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PubMed2003

Flow-cytometric analysis of T-lymphocyte subsets after different treatment methods in smokers and non-smokers with chronic periodontitis.

AIM: To determine any change in T-lymphocyte subsets after applying different treatment methods in smokers and non-smokers with chronic periodontitis. PARTICIPANTS: 50 adults with chronic periodontitis. METHOD: The subjects were divided into smokers and non-smokers. Biopsy samples were taken from the gingival pocket wall tissues at sites with chronic periodontitis before treatment, after initial treatment, after curettage and after flap operation and tested for CD4+, CD8+ lymphocyte and CD4/ CD8 ratio values. Gingival pocket depth, gingival index (GI-Löe-Silness) and plaque index (PI-Silness-Löe) scores were also recorded. Analysis aimed at determining the relation between the clinical measurements and the laboratory results. RESULTS: Flow cytometry findings in both groups showed that CD4+ and CD8+ lymphocyte values before treatment were under the normal value while the CD4+/CD8+ ratio was within normal distribution interval. The lymphocyte values observed in the smokers were found to be lower than those in the non-smokers. After treatment the difference between the lymphocyte values in smokers and non-smokers was found to be statistically significant. However, the difference between the CD4/CD8 rate obtained in smokers and non-smokers was not found to be statistically significant. CONCLUSIONS: The lymphocyte values observed in smokers were found to be lower than those in non-smokers after applying different treatment methods and the local immune response was poor in the smokers.

Adult↗
PubMed2004

Response of choroidal blood flow to carbogen breathing in smokers and non-smokers.

AIM: To investigate a potential difference in ocular vascular reactivity during carbogen breathing in optic nerve head, choroid, and retina between healthy smokers and non-smokers. METHODS: 25 (13 smokers and 12 non-smokers) healthy male volunteers participated in this observer masked, two cohort study. During inhalation of carbogen (5% CO(2) and 95% O(2)) over 10 minutes measurements were taken using laser Doppler flowmetry to assess submacular choroidal and optic nerve head blood flow, laser interferometry to assess fundus pulsation amplitudes, and retinal vessel analyser (RVA) to assess retinal vessel diameters. RESULTS: At baseline choroidal blood flow was higher (p = 0.018, ANOVA) in smokers than in non-smokers. During administration of carbogen the response in choroidal blood flow was significantly different between the two groups: there was an increase in non-smokers after carbogen breathing (p = 0.048) compared with relatively stable blood flow in smokers (p = 0.049 between groups, ANOVA). A similar response pattern was seen for fundus pulsation amplitude, which increased notably after carbogen breathing in non-smokers but not in smokers (p<0.001 between groups, ANOVA). Optic nerve head blood flow and retinal vessel diameters were reduced in both groups to a comparable degree during carbogen breathing. CONCLUSION: The study indicated abnormal choroidal vascular reactivity in chronic smokers. These early haemodynamic changes may be related to the increased risk to smokers of developing ocular vascular diseases. The specific mechanisms underlying abnormal choroidal vascular reactivity in chronic smokers remain to be characterised.

Adult↗
PubMed1983

Packed cell volume, haemoglobin, and oxygen saturation changes in healthy smokers and non-smokers.

We have investigated the relationship between cigarette smoking, packed cell volume, haemoglobin concentration, and arterial oxygen saturation (SaO2) in 114 non-smokers, 66 light smokers (1-20 cigarettes a day), and 50 heavy smokers (over 20 cigarettes a day) aged 20-75 years. Packed cell volume was greater in female heavy smokers (p less than 0.001) over 40 years of age and in all female smokers over 60 years (p less than 0.001) than in non-smoking contemporaries. Haemoglobin concentrations were higher in 40-59 year old female heavy smokers (p less than 0.05) and in male and female light (p less than 0.05) and heavy smokers (p less than 0.001) over 60 years of age than in non-smoking contemporaries. SaO2 was lower in 20-39 year old male heavy smokers (p less than 0.02) and female (p less than 0.05) light smokers and also in 40-59 year old male light and heavy smokers (p less than 0.001) and female light smokers (p less than 0.02) than in non-smoking contemporaries. It was also lower in female light (p less than 0.05) and heavy (p less than 0.02) smokers over 60 years, whereas it was higher in male light smokers over 60 (p less than 0.001). Changes in SaO2 were seen at a younger age than changes in haemoglobin concentration and packed cell volume.

Adult↗
PubMed1988

Changes in bronchial responsiveness to inhaled histamine over four years in middle aged male smokers and ex-smokers.

Bronchial hyperresponsiveness to inhaled histamine in smokers is associated with an accelerated annual decline in FEV1 and low baseline FEV1 values. The evolution of bronchial hyperresponsiveness and whether it precedes or follows the accelerated decline in FEV1 and reduction in FEV1 is unknown. Measurements of the provocative concentration of inhaled histamine required to reduce FEV1 by 20% (PC20) were repeated after a four year interval in 27 male smokers (mean age 59 years, smoking on average 27 cigarettes a day in 1986) and 16 men who were ex-smokers in 1982 and who remained non-smokers until 1986 (mean age 53 years in 1986). These men were originally recruited to a prospective study in 1974 and had their first PC20 measurement in 1982. PC20 was positively related to baseline FEV1 in both smokers and ex-smokers in both 1982 and 1986 (r ranging from 0.56 to 0.76, p less than 0.01). In smokers mean FEV1 fell from 83% to 77% predicted (p less than 0.001) and geometric mean PC20 from 7.11 to 3.27 mg/ml (p less than 0.001) between 1982 and 1986. The change in PC20 in individual smokers over the four years was related to change in FEV1 (p = 0.012). In ex-smokers mean FEV1 was 93% predicted both in 1982 and in 1986 and there was no significant difference in geometric mean PC20 between 1982 (6.68 mg/ml) and 1986 (5.98 mg/ml). Thus in smokers there was an accelerated annual decline in FEV1 and an increase in bronchial hyperresponsiveness as FEV1 fell. The ex-smokers had comparable levels of bronchial hyperresponsiveness in 1982. Mean PC20 values were unchanged in 1986 in these men, who showed a normal age related decline in FEV1. These longitudinal results emphasise the importance of baseline airway geometry in influencing bronchial hyperresponsiveness to histamine in middle aged smokers and ex-smokers.

Airway Resistance↗
PubMed1991

Difference in pulmonary absorption of inhaled terbutaline in healthy smokers and non-smokers.

Pathophysiological studies have shown that the alveolocapillary transfer of small solutes is much faster in healthy smokers than in non-smokers. The effects of smoking on the pulmonary absorption of inhaled terbutaline were examined in normal subjects. Nine healthy smokers and 13 healthy non-smokers inhaled nebulised terbutaline and dry terbutaline powder on two study days. Plasma concentrations of terbutaline were measured up to 240 minutes after the inhalation. The plasma concentration of terbutaline rose much faster in smokers than in non-smokers, the mean time to peak terbutaline concentration being 17 minutes in the smokers and 50 minutes in the non-smokers. The peak plasma concentration was nearly twice as high in the smokers as in the non-smokers, being 21 mmol/l and 23 mmol/l for the dry powder inhalation and nebuliser respectively in the smokers and 12 mmol/l and 14 mmol/l in the non-smokers. It is concluded that smoking increases the rate of terbutaline absorption and the peak plasma concentration achieved. The rapid pulmonary absorption of terbutaline in smokers may affect the onset of action of the drug and the duration of its therapeutic effects.

Administration, Inhalation↗
PubMed1997

Differential inhibition of inflammatory cytokine release from cultured alveolar macrophages from smokers and non-smokers by NO2.

Human alveolar macrophages (AMs) obtained from smokers and non-smokers by bronchoalveolar lavage (BAL) were subjected to various concentrations of NO2 in an inverted monolayer exposure model. Culture supernatants were collected 4 h after the exposure and assayed for secreted TNF-alpha, IL-1 beta, IL-8 and MIP-1 alpha. The steady state levels of the mRNAs for these cytokines were also analysed in the cells. The adherence of BAL cells to plastic prior to exposure to the gas elevated the steady state mRNA levels of all four cytokines tested in smoker's cells and that of TNF-alpha and IL-1 beta, but not IL-8 (MIP-1 alpha not tested), in non-smoker's cells. Interestingly, adherent cells from non-smokers released circa 15-, 3-, 1.5- and 3-fold the amounts of IL-1 beta, IL-8, TNF-alpha and MIP-1 alpha, respectively, than smoker's cells during control incubation or exposure to air. A 20 min exposure to NO2 (5 or 20 p.p.m.) did not increase the secretion of any of the cytokines from either cell type. In contrast, NO2 caused a concentration-dependent inhibition of the secretion of all cytokines except IL-1 beta from smoker's cells. Additionally, NO2 greatly diminished the release of all cytokines in response to further treatment with lipopolysaccharide (LPS). In contrast, only the secretion of TNF-alpha from non-smoker's cells was inhibited by the gas in a concentration-dependent manner, whilst LPS-induced secretion of the cytokines was not affected by the gas. The steady state levels of the respective mRNAs for each of the cytokines were not significantly affected in smoker's cells by exposure to NO2, except for a negative, dose-dependent trend in the case of TNF-alpha. Nitrogen dioxide also failed to elevate the levels of the mRNAs in non-smoker's cells but, again, tended to diminish the levels, particularly of IL-1 beta mRNA. However, exposure to the gas inhibited LPS-induced accumulation of cytokine mRNAs in smoker's cells only. The data suggest that macrophage-derived cytokine mediators of the sepsis response may not play a role in the generation of NO2-induced inflammation in the human lung. Conversely, the gas seems to non-specifically inhibit the release and/or production of cytokines, particularly from smoker's cells, at the post-transcriptional level, and impairs the ability of the cells to increase the transcription and release of the cytokines in response to bacterial LPS. The fact that NO2 seriously impaired the already diminished capacity of smoker's cells to release several important pro-inflammatory cytokines, both under control conditions and in response to LPS, strongly suggest that the inhalation of NO2 in cigarette smoke may contribute to impairing host defence against infection in the lung.

Adult↗
PubMed2003

Promoter hypermethylation of the O6-methylguanine-DNA methyltransferase gene: more common in lung adenocarcinomas from never-smokers than smokers and associated with tumor progression.

Adenocarcinoma (AC) is the most common type of lung cancer diagnosed in the United States, comprising up to 40% of tumors in smokers and 50-80% of tumors in never-smokers. Exposures to cigarette smoke, direct or second-hand, and radiation in the form of radon progeny are the major risk factors for lung AC in both smokers and never-smokers. The goal of the current study was to determine the prevalence for O(6)-methylguanine-DNA methyltransferase (MGMT) promoter methylation in a large sample of central or peripheral ACs from smokers (n = 157), former uranium miners (n = 34), and never-smokers (n = 46). The mutation rate at codon 12 of the K-ras gene was determined to assess whether activation of this oncogene was associated with MGMT methylation. The overall prevalence for MGMT methylation was 51%. Significantly more tumors from never-smokers than smokers exhibited MGMT methylation (66 versus 47%, respectively). In contrast, exposure to radon through uranium mining did not affect the prevalence for methylation. The frequency of MGMT methylation was increased significantly in association with tumor stage. K-ras mutations were detected in 24% of all ACs and 22, 24, and 28% of tumors from never-smokers, smokers, and miners, respectively. Alterations in both the K-ras and MGMT genes were seen in only 11% of ACs. Kaplan-Meier survival estimates did not reveal any difference between patient survival with or without MGMT methylation. In contrast, survival was significantly reduced over the initial 60 months after diagnosis for patients with a transition mutation in the K-ras gene compared with those with a transversion mutation. This investigation demonstrates that MGMT promoter hypermethylation is a common event in the progression of early stage AC of the lung. We have shown that the incidence of MGMT methylation was significantly higher in never-smokers than smokers and have detected a higher frequency of mutations within the K-ras gene than previously reported in never-smokers. This study also suggests that K-ras activation is independent of MGMT methylation.

Adenocarcinoma↗
PubMed1996

[Comparison of life habits and health examination data between smokers and ex-smokers].

Health practice and health examination data were compared between smokers and ex-smokers in 6,076 male subjects, whose ages ranged from 40 to 59 years, who participated in health examinations in 1993 in 17 towns of Gunma Prefecture. A total of 4,629 (76.2%) subjects replied to the interview on health practice and also had health examination data that could be used. The numbers of smokers and ex-smokers were 2,681 and 245, respectively for a total of 2,926 target population. The percentage for those having breakfast daily was significantly higher in ex-smokers than in smokers in the age 40's group (p < 0.01). The percentage for those doing exercise more than one day a week was significantly higher in ex-smokers than in smokers in the age 50's group (p < 0.05). Mean body mass index (BMI) was significantly higher in ex-smokers than in smokers in the age 40's and 50's groups, with p < 0.05 and p < 0.01, respectively. Mean high-density lipoprotein cholesterol (HDLC) was significantly higher in ex-smokers than in smokers in the age 40's group (p < 0.05). The two way analysis of variance on BMI and HDLC was conducted by smoking and drinking factors. BMI was related to only smoking in the age 40's and 50's groups. Smoking and drinking habit related to HDLC in the age 40's group and the latter habit had a relatively large association to HDLC. From the association between BMI and smoking habit, we speculate that exercise was practiced by ex-smokers due to the obesity potential of the ex-smoking status.

Adult↗
PubMedDate not supplied

DNA adducts in cervical tissue of smokers and non-smokers.

Cervical biopsy samples were taken from 40 women, aged between 31 and 72, undergoing hysterectomies. Twenty-two of the women were smokers, four were ex-smokers and 14 were non-smokers. DNA was isolated and analysed using 32P-postlabelling, after butanol extraction or nuclease P1 digestion enhancement of the adducts. Resolution of the adducts was by thin-layer chromatography on polyethyleneimine (PEI)-cellulose. The pattern of adducts seen was similar to smoking-related adducts detected in other tissues and consisted mainly of a diagonal zone of radioactivity. With the butanol extraction enrichment method, the levels of adducts in DNA from the 22 smokers ranged from 1.65 to 6.04 adducts/10(8) nucleotides (mean = 3.70, SD = 1.36), in DNA from non-smokers from 1.16 to 3.98 (mean = 2.04, SD = 0.77) and in samples from ex-smokers from 2.57 to 3.35 (mean = 2.86, SD = 0.37). The increase in adduct levels in smokers compared with non-smokers was highly significant (Mann-Whitney test p = 0.0005, two-tailed). When analysed by the nuclease P1 digestion enhancement method, total adduct levels in samples from smokers (mean = 2.95, SD = 1.77) were not significantly different (p = 0.3, two-tailed) from levels in non-smokers (mean = 2.34, SD = 0.96). However, the level of a minor discrete adduct spot was significantly lower (p = 0.02, two-tailed) in smokers (mean = 0.19, SD = 0.36) than in non-smokers (mean = 0.39, SD = 0.41). The results indicate that some of the DNA adducts detected in cervical epithelium correlate with tobacco smoking and support the hypothesis that smoking-related cervical cancer results from exposure to genotoxic components of cigarette smoke that become activated to DNA-binding products in this tissue.

Adult↗
PubMed2006

Acute smoke-induced endothelial dysfunction is more prolonged in smokers than in non-smokers.

BACKGROUND: The aim of the study was to compare acute endothelial dysfunction caused by smoking one cigarette between smokers and non-smokers. METHODS: Thirty volunteers, 15 smokers and 15 non-smokers, were asked to smoke the same type of cigarette and endothelial function was assessed by FMD (flow mediated dilatation) at fast, 30, 60 and 90 min post-smoking. RESULTS: Overall response of FMD after smoking was significantly different between smokers and non-smokers (p=0.011). Endothelial dysfunction after smoking remained significant for 1-h in smokers (p=0.002), but only for 30 min in non-smokers (p=<0.001). FMD 1-h after smoking was significantly higher in non-smokers than in smokers (p=0.002). CONCLUSIONS: Smokers seem to have sustained and more intensive unfavourable effects in endothelial function than non-smokers after smoking one cigarette. It is possible that long-term smoking diminishes the capacity of endothelium to counterbalance external factors that cause endothelial dysfunction.

Adult↗
PubMed1998

Effect of oral contraceptives containing 20 and 35 µg ethinyl estradiol on urinary prostacyclin and thromboxane levels in smokers and non-smokers.

Objective: Several observational epidemiological studies have shown an increased risk of myocardial infarction (MI) in oral contraceptive (OC) users who smoke cigarettes. Nearly a quarter of all OC users are smokers. The etiology of MI in OC users has been shown to be thrombotic, and the thrombogenic effect of OCs appears to be due to the estrogen component of the formulation. There are epidemiologic data that indicate that decreasing the estrogen dosage in OCs decreases the risk of thrombosis. Smoking may enhance thrombosis in OC users by decreasing prostacyclin levels. The objective of the present study was to investigate the interaction between smoking and OC use with respect to thrombogenesis by studying the effects of OCs and smoking on urinary levels of prostacyclin PGI and thromboxane A(2) TX in smokers and non-smokers.Study Design: A total of 60 healthy women, aged 19-32 years, who were not taking any hormonal treatment for at least 3 months prior to initiating the study were divided into three equal groups: A) OC users who smoked (N = 20), B) OC users who did not smoke (N = 20), and a control group of 10 smokers and 10 non-smokers. To be eligible to participate in the study, all smokers had to smoke at least one pack of cigarettes per day. Each OC treatment group was randomized to receive either norethindrone (NET) acetate (1 mg)/ethinyl estradiol (EE(2)) (0.035 mg) (N = 10) or NET acetate (1 mg)/EE(2) (0.02 mg) (N = 10) daily for 3 months. Overnight urine collections and fasting blood samples were obtained at baseline and at 3 months prior to taking the last OC. Serum levels of NET and EE(2), as well as urinary levels of cotinine and the stable metabolites of prostacyclin and thromboxane A(2) (6-keto-prostaglandin F(1alpha) and thromboxane B(2), respectively), were measured by specific immunoassays.Results: Study subjects showed compliance with respect to smoking and OC use as determined by the levels of serum NET, EE(2), and cotinine. Comparing mean levels of PGI metabolites in the two groups of OC smokers, those taking 35 µg EE(2) showed a significant decrease in PGI. Comparing the ratio of PGI/TX in all smokers, only the smokers on the 35 µg formulation showed a significant decrease in the ratio, while there was no change in the 20 µg group. No significant changes in the ratio PGI/TX during the same time interval in smoking and non-smoking controls and OC non-smokers were observed.Conclusions: Women smokers taking 20 µg EE(2) OC had no thrombophilic changes of PGI and TXA(2) metabolites. Women smokers taking 35µg EE(2) oral contraceptive had thrombophilic changes in PGI/TXA metabolite ratio. Women smokers who use oral contraceptives may have less thrombotic risk taking formulations with 20µg EE(2) than 35µg EE(2).

Journal Article↗
PubMed1999

Non-surgical periodontal treatment with and without adjunctive metronidazole in smokers and non-smokers.

AIM: To determine whether adjunctive metronidazole therapy would compensate for the poorer treatment response to scaling and root planing reported in smokers. METHOD: A single-blind, randomised clinical trial of 28 smokers and 56 non-smokers, stratified for periodontitis disease severity and randomly allocated to 3 treatment groups: (1) Scaling and root planing using an ultrasonic scaler with local anaesthesia (SRP), (2) SRP+ metronidazole tabs 200 mg tds for 7 days, (3) SRP + 2 subgingival applications of 25% metronidazole gel. Probing depths (PD) and attachment levels (AL) were recorded with a Florida probe at baseline, 2 months and 6 months post treatment by a single examiner who was unaware of the treatment modality. Results were analysed for all sites with baseline probing depths equal to or greater than Florida probe recordings of 4.6 mm using analysis of variance. RESULTS: Reductions in probing depth at 6 months were significantly less (p < 0.001) in the smokers (mean 1.23 mm, 95% confidence intervals = 1.05 to 1.40 mm) than in the non-smokers (1.92, 1.75 to 2.09 mm). Attachment level gains were approximately 0.55 mm and there was no statistically significant difference between smokers and non-smokers. There were no differences in any clinical measure in response to the three treatment regimens at 2 or 6 months for either smokers or non-smokers. A reduction in the proportion of spirochaetes was observed at 6 months which was less in smokers than in non-smokers (p = 0.034). Multiple linear regression analysis on probing depth at 6 months demonstrated that smoking was a significant explanatory factor (p < 0.001) for poor treatment outcome, whilst the presence or absence of adjunctive metronidazole was not (p = 0.620). CONCLUSION: This study confirms that smokers have a poorer treatment response to SRP, regardless of the application of either systemic or locally applied adjunctive metronidazole.

Administration, Oral↗
PubMed2001

Periodontitis in smokers and non-smokers: intra-oral distribution of pockets.

AIM: The purpose of the present study was to establish retrospectively whether the disease severity differs between smokers and non-smokers. METHODS: The study population consisted of 183 periodontitis patients, 79 smokers and 104 non-smokers. These subjects had been referred by general dentists to the Clinic for Periodontology, Utrecht, because of periodontal problems and were selected on the basis of the clinical diagnosis: adult periodontitis. The proportion of bleeding sites and the intra-oral distribution of probing pocket depth was evaluated. RESULTS: No statistically-significant differences between smokers (SM) and non-smokers (NSM) were found regarding the mean % of sites that bled upon probing (SM=76%, NSM=72%). Overall differences in the prevalence of probing depths > or =5 mm between smokers and non-smokers were found (SM=44%, NSM=34%). The proportion of sites with a probing pocket depth of > or =5 mm was consistently higher in smokers in the anterior, premolar and molar regions. The data also show that in the upper jaw at the anterior and premolar teeth, the largest differences are found between smokers and non-smokers. Smokers have more sites with a pocket depth > or =5 mm, especially on the lingual surfaces of these teeth. CONCLUSIONS: The present study indicates that cigarette smoking is a factor associated with deeper periodontal pockets and an intra-oral distribution that is suggestive of a local effect.

Adult↗
PubMed2000

Ibuprofen inhibits adhesiveness of monocytes to endothelium and reduces cellular oxidative stress in smokers and non-smokers.

BACKGROUND: Cigarette smoking is a major risk factor in atherosclerosis and a useful model from which to study chronic inflammation. We compared monocyte function, lipid profiles and inflammatory markers in smokers and non-smokers, before and after oral ibuprofen intake. The adhesion of freshly isolated monocytes to native and tumour necrosis factor alpha (TNFalpha) stimulated human umbilical vein endothelial cells (HUVEC), as well as superoxide anion (O2-) levels and hydrogen peroxide (H2O2) production in resting and phorbol myristate acetate (PMA) stimulated monocytes were determined. MATERIALS AND METHODS: A group of nine smokers without any other coronary risk factor was compared with an age-matched group of 9 non-smokers. Tests were performed before and after a two-week course of oral ibuprofen (600 mg day-1). RESULTS: In smokers before ibuprofen, monocyte adhesion to native and TNFalpha-stimulated HUVEC was increased (P < 0001 and P < 0.01, respectively), and so were O2- levels in native and PMA-stimulated monocytes (P < 0.01 and P < 0.001, respectively). Ibuprofen reduced the adhesion of monocytes to native and stimulated HUVEC (P < 0.001) and O2- generation by resting and PMA-stimulated cells (P < 0.01) in both groups. H2O2 production by resting and PMA-stimulated monocytes was reduced in smokers and non-smokers (P < 0.01). Interestingly, ibuprofen increased HDL cholesterol levels in smokers (P < 0.01) and non-smokers (P < 0.001), and reduced the level of triglycerides in smokers (P < 0.05). CONCLUSION: Oral administration of ibuprofen reduced the adhesion of monocytes to HUVEC, suppressed oxidative stress and increased HDL cholesterol levels in smokers and non-smokers.

Adult↗
PubMed1991

Antioxidant vitamin intakes assessed using a food-frequency questionnaire: correlation with biochemical status in smokers and non-smokers.

The increasing interest in the possible role of antioxidant vitamins in many disease states means that methods of assessing vitamin intakes which are suitable for large-scale investigations are now required. The suitability of the food-frequency questionnaire, which was developed by the Medical Research Council - Cardiff Group, for determining dietary intake of antioxidant vitamins in epidemiological studies was investigated in 196 Scottish men. The validity of the dietary data was assessed by comparison with serum vitamin concentrations, and separate analyses were performed for current smokers and non-smokers. The results showed that total energy intake and the percentage of energy derived from sugar were higher in smokers, and that both dietary and serum values of vitamin C, beta-carotene and vitamin E were lower in smokers than non-smokers. After adjustment for serum lipids, energy intake and body mass index, correlation coefficients between dietary and serum vitamins C and E were similar for smokers (r 0.555 and 0.25 respectively) and non-smokers (r 0.58 and 0.32 respectively). Correlation between dietary and serum carotenes was reduced from 0.28 in non-smokers to 0.09 in smokers and correlations for retinol and total vitamin A were weakly significant only for non-smokers. The food-frequency questionnaire assigned greater than 70% of subjects correctly into the upper or lower plus adjacent tertiles of serum vitamin values, with the exception of beta-carotene and total vitamin A for smokers. Thus, the food-frequency questionnaire appeared to be an adequate tool for assigning individuals into tertiles of serum antioxidant vitamins with the main exception of beta-carotene for smokers. Marked differences do occur between the vitamins and between the smoking groups which may reflect reduced accuracy of reporting on the food-frequency questionnaire or differential absorption and metabolism of the vitamins.

Adult↗
PubMed2005

Differential expression of biomarkers in lung adenocarcinoma: a comparative study between smokers and never-smokers.

BACKGROUND: Non-small-cell lung cancer arising in never-smokers is usually of adenocarcinoma subtype. The oncogenic pathway of such tumors is poorly understood. To better define the biological characteristics of these tumors, we have compared the expression of a panel of epidermal growth factor receptor (EGFR)-related biomarkers in lung adenocarcinomas from smokers versus those in never-smokers. PATIENTS AND METHODS: Using immunohistochemical analysis, we retrospectively analyzed EGFR, pAKT, PTEN, Ki-67, p27 and hTERT expression in specimens from 190 patients with completely resected lung adenocarcinomas (43 never-smokers and 147 smokers). These analyses were performed on tissue microarrays. RESULTS: EGFR expression was higher in tumors from smokers (P < 0.01), while pAKT was overexpressed mainly in tumors from never-smokers (P = 0.01). As expected, the tumors from smokers presented a higher expression of Ki-67 and a more frequent loss of expression of p27 (P < 0.01). In a multivariate model, two biological factors (p27 and Ki-67) and two clinical factors (age and sex) showed independent significant correlation with never-smoking status. CONCLUSIONS: Lung adenocarcinomas in never-smokers have a very distinct immunohistochemical expression profile of EGFR-related biomarkers as compared with lung adenocarcinomas in smokers. High levels of EGFR and Ki-67 are observed in smokers, while never-smokers are characterized by high levels of pAKT and p27.

Adenocarcinoma↗
PubMed1991

A comparison of the diets of non-smokers and smokers.

Dietary data, mostly in the form of the frequency of consumption of foods, from the 9003 respondents in the Health and Lifestyle Survey were used to compare lifetime non-smokers with light, heavy and ex-smokers, taking account of age and social class. Non-smokers, of both sexes, were significantly more likely than smokers to consume, frequently, fresh fruit in summer and winter, fruit juice, cooked and canned fruit, salads in summer and winter, breakfast cereals, cakes, biscuits, puddings, pasta, poultry, light desserts and preserves. They were also more likely to choose 'brown' bread, semi- or skimmed milk, low fat or polyunsaturated spread and to eat breakfast. Smokers were likely to consume chips and processed meats frequently, to drink more alcohol, more cups of tea and coffee and take sugar in these beverages. The differences from the non-smokers were more marked in the heavy smokers. Ex-smokers only differed from non-smokers in consuming more alcohol, tea and coffee, and nuts, in consuming cakes and soft drinks less frequently and in being more likely to choose skimmed or semi-skimmed milk. The results extend previous findings, and suggest that the eating patterns of non-smokers are more in line with current dietary recommendations than those of light smokers or, more particularly, heavy smokers.

Adolescent↗
PubMed1997

The effects of local anesthetic containing adrenaline on gingival blood flow in smokers and non-smokers.

Recent evidence suggests that fundamental differences exist in the development of gingival and periodontal diseases in smokers versus non-smokers. In part, these differences may be attributable to smoking-induced differences in the vascular dynamics of the periodontium. This study monitored gingival blood flow when challenged by a local anesthetic-containing adrenaline in 20 smokers and 20 non-smokers using laser Doppler flowmetry (LDF). The dosage of local anesthetic used (0.5 ml lignocaine hydrochloride 2% with adrenaline 1:80,000) was calculated after establishing a dose-response curve (DRC) for 3 subjects (2 non-smokers and 1 smoker). Plain lignocaine and normal saline were used as controls. The injection of lignocaine-containing adrenaline had little effect on LDF signals when different doses were injected at frequent short intervals, indicating that tolerance to adrenaline had rapidly developed in the receptors of gingival blood vessels. Injection of local anesthetics containing adrenaline consistently resulted in a marked and significant drop (average: 46%, sd;13.5) in the LDF output signals from gingiva; smokers and non-smokers responded similarly. The significant finding of this study was that the recovery of LDF signals to baseline took considerably longer in smokers than in non-smokers. This provides further evidence that gingival blood vessels in smokers with healthy gingival conditions respond differently to those of non-smokers.

Adolescent↗