Childhood Poverty and Health Cumulative Risk Exposure and Stress Dysregulation

A massive literature documents the inverse association between poverty or low socioeconomic status and health, but little is known about the mechanisms underlying this robust relation. We examined longitudinal relations between duration of poverty exposure since birth, cumulative risk exposure, and physiological stress in two hundred seven 13-year-olds. Chronic stress was assessed by basal blood pressure and overnight cortisol levels; stress regulation was assessed by cardiovascular reactivity to a standard acute stressor and recovery after exposure to this stressor. Cumulative risk exposure was measured by multiple physical (e.g., substandard housing) and social (e.g., family turmoil) risk factors. The greater the number of years spent living in poverty, the more elevated was overnight cortisol and the more dysregulated was the cardiovascular response (i.e., muted reactivity). Cardiovascular recovery was not affected by duration of poverty exposure. Unlike the duration of poverty exposure, concurrent poverty (i.e., during adolescence) did not affect these physiological stress outcomes. The effects of childhood poverty on stress dysregulation are largely explained by cumulative risk exposure accompanying childhood poverty. Poverty during early childhood is associated with increased morbidity and decreased life span in adulthood (Blane, Bartley, & Davey-Smith, 1997; Lawlor, Ronalds, Macintyre, Clark, & Leon, 2006). This association occurs irrespective of adults’ social status (Kuh, Hardy, Langenberg, Richards, & Wadsworth, 2002; Poulton et al., 2002). Something in the early life experiences of low-income individuals sets them on a life trajectory of impaired health. Our focus in this article is on why this occurs. We suggest that poverty in early childhood harms health because stress regulatory mechanisms are damaged by excessive exposure to cumulative environmental risks during childhood. We tested this hypothesis by examining neuroendocrine and cardiovascular markers of stress regulation and cumulative physical and social risk exposure in a longitudinal sample of lowand middle-income adolescents. Poverty and low socioeconomic status (SES) are associated with elevated basal measures of blood pressure in children under the age of 13 (Chen, Matthews, & Boyce, 2002). This link between poverty and blood pressure vanishes by adolescence, although it reappears in adulthood (Chen et al., 2002). Two crosssectional studies also have revealed elevated hypothalamicpituitary-adrenocortical (HPA) axis activity among low-income, elementary-school-age children (Evans & English, 2002; Lupien, King, Meaney, & McEwen, 2000). These findings leave open a critical question: Why does poverty in early childhood lead to stress dysregulation? One plausible explanation is that risk exposure may be heightened among poor children relative to more affluent children. Low-income children confront significantly more physical and social risk factors than their wealthier counterparts (Taylor, Repetti, & Seeman, 1997). Income-related physical risks include substandard housing, low neighborhood quality, toxins, ambient pollutants, noise, and crowding (Evans, 2004). Also, the families of poor children tend to have heightened levels of conflict, greater risk of dissolution, and harsher and more unresponsive parenting (Repetti, Taylor, & Seeman, 2002). Research has also shown that several of these physical and social environmental risk factors potentiate physiological stress. Both noise and crowding increase blood pressure and activate the HPA in children (Evans, 2006). Early exposure to family instability, turmoil, and harsh, unresponsive parenting is linked to similar physiological outcomes (Repetti et al., 2002). Although elevated resting levels of blood pressure and HPA activity are associated with morbidity, recent physiological stress research implicates damage to stress regulation as the principle mechanism underlying disease etiology (McEwen, 1998, 2000). Thus, we hypothesized that the effect of childhood poverty on subsequent health is due to elevated HPA activity plus reduced efficiency of the cardiovascular response to stress. We examined the efficiency of stress regulation by assessing Address correspondence to Gary W. Evans, Departments of Design & Environmental Analysis and of Human Development, Cornell University, Ithaca, NY 14853-4401, e-mail: gwe1@cornell.edu. PSYCHOLOGICAL SCIENCE Volume 18—Number 11 953 Copyright r 2007 Association for Psychological Science blood pressure reactivity and recovery after exposure to an acute stressor. Given the epidemiological literature, however, we expected no effects of poverty on sympathetic activation in young adolescents (Chen et al., 2002). Moreover, we expected the adverse effects of childhood poverty on stress regulatory mechanisms to be mediated by elevated cumulative risk exposure.