Abstract
1-Hydroxypyrene (1-OHP) urinary excretion has been studied in subjects exposed to polycyclic aromatic hydrocarbons (PAH) from different sources (urban air pollution, cigarette smoking, food contamination or occupational exposure). In Study A, statistically significant differences among subjects categorized according to daily cigarette consumption were observed: 1-OHP median excretion of heavy smokers (more than 20 cigarettes per day; 1-OHP=371 ng l-1; n=6) was significantly increased over that of non-smokers (1-OHP=160 ng l-1; n=79), light smokers (less than 10 cigarettes per day,1-OHP=157 ng l-1; n=7) and also medium smokers (10-20 cigarettes per day, 1-OHP=154 ng l-1; n=13) (p<0.04). In smokers, 1-OHP excretion (y, ng l-1) increased with the intensity of cigarette consumption and was associated with self-reported number of cigarettes smoked daily (x, n) (y=20+16.6x; r=0.58, n=22, p<0.01), urinary thiocyanate (x, µmoll-1) (y=55+2.6x; r=0.57, n=20, p<0.01) and cotinine (x, µg l-1) (y=89+0.23x; r=0.62, n=17, p<0.01). In Study B the influence of smoked food consumption on 1-OHP excretion was evaluated: 1-OHP excretion began to increase as soon as 3 h after a PAH-rich meal and peak values were reached between 6 and 9 h after lunch. Maximum excretion mean values were respectively 525 ng l-1 for non-smokers (n=8) and 650 ng l-1 for smokers (n= 4). 1-OHP concentrations in next-morning samples were back to pre-lunch levels both for non-smokers and smokers. In Study C non-smoker workers (n=28) occupationally exposed to PAH in a steel plant were investigated. At values of airborne pyrene ranging between 6 and 30 µg m-3, excretion values of 1-OHP up to 80000 ng l-1 were observed. The use of urinary 1-OHP as a screening test to discriminate between smokers and non-smokers in the presence of uncorrected dietary influence has been calculated according to a cut-off value of 461 ng l-1 (reference group upper limit): the 1-OHP positive predictive value is 57%, its predictive negative value is 77%, sensitivity is 15% and specificity is 96%. In conclusion, 1-OHP appears to be a valuable biomarker of pyrene exposure. It will be nevertheless more accurate in assessing human PAH exposure from multiple sources if the influence of different kinetics for inhaled (particulate or gaseous) or ingested PAH are considered and if the role of oxidative polymorphism is adequately elucidated. The possibility of using 1-OHP to estimate the total burden of PAH from different sources or of screening groups with different PAH exposure appears to be a possible approach. However, the use of 1-OHP to evaluate the associated risk of cancer is still a premature target.
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