Dimethoate is a widely used organophosphorus (OP) insecticide applied to kill mites and insects systemically and on contact(1). It was introduced in the 1950s, originally patented by American Cyanamid(2), and is now produced by 39 companies around the world(3). Dimethoate is used against a broad range of insects such as thrips, aphids, mites, and whiteflies(4), and on a number of crops including citrus, cotton, fruit, olives, potatoes, tea, tobacco and vegetables(5). It is also permitted for the control of the flies in livestock accommodation(6), home gardens and food storage(7) . Like all OPs, dimethoate acts by interfering with the activities of cholinesterase, an enzyme essential for the proper functioning of the nervous system of insects and humans(8).
Production and use
Dimethoate is used in a large number of products. In the US, it has 166 approved labels(9). Its trade names include Afidox (produced by Lucava), Cekutoate (Cequisa), Perfekthion (BASF), Rogor (Isagro), Dimezyl (Agriphar), Hilthioate (Hindustan), and Teeka (Nagarjuna Agrichem)(10). The large number of producers and products reflect the fact that it is one of the most commonly used insecticides in agriculture. In 1998, there were 16,250 metric tonnes of sales globally, with a value of $US 180 million(11).
In 1993, dimethoate applications to orchard crops in the US accounted for 35% of the total active ingredient used in agricultural applications, totaling approximately 725,000 pounds (329,000 kg)(12). Applications made to 10 crops accounted for more than 80% of the total dimethoate applied in the US during 1993. These crops included cotton (17.1%), alfalfa (15.4%), oranges (7.7%), wheat (7.0%), apples (6.9%), grapefruit (6.9%), lemons (6.4%), peas/beans (5.68%), lettuce (3.9%) and field maize (3.1%)(13).
In the UK, dimethoate use in 1998 was 377,030 spray hectares on arable crops(14), an increase from 291,578 treated hectares in 1996(15). It is mostly used against aphids on wheat (322,883 spray hectares in 1998), making it the second most widely used insecticide in wheat (accounting for 14% of all insecticides used), and the 23rd most widely used active substance in UK agriculture in 1998(16).
Dimethoate is moderately toxic (World Health Organisation class II) by ingestion, inhalation and dermal absorption(17). Most oral LD50s (dose at which half the sample is dead) in rats range from 150-400 mg/kg body weight(18). For mice, rabbits and guinea pigs, the LD50s are 160, 300 and 350 mg/kg respectively(19). As with all OPs, dimethoate is rapidly absorbed through the skin, and easily absorbed through the lungs(20).
The population as a whole is not generally subject to exposure to dimethoate from air, water or food(21); however occupational exposure may occur during manufacture, formulation and use. This mainly occurs through inhalation and dermal absorption, although occupational exposure can occur by accident or as a result of incorrect handling(22).
Where humans are exposed to dimethoate, there are many effects: when inhaled, the first effects are usually respiratory and may include a bloody or runny nose, coughing, chest discomfort, difficult or short breath, and wheezing due to constriction or excess fluid in the bronchial tubes. Skin contact may cause skin sensitisation. Eye contact will cause pain, bleeding, tears, pupil constriction and blurred vision. Following exposure by any route, other systemic effects may begin within a few minutes or be delayed for up to 12 hours. These may include pallor, nausea, vomiting, diarrhoea, abdominal cramps, headache, dizziness, eye pain, and blurred vision. Severe poisoning will affect the central nervous system producing lack of coordination, 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(23).
In humans, repeated or prolonged exposure to OPs may result in the same effects as acute exposure, including the delayed symptoms. Other effects reported in workers repeatedly exposed include impaired memory and concentration, disorientation, severe depressions, irritability, confusion, headache, speech difficulties, delayed reaction times, nightmares, sleepwalking and drowsiness or insomnia(24).
Teratogenicity (birth defects)
Dimethoate is a suspected human teratogen(25). It has been demonstrated as teratogenic in dogs and cats: for example, one study found that a dosage of 12 mg/kg/day given to pregnant cats increased the incidence of extra toes on kittens. The same dosage given to pregnant rats produced both birth defects related to bone formation, stunting and defects related to malfunction of the bladder(26). These results contradict previous statements made, for example, the UK Advisory Committee on Pesticides (ACP) evaluation in 1993 concluded ‘dimethoate was not overtly teratogenic in rats or rabbits’(27), and in 1988 the International Programme on Chemical Safety (IPCS) stated ‘on the basis of available data on experimental animals, dimethoate is not considered to be a teratogen’(28). In 1994, BASF rejected claims made in Chile of a link between unusually high levels of genetic defects among babies born in the fruit-growing region of Rancagua with the usage of the insecticide dimethoate. BASF denied there was any evidence to support the claim(29).
Dimethoate may affect reproduction: in a multiple generation study in mice, reproductive performance was impaired at high doses but only in the presence of marked cholinergic effects. In an inadequate mouse multigeneration study in 1965, there was no overt effect on reproductive capacity at dietary levels up to 50 ppm(30). However, another study showed that dimethoate at 60 mg/litre drinking water did affect mating of five generations of mice tested(31).
There is no consensus on mutagenicity. In 1989, the WHO concluded that dimethoate was found to be mutagenic in a variety of in vitro and in vivo studies(32). In contrast, the various mutagenicity studies reviewed during ACP evaluation indicated that dimethoate possesses mutagenic potential in vitro, but is not mutagenic in vivo(33). One study found dimethoate to be mutagenic in a continuous four generation in vivo experiment(34), contradicting the previous statement, whilst the US Environmental Protection Agency stated there was positive mutagenicity associated with dimethoate(35).
Dimethoate is classified as a possible human carcinogen by the US EPA, based on tumors in mice, the compound-related (no dose response) weak effect of combined spleen, skin and lymph tumors in male rats, and positive mutagenic activity associated with dimethoate(36). The IPCS concluded in 1989 that the available data were inadequate to assess the carcinogenic potential of the compound. The ACP 1993 evaluation concluded that dimethoate was not carcinogenic in rats or mice(37), however, an increase in malignant tumours has been reported in rats given oral doses of five,15 or 30 mg/kg dimethoate for 511 to 627 days(38). It seems there is a lack of data assessing the carcinogenic potential of dimethoate.
Effects on wildlife
The toxicity of dimethoate for aquatic organisms and birds is moderate to high(39). One study found that it causes temporary rhythm alterations in some bird seed-eating species. Whilst these effects may not be fatal, they may be critical for the birds’ food-finding ability and in making them more vulnerable to predators(40). Dimethoate has also been found to affect wood mice behaviour(41) and to cause jumping, erratic movement imbalance and death in fish(42).
Dimethoate is highly toxic to bees on an acute contact basis(43), particular concern has been expressed over this(44). The LD50 (oral and topical) for bees is 0.1-0.2 µg/bee(45). Products containing dimethoate warn not to apply to crops in open flower nor when flowering weeds are present(46).
Fate in the environment
Dimethoate is a mobile, yet relatively non-persistent OP insecticide. The primary route of dissipation appears to be microbially-mediated degradation in anaerobic (oxygen-rich) soil, particularly under moist conditions, with a half-life (time taken to degrade to half its initial strength) of 2.4 days(47). The 1999 ACP review discussed its previous concerns over environmental fate and behaviour. They concluded that dimethoate was unlikely to leach because it is so rapidly degraded in soil, is non-volatile, was slightly persistent in sediment/water systems with a DT50 of 13-17 days and did not significantly partition to sediment(48).
The peach potato aphid is known to be resistant to dimethoate in the UK. However, other aphid species and leaf miner do not exhibit such resistance(49).
The cocktail effect
It appears dimethoate creates a metabolite called demethoxon that plays a dominant role in the toxicity of dimethoate for insects and mammals. Dimethoxon is also used as an insecticide known as omethoate. Omethoate, is about 10 times more toxic and is more of a potential inhibitor to cholinesterase activity than dimethoate(50). This is an important issue as, in the past, the intake of dimethoate and omethoate have been considered separately, and consumer exposure from individual crop uses has remained below the Acceptable Daily Intake (ADI). However, if the total diet is taken into account, the ADI could be exceeded for toddlers by both dimethoate and omethoate residues and for infants by dimethoate residues. The Pesticides Safety Directorate is in the UK is currently examining the issue of combined residues(51).
Unlike organochlorine pesticides, OPs such as dimethoate do not persist in the environment. Instead, their problem lies in their health effects on humans and other organisms. There is little concrete evidence regarding the chronic effects of dimethoate, for example on its carcinogenicity, however its acute effects on the nervous systems of humans and wildlife have been widely observed. Even though safer alternatives to OP insecticides are available, dimethoate still remains one of the most widely used insecticides in the world. Further safer alternatives should be developed, and an alternative approach based on the encouragement of natural pest enemies widely adopted. (HM)
1. Pesticide Management Information Programme ‘Dimethoate’ EXTOXNET Pesticide Information Notebook, Cornell University, New York, 1993.
2. CDS Tomlin (Ed), Pesticides Manual, Twelfth Edition, British Crop Protection Council, 2000.
3. Farm Chemicals International, November 1999, WOW! 2000.
4. EXTOXNET, Op. cit. 1.
5. Tomlin, Op. cit. 2.
6. Tomlin, ibid.
7. ACP, Evaluation on Dimethoate, Evaluation of Fully Approved or Provisionally Approved Products No. 86, Pesticides Safety Directorate, Ministry of Agriculture, Fisheries and Food, London, 1993.
8. EXTOXNET, Op. cit. 1.
10. Tomlin, Op. cit. 2.
11. Farm Chemicals International, Op. cit. 3.
12. USEPA, Op. cit. 9.
13. USEPA, ibid.
14. Pesticide Usage Survey Report, Arable Farm Crops in Great Britain. Number 159, Ministry of Agriculture, Fisheries and Food and Scottish Office Agriculture, Environment and Fisheries Department, 1998.
15. Pesticide Usage Survey Report, Arable Farm Crops in Great Britain. Number 14, Ministry of Agriculture, Fisheries and Food and Scottish Office Agriculture, Environment and Fisheries Department, 1996.
16. MAFF, Op. cit 14.
17. IPCS, The WHO recommended classification of pesticides by hazard and guidelines to classification 1998-1999, WHO/PCS/98.21.
18. IPCS, Environmental Health Criteria 90 Dimethoate, WHO Geneva, 1989.
19. Tomlin, Op. cit. 2.
20. EXTOXNET, Op. cit. 1.
21. Tomlin, Op. cit. 2.
22. IPCS, Op. cit. 18.
23. EXTOXNET, Op. cit. 1.
24. EXTOXNET, ibid.
25. S A Briggs, Basic guide to pesticides: Their characteristics and hazards, Rachel Carson Council, Hemisphere Publishing Corporation, 1992.
26. Hayes, cited by EXTOXNET Information Notebook (Op. cit. 1).
27. ACP, Op. cit. 7.
28. IPCS, Dimethoate Health and Safety Guide. Health and Safety Guide No. 20. WHO, 1992 .
29. Agrow No. 211, p. 22 ‘BASF sets dimethoate record straight’, July 1994.
30. ACP, Op. cit. 7.
31. IPCS, Op. cit. 18.
32. IPCS, ibid.
33. ACP, Op. cit 7.
34. M Nehez and I Desi, The Effect of Dimethoate on Bone Marrow Cell Chromosomes of Rats in Subchronic Four-Generation Experiments. Ecotoxicology and Environmental Safety 33, 103-109, 1996.
35. Reregistration Eligibility Decision Document. United States Environmental Protection Agency 1999, www.epa.gov/pesticides/op/dimethoate/hedrra.pdf
36. USEPA, ibid.
37. ACP, Op. cit. 7.
38. EXTOXNET, Op. cit. 1.
39. IPCS, Op. cit. 28.
40. R Brunet and A Cyr, The impact of dimethoate on rhythms of three granivorous bird species, Agriculture, Ecosystems and Environment, 41, 327-336, 1992.
41. G Dell’Omo and R Shore, Behavioural and Physiological Effects of Acute Sublethal Exposure to Dimethoate on Wood Mice Apodemus sylvaticus, Arch. Environ. Contam. Toxicol. 31, 91-97, 1996.
42. IPCS, Op. cit. 18.
43. USEPA, Op. cit. 9.
44. ACP, Annual Report. Ministry of Agriculture, Food and Fisheries, 1999.
45. Tomlin, Op. cit. 2.
46. Dimethoate product label.
47. IPCS, Op. cit. 18.
48. ACP, Op. cit 44.
49. ACP, Op. cit. 7.
50. IPCS, Op. cit. 28.
51. Note of the Dimethoate Stakeholder’s Forum, 19 March 2001, www.pesticides.gov.uk/ec_process/
[This article first appeared in Pesticides News No. 55, March 2002, pages 20-21]