Background and Purpose: Liquid gasoline (CAS 86290-81-5) is produced by the fractional distillation of crude oil and mainly consists of volatile organic compounds; finished automotive gasoline products may also include various additives. The objective of this study was to review mechanistic data on automotive gasoline potentially associated with mutagenic or genotoxic endpoints, as well as indications suggestive of immunosuppressive and/or epigenetic activity pertaining to possible carcinogenic potential in humans. Methods: Literature searches were conducted in PubMed and Embase on August 12, 2025 and October 29, 2024. The search strategy consisted of terms associated with automotive gasoline, cancer and mechanistic data in occupationally-exposed human subjects, mammalian in vivo models and in vitro models. Study quality was determined using Klimisch scores (animal and in vitro studies) or using a modification of the National Toxicology Program (NTP)’s Office of Health Assessment and Translation (OHAT) Risk of Bias (RoB) approach (human subjects). Results: Based on TiAb review, a total of 2,630 papers were identified as containing a potential exposure to automotive gasoline and data relevant to cancer pathways. From these, 57 papers were confirmed (at full text) as studies of genotoxicity, 22 papers as studies of immunosuppression and 9 as studies of epigenetic alterations in exposed human subjects. All studies were conducted in fuel station attendants assumed to be occupationally exposed to gasoline. Following study quality appraisal, six reliable observational studies showed a significantly elevated frequency of genetic damage in workers compared to controls and two studies showed no elevated frequency of genetic damage in fuel stations workers. Animal model and human cell line studies, with a better characterized exposure, did not produce consistent evidence of genotoxic activity. Insufficient reliable studies existed to conclude whether occupational exposure to gasoline resulted in immunosuppressive or epigenetic changes. Conclusions: This analysis provides some evidence of genotoxic activity in fuel station attendants exposed to a poorly characterized complex mixture of chemicals (e.g., including automotive fuel, diesel and gasoline engine exhaust, rubber and metal particles from tire wear, and asphalt particulates from road wear) containing a mixture of known genotoxic substances and recognized human carcinogens. In summary, due to the poor characterization of the chemical mixture to which people were occupationally exposed, there is insufficient evidence to conclude that genotoxic activity observed in occupationally-exposed human subjects should be directly attributed to automotive gasoline alone.