Chitotriosidase is a Biomarker for the Resistance to World Trade Center Lung Injury in New York City Firefighters
Supporting Files
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8 2013
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File Language:
English
Details
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Alternative Title:J Clin Immunol
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Personal Author:
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Description:Purpose
World Trade Center (WTC) exposure caused airflow obstruction years after exposure. Chitinases and IgE are innate and humoral mediators of obstructive airway disease. We investigated if serum expression of chitinases and IgE early after WTC exposure predicts subsequent obstruction.
Methods
With a nested case-control design, 251 FDNY personnel had chitotriosidase, YKL-40 and IgE measured in serum drawn within months of 9/11/2001. The main outcome was subsequent Forced Expiratory Volume after one second/Forced Vital Capacity (FEV1/FVC) less than the lower limit of normal (LLN). Cases (N=125) had abnormal FEV1/FVC whereas controls had normal FEV1/FVC (N=126). In a secondary analysis, resistant cases (N=66) had FEV1 (≥107%) one standard deviation above the mean. Logistic regression adjusted for age, BMI, exposure intensity and post-exposure FEV1/FVC modeled the association between early biomarkers and later lung function.
Results
Cases and Controls initially lost lung function. Controls recovered to pre-9/11 FEV1 and FVC while cases continue to decline. Cases expressed lower serum chitotriosidase and higher IgE levels. Increase in IgE increased the odds of airflow obstruction and decreased the odds of above average FEV1. Alternately, increasing chitotriosidase decreased the odds of abnormal FEV1/FVC and increased the odds of FEV1≥107%. Serum YKL-40 was not associated with FEV1/FVC or FEV1 in this cohort.
Conclusions
Increased serum chitotriosidase reduces the odds of developing obstruction after WTC-particulate matter exposure and is associated with recovery of lung function. Alternately, elevated IgE is a risk factor for airflow obstruction and progressive lung function decline.
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Subjects:
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Keywords:
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Source:J Clin Immunol. 33(6):1134-1142
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Pubmed ID:23744081
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Pubmed Central ID:PMC3722498
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Document Type:
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Funding:U01CA008617/CA/NCI NIH HHSUnited States/ ; U10 OH008243/OH/NIOSH CDC HHSUnited States/ ; AL080298A/PHS HHSUnited States/ ; 1 UL1RR029893/RR/NCRR NIH HHSUnited States/ ; T32 ES007267/ES/NIEHS NIH HHSUnited States/ ; K23HL084191/HL/NHLBI NIH HHSUnited States/ ; U10-OH008242/OH/NIOSH CDC HHSUnited States/ ; UL1TR000038/TR/NCATS NIH HHSUnited States/ ; K24A1080298/PHS HHSUnited States/ ; U10-OH008243/OH/NIOSH CDC HHSUnited States/ ; TL1 RR029892/RR/NCRR NIH HHSUnited States/ ; HL090316/HL/NHLBI NIH HHSUnited States/ ; K23 HL084191/HL/NHLBI NIH HHSUnited States/ ; TL1RR029892/RR/NCRR NIH HHSUnited States/ ; U10 OH008242/OH/NIOSH CDC HHSUnited States/ ; R01HL090316/HL/NHLBI NIH HHSUnited States/ ; R01HL057879/HL/NHLBI NIH HHSUnited States/ ; UL1 RR029893/RR/NCRR NIH HHSUnited States/ ; R01 HL090316/HL/NHLBI NIH HHSUnited States/ ; K24 AI080298/AI/NIAID NIH HHSUnited States/ ; UL1 TR000038/TR/NCATS NIH HHSUnited States/ ; R01 HL057879/HL/NHLBI NIH HHSUnited States/
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Volume:33
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Issue:6
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Collection(s):
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Main Document Checksum:urn:sha256:49c2d5cb13f0f2271ccb657f4a9f2eeec0cdb020051115fe4989e2ed3d6684e1
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Download URL:
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File Type:
Supporting Files
File Language:
English
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