Secondhand Smoke Tied to Teens' Hearing Loss
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#1 Jul 19, 2011
Teens who are exposed to secondhand smoke may be at a higher risk of hearing loss, researchers have found.
The findings, which one expert called "surprising," can't prove that secondhand smoke causes hearing loss.
MORE BULLCHIT FROM TOBACCO CONTROL!
USING CONTININE LEVELS AS A BIO-MARKER OF EXPOSURE LMAO!
NO NOTE OF THEY GAVE THEM A DIETARY SCHEDULE TO FOLLOW TO MAKE SURE FOOD BORNE NICOTINE WASNT IN THEIR BLOOD OR URINE!
#2 Jul 20, 2011
Well, here's some input regarding the effect of dietary nicotine on SALIVARY cotinine levels.
"A large number of samples was investigated, but cotinine was not detected in any of the samples, although very high sensitivity could be achieved. Based on the results, we report a Monte Carlo simulation of salivary cotinine levels obtained utilising dietary nicotine, food consumption data, and the variance in these parameters. In this estimate, a mean salivary cotinine concentration of 0.022 ng ml−1 is predicted from dietary sources. This level is below the limit of detection for traditional analytical methods, but perhaps not for newly-developed methods."
That, of course, may be a case of author bias, since it comes from that rabid anti-smoking group, Philip Morris.
#3 Jul 20, 2011
The study is junk AND iVE GOT OTHER CONTININE STUDYS THAT FIND HIGHER LEVELS FROM FOOD SOURCES!
What theyve been doing is tossing in any subject matter and measuring continine levels to make a claim...total B.S.
I could say being exposed to the smell of human waste causes a hearing loss in kids when measured against BLOOD LEVELS OF methane gas exposed children!
Its all B.S.
#4 Jul 20, 2011
#5 Jul 20, 2011
Dietary nicotine: a source of urinary cotinine.
Davis RA, Stiles MF, deBethizy JD, Reynolds JH.
SourceBiochemical/Biobehaviora l R&D, R. J. Reynolds Tobacco Company, Winston-Salem, NC 27102.
Foods, principally from plants in the family Solanaceae, and a number of teas were examined for the presence of nicotine. Dietary nicotine would give rise to cotinine in urine and compromise estimates of exposure to tobacco smoke that depend on urinary cotinine. All foods were homogenized, extracted and analysed for nicotine and cotinine by gas chromatography with nitrogen-sensitive detection (GC) and/or GC/MS (mass spectrometry). Weak acid and aqueous extracts of the teas were analysed in a similar manner. Nicotine was not detected (less than 1 ng/ml of extract) in egg plant or green pepper. The average values for nicotine in tomato and potato were 7.3 ng/g wet weight and 15 ng/g wet weight, respectively. Black teas, including regular and decaffeinated brands, had nicotine contents ranging from non-detectable to greater than 100 ng/g wet weight. Instant teas yielded the highest nicotine contents observed (up to 285 ng/g wet weight). The possible sources of nicotine in these foods are discussed. A range of potential values for urinary cotinine concentrations (0.6 to 6.2 ng/ml) was calculated based upon estimated average and maximal consumptions of these foods and beverages. Because of the potential for exposure to nicotine by way of these routes, the use of urinary cotinine as a biomarker of exposure to environmental tobacco smoke may be compromised.
(0.6 to 6.2 ng/ml)
#6 Jul 20, 2011
It doesnt list any continine levels anywhere!
Hughjass dont you think its about time to cry foul on studies like this...
I mean come on its really scraping the the limits of imagination!
#7 Jul 20, 2011
People even defending junk science like this leave themselve looking like a Hugh Jass!
#8 Jul 20, 2011
Heres what the scotland nazis were told about shs enforcement when their smoking ban law went into effect!
NOT FOR PUBLIC EYES: Tobacco Control Division, Health and Safety Executive, 2006 Guide Circular to Inspectors, HSAOS, Complaint Officers, regarding enforcement of the Scotland Health and Safety at Work Act, Item 9, "The evidential link between individual circumstances of exposure to risk in exempted premises will be hard to establish. In essence, HSE cannot produce epidemiological evidence to link levels of exposure to SHS to the raised risk of contracting specific diseases and it is therefore difficult to prove health-related breaches of the Health and Safety at Work Act. Inspectors are therefore urged to exercise caution in considering any formal enforcement action in relation to SHS."
#9 Jul 20, 2011
Let's see, first you scream that cotinine levels are meaningless and now you are screaming that they aren't provided in the abstract.
Maybe you should take a break (and your meds).
#10 Jul 20, 2011
While nothing is perfect, a study examining biomarkers for nicotine exposure included this in its report:
"Traditional measures for nicotine dependence are the number of cigarettes smoked per day, nicotine intake expressed as mg per day, Fagerstr m questionnaire, expired air carbon monoxide, thiocyanates and cotinine levels in biological fluids. Urinary cotinine measurement is the most useful for the follow-up of smoking cessation including adjustment of nicotine replacement therapy, especially after a clinical event or for the follow-up of smoking pregnant women. It allows the detection of passive smoke exposure in children who are hospitalized for recurrent respiratory illnesses."
( http://www.ncbi.nlm.nih.gov/pubmed/12050041 )
Credibility check #1--tobacco industry propaganda
Nicotine in food would only become cotinine--in urine or anywhere else--IF the nicotine were metabolized.
The nicotine content in tomatoes, at least, varies depending on ripeness and on inclusion/exclusion of any of the green portion of the plants. Did RJR adjust for this?
Here's the entire bit, hosted by the Legacy library.
It contains this comment:
"There was no cotinine observed in any of the vegetables or
The authors of your touted study list a number of assumptions made in their work. One of them involves oral intake of nicotine from tobacco. Oral intake from tobacco is generally a question of prolonged exposure of the membranes in the mouth to fairly high concentrations of nicotine compared to what would be the case for foods in the stomach, where a completely different set of chemical reactions takes place and where the concentration within the food is far lower--and therefore less of the nicotine would be in contact with the stomach wall at any given time even if the gastric fluid production WERE as low-volume as salivary excretion.
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