Invited Perspective: Temporality and Recursive Dynamics in Stress-Pollution Interactions.

Abstract

Vol. 130, No. 12 Invited PerspectiveOpen AccessInvited Perspective: Temporality and Recursive Dynamics in Stress–Pollution Interactionsis accompanied byStress Drivers of Glucose Dynamics during Ozone Exposure Measured Using Radiotelemetry in Rats Jane E. Clougherty Jane E. Clougherty Address correspondence to Jane E. Clougherty, Dornsife School of Public Health, Drexel University, Philadelphia, PA 19104 USA. Telephone: 617-816-7717. Email: E-mail Address: [email protected] https://orcid.org/0000-0002-9911-1565 Dornsife School of Public Health, Drexel University, Philadelphia, Pennsylvania, USA Urban Health Collaborative (UHC), Drexel University, Philadelphia, Pennsylvania, USA Search for more papers by this author Published:21 December 2022CID: 121302https://doi.org/10.1289/EHP12416AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit Over the past two decades, a body of epidemiologic evidence has suggested that chronic psychosocial stress may increase susceptibility to environmental pollutants,1–4 an effect plausibly mediated via stress-related impacts on immune, endocrine, and metabolic function. Much of the early research on stress–pollution interactions focused on stress as a modifier of air pollution effects on respiratory1,5,6,2 and cardiovascular3,4,7,8 outcomes, or on lead or other heavy metal exposures on cognitive and neurodevelopmental outcomes.9–11 In recent years, however, the literature has expanded to consider outcomes and pathways as diverse as DNA methylation,12 birth outcomes,13,14 brain structural development,15 and circadian rhythm.16 Finally, toxicologic experiments17 and controlled human studies have suggested that some pollutants may directly affect stress pathways, particularly the hypothalamic–pituitary–adrenal (HPA) axis, which organizes the acute stress response.18–21These varied interactions between pollution and stress are critical because they speak directly to health disparities,22 given that many communities of lower socioeconomic position (SEP) bear disproportionate exposures to both environmental pollution23–25 and chronic social stressors (e.g., poverty, violence).9,26–30 As long argued by the environmental justice movement, for example, industrial facilities are disproportionately sited in or near minoritized and lower-income communities, increasing local pollution exposures.31 Finally, this stress-related susceptibility may be particularly important in settings with low-level chronic pollution exposures, where overall effects may not be apparent, though impacts among susceptible populations may be substantial.Given this growing evidence, and a desire on the part of the public health community, policy makers, and local governments to identify efficacious interventions to reduce health disparities, it has become pertinent to better understand directionality in stress–pollution interactions. More specifically, does chronic stress shape physiologic response to pollution, or, rather, do pollution exposures alter physiologic response to stress? Alternatively, if both are true, we may learn that stress–pollution interactions are indeed cyclical—with one exposure iteratively altering response to the other, creating an interplay among social and environmental exposures that may be more profoundly complicated than previously understood.The study by Henriquez et al., presented in this issue of Environmental Health Perspectives, makes a critical contribution to this science, by demonstrating the central role of “stress” processes in mediating impacts of ozone exposures on metabolic function.32 Specifically, pollutants that are strong respiratory irritants, such as ozone or acrolein inflame lung tissue, triggered a cascade of stress hormones produced via the HPA axis and ultimately led to downstream impacts on glucose dynamics, a key aspect of metabolic function. Metabolic function, likewise, is shown to be influenced by some pollutant exposures, in both children33 and adults,34–36 which, in turn, can also influence pollution response.37Henriquez et al. demonstrated this effect of ozone on stress regulation, by detailing the time course of glucose changes following ozone exposures in Wistar Kyoto rats that had been either adrenalectomized or not. They found that ozone-induced changes in glucose production were profoundly dampened in adrenalectomized rats, demonstrating that ozone affects metabolic function predominantly via “stress” pathways.The lack of response to ozone shown in adrenalectomized rats (those that cannot produce “stress” hormones) may revolutionize our understanding of the biological processes through which ozone influences metabolic dysfunction and health; it may, in fact, reveal that much of its impact appears to operate through mechanisms we normally associate with psychosocial stress. The results further point to important nuances in the interactions among stress and pollution that have not yet been fully appreciated. Together, this evidence depicts a profoundly complex system of recursive impacts among pollutants and stressors, with tremendous nuance in both temporality and intensity of joint effects.Given the importance of this finding and the temporal nuances at play, Henriquez et al. ultimately call attention to the great need for closer alignment between epidemiologic and toxicologic approaches for understanding the joint effects of pollution and chronic stressors on health.32 This literature has matured to the point of revealing nonlinearities, thresholds, and saturation effects,15 as well as nuanced temporalities in joint effects,1 each of which will require dedicated animal models to help guide epidemiologic model structure and to more accurately interpret epidemiologic results.