Do menthol smokers inhale more nicotine and toxins?

I have previously discussed some studies conducted at UMDNJ suggesting that under certain conditions menthol smokers inhale more nicotine and carbon-monoxide from their cigarettes and have a lower quit rate when attending our tobacco dependence treatment clinic.

The pattern of results we have observed suggest that it may not be a simple effect of menthol causing smokers to inhale more smoke. Rather, we have proposed that in circumstances requiring the smoker to reduce their cigarette consumption (e.g. when price increases affect affordability in a low-income smokers) menthol enables the smoker to increase the amount of smoke and nicotine they inhale per cigarette, by reducing the harshness.

Now clearly manufacturers of menthol cigarettes have an interest in this issue. In particular, the Lorrilard Tobacco Company, who depend on sales of Newport cigarettes for most of their profits, have an interest. So I was interested to read a paper by Dr Daniel Heck of Lorrilard Tobacco Company, on biomarkers of smoke exposure on menthol and nonmenthol smokers.

The study recruited 54 monthol smokers and 58 non-menthol smokers, provided them with preference-matched standard menthol or nonmenthol for a 1-week study period and menthol smokers were also given free menthol cigarettes for 2 weeks prior to the study period to allow them to acclimatize to the study menthol cigarettes.

For one day at the start of the one week study period and another day at the end, participants were allowed to smoke normally but blood and urine was taken in order to measure a variety of indicators of smoke exposure. The main result was that there were no consistent differences in markers of smoke exposure between menthol and nonmenthol smokers.

I am not writing to dispute the findings or even the measures used in the study (although Id have preferred if blood nicotine concentration had been measured). Rather I want to point out some characteristics of the study population and study procedures that make it unsurprising that they didn’t find any differences.

First of all, the study sample smoked an average of 27 cigarettes per day (both menthol and nonmenthol smokers). This a very high cigarette consumption, and extremely unusual for current African American menthol cigarette smokers. Just for comparison, among smokers attending our clinic (who are heavier than average smokers), AA menthol smokers smoked under 16 cigarettes per day.

Secondly, providing the sample of menthol smokers with free access to the study menthol cigarettes for 3 weeks, including the study week, detracts from the financial reality facing many smokers just now, and could have altered the way they smoked the cigarettes.

It is a pity this study did not recruit a more representative sample of US smokers and allow them to smoke their own, paid-for cigarettes.


Heck JD. Smokers of menthol and nonmenthol cigarettes exhibit similar levels of biomarkers of smoke exposure. Cancer Epidemiol Biomarkers Prev. 2009 Feb;18(2):622-9.

Labels: biomarkers, cancer, cigarette, cigarette smoking, jonathan foulds, menthol, toxins

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What is in cigarette smoke?

More than 4000 different chemicals have been identified in cigarette smoke. Most of us have a very basic idea that these chemicals can be harmful to health and that the mechanisms whereby this complex mixture of toxins contained in tobacco smoke leads to specific diseases are complex. However, I thought it might be helpful to some readers to provide a very basic description of the ways in which some of these components of cigarette smoke cause ill-health.

The simplest categorization of the components if cigarette smoking identifies 3 major components: tar, nicotine, and cabon-monoxide (CO).

Tar is the black sticky mass that coats the lungs and the airways. There are many hundreds of different chemicals within the tar, some of which have been shown to be carcinogenic in animals and/or humans. The deposition of particles of tar in the lungs and upper airways leads to the blocking of airways and to serious breathing problems, including Chronic Obstructive Pulmonary Disease (COPD). The toxic chemicals also cause inflammation and reduce the elasticity of the lungs and hence the ability to inhale and exhale normally.

The carbon-monoxide in smoke replaces oxygen in the hemoglobin (a component of blood), adversely affecting oxygen transport and energy supply, and requiring the heart to do more work to supply the same amount of oxygen to the body. A large number of smoke constituents, and particularly components of the gaseous phase of the tobacco smoke, cause immunologic responses and inflammation in the cells. This causes increased stickiness of the blood which increases the risk of clots. These processes increase the likelihood of a heart attack, stroke or other problems with the cardiovascular system.

Irritants such as nitric oxide cause hypersecretion of mucus and substances such as acrolein, acetone and acetaldehyde cause damage to the small hair-like strands that line the airways (cilia). This damage to the cilia impairs the ability of the cilia to clear mucus, causing breathi9ng difficulties. Years of smoking and daily coating of the lungs and airways in tar leads to irreversible lung damage and ultimately death from COPD .

Acute nicotine (critical for the development of addiction), increases heart rate, blood pressure and causes peripheral vasoconstriction (i.e. impairs peripheral circulation and thus exacerbates Reynauds’ Disease and erectile dysfunction). However, studies of smokeless tobacco users (who have high nicotine exposure like smokers, but without the smoke) compared with smokers, suggest that most of the cardiovascular problems are not caused by nicotine. It therefore appears that it is the thrombogenic effects of tobacco smoke exposure (primarily oxidant gases), combined with reduced oxygen supply (carbon monoxide) and increased myocardial oxygen demand (nicotine) that cause the cardiovascular harms from smoking.

Some of the chemicals found in cigarette smoke are listed below.

Carbonyls
Formaldehyde, Acetaldehyde, Acetone, Acrolein, Propionaldehyde, Crotonaldehyde, Methyl-Ethyl-Ketone, Butyraldehyde
Phenolics
Hydroquinone, Resorcinol, Catechol, Phenol, Cresol (m+p and o)
Aromatic Amines
3- and 4-aminobiphenyl, 1- and 2- aminonapthlene, o-toluidine, o-anisidine
Oxides of Nitrogen NO,
Hydrogen Cyanide
Ammonia
Volatiles
Benzene, Toluene, 1,3-butadiene, Isoprene, Acrylonitrile
Semi-Volatiles
Pyridine, Quinoline, Styrene
Trace Metals
Nickel (Ni), Cadmium (Cd) Lead (Pb) Chromium (Cr) Arsenic (As) Selenium (Se), Mercury (Hg)
Tobacco Specific Nitrosamines
N-Nitrosonornicotine (NNN)N-Nitrosoanabasine (NAB) Nitrosoanatabine (NAT)4-(N-nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK)
Volatile Nitrosamines
N,N-Nitrosodimethylamine (NDMA)N-Nitrosopyrrolidine (NPYR), N,N-Nitrosodiethylamine (NDEA)N,N-Nitrosoethylmethylamine (NEMA), N,N-Nitrosodipropylamine (NDPA)N,N-Nitrosodibuthylamine (NDBA), N-Nitrosopiperidine (NPIP)
Polycyclic Aromatic Hydrocarbons
Naphthalene, 1-Methylnaphthalene, 2-methylnaphthalene, AcenaphthyleneAcenaphthene, Fluorene, Phenanthrene, Anthracene, FluoranthenePyrene, Benzo(a)anthracene, Chrysene, Benzo(b)fluorantheneBenzo(k)fluoranthene, Benzo(j)fluoranthene, Benzo(g,h,l)peryleneBenzo(e)pyrene, Benzo(a)pyrene, PeryleneIndeno(1,2,3,-cd)pyrene, Dibenzo(a,h)anthraceneDibenz(a,j)acridine, Dibenz(a,h)acridine, Dibenz(a,e)pyreneDibenz(a,h)pyrene, Dibenz(a,i)pyrene, Dibenz(a,l)pyrene7H-Dibenzo(c,g)carbazole,
Heterocyclic Aromatic Amines
2-Amino-3-methylimidaszo(4,5-f)quinoline (IQ)2-Amino-3,4-dimethylimidazo(4,5-f)quinoline (MeIQ)2-Amino-3-methyl-9H-pyrido(2,3-b)indole (MeAaC)2-Amino-9H-pyrido(2,3-b)indole (AaC)1-Methyl-9H-pyridol(3,4-b)indole (Harman)9H-Pyrido(3,4-b)indole (Norharman)

Labels: cancer, chemicals, cigarette, jonathan foulds, nicotine, smoke, tar, toxins

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