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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Toxicological information

Neurotoxicity

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Administrative data

Description of key information

Exposure to high levels of gasoline can produce acute central nervous system depression in humans and experimental animals.

Repeated exposure at lower, occupational levels of gasoline produced little evidence of chronic neurological effects in humans or in experimental animals.

Key value for chemical safety assessment

Effect on neurotoxicity: via oral route

Endpoint conclusion
Endpoint conclusion:
no study available

Effect on neurotoxicity: via inhalation route

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed

Effect on neurotoxicity: via dermal route

Endpoint conclusion
Endpoint conclusion:
no study available

Additional information

Both the human and animal data indicate that exposure to high levels of gasoline can produce acute central nervous system depression. There is also evidence from the clinical literature that repeated exposure to gasoline at very high levels, under abuse conditions, can produce more profound central nervous system effects. Less clear is the degree to which these effects may have been due to the lead additives as opposed to the hydrocarbon constituents. There is little evidence of chronic neurological effects in humans exposed repeatedly at lower, occupational levels. The animal data provide little experimental support for chronic neurological effects from either unleaded gasoline or naphtha blending stocks. Initial studies with wholly vaporized unleaded gasoline provided evidence of exacerbation of normal, age-related changes. However, subsequent studies with gasoline vapor and naphtha blending stocks had no clear or reproducible effects on motor activity, produced no functional changes, and did not induce histological changes in the nervous system. It is not known to what extent the differences between these studies, if real, were due to differing experimental conditions (i.e., subchronic versus chronic exposures) or specific constituents contributing to exposure (gasoline vapor versus wholly vaporized gasoline).

Justification for selection of effect on neurotoxicity via inhalation route endpoint:

one of 3 studies investigating the neurotoxicity of gasoline

Justification for classification or non-classification