Chest
Opinions and HypothesesCOPD: A Dust-Induced Disease?
Section snippets
Respiratory Bronchiolitis and the Pathogenesis of COPD: Anatomic and Physiologic Correlations
The respiratory bronchioles are the “bridge” between bronchioles and alveolar spaces and serve both air-conducting and gas exchange functions. In 1957, Leopold and Gough22 described the anatomic link between respiratory bronchiolitis and emphysema in postmortem studies. In 1974, Niewoehner et al23 reported the consistent finding of respiratory bronchiolitis in young asymptomatic smokers. In the largest published clinicopathologic study of current and ex-smokers, Fraig and colleagues24 confirmed
Respiratory Bronchiolitis and the Pathogenesis of COPD: Radiologic and Histologic Correlations
Early, subclinical COPD and its accompanying small airway disease and emphysema are grossly underestimated by currently available insensitive techniques: chest radiographs and pulmonary function tests (PFTs).23464748 The high-resolution CT scan (HRCT) identifies abnormalities within the secondary pulmonary lobule with detection of structures as small as 0.5 mm in size. The normal respiratory bronchioles, at 0.3 to 0.5 mm, are below the HRCT sensitivity. Nevertheless, inflammation of the
Is Respiratory Bronchiolitis Merely a Surrogate Marker of Cigarette Smoking or Is It Pathogenic for COPD?
Respiratory bronchiolitis is found in the majority of smokers.2324255253 Nevertheless, most smokers (> 70%) do not have clinically significant COPD or airway obstruction.54 This suggests that respiratory bronchiolitis with its accumulation of atypical macrophages in the distal lung may be a marker of cigarette smoking and not a pathogenic step in the development of COPD.24 Nevertheless, a simple explanation for this apparent paradox is proposed. COPD is a complex disease influenced by multiple
Cigarette Smoke Induces Inflammatory Cell Influx Into the Peripheral Lung
The mechanisms for cigarette smoke-induced inflammatory cell and macrophage influx into the lung are various and have been reviewed.411121659 Snider59 has elucidated the cytokines and macrophage products essential to inflammatory cell chemotaxis into the lung.59 Cigarette smoke triggers the activation of nuclear factor-κB in pulmonary epithelial and resident macrophages, promoting transcription of inflammatory genes such as chemoattractant proteins, adhesion molecules, and proinflammatory
Kaolinite Is the Main Component of Intracellular Inclusions in Pulmonary Macrophages
An important clue to the molecule or particulate matter responsible for the inflammatory effect of cigarette smoke comes from the macrophages themselves. The macrophages of smokers contain characteristic brown-pigmented cytoplasmic inclusions believed to be byproducts of cigarette smoke. Brody and Craighead26 performed electron microscopy of the atypical pulmonary macrophages isolated from human smokers. The needle-shaped inclusions, as previously detected by light microscopy, were shown to be
Kaolinosis, a Predominantly Nodular and Fibrotic Pneumoconiosis
Kaolin is mined for commercial use in the preparation of glossy paper, ceramics, adhesives, rubber products, and plastics.73 Mining in the United States is located along a “fall line” that separates the Piedmont plateau and the coastal planes from Georgia to South Carolina.87 Kaolinosis is an occupational lung disease associated with mining and processing of kaolin and kaolinite. Clay obtained during mining is dehydrated by vacuum filtration, air-dried, and purified into kaolin. The respirable
Conclusion
Respiratory bronchiolitis is associated with early emphysema and is perhaps the most common pathologic lesion of human lung. It is a lesion that appears to be reversible on smoking cessation.23245299 We suggest that kaolinite is the inorganic dust component of cigarette smoke that is responsible for the cellular and cytokine responses necessary for the development of a chronic respiratory bronchiolitis. In the proper detrimental genetic and environmental context, a natural progression from
References (99)
- et al.
Estimates of global mortality attributable to smoking in 2000
Lancet
(2003) - et al.
Chronic obstructive pulmonary disease
Lancet
(2003) Cigarette smoke-induced airway inflammation as sampled by the expired breath condensate
Am J Med Sci
(2003)Evolving concepts in the pathogenesis of chronic obstructive pulmonary disease
Clin Chest Med
(2000)- et al.
Electron microscopic observations on pulmonary fibrosis and emphysema in smoking dogs
Exp Mol Pathol
(1971) - et al.
Contribution of emphysema and small airways in COPD
Chest
(1996) Overview of the pathology of pulmonary emphysema in the human
Clin Chest Med
(1983)- et al.
The epidemiology of emphysema
Clin Chest Med
(1983) Imaging of small airways diseases
Clin Chest Med
(1993)- et al.
Small airway diseases
Radiol Clin North Am
(1998)
Genetic influences in the development of emphysema in persons with normal serum proteins
Clin Chest Med
Changing smoking patterns and mortality from chronic obstructive pulmonary disease
Prev Med
Macrophages and the pathogenesis of COPD
Chest
Oxidative metabolism of alveolar macrophages from young asymptomatic cigarette smokers: increased superoxide anion release and its potential consequences
Chest
Respiratory bronchiolitis-associated interstitial lung disease
Clin Chest Med
Respiratory bronchiolitis-associated interstitial lung disease and its relationship to desquamative interstitial pneumonia
Mayo Clin Proc
Evidence-based health policy: lessons from the Global Burden of Disease Study
Science
Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop summary
Am J Respir Crit Care Med
Emphysema: the first two centuries–and beyond; a historical overview, with suggestions for future research: part 1
Am Rev Respir Dis
Smoking and health. Report of the Advisory Committee to the Surgeon General of the Public Health Service
Effect of cigarette smoking on evolution of ventilatory lung function in young adults: an eight year longitudinal study
Thorax
Cigarette smoking: objective evidence for lung damage in teen-agers
Science
Emphysema: the first two centuries–and beyond; a historical overview, with suggestions for future research: part 2
Am Rev Respir Dis
New concepts in chronic obstructive pulmonary disease
Ann Rev Med
Cellular and structural bases of chronic obstructive pulmonary disease
Am J Respir Crit Care Med
Chronic obstructive pulmonary disease
N Engl J Med
Inhibition of VEGF receptors causes lung cell apoptosis and emphysema
J Clin Invest
Role of latent viral infections in chronic obstructive pulmonary disease and asthma
Am J Respir Crit Care Med
Hypothesis: does COPD have an autoimmune component?
Thorax
The nature of small-airway obstruction in chronic obstructive pulmonary disease
N Engl J Med
On the progressive nature of emphysema: roles of proteases, inflammation, and mechanical forces
Am J Respir Crit Care Med
The centrilobular form of hypertrophic emphysema and its relation to chronic bronchitis
Thorax
Pathologic changes in the peripheral airways of young cigarette smokers
N Engl J Med
Respiratory bronchiolitis: a clinicopathologic study in current smokers, ex-smokers, and never-smokers
Am J Surg Pathol
Cigarette smoking, lung inflammation, and the development of emphysema
J Lab Clin Med
Cytoplasmic inclusions in pulmonary macrophages of cigarette smokers
Lab Invest
Bronchiolar inflammation and fibrosis associated with smoking: a morphologic cross-sectional population analysis
Am Rev Respir Dis
Pathogenesis of lesions induced in rat lung by chronic tobacco smoke inhalation
J Natl Cancer Inst
Small airways in COPD
N Engl J Med
The relations between structural changes in small airways and pulmonary-function tests
N Engl J Med
Correlation between the function and structure of the lung in smokers
Am Rev Respir Dis
Morphologic and morphometric effects of prolonged cigarette smoking on the small airways
Am Rev Respir Dis
Morphology of peripheral airways in current smokers and ex-smokers
Am Rev Respir Dis
The detection of small airways disease
Am Rev Respir Dis
Density-dependence of maximal expiratory flow and its correlation with small airway disease in smokers
Am Rev Respir Dis
Radial traction and small airways disease in excised human lungs
Am Rev Respir Dis
Small airways disease in patients without chronic air-flow limitation
Am Rev Respir Dis
Cited by (27)
Differential expression of caveolin-1 during pathogenesis of combined pulmonary fibrosis and emphysema: Effect of phosphodiesterase-5 inhibitor
2020, Biochimica et Biophysica Acta - Molecular Basis of DiseaseCitation Excerpt :Sildenafil treatment significantly decreased the oxidant, ROS and XO levels from 8th to 12th week (Figs. 11b and 12b respectively). Cigarette smoke induced lung diseases are a complex group of disorders that include respiratory bronchiolitis [37], chronic obstructive pulmonary disease (COPD) [38], interstitial lung diseases (ILD), lung cancer, smoking related interstitial fibrosis (SRIF) and the recently described combined pulmonary fibrosis and emphysema (CPFE). Caveolin-1 is differentially expressed in chronic lung diseases.
Pro-inflammatory effects of metals in persons and animals exposed to tobacco smoke
2015, Journal of Trace Elements in Medicine and BiologyCitation Excerpt :In leukocytes, caspase 1 (EC 3.4.22.36) activates IL-18, which acts on several types of cells and stimulates them to produce TNFα [25]. In vitro studies also demonstrated that the exposure of macrophages to kaolinite – a compound of aluminum and silicon – can lead to the production of TNF-α, which intensifies the inflammatory response [84]. It was shown that Al inhaled from tobacco smoke in the form of kaolinite accumulated at the bottom section of the lungs, which could contribute to the recruitment of macrophages in the distal sections of the respiratory tract, leading to their activation and ineffective phagocytosis.
Respiratory consequences of red sludge dust inhalation in rats
2012, Toxicology LettersCitation Excerpt :Since a substantial proportion of the particles in our study were in this size range, the involvement of this mechanism is expected. Chronic dust inhalation drives the influx of macrophages and other inflammatory cells, and these factors may lead to the progress of chronic lung diseases such as asthma (Andersen et al., 2008; Dong et al., 2005), emphysema, bronchiolitis (Girod and King, 2005) or fibrosis (Oberdorster et al., 1992). The present study investigated the short-term pulmonary consequences of exposure to a high dose of RSD in healthy adult rats, an adequate model of long-term RSD inhalation in adult individuals with normal lungs.
Combination of pulmonary fibrosis and emphysema: Is tobacco once again the protagonist?
2011, Medicina ClinicaCombined Pulmonary Fibrosis and Emphysema
2010, Archivos de BronconeumologiaRapid decline in forced expiratory volume in 1 second (FEV1) and the development of bronchitic symptoms among new chinese coal miners
2007, Journal of Occupational and Environmental Medicine
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