MASAES
Mechanisms by Which Air Pollutants Exacerbate Asthma in Mild and Moderate to Severe Asthmatics
The project aims to clarify discrepancies between epidemiological studies that investigate the effects of air pollution on asthma exacerbations and include all asthmatics, and challenge studies that include only mild asthmatics.
MASAES
Mechanisms by Which Air Pollutants Exacerbate Asthma in Mild and Moderate to Severe Asthmatics
The project aims to clarify discrepancies between epidemiological studies that investigate the effects of air pollution on asthma exacerbations and include all asthmatics, and challenge studies that include only mild asthmatics.
Overview
Several epidemiological studies have shown that various air pollutants (including ozone and particulate matter) can induce acute exacerbations of asthma, suggesting that asthmatics may have increased susceptibility to ambient air pollutants. It has also been observed that those with disease moderate to severe enough to require corticosteroids may be at more risk than milder asthmatics. However, controlled human exposure studies, which are restricted to mild asthmatics due to ethical and safety considerations, do not always demonstrate increased response to pollutants. We hypothesize that moderate to severe asthmatics are more susceptible to the effect of air pollutants, due at least in part to the enhancement of IgE mediated inflammation.
- To determine if moderate to severe asthmatics respond more severely to air pollution than non-asthmatics and those with mild asthma:
- To better understand the mechanisms by which asthmatics are more susceptible to air pollution than the general populat
The MASAES panel study recruited 63 participants from the Raleigh-Durham-Chapel Hill area of North Carolina, U.S., consisting of 23 non-asthmatics, 16 mild asthmatics (controlled with bronchodilators), and 24 moderate to severe asthmatics (controlled with steroids). All participants attended up to five study visits during February 2008 and February 2012. At each visit, lung function, heart rate variability (HRV), and venous blood biomarkers were measured.
U.S. Environmental Protection Agency (funding period: 2008 – ongoing)
- U.S. Environmental Protection Agency (EPA) –National Health and Environmental Effects Research Laboratory (NHEERL), Environmental Public Health Division (EPHD): Ana Grohovac Rappold (PI)
- Helmholtz Zentrum München - Institute of Epidemiology: Alexandra Schneider, Susanne Breitner, Siqi Zhang
Several epidemiological studies have shown that various air pollutants (including ozone and particulate matter) can induce acute exacerbations of asthma, suggesting that asthmatics may have increased susceptibility to ambient air pollutants. It has also been observed that those with disease moderate to severe enough to require corticosteroids may be at more risk than milder asthmatics. However, controlled human exposure studies, which are restricted to mild asthmatics due to ethical and safety considerations, do not always demonstrate increased response to pollutants. We hypothesize that moderate to severe asthmatics are more susceptible to the effect of air pollutants, due at least in part to the enhancement of IgE mediated inflammation.
- To determine if moderate to severe asthmatics respond more severely to air pollution than non-asthmatics and those with mild asthma:
- To better understand the mechanisms by which asthmatics are more susceptible to air pollution than the general populat
The MASAES panel study recruited 63 participants from the Raleigh-Durham-Chapel Hill area of North Carolina, U.S., consisting of 23 non-asthmatics, 16 mild asthmatics (controlled with bronchodilators), and 24 moderate to severe asthmatics (controlled with steroids). All participants attended up to five study visits during February 2008 and February 2012. At each visit, lung function, heart rate variability (HRV), and venous blood biomarkers were measured.
U.S. Environmental Protection Agency (funding period: 2008 – ongoing)
- U.S. Environmental Protection Agency (EPA) –National Health and Environmental Effects Research Laboratory (NHEERL), Environmental Public Health Division (EPHD): Ana Grohovac Rappold (PI)
- Helmholtz Zentrum München - Institute of Epidemiology: Alexandra Schneider, Susanne Breitner, Siqi Zhang
