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 RESEARCH ARTICLE

Physiological reactivity in children of Oklahoma City bombing survivors 7 years postdisaster: A pilot study

Betty Pfefferbaum, MD, JD

Department of Psychiatry, and Behavioral Sciences, University of Oklahoma College of Medicine, Oklahoma City, OK, USA

Phebe Tucker, MD

Department of Psychiatry, and Behavioral Sciences, University of Oklahoma College of Medicine, Oklahoma City, OK, USA

Carol S. North, MD, MPE

North Texas VA Health Care System, Departments of Psychiatry and Surgery/Division of Emergency Medicine, University of Texas Southwestern, Medical Center, Dallas, TX, USA

Haekyung Jeon-Slaughter, PhD

Department of Psychiatry, and Behavioral Sciences, University of Oklahoma College of Medicine, Oklahoma City, OK, USA

BACKGROUND: Relatively few studies of children exposed to trauma have used objective indicators such as heart rate and blood pressure measurements to assess physiological reactivity.

METHODS: This pilot study examined physiological reactivity (heart rate, systolic blood pressure, and diastolic blood pressure) and emotional indicators (posttraumatic stress and depressive symptoms) in 17 children of directly exposed Oklahoma City bombing survivors and in 17 demographically matched community comparison children, 7 years after the incident.

RESULTS: Despite generally low levels of subjectively reported posttraumatic stress and depressive symptoms 7 years after the disaster, the children of survivors showed heightened objectively measured physiological reactivity relative to the comparison group. The extent to which this heightened physiological reactivity in the children of survivors was pathologic is unclear. Only 1 participant reported high levels of posttraumatic stress and depressive symptoms; this individual also demonstrated physiological reactivity.

CONCLUSIONS: Results suggest children of disaster survivors may experience physiological reactivity despite absence of direct exposure to the trauma or acknowledgement of symptoms. These findings indicate the physiological effects of trauma may endure separate from subjective affect in the offspring of highly exposed disaster survivors. More research is needed to determine the potential consequences of persistent physiological reactivity.

KEYWORDS: disaster, indirect trauma exposure, physiological reactivity, posttraumatic stress, terrorism, trauma, Oklahoma City bombing

ANNALS OF CLINICAL PSYCHIATRY 2011;23(3):202-207

  INTRODUCTION

Physiological reactivity, a symptom of posttraumatic stress disorder (PTSD), is typically assessed by subjective report of personal experiences rather than objective laboratory measurement. Research using objective physiological measures has documented increased reactivity in individuals exposed to various forms of trauma,1-3 including disasters,4,5 relative to comparison samples. For example, physically healthy Oklahoma City bombing survivors experienced elevations in heart rate (HR) and blood pressure (BP) in response to an interview about the disaster 7 years after the incident.4 Although PTSD symptoms were below levels considered clinically relevant, these survivors had significantly greater autonomic reactivity than sex- and age-matched comparison participants who were not disaster survivors, were not related to deceased victims, and did not participate in rescue/recovery efforts.4

Relatively few studies of children exposed to trauma have used objective indicators such as HR and BP measurements to assess physiological reactivity. HR has been studied as an objective predictor of posttraumatic stress in children after accidental injury.6-8 Scheeringa and colleagues9 found young children (n = 62, age 1.5 to 6 years) who developed PTSD symptoms after exposure to a traumatic event (eg, accidents, witnessing domestic violence, medical procedures) exhibited objective signs of physiological reactivity relative to a matched control group of children without trauma exposure. Reactivity was measured through electrocardiogram (EKG) heart period (interbeat interval) in response to memories of the traumatic event.

To augment the sparse literature, we used objective measures to examine physiological reactivity in a pilot sample of 17 children of Oklahoma City bombing survivors studied 7 years after the disaster. We also enrolled a community comparison group of children matched for sex, age, and race/ethnicity.

  METHODS

Participants

Our sample included 17 volunteer children of directly exposed survivors of the Oklahoma City bombing. At assessment, 10 participants were adolescents age 13 to 17 (mean = 15.3, standard deviation [SD] = 1.5) and 7 participants were young adults age 18 to 25 (mean = 22.1, SD = 2.6). During the bombing 7 years prior, the 10 adolescents had been age 6 to 10 (mean = 8.3, SD = 1.5) and the 7 young adults had been age 11 to 18 (mean = 14.7, SD = 2.6).

All participants were children of bombing survivors who had been in the direct path of the bomb blast, either in the Alfred P. Murrah Federal Building or surrounding buildings, during the disaster. North and colleagues10 conducted an index study of 182 Oklahoma City bombing survivors approximately 6 months after the event; 113 of these participated in our follow-up study between November 2001 and October 2002, approximately 7 years after the bombing (mean = 83.5 months, SD = 3.4, median = 83 months).11

The current sample of adolescent and young adult children of bombing survivors was recruited through their parents, who were among the 113 adult survivors in the follow-up study.11 Of the 113 survivors, 36 had a total of 59 study-eligible children in the age range we were investigating. Twenty-seven agreed to participate in the study and completed physiological assessments. Of these, 17 were matched with community participants. The final group of 17 study participants included 3 sibling pairs (2 children per family for a total of 6 children) and 11 children from different families. Exclusion criteria eliminated potential participants with a medical illness and those taking medications associated with potential changes in physiological functioning. Only 1 potential young adult participant who was on psychotropic medication was excluded.

Community comparison participants were matched with children of survivors on measures of sex, age, and race/ethnicity (with the exception of 1 pair, in which a white child was matched with a Korean-American comparison participant; they were matched on sex and age). Comparison participants were initially recruited by asking participating children of survivors to identify a peer from the community who had no direct exposure to the bombing and whose family members were not involved. Additional participants were recruited through less formal mechanisms, such as fliers and word of mouth. All community comparison participants resided in the Oklahoma City metropolitan area at the time of the bombing. None were in the immediate vicinity of the blast and none were related to bombing victims or to rescue or recovery workers.

Of the survivors’ children in the physiological reactivity study sample, 10 were male and 7 were female. The majority (n = 16) of survivors’ children were white and 1 was African American. The majority of the community comparison participants were white; 1 was African American and 1 was Korean American.

None of the participants in the current study had been physically present at the site of the Oklahoma City bombing. Of the community control group, none reported immediate or distant family members killed or injured; however, 4 reported a friend or acquaintance killed in the bombing and 4 reported a friend or acquaintance injured.

Procedures

The University of Oklahoma Health Sciences Center and Washington University School of Medicine Institutional Review Boards (IRBs) approved the index10 and follow-up studies4,5,11; the University of Texas Southwestern Medical Center IRB approved additional data analyses for these studies. Potential participants for the follow-up study were contacted by letter and/or telephone call. All adult participants provided informed consent. Participants age <18 provided assent and their parents provided consent. Participants were paid $125 to compensate for their time and effort.

The 34 adolescent and young adult participants in this study were assessed approximately 7 years after the bombing (mean = 71.3 months, range = 65 to 84 months). Participants completed a physiological assessment and a self-report questionnaire to assess posttraumatic stress and depressive responses.

Physiological assessment

The physiological assessment was conducted before all psychometric assessments. Participants first were shown the physiological equipment to reduce potential anxiety about the procedure. Each participant was seated in a comfortable chair in a private testing room, with a BP cuff placed on the left arm and EKG electrodes appropriately placed. A Lablink Modular Instrument System (Biopac Systems Inc., Goleta, CA) recorded HR via standard EKG lead 2 placement. A Critikon Dinamap Vital Signs Monitor (1846 SX; Johnson & Johnson, Tampa, FL) recorded systolic blood pressure (SBP) and diastolic blood pressure (DBP). A Compaq computer interfaced with all equipment. All autonomic measurements were assessed for 4 minutes during a resting phase (pretest phase), for 4 minutes during a semi-structured interview about the bombing (test phase), and for 4 minutes after the interview was completed (posttest phase).

The semi-structured interview lasted for 3 minutes during the testing phase only. All participants, including those in the comparison group were asked to describe how they felt after learning about the bombing, if they knew anyone injured or killed in the incident, and if “anything jumped into (their) mind when thinking about the bombing.” Participants were prompted to continue talking during the assessment so the length of the interview was consistent for all participants. Participants were not queried about exposure or reaction to other traumatic events.

Emotional indicators

Posttraumatic stress was measured using a modified version of the self-report Impact of Event Scale-Revised (IES-R).12,13 The scale assessed how often participants experienced each of 22 posttraumatic stress responses in the preceding 7 days using a 4-point scale (1 = not at all, 2 = rarely, 3 = sometimes, 4 = often).

Depressive symptoms in the last 2 weeks were measured using the Beck Depression Inventory (BDI).14 This self-report inventory consists of 21 items each scored from 0 to 3, with 3 representing the most severe score. Total scores of 0 to 9 are considered clinically insignificant, 10 to 18 indicates mild-to-moderate depressive symptom levels, 19 to 29 suggests moderate-to-severe depressive symptom levels, and 30 to 63 indicates severe depressive symptom levels.

One survivor’s child did not complete the modified IES-R and 3 comparison children did not complete the modified IES-R or the BDI.

Data analysis

Wilcoxon rank-sum tests were used to compare children of survivors and children in the community comparison group on mean modified IES-R and BDI scores and on physiological measures. Means and SDs for each physiological variable—HR, SBP, and DBP—were calculated for both groups during the pretest, test, and posttest phases. Autonomic reactivity scores were calculated by subtracting pretest from test scores in measures of HR, SBP, and DBP. Spearman correlations examined the association between autonomic reactivity difference scores (test minus pretest values for HR, SBP, and DBP), and for posttraumatic stress and depressive responses measured by the modified IES-R and BDI, respectively. Analysis of variance F test was used to examine family effects and to compare children who did and did not know deceased or injured victims on variables of interest. Statistical significance was set at <.05 for 2-tailed tests.

  RESULTS

There were no significant sex or age (young adults versus adolescents) differences in HR, SBP, or DBP in any time periods or in autonomic reactivity. There were no significant differences in physiological variables based on family effects, or in physiological reactivity between children who did and did not know deceased or injured victims.

The mean modified IES-R score for children of survivors was 28.50 (SD = 10.02) with a range of 22 to 62. The mean modified IES-R score for the comparison group was 27.64 (SD = 7.26) with a range of 22 to 48. There was no significant difference in mean modified IES-R score between the survivors’ children and the community comparison group; these scores were low, reflecting general endorsement of symptoms between “never” and “rarely.”

The mean BDI score for survivors’ children was 3.53 (SD = 5.87), well within the clinically insignificant category, with a range of 0 to 25. Among children of survivors, 1 scored in the moderate-to-severe range of depression, with a BDI score of 25; the rest of the sample (n = 16) scored in the clinically insignificant range (0 to 9). There was no significant difference between the participant with moderate-to-severe depressive symptoms and those without depression in HR, SBP, or DBP or reactivity in these measures when assessed with the bombing reminder interview. The mean BDI score for the comparison group was 3.35 (SD = 4.43) with a range of 0 and 15. Among comparison children, 1 scored in the mild-to-moderate range of depression, with a BDI score of 15; the rest of the group (n = 13) scored in the clinically insignificant range (0 to 9). There was no significant difference in mean BDI scores between the survivors’ children and the comparison group. There was no significant correlation between modified IES-R and BDI scores for the children of survivors or for the comparison children.

The accompanying TABLE presents physiological data for the children of survivors and the comparison children. There was no significant difference between the 2 groups in baseline HR or SBP during pretest, test, and posttest phases. DBP during the test phase for children of survivors was significantly higher than for comparison children, but there were no significant differences in DBP during pre- and posttest phases. Notably, relative to comparison children, the children of survivors showed significantly higher physiological reactivity in HR, SBP, and DBP.

Among children of survivors, the modified IES-R score was positively correlated with HR reactivity to the bombing reminder interview (r = 0.49; P = .0447); in contrast, the modified IES-R score and HR reactivity for children in the comparison group were not correlated. The modified IES-R score was not significantly correlated with either SBP reactivity or DBP reactivity or with HR, SBP, or DBP during the pretest, test, and posttest phases for both the survivors’ children and the children in the comparison group.

Most of the children of survivors we studied reported few posttraumatic stress symptoms on the modified IES-R. The only participant with a score >37 on the modified IES-R received a score of 62. He also scored in the moderate-to-severe range of depressive symptoms, with a BDI score of 25. His father, a bombing survivor, had experienced bombing-related PTSD as well as prior trauma exposure while serving in the military but had no pre-bombing psychiatric disorders. The participant was age 18 at the time of the assessment, and had been at school during the bombing. His HR, SBP, and DBP were reactive to the trauma interview (pretest HR = 61, SBP = 98, DBP = 52; test HR = 70, SBP = 106, DBP = 56; posttest HR = 65, SBP = 97, DBP = 49).


TABLE

Physiological reactivity in children of trauma survivors and community comparison groups

  Children of survivors (n = 17) Community comparison (n = 17)  
Physiological reactivity Mean (SD) Mean (SD) P value
HR
   Pretest 71.06 (10.06) 70.94 (20.80) P = .6818
   Test 77.74 (11.68) 74.79 (13.33) P = .5621
   Posttest 73.41 (10.94) 74.09 (15.20) P = .9182
   Test – Pretest 6.68 (6.44) 3.85 (11.91) P = .0498
SBP
   Pretest 113.44 (10.48) 115.24 (13.30) P = .8912
   Test 121.85 (14.09) 117.32 (13.59) P = .3586
   Posttest 113.35 (11.33) 111.85 (12.32) P = .4742
   Test – Pretest 8.41 (7.93) 2.09 (6.15) P = .0215
DBP
   Pretest 65.47 (7.00) 62.44 (8.88) P = .1935
   Test 74.12 (10.99) 66.59 (8.53) P = .0208
   Posttest 64.85 (7.87) 63.21 (8.65) P = .4954
   Test – Pretest 8.65 (6.21) 4.15 (5.15) P = .0357
DBP: diastolic blood pressure; HR: heart rate; SBP: systolic blood pressure; SD: standard deviation.

  Discussion

For the most part, the children of survivors we studied were free of psychological symptoms. Only 1 evidenced what might qualify as high levels of posttraumatic stress responses; this child and 1 comparison child reported clinical levels of depressive symptoms.

Studies of traumatized children have demonstrated relationships between early post-event objective autonomic measures (eg, HR) and later subjective symptoms over relatively short time periods (eg, 6 months).6-8 Our results, nearly 7 years after the Oklahoma City bombing, suggest longstanding heightened physiological reactivity may occur in indirectly exposed children of trauma survivors. At the same time, baseline HR and BP measurements did not differ across groups, suggesting children of survivors did not experience chronically elevated physiological arousal, but rather heightened physiological reactivity, in response to specific reminders of their parents’ trauma and their own indirect exposure to that trauma. Levels of subjectively reported posttraumatic stress responses and depressive symptoms generally were low. However, the objectively measured heightened HR, SBP, and DBP reactivity to reminiscence of the disaster in children of survivors relative to the comparison group, persisted nearly 7 years after the disaster, and HR reactivity correlated with modified IES-R scores in children of survivors.

The children of survivors we studied would qualify as “close associates” for meeting the exposure criterion for a diagnosis of PTSD.15 The results may reflect indirect exposure associated with learning about the incident and the involvement of a parent, and from knowing, and maybe even imagining, details about the parent’s suffering. Our findings suggest rather than manifesting subjective symptoms, the reactions to this indirect exposure were expressed physiologically. Unfortunately, we do not have information about the subjective or physiological reactions of the study participants early in the postdisaster course, when they may have been symptomatic. Failure to find symptoms at 7 years is not surprising, given the participants were not directly exposed to the bombing, several years had elapsed since the event, and a potential bias was created by limiting participation to individuals who were free of medical conditions or use of medications that might affect physiological functioning.

The extent to which the heightened physiological reactivity in the children of survivors was pathologic or a reason for concern is unclear. Only 1 participant reported high levels of posttraumatic stress and depressive symptoms and he demonstrated increased physiological reactivity to the trauma interview. Nonetheless, our results demonstrate children of disaster survivors may experience heightened physiological reactivity despite their lack of direct exposure, or recognition/acknowledgement of symptoms. This suggests the physiological effects of trauma may endure separate from subjectively experienced effects in the offspring of highly exposed disaster survivors. This heightened reactivity to cues or reminders of the event does not represent increased response to stress in general. More research is needed to determine the potential physical and mental health consequences of enduring physiological reactivity (eg, cardiovascular and/or psychiatric effects associated with chronic stress reactions). For example, offspring with greater physiological reactivity to reminders of indirectly experienced early trauma may be more susceptible to mental illness in response to later life stressors or trauma, or to cardiovascular problems later in life. Arguing against the latter possibility, it is notable the offspring of survivors studied did not evidence higher baseline autonomic measures that would predict future problems from sustained elevated HRs or BPs. In addition, physiologically reactive offspring may be more vigilant and better able to mount a protective “fight or flight” response to subsequent trauma.

We cannot discount the possibility of type II errors due to the small sample size we studied. Other significant limitations to this study include the small non-representative sample and the possibility of selection bias created by excluding potential participants with a medical illness and those taking medications known to affect physiological or psychological functioning. Without these restrictions, more dramatic differences may have been observed between children of survivors and the comparison group in both objectively measured physiological reactivity and subjectively experienced emotional reactions. Recruitment of controls may have selected comparison participants who differed from survivors’ children in unknown ways beyond their disaster exposure, which could explain differences between the 2 groups.

This investigation was scheduled for implementation in early September 2001. Because of the September 11 attacks, data collection was delayed until November 2001, but it is possible temporal proximity to the September 11 attacks influenced the reactions of our participants. In addition, studying the children of survivors earlier in the postdisaster course might have shown symptoms that we failed to detect at 7 years and that might have correlated with physiological reactivity. Following the children longitudinally beginning soon after the event and for a longer period of time would provide opportunities to examine the course of recovery and potential consequences of heightened physiological reactivity. Finally, the measures we used to quantify posttraumatic stress responses and depressive symptoms were not diagnostic measures, thus limiting our ability to draw conclusions about the clinical significance of our findings. Future studies are needed to examine these issues.

  Conclusions

Our findings suggest potential biologic effects of trauma over time and the long-term nature of reactions in children of survivors that warrant exploration.

ACKNOWLEDGEMENTS: This work was supported by Award No. MIPT106-113-2000-020 from the Oklahoma City National Memorial Institute for the Prevention of Terrorism (MIPT) and the Office of Justice Programs, National Institute of Justice, Department of Justice, to Dr. Pfefferbaum, and by National Institute of Mental Health (NIMH) grants MH40025 and MH68853 awarded to Dr. North. Points of view in this manuscript are those of the authors and do not necessarily represent the official position of the Oklahoma City MIPT, U.S. Department of Justice, NIMH, Department of Veterans Affairs, or US Government.

DISCLOSURES: The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products. Dr. Pfefferbaum receives research/grant support from the University of Maryland National Consortium for the Study of Terrorism and Responses to Terrorism and the Substance Abuse and Mental Health Services Administration.

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CORRESPONDENCE: Betty Pfefferbaum, MD, JD Department of Psychiatry and Behavioral Sciences, University of Oklahoma College of Medicine, WP 3470, PO Box 26901, Oklahoma City, OK 73126 USA, E-MAIL: betty-pfefferbaum@ouhsc.edu