Comparative dermal absorption of 2,3,7,8-tetrachlorodibenzo-p-dioxin and three polychlorinated dibenzofurans

Brewster, David; Banks, Yolanda B.; Clark, Ann-Marie; Birnbaum, Linda S.

doi:10.1016/0041-008x(89)90064-1

Cited by 38 publications

(16 citation statements)

References 21 publications

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“…Only a handful of absorption experiments have been conducted at loads under 200 ng/cm 2 . These include the in vitro mouse TDCP experiments of Hughes et al (2001), the in vitro human DEET experiments of Santhanam et al (2005) and some early dioxin/dibenzofuran experiments using rats in vivo (Brewster et al, 1989;Banks and Birnbaum, 1991). Santhanam et al (2005) found relatively low fractional absorption at low loads, a result that is attributable to the relatively high vapor pressure of DEETand the long duration of the experiments.…”

Section: Discussionmentioning

confidence: 99%

The mismeasure of dermal absorption

Kissel

2010

J Expo Sci Environ Epidemiol

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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.

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Section: Discussionmentioning

confidence: 99%

The mismeasure of dermal absorption

Kissel

2010

J Expo Sci Environ Epidemiol

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“…For a number of dioxin-related compounds, both oral and dermal absorption has been shown to be dose-dependent (122,123,124). Relative absorption decreases as the dose is increased.…”

Section: Toxiic Equivalencymentioning

confidence: 99%

The mechanism of dioxin toxicity: relationship to risk assessment.

Birnbaum

1994

Environ Health Perspect

298

147

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Risk characterization involves hazard identification, determination of dose-response relationships, and exposure assessment. Improvement of the risk assessment process requires inclusion of the best available science. Recent findings in the area of dioxin toxicity have led to a major effort to reassess its risk. 2,3,7,, commonly referred to as "dioxin," is the most toxic member of a class of related chemicals including the polyhalogenated dibenzo-p-dioxins, dibenzofurans, biphenyls, naphthalenes, azo-and azoxy-benzenes, whose toxicities can be expressed as fractional equivalencies of TCDD. These chemicals exert their effects through interaction with a specific intracellular protein, the Ah receptor. While binding to the receptor is necessary, it is not sufficient to bring about a chain of events leading to various responses including enzyme induction, immunotoxicity, reproductive and endocrine effects, developmental toxicity, chloracne, tumor promotion, etc. Some of these responses appear to be linear at low doses. Immunotoxicity and effects on the reproductive system appear to be among the most sensitive responses. The Ah receptor functions as a transcriptional enhancer, interacting with a number of other regulatory proteins (heat shock proteins, kinases, translocases, DNA binding species). Interaction with specific base sequences in the DNA appear to be modulated by the presence of other growth factors, hormones, and their receptors as well as other regulatory proteins. Thus, dioxin appears to function as a hormone, initiating a cascade of events that is dependent upon the environment of each cell and tissue. While Ah receptor variants exist, all vertebrates examined have demonstrated such a protein with similar numbers of receptors and binding affinity for TCDD. Most species respond similarly to dioxin and related compounds. While a given species may be an outlier for a given response, it will behave like other animals for other responses. For both in vivo and in vitro end points where animal and human data exist, such as enzyme induction, chloracne, immunotoxicity, developmental toxicity, and cancer, the sensitivity of humans appears similar to that of experimental animals. Current levels of environmental exposure to this class of chemicals may be resulting in subtle responses in populations at special risk such as subsistence fisherman and the developing infant, as well as in the general population. Increased understanding of the mechanism of dioxin's effects as well as elucidation of exposure-dose relationships is leading to the development of a biologically based dose-response model in the ongoing process of incorporating the best science into the risk assessment of TCDD and related compounds.-Environ Health Perspect 102(Suppl 9) 157-167(1994)

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“…Their model indicates that, even as the magnitude of uptake increases, the efficiency of uptake can go down when the thickness of the soil layer (i.e., the magnitude of applied dose) increases. This effect has been measured by Brewster et al (26) who observed that dioxins and furans penetrate rat skin more easily at lower doses. For example, they found that 40% of the TCDD placed on skin passes through at an applied dose of 0.3 p.g/kg (soil) but uptake falls to half that much at applied doses between 32 and 320 kglkg(soi1).…”

Section: Dermal Uptake Modelmentioning

confidence: 84%

Dermal Uptake of Organic Chemicals from a Soil Matrix

McKone

1990

Risk Analysis

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Uptake of chemicals from soil on human skin is considered. Based on a review of literature on the structure of human skin, the processes by which chemicals pass through this boundary, and experiments that reveal the rate and magnitude of this transport process; a two-layer model is presented for estimating how chemical uptake through the stratum corneum depends on chemical properties, skin properties, soil properties and exposure conditions. The model is applied to two limiting scenarios--(1) continuous deposition and removal of soil on the skin surface and (2) a one-time deposition of soil onto the skin surface. The fraction of soil-bound chemical that passes through the stratum corneum is dependent on the skin-soil layer thickness; the dimensionless Henry's law constant, Kh and the octanol-water partition coefficient, Kow of the soil-bound chemical. The nature of this dependence is discussed.

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Comparative dermal absorption of 2,3,7,8-tetrachlorodibenzo-p-dioxin and three polychlorinated dibenzofurans

Cited by 38 publications

References 21 publications

The mismeasure of dermal absorption

The mismeasure of dermal absorption

The mechanism of dioxin toxicity: relationship to risk assessment.

Dermal Uptake of Organic Chemicals from a Soil Matrix

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