Abstract  A common dermal exposure assessment strategy estimates the systemic uptake of chemical in contact with skin using the fixed fractional absorption approach: the dermal absorbed dose is estimated as the product of exposure and the fraction of applied chemical that is absorbed, assumed constant for a given chemical. Despite the prominence of this approach there is little guidance regarding the evaluation of experiments from which fractional absorption data are measured. An analysis of these experiments is presented herein, and limitations to the fixed fractional absorption approach are discussed. The analysis provides a set of simple algebraic expressions that may be used in the evaluation of finite dose dermal absorption experiments, affording a more data-driven approach to dermal exposure assessment. Case studies are presented that demonstrate the application of these tools to the assessment of dermal absorption data.

Abstract  The results of dermal absorption experiments are routinely and often exclusively reported in terms of fractional absorption. However, fractional absorption is not generally independent of skin loading conditions. As a consequence, experimental outcomes are commonly misinterpreted. This can lead in turn to poor estimation of exposures under field conditions and inadequate threat assessment. To aid interpretation of dermal absorption-related phenomena, a dimensionless group representing the ratio of mass delivery to plausible absorptive flux under experimental or environmental conditions is proposed. High values of the dimensionless dermal number (N(DERM)) connote surplus supply (i.e., flux-limited) conditions. Under such conditions, fractional absorption will generally depend on load and should not be assumed transferable to other conditions. At low values of N(DERM), dermal absorption will be delivery-limited. Under those conditions, high fractional absorption is feasible barring maldistribution or depletion due to volatilization, washing, mechanical abrasion or other means. Similar logic also applies to skin sampling and dermal toxicity testing. Skin surface sampling at low N(DERM) is unlikely to provide an appropriate measure of potential dermal dose due to depletion, whereas dermal toxicity testing at high N(DERM) is unlikely to show dose dependence due to saturation.

Abstract  Developmental health risks of chronical exposure to low doses of foodborne persistent organic pollutants (POP)are recognized but still largely uncharacterized. Juvenile female BALB/c mice exposed to either HBCD, CB-153 or TCDD at doses relevant to human dietary exposures (49.5 μg, 1.35 μg and 0.90 ng kg−1 bw−1 day−1, respectively) for 28 days displayed histopathological changes in liver (HBCD, CB-153, TCDD), thymus (HBCD, CB-153) and uterus (HBCD), reduced serum oestradiol 17β (E2) levels (HBCD), increased serum testosterone (T)levels (CB-153) and an increased T/E2 ratio (HBCD). Proteomics analysis of brain provided molecular support for the HBCD-induced reduction in E2. Neural gene expression analysis, confirmed effects on 18 out of 30 genes previously found to be affected after exposure to higher doses to the same pollutants. Our findings indicate that exposure to POP at low doses is associated with subtle, but toxicological relevant effects on post-natal development in female mice.