Higher Pack-years Research Articles

Gender Differences in the Association of Smoking and Drinking with the Development of Cognitive Impairment

Modifiable lifestyle-related factors such as smoking and alcohol drinking are associated with cognitive impairment in the elderly population but the relationships have shown various results. To evaluate the relationship of alcohol drinking and smoking in the early 60 s with the risk of developing incident cognitive impairment. In 1999, we evaluated cognitive function, smoking, and drinking status in 3,174 inhabitants aged 60–64 years in a rural area of Korea, with a follow-up assessment of cognitive function 7 years later. A total of 1,810 individuals who did not show cognitive impairment at baseline were included. A stratified analysis was applied to evaluate how smoking and alcohol drinking affected the risk of developing cognitive impairment based on gender. Current smokers showed a higher risk for developing cognitive impairment than did never smokers (odds ratio [OR], 1.53; 95% confidence interval [CI], 1.09–2.15). The OR for female current smokers compared with never smokers was 1.62 (95% CI, 1.05–2.52), and smokers with higher pack-years were more likely to develop cognitive impairment than never smokers, showing a dose–response relationship (P for trend = 0.004). Frequent alcohol consumption increased the risk of developing cognitive impairment (OR, 1.68; 95% CI, 1.01–2.78), and a dose–response relationship was observed among male subjects (P for trend = 0.044). Infrequent drinking in females decreased the odds of developing cognitive impairment (OR, 0.67; 95% CI, 0.42–1.00), whereas frequent drinking tended to increase the odds, although this trend was not significant, suggesting a U-shaped relationship. Although the sample was small for some analyses, especially in female, our data suggest that smoking and drinking in the early 60 s are associated with a risk of developing cognitive impairment, and this relationship is characterized by gender differences.

Histology and Smoking Status Predict Survival of Patients with Advanced Non–Small-Cell Lung Cancer: Results of West Japan Oncology Group (WJOG) Study 3906L

Smoking status is one of the prognostic factors in advanced non-small-cell lung cancer (NSCLC). Currently, adenocarcinoma (Ad) histology is considered a predictive factor in advanced NSCLC. We investigated the correlation between histology or smoking status and survival of NSCLC patients receiving chemotherapy. We retrospectively reviewed clinical data from stage IIIB or IV NSCLC patients who started first-line chemotherapy at affiliated institutions of West Japan Oncology Group from 2004 to 2005. We also collected information on pack-years of cigarette smoking and years since cessation. Overall survival was compared using log-rank test, and Cox regression analysis was used to identify independent prognostic factors. In total, 2542 consecutive patients were enrolled at 40 institutions. Of those, 71 were excluded because of unknown smoking history. The median overall survival of nonsmoking Ad patients (593 days) was longer than that of smoking Ad, nonsmoking non-Ad, and smoking non-Ad patients (384, 374, and 319 days, respectively; p < 0.001). In Cox regression with sex, age, stage, performance, and treatment as covariates, we found significant interaction (p = 0.039) between histology (Ad/non-Ad) and smoking status (smoker/nonsmoker); smoking conferred a hazard ratio of 1.34 (95% confidence interval, 1.15-1.55) in Ad, but only 0.99 (0.75-1.31) in non-Ad. Higher pack-years and shorter period since cessation were significantly associated with poorer survival in Ad (p < 0.001), but not in non-Ad (p ≥ 0.434). Ad histology is associated with better prognosis, and only smoking status had a prognostic impact in Ad.

SAT0293 High Prevalence of Metabolic Syndrome in Psoriatic Arthritis Patients is Associated With Severity of Underlying Psoriatic Disease

BackgroundWhile Psoriatic Arthritis (PsA) is characterized by inflammation of both skin and joints there has been an increased recognition that PsA is associated with modest increase in the risk of...

Electrocardiographic Changes Associated with Smoking and Smoking Cessation: Outcomes from a Randomized Controlled Trial

IntroductionCardiovascular disease (CVD) can be detected and quantified by analysis of the electrocardiogram (ECG); however the effects of smoking and smoking cessation on the ECG have not been characterized.MethodsStandard 12-lead ECGs were performed at baseline and 3 years after subjects enrolled in a prospective, randomized, placebo-controlled clinical trial of smoking cessation pharmacotherapies. ECGs were interpreted using the Minnesota Code ECG Classification. The effects of (i) smoking burden on the prevalence of ECG findings at baseline, and (ii) smoking and smoking cessation on ECG changes after 3 years were investigated by multivariable and multinomial regression analyses.ResultsAt baseline, 532 smokers were (mean [SD]) 43.3 (11.5) years old, smoked 20.6 (7.9) cigarettes/day, with a smoking burden of 26.7 (18.6) pack-years. Major and minor ECG criteria were identified in 87 (16.4%) and 131 (24.6%) of subjects, respectively. After adjusting for demographic data and known CVD risk factors, higher pack-years was associated with major ECG abnormalities (p = 0.02), but current cigarettes/day (p = 0.23) was not. After 3 years, 42.9% of subjects were abstinent from smoking. New major and minor ECG criteria were observed in 7.2% and 15.6% of subjects respectively, but in similar numbers of abstinent subjects and continuing smokers (p>0.2 for both). Continuing smokers showed significant reduction in current smoking (–8.4 [8.8] cigarettes/day, p<0.001) compared to baseline.ConclusionsIn conclusion, major ECG abnormalities are independently associated with lifetime smoking burden. After 3 years, smoking cessation was not associated with a decrease in ECG abnormalities, although cigarettes smoked/day decreased among continuing smokers.

Body mass index is associated with lumbar disc degeneration in young Finnish males: subsample of Northern Finland birth cohort study 1986

BackgroundThe role of environmental factors in lumbar intervertebral disc degeneration (DD) in young adults is largely unknown. Therefore, we investigated whether body mass index (BMI), smoking, and physical activity are associated with lumbar DD among young adults.MethodsThe Oulu Back Study (OBS) is a subpopulation of the 1986 Northern Finland Birth Cohort (NFBC 1986) and it originally included 2,969 children. The OBS subjects received a postal questionnaire, and those who responded (N = 1,987) were invited to the physical examination. The participants (N = 874) were invited to lumbar MRI study. A total of 558 young adults (325 females and 233 males) underwent MRI that used a 1.5-T scanner at the mean age of 21. Each lumbar intervertebral disc was graded as normal (0), mildly (1), moderately (2), or severely (3) degenerated. We calculated a sum score of the lumbar DD, and analyzed the associations between environmental risk factors (smoking, physical activity and weight-related factors assessed at 16 and 19 years) and DD using ordinal logistic regression, the results being expressed as cumulative odds ratios (COR). All analyses were stratified by gender.ResultsOf the 558 subjects, 256 (46%) had no DD, 117 (21%) had sum score of one, 93 (17%) sum score of two, and 92 (17%) sum score of three or higher. In the multivariate ordinal logistic regression model, BMI at 16 years (highest vs. lowest quartile) was associated with DD sum score among males (COR 2.35; 95% CI 1.19-4.65) but not among females (COR 1.29; 95% CI 0.72-2.32). Smoking of at least four pack-years was associated with DD among males, but not among females (COR 2.41; 95% CI 0.99-5.86 and 1.59; 95% 0.67-3.76, respectively). Self-reported physical activity was not associated with DD.ConclusionsHigh BMI at 16 years was associated with lumbar DD at 21 years among young males but not among females. High pack-years of smoking showed a comparable association in males, while physical activity had no association with DD in either gender. These results suggest that environmental factors are associated with DD among young males.

Influence of cigarette smoking on coronary artery and aortic calcium among random samples from populations of middle-aged Japanese and Korean men

BackgroundCigarette smoking is a risk factor of coronary heart disease. Vascular calcification such as coronary artery calcium (CAC) and aortic calcium (AC) is associated with coronary heart disease. The authors...

Abstract 664: Menthol cigarettes in relation to breast cancer incidence in African American women

Abstract The Tobacco Products Scientific Advisory Committee has found that smokers of menthol cigarettes have an earlier age at smoking initiation, less success in smoking cessation, and are more likely to be African American than smokers of non-menthol cigarettes. However, whether menthol cigarettes are associated with higher cancer risk relative to non-menthol cigarettes is unclear. Recent studies of smoking and breast cancer suggest that long-term smoking may associated with a small increase in risk, but no data are available on type of cigarette. We assessed the relative effects of menthol and non-menthol cigarettes on incidence of breast cancer in a large prospective cohort of African American women. The Black Women's Health Study has followed approximately 59,000 women with biennial questionnaires since enrollment in 1995. Beginning in 2003, data has been collected on whether cigarettes smoked were menthol or non-menthol; menthol cigarettes were reported by 64.7% of smokers who provided information. During follow-up from 2003 through 2010, 739 incident breast cancer cases occurred. In proportional hazard models that controlled for age and numerous breast cancer risk factors, hazard ratios (HR) were computed for categories of pack-years of smoking of the two types of cigarettes relative to a reference group of never-smokers who reported no regular exposure to second-hand smoke. The HR for β20 pack-years of smoking non-menthol cigarettes was 1.70 (95% confidence interval (CI) 1.04-2.76); for β20 pack-years of smoking menthol cigarettes, the HR was 1.14 (95% CI, 0.72-1.82). Our findings suggest that, to the extent that higher pack-years of smoking may be associated with breast cancer, smoking menthol cigarettes is not more harmful than smoking non-menthol cigarettes. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 664. doi:1538-7445.AM2012-664

Do lutein, zeaxanthin and macular pigment optical density differ with age or age-related maculopathy?

Background and aims Current age-related macular disease (ARMD) treatment includes antioxidant supplementation. Lutein (L) and zeaxanthin (Z) are antioxidants that make up macularpigment within the retina and may reduce the risk of developing ARMD. Ageing and smoking are leading risk factors for developing ARMD. We investigated differences in dietary, supplemental and retinal L and Z, and smoking habits in healthy younger eyes (HY), healthy older eyes (HO) and eyes with an early form of ARMD called age-related maculopathy (ARM). Methods HO, HY and ARM groups were assessed for dietary intakes of L and Z using food diaries. Smoking habits and self-administered quantities of L and Z were obtained via questionnaire. Retinal L and Z levels (macularpigmentopticaldensity, or MPOD) were determined using heterochromatic flicker photometry. Results No significant difference was demonstrated for dietary L and Z intake (?2 = 4.983, p = 0.083) or for MPOD between groups (F = 0.40, p = 0.67). There was a significant difference between the HY (mean ± sd: 1.20 ± 2.99), HO (4.51 ± 7.05) ARM groups (9.15 ± 12.28) for pack years smoked (?2 = 11.61, p = 0.03). Conclusions Our results do not support the theory that ARM develops as a result of L and Z deficiency. Higher pack years smoked may be a factor in disease development. Dietary and supplementary L and Z levels must be obtained when assessing MPOD between groups or over time.

640 Poor Pre-Operative Pulmonary Function Tests (PFT) Do Not Predict Worse Outcomes in Patients Undergoing LVAD Placement

Purpose: Poor preoperative pulmonary function has been identified as a risk factor for poor outcomes following cardiac surgery, but this has not been well described in patients undergoing LVAD placement. The objective is to examine the relationship between preoperative pulmonary function and outcomes after LVAD implantation. Methods: We evaluated patients who underwent HeartMate II as intent for BTT at a single center from 10/2005 to 7/2014. Moderate to severe obstructive pulmonary disease was defined as a forced expiratory volume in 1s (FEV1) to forced vital capacity ratio (FEV1/FVC) < 0.7 and FEV1 < 80%. Results: 183 patients were evaluated; of these, 122 had preoperative PFTs; 61 patients had PFTs deferred due to heart failure exacerbation. Of these 122 patients, 47 had moderate to severe obstructive PFTs (group 1) and 75 patients had normal to mild obstructive PFTs. The mean % predicted FEV1 was 56 ± 12L in group 1 and 72± 17L (p = 0.001) in group 2. The FEV1/ FVC ratio was 0.63 ± 0.1 in group 1 and 0.80 ± 0.05 in group 2 (p = 0.0001). There were no significant differences in age, etiology, gender, INTERMACS profiles, or baseline hemodynamics (p = NS). Patients in group 1 were significantly more likely to have a smoking history (64% vs 35%, p = 0.03) higher pack years of smoking (39 vs 23, p = 0.02), and prior history of COPD (23% vs 5%, 0.004). There was no significant differences in days of ventilation, reintubation, right heart failure, ICU length of stay, length of stay, or LVAD duration of support between group 1 or 2 (p = NS). Actuarial survival at 1 year was 81% in group 1 and 89.5% in group 2 (log rank p = NS). Conclusion: Patients with moderate to severe obstruction on PFTs prior to LVAD placement do not have worse outcomes than those patients with normal PFTs. In patients with end-stage heart failure, poor pulmonary function may be a reflection of decompensated heart failure. Therefore, poor PFTS should not be considered an absolute contraindication to LVAD placement.

Active smoking and secondhand smoke increase breast cancer risk: the report of the Canadian Expert Panel on Tobacco Smoke and Breast Cancer Risk (2009)

Four authoritative reviews of active smoking and breast cancer have been published since 2000, but only one considered data after 2002 and conclusions varied. Three reviews of secondhand smoke (SHS) and breast cancer (2004-2006) each came to different conclusions. With 30 new studies since 2002, further review was deemed desirable. An Expert Panel was convened by four Canadian agencies, the Ontario Tobacco Research Unit, the Public Health Agency of Canada, Physicians for a Smoke-Free Canada and the Canadian Partnership Against Cancer to comprehensively examine the weight of evidence from epidemiological and toxicological studies and understanding of biological mechanisms regarding the relationship between tobacco smoke and breast cancer. This article summarises the panel's full report (http://www.otru.org/pdf/special/expert_panel_tobacco_breast_cancer.pdf). There are 20 known or suspected mammary carcinogens in tobacco smoke, and recognised biological mechanisms that explain how exposure to these carcinogens could lead to breast cancer. Results from the nine cohort studies reporting exposure metrics more detailed than ever/never and ex/current smoker show that early age of smoking commencement, higher pack-years and longer duration of smoking increase breast cancer risk 15% to 40%. Three meta-analyses report 35% to 50% increases in breast cancer risk for long-term smokers with N-acetyltransferase 2 gene (NAT2) slow acetylation genotypes. The active smoking evidence bolsters support for three meta-analyses that each reported about a 65% increase in premenopausal breast cancer risk among never smokers exposed to SHS. The Panel concluded that: 1) the association between active smoking and breast cancer is consistent with causality and 2) the association between SHS and breast cancer among younger, primarily premenopausal women who have never smoked is consistent with causality.

Smoking Affects Diagnostic Salivary Periodontal Disease Biomarker Levels in Adolescents

The effects of smoking on periodontal biomarkers in adolescents are unknown. This study investigates matrix metalloproteinase (MMP)-8 and polymorphonuclear leukocyte elastase levels in saliva together with periodontal health indices accounting for body mass index and smoking in a birth cohort from Finland. The oral health of boys (n = 258) and girls (n = 243) aged 15 to 16 years was examined clinically. Health habits were assessed by questionnaire. Saliva samples were collected and analyzed by immunofluorometric and peptide assays for MMP-8 levels and polymorphonuclear leukocyte elastase activities, and investigated statistically with the background factors. Median MMP-8 values of male smokers were 112.03 microg/l compared to 176.89 microg/l of non-smokers (P = 0.05). For female smokers corresponding values were 170.88 microg/l versus 177.92 microg/l in non-smokers (not statistically significant). Elastase values in male smokers were 5.88 x 10(-3) Delta OD(405)/h versus 11.0 x 10(-3) Delta OD(405)/h in non-smokers (P = 0.02), and in female smokers 9.16 x 10(-3) Delta OD(405)/h versus 10.88 x 10(-3) Delta OD(405)/h in non-smokers (P = 0.72). The effect was strengthened by high pack-years of smoking (MMP-8, P = 0.04; elastase, P = 0.01). Both biomarkers increased with gingival bleeding. However, statistically significant associations were observed with bleeding on probing and MMP-8 (P = 0.04); MMP-8 was suggestively associated with probing depth (P = 0.09) in non-smoking boys. In smokers with calculus, MMP-8 increased after adjusting with body mass index (P = 0.03). No corresponding differences were seen in girls. Smoking significantly decreased both biomarkers studied. Compared to girls, boys seem to have enhanced susceptibility for periodontitis as reflected in salivary MMP-8 values.

Abstract 1865: ERCC2 polymorphisms, smoking, and risk of breast cancer

Abstract The nucleotide excision repair (NER) pathway is important in the repair of bulky DNA lesions, including those that may be induced by cigarette smoking. Excision Repair Cross-Complementing Rodent Repair Deficiency, Complementation Group 2 (ERCC2) is an important gene in the NER pathway. Previous research suggests that polymorphisms in this gene may be associated with altered DNA repair capacity, cancer risk and treatment outcome. This study investigated whether two common single nucleotide polymorphisms (SNPs) in ERCC2 (ERCC2 Asp312Gln and ERCC2 Lys751Gln) were associated with risk of breast cancer, or modified a breast cancer risk associated with smoking. We used data previously collected from a primarily Caucasian population in northeastern Ontario Canada of 347 women diagnosed (2002-2004) with breast cancer and 775 population-based controls. The mailed study package contained a questionnaire that provided information on known breast cancer risk factors and lifetime residential and occupational history of exposure to passive and active smoking, and a buccal swab for genetic analyses. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using unconditional logistic regression, and used a refined referent group that excluded women with substantial exposure to passive smoke and who were never active smokers. Both SNPs were in Hardy-Weinburg Equilibrium (HWE) in controls. Overall, there was no significant association with either SNP and risk of breast cancer. Women who were active smokers of long duration (&amp;gt; 29 years), or high (&amp;gt;20) pack-years, were at significantly increased risk of breast cancer if they carried the G allele of ERCC2Asp312Gln, with ORs of 1.72 (95% CI 1.10-2.68) and 1.68 (95% CI 1.09-2.61) and p=0.03 and 0.007 for trend, respectively. Similar significantly increased risks were observed in women who carried the A allele of ERCC2 Lys751Gln, with ORs of 1.77 (95% CI 1.14-2.76) and 1.67 (95% CI 1.08-2.58) and p=0.02 and 0.01 for trend, respectively. In conclusion, our data suggest that polymorphisms in the NER pathway may modify a smoking-breast cancer relationship. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1865.

NAT2 polymorphisms combining with smoking associated with breast cancer susceptibility: a meta-analysis

To derive a more precise estimation of the relationship between the slow or rapid acetylation resulting from N-acetyltransferase 2 (NAT2) polymorphisms and breast cancer risk, a meta-analysis was performed. PubMed, Medline, Embase, and Web of Science were searched. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess strength of association. The pooled ORs were performed for slow versus rapid acetylation genotypes. A total of 26 studies including 9,215 cases and 10,443 controls were included in the meta-analysis. Overall, no significantly elevated breast cancer risk was associated with NAT2 slow genotypes when all studies were pooled into the meta-analysis (OR = 1.026, 95% CI = 0.968-1.087). In the subgroup analysis by ethnicity, increased risks were not found for either Caucasians (OR = 1.001, 95% CI = 0.938-1.068) or Asians (OR = 1.155, 95% CI = 0.886-1.506). When stratified by study design, statistically significantly elevated risk associated with NAT2 slow genotypes was only found among hospital-based studies (OR = 1.178, 95% CI = 1.037-1.339). In the subgroup analysis by menopausal status, no statistically significantly increased risk was found in either premenopausal (OR = 1.053, 95% CI = 0.886-1.252) or postmenopausal women (OR = 0.965, 95% CI = 0.844-1.104). When stratified by cumulative smoking exposure, in the subgroup of smokers with high pack-years, NAT2 slow genotypes were significantly associated with increased breast cancer risk (OR = 1.400, 95% CI = 1.099-1.784). In conclusion, this meta-analysis suggested that there is overall lack of association between NAT2 genotypes and breast cancer risk, however, NAT2 polymorphisms when combining with heavy smoking history may contribute to breast cancer susceptibility.

Eosinophils in induced sputum from asymptomatic smokers with normal lung function

Cigarette smoking is the dominant risk factor for chronic obstructive pulmonary disease (COPD). However, only 10–15% of smokers develop the disease and early changes within the airways are poorly defined. We aimed to compare cell profiles in induced sputum (IS) from asymptomatic smokers to that from healthy subjects, and to ascertain whether or not inflammatory cells in IS are related to lung function and smoking habit. We recruited 34 heavy, non-allergic asymptomatic smokers with normal lung function and 15 healthy volunteers, who performed lung function tests and IS by hypertonic saline (3%) solution. In smokers, significant correlation between pack-years and FEF25–75(rs=−0·43, P<0·02) was found. In IS, smokers had higher counts of macrophages (P<0·01) and eosinophils (P<0·02), when compared to those of healthy subjects. Additionally, eosinophils were found in IS of 14 out of 34 smokers, with eosinophils had a higher pack-years (31±25 vs. 13±10, P=0·02) and lower FEF25–75%value (78%±34 vs. 100%±23, P<0·04), when compared to smokers without eosinophils. Additionally, on the basis of regression equations by stepwise multiple regression analysis, eosinophils were predicted by pack-years (r2=0·41). Our results showed that asymptomatic smokers have evidence of inflammatory cells in IS samples. In addition, we found that the degree of eosinophilic inflammation is related to early changes of lung function and can be predicted by smoking habit.

Glutathione S-transferase T1-null genotype interacts synergistically with heavy smoking on lung cancer risk.

We studied the influence of genotype for glutathione S-transferase T1 (GSTT1) on susceptibility to lung cancer among 184 Swedish lung cancer patients (88 never-smokers and 96 ever-smokers) and 162 matched population controls (79 never-smokers and 83 ever-smokers), with special emphasis on gene-environment interactions. Cases had significantly lower frequency of the GSTT1-null genotype than that of controls among never-smokers (4.6 vs. 16.5%, P = 0.02), whereas the frequencies were very close to each other among smokers (7.4 vs. 7.2%). Cases with high packyears of smoking, however, had a significantly higher frequency of the GSTT1-null genotype compared to that of cases with low packyears (18.3 vs. 5.6%, P = 0.005). Adjusted for age and gender, the GSTT1-null genotype appeared to be protective against lung cancer among never-smokers (odds ratio [OR] = 0.2, 95% confidence interval [CI] = 0.07-0.7), although it was associated with an increased risk for lung cancer among smokers (OR = 2.1, 95% CI = 0.8-5.9), mainly attributed to the group of heavy smokers (>23 packyears; OR = 3.5, 95% CI = 0.7-17.3). Heavy smoking conferred a threefold increased risk for lung cancer (OR = 2.6, 95% CI = 1.3-5.0) among GSTT1-positive individuals, but a ninefold increased risk when combined with the GSTT1-null genotype (OR = 9.3, 95% CI = 1.9-46.3, relative to GSTT1-positive light smokers). This joint effect was further demonstrated by a positive interaction between the GSTT1-null genotype and packyears of smoking. The risk of lung cancer increased steeply with increasing packyears among GSTT1-null smokers, whereas no such effect was seen among GSTT1-positive smokers. We conclude that the GSTT1-null genotype may strengthen the effect of heavy smoking on lung cancer risk.