Lack of a distinct gradient in biomarker responses in small mammals collected at different distances from a highway.
This study describes biomarker effects in small mammals exposed to traffic emissions. Animals were collected at 10-50 m (site 1), 150-200 m (site 2), and 5 km (site 3) from a very busy highway (A2). To distinguish between routes of exposure, strictly carnivorous common shrews ( Sorex araneus) and predominantly herbivorous bank voles ( Clethrionomys glareolus) were collected. As a measure of exposure to polycyclic aromatic hydrocarbons (PAHs), aromatic DNA adduct levels were determined by (32)P-postlabeling techniques in tissue from heart, lung, and liver. Lead (Pb), cadmium (Cd), and copper (Cu) levels were analyzed in kidney as a measure of exposure to heavy metals. EROD and PROD activity and retinoid levels were determined in liver as effect biomarkers for exposure to PAHs and polyhalogenated aromatic hydrocarbons (PHAHs). Relatively high Cd levels in S. araneus and in particular elevated DNA adduct levels in C. glareolus indicated that small mammals at site 3 were exposed to more compounds than at sites 1 and 2 (3 > or = 1 > 2). The latter effect is probably due to an incidental and actual input of airborne pollutants that is deposited on plant surfaces. By consumption of above-ground vegetation, voles are chronically exposed to this pollution. Relatively high background input of PAHs probably hinders that the traffic-related gradient of airborne PAH concentrations found in an earlier study is reflected in DNA adduct levels in small mammals in the present study. Moreover, historical biomarkers for exposure to traffic emissions, such as increased kidney Pb levels, increased hepatic EROD activity, and disturbed hepatic vitamin A homeostasis are no longer applicable to indicate differences in exposure. This is a result of the ban on addition of Pb and chlorinated scavengers to gasoline and of cleaner combustion techniques, which were enforced by law over the past decade. Finally, it is advisable to use only juvenile small mammals for in situ monitoring of diffuse pollution because DNA adduct levels increased with age.
Hamers
T
T
Wageningen University-Toxicology Group, P.O. Box 8000, 6700 EA Wageningen, The Netherlands. timo.hammers@algemeen.tox.wau.nl
Smit
L A M
LA
Bosveld
A T C
AT
van den Berg
J H J
JH
Koeman
J H
JH
van Schooten
F J
FJ
Murk
A J
AJ
D000367:Age Factors; D000393:Air Pollutants / Q000032:analysis*; D000818:Animals; D003411:Arvicolinae; D015415:Biomarkers / Q000097:blood*; D019363:Cytochrome P-450 CYP1A1 / Q000494:pharmacology; D019362:Cytochrome P-450 CYP2B1 / Q000494:pharmacology; D018736:DNA Adducts; D004781:Environmental Exposure; D004784:Environmental Monitoring / Q000379:methods; D005260:Female; D006706:Homeostasis; D008297:Male; D011084:Polycyclic Aromatic Hydrocarbons / Q000097:blood*; D012788:Shrews; D014018:Tissue Distribution; D001335:Vehicle Emissions / Q000032:analysis*; D014801:Vitamin A / Q000378:metabolism
D000393:Air Pollutants; D015415:Biomarkers; D018736:DNA Adducts; D011084:Polycyclic Aromatic Hydrocarbons; D001335:Vehicle Emissions; D014801:Vitamin A; D019363:Cytochrome P-450 CYP1A1; D019362:Cytochrome P-450 CYP2B1