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Background: Chronic obstructive pulmonary disease (COPD) is associated with many comorbidities, but the percentage of COPD patients who develop comorbidities has not been clearly defined. Objectives: We aimed to examine the relationship between COPD and comorbidities using information obtained from the Health Search Database (HSD) owned by the Italian College of General Practitioners (SIMG), which stores information on about 1.5% of the total Italian population served by general practitioners. Methods: We conducted a population-based retrospective study using information obtained from the HSD. The software system used codes all the diagnostic records using the 9th Revision of the International Classification of Diseases. Results: Compared to the non-COPD people, COPD patients were at increased risk for cardiovascular events [ischemic heart disease (6.9% in the general population vs. 13.6% in COPD patients), cardiac arrhythmia (6.6% in the general population vs. 15.9% in COPD patients), heart failure (2.0% in the general population vs. 7.9% in COPD patients), and other forms of heart disease (10.7% in the general population vs. 23.1% in COPD patients); with a higher impact of COPD in the elderly]; non-psychotic mental disorders, including depressive disorders (29.1% in the general population vs. 41.6% in COPD patients; with a higher impact of COPD on women aged <75 years); diabetes mellitus (10.5% in the general population vs. 18.7% in COPD patients); osteoporosis (10.8% in the general population vs. 14.8% in COPD patients), with a higher impact of COPD on women aged <75 years, and malignant pulmonary neoplasms (0.4% in the general population vs. 1.9% in COPD patients). Conclusions: Our results indicate that COPD is a risk factor for these comorbid conditions.

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Nitrogen dioxide (NO2) is a free radical and a common oxidant in polluted air. Here we present data on the time course of inflammation after NO2 exposure, as reflected in bronchial biopsy and airway lavage specimens. Healthy, nonsmoking subjects were exposed to air or 2 ppm NO2 for 4 h in random order on separate occasions. Endobronchial biopsies, bronchial washing (BW), and bronchoalveolar lavage (BAL) were done at 1.5 h (n = 15) or 6 h (n = 15) after exposure. In BW, exposure to NO2 induced a 1.5-fold increase in interleukin-8 (IL-8) (p < 0.05) at 1.5 h and a 2.5-fold increase in neutrophils (p < 0.01) at 6 h. In BAL fluid (BALF), small increases were observed in CD45RO+ lymphocytes, B-cells, and natural killer (NK) cells only. Immunohistologic examination of bronchial biopsy specimens showed no signs of upregulation of adhesion molecules, and failed to reveal any significant changes in inflammatory cells at either time point after NO2 exposure. In summary, NO2 induced a neutrophilic inflammation in the airways that was detectable in BW at 6 h after NO2 exposure. The increase in neutrophils could be related to the enhanced IL-8 secretion observed at 1.5 h after exposure. The absence of adhesion-molecule upregulation or cellular inflammation in mucosal biopsy specimens indicates that the major site of inflammation following exposure to NO2 may be in the smaller airways and not in the alveoli.