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An Experimental Examinationof Stress Reactivity inAdolescents and Young AdultsWith AsthmaAngelica R. Eddington a , Larry L. Mullins a , JenniferByrd-Craven a & John M. Chaney aa Department of Psychology, Oklahoma StateUniversity, Stillwater, OK
Available online: 17 Feb 2012
To cite this article: Angelica R. Eddington, Larry L. Mullins, Jennifer Byrd-Craven& John M. Chaney (2012): An Experimental Examination of Stress Reactivity inAdolescents and Young Adults With Asthma, Children's Health Care, 41:1, 16-31
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Children’s Health Care, 41:16–31, 2012
Copyright © Taylor & Francis Group, LLC
ISSN: 0273-9615 print/1532-6888 online
DOI: 10.1080/02739615.2012.643287
An Experimental Examination of StressReactivity in Adolescents and Young
Adults With Asthma
Angelica R. Eddington, Larry L. Mullins,Jennifer Byrd-Craven, and John M. Chaney
Department of Psychology, Oklahoma State University, Stillwater, OK
Despite advancements in treatment for asthma, the adolescent and young adult
(AYA) population continues to face a host of psychological challenges when com-
pared to healthy controls. In addition, unusually high mortality and morbidity rates
for asthma are present in the AYA population. Some researchers have suggested an
examination of stress reactivity to shed light on these differences. Using a learned
helplessness task, this study investigated the differences in cortisol elevation in
a sample of college students with asthma and their healthy controls. Results
supported an initial elevation of cortisol in asthma participants not evident in
the healthy control population. Notably, neither college students with asthma nor
healthy controls perceived the learned helplessness task to be stressful. Findings
suggest that college students with asthma may be more reactive to novel envi-
ronments when compared to healthy controls, as evidenced by increased cortisol
levels. Future studies on the differences in stress reactivity in individuals with
asthma are warranted.
Asthma, the most common chronic illness in the United States, is a chronic
inflammatory disorder of the airway in which individuals experience recurrent
episodes of wheezing, breathlessness, chest tightness, and cough (National Heart,
Lung, and Blood Institute [NHLBI], 2008). Traditionally viewed as an illness of
younger children, recent studies have clearly demonstrated high asthma preva-
Correspondence should be addressed to Angelica R. Eddington, Department of Psychology,
Oklahoma State University, 116 North Murray Hall, Stillwater, OK 74078. E-mail: angelica.
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STRESS REACTIVITY 17
lence rates in older children and young adolescents aged 11 to 17 (Akinbami,
Moorman, Garbe, & Sondik, 2009). Although some individuals report that
they experience a reduction in symptoms as they enter adolescence, studies
have documented that this decrease does not happen as often as once thought
(Carpentier, Mullins, & Van Pelt, 2007).
Unfortunately, little research has focused on psychosocial aspects of asthma
in the adolescent and young adult (AYA) population, although studies have
shown that, as a group, they still experience significant life challenges (e.g.,
Hommel et al., 2003; Mullins, Chaney, Pace, & Hartman, 1997; Perez-Yarza,
1996). Adults and adolescents with asthma have been documented to be at
greater risk for engaging in substance abuse (Forero, Bauman, Young, Booth, &
Nutbeam, 1996), experience high rates of school absenteeism (American Lung
Association, 2007), and struggle with unemployment (Taitel, Allen, & Creer,
1998) when compared to same-aged peers. Notably, a significant number of
college students are hospitalized each year for reasons secondary to their asthma
(Jolicoeur, Pharm, Boyer, Reeder, & Turner, 1994). At the same time, 40% of
college students with asthma report that they do not seek medical attention even
if they feel that their symptoms are severe enough for medical care (Jolicoeur
et al., 1994). Thus, it would appear that older AYAs continue to face a host
of challenges related to the experience of asthma. As a result, researchers have
increasingly turned to the examination of factors that place these individuals
at risk.
In this vein, a number studies have investigated cognitive deficits in function-
ing that potentially result from the unpredictable nature of asthma. One line of
research has utilized “learned helplessness theory” as a means of understanding
the impact of the unpredictability of asthma and the stress that accompanies
this disease (Chaney et al., 1999; Mullins et al., 1997). Using an experimentally
induced learned helplessness paradigm, Chaney et al. provided evidence that
older adolescents with childhood-onset asthma, who had experienced a non-
contingent computer (i.e., non-controllable/unsolvable) concept formation task,
demonstrated more performance deficits on a subsequent anagram task than age-
matched healthy controls. In addition, a pre–post examination of causal attribu-
tions revealed an increase in internal attributions among college students with
asthma in the uncontrollable condition, whereas healthy controls displayed more
external attributions for failure (Chaney et al., 1999). Such results suggest that
the unpredictable and variable nature of asthma may indeed lead to an increased
cognitive vulnerability to helplessness under conditions of non-contingency or
stress. It is interesting to note that little research, to date, has focused on the
psycho-physiologic aspects of stress reactivity in youth with asthma, particularly
within an experimental context. Thus, it remains to be seen whether individuals
with asthma also respond differentially in terms of their physiological responses
to stress compared to healthy controls.
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18 EDDINGTON ET AL.
To date, stress reactivity and associated cortisol elevations have witnessed
limited research in youth with chronic illnesses. Although stress reactivity may
include many complex patterns, its most basic definition applies to the difference
between baseline arousal and stress-induced arousal (Bauer, Quas, & Boyce,
2002). Although still developing, research suggest that stress has been linked
to the onset, development, and morbidity of asthma in children (Mrazek et al.,
1999; Randolph & Fraser, 1999; Wade et al., 1997), as well as exacerbation of
symptoms (Joachim et al., 2003). In recent years, researchers have increasingly
utilized salivary cortisol, a biomarker of hypothalamic–pituitary–adrenal (HPA)
axis activity often initiated by psychosocial stress (Aardal-Eriksson, Karlberg,
& Holm, 1998; Kirschbaum & Hellhammer, 1994; Masharani, et al., 2005), as
a measure of stress reactivity. The degree of activation depends, in part, on
the unpredictable, uncontrollable, or novel nature of a situation, anticipation,
or ego involvement (Kudielka, Hellhammer, & Kirschbaum, 2007). Vedhara
et al. (2007) hypothesized that early childhood illness could have a long-lasting
effect on activity of the HPA axis in adulthood, and increased activity of the
HPA axis following stressors. It is interesting to note that they found that
childhood respiratory illnesses were associated with reduced HPA axis activity
later in adulthood. Recently, cortisol secretion has been studied in populations of
individuals with asthma. Masharani et al. found support for the normal diurnal
pattern of cortisol secretion in a sample of adults with varying asthma severity.
In addition, after collecting salivary cortisol samples from the participants 30
min and then 12 hr after awakening, they found significantly higher cortisol
levels in the morning samples. They also investigated the impact of prescribed
glucocorticoid from inhaled, nasal, or oral usage on cortisol secretion. The results
showed that external glucocorticoid use suppressed salivary cortisol secretion,
especially in the 30-min-after-awakening samples. Such results suggest that indi-
viduals with asthma demonstrate similar cortisol patterns, as healthy controls and
glucocorticoid use is effective, as should be, in suppressing cortisol elevations.
Hence, increases in cortisol among individuals with asthma should be attributed
to other factors.
Wolf, Nicholls, and Chen (2008) investigated cortisol levels, salivary ˛-
amylase (an enzyme that reflects stress-responsive sympatho-adrenal medullary
[SAM] axis activity) levels, and stress in healthy children and adolescents
and children and adolescents with asthma. In healthy children, chronic stress
was associated with flatter cortisol slopes. Higher chronic stress among chil-
dren with asthma was associated with lower daily ˛-amylase, thus indicat-
ing lower sympathetic activity and implying increased susceptibility to symp-
tom exacerbations. In addition, their study supported a reversed secretion pat-
tern of cortisol and ˛-amylase, and that only salivary ˛-amylase patterns dif-
fered between children with asthma and healthy children, with asthmatic chil-
dren showing lower levels. Wolf et al. hypothesized that increased sympathetic
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STRESS REACTIVITY 19
system activity could potentially protect against asthma symptom exacerba-
tions.
Researchers have suggested that the use of self-report inventories alone may
limit the conclusions that we can draw concerning the psychological effects of
having asthma (Gillaspy, Hoff, Mullins, Van Pelt, & Chaney, 2002; Mullins,
Chaney, Balderson, & Hommel, 2000); therefore, the use of salivary cortisol to
investigate psycho-physiological outcomes appears to be warranted. Indeed, in
the context of asthma, a better understanding of stress reactivity would yield
important information about the potential long-term physical and psychological
outcomes, especially because psychological risk factors have been postulated to
account for increased morbidity and mortality rates (Kang & Fox, 2000). Thus,
the primary aim of this study was designed to extend the work of Chaney et al.
(1999) in a sample of college students with asthma utilizing salivary cortisol as
a measure of stress reactivity.
In this study, we used a learned helplessness paradigm task with either a
controllable (contingent) or uncontrollable (non-contingent) condition. Cortisol
levels were taken at three different time points (prior to the manipulation [T1],
immediately after manipulation [T2], and 15 min post manipulation [T3]). Given
that cortisol is a biomarker of psychosocial (Kirschbaum & Hellhammer, 1994)
and uncontrollable stress (de Boer, de Beun, Slangen, & Van der Gugten, 1990;
Henry, 1986; Huether, 1998; Vogel, 1985), we hypothesized different cortisol
elevation patterns for participants with asthma and their healthy controls for each
collection point during the learned helplessness task (Chaney et al., 1999) as a
function of the experimental manipulation. Because stress has been associated
with the development of asthma and maintenance of symptoms (Randolph &
Fraser, 1999; Wade et al., 1997), we hypothesized, at the first collection point
(T1), that college students with childhood-onset asthma would exhibit higher
cortisol levels than healthy controls in both experimental conditions. In the non-
contingent condition, we predicted that cortisol levels at T2 would increase in
both college students with childhood-onset asthma and their healthy controls in
response to the uncontrollable stress (Vogle, 1985), with steeper elevations in
participants with asthma given that healthy controls have been found to exhibit
lower cortisol levels when exposed to stress than individuals with asthma (Wolf
et al., 2008). We expected this increase in both participant groups in the non-
contingent condition to decrease at T3, as research has supported a decline of
cortisol within 10 to 15 min after a stressor (Sapolsky, Romero, & Munck,
2000).
In the contingent (controllable) condition, we predicted that cortisol levels of
both college students with childhood-onset asthma and healthy controls would
not show increases at T2, assuming that this condition will elicit less stress or
learned helplessness in the participants (see Chaney et al., 1999). In addition,
in the contingent condition, we expected T2 and T3 cortisol levels for both
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20 EDDINGTON ET AL.
participants with asthma and healthy controls to remain fairly consistent with
T1 cortisol levels, also assuming that this condition will elicit less stress and,
hence, be less cortisol reactive (de Boer et al., 1990; Henry, 1986; Huether,
1998; Vogel, 1985).
METHOD
Participants
College students with and without a history of asthma were recruited from a
Midwestern university through psychology courses or the health center. Partic-
ipants in the asthma group were 30 college students between the ages of 18
and 24 (M D 20:00, SD D 1:39), who self-identified as having childhood-
onset asthma (prior to the age of 12). Using a self-report, 7-point Likert scale
of asthma severity based on NHLBI (2008) guidelines, 46.7% of participants
with asthma reported having intermittent symptoms, 23.3% reported having mild
symptoms, 10% reported having moderate symptoms, and 5% reported having
severe symptoms associated with asthma. In addition, 83.3% of the chronic
population reported currently taking medication for their asthma, and 46.7%
reported currently receiving medical treatment from a physician. Most of the
sample (90%) reported that their symptoms were controllable. The group with
asthma included 18 women (60.0%) and 12 men (40.0%). The majority of
participants self-identified as Caucasian (83.3%; n D 25), followed by Native
American (13.3%; n D 4).
Participants in the control group were 30 college students between the ages
of 18 and 24 (M D 19:70, SD D 1:34), who denied any history of asthma or
major chronic illnesses. The control group included 18 women (60.0%) and 12
men (40.0%). The majority of participants self-identified as Caucasian (80.0%;
n D 24), followed by Native Americans (10.0%; n D 3) and Hispanics/Latinos
(6.7%; n D 2). The distribution of ethnicities reflects the demographic makeup
of the larger college population at this particular institution.
Materials
Demographic form. A demographic questionnaire was designed for this
study that inquired about the participant’s gender, age, ethnicity, number of
years of education completed, household income, marital status, current chronic
illness, and medication history.
Zung Self-Rating Anxiety Scale (SAS; Zung, 1971). The SAS is a
20-item (e.g., “I feel afraid for no reason at all,” and “I can feel my heart
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STRESS REACTIVITY 21
beating fast”), self-report measure that assessed anxiety. Each question infers
about anxious behavior, and is scored on a 4-point scale ranging from 1 (none
or a little of the time), 2 (some of the time), 3 (a good part of the time),
to 4 (most of the time). The overall score from the SAS was used to assess
participants’ levels of anxiety, with higher scores reflecting greater anxiety.
Scores range from 20 to 80, with 20 through 44 indicating normal anxiety
levels, 45 through 59 indicating mild to moderate anxiety levels, 60 through
74 indicating marked to severe anxiety levels, and 75 through 80 indicating
extreme anxiety levels. This measure has been found to have high internal
consistency in community samples (.79; Knight, Waal-Manning, & Spears, 1983)
and depressed patients (.88; Gabreys & Peters, 1985). Cronbach’s alpha for this
sample was .82.
Center for Epidemiologic Studies–Depression (CES–D) Scale (Radloff,1977). The CES–D is a 20-item, self-report measure that assesses depressive
symptoms and behaviors during the past week. For each item, the respondents
rate how much they experienced depressive and non-depressive feelings during
the week (e.g., “I did not feel like eating; my appetite was poor,” and “I felt
I was just as good as other people”). All 20 items were summed to reflect a
total score. The total score is used to assess participants’ levels of depression,
with higher scores being indicative of greater levels of depression. A score > 16
indicates a clinically significant level of psychological distress. The measure has
demonstrated high internal consistency estimates (.85–.90) in general and patient
populations (Radloff, 1977). This sample had a Cronbach’s alpha of .89.
Saliva collection materials and sampling. All salvia collections were
taken between 12:00 p.m. and 5:00 p.m. to control the influence of the natural
diurnal pattern (Gibson et al., 1999). Because it is well-established that cortisol
levels can peak and decline within 10 to 15 min (Sapolsky et al., 2000), saliva
samples were taken at three different time points (T1 D prior to experimental
task, T2 D immediately following the experimental task, and T3 D 15 min after
the experimental task) during the first session of the study. The participants were
given three oral swabs, each located inside one of the three swab storage tubes
(from Salimetrics Testing Services, Inc., State College, PA). The participants
were instructed to saturate the oral swabs with saliva while inside their mouths.
Each storage tube had the participant’s subject number and the abbreviation for
when to swab their mouths (T1, T2, and T3). A timer was used to time 15 min
between T2 and T3 collection points.
Oral swab samples were stored at �20ıC in an on-site freezer until analysis.
After all samples had been taken, samples were packed on dry ice and shipped
to Salimetrics and assayed in singulate using enzymatic immunoassay (EIA)
following standard procedures outlined by Salimetrics. The EIA kit included
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22 EDDINGTON ET AL.
a microtitre plate with monoclonal antibodies to cortisol, and was designed to
capture 0.0003 to 3.00 �g/dL of cortisol. Standard cortisol levels from Sali-
metrics and study samples competed with cortisol linked horse radishperoxidase
for the antibody binding sites. The cortisol standards, controls, and samples
were then pipetted into appropriate wells on the microtitre plate. Assay diluents
were used to serve as the zero for comparison purposes. A dilution of the
enzyme conjugate was immediately pipetted into each well using a multichan-
nel pipette. After mixing the plate, it was incubated at room temperature for
55 min.
After washing unbound components, the substrate tetramethylbenzidine
(TMB) was added, and the solution was mixed on a plate rotator for 5 min
at 500 rpm and placed in the dark at room temperature for an additional 25 min.
Fifty �L of solution was added to each well to stop the enzymatic reaction, and
then mixed on a plate rotator for 3 min. The plate was placed on a plate reader
within 10 min of adding the stop solution. Bound cortisolperoxidase was then
measured by optical density color differences produced by the reaction of the
peroxidase enzyme on the substrate TMB.
Referral sheet. Because the tasks and measures in the study could have
elicited some distress in the participants, a list of available psychological support
services was issued to each person.
Procedure
Institutional review board approval for the protection of human participants was
obtained, and the study was advertised online through a chronic health screener
for enrolled undergraduate students, as well as through flyers. All participants
voluntarily consented to the study via e-mail. Verbal and written informed
consent was obtained at the beginning of the first session after explaining the
purpose of the study. All participants were above the age of 18; therefore, the
protocol for obtaining consent for minors was not necessary. Participants were
matched by age and gender after data collection. Participants received course
credit and monetary compensation. The study consisted of two sessions, with
the first lasting 1 1
2hr and the second lasting approximately 1 hr. In the first
session, after filling out the consent form, the first saliva sample was collected
(T1). Then, participants were assigned (before arrival) by the experimenter to
either a contingent or non-contingent condition for the computerized experi-
mental (learned helplessness) task. Participants were read a script of examples
of the tasks and how they work. After the examples, a computer presented
the participants with a concept-formation task involving 40 stimulus patterns
grouped into four sets of 10 problems (for a complete description, see Chaney
et al., 1999). The experimental manipulation involved one-half of the participants
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STRESS REACTIVITY 23
receiving positive feedback from the computer screen, which allowed successful
completion of the task (contingent or controllable condition); and the other
half of the participants receiving random, negative feedback from the computer
screen, which prevented successful completion of the task (non-contingent or
non-controllable condition).
As part of the standardized instructions, all participants were led to believe
that the task was solvable and that determining the correct stimulus dimension
was attainable. However, only participants in the contingent-feedback condition
were given solvable problems with response-contingent correct and incorrect
feedback about their performance. In addition, after the computer task, research
assistants verbally commented with similar positive feedback or random, nega-
tive feedback, depending on the experimental condition, to the participant about
his or her performance. As soon as the feedback was given, the participant was
asked to give saliva sample T2, and the experimenter started the timer for 15 min.
Following the administration of the computer task, participants were asked to
complete an anagram task containing 20 anagrams with five letters per anagram,
and were given 100 sec to solve each anagram. The program was conducted on
the same computer as the experimental task. The purpose of this task was to
measure changes in performance and motivation following experiencing non-
contingency in the earlier task. After the task was over, a score was presented
on the screen. The experimenter documented this score. Next, the experimenter
gave the participant the demographic form to fill out (allowing 15 min to pass).
After 15 min passed, the T3 saliva sample was taken. If the participant did not
fill out the demographic form before the 15 min, the experimenter took the saliva
sample, and then allowed the participant to fill out the form afterward.
Following the completion of the experiment, participants were given an
explanation regarding the deceptive aspects of the study and the expected results
to be gained from the research. In the second session, the experimenter re-
introduced the study to the participants. All participants were asked to complete
a series of questionnaires concerning anxiety, depression, and other psychosocial
concepts.
RESULTS
Preliminary Results
Because HPA axis over-activity and more frequent and longer cortisol elevations
have been associated with mental disorders, like depression (Burke, Davis, Otte,
& Mohr, 2005), descriptive statistics were conducted to determine the percentage
of college students with asthma and the healthy controls that met clinically sig-
nificant criteria for depression or scored in the severe to extremely severe range
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24 EDDINGTON ET AL.
for anxiety. Results revealed that 23.2% of participants with asthma and 30% of
the healthy controls scored in the clinically significant range for depression (> 16
for the CES–D; Radloff, 1977). In addition, 26.7% of participants with asthma
and 46.8% of healthy controls scored in the moderate range of depression (7–10
for the CES–D). For anxiety, 3.3% of college students with asthma and 3.3% of
healthy controls scored in the severe to extreme range (between 60 and 80 on the
SAS; Zung, 1971). Further, 93.3% of college students with asthma and 93.3%
of healthy controls reported anxiety levels in the normal range (between 20 and
44 on the SAS; Zung, 1971). In addition, an independent t test revealed that
college students with asthma did not differ from healthy controls on self-ratings
of anxiety, t.58/ D 0:88, p D :383 (d D 0:15); and depression, t.58/ D �0:03,
p D :977 (d D 0:01). In sum, college students with asthma and their healthy
controls did not self-report significant differences in levels of either depression
or anxiety.
Primary Results
To address the primary hypothesis in this study, a 2 (Illness Status) � 3 (Saliva
Measurement Times) � 2 (Experimental Condition) mixed analysis of variance
design was used to assess the level of cortisol after the experimental ma-
nipulation. Analysis revealed a significant main effect of measurement times,
F.1:54; 84:92/ D 7:53, p D :002 .d D 0:12/. Bonferroni-corrected post hoc
tests showed that measurement time T2 .M D 0:32/ was significantly higher
than measurement time T3 .M D 0:28/; T1 measurements were not significantly
different from T2 .p > :05/ or T3 .p > :05/ measurements. There was no
main effect for illness status, F.1; 55/ D 3:32, p D :74 .d D 0:06/; or
experimental condition, F.1; 55/ D 0:58, p D :45 .d D 0:01/, thus indicating
that neither illness status nor experimental condition alone had an effect on
cortisol levels. There was an interaction between measurement times and illness,
F.1:54; 84:92/ D 3:42, p D :049 .d D 0:06/, indicating that the differences
between measurement times differed by illness group. To break down this
interaction, simple contrasts were conducted to compare the three measurement
times across illness statuses. The contrasts revealed that at T1, cortisol levels
for asthma participants (M D 0:29; SD D 0:18) were significantly higher than
age-gendered healthy controls (M D 0:20, SD D 0:10), F.1; 58/ D 5:94,
p D :018. Among asthma participants and same age-gendered healthy controls,
cortisol levels were not significantly different at T2, F.1; 58/ D 3:16, p D :081;
or at T3, F.1; 58/ D 0:82, p D :370. There was no interaction between
experimental condition and illness, F.1; 55/ D 0:73, p D :40 .d D 0:01/;
between measurement time and experimental condition, F.1:54; 84:92/ D 0:90,
p D :39 .d D 0:02/; or between measurement time, experimental condition,
and illness, F.1:54; 84:92/ D 1:43, p D :24 .d D 0:03/.
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STRESS REACTIVITY 25
FIGURE 1 Cortisol levels of participants with asthma and same age-gendered controls as
a function of the learned helplessness task (color figure available online).
Thus, to summarize, the only significant effects on cortisol levels were mea-
surement times and the interaction of measurement times and illness condi-
tions. The stressor from the learned helplessness task did not account for the
significant elevations in cortisol levels in college students with asthma com-
pared to healthy controls. Overall, T2 cortisol levels were significantly higher
than T3 cortisol levels for both college students with asthma and healthy con-
trols. In addition, the interaction indicated that participants with asthma had
overall higher T1 cortisol levels than same age-gendered healthy controls (see
Figure 1).
DISCUSSION
The primary aim of this study was to determine if college students with asthma
would evidence higher cortisol levels (and, hence, greater stress reactivity)
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26 EDDINGTON ET AL.
following a helplessness induction task when compared to same age-gendered
healthy controls. With regard to the primary aim, results supported the hypothesis
as it pertains to demonstrating higher cortisol levels in college students with
asthma at T1 in both the contingent and non-contingent condition. However,
although post hoc testing revealed that T2 cortisol was significantly higher than
T3 for both participants with asthma and healthy controls, simple contrasts
suggested that the increase was not due to the experimental manipulation of
the learned helplessness task. In addition, it would appear that T1 levels of
cortisol were initially elevated for college students with asthma and seemed
to decline (see Figure 1); therefore, the results cannot be interpreted that this
elevation in cortisol levels at T2 was a response to the stress task in either
college students with asthma or to healthy controls. Cortisol levels in the non-
contingent condition did decline from T2 to T3 in college students with asthma,
but showed little variability in the healthy controls, as evidenced by remaining
fairly consistent with T1 levels (see Figure 1).
Notably, in the contingent or controllable condition, cortisol levels showed
little variability across the three time points and, hence, did support the hypoth-
esis of cortisol levels remaining fairly consistent from T1 to T2 and T3 in both
the asthma and healthy control groups. More important, it should be noted that
the non-contingent or non-controllable condition of the learned helplessness
task did not elicit increased cortisol secretion in either college students with
childhood-onset asthma or their matched controls, as predicted by previous
research (Chaney et al., 1999). Several factors could have contributed to this
lack of a manipulation effect. A primary explanation for this finding might
be the dated design of the computerized learned helplessness task, which may
not have been perceived by the participants as valid and, hence, non-stressful.
The experimental task used in this study was developed from older studies
from the 1970s (e.g., Benson & Kennelly, 1976; Hiroto & Seligman, 1975;
Levine, 1971) and implemented with 1980 computer software. Participants in
this sample were born between 1985 and 1991, and the older task may have
looked dated to them, contributing to the lack of effective manipulation in both
populations. Second, despite extensive training and modeling, poorly executed
feedback from the computer-generated data and corresponding verbal responses
of the research assistants after the experimental task may be another factor
that could have contributed to the unexpected cortisol pattern. Indeed, a key
factor for the contingent/non-contingent feedback relied on verbal reiteration
from research assistants after the computer task. To the extent that the feedback
was not convincingly delivered, the T2 cortisol level would not be influenced.
Although research has found support for normal diurnal patterns of cortisol
in adults with asthma (Masharani et al., 2005), there has been limited research
comparing cortisol levels among individuals with a chronic illness and their
healthy controls. Also, although this study did show a significant decrease
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STRESS REACTIVITY 27
in cortisol levels 15 min after the stress task (T3), for college students with
childhood-onset asthma in the non-contingent condition, as mentioned earlier,
the decrease did not appear to be an effect of the non-contingent aspect of
the learned helplessness task. The cortisol levels were significantly elevated at
the start of the experiment, and tapered off toward T3 in college students with
childhood-onset asthma. The observed decrease in cortisol in participants with
asthma in this study is consistent with adaptive reorganization to a stressor (i.e.,
adapting to an unfamiliar event or context, such as being part of an experiment),
which was later reappraised and perceived as non-threatening (i.e., Abramson,
Seligman, & Teasdale, 1978) and, hence, reflects habituation to the environment.
Although speculative, the initial elevation noticed in the participants with asthma
in the contingent and non-contingent conditions could also be the result of
a pre-experimental “anticipation” response. Supporting this proposition, this
anticipation response was not seen in the healthy control population in either the
contingent or non-contingent conditions (see Figure 1). Similarly, these results
are also consistent with the reactivity and then, later, recovery phases of the HPA
axis (McEwen, 1998), and suggests that individuals with asthma may be more
reactive to novel situations. With more research, positive biological reactivity
may be highlighted as a prevented tactic or skill to foster in college students
with asthma.
This study has a number of limitations. First, asthma diagnosis and severity
were subjective, based on self-report, and was not verified by a medical profes-
sional. Furthermore, knowledge about prescribed glucocorticoid from inhaled,
nasal, or oral usage was not analyzed. In addition, most of the individuals with
asthma reported mild severity (see Table 1); thus, these results may not generalize
when compared to populations with more severe asthma. Also, all participants
were college students, and the majority were Caucasian, thereby limiting gen-
eralizability, particularly given that statistics show that Puerto Ricans have the
TABLE 1
Description of Self-Report Asthma Severity Ratings
Description Frequency %
Very mild 14 46.7
Mild 7 23.3
Very moderate 3 5.0
Moderate 3 5.0
Severe 3 5.0
Extremely severe 0 0.0
Respiratory failure 0 0.0
Note. N D 30 college students with asthma.
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28 EDDINGTON ET AL.
highest current asthma prevalence rates, followed by non-Hispanic Blacks and
non-Hispanic American Indians (National Center for Health Statistics, 2006).
The small sample size limits the ability to find significant effects. Finally, salivary
cortisol measurements were not assayed in duplicate for average variability for
each assay. More accurate ratings could have been achieved with duplicate
assays.
Despite these limitations, several strengths should be acknowledged. First,
this study is an initial step in highlighting cortisol differences in individuals
with chronic illnesses. To our knowledge, this study is the first to find signif-
icant differences in cortisol levels of college students with asthma and their
healthy controls. The results provide evidence that stress levels may be initially
elevated in individuals with asthma due to anticipation of novel situations or
environments.
Because the method of stress induction used in this study (i.e., the learned
helplessness task) did not appear to elicit stress, a more effective methodology
should be used in the future. The Trier Social Stress Test (Kirschbaum, Pirke, &
Hellhammer, 1993) has been utilized and validated in cortisol research, and
would mostly likely elicit stress in this population. Further examination of
cortisol levels in individuals with a chronic illness across different illnesses,
genders, and varying ethnicities would be helpful in future research, especially
because several disparities have been documented in mortality, morbidity, and
prevalence rates among individuals with asthma (Centers for Disease Control,
1998). In addition, verification of asthma diagnosis, severity of asthma symp-
toms, and physician visits should be confirmed with additional independent
physician ratings. Including evaluation of salivary ˛-amylase (SAM) would be
quite beneficial to future research (Baum, 1993).
Implications for Practice
Evidence for the peak, then decline, of cortisol levels in individuals with asthma
could have a number of implications for future research and practice. These
data indeed suggest that college students with asthma are more reactive to stress.
More knowledge about the pattern of cortisol levels and its impact on individuals
with asthma would be beneficial for understanding the health and lifestyle of
individuals with asthma or with other chronic illnesses. This information would
be helpful in treatment planning and recommendations for young adults with
asthma. Furthermore, Chaney et al. (1999) documented a pre–post increase in
internal attributions among college students with asthma in the uncontrollable
condition, whereas this study demonstrated a pre–post decline in cortisol levels.
Hommel, Chaney, Wagner, & Jarvis (2006) found more external attributions
after an uncontrollable event in adolescents with juvenile rheumatic disease.
Evaluation of an inverse relation between cortisol levels and internal or external
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attributions may explain physiological components to stress habituation. Indeed,
it would be intriguing to see if attributing stress to internal versus external
sources is linked to a decrease in cortisol levels in individuals with asthma.
Overall, future efforts examining the differences in stress reactivity among
individuals with asthma and healthy controls seems warranted.
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