Organic solvents are a class of chemical substances that are widely used in large volume in various manufacturing plants. Due to their high lipophilicity, organic solvents may produce physicochemical damage to renal glomeruli and tubuli. Many reports have been published abroad, though only a few in Japan, on organic solvent-induced nephropathy such as Goodpasture syndrome, a form of renal damage mediated by anti-basement membrane antibodies. This article reviews the epidemiological studies published in the literature and stresses that organic solvent exposure is one of the etiological factors involved in the development of chronic nephropathy. At present in Japan there are 60, 000 patients with terminal renal failure undergoing hemodialysis, 50, 000 young men placed under observation each year for abuse of organic solvents, and one million workers exposed to organic solvents in factories. Attention should be focused on the occurrence of renal damage due to organic solvents in Japan.

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A study was made on the possibility of synergistic effects of ethyl alcohol and lead on porphyrin metabolism in rabbits.
Experimental rabbits were divided into 4 groups. Group A was the control group not given any treatment, and the other 3 groups (Groups B, C and D) were treated with ethyl alcohol, lead, and ethyl alcohol and lead respectively, for 2 months. Ethyl alcohol solution (5%) was administered to rabbits in Groups B and D as drinking water on every weekday. The average dose of alcohol was 6 ml/kg/day (18 ml/cap/day). Lead was injected intravenously to rabbits in Groups C and D at a dose of 0.5 mg Pb/kg on alternate days (3 times per week). Furthermore, a large dose of Pb was administered to other rabbits (Group C').
In rabbits treated with alcohol alone (Group B), no effect was observed in the biochemical indicators related to porphyrin metabolism. In the groups treated with lead (Groups C and C') and with lead and alcohol combined (Group D), some biochemical changes in porphyrin metabolism developed with increase of Pb-B, i.e. increase of ALA-S activity and total porphyrin content in the bone marrow, elevation of FEP level, increase of ALA-U and CP-U, and decrease of ALA-D activity in erythrocytes. Camparison of Groups C and D showed that CP-U and ALA-U increased significantly in Group D, but no significant difference was observed between both groups in FEP and in ALA-S activity in the bone marrow and liver. The other laboratory measurements, such as total porphyrin contents in the liver and plasma, and GOT or GPT level in serum, showed no significant change in all the groups.
In the present study, the biochemical changes suggesting synergism of lead and ethyl alcohol were observed slightly in ALA-U and CP-U but not in ALA-S and FEP. These results suggest that these changes are essentially due to lead rather than mutual enhancement of the direct effects of these two toxins on porphyrin metabolism. However, it still remains to be determined whether or not ethyl alcohol affects the liver and kidney functions which may be related to ALA and CP excretion.

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Rabbit eyes were irradiated by an ultraviolet laser beam in with to investigate its effects on the corneal endothelium, thickness of the cornea, and lens. An Excimer laser beam (gas; XeCl) with wave length of 308 nm and with energy intensity of 0.02, 0.07, 0.2, 0.6, 1.7, 3.0, 4.0, or 5.1 J/cm² was irradiated to the right eye using 3 rabbits for each energy intensity (24 rabbits in all) in order to examine changes occurring in the right eye compared with the left eye from immediately after irradiation to 32 days thereafter.
The results obtained were as follows:
1. Corneal thickness
UV laser beam irradiation at 0.02, 0.07, and 0.6 J/cm² caused immediate thickening of the cornea (p<0.01). The cornea thickness returned to normal 14 days later. Irradiation at 3.0 and 4.0 J/cm² resulted in remarkable thickening, which returned to normal 28 days after irradiation. By irradiation at 5.1 J/cm², the corneal thickness increased markedly (0.333±0.019 mm in control eyes and 0.405±0.05 mm in irradiated eyes) immediately after irradiation.
It tended to gradually return to normal and was reduced to the pre-irradiation thickness on the 32nd day after irradiation.
2. Corneal endothelial area and morphology (the number of angles)
The area of the corneal endothelium increased after irradiation. However, no significant differences were noted at any energy intensity, because of the larger scattering of the values in the control eyes. The ratio of hexagonal cells tended to decrease even by energy intensities, above 0.7 J/cm². However, no significant differences were found at any energy intensity level.
3. Scanning electron microscopic observation
The corneal endothelium at 32 days after 5.1 J/cm² irradiation showed a number of invaginations over a plurality of cells.
4. Development of the cataract
Irradiation at intensities below 1.7 J/cm² induced no abnormality in the lens. Intensities above 3.0 J/cm² produced disk-shaped whitish opacity under the anterior vesicle and intensification of radiation energy increased the degree of opacity.

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Ethanol-treated and ethanol-nontreated rats were exposed to 0, 500, 1, 000, 2, 000, 4, 000 and 8, 000 ppm of trichloroethylene for 2 h in order to evaluate the metabolic (metabolic rate of styrene) and morphologic changes in the lung. The exposure resulted in dose-dependent decrease of styrene metabolism. By MPA (Maclura pomifera agglutinin) stain it was revealed by light microscopy that trichloroethylene caused a highly selective damage to nonciliated bronchiolar epithelial (Clara) cells, which were characterized by flattened cells. The ratios of the length of apical surface (a) to the length of the base (b) of Clara cells analyzed morphometrically decreased dependent on trichloroethylene dose. Electron microscopy showed that the bronchiolar luminal surface was covered by flattened and dilated endoplasmic reticulum and that destruction of mitochondrial crista and disappearance of secretory granules were dependent on increase in trichloroethylene concentration. Time-course studies conducted with exposure of 8, 000 ppm of trichloroethylene to ethanol-treated rats demonstrated that maximal Clara cell damage occurred between 8 and 22 h after exposure, and that the cells appeared to be virtually identical to these of the control by 4 wk after exposure. Ethanol ingestion slightly increased Clara cell damage induced by trichloroethylene.

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