Rev Prat. 2005 Jan 15;55(1):41-9.

[Adverse effects of marijuana].

[Article in French]
Mallaret M, Dal'Bo-Rohrer D, Demattis M.

Source
Centre d'valuation et d'information sur la pharmacodpendance, CHU Grenoble, 38043 Grenoble. mmallaret@chugrenoble.fr

Abstract
When admitted in an emergency unit, young patients often present acute neurological effects of
smoked marijuana. Other chronic adverse effects of marijuana are probably underestimated: postural
syncope, arteritis, chronic bronchitis, amnesia. Marijuana may trigger a myocardial infarction and
have a vasospastic effect. Marijuana has impairing effects on driving ability. Smoked marijuana is a
potential respiratory tract carcinogen.

[Cognitive abnormalities and cannabis use].

[Article in Portuguese]
Solowij N, Pesa N.

Source
School of Psychology, University of Wollongong, Wollongong, Austrlia. nadia@uow.edu.au

Abstract
OBJECTIVE:
Evidence that cannabis use impairs cognitive function in humans has been accumulating in recent
decades. The purpose of this overview is to update knowledge in this area with new findings from the
most recent literature.
METHOD:
Literature searches were conducted using the Web of Science database up to February 2010. The
terms searched were: "cannabi*" or "marijuana", and "cogniti*" or "memory" or "attention" or
"executive function", and human studies were reviewed preferentially over the animal literature.
DISCUSSION:
Cannabis use impairs memory, attention, inhibitory control, executive functions and decision making,
both during the period of acute intoxication and beyond, persisting for hours, days, weeks or more
after the last use of cannabis. Pharmacological challenge studies in humans are elucidating the
nature and neural substrates of cognitive changes associated with various cannabinoids. Long-term
or heavy cannabis use appears to result in longer-lasting cognitive abnormalities and possibly
structural brain alterations. Greater adverse cognitive effects are associated with cannabis use
commencing in early adolescence.
CONCLUSION:
The endogenous cannabinoid system is involved in regulatory neural mechanisms that modulate
processes underlying a range of cognitive functions that are impaired by cannabis. Deficits in human
users most likely therefore reflect neuroadaptations and altered functioning of the endogenous
cannabinoid system.

J Clin Pharmacol. 2002 Nov;42(11 Suppl):64S-70S.

Cardiovascular consequences of marijuana use.

Sidney S.

Source
Kaiser Permanente Medical Care Program, Division of Research, Oakland, California 94612, USA.

Abstract
This review describes what is known about effects of marijuana and cannabinoids in relation to
human physiological and disease outcomes. The acute physiological effects of marijuana include a
substantial dose-dependent increase in heart rate, generally associated with a mild increase in blood
pressure. Orthostatic hypotension may occur acutely as a result of decreased vascular resistance.
Smoking marijuana decreases exercise test duration in maximal exercise tests, increases the heart
rate at submaximal levels of exercise. Tolerance develops to the acute effects of marijuana smoking
and delta9-tetrahydrocannibol (THC) over several days to a few weeks. The cardiovascular
responses that occur in response to THC are mediated by the autonomic nervous system, with recent
findings also demonstrating that the human cannabinoid receptor system plays a role in regulating the
cardiovascular response. Although several mechanisms exist by which marijuana use might
contribute to the development of chronic cardiovascular conditions or acutely trigger cardiovascular
events, there are few data regarding marijuana/THC use and cardiovascular disease outcomes. A
large cohort study showed no association of marijuana use with cardiovascular disease
hospitalization or mortality. However, acute effects of marijuana use include a decrease of the time
until the onset of chest pain in patients with angina pectoris; one study has shown that marijuana may
trigger the onset of myocardial infarction. Patients who have coronary heart disease or are at high risk
for the development of CHD should be cautioned about the potential hazards of marijuana use as a
precipitant for clinical events. Research directions might include more studies of cardiovascular
disease outcomes and relationships of marijuana with cardiovascular risk factors, studies of metabolic
and physiologic effects of chronic marijuana use that may affect cardiovascular disease risk,
increased understanding of the role of the cannabinoid receptor system in cardiovascular regulation,
and studies to determine if there is a therapeutic role for cannabinoids in blood pressure control or for
neuroprotection after stroke.

J Clin Pharmacol. 2002 Nov;42(11 Suppl):58S-63S.

Cardiovascular system effects of marijuana.

Jones RT.

Source
Langley Porter Psychiatric Institute, Department of Psychiatry, University of California, San Francisco 94143-0984,
USA.

Abstract
Marijuana and delta9-tetrahydrocannabinol (THC) increase heart rate, slightly increase supine blood
pressure, and on occasion produce marked orthostatic hypotension. Cardiovascular effects in animals
are different, with bradycardia and hypotension the most typical response. Cardiac output increases,
and peripheral vascular resistance and maximum exercise performance decrease. Tolerance to most
of the initial cardiovascular effects appears rapidly. With repeated exposure, supine blood pressure
decreases slightly, orthostatic hypotension disappears, blood volume increases, heart rate slows, and
circulatory responses to exercise and Valsalva maneuver are diminished, consistent with centrally
mediated, reduced sympathetic, and enhanced parasympathetic activity. Receptor-mediated and

probably nonneuronal sites of action account for cannabinoid effects. The endocannabinoid system
appears important in the modulation of many vascular functions. Marijuana's cardiovascular effects
are not associated with serious health problems for most young, healthy users, although occasional
myocardial infarction, stroke, and other adverse cardiovascular events are reported. Marijuana
smoking by people with cardiovascular disease poses health risks because of the consequences of
the resulting increased cardiac work, increased catecholamine levels, carboxyhemoglobin, and
postural hypotension.

Clin Rev Allergy Immunol. 1997 Fall;15(3):243-69.

Marijuana. Respiratory tract effects.

Van Hoozen BE, Cross CE.

Source
Division of Pulmonary and Critical Care Medicine, University of California at Davis, Sacramento 95817, USA.

Abstract
Daily marijuana smoking has been clearly shown to have adverse effects on pulmonary function and
produce respiratory symptomatology (cough, wheeze, and sputum production) similar to that of
tobacco smokers. Based on the tobacco experience, decrements in pulmonary function may be
predictive of the future development of chronic obstructive pulmonary disease (COPD). However, in
the absence of alpha-1-antitrypsin deficiency, the habitual marijuana-only smoker would likely have to
smoke 4-5 joints per day for a span of at least 30 yr in order to develop overt manifestations of COPD.
The mutagenic/carcinogenic properties of marijuana smoke are also well-established. The potential
for induction of laryngeal, oropharyngeal, and possibly bronchogenic carcinoma from marijuana has
been documented by several case reports and observational series. Despite this, a relative risk ratio
for the development of these tumors has not yet been quantified. Based on a higher frequency of
case reports for upper airway cancer compared to bronchogenic carcinoma, marijuana smoking may
have a more deleterious effect on the upper respiratory tract. However, this hypothesis remains
speculative at best, pending confirmation by longitudinal studies.

Effects of smoking cannabis on lung function.

Lee MH, Hancox RJ.

Source
Department of Respiratory Medicine, Waikato Hospital, Pembroke St, Hamilton, New Zealand.

Abstract
Although cannabis (or marijuana) is the world's most widely-used illicit drug, there has been
surprisingly little research into its effects on respiratory health. Part of the problem is the inherent
difficulty of studying the long-term effects of an illegal habit. It has often been assumed that smoking
cannabis will have similar long-term effects to smoking tobacco. Several recent observational studies
suggest that this is not the case and that cannabis has quite different effects on the lung function.
There are consistent findings that smoking cannabis is associated with large airway inflammation,
symptoms of bronchitis, increased airway resistance and lung hyperinflation. The evidence that
smoking cannabis leads to features of chronic obstructive pulmonary disease, such as airflow
obstruction and emphysema is not convincing. However, there are numerous case reports of bullous
emphysema among cannabis smokers. These findings have not been confirmed in systematic
analytical studies and probably represent uncommon adverse effects in very heavy cannabis

smokers. There is now additional controversial evidence that cannabis is at least an occasional cause
of respiratory malignancies, but again the evidence is inconclusive.

Thorax. 2007 Dec;62(12):1058-63. Epub 2007 Jul 31.

Effects of cannabis on pulmonary structure, function and

symptoms.
Aldington S, Williams M, Nowitz M, Weatherall M, Pritchard A, McNaughton A, Robinson G, Beasley R.

Source
Medical Research Institute of New Zealand, P O Box 10055, Wellington 6143, New Zealand.

Erratum in

Thorax. 2008 Apr;63(4):385.

Abstract
BACKGROUND:
Cannabis is the most widely used illegal drug worldwide. Long-term use of cannabis is known to
cause chronic bronchitis and airflow obstruction, but the prevalence of macroscopic emphysema, the
dose-response relationship and the dose equivalence of cannabis with tobacco has not been
determined.
METHODS:
A convenience sample of adults from the Greater Wellington region was recruited into four smoking
groups: cannabis only, tobacco only, combined cannabis and tobacco and non-smokers of either
substance. Their respiratory status was assessed using high-resolution CT (HRCT) scanning,
pulmonary function tests and a respiratory and smoking questionnaire. Associations between
respiratory status and cannabis use were examined by analysis of covariance and logistic regression.
RESULTS:
339 subjects were recruited into the four groups. A dose-response relationship was found between
cannabis smoking and reduced forced expiratory volume in 1 s to forced vital capacity ratio and
specific airways conductance, and increased total lung capacity. For measures of airflow obstruction,
one cannabis joint had a similar effect to 2.5-5 tobacco cigarettes. Cannabis smoking was associated
with decreased lung density on HRCT scans. Macroscopic emphysema was detected in 1/75 (1.3%),
15/92 (16.3%), 17/91 (18.9%) and 0/81 subjects in the cannabis only, combined cannabis and
tobacco, tobacco alone and non-smoking groups, respectively.
CONCLUSIONS:
Smoking cannabis was associated with a dose-related impairment of large airways function resulting
in airflow obstruction and hyperinflation. In contrast, cannabis smoking was seldom associated with
macroscopic emphysema. The 1:2.5-5 dose equivalence between cannabis joints and tobacco
cigarettes for adverse effects on lung function is of major public health significance.

Comment in

Cannabis and the lung. [Thorax. 2007]

Clin Rev Allergy Immunol. 1997 Fall;15(3):243-69.

Marijuana. Respiratory tract effects.

Van Hoozen BE, Cross CE.

Source
Division of Pulmonary and Critical Care Medicine, University of California at Davis, Sacramento 95817, USA.

Abstract
Daily marijuana smoking has been clearly shown to have adverse effects on pulmonary function and
produce respiratory symptomatology (cough, wheeze, and sputum production) similar to that of
tobacco smokers. Based on the tobacco experience, decrements in pulmonary function may be
predictive of the future development of chronic obstructive pulmonary disease (COPD). However, in
the absence of alpha-1-antitrypsin deficiency, the habitual marijuana-only smoker would likely have to
smoke 4-5 joints per day for a span of at least 30 yr in order to develop overt manifestations of COPD.
The mutagenic/carcinogenic properties of marijuana smoke are also well-established. The potential
for induction of laryngeal, oropharyngeal, and possibly bronchogenic carcinoma from marijuana has
been documented by several case reports and observational series. Despite this, a relative risk ratio
for the development of these tumors has not yet been quantified. Based on a higher frequency of
case reports for upper airway cancer compared to bronchogenic carcinoma, marijuana smoking may
have a more deleterious effect on the upper respiratory tract. However, this hypothesis remains
speculative at best, pending confirmation by longitudinal studies.

Monaldi Arch Chest Dis. 2005 Jun;63(2):93-100.

Smoked marijuana as a cause of lung injury.

Tashkin DP.

Source
Division of Pulmonaiy & Critical Care Medicine, Department of Medicine, David Geffen School of Medicine, UCLA, Los
Angeles, CA 90095-1690, USA. dtashkin@mednet.ucla.edu

Abstract
In many societies, marijuana is the second most commonly smoked substance after tobacco. While
delta9-tetrahydrocannabinol (THC) is unique to marijuana and nicotine to tobacco, the smoke of
marijuana, like that of tobacco, consists of a toxic mixture of gases and particulates, many of which
are known to be harmful to the lung. Although far fewer marijuana than tobacco cigarettes are
generally smoked on a daily basis, the pulmonary consequences of marijuana smoking may be
magnified by the greater deposition of smoke particulates in the lung due to the differing manner in
which marijuana is smoked. Whereas THC causes modest short-term bronchodilation, regular
marijuana smoking produces a number of long-term pulmonary consequences, including chronic
cough and sputum, histopathologic evidence of widespread airway inflammation and injury and
immunohistochemical evidence of dysregulated growth of respiratory epithelial cells, that may be
precursors to lung cancer. The THC in marijuana could contribute to some of these injurious changes
through its ability to augment oxidative stress, cause mitochondrial dysfunction, and inhibit apoptosis.
On the other hand, physiologic, clinical or epidemiologic evidence that marijuana smoking may lead to
chronic obstructive pulmonary disease or respiratory cancer is limited and inconsistent. Habitual use
of marijuana is also associated with abnormalities in the structure and function of alveolar
macrophages, including impairment in microbial phagocytosis and killing that is associated with
defective production of immunostimulatory cytokines and nitric oxide, thereby potentially predisposing

to pulmonary infection. In view of the growing interest in medicinal marijuana, further epidemiologic
studies are needed to clarify the true risks of regular marijuana smoking on respiratory health.
PMID:

16128224

[PubMed - indexed for MEDLINE]

Monaldi Arch Chest Dis. 2005 Jun;63(2):93-100.

Smoked marijuana as a cause of lung injury.

Tashkin DP.

Source
Division of Pulmonaiy & Critical Care Medicine, Department of Medicine, David Geffen School of Medicine, UCLA, Los
Angeles, CA 90095-1690, USA. dtashkin@mednet.ucla.edu

Abstract
In many societies, marijuana is the second most commonly smoked substance after tobacco. While
delta9-tetrahydrocannabinol (THC) is unique to marijuana and nicotine to tobacco, the smoke of
marijuana, like that of tobacco, consists of a toxic mixture of gases and particulates, many of which
are known to be harmful to the lung. Although far fewer marijuana than tobacco cigarettes are
generally smoked on a daily basis, the pulmonary consequences of marijuana smoking may be
magnified by the greater deposition of smoke particulates in the lung due to the differing manner in
which marijuana is smoked. Whereas THC causes modest short-term bronchodilation, regular
marijuana smoking produces a number of long-term pulmonary consequences, including chronic
cough and sputum, histopathologic evidence of widespread airway inflammation and injury and
immunohistochemical evidence of dysregulated growth of respiratory epithelial cells, that may be
precursors to lung cancer. The THC in marijuana could contribute to some of these injurious changes
through its ability to augment oxidative stress, cause mitochondrial dysfunction, and inhibit apoptosis.
On the other hand, physiologic, clinical or epidemiologic evidence that marijuana smoking may lead to
chronic obstructive pulmonary disease or respiratory cancer is limited and inconsistent. Habitual use
of marijuana is also associated with abnormalities in the structure and function of alveolar
macrophages, including impairment in microbial phagocytosis and killing that is associated with
defective production of immunostimulatory cytokines and nitric oxide, thereby potentially predisposing
to pulmonary infection. In view of the growing interest in medicinal marijuana, further epidemiologic
studies are needed to clarify the true risks of regular marijuana smoking on respiratory health.
PMID:

16128224

[PubMed - indexed for MEDLINE]

Expert Rev Respir Med. 2011 Aug;5(4):537-46; quiz 547.

Effects of smoking cannabis on lung function.

Lee MH, Hancox RJ.

Source
Department of Respiratory Medicine, Waikato Hospital, Pembroke St, Hamilton, New Zealand.

Abstract
Although cannabis (or marijuana) is the world's most widely-used illicit drug, there has been
surprisingly little research into its effects on respiratory health. Part of the problem is the inherent
difficulty of studying the long-term effects of an illegal habit. It has often been assumed that smoking
cannabis will have similar long-term effects to smoking tobacco. Several recent observational studies
suggest that this is not the case and that cannabis has quite different effects on the lung function.
There are consistent findings that smoking cannabis is associated with large airway inflammation,
symptoms of bronchitis, increased airway resistance and lung hyperinflation. The evidence that
smoking cannabis leads to features of chronic obstructive pulmonary disease, such as airflow
obstruction and emphysema is not convincing. However, there are numerous case reports of bullous
emphysema among cannabis smokers. These findings have not been confirmed in systematic
analytical studies and probably represent uncommon adverse effects in very heavy cannabis
smokers. There is now additional controversial evidence that cannabis is at least an occasional cause
of respiratory malignancies, but again the evidence is inconclusive.

CMAJ. 2009 Apr 14;180(8):814-20.

Marijuana and chronic obstructive lung disease: a populationbased study.

Tan WC, Lo C, Jong A, Xing L, Fitzgerald MJ, Vollmer WM, Buist SA, Sin DD; Vancouver Burden of
Obstructive Lung Disease (BOLD) Research Group.

Collaborators (14)

Source
iCapture Centre for Cardiovascular and Pulmonary Research, St. Paul's Hospital and the University of British Columbia,
Vancouver, Canada. wtan@mrl.ubc.ca

Abstract
BACKGROUND:
Our aim was to determine the combined and independent effects of tobacco and marijuana smoking
on respiratory symptoms and chronic obstructive pulmonary disease (COPD) in the general
population.
METHOD:
We surveyed a random sample of 878 people aged 40 years or older living in Vancouver, Canada,
about their respiratory history and their history of tobacco and marijuana smoking. We performed
spirometric testing before and after administration of 200 microg of salbutamol. We examined the
association between tobacco and marijuana smoking and COPD.
RESULTS:
The prevalence of a history of smoking in this sample was 45.5% (95% confidence interval [CI]
42.2%-48.8%) for marijuana use and 53.1% (95% CI 49.8%-56.4%) for tobacco use. The prevalence
of current smoking (in the past 12 months) was 14% for marijuana use and 14% for tobacco use.
Compared with nonsmokers, participants who reported smoking only tobacco, but not those who
reported smoking only marijuana, experienced more frequent respiratory symptoms (odds ratio [OR]
1.50, 95% CI 1.05-2.14) and were more likely to have COPD (OR 2.74, 95% CI 1.66-4.52).
Concurrent use of marijuana and tobacco was associated with increased risk (adjusted for age,
asthma and comorbidities) of respiratory symptoms (OR 2.39, 95% CI 1.58-3.62) and COPD (OR

2.90, 95% CI 1.53-5.51) if the lifetime dose of marijuana exceeded 50 marijuana cigarettes. The risks
of respiratory symptoms and of COPD were related to a synergistic interaction between marijuana
and tobacco.
INTERPRETATION:
Smoking both tobacco and marijuana synergistically increased the risk of respiratory symptoms and
COPD. Smoking only marijuana was not associated with an increased risk of respiratory symptoms or
COPD.

Life Sci. 1995;56(23-24):2185-91.

The relationship of tobacco and marijuana smoking

characteristics.
Simmons MS, Tashkin DP.

Source
Dept. of Medicine, UCLA School of Medicine 90095, USA.

Abstract
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.

Lancet. 2009 Oct 17;374(9698):1383-91.

Adverse health effects of non-medical cannabis use.

Hall W , Degenhardt L.

Source
School of Population Health, University of Queensland, Herston, QLD, Australia. w.hall@sph.uq.edu.au

Abstract
For over two decades, cannabis, commonly known as marijuana, has been the most widely used illicit
drug by young people in high-income countries, and has recently become popular on a global scale.
Epidemiological research during the past 10 years suggests that regular use of cannabis during
adolescence and into adulthood can have adverse effects. Epidemiological, clinical, and laboratory
studies have established an association between cannabis use and adverse outcomes. We focus on
adverse health effects of greatest potential public health interest-that is, those that are most likely to
occur and to affect a large number of cannabis users. The most probable adverse effects include a

dependence syndrome, increased risk of motor vehicle crashes, impaired respiratory function,
cardiovascular disease, and adverse effects of regular use on adolescent psychosocial development
and mental health.

J Addict Med. 2011 Mar;5(1):1-8.

An evidence based review of acute and long-term effects of

cannabis use on executive cognitive functions.
Crean RD, Crane NA, Mason BJ.

Source
Committee on the Neurobiology of Addictive Disorders; The Scripps Research Institute; La Jolla, CA 92037, USA.

Abstract
Cannabis use has been shown to impair cognitive functions on a number of levels-from basic motor
coordination to more complex executive function tasks, such as the ability to plan, organize, solve
problems, make decisions, remember, and control emotions and behavior. These deficits differ in
severity depending on the quantity, recency, age of onset and duration of marijuana use.
Understanding how cannabis use impairs executive function is important. Individuals with cannabisrelated impairment in executive functions have been found to have trouble learning and applying the
skills required for successful recovery, putting them at increased risk for relapse to cannabis use.
Here we review the research on the acute, residual, and long-term effects of cannabis use on
executive functions, and discuss the implications for treatment.

Monaldi Arch Chest Dis. 2005 Jun;63(2):93-100.

Smoked marijuana as a cause of lung injury.

Tashkin DP.

Source
Division of Pulmonaiy & Critical Care Medicine, Department of Medicine, David Geffen School of Medicine, UCLA, Los
Angeles, CA 90095-1690, USA. dtashkin@mednet.ucla.edu

Abstract
In many societies, marijuana is the second most commonly smoked substance after tobacco. While
delta9-tetrahydrocannabinol (THC) is unique to marijuana and nicotine to tobacco, the smoke of
marijuana, like that of tobacco, consists of a toxic mixture of gases and particulates, many of which
are known to be harmful to the lung. Although far fewer marijuana than tobacco cigarettes are
generally smoked on a daily basis, the pulmonary consequences of marijuana smoking may be
magnified by the greater deposition of smoke particulates in the lung due to the differing manner in
which marijuana is smoked. Whereas THC causes modest short-term bronchodilation, regular
marijuana smoking produces a number of long-term pulmonary consequences, including chronic
cough and sputum, histopathologic evidence of widespread airway inflammation and injury and
immunohistochemical evidence of dysregulated growth of respiratory epithelial cells, that may be
precursors to lung cancer. The THC in marijuana could contribute to some of these injurious changes
through its ability to augment oxidative stress, cause mitochondrial dysfunction, and inhibit apoptosis.
On the other hand, physiologic, clinical or epidemiologic evidence that marijuana smoking may lead to
chronic obstructive pulmonary disease or respiratory cancer is limited and inconsistent. Habitual use
of marijuana is also associated with abnormalities in the structure and function of alveolar

macrophages, including impairment in microbial phagocytosis and killing that is associated with
defective production of immunostimulatory cytokines and nitric oxide, thereby potentially predisposing
to pulmonary infection. In view of the growing interest in medicinal marijuana, further epidemiologic
studies are needed to clarify the true risks of regular marijuana smoking on respiratory health.