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Letters To The Editor |
Department of Medicine
College of Physicians and Surgeons
Columbia University
New York, NY 10032
E-mail: rj2136{at}columbia.edu
Channing Laboratory
Department of Medicine
Brigham & Women's Hospital
Harvard Medical School
Boston, MA
Department of Nutrition
Harvard School of Public Health
Boston, MA
Department of Ophthalmology
College of Physicians and Surgeons
Columbia University
New York, NY
Dear Sir:
We thank Chow for his letter and his interest in our study (1). We agree with Chow that a critical evaluation of available information is needed to determine whether consumption of cured meats is associated with an increased risk of chronic obstructive pulmonary disease (COPD), but we disagree on several points he raised in his letter.
First, it is true that 
25% of ingested nitrate mostly from vegetables will be secreted through the salivary glands and that oral flora with nitrate reductase capability leads to an elevation of salivary nitrite concentrations. Such salivary nitrite could, in principle, contribute to systemic nitrite exposure. However, to what extent such salivary nitrite is absorbed systemically is far from clear. It has been shown that ingestion of high nitrate loads in persons with normal acidic gastric pH, but a high secretion of salivary nitrite, does not cause the expected elevated gastric nitrite concentrations (2, 3). This has been attributed to the acidic environment of the stomach, which promotes the formation of nitrous acid and related nitrosating species, such as nitrosonium ion and dinitrogen trioxide, in addition to nitric oxide. These findings are supported by studies in which dietary nitrate loading via foodstuffs in healthy human volunteers resulted in large increases in serum nitrate and salivary nitrite, but no appreciable change in serum nitrite (4). Although endogenous exposures to nitrite via the production of nitric oxide gas in inflammatory states can be significant, the low nanomolar concentrations resulting from constitutive nitric oxide production as part of normal metabolic processes is miniscule by comparison. Thus, upregulation of inducible nitric oxide synthases during inflammation may contribute in a meaningful way to pathologic connective tissue protein damage in the lung.
Second, the positive association between cured meat consumption and risk of newly diagnosed COPD observed in our study was independent of total energy intake, physical activity, BMI, smoking history (smoking status, pack-years, and exposure to secondhand tobacco), and several other factors considered to be related to lifestyle, such as multivitamin supplement use and intake of fish, fruit, and vegetables (listed in the footnote of Table 2, p 2005). The correlation between cured meat consumption and pack-years among ever smokers was weak (r = 0.08), which suggests that the residual confounding by smoking was probably small. There was no evidence of a significant association among never smokers, which is not surprising given that few never smokers develop COPD and therefore we did not have sufficient power to examine the association.
Third, the source of nitric oxide detected in the expired air is unclear. It is thought that inducible nitric oxide synthase activity within the airways, and not the lung parenchyma, contributes most to exhaled nitric oxide in COPD. Sterk et al pointed out in their editorial that studies of exhaled nitric oxide values in COPD have yielded inconsistent results (5). Some found that exhaled nitric oxide is higher in patients with COPD than in healthy control subjects, but others observed no difference in exhaled nitric oxide between COPD patients and healthy control subjects. Several possible explanations have been proposed for the inconsistent results (5, 6). First, the techniques for measuring exhaled nitric oxide of lower airway origin were not standardized. Second, most studies have measured exhaled nitric oxide in relatively small numbers of subjects. Third, several studies were confounded by the inclusion of current smokers among the study populations. Tobacco smoking down-regulates endothelial nitric oxide synthase and masks any tendency toward a disease-related rise in exhaled nitric oxide concentrations.
Fourth, it is commonly known that nitrite is a precursor of nitrogen dioxide. In fact, nitrite serves as a reactive substrate for reactions involving hydrogen peroxide/myeloperoxidase, hydrogen peroxide/Fenton chemistry, and hydrogen peroxide/hypochlorous acid by virtue of its transformation into a free radical–nitrating species, nitrogen dioxide. Hence, our findings are consistent with the existing literature. Further studies are underway to elucidate the role of cured meat consumption and nitrites in the etiology of COPD.
ACKNOWLEDGMENTS
No conflicts of interest were reported.
REFERENCES
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