Chronic traffic-related air pollution and stress interact to predict biologic and clinical outcomes in asthma

Edith Chen, Hannah M.C. Schreier, Robert C. Strunk, Michael Brauer

Research output: Contribution to journalArticle

98 Citations (Scopus)

Abstract

Background: Previous research has documented effects of both physical and social environmental exposures on childhood asthma. However, few studies have considered how these two environments might interact to affect asthma. Objective: This study aimed to test interactions between chronic exposure to traffic-related air pollution and chronic family stress in predicting biologic and clinical outcomes in children with asthma. Method: Children with asthma (n = 73, 9-18 years of age) were interviewed about life stress, and asthma-relevant inflammatory markers [cytokine production, immunoglobulin E (IgE), eosinophil counts] were measured. Parents reported on children's symptoms. Children completed daily diaries of symptoms and peak expiratory flow rate (PEFR) measures at baseline and 6 months later. Exposure to traffic related air pollution was assessed using a lahd use regression model for nitrogen dioxide was concentrations. Results: NO2 by stress interactions were found for interleukin-5 (β for interaction term = -0.31, p = 0.02), IgE (interaction β = -0.29, p = 0.02), and eosinophil counts (interaction β = -0.24, p = 0.04). These interactions showed that higher chronic stress was. associated with heightened inflammatory profiles as pollution levels decreased. Longitudinally, NO2 by stress interactions emerged for daily diary symptoms (interaction β = -0.28, p = 0.02), parent-reported symptoms (interaction β = -0.25, p = 0.07), and PEFR (interaction β = -0.30, p = 0.03). These interactions indicated that higher chronic stress was associated with incrcases over time in symptoms and decreases over time in PEFR as pollution levels decreased. Conclusions: The physical and social environments interacted in predicting both biologic and clinical outcomes in children with asthma, suggesting that when pollution exposure is more modest, vulnerability to asthma exacerbations may be heightened in children with higher chronic stress.

Original languageEnglish (US)
Pages (from-to)970-975
Number of pages6
JournalEnvironmental health perspectives
Volume116
Issue number7
DOIs
StatePublished - Jul 1 2008

Fingerprint

asthma
Air Pollution
Air pollution
atmospheric pollution
Asthma
Peak Expiratory Flow Rate
Pollution
peak flow
Flow rate
Immunoglobulin E
Eosinophils
Nitrogen Dioxide
Interleukin-5
pollution exposure
pollution
Social Environment
Environmental Exposure
nitrogen dioxide
traffic
Psychological Stress

All Science Journal Classification (ASJC) codes

  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis

Cite this

@article{7b11c86943594709ac1b986d90b61644,
title = "Chronic traffic-related air pollution and stress interact to predict biologic and clinical outcomes in asthma",
abstract = "Background: Previous research has documented effects of both physical and social environmental exposures on childhood asthma. However, few studies have considered how these two environments might interact to affect asthma. Objective: This study aimed to test interactions between chronic exposure to traffic-related air pollution and chronic family stress in predicting biologic and clinical outcomes in children with asthma. Method: Children with asthma (n = 73, 9-18 years of age) were interviewed about life stress, and asthma-relevant inflammatory markers [cytokine production, immunoglobulin E (IgE), eosinophil counts] were measured. Parents reported on children's symptoms. Children completed daily diaries of symptoms and peak expiratory flow rate (PEFR) measures at baseline and 6 months later. Exposure to traffic related air pollution was assessed using a lahd use regression model for nitrogen dioxide was concentrations. Results: NO2 by stress interactions were found for interleukin-5 (β for interaction term = -0.31, p = 0.02), IgE (interaction β = -0.29, p = 0.02), and eosinophil counts (interaction β = -0.24, p = 0.04). These interactions showed that higher chronic stress was. associated with heightened inflammatory profiles as pollution levels decreased. Longitudinally, NO2 by stress interactions emerged for daily diary symptoms (interaction β = -0.28, p = 0.02), parent-reported symptoms (interaction β = -0.25, p = 0.07), and PEFR (interaction β = -0.30, p = 0.03). These interactions indicated that higher chronic stress was associated with incrcases over time in symptoms and decreases over time in PEFR as pollution levels decreased. Conclusions: The physical and social environments interacted in predicting both biologic and clinical outcomes in children with asthma, suggesting that when pollution exposure is more modest, vulnerability to asthma exacerbations may be heightened in children with higher chronic stress.",
author = "Edith Chen and Schreier, {Hannah M.C.} and Strunk, {Robert C.} and Michael Brauer",
year = "2008",
month = "7",
day = "1",
doi = "10.1289/ehp.11076",
language = "English (US)",
volume = "116",
pages = "970--975",
journal = "Environmental Health Perspectives",
issn = "0091-6765",
publisher = "Public Health Services, US Dept of Health and Human Services",
number = "7",

}

Chronic traffic-related air pollution and stress interact to predict biologic and clinical outcomes in asthma. / Chen, Edith; Schreier, Hannah M.C.; Strunk, Robert C.; Brauer, Michael.

In: Environmental health perspectives, Vol. 116, No. 7, 01.07.2008, p. 970-975.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Chronic traffic-related air pollution and stress interact to predict biologic and clinical outcomes in asthma

AU - Chen, Edith

AU - Schreier, Hannah M.C.

AU - Strunk, Robert C.

AU - Brauer, Michael

PY - 2008/7/1

Y1 - 2008/7/1

N2 - Background: Previous research has documented effects of both physical and social environmental exposures on childhood asthma. However, few studies have considered how these two environments might interact to affect asthma. Objective: This study aimed to test interactions between chronic exposure to traffic-related air pollution and chronic family stress in predicting biologic and clinical outcomes in children with asthma. Method: Children with asthma (n = 73, 9-18 years of age) were interviewed about life stress, and asthma-relevant inflammatory markers [cytokine production, immunoglobulin E (IgE), eosinophil counts] were measured. Parents reported on children's symptoms. Children completed daily diaries of symptoms and peak expiratory flow rate (PEFR) measures at baseline and 6 months later. Exposure to traffic related air pollution was assessed using a lahd use regression model for nitrogen dioxide was concentrations. Results: NO2 by stress interactions were found for interleukin-5 (β for interaction term = -0.31, p = 0.02), IgE (interaction β = -0.29, p = 0.02), and eosinophil counts (interaction β = -0.24, p = 0.04). These interactions showed that higher chronic stress was. associated with heightened inflammatory profiles as pollution levels decreased. Longitudinally, NO2 by stress interactions emerged for daily diary symptoms (interaction β = -0.28, p = 0.02), parent-reported symptoms (interaction β = -0.25, p = 0.07), and PEFR (interaction β = -0.30, p = 0.03). These interactions indicated that higher chronic stress was associated with incrcases over time in symptoms and decreases over time in PEFR as pollution levels decreased. Conclusions: The physical and social environments interacted in predicting both biologic and clinical outcomes in children with asthma, suggesting that when pollution exposure is more modest, vulnerability to asthma exacerbations may be heightened in children with higher chronic stress.

AB - Background: Previous research has documented effects of both physical and social environmental exposures on childhood asthma. However, few studies have considered how these two environments might interact to affect asthma. Objective: This study aimed to test interactions between chronic exposure to traffic-related air pollution and chronic family stress in predicting biologic and clinical outcomes in children with asthma. Method: Children with asthma (n = 73, 9-18 years of age) were interviewed about life stress, and asthma-relevant inflammatory markers [cytokine production, immunoglobulin E (IgE), eosinophil counts] were measured. Parents reported on children's symptoms. Children completed daily diaries of symptoms and peak expiratory flow rate (PEFR) measures at baseline and 6 months later. Exposure to traffic related air pollution was assessed using a lahd use regression model for nitrogen dioxide was concentrations. Results: NO2 by stress interactions were found for interleukin-5 (β for interaction term = -0.31, p = 0.02), IgE (interaction β = -0.29, p = 0.02), and eosinophil counts (interaction β = -0.24, p = 0.04). These interactions showed that higher chronic stress was. associated with heightened inflammatory profiles as pollution levels decreased. Longitudinally, NO2 by stress interactions emerged for daily diary symptoms (interaction β = -0.28, p = 0.02), parent-reported symptoms (interaction β = -0.25, p = 0.07), and PEFR (interaction β = -0.30, p = 0.03). These interactions indicated that higher chronic stress was associated with incrcases over time in symptoms and decreases over time in PEFR as pollution levels decreased. Conclusions: The physical and social environments interacted in predicting both biologic and clinical outcomes in children with asthma, suggesting that when pollution exposure is more modest, vulnerability to asthma exacerbations may be heightened in children with higher chronic stress.

UR - http://www.scopus.com/inward/record.url?scp=46749146184&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=46749146184&partnerID=8YFLogxK

U2 - 10.1289/ehp.11076

DO - 10.1289/ehp.11076

M3 - Article

C2 - 18629323

AN - SCOPUS:46749146184

VL - 116

SP - 970

EP - 975

JO - Environmental Health Perspectives

JF - Environmental Health Perspectives

SN - 0091-6765

IS - 7

ER -