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[Ascorbic acid consumption and serum levels in smokers and non-smokers adult men in Hermosillo, Sonora, México].

Ascorbic acid is one of the important antioxidant nutrients that can aid in the prevention of oxidative cellular damage. Adequate dietary intake is essential as humans can not synthesize this vitamin. It has been reported that smokers require higher dietary intakes to maintain their serum levels. The objective of this study was to determine serum levels of ascorbic acid in young male smokers and non smokers in the city of Hermosillo, Sonora, Mexico. In addition, their dietary intake of ascorbic acid was determined by a 24 h dietary recall. The dietary intake of ascorbic acid in 12 smokers was 64 +/- 11 mg/d and in 13 non smokers it was 70 +/- 12 mg/d. The smokers in this study did not meet the dietary recommendation of 100 mg/d. Serum ascorbic acid values in smokers and non smokers were 24.2 +/- 6.9 mumol/L and 30.9 +/- 3.7 mumol/L respectively. No significant difference was found among the 2 groups. Although the average serum ascorbic acid values fell within the range considered normal, 50% of the smokers had individual values that were below 23 mumol/L, indicating that these subjects have hipovitaminosis. A positive correlation between intake and serum levels was obtained for smokers (r = 0.71; p = 0.03). The results of this study suggest smokers may be at increased risk for chronic diseases due to their low intake and low serum levels of ascorbic acid.

Adolescent↗

Expression of CYP1A1, CYP1B1 and CYP3A, and polycyclic aromatic hydrocarbon-DNA adduct formation in bronchoalveolar macrophages of smokers and non-smokers.

Variability in the expression of enzymes metabolizing carcinogens derived from cigarette smoke may contribute to individual susceptibility to pulmonary carcinogenesis. This study was designed to determine the effects of smoking and 3 major cytochrome P450 (CYP) enzymes, i.e., CYP1A1, CYP1B1 and CYP3A, which metabolize polycyclic aromatic hydrocarbons (PAH) on PAH-DNA adduct formation in the bronchoalveolar macrophages (BAM) of 31 smokers and 16 non-smokers. CYP protein levels were determined by immunoblotting and PAH-DNA adduct levels by the nuclease P1 enhanced (32)P-postlabeling method. The expression of specific CYP forms was confirmed by reverse transcriptase-polymerase chain reaction (RT-PCR) from 10 additional samples. CYP3A protein, CYP3A5 by RT-PCR, was detected in the majority of samples from smokers and non-smokers. The levels of CYP3A appeared to be lower in active smokers than in ex-smokers (p = 0.10) or never smokers (p = 0.02). CYP1A1 was not detectable by either immunoblotting or RT-PCR. The expression of CYP1B1 was low or undetectable in most samples. The PAH-DNA adduct levels were higher (mean 1.57/10(8) nucleotides) in samples from smokers compared with non-smokers (mean 0.42/10(8) nucleotides, p < 0.001) and the number of adducts correlated with the number of cigarettes smoked daily (regression analysis, p < 0. 001). Higher levels of adducts were detected in samples from smokers with a high level of CYP3A compared with those with a low level (regression analysis, p = 0.002). As CYP3A5 is abundant in both lung epithelial cells and BAM, its association with adduct formation suggests that this CYP form may be important in the activation of cigarette smoke procarcinogens.

Adult↗

Comparison of an oxidative stress biomarker "urinary8-hydroxy-2'-deoxyguanosine," between smokers and non-smokers.

A great deal of effort has been made on the effect of oxidative stress for smokers. What seems to be lacking, however, is its evidence. Analyzing 1076 participants (age 35.9 +/- 12.9, urinary8-OHdG Mean +/- S.D., 11.4 +/- 6.7, n = 1076), our study found the significant increase in a biomarker of DNA damage urinary 8-OHdG/creatinine among smokers (7.75 +/- 2.8 ng/ml x CRE (n = 154) and 7.36 +/- 2.5 ng/ml x CRE (n = 627) (p < 0.05), Relative Risk = 2.9 (1.4-6.2) sex and age +/- 2 matching 105 male smokers and non-smokers. There was no significance on the comparison between female smokers and non-smokers. Smokers have significantly decreased serum alpha-tocopherol (1012 +/- 455, 1152 +/- 857, p < 0.03). The amount of serum ascorbate did not change. Smokers lowered serum HDL-cholesterol compared to non-smokers (59.3 +/- 11.8, 63.9 +/- 13.3, p < 0.05). The result of oxidative stress profile (OSP) also indicated that the increase of oxidative stress to smokers (p < 0.05). The calculated value of oxygen radical absorbance capacity (ORAC) of the meal for subjects was 1600 ORAC units.

8-Hydroxy-2'-Deoxyguanosine↗

Levels of matrix metalloproteinase-2, -9 and -8 in the skin, serum and saliva of smokers and non-smokers.

Smoking induces skin ageing, affects wound healing and inflammatory responses in skin and mucous membranes but the mechanisms behind these adverse effects of smoking are not clear. The objective was to elucidate the mechanisms of smoking-related tissue damage, by comparing the levels of matrix metalloproteinases (MMPs) -2, -9, and -8 in the skin, serum and saliva of smokers and non-smokers. The study population consisted of 47 current smokers and 51 non-smokers, all males of Finnish origin. Skin samples from the upper inner arm were frozen in liquid nitrogen. Levels of MMP-2 and MMP-9 protein in the skin were assessed by zymography and MMP-8 isoforms were determined by Western blotting. From the serum samples, MMP-2 and MMP-9 were assessed by zymography and MMP-8 levels by time-resolved immunofluorometric assay (IFMA). From the salivary samples, MMP-8 levels were analysed by IFMA and MMP-9 levels by capture activity assay. In skin tissue, lower levels of both the pro and active forms of MMP-9 and of the active forms of MMP-8 were found in the smokers compared to the non-smokers. In serum, higher levels of proMMP-2 and proMMP-9 were found in the smokers compared to the non-smokers (P=0.001 and P<0.001, respectively), whereas MMP-8 levels did not differ significantly between the groups. Active forms of MMP-9 and MMP-2 could not be found in serum. In saliva, the amount of total MMP-9 was significantly lower in the smokers (156.0 U/ml) compared to the non-smokers (223.9 U/ml, P=0.032), whereas the levels of MMP-8 or active MMP-9 did not differ significantly between the groups. We conclude that smoking alters the levels of matrix metalloproteinases in skin tissue, serum and saliva, which may affect the turnover of extracellular matrix of skin even though the clinical impact of our findings is not clear.

Finland↗

Radon-induced lung cancer in smokers and non-smokers: risk implications using a two-mutation carcinogenesis model.

Three sets of data (population statistics in non-smokers, data from an investigation of the smoking habits of British doctors and a study of Colorado uranium miners) were used to analyse lung cancer in humans as a function of exposure to radon and smoking. One of the aims was to derive implications for radon risk estimates. The data were analysed using a two-mutation radiation carcinogenesis model and a stepwise determination of the model parameters. The basic model parameters for lung cancer were derived from the age dependence fit of the spontaneous lung cancer incidence in non-smokers. The effect of smoking was described by two additional parameters and, subsequently, the effect of radon by three other parameters; these five parameters define the dependence of the two mutation steps on smoking and exposure to radon. Using this approach, a consistent fit and comprehensive description of the three sets of data have been achieved, and the parameters could, at least partly, be related to cellular radiobiological data. The model results explain the different effect of radon on non-smokers and smokers as seen in epidemiological data. Although the analysis was only applied to a limited number of populations, lung cancer incidence as a result of radon exposure is estimated to be about ten times higher for people exposed at the age of about 15 than at about 50, although this effect is masked (especially for smokers) by the high lung cancer incidence from smoking. Using the model to calculate the lung cancer risks from lifetime exposure to radon, as is the case for indoor radon, higher risks were estimated than previously derived from epidemiological studies of the miners' data. The excess absolute risk per unit exposure of radon is about 1.7 times higher for smokers of 30 cigarettes per day than for non-smokers, even though, as a result of the low spontaneous tumour incidence in the non-smokers, the excess relative risk per unit exposure for the smokers is about 20 times lower than for the non-smokers. This prediction could have serious consequences for the transfer of risk estimates between populations. Although the solution of the model presented here is not unique but dependent on the model assumptions, the predictions and risk implications are sufficiently supported to justify a thorough investigation of the applicability of the model to other radon data sets.

Adolescent↗

Fibrinogen levels in hypercholesterolemic smokers and non-smokers in relation to age and gender.

Elevated total cholesterol and plasma fibrinogen levels and smoking are risk factors for cardiovascular disease, whose inter-relationships are influenced by both gender and age. The aim of this study was to investigate the effect of smoking on fibrinogen levels in a hypercholesterolemic population subdivided on the basis of gender and age. The study included 492 hypercholesterolemic subjects, divided into four subpopulations: men and women, aged 26-49 and 50-66 years. Mean fibrinogen levels among smokers and non-smokers in the four subpopulations of this hypercholesterolemic cohort followed mean total cholesterol levels. Three subpopulations (men <50 years, men >/=50 years and women >/=50 years) showed differences in mean total cholesterol and fibrinogen values between smokers and non-smokers (total cholesterol 7.23+/-0.54 vs. 7.40+/-0.93 mmol/l and fibrinogen 2.79+/-0.48 vs. 3.23+/-0.72 g/l in men <50 years; total cholesterol 7.17+/-0.43 vs. 7.50+/-0.60 mmol/l and fibrinogen 3.11+/-0.44 vs. 3.68+/-0.66 g/l in men >/=50 years and 7.41+/-0.59 vs. 7.65+/-0.73 mmol/l and fibrinogen 3.29+/-0.61 vs. 3.58+/-0.71 g/l in women >/=50 years). These values correspond to a percentage difference between smokers and nonsmokers in total cholesterol and fibrinogen of 2.4% and 15.8% in men <50 years, 4.6% and 18.3% in men >/=50 years and 3.2% and 8.8% in women >/=50 years. All differences were significant ( P<0.05), except for total cholesterol in the younger men (<50 years). No differences between smokers and non-smokers were observed in the younger female group (<50 years). Except in the younger female group (<50 years), significant differences between smokers and non-smokers were also observed in the number of subjects exceeding the upper reference value of fibrinogen (>4.0 g/l), the highest percentage being found for the older women smokers (>/=50 years) (29%). In Conclusion, smoking elevates fibrinogen levels in hypercholesterolemic men (<50 years; >/=50 years) and older women (>/=50 years), but not in younger women (<50 years).

Adult↗

Beta-carotene concentrations in maternal and cord blood of smokers and non-smokers.

BACKGROUND: Smoking in pregnancy can cause a reduction in the transport of beta-carotene across the placenta, consequently reflecting on the concentrations of this micronutrient in the newborn baby. AIMS: This study determined the concentrations of beta-carotene in maternal blood and umbilical cord blood in a group of smokers and non-smokers. DESIGN AND SUBJECTS: A total of 215 women and respective newborn babies were selected from a hospital in Joinville city, Brazil, between July and November 2002. Women were divided in two groups according to their smoking habits. beta-Carotene concentration was determined by high-performance liquid chromatography (HPLC). The difference between mean concentrations of beta-carotene in maternal blood and cord blood, in smokers and non-smokers, was determined by analysis of variance (ANOVA). The Student's t-test compared mean concentrations of beta-carotene in maternal blood and cord blood, and the mean ingestion of foods rich in beta-carotene by smokers and non-smokers. RESULTS: There was a statistical significant difference between the concentrations of beta-carotene in maternal blood (S=0.271 micromol/L, NS=0.450 micromol/L; P=0.001) and cord blood (S=0.028 micromol/L, NS=0.045 micromol/L; P=0.001) in smokers (S) and non-smokers (NS). The mean concentration of beta-carotene was significantly higher in maternal blood (0.398 micromol/L) than in cord blood (0.041 micromol/L) (P<0.001). The intake of foods rich in beta-carotene was lower in smokers, than in non-smokers (P=0.04). CONCLUSIONS: The concentrations of beta-carotene in maternal blood and cord blood were influenced by the use of tobacco.

Adolescent↗

Mitochondrial DNA mutations in the parotid gland of cigarette smokers and non-smokers.

It has previously been demonstrated that mitochondrial DNA (mtDNA) mutations accumulate in the lung and increase in frequency with age. It has also been shown that the level of mtDNA mutations including deletions and base substitutions are elevated in lung tissue of smokers relative to non-smokers. We have previously shown that the 'common' 4977 bp mtDNA deletion is present in the parotid (salivary) gland of smokers and non-smokers and that there is a significant increase in the level of this deletion in Warthins tumour, an oncocytoma of the parotid gland. In this study we used semi-quantitative PCR to confirm the presence of 4977 bp mtDNA deletion in the parotid gland of non-smokers and smokers. Importantly, we show that the deletion accumulates with age regardless of smoking status and that there was no significant difference in the level of the 4977 bp deletion in parotid tissue of smokers and non-smokers. Using strand conformational polymorphism (SSCP) and direct sequencing we also found 5/23 smokers had parotid tissue specific base substitutions: either an A/T to G/C transition at A4767 or a G/C to A/T transition at G4853. These results are evidence of age related increase in the 4977 bp deletion and a higher level of mutations, probably due to oxidative damage, in the parotid gland of smokers.

Adenolymphoma↗

Smokers have less reductions in probing depth than non-smokers following nonsurgical periodontal therapy.

DATA SOURCES: Studies were located using Medline, Embase and the Cochrane Central Register of Controlled Clinical Trials, as well as searching bibliographies of identified references, review articles and consensus statements by hand. STUDY SELECTION: As the habit of smoking cannot be randomised, studies included were both controlled clinical trials and arms of randomised controlled trials investigating the effects of nonsurgical periodontal treatment, which reported results separately for smokers and nonsmokers. Other inclusion criteria were that studies should assess otherwise healthy people who had been diagnosed with chronic or adult periodontitis and that the patient was the unit of analysis (rather than a tooth- or site-based analysis). Studies were not excluded on the basis of quality, only on whether they fulfilled the inclusion criteria for entry. DATA EXTRACTION AND SYNTHESIS: General information about the paper, study characteristics, outcome measures, treatment characteristics and quality assessment was extracted independently, in duplicate. Where disagreement arose, this was resolved by discussion. Meta-analysis of data was performed and heterogeneity between studies was investigated using meta-analysis regression. RESULTS: Out of the 330 studies initially identified, 13 were considered eligible for inclusion. No studies reported data on tooth loss. For all sites, the reduction in probing depth (PD) was 0.13 mm greater in nonsmokers than in smokers (six studies) and there was no evidence to suggest that the studies were dissimilar in their estimates of this result (no evidence of heterogeneity; P>0.05). For sites with an initial PD of 5.00 mm (eight studies), a random-effects meta-analysis indicated a weighted mean difference in PD reduction of 0.43 mm favouring nonsmokers (95% confidence interval (CI), 0.24-0.63; P<0.001). Because of significant heterogeneity between studies, only a cautious observation can be made but, with one exception, all studies produced a summary estimate favouring nonsmokers. Meta-analysis of the two studies that compared the change in clinical attachment level between nonsmokers and ex-smokers, who had given up their habit, in sites with an initial PD of +/-5.00 mm, showed a difference in clinical attachment level gain of 1.34 mm favouring the nonsmokers (95% CI, 0.65-2.03; P<0.001; chi(2) test for heterogeneity, 7.47 with 1 degree of freedom; P=0.006). In both of these analyses, the degree of heterogeneity is a cause for concern. Bleeding was assessed after therapy in seven studies but meta-analysis was not performed because of great heterogeneity in the methods used to assess bleeding. No statistically significant differences in bleeding were found between smokers and nonsmokers either at baseline or after therapy in most of the studies. One study found significantly less bleeding in smokers than in nonsmokers at baseline and another found a reduced response in terms of bleeding in smokers than in nonsmokers. Two studies evaluating the change in bleeding in ex-smokers found no statistically significant difference after treatment. No data were reported for any of the included studies on patient-centred outcomes such as quality of life, ease of maintenance, changes in aesthetic appearance, or patient experience. CONCLUSIONS: Following nonsurgical periodontal therapy, people who smoke will experience less reduction in PD than nonsmokers. There is no evidence of a difference in gain in clinical attachment between smokers and nonsmokers or a reduction of bleeding on probing between smokers and nonsmokers. Differences in study design and lack of data precluded an adequate and complete pooling of data for a more comprehensive analysis. In short-term studies, it is unclear whether people who stop smoking will respond as favourably to nonsurgical therapy as those who have never been smokers. Progress in understanding the effects of smoking on periodontal therapy will require the evaluation of objective measures of smoking such as nicotine exposure and exhaled carbon monoxide in place of sole reliance on patient-reported information.

Comment↗

Expression of ICAM-1 and E-selectin in gingival tissues of smokers and non-smokers with periodontitis.

BACKGROUND: Tobacco smoking affects systemic concentrations of soluble intercellular adhesion molecule (ICAM)-1, but its effect on local expression of adhesion molecules in gingival tissue has not been studied previously. METHODS: E-selectin and ICAM-1 expression on small blood vessel endothelia in gingival biopsies obtained from smokers (n=17) and non-smokers (n=17) with periodontitis was examined with immunohistochemistry. Blood vessels were identified with monoclonal antibody for von Willebrand's factor. RESULTS: A significantly larger number of vessels were observed in inflamed tissues of non-smokers than smokers (P<0.05). The number and proportion of vessels expressing both ICAM-1 and E-selectin was greater in sites with inflammation compared to non-inflamed sites in both smokers and non-smokers (P<0.05). The proportion of the total number of vessels expressing ICAM-1 in non-inflamed sites was greater in non-smokers compared with smokers (P<0.05). CONCLUSIONS: These results suggest that the inflammatory response in smokers with periodontitis may not be accompanied by an equivalent increase in vascularity. Reduced ICAM-1 expression in non-inflamed areas of smokers could reflect a systemic effect of tobacco smoking on ICAM-1 independent of inflammation.

Adult↗

Respiratory symptoms relate to physiological changes and inflammatory markers reflecting central but not peripheral airways. A study in 60-year-old 'healthy' smokers and never-smokers.

The aim of this study was to evaluate the relationship between respiratory symptoms, lung function and inflammatory markers in 'healthy' smokers. The study population was recruited from an epidemiological study with subjects of the same age, 60 years. Only smokers who considered themselves healthy (n=58) and a random sample of never-smokers (n=34) were investigated. All subjects underwent lung function tests--spirometry, carbon monoxide transfer (DLco) and the single-breath N2 method (N2 test)--together with high-resolution computed tomography (HRCT). A flexible bronchoscopy with a bronchoalveolar lavage (BAL) was performed in 30 smokers and 18 never-smokers. Bronchial biopsies were also taken. Smokers who reported non-specific respiratory problems, chronic bronchitis and wheezing in a symptom questionnaire had a lower forced expiratory volume in 1 sec (FEV1), FEV% and specific airway conductance (sGaw), lung function tests supposed to reflect the more central airways, than smokers without respiratory symptoms. A limited number of smokers with occasional non-specific respiratory problems also had more cytotoxic T cells (CD8) in bronchial biopsies. No differences were found in DLCO and the N2 test, lung function tests supposed to reflect the more peripheral airways including the alveoli, HRCT-diagnosed emphysema or inflammatory markers in blood and BAL between smokers with and without respiratory symptoms. It is concluded that even when smokers consider themselves 'healthy' they have mild symptoms that are related more to physiological changes and inflammatory markers that may reflect events in the central airways than to changes that may reflect events in the peripheral airways.

Biopsy↗

Comparison of clinical and computerized image analyses in the assessment of skin ageing in smokers and non-smokers.

Tobacco smoke and UV radiation are extrinsic risk factors for accelerated skin ageing. In this study the effects of smoking on wrinkling and ageing were assessed in males living in Northern Finland, where cumulative sun exposure is low. Smoking habits, age and facial wrinkling were estimated from facial photographs of 41 smokers and 48 non-smokers by eight panellists, using a blinded standardized assessment. Wrinkling of 26 smokers and 31 non-smokers was also assessed by computerized image analysis. The panellists identified 68% of the smokers correctly as being smokers and the smokers were estimated as being an average of 2.1 years older than their age by the panellists, whereas the non-smokers were estimated as being an average of 0.7 years younger than their age (p < 0.05). No significant difference in skin wrinkling was found between the groups by either clinical assessment or by computerized image analysis. In conclusion, even in the absence of increased wrinkling, the smokers looked older than their age and a majority of them could be identified as smokers by their facial features alone.

Adult↗

Neutrophil elastase activity, levels of prostaglandin E2, and matrix metalloproteinase-8 in refractory periodontitis sites in smokers and non-smokers.

The study was aimed to determine elastase activity, levels of prostaglandin E2 (PGE2), and matrix metalloproteinase-8 (MMP-8) in gingival crevicular fluid (GCF) in 20 smokers and 20 non-smokers, mean age 47.4 (+/-2.9 SD) years with refractory periodontal diseases. GCF was collected with intracrevicular washing from four sites in each subject. Clinical assessments, included gingival index, probing depth, clinical attachment level, bleeding on probing, bone height, and plaque accumulation. Smokers had a significantly higher percentage of the gingival margin covered by plaque (P%Im), higher number of sites with probing pocket depth > or = 5 mm, higher mean values of probing pocket depth and probing attachment level (P< 0.01). Smokers had significantly higher mean levels of neutrophil elastase activity (P< 0.01) in the supernatants than non-smokers did. In sites with matching pocket depths, neutrophil elastase activity was significantly higher in smokers (P< 0.001) than in non-smokers. In sites with high levels of MMP-8 the PGE2 levels were significantly (P< 0.001) higher compared to sites with low levels in smokers as well as in non-smokers. A significant correlation was found between probing pocket depth and levels of MMP-8 (P< 0.001) and in non-smokers between probing pocket depth and levels of PGE2 (P< 0.05).

Biomarkers↗

High-resolution computed tomography in healthy smokers and never-smokers: a 6-year follow-up study of men born in 1933.

PURPOSE: To elucidate whether emphysematous lesions and other high-resolution computed tomography (HRCT) findings considered associated with smoking are part of a progressive process, and to measure the extent to which similar changes are found in never-smokers. MATERIAL AND METHODS: Healthy smokers and never-smokers were recruited from a randomized epidemiological study and investigated with a 6-year interval. Emphysema, parenchymal and subpleural nodules, ground-glass opacities, bronchial alterations, and septal lines were evaluated in 66 subjects (40 smokers, 11 of whom had stopped smoking in the interval, and 26 never-smokers). Lung function was tested. RESULTS: All except emphysematous lesions were present to some extent in never-smokers. Emphysema, parenchymal nodules, and septal lines occurred significantly more in current smokers, and a progression in extent of emphysema, ground-glass opacities, bronchial alterations and septal lines was seen. There was no significant change among those who stopped and never-smokers except for bronchial alterations, which progressed in never-smokers. CONCLUSION: In healthy, elderly never-smokers a low extent of various HRCT findings has to be considered normal. Emphysema, parenchymal nodules, and ground-glass opacities are indicative of smoking-induced disease. Further progress may cease if smoking is stopped.

Aged↗

Association of serotonin transporter genotype with selective processing of smoking-related stimuli in current smokers and ex-smokers.

We sought to determine whether polymorphism in the serotonin transporter (5HTT) gene is associated with attentional bias toward smoking-related stimuli in current smokers and ex-smokers, using a modified Stroop task and an attentional blink task to measure selective processing of smoking-related stimuli. All participants attended a single testing session during which they completed the modified Stroop and attentional blink tasks to index attentional bias for smoking-related stimuli, in counterbalanced order. The experimental design included two between-subjects factors of smoking status (current smoker, ex-smoker) and 5HTT genotype (short, long). Smoking status x genotype interactions were significant on both the modified Stroop (p = .046) and the attentional blink (p = .006) tasks. On the modified Stroop task, we found a significant effect of 5HTT genotype on color-naming interference among ex-smokers (p = .018) but not current smokers (p = .989). On the attentional blink task, we found a significant effect of 5HTT genotype for current smokers (p = .028), whereas among ex-smokers this effect did not reach statistical significance, although it constituted a trend (p = .086). Our data provide tentative support for a moderating influence of 5HTT genotype on attentional bias for smoking-related stimuli in ex-smokers. This finding may account for inconsistent reports of attentional bias among ex-smokers.

Adult↗

Responsiveness of homocysteine concentrations to food and supplemental folate intakes in smokers and never-smokers enrolled in a diet intervention trial.

We investigated circulating homocysteine concentrations in relation to smoking, folate intake (from food and supplements), serum folate concentrations, and other dietary variables. The present study is part of a parent trial assessing the effects of increasing vegetable, fruit, and fiber intakes and reducing the percentage of energy obtained from fat on breast cancer recurrence in 3,088 women previously diagnosed with breast cancer. Of the 121 smokers enrolled in the parent trial, 85 were available at baseline for the present study and were randomly matched to 85 never-smokers on baseline folate intake, age, and intervention status. Follow-up data were available on 53 smokers (22 intervention and 31 comparison) and 56 never-smokers (24 intervention and 32 comparison). No significant differences in circulating homocysteine and folate concentrations were observed between smokers and never-smokers at baseline. For smokers, significant decreases in circulating homocysteine and significant increases in folate concentrations (p < .05) from baseline to 12 months were observed in the comparison group. For never-smokers, significant decreases in circulating homocysteine and significant increases in folate concentrations were observed in the intervention and comparison groups (p < .05). In the multivariate analysis, changes in serum folate concentration and supplemental folic acid were significantly associated with change in plasma homocysteine concentrations (p < .05). These findings show that increasing supplemental folic acid can reduce homocysteine concentrations, which may have implications for lowering cardiovascular disease risk for smokers and never-smokers.

Adult↗

Comparison of pulmonary DNA adduct levels, measured by 32P-postlabelling and aryl hydrocarbon hydroxylase activity in lung parenchyma of smokers and ex-smokers.

In order to compare pulmonary DNA adducts and aryl hydrocarbon hydroxylase (AHH) activity, we have measured these two parameters in non-neoplastic surgical lung parenchymal samples from four ex-smokers and 19 smokers, out of 20 patients operated for lung cancer, and three for nonmalignant lung diseases. DNA adducts were determined by scintillation counting after 32P-postlabelling analysis. The microsomal fractions of the same lung specimen were assayed for AHH activity by a fluorometric method. Autoradiograms of DNA adducts found in lungs of smokers revealed two distinct diagonal radioactive zones that were absent in ex-smokers. The smokers had significantly higher levels (1.68-13.4 DNA adducts/10(8) nucleotides; mean +/- SD 5.38 +/- 3.19) than ex-smokers (0.23-2.21; 1.09 +/- 0.84). AHH activity in smokers ranged from 0.01 to 0.69 pmol/min/mg. This activity was significantly (P less than 0.05) higher in smokers (0.26 +/- 0.26) who had smoked until 1 week before surgery than in those who had stopped smoking for greater than 7 days (0.11 +/- 0.11). A positive linear correlation between DNA adduct levels and AHH activity (r = 0.69; P less than 0.001; n = 19) was found in smokers. This relationship could explain why AHH inducibility appears to be a crude marker for lung cancer risk in smokers.

Adult↗

Perceptions of risk of cervical cancer and attitudes towards cervical screening: a comparison of smokers and non-smokers.

OBJECTIVES: The aim of this study was to compare smokers' and non-smokers' perceptions of risks of cervical cancer and attitudes towards cervical screening. METHODS: A cross-sectional descriptive study was carried out in 722 women aged between 20 and 64 years. RESULTS: While smokers perceived their relative risk of heart disease to be greater than that of non-smokers, they did not perceive their risks of cervical cancer to be greater. Smokers held less positive attitudes towards cervical screening than did non-smokers. Smokers and non-smokers did not differ in their intentions to attend for cervical screening: for both groups, intentions were very high. Using logistic regression analysis, both attitudes towards cervical screening [odds ratio (OR) 1.9; 95% confidence interval (CI) 1.7-2.2] and perceived relative risk of developing cervical cancer (OR 1.5; 95% CI 1.0-2.1) were predictive of intentions to attend for screening, as well as educational level (OR 3.8; 95% CI 1.2-11.3) and marital status (OR 0.6; 95% CI 0.3-0.9). CONCLUSIONS: Smokers seem unaware of their increased risks of cervical cancer and hence the increased value for them of regular smears. Evaluations are needed to determine the effectiveness of interventions delivered in the context of cervical screening aimed at (i) raising smokers' awareness of their increased risk of cervical cancer and (ii) stopping smoking.

Adult↗