Quitting smoking reverses nasal mucosal changes (original) (raw)
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Nasal and systemic inflammatory profile after short term smoking cessation
Respiratory Medicine, 2014
Results: There was a decrease of TNF-a level only in blood serum at 30 days of abstinence compared to current smokers. The mucociliary clearance improved and there was a reduction in exCO and HbCO (p < 0.05 for all) after 30 days of smoking cessation. Conclusion: The short term smoking abstinence decreased systemic inflammation and improved nasal mucociliary clearance, despite not having changed the nasal inflammation. ª
Effect of passive smoking on the ultrastructure of the nasal mucosa in children
The Laryngoscope, 2012
Objectives/Hypothesis: Passive exposure to cigarette smoke has been implicated in a number of respiratory childhood disorders. Most studies concerning smoking were directed to its carcinogenic effect on the lungs. However, the effects of smoking on nasal respiratory mucosa have not been widely studied. The aim of the present study was, therefore, to study the ultrastructural changes in the nasal mucosa of a pediatric population exposed to passive smoking.
Smoking-associated Squamous Metaplasia in Olfactory Mucosa of Patients with Chronic Rhinosinusitis
Toxicologic Pathology, 2009
Few studies have examined the induction of squamous metaplasia in human olfactory nasal tissue caused by tobacco use and the implications it may have for olfaction, particularly when there are pre-existing insults, such as chronic rhinosinusitis (CRS). Quantitative histopathological analyses were performed on Alcian blue-and H&E-stained sections of nasal biopsies taken from the upper aspect of the middle turbinate of CRS patients. Chronic rhinosinusitis patients who were current smokers had a predominance of squamous metaplasia in the olfactory sensory epithelium, whereas CRS patients who were nonsmokers and were not exposed to secondhand cigarette smoke had a prevalence of goblet cell hyperplasia. In spite of this difference, the groups did not differ significantly in olfactory threshold sensitivity. The impact of primary cigarette smoke on olfaction and a possible role of squamous metaplasia in preserving olfactory neurogenesis are discussed.
Evaluation of Smoking as a Modifying Factor in Chronic Rhinosinusitis
JAMA Otolaryngology–Head & Neck Surgery, 2021
Key points: 1)This study sought to determine whether smoking was a risk factor for CRS and whether it has an impact on disease specific quality of life. 2) We found no significant difference in active smoking prevalence by CRS disease (CRSsNPs and CRSwNPs) vs controls. We were able however to demonstrate a significant symptom burden associated with smoking, with significantly worse SNOT-22 scores in the smoking cohort by a mean magnitude of 10 points. 3) Cigarette smoke has a deleterious effect on the quality of life and symptom burden of patients with CRS and clinicians should encourage smoking cessation alongside general CRS medical management.
International Journal of Morphology, 2012
The objective of this study was to evaluate the histopathologic effects of systemic use of nicotine on the rat nasal mucosa. Twelve adult Sprague-Dawley rats weighing 180-220 g, were used as experimental animals. The rats were divided into Nicotine and control groups. The rats of Nicotine groups (n=6) were administered 2mg/kg Nicotine sulphate for 28 days. The rats of control group (n=6) were only administered 1,5 ml physiologic saline solution subcutaneously for 28 days. All animals were sacrified at the end of the study and nasal tissue samples were removed and prepared for histologic examination. The sections were stained with Hematoxylin and Eosin (H-E) and Periodic acid-Schiff (PAS) and Trichrome-Masson were observed under light microscope. E-cadherin immunreactivity of pseudostrafied epithelial cells of nasal mucosa was assessed by immunohistochemical staining. There were significant differences in average histopathological score between the groups treated and non-treated to nicotine. In nicotine group, degenerative change of epithelial cells and hypertrophy of goblet cells were observed. Leukocytes infiltration was observed in significant areas of connective tissue. Ecadherin expression was significantly decreased in epithelial cells of the nasal mucosa of Nicotine group.
Inflammatory features of nasal mucosa in smokers with and without COPD
Thorax, 2004
To investigate whether nasal and bronchial inflammation coexists in chronic obstructive pulmonary disease (COPD), nasal and bronchial biopsy specimens from seven control subjects, seven smokers without COPD, and 14 smokers with COPD were studied. Nasal and bronchial biopsy specimens were taken from the same patients during bronchoscopy and squamous cell metaplasia and the thickness of the epithelium and basement membrane were measured. The numbers of eosinophils (EG2), neutrophils (elastase), macrophages (CD68), and CD8 T lymphocytes (CD8/144B) were assessed by immunohistochemistry. Smokers with and without COPD had squamous metaplasia in the nasal and bronchial epithelium. In all groups the thickness of the nasal epithelium was greater than that of the bronchial epithelium. The thickness of the basement membrane was similar in nasal and bronchial biopsy specimens from smokers with and without COPD, but was greater in the bronchi than in the nasal epithelium of controls. Eosinophil number was higher in the nasal and bronchial mucosa of smokers without COPD than in smokers with COPD or controls. Neutrophil number was higher in the nasal and bronchial mucosa of smokers with COPD than in smokers without COPD or controls. CD8 T lymphocyte numbers were similar in smokers with and without COPD and higher than in controls. There were fewer macrophages in nasal and bronchial biopsy specimens from smokers without COPD than in those with COPD. Nasal and bronchial inflammation coexists in smokers and is characterised by infiltration of CD8 T lymphocytes. In smokers without COPD this feature is associated with an increased number of eosinophils, while in those with COPD it is linked to an increased number of neutrophils in both nasal and bronchial biopsy specimens.
2017
Aim: To evaluate the association between active smoking, second hand tobacco smoke (SHS) exposure and chronic rhinosinusitis (CRS). Material and methodology: 100 cases with a confirmed diagnosis of CRS, were evaluated with anterior rhinoscopy, nasal endoscopy and plain radiography & CT scans of paranasal sinuses. A validated questionnaire was used to assess past and present active smoking and SHS. Results: CRS cases exposed to active smoking (n=21) and SHS (n=28) had worse mean scores in nasal endoscopy Lund-Kennedy scores, being 8.61 for active smokers and 8.07 for SHS, than cases without smoking exposure (n=51) being 7.30. CRS cases exposed to active smoking (n=21) and SHS (n=28) had worse mean scores in Lund-Mackay staging system on CT Scans, being 10.43 for active smokers and 9.37 for SHS, than cases without Smoking exposure (n=51) for which it was 7.67. Conclusion: Tobacco smoke exposure has been found to a significant risk factor for CRS. Cigarette smoke, either through active...
Detection of Cytomorphological Changes in Nasal Cavity amongSudanese Cigarette Smokers
IOSR Journal of Dental and Medical Sciences, 2016
A case-control study of cytological changes in nasal cavity smear among smokers people was conducted to test the hypothesis that exposure to cigarette tobacco smoke can make cytological change in nasal cavity. This study was conducted in eastern Sudan in Port – Sudan city during 9th of January 2016 to 30 may 2016. Include 140 people, 70 smoker people considered to be the case group and 70 non-smoker considered to be control group. Nasal mucosal smear using different method of stain (papanicolaou and grun Wald Giemsa stain). The result obtained indicated smoking causes change on the cells we found many cytological changes among case group ranged from 5% metaplasia change , 25% micro nuclear change and 20% normal epithelial cells in case group ,while 49% normal epithelial cell , 1% micro nuclear changes there was no metaplastic changes showed in control group . In conclusion, the results of current study indicate different rates of epithelial change in nasal cavity among smokers and nonsmokers and higher proliferative activity in cigarettes smoking compared to nonsmoking .Also, our results suggest a possible relationship between the number of cigarettes per day and duration can increase in the rate of cellular proliferation.
Respirology, 2011
Methods: Thirty-three current smokers enrolled in a SC intervention programme were evaluated after they had stopped smoking. Smoking history, Fagerström's test, lung function, exhaled carbon monoxide (eCO), carboxyhaemoglobin (COHb) and nasal MC as assessed by the saccharin transit time (STT) test were evaluated. All parameters were also measured at baseline in 33 matched non-smokers. Results: Smokers (mean age 49 Ϯ 12 years, mean pack-year index 44 Ϯ 25) were enrolled in a SC intervention and 27% (n = 9) abstained for 180 days, 30% (n = 11) for 120 days, 49.5% (n = 15) for 90 days or 60 days, 62.7% (n = 19) for 30 days and 75.9% (n = 23) for 15 days. A moderate degree of nicotine dependence, higher education levels and less use of bupropion were associated with the capacity to stop smoking (P < 0.05). The STT was prolonged in smokers compared with non-smokers (P = 0.002) and dysfunction of MC was present at baseline both in smokers who had abstained and those who had not abstained for 180 days. eCO and COHb were also significantly increased in smokers compared with non-smokers. STT values decreased to within the normal range on day 15 after SC (P < 0.01), and remained in the normal range until the end of the study period. Similarly, eCO values were reduced from the seventh day after SC. Conclusions: A SC programme contributed to improvement in MC among smokers from the 15th day after cessation of smoking, and these beneficial effects persisted for 180 days.
Characterization of Smoking-Induced Nasopharyngeal Lymphoid Hyperplasia
The Laryngoscope, 1997
The frequency of smoking-induced nasopharyngeal lymphoid hyperplasia in heavy smokers and its potential clinical implications are still unknown. Precise criteria to differentiate this entity from other types of nasopharyngeal lymphoid hyperplasia are needed. A prospective clinicopathological study of smoking-induced nasopharyngeal lymphoid hyperplasia was conducted in 17 heavy smokers. Ten nonsmoking patients, five of them with chronic sinusitis, three with adult-onset adenoid hypertrophy, and two children with adenoidal hypertrophy served as a control group. Both in smokers and in nonsmokers, lymphocytic infiltration of the mucosa was characterized immunohistochemically as T cells. In smokers, semithin (1 micron) sections revealed deformed and migrating cytotoxic lymphocytes in the nasopharyngeal mucosa. The lymphocytes were attached to epithelial, ciliated, and goblet cells, resulting in cell damage. Transmission electron microscopy of biopsies from smokers revealed emperipolesis, characterized by mucosal invasion and epithelial cell damage by an unusual population of migrating T lymphocytes that penetrate them. These findings confirm a direct effect of smoking on the nasopharyngeal lymphoid tissue, which forms part of the immune system. It is concluded that the diagnostic evaluation and therapeutic approach of heavy smokers with otological and airway symptoms should be based on thorough endoscopic examination of the nasopharynx. When the diagnosis is not clear-cut, selective tele-endoscopic biopsy and electron microscopic examination are recommended. This entity should be added to the list of known clinical manifestations of the smoking habit.