Ignite Creation Date:
2025-12-25 @ 2:29 AM
Ignite Modification Date:
2025-12-27 @ 10:53 PM
Study NCT ID:
NCT01874834
Status:
COMPLETED
Last Update Posted:
2013-06-11
First Post:
2013-06-07
Is NOT Gene Therapy:
True
Has Adverse Events:
False
Brief Title:
Cardiopulmonary Responses to Exposure to Ozone and Diesel Exhaust
Sponsor:
Environmental Protection Agency (EPA)
Organization:
Study Overview
Official Title:
Cardiopulmonary Responses to Exposure to Ozone and Diesel Exhaust With Moderate Exercise in Healthy Adults
Status:
COMPLETED
Status Verified Date:
2013-06
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
DEPOZ
Brief Summary:
The US EPA Clean Air Multiyear research program is moving toward a multi-pollutant approach to the assessment of air pollution in response to recommendations by the NRC 2004 and the BOSC in 2005. Such an approach better reflects the complexity of real-world air pollution problems and parallels evolving scientific and regulatory considerations. Ozone (O3) and diesel exhaust (DE) generally are major and important components of ambient air pollution. This proposed study will address the agency's goals by investigating the cardiopulmonary health effects in healthy human subjects co-exposed to O3 and DE. The findings derived from these exposures will provide NCEA findings for risk assessments of O3 and DE, as well as the Office of Air and Radiation (includes OTAQ and OAQPS) with information relevant to possible modulation of PM-induced health effects and responses by a gaseous co-pollutant for potential standard setting. Additionally the findings will address the fundamental driving principle of the Clean Air Research strategy related to reduction of health due to air pollutant exposures.
Detailed Description:
Numerous epidemiological studies have demonstrated an association between acute and chronic exposure to air pollution and various adverse cardiopulmonary effects including mortality, respiratory tract infections, exacerbation of asthma symptoms, chronic bronchitis, ischemic heart disease, and stroke \[1\] and other health effects. Understanding the components responsible for these effects is difficult because ambient air pollution is a complex mixture of gases and particulate matter (PM). In this complex mixture of ambient air pollution, ozone (O3) and diesel exhaust (DE) are generally major and important components. Controlled exposure of volunteers to either pollutant have resulted in biological effects such as lung physiological changes. However it is not known if co-exposure to both pollutants, similar to polluted ambient air, can induce additive or synergistic effects. Additionally it is also uncertain if exposure to DE, or DE with O3, can alter a subsequent exposure to O3 similar to multiple day exposures that the general population receives. This study proposes to examine whether co-exposures to O3 and DE can induce additive or synergistic effects, and whether a previous DE exposure alters a response upon subsequent exposure to O3. The potential effects of O3 on cardiac electrophysiology are also not clear.
Approximately 15 healthy non-smoking volunteers between the ages of 18 and 55 will be exposed in a controlled manner to O3 (approximately mean concentration of 0.3 ppm over the 2 hr exposure period), or diesel exhaust (DE; \~300 µg/m3), or a combined O3 and DE exposure while undergoing moderate intermittent exercise at the EPA Human Studies Facility. A clean air exposure will serve as a control. Primary endpoints for evaluating health effects and surrogate responses are changes in lung function and heart rate variability. In addition, other cardiopulmonary and vascular biological endpoints will be measured, as well as markers of exposure and genetic markers of susceptibility.
Approximately 15 healthy non-smoking volunteers between the ages of 18 and 55 will be exposed in a controlled manner to O3 (approximately mean concentration of 0.3 ppm over the 2 hr exposure period), or diesel exhaust (DE; \~300 µg/m3), or a combined O3 and DE exposure while undergoing moderate intermittent exercise at the EPA Human Studies Facility. A clean air exposure will serve as a control. Primary endpoints for evaluating health effects and surrogate responses are changes in lung function and heart rate variability. In addition, other cardiopulmonary and vascular biological endpoints will be measured, as well as markers of exposure and genetic markers of susceptibility.
Study Oversight
Has Oversight DMC:
False
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?: