NOT PEER REVIEWED This paper, although the authors may well have found evidence in line with their intent, could also open our eyes to another distinct and obvious perspective. One which may well be glossed over, in our determination to find the target perspective many seek. What if a smoke free environment could substantially increase population mortality and morbidity health risks? Is it too late to rethink our position, or to mitigate that risk? The idea is most often met with immediate dismissal. However there is indeed biological plausibility and physical routes by which the argument could be made and made quite convincingly.

The sediment studied in this paper adds significantly to that argument, by the measures of physical evidence which were found, although viral matter or sub micron toxic particulate from ambient air sources was not thoroughly investigated. It is a perspective we have been neglecting by lack of investigation. When people congregate, if one in the room carries a contagious disease and he coughs or sneezes, emitting into the room a virus that would then be inhaled by others within the room, the virus spreads infecting others exponentially. Cigarette smoke acts by its physical properties as a sticky mask that hangs in the air, collecting sub micron particulate and biological toxins. Which even if inhaled could be rendered to the larger extent, ineffective in promoting harms.

Fine particulate cigarette smoke is sticky in nature, in the 2-3 micron range with a capacity to collect large amounts of sub micron particles, with unique velocities and trajectories swirling around within that space. Considering the increased mass by combining the virus or sub micron particulate with tobacco smoke; viral and ultra fine particulate matter in the majority is either excavated from the room by increased ventilation potentials or earned filtering potentials. Within systems which otherwise would have no effect, or even a contributing effect to the toxic particle volumes contained in that space. Traditionally ventilation rates have been increased to limit the tobacco smoke odors and are in turn decreased when it is less pervasive or not noticeable. The viral or sub micron particulate is either evacuated more efficiently in a smoking allowed environment, or is attached firmly to any solid object in the room, as demonstrated by the authors herein. As the study indicates that adhesion will last for months after smoking has ceased which is well beyond the lifespan of the hardiest of viruses.

Thus we see a large degree of mitigation, of both harm and risk. With smoke in the room the chances are much less that someone in that room will become infected by contagions, or poisoned by the most dangerous of non ETS ambient air contaminants, compared to the substantial increased risk without the smoke. The same arguments could be made in relation to any sub micron particulate, with a large array of carcinogens and toxins found in ambient air which have no proper risk assessment to date, which will only increase the potential for adverse effects. The limited evidence of increased risk by Environmental Tobacco Smoke [ETS] is based primarily in "lifetime exposure" estimates. Most within the precautionary principle of assessment, or "worst case", with few of the immediate variety of health risks, demonstrating any substantial or significant numeric effect, which could be remotely comparable to a larger effect by pollen or Diesel exhaust, which are for the most part unavoidable.

According to the American CDC; the common Flu alone kills more than 35,000 annually within the American population, a risk that is immediate and sees its effect within hours or a few days. Can we simply dismiss that immediate risk as implausible? Were the numeric value increased, by what ever means, the mortality impact among the millions at risk would be substantial. The actual population risks understandably carry a potential to provide a much more devastating risk than anything surmised by the most aggressive estimate of mortality and morbidity, which could possibly be caused by tobacco smoke or its sediments.

Unintended consequence is an argument in need of discussion and investigation, evolved by the warning; "be careful what you wish for, because you just might get it".

Conflict of Interest:

None declared

Matt et al's demonstration that nicotine can be detected in house dust, on surfaces and on fingers in homes formerly occupied by smokers[1] is used as a springboard to promote concern about third hand smoke(THS)[2]. Given the rudimentary nature of most domestic cleaning and the common experience of the distinctive smell of stale tobacco smoke, few will find it surprising that traces of nicotine can be found in smokers' homes long after they have vacated them.

While Schick notes several times that the health consequences of this level of exposure are unknown, the title of her editorial says that THS is "here to stay"[2], presumably an intended pun suggesting that concerns about the health implications of THS are now established. Schick notes that nicotine "and all the other things that go along with it" can pollute houses. But the soup of gases, fine and ultra-fine particles in tobacco smoke that include irritants, toxins and carcinogens has much in common with smoke emitted as pyrolisis products from the combustion of other organic matter: when you breath wood smoke[3], cooking smoke[4] or petroleum smoke[5], you are exposed to many of the very same irritants and carcinogens that are also in tobacco smoke.

So why did Matt et al consider only nicotine? There is not a house anywhere that is not finely carpeted with many of the very same pyrolysis compounds "that go along with" nicotine but which originate from everyday activities like heating, cooking, candles, electrical appliances, and leaving windows and doors open to allow household exposure to motor transport fumes. Had they done so, equally "alarming" information about all our houses would have emerged to give their findings some important perspective.

The evidence base that has supported indoor smoking restrictions is concentrated around fine particle (PM2.5) concentrations emitted in unhealthy abundance by smoking[6] and on the evidence of harm from particularly chronic exposure to those particles and what they contain. While nicotine is often used as a marker for secondhand smoke exposure and not benign[7], nicotine is far from being the chief health concern.

Ott and Seigmann[8] and Wallace and Ott[9] provide data on fine and ultra-fine particle emissions from different sources: "Controlled experiments with 10 cigarettes averaged 0.15 ng mm-2 ... ambient wood smoke averaged 0.29 ng mm-2 or about twice those of cigarettes and cigars ... In-vehicle exposures measured on 43 and 50 min drives on a California arterial highway gave PC/DC ratios of 0.42 and 0.58 ng mm-2 ... Interstate highways had PC/DC ratios of approximately 0.5 ng mm-2 with ratios above 1 ng mm-2 when driving behind diesel trucks. These PC/DC ratios were higher than the ''signature'' value of the cigarette (0.11-0.19 ngmm-2)measured in a large Indian gaming casino with smoking." [8]

Tobacco smoke also contains ultra-fine particles. Other sources of ultra-fine particles (UFPs) include "laser printers, fax machines, photocopiers, the peeling of citrus fruits, cooking, penetration of contaminated outdoor air, chimney cracks and vacuum cleaners."[8] Wallace and Ott's data on concentrations of UFPs in restaurants and cars found "cooking on gas or electric stoves and electric toaster ovens was a major source of UFP, with peak personal exposures often exceeding 100,000 particles/cm3 .... Other common sources of high UFP exposures [in restaurants] were cigarettes, a vented gas clothes dryer, an air popcorn popper, candles, an electric mixer, a toaster, a hair dryer, a curling iron, and a steam iron."[9]

It is important that research documents residuals from tobacco smoke. But it is equally important that consumers and policy makers are not led to believe that the chemical compounds thus located are somehow unique to tobacco smoke. Unless in the extremely unlikely event that residents burn copious quantities of solanaceous vegetables (aubergine, tomato) which contain small amounts of nicotine, tobacco is going to be the only source of nicotine in homes. But it will not by any means be the only source of many of the ingredients of "third hand smoke" that the unwitting or the fumophobic may believe are attributable only to smoking. The omission of this information in such reports risks harming the credibility of tobacco control.

References

1. Matt, G.E., et al., When smokers move out and non-smokers move in: residential thirdhand smoke pollution and exposure. Tob Control, 2011. 20(1): p. e1.

2. Schick, S., Thirdhand smoke: here to stay. Tob Control, 2011. 20(1): p. 1-3.

3. Naeher, L.P., et al., Woodsmoke health effects: a review. Inhal Toxicol, 2007. 19(1): p. 67-106.

4. Lijinsky, W., The formation and occurrence of polynuclear aromatic hydrocarbons associated with food. Mutat Res, 1991. 259(3-4): p. 251-61.

5. Mehlman, M.A., Dangerous properties of petroleum-refining products: carcinogenicity of motor fuels (gasoline). Teratog Carcinog Mutagen, 1990. 10(5): p. 399-408.

6. Hyland, A., et al., A 32-country comparison of tobacco smoke derived particle levels in indoor public places. Tobacco Control, 2008. 17(3): p. 159-65.

7. Sleiman, M., et al., Formation of carcinogens indoors by surface- mediated reactions of nicotine with nitrous acid, leading to potential thirdhand smoke hazards. Proc Natl Acad Sci U S A, 2010. 107(15): p. 6576- 81.

8. Ott, W. and M. Siegmann, Using multiple continuous fine particle monitors to characterize tobacco, incense, candle, cooking, wood burning, and vehicular sources in indoor, outdoor, and in-transit settings. Atmospheric Environment, 2006. 40: p. 821-843.

9. Wallace, L. and W. Ott, Personal exposure to ultrafine particles. Journal of Exposure Science and Environmental Epidemiology 0, 2011. 21: p. 20-30.

Conflict of Interest:

None declared