The gasoline discussed in this fact sheet
is automotive used as a fuel for engines in cars. Gasoline
is a colorless, pale brown, or pink liquid, and is very flammable.
Gasoline is a manufactured mixture that
does not exist naturally in the environment. Gasoline is produced
from petroleum in the refining process.
Typically, gasoline contains more than
150 chemicals, including small amounts of benzene, toluene,
automotive gasolineylene, and sometimes lead. How the gasoline
is made determines which chemicals are present in the gasoline
mixture and how much of each is present. The actual composition
varies with the source of the crude petroleum, the manufacturer,
and the time of year.
U.S. gasoline contains about 1% benzene and about 1% n-hexane. Gasoline additives include organic lead, ethylene dibromide, ethanol, methanol, methyl tertiary butyl ether (MTBE), and tertiary butyl ether (TBE). In some countries Benzene content may be as high as 30%! For more specific information about the hazards of Benzene visit our Benzene Bible which includes complete Benzene MSDS, public health FAQs, and toxicological information.
Gasoline may also be referred to as: Motor fuel, Motor spirits, Natural gasoline, Petrol [Note: A complex mixture of volatile hydrocarbons (paraffins, cycloparaffins & aromatics).] Antiknock gasoline, Benzin (German), Casing head gasoline, Cracked gasoline, EINECS 232-349-1, HSDB 6477, Mogas (short for motor gasoline), Gasolina (spanish), Benzin (German), High-octane gasoline, Light gasoline, Natural gasoline, Natural gasoline (natural gas), Petrol (British), natural Petrol, Petroleum distillates, Polymer gasoline, Pyrolysis gasoline, Reformed gasoline, Straight-run gasoline, UN 1203, White gasoline, natural Gasoline, Gasoline (casinghead), Gasoline [UN1203][Flammable liquid], Unleaded gasoline (wholly vaporized).
A major hazard associated with automotive gasoline is Benzene. Benzene was used in the past as a solvent in inks, rubber, lacquers, and paint removers. Today, it is used mainly in closed processes to synthesize organic chemicals. Gasoline in some countries contains a high concentration of benzene (as high as 30%); the U.S. average is 1-3%. Workers who remove or clean underground storage tanks may be exposed to significant levels.
Many of the harmful effects seen after
exposure to gasoline are due to the individual chemicals in
the gasoline mixture, such as benzene and lead. Inhaling or
swallowing large amounts of gasoline can cause death.
Inhaling high concentrations of gasoline
is irritating to the lungs when breathed in and irritating
to the lining of the stomach when swallowed. Gasoline is also
a skin irritant. Breathing in high levels of gasoline for
short periods or swallowing large amounts of gasoline may
also cause harmful effects on the nervous system.
Serious nervous system effects include
coma and the inability to breathe, while less serious effects
include dizziness and headaches.
There is not enough information available
to determine if gasoline causes birth defects or affects reproduction.
The systemic symptoms of acute solvent poisoning from Automobile Gasoline may resemble those of intoxication from alcoholic beverages. Like HARD liquor, organic solvents can cause: Toxicity to Liver (Hepatotoxicity), Heart sensitization, Anesthesia, Respiratory irritation, Reaction time increased, and Dermatitis. Biological monitoring of exposed workers may be preferable to air monitoring because solvent uptake is greatly influenced by workload.
Other syptoms of Acute Toxic Solvent Poisoning from Automotive Gasoline may include:
- arrhythmia
- confusion
- dermatitis
- dizziness
- fatigue
- headache
- incoordination
- inebriation
- irritability
- lethargy
- liver function test, abnormal
- speech, impaired
- stupor and coma
Common Automotive Gasoline Additives Which May Cause Additional Health Hazards:
Aromatic Hydrocarbons as replacements for Tetra-ethyl lead - Ethers and Alcohols such as Ethanol or Methanol which help to reduce "engine-knocking" or "pinging" noises.
Methylcyclopentadienyl manganese tricarbonyl (MMT)- to boost octane and help older cars originally designed to run leaded gas use unleaded gas without the need for fuel additives to prevent valve problems.
MTBE, Ethanol and ETBE - to introduce oxygen to gas which reduces the amount of carbon monoxide and unburned fuel in the exhaust gas, thus reducing smog.
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The Department of Health and Human Services
(DHHS) and the International Agency for Research on Cancer
(IARC) have not classified automotive gasoline for carcinogenicity.
Automotive gasoline is currently undergoing review by the
EPA for cancer classification.
Some laboratory animals that breathed
high concentrations of unleaded gasoline vapors continuously
for 2 years developed liver and kidney tumors. However, there
is no evidence that exposure to gasoline causes cancer in
humans.
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Laboratory tests are available that can
measure elevated blood or urine levels of lead (as an indication
of exposure to leaded gasoline only), benzene, or other substances
that may result from exposure to gasoline or other sources.
These methods are sensitive enough to measure background levels
and levels where health effects may occur. These tests aren't
available in most doctors' offices, but can be done at special
laboratories that have the right equipment.
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The EPA has established many regulations
to control air pollution. These are designed to protect the
public from the possible harmful health effects of gasoline.
The American Conference of Governmental
Industrial Hygienists (ACGIH) set a maximum level of 890 milligrams
of gasoline per cubic meter of air (890 mg/m³) for an
8-hour workday, 40-hour workweek.
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Carcinogenicity: Ability to cause cancer.
CAS: Chemical Abstracts Service.
Crude petroleum: Petroleum that has not
been processed.
Dissolve: To disappear gradually.
Evaporate: To change into a vapor or
a gas.
Irritant: A substance that causes an
abnormal reaction.
Mixture: A combination of two or more
components.
Refining process: The process by which
petroleum is purified to form gasoline.
Tumor: An abnormal mass of tissue.
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Agency for Toxic Substances and Disease
Registry (ATSDR). 1996. Managing Hazardous Materials Incidents.
Volume III – Medical Management Guidelines for Acute
Chemical Exposures: Automotive Gasoline. Atlanta,
GA: U.S. Department of Health and Human Services, Public Health
Service.
Agency for Toxic Substances and Disease
Registry (ATSDR). 1995. Toxicological
Profile for automotive gasoline. Atlanta, GA: U.S. Department
of Health and Human Services, Public Health Service.
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ATSDR can tell you where to find occupational
and environmental health clinics. Their specialists can recognize,
evaluate, and treat illnesses resulting from exposure to hazardous
substances. You can also contact your community or state health
or environmental quality department if you have any more questions
or concerns.
For more information, contact:
Agency for Toxic Substances and Disease Registry
Division of Toxicology
1600 Clifton Road NE, Mailstop F-32
Atlanta, GA 30333
Phone: 1-888-42-ATSDR (1-888-422-8737)
FAX: (770)-488-4178
Email: ATSDRIC@cdc.gov
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Automotive Gasoline MSDS Information
SECTION I - Material Identity
| Item Name............................... |
GASOLINE, AUTOMOTIVE |
| Part Number/Trade Name.................. |
GASOLINE |
| National Stock Number................... |
9130001487103 |
| CAGE Code............................... |
0A0Y5 |
| Part Number Indicator................... |
A |
| MSDS Number............................. |
93218 |
| HAZ Code................................ |
B |
SECTION II - Manufacturer's Information
| Manufacturer Name....................... |
FRONTIER OIL AND REFINING COMPANY |
| Street.................................. |
1600 BROADWAY |
| City.................................... |
DENVER |
| State................................... |
CO |
| Country................................. |
US |
| Zip Code................................ |
80202 |
| Emergency Phone......................... |
307-634-3551 CHEMTREC 800-424-9300 |
| Information Phone....................... |
307-634-3551 |
MSDS Preparer's Information
| Date MSDS Prepared/Revised.............. |
UNDATED |
| Date of Technical Review................ |
28APR93 |
| Active Indicator........................ |
N |
| Item Manager............................ |
KY |
Alternate Vendors
| Vendor #5 CAGE.......................... |
BQMYS |
SECTION III - Physical/Chemical Characteristics
| Specification Number.................... |
VV-G-1690 |
| Specification Type/Grade/Class.......... |
REGULAR, UNLEADED |
| Hazard Storage Compatibility Code....... |
F2 |
| NRC License Number...................... |
N/R |
| Net Propellant Weight (Ammo)............ |
N/R |
| Appearance/Odor......................... |
WATER WHITE TO STRAW YELLOW LIQUID, GASOLINE ODOR. |
| Boiling Point........................... |
85.0F,29.4C |
| Melting Point........................... |
<-76F,<-60C |
| Vapor Pressure.......................... |
275-475MMH |
| Vapor Density........................... |
>1 |
| Specific Gravity........................ |
O.70-0.77 |
| Decomposition Temperature............... |
UNKNOWN |
| Evaporation Rate........................ |
<1 (ETHER=1) |
| Solubility in Water..................... |
INCOLUBLE |
| Percent Volatiles by Volume............. |
100 |
| Chemical pH............................. |
N/R |
| Corrosion Rate.......................... |
UNKNOWN |
| Container Type.......................... |
R |
| Container Pressure Code................. |
4 |
| Temperature Code........................ |
8 |
| Product State Code...................... |
L |
SECTION IV - Fire and Explosion Hazard Data
| Flash Point............................. |
-50 |
| Flash Point Method...................... |
TCC |
| Lower Explosion Limit................... |
<1% |
| Upper Explosion Limit................... |
8% |
| Extinguishing Media..................... |
USE CARBON DIOXIDE, FOAM, HALON OR DRY CHEMICAL. USE WATER FOG TO COOL SRROUNDING CONTAINERS. |
| Special Fire Fighting Procedures........ |
WEAR FIRE FIGHTING PROTECTIVE EQUIPMENT AND A FULL FACED SELF CONTAINED BREATHING APPARATUS. EVACUATE AREA. COOL FIRE EXPOSED CONTAINERS WITH WATER SPRAY. |
| Unusual Fire/Explosion Hazards.......... |
VAPORS ARE HEAVIER THAN AIR AND MAY TRAVEL A CONSIDERABLE DISTANCE TO SOURCE OF IGNITION AND FLASH BACK. |
SECTION V - Reactivity Data
| Stability............................... |
YES |
| Stability Conditions to Avoid........... |
HIGH HEAT, OPEN FLAMES AND OTHER SOURCES OF IGNITION |
| Materials to Avoid...................... |
STRONG OXIDIZING AGENTS, STRRONG ACIDS & ALKALIS, AND HALOGENS. |
| Hazardous Decomposition Products........ |
CARBON MONOXIDE, CARBON DIOXIDE AND OTHER HYDROCARBON COMPOUNDS DURING COMBUSTION. |
| Hazardous Polymerization................ |
NO |
| Polymerization Conditions to Avoid...... |
NOT APPLICABLE |
| LD50 - LD50 Mixture..................... |
ORAL LD50 (RAT) IS UNKNOWN |
SECTION VI - Health Hazard Data
| Route of Entry: Skin.................... |
YES |
| Route of Entry: Ingestion............... |
NO |
| Route of Entry: Inhalation.............. |
YES |
| Health Hazards - Acute and Chronic...... |
ACUTE-INHALATION:CENTRAL NERVOUS SYSTEM DEPRESSION, NARCOSIS, UNCONSCIOUSNESS, ASPHYXIATION. EYE:IRRITATION. SKIN:DEFATING, IRRITATION. INGESTION: GI DISTURBANCES, ASPIRATION PNEUMONITIS. CHRONIC: DERMATITIS, ANEMIA, PULMONARY EDEMA, LIVER AND KIDNEY DAMAGE. |
| Carcinogenity: NTP...................... |
YES |
| Carcinogenity: IARC..................... |
YES |
| Carcinogenity: OSHA..................... |
YES |
| Explanation of Carcinogenity............ |
CONTAINS Benzene 9-43-2 WHICH IS LISTED BY NTP AND IARC AND REGULATED BY OSHA AS A CARCINOGEN. |
| Symptoms of Overexposure................ |
RESPIRATORY IRRITATION, COUGHING, DIFFICULTY IN BREATHING, NAUSEA, VOMITING, FATIGUE, BLURRED VISION, DIZZINESS, HEADACHES, UNCONSCIOUSNESS, EYE IRRITATION, REDNESS, DRY SKIN. |
| Medical Cond. Aggrevated by Exposure.... |
SKIN AND RESPIRATORY DISORDERS. |
| Emergency/First Aid Procedures.......... |
SKIN: REMOVE CONTAMINATED CLOTHING. WASH WITH SOAP AND WATER. GET MEDICAL ATTENTION IF IRRITATION PERSISTS. INHALATION: REMOVE TO FRESH AIR & RESTORE BREATHING IF NECESSARY. GET MEDICAL ATTENTION. EYE: IMMEDIATELY FLUSH WITH WATER FOR 15 MINUTES WHILE HOLDING EYELIDS OPEN. GET MEDICAL ATTENTION. INGESTION: GET IMMEDIATE MEDICAL ATTENTION. DO NOT INDUCE VOMITING. NOTHING BY MOUTH IF UNCONSCIOUS. |
SECTION VII - Precautions for Safe Handling and Use
| Steps if Material Released/Spilled...... |
MINOR: ABSORB MATERIAL WITH CLAY, VERMICULITE, OR SIMILAR ABSORBENT MATERIAL. PLACE IN DISPOSAL CONTAINERS. MAJOR: DIKE & CONTAIN SPILL. ELIMINATE SOURCES OF IGNITION. SHUT OFF LEAKS. REMOVE LIQUID BY VACUUM OR ABSORBENT. |
| Neutralizing Agent...................... |
NOT APPLICABLE |
| Waste Disposal Method................... |
WASTE MAY BE BURNED IN AN APPROVED INCINERATOR OR DISPOSED OF IN ACCORDANCE WITH ALL APPLICABLE LOCAL, STATE AND FEDERAL LAWS AND REGULATIONS. |
| Handling and Storage Precautions........ |
RE IN A COOL, VENTILATED WORK AREA. KEEP CONTAINERS CLOSED WHEN NOT IN USE. FLAMMABLE LIQUID; EMPTY CONTAINERS CAN BE HAZARDOUS. EX |
| Other Precautions....................... |
EXTREMELY FLAMMABLE LIQUID AND VAPOR. HIGHLY VOLATILE. VAPOR MAY CAUSE FLASH FIRE. VAPORS MAY SPREAD LONG DISTANCES AND IGNITE. KEEP AWAY FROM HEAT, SPARKS, AND FLAME. KEEP CONTAINER CLOSED. USE WITH ADEQUATE VENTILATION. |
SECTION VIII - Control Measures
| Respiratory Protection.................. |
USE NIOSH APPROVED RESPIRATOR. AIR-SUPPLIED OR FILTERING TYPE WITH ORGANIC VAPOR CARTRIDGES ARE RECOMMENDED. |
| Ventilation............................. |
LOCAL AND MECHANICAL EXHAUST RECOMMENDED. AVOID OPEN ELECTRICAL SOURCES NEAR PRODUCT VAPOR AREAS. |
| Protective Gloves....................... |
NEOPRENE, NITRILE, OR POLYVINYL ALCOHOL |
| Eye Protection.......................... |
USE CHEMICAL SAFETY GOGGLES & FACESHIELD |
| Other Protective Equipment.............. |
EYE WASH STATION & SAFETY SHOWER. |
| Work Hygenic Practices.................. |
DO NOT TAKE INTERNALLY. AVOID SKIN CONTACT. WASH SKIN AFTER USING PRODUCT. DO NOT EAT, DRINK OR SMOKE IN WORK AREA. |
| Supplemental Health/Safety Data......... |
NONE |
| Disposal Code........................... |
O |
SECTION IX - Label Data
| Protect Eye............................. |
YES |
| Protect Skin............................ |
YES |
| Protect Respiratory..................... |
YES |
| Chronic Indicator....................... |
UNKNOWN |
| Contact Code............................ |
MODERATE |
| Fire Code............................... |
UNKNOWN |
| Health Code............................. |
UNKNOWN |
| React Code.............................. |
UNKNOWN |
SECTION X - Transportation Data
| Container Quantity...................... |
5 |
| Unit of Measure......................... |
GL |
SECTION XI - Site Specific/Reporting Information
| Volatile Organic Compounds (P/G)........ |
6.4253 |
| Volatile Organic Compounds (G/L)........ |
770 |
SECTION XII - Ingredients/Identity Information
| Ingredient #............................ |
01 |
| Ingredient Name......................... |
MIXTURE OF PETROLEUM HYDROCARBONS (AROMATIC AND PARAFFINIC HYDROCARBONS) |
| NIOSH Number............................ |
1009503PH |
| Proprietary............................. |
NO |
| Percent................................. |
N/K |
| OSHA PEL................................ |
300 PPM TWA GASOLINE |
| ACGIH TLV............................... |
300 PPM TWA GASOLINE |
| Recommended Limit....................... |
NONE RECOMMENDED |
| Ingredient #............................ |
02 |
| Ingredient Name......................... |
BENZENE (ESTIMATE 2%) |
| CAS Number.............................. |
71432 |
| NIOSH Number............................ |
CY1400000 |
| Proprietary............................. |
NO |
| Percent................................. |
2 |
| OSHA PEL................................ |
1PPM/5STEL;1910.1028 |
| ACGIH TLV............................... |
10 PPM; A2; 9293 |
| Recommended Limit....................... |
NONE RECOMMENDED |
Gasoline MSDS DISCLAIMER
Employers, employees, and anyone else should use this information only as a supplement to other information gathered by them, and should make independent judgement of suitability of this information to ensure proper use and protect health and safety. This information is furnished without warranty, and any use of the product not in conformance with this Material Safety Data Sheet, or in combination with any other product or process, is the responsibility of the user.
|
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Gasoline Toxicological Information
Human Health Effects
Evidence for Carcinogenicity
Human Toxicity Excerpts
Human Toxicity Values
Skin, Eye and Respiratory Irritations
Probable Routes of Human Exposure
Emergency Medical Treatment
Emergency Medical
Treatment
Antidote and Emergency Treatment
Animal Toxicity Studies
Evidence
for Carcinogenicity
Non-Human Toxicity
Excerpts
Ecotoxicity Excerpts
Non-Human Toxicity Values
Ecotoxicity Values
Metabolism/Pharmacokinetics
Metabolism/Metabolites
Absorption,
Distribution & Excretion
Biological
Half-Life
Mechanism of Action
Interactions
Pharmacology
Interactions
Environmental Fate
& Exposure
Environmental Fate/Exposure
Summary
Probable Routes of Human Exposure
Artificial Pollution Sources
Environmental Fate
Environmental Biodegradation
Environmental Abiotic Degradation
Environmental Bioconcentration
Soil Adsorption/Mobility
Volatilization from Water/Soil
Environmental Water Concentrations
Effluent Concentrations
Sediment/Soil Concentrations
Atmospheric Concentrations
Food Survey Values
Environmental
Standards & Regulations
Federal Drinking
Water Guidelines
State Drinking Water
Guidelines
Chemical/Physical Properties
Molecular Formula
Color/Form
Odor
Boiling Point
Melting Point
Density/Specific Gravity
Solubilities
Spectral Properties
Vapor Density
Vapor Pressure
Chemical Safety
& Handling
DOT Emergency Guidelines
Skin, Eye and Respiratory Irritations
Fire Potential
NFPA Hazard Classification
Flammable Limits
Flash Point
Autoignition Temperature
Fire Fighting Procedures
Firefighting Hazards
Hazardous Reactivities &
Incompatibilities
Other Hazardous Reaction
Protective Equipment & Clothing
Preventive Measures
Shipment Methods and Regulations
Storage Conditions
Cleanup Methods
Disposal Methods
Occupational
Exposure Standards
OSHA Standards
Threshold Limit Values
Manufacturing/Use Information
Major Uses
Manufacturers
Methods of Manufacturing
General Manufacturing Information
Formulations/Preparations
U. S. Production
U. S. Imports
U. S. Exports
Laboratory Methods
Clinical Laboratory Methods
Analytic Laboratory Methods
Special References
Special Reports
Synonyms and Identifiers
Related HSDB Records
Synonyms
Associated Chemicals
Formulations/Preparations
Shipping Name/
Number DOT/UN/NA/IMO
GASOLINE
CASRN: 8006-61-9
According to the U.S. Environmental Protection Agency, reformulated gasoline (RFG) is gasoline blended such that, on average, it significantly reduces Volatile Organic Compounds (VOC) and air toxics emissions relative to conventional gasolines. The majority of air toxics emission reductions from RFG are from benzene. Oxygenates are added to RFG as octane extenders and for controlling carbon monoxide emissions. The majority of the oxygenates are methyl tertiary-butyl ether (MTBE) and ethanol. This record does not address RFG; information on oxygenates can be obtained from records on each individual compound. Motor vehicles also emit a variety of toxic air pollutants as the result of the fuel combustion process. The three major pollutants are hydrocarbons, nitrogen oxides, and carbon monoxide, also because of their health effects, benzene, formaldehyde, acetaldehyde, 1,3-butadiene, and particulate organic matter are also of concern.This record does not address the release of those pollutants, the records for the those individual chemicals would provide the relevant information.
For other data, click on the Table of ContentsHuman Health Effects:
Evidence for Carcinogenicity:
Classification of carcinogenicity: 1) evidence in humans: inadequate; 2) evidence in animals: limited. Overall summary evaluation of carcinogenic risk to humans is Group 2B: The agent is possibly carcinogenic to humans. /SRP: Compounds in gasoline are known to induce alpha-2u-globulin nephropathy in male rats, a process that does not occur in humans, suggesting that renal tumors in male rats from gasoline exposure may lack relevance to humans./
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V45 194 (1989)]**PEER REVIEWED**
Human exposure to gasoline and d-limonene is particularly interesting I the light of these agents' ability to induce alpha-2u-globulin nepthropathy and renal tumors in male rats. Although some case-control studies have found an approximately 50% increase in risk among individuals exposed to gasoline after adjustment for other risk factors, other studies gave negative results and cohort studies of refinery workers and gasoline station attendants have yielded inconsistent findings. Furthermore, no studies have looked at leaded and unleaded gasoline separately.
[Capen, C.C., E. Dybing, J.M. Rice, and J.D. Wilbourn (eds.) , Species Differences in Thyroid, Kidney and Urinary Bladder Carcinogenesis. IARC Scientific Publication No. 147. Lyon, France: International Agency for Research on Cancer. Available from: http://www.cie.iarc.fr/htdocs/iaarcpubs/pub147 as of January 9, 2004 ]**PEER REVIEWED**
A3; Confirmed animal carcinogen with unknown relevance to humans.
[ American Conference of Governmental Industrial Hygienists TLVs and BEIs. Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinnati, OH, 2005, p. 31]**QC REVIEWED**
Human Toxicity Excerpts:
/HUMAN EXPOSURE STUDIES/ Inhalation of >/= 5,000 ppm gasoline vapor (20,000 ppm for 5 minutes) has been shown to be lethal. It has been postulated that the cause of death following inhalation of high concentrations of gasoline vapors is either central nervous system depression due to asphyxia leading to respiratory failure, or cardiac sensitization to circulating catecholamines leading to a fatal arrhythmia.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.11 (1995) ]**PEER REVIEWED**
/HUMAN EXPOSURE STUDIES/ Experimental exposure of human volunteers to vapors of gasoline indicates essentially no ocular irritation at a concentration of 140 ppm in air, but a detectable sensation of irritation of eyes and throat at 270 to 900 ppm. This sensation is perceived by the subject before signs of irritation, such as conjunctival hyperemia, are visible.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 714]**PEER REVIEWED**
/HUMAN EXPOSURE STUDIES/ Eye irritation was the only significant effect reported among volunteers exposed for 30 min to gasoline vapor at concentrations of about 200, 500 and 1000 ppm ( approx 600, 1,500 and 3,000 mg/cu m) in air; the highest concentrations had the most severe effects.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V45 181 (1989)]**PEER REVIEWED**
/HUMAN EXPOSURE STUDIES/ Young male volunteers were exposed in a chamber to a range of concentrations of vapor from commercial gasoline. Initial central nervous system symptoms started at concentrations between 700 (0.07%) and 2,800 0.28%) ppm (approx 2,100 and 8,400 mg/cu m); exposure to 1000 ppm (0.1%) (approx 3,000 mg/cu m) gasoline vapor caused serious central nervous system symptoms; and , at 10,000 ppm (1%) (approx 30,000 mg/cu m), dizziness and drunkenness started after about 5 minutes of exposure.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V45 181 (1989)]**PEER REVIEWED**
/SIGNS AND SYMPTOMS/ Repeated or chronic dermal contact may result in drying of the skin, lesions, and other dermatological conditions.
[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V1 788]**PEER REVIEWED**
/SIGNS AND SYMPTOMS/ Acute toxicity is similar for all gasolines. They act generally as an anesthetic and are mucous membrane irritants. The hazard is high because of the ease in which harmful concentration may develop. Inhalation is the most important route of occupational entry... Reported responses to gasoline vapors are: 160-270 ppm causes eye and throat irritation in several hours; 500-900 ppm causes eye, nose and throat irritation, and dizziness in 1 hour; and 2000 ppm produces mild anesthesia in 30 minutes. Higher concentrations are intoxicating in 4-10 minutes. The threshold for immediate mild toxic effect is 900-1000 ppm.
[American Conference of Governmental Industrial Hygienists. Documentation of Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices for 2001. Cincinnati, OH. 2001., p. 3]**PEER REVIEWED**
/SIGNS AND SYMPTOMS/ In human beings, inhaling gasoline vapor may cause inebriation and may lead to unconsciousness. During inebriation, miosis has been noted, and in comatose individuals, mydriasis and nystagmus.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 714]**PEER REVIEWED**
/SIGNS AND SYMPTOMS/ Intoxication by ingestion of gasoline and kerosene resembles that from ethyl alcohol. Signs and symptoms include incoordination, restlessness, excitement, confusion, disorientation, ataxia, delirium, and finally coma, which may last a few hours or several days.
[Hardman, J.G., L.E. Limbird, P.B., A.G. Gilman. Goodman and Gilman's The Pharmacological Basis of Therapeutics. 10th ed. New York, NY: McGraw-Hill, 2001., p. 1884]**PEER REVIEWED**
/SIGNS AND SYMPTOMS/ Gasoline vapor acts as a central nervous system depressant. Exposure to low concentrations may produce flushing of the face, staggering gait, slurred speech, and mental confusion. In high concentrations, gasoline vapor may cause unconsciousness, coma, and possible death resulting from respiratory failure. Other signs also may develop following acute exposure. These signs are early acute hemorrhage of the pancreas, centrilobular, cloudy swelling and fatty degeneration of the liver, fatty degeneration of the proximal convoluted tubules and glomeruli of the kidneys, and passive congestion of the spleen. /Leaded gasoline/
[Sittig, M. Handbook of Toxic And Hazardous Chemicals. Park Ridge, NJ: Noyes Data Corporation, 1981., p. 348]**PEER REVIEWED**
/SIGNS AND SYMPTOMS/ Acute exposure of humans to high levels of gasoline vapors is characterized by a spectrum of neurological effects that progress in severity with increasing dose and duration and can include dizziness, headaches, giddiness, euphoria, vertigo, blurred vision, nausea, numbness, drowsiness, anesthesia, and coma. Chronic exposure to gasoline (i.e., in those individuals who habitually sniff gasoline for its euphoric/hallucinogenic effects and in those occupationally exposed to gasoline) is associated with neurological effects as well.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.32 (1995) ]**PEER REVIEWED**
/CASE REPORTS/ A 14 year-old male who inhaled gasoline 10-20 times a day complained of a loss of strength and paresthesia in the limbs. Motor nerve conduction velocity was slowed on his right side, and Wallerian degeneration and segmental demyelination were reported.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.33 (1995) ]**PEER REVIEWED**
/CASE REPORTS/ The polyneuropathy caused by chronic gasoline inhalation is reported to be a gradually progressive, symmetric, sensorimotor polyneuropathy. ... /A case of/ unleaded gasoline sniffing by a female 14 years of age that precipitated peripheral neuropathy /is reported/. In contrast with the previously reported presentation of peripheral neuropathy in gasoline inhalation, /this/ patient developed multiple mononeuropathies superimposed on a background of sensorimotor polyneuropathy. The patient illustrates that gasoline sniffing neuropathy may present with acute multiple mononeuropathies resembling mononeuritis multiplex, possibly related to increased peripheral nerve susceptibility to pressure in the setting of neurotoxic components of gasoline. The presence of tetraethyl lead, which is no longer present in modern gasoline mixtures, is apparently not a necessary factor in the development of gasoline sniffer's neuropathy.
[Burns TM et al; Pediat Neurol 25(5): 419-421 (2001) ]**PEER REVIEWED**
/CASE REPORTS/ In adults, ingestion of 20-50 g of gasoline may produce symptoms of poisoning. Accidental ingestion of gasoline from a pop bottle by an adult human caused immediate severe burning of the pharynx and gastric region. With immediate gastric lavage, no general symptomatic effects were noted, except for clinical findings of temporary galactose excretion of 10.6 g and slightly increased liver function results. The transient hepatic damage was probably due to the gasoline's lipid solubility.
[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V1 787]**PEER REVIEWED**
/CASE REPORTS/ A 12 year old boy who was partially immersed in a pool of gasoline for an hour presented with hypotension and a "scald" of 50% of his body surface. Transient hematuria occurred, followed by abdominal tenderness, an elevated blood level of amylase, disseminated intravascular coagulation and nonoliguric renal failure. Autopsy revealed epidermal loss of skin, cerebral edema, diffuse bilateral pneumonia, biventricular cardiac enlargement, toxic nephrosis, fatty infiltration of the liver and peripancreatic fat necrosis.
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-221]**PEER REVIEWED**
/CASE REPORTS/ Adverse respiratory effects were described in one case report of inhalation of gasoline vapors that resulted in death. In this case, a 3-year-old boy was found with his head lying in a pool of gasoline, and he died shortly thereafter. Autopsy revealed pulmonary congestion, edema, and intrapulmonary hemorrhage. Hyperemia was evident in the tracheal and bronchial mucosa, and there was hemorrhagic fluid in the bronchi. Intraalveolar hemorrhage and alveolar necrosis were seen upon histopathological evaluation. According to the report, these effects were the result of inhalation of gasoline fumes. No gasoline was found in the stomach, and there was no evidence of oral or pharyngeal mucosal damage, thus ruling out the possibility that the lung damage was due to aspiration of ingested gasoline.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.12 (1995) ]**PEER REVIEWED**
/CASE REPORTS/ An 18-year-old male with a history of sniffing leaded gasoline vapors was admitted to the hospital on two occasions complaining of muscle weakness and pain. He claimed to sniff l-l.5 liters at a time irregularly over the past year. Neurological examinations were normal on both hospital admissions, but his serum creatinine kinase was markedly elevated, and his urine was positive for myoglobin. Furthermore, his blood and urine lead levels were also elevated. /Leaded gasoline/
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.28 (1995) ]**PEER REVIEWED**
/EPIDEMIOLOGY STUDIES/ Gasoline is widely used as a solvent in industry. To study its adverse effects on the skin and to understand their mechanisms, a matched epidemiological study (1:1, 52 exposed workers and 52 control subjects) was developed. Information about general conditions, history of dermatosis, changes in skin after exposure to gasoline, etc., was obtained. Ceramide, fatty acid and cholesterol collected from the backs of the hands were analyzed by high-performance thin-layer chromatography (HPTLC), because stratum corneum lipids play a predominant role in maintaining the physiological function of skin. The results showed that prevalences of hyperkeratosis, dryness, onychosis and dermatitis were clearly higher in exposed workers than in the control group, prevalence ratios being 3.33 (p<0.05), 3.00 (p<0.001), 11.25 (p<0.001), 5.00 (p<0.001), respectively. Fissures and onychorrhexis were the common symptoms in exposed workers. The stratum corneum lipid levels of ceramide, fatty acid and cholesterol were significantly lower in the exposed group than in the control group (p<0.05).
[Jia X et al; Contact Dermatitis 46 (1): 44-7 (2002) ]**PEER REVIEWED**
/EPIDEMIOLOGY STUDIES/ A retrospective study was conducted at the Beijing Yanshan Petrochemical Corporation located in Beijing, China, concerning the association between exposure to specific petrochemicals and the frequency of fetal loss. The study group included 2,853 women workers at the petrochemical complex who had at least one pregnancy and had completed information on covariates and reproductive outcomes. Of this number, 568 reported two pregnancies and 161 reported three or more. Of the 2,853 women analyzed, 1,620 (57%) reported exposure to any chemicals during the first trimester of their pregnancy, and 485 (17%) had exposure to benzene (71432). The overall mean rates of spontaneous abortion for first pregnancies for all the study sample was 6.1%. An increased risk of spontaneous abortion was noted in facilities that used petrochemicals, 8.8%. Women working in a chemical environment had a 2.9% rate compared to 1.8% among women working in a nonchemical environment. Seven frequently exposed chemicals or dusts were identified from information on job history. ... The link between spontaneous abortion and exposure to benzene, gasoline, and hydrogen-sulfide was particularly strong. An exposure response trend was noted for increased risk of spontaneous abortion with increasing exposure to petrochemicals, based on interview information.
[Xu X, Cho SI; Occup Environ Med 55(1): 36-36 (1998) ]**PEER REVIEWED**
/EPIDEMIOLOGY STUDIES/ Epidemiological studies on the health experience of workers involved in the manufacture and distribution of gasoline were reviewed. For all causes of mortality, there was a consistent deficit for petroleum workers ranging from a standardized mortality ratio of 0.43 to 1.04, although the bias of the healthy worker effect was clearly a factor. With respect to grouping of "all cancers" was a deficit, with standardized morality ratios of 0.58 to 1.29. Known carcinogens such as benzene and the polynuclear aromatics resulted in excess of leukemia and skin cancer in limited numbers of petroleum workers, but the findings were not consistent across even the best designed studies. An excess risk for pancreatic cancer was rarely statistically significant; however, ten cohort studies have shown standardized mortality ratios of 1.08 to 1.38. With respect to nonmalignant diseases, mortality studies predominated. Low rates for the main causes of death and disease were almost uniformly reported, although there was a question of whether occupational factors were active in the pathogenesis of glomerulonephritis and chronic neuropsychiatric syndromes. The evidence for occupational causation of abnormal pregnancy and chromosomal aberrations was weaker still. It was concluded that despite a generally favorable health experience of gasoline exposed workers, there remains some concern over a number of specific malignant, premalignant, and nonmalignant diseases, and that additional and more carefully designed studies are needed to evaluate the significance, if any, of leukemia, melanoma, and cancers of the renal system, brain, and pancreas.
[Harrington JM; COCAWE, The Oil Companies' European Organization for Environmental and Health Protection #2/87 51pp (1987) ]**PEER REVIEWED**
/BIOMONITORING/ A group of 16 tank cleaners were studied for cytogenetic changes; a subgroup of four men who had cleaned gasoline tanks over the preceding ten months was also included. Micronuclei in bone-marrow cells and chromosomal aberrations in peripheral blood lymphocytes were reported to be significantly more prevalent in the whole group than in the control group.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V45 183 (1989)]**PEER REVIEWED**
/BIOMONITORING/ Leukocytopenia (13%), thrombocytopenia (7%) and small-diameter erythrocytes were observed among 200 crewmen on gasoline tankers operating mainly in the Black Sea basin. A relationship was seen between length of service of sailors on tankers and the hematological changes. Hematological changes were also observed in a group of painters who used gasoline diluents for paints.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V45 182 (1989)]**PEER REVIEWED**
/BIOMONITORING/ Urinary thioether excretion was increased in 35 gasoline service station attendants and in 13 workers in self-service stations when samples taken before and after work were compared. The difference between the samples was greater in persons working in attendant operated service stations than in those in self-service outlets. Cigarette smokers, in general, excreted higher levels of thioethers in samples taken both before and after work.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V45 181 (1989)]**PEER REVIEWED**
/OTHER TOXICITY INFORMATION/ If aspirated into the lungs, gasoline may produce pulmonary epithelial damage, edema, and pneumonitis.
[Klaassen, C.D. (ed). Casarett and Doull's Toxicology. The Basic Science of Poisons. 6th ed. New York, NY: McGraw-Hill, 2001., p. 900]**PEER REVIEWED**
/OTHER TOXICITY INFORMATION/ Intentional or accidental ingestion of gasoline often results in aspiration of the gasoline into the lungs because of its high volatility and low surface tension. Therefore, the most common effect associated with acute gasoline ingestion in humans is aspiration pneumonia which is often accompanied by respiratory distress, pulmonary edema, emphysema, and focal alveolar hemorrhage. Death from asphyxia is often the result in cases of gasoline ingestion when the aspiration pneumonia becomes severe.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.53 (1995) ]**PEER REVIEWED**
/OTHER TOXICITY INFORMATION/ High test gasoline can cause smarting and pain on splash contact with the eye, but only slight transient corneal epithelium disturbance.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 714]**PEER REVIEWED**
/OTHER TOXICITY INFORMATION/ Inhalation of high concentrations of gasoline vapors, as by workmen cleaning storage tanks, can cause immediate death. Gasoline vapors sensitize the myocardium such that small amounts of circulating epinephrine may precipitate ventricular fibrillation ... . High concentrations of gasoline vapor may also lead to rapid depression of the CNS and death from respiratory failure. ...
[Hardman, J.G., L.E. Limbird, P.B., A.G. Gilman. Goodman and Gilman's The Pharmacological Basis of Therapeutics. 10th ed. New York, NY: McGraw-Hill, 2001., p. 1884]**PEER REVIEWED**
/OTHER TOXICITY INFORMATION/ Ingestion is more hazardous /than inhalation/, because the liquids have a low surface tension and can be easily aspirated into the respiratory tract by vomiting or eructation. Morbidity is attributed to aspiration whether it occurs at the time of ingestion or during treatment. Pulmonary damage does not result from gastrointestinal absorption of gasoline... Chemical pneumonitis, complicated by secondary bacterial pneumonia and pulmonary edema, is the most serious sequel to aspiration. Death is caused by hemorrhagic pulmonary edema usually occurs in 16 to 18 hours and seldom later than 24 hours after aspiration.
[Hardman, J.G., L.E. Limbird, P.B., A.G. Gilman. Goodman and Gilman's The Pharmacological Basis of Therapeutics. 10th ed. New York, NY: McGraw-Hill, 2001., p. 1884]**PEER REVIEWED**
Human Toxicity Values:
Human oral 10-15 g of gasoline is lethal in children.
[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V1 787]**PEER REVIEWED**
Human inhalation (acute) 2000 ppm (approx 7.6 mg/L)/1 hr. Effects: dizziness, mucous membrane irritation, and anesthesia. /From table/
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 3374]**PEER REVIEWED**
Human inhalation (chronic) >500 ppm (approx 1.8 mg/L)/ day. Effects: May cause vomiting, diarrhea, insomnia, headache dizziness, anemia, muscle & neurological symptoms. /From table/
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 3374]**PEER REVIEWED**
Skin, Eye and Respiratory Irritations:
Irritating to skin, conjuctiva, and mucous membranes. ...
[Sittig, M. Handbook of Toxic And Hazardous Chemicals. Park Ridge, NJ: Noyes Data Corporation, 1981., p. 348]**PEER REVIEWED**
Vapor irritating to eyes, nose, and throat. Liquid irritating to skin and eyes.
[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5., p. ]**PEER REVIEWED**
Experimental exposure of human volunteers to vapors of gasoline indicates essentially no ocular irritation at a concentration of 140 ppm in air, but a detectable sensation of irritation of eyes and throat at 270 to 900 ppm. This sensation is perceived by the subject before signs of irritation, such as conjunctival hyperemia, are visible.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 714]**PEER REVIEWED**
Probable Routes of Human Exposure:
Personal air sample measurements of employees at a high-volume service station in Pennsylvania for 1 week in May showed geometric mean total gasoline vapor time-weighted average (TWA) exposures of employees ranged from 2.9 to 5.2 mg/cu m(1). Geometric mean personal short-term exposures to gasoline vapor ranged from 12.7 to 24.7 mg/cu m(1). Actual exposure concns during refueling ranged from not detected (detection limit of 10 mg/liter extraction solvent) to 116.3 mg/cu m(1). Component analysis of personal long-term samples showed that 2-methyl butane and pentane were the most prevalent hydrocarbons and were detected in all 18 samples at concentrations ranging from 0.1 to 1.7 ppm(1). Another survey of service station employees conducted from March to June at seven service stations located throughout the United States (Houston, Texas, Manhattan Beach, California, New Britain, Connecticut, New Orleans, Louisiana, Plantation, Florida, Stickney, Illinois, and Walnut Creek, California) showed that mean TWA attendant exposures ranged from 3.63 to 22.3 ppm for gasoline vapor and 0.02-0.24 ppm for benzene(1). Monitoring of service station personnel responsible for refueling operations at 2 gas stations located near a major expressway, revealed a geometric mean 8-hour TWA of 4.0 mg/cu m (range of 1.1-130.3 mg/cu m)(1).
[(1) ATSDR; Toxicological Profile for Automotive Gasoline. Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) ]**PEER REVIEWED**
Emergency Medical Treatment:
Emergency Medical Treatment:
For more information consult the Automotive Gasoline MSDS Information above.
Antidote and Emergency Treatment:
Provide basic supportive care for all symptomatic patients, whether from aspiration, ingestion, or inhalation. (1) Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen. (2) Monitor arterial blood gases or oximetry, chest x-ray, and ECG and admit symptomatic patients to intensive care setting. (3) Use epinephrine and other sympathomimetic amines with caution in patients with significant hydrocarbon intoxication, because arrhythmias may be induced. Patients who remain asymptomatic after 4-6 hours of observation may be discharged. In contrast, if the patient is coughing on arrival, aspiration has probably occurred. Administer supplemental oxygen, and treat bronchospasm, hypoxia, and pneumonia if they occur. Do not use steroids or prophylactic antibiotics. /hydrocarbons/
[ Olson, K.R. (ed.) Poisoning & Drug Overdose. 3rd edition. Lange Medical Books/McGraw-Hill, New York, NY. 1999., p. 185]**PEER REVIEWED**
Symptomatic and supportive care is probably the best treatment for intoxication by gasoline or kerosene. Because of the danger of aspiration, emesis or gastric lavage should be avoided unless the risks are justified by the presence of additional toxic substances in the petroleum. Catharsis may be included with magnesium or sodium sulfate. Antibiotics are used if there is a specific indication, such as bacterial pneumonitis. Epinephrine and related substances should be avoided because they may induce cardiac arrhythmias. Treatment should include correction of imbalances of fluid and electrolytes.
[Hardman, J.G., L.E. Limbird, P.B., A.G. Gilman. Goodman and Gilman's The Pharmacological Basis of Therapeutics. 10th ed. New York, NY: McGraw-Hill, 2001., p. 1884]**PEER REVIEWED**
The primary threat to life from pure petroleum distillate ingestion is respiratory failure. Patients should be quickly evaluated for signs of respiratory distress (eg, cyanosis, tachypnea, intercostal retractions, obtundation) and given oxygen. Patients with inadequate tidal volumes or poor arterial blood gases (PO2 <50 mm Hg or PCO2 >50 mm Hg) should be intubated. Since arrhythmias complicate some hydrocarbon ingestions and electrocardiographic evidence of myocardial injury has been reported, intravenous lines and cardiac monitors should be established in obviously symptomatic patients. A chest x-ray should be taken immediately after stabilization of breathing and circulation to document aspiration and detect the presence of pneumothorax. Continuous positive airway pressure or positive end expiratory pressure and intubation may be necessary in severe cases to maintain adequate oxygenation, but careful observation for the development of pneumothorax must be made during therapy. Inhaled cardioselective bronchodilators (eg, Alupent, salbutamol) are the preferred bronchodilator agents, with aminophylline a second choice. /Hydrocarbons/
[Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 1425]**PEER REVIEWED**
Gasoline contact may cause significant full-thickness /third degree/ burn injuries. Systemic complications may result from the absorption of hydrocarbons through the skin. Regional neuromuscular absorption may produce transient or even permanent impairment.
[Schneider MS et al; J Burn Care Rehabil 12(2): 140-3 (1991) ]**PEER REVIEWED**
Basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 m/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . /Hydrocarbon Blends, Mixtures, and Related Compounds/
[Bronstein, A.C., P.L. Currance; Emergency Care for Hazardous Materials Exposure. 2nd ed. St. Louis, MO. Mosby Lifeline. 1994., p. 215]**PEER REVIEWED**
Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, is in respiratory arrest, or has severe pulmonary edema. Positive pressure ventilation techniques with a bag valve mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start an IV with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. Consider drug therapy for pulmonary edema ... . For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of pulmonary edema ... . Treat seizures with diazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Hydrocarbon Blends, Mixtures, and Related Compounds/
[Bronstein, A.C., P.L. Currance; Emergency Care for Hazardous Materials Exposure. 2nd ed. St. Louis, MO. Mosby Lifeline. 1994., p. 216]**PEER REVIEWED**
Animal Toxicity Studies:
Evidence for Carcinogenicity:
Classification of carcinogenicity: 1) evidence in humans: inadequate; 2) evidence in animals: limited. Overall summary evaluation of carcinogenic risk to humans is Group 2B: The agent is possibly carcinogenic to humans. /SRP: Compounds in gasoline are known to induce alpha-2u-globulin nephropathy in male rats, a process that does not occur in humans, suggesting that renal tumors in male rats from gasoline exposure may lack relevance to humans./
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V45 194 (1989)]**PEER REVIEWED**
Human exposure to gasoline and d-limonene is particularly interesting I the light of these agents' ability to induce alpha-2u-globulin nepthropathy and renal tumors in male rats. Although some case-control studies have found an approximately 50% increase in risk among individuals exposed to gasoline after adjustment for other risk factors, other studies gave negative results and cohort studies of refinery workers and gasoline station attendants have yielded inconsistent findings. Furthermore, no studies have looked at leaded and unleaded gasoline separately.
[Capen, C.C., E. Dybing, J.M. Rice, and J.D. Wilbourn (eds.) , Species Differences in Thyroid, Kidney and Urinary Bladder Carcinogenesis. IARC Scientific Publication No. 147. Lyon, France: International Agency for Research on Cancer. Available from: http://www.cie.iarc.fr/htdocs/iaarcpubs/pub147 as of January 9, 2004 ]**PEER REVIEWED**
A3; Confirmed animal carcinogen with unknown relevance to humans.
[ American Conference of Governmental Industrial Hygienists TLVs and BEIs. Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinnati, OH, 2005, p. 31]**QC REVIEWED**
Non-Human Toxicity Excerpts:
For more information consult the Automotive Gasoline MSDS Information above.
/LABORATORY ANIMALS: Acute Exposure/ /Draize Test - Rabbit/ 0.5 mL of undiluted test material was applied to the shorn skin in two areas on each of 3 male and 3 female rabbits. One area was intact and the other abraded skin. The treated area was then covered with an occlusive dressing. After 24 hours the dressing was removed and the treated skin was wiped to remove any residue of test material. The degree of erythema and edema was recorded according to the Draize scale. A second reading of skin responses was made at 72 hours and again at 96 hours, 7 and 14 days. Results of the 24 and 72 hour readings were used to determine the Primary Irritation Index. ...Primary irritation score = 0.98. Edema but no erythema was noted at 24 hours, although the test area was whiter than the surrounding skin. At 72 hours erythema and edema were observed. By 7 days almost all erythema had cleared but some edema was still present and the test site was dry and flaky. By day 14 all edema and erythema had cleared but there was no hair growth at this time.
[EPA/Office of Pollution Prevention and Toxics; High Production Volume (HPV) Challenge Program's Robust Summaries and Test Plans. Available from: http://www.epa.gov/chemrtk/viewsrch.htm on Paraffinic Naphthas as of May 6, 2004 ]**PEER REVIEWED**
/LABORATORY ANIMALS: Acute Exposure/ Experimental exposure of rabbit eyes to gasoline with and without tetraethyl lead have been carried out, and the effects have been evaluated by biomicroscope and by testing with fluorescein. A single drop applied without local anesthetic caused obvious discomfort and immediate blepharospasm which lasted several minutes. The conjunctiva became mildly hyperemic and the corneal epithelium stained faintly, but all returned rapidly to normal. Ten drops applied during five minutes after induction of local anesthesia by means of topical proparacaine hydrochloride caused blepharospasm lasting fifteen minutes. The conjunctiva became moderately edematous and hyperemic. The cornea stained definitely with fluorescein, but the injury was superficial and transient. Recovery was prompt and complete. Gasoline containing tetraethyl lead caused no more injury than plain gasoline.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 714]**PEER REVIEWED**
/LABORATORY ANIMALS: Acute Exposure/ Male albino (Wistar) rats given a single dose of 2.0 mL/kg body weight gasoline (Indian Oil Corp.) by intraperitoneal injection showed increased lipid peroxidation in the liver after 24 hours. Female Wistar rats administered 1.0 mL/kg body weight gasoline intraperitoneally had depressed activities of hepatic delta-aminolevulinic acid synthetase and dehydratase within 20 hours.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V45 177 (1989)]**PEER REVIEWED**
/LABORATORY ANIMALS: Acute Exposure/ A single 2-hour exposure to 70,180 ppm leaded gasoline vapors was reported to induce ECG changes and disturbances in myocardial enzyme activities and electrolyte levels in rabbits. The ECG readings were taken from the animals prior to exposure while they were anesthetized with evipan and again immediately after intoxication (elapsed time not specified). Exposure to leaded gasoline vapor resulted in a slowing of heart rate in all exposed animals and evidence of disturbed ventricular repolarization such as flattening of the T-wave (10/20), inverted T-wave (7/20), biphasic T-wave (3/20), ST depression (10/20), prolongation of the QT interval (16/20), and prolongation of the QRS complex (7/20). Decreased myocardial acid phosphatase, decreased myocardial sodium, potassium, and magnesium levels, and altered acid phosphatase and ATPase (adenosinetriphosphatase) activity in the myocardium were also observed. A decrease seen in myocardial alkaline phosphatase was not statistically significant.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.26 (1995) ]**PEER REVIEWED**
/LABORATORY ANIMALS: Acute Exposure/ The frequency and physical sites involved by amyloid deposits were examined in domesticated rabbits in which amyloidosis had been induced by intramuscular injections of low molecular weight hydrocarbons, including gasoline, which is a mixture of such hydrocarbons. ... Amyloid deposits were clearly recognized following daily injections for 6 weeks of various gasolines refined in Japan and for 10 weeks in the low molecular weight hydrocarbon group. The amyloid protein in this amyloidosis was /amyloid protein A/ (AA). The main sites of amyloid deposit were splenic red pulp in the case of the spleen, around sinusoids in the liver, while it was in the glomerular tuft, interstitium of the medulla and urinary tubular epithelium in the kidney, the interstitium of the lamina propria mucosae in the stomach, surrounding capillary vessels in the adrenal cortex, mainly centered on the inner zone of the zona fasciculata, and small vessels inside and outside splenic follicle.
[Sassa H et al; J Tokyo Med Coll 49 (4): 457-463 (1991) ]**PEER REVIEWED**
/LABORATORY ANIMALS: Acute Exposure/ 0.1 mL of undiluted test material was applied to the corneal surface of one eye of each of 9 rabbits (4 male, 5 female), the other eye was untreated and served as control. After 20 to 30 seconds the treated eyes of 3 rabbits were washed with lukewarm water for 1 minute. Eyes of the other 6 rabbits were not washed. Readings of ocular lesions for all animals were made at 1, 24, 48, 72 hours and 7 days after treatment. Sodium fluorescein was used to aid in revealing possible corneal injury. No irritation was observed in any animal at any of the three observation times. Animals whose eyes had been irrigated following instillation of test material were no different from those whose eyes had not been washed /API PS-6/.
[EPA/Office of Pollution Prevention and Toxics; High Production Volume (HPV) Challenge Program's Robust Summaries and Test Plans. Available from: http://www.epa.gov/chemrtk/viewsrch.html on Paraffinic Naphthas as of May 6, 2004 ]**PEER REVIEWED**
/LABORATORY ANIMALS: Acute Exposure/ ...Unleaded gasoline (UG) ... induced cell proliferation and cytochrome P-450-related enzyme activities in mouse liver, properties commonly associated with liver tumor promoters. To determine if the mitogenic and/or cytochrome P-450-inducing properties of unleaded gasoline (UG) reside in individual fractions of UG, UG was separated into four fractions on the basis of boiling point (BP): fraction 1, BP<66 deg C; fraction 2, 66 deg C < BP<100 deg C; fraction 3, 100 deg C < BP<132 deg C; fraction 4, BP>132 deg C. Fractions 1 and 2 were combined to form "light UG" (BP<100 deg C), and fractions 3 and 4 were combined to form "heavy UG" (BP>100 deg C). Female B6C3F1 mice were implanted with osmotic pumps containing 5-bromo-2'-deoxyuridine (BrdU) on day 1, treated by intragastric intubation with corn oil or 3000 mg/kg/day of light, heavy, or whole UG on day 2-4, and euthanized on day 5. Pentoxyresorufin O-dealkylase (PROD) and ethoxyresorufin O-deethylase (EROD) activities were assayed in hepatic microsomes, and hepatocyte BrdU labeling index (LI) was determined in liver sections. Whole UG and heavy UG caused comparable increases in hepatic PROD and EROD activities and the hepatocyte LI. Light UG caused relatively small increases in hepatic PROD and EROD activities and did not increase the hepatocyte LI. When fractions 3 and 4 were tested separately in the above treatment protocol, both fractions strongly induced hepatic PROD and weakly induced hepatic EROD activities. However, only fraction 3 increased the hepatocyte LI. To isolate mitogenic components in fraction 3, equimolar doses of individual chemicals in fraction 3 were tested in the above treatment protocol. Toluene did not increase the hepatocyte LI, whereas 2,2,3-trimethylpentane (TMP), 2,2,4-TMP, and 2,3,4-TMP all dramatically increased the hepatocyte LI. Thus, while the hepatic cytochrome P-450-inducing activity of UG was concentrated in components of UG with BPs>100 deg C, this activity apparently resides in UG components with a wide range of BPs. The mitogenic activity of UG, in contrast, was highly concentrated in components of UG with BPs ranging from approximately 100 to 132 deg C, an
