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Skin Absorption
Skin Absorption
Skin Absorption refers to the process by which substances penetrate the skin and enter the body's circulatory system.
This includes the absorption of topically applied drugs, cosmetics, and other chemicals through the epidermis and underlying layers of the skin.
Factors that influence skin absorption include the physiochemical properties of the substance, the condition of the skin, and environmental conditions.
Understanding skin absorption is crucial for developing effective and safe topical treatments, as well as for evaluating the potential health impacts of dermal exposure to chemicals.
Researchers utilize a variety of in vitro and in vivo methods to study and optimize skin absorption, including comparartive analysis of different protocols and formulations.
Publcompare.ai, the leading AI-driven platform for protocol comparision and reproducibility, can help streamline this research and drive more reproducible results.
This includes the absorption of topically applied drugs, cosmetics, and other chemicals through the epidermis and underlying layers of the skin.
Factors that influence skin absorption include the physiochemical properties of the substance, the condition of the skin, and environmental conditions.
Understanding skin absorption is crucial for developing effective and safe topical treatments, as well as for evaluating the potential health impacts of dermal exposure to chemicals.
Researchers utilize a variety of in vitro and in vivo methods to study and optimize skin absorption, including comparartive analysis of different protocols and formulations.
Publcompare.ai, the leading AI-driven platform for protocol comparision and reproducibility, can help streamline this research and drive more reproducible results.
Most cited protocols related to «Skin Absorption»
Chlorpyrifos
Creatinine
factor A
Factor VII
Homo sapiens
No-Observed-Adverse-Effect Level
Occupational Exposure
Skin
Skin Absorption
Urine
Workers
BLOOD
Blood Circulation
Carotenoids
Diet
Fingers
Fruit
Medical Devices
Pressure
Self-Assessment
Skin
Skin Absorption
Sodium Chloride, Dietary
Spectrum Analysis, Raman
Vegetables
Vibration
PB (99.4%) was purchased from Fisher Scientific (Hanover Park, IL), and permethrin (PER) (98.3% mixture of 27.2% cis and 71.1% trans isomers) was purchased from Sigma Aldrich (St. Louis, MO). As there is no information currently available on the exact cis/trans ratio of PER that was used in the 1990–1991 Gulf War, we used this commercially available ratio since it was similar to that recommended by the World Health Organization (25% cis and 75% trans; WHO, 2009 ). We used 0.7 mg/kg of PB and 200 mg/kg of PER doses that have been used in previous mouse studies showing adverse behavioral or pathological outcomes (Gillette and Bloomquist, 2003 (link); Abdullah et al., 2011 (link); Ojo et al., 2013 (link); Zakirova et al., 2015 (link)).
We acknowledge the limitations of this animal model of GW agent exposure, specifically, the route of administration of GW agents, PB and PER, via intraperitoneal administration. Given that, clinical literature on GWI reports that PB was taken orally by GWVs, and that PER exposure likely occurred through inhalation and/or through skin exposure. However, we would like to reiterate that this work was an extension of our previously published model. A daily consumption of 120 mg of PB for an average weight of 75 kg per individual would approximate 1.6 mg/kg. This higher dose range has been shown to inhibit AChE and activate pathways involved in long-term memory retention (Friedman et al., 1996 (link); Vythilingam et al., 2005 (link)). However, for our current studies the dose of PB was systematically scaled down from 2 to 0.7 mg/kg in the C57BL6/J mice as higher dose(s) of PB caused insurmountable death in these mice (Dr. Ait-Ghezala, pers. comm.), this is due to the fact that the C57BL6/J mouse strain is known to exhibit cholinergic deficits (Schwab et al., 1990a (link),b (link)). PER was provided to enlisted personnel as 0.5% spray, and its usage far exceeded that recommended on the PER label (Binns et al., 2008 ). Given the paucity of information on doses and routes (i.e., inhaled, skin absorption) of PER delivery, there is no accurate way of estimating the exact dose of PER exposure to GW veterans. Thus, we used 200 mg/kg of PER to mimic a high-level exposure that is similar to doses administered to mice in previous studies showing adverse behavioral or pathological outcomes (Pittman et al., 2003 (link); Dodd and Klein, 2009 (link)). While we agree that investigation into the effects of different doses of GW agents in different preclinical models is critical in order to fully capture the heterogeneity of exposure and to recapitulate the clinical presentation seen in veterans with GWI, the doses for PB and PER used in this study are approximately less than one fifth and less than half of the reported LD50 dose for mice, respectively (Williamson et al., 1989 (link); Chaney et al., 2002 (link))and are therefore relevant to modeling GWI disease pathophysiology.
We acknowledge the limitations of this animal model of GW agent exposure, specifically, the route of administration of GW agents, PB and PER, via intraperitoneal administration. Given that, clinical literature on GWI reports that PB was taken orally by GWVs, and that PER exposure likely occurred through inhalation and/or through skin exposure. However, we would like to reiterate that this work was an extension of our previously published model. A daily consumption of 120 mg of PB for an average weight of 75 kg per individual would approximate 1.6 mg/kg. This higher dose range has been shown to inhibit AChE and activate pathways involved in long-term memory retention (Friedman et al., 1996 (link); Vythilingam et al., 2005 (link)). However, for our current studies the dose of PB was systematically scaled down from 2 to 0.7 mg/kg in the C57BL6/J mice as higher dose(s) of PB caused insurmountable death in these mice (Dr. Ait-Ghezala, pers. comm.), this is due to the fact that the C57BL6/J mouse strain is known to exhibit cholinergic deficits (Schwab et al., 1990a (link),b (link)). PER was provided to enlisted personnel as 0.5% spray, and its usage far exceeded that recommended on the PER label (Binns et al., 2008 ). Given the paucity of information on doses and routes (i.e., inhaled, skin absorption) of PER delivery, there is no accurate way of estimating the exact dose of PER exposure to GW veterans. Thus, we used 200 mg/kg of PER to mimic a high-level exposure that is similar to doses administered to mice in previous studies showing adverse behavioral or pathological outcomes (Pittman et al., 2003 (link); Dodd and Klein, 2009 (link)). While we agree that investigation into the effects of different doses of GW agents in different preclinical models is critical in order to fully capture the heterogeneity of exposure and to recapitulate the clinical presentation seen in veterans with GWI, the doses for PB and PER used in this study are approximately less than one fifth and less than half of the reported LD50 dose for mice, respectively (Williamson et al., 1989 (link); Chaney et al., 2002 (link))and are therefore relevant to modeling GWI disease pathophysiology.
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Animal Model
Cardiac Arrest
Cholinergic Agents
Genetic Heterogeneity
Injections, Intraperitoneal
Isomerism
Memory, Long-Term
Mice, House
Obstetric Delivery
Pain
Permethrin
Permethrin, (cis)-Isomer
Retention (Psychology)
Skin
Skin Absorption
SOCS2 protein, human
Strains
Veterans
Vision
The ex vivo permeation of ATR from different preparations was determined using previously described diffusion cells [29 (link)]. The skin membranes were mounted in the diffusion cell, where the stratum corneum side faced the donor (drug-loaded system) and the dermal side faced the receptor compartment which contained 100 mL phosphate buffer (pH 7.4) and 0.02% sodium azide at 37 ± 0.5 °C. Then, 0.2 g of each tested formulations were placed separately into membrane holders and fixed to the glass tubes; skin membranes were used to cover the preparations with the stratum corneum side face. The tubes were attached to the dissolution apparatus with Parafilm (Bemis, Oshkosh, WI, USA) to avoid water evaporation, then they were allowed to stir at 100 rpm. At 0.5, 1, 2, 3, 4, 5, and 6 h after starting the experiment, 1 mL aliquots were sampled from the receptor compartment with the fresh buffer replacement. Samples were analyzed spectrophotometrically (Jenway 6305 spectrophotometer, Jenway, Staffordshire, UK) at 241 nm. Samples collected from permeation of drug-free systems were used as a blank [30 ]. Ex vivo permeation parameters including steady state transdermal flux (SSTF), lag time, and enhancement ratio (ER) for percutaneous absorption of ATR across rat skin were estimated for different formulations.
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Buffers
Cells
Diffusion
Face
Phosphates
Skin
Skin Absorption
Sodium Azide
Tissue, Membrane
Tissue Donors
HMMs are introduced into the body by various pathways, with ingestion—the most frequent route of water consumption—as a common pathway resulting from oral human exposure. The CDI quantifies the extent of pollution absorbed by the human body and specifies the pollutant dosage per kilogram of body weight per day as received by direct eating, dermal absorption, or inhalation, as suggested by the USEPA. The CDI of water ingestion can be calculated using Equation (5) [35 (link)]:
where CDIin is the exposure doses from ingestion of water in gram/kilogram-day and Ci is the mean concentration of the ith HMM in water (micrograms/liter) [36 (link)]. Additional amounts and units of other parameters in the computation of CDI are presented inTable 3 .
The relevant RfD was compared to the exposure or mean intake of hazardous elements to determine the probability on noncarcinogenic substances. The noncancer risk was quantified using the hazard quotient (HQ) for a single chemical or the hazard index (HI) for multiple substances and exposure routes. Concerns about possible noncarcinogenic consequences may arise if exposure to a chemical exceeds the corresponding RfD, i.e., if HQ exceeds 1 [43 (link)] as shown as Equation (6).
Table 4 presents the toxicity reactions of HMMs for RfD values for both oral and dermal exposure route as well as the oral slope factor (SF).
The total potential for non-CRs influenced by calculating chemicals can be evaluated by the HI, which is the sum of each computed HQ. Equation (7) displays the formula for calculating the hazard index.
It is recommended to have even greater probabilities of harmful health effects when the HI is greater than 1. At the same time, no chronic risks were expected to transpire at the site when HI was less than 1 [48 (link)].
The USEPA defined CRs as the cumulative risk of a person developing cancer because of exposure to a probable cancer-causing agent. The cancer risk was calculated by Equation (8):
The total cancer risk (TCR) is the sum of the cancer risks due to the ingestion exposures to multiple HMMs of concern. The TCR can be evaluated through Equation (9), and the risk value levels are shown inTable 5 .
where CDIin is the exposure doses from ingestion of water in gram/kilogram-day and Ci is the mean concentration of the ith HMM in water (micrograms/liter) [36 (link)]. Additional amounts and units of other parameters in the computation of CDI are presented in
The relevant RfD was compared to the exposure or mean intake of hazardous elements to determine the probability on noncarcinogenic substances. The noncancer risk was quantified using the hazard quotient (HQ) for a single chemical or the hazard index (HI) for multiple substances and exposure routes. Concerns about possible noncarcinogenic consequences may arise if exposure to a chemical exceeds the corresponding RfD, i.e., if HQ exceeds 1 [43 (link)] as shown as Equation (6).
The total potential for non-CRs influenced by calculating chemicals can be evaluated by the HI, which is the sum of each computed HQ. Equation (7) displays the formula for calculating the hazard index.
It is recommended to have even greater probabilities of harmful health effects when the HI is greater than 1. At the same time, no chronic risks were expected to transpire at the site when HI was less than 1 [48 (link)].
The USEPA defined CRs as the cumulative risk of a person developing cancer because of exposure to a probable cancer-causing agent. The cancer risk was calculated by Equation (8):
The total cancer risk (TCR) is the sum of the cancer risks due to the ingestion exposures to multiple HMMs of concern. The TCR can be evaluated through Equation (9), and the risk value levels are shown in
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Body Weight
Environmental Pollutants
Hazardous Chemicals
Hazardous Substances
Homo sapiens
Human Body
Hypertelorism, Severe, With Midface Prominence, Myopia, Mental Retardation, And Bone Fragility
Inhalation
Malignant Neoplasms
Skin
Skin Absorption
Water Consumption
Most recents protocols related to «Skin Absorption»
Daily intake
(EDI) of plasticizers via dust ingestion or dermal contact was determined
using the following equations29 (link),45 (link) where EDI is the estimated daily intake (ng/kg body weight/day), C is the concentration of a chemical in house dust (ng/g),
IEF is the indoor exposure fraction (hours spent over a day in homes),
DIR is the dust ingestion rate (g/day), BW is body weight (kg), BSA
is body surface area (cm2/day), SAS is the amount of solid
particles adhered onto skin (mg/cm2), and FA is the fraction
of a chemical absorbed through the skin. We assumed a 100% absorption
of chemicals from ingested dust. Due to the lack of experimental and
model data of skin absorption of NPPs, the skin absorption fraction
of NPPs was assumed to be 0.000031 (low exposure) or 0.01025 (high
exposure) according to the experimental data of PAEs (0.000031–0.01025).46 (link) Other parameters included in the equations are
summarized inTable S3 .
The hazard
quotient (HQ) was determined to assess human exposure risks via dust
ingestion and dermal absorption. Only chemicals with a DF of >70%
in at least four of the five regions were included for HQ estimation47 where RfD
represents the reference dose of a target chemical. For an analyte
without an appropriate RfD, its nonobserved-adverse-effect-level
(NOAEL) or lethal dose (LD50) adjusted with an uncertainty
factor was applied (Table S4 ). A hazard
index (HI) was also calculated by summing the HQs for individual analytes.
For a target analyte with a detection frequency (DF) > 70%,
an
LOQ/√2 was assigned to any measurements below the LOQ for statistical
analysis. Statistical analyses and data visualization were conducted
using Origin version 9.0 or PASW Statistics 18.0. Differences among
chemical groups or regions were determined using a Kruskal–Wallis
analyses of variance (ANOVA) followed by a Mann–Whitney test.
Spearman’s correlation analyses were used to determine the
relationships between individual plasticizers in house dust. The level
of significance was set at α = 0.05.
(EDI) of plasticizers via dust ingestion or dermal contact was determined
using the following equations29 (link),45 (link) where EDI is the estimated daily intake (ng/kg body weight/day), C is the concentration of a chemical in house dust (ng/g),
IEF is the indoor exposure fraction (hours spent over a day in homes),
DIR is the dust ingestion rate (g/day), BW is body weight (kg), BSA
is body surface area (cm2/day), SAS is the amount of solid
particles adhered onto skin (mg/cm2), and FA is the fraction
of a chemical absorbed through the skin. We assumed a 100% absorption
of chemicals from ingested dust. Due to the lack of experimental and
model data of skin absorption of NPPs, the skin absorption fraction
of NPPs was assumed to be 0.000031 (low exposure) or 0.01025 (high
exposure) according to the experimental data of PAEs (0.000031–0.01025).46 (link) Other parameters included in the equations are
summarized in
The hazard
quotient (HQ) was determined to assess human exposure risks via dust
ingestion and dermal absorption. Only chemicals with a DF of >70%
in at least four of the five regions were included for HQ estimation47 where RfD
represents the reference dose of a target chemical. For an analyte
without an appropriate RfD, its nonobserved-adverse-effect-level
(NOAEL) or lethal dose (LD50) adjusted with an uncertainty
factor was applied (
index (HI) was also calculated by summing the HQs for individual analytes.
For a target analyte with a detection frequency (DF) > 70%,
an
LOQ/√2 was assigned to any measurements below the LOQ for statistical
analysis. Statistical analyses and data visualization were conducted
using Origin version 9.0 or PASW Statistics 18.0. Differences among
chemical groups or regions were determined using a Kruskal–Wallis
analyses of variance (ANOVA) followed by a Mann–Whitney test.
Spearman’s correlation analyses were used to determine the
relationships between individual plasticizers in house dust. The level
of significance was set at α = 0.05.
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Body Surface Area
Body Weight
Homo sapiens
House Dust
Nandrolone
neuro-oncological ventral antigen 2, human
No-Observed-Adverse-Effect Level
phenyl-2-aminoethyl sulfide
Plasticizers
Skin
Skin Absorption
Validation was conducted using in silico data generated with Monte-Carlo Extreme (MCX) in an adult head model at various skin and brain oxygen saturations (Fang and Boas, 2009 (link); Yan and Fang, 2020 (link)). Using in silico data allows for direct comparison of the results of the algorithm with the “ground truth” inputted parameters while maintaining realistic geometry and optical properties. To better mimic experimental conditions, we segmented an MRI of an adult head into four tissue types: scalp, skull, cerebrospinal fluid (CSF), and brain using 3DSlicer (Kikinis et al., 2014 (link)). Brain and scalp oxygen saturations were varied independently from 40 to 80% and 50 to 70%, respectively, in 2% increments. The wide range of scalp oxygen saturations were simulated to investigate the confounding effects of changing scalp SO2 on the accuracy of estimating brain SO2. 126 simulations were conducted for each brain-skin pair, corresponding to the wavelength range of 680 to 930 nm, in 2 nm increments. In total, we completed 8,316 simulations for this validation. The source was positioned on the right side of the head with the detectors placed 2 and 3 cm toward the forehead, as shown in Figure 3 . Each simulation had a total of 3 billion photons with random seeds, ensuring realistic photon statistics with high SNR at both detectors. The optical properties of bone and CSF, the scattering coefficient, anisotropy factor, and refractive indices of the skin and brain, were obtained from literature (Firbank et al., 1993 (link); Jacques, 2013 (link)). Absorption coefficients of skin and brain were computed using Eq. 2 for each oxygen saturation in the aforementioned range. Total hemoglobin in the skin and brain were set to 12.4 and 55 μMol, respectively, for all the simulations (Luttkus et al., 1995 (link); Kanti et al., 2014 (link); Auger et al., 2016 (link); Farzam et al., 2017 (link)).
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Adult
Anisotropy
Boa
Bones
Brain
Cerebrospinal Fluid
Cranium
Forehead
Head
Hemoglobin
Histocompatibility Testing
Oxygen Saturation
Plant Embryos
Scalp
Skin
Skin Absorption
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Absence of Tibia
Body Weight
carboxyaminoimidazole ribotide
Environmental Pollutants
Health Risk Assessment
Homo sapiens
Inhalation
Inhalation Exposure
Malignant Neoplasms
Permeability
Respiratory Rate
Risk Management
Skin
Skin Absorption
The health risk assessment of the investigated phthalate esters based on systemic exposure was performed. The non-cancer risk assessment was expressed as the margin of safety (MOS) according to the following equation:
where NOAEL is the no observed adverse effect level and SED is the systemic exposure dose. The NOAEL values of the investigated phthalates were identified in various studies such as ref. [20 ,21 ,22 (link),23 (link),24 (link)]. MOS values greater than 100 are known to be safe and values below 100 indicate a possibility of causing health risk to consumers.
Additionally, SED (systemic exposure dose) (mg/kg/day) was calculated using the following equation [25 (link)]:
where A is the cosmetic usage per day (g/day), C (%) is concentration of phthalate esters in perfumes determined by GC-MS, D (%) is the dermal absorption rate and BW is the body weight (kg). The consumption use of perfumes per day is 0.75 [26 (link)]. SED values were calculated using the average detected concentrations, and the maximum concentrations as well, in order to represent the worst-case exposure scenario. The dermal absorption rates of the investigated phthalate esters were 5%, except for DBP, which was 10% [26 (link)]. The average body weight of Saudi males was 67.4 kg and the average body weight for Saudi females was 61.9 kg [27 ].
The carcinogenic risk for DEHP was expressed as lifetime cancer risk (LCR) according to the following equation:
where human T25 (HT25) is a toxicity value that relates to a chronic dose which causes tumors at a specific tissue region in 25% of experimental animals, after correcting the rate using spontaneous carcinogenesis factor [28 (link)]. The HT25 value for DEHP determined in other studies was 95.73 [26 (link),29 (link)]. LCR values of ≤ 10−5 indicate safety [25 (link),30 (link),31 ]. As a result, any value greater than 10−5 indicates that there is some carcinogenic risk to human health [25 (link)].
where NOAEL is the no observed adverse effect level and SED is the systemic exposure dose. The NOAEL values of the investigated phthalates were identified in various studies such as ref. [20 ,21 ,22 (link),23 (link),24 (link)]. MOS values greater than 100 are known to be safe and values below 100 indicate a possibility of causing health risk to consumers.
Additionally, SED (systemic exposure dose) (mg/kg/day) was calculated using the following equation [25 (link)]:
where A is the cosmetic usage per day (g/day), C (%) is concentration of phthalate esters in perfumes determined by GC-MS, D (%) is the dermal absorption rate and BW is the body weight (kg). The consumption use of perfumes per day is 0.75 [26 (link)]. SED values were calculated using the average detected concentrations, and the maximum concentrations as well, in order to represent the worst-case exposure scenario. The dermal absorption rates of the investigated phthalate esters were 5%, except for DBP, which was 10% [26 (link)]. The average body weight of Saudi males was 67.4 kg and the average body weight for Saudi females was 61.9 kg [27 ].
The carcinogenic risk for DEHP was expressed as lifetime cancer risk (LCR) according to the following equation:
where human T25 (HT25) is a toxicity value that relates to a chronic dose which causes tumors at a specific tissue region in 25% of experimental animals, after correcting the rate using spontaneous carcinogenesis factor [28 (link)]. The HT25 value for DEHP determined in other studies was 95.73 [26 (link),29 (link)]. LCR values of ≤ 10−5 indicate safety [25 (link),30 (link),31 ]. As a result, any value greater than 10−5 indicates that there is some carcinogenic risk to human health [25 (link)].
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Animals, Laboratory
Body Weight
Carcinogenesis
Carcinogens
Diethylhexyl Phthalate
Esters
Females
Gas Chromatography-Mass Spectrometry
Health Risk Assessment
Homo sapiens
Males
Malignant Neoplasms
Neoplasms
No-Observed-Adverse-Effect Level
phthalate
Safety
Skin Absorption
Tissues
The human health risk of the heavy metals was assessed using the method recommended by the U.S. Environmental Protection Agency. Non-carcinogenic risk (NCR) and carcinogenic risk (CR) were considered with this method. Human exposure to metals can occur through three main pathways: (i) oral ingestion via the mouth, (ii) inhalation via the nose and (iii) dermal absorption via the skin. Among these routes, only the ingestion route, which is usually significant, was considered in the current study in both the NCR and CR assessments. To assess the CR and NCR from ingesting soil in children and adults, the average daily exposure dose via ingestion (ADDing) of heavy metals was measured, following which risk characteristics were evaluated. The non-carcinogenic risk hazard quotient (HQ) and the carcinogenic risk were calculated via reference doses (RfDs) and the cancer slope factor (CSF), respectively. To determine the overall non-carcinogenic risk posed by all the metals, the hazard index (HI) was calculated (Equations (6)–(9)) [74 (link),76 ]:
where C is the mean concentration of the metals in soil (mg/kg); IR is the ingestion rate (100 mg/day for adults and 200 mg/day for children); CF is the conversion factor (10−6, kg/mg); EF is the exposure frequency (350 days/year); ED is the exposure duration (24 years for adults and 6 years for children); BW is the body weight (70 kg for adults and 15 kg for children); AT is the average time (365 × ED days for non-carcinogenic risk and 72 × 365 days for carcinogenic risk); and CSF represents the cancer slope factor (mg/kg.day) [74 (link),76 ].
where C is the mean concentration of the metals in soil (mg/kg); IR is the ingestion rate (100 mg/day for adults and 200 mg/day for children); CF is the conversion factor (10−6, kg/mg); EF is the exposure frequency (350 days/year); ED is the exposure duration (24 years for adults and 6 years for children); BW is the body weight (70 kg for adults and 15 kg for children); AT is the average time (365 × ED days for non-carcinogenic risk and 72 × 365 days for carcinogenic risk); and CSF represents the cancer slope factor (mg/kg.day) [74 (link),76 ].
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Adult
Body Weight
Carcinogens
Child
Health Risk Assessment
Homo sapiens
Inhalation
Limulus clotting factor C
Malignant Neoplasms
Metals
Metals, Heavy
Nose
Oral Cavity
Skin Absorption
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