Occupational exposure neurotoxic effects

Ross WD, Emmett EA, Steiner J, Tureen R (1981) Neurotoxic effects of occupational exposure to organotins. American Journal of Psychiatry, 138 1092-1095. 

Mineral Oil Hydraulic Fluids. There is limited information on the toxicity of mineral oil hydraulic fluids in humans. A single case report of a child accidentally ingesting a single dose of automotive transmission fluid provides limited information on death and systemic effects. A case-control study provides some information on the carcinogenicity of mineral oil hydraulic fluids. The study population was exposed via inhalation and dermal routes. An occupational exposure study provides information on neurotoxicity following chronic dermal exposure. Information on the toxicity of mineral oil hydraulic fluids is limited to a series of inhalation, oral, and dermal acute-duration exposures. These studies provide information on death, systemic effects, and neurotoxicity by inhalation, oral, and dermal routes, and immunotoxicity following dermal exposure. 

Seppalainen AM, Hemberg S, Vesanto R, et al. 1983. Early neurotoxic effects of occupational lead exposure A prospective study. Neurotoxicology 4 181-192. 

Effect of Dose and Duration of Exposure on Toxicity. No studies were located where -hexane concentration was measured in workplace air before workers became ill, so no dose-response relationship can be defined for human neurotoxicity as the result of -hexane exposure. Information on duration of exposure leading to toxicity is available from some case series reports. An occupational exposure caused sensory disturbances in the lower extremities after approximately 2 months (Herskowitz et al. 1971). A case of peripheral neuropathy after 7 months of exposure was reported among press-proofing workers in Taipei (Wang et al. 1986) a serious case resulting in quadriplegia after 8 months of exposure was reported among sandal workers in Japan (Yamamura 1969). Based on case reports, it can be estimated... 

Comparative Toxicokinetics. The toxicokinetic studies available indicate that the rat is a good model for human neurotoxicity observed after occupational exposure to 77-hexane. Mild signs can be produced in chickens and mice, but these do not progress to the serious neurotoxicity observed in humans and rats. Toxicokinetic data from other species (absorption, distribution, metabolism, excretion) could provide insight on the molecular mechanism(s) of the species specificity of 77-hexane toxicity and would be valuable for predicting toxic effects in humans. 

Neurotoxicity. The only human data on neurotoxicity come from case reports of occupational exposures to chlordane in which the route was not specified, and for which the effects could not be related directly to heptachlor or heptachlor epoxide alone (Dadey and Kammer 1953). Signs of neurotoxicity, such as irritability, salivation, lethargy, dizziness, labored respiration, muscle tremors, and convulsions, were reported. No data exist describing neurologic effects in animals following inhalation exposure of any duration. Acute and intermediate oral studies in animals provide support for the supposition that the neurotoxicity of chlordane seen in humans may be due in part to heptachlor or heptachlor epoxide. Although there are no reasons to suspect that neurotoxic effects... 

Tsai S-Y, ChenJ-D Neurobehavioral effects of occupational exposure to low-level styrene. Neurotox Terat 18(4) 463-9, 1996... 

Most of the Al absorbed from the respiratory tract accumulates in the lungs. Pulmonary lesions have been described in employees of Al processing or manufacturing industries and encephalopathy after Al inhalation has been reported. Al is widely distributed and has many industrial uses, and toxicity from occupational exposure is assumed to be extremely rare [2, 177]. Nevertheless, a recent study investigating adverse effects on the central nervous system of Al welders found an Al-exposure-related increase in blood and urine Al concentrations, deficits in neuropsychological test performance and mild diffuse EEG abnormalities. Therefore, the potential for Al-induced neurotoxicity in those occupationally exposed to Al fumes may be greater than previously suspected [177]. 

Occupational exposure to neurotoxic chemicals before and after conception has been reported to produce a wide range of adverse effects on reproduction. Studies in the United States and Europe have shown increased risk of congenital malformations and reductions in birth weight among infants born to parents living near hazardous... 

London, L. and J.E. Meyers (1998). Use of a crop and job specific exposure matrix for retrospective assessment of long term exposure in studies of chronic neurotoxic effects of agrichemicals, Occup. Environ. Med., 55, 194-201. 

Incendiary and explosive devices are used in most terrorist attacks. As a result of combustion of fuel and hazardous materials, PAHs are released in high volumes. Exposure of civilians or deployed personnel to fumes containing PAHs constitutes an acute exposure scenario. Additionally, defense forces involved in extinguishing oil well fires, and cleanup tasks are exposed to low levels of PAHs over a more protracted time period. In addition, over 1.3 million civilian and military personnel are occupationally exposed to hydrocarbon fuels, particularly gasoline, jet fuel, diesel fuel, or kerosene on a near daily basis. Studies have reported acute or persisting neurotoxic effects from acute, subchronic, or chronic exposure of humans or animals to hydrocarbon fuels (Ritchie et n/., 2001), specifically burning of jet fuels, which release PAHs in considerable proportions. 

The neurotoxic effects after 10 years or more of long-term, low-level occupational exposure to carbon disulfide in workers at a viscose rayon plant were examined by assessing markers of the peripheral and autonomic nervous system (Ruijten et al. 1990, 1993). Reinvestigation of 44 of 45 exposed and 31 of 37 matched control workers revealed changes in the motor nerve conduction velocity (Ruijten et al. 1993). The exposure concentration in the two studies varied from 1 to 30 ppm. For peripheral nerves, a decrease in the conduction velocity in both fast and slow motor nerve fibers (peroneal nerve) was observed in exposed workers. Sensory conduction velocities were reduced and the refractory period of the sural nerve was increased. The effects on the sural nerve were pronounced. A small decrease in conduction velocities in the absence of symptoms of neuropathy and decreased response amplitudes suggest a mild presymptomatic nerve impairment. 

Animal studies on the neurotoxicity of carbon disulfide have usually been done in rats and provide histopathologic and neurochemical data that support a neurotoxic effect for carbon disulfide. In general, the doses used in these animal studies are considerably higher than the occupational exposures seen in epidemiological studies. 

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