Thanks Sal (and Joel, and Kat)--
This thread helps, answering yet another question that arises in the midst of a quit. Second-hand smoke will not let the nicotine back into my system-- those smoke-filled rooms are to be avoiding for the other 3999 poisons, then :-).
It is much better to be asking these questions and continuing education, rather than residing in the state-of-denial necessary to allow indulging my nicotine addiction.
Jim (11 days)
- Joined: 18 Dec 2008, 23:57
|Video Title||Dial Up||High Speed||MP3||Length||Created|
|The Palmolive bottle demonstration||2.84mb||19.1mb||3.55mb||07:45||10/11/06|
|See how smoking destroys the lungs||1.55mb||4.59mb||1.87mb||04:13||11/27/06|
These three videos, especially the first one illustrate the differences between second hands smoke and you smoking yourself.
- Joined: 18 Dec 2008, 23:57
- Joined: 16 Jan 2003, 08:00
- Joined: 11 Nov 2008, 19:22
Part of the below study examined cotinine levels (primary chemical nicotine breaks down into) in both smokers and those breathing passive or second hand smoke. If I'm reading this correctly the cotinine level in the urine of smokers was 634 times greater than in passive smokers. If worried about passive smoking causing relapse, cotinine levels are a marker of where nicotine has been. Hopefully this finding helps give you peace of mind, at least in regard to relapse.
Urine cotinine underestimates exposure to tobacco-derived
lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone
(NNK) in passive compared to active smokers
Cancer Epidemiology, Biomarkers & Prevention
Published OnlineFirst August 30, 2010.
Neal L. Benowitz, Maciej Goniewicz, Mark Eisner, Eduardo Lazcano-Ponce, Wioleta Zielinska-Danch, Bartosz Koszowski, Andrzej Sobczak, Chis Havel and Peyton Jacob III
Objectives: Cotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) are widely used biomarkers for tobacco-derived nicotine and the lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), respectively. The discrepancy between cotinine levels in relation to disease risk comparing active vs. passive smoking suggests a non-linear tobacco smoke dose-response and/or that cotinine is not providing an accurate measure of exposure to tobacco smoke toxic constituents from secondhand smoke.
Methods: Cotinine and NNAL were measured in urine of 373 active smokers and 228 passive smokers.
Results: Average cotinine levels were 1,155 (IQR 703-2,715) for active smokers and 1.82 (0.45-7.33) ng/mg creatinine for passive smokers. Average NNAL levels were 183 (103-393) and 5.19 (2.04-11.6) pg/mg creatinine, respectively. NNAL/cotinine ratio in urine was significantly higher for passive smokers when compared to active smokers (2.85×103 vs. 0.16×103, p<0.0001).
Conclusions: Cotinine measurement leads to an underestimation of exposure to the carcinogen NNK from second-hand smoke when compared with active smoking.
http://cebp.aacrjournals.org/content/ea ... PI-10-0497