In contrast to lung fibroblasts--no signs of senescence in skin fibroblasts of patients with emphysema

Smoking is known to be linked to skin ageing and there is evidence for premature senescence of parenchymal lung fibroblasts in emphysema. To reveal whether the emphysema-related changes in cellular phenotype extend beyond the lung, we compared the proliferation characteristics of lung and skin fibroblasts between patients with and without emphysema. Parenchymal lung fibroblasts and skin fibroblasts from the upper torso (thus limiting sun exposure bias) were obtained from patients without, or with mild, or with moderate to severe emphysema undergoing lung surgery. We analysed proliferation rate, population doublings (PD), staining for senescence-associated beta-galactosidase (beta-gal) and gene expression of IGFBP-3 and IGFBP-rP1. Population doubling time of lung fibroblasts differed between control, mild, and moderate to severe emphysema (median (IQR) 29.7(10.0), 33.4(6.1), 44.4(21.2) h; p=0.012) and staining for beta-gal was elevated in moderate to severe emphysema. Compared to control subjects, skin fibroblasts from patients with emphysema did not differ with respect to proliferation rate, PD and beta-gal staining, and showed a lower abundance of mRNA for IGFBP-3 and -rP1 (p<0.05, each). These results suggest that the induction of a senescent fibroblast phenotype by cigarette smoke, as observed in emphysema, primarily occurs in the lung.

ACETYL RADICAL IN TOBACCO SMOKE: DETECTION, QUANTIFICATION AND SIMULATION

Free radicals are present in cigarette smoke and can have a negative effect on human health by attacking lipids, nucleic acids, proteins and other biologically important species. However, because of the complexity of the tobacco smoke system and the dynamic nature of radicals, little is known about the identity of the radicals, and debate continues on the mechanisms by which those radicals are produced. In this study, acetyl radicals were trapped from the gas phase using 3-amino-2, 2, 5, 5- tetramethyl-proxyl (3AP) on solid support to form stable 3AP adducts for later analysis by high performance liquid chromatography (HPLC), mass spectrometry/tandem mass spectrometry (MS-MS/MS) and liquid chromatography- mass spectrometry (LC-MS). Simulations of acetyl radical generation were performed using Matlab and the Master Chemical Mechanism (MCM) programs. A range of 10- 150 nmol/cigarette of acetyl radical was measured from gas phase tobacco smoke of both commerial and research cigarettes under several different smoking conditions. More radicals were detected from the puff smoking method compared to continuous flow sampling. Approximately twice as many acetyl radicals were trapped when a GF/F particle filter was placed before the trapping zone. Computational simulations show that NO/NO2 reacts with isoprene, initiating chain reactions to produce a hydroxyl radical, which abstracts hydrogen from acetaldehyde to generate acetyl radical. With initial concentrations of NO, acetaldehyde, and isoprene in a real-world cigarette smoke scenario, these mechanisms can account for the full amount of acetyl radical detected experimentally. This study contributes to the overall understanding of the free radical generation in gas phase cigarette smoke.

[Abdominal aortic aneurysm]

Abdominal aortic aneurysms (AAA) confer a substantial healthcare burden in the Western world. Surgical or endovascular therapy is indicated in patients with a maximum diameter exceeding 5.5 cm. Patients with smaller AAA must undergo a specific ultrasound surveillance program aimed at avoiding exposure to an increased risk of rupture once their AAA exceeds the threshold for active treatment. Based on improved understanding of the pathophysiology of AAA, recent years provided initial insight into potential medical treatment options. The presence of AAA is currently regarded a coronary artery disease risk equivalent. ACE inhibitors, statins and JNK-inhibitors were shown to have the potential to slow down progression. Since cigarette smoking is the main risk factor for both the development and progression of AAA, smoking cessation remains a key goal. Further prospective studies will assess the clinical efficacy of various promising drug treatment approaches aimed at slowing disease progression of small AAA and after endovascular therapy.

SerpinB1 deficiency is not associated with increased susceptibility to pulmonary emphysema in mice

Chronic obstructive pulmonary disease (COPD) is characterized by emphysema and chronic bronchitis and is a leading cause of morbidity and mortality worldwide. Tobacco smoke and deficiency in α1-antitrypsin (AAT) are the most prominent environmental and genetic risk factors, respectively. Yet the pathogenesis of COPD is not completely elucidated. Disease progression appears to include a vicious circle driven by self-perpetuating lung inflammation, endothelial and epithelial cell death, and proteolytic degradation of extracellular matrix proteins. Like AAT, serpinB1 is a potent inhibitor of serine proteases including neutrophil elastase and cathepsin G. Because serpinB1 is expressed in myeloid and lung epithelial cells and is protective during lung infections, we investigated the role of serpinB1 in preventing age-related and cigarette smoke-induced emphysema in mice. Fifteen-month-old mice showed increased lung volume and decreased pulmonary function compared with young adult mice (3 mo old), but no differences were observed between serpinB1-deficient (KO) and wild-type (WT) mice. Chronic exposure to secondhand cigarette smoke resulted in structural emphysematous changes compared with respective control mice, but no difference in lung morphometry was observed between genotypes. Of note, the different pattern of stereological changes induced by age and cigarette smoke suggest distinct mechanisms leading to increased airway volume. Finally, expression of intracellular and extracellular protease inhibitors were differently regulated in lungs of WT and KO mice following smoke exposure; however, activity of proteases was not significantly altered. In conclusion, we showed that, although AAT and serpinB1 are similarly potent inhibitors of neutrophil proteases, serpinB1 deficiency is not associated with more severe emphysema.

Xenobiotic Metabolism Genes and Clubfoot

Idiopathic or isolated clubfoot is a common orthopedic birth defect that affects approximately 135,000 children worldwide. It is characterized by equinus, varus and adductus deformities of the ankle and foot. Correction of clubfoot involves months of serial manipulations, castings and bracing, with surgical correction needed in forty percent of cases. Multifactorial etiology has been suggested in numerous studies with both environmental and genetic factors playing an etiologic role. Maternal smoking during pregnancy is the only common environmental factor that has consistently been shown to increase the risk for clubfoot. Moreover, a positive family history of clubfoot and maternal smoking increases the risk of clubfoot twenty fold. These findings suggest that genetic variation in smoking metabolism genes may increase susceptibility to clubfoot. Based on this reasoning, we interrogated eight candidate genes, chosen based on their involvement in phase 1 and 2 cigarette smoke metabolism. Twenty-two SNPs and two null alleles in eight genes (CYP1A1, CYP1A2, CYP1B1, CYP2A6, EPHX1, NAT2, GSTM1 and GSTT1) were genotyped in a dataset composed of nonHispanic white and Hispanic multiplex and simplex families. Only one SNP in CYP1A1, rs1048943, had significantly altered transmission in the aggregate and multiplex NHW datasets (p=0.003 and p=0.009). Perturbation of CYP1A1 by rs1048943 polymorphism causes an increase in the amount of harmful, adduct forming metabolic intermediates. A significant gene interaction between EPHX1 and NAT2 was also found (p=0.007). This interaction may affect the metabolism of harmful metabolic intermediates. Additionally, marginal interactions were found for other xenobiotic genes and these interactions may play a contributory role in clubfoot. Importantly, for CYP1A2, significant maternal (p=0.03; RR=1.24; 95% CI: 1.04-1.44) and fetal (p=0.01; RR=1.33; 95% CI: 1.13-1.54) genotypic effects were identified suggesting that both maternal and fetal genotypes impact normal limb development. No association was found for maternal smoking status and tobacco metabolism genes. Together, these results suggest that xenobiotic metabolism genes may play a contributory role in the etiology of clubfoot regardless of maternal smoking status and may impact foot development through perturbation of tobacco metabolic pathways.

Ultrasound feedback and motivational interviewing targeting smoking cessation in the second and third trimesters of pregnancy.

INTRODUCTION: Cigarette smoking during pregnancy is associated with poor maternal and child health outcomes. Effective interventions to increase smoking cessation rates are needed particularly for pregnant women unable to quit in their first trimester. Real-time ultrasound feedback focused on potential effects of smoking on the fetus may be an effective treatment adjunct, improving smoking outcomes. METHODS: A prospective randomized trial was conducted to evaluate the efficacy of a smoking cessation intervention consisting of personalized feedback during ultrasound plus motivational interviewing-based counseling sessions. Pregnant smokers (N = 360) between 16 and 26 weeks of gestation were randomly assigned to one of three groups: Best Practice (BP) only, Best Practice plus ultrasound feedback (BP+US), or Motivational Interviewing-based counseling plus ultrasound feedback (MI+US). Assessments were conducted at baseline and end of pregnancy (EOP). RESULTS: Analyses of cotinine-verified self-reported smoking status at EOP indicated that 10.8% of the BP group was not smoking at EOP; 14.2% in the BP+US condition and 18.3% who received MI+US were abstinent, but differences were not statistically significant. Intervention effects were found conditional upon level of baseline smoking, however. Nearly 34% of light smokers (< or =10 cigarettes/day) in the MI+US condition were abstinent at EOP, followed by 25.8% and 15.6% in the BP+US and BP conditions, respectively. Heavy smokers (>10 cigarettes/day) were notably unaffected by the intervention. DISCUSSION: Future research should confirm benefit of motivational interviewing plus ultrasound feedback for pregnant light smokers and explore mechanisms of action. Innovative interventions for pregnant women smoking at high levels are sorely needed.

A case-control study of hepatitis C virus and its interaction with hepatitis B virus on the development of hepatocellular carcinoma in the USA

Objective. The aim of this study was to assess the independent risk of hepatitis C virus (HCV) infection in the development of hepatocellular carcinoma (HCC). The independent risk of hepatitis B virus (HBV), its interaction with hepatitis C virus and the association with other risk factors were examined.^ Methods. A hospital-based case-control study was conducted between January 1994 and December 1995. We enrolled 115 pathologically confirmed HCC patients and 230 nonliver cancer controls, who were matched by age ($\pm$5 years), gender, and year of diagnosis. Both cases and controls were recruited from The University of Texas M. D. Anderson Cancer Center at Houston. The risk factors were collected through personal interviews and blood samples were tested for HCV and HBV markers. Univariate and multivariate analyses were performed through conditional logistic regression.^ The prevalence of anti-HCV positive is 25.2% in HCC cases compared to 3.0% in controls. The univariate analysis showed that anti-HCV, HBsAg, alcohol drinking and cigarette smoking were significantly associated with HCC, however, family history of cancer, occupational chemical exposure, and use of oral contraceptive were not. Multivariate analysis revealed a matched odds ratio (OR) of 10.1 (95% CI 3.7-27.4) for anti-HCV, and an OR of 11.9 (95% CI 2.5-57.5) for HBsAg. However, dual infection of HCV and HBV had only a thirteen times increase in the risk of HCC, OR = 13.9 (95% CI 1.3-150.6). The estimated population attributable risk percent was 23.4% for HCV, 12.6% for HBV, and 5.3% for both viruses. Ever alcohol drinkers was positively associated with HCC, especially among daily drinkers, matched OR was 5.7 (95% CI 2.1-15.6). However, there was no significant increase in the risk of HCC among smokers as compared to nonsmokers. The mean age of HCC patients was significantly younger among the HBV(+) group and among the HCV(+)/HBV(+) group, when compared to the group of HCC patients with no viral markers. The association between past histories of blood transfusion, acupuncture, tattoo and IVDU was highly significant among the HCV(+) group and the HBV(+)/HCV(+) group, as compared to HCC patients with no viral markers. Forty percent of the HCC patients were pathologically or clinically diagnosed with liver cirrhosis. Anti-HCV(+) (OR = 3.6 95% CI 1.5-8.9) and alcohol drinking (OR = 2.7 95% CI 1.1-6.7), but not HBsAg, are the major risk factors for liver cirrhosis in HCC patients.^ Conclusion. Both hepatitis B virus and hepatitis C virus were independent risk factors for HCC. There was not enough evidence to determine the interaction between both viruses. Only daily alcoholic drinkers showed increasing risk for HCC development, as compared to nondrinkers. ^

The angiotensin-converting enzyme insertion/deletion polymorphism and its associations with carotid artery wall thickness and coronary heart disease: The atherosclerosis risk in communities study

Coronary heart disease (CHD) is the leading cause of death in the United States. Recently, renin-angiotensin system (RAS) was found associated with atherosclerosis formation, with angiotensin II inducing vascular smooth muscle cell growth and migration, platelet activation and aggregation, and stimulation of plasminogen activator inhibitor-1. Angiotensin II is converted from angiotensin I by angiotensin I-converting enzyme (ACE) and this enzyme is mainly genetically determined. The ACE gene has been assigned to chromosome 17q23 and an insertion/deletion (I/D)polymorphism has been characterized by the presence/absence of a 287 bp fragment in intron 16 of the gene. The two alleles form three genotypes, namely, DD, ID and II and the DD genotype has been linked to higher plasma ACE levels and cell ACE activity.^ In this study, the association between the ACE I/D polymorphism and carotid artery wall thickness measured by B-mode ultrasound was investigated in a biracial sample, and the association between the gene and incident CHD was investigated in whites and if the gene-CHD association in whites, if any, was due to the gene effect on atherosclerosis. The study participants are from the prospective Atherosclerosis Risk in Communities (ARIC) Study, including adults aged 45 to 65 years. The present dissertation used a matched case-control design for studying the associations of the ACE gene with carotid artery atherosclerosis and an unmatched case-control design for the association of the gene with CHD. A significant recessive effect of the D allele on carotid artery thickness was found in blacks (OR = 3.06, 95% C.I: 1.11-8.47, DD vs. ID and II) adjusting for age, gender, cigarette smoking, LDL-cholesterol and diabetes. No similar associations were found in whites. The ACE I/D polymorphism is significantly associated with coronary heart disease in whites, and while stratifying data by carotid artery wall thickness, the significant associations were only observed in thin-walled subgroups. Assuming a recessive effect of the D allele, odds ratio was 2.84 (95% C.I:1.17-6.90, DD vs. ID and II) and it was 2.30 (95% C.I:1.22-4.35, DD vs. ID vs. II) assuming a codominant effect of the D allele. No significant associations were observed while comparing thick-walled CHD cases with thin-walled controls. Following conclusions could be drawn: (1) The ACE I/D polymorphism is unlikely to confer appreciable increase in the risk of carotid atherosclerosis in US whites, but may increases the risk of carotid atherosclerosis in blacks. (2) ACE I/D polymorphism is a genetic risk factor for incident CHD in US whites and this effect is separate from the chronic process of atherosclerosis development. Finally, the associations observed here are not causal, since the I/D polymorphism is in an intron, where no ACE proteins are encoded. ^

EMPLOYMENT AND EXPOSURES IN THE PETROLEUM REFINING AND PETROCHEMICAL INDUSTRIES AND THE RISK OF LUNG CANCER (EPIDEMIOLOGY, ASSESSMENT)

This dissertation addresses the risk of lung cancer associated with occupational exposures in the petroleum refining and petrochemical industries. Earlier epidemiologic studies of this association did not adjust for cigarette smoking or have specific exposure classifications. The Texas EXposure Assessment System (TEXAS) was developed with data from a population-based, case-comparison study conducted in five southeast Texas counties between 1976 and 1980. The Texas Exposure Assessment System uses job and process categories developed by the American Petroleum Institute, as well as time-oriented variables to identify high risk groups.^ An industry-wide, increased risk for lung cancer was associated with jobs having low-level hydrocarbon exposure that also include other occupational inhalation exposures (OR = 2.0--adjusted for smoking and latency effects). The prohibition of cigarette smoking for jobs with high-level hydrocarbon exposure might explain part of the increased risk for jobs with low-level hydrocarbon exposures. Asbestos exposure comprises a large part of the risk associated with jobs having other inhalation exposures besides hydrocarbons. Workers in petroleum refineries were not shown to have an increased, occupational risk for lung cancer. The increased risk for lung cancer among petrochemical workers (OR = 3.1--smoking and latency adjusted) is associated with all jobs that involve other inhalation exposure characteristics (not only low-level hydrocarbon exposures). Findings for contract workers and workers exposed to specific chemicals were inconclusive although some hypotheses for future research were identified.^ The study results demonstrate that the predominant risk for lung cancer is due to cigarette smoking (OR = 9.8). Cigarette smoking accounts for 86.5% of the incident lung cancer cases within the study area. Workers in the petroleum industry smoke significantly less than persons employed in other industries (p << 0.001). Only 2.2% of the incident lung cancer cases may be attributed to petroleum industry jobs; lifestyle factors (e.g., nutrition) may be associated with the balance of the cases. The results from this study also suggest possible high risk time periods (OR = 3.9--smoking and occupation adjusted). Artifacts in time-oriented findings may result because of the latency interval for lung cancer, secular peaks in age-, sex-specific incidence rates, or periods of hazardous exposures in the petroleum industry. ^

Assessment of smoking behaviour in a dental setting: a 1-year follow-up study using self-reported questionnaire data and exhaled carbon monoxide levels.

OBJECTIVES This study analyses the changes in smoking habits over the course of 1 year in a group of patients referred to an oral medicine unit. MATERIALS AND METHODS Smoking history and behaviour were analysed at baseline and after 1 year based on a self-reported questionnaire and on exhaled carbon monoxide levels [in parts per million (ppm)]. During the initial examination, all smokers underwent tobacco use prevention and cessation counselling. RESULTS Of the initial group of 121 patients, 98 were examined at the follow-up visit. At the baseline examination, 33 patients (33.67 %) indicated that they were current smokers. One year later, 14 patients (42.24 % out of the 33 smokers of the initial examination) indicated that they had attempted to stop smoking at least once over the follow-up period and 15.15 % (5 patients) had quit smoking. The mean number of cigarettes smoked per day by current smokers decreased from 13.10 to 12.18 (p = 0.04). The exhaled CO level measurements showed very good correlation with a Spearman's coefficient 0.9880 for the initial visit, and 0.9909 for the follow-up examination. For current smokers, the consumption of one additional cigarette per day elevated the CO measurements by 0.77 ppm (p < 0.0001) at the baseline examination and by 0.84 ppm (p < 0.0001) at the 1-year follow-up. CONCLUSIONS In oral health care, where smoking cessation is an important aspect of the treatment strategy, the measurement of exhaled carbon monoxide shows a very good correlation with a self-reported smoking habit. CLINICAL RELEVANCE Measurement of exhaled carbon monoxide is a non-invasive, simple and objective measurement technique for documenting and monitoring smoking cessation and reduction.

Prevalence and Risk Factors for Therapy Escalation in Ulcerative Colitis in the Swiss IBD Cohort Study.

BACKGROUND Physicians traditionally treat ulcerative colitis (UC) using a step-up approach. Given the paucity of data, we aimed to assess the cumulative probability of UC-related need for step-up therapy and to identify escalation-associated risk factors. METHODS Patients with UC enrolled into the Swiss IBD Cohort Study were analyzed. The following steps from the bottom to the top of the therapeutic pyramid were examined: (1) 5-aminosalicylic acid and/or rectal corticosteroids, (2) systemic corticosteroids, (3) immunomodulators (IM) (azathioprine, 6-mercaptopurine, methotrexate), (4) TNF antagonists, (5) calcineurin inhibitors, and (6) colectomy. RESULTS Data on 996 patients with UC with a median disease duration of 9 years were examined. The point estimates of cumulative use of different treatments at years 1, 5, 10, and 20 after UC diagnosis were 91%, 96%, 96%, and 97%, respectively, for 5-ASA and/or rectal corticosteroids, 63%, 69%, 72%, and 79%, respectively, for systemic corticosteroids, 43%, 57%, 59%, and 64%, respectively, for IM, 15%, 28%, and 35% (up to year 10 only), respectively, for TNF antagonists, 5%, 9%, 11%, and 12%, respectively, for calcineurin inhibitors, 1%, 5%, 9%, and 18%, respectively, for colectomy. The presence of extraintestinal manifestations and extended disease location (at least left-sided colitis) were identified as risk factors for step-up in therapy with systemic corticosteroids, IM, TNF antagonists, calcineurin inhibitors, and surgery. Cigarette smoking at diagnosis was protective against surgery. CONCLUSIONS The presence of extraintestinal manifestations, left-sided colitis, and extensive colitis/pancolitis at the time of diagnosis were associated with use of systemic corticosteroids, IM, TNF antagonists, calcineurin inhibitors, and colectomy during the disease course.

Associations Between Cardiovascular Risk Factors, Inflammation, and Progression of Carotid Atherosclerosis Among Smokers

INTRODUCTION The high risk of cardiovascular events in smokers requires adequate control of other cardiovascular risk factors (CVRFs) to curtail atherosclerosis progression. However, it is unclear which CVRFs have the most influence on atherosclerosis progression in smokers. METHODS In 260 smokers aged 40-70 included in a smoking cessation trial, we analyzed the association between traditional CVRFs, high-sensitivity C-reactive protein (hs-CRP), smoking cessation and 3-year progression of carotid intima-media thickness (CIMT, assessed by repeated ultrasound measurements) in a longitudinal multivariate model. RESULTS Participants (mean age 52 years, 47% women) had a mean smoking duration of 32 years with a median daily consumption of 20 cigarettes. Baseline CIMT was 1185 μm (95% confidence interval [CI]: 1082-1287) and increased by 93 μm (95% CI: 25-161) and 108 μm (95% CI: 33-183) after 1 and 3 years, respectively. Age, male sex, daily cigarette consumption, systolic blood pressure (SBP), but neither low-density lipoprotein cholesterol nor hs-CRP, were independently associated with baseline CIMT (all P ≤ .05). Baseline SBP, but neither low-density lipoprotein cholesterol nor hs-CRP, was associated with 3-year atherosclerosis progression (P = .01 at 3 years). The higher the SBP at baseline, the steeper was the CIMT increase over 3-year follow-up. We found an increase of 26 μm per each 10-mmHg raise in SBP at 1 year and an increase of 39 μm per each 10 mmHg raise in SBP at 3 years. Due to insufficient statistical power, we could not exclude an effect of smoking abstinence on CIMT progression. CONCLUSION Control of blood pressure may be an important factor to limit atherosclerosis progression in smokers, besides support for smoking cessation. IMPLICATIONS Among 260 smokers aged 40-70 years with a mean smoking duration of 32 years, baseline SBP was associated with atherosclerosis progression over 3 years, as measured by CIMT (P = .01 at 3 years), independently of smoking variables and other CVRFs. The higher the SBP at baseline, the steeper was the CIMT increase over 3-year follow-up. Our findings emphasize the importance of focusing not only on smoking cessation among smokers, but to simultaneously control other CVRFs, particularly blood pressure, in order to prevent future cardiovascular disease.

Effect of maternal weight status on the relationship between prenatal smoking and infant birth weight

The purpose of this study was to assess the effect of maternal pre-pregnancy weight status on the relationship between prenatal smoking and infant birth weight (IBW). Prenatal cigarette smoking and maternal weight exert opposing effects on IBW; smoking decreases birth weight while maternal pre-pregnancy weight is positively correlated with birth weight. As such, mutual effect modification may be sufficiently significant to alter the independent effects of these two birth weight correlates. Finding of such an effect has implications of prenatal smoking cessation education. Perception of risk is an important determinant of smoking cessation, and reduced or low birth weight (LBW) as a smoking-associated risk predominates prenatal smoking counseling and education. In a population such as the US, where obesity is becoming epidemic, particularly among minority and low-income groups, perception of risk may be lowered should increased maternal size attenuate the effect of smoking. Previous studies have not found a significant interaction effect of prenatal smoking and maternal pre-pregnancy weight on IBW; however, use of self-reported smoking status may have biased findings. Reliability of self-reported smoking status reported in the literature is variable, with deception rates ranging from a low of 5% to as high as 16%. This study, using data from a prenatal smoking cessation project, in which smoking status was validated by saliva cotinine, was an opportunity to assess effect modification of smoking and maternal weight using biochemically determined smoking status in lieu of self report. Stratified by saliva cotinine, 151 women from a prenatal smoking cessation cohort, who were 18 years and older and had full-term, singleton births, were included in this study. The effect of smoking in terms of mean birth weight across three levels of maternal pre-pregnancy weight was assessed by general linear modeling procedures, adjusting for other known correlates of IBW. Effect modification was marginally significant, p = .104, but only with control for differential effects among racial/ethnic groups. A smaller than planned sample of nonsmokers, or women who quit smoking during the pregnancy, prohibited rejection of the null hypothesis of no difference in the effect of smoking across levels of pre-pregnancy weight. ^

The role of smoking status on postoperative complications and survival in lung cancer patients presenting to M.D. Anderson Cancer Center

It is estimated that 50% of all lung cancer patients continue to smoke after diagnosis. Many of these lung cancer patients who are current smokers often experience tremendous guilt and responsibility for their disease, and feel it might be too late for them to quit smoking. In addition, many oncologists may be heard to say that it is 'too late', 'it doesn't matter', 'it is too difficult', 'it is too stressful' for their patients to stop smoking, or they never identify the smoking status of the patient. Many oncologists feel unprepared to address smoking cessation as part of their clinical practice. In reality, physicians can have tremendous effects on motivating patients, particularly when patients are initially being diagnosed with cancer. More information is needed to convince patients to quit smoking and to encourage clinicians to assist patients with their smoking cessation. ^ In this current study, smoking status at time of lung cancer diagnosis was assessed to examine its impact on complications and survival, after exploring the reliability of smoking data that is self-reported. Logistic Regression was used to determine the risks of smoking prior to lung resection. In addition, survival analysis was performed to examine the impact of smoking on survival. ^ The reliability of how patients report their smoking status was high, but there was some discordance between current smokers and recent quitters. In addition, we found that cigarette pack-year history and duration of smoking cessation were directly related to the rate of a pulmonary complication. In regards to survival, we found that current smoking at time of lung cancer diagnosis was an independent predictor of early stage lung cancer. This evidence supports the idea that it is "never too late" for patients to quit smoking and health care providers should incorporate smoking status regularly into their clinical practice.^

The association between smoking marijuana and the occurrence of lung cancer

It is still unclear if an association exists between the smoking of marijuana and the occurrence of lung cancer although one clearly exists between cigarette smoking and lung cancer. The objective of this study was to systematically review the literature in order to assess the impact of marijuana smoking, which is increasingly becoming a significant public health issue, on the occurrence of the number one killing cancer, lung cancer. ^ Method. Selected studies in the English language conducted on humans that assess the impact of marijuana smoking on lung cancer were identified from EBSCO MEDLINE, PUBMED, and GOOGLE databases. The search keywords were marijuana, cannabis, hashish, kif, and lung cancer with selection criteria including studies in the English language identified from 1950 to April 2008. Excluded were non-research studies such as editorials, letters, and reviews. Also excluded were studies that did not involve humans with direct intentional marijuana smoking or in vivo studies with mice. Case report studies or case series studies involving less than 10 patients were also excluded as well as studies that did not examine lung conditions related to premalignant or cancerous changes. ^ Results. Ten studies met the selection criteria and were analyzed. The ten studies in this review overall offer biological evidence of the potential association between marijuana smoking and premalignant lung findings but no overwhelming conclusive evidence for the association between marijuana smoking and the occurrence of lung cancer. Two of the observational studies [1, 2] failed to demonstrate an association between marijuana and lung cancer, but the remaining studies supported an association between marijuana smoking and premalignant or malignant lung findings. ^ Conclusion. It must, therefore, be concluded that no convincing evidence exists, based on the existing data, for an association between marijuana smoking and the occurrence of lung cancer even though the few observational studies failing to report such an association may be due to certain limitations particularly the relative young age of the participants precluding sufficient lag time for the identification of lung cancer outcome as explained in other sections of this paper. ^ Further research is, therefore, necessary to better evaluate this critical issue, while recommendations against smoking marijuana because of its potential harmful effects, including the potential for premalignant lung changes as noted in this review, should continue to be made. ^ In the future, large prospective studies with study participants representing a much wider spectrum of ages, and longer follow-up periods, with detailed assessment of marijuana exposure and definitive pathologic diagnosis of lung cancer are necessary^