Total Pack-years Of Smoking Research Articles

Chronic Obstructive Pulmonary Disease and Smoking in India: A Meta-Analysis

Introduction: WHO estimates show Chronic obstructive pulmonary disease [COPD] as a growing major global cause of morbidity as well as mortality. An estimated 90% of COPD- related deaths occur in low/middle income countries. India and China together constitutes about one third of the total humanpopulation, accounting for 66% of COPD mortality globally. In the south east Asia region, COPD associated mortality is projected to grow by 160% in the decades ahead. Much of this projection holds pansexual cigarette smoking, improved life expectancy, bulging geriatric population and high levels ofsmall particle pollution, as major causes behind increase in COPD case burden. Methods: The aim of the meta-analysis was to investigate association between COPD and risk factors by pooled and subgroup analysis. We searched for case control studies and studies which are meeting the inclusion criteria. The publications listed in the NCBI PubMed and Cochrane library were searched using the following combination of the key words “COPD”; “smokers”; “health”; “risk” or “factors”;“diagnostic”; “burden”; “exposure”; “disease” or “prevalence” or “morbidity ” or “mortality”; “tobacco”; “smoking”; “smoke”, “India”. Random effects meta-analysis was applied to generate pooled SMD by using CMA software. Results: Data base search identified twenty-nine thousand two hundred twenty-two records and 14 articles made to the cut after implementing the inclusion and exclusion criteria. Main risk factors for COPD were higher age [SMD=0.53, CI= (0.0018-1.05)], total pack years of Smoking [SMD=13.83,CI (10.060-17.616)], FEV1 [SMD=-13.15, CI= (-16.234 to -10.085) and FEV/FVC ratio [SMD=0.915.CI= (0.767-1.063)]. Higher age, smoking, low values of FEV1 and FEV/FVC ratio is directly associated with high risk of COPD. Discussions: The findings of the study shows evidence of smoking history in terms of pack of years as a major risk factor for COPD prevalence. Further research is needed on COPD prevalence andincidence associated with other chemical exposure, to identify how to effectively reduce risks fromexposure to smoking.

Interest in cessation treatment and survival among smokers in a community-based multidisciplinary thoracic oncology program.

2028 Background: Tobacco cessation is essential to high quality oncology care. Many patients smoke when diagnosed and continue to smoke during treatment, which adversely affects treatment response and survival. Although most patients are motivated to quit, few receive effective cessation therapy. The multidisciplinary clinic (MDC), where patients, their caregivers, and key specialists coordinate care, is an ideal setting to integrate a cessation program. To assess the need for cessation services within a MDC setting, we surveyed incoming patients about their smoking status, interest in quitting, and willingness to participate in a clinic-based cessation program. Methods: The study was conducted in the Multidisciplinary Thoracic Oncology Program at Baptist Cancer Center, Memphis TN. We evaluated sociodemographic/clinical characteristics, smoking status, and tobacco dependence of consecutive new patients diagnosed with lung cancer from 2014-2019, who completed a social history questionnaire. Current smokers reported their interest in quitting and their willingness to participate in a cessation program. Chi square tests and logistic regression models were used to compare characteristics of those who would participate vs. those who would not/were unsure. Kaplan-Meier curves and multivariable Cox regression were used to evaluate the association between willingness to participate in a cessation program and overall survival, adjusted for age, sex, race, and total pack-years of smoking. Results: Of 641 patients, the average age was 69 years (range: 32-95), 47% were men, 64% white/34% black, and 17% college graduates; 90% had ever smoked, 34% currently smoked, and 24% quit smoking within the past year. Among current smokers, 60% were very interested in quitting and 37% would participate in a clinic-based cessation program. Willingness to participate was associated with greater interest in quitting (p = 0.0010) and greater overall survival (log rank p = 0.01;HR: 0.48, 95% CI: 0.24-0.95) but was not associated with any sociodemographic, clinical, or smoking-related characteristics. Conclusions: Over half (58%) of patients in a community-based MDC program were current smokers/recent quitters. Willingness to participate in a cessation program was associated with improved survival, suggesting patients with favorable prognoses are especially interested in receiving cessation support. There is considerable need for cessation services and relapse-prevention support within a coordinated, MDC lung cancer care setting.

P6136Intense daily cigarette smoking accelerates vascular damage of smokers with a moderate cumulative tobacco smoke exposure

Abstract Purpose Coronary artery disease death has been associated with increased cigarette smoking intensity. Aim of the study is to investigate the impact of cigarette smoking intensity on vascular function and structure changes among male smokers with similar age at starting smoking and moderate cumulative tobacco smoke exposure. Methods Indices of vascular function and structure including carotid-femoral pulse wave velocity (PWV), brachial flow-mediated dilation (bFMD), carotid intima media thickness (cIMT) and microvascular damage (penile vasculature) were measured in 118 smokers consuming up to 1 pack (20 cigarettes)/day and 58 patients smoking >1 pack (20 cigarettes)/day. The two groups had a similar mean cigarette smoking exposure (32 pack/years). Microvascular damage was examined by measuring penile peak systolic velocity (PSV) with a dynamic penile color Doppler ultrasonography after intracavernous injection of prostanglandin E1. Lower PSV values indicate severe penile vascular disease. Results The individuals smoking more than 1 pack/day were 10 years younger than smokers consuming up to 1 pack/day, however systolic, diastolic blood pressure, body-mass index, fasting blood glucose levels, lipid profile, C-reactive protein and total testosterone concentration were similar between the two groups. Figure shows mean bFMD, penile PSV, PWV and cIMT of the two groups. Interestingly, despite the similar cumulative smoking exposure between the two groups, the younger in age individuals with the intense cigarette smoking history had significantly lower mean bFMD and penile PSV (all P<0.05) and similar PWV and cIMT compared to the mean values of older subjects smoking up to 1 pack/day. Smoking intensity and vascular changes Conclusions Intense daily smoking accelerates damage of large arteries and significantly impairs microvascular and systemic endothelial function. Considering the predictive value of vascular biomarkers, the findings of this study imply the possibility that baseline daily smoking intensity could be a better summary measure of smoking-related cardiovascular risk among young heavy smokers, relative to total pack-years of smoking.

Tobacco smoking, family history, and the risk of nasopharyngeal carcinoma: a case-referent study in Hong Kong Chinese.

This study aimed to investigate the associations of tobacco smoking and family history of nasopharyngeal carcinoma (NPC) with the risk of NPC in Hong Kong Chinese. Between June 2010 and December 2012, we conducted a case-referent study with 352 incident cases and 410 referents in Hong Kong. We collected information on tobacco smoking and family history of NPC via face-to-face interviews. There were 174 (49.4%) and 131 (32.0%) ever-smokers among cases and referents, respectively. The adjusted odds ratio (OR) for NPC related to current smoking was 1.67 [95% confidence interval (CI) 1.06, 2.61]. Exposure-response relationships were observed between years and total pack-years of smoking, and NPC risk (p = 0.001 and p = 0.018, respectively). History of NPC in first-degree relatives was associated with an increased NPC risk (adjusted OR = 4.52, 95% CI 2.39, 8.55). The increased NPC risk associated with sibling history (adjusted OR = 6.80, 95% CI 2.63, 17.56) was higher than that for parental history (adjusted OR = 3.04, 95% CI 1.27, 7.25). The adjusted OR for ever-smokers with family history using never-smokers without family history as the reference was 4.54 (95% CI 1.67, 12.34). This study verified the important roles of tobacco smoking and family history on NPC risk among Hong Kong Chinese. The provided evidence supported the knowledge that both environmental exposures and inherited susceptibility contributed to the risk of NPC.

Correlates of Severity of Smoking Among Persons with Severe Mental Illness

Individuals with schizophrenia and severe mental illness smoke cigarettes at rates that well exceed the general population. Little is known about the correlates and sequelae of increased smoking severity on persons with severe mental illness. A total of 304 smokers from six community mental health centers were assessed for smoking history, psychiatric symptoms, co-occurring disorders, subjective quality of life, and expired carbon monoxide (CO). Statistical analyses identified correlates of smoking severity, as assessed by number of cigarettes smoked per week. The average number of cigarettes smoked per week was 136+/-83. Increased smoking was associated with higher levels of expired CO and being Caucasian, and with a greater likelihood of a current diagnosis of hypertension and oral/gum disease. Greater smoking severity was also associated with greater perceived stress, poorer overall subjective quality of life, and lower satisfaction with finances, health, leisure activities, and social relationships. This study confirms high rates of heavy smoking among persons with severe mental illness. The association of increased quantity of cigarettes smoked with being Caucasian is consistent with previous reports in mentally ill and non-mentally ill populations. The linkage of heavy smoking with poorer quality of life and co-occurring medical disorders suggests the importance of smoking reduction and cessation strategies to reduce smoking and decrease patients' total pack years of smoking.

Smoking and Risk of Acute Myeloid leukemia in Adults

In recently published results from a Canadian case–control study on lifestyle factors and risk of adult leukemia, Kasim et al. reported a significantly increased risk of acute myeloid leukemia (AML) associated with cigarette smoking, based on 307 AML cases [1]. Specifically, they observed an odds ratio (OR) of 1.4 [95% confidence interval (CI) = 1.1, 1.8] for current smokers compared to neversmokers and positive trends relating smoking status (never, ex, current) and total pack-years of smoking with AML risk. Smoking was not associated with other forms of adult leukemia (acute lymphoid, chronic myeloid, chronic lymphoid, hairy cell). In a case–control study of AML conducted in Los Angeles, California, we observed increased risks associated with smoking that were particularly strong for French–American–British (FAB) subtype M2; OR for ‘ever smoked’ was 1.2 (CI = 0.9, 1.6) among all cases and 2.3 (CI = 1.1, 4.4) among M2 cases [2]. Among all cases, we observed weak evidence of dose-response. However, among M2 cases we observed significant doseresponse for total number of years smoked, average cigarettes/day, and type of product smoked (filtered versus non-filtered). In general, results were stronger for older cases (‡60 years). We hypothesized that the age effect may be due to decreased ability to repair DNA damage in older subjects, higher exposure levels among older subjects due to smoking habits that differed from those of younger subjects, and long latency for the smoking effect

Fibrinogen and cigarette smoking in men and women in the European Prospective Investigation into Cancer in Norfolk (EPIC-Norfolk) population

Plasma fibrinogen may be an independent risk factor for cardiovascular disease. Cigarette smoking is a well-recognized determinant of plasma fibrinogen however it remains unclear how fibrinogen levels relate to the degree and duration of smoking, or to time since smoking cessation. In a population-based study of 11 059 men and women aged 45-74 years, we examined the cross-sectional relationship between plasma fibrinogen and cigarette smoking habit. Mean fibrinogen concentrations were higher in current smokers compared to non-current smokers (men: 3.13+/-0.77 versus 2.80+/-0.71 g/l, P<0.0001; women: 3.03+/-0.72 versus 2.95+/-0.71 g/l, P=0.01), independent of age, body mass index and hormone replacement therapy in women In men, fibrinogen concentrations declined with years since stopping smoking but remained higher than in life-long non-smokers for 15 years. No relationship between fibrinogen and duration of smoking cessation was observed in women. On multivariate analysis, age, body mass index, use of hormone-replacement therapy, smoking status and pack-years of smoking were independent predictors of plasma fibrinogen. Plasma fibrinogen is strongly associated with cigarette smoking with a dose-response relationship with total pack-years of smoking. In men who stop smoking plasma fibrinogen may remain elevated for several years after cessation.

The Overlap Between Respiratory Bronchiolitis and Desquamative Interstitial Pneumonia in Pulmonary Langerhans Cell Histiocytosis: High-Resolution CT, Histologic, and Functional Correlations

To characterize the histologic, high-resolution CT (HRCT), and functional correlates of respiratory bronchiolitis (RB)/desquamative interstitial pneumonia (DIP)-like changes in biopsy specimens of adults with pulmonary Langerhans cell histiocytosis (PLCH). We retrospectively identified 14 adult patients with histologically proven PLCH (all smokers) in whom both biopsy specimens and HRCT were available for review. The presence and extent of RB/DIP-like changes on lung biopsy specimens of patients with PLCH were correlated with total pack-years of smoking, lung function variables, and the presence of ground-glass attenuation on HRCT. Varying degrees of RB/DIP-like changes were identified in all biopsy specimens. The extent of involvement with RB/DIP-like changes correlated with the cumulative exposure to cigarettes smoked at the time of biopsy (r = 0.61, p = 0.03). Ground-glass attenuation was detected in three HRCTs, two of which had extensive RB/DIP-like changes (> or = 70% involvement) on histology, suggesting that substantial smoking-induced RB/DIP-like changes may be the cause of ground-glass attenuation on the HRCT of patients with PLCH. No correlation was found between the extent of RB/DIP-like changes and total lung capacity, FEV(1), or diffusion capacity of the lung for carbon monoxide. RB/DIP-like changes are exceedingly common in PLCH, may be sufficiently severe to cause the appearance of ground-glass attenuation on HRCT, and correlate with the cumulative exposure to cigarettes smoked. This study provides additional evidence that PLCH, RB, and DIP form a spectrum of interstitial patterns of lung injury to cigarette smoke.

Cardiovascular risk factors and increased carotid intima-media thickness in healthy young adults: the Atherosclerosis Risk in Young Adults (ARYA) Study.

The relation between cardiovascular risk factors and extent of atherosclerosis in middle-aged and elderly populations is well established. Autopsy studies have suggested that similar associations may be present at a young age. We evaluated the relationship between conventional risk factors and increased carotid intima-media thickness (CIMT) in 750 healthy young adults, aged 27 to 30 years. All participants completed a questionnaire on cardiovascular risk factors, had a fasting blood sample drawn, and underwent an ultrasonographic examination of both common carotid arteries to assess common CIMT (CCIMT). Age (11.2 micro m/SD), body mass index (10.3 micro m/SD), pulse pressure (5.0 micro m/SD), sex (4.8 micro m/SD), and low-density lipoprotein cholesterol level (4.3 micro m/SD) were independent determinants of increased CCIMT in young adults (R2 = 0.36). Total pack-years of smoking, adjusted for age and sex, showed a linear trend with increased CCIMT (P =.02), which attenuated after further adjustment for body mass index. Common CIMT increased gradually and significantly with the number of cardiovascular risk factors present. The estimated absolute risk, based on the Framingham risk function, for development of coronary heart disease within 20 years was 2.5 times higher in individuals with mean CCIMT in the highest quartile compared with those in the lowest quartile of the distribution. An unfavorable cardiovascular risk profile is associated with a marked increase in CCIMT in young adulthood. Efforts to change modifiable risk factors early in life may retard atherosclerosis development and hence delay the onset of clinical cardiovascular disease later in life.

Relation Between Lung Function and RBC Distribution Width in a Population-Based Study

Pulmonary function is dependent not only on smoking, but also on nutritional status. Since an increased RBC distribution width (RDW) has been associated with nutritional deficiencies, we postulated that RDW has an inverse relation to pulmonary function. The purpose of this study was to test this hypothesis. A cross-sectional study was conducted of a random sample of the general population in western New York. A total of 1,616 subjects of both genders who were aged 35 to 79 years and were free of respiratory disease. None. Pulmonary function was assessed from FEV(1), FVC, height, body weight, total pack-years of smoking, smoking status, hemoglobin concentration, and hematologic indexes, eosinophil count, education, and blood levels of retinol, beta-cryptoxanthin, and vitamin E. We found a direct relation between RDW and the number of pack-years of smoking and smoking status, and an inverse relation between FEV(1) and FVC with RDW, even when potentially confounding variables such as smoking were taken into account. When the variability of FEV(1) due to smoking was used for comparison, an additional 27% of that variability in FEV(1) was explained by variations in antioxidant vitamin levels, and another 24% by RDW. The results confirmed our hypothesis that there is an inverse relation between RDW and pulmonary function, and raise the possibility that RDW may be a biomarker for as-yet unidentified nutrients that affect pulmonary function.

The Difference of Lung Cancer Prevalence According to Smoking Habits

Background : The purpose of this study was to analyze the smoking habits in patients with lung cancer and identify any difference of prevalence according to histologic types of lung cancer. Methods : The data were calculated by total amounts of tar and nicotine inhaled during the whole lifetime according to variation of smoking habits. This study was to investigated any difference of prevalence in lung cancer according to smoking habits. The subjects comprised 150 lung cancer cases and 300 hospital control cases that were matched by age and sex. Smoking habits during the whole lifetime were surveyed by standardized questionnaire. Odds ratios were estimated by unconditional logistic regression analysis. Results : There were 104 male and 34 female lung cancer cases. By histologic type, there were 53 cases of squamous cell carcinoma, 67 of adenocarcinoma and 30 of small cell lung carcinoma. The differences between lung cancer cases and controls according to smoking habits were total duration of smoking, total pack years of smoking and number of cigarettes smoked per day during the previous two years.

Expression of p27Kip1 and bcl-2, cigarette smoking, and colorectal cancer risk

Although a positive association between cigarette smoking and colorectal adenoma development is consistently found, the association with colorectal cancer remains controversial. We evaluated the potential roles of p27Kip1 and bcl-2 protein expressions in conjunction with cigarette smoking exposure and colorectal cancer risk in a hospital-based case-control study. A total of 163 colorectal cancer patients from Roswell Park Cancer Institute and Buffalo General Hospital and 326 healthy controls responded to a standardized questionnaire on colorectal cancer risk factors including detailed information on their history of cigarette smoking; 110 of the patients' tumours were available for immunohistochemical analysis of p27Kip1 and bcl-2 protein overexpression. An avidin-biotin immunoperoxidase procedure was used to determine expression after incubation with mouse monoclonal p27Kip1 and mouse monoclonal bcl-2 antibodies, respectively. A statistically significant trend for total pack-years of smoking was found when p27Kip1 positive cases were compared with p27Kip1 negative cases (trend test, p = 0.007). Although a weak inverse association was observed with smoking exposure among p27Kip1 negative tumour cases in comparison to controls, a significant dose-response association was seen with p27Kip1 positive tumours. The relative risk of developing a p27Kip1 positive tumour was estimated to be 1.17 (95% CI 0.54-2.54) for those with less than 20 pack-years, 1.95 (95 % CI 0.95-3.97) for those with 20-39 pack-years, and 2.25 (95% CI 1.14-4.45) for those with greater than 39 pack-years of smoking exposure (trend test, p = 0.009) when compared with controls. When cases with bcl-2 expression were compared with cases without bcl-2 expression, suggestion of a trend was also observed with pack-years smoked (trend test, p = 0.09). In our study of 110 patients with sporadic colorectal cancer and 326 controls, we observed differences in associations between cigarette smoking and expressions in p27Kip1 and bcl-2. Our data suggest that bcl-2 overexpression (or a bcl-2 dependent pathway) is associated with cigarette smoking in the development of colorectal cancer, whereas a loss of p27Kip1 expression is not. These associations indicate that there is aetiological heterogeneity in colorectal cancer development, and that they can indirectly allude to where these changes in protein expression occur in the adenoma-carcinoma sequence (i.e. early versus late events).

The relationship between smoking exposure and p53 overexpression in colorectal cancer

Although epidemiological studies of the relationship between cigarette smoking and colorectal cancer risk have been equivocal, a positive association is consistently found for colorectal adenoma development. We performed an epidemiological study to determine whether p53 protein overexpression, in tumours obtained at the time of resection, is associated with cigarette exposure in colorectal cancer. A total of 163 colorectal cancer cases and 326 healthy controls responded to a standardised questionnaire on colorectal cancer risk factors including detailed information on their history of cigarette smoking. All patients' tumours were analysed immunohistochemically for p53 overexpression using an avidin-biotin immunoperoxidase procedure and polyclonal anti-p53 antibody CM1. Comparison of colorectal cases with controls revealed an elevated risk for ex-smokers (OR = 1.34, 95% CI 0.85-2.12) and current smokers (OR = 1.13, 95% CI 0.63-2.02) when compared with non-smokers. No dose-response relationship was found for total pack-years of smoking (trend test: P = 0.19). However, a trend for total pack-years of smoking was found when p53-positive cases were compared with p53-negative cases suggesting aetiological, heterogeneity (trend test: P = 0.06). Estimating the individual relative risk of developing a p53-positive tumour relative to controls showed no associations for smoking status or total pack-years of smoking. However, when p53-negative cases were compared with controls, an elevated risk was found for ex-smokers (OR = 1.84, 95% CI 1.00-3.37) and current years of smoking (trend test: P = 0.03). Colorectal tumours developing through p53-positive dependent pathways were not associated with smoking exposure. A significant increase in risk was observed for the p53-negative independent pathway with smoking. p53 overexpression appears to be associated with smoking exposure in colorectal cancer.

Renovascular disease in older patients beginning renal replacement therapy

Renovascular disease (RVD) in older patients can cause progressive renal insufficiency and even end-stage renal disease (ESRD). The frequency of this clinical problem is not well defined. Renal duplex sonography (RDS) correctly identifies the presence of RVD with an overall accuracy of approximately 95%. Therefore, the purpose of this study was to utilize RDS as a noninvasive tool to identify the presence of critical RVD (> or = 60% diameter-reducing stenosis or occlusion) in patients 50 years of age or older beginning renal replacement therapy. A total of 53 consecutive participating patients were prospectively interrogated. Complete interrogations occurred in 45 of the 53 patients (85%), and 92 of the 103 kidneys (89%). Critical RVD was noted in 10 of 45 patients (22%). RVD was bilateral in 5 patients, unilateral in 5 patients, and there were 4 renal artery occlusions noted. All patients with critical RVD were white (10 of 25 white patients or 40%). Total pack years of smoking as well as associated cardiovascular and cerebrovascular conditions were greater in those patients with critical RVD compared to those without. These results indicate that RDS remains technically feasible as renal blood flow and function decline. Unsuspected RVD possibly contributory to renal insufficiency exists in a significant number of primarily white patients 50 years of age or older beginning renal replacement therapy. These patients are generally smokers with a high frequency of associated extrarenal atherosclerosis The addition of RVD as a separate category of disease causing ESRD would improve U.S. Renal Data System ESRD classification. RVD should be recognized as a cause of ESRD.

Measurement of 4-aminobiphenyl-hemoglobin adducts in lung cancer cases and controls : Weston A, Caporaso NE, Taghizadeh K, Hoover RN, Tannenbaum SR, Skipper PL et al. Building 37, Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Ccancer Res 1991;51:5219–23

Hemoglobin adducts of the activated carcinogenic aromatic amine 4-aminobiphenyl have been measured in a case-control study of lung cancer. Data obtained for lung cancer cases are compared to those obtained for controls that consisted of patients with either chronic obstructive pulmonary disease or non-pulmonary cancers. Both simple and multivariate analysis found a positive association of 4-aminobiphenyl-hemoglobin adducts with the quantity of tobacco smoked as determined by either urine cotinine or questionnaire data. No association was found between 4-aminobiphenyl-hemoglobin adducts and cancer diagnosis, and adduct levels were not related to remote tobacco use, i.e., total pack years of smoking. There was no association between the levels of adducts detected and the ability of an individual to metabolize debrisoquine (debrisoquine metabolic phenotype, CYP2D6). Whereas 4-aminobiphenyl-hemoglobin adduct levels reflected recent tobacco smoking, they were not correlated with lung cancer risk.