Ignite Creation Date:
2024-05-06 @ 3:07 AM
Last Modification Date:
2024-10-26 @ 11:28 AM
Study NCT ID:
NCT02206750
Status:
COMPLETED
Last Update Posted:
2017-07-26
First Post:
2014-07-30
Brief Title:
The Interaction of Social Factors With Air Pollution
Sponsor:
Environmental Protection Agency EPA
Organization:
Environmental Protection Agency EPA
Study Overview
Official Title:
The Interaction of Social Factors With Air Pollution
Status:
COMPLETED
Status Verified Date:
2017-07
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:
SOZIAL
Brief Summary:
Purpose
The purpose of this protocol is to understand how social factors such as psychosocial stress may modify how people respond to air pollution Ultimately this will help us understand health disparities from poor air quality
Participants
Up to 40 healthy adults18-33 years old with different perception of stress will participate and complete this study
Procedures methods
Subjects will be exposed to clean air and to ozone 300ppb for 2 hours in a controlled environment chamber Cardiac vascular pulmonary and cognitive function will be evaluated pre immediately post and 18 hr post exposure
The primary endpoint will be Heart Rate Variability Secondary endpoints will include pulmonary function analysis of blood clottingcoagulation factors biomarkers of stress cognitive function radial artery pulse wave measurements and analysis of soluble factors present in plasma
The purpose of this protocol is to understand how social factors such as psychosocial stress may modify how people respond to air pollution Ultimately this will help us understand health disparities from poor air quality
Participants
Up to 40 healthy adults18-33 years old with different perception of stress will participate and complete this study
Procedures methods
Subjects will be exposed to clean air and to ozone 300ppb for 2 hours in a controlled environment chamber Cardiac vascular pulmonary and cognitive function will be evaluated pre immediately post and 18 hr post exposure
The primary endpoint will be Heart Rate Variability Secondary endpoints will include pulmonary function analysis of blood clottingcoagulation factors biomarkers of stress cognitive function radial artery pulse wave measurements and analysis of soluble factors present in plasma
Detailed Description:
Over the past decades air quality in the US has improved significantly Even so millions of people in the US still live in counties that do not meet air quality standards for one or more pollutants Ozone is a major component of photochemical smog and is one of the most thoroughly studied gaseous pollutants Controlled human exposure studies have been critical in demonstrating that it can cause airway inflammation 1-3 including increases in neutrophil infiltration into the lung and the production of pro-inflammatory mediators 45 and ultimately decrements in lung function reviewed in 6 More recent studies have shown that ozone can also increase vascular inflammation as well as alter autonomic nervous system control of heart rate and cardiac repolarization 7 Numerous epidemiological studies have also demonstrated an association between acute and chronic exposure to ambient levels of ozone and various health effects most notably asthma 6 These studies have also highlighted a need to incorporate social and nonchemical factors into risk assessments 8 Similarly social factors such as psychological stress are now regarded as important contributors to asthma outcomes 910 This protocol is aimed at investigating how stress impacts health responses to air pollutants Since psychosocial stress-related susceptibility has been proposed to explain social disparities this will help us understand which populations and individuals are at increased risk from air pollution
This protocol is designed to determine whether nonchemical stressors exacerbate ozone effects In particular we will focus on elevated psychosocial stress as it has been shown to contribute to several adverse health outcomes most notably to cardiovascular disease The physiological mechanism by which psychosocial stress leads to health effects is due at least in part to elevated circulating glucocorticoids or stress hormones which are regulated by the hypothalamic-pituitary-adrenal HPA In the last 30 years the concept of allostasis has evolved Allostasis is the process whereby an organism adapts to the demands of the environment An allostatic load model applies this concept to chronic stress11 In this model the perception of threat over long time intervals perceived stress can cause over-activation of the HPA-axis resulting in changes in physiological systems as chemical imbalances in autonomic nervous system central nervous system neuroendocrine and immune system activity Factors such as genetics behavior life events and diet can impact this model To our knowledge no clinical study has investigated the link between air pollution effects on cardiovascular disease and psychosocial stress However several studies have now shown an association between stress and respiratory outcomes to air pollution Claugherty and colleagues 2007 found an association between traffic-related air pollution and asthma solely among children exposed to violence 12 Shankardass and colleagues demonstrated that children from stressful households are more susceptible to the effects of traffic-related pollution on the development of asthma 13 In that study stress was evaluated using the Perceived Stress Scale PSS developed by Dr Sheldon Cohen of Carnegie Mellon University This is the most widely used psychological instrument for measuring the perception of stress and has been validated in multiple studies We will use this scale to evaluate the degree to which subjects appraise situations in their life as stressful Heart rate variability HRV is considered to be a reliable biomarker of stress Chronic stress has been shown to be associated with decreases in HRV 14 Since acute ozone exposure can also cause changes in HRV we have chosen HRV as our primary endpoint We hypothesize that the imbalance between the sympathetic and the parasympathetic nervous system caused by chronic stress will result in altered responses to ozone exposure that will be reflected by HRV
This protocol is designed to determine whether nonchemical stressors exacerbate ozone effects In particular we will focus on elevated psychosocial stress as it has been shown to contribute to several adverse health outcomes most notably to cardiovascular disease The physiological mechanism by which psychosocial stress leads to health effects is due at least in part to elevated circulating glucocorticoids or stress hormones which are regulated by the hypothalamic-pituitary-adrenal HPA In the last 30 years the concept of allostasis has evolved Allostasis is the process whereby an organism adapts to the demands of the environment An allostatic load model applies this concept to chronic stress11 In this model the perception of threat over long time intervals perceived stress can cause over-activation of the HPA-axis resulting in changes in physiological systems as chemical imbalances in autonomic nervous system central nervous system neuroendocrine and immune system activity Factors such as genetics behavior life events and diet can impact this model To our knowledge no clinical study has investigated the link between air pollution effects on cardiovascular disease and psychosocial stress However several studies have now shown an association between stress and respiratory outcomes to air pollution Claugherty and colleagues 2007 found an association between traffic-related air pollution and asthma solely among children exposed to violence 12 Shankardass and colleagues demonstrated that children from stressful households are more susceptible to the effects of traffic-related pollution on the development of asthma 13 In that study stress was evaluated using the Perceived Stress Scale PSS developed by Dr Sheldon Cohen of Carnegie Mellon University This is the most widely used psychological instrument for measuring the perception of stress and has been validated in multiple studies We will use this scale to evaluate the degree to which subjects appraise situations in their life as stressful Heart rate variability HRV is considered to be a reliable biomarker of stress Chronic stress has been shown to be associated with decreases in HRV 14 Since acute ozone exposure can also cause changes in HRV we have chosen HRV as our primary endpoint We hypothesize that the imbalance between the sympathetic and the parasympathetic nervous system caused by chronic stress will result in altered responses to ozone exposure that will be reflected by HRV
Study Oversight
Has Oversight DMC:
None
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?:
None