Research Report

Childhood Poverty and HealthCumulative Risk Exposure and Stress DysregulationGary W. Evans and Pilyoung Kim

Department of Design and Environmental Analysis and Department of Human Development, Cornell University

ABSTRACT—A massive literature documents the inverse

association between poverty or low socioeconomic status

and health, but little is known about the mechanisms un-

derlying 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 mul-

tiple 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 over-

night cortisol and the more dysregulated was the cardio-

vascular response (i.e., muted reactivity). Cardiovascular

recovery was not affected by duration of poverty exposure.

Unlike the duration of poverty exposure, concurrent pov-

erty (i.e., during adolescence) did not affect these physi-

ological stress outcomes. The effects of childhood poverty

on stress dysregulation are largely explained by cumula-

tive 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’ so-

cial status (Kuh, Hardy, Langenberg, Richards, & Wadsworth,

2002; Poulton et al., 2002). Something in the early life experi-

ences 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 expo-

sure to cumulative environmental risks during childhood. We

tested this hypothesis by examining neuroendocrine and car-

diovascular markers of stress regulation and cumulative phys-

ical and social risk exposure in a longitudinal sample of low- and

middle-income adolescents.

Poverty and low socioeconomic status (SES) are associated

with elevated basal measures of blood pressure in children un-

der the age of 13 (Chen, Matthews, & Boyce, 2002). This link be-

tween poverty and blood pressure vanishes by adolescence,

although it reappears in adulthood (Chen et al., 2002). Two cross-

sectional studies also have revealed elevated hypothalamic-

pituitary-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 pover-

ty 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, CornellUniversity, Ithaca, NY 14853-4401, e-mail: gwe1@cornell.edu.

PSYCHOLOGICAL SCIENCE

Volume 18—Number 11 953Copyright r 2007 Association for Psychological Science

blood pressure reactivity and recovery after exposure to an acute

stressor. Given the epidemiological literature, however, we ex-

pected 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 mecha-

nisms to be mediated by elevated cumulative risk exposure.

METHOD

Participants

Two hundred seven young adolescents (M 5 13.4 years; 52%

male) who had complete physiological data in the second wave

of a longitudinal study (M 5 9.2 years at Wave 1) were included

in the sample. At initial recruitment, 53% of the sample lived at

or below the federal poverty line. The sample was Caucasian,

and all the children resided in rural areas of upstate New York.

(See Evans, 2003, for further details on the sample and the

procedures for data collection.)

Each youth and his or her mother were tested independently

by two trained interviewers in the home. A standard protocol was

used to collect sociodemographic information, data on risk ex-

posure, a host of questionnaire and behavioral indices of so-

cioemotional development, and physiological stress indicators.

Measures

Poverty

The duration of lifetime exposure to poverty was defined as the

proportion of years each adolescent had lived in poverty since

birth. Poverty was operationalized as an income-to-needs ratio

of less than or equal to 1.0. This ratio is an annually adjusted, per

capita index of income that the U.S. Census Bureau calculates

using a standardized formula.

Physiological Stress

Twelve-hour, overnight urinary free cortisol was calculated by a

radioimmune assay at both Wave 1 and Wave 2 (Contreras, Hane,

& Tyrrell, 1986). Creatinine was also measured to control for

differences in body size and incomplete voiding (Tietz, 1976).

We also assayed overnight urinary catecholamines; we do not

discuss these data here, however, because urinary catechola-

mines are indices of sympathetic activation, which does not

show effects of poverty in adolescents.

At both waves, basal blood pressure was monitored (Dinamap

Pro 100, Tampa, FL) every 2 min over a 14-min period while the

youth sat quietly and read. The mean of the second through

seventh readings was used as the index of basal blood pressure

(Kamarck et al., 1992), which was not expected to be related to

exposure to poverty. Cardiovascular reactivity and recovery

were measured at Wave 2 only. Immediately following the sev-

enth reading, the youth was told without warning that he or she

would now take a math test. The task was to mentally subtract a

two-digit number from a series of four-digit numbers without

writing down any calculations. Every 4 min, the two-digit

number was changed. This reactivity phase lasted for 12 min,

with blood pressure monitored every 2 min. Thirty seconds after

the test was completed, the first of five additional readings (at 2-

min intervals) was taken while the youth again sat quietly and

read for a period of 10 min. This constituted the recovery phase

of the protocol. At the end of the test, the participant was assured

that no more tests would be given, and that he or she could relax

and read while the blood pressure monitoring continued. Mental

arithmetic is a standard stress-induction protocol used in re-

activity studies with children and adults (Gump & Matthews,

1999; Matthews, Gump, Block, & Allen, 1997).

Cumulative Risk Exposure

Cumulative risk was calculated from birth to the initial wave

of data collection and for the time interval between Wave 1

and Wave 2. The six risk factors included three physical risks,

crowding (people/room), noise (average decibel level in the

home over a 2-hr period), and substandard housing (assessed

using a standardized, rater-based instrument; Evans, Wells, Chan,

& Saltzman, 2000), and three social risks, family turmoil, child’s

separation from parents, and exposure to violence. At Wave 1,

exposure to social risks was determined from mothers’ reports on

the Life Events and Circumstances (LEC) checklist (Work,

Cowen, Parker, & Wyman, 1990); at Wave 2, youths’ self-reports

on the Adolescent Perceived Events Scale (Compas, 1997) were

also included (an event was counted a single time if it was re-

ported by the youth, the mother, or both). Multiple items (yes/no)

made up each social risk factor. Exposure to physical risks was

calculated identically at each wave of data collection.

For each of the six individual risk domains, risk was coded

dichotomously at each wave. A score of 1 was given if the youth’s

exposure at a given wave was more than 1 standard deviation

above the mean for the entire sample’s distribution of continuous

exposure at that wave, and a score of 0 was given in all other

cases. Cumulative risk exposure (0–6) was then calculated for

each wave of data collection by summing across the six singular

risk factors.

RESULTS

Data-Analytic Strategy

Ordinary least squares regression was employed to analyze how

the duration of lifetime exposure to poverty was related to cor-

tisol levels, baseline blood pressure, and cardiovascular reac-

tivity assessed in early adolescence in Wave 2 of this longi-

tudinal study. Cardiovascular reactivity was operationalized by

subtracting the mean of the six baseline readings from the mean

of the six readings during the acute stressor. Recovery was an-

alyzed with multilevel, hierarchical linear modeling (Singer &

Willett, 2003). For overnight cortisol, prior cortisol levels, as-

sessed at age 8, were included in the model. For the reactivity

and recovery indices, no prior physiological data were available;

954 Volume 18—Number 11

Childhood Poverty and Health

thus, these analyses are cross-sectional. To examine the hy-

pothesized mediational role of cumulative risk exposure, we

repeated each of the regression equations with two additional

terms in the model, Wave 1 and Wave 2 cumulative risk. The

change in the b weight for poverty between the first regression

model (cumulative risk not included) and the second regression

model (cumulative risk included) was the prime indicator of

mediation.

Table 1 displays descriptive information and the zero-order

correlation matrix for duration of poverty exposure, cumulative

risk, and the physiological stress measures.

Chronic Physiological Stress

Overnight urinary free cortisol (controlling for Wave 1 cortisol)

was significantly elevated by longer duration of exposure to

poverty in childhood, b 5 0.02 (SE 5 0.01), p< .01, prep 5 .97,

f 2 5 .05. As expected, adolescents’ basal blood pressure, con-

trolling for Wave 1 levels, was unaffected by exposure to poverty.

To examine whether the effects of poverty duration on chronic

physiological stress were mediated by cumulative risk exposure,

we initially examined whether duration of poverty was related to

the hypothetical mediator, cumulative risk exposure. Duration

of poverty was significantly related to cumulative risk exposure

at Wave 1, b 5 0.80 (SE 5 0.16), p < .001, prep 5 1.00, f 2 5

.11, and at Wave 2, b 5 1.05 (SE 5 0.14), p< .001, prep 5 1.00,

f 2 5 .25. We next examined whether the significant relation

between poverty duration and overnight cortisol was attenuated

when cumulative risk was included in the equation. Contrary to

our hypothesis, the covariance between poverty duration and

elevated cortisol was not affected by the inclusion of the me-

diator, cumulative risk, in the regression model, b 5 0.02.

Stress Regulation

The greater the duration of exposure to poverty, the less robust

was the response to the acute stressor. Both diastolic and systolic

blood pressure reactivity were significantly lower for children

who had spent a greater proportion of their lives in poverty,

b 5 �1.62 (SE 5 0.77), p < .03, prep 5 .90, f 25 .02, and

b 5 �3.62 (SE 5 1.05), p < .01, prep 5 .99, f 2 5 .06, respec-

tively. The effects of duration of poverty exposure on diastolic

and systolic blood pressure recovery were not significant. The

significant relations between duration of poverty and cardio-

vascular reactivity became nonsignificant when the effects of

cumulative risk were partialed out of each equation, bdiastolic 5

�1.06, bsystolic 5 �2.75.

Timing of Poverty Exposure

Because of the longitudinal nature of our research design, we

could also examine whether the chronic effects of poverty du-

ration on stress dysregulation were largely due to exposure to

poverty at the time of Wave 2 assessment. They were not. Poverty

at Wave 2 had no significant effects on any of the measures of

stress dysregulation. Moreover, the significant impacts of pov-

erty duration on cortisol and cardiovascular reactivity all re-

mained statistically significant when poverty at Wave 2 was

added to the equation.

DISCUSSION

In this sample of young adolescents, the greater the proportion of

their lives they had spent living in poverty, the higher their

levels of chronic HPA activity. These are the only prospective,

longitudinal data on poverty and physiological stress, and

they replicate two prior cross-sectional studies of childhood

poverty and HPA activity (Evans & English, 2002; Lupien et al.,

2000). Also, for the first time, we have shown that poverty during

childhood is linked to a dysregulated stress response to an acute

stressor. The more time 13-year-old children have spent living in

poverty since birth, the more muted their cardiovascular reac-

tivity to a standard acute-stressor protocol. Although we had also

expected to see a less efficient (i.e., slower) pattern of cardio-

vascular recovery among chronically poorer children following

cessation of the acute stressor, we did not. One reason for this

result might be the significantly lower level of reactivity in the

children with greater exposure to poverty. Another possibility is

that chronically impoverished children have an elevated degree

of variability during the recovery period. The pattern of chron-

ically elevated cortisol coupled with muted reactivity to an acute

stressor is indicative of damage to stress regulatory mechanisms

TABLE 1

Descriptive Statistics and Zero-Order Correlations for This Study

Variable Mean (SD)

Correlation

2 3 4 5 6

1. Poverty duration .40 (.46) .32nn .44nn .21n �.13n �.23nn

2. Cumulative risk: Wave 1 1.41 (1.50) .38nn �.04 �.05 �.06

3. Cumulative risk: Wave 2 0.92 (1.06) �.03 �.12n �.20nn

4. Cortisol (mg/mg creatinine) 0.11 (0.05) �.02 �.02

5. Diastolic reactivity 4.43 (5.04) .61nn

6. Systolic reactivity 4.52 (7.19)

np < .05. nnp < .01.

Volume 18—Number 11 955

Gary W. Evans and Pilyoung Kim

that portends long-term morbidity (McEwen, 1998, 2000). The

finding that these results are due to chronic poverty exposure

rather than concurrent poverty exposure during adolescence is

important as well. Many epidemiological studies have uncov-

ered little or no relation between poverty and blood pressure

among adolescents (Chen et al., 2002).

Our results also provide longitudinal evidence that some of

the apparent ill effects of childhood poverty on stress regulation

are due to elevated cumulative risk exposure. These longitudi-

nal data on poverty and cumulative risk exposure extend the

results of prior cross-sectional studies showing elevated expo-

sure to single physical and social risks among low-income

children (Repetti et al., 2002; Taylor et al., 1997). Moreover, we

have demonstrated that elevated cumulative risk exposure during

early childhood compromises the ability of the body to handle

environmental demands efficiently. One possible reason why

cumulative risk exposure had significant mediational effects on

cardiovascular reactivity but not on the HPA axis may be found

in allostatic-load theory. Elevated HPA activity from chronic

stress is viewed as an early marker of allostatic load, whereas

alterations in dynamic stress regulation, such as reactivity to

an acute stressor, are posited to occur later in the etiology of

allostatic load (McEwen, 1998, 2000). It is interesting to note in

this regard that the cumulative risk index mediated the effects of

poverty on cortisol in this same sample of children at Wave 1,

when they were 9 years old (Evans & English, 2002). Unfortu-

nately, dynamic cardiovascular responses were not assessed in

the first wave of this study. It is also worth repeating that the well-

documented associations between childhood social class and

adult morbidity and mortality occur irrespective of adults’ social

class (Kuh et al., 2002; Poulton et al., 2002). An early history of

poverty appears to set children on a life-course trajectory of ill

health.

The overall pattern of chronically elevated HPA activity, in-

efficient cardiovascular mobilization, and elevated cumulative

risk exposure accompanying childhood poverty is consistent

with the findings of two epidemiological studies of early-child-

hood risk and adult health. The accumulation of risk factors

beginning in childhood (e.g., not owning a home at age 11) re-

lated prospectively to self-reported health at age 23 in a national

birth cohort in Britain (Power & Matthews, 1998). Felitti et al.

(1998) showed that the 10 major causes of adult mortality were

associated with retrospective reports of early-childhood risks

(e.g., domestic violence). Although these two epidemiological

studies and the present results suggest linkages among poverty

in early childhood, elevated cumulative risk exposure, and

eventual morbidity, more definitive results will require contin-

ued prospective tracking of disease outcomes in the present

sample as these individuals develop over the life course.

Acknowledgments—We are grateful to the many families who

have participated throughout this research and to Jana Coo-

perman, Kim English, Missy Globerman, Tina Merilees, Cha-

nelle Richardson, Adam Rokhsar, and Amy Schreier for their

assistance with data collection. This work has been supported

by the W.T. Grant Foundation and the John D. and Catherine

T. MacArthur Foundation Network on Socioeconomic Status and

Health and by the Virginia F. Cutler, Martha E. Roulk, Flora

Rose, and Anna Cora Smith Graduate Fellowships from Cornell

University.

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(RECEIVED 1/10/07; REVISION ACCEPTED 3/21/07;FINAL MATERIALS RECEIVED 3/23/07)

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