Periodical Multiphasic Screening and Lung Cancer Prevention

AbstractThe purpose of this work is to evaluate the utilization of information gathered by multiphasic screening with respect to lung cancer detection and smoking cessation techniques. A cohort (follow-up) study is reported in which cancer incidence and factors affecting its occurrence are evaluated in a group of about 20,000 presumably healthy adults along a period of approximately 10 years following comprehensive multiphasic health examinations. Lung cancer occurrence is primarily related to smoking. The risk is higher in smokers and is dose-dependent; OR = 0.21, (CI = 0.08,.53) in never smokers, OR = 1.53 (CI = 0.8,3.2) in past and current moderate smokers, OR = 4.92 (CI = 2.18,11.11) in current heavy smokers. Moreover, smokers with compromised pulmonary function (FEVI/FVC < 75%) are at an even higher risk of developing lung cancer OR = 4.22 (CI = 2.2, 8.2) for past and current moderate smokers; and OR = 10.7 (CI-2.5, 38.6) in current heavy smokers. Information gathered in periodical multiphasic health examinations could be utilized by health professionals to encourage smoking cessation and smoking prevention in the appropriate screenees. Various elements of the multiphasic test results could contribute to such prevention efforts. While every smoker should receive appropriate evaluation and consultation regarding nicotine dependence, smokers with reduced pulmonary function represent an extra high risk group to which special attention should be given.

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Developing a comprehensive smoking cessation program in patients with lung cancer: The role of social smoking environments.

Journal of Clinical Oncology ◽

10.1200/jco.2012.30.34_suppl.75 ◽

2012 ◽

Vol 30 (34_suppl) ◽

pp. 75-75

Author(s):

Lawson Eng ◽

Jie Su ◽

Xin Qiu ◽

Prakruthi R. Palepu ◽

Henrique Hon ◽

...

Keyword(s):

Lung Cancer ◽

Smoking Cessation ◽

Cancer Patients ◽

Past History ◽

Lung Cancer Patients ◽

Quitting Smoking ◽

Key Factor ◽

History Of ◽

Never Smokers

75 Background: Smoking during cancer treatment negatively impacts outcome, survival, and quality of life. Social smoking environments (SSEs) (i.e., smoking in household, peers, and spouse) influence cessation rates in non-cancer patients, but are understudied in cancer patients. Methods: Lung cancer patients, recruited from Princess Margaret Hospital (2006-2012) were given baseline and follow-up questionnaires (median of 2 years apart) evaluating changes in smoking habits and SSEs. Multivariate logistic regression and Cox-proportional hazard models evaluated the association of socio-demographics, clinicopathological and SSE factors with smoking cessation and time to quitting, respectively. Results: 721 patients completed both questionnaires. Of the 261 current smokers at diagnosis, 180 (69%) had quit by follow-up. Among 318 ex-smokers, 5 re-started smoking after diagnosis. All of the 140 never smokers remained non-smoking. Home smoke exposure (OR=9.4; 95% CI: 3.4-26.2; p=2.0 x 10E-5), spousal smoking (OR=4.7, 95% CI:1.7-12.6; p=3.0 x 10E-3) and peer smoking (OR=2.6; 95% CI:1.1-6.1; p=0.03) were each associated with reduced cessation, adjusted for a base multivariate model that included education and past history of depression. Individuals with no SSE factors had a much higher chance of quitting smoking when compared to patients with multiple areas of SSEs (0 vs. 3, OR=16.4; 95% CI: 4.1-66.7; p=7.3 x 10E-5). Similar results were seen when using time-to-quitting as the outcome (0 vs 3, OR=4.4, 95% CI=1.4-14.1, p=0.01). Time to quitting analysis found that 60% of patients with at least one SSE who did quit, did so within 6 months of diagnosis. Subgroup analysis revealed similar associations in early- and late-stage patient groups. Conclusions: SSE is a key factor in smoking cessation, where household smoke exposures reduces the chance of quitting up to 9-fold. SSEs should be a key consideration when developing smoking cessation programs in lung cancer patients, as part of quality improvement strategies. Approaches incorporating household members or spouses into the smoking cessation intervention, around the time of diagnosis, should be researched further. GL and WX are co-senior authors.

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Social environment as a predictor of smoking cessation and recidivism in lung cancer survivors.

Journal of Clinical Oncology ◽

10.1200/jco.2012.30.15_suppl.9032 ◽

2012 ◽

Vol 30 (15_suppl) ◽

pp. 9032-9032

Author(s):

Lawson Eng ◽

Jie Su ◽

Prakruthi R. Palepu ◽

Henrique Hon ◽

Ehab Fadhel ◽

...

Keyword(s):

Lung Cancer ◽

Smoking Cessation ◽

Cancer Patients ◽

Social Environment ◽

Smoking History ◽

Recidivism Rates ◽

Lung Cancer Patients ◽

Never Smokers ◽

At Home

9032 Background: Smoking during cancer treatment negatively impacts treatment, survival and quality of life. Lung cancer patients with a smoking history often continue to smoke; some ex-smokers re-start after diagnosis. Social environment impacts cessation and recidivism rates in non-cancer patients. We assessed whether the same influences occur among lung cancer patients. Methods: Lung cancer patients, recruited from Princess Margaret Hospital, completed a baseline questionnaire about their demographics and smoking history (at diagnosis). A follow-up questionnaire was administered at a median of two years, assessing changes in smoking habits, exposure at home/work/among friends, healthcare use, social support and alcohol use since diagnosis. The relationship between each variable with cessation/recidivism was analyzed. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated. Results: 478 patients completed both questionnaires. Of the 100 current smokers at diagnosis; 52 quit by the time of the follow-up questionnaire. Among 294 ex-smokers, 15 started to smoke after diagnosis. None of the 84 never smokers at baseline started to smoke after diagnosis. Exposure to smoking at home was associated with continued smoking and relapse (OR=5.1, 95% CI: 1.8–14.3, p=0.001; and OR=3.9, 95% CI: 0.8–14.4, p=0.04, respectively). Specifically, spousal smoking was associated with both continued smoking (OR=7.3, 95% CI: 2.4–21.7, p=2.0E-04) and recidivism (OR=3.7, 95% CI: 0.6–16.6, p=0.08). Having more than a few friends who smoke is associated with continued smoking (OR=3.5, 95% CI: 1.4–8.7, p=0.005) and relapse (OR=4.8, 95% CI: 1.5–15.0, p=0.004). Not completing high school was also associated with continued smoking (OR=3.0, 95% CI: 1.2–7.6, p=0.02). Multivariate analysis identified spousal smoking as the major single predictor of continued smoking (OR=8.8, 95% CI: 2.2–34.8, p=0.002). Conclusions: Smoking cessation programs for lung cancer patients should not only target the patient but also include the immediate family, consider a patient’s peers and be tailored to the patient’s education level. Involvement of the immediate family and consideration of peers may help prevent smoking relapse.

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Smoking cessation, decline in pulmonary function and total mortality: a 30 year follow up study among the Finnish cohorts of the Seven Countries Study

Thorax ◽

10.1136/thx.56.9.703 ◽

2001 ◽

Vol 56 (9) ◽

pp. 703-707

Author(s):

M Pelkonen ◽

I-L Notkola ◽

H Tukiainen ◽

M Tervahauta ◽

J Tuomilehto ◽

...

Keyword(s):

Smoking Cessation ◽

Pulmonary Function ◽

Total Mortality ◽

Forced Expiratory Volume ◽

Rapid Decline ◽

Seven Countries Study ◽

Never Smokers ◽

The Relationship

BACKGROUNDPermanent smoking cessation reduces loss of pulmonary function. Less is known in the long term about individuals who give up smoking temporarily or quitters with lower initial pulmonary function. Little is known also about the relationship between decline in pulmonary function and mortality. We examined these aspects and the association between smoking, decline in pulmonary function, and mortality.METHODSTwo middle aged male Finnish cohorts of the Seven Countries Study and their re-examinations on five occasions during a 30 year period of follow up were analysed.RESULTSDuring the first 15 years (n=1007) adjusted decline in forced expiratory volume in 0.75 seconds (FEV0.75) was 46.4 ml/year in never smokers, 49.3 ml/year in past smokers, 55.5 ml/year in permanent quitters, 55.5 ml/year in intermittent quitters, and 66.0 ml/year in continuous smokers (p<0.001 for trend). Quitters across the entire range of baseline FEV0.75 had a slower decline in FEV0.75 than continuous smokers. Among both continuing smokers and never smokers, non-survivors had a significantly (p<0.001) more rapid decline in FEV0.75 than survivors. The adjusted relative hazard for total mortality was 1.73 (95% confidence interval (CI) 1.41 to 2.11) and 1.24 (95% CI 1.02 to 1.52) in the lowest and middle tertiles of decline in FEV0.75. Never smokers, past smokers, and quitters had significantly lower total mortality than continuous smokers, partly because of their slower decline in FEV0.75.CONCLUSIONThese results highlight the positive effect of smoking cessation, even intermittent cessation, on decline in pulmonary function. Accelerated decline in pulmonary function was found to be a risk factor for total mortality. The beneficial effect of smoking cessation on mortality may partly be mediated through a reduced decline in pulmonary function.

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Factors affecting success and abstinence within a smoking cessation clinic: A one-year follow-up study in Turkey

Tobacco Prevention & Cessation ◽

10.18332/tpc/130471 ◽

2020 ◽

Vol 6 (December) ◽

pp. 1-8

Author(s):

Ayse Esen ◽

Yuksel Soylem ◽

Secil Arica ◽

Gulten Belgin ◽

Nadire Gonultas

Keyword(s):

Smoking Cessation ◽

Factors Affecting ◽

Follow Up Study ◽

One Year ◽

Cessation Clinic ◽

Smoking Cessation Clinic

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Lifestyle and Long-Term Smoking Cessation

Tobacco Use Insights ◽

10.1177/1179173x20963062 ◽

2020 ◽

Vol 13 ◽

pp. 1179173X2096306

Author(s):

Tove Sohlberg ◽

Karin Helmersson Bergmark

Keyword(s):

Smoking Cessation ◽

Smoking Initiation ◽

Lifestyle Changes ◽

Factors Affecting ◽

Quit Smoking ◽

Swedish Health Care ◽

The Impact ◽

Term Maintenance

Background: Since smoking is the leading cause of preventable death, discouraging smoking initiation, encouraging smoking cessation, and exploring factors that help individuals to stay smoke free are immensely important. One such relevant factor may be the impact of lifestyle for long-term smoking cessation. Method: A representative sample of successful quitters was recruited for a study about smoking cessation. These respondents are now part of a 7-year follow-up with the overall aim of revealing factors affecting long-term smoking cessation. Descriptive analyses were carried out at baseline and at follow-up, as well as a further two-step cluster analysis to explore profiles of long-term smoke-free individuals. Results: A majority did not make any particular lifestyle changes, but among those who did, most adopted a healthier lifestyle and/or increased their quota of physical training, where permanent changes in this direction seem to promote a more enduring smoke-free life. Conclusions: Individuals who want to quit smoking should be encouraged to increase their level of physical activity. Swedish health care institutions should be able to provide support for this both initially and over time to promote the long-term maintenance of a smoke-free lifestyle.

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Chronic obstructive pulmonary disease and lung cancer incidence in never smokers: a cohort study

Thorax ◽

10.1136/thoraxjnl-2019-213732 ◽

2020 ◽

Vol 75 (6) ◽

pp. 506-509 ◽

Cited By ~ 3

Author(s):

Hye Yun Park ◽

Danbee Kang ◽

Sun Hye Shin ◽

Kwang-Ha Yoo ◽

Chin Kook Rhee ◽

...

Keyword(s):

Lung Cancer ◽

Chronic Obstructive Pulmonary Disease ◽

Cohort Study ◽

Pulmonary Disease ◽

Cancer Incidence ◽

Chronic Obstructive ◽

Lung Cancer Incidence ◽

Obstructive Pulmonary Disease ◽

Never Smokers

There has been limited evidence for the association between chronic obstructive pulmonary disease (COPD) and the incidence of lung cancer among never smokers. We aimed to estimate the risk of lung cancer incidence in never smokers with COPD, and to compare it with the risk associated with smoking. This cohort study involved 338 548 subjects, 40 to 84 years of age with no history of lung cancer at baseline, enrolled in the National Health Insurance Service National Sample Cohort. During 2 355 005 person-years of follow-up (median follow-up 7.0 years), 1834 participants developed lung cancer. Compared with never smokers without COPD, the fully-adjusted hazard ratios (95% CI) for lung cancer in never smokers with COPD, ever smokers without COPD, and ever smokers with COPD were 2.67 (2.09 to 3.40), 1.97 (1.75 to 2.21), and 6.19 (5.04 to 7.61), respectively. In this large national cohort study, COPD was also a strong independent risk factor for lung cancer incidence in never smokers, implying that COPD patients are at high risk of lung cancer, irrespective of smoking status.

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Personalized Risk Assessment in Never, Light, and Heavy Smokers in a prospective cohort in Taiwan

Scientific Reports ◽

10.1038/srep36482 ◽

2016 ◽

Vol 6 (1) ◽

Cited By ~ 8

Author(s):

Xifeng Wu ◽

Chi Pang Wen ◽

Yuanqing Ye ◽

MinKwang Tsai ◽

Christopher Wen ◽

...

Keyword(s):

Lung Cancer ◽

Family History ◽

Lung Function ◽

Risk Prediction ◽

Prospective Cohort ◽

Lung Function Test ◽

Function Test ◽

History Of ◽

Never Smokers ◽

Heavy Smokers

Abstract The objective of this study was to develop markedly improved risk prediction models for lung cancer using a prospective cohort of 395,875 participants in Taiwan. Discriminatory accuracy was measured by generation of receiver operator curves and estimation of area under the curve (AUC). In multivariate Cox regression analysis, age, gender, smoking pack-years, family history of lung cancer, personal cancer history, BMI, lung function test, and serum biomarkers such as carcinoembryonic antigen (CEA), bilirubin, alpha fetoprotein (AFP), and c-reactive protein (CRP) were identified and included in an integrative risk prediction model. The AUC in overall population was 0.851 (95% CI = 0.840–0.862), with never smokers 0.806 (95% CI = 0.790–0.819), light smokers 0.847 (95% CI = 0.824–0.871), and heavy smokers 0.732 (95% CI = 0.708–0.752). By integrating risk factors such as family history of lung cancer, CEA and AFP for light smokers, and lung function test (Maximum Mid-Expiratory Flow, MMEF25–75%), AFP and CEA for never smokers, light and never smokers with cancer risks as high as those within heavy smokers could be identified. The risk model for heavy smokers can allow us to stratify heavy smokers into subgroups with distinct risks, which, if applied to low-dose computed tomography (LDCT) screening, may greatly reduce false positives.

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Second-Hand Smoke As a Predictor of Smoking Cessation Among Lung Cancer Survivors

Journal of Clinical Oncology ◽

10.1200/jco.2013.50.9695 ◽

2014 ◽

Vol 32 (6) ◽

pp. 564-570 ◽

Cited By ~ 44

Author(s):

Lawson Eng ◽

Jie Su ◽

Xin Qiu ◽

Prakruthi R. Palepu ◽

Henrique Hon ◽

...

Keyword(s):

Lung Cancer ◽

Smoking Cessation ◽

Cancer Survivors ◽

Second Hand Smoke ◽

Proportional Hazard ◽

Cox Proportional Hazard ◽

Cox Proportional Hazard Models ◽

Peer Smoking ◽

After Cancer

Purpose Second-hand smoke (SHS; ie, exposure to smoking of friends and spouses in the household) reduces the likelihood of smoking cessation in noncancer populations. We assessed whether SHS is associated with cessation rates in lung cancer survivors. Patients and Methods Patients with lung cancer were recruited from Princess Margaret Cancer Centre, Toronto, ON, Canada. Multivariable logistic regression and Cox proportional hazard models evaluated the association of sociodemographics, clinicopathologic variables, and SHS with either smoking cessation or time to quitting. Results In all, 721 patients completed baseline and follow-up questionnaires with a mean follow-up time of 54 months. Of the 242 current smokers at diagnosis, 136 (56%) had quit 1 year after diagnosis. Exposure to smoking at home (adjusted odds ratio [aOR], 6.18; 95% CI, 2.83 to 13.5; P < .001), spousal smoking (aOR, 6.01; 95% CI, 2.63 to 13.8; P < .001), and peer smoking (aOR, 2.49; 95% CI, 1.33 to 4.66; P = .0043) were each associated with decreased rates of cessation. Individuals exposed to smoking in all three settings had the lowest chances of quitting (aOR, 9.57; 95% CI, 2.50 to 36.64; P < .001). Results were similar in time-to-quitting analysis, in which 68% of patients who eventually quit did so within 6 months after cancer diagnosis. Subgroup analysis revealed similar associations across early- and late-stage patients and between sexes. Conclusion SHS is an important factor associated with smoking cessation in lung cancer survivors of all stages and should be a key consideration when developing smoking cessation programs for patients with lung cancer.

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Immune-mediated genetic pathways resulting in pulmonary function impairment increase lung cancer susceptibility

10.1101/635318 ◽

2019 ◽

Author(s):

Linda Kachuri ◽

Mattias Johansson ◽

Sara R. Rashkin ◽

Rebecca E. Graff ◽

Yohan Bossé ◽

...

Keyword(s):

Lung Cancer ◽

Pulmonary Function ◽

Cancer Susceptibility ◽

Forced Expiratory Volume ◽

Lung Carcinogenesis ◽

Cancer Etiology ◽

Impaired Lung Function ◽

Never Smokers ◽

The Uk ◽

Lung Cancer Susceptibility

ABSTRACTImpaired lung function is often caused by cigarette smoking, making it challenging to disentangle its role in lung cancer susceptibility. Investigation of the shared genetic basis of these phenotypes in the UK Biobank and International Lung Cancer Consortium (29,266 cases, 56,450 controls) shows that lung cancer is genetically correlated with reduced forced expiratory volume in one second (FEV1: rg=0.098, p=2.3×10−8) and the ratio of FEV1 to forced vital capacity (FEV1/FVC: rg=0.137, p=2.0×10−12). Mendelian randomization analyses demonstrate that reduced FEV1 increases squamous cell carcinoma risk (odds ratio (OR)=1.51, 95% confidence intervals: 1.21-1.88), while reduced FEV1/FVC increases the risk of adenocarcinoma (OR=1.17, 1.01-1.35) and lung cancer in never smokers (OR=1.56, 1.05-2.30). These findings support a causal role of pulmonary impairment in lung cancer etiology. Integrative analyses reveal that pulmonary function instruments, including 73 novel variants, influence lung tissue gene expression and implicate immune-related pathways in mediating the observed effects on lung carcinogenesis.

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