Grantee Research Project Results
Final Report: Effects of Stress and Traffic Pollutants on Childhood Asthma in an Urban Community
EPA Grant Number: R834579Title: Effects of Stress and Traffic Pollutants on Childhood Asthma in an Urban Community
Investigators: Laumbach, Robert , Kipen, Howard , Greenberg, Molly , Fiedler, Nancy , Ohman-Strickland, Pamela
Institution: University of Medicine and Dentistry of New Jersey , Rutgers , Ironbound Community Corporation , Robert Wood Johnson Medical School
Current Institution: University of Medicine and Dentistry of New Jersey , Ironbound Community Corporation , Robert Wood Johnson Medical School , Rutgers
EPA Project Officer: Hahn, Intaek
Project Period: June 1, 2010 through June 30, 2014 (Extended to June 30, 2016)
Project Amount: $1,249,960
RFA: Understanding the Role of Nonchemical Stressors and Developing Analytic Methods for Cumulative Risk Assessments (2009) RFA Text | Recipients Lists
Research Category: Human Health
Objective:
Air pollution risk assessments and public health interventions that take into account the increased susceptibility of people with asthma would be improved by a better understanding of how SES, race, and/or other nonchemical factors interact with exposure to air pollutants. Asthma disproportionately affects children of color living in urban areas and in poverty. Although the susceptibility and vulnerability factors underlying this disparity are complex, psychosocial stress may be a common pathway by which multiple factors related to race and social class may modify responses to air pollution and other chemical environmental factors that exacerbate asthma. Exposures to traffic air pollutants and psychosocial stress often occur together in urban communities, suggesting that interactions between these factors are likely to be important. This project examined how exposure to traffic air pollutants, combined with chronic and episodic psychosocial stress, can affect exacerbation of asthma in a panel study of children in a diverse, low-income urban community.
We are testing a hypothesis about the biological pathways by which stress may "get into the body" and modify associations between air pollution and asthma exacerbation among children. Specifically, we are testing how stress may modify inflammatory and pulmonary function effects of acute exposures to traffic-related air pollutants via attenuation of the normally homeostatic roles of the hypothalamic pituitary adrenal (HPA) and/or sympathetic adrenal medullary (SAM) axes in acute asthma exacerbation. Our primary outcomes were measurement of acute changes in exhaled nitric oxide (eNO)—a marker of pulmonary inflammation, and forced expiratory volume in one second (FEV1)—a measure of obstructed lung function. Pulmonary inflammation and/or pulmonary function decrements in response to traffic air pollution are expected to be greater in children with asthma who have had high chronic and episodic life stressors during the previous 6 months compared to children with lower levels of these stressors. We assessed HPA and SAM responsiveness non-invasively with measurement of 1) salivary cortisol and alpha-amylase (a marker of sympathetic activation) levels following an acute experimental stressor, and 2) the pattern of daily salivary cortisol and a-amylase levels. We proposed that chronic stress attenuates acute sympathetic nervous system activation that is normally protective against asthma. These acute stress responses include endogenous cortisol and sympathetic nervous system responses, which are anti-inflammatory and bronchodilatory, respectively. Down-regulation of these protective responses to the acute stress of an asthma exacerbation may worsen the acute asthma response to asthma triggers, such as air pollutants. We hypothesized that blunting of HPA and SAM responses by chronic and episodic stress mediates the modification of asthma responses to air pollution that has been suggested by other studies.
This project was conceived, designed, and carried out as a community-based participatory research project by Ironbound Community Corporation (ICC) leaders and Rutgers University (formerly University of Medicine and Dentistry of New Jersey) faculty. The Ironbound community is adjacent to the largest seaport on the east coast, Liberty International Airport, and major interstate highways. The community has had a long-standing concern about the impacts of diesel truck traffic, particularly port drayage trucks, on the health of residents, especially children. Asthma among children was recognized as especially burdensome in this community. Together, ICC and Rutgers investigators developed the plan to conduct a study of exacerbation of asthma by exposure to diesel exhaust and other traffic pollutants among a panel of children with asthma. We would conduct personal monitoring for black carbon and nitrogen dioxide, and daily measurements of asthma, as well as measurements of chronic stress and responses to acute stress.
Summary/Accomplishments (Outputs/Outcomes):
Our original goal was to recruit 40 participants aged 9-14 and parent/caregiver to participate in the study. Thirty-seven subjects completed participation in data collection activities for up to 30 days, for approximately 1,100 person-days of personal air pollutant exposure and asthma outcomes. The personal exposure data included daily, 24-hour, 1-minute black carbon (BC) recorded for up to 30 consecutive days, and daily 24-hour integrated nitrogen dioxide (NO2). Daily asthma status data included thrice daily spirometry with peak flow and FEV1 and other parameters, daily exhaled nitric oxide, symptoms, and medication use. Daily time-activity logs were confirmed with GPS location coordinates with a tracker co-located with the micro-aethalometer. No serious problems or adverse events have been observed.
We demonstrated the feasibility of using microaethalometers for personal monitoring of exposure to BC among children. However, motion artifact and effects of sudden changes in humidity necessitated use of algorithms (Cai, 2014) to identify and eliminate artifact on continuous 24 hour x 30-day data. As planned, personal NO2 monitoring using Ogawa passive monitors for integrated 24-hour measurements was completed. Central-site air monitoring data also are being compiled. A GPS tracker that accompanied the monitors provided time-location data, supplemented by daily time-activity logs.
Daily asthma outcomes measured as exhaled nitric oxide using a NIOX Mino (Aerocrine) instrument were taken on 5 weekdays per week of subject participation. Spirometry with a portable spirometer (EasyOne) was measured three times per day (morning, afternoon, evening). Asthma symptom and medication use logs were collected daily.
Chronic stress was assessed with the UCLA Chronic and Episodic Stress Interview for Children during the study period for each participant and a primary parent/caregiver. Ratings in five domains (academic, school behavior, social, household, and neighborhood) for each participant and parent were recorded. Three pairs of morning and bed-time saliva samples were collected for each subject to assess diurnal variability in salivary cortisol, measured with an ELISA assay (Salimetrics Inc). Responses to acute stress also were measured with salivary cortisol and amylase before and after a modified TRIER social stress test was administered. Analysis by ELISA was conducted to meet quality control standards of intra-assay variability (coefficient of variation ≤ 15%) and inter-assay variability (coefficient of variation ≤ 20%).
Demographic data on age, sex, race, ethnicity, height, body weight, school grade, maternal education, and family income were collected to be used in data analysis.
We developed mixed linear regression models to test the hypothesis that exposure to diesel exhaust, measured as daily personal exposure to BC, is associated with asthma exacerbation, measured as daily exhaled nitric oxide (eNO) levels, spirometry (FEV-1 and FVC), symptoms and/or medication use (Aim 1). Real-time, personal BC data for 20 subjects have been reviewed and cleaned using the method of Cai, et al. (2014). Preliminary analysis of the relationships between personal BC and NO2 and eNO has been completed for these subjects in order to test the methods. Multiple imputation was used to deal with missing data (primarily due to weekends and difficulties that some subjects had with adherence to the protocol). The results of an initial analysis of the first six subjects were presented at the International Society for Environmental Epidemiology (ISEE) conference on September 1, 2016. In this analysis, mean previous 24-hour black carbon was associated with increase in eNO (2.7%, 95% CI -1.3 to 6.8%), which was not statistically significant, but there was low statistical power to detect effects in this small subset of study data. Unpublished analysis results indicate a statistically significant increase in eNO with increased exposure to BC in the first 20 subjects. Additional asthma outcomes (spirometry, symptoms, medication use) will be analyzed with similar approaches in the full data set.
Analysis of data for Aim 2 to determine if chronic stress modifies relationships between exposure to traffic pollutants and asthma outcomes awaits completion of analyses for Aim 1. We have collected stress scores (1-5 scale) from the UCLA Chronic and Episodic Stress interview of the participant and primary caregiver. Frequency distributions of the scores were plotted as histograms in each category. These figures were presented at the grant review meeting in May 2016.
Analysis for Aim 3, determining the relationships between chronic stress, HPA, SAM, and air pollutants on exacerbation of asthma, also is ongoing. Salivary cortisol and amylase from three evening-morning pairs from each participant have been collected and analyzed, as well as prior to and after the experiment's stressor (Trier Social Stress Test). These will be entered into statistical models to test for modification of the effect of the traffic air pollutants on asthma outcomes.
Conclusions:
This community-based participatory research project was conceived, designed, and implemented as a partnership between the Ironbound Community Corporation and investigators from Rutgers University School of Public Health. The project resulted in increased knowledge and community infrastructure to actively engage in scientific research within this environmental justice community. The ability of community members to interpret and apply scientific knowledge to environmental health problems in the community also was increased. Initial results indicate that there was an association between exposure to black carbon—a marker for diesel exhaust, and exhaled nitric oxide—a marker for airway inflammation in children with asthma. This project is contributing to the body of knowledge about how short-term changes in air quality can affect asthma exacerbation in children, using gold-standard personal exposure measurements. The project also is contributing to understanding how chronic psychosocial stress may interact with exposure to air pollution to contribute to disparities in asthma in urban communities, especially environmental justice communities with multiple environmental and social stressors. Study data collected on exposure to air pollutants, asthma outcomes, and psychosocial stress provide a rich data set for analysis of relationships between air pollutants, stress, and asthma outcomes in children.
Journal Articles on this Report : 3 Displayed | Download in RIS Format
Other project views: | All 4 publications | 3 publications in selected types | All 3 journal articles |
---|
Type | Citation | ||
---|---|---|---|
|
Ji N, Baptista A, Yu C, Cepeda C, Green F, Greenberg M, Mincey I, Ohman-Strickland P, Fielder N, Kipen H, Laumbach R. Traffic-related air pollution, chronic stress, and changes in exhaled nitric oxide and lung function among a panel of children with asthma living in an underresourced community. SCIENCE OF THE TOTAL ENVIRIONMENT 2023;912(168984) |
R834579 (Final) |
Exit |
|
Laumbach RJ, Kipen HM. Respiratory health effects of air pollution: Update on biomass smoke and traffic pollution. Journal of Allergy and Clinical Immunology 2012;129(1):3-11. |
R834579 (Final) |
Exit Exit |
|
Payne-Sturges DC, Korfmacher KS, Cory-Slechta DA, Jimenez M, Symanski E, Carr Shmool JL, Dotson-Newman O, Cloughtery JE, French R, Levy JI, Laumbach R, Rodgers K, Bongiovanni R, Scammell MK. Engaging communities in research on cumulative risk and social stress-environment interactions: lessons learned from EPA's STAR Program. Environmental Justice 2015;8(6):203-212. |
R834579 (Final) R834576 (Final) R834577 (Final) R834578 (Final) R834580 (Final) R834581 (Final) R834582 (Final) |
Exit Exit Exit |
Supplemental Keywords:
Health, Scientific Discipline, ENVIRONMENTAL MANAGEMENT, Risk Management, Health Risk Assessment, Risk Assessments, Environmental Monitoring, Biology, cumulative risk, anthropogenic stress, asthma, children's health, lung disease, allergic airway disease, airway disease, air pollution, ambient particle health effects, airshed modeling, allergens, inhalation study, exposure assessmentProgress and Final Reports:
Original AbstractThe perspectives, information and conclusions conveyed in research project abstracts, progress reports, final reports, journal abstracts and journal publications convey the viewpoints of the principal investigator and may not represent the views and policies of ORD and EPA. Conclusions drawn by the principal investigators have not been reviewed by the Agency.
Project Research Results
- 2015 Progress Report
- 2014
- 2013 Progress Report
- 2012 Progress Report
- 2011 Progress Report
- 2010 Progress Report
- Original Abstract
3 journal articles for this project