Pollution of surface soils by traffic, especially along major highways, can be a significant issue. Numerous studies have demonstrated traffic to be an important source of particulate matter and gas-phase organic air pollutants that produce many types of deleterious effects. This article brings original information about the presence of contaminants with specific mechanisms of action in traffic-influenced soils as determined by bioanalytical approaches and instrumental analyses. The initial phase of the study aimed to compare contamination of soils near highways with those from reference localities, whereas the second phase of the study investigated the influence of traffic pollution in soils at various distances from highways. For the reference areas, forest soils contained greater concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents (TCDD-EQs; 483 to 2094 pg/g) than did arable soils (96 to 478 pg/g), which represent the relevant reference for the studied soils along highways. The total concentration of TCDD-EQs determined in the in vitro transactivation assay ranged from 225 to 27,700 pg/g in traffic-affected soils. The greatest concentration of TCDD-EQs among the studied sites was observed in soils collected near highway D1, which is the primary thoroughfare in the Czech Republic. The concentrations of TCDD-EQs in roadside soils were the greatest and decreased with increased distance from highways, and this spatial distribution corresponded with the levels of polycyclic aromatic hydrocarbons (PAHs). Soils collected 100 m away from highways in most cases contained concentrations of TCDD-EQs similar to background values. Most TCDD-EQ presence was caused by nonpersistent compounds in soils, with a significant contribution from PAHs as well as other unknown nonpersistent chemicals. Extracts from most soils collected near highways exhibited antiestrogenic and in some cases antiandrogenic activities; for several sites the activity was also detected in soils farther from highways. The presence of TCDD-EQs and antihormonal activity in highway-affected soils points to traffic as a source of polluting compounds having specific effects.

• MeSH
• Dioxins analysis   MeSH
• Endocrine Disruptors analysis   MeSH
• Soil Pollutants analysis   MeSH
• Environmental Monitoring MeSH
• Motor Vehicles MeSH
• Soil analysis   standards   MeSH
• Publication type
• Research Support, Non-U.S. Gov't MeSH
• Geographicals
• Czech Republic MeSH

Retinoids are known to regulate important processes such as differentiation, development, and embryogenesis. Some effects, such as malformations in frogs or changes in metabolism of birds, could be related to disruption of the retinoid signaling pathway by exposure to organic contaminants. A new reporter gene assay has been established for evaluation of the modulation of retinoid signaling by individual chemicals or environmental samples. The bioassay is based on the pluripotent embryonic carcinoma cell line P19 stably transfected with the firefly luciferase gene under the control of a retinoic acid-responsive element (clone P19/ A15). The cell line was used to characterize the effects of individual chemicals and sediments extracts on retinoid signaling pathways. The extracts of sediments from the River Kymi, Finland, which contained polychlorinated dioxins and furans and polycyclic aromatic hydrocarbons (PAHs), significantly increased the potency of all-trans retinoic acid (ATRA), while no effect was observed with the extract of the sediment from reference locality. Considerable part of the effect was caused by the labile fraction of the sediment extracts. Also, several individual PAHs potentiated the effect of ATRA; on the other hand, 2,3,7,8-tetrachlorodibenzo-p-dioxin and several phthalates showed slightly inhibiting effect. These results suggest that PAHs could be able to modulate the retinoid signaling pathway and that they could be responsible for a part of the proretinoid activity observed in the sediment extracts. However, the effects of PAHs on the retinoic acid signaling pathways do not seem to be mediated directly by crosstalk with aryl hydrocarbon receptor.

• MeSH
• Biological Assay methods   MeSH
• Dioxins analysis   toxicity   MeSH
• Carcinoma, Embryonal pathology   MeSH
• Financing, Organized MeSH
• Furans analysis   toxicity   MeSH
• Geologic Sediments chemistry   MeSH
• Risk Assessment MeSH
• Phthalic Acids analysis   toxicity   MeSH
• Environmental Pollutants analysis   toxicity   MeSH
• Luciferases, Firefly genetics   MeSH
• Cell Line, Tumor MeSH
• Polycyclic Aromatic Hydrocarbons analysis   toxicity   MeSH
• Genes, Reporter MeSH
• Retinoids genetics   metabolism   MeSH
• Signal Transduction MeSH
• Tretinoin analysis   toxicity   MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Geographicals
• Finland MeSH