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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A method of assessing "buffering capacity" is described for comparison of the degree of acidity of alkalinity of the smoke of different tobaccos as presented to the oral and respiratory tracts of the smoker. Nicotine is more readily absorbed from an alkaline than from an acid smoke. The smoker of tobaccos giving a smoke of acid buffering capacity, in order to achieve full nicotine satisfaction, tends to smoke more and to inhale more, thus increasing lung cancer risks, than the smoker of tobaccos giving smoke of less acid or of alkaline buffering capacity.
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PMID:Buffering capacity of the smoke of different tobaccos in relation to lung cancer risks. 1 26

Over one quarter of the risk of death due to the sudden infant death syndrome (cot death) is attributable to maternal smoking. Maternal smoking during pregnancy and infancy is one of the most important avoidable risk factors for infant death. Nicotine is a drug of addiction. Many young smokers are addicted to nicotine and develop withdrawal symptoms on stopping. Smoking is an important marker for other types of drug abuse, e.g. alcohol, cannabis and cocaine. The earlier children start smoking, the greater the risk of lung cancer and heart disease. Smoking affects immunity and has been associated with an increased risk of acquiring human immunodeficiency virus-1 infection.
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PMID:Smoking and the young. 146 39

Cigarette smoking has been established as a major risk factor for atherosclerosis and also for lung cancer. Nicotine is one of the major components of cigarette smoke which is believed to be partly responsible for the deleterious effect of cigarette smoke. There was significant alteration in the concentration of glycosaminoglycans (GAG) in rats exposed to cigarette smoke. Administration of nicotine to rats has been found to decrease many of GAG fractions in the aorta, liver and heart and increase in the lungs. The increase in GAG now observed in lung tissue in rats administered nicotine and those exposed to cigarette smoke may be involved in the increased incidence of lung cancer in smokers. Increased activity of many of GAG hydrolysing enzymes indicates increased degradation of GAG. Sulphate metabolism in the liver is also significantly altered by nicotine. Thus administration of nicotine to rats caused alteration in the metabolism of GAG which are similar to those observed on exposure of rats to cigarette smoke, indicating that nicotine content of the tobacco smoke may partly be responsible for the effect on GAG observed on exposure to cigarette smoke.
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PMID:Effect of nicotine on glycosaminoglycan metabolism in rats. 151 30

Using specific ligands, we find that lung cancer cell lines of diverse histologic types express multiple, high-affinity (Kd = 10(-9)-10(-10) M) membrane receptors for mu, delta, and kappa opioid agonists and for nicotine and alpha-bungarotoxin. These receptors are biologically active because cAMP levels decreased in lung cancer cells after opioid and nicotine application. Nicotine at concentrations (approximately 100 nM) found in the blood of smokers had no effect on in vitro lung cancer cell growth, whereas mu, delta, and kappa opioid agonists at low concentrations (1-100 nM) inhibited lung cancer growth in vitro. We also found that lung cancer cells expressed various combinations of immunoreactive opioid peptides (beta-endorphin, enkephalin, or dynorphin), suggesting the participation of opioids in a negative autocrine loop or tumor-suppressing system. Due to the almost universal exposure of patients with lung cancer to nicotine, we tested whether nicotine affected the response of lung cancer cell growth to opioids and found that nicotine at concentrations of 100-200 nM partially or totally reversed opioid-induced growth inhibition in 9/14 lung cancer cell lines. These in vitro results for lung cancer cells suggest that opioids could function as part of a "tumor suppressor" system and that nicotine can function to circumvent this system in the pathogenesis of lung cancer.
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PMID:Opioid and nicotine receptors affect growth regulation of human lung cancer cell lines. 215 43

Diesel exhaust is a known mutagen and a potential human carcinogen. Recent epidemiological studies have demonstrated a small increase in the risk of lung cancer from diesel exhaust exposure. However, many epidemiological studies have used crude estimates of exposure, and even accurate measures of exposure may not be accurate estimates of the internal dose received. Measurement of diesel exhaust exposure also has been limited by the absence of a standard marker. This study was undertaken to evaluate the usefulness of urinary mutagenicity as a biological marker of diesel exhaust exposure in the workplace. We measured the exposure of individual railroad workers to diesel exhaust by using personal air samples taken over two consecutive work shifts. Nicotine in the samples was measured to adjust the respirable particle concentrations for active and passive cigarette smoking. Urine samples were collected at the end of the study work shifts and were analyzed for markers of cigarette smoking (nicotine, cotinine) and for mutagenicity, using a sensitive microsuspension assay (micro preincubation assay; Salmonella strain TA98 with or without S9 enzyme). The number of cigarettes smoked on the study shift was recorded, and subjects completed a questionnaire at the end of the second day on personal habits and exposures at home and work. Multiple regression analyses were used to analyze independent determinants of urinary mutagenicity, including a generalized least-squares analysis that divided residual variation into between- and within-person components. Eighty-seven subjects completed 151 two-day protocols; an additional four subjects provided usable data for a single day (n = 306 samples). Respirable particle concentration was not a good marker of diesel exhaust exposure when contamination by environmental tobacco smoke existed in the work location, but respirable particle concentration that was adjusted for environmental tobacco smoke correlated with a priori assessments of diesel exhaust exposure by job grouping. Phenanthrene concentration, as a potential marker, was measured in a subset of personal samples, and correlated with known diesel exhaust exposure by job grouping. A constant ratio of phenanthrene to respirable particles in area samples from diesel exhaust-exposed work locations suggested that phenanthrene is promising as a marker for diesel exhaust. Mutagenic activity was also measured from extracts of respirable particles in a few personal filter samples, and this technique may be useful for further investigation in epidemiological studies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Markers of exposure to diesel exhaust in railroad workers. 226 34

Recent studies indicate that nonsmokers exposed to environmental tobacco smoke (ETS) acquire an impaired lung function and run an increased risk of lung cancer. These findings have been questioned mainly on the basis that the amount of ETS received by the nonsmoker has remained unquantified. The factural risk of ETS exposure could possibly be estimated by measuring the absorption of tobacco smoke products by nonsmokers. Nicotine, which is specific to tobacco, and its main metabolite, cotinine, have been used for this purpose. The usefulness of these markers based on data obtained for different body fluids from nonsmokers exposed to ETS under experimental as well as field conditions is discussed.
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PMID:Monitoring absorption by means of determination of nicotine and cotinine. 346 33

Despite major changes in the patterns of cigarette consumption in the United States in the last two decades, cigarette smoking remains a widespread practice. Many studies show a strong association between cigarette smoking and chronic obstructive lung disease, but only recently have mechanisms been elucidated to explain this association, particularly in the case of emphysema. The exact mechanism of chronic bronchitis is less well defined. The mortality rate for lung cancer continues to increase in this country, particularly among women. Compelling evidence associates lung cancer with cigarette smoking, although animal models have not been very successful. Recently, concern has been raised about the effects of passive smoking. There are substantial data available to suggest that passive smoking results in pulmonary infections and abnormal pulmonary function in children of smokers. The data are less clear-cut for pulmonary functional impairment in adults and for lung cancer in the spouses of smokers. Although the concept of "safer" cigarettes has been widely accepted by the American public, these cigarettes may not be as safe as is widely assumed. Clearly, they are far inferior to total smoking cessation. Nevertheless, smoking cessation remains difficult for many Americans, despite a number of methods that have been used to help smokers quit. Nicotine chewing gum, which has recently become available for use in the United States, has shown some efficacy in helping well-motivated, nicotine-dependent smokers quit smoking. Although some inroads have been made into the occurrence of smoking related diseases in the United States, many unnecessary deaths continue to occur.
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PMID:Cigarette smoking and lung disease. 351 99

Nicotine and the minor tobacco alkaloids give rise to tobacco-specific N-nitrosamines (TSNA) during tobacco processing and during smoking. Chemical-analytical studies led to the identification of seven TSNA in smokeless tobacco (< or = 25 micrograms/g) and in mainstream smoke of cigarettes (1.3 micrograms TSNA/cigarette). Indoor air polluted by tobacco smoke may contain up to 24 pg/L of TSNA. In mice, rats, and hamsters, three TSNA, N'-nitrosonornicotine (NNN), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), are powerful carcinogens; two TSNA are moderately active as carcinogens; and two TSNA appear not to be carcinogenic. The TSNA are procarcinogens, agents that require metabolic activation. The active forms of the carcinogenic TSNA react with cellular components, including DNA, and with hemoglobin (Hb). The Hb adducts in chewers and smokers serve as biomarkers for the uptake and metabolic activation of carcinogenic TSNA and the urinary excretion of NNAL as free alcohol and as glucuronide for the uptake of TSNA. The review presents evidence that strongly supports the concept that TSNA contribute to the increased risk for cancer of the upper digestive tract in tobacco chewers and for the increased risk of lung cancer, especially pulmonary adenocarcinoma, in smokers. The high incidence of cancer of the upper digestive tract especially among men on the Indian subcontinent has been causally associated with chewing of betel quid mixed with tobacco. In addition to the TSNA, the betel quid chewers are exposed to four N-nitrosamines that are formed during chewing from the Areca alkaloids, two of these N-nitrosamines are carcinogens. The article also reviews approaches toward the reduction of the carcinogenic potency of smokeless tobacco, betel quid-tobacco mixtures, and cigarette smoke. Although the safest way to reduce the risk for tobacco-related cancers is to refrain from chewing and smoking, modifications of smokeless tobacco and of cigarettes are indicated to lead to less toxic products. Another more recent approach for reducing the carcinogenic effect of tobacco products is the application of chemopreventive agents, primarily of micronutrients. Future aspects in tobacco carcinogenesis, especially as it relates to TSNA, are expected in the field of molecular biochemistry and in biomarker studies, with the goal of identifying those tobacco and betel quid chewers and tobacco smokers who are at especially high risk for cancer.
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PMID:Tobacco-specific N-nitrosamines and Areca-derived N-nitrosamines: chemistry, biochemistry, carcinogenicity, and relevance to humans. 827 23

Nicotine, a major component of cigarette smoke, plays an important role in the development of cardiovascular disease and lung cancer in smokers. Lipid peroxidation is a process associated with the pathogenesis of atherosclerosis and the level of lipid peroxides is increased in smokers. In rats fed a high-fat diet, the tissue concentration of lipid peroxides was found to be increased. On nicotine administration along with a high-fat diet an additive effect was observed in lipid peroxidation and free radical scavengers. The activities of scavenging enzymes superoxide dismutase, catalase and glutathione reductase were found to be decreased, while the glutathione concentration and activity of glutathione peroxidase were enhanced.
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PMID:Effect of nicotine on antioxidant defence mechanisms in rats fed a high-fat diet. 884 84

Cigarette smoking has been established as a major risk factor for atherosclerosis and also for lung cancer. Nicotine is one of the major toxic components of cigarette smoke that is believed to be partly responsible for the deleterious effect of cigarette smoke. Alcohol intake is another major risk factor for the development of cardiovascular disease. Lipid peroxidation is a process associated with the pathogenesis of atherosclerosis. The concentration of lipid peroxides is found to be increased in alcohol-treated rats. On nicotine administration along with alcohol, an additive effect was observed in lipid peroxidation and the antioxidant defence mechanism. The activity of scavenging enzymes superoxide dismutase, catalase and glutathione reductase was found to be decreased, while the activity of glutathione peroxidase and the concentration of glutathione were increased.
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PMID:Additive effect of alcohol and nicotine on lipid peroxidation and antioxidant defence mechanism in rats. 885 16


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