Examination of various biomarkers measuring genotoxic endpoints from Barcelona airport personnel

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Abstract

Three different biomarkers: sister-chromatid exchanges (SCE), micronuclei (MN), and the Comet assay, were used to evaluate different kinds of genetic damage in peripheral blood lymphocytes from 34 male workers at Barcelona airport, exposed to low levels of hydrocarbons and jet fuel derivatives. The control group consisted of 11 unexposed men. We also investigated the ras p21 protein levels in plasma, in order to evaluate whether the ras gene could serve as a suitable potential marker of carcinogenic pollution in occupationally exposed cohorts. SCE and MN analyses failed to detect any statistically significant increase in the airport workers when compared with the controls, and in fact, the frequency of binucleated cells with MN in the exposed group was significantly lower than that obtained in the control. However, slight but significant differences in the mean comet length and genetic damage index were observed between the exposed and control groups when using the Comet assay. There were no statistically significant differences between both groups in p21 plasma levels. Smoking was shown to affect significantly both SCE and high frequency cells (HFC) in the exposed group.

Introduction

In the early 19th century, benzene, toluene, xylenes and other alkyl benzenes were shown to be the major constituents of coal tar naptha, a by-product of coal gas manufacture, that was used as a solvent for rubber. The value of the alkyl benzenes and other aromatic hydrocarbons both as solvents and starting materials in many industrial processes was soon realised. In the 20th century, crude oil or petroleum was also shown to be a rich source of aromatics. Vast and diverse applications were found for these valuable chemicals. An extensive literature describes investigations into the toxicology and biochemistry of these compounds 1, 2, 3, 4, 5, 6. Benzene is an established human carcinogen and is genotoxic in vivo 7, 8. Epidemiological data on leukaemia incidence in benzene exposed workers have been used to derive the unit risk, i.e., the risk for a lifetime exposure to 1 μg/m3. Current estimates are in the range from 4×10−6 to 3×10−5 9, 10. The health effects of benzene pollution are consequently a matter of some concern and the reduction of environmental benzene is regarded as a priority goal in the field of environmental safety. Most environmental benzene comes from the use of petroleum and exposure to petroleum fuels and to exhausts from engines operating on gasoline is also considered as possibly carcinogenic to humans [11].

In addition to the hazard to the general population, the consequences of occupational exposure to benzene is a cause for concern and exposure limits to benzene usually above 1 ppm (3.2 mg/m3) as 8 h TWA have been established [12]. However, the possible risks related to low dose exposures (below 1 ppm), such as those associated with fuel delivery are not yet elucidated [13]. Epidemiological studies point to an increased cancer risk in these workers 14, 15. The present study, therefore, investigated the effects on various biomarkers of low level exposure to benzene and related alkyl benzenes in workers from the Barcelona airport by comparison with unexposed controls.

Section snippets

Subjects investigated

Thirty-nine male workers from the Barcelona airport personnel, probably exposed to petroleum derivatives and engine exhausts, were examined. These workers assisted during charge and discharge of the aeroplanes, sometimes even during the activity of refuelling their tanks. A questionnaire was prepared to collect relevant information about confounding factors that can affect the different parameters investigated, as well as information concerning potential exposure at the work place. This group

Results

The characteristics of both control and exposed groups are shown in Table 1. Table 2 shows the levels of benzene, toluene and xylenes measured in the airport during an 8-h workshift by comparison with those previously found in other Barcelona environments [16]. It can be seen that the 8-h TWA levels (mg/m3) of the three compounds for the airport workers are similar to those found in some Barcelona streets with intense moving traffic. Although the control individuals are living in the

Discussion

The lack of a genotoxic effect due to occupational exposure to benzene or jet fuel derivatives in the airport workers, as measured by SCE and MN in this study, was not unexpected in view of the fact that very low exposure levels were recorded for benzene (0.03 ppm), toluene (0.04 ppm), and xylenes at the airport of Barcelona. These levels were lower than those previously measured at petrol stations, and similar to the levels in some streets of Barcelona. Our SCE and MN results are in accordance

Acknowledgements

This investigation was supported in part by the European Union (EU, EV5V-CT92-0221), the Spanish Ministry of Education and Science (CICYT, SAF95-0813) and the Generalitat de Catalunya (CIRIT, SGR95-00512). We are grateful to the Universitat Autònoma de Barcelona for supporting M. Pitarque's stay at BIBRA International. We would like to thank T. Amador, A. Corral, and G. Umbert for their expert technical assistance in the processing and scoring of the samples. The collaboration of the Centre de

References (47)

  • L. Liu et al.

    The study of DNA oxidative damage in benzene-exposed workers

    Mutat. Res.

    (1996)
  • C. Andreoli et al.

    Detection of DNA damage in human lymphocytes by alkaline single cell gel electrophoresis after exposure to benzene or benzene metabolites

    Mutat. Res.

    (1997)
  • F. Sarto et al.

    Aging and smoking increase in the frequency of sister-chromatid exchanges (SCE) in man

    Mutat. Res.

    (1985)
  • C. Bolognesi et al.

    Sister chromatid exchange induction in peripheral blood lymphocytes of traffic police workers

    Mutat. Res.

    (1997)
  • L. Migliore et al.

    Micronucleated lymphocytes in people occupationally exposed to potential environmental contaminants: the age effect

    Mutat. Res.

    (1991)
  • M. Fenech

    Important variables that influence base-line micronucleus frequency in cytokinesis-blocked lymphocytes—a biomarker for DNA damage in human populations

    Mutat. Res.

    (1998)
  • M. Fenech

    The advantages and disadvantages of the cytokinesis-block micronucleus method

    Mutat. Res.

    (1997)
  • A. Tompa et al.

    Monitoring of benzene-exposed workers for genotoxic effects of benzene

    Mutat. Res.

    (1994)
  • D. Anderson et al.

    An examination of DNA strand breakage in the Comet assay and antioxidant capacity in diabetic patients

    Mutat. Res.

    (1998)
  • D. Anderson et al.

    Ras oncoproteins in human plasma from lung cancer patients and healthy controls

    Mutat. Res.

    (1996)
  • L. Fishbein

    Genetic effects of benzene, toluene and xylene

    IARC Sci. Publ.

    (1988)
  • R. Snyder et al.

    The toxicology of benzene

    Environ. Health Perspect.

    (1993)
  • IPCS/WHO Environmental Health Criteria Document 150, Benzene, World Health Organization, Geneve,...
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