Eye Toxicity Flashcards
(111 cards)
1
Q
What are common toxic agents for eye toxicity?
A
Methanol, chloroquine, UV radiation, lead, corticosteroids, ethambutol, tamoxifen, cisplatin, organophosphates, digoxin.
2
Q
What is the mechanism of methanol-induced eye toxicity?
A
Metabolized to formic acid, disrupts optic nerve metabolism, causing retinal edema and blindness.
3
Q
What is the mechanism of chloroquine-induced eye toxicity?
A
Binds melanin in retina, causes phospholipidosis and retinal degeneration.
4
Q
What is the mechanism of UV radiation eye toxicity?
A
Generates ROS, causes DNA damage in lens epithelial cells, leading to cataracts.
5
Q
What are biomarkers for eye toxicity?
A
Reduced visual acuity, color vision deficits (Ishihara test), abnormal ERG, VEP changes.
6
Q
What are testing methods for eye toxicity?
A
Ophthalmoscopy, slit-lamp examination, fluorescein angiography, electroretinogram (ERG).
7
Q
What are endpoints for eye toxicity?
A
Blindness, retinal degeneration, cataracts, glaucoma, corneal opacity.
8
Q
How do corticosteroids cause eye toxicity?
A
Increase intraocular pressure, leading to glaucoma.
9
Q
What is the role of lead in eye toxicity?
A
Induces retinal apoptosis, contributes to cataracts.
10
Q
How is ethambutol toxic to the eyes?
A
Causes optic neuropathy, leading to visual field loss.
11
Q
What is the primary toxicological concern for the cornea?
A
The cornea is prone to chemical burns, ulceration, and opacification due to its direct exposure to xenobiotics. Alkaline chemicals (e.g., sodium hydroxide) cause severe damage by penetrating deep into tissues, leading to necrosis and potential perforation. Acid burns, while painful, are typically less penetrating. Example: Ammonia exposure can cause corneal clouding (Web: EPA, 2023).
12
Q
Define conjunctival toxicity.
A
Conjunctival toxicity involves inflammation (conjunctivitis) or irritation of the conjunctiva due to chemical exposure. Symptoms include redness, swelling, and discharge. Example: Formaldehyde exposure causes conjunctival irritation, often seen in occupational settings (Web: ATSDR, 2024).
13
Q
What is keratitis?
A
Keratitis is inflammation of the cornea, often resulting from chemical exposure or infection, leading to pain, photophobia, and vision impairment. Toxicants like organic solvents (e.g., methanol) can cause keratitis by disrupting corneal epithelial integrity (Web: NIH, 2025).
14
Q
How do corticosteroids cause ocular toxicity?
A
Corticosteroids (e.g., prednisone) can induce cataracts and glaucoma. Prolonged use increases intraocular pressure (IOP) by altering trabecular meshwork function and can cause posterior subcapsular cataracts due to protein aggregation in the lens (Document: Eye Tab; Web: FDA, 2024).
15
Q
What is the Draize Test?
A
The Draize Test assesses ocular irritation in rabbits by applying chemicals to the eye and scoring effects like redness, swelling, and corneal opacity. It’s widely used but criticized for ethical concerns. Alternatives like in vitro models are now preferred (Document: Principles & Mechanisms; Web: OECD, 2024).
16
Q
How does methanol affect the eye?
A
Methanol toxicity leads to optic neuropathy and retinal damage due to its metabolite, formic acid, which inhibits cytochrome oxidase, causing retinal ganglion cell death and optic disc edema. Symptoms include blurred vision and blindness (Document: Eye Tab; Web: CDC, 2024).
17
Q
How does chloroquine affect the eye?
A
Chloroquine, an antimalarial, causes corneal deposits and retinopathy. It accumulates in the retinal pigment epithelium, leading to a bull’s-eye maculopathy, which can result in irreversible vision loss (Document: Eye Tab; Web: NIH, 2025).
18
Q
What is the mechanism of ethanol-induced ocular toxicity?
A
Ethanol can cause optic neuropathy and corneal damage by disrupting cellular metabolism and generating reactive oxygen species (ROS). Chronic exposure leads to blurred vision and photophobia (Document: Eye Tab; Web: PubMed, 2024).
19
Q
Describe the ocular toxicity of ethylene glycol.
A
Ethylene glycol metabolites (e.g., oxalic acid) form calcium oxalate crystals, which can deposit in the retina, causing retinal edema and vision impairment. It also disrupts retinal metabolism (Document: Eye Tab; Web: ToxNet, 2023).
20
Q
What is the role of the blood-ocular barrier in toxicity?
A
The blood-ocular barrier (similar to the blood-brain barrier) limits xenobiotic entry into the eye. Disruption by toxicants like lead increases retinal exposure, leading to toxicity (Document: Eye Tab; Web: ATSDR, 2024).
21
Q
How does lead affect the eye?
A
Lead causes optic neuropathy and retinal degeneration by disrupting neuronal signaling and generating ROS. Children are more susceptible due to an immature blood-ocular barrier (Document: Eye Tab; Web: EPA, 2023).
22
Q
What ocular effects are associated with organophosphates?
A
Organophosphates (e.g., chlorpyrifos) inhibit acetylcholinesterase, causing miosis (pupil constriction) and blurred vision due to excessive acetylcholine at muscarinic receptors (Document: Eye Tab; Web: NIH, 2025).
23
Q
How does amiodarone cause ocular toxicity?
A
Amiodarone, an antiarrhythmic, causes corneal microdeposits (verticillata) due to its cationic amphiphilic nature, leading to lysosomal accumulation. It rarely affects vision but is a common side effect (Document: Eye Tab; Web: FDA, 2024).
24
Q
What is the significance of retinal pigment epithelium in toxicity?
A
The retinal pigment epithelium (RPE) is critical for retinal function but is a target for toxicants like chloroquine, which accumulate and cause RPE degeneration, leading to retinopathy (Document: Eye Tab; Web: PubMed, 2024).
25
How does digoxin affect the eye?
Digoxin, a cardiac glycoside, causes color vision disturbances (xanthopsia, yellow-tinted vision) by affecting retinal cone function and sodium-potassium ATPase activity (Document: Eye Tab; Web: NIH, 2025).
26
What is the ocular impact of carbon disulfide?
Carbon disulfide, an industrial solvent, causes optic neuropathy and retinal damage by disrupting axonal transport and generating ROS, leading to vision loss (Document: Eye Tab; Web: ATSDR, 2024).
27
How does formaldehyde affect the eye?
Formaldehyde causes conjunctival irritation and lacrimation due to its reactivity with mucosal tissues. Chronic exposure may lead to corneal damage (Document: Eye Tab; Web: EPA, 2023).
28
What is the mechanism of tamoxifen-induced ocular toxicity?
Tamoxifen, an anti-estrogen, causes crystalline retinopathy and corneal opacities by accumulating in the retina and disrupting lipid metabolism (Document: Eye Tab; Web: FDA, 2024).
29
How does UV radiation contribute to ocular toxicity?
UV radiation causes photokeratitis and cataracts by generating ROS, which damage corneal epithelium and lens proteins. Chronic exposure increases cataract risk (Document: Eye Tab; Web: NIH, 2025).
30
What is photokeratitis?
Photokeratitis is a painful corneal condition caused by UV exposure (e.g., from welding arcs), resulting in epithelial damage and inflammation, often resolving within days (Document: Eye Tab; Web: CDC, 2024).
31
How does arsenic affect the eye?
Arsenic causes conjunctivitis and optic neuropathy by generating ROS and disrupting cellular metabolism, leading to vision impairment (Document: Eye Tab; Web: ATSDR, 2024).
32
What ocular effects are seen with mercury exposure?
Mercury causes lens opacities and optic neuropathy due to its accumulation in ocular tissues, disrupting protein structure and neuronal function (Document: Eye Tab; Web: EPA, 2023).
33
How does cisplatin cause ocular toxicity?
Cisplatin, a chemotherapeutic, causes retinal toxicity and optic neuritis by inducing oxidative stress and apoptosis in retinal cells (Document: Eye Tab; Web: PubMed, 2024).
34
What is the role of oxidative stress in ocular toxicity?
Oxidative stress, caused by ROS from toxicants like methanol or UV radiation, damages ocular tissues (cornea, lens, retina) by oxidizing proteins, lipids, and DNA, leading to cataracts and retinopathy (Document: Eye Tab; Web: NIH, 2025).
35
How does ethambutol affect the eye?
Ethambutol, an anti-tuberculosis drug, causes optic neuropathy by chelating zinc, disrupting retinal ganglion cell function, and causing color vision defects (Document: Eye Tab; Web: FDA, 2024).
36
What is the ocular toxicity of isoniazid?
Isoniazid, a tuberculosis drug, causes optic neuritis by depleting vitamin B6, which is essential for retinal health, leading to vision loss if untreated (Document: Eye Tab; Web: NIH, 2025).
37
How does sildenafil affect vision?
Sildenafil, a PDE5 inhibitor, causes transient blue-tinted vision (cyanopsia) by inhibiting PDE6 in retinal photoreceptors, affecting color perception (Document: Eye Tab; Web: FDA, 2024).
38
What is the significance of the lens in ocular toxicity?
The lens is susceptible to opacification (cataracts) from toxicants like corticosteroids or UV radiation, which disrupt protein structure and cause aggregation (Document: Eye Tab; Web: NIH, 2025).
39
How does vincristine cause ocular toxicity?
Vincristine, a chemotherapeutic, causes cranial nerve palsies and optic neuropathy by disrupting microtubule function in neurons, affecting eye movement and vision (Document: Eye Tab; Web: PubMed, 2024).
40
What is the effect of carbon monoxide on the eye?
Carbon monoxide causes retinal hypoxia by binding hemoglobin, reducing oxygen delivery, leading to blurred vision and optic neuropathy (Document: Eye Tab; Web: CDC, 2024).
41
How does acrylamide affect the eye?
Acrylamide causes optic neuropathy by disrupting axonal transport, leading to retinal ganglion cell damage and vision impairment (Document: Eye Tab; Web: ATSDR, 2024).
42
What is the ocular toxicity of quinine?
Quinine causes retinal toxicity (cinchonism), leading to blurred vision, constricted visual fields, and potential blindness due to vascular constriction and photoreceptor damage (Document: Eye Tab; Web: NIH, 2025).
43
How does tobacco smoke affect the eye?
Tobacco smoke causes cataracts and macular degeneration by generating ROS and heavy metals (e.g., cadmium), damaging lens proteins and retinal tissues (Document: Eye Tab; Web: CDC, 2024).
44
What is the role of P-glycoprotein in ocular toxicity?
P-glycoprotein (Pgp) in the blood-ocular barrier effluxes xenobiotics, reducing ocular toxicity. Inhibition (e.g., by cyclosporine) increases toxicant accumulation in the eye (Document: Eye Tab; Web: PubMed, 2024).
45
How does cyclosporine affect the eye?
Cyclosporine, an immunosuppressant, causes conjunctival irritation and optic neuropathy by inhibiting Pgp, increasing xenobiotic accumulation in ocular tissues (Document: Eye Tab; Web: FDA, 2024).
46
What is the ocular impact of cadmium?
Cadmium causes lens opacities and retinal damage by accumulating in ocular tissues, generating ROS, and disrupting cellular homeostasis (Document: Eye Tab; Web: ATSDR, 2024).
47
How does digitalis affect the eye?
Digitalis (digoxin) causes xanthopsia (yellow vision) by inhibiting sodium-potassium ATPase, disrupting retinal cone function (Document: Eye Tab; Web: NIH, 2025).
48
What is the mechanism of benzene-induced ocular toxicity?
Benzene causes retinal damage and optic neuropathy by generating ROS and disrupting hematopoietic cells, affecting retinal blood supply (Document: Eye Tab; Web: EPA, 2023).
49
How does methotrexate affect the eye?
Methotrexate, a chemotherapeutic, causes conjunctivitis and optic neuropathy by inhibiting folate metabolism, leading to cellular damage in ocular tissues (Document: Eye Tab; Web: PubMed, 2024).
50
What is the ocular toxicity of indomethacin?
Indomethacin, an NSAID, causes corneal deposits and retinal toxicity by altering lipid metabolism and inducing oxidative stress (Document: Eye Tab; Web: FDA, 2024).
51
How does chlorpromazine affect the eye?
Chlorpromazine, an antipsychotic, causes corneal and lens opacities due to its cationic amphiphilic nature, leading to lysosomal accumulation and phospholipidosis (Document: Eye Tab; Web: NIH, 2025).
52
What is the effect of aminoglycosides on the eye?
Aminoglycosides (e.g., streptomycin) cause optic neuropathy by disrupting mitochondrial function in retinal ganglion cells, leading to vision loss (Document: Eye Tab; Web: PubMed, 2024).
53
How does toluene affect the eye?
Toluene, a solvent, causes optic neuropathy and color vision defects by disrupting neuronal membranes and generating ROS (Document: Eye Tab; Web: ATSDR, 2024).
54
What is the ocular impact of thallium?
Thallium causes optic neuropathy and vision loss by disrupting mitochondrial function and generating ROS in retinal cells (Document: Eye Tab; Web: EPA, 2023).
55
How does bisphenol A affect the eye?
Bisphenol A, an endocrine disruptor, may cause retinal damage by mimicking estrogen, altering retinal cell signaling, and inducing oxidative stress (Document: Eye Tab; Web: NIH, 2025).
56
What is the role of glutathione in ocular protection?
Glutathione detoxifies ROS in the eye, protecting the cornea, lens, and retina from oxidative damage by toxicants like methanol or UV radiation (Document: Eye Tab; Web: PubMed, 2024).
57
How does phenytoin affect the eye?
Phenytoin, an anticonvulsant, causes nystagmus and diplopia by altering neuronal signaling and affecting extraocular muscle control (Document: Eye Tab; Web: FDA, 2024).
58
What is the ocular toxicity of vigabatrin?
Vigabatrin, an anticonvulsant, causes visual field defects by inhibiting GABA transaminase, leading to retinal toxicity and photoreceptor damage (Document: Eye Tab; Web: NIH, 2025).
59
How does hydroxychloroquine affect the eye?
Hydroxychloroquine causes retinal toxicity (bull’s-eye maculopathy) by accumulating in the retinal pigment epithelium, disrupting lysosomal function (Document: Eye Tab; Web: FDA, 2024).
60
What is the significance of the corneal epithelium in toxicity?
The corneal epithelium is the first barrier to xenobiotics, susceptible to irritation and erosion by chemicals like formaldehyde, leading to keratitis or ulceration (Document: Eye Tab; Web: CDC, 2024).
61
What considerations are critical when designing a study to assess corneal toxicity? (Domain I.A)
When designing a study for corneal toxicity, consider dose/concentration, exposure duration, route (e.g., topical), and endpoints like opacity or ulceration. Select appropriate species (e.g., rabbits for Draize test) and comply with OECD Test No. 437 (BCOP assay) for in vitro alternatives, applying 3Rs principles to reduce animal use (ABT Handbook, Domain I.A; Web: OECD, 2024).
62
How does methanol cause optic neuropathy, and what molecular pathways are involved? (Domain II)
Methanol’s metabolite, formic acid, inhibits cytochrome oxidase, disrupting ATP production in retinal ganglion cells, leading to optic neuropathy. This involves mitochondrial dysfunction and oxidative stress pathways, causing vision loss (ABT Handbook, Domain II.C; Document: Eye Tab; Web: CDC, 2024).
63
What endpoints are used to identify ocular hazards in acute toxicity studies? (Domain III.A)
Ocular hazard endpoints include corneal opacity, conjunctival redness, iritis, and chemosis, measured in acute studies (e.g., OECD Test No. 405). These indicate local effects and guide hazard identification for chemicals like ammonia (ABT Handbook, Domain III.A; Web: NIH, 2025).
64
How is exposure to formaldehyde assessed in occupational settings for ocular irritation? (Domain III.B)
Exposure is assessed via air sampling for formaldehyde concentration (ppm) and biomonitoring for eye irritation (e.g., tear film analysis). Occupational exposure limits (e.g., OSHA PEL) guide risk assessment for conjunctival irritation (ABT Handbook, Domain III.B; Web: ATSDR, 2024).
65
How does chloroquine’s mode of action lead to retinal toxicity? (Domain II)
Chloroquine accumulates in the retinal pigment epithelium, disrupting lysosomal function and lipid metabolism, causing bull’s-eye maculopathy. This involves receptor-level interactions and secondary photoreceptor damage (ABT Handbook, Domain II.D; Document: Eye Tab; Web: FDA, 2024).
66
What is the role of in vitro models in studying corneal toxicity? (Domain I.B)
In vitro models like the BCOP assay (OECD Test No. 437) characterize corneal toxicity by measuring opacity and permeability after chemical exposure, ensuring GLP compliance. They reduce animal use and assess endpoints like epithelial damage (ABT Handbook, Domain I.B; Web: OECD, 2024).
67
How does UV radiation contribute to cataracts, and what are the susceptibility factors? (Domain II)
UV radiation generates ROS, oxidizing lens proteins and causing cataracts. Susceptibility factors include age, genetic polymorphisms (e.g., GSTM1), and chronic exposure, impacting lens transparency (ABT Handbook, Domain II.C; Document: Eye Tab; Web: NIH, 2025).
68
What is the significance of dose-response assessment in evaluating corticosteroid-induced glaucoma? (Domain III.C)
Dose-response assessment for corticosteroids (e.g., prednisone) quantifies intraocular pressure (IOP) increases with dose, using threshold models. NOAEL and BMD identify safe doses to minimize glaucoma risk (ABT Handbook, Domain III.C; Document: Eye Tab; Web: FDA, 2024).
69
How are ocular risks from organophosphates characterized in risk assessment? (Domain III.D)
Ocular risks (e.g., miosis from chlorpyrifos) are characterized using hazard quotients (HQ) and margins of exposure (MOE), integrating animal data (e.g., pupil constriction) with human exposure levels to inform safety limits (ABT Handbook, Domain III.D; Web: EPA, 2023).
70
How does applied toxicology address public health concerns from ocular irritants? (Domain IV)
Applied toxicology evaluates irritants (e.g., formaldehyde) via biomonitoring and epidemiological studies, developing exposure limits and mitigation strategies (e.g., ventilation) to protect workers and communities (ABT Handbook, Domain IV.A; Web: CDC, 2024).
71
How is the Draize test designed to comply with regulatory guidelines? (Domain I.A)
The Draize test (OECD Test No. 405) assesses ocular irritation in rabbits, scoring corneal opacity, conjunctival redness, and iritis. It complies with GLP and ICH S7A guidelines, ensuring standardized endpoints (ABT Handbook, Domain I.A; Web: OECD, 2024).
72
What mechanistic role does oxidative stress play in ethanol-induced ocular toxicity? (Domain II)
Ethanol generates ROS, damaging corneal epithelium and retinal cells via lipid peroxidation and protein oxidation, leading to blurred vision and photophobia (ABT Handbook, Domain II.A; Document: Eye Tab; Web: PubMed, 2024).
73
How are ocular endpoints interpreted in repeat-dose toxicity studies? (Domain I.C)
Ocular endpoints (e.g., lens opacity, retinal degeneration) are analyzed using histopathology and clinical observations, integrating with systemic data to identify target organ effects and reversibility (ABT Handbook, Domain I.C; Web: NIH, 2025).
74
What biomarkers are used to assess ocular exposure to mercury? (Domain III.B)
Biomarkers include mercury levels in tears or aqueous humor, reflecting exposure and correlating with lens opacities or optic neuropathy. Biomonitoring ensures accurate exposure assessment (ABT Handbook, Domain III.B; Document: Eye Tab; Web: ATSDR, 2024).
75
How does tamoxifen’s toxicity manifest in the retina, and what is its adverse outcome pathway? (Domain II)
Tamoxifen causes crystalline retinopathy by accumulating in retinal lipids, disrupting metabolism. The AOP involves lysosomal dysfunction, leading to photoreceptor damage and vision impairment (ABT Handbook, Domain II.D; Document: Eye Tab; Web: FDA, 2024).
76
How are in silico methods used to predict ocular toxicity? (Domain I.B)
In silico methods like QSAR model chemical structure-activity relationships to predict ocular irritation (e.g., for solvents), reducing reliance on animal testing and guiding study design (ABT Handbook, Domain I.B; Web: EPA, 2023).
77
What genetic factors influence susceptibility to lead-induced optic neuropathy? (Domain II)
Genetic polymorphisms (e.g., ALAD gene variants) increase susceptibility to lead’s neurotoxic effects on the optic nerve, exacerbating ROS-mediated damage (ABT Handbook, Domain II.C; Document: Eye Tab; Web: NIH, 2025).
78
How is the benchmark dose (BMD) applied to ethylene glycol’s ocular effects? (Domain III.C)
BMD models retinal edema from ethylene glycol’s oxalic acid crystals, establishing a point of departure (POD) for safe exposure levels, adjusted for interspecies differences (ABT Handbook, Domain III.C; Document: Eye Tab; Web: ToxNet, 2023).
79
How does weight of evidence (WoE) integrate data for ocular risk characterization? (Domain III.D)
WoE integrates animal (e.g., Draize), in vitro (e.g., BCOP), and epidemiological data to characterize ocular risks, using Bradford Hill criteria to assess causation and inform mitigation (ABT Handbook, Domain III.D; Web: EPA, 2023).
80
How does applied toxicology evaluate ocular risks from environmental pollutants? (Domain IV)
Applied toxicology assesses pollutants (e.g., cadmium) via ecotoxicological studies, identifying retinal damage risks and developing health-based guidance values (e.g., EPA PALs) for public protection (ABT Handbook, Domain IV.A; Web: ATSDR, 2024).
81
What statistical methods are used to analyze ocular toxicity study results? (Domain I.C)
Statistical methods include ANOVA for comparing corneal opacity scores and logistic regression for dose-response modeling, ensuring robust interpretation of ocular endpoints (ABT Handbook, Domain I.C; Web: PubMed, 2024).
82
How does amiodarone’s mechanism lead to corneal microdeposits? (Domain II)
Amiodarone’s cationic amphiphilic structure causes lysosomal accumulation in corneal epithelium, forming microdeposits (verticillata), with minimal visual impact (ABT Handbook, Domain II.A; Document: Eye Tab; Web: FDA, 2024).
83
How are ocular hazards from pesticides identified in regulatory studies? (Domain III.A)
Pesticide ocular hazards (e.g., conjunctivitis) are identified via OECD Test No. 405 or in vitro assays, focusing on local effects and systemic absorption (ABT Handbook, Domain III.A; Web: EPA, 2023).
84
What exposure metrics are used for UV radiation’s ocular effects? (Domain III.B)
Exposure metrics include UV dose (J/m²) and duration, measured via environmental monitoring or personal dosimeters, correlating with photokeratitis risk (ABT Handbook, Domain III.B; Web: NIH, 2025).
85
How does digoxin’s toxicity affect retinal function mechanistically? (Domain II)
Digoxin inhibits sodium-potassium ATPase in retinal cones, disrupting color perception and causing xanthopsia (yellow vision), a direct receptor-level effect (ABT Handbook, Domain II.E; Document: Eye Tab; Web: NIH, 2025).
86
How are alternative testing methods validated for ocular irritation? (Domain I.A)
Alternative methods (e.g., BCOP, EpiOcular) are validated per OECD standards, ensuring specificity, sensitivity, and reproducibility compared to in vivo data (ABT Handbook, Domain I.A; Web: OECD, 2024).
87
What role do species differences play in arsenic’s ocular toxicity? (Domain II)
Species differences in arsenic metabolism (e.g., methylation efficiency) affect conjunctival and optic nerve toxicity, with humans more susceptible due to slower clearance (ABT Handbook, Domain II.B; Document: Eye Tab; Web: ATSDR, 2024).
88
How is the margin of safety (MOS) calculated for cisplatin’s retinal toxicity? (Domain III.D)
MOS is calculated as the ratio of NOAEL (from animal retinal studies) to human exposure levels, ensuring safe chemotherapeutic dosing to minimize optic neuritis (ABT Handbook, Domain III.D; Web: PubMed, 2024).
89
How does applied toxicology address ocular risks in occupational settings? (Domain IV)
Applied toxicology develops exposure limits (e.g., OSHA PELs) and engineering controls (e.g., ventilation) to mitigate ocular irritation from chemicals like toluene in workplaces (ABT Handbook, Domain IV.C; Web: CDC, 2024).
90
What is the role of P-glycoprotein in reducing ocular toxicity? (Domain II)
P-glycoprotein effluxes xenobiotics at the blood-ocular barrier, reducing retinal accumulation of toxicants like cyclosporine, which can otherwise cause optic neuropathy (ABT Handbook, Domain II.A; Document: Eye Tab; Web: PubMed, 2024).
91
How are ocular study results communicated to regulatory bodies? (Domain I.C)
Ocular study results are reported in standardized formats (e.g., OECD templates), including tabular endpoint data (e.g., corneal opacity scores) and narratives for EPA or FDA submissions (ABT Handbook, Domain I.C; Web: EPA, 2023).
92
How does carbon disulfide’s mechanism cause retinal damage? (Domain II)
Carbon disulfide disrupts axonal transport and generates ROS in retinal ganglion cells, causing optic neuropathy and vision loss, a primary toxic effect (ABT Handbook, Domain II.E; Document: Eye Tab; Web: ATSDR, 2024).
93
What ecotoxicological endpoints are relevant for ocular toxicity? (Domain III.A)
Ecotoxicological endpoints include fish corneal damage from pollutants (e.g., cadmium), assessed via OECD Test No. 203, indicating environmental ocular hazards (ABT Handbook, Domain III.A; Web: OECD, 2024).
94
How is internal ocular exposure to lead measured? (Domain III.B)
Internal exposure is measured via lead levels in aqueous humor or retinal tissue, using ICP-MS, correlating with optic neuropathy risk (ABT Handbook, Domain III.B; Document: Eye Tab; Web: EPA, 2023).
95
How does ethambutol’s toxicity affect optic nerve function? (Domain II)
Ethambutol chelates zinc, disrupting retinal ganglion cell function, causing optic neuropathy and color vision defects via mitochondrial pathways (ABT Handbook, Domain II.A; Document: Eye Tab; Web: FDA, 2024).
96
How is the therapeutic index (TI) used for sildenafil’s ocular effects? (Domain III.C)
TI compares sildenafil’s therapeutic dose to the dose causing cyanopsia (blue-tinted vision), ensuring safe PDE5 inhibitor use with minimal retinal impact (ABT Handbook, Domain III.C; Web: FDA, 2024).
97
How does applied toxicology mitigate ocular risks from consumer products? (Domain IV)
Applied toxicology evaluates product ingredients (e.g., bisphenol A) for ocular irritation, using tiered testing and labeling to reduce consumer exposure risks (ABT Handbook, Domain IV.C; Web: NIH, 2025).
98
What are the limitations of in vitro ocular toxicity assays? (Domain I.B)
In vitro assays (e.g., BCOP) lack systemic metabolism and vascular responses, limiting extrapolation to in vivo ocular effects, though they excel in irritation screening (ABT Handbook, Domain I.B; Web: OECD, 2024).
99
How does hydroxychloroquine’s retinal toxicity inform risk assessment? (Domain III.D)
Hydroxychloroquine’s bull’s-eye maculopathy risk is assessed via cumulative dose-response models, integrating clinical data to set safe exposure thresholds (ABT Handbook, Domain III.D; Document: Eye Tab; Web: FDA, 2024).
100
What is the role of omics in studying ocular toxicity mechanisms? (Domain II)
Omics (e.g., proteomics) identifies molecular pathways (e.g., ROS signaling) in corneal or retinal toxicity, informing mechanistic hypotheses for chemicals like methanol (ABT Handbook, Domain II.F; Web: PubMed, 2024).
101
How are ocular effects of tobacco smoke assessed in epidemiological studies? (Domain IV)
Epidemiological studies (e.g., NHANES) correlate tobacco smoke exposure with cataracts and macular degeneration, using biomonitoring data to assess public health risks (ABT Handbook, Domain IV.E; Web: CDC, 2024).
102
What analytical methods characterize test agents for ocular studies? (Domain I.A)
HPLC and MS analyze test agent stability and impurities (e.g., ICH Q3A[R2]) for ocular studies, ensuring accurate dosing for chemicals like formaldehyde (ABT Handbook, Domain I.A; Web: FDA, 2024).
103
How does quinine’s retinal toxicity manifest, and what is its AOP? (Domain II)
Quinine causes retinal toxicity (cinchonism) via vascular constriction and photoreceptor damage, with an AOP involving G-protein-coupled receptor disruption (ABT Handbook, Domain II.D; Document: Eye Tab; Web: NIH, 2025).
104
What is the role of PBPK modeling in ocular dose-response assessment? (Domain III.C)
PBPK modeling predicts ocular tissue concentrations of toxicants (e.g., ethylene glycol), refining dose-response curves and interspecies extrapolations for retinal effects (ABT Handbook, Domain III.C; Web: EPA, 2023).
105
How does applied toxicology address emerging ocular risks from nanomaterials? (Domain IV)
Applied toxicology evaluates nanomaterials (e.g., titanium dioxide) for corneal irritation via in vitro and ecotoxicological studies, developing safety standards for consumer products (ABT Handbook, Domain IV.B; Web: NIH, 2025).
106
How are systemic and local ocular effects distinguished in study interpretation? (Domain I.C)
Systemic effects (e.g., lead’s optic neuropathy) involve multi-organ toxicity, while local effects (e.g., formaldehyde’s conjunctivitis) are confined to the eye, assessed via targeted endpoints (ABT Handbook, Domain I.C; Web: ATSDR, 2024).
107
What factors increase ocular susceptibility to carbon monoxide? (Domain II)
Susceptibility factors include hypoxia sensitivity, age, and pre-existing retinal conditions, exacerbating carbon monoxide’s retinal hypoxia and optic neuropathy (ABT Handbook, Domain II.C; Document: Eye Tab; Web: CDC, 2024).
108
How is the precautionary principle applied to ocular risk management? (Domain III.D)
The precautionary principle sets conservative exposure limits for ocular irritants (e.g., ammonia) when data is uncertain, prioritizing public safety via engineering controls (ABT Handbook, Domain III.D; Web: EPA, 2023).
109
What clinical signs indicate ocular toxicity in poisoning incidents? (Domain IV)
Clinical signs include blurred vision, miosis, or conjunctival redness, guiding antidote use (e.g., atropine for organophosphates) based on toxicological mechanisms (ABT Handbook, Domain IV.K; Web: NIH, 2025).
110
How does green chemistry reduce ocular toxicity risks in product design? (Domain IV)
Green chemistry principles minimize ocular irritants (e.g., volatile solvents) in consumer products, using benign-by-design approaches to reduce toxicity risks (ABT Handbook, Domain IV.G; Web: EPA, 2023).
111
What are the regulatory standards for ocular toxicity testing? (Domain IV)
Regulations like REACH and TSCA require ocular toxicity testing (e.g., OECD Test No. 405) for chemicals, ensuring consumer and occupational safety from irritants (ABT Handbook, Domain IV.L; Web: EPA, 2023).
