Combination Of Cigarette Smoke Research Articles

Cigarette Smoking and Alcohol Consumption as Risk Factors for Colorectal Adenomatous Polyps

Results of epidemiologic studies suggest that there is limited evidence for the association between cigarette smoking and risk of colorectal cancer. Cigarette smoking has been shown to increase the risk of colorectal adenomatous polyps, which are recognized as precursors of colorectal cancer, while few studies have examined the association between alcohol consumption and the development of adenomatous polyps. We examined the association between cigarette smoking, alcohol consumption, and the presence of colorectal adenomatous polyps. Analyses were based on data from a case-control study of dietary and other lifestyle factors for colorectal adenomatous polyps. We assessed the risk of adenomatous polyps associated with total number of years of smoking, number of cigarettes smoked per day, and pack-years of smoking for past and current smokers separately. We also assessed the joint association between cigarette smoking and alcohol consumption on the risk of adenomatous polyps. Current smokers who smoked more than 20 pack-years were at significantly higher risk of adenomatous polyps compared with never smokers (odds ratio [OR] = 2.56; 95% confidence interval [CI] = 1.28-5.14). Past smokers also had an increased risk of having adenomatous polyps, but no clear trend was observed for pack-years of smoking. Alcohol consumption was positively associated with risk of adenomatous polyps. Compared with nondrinkers, the strongest risk was observed for individuals who consumed 2.31-9.46 g alcohol per day (OR = 2.23; 95% CI = 1.29-3.83), and a decrease in risk was observed for individuals who consumed 9.47-67.36 g alcohol per day (OR = 1.63; 95% CI = 0.92-2.88). Among current smokers, a joint effect was observed for individuals who smoked and drank compared with those who never smoked and were not current drinkers (OR = 4.21; 95% CI = 1.88-9.41). For past smokers, a significant joint effect of smoking and current alcohol consumption was also observed, but the risk was not as strong as that for current smokers (OR = 2.61; 95% CI = 1.40-4.87). These data provide further evidence of the positive association between cigarette smoking and the development of colorectal adenomatous polyps. The combination of cigarette smoking and alcohol consumption increased the risk of adenomatous polyps. Future research should focus on the understanding of the role of cigarette smoking and alcohol consumption as these two factors relate to the evolution of colorectal adenomatous polyps and subsequent carcinogenesis.

Congenital cutis laxa with a dominant inheritance and early onset emphysema.

Two cases (mother and daughter) are reported of autosomal dominant cutis laxa which are unusual in being associated with early onset emphysema. Both mother and daughter have been smokers and are heterozygotes for the alpha 1 antitrypsin genotype. The combination of cigarette smoking and subnormal alpha 1 antitrypsin levels may explain the pulmonary spread in these two women who have what is usually a benign form of cutis laxa limited to the skin.

Coffee consumption and risk of acute myocardial infarction in Italian males

The relationship between coffee consumption and acute myocardial infarction (AMI) was analyzed using data from a case-control study conducted in 1988 to 1989 within the framework of the GISSI-2 trial on streptokinase versus alteplase and heparin versus no heparin in the treatment of AMI. A total of 801 male patients with AMI and 792 control subjects who were hospitalized in several Italian regions for diseases unrelated to known or potential risk factors for cardiovascular diseases were included. Compared with coffee nondrinkers, the multivariate relative risks (RRs), after allowance for age, education, body mass index, smoking habits, alcohol consumption, family history of AMI, cholesterol level, history of diabetes, and hypertension, were 0.8 (95% confidence interval (CI), 0.5 to 1.2) for consumption of one cup/d, 1.3 (95% CI, 0.9 to 2.0) for two cups/d, 1.8 (95% CI, 1.1 to 2.7) for three cups, 2.5 (95% CI, 1.5 to 4.1) for four cups, and 2.6 (95% CI, 1.6 to 4.2) for five cups or more. The trend in risk with dose was statistically significant (P < 0.001). Duration of coffee consumption was not associated with the risk of AMI. The RRs for daily coffee consumption were elevated across strata of various covariates, including age, smoking habits, cholesterol level, diabetes, and hypertension, with a particularly elevated (although not significantly heterogeneous) estimate in patients younger than 50 years (RR, 5.7; 95% CI, 3.0 to 10.9 for four or more cups/d). The RR in patients who drank four or more cups of coffee per day and were current smokers was 8.1 (95% CI, 5.1 to 13.0), suggesting an unfavorable effect on the combination of cigarette smoking and high coffee intake on the risk of AMI.

Rat Pleural Mesothelial Cells Show Damage after Exposure to External but Not Internal Cigarette Smoke

The combination of cigarette smoke and high-level occupational asbestos exposure produces a synergistic increase in the incidence of lung cancer; however, smoking does not affect the incidence of mesothelioma. Here we present the results of tests of two theories that have been proposed to explain this phenomenon; namely, that pleural mesothelial cells are resistant to cigarette smoke-induced damage and that the pleural connective tissue acts as a barrier that prevents smoke from reaching the mesothelial cells. To test these hypotheses, excised whole rat lung preparations were exposed to either internal (intratracheal) or external (pleural surface) smoke. For comparison, additional excised lung preparations were exposed to solutions of hydrogen peroxide either externally or intratracheally. Mesothelial cells exposed to external smoke showed widespread, dose-dependent uptake of Trypan blue. Mesothelial cells did not take up Trypan blue after exposure to internal smoke. Bronchial epithelial cells exposed to internal smoke did show uptake, but to a lesser degree than externally exposed mesothelial cells. Examination by scanning and transmission electron microscopy showed that internal smoke did not affect mesothelial cell ultrastructure, whereas external smoke produced obvious mesothelial cell damage and mesothelial cell detachment. Catalase and deferoxamine, scavengers of active oxygen species, provided protection against smoke-induced mesothelial cell injury, but inactivated catalase did not. External hydrogen peroxide produced a very similar, dose-dependent pattern of Trypan blue uptake and ultrastructural changes. Intratracheal hydrogen peroxide also damaged mesothelial cells, but the extent of damage was always less than with comparable concentrations of external hydrogen peroxide.(ABSTRACT TRUNCATED AT 250 WORDS)

Factors Related to Treatment Resistance in Hypertension

Hypertension which is resistant to treatment carries a relatively bad prognosis. Factors associated with treatment resistance were examined in a case-control study in a hospital hypertension clinic. Patients with resistant hypertension had more severe hypertension and more frequently had evidence of end-organ damage on presentation to the clinic. The prevalence of accelerated phase hypertension, renovascular disease and impaired renal function was also higher in these patients. Cigarette smoking, and the combination of cigarette smoking and heavy caffeine use, were greater in patients with resistant hypertension. Resistant hypertension did not appear to be associated with older age, obesity, regular alcohol use, various psychological factors or non-compliance. These findings support an aggressive investigation policy in resistant hypertension, and underline the harmful effects of cigarette smoking to hypertensive subjects.

Bronchoalveolar lavage fluid neutrophils increase after corticosteroid therapy in smokers with idiopathic pulmonary fibrosis.

Patients with idiopathic pulmonary fibrosis (IPF) are often cigarette smokers and are often being treated with corticosteroids at the time of bronchoalveolar lavage. We addressed the question of whether or not the bronchoalveolar lavage fluid (BALF) neutrophil content of patients with IPF undergoes changes in smokers different from those in nonsmokers after institution of corticosteroids. Eighteen patients were studied (10 smokers and 8 nonsmokers). Fourteen patients (6 smokers and 8 nonsmokers) were treated orally with prednisone. The histologic assessment of alveolar inflammation and inflammatory small airways disease was no different in smokers than in nonsmokers. None of the smokers treated with prednisone had pathologic evidence of emphysema in addition to IPF. Five of 6 smokers showed an increase in BALF neutrophils after 3 months of prednisone (p less than 0.05), whereas the nonsmokers' BALF neutrophils decreased or remained unchanged. This increase in BALF neutrophils in smokers was not associated with concomitant or subsequent clinical deterioration but, in fact, with clinical improvement after 3 months of therapy. These data indicate that the combination of cigarette smoking and corticosteroid therapy influences the BALF neutrophil content in patients with IPF and suggest that interval changes in BALF neutrophil content may not reflect the status of the inflammatory process or structural derangements in the lungs of some patients with IPF.

The effects of a combination of cigarette smoking and oral contraception on coagulation and fibrinolysis in human females.

Oral contraception as well as cigarette smoking influence haemostasis. The simultaneous effect of both on blood coagulation and fibrinolysis was studied in nine female smokers. While continuing oral contraception after a 4-week abstinence from smoking the concentration of fibrinogen, antithrombin III and alpha 1-Antitrypsin decreased (P less than 0.01 or P less than 0.04) and of plasminogen increased (P less than 0.03). The other coagulation parameters remained unchanged. Although all determinations of these parameters were in the normal range, the observed trends were statistically significant. The concentrations of the fibrinopeptide A and B 15-42 did not differ. It is concluded that the observed alteration is caused by cessation from cigarette smoking.

Myocardial infarction, oral contraception, cigarette smoking, and coronary artery spasm in young women

Previous research has suggested that the combination of cigarette smoking and oral contraceptive (OC) use provides a strong stimulus for platelet aggregation coronary spasm and thrombosis. This paper presents the cases of 2 patients with myocardial infarction (MI) in whom smoking and OC use appeared to be contributory factors. The cases were part of a series of 65 women with atypical chest pains and normal coronary arteriograms who were followed in 1977-79. The 1st case a previously healthy 28-year old had been taking Ortho-novum 1-50 for 4 years and had smoked 40 cigarettes/day for 12 years prior to MI. No other risk factors for premature atherosclerosis were present. The electrocardiogram (ECG) revealed transmural inferior and anteroapial MI. Left ventricular angiography showed an anteroapial aneurysm with a large thrombus; the ejection fraction was 39%. Ergovine testing was positive. Cornonary arteriography showed normal coronary arteries except for a catheter-induced spasm of the proximal right coronary artery and segmental narrowing of the distal two thirds of the left anterior descending artery. OC use was discontinued and oral anticoagulants were administered. 2 years later the thrombus was not detectable. The 2nd case 39 years old took OCs for 9 months 15 years prior to admission and smoked 50 cigarettes/day for 20 years. ECG revealed an old inferior MI. Angiocardiography showed left ventricular enlargement and an ejection fraction of 51%. The coronary arteriogram revealed noncritical fixed lesions (40%) of the left circumflex diagonal branch and right coronary arteries. Only a 25% caliber reduction was induced by ergovine. It is hypothesized that cigarette smoking precipitated coronary artery spasm in the 1st case through the nicotine-induced release of norepinephrine and diminished prostacyclin/thromboxane A2 ratio. The combination of cigarette smoking and estrogen may have created a cycle of platelet aggregation vasoconstriction and thrombosis leading to MI. Although further studies are needed to confirm this hypothesis the reports suggest that provocative testing for coronary spasm should be considered in young women with MI or angina and normal or near normal arteries.

Epidemiology of radiation-induced cancer.

The epidemiology of radiation-induced cancer is important for theoretical and practical insights that these studies give to human cancer in general and because we have more evidence from radiation-exposed populations than for any other environmental carcinogen. On theoretical and experimental grounds, the linear no-threshold dose-response relationship is a reasonable basis for extrapolating effects to low doses. Leukemia is frequently the earliest observed radiogenic cancer but is now considered to be of minor importance, because the radiation effect dies out after 25 or 30 years, whereas solid tumors induced by radiation develop later and the increased cancer risk evidently persists for the remaining lifetime. Current estimates of the risk of particular cancers from radiation exposure cannot be fully evaluated until the population under study have been followed at least 40 or 50 years after exposure. Recent evidence indicates that for lung cancer induction, combination of cigarette smoking and radiation exposure leads to risks that are not multiplicative but rather nearly additive.

Tolbutamide, smoking, and cardiac arrhythmia. A case report

RECENTLY reported analyses of the mortality data of the University Group Diabetes Program (UGDP) study¹have prompted a reassessment of the role of oral hypoglycemic agents and other factors in ischemic heart disease in patients with diabetes. We describe a patient in whom the occurrence of premature ventricular contractions appeared to be associated with the combination of cigarette smoking and long-term treatment with tolbutamide. <h3>Report of a Case</h3> A 58-year-old woman was admitted to the Clinical Research Center as a volunteer subject in a continuing study of the pharmacogenetics of tolbutamide metabolism.^2,3She gave a reliable medical history of mild glucose intolerance and hypertension since 1968 but volunteered no complaints referable to these problems. The glucose intolerance was established by an oral glucose tolerance test (OGTT) in 1968, and repeated testing by her private physician in 1973 again showed blood glucose levels in the diabetic range. In addition,

Tolbutamide, Smoking, and Cardiac Arrhythmia

RECENTLY reported analyses of the mortality data of the University Group Diabetes Program (UGDP) study 1 have prompted a reassessment of the role of oral hypoglycemic agents and other factors in ischemic heart disease in patients with diabetes. We describe a patient in whom the occurrence of premature ventricular contractions appeared to be associated with the combination of cigarette smoking and long-term treatment with tolbutamide. Report of a Case A 58-year-old woman was admitted to the Clinical Research Center as a volunteer subject in a continuing study of the pharmacogenetics of tolbutamide metabolism. 2,3 She gave a reliable medical history of mild glucose intolerance and hypertension since 1968 but volunteered no complaints referable to these problems. The glucose intolerance was established by an oral glucose tolerance test (OGTT) in 1968, and repeated testing by her private physician in 1973 again showed blood glucose levels in the diabetic range. In addition,

Risk factors and angiographic coronary artery disease: a report from the coronary artery surgery study (CASS).

The findings for 14 risk variables were correlated with the results of coronary arteriography in 8807 patients registered in the interinstitutional Coronary Artery Surgery Study (CASS). Discriminant-function analysis revealed that age, sex, cigarette smoking and the level of blood cholesterol best distinguished between the groups with (6688 patients) and without (2119 patients) coronary artery disease. A family history of coronary artery disease and the presence of hypertension or diabetes were of addition, but less, discriminating value. The relative risk for coronary artery disease in patients with the combination of cigarette smoking and an elevated cholesterol level was high (> 4) in females age 55 years or younger and in males age 35 years or younger. Few females age 45 years or younger (seven of 97) had coronary artery disease when both of these risk factors were absent. In spite of these correlations, only limited gains accrued from the use of discriminant-function analysis in correctly allocating patients into disease and nondisease groups. This indicates that, while certain factors are significantly correlated with coronary arteriographic findings, their value for predicting the presence of coronary artery disease is limited.

Bronchitis in men employed in the coke industry.

<b>Walker, D. D., Archibald, R. M., and Attfield, M. D. (1971).</b><i>Brit. J. industr. Med.,</i><b>28,</b> 358-363. <b>Bronchitis in men employed in the coke industry.</b> An epidemiological survey to determine the prevalence of bronchitis in men employed at two of the National Coal Board9s coking plants is described. Eight hundred and eighty-one men (91%) of the total working population were examined. A strong association was found between bronchitis prevalence and cigarette smoking (P &lt; 0·001). In addition, men who smoked and who were exposed to high temperatures, dust, and fumes in the environment of the coke-ovens had more bronchitis than men who worked elsewhere in the cokeworks (P &lt; 0·02). Both the presence of bronchitis and employment in the environment of the coke-ovens had significant and independent effects on ventilatory capacity. The combination of cigarette smoking and previous employment in a dusty industry also had a significant effect on ventilatory capacity. The investigation suggests that cigarette smoking, and the combination of smoking and pollution from the coke-ovens and previous occupation, appear to be important factors in the aetiology of bronchitis and reduced ventilatory capacity in men employed in the coke manufacturing industry.