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Smoking/smokers

Effects of smoking Smokers had a 25% increase in the metabolism of fluvoxamine compared with nonsmokers. [Pg.1084]

COMPENSATORY SMOKING Smokers puff harder, deeper, and more frequently to obtain desired amounts of nicotine from fewer cigarettes or from low-nicotine cigarettes. Smokers may also hold the smoke in the lungs longer before exhaling and smoke the cigarette further down. [Pg.363]

Dust particles inhaled in tobacco smoke, together with bronchial mucus, must be removed by the ciliated epithelium from the airways. However, ciliary activity is depressed by tobacco smoke and mucociliary transport is impaired. This favors bacterial infection and contributes to the chronic bronchitis associated with regular smoking (smoker s cough). Chronic injury to the bronchial mucosa could be an important causative factor in increasing the risk in smokers of death from bronchial carcinoma. [Pg.114]

Blood-cyanide concentrations of up to 0.02 iLig/ml may be found in normal individuals who do not smoke smokers may have concentrations of up to about 0.05 LLg/ml. Acute toxicity is associated widi blood concentrations of 0.5 iLig/ml or more such concentrations may be encountered during sodium nitroprusside therapy for hypertension. Concentrations above 1 iLig/ml have been reported in fatalities. Cyanide is concentrated in the erythrocytes. [Pg.66]

According to the U.S. Environmental Protection Agency (EPA) in 2010, radon gas in people s homes may cause as many as 20,000 deaths due to lung cancer annually. This makes radon the second-leading cause of this disease in the United States, after smoking. The people most in danger from radon are those who also smoke. Smokers are threatened both by radon and by cigarette smoke. [Pg.489]

Individual differences in nicotine kinetics and metabolism could affect smoking behavior in two ways. First, an individual s rate of nicotine metabolism could affect how much a person smokes. Smokers tend to... [Pg.48]

Low concentrations of cyanide can be found in human blood it has been estimated that normal blood cyanide levels can be 0.4 mg/L blood (Ellenhom and Barceloux 1988). A nonoccupational source of cyanide is smoking. Smokers tend to have higher thiocyanate, a metabolite of cyanide, concentrations in their urine and plasma than nonsmokers (Hartung 1991). [Pg.326]

Tobacco smoke contains a variety of air pollutants. In a survey of 80 homes ia an area where the outdoor TSP varied between 10—30 lg/m, the iadoor TSP was the same, or less, ia homes having ao smokers. la homes having oae smoker, the TSP levels were betweea 30—60 lg/m, while ia homes having two or more smokers, the levels were betweea 60—120 lg/m (64). la other studies, iadoor TSP levels exceeding 1000 lg/m have beea fouad ia homes with aumerous smokers. la additioa to TSP, burning tobacco emits CO, NO formaldehyde [50-00-0] bea2opyreaes, nicotine [54-11-5] pheaols, and some metals such as cadmium [7440-43-9] and arsenic [7440-38-2] (65). [Pg.381]

There are no significant health hazards arising from exposure to poly(vinyl chloride) at ambient temperature (154—158). However, a British study has found a small decrease in breathing capacity for workers who smoked and were exposed to vinyl resin dust (159). This decrease was about one-seventh of that caused by normal aging and about equal to that expected with a one-pack-a-day cigarette smoker. [Pg.508]

Nicotine Delivery Systems. For all transdermal nicotine products, the hypothesis is that continuous deflvery of nicotine [34-11-3] ne t trough levels during smoking should alleviate physical nicotine withdrawal symptoms and allow the smoker to concentrate on eliminating the behavioral aspects of addiction. [Pg.230]

Environmental Tobacco Smoke (ETS) mixture of smoke from the burning end of a cigarette, pipe, or cigar and smoke exhaled by the smoker (also secondhand smoke or passive smoking). [Pg.529]

Environmental tobacco smoke (ETS) is the diluted mixture of pollutants caused by smoking of tobacco and emitted into the indoor air by a smoker. Constituents of ETS include submicron-size particles composed of a large number of chemicals, plus a large number of gaseous pollutants. Fibers in indoor air include those of asbestos, and man-made mineral fibers such as fiberglass, and glass wool. [Pg.56]

Certain compounds of this type are potent carcinogens. One of the most dangerous is benzo[a]pyrene, which has been detected in cigarette smoke. It is believed to be a cause of lung cancer, to which smokers are susceptible. [Pg.590]

The monomeric non-polar molecular structure enables it to pass through cell walls relatively easily (myocrisin passes easily into the red blood cells of smokers, possibly owing to ingested cyanide in the smoke reacting to form monomeric Au(SR)CN ). [Pg.325]

Chronic obstructive pulmonary disease (COPD) affects over 5% of the adult population, is the fourth leading cause of death worldwide and is the only major cause of mortality that is increasing worldwide. It is an inflammatory disorder of the lungs, caused mainly, but not exclusively, by cigarette smoking. 15-20% of smokers develop COPD. [Pg.362]

Nicotine nasal spray delivers nicotine through the nasal mucosa. One advantage of nicotine nasal spray is that it relieves tobacco cravings quickly. One study found that nicotine nasal spray was 2.6 times more likely to produce smoking cessation, compared with placebo, at 1 year (Sutherland et al. 1992). The active spray was also the most beneficial among highly dependent smokers (Sutherland et al. 1992). [Pg.319]

Efficacy. A pivotal study by Hurt et al. (1997) established the efficacy and safety of bupropion SRfor treatment of nicotine dependence, which led to its approval for this indication by the FDA in 1998. This study was a 7-week, double-blind, placebo-controUed, multicenter trial of three doses of bupropion SR (100 mg/day, 150 mg/day, or 300 mg/day in twice daily dosing). Patients were 6l5 cigarette smokers who smoked at least 15 cigarettes/day. The medication was administered in combination with weekly individual cessation counseling. End-of-trial 7-day point prevalence cessation rates were 19.0% for placebo and 28.8%, 38.6%, and 44.2% for the 100 mg/day, 150 mg/day, and 300 mg/day bupropion doses, respectively. At 1-year follow-up, cessation rates were 12.4% for placebo and 19.6%, 22.9%, and 23.1% for the 100 mg/day,... [Pg.322]

Nortriptyline. Nortriptyhne, a tricychc antidepressant, has been shown in double-blind, placebo-controlled randomized trials to be superior to placebo for smoking cessation (Prochazka et al. 1998). Nortriptyline appears to have efficacy comparable to that of bupropion for smoking cessation (Hall et al. 2002). The efficacy of this agent may be improved with more intensive behavioral therapies (Hall et al. 1998). Nortriptyline s mechanism of action is thought to relate to its noradrenergic and serotonergic reuptake blockade, because these two neurotransmitters have been implicated in the neurobiology of nicotine dependence. Side effects of nortiptyline are typical of tricyclic antidepressants and include dry mouth, blurred vision, constipation, and orthostatic hypotension. Nortriptyline appears to have some utility for smokers with a past history of major depression, and it can be recommended as a second-... [Pg.325]


See other pages where Smoking/smokers is mentioned: [Pg.766]    [Pg.178]    [Pg.203]    [Pg.175]    [Pg.199]    [Pg.262]    [Pg.766]    [Pg.178]    [Pg.203]    [Pg.175]    [Pg.199]    [Pg.262]    [Pg.59]    [Pg.389]    [Pg.391]    [Pg.452]    [Pg.148]    [Pg.867]    [Pg.859]    [Pg.867]    [Pg.868]    [Pg.198]    [Pg.167]    [Pg.315]    [Pg.316]    [Pg.317]    [Pg.318]    [Pg.319]    [Pg.321]    [Pg.322]    [Pg.322]    [Pg.323]    [Pg.324]    [Pg.324]    [Pg.326]    [Pg.327]    [Pg.327]   


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