NO—CADMIUM IN TOBACCO
SMOKE IS NOT A LIKELY CAUSE
OF EMPHYSEMA
If cadmium is a constituent of tobacco
smoke, it is to be expected that urinary
cadmium levels will increase as pack
years accumulate. It may simply be an
innocent marker of cumulative exposure
to tobacco smoke, much as expired
carbon monoxide, blood carboxyhaemoglobin,
serum thiocyanate, or serum/
urinary/salivary cotinine are innocent
markers of acute exposure.
In the NHANES III population the
mean creatinine adjusted urinary cadmium
levels of current and former
smokers (0.46 and 0.32 mg/g creatinine,
respectively) were no more than 2.0-
and 1.4-fold that of the never smokers
(0.23 mg/g creatinine). The level among the smokers was thus twice that of the
never smokers—and so consistent with
general experience—but it was very low
indeed compared with working populations
exposed to cadmium, even populations
without any apparent adverse
effect on kidneys or lungs. If urinary
cadmium provides a reliable measure of
the cumulative dose of cadmium
absorbed by the lungs and gut, and if
cadmium delivered to the lungs through
the circulation is as hazardous as
cadmium delivered in inspired air, these
observations imply a ‘‘dose’’ threshold
for inducing emphysema that is similar
to, or only marginally above, the average
dose retained without apparent ill effect
in the population at large from food and
water. This is just plausible, but it is not
likely.
NO—CADMIUM IN TOBACCOSMOKE IS NOT A LIKELY CAUSEOF EMPHYSEMAIf cadmium is a constituent of tobaccosmoke, it is to be expected that urinarycadmium levels will increase as packyears accumulate. It may simply be aninnocent marker of cumulative exposureto tobacco smoke, much as expiredcarbon monoxide, blood carboxyhaemoglobin,serum thiocyanate, or serum/urinary/salivary cotinine are innocentmarkers of acute exposure.In the NHANES III population themean creatinine adjusted urinary cadmiumlevels of current and formersmokers (0.46 and 0.32 mg/g creatinine,respectively) were no more than 2.0-and 1.4-fold that of the never smokers(0.23 mg/g creatinine). The level among the smokers was thus twice that of thenever smokers—and so consistent withgeneral experience—but it was very lowindeed compared with working populationsexposed to cadmium, even populationswithout any apparent adverseeffect on kidneys or lungs. If urinarycadmium provides a reliable measure ofthe cumulative dose of cadmiumabsorbed by the lungs and gut, and ifcadmium delivered to the lungs throughthe circulation is as hazardous ascadmium delivered in inspired air, theseobservations imply a ‘‘dose’’ thresholdfor inducing emphysema that is similarto, or only marginally above, the averagedose retained without apparent ill effectin the population at large from food andwater. This is just plausible, but it is notlikely.
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