Lower respiratory tract iron burden is increased in association with cigarette smoking

A. B. Thompson, T. Bohling, A. Heires, J. Linder, S. I. Rennard

Research output: Contribution to journalArticle

104 Scopus citations

Abstract

Iron, by catalyzing the generation of the hydroxyl radical via the Haber-Weiss reaction, may participate in oxidant tissue injury. To determine whether iron might contribute to cigarette smoke-induced lung injury, we estimated the iron content of the lower respiratory tract by measuring intracellular iron content of pulmonary macrophages and extracellular iron content of bronchoalveolar lavage fluid from cigarette smokers and nonsmokers. Bronchoalveolar lavage was performed by using methods that allow for recovery of samples enriched for bronchial and alveolar contents. The intracellular iron content of the alveolar macrophages was determined by staining cytocentrifuged, air-dried pulmonary macrophages with a modified Prussian blue stain and assigning a score of 0 to 3 (0 = no stain, 3 = dense staining throughout the cytoplasm) to 100 macrophages. The extracellular iron level of bronchoalveolar lavage fluid was determined by using modifications of the Ferrozine method of Carter. Macrophage intracellular iron content was measured in a group of cigarette smokers with chronic bronchitis (n = 17), in smokers without chronic bronchitis (n = 15), and in normal volunteers (n = 15). Extracellular iron concentration was determined in a subset of the subjects with chronic bronchitis (n = 12) and in a separate group of normal volunteers (n = 5). The intracellular iron score was elevated in the bronchial sample lavage fluid in both the smokers with chronic bronchitis (45.3 ± 13.9) and the asymptomatic smokers (26.6 ± 8.0) compared with the normal individuals (8.1 ± 1.7, p < 0.03, both comparisons), but did not differ between the two groups of cigarette-smoking subjects (p = 0.68). Likewise, in the alveolar sample, the intracellular iron scores were elevated in both the smokers with chronic bronchitis (25.8 ± 9.8) and asymptomatic smokers (21.7 ± 5.6) compared with normal volunteers (5.5 ± 1.5, p < 0.05). In contrast, the extracellular iron content of the bronchial sample from the subjects with chronic bronchitis was not elevated compared with the normal levels. However, in the alveolar samples, the extracellular iron level was elevated in the subjects with chronic bronchitis (48.3 ± 10.5 ng/ml) compared with the normal subjects (7.2 ± 2.8 ng/ml, p = 0.002). The elevation of extracellular iron was noted after normalization of the results to albumin (p = 0.006) and estimation of the epithelial lining fluid concentration (p = 0.03). Thus, the iron burden in the lower respiratory tract was found to be elevated in association with cigarette smoking, suggesting that iron may contribute to the pathogenesis of cigarette smoke-induced lung injury.

Original languageEnglish (US)
Pages (from-to)493-499
Number of pages7
JournalJournal of Laboratory and Clinical Medicine
Volume117
Issue number6
StatePublished - 1991

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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