Rotenone
| 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/CIRCUMSTANCES OF POISONING |
| 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 ENTRY |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Others |
| 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 by route of exposure |
| 7. TOXICOLOGY |
| 7.1 Mode of Action |
| 7.2 Toxicity |
| 7.2.1 Human data |
| 7.2.1 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 Others |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatological |
| 9.4.9 Eye, ears, 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 Others |
| 9.6 Summary |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Life supportive procedures and symptomatic 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) |
ROTENONE
International Programme on Chemical Safety
Poisons Information Monograph 474
Chemical
1. NAME
1.1 Substance
Rotenone
1.2 Group
Insecticide
1.3 Synonyms
Derrin;
Nicouline;
Rotenonum;
Tubatoxin;
1.4 Identification numbers
1.4.1 CAS number
83-79-4
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
Inhalation or ingestion of large doses may cause
numbness of oral mucous membranes, nausea and vomiting,
muscle tremors, tachypnea. With lethal doses respiratory
paralysis occurs. Chronic poisoning may produce fatty
changes in liver and kidneys. Direct contact occasionally
causes mild irritation of skin or eyes. Rotenone is more
toxic when inhaled than when ingested.
Target organs: central nervous system, skin, mucous
membrane.
2.2 Summary of clinical effects
Respiratory effects mainly after inhalation are
coughing, sneezing, rhinorrhoea, respiratory stimulation
followed by depression, and severe pulmonary irritation from
inhalation of dusts. Pulmonary oedema and pneumonitis may
occur due to the aspiration of solvents or vehicle, which is
often kerosene. The immediate cause of death is
asphyxia.
Digestive symptoms include numbness of oral mucous membranes,
vomiting, and gastric pain.
Central nervous manifestations are muscle tremors,
incoordination, clonic convulsions, and lethargy. Skin and
conjunctival irritation from local contact.
2.3 Diagnosis
Nausea, vomiting, abdominal pain, numbness of the oral
mucosa, respiratory depression, tremors, lethargy and
convulsions occur following ingestion or inhalation.
Laboratory analysis of blood may show hypoglycaemia.
Vomitus or gastric aspirate should be collected in clean
bottles for identification.
2.4 First-aid measures and management principles
Ingestion: Induce vomiting unless the product vehicle
is a petroleum distillate (see the treatment protocol on
decontamination procedures)
Gastric lavage may be performed if a large amount of rotenone
was ingested even if it is dissolved in kerosene or a related
petroleum distillate.
A slurry of powdered activated charcoal in water should be
given by mouth after vomiting, or after about 30 minutes if
the patient does not vomit. Avoid ingestion of oils and fats,
which promote the absorption of rotenone.
Administer glucose intravenously.
If agitation or seizures occur, administer diazepam IV.
Inhalation: Provide symptomatic and supportive treatment.
Ensure patient's airway and ventilation.
Skin and eye contact: Wash thoroughly with water.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Rotenone is extracted from plants, particularly from
Derris spp grown in Malaya, East Indies, and South America,
and Lonchocarpus also known as "cubé", grown in Central and
South America. Examples are e.g Derris Amazonica Killip and
Derris Pterocarpus Killip. Other genera are Tephrosia,
Milletia, Mundulea, Spatholobus, and Pachyrhizus. These
plants have been known for centuries to be toxic to fish and
used to poison arrowheads. Rotenone is present mainly in the
roots of the plants. The roots are dried, ground, and the
active principle extracted with solvents such as chloroform
and benzene (Gosselin, 1984; Hayes, 1982).
3.2 Chemical structure
Chemical name: [2R-(2a, 6a alpha, 12a alpha)] - 1, 2,
12, 12a-tetrahydro-8,9-dimethoxy-2-(1-methylethyl)[I]
benzopyranol [3,4-b] furo 12,3-h] [I]benzopyran-6(6aH)-one
(Windholz, 1983).
Molecular weight = 394, 41
(C 70.04% H 5.62% 0 24.34%)
Structural formula:
3.3 Physical properties
3.3.1 Colour
3.3.2 State/Form
3.3.3 Description
Melting points 165 to 166°C (dimorphic form 181'C)
Vapour pressureless than 0.00001 mbar at 20°C
SolubilityPractically insoluble in water;
soluble 1 in 300 of alcohol, 1 in 12 of acetone, 1 in 3 of
chloroform, and 1 in 200 of ether (Reynolds, 1989).
3.4 Hazardous characteristics
The normal state at room temperature is colourless to
brownish crystals, or a white or brownish-white, odourless,
tasteless, crystalline powder. Unstable in the presence of
air or light. Colourless solutions of rotenone in organic
solvent, when exposed, become successively yellow, orange,
and finally deep red as a result of oxidation. Rotenone is
readily racemised by alkali and readily oxidized especially
in the presence of light and alkali. Store in airtight
container in temperatures not exceeding 25°C and protect from
light.
Environmental risks: the effects are short-lived. Rotenone
is not toxic to plants but extremely toxic to fish. Residues
must not be allowed to drain into streams (Windholz, 1983;
Reynolds, 1989; Hayes, 1982).
4. USES/CIRCUMSTANCES OF POISONING
4.1 Uses
4.1.1 Uses
4.1.2 Description
Rotenone is a widely used insecticide of
botanical origin. It is a selective non-systemic
insecticide with some acaricidal properties. Rotenone
is used alone or in combination with pyrethrins,
pyrethrum, and piperonyl butoxide to control a wide
variety of insects on food crops. In human and
veterinary medicine the compound has been applied
directly to treat lice, ticks, scabies and other
ectoparasites.
4.2 High risk circumstance of poisoning
Rotenone is a very safe compound when properly used.
The formulations are presented in low concentrations, (1 to
5%), have low solubility in water, and decompose rapidly when
exposed to light and air. The irritating properties to
mucous membranes provoke prompt vomiting, avoiding further
absorption.
Accidents have been reported in children who ingest large
doses. Gosselin (1984) reported no fatalities. De Wilde
(1986) reported one death in a child.
4.3 Occupationally exposed populations
Agricultural workers and pesticide applicators are
occupationally exposed. Factory workers processing rotenone
without proper protection have developed rhinitis and
dermatitis (Hayes, 1982).
5. ROUTES OF ENTRY
5.1 Oral
Accidental or deliberate ingestion of the product may
occur.Gastrointestinal absorption is slow and incomplete. Its
irritant effect on mucous membranes induces immediate
vomiting (Gosselin, 1984).
5.2 Inhalation
Inhalation of dusts of rotenone produces is a more
common cause of poisoning than ingestion and causes severe
pulmonary irritation (Gosselin, 1984).
5.3 Dermal
Direct contact with the skin occasionally causes mild
irritation.
5.4 Eye
Direct eye contact occasionally causes mild irritation
of conjunctiva.
5.5 Parenteral
Unknown
5.6 Others
Unknown
6. KINETICS
6.1 Absorption by route of exposure
Gastrointestinal absorption is low and incomplete. In
animals, rotenone is hundreds of times more toxic
intravenously than orally. Fats and oils increase absorption
(Gosselin, 1984).
Inhalation of dusts or fine powders cause immediate pulmonary
irritation. Data on pulmonary or dermal absorption are not
available.
6.2 Distribution by route of exposure
No data are available concerning distribution after oral
ingestion or inhalation or dermal exposure.
6.3 Biological half-life by route of exposure
Unknown
6.4 Metabolism
Rotenone is metabolized by the liver. It inhibits the
oxidation of NADH to NAD, and blocks the oxidation by NAD of
substrates such as glutamate, alpha-ketoglutarate, and
pyruvate (Goodman, 1985).
After intravenous injection in the rat and mouse, rotenone is
metabolized by NADP-linked hepatic microsomal enzymes.
Several metabolites have been identified as rotenoids
(rotenolone I and II, hydroxy and dihydroxyrotenones, etc.)
with a toxicity similar to rotenone. One mechanism of
metabolism was demethylation (Hayes, 1982; Gosselin,
1984).
6.5 Elimination by route of exposure
In the mouse and rat, approximately 20% of a dose is
recovered in urine within 24 hours of oral administration
(Hayes, 1982).
7. TOXICOLOGY
7.1 Mode of Action
Rotenone inhibits the oxidation of NADH to NAD, blocking
the oxidation by NAD of substrates such as glutamate,
alpha-ketoglutarate, and pyruvate. Rotenone inhibits the
mitochondrial respiratory chain between diphosphopyridine
nucleotide and flavine. This blockade is overcome by Vitamin
K3 (menadione sodium bisulphite), which apparently activates
a bypass of the rotenone sensitive site. Rotenone is a
powerful inhibitor of mitochondrial electron transport. The
regulation of fatty acid synthesis in mitochondria by
rotenone may be altered after chronic administration,
resulting in fatty changes in the liver (Hayes, 1982;
Gosselin, 1984; Goodman & Gilman, 1985).
7.2 Toxicity
7.2.1 Human data
7.2.1 Adults
<7.2.1.>Mean lethal oral dose is about 0.3 to 0.5 g/kg
(Gosselin, 1984).
7.2.1.2 Children
Mean lethal oral dose is estimated
from 0.3 to 0.5 g/kg (Gosselin, 1984).
In one fatal case, postmortem concentrations
of rotenone in the stomach and blood were
1,260 and 2.4 ppm (De Wilde, 1986).
7.2.2 Relevant animal data
The lethal dose in mammals range from 50 mg to
3000 g/kg (Ellenhorn and Barceloux, 1988).
Lethal Dose 50 (mg/kg)
Rat (oral) 60 to 132
Rat (intravenous) 0.2 to 0.3
Mouse (intraperitonial) 5.4
Rabbit (oral) 1.5
Rabbit (dermal) 100 to 200
Rabbit (intravenous) 0.35 to 0.65 (Hayes, 1982)
In the rat and dog, experimental inhalation of
rotenone dust produced symptoms within minutes. The
onset of poisoning was more rapid than after oral
administration and the fatal dose was lower (Hayes,
1982).
Rotenone is highly toxic to fish.
7.2.3 Relevant in vitro data
In isolated rat liver mitochondria, the aerobic
oxidation of pyruvate is almost completely inhibited
by rotenone. yolitic effects are also described
(Hayes, 1982).
7.2.4 Workplace standards
The TLV-TWA (Threshold limit Value-time
Weighted Average) for commercial rotenone is 5 mg/m3
(American Conference of Governmental Industrial
Hygienists, 1987-8). This indicates that an
occupational intake of 0.7 mg/kg/day is considered
safe (Hayes, 1982).
7.2.5 Acceptable daily intake (ADI)
The proposed No-Adverse-Response Level (SNARL)
for chronic exposure to rotenone: 0.014 mg/l
(National Research Council, 1983).
7.3 Carcinogenicity
The carcinogenicity of rotenone is a controversial
issue. It has been suggested that rotenone may cause tumours
only in vitamin-deficient animals (Gosalvez, 1983).
7.4 Teratogenicity
No data available.
7.5 Mutagenicity
No mutagenic effects were reported in mouse bone marrow
(Waters et al, 1982). Rotenone is non-mutagenic in bacterial
reversion tests (Moriya et al, 1983)
7.6 Interactions
When applied in low concentrations to plant foliage,
rotenone catalyses photoisomerization of dieldrin and other
cyclodiene insecticide residues. However, photodecomposition
was a predominant effect when residues of rotenone were
combined with those of methylcarbamate and phosphothionate
insecticides (Hayes, 1975).
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
Sample collection
Collect blood and gastric aspirate/vomitus for analysis.
Biomedical analysis
Determine blood glucose, acid base status, and serum
electrolytes.
Blood: Full blood count (red cells), white cell and platelet
count).
Urine: Urinalysis to detect red and white blood cells.
In animals, chemical investigations in blood and urine showed
severe hypoglycaemia. In man, electrolytes may be altered
after convulsions. Liver failure has been reported in
animals.
Arterial blood gases and acid-base balance may be altered
because severe overdoses may cause hypoxemia and hypercapnia
due to respiratory depression and seizures. Acid-base
abnormalities follow hypoxemia.
Experimentally, myocardial contractile force is impaired
(Hayes, 1982).
Toxicological analysis
No information available.
Other investigations
No information available.
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
After ingestion, signs and symptoms are:
numbness of oral mucous membranes, pharyngitis,
nausea, vomiting, and gastric pain. Muscle tremors,
lethargy, respiratory stimulation followed by
depressed respiration (Hayes, 1982; Gosselin, 1984).
In one case (De Wilde, 1986 cardiopulmonary arrest was
the cause of death. Animal experiments indicate that
hypoglycaemia may occur.
9.1.2 Inhalation
Rhinitis, coughing, and sneezing occur. In
experimental acute poisoning, onset of symptoms is
fast when dusts or fine powders are inhaled. Severe
pulmonary irritation and asphyxia were present (Hayes,
1982).
9.1.3 Skin exposure
Skin irritation is observed after local
application.
9.1.4 Eye contact
Conjunctivitis and photophobia.
9.1.5 Parenteral exposure
Experimentally: vomiting, incoordination,
muscle tremors, clonic convulsions, and respiratory
failure (Gosselin, 1984).
9.1.6 Other
No data available.
9.2 Chronic poisoning
9.2.1 Ingestion
In animals, chronic ingestion causes growth
depression (Gosselin, 1984).
9.2.2 Inhalation
Ulcerative rhinitis and complete but transient
loss of smell. Irritation of the throat with partial
destruction of the soft palate as well as of the
anterior pillars (Hayes, 1982).
9.2.3 Skin exposure
Occupational chronic exposure produces
important immediate dermatitis characterized by a
red-violet colour, slight oedema, and some itching.
If contact is stopped, desquamation occurs and
dermatitis became worse,with large papules (Hayes,
1982).
9.2.4 Eye contact
Conjunctivitis
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
Exposure to low doses of rotenone causes numbness of
oral mucous membranes, nausea, vomiting, and gastric pain.
In acute cases, large doses cause early respiratory
stimulation followed by depression and stupor. Terminal
symptoms of rotenone poisoning involve convulsions and
cardiorespiratory arrest (Gosselin, 1984; Ellenhorn, 1988).
In animals, most effects are due to severe
hypoglycaemia.
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Acute: Tachycardia, hypotension, impaired
myocardial contractility (experimentally).
Chronic: No data available.
9.4.2 Respiratory
Acute: tachypnea, followed by respiratory
depression, cyanosis, hypoxemia, mainly after
convulsions. Asphyxia from respiratory arrest.
Severe pulmonary irritation from inhalation of dusts
or fine powders.
Chronic: Pharyngitis, bronchitis.
9.4.3 Neurological
9.4.3.1 Central Nervous System (CNS)
Acute: Incoordination, tremors,
clonic convulsions, stupor.
Chronic: No data available.
9.4.3.2 Peripheral nervous system
Rotenone causes a definite
anaesthetic effect when brought into intimate
contact with nerve axon, efferent fibres
being more sensitive than efferent ones
(Hayes, 1982).
9.4.3.3 Autonomic nervous system
No data available.
9.4.3.4 Skeletal and smooth muscle
Muscular tremor.
9.4.4 Gastrointestinal
Acute: Nausea, vomiting, abdominal cramps.
9.4.5 Hepatic
Chronic poisoning may produce fatty changes in
liver (Windholz, 1983).
9.4.6 Urinary
9.4.6.1 Renal
Chronic poisoning may produce fatty
changes in the kidneys (Windholz,
1983).
9.4.6.2 Others
No data available.
9.4.7 Endocrine and reproductive systems
No data available.
9.4.8 Dermatological
Acute: skin irritation results from local
application.
Chronic: contact dermatitis with erythema, itching,
desquamation, papules.
9.4.9 Eye, ears, nose, throat: local effects
Acute: rhinitis, sneezing, irritation of the
conjunctiva.
Chronic: sneezing and coryza-like symptoms. Severe
irritation of the throat, partial destruction of the
soft palate and anterior pillars.
Ulcerative keratitis.
9.4.10 Haematological
No data available.
9.4.11 Immunological
No data available.
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
Acid-base disturbances may occur
after hypoxemia following
seizures.
9.4.12.2 Fluid and electrolyte disturbances
Vomiting may result in loss of
fluids in severe poisoning.
9.4.12.3 Others
No data available.
9.4.13 Allergic reactions
Skin sensitization after local contact.
9.4.14 Other clinical effects
No data available.
9.4.15 Special risks
No data available.
9.5 Others
No data available.
9.6 Summary
10. MANAGEMENT
10.1 General principles
Remove from exposure. Wash contaminated skin or eyes
thoroughly. Maintain airway and respiration. Administer
oxygen if cyanosis is present. If large amounts have been
ingested, perform cautious gastric lavage after intubation.
Emesis is contraindicated in case of convulsions or when the
product contains a petroleum distillate. Control agitation
and seizures with diazepam. Administer intravenous glucose
and vitamin K3 (menadione). Correct dehydration. Do not
administer lipids. After chronic poisoning, discontinue
exposure.
10.2 Life supportive procedures and symptomatic treatment
Assess the airway, respiration, circulation and
neurological status of the patient.
Monitoring cardiac rhythm, respiration and blood pressure.
Monitor fluid and electrolyte balance and acid-base balance.
If respiration is impaired maintain clear airway, aspirate
secretions, administer oxygen and support ventilation using
appropriate mechanical device.
Control convulsions with intravenous diazepam.
If cardiac arrest develops perform cardio-respiratory
resuscitation.
10.3 Decontamination
Gastric lavage may be indicated if a large amount of
rotenone was ingested, even if the product contains kerosene
or other petroleum distillate (Gosselin, 1984) (consult the
treatment protocol on decontamination procedures).
A slurry of activated charcoal in water is administered by
mouth or gastric lavage hose after emesis or lavage (or after
20 minutes if vomiting did not occur). The usual dose of 1
g/kg body weight in a dilution at least of 1.4 in water.
Avoid administration of oils and fats, which promote
absorption of rotenone. After inhalation, management is
symptomatic and supportive: remove from exposure, ensure a
clear airway and ventilate. Supportive measures include
oxygen and artificial respiration.
Wash skin and eyes thoroughly with running water. Control of
agitation and seizures with intravenous diazepam. Correct
hypoglycaemia with IV glucose 5%.
10.4 Enhanced elimination
No data available.
10.5 Antidote treatment
10.5.1 Adults
There is no specific antidote available.
10.5.2 Children
There is also no specific antidote available.
10.6 Management discussion
Management is mainly symptomatic. Experimentally,
menadione (Vitamin K3) antagonises the inhibition by rotenone
of mitochondrial respiration. Some authors therefore propose
a trial with large doses of menadione (Gosselin, 1984).
Hypoglycaemia has not been reported in man, but in the rabbit
and dog some of the neurological effects are due to severe
hypoglycaemia (Gosselin, 1984).
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
A 3.5 year-old child swallowed a pesticide containing
rotenone and developed stupor, vomiting, and depressed
respiration. At hospital, she had a cardiopulmonary arrest.
The postmortem concentrations of rotenone in the stomach and
blood were 1260 and 2.4 ppm (De Wilde, 1986).
Some cases of ingestion of the roots of plants (mainly
"derris") are reported by Hayes (1982) as common means of
suicide by natives of New Ireland. Acute congestive heart
failure was found at autopsy.
12. ADDITIONAL INFORMATION
12.1 Specific preventive measures
Wear suitable protective equipment (dust mask)
Do not work in strong winds
Do not blow out clogged nozzles with the mouth
Avoid all contact by mouth
Avoid contact with skin and eyes
Wash off splashes immediately
Avoid inhaling spray or dusts
Wash hands and exposed skin after use
Keep away from children
Keep away from food and drink
Keep in closed original containers, and store in a safe place
Wash out container thoroughly and dispose of safely
Ensure that all the safety precautions on the product label
are observed
In case of accident, seek medical advice immediately
12.2 Other
No data available.
13. REFERENCES
American Conference of Governmental Industrial Hygienists
(1987) Threshold Limit Values and Biological Exposures Indices
for 1987-1988. Cincinnati, Ohio 114p.
De Wilde AR, Heyndrickx A, Carton D (1986) A case of fatal
rotenone poisoning in a child. J Forensic Sci, 31:1492-8.
Ellenhorn MJ and Barceloux DG (1988). Medical Toxicology.
Diagnosis and treatment of human poisoing. New York. Elsevier
Goodman LS, Gilman AG, Rall TW, Murad F (1985) Goodman and
Gilman's The Pharmacological Basis of Therapeutics 7th ed. New
York, Toronto, London: Macmillan 1839 p.
Gosalvez M (1983). Carcinogenesis with the insecticide rotenone.
Life Science. 32: 809 - 816.
Gosselin RE, Smith RP, Hodge HC (1984) Clinical Toxicology of
Commercial Products. 5th ed. Baltimore/London: Williams &
Wilkins, p.111-366-7.
Hayes WJ Jr (1982) Pesticides studied in man. Baltimore/London:
Williams & Wilkins, 81-6.
Hayes Jr WJ (1975) Toxicology of pesticides. Baltimore:
Williams & Wilkins, p 271.
Moriya M, Ohta T, Watanabe K et al (1983). Further mutagenicity
studies on pesticides in bacterial reversion assay system. Mutat.
Res. 116: 185 - 216.
Reynolds JEF (1989) Martindale The Extra Pharmacopoeia. 29th ed.
London, Pharmaceutical Press, 1896 p.
National Research Council (1983) Drinking Water and Health Vol. 5
Washington, D.C.: National Academy Press p.98.
Waters MD, Sandhu SS, Simon VF et al. (1982) Study of pesticide
genotoxicity. Basic Life Sci. 21; 275 - 326.
Windholz M. (1983) The Merck Index: an encyclopedia of chemicals,
drugs, and biologicals. 10th ed. Rahway, New Jersey, Merck and
Co., Inc.
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: Prof. Alberto Furtado Rahde
Poison Centre of Porto Alegre
Rua Riachuelo 677, ap. 201
90010 Porto Alegre
Brazil
Tel: 0512 275 419
Fax: 55 512 391 564
Date: December 1989
Revised: London Group
Date: March 1990
Revised: Prof. A.F. Rahde
Date: April 1990.