Recent trends in lung cancer mortality in the United States.
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BACKGROUND: Previous age-period-cohort analyses of lung cancer incidence and mortality rates in the United States have demonstrated a decrease in risk by birth cohort through 1950, consistent with declining trends in smoking prevalence. This study was conducted to examine recent lung cancer trends, including trends among the cohorts born after 1950. METHODS: Lung cancer mortality rates from 1970 through 1997 for whites aged 24--83 years and for blacks aged 30--83 years were investigated. Using age--period--cohort analyses with 2-year age and 2-year calendar-period intervals, we examined changes in the slope of the trends in birth-cohort and calendar-period effects. All statistical tests are two-sided. RESULTS: There was an unexpected, statistically significant moderation in the rate of decrease of the birth-cohort trend in lung cancer mortality for whites born after 1950, with a corresponding smaller and statistically nonsignificant moderation for blacks. These data are consistent with smoking initiation rates: Rates of both cigarette and marijuana smoking initiation increased for children aged 12--17 years from 1965 through 1977. There was a statistically significant decrease in the slope of the calendar-period trend for lung cancer mortality in 1990 for both whites and blacks that was observed primarily in people 55 years of age and older. CONCLUSIONS AND IMPLICATIONS: The birth-cohort pattern of lung cancer mortality after 1950 appears to reflect the early impact of teenage cigarette smoking on lung cancer risk in people under the age of 45 years, although a contribution from marijuana smoking cannot be ruled out. This result provides additional support for increasing smoking cessation and prevention programs for teenagers. The calendar-period decrease in lung cancer mortality after 1990 may reflect the long-term benefits of reductions in tobacco carcinogens in cigarettes and increases in smoking cessation beginning around 1960. (+info)
Paroxysmal atrial fibrillation in a young female patient following marijuana intoxication--a case report of possible association.
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Marijuana is one of the most popular drugs legally admitted for general sale in many countries. To consider it safe and unlikely to develop drug dependence is abusive. The use of marijuana as a herbal medication is being widely discussed in literature. The most promising effect of delta-9-etrahydrocannabinol seems to be observed in the case of nausea, following cancer chemotherapy. Despite its positive action on the human organism, marijuana smoking has been shown to exert adverse effects on the cardiovascular system causing well-tolerated tachycardia and/or hypotension. We also observed that marijuana abuse was associated with an increased risk of paroxysmal atrial fibrillation. The report presents a case of young healthy white subject suffering from paroxysmal atrial fibrillation following marijuana intoxication. The abuse of this substance was the most possible and identifiable risk factor for observed paroxysmal atrial fibrillation. (+info)
Variation in youthful risks of progression from alcohol and tobacco to marijuana and to hard drugs across generations.
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OBJECTIVES: Much research has documented that youthful substance use typically follows a sequence starting with use of alcohol or tobacco or both and potentially proceeding to marijuana and then hard drug use. This study explicitly examined the probabilities of progression through each stage and their covariates. METHODS: A secondary analysis of data from the National Household Survey on Drug Abuse (1979-1997) was conducted with particular sensitivity to the nature of substance use progression, sampling procedures, and reliability of self-report data. RESULTS: Progression to marijuana and hard drug use was uncommon among persons born before World War II. The stages phenomenon essentially emerged with the baby boom and rose to a peak among persons born around 1960. Subsequently, progression risks at each stage declined. Progression risks were also higher among younger initiators of alcohol, tobacco, or marijuana use. CONCLUSIONS: The recent increase in youthful marijuana use has been offset by lower rates of progression to hard drug use among youths born in the 1970s. Dire predictions of future hard drug abuse by youths who came of age in the 1990s may be greatly overstated. (+info)
Television campaigns and adolescent marijuana use: tests of sensation seeking targeting.
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OBJECTIVES: This study evaluated the effectiveness of targeted televised public service announcement campaigns in reducing marijuana use among high-sensation-seeking adolescents. METHODS: The study used a controlled interrupted time-series design in 2 matched communities. Two televised antimarijuana campaigns were conducted in 1 county and 1 campaign in the comparison community. Personal interviews were conducted with 100 randomly selected teenagers monthly in each county for 32 months. RESULTS: All 3 campaigns reversed upward developmental trends in 30-day marijuana use among high-sensation seekers (P < .002). As expected, low-sensation seekers had low use levels, and no campaign effects were evident. CONCLUSIONS: Televised campaigns with high reach and frequency that use public service announcements designed for and targeted at high-sensation-seeking adolescents can significantly reduce substance use in this high-risk population. (+info)
Effects of prenatal exposure to marijuana.
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QUESTION: I am treating a 27-year-old woman who is now in her 10th week of pregnancy. She smokes marijuana two to three times a week, but does not use other drugs. She also smokes 20 cigarettes a day. I am concerned about the effects of marijuana exposure on her baby. ANSWER: It is not always possible to isolate the effect of marijuana exposure from other possible confounders on pregnancy outcome. Although marijuana is not an established human teratogen, recent well conducted studies suggest it might have subtle negative effects on neurobehavioural outcomes, including sleep disturbances, impaired visual problem solving, hyperactivity, impassivity, inattention, and increased delinquency. (+info)
Triggering myocardial infarction by marijuana.
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BACKGROUND: Marijuana use in the age group prone to coronary artery disease is higher than it was in the past. Smoking marijuana is known to have hemodynamic consequences, including a dose-dependent increase in heart rate, supine hypertension, and postural hypotension; however, whether it can trigger the onset of myocardial infarction is unknown. METHODS AND RESULTS: In the Determinants of Myocardial Infarction Onset Study, we interviewed 3882 patients (1258 women) with acute myocardial infarction an average of 4 days after infarction onset. We used the case-crossover study design to compare the reported use of marijuana in the hour preceding symptoms of myocardial infarction onset to its expected frequency using self-matched control data. Of the 3882 patients, 124 (3.2%) reported smoking marijuana in the prior year, 37 within 24 hours and 9 within 1 hour of myocardial infarction symptoms. Compared with nonusers, marijuana users were more likely to be men (94% versus 67%, P<0.001), current cigarette smokers (68% versus 32%, P<0.001), and obese (43% versus 32%, P=0.008). They were less likely to have a history of angina (12% versus 25%, P<0.001) or hypertension (30% versus 44%, P=0.002). The risk of myocardial infarction onset was elevated 4.8 times over baseline (95% confidence interval, 2.4 to 9.5) in the 60 minutes after marijuana use. The elevated risk rapidly decreased thereafter. CONCLUSIONS: Smoking marijuana is a rare trigger of acute myocardial infarction. Understanding the mechanism through which marijuana causes infarction may provide insight into the triggering of myocardial infarction by this and other, more common stressors. (+info)
Detection of marijuana use by oral fluid and urine analysis following single-dose administration of smoked and oral marijuana.
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We compared oral fluid testing to urine testing in subjects who were administered single doses of marijuana by smoked and oral routes. Oral fluid specimens were collected with the Intercept DOA Oral Specimen Collection Device, screened for THC with the Cannabinoids Intercept MICRO-PLATE Enzyme Immunoassay (EIA) utilizing a 1.0-ng/mL cutoff concentration, and confirmed for THC by gas chromatography-tandem mass spectrometry (GC-MS-MS) with a 0.5-ng/mL cutoff concentration. Urine specimens were screened for 11-nor-carboxy-delta9-tetrahydrocannabinol (THCCOOH) by immunoassay utilizing a 50-ng/mL cutoff concentration and confirmed for THCCOOH by GC-MS with a 15-ng/mL cutoff concentration. Oral fluid specimens tested positive following smoked marijuana (N = 10) consecutively for average periods (+/-SEM; range) of 15 (+/-2; 1-24) and 13 h (+/-3; 1-24) by EIA and GC-MS-MS, respectively. The average THC detection times of the last oral fluid positive specimen following smoked marijuana by EIA and GC-MS-MS were 31 (+/-9; 1-72) and 34 h (+/-11; 1-72), respectively. In comparison to oral fluid, urine specimens generally tested negative for THCCOOH immediately after marijuana use. The average times to detection of the first urine specimen positive for THCCOOH by EIA and GC-MS were 6 (+/-2; 1-16) and 4 h (+/-1; 2-8), respectively. Urine specimens tested positive consecutively for average periods of 26 (+/-9; 2-72) and 33 h (+/-10; 4-72) for EIA and GC-MS, respectively. The average THCCOOH detection times of the last specimen by EIA and GC-MS were 42 (+/-10; 2-72) and 58 h (+/-6; 16-72), respectively. Considering the noninvasive nature of oral fluid collection and improved detection of recent marijuana use compared to urine testing, it was concluded that oral fluid testing for THC offers specific advantages over other means of marijuana testing when used in safety-sensitive testing programs. (+info)
Simultaneous determination of delta9-tetrahydrocannabinol and 11-nor-9-carboxy-delta9-tetrahydrocannabinol in human plasma by solid-phase extraction and gas chromatography-negative ion chemical ionization-mass spectrometry.
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Delta9-tetrahydrocannabinol (THC) and 11-nor-9-carboxy-delta9-tetrahydrocannabinol (THCA) in human plasma can be simultaneously detected using solid-phase extraction with gas chromatography and negative ion chemical ionization mass spectrometry. THC-d3 and THCA-d3 are added as internal standards; protein is precipitated with acetonitrile and the resulting supernatants diluted with 0.1 M sodium acetate (pH 7.0) prior to application to the solid-phase extraction columns. THC and THCA were eluted separately and then pooled, dried under air, and derivatized with trifluoroacetic anhydride and hexafluoroisopropanol. The derivatized THC-d0 gives abundant molecular anions (m/z 410), and the derivatized THCA-d0 gives abundant fragment ions (m/z 422) formed by loss of (CF3)2CHOH from its molecular anion. The recoveries of THC and THCA were 74% and 17%, respectively. The lower and upper limits of quantitation were 0.5 and 100 ng/mL for THC and 2.5 ng/mL and 100 ng/mL for THCA. The within-run accuracy and precision for THC (measured at 0.5, 1, 10 and 75 ng/mL) ranged from 98 to 106% (% target) and 4.1 to 9.5 (%CV), respectively. For THCA, the within-run accuracy and precision (measured at 2.5, 5, 10, and 75 ng/mL) ranged from 89 to 101% and 4.3 to 7.5%, respectively. The between-run accuracy and precision for THC ranged from 92 to 110% and 0.4 to 12.4%, respectively. The between-run accuracy and precision for THCA ranged from 97 to 103% and 6.5 to 12.3%, respectively. In processed samples stored in reconstituted form at -20 degrees C, THC and THCA were stable for at least three days. THC and THCA stored in plasma were stable following three freeze/thaw cycles. THC and THCA in whole blood at room temperature for 6 h, or in plasma stored at room temperature for 24 h, did not show significant change. Storage in polypropylene containers for 7 days at -20 degrees C and the presence of 1% sodium fluoride or the cannabinoid receptor antagonist, SR141716, at 1 microg/mL did not interfere with the quantitation of THC and THCA. In three individuals who smoked marijuana under controlled dosing conditions, peak THC concentrations of 151, 266, and 99 ng/mL were seen in the first plasma samples drawn immediately after the end of smoking, and corresponding peak THCA concentrations of 41, 52, and 17 ng/mL occurred at 0.33 to 1 h after cessation of smoking. (+info)