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* From the Departments of Respiratory Medicine (Drs. Cunnington, Teichtahl, and Hunt) and Pathology (Drs. Dow and Valentine), Western Hospital, Melbourne, Australia.
Correspondence to: David Cunnington, MB,BS, Department of Respiratory Medicine, Western Hospital, Gordon St, Footscray 3011, Australia; e-mail: david.cunnington{at}nwhcn.org.au
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Abstract |
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Key Words: granuloma • marijuana • pulmonary • tobacco
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Introduction |
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As the prevalence of marijuana smoking is not declining, and indeed is rising in adolescents, we believe it is important to highlight the potential hazards of habitual marijuana smoking.
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Case Report |
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For 5 years, the patient had been a heavy marijuana user, smoking 2 to 3 g of marijuana a day via a water pipe. The marijuana she smoked was illicit, and she was unaware of the conditions under which it was grown, or any details about its drying and preparation. In addition, she smoked 5 to 10 tobacco cigarettes per day, and had used IV heroin for a short period 2 years prior to this presentation. There was no history of crack cocaine use.
The patient had cutaneous varicella 6 months prior to presentation. At that time, she had widespread skin lesions but no respiratory or neurologic symptoms. She is a single mother of four children and keeps a dog and a cat, but has never kept birds.
Physical examination was unremarkable, except for a resting tachypnea with a respiratory rate of 24 breaths/min. The patient’s temperature was 36.9°C. Auscultation of the lung fields was normal, and there was no cyanosis or clubbing. Cardiovascular examination was normal, with no evidence of endocarditis. There was no hepatomegaly or signs of chronic liver disease, and no evidence of recent use of illicit IV drugs.
The chest radiograph showed a bilateral lung infiltrate, with diffuse small nodules evenly distributed throughout both lungs. High-resolution CT scanning of the chest confirmed the presence of bilateral diffuse lung nodules, 1 to 4 mm in diameter (Fig 1 ). A full blood examination was normal with no eosinophilia. The erythrocyte sedimentation rate was not elevated, and serum calcium and angiotensin-converting enzyme levels were normal. Antinuclear antibody was present at a titer of 1:160 with a nucleolar pattern; however, double-stranded DNA and antineutrophil cytoplasmic antibodies were negative. She had chronic hepatitis-C infection but normal liver function tests and had not received treatment for this. HIV and hepatitis-B serologies were negative. Mantoux testing (10-U purified protein derivative) and serum aspergillus precipitins were negative. Sputum microscopy and culture for bacteria, acid fast bacilli, fungi and viruses were negative.
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The patient underwent fiberoptic bronchoscopy that revealed generalized tracheobronchitis but no other endobronchial abnormality. BAL fluid contained green-black pigmented material (Fig 2 ) and had a cell count of 85% macrophages, 13% neutrophils, and 2% lymphocytes. Most of the alveolar macrophages were laden with carbon pigment. A transbronchial biopsy could not be performed, as the patient became hypotensive and bronchoscopy had to be abandoned. Subsequently, a video-assisted thoracoscopic biopsy of the right lung was performed. At surgery, the right lung was blackened with miliary white nodules over the entire lung surface. Microscopy of lung sections showed numerous well-circumscribed necrotizing granulomata, which contained histiocytes and scattered multinucleated giant cells (Fig 3 ). There were no acid-fast bacilli, or birefringent foreign materials seen within the granulomata, and no evidence of vasculitis. A single fungal element was seen on one section only within the lung parenchyma (Fig 4 ). Elsewhere there was a florid alveolar exudate of carbon-laden macrophages that appeared to coat the alveolar membrane (Fig 5 ). Culture of lung tissue was negative for bacteria, acid-fast bacilli, fungi, and viruses.
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Discussion |
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Tobacco smoking alone can cause an accumulation of pigmented macrophages in alveolar spaces, as described with respiratory bronchiolitis-associated interstitial lung disease.12 However, marijuana smoking has also been shown to increase respiratory tract inflammation and alveolar macrophages in BAL fluid, an effect that was additive to that of tobacco smoking.13 It is unclear which component of marijuana smoke induces this exudate of alveolar macrophages, but as the macrophages are carbon laden, the increased tar and carbon retention associated with marijuana smoking may be the cause. A similar exudate of alveolar macrophages has been shown in primates exposed to 12 months of daily marijuana smoke inhalation, and in a human postmortem series of heavy marijuana smokers.14 15 In the latter series, all 13 individuals had a dose-related alveolar infiltrate of pigmented macrophages similar to that seen in this case (Fig 5) .15 This exudate of alveolar macrophages contributes to the reduction in single-breath carbon monoxide diffusing capacity seen with chronic marijuana smoking and seen in our patient.16
Blackened BAL fluid has been described principally in association with crack cocaine smoking; however, this patient had no history of crack cocaine use and it is a very uncommon illicit drug in Australia.11 This patient smoked marijuana predominantly via a water pipe that does not filter particulate-phase smoke toxins such as tar from marijuana smoke.17 In addition, smoking marijuana via a water pipe can result in a buildup of carbonaceous residue within the water pipe, similar to that seen with crack smoking. This residue is believed to be responsible for the blackened BAL fluid seen in crack smokers; but water pipes, if used correctly, do not allow inhalation of particulate matter from marijuana smoke.11 18 This makes the cause of the blackened BAL fluid in our patient unclear. However, it is most likely due to a combination of tar and particulate matter inhaled with marijuana smoke, incorrect water pipe use, or use of a homemade water pipe without a consistent water seal.
Tobacco smoking alone has not been associated with granulomatous inflammation in humans. Respiratory bronchiolitis-associated interstitial lung disease is the only interstitial lung disease thought to be directly related to tobacco smoking.12 However, granulomatous inflammation has been shown to occur in primates exposed to marijuana smoke. The granulomata seen in these primates generally had birefringent material or foreign bodies within them.14 In our patient, there were no birefringent materials or foreign bodies within the granulomata, so it is unlikely that talc or starch granules inadvertently injected with IV opioid abuse caused the granulomata.
Although persistent pulmonary granulomata have been described following varicella pneumonia, this is unlikely to have caused the granulomata in this case.19 Our patient did not have symptoms of lung involvement at the time of varicella infection, and the granulomata lacked the fibrous capsule usually seen surrounding the granulomata in post varicella granulomatous lung disease. Necrotizing sarcoid granulomatosis can cause lesions very similar to those seen in our patient. This is unlikely, however, given that the patient had no systemic symptoms of sarcoidosis, normal erythrocyte sedimentation rate and angiotensin-converting enzyme level, and no evidence of vasculitis involving arteries or veins, as would be expected in necrotizing sarcoid granulomatosis.
Infection is a common cause of pulmonary granulomata, and is potentially involved in the pathogenesis of our case. Mycobacterial infection is unlikely, given the negative Mantoux and sputum and lung cultures. Bacteria have been shown to contaminate marijuana, with Gram-negative bacilli being the most common organisms.17 Despite this, pulmonary bacterial infection from marijuana smoking is not a clinical problem, which probably relates to killing of bacteria during combustion of marijuana. Marijuana is often contaminated with fungal spores that are respirable in marijuana smoke from either cigarettes or water pipes. These spores do not appear to be inactivated during the combustion of marijuana and are not filtered from marijuana smoke by water pipes.20 The most common fungi are Aspergillus and Mucor species, but many other fungal species such as Thermoactinomyces, Micropolyspora, Penicillium, and Rhizophus contaminate marijuana.17 Fungi inhaled with marijuana smoke are known to cause disease in immunocompromised individuals. Invasive pulmonary aspergillosis has been described in immunocompromised individuals smoking marijuana.21 In a series of immunocompetent marijuana smokers, 11 of 21 had serum precipitins to aspergillus, compared to 1 of 10 control subjects.20 The clinical significance of this is not clear; however, it is clear that fungi contaminate marijuana and are inhaled with marijuana smoke, leading to potential fungal infection or hypersensitivity to inhaled fungi. In our case, serum precipitins to aspergillus were not detected, and there was only a single fungal element seen in the lung on biopsy. We were unable to culture fungus from lung biopsy specimens, and the patient was not significantly immunocompromised. Although we have been unable to conclusively demonstrate the presence of fungal infection in our patient, we believe fungal infection or hypersensitivity to inhaled fungi are the most likely cause of the necrotizing granulomata seen in our case.
This case highlights some of the pulmonary hazards of chronic marijuana smoking. To our knowledge, this case represents the first reported demonstration of necrotizing granulomata in the setting of heavy marijuana smoking. Even though the exact cause for these remains unclear, it is likely that these granulomata are a result of chronic marijuana smoking and perhaps the inhalation of a contaminant such as a fungus with the marijuana smoke. This etiology should be considered in other patients who are chronic marijuana smokers with radiologic changes of diffuse pulmonary nodules.
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Footnotes |
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Received for publication June 28, 1999. Accepted for publication October 20, 1999.
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This article has been cited by other articles:
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  A. Sakkour, T. Wang, and D. Tashkin A 56-Year-Old Woman With COPD and Multiple Pulmonary Nodules Chest, February 1, 2008; 133(2): 566 - 569. [Full Text] [PDF]
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H. Teichtahl, D. Wang, D. Cunnington, T. Quinnell, H. Tran, I. Kronborg, and O. H. Drummer Ventilatory Responses to Hypoxia and Hypercapnia in Stable Methadone Maintenance Treatment Patients Chest, September 1, 2005; 128(3): 1339 - 1347. [Abstract] [Full Text] [PDF]
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