What are the Pulmonary Effects of Smoking Marijuana?

Current studies show that marijuana smoking is also associated with pulmonary fibrosis and lung bullae. As stated by Phan et al (2005), a case of twenty six years old Caucasian man presented with a history of exertional dyspnoea and dry cough for eight months had been smoking 10 cigarettes per day for 2 years and 10 pipes of marijuana per day for five years. The case report also indicated that the twenty six year old had no history of animal or occupational exposure, medications use or i.v. drugs use (Phan et al, 2005). The examination of this patient showed bilaterally reduced breath sounds that is an evidence of hyper-inflated lungs. This study also revealed that there was no cyanosis or clubbing and was a febrile. A radiograph examination of the patients’ chest also showed that there are widespread of opacities throughout the lungs. This case shows that marijuana smoking results into cystic changes which were particularly large in the lower zones in both lungs. There were extensive interstitial opacities throughout the lungs which included the upper mid and lower zones.

The case presented above shows that marijuana can result into extensive damage onto lungs and the lower parts of the pulmonary system. As stated by Winger et al (2004), smoking marijuana often lead to a number of deformities; radiology, histology and lung function which all are related to heavy marijuana smoking. The combination of advanced pulmonary fibrosis, combination of lung bullae and heavy pigmented macrophage infiltration is unique (Phan et al, 2005). This study reveals the adverse effects of marijuana not only to the lungs but also to the other parts of the respiratory tract system. The destruction of marijuana by toxic chemicals resulting from marijuana is evident among both regular and long to short term smokers of marijuana.

Milroy & Parai (2011) conducted an autopsy study which involved up to 13 marijuana smokers who suddenly died from accidental causes. This study revealed that the pigmented macrophages from marijuana infiltrated into the alveoli and interstitial of the lungs which is related to pulmonary fibrosis, emphysema and eventually chronic obstructive pulmonary disease (COPD) (ElSohly, 2007). The dose of marijuana also played a vital role in adverse effects that result into patients suffering COPD (Milroy & Parai, 2011). According to ElSohly (2007), the intensity of the infiltration of macrophages was closely related to the doses of marijuana smoked by the affected patients. This is because pigmented macrophages exhibit pulmonary toxicity hence causes tissue fibrosis. Other researchers have also confirmed these findings with very little variations with respect to lung damage. Milroy & Parai (2011) also reported six cases of young men who were significantly exposed to marijuana having lung bullae than those who were exposed to tobacco. In this respect, new findings are linking marijuana to not only severe cases of damage to the lower respiratory tract systems, but also to the pulmonary system (Onaivi, 2006). 

Emerging research reveal that smoking of marijuana is also linked to incidences of tuberculosis.  Thu et al (2013) reported three cases of cavitating disease which were associated with common illicit smoking of marijuana using makeshifts and bong. As stated in this study the total number of positives contacts were 34 and out of 34 cases and among those sharing bong with an index case was associated with a six fold risk of transmission. As stated by, when tuberculosis is detected among young people in Australia, marijuana is most likely to be a possible risk factor. Even though this report is observational, it gives devastating effects of marijuana that includes predisposing individuals to other infectious diseases. While tuberculosis is caused by a strain of bacteria known as mycobacterium tuberculosis, it is important to note that the smoke of marijuana affects the body immunity system thus predisposes the body to other opportunistic infections (Rosenow & Camus, 2008).

Several studies involving in vivo and in vitro research in both human and animal experiments, the smoke of marijuana compromises the natural defense mechanisms as well as the immunity of the body (Bedi et al, 2013). As stated by Onaivi (2006), smoking marijuana affects the tracheobronchial epithelial function thus interferes with clearance of mucus from the trachea. The smokers of marijuana also have their alveolar macrophages’ capacity to phagocytose Staphylococcus aureus compromised hence they produce reduced amounts of tumoour necrosis factor alpha, granulocyte-macrophage colony-stimulating factor and interleukin-6 (Bedi et al, 2013). It is these deficiencies that that could be predicted to improve the susceptibility to mycobacterial infection. This studies show that effects of marijuana is not only limited to the effects of the smoke itself, but the chemicals could interfere with body defense mechanism thus predisposes individuals to other infectious diseases of the pulmonary system.

The pulmonary consequences of smoking marijuana and tobacco were compared by Gilbert et al (2013) by characterising the relative pressure of insoluble particles and carbon monoxide from smoke to the lungs of the same amounts of tobacco and marijuana. Before and after smoking, 15 men who had habitually smoked cigarettes and weed for more than five years were checked for carboxyhemoglobin levels in their blood. Tobacco and marijuana were inhaled and stored inside the respiratory tract. This research showed that consuming pot, unlike cigarettes, was correlated with up to a fivefold rise in the volume of carboxyhemoglobin in the blood. The findings of this analysis have showed that the volume of tar inhaled and stored inside the respiratory tract has risen threefold. There are major variations in the smoking of marijuana in this respect.

The impact of marijuana on airway epithelium inflammation and atypia, followed by signs of recurrent bronchitis, were examined by Sarafian et al (2006). In this report, the researchers hypothesised that the primary ingredient and psychoactive portion of marijuana, Delta 9-tetrahydrocannabinol (THC), is likely to result in the above findings by impairing mitochondrium activity and impairing cellular capacity. By analysing the particulate samples of smoke from cigarette smoke from tobacco and alcohol as well as placebo marijuana cigarettes, the researchers checked this theory for the impact on the mitochondrial structure of the in vitro A549 cells. The implications of this research show that only weed extracts have killed the mitochondrion. This indicates that pot smoking has an overall impact on the energy of airway epithelial cells, and is likely to have detrimental pulmonary effects (Sarafian et al, 2006). This shows that smoking marijuana can contribute to pulmonary failure and is a health danger to the pulmonary system.