Phenanthrene metabolites (phenols and dihydrodiols) and l-hydroxypyrene exc
reted in the 24-h urine of smokers, non-smokers and lung cancer patients, w
ho after heavy smoking became light smokers, were determined and compared.
In contrast to 1-hydroxypyrene, no significant differences of the absolute
amounts of phenanthrene metabolites were found between smokers and non-smok
ers. A ratio phenanthrene metabolites/1-hydroxypyrene of 10.4 was observed
for non-smokers and 9.9 for lung cancer patients, but 4.2 for smokers. Sign
ificantly different ratios for the regiospecific oxidation of phenanthrene
were found for smokers when compared with non-smokers (1,2-oxidation vs 3,4
-oxidation was 1.45 in the case of smokers, but 2.34 in the case of non-smo
kers) indicating a cigarette smoke- but not PAM-caused induction of CYP 1A2
in smokers. As a consequence of the degree of PAH exposure the ratio dihyd
rodiols/phenols depends on the total amount of metabolites excreted. Phenol
s predominate, equally in smokers and non-smokers after low exposure, while
dihydrodiols become more prominent in highly exposed persons (coke plant w
orkers). Both (i) the regiospecific oxidation of PAH and (ii) the ratio of
dihydrodiol vs phenol formation may be recognized from the urinary phenanth
rene metabolite profile. This pattern mirrors the enzymatic status (balance
of the CYP isoforms and epoxide hydrolase) in individuals. Accordingly, mo
re detailed information may be obtained from the urinary metabolite pattern
than from 1-hydroxypyrene, commonly used in PAH biomonitoring.