BACKGROUND: Our study investigated the presence, type and quantity of silicon in the human cornea. We report the results of silicon measurements in the corneas of silicotic individuals, bricklayers and apparently normal human individuals and offer a hypothesis for the mechanism of silicon deposition in the human cornea. METHODS: We examined corneas from 13 decreased subjects who suffered from silicosis, 2 bricklayers and 6 apparently healthy subjects. Cornea samples were examined by energy-dispersive x-ray analysis (EDXA) under calibrated conditions in a scanning electron microscope (SEM). The EDXA detector was a silicon-free germanium crystal. Five distinct layers (epithelium, Bowman's membrane, central stroma. Descemet's membrane and endothelium) were analyzed in each cornea. The method allows simultaneous semiquantitative analysis of, among other elements, silicon, calcium and oxygen. We measured amorphous silicon and visible particles of silicon. RESULTS: We found amorphous silicon in low concentrations in 38% of the silicotic corneas and in very low concentrations in 29% of the healthy corneas. Bricklayers showed high concentrations of amorphous silicon. These accumulations of silicon were predominantly located in Descemet's membrane. Silicotic corneas showed significantly more silicon-containing particles than corneas of healthy controls (chi 2-test, P < 0.01). CONCLUSION: Normal corneas contain very low amounts of silicon. Longterm exposure to inhalative silicon dusts results in only very slightly increased levels of amorphous silicon in the cornea. However, silicon-containing particles accumulate in the cornea of silicotic individuals. Bricklayers incorporate more amorphous silicon into the cornea.
BACKGROUND: Our study investigated the presence, type and quantity of silicon in the human cornea. We report the results of silicon measurements in the corneas of silicotic individuals, bricklayers and apparently normal human individuals and offer a hypothesis for the mechanism of silicon deposition in the human cornea. METHODS: We examined corneas from 13 decreased subjects who suffered from silicosis, 2 bricklayers and 6 apparently healthy subjects. Cornea samples were examined by energy-dispersive x-ray analysis (EDXA) under calibrated conditions in a scanning electron microscope (SEM). The EDXA detector was a silicon-free germanium crystal. Five distinct layers (epithelium, Bowman's membrane, central stroma. Descemet's membrane and endothelium) were analyzed in each cornea. The method allows simultaneous semiquantitative analysis of, among other elements, silicon, calcium and oxygen. We measured amorphous silicon and visible particles of silicon. RESULTS: We found amorphous silicon in low concentrations in 38% of the silicotic corneas and in very low concentrations in 29% of the healthy corneas. Bricklayers showed high concentrations of amorphous silicon. These accumulations of silicon were predominantly located in Descemet's membrane. Silicotic corneas showed significantly more silicon-containing particles than corneas of healthy controls (chi 2-test, P < 0.01). CONCLUSION: Normal corneas contain very low amounts of silicon. Longterm exposure to inhalative silicon dusts results in only very slightly increased levels of amorphous silicon in the cornea. However, silicon-containing particles accumulate in the cornea of silicotic individuals. Bricklayers incorporate more amorphous silicon into the cornea.