Chest
Volume 142, Issue 2, August 2012, Pages 412-418
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Original Research
Occupational and Environmental Lung Diseases
Inflammatory Biomarkers Predict Airflow Obstruction After Exposure to World Trade Center Dust

https://doi.org/10.1378/chest.11-1202Get rights and content

Background

The World Trade Center (WTC) collapse on September 11, 2001, produced airflow obstruction in a majority of firefighters receiving subspecialty pulmonary evaluation (SPE) within 6.5 years post-September 11, 2001.

Methods

In a cohort of 801 never smokers with normal pre-September 11, 2001, FEV1, we correlated inflammatory biomarkers and CBC counts at monitoring entry within 6 months of September 11, 2001, with a median FEV1 at SPE (34 months; interquartile range, 25-57). Cases of airflow obstruction had FEV1 less than the lower limit of normal (LLN) (100 of 801; 70 of 100 had serum), whereas control subjects had FEV1 greater than or equal to LLN (153 of 801; 124 of 153 had serum).

Results

From monitoring entry to SPE years later, FEV1 declined 12% in cases and increased 3% in control subjects. Case subjects had elevated serum macrophage derived chemokine (MDC), granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating factor, and interferon inducible protein-10 levels. Elevated GM-CSF and MDC increased the risk for subsequent FEV1 less than LLN by 2.5-fold (95% CI, 1.2-5.3) and 3.0-fold (95% CI, 1.4-6.1) in a logistic model adjusted for exposure, BMI, age on September 11, 2001, and polymorphonuclear neutrophils. The model had sensitivity of 38% (95% CI, 27-51) and specificity of 88% (95% CI, 80-93).

Conclusions

Inflammatory biomarkers can be risk factors for airflow obstruction following dust and smoke exposure. Elevated serum GM-CSF and MDC levels soon after WTC exposure were associated with increased risk of airflow obstruction in subsequent years. Biomarkers of inflammation may help identify pathways producing obstruction after irritant exposure.

Section snippets

Study Design and Participants

The study cohort was derived from subjects (N = 1,720) entering SPE between October 1, 2001, and March 10, 2008,15 if they met the following criteria: never smokers (consistently reported not smoking on all health screens); male; had reliable National Health and Nutrition Examination Survey (NHANES) normative data for predicted FEV1; had post-September 11, 2001, FDNY-Bureau of Health Services pulmonary function test (PFTs) within 200 days of September 11, 2001; and had pre-September 11, 2001,

Participants

This nested case-control study was drawn from a population of 801 never smokers with normal pre-September 11, 2001, PFTs. Derivation of baseline cohort, cases, and control subjects from the cohort that received SPE is described in Figure 1. Control subjects had similar FEV1 at MME when compared with the larger never smoker baseline cohort (n = 801) and to the original SPE cohort (n = 1,720). Airflow obstruction case and control subjects had similar WTC exposure; time from September 11, 2001, to

Discussion

This study was designed to identify risk factors of susceptibility to WTC-related airflow obstruction early in the disease process. We measured biomarkers in blood from the first post-September 11, 2001, monitoring evaluation done within 6 months of exposure and used subsequent lung function to define disease status. Case subjects had FEV1 less than LLN at pulmonary evaluation within 6.5 years of September 11, 2001, whereas control subjects had FEV1 greater than or equal to LLN. From the first

Acknowledgments

Author contributions: Drs Nolan and Weiden had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Dr Nolan: contributed to study design; data collection and analysis; manuscript writing and preparation; and reviewing, editing, and approving the manuscript.

Dr Naveed: contributed to data collection and analysis; and reviewing, editing, and approving the manuscript.

Ms Comfort: contributed to data collection and

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  • Cited by (0)

    For editorial comment see page 278

    Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.

    Funding/Support: This work was supported by the National Institutes of Health [Grants K23HL084191 (Dr Nolan), K24A1080298 (Dr Weiden), UL1 RR029893, T32-ES007267 (Drs Naveed and Ferrier), U01CA008617, RO1HL090316 (Dr Rom), and 1UL1RR029893 (New York University, Clinical and Translational Science Institute)] and the National Institute for Occupational Safety and Health [Grants U10-OH008243, U10-OH008242 (Dr Prezant)].

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