Search

Circadian variations in immune defense and tissue repair may interfere with shift effects of occupational exposure when investigating biomarkers in cross-shift studies. This investigation compared biomarkers of inflammation and DNA damage in 59 nonsmoking and 59 smoking male construction workers pre- (6-10 a.m.) versus postshift (4-7 p.m.). Cellular compositions were analyzed in blood, induced sputum (IS), and nasal lavage fluid (NALF) and soluble inflammatory biomarkers were analyzed in IS and NALF. DNA damage was measured as 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) adducts and DNA strand breaks (alkaline Comet assay) in white blood cells (WBC). Apoptosis was quantified as percent apoptotic cells by annexin V and 7-amino-actinomycin staining in blood lymphocytes using flow cytometry. In nonsmokers higher preshift than postshift levels of interleukin-8 (IL-8) in IS and more DNA strand breaks were detected. However, more DNA adducts were found postshift. Among smokers, the cellular composition of IS and NALF differed between pre- and postshift samples, in particular more neutrophils pre- than postshift. In contrast, more cells in early apoptosis were observed post shift in both smokers and nonsmokers. These results indicate a potential influence of circadian rhythms on several biomarkers used in epidemiological studies. Data suggest interference with shift-work effects of occupational exposure in cross-shift studies and also the need to consider smoking as a modifying variable.

Urinary hydroxylated metabolites of polycyclic aromatic hydrocarbons (PAH) were investigated as potential biomarkers of bitumen exposure in a cross-shift study in 317 exposed and 117 non-exposed workers. Personal measurements of the airborne concentration of vapours and aerosols of bitumen during a working shift were weakly associated with post-shift concentrations of 1-hydroxypyrene (1-OHP) and 1-, 2+9-, 3- and 4-hydroxyphenanthrenes (further referred to their sum as OHPHE), but not 1- and 2-hydroxynaphthalene (OHNA). Smoking showed a strong influence on the metabolite concentrations, in particular on OHNA. Pre-shift concentrations of 1-OHP and OHPHE did not differ between the study groups ( P = 0.16 and P = 0.89, respectively). During shift, PAH metabolite concentrations increased in exposed workers and non-exposed smokers. Statistical modelling of post-shift concentrations revealed a small increase in 1-OHP by a factor of 1.02 per 1 mg/m bitumen ( P = 0.02) and 1.04 for OHPHE ( P < 0.001). A group difference was observed that was diminished in non-smokers. Exposed non-smokers had a median post-shift 1-OHP concentration of 0.42 μg/l, and non-smoking referents 0.13 μg/l. Although post-shift concentrations of 1-OHP and OHPHE were slightly higher than those in the general population, they were much lower than in coke-oven workers. The small content of PAHs in vapours and aerosols of bitumen, the increasing use of additives to asphalt mixtures, the strong impact of smoking and their weak association with airborne bitumen limit the use of PAH metabolites as specific biomarkers of bitumen exposure. [ABSTRACT FROM AUTHOR]

Contaminated soils represent a potential health risk for the human population. Risk assessment for humans requires specific methods, which must reflect the peculiarities of human behaviour, physiology and biochemistry with respect to contaminant uptake and processing. Biomarkers of effect or exposure have become an appropriate tool. Organic pollutants influence the expression profile of cytochromes P450 (CYP), and CYP1A1 has been shown to be a suitable biomarker for polycyclic aromatic hydrocarbons (PAH). The latter are widely distributed in soils and constitute an important soil contamination. Upon intake of PAH-contaminated soils, CYP1A1 is induced in various organs of rats and minipigs. Increased CYP1A1-levels in lung, kidney and spleen, after oral soil intake, indicate that contaminants escape the primary duodenal and hepatic metabolism and reach further organs. Dose–response relationships reveal that induction effects are to be expected in children based on known exposure conditions. Generally, CYP1A1-induction does not correlate with results of toxicity tests with lower organisms, performed with the same soils. The organic carbon content is largely responsible for this discrepancy. It severely affects the toxicity of soil bound PAH for microorganisms, but obviously affects the mobilization efficiency for PAH in the gastro-intestinal tract of mammals to a minor extent. Soil remediation by different methods may result in a significant reduction of the PAH content and of toxicity. Ingestion of remediated soils by rats shows, however, that the induction potential for CYP1A1 is only slightly decreased after remediation. This means that the major inducing components resist biological remediation or soil washing and remain in the soil. Because data obtained with experimental animals form the guiding principle for in vitro tests to be developed, the suitability of the animal model used for extrapolations to humans has to be proven. Upon soil ingestion, minipigs show a tissue-specific response pattern, which substantially differs from that of rats, which are widely used as animal models. It is not known which response pattern resembles that of man. In summary, cytochromes P450, in particular CYP1A1, are suitable biomarkers to assess the bioavailability of soil bound contaminants and their effects on mammalian species. There are, however, a number of questions to be answered in order to develop an in vitro test for human risk assessment. This concerns, for example, the identification of the suitable animal model, the identification of biomarkers for other contaminants and concepts to transpose the in vivo data to in vitro technologies or to mathematical modelling. [Copyright &y& Elsevier]