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We observed a dose-dependent increase in benzene-induced chromosomal damage and estimated a benchmark concentration limit of 0.205 ppm benzene using DO mice.
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Additionally it is also a prerequisite for estimating a benchmark dose.
The current standard NTP bioassay provides sufficient data to estimate a benchmark dose associated with a specified low tumor incidence to be used as a point-of-departure for cancer risk assessments.
(National Institute for Clinical Excellence 2008) recommends using 40 per 1,000 deliveries in estimating a benchmark for referral to a specialist perinatal mental health team.
In the present study we used DO mice to assess a toxicity response to benzene exposure and to estimate a benchmark concentration (BMC) of benzene exposure that is likely to result in a 10% increase in chromosomal damage over baseline.
In their investigation about toxicity study designs, Slob et al. (2005) use a computer simulation approach to investigate the performance of the typical dose response study design for determination of the no-observed-adverse-effect-level (NOAEL), when the study aim is to estimate a benchmark dose (BMD) in continuous endpoints.
Luebker et al. (2005b) estimated a lower bound of the benchmark dose correlated with a 5% change in response for PFOS and birth weight in rats of 0.39 mg/kg/day, equivalent to rat fetal serum concentrations of 34,000 ng/mL.
To compare our position estimates to a benchmark, we compute the localization Cramer-Rao lower bound as in [20].
Overall, benchmark dose analysis estimated a BMDL of 1857 mg/kg/day based on increased serum ALT.
The distance cutoff in the scoring function defining which pairwise interactions are taken into account when estimating the binding affinity was estimated based on a benchmark set of MHC class I binding data described in the methods section.
We used these estimates as a benchmark for the ISOpure estimate of tumor purity.
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