Parental Stress Increases the Detrimental Effect of

Traffic Exposure on Children’s Lung Function

Talat Islam1, Robert Urman1, W. James Gauderman1, Joel Milam1, Fred Lurmann2, Ketan Shankardass3,

Ed Avol1, Frank Gilliland1, and Rob McConnell1

1

Department of Preventive Medicine, Keck School of Medicine, Los Angeles, California; 2Sonoma Technology Inc, Petaluma, California;

and 3

Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada

Rationale: Emerging evidence indicates that psychosocial stress

enhances the effect of traffic exposure on the development of

asthma.

Objectives: We hypothesized that psychosocial stress would also

modify the effect of traffic exposure on lung function deficits.

Methods: We studied 1,399 participants in the Southern California

Children’s Health Study undergoing lung function testing (mean

age, 11.2 yr). We used hierarchical mixed models to assess the joint

effect of traffic-related air pollution and stress on lung function.

Measurements and Main Results: Psychosocial stress in each child’s

householdwas assessed based on parental response to the perceived

stress scale (range, 0–16) at study entry. Exposures to nitric oxide,

nitrogen dioxide, and total oxides of nitrogen (NOx), surrogates of

the traffic-related pollution mixture, were estimated at schools and

residences based on a land-use regression model. Among children

from high-stress households (parental perceived stress scale .4)

deficits in FEV1 of 4.5 (95% confidence interval, 26.5 to 22.4) and

of 2.8% (25.7 to 0.3) were associated with each 21.8 ppb increase in

NOx at homes and schools, respectively. These pollutant effects were

significantly larger in the high-stress compared with lower-stress

households (interaction P value 0.007 and 0.05 for residential and

school NOx, respectively). No significant NOx effects were observed

in children from low-stress households. A similar pattern of association was observed for FVC. The observed associations for FEV1 and

FVC remained after adjusting for sociodemographic factors and after

restricting the analysis to children who do not have asthma.

Conclusions: A high-stress home environment is associated with increased susceptibility to lung function effects of air pollution both at

home and at school.

Keywords: parental stress; traffic exposure; lung function; children

Exposure to air pollution, especially to local particulate and the

traffic-related air pollution (TRP) mixture near children’s homes,

has been associated with asthma prevalence, incidence, and exacerbation, and with lung function deficits (1–8). Genetic and

toxicologic studies suggest that these relationships are causal

(9–12). Emerging evidence indicates that the susceptibility to

health effects caused by air pollution is greater among socially

deprived populations (13–15), which might be because of psychosocial stress (13). Although the exact mechanism for this susceptibility remains unknown, one possible explanation is synergistic

psychosocial stress-induced and TRP-induced oxidative stress,

a common biologic effect of both exposures, resulting in airway

inflammation (11, 16).

Psychosocial stress is associated with high-level endogenous

steroid production, which leads paradoxically to steroid resistance

and a diminished antiinflammatory effect of cortisol (17). Diminished production of antiinflammatory IL-5 and IFN-g from peripheral blood mononuclear cells, and an increase in eosinophils

(18), has been reported from children with asthma who perceived

low parental support (a proxy for psychosocial stress). Because

psychosocial stress can provide a milieu that can augment the

effect of inflammatory and oxidative stressors present in TRP

(19–21), we hypothesized that children exposed to high level of

chronic stress would be more susceptible to the detrimental effect

of TRP on lung function deficits in children.

We investigated our hypothesis in a large cohort of Children’s

Health Study (CHS) participants, for who detailed sociodemographic household information, markers of perceived parental

stress as a proxy for children’s psychosocial stress, lung function

measurements, and validated residential and school TRP exposure estimates were available. Some of the results of these studies

have been previously reported in the form of an abstract (22).

METHODS

Study Population

Characteristics of the study population have been described previously

(6). The current analysis involves 1,399 children (mean age,11.2;

SD 0.63) from eight communities in Southern California. These

(Received in original form April 20, 2011; accepted in final form May 17, 2011)

Supported by grants 5P30ES007048, 5P01ES009581, 5P01ES011627,

5R01ES016535, and 5R03ES014046 from the National Institute of Environmental

Health Sciences; grants 5R01HL061768, 5R01HL076647, 5R01HL087680, and

1RC2HL101651 from the National Heart, Lung and Blood Institute; grants R831845,

R826708, and RD831861 from the Environmental Protection Agency; and the Hastings

Foundation.

Author Contributions: T.I. assisted R.U. in statistical analysis, planned the analysis,

and prepared the manuscript. R.U. conducted the statistical analysis of the manuscript and contributed in revising the manuscript. W.J.G., J.M., F.L., K.S., E.A.,

F.G., and R.M. assisted in interpreting the results and contributed to revising the

manuscript. W.J.G., E.A., F.G., and R.M. conceived and designed the study.

Correspondence and requests for reprints should be addressed to Talat Islam,

M.B.B.S., M.S., 1540 Alcazar Street, CHP 236, Keck School of Medicine, Los

Angeles, CA 90033. E-mail: islam@usc.edu

This article has an online supplement, which is accessible from this issue’s table of

contents at www.atsjournals.org

Am J Respir Crit Care Med Vol 184. pp 822–827, 2011

Originally Published in Press as DOI: 10.1164/rccm.201104-0720OC on July 14, 2011

Internet address: www.atsjournals.org

AT A GLANCE COMMENTARY

Scientific Knowledge on the Subject

Traffic exposure has been shown to be associated with

asthma risk and lung function in children. Psychosocial

stress increases susceptibility to the detrimental effects of

traffic exposure–mediated asthma risk in children. Currently, the role of stress on lung function levels in healthy

children remains unknown.

What This Study Adds to the Field

This study shows that children who grow up in households

with high levels of psychosocial stress are more susceptible

to the detrimental effects of traffic exposure on lung

function compared with children who grow up in households

with low parental stress.
communities were selected to reflect a broad range of regional air

pollutant exposures across communities and large gradients in traffic

exposure within communities. Children underwent spirometric lung

function testing during the 2008–2009 school year. Information about

respiratory illness and environmental exposures was provided by

parents in a questionnaire sent home with children at the time of spirometric testing. Additional information, including sociodemographic characteristics and parental psychosocial stress, was available from

a questionnaire parents completed at the time of enrollment of this cohort in 2002–2003. Parents provided informed consent (see the online

supplement).

Parental Stress

The perceived stress scale (PSS), which was used to measure parental

stress, has been validated as a measure of negative affective states and

physical symptoms of stress (23). We used a four-item version of the

scale that has been used previously to predict incidence of wheeze and

asthma in children (24, 25). Items included: “In the last month, how

often have you felt” (1) “that you were unable to control the important

things in your life”; (2) “confident about your ability to handle your

personal problems”; (3) “that things were going your way”; and (4)

“your difficulties were piling up so high that you could not overcome

them.” Each item was scored on a scale of 0–4, with larger values

indicating higher stress levels. The PSS gives equal weight to each item,

resulting in an overall score ranging from 0–16. The PSS was also dichotomized at its sample median into high (.4) and low (< 4) parental stress.

Other Covariates

Sociodemographic characteristics (i.e., race, income, and insurance),

secondhand exposure to tobacco smoke, health insurance, housing characteristics, history of allergy, and child and parental asthma were

assessed by questionnaire (see the online supplement).

Local TRP

Exposure to nitric oxide (NO), nitrogen dioxide (NO2), and total oxides of

nitrogen (NOx) was estimated based on measurements of these pollutants at 940 locations in CHS communities during 2 weeks in each of the

two Southern California seasons. A prediction model was developed

based on distance to traffic corridors, traffic volume, average vehicle

NOx emission rates, wind speed and direction and height of the mixing

layer, and elevation and population density (26). Cross-validation analysis showed that this model was able to predict 68%, 61%, and 72% of the

local variation in average levels of NO2, NO, and NOx, respectively (26).

This model was used to predict concentrations of these pollutants at the

homes and schools of study participants.

Lung Function Measurements

Maximal-effort spirometry and standing height and weight were measured by trained field technicians, using previously described procedures

(7). We evaluated three measures of lung function in this analysis: (1)

FVC, (2) FEV1, and (3) forced expiratory flow over the mid-range of

expiration (FEF25–75).

Asthma

Lifetime asthma at study entry was assessed based on parental report of

physician-diagnosed asthma. Children who were asthma-free at study entry were classified as having new-onset asthma when a parent reported

physician-diagnosed asthma on the annual follow-up questionnaire. Because low lung function is associated with asthma and we have previously

reported that TRP exposure was associated with increased risk of newonset asthma in children residing in high-stress households (25), we conducted sensitivity analyses restricted to children without any history of

asthma.

Statistical Methods

We evaluated the determinants of high parental stress using univariate

logistic regression models. We used hierarchical two-stage multivariate

regression models to assess the joint effect of TRP and stress on lung

function levels with interaction terms after accounting for clustering

at community and school levels with adjustments for known determinants of lung function (see the online supplement). Heterogeneity of

TRP effects by PSS was assessed by comparing nested models using

a partial likelihood ratio test with and without appropriate interaction

terms (i.e., for PSS with TRP). We fitted the following model:

LF 1⁄4 a 1 b1TRPi 1 b2TRPs 1 b3PSS 1 g1PSSTRPi 1 g2PSSTRPs 1 C 1 es;

ðEq:1Þ

where LF represented one of the lung function measurements, and TRPi

(residential TRP centered to local school TRP) and TRPs represented

one of the TRPs at the residence and school level, respectively. The

parameters g1 and g2 quantify modifying effects of stress on the association between LF and residential and school level TRP, respectively.

The model included school-specific (es) random effects and adjustments

for several potential confounders (C) including community of residence

as fixed effects. The approximately orthogonal relationship between

school and deviated residential TRPs allowed us to assess the joint effect of both exposures in the same model. Effect estimates for both

residential and school TRPs were scaled to an increase in exposure

equivalent to 2 SD based on the distribution of residential TRP.

We were concerned that the modifying effects of PSS (captured by g1

and g2) could be confounded by other social factors. We addressed this

issue by including additional interaction terms between TRP and other

social factors in the above model. We determined whether the estimates of g1 and g2 changed by at least 10% on including any of these

additional interaction terms.

All analyses were performed using Statistical Analysis System software (SAS version 9.2; SAS Institute Inc., Cary, NC). A two-tailed alternative hypothesis was assumed in all analyses with significance being

claimed at the 0.05 probability level.

RESULTS

We observed a wide range of variation in parental stress among

the participants’ parents. The observed PSS values ranged from

0–16, with mean of 3.9 (SD 2.8) and median of 4. Approximately 11.5% (n 1⁄4 156) of parents reported no stress in their

life (PSS 1⁄4 0). Less than 25% of the parents reported PSS less

than two (23%) or PSS greater than seven (20%). High parental

PSS varied by sociodemographic and personal factors (Table 1).

Compared with whites, Asian and Hispanic households had

higher levels of PSS. Among Hispanics, completion of the questionnaire in Spanish was associated with an increased risk of

high parental stress. Neither parental nor child’s asthma status

was associated with parental stress. Characteristics suggestive of

low socioeconomic status were associated with increased parental stress, including low parental education, annual household

income less than $30,000, lack of health insurance, and no airconditioner in the home. In this cohort, 6.4% of children did not

have health insurance, 17.4% had parents with less than a high

school education, and 18.8% did not live in a single-family

home, characteristics that were associated with high parental

stress. About 5.3% of the parents reported at least one smoker

at home and 6.1% of children had in utero exposure to maternal

smoking. Although maternal smoking during pregnancy was not

associated with parental stress, a smoker in the home was associated with a 1.7-fold increased risk of high parental stress.

The TRPs had a wide range of variability for both homes and

schools. For example, the mean residential and school NOx were

46.7 ppb (SD 19.6) and 49.7 (SD 19.2) ppb, with ranges of 101.6

and 61.8, respectively (Table 2). In the neighborhood of children’s homes around each school, residential NOx ranged from

55.5 ppb less than to 52.7 ppb greater than the school estimate

(SD 10.9; data not shown). Similar ranges in the distribution of

NO and NO2 were observed.

Islam, Urman, Gauderman, et al.: Stress, Traffic, and Lung Function 823
On average the lung volume and flows were larger for boys

than girls; however, the effect of TRP did not differ by sex (interaction P value . 0.10 for all TRP), so we combined girls and

boys in analyses of lung function. In models adjusted for sex and

other relevant covariates, we observed a detrimental effect of

TRPs on lung function. For example, each 21.8 ppb (2 SD [10.9]

of average school-deviated residential NOx) increase in residential NOx was associated with 2.31% (P value , 0.001) and

1.85% (P value , 0.001) decrease in FVC and FEV1, respectively (Table 3). No statistically significant association was observed between any TRP and FEF25–75. A similar pattern of

associations was observed for NO and NO2; however, the effect

of NO was modestly larger and more significant than NOx or

NO2. We did not observe any statistically significant associations between lung function measures and TRP at school.

We did not observe any statistically significant associations

between PSS and lung function levels (see Table E1 in the

online supplement). However, strong modifying effects of PSS

on the association between FVC and FEV1 and both home and

school TRPs were observed (Table 3). The adverse effect of

TRP was restricted to children from high-stress households

and these associations were most strongly associated with predicted NO. For example, among children with high parental

stress, each 21.8 ppb increase of residential and school NOx

was associated with 4.5% (95% confidence interval [CI], 26.7

to 22.4) and 2.8% (95% CI, 25.7 to 0.28) deficits in FEV1,

respectively. A stronger and more significant interaction was

observed between household stress and NO level at homes

and schools. No significant associations with TRP were observed in low-stress households. Although a similar pattern

was observed for FEF25–75, the interactions between stress and

TRPs were not statistically significant.

We evaluated whether the modifying effect of PSS could be

explained by other factors that were associated with PSS (Table

1). Lack of health insurance (n 1⁄4 93) modified the association of

FEV1 with residential NOx (interaction P value 1⁄4 0.04) but not

with school NOx (interaction P value 1⁄4 0.59; see Table E2). For

each 21.8 ppb increase in NOx, the FEV1 deficit was 9.03%

(95% CI, 213.4 to 23.8) for children without health insurance

and 21.3% (95% CI, 22.9 to 0.25) for children with health

insurance. However, the joint effects of health insurance and

NOx did not fully explain the observed modifying effect of PSS

on lung function. The interaction between PSS and NOx

remained significant (P value 1⁄4 0.01) and the interaction between health insurance and NOx was attenuated and marginally

significant (P value 1⁄4 0.07) when both terms were included in

the same model. Even after restricting the analysis to children

with health insurance, we observed that each 21.8 ppb increase

in NOx was associated with 3.7% (95% CI, 25.86 to 21.49)

deficit in FEV1 among children from high-stress households

compared with those from low-stress households (see Table E3).

Another possible explanation of our findings is that the lung

function deficits were caused by differential risk of TRP by

asthma status in this population (25). To address this concern,

we performed sensitivity analysis by excluding all prevalent

(n 1⁄4 173) and new-onset asthma cases (n 1⁄4 165). Among the

children without any asthma diagnosis (n 1⁄4 1,061), we observed

a modifying effect of household stress on the association between lung function and TRP exposure at home and school

(Table 4) that was similar to that observed in the entire sample.

Each 21.8 ppb increase of residential and school NOx was associated with a 4.3% (95% CI, 26.55 to 22.07) and 3.5% (95%

CI, 26.68 to 20.14) decrease in FEV1, respectively, among

children with high parental stress.

DISCUSSION

To our knowledge, this is the first study demonstrating that growing up in a stressful household was associated with larger TRPinduced lung function deficits in children. Children whose

parents reported a stressful life early in the child’s school years

experienced a detrimental effect associated with exposure to

both residential and school TRP on their lung function volume

and flow in large airways. The observed pattern of effects in

these children could not be explained by asthma or by a range

TABLE 1. SUBJECT CHARACTERISTICS AND ASSOCIATIONS WITH

PARENTAL STRESS

Risk Factor N (%)

High Parental

Stress OR (95% CI)

Subject characteristics

Male 672 (48) 0.90 (0.73–1.12)

Race and ethnicity

White 629 (45) 1.00

Asian 64 (4.6) 2.67 (1.5–4.6)

African American 22 (1.6) 0.84 (0.4–2)

Do not know 149 (10.7) 2.41 (1.7–3.5)

Mixed 194 (13.9) 0.95 (0.7–1.3)

Other or Native American Indian 341 (24.4) 1.83 (1.4–2.4)

Hispanicity

Not Hispanic 595 (42.5) 1.00

Hispanic 769 (55) 1.52 (1.2–1.9)

Do not know 35 (2.5) 2.99 (1.4–6.3)

Spanish language questionnaire

(among Hispanic whites)

288 (38) 1.79 (1.3–2.4)

Asthma in children 173 (13.1) 0.91 (0.7–1.3)

Parental history of asthma 293 (22.3) 1.06 (0.8–1.4)

Sociodemographic factors

Parental education

At least college diploma 419 (30.8) 1.00

High school or some college 704 (51.8) 2.04 (1.5–2.8)

Did not finish high school 236 (17.4) 3.04 (2.3–4.5)

Household income

>$30,000 913 (74.7) 1.00

,$30,000 309 (25.3) 2.44 (1.9–3.2)

Health insurance

Yes 1,231 (88) 1.00

No 93 (6.6) 1.49 (1–2.2)

Home characteristics

Mildew at home 348 (27.2) 1.20 (0.9–1.5)

Cats at home 248 (18.1) 0.68 (0.5–0.9)

Dogs at home 388 (28.4) 0.87 (0.7–1.1)

Cockroaches in home 141 (10.4) 1.79 (1.3–2.6)

In utero smoking 83 (6.1) 1.06 (0.7–1.7)

Any smoker inside home 73 (5.3) 1.72 (1.1–2.8)

Air conditioning at home 900 (65.2) 0.53 (0.4–0.7)

Type of home

Single family house 1,114 (81.2) 1.00

Apartment (2–10 units) 191 (13.9) 2.46 (1.8–3.4)

Apartment (.10 units) 45 (3.3) 2.20 (1.2–4.1)

Mobile home 22 (1.6) 1.92 (0.8–4.6)

Definition of abbreviations: CI 1⁄4 confidence interval; OR 1⁄4 odds ratio.

TABLE 2. DISTRIBUTION OF ANNUAL AVERAGE RESIDENTIAL

TRAFFIC MODELED POLLUTION

TRP* Location Mean (SD) Median (IQR) Min Max Range

NOx Home 46.7 (19.6) 44.3 (31.7) 6.15 107.7 101.5

School 49.7 (19.2) 49.1 (27.8) 16.6 78.3 61.8

NO2 Home 23.2 (6.96) 24.3 (10.6) 3.70 41.5 37.8

School 23.8 (6.73) 24.7 (7.8) 8.25 33.7 25.5

NO Home 23.4 (14.3) 19.1 (20.3) 2.11 77 74.9

School 25.8 (14) 21.4 (24.2) 5.84 51.4 45.5

Definition of abbreviations: IQR 1⁄4 interquartile range; NO 1⁄4 nitric oxide; NO2 1⁄4

nitrogen dioxide; NOx 1⁄4 total oxides of nitrogen.

* Traffic-related pollution (oxides of nitrogen) in parts per billion.

824 AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL 184 2011
of behavioral, socioeconomic, or environmental factors associated with stress.

Over the last decade intensive investigation indicates that

traffic-related particulate or gaseous pollutants result in adverse

effects on respiratory health in children (3, 7, 11, 12, 27, 28). In

the CHS we have shown that particulate matter and ambient

NO2 (28), and living close to a freeway, were associated with

a significant decrease in lung function growth in children 10–18

years of age (7). Emerging evidence indicates that these exposures result in formation of radical oxygen species leading to

inflammation-mediated injury to lung tissue (29, 30). Furthermore, TRP exposure has been shown to have direct proinflammatory effects by enhancing mast cell degranulation and

cytokine release (31, 32).

A potential explanation for the stress-related pattern of TRP

respiratory effects is the biologic pathways common to effects of

TRP and stress (13). Psychosocial stress has been linked to inflammation and oxidative stress (16). These common biologic

pathways may explain the recent epidemiologic studies demonstrating that the risk of TRP-associated asthma was larger in

children in high-stress homes or with a history of exposure to

violence (20, 25). Although the epidemiologic studies have

largely examined modifying effects of stress on the relationship

between TRP and asthma, one toxicologic study found that

stress modified the effect of pollution on lung function (21).

In a rat model, low respiratory flows and volumes resulting from

exposure to ambient fine particles occurred only in stressed

animals. Moreover, markers of systemic inflammation, such as

tumor necrosis factor-a, C-reactive protein, white blood count,

and absolute monocyte and lymphocyte counts, were on average higher among the stressed animals compared with the nonstressed control animals. Psychosocial stress-induced heightened

inflammatory status in CHS participants is one possible explanation for the findings of the current study. Further studies are

warranted to delineate the involved biologic pathways.

Another unique finding of this study was that stress-related

susceptibility was related to TRP exposure effects both at home

and at school. Children in this age group spend almost one-third

of their daytime hours at school so exposure at school is an important contributor to total exposure. Because the residential

TRP levels were deviated from the corresponding school TRP

level, effects could be assessed jointly in the regression model.

The observed consistent pattern of TRP susceptibility among

children growing up in a high-stress household regardless of

the location of TRP exposure also strengthens a causal interpretation of the observed lung function associations with TRP exposure. Furthermore, the higher effect estimates and lower P

values in the order of NO, NOx, and NO2 suggest that reactive

primary traffic emissions were better reflected by NO and it

might be of etiologic importance.

Emerging evidence suggests that social deprivation promotes

the adverse effect of air pollution on respiratory health outcomes

(20, 33, 34), and psychosocial stress associated with deprivation

is one possible explanation for this effect (9, 13, 19, 35, 36). In

this study markers of social deprivation (i.e., low socioeconomic

status; lack of health insurance; and housing characteristics, such

as secondhand smoke exposure, cockroaches in the home, and

lack of air conditioning) were associated with higher household

stress (Table 1). However, none of those factors explained the

large TRP-related health effects we observed in children with

high household stress. Although lack of health insurance, a marker

of low socioeconomic status, increased the susceptibility to TRP

exposure (Table E3), the modifying effect of stress was still evident even among children who had health insurance (Table E4).

A major strength of the study was the use of predicted TRP

exposures that were calibrated from models based on actual

measurement of NO, NO2, and NOx at a large number of

homes and schools in the study communities. The final exposure

model accounted for traffic distance and volume, meteorology,

and other characteristics of nearby land use (26). Approximately two-thirds of the within-community variability in these

TRPs was explained by the model.

There are some limitations to these data. The TRP exposure

was estimated at the center point of the school buildings, but

TABLE 3. EFFECT OF TRP ON LUNG FUNCTION MEASUREMENTS, STRATIFIED BY PARENTAL STRESS LEVEL (HIGH OR LOW)*

TRP Location

Main Effect %

Change (95% CI)

Low Parental Stress %

Change (95% CI)

High Parental Stress %

Change (95% CI)

Interaction

P Value

FVC

NOx Home 22.31 (23.8 to 20.8) 0.02 (22.1 to 2.2) 24.73 (26.7 to 22.7) ,0.01

School 20.98 (23 to 1) 1.04 (21.7 to 3.9) 23.01 (25.9 to 20.1) 0.07

NO Home 22.60 (24.2 to 21) 20.04 (22.4 to 2.4) 24.84 (26.9 to 22.8) ,0.01

School 21.39 (23.5 to 0.8) 0.82 (22.2 to 4) 23.30 (26.3 to 20.2) 0.04

NO2 Home 22.00 (23.4 to 20.6) 0.07 (21.9 to 2) 24.55 (26.5 to 22.6) 0.02

School 20.59 (22.5 to 1.3) 1.29 (21.3 to 4) 22.68 (25.4 to 0.1) .0.10

FEV1

NOx Home 21.85 (23.3 to 20.4) 0.62 (21.6 to 2.9) 24.47 (26.5 to 22.4) ,0.01

School 20.15 (22.2 to 1.9) 2.52 (20.3 to 5.5) 22.77 (25.7 to 0.3) 0.07

NO Home 22.09 (23.7 to 20.5) 0.75 (21.7 to 3.3) 24.61 (26.7 to 22.5) ,0.01

School 20.40 (22.6 to 1.8) 2.62 (20.5 to 5.8) 23.03 (26.1 to 0.2) 0.04

NO2 Home 21.60 (23 to 20.2) 0.54 (21.4 to 2.5) 24.31 (26.3 to 22.3) 0.02

School 0.06 (21.9 to 2) 2.43 (20.3 to 5.2) 22.48 (25.3 to 0.4) .0.10

MMEF

NOx Home 20.72 (23.7 to 2.4) 0.85 (23.4 to 5.3) 22.57 (26.7 to 1.8) .0.10

School 1.21 (22.9 to 5.5) 3.28 (22.4 to 9.2) 20.82 (26.8 to 5.6) .0.10

NO Home 21.09 (24.3 to 2.2) 0.77 (24 to 5.8) 22.90 (27.2 to 1.6) .0.10

School 0.95 (23.4 to 5.5) 3.39 (22.7 to 9.9) 21.15 (27.5 to 5.6) .0.10

NO2 Home 20.55 (23.4 to 2.4) 0.88 (23 to 4.9) 22.60 (26.7 to 1.7) .0.10

School 1.19 (22.7 to 5.3) 2.99 (22.3 to 8.6) 20.76 (26.5 to 5.4) .0.10

Definition of abbreviations: CI 1⁄4 confidence interval; MMEF 1⁄4 FEF25–75; NO 1⁄4 nitric oxide; NO2 1⁄4 nitrogen dioxide; NOx 1⁄4 total oxides of nitrogen; TRP 1⁄4 trafficrelated pollution.

* Models adjusted for log height and square term for log height, body mass index and square term for body mass index, sex, age, age–sex interaction, race, Hispanic

ethnicity, respiratory illness at time of lung function, field technician, and community. Percent (%) change was scaled to 2 SD (NOx 1⁄4 21.8 ppb; NO 1⁄4 16.2 ppb; and

NO2 1⁄4 7.3 ppb) of the TRP difference between home and school (averaged across schools).

Islam, Urman, Gauderman, et al.: Stress, Traffic, and Lung Function 825
these TRP can have high variability on a small spatial scale.

Therefore, children’s true exposure at school may have been

substantially different when they were outdoors exercising, a period of likely greatest vulnerability to TRP exposure because of

increased ventilation rates and consequent increased lung dose.

If the observed associations were causal, it is likely that accounting for this exposure uncertainty would have resulted in a larger

estimated health effect. The use of parental stress as a proxy for

psychosocial stress in the child limits our ability to differentiate

between the effects of household and personal stress in these

children. Parental stress has been shown to be indicative of

stress in children (37, 38), and at the time of assessment of early

life stress at study enrollment, these children were too young to

provide reliable questionnaire information on their own stress

levels. Studies with longitudinal measurement of parental stress,

personal stress, and lung function measurement are needed to

clarify the role of the psychologic stressors on lung function and

lung function growth.

Findings of this study suggest that psychosocial stress may increase the susceptibility of the lung to the detrimental effect of

TRP, resulting in decreased lung volume (FVC) and flow in the

larger airways (FEV1). Further research is warranted to identify

the biologic pathways involved in the augmentation of the detrimental effect of TRP in children exposed to household stress.

Beyond this etiologic importance, our findings also have potentially important public health implications. The magnitude of

the TRP-associated deficits in FEV1 and FVC levels in children

growing up in high-stress households was larger than deficits

reported for children exposed to maternal smoking during pregnancy and secondhand tobacco smoke (39, 40). Hispanic white

children living in low income households have been reported to

be exposed to high levels of TRP (41) and in our sample they

also had higher levels of household stress. Therefore, these children may be a group at particularly high risk of preventable

TRP-associated deficits in lung function. Furthermore, children

spend a substantial amount of time at school where they are also

exposed to TRP. In California, more than 10% of the public

schools are within 150 m of major roadways with more than

25,000 daily vehicular traffic (42) and a similar pattern of heavy

school-related traffic exposure has been reported in other major

metropolitan areas across the United States (43). Our findings

suggest that by regulating TRP levels around residential areas

and schools, the adverse effect of TRP on lung function among

vulnerable children could be reduced.

Author Disclosure: T.I., R.U., W.J.G., J.M., K.S., E.A., and F.G. do not have a financial relationship with a commercial entity that has an interest in the subject of this

manuscript. F.L. is employed by Sonoma Technology Inc. R.M. received an award

to examine the risk of traffic-related air pollution that resulted from a competitive

application submitted to and selected by the California State South Coast Air

Quality Management District. The award was made with funds from settlement

with the District by BP for violation of air quality standards.

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TABLE 4. EFFECT OF TRP ON LUNG FUNCTION MEASUREMENTS AMONG CHILDREN WITHOUT ANY HISTORY OF ASTHMA

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NOx Home 22.49 (24.1 to 20.9) 20.47 (22.9 to 2) 24.72 (26.9 to 22.5) 0.05

School 20.85 (23.1 to 1.4) 1.39 (21.7 to 4.6) 23.74 (26.9 to 20.4) 0.05

NO Home 22.93 (24.7 to 21.2) 20.80 (23.5 to 2) 24.94 (27.2 to 22.6) 0.06

School 21.32 (23.7 to 1.1) 1.05 (22.3 to 4.6) 24.12 (27.5 to 20.7) 0.04

NO2 Home 22.01 (23.5 to 20.5) 20.18 (22.3 to 2) 24.39 (26.6 to 22.2) 0.09

School 20.39 (22.5 to 1.8) 1.66 (21.3 to 4.7) 23.26 (26.4 to 20.1) .0.10

FEV1

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School 0.09 (22.2 to 2.4) 3.32 (0.1 to 6.7) 23.46 (26.7 to 20.1) 0.03

NO Home 22.24 (24 to 20.5) 0.55 (22.2 to 3.4) 24.57 (26.8 to 22.2) 0.06

School 20.23 (22.6 to 2.2) 3.37 (20.2 to 7) 23.81 (27.2 to 20.3) 0.02

NO2 Home 21.50 (23 to 0.1) 0.63 (21.6 to 2.9) 24.06 (26.3 to 21.8) 0.06

School 0.37 (21.8 to 2.6) 3.22 (0.2 to 6.4) 23.06 (26.2 to 0.2) .0.10

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NOx Home 0.24 (23.1 to 3.7) 2.33 (22.5 to 7.4) 21.31 (26.1 to 3.7) .0.10

School 2.13 (22.5 to 7) 5.43 (21 to 12.3) 20.83 (27.6 to 6.5) .0.10

NO Home 20.10 (23.7 to 3.7) 2.40 (23.1 to 8.1) 21.64 (26.5 to 3.5) .0.10

School 1.89 (23.1 to 7.1) 5.74 (21.2 to 13.2) 21.20 (28.3 to 6.4) .0.10

NO2 Home 0.32 (22.8 to 3.6) 2.12 (22.2 to 6.6) 21.35 (26 to 3.5) .0.10

School 2.12 (22.3 to 6.8) 4.93 (21.1 to 11.3) 20.72 (27.3 to 6.3) .0.10

Definition of abbreviations: CI 1⁄4 confidence interval; MMEF 1⁄4 FEF25–75; NO 1⁄4 nitric oxide; NO2 1⁄4 nitrogen dioxide; NOx 1⁄4 total oxides of nitrogen; TRP 1⁄4 trafficrelated pollution.

* Models adjusted for log height and square term for log height, body mass index and square term for body mass index, sex, age, age–sex interaction, race, Hispanic

ethnicity, respiratory illness at time of lung function, field technician, and community. Percent (%) change was scaled to 2 SD (NOx 1⁄4 21.8 ppb; NO 1⁄4 16.2 ppb; and

NO2 1⁄4 7.3 ppb) of the TRP difference between home and school (averaged across schools).

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