...I will make secondhand smoke travel through a wall.
The majority of children living in apartments are exposed to secondhand smoke, even when they don’t live with smokers.
Do go on.
“We are starting to understand the role that seepage through walls and through shared ventilation may impact tobacco smoke exposure in apartments,” said Karen Wilson, M.D., MPH, author of the study and an assistant professor of Pediatrics at the University of Rochester Medical Center’s Golisano Children’s Hospital.
Among children who lived in an apartment, 84 percent had been exposed to tobacco smoke, according to the level of a biomarker (cotinine) in their blood that indicates exposure to nicotine found in tobacco, and this included more than 9 of 10 African-American and white children.
Even among children who lived in detached houses, 70 percent showed evidence of exposure.
A bit of a hole in the theory, that, isn't it? Clearly the cotinine is not coming from tobacco smoke "seeping through walls and ventilation".
I won't bother fisking this in full—the press release is here—suffice to say that the levels of cotinine found are risibly small and there is absolutely no suggestion of any health risk. As usual, it is a case of the policy leading the evidence; the policy being...
A smoking ban within multi-unit, subsidized housing could further reduce the tobacco smoke exposure for children and reduce smoking rates among residents.
The positive aspect of this story is that it has gone almost completely unreported in the mainstream media (ASH have reported it, naturally). Perhaps the junk scientists have finally stretched the public's credulity too far? Not before time, some would say.
H/T Dick Puddlecote
Go on Debs keep it on your quango website so we can all have a laugh.
ReplyDeleteThat's if your still in business next week.
LOL
Thanks to the anti-smoker cartel we know now that molecules can seep through walls, be transported by copper wires (also between detached houses) and be ejected from power outlets.
ReplyDeleteBut then, those with a minimum of logic know that ventilation systems extract air, they don't blow air in. For the simple reason that nobody in a multi-apartment building would like to smell the fish cooking in the kitchen of a distant or close neighbor. Let alone the odors coming from the neighbors WC.
Hmmm, I live in a block of flats, I smoke like a trooper and I've often wondered why my neighbours are dropping dead like flies...Now I know!
ReplyDeleteIn the thirty odd years I've been living here not one of the neighbours who died were under eighty years old...I should be so lucky to live that long eh.
Oh and Debs, you are up for a Hitler parody.
I've seen it coming through my walls !!
ReplyDeleteAlthough I live miles from the nearest house.
A car went past last week and someone must have been smoking as my kitchen filled with smoke.
The wife was cooking chips, but it couldn't have been that...could it ???
Years and years ago, I did a short-term contract for a big bio-pharmaceuticals company based in a noted spar town (Yes, you can work it out, but shush), working on detecting levels of cotinine in saliva (equivalent to blood levels, but easier to work with). I am a non-smoker; this was inportant for that job because apparently they'd already run the trial once and found that vapour contamination from the breath of the one smoker in the lab was queering their results.
ReplyDeleteAnyway, the method used was pretty usual; take a saliva sample with a tampon-like thing which tasted appalling, bung that in a sample tube, centrifuge the saliva out, spike it with a known quantity of radiolabelled cotinine (deuterated cotinine, which is mindbogglingly expensive) and run it through an initial concentration stage with a vac-elut system. That got you from 1ml saliva to 25 microlitres of fairly clean liquid, which you then ran through LC/MS.
The liquid chromatograph separated out the cotinine from the mixture, and the mass spectrometer which was one of the scanning variety compared the ratio of heavy cotinine to normal cotinine. You already knew how much heavy stuff was in the sample, so used area under graph measurement to work out how much cotinine was in the original sample.
Detection levels were down to about 3 or 4 picogrammes of cotinine per ml original matrix. A non-smoker usually showed up at between 10 and 20 picogrammes/ml, depending on how much chilli, tomatoes etc. they'd eaten lately. Non-smokers who lived with smokers were very hard to find, but came in at 30 or 40 picogrammes/ml if memory serves; the levels were VERY variable here.
Smokers came in at levels from a couple of hundred picogrammes/ml upwards; so high that you didn't want to run a sample from a smoker in with the non-smoker samples for fear of cross-contamination. This, BTW, was the big bogey in all of this work; I seemed to spend fully half my time swabbing down the bench to get rid of possible cotinine contamination on my workspace.
What all these levels mean I don't really know, save to say the levels of nicotine a non-smoker experiences even when sitting right next to a smoker are miniscule compared to what the smoker actually experiences, and whilst smoking does make most ailments, especially lung and circulatory diseases worse, it is hard to see how you could separate the effects of secondhand smoke out of background noise for non-smokers.
By background noise, I'm talking about diesel engine smoke, domestic heating pollutants, environmental toxins and phytotoxins from food, any one of which could conceivably produce effects way in excess of the secondhand smoke. Interestingly a World Health Organisation report from some years ago seemed to show a mildly protective effect where secondhand exposure to tobacco smoke was checked in children; certainly no harmful effects could be detected. The report was surpressed, if I recall, for not showing the right conclusions (though it did show that smoking isn't very good for you).