Health Psychology © 2017 American Psychological Association

2017, Vol. 36, No. 11, 1047–1058 0278-6133/17/$12.00 http://dx.doi.org/10.1037/hea0000540

Resilience and Biomarkers of Health Risk in Black Smokers

and Nonsmokers

Carla J. Berg, Regine Haardörfer, Aliza P. Wingo

Colleen M. McBride, Varun Kilaru, and Emory University and Atlanta Veterans Affairs Medical Center,
Kerry J. Ressler Decatur, Georgia
Emory University

Nabil F. Saba, Jackelyn B. Payne, and Alicia Smith

This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

Emory University
This document is copyrighted by the American Psychological Association or one of its allied publishers.

Objectives: Blacks are disproportionately affected by tobacco-related illnesses as well as traumatic events
associated with psychiatric conditions and smoking. We examined the potential protective nature of
resilience within this context, hypothesizing resilience differentially moderates the associations of
traumatic experiences to depressive symptoms and to biomarkers of health risk among Black ever versus
never smokers. Method: Measures of resilience, traumatic experiences, depressive symptoms, and
biomarkers (interleukin-6 [IL-6], C-reactive protein [CRP], allostatic load) were obtained among 852
Blacks recruited from Grady Memorial Hospital in Atlanta. Results: Ever smokers experienced more
trauma (p ⬍ .001) and depressive symptoms (p ⫽ .01). Structural equation modeling indicated that, in
ever smokers, childhood trauma was positively associated with depressive symptoms (p ⬍ .001);
resilience was negatively associated with depressive symptoms (p ⫽ .01). Depressive symptoms were
positively associated with IL-6 (p ⫽ .03), which was positively associated with allostatic load (p ⫽ .01).
Adulthood trauma was associated with higher CRP levels (p ⫽ .03). In never smokers, childhood (p ⬍
.001) and adulthood trauma (p ⫽ .01) were associated with more depressive symptoms. Adulthood
trauma was also associated with higher CRP levels (p ⬍ .001), which was positively associated with
allostatic load (p ⬍ .001). Never smokers with higher resilience had a negative association between
childhood trauma and depressive symptoms whereas those with lower resilience had a positive associ-
ation between childhood trauma and depressive symptoms. Resilience was negatively associated with
CRP levels (p ⬍ .001). Conclusions: Interventions targeting resilience may prevent smoking and adverse
health outcomes.

Keywords: tobacco use, health disparities, trauma, depression, resilience

Health is affected by social environment, health behaviors, and
endogenous biological responses that occur across the life span, a
complement that is increasingly referred to as the exposome
(Miller & Jones, 2014). The exposome comprises overlapping
domains that include (a) general external environments (e.g., ur-
banicity, social capital, interpersonal relationships), (b) specific
external environments (e.g., dietary habits, tobacco use), and (c)
internal biological environments (e.g., metabolic factors, inflamma-
tion, oxidative stress; Miller & Jones, 2014). These environmental
domains interact with each other to affect health outcomes (Miller &
Jones, 2014; Wild, 2012). The public health exposome model con-
ceptualizes these pathways to include environmental exposures, per-

This article was published Online First August 21, 2017.
Carla J. Berg, Regine Haardörfer, and Colleen M. McBride, Department of
Behavioral Sciences and Health Education, Rollins School of Public Health,
Emory University; Varun Kilaru, Department of Gynecology and Obstetrics,
School of Medicine, Emory University; Kerry J. Ressler, Departments of
Psychiatry and Behavioral Sciences, School of Medicine and Yerkes National
Primate Research Center, Emory University; Aliza P. Wingo, Departments of
Psychiatry and Behavioral Sciences, School of Medicine, Emory University,
and Atlanta Veterans Affairs Medical Center, Decatur, Georgia; Nabil F. Saba,
Department of Hematology and Medical Oncology, Winship Cancer Institute,
Emory University; Jackelyn B. Payne, Department of Behavioral Sciences and
Health Education, Rollins School of Public Health, Emory University; Alicia
Smith, Department of Gynecology and Obstetrics, School of Medicine, Emory
University.
This work was primarily supported by the NationalInstitute of Mental
Health (MH071537, MH100122, MH102890, MH096764) and the Na-
tional Institute of Child Health and Human Development (HD071982).
Support also included the Emory and Grady Memorial Hospital General
Clinical Research Center, the National Institute of Health National
Centers for Research Resources (M01 RR00039), the Burroughs Wel-
come Fund, and Emory University’s Winship Cancer Institute (co-
principal investigators: Colleen M. McBride, Carla J. Berg). Aliza P.
Wingo is supported by Veterans Affairs Grant IK2CX000601.
Correspondence concerning this article should be addressed to Carla J.
Berg, Department of Behavioral Sciences and Health Education, Rollins
School of Public Health, Emory University, 1518 Clifton Road, Northeast,
Room 524, Atlanta, GA 30322. E-mail: cjberg@emory.edu

1047
 1048
sonal characteristics, and moderating factors that, in turn, are associ-
ated with health disparities among communities at greatest risk
(Juarez & 2013). One such community is Blacks in the United
States. Indeed, it is this chronicity of lifetime exposures that
Geronimus and colleagues posited in their “weathering hypothe-
sis”: Blacks show higher cumulative risk measurements than
Whites, and these differences are not explained by poverty alone
(Geronimus, Bound, Waidmann, Hillemeier, & Burns, 1996;
Geronimus, Hicken, Keene, & Bound, 2006). This hypothesis
provides a framework for examining the impact of exposure fac-
tors with greater prevalence among Blacks that may together
influence health outcomes.
An important exposure associated with multiple negative
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
health outcomes is the experience of traumatic events (e.g.,
This document is copyrighted by the American Psychological Association or one of its allied publishers.
experiencing, witnessing, or being confronted with death, seri-
ous injury, or physical threat to self or others; American Psy-
chological Association [APA], 1994), particularly those that
occur in childhood. Such trauma has been associated with the
development of substance abuse and dependence, including
cigarette smoking (Hovdestad, Campeau, Potter, & Tonmyr,
2015; Simpson & Miller, 2002), as well as mental health
problems (e.g., depression, anxiety, suicidality; Enns et al.,
2006; Gilbert et al., 2009; Kessler, Davis, & Kendler, 1997;
MacMillan et al., 2001; Scott, Smith, & Ellis, 2010), interpersonal
difficulties (Jaffee & Gallop, 2007; Wolfe, Scott, Wekerle, &
Pittman, 2001), compromised academic and occupational func-
tioning (Cicchetti & Rogosch, 1997; Gilbert et al., 2009), aggres-
sion, violence, and criminal behaviors (Casiano, Mota, Afifi, Enns,
& Sareen, 2009; Gilbert et al., 2009; Ou & Reynolds, 2010).
Cumulatively, the impact of traumatic experiences on health are
significant and multidimensional. Blacks are disproportionately
exposed to traumatic events of various types (Breslau, Davis, &
Andreski, 1995; Green, Grace, Lindy, & Leonard, 1990). Com-
pared with Whites, Blacks are more likely to report higher rates of
childhood trauma, including parental death and severe alcoholism,
as well as extreme economic deprivation (Breslau et al., 1995;
Green et al., 1990). Blacks experience more traumatic events in
adulthood, such as being attacked or raped, threatened with a
weapon, or witnessing an injury or murder (Breslau et al., 1995).
Blacks also have higher lifetime and current rates of posttraumatic
stress disorder (Breslau et al., 1995; Green et al., 1990).
Blacks are disproportionately affected by tobacco-related ill-
nesses. Each year, approximately 45,000 Blacks die from
smoking-related disease (American Cancer Society [ACS], 2016;
Centers for Disease Control and Prevention [CDC], 1998).
Smoking-related illnesses are the number one cause of death in the
Black community, surpassing all other causes of death, including
AIDS, homicide, diabetes, and accidents (ACS, 2016). Blacks
suffer disproportionate tobacco-related morbidity and mortality
although they tend to smoke fewer cigarettes per day and begin
smoking later in life (Alexander et al., 2016). This phenomenon
remains unexplained but has been attributed to various factors
including stress associated with living in conditions of socioenvi-
ronmental disadvantage. In addition, Blacks are less likely to quit
smoking than Whites, resulting in sustained exposure to tobacco
smoke for a longer period of their life (Holford, Levy, & Meza,
2016).
The disproportionate burden of smoking-related diseases among
Blacks is further compounded by the co-occurrence of smoking
BERG ET AL.
and depression that can result from trauma. Studies have shown an
increased risk of nicotine dependence among individuals who
report exposure to trauma or adverse events (Al Mamun et al.,
2007; Breslau, Davis, & Schultz, 2003; Hapke et al., 2005), an
association that may be particularly unique to smoking. For ex-
ample, Breslau and colleagues (2003) found an association be-
tween trauma exposure and 10-year cumulative incidence of nic-
otine dependence but no association between trauma exposure and
alcohol use. Depressive symptoms also commonly co-occur
among those who have been exposed to a traumatic life event
(Fergusson, Horwood, & Lynskey, 1996; O’Donnell, Creamer, &
Pattison, 2004). Depressive symptoms are strongly associated with
nicotine dependence (Breslau et al., 1998; Fergusson et al., 1996;
Windle & Windle, 2001).
Resilience is a personal characteristic that may account for
differential health outcomes among people with histories of
trauma. Definitions of resilience have included positive outcomes
despite serious threats to adaptation and development (Masten,
2001), the absence of a particular negative outcome in at-risk
populations (e.g., absence of psychiatric disorder or suicidality;
Collishaw et al., 2007), or a composite score based on indices of
functioning reflecting both positive outcomes (e.g., educational
attainment, employment history) and a lack of negative outcomes
(e.g., homelessness, substance use; McGloin & Widom, 2001).
The Connor-Davidson Resilience Scale (CD-RISC) is a compre-
hensive assessment of personal strengths that contribute to positive
outcomes among individuals faced with adversity. The CD-RISC
is one of few multidimensional measures available for use with
adults and includes personal competence, perseverance, tolerance
of negative affect, acceptance of change, sense of social support,
trust in one’s instincts, spiritual faith, and an action-oriented ap-
proach to solving problems (Campbell-Sills & Stein, 2007; Connor
& Davidson, 2003). Prior research has found that this measure of
resilience may buffer the effects of traumatic experiences on
mental health and cigarette smoking (Campbell-Sills & Stein,
2007; Goldstein, Faulkner, & Wekerle, 2013). However, no pre-
vious research has examined the differential role of resilience on
depressive symptoms and smoking among Blacks, which is par-
ticularly relevant given the range of sociodemographic and psy-
chosocial differences between smokers and nonsmokers (e.g., ed-
ucational attainment, income levels, age; Agaku, King, Dube, &
the CDC, 2014; Agaku, King, Husten, et al., 2014).
In addition, although resilience has frequently been examined in
terms of mental health outcomes, it has been infrequently exam-
ined in relation to the internal environmental component of the
exposome, such as physiological biomarkers associated with ill-
ness or disease (e.g., cancer risk). Such biomarkers might include
interleukin-6 (IL-6), C-reactive protein (CRP), and allostatic load.
IL-6 is an interleukin that acts as both a proinflammatory and
anti-inflammatory cytokine (Ferguson-Smith et al., 1988). It is
secreted by T cells and macrophages to stimulate immune response
(e.g., during infection and after trauma) and has been found to be
associated with several types of chronic diseases, including car-
diovascular disease and cancer, as well as increased mortality
(Volpato et al., 2001). CRP is a sensitive marker of systemic
low-grade inflammation and is currently recommended as the
principal inflammatory marker in research and clinical practice
(Pearson et al., 2003). Elevated plasma levels of CRP have been
associated with an increased risk of coronary heart disease (Koenig
 RESILIENCE IN AFRICAN AMERICANS
et al., 1999; Ridker, Rifai, Rose, Buring, & Cook, 2002), ischemic
stroke (Rost et al., 2001), peripheral artery disease (Ridker, Cush-
man, Stampfer, Tracy, & Hennekens, 1998), hypertension (Sesso
et al., 2003), and any cardiovascular disease (Ridker, Buring,
Cook, & Rifai, 2003; Ridker et al., 2002) in individuals who have
no prior cardiovascular disease. CRP has also been found to
predict the risk of recurrent myocardial infarction (Ridker, 1998)
and mortality (Lindahl, Toss, Siegbahn, Venge, & Wallentin,
2000) in patients with coronary heart disease and is also associated
with cancer risk (Chaturvedi et al., 2010; Trichopoulos, Psalto-
poulou, Orfanos, Trichopoulou, & Boffetta, 2006). Moreover, el-
evated plasma CRP levels have been associated with obesity,
insulin resistance, the metabolic syndrome, endothelial dysfunc-
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
tion, and an increased risk of developing type 2 diabetes (Festa et
This document is copyrighted by the American Psychological Association or one of its allied publishers.
al., 2000; Freeman et al., 2002; Ridker et al., 2003; Yudkin,
Stehouwer, Emeis, & Coppack, 1999). Allostatic load is one
biomarker that captures the “weathering” the body experiences as
it strives to achieve stability in disruptive environments, and ele-
vated IL-6 and CRP levels may be precursors to increased allo-
static load (McEwen, 1998). Allostatic load is commonly concep-
tualized as an aggregate measure of disease risk markers, such as
blood pressure, body mass index (BMI), waist circumference, and
blood glucose (Barboza Solis et al., 2015; Seeman, Singer, Rowe,
Horwitz, & McEwen, 1997). Having a history of smoking has been
associated with IL-6 (Bermudez, Rifai, Buring, Manson, & Ridker,
2002), CRP (Ohsawa et al., 2005), and allostatic load (McEwen,
1998); thus, those with a history of smoking should be examined
separately from those without such a history in terms of other
environmental exposures related to these outcomes.
Consistent with the weathering framework, we examined
whether the association of exposure to traumatic experiences with
depressive symptoms and, in turn, allostatic load would be mod-
erated by resilience in a heterogeneous cohort of Black adults (see
Figure 1). In addition, we hypothesized that these associations may
differ for smokers and nonsmokers. Our assumptions in testing the
models were that childhood traumatic experiences predate tobacco
initiation and ongoing use as well as depressive symptoms. How-
ever, the availability of additional measures of adult exposure to
traumatic experiences provides a lifetime exposome indicator that
has not been available in other studies. Given consistent evidence
of positive associations between smoking and trauma exposure as
well as depression, we hypothesized that their joint influences on
weathering might differ for smokers and nonsmokers. We tested
structural equation models to capture the complexity of the poten-
tial associations among these factors. Such approaches are essen-
Figure 1. Conceptual framework examining exposures across the expo-
some and impact on health risk biomarkers.
1049
tial for sorting out the complex and interdependent factors that are
likely to contribute to health disparities. Characterizing groups for
whom the link between depression and resilience is most pro-
nounced could inform future interventions for tobacco users.
Method
Participants and Procedures
This analysis was part of a larger study investigating genetic and
trauma-related risk factors for posttraumatic stress disorder and
depression in a population of urban, low-income, highly trauma-
tized, predominantly Black men and women (Binder et al., 2008;
Bradley et al., 2008). Inclusion criteria included ages 18 –75 years,
understanding English, and ability to give informed consent. The
study was approved by the Emory University Institutional Review
Board.
Members of the research team approached adult patients waiting
for their outpatient appointments at the primary medical care or
obstetrical-gynecological clinics of Grady Memorial Hospital in
Atlanta, Georgia, to solicit for study participation (Binder et al.,
2008; Bradley et al., 2008). If the first participant that the staff
approached in the waiting room did not agree to do the study, then
the staff approached at least two additional possible participants.
Of those approached first by staff, 58% agreed, and a cumulative
percentage of 84% and 91%, respectively, of the second and third
participants approached agreed if the initial participant approached
did not participate. Participants gave informed consent and com-
pleted a battery of self-report measures. Because of variation
between participants with respect to literacy, all self-report mea-
sures were obtained by interview. Blood pressure, weight (kg),
height (cm), and waist circumference (cm) were obtained by
trained nursing staff at the Grady Hospital Clinical Research
Center. Current analyses focused on all Black participants with
data available regarding smoking history; traumatic experiences;
depression; resilience; and measures of IL-6, CRP, and physiolog-
ical measures used to calculate allostatic load (n ⫽ 852).
Measures
Lifetime history of smoking was assessed using responses from
the Kreek-McHugh-Schluger-Kellogg (KMSK) Scale (Kellogg et
al., 2003). Participants were grouped into “never smokers” and
“ever smokers” for structural equation modeling.
Covariates and Predictors
Sociodemographics included age, sex, education, income, em-
ployment, and disability.
Childhood Trauma Questionnaire. Childhood abuse was as-
sessed retrospectively using the 28-item Childhood Trauma Ques-
tionnaire (CTQ; Bernstein & Fink, 1998; Bernstein et al., 2003).
This scale uses a 5-point Likert scale that ranged from 1 (never
true) to 5 (very often true). Reliability for the CTQ is good with
high internal consistency scores. Sexual Abuse, Emotional Ne-
glect, Emotional Abuse, and Physical Abuse have reported coef-
ficients of .93–.95, .88 –.92, .84 –.89, and .81–.86, respectively.
Over a 3-month period, the test–retest coefficient was 0.80. Factor
analysis on the five-factor CTQ model showed structural invari-
 1050 BERG ET AL.
ance, demonstrating good validity (Bernstein & Fink, 1998; Bern-
stein et al., 2003).
Traumatic Events Inventory. Adulthood trauma was as-
sessed using the Traumatic Events Inventory (TEI; Gillespie et
al., 2009; Schwartz, Bradley, Sexton, Sherry, & Ressler, 2005).
This instrument screens for lifetime exposure to different cat-
egories of trauma, including natural disaster, serious accident or
injury, sudden life-threatening illness, military combat, being
attacked with a weapon, witnessing a family member or friend
being attacked with a weapon, being attacked without a
weapon, witnessing a family member or friend being attacked
without a weapon, witnessing the murder of a friend or family
member, or being sexually assaulted under duress. For each
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
category of the instrument, having had the exposure was scored
This document is copyrighted by the American Psychological Association or one of its allied publishers.
as 1 and no exposure as 0. Score ranges from 0 to 15 for
adulthood trauma, with higher scores reflecting exposure to
more types of trauma. The childhood trauma items in this
inventory were excluded to avoid overlap with the information
collected with the CTQ.
Beck Depression Inventory. Depression was measured with
the 21-item Beck Depression Inventory (BDI), which has a high
degree of reliability and validity (Beck, Ward, Mendelson, Mock,
& Erbaugh, 1961). Items were rated on a four-point Likert scale of
0 to 3; total score ranges from 0 to 63, with higher scores reflecting
higher levels of depression. Levels of depression severity are
suggested by the following score ranges: ⱕ9 reflects no depressive
symptoms, 10 –18 reflects mild symptoms, and ⱖ19 reflects mod-
erate to severe depressive symptoms (Beck et al., 1961). This
variable was operationalized as a continuous variable.
Moderator
CD-RISC. Resilience was assessed with the 10-item CD-
RISC (Campbell-Sills & Stein, 2007; Connor & Davidson, 2003).
Example items include “can deal with whatever comes” and “think
of self as strong person.” In prior research (e.g., Campbell-Sills &
Stein, 2007; Connor & Davidson, 2003), the full CD-RISC was
found to have an unstable structure across two demographically
equivalent samples; thus, it was modified into a 10-item scale with
good internal consistency, construct validity, and excellent psy-
chometric properties for efficient measurement of resilience (e.g.,
Cronbach’s ␣ ⫽ .91 and item separation reliability ⫽ .98; Gon-
zalez, Sierra, Martinez, Martinez-Molina, & Ponce, 2015; high
content validity; Windle, Bennett, & Noyes, 2011). Items were
rated on a 5-point Likert scale, ranging from 0 (not true at all) to
4 (true nearly all the time). Scores range from 0 to 40, with a
higher score reflecting greater resilience.
Biomarker Outcomes
IL-6 and CRP. Whole blood was collected under fasting
conditions between 8:00 a.m. and 9:00 a.m. and processed by
centrifugation to separate the plasma from the buffy coat. Plasma
samples were used to assess IL-6 and CRP as well as cortisol (used
in the measure of allostatic load described next).
Allostatic load. Allostatic load was operationalized as an ag-
gregate measure of biomarkers of disease risk. Individual bio-
marker scores were standardized and summed, creating a cumula-
tive allostatic load score. We adapted our measure from Seeman
and colleagues’ (1997) seminal measure of allostatic load to in-
clude a culmination of biomarkers known to be linked with various
health outcomes. This is a standard way to measure allostatic load
in the literature because sums across physiological systems are
better indicators of cumulative dysregulation than individual bio-
marker scores (Geronimus et al., 2006; Karlamangla, Singer, Mc-
Ewen, Rowe, & Seeman, 2002; Seeman, McEwen, Rowe, &
Singer, 2001; Seeman et al., 1997). This approach has been studied
in population-based survey research and indicated that higher
allostatic load scores were associated with higher morbidity and
mortality (Seeman et al., 1997, 2001). Moreover, lower allostatic
load scores were associated with higher educational levels and
better psychosocial factor scores (Seeman et al., 2004; Seeman,
Singer, Ryff, Dienberg Love, & Levy-Storms, 2002).
The five factors comprising the allostatic load measure were
cortisol, systolic blood pressure, diastolic blood pressure, BMI,
and waist-to-hip circumference. We selected these biomarkers
from available data on the basis of their roles as indicators of
disease risk and use in prior allostatic load research (Doamekpor &
Dinwiddie, 2015; Mauss, Li, Schmidt, Angerer, & Jarczok, 2015;
Seeman et al., 1997; Steptoe et al., 2014; Upchurch et al., 2015).
For each factor, the following dichotomizations were made: (a)
cortisol ⱖ16.6 mg/dL, which represents the highest quartile of
this cohort; (b) systolic blood pressure ⱖ140 mmHg; (c) dia-
stolic blood pressure ⱖ90 mmHg; (d) BMI ⱖ30 kg/m2; and (e)
abdominal obesity based on a waist circumference of ⬎102 cm
for men or ⬎88 cm for women. A point was assigned for each
criterion, yielding scores of 0 to 5, with 5 indicating highest
risk.
Data Analysis
Descriptive univariate analyses were conducted to assess distri-
butions and the extent of missing data. Bivariate analyses were
used to examine the differences between ever smokers and never
smokers. These were followed by analyses into the patterns of
missing data and multivariable regression analyses (including re-
sidual analyses) for each of the endogenous constructs (e.g., de-
pression, IL-6, allostatic load). Joint normality was assessed.
Structural equation modeling was then conducted to examine the
mediating role of depressive symptoms as well as the moderating
role of resilience comparing relationships between ever and never
smokers. Age and sex were included as covariates for IL-6, CRP,
and allostatic load. Estimation for the two-group model used
maximum likelihood with missing values. No auxiliary variables
were included because missingness in the data was due to admin-
istration of different modules at different times independent of
specific participant characteristics; thus, they were assumed to be
missing completely at random. Indices used to assess model fit
were ␹2, the root mean square error of approximation (RMSEA),
and the comparative fit index (CFI). After structural equation
modeling, residuals were inspected. Data were cleaned and de-
scriptive, univariate, bivariate, and multivariable analyses were
conducted using SAS 9.4. Structural equation modeling analyses
were conducting using Stata 14. Age and sex were included as
covariates in the structural equation model on the basis of results
from the bivariate analyses.
 RESILIENCE IN AFRICAN AMERICANS 1051

Results
Participant Characteristics
Ever smokers and never smokers differed across all sociodemo-
graphic dimensions, with ever smokers being older, more likely to
be male, less educated, lower income earners (p ⬍ .001), more
likely to be unemployed (p ⫽ .02), and more likely to receive
disability (p ⫽ .04; Table 1). As the literature would suggest, ever
smokers also reported experiencing more childhood and adulthood
trauma (p ⬍ .001) and depressive symptoms (p ⫽ .01).
Structural Equation Model Results
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
of health risk (i.e., IL-6, CRP, and allostatic load) among ever and
never smokers, respectively. In ever smokers, childhood trauma
was positively associated with depressive symptoms (p ⬍ .001);
resilience was negatively associated with depressive symptoms
(p ⫽ .01). Depressive symptoms were positively associated with
IL-6 (p ⫽ .03), which was positively associated with allostatic
load (p ⫽ .01). Adulthood trauma was positively associated
with CRP levels (p ⫽ .03). Older age was also associated with
higher IL-6, and being female was associated with higher
allostatic load.
In never smokers, childhood and adulthood trauma were positively
associated with depressive symptoms (p ⬍ .001, p ⫽ .01). Adulthood
trauma was also associated with higher CRP levels (p ⬍ .001), which

The final structural equation model presented had good model was positively associated with allostatic load (p ⬍ .001). Never
This document is copyrighted by the American Psychological Association or one of its allied publishers.

fit: ␹2(30) ⫽ 46.501, p ⫽ .03 overall, ␹2(15) ⫽ 8.156, p ⫽ .92 for
ever smokers, ␹2(15) ⫽ 38.345, p ⫽ .001 for never smokers,
RMSEA ⫽ 0.036, CFI ⫽ 0.950. The overall coefficient of deter-
mination (CD) was 0.532, with CD ⫽ 0.426 and 0.683 for ever and
never smokers, respectively.
Table 2 and Figure 2 display the results of the structural equa-
tion models examining the impact of childhood and adulthood
trauma (per the CTQ and TEI, respectively), resilience (per the
CD-RISC), and depressive symptoms (per the BDI) on biomarkers
smokers with higher resilience showed a negative association between
childhood trauma and depressive symptoms, whereas those with
lower resilience showed a positive association between childhood
trauma and depressive symptoms (see Figure 3). Resilience was
negatively associated with CRP levels (p ⬍ .001). Older age and
being female was also associated with higher CRP.
In comparing coefficients across groups, differences were found
regarding the interaction of childhood trauma and resilience on
depressive symptoms (p ⫽ .03), adulthood trauma on CRP levels

Table 1
Participant Characteristics and Bivariate Analyses Examining Differences Between Ever Smokers and Never Smokers

Total Ever smoker Never smoker

Variable M/N SD/% M/N SD/% M/N SD/% p

Sample size 852 100 608 71.36 244 28.64

Sociodemographics
Age 44.32 11.62 44.32 11.62 38.14 13.39 ⬍.0001
Gender ⬍.0001
Male 302 35.53 246 40.53 56 23.05
Female 548 64.47 361 59.47 187 76.95
Education ⬍.0001
Less than 12th grade 207 24.64 172 28.67 35 14.58
12th grade or high school graduate 294 35.00 193 32.17 101 42.08
GED 54 6.43 45 7.50 9 3.75
Some college/tech school 186 22.14 124 20.67 62 25.83
Tech school graduate 32 3.81 24 4.00 8 3.33
College graduate 57 6.79 34 5.67 23 9.58
Graduate degree 10 1.19 8 1.33 2 .83
Monthly household income ⬍.0001
Less than $250 274 33.29 216 36.61 58 24.89
$250–$499 87 10.57 62 10.51 25 10.73
$500–$999 235 28.55 163 27.63 72 30.90
$1000–$1999 163 19.81 108 18.31 55 23.61
$2000 or more 64 7.78 41 6.95 23 9.87
Employment status (no reported) 668 79.43 490 81.53 178 74.17 .02
Received disability (yes reported) 210 25.06 162 27.00 48 20.17 .04
Primary predictors
CTQ 43.62 18.26 45.20 19.32 39.72 14.65 ⬍.0001
TEI 3.59 2.51 3.95 2.55 2.64 2.14 ⬍.0001
CD-RISC 30.88 8.32 30.87 8.15 30.90 8.78 .98
BDI 15.93 12.54 16.69 12.65 13.97 12.06 .01
Outcomes
IL-6 1.35 1.42 1.34 1.32 1.41 1.73 .73
CRP 5.91 8.77 5.70 8.44 6.41 9.52 .47
Allostatic load 2.08 1.34 2.04 1.36 2.18 1.28 .21
Note. CTQ ⫽ Childhood Trauma Questionnaire; TEI ⫽ Traumatic Events Inventory; CRP ⫽ C-reactive protein; BDI ⫽ Beck Depression Inventory;
CD-RISC ⫽ The Connor-Davidson Resilience Scale.
 This document is copyrighted by the American Psychological Association or one of its allied publishers.
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

1052

Table 2
Equation Estimates for Structural Equation Models for Ever Smokers and Never Smokers, Respectively, and Comparisons of Coefficients Across Groups

Ever smokers Never smokers

Unstandardized Standardized Unstandardized Standardized
Variable coefficient SE Z p 95% CI coefficient coefficient SE Z p 95% CI coefficient pa

CTQ ¡ BDI 0.17 0.03 5.66 <.001 0.11 0.23 0.35 0.21 0.06 3.48 <.001 0.09 0.33 0.40 .55
TEI ¡ BDI 0.33 0.22 1.49 .14 ⫺0.10 0.77 0.15 1.05 0.42 2.50 .01 0.23 1.87 0.33 .13
CDR ¡ BDI ⫺0.44 0.18 ⫺2.46 .01 ⫺0.79 ⫺0.09 ⫺0.06 0.22 0.35 0.62 .53 ⫺0.47 0.92 0.67 .10
CTQ ⫻ CDR ¡ BDI 0.06 0.41 0.15 .88 ⫺0.74 0.87 0.33 ⫺2.35 1.00 ⫺2.35 .02 ⫺4.30 ⫺0.39 ⫺0.12 .03
TEI ⫻ CDR ¡ BDI ⫺5.96 3.68 ⫺1.62 .11 ⫺13.18 1.25 0.04 8.43 7.55 1.12 .26 ⫺6.38 23.23 0.45 .09
BDI ¡ CRP ⫺0.10 0.05 ⫺1.91 .06 ⫺0.20 0.00 0.00 ⫺0.08 0.08 ⫺0.97 .33 ⫺0.23 0.08 0.10 .82
TEI ¡ CRP 0.44 0.21 2.12 .03 .003 0.85 0.26 ⫺2.01 0.45 ⫺4.51 <.001 ⫺2.88 ⫺1.13 ⫺0.26 <.001
CDR ¡ CRP ⫺0.05 0.14 ⫺0.38 .71 ⫺0.33 0.23 0.17 ⫺0.99 0.15 ⫺6.64 <.001 ⫺1.29 ⫺0.70 0.40 .07
TEI ⫻ CDR ¡ CRP ⫺1.54 2.92 ⫺0.53 .60 ⫺7.25 4.18 0.22 35.13 6.40 5.49 <.001 22.60 47.67 ⫺0.64 <.001
Age ¡ CRP 0.04 0.04 0.94 .35 ⫺0.04 0.12 0.21 0.17 0.06 2.86 <.001 0.05 0.29 1.13 <.001
Female ¡ CRP 0.77 1.10 0.69 .49 ⫺1.40 2.93 0.17 3.68 1.83 2.01 .04 0.09 7.27 0.31 .17
BDI ¡ IL-6 0.01 0.01 2.16 .03 0.00 0.03 0.27 ⫺0.01 0.01 ⫺0.60 .55 ⫺0.04 0.02 0.14 .15
Age ¡ IL-6 0.02 0.01 2.35 .02 0.00 0.03 0.25 0.04 0.02 2.36 .02 0.01 0.07 0.50 .21
Female ¡ IL-6 0.21 0.16 1.31 .19 ⫺0.10 0.52 0.19 ⫺0.04 0.48 ⫺.08 .94 ⫺0.98 0.91 0.22 .63
BDI ¡ Allostatic load ⫺0.01 0.00 ⫺1.59 .11 ⫺0.02 0.00 0.02 0.00 0.01 0.37 .71 ⫺0.01 0.02 0.18 .25
BERG ET AL.

CRP ¡ Allostatic load 0.02 0.01 1.62 .11 0.00 0.04 0.22 0.04 0.01 3.05 <.001 0.01 0.06 0.44 .20
IL-6 ¡ Allostatic load 0.16 0.06 2.68 .01 0.04 0.28 0.27 0.09 0.09 1.06 .29 ⫺0.08 0.26 0.36 .51
Age ¡ Allostatic load 0.00 0.01 0.89 .37 ⫺0.01 0.02 0.13 0.01 0.01 0.85 .40 ⫺0.01 0.02 0.23 .85
Female ¡ Allostatic load 0.55 0.12 4.48 <.001 0.31 0.79 0.28 0.22 0.23 0.94 .35 ⫺0.23 0.67 0.22 .20

Equation-level goodness
of fit r2 mc mc2 r2 mc mc2

BDI .366 .605 .366 .312 .559 .312

CRP .035 .188 .035 .497 .705 .497
IL-6 .042 .205 .042 .083 .288 .083
Allostatic load .082 .286 .082 .110 .331 .110
Overall .426 .683
Note. Bold text indicates significant p-values. mc ⫽ correlation between the dependent variable and its prediction; mc2 ⫽ Bentler Raykov squared multiple correlation coefficient; CI ⫽ confidence
interval; CTQ ⫽ Childhood Trauma Questionnaire; TEI ⫽ Traumatic Events Inventory; CRP ⫽ C-reactive protein; BDI ⫽ Beck Depression Inventory; CD-RISC ⫽ The Connor-Davidson Resilience
Scale.
a
Comparing coefficients across groups.
 RESILIENCE IN AFRICAN AMERICANS 1053
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
This document is copyrighted by the American Psychological Association or one of its allied publishers.

Figure 2. Structural equation models examining the impact of trauma, resilience, and depressive symptoms on
biological outcomes among ever smokers and never smokers, respectively. Solid black lines indicate significant
associations whereas gray lines indicate insignificant associations.

(p ⬍ .001), the interaction between adulthood trauma and resil-
ience on CRP (p ⬍ .001), and age on CRP levels (p ⬍ .001).
Discussion
The current study examined the role of resilience in moderating
the impact of trauma exposure, depression, and resilience on
biomarkers of “weathering” among Black ever versus never smok-
ers. Examining these groups separately is critical because our
results and the prior literature (Agaku, King, Dube, et al., 2014;
Agaku, King, Husten, et al., 2014) have demonstrated marked
differences in the range of exposures across the exposome (e.g.,
sociodemographic, sociocontextual, psychological characteristics),
with smokers experiencing more risk exposures across these di-
mensions (Al Mamun et al., 2007; APA, 1994; Breslau et al., 2003;
Hapke et al., 2005). As anticipated, resilience served as a buffer
between specific upstream risk factors (i.e., traumatic experiences)
and downstream risk factors (i.e., depressive symptoms, health risk
biomarkers). In addition, our hypothesis that resilience would
differentially moderate the associations among traumatic experi-
ences, depressive symptoms, and health risk biomarkers among
ever versus never smokers was also supported.
First, these findings highlight the need for early intervention
among Blacks experiencing childhood trauma. Our results show
that, among ever smokers, childhood trauma— but not adulthood
trauma—was associated with higher depressive symptoms. This
finding points to biological embedding (Hertzman, 1999, 2012).
Biological embedding suggests that long-term and stable differ-
ences in experience, under different nurturant conditions, lead to
differences in learning and behavior over the life course. These
differences can impact the weathering process and ultimately
health outcomes (Essex et al., 2013). Our data indicate that child-
hood trauma leads to higher depressive symptoms. These higher
depressive symptoms put one at risk for smoking initiation, which,
in turn, can increase depressive symptoms (Windle & Windle,
2001) and consequently reduce the odds of successful cessation
(Brody, Hamer, & Haaga, 2005; Catley, Ahluwalia, Resnicow, &
Nazir, 2003; Chen, White, & Pandina, 2001; Covey, Glassman, &
Stetner, 1990; Husky, Mazure, Paliwal, & McKee, 2008). This line
of downstream consequences potentially prompted by early child-
hood environmental factors—specifically trauma— has long-term
and potentially difficult-to-modify consequences, both in terms of
depressive symptoms and health risk biomarkers, specifically IL-6
 1054
30
20
Impact on depression score
10
0
3 4 5 6 7 8 9 10 11 12
-10
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
This document is copyrighted by the American Psychological Association or one of its allied publishers.
-20
-30
Childhood trauma quesonnaire (CTQ) score
Figure 3. Resilience moderating the relationship between childhood
trauma and depression among never smokers. No relationship among ever
smokers (figure not shown).
and allostatic load. However, resilience was associated with de-
creased depressive symptoms in ever smokers. This suggests the
potential importance of promoting resilience as a construct among
young people who have experienced traumatic events to prevent
biological embedding that may directly lead to depression and
indirectly to smoking initiation and progression (Brody et al.,
2005; Catley et al., 2003; Chen et al., 2001; Covey et al., 1990;
Husky et al., 2008).
Among never smokers, both childhood and adulthood trauma
were associated with higher depressive symptoms. Whereas resil-
ience was not significantly associated with depressive symptoms
(as with ever smokers), it did serve as a moderator between
childhood trauma and depressive symptoms in never smokers.
Specifically, those with greater resilience demonstrated a negative
association between levels of childhood trauma and depressive
symptoms, whereas those with less resilience demonstrated a pos-
itive association between levels of childhood trauma and depres-
sive symptoms. It is interesting to note that resilience was nega-
tively associated with CRP levels among never smokers, indicating
that resilience may particularly serve as a buffer for disease risk
among Blacks who have never smoked.
The distinct roles of resilience among ever versus never smokers
are difficult to interpret. One explanation is that relative to non-
smokers, smokers have a complement of interdependent vulnera-
bilities (e.g., less educated, lower income, unemployed; Al Mamun
et al., 2007; APA, 1994; Breslau et al., 2003; Hapke et al., 2005)
along with their experiences of depression and trauma history. As
such, the earlier childhood experiences of this group may have
shaped their subsequent behaviors (e.g., substance use, academic
performance). Those with higher levels of childhood trauma may
have engaged in these damaging behaviors, which resulted in
poorer quality of life. However, a higher resilience within this
high-risk group may contribute to lower levels of depressive
symptoms despite these vulnerabilities. On the other hand, indi-
viduals who never engaged in cigarette smoking, and who were
BERG ET AL.
less vulnerable in terms of sociodemographics and psychosocial
experiences, were differentially affected by childhood trauma.
However, our cross-sectional data did not allow us to test this
assumption. The impact of childhood traumatic events on depres-
sive symptoms may have been mitigated by higher resilience.
Another finding that is interesting to note is that the two groups
showed different associations between experiencing traumatic
1SD above mean
resilience
events in adulthood and CRP levels, such that experiencing greater
adulthood traumatic events was associated with higher CRP levels
Mean resilience
in smokers whereas less adulthood trauma was associated with
1SD below mean higher CRP levels in never smokers. These findings warrant rep-
resilience lication to ensure that these were not spurious findings and, if
replicated, additional research to understand the differential mech-
anisms affecting the relationship between adulthood trauma and
CRP levels in ever versus never smokers.
These findings collectively suggest that increasing resilience
may buffer the impact of environmental risk factors. Further pro-
spective study designs will be needed to confirm this. This re-
search could take the form of randomized intervention trials that
vary resilience-building activities in groups at high risk of accel-
erated weathering. Limited research has examined the utility of
interventions targeting resilience to prevent or treat substance use,
specifically smoking or nicotine dependence. Although there is
some controversy regarding whether resilience is a personality trait
or a characteristic amenable to intervention (Yilmaz, Unal, Gencer,
Aydemir, & Selcuk, 2015), some research indicates the promise of
intervening on resilience. For example, some intervention research
has shown that attempts to increase resilience in young adults have
been effective in not only increasing resilience but also increasing
coping skills and protective factors (e.g., positive affect, self-
esteem) and decreasing symptoms of depression, stress, and neg-
ative affect (Steinhardt & Dolbier, 2008). Other research using a
family-based resilience intervention has documented reductions in
alcohol use among adolescents (Toumbourou, Gregg, Shortt,
Hutchinson, & Slaviero, 2013). Indeed, there have been recent
calls for social policies that promote resilience to decrease sub-
stance use and related costs (Luthar, Cicchetti, & Becker, 2000)
and for interventions to increase resilience among youth that are
multilevel, coordinated, continuous over time, and shown to be
effective to meet the long-term needs of youth facing the cumu-
lative disadvantages of family, community, school, and individual
challenges (Ungar, Liebenberg, Landry, & Ikeda, 2012).
Limitations
Several study limitations are worth noting. First, the cross-
sectional nature of this study and the use of retrospective self-
reports prohibits us from making causal attributions and is vulner-
able to bias. Prospective, longitudinal studies are required to
examine the temporality of trauma in relation to smoking, depres-
sive symptoms, and resulting health outcomes as well as the
impact of resilience on these outcomes. Another limitation is that
our sample was disproportionately female and low income, and we
do not yet have the data to demonstrate if these findings would
apply in other segments of the Black population. However, this
weakness is counterbalanced by the public health importance of
studying these variables in an often underresearched and under-
served population with disproportionally high rates of trauma
exposure as well as mental and physical health problems. In
 RESILIENCE IN AFRICAN AMERICANS
addition, this is a study exclusively of Blacks. Thus, it is not
possible to infer from the current analyses whether the documented
associations would also be demonstrated within other racial or
ethnic groups. Finally, it is important to note that several of our
hypothesized associations were not significant. The strongest as-
sociations were found in the model representing never smokers,
particularly the moderating effect of resilience on the relationship
between childhood trauma experiences and depressive symptoms.
The model representing ever smokers showed less robust associ-
ations, with the strongest associations being those between adult-
hood traumatic events and CRP levels as well as between resil-
ience and depressive symptoms. As such, these analyses warrant
replication in similar samples and in other more representative
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
samples to establish which relationships are most robust, both in
This document is copyrighted by the American Psychological Association or one of its allied publishers.
this population and in others.
Conclusions
The current findings point to the distinct role of resilience in
buffering the impact of environmental stressors in Black ever
versus never smokers. Although resilience did not moderate the
association between trauma and depressive symptoms in ever
smokers, it was directly related to lower levels of depressive
symptoms. In contrast, resilience was not directly related to de-
pressive symptoms in never smokers but rather buffered the impact
of traumatic experiences on depressive symptoms. In addition,
resilience directly affected specific health risk biomarkers in never
smokers but only indirectly affected specific health risk biomark-
ers in smokers via depressive symptoms. Ultimately, this study
highlights the importance of resilience in preventing adverse
health outcomes and provides a basis for understanding the mech-
anisms of change that might result from interventions targeting
resilience in Black ever versus never smokers.
References
Agaku, I. T., King, B. A., Dube, S. R., & the Centers for Disease Control
and Prevention (CDC). (2014). Current cigarette smoking among
adults—United States, 2005–2012. MMWR. Morbidity and Mortality
Weekly Report, 63, 29 –34.
Agaku, I. T., King, B. A., Husten, C. G., Bunnell, R., Ambrose, B. K., Hu,
S. S., . . . the Centers for Disease Control and Prevention (CDC). (2014).
Tobacco product use among adults—United States, 2012–2013. MMWR.
Morbidity and Mortality Weekly Report, 63, 542–547.
Alexander, L. A., Trinidad, D. R., Sakuma, K. L., Pokhrel, P., Herzog,
T. A., Clanton, M. S., . . . Fagan, P. (2016). Why we must continue to
investigate menthol’s fole in the African American smoking paradox.
Nicotine & Tobacco Research, 18(Suppl. 1), S91–S101. http://dx.doi
.org/10.1093/ntr/ntv209
Al Mamun, A., Alati, R., O’Callaghan, M., Hayatbakhsh, M. R.,
O’Callaghan, F. V., Najman, J. M., . . . Bor, W. (2007). Does childhood
sexual abuse have an effect on young adults’ nicotine disorder (depen-
dence or withdrawal)? Evidence from a birth cohort study. Addiction,
102, 647– 654. http://dx.doi.org/10.1111/j.1360-0443.2006.01732.x
American Cancer Society. (2016). Cancer facts and figures, 2016. Atlanta,
GA: Author. Retrieved from https://www.cancer.org/content/dam/
cancer-org/research/cancer-facts-and-statistics/annual-cancer-facts-and-
figures/2016/cancer-facts-and-figures-2016.pdf
American Psychological Association. (1994). Diagnostic and statistical
manual of mental disorders (4th ed.). Washington, DC: Author.
Barboza Solis, C., Kelly-Irving, M., Fantin, R., Darnaudery, M., Torrisani,
J., Lang, T., & Delpierre, C. (2015). Adverse childhood experiences and
1055
physiological wear-and-tear in midlife: Findings from the 1958 British
birth cohort. Proceedings of the National Academy of Science USA, 112,
E738 –E746. http://dx.doi.org/10.1073/pnas.1417325112
Beck, A. T., Ward, C. H., Mendelson, M., Mock, J., & Erbaugh, J. (1961).
An inventory for measuring depression. Archives of General Psychiatry,
4, 561–571. http://dx.doi.org/10.1001/archpsyc.1961.01710120031004
Bermudez, E. A., Rifai, N., Buring, J., Manson, J. E., & Ridker, P. M.
(2002). Interrelationships among circulating interleukin-6, C-reactive
protein, and traditional cardiovascular risk factors in women. Arterio-
sclerosis, Thrombosis, and Vascular Biology, 22, 1668 –1673. http://dx
.doi.org/10.1161/01.ATV.0000029781.31325.66
Bernstein, D., & Fink, L. (1998). Childhood Trauma Questionnaire man-
ual. San Antonio, TX: Psychological Corporation.
Bernstein, D. P., Stein, J. A., Newcomb, M. D., Walker, E., Pogge, D.,
Ahluvalia, T., . . . Zule, W. (2003). Development and validation of a
brief screening version of the Childhood Trauma Questionnaire. Child
Abuse & Neglect, 27, 169 –190. http://dx.doi.org/10.1016/S0145-2134
(02)00541-0
Binder, E. B., Bradley, R. G., Liu, W., Epstein, M. P., Deveau, T. C.,
Mercer, K. B., . . . Ressler, K. J. (2008). Association of FKBP5
polymorphisms and childhood abuse with risk of posttraumatic stress
disorder symptoms in adults. Journal of the American Medical Associ-
ation, 299, 1291–1305. http://dx.doi.org/10.1001/jama.299.11.1291
Bradley, R. G., Binder, E. B., Epstein, M. P., Tang, Y., Nair, H. P., Liu, W.,
. . . Ressler, K. J. (2008). Influence of child abuse on adult depression:
Moderation by the corticotropin-releasing hormone receptor gene. Ar-
chives of General Psychiatry, 65, 190 –200. http://dx.doi.org/10.1001/
archgenpsychiatry.2007.26
Breslau, N., Davis, G. C., & Andreski, P. (1995). Risk factors for PTSD-
related traumatic events: A prospective analysis. The American Journal
of Psychiatry, 152, 529 –535. http://dx.doi.org/10.1176/ajp.152.4.529
Breslau, N., Davis, G. C., & Schultz, L. R. (2003). Posttraumatic stress
disorder and the incidence of nicotine, alcohol, and other drug disorders
in persons who have experienced trauma. Archives of General Psychi-
atry, 60, 289 –294. http://dx.doi.org/10.1001/archpsyc.60.3.289
Breslau, N., Kessler, R. C., Chilcoat, H. D., Schultz, L. R., Davis, G. C.,
& Andreski, P. (1998). Trauma and posttraumatic stress disorder in the
community: The 1996 Detroit Area Survey of Trauma. Archives of
General Psychiatry, 55, 626 – 632. http://dx.doi.org/10.1001/archpsyc
.55.7.626
Brody, C. L., Hamer, D. H., & Haaga, D. A. (2005). Depression vulnera-
bility, cigarette smoking, and the serotonin transporter gene. Addictive
Behaviors, 30, 557–566.
Campbell-Sills, L., & Stein, M. B. (2007). Psychometric analysis and
refinement of the Connor-Davidson Resilience Scale (CD-RISC): Val-
idation of a 10-item measure of resilience. Journal of Traumatic Stress,
20, 1019 –1028. http://dx.doi.org/10.1002/jts.20271
Casiano, H., Mota, N., Afifi, T. O., Enns, M. W., & Sareen, J. (2009).
Childhood maltreatment and threats with weapons. Journal of Nervous
and Mental Disease, 197, 856 – 861. http://dx.doi.org/10.1097/NMD
.0b013e3181be9c55
Catley, D., Ahluwalia, J. S., Resnicow, K., & Nazir, N. (2003). Depressive
symptoms and smoking cessation among inner-city African Americans
using the nicotine patch. Nicotine and Tobacco Research, 5, 61– 68.
http://dx.doi.org/10.1080/1462220021000060464
Centers for Disease Control and Prevention. (1998). Tobacco use among
U.S. racial/ethnic minority groups—African Americans, American In-
dians and Alaska Natives, Asian Americans and Pacific Islanders, His-
panics. A Report of the Surgeon General. Executive summary. MMWR:
Recommendations and Reports, 47(RR-18), v–xv, 1–16.
Chaturvedi, A. K., Caporaso, N. E., Katki, H. A., Wong, H. L., Chatterjee,
N., Pine, S. R., . . . Engels, E. A. (2010). C-reactive protein and risk of
lung cancer. Journal of Clinical Oncology, 28, 2719 –2726. http://dx.doi
.org/10.1200/JCO.2009.27.0454
 1056 BERG ET AL.
Chen, P. H., White, H. R., & Pandina, R. J. (2001). Predictors of smoking
cessation from adolescence into young adulthood. Addictive Behaviors,
26, 517–529. http://dx.doi.org/10.1016/S0306-4603(00)00142-8
Cicchetti, D., & Rogosch, F. A. (1997). The role of self-organization in the
promotion of resilience in maltreated children. Development and Psy-
chopathology, 9, 797– 815. http://dx.doi.org/10.1017/S09545794
97001442
Collishaw, S., Pickles, A., Messer, J., Rutter, M., Shearer, C., & Maughan,
B. (2007). Resilience to adult psychopathology following childhood
maltreatment: Evidence from a community sample. Child Abuse &
Neglect, 31, 211–229. http://dx.doi.org/10.1016/j.chiabu.2007.02.004
Connor, K. M., & Davidson, J. R. (2003). Development of a new resilience
scale: The Connor-Davidson Resilience Scale (CD-RISC). Depression
and Anxiety, 18, 76 – 82. http://dx.doi.org/10.1002/da.10113
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
Covey, L. S., Glassman, A. H., & Stetner, F. (1990). Depression and
This document is copyrighted by the American Psychological Association or one of its allied publishers.
depressive symptoms in smoking cessation. Comprehensive Psychiatry,
31, 350 –354.
Doamekpor, L. A., & Dinwiddie, G. Y. (2015). Allostatic load in foreign-
born and US-born blacks: Evidence from the 2001–2010 National
Health and Nutrition Examination Survey. American Journal of Public
Health, 105, 591–597. http://dx.doi.org/10.2105/AJPH.2014.302285
Enns, M. W., Cox, B. J., Afifi, T. O., De Graaf, R., Ten Have, M., &
Sareen, J. (2006). Childhood adversities and risk for suicidal ideation
and attempts: A longitudinal population-based study. Psychological
Medicine, 36, 1769 –1778. http://dx.doi.org/10.1017/S003329170
6008646
Essex, M. J., Boyce, W. T., Hertzman, C., Lam, L. L., Armstrong, J. M.,
Neumann, S. M. A., & Kobor, M. S. (2013). Epigenetic vestiges of early
developmental adversity: Childhood stress exposure and DNA methyl-
ation in adolescence. Child Development, 84, 58 –75. http://dx.doi.org/
10.1111/j.1467-8624.2011.01641.x
Ferguson-Smith, A. C., Chen, Y. F., Newman, M. S., May, L. T., Sehgal,
P. B., & Ruddle, F. H. (1988). Regional localization of the interferon-
beta 2/B-cell stimulatory factor 2/hepatocyte stimulating factor gene to
human chromosome 7p15-p21. Genomics, 2, 203–208. http://dx.doi.org/
10.1016/0888-7543(88)90003-1
Fergusson, D. M., Horwood, L. J., & Lynskey, M. T. (1996). Childhood
sexual abuse and psychiatric disorder in young adulthood: II. Psychiatric
outcomes of childhood sexual abuse. Journal of the American Academy
of Child & Adolescent Psychiatry, 35, 1365–1374. http://dx.doi.org/10
.1097/00004583-199610000-00024
Festa, A., D’Agostino, R., Jr., Howard, G., Mykkänen, L., Tracy, R. P., &
Haffner, S. M. (2000). Chronic subclinical inflammation as part of the
insulin resistance syndrome: The Insulin Resistance Atherosclerosis
Study (IRAS). Circulation, 102, 42– 47. http://dx.doi.org/10.1161/01
.CIR.102.1.42
Freeman, D. J., Norrie, J., Caslake, M. J., Gaw, A., Ford, I., Lowe, G. D.,
. . . the West of Scotland Coronary Prevention Study. (2002). C-reactive
protein is an independent predictor of risk for the development of
diabetes in the West of Scotland Coronary Prevention Study. Diabetes,
51, 1596 –1600. http://dx.doi.org/10.2337/diabetes.51.5.1596
Geronimus, A. T., Bound, J., Waidmann, T. A., Hillemeier, M. M., &
Burns, P. B. (1996). Excess mortality among blacks and whites in the
United States. The New England Journal of Medicine, 335, 1552–1558.
http://dx.doi.org/10.1056/NEJM199611213352102
Geronimus, A. T., Hicken, M., Keene, D., & Bound, J. (2006). “Weath-
ering” and age patterns of allostatic load scores among blacks and whites
in the United States. American Journal of Public Health, 96, 826 – 833.
http://dx.doi.org/10.2105/AJPH.2004.060749
Gilbert, R., Widom, C. S., Browne, K., Fergusson, D., Webb, E., & Janson,
S. (2009). Burden and consequences of child maltreatment in high-
income countries. Lancet, 373, 68 – 81. http://dx.doi.org/10.1016/S0140-
6736(08)61706-7
Gillespie, C. F., Bradley, B., Mercer, K., Smith, A. K., Conneely, K.,
Gapen, M., . . . Ressler, K. J. (2009). Trauma exposure and stress-related
disorders in inner city primary care patients. General Hospital Psychi-
atry, 31, 505–514. http://dx.doi.org/10.1016/j.genhosppsych.2009.05
.003
Goldstein, A. L., Faulkner, B., & Wekerle, C. (2013). The relationship
among internal resilience, smoking, alcohol use, and depression symp-
toms in emerging adults transitioning out of child welfare. Child Abuse
& Neglect, 37, 22–32. http://dx.doi.org/10.1016/j.chiabu.2012.08.007
Gonzalez, V. B. A., Sierra, M. T. C., Martinez, B. A., Martinez-Molina, A.,
& Ponce, F. P. (2015). An in-depth psychometric analysis of the Connor-
Davidson Resilience Scale: Calibration with Rasch-Andrich model.
Health and Quality of Life Outcomes, 13, 154. http://dx.doi.org/10.1186/
s12955-015-0345-y
Green, B. L., Grace, M. D., Lindy, J. D., & Leonard, A. C. (1990). Race
differences in response to combat stress. Journal of Traumatic Stress, 3,
379 –393. http://dx.doi.org/10.1002/jts.2490030307
Hapke, U., Schumann, A., Rumpf, H. J., John, U., Konerding, U., &
Meyer, C. (2005). Association of smoking and nicotine dependence with
trauma and posttraumatic stress disorder in a general population sample.
Journal of Nervous and Mental Disease, 193, 843– 846. http://dx.doi
.org/10.1097/01.nmd.0000188964.83476.e0
Hertzman, C. (1999). The biological embedding of early experience and its
effects on health in adulthood. Annals of the New York Academy of
Sciences, 896, 85–95. http://dx.doi.org/10.1111/j.1749-6632.1999
.tb08107.x
Hertzman, C. (2012). Putting the concept of biological embedding in
historical perspective. PNAS Proceedings of the National Academy of
Sciences of the United States of America, 109(Suppl. 2), 17160 –17167.
http://dx.doi.org/10.1073/pnas.1202203109
Holford, T. R., Levy, D. T., & Meza, R. (2016). Comparison of smoking
history patterns among African American and White cohorts in the
United States born 1890 to 1990. Nicotine & Tobacco Research,
18(Suppl. 1), S16 –S29. http://dx.doi.org/10.1093/ntr/ntv274
Hovdestad, W., Campeau, A., Potter, D., & Tonmyr, L. (2015). A system-
atic review of childhood maltreatment assessments in population-
representative surveys since 1990. PLoS ONE, 10, e0123366. http://dx
.doi.org/10.1371/journal.pone.0123366
Husky, M. M., Mazure, C. M., Paliwal, P., & McKee, S. A. (2008). Gender
differences in the comorbidity of smoking behavior and major depres-
sion. Drug and Alcohol Dependence, 93, 176 –179. http://dx.doi.org/10
.1016/j.drugalcdep.2007.07.015
Jaffee, S. R., & Gallop, R. (2007). Social, emotional, and academic
competence among children who have had contact with child protective
services: Prevalence and stability estimates. Journal of the American
Academy of Child & Adolescent Psychiatry, 46, 757–765. http://dx.doi
.org/10.1097/chi.0b013e318040b247
Juarez, P., & Hood, D. B. (2013). Sequencing the public health genome.
Journal of Health Care for the Poor and Underserved, 24, 114 –120.
http://dx.doi.org/10.1353/hpu.2013.0035
Karlamangla, A. S., Singer, B. H., McEwen, B. S., Rowe, J. W., & Seeman,
T. E. (2002). Allostatic load as a predictor of functional decline Mac-
Arthur studies of successful aging. Journal of Clinical Epidemiology, 55,
696 –710.
Kellogg, S. H., McHugh, P. F., Bell, K., Schluger, J. H., Schluger, R. P.,
LaForge, K. S., . . . Kreek, M. J. (2003). The Kreek-McHugh-Schluger-
Kellogg scale: A new, rapid method for quantifying substance abuse and
its possible applications. Drug and Alcohol Dependence, 69, 137–150.
http://dx.doi.org/10.1016/S0376-8716(02)00308-3
Kessler, R. C., Davis, C. G., & Kendler, K. S. (1997). Childhood adversity
and adult psychiatric disorder in the US National Comorbidity Survey.
Psychological Medicine, 27, 1101–1119. http://dx.doi.org/10.1017/
S0033291797005588
 RESILIENCE IN AFRICAN AMERICANS
Koenig, W., Sund, M., Fröhlich, M., Fischer, H. G., Löwel, H., Döring, A.,
. . . Pepys, M. B. (1999). C-reactive protein, a sensitive marker of
inflammation, predicts future risk of coronary heart disease in initially
healthy middle-aged men: Results from the MONICA (Monitoring
Trends and Determinants in Cardiovascular Disease) Augsburg Cohort
Study, 1984 to 1992. Circulation, 99, 237–242. http://dx.doi.org/10
.1161/01.CIR.99.2.237
Lindahl, B., Toss, H., Siegbahn, A., Venge, P., & Wallentin, L. (2000).
Markers of myocardial damage and inflammation in relation to long-
term mortality in unstable coronary artery disease. FRISC Study Group.
Fragmin during Instability in Coronary Artery Disease. The New Eng-
land Journal of Medicine, 343, 1139 –1147. http://dx.doi.org/10.1056/
NEJM200010193431602
Luthar, S. S., Cicchetti, D., & Becker, B. (2000). The construct of resil-
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
ience: A critical evaluation and guidelines for future work. Child De-
This document is copyrighted by the American Psychological Association or one of its allied publishers.
velopment, 71, 543–562. http://dx.doi.org/10.1111/1467-8624.00164
MacMillan, H. L., Fleming, J. E., Streiner, D. L., Lin, E., Boyle, M. H.,
Jamieson, E., . . . Beardslee, W. R. (2001). Childhood abuse and lifetime
psychopathology in a community sample. The American Journal of
Psychiatry, 158, 1878 –1883. http://dx.doi.org/10.1176/appi.ajp.158.11
.1878
Masten, A. S. (2001). Ordinary magic. Resilience processes in develop-
ment. American Psychologist, 56, 227–238. http://dx.doi.org/10.1037/
0003-066X.56.3.227
Mauss, D., Li, J., Schmidt, B., Angerer, P., & Jarczok, M. N. (2015).
Measuring allostatic load in the workforce: A systematic review. Indus-
trial Health, 53, 5–20. http://dx.doi.org/10.2486/indhealth.2014-0122
McEwen, B. S. (1998). Stress, adaptation, and disease. Allostasis and
allostatic load. Annals of the New York Academy of Sciences, 840,
33– 44. http://dx.doi.org/10.1111/j.1749-6632.1998.tb09546.x
McGloin, J. M., & Widom, C. S. (2001). Resilience among abused and
neglected children grown up. Development and Psychopathology, 13,
1021–1038. http://dx.doi.org/10.1017/S095457940100414X
Miller, G. W., & Jones, D. P. (2014). The nature of nurture: Refining the
definition of the exposome. Toxicological Sciences, 137, 1–2. http://dx
.doi.org/10.1093/toxsci/kft251
O’Donnell, M. L., Creamer, M., & Pattison, P. (2004). Posttraumatic stress
disorder and depression following trauma: Understanding comorbidity.
The American Journal of Psychiatry, 161, 1390 –1396. http://dx.doi.org/
10.1176/appi.ajp.161.8.1390
Ohsawa, M., Okayama, A., Nakamura, M., Onoda, T., Kato, K., Itai, K.,
. . . Hiramori, K. (2005). CRP levels are elevated in smokers but
unrelated to the number of cigarettes and are decreased by long-term
smoking cessation in male smokers. Preventive Medicine, 41, 651– 656.
http://dx.doi.org/10.1016/j.ypmed.2005.02.002
Ou, S. R., & Reynolds, A. J. (2010). Childhood predictors of young adult
male crime. Children and Youth Services Review, 32, 1097–1107. http://
dx.doi.org/10.1016/j.childyouth.2010.02.009
Pearson, T. A., Mensah, G. A., Alexander, R. W., Anderson, J. L., Cannon,
R. O., III, Criqui, M., . . . American Heart Association. (2003). Markers
of inflammation and cardiovascular disease: Application to clinical and
public health practice: A statement for healthcare professionals from the
Centers for Disease Control and Prevention and the American Heart
Association. Circulation, 107, 499 –511. http://dx.doi.org/10.1161/01
.CIR.0000052939.59093.45
Ridker, P. M. (1998). Inflammation, infection, and cardiovascular risk:
How good is the clinical evidence? Circulation, 97, 1671–1674. http://
dx.doi.org/10.1161/01.CIR.97.17.1671
Ridker, P. M., Buring, J. E., Cook, N. R., & Rifai, N. (2003). C-reactive
protein, the metabolic syndrome, and risk of incident cardiovascular
events: An 8-year follow-up of 14 719 initially healthy American wom-
en. Circulation, 107, 391–397. http://dx.doi.org/10.1161/01.CIR
.0000055014.62083.05
1057
Ridker, P. M., Cushman, M., Stampfer, M. J., Tracy, R. P., & Hennekens,
C. H. (1998). Plasma concentration of C-reactive protein and risk of
developing peripheral vascular disease. Circulation, 97, 425– 428. http://
dx.doi.org/10.1161/01.CIR.97.5.425
Ridker, P. M., Rifai, N., Rose, L., Buring, J. E., & Cook, N. R. (2002).
Comparison of C-reactive protein and low-density lipoprotein choles-
terol levels in the prediction of first cardiovascular events. The New
England Journal of Medicine, 347, 1557–1565. http://dx.doi.org/10
.1056/NEJMoa021993
Rost, N. S., Wolf, P. A., Kase, C. S., Kelly-Hayes, M., Silbershatz, H.,
Massaro, J. M., . . . Wilson, P. W. (2001). Plasma concentration of
C-reactive protein and risk of ischemic stroke and transient ischemic
attack: The Framingham study. Stroke, 32, 2575–2579. http://dx.doi.org/
10.1161/hs1101.098151
Schwartz, A. C., Bradley, R. L., Sexton, M., Sherry, A., & Ressler, K. J.
(2005). Posttraumatic stress disorder among African Americans in an
inner city mental health clinic. Psychiatric Services, 56, 212–215. http://
dx.doi.org/10.1176/appi.ps.56.2.212
Scott, K. M., Smith, D. R., & Ellis, P. M. (2010). Prospectively ascertained
child maltreatment and its association with DSM–IV mental disorders in
young adults. Archives of General Psychiatry, 67, 712–719. http://dx
.doi.org/10.1001/archgenpsychiatry.2010.71
Seeman, T. E., Crimmins, E., Huang, M. H., Singer, B., Bucur, A.,
Gruenewald, T., . . . Reuben, D. B. (2004). Cumulative biological risk
and socio-economic differences in mortality: MacArthur studies of suc-
cessful aging. Social Science & Medicine, 58, 1985–1997. http://dx.doi
.org/10.1016/S0277-9536(03)00402-7
Seeman, T. E., McEwen, B. S., Rowe, J. W., & Singer, B. H. (2001).
Allostatic load as a marker of cumulative biological risk: MacArthur
studies of successful aging. Proceedings of the National Academy of
Sciences of the United States of America, 98, 4770 – 4775. http://dx.doi
.org/10.1073/pnas.081072698
Seeman, T. E., Singer, B. H., Rowe, J. W., Horwitz, R. I., & McEwen, B. S.
(1997). Price of adaptation—Allostatic load and its health consequences.
MacArthur studies of successful aging. Archives of Internal Medicine,
157, 2259 –2268. http://dx.doi.org/10.1001/archinte.1997.004404001
11013
Seeman, T. E., Singer, B., Ryff, C., Dienberg Love, G., & Levy-Storms, L.
(2002). Social relationships, gender, and allostatic load across two age
cohorts. Psychosomatic Medicine, 64, 395– 406. http://dx.doi.org/10.1097/
00006842-200205000-00004
Sesso, H. D., Buring, J. E., Rifai, N., Blake, G. J., Gaziano, J. M., &
Ridker, P. M. (2003). C-reactive protein and the risk of developing
hypertension. Journal of the American Medical Association, 290, 2945–
2951. http://dx.doi.org/10.1001/jama.290.22.2945
Simpson, T. L., & Miller, W. R. (2002). Concomitance between childhood
sexual and physical abuse and substance use problems. A review.
Clinical Psychology Review, 22, 27–77. http://dx.doi.org/10.1016/
S0272-7358(00)00088-X
Steinhardt, M., & Dolbier, C. (2008). Evaluation of a resilience interven-
tion to enhance coping strategies and protective factors and decrease
symptomatology. Journal of American College Health, 56, 445– 453.
http://dx.doi.org/10.3200/JACH.56.44.445-454
Steptoe, A., Hackett, R. A., Lazzarino, A. I., Bostock, S. L. A., Marca, R.,
Carvalho, L. A., & Hamer, M. (2014). Disruption of multisystem re-
sponses to stress in type 2 diabetes: Investigating the dynamics of
allostatic load. PNAS Proceedings of the National Academy of Sciences
of the United States of America, 111, 15693–15698. http://dx.doi.org/10
.1073/pnas.1410401111
Toumbourou, J. W., Gregg, M. E., Shortt, A. L., Hutchinson, D. M., &
Slaviero, T. M. (2013). Reduction of adolescent alcohol use through
family-school intervention: A randomized trial. Journal of Adolescent
Health, 53, 778 –784. http://dx.doi.org/10.1016/j.jadohealth.2013.07
.005
 1058 BERG ET AL.
Trichopoulos, D., Psaltopoulou, T., Orfanos, P., Trichopoulou, A., &
Boffetta, P. (2006). Plasma C-reactive protein and risk of cancer: A
prospective study from Greece. Cancer Epidemiology, Biomarkers and
Prevention, 15, 381–384. http://dx.doi.org/10.1158/1055-9965.EPI-05-
0626
Ungar, M., Liebenberg, L., Landry, N., & Ikeda, J. (2012). Caregivers,
young people with complex needs, and multiple service providers: A
study of triangulated relationships. Family Process, 51, 193–206. http://
dx.doi.org/10.1111/j.1545-5300.2012.01395.x
Upchurch, D. M., Stein, J., Greendale, G. A., Chyu, L., Tseng, C. H.,
Huang, M. H., . . . Seeman, T. (2015). A longitudinal investigation of
race, socioeconomic status, and psychosocial mediators of allostatic load
in midlife women: Findings from the Study of Women’s Health Across
the Nation. Psychosomatic Medicine, 77, 402– 412. http://dx.doi.org/10
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
.1097/PSY.0000000000000175
Volpato, S., Guralnik, J. M., Ferrucci, L., Balfour, J., Chaves, P., Fried,
This document is copyrighted by the American Psychological Association or one of its allied publishers.
L. P., & Harris, T. B. (2001). Cardiovascular disease, interleukin-6, and
risk of mortality in older women: The Women’s Health and Aging
Study. Circulation, 103, 947–953. http://dx.doi.org/10.1161/01.CIR.103
.7.947
Wild, C. P. (2012). The exposome: From concept to utility. International
Journal of Epidemiology, 41, 24 –32. http://dx.doi.org/10.1093/ije/dyr236
Windle, G., Bennett, K. M., & Noyes, J. (2011). A methodological review
of resilience measurement scales. Health and Quality of Life Outcomes,
9, 8. http://dx.doi.org/10.1186/1477-7525-9-8
Windle, M., & Windle, R. C. (2001). Depressive symptoms and cigarette
smoking among middle adolescents: Prospective associations and intrap-
ersonal and interpersonal influences. Journal of Consulting and Clinical
Psychology, 69, 215–226. http://dx.doi.org/10.1037/0022-006X.69.2
.215
Wolfe, D. A., Scott, K., Wekerle, C., & Pittman, A. L. (2001). Child
maltreatment: Risk of adjustment problems and dating violence in ado-
lescence. Journal of the American Academy of Child & Adolescent
Psychiatry, 40, 282–289. http://dx.doi.org/10.1097/00004583-
200103000-00007
Yilmaz, E. D., Unal, O., Gencer, G. G., Aydemir, O., & Selcuk, Z. (2015).
Static/unchangeable and dynamic/changeable nature of personality ac-
cording to the nine types temperament model: A proposal. International
Journal of Emergency Mental Health and Human Resilience, 17, 298 –
303.
Yudkin, J. S., Stehouwer, C. D., Emeis, J. J., & Coppack, S. W. (1999).
C-reactive protein in healthy subjects: Associations with obesity, insulin
resistance, and endothelial dysfunction: A potential role for cytokines
originating from adipose tissue? Arteriosclerosis, Thrombosis, and Vas-
cular Biology, 19, 972–978. http://dx.doi.org/10.1161/01.ATV.19.4.972
Received December 26, 2016
Revision received March 28, 2017
Accepted June 4, 2017 䡲