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DABT 2025 > Skin Toxicity > Flashcards

Skin Toxicity Flashcards

(61 cards)

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1
Q

What are common toxic agents for skin toxicity?

A

Urushiol (poison ivy), nickel, chromium, formaldehyde, toluene diisocyanate, TCDD, arsenic, UV radiation, coal tar, psoralens.

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2
Q

What is the mechanism of urushiol-induced skin toxicity?

A

Forms haptens, triggers allergic contact dermatitis via immune response.

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3
Q

What is the mechanism of TCDD-induced skin toxicity?

A

Activates AhR, causing chloracne through altered keratinocyte differentiation.

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4
Q

What is the mechanism of UV radiation skin toxicity?

A

Generates ROS, causes DNA damage, leading to skin cancer.

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5
Q

What are biomarkers for skin toxicity?

A

Erythema, edema, vesiculation, scaling, histopathological lesions.

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6
Q

What are testing methods for skin toxicity?

A

Draize test, Buehler test, local lymph node assay (LLNA), HRIPT, 3T3 neutral red assay.

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7
Q

What are endpoints for skin toxicity?

A

Dermatitis (irritant/allergic), chemical burns, photosensitivity, skin cancer (e.g., melanoma).

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8
Q

How does nickel cause skin toxicity?

A

Induces allergic contact dermatitis via T-cell activation.

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9
Q

What is the role of arsenic in skin toxicity?

A

Causes hyperkeratosis and pigmentation changes via endothelial damage.

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10
Q

How is formaldehyde toxic to the skin?

A

Acts as a sensitizer, causing irritant and allergic dermatitis.

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11
Q

What factors are critical when designing a study to assess skin irritation? (Domain I.A)

A

Study design for skin irritation includes dose/concentration, exposure duration, and endpoints like erythema or edema. Use OECD Test No. 404 (in vivo) or 439 (in vitro, RhE) with GLP compliance and 3Rs principles to select appropriate models (e.g., reconstructed human epidermis) (ABT Handbook, Domain I.A; Web: OECD, 2024).

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12
Q

How does formaldehyde cause skin sensitization, and what molecular pathways are involved? (Domain II)

A

Formaldehyde acts as a hapten, binding skin proteins to trigger T-cell activation via the NLRP3 inflammasome pathway, leading to allergic contact dermatitis (ACD) (ABT Handbook, Domain II.C; Document: Skin Tox Tab; Web: NIH, 2025).

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13
Q

What endpoints are used to identify skin hazards in acute dermal toxicity studies? (Domain III.A)

A

Endpoints include erythema, edema, necrosis, and corrosion, assessed per OECD Test No. 402. These indicate local effects for chemicals like sodium hydroxide (ABT Handbook, Domain III.A; Web: EPA, 2023).

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14
Q

How is occupational exposure to benzene assessed for skin irritation? (Domain III.B)

A

Exposure is measured via air sampling (ppm) and skin patch testing for benzene, with biomonitoring for urinary metabolites (e.g., phenol) to correlate with irritation (ABT Handbook, Domain III.B; Web: ATSDR, 2024).

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15
Q

How does nickel’s mode of action lead to skin sensitization? (Domain II)

A

Nickel ions bind to skin proteins, activating dendritic cells and T-cells via TLR4 signaling, causing ACD. This involves direct hapten-mediated immune responses (ABT Handbook, Domain II.D; Document: Skin Tox Tab; Web: PubMed, 2024).

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16
Q

How are in vitro models used to study skin corrosion? (Domain I.B)

A

In vitro models like RhE (OECD Test No. 431) measure cell viability after chemical exposure to assess corrosion, ensuring GLP compliance and reducing animal use (ABT Handbook, Domain I.B; Web: OECD, 2024).

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17
Q

What susceptibility factors influence UV radiation-induced skin damage? (Domain II)

A

Susceptibility factors include skin phototype (e.g., Fitzpatrick scale), genetic polymorphisms (e.g., MC1R), and chronic exposure, increasing photocarcinogenesis risk (ABT Handbook, Domain II.C; Document: Skin Tox Tab; Web: NIH, 2025).

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18
Q

How is dose-response assessment applied to corticosteroid-induced skin atrophy? (Domain III.C)

A

Dose-response assessment quantifies skin thinning with corticosteroid dose, using threshold models. BMD and NOAEL establish safe topical doses (ABT Handbook, Domain III.C; Document: Skin Tox Tab; Web: FDA, 2024).

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19
Q

How are skin risks from isothiazolinones characterized in risk assessment? (Domain III.D)

A

Risks (e.g., ACD from methylisothiazolinone) are characterized using hazard quotients (HQ) and margins of exposure (MOE), integrating animal and human patch test data (ABT Handbook, Domain III.D; Web: ECHA, 2024).

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20
Q

How does applied toxicology address public health concerns from skin sensitizers? (Domain IV)

A

Applied toxicology evaluates sensitizers (e.g., fragrance allergens) via biomonitoring and epidemiology, developing exposure limits and labeling for consumer safety (ABT Handbook, Domain IV.A; Web: CDC, 2024).

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21
Q

How is the Local Lymph Node Assay (LLNA) designed to comply with regulations? (Domain I.A)

A

The LLNA (OECD Test No. 429) assesses skin sensitization in mice, measuring lymph node proliferation. It complies with GLP and ICH S8 guidelines for immunotoxicity (ABT Handbook, Domain I.A; Web: OECD, 2024).

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22
Q

What mechanistic role does oxidative stress play in arsenic-induced skin toxicity? (Domain II)

A

Arsenic generates ROS, causing keratinocyte apoptosis and hyperkeratosis via MAPK signaling, leading to skin lesions (ABT Handbook, Domain II.A; Document: Skin Tox Tab; Web: ATSDR, 2024).

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23
Q

How are skin endpoints interpreted in repeat-dose dermal studies? (Domain I.C)

A

Endpoints like epidermal hyperplasia or dermatitis are analyzed via histopathology and clinical scores, integrating with systemic data to assess target organ effects (ABT Handbook, Domain I.C; Web: NIH, 2025).

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24
Q

What biomarkers assess skin exposure to mercury? (Domain III.B)

A

Biomarkers include mercury levels in skin biopsies or sweat, correlating with hyperpigmentation or dermatitis, ensuring accurate exposure assessment (ABT Handbook, Domain III.B; Document: Skin Tox Tab; Web: EPA, 2023).

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25
How does paraphenylenediamine (PPD) cause skin sensitization, and what is its AOP? (Domain II)
PPD forms haptens with skin proteins, activating dendritic cells via Nrf2/Keap1 pathways, leading to ACD. The AOP involves immune cell activation and cytokine release (ABT Handbook, Domain II.D; Document: Skin Tox Tab; Web: PubMed, 2024).
26
How are in silico methods used to predict skin sensitization? (Domain I.B)
QSAR models predict skin sensitization by analyzing chemical structures (e.g., TIMES-SS), guiding study design and reducing animal testing (ABT Handbook, Domain I.B; Web: ECHA, 2024).
27
What genetic factors influence susceptibility to chromium-induced ACD? (Domain II)
Polymorphisms in HLA genes increase susceptibility to chromium’s hapten-mediated ACD, enhancing T-cell responses (ABT Handbook, Domain II.C; Document: Skin Tox Tab; Web: NIH, 2025).
28
How is the benchmark dose (BMD) applied to formaldehyde’s skin effects? (Domain III.C)
BMD models erythema from formaldehyde exposure, establishing a POD for safe exposure levels, adjusted for human variability (ABT Handbook, Domain III.C; Document: Skin Tox Tab; Web: EPA, 2023).
29
How does weight of evidence (WoE) integrate data for skin risk characterization? (Domain III.D)
WoE integrates LLNA, in vitro (e.g., h-CLAT), and human patch test data, using Bradford Hill criteria to assess causation for sensitizers like nickel (ABT Handbook, Domain III.D; Web: ECHA, 2024).
30
How does applied toxicology evaluate skin risks from environmental pollutants? (Domain IV)
Ecotoxicological studies assess pollutants (e.g., PAHs) for skin damage, developing health-based guidance values (e.g., EPA AEGLs) for public protection (ABT Handbook, Domain IV.A; Web: ATSDR, 2024).
31
What statistical methods analyze skin toxicity study results? (Domain I.C)
ANOVA compares erythema scores, and logistic regression models dose-response for skin irritation, ensuring robust interpretation (ABT Handbook, Domain I.C; Web: PubMed, 2024).
32
How does cobalt’s mechanism lead to skin sensitization? (Domain II)
Cobalt ions bind skin proteins, activating T-cells via NF-κB pathways, causing ACD with direct immune activation (ABT Handbook, Domain II.A; Document: Skin Tox Tab; Web: NIH, 2025).
33
How are skin hazards from pesticides identified in regulatory studies? (Domain III.A)
Pesticide hazards (e.g., dermatitis) are identified via OECD Test No. 404 or in vitro RhE assays, focusing on local and systemic effects (ABT Handbook, Domain III.A; Web: EPA, 2023).
34
What exposure metrics assess UV radiation’s skin effects? (Domain III.B)
UV dose (J/m²) and exposure duration are measured via dosimeters, correlating with erythema or photocarcinogenesis risk (ABT Handbook, Domain III.B; Web: NIH, 2025).
35
How does hydroquinone’s toxicity affect skin melanocytes mechanistically? (Domain II)
Hydroquinone inhibits tyrosinase, disrupting melanin synthesis and causing depigmentation via oxidative stress in melanocytes (ABT Handbook, Domain II.E; Document: Skin Tox Tab; Web: FDA, 2024).
36
How are alternative testing methods validated for skin sensitization? (Domain I.A)
Methods like h-CLAT (OECD Test No. 442E) are validated for specificity and sensitivity against LLNA data, ensuring reliable sensitization predictions (ABT Handbook, Domain I.A; Web: OECD, 2024).
37
What role do species differences play in mercury’s skin toxicity? (Domain II)
Species differences in skin permeability and metabolism affect mercury’s dermal toxicity, with humans more prone to hyperpigmentation due to slower clearance (ABT Handbook, Domain II.B; Document: Skin Tox Tab; Web: ATSDR, 2024).
38
How is the margin of safety (MOS) calculated for retinoid-induced skin irritation? (Domain III.D)
MOS is the ratio of NOAEL (from animal irritation studies) to human exposure levels, ensuring safe topical retinoid use (ABT Handbook, Domain III.D; Web: FDA, 2024).
39
How does applied toxicology address skin risks in occupational settings? (Domain IV)
Exposure limits (e.g., OSHA PELs) and PPE (e.g., gloves) mitigate skin irritation from chemicals like solvents in workplaces (ABT Handbook, Domain IV.C; Web: CDC, 2024).
40
What is the role of skin barrier function in reducing toxicity? (Domain II)
The stratum corneum limits xenobiotic penetration, reducing toxicity from agents like arsenic, though disruption (e.g., by solvents) increases risk (ABT Handbook, Domain II.A; Document: Skin Tox Tab; Web: PubMed, 2024).
41
How are skin study results communicated to regulatory bodies? (Domain I.C)
Results are reported in OECD-compliant formats, with tabular data (e.g., erythema scores) and narratives for EPA or ECHA submissions (ABT Handbook, Domain I.C; Web: ECHA, 2024).
42
How does TCDD’s mechanism cause chloracne? (Domain II)
TCDD activates the AhR pathway, altering keratinocyte differentiation and causing chloracne with hyperkeratosis (ABT Handbook, Domain II.E; Document: Skin Tox Tab; Web: ATSDR, 2024).
43
What ecotoxicological endpoints are relevant for skin toxicity? (Domain III.A)
Endpoints include amphibian skin lesions from pollutants (e.g., pesticides), assessed via OECD Test No. 202, indicating environmental dermal hazards (ABT Handbook, Domain III.A; Web: OECD, 2024).
44
How is internal skin exposure to cadmium measured? (Domain III.B)
Cadmium levels in skin tissue are measured via ICP-MS, correlating with dermatitis or hyperpigmentation risk (ABT Handbook, Domain III.B; Document: Skin Tox Tab; Web: EPA, 2023).
45
How does SLS’s toxicity affect skin barrier function? (Domain II)
Sodium lauryl sulfate (SLS) disrupts lipid bilayers in the stratum corneum, increasing permeability and causing irritation via direct cytotoxicity (ABT Handbook, Domain II.A; Document: Skin Tox Tab; Web: PubMed, 2024).
46
How is the therapeutic index (TI) used for topical corticosteroid effects? (Domain III.C)
TI compares therapeutic doses to those causing skin atrophy, ensuring safe use with minimal dermal side effects (ABT Handbook, Domain III.C; Web: FDA, 2024).
47
How does applied toxicology mitigate skin risks from consumer products? (Domain IV)
Ingredient testing (e.g., parabens) for irritation and labeling requirements reduce consumer exposure risks (ABT Handbook, Domain IV.C; Web: ECHA, 2024).
48
What are the limitations of in vitro skin toxicity assays? (Domain I.B)
In vitro assays (e.g., RhE) lack systemic metabolism and immune responses, limiting extrapolation to in vivo sensitization effects (ABT Handbook, Domain I.B; Web: OECD, 2024).
49
How does benzophenone’s skin toxicity inform risk assessment? (Domain III.D)
Benzophenone’s photoallergic potential is assessed via dose-response models, integrating patch test data to set safe exposure thresholds (ABT Handbook, Domain III.D; Document: Skin Tox Tab; Web: FDA, 2024).
50
What is the role of omics in studying skin toxicity mechanisms? (Domain II)
Proteomics identifies pathways (e.g., cytokine signaling) in ACD from sensitizers like PPD, informing mechanistic hypotheses (ABT Handbook, Domain II.F; Web: PubMed, 2024).
51
How are skin effects of air pollutants assessed in epidemiological studies? (Domain IV)
Studies (e.g., NHANES) correlate PM2.5 exposure with dermatitis, using biomonitoring to assess public health risks (ABT Handbook, Domain IV.E; Web: CDC, 2024).
52
What analytical methods characterize test agents for skin studies? (Domain I.A)
HPLC and GC-MS analyze test agent stability and impurities (e.g., ICH Q3A[R2]) for dermal studies, ensuring accurate dosing (ABT Handbook, Domain I.A; Web: FDA, 2024).
53
How does dinitrochlorobenzene’s mechanism cause ACD? (Domain II)
Dinitrochlorobenzene (DNCB) forms haptens, activating T-cells via NF-κB pathways, leading to ACD with immune-mediated inflammation (ABT Handbook, Domain II.D; Document: Skin Tox Tab; Web: NIH, 2025).
54
What is the role of PBPK modeling in skin dose-response assessment? (Domain III.C)
PBPK models predict dermal absorption of toxicants (e.g., formaldehyde), refining dose-response curves for irritation endpoints (ABT Handbook, Domain III.C; Web: EPA, 2023).
55
How does applied toxicology address emerging skin risks from nanomaterials? (Domain IV)
Nanomaterial (e.g., nanosilver) irritation is evaluated via in vitro and ecotoxicological studies, developing safety standards for cosmetics (ABT Handbook, Domain IV.B; Web: NIH, 2025).
56
How are systemic and local skin effects distinguished in study interpretation? (Domain I.C)
Systemic effects (e.g., mercury’s hyperpigmentation) involve multi-organ toxicity, while local effects (e.g., SLS irritation) are dermal, assessed via specific endpoints (ABT Handbook, Domain I.C; Web: ATSDR, 2024).
57
What factors increase skin susceptibility to PAHs? (Domain II)
Susceptibility factors include skin barrier defects, genetic polymorphisms (e.g., CYP1A1), and occupational exposure, increasing dermatitis risk (ABT Handbook, Domain II.C; Document: Skin Tox Tab; Web: ATSDR, 2024).
58
How is the precautionary principle applied to skin risk management? (Domain III.D)
Conservative exposure limits for sensitizers (e.g., isothiazolinones) are set when data is uncertain, prioritizing safety via product reformulation (ABT Handbook, Domain III.D; Web: ECHA, 2024).
59
What clinical signs indicate skin toxicity in poisoning incidents? (Domain IV)
Signs include erythema, urticaria, or necrosis, guiding treatments (e.g., decontamination for corrosives) based on toxicological mechanisms (ABT Handbook, Domain IV.K; Web: NIH, 2025).
60
How does green chemistry reduce skin toxicity risks in product design? (Domain IV)
Green chemistry minimizes irritants (e.g., phthalates) in cosmetics, using benign-by-design principles to reduce dermal toxicity (ABT Handbook, Domain IV.G; Web: EPA, 2023).
61
What are the regulatory standards for skin toxicity testing? (Domain IV)
REACH and CPSC require skin toxicity testing (e.g., OECD Test No. 439) for chemicals, ensuring safety from irritants and sensitizers (ABT Handbook, Domain IV.L; Web: ECHA, 2024).

DABT 2025 (16 decks)

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