2,2,4-Trimethylpentane is a colorless, transparent liquid at room temperature with a characteristic gasoline odor. It is miscible with any hydrocarbons and ethers. As a highly branched alkane, it exhibits excellent chemical stability and outstanding anti-knock properties. It serves as the reference standard for gasoline octane rating, with a specified octane number of 100. It is primarily used for fuel quality calibration, as an organic solvent, and as a raw material for organic synthesis. This product is highly flammable, and its vapors are explosive when exposed to open flames.

2,2,4-Trimethylpentane inhalation affects visual electrophysiology and behavioral detection

The U.S. Environmental Protection Agency (EPA) Office of Transportation and Air Quality has identified over 1,000 hydrocarbon substances arising from the evaporative or combustive emissions of gasoline and diesel engines. One substance that typically constitutes about 2.5–4.0% of gasoline is 2,2,4-trimethylpentane (TMP), also known as “isooctane”. Gasoline is commonly graded using an “octane rating” scale in which the burning efficiency of n-heptane is assigned a value of 0 and TMP (isooctane) a value of 100. A survey of the indoor air of 100 suburban and rural homes where there was no known contamination of soil or groundwater found 2,2,4-trimethylpentane above the minimum detection level (2.3 μg/m3) in 27% of the homes, with a maximum value of 140 μg/m3. As such, TMP is a common constituent of gasoline to which people may be exposed, and it is therefore important to understand the potential for toxic effects resulting from such exposures. Behavioral assessments involved quantifying the accuracy and speed with which rats performed a visual signal detection task while inhaling TMP. The task was designed to assess sustained attention: both rats and humans have been shown to vary their choice accuracy similarly in response to parametric manipulations known to affect attention in humans. The PBPK model for TMP was used to estimate the concentrations of 2,2,4-trimethylpentane in the brain at the time of testing, to enable determination of dose–response relationships between internal dose and VEP amplitude, and between internal dose and the accuracy and speed of performing a signal detection task. Scientists hypothesized that acute inhalation of TMP would reduce VEP F2 amplitude, reduce signal detection accuracy, and increase signal detection response latency as a direct function of the estimated concentration of 2,2,4-trimethylpentane in the brain at the time of testing.[1]

TMP is an important constituent of gasoline and its vapors are present in the evaporative emissions from gasoline and gasoline engines. Combustion emissions from gasoline engines may also contain traces of 2,2,4-trimethylpentane. TMP is among the substances detected in the air alongside busy roadways, where a substantial segment of the population resides. TMP is also detectable in the air of typical US suburban homes. For these reasons, it is important to understand the potential risks posed by inhalation exposure to TMP. One of the common health outcomes from acute inhalation of volatile organic compounds is impaired function of the central nervous system. In summary, the relatively low penetration of 2,2,4-trimethylpentane into the brain appears to determine that acute neurological impairments from exposure to this substance alone are unlikely to be as severe as those caused by other volatile components of gasoline, such as toluene. In addition, the TMP concentrations in this study were higher than those anticipated for most exposed populations. TMP, however, is only one of many volatile hydrocarbons present in gasoline. Because TMP did cause effects resembling those of other VOCs, it would be reasonable to expect additivity of internal doses of 2,2,4-trimethylpentane in combination with other organic vapors emitted from gasoline. Therefore, a risk assessment of acute exposures to gasoline vapors as a whole should consider the contribution of 2,2,4-trimethylpentane among the other constituents in proportion to its expected relative concentration in brain tissue.

Improved microbial tolerance to 2,2,4-trimethylpentane

Microbial tolerance to hydrocarbons has been studied in an effort to improve the productivity of biochemical processes and to enhance the efficiency of hydrocarbon bioremediation. Despite these studies, few attempts have been made to design rational strategies to improve microbial tolerance to hydrocarbons. Herein, we present an engineering framework that enables us to harness our understanding of genetic regulatory networks to improve hydrocarbon tolerance. In this study, 2,2,4-trimethylpentane was used as a representative hydrocarbon due to its use in petroleum refining and in biochemical processes. To increase isooctane tolerance, we first identified essential transcriptional determinants and genetic regulatory networks underlying cellular responses to isooctane in Escherichia coli using genome-wide microarray analysis. Based on functional transcriptome and bioinformatics analysis, a range of combinations of transcription factors whose activity was predictably perturbed by isooctane were knocked out and overexpressed to reconstitute the regulatory networks. We demonstrated that the reconstitution of the regulatory networks led to a significant improvement in 2,2,4-trimethylpentane tolerance, and especially, engineered E. coli strains lacking and overexpressing some of the perturbed transcription factors showed 3- to 5-fold improvement. This microbe with high tolerance to 2,2,4-trimethylpentane can be harnessed for biochemical processes, fuel oil bioremediation and metabolic engineering for biofuel production. Furthermore, we envision that the engineering framework employed to improve the tolerance in this study can be exploited for developing other microbes with desired phenotypes.[2]

References

[1]Boyes WK, Oshiro WM, El-Masri H, Degn LL, Bercegeay M, Krantz QT, Bushnell PJ. Acute inhalation of 2,2,4-trimethylpentane alters visual evoked potentials and signal detection behavior in rats. Neurotoxicol Teratol. 2010 Sep-Oct;32(5):525-35. doi: 10.1016/j.ntt.2010.04.055. Epub 2010 May 11. PMID: 20438835.

[2]Kang A, Chang MW. Identification and reconstitution of genetic regulatory networks for improved microbial tolerance to isooctane. Mol Biosyst. 2012 Apr;8(4):1350-8. doi: 10.1039/c2mb05441h. Epub 2012 Feb 10. PMID: 22328008.