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Pseudmonas aeruginosa in tobacco

Question
In the health section of a large German newspaper there has been a citation last week from the university of Kentucky, in which PsA has been detected beneath many other germs in tobacco. It has been mentioned, that it is supected, that PsA can survive the process of smoking and therefore be inhaled from the smoker and also the non-smoker.
How do you judge the danger, which arises for CF patients in this context from passive smoking? Are there probably observations about a decreasing number of new infections due to the gouvernmental ban of smoking?
Answer
Hello,
the in the question mentioned study by Sapkota, Berger and Vogel (Environmental Health Perspectives, 2009) has shown, that cigarette tobacco can be "loaded" with a number of bacteria. Among those bacteria there were germs, which can cause infections in human beings, as e.g. P. aeruginosa (detected in over 90% of the samples). The authors conclude from this data, that via active and passive smoking it could come to a transfer of bacteria and as a consequence to an infection of the airways.
Restrictively it has to be said, that exactly those questions have not been investigated directly in the study and therefore can not be proven. In the investigated tobacco, the genetic substance of the bacteria has been detected (DNA). This method can not distinguish between alive and dead bacteria. This very important question, if the identified bacteria are capable to live, to multiply and therefore be infectious, remains unanswered.
How many bacteria are in the tobacco, which sorts predominate quantitatively, to which extent the bacteria survive the burning process during smoking and if those are then transported to the lungs while smoking or passively smoking, in order to cause an infection, is unclear. Only with additional investigations, e.g. of the smoke of the cigarette, the risk of infection of smoking can be judged reliably.
Estimation of the risk: How and when the bacteria come into the tobacco, can not be answered clearly. The found bacteria are present however in the environment and can not unexpectedly be found already on the tobacco plants. The number of bacteria pro gram of tobacco is hereby with 0 (more often) - 10000 (more seldom) very variable. In general, the charge of the tobacco plants decreases again distinctly during the process of drying of the plants (Larsson 2008). P. aeruginosa is an environmental resp. a humid-germ, which is found widely spread in the earth, in water and on plants, which explains the finding of P. aeruginosa DNA in tobacco sufficiently. However, in cigarette-filters bacteria capable of multiplying (Bacillus spp.) have been found, which shows only, that at least those especially resistant bactiera (capable of making spores) can survive the process of burning. These results however are not transferable to other germs, like P. aeruginosa. Especially P. aeruginosa is particularly sensitive against drying-out, so that a marked load of tobacco with this germ is not to be expected. Under the many possible and quite more charged sources of infection (humid areas), it seems to be rather improbable, that tobacco smoke plays a central role at the transfer to CF-patients. According to the latest knowledge, it can not totally be excluded. The detection of P. aeruginosa DNA in the tobacco does however not allow any conclusion about the real risk of infection, which can be judged especially with the passive smoke as very improbable.
Smoking is without doubt a health risk. Hereby the harmful effect of the 4000 different substances which are present in the tobacco smoke are predominant. Smoking can furthermore support the colonization of the airways with bacteria, as smoking inhibits the function of the cilia in the airways and inhaled particles like bateria are cleared less sufficiently. Persons with diseases of the lung should therefore avoid an exposition to tobacco smoke. Furthermore there are a number of hints that passive smoking, which is not always avoidable, represents a health risk, however to a much lesser extent (biomarkers of a smoke exposition like nicotin or cotinin in hairs or urine are at passive-smokers reduced about the factor 10 (hairs) resp. 100-1000 (urine)). Even with a risk of infection via inhalation of smoke which can not completely be ruled out, this should be even much less via passive smoking.
At the moment there are therefore no concrete hints which can be proven scientifically that when smoking, P. aeruginosa is transmitted with the inhaled tobacco smoke into the airways reps. that this represents a risk of infection. This is especially true for passive smoking. Due to insufficient available data this can not be excluded totally. Persons with a prexsisting lung disease should be discouraged from smoking independently of this.

Final comment: in the media reports about the study the detction of an extremely infectious anthrax germ has been emphasized among others. In Germany there is not a singel infection with lung anthrx while there is a consumption of about 140 billions cigarettes/year.

Yours sincerely,
Dr. M. Hogardt

28.01.2010