Genotoxicity 7,8- from

No information regarding the genotoxicity of HCN in animals was located in the available literature. Studies that addressed genotoxicity from other... 

Mazzullo, M., Colacci, A., Grilli. S., Prodi, G. Arefellini, G. (1986) 1,1,2-Trichloroethane evidence of genotoxicity from short-tcnn tests. Jpn. J. Cancer Res. (Gann), Tl, 532-539... 

Because uranium is a predominantly alpha-emitting radionuclide, current theories on gene mutation and chromosomal aberrations by high-LET alpha radiation suggest a potential for genotoxicity from uranium s radioactivity (BEIR 1980,1988,1990 Leach et al. 1970 Morris et al. 1990 Muller et al. 1967 Otake and Schull 1984 Sanders 1986 Stokinger et al. 1953 UNSCEAR 1982,1986,1988) (see Appendix D for a review of the hazards associated with radionuclide exposure). Other genotoxicity studies are discussed in Section 2.5. 

Researchers have reported the following evidence of genotoxicity from wood dust exposures. 

Mazzullo M, Colacci A, Grilli S, et al. 1986.1,1,2-Trichloroethane Evidence of genotoxicity from short-term tests. Jpn J Cane Res 77 532-539. 

The weight of the evidence from a variety of in vitro and in vivo test indicates a lack of genotoxicity for BP, and no evidence of genotoxicity from micronucleus test for 4-MBP. Additional smdies are needed to clarify the presence of and capacity for genotoxicity of other BP-related chemicals used as amine synergists in print ink (including MK, DEAB, and DMAB) that have been identified in recycled paperboard products. 

Simultaneous presence of several of these compoimds in the environment makes the assessment of their genotoxicities from environmental samples, very difficult, besides also difficulting the eorrelation studies between the exposition via and the observed carcinogenic effect (Tuvikene, 1995). These characteristies vary from one species to another but, in the human species, the respiratory via is eonsidered the most important, particularly for individuals occupationally exposed, although, in several cases, the dermic via is so or more important (Harvey and Dune, 1978). 

However, for some type of adverse effects, such as genotoxicity, carcinogenicity, and respiratory sensitization, it may not be possible from present knowledge to define this threshold of activity, so we may conclude that any level of exposure might carry some finite risk. In this case, OELs should be established at levels sufficiently low to avoid risks these are called pragmatic OELs. 

Recently, 202 and 203 were found to significantly reduce the mutation frequency induced by BaP in vivo as well (00UP3). Previously, flie same group had pointed out that some genotoxic effects could result from UV irradiation of tryptophan, but this had not been attributed to lipophilic substances like 202 and 203 (94MI5). 

Genotoxicity studies are required to identify compounds that can induce genetic damage ranging from single point gene mutations to gross alterations of chromosomal structure. Such effects are taken as indicative of the potential to cause cancer or heritable defects in humans. A standard battery of three types of test is recommended ... 

The vast majority of in vivo tests show no genotoxicity of mono- and dialkyltins. Results from in vitro tests are variable, with little indicahon of DNA reactivity. There are, however, indications of clastogenicity and effects on spindle formation in mitosis in viho. 

Klopman G, Contreras R, Rosenkranz HS, et al. 1985. Stmcture-genotoxic activity relationships of pesticides Comparison of the results from several short-term assays. Mutat Res 147 343-356. 

The chapter covers end points in the same order they appear within the Discussion of Health Effects by Route of Exposure section, by route (inhalation, oral, dermal) and within route by effect. Human data are presented first, then animal data. Both are organized by duration (acute, intermediate, chronic). In vitro data and data from parenteral routes (intramuscular, intravenous, subcutaneous, etc.) are also considered in this chapter. If data are located in the scientific literature, a table of genotoxicity information is included. 

The carcinogenic potential of the profiled substance is qualitatively evaluated, when appropriate, using existing toxicokinetic, genotoxic, and carcinogenic data. ATSDR does not currently assess cancer potency or perform cancer risk assessments. Minimal risk levels (MRLs) for noncancer end points (if derived) and the end points from which they were derived are indicated and discussed. 

Genotoxic effects of crnde jnices from Brassica vegetables andjnices and extracts from ph)dopharmaceutical preparations and spices of cruciferous plants origin in bacterial and mammalian cells , Chemico-Biological Interact, 102 1-16. 

In contrast, the calculation of human risk for genotoxic carcinogens from... 

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