Pathologic Changes in the Peripheral Airways of Young Cigarette Smokers

Niewoehner, Dennis E.; Kleinerman, Jerome; Rice, Donald B.

doi:10.1056/nejm197410102911503

Cited by 851 publications

(420 citation statements)

References 14 publications

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“…SOBONYA and KLEINERMAN [38] found that the percentage of the wall in central airways that was occupied by smooth muscle ranged from 3.5±8% in smokers (mean age 32 yrs) and controls (mean age 26 yrs) with no significant difference between the two groups. An earlier study [39] found no increase in scores for amounts of smooth muscle in the small airways of young smokers, compared with nonsmokers, although higher scores for inflammation were observed. Using similar methods, COSIO et al [31] showed that higher scores for inflammation and for smooth muscle were present in older smokers; however, some of these patients had developed emphysema too, and fibrosis of the small airways was increased.…”

Section: Chronic Obstructive Pulmonary Disease and Chronic Bronchitismentioning

confidence: 69%

Airway smooth muscle in health and disease; methods of measurement and relation to function

James¹,

Carroll²

2000

Eur Respir J

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Smooth muscle is present and probably functional in the airways in utero and increases in absolute area during growth with little further change during adulthood. It encircles the entire airway below the level of the main bronchus, in a roughly circular orientation, except at high lung volumes. It occupies relatively more of the airway wall in the peripheral airways, reaching a maximum in the membranous bronchioles. Measurement of smooth muscle area in the airway wall is confounded by clinical classification of cases, methods of tissue retrieval and preparation, staining and orientation of sections, magnification, image analysis and statistical methods of comparison between groups. Airway smooth muscle area is pathologically increased in inflammatory conditions of the airways such as chronic obstructive pulmonary disease, in relation to airways obstruction, and asthma, in relation to severity and airway size (between 25 and 250% compared with control cases). It is increased in sudden infant death syndrome, but there are few studies in other conditions such as bronchiectasis. In asthma, smooth muscle must shorten (not necessarily to an abnormal degree) for the structural abnormalities of the airway to manifest as excessive airway narrowing. Not surprisingly there is renewed interest in the relationships between the mechanical and contractile properties of smooth muscle, parenchymal properties and lung volume and how these interact to determine smooth muscle length. The relative importance of smooth muscle area and mechanical properties, altered airway structure and airway inflammation in disease are yet to be determined.

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Section: Chronic Obstructive Pulmonary Disease and Chronic Bronchitismentioning

confidence: 69%

Airway smooth muscle in health and disease; methods of measurement and relation to function

James¹,

Carroll²

2000

Eur Respir J

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“…13 Finally, post-mortem examinations have shown that many smokers have histopathological features of respiratory bronchiolitis. 31 …”

Section: Limitationsmentioning

confidence: 99%

Evaluation of Electronic Cigarette Liquids and Aerosol for the Presence of Selected Inhalation Toxins

Farsalinos

Kistler

Gillman

et al. 2014

Nicotine &Amp; Tobacco Research

271

217

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Introduction: The purpose of this study was to evaluate sweet-flavored electronic cigarette (EC) liquids for the presence of diacetyl (DA) and acetyl propionyl (AP), which are chemicals approved for food use but are associated with respiratory disease when inhaled. Methods: In total, 159 samples were purchased from 36 manufacturers and retailers in 7 countries. Additionally, 3 liquids were prepared by dissolving a concentrated flavor sample of known DA and AP levels at 5%, 10%, and 20% concentration in a mixture of propylene glycol and glycerol. Aerosol produced by an EC was analyzed to determine the concentration of DA and AP. Results: DA and AP were found in 74.2% of the samples, with more samples containing DA. Similar concentrations were found in liquid and aerosol for both chemicals. The median daily exposure levels were 56 μg/day (IQR: 26-278 μg/day) for DA and 91 μg/day (IQR: 20-432 μg/day) for AP. They were slightly lower than the strict NIOSH-defined safety limits for occupational exposure and 100 and 10 times lower compared with smoking respectively; however, 47.3% of DA and 41.5% of AP-containing samples exposed consumers to levels higher than the safety limits. Conclusions: DA and AP were found in a large proportion of sweet-flavored EC liquids, with many of them exposing users to higher than safety levels. Their presence in EC liquids represents an avoidable risk. Proper measures should be taken by EC liquid manufacturers and flavoring suppliers to eliminate these hazards from the products without necessarily limiting the availability of sweet flavors.

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“…It has become apparent that these two pathological alterations can be found in many patients with COPD [2] . Niewoehner and coworkers demonstrated that early structural changes in the small airways existed even before the establishment of COPD [3] . Subsequent studies consistently showed that small airway remodeling was pivotal in causing airflow limitation in patients with COPD [4][5][6] .…”

Section: Introductionmentioning

confidence: 99%

Chemokine receptor CXCR3 is important for lung tissue damage and airway remodeling induced by short-term exposure to cigarette smoking in mice

et al. 2010

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Aim: To investigate the role of chemokine receptor CXCR3 in cigarette smoking (CS)-induced pulmonary damage. Methods: CXCR3 knockout (CXCR3-/-) mice were used. Differences in airspace enlargement, mRNA expression of matrix metalloproteinases (MMPs), transforming growth factor (TGF) β1, CXCL10 in lung homogenates, and CXCL10 content in bronchoalveolar lavage (BAL) fluids and homogenates were compared between CXCR3-/-mice and wild-type (WT) mice three days after three-day CS exposures. Results: The linear intercept was significantly less in CXCR3-/-mice than in WT mice (30.1±0.9 µm vs 40.3±2.4 µm, P<0.01). Morphologically, collagen was deposited less around airways and vessels in CXCR3-/-mice. The lung hydroxyproline content was significantly lower in CXCR3-/-mice than in WT mice (6.0±1.0 µg/mL vs 12.0±1.6 µg/mL, P<0.05). Profoundly lower mRNA expression of MMP2, MMP12, TGFβ1, and CXCL10 was seen in lung homogenates from CXCR3-/-mice. CXCL10 concentrations in BAL fluid and lung homogenates were significantly lower in CXCR3-/-mice than in WT mice (BAL fluid: 19.3±1.4 pg/mL vs 24.8±1.6 pg/mL, P<0.05; lung homogenates: 76.6±7.0 pg/mL vs 119.5±15.9 pg/mL, P<0.05). Conclusion: CXCR3 is important in mediating lung tissue damage and airway remodeling following a short-term CS insult, possibly through up-regulation of CXCL10 and inducement of mRNA expression of MMPs. Targeting CXCR3 may be helpful for prevention of CSinduced pulmonary pathology.

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Pathologic Changes in the Peripheral Airways of Young Cigarette Smokers

Cited by 851 publications

References 14 publications

Airway smooth muscle in health and disease; methods of measurement and relation to function

Airway smooth muscle in health and disease; methods of measurement and relation to function

Evaluation of Electronic Cigarette Liquids and Aerosol for the Presence of Selected Inhalation Toxins

Chemokine receptor CXCR3 is important for lung tissue damage and airway remodeling induced by short-term exposure to cigarette smoking in mice

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