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We found VOC concentrations to be generally lower than human-health benchmarks; concentrations of six VOCs in 1.2% of the samples were of potential human-health concern because their concentrations were greater than MCLs.
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Variability of the benchmark concentration of 25%% or even more is possible.
Estimates of benchmark concentrations for three example responses of interest (induction of cytochrome P4501A2 activity, dental anomalies, and neonatal thyroid hormone alterations) were derived based on selected human studies.
Statistical methods can then be used to evaluate benchmark concentrations for adaptive and adverse responses and to assess point-of-departure concentrations (Burgoon and Zacharewski 2008; Parham et al. 2009; Sand et al. 2011; Wignall et al. 2014).
Outdoor concentrations of air toxics were compared to previously defined benchmark concentrations for cancer and noncancer health effects.
Estimated concentrations of benzene, formaldehyde, and 1,3-butadiene were greater than cancer benchmark concentrations in over 90% of the census tracts.
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.
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.
The number of benchmark concentrations exceeded by modeled concentrations ranged from 8to3232 per census tract, with a mean of 14.
Twenty-two pollutants with chronic toxicity benchmark concentrations had modeled concentrations in excess of these benchmarks, and approximately 200 census tracts had a modeled concentration 100 times the benchmark for at least one of these pollutants.
Rather, HBSLs are nonenforceable benchmark concentrations in water that, when exceeded, may be of potential human-health concern.
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