Chitotriosidase is a Biomarker for the Resistance to World Trade Center Lung Injury in New York City Firefighters

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 (FEV 1 /FVC) less than the lower limit of normal (LLN). Cases ( N = 125) had abnormal FEV 1 /FVC whereas controls had normal FEV 1 /FVC ( N = 126). In a secondary analysis, resistant cases ( N = 66) had FEV 1 (≥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 FEV 1 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 FEV 1 . Alternately, increasing chitotriosidase decreased the odds of abnormal FEV 1 /FVC and increased the odds of FEV 1 ≥ 107 %. Serum YKL-40 was not associated with FEV 1 /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.