To our knowledge, this is the first study demonstrating that growing up in a stressful household was associated with larger TRP-induced 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 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
). In the CHS we have shown that particulate matter and ambient NO2
), 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
). Furthermore, TRP exposure has been shown to have direct proinflammatory effects by enhancing mast cell degranulation and cytokine release (31
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
). 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-α, 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
), and psychosocial stress associated with deprivation is one possible explanation for this effect (9
). 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 (). 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 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
), 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
). 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.