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.

CDC Public Access

1 UL1RR029893/RR/NCRR NIH HHS/United States
AL080298A/PHS HHS/United States
HL090316/HL/NHLBI NIH HHS/United States
K23 HL084191/HL/NHLBI NIH HHS/United States
K23HL084191/HL/NHLBI NIH HHS/United States
K24 AI080298/AI/NIAID NIH HHS/United States
K24A1080298/PHS HHS/United States
R01HL057879/HL/NHLBI NIH HHS/United States
R01HL090316/HL/NHLBI NIH HHS/United States
T32 ES007267/ES/NIEHS NIH HHS/United States
TL1RR029892/RR/NCRR NIH HHS/United States
U01CA008617/CA/NCI NIH HHS/United States
U10-OH008242/OH/NIOSH CDC HHS/United States
U10-OH008243/OH/NIOSH CDC HHS/United States
UL1TR000038/TR/NCATS NIH HHS/United States