Abstract

From the Authors: We thank Drs. Joppa, Pobeha, and Tkacova for their interest in our article (1). The patients who are described in the letter of Joppa and colleagues are different in many ways from the cases of abnormal FEV1 that our group has studied in the Fire Department of New York cohort (1). The 71 Fire Department of New York cases were never smokers with median body mass index of 30 and FEV1 of 73% predicted at subspecialty pulmonary evaluation. They had normal FEV1 prior to World Trade Center exposure. We provided evidence that dyslipidemia, with high-density lipoprotein less than 40 mg/dl and triglycerides greater than 150 mg/dl, increased the odds of progressing to abnormal FEV1 within 6.5 years of an irritant exposure (1, 2). The work of Joppa and colleagues describes a cohort of 29 heavy smokers with mean 35.5 ± 25.7 pack-years of cigarette consumption and advanced chronic obstructive pulmonary disease with FEV1 52.9 ± 24.5%. The body mass index of the cohort was 25.4 ± 5.5, so few of the patients were obese (3). Joppa and coworkers state that baseline triglyceride and total cholesterol levels were inversely related to the decline in FEV1 with a similar proportion of the cohort with dyslipidemia as in our cohort (1). In advanced obstructive lung disease, malnutrition and associated weight loss is a poor prognostic indicator (4–7). The “obesity paradox” mentioned by Joppa and colleagues is likely related to the differences in the study populations. Our report was intended to provide insight on how the obesity epidemic in developed nations may contribute to development of lung disease in patients with normal lung function. It is not surprising that biomarkers of a high-calorie Western diet identify a subgroup with better outcome in advanced smoking-related obstructive lung disease. The report of Joppa and colleagues is likely to reflect the interaction of nutrition with lung function in these “obesity paradox” patients. There is still much work that needs to be done to clarify a relationship between metabolic syndrome and lung function loss. However, we stand by the conclusion of our paper that there is a correlation between biomarkers of metabolic syndrome and eventual decline in FEV1 in the never-smoking World Trade Center–exposed firefighter cohort. A better understanding of the impact of dyslipidemia on lung function at different stages of disease needs further investigation.

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