Studies about the effect of organic solvents in biological systems are more frequent in occupational medicine, and most commonly the intoxication is occupational and caused by solvent mixtures [¹–⁷]. In addition, inhalation is the major pathway of intoxication in occupational environment [⁸–¹⁰].

Occupational exposure to organic solvents can cause damage in both central and peripheral nervous system [¹¹–¹⁴], and the visual system is one of the main targets of organic solvent intoxication [¹⁵]. As a result, acquired dyschromatopsias usually have been found in chronically exposed subjects to organic solvent mixtures [³, ¹⁶–¹⁹], as well as to specific solvents as n-hexane, styrene, and toluene [²⁰–²⁵]. Most color vision deficiencies due to exposure to solvents have subclinical symptoms, and a loss of the blue-yellow discrimination has been the most frequently reported impairment [³, ¹⁶, ¹⁸, ²⁰–²², ²⁴, ²⁶–³⁰], although some studies described altered red-green discrimination [³, ³¹].

It has been described that chronic exposure to n-hexane may cause color discrimination losses, associated with maculopathy [³²] and visual perimetry losses at the periphery, with optic nerve atrophy and retrobulbar neuritis [³³]. Optic neuropathy is a finding associated with polyneuropathy in cases of alcohol, methanol, styrene, toluene, trichloroethylene, and solvent misture intoxication [³⁴]. Decreased spatial contrast sensitivity in the middle range (6–12 cpd) of spatial frequencies associated to normal visual acuity seems to be an indicator of visual impairment induced by chronic exposure to styrene, acute exposure to tetrachloroethylene or triethylamine [²¹, ²⁵, ³⁵] and organic solvent mixtures [⁶, ³⁶–³⁸]. Losses of spatial vision can be dependent of the intoxication level [³⁸–⁴⁰].

Painters, factory workers, and cleaners are subject to continuous exposure to organic solvents. Investigation of their visual system to look for functional deficits has been performed by several authors, showing the impact of this exposure [⁶, ⁷, ²⁵, ³⁰, ⁴¹]. In some countries, Brazil included, automobile tanks are filled by gas station workers. Therefore, in this job the person is subject to a long period of organic solvent exposure. Automobile fuel is composed of a mixture of organic solvent including gasoline, alcohol, and diesel oil. They are composed by several hydrocarbons such as methane, ethane, propane, pentane, methanol, ethanol, propanol, methyl tertiary butyl ester, benzene, toluene, and xylene.

Thirty-one gas station workers agreed to participate in the study. Two subjects were excluded due to congenital red-green dyschromatopsia. Twenty-nine (27 males, 31.5 ± 8.4 years old) workers were evaluated. All procedures were evaluated by Ethical Committee in Research in Humans of the Tropical Medicine Nucleus of Federal University of Pará (Protocol no. 075/2006-CEP/NMT). These subjects had normal visual acuity or corrected to 20/20 (Snellen test).

Gas station workers participated in the current work according to their availability and in some cases they were unable to do all the tests due to their heavy work schedule. Control group for each psychophysical test was composed by the same number of subjects as the exposed group, matched in age and gender (32.8 ± 9.5 years old). The control subjects worked in environments free of solvent exposure.

In the present study we assessed visual functions of gas station workers. In this profession, common in some countries, the job of the worker is to fill the automobile gas tanks. The worker is thus continuously exposed to a mixture of organic solvents throughout his work shift. We observed that twenty-five out of twenty-nine gas station workers had some kind of visual loss evaluated by psychophysical methods.

Many studies have demonstrated that workers exposed to organic solvent have visual impairments, mainly in color vision [³, ¹⁶–²⁵, ⁴⁵]. The mechanisms of neuronal dysfunction elicited by exposure to organic solvents are still unclear, but the affinity of organic solvent to lipid enriched tissues is well known. The nervous system is therefore a potential target of the solvent intoxication [⁴⁶].

Most color vision studies have reported mainly blue-yellow color vision losses, and a secondary red-green color dyschromatopsia as shown in the present study [³, ¹⁶–²⁵, ²⁷–³¹]. Previous studies have investigated the color vision of solvent exposed workers using color arrangement test as FM100 test or Lanthony D15. As far we know, the present study is the first time that color discrimination ellipses test was applied in the solvent exposed subjects [¹⁶, ²³–²⁵, ²⁷, ²⁸, ³⁰, ³¹, ³⁸, ⁴⁷–⁵¹]. As the tasks of color discrimination and FM100 test are quite different it is difficult to assert which test would be best to evaluate the color vision of the workers. This acquired dyschromatopsia might be the result of optics and neural causes [⁵², ⁵³]. Aging can also lead to macular degeneration [⁵², ⁵³]. The present study did not find worker diagnosed with any change in the ophthalmic clinical evaluation, suggesting that the color vision losses have neural predominant origin [³¹, ⁵⁴].

Study in rats and nonhuman primates demonstrated an accumulation of metabolites from methanol in the vitreous and retina [⁵⁵, ⁵⁶], which could cause degeneration of outer nuclear layer and ganglion cell layer suggested for histopathologic studies by Potts and colleges [⁵⁷]. For Köllner [⁵⁸] blue-yellow color vision loss reflects changes in outer retina whilst losses in the red-green axes reflect abnormalities in the inner retina or optic nerve. This became known as Köllner's rule. Muttray et al. [²²] argued that Köllner rule [⁵⁸] could be combined with more recent findings [⁵⁹], considering that outer retinal damage in the central retina would lead the subject to fixate at more eccentric retinal points. We agreed with Muttray's argument, because the pathologic eccentric fixation could result in impairment of red-green discrimination.

Dyschromatopsia associated to organic solvents intoxication has been attributed to maculopathies caused by damage in cone photoreceptors, ganglion cells and optic nerve demielinization [²⁰, ³², ⁶⁰]. Blain and Mergler [⁶¹] suggested that the fact solvent intoxication led to blue-yellow color vision losses and later may develop to red-green color vision loss, reflects progressive degeneration from outer retina to optic nerve [⁶¹]. Cortical changes in the visual processing can occur after organic solvent intoxication [¹⁶, ²⁰, ³², ⁶⁰, ⁶²–⁶⁴]. We described diffuse color vision losses, with no preferences for blue-yellow or red-green chromatic axes. This kind of color vision loss is associated to high exposure to organic solvents [¹⁶, ⁵⁴].

Eight out of 25 gas station workers had luminance spatial contrast sensitivity lower than the tolerance limits defined by the control group. There was statistical difference between the organic solvent exposed workers and the control group at 20 and 30 cpd, but there was no change in their Snellen visual acuity. Boeckelmann and Pfister [⁶] and Järvinen and Hyvärinen [³⁵] suggested measuring contrast sensitivity at low and intermediate spatial frequencies which reflect changes in the neural processing whereas loss of contrast sensitivity at high spatial frequencies reflects impairment of the optics of the eye. In the present work, all subjects had normal or corrected visual acuity to 20/20. Other studies on intoxication by organic solvents intoxication showed spatial vision impairments without changes of visual acuity [⁶, ²¹, ²⁵, ³⁵–⁴⁰]. We found no impairments in the temporal contrast sensitivities in the organic solvent exposed workers.

Our results of visual field losses are similar to the findings of Yamamura [³³]. Six out of 21 gas station workers had impairment of contrast sensitivity in eccentricities above 10°. Even the workers who were in the normal range of contrast sensitivity in eccentricities that ranged between 10°–60°, there was significant decreasing between the values of the exposed group and control group. This impairment is detected by MD (low values) and PSD (high values) analysis, reflecting in altered visual field with constriction of the visual field towards the central field. Grant and Schuman [³⁴] suggest that this type of visual loss indicates a beginning process of optical neuropathy after exposure to methanol, styrene, toluene, trichloroethylene, and organic solvents mixtures.

In the present study, the exposed subjects have worked at the gas station from one month to twenty-one years (47.4 ± 61.7 months) and the period of exposure varied from 36 to 48 hours a week (45.23 ± 4.4 hours a week). Three subjects reported that they used protective safety equipment, but they lack specific training for use of this kind of equipment. Some studies found weak correlation between psychophysical performance of exposed subjects and their exposure to organic solvent mixtures, styrene, perchloroethylene, or benzene [²², ²⁴, ⁶⁵]. Although we also expected to find some correlation between total time of exposure and/or amount of daily exposure and the performance of exposed subjects in the psychophysical tests that we used, that was not the case. We did not find any significant correlation between the exposed subject performances and the duration or amount of exposure to organic solvents.

Concentration of organic solvents or their metabolites in tissues are not directly related to time of exposure. There are genes that code enzymes that work in the metabolism of organic solvents in the organisms, and gene polymorphism modifies the absorption and the neurotoxicity effects of the organic solvents [²⁵, ⁶⁶]. We suggest that visual system damage probably occurred at early moment of solvent exposure, and the intersubject variability in the psychophysical tests could be explained by individual genetic predisposition.

The current study investigated psychophysically the achromatic and chromatic vision of gas station workers, and correlated the psychophysical results with time of exposure. These results have previously been published as abstracts [⁶⁷].

The authors declare no conflict of interests.

All procedures were evaluated by Ethical Committee in Research in Humans of the Tropical Medicine Nucleus of Federal University of Pará (protocol no. 075/2006-CEP/NMT).

This paper is supported by FINEP IBN Net; CNPq-PRONEX/FAPESPA #2268 and #316799/2009; CNPq #486351/2006-8, #476744/2009-1, and #620037/2008-3; CAPES-PROCAD #182/2007. D. F. Ventura and L. C. L. Silveira are CNPq research fellows.