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Anxiety, Stress, & Coping, 2013

Vol. 26, No. 3, 241253, http://dx.doi.org/10.1080/10615806.2012.672976

Predicting emotional responses to potentially traumatic events from


pre-exposure waking cortisol levels: a longitudinal study of police and
firefighters
Suzanne L. Pinelesa,b, Ann M. Rasmussona,b, Rachel Yehudac,d, Natasha B. Laskoe,f,
Michael L. Macklinf, Roger K. Pitmane and Scott P. Orre,f*
a
Women’s Health Sciences Division, National Center for PTSD, VA Boston Healthcare System,
Boston, MA, USA; bDepartment of Psychiatry, Boston University School of Medicine, Boston,
MA, USA; cDepartment of Psychiatry and Neurobiology, Mount Sinai School of Medicine,
Bronx, NY, USA; dDepartment of Psychiatry, James J. Peters Bronx VA, Bronx, NY, USA;
e
Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School,
Boston, MA, USA; fResearch Service, Veterans Affairs Medical Center, Manchester, NH, USA
(Received 30 September 2011; final version received 2 March 2012)

There is a large literature demonstrating that individuals who have experienced


traumatic events have alterations in the hypothalamic-pituitary-adrenal (HPA)
axis. However, the existing literature does not address the extent to which these
alterations represent pre-existing risk factors for developing psychopathology
upon exposure to a significant stressor. In the current study, we examined the
relationship between waking salivary cortisol level and physiological, personality,
and psychological measures in 60 firefighters and police trainees during training,
and then again after exposure to a highly stressful, potentially traumatic event
(PTE). Waking cortisol was negatively associated with neuroticism, but positively
associated with physiological reactivity to loud tones and fear conditioning
when assessed during training. Longitudinally, there were significant negative
correlations between pre-PTE waking cortisol and post-PTE negative mood and
anxiety symptoms, but a positive correlation (trend) between pre-PTE waking
cortisol and post-PTE physiological reactivity during recollection of the PTE.
Thus, waking cortisol level may serve to predict divergent types of emotional
sequelae following PTEs.
Keywords: cortisol; psychophysiology; trauma; negative affect; neuroticism; stress

Introduction
Cross-sectional research has identified several psychophysiological, neuroendocrine,
and psychological outcomes that are associated with individual responses to stressful
events (Charney, 2004; Pole, 2007; Resick, 2001; Yehuda & LeDoux, 2007). However,
it is unclear which, if any, of these correlates represent risk factors for experiencing
greater distress following stressful or potentially traumatic events (PTEs). Research
that uses a longitudinal design and includes assessment prior to exposure to a
stressful event can help inform this issue.
Rates of posttraumatic stress disorder (PTSD) highlight individual differences in
reactions to traumatic events. Although as many as 90% of individuals in the general

*Corresponding author. Email: scott_orr@hms.harvard.edu


# 2013 Taylor & Francis
242 S.L. Pineles et al.

population experience at least one traumatic event in their lifetimes (Breslau et al.,
1998), prevalence estimates of 12-month and lifetime PTSD are only 3.5% (Kessler,
Chui, Demler, & Walters, 2005) and 6.8% respectively (Kessler, Berglund, et al.,
2005). The disparity between the large percentage of people who experience
traumatic events and the relatively small percentage of individuals who ultimately
meet diagnostic criteria for a disorder such as PTSD, suggests that there may be
traits that place some individuals at increased risk for developing posttraumatic
psychopathology or that protect other individuals against it.
When individuals are exposed to a stressful event, the hypothalamic-pituitary-
adrenal (HPA) axis is typically activated and contributes to a constellation of
physiological, emotional, and behavioral responses (Munck, Guyre, & Holbrook,
1984; Sapolsky, Romero, & Munck, 2000). As part of the HPA axis response, cortisol
is released into the bloodstream, making it a potentially useful index of HPA axis
functioning. Higher cortisol levels have been shown to be associated with stronger
fear conditioning, especially in men (Grillon et al., 2006; Jackson, Payne, Nadel, &
Jacobs, 2006; Zorawski, Blanding, Kuhn, & LaBar, 2006; Zorawski, Cook, Kuhn, &
Labar, 2005), whereas low cortisol levels have been associated with emotional
numbing and disengagement (Mason et al., 2001).
Individuals who have experienced extremely stressful or traumatic events, in
particular those with PTSD, have been found to have alterations in HPA axis
regulation with some individuals with PTSD showing lower, higher, or similar basal
cortisol levels as compared to control groups (Handwerger, 2009; Mason, Giller,
Kosten, Ostroff, & Podd, 1986; Meewisse, Reitsma, De Vries, Gersons, & Olff, 2007;
Rasmusson, Vythilingam, & Morgan, 2003; Yehuda, 2006; Yehuda, Teicher,
Trestman, Levengood, & Siever, 1996). This mixed pattern of results has been found
across studies using a variety of cortisol measures including those using a single
measure of salivary cortisol at awakening (Anisman, Griffiths, Matheson, Ravin-
dran, & Merali, 2001; de Kloet et al., 2007; Kellner, Baker, & Yehuda, 1997;
Lindauer, Olff, van Meijel, Carlier, & Gersons, 2006; Yehuda, Golier, & Kaufman,
2005). However, it is unclear whether any of these alterations in cortisol reflect risk
factors for developing psychopathology or result from exposure to a significant
stressor. Thus far, two studies have assessed pre-PTE cortisol awakening response
(CAR) (i.e., the rapid rise in cortisol levels occurring approximately 2030 minutes
after awakening) as a predictor of PTSD symptoms following PTE exposure and
both reported null results (Heinrichs et al., 2005; van Zuiden et al., 2011). More
research on this topic is clearly needed and prospective waking cortisol levels provide
an index that lends itself to examination for associations between HPA axis activity
and various measures of emotional reactivity prior to, and following, exposure to a
highly stressful event.
The current study prospectively examined associations of pre-exposure waking
salivary cortisol levels with (1) concurrently ascertained physiological, personality,
and psychological measures of emotional distress and (2) physiological and
psychological measures of emotional distress following exposure to a highly stressful,
potentially traumatic event. In this study, medically healthy, medication-free
firefighter and police trainees without psychiatric disorders completed a battery of
physiological and psychometric measures and provided waking salivary cortisol
samples during their professional training. Because the parent study was designed to
test a variety of potential predictors that would be easily administered, waking
Anxiety, Stress, & Coping 243

cortisol consisted of a single saliva sample. Subsequent to this training and


assignment to jobs in the field, the trainees were carefully followed for the occurrence
of a PTE. Those who experienced such an event were asked to participate in a second
set of assessments. We expected that baseline cortisol would show significant
relationships with initial and post-PTE measures of emotional distress and
psychophysiological reactivity. However, given the mixed findings regarding whether
traumatic stress is associated with elevated or reduced cortisol levels, we did not have
directional hypotheses regarding the nature of these relationships.

Method
Participants
Written informed consent was obtained from all participants in accordance with the
requirements of the Partners Healthcare System Human Research Committee. Study
participants included 60 police (n 38; 63%) and firefighter (n  22; 37%) trainees
from New England (8% female,1 80% Caucasian) who participated in a larger
prospective study examining risk factors for developing PTSD (Orr et al., Under
Review). Participants were included in the current study if they provided salivary
samples (27% of the larger sample). Mean age and educational level were 28.6
(SD  5.2) and 14.7 (SD 1.9) years, respectively. The sample was psychologically
healthy; with the exception of one participant who met criteria for a current eating
disorder, no participants met criteria for any other Axis I diagnosis at the pre-PTE
assessment (see in the following section). Mean scores on the Beck Depression
Inventory-II (BDI-II; Beck, Rush, Shaw, & Emery, 1979) were 2.7 (SD 2.7) at the
pre-PTE assessment and 2.9 (SD  3.2) post-PTE. Mean score on the one-month
Clinician-Administered PTSD Scale (CAPS; Blake et al., 1995) was 4.5 (SD 9.5)
post-PTE. No participants reported using psychiatric medications or tobacco
products. None of the women used hormonal birth control.

Measures and procedures


Pre-PTE diagnostic assessment and psychometrics
Current and lifetime Axis I diagnoses were assessed with the Structured Clinical
Interview for DSM-IV (SCID; First, Spitzer, Williams, & Gibbon, 1995) and CAPS.
Several other instruments were administered including the: (1) Revised NEO
Personality Inventory (NEO-PI-R; Costa & McCrae, 1992), which measures the
‘‘Big 5’’ personality dimensions of neuroticism, introversion, conscientiousness,
agreeableness, and openness to experience; (2) Symptom Check List 90-Revised
(SCL-90-R; Derogatis, 1983), which measures a wide range of psychiatric symptoms;
(3) State-Trait Anxiety Inventory (STAI; Spielberger, Gorsuch, & Lushene, 1970);
and (4) BDI-II (Beck et al., 1979).

Pre-PTE psychophysiologic assessment


Two psychophysiological tasks were administered during the pre-PTE assessment in
the morning.
244 S.L. Pineles et al.

Loud-tones procedure
During the loud-tones procedure, left orbicularis oculi EMG (O-EMG), skin
conductance (SC), and heart rate (HR) responses were recorded during and
following binaural presentations of 15, 95-dB, 1000-Hz pure tones with 0-ms rise
and fall times lasting 500-ms over headphones, with intertrial intervals (ITIs) ranging
from 27 to 52s. Before engaging in the loud-tone task, participants were given
standardized instructions and there was a 5-min resting period. This procedure has
been used in previous studies of PTSD (Orr, Lasko, Shalev, & Pitman, 1995).
Left O-EMG, SC, and HR were recorded using a Coulbourn Lablinc V modular
instrument system (Coulbourn Instruments LLC, Whitehall, PA, USA). EMG
signals were amplified, filtered to include the 901000 Hz range, and integrated using
a 10-ms time constant. For EMG, the skin was abraded and 4-mm (sensor diameter)
Invivo Metric Ag/AgCl electrodes filled with electrolyte paste were placed over the
left O-EMG muscle site according to published specifications (Fridlund & Cacioppo,
1986). SC was measured directly using a constant .5 V through 9-mm (sensor
diameter) Invivo Metric Ag/AgCl electrodes placed on the hypothenar surface of the
participant’s non-dominant hand in accordance with published guidelines (Fowles et
al., 1981). HR was converted from interbeat interval (IBI) recorded from standard
limb electrocardiogram leads. For HR recording, the skin was abraded and 9-mm
(sensor diameter) Invivo Metric Ag/AgCl electrodes filled with electrolyte paste.
All psychophysiologic analog signals were digitized at 1000 Hz.
Psychophysiologic responses to the loud tones were quantified using previously
described methods (Orr et al., 1995). The eyeblink (O-EMG) response was calculated
for each trial by subtracting the average O-EMG level during the 1-sec interval
immediately preceding tone onset from the highest O-EMG value within 40200
msec following tone onset. SC response (SCR) was calculated for each tone trial by
subtracting the average SC level during the 1 sec immediately preceding tone onset
from the highest SC value within 14 sec following tone onset. Accelerative
HR response was calculated for each tone trial by subtracting the average HR,
as determined from the two heart beats immediately preceding tone onset, from the
highest HR value (i.e., shortest IBI) within 14 sec following tone onset. Square-root
transformations were performed for all responses. Response scores comprised HR,
SC, and O-EMG responses averaged across the 15 tones. Habituation of responses
was measured in two ways. Absolute habituation of SC and O-EMG responses was
assessed by counting the number of trials before reaching a criterion of two
successive non-response trials (SC 5.05 mS; EMG 5.30 mV). Relative habituation
was calculated for SCR from the slope of the regression equation Y  bx  a for
Trials 215, whereby Y is the square root of the SCR score, and x is the log trial
number.

Conditioning procedure
The procedure for this task was identical to those used in previous published
research (Orr et al., 2000). In this discrimination fear-conditioning task, the CS
(i.e., stimulus paired with an unconditioned aversive stimulus) and CS (i.e., stimulus
not paired with the unconditioned aversive stimulus) were represented by 6-inch
diameter blue and white circles, respectively, displayed on a computer screen.
Anxiety, Stress, & Coping 245

The unconditioned stimulus (US) was a 500-msec electric shock previously set by
each participant to be ‘‘highly annoying but not painful.’’ The US was delivered
through electrodes attached to the second and fourth fingers of the dominant hand.
It was generated by a Coulbourn Transcutaneous Aversive Finger Stimulator using
a 9-V dry cell battery that produced electric stimuli ranging from .2 to 4.0
milliamperes.
This task consisted of a 5-minute baseline recording period, followed by three
phases of the conditioning task: habituation, acquisition, and extinction. Partici-
pants were instructed that they could only receive shocks during the acquisition
phase. Habituation consisted of five presentations each of the to-be CS and CS in
pseudo-random order. The CS duration was 8 sec, with ITIs of 2095 sec.
Acquisition consisted of five similar presentations of each stimulus type in pseudo-
random order; the US occurred immediately following each CS offset. Extinction
consisted of 10 similar, non-reinforced presentations each of the CS and CS in
pseudo-random order.
Skin conductance (SC) was recorded throughout the conditioning procedure
using the same parameters as the loud-tones task. In each phase, SC was sampled
and stored at 10 Hz, beginning 4 sec prior to CS onset and ending 6 sec following CS
offset. A SCR score for each trial was calculated by subtracting average SC level
during the 2-sec interval immediately preceding CS onset from the highest SC value
during the 8-sec CS interval (Carson et al., 2000; Pineles, Orr, & Orr, 2009).
Differential SCR scores were calculated by subtracting the average SCR to CS trials
from the average SCR to CS trials. This was done separately for the habituation,
acquisition, and extinction phase. An unconditioned response (UR) score was
calculated by subtracting average SC level during the 2 sec immediately preceding US
onset from the highest SC value during the 06 sec following US offset. An orienting
score was calculated by averaging the SCR to the first CS and first CS trials
during the habituation phase.

Pre-PTE assessment of salivary cortisol


Participants were provided with salivary specimen tubes along with prepaid mailers
and written instructions. Participants were instructed to provide a saliva sample
immediately after wakening and to not exercise, engage in sexual activity, eat or drink
(except water) prior to collection. Women were also instructed to start collection on
menstrual cycle day 10. Salivary cortisol was quantified by radioimmunoassay (RIA)
according to a previously published method (Yehuda, Boisoneau, Lowy, & Giller,
1995). The detection limit was .1 mg/l, and the intra- and inter-assay variability were
7.7% and 11.9%, respectively. For the current study, the cortisol level obtained at
waking was the measure of interest. The group mean waking cortisol level was
.572 mg/l (SD .333).

Monitoring participant for the occurrence of a PTE


Participants were contacted by mail on a bi-monthly basis to inquire as to the
occurrence, during the previous two months, of a PTE that met the DSM-IV PTSD
Category A1 criterion (Weathers & Pitman, 1996). Specifically, a PTE was deemed to
have occurred when an individual indicated that he/she had experienced, witnessed,
246 S.L. Pineles et al.

or was confronted with an event(s) involving threat of death, serious injury, or


physical integrity (American Psychiatric Association, 2000).

Post-PTE diagnostic assessment and psychometrics


Thirty-seven participants (6% female) who experienced a PTE completed the post-
PTE assessment. The mean time between pre-PTE assessment and the reported PTE
was 18.97 months (SD 14.09), and the mean time between the PTE and the post-
PTE assessment was 14.93 months (SD  14.25). During the post-PTE assessment,
the CAPS, SCID, SCL-90-R, BDI-II, and STAI were re-administered. Participants
also completed the Peritraumatic Emotional Distress Scale (PEDS; Brunet, Weiss,
Best, & Marmar, 1998), Impact of Event Scale-Revised (IES-R; Weiss & Marmar,
1997), and Mississippi Scale for Civilian PTSD (C-Mississippi Scale; Keane, Caddell,
& Taylor, 1988). Psychophysiologic reactivity during script-driven imagery was
performed according to standard procedures (Orr, Pitman, Lasko, & Herz, 1993).
Personalized ‘‘scripts’’ approximately 30 seconds in length were created for each
individual’s PTE. Scripts were recorded and played back to participants who were
asked to vividly imagine each event, while HR, SC, and facial EMG (left lateral
frontalis, LF-EMG) responses were measured. A composite measure of psychophy-
siologic reactivity during PTE-related script-driven imagery was determined by
applying an a priori discriminant function, derived from psychophysiologic (HR, SC,
and LF-EMG) responses of previously studied individuals with and without PTSD
to the participants’ responses, yielding a ‘‘posterior probability’’ for the presence of
PTSD (Carson et al., 2000; Orr et al., 1993, 1998; Pitman & Orr, 1990).

Results
Associations between pre-PTE waking cortisol and pre-PTE psychometric and
physiologic measures
Pearson product-moment correlation coefficients were used to assess the relationship
between waking cortisol and concurrent measures of personality, psychological
symptoms, physiological reactivity to loud tones, and conditioning (Table 1). Waking
cortisol level was negatively associated with neuroticism but positively associated with
several measures of psychophysiological reactivity and conditioning, including HR
response during the loud-tone task, delayed absolute SC habituation (i.e., greater
number of trials to SC habituation during the loud-tone task), magnitude of the SC
orienting response during the conditioning task, and differential SCR to the
CS and CS during acquisition.

Associations between pre-PTE waking cortisol and post-PTE psychometric and


physiologic measures
Longitudinal associations between pre-PTE waking cortisol and post-PTE psycho-
logical symptoms and psychophysiological reactivity to PTE-related scripts were
assessed using Pearson correlations (Table 2). There were several significant negative
correlations between pre-PTE waking cortisol and post-PTE measures of mood and
anxiety symptoms. In contrast, there was a positive trend for the correlation between
Anxiety, Stress, & Coping 247

Table 1. Pearson product-moment correlations between pre-PTE waking cortisol and pre-
PTE psychometric and physiologic measures.

Waking cortisol n

BDI-II .07 57
STAI-S .04 58
STAI-T .05 58
Neuroticism .38* 40
Extraversion .15 40
Openness .14 40
Agreeableness .00 40
Conscientiousness .01 40
Loud-tone task
HRR mean .27* 54
SCR mean .11 54
O-EMGR mean .06 53
SCR slope .04 54
SC Trials to Habit. Crit. .31* 54
O-EMG Trials to Habit.Crit. .11 53
Aversive conditioning task
SC orienting .27* 54
SCDIFF_H .10 54
SCDIFF_A .26* 54
SCDIFF_E .13 53
SC_UR .02 54
Note: Neuroticism, extraversion, openness, agreeableness, and conscientiousness all are NEO PI-R
domain scores.
PTE, potentially traumatic event; BDI-II, Beck Depression Inventory; STAI-S, State/Trait Anxiety
Inventory-State score; STAI-T, State/Trait Anxiety Inventory-Trait score.
Loud-tone assessment measures: HRR Mean, mean HR acceleratory response; SCR Mean, mean SC
response; O-EMGR Mean, mean orbicularis oculi EMG response; SCR Slope, SC response slope; SC
Trials to Habit. Crit., SC trials to criterion to habituation; O-EMG Trials to Habit. Crit., orbicularis oculi
EMG trials to criterion to habituation.
Aversive conditioning measures: SC Orienting, SC orienting response, mean response to first presentation
of the CS  and the CS during the habituation phase; SCDIFF_H, differential response during
habituation, SCDIFF_A, differential response during acquisition; SCDIFF_E, differential response
during extinction; SC_UR, mean unconditioned response for CS  trials during the acquisition phase.
*p B.05; **pB.01.

pre-PTE waking cortisol and post-PTE physiological reactivity during recollection of


the PTE. Because of the substantial variability in the time lag between the traumatic
event and the post-trauma assessment, a series of partial correlation coefficients were
calculated between pre-trauma waking cortisol and post-trauma psychometric and
physiologic measures, controlling for the duration between the trauma and post-
trauma assessment. These partial correlation coefficients were of similar magnitude
to those presented in Table 2 (results available upon request).

Discussion
Our findings suggest that waking cortisol level has divergent relationships with
psychometric measures of mood and anxiety symptoms versus physiological
248 S.L. Pineles et al.

Table 2. Pearson product-moment correlations between pre-PTE baseline waking cortisol and
post-PTE psychometric measures and composite psychophysiological response measure
during script-driven imagery.

Waking cortisol n

CAPS .07 36
BDI-II .39* 27
STAI-S .40* 32
STAI-T .25 33
PEDS .35* 33
C-Mississippi Scale .37* 33
IES-R .04 35
Psychophysiological Posterior Probability .28$ 36
Note: Psychophysiological Posterior Probability was derived from script-driven imagery assessment data.
PTE, potentially traumatic event; CAPS, Clinician Administered PTSD Scale total score for Current
PTSD symptoms; BDI-II, Beck Depression Inventory; STAI-S, State/Trait Anxiety Inventory-State score;
STAI-T, State/Trait Anxiety Inventory-Trait score; PEDS, Peritraumatic Dissociation Scale; IES-R,
Impact of Event Scale-Revised total score; C-Mississippi, Mississippi Scale for Civilian PTSD.
*p B.05; $p B.10.

reactivity to loud tones, aversive conditioning, and PTE-related imagery (trend).


Lower pre-PTE waking cortisol was associated with higher pre-PTE neuroticism  a
well-established risk factor for psychopathology (Mineka, Watson, & Clark, 1998).
Lower pre-PTE waking cortisol also was associated with higher post-PTE
peritraumatic distress, anxiety, depression (trend), and symptoms measured by the
C-Mississippi Scale. Although the Mississippi Scale was originally developed as a
measure of PTSD symptoms, several researchers now suggest that this scale is more
accurately conceptualized as a measure of general psychopathology (Lauterbach,
Vrana, King, & King, 1997; Vreven, Gudanowski, King, & King, 1995). The above
relationships between psychometric measures and cortisol level provide some
support for a predictive relationship between lower pre-PTE waking cortisol and
increased negative mood and anxiety following exposure to a potentially traumatic
event. Thus, the relationship between pre-PTE cortisol level and neuroticism suggests
that lower waking cortisol level is associated with a general dispositional factor such
as negative affectivity (Clark, Watson, & Mineka, 1994) that is predictive of
increased negative mood and anxiety following exposure to a PTE. Because there
was not a large range in PTSD or depression symptoms, it would be important to
re-examine the associations tested here in a larger sample of subjects with a broader
range of emotional distress/pathology, including PTSD. However, as noted above,
two other studies did not find pre-PTE cortisol to significantly predict PTSD
symptoms after a PTE (Heinrichs et al., 2005; van Zuiden et al., 2011).
In this healthy sample, pre-PTE waking cortisol level was positively associated
with pre-PTE measures of psychophysiological reactivity and conditioning, including
acquisition of conditioned fear responses and orienting response, as well as slower
skin conductance habituation and larger mean HR responses to loud tones. Finally,
there was a trend for a positive association between pre-PTE waking cortisol and
increased psychophysiological reactivity while recalling the PTEs during the script-
driven imagery task. Thus, the pattern of findings supports an association between
higher waking cortisol level and greater emotional responsiveness, as indexed by
Anxiety, Stress, & Coping 249

psychophysiologic reactivity. These findings align with research in animals demon-


strating that cortisol has been found to sensitize the amygdala, leading to increased
anxiety-like behavior (Shepard, Barron, & Myers, 2000, 2003). The present findings
for waking cortisol raise the possibility that an individual’s pre-PTE cortisol level
represents a disposition towards the type of psychological symptoms that may
manifest following exposure to a PTE. Specifically, individuals with higher pre-PTE
cortisol may be disposed to developing PTSD that is characterized by heightened
psychophysiologic reactivity, whereas individuals with lower pre-PTE cortisol level
(and increased ‘‘negative affectivity’’) may be disposed to emotional numbing,
possibly accompanied by comorbid mood disorder.
These opposite associations are interesting to consider in the context of HPA axis
alterations in PTSD. Individuals with PTSD can show a variety of PTSD symptom
constellations, which could include variations in the relative dominance of
psychological distress versus physiological reactivity symptoms. Furthermore, a
given individual may present with variations in the relative amounts of blunting
versus reactivity symptoms at different points in time. We believe that it is important
to focus more selectively on particular symptoms or symptom constellations, such as
undertaken by the current study, to begin to disentangle these seemingly elusive
relationships (Sanislow et al., 2010). Addressing these issues in a more definitive way
will require prospective studies that have a higher prevalence of the PTSD outcome.
It is important to acknowledge several significant limitations of the present work.
First, the cohorts of firefighters and police were psychologically healthy. Conse-
quently, the correlations may actually underestimate the relationships amongst
variables due to truncated ranges of symptoms. Furthermore, because the sample
providing saliva for cortisol measures was self-selected, it may neither represent
the larger population of firefighters and police nor the general population. The
variability in time between the experience of a PTE and the post-PTE assessment
may have contributed to the low symptom levels we observed. However, the impact
of this potential limitation is mitigated by the fact that when we adjusted for the
amount of time that lapsed between the PTEs and post-PTE assessment the
magnitude of the correlation coefficients remained essentially unchanged. Another
potential limitation is the use of a single sample to measure waking cortisol level.
Because the parent study was designed to test a variety of potential predictors that
would be easily administered in the field, waking cortisol consisted of a single saliva
sample rather than several collections within the first hour of waking, which
precluded assessment of the CAR. Morning awakening curve is the current standard
for measuring waking cortisol and a single sample of cortisol may be a less
reliable measure. However, this limitation is tempered by the consideration that
correlations ought to become stronger when a more reliable measure of CAR is used,
that is, one based on multiple samples. Furthermore, there is precedent for use of a
single cortisol sample in studies of post-trauma sequelae. Findings of studies using a
single cortisol sample parallel findings in the broader cortisol and PTSD literature
(Anisman et al., 2001; de Kloet et al., 2007; Kellner et al., 1997; Lindauer et al., 2006;
Yehuda et al., 2005). Thus, although the single cortisol measure used in the study
cannot be said to directly represent the CAR, we believe the results to be interesting
and useful in their own right. Finally, in order to provide a comprehensive
assessment, a number of outcome measures were included and may have increased
the chance of Type I error. For these reasons, the present results should be regarded
250 S.L. Pineles et al.

as suggestive rather than definitive, in accord with the hypothesis-generating aims of


the study. Future research is needed to test the newly generated hypothesis that
pre-PTE cortisol level has opposite predictive value for subjective measures of
psychological distress and psychophysiologic measures of reactivity.

Acknowledgements
This research was supported by U.S. Public Health Service grant R01-MH60315 and
Department of Veterans Affairs Merit Review grant to Scott P. Orr. Additional support
was provided to Suzanne Pineles through a VA Career Development Award, Department of
Veterans Affairs. Portions of these results were presented at the Society for Psychophysiolo-
gical Research 50th Annual Meeting (October, 2010) in Portland, OR. We thank Margaret
Bauer; Heike Croteau; Sgt. Thomas Fleming, Director, Lowell Police Academy, Lowell, MA;
Dr. John Connell and Gary Courtney, Fire Technologies Program, Lakes Region Community
College, Laconia, NH; and Captain/Drillmaster Hugh Duffy, Boston Fire Academy, Boston
Fire Department, Boston, MA for their invaluable assistance with this project. We would also
like to express our appreciation to the police and firefighters for their willingness to
participate.

Note
1. Analyses including only men reflected a similar pattern of results.

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