Toxic Chemicals ....(news and articles)

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Frying pan fumes 'kill canaries'

Thursday, 29 January, 2004
By Alex Kirby
BBC News Online environment correspondent

Fumes given off by cancer-causing chemicals used to make non-stick frying pans are killing hundreds of pet birds every year, environmentalists say.

http://newsimg.bbc.co.uk/media/images/39797000/jpg/_39797757_budgie1_bbc_203.jpg
New chemicals "threaten" caged birds, WWF says

The Worldwide Fund for Nature says it is hearing reports that many US caged birds are being killed by the fumes.

It says the chemicals, perfluorinated compounds, are also contaminating both people and wildlife with grave effects.

The chemicals industry says it doubts that birds exposed to ordinary levels of the compounds could die from them.

Guilty till proved harmless

In a report, Causes For Concern: Chemicals and Wildlife, WWF says the compounds, also used in some textiles and food packaging, are among "the most prominent new toxic hazards".

It says: "Scientists have found perfluorinated compounds, classified as cancer-causing chemicals by the US Environmental Protection Agency, in dolphins, whales and cormorants in the Mediterranean; seals and sea eagles in the Baltic; and polar bears."

Elizabeth Salter-Green, head of WWF's toxics programme, said: "Years ago, coal miners took canaries with them down the pits to detect lethal gases.

"Now, canaries are dying in our kitchens, but no action is being taken about the suspect chemicals.

"The global production of chemicals is increasing, and at the same time we have warning signals that a variety of troubling threats to wildlife and human health are becoming more prevalent.

"It is reckless to suggest there is no link between the two and give chemicals the benefit of the doubt."

WWF says while the harmful effects of chemicals like DDT and polychlorinated biphenyls have been documented, recent studies of other chemicals on sale today show the dangers to people and wildlife.

It says: "As well as perfluorinated compounds other harmful man-made chemicals still in use today include phthalates, phenolic compounds - such as bisphenol A - and brominated flame retardants (BFRs).

"Phthalates can be found in plastics (including PVC), phenolic compounds in food cans, plastic bottles and computer casings, and BFRs in fabrics and TVs.

Brussels' approach defended

"These toxic compounds, which contaminate a wide range of animals, can cause severe health disorders such as cancer, damage to the immune system, behavioural problems, hormone disruption, or even feminisation."

WWF says the European Union's planned legislation, Reach (Registration, Evaluation, Authorisation and Restriction of Chemicals) does not go far enough.

It says Reach "falls short of ensuring that hazardous chemicals are replaced with safer alternatives".

Judith Hackitt, director-general of the UK's Chemical Industries Association, told BBC News Online: "It sounds highly unlikely to me that birds exposed to perfluorinated compounds in normal household conditions would be killed.

"With them and the other chemicals WWF is concerned about, the industry is spending a lot on investigating them.

"And with Reach, it's a big assumption to say replacement won't happen - I think it will."

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NTN produces Chemical Information sheets and distributes related community information as HTML documents. Click on the Chemical Names to see the Material Safety Data Sheet (MSDS).

BENZENE

RECORD NUMBER: 203-170491
CAS REGISTRY NUMBER: 71-43-2

CHEMICAL FAMILY: Aromatic hydrocarbon

MOLECULAR FORMULA: C6-H6


DESCRIPTION: Clear, colourless liquid with an aromatic odour.

Agricultural - Solvent for pesticides

Industrial - Predominantly industrial Solvent

Domestic -



USAGE: Used in the manufacture of medicinal chemicals, dyes, plastics, textiles, detergents, artificial leather, varnishes, paints, lacquers, waxes and many other materials. Solvent for inks, paints, rubber, adhesives, coatings, detergent and pesticides. Benzene is found in coal tar distillates, petroleum naphtha and gasoline.

TOLERANCE & EXPOSURE LEVELS: Odour Threshold 5 ppm (Canada)

ROUTES OF EXPOSURE: The primary routes of exposure are inhalation of contaminated air (areas of high traffic, filling stations, industry, cigarette smoke) and consumption of contaminated drinking water (leaking underground petrol tanks). Benzene is detected in various foods. (5)

HEALTH EFFECTS:

SHORT-TERM: Benzene is a fat solvent that causes CNS dysfunction and the destruction of other tissues.(2) Short term exposure can cause drowsiness, dizziness, headache, lightheadedness, nausea, and decreased coordination. Benzene vapour can cause mild irritation of the respiratory tract. Absorbed slightly through the skin. (1) Other acute effects include anorexia, bone marrow depression, eye irritation, hallucinations and muscle twitching. (2)

LONG-TERM: Benzene can impair the formation of red and white blood cells and platelets. Prolonged low level exposure can damage the nervous system and may also cause lesions resembling first or second degree burns. (1) Other chronic effects are cardiac sensitisation, CNS injury, hepatic damage, internal hemorrhage, disturbed iron metabolism, spleno-adrenomegaly and myocardial changes.(2)

CARCINOGENICITY: Can cause cancers of the white blood cells (leukemias). Carcinogen A2 (1) IARC Classification: Group 1

MUTAGENICITY: Benzene can cause chromosomal aberrations in heavily- exposed workers. (1)

REPRODUCTIVE EFFECTS: Benzene can cross the placental barrier and can be present in the fetal blood. It can also cause menstrual disorders. (1)

BIO-ACCUMULATION: Benzene can be stored temporarily in fat. Elimination may take more than five days after exposure has stopped.(1) Detected in 8 samples of mothers milk in U.S urban areas. Using whole blood, 250 subjects ranged from not detected to 5.9ppb, 0.8ppb average. In U.S. National Human Adipose Tissue Survey, 46 specimens had 96% had >4ppb with a maximum of 97ppb.(5) Detected in breath of person without specific exposure at 8-20ppb. (5) Detected in blood samples from children on the North Coast,NSW. (3)
Suspected Effects:Bronchiogenic carcinoma, Hodgkins disease, lymphosarcoma malignant lymphoma, multiple myeloma, mutagenisis, myeloid metaplasia, myocardial sensitisation to epinephrine, paroxysmal nocturnal hemoglobinuria, prenatal damage, postnatal damage and reproductive system damage.(2)


ANIMAL TOXICITY DATA: LD50 (oral, rat): 4894 mg/kg LD50 (oral, rat): 5.6 g/kg LC50 (rat): 16000 ppm/4 hr LC50 (rat): 10000 ppm/7 hr Rats exposed to 20ppm, 8hours per day, 5 days per week for 90 days developed a severe decrease in the number of white blood cells. (1)

REPRODUCTIVE EFFECTS: May cause reduced fetal weight and growth. There is some indication of fetotoxicity with doses which are not necessarily toxic to the dam. (1)

MUTAGENICITY: Wildlife Data: Benzene is not expected to bioconcentrate in aquatic organisms. (5)

ENVIRONMENTAL EFFECTS: Environmental Fate: When released into the atmosphere, gas phase benzene will react with photochemically produced hydroxyl radicals and have a half life of 13.4 days. In polluted atmospheres reaction time is accelerated and half life is 4-6 hours. Products of photooxidation include phenols, nitrophenols, nitrobenzenes, formic acid and peroxyacetyl nitrate. (5) U.S. atmospheric concentrations:Rural: 1.4ppb avg. ('77-80,100sample) Urban: 2.8ppb avg. ('77-80,2292sample) Benzene is fairly soluble in water and is removed from air by rain. In a marine environment, half lives varied from 3.1 days in summer to 23 days in spring. Little degradation occurring in winter. (5) When spilt on soil benzene will rapidly volatilise near the surface. What isn't evaporated will be highly to very highly mobile in soil and will leach to groundwater. (5)

EPA DATA GAPS:


NOTES: Restricted usage in 6 countries. (4)

** Disclaimer: These sheets are designed as summary information and as such are a guide only. The information is compiled from publicly available references which can be supplied on request.

References:

1.Canadian Centre of Occupational Health Database - CCINFO

2.Pesticides and Human Health, W.H.Hallenbeck&K.M.Cunningham-Burns School of Public Health, Uni. of Illinois Chicago, Springer-Verlag

3.Coffs Harbour Chemical Data Base 1991

4.Consolidated List of Products whose Consumption &/or Sale have been Banned, Withdrawn, Severely restricted or not approved by Governments.

5.Handbook of Environmental Fate and Exposure Data for Organic Chemicals, Vol1 Large Production and Priority Pollutants., Philip H. Howard 1989 Lewis Publishers Inc. USA

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CHLORPYRIFOS

Chemical Name : 0,0-diethyl O-(3,5,6-trichloro-2-pyridyl) phosphorothioate

Category: Organophosphate

Physical Properties:

CAS Number: 2921-88-2
Description: Technical chlorpyrifos is an amber to white crystalline solid with a mild sulfur odor
Molecular formula: C9H11Cl3N03PS
Molecular weight: 350.62
Melting point/Boiling point: 41.5-44 C
Solubility: water: 2 mg/L @ 25 C; Soluble in organic solvents.
Vapour Pressure: 2.5 mPa @ 25 C [13]

Usage:

Chlorpyrifos is a broad spectrum insecticide used on wide variety of crop types, for the control of locusts and is present in some cattle dips for the control of ticks and lice.

Chlorpyrifos is also used in domestic gardens; as indoor insect control, as a termiticide, and for pet products.

Regulatory Standards:

AUSTRALIAN GUIDELINES
TWA: 0.2 mg/m3
STEL: no guideline

OVERSEAS GUIDELINES
0.2 mg/m3 OSHA TWA (skin)
0.2 mg/m3 ACGIH TWA (skin) (9)

The US EPA has established a 24-hour reentry interval for crop areas treated with emulsifiable concentrate or wettable powder formulations of chlorpyrifos unless workers wear protective clothing.(13)

HEALTH EFFECTS:

Acute Toxicity

Chlorpyrifos is very toxic to humans, between 1 teaspoon and 1 ounce may be fatal. (6) Chlorpyrifos toxicity is considerably greater if administered orally compared to dermal exposure. (8) Primary routes of exposure are inhalation, skin or eye contact. Inhalation exposure to high concentration may cause upper respiratory irritation, central nervous system depression, headache, dizziness, increased sensitivity to epinephrine, irregular heartbeats, incoordination, muscle twitching, tremor, pinpoint pupils, blurred vision, tightness in chest, and convulsions. Eye contact may cause pain, moderate irritation.(6)

Poisoning may impair Central Nervous System. (2)



Chronic Toxicity

Continual absorption at intermediate dosage may cause an influenza-like illness which includes symptoms like weakness, anorexia and malaise.(2, 13) Other chronic exposure effects may include behavioural neurotoxicity and organo-phosphate induced delayed neuropathy. (8)

Repeated or prolonged exposure to organophosphates may result in the same effects as acute exposure. Other effects reported in workers repeatedly exposed include impaired memory and concentration, disorientation, severe depressions, irritability, confusion, headache, speech difficulties, delayed reaction times, nightmares, sleepwalking and drowsiness or insomnia. An influenza-like condition with headache, nausea, weakness, loss of appetite and malaise has also been reported (13).

Carcinogenicity

Chlorpyrifos is not considered to be a carcinogen by the National Toxicology Program, the International Agency for Research on Cancer, or the Occupational Safety and Health Administration. (1)

Mutagenicity

US EPA classifies chlorpyrifos as not mutagenic, though mutagenic effects were observed in fruit flies given oral concentrations of 50 parts per billion of chlorpyrifos for 3 days (13).

Chlorpyrifos was also mutagenic in microbial inhibition assays.(5)

Teratogenicity and Reproductive effects

US EPA has determined that chlorpyrifos is not teratogenic. (2)

In one experiment developmental NOEL was 10mg/kg/day (13).

An experimental teratogen (7)



US EPA has determined that chlorpyrifos does not adversely affect reproduction. In two studies reviewed by the US EPA, no effects were seen in the animals tested at dose levels up to 1.2 mg/kg/day (13).

Fate in Humans

Animal studies suggest that Chlorpyrifos is rapidly absorbed and metabolised to 3,5,6-trichloro-2-pyridinal (TCP) with the parent compound and metabolite being excreted in the urine. (2)

Yet, the metabolite 3,5,6-trichloro-2-pyridinol was detected in urine of 5.8% of 6990 samples from general population (1976-80) with a mean in urine of pest controllers in Texas of 5.6-8.3 ug/l.(10)

More recent sampling from the US Environment Protection Agency Preliminary Risk Assessment October 1999, reports “measurable concentrations of the primary metabolite, 3,5,6-trichloro-2-pyridinal (TCP) in the urine of 92% of adults and 89% of children tested. (14)

ACTION ON ANIMALS
Chlorpyrifos is very highly toxic to freshwater fish, aquatic invertebrates and estuarine and marine organisms and moderately to very highly toxic to birds. (2)

Aquatic and general agricultural uses of chlorpyrifos pose a serious hazard to wildlife and honeybees. (10)

Chlorpyrifos was detected in 1990 sampling of three eggs of Little Terns (0.06-0.36ppm), one liver sample from Little Terns (0.02ppm) and one Pelican egg (0.5ppm) from the Wallace Lake Colony, central coast of NSW. (12)

When applied to freshwater ponds, cladocerans and copepods were killed and a 42% mortality rate in Mallard ducklings. (8)

Chlorpyrifos residues have been detected in the kidney and fat from cattle dipped once in a 0.025% emulsion. Fats of Australian cattle contained the breakdown product, 0,0-diethyl 0-(3,6-dichloro-2-pyridyl) phosphothioate after being treated with chlorpyrifos for cattle tick.(8)

Animal Toxicity Data

Acute Oral 163mg/kg Toxicity Category 11

Acute Dermal 1505mg/kg Toxicity Category 11

Avian Oral 76mg/kg

Freshwater fish : Rainbow Trout 3ppm



Two studies carcinogenicity studies were submitted were to USA EPA, neither suggest

carcinogenicity. (2)

EPA evaluated 3 reproductive health studies and determined that Chlorpyrifos is not teratogenic at levels up to 25mg/kg. Chlorpyrifos does not produce reproductive effects at dose levels up to 1.2mg/kg/day. (2)

Two assays in bacterial systems are weakly positive for DNA damage. (3)

Action on Plants
Chlorpyrifos may be toxic to some plants, such as head lettuce. Residues remain on plant surfaces for approximately 10-14 days. Data indicate that this insecticide and/or its soil metabolites can accumulate in certain crops (13).

FATE IN THE ENVIRONMENT
US EPA considers that there is insufficient data to fully assess the environmental fate of Chlorpyrifos. (2)

Chlorpyrifos is tightly adsorbed by soil and not expected to leach significantly. Volatilisation from soil surface will contribute to loss (10). Depending on soil type, microbial metabolism of Chlorpyrifos may have a half-life of up to 279 days.(2) Higher soil temperatures, lower organic content and lower acidity increases degradation of chlorpyrifos.

When applied to sandy soil, a 50% loss was noted after 2 weeks and when applied to high organic matter soil, a 50% loss was noted after 8 weeks. (8)

Chlorpyrifos inhibits nitrification and nitrogen fixation marginally, many bacterial strains were unable to degrade it but some micro-organisms can use chlorpyrifos as their only source of carbon and nitrogen.(8)

If released to water, chlorpyrifos partitions significantly from water column to sediments. Hydrolysis half-life at 25C in neutral conditions is 35-78 days. Photolysis half-life at water surface in mid-summer is approx. 3-4 weeks. The desorption from sediment can contribute to long term residual concentration in water column. (10)

If released to air will react in vapor phase with photochemically produced hydroxyl radicals with half life 6.34 hours. Detected in 14/123 ambient air samples collected at 10 U.S. locations (1980) with maximum concentration of 100ng/m3 and mean of 2.1ng/m3. (10)

Air in 16 houses treated for subterranean termites according to label instructions average 1.38-3.07 ug/m3 one year after treatment and 1.32-1.82 ug/m3, 2 years after treatment. These were above the air equivalent of Acceptable Daily Intake set by New York Department of Health: 1.0ug/m3 (adult) and 0.49 ug/m3 (child). (11)



* Disclaimer: These sheets are designed as summary information and as such

are a guide only.

References:

1. Canadian Centre of Occupational Health Database - CCINFO 1991.

2. EPA Pesticide Fact Sheet, Chlorpyrifos 1984

3. EPA Chlordane, Heptachlor Aldrin & Dieldrin 1987 Technical Support

Document.

4. Pesticides and Human Health, W.H.Hallenbeck&K.M.Cunningham-Burns School

of Public Health, University of Illinois Chicago, Springer-Verlag 1985

5. Contemporary Issues in Pesticide Toxicology & Pharmacology, Dr Judith

Marquis, Associate Professor of Pharmacology,Boston Uni. Karger 1986

6. Oil & Hazardous Materials - Technical Assistance Data System, US EPA

7. Irving Sax, N. & Lewis, R.J. “Dangerous Properties of Industrial Materials” Seventh Edition , Van Nostrand Reinhold 1989 N.Y. USA



8. Centre for Human Aspects of Science and Technology, Pub 1., Chlorpyrifos

9. Exposure Standards for Atmospheric Contaminants in the Occupational Environment

[NOHSC:3008(1995)] http://www.nohsc.gov.au/databases/exp/az/chlorpyrifos.htm

10. Handbook of Environmental Fate and Exposure Data for Organic Chemicals,

Ed. P.H.Howard Lewis Pub. Michigan 1991

11. Dr Mary O'Brien , Chlorpyrifos, Journal of Pesticide Reform, Vol8 No4 1989

12. NSW Department of Agriculture, Pesticide Analysis No. CP90/633-635

Re: Pelican Eggs, Little Tern - Wallace Lake Colony

13. E X T O X N E T, Extension Toxicology Network Pesticide Information Profiles

A Pesticide Information Project of Cooperative Extension Offices of Cornell University, Oregon State University, the University of Idaho, and the University of California at Davis and the Institute for Environmental Toxicology, Michigan State University. Major support and funding was provided by the USDA/Extension Service/National Agricultural Pesticide Impact Assessment Program available at

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Diazinon


Chemical Name:

O,O-diethyl 0-2-isopropyl-6-methyl(pyrimidine-4-yl) phosphorothioate
Category : Organophosphate

Physical Properties

CAS Number: 333-41-5

Description: Diazinon is a colorless to dark brown liquid. It has a flashpoint of 180 F

Molecular formula: C12H21N2O3PS

Molecular weight: 304.35

Melting point: decomposes >120 C

Solubility: water - 40 mg/L @ 20 C, Miscible in organic solvents

Vapour Pressure: 0.097 mPa @ 20 C

Usage :

Diazinon is a persistent, broad spectrum organophosphate insecticide used on a wide variety of crops and plants to control sucking and leaf eating insects. It is also used for the control of insects on stock (lice and ticks) particularly, fly strike on sheep.

In the home diazinon is often used as an ant killer and for the control of fleas and ticks on domestic pets.

Regulatory Status:

AUSTRALIAN GUIDELINES
TWA: 0.1 mg/m3

STEL: no guideline

OVERSEAS GUIDELINES
ACGIH TLV: TWA 0.1 mg/m3 (8)

In the United States, Diazinon is classified as a Restricted Use Pesticide (RUP) and is for professional pest control operator use only. In 1988, US EPA canceled registration of diazinon for use on golf courses and sod farms because of die offs of birds that often congregated in these areas.(10)

HEALTH EFFECTS:

Acute Toxicity

As an organophosphate, Diazinon inhibits the enzyme, acetylcholinesterase and causes depression of the Central Nervous System. It is easily absorbed through the skin. Ingestion or inhalation may cause headaches, giddiness, blurred vision, confusion, weakness, cramps, diarrhea, respiratory problems, sweating, vomiting, muscle twitches, convulsions, coma, renal or hepatic damage. (4) (5)

Fatal dose in man estimated to be 360mg/kg. (6)

Diazinon is classified as slightly toxic to moderately toxic depending on the formulation. Diazinon itself is not a potent cholinesterase inhibitor. However, in animals, it is converted to diazoxon, a compound that is a strong enzyme inhibitor. (10)

Chronic Toxicity

Chronic exposure may result in above symptoms plus frontal lobe impairment. (4)

No-effect doses have ranged from 0.02 mg/kg/day in humans to 0.1 mg/kg/day in rats. These values are based on inhibition of the enzyme acetylcholinesterase. Enzyme inhibition has been documented in red blood cells, in blood plasma, and in brain cells at varying doses and with different species (10).

Chronic effects have been observed at doses ranging from10 mg/kg/day for swine to 1,000 mg/kg/day for rats. These effects included only visibly recognisable symptoms of toxicity (gross toxicities). Certain effects such as the inhibition of red blood cell cholinesterase, and enzyme response occurred at much lower doses in the rats.(10)

Carcinogenicity:

Based on animal tests Diazinon does not appear to be carcinogenic.

Diazinon has not been evaluated by International Agency for Research on Cancer. (2)

Mutagenicity:

Chromosone aberrations were produced in human lymphocytes at a dose of 0.5mg/l (6)



Teratogenicity and Reproductive effects:

The data on reproductive and developmental effects due to chronic exposure is limited. (10)

An experimental teratogen and experimental reproductive effects (1)

Fate in humans :

The half-life of diazinon in animals is about 12 hours. The product is passed out of the body through urine and in the feces. The metabolites account for about 70% of the total amount excreted. (10)

ACTION ON ANIMALS

Diazinon has a high to very high freshwater fish acute toxicity.

Freshwater Fish Acute Toxicity Coldwater

LC50 90ug/l (Rainbow Trout) (2)

There is some evidence that saltwater fish are more susceptible than freshwater fish.

Bioconcentration ratios range from 200 in minnows to 17.5 for guppies (10)

Diazinon is very highly toxic to birds. (2)

Avian acute toxicity 6.3mg/kg (Mallard Duck)

Avian dietary toxicity <47ppm (Mallard Duck)



Honey Bees Contact LD 50 0.22ug

The US EPA in 1988 concluded that the use of diazinon in turf and golf course treatment poses a "widespread and continuous hazard" to birds. (10)

Two mice studies indicate Diazinon is not carcinogenic.(2)

Rabbit and rat studies showed no developmental toxicity up to and including dose 100mg/kg. (2)

Tests with Rabbits and hamsters were negative for teratology but tests with chicks produced congenital malformations. (6)

Diazinon injected into chicken eggs resulted in skeletal and spinal deformities in the chicks. Bobwhite quail born from eggs treated in a similar manner showed skeletal deformities but no spinal abnormalities but Acetylcholine was significantly affected. (10)

Tests with dogs and pigs at higher levels (1.0 10.0 mg/kg/day) revealed gross abnormalities (10)

Cattle exposed to diazinon may store it in their fat for a short term. One study showed that the cows excreted the compound within 2 weeks after spraying stopped. (10)

ACTION ON PLANTS
In plants, a lower temperature and a high oil content tend to increase the persistence of diazinon. Generally the half-life is rapid in leafy vegetables, forage crops and grass, ranging from two days to 14 days. Diazinon is absorbed by plant roots when applied to the soil and translocated to other parts of the plant (10).

ENVIRONMENTAL FATE

Diazinon is persistent in the soil for approximately 12 weeks. The major soil degradate, oxypyrimidine is more persistent than the original compound. (2) Diazinon is not expected to bind to soil and but exhibit moderate mobility. Biodegradation is major fate process with half life of <1 - 5 weeks in non sterile soils and half lives of 6 - 12.5 weeks in sterile soils. (9)

Diazinon seldom migrates below the top 1.3 centimetres in soil but can stay biologically available for six months under conditions of low temperature and low moisture. The average time for 50% degradation in soil is two to four weeks. (10)

The breakdown rate is dependent on the acidity of water. At highly acidic levels, one half of the

compound disappeared within 12 hours while in a neutral solution, the pesticide took six months to degrade to one half of the original concentration (10).

When released to water, diazinon may sorb to sediments moderately but should not significantly bioconcentrate in aquatic organisms. Reported half lives in water (20C): 31 days- pH 5, 185 days- pH 7.4, 136 days- pH 9. Volatilisation from water can be important transport process. In sampling of US surface and ground water Diazinon was detected in 6,026 of 22,291 surface water samples from 3,555 locations with a maximum concentration of 33,400ug/l. It was also detected in 74 of the 3,633 ground water samples taken in 2,835 locations. The maximum concentration in ground water was 84ug/l. (3)

When released to atmosphere, it is expected to survive in vapour phase (expected half-life: 4.1 hours) and particulate phase. Detected in 61% of 787 ambient air samples from 14 states in 1970 US National Monitoring Programs, max concentration was 62.2 ng/m3, average: 3.0 ng/m3. (9)

FURTHER INFORMATION

US EPA identified 5 major data gaps including toxicology, environmental fate and effects, and residue chemistry. (2)

International Organisation of Consumers Union (IOCU) warns of the possibility of the highly toxic contaminant Sulfotepp in old stock, particularly opened containers.IOCU recommends the removal of children and animals from area for 4

hours after spraying. (7)

* Disclaimer: These sheets are designed as summary information and as such

are a guide only.

References:

1.Irving Sax, N. & Lewis, R.J. “Dangerous Properties of Industrial Materials” Seventh Edition , Van Nostrand Reinhold 1989 N.Y. USA

2.EPA Pesticide Fact Sheet, Diazinon 1988

3.EPA Health Advisory, Office of Drinking Water US EPA Aug 1988

4.Pesticides and Human Health, W.H.Hallenbeck&K.M.Cunningham-Burns School

of Public Health, University of Illinois Chicago, Springer-Verlag

5.Chemical Hazard Response Information System, US Dept. of Transportation.

6.Oil & Hazardous Materials - Technical Assistance Data System, US EPA

7.The Pesticide Handbook, Profiles for Action. International Organisation

of Consumers Union, 1986

8. Exposure Standards for Atmospheric Contaminants in the Occupational Environment

[NOHSC:3008(1995)] http://www.nohsc.gov.au/databases/exp/az/Diazinon.htm

9.Handbook of Environmental Fate and Exposure Data for Organic Chemicals,

Ed. P.H.Howard Lewis Pub. Michigan 1991

10. E X T O X N E T, Extension Toxicology Network Pesticide Information Profiles

A Pesticide Information Project of Cooperative Extension Offices of Cornell University, Oregon State University, the University of Idaho, and the University of California at Davis and the Institute for Environmental Toxicology, Michigan State University. Major support and funding was provided by the USDA/Extension Service/National Agricultural Pesticide Impact Assessment Program available at http://ace.orst.edu/cgi-bin/mfs/01/pips/

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Endosulphan

RECORD NUMBER: 19-010991

CHEMICAL NAME: ENDOSULFAN

(6,7,9,10,10-hexachloro-1,5,5a,6,9,9a-hexahydro-6,9-methano-2,4,3-benzodioxathiepin-3-oxide).

CAS REGISTRY NUMBER: 0115-29-7

CHEMICAL FAMILY: Organo-chlorine

MOLECULAR FORMULAE: C9 H6 Cl6 O3 S

DESCRIPTION: Colourless crystals. Technical endosulfan is composed of alpha and beta endosulfan.

USAGE: A Schedule 6 (PESKEM) non-systemic insecticide and acaricide with contact and stomach action registered for use on a wide variety of food and non-food crops including ornamentals.

Agricultural - insecticide

Industrial -

Domestic - insecticide

TOLERANCE & EXPOSURE LEVELS:

HEALTH EFFECTS:

SHORT TERM: Organo-chlorines interfere with the transmission of nerve impulses, disrupting the nervous system particularly,

Central Nervous System. They can induce changes in the liver enzymes and affect the synthesis of proteins and fats.(3) Workers have reported symptoms of malaise, vomiting, dizziness, weakness, confusion, dull headache, anorexia and abdominal discomfort. (5)

Other acute exposure effects to organo-chlorines include behavioural and EEG disturbances, cardiac arrhythmias, central nervous system stimulation and depression, dermatitis, diarrhea, visual disturbances, hepatic and renal injury, insomnia, mucous membrane irritation, respiratory difficulties and muscle twitching.(3)

LONG TERM: Chronic exposure to organo-chlorines may result in abdominal pain and anorexia, chest pain, visual disturbances, hepatic and renal degeneration, joint pain, insomnia, mental changes, hormonal disturbances, paralysis, peripheral neuropathy, splenomegaly, tremor and weakness. (3)

CARCINOGENICITY:

MUTAGENICITY: Some experimental mutagenicity has been observed at high doses of endosulfan. (1) Endosulfan was mutagenic in bacterial and bone marrow tests. (5)

REPRODUCTIVE EFFECTS:

BIO-ACCUMULATION: When administered to rats orally, endosulfan is metabolised to alpha-hydroxyendosulfan and endosulfandiol, which are then excreted in the urine. (2)

Suspected Effects: Endosulfan is suspected of being a carcinogen, teratogen and causing embryotoxicity. (7)

ANIMAL TOXICITY DATA:

** The Lethal Dose 50 varies considerable according to the source.

Acute Oral (rat) LD50: 18mg/kg

Acute dermal(rat)LD50: 74mg/kg (7)

Acute Oral (rat) LD50: 70mg/kg (aqueous solution)

110mg/kg (in oil)

Acute Oral (dog) LD50: 77mg/kg

Acute dermal (rabbit) LD50:359mg/kg (in oil)

Acute Inhalation (rat)LC50:>21mg/litre (1hr) (2)

In 2 year feeding trials, rats and dogs recieving 30 mg/kg diet showed no ill effects. (2) Test animals fed high dosages showed evidence of liver changes,(6) and changes in blood and kidneys. (5)

CARCINOGENICITY:

MUTAGENICITY: Some experimental mutagenicity has been observed at high doses of endosulfan. (1) Endosulfan was mutagenic in bacterial and bone marrow tests. (5)

REPRODUCTIVE EFFECTS: Some reproductive effects observed in experimental animals at levels of endosulfan around the LD50 dose. (1)

Wildlife Data: Acute Avian Oral Toxicity LD50: 205-245mg/kg

Toxicity to fish (96hrs) LC50: 0.002mg/l. (2)

(96 hr) LC 50: 2.0-4.6 ug/l (mosquito fish) (8)

Residues in fish were dependent on concentration and duration of exposure. Toxicity to mosquito fish of endosulfan increased with temperature. (8) Endosulfan is toxic to aquatic organisms at low concentrations and short durations. Fish accumulate endosulfan directly from surrounding water, with the liver the main site of detoxification and having the highest residues. Results from sampling wild catfish Gwydir River NSW, showed a significant increase in endosulfan residues and its metabolites, endosulfan sulfate and isomers, in fish livers during Summer with a total range of 147.7 - 307.2 ug/kg. (9)

Detected in salmon eggs from females returning from Lake Michigan at concentrations 0.6-27.8 ug/kg. (10)

ENVIRONMENTAL EFFECTS:

Environmental Fate: In plants endosulfan is metabolised to the corresponding sulphate. (2) Release of endosulfan isomers to soil will probably result in biodegradation and hydrolysis, particularly in alkaline conditions.

Isomers may also photolyze. Volatilisation and leaching will not be significant. (10)

When released to water endosulfan isomers should hydrolyse readily in alkaline conditions and more slowly in neutral and acidic pH conditions; alpha halflife: 35.4 [pH7] - 150.6 days [pH5.5] beta halflife: 37.5 [pH7] - 187.3 days [pH5.5]

Volatilisation and biodegradation expected to be significant.

Bioconcentration is expected to be significant. Endosulfan isomers regularly detected in groundwater, surface water, sediment and rain and snow samples.(10)

When released to air, endosulfan will react with hydroxyl radicals with est. half life of 1.23 hours. Adsorption to atmospheric particulate matter will increase half life. Detected in 2.11% of ambient air samples from 14 U.S. States (1970). (10)

The manufacturer includes these warnings for the formulated product

THIODAN 50 W P (Thiodan (R)) [47% Endosulfan] :Toxic to fish. Avoid direct run-off of material into sewers, waterways, lakes or ponds. Do not exceed prescribed application rates. Do not apply insecticides to fields under irrigation where run-off can enter streams, canals, ditches or lakes containing fish. This product does not degrade easily in water treatment plants. Product should not be released into sewers or surface water. (1)

Water MRL: 0.04ppm

Milk (fat) MRL: 0.5ppm

Meat (fat) MRL: 0.2ppm

Fruit MRL: 2.0ppm

Tea MRL: 30.0ppm (4)

35% of tomatoes tested by NSW Dept of Health in "Pesticide Residues in Food and Water 1986-87" Survey had endosulfan residues 0.014-0.57mg/kg.

US EPA DATA GAPS:

NOTES: Endosulfan is severely restricted or banned in Great Britain, Canada, Denmark, Finland, Hungary, India, Israel, Philipines, Sweden, Thailand, Bulgaria. (7)

** Disclaimer: These sheets are designed as summary information and as such are a guide only.

References:

1.Canadian Centre of Occupational Health Database - CCINFO 1991.

2.The Agrochemicals Handbook, 2nd Edition, Royal Society of Chemistry

Information Services The University. Nottingham England. Aug 87.

3.Pesticides and Human Health, W.H.Hallenbeck&K.M.Cunningham-Burns School

of Public Health, Uni. of Illinois Chicago, Springer-Verlag 1985

4.NH&MRC MRL Standards Draft 1989

5.Pesticides Studied in Man, W.J.Hayes. Williams and Wilkins, Baltimore and

London 1982

6 UNEP/IRPTC Data Profile on Endosulfan 1985 Geneva.

7.The Pesticides Handbook, Profiles for Action, 2nd Edition International

Organisation of Consumers Unions.1986

8. Toxicity and bioaccumulation of Endosulfan to Mosquito Fish. B,Nowak,

R.I.M.Sunderam, Uni. of Sydney, Centre for Environmental Toxicology,

SPCC and the University of Technology. 1989

9. Residues of Endosulfan in the livers of wild catfish from a cotton

growing area. Barbara Nowak Uni. of Sydney 1988

10.Handbook of Environmental Fate and Exposure Data for Organic Chemicals,

Ed. P.H.Howard Lewis Pub. Michigan 1991

[accuracy]

Ethylene Glycol MonoButyl Ether


RECORD NUMBER : 32

SYNONYM(S) :

* 2-Butoxyethanol

* Ethylene glycol n-butyl ether

* Ether monobutylique de l'ethylene glycol

TRADE NAME(S) : Butyl Cellosolve

CAS REGISTRY NUMBER : 111-76-2

PIN - UN/NA NUMBER(S) : 2369

RTECS NUMBER(S) : KJ8575000

CHEMICAL FAMILY : Glycol ether / alkoxy alcohol

MOLECULAR FORMULA : C6-H14-O2

STRUCTURAL FORMULA : CH3-CH2-CH2-CH2-O-CH2-CH2-OH

LAST REVISION DATE : 1989-04-26

*** DESCRIPTION ***

APPEARANCE AND ODOUR : Colourless liquid with a mild odour

ODOUR THRESHOLD : Approx 0.4 ppm

WARNING PROPERTIES (ODOUR AND IRRITATION) : Good - odour is normally detectable below the exposure limit

USES AND OCCURRENCES : Solvent for nitrocellulose, natural and synthetic resins, soluble oils, lacquers, varnishes and enamels Also used in textile dyeing and printing, in the treatment of leather, in the production of plasticizers, as a stabilizer in metal cleaners and household cleaners, and in hydraulic fluids, insecticides, herbicides and rust removers.

*** HUMAN HEALTH HAZARD DATA ***

* EFFECTS OF SHORT-TERM (ACUTE) EXPOSURE *

INHALATION :

Nose and throat irritation; a metallic taste in the mouth; and headache.

Exposure to high concentrations, probably in the range of 300 to 600 ppm,

for several hours, may cause respiratory tract irritation, unconsciousness,

and kidney and liver damage.

EYE CONTACT :

Vapour can irritate the eyes The liquid can cause irritation, pain,

reddening, and corneal injury which heals within a few days.

SKIN CONTACT :

Mild irritation

INGESTION :

No specific data Probably can cause irritation and effects described for

inhalation.

* EFFECTS OF LONG-TERM (CHRONIC) EXPOSURE *

HEALTH EFFECTS :

Some reports of respiratory tract and eye irritation, damage to blood

cells, and blood in urine.

CARCINOGENICITY :

Insufficient data

TERATOGENICITY AND EMBRYOTOXICITY :

Animal tests to date have not found severe effects seen in tests with

certain other glycol ethers.

MUTAGENICITY :

Insufficient data

POTENTIAL FOR ACCUMULATION :

Slight - eliminated via lungs; also changed to butoxyacetic acid and eliminated via kidneys.

*** FIRST AID ***

INHALATION :

Remove source of contamination or move victim to fresh air If breathing has stopped, properly trained personnel should begin rtificial respiration or cardiopulmonary resuscitation (CPR) immediately Obtain medical attention immediately.

EYE CONTACT :

Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for 20 minutes, by the clock, holding the eyelid(s) pen Obtain medical attention immediately.

SKIN CONTACT :

As quickly as possible, flush contaminated area with lukewarm, gently running water for at least 20 minutes, by the clock Under unning water, remove contaminated clothing, shoes, and leather goods (e.g watchbands, belts) Obtain medical advice mmediately Completely decontaminated clothing, shoes and leather goods before re-use or discard. 2-Butoxyethanol can be absorbed through skin in toxic amounts.

INGESTION :

Do not induce vomiting or give anything by mouth Obtain medical attention immediately.

FIRST AID COMMENTS :

Provide general supportive measures (comfort, warmth, rest) Consult a physician and/or the nearest Poison Control Centre for all exposure except minor instances of inhalation or skin contact.

*** ANIMAL TOXICITY DATA ***

ANIMAL TOXICITY DATA :

NOTE: Toxicity may differ significantly depending upon the age of the animals studied Weanling rats are less sensitive than older ones.
LD50 (oral, weanling rat): 3000 mg/kg LD50 (oral, 6 week old rat): 2400 mg/kg
LD50 (oral, 1 year old rat): 560 mg/kg LD50 (oral, mouse): 1200 mg/kg
LD5 (oral, rabbit): 320 mg/kg LD50 (dermal, rabbit): 0.40 g/kg (material confined to the skin for 24 hours) LD50 (dermal, rabbit): 1.8 g/kg (material applied by gentle massage) LD50 (dermal, rabbit): 0.11 mL/kg LC50 (inhalation, rat): 500 ppm;/duration of exposure: 4 hours LC50 (inhalation, mouse): 700 ppm;/ duration of exposure: 7 hours.

ACUTE TOXICITY COMMENTS: Changes in the kidney, liver, spleen, and lung were found in animals exposed by ingestion, inhalation, and skin absorption Deaths usually resulted from central nervous system depression, lung damage, and kidney injury.

EFFECTS OF BLOOD CELLS: Long-term exposure to 2-butoxyethanol can cause blood changes, including anemia, in rats Both 2-butoxyethanol and its metabolite butoxyacetic acid can cause breakdown of red blood cells Humans appear to be less sensitive to this effect than rats.

REPRODUCTIVE EFFECTS: 2-Butoxyethanol has been found to produce toxic effects in pregnant rats at about 200 ppm, with no apparent increase in congenital defects among the offspring It did not cause testicular atrophy in males.

*** OCCUPATIONAL EXPOSURE LIMITS ***

* THRESHOLD LIMIT VALUES (TLVS) / AMERICAN CONFERENCE OF

GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH) / 1987-88 *

TIME-WEIGHTED AVERAGE (TLV-TWA) : 25 ppm (120 mg/m3) - skin

EXPOSURE LIMIT COMMENTS :

SKIN NOTATION -- Absorption through intact skin, eyes, or mucous membranes may contribute to the overall exposure Prevent absorption by these routes.

NOTE: In many Canadian jurisdictions, exposure limits are similar to the ACGIH TLVs Since the manner in which exposure limits are established, interpreted, and implemented can vary, obtain detailed information from the appropriate government agency in each jurisdiction.

*** SAMPLING AND ANALYSIS ***

SAMPLING & ANALYSIS :

DETECTOR TUBES: Short- and long-term sampling INFRARED: Continuous monitoring

GAS CHROMATOGRAPHY: Continuous monitoring PASSIVE DOSIMETER:

Long-term sampling NIOSH METHOD: 1403 - NIOSH Manual of Analytical Methods

3rd ed Vol 1

*** EXPOSURE CONTROL ***

* Note: Exposure to this material can be controlled in many ways. The measures appropriate for a particular worksite depend on how this material is used and on the extent of exposure. Use this general information to help develop specific control measures. Ensure that control systems are properly designed and maintained. Comply with occupational, environmental, fire, and other applicable regulations. *

* ENGINEERING CONTROLS *

ENGINEERING CONTROLS :

Local exhaust ventilation is normally required when used in small quantities Process enclosure or worker isolation are preferred when used in large quantities.

* PERSONAL PROTECTIVE EQUIPMENT *

RESPIRATORY PROTECTION :

Not normally required if engineering controls are adequate If concentration of airborne contaminant exceeds the recommended exposure limit, wear appropriate approved respiratory protection Emergency respirators should be available in case of leak or spill.

RESPIRATORY PROTECTION GUIDELINES :

NIOSH RECOMMENDATIONS FOR 2-BUTOXY ETHANOL CONCENTRATIONS IN AIR: UP TO

250 ppm: SAR; or SCBA. UP TO 625 ppm: Powered air-purifying respirator with organic vapour cartridge(s); or SAR operated in a continuous flow mode. UP TO 700 ppm: Gas mask with organic vapour canister; or full-facepiece chemical cartridge respirator with organic vapour cartridge(s); or full-facepiece SAR; or full-facepiece SCBA.

EMERGENCY OR PLANNED ENTRY IN UNKNOWN CONCENTRATION OR IDLH CONDITIONS: Positive pressure, full-facepiece SCBA; or positive pressure, full-facepiece SAR with an auxiliary positive pressure SCBA. ESCAPE: Gas mask with organic vapour canister; or escape-type SCBA.
NOTE: The IDLH concentration for 2-Butoxy ethanol is 700 ppm. NOTE: Substance reported to cause eye irritation or damage; may require eye protection.

ABBREVIATIONS: SAR = supplied-air respirator; SCBA = self-contained breathing apparatus IDLH = Immediately Dangerous to Life or Health.
NOTE: In these recommendations the IDLH concentration is defined as the maximum concentration which would not cause any escape-impairing symptoms or irreversible health effects to a person exposed for 30 minutes if the respirator failed.

EYE/FACE PROTECTION :

Chemical splash goggles or face shields (eight inch minimum), as required

SKIN PROTECTION :

Impervious gloves, coveralls, boots, and/or other resistant protective clothing Have a safety shower/eye-wash fountain readily available in the immediate work area.

RESISTANCE OF MATERIALS FOR PROTECTIVE CLOTHING :

GOOD - Polyvinyl alcohol (PVA) NOTE: Some types of rubber and plastics are non-resistant. NOTE: Resistance of specific materials can vary from product to product. Evaluate resistance under conditions of use and maintain clothing carefully.

PERSONAL PROTECTION COMMENTS :

Remove contaminated clothing promptly Keep contaminated clothing in closed containers Discard or launder before rewearing Inform laundry personnel of contaminant's hazards. Do not smoke, eat or drink in work areas Wash hands thoroughly after handling this material Maintain good housekeeping.

*** STORAGE AND HANDLING ***

STORAGE CONDITIONS :

2-Butoxyethanol should be stored in tightly closed, grounded containers in a cool area with adequate ventilation, away from normal work areas and sources of heat and sparks Fans and other electrical equipment should be spark-resistant Approved safety solvent containers are preferred. Containers should be covered when not in use and stored in a fire-resistant grounded cabinet Use solvent resistant materials in storage and handling area.

HANDLING :

Use 2-butoxyethanol in minimal quantities in designated areas with adequate ventilation and away from sources of heat or sparks Whenever possible, fire-resistant containers should be used Wear appropriate protective equipment to prevent skin and eye contact.

*** SPILL AND LEAK PROCEDURES ***

PRECAUTIONS :

Restrict access to area Provide adequate protective equipment and ventilation Remove sources of heat and flame Only trained personnel should perform or supervise clean-up operations.

CLEANUP :

Stop or reduce discharge if it can be done safely Contain material. Material should be recovered if possible or collected on absorbent materials such as dry clay, sand, or sawdust Prevent entry into water or sewer systems Notify appropriate environmental authorities in the event of any significant release of this material into the environment Some companies sell cleanup kits which may be appropriate for small spills involving this material.

*** DISPOSAL ***

DISPOSAL :

Review federal, provincial and local regulations prior to disposal Dispose of in a designated landfill site or burn in an approved incinerator.

*** FIRE AND EXPLOSION ***

FLASH POINT : 61 deg C (142 deg F)

LOWER EXPLOSIVE LIMIT (LEL) : 1.1%

UPPER EXPLOSIVE LIMIT (UEL) : 10.1%

AUTOIGNITION TEMPERATURE :

244 deg C (472 deg F)

FIRE EXTINGUISHING AGENTS :

Carbon dioxide, dry chemical, alcohol foam

FIRE FIGHTING PROCEDURES :

Water spray can be used to cool 2-butoxyethanol below its flash point. Vapours can accumulate in low areas.

COMBUSTION (THERMAL DECOMPOSTITION) PRODUCTS :

Carbon monoxide, carbon dioxide

* NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD INDEX *

HEALTH : 2 - Hazardous to health

FIRE : 2 - Must be moderately heated before ignition will occur

REACTIVITY : 0 - Normally stable

*** CHEMICAL REACTIVITY ***

STABILITY : Normally stable

INCOMPATIBILITY - MATERIALS TO AVOID :

Avoid contact with strong oxidizing agents and strong caustics Attacks some types of rubber, plastics and coatings.

HAZARDOUS POLYMERIZATION : Does not occur

CORROSIVITY TO METALS :Not corrosive

*** PHYSICAL PROPERTIES ***

MOLECULAR WEIGHT : 118.17

CONVERSION FACTOR :1 ppm = 4.8 mg/m3 @ 25 deg C

BOILING POINT : 171.2 deg C (340 deg F)

RELATIVE DENSITY (SPECIFIC GRAVITY) :0.90 (water = 1)

SOLUBILITY IN WATER :Soluble

SOLUBILITY IN OTHER LIQUIDS :Soluble in alcohol, ether

VAPOUR DENSITY : 4.1 (air = 1)

VAPOUR PRESSURE : 0.76 mm Hg @ 20 deg C

SATURATION VAPOUR CONCENTRATION : Approximately 1,000 ppm (0.1%)

EVAPORATION RATE : 0.1 (butyl acetate = 1)

*** WORKPLACE HAZARDOUS MATERIALS INFORMATION SYSTEM (WHMIS)

CLASSIFICATION ***

WHMIS INGREDIENT DISCLOSURE LIST : Confirmed A; meets criteria for disclosure at 1% or greater

*** TRANSPORTATION OF DANGEROUS GOODS (TDG) SHIPPING INFO ***

* (Source: Transport Canada, Transportation of Dangerous Goods Regulations) *

TDG INFORMATION : SHIPPING NAME AND DESCRIPTION: Ethylene glycol monobutyl ether

PRODUCT IDENTIFICATION NUMBER (PIN): 2369

CLASSIFICATION: 6.1 - Poisonous substance

SPECIAL PROVISIONS: ---

IMO CLASSIFICATION: 6.1; 3

ICAO CLASSIFICATION: 6.1

PACKING GROUP: III

*** SELECTED BIBLIOGRAPHY ***

BIBLIOGRAPHY :

2-Butoxyethanol : chemical hazard summary : no 3. Hamilton, Ontario : CCOHS, 1984

NIOSH pocket guide to chemical hazards (Repr with corr.) NIOSH, Feb.1987. p 62-63

[accuracy]

FENITROTHION

Record No: 161-161091
Chemical Name: 0,0-dimethyl 0-(4-nitro-m-tolyl) phosphorothioate
CAS REGISTRY NUMBER: 122-14-5
CHEMICAL FAMILY: Organo-phosphate insecticide
MOLECULAR FORMULAE: C9 H12 NO5 PS

DESCRIPTION: Technical grade is an oily liquid, yellowish/brown in colour.

USAGE: A Schedule 6 insecticide registered for a wide variety of crop and noncrop uses including buildings, apples, stored grain and tobacco. (Fenitrothion is not registered for food usage in U.S.) (1)

Agricultural - insecticide

Industrial -

Domestic - insecticide

TOLERANCE & EXPOSURE LEVELS:

HEALTH EFFECTS:

SHORT TERM: Acute exposure effects of organo-phosphates include cholinesterase inhibition, Central Nervous System damage, anorexia, confusion, convulsions, dermatitis, EEG and EMG disturbances, visual and eye damage, renal and hepatic damage, hyperglycemia, muscle twitching and atrophy, respiratory problems, insomnia, sweating, vomiting, weakness, headache, hallucinations and psychosis. (4)

LONG TERM: Human epidemiological evidence indicates fenitrothion causes eye effects such as retinal degeneration and myopia. (1)

Chronic exposure to organo-phosphates can cause frontal lobe impairment. (4)

CARCINOGENICITY:

MUTAGENICITY:

REPRODUCTIVE EFFECTS:

BIO-ACCUMULATION:

Suspected Effects: Organo-phosphates are suspected of causing neurologic deficits. (4)

ANIMAL TOXICITY DATA: Oral rat LD 50: 250mg/kg (PESKEM)

Acute Oral LD 50: 800mg/kg (male rat)

330mg/kg (female rat)

Acute Dermal LD 50: 1200mg/kg (female rat)

890mg/kg (male rat)

Acute Inhalation: 5mg/l in rats.

Fenitrothion is mildly irritating to eyes and skin. It was not a skin sensitiser and did not cause delayed neurotopxicity in hen study. In chronic feeding studies a No Observable Effect Level (NOEL) for brain and red bllod cell cholinesterase in rats: 10ppm

Systemic NOEL : 5ppm (dog)

Chronic dog feeding studies have implicated fenitrothion in causing eye effects. (1)

CARCINOGENICITY:

MUTAGENICITY: Datagap (1)

REPRODUCTIVE EFFECTS: Datagap (1)

Wildlife Data: Laboratory data show that fenetrothion is potentially highly to very highly toxic to birds, fish and aquatic invertebrates including some endangered species.

Freshwater Fish acute toxicity: (96 hrs) LC50 :1.7ppm (brook trout)

3.8ppm (bluegill)

Very highly toxic to aquatic invertebrates:

(48/96hrs) EC50 :3ppb (Gammarus fasciatus) (1)

Highly toxic to honey bees. U.S. requires endangered species label restrictions. (1)

ENVIRONMENTAL EFFECTS:

Environmental Fate: U.S.EPA state there are datagaps for most environmental characteristics studies. Preliminary data indicates fairly rapid degradation in soils with a half life of <week in nonsterile muck and sandy loam soils. Fenitrothion appears to be mobile in a variety of soils. Potential to contaminate groundwater is unable to be assessed due to datagaps. (1)

Breakdown products include fenitrooxon, p-nitrocresol and desmethyl fenitrothion. (1)

Water MRL: 0.02mg/l

Cerial grain MRL:10.0 mg/kg

Milk fat MRL: 0.05mg/kg

Apples MRL: 0.5 mg/kg

Wheat bran: 20.0 mg/kg (3)

Fenitrothion was detected at above Maximum Residue Levels in wheat, barley, oats, sorghum, malted grain, bran, eggs and fiels peas. (2) A U.S. EPA provisional Acceptable Daily Intake (PADI) was calculated at 0.004mg/kg/day. (based on a 1yr dog study with a NOEL of 0.125mg/kg/day using a 30-fold safety factor) fold safety factor. (1)

EPA DATA GAPS:

NOTES: There are no domestic uses for fenitrothion on food or feed commodities in the U.S., yet one food additive tolerance is established for wheat gluten imported from Australia (resulting from Australia's treatment of stored grain with fenitrothion). (1)

** Disclaimer: These sheets are designed as summary information and as such are a guide only.

References:

1. EPA Pesticide Fact Sheet 142 Fenitrothion 1987

2. Report on National Residue Survey 1987-88, Bureau of Rural Resources.

3. NHMRC MRL Standard Draft 1989

4. Pesticides and Human Health, W.H.Hallenbeck&K.M.Cunningham-Burns School

of Public Health, Uni. of Illinois Chicago, Springer-Verlag 1985

[accuracy]

FLUPROPANATE, TETRAPION (Frenock)

RECORD NUMBER: 107-250391

CHEMICAL NAME: FLUPROPANATE, TETRAPION (Frenock)

Sodium 2,2,3,3-tetra fluoropropinate

CAS REGISTRY NUMBER: 22898-01-7

CHEMICAL FAMILY: Not available

MOLECULAR FORMULAE:

DESCRIPTION: Pale amber liquid, soluble in water, ethanol, methanol and acetone. Insoluble in most other organic solvents.

USAGE: Frenock (formulated product) is an organic compound used as a selective translocated herbicide for the control of Parrammatta Grass.(2) It is Schedule 6 poison.

Agricultural - Herbicide

Industrial -

Domestic -

TOLERANCE & EXPOSURE LEVELS: Acceptable Daily Intake: 0.0025 mg/kg

HEALTH EFFECTS:

SHORT TERM: Short term exposure by all routes is considered harmful.

Skin and eye contact may result in mild irritation.

Inhalation can produce respiratory irritation.

Ingestion may cause sluggishness and diarrhoea. (1)

LONG TERM: Prolonged skin contact may lead to dermatitis effects and may lead to absorption through the skin with resultant toxic effects. (1) No long term studies carried out other than 90 day feeding study. (6)

CARCINOGENICITY: No data available.

MUTAGENICITY: Animal tests indicate it is not mutagenic. (1)

REPRODUCTIVE EFFECTS:

BIO-ACCUMULATION: No data available.

Suspected Effects:

ANIMAL TOXICITY DATA: Oral Rat LD 50: >8000mg/kg

Dermal Rabbit LD 50: >4000mg/kg (1)

NOEL (rat) is 100ppm or 5mg/kg in a 90 day feeding study.(1)

* No long term studies carried out other than a 90 day feeding study.

CARCINOGENICITY: No data available.

MUTAGENICITY: Negative in IN VITRO mutagenicity assays. (1)

REPRODUCTIVE EFFECTS:Manufacturers state that Frenock is negative in teratogenic tests in rats at dose levels up to 100mg/kg (1)

BIO-ACCUMULATION: Withholding period for stock is 14 days for spot spraying and 4 months for blanket spraying of Frenock.(5) No other data available.

Wildlife Data: Low toxicity to fish.(1)

ENVIRONMENTAL EFFECTS:

Environmental Fate: Very slow rate of biodegradation. (1) Frenock is residual to some extent in soil and plant tissue. It is removed by leaching and broken down rapidly under anaerobic conditions in subsoil.

Frenock has a long lifespan in plant tissue and persists in susceptible species until plant dies and decays. (5)

Water MRL: No MRL set.

EPA DATA GAPS:

NOTES: Lactating dairy cows or goats must not be grazed on Frenock treated areas as no MRL has been set for Frenock in milk. (5) No further testing including chronic studies will be carried out and no MRL for milk will be assigned as chemical usage will remain for non-food use.(6)

** Disclaimer: These sheets are designed as summary information and as such are a guide only.

References:

1. ICI Data Sheet 11.89

2. Agricultural Chemicals, Book 4 Fungicides 1982-83 Revision WT Thomson.

3. Correspondence ICI Mr Alan Jacques. 6 Aug 1986

4. Correspondence ICI Mr Susan Taplin. 27 June 1988

5. Comparative Analysis of Frenock and 2,2-DPA. NSW Dept of Agriculture &

Fisheries.

6. Pers. Communication: Mr Don Mathews ICI, 12.2.91

[accuracy]

GLYPHOSATE

CHEMICAL NAME: GLYPHOSATE Isopropylamine salt of N-(phosphonomethyl) glycine

CAS REGISTRY NUMBER: 1071-83-6

CHEMICAL FAMILY: Phosphonate/organic phosphorus compound

MOLECULAR FORMULA: C3 H8 NO5 P

DESCRIPTION: Colourless or white, odourless crystals

USAGE: A Schedule 5 herbicide in the form of the mono(isopropyl ammonium) salt. A broad spectrum (non selective) post-emergent plant growth regulator used for the control of grasses, sedges and broadleaved weeds.

A systemic herbicide that translocates to the roots of plants. Used as the active constituent in many commercial herbicide products. Formerly a Monsanto-held patent, glyphosate products are now formulated by a number of pesticide producers. Used in forestry, farming and pastoral activities, local councils, weed control and transport agencies, as well as domestic and industrial uses.

HEALTH EFFECTS: HUMAN AND TEST ANIMAL DATA

Short Term (Acute Toxicity)

Acute Toxicity (standard animal tests) : Oral Toxicity: low

LD50 (rat, oral): 4873 mg/kg. LD50 (mouse, oral): 1568 mg/kg.

Lethal oral doses produce severe stress, breathing difficulties, blood in the lungs, convulsions and death.

LD50 (rabbit, dermal): Greater than 5000 mg/kg.

LC50 (rat): greater than 12.2 mg/kg in air (4 hour exposure)

Can cause slight skin irritation, severe eye irritation. Dust may cause mild to moderate irritation of nose and throat.

Toxicity of glyphosate formulations may be due to presence of surfactants and other additives/contaminants.

Long Term (Chronic Toxicity)

No chronic effects from human exposure reported in peer reviewed literature. [1]

Mouse feeding studies noted non-neoplastic changes including necrosis of hepatocytes male mice and hypertrophy in female mice.[2] (Non-cancerous liver damage) potential for adverse human health impacts of glyphosate formulations requires more investigation.

Carcinogenicity

Long term animal studies did not show carcinogenic activity.[3]

No information on human cancer risk is available.

Glyphosate is readily nitrosated to N-nitrosoglyphosate. Whilst this compound has not been assessed for carcinogenicity potential, at least 3/4 of another 120 N-nitroso compounds showed carcinogenic potential. Nitrosation occurs in the stomach by reaction of nitrite in human saliva. Standard carcinogenic tests using rats would not detect this effect since rats do not secrete nitrite in their saliva.[4]

In 1986, the oncogenic potential of glyphosate was not fully understood. A review of a mouse cancer study noted a slight increase in renal tubular adenomas and a one- year feeding study in dogs observed a reduction of weight of pituitary gland in mid to high doses. The United States Environment Protection Agency reveiwed thses studies and concluded that the mice feeding study did not represent a safety concern because such high doses of glyphosate had been administered to the test animals. (up to 3% of total diet). They did require an additional rat study conducted at high dose levels.

In 1991, following review of the new rat study, the US EPA placed glyphosate in Group E. Evidence of non-carcinogenciity for humans.[5]

Reproductive Effects

Animal studies did not produce any effects. Diets of up to 30 mg/day did not produce any reproductive effects in male or female rats, over three generations. No teratogenic effects were observed in rabbits given up to 350 mg/kg/day on days 6-27 of pregnancy. Toxic effects noted at the highest dose in both treated animals and their offspring. [6]

No information on human reproductive risk is available.

Mutagenicity

Not mutagenic in a standardised series of tests using bacteria, cultured mammalian cells and whole animals.[7] One study showed very weak mutagenic activity in an in vitro mammalian cell test. [8]

No information on human genetic risk.



Damage to cell structure and function

Glyphosate, or some additive to commercial glyphosate products, may cause damage to DNA via sister chromatid exchange. [9]

Glyphosate can affect the capacity of cells to produce energy. This occurs due to disruption of cell membrane structure. [10]

Further investigation of potential for cell and sub-cellular impacts is required

Synergism Potential

All commercial pesticide products are mixtures of chemical compounds. They contain the active constituent/s (a.i.) and other compounds such as solvents, surfactants, lubricants, preservatives, solubilizers and suspending agents. They may also contain impurities and/or contaminants. Some commercial glyphosate products contain the solvent POEA, which is contaminated with the carcinogen 1,4-dioxane, a common solvent used in laboratories and contained in many consumer products. According to the manufacturer, the levels of this contaminant are kept below 1 part per million ( ppm). Another contaminant is N-Nitrosoglyphosate. According to the manufacturer, levels of this contaminant are kept below 0.1 ppm.

No information is available on the human toxicity of pesticide mixtures containing glyphosate. It is often mixed with other pesticides. [11]

HEALTH EFFECTS: WILDLIFE

General Toxicity

The US EPA regards glyphosate as being slightly toxic to birds, aquatic vertebrates and fish and moderately toxic to embryo and larvae.

Acute toxicity to freshwater fish: Rainbow trout 86 mg/L.

Chronic toxicity to freshwater fish: Fathead minnow with maximum threshold concentration (MATC). >25.7 mg/L.

Avian toxicity (reproductive study): Mallard ducks > 1000ppm.

The use of glyphosate for vegetation control and the resulting decreased habitat complexity caused a decrease in invertebrate populations and songbird numbers (especially insectivores). One US study found the total abundance of songbirds was 36% lower on clear-cut treated with herbicides for at least three years. The effect related to the complexity of vegetation.[12]

Frog Toxicity

Toxicity to wildlife has mainly focussed on its acute toxicity to frogs. The Final Report, Acute toxicity of a herbicide to selected frog species[13] investigated the toxicity of technical grade glyphosate and the glyphosate-based herbicide, Roundup 360. The method used was through acute bioassays with frog species common to the south-west of Western Australia. The report found that:

technical grade glyphosate and Roundup 360 can be acutely toxic to adult frogs and tadpoles in laboratory bioassays tadpoles were many times more sensitive to the herbicide formulation tested than adult frogs tadpoles were approximately an order of magnitude more sensitive to the formulation than to technical grade glyphosate the above results and the results of other studies reported in the literature tend to suggest that the surfactant used in the formulation is more harmful to aquatic animals than the glyphosate The report also stated that:

the acute toxicity value ( 48 hour LC50 or Lethal Concentration) to the juvenile Crinia insignifera was 51.8 mg/L for Roundup 360 (the commercial formulation containing the solvent) the acute toxicity value ( 48 hour LC50 or Lethal Concentration) to the juvenile Crinia insignifera was 83.6 mg/L for glyphosate alone the toxicity of Roundup to fish changes significantly with temperature and pH, with greatest toxicity at high temperature and pH. A potential hazard exists for frogs and tadpoles in shallow water bodies. Further study is required to determine the actual concentrations and persistence of the formulation in aquatic environments As a result of this study, commercial herbicide products containing the herbicide glyphosate have been reformulated, with the toxic surfactant replaced by another compound/s.

Limitations of the study : Replicating real world conditions in a laboratory is impossible and as a result, laboratory studies can only provide a guide to toxicity potential, not a definitive prediction. Professor Tyler of the University of Adelaide (Zoology) noted: [14]

The WA toxicity trial involved placing the animals in an exposure chamber where there would be some skin contact with the solution. However, under normal application in the environment, the application method (of boom spraying) may result in atomised spray, which may increase overall exposure potential for the animals.

All bioassays were conducted at 20 +/- 2 degrees C under ambient laboratory light. Temperatures in real world conditions may be as high as 42 degrees C (in the Northern Territory) and certainly well above 30 degrees C in northern NSW summer months.

The WA study looked at three frog species, with the bulk of the investigation focussed on two species, Crinia insignifera and Litoria moorei. Under real world conditions, many thousands of species of amphibians, invertebrates and other aquatic creatures may be exposed to herbicides and risks to the viability of their communities is not well understood. The studies have not been done.

Australia’s biodiversity is well documented and to assert negligible risk to the environment based on a small laboratory study on two localised frog species is not scientifically defensible.

The WA study investigated acute poisoning potential only. No attempt was made to investigate sub-lethal, chronic, reproductive, endocrinal or immunological effects, which may also pose significant risks to the viability of aquatic communities.

The WA study did indicate a 48 hour LC50 of 83.6 mg/L for glyphosate alone for Crinia insignifera. This is a significant level if reproduced by normal applications in the environment. Thus it is not just the formulation that may pose unacceptable risks to wildlife. The data generated by the WA study indicates both commercial formulation and the active constituent alone pose risks.

ENVIRONMENTAL IMPACTS: PLANT RESISTANCE

Australian research [15] reports that fescue and perennial ryegrass cultivars, soybean and convolvulus arvenis L. Lines displayed varying degrees of resistance to glyphosate. Genetic engineering of crops such as soy now allows this and other commercially important food crops to be sprayed with glyphosate, thus extending the potential global market for glyphosate-based products.

ENVIRONMENTAL FATE AND TRANSPORT

Elimination, Bioaccumulation and Residues in Food and Animals.

Slowly absorbed through the digestive system and rapidly eliminated.[16] A urine test for glyphosate in urine is available.

Does not bio-accumulate in animal tissue but residues can be detected after exposure. Glyphosate and its metabolite, aminomethylphosphonic acid (AMPA) have been identified in the tissues, urine and faeces of rats and rabbits, in the liver in poultry, pigs and cattle and the kidney of pigs and cattle.[17] Has been detected in rice. [18]

Persistence

The persistence of glyphosate in the environment is variable. It is strongly bound to clay particles and is considered moderately persistent in soil. Degradation via microbial action is moderately slow. Half lives range from a few days to several months or years. The more sand in the soil, the slower the inactivation via the bounding to clay.

Application of glyphosate to sandy loam resulted in weakening of subclover planted 120 days after application. A significant decrease in nodule numbers and root weights of the plants was observed. This indicated that breakdown of glyphosate in soils with a high sand content is slow. Study recommended care in advocating glyphosate use in soils with high (>80%) sand content. [19]

Nitrosation: N-nitrosoglyphosate was generated in soils treated with sodium nitrate (20 ppm) and glyphosate (740 ppm) at elevated levels. The highest level generated was noted in soil of low organic matter and clay content. The formation of N-nitrosoglyphosate was not observed in soils treated with lower levels, nitrite nitrogen (2ppm) and glyphosate (5ppm).[20]

The manufacturer claims that the product is completely biodegradable, breaking down into natural products in both soil and water. Stated half-life of 60 days in the soil, a time frame described as rapid by manufacturer. Other information indicates that breakdown time is extremely variable from a half-life of 24 days in forest soils in Ontario to 249 days in Finland.[21]

Very little leaching capacity. Low potential to contaminate ground water as it is tightly bound to soil

Glyphosate and its metabolites are considered as residues of concern in plants. [22] Maximum Residue Limits (in mg/kg or parts per million/ppm) have been set for a number of commodities.

GENETICALLY ENGINEERED RESISTANCE TO GLYPHOSATE
Resistance has been genetically engineered into food crops such as soya beans so that this core food crop can be sprayed with glyphosate without killing it. This means that up to 200 times more glyphosate residue may be present in soy-based foods.

MANUFACTURER AGREES TO CHANGE ADS

In the USA, Monsanto has agreed to change its advertisements for glyphosate-based products. As part of the agreement, Monsanto will discontinue the use of the terms “biodegradable” and “environmentally friendly “ in all advertising in New York State.



--------------------------------------------------------------------------------

[1]. Canadian Centre of Occupational Health Database, CCINFO 1991. Glyphosate, 1,4-Dioxane

[2]. US EPA. Pesticide Fact Sheet, Glyphosate. June 1986.

[3].US EPA. Health Advisory, Glyphosate. Office of Drinking Water. August 1988.

[4]. Shearer R. Consultant in genetic toxicology. Health effects of glyphosate. 1984.

[5]. 1) Pers. Com. Mick Tydens, Monsanto. 2) Monsanto Backgrounder Roundup Herbicide by Monsanto 3) Reregistration Eligibility Document for Glyphosate, (EPA 738-R-93-014). United States Environment Protection Agency, Washington, September 1993.

[6].Canadian CCINFO 1991.

[7]US EPA. 1986.

[8]. Canadian CCINFO (1991).

[9]. Vifusson @ Vyse. The effect of pesticides Dexon, captan and Roundup on sister chromatid exchange in human lymphocytes in vitro in Mutation Research (1980) 79, pp59-72.

[10]. For discussion of the biological mechanism (uncoupling of mitochondrial oxidative phosphorylation) see Clorunsungo, Bababunmi and Basair , 1979. Effect of glyphosate on rat liver mitochondria in vivo in Bull. Env. Contam. Toxicol. 22. pp. 357-364. This study does not meet US EPA requirements for toxicity assessment since the herbicide was given by injection, which is considered an inappropriate exposure route for humans. See also Pollak, J.K. The Toxicity of Chemical Mixtures; An Introduction to Recent Developments in Toxicology. CHAST, The University of Sydney 1993.

[11].Quite apart from their own toxicity, the additives that are contained in many pesticide products may cause metabolic reactions and in this way significantly enhance the toxicity of the formulation.

For example, when four organochlorine pesticides, dieldrin, endosulfan, toxaphene and chlordane were tested individually they were found to be weakly estrogenic. When two of these pesticides applied in combination, their activity increased between 160 and 1600 fold. Science 7/6/96.

[12]Roundup Information Summary. Soil and Health Association of New Zealand Inc. September 1993.

[13].Department of Environment Protection, Perth, Western Australia. Technical Series 79. June 1995.

[14].Pers, Corr. November 1996.

[15].Powles S. B. And Holtum J.A.M. (Eds) Herbicide Resistance in Plants: Biology and Biochemistry. Lewis Publishers, Boca Raton. 1994. Pp. 231-235.

[16]. Canadian CCINFO (1991)

[17]. US EPA(1986)

[18].Short, K. Quick Poison, Slow Poison. Pesticide Risk in the Lucky Country Envirobook, Sydney. 1994. p.69.

[19]. Eberbach P.L. and Douglas L.A. Persistence of Glyphosate in Sandy Loam. School of Agriculture and Forestry, The University of Melbourne 1983.

[20]. Khan and Young. N-nitrosamine formation in soil from the herbicide glyphosate. Agric. Food Chem. Vol. 25, no.6. 1977.

[21]. Short (1994) p. 69.

[22]. US EPA (1986)

[accuracy]

TOLUENE

RECORD NUMBER: 202-17049

CAS REGISTRY NUMBER: 108-88-3
CHEMICAL FAMILY Aromatic hydrocarbon

MOLECULAR FORMULA: C7-H8

DESCRIPTION: Clear, colourless liquid with characteristic odour.

USAGE: Used to make chemicals (examples: benzene, toluene diisocyanate, benzoic acid), explosives, dyes and many other compounds. Used as a solvent for inks, paints, lacquers, resins, cleaners, glues and adhesives. Found in gasoline and aviation fuel.

Agricultural -

Industrial - Predominant usage as solvent

Domestic -

ROUTES OF EXPOSURE: Main route of exposure is through ambient air, particularly areas of heavy traffic and around filling stations, also from areas where solvents are used, near cigarettes and glue sniffing. (4)

TOLERANCE & EXPOSURE LEVELS: ODOUR THRESHOLD: Approximately 2 ppm

TIME-WEIGHTED AVERAGE (TLV-TWA) : 100 ppm (375 mg/m3)

HEALTH EFFECTS:

SHORT-TERM: Toluene is a fat solvent that causes a CNS dysfunction and the destruction of other tissues.(2) Inhalation of high vapour concentrations (greater than 200 ppm for 8 hours) affects the central nervous system. Symptoms include tiredness, muscle weakness, headache, dizziness, confusion, poor coordination, nausea and vomiting (1) Massive over-exposures have resulted in loss of consciousness and death. Liver injury has been reported in survivors of serious over-exposures.

Toluene vapour is mildly irritating to the nose, throat and eyes.

Prolonged skin contact can cause dry, irritated skin.

Toluene vapour is poorly absorbed through the skin (1).

LONG-TERM: Workers exposed to between approximately 200 and 430 ppm toluene for periods from 17 to 33 years showed disturbances in memory, thinking ability, emotions and coordination. Increased levels of liver enzymes and enlarged livers were seen in some studies.(1)

Other chronic exposure effects are anaemia, anorexia, renal damage and toluene in the blood. (2)

REPRODUCTIVE EFFECTS: Limited evidence that exposed women may have an increased incidence of menstrual disorders. It is likely that absorbed toluene would be transferred from a pregnant woman to her unborn child. (1)

CARCINOGENICITY: No evidence to suggest that toluene is carcinogenic in humans. (1)

TERATOGENICITY AND EMBRYOTOXICITY :

MUTAGENICITY: Studies have suggested that toluene is not mutagenic.(1)

BIO-ACCUMULATION: Absorbed toluene is changed by the liver to hippuric acid and benzoylglucuronide which are excreted in the urine.

Toluene can be stored for several days in body fat with a biological half-life is 3 days. (1)

Detected in all 8 U.S. samples of breast milk from 4 urban areas. 250 whole blood samples: 100% positive with a range of 0.2ppb-38ppb with an av.1.5ppb. Detected in 91% in U.S. National Human Adipose Tissue Survey: 250ppb max.(4)

Toluene has been detected in the blood of children from the North Coast of NSW. (3)

Suspected Effects:
Aplastic anaemia, cardiac sensitivity, cerebellar dystropy, hepatic damage, learning capacity decreased, mutagenisis, neural dystrophy, prenatal damage, phagocytic activity of leukocytes depressed, serum albumin depression, adrenal hypertrophy, plasma hydrocorticoid elevation. (2)


ANIMAL TOXICITY DATA: LD50 (oral, rat) 2500 mg/kg (5,000mg/kg)

LD50 (dermal, rabbit): 14000 mg/kg

LC50 (rat): 8000 ppm; 4-hr exposure

CARCINOGENICITY: No data available.(1)

REPRODUCTIVE EFFECTS: Rats, exposed to 266 ppm for 8 hours/day on days 1-21 of pregnancy had offspring which were slightly underweight. Bone formation was delayed Toluene did not cause birth defects (1).

MUTAGENICITY: Toluene was not mutagenic in short-term tests using three types of bacteria.(1) Chromosome abnormalities were reported in two early Russian studies using very high doses, but have not been reproduced in recent tests.(1)

Wildlife Data: Detected in U.S. oysters:3.4ppb, clams (2 sites) 11ppb and 18ppb. (4)

ENVIRONMENTAL EFFECTS:

Environmental Fate: When released into soil, toluene will evaporate from near surface soil and leach into groundwater. Biodegradation occurs in both soil and water but is slow particularly at high concentrations.

This may be due to toluene's toxicity to microorganisms. U.S.EPA database: 397 soil/sediment sample points: 17% positive with 5ppb median. (4)

When released into water, its removal depends on temperature, mixing conditions and microorganisms. It will not be significantly absorbed to sediment or bioconcentrate in aquatic organisms. U.S.Groundwater Supply Survey 1982: 466 drinking water supplies: 1.3% positive with 0.8ppb av. (4)

When released to atmosphere it will degrade by reaction with photochemically produced hydroxyl radicals or wash out with rain, with half life of 3hours to over one day.

Atmospheric Concentrations: Rural: 0.66ppb median (115 samples, 1978)

Urban: 11ppb median,max 85ppb (3195samples) (4)

Water MRL:

EPA DATA GAPS:

NOTE: Toluene is often contaminated with benzene.

** Disclaimer: These sheets are designed as summary information and as such are a guide only. The information is compiled from publicly available references which can be supplied on request.



References:

1.Canadian Centre of Occupational Health Database - CCINFO

2.Pesticides and Human Health, W.H.Hallenbeck&K.M.Cunningham-Burns School

of Public Health, Uni. of Illinois Chicago, Springer-Verlag 1985

3.Coffs Harbour Chemical Data Base 1991

4.Handbook of Environmental Fate and Exposure Data for Organic Chemicals,

Vol1 Large Production and Priority Pollutants., Philip H. Howard 1989

Lewis Publishers Inc. USA

[accuracy]

TOLUENE



This product (and also Glue Rid ) is now over the counter sale, as a detterrent for
the "sniffers" (largely by Aboriginals) for their cheap quick "fix"!

[accuracy]

1,1,1-TRICHLOROETHANE

RECORD NUMBER: 200-170491

CAS REGISTRY NUMBER: 71-55-6

CHEMICAL FAMILY: Halogenated hydrocarbon / Chlorinated alkane

MOLECULAR FORMULA: C2-H3-Cl3

DESCRIPTION: Colourless, volatile liquid with a sweetish, chloroform-like odour.

USAGE: Used as a solvent for metal degreasing, natural and synthetic resins, oils, waxes, tar and alkaloids; for adhesives and coatings; for textile-dyeing operations; used in dry-cleaning operations; cleaning electrical machinery; coolant and lubricant in metal-cutting oils; and as extraction solvent and chemical intermediate in the chemical industry.

Agricultural - Additive to pesticides.

Industrial - Predominant usage as solvent.

Domestic - White out.

TOLERANCE & EXPOSURE LEVELS: Odour Threshold - 44-100 ppm

ROUTES OF EXPOSURE: Humans can be exposed dermally and by inhalation of air at occupational sites, from ambient air, household products containing 1,1,1-Trichloroethane (cleansers, polishes, lubricants, paint removers) or ingestion of contaminated food and water. (4)

HEALTH EFFECTS:

SHORT TERM: Acute exposure to high levels (above 900 ppm) of 1,1,1- trichloroethane can depress the nervous system and cause headache, dizziness and fatigue. Short term impaired performance of behavioural tests was also reported. At high levels (greater than 5000 ppm), 1,1,1- trichloroethane can cause unconsciousness, respiratory depression and death. Ingestion can cause severe gastrointestinal irritation characterized by vomiting and diarrhea. Contact with eyes or skin can result in mild irritation.(1) Other acute exposure effects are renal and hepatic damage.(2)

LONG TERM: Little information available. Volunteers exposed to 500 ppm 7hrs/day for 5 days felt tired and had slight problems with balance. Prolonged exposure has caused skin burns.(1) Chronic exposure may result in paralysis and increased susceptibility to viral hepatitis. (2)

1,1,1-Trichloroethane exposure can cause sensitisation of the heart to epinephrine.(2)

CARCINOGENICITY: No human data. Animal studies are inconclusive. (1)



MUTAGENICITY: No human data. Animal and cell studies indicate that 1,1,1-trichloroethane is probably not mutagenic.(1)

REPRODUCTIVE EFFECTS: No human data

BIO-ACCUMULATION: Eliminated mainly in the exhaled air and in the urine, breakdown products (as trichloroethanol and trichloroacetic acid) were detected in the urine up to 12 days after exposure had stopped. Stored in the fat tissues temporarily. (1)

Detected in 8/8 U.S. breast milk samples from urban areas. Detected in whole blood, in 59% of non occupationally exposed West Germans, <0.1-3.4ppb, with a median of 0.2ppb. (4) Detected in blood samples from children in Northern NSW.(3)

Suspected effects: Carcinogenisis, mutagenisis and prenatal damage.(2)

ANIMAL TOXICITY DATA: LD50 (oral, rat): 10 300 mg/kg

LD50 (skin, rabbit): about 15 000 mg/kg (Dow)

LC50 (rat): 24 000 ppm/1-hr exposure;

18 400 ppm/4-hr exposure;

Rats exposed to 12 000 ppm of 1,1,1-trichloroethane

for 7 hours showed slight liver damage. (1)

CARCINOGENICITY: A feeding study in rats and mice gave inconclusive results; a few liver tumours were seen in treated mice, but survival of treated animals was low. (1) IARC considered the available information inadequate for evaluation.

REPRODUCTIVE EFFECTS: Birth defects were not observed in the rodent offspring. At high levels some indication of fetotoxicity.(1)

MUTAGENICITY: Some limited positive results and many negative results have been reported from tests in bacteria. It appears that 1,1,1-trichloroethane is probably not mutagenic. (1)

Wildlife Data:

ENVIRONMENTAL EFFECTS:

Environmental Fate: When released into surface water 1,1,1 Trichloroethane will decrease in concentration due to evaporation. Detected in 133 US cities finished surface water at 0.4ppb median and 23 US cities finished groundwater at 2.1ppb median. (22% of sample positive) (4)

When spilt on soil it will volatilize and percolate into groundwater, with very slow degradation in subsoils (no degradation was observed in subsurface soils in 27 weeks).

Average U.S. background levels; in soil: 0.42ppb in sediment: 0.45ppb (4)

When released into air it will be transported long distances (half life of 6 months to 25 years)and return to earth in rain.

Atmospheric Concentrations: U.S. Rural: av. 110 ppt [1977-80] Urban: av. 420ppt (max 700-8000ppt)

(4)

Water MRL:

EPA DATA GAPS:



NOTES: Those with heart condition should avoid exposure. (1)

COMBUSTION (THERMAL DECOMPOSITION) PRODUCTS : Hydrogen chloride (HCl)

and trace amounts of phosgene at 500 deg C (932 deg F) (1)



** Disclaimer: These sheets are designed as summary information and as such

are a guide only. The information is compiled from publicly available references which can

be supplied on request.



References:

1.Canadian Centre of Occupational Health Database - CCINFO

2.Pesticides and Human Health, W.H.Hallenbeck&K.M.Cunningham-Burns School

of Public Health, Uni. of Illinois Chicago, Springer-Verlag 1986

3.Coffs Harbour Chemical Data Base

4.Handbook of Environmental Fate and Exposure Data for Organic Chemicals,

Vol1 Large Production and Priority Pollutants., Philip H. Howard 1989

Lewis Publishers Inc. USA

[accuracy]

1,2-XYLENE

RECORD NUMBER: 204-150591

CHEMICAL NAME: (Dimethylbenzene, xylol, o-Xylene) Three chemical forms of xylene exist (o-, m-, p-isomers)

CAS REGISTRY NUMBER: 95-47-6

CHEMICAL FAMILY:

MOLECULAR FORMULAE: C8 H10

Agricultural - solvent

Industrial - solvent

Domestic - component of petrol

DESCRIPTION: Colourless liquid with strong, sweetish, aromatic odour. Commercial xylene is a mixture of the three isomers.

Xylene contains toluene, trimethylbenzenes, benzene and other hydrocarbons

USAGE: Xylene is used extensively as feedstock in manufacture of dyes, pharmaceuticals, plastics, as a solvent for paints, lacquers, resins, inks, adhesives, cleansers, degreasers, pesticides, paint strippers and in laboratories.

TOLERANCE & EXPOSURE LEVELS:

Time Weighted Average Exposure-(TWA):100ppm or 435 mg/m3

Short Term Exposure Limit-(STEL): 150ppm or 655 mg/m3

ROUTES OF EXPOSURE: Exposure is primarily inhalation in areas of heavy traffic, filling stations, industrial refineries or where solvents, Agricultural sprays, wood burning stoves & fires, glue for wallpaper and carpet are used or drinking contaminated underground water (leaking underground petrol tanks).

Av. Daily Intake: air-106ppb, water-2ppb (2)

Skin absorption (damaged skin enhance uptake) and ingestion can occur.(1)

HEALTH EFFECTS:

SHORT TERM: Xylene is a fat solvent that causes Central Nervous System dysfunction and destruction of other tissues. (3)

One of earliest effects of exposure to xylene is increase in liver enzymes. Other effects of a single or short term exposure include irritation of nose, throat and eyes, headache ,nausea, vomiting, dizziness, fatigue, light headedness, irritability, abdominal pain, loss of appetite, reduced coordination, loss of consciousness. (1)

Other acute exposure effects include amnesia, brain hemorrhage, cardiac stress, dermatitis, liver and kidney damage, respiratory difficulties, tremor and xylene in blood and exhaled air. (3)

Alcohol enhances toxic effects of xylene. (1)

LONG TERM: Effects of long term or chronic exposure include inflammation of skin including dryness and cracking, reversible kidney and liver damage.

(1) Other chronic effects include anorexia, apprehension, bone marrow hyperplasia, CNS excitation and depression, dermatitis, drowsiness, eye injury, flatulence, gastrointestinal pain, memory impairment, hepatic damage, mucosal hemorrhage, nausea, red and white blood cell abnormalities [may be due to benzene contaminant, tremor and weakness. (3) Abnormal heartbeat in laboratory workers was associated with long term exposure to xylene.(1)

CARCINOGENICITY: Studies indicate xylene is not a carcinogen. (1)

MUTAGENICITY: Studies indicate xylene is not a mutagen. (1)

REPRODUCTIVE EFFECTS: Available data indicates xylene does not cause permanent structural defects in off spring but is toxic to embryo or fetus and may reduce fertility. (1)

BIO-ACCUMULATION: Most of absorbed xylene is rapidly metabolised and eliminated in urine within a few hours, some exhaled. Metabolites are methylhippuric acids. Alcohol delays metabolism and excretion. Small amount is stored in fatty tissues from which it is slowly released. Repeated or prolonged exposure can result in accumulation of xylene in fatty tissues. (1)

Blood of 35 occupationally exposed men: av.26.6ppb (2)

Detected in the blood of North Coast NSW children in levels above USA average. (4)

Suspected Effects: Xylene is suspected of causing cholinesterase depression, epilepsy, fatty liver, hyperplasia, mutagenisis, prenatal damage, reproductive systems effects. (3)

Nervous system damage. (1)

ANIMAL TOXICITY DATA: Oral rat LD 50: 4,300 mg/kg

Inhalation rat LC50: 29.000mg/m3

Rats and dogs exposed to xylene vapour for 13 weeks at 180-810ppm showed no adverse effects related to dose or time of treatment. (1)

CARCINOGENICITY: One study indicated the irritant action of xylene on the skin increased frequency of skin tumours in animals also treated with a carcinogen. (1)

MUTAGENICITY:

REPRODUCTIVE EFFECTS: Female rats inhaling toxic levels of 700ppmn had reduced litter size, retarded development of fetus and an increase in anomolies (minor defect). (1)

Wildlife Data: Detected in rainbow trout in Colorado R. USA. (not quantified) (2)

ENVIRONMENTAL EFFECTS:

Environmental Fate: When released to air, o-xylene may degrade by reacting with hydroxyl radicals (produced photochemically) with half life of 1.5 hr in summer and 15 hr in winter.

Detected in 114 U.S. rural areas: av-0.5ppb, max-37ppb

1885 U.S. urban : av-1.9ppb, max-89ppb (2)

When spilt on land o-xylene will volatilise and leach into ground where it will degrade in either aerobic (70% degradation after 10 days) or anaerobic (6 months before degradation starts) denitrifying conditions.

Soil type and microbial acclimatization affect extent of degradation.(2)

If released to surface water, volatilisation is main removal process with a half life of 1-5 days. Absorption to sediment will occur.

Regularly detected in U.S.treated drinking water, groundwater,surface water.

Water MRL:

EPA DATA GAPS:

** Disclaimer: These sheets are designed as summary information and as such are a guide only. The information is compiled from publicly available references which can be supplied on request.



References:

1.Canadian Department of Occupational Health Database, CCINFO Xylene 1991

2.Handbook of Environmental Fate and Exposure Data for Organic Chemicals,

Vol 1, Large Production and Priority Pollutants, Philip H.Howard

Lewis Pub.1989

3.Pesticides and Human Health, W.H.Hallenbeck&K.M.Cunningham-Burns School

of Public Health, Uni. of Illinois Chicago, Springer-Verlag 1985

4.Coffs Harbour Chemical Data base 1991