In this exclusive HIGH TIMES interview, Dr. Donald Tashkin, the UCLA lung specialist behind one of the most comprehensive cannabis/lung cancer studies in history, explains how his research has failed to link marijuana use to lung cancer.

HIGH TIMES: Can you give me a brief overview of your research over the last thirty years regarding cannabis use versus lung health?

Donald Tashkin: Let me take a stab at it, because I think it is important. We recruited heavy habitual smokers of marijuana, by which we meant smokers of at least one joint per day for on the average the last ten to fifteen years. The average marijuana use by the subjects that we recruited into our study to look at the impact of marijuana on lung health was about three joints a day for around fifteen years, so these were what we would consider heavy habitual smokers of marijuana. We also recruited non-marijuana smokers as controls and we also adjusted for tobacco. So about half of the marijuana smokers smoked tobacco and the other half didn’t, and we also recruited tobacco only smokers as tobacco controls. We asked the subjects to undergo a variety of procedures, including an extensive interview with regard to respiratory symptoms to other aspects of their health and also their use of tobacco, marijuana, and other substances. We performed a battery of lung function tests; we had not only additionally but longitudinally over time looked at the progression of any abnormalities that might be detected. We subjected some of the subjects to bronchoscope so that we could biopsy cells lining the airway to determine if smoking marijuana was associated with evidence of airway injury. We rinsed out the cells from their lungs to see whether or not marijuana smoking had any impact on the inflammatory cells in the lung that are responsible for defending the lung against infection and other insults. Our findings were quite interesting. We found that smoking marijuana regularly was associated with an increased frequency of cough and sputum on most days. So these marijuana smokers often had chronic bronchitis, about twenty percent of them, compared to about twenty-five percent of tobacco only smokers. They also had an increased frequency of acute chest cold, defined as an increase in cough and sputum that lasts a certain number of days. They also reported more wheezing than non-marijuana smokers. So there’s definitely some impact on respiratory symptoms. When we biopsied the airways, the tissue lining, widespread evidence of injury. Very similar to the damage that we saw in tobacco smokers. I don’t want to use technical terms, but the cells that normally line the airways have a certain shape and they have cilia. The purpose of the cilia is to move mucus up from the lung into the mouth in order to cleanse the lung of mucus it’s produced and we found that the cilia cells were often lost and replaced by non-cilia cells, or sometimes the cells will form patterns that we call ‘squeamish,’ it looks like skin. These are changes in the appearance of the nuclei. These are changes that have been found to be precancerous. They are changes that in tobacco smokers preceded the subsequent development of lung cancer.

HT: Isn’t the term precancerous used for any inflammation or abrasion in or on the body that is not cancerous? Have any of these changes in the cilia gone on to be proven negative for marijuana only smokers?

DT: Yeah, that’s a good point, and they are precancerous in a sense that those who go on to develop lung cancer exhibit these changes, but we don’t know, any particular individual who exhibits these changes may be at increased risk, but will not go on to develop cancer. So the assumption is that the presence of these symptoms represents an increased risk, but doesn’t necessarily mean that an individual exhibiting these changes will go on to develop cancer.

HT: Were individuals selected based on their susceptibility to developing cancer?

DT: No. They were not selected.

HT: Not by age or anything?

DT: They were young, so we didn’t follow them along enough to observe subsequent risk of developing cancer. Even if we did, the sample was too small to assess the risk of cancer. So that really wasn’t our intent, our intent was to describe what changes are proven and then to relate those changes to risks that have been associated with those changes in other studies, not in our study.

HT: But you did show that marijuana smoking had no positive association with cancer…

DT: That’s getting ahead of the game. That’s a recent study. What you really need is an epidemiological study in order to test that hypothesis, and that’s a real world study. We carried out such a study involving roughly 600 lung cancer cases in Los Angeles County over the period of a few years. Also about 600 cases of head and neck cancer cases and about 1,040 controls that were matched to the cases, and we used classical case control experimental design, epidemiologic design, so that both the cases and controls were interviewed face to face and administered a detailed questionnaire on their history of tobacco, marijuana, and other drug use in their life-time, other factors that might be related to cancer such as a family history, diet, occupational exposures, socioeconomic status, etc. We simply used a common statistical tool known as logistic regression analysis controlling for all the known or imputed risk factors that we had information on and failed to find any positive association between marijuana use and either lung cancer or head and neck cancer; that was the bottom line.

HT: And you were surprised by these results?

DT: Yes, we were.

HT: Did you have any personal interest or experiences that led you to this field of research?

DT: No, not at all. My involvement in this type of research was purely coincidental. A psychiatrist who was interested in marijuana and particularly its effects on behavior had a large grant, and he asked me to look at the effects on the lungs because he assumed that smoking any substance might harm the lung and that’s how I got started.

HT: As more studies come out on cannabinoids and cannabinoid receptors and how their stimulation is beneficial for a variety of illnesses including wasting syndrome, do you at all feel like a pioneer in finding these positive results?

DT: I wouldn’t consider these positive results. I would consider these to be neutral results; we failed to find a positive association, so I don’t think that’s a positive result. You could consider it to be a negative result, but you know you can never prove the negative; you can only fail to prove the positive. I don’t consider this to be a definitive study; there are a lot of limitations in this study. One is that there was a higher rate of refusal among the cases, so there could have been a selection bias. And the other is that the recall of marijuana use could have been erroneous. The patients may have reported that they used more than they really did or less than they really did and that over and under reporting could have differed between different cases and controls and that could have affected the results. So it’s not a conclusive study, but it is, I think, an important study because the fact that it was designed as well as we could to minimize the biases and we failed to find a positive association.

HT: And what was and is your interaction with the Federal Government?

DT: This study was supported by the National Institute of Health and the National Institute on Drug Abuse, as have all my studies over the past thirty years.

HT: Has there ever been any pressure for the results to lean a certain way?

DT: Absolutely not.

HT: Have you considered the severe lack of anecdotal evidence of a cancer link given the millions of marijuana smokers in America not getting lung cancer?

DT: Well, I think that people who have smoked marijuana a lot and are worried about cancer development might or probably will feel some relief that there is some evidence not supporting that link but I still feel that the heavy smoker might be at risk. The fact that we didn’t find, or failed to find an association doesn’t mean there isn’t one. I would be concerned if I smoked a lot of marijuana about this possibility and also it does have other effects on the lung as demonstrated by the bronchoscope. It does injure the lung and injure the ability of the cells to protect the lung against infection. I didn’t mention that it also depresses the activity of the major inflammatory cell in the lung which is called the alveolar macrophage; it interferes with the ability of the inflammatory cells to fight bacteria. Which might increase susceptibility of the lung to pneumonia, particularly if you have an underlying immunosuppressive disorder such as AIDS or cancer treated with chemotherapy which is often immunosuppressive, so there could be negative health impacts, particularly individuals who might use marijuana medicinally.

HT: So, as a doctor, you believe that the possibility of infection outweighs the benefits of appetite stimulation, pain suppression, and the reduction of insomnia?

DT: I’m not saying that. The risk/benefit has to be assessed in any given individual. If there is more potential benefit than risk in an individual and nothing else works, then I think it’s reasonable to use a risky drug. But if you have a trivial problem for which the benefit is uncertain, then I think that the risk may outweigh the benefit.

HT: Were you aware at the initial time of the studies of the research conducted previously by Vera Ruben with the Rastafarians in Jamaica?

DT: Yes, I am. That’s a really old study, three decades at least. Yes, I am familiar with that study and in those studies very little negative outcomes were actually found, and these were among individuals in Jamaica, I believe, who smoke a lot of marijuana, but those studies were really not carefully done and I’m concerned about selection bias and the compounding affect of tobacco, which was not even a consideration in the Ruben studies.

HT: In 1981 Jack Herer met with you and said that marijuana would have no ill affect on the lungs and maintained that smoking would even help you to live longer. Did this meeting and the subsequent meetings with Herer affect or inspire your research?

DT: No, Jack is a really nice fellow and I appreciate his participation in our studies. My personal interaction had no affect on my interpretations or findings. I have always tried to keep an open mind about the data. We have some expectation of the result going one way or the other, but we have no preconceptions and my interpretations are not slanted by my preconceptions.

HT: Have you been contacted by “big tobacco” regarding your study results?

DT: No.

HT: Not at all?

DT: No. I have not been contacted by any representative of the tobacco industry recently. I was involved as an expert witness in a case a few years ago that had a marijuana relationship, but that far preceded the presentation of the results of the study.

HT: How do you plan to expand your research?

DT: We are looking at, we did collect smears from the cheeks, what we call ‘buckle smears’ of nearly all our cases and controls, and we’re looking at markers for genetic susceptibility to cancer and we’re going to stratify our results based upon those susceptibilities. We’re also looking at the possibility that exposure to marijuana or tobacco might lead to some alteration, some genetic abnormalities. We can asses these by examining the material that we have gained from our cases and controls.

HT: So you are continuing cannabis research?

DT: Yes. We’re looking at a lot of things. We’re mainly interested right now on the effects of marijuana on the immune system. It is a very powerful immune modulator and that’s the major direction of our research right now. Whether or not it affects, for example, the ability to milk a response to a vaccination, let’s say a vaccination against Hepatitis B or Hepatitis C.

HT: Has your research changed your view on marijuana prohibition over the years?

DT: Well, I still maintain that, in terms of safety and health effects, I believe that smoking any substance is not good for your health, but there could be in certain desperate situations where no other remedy is available, there might be an indication, on a case by case basis, for smoking a substance that may have more benefit than harm.

HT: Aside from smoking, how do you see marijuana as a “risky” medicine?

DT: Outside of the smoking factor? I’m not an expert in that area. I think you need to talk to a behavioral psychologist or someone interested in the effects on cognition. This is an area I really have no expertise in and I prefer not to comment on it.