Rafael E de la Hoz1,2, Yunho Jeon1, Anthony P Reeves3, Raúl San José Estépar4, Xiaoyu Liu5, John T Doucette1, Juan C Celedón6, Anna Nolan7. 1. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York. 2. Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York. 3. School of Electrical and Computer Engineering, Cornell University, Ithaca, New York. 4. Department of Radiology, Brigham and Women's Hospital, Boston, Massachusetts. 5. Department of Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York, New York. 6. Division of Pediatric Pulmonary Medicine, Children's Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, Pennsylvania. 7. Department of Medicine, New York University School of Medicine, New York, New York.
Abstract
RATIONALE: Occupational exposures at the WTC site after September 11, 2001 have been associated with several presumably inflammatory lower airway diseases. Pulmonary arterial enlargement, as suggested by an increased ratio of the diameter of the pulmonary artery to the diameter of the aorta (PAAr) has been reported as a computed tomographic (CT) scan marker of adverse respiratory health outcomes, including WTC-related disease. In this study, we sought to utilize a novel quantitative CT (QCT) measurement of PAAr to test the hypothesis that an increased ratio is associated with FEV1 below each subject's statistically determined lower limit of normal (FEV1 < LLN). METHODS: In a group of 1,180 WTC workers and volunteers, we examined whether FEV1 < LLN was associated with an increased QCT-measured PAAr, adjusting for previously identified important covariates. RESULTS: Unadjusted analyses showed a statistically significant association of FEV1 < LLN with PAAr (35.3% vs 24.7%, P = 0.0001), as well as with height, body mass index, early arrival at the WTC disaster site, shorter WTC exposure duration, post-traumatic stress disorder checklist (PCL) score, wall area percent and evidence of bronchodilator response. The multivariate logistic regression model confirmed the association of FEV1 < LLN with PAAr (OR 1.63, 95% CI 1.21, 2.20, P = 0.0015) and all the unadjusted associations, except for PCL score. CONCLUSIONS: In WTC workers, FEV1 < LLN is associated with elevated PAAr which, although likely multifactorial, may be related to distal vasculopathy, as has been hypothesized for chronic obstructive pulmonary disease.
RATIONALE: Occupational exposures at the WTC site after September 11, 2001 have been associated with several presumably inflammatory lower airway diseases. Pulmonary arterial enlargement, as suggested by an increased ratio of the diameter of the pulmonary artery to the diameter of the aorta (PAAr) has been reported as a computed tomographic (CT) scan marker of adverse respiratory health outcomes, including WTC-related disease. In this study, we sought to utilize a novel quantitative CT (QCT) measurement of PAAr to test the hypothesis that an increased ratio is associated with FEV1 below each subject's statistically determined lower limit of normal (FEV1 < LLN). METHODS: In a group of 1,180 WTC workers and volunteers, we examined whether FEV1 < LLN was associated with an increased QCT-measured PAAr, adjusting for previously identified important covariates. RESULTS: Unadjusted analyses showed a statistically significant association of FEV1 < LLN with PAAr (35.3% vs 24.7%, P = 0.0001), as well as with height, body mass index, early arrival at the WTC disaster site, shorter WTC exposure duration, post-traumatic stress disorder checklist (PCL) score, wall area percent and evidence of bronchodilator response. The multivariate logistic regression model confirmed the association of FEV1 < LLN with PAAr (OR 1.63, 95% CI 1.21, 2.20, P = 0.0015) and all the unadjusted associations, except for PCL score. CONCLUSIONS: In WTC workers, FEV1 < LLN is associated with elevated PAAr which, although likely multifactorial, may be related to distal vasculopathy, as has been hypothesized for chronic obstructive pulmonary disease.
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