7 Major Ophthalmic Toxic Effects | Eyes | Toxicology

The following points highlight the seven major ophthalmic toxic effects. The effects are: 1. Effects on Cornea 2. Effects on Iris 3. Effects on Aqueous Humor 4. Effects on Ciliary Body 5. Effects on Lens 6. Effects on Retina 7. Effects on Optic Nerve.

1. Effects on Cornea:

This delicate structure is subjected to toxic effects of xenobiotics chiefly through external exposures. Xenobiotics that impair the cornea function include acids and alkalis, detergents, organic solvents, and smog. Acids and alkalis can readily damage the cornea. The extent of damage ranges from minor, superficial destruction of the tissue, which heals completely, to opacity of the cornea or even perforation.

Acid burns are related to the low pH as well as the affinity of the anion for the corneal tissue. The effects of alkalis usually have slower onset than those caused by acids and essentially pH-dependent. However, ammonium ion, which is present in many household products, penetrates the cornea more readily and can thereby affect the iris.

The nonionic detergents are less damaging than the ionic agents, and the cationics are more damaging than the anionics.

Organic solvents, viz. acetone, hexane and toluene, may enter the eye as a result of industrial or laboratory accidents. These xenobiotics may dissolve lipid and damage the corneal epithelial cells.

Industrial smoke and fog combine to form smog. It adversely affects the respiratory tract, but, even at low concentrations, it irritates the corneal sensory nerve endings and cause reflex lacrimation.

Other xenobiotics may adversely affect the cornea following systemic administration. These include quinacrine, chloroquine, and chlorpromazine.

2. Effects on Iris:

The iris is susceptible to physical trauma and chemical irritations because of its proximity to the cornea. The effects of such irritation consists of leakage of serum proteins and fibrin from the blood vessels as well as leukocytes. These may be followed by fibroblast metaplasia. Severe damages to the iris cause liberation of melanin granules from the posterior epithelium of the iris.

Since the iris is innervated by sympathetic (for the dilator muscles) and the parasympathetic nerves (for the constrictor muscles), the pupil can be dilated by toxic chemicals that are sympathomimetic or para-sympatholytic. Likewise, the pupil can be constricted by para-sympathomimetic and sympatholytic chemicals. Furthermore, the size of the pupil can be altered via the central nervous system by chemicals such as morphine and general anesthetics.

3. Effects on Aqueous Humor:

The aqueous humor is secreted into the posterior chamber by the epithelium of the ciliary body. It flows into the anterior chamber through the pupil and drains through the canal of Schlemm at the angle of the anterior chamber. Inflammatory alterations of the iris may block the drainage of the fluid through the canal of Schlemm and raise the intraocular pressure, thereby inducing glaucoma. Atropine and other mydriatics may also precipitate glaucoma by blocking the drainage.

4. Effects on Ciliary Body:

Ciliary body contains the ciliary muscle. Its contraction allows relaxation of the ciliary zonule, which, in turn, allows the lens capsule to assume a more spherical form. Ciliary muscle is para-sympathetically innervated, there cholinesterase inhibitors and parasympathetic agents like atropine can cause the lens to be fixed in different state of accommodation.

5. Effects on Lens:

Various xenobiotics are known to alter the lenticular transparency, resulting in the formation of cataract. Examples are 2, 4-dinitrophenol, corticosteroids, triparanol, thallium, busulfan, alkylating agents, naphthalene, iodoacetic acid, DMSO (Dimethyl sulphoxide) etc. Their cataractogenic property has been reported in humans and other animals, such as rat, rabbit and young fowl. The effects usually follow systemic exposure, but with certain chemicals viz., corticosteroids, anticholinesterases, etc. they may occur after topical application.

Gehring (1971) reported that deficiencies of certain nutrients viz., tryptophan, proteins, vit. E, riboflavin and folic acid may also induce cataract.

The causo-mechanism underlying the formation of cataract is not fully known to date. It is likely that it varies with the nature of the xenobiotics. For example, corticosteroid cataract may be mediated through an inhibition of protein synthesis in the lens. Triparanol may interfere with the Na⁺ pump resulting in an increase of Na⁺ and water in the lens.

Besides cataractogenic effects, transient lens opacity may be induced by certain xenobiotics like diisophenol. In addition, the transparency and refraction of the lens may also be altered by dimethyl sulphoxide and p-chlorophenylalanine.

6. Effects on Retina:

Retinopathy in humans and other animals have been reported to be induced by certain polycyclic chemical compounds such as chloroquine, hydroxychloroquine, and thioridazine.

These compounds affect the visual acuity, dark adaptation, and retinal pigment pattern. Hyperoxia and iodate may also induce retinal changes. Other retinal effects include hemorrhage from rupture of blood vessels or disturbance of blood clotting mechanism and exudates, which may cause partial detachment of retina.

7. Effects on Optic Nerve:

Xenobiotics at one time may affect either the ganglion cells or the optic nerve. Damage to one of them results in the degeneration of the other. Certain toxicants affect mainly the central vision.

The most notable example is methanol (CH₃OH). Others include CS₂, disulphuran, ethambutol and thallium. On the other hand, quinine, chloroquine, arsenic⁺⁵, and CO cause constriction of visual fields by damaging the structures responsible for peripheral vision. However, nitrobenzol affects both the central and peripheral vision.

It would not be out of place to mention that certain organic solvents viz., trio-cresyl phosphate, acrylamide, n-hexane, and methyl n-butyl ketone can induce peripheral neuropathy but spare the visual system.

The mode of action of these toxicants is not well understood, however, quinine appears to act through an inhibition of DNA, which, in turn, inhibits RNA transcription and protein synthesis. As⁺⁵ appears to act on the ganglion cell neurons.