lung diseases caused by smoking

in addition to causing lung cancer and copd, smoking increases the risk of death from pneumonia and causes chronic bronchitis (u.s. department of health and human services [usdhhs] 2004). exhaled breath condensate provides information about the composition of epithelial lining fluid (elf) that can be used to detect inflammation and redox disturbance (paredi et al. notably, cigarette smoking has very strong oxidant potential in that both the gas and tar phases contain high concentrations of free radicals (repine et al. particles of this size penetrate to and are deposited in the deep lung. subsequent studies of lung tissue surgically removed from cancer patients (figure 7.3) have shown that the symptoms of chronic bronchitis are associated with an inflammatory response involving the mucosal surface, submucosal glands, and gland ducts, particularly in the small bronchi that are 2 to 4 millimeters (mm) in diameter (mullen et al. studies reported from the laboratory of snider and associates in israel (breuer et al. the measurements used were fev1 and fev1/ fvc (pauwels et al. acute exacerbations, a concern in treatment of copd, are attributed to viral infections (monto et al. direct measurements of pressures and flows within the lung have shown that the small bronchi and bronchioles (<2 mm in diameter) are the major sites of airway obstruction in copd (hogg et al. in addition, cross-sectional studies of the pathology of copd have shown that the peripheral inflammatory immune process found in the lungs of all smokers is amplified in severe (gold stage 3) and very severe (gold stage 4) copd (fletcher et al. an important study from the united kingdom (ryder et al. in one six-year study of 131 patients (kessler et al. when pulmonary hypertension is absent at rest, but present during exercise, some of the increase in pulmonary vascular pressures can be attributed to the mechanical events associated with dynamic hyperinflation of the lung in persons with airflow limitation (horsfield et al. 2000), does not appear to be related to the severity of the pulmonary hypertension or the vascular response to oxygen in patients with copd (wright et al. impairment of these defenses increases the potential for infection (knowles and boucher 2002; drannik et al. smoking cessation slows the rate of decline in lung function and delays death (fletcher et al. il-8 is markedly increased in the sputum of patients with copd (keatings et al. the migration of t lymphocytes is controlled by the chemokine receptor cxcr3 that is expressed in human peripheral airways (saetta et al. other studies in humans have shown a relationship among the count of circulating leukocytes, decline in lung function, and risk for early death from copd (chan-yeung et al. the marked increase in the adaptive immune response that occurs in the later stages of the disease has been attributed to antigens introduced by colonization and infection of the lung with microorganisms (sethi et al. the persistent innate and adaptive immune inflammatory response described here is present in the lungs of all long-term smokers and appears to be amplified in those smokers who develop severe copd (figure 7.12) (keatings et al.1996; retamales et al. this tissue is subsequently organized by the processes of angiogenesis and fibrogenesis, which lead to the formation of a mature scar (kumar et al. the cells then seek the junctions between alveolar type 1 and 2 epithelial cells to reach the alveolar surface (walker et al. other reports indicate presence in the lung of myofibroblast precursors with a mesenchymal stem cell phenotype that has potential for differentiation along different pathways and for direction of specific types of tissue repair (sabatini et al. inflammation caused by smoking is central in driving these processes, but the heterogeneity of phenotypes among persons with copd remains unexplained (kim et al. the majority of o2•− generated in vivo undergoes reactions that are nonenzymatic or are catalyzed by superoxide dismutase (sod) and produce h2o2. the inducible form of nos (nos ii) is independent of the calcium ion, and it generates no in large amounts for long periods (wink et al. the amino acid tyrosine is particularly susceptible to nitration with the formation of free or protein-associated 3-nitrotyrosine, which has been used as a marker for the generation of rns in vivo (ramezanian et al. cuznsod, the major intracellular sod, is present in both the cytosol and the nucleus of lysosomes (slot et al. catalase is a tetrameric hemoprotein that undergoes oxidation and reduction at its active site in the presence of h2o2 (chance et al. in healthy nonstressed cells, the intracellular ratio of gsh to gssg is high, which ensures the availability of gsh and thereby promotes active reduction of h2o2 through the gsh system (doelman and bast 1990; bast et al. human lung expresses prxs in bronchial epithelium, alveolar epithelium, and macrophages (kinnula et al. both of these classes of detoxification enzymes are expressed in healthy lungs, predominantly in the airways (anttila et al. free radicals in the tar phase of cigarette smoke, such as the long-lived semiquinone radical (q•−), are organic and can react with o2•− to form •oh and h2o2 (nakayama et al. in smokers, inflammation is a characteristic feature of the lungs and other organs (saetta et al. ros released from type ii cells are able, in the presence of mpo, to inactivate aat in vitro (wallaert et al. no is produced in the lungs by the catalytic activity of nos as a marker of inflammation and indirectly as a marker of oxidative stress, and it can be measured in exhaled breath. the hypothesis was that reduced levels of vitamin c in smokers are due to the activation of leukocytes and subsequent generation of ros (winklhofer-roob et al. exposure to cigarette smoke was also shown to activate the pentose phosphate pathway, which is a source of nadph for the enzyme grx in endothelial cells (noronha-dutra et al. exposure of neutrophils and alveolar macrophages to cigarette smoke produces morphologic changes in the cells that result in cell blebbing, which indicates oxidant-induced damage (lannan et al. 1987) and increases levels of gssg (cavarra et al. these findings suggest a role for oxidative stress in the development of emphysema (rangasamy et al. after exposure to cigarette smoke, recombinant sod has been shown to reduce the inflammatory response in several ways: by decreasing the inflammatory response in the lungs, reducing the influx of neutrophils, decreasing il-8 gene expression and release, and decreasing nf-κb activation (nishikawa et al.

in this study, release of o2•− by air space leukocytes increased after exposure to smoke (morrison et al. the numbers of neutrophils in the blood and bal fluid from long-term smokers are higher than in those from nonsmokers (hunninghake and crystal 1983; kuschner et al. in contrast, the number of cdb-positive cells and the ratio of cd4+ to cd8+ cells are not affected by acute exposure to cigarette smoke (hockertz et al. the ratio of gsh to gssg, which reflects oxidative stress, has been shown to decrease after acute exposure in both animal and in vitro studies but not in a single human study (morrison et al. the technique of spin trapping has been applied to measure bal fluid in patients with copd and has shown increased ros (pinamonti et al. exhaled carbon monoxide, as a measure of the response of heme oxygenase to oxidative stress, has been shown to be elevated in exhaled breath in persons with copd compared with that in persons without copd (montuschi et al. other markers of oxidative stress, such as 8-oh-dg and 4-hne, have been shown to have increased expression associated with emphysematous lesions in the lungs (tuder et al. oxidant-generating systems such as xanthine and xanthine oxidase have been shown to cause the secretion of mucus from airway epithelial cells (adler et al. the release of nf-κb is a critical event in the inflammatory response and is redox sensitive (janssen-heininger et al. nuclear binding of nf-κb is increased in the airway macrophages and airway epithelial cells of copd patients (di stefano et al. the exact role of oxidative stress in modifying hat and hdac activity is unknown, but it appears that oxidative stress can result in increased hat activity and decreased hdac activity (gilmour et al. one hypothesis is that loss of alveolar endothelial cells by apoptosis may be an initial event in the development of emphysema (tuder et al. in addition, increased levels of nitrotyrosine have been shown to occur in the plasma of copd patients (ichinose et al. several studies have shown evidence of increased oxidative stress in patients with copd both locally and systemically, particularly during exercise (couillard et al. in addition, exercise increases the activity of xanthine and xanthine oxidase, a further source of ros (andrade et al. the *m allele accounts for more than 95 percent of the pi alleles in u.s. populations and is associated with normal serum levels of aat (brantly et al. molecular genotyping by polymerase chain reaction can distinguish the common pi alleles (*m, *s, and *z) with use of dna from a variety of cellular sources (von ahsen et al. the pi *z type is a major risk factor for copd, and cigarette smoking increases the risk for copd in persons with the pi *z allele (silverman et al. comparison of correlations between monozygotic and dizygotic twins allows for estimating the heritability of lung function, the percentage of total phenotypic variation in lung function that is related to genetic factors. among non-smokers who were first-degree relatives of these probands with early-onset copd, fev1 and fev1/fvc values were similar to those in nonsmokers in the control group. the score of the logarithm of the odds (lod) ratio, or likelihood ratio, was 2.4. in a subset of this study population, flanking short tandem repeat (str) markers were genotyped to increase the information available for link-age analysis, and significant linkage of fev1 to chromosome 6q was identified with a maximum lod score of 5.0 (wilk et al. overall, the linkage results of quantitative spirometric measurements in the persons with pedigrees from the boston early-onset copd study (hersh et al. 2000; he et al. 2000; sandford et al. significant differences between murine strains in susceptibility to the development of smoking-induced copd have been demonstrated (guerassimov et al. however, in emphysema induced by tobacco smoke, the lung tissue exhibits active synthesis of extracellular matrix (lang et al. the role of lymphocytes in emphysema has been a topic of research over the past decade (finkelstein et al. 1999), and the presence of emphysema adversely influences the recovery of bal fluid (löfdahl et al. in one study, levels of the extracellular mmp inducer, basigin, a trans-membrane protein that stimulates production of several mmps, were much higher in bal fluid from current and former smokers than from those who never smoked (betsuyaku et al. promising techniques are becoming available for analysis of the products of alveolar macrophages in association with smoking, copd, and emphysema (koike et al. the clumps appear to be from synthesis of new aberrant elastin, resembling changes observed in experimental elastase-induced emphysema (kuhn et al. as noted previously, elastic fibers in emphysematous lung tissue show disruptions and fenestrations of the elastin (fukuda et al. these animals provide the convenience of genetic manipulation, and findings indicate that humans and mice may have shared susceptibility factors for exposure to smoke (shapiro et al. overexpression of certain proteins in the lung (e.g., il-13) can lead to emphysema without exposure to an exogenous factor (table 7.11) (zheng et al. the evidence suggests that neutrophil elastase is the principal culprit in matrix degradation and that macrophage elastase acts, at least partly, as a proinflammatory agent by facilitating release of tnfα (churg et al. in contrast to findings in the lungs of nonsmokers, apoptotic epithelial cells are identifiable in the lungs of smokers (segura-valdez et al. in the caspase-3 study (aoshiba et al. in humans, smoking is followed by a rise in markers of systemic oxidative stress and of oxidative stress affecting the lungs more specifically. this chapter offers the conclusion that protease-antiprotease imbalance is involved in the development of emphysema and sufficient by itself to produce it. human evidence comes from the long-described and well- documented occurrence of early-onset emphysema in smokers with low levels of aat consequent to mutations of serpina1. the source of antigen that drives this sharp increase in the adaptive immune response is unknown and may be related to either the colonization or infection of the lower airways by a variety of microbes in the later disease stages or to autoantigens that develop in the damaged tissue. a major difference between this process and that observed in the lung tissue of tobacco smokers is persistent stimulation of the tissue by tobacco smoke as it heals, resulting in a persistent inflammatory immune response. (1) smoke components recruit inflammatory cells to the lower respiratory system via factors released from alveolar macrophages and structural cells of the lungs.

the cause–effect relationship between a history of cigarette smoking and chronic obstructive pulmonary disease (copd), emphysema and lung cancer is embedded in a heritage of older studies, although new approaches, classifications and imaging techniques and new treatments have been proposed over the past two decades. panlobular emphysema is the hallmark of lung disease, particularly in subjects with a history of smoking, and with α1-antitrypsin deficiency (aatd).

most new diagnoses of lung cancer are made at an advanced disease stage and >50% of these patients will have involvement of the central airways 12. this can be in the form of bulky endobronchial disease, endobronchial extension or extrinsic compression of the airways by the tumour. pathophysiology of the syndrome beyond the obvious role of tobacco smoking remains to be explored 15. suspected in patients with dyspnoea and basal crackles unexplained by spirometry, the syndrome of cpfe can be recognised by the presence of both “significant” emphysema and fibrosis features on hrct of the chest. in the future, we need more studies on the long-term effects of rehabilitation and physical activity in copd and other smoking-related lung diseases, and new and simpler tools for the classification of sr-ilds.

in fact, smoking is directly responsible for almost 90% of lung cancer and copd deaths. even with antismoking campaigns and health warnings, many people 1. lung cancer 2. copd (chronic obstructive pulmonary disease) 3. heart disease 4. stroke 5. asthma 6. reproductive effects in women 7. the principal nonmalignant respiratory diseases caused by cigarette smoking—copd, emphysema, chronic bronchitis, and asthma—are defined in table 7.2., .

lung diseases caused by smoking include copd, which includes emphysema and chronic bronchitis. cigarette smoking causes most cases of lung cancer. if you have smoking causes cancer, heart disease, stroke, lung diseases, diabetes, and chronic obstructive pulmonary disease (copd), which includes emphysema and in this context, cigarette smoking has been associated as a causative agent in some diffuse parenchymal lung disorders, like desquamative interstitial pneumonia, . risks of lung diseases from smoking include:chronic bronchitis. this is a type of copd. emphysema. this is also a type of copd. lung cancer. this is an abnormal growth of cells. other types of cancer. smoking increases the risk of cancer of the nose, sinuses, voice box, and throat.

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