What is bendiocarb?
Bendiocarb is a carbamate insecticide. Like other carbamates, it reversibly inhibits acetylcholinesterase, an enzyme required for normal transmission of nerve impulses. Bendiocarb binds to the active site of this enzyme leading to an accumulation of acetylcholine, required for the transmission of nerve impulses in the body, at nerve muscle
sites(1).
Use
Bendiocarb has both public health and agricultural uses. It is used to control household pests, ornamental plant pests, mosquitoes, fire ants and other pests in industrial facilities and food storage
sites(2). In agriculture it is used against a variety of insects, particularly those in soil. It is also used as a seed treatment on sugar beets and maize and against snails and
slugs(3). Bendiocarb is also used as a residual spray against the malaria mosquito vector
Anopheles culicifacies. A recent study showed that bendiocarb 80% WP at 0.2 g/m2 produced effective control of
A. culicifacies resistant to other insecticides, provided that more than 95 % human-dwelling room coverage is achieved in both first and second round of spraying at an interval of 10 weeks in areas where malaria is a seasonal
problem(4).
Bendiocarb is manufactured for use in several forms; as granules, wettable powder, dust, pellets, pressurised liquids and pet collars, and is applied by broadcast, band treatment, foliar application, dusting, crack and crevice, premises treatment and mound drench.
The global non-crop market is currently estimated around US$16 million at end user level and around 90 metric tonnes of active ingredient are
sold(5).
Manufacturing
Bendiocarb was reported in 1971 and was introduced onto the market by Fison Ltd, Agrochemical Division. It is currently marketed by Bayer CropScience and Kuo
Ching(6) under various trade names: Ficam, Dycarb, Garvox, Turcam, Niomil, Seedox, Tattoo.
Regulatory status
Bendiocarb is registered for use in Canada, Australia, India, New Zealand, the Philippines, Tanzania and a number of countries in Europe (UK, Germany and Hungary). Pesticides used in Europe are currently being reviewed under two separate EU directives. Agricultural uses (including garden uses) are being reviewed under directive 91/414/EEC. Bendiocarb’s use was not supported through this review and agricultural and garden uses were withdrawn throughout EU member states in 2003. Bendiocarb is, however, still registered for use as an indoor insecticide. This is defined as a biocidal use and this use will be defended by the industry under the Biocidal Products Directive.
Bendiocarb was registered for use in the United States until recently. On 18 August 1999, the registrant AgrEvo (subsequently Aventis and now part of Bayer CropScience) voluntarily cancelled the registration of all bendiocarb products as part of the Food Quality Protection Act re-registration process. The United States Environmental Protection Agency’s (EPA) preliminary risk assessment showed that applicators (including homeowners) were at risk when mixing or applying the
pesticide(7). Bendiocarb can no longer be sold for any use in the US.
Acute toxicity
Bendiocarb is in World Health Organisation (WHO) class II for acute toxicity indicating that it is moderately hazardous to humans if ingested or absorbed through the
skin(8). It is in the EPA’s Acute Toxicity Category I for oral exposure, which is the highest of four categories for this effect. For dermal and inhalation routes of exposure bendiocarb is in Acute Toxicity Category II, for primary dermal irritation in Acute Toxicity Category III and for primary eye irritation in Acute Toxicity Category
IV(9). For rats, the oral LD50 is 34-156 mg/kg and the dermal LD50 is 566 mg/kg. For rabbits the oral LD50 is 35-40 mg/kg and for guinea pigs it is 35
mg/kg(10).
Chronic effects
Chronic exposure to bendiocarb can cause the same symptoms as acute exposure. Sub chronic and chronic studies have shown that bendiocarb inhibits cholinesterase activity in whole blood, plasma, and brain in rats, mice and
dogs(11). A two-year study with dogs fed doses of 12.5 mg/ kg resulted in increased levels of serum cholesterol and decreased levels of calcium in the blood
stream(12).
Human poisonings
Symptoms of bendiocarb poisoning are weakness, blurred vision, headache, nausea, abdominal cramps, low blood pressure, muscle tremors, uncoordination and heart irregularities. Death can result from discontinued breathing, paralysis of muscles of the respiratory system, and/or intense constriction of the openings of the
lung(13). Poisonings can be treated with atropine. Carbamates do not generally accumulate in mammalian tissue and the cholinesterase inhibition reverses rapidly once exposure ceases. In non-fatal cases symptoms usually last less than 24
hours(14).
The threshold dose for blood cholinesterase inhibition and mild symptoms lies between 0.15 and 0.20 mg a.i./kg, for humans for the oral route. When doses of 0.20 mg a.i./kg were taken some symptoms such as mild vertigo, nausea and sweating followed rapidly. The effects started subsiding 30 minutes after exposure and were completely gone within four
hours(15).
Carbamate poisonings are frequently reported to the American Association of Poison Control Centres. In 1996, a total of 1030 carbamate poisoning cases including 202 cases involving children were reported. Not every poisoning is reported so it is likely that there are far more poisonings each year than are actually
recorded(16).
In one case a man was applying bendiocarb when he experienced a severe headache, vomiting, excessive salivation and his cholinesterase level was depressed by 63%. Less than three hours after exposure the man recovered with no medical treatment and his cholinesterase level returned to normal within 24 hours. In another case an applicator was not wearing protective clothing when trying to clean contaminated equipment. The victim experienced nausea, vomiting, uncoordination, pain in his arms, hands and legs, muscle spasms and breathing difficulty. All of these symptoms abated within two hours after decontamination and treatment with atropine. The victim had recovered the following
day(17).
Poisoning records frequently state a class of pesticides rather than a specific active ingredient. One study looked at poisonings reported to the Poison Control Centre in Rio de Janeriro. In 1993, there were 189 cases of carbamate poisoning in the city. The poisonings were due to illegal use of carbamates as a rodenticide. The causes of carbamates poisoning were suicide attempts (65%) and accidental ingestions (35%). Of the accidental poisonings 83% were of children under the age of five years. The symptoms were similar to the ones described above, however, despite treatment with an antidote atropine eight people
died(18).
A recent study of pesticide-related illness in Catalunya, Spain, indicates that bendiocarb may be causing serious health problems in workers exposed after professional pest control
operations(19).
The US EPA preliminary risk assessment under the Food Quality Protection Act re-registration process showed that applicators (including homeowners) were at risk when mixing or applying the
pesticide(20). Post application exposure, particularly in children, is often through hand-to-mouth transfer after coming in contact with treated carpets or other indoor surfaces, or treated lawns
outdoors(21). A study based on 230 mother and newborn pairs enrolled in the Columbia Centre for Children, US, showed that residential pesticides such as carbamates, particularly bendiocarb, are readily transferred to the developing foetus during
pregnancy(22). Residential pesticide use is widespread in the US, with approximately 80-90% of American households using pesticides.
Reproductive effects
In a three-generation study with rats, fertility and reproduction were not affected by bendiocarb at dietary levels of up to 12.5 mg/kg. Although prenatal and postnatal doses of 40 mg/kg did affect reproductive success, it led to reduced pup weight and survival rates. Increased eye abnormalities and underdeveloped pubic bones were
detected(23,24).
Teratogenic effects
No teratogenic effects were detected in studies carried out on the offspring of rats fed 4 mg/kg/day or in the offspring of rabbit’s given 5
mg/kg/day(25).
Ecological effects
Carbamate insecticides have a mode of action similar to the organophosphates and, like the organophosphates, some kill birds at low doses. Bendiocarb is highly toxic to birds. The oral LD50 for mallard ducks is 3.1 mg a.i./ kg body weight (bw) and for bobwhite quail is 16.0 mg a.i./ kg bw. Granular formulations of a number of carbamates have been found to be particularly hazardous to birds since they are of a similar size as their natural feed. A study showed that over half of house sparrows fed granular formulations of three carbamates (bendiocarb, aldicarb and carbofuran) were killed by ingestion of just one granule and only five to ten granules killed red-winged blackbirds. Bird deaths have also been recorded on several locations. However, birds normally hide when not feeling well and often die in forests where they are eaten or degraded making it impossible to obtain accurate estimates of numbers of birds actually
killed(26).
A single broadcast application of bendiocarb on turf could result in high acute risks to birds with levels of concern being exceeded at the registered maximum application rate accordingly to the EPA risk
assessment(27). There is also an acute risk to mammals when bendiocarb is used at maximum registered application rate.
Deliberate and accidental poisonings of birds with bendiocarb have been recorded in the UK. For example, someone placed bread laced with bendiocarb on their balcony to poison birds. Both sparrows and blackbirds died in addition to a dog that accidentally ate the bread crumbs when the aluminium foil tray with the bread crumbs most probably blew down from the persons
balcony(28). In another case a green woodpecker died after a house owner applied Ant Stop Powder, to her garden path. This pesticide contained bendiocarb as the active ingredient. Despite its high toxicity to birds bendiocarb has been sold to households in the UK without appropriate label warnings. The UK governments Health and Safety Executive recently required a change to labelling of amateur use products in the UK as a result of the incident to highlight the risk to
birds(29).
Bendiocarb poses acute risks to freshwater fish. The LC50 (96 hour) for fish ranges from 0.4-1.8 mg/litre. Bendiocarb poses both acute and chronic risks to freshwater invertebrates when applied at the registered maximum rate. In Daphnia, it has a 24 hour LC50 (96 hour) of 0.33 mg/l and a 48 hour LC50 is 0.16
mg/l(30). The estuarine and marine animals are also at acute risk from the use of bendiocarb indicates the risk assessment. Due to lack of data no chronic risks for them have been possible to calculate.
Bendiocarb is also toxic to some beneficial organisms such as honeybees, earthworms and predators of plant
pest(31). The oral LD50 for honeybees are 0.1 µg/ bee(32). There had been a number of bendiocarb related deaths reported to the Wildlife Incident Investigation Scheme, run by the UK government’s Department for the Environment Food and Rural Affairs. Although reporting to this scheme is low. It has been confirmed that from 1999 to 2003, the use of bendiocarb has caused the death of 53 colonies in the
UK(33). For earthworms bendiocarb is extremely toxic, in one study a standard rate was applied and it reduced the population by
90%(34).
Environmental fate
Bendiocarb half-life varies with soil type from less than a week to up to four
weeks(35,36). The amount of bendiocarb leaching through soil is inversely proportional to the organic matter content of the soil. Bendiocarb is degraded in soil to NC 7312 (2,2-dimethyl-1,3-benzodioxol-4-ol,) a phenol that is much less likely to leach significantly.
In water bendiocarb is degraded in solution by hydrolysis, its half-life in aqueous systems is relatively stable. The half-life varies in water with the pH conditions, in more acidic waters the half-time is longer, pH 5 half-life is 48 days, compared with 81 hours in water with pH 7. It does not accumulate in water, soil or
plants(37).
Conclusion
Bendiocarb is a highly acute toxic insecticide both to humans, birds, fish and freshwater invertebrates. It causes identical symptoms as organophosphates poisonings although poisoning symptoms generally subside more rapidly. It has been found to readily transfer to the foetus. Bendiocarb has been voluntarily cancelled by its registrants as part of the Food Quality Protection Act re-registration process in US. In UK it is still registered as a biocide and amateurs can use it even though it lacks proper warning labels.
(LI)
1. The Pesticide Manual, thirteenth edition, 2003, ed Tomlin CDS, BCPC.
2. EPA, R.E.D. FACTS Bendiocarb.
3. Toxin (www.nccnsw.org.au/member/tec/project/tcye/tox/bendiocarb_01.html).
4. Ansari MA and Razdan RK, Impact of residential spraying of bendiocarb against the malaria vector Anopheles culicifacies in selected villages of Gaziabad District, Uttar Pradesh, India.
5. Rod Parker, Agricultural Information Services, personal communication.
6. Op cit 1, BCPC.
7. Delahaut KA, IPM Outreach Specialist, Bendiocarb to lose registration, 31 December 2001. University of Wisconsin Urban Horticultural Website.
8. The WHO recommended classification of pesticides by hazard and guidelines to classification: 2004, http://www.who.int/ipcs/
publications/pesticides_hazard/en/
9. Op cit 2, EPA
10. The Pesticide Manual, twelfth edition, 2000, ed Tomlin CDS, BCPC.
11. Beyond Pesticides, Chemicalwatch factsheet, Bendiocarb, 2001.
12. Op cit 3, Toxin.
13. TOXNET, 1985, National library of medicine’s toxicology data network, Hazardous Substances Databank, Public Health Service, National Institute of Health, U.S. Department of Health and Human Services, Bethesda, MD: NLM.
14. Op cit 2, EPA.
15. WHO and FAO, VBC/DS/82.52 Rev.1.
16. Reigart J, MD et al, Recognition and management of pesticides Poisonings, EPA, 1999.
17. Op cit 2, EPA.
18. Lima JS, Reis CA, Journal of Toxicology-Clinical Toxicology, 1995, 33(6):687-690.
19. Crespí FL, Luengo JB and Quinto JO, Urban pesticide exposure disables workers in Catalunya, Pesticides News, 2005, 68:12-14.
20. Op cit 7, Delahaut KA.
21. Op cit 7, Delahaut KA.
22. Whyatt RM, Barr DB, Camann DE, Kinney PL, Barr JR, Andrews HF, Hoepner LA, Garfinkel R, Hazi Y, Reyes A, Ramirez J, Cosme Y and Perera FP, Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Environmental Health Perspectives, vol 111, No 5, May 2003.
23. Op cit 2, EPA.
24. National Pesticide Information Center (NPIC), Technical Fact Sheet, http://npic.orst.edu/factsheets/bendiotech.pdf
25. Op cit 2, EPA.
26. Cox C, Pesticides and Birds: From DDT to today’s poisons. Journal of pesticide reform, winter 1991, Vol. 11, No. 4.
27. Op cit 2, EPA.
28. Humphreys DJ, and Stodulski JBJ, Bendiocarb poisoning in birds and a dog, Journal of Applied Toxicology, Vol. 1, No. 6, 1981.
29. Fletcher MR and Barnett EA, Bendiocarb poisoning in a woodpecker, The Veterinary Record, 16 October 2004, 503-504.
30. NPIC, op cit 23.
31. Op cit 4, Ansari MA.
32. Op cit 25, Cox C.
33. Pesticides poisonings of animals reports, Wildlife Incident Investigation Scheme, Environmental Panel of the Advisory Committee on Pesticides, DEFRA, www.pesticides.gov.uk/environment.asp?id=58
34. Op cit 25, Cox C.
35. Canadian www.pmra-arla.gc.ca/
36.www.doff.co.uk/pdf/Bendiocarb/DoffWoodliceKiller.pdf
37. Op cit 32, www.pmra-arla.gc.ca/[This article first appeared in Pesticides News No. 68, June 2005, pages 20-21]