Roman Kotov1, Evelyn J Bromet, Clyde Schechter, Julie Broihier, Adriana Feder, George Friedman-Jimenez, Adam Gonzalez, Kathryn Guerrera, Julia Kaplan, Jacqueline Moline, Robert H Pietrzak, Dori Reissman, Camilo Ruggero, Steven M Southwick, Iris Udasin, Michael Von Korff, Benjamin J Luft. 1. From the Departments of Psychiatry (Kotov, Bromet, Gonzalez) and Medicine (Broihier, Guerrera, Luft), Stony Brook University, Stony Brook, New York; Department of Family & Social Medicine (Schechter), Albert Einstein College of Medicine, New York, New York; Departments of Psychiatry (Feder, Pietrzak, Southwick) and Preventive Medicine (Kaplan), Mount Sinai School of Medicine, New York, New York; Departments of Population Health (Epidemiology), Medicine and Environmental Medicine (Friedman-Jimenez), New York University School of Medicine and Bellevue Hospital Center, New York, New York; Department of Population Health (Moline), North Shore-LIJ Health System, Great Neck, New York; Department of Psychiatry (Pietrzak, Southwick), Yale University School of Medicine, National Center for Posttraumatic Stress Disorder, VA Connecticut Healthcare System, West Haven, Connecticut; Office of the Director National Institute for Occupational Safety and Health (Reissman), Washington, DC; Department of Psychology (Ruggero), University of North Texas, Denton, Texas; Environmental and Occupational Health Sciences Institute (Udasin), University of Medicine & Dentistry of New Jersey, Piscataway, New Jersey; and Group Health Research Institute (Von Korff), Group Health Cooperative, Seattle, Washington.
Abstract
OBJECTIVE: Posttraumatic stress disorder (PTSD) is associated with high medical morbidity, but the nature of this association remains unclear. Among responders to the World Trade Center (WTC) disaster, PTSD is highly comorbid with lower respiratory symptoms (LRS), which cannot be explained by exposure alone. We sought to examine this association longitudinally to establish the direction of the effects and evaluate potential pathways to comorbidity. METHODS: 18,896 responders (8466 police and 10,430 nontraditional responders) participating in the WTC-Health Program were first evaluated between 2002 and 2010 and assessed again 2.5 years later. LRS were ascertained by medical staff, abnormal pulmonary function by spirometry, and probable WTC-related PTSD with a symptom inventory. RESULTS: In both groups of responders, initial PTSD (standardized regression coefficient: β = 0.20 and 0.23) and abnormal pulmonary function (β = 0.12 and 0.12) predicted LRS 2.5 years later after controlling for initial LRS and covariates. At follow-up, LRS onset was 2.0 times more likely and remission 1.8 times less likely in responders with initial PTSD than in responders without. Moreover, PTSD mediated, in part, the association between WTC exposures and development of LRS (p < .0001). Initial LRS and abnormal pulmonary function did not consistently predict PTSD onset. CONCLUSIONS: These analyses provide further evidence that PTSD is a risk factor for respiratory symptoms and are consistent with evidence implicating physiological dysregulation associated with PTSD in the development of medical conditions. If these effects are verified experimentally, treatment of PTSD may prove helpful in managing physical and mental health of disaster responders.
OBJECTIVE:Posttraumatic stress disorder (PTSD) is associated with high medical morbidity, but the nature of this association remains unclear. Among responders to the World Trade Center (WTC) disaster, PTSD is highly comorbid with lower respiratory symptoms (LRS), which cannot be explained by exposure alone. We sought to examine this association longitudinally to establish the direction of the effects and evaluate potential pathways to comorbidity. METHODS: 18,896 responders (8466 police and 10,430 nontraditional responders) participating in the WTC-Health Program were first evaluated between 2002 and 2010 and assessed again 2.5 years later. LRS were ascertained by medical staff, abnormal pulmonary function by spirometry, and probable WTC-related PTSD with a symptom inventory. RESULTS: In both groups of responders, initial PTSD (standardized regression coefficient: β = 0.20 and 0.23) and abnormal pulmonary function (β = 0.12 and 0.12) predicted LRS 2.5 years later after controlling for initial LRS and covariates. At follow-up, LRS onset was 2.0 times more likely and remission 1.8 times less likely in responders with initial PTSD than in responders without. Moreover, PTSD mediated, in part, the association between WTC exposures and development of LRS (p < .0001). Initial LRS and abnormal pulmonary function did not consistently predict PTSD onset. CONCLUSIONS: These analyses provide further evidence that PTSD is a risk factor for respiratory symptoms and are consistent with evidence implicating physiological dysregulation associated with PTSD in the development of medical conditions. If these effects are verified experimentally, treatment of PTSD may prove helpful in managing physical and mental health of disaster responders.
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