Toxicological Significance (toxicological + significance)

Distribution by Scientific Domains


Selected Abstracts


DNA damage in mice treated with sulfur dioxide by inhalation

ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 3 2005
Ziqiang Meng
Abstract Sulfur dioxide (SO2) is a ubiquitous air pollutant produced by the burning of fossil fuels. In this study, single-cell gel electrophoresis (the Comet assay) was used to evaluate the DNA damage produced by inhalation exposure of mice to SO2. Male and female mice were housed in exposure chambers and treated with 14.00 ± 1.25, 28.00 ± 1.98, 56.00 ± 3.11, and 112.00 ± 3.69 mg/m3 SO2 for 6 hr/day for 7 days, while control groups were exposed to filtered air. Comet assays were performed on blood lymphocytes and cells from the brain, lung, liver, spleen, kidney, intestine, and testicles of the animals. SO2 caused significant, dose-dependent increases in DNA damage, as measured by Olive tail moment, in all the cell types analyzed from both sexes of mice. The results indicate that inhalation exposure to SO2 damages the DNA of multiple organs in addition to the lung, and suggests that this damage could result in mutation, cancer, and other diseases related to DNA damage. Further work will be required to understand the ultimate toxicological significance of this damage. These data also suggest that detecting DNA damage in blood lymphocytes, using the Comet assay, may serve as a useful tool for evaluating the impact of pulmonary SO2 exposure in human biomonitoring studies. Environ. Mol. Mutagen., 2005. © 2005 Wiley-Liss, Inc. [source]


Pharmaceutical metabolites in the environment: Analytical challenges and ecological risks,

ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 12 2009
Mary D. Celiz
Abstract The occurrence of human and veterinary pharmaceuticals in the environment has been a subject of concern for the past decade because many of these emerging contaminants have been shown to persist in soil and water. Although recent studies indicate that pharmaceutical contaminants can pose long-term ecological risks, many of the investigations regarding risk assessment have only considered the ecotoxicity of the parent drug, with very little attention given to the potential contributions that metabolites may have. The scarcity of available environmental data on the human metabolites excreted into the environment or the microbial metabolites formed during environmental biodegradation of pharmaceutical residues can be attributed to the difficulty in analyzing trace amounts of previously unknown compounds in complex sample matrices. However, with the advent of highly sensitive and powerful analytical instrumentations that have become available commercially, it is likely that an increased number of pharmaceutical metabolites will be identified and included in environmental risk assessment. The present study will present a critical review of available literature on pharmaceutical metabolites, primarily focusing on their analysis and toxicological significance. It is also intended to provide an overview on the recent advances in analytical tools and strategies to facilitate metabolite identification in environmental samples. This review aims to provide insight on what future directions might be taken to help scientists in this challenging task of enhancing the available data on the fate, behavior, and ecotoxicity of pharmaceutical metabolites in the environment. [source]


Assessing trace-metal exposure to American dippers in mountain streams of southwestern British Columbia, Canada

ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 4 2005
Christy A. Morrissey
Abstract To develop a suitable biomonitor of metal pollution in watersheds, we examined trends in exposure to nine trace elements in the diet (benthic invertebrates and fish), feathers (n = 104), and feces (n = 14) of an aquatic passerine, the American dipper (Cinclus mexicanus), from the Chilliwack watershed in British Columbia, Canada. We hypothesized that key differences may exist in exposure to metals for resident dippers that occupy the main river year-round and altitudinal migrants that breed on higher elevation tributaries because of differences in prey metal levels between locations or possible differences in diet composition. Metals most commonly detected in dipper feather samples in decreasing order were Zn > Cu > Hg > Se > Pb > Mn > Cd > Al > As. Resident dipper feathers contained significantly higher mean concentrations of mercury (0.64 ,g/g dry wt), cadmium (0.19 ,g/g dry wt), and copper (10.8 ,g/g dry wt) relative to migrants. Mass balance models used to predict daily metal exposure for dippers with different diets and breeding locations within a watershed showed that variation in metal levels primarily was attributed to differences in the proportion offish and invertebrates in the diet of residents and migrants. In comparing predicted metal exposure values to tolerable daily intakes (TDI), we found that most metals were below or within the range of TDI, except selenium, aluminum, and zinc. Other metals, such as cadmium, copper, and arsenic, were only of concern for dippers mainly feeding on insects; mercury was only of concern for dippers consuming high fish diets. The models were useful tools to demonstrate how shifts in diet and breeding location within a single watershed can result in changes in exposure that may be of toxicological significance. [source]


Chronic toxicity/oncogenicity study of styrene in cd-1 mice by inhalation exposure for 104 weeks

JOURNAL OF APPLIED TOXICOLOGY, Issue 3 2001
George Cruzan
Abstract Groups of 70 male and 70 female Charles River CD-1 mice were exposed whole body to styrene vapor at 0, 20, 40, 80 or 160 ppm 6 h per day 5 days per week for 98 weeks (females) or 104 weeks (males). The mice were observed daily; body weights, food and water consumption were measured periodically, a battery of hematological and clinical pathology examinations were conducted at weeks 13, 26, 52, 78 and 98 (females)/104 (males). Ten mice of each gender per group were pre-selected for necropsy after 52 and 78 weeks of exposure and the survivors of the remaining 50 of each gender per group were necropsied after 98 or 104 weeks. An extensive set of organs from the control and high-exposure mice were examined histopathologically, whereas target organs, gross lesions and all masses were examined in all other groups. Styrene had no effect on survival in males. Two high-dose females died (acute liver toxicity) during the first 2 weeks; the remaining exposed females had a slightly higher survival than control mice. Levels of styrene and styrene oxide (SO) in the blood at the end of a 6 h exposure during week 74 were proportional to exposure concentration, except that at 20 ppm the SO level was below the limit of detection. There were no changes of toxicological significance in hematology, clinical chemistry, urinalysis or organ weights. Mice exposed to 80 or 160 ppm gained slightly less weight than the controls. Styrene-related non-neoplastic histopathological changes were found only in the nasal passages and lungs. In the nasal passages of males and females at all exposure concentrations, the changes included respiratory metaplasia of the olfactory epithelium with changes in the underlying Bowman's gland; the severity increased with styrene concentration and duration of exposure. Loss of olfactory nerve fibers was seen in mice exposed to 40, 80 or 160 ppm. In the lungs, there was decreased eosinophilia of Clara cells in the terminal bronchioles and bronchiolar epithelial hyperplasia extending into alveolar ducts. Increased tumor incidence occurred only in the lung. The incidence of bronchioloalveolar adenomas was significantly increased in males exposed to 40, 80 or 160 ppm and in females exposed to 20, 40 and 160 ppm. The increase was seen only after 24 months. In females exposed to 160 ppm, the incidence of bronchiolo-alveolar carcinomas after 24 months was significantly greater than in the controls. No difference in lung tumors between control and styrene-exposed mice was seen in the intensity or degree of immunostaining, the location of tumors relative to bronchioles or histological type (papillary, solid or mixed). It appears that styrene induces an increase in the number of lung tumors seen spontaneously in CD-1 mice. Copyright © 2001 John Wiley & Sons, Ltd. [source]