Marcy I. Banton

TL;DR: The model provides a validated framework for performing chemical-specific route-to-route extrapolation and cross-species dosimetry, which can be used in place of generic default calculations in support of risk assessments for IPA and acetone.

TL;DR: It is concluded that styrene respiratory tract toxicity in mice and rats, including mouse lung tumors, are mediated by CYP2F-generated metabolites, and the PBPK model predicts that humans do not generate sufficient levels of these metabolites in the terminal bronchioles to reach a toxic level.

TL;DR: It is unlikely several chemicals that cause mouse lung tumors via CYP2F2 metabolism will cause lung tumors in humans, because human lungs contain far fewer of Clara cells than rats or mice, and human lung microsomes failed to metabolize these compounds, which make humans much less sensitive to toxicity due to reactive metabolites.

TL;DR: The weight of evidence suggests that benign tumors found in rats and mice are likely not relevant to human health, but instead secondary to rodent-specific modes of action, and THF is inherently biodegradable, thus is not expected to be environmentally persistent.

TL;DR: The larger data set indicates that these compounds have low sensitization potential in animal studies, and therefore are unlikely to represent human allergens, and the existing safety evaluations of the FDA, USEPA, NTP and ATSDR for these compounds are consistent and point to the conclusion that the propylene glycols present a very low risk to human health.