Subscribe To This Site

Automobile Gasoline MSDS (Material Safety Data Sheet), Testing, Air Purification, and Public Health Information

Complete Gasoline MSDS information plus answers to frequently asked questions is found below. Improper gasoline storage near your home can actually raise your risk of Leukemia, so always keep gasoline totally separated from in, around, or under your home.

I especially hope anyone living in an apartment above a garage uses the information here to limit their exposure to exhaust and gasoline fumes which may be entering your living space from below.

Gas fume inhalation is a more common problem than most people realize. I would never live above a garage unless is was not being used to store anything (including chemicals or anything having a combustion engine). Ventilation sometimes is not enough.

If you are one of the many with concerns about the health effects of breathing gasoline, this page will help you mitigate the hazard.

Automotive Gasoline is dangerous. It may cause both chronic and acute health effects

try not to breath fumes while you're pumping gas at the gas pump

Danger Gasoline contains Benzene, check the Gasoline MSDS for exact percentages

Gas, benzene, Carbon Monoxide, and volatile organic compounds (VOCs) is one of the most common concerns I get contacted about either because someone's living space is being contaminated with fumes from an actively used garage area below or because a fuel spill has made a property unlivable.

Never ever store gasoline or power equipment like lawnmowers in your crawlspace or basement. keep all fuels outside in a well ventilated storage area unconnected to your home.

Even power equipment with a small amount of gasoline in the capped tank will quickly vaporize and rise up through your floor boards and into your house where it can contribute to Sick Building Syndrome or worse.

Trust me, I speak from experience having suffered from this very scenario for many years without realizing it.

I hope you will also follow the above advice when it comes to pool chemicals like Chlorine tablets or anything else that can emit toxic gases into your home from below. Never assume your floor will act as a vapor barrier because it WILL NOT.

Fumes such as from Gasoline, chemicals, and Radon will always follow the path of least resistance from high pressure to low pressure. The inside of your home is often at a lower pressure than below due to the chimney effect and because warmer air rises and causes a draft upwards from below.

Be extra cautious if gasoline is stored in any way, shape, or form anywhere under your roof or near your home. It does not take much to affect your health negatively.

The Best Chemical Air Purifier for Gasoline Fume Removal, Odor Control, and Particle Filtration:
IQAir GC Multigas Air Purifier

The best air purifier for controlling Gasoline fumes that may be continuously reintroduced into rooms from source materials such as gas cans or power equipment is one that has a high amount of special chemical gas filtering media such as Activated Carbon Potassium Permanganate filtration such as what is found in professional gas mask cartridges.

Since tiny gas molecules such as Gasoline and Formaldehyde will pass right through HEPA filters, air cleaners for Gasoline removal must contain advanced gas filters besides just efficient air purifier HEPA filters which catch the tiniest of particulates, but not gases.

With this in mind, the best of breed air purifier for Gasoline removal from indoor air is IQAir GC Chemisorber Multigas or VOC. It is proven to be one of the most effective air cleaners on the market today and will likely clean your air of both solids and gases such as Gasoline and Formaldehyde with the highest efficiency compared to other air purifiers.

IQ Air GC Chemisorber contains an impressive 12 pounds of the advanced Carbon-Potassium Permanganate filter media and has a very sophisticated gas filtration cartridge system plus highly efficient HEPA filtration for the removal of the tiniest of solid particulates as well.

IQAir GC Multigas Air Purifier: Powerfully Efficient Air Cleaning of Solids and Gases

Chemical Vapors Such as from Gasoline and Formaldehyde Are Destroyed Via Oxidation Inside Active Alumina Pellet Filter Media

Micro-charged Filtration Technology With Charged Fiber Structure for Particle Elimination

Ultra-small Nano-particle Filtration of Solid Indoor Air Pollutants Such as Viruses, Smoke, and Microorganisms

Advanced Activated Carbon Cartridge Filtration for Adsorption of Odors and Volatile Organic Compounds

Efficiently filters out mold spores, pet dander, wildfire / cooking / cigarette smoke, pollen, most odors, chemical molecules such as Benzene, and most general indoor air pollutants.

The IQ Air GC MultiGas is a Top Rated Air Purifier for Multiple Chemical Sensitivity (MCS).

Public Health Statement for Automobile Gasoline

Automotive Gasoline (Gasolina de Automóvil) CONTENTS:

Summary

What is automotive gasoline?

What happens to automotive gasoline when it enters the environment?

How might I be exposed to automotive gasoline?

How can automotive gasoline affect my health?

How likely is automotive gasoline to cause cancer?

Is there a medical test to show whether I've been exposed to automotive gasoline?

Has the federal government made recommendations to protect human health against Automotive Gasoline?

Glossary of Terms

Gasoline References

Contact Information

Automotive Gasoline MSDS Information

Automotive Gasoline Toxicological Information

This fact sheet answers the most frequently asked health questions about automotive gasoline.

SUMMARY:

Exposure to automotive gasoline most likely occurs from breathing its vapor at a service station while filling a car's fuel tank. At high levels, automotive gasoline is irritating to the lungs when breathed in and irritating to the lining of the stomach when swallowed. Exposure to high levels may also cause harmful effects to the nervous system. Automotive gasoline has been found in at least 23 of the 1,430 National Priorities List sites identified by the Environmental Protection Agency (EPA).

What is automotive gasoline?

Automotive Gasoline is a flammable petroleum distillate and solvent

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.

TSCA Definition of Automotive Gasoline 2005: A complex combination of hydrocarbons separated from natural gas by processes such as refrigeration or absorption. It consists predominantly of saturated aliphatic hydrocarbons having carbon numbers predominantly in the range of C4 through C8 and boiling in the range of approximately minus 20.degree.C to 120.degree.C (-4.degree.F to 248.degree.F).

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 Guide 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).

If you are concerned about Gasoline fumes, toxic black mold, toxins from cigarette smoke, or if you would like to know which of over 400 volatile organic compounds like Gasoline may be contaminating your indoor air, I recommend you easily and accurately test your indoor air using a high quality indoor air quality test kit

back to top

What happens to automotive gasoline when it enters the environment?

Small amounts of the chemicals present in gasoline evaporate into the air when you fill the gas tank in your car or when gasoline is accidentally spilled onto surfaces and soils or into surface waters.
Other chemicals in gasoline dissolve in water after spills to surface waters or underground storage tank leaks into the groundwater.
In surface releases, most chemicals in gasoline will probably evaporate; others may dissolve and be carried away by water; a few will probably stick to soil.
The chemicals that evaporate are broken down by sunlight and other chemicals in the air.
The chemicals that dissolve in water also break down quickly by natural processes.

How might I be exposed to automotive gasoline?

Breathing vapors at a service station when filling the car's fuel tank is the most likely way to be exposed.
Gasoline inhalation exposures to the general public during self-service automobile refueling do not appear to be a significant health risk--2 minute exposures to approximately 200 ppm gasoline and 1 ppm benzene. (15 min. Short-term exposure limits (STELs) are 500 ppm and 5 ppm, respectively.) Misuse of gasoline as a solvent or cleaner can cause skin and eye irritation and CNS toxicity after extensive overexposure. Gasoline is in the list of "Some volatile substances which may be abused by inhalation" published on the web site of the U.N. International Drug Control Programme, indicating its potential to cause narcosis in workers.
Working at a service station.
Using equipment that runs on gasoline, such as a lawn mower.
Drinking contaminated water.
Being close to a spot where gasoline has spilled or leaked into the soil.

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.

Household Products that contain Gasoline-like chemicals:
These Gasoline-like compounds may also be known as: Petroleum distillate(s), JP5 Jet fuel, Aliphatic petroleum distillate, Kerosene, Fuel oil no. 1, Deodorized kerosene, hydrodesulfurized Kerosine, Jp-5 navy fuel/marine diesel fuel, petroleum, Hydrocarbon propellant (1), Petroleum products, liquefied gas, Petroleum gas (liquefied), Liquefied petroleum gas (2), Petroleum gases, liquefied sweetened Petroleum gas, or liquified Petroleum gases.

As One Example, BP Unleaded Gasolines contain:

Gasoline 99.9-100%
Benzene 0-3%
Butane 4-6%
Cyclohexane 0-1%
Ethylbenzene 0-2%
Heptane 6-8%
Hexane 8-10%
Pentane 9-11%
Toluene 10-12%
Trimethylbenzene 0-3%
Xylene 8-10%

Below is the household product brand, category, form, and percent of chemical

Eagle One Wet Look Paste Auto products liquid
Tribotech IJP Lubricant Auto products liquid
Gumout Winter Fuel Injector Cleaner Auto products liquid 40-70
STP 4 Cylinder Oil Treatment-04/01/2003 Auto products liquid 1-5
STP Oil Treatment-04/01/2003 Auto products liquid 10-30
Armor All Leather Care-01/01/1998 Auto products liquid 1-5
Alemite Gas Treatment Auto products liquid
Nevr Dull Wadding Auto Polish Auto products liquid
Turtle Wax Color Enriched Car Polish Auto products liquid
Snap Engine Degreaser Professional Strength Auto products aerosol 65-80
STP Octane Performance Booster-12/01/2003 Auto products liquid 90-100
STP Stop Smoke Oil Additive-10/01/2003 Auto products liquid 10-30
STP Engine Stop Leak 14 Fl. Oz. Auto products liquid 5-10
Martin Weber RapiDry Quick Drying Oil Medium Hobby/Craft liquid 68
Rubberize It Rubberized Plastic Coating, Blue Hobby/Craft aerosol
Martin Weber Cleaning Solution Hobby/Craft liquid 35
Weiman Candle Wax Remover Home inside liquid
Martin Weber Synvar Varnish Home maintenance liquid 58
Martin Weber LiquiGlaze Home maintenance liquid 56
Martin Weber Sphinx Retouch Varnish Home maintenance liquid 67
Max Factor Lashfinity Personal care/use pencil
Cover Girl Marathon Waterproof Mascara Personal care/use semi-solid
Cover Girl Pure Magic Body Art Personal care/use cream
Cover Girl Professional Advanced Waterproof Mascara, Black Personal care / use solid
Cover Girl Professional Advanced Waterproof Mascara Personal care/use semi-solid
Cover Girl Remarkable Washable/Waterproof Mascara Personal care/use semi-solid
Cover Girl Professional Advanced Waterproof Mascara, Black Brown Personal care / use solid
Ortho Roach, Ant & Spider Killer Pesticides aerosol 99.62
Ortho Garden Care Pesticides liquid
Bonide Mosquito Beater Propane Flying Insect Fog Pesticides liquid 99.80
Bonide Fruit Tree Spray Concentrate Pesticides liquid
Diazinon 25E Lawn and Garden Insect Control Pesticides liquid
Flys Off Lotion Insect Repellent for Dogs Pet Care liquid 1.0-8.0
Simoniz Advanced Total Car Finish/Polish Auto products liquid <5-10
Mothers Pure Carnauba Cleaner Wax Auto products liquid
Classic Liquid Carnauba Auto Polish Auto products liquid
Mothers Magnesium/Aluminum Polish Auto products liquid
Gumout Professional Fuel System Cleaner Auto products liquid 40-45
Gumout Emissions Reducer Auto products pump spray <85
Gumout Gas Treatment Auto products liquid 95-99
Wet Wax-01/24/2002 Auto products liquid 2-5
Foamy Engine Brite Degreaser-03/01/1999 Auto products liquid 5-6
Liquid Wrench Super Penetrant-06/01/2000 Auto products aerosol 85-90
Westleys Concentrated Liquid Auto Polish-06/17/2002 Auto products liquid 1-5
Gumout Carb/Fuel Injector Cleaner-10/22/2002 Auto products aerosol 95-99
Snap Concentrated Engine Flush Auto products liquid 99-100
Snap Gas Treatment Auto products liquid 95-100
Armor All No. 7 Rubbing Compound Auto products paste 20-30
Rally Liqui-Car Wax Auto products thick liquid 1-5
STP Fuel Injector/Carburetor Cleaner-08/07/1998 Auto products liquid 75-100
STP Gas Treatment-09/30/1998 Auto products liquid 65-95
STP Octane Performance Booster-11/13/1998 Auto products liquid 60-80
STP Oxygenated Gas Treatment-12/24/1998 Auto products liquid 70-95
STP Super Concentrated Intake Valve Cleaner Auto products liquid 0-60
STP Gas Treatment-08/03/2000 Auto products liquid 90-100
STP Super Concentrated Fuel Injector Cleaner-07/06/1999 Auto products liquid 80-100
STP Fuel Injector and Carburetor Treatment 12 Fl. Oz. Auto products liquid <75-100
Simoniz Super Blue Liquid Car Wax Auto products liquid 0-5
Mothers California Gold Sealer & Glaze Auto products liquid
Classic Carnauba Car Wax Auto products liquid
Turtle Wax Chrome Polish Auto products liquid 12-15
Gumout Octane Booster Auto products liquid 95-99
Gumout Xtra Concentrated Fuel System Cleaner Auto products liquid 85-95
Gumout 2 Part Professional Fuel System Cleaner, Step 2 Auto products liquid 40-45
Champion Sprayon Flush Off Degreaser Auto products aerosol
Rain X Ultra Paste Wax-05/09/2002 Auto products paste 1-5
Gunk Diesel Fuel Anti Gel Additive-01/01/1999 Auto products liquid 30-40
Westleys Bug & Tar Remover-06/19/2002 Auto products liquid <35
Gumout 2 Part Professional Fuel System Cleaner-Step 2-03/06/2002 Auto products liquid 55-65
Regane Complete Fuel System Cleaner Auto products liquid 60-70
Snap Emissions Reducer Auto products liquid 90-99
Snap Super Octane Booster Auto products liquid 95-99
Armor All No. 7 White Polishing Compound Auto products paste 20-30
Rally Cream Car Wax Auto products paste 5-10
STP Fuel Injector/Carburetor Cleaner Auto products liquid <75-95
STP Gas Treatment Auto products liquid <50-80
STP Octane Performance Booster Auto products liquid <70-90
STP Oxygenated Gas Treatment Auto products liquid <50-80
STP Super Concentrated Fuel Injector Cleaner Auto products liquid <75-85
Westleys Bug & Tar Remover Auto products liquid <10
STP Fuel Injector/Carburetor Cleaner-01/18/2000 Auto products liquid 95-100
Cabot O.V.T. Solid Color Oil Stains, 0500 Series Home maintenance liquid
Cabot Semi Transparent Stains, 0300 Series Home maintenance liquid
Cabot Semi Solid Stains, 0100 Series Home maintenance liquid
Fletco Liquid Plastic Semi Gloss Home maintenance liquid 5.0
Cabot 0241 Bleaching Oil Home maintenance liquid
Cabot Semi Solid Stains, Low VOC CA, 6100 Series Home maintenance liquid
Sakrete Blacktop Patch, Ready-to-Use Packaged Asphalt for Patching & Repairing Landscaping / Yard semi-solid
Chaser Turf Herbicide (Industrial) Pesticides liquid <49.10
Castrol GTX Motor Oil SAE 10W-40W Auto products liquid 60-100
Rust Oleum Premium Stops Rust Protective Enamel Spray 7798 Semi Gloss Black Hobby / Craft aerosol 30
Rust Oleum Premium Textured Aerosol 7221 Dark Pewter Hobby / Craft aerosol 30
Rust Oleum Premium Textured Aerosol 7223 Sandstone Hobby / Craft aerosol 25
Rust Oleum Premium Textured Aerosol 7225 White Hobby / Craft aerosol 25
Rust Oleum Premium Hammered Finish Aerosol 7211 Deep Green Hobby / Craft aerosol 25
Rust Oleum Premium Hammered Finish Aerosol 7213 Silver Hobby / Craft aerosol 25
Rust Oleum Premium Hammered Finish Aerosol 7215 Black Hobby / Craft aerosol 25
Rust Oleum Premium Hammered Finish Aerosol 7217 Bright Red Hobby / Craft aerosol 25
Rust Oleum Premium Hammered Finish Aerosol 7219 Verde Green Hobby / Craft aerosol 25
Rust Oleum Premium Stops Rust Protective Enamel Spray 7721 Fresh Blue Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7723 Navy Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7727 Royal Blue Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7731 Grass Green Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7738 Hunter Green Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7754 Anodized Bronze Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7762 Sunrise Red Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7768 Burgundy Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7771 Sand Hobby/Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7763 Carnival Red Hobby / Craft aerosol 30
Rust Oleum Premium Textured Aerosol 7220 Black Hobby/Craft aerosol 25
Rust Oleum Premium Textured Aerosol 7222 Forest Green Hobby/Craft aerosol 30
Rust Oleum Premium Textured Aerosol 7224 Nickel Hobby/Craft aerosol 30
Rust Oleum Premium Hammered Finish Aerosol 7210 Gold Hobby/Craft aerosol 25
Rust Oleum Premium Hammered Finish Aerosol 7212 Light Blue Hobby/Craft aerosol 25
Rust Oleum Premium Hammered Finish Aerosol 7214 Gray Hobby / Craft aerosol 25
Rust Oleum Premium Hammered Finish Aerosol 7216 Deep Blue Hobby / Craft aerosol 25
Rust Oleum Premium Hammered Finish Aerosol 7218 Dark Bronze Hobby / Craft aerosol 25
Rust Oleum Premium Stops Rust Protective Enamel Spray 7701 Crystal Clear Hobby / Craft aerosol 25
Rust Oleum Premium Stops Rust Protective Enamel Spray 7722 Harbor Blue Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7724 Sail Blue Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7729 Teal Gloss Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7733 Dark Hunter Green Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7747 Sunburst Yellow Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7755 Light Olive Green Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7765 Regal Red Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7770 Almond Hobby / Craft aerosol 30
Rust Oleum Premium Stops Rust Protective Enamel Spray 7797 Semi Gloss White Hobby / Craft aerosol 30
Rust Oleum Stops Rust, Crystal Clear Spray Home inside aerosol 25.0
Rust Oleum Specialty High Heat Resistant, White Home inside aerosol 35.0
Rust Oleum Premium Hammered Unique Hammered Finish, Light Blue Home inside aerosol 25
Painters Touch by Rust Oleum Multi Purpose Paint, Matte Clear Home inside aerosol 25.0
American Accents by Rust Oleum, Clear Top Coat Home inside aerosol 25.0
Schultz Houseplants and Garden Bug Spray, Whitefly and Mealy Bug Home inside aerosol 5-40
Dow Heavy Duty Oven Cleaner Home inside aerosol
K2r Spot Lifter Home inside liquid <45
Rust Oleum Textured Spray Paint, White Home inside aerosol 25.0
Rust Oleum Painters Touch, Gold Metallic Home inside aerosol 35.0
Painters Touch by Rust Oleum Sandable Primer, Red Primer Home inside aerosol 30.0
Americas Finest by Rust Oleum, Fast Dry All Purpose Int./Ext, Flat White Home inside aerosol 25.0
Rust Oleum Painters Touch Specialty, Fluorescent Green Home inside aerosol 30.0
Purex Magic Sizing Home inside aerosol
Klean Strip Graffiti Remover Home maintenance aerosol 15-20
Foam Plus Insulation/Sealant Home maintenance aerosol
Rust Oleum Bright Coat Metallic Finish, Chrome Home maintenance aerosol 35.0
Rust Oleum Painters Touch, Frosted Glass Finish Home maintenance aerosol 15.0
Great Stuff Insulation/Sealant Home maintenance aerosol 10-30
Rust Oleum Professional High Performance Enamel, Gloss White Home maintenance aerosol 30.0
Rust Oleum Premium Satin Aerosol 7720 Sage Home maintenance aerosol 25
Rust Oleum Premium Satin Aerosol 7728 Navy Blue Home maintenance aerosol 30
Rust Oleum Premium Satin Aerosol 7732 Hunter Green Home maintenance aerosol 30
Rust Oleum Premium Satin Aerosol 7739 Charcoal Green Home maintenance aerosol 30
Rust Oleum Premium Satin Aerosol 7740 Mediterranean Teal Home maintenance aerosol 30
Rust Oleum Premium Satin Aerosol 7760 Heritage Red Home maintenance aerosol 30
Rust Oleum Premium Satin Aerosol 7767 Redwood Home maintenance aerosol 30
Rust Oleum Premium Satin Aerosol 7791 Satin White Home maintenance aerosol 30
Water White Rubbed Effect Clear Lacquer (Professional) Home maintenance aerosol 25.97
Rust Oleum Premium Stops Rust Clean Metal Primer, White Home maintenance aerosol 30.0
Rust Oleum Professional Primer, Gray Primer Home maintenance aerosol 30.0
Rust Oleum Professional Spray Enamel, Cold Galvanizing Compound Home maintenance aerosol 15.0
Rust Oleum Premium Satin Aerosol 7725 Federal Blue Home maintenance aerosol 30
Rust Oleum Premium Satin Aerosol 7730 Teal Home maintenance aerosol 30
Rust Oleum Premium Satin Aerosol 7737 Spruce Green Home maintenance aerosol 30
Rust Oleum Premium Satin Aerosol 7742 Summer Straw Home maintenance aerosol 30
Rust Oleum Premium Satin Aerosol 7744 Cornmeal Home maintenance aerosol 25
Rust Oleum Premium Satin Aerosol 7761 Outdoor Decor Red Primer Home maintenance aerosol 30
Rust Oleum Premium Satin Aerosol 7777 Satin Black Home maintenance aerosol 30
Mitchellace Shine Rite Rain And Stain Repellent 5.5oz. Personal care/use aerosol
Enforcer Crack and Crevice Fumigator Pesticides aerosol 5-15
Deep 6 Flying Insect Killer Pesticides emulsion 15.00-40.00
Deep 6 Flea Killer Plus Fogger Pesticides emulsion 15.00-40.00
Raid MAX Large Roach Killer 7 Pesticides aerosol spray 7-13
Fiberglass Magic Cleaner Auto products aerosol
Westleys Rubberized Undercoating-06/25/2002 Auto products aerosol 10
Number 7 Tar And Bug Remover Auto products liquid 12
Classic Aerosol Wax Auto products aerosol 10-15
Fiberglass Magic Cleaner-02/01/2000 Auto products aerosol <10
Stainless Steel Magic Cleaner Home inside aerosol
Furniture Magic Home inside aerosol <18.0
Kitchen Magic Home inside aerosol <13.0
Magic Shock Free Home inside aerosol <14.0
Magic American Marble & Granite Magic Home inside aerosol <20.0
Oust Air Sanitizer, Floral Scent Home inside aerosol 25-35
Pledge Grab It Go Mop Foam Floor Cleaner Home inside aerosol 3-7
Spot Shot Carpet Stain Remover Home inside aerosol <10
Tile & Grout Magic Cleaner Home inside aerosol
Panel Magic Home inside aerosol <18.0
Stainless Steel Magic Home inside aerosol <15.0
Oust Air Sanitizer, Citrus Scent Home inside aerosol 25-35
Oust Air Sanitizer, Outdoor Scent Home inside aerosol 25-35
Glade Candle Scent Rainshower (aerosol) Home inside aerosol 20-30
Klean Strip Deep Down Stain Stripper Home maintenance aerosol 20-25
Rust Oleum Metallic Topcoats Home maintenance aerosol 30
Paint & Varnish Remover No. 2600, Aerosol Home maintenance aerosol
Kilz Universal Sealer Primer Stain Blocker Home maintenance aerosol
Kilz UpShot Overhead Stain Sealer Home maintenance aerosol 24.00
Kilz Aerosol Spray Primer Home maintenance aerosol 24.00
Garage Magic Home maintenance aerosol <12.5
Cabot Oil Based Polyurethane Varnish, 2300 Series Home maintenance liquid
Ortho Flying Insect Killer Pesticides aerosol
Pennzoil Motor Oil HD SAE30 Auto products liquid
Flood Penetrol Paint Oil Home maintenance liquid 65
DAP 33 Glazing Paste Home maintenance paste
Slick 50 Engine Formula Care-05/31/2002 Auto products liquid 90-99
Bonide All Seasons Horticultural & Dormant Spray Oil Pesticides pump spray 98
Bonide Oil and Lime Sulphur Spray Pesticides spray 80.0
Super Glaze Car Care Auto products liquid
STP Fuel Injector/Carburetor Cleaner-08/07/1998 Auto products liquid 75-100
STP Gas Treatment-09/30/1998 Auto products liquid 65-95
STP Oxygenated Gas Treatment Auto products liquid <50-80
STP Super Concentrated Fuel Injector Cleaner Auto products liquid <75-85
STP Fuel Injector/Carburetor Cleaner-01/18/2000 Auto products liquid 95-100
STP Complete Fuel System Cleaner Auto products liquid 60-80
STP Fuel Injector/Carburetor Cleaner Auto products liquid <75-95
STP Gas Treatment Auto products liquid <50-80
STP Octane Performance Booster-11/13/1998 Auto products liquid 60-80
STP Oxygenated Gas Treatment-12/24/1998 Auto products liquid 70-95
STP Gas Treatment-08/03/2000 Auto products liquid 90-100
STP Super Concentrated Fuel Injector Cleaner-07/06/1999 Auto products liquid 80-100
STP Fuel Injector and Carburetor Treatment 12 Fl. Oz. Auto products liquid <75-100

How can automotive gasoline affect my health?

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.

Diseases associated with exposure to Automotive Gasoline:

Chronic Solvent Encephalopathy

Chronic solvent encephalopathy or "chronic painters' syndrome" refers to a central nervous system disorder that can follow many years of heavy exposure to solvents such as Automotive Gasoline. It is difficult to distinguish this disorder from depression, conversion reaction, malingering, and other injuries to the brain. Symptoms include difficulty concentrating, dementia, mememory loss, or mood disturbance. A study of 85 painters by Mikkelsen showed that changes in neurobehavioral dysfunction were related to the degree of past solvent exposure. There was little risk of organic brain damage in workers with fewer than 13 years of exposure to the equivalent of a time-weighted average of 40 ppm of white spirit. [Mixed solvent exposure and organic brain damage. A study of painters. Acta Neurol Scand Suppl 1988;118:1-143] A workshop of the World Health Organization described three effects from chronic exposure to organic solvents: 1) organic affective syndrome (reversible irritability, fatigue and difficulty concentrating , 2) mild chronic toxic encephalopathy (sustained mood changes and impairment of intellectual function), and 3) severe chronic toxic encephalopathy (irreversible dementia characterized by deterioration of memory and cognitive function). Haz-Map lists over 150 organic solvents that could cause acute solvent syndrome, or after chronic heavy exposure, chronic toxic encephalopathy. The most hazardous solvents such as Automotive Gasoline are volatile at room temperature. They are or were commonly used in open processes such as degreasing metals and thinning paints. They are not obnoxious in smell or irritating effects--workers could tolerate high concentrations on a daily basis.

Acute Toxic Solvent Effects:

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.

How likely is automotive gasoline to cause cancer?

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.

Is there a medical test to show whether I've been exposed to automotive gasoline?

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.

Has the federal government made recommendations to protecthuman health against Automotive Gasoline exposure?

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.

Glossary of Terms

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.

Automotive Gasoline References

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.

Where can I get more information about Automotive Gasoline?

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

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.

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 Contents

Human 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:

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:

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, and quite possibly in specific TMPs.
[Standeven AM, Goldsworthy TL; J Toxicol Environ Health 43 (2): 213-24 (1994) ]**PEER REVIEWED**

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ The short term inhalation toxicity of methanol and gasoline was studied in rats. Sprague-Dawley-rats were exposed to 0 or 2,500 ppm methanol or 3,200 ppm gasoline vapor alone, or 570 or 2,500 ppm methanol in combination with 3,200 ppm gasoline vapor for 6 hours/day, 5 days/week for 4 weeks. Rats were observed for clinical signs of toxicity. They were killed at the end of exposure and necropsied. The necropsies included determinations of standard hematologic, serum and urine chemistry parameters, hepatic mixed-function-oxidase (MFO) enzymes, and urine ascorbic-acid and hippuric-acid concentrations. All rats survived until the end of the study and none showed any signs of toxicity. Relative liver weights were significantly increased in all rats exposed to gasoline with or without methanol. Absolute and relative kidney weights were increased in female rats exposed to gasoline with or without methanol, and relative kidney weights were increased in males exposed to the methanol plus gasoline mixtures. Exposure to the gasoline and methanol mixtures caused a six fold increase in urinary ascorbic-acid and a three to four fold increase in hippuric-acid excretion. Hemoglobin values were significantly increased in female rats exposed to gasoline and the 570 ppm methanol and gasoline mixture. Exposure to gasoline with or without methanol significantly increased aniline-hydroxylase and other hepatic MFO enzyme activities. Mild panlobular vacuolation was observed following exposure to methanol or gasoline alone. Mild histopathological changes such as minimal epithelial degeneration in the nasolacrimal duct of male rats and mucous cell metaplasia in the nasal septum in both sexes were seen following exposure to gasoline alone. Uterine eosinophilia was suppressed in female rats exposed to methanol or the 2,500 ppm methanol plus gasoline mixture. /Thus,/ ... 4 weeks of exposure to gasoline and methanol vapor alone or in combination causes mild changes in nasal passages, hepatomegaly, and changes in the hepatic MFO system.
[Poon R, Chu I; Toxicol Ind Health 11 (3): 343-361 (1995) ]**PEER REVIEWED**

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ... Female Wistar-rats inhaled air containing 4mg/m3 /unleaded gasoline/ UG having an octane number of 80.5, an aromatic content of 27.2%, and an olefin content of 0.7% for 8 hours/day, 5 days a week for 60 days. Twenty four hour urine samples were collected after 1 and 2 months (mo) of exposure and analyzed for total protein, lactate-dehydrogenase (LDH), lysozyme, beta2-microglobulin (b2MG), and albumin. Glomerular filtration rates (GFRs) were determined by measuring the rate of clearance of chromium-51 tagged ethylenediaminetetraacetic-acid. Exposure to UG vapor increased urinary excretion of b2MG, lysozyme, LDH, and total protein at both time points. Only the increase in b2MG excretion at 2 mo was statistically significant. No treatment related changes in urinary albumin excretion or GFR were observed.
[Vyskocil A, Cizkova M; J Appl Toxicol 16(1): 55-56 (1996) ]**PEER REVIEWED**

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ... Twelve-day-old male B6C3F1 mice were injected with N-nitrosodiethylamine (N-nitrosodiethylamine; 5 mg/kg, intraperitoneally) or vehicle. Starting at 5-7 weeks of age, mice were exposed by inhalation 6 hr/day, 5 days/week for 16 weeks to 0 or 2046 ppm of PS-6 blend unleaded gasoline. Unleaded gasoline treatment caused a significant 2.3-fold increase in the number of macroscopic hepatic masses in N-nitrosodiethylamine-initiated mice, whereas no macroscopic masses were observed in non-initiated mice. Altered hepatic foci (AHF), which were predominantly basophilic in phenotype, were found almost exclusively in N-nitrosodiethylamine-initiated mice. unleaded gasoline treatment significantly increased both the mean volume (threefold) and the volume fraction (twofold) of the altered hepatic foci without increasing the number of altered hepatic foci per unit area. Unleaded gasoline also induced hepatic pentoxyresorufin-O-dealkylase (PROD) activity, a marker of CYP2B, by more than 12-fold over control with or without N-nitrosodiethylamine cotreatment.
[Standeven AM et al; Environ Health Perspect 103 (7-8): 696-700 (1995) ]**PEER REVIEWED**

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ... Twelve-day-old female C57BL/6 x C3H F1 mice (hereafter called B6C3F1) received i.p. injections of N-nitrosodiethylamine (5 mg/kg) or vehicle. Beginning at 5-7 weeks of age, mice were exposed to 0, 292, or 2056 ppm of PS-6 blend UG vapor for 6 h/day, 5 days/week for 16 weeks, 1 ppm ethinyl estradiol (EE2) in the diet, or 2056 ppm UG vapor and 1 ppm EE2 in the diet. Treatment with 2026 ppm UG but not 292 ppm UG increased relative liver weight, the number of macroscopic hepatic neoplasms, and the size and volume fraction of altered hepatic foci in N-nitrosodiethylamine-initiated mice. Treatment with 2056 ppm UG reduced relative uterus, ovary, and pituitary weights but did not change serum 17 beta-estradiol levels, uterine peroxidase activity, or uterine cytosolic estrogen receptor levels. EE2 treatment reduced the number and size of altered hepatic foci in N-nitrosodiethylamine-initiated mice, caused weight loss, anestrus, vaginal keratinization, decreased uterine peroxidase activity, and decreased uterine cytosolic estrogen receptor levels. UG/EE2 co-treatment attenuated the weight loss, anestrus, and vaginal keratinization caused by EE2 treatment alone but dramatically increased the number of macroscopic hepatic neoplasms and the size and volume fraction of altered hepatic foci as compared to UG treatment alone. Thus, in this two-stage model of carcinogenesis (a) 2056 ppm UG had antiestrogenic effects, particularly with respect to pharmacological actions of EE2; (b) 2056 ppm UG but not 292 ppm UG acted as a liver tumor promoter; (c) EE2 inhibited liver tumor promotion; and (d) EE2 strongly potentiated liver tumor promotion by UG. These data demonstrate significant individual and interactive effects of UG vapor and estrogens in liver tumor promotion in female mice.
[Standeven AM et al; Cancer Res 54(5): 1198-204 (1994) ]**PEER REVIEWED**

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ An initiation-promotion protocol was used to test the hypothesis that unleaded gasoline (UG) vapor acts as a liver tumor promoter in female mice under exposure conditions in which UG was hepatocarcinogenic in a cancer bioassay. Twelve day old female B6C3F1 mice were injected with N-nitrosodiethylamine (DEN, 5 mg/kg, ip) or vehicle. Starting at 5-7 weeks of age, mice were exposed by inhalation 6 hr/day, 5 days/week for 13 weeks to 0 or 2039 ppm of PS-6 blend UG, the same gasoline blend used in the cancer bioassay. Putative preneoplastic lesions in liver, characterized mainly as basophilic foci in H&E-stained liver sections, were found exclusively in mice treated with DEN. While similar numbers of altered hepatic foci were found in DEN-initiated mice treated with 0 or 2039 ppm UG, UG treatment significantly increased both the mean volume (3.2-fold) and the volume fraction (3.6-fold) of the foci. To determine if UG induced CYP2B, a subfamily of cytochrome P450 commonly induced by liver tumor promoters in rodents, pentoxyresorufin-O-dealkylase (PROD) activity was assayed in hepatic microsomes derived from the above livers. UG vapor increased hepatic PROD activity approximately 8-fold, while increasing cytochrome P450 content only approximately 30%.
[Standeven AM, Goldsworthy TL; Carcinogenesis 14 (10): 2137-41 (1993) ]**PEER REVIEWED**

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ 20 rats and 4 monkeys of each sex were housed in ... exposure chambers 24 hours a day and were only removed for cleaning purposes. Target exposure vapor concentrations of the test materials were: Unleaded gasoline: 400 and 1500 ppm; Leaded gasoline: 100 and 400 ppm. A control group of 20 rats and 4 monkeys of each sex wasxposed to air only. Exposures were for 6 hours each day, 5 days each week for 13 weeks. ... Three rats at different dose levels and three monkeys also at different dose levels died during the study. These deaths were not considered to be treatment-related. Two female monkeys in each of the high dose groups exhibited emesis, 13 and 17 days after commencing exposure for the 1500 ppm unleaded and 400 ppm leaded groups, respectively. Although there was a/n initial/ reduction in body weights in males in the lowest dose group of each of the test materials... by the end of the study they were demonstrating increased weights. No differences were observed in any of the other treated groups. The hematological values for the monkeys exposed to either test material at either dose level were similar to those of the control animals. In the rats, the only changes observed were: unleaded (1500 ppm males) - 64% increase in thrombocytes; unleaded (1500 ppm females) - 150% increase in reticulocytes; leaded (400 ppm males) - 4% decrease in MCHC /mean corpuscular hemoglobin concentration/; leaded (400 ppm females) - 10% increase in hematocrit; leaded (400 ppm females) - 11% increase in MCV /mean corpuscular volume/;29 / 51 leaded (400 ppm females) - decrease in WBC /white blood count/. Mean flash-evoked response time for the monkeys was ... unaffected by exposure. The results of the mean pulmonary function data are summarized: /Changes reported were: Respiratory Rate for unleaded 1500 ppm males, 21% decrease at 42 days; Tidal volume for unleaded 1500 ppm females of 22% decrease at 90 days; Minute Volume - 36% increase in unleaded 1500 ppm males and 53% increase in leaded 400 ppm males at 90 days./ from table/ There were no effects on airway resistance, dynamic compliance or breaths to 1% nitrogen. Urinalysis showed no differences between treated and control animals in either species. There was no evidence of IgG deposition in the kidneys of rats or monkeys of either sex following exposure to the test materials for 90 days. ... No actual values are given on organ weights or organ/body weight ratios but the following effects are reported: increased liver weights in the unleaded 400 ppm males and leaded 100 ppm males, and increased kidney weights in leaded 100 ppm females /from table/ /In monkeys, thyroid weights increased in unleaded 400 ppm males and unleaded 1500 ppm males; kidney weights decreased in 400 ppm males /from table/. Organ weights were also expressed as % of body weight and the following effects were recorded. (1) Rats: Decreased heart weight in both male leaded groups; decreased brain weight in both male unleaded groups; decreased liver weight in 400 ppm female leaded group; decreased adrenal weight in 1500 ppm female unleaded group. (2) Monkeys: Decreased kidney weight in 400 ppm male unleaded group /from table/. No evidence of treatment-related histopathology was observed in either rats or monkeys, with the exception of lesions noted in the kidneys of all male rats. The lesions were characterized by subtle but discernible increases in the incidence and severity of regenerative epithelium and dilated tubules. The latter were seen to contain protein in their lumens.
[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: Subchronic or Prechronic Exposure/ ... To directly test the hypothesis that UG-induced tumor-promoting ability is secondary to its interaction with the mouse liver tumor inhibitor, estrogen, we compared the tumor-promoting ability of UG in ovariectomized (Ovex) mice with the hepatic tumor-promoting ability of UG in intact mice. Ovaries were surgically removed at 4 weeks of age. Exposure to wholly vaporized UG (2018 ppm) under bioassay and tumor-promoting conditions began at 8 weeks of age. After 4 months of exposure, UG increased relative liver weight and hepatic microsomal cytochrome P450 pentoxyresourfin-O-dealkylase and ethoxyresorufin-O-deethylase activity to a similar extent in intact and Ovex mice. Non-focal hepatocyte proliferation, as measured by the incorporation of bromo-deoxyuridine, was not changed by UG exposure and was similar in all treatment groups. After 4 months of exposure to DEN-initiated mice, UG significantly increased the volume fraction of liver occupied by foci (three-fold) as compared to control intact mice. As expected, volume of foci was elevated in DEN/Ovex/control mice as compared to DEN/intact/control mice. In DEN/Ovex mice UG did not significantly increase the focal volume fraction. Thus, the tumor promoting activity of UG, as demonstrated by increased volume fraction of liver occupied by hepatic foci in intact mice, is greatly attenuated in Ovex mice. The volume fraction data in Ovex mice support the hypothesis that the tumor promoting activity of UG is dependent upon the interaction of UG with ovarian hormones. These data also indicate that hepatic microsomal cytochrome P450 PROD and EROD induction, hepatomegaly and non-focal hepatic LI are not specific markers of hepatic tumor promoting activity of UG.
[Moser GJ et al; Carcinogenesis 18(5): 1075-83 (1997) ]**PEER REVIEWED**

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Male and female Sprague-Dawley rats exposed to 29, 416, or 3316 ppm (0.11, 1.58, or 12.61 mg/L TWA) unleaded gasoline blend by inhalation for 6 hr/day on five days/wk for 21 days developed mild renal tubular degenerative and regeneration changes, including increased levels of hyaline droplet formation, necrosis and degeneration of the proximal convoluted tubule of the renal cortex in males only. When exposure was extended to 90 days at concentrations of 40, 379, or 3866 ppm (0.15, 1.44, or 14.70 mg/L), a concentration-related incidence of tubular dilatation and necrosis at the corticomedullary junction was observed in male rats only.
[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 178 (1989)]**PEER REVIEWED**

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Male Sprague-Dawley rats exposed to 1552 ppm (approx 4650 mg/cu m) unleaded gasoline vapor for 6 hr/day on 5 days/wk for 90 days had regenerative epithelium and dilatation of kidney tubules. These effects were not seen in females and were not seen with leaded gasoline in animals of either sex.
[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 179 (1989)]**PEER REVIEWED**

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ...Male and female B6C3F1-mice were exposed to 0, 67, 292, or 2056 parts per million (ppm) of PS-6 blend gasoline vapor 6 hours/day, 5 days/week for up to 13 weeks. They were implanted with osmotic minipumps to deliver 5-bromo-2'-deoxyuridine (BrdU) for labeling DNA synthesizing cells 3 days before the scheduled sacrifice times at week one, three, six, or 13. Blood samples were assayed for serum alanine-aminotransferase (ALT) and aspartate-aminotransferase (AST). The extent of hepatocellular proliferation was assessed by determining the proportion of BrdU labeled liver cells. Unleaded gasoline did not significantly affect serum ALT and AST activity or cause any histological changes in the liver. The 2056ppm exposure significantly increased absolute and relative liver weights in mice of both sexes at all time points. The extent of BrdU hepatocyte labeling was significantly increased by 2056ppm in male and female mice after 1 week of exposure. The extent of labeling returned to the control value at later times.
[Tilbury L et al; J Toxicol Environ Health 38(3): 293-307 (1993) ]**PEER REVIEWED**

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ /The/ effect in male rats of unleaded gasoline and hormonal modulation on the renal accumulation of alpha2u-globulin and hyaline droplets /was studied/. Animals were dosed by daily gavage for up to 9 days and were studied for hyaline droplet decay at 3,6, and 9 days postexposure. Gasoline increased renal alpha2u-globulin accumulation, which was paralleled by hyaline droplet accumulation in renal tissue. Gasoline administration had no significant effect on hepatic alpha2u-globulin levels at any time. Estradiol treatment plus the unleaded gasoline reduced hepatic and renal alpha2u-globulin levels by 74% and 25 %, respectively, on postexposure day 3 and accelerated the renal decay of hyaline droplets... Gasoline induced significant renal accumulation of alpha2u-globulin and hyaline droplets that was reversible and dependant on maintenance on normal constitutive levels of circulating alpha2u-globulin.
[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. 2]**PEER REVIEWED**

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ When the lungs of rats exposed to 100 ppm of gasoline vapors for 12 weeks were examined by electron microscopy, a progression of lesions characteristic of fibrosing alveolitis (interstitial fibrosis and alveolar collapse) was observed. These lesions were not apparent at the light microscopic level. The animals began to exhibit signs of respiratory distress in this study after about 7 weeks of exposure, which is consistent with the alveolar collapse seen.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.25 (1995) ]**PEER REVIEWED**

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Treatment of male Fischer 344 rats by gavage with 0.04-2.0 mL/ kg bw unleaded gasoline daily for nine days markedly increased the number and size of hyaline droplets in cells of the renal proximal convoluted tubules. The renal content of the male rat-specific low molecular protein alpha2u-globulin was increased up to 4.4 fold.
[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 178 (1989)]**PEER REVIEWED**

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Groups of 100 / F344/ rats of each sex and 100 /B6C3F/ mice of each sex were exposed /for 6 hr per day, 5 days per wk for up to 113 wks / to wholly vaporized /API PS-6/ gasoline at nominal concentrations of 50, 275 and 1500 ppm. 100 mice and 100 rats of each sex were exposed to air only and served as controls. ... All animals were examined once per month for clinical signs and palpable tissue masses. Body weights were recorded monthly for the first 17 months and bi-weekly thereafter. After approximately 18 and 24 months exposure 7 male and 7 female rats from each dose group were selected and hematological and clinical evaluations were conducted...After 3, 6,12 and 18 months exposure 10 rats and 10 mice of each sex from each dose group were sacrificed and underwent complete post mortem examinations. At study termination all surviving animals were sacrificed ... and after gross examination a wide range of organs/tissues were ... fixed for subsequent histopathological examination. Monitoring of the exposure chamber concentrations established that actual concentrations for the study were: 0, 67, 292 and 2056 ppm. Results of study in rats: There were /no treatment-related/ ... pharmacotoxic signs... . Mortality rates were also unaffected by exposure to gasoline vapor. Male rats in the highest dose group had lower body weights than controls from week 5 throughout the study. ... Females at the highest dose also weighed less than controls. ...The few differences in hematological data between controls and several treatment groups were within the normal range for rats of similar age and not considered to be treatment-related. Similarly, small changes in a few clinical chemical parameters were not considered to be treatment-related. At gross necropsy at the 3, 6 12 and 18 month sacrifice the only significant macroscopic findings were in the kidneys of the high dose group male rats and these consisted of tan color, foci, mottling, discolored and granular surface. Although the incidence was small it was considered significant in the light of the histopathology findings. Additionally, masses or nodules were observed in /kidneys of/ mid (3 masses/nodules) and high (5 masses/nodules) dose males that died between 18 months and study termination. There were no other gross findings. Microscopic pathology examination revealed an increase in the incidence of renal disease with tubular degeneration and regeneration or cystic dilatation in the mid and high dose males from 3 months onwards. At 24 months primary renal neoplasms were observed in the following incidence: 0 ppm, none in males or females; 50 ppm 1 renal carcinoma in a male rat; 275 ppm 2 renal adenomas, 2 renal carcinomas, and 1 renal sarcoma in male rats and 1 renal sarcoma in a female rat; 2056 ppm 6 renal carcinomas in male rats with 1 renal adenoma detected at 18 months /from table/. Results of study in mice: There were no consistent signs of toxicity attributable to treatment and mortality rates were considered to be unaffected by treatment. Growth rates were similar for treated and control groups up until approximately week 70 after which the highest dose group males and females had lower body weights than controls. ... Organ weights were unaffected by treatment. There was an increased incidence of liver nodules and masses in treated females in the high dose group that died on the study from 18 months to termination and which were terminally sacrificed. The incidence is tabulated as follows: Males: Total (18 mo to termination) 17/51 in control animals; 14/42 at 67 ppm; 16/44 at 292 ppm, and 25/54 at 2056 ppm; Females: Total (18 mo to termination) 9/57 in control animals; 10/ 52 at 67 ppm; 15/57 at 292 ppm; and 26/56 at at 2056 ppm /from table/. There was a possible reduction in the incidence of cystic or enlarged uteri for female mice. ...There were no other treatment-related findings at necropsy. Microscopic examination of the tissues of animals up to and including the 18 month sacrifice did not reveal any compound-related effects. At 24 months, however, there was an increased incidence of hepatocellular tumors in the high dose group females when compared to controls. The actual incidence of liver tumors /adenomas and carcinomas/ was: 8/57 in controls; 10/52 at 67 ppm; 12 of 57 at 292 ppm and 27/56 at 2056 ppm /from table/. Some animals had more than 1 tumor.
[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: Chronic Exposure or Carcinogenicity/ In experiments on rats..., chronically inhaling gasoline vapor (1 g/cu m) is reported to have caused damage to cornea, retina and ciliary body in 6 to 9 months, with reversible damage to blood vessels of the eye being particularly noted.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 714]**PEER REVIEWED**

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ In a long term study, groups of male and female Fischer 344 rats were exposed to 67, 292 or 2056 (approx 200, 870, 6170 mg/cu m) unleaded gasoline vapors for 6 hr per day on five days per week for three, six, 12, 18, and 24 months. After three, six, and 12 months at the highest doses, the males had increased foci of regenerative epithelium in the renal cortex and dilated tubules. Both exposed and control rats developed spontaneous chronic progressive nephropathy after 18 and 24 months' exposure. However, male rats exposed to 292 and 2056 ppm for 12, 18, and 24 months had linear mineral deposits in the renal medullae.
[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 179 (1989)]**PEER REVIEWED**

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Groups of 100 male and 100 female B6C3F1 mice, six weeks of age, were exposed to 0, 67, 292, or 2056 ppm (0, approx 200, 870, or 6170 mg/cu m) totally volatilized unleaded gasoline (benzene content, 2%) by inhalation for 6 hr per day on five days per week for 103 to 113 weeks. ...Ten male and ten female mice from each group were killed at three, six, 12, and 18 months and the remainder at the end of the study. Survival in the groups of exposed female mice was not significantly different from that of controls (rates not reported). That of the low- and medium-dose male mice was significantly higher than that in controls, although survival of high-dose males was lower than that of controls (rates not reported). The incidences of hepatocellular adenomas and carcinomas were increased in exposed females. In mice killed at 18 to 24 months, the percentages of animals with liver tumors were: controls, 14%; low dose, 19%; medium dose, 21%; high dose, 48% (ratio of benign to malignant tumors unspecified). The incidence of hepatocellular tumors was not increased in treated male mice. A renal adenoma occurred in one high-dose female and a bilateral renal tubular adenocarcinoma in another.
[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 176 (1989)]**PEER REVIEWED**

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ When male F344 rats inhaled 300 ppm unleaded gasoline for 48 weeks, H-labeled-thymidine indices in the renal proximal tubule were 4- to 6-fold higher in treated rats than in control rats; the extent and severity of renal pathology (hyaline droplet accumulation and localized tubular proliferation) paralleled the labeling dose-response data.
[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. 2]**PEER REVIEWED**

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Groups of 100 male and 100 female Fischer 344 rats, six weeks of age, were exposed to 0, 67, 292, or 2056 ppm (0, approx 200, 870 or 6170 mg/cu m) totally volatilized unleaded gasoline (benzene content, 2%) by inhalation for 6 hr per day on five days per week for 107 or 109 weeks. Ten males and ten females from each group were killed at 3, 6, 12 and 18 months and the remainder at the end of the study. Survival in the groups of exposed female rats was not significantly different from that of controls (rates not reported). That of control male rats was significantly higher than that of any of the exposed groups after week 80 (rates not reported). Increased incidences of renal tumors were observed in male rats: renal adenomas -- controls, 0; low-dose, 0; medium-dose, 2; high-dose 1; renal carcinomas -- control, 0; low-dose, 1; medium-dose, 2; high-dose, 6. No renal adenomas or carcinoma was observed in female rats. Renal sarcomas occured in one medium-dose male and in one medium-dose female.
[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: Chronic Exposure or Carcinogenicity/ A study was conducted on a possible relationship between the induction of liver tumors in female mice following exposure to 2,056 ppm of vaporized unleaded gasoline and the coincident finding of a decreased incidence of enlarged/cystic uteri. Tissues obtained from B6C3F1-mice ... exposed for 3, 6, 12, or 18 months to 0, 67, 292, or 2,056 ppm gasoline by inhalation were evaluated. Cystic endometrial hyperplasia was identified in the uteri of most of the mice examined. It was much more severe in ... mice exposed to low doses of gasoline compared with those exposed to the middle or high doses. There was a tendency for the severity of the endometrial lesions to be milder in mice with liver tumors. Uterine atrophy was seen almost exclusively in mice in the highest dose group.
[MacGregor JA et al; J Am Coll Toxicol 12 (2): 119-126 (1993) ]**PEER REVIEWED**

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ The long term carcinogenic effects of gasoline, related fuels, and aromatic gasoline components were examined in rats. Male and female Sprague-Dawley-rats were exposed daily to unleaded gasoline, leaded gasoline, diesel, kerosene, toluene, xylene, ethylbenzene, and 1,2,4-trimethylbenzene doses of 0 to 800 mg/kg 4 days per week for 104 weeks. Chemicals were administered via stomach tube. Controls received vehicle only. The rats were observed until death, up to 123 or 145 weeks. Upon necropsy, numerous tissues were analyzed microscopically for histopathological changes. Among males, survival was slightly or moderately reduced by exposure to unleaded gasoline, diesel, kerosene, toluene, ethylbenzene, and 1,2,4-trimethylbenzene. Survival was markedly reduced by leaded gasoline and xylene. Among females, survival was slightly or moderately reduced by exposure to leaded gasoline, toluene, ethylbenzene, and 1,2,4-trimethylbenzene. Survival was markedly reduced by unleaded gasoline, diesel, kerosene, and xylene. Survival was often dose dependent. Exposure to either unleaded or leaded gasoline increased the number of total malignant tumors in males and females, the number of mammary tumors and malignant uterine/vaginal tumors in females, and the number of head cancers in males.
[Maltoni C, Ciliberti A; Ann NY Acad Sci 837: 15-52 (1997) ]**PEER REVIEWED**

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ ...Unleaded gasoline (UG), a complex mixture of over 300 hydrocarbons, induced liver tumors selectively in female mice and exhibited liver tumor promoting activity.
[Standeven AM, Goldsworthy TL; J Toxicol Environ Health 43 (2): 213-24 (1994) ]**PEER REVIEWED**

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ To evaluate the potential of unleaded gasoline vapor for developmental toxicity, a sample was prepared by slowly heating API 94-02 (1990 industry average gasoline) and condensing the vapor. At a final vapor temperature of 130 degrees F, 10.4% (by volume) of the starting gasoline was recovered as vapor condensate. The composition of this vapor condensate is representative of real-world exposure to gasoline vapor encountered at service stations and other occupational settings. In a dose range-finding study, pregnant Sprague-Dawley rats and CD-1 mice (10/group/species) were exposed for 6 hr/day via whole-body inhalation on gestation days 6-19 (rats) or 6-17 (mice) to concentrations of 0, 300, 1000, 3000, and 9000 ppm (9000 ppm = 75% Lower Explosive Limit). No developmental or maternal toxicity was observed in mice. In rats, no developmental toxicity was observed, but maternal body weight gain appeared reduced at 9000 ppm. Since no effects were observed in mice, the definitive study was conducted in rats. In the definitive study, groups of pregnant rats (n = 24/group) were exposed to 0, 1000, 3000, or 9000 ppm unleaded gasoline vapor for 6 hr/day on gestation days 6-19. All rats were sacrificed on gestation day 20. No maternal toxicity was observed. Developmentally, there were no differences between treated and control groups in malformations, total variations, resorptions, fetal body weight, or viability. The maternal and developmental NOELs were 9000 ppm.
[Roberts L, Schroeder R; Toxicologist 36(1 pt 2); 259 (1997) ]**PEER REVIEWED**

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ A 2-generation study was conducted on gasoline vapor to assess its reproductive toxicity potential. The test material was collected from vapor recovery units of a gasoline distribution terminal and was shown to be similar in composition to vapors to which humans are exposed through occupational or public contact. In the two-generation reprotoxicity study, groups of male and female Sprague-Dawley rats were exposed daily for 6 hours to gasoline vapor at concentrations up to 20,000 mg/cu m. This dose is approximately 50% of the lower explosive limit and the highest level considered safe to test. There were no treatment-related effects in parental animals, and no microscopic changes other than hyaline droplet nephropathy in the kidneys of male rats. There were no effects on fertility and reproductive parameters, and no fetal effects. Additionally, there was no evidence of endocrine modulating activity as indicated by a lack of effect on estrous cycling, sperm count and quality, quantification of primordial oocytes, and no changes in any specific landmarks related to sexual development in either generation. Thus, no toxicologically important findings were identified in this study, and the NOAEL for reproductive effects for gasoline vapor was 20,000 mg/cu m.
[Riley AJ et al; Toxicologist 54(1): 395 (2000) ]**PEER REVIEWED**

/GENOTOXICITY/ The genotoxic potential of unleaded gasoline and 2,2,4-trimethylpentane, a component of unleaded gasoline, were investigated in vivo and in vitro in hepatocytes using unscheduled DNA synthesis as an indicator of genotoxic activity and replicative DNA synthesis as an indicator of cell proliferation. For the in vitro study, primary hepatocyte cultures prepared from Fischer 344 rats, B6C3F1 mice, or human surgical material were incubated with tritium labeled thymidine and one of the test agents. For the in vivo study, male and female B6C3F1/Cr1BR mice and male Fischer 344/Cr1BR rats were administered 100 to 5000 mg/kg unleaded gasoline or 500 mg/kg 2,2,4-trimethylpentane by gavage. Hepatocytes isolated from treated rats and mice were cultured in the presence of tritium labeled thymidine. Unscheduled DNA synthesis and replicative DNA synthesis were measured in rat and mouse hepatocytes exposed either in vitro or in vivo. In rat hepatocytes treated in vitro with 0.05 to 0.10% unleaded gasoline, there was a dose dependent increase in unscheduled DNA synthesis; these doses were toxic in mouse and human hepatocyte cultures. 2,2,4-Trimethylpentane did not induce unscheduled DNA synthesis in rat hepatocytes exposed in vitro or in vivo. The percentage of cells in S-phase 24 hours after treatment with 2,2,4-trimethylpentane increased 20 fold in male mice, four fold in female mice, and five fold in male rats. The percentage of S-phase cells in male mice increased nine fold in male mice treated with unleaded gasoline, but there was no induction of replicative DNA synthesis in female mice. It was concluded that the lack of unscheduled DNA synthesis activity observed in the DNA repair assay is consistent with the lack of liver tumors observed in rats following chronic exposure to unleaded gasoline in previous studies. While genotoxicity may be one of the factors contributing to hepatocarcinogenic activity of unleaded gasoline in the mouse, the mechanism underlying the particular susceptibility of the female mouse liver is still unknown.
[Loury DJ et al; Toxicol and Appl Pharmacol 85 (1): 11-23 (1986) ]**PEER REVIEWED**

/GENOTOXICITY/ Studies of unleaded gasoline in Salmonella typhimurium, in L5178Y cells, and the mouse dominant lethal and bone marrow cytogenicity assays failed to demonstrate a significant mutagenic response... Unscheduled DNA synthesis (UDS) occurred upon addition of unleaded gasoline to rat, mouse , and human hepatocytes. Gasoline inhalation or gavage in male rats failed to elicit UDS in kidney or liver, but UDS was elevated in mouse liver after gasoline gavage
[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**

/GENOTOXICITY/ Unleaded gasoline (containing 2% benzene; boiling range, 31-192 deg C; 39% aromatics) did not induce mutation in Salmonella typhimurium TA1535, TA1537, TA1538, TA98 or TA100 in the presence or absence of an exogenous metabolic system from rat liver using either the plate incorporation (0.001-5 l/plate) or suspension method (3.75-30 l/ml ... .
[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 179 (1989)]**PEER REVIEWED**

/GENOTOXICITY/ Unleaded gasoline (PS-6; with 2% benzene w/w) induced unscheduled DNA synthesis in vivo in hepatocytes from male and female B6C3F1/CrlBR mice 12 h after treatment with 2000 mg/ kg bw by gavage. The percentage of S-phase cells in the hepatocytes of male, but not female, mice also increased. No increase was observed in unscheduled DNA synthesis in vivo in hepatocytes from male Fischer-344/ CrlBR rats 2-48 hr after gavage treatment at 100-5000 mg/ kg bw. However, the percentage of S-phase cells was increased 24-48 hr after treatment with 2000 mg/ kg bw.
[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 180 (1989)]**PEER REVIEWED**

/GENOTOXICITY/ Mouse lymphoma assay; forward mutation assay using cell line L5178Y TK+/-; with and without /rat liver S-9/; negative
[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**

/GENOTOXICITY/ Dominant lethal assay: Mouse (Male/female) CD-1; Inhalation, 6 hours/day, 5 days/week for 8 weeks at 400 &1600 ppm; Negative/API PS-6 unleaded gasoline/
[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**

/GENOTOXICITY/ The abilities of unleaded gasoline and 2,2,4-trimethylpentane which comprises about 10% of unleaded gasoline to induce gene locus mutation and sister chromatid exchange in a human lymphoblast system were investigated TK6 human lymphoblastoid cells were used. The cytotoxic effects of medium saturated with these agents were first determined by monitoring cell growth following treatment. For cell exposures, a hydrocarbon saturated medium was mixed in different ratios with normal medium containing the cells. Exposures were for 3 hours. For unleaded gasoline, ratios were 1:7 or 1:3 (saturated/normal); for 2,2,4-trimethylpentane, 1:1 or no dilution concentrations were used. Incubations were performed with and without S9. Benzo(a)pyrene was used as a positive control and to test the bioactivating ability of S9 in the presence of the treatment agents. Unleaded gasoline in a 1:1 ratio dissolved TK6 cells. A reduction to 1:3 increased cell survival to approximately 70 %. Greater than 60% of cells survived treatment in the 2,2,4-trimethylpentane saturated medium. Neither unleaded gasoline at its maximum tolerated concentration, nor 2,2,4-trimethylpentane at its limit of solubility, induced mutation at the thymidine kinase locus. Negative results were seen both in the presence and absence of the rat liver homogenate metabolizing system. Sister chromatid exchange analyses were also negative for both agents. The expected frequency of mutation was observed with BaP in the presence of the bioactivating system indicating that no inhibition of metabolism was taking place. It was concluded that the carcinogenicity and nephrotoxicity of these agents observed in-vivo do not correlate with any marked genotoxicity in-vitro.
[Richardson KA et al; Toxicol and Appl Pharmacol 82 (2): 316-22 (1986) ]**PEER REVIEWED**

/GENOTOXICITY/ Male Sprague-Dawley rats were treated orally with API-PS-6 /American Petroleum Institute's PS-6 unleaded gasoline/ (500, 750, 1000 mg/kg/day) for 5 consecutive days, treated with colchicine 4 hours following the last treatment, and sacrificed 2 hours later. No chromosome aberrations were seen in bone marrow cells from rats treated with 500 or 750 mg/kg/day API-PS-6 and only two aberrations were observed in rats receiving 1000 mg/kg/day; the aberrations did not represent a statistically significant increase over control values. A dimethylsulfoxide extract of API-PS-6 had no effect on the number of revertants seen in a modified Ames assay except at the highest concentration where a slight reduction was observed. Evaporative residues of API-PS-6 (50 to 10,000 ug/plate) produced slight increases in revertant recovery at two nontoxic concentrations. The mouse lymphoma mutagenesis assay showed that API-PS-6 did not produce a significant increase in mutant frequency at concentrations yielding total growths of greater than 10% with or without metabolic activation. However, concentrations yielding total growths of less than 10% did increase mutant frequency two fold or more with and without activation. The dimethylsulfoxide extract was mutagenic without metabolic activation while the evaporative residue was mutagenic with metabolic activation. It was concluded that whole API-PS-6 is not mutagenic in the test systems used, however, this gasoline does contain at least two mutagenic components.
[Dooley JF et al; Polynuclear Aromatic Hydrocarbons: A Decade of Progress, Proceedings of the 10th International Symposium p.179-94 (1988) ]**PEER REVIEWED**

Ecotoxicity Excerpts:

Unleaded gasoline is potentially toxic to freshwater and saltwater ecosystems. Various grades of gasoline exhibited range of lethal toxicity (LC100) from 40 PPM to 100 PPM in ambient stream water with Rainbow Trout (Salmo irideus). A 24-hour TLm (Median Toxic Limit) was calculated to be 90 PPM with juvenile American Shad (Squalius cephalus). Using Bluegill Sunfish (Lepomis macrochirus), Grey Mullet (Chelon labrosus) and Gulf Menhaden (Brevoortia patronus), gasoline exhibited a 96-hour LC50 of 8 PPM, 2 PPM, and 2 PPM, respectively.
[CITGO Pertoleum Corp. Material Safety Data Sheet CITGO Gasolines, All Grades Unleaded. Tulsa, OK, 2001 ]**PEER REVIEWED**

This material is expected to be toxic to aquatic organisms. Gasoline studies have been conducted in the laboratory under a variety of test conditions with a range of fish and invertebrate species. An even more extensive database is available on the aquatic toxicity of individual aromatic constituents. The majority of published studies do not identify the type of gasoline evaluated, or even provide distinguishing characteristics such as aromatic content or presence of lead alkyls. As a result, comparison of results among studies using open and closed vessels, different ages and species of test animals and different gasoline types, is difficult. The bulk of the available literature on gasoline relates to the environmental impact of monoaromatic (BTEX) and diaromatic (naphthalene, methylnaphthalenes) constituents. In general, non-oxygenated gasoline exhibits some short-term toxicity to freshwater and marine organisms, especially under closed vessel or flow-through exposure conditions in the laboratory. The components which are the most prominent in the water soluble fraction and cause aquatic toxicity, are also highly volatile and can be readily biodegraded by microorganisms.
[Chevron/ Material Safety Data Sheet Chevron Regular Unleaded Gasoline. MSDS Coordinator, San Ramon, CA (2004) ]**PEER REVIEWED**

Non-Human Toxicity Values:

LD50 Sprague-Dawley rat (m,f) acute oral 18.75 mL/kg (95% confidence limit 16.3-21.6 mL/kg /API PS-6 gasoline/
[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 5, 2004 ]**PEER REVIEWED**

LD50 Rat acute oral 14,063 mg/kg
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.47 (1995) ]**PEER REVIEWED**

LD50 New Zealand white rabbit (m,f) acute dermal /24 hrs/ >5 mL/kg /API PS-6 gasoline/
[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 5, 2004 ]**PEER REVIEWED**

Ecotoxicity Values:

LC50 Oncorhynchus mykiss (Rainbow trout) 16 mg/L/96 hr (99% confidence interval: 10-25 mg/L); static; CAS No. 86290-81-5
[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**

LC50 Oncorhynchus mykiss (Rainbow trout) 11 mg/L/96 hr (95% confidence interval: 8.7-16 mg/L); static; CAS No. 86290-81-5
[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**

EC50 Daphnia magna (water flea) (acute immobilization) 12 mg/L/48 hr (95% confidence interval: 7.3-22 mg/L); static; CAS No. 86290-81-5
[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**

EC50 Daphnia magna (water flea) (acute immobilization) 7.6 mg/L/48 hr (95% confidence interval: 6.4-9.3 mg/L); static; CAS No. 86290-81-5
[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**

Metabolism/Pharmacokinetics:

Metabolism/Metabolites:

The metabolism of gasoline is not known, although it is expected that the interaction of the various components of gasoline may affect the metabolic products that are formed. The interaction of the components of gasoline is likely to influence the metabolizing enzymes such that the elimination rate of a compound may be altered. The increased metabolism of antipyrine suggested that mixed function oxygenase activity was induced after inhalation of gasoline vapors in humans (43-1,312 mg/cu m) and in rats (5,000 mg/cu m).
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.65 (1995) ]**PEER REVIEWED**

Although there are no specific data on the elimination of gasoline following inhalation, oral, or dermal exposure, the elimination rate of the components of gasoline probably varies because of the metabolism of the gasoline components by the hepatic enzymes. Metabolites of benzene, toluene, and xylene are known to be excreted primarily in the urine.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.63 (1995) ]**PEER REVIEWED**

Absorption, Distribution & Excretion:

Although there are no data on the absorption rate of gasoline, indirect evidence from case reports of gasoline sniffers indicates that it can be absorbed following inhalation exposure. The increases in blood and urinary lead levels, as well as the characteristic neurological signs, are indicators of exposure. Because gasoline is a mixture, the pattern of absorption following inhalation varies for the individual components. The compounds with higher blood/gas coefficients (e.g., xylene, benzene, toluene) have a higher rate of absorption than the compounds with lower coefficients (e.g., cyclohexane, ethane, ethylene)
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.63 (1995) ]**PEER REVIEWED**

After pregnant women working in a chemical industry were exposed to gasoline fumes, gasoline was found in fetal and neonatal tissues; neonatal blood concentrations of gasoline were about double the maternal blood concentrations.
[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**

An initial concentration of 247 ug/mL gasoline was estimated from blood samples of an adult male who was found unconscious in a gasoline-vapor-filled car. However, the patient was also exposed dermally to gasoline. The estimated half-life of the gasoline was 16.9 hours.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.64 (1995) ]**PEER REVIEWED**

There is no quantitative information on the absorption of gasoline following oral exposure in humans and animals. However, the absorption is believed to be relatively complete because of the high lipophilicity of the hydrocarbon compounds, the large surface area of the gastrointestinal tract, and the long resident time in the tract.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.63 (1995) ]**PEER REVIEWED**

There are limited data on the distribution pattern of gasoline in humans and animals. The distribution of gasoline (gasoline concentration measured as the ratio of the concentrations of (2-methylpentane/2,2-dimethylbutane) in sample/(2-methylpentane/2,2-dimethylbutane) in standard) was determined in a male who died following accidental ingestion of gasoline. The liver, gastric wall, and lungs had the highest gasoline concentrations at 663, 324, and 457 ppm, respectively. The brain, bile, and kidney contained 44.2, 59, and 51.5 ppm, respectively, while the concentrations in the blood from the brain, lungs, and heart were 29.4, 132, and 51.5 ppm, respectively. Autopsies of humans who were apparently exposed to gasoline indicated elevated blood levels of hydrocarbons such as benzene, toluene, pentane, and hexane.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.64 (1995) ]**PEER REVIEWED**

Biological Half-Life:

Mechanism of Action:

For more information consult the Automotive Gasoline MSDS Information above.

Investigations of mechanisms of the nephropathy and renal tumors included an assessment of unscheduled (a measure of genotoxicity) and replicative DNA synthesis (a measure of cell proliferation) in rat kidney cells exposed in vitro and in vivo to unleaded gasoline. No unscheduled DNA synthesis occurred, even at a tumorigenic dose, while a five-to eightfold increase in cell proliferation was observed. ...Unleaded gasoline /exposure/ was reported to result in an increase in hyaline droplets harboring large accumulations of alpha2u-globulin within proximal convoluted tubule epithelial cells. It was hypothesized that alpha2u-globulin accumulated secondary to a defect in renal lysosomal degradation of the protein. Supportive evidence for this hypothesis came from /a study that/... demonstrated that inhibition of the lysosomal peptidase cathepsin B caused a rapid accumulation of phagolysosomes and alpha2u-globulin in the kidney similar to that of gasoline. Further progress in elucidating the mechanism of alpha2u-globulin nephropathy came from the demonstration that the unleaded gasoline component, 2,2,4-trimethylpentane (TMP), itself an inducer of alpha2u-globulin nephropathy, was metabolized to 2,4,4-trimethyl-2-pentanol (TMPOH), which was selectively retained by the kidney of male rats. Subsequently, it was demonstrated that the sex-specific retention of TMPOH in the kidney was due to reversible binding with alpha2u-globulin. This binding rendered the protein less digestible by lysosomal enzymes, which accounted for its accumulation. This accumulation, in turn, led to cellular degeneration and necrosis, primarily in the P2 segment of the proximal tubule. In response, regenerative proliferation occurs and promotes formation of renal cell tumors by irreversibly "fixing" spontaneously altered DNA and clonally expanding initiated cells.
[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**

To study the cellular and molecular mechanism of gasoline-induced adverse effects on skin, particularly on keratinocyte and fibroblast in vitro. The primary cell culture of keratinocyte and fibroblast were treated with 0, 0.001%, 0.01%, 0.1% and 1.0% gasoline, respectively. (3)H-thymidine ((3)H-TdR), (3)H-leucine ((3)H-Leu), (3)H-proline ((3)H-Pro) and (14)C-linoleic acid incorporation tests were applied to elucidate their capacity of synthesizing DNA, protein and sebum. The incorporation of (3)H-TdR in keratinocyte and (3)H-TdR and (3)H-Pro in fibroblast inhibited significantly after exposure to 0.01% gasoline (P < 0.05), with inhibition rates 68.5%, 45.1% and 40.6% for (3)H-TdR in keratinocyte, and (3)H-TdR and (3)H-Pro in fibroblast, respectively. Significant depression in incorporation of (3)H-Leu and (14)C-linoleic acid in keratinocyte were found even in the group treated with 0.001% gasoline (P < 0.05), with inhibition rates of 20.2% and 41.2%, respectively. Solvent gasoline has certain toxic effect on keratinocyte and fibroblast, intervening their normal metabolic and physiological process and affecting their ability of synthesizing DNA, protein and sebum, and their physiological functions, which could be one of the mechanisms causing skin damage by gasoline. The results also indicated that keratinocyte was more susceptible to gasoline than fibroblast.
[Jia X et al; Zhonghua Yu Fang Yi Xue Za Zhi 36(4): 261-3 (2002) ]**PEER REVIEWED**

The antiestrogenic effects of unleaded gasoline have been proposed as a possible underlying mechanism of female mouse liver tumor induction by this chemical.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.66 (1995) ]**PEER REVIEWED**

... To directly test the hypothesis that UG-induced tumor-promoting ability is secondary to its interaction with the mouse liver tumor inhibitor, estrogen, ...the tumor-promoting ability of UG in ovariectomized (Ovex) mice with the hepatic tumor-promoting ability of UG in intact mice. ... Non-focal hepatocyte proliferation, as measured by the incorporation of bromo-deoxyuridine, was not changed by UG exposure and was similar in all treatment groups. After 4 months of exposure to DEN-initiated mice, UG significantly increased the volume fraction of liver occupied by foci (three-fold) as compared to control intact mice. As expected, volume of foci was elevated in DEN/Ovex/control mice as compared to DEN/intact/control mice. In DEN/Ovex mice UG did not significantly increase the focal volume fraction. ...The volume fraction data in Ovex mice support the hypothesis that the tumor promoting activity of UG is dependent upon the interaction of UG with ovarian hormones. These data also indicate that hepatic microsomal cytochrome P450 PROD and EROD induction, hepatomegaly and non-focal hepatic LI are not specific markers of hepatic tumor promoting activity of UG.
[Moser GJ et al; Carcinogenesis 18 (5): 105-83 (1997) ]**PEER REVIEWED**

Interactions:

Twelve-day-old female C57BL/6 x C3H F1 mice (hereafter called B6C3F1) received i.p. injections of N-nitrosodiethylamine (5 mg/kg) or vehicle. Beginning at 5-7 weeks of age, mice were exposed to 0, 292, or 2056 ppm of PS-6 blend UG vapor for 6 h/day, 5 days/week for 16 weeks, 1 ppm ethinyl estradiol (EE2) in the diet, or 2056 ppm UG vapor and 1 ppm EE2 in the diet. ... in this two-stage model of carcinogenesis (a) 2056 ppm UG had antiestrogenic effects, particularly with respect to pharmacological actions of EE2; (b) 2056 ppm UG but not 292 ppm UG acted as a liver tumor promoter; (c) EE2 inhibited liver tumor promotion; and (d) EE2 strongly potentiated liver tumor promotion by UG. These data demonstrate significant individual and interactive effects of UG vapor and estrogens in liver tumor promotion in female mice.
[Standeven AM et al; Cancer Res 54 (5): 1198-204 (1994) ]**PEER REVIEWED**

Twelve-day-old male B6C3F1 mice were injected with N-nitrosodiethylamine (N-nitrosodiethylamine; 5 mg/kg, intraperitoneally) or vehicle. Starting at 5-7 weeks of age, mice were exposed by inhalation 6 hr/day, 5 days/week for 16 weeks to 0 or 2046 ppm of PS-6 blend unleaded gasoline. Unleaded gasoline treatment caused a significant 2.3-fold increase in the number of macroscopic hepatic masses in N-nitrosodiethylamine-initiated mice, whereas no macroscopic masses were observed in non-initiated mice.
[Standeven AM et al; Environ Health Perspect 103 (7-8); 696=700 (1995) ]**PEER REVIEWED**

The tumor promoting activity of /unleaded gasoline/ UG, as demonstrated by increased volume fraction of liver occupied by hepatic foci in intact mice /initiated with diethylnitrosamine/, is greatly attenuated in /ovariectomized/ Ovex mice.
[Moser GJ et al; Carcinogenesis 18 (5): 1075-83 (1997) ]**PEER REVIEWED**

Twelve day old female B6C3F1 mice were injected with N-nitrosodiethylamine (DEN, 5 mg/kg, ip) or vehicle. Starting at 5-7 weeks of age, mice were exposed by inhalation 6 hr/day, 5 days/week for 13 weeks to 0 or 2039 ppm of PS-6 blend /unleaded gasoline/ UG.. Putative preneoplastic lesions in liver, characterized mainly as basophilic foci ... were found exclusively in mice treated with DEN. While similar numbers of altered hepatic foci were found in DEN-initiated mice treated with 0 or 2039 ppm UG, UG treatment significantly increased both the mean volume (3.2-fold) and the volume fraction (3.6-fold) of the foci.
[Standeven AM, Goldsworthy TL; Carcinogenesis 14 (10): 2137-41 (1993) ]**PEER REVIEWED**

Iron-deficiency anemia induced in the maternal organism markedly enhances embryotoxic and teratogenic effects of ... gasoline ... . The prenatal effects ... against the background of iron-deficiency state in pregnant females leads to development of the main feature of the tissue hypoxia, decompensated metabolic acidosis, in both the maternal organism and 20-day embryos.
[Senichenkova IN, Chebotar' NA ; Ontogenez. 27 (2): 108-13 (1996) ]**PEER REVIEWED**

Pharmacology:

Interactions:

Environmental Fate & Exposure:

Environmental Fate/Exposure Summary:

Gasoline consists of over 150 individual C4-C12 hydrocarbons with boiling range 32-210 deg C. The individual components of gasoline include paraffins, olefins, aromatics, and oxygenated additives. Gasoline's production and use as a fuel source has resulted in its release to the environment through various waste streams including emissions, spills and storage tank leakage. The individual components of gasoline exist solely as a vapor in the ambient atmosphere. Vapor-phase gasoline will be degraded in the atmosphere by reaction with hydroxyl radicals, nitrate radicals and ozone. The rate of this reaction varies depending upon the chemical structure of the individual components. Alkanes, isoalkanes, and cycloalkanes have half-lives on the order of l-10 days, whereas alkenes, cycloalkenes, and substituted benzenes have half-lives of 1 day or less. If released to soil, the components of gasoline are expected to have high to no mobility based upon log Koc values in the range of 1.81 to 4.56. Volatilization from moist and dry soils is expected to be an important fate process for gasoline. The individual components of gasoline undergo biodegradation in soils and water; however, the rate of degradation is greatly influenced by the amount of the hydrocarbon substrate and a number of site-specific environmental factors, including temperature, oxygen content, moisture content, nutrient content, salinity, and pH. Volatilization from water surfaces is expected to be an important fate process for gasoline. The estimated volatilization half-lives for alkanes and benzene, toluene, ethylbenzene, xylene (BTEX) components were predicted as 7 days in ponds, 1.5 days in rivers, and 6 days in lakes. The bioconcentration potential of the major components of gasoline range from low to high. Alkenes have estimated BCF values of about 10; aromatics have BCF values in the range of 20-200, while C5 and greater alkanes have fairly large BCF values in the range of 100-1,500. Hydrolysis is not expected to be an important fate process since gasoline contains no chemicals with functional groups that hydrolyze under environmental conditions. Occupational exposure to gasoline may occur through inhalation and dermal contact with this compound at workplaces where gasoline is produced, used or distributed. The general population is exposed through inhalation of gasoline vapors in the ambient air, particularly near refueling stations. The general population is also exposed through the ingestion of drinking water and food sources that contain the individual components of gasoline. (SRC)
**PEER REVIEWED**

Probable Routes of Human Exposure:

For more information consult the Automotive Gasoline MSDS Information above.

Artificial Pollution Sources:

Gasoline's production and use as a fuel source in the internal combustion engine has resulted in its release to the environment from various waste streams including emissions, spills and storage tank leakage(1).
[(1) ATSDR; Toxicological Profile for Automotive Gasoline. Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) ]**PEER REVIEWED**

Environmental Fate:

TERRESTRIAL FATE: Log Koc values for the individual components of gasoline have been reported to range from 1.81-4.56(1). Based upon a classification scheme(2), this range of Koc values indicates that the components of gasoline will have high to no mobility in soil(SRC). The Henry's law constants for the constituents of gasoline range from about 5X10-4 to 4 atm-cu m/mol(1), which suggests that volatilization from soil surfaces is an important environmental fate process(SRC). The volatilization half-lives for the individual components of a synthetic gasoline from 3 soils ranged from about 50-200 hours depending upon the soil type, initial gasoline concentration, temperature and moisture content(3). The individual components of gasoline undergo biodegradation in soils; however the rate of degradation is greatly influenced by the amount of the hydrocarbon substrate and a number of site-specific environmental factors, including temperature, oxygen content, moisture content, nutrient content, salinity, and pH(1).
[(1) ATSDR; Toxicological Profile for Automotive Gasoline. Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) (2) Swann RL et al; Res Rev 85: 17-28 (1983) (3) Gidda T et al; J Contam Hydrol 39: 137-159 (1999) ]**PEER REVIEWED**

AQUATIC FATE: Log Koc values for the individual components of gasoline have been reported to range from 1.81-4.56(1). Based upon a classification scheme(2), this range of Koc values indicates that many of the components of gasoline will adsorb to suspended solids and sediment in the water column(SRC). Volatilization from water surfaces is expected(3) based upon a range of Henry's Law constants 5X10-4 to 4 atm-cu m/mol(1). The volatilization rate of 3 distillate fuels (JP-4, JP-5, and JP-8) was studied in deionized water at 3 stirring rates in order to estimate the volatilization half-lives that might be observed in the environment(4). The estimated volatilization half-lives for alkanes and benzene, toluene, ethylbenzene, xylene (BTEX) components were predicted as 7 days in ponds, 1.5 days in rivers, and 6 days in lakes(4). The volatilization rate of naphthalene and its substituted derivatives were estimated to be slower(4). The bioconcentration potential of the major components of gasoline range from low to high(SRC). Some higher molecular weight components (e.g., naphthalene and substituted naphthalenes) may be taken up by fish and domestic animals and bioconcentrated if they persist in environmental media(1). Alkenes have low log octanol/water partition coefficients (Kow) of about 1 and estimated bioconcentration factors (BCF) of about 10; aromatics have intermediate values (log Kow values of 2-3 and BCF values of 20-200), while C5 and greater alkanes have fairly high values (log Kow values of about 3-4.5 and BCF values of 100-1,500)(1). Hydrolysis is not expected to be an important environmental fate process since gasoline does not contain any constituents with hydrolyzable functional groups(3). Tri-substituted benzenes and naphthalenes contained in a distillate fuel (JP-4) were shown to undergo photolysis with half-lives on the order of a few days in seawater and pondwater, while the alkanes, benzene, toluene, mono-, and di-substituted benzenes were reported to be stable over a 21 day period(4). Many of the hydrocarbon components of gasoline have been found to undergo biodegradation in surface waters and sediment, but the rate is highly dependent upon the environmental conditions of the aquatic system and the concentration of the hydrocarbons(1). Degradation of gasoline hydrocarbons in surface waters is expected to be rapid under conditions favorable to microbial activity; however, it may be slow or limited under unfavorable conditions, such as low pH, low temperature, low oxygen levels, or high salinity, or where populations of degrading microbes are low(1).
[(1) ATSDR; Toxicological Profile for Automotive Gasoline. Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) (2) Swann RL et al; Res Rev 85: 17-28 (1983) (3) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 4-9, 15-1 to 15-29 (1990) (4) Smith JH, Harper JC; pp. 336-53 in Proc 12th Conf Environ Toxicol 3, 4, and 5 Nov. 81. Air Force Aerospace Medical Research Laboratory, Ohio (1982) ]**PEER REVIEWED**

ATMOSPHERIC FATE: The majority of gasoline's individual components will exist in the vapor-phase in the ambient atmosphere where they will be degraded by reacting with atmospheric oxidants such as hydroxyl radicals, nitrate radicals and ozone(1). The rate of this reaction varies depending upon the chemical structure of the individual components. Alkanes, isoalkanes, and cycloalkanes have half-lives on the order of l-10 days, whereas alkenes, cycloalkenes, and substituted benzenes have half-lives of 1 day or less(1). Photochemical oxidation products include aldehydes, hydroxy compounds, nitro compounds, and peroxyacyl nitrates(1). Alkenes, certain substituted aromatics, and naphthalene are potentially susceptible to direct photolysis(1).
[(1) ATSDR; Toxicological Profile for Automotive Gasoline. Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) ]**PEER REVIEWED**

For more information consult the Automotive Gasoline MSDS Information above.

Environmental Biodegradation:

Hydrocarbons in the C5-C9 range are biodegradable only at low concentrations since at higher concentrations they exhibit membrane-solvent toxicity to soil microbes(1). Hydrocarbons with condensed ring structures, such as polyaromatic hydrocarbons (PAHs), and cycloalkanes are relatively resistant to biodegradation(1). A 49% loss of n-octane occurred within 5 days and completely disappeared within 15 days from 1 ml of crude oil added to a 100 ml simulated seawater soln inoculated with sediment samples from Fukae of Kobe harbor, Japan, and incubated at 20 deg C(2). n-Hexane present at 500 mg/liter achieved 4.1, 7.6 and 16.9% of its theoretical BOD using a benzene acclimated activated sludge at 2,500 mg/liter after 6, 24, and 72 hours, respectively(3). n-Hexane at 500 mg/liter was toxic to microorganisms using 50 mg municipal sludge obtained at a sewage treatment facility(4). n-Heptane present at 500 mg/liter achieved 0.7, 4.3 and 23.4% of its theoretical BOD using a benzene acclimated activated sludge at 2,500 mg/liter after 6, 24, and 72 hours, respectively(3). n-Octane present at 500 mg/liter achieved 1, 4.6 and 28.4% of its theoretical BOD using a benzene acclimated activated sludge at 2,500 mg/liter after 6, 24, and 72 hours, respectively(3). Other constituents of gasoline such as benzene, toluene, ethylbenzene and xylenes are more biodegradable(SRC). The biodegradation half-life of toluene in various soils was reported as several hours to 71 days(5). Using a standard BOD dilution technique and a sewage inoculum, a theoretical BOD of 52, 80 and 44% was observed over a 5 day incubation period for 2-, 3-, and 4-xylene, respectively(6). Benzene present at 100 mg/liter achieved 39-41% of its theoretical BOD using an activated sludge inoculum at 30 mg/liter and the Japanese MITI test(7). Toluene present at 100 mg/liter achieved 112-129% of its theoretical BOD using an activated sludge inoculum at 30 mg/liter and the Japanese MITI test(7). Ethylbenzene present at 100 mg/liter achieved 81-126% of its theoretical BOD using an activated sludge inoculum at 30 mg/liter and the Japanese MITI test(7). Naphthalene present at 100 mg/liter achieved 2% of its theoretical BOD using an activated sludge inoculum at 30 mg/liter and the Japanese MITI test(7).
[(1) ATSDR; Toxicological Profile for Automotive Gasoline. Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) (2) Nagata S, Kondo G; pp. 617-20 in Proc 1977 Oil Spill Conf, Am Petrol Inst (1977) (3) Malaney GW, McKinney RE; Water Sewage Works 113: 302-9 (1966) (4) Gerhold RM, Malaney GW; J Water Pollut Contr Fed 38: 562-79 (1966) (5) Aronson D et al; Aerobic biodegradation of organic chemicals in environmental media: a summary of field and laboratory studies. 1999. Available at http://esc.syrres.com as of Nov 21, 2003. (6) Bridie AL et al; Water Res 13: 627-30 (1979) (7) Chemicals Inspection and Testing Institute. Japan Chemical Industry Ecology - Toxicology and Information Center. ISBN 4-89074-101-1 (1992) ]**PEER REVIEWED**

Environmental Abiotic Degradation:

Gasoline consists of over 150 identifiable C4-C12 hydrocarbons with boiling range 32-210 deg C(1). The individual components of gasoline include paraffins, olefins, aromatics, and oxygenated additives(2). The components of gasoline are expected to be degraded in air by atmospheric oxidants such as hydroxyl radicals, nitrate radicals and ozone(3,4). The rate of this reaction varies depending upon the chemical structure of the individual components. Alkanes, isoalkanes, and cycloalkanes have half-lives on the order of l-10 days, whereas alkenes, cycloalkenes, and substituted benzenes have half-lives of 1 day or less(3). Photochemical oxidation products include aldehydes, hydroxy compounds, nitro compounds, and peroxyacyl nitrates(3). Alkenes and substituted aromatics, including naphthalene are potentially susceptible to direct photolysis(3). The water soluble components of a distillate fuel were studied for photolysis and the alkane, benzene, toluene, mono-, and di-substituted benzenes were reported to be stable over a 21 day period(5). Tri-substituted benzenes and naphthalenes underwent photolysis with half-lives on the order of a few days in seawater and pondwater(5). Gasoline is not expected to undergo hydrolysis in the environment because it contains no chemicals with hydrolyzable functional groups(6).
[(1) Neimeier RW; in Pattys Toxicology 5th ed. Bingham E et al, eds. NY, NY: John Wiley & Sons 1: 776 (2001) (2) Hochhauser A; in Kirk-Othmer Encycl Chem Technol. Kroschwitz JI, ed. NY, NY: John Wiley & Sons 12: (1994) (3) ATSDR; Toxicological Profile for Automotive Gasoline. Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) (4) ATSDR; Toxicological Profile for Methyl Tertiary Butyl Ether (MTBE). Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) (5) Smith JH, Harper JC; pp. 336-53 in Proc 12th Conf Environ Toxicol 3, 4, and 5 Nov. 81. Air Force Aerospace Medical Research Laboratory, Ohio (1982) (6) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 7-4, 7-5 (1990) ]**PEER REVIEWED**

Environmental Bioconcentration:

The bioaccumulation potentials of the major components of gasoline range from low to high(SRC). Some higher molecular weight components (e.g., naphthalene and substituted naphthalenes) may be taken up by fish and domestic animals and bioconcentrated if they persist in environmental media(1). Alkenes have low log octanol/water partition coefficients (Kow) of about 1 and estimated bioconcentration factors (BCF) of about 10; aromatics have intermediate values (log Kow values of 2-3 and BCF values of 20-200), while C5 and greater alkanes have fairly high values (log Kow values of about 3-4.5 and BCF values of 100-1,500)(1).
[(1)ATSDR; Toxicological Profile for Automotive Gasoline. Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) ]**PEER REVIEWED**

Soil Adsorption/Mobility:

Gasoline consists of over 150 identifiable C4-C12 hydrocarbons with boiling range 32-210 deg C(1). The individual components of gasoline include paraffins, olefins, aromatics, and oxygenated additives(2). The relatively low water solubility and large log Kows for the paraffins, olefins, and some aromatics suggest that these compounds will possess low to moderate mobility in soil(3). Log Koc values for the individual components of gasoline have been reported to range from 1.81-4.56(3). Based on a classification scheme(4), these Koc values suggest the components of gasoline will have high to no mobility in soil(SRC). Oxygenated compounds such as methyl tertiary butyl ether (MTBE) which are added to automotive gasoline in order to improve fuel combustion, have very high mobility in soil and often contaminate groundwater(5).
[(1) Neimeier RW; in Pattys Toxicology 5th ed. Bingham E et al, eds. NY, NY: John Wiley & Sons 1: 776 (2001) (2) Hochhauser A; In Kirk-Othmer Encycl Chem Technol Kroschwitz JI, ed. NY, NY: John Wiley & Sons 12: (1994) (3) ATSDR; Toxicological Profile for Automotive Gasoline. Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) (4) Swann RL et al; Res Rev 85: 17-28 (1983) (5) ATSDR; Toxicological Profile for Methyl Tertiary Butyl Ether (MTBE). Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) ]**PEER REVIEWED**

For more information consult the >Automotive Gasoline MSDS Information above.

Volatilization from Water/Soil:

Gasoline consists of over 150 identifiable C4-C12 hydrocarbons with boiling range 32-210 deg C(1). The individual components of gasoline include paraffins, olefins, aromatics, and oxygenated additives(2). The Henry's law constants for these components range from about 5X10-4 to 4 atm-cu m/mol(3), which suggests that volatilization from moist soil and water surfaces will be an important environmental fate process. The volatilization rate of 3 distillate fuels (JP-4, JP-5, and JP-8) was studied in deionized water at 3 stirring rates in order to estimate the volatilization half-lives that might be observed in the environment(4). The estimated volatilization half-lives for alkanes and BTEX components was 7 days in ponds, 1.5 days in rivers, and 6 days in lakes(4). The volatilization rate of naphthalene and its substituted derivatives were estimated to be slower(4).
[(1) Neimeier RW; in Pattys Toxicology 5th ed. Bingham E et al, eds. NY, NY: John Wiley & Sons 1: 776 (2001) (2) Hochhauser A; in Kirk-Othmer Encycl Chem Technol Kroschwitz JI ed. NY, NY: John Wiley & Sons 12: (1994) (3) ATSDR; Toxicological Profile for Automotive Gasoline. Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) (4) Smith JH, Harper JC; pp. 336-53 in Proc 12th Conf Environ Toxicol 3, 4, and 5 Nov. 81. Airforce Aerospace Medical Research Laboratory, Ohio (1982) ]**PEER REVIEWED**

The volatilization rate of a synthetic gasoline was studied in a sandy loam, silty loam and a clay loam at varying temperatures, moisture content and initial gasoline/soil concentration(1). In general, volatilization for the individual components occurred rapidly with half-lives around 50-200 hours depending upon the soil type, initial gasoline concentration, temperature and moisture content(1). Volatilization occurred more readily at higher temperatures and also increased with moisture content for the sandy and silty loams, but decreased for the clay loam(1). A synthetic gasoline consisting of n-heptane, n-octane, toluene, ethylbenzene, m-xylene and n-hexadecane (which was used as a tracer) was employed to study the volatilization rate of gasoline from 2 sandy soils and a silt loam(2). After incorporating the synthetic gasoline in each soil at a depth of 50 mm, volatilization half-lives of about 25-150 hours were observed for the individual components except n-hexadecane which did not volatilize(2). Volatilization rates were greater for the 2 sandy soils as compared to the silty loam(2).
[(1) Gidda T et al; J Contam Hydrol 39: 137-159 (1999) (2) Arthurs P et al; J Soil Contam 4: 123-135 (1995) ]**PEER REVIEWED**

Environmental Water Concentrations:

GROUNDWATER: Following the accidental release of 1,900 metric tons of gasoline into the water at Block Island Sound, Rhode Island, total levels of C8-C12 hydrocarbons at three sites close to the spill ranged from 5 to 20 ug/liter at a depth of 3.5 meters in the water column 1 day postspill(1). Following the spillage of a JP-4 fuel in East Anglia, UK the following gasoline components were detected in groundwater: benzene (40-1,250 ug/liter); heptane isomers (3-85 ug/liter); toluene (0.2-2,140 ug/liter); ethylbenzene (7.5-1,110 ug/liter); xylenes (0.2-1,550 ug/liter); cumene (1.3-30 ug/liter); n-propylbenzene (2.8-195 ug/liter); m-ethyltoluene (0.2-1,060 ug/liter); p-ethyltoluene (0.2-560 ug/liter); 1,2,4-trimethylbenzene (0.2-1,530 ug/liter); 1,2,3-trimethylbenzene (1.2-445 ug/liter); methylstyrene or indan (2.4-130); naphthalene (1-153 ug/liter); 2-methylnaphthalene (2-40 ug/liter); 1-naphthalene (8-25 ug/liter); cyclohexane (10 ug/liter)(2).
[(1) ATSDR; Toxicological Profile for Automotive Gasoline. Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) (2) Tester DJ, Harker RJ; Water Pollut Control 80: 614-31 (1981) ]**PEER REVIEWED**

DRINKING WATER: Several components of gasoline are frequently detected in drinking water, although the source of contamination is often unclear(SRC). Benzene has been detected in well water at concns of about 5 ng/liter(1). Toluene was detected in 14% of the samples of drinking water in the US at concns of less than 1 part per trillion(2). In a survey of 30 Canadian water treatment facilities, the average value of 4-xylene combined with ethyl benzene was 1 ppb with a maximum value of 10 ppb(3). n-Octane was identified, not quantified, in 4 of 14 treated water supplies in England(4).
[(1) Wallace L; Environ Health Perspect 104: 1129-1136 (1996) (2) NAS; The Alkyl Benzene USEPA Contract No. 68-02-4655 (1980) (3) Otson R et al; J Assoc Off Anal Chem 65: 1370-4 (1982) (4) Fielding M et al; Organic Pollutants in Drinking Water. Medmenham, UK: Water Res Cent TR-159 p. 49 (1981) ]**PEER REVIEWED**

SURFACE WATER: Several components of gasoline are frequently detected in surface water, although the source of contamination is often unclear(SRC). Toluene was detected in 31 of 204 sites at concns of 1-5 ppb in 14 heavily industrialized river basins in the US(1). 4-Xylene was detected in the raw water supplies for 30 Canadian treatment facilities, 23% contained a combination of p-xylene and ethyl benzene which averaged <1 ppb and whose maximum value was <1 ppb in summer and 2 ppb in winter(2). Xylenes were detected in only 1 of 204 surface water samples in the USA(1).
[(1) Ewing BB et al; Monitoring to detect previously unrecognized pollutants in surface waters USEPA 560/6-77-015 (appendix USEPA 560/6-77-015a) (1977) (2) Otson R et al; J Assoc Off Anal Chem 65: 1370-4 (1982) ]**PEER REVIEWED**

Effluent Concentrations:

Gasoline vapors are released to the air during refueling of gasoline-powered vehicles, bulk transfer of gasoline at distribution terminals, leaks from storage containers and loading equipment, and during removal and maintenance of underground storage tanks (1). It has been estimated that 75,000-100,000 tanks leak millions of gallons of gasoline to groundwater each year in the US(1). The state of Maine has estimated that leaking underground tanks release approximately 11 million gallons of gasoline annually(1). A leak from a pipeline or underground storage tank contaminated groundwater in the north Los Angeles area of California with an estimated 100,00-250,000 gallons of gasoline(1). The US Coastguard estimated that 48,816 gallons of gasoline were accidentally discharged to New Jersey's Newark Bay and associated major tributaries from 1982 to 1991(1).
[(1) ATSDR; Toxicological Profile for Automotive Gasoline. Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) ]**PEER REVIEWED**

Sediment/Soil Concentrations:

Several components of gasoline are frequently detected in soil and sediment, although the source of contamination is often unclear(SRC). Toluene was detected in 67 of 397 sediment samples at a median concentration of 5.0 ppb dry weight in the EPA STORET Database(1). Benzene was detected in 32 out of 355 samples tested in the EPA STORET Database at a median concn of <5.0 ppb dry weight(1). Ethylbenzene was detected in 38 of 350 sediment samples at a median concn of 5.0 ppb dry weight in the EPA STORET Database(1). Naphthalene was detected in 32 out of 355 samples tested in the EPA STORET Database at a median concn of <500.0 ppb dry weight(1).
[(1) Staples CA et al; Environ Toxicol Chem 4: 131-42 (1985) ]**PEER REVIEWED**

Atmospheric Concentrations:

Levels of gasoline vapor have been measured in air at service stations in several areas of the country. Area air samples taken in the vicinity of a high-volume service station in Pennsylvania during 1 week in May showed concentrations of gasoline vapor ranging from not detected (detection limit of 0.4 mg/cu m) to 28 mg/cu m (1). Air levels of gasoline vapor measured at seven different service stations in the United States (Houston, Texas; Manhattan Beach, California; New Britain, Connecticut; New Orleans, Louisiana; Plantation, Florida; Stickney, Illinois; and Walnut Creek, California) from March to June ranged from 1.81 to 99.2 ppm (1). Corresponding concentrations of benzene ranged from <0.01 to 1.21 ppm(1).
[(1) ATSDR; Toxicological Profile for Automotive Gasoline. Atlanta, GA: Agency for Toxic Substances and Disease Registry (1996) ]**PEER REVIEWED**

Food Survey Values:

Several components of gasoline are frequently detected in food sources, although the source of contamination is unclear(SRC). Toluene was identified, not quantified, in baked potatoes(1), mountain cheese(2), fried bacon(3), fried chicken(4), peanut oil(5) and raw beef(6). Unspecified concentrations of xylenes were detected in cheese products obtained from dairy cattle in the French Alps(7). Benzene was found in both heat treated and canned beef at 2 ug/kg; in Jamaican rum at 120 ug/kg; in eggs ranging from 500-1900 ug/kg; and it was detected (concns not specified) in fruits, nuts, vegetables, dairy products, meat, fish, poultry, eggs, and beverages(8).
[(1) Coleman EC et al; J Agric Food Chem 29: 42-8 (1981) (2) Dumont JP, Adda J; J Agric Food Chem 26: 364-7 (1978) (3) Ho CT et al; J Agric Food Chem 31: 336-42 (1983) (4) Tang JT et al; J Agric Food Chem 31: 1287-92 (1983) (5) Chung TY et al; J Agric Food Chem 41:1467-70 (1993) (6) King MF et al; J Agric Food Chem 41: 1974-81 (1993)(7) Dumont JP, Adda J; J Agric Food Chem 26:364-367 (1978) (8) USEPA; Ambient Water Quality Criteria: Benzene p. C-5 USEPA-440/5-80-018 (1980) ]**PEER REVIEWED**

Environmental Standards & Regulations:

Federal Drinking Water Guidelines:

EPA 5 ug/L
[USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee (FSTRAC). Summary of State and Federal Drinking Water Standards and Guidelines (11/93), p. ]**QC REVIEWED**

State Drinking Water Guidelines:

(ME) MAINE 50 ug/L
[USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee (FSTRAC). Summary of State and Federal Drinking Water Standards and Guidelines (11/93), p. ]**QC REVIEWED**

Chemical/Physical Properties:

Molecular Formula:

UVCB
**PEER REVIEWED**

Color/Form:

Mobile liquid
[O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 776]**PEER REVIEWED**

Odor:

Characteristic odor
[O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 776]**PEER REVIEWED**

Boiling Point:

32-210 deg C
[O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 776]**PEER REVIEWED**

Melting Point:

-90.5 to -95.4 deg C
[ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1988., p. 255]**PEER REVIEWED**

Density/Specific Gravity:

0.70-0.80
[ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1988., p. 255]**PEER REVIEWED**

Solubilities:

Insol in water; freely sol in absolute alcohol, ether, chloroform, benzene.
[O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 776]**PEER REVIEWED**

Spectral Properties:

Index of Refraction: 1.375-1.388
[ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1988., p. 255]**PEER REVIEWED**

Vapor Density:

3-4 (Air= 1)
[ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1988., p. 255]**PEER REVIEWED**

Vapor Pressure:

304-684 mm Hg @ 37.8 deg C
[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 (1989) 159-99]**PEER REVIEWED**

Chemical Safety & Handling:

DOT Emergency Guidelines:

For more information consult the Automotive Gasoline MSDS Information above.

/GUIDE 128: FLAMMABLE LIQUIDS (NON-POLAR/WATER-IMMISCIBLE)/ Fire or Explosion: HIGHLY FLAMMABLE: Will be easily ignited by heat, sparks or flames. Vapors may form explosive mixtures with air. Vapors may travel to source of ignition and flash back. Most vapors are heavier than air. They will spread along ground and collect in low or confined areas (sewers, basements, tanks). Vapor explosion hazard indoors, outdoors or in sewers. Those substances designated with a "P" may polymerize explosively when heated or involved in a fire. Runoff to sewer may create fire or explosion hazard. Containers may explode when heated. Many liquids are lighter than water. Substances may be transported hot.
[U.S. Department of Transportation. 2004 Emergency Response Guidebook. A Guide book for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident. Washington, D.C. 2004G-128]**QC REVIEWED**

/GUIDE 128: FLAMMABLE LIQUIDS (NON-POLAR/WATER-IMMISCIBLE)/ Health: Inhalation or contact with material may irritate or burn skin and eyes. Fire may produce irritating, corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff from fire control or dilution water may cause pollution.
[U.S. Department of Transportation. 2004 Emergency Response Guidebook. A Guide book for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident. Washington, D.C. 2004G-128]**QC REVIEWED**

/GUIDE 128: FLAMMABLE LIQUIDS (NON-POLAR/WATER-IMMISCIBLE)/ Public Safety: CALL Emergency Response Telephone Number ... . As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces before entering.
[U.S. Department of Transportation. 2004 Emergency Response Guidebook. A Guide book for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident. Washington, D.C. 2004G-128]**QC REVIEWED**

/GUIDE 128: FLAMMABLE LIQUIDS (NON-POLAR/WATER-IMMISCIBLE)/ Protective Clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Structural firefighters' protective clothing will only provide limited protection.
[U.S. Department of Transportation. 2004 Emergency Response Guidebook. A Guide book for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident. Washington, D.C. 2004G-128]**QC REVIEWED**

/GUIDE 128: FLAMMABLE LIQUIDS (NON-POLAR/WATER-IMMISCIBLE)/ Evacuation: Large spill: Consider initial downwind evacuation for at least 300 meters (1000 feet). Fire: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.
[U.S. Department of Transportation. 2004 Emergency Response Guidebook. A Guide book for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident. Washington, D.C. 2004G-128]**QC REVIEWED**

/GUIDE 128: FLAMMABLE LIQUIDS (NON-POLAR/WATER-IMMISCIBLE)/ Fire: Caution: All these products have a very low flash point: Use of water spray when fighting fire may be inefficient. CAUTION: For mixture containing a high percentage of an alcohol or polar solvent, alcohol-resistant foam may be more effective. Small fires: Dry chemical, CO2, water spray or regular foam. Large fires: Water spray, fog or regular foam. Use water spray or fog; do not use straight streams. Move containers from fire area if you can do it without risk. Fire involving tanks or car/trailer loads: Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.
[U.S. Department of Transportation. 2004 Emergency Response Guidebook. A Guide book for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident. Washington, D.C. 2004G-128]**QC REVIEWED**

/GUIDE 128: FLAMMABLE LIQUIDS (NON-POLAR/WATER-IMMISCIBLE)/ Spill or Leak: ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). All equipment used when handling the product must be grounded. Do not touch or walk through spilled material. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. A vapor suppressing foam may be used to reduce vapors. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. Use clean non-sparking tools to collect absorbed material. Large spills: Dike far ahead of liquid spill for later disposal. Water spray may reduce vapor; but may not prevent ignition in closed spaces.
[U.S. Department of Transportation. 2004 Emergency Response Guidebook. A Guide book for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident. Washington, D.C. 2004G-128]**QC REVIEWED**

/GUIDE 128: FLAMMABLE LIQUIDS (NON-POLAR/WATER-IMMISCIBLE)/ First Aid: Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Wash skin with soap and water. Keep victim warm and quiet. In case of burns, immediately cool affected skin for as long as possible with cold water. Do not remove clothing if adhering to skin. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
[U.S. Department of Transportation. 2004 Emergency Response Guidebook. A Guide book for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident. Washington, D.C. 2004G-128]**QC 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**

Fire Potential:

Volatile liquid
[Association of American Railroads/Bureau of Explosives; Emergency Handling of Hazardous Materials in Surface Transportation. Association of American Railroads. Pueblo, CO. 2002., p. 466]**PEER REVIEWED**

NFPA Hazard Classification:

Health: 1. 1= Materials that, on exposure, would cause significant irritation, but only minor residual injury, including those requiring the use of an approved air-purifying respirator. These materials are only slightly hazardous to health and only breathing protection is needed.
[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 325-68]**PEER REVIEWED**

Flammability: 3. 3= This degree includes Class IB and IC flammable liquids and materials that can be easily ignited under almost all normal temperature conditions. Water may be ineffective in controlling or extinguishing fires in such materials.
[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 325-68]**PEER REVIEWED**

Instability: 0. 0= This degree includes materials that are normally stable, even under fire exposure conditions, and that do not react with water. Normal fire fighting procedures may be used.
[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 325-68]**PEER REVIEWED**

Flammable Limits:

Lower flammable limit: 1.4% by volume; Upper flammable limit: 7.8% by volume /56-60 Octane, 73 Octane, 92 Octane, 100 Octane/
[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 325-68]**PEER REVIEWED**

Lower flammable limit: 1.3% by volume; Upper flammable limit: 7.1% by volume /100-130 (Aviation Grade)/
[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 325-68]**PEER REVIEWED**

Lower flammable limit: 1.2% by volume; Upper flammable limit: 7.1% by volume /115-145 (Aviation Grade)/
[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 325-68]**PEER REVIEWED**

Flash Point:

-45 deg F (-43 deg C); -36 deg F (-38 deg C) (Closed cup) /56-60 Octane, 73 Octane, 92 Octane, 100 Octane/
[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 325-68]**PEER REVIEWED**

-50 deg F (-46 deg C) approx (Closed cup) /100-130 (Aviation Grade)/
[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 325-68]**PEER REVIEWED**

-50 deg F (-46 deg C) approx (Closed cup) /115-145 (Aviation Grade)/
[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 325-68]**PEER REVIEWED**

Autoignition Temperature:

536 deg F (280 deg C), 853 deg F (456 deg C) /56-60 Octane, 73 Octane, 92 Octane, 100 Octane/; 824 deg F 440 deg C) /100-130 (Aviation Grade)/; 880 deg F (471 deg C) /115-145 (Aviation Grade)/
[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 325-68]**PEER REVIEWED**

Fire Fighting Procedures:

If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped. Use water in flooding quantities as fog. Solid streams of water may spread fire. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible. Use foam, dry chemical, or carbon dioxide.
[Association of American Railroads/Bureau of Explosives; Emergency Handling of Hazardous Materials in Surface Transportation. Association of American Railroads. Pueblo, CO. 2002., p. 466]**PEER REVIEWED**

Evacuation: If fire becomes uncontrollable or container is exposed to direct flame -- consider evacuation of one-third (1/3) mile radius.
[Association of American Railroads/Bureau of Explosives; Emergency Handling of Hazardous Materials in Surface Transportation. Association of American Railroads. Pueblo, CO. 2002., p. 466]**PEER REVIEWED**

Use carbon dioxide, dry chemical, or "alcohol" foam. Water spray is not effective for extinguishing, but effective to keep fire-exposed containers cool. If a leak or spill has not ignited, use water to disperse the vapor and to protect men attempting to stop the leakage.
[ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1988., p. 255]**PEER REVIEWED**

Firefighting Hazards:

Vapors from this commodity may travel to a source of ignition and then flash back to the source of the leak.
[Association of American Railroads/Bureau of Explosives; Emergency Handling of Hazardous Materials in Surface Transportation. Association of American Railroads. Pueblo, CO. 2002., p. 466]**PEER REVIEWED**

Hazardous Reactivities & Incompatibilities:

...can react vigorously with oxidizing materials.
[Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 1720]**PEER REVIEWED**

Other Hazardous Reaction:

Any /statically charged/ clothing system that produces a potential exceeding 3000 volts on a man is hazardous, since it can cause the ignition of gasoline-air mixtures.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V3 153 (1978)]**PEER REVIEWED**

For more information consult the Automotive Gasoline MSDS Information above.

Protective Equipment & Clothing:

Protective goggles, gloves.
[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**

Wear goggles, or rubber gloves, a chemical cartridge respirator and coveralls.
[ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1988., p. 255]**PEER REVIEWED**

For more information consult the Gasoline MSDS included above.

Preventive Measures:

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.
**PEER REVIEWED**

If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers. Build dikes to contain flow as necessary. Attempt to stop leak if without undue personnel hazard. Use water spray to knock-down vapors.
[Association of American Railroads/Bureau of Explosives; Emergency Handling of Hazardous Materials in Surface Transportation. Association of American Railroads. Pueblo, CO. 2002., p. 466]**PEER REVIEWED**

Personnel protection: Avoid breathing vapors. Keep upwind. ... Do not handle broken packages unless wearing appropriate personal protective equipment. Wash away any material which may have contacted the body with copious amounts of water or soap and water.
[Association of American Railroads/Bureau of Explosives; Emergency Handling of Hazardous Materials in Surface Transportation. Association of American Railroads. Pueblo, CO. 2002., p. 466]**PEER REVIEWED**

Evacuation: IF material leaking (not on fire) consider evacuation from downwind area based on amount of material spilled, location and weather conditions.
[Association of American Railroads/Bureau of Explosives; Emergency Handling of Hazardous Materials in Surface Transportation. Association of American Railroads. Pueblo, CO. 2002., p. 466]**PEER REVIEWED**

Shipment Methods and Regulations:

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
[49 CFR 171.2; U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from:http://www.gpoaccess.gov/ecfr/ as of October 22, 2002]**PEER REVIEWED**

The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials.
[International Air Transport Association. Dangerous Goods Regulations. 47th Edition. Montreal, Quebec Canada. 2006., p. 197]**QC REVIEWED**

The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article.
[International Maritime Organization. International Maritime Dangerous Goods Code. London, UK. 2004., p. 51]**QC REVIEWED**

Marine pollutant /Gasoline, leaded/
[49 CFR 172.101, Appendix B; U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from: http://www.gpoaccess.gov/ecfr/ as of November 10, 2003 ]**PEER REVIEWED**

For more information consult the Automotive Gasoline MSDS Information above.

Storage Conditions:

Keep bottles, cans and drums closed and avoid direct sunlight. Protect containers against physical damage. No fire. Outdoor or detached storage is preferred. For indoor storage, use standard combustible liquid storage rooms or cabinets.
[ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1988., p. 255]**PEER REVIEWED**

Because rusting and corrosion can cause problems in storage tanks, pipelines, tankers, and the fuel systems of engines, several types of hydrocarbon soluble compounds are used in gasolines as rust inhibitors. Most of these compounds, which include various fatty acid amines, sulfonates, alkyl phosphates, and amine phosphates, function by coating metal surfaces with a very thin protective film that keeps water from contacting the surfaces. This surface active property also helps in preventing buildup of gummy deposits in the carburetor and combats carburetor iceup during cold weather.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V11 668 (1980)]**PEER REVIEWED**

Cleanup Methods:

Absorb on paper. Evaporate on a glass or iron dish in hood. Burn the paper.
[ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1988., p. 255]**PEER REVIEWED**

Disposal Methods:

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.
**PEER REVIEWED**

Occupational Exposure Standards:

OSHA Standards:

Vacated 1989 OSHA PEL TWA 300 ppm (900 mg/cu m); STEL 500 ppm (1500 mg/cu m) is still enforced in some states.
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997., p. 365]**PEER REVIEWED**

Threshold Limit Values:

8 hr Time Weighted Avg (TWA): 300 ppm; 15 min Short Term Exposure Limit (STEL): 500 ppm. /Gasoline, CAS# 86290-81-5/
[ 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**

A3; Confirmed animal carcinogen with unknown relevance to humans. /Gasoline, CAS# 86290-81-5/
[ 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**

For more information consult the Gasoline MSDS included above.

Manufacturing/Use Information:

Major Uses:

As fuel in internal combustion engines of the spark-ignited, reciprocating type. /Gasoline, CAS# not specified/
[O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 777]**PEER REVIEWED**

Fuel, fats, extractant or dilutant for essential oils; solvent for rubber adhesives; detergent for precision instruments. Finishing agent for artificial leathers.
[ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1988., p. 254]**PEER REVIEWED**

Manufacturers:

BP (formerly BP Amoco), 150 West Warrenville Rd., Naperville, IL 60563, (877) 701-2726
[SRI Consulting. 2003 Directory of Chemical Producers. SRI International, Menlo Park, CA. 2003, p. 63]**PEER REVIEWED**

Conoco Phillips, 600 North Dairy Ashford, Houston, TX 77079, (281) 293-1000.
[SRI Consulting. 2003 Directory of Chemical Producers. SRI International, Menlo Park, CA. 2003, p. 96]**PEER REVIEWED**

Exxon Mobil Corp., 13501 Katy Freeway, Houston, TX 77079, (281) 870-6000
[SRI Consulting. 2003 Directory of Chemical Producers. SRI International, Menlo Park, CA. 2003, p. 152]**PEER REVIEWED**

Shell Oil Products US., 1100 Louisiana St., Houston, TX 77002, (713) 277-7000
[SRI Consulting. 2003 Directory of Chemical Producers. SRI International, Menlo Park, CA. 2003, p. 351]**PEER REVIEWED**

Methods of Manufacturing:

Hydrocracking, which consists of cracking in the presence of added hydrogen.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V11 662 (1980)]**PEER REVIEWED**

Early in the history of petroleum refining, it was found that higher boiling hydrocarbons could be broken down, or cracked, into lower boiling ones by subjecting them to high temperatures for an appreciable length of time. ... Because temperatures as high as 540 deg C are required for such thermal breakdown, pressures of 2.4-6.9 MPa (300-1000 psi) are used to keep the feedstock largely in the liquid phase while it undergoes the cracking reactions. Such high pressures are not required, however, when cracking is conducted in the presence of a catalyst. The catalyst, which may consist of naturally occurring clays or synthetic compounds containing silica and alumina, offers a large surface area on which the cracking reactions take place. Modern catalytic cracking units employ catalysts in the form of small beads or finely divided, fluidized powder. The carbon deposits formed on the surface of these catalysts during cracking are burned off (thereby regenerating the catalyst) by subjecting the hot catalyst to a stream of air in a separate catalyst regeneration step. Continuous operation is attained by constantly circulating a portion of the catalyst from the reaction zone, through the regenerator, and back to the reaction zone.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V11 661 (1980)]**PEER REVIEWED**

Petroleum refining begins with the distillation of crude oil into fractions of different boiling ranges. The crude oil is heated to 370-430 deg C, pumped into a fractionating tower, and separated into light naphtha, heavy naphtha, kerosene, light gas oil, heavy gas oil, and reduced crude. Because they are naturally occurring fractions of crude oil, the naphtha fractions obtained by distillation are called virgin naphtha, or straightrun gasoline. Both the amounts of these naphthas and their hydrocarbon compositions depend on the type of crude oil being distilled. Thus, straightrun gasolines differ widely in such properties as specific gravity, vaporization characteristics, and antiknock quality. The light naphtha fraction is usually of sufficiently high octane number to be used as a component of finished gasoline without any more refining than is needed to remove undesirable impurities. The heavy naphtha is catalytically reformed to higher octane blending stock. The kerosene and light gas-oil fractions, referred to collectively as middle distillates, are used in the production of kerosene, jet fuel, diesel fuel, and furnace oils. The heavy gas-oil fraction may be used in heavy diesel fuel, industrial fuel oil, and bunker oil.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V11 660 (1980)]**PEER REVIEWED**

... Gasolines are blended from several petroleum refinery process streams that are derived by the following methods: direct distillation of crude oil, catalytic and thermal cracking, hydrocracking, catalytic reforming, alkylation, and polymerization. ... After the various gasoline streams have been blended, foul-smelling, corrosive, sulfur compounds are removed by hydrogenation. Additives and blending agents are added to improve the performance and stability of gasoline. These compounds include anti-knock agents, anti-oxidants, metal deactivators, lead scavengers, anti-rust agents, anti-icing agents, upper-cylinder lubricants, detergents, and dyes. At the end of the refining process, finished gasoline typically contains more than 150 separate compounds although as many as 1,000 compounds have been identified in some blends /Conventional gasoline/
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.113 (1995) ]**PEER REVIEWED**

Gasoline ... has been produced from /petroleum/, shale oil, Athabasca tar sands, and by hydrogenation or gasification of coal.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.114 (1995) ]**PEER REVIEWED**

General Manufacturing Information:

Gasoline is a complex combination of hydrocarbons consisting primarily of paraffins, cycloparaffins, aromatic and olefinic hydrocarbons having carbon numbers predominantly greater than C3 and boiling in the range of 30 degree C to 260 degree C. To achieve acceptable physical and combustion properties, gasoline is prepared by blending naphtha streams. The streams normally used are paraffinic streams, olefinic streams,naphthenic streams, and aromatic streams. Motor gasoline (CAS No. 8006-61-9) is considered a mixture; the product specifications of refinery blended motor gasoline (CAS No. 86290-81-5) sold in different areas of the country depend on applicable Federal and State regulations.
[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**

The American Petroleum Institute prepared a blend of naphtha streams considered typical of US gasoline in the middle 1970s. The blend was designated PS-6 gasoline. ... The proportions of the various naphtha streams used to prepare the PS-6 gasoline blend were: paraffiic naphtha streams 22.0 % vol., olefinic naphtha streams 52.1% vol., aromatic naphtha streams 21.3% vol., benzene 0.8% vol., and n-butane 3.8% vol. /from table/
[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**

.... The composition of gasoline varies as a function of the crude oil, the refinery process, the gasoline blending makeup for different grades, the grade of the gasoline, the climate of the marketing region, and the brand.
[National Research Council. Drinking Water & Health, Volume 4. Washington, DC: National Academy Press, 1981., p. 248]**PEER REVIEWED**

It consists predominantly of saturated aliphatic hydrocarbons having carbon numbers predominantly in the range of C4 through C8 and boiling in the range of approximately minus 20 deg C to 120 deg C (-4 deg F to 248 deg F).
[USEPA; Toxic Substances Control Act Chemical Substances Inventory, Volume 1 TSCA Inventory: 1985 ed, p.3A ]**PEER REVIEWED**

... Foul smelling, corrosive sulfur compounds in gasoline can either be removed or be converted to less objectionable forms, removal being preferred. ... Sulfur removal usually is accomplished by hydrogen treating, wherein hydrogen reacts with the sulfur in objectionable compounds, forming easily removable hydrogen sulfide. Hydrogen treating is conducted at moderate temperatures, 250-450 deg C, and pressures, 2.0-5.5 MPa (300-800 psi), using oxides of cobalt and molybdenum as catalyst. The range of operating conditions is wide, because the purposes vary from mild treatment of reformer feedstock to severe hydrogenation of heavy fractions.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V11 664 (1980)]**PEER REVIEWED**

In 1989, the 10 US companies leading gasoline sales were the following (in descending order of sales): Shell, Amoco, Exxon, Mobil, Chevron, Texaco, Unocal, BP Ameriica, Sun, and Phillips.
[ATSDR; Toxicological Profile for Automotive Gasoline. June 1995. Washington, DC: Agency for Toxic Substances and Disease Registry. Available at http://atsdr1.atsdr.cdc.gov/toxprofiles/tp72.html as of Oct 21, 2004. ]**PEER REVIEWED**

Formulations/Preparations:

To help lubricate cylinders and top piston rings, to prevent valve and ring sticking, and to reduce intake-system deposits, refiners often include small amounts of a light lubricant in their gasolines.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V11 669 (1980)]**PEER REVIEWED**

Because copper accelerates gum formation by acting as a catalyst in gasoline oxidation, metal deactivators (the Schiff's base, N,N'-disalicylidene-1,2-diaminopropane) are often added along with an antioxidant. Trace amounts of copper, picked up from piping or engine fuel systems, so powerfully promote oxidation that even the most effective antioxidant might not be able to provide adequate fuel stability without the help of a metal deactivator. The tiny amount of chelating agent added for this purpose functions by tying up trace copper in stable compounds that have no catalytic effect on oxidation.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V11 668 (1980)]**PEER REVIEWED**

Many refiners now use a multipurpose additive that combines detergent, deicing, and anticorrosion properties in a single formulation. Most of the action of such an additive comes from its surface-active ingredients, typically amino hydroxy amides. However, isopropyl alcohol, which is also included, contributes to anti-icing effectiveness.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V11 669 (1980)]**PEER REVIEWED**

To prevent formulation of /contaminants/ and to remove them from dirty carburetors, many refiners include a detergent additive in their gasolines. The effectiveness of these detergents, which include amides and alkylammonium dialkyl phosphates, stems from their surface-active properties.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V11 669 (1980)]**PEER REVIEWED**

Hydrocarbon-soluble organic dyes have long been added to gasolines to indicate the presence of antiknock compound, to increase sales appeal, and to identify various brands or grades of gasoline.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V11 669 (1980)]**PEER REVIEWED**

... The two common grades of ... gasoline, premium and regular, differ in their anti-knock quality. Better anti-knock quality is indicated by a higher octane number /Conventional gasoline/
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.114 (1995) ]**PEER REVIEWED**

U. S. Production:

The U.S. production volume of motor gasoline has steadily increased between 1983 and 1989 from 277.2 million gallons/day to 306.6 million gallons/day.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.115 (1995) ]**PEER REVIEWED**

(2003) 2,997.3 million barrels (Data include straight-run and cracked gasoline (including aviation gasoline) and natural gas liquids blended to produce motor fuel.)
[MP Malveda; CEH Prouct Review: Crude Petroleum and Petroleum Products 2004. Available on CD-Rom from SRI Consulting, Menlo Park, CA. ]**PEER REVIEWED**

U. S. Imports:

Between 1988 and 1989, net U.S. imports of gasoline declined by 14% to an average of 13.0 million gallons/day. By 1990, imports were up to an average of 14.3 million gallons/day. Typically net U.S. imports of gasoline account for 4-5% of demand.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.115 (1995) ]**PEER REVIEWED**

U. S. Exports:

Between 1988 and 1989, U.S. exports of finished motor gasoline increased from 924,000 gallons/day to 1.6 million gallons/day. Exports reached the highest point ever in 1989 at 2.4 million gallons/day.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.115 (1995) ]**PEER REVIEWED**

Laboratory Methods:

Clinical Laboratory Methods:

Method: GC/MS; Analyte: gasoline; Matrix: blood (aromatic and aliphatic hydrocarbons); Detection Level: 0.01 ug.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.143 (1995) ]**PEER REVIEWED**

Method: High Resolution GC/Atomic Absorption Spectrometry; Analyte: gasoline; Matrix: blood (tetramethyl lead); Detection Level: 10-100 ppb.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.143 (1995) ]**PEER REVIEWED**

Method: GC/Flame Ionization Detection; Analyte: gasoline; Matrix: urine (benzene metabolites); Detection Level: 1 mg/l.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.144 (1995) ]**PEER REVIEWED**

Method: HPLC/UV; Analyte: gasoline; Matrix: urine (toluene metabolite); Detection Level: 30 mg/l.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.144 (1995) ]**PEER REVIEWED**

Method: Anodic Stripping Voltammetry; Analyte: gasoline; Matrix: urine (lead); Detection Level: 4 ug/l.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.144 (1995) ]**PEER REVIEWED**

Method: High Resolution GC/Flame Ionization Detector; Analyte: gasoline; Matrix: tissues (blood, brain, and lung); Detection Level: nor reported
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.145 (1995) ]**PEER REVIEWED**

Analytic Laboratory Methods:

... Gasoline is composed of a complex mixture of hydrocarbons, there are few methods for the environmental analysis of gasoline as an entity, but many methods are reported for the analysis of its component hydrocarbons. These methods are used to identify or fingerprint the origin of a specific gasoline sample on the basis of the proportion of its component hydrocarbons.
[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 175 (1989)]**PEER REVIEWED**

Method: GC/Flame Ionization Detection; Analyte: gasoline; Matrix: air; Detection Level: 0.03 mg/cu m total hydrocarbon.
[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 176 (1989)]**PEER REVIEWED**

Method: GC/FID; Analyte: gasoline; Matrix: air (benzene, ethylbenzene); Detection Level: 10-100 ppb.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.148 (1995) ]**PEER REVIEWED**

Method: GC/Photoioniztion-Ion Mobility Spectrometry; Analyte: gasoline; Matrix: soil (volatile aromatics); Detection Level: 0.18 mg/kg.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.150 (1995) ]**PEER REVIEWED**

Method: GC/FID; Analyte: gasoline; Matrix: air (toluene); Detection Level: 0.01 mg.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.148 (1995) ]**PEER REVIEWED**

Method: GC/Photoionization Detection; Analyte: gasoline; Matrix: air (benzene); Detection Level: 50 ppb.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.148 (1995) ]**PEER REVIEWED**

Method: High Resolution GC/Flame Ionization Detector; High Resolution GC/MS; Analyte: gasoline; Matrix: air (benzene); Detection Level: not reported.
[DHHS/ATSDR; Toxicological Profile for Automotive Gasoline p.148 (1995) ]**PEER REVIEWED**

Method: OSHA PV2028, Gas Chromatography using Flame Ionization Detector; Analyte: gasoline; Matrix: air; Detection Level: 9.0 ug/injection.
[U.S. Department of Labor/Occupational Safety and Health Administration's Index of Sampling and Analytical Methods. Available from: http://www.osha.gov/dts/sltc/methods/toc.html on Gasoline (8006-61-9) as of November 10, 2003 ]**PEER REVIEWED**

Determination of gasoline hydrocarbons in industrial air by two stage (chromosorb/charcoal) adsorption, thermal desorption and capillary gas chromatography.
[Brown RH; IARC Sci Publ 85 (Environ Carcinogen): Methods Anal Exposure Meas 10 243-51 (1988)]**PEER REVIEWED**

Extraction of gasoline constituents from soil by using a sonication/extraction method. Recovery of unleaded gasoline from a dry, spiked soil was 43.2% when expressed on a total petroleum hydrocarbon basis and recovery from a wet, spiked soil was 21.8%.
[Donaldson SG et al; J Assoc Off Anal Chem 73 (2): 306-11 (1990)]**PEER REVIEWED**

Analysis of gasoline hydrocarbons in relation to industrial airby using a monitoring method giving detailed composition.
[Coker DT et al; Ann Occup Hyg 33 (1): 15-26 (1989)]**PEER REVIEWED**

Special References:

Special Reports:

WHO; Environmental Health Criteria 119: Principles and Methods for the Assessment of Nephrotoxicity Associated with Exposure to Chemicals (1991)

USEPA; Evaluation of the Carcinogenicity of Unleaded Gasoline (1987) EPA 600/6-87-001. A comprehensive review of the carcinogenicity of unleaded gasoline vapors to humans. All recent relevant animal and epidemiological studies of unleaded gasoline exposure were evaluated.

U.S. Dept Health & Human Services/Agency for Toxic Substances Disease Registry; Toxicological Profile for Automotive Gasoline (1995) NTIS # PB/95/264206/AS

Synonyms and Identifiers:

Related HSDB Records:

903 [CARBON MONOXIDE] (By-product (Combustion))

230 [ACETALDEHYDE] (Hazardous Component)

164 [FORMALDEHYDE] (Hazardous Component)

181 [1,3-BUTADIENE] (Hazardous Component)

121 [TOLUENE] (Hazardous Component)

84 [ETHYLBENZENE] (Hazardous Component)

5293 [1,2,4-TRIMETHYLBENZENE] (Hazardous Component)

60 [CYCLOHEXANE] (Hazardous Component)

35 [BENZENE] (Hazardous Component)

91 [n-HEXANE] (Hazardous Component)

4500 [XYLENE] (Hazardous Component)

184 [NAPHTHALENE] (Hazardous Component)

5847 [METHYL T-BUTYL ETHER] (Mixture Component)

Synonyms:

Antiknock gasoline
**PEER REVIEWED**

Benzin (German)
**PEER REVIEWED**

Casing head gasoline
**PEER REVIEWED**

Cracked gasoline
**PEER REVIEWED**

Lead-free gasoline
**PEER REVIEWED**

Natural gasoline
**PEER REVIEWED**

Petrol (British)
**PEER REVIEWED**

Polymer gasoline
**PEER REVIEWED**

Pyrolysis gasoline
**PEER REVIEWED**

Straight-run gasoline
**PEER REVIEWED**

White gasoline
**PEER REVIEWED**

Associated Chemicals:

API PS-6; 86290-81-5
Refinery-blended motor gasoline; 86290-81-5
Conventional gasoline; 86290-81-5

Formulations/Preparations:

Shipping Name/ Number DOT/UN/NA/IMO:

UN 1203; Gasoline

IMO 3.1; Gasoline

For more specific material safety information for automotive Gasoline, please consult the Automotive Gasoline MSDS Information above.

Top of Page

Return to Home Page of Home Air Purifier Expert from Automotive Gasoline MSDS

Best Indoor Air Quality Test Kit for Gasoline Compound Testing

Learn more about leukemia causing Benzene found in many fuels such as gas

Share this page:

What’s this?

Enjoy this page? Please pay it forward. Here's how...

Would you prefer to share this page with others by linking to it?

Click on the HTML link code below.
Copy and paste it, adding a note of your own, into your blog, a Web page, forums, a blog comment, your Facebook account, or anywhere that someone would find this page valuable.

Air Purifier Advice

Test Your Air

Source Control

Hazardous Products

Toxic Compounds

Respiratory Health

New Updates

About

Automobile Gasoline MSDS (Material Safety Data Sheet), Testing, Air Purification, and Public Health Information

The Best Chemical Air Purifier for Gasoline Fume Removal, Odor Control, and Particle Filtration:
IQAir GC Multigas Air Purifier

IQAir GC Multigas Air Purifier: Powerfully Efficient Air Cleaning of Solids and Gases

Public Health Statement for Automobile Gasoline

SUMMARY:

What is automotive gasoline?

What happens to automotive gasoline when it enters the environment?

How might I be exposed to automotive gasoline?

How can automotive gasoline affect my health?

Diseases associated with exposure to Automotive Gasoline:

How likely is automotive gasoline to cause cancer?

Is there a medical test to show whether I've been exposed to automotive gasoline?

Has the federal government made recommendations to protecthuman health against Automotive Gasoline exposure?

Glossary of Terms

Automotive Gasoline References

Where can I get more information about Automotive Gasoline?

Automotive Gasoline MSDS Information

Gasoline Toxicological Information

Air Purifier Advice

Test Your Air

Source Control

Hazardous Products

Toxic Compounds

Respiratory Health

New Updates

About

Automobile Gasoline MSDS (Material Safety Data Sheet), Testing, Air Purification, and Public Health Information

The Best Chemical Air Purifier for Gasoline Fume Removal, Odor Control, and Particle Filtration: IQAir GC Multigas Air Purifier

IQAir GC Multigas Air Purifier: Powerfully Efficient Air Cleaning of Solids and Gases

Public Health Statement for Automobile Gasoline

Diseases associated with exposure to Automotive Gasoline:

Automotive Gasoline MSDS Information

Gasoline Toxicological Information

The Best Chemical Air Purifier for Gasoline Fume Removal, Odor Control, and Particle Filtration:
IQAir GC Multigas Air Purifier