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1.
Environ Toxicol Chem ; 42(5): 1049-1060, 2023 05.
Article in English | MEDLINE | ID: mdl-36848322

ABSTRACT

Treated seeds and their cotyledons can present a toxicological risk to seed-eating birds. To assess whether avoidance behavior limits exposure and consequently the risk to birds, three fields were sown with soybeans. Half of the surface of each field was sown with seeds treated with 42 g/100 kg seed of insecticide imidacloprid (T plot, treated) and the other half with seeds without imidacloprid (C plot, control). Unburied seeds were surveyed in C and T plots at 12 and 48 h post-sowing. Damaged seedlings were surveyed in C and T plots at 12 days post-sowing. The abundance and richness of birds was surveyed at the field level (without distinguishing between C and T plots) before, during, and after sowing, and 12 days post-sowing. Unburied seed density was higher in the headlands of the T plots than in the C plots, but did not differ between 12 and 48 h. The damage to cotyledons of seedlings was 15.4% higher in C plots than in T plots. The abundance and richness/ha of birds that eat seeds and cotyledons were lower after sowing, indicating a deterrent effect on birds by sowing imidacloprid-treated seeds. Although the variation in seed density over time does not allow solid conclusions to be drawn about the avoidance of seeds treated by birds, the seedling results suggest an aversive effect of imidacloprid-treated soybeans on birds. The dominant species was the eared dove (Zenaida auriculata), whose risk of acute poisoning by imidacloprid in soybean seeds and cotyledons was low, according to its toxicity exposure ratio, foraged area of concern, and foraged time of concern. Environ Toxicol Chem 2023;42:1049-1060. © 2023 SETAC.


Subject(s)
Glycine max , Insecticides , Animals , Cotyledon/chemistry , Neonicotinoids/toxicity , Insecticides/analysis , Nitro Compounds/toxicity , Seeds/chemistry , Birds , Seedlings
2.
Sci Total Environ ; 650(Pt 1): 1158-1172, 2019 Feb 10.
Article in English | MEDLINE | ID: mdl-30308804

ABSTRACT

Tissue-based burdens of polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs) were integrated with ethoxyresorufin-O-deethylase (EROD) and glutathione S-transferase (GST) enzyme activity in bull (Carcharhinus leucas), blacktip (Carcharhinus limbatus), and bonnethead (Sphyrna tiburo) sharks from Galveston Bay, TX. The potential toxicity of these burdens was evaluated by calculation of toxic equivalents (TEQs). Concentrations of total PAHs (∑PAHs) were significantly greater in blacktip and bonnethead sharks than bull sharks in liver, but did not exhibit differences in muscle among species. Hepatic concentrations of ∑PAHs in these sharks (range of means: 1560-2200 ng/g wet wt.) were greater than concentrations previously reported in oysters from Galveston Bay (range of means: 134-333 ng/g dry wt.), which suggests that trophic dilution of PAHs may not be reflected in sharks. Total PCBs (∑PCBs) were significantly greatest in bull sharks and lowest in bonnetheads, while blacktips were intermediate to these species. EROD activity was greater in bonnetheads than the other species, whereas GST activity was significantly higher in blacktips and bonnetheads than in bull sharks. Integration of hepatic burdens with biomarker activity via constrained multivariate analysis found correlations for only a small number of individual PAH/PCB congeners. Hepatic TEQ measurements suggest potential physiological effects of these burdens compared to established TEQ thresholds for other taxa, although the likelihood of similar effects in sharks requires further study and the inclusion of toxic endpoints. Our findings indicate that sharks may be prone to the accumulation of PAHs and PCBs, which may result in negative health outcomes for these cartilaginous fishes.


Subject(s)
Environmental Monitoring , Polychlorinated Biphenyls/metabolism , Polycyclic Aromatic Hydrocarbons/metabolism , Sharks/metabolism , Water Pollutants, Chemical/metabolism , Animals , Biomarkers/metabolism , Cytochrome P-450 CYP1A1/metabolism , Gulf of Mexico
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