For those that are new or may have forgotten, this is one confounder in measuring SHS exposure in non-smokers.


Relevance of nicotine content of common vegetables to the
identification of passive tobacco smokers
E.F. Domino, E. Hombach and T. Demana
Department of Pharmacology, University of Michigan. Ann Arbor. MI48109-0626, USA

The presence of nicotine and cotinine in body fluids of nonsmokers is usually taken as evidence of passive smoking exposure.

This is because nicotine when present in air is
almost always due to contamination by tobacco smoke.

Dietary sources of nicotine in common foods could be responsible for the nicotine and cotinine concentrations in the body fluids of some nonsmokers.

Nicotine is used throughout the world as an insecticide and can contaminate dietary food. It is no surprise that nicotine has been found in a variety of human foods, either from
contamination or its actual synthesis by plants.

There has been considerable evidence over the years that nicotine is present in certain foods,especially plants from the family
Solanaceac.

If you spend three hours in a room with minimal tobacco smoke, you get about the same amount of nicotine in 5 oz. of potatoes, 8 1/2 oz. ripe tomatoes, 9 1/2 oz. cauliflower, and 1/3 oz. eggplant.

It appears that the dietary intake of nicotine in nonsmokers is of practical importance in the interpretation of passive smoke inhalation by nonsmokers when determining blood and urinary nicotine and cotinine levels.

http://www.bmj.com/cgi/eletters/bmj.38146.427188.55v1
The only reason cotinine (a harmless metabolite of nicotine and other nightshade vegetables) is used as a marker for exposure to ETS is because... it's the only thing that's possible to measure. For all the hot talk about "4000 chemicals" in secondhand smoke, most of them exist in such miniscule proportions that they can't be detected (even in the air!); rather, their presence can merely be merely deduced or perhaps just supposed.

The question then arises: What does the presence of cotinine measure? Answer: it measures the presence of cotinine. Even the California EPA Report (also known as WHO's "Monograph 10") admits that "cotinine does not serve well as a marker for the presence of other tobacco smoke compounds," an assertion one finds in virtually all the literature on secondhand smoke.

Then, too, there's this:

"There exists between individuals a genetically determined variation (up to 50 fold) in the level of metabolism to cotinine from a given exposure." (Nyberg et al, "Misclassification of Smoking Status," Epidemiology, 5/97)

And this:

Men metabolize cotinine faster than women, and whites faster than blacks (by 30%). This would also apply to the cotinine metabolized out of potatoes. And would indicate that either-- and/or-- women and blacks would register higher levels than their white/male counterparts to identical exposure. Further, eating a meal (consisting of anything) can also affect the metabolic speed. (Ahjevych et al, "Nicotine Metabolism Variables," Agency for Health Care Policy.)

Nevertheless, it's used as a marker (?)

Here's another angle that relates to the study that's now under discussion-- in which serum cotinine at levels of ...what?....8-10 ng/ml are fingered as risky (1.6 RR) for eventual Coronary Heart Disease.

According to a study sponsored by the American Lung Assn (Ahjevych et al, in Addiction Behaviors, 2/99) the blood cotinine levels that were measured in LESS than pack-a-day smokers ranged from 182 - 249 ng/ml. And the generally- accepted RR for CHD among first-hand smokers is 1.7.

So why are we to believe (by what strange logic?) that serum levels of 8-14 produce a risk almost as high?

And cotinine (have I mentioned?) is a harmless metabolite that indicates nothing except exposure to nicotine or nightshade vegetables. But, hey, I'll let Nyberg mention it again:

"It is not known how levels of cotinine measured relate to the biologically important components of ETS other than nicotine." (Op cit)

so if one had a steady diet of potatoes and was a non smoker being tested by a company for cotinine levels the company wouldn't hire cause the person LIED about being a non-smoker

either that the banners should ban potatoes

Looked into this and No, the cotinine levels would not be as high as a smoker's.

This could mess up tests for SHS exposure tho.

Gary K.