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Selection of chemicals in each dataset was based on the availability of experimental in vivo carcinogenicity data [obtained from the Carcinogenic Potency Database and Chemical Carcinogenesis Research Information System (CCRIS [40])] and predictions from all four QSAR tools.
A simple example is representing carcinogenicity data from two public datasets, DSSTox CPDBAS: Carcinogenic Potency Database [40] (Appendix 7) and ISSCAN: Chemical Carcinogens Database [41].
We have highlighted the considerations and challenges associated with calculating ADIs based on available carcinogenicity data.
The genotoxicity and carcinogenicity data are summarised and the approach used to derive an acceptable daily intake (ADI) is described for each chemical.
The carcinogenicity data involved in this study has been used in QSAR studies mostly as a source of further data retrieval.
Table 3 Risk characterization for acceptable intake levels TTC-based acceptable intakes Develop compound-specific limits when carcinogenicity data available Acceptable intakes based on compound-specific risk assessments Acceptable intakes based on Less than lifetime (staged TTC) limit concept Acceptable total daily intakes for multiple impurities Exceptions and flexibility in approaches.
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Regulatory agencies currently rely on rodent carcinogenicity bioassay data to predict whether or not a given chemical poses a carcinogenic threat to humans.
Data from the Salmonella assay were used by Ashby (1985) to identify structural alerts for potential carcinogenicity, providing critical data for the development of computerized structure activity methods for carcinogenicity prediction (Richard 1998).
Epigenetic effects might therefore partly explain cadmium's toxicity, including its carcinogenicity; however, human data on epigenetic effects are lacking.
Among the many substances in the industrial environment for which there are no human data concerning carcinogenicity, there are hundreds that have been shown to be carcinogenic in some animal species and thousands that have been shown to have some effect in assays of mutagenicity or genotoxicity.
This is based on inadequate data of carcinogenicity in humans exposed to naphthalene via the oral or inhalation routes, and the limited evidence of carcinogenicity in animals via the inhalation route".
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