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[*] Chaouachi K. False positive result in study on hookah smoking and cancer in Kashmir: measuring risk of
poor hygiene is not the same as measuring risk of inhaling water filtered tobacco smoke all over the world.
Br J Cancer. 2013 Apr 2;108(6):1389-90. doi: 10.1038/bjc.2013.98. Epub 2013 Mar 7.
http://www.nature.com/bjc/journal/vaop/ncurrent/full/bjc201398a.html
http://www.ncbi.nlm.nih.gov/pubmed/23470468
All users of the fashionable hookah across the world, except in rare cases, do change the water of the pipe
basin after each smoking session (or get it changed). This is a well-established fact as the following note a
physician in Nepal early wrote in the British Medical Journal shows: “water is changed each time smoking is
carried out” (Pande, 1962). As for the cancer risk, there is actually an extensive literature suggesting a null
or weaker association than the one usually measured when it comes to tobacco use in general (Chaouachi &
Sajid, 2010). Among others, let us cite an early study published in this very journal (Rakower & Fatal, 1962),
another one in India (Sanghvi,1981) and the most recent one in Punjab, Pakistan (Sajid et al, 2008).
Interestingly, the latter, which was carried out on the other side of the national border, actually represents
the same geographical, human and cultural environment as Kashmir in which the Dar et al study was
conducted (2012).
However, Dar et al.’s paper offers a false-positive result regarding hookah smoking. It is based on a serious
misinterpretation which could have easily been avoided if the authors had paid more attention to a recent
lung cancer study in the very same region, Kashmir, and a subsequent important clarification published by
its senior author (Koul et al, 2011; Koul & Chaouachi, 2011). None of the Kashmiri participants changed the
water after each session. A rarely-cited 84-page WHO Egyptian report on shisha smoking was quoted,
highlighting the filtering effect of water (Koul & Chaouachi, 2011). Amazingly, in a recent relevant review,
Maziak (2012) cites that very study in Kashmir while ignoring the above important clarification by Koul &
Chaouachi. Furthermore, because the setup (e.g., smoking mixture not described by Dar et al (2012)),
smoke chemistry and smoking behaviour of a Kashmiri hookah are completely different from those of the
fashionable shisha used these days in Washington or London, both Dar et al and Maziak in his biased review
extrapolate false-positive findings to the whole world. Such a wide confusion is also fuelled by the
widespread nominalist use of the ««waterpipe»» neologism since all water pipes of the world have almost
nothing in common but that name imposed one decade ago (Chaouachi & Sajid, 2010).
Yet, the water “detail” already led astray Maziak in a previous review when warning against aspergillosis. In
fact, the cited study (Szyper-Kravitz et al, 2001) showed that the patient had not changed the water of his
hookah for weeks. In sum, measuring a risk due to the blatant lack of primary hygiene (water, but also
suction hose) is one thing and measuring the real “corrected” risk (that of inhaling hookah smoke) is
something else. Similarly, the study on ESCC, opium and tobacco use in Iran cited by Dar et al, and on which
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we already commented (Chaouachi, 2009), may have simply measured the same lack of hygiene (water,
hose).
Another source of confusion in Dar et al.’s study appears when its authors state that "hookah smokers seem
to be exposed to [as] many toxic compounds as cigarette smokers”, citing exclusively for this purpose
studies by the US-American University of Beirut (US-AUB). First, the Kashmiri hookah is not the growingly
popular shisha targeted by antismoking research (different smoking product, chemistry, puffing, etc.). Then,
the cited experiments rely on machine smoking, not on human subjects. Cigarette smoking machines (used
for about 5 minutes at a pace of 1 puff/min. on average) have been widely criticised over the past half
century (including by the WHO) for greatly distorting the reality of actual human cigarette smoking. Quite
astoundingly, their use for hookah smoking “simulation” (about 60 minutes of puffs arbitrarily and
periodically drawn every 17s) has been virtually imposed to research for almost one decade now. Here, the
first unavoidable question is: where does the demonstrated relevance of the latter machine lie if the former
one (for much shorter periods) has failed?
Furthermore, the setup (cramming of the smoking mixture inside the bowl, its systematic charring with a
piece of charcoal kept in place over the same point for one full hour, etc.) represents at best a model about
how not to smoke a hookah (Chaouachi & Sajid, 2010).
Admitting (absurd hypothesis) that such a “protocol” were realistic, why did a German team find acrolein at
levels 66 times lower (6 times lower for formaldehyde and acetaldehyde) and benzo[a]pyrene 20 times
lower than in the studies by the US-AUB cited by Dar et al and Maziak? Yet, both used a shisha smoking
machine with similar parameters (notably, inter-puff time). The German scientists said they have “fully
validated [their] approach” (Schubert et al, 2011b, 2012). In these conditions, is it scientifically acceptable
to hype this way the hazards of hookah smoking on a global scale?
The assessment of related biomarkers supports the need for questioning such methods as studies in the
USA, Germany and Pakistan show (Jacob et al, 2011; Schubert et al 2011a, 2012; Sajid et al, 2008). Biological
levels of blood nicotine and urine cotinine of shisha (with Moassel) users are generally similar to those
found in cigarette smokers after having smoked 1 single (2 at the most) cigarette(s), which obviously does
not mean that a hookah session is equivalent to smoking 20 cigarettes or more.
As for nitrosamines, polycyclic aromatic hydrocarbons, primary aromatic amines, carbonyls, etc., their
metabolites are generally found in very much lower quantities in shisha users than among cigarette smokers
(Schubert et al, 2011a, 2011b, 2012; Jacob et al, 2011). The German group even found no difference in
urinary NNAL between shisha smokers and non-smokers (Schubert et al, 2011b). As for urinary
concentrations of PAH metabolites, they were much less important in shisha smokers than in cigarette
smokers by factors ranging from about 1.5 to 5 (Jacob et al, 2011). From there, statements asserting “the
similarity of biological consequences of waterpipe and cigarette smoking” (Dar et al, 2012) are groundless.
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Finally, “systematic reviews” and “meta-analyses” have fallen prey to the same errors discussed above. Dar
et al cite one of them but ignore a methodological critique of such biased literature and the global
confusion it has contributed to fuel in this field of research (Chaouachi, 2011).
References
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Chaouachi K (2009). Hookah, opium and tobacco smoking in relation to oesophageal squamous cell
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mainstream waterpipe smoke using liquid chromatography-electrospray ionization tandem mass
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Does this environmental matrix reveal as significant source of toxic compounds? Toxicol Lett. 205:279-84.
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Competing interests: I have no competing interests. I have never received direct or indirect funding, either
from pharmaceutical companies or the tobacco industry.