The following post first appeared in my January 30, 2012 blog post
When I started growing tomatoes for sale, many years ago, I read quite a bit about tomato diseases. While there are many diseases of tomatoes, the Tobacco Mosaic Virus Disease stood out in my mind because many experts mentioned that TMV (Tobacco Mosaic Virus), which is found in ALL tobacco products, can devastate tomato plants (and some other plants such as peppers and eggplants) and is especially damaging to young plants grown in greenhouses. The potential for serious problems is so great that growers are cautioned to not let visitors enter their greenhouse if they smoked cigarettes, pipes or cigars recently. This knowledge is what set my mind thinking…
Is the Common TMV (Tobacco Mosaic Virus) a Possible Agent that is Responsible for Some Lung, Oral and Throat Cancers?
The TMV virus, which infects many tobacco plants, resists tobacco manufacturing processes to such a degree that most commercial growers will not allow those who have recently used tobacco products to enter their greenhouse if plants from the nightshade family (e.g. tomatoes and peppers) are growing. Many growers also do not allow tobacco use in their tomato, potato, pepper and eggplant fields. These growers know that the TMV from tobacco will devestate their crops. While plant viruses, such as TMV, aren’t believed to be able to replicate in human cells, Didier Raoult of the University of the Mediterranean in Marseilles, France, believes he had found evidence in 2010 that the PMMV (Pepper Mild Mottle Virus) can cause fever, aches and itching in humans. Raoult doesn’t claim he discovered direct infection of human cells by the virus, but viral RNA (ribonucleic acid) accidental interfering with the human RNA. The possibility of TMV being involved in the etiology of lung cancer has been discussed as long ago as 1960 when P.W. Bothwell (M.D. D.P.H. Univ. of Birmingham, England ) speculated in The Lancet that perhaps the combustion processes of tobacco burning might provide the media for modifying the TMV so that it could upset the normal RNA/protein mechanism in lung cells. While this is an interesting hypothesis, it doesn’t seem to fit the likely scenario since it has been found that smokeless tobacco use, especially snuff dipping, is also associated with above normal oral cancer rates. Alternatively, some may argue against TMV being involved in the etiology of smoking tobacco since, they argue, the high temperatures would destroy the viruses. This is probably true. However, the smoke that is drawn through the non-burning part of the tobacco could easily dislodge the viral particles from the tobacco and carry it to the user. In other words, the problem could be the non-burning part of the tobacco and not directly by the burning tobacco.
Research has indicated that Benzo[a]pyrene is a carcinogen and is found in tobacco smoke. Benzo[a]pyrene is also found in many foods such as overdone charcoal broiled steak and burnt toast. Benzo[a]pyrene, found in tobacco smoke (including cigarette smoke), was shown to cause genetic damage in lung cells that was identical to the damage observed in the DNA of most malignant lung tumors. Since DNA damage is believed to be the underlying cause of mutations leading to cancer, it follows that it is thought that benzo[a]pyrene, may be an important etiologic agent of lung cancer. Nonetheless, the high oral cancer rate (especially cheek and gum cancers) among snuff dippers, compared to nontobacco users, implies that tobacco itself, and not just tobacco smoke, is a carcinogen. The chemical family of nitrosomenes occurs in both tobacco smoke and tobacco itself. In 1956, two British scientists, John Barnes and Peter Magee, reported that dimethylnitrosamine produced liver tumours in rats. Research was undertaken and approximately 90% of nitrosamine compounds were deemed to be carcinogenic. The problem is that nitrosomenes are found in many foods and other consumables that are consumed by both tobacco and nontobacco users. It seems logical to assume there is something unique to tobacco that is the cause of enormously high (some data suggests a 50 fold increase!) cheek and gum cancer rates in those people who are long term snuff dippers. While some data suggests that nitrosamines may be responsible for this increase — the Swedish usually use a pasteurizing technique, (instead of heat treating it) of curing the tobacco for snuff use (they call it snus) which results in lower nitrosamines and apparently lower cancer rate. However, it is just possible that this unique curing technique also results in damaging or even destroying the tobacco’s TMV. The traditional heat treatment of curing tobacco does not destroy the TMV since this method uses a maximum temperature of 72C and it is known that TMV can survive at a temperature as high as 79C. While nitrosamines, like TMV, do contact the cells of both smokers and nonsmokers, Health New Zealand concluded, in their study, that carcinogens and toxicants were present only below harmful levels in “smokeless” tobacco products. This data seems to point to an unknown etiologic agent that is responsible for most tobacco related cancers. Logically, this points to the need for serious studies to determine if TMV could be this unknown etiologic agent. If it is, the risk associated with the use of tobacco products could be reduced by the removal of or destruction of the TMV before use.
I am not implying here with this discussion that TMV can replicate itself in a human cell or that it is infectious in a manner similar to the influenza virus. In a way it might be appropriate to think of TMV as an environmental, natural occurring chemical that when in sufficient concentrations can damage human cell’s DNA. Also possible is that the TMV can affect negatively the cell’s DNA repair enzymes.
One test of this theory is to eliminate the TMV by heating the tobacco to temperatures in excess of 81C. Sterilization via irradiation is another option. The TMV eliminated tobacco can then be available for research trials. Before this is done, however, the Swedish Snus should be tested for active TMV. If there is a reduction in TMV levels this would seem to indicate an increase in probability that TMV is an important etiological agent for cancer and it would be fitting and proper to go ahead with the appropriate trials.