Cigarette smoking: Carboxyhemoglobin, plasma nicotine, cotinine and thiocyanate vs self-reported smoking data and cardiovascular disease

doi:10.1016/0021-9681(83)90136-4

Journal of Chronic Diseases

Volume 36, Issue 6, 1983, Pages 439-449

Journal of Chronic D...

https://doi.org/10.1016/0021-9681(83)90136-4 Get rights and content

Abstract

Measurement of the absorption of cigarette smoke constituents were compared with self-reported daily consumption from 450 smokers to determine the most reliable dose dependent indicator of smoke inhalation and risk for coronary heart disease. A plateau of plasma nicotine and cotinine concentration at levels above 20 cigarettes per day with a continued increase of carboxyhemoglobin and thiocyanate with increasing consumption of cigarettes occurred. Classification of smokers into groups smoking cigarettes yielding more or less than 1 mg nicotine showed that smokers of low yield brands had lower plasma levels of nicotine and cotinine, but comparable levels of carboxyhemoglobin and thiocyanate. Plasma nicotine bore no relationship to smoke inhalation, while the number of cigarettes consumed per day showed a weak correlation to smoke inhalation. Despite the lower nicotine yield of cigarettes, modification in smoking behaviour enabled the smoker to derive as much carbon monoxide and thiocyanate constituents from low and high yield cigarettes; thus counteracting the advantage of low nicotine yield brands. The relationship of these parameters to the risk of coronary heart disease is discussed.

References (58)

SS Ahmed et al.
Cardiovascular effects of long term cigarette smoking and nicotine administration
Am J Cardiol
(1976)
P Hill et al.
Smoking and cardiovascular disease: effect of nicotine on the serum epinephrine and norepinephrine in man
Am Heart J
(1974)
NJ Vetter et al.
Initial metabolic and hormonal response to acute myocardial infarction
Lancet
(1974)
Mah Russell et al.
Comparison of increases in carboxyhemoglobin after smoking “extra mild” and “non-mild” cigarettes
Lancet
(1973)
WB Kannel
Update on the role of cigarette smoking in coronary artery disease
Am Heart J
(1981)
MAH Russell et al.
Blood and urinary nicotine in non-smokers
Lancet
(1975)
DM Prue et al.
A critical evaluation of thiocyanate as a biochemical index of smoking exposure
Behav Ther
(1980)
JA Turner et al.
Some effects of changing to low tar and low nicotine cigarettes
Lancet
(1974)
N Wald et al.
Carboxyhemoglobin levels in smokers of filter and plain cigarettes
Lancet
(1977)
K Ball et al.
Smoking and the heart
Lancet
(1974)

WP Castelli et al.

The filter cigarettes and coronary heart disease: The Framingham Study

Lancet

(1981)

R Doll et al.

Mortality in relation to smoking: 10 years observation of British doctors

Br Med J

(1964)

EC Hammond et al.

Coronary heart disease, stroke and aortic aneurism

Arch Environ Hlth

(1969)

L Rosenberg et al.

Cigarette smoking in relation to the risk of myocardial infarction in young women. Modifying influence of age and predisposing factors

Int J Epid

(1980)

Cigarette smoking as a risk factor in men with a prior history of myocardial infarction

J Chron Dis

(1979)

MH Criqui et al.

Cigarette smoking and plasma high density lipoprotein cholesterol

Am Heart Assoc Monogr No 73

(1980)

WB Kannel et al.

Pressures of sudden coronary death

Circulation

(1975)

J Rosenberg et al.

Disposition kinetics and effects of intravenous nicotine

Clin Pharmac Ther

(1980)

BR Lucchesi et al.

The role of nicotine as a determinant of cigarette smoking frequency in man with observations of certain cardiovascular effects associated with the tobacco alkaloid

Clin Pharmac Ther

(1980)

RT Jones et al.

Tobacco smoking and nicotine tolerance in self-administration of abused substances. Methods of study

Nat Inst Drug Abuse Res

(1978)

RD Rabinowitz et al.

Acute hemodynamic effects of cigarette smoking in man assessed by systolic time intervals and echocardiography

Circulation

(1979)

N Wald et al.

Association between atherosclerosis diseases and carboxyhemoglobin levels in tobacco smokers

Br Med J

(1973)

WB Kannel et al.

Diet factors in heart disease. An evaluation of serum lipids as predictors of coronary heart disease

Ann Int Med

(1964)

Advance data

EL Wynder et al.

Impact of long-term filter cigarette usage on lung and larynx cancer risk. A case control study

J Nat Canc Inst

(1979)

N Wald et al.

Trends in tar. nicotine and carbon monoxide yields of UK cigarettes manufactured since 1934

Br Med J

(1981)

Mah Russell

Low tar-medium nicotinc cigarettes: A new approach to safer smoking

Br Med J

(1976)

R Stepney

Would a medium-nicotine, low tar cigarette be less hazardous to health?

Br Med J

(1981)

Mah Russell et al.

Plasma nicotine levels after smoking cigarettes with high, medium and low nicotine yields

Br Med J

(1975)

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Original articleCigarette smoking: Carboxyhemoglobin, plasma nicotine, cotinine and thiocyanate vs self-reported smoking data and cardiovascular disease

Abstract

Am J Cardiol

Am Heart J

Lancet

Lancet

Am Heart J

Lancet

Behav Ther

Lancet

Lancet

Lancet

Lancet

Mortality in relation to smoking: 10 years observation of British doctors

Br Med J

Coronary heart disease, stroke and aortic aneurism

Arch Environ Hlth

Cigarette smoking in relation to the risk of myocardial infarction in young women. Modifying influence of age and predisposing factors

Int J Epid

Cigarette smoking as a risk factor in men with a prior history of myocardial infarction

J Chron Dis

Cigarette smoking and plasma high density lipoprotein cholesterol

Am Heart Assoc Monogr No 73

Pressures of sudden coronary death

Circulation

Disposition kinetics and effects of intravenous nicotine

Clin Pharmac Ther

The role of nicotine as a determinant of cigarette smoking frequency in man with observations of certain cardiovascular effects associated with the tobacco alkaloid

Clin Pharmac Ther

Tobacco smoking and nicotine tolerance in self-administration of abused substances. Methods of study

Nat Inst Drug Abuse Res

Acute hemodynamic effects of cigarette smoking in man assessed by systolic time intervals and echocardiography

Circulation

Association between atherosclerosis diseases and carboxyhemoglobin levels in tobacco smokers

Br Med J

Diet factors in heart disease. An evaluation of serum lipids as predictors of coronary heart disease

Ann Int Med

Advance data

Impact of long-term filter cigarette usage on lung and larynx cancer risk. A case control study

J Nat Canc Inst

Trends in tar. nicotine and carbon monoxide yields of UK cigarettes manufactured since 1934

Br Med J

Low tar-medium nicotinc cigarettes: A new approach to safer smoking

Br Med J

Would a medium-nicotine, low tar cigarette be less hazardous to health?

Br Med J

Plasma nicotine levels after smoking cigarettes with high, medium and low nicotine yields

Br Med J

Original article
Cigarette smoking: Carboxyhemoglobin, plasma nicotine, cotinine and thiocyanate vs self-reported smoking data and cardiovascular disease