Chitotriosidase is a biomarker for the resistance to world trade center lung injury in New York City firefighters

Soo Jung Cho, Anna Nolan, Ghislaine C. Echevarria, Sophia Kwon, Bushra Naveed, Edward Schenck, Jun Tsukiji, David J. Prezant, William N. Rom, Michael D. Weiden

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

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 1 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 FEV 1/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 FEV 1/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 FEV 1 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.

Original languageEnglish (US)
Pages (from-to)1134-1142
Number of pages9
JournalJournal of Clinical Immunology
Volume33
Issue number6
DOIs
StatePublished - Aug 2013

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Firefighters
Lung Injury
Immunoglobulin E
Biomarkers
Vital Capacity
Forced Expiratory Volume
Chitinases
Serum
Lung
Particulate Matter
Recovery of Function
chitotriosidase
Logistic Models

Keywords

  • Chitotriosidase
  • immunoglobulin E
  • pulmonary function testing
  • WTC particulate matter

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Cho, S. J., Nolan, A., Echevarria, G. C., Kwon, S., Naveed, B., Schenck, E., ... Weiden, M. D. (2013). Chitotriosidase is a biomarker for the resistance to world trade center lung injury in New York City firefighters. Journal of Clinical Immunology, 33(6), 1134-1142. https://doi.org/10.1007/s10875-013-9913-2

Chitotriosidase is a biomarker for the resistance to world trade center lung injury in New York City firefighters. / Cho, Soo Jung; Nolan, Anna; Echevarria, Ghislaine C.; Kwon, Sophia; Naveed, Bushra; Schenck, Edward; Tsukiji, Jun; Prezant, David J.; Rom, William N.; Weiden, Michael D.

In: Journal of Clinical Immunology, Vol. 33, No. 6, 08.2013, p. 1134-1142.

Research output: Contribution to journalArticle

Cho, SJ, Nolan, A, Echevarria, GC, Kwon, S, Naveed, B, Schenck, E, Tsukiji, J, Prezant, DJ, Rom, WN & Weiden, MD 2013, 'Chitotriosidase is a biomarker for the resistance to world trade center lung injury in New York City firefighters', Journal of Clinical Immunology, vol. 33, no. 6, pp. 1134-1142. https://doi.org/10.1007/s10875-013-9913-2
Cho, Soo Jung ; Nolan, Anna ; Echevarria, Ghislaine C. ; Kwon, Sophia ; Naveed, Bushra ; Schenck, Edward ; Tsukiji, Jun ; Prezant, David J. ; Rom, William N. ; Weiden, Michael D. / Chitotriosidase is a biomarker for the resistance to world trade center lung injury in New York City firefighters. In: Journal of Clinical Immunology. 2013 ; Vol. 33, No. 6. pp. 1134-1142.
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abstract = "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 1 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 FEV 1/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 FEV 1/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 FEV 1 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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AU - Nolan, Anna

AU - Echevarria, Ghislaine C.

AU - Kwon, Sophia

AU - Naveed, Bushra

AU - Schenck, Edward

AU - Tsukiji, Jun

AU - Prezant, David J.

AU - Rom, William N.

AU - Weiden, Michael D.

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N2 - 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 1 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 FEV 1/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 FEV 1/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 FEV 1 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.

AB - 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 1 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 FEV 1/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 FEV 1/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 FEV 1 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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