so why not just go back to smoking."
"Contrary to popular opinion or misconceptions, the risks of secondhand smoke exposure are nothing compared to actually smoking yourself," writes Joel.
"As far as causing a relapse to needing nicotine, it can't do that. The trace amount of nicotine that can be absorbed from secondhand smoke exposure is usually under 1% of what a smoker gets from smoking."
The primary metabolite that nicotine breaks down into is called cotinine. The benefit of researchers looking at cotinine levels in saliva, blood, and urine, instead of nicotine, is that nicotine has a relatively short elimination half-life of about 2 hours. Cotinine's 17-hour half-life makes it a more stable indicator that nicotine was present.
The average of three studies reporting cotinine levels in the saliva of smokers was 260 ng/ml in women and 337 ng/ml in men.[1] Ng/ml stands for nanograms per milliliter. A nanogram is one billionth of a gram and a milliliter is one-thousandth of a liter.
A 2006 study used spectrometry (a scope that measures wavelengths or frequency) to analyze cotinine levels of non-smokers after spending 3 hours in a smoke-filled bar.
Although they experienced an 8-fold increase in cotinine levels, their total average increase was still only 0.66 ng/ml or a little more than half of a nanogram.[2] That's nearly 400 times lower than the 260 ng/ml found in the saliva of female smokers in the above study.
Let me quote from a 1979 Surgeon General report:
"Several researchers have attempted to measure the amount of nicotine absorbed by nonsmokers in involuntary smoking situations. Cano, et al. studied urinary excretion of nicotine by persons on a submarine. Despite very low levels measured in the air (15 to 32ug/ma), nonsmokers showed a small rise in nicotine excretion; however, the amount excreted was still less than 1 percent of the amount excreted by smokers."
"Harke measured nicotine and its main metabolite, cotinine, in the urine of smokers and nonsmokers exposed to a smoke-filled environment and reported that nonsmokers excreted less than 1 percent of the amount of nicotine and cotinine excreted by smokers. He concluded that at this low-level of absorption nicotine is unlikely to be a hazard to the nonsmoker."[3]
What about inhaling secondhand e-cigarette vapor instead of cigarette smoke? A 2014 study found that, as with cigarettes, e-cig cotinine levels were roughly 100 times lower in exposed non-users than commonly seen in smokers.
"We did not find statistically significant differences in cotinine concentrations from the non-smokers exposed to e-cigarette vapour versus those exposed to tobacco smoke. This is also in agreement with a laboratory study from Flouris et al (2013) that found that e-cigarettes and tobacco cigarettes generated similar effects on serum cotinine levels after a passive exposure of one hour (2.4 vs. 2.6 ng/ml respectively)."[4]
An e-cigarette industry marketing ploy is to entice teens and comfort e-cig users by teaching them that nicotine is also found in nightshade vegetables (tomatoes, potatoes, eggplant, and peppers).
A 1999 study of nicotine in nightshade vegetables found that "on the basis of the observed concentrations and the respective food consumption data for different countries, a distributive analysis of the results suggests that the mean daily dietary nicotine intake for the population of the countries for which consumption data were available is approximately 1.4 micrograms per day."[5]
Contrast this study's 1.4 micro-gram figure (.0000014) for total daily dietary nicotine intake from nightshade veggies to the 1 milligram of nicotine (.001) that enters the smoker's bloodstream after smoking a single cigarette. That one cigarette alone introduces 714 times more nicotine than a daily diet that includes nightshade veggies.
Still, a critical fact that bears repeating is that just one puff of mainstream nicotine is enough to stimulate up to 50 percent of the brain receptors that sustain nicotine addiction.[6] And once "cheating" rings dependency's bell it cannot be un-rung.
Breathing secondhand smoke introduces vastly more nicotine than nightshade veggies yet vastly less than taking a puff from a lit cigarette. One puff is sufficient to foster relapse while secondhand smoke cannot.
According to Joel, "as far as secondhand smoke and nicotine go, you would have to be in a smoke-filled room, non-stop for 100 hours, yes I am saying over 4 days to get the equivalent dose of nicotine delivered to a smoker from one cigarette."[7]
"Other chemicals in secondhand smoke can reach some pretty toxic levels much quicker than that, in minutes not days. The side effects felt from being exposed to secondhand smoke are from carbon monoxide, hydrogen cyanide, and some other noxious chemicals that can reach levels that are well above OSHA standards for safety," explains Joel.
But as many newbies discover, being forced to breathe secondhand smoke during recovery can be demoralizing. Breathing it can become a source of junkie-thinking during times of challenge. "I have to breathe it anyway so why not just go back to smoking."
What this addict is really saying is, "I'm so concerned about the lesser harms of secondhand smoke and the damage it inflicts that "I'm going to suck main-stream smoke into my lungs and bloodstream, smoke that I know will cause far greater harm."
What they're saying is, "I'm so concerned about a risk that is many times less than I used to face, that I'm going to relapse back to the greater risk and take a 50% chance that I'll smoke myself to death 13 to 14 years early.[8]
Such thinking makes you wonder why it never, ever occurs to non-smokers to take up smoking for the same reason. Such logic only makes sense to an addict.
What such junkie-thinking is saying is that, "I'm going to again become part of the problem and at times expose others to the smoke, smells, and chemicals that my once again badly damaged senses will by then no longer find offensive."
Why allow such smoke-screen junkie-thinking obscure the path home? Just one challenge at a time "endeavor to persevere," strive to see through it!
References:
2. Fowles J, et al, Secondhand tobacco smoke exposure in New Zealand bars: results prior to implementation of the bar smoking ban, The New Zealand Medical Journal, April 21, 2006, Volume 119, Page U1931.
3. US Surgeon General, Smoking and Health: A Report of the Surgeon General, 1979, Chapter 11, Page 24.
4. Ballbè M, Martínez-Sánchez JM, Sureda X, et al. Cigarettes vs. e-cigarettes: Passive exposure at home measured by means of airborne marker and biomarkers. Environmental Research, 2014, Volume 135, Pages 76-80.
5. Siegmund B, et al, Determination of the nicotine content of various edible nightshades (Solanaceae) and their products and estimation of the associated dietary nicotine intake, Journal of Agriculture and Food Chemistry, August 1999, Volume 47(8), Pages 3113-3120.
6. Brody AL et al, Cigarette smoking saturates brain alpha 4 beta 2 nicotinic acetylcholine receptors, Archives of General Psychiatry, August 2006, Volume 63(8), Pages 907-915.
7. Spitzer, J, Can secondhand smoke cause relapse? 11/21/01 https://whyquit.com/joels-videos/can-second-hand-smoke-cause-relapse/
8. Wald NJ and Hackshaw AK, Cigarette smoking: an epidemiological overview, British Medical Bulletin, January 1996, Volume 52(1), Pages 3-11.
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