Triazine herbicides
| 1. NAME |
| 1.1 Substance |
| 1.2 Group |
| 1.3 Synonyms |
| 1.4 Identification numbers |
| 1.4.1 CAS number |
| 1.4.2 Other numbers |
| 1.5 Main brand names, main trade names |
| 1.6 Main manufacturers, main importers |
| 2. SUMMARY |
| 2.1 Main risks and target organs |
| 2.2 Summary of clinical effects |
| 2.3 Diagnosis |
| 2.4 First aid measures and management principles |
| 3. PHYSICO-CHEMICAL PROPERTIES |
| 3.1 Origin of the substance |
| 3.2 Chemical structure |
| 3.3 Physical properties |
| 3.3.1 Colour |
| 3.3.2 State/Form |
| 3.3.3 Description |
| 3.4 Hazardous characteristics |
| 4. USES |
| 4.1 Uses |
| 4.1.1 Uses |
| 4.1.2 Description |
| 4.2 High risk circumstance of poisoning |
| 4.3 Occupationally exposed populations |
| 5. ROUTES OF EXPOSURE |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Other |
| 6. KINETICS |
| 6.1 Absorption by route of exposure |
| 6.2 Distribution by route of exposure |
| 6.3 Biological half-life by route of exposure |
| 6.4 Metabolism |
| 6.5 Elimination and excretion |
| 7. TOXICOLOGY |
| 7.1 Mode of action |
| 7.2 Toxicity |
| 7.2.1 Human data |
| 7.2.1.1 Adults |
| 7.2.1.2 Children |
| 7.2.2 Relevant animal data |
| 7.2.3 Relevant in vitro data |
| 7.2.4 Workplace standards |
| 7.2.5 Acceptable daily intake (ADI) |
| 7.3 Carcinogenicity |
| 7.4 Teratogenicity |
| 7.5 Mutagenicity |
| 7.6 Interactions |
| 8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS |
| 8.1 Material sampling plan |
| 8.1.1 Sampling and specimen collection |
| 8.1.1.1 Toxicological analyses |
| 8.1.1.2 Biomedical analyses |
| 8.1.1.3 Arterial blood gas analysis |
| 8.1.1.4 Haematological analyses |
| 8.1.1.5 Other (unspecified) analyses |
| 8.1.2 Storage of laboratory samples and specimens |
| 8.1.2.1 Toxicological analyses |
| 8.1.2.2 Biomedical analyses |
| 8.1.2.3 Arterial blood gas analysis |
| 8.1.2.4 Haematological analyses |
| 8.1.2.5 Other (unspecified) analyses |
| 8.1.3 Transport of laboratory samples and specimens |
| 8.1.3.1 Toxicological analyses |
| 8.1.3.2 Biomedical analyses |
| 8.1.3.3 Arterial blood gas analysis |
| 8.1.3.4 Haematological analyses |
| 8.1.3.5 Other (unspecified) analyses |
| 8.2 Toxicological Analyses and Their Interpretation |
| 8.2.1 Tests on toxic ingredient(s) of material |
| 8.2.1.1 Simple Qualitative Test(s) |
| 8.2.1.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.1.3 Simple Quantitative Method(s) |
| 8.2.1.4 Advanced Quantitative Method(s) |
| 8.2.2 Tests for biological specimens |
| 8.2.2.1 Simple Qualitative Test(s) |
| 8.2.2.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.2.3 Simple Quantitative Method(s) |
| 8.2.2.4 Advanced Quantitative Method(s) |
| 8.2.2.5 Other Dedicated Method(s) |
| 8.2.3 Interpretation of toxicological analyses |
| 8.3 Biomedical investigations and their interpretation |
| 8.3.1 Biochemical analysis |
| 8.3.1.1 Blood, plasma or serum |
| 8.3.1.2 Urine |
| 8.3.1.3 Other fluids |
| 8.3.2 Arterial blood gas analyses |
| 8.3.3 Haematological analyses |
| 8.3.4 Interpretation of biomedical investigations |
| 8.4 Other biomedical (diagnostic) investigations and their interpretation |
| 8.5 Overall interpretation of all toxicological analyses and toxicological investigations |
| 8.6 References |
| 9. CLINICAL EFFECTS |
| 9.1 Acute poisoning |
| 9.1.1 Ingestion |
| 9.1.2 Inhalation |
| 9.1.3 Skin exposure |
| 9.1.4 Eye contact |
| 9.1.5 Parenteral exposure |
| 9.1.6 Other |
| 9.2 Chronic poisoning |
| 9.2.1 Ingestion |
| 9.2.2 Inhalation |
| 9.2.3 Skin exposure |
| 9.2.4 Eye contact |
| 9.2.5 Parenteral exposure |
| 9.2.6 Other |
| 9.3 Course, prognosis, cause of death |
| 9.4 Systematic description of clinical effects |
| 9.4.1 Cardiovascular |
| 9.4.2 Respiratory |
| 9.4.3 Neurological |
| 9.4.3.1 Central nervous system (CNS) |
| 9.4.3.2 Peripheral nervous system |
| 9.4.3.3 Autonomic nervous system |
| 9.4.3.4 Skeletal and smooth muscle |
| 9.4.4 Gastrointestinal |
| 9.4.5 Hepatic |
| 9.4.6 Urinary |
| 9.4.6.1 Renal |
| 9.4.6.2 Other |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatological |
| 9.4.9 Eye, ear, nose, throat: local effects |
| 9.4.10 Haematological |
| 9.4.11 Immunological |
| 9.4.12 Metabolic |
| 9.4.12.1 Acid-base disturbances |
| 9.4.12.2 Fluid and electrolyte disturbances |
| 9.4.12.3 Others |
| 9.4.13 Allergic reactions |
| 9.4.14 Other clinical effects |
| 9.4.15 Special risks |
| 9.5 Other |
| 9.6 Summary |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Life supportive procedures and symptomatic/specific treatment |
| 10.3 Decontamination |
| 10.4 Enhanced elimination |
| 10.5 Antidote treatment |
| 10.5.1 Adults |
| 10.5.2 Children |
| 10.6 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from literature |
| 12. Additional information |
| 12.1 Specific preventive measures |
| 12.2 Other |
| 13. REFERENCES |
| 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES) |
Triazine Herbicides
International Programme on Chemical Safety
Poisons Information Monograph G013 (Group PIM)
Chemical
This Monograph has the following sections
completed: 1, 2, 3, 4, 5, 7, 9, & 10.
1. NAME
1.1 Substance
Triazine herbicides
1.2 Group
This group includes amitrole (aminotriazole), atrazine,
cyanazine, simazine and trietazine.
1.3 Synonyms
Amitrole:
Amerol; Amino triazole weedkiller 90;
Aminotriazol-spritzpulver;
Aminotriazole; Amitol;
Amitril; Amitril T.L.;
Amitrol; Amitrol 90;
Amitrol-T; Amizol; Amizol D;
Amizol DP NAU; Amizol F;
AT; AT liquid; AT-90;
ATA; Azaplant;
Azaplant kombi; Azolan;
Azole; Campaprim A 1544;
Cytrol; Cytrol amitrole-T;
Cytrole; Diurol;
Diurol 5030; Domatol;
Domatol 88; Elmasil; Emisol;
Emisol 50; Emisol F;
ENT 25445; Fenamine;
Fenavar; Herbidal total;
Herbizole; Kleer-lot;
Orga-414; Radoxone TL;
Ramizol; RCRA waste number U011;
Simazol; Solution concentree T271;
Triazolamine; USAF XR-22;
Vorox; Vorox AA; Vorox AS;
Weedar ADS; Weedar AT;
Weedazin; Weedazin arginit;
Weedazol; Weedazol GP2;
Weedazol super; Weedazol T;
Weedazol TL; Weedex granulat;
Weedoclor; X-All liquid;
Atrazine:
A 361; Aatram 20G; Aatrex;
Aatrex 4L; Aatrex 80W;
Aatrex nine-O; Aktikon;
Aktikon PK; Aktinit A;
Aktinit PK; Aneldazin;
Argezin; Atazinax; Atranex;
Atrasine; Atratol A;
Atrazin; Atred; Atrex;
Candex; Cekuzina-T;
Chromozin; Crisatrina;
Crisazine; Cyazin;
Farmco atrazine; Fenamin;
Fenamine; Fenatrol; G 30027;
Geigy 30,027; Gesaprim;
Gesoprim; Giffex 4L;
Griffex; Herbatoxol;
Hungazin; Hungazin PK;
Inakor; Oleogesaprim;
Primatol; Primatol A;
Primaze; Radazin; Radizine;
Shell atrazine herbicide; Strazine;
Triazine A 1294; Vectal;
Vectal SC; Weedex A; Wonuk;
Zeaphos; Zeapos; Zeazin;
Zeazine; Zeopos;
Cyanazine:
Bladex; Bladex 80WP;
Blanchol; DW3418; Fortrol;
Payze; Propanenitrile; SD
15418; WL 19805;
Simazine:
A 2079; Aktinit S; Aquazine;
Azotop; Batazina; Bitemol;
Bitemol S 50; CAT; CDT;
Cekusan; Cekusima;
Cekuzina-S; CET; Framed;
G 27692; Geigy 27,692;
Gesaran; Gesatop;
Gesatop 50; H 1803;
Herbatoxol S; Herbazin;
Herbazin 50; Herbex;
Herboxy; Hungazin DT;
Premazine; Primatol S;
Princep; Printop; Radocon;
Radokor; Simadex; Simanex;
Simatsin-neste; Simazin;
Simazine; Simazine 80W;
Symazine; Tafazine;
Tafazine 50-W; Taphazine;
Triazine A 384; W 6658;
Weedex; Yrodazin; Zeapur;
Trietazine:
Aventox; Bronox; 27901;
Gesafloc; NC 1667; Remtal;
1.4 Identification numbers
1.4.1 CAS number
Amitole: 61-82-5
Atrazine: 1912-24-9
Cyanazine: 21725-46-2
Simazine: 122-34-9
Trietazine: 1912-26-1
1.4.2 Other numbers
Amitrole NIOSH/RTECS: XZ3850000
Simazine NIOSH/RTYECS: XY5250000
Trietazine NIOSH/RTECS: XY5425000
1.5 Main brand names, main trade names
1.6 Main manufacturers, main importers
2. SUMMARY
2.1 Main risks and target organs
Triazine herbicides are of low toxicity to humans.
2.2 Summary of clinical effects
Ingestion: Nausea, vomiting, diarrhoea, abdominal pain
and a burning sensation in the mouth.
However, due to the lack of clinical data serious effects
cannot be excluded from large dose deliberate ingestions. In
the case of products with organic solvents, aspiration can
develop. Ataxia, anorexia, dyspnoea and muscle spasms have
all been reported in animal studies but have not been seen in
humans.
Inhalation: There may be irritation from fine dust and some
preparations may contain organic solvents.
Skin: Although triazine herbicides are thought to be non
irritant, there are a few reports of contact dermatitis in
the literature.
Eye: Triazine herbicides may be slightly irritant to the
eye.
2.3 Diagnosis
History of exposure to triazine herbicides, and
gastrointestinal (GI) irritation, are sufficient for the
diagnosis.
2.4 First aid measures and management principles
Ingestion: In most cases there is probably no need for
anything other than oral fluids and reassurance. If a very
large amount has been ingested then consider:
adult: gastric lavage (with a cuffed endotracheal tube if an
organic solvent is involved) followed by 50 g activated
charcoal,
child: 1 g/kg activated charcoal. Do not induce vomiting if
product contains an organic solvent. Observe the patient if a
large dose has been ingested. Symptomatic and supportive
care.
Inhalation: Remove to fresh air. Give oxygen if necessary.
Bronchodilators may be given if indicated. Otherwise treat
for the particular solvent involved.
Skin: Wash with copious amounts of water and prevent
drying/cracking (due to solvent) with an emollient such as
E45 cream.
Eye: Irrigate for 15 to 20 minutes with running water or
saline. Refer to an ophthalmologist.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Synthetic
3.2 Chemical structure
Amitrole
Chemical Name:
3-Amino-s-triazole;
1-H-1,2,4-triazol-3-ylamine (IUPAC chemical name);
1H-1,2,4-Triazol-3-Amine (CAS chemical name);
2-Amino-1,3,4-triazole;
2-Aminothiazole;
2-Aminotriazole;
3,A-T; 3-Amino-1,2,4-triazole;
3-Amino-1H-1,2,4-triazole;
3-Amino-s-triazole;
3-Aminotriazole
Molecular formula: C2H4N4
Molecular weight: 84.08
Atrazine
Chemical names:
1,3,5-Triazine-2,4-Diamine;
6-Chloro-N-Ethyl-N'-(1-Methylethyl)-;
1,3,5-Triazine-2,4-diamine;
6-chloro-N-ethyl-N'-(1-methylethyl)- (9CI);
1-Chloro-3-Ethylamino-5-Isopropylamino-2,4,6-Triazine;
1-Chloro-3-Ethylamino-5-Isopropylamino-S-Triazine;
2-Aethylamino-4-chlor-6-isopropylamino-1,3,5-triazin;
2-Aethylamino-4-Chlor-6-Isopropylamino-1,3,5-Triazin
(German);
2-Aethylamino-4-isopropylamino-6-chlor-1,3,5-triazin;
2-Chloro-4-(2-Propylamino)-6-Ethylamino-S-Triazine;
2-Chloro-4-ethylamineisopropylamine-s-triazine;
2-Chloro-4-Ethylamino-6-Isopropylamino-1,3,5-Triazine;
2-Chloro-4-ethylamino-6-isopropylamino-s-triazine;
2-Chloro-4-ethylamino-6-isorpopylamino-s-triazine;
6-Chloro-N-ethyl-N'-(1-methylethyl)-1,3,5-triazine-2,4-
diamin;
Cyanazine:
Chemical names:
2-((4-Chloro-6-(ethylamino)-s-triazin-2-yl)amino)-2-
methylproionitrile
2-(4-Chloro-6-ethylamino-1,3,5-triazine-2-ylamino)-2-
methylprpionitrile
2-(4-Chloro-6-ethylamino-s-triazine-2-ylamino)-2-methyl-
propinitrile
2-Chloro-4-(1-cyano-1-methylethylamino)-6-ethylamino-1,3,5-
trazine
2-((4-chloro-6-(ethylamino)-1,3,5-triazin-2-yl)amino)-2-
methy-s-Triazine
2-chloro-4-ethylamino-6-(1-cyano-1-methyl)ethylamino
Simazine:
Chemical names:
1,3,5-Triazine-2,4-diamine, 6-chloro-N,N'-diethyl-
1-Chloro, 3,5-bisethylamino-2,4,6-triazine
2,4-Bis(aethylamino)-6-chlor-1,3,5-triazin
2,4-Bis(ethylamino)-6-chloro-s-triazine
2-Chloro-4,6-bis(ethylamino)-1,3,5-triazine
2-Chloro-4,6-bis(ethylamino)-s-triazine
4,6-Bis(ethylamino)-2-chlorotriazine
6-Chloro-N,N'-diethyl-1,3,5-triazine-2,4-diamine
Trietazine
Chemical names:
s-Triazine, 2-chloro-4-(diethylamino)-6-(ethylamino)-
1,3,5-Triazine-2,4-diamine, 6-chloro-N,N,N'-triethyl-
2-Chloro-4-(diethylamino)-6-(ethylamino)-s-triazine
2-Ethylamino-4-diethylamino-6-chloro-s-triazine
6-Chloro-N(sup 2),N(sup 2),N(sup
4)-triethyl-1,3,5-triazine-2,4-diamine (IUPAC)
6-Chloro-N,N,N'-triethyl-1,3,5-triazine-2,4-diamine
3.3 Physical properties
3.3.1 Colour
See section 3.3.3
3.3.2 State/Form
See section 3.3.3
3.3.3 Description
Most are poorly soluble in water and only
slightly soluble in organic solvents. They are
available as solutions (some in organic solvents),
suspensions or as dispersable powders and may be
combined with other herbicides (such as
phenoxyacetates, sodium chlorate or paraquat) or
fungicides.
Amitrole
Pure amitrole is a colourless crystalline powder with
a bitter taste. It is a strong chelating agent with a
melting point of 153 to 159°C and a specific gravity
of 1.138 at 20°C.
Solubility: 300 g/L water at 20°C;
260 g/kg ethanol at 75°C;
moderately soluble in methylene chloride,
chloroform; insoluble in acetone, diethyl
ether and hydrocarbons.
Stability: Amitrole is thermally stable. It is also
stable in neutral or alkaline media, but it forms
salts. It breaks down in ultraviolet light. Forms
chelates with metals, and is thus corrosive to
aluminium, copper and iron.
(WHO/FAO, 1994)
3.4 Hazardous characteristics
Amitrole:
The substance decomposes on heating producing toxic fumes of
nitrogen oxides. Amitrole is a weak base. It reacts with
strong acids, strong oxidants, acid chlorides and acid
anhydrides. It attacks iron, copper and aluminium.
4. USES
4.1 Uses
4.1.1 Uses
Pesticide for use on plants
Herbicide
4.1.2 Description
Triazine herbicides are used as selective
weedkillers.
They act by inhibiting photosynthesis.
4.2 High risk circumstance of poisoning
4.3 Occupationally exposed populations
Manufacturers and packers of the herbicides.
Those mixing and using the herbicides.
5. ROUTES OF EXPOSURE
5.1 Oral
Triazine herbicides are available as water soluble powders.
5.2 Inhalation
Risk of inhalation ofthe powder.
5.3 Dermal
Exposure can occur due to the liquid formulation.
5.4 Eye
Exposure can occur due to the liquid formulation.
5.5 Parenteral
Not known.
5.6 Other
Not known.
6. KINETICS
6.1 Absorption by route of exposure
6.2 Distribution by route of exposure
6.3 Biological half-life by route of exposure
6.4 Metabolism
6.5 Elimination and excretion
7. TOXICOLOGY
7.1 Mode of action
Amitrole has been shown to be goitrogenic in a number of
animal species. Amitole reduces thyroid uptake of iodine and
inhibits the peroxidase activity of the thyroid. The
resulting reduction of thyroid hormones induces a
hypothalamus mediated TSH stimulation on the thyroid itself.
This prolonged stimulation is thought to be responsible for
the induction of thyroid cancers in animals treated with high
doses of amitrole (WHO/FAO, 1994).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
There are no reports of fatalities
from ingestion of triazines in the
literature. One patient developed gastritis
after ingesting 400 mL of an unknown
concentration of atrazine + aminotriazole
(amitrole) (NPIS, 1997).
A single case report describes the
development of a chemical pneumonitis after
one exposure to an amitrole spray containing
19% aminotriazole, 17% ammonium thiocyanate,
less than 1% sodium diethylsulfosuccinate and
less than 1% ethylene oxide (WHO/FAO, 1994).
At an estimated dermal exposure of 340
mg/day/man over a 10 day spraying operation
no thyroid dysfunctions were detected
(WHO/FAO, 1994).
Prolonged exposure for up to 16 years to
unknown levels of amitrole during its
production and packaging did not cause
thyroid disfunction (WHO/FAO, 1994).
Observations in occupationally exposed
workers:
Observations on volunteers: A single oral
dose of 100 mg of amitrole inhibited 131I
intake of the thyroid for 24 hours in healthy
and hyperthyrotid individuals. A dose of 10
mg produced only slight effects (WHO/FAO,
1994).
Amitrole had no irritant effect in a 4 to 8
hour exposure dermal patch test, and had only
slight irritancy after 24 hours exposure
(WHO/FAO, 1994).
7.2.1.2 Children
7.2.2 Relevant animal data
Chronic high dose triazine administration in
rats has resulted in growth retardation, slight
leucopaenia and modification of liver metabolism.
Aminotriazole or amitrole is reported to have
antithyroid effects in laboratory animals but this has
not been demonstrated in humans.
Oral LD50
Rat 5 000 mg/kg b.w.
Rat 25 000 mg/kg b.w.
Mouse 11 000 to 14 700 mg/kg b.w.
Rabbit >2 150 mg/kg b.w.
Intraperitoneal LD50
Mouse >4 000 mg/kg b.w.
Intravenous LD50
Mouse 5 000 mg/kg b.w.
Rat >2 500 mg/kg b.w.
Dermal LD50 (24h)
Rabbit >10 000 mg/kg b.w.
Inhalation LC50 (4h)
Rat >439 mg/L
(WHO/FAO, 1994)
7.2.3 Relevant in vitro data
7.2.4 Workplace standards
Exposure Limits TLV: ppm: 0.2 mg/m3 (as TWA)
(WHO/FAO, 1994)
7.2.5 Acceptable daily intake (ADI)
7.3 Carcinogenicity
High doses of amitrol induce thyroid cancers in
experimental animals (WHO/FAO, 1994).
7.4 Teratogenicity
No teratogenic effects have been detected in rats given
up to 1000 mg/kg body weight day on days 6 to 15 gestation
(WHO/FAO, 1994).
7.5 Mutagenicity
Amitrole was not mutagenic to the repair deficient
strains of Escherichia coli nor to several strains of
Salmonella typhimurium with or without metabolic
activation. Weak mutagenic activity was observed with
Streptomyces coelicolor . No evidence of chromosomal damage
was observed following in vitro incubation of human
leucocytes with 0.2 to 1% (w/v) amitrole. Concentrations
over 0.2% were cytotoxic, inhibiting lymphoblast
transformation.
Male and female Drosophila melanogaster reared on 10 mg
amitrole/kg media showed no evidence of amitrole induced
sex-chromosome non-disjunction or sex-linked dominant lethal
mutations (WHO/FAO, 1994).
7.6 Interactions
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.2 Urine
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
interpretation
8.5 Overall interpretation of all toxicological analyses and
toxicological investigations
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Nausea, vomiting, diarrhoea, abdominal pain and
a burning sensation in the mouth.
However due to the lack of clinical data serious
effects cannot be excluded from large dose deliberate
ingestions. In the case of organic solvent containing
products, aspiration can develop. Ataxia, anorexia,
dyspnoea and muscle spasms have all been reported in
animal studies but have not been seen in humans.
9.1.2 Inhalation
There may be irritation from fine dust in some
preparations. Some preparations may contain organic
solvents.
9.1.3 Skin exposure
Although triazine herbicides are thought to be
non irritant, there are a few reports of contact
dermatitis in the literature (Schlicher & Beat, 1972).
9.1.4 Eye contact
Triazine herbicides may be slightly irritant to
the eye.
9.1.5 Parenteral exposure
Not known.
9.1.6 Other
Not known.
9.2 Chronic poisoning
9.2.1 Ingestion
9.2.2 Inhalation
9.2.3 Skin exposure
9.2.4 Eye contact
9.2.5 Parenteral exposure
9.2.6 Other
9.3 Course, prognosis, cause of death
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
9.4.2 Respiratory
9.4.3 Neurological
9.4.3.1 Central nervous system (CNS)
9.4.3.2 Peripheral nervous system
9.4.3.3 Autonomic nervous system
9.4.3.4 Skeletal and smooth muscle
9.4.4 Gastrointestinal
9.4.5 Hepatic
9.4.6 Urinary
9.4.6.1 Renal
9.4.6.2 Other
9.4.7 Endocrine and reproductive systems
9.4.8 Dermatological
9.4.9 Eye, ear, nose, throat: local effects
9.4.10 Haematological
9.4.11 Immunological
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
9.4.12.2 Fluid and electrolyte disturbances
9.4.12.3 Others
9.4.13 Allergic reactions
9.4.14 Other clinical effects
9.4.15 Special risks
9.5 Other
9.6 Summary
10. MANAGEMENT
10.1 General principles
Ingestion: In most cases there is probably no need
for anything other than oral fluids and reassurance. If a
very large amount has been ingested then consider for:
adult: gastric lavage (with a cuffed endotracheal tube if an
organic solvent is involved) followed by 50 g activated
charcoal.
child: 1 g/kg activated charcoal. Do not induce vomiting if
product contains an organic solvent. Observe the patient if a
large dose has been taken. Symptomatic and supportive
care.
Inhalation: Remove to fresh air. Give oxygen if necessary.
Bronchodilators may be given if indicated. Otherwise treat
for the particular solvent involved.
Skin: Wash with copious amounts of water and prevent
drying/cracking (due to solvent) with an emollient such as
E45 cream.
Eye: Irrigate for 15-20 min with running water or saline.
Refer to an ophthalmologist.
10.2 Life supportive procedures and symptomatic/specific treatment
See section 10.1
10.3 Decontamination
If a very large amount has been ingested then consider
for:
adult: gastric lavage (with a cuffed endotracheal tube if an
organic solvent is involved) followed by 50 g activated
charcoal.
child: 1 g/kg activated charcoal. Do not induce vomiting if
product contains an organic solvent. Observe the patient if a
large dose has been taken. Symptomatic and supportive
care.
10.4 Enhanced elimination
See section 10.1
10.5 Antidote treatment
10.5.1 Adults
No antidote available.
10.5.2 Children
No antidote available.
10.6 Management discussion
See section 10.1
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
12. Additional information
12.1 Specific preventive measures
12.2 Other
13. REFERENCES
NPIS (1997) National Poisons Information Service, London, UK.
Schlicher J.E. & Beat V.B. (1972) Dermatitis resulting from
herbicide use - a case study. J. Iowa Med. Soc. 62(8): 419-420
WHO/FAO (1994) Amitrole Data Sheet on Pesticides No.79. World
Health Organization, Geneva, Switzerland
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: Medical Toxicology Unit,
Guyœs and St Thomasœ Trust
Avonley Road, London SE14 5ER, UK
Date: March, 1997
Review: As for author. 1997
Peer review: INTOX meeting, March 1998, London, UK
(Members of group: Drs G. Allridge, L.
Lubomovir, R. Turk, C. Alonso, S. de Ben, K.
Hartigan-Go, N. Bates)
Editor: Dr M.Ruse (September, 1998)