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PYRETHRIN

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 Trade Names
   1.6 Main manufacturers, 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. PHYSIO-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 circumstances of poisoning
   4.3 Occupationally exposed population
5. ROUTES OF EXPOSURE
   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 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
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
   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 & 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 &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 & 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 investigations
   8.5 Overall Interpretation
   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 Contact
      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
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary
      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
      9.4.13 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 support 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 the literature
12. ADDITIONAL INFORMATION
   12.1 Specific Preventative Measures
   12.2 Other
13. REFERENCES

International programme on Chemical Safety

Poisons Information Monograph G 026

Chemical

1. NAME

1.1 Substance

Pyrethrin

1.2 Group

Pyrethrins

1.3 Synonyms

Pyrethrum Extract

Pyrethrum Oleoresin

and contents of extracts include

Buhach

Chrysanthemum cinerareaefolium

Cinerin I or II

Dalmatian insect powder

Dalmation insect flowers

Firmotox

Jasmolin I or II

Persian insect powder

Prentox pyrethrum extract

Pyrenone

Pyrethre

Pyrethrin

Pyrethrin I or II

Pyrethrines

Pyrethrins Pyrethrum

Pyrethrum (insecticide)

Pyrocide

Pyronyl

Trieste flowers

1.4 Identification Numbers

1.4.1 CAS number

8003-34-7

1.4.2 Other Numbers

OTHER CAS REG NUMBER: 12768-73-9

1.5 Trade Names

1.6 Main manufacturers, Importers

2. SUMMARY

2.1 Main Risks and Target Organs

Pyrethrins rarely cause systemic toxicity in adults; they can however induce hypersensitivity.

2.2 Summary of clinical effects

Topical exposure can result in a mild erythematous dermatitis. Large oral doses commonly produce nausea and vomiting. Once systemically absorbed symptoms of pyrethrin poisoning follow the typical pattern of nerve poisoning: (1) excitation, (2) convulsions, (3) paralysis, and (4) death. Infants and children appear to be at greater risk than adults.

Hypersensitivity reactions from exposure to pyrethrins range from allergic rhinitis, bronchitis, and bronchial asthma to anaphylactic shock. Contact dermatitis can also occur.

Pyrethrins are often dissolved in organic solvents, which may have significant toxicity.

2.3 Diagnosis

Diagnosis is made following known exposure to the insecticide. There is no specific investigation.

2.4 First-aid measures and management principles

Patients should be removed from exposure, and contaminated clothing should be removed. Skin decontamination is by washing with soap and tepid water. In patients with clinical evidence of toxicity, treatment is symptomatic. The airway should be maintained in unconscious patients. Seizures should be treated with anticonvulsants such as diazepam. Hypersensitivity reactions should be treated with antihistamines, corticosteriods, and bronchodilators as required. Epinephrine should be used as indicated.

3. PHYSIO-CHEMICAL PROPERTIES

3.1 Origin of the substance

Natrual

Pyrethrins are extracts of the pyrethrum flower, largely Chrysanthemum cinerariaefolium. Extracts contain 20-50% total pyrethrins, the main active constituents being pyrethrin I (P1) and pyrethrin II (PII), with smaller amounts of the related cinerins and jasmolins.

3.2 Chemical structure

Pyrethrin I

C21H28O3

328.4

Pyrethrin II

C22H28O5

372.4

Jasmolin I

C21H30O3

330.4

Jasmolin II

C22H30O5

374.4

Cinerin I

C20H28O3

316.4

Cinerin II

C21H28O5

360.4

3.3 Physical Properties

3.3.1 Colour

Brown

3.3.2 State/Form

Liquid-viscous fluid

3.3.3 Description

PI b.p. 170C at 0.1 mmHg with decomposition

PII b.p. 200C at 0.1 mmHg with decomposition

Solubility: Virtually insoluble in water at 20C: soluble in alcohol, acetone, kerosene, carbon tetrachloride, nitromethane, ethylene dichloride, and many other organic solvents.

Vapour Pressure Approximately 0 Torr at 20C.

Stability: rapidly oxidised and inactivated in sunlight: decomposed by exposure to light with loss of insecticidal activity. Rapidly hydrolysed by alkali.

3.4 Hazardous Characteristics

Often combined with other insecticides such as organophosphates or carbamates.

Pyrethrins burn with difficulty, though solvent may burn readily. Contact with strong oxidizers may cause fires and explosions.

4. USES

4.1 Uses

4.1.1 Uses

Pesticide

4.1.2 Description

Insecticide used for indoor pest control. Also used commercially as a pesticide for pre-harvest treatment on growing bush and vine fruits, deciduous fruits and nuts, forage crops and vegetables and ornamentals (Reigart and Roberts 1999).

Pyrethrins often combined with piperonyl butoxide are used for the topical treatment of pediculosis. Owing to its low mammalian toxicity this preparation has been advocated in pregnancy and young children (McEvoy 1992).

Pyrethrins have also been used orally as an anthelmintic without adverse effects at a recommended dose in adults of 20mg and in children 10mg, given as a three-day course, in the form of an emulsion formed by adding an alcoholic solution to water (Hayes JW 1982).

4.2 High risk circumstances of poisoning

Unintentional exposure to spray during field application. Accidental or intentional ingestion by children or adults. In persons with acute and chronic respiratory disease the inhalation of pyrethrins may exacerbate symptoms due to its sensitising properties (Mackison FW et al 1981).

4.3 Occupationally exposed population

Those engaged in the isolation, formulation or application of pyrethrins (Sittig M 1985), principally farm workers, gardeners and pet-groomers (Mehler L et al 1999).

5. ROUTES OF EXPOSURE

5.1 Oral

Oral ingestion has been described.

5.2 Inhalation

Cases of inhalational exposure have been reported.

5.3 Dermal

Pyrethrins are poorly absorbed via the dermal route, however may cause irritation.

5.4 Eye

Eye irritation has been described.

5.5 Parenteral

No data available

5.6 Others

6. KINETICS

6.1 Absorption by route of exposure

Absorbed by the respiratory route. Poorly absorbed via the gastro-intestinal and dermal routes (Reigart and Roberts 1999).

6.2 Distribution by route of exposure

Pyrethrins or their metabolites do not appear to be stored in the body. It is thought that they are not excreted in breast milk though modern studies are lacking to exclude this route of excretion completely (Hayes and Wayland 1982). Tracer studies in mice suggest that certain pyrethrins and their metabolites may be stored in skin and animal hair (Gong ZC et al 1990).

6.3 Biological half-life by route of exposure

No Data Available

6.4 Metabolism

Pyrethrum is metabolised by oxidation of the isobutenyl side chain of the acid moiety. This reaction can take place in both the liver and the plasma and is followed by hydroxylation and conjugation to glucuronides or sulphates, which are excreted in the urine (Hayes and Laws 1991a).

6.5 Elimination and excretion

Oxidation and hydrolysis products are excreted in the urine. Oxidation of the isobutenyl side change of the chrysanthemumic acid portion of the molecule may be a more important route to detoxification than hydrolysis of the ester linkage. Some pyrethrins are also excreted unchanged (Hayes and Laws 1991a).

7. TOXICOLOGY

7.1 Mode of action

In insects pyrethrins prolong the opening of the sodium channel, and produce instant paralysis. Nervous system stimulation proceeds from excitation to convulsions and tetanic paralysis. Muscular fibrillation and death may occur as with DDT (Hayes and Laws 1991a).

7.2 Toxicity

7.2.1 Human Data

7.2.1.1 Adults

Pyrethrins have a wide margin of safety when used judiciously, and there are few adequately documented cases of fatal pyrethrin poisoning in man. It appears that the main toxicity to humans is related more to the solvent vehicle (Gosselin et al 1984).

Injury is more likely to result from allergy than direct toxicity.

Amount immediately dangerous to life or health: 5000 mg/cubic metre (NIOSH 1997)

Minimal lethal dose of pyrethrins is probably in the region of 10 to 100 grams

7.2.1.2 Children

Animal studies suggest that the young are at greater risk than adults.

A 2 yr old girl died having ingested 15g of pyrethrum concentrate and an 11 month old baby whose mouth, nostrils and entire face were covered with pyrethrum powder had severe breathing difficulties. These effects had subsided within 1.5 hours (Hayes, WJ.. 1982).

7.2.2 Relevant animal Data

In mammals pyrethrum is only weakly toxic.

 

Formulation

Oral
LD50
mg/kg

Dermal
LD50
mg/kg

Rat

Solution
(irrespective of solvent)

584 to 900

>1500

Mouse

Solution
(irrespective of solvent)

273 to 796

375

Rabbit

Purified Extract

-

2060

(Hayes, WJ.1982; Spencer, EY 1982)

When rats were fed 1000-5000 ppm for 2 years, liver lesions consisting of bile duct proliferation and focal necrosis of liver cells were observed (Hayes WJ, Laws ER 1991b).

7.2.3 Relevant in vitro data

No data available

7.2.4 Workplace standards

MAC 8-hr time weighted average: 5 mg/cubic metre

MAC 10-hr time weighted average: 5 mg/cubic metre (NIOSH 1997)

7.2.5 Acceptable daily intake

No data available

7.3 Carcinogenicity

Not classifiable as a human carcinogen (American Conference of Governmental Industrial Hygienists 1998).

7.4 Teratogenicity

No known human data.

In rats fed 5000 ppm beginning 3 weeks prior to mating, reproductive performance was not reduced, but weights of weanling were significantly lower than those of controls (Hayes JW 1982).

7.5 Mutagenicity

No data available.

7.6 Interactions

Often used with synergists to increase insecticidal efficacy. Common synergists include piperonyl butoxide, or n-octyl bicycloheptene dicarboximide. Has also been used with organophosphates and carbamates.

Preparations may also contain antioxidants to protect against the effects of sunlight.

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 & 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 &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 & 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 investigations

8.5 Overall Interpretation

8.6 References

9. CLINICAL EFFECTS

9.1 Acute poisoning

9.1.1 Ingestion

Pyrethrum may be taken orally as an anthelmintic with minimal adverse effects (20mg in adults, 10mg in childrem), as oral absorption is low. Once systemically absorbed symptoms of pyrethrin poisoning follow the typical pattern of nerve poisoning: (1) excitation, (2) convulsions, (3) paralysis, and (4) death (Matsumura, F 1985). In dogs fed extraordinarily high doses tremor, ataxia, laboured breathing and salivation have been recorded. If a sufficiently high dose was taken such effects may also be expected in man, however neurotoxicity is rare.

9.1.2 Inhalation

Crude pyrethrum is a respiratory allergen, probably due to non-insecticidal ingredients. Although pyrethrum may be absorbed across the pulmonary mucosa, it is rapidly hydrloyzed to inert products by mammalian liver enzyme systems minimising systemic effects. Following inhalation, a stuffy, runny nose and itchy throat are common. Hypersensitivity reactions may occur.

9.1.3 Skin Exposure

Crude pyrethrum is a dermal allergen, probably due to non-insecticidal ingredients, containing sensitising sesquiterpene lactones contained within the crude extract. Modern pyrethrum-containing insecticides should not contain them. (Zenz C 1988). The usual lesion is a mild erythematous dermatitis with vesicles, intense puritis and a bullous dermatitis. Persons sensitive to ragweed pollen are particularly prone to such reactions.

Pyrethrins especially if mixed with piperonyl butoxide should not be applied directly to acutely inflammed skin or raw weeping surfaces (McEvoy 1992).

9.1.4 Eye contact

Crude pyrethrum may act as an irritant. Slight corneal erosions and stromal oedema may occur (McEvoy 1992).

9.1.5 Parenteral Exposure

No known Data

9.1.6 Other

Contact dermatitis and allergic respiratory reactions (rhinitis and asthma) have occurred following exposures. Single cases exhibiting anaphylactic and pneumonitic manifestations have also been reported.

Commercial products containing pyrethrums are often combined with other pesticides to increase their insecticidal activity. Common preparations contain piperonyl butoxide and n-octyl bicycloheptene dicarboximide with low toxic potential as well as organophosphates and carbamates with high potential toxicity.

9.2 Chronic poisoning

9.2.1 Ingestion

No known data

9.2.2 Inhalation

No known data

9.2.3 Skin Contact

Repeated contact may produce an erythema that mimics sunburn.

9.2.4 Eye Contact

No known data

9.2.5 Parenteral exposure

No known data

9.2.6 Other

9.3 Course, prognosis, cause of death

Poisoning from pyrethrins is often mild and only symptomatic treatment is required. Severe poisonings may present with numbness of lips and tongue with nausea and vomiting, sneezing and diarrhoea, followed by headache restlessness, tinnitis, incoordination, convulsions and eventually death due to respiratory paralysis (Gosselin 1984).

Allergic type reactions can occur in the absence of overt chemical toxicity.

9.4 Systematic description of clinical effects

9.4.1 Cardiovascular

Hypotension and tachycardia may occur as a result of anaphylaxis.

9.4.2 Respiratory

Hypersensitivity reactions can occur, presenting as cough, wheeze, dyspnoea, bronchospasm or pulmonary oedema.

9.4.3 Neurological

9.4.3.1 Central Nervous System

Paraesthesiae, headaches and dizziness are common. Massive exposure may potentially lead to seizures and coma.

9.4.4 Gastrointestinal

Nausea and vomiting may develop post ingestion. Abdominal cramps, tenesmus and gastritis have also been reported.

9.4.5 Hepatic

No data available

9.4.6 Urinary

No data available

9.4.7 Endocrine and Reproductive systems

No data available

9.4.8 Dermatological

Contact and irritant dermatitis may occur.

9.4.9 Eye, Ear, Nose, Throat: local effects

Local symptoms include a stuffy, runny nose, and dry throat.

9.4.10 Haematological

No data available

9.4.11 Immunological

Anaphylaxis and anaphylactoid reactions may occur following pyrethrum inhalation.

9.4.12 Metabolic

No data available

9.4.13 Allergic Reactions

Anaphylaxis and anaphylactoid reactions may occur following pyrethrum inhalation.

9.4.14 Other Clinical Effects

9.4.15 Special Risks

9.5 Other

9.6 Summary

10. MANAGEMENT

10.1 General principles

Treatment for pyrethrum poisoning is largely supportive. If a patient suspected of pyrethrin poisoning is severely ill, the physician should consider other substances such as organophosphates or carbamates that pyrethrins may be mixed with. Emesis is contra-indicated owing to the risk of seizures.

10.2 Life support procedures and symptomatic/specific treatment

Make a proper assessment of airway, breathing, circulation and neurological status of patient.

Maintain a clear airway.

Aspirate secretions from airway.

Control convulsions with appropriate drug regimen.

Treat anaphylaxis by appropriate means.

10.3 Decontamination

Remove and discard contaminated clothing.

Eye and skin contact to be washed with copious amounts of water.

Emesis is contra-indicated.

If large amounts have been ingested and the patient presents within one hour, gastric emptying may be considered.

Activated charcoal may be helpful.

10.4 Enhanced elimination

No known data.

10.5 Antidote treatment

10.5.1 Adults

No specific antidote exists. Treatment is largely supportive.

Allergic reactions may be treated with antihistamines and if necessary corticosteriods. Anaphylaxis may require adrenaline. Contact dermatitis can be treated using local corticosteroids.

10.5.2 Children

No specific antidote exists. Treatment is largely supportive.

Allergic reactions may be treated with antihistamines and if necessary corticosteriods. Anaphylaxis may require adrenaline. Contact dermatitis can be treated using local corticosteroids.

10.6 Management discussion

Pyrethrum poisonings usually present little risk. Treatment is mainly supportive. Diagnosis is important to differentiate pyrethrin from pyrethroids and other more toxic compounds.

11. ILLUSTRATIVE CASES

11.1 Case reports from the literature

43 year old women experienced an anaphylactoid reaction after self medicating with a shampoo containing pyrethrin I for the treatment of headlice. Periorbital oedema developed within 1 hour of application. The following morning, the patient developed shortness of breath, chest tightness and numbness and became unresponsive. Treatment consisted of naloxone, epinephrine, dextrose, aminophylline, salbutamol (albuterol), methylprednisolone and prednisone (Culver et al 1988).

A 24 year old male sprayed his dog with a flea killing spray containing pyrethrins 0.15percent in a coconut oil base with aloe. Within 30 minutes he started to complain of the following symptoms: shortness of breath, abdominal cramp and repeated vomiting. Within 2 hours his symptoms had settled and he returned rapidly to normal (Paton DL, Walker JS 1988).

Fatality associated with inhalational exposure of pyrethrin based shampoo secondary to an acute allergic reaction causing irreversible bronchospasm (Wax and Hoffman 1994).

Death occurred in a 2 year old child following ingestion of approximately 14g of pyrethrum powder (1-3% pyrethrins) (McEvoy 1992)

12. ADDITIONAL INFORMATION

12.1 Specific Preventative Measures

Those persons exhibiting atopy, especially to ragweed should avoid exposure to pyrethrins.

12.2 Other

Pyrethrins are unstable in the presence of light moisture and air. It is rapidly oxidised and inactivated by air especially in the presence of alkalis.

Pyrethroids are synthetic analogues of pyrethrins and produce severer toxicity to mammals than pyrethrins.

13. REFERENCES

American Conference of Governmental Industrial Hygienists (1998). Threshold limits values (TLV) for chemical substances and physical agents biological exposure indices for 1998. Cincinnati, OH: ACGIH

Culver CA, Malina JJ,Talbert RL.(1988) Probable anaphylactoid reaction to a pyrethrin pediculicide shampoo. Clin Pharm 7:846-9

Gong ZC et al (1990). Chin J Prev Med;24:277-80.

Gosselin, RE, Smith RP, Hodge HC.(1984) Clinical Toxicology of Commercial Products. 5th Edition. Baltimore. Wilkins and Williams. pIII-353-4.

Hayes WJ, Laws ER. (1991a) eds Handbook of pesticide toxicology Vol 2. p 588.

Hayes WJ, Laws ER. (1991b) eds Handbook of pesticide toxicology vol 2 p952

Hayes, WJ. (1982) Pesticides Studied in Man. Baltimore/London. Williams and Wilkins p. 77-78

Mackison FW, Stricoff RS, Partridge LJ (eds) (1981) NIOSH/OSHA-Occupational Health Guidelines for Chemical Hazards. DHHS (NIOSH) Publication Number 81-123 (3 vols). Washington, DC. US Government Printing Office

Matsumura, F. (1985) Toxicology of Insecticides. 2nd ed. New York, NY:Plenum Press,. 147

McEvoy GK. Ed (1992) American Hospital Formulary Service-Drug Information 92. Bethsada, MD; American Society of Hospital Pharmacists, Inc. p2125-6.

Mehler L, Shannon J (1999) Illnesses associated with occupational use of flea-control products-California, texas, and Washington, 1989-1997. Morbidity and Mortality Weekly Report (MMWR) 48 (21);443-447

NIOSH. (1997) NIOSH pocket guide to chemical hazards. DHHS (NIOSH) Publication number 97-140. Washington DC. US Government printing office. 270.

Paton DL, Walker JS (1988). Pyrethrin poisoning from commercial strength flea and tick spray. American journal of emergency medicine 6:232-5

Routt Reigart J, Roberts JR. (1999). eds Recognition and Management of Pesticide Poisonings 5th Edition United States Environmental Protection Agency p68-69

Sittig M (1985) Handbook of toxic and hazardous chemicals and carcinogens. 2nd edn Park Ridge. NJ Noyes Data Corporation. p 761

Spencer, E.Y. (1982). Guide to the chemicals used in crop protection. 7th Edition. Publication 1093. Research institute, Agriculture Canada, Ottowa, Canada: Information Canada. p 495

Wax PM, Hoffman RS (1994). Fatality associated with inhalation of a pyrethrin shampoo. J Toxicol Clin Tox 32 (4) 457-460.

Zenz, C (1988). Occupational Medicine-Principles and practical applications. 2nd Edn. St. Louis, MO:Mosby-Yearbook Inc. 146

14. AUTHOR(S), REVIEWER(S), DATES
(INCLUDING UPDATES), COMPLETE ADDRESS(ES)

Authors

NJ Langford, RE Ferner
West Midlands Centre for Adverse Drug Reaction Reporting
City Hospital
Dudley Road
Birmingham
B18 7QH
United Kingdom
E-mail n.j.langford@bham.ac.uk
r.e.ferner@bham.ac.uk

Date

September 2001

PEER REVIEWED GROUP

Ligia Fruchtengarten, Mahdi Balali-Mood, Wayne Temple, Nigel Langford

Edinburgh September 2001



    See Also:
       Toxicological Abbreviations