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Octane
Octane SR Clough, Haley & Aldrich, Inc., Bedford, NH, USA Ó 2014 Elsevier Inc. All rights reserved. l l l l l l
Name: Octane Chemical Abstracts Service Registry Number: 111-65-9 Synonyms: n-Octane (UN1262, DOT), Oktan (Polish), Oktanen (Dutch), Ottani (Italian) Chemical/Pharmaceutical/Other Class: Aliphatic hydrocarbon (C8) Molecular Formula: C8H18 Chemical Structure: H3C
CH3
n-Octane
CH3
CH3
H3C
CH3 CH3
Isooctane (2,2,4-trimethylpentane)
Uses n-Octane is used as a solvent and raw material for organic synthesis reactions and is a very important chemical in the petroleum industry. It is also widely used in the rubber and paper processing industries. Isooctane, along with other nalkanes and isoparaffins, is used in the blending of fuels to achieve desired antiknock properties.
Environmental Fate and Behavior Octane is an eight carbon aliphatic compound that is a natural constituent of the major paraffin fraction of crude oil and also found in natural gas. A total of 17 isomers of octane are known to exist and differ by the amount and location of branching in the carbon chain. Isooctane (2,2,4-trimethylpentane) is a principal ingredient of gasoline and is used as a standard in the octane rating of gasoline. Pure n-octane is a colorless liquid that is highly flammable and lighter than water. It has a gasolinelike odor with an olfactory threshold around 400 ppm. Octane has a molecular weight of 114.23 g mol1. At 20 C, n-octane has a solubility of 0.66 mg l1 in water and a Henry’s law constant of 3.2 atm m3 mol1 (USEPA, 2011). The log octanol/water partition coefficient is 5.18. Conversion factors for n-heptane in air are as follows: 1 mg m3 ¼ 0.21 ppm; 1 ppm ¼ 4.67 mg m3. If released to air, a vapor pressure of 14.1 mmHg at 25 C indicates n-octane will exist solely as a vapor in the ambient atmosphere. Vapor-phase n-octane will be degraded in the atmosphere by reaction with photochemically produced
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hydroxyl radicals; the half-life for this reaction in air is estimated to be 44 h (USEPA, 2011). Vapor-phase n-octane will not undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups nor photolyze due to the lack of absorption in the ultraviolet spectrum (>290 nm). Experimental data showed that w33% of the n-octane fraction in a dark chamber reacted with nitrate radical to form the corresponding alkyl nitrate, suggesting nighttime reactions with nitrate radicals may contribute to the atmospheric transformation of n-octane, especially in urban environments (HSDB, 2011). The Henry’s law constant for n-octane indicates that it is expected to volatilize rapidly from water surfaces. Based on this Henry’s law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m s1, wind velocity of 3 m s1) is estimated as 1.1 h. The volatilization half-life from a model lake (1 m deep, flowing 0.05 m s1, wind velocity of 0.5 m s1) is estimated as 4.2 days (USEPA, 2011). Volatilization from water surfaces may be attenuated by adsorption to suspended sediment in the water. The estimated volatilization half-life from a model pond is 11 months if adsorption is considered. However, in a study using a jet fuel mixture and sterile freshwater controls from the Escambia River (Florida), a 99% loss of n-octane was attributed to evaporation at 25 C. If released to soil, n-octane is expected to have very low mobility based upon an estimated Koc of 16 000. Volatilization from moist soil surfaces is expected to be an important fate process based upon the estimated Henry’s law constant. However, adsorption to soil is expected to attenuate volatilization. n-Octane would also be expected to volatilize from dry soil surfaces based upon its vapor pressure. Octane is expected to biodegrade in soil under aerobic conditions (HSDB, 2011). Using a measured log Kow of 5.18, the United States Environmental Protection Agency’s EPI Suite computer program estimates a bioconcentration factor and a bioaccumulation factor of 1086 and 1155, respectively (USEPA, 2011). Although these predicted bioaccumulation and biomagnifications appear relatively high, n-octane would not be expected to be found in the tissues of fish or wildlife as (1) n-octane contains no persistent functional groups (e.g., chlorine, bromine), (2) exposure would be expected to be low based on a low half-life in the environment, and (3) subsequent to exposure, n-octane would be rapidly metabolized by the liver (similar to what is seen with other organic compounds, such as polycyclic aromatic hydrocarbons).
Exposure and Exposure Monitoring Because n-octane can exist as a liquid or vapor at normal temperature and pressure, the most probable route of exposure, as seen in most occupational settings, would occur by either dermal contact or inhalation. Oral exposure would most likely be either incidental or accidental. Isooctane, an n-octane
Encyclopedia of Toxicology, Volume 3
http://dx.doi.org/10.1016/B978-0-12-386454-3.00416-4
Octane
isomer, can comprise up to 1% of the total hydrocarbons emitted from the exhaust of diesel and gasoline engines. NIOSH has estimated >9000 workers are potentially exposed to n-octane in the United States. Occupational exposure to n-octane may occur through inhalation and dermal contact with this compound at workplaces where n-octane is produced or used. At automobile repair shops, petroleum refineries, or rubber industries requiring vulcanization processes, n-octane air concentrations can range from 0 to 300 mg m3. Octane has been measured in air down to levels as low as 0.1 ppb. It has been measured and detected in both indoor air (ND–533 mg m3) and outdoor air (<0.3–1 mg m3) with the latter typically a result of automobile emissions (Verschueren, 1996). A review of indoor air concentrations of volatile organic compounds in North America (Hodgson and Levin, 2003) also found an average n-octane in ‘existing’ residences of 0.7 ppb (3.3 mg m3) and 0.11 ppb (0.5 mg m3) in office buildings.
Toxicokinetics Inhaled n-octane is rapidly distributed from the blood to different organs and tissues, particularly those with high fat content. After absorption, n-octane is most likely converted to a hydroxy derivative (e.g., alcohol) via the cytochrome P450 oxidase system. The 1-octanol formed is conjugated with glucuronic acid or undergoes further oxidation to octanoic acid. The urinary metabolites of n-octane in Fischer 344 rats given the n-octane by gavage included 2-octanol, 3-octanol, 5oxohexanoic acid, and 6-oxoheptanoic acid. The sex of the animals influenced the relative amounts of metabolites formed. This was the first reported finding of keto acids in hydrocarbon oxidative metabolism. No kidney damage was found as a result of n-octane dosing although the 2,2,4-trimethylpentane (isooctane) isomer does cause kidney lesions in male rats.
Mechanism of Toxicity The mechanism of toxicity is suspected to be similar to other solvents that rapidly induce anesthesia-like effects, i.e., a ‘nonspecific narcosis’ due to disruption (solvation) of the integrity of the cellular membranes of the central nervous system (CNS). Octane is generally considered to be relatively nontoxic relative to the effect seen following exposure to other aliphatic hydrocarbons. This is probably due to the fact that it is less volatile than the shorter chain aliphatic hydrocarbons (e.g., pentane or heptane) and may not be as readily transferred across either the pulmonary alveoli or the blood–brain barrier. If it is aspirated into the lungs, however, n-octane will cause adverse effects similar to effects seen following aspiration of other petroleum distillates or compounds.
Acute and Short-Term Toxicity (Animal/Human) CNS depression was produced in mice in 30–90 min when exposed at 6600–13 700 ppm n-octane in air. Respiratory arrest occurred in 1 of 4 mice within 5 min at 16 000 ppm and in 4 of 4 mice within 3 min when exposed at 32 000 ppm. The
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CNS depressant potential of n-octane is approximately equivocal to heptane, but does not appear to exhibit other CNS effects seen in lower homologs. Octane does not cause nerve degeneration. The reported LC50 following a 4 h exposure of rats to noctane via inhalation is 118 g m3. A concentration of 35 mg l1 resulted in the loss of righting reflexes in mice and 50 mg l1 caused a total loss of reflexes. A concentration of 9.5% causes loss of reflexes in mice in 125 min; however, less than or equal to 1.9% is easily tolerated for 143 min, and the effects are reversible (HSDB, 2011). For 2,5-dimethylhexane (an octane isomer), the narcotic concentration in mice was 70 000–80 000 mg m3 (14 980–17 120 ppm), and the effects were less severe than those seen for n-octane. In rats, oral administration of isooctane caused moderate toxicity, and pulmonary lesions were observed following aspiration of octane into the lungs. None of the branched octane isomers is known to have neurotoxic properties. Acute adverse effects to humans would be expected to be similar to those seen in laboratory animals that are acutely exposed to petroleum solvents. Humans who are acutely exposed to hydrocarbon solvents show, in general order of increasing exposure, disorientation, euphoria, giddiness, confusion, unconsciousness, paralysis, convulsion, and death. Octane is moderately toxic if taken orally and more toxic than the lower molecular weight analogs by this route. It is similar in potency to heptane (especially with regard to narcotic effects) but is apparently without the associated peripheral neurotoxic signs of heptane and hexane. If it is aspirated into the lungs, it may cause rapid death due to cardiac arrest, respiratory paralysis, and asphyxia. At high air concentrations (generally between 5000 and 13 700 ppm for 30 min), it will have an acute narcotic effect but no adverse effects are apparent in humans at concentrations below 500 ppm.
Chronic Toxicity (Animal/Human) A comprehensive search on the adverse effects of n-octane following chronic exposure could not be found in the public domain. In subchronic (prechronic) exposures, daily intraperitoneal injections of n-octane (1.0 ml kg1) to rats for 7 days resulted in a decrease in body weight. In addition, liver enlargement was seen and there was a loss in drug metabolizing capability as phenobarbital sleep time was increased as a result of the diminished drug metabolizing activity of the liver (HSDB, 2011).
Immunotoxicity A comprehensive search on the adverse effects of n-octane on the immune system could not find any studies in the public domain. Pregnant women should, however, avoid inhalation of any type of petroleum solvent vapors.
Reproductive Toxicity A comprehensive search on the adverse reproductive effects of n-octane could not find any studies in the public domain.
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Octane
Pregnant women should, however, avoid inhalation of any type of petroleum solvent vapors.
Carcinogenicity Octane is not listed as a carcinogen by the National Toxicology Program, the Occupational Safety & Health Administration (OSHA), or the International Agency for Research on Cancer.
Clinical Management Persons who are exposed to high concentrations of n-octane in air should vacate or be removed from the source and seek fresh air. Upon oral ingestion, vomiting should not be induced as pulmonary aspiration may occur, resulting in severe pneumonitis and/or death. In areas of expected increased concentration, extreme care must be taken to use explosion-proof apparatus and keep the areas free from ignition sources, such as sparks from static electricity.
Industrial Hygienists (ACGIH) 8-h TWA is 300 ppm (excursions in worker exposure levels may exceed three times the TLV–TWA for not more than a total of 30 min during a workday, and it is recommended that under no circumstances should they exceed five times the TLV–TWA, provided that the TLV–TWA is not exceeded). NIOSH’s recommended exposure limit is a 10-h TWA of 75 ppm (350 mg m3) with a 15 min ceiling value of 385 ppm (1800 mg m3). The level that would be ‘immediately dangerous to life or health’ is 1000 ppm (based on 10% of the lower explosion limit for safety considerations even though the relevant toxicological data indicated that irreversible health effects or impairment of escape existed only at higher concentrations.)
See also: Decane; Gasoline; Heptane; Hexane; Petroleum Distillates; Petroleum Hydrocarbons; Pentane; Polycyclic Aromatic Hydrocarbons (PAHs).
Further Reading Ecotoxicology No significant mortalities were reported for young coho salmon (Oncorhynchus kisutch) exposed to 100 mg l1 in artificial seawater after 96 h at 8 C (Verschueren, 1996). No significant mortality of the eggs of the Pacific oyster was seen at concentrations <3500 mg l1. An EC50 of 120 mg l1 was calculated based on the effects on the feeding behavior of a test population of blue mussels. Some types of soil-dwelling bacteria can exist using branched chain octanes as the sole carbon sources.
Other Hazards Extreme care must be taken to keep areas of expected high concentration free from ignition sources; for example, sparks from static electricity. Only explosion-proof equipment should be used in these areas. The lower and upper explosive limits for n-octane are 1 and 4.7% by volume, respectively.
Exposure Standards and Guidelines Octane has an OSHA 8-h time weighted average (TWA) of 500 ppm (2350 mg m3). The American Conference of
Hodgson, A.T., Levin, H., 2003. Volatile Organic Compounds in Indoor Air: A Review of Concentrations Measured in North America Since 1990. LBNL-51715. Revised Oct. 2003. http://energy.lbl.gov/ied/pdf/LBNL-51715.pdf Kim, S.J., Rim, K.T., Kim, H.Y., Yang, J.S., August 2010. Mutagenicity of octane and tetrasodium pyrophosphate in bacterial reverse mutation (Ames) test. J. Toxicol. Sci. 35 (4), 555–562. Schultz, T.W., 1989. Nonpolar narcosis: a review of the mechanisms of action for baseline aquatic toxicity. ASTM STP 1027. In: Cowgill, U.M., Williams, L.R. (Eds.), Aquatic Toxicology and Hazard Assessment, vol. 12. American Society for Testing and Materials, Philadelphia, pp. 104–109. Verschueren, K., 1996. Handbook of Environmental Data on Organic Chemicals, third ed. Van Nostrand Reinhold, NY, ISBN 0-442-01916-5.
Relevant Websites http://www.toxnet.nlm.nih.gov – HSDB, 2011. Octane. Hazardous Substances Data Bank, National Library of Medicine TOXNET System (Record No. 108). Searched 24 October 2011. http://www.epa.gov/oppt/exposure/pubs/episuite.htm – USEPA, 2011. United States Environmental Protection Agency, Office of Pollution Prevention Toxics and Syracuse Research Corporation. EPI Suite Quantitative Structure Activity Relationship Computer Program.
Name: Octane Chemical Abstracts Service Registry Number: 111-65-9 Synonyms: n-Octane (UN1262, DOT), Oktan (Polish), Oktanen (Dutch), Ottani (Italian) Chemical/Pharmaceutical/Other Class: Aliphatic hydrocarbon (C8) Molecular Formula: C8H18 Chemical Structure: H3C
CH3
n-Octane
CH3
CH3
H3C
CH3 CH3
Isooctane (2,2,4-trimethylpentane)
Uses n-Octane is used as a solvent and raw material for organic synthesis reactions and is a very important chemical in the petroleum industry. It is also widely used in the rubber and paper processing industries. Isooctane, along with other nalkanes and isoparaffins, is used in the blending of fuels to achieve desired antiknock properties.
Environmental Fate and Behavior Octane is an eight carbon aliphatic compound that is a natural constituent of the major paraffin fraction of crude oil and also found in natural gas. A total of 17 isomers of octane are known to exist and differ by the amount and location of branching in the carbon chain. Isooctane (2,2,4-trimethylpentane) is a principal ingredient of gasoline and is used as a standard in the octane rating of gasoline. Pure n-octane is a colorless liquid that is highly flammable and lighter than water. It has a gasolinelike odor with an olfactory threshold around 400 ppm. Octane has a molecular weight of 114.23 g mol1. At 20 C, n-octane has a solubility of 0.66 mg l1 in water and a Henry’s law constant of 3.2 atm m3 mol1 (USEPA, 2011). The log octanol/water partition coefficient is 5.18. Conversion factors for n-heptane in air are as follows: 1 mg m3 ¼ 0.21 ppm; 1 ppm ¼ 4.67 mg m3. If released to air, a vapor pressure of 14.1 mmHg at 25 C indicates n-octane will exist solely as a vapor in the ambient atmosphere. Vapor-phase n-octane will be degraded in the atmosphere by reaction with photochemically produced
652
hydroxyl radicals; the half-life for this reaction in air is estimated to be 44 h (USEPA, 2011). Vapor-phase n-octane will not undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups nor photolyze due to the lack of absorption in the ultraviolet spectrum (>290 nm). Experimental data showed that w33% of the n-octane fraction in a dark chamber reacted with nitrate radical to form the corresponding alkyl nitrate, suggesting nighttime reactions with nitrate radicals may contribute to the atmospheric transformation of n-octane, especially in urban environments (HSDB, 2011). The Henry’s law constant for n-octane indicates that it is expected to volatilize rapidly from water surfaces. Based on this Henry’s law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m s1, wind velocity of 3 m s1) is estimated as 1.1 h. The volatilization half-life from a model lake (1 m deep, flowing 0.05 m s1, wind velocity of 0.5 m s1) is estimated as 4.2 days (USEPA, 2011). Volatilization from water surfaces may be attenuated by adsorption to suspended sediment in the water. The estimated volatilization half-life from a model pond is 11 months if adsorption is considered. However, in a study using a jet fuel mixture and sterile freshwater controls from the Escambia River (Florida), a 99% loss of n-octane was attributed to evaporation at 25 C. If released to soil, n-octane is expected to have very low mobility based upon an estimated Koc of 16 000. Volatilization from moist soil surfaces is expected to be an important fate process based upon the estimated Henry’s law constant. However, adsorption to soil is expected to attenuate volatilization. n-Octane would also be expected to volatilize from dry soil surfaces based upon its vapor pressure. Octane is expected to biodegrade in soil under aerobic conditions (HSDB, 2011). Using a measured log Kow of 5.18, the United States Environmental Protection Agency’s EPI Suite computer program estimates a bioconcentration factor and a bioaccumulation factor of 1086 and 1155, respectively (USEPA, 2011). Although these predicted bioaccumulation and biomagnifications appear relatively high, n-octane would not be expected to be found in the tissues of fish or wildlife as (1) n-octane contains no persistent functional groups (e.g., chlorine, bromine), (2) exposure would be expected to be low based on a low half-life in the environment, and (3) subsequent to exposure, n-octane would be rapidly metabolized by the liver (similar to what is seen with other organic compounds, such as polycyclic aromatic hydrocarbons).
Exposure and Exposure Monitoring Because n-octane can exist as a liquid or vapor at normal temperature and pressure, the most probable route of exposure, as seen in most occupational settings, would occur by either dermal contact or inhalation. Oral exposure would most likely be either incidental or accidental. Isooctane, an n-octane
Encyclopedia of Toxicology, Volume 3
http://dx.doi.org/10.1016/B978-0-12-386454-3.00416-4
Octane
isomer, can comprise up to 1% of the total hydrocarbons emitted from the exhaust of diesel and gasoline engines. NIOSH has estimated >9000 workers are potentially exposed to n-octane in the United States. Occupational exposure to n-octane may occur through inhalation and dermal contact with this compound at workplaces where n-octane is produced or used. At automobile repair shops, petroleum refineries, or rubber industries requiring vulcanization processes, n-octane air concentrations can range from 0 to 300 mg m3. Octane has been measured in air down to levels as low as 0.1 ppb. It has been measured and detected in both indoor air (ND–533 mg m3) and outdoor air (<0.3–1 mg m3) with the latter typically a result of automobile emissions (Verschueren, 1996). A review of indoor air concentrations of volatile organic compounds in North America (Hodgson and Levin, 2003) also found an average n-octane in ‘existing’ residences of 0.7 ppb (3.3 mg m3) and 0.11 ppb (0.5 mg m3) in office buildings.
Toxicokinetics Inhaled n-octane is rapidly distributed from the blood to different organs and tissues, particularly those with high fat content. After absorption, n-octane is most likely converted to a hydroxy derivative (e.g., alcohol) via the cytochrome P450 oxidase system. The 1-octanol formed is conjugated with glucuronic acid or undergoes further oxidation to octanoic acid. The urinary metabolites of n-octane in Fischer 344 rats given the n-octane by gavage included 2-octanol, 3-octanol, 5oxohexanoic acid, and 6-oxoheptanoic acid. The sex of the animals influenced the relative amounts of metabolites formed. This was the first reported finding of keto acids in hydrocarbon oxidative metabolism. No kidney damage was found as a result of n-octane dosing although the 2,2,4-trimethylpentane (isooctane) isomer does cause kidney lesions in male rats.
Mechanism of Toxicity The mechanism of toxicity is suspected to be similar to other solvents that rapidly induce anesthesia-like effects, i.e., a ‘nonspecific narcosis’ due to disruption (solvation) of the integrity of the cellular membranes of the central nervous system (CNS). Octane is generally considered to be relatively nontoxic relative to the effect seen following exposure to other aliphatic hydrocarbons. This is probably due to the fact that it is less volatile than the shorter chain aliphatic hydrocarbons (e.g., pentane or heptane) and may not be as readily transferred across either the pulmonary alveoli or the blood–brain barrier. If it is aspirated into the lungs, however, n-octane will cause adverse effects similar to effects seen following aspiration of other petroleum distillates or compounds.
Acute and Short-Term Toxicity (Animal/Human) CNS depression was produced in mice in 30–90 min when exposed at 6600–13 700 ppm n-octane in air. Respiratory arrest occurred in 1 of 4 mice within 5 min at 16 000 ppm and in 4 of 4 mice within 3 min when exposed at 32 000 ppm. The
653
CNS depressant potential of n-octane is approximately equivocal to heptane, but does not appear to exhibit other CNS effects seen in lower homologs. Octane does not cause nerve degeneration. The reported LC50 following a 4 h exposure of rats to noctane via inhalation is 118 g m3. A concentration of 35 mg l1 resulted in the loss of righting reflexes in mice and 50 mg l1 caused a total loss of reflexes. A concentration of 9.5% causes loss of reflexes in mice in 125 min; however, less than or equal to 1.9% is easily tolerated for 143 min, and the effects are reversible (HSDB, 2011). For 2,5-dimethylhexane (an octane isomer), the narcotic concentration in mice was 70 000–80 000 mg m3 (14 980–17 120 ppm), and the effects were less severe than those seen for n-octane. In rats, oral administration of isooctane caused moderate toxicity, and pulmonary lesions were observed following aspiration of octane into the lungs. None of the branched octane isomers is known to have neurotoxic properties. Acute adverse effects to humans would be expected to be similar to those seen in laboratory animals that are acutely exposed to petroleum solvents. Humans who are acutely exposed to hydrocarbon solvents show, in general order of increasing exposure, disorientation, euphoria, giddiness, confusion, unconsciousness, paralysis, convulsion, and death. Octane is moderately toxic if taken orally and more toxic than the lower molecular weight analogs by this route. It is similar in potency to heptane (especially with regard to narcotic effects) but is apparently without the associated peripheral neurotoxic signs of heptane and hexane. If it is aspirated into the lungs, it may cause rapid death due to cardiac arrest, respiratory paralysis, and asphyxia. At high air concentrations (generally between 5000 and 13 700 ppm for 30 min), it will have an acute narcotic effect but no adverse effects are apparent in humans at concentrations below 500 ppm.
Chronic Toxicity (Animal/Human) A comprehensive search on the adverse effects of n-octane following chronic exposure could not be found in the public domain. In subchronic (prechronic) exposures, daily intraperitoneal injections of n-octane (1.0 ml kg1) to rats for 7 days resulted in a decrease in body weight. In addition, liver enlargement was seen and there was a loss in drug metabolizing capability as phenobarbital sleep time was increased as a result of the diminished drug metabolizing activity of the liver (HSDB, 2011).
Immunotoxicity A comprehensive search on the adverse effects of n-octane on the immune system could not find any studies in the public domain. Pregnant women should, however, avoid inhalation of any type of petroleum solvent vapors.
Reproductive Toxicity A comprehensive search on the adverse reproductive effects of n-octane could not find any studies in the public domain.
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Octane
Pregnant women should, however, avoid inhalation of any type of petroleum solvent vapors.
Carcinogenicity Octane is not listed as a carcinogen by the National Toxicology Program, the Occupational Safety & Health Administration (OSHA), or the International Agency for Research on Cancer.
Clinical Management Persons who are exposed to high concentrations of n-octane in air should vacate or be removed from the source and seek fresh air. Upon oral ingestion, vomiting should not be induced as pulmonary aspiration may occur, resulting in severe pneumonitis and/or death. In areas of expected increased concentration, extreme care must be taken to use explosion-proof apparatus and keep the areas free from ignition sources, such as sparks from static electricity.
Industrial Hygienists (ACGIH) 8-h TWA is 300 ppm (excursions in worker exposure levels may exceed three times the TLV–TWA for not more than a total of 30 min during a workday, and it is recommended that under no circumstances should they exceed five times the TLV–TWA, provided that the TLV–TWA is not exceeded). NIOSH’s recommended exposure limit is a 10-h TWA of 75 ppm (350 mg m3) with a 15 min ceiling value of 385 ppm (1800 mg m3). The level that would be ‘immediately dangerous to life or health’ is 1000 ppm (based on 10% of the lower explosion limit for safety considerations even though the relevant toxicological data indicated that irreversible health effects or impairment of escape existed only at higher concentrations.)
See also: Decane; Gasoline; Heptane; Hexane; Petroleum Distillates; Petroleum Hydrocarbons; Pentane; Polycyclic Aromatic Hydrocarbons (PAHs).
Further Reading Ecotoxicology No significant mortalities were reported for young coho salmon (Oncorhynchus kisutch) exposed to 100 mg l1 in artificial seawater after 96 h at 8 C (Verschueren, 1996). No significant mortality of the eggs of the Pacific oyster was seen at concentrations <3500 mg l1. An EC50 of 120 mg l1 was calculated based on the effects on the feeding behavior of a test population of blue mussels. Some types of soil-dwelling bacteria can exist using branched chain octanes as the sole carbon sources.
Other Hazards Extreme care must be taken to keep areas of expected high concentration free from ignition sources; for example, sparks from static electricity. Only explosion-proof equipment should be used in these areas. The lower and upper explosive limits for n-octane are 1 and 4.7% by volume, respectively.
Exposure Standards and Guidelines Octane has an OSHA 8-h time weighted average (TWA) of 500 ppm (2350 mg m3). The American Conference of
Hodgson, A.T., Levin, H., 2003. Volatile Organic Compounds in Indoor Air: A Review of Concentrations Measured in North America Since 1990. LBNL-51715. Revised Oct. 2003. http://energy.lbl.gov/ied/pdf/LBNL-51715.pdf Kim, S.J., Rim, K.T., Kim, H.Y., Yang, J.S., August 2010. Mutagenicity of octane and tetrasodium pyrophosphate in bacterial reverse mutation (Ames) test. J. Toxicol. Sci. 35 (4), 555–562. Schultz, T.W., 1989. Nonpolar narcosis: a review of the mechanisms of action for baseline aquatic toxicity. ASTM STP 1027. In: Cowgill, U.M., Williams, L.R. (Eds.), Aquatic Toxicology and Hazard Assessment, vol. 12. American Society for Testing and Materials, Philadelphia, pp. 104–109. Verschueren, K., 1996. Handbook of Environmental Data on Organic Chemicals, third ed. Van Nostrand Reinhold, NY, ISBN 0-442-01916-5.
Relevant Websites http://www.toxnet.nlm.nih.gov – HSDB, 2011. Octane. Hazardous Substances Data Bank, National Library of Medicine TOXNET System (Record No. 108). Searched 24 October 2011. http://www.epa.gov/oppt/exposure/pubs/episuite.htm – USEPA, 2011. United States Environmental Protection Agency, Office of Pollution Prevention Toxics and Syracuse Research Corporation. EPI Suite Quantitative Structure Activity Relationship Computer Program.