Ocular Effects of Exposure to Industrial Chemicals: Clinical Management and Proteomic Approaches to Damage Assessment

Abstract

Industrial chemicals in a variety of applications are often found in highly populated areas and their presence carries risks. The threat of serious consequences from inadvertent or intentional events involving hazardous chemicals is a possibility. Extremism and/or other illicit activities pose environmental threats from chemical exposures. We present here a review of the threat of ocular injury in small-and large-scale chemical releases and discuss mechanisms of damage and repair to the eyes. The emerging field of proteomics has been described in relation to its potential role in the assessment of ocular changes following chemical exposures and management of ocular trauma.

Proteomic Analyses of Corneal Tissue Subjected to Alkali Exposure

“…Our selection of alkali was based on the fact that several alkaline materials are valuable industrial chemicals, often stored in large amounts in areas adjacent to and transported through populated areas. 2 Sodium and ammonium hydroxide are used in a number of industrial processes, 1 and calcium hydroxide is used as quicklime for white wash and painting and as an edible paste that has been known to cause accidental corneal burns. 28,29 Alkali damages are usually more penetrating and more severe than acid damages.…”

“…1 Traumatic exposure to chemicals may be unintentional or intentional. 1,2 With the advent of industrialization, chemicals are often stored or transported through populated areas, 2 creating the possibility for accidents; therefore, changes associated with exposure to chemicals must be studied so we may better understand the resultant damage and design better medical treatment.…”

“…3 Many physical and chemical factors determine the type of tissue damage that results from chemical exposure. 2,4,5 Although acidic agents, primarily organic acids, can penetrate the eye, alkaline agents more rapidly penetrate the cornea and saponify cellular membrane lipids. 6 -9 The acidic injuries tend to result in local coagulation-necrosis, whereas alkali injuries tend to be gelatinous and liquefactive.…”

Late-onset Peripheral Ulcerative Sclerokeratitis Associated With Alkali Chemical Burn

“…Ammonium hydroxide, the toxic byproduct of ammonia, causes saponification of the lipid layer of cell membranes with consequent liquefactive necrosis and release of various proteins normally sequestered in subcellular compartments. 6,16,17 Ammonium hydroxide also produces alkaline proteinases, which permanently alter the structure of proteins. Both released and altered proteins may function as autoantigens.…”

“…Both released and altered proteins may function as autoantigens. 6,16,17 Professional (polymorphonuclear leucocytes, monocytes) and nonprofessional (keratocytes expressing class II major histocompatibility complex) antigen-presenting cells (APCs) have both been found in alkali-burned corneas very shortly after the injury. 18 Also, formation in the cornea of new blood and lymphatic vessels has been shown following alkali injuries.…”