The smoking of cannabis and tobacco is common in many countries. In contrast to tobacco, which is an established risk factor for the sudden infant death syndrome (SIDS), nothing is known about cannabis and its effects on SIDS risk. We analysed data collected in a nation-wide case control study in New Zealand (393 cases, 1592 controls) to determine if there is any association between maternal cannabis use and SIDS risk. Adjusting for ethnicity and maternal tobacco use, the SIDS odds ratio for >weekly maternal cannabis use since the infant's birth was 2.23 (95% CI = 1.39, 3.57) compared to non-users; and the multivariate odds ratio was 1.55 (95% CI = 0.87, 2.75). We conclude that frequent maternal cannabis use may be a weak risk factor for SIDS, but this finding requires further research.
The purpose of this study was to determine whether marijuana produced dose-dependent antinociception in humans and, if so, whether endogenous opiates modulate this effect. A total of five male regular marijuana users participated in three test sessions during which they smoked cigarettes containing 0% (placebo) and 3. 55% Delta(9)-tetrahydrocannabinol (Delta(9)-THC) (active). Each of four controlled smoking bouts per session, spaced at 40-min intervals, consisted of nine puffs from active and placebo cigarettes (three cigarettes, three puffs per cigarette, one puff per min). During successive bouts, participants smoked 0, 3, 6 and 9 (0, 3, 9 and 18 cumulative) puffs from active marijuana cigarettes, with the remainder of puffs from placebo cigarettes. Test sessions were identical, except for naltrexone 0, 50 or 200 mg p.o. (randomized, double-blind) administration 1 h before the first smoking bout on the different days. Before smoking, between smoking bouts and postsmoking, participants completed an assessment battery that included antinociceptive (finger withdrawal from radiant heat stimulation), biological, subjective, observer-rated signs and performance measures. Marijuana produced significant dose-dependent antinociception (increased finger withdrawal latency) and biobehavioral effects. Naltrexone did not significantly influence marijuana dose-effect curves, suggesting no role of endogenous opiates in marijuana-induced antinociception under these conditions.
AIM: To evaluate the relationship between cannabis dependence and respiratory symptoms and lung function in young adults, while controlling for the effects of tobacco smoking.
SETTING AND PARTICIPANTS: Nine hundred and forty-three young adults from a birth cohort of 1037 subjects born in Dunedin, New Zealand in 1972/1973 were studied at age 21.
MEASUREMENTS: Standardized respiratory symptom questionnaires were administered. Spirometry and methacholine challenge tests were undertaken. Cannabis dependence was determined using DSM-III-R criteria. Descriptive analyses and comparisons between cannabis-dependent, tobacco-smoking and non-smoking groups were undertaken. Adjusted odds ratios for respiratory symptoms, lung function and airway hyper-responsiveness (PC20) were measured.
FINDINGS: Ninety-one subjects (9.7%) were cannabis-dependent and 264 (28.1%) were current tobacco smokers. After controlling for tobacco use, respiratory symptoms associated with cannabis dependence included: wheezing apart from colds, exercise-induced shortness of breath, nocturnal wakening with chest tightness and early morning sputum production. These were increased by 61%, 65%, 72% (all p < 0.05) and 144% (p < 0.01) respectively, compared to non-tobacco smokers. The frequency of respiratory symptoms in cannabis-dependent subjects was similar to tobacco smokers of 1-10 cigarettes/day. The proportion of cannabis-dependent study members with an FEV1/FVC ratio of < 80% was 36% compared to 20% for non-smokers (p = 0.04). These outcomes occurred independently of co-existing bronchial asthma.
CONCLUSION: Significant respiratory symptoms and changes in spirometry occur in cannabis-dependent individuals at age 21 years, even although the cannabis smoking history is of relatively short duration.
Blood samples from 2,500 injured drivers were analysed for alcohol, cannabinoids (measured by the presence of THC), benzodiazepines and stimulants. The relationship between the prevalence and concentration of drugs and the culpability of the driver was examined using an objective method for assessing culpability. There were no significant differences between males and females with respect to culpability. However, there was a relationship between age and culpability: drivers under 26 years and over 60 years were more likely to be culpable. Drivers who tested positive for alcohol only, benzodiazepines only and the combinations of alcohol and THC and alcohol and benzodiazepines were significantly more likely to be culpable for the crash compared with the drug-free group. Conversely, a lower percentage of drivers who only tested positive for THC were culpable for the crash compared with drug-free drivers. This difference was not statistically significant. For car drivers in single-vehicle crashes, the majority of drivers were judged culpable irrespective of drug use. In multiple-vehicle crashes, car drivers testing positive for alcohol only or benzodiazepines only were more likely to be culpable for the crash compared with drug-free drivers. For motorcycle riders in both single- and multiple-vehicle crashes, there were no significant differences between the drug-positive and drug-free groups. A higher percentage of drug-free riders in multiple-vehicle crashes were culpable compared with riders who only tested positive for THC, but this difference was not statistically significant. There was a significant concentration-dependent relationship between alcohol and culpability: as blood alcohol concentration increased, so did the percentage of culpable drivers. When THC was used alone, there was no significant increase in culpability. For those drivers with benzodiazepines at therapeutic concentrations and above, there was a significant increase in culpability. The relationship between stimulants and culpability was not significant, although a higher proportion of stimulant-positive drivers were culpable compared with drug-free drivers. The combinations of alcohol and THC, and alcohol and benzodiazepines also produced a significant increase in culpability, but this increase was not significantly greater than that produced by alcohol alone.
This is a prospective study of the effects of prenatal marijuana exposure on child behavior problems at age 10. The sample consisted of low-income women attending a prenatal clinic. Half of the women were African-American and half were Caucasian. The majority of the women decreased their use of marijuana during pregnancy. The assessments of child behavior problems included the Child Behavior Checklist (CBCL), Teacher's Report Form (TRF), and the Swanson, Noland, and Pelham (SNAP) checklist. Multiple and logistic regressions were employed to analyze the relations between marijuana use and behavior problems of the children, while controlling for the effects of other extraneous variables. Prenatal marijuana use was significantly related to increased hyperactivity, impulsivity, and inattention symptoms as measured by the SNAP, increased delinquency as measured by the CBCL, and increased delinquency and externalizing problems as measured by the TRF. The pathway between prenatal marijuana exposure and delinquency was mediated by the effects of marijuana exposure on inattention symptoms. These findings indicate that prenatal marijuana exposure has an effect on child behavior problems at age 10.
Journal»Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
Marijuana is the most commonly used illegal drug in the United States. In some subcultures, it is widely perceived to be harmless. Although the carcinogenic properties of marijuana smoke are similar to those of tobacco, no epidemiological studies of the relationship between marijuana use and head and neck cancer have been published. The relationship between marijuana use and head and neck cancer was investigated by a case-control study of 173 previously untreated cases with pathologically confirmed diagnoses of squamous cell carcinoma of the head and neck and 176 cancer-free controls at Memorial Sloan-Kettering Cancer Center between 1992 and 1994. Epidemiological data were collected by using a structured questionnaire, which included history of tobacco smoking, alcohol use, and marijuana use. The associations between marijuana use and head and neck cancer were analyzed by Mantel-Haenszel methods and logistic regression models. Controlling for age, sex, race, education, alcohol consumption, pack-years of cigarette smoking, and passive smoking, the risk of squamous cell carcinoma of the head and neck was increased with marijuana use [odds ratio (OR) comparing ever with never users, 2.6; 95% confidence interval (CI), 1.1-6.6]. Dose-response relationships were observed for frequency of marijuana use/day (P for trend <0.05) and years of marijuana use (P for trend <0.05). These associations were stronger for subjects who were 55 years of age and younger (OR, 3.1; 95% CI, 1.0-9.7). Possible interaction effects of marijuana use were observed with cigarette smoking, mutagen sensitivity, and to a lesser extent, alcohol use. Our results suggest that marijuana use may increase the risk of head and neck cancer with a strong dose-response pattern. Our analysis indicated that marijuana use may interact with mutagen sensitivity and other risk factors to increase the risk of head and neck cancer. The results need to be interpreted with some caution in drawing causal inferences because of certain methodological limitations, especially with regard to interactions.
The purpose of this study was to investigate possible adverse effects of cannabis use on cognitive decline after 12 years in persons under age 65 years. This was a follow-up study of a probability sample of the adult household residents of East Baltimore. The analyses included 1,318 participants in the Baltimore, Maryland, portion of the Epidemiologic Catchment Area study who completed the Mini-Mental State Examination (MMSE) during three study waves in 1981, 1982, and 1993-1996. Individual MMSE score differences between waves 2 and 3 were calculated for each study participant. After 12 years, study participants' scores declined a mean of 1.20 points on the MMSE (standard deviation 1.90), with 66% having scores that declined by at least one point. Significant numbers of scores declined by three points or more (15% of participants in the 18-29 age group). There were no significant differences in cognitive decline between heavy users, light users, and nonusers of cannabis. There were also no male-female differences in cognitive decline in relation to cannabis use. The authors conclude that over long time periods, in persons under age 65 years, cognitive decline occurs in all age groups. This decline is closely associated with aging and educational level but does not appear to be associated with cannabis use. Am J Epidemiol 1999;149:794-800.
Previous experimental and epidemiological studies failed to provide unequivocal evidence that marijuana, either alone or in combination with alcohol, impairs a driver's performance to the extent that it will compromise traffic safety. We investigated the effects of marijuana, alone and in combination with alcohol, on actual driving in four, single-blind, randomized, cross-over studies. In Study 1, 24 subjects performed a road-tracking test on a closed segment of a primary highway after smoking marijuana that contained 0, 100, 200 and 300 μg/kg Δ9-tetrahydrocannabinol (THC). In Study 2, 16 new subjects smoked the same THC doses before they performed a road-tracking and a car-following test; however, this time in the presence of other traffic. In Study 3, two groups of 16 subjects performed a city driving test. One group smoked marijuana delivering 0 and 100 μg/kg THC prior to driving; the other group drunk orange juice mixed with or without a low dose of alcohol. In Study 4, 18 subjects performed a road-tracking and a car-following test in each of six conditions where they smoked marijuana with 0, 100, or 200 μg/kg THC after they had consumed orange juice with or without alcohol. In these studies, marijuana alone significantly increased lateral position variability in the road-tracking test and distance variability during deceleration manoeuvres in the car-following test. Reaction times during car-following were not significantly affected, and a THC dose of 100 μg/kg did not impair city driving performance. Blood plasma concentrations of THC and THC-COOH were not related to the degree of impairment. A low dose of alcohol (i.e. blood alcohol concentrations around 0.04%) impaired performance in all driving tests. Whereas marijuana's effects on driving performance were small (100 μg/kg THC) or moderate (200 and 300 μg/kg) when taken alone, they were severe when combined with a low dose of alcohol. In conclusion, marijuana alone impairs driving performance, with the degree of impairment increasing from small to moderate as the THC dose increases from 100 to 300 μg/kg. However, when low to moderate doses of THC (100 and 200 μg/kg) are taken in combination with a low dose of alcohol sufficient for attaining a BAC of about 0.04% actual driving is severely impaired.
BACKGROUND: Cognitive correlates of long-term cannabis use have been elusive. We tested the hypothesis that long-term cannabis use is associated with deficits in short term memory, working memory, and attention in a literate, westernized culture (Costa Rica) in which the effects of cannabis use can be isolated.
METHODS: Two cohorts of long-term cannabis users and nonusers were studied. Within each cohort, users and nonusers were comparable in age and socioeconomic status. Polydrug users and users who tested positive for the use of cannabis at the time of cognitive assessment after a 72-hour abstention period were excluded. The older cohort (whose age was approximately 45 years) had consumed cannabis for an average of 34 years, and comprised 17 users and 30 nonusers, who had been recruited in San José, Costa Rica, and had been observed since 1973. The younger cohort (whose age was approximately 28 years) had consumed cannabis for an average of 8 years, and comprised 37 users and 49 nonusers. Short-term memory, working memory, and attentional skills were measured in each subject.
RESULTS: Older long-term users performed worse than older nonusers on 2 short-term memory tests involving learning lists of words. In addition, older long-term users performed worse than older nonusers on selective and divided attention tasks associated with working memory. No notable differences were apparent between younger users and nonusers.
CONCLUSION: Long-term cannabis use was associated with disruption of short-term memory, working memory, and attentional skills in older long-term cannabis users.
The smoking of cannabis and tobacco is common in many countries. In contrast to tobacco, which is an established risk factor for the sudden infant death syndrome (SIDS), nothing is known about cannabis and its effects on SIDS risk. We analysed data collected in a nation-wide case control study in New Zealand (393 cases, 1592 controls) to determine if there is any association between maternal cannabis use and SIDS risk. Adjusting for ethnicity and maternal tobacco use, the SIDS odds ratio for >weekly maternal cannabis use since the infant's birth was 2.23 (95% CI = 1.39, 3.57) compared to non-users; and the multivariate odds ratio was 1.55 (95% CI = 0.87, 2.75). We conclude that frequent maternal cannabis use may be a weak risk factor for SIDS, but this finding requires further research.
