Effects of Stress and Traffic Pollutants on Childhood Asthma in an Urban CommunityEPA Grant Number: R834579
Title: Effects of Stress and Traffic Pollutants on Childhood Asthma in an Urban Community
Investigators: Laumbach, Robert , Baptista, Ana , Fiedler, Nancy , Kipen, Howard , Ohman-Strickland, Pamela , Zhang, Junfeng
Current Investigators: Laumbach, Robert , Baptista, Ana , Fan, Zhi-Hua (Tina) , Fiedler, Nancy , Kipen, Howard , Ohman-Strickland, Pamela
Institution: University of Medicine and Dentistry of New Jersey
Current Institution: University of Medicine and Dentistry of New Jersey , UMDNJ - Robert Wood Johnson Medical School
EPA Project Officer: Breville, Maggie
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: Health Effects , Human Health Risk Assessment , Health
Higher levels of exposure to air pollutants and stress may contribute to asthma disparities in urban communities. Recent epidemiological evidence suggests that psychosocial stress may modify the effects of traffic-related air pollution on asthma. We will test a model in which chronic stress modifies the effects of acute exposures to traffic-related air pollutants by blunting the normally protective roles of the hypothalamic-pituitary-adrenal (HPA) and/or sympathetic-adrenal-medullary (SAM) axes in acute asthma exacerbation. We propose to test these hypotheses: 1) Exposure to the traffic pollution markers nitrogen dioxide (NO2) and black carbon (BC) will be inversely correlated with lung function (FEV1) and positively correlated with fraction exhaled nitric oxide (FENO), a marker of pulmonary inflammation. 2) Individual levels of chronic and episodic stress, assessed by interview, will modify the correlations between air pollutant levels and FEV1 and FENO. 3) The degree to which HPA and SAM responses are blunted will be correlated with the level of chronic and episodic stress obtained from the stress interviews. 4) The degree to which HPA and SAM responses are blunted will have a stronger modifying effect than the interview variables on the relationships between air pollution and asthma exacerbation.
A panel of 40 volunteers in Newark, NJ with mild-to-moderate, persistent asthma, aged 9-14 years old, will participate in a study monitoring personal exposure to traffic-related pollutants and acute changes in asthma status. We will assess asthma status as daily medication use, forced expiratory volume in one second (FEV1) measured three times per day, and FENO measured once per day, for 10 consecutive days. We will measure personal exposure to traffic pollution as 24-hr-average NO2 and real-time, 5-min average BC concentrations over the 10-day period. We will evaluate correlations between changes in asthma status and changes in prior NO2 and BC exposure concentrations. We will assess chronic and episodic psychosocial stress during the previous 6-month period in asthmatics using the UCLA Life Stress Interview for Children. We will evaluate blunting of the HPA and SAM axes by chronic and episodic stress by measuring a) diurnal variation in salivary cortisol and a-amylase and b) salivary cortisol and α-amylase response to a standardized acute stressor, the Trier Social Stress Test for Children, in each subject.
We will test a plausible mode of action by which psychosocial stress may worsen asthma responses to air pollution. Improved understanding of how chronic stress may increase susceptibility to air pollutants among people with asthma is important for understanding cumulative risk in urban and other communities. Ultimately, better understanding of modes of action of stress on pollution-health associations will lead to improved characterization of risk among susceptible populations. Additional long-term outcomes may include support for better-integrated public health interventions that address both environmental pollution and nonchemical stressors.
Supplemental Keywords:Air, vulnerability, human health, community-based, psychological, toxics, nitrogen oxides, particulates, midatlantic, New Jersey, N.J., EPA Region 2;, Health, Scientific Discipline, ENVIRONMENTAL MANAGEMENT, Risk Management, Health Risk Assessment, Risk Assessments, Environmental Monitoring, Biology, asthma, cumulative risk, anthropogenic stress, children's health, lung disease, airway disease, allergic airway disease, air pollution, ambient particle health effects, airshed modeling, allergens, inhalation study, exposure assessment
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