Chronic bronchitis is a descriptive term, when used pathologically, that indicates chronic inflammation of large airways of any cause (Fig. 30.1). In clinical practice, it refers to a constellation of symptoms related to inflammation and hypersecretion in large and small airways, often sharing causes that result in emphysema and/or asthma (Table 30.1). Interestingly, although the inflammatory component of chronic obstructive lung disease (COPD) involves small airways as prominently as bronchi, the term “chronic bronchiolitis” is generally used for processes restricted to small airways (such as obliterative, constrictive, and follicular bronchiolitis) and not in the context of COPD. The pathologic findings that are specific for asthma or emphysema are described in subsequent chapters.

Chronic bronchitis is characterized pathologically by chronic inflammation and mucous gland hyperplasia resulting in narrowing of the airway and hypersecretion and involves bronchioles as well as bronchi.¹ Chronic bronchitis is a complication of exposures to particulate matter, especially tobacco smoke, but may also result from allergic hyperreactive airway disease (chronic asthma). Regardless of the cause, recurrent infections frequently exacerbate the condition and contribute to gradual decline in lung function. Airflow obstruction results from physical narrowing of the airway, epithelial remodeling, and airway collapse secondary to alteration of airway surface tension. Chronic bronchitis is at one end of the classic COPD spectrum, with emphysema on the other, and most patients lie somewhere in between.² Studies in animal models suggest that chronic bronchitis resembles the natural defense against viral infection and therefore is in a way an exaggerated normal immune response.³

The diagnosis of chronic bronchitis is entirely clinical and is based on symptoms of bronchial hypersecretion, chronic productive cough, expectoration, and phlegm production. A generally held definition for chronic bronchitis is chronic cough and sputum production for at least 3 months per year for at least two consecutive years, in the absence of other known causes.² It is often separated into patients with or without airway obstruction on pulmonary function tests and presence of asthma or emphysema. Population estimates of the prevalence of chronic bronchitis vary by population and definition, and range from 3.4% to 22% of the population, with current and former smokers at the higher end.²

Acute exacerbations of chronic bronchitis affect a significant proportion of patients with chronic bronchitis and are usually related to bacterial infection.⁴ Patients with chronic bronchitis are more susceptible to this than those at the emphysema or asthma ends of the spectrum.⁵

Neither chest radiograph nor high-resolution computed tomography is particularly useful in the diagnosis of patients with chronic bronchitis, other than excluding other diseases. A variety of computed tomography findings can be observed, but they are considered nonspecific, subjective, and poorly reproducible. The finding of bronchial wall thickening, for example, is neither particularly sensitive nor specific for chronic bronchitis.⁶

Because chronic bronchitis is clinically diagnosed, tissue sampling is not performed for establishing the diagnosis. However, transbronchial biopsies may be performed to rule out specific infections, eosinophilic bronchitis or bronchiolitis, or other causes of airway inflammation, such as sarcoidosis. The general features of chronic bronchitis and bronchiolitis are chronic inflammation in the respiratory epithelium, extending into the submucosa and smooth muscle, with increase in submucosal glands and goblet cells, especially in the distal bronchioles (Figs. 30.2 and 30.3). There may be superimposed acute inflammation corresponding typically to bacterial superinfection (Fig. 30.4). Although there are frequently coexisting features of asthma, including mucous plugging and thickened basement membrane, eosinophilic inflammation of the lamina propria is only mild. Increased mucous production may result in extravasation into the surrounding airspaces, in which case a mucinous adenocarcinoma should be excluded by careful histologic inspection (Fig. 30.5). Airway mucus attracts neutrophils, and presence of neutrophils within luminal mucus does not imply acute bronchitis/bronchiolitis.

There have been several studies investigating the histologic findings in chronic bronchitis, generally in the patients with COPD. Tissue samples in these studies are not procured for diagnostic purposes, but for a variety of indications, such as volume reduction, or removal of masses. Patients with chronic bronchitis have greater mucosal inflammation in airways >2 mm luminal diameter and greater submucosal inflammation around mucous glands in bronchi larger than 4 mm diameter.¹ In studies of smaller airways (bronchioles), smokers without chronic bronchitis had more neutrophils, CD8-positive T lymphocytes, and macrophages compared to nonsmokers with and smokers with chronic bronchitis.⁷ Bronchiolar lymphocytic inflammation is related to mucous metaplasia (increase in goblet cells).⁸ In the small airways, the degree of inflammation (including neutrophils, macrophages, T lymphocytes, B lymphocytes, and lymphoid follicles) and amount of luminal mucus show a stepwise increase with the progression of COPD.⁹ A link between epithelial mucin dysregulation and airflow obstruction has been established.¹⁰