Biomarkers of environmental benzene exposure.

Abstract

Environmental exposures to benzene result in increases in body burden that are reflected in various biomarkers of exposure, including benzene in exhaled breath, benzene in blood and urinary trans-trans-muconic acid and S-phenylmercapturic acid. A review of the literature indicates that these biomarkers can be used to distinguish populations with different levels of exposure (such as smokers from nonsmokers and occupationally exposed from environmentally exposed populations) and to determine differences in metabolism. Biomarkers in humans have shown that the percentage of benzene metabolized by the ring-opening pathway is greater at environmental exposures than that at higher occupational exposures, a trend similar to that found in animal studies. This suggests that the dose-response curve is nonlinear; that potential different metabolic mechanisms exist at high and low doses; and that the validity of a linear extrapolation of adverse effects measured at high doses to a population exposed to lower, environmental levels of benzene is uncertain. Time-series measurements of the biomarker, exhaled breath, were used to evaluate a physiologically based pharmacokinetic (PBPK) model. Biases were identified between the PBPK model predictions and experimental data that were adequately described using an empirical compartmental model. It is suggested that a mapping of the PBPK model to a compartmental model can be done to optimize the parameters in the PBPK model to provide a future framework for developing a population physiologically based pharmacokinetic model.

Urinary Phenylmercapturic Acid as a Marker of Occupational Exposure to Benzene.

“…The reported values for PMA corresponding to 1 ppm benzene cluster around 40 µg/g cr with two extremes of 12 and 58 µg/g cr. In making comparison with the present observation (Table 4), it should be noted that the benzene exposure in the present study (up to 210 ppm) is much higher than the levels reported for the populations in literature (up to 20 ppm), and that possibility exists that the metabolism of benzene may vary depending on the exposure intensity 34) . Nevertheless, it appears likely that there is a general agreement between the present observation and findings available in literature, when urinary PMA level corresponding to 1 ppm benzene exposure is estimated from individual regression equations (the rightmost column in Table 4).…”

Analysis of urinary S-phenylmercapturic acid and trans,trans-muconic acid as exposure biomarkers of benzene in petrochemical and industrial areas of Korea

“…Recently, in a number of countries, the occupational exposure limit for airborne benzene has been lowered to 1 ppm (8-hour time-weighted average). Weisel et a1 (7) reported that automobile mechanics were exposed to a mean concentration of 1 ppm, and workers at a chemical plant had benzene exposure with a geometric mean level of 0.1 ppm for both smokers and nonsmokers. Therefore, it is very meaningful to verify the suitability of S-PMA and t,t-MA as exposure biomarkers which allow the detection of low concentrations of benzene and to apply their biomonitoring for the monitoring of occupational exposure and environmental pollution from benzene in Korea.…”

Environmental, dietary, demographic, and activity variables associated with biomarkers of exposure for benzene and lead

“…However, biomarker data are often difficult to obtain, and the relationship between biomarkers of exposure and dose is usually not straightforward (Weisel et al, 1996;Roy and Georgopoulos, 1998), as is evident by considering the factors that affect the blood concentrations of benzene and lead. Exposure to benzene generally occurs via inhalation, which has an immediate impact on blood concentrations, whereas lead exposure generally occurs via ingestion, which has a delayed effect on blood concentration, as the ingested lead is absorbed into systemic circulation over a period of time.…”