: this is subproject number 002 , established and managed by the Center Director under grant RD834515
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: Denver Children’s Environmental Health Center - Environmental Determinants of Airway Disease in Children
Center Director: Schwartz, David A
Title: Environmental Determinants of Early Host Response to RSV
Investigators: Schwartz, David A
Institution: National Jewish Health
EPA Project Officer: Louie, Nica
Project Period: June 22, 2010 through June 21, 2015 (Extended to June 21, 2017)
RFA: Children's Environmental Health and Disease Prevention Research Centers (with NIEHS) (2009) RFA Text | Recipients Lists
Research Category: Children's Health , Health
Inhaled air pollutants such as ozone are known to exacerbate asthma and may play a potential role in the development of reactive airway disease such as asthma in early life. While ozone can cause significant respiratory health problems in the majority of exposed individuals, young children are particularly at risk for developing serious adverse health effects from ozone exposure. This is because their lungs are still rapidly developing, and exposures during this critical time period of susceptibility may alter lung development, resulting in permanent respiratory health problems. Air pollutants may also influence the developing immune system in young children, increasing susceptibility to infection and promoting airway sensitization to common airborne allergens. The overall objective of this project is to define how ozone influences children’s lung development and immune system response early in life. Our general hypothesis is that ozone exposure in the early period after birth alters lung development and modifies the child’s immune response to early life viral infection and allergen exposure, thereby contributing to the development of reactive airway disease such as asthma.
To test this hypothesis, we will pursue the following aims: 1. To define the influence of ozone on innate immune response, airway structure and function. Studies are designed to identify which toll-like receptors (TLRs) are modified following postnatal ozone exposure, to define the changes in airway structure and function, and to determine the role of TLR-4 in these responses. 2. To define the influence of ozone on the early response to respiratory syncytial virus (RSV) infection and house dust mite (HDM) allergen exposure.
The proposed studies will determine how ozone modifies the host response to RSV and HDM just after birth and will define the associated changes in airway structure and function and the role of TLR-4 in these responses. 3. To determine how lipopolysaccharide (LPS), an air contaminant from bacterial endotoxin that interacts with TLR-4, modifies the host response to RSV and HDM following postnatal ozone exposure. We will determine how LPS modifies the early host response to RSV and HDM, and associated changes in airway structure and function, following postnatal ozone exposure.
Publications and Presentations:Publications have been submitted on this subproject: View all 23 publications for this subproject | View all 34 publications for this center
Journal Articles:Journal Articles have been submitted on this subproject: View all 13 journal articles for this subproject | View all 17 journal articles for this center
Supplemental Keywords:Endotoxin, exposure, children, asthma, risk, health effects, susceptibility, sensitive populations, genetic pre-disposition, genetic polymorphism, indoor air, dose-response, ozone, remediation, human health, Scientific Discipline, Health, Health Effects, Biology, Health Risk Assessment, Allergens/Asthma, asthma indices, intervention, endotoxin, sensitive populations, children, asthma triggers, allergic response, asthma, airway inflammation, Health, Scientific Discipline, HUMAN HEALTH, Health Risk Assessment, Allergens/Asthma, Health Effects, Biology, asthma, sensitive populations, asthma triggers, endotoxin, asthma indices, children, airway inflammation, allergic response
Progress and Final Reports:2010 Progress Report
2014 Progress Report
Main Center Abstract and Reports:RD834515 Denver Children’s Environmental Health Center - Environmental Determinants of Airway Disease in Children
Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
RD834515C001 Endotoxin Exposure and Asthma in Children
RD834515C002 Environmental Determinants of Early Host Response to RSV
RD834515C003 Environmental Determinants of Host Defense