Neighborhood Disadvantage and Environmental Toxins Predict Elevated Immunological and Suppressed Adrenocortical Functioning in Mexican-origin Youth

• In Event: Inequities in Children’s Environmental Exposures: Integrating Toxicant, Social, and Structural Influences on Children’s Physical Health

Abstract

Social disadvantage, such as socioeconomic inequality and residential segregation, often co-occurs with increased pollution exposure, contributing to adverse health outcomes across the lifespan (Morello-Frosch et al., 2011). Disruptions to biological stress responsivity including the hypothalamic–pituitary–adrenal (HPA) axis and inflammation are key mechanisms conveying the effects of chronic stress on health problems (Kraft & Kraft, 2021). Yet, studies have measured only one aspect of social disadvantage, typically either poverty or pollution (Trentacosta et al., 2016). Given the co-occurrence of environmental stressors, the effect of a single stressor may be driven by the effect of an associated but unmeasured stressor. Additionally, studies have examined a single physiological system. Exploring joint HPA-inflammatory stress response profiles may clarify response patterns that signal well-regulated versus dysregulated functioning. Based on Allostatic Load theory (McEwen, 2007), and the immunosuppressive effects of cortisol, we expected that family poverty, adverse neighborhood conditions, and air and water toxins would additively predict hypocortisolism paired with heightened inflammation both at baseline and in response to a stressor.
Adversities were measured annually from ages 10 to 16 years for 229 Mexican-origin adolescents (48.6% female). Family income-to-needs was calculated from parents reported total household income (M =$30,000-$35,000 at age 10) and household roster (M =5.47 people at age 10). Neighborhood housing burden (proportion of low-income households with 50% of income spent on rent), low education (% of population without a bachelor’s degree), unemployment, water pollutant levels, and fine particulate matter (PM 2.5) concentration in air were assessed by matching participants’ census tracts with administrative data. At 17 years, adolescents completed Cyberball, a social exclusion simulation task, while undergoing magnetic resonance imaging. Saliva samples were collected prior to the task and five times over a 50-minute period following the MRI scan, and assayed for cortisol and interleukin-6 (IL-6).
Using structural equation modeling to examine predictors simultaneously and correcting for census-tract clustering, we found that worse drinking water quality predicted both heightened IL-6 and reduced cortisol at baseline and post-Cyberball (Figure 1). Greater PM 2.5 exposure predicted reduced peak cortisol reactivity. Lower education predicted heightened IL-6 at baseline and peak. Unexpectedly, unemployment, and housing burden predicted lower baseline IL-6. Conversely, low family income-to-needs predicted reduced baseline cortisol.
Altogether, results provide support for additive and convergent effects of pollutants on adolescent stress and immune physiology, while effects of neighborhood conditions were mixed. Results of toxins reinforce the importance of considering developing neurobiology as a possible mechanism linking multidimensional environmental risk with later health problems. Evidence of cumulative exposure to air and water pollutants, neighborhood education disadvantage, and low family income generally driving up inflammation and suppressing HPA activity supports the allostatic load model. Although unexpected, the protective effects of housing burden on inflammation are in line with previous findings with this sample, wherein housing burden was related to better autonomic regulation. The implications of unemployment linked to lower inflammation will be addressed in the discussion. These findings may inform developmental models integrating social disadvantage and environmental influences with multisystem neurobiology and related health risks.

Authors

• Elisa Ugarte, University of California - Davis
  Presenting Author

• Lisa Johnson, University of California - Davis

• Luis A Parra, Washington University in Saint Louis

• Richard Whitney Robins, University of California - Davis

• Amanda E Guyer, University of California - Davis

• Paul David Hastings, University of California - Davis