Traffic-Related Air Pollution and Stress: Effects on Asthma
Environ Health Perspect. doi:10.1289/ehp.11863 available via http://dx.doi.org [Online 29 August 2008]
Referencing: Chronic Traffic-Related Air Pollution and Stress Interact to Predict Biologic and Clinical Outcomes in Asthma
Chen et al. (2008) examined the potential for social stressors to influence responsiveness to environmental pollution. Contrary to their initial hypothesis, and to results we reported previously (Clougherty et al. 2007), their findings indicated that chronic stress was associated with asthma symptoms and heightened inflammatory profiles only in low nitrogen dioxide areas. We would like to note several key issues in the emerging research on social susceptibility to environmental pollutants that should be considered as research on this work moves forward.
One key issue is that the relative timing of psychosocial stressors and physical exposures, which Chen et al. (2008) did not present, is critical for at least two reasons:
- Acute and chronic stress produce substantively different physiologic sequelae. Acute stress can induce bronchodilation with elevated cortisol (possibly masking short-term detrimental respiratory effects of pollution), whereas chronic stress can result in cumulative wear and tear (allostatic load) and suppressed immune function over time, increasing general susceptibility (McEwen and Seeman 1999).
- Temporal relationships between stress and pollution exposures matter. Depending on when measures are obtained, exposure misclassification is possible, which may influence the directionality of observed interactions. Chen et al. (2008) stated that the measured 6-month stress and NO2 periods do not overlap, but they did not specify whether the stress measure preceded the 1998–2003 NO2 exposure window or the amount of time that passed between exposures. If the stress interval occurred first, some increased susceptibility to subsequent pollution is plausible, provided that chronic stress effects predominate over acute effects. If, however, the stress interval occurred after NO2 exposures, the interaction is potentially problematic, because we must then assume that stress levels measured after the 6-year NO2 period (1998–2003) are relevant for the earlier time, which may not be the case. If, for example, respondents compared current stress to prior experience, an individual reporting high stress for one interval may have experienced lower stress previously, during those "reference" periods corresponding to the NO2 window—potentially producing a negative interaction, as Chen et al. (2008) observed. More broadly, careful attention to relative timing and durations of stress and pollution exposures is critical in maintaining directionality and interpretability as we progress with this research.
Second, Chen et al.'s finding of significant effects of stress only in low-NO2 areas (Chen et al. 2008) points to the possibility of nonlinear interactions and saturation effects at high exposures. Similarly, our group (Clougherty et al. 2006) reported that asthmatic children of families reporting higher fear of violence showed less symptom improvement in response to allergen-reducing indoor environmental interventions. Our results, counter to our initial hypotheses, suggested a saturation effect in our very high-exposure public housing cohort, where either high exposure alone may have been adequate to induce or maintain symptoms.
Third, Chen et al. (2008) did not address the spatial covariance among stress, socioeconomic status, and pollution, which can confound geographic information system–based air pollution epidemiology. In particular, communities near highways, with higher traffic-related pollution and lower property values, may be disproportionately composed of families having lower socioeconomic status. Because of this potential for spatial autocorrelation and thus confounding, accurate fine-scale exposure measurement is critical. However, Chen et al. (2008) did not present pollution or stress maps, the NO2 model was not formally validated to this cohort's specific spatial characteristics, and spatial patterns in stress were not explored; thus we are left wondering whether, and how, spatial misclassification and confounding may be at play. Relatedly, social–physical correlations may vary by geographic scale (e.g., across vs. within neighborhoods); although a given neighborhood may have high mean pollution and stress, it is harder to argue that particular individuals (or residences) within these neighborhoods would be relatively more exposed to both (i.e., individuals living closer to highways are not necessarily more exposed to violence or family stress than are other community members).
Fourth, Chen et al. (2008) reported results for 73 asthmatic children. However, in the absence of information on disease chronicity, severity, or adequacy of medical treatment, it may be difficult to truly assess the influence of either stress or traffic-related pollution. Relatedly, it is important to distinguish between processes related to illness onset from those related to progression or exacerbation, and whether the negative interaction observed in their study could be expected in healthy adolescents.
Finally, the cohort studied by Chen et al. (2008) varied considerably in age (9–18 years), but the authors did not consider age-related asthma characteristics and responsiveness to family stressors and air pollution. Age stratification should have been used to compare the strength of individual and combined effects at multiple ages. It would also be interesting to know whether non–family-related stressors would produce similar interactions at all ages.
The issues we have highlighted—temporal relationships between stressors and pollution, nonlinearity and saturation effects, spatial correlations, age-related susceptibility, and distinctions between illness etiology and exacerbation—will be critical in the further study of social–environmental interactions. These effects may distort observed associations (e.g., saturation effects may reverse interactions at high exposures), but with sustained attention to these issues, we can better understand joint effects of social and physical environments on health.
The authors declare they have no competing financial interests.
Jane E. Clougherty
Laura D. Kubzansky
Harvard School of Public Health
Boston, Massachusetts
References
Chen E, Schreier HMC, Strunk R, Brauer M. 2008. Chronic traffic-related air pollution and stress interact to predict biologic and clinical outcomes in asthma. Environ Health Perspect 116:970–975.
Clougherty JE, Levy JI, Hynes HP, Spengler JD. 2006. A longitudinal analysis of the efficacy of environmental interventions on asthma-related quality of life and symptoms among children in urban public housing. J Asthma 43:335–343.
Clougherty JE, Levy JI, Kubzansky LD, Ryan PB, Suglia SF, Canner MJ, et al. 2007. Synergistic effects of traffic-related air pollution and exposure to violence on urban asthma etiology. Environ Health Perspect 115:1140–1146.
McEwen BS, Seeman TE. 1999. Protective and damaging effects of mediators of stress. Elaborating and testing the concepts of allostasis and allostatic load. Ann NY Acad Sci 896:30–47.
Traffic-Related Air Pollution and Stress: Chen and Brauer Respond
Environ Health Perspect. doi:10.1289/ehp.11863R available via http://dx.doi.org [Online 29 August 2008]
We thank Clougherty and Kubzansky for their thoughtful review of our article (Chen et al. 2008). We view our article, as well as their article on exposure to violence, air pollution, and asthma etiology (Clougherty et al. 2007), as suggestive regarding how the social and physical environments operate in asthma. Although the nature of the interaction effects were different in these two studies, the broader point—that there are interactive effects between the social and physical environments in asthma —is consistent and is the key message that we wish to emphasize.
We would like to address their specific comments. First, regarding temporal issues, Clougherty and Kubzansky raise the possibility that stress increases susceptibility to subsequent pollution. We agree that this is possible; we also recognize the possibility that chronic pollution exposure could heighten responses to subsequent stressors. As we stated in our "Discussion" (Chen et al. 2008), the time frame of assessments that were available to us for these analyses was not ideal, and future studies should more specifically coordinate the timing of exposures to both stress and air pollution.
Second, we agree it is possible that saturation effects may occur at high levels of pollution exposure. However, because pollution levels in Vancouver (British Columbia, Canada) are not extreme (the range in our sample was 10–30 ppb nitrogen dioxide), we think this is an unlikely explanation.
Third, regarding spatial covariance, in our study (Chen et al. 2008), family stress was measured at the individual level; thus, we do not have neighborhood-level stress maps or information on spatial patterns in stress. Although spatial covariance between socioeconomic status and air pollution has the potential to lead to confounding, the availability of individual measures of stress and air pollution exposure estimates at the resolution of individual addresses allowed us to evaluate interactions. Our longitudinal findings also diminish the likelihood of confounding. Further, previously published pollution maps (Henderson et al. 2007) have shown that, in our study area, air pollution levels are not spatially correlated with neighborhood socioeconomic status [e.g., see UBC (University of British Columbia) Centre for Health and Environment Research 2008].
Fourth, we presented information about disease characteristics in Table 1 (Chen et al. 2008). We also controlled for asthma severity and medication use in all analyses, as described in our article under "Potential confounders."
Finally, we agree that it would be interesting to know whether stress by air pollution effects vary by age. However, given the limited sample size in our study, we were unable to test this possibility.
The authors declare they have no competing financial interests.
Edith Chen
Michael Brauer
University of British Columbia
Vancouver, British Columbia, Canada
References
Chen E, Schreier HMC, Strunk R, Brauer M. 2008. Chronic traffic-related air pollution and stress interact to predict biologic and clinical outcomes in asthma. Environ Health Perspect 116:970–975.
Clougherty JE, Levy JI, Kubzansky LD, Ryan PB, Suglia SF, Canner MJ, et al. 2007. Synergistic effects of traffic-related air pollution and exposure to violence on urban asthma etiology. Environ Health Perspect 115:1140–1146.
Henderson SB, Beckerman B, Jerrett M, Brauer M. 2007. Application of land use regression to estimate long-term concentrations of traffic-related nitrogen oxides and fine particulate matter. Environ Sci Technol 41: 2422–2428.
UBC (University of British Columbia) Centre for Health and Environment Research. 2008. Annual Average Air Pollution Levels, Asthma Rates and Neighbourhood Income Levels in Vancouver. Available: http://www.cher.ubc.ca/UBCBAQS/images/Asthma_Vancouver.gif [accessed 21 July 2008].