Monocrotophos

Monocrotophos is an organophosphorus (OP) insecticide, developed by Ciba-Geigy (now Novartis) and first registered in 1965. It is a hazardous chemical especially for conditions of use in developing countries.

What is monocrotophos?
This non-specific systemic insecticide and acaricide, used to control common mites, ticks and spiders with contact and stomach action, quickly penetrates plant tissue(1). In common with other OPs, its toxic action is achieved by inhibiting acetylcholinesterase, an enzyme essential for normal nerve impulse transmission. It is widely used, mainly for foliar application to cotton. Monocrotophos is corrosive(2), and stable when stored in glass or polyethylene containers(3).

Production
The pesticide is now out of patent, and is produced by at least 15 manufacturers, although Novartis still produces an estimated 40% of total annual production(4). Monocrotophos is also manufactured and exported by companies in India, China, Brazil and Argentina. In India, for example, DowElanco makes monocrotophos in a joint venture with the Indian company NOCIL(5).

Uses and usage
The total sales of this widely-used pesticide is roughly 3% of all insecticide products.(6) It is registered in approximately 60 countries. Eight of these, accounting for 60% of sales, require detailed data on performance, chemistry, safety and environmental aspects(7). The remaining 40% are in countries which require only assessments, summaries, or very limited data. The product was withdrawn from use in the US, and in the European Union is registered in Austria, France, Spain, Italy and Greece(8).
    While mainly applied against cotton pests, it is used on citrus, olives, rice, maize, sorghum, sugar cane, sugar beet, peanuts, potatoes, soya beans, vegetables, ornamentals and tobacco.

Acute toxicity
Monocrotophos is classified WHO Ib, highly hazardous, and has been responsible for deaths resulting from accidental or intentional exposure. It is highly toxic orally, as well by inhalation or absorption through the skin. Early symptoms of poisoning may include excessive sweating, headache, weakness, giddiness, nausea, vomiting, hypersalivation, abdominal cramps, diarrhoea, blurred vision and slurred speech. Inhalation or skin contact may increase the susceptibility to the pesticide without showing immediate symptoms(9). The acute oral toxicity for rats (LD50) is 23mg/kg (males) and 18 mg/kg (females). The acute dermal toxicity for a rats is 354 mg/kg(10). Tests on rabbits indicate it is slightly irritating to eyes and causes reversible corneal opacity: reports on human health indicate eye contact will cause pain, bleeding, tears, pupil constriction and blurred vision.
    Severe poisoning will affect the central nervous system, producing inco-ordination, slurred speech, loss of reflexes, weakness, fatigue, involuntary muscle contractions, twitching, tremors of the tongue or eyelids and eventually paralysis of the body extremities and the respiratory muscles. In severe cases there may also be involuntary defecation or urination, psychosis, irregular heart beat, unconsciousness, convulsions and coma. Ingestion of 120 mg monocrotophos can be fatal(11).
    Like other OPs, monocrotophos is a potent cholinesterase inhibitor. The no effect level (NOEL) is 0.03 ppm in rats. It is slightly irritating to the skin and mildly irritating to the eyes(12,13).

Chronic effects
Monocrotophos has also been shown to cause delayed neuropathy (see page 6 for more details)(14). A study in Egypt of farmers using OPs, including monocrotophos, found that 50% of the workers showed signs of neurological effects such as superficial or deep sensory loss and decrease or lost reflexes in their ankle or ankle and knee(15). (See Pesticides Trust [now PAN UK] OP fact sheet for more data on neurological effects(16).)

Cancer
Monocrotophos is not carcinogenic in rats at 0.45 mg/kg/day, the highest dose tested(17). No significant carcinogenic lesions were observed when rats were exposed to monocrotophos aerosol at concentrations from 97-308 mg/m3 for one hour(18).

Reproductive effects
Researchers have generated a rat reproductive (and offspring) NOEL of 2.7 ppm, evidenced by decreased fertility, pup viability and weight, partly attributed to depressed maternal lactation(19).

Teratogenicity (birth defects)
Rats which received doses of 2 mg/kg per day of monocrotophos produced foetuses with lower than average length and weight and maternal toxicity in the form of reduced body weight gain in pregnancy at 1.0 mg/kg. No teratogenic effects were found at 2 mg /kg/day in rats, the highest dose tested(20).

Key health issues
Concerns about the safety of monocrotophos has led to its inclusion in the Prior Informed Consent (PIC) procedure (see page 16 for more on PIC). Governments are informed that formulations which exceed 600 g/litre of active ingredient may not be safe because of their impact on human health under conditions of use in developing countries. Governments which wish to prohibit these formulations can notify the PIC secretariat. Their decisions will be circulated to exporting countries(21).
    Many incidents in developing countries have been linked to monocrotophos. It is often difficult to trace an incident to a particular active ingredient: frequently a 'block' of pesticides commonly used in a region may be linked to a survey indicating occupational and other health impacts in the area. Monocrotophos has been pointed to as a cause, in the following:

• Brazil, Parana State Monocrotophos caused 107 of 412 reported incidents analysed in 1990, and the toxicology centre and health clinics also noted 1,650 incidents involving monocrotophos between 1982 and 1991(22).
• Paraguay In a region where monocrotophos is one of the most commonly used active ingredients there have been numerous cases of pesticide poisoning; monocrotophos was identified as the cause of paralysis in children in cotton-growing areas by the Ministry of Public Health and Welfare which found that 2-3 weeks of frequent exposure caused paralysis in children and acute poisoning in adults(23).
• Egypt In a cotton growing region of Egypt the health of 14 farmers who spray was compared with a control group from the same region. Monocrotophos is widely used and 61% of those surveyed showed symptoms of chronic pesticide poisoning(24).
• Philippines, Cordillera region Monocrotophos was one of the pesticides widely used by farmers in a survey that found all farmers suffered some adverse health effects(25).
• Indonesia In observations of 906 spray operations of 214 farmers commonly using monocrotophos and other OPs, over a three-month period, researcher found a significant increase-from two to fifty-fold-in the symptoms of pesticide toxicity during the spraying period. Of these spray operations, 21% brought on three or more neurobehavioural and intestinal signs of poisoning(26).

Fate in the environment
The EU has classified monocrotophos as dangerous for the environment(27). Monocrotophos has a half life of 14-21 days at pH9 and 25oC, with the rate decreasing at lower pH's and increasing at higher temperatures. Degradation on soil exposed to natural sunlight is rapid (half life less than 7 days) and on dark control samples is slower (half-life approximately 30 days). Monocrotophos is mobile in soil, and although it degrades rapidly it may possess potential for groundwater contamination.(28)

Wildlife
Monocrotophos is one of the most toxic pesticides to birds and is extremely toxic other wildlife, highly toxic to bees. It is toxic to shrimps and crabs, moderately toxic for fish and non-toxic for microorganisms. The acute LD50 for birds ranges from 0.9-6.7 mg/kg body weight, and for honey bees 33-84 ug/bee(29).
    There are numerous reports of avian mortality attributed to monocrotophos. The most recent occurred in Argentina, where an estimated 20,000 hawks died over an area of approximately 200km by 250 km in 1996. More than 700 dead hawks were found in one roost. Ornithologists suggested that monocrotophos used against grasshopper pests in the region was responsible, with hawks affected by direct exposure to the spray or secondary poisoning through eating contaminated grasshoppers. Scientists from Canada and the US had observed that smaller numbers of hawks were returning after migrating to South America. Miniature satellite transmitters attached to hawks led to the discovery. The major manufacturer, Novartis, joined meetings which agreed not to use monocrotophos in the region and encouraged other local distributors to stop selling the pesticide. A campaign to inform farmers was also supported by Novartis(30).

Food residues
OPs do not have long persistence and are generally found at low levels in food. Monocrotophos is not used in the UK, and testing imported food in 1996 found low levels (0.03 mg/kg) in one sample of dried currants (of eight tested) imported from Greece. Testing by UK food industry sources found monocrotophos residues in dwarf beans (0.07 mg/kg)(31). Maximum residue limits have been set in some products in the range of 0.02-1 mg/kg, and the acceptable daily take is 0.0006 mg/kg body weight(32).
    Monocrotophos and some of its metabolites have been identified in the milk, muscle, and liver of cows and in the milk of goats following ingestion of this chemical(33).
    Pre-harvest intervals have been set in several countries and are generally in the order of 7-15 days for vegetables and potatoes, maize and citrus and 28-30 days for other crops(34).

Ways to reduce exposure
Full protective clothing should be worn, including a respirator when mixing and spraying tall crops. Use of flaggers should be avoided. All equipment and protective clothing should be washed thoroughly after use and clothing should be laundered separately from family clothing. Unprotected workers should be kept out of treated areas for 48 hours37. Manufacture, formulation, agricultural use and disposal of monocrotophos should be carefully managed to minimize contamination of the environment.
    In view of the high toxicity of monocrotophos, it should not be considered in hand-applied ULV spraying practices38.

Conclusions
Monocrotophos is a widely used, and extremely dangerous insecticide. It has now been included in the PIC procedure, in recognition of the health problems caused by formulations with a high percentage of the active ingredient. Its low cost and many applications will present a challenge to users looking for safer alternatives, or measures which will protect health.

Control actions(37)
Germany May not be handled by adolescents and pregnant and nursing women.
Indonesia Monocrotophos was banned for use in rice in 1986 because of insect resistance and certain formulations phased out in 1994.
Kuwait Severely restricted: to use on plants up to the flowering stage only.
Malaysia Registration for use only on coconut and oil palm by trunk injection.
Philippines In 1990 the Fertilizer and Pesticide Authority issued Circular No. 01, which included a severe restriction on monocrotophos for use only in bean fly control. A six month phase out period took effect from 29 September 1993.
Sri Lanka Severely restricted. Import prohibited since July 1995.
US Voluntarily withdrawn by the registrant in 1989. Before withdrawal it could be used only by certified applicators. No remaining uses are allowed. Main concern is toxicity to non-target species, especially birds.

References
1. Tomlin, C. (ed), The Pesticide Manual, Tenth Edition, Crop Protection Publications. British Crop Protection Council and Royal Society of Chemistry, 1994.
2. IPCS, Monocrotophos Health and Safety guide, No. 80, IPCS International Programme on Chemical Safety, UNEP and ILO, WHO, Geneva, 1993.
3. EPA Pesticide Fact Sheet No. 72, US Environment Protection Agency, 1985
4. Ciba, Monocrotophos: Information for participants at the fifth FAO/UNEP joint meeting on PIC, Rome, October 1992.
5. Dinham, B., The Pesticide Trail: The impact of trade controls on reducing pesticide hazards in developing countries, The Pesticides Trust [now PAN UK], London, January 1995.
6. Op. cit. 4.
7. Op. cit. 4.
8. Active Substances Authorized by Plant Protection Products, DOC.3010/VI/91-Rev.12, September 1995.
9. Watterson , A., Pesticide Users' Health and Safety Handbook: An international guide, Gower Technical, Aldershot, UK, 1988.
10. Op. cit. 3.
11. FAO/UNEP, PIC Decision Guidance Document, Monocrotophos, June 1997.
12. Op. cit. 3.
13. Op. cit. 2.
14. Hill v Tomkins, Judgement of HH Smith, J (QBD) delivered on 17 October 1997.
15. Amr, M. et. al. 'Neurological effects of pesticides', study by the Industrial Medicine and Occupational Diseases Faculty of Medicine, Cairo University, reported in Pesticides News 30, December 1995.
16. Pesticides News, 'Fact sheet-Organophosphate insecticides' No. 34, December 1996, p. 20.
17. Op. cit. 3.
18. EXTOXNET Pesticide Information Notebook, Cornell University, Ithaca, USA, 1995.
19. Op. cit. 3.
20. Op. cit. 3.
21. Op. cit 11.
22. Dinham, B., The Pesticide Hazard: A global health and environmental audit, Zed Books, London and New Jersey, 1993, pp 87-88.
23. Ibid. pp120-121.
24. Op. cit. 15.
25. Cheng, Dr. Charles L., Medical Director, Baguio Philipino-Chinese General Hospital, Baguio city, Philippines 'Pesticides and Hazardous Effects on the Benguet Vegetable Farmers, 1993, (In Dinham, 1995 pp 76-7. Op. cit. 22.)
26. Hirschhorn, Norbert, 'Study of the Occupational Health of Indonesian Farmers who Spray Pesticides, the Indonesian National IPM Program', FAO (UTF/INS/067/INS), Jakarta, August 1993 (In Dinham, 1995, pp 59-60). Op. cit 5.)
27. Op. cit. 11
28. Op. cit. 3.
29. Op. cit. 2.
30. 'Action to halt hawk deaths', Pesticides News 35, March 1997, p. 6.
31. MAFF/HSE, Annual Report of the Working Party on Pesticide Residues: 1996, MAFF, London 1997.
32. FAO/WHO, Pesticide Residues in Food, 1993 Evaluations, Joint Meeting on Pesticide Residues (JMPR), FAO, Rome, Plant Production Paper Monocrotophos.
33. Op. cit. 3.
34. Op. cit. 11.
35. Denholm, I, and Devonshire, AL (Eds), Resistance '91, Elsevier, London and New York, 1991.
36. Metcalf, RL, Insect Resistance to Insecticides, Pesticide Science, Vol 26, 1989, pp 333-358.
37. Guidelines for personal protection when working with pesticides in tropical countries, FAO, 1990.
38. Op. cit. 2.
39. Control actions in Germany, Kuwait, Malaysia, Sri Lanka and the US see PIC DGD (op. cit. 11), and control actions in Philippines and Indonesia see The Pesticide Trail (op. cit. 5.), pp 79 and 56 respectively.

[This article first appeared in Pesticides News No.38, December 1997, p20-21]