Medicinal marijuana?
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AIDS-Related Opportunistic Infections↗
Biomedical subjects
D P Tashkin
Publications and source records attributed to D P Tashkin.
Comparative efficacy and safety of twice daily fluticasone propionate powder versus placebo in the treatment of moderate asthma.
BACKGROUND: Fluticasone propionate, an inhaled corticosteroid with negligible systemic bioavailability via the oral route, is efficacious in the treatment of asthma when administered via metered-dose inhaler. OBJECTIVE: To evaluate the efficacy and safety of inhaled fluticasone propionate powder in patients with moderate asthma previously treated with an inhaled corticosteroid. METHODS: This was a randomized, double-blind, placebo-controlled, parallel-group, multicenter study of 342 adolescent and adult patients with moderate asthma [forced expiratory volume in 1 second (FEV1) between 50% and 80% of predicted] treated previously by beclomethasone dipropionate or triamcinolone acetonide. Patients received fluticasone propionate powder 50 micrograms, 100 micrograms, 250 micrograms, or placebo via a breath-actuated inhalation device, the Diskhaler, twice daily for 12 weeks. RESULTS: Patients in the fluticasone propionate groups experienced a mean increase from baseline to endpoint in FEV1 ranging from 0.43 L to 0.47 L. Patients in the placebo group experienced a mean decrease from baseline of 0.22 L (P < .001). The probability of patients remaining in the study over time without developing signs of exacerbating asthma was significantly greater in the fluticasone propionate groups than in the placebo group (P = .001). Asthma symptom scores, supplemental rescue albuterol use, and number of nighttime awakenings due to asthma requiring treatment also improved significantly with all fluticasone propionate treatment regimens compared with placebo (P < .001). There were no statistically significant differences at endpoint among the three fluticasone propionate groups. No serious drug-related adverse events occurred. CONCLUSIONS: Fluticasone propionate powder (50, 100, and 250 micrograms) was well-tolerated and significantly improved lung function in patients with moderate asthma.
Administration, Inhalation↗
Heavy habitual marijuana smoking does not cause an accelerated decline in FEV1 with age.
To assess the possible role of daily smoking of marijuana in the development of chronic obstructive pulmonary disease (COPD), we evaluated the effect of habitual use of marijuana with or without tobacco on the age-related change in lung function (measured as FEV1) in comparison with the effect of nonsmoking and regular tobacco smoking. A convenience sample of 394 healthy young Caucasian adults (68% men; age: 33 +/- 6 yr; mean +/- SD) including, at study entry, 131 heavy, habitual smokers of marijuana alone, 112 smokers of marijuana plus tobacco, 65 regular smokers of tobacco alone, and 86 nonsmokers of either substance were recruited from the greater Los Angeles community. FEV1 was measured in all 394 participants at study entry and in 255 subjects (65 %) on up to six additional occasions at intervals of > or = 1 yr (1.7 +/- 1.1 yr) over a period of 8 yr. Random-effects models were used to estimate mean rates of decline in FEV1 and to compare these rates between smoking groups. Although men showed a significant effect of tobacco on FEV1 decline (p < 0.05), in neither men nor women was marijuana smoking associated with greater declines in FEV1 than was nonsmoking, nor was an additive effect of marijuana and tobacco noted, or a significant relationship found between the number of marijuana cigarettes smoked per day and the rate of decline in FEV1. We conclude that regular tobacco, but not marijuana, smoking is associated with greater annual rates of decline in lung function than is nonsmoking. These findings do not support an association between regular marijuana smoking and chronic COPD but do not exclude the possibility of other adverse respiratory effects.
Adult↗
Nonspecific airway hyperresponsiveness in HIV disease. Pulmonary Complications of HIV Infection Study Group.
OBJECTIVES: HIV disease is frequently complicated by episodic acute bronchitis, suggesting the presence of chronic bronchial inflammation. To further examine this concept, we investigated the possible association of nonspecific airway hyperresponsiveness (AHR) and HIV disease. DESIGN: Methacholine inhalation challenge studies were performed on 66 HIV-seropositive and 8 HIV-seronegative members of the Pulmonary Complications of HIV Infection Study Cohort. AHR was defined as 20% or more decline in FEV1 from the postdiluent value after inhalation of 125 or less cumulative breath units. The prevalence of AHR in HIV-seropositive cohort members was compared with that in matched control subjects who had undergone methacholine challenge testing for two unrelated studies. Demographic, behavioral, and clinical features in HIV cohort members with and without AHR were contrasted. The relationship between AHR and the occurrence of episodic airway disease or symptoms suggestive of airway disease was examined. RESULTS: AHR was not more prevalent in HIV-seropositive cohort members than control subjects (19.3% vs 12.9%; p > 0.1). Within the cohort, AHR was detected more frequently in members with than without a history of asthma (60% vs 16%; p < 0.05). A greater proportion with than without AHR had 1 or more episode of pneumonia within 2 years (46% vs 9%; p < 0.01), 1 or more asthma episode during the study period (39% vs 1.9%; p < 0.001), or wheeze noted during clinic visits (62% vs 17%; p < 0.01). The proportion that experienced acute bronchitis did not differ in the two groups. CONCLUSIONS: This study suggest that HIV-infected persons do not have increased prevalence of nonspecific AHR. In HIV disease, AHR is associated asthma, but not episodic acute bronchitis. Thus, the possibility that airway injury without demonstrable AHR might complicate HIV disease remains.
Adult↗
Acute effects of intravenous cocaine on pulmonary artery pressure and cardiac index in habitual crack smokers.
BACKGROUND: Some habitual crack cocaine smokers who deny IV drug abuse show decreased pulmonary transfer of carbon monoxide (DCO). We speculated that repeated elevations in pulmonary artery pressure (PAP) might cause pulmonary capillary damage and result in a lowered DCO, or that the reduction could be due to anoxic lung injury secondary to repeated episodes of cocaine-induced pulmonary vascular constriction. STUDY OBJECTIVE: Compare the acute effects of i.v. cocaine HCl and placebo on PAP, cardiac stroke volume, and cardiac output estimated indirectly by continuous Doppler echocardiography. DESIGN: A single-blind crossover study in which placebo always preceded the active drug. SUBJECTS: Ten current crack-smoking subjects, 32 to 47 years of age, with a history of limited previous i.v. cocaine use. METHODS: PAP, cardiac stroke volume, heart rate, and BP were measured continuously after injection of placebo followed by cocaine HCl (0.5 mg/kg). RESULTS: i.v. cocaine resulted in no significant change in PAP (-0.14 +/- 3.3[SD] mm Hg, 95% confidence interval [CI] for difference -2.48, +2.21). Stroke volume index showed no significant change after cocaine (-0.1 +/- 2.0 mL; 95% CI, -1.5, +1.3). Heart rate showed a significant increase (10.0 +/- 7.2 min-1; p = 0.0017, 95% CI, +4.9, +15.1). Cardiac index showed a significant increase (0.48 +/- 0.32 L/min; p = 0.0012, 95% CI, +0.25, +0.71). Pulmonary vascular resistance showed no significant change (-44 +/- 101 dyne.s.cm-5/m2, 95% CI, -116, +29). CONCLUSIONS: i.v. cocaine HCl does not cause short-term increases in PAP or stroke volume index, but causes an increase in cardiac index due to its chronotropic effect.
Adult↗
Acute activation of circulating polymorphonuclear neutrophils following in vivo administration of cocaine. A potential etiology for pulmonary injury.
Crack cocaine has become a major drug of abuse in the United States and its use is associated with a broad spectrum of pulmonary complications. The present study was conducted to determine whether controlled in vivo administration of cocaine (inhaled or IV) alters the function of circulating inflammatory cells in a manner capable of contributing to acute lung injury. Subjects who regularly smoked crack cocaine were asked to abstain from illicit drug use for at least 8 h, and were then administered one of the following treatments on each of 4 study days: inhaled cocaine base (45 mg), inhaled placebo (4.5 mg cocaine base, a subphysiologic dose), IV cocaine HCl (0.35 to 0.50 mg/kg), or IV placebo (saline solution). Samples of blood were obtained from a peripheral venous catheter and blood cells were isolated before and 10 to 45 min after treatment. The administration of either cocaine base or cocaine HCl, but not their corresponding placebos, resulted in the activation of circulating polymorphonuclear neutrophils (PMNs). Exposure to cocaine in vivo enhanced the antibacterial activity of PMNs, as measured by their ability to kill Staphylococcus aureus. Antitumor activity, as measured in an antibody-dependent cell-mediated cytotoxicity assay, also increased following short-term administration of cocaine. Finally, short-term exposure to cocaine enhanced production of interleukin 8, a potent PMN chemoattractant and neutrophil-activating factor associated with both acute and chronic lung injury. These studies demonstrate that short-term in vivo exposure to cocaine activates the effector function and cytokine production of circulating PMNs. Therefore, it is possible that bursts of acute inflammatory activity resulting from crack use could contribute to lung injury.
Administration, Inhalation↗
Cocaine down-regulates IL-2-induced peripheral blood lymphocyte IL-8 and IFN-gamma production.
Cocaine has multiple immunomodulatory effects, including the ability to influence cytokine release in immunoeffector cells. Little is known, however, regarding the effects of cocaine on cytokine production by human peripheral blood lymphocytes (PBL). The effect of cocaine on PBL cytokine profiles and the molecular mechanisms responsible for the modulation of cytokine mRNA expression were investigated. To evaluate the effects of cocaine on cytokine production, conditioned supernatant from IL-2-stimulated PBL was evaluated by cytokine-specific ELISA (IL-4, IL-5, IL-8, IL-10, IFN-gamma, and TGF-beta) following in vitro cocaine exposure. Cocaine abrogated the IL-2-induced production of IFN-gamma and IL-8 in a dose-responsive manner. Cocaine also decreased PBL IFN-gamma and IL-8 mRNA expression as determined by Northern blot and slot blot analysis. Cocaine did not affect the stability of the IFN-gamma and IL-8 mRNA. Nuclear run-on assays revealed that cocaine down-regulated the rate of IFN-gamma and IL-8 transcription. These findings suggest that the immunomodulatory effects of cocaine may be mediated, in part, by modification of lymphocyte cytokine production.
Cocaine↗
Results of a multicenter study of nebulized inhalant bronchodilator solutions.
The efficacy, persistence of bronchodilator action, and safety of the quaternary ammonium anticholinergic agent, ipratropium bromide (500 microgram), and placebo were compared when each was added in solution form to the beta-adrenergic agonist solution, metaproterenol sulfate (15 mg), and administered three times daily for 12 weeks to a total of 213 patients with chronic obstructive pulmonary disease (COPD). Subjects had a mean forced expiratory volume in 1 second (FEV1) of approximately 1 liter (37% of predicted) and were permitted to use nonanticholinergic therapy for COPD throughout the trial. The study was a randomized, double-blind, 85-day, parallel-group, eight-center study. On a 3 test days, 1, 43, and 85, mean peak responses for FEV1 and forced vital capacity and mean area under the curve were significantly higher for the iprathropium bromide-metaproterenol combination than for metaproterenol only. Duration of action was also significantly longer for the combination therapy than for the beta-agonist alone on test days 1 and 43. Neither treatment regimen produced an demonstrable effect on daily morning peak expiratory flow rates, reported respiratory symptoms, or quality of life. Both treatment regimens were similarly well tolerated with a comparable frequency of adverse events. These results suggest that the combination of iprathropium bromide and metaproterenol inhalation solutions offers a potential therapeutic advantage to patients with symptomatic COPD over nebulized metaproterenol alone without the risk of increased side effects.
Administration, Inhalation↗
Methacholine reactivity predicts changes in lung function over time in smokers with early chronic obstructive pulmonary disease. The Lung Health Study Research Group.
As part of a clinical trial of early intervention in chronic obstructive pulmonary disease (COPD) (the Lung Health Study), 5,733 smokers with mild to moderate airflow obstruction underwent methacholine challenge tests at baseline. All participants were randomized to receive either usual care (no intervention) or special intervention, consisting of intensive smoking cessation counseling and the prescription of a metered-dose inhaler containing either ipratropium bromide or placebo (two inhalations three times daily). For this report, we analyzed the relationship between baseline methacholine reactivity and subsequent change in lung function. Methacholine reactivity was expressed as a logarithmic function of the two-point slope of percent decline in FEV1 over the concentration of methacholine (LMCR). Using a random effects linear model, LMCR was found to be a strong predictor of change in FEV1% predicted, after controlling for baseline lung function, age, sex, baseline smoking history, and changes in smoking status. Significant interactions were found between reactivity and smoking behavior. In the first year, participants who quit smoking showed improvement in FEV1, whereas continuing smokers showed worsening, and between Years 1 and 5, lung function declined to a greater extent in continuing smokers than in sustained quitters. For both time periods, these quitter/smoker differences increased as a function of airway reactivity. These findings indicate that methacholine reactivity is an important predictor of progression of airway obstruction in continuing smokers with early COPD, independent of the baseline level of obstruct.
Bronchoconstrictor Agents↗
Contribution of emphysema and small airways in COPD.
BACKGROUND: The contribution and role of emphysema and small airways disease in causing expiratory airflow limitation in COPD is controversial. METHODS: We obtained high-resolution thin-section 2-mm CT scans of the lung for emphysema grading and lung function in 116 consecutively seen COPD outpatients with fixed expiratory airflow limitation. In this group, inflated whole lung(s) were subsequently obtained in 24 patients (23 autopsy, 1 surgery) for morphologic studies and results compared with lung CT. Airway histologic condition was studied in 17 of the 24 patients. RESULTS: There was fair to weak negative correlation between CT emphysema score and either FEV1/FVC percent (r = -0.51, p = 0.001) or FEV1 percent predicted (r = -0.31, p = 0.001). In only 24 of the 81 patients (30%) with FEV1 less than 50% predicted, the CT emphysema score was 60 or more, indicating severe emphysema. In the 24 patients studied, there was a good correlation (r = 0.86, p = 0.001) between CT and pathologic grade of emphysema. While respiratory bronchioles (RBs) and membranous bronchioles (MBs) demonstrated marked morphologic abnormalities, there was a weak correlation with emphysema grade (for RB, r = 0.36, p = 0.16; for MB, r = 0.41, p = 0.10) or with FEV1 percent predicted (for RB, r = -0.21, p = 0.42; for MB, r = -0.28, p = 0.28). There was no correlation between emphysema and FEV1 percent predicted (r = -0.13, p = 0.54). CONCLUSIONS: High-resolution CT lung scans are an in vivo surrogate to quantitate moderate to severe morphologic emphysema. Emphysema does not appear to be primarily responsible for severe expiratory airflow limitation in most patients with severe COPD. There was no correlation between severity of small airway histologic condition and emphysema or FEV1 percent predicted. The causes of the lesions responsible for small airways obstruction need to be identified.
Aged↗
Cumulative dose-response study of non-CFC propellant HFA 134a salbutamol sulfate metered-dose inhaler in patients with asthma.
STUDY OBJECTIVE: This study compares the safety and efficacy of HFA 134a salbutamol sulfate (Airomir in the 3M CFC-free system [3M Pharmaceuticals]) and CFC 11/12 salbutamol (Ventolin [Allen & Hanburys]) in a cumulative dose-response (1, 1, 2, 4, 8 inhalations at 30-min intervals) study in asthmatic patients. DESIGN: Randomized, single-blind, two-period cross-over study. PARTICIPANTS: Twenty-four stable mild to moderate asthmatics. MEASUREMENTS AND RESULTS: At all cumulative inhalations, the changes in FEV1 (absolute, percent, and percent predicted) and FVC were equivalent. There was also no significant difference in heart rate, serum potassium level, BP, 12-lead ECG, Holter monitor recordings, or adverse events. Both HFA 134a salbutamol sulfate and CFC 11/12 salbutamol displayed a significant dose-response for FEV1, FEF25-75%, FVC, serum potassium, heart rate, and systolic BP. CONCLUSIONS: HFA 134a salbutamol sulfate and CFC 11/12 salbutamol produced clinically and statistically similar airway responses and side effects. These results indicate that HFA 134a salbutamol sulfate would be a safe and effective substitute for CFC 11/12 salbutamol.
Administration, Inhalation↗
Trends in compliance with bronchodilator inhaler use between follow-up visits in a clinical trial.
STUDY OBJECTIVE: To assess objectively measured, long-term trends in compliance with physician-prescribed metered-dose inhaler (MDI) use during a clinical trial. DESIGN: A prospective study. SETTING: The Lung Health Study, a 5-year clinical trial to determine the effect of special intervention with an intensive smoking cessation program and bronchodilator therapy in cigarette smokers 35 to 60 years of age with minimal to moderate airflow limitation due to COPD. PARTICIPANTS: Two hundred thirty-one participants who were issued an MDI with an attached Nebulizer Chronolog (NC) (Forefront Technologies Inc; Lakewood, Colo) which electronically records the date and time of each MDI actuation. One hundred two participants were not informed of the recording capabilities of the attached NC, while 129 participants were aware of the NC's monitoring function. INTERVENTION: Following an initial 12-week period of counseling, participants returned to the clinic every 4 months. MEASUREMENTS AND RESULTS: Analysis of the data from the NC collected over a period of 2 years indicates that compliance with the prescribed medication regimen was best immediately following each follow-up visit and gradually declined during the interval between follow-up visits. The level of compliance after each visit was lower for each successive follow-up. These trends could not be observed from self-report or weighting the medication canisters at follow-up visits. The participants who were informed of the NC's function and who were provided with detailed feedback about their inhaler use generally showed better compliance.
Adult↗
Acute effects of inhaled and i.v. cocaine on airway dynamics.
BACKGROUND: Wheezing has been reported by 32% of habitual smokers of crack cocaine, and several cases of crack-related acute exacerbations of asthma have been reported. STUDY OBJECTIVE: To compare the acute effects of physiologically active doses of smoked cocaine base and, i.v. cocaine hydrochloride (HCl), a subphysiologic dose of cocaine base (smoked "placebo"), and i.v. saline solution placebo on bronchomotor tone, subjective level of intoxication, and cardiovascular responses in healthy habitual crack users. DESIGN: A single-blind crossover study in which the order of route of administration (inhaled vs i.v.) was random but placebo always preceded the active drug. SUBJECTS: Fourteen healthy, nonasthmatic current crack-smoking subjects, 34 to 48 years of age, with a history of previous i.v. cocaine use (1 to 12 times per lifetime). METHODS: Heart rate, BP, self-rated level of intoxication (scale of 0 to 10), and measurements of airway resistance (Raw) and specific airway conductance (SGaw) were recorded during separate sessions before and 3 to 5, 10, 15, and 30 min after administration of smoked cocaine base (38.5 +/- 2.3 [SEM] mg), smoked placebo (2.3 +/- 0.9 mg cocaine base), i.v. cocaine HCl (30.0 +/- 2.0 mg), and i.v placebo (saline solution). RESULTS: Both smoked active cocaine and i.v. cocaine HCl caused comparable, significant (p < 0.05) peak levels of acute intoxication (6.7 +/- 0.7 and 7.3 +/- 0.8, respectively) and increases in heart rate from baseline (29.6 +/- 2.9% and 21.4 +/- 3.7%, respectively, at 5 min). However, only smoked active cocaine caused significant decreases from baseline in SGaw (25.4 +/- 6.3% at 5 min), in contrast to nonsignificant changes after i.v. cocaine HCl (5.6 +/- 7.0% increase) and smoked placebo (10.2 +/- 6.0% decrease). CONCLUSIONS: Smoked cocaine base, but not systemically administered cocaine HCl, causes acute bronchoconstriction that is probably mediated by local airway irritation and could account for reports of crack-induced wheezing and asthma attacks in nonasthmatic and asthmatic individuals, respectively.
Administration, Inhalation↗
Mentholated cigarette use and lung cancer.
BACKGROUND: Menthol combustion produces carcinogenic compounds such as benzo[a]pyrenes. Mentholated cigarettes are much more commonly smoked by black individuals than by white individuals. The incidence of lung cancer is much higher (60%) in black men than in white men, but it differs little by race in women. We examined the association of mentholated cigarette use with lung cancer in men and women because mentholated cigarette use could help to explain the higher incidence rate of lung cancer in black men than in white men. METHODS: The study population consisted of 11,761 members of the Northern California Kaiser Permanente Medical Care Program, Oakland (5771 men and 3990 women), aged 30 to 89 years, who underwent a multiphasic health checkup in 1979 through 1985 and reported that they were current cigarette smokers who had smoked for at least 20 years. Data were collected about current cigarette brand, duration of mentholated cigarette use, and other smoking characteristics. Follow-up for incident lung cancer cases (n = 318) was carried out through 1991. RESULTS: The relative risk of lung cancer associated with mentholation compared with nonmentholated cigarettes was 1.45 in men (95% confidence interval, 1.03 to 2.02) and it was 0.75 in women (95% confidence interval, 0.51 to 1.11), adjusted for age, race, education, number of cigarettes smoked per day, and duration of smoking. Further adjustment for tar content and self-reported smoking intensity characteristics did not substantially alter the estimate of relative risk. A graded increase in risk of lung cancer with increasing duration of mentholated cigarette use was present in men. CONCLUSION: This study suggests that there is an increased risk of lung cancer associated with mentholated cigarette use in male smokers but not in female smokers.
Adult↗
The relationship of tobacco and marijuana smoking characteristics.
In an ongoing study of the pulmonary effects of heavy, habitual marijuana smoking, detailed marijuana and tobacco smoking histories were obtained from 467 adult regular smokers of marijuana and/or tobacco. Frequency and cumulative amounts of tobacco and marijuana smoking were similar for smokers and nonsmokers of tobacco, except that pack-years and cigarettes/day at the time of the interview were both significantly less for tobacco smokers who also smoked marijuana compared those who did not. For all subjects who smoked both substances at any time, changes in tobacco and marijuana smoking amounts after commencement of regular smoking of the other substance were similar for tobacco and marijuana; the existing smoking habit decreased in approximately one third of the subjects and remained the same in slightly more than one half of the subjects. Of the dual smokers, 49% began smoking tobacco before marijuana, while 33% began smoking marijuana first; 85% of marijuana smokers who quit tobacco smoking did so after beginning regular marijuana smoking. Self-reported depth of inhalation and breath-holding time of marijuana smoke were similar for tobacco and non-tobacco smokers; smoking topography for tobacco was also comparable for smokers and non-smokers of marijuana.
Adult↗
Acute and chronic effects of marijuana smoking on pulmonary alveolar permeability.
Pulmonary clearance of technetium (99mTc)-labeled diethylene triamine pentaacetate (DTPA), a sensitive test of alveolar epithelial permeability, was measured twice in 34 healthy subjects, including 10 control nonsmokers (NS), 10 habitual smokers of marijuana alone (MS) (> or = 10 joints/wk), 9 regular smokers of tobacco alone (TS) (> or = 15 cigarettes/day) and 4 habitual smokers of both marijuana and tobacco (MTS). In smokers, the first study was performed after > or = 12 hrs of abstinence from smoking to assess chronic effects of marijuana and/or tobacco smoking on alveolar permeability; the second study was performed within 15 min of smoking to assess possible acute effects. TS exhibited abnormally rapid 99mTc-DTPA clearance after > or = 12 hours of abstinence, indicating an increase in pulmonary epithelial permeability, consistent with chronic tobacco-induced lung injury. MS showed a more modest and less consistent chronic effect than TS on 99mTc-DTPA clearance, suggesting a more variable and smaller degree of marijuana-induced lung injury. No acute effect of tobacco or marijuana smoking on 99mTc-DTPA clearance was apparent. Concomitant habitual smoking of marijuana and tobacco had no additive effect on alveolar permeability.
Adult↗
Effects of smoking marijuana, tobacco or cocaine alone or in combination on DNA damage in human alveolar macrophages.
This study examined the role of marijuana smoking in the pathogenesis of human lung cancer by measuring DNA damage in alveolar macrophages (AM). The alkaline unwinding method was used to determine DNA single-strand breaks in AM lavaged from non-smokers [NS] and smokers of marijuana [MS], tobacco [TS] or cocaine [CS], either alone or in combination. DNA damage was related to superoxide anion (O2-) production by AM stimulated with phorbol myristate acetate (PMA) and to nitric oxide content of smoke using cellular nitrite (NO2-) concentrations. The percentage of double-stranded DNA present after alkaline unwinding was higher in AM of NS (41 +/- 5% [11]) and CS (41 +/- 4% [9]) versus that of MS (31 +/- 4% [8]), TS (35 +/- 3% [11]), MTS (26 +/- 4% [3]), and CTS (27 +/- 5%* [10]), mean +/- SEM [n], * = p < 0.1 vs. NS). PMA stimulated O2- production by AM from NS and CS was lower than that of other smokers, but the differences were not significant. O2- release, however, had an inverse correlation with DNA single-strand breaks (r = -0.38, p = 0.009). Nitrite content of AM from NS and CS was less than that of other smokers' cells (p < 0.1 for TS & CTS vs. NS), but DNA damage had no relationship to NO2- concentration. We conclude that AM recovered from MS, either alone or in combination with tobacco smoking, show a trend towards DNA damage. Studies utilizing a larger population should verify our findings and further define its relationship to enhanced oxidant production by macrophages.
Cocaine↗
Predictors of initial smoking cessation and relapse through the first 2 years of the Lung Health Study.
Analyses were made separately for men and women of the predictors of end-of-treatment (4 months) smoking cessation and subsequent relapse at 12 and 24 months among 3,923 participants enrolled in the Lung Health Study's 12-week cognitive-behavioral group smoking cessation program. Nicotine gum (2 mg) was available to all participants. Men were more likely than women to quit smoking initially, but relapse rates were similar for both genders. Baseline variables associated with initial quitting for both genders included greater education, lower nicotine dependence, and fewer respiratory symptoms. The best predictor of relapse between 4 and 12 months was smoking at least 1 cigarette between quit day and 4 months. Nicotine gum use at 12 months predicted relapse by 24 months for both genders. Greater social and environmental support for quitting smoking were the only factors that predicted both initial quitting and relapse for both genders. Clinical implications are discussed.
Adult↗