Clougherty and Kubzansky exposures for stay-at-home parents (usually mothers) than for working adults (Dietrich et al. 2008; Jedrychowski and Krzyzanowski 1989). Physiologic stress responses differ by sex (Sundaram et al. 2004; Taylor et al. 2000), as does observed effect modification by SES (Wheeler and Ben-Shlomo 2005), such that gendered stress assessment may be needed to fully understand stress-linked effect modification for air pollution. To what extent are the effects of SES attributable to stress? As described, there is growing evidence of SES effect modifica- tion in the air pollution–disease relationship. ACS studies reported stronger health effects of air pollution among less-educated adults (Krewski et al. 2000), and time-series studies report the same (Jerrett et al. 2004; Kan et al. 2008; Lin et al. 2004; Martins et al. 2004), although these air pollution studies have not identified causal components of SES shap- ing susceptibility. Like air pollution, SES is a complex exposure mix accumulated over the life course, potentially including poorer- quality education; nutrition; housing; health care; health behaviors; pollution exposures in the home, community, and workplace; per- ceived social position; and other stressors. Indeed, newer variants of the allostatic load model incorporate primary (e.g., perceived stress, psychological response) and secondary (e.g., smoking, sleep, dietary behaviors) mani- festations of stress (McEwen 2006). Growing evidence links low SES to perceived stress and distress (Adler et al. 1994; Miller and Chen 2007) and to biological markers of stress-re- lated susceptibility (Lupien et al. 2001). Some of these studies used allostatic load models to link SES to distress and markers of disease risk (e.g., metabolic dysregulation) (Kubzansky et al. 2000). Other studies link allostatic load parameters to morbidity and mortality, sug- gesting that allostatic load may mediate rela- tionships between SES and mortality, after accounting for demographic characteristics and physician-diagnosed illness (Seeman et al. 2004). Among children, low SES may be a marker of early exposure to adversity. Recent studies link low childhood SES to epigenetic changes in messenger ribonucleic acid (mRNA) for the glucocorticoid receptor and toll-like recep- tor 4, indicative of proinflammatory profiles associated with asthma and allergic illness (Miller and Chen 2007). Low-SES children 6–10 years of age have shown higher basal cor- tisol levels than higher-SES children (Lupien et al. 2001). Children of parents reporting higher stress display physiologic hyperrespon- siveness, and low-income children of depressed m o t h e r s s h o w s e x - s p e c i f i c p h y s i o l o g i c responses: elevated cortisol in girls, HPA-axis hypoactivity in boys (Fernald et al. 2008). Children of depressed mothers can display 1356 ovlume 117 | number 9 | September 2009 • Environmental Health Perspectives altered adrenocorticotropic hormone and corticotropin-releasing hormone production into young adulthood (Ronsaville et al. 2006). Evidence suggesting that stress is a key media- tor for SES effects on health is not universally endorsed, and associations between SES and stress-related biological changes are not always positive (Dowd and Goldman 2006). Authors have argued that psychosocial factors are inex- tricably bound to material factors in developed countries; therefore, the accumulated evidence does not unequivocally demonstrate an inde- pendent pathway by which psychosocial stress may link SES to physical health (Macleod and Davey Smith 2003). Other aspects of SES (e.g., nutrition, health care) may also influ- ence pollution susceptibility, and methods are needed to determine their effects. We believe that the evidence to date is broadly suggestive of a link between SES and physiologic suscep- tibility, a significant portion of which may be explained by life stress. Continued research in this area is valuable, especially as it improves our understanding of the pathways through which physical exposures, including pollu- tion, may differently impinge on the health of vulnerable populations. Conclusions There is tremendous potential, although much work still to be done, in understanding com- bined effects of social and physical environ- mental exposures. These topics are exceedingly complicated. Accurately characterizing both social and physical exposures is a significant challenge that must be performed carefully, especially in light of potential confounding across the exposures of interest, before analyz- ing and interpreting interactions. The issues we have highlighted here— temporal relationships between stressors and pollution; nonlinearity and saturation effects; spatial colinearity across exposures; age-related susceptibility and critical periods; and dis- tinctions between processes related to illness etiology and exacerbation—will be critical in exploring social–environmental interactions. 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