This fact sheet summaries the important health and environment effects of
the fungicide benomyl. It came to the public's attention in the early 1990s
because the exposure of pregnant women to benomyl was linked with subsequent eye
defects in the foetus.
What is benomyl
Benomyl was first reported as a fungicide in 1968 and
introduced onto the UK market in 1971 by the US company Du Pont(1). It is a
systemic benzimidazole fungicide that is selectively toxic to micro-organisms
and to invertebrates, especially earthworms(2).
Benomyl and its main metabolite
carbendazim bind to microtubules (an essential structure of all cells) and
therefore interfere with cell functions such as cell division and intracellular
transportation. The selective toxicity of benomyl as a fungicide is possibly due
to its heightened effect on fungal rather than mammalian microtubules(3).
Uses and usage
Benomyl is used as a pre-harvest systemic fungicide, and as a post-harvest dip
or dust. It combats a wide range of fungal diseases of arable and vegetable
crops, apples, soft fruit, nuts, ornamentals, mushrooms, lettuce, tomatoes and
turf. It is also available widely for amenity and amateur garden use(4).
Benomyl's principal trade name is Benlate.
The basic manufacturer is Du Pont
Agricultural Products, based in Wilmington, Delaware. Global figures of benomyl
usage are not widely available. In Britain benomyl was applied to 22,157 ha of
top fruit crops (1992)(5); 2,957 ha of bulb and flower crops (1994)(6); 1,359 ha
of outdoor vegetable crops (1995)(7) and 1,033 ha of hardy nursery stock
Benomyl is of such a low acute toxicity to mammals that it
has been impossible or impractical to administer doses large enough to establish
an LD50. It therefore has an arbitrary LD50 that is 'greater than 10,000
mg/kg/day for rats'. However, skin irritation may occur with workers exposed to
benomyl(9). It is a mild to moderate eye irritant and is a skin sensitiser.
Florists, mushroom pickers and flower growers have reported allergic reactions
In 1992, benomyl exposure caused
adverse occupational health effects (headaches, diarrhoea and sexual
dysfunction) in agricultural workers in Florida(11).
In a laboratory study, dogs fed benomyl in their diets for three months
developed no major toxic effects but did show evidence of altered liver function
at the highest dose (150 mg/kg). With longer exposure, more severe liver damage
occurred including cirrhosis after two years(12).
The US Environmental Protection Agency classified benomyl as a possible human
carcinogen(13). There is an element of doubt in this classification because
carcinogenic studies have produced conflicting results. A two year experimental
mouse study has shown it probably caused an increase in liver tumours. The
Ministry of Agriculture Fisheries and Food (MAFF) takes the view that this was
bought about by the hepatoxic effect of benomyl(14).
Tests on laboratory animals have shown benomyl can have an effect on
reproduction. In one rat study, where the mothers were fed 1,000 mg/kg/day for
four months, the offspring showed a decrease in viability and fertility(15). In
studies to investigate the effects of benomyl on male reproductive performance,
fertility was reduced at all dose levels tested. In another study a no-effect
level of 15mg/kg/day was established based on testicular abnormalities(16).
Permanent reductions occurred in the
size of testes and male accessory glands in 100 day-old offspring from female
laboratory rats receiving 31.2 mg benomyl/kg body weight per day. Rats developed
a reduced sperm activity following acute inhalation exposure, acute and
sub-chronic oral exposure. The same effect occurred in dogs following a single
four hour inhalation exposure(17).
In 1993, the Observer, a UK national newspaper, published the first in a
series of articles alleging a possible link between exposure of pregnant mothers
to benomyl and their children being born without eyes (anophthalmia) or with
related syndromes including reduced eyes and blindness due to severe damage of
the optic stem(18). The newspaper cited a number of suspected clusters in the UK
that may have corresponded to areas of benomyl use.
Government officials at MAFF made an
assessment of the claims but concluded it was doubtful there was a link. They
said likely benomyl exposure in the pregnant mothers was not sufficiently high
to cause developmental eye problems in their children. MAFF concluded: "The
no effect level for teratogenicity based on all the available data was
30mg/kg/day. The exposure of both operators and consumers is several orders of
magnitude lower than this no-effect level. It is therefore difficult to see how
any link can be made with eye defects and exposure to benomyl."(19)
Studies have shown that eye defects can
occur at relatively high doses. A test in which rats were dosed orally
demonstrated evidence of microphthalmia at dose levels of 62.5 mg/kg and
At the height of concern over benomyl,
councillors on Lincoln's Environmental Committee urged local farmers to adopt a
voluntary ban on the use of benomyl.
In 1996 a Miami jury awarded US$4
million to a child whose mother was exposed in pregnancy to Benlate. The child
was born without eyes. The mother in this case was subject to an unusually high
dose of Benlate. The case is on appeal by the manufacturers. An important issue
in the case is whether the timing of exposure - during the formation of the
optic nerve in the foetus - is critical as well as the magnitude of exposure. A
Benlate compensation case involving an English boy from Essex born without eyes
is also due to be heard shortly in the US(21).
There are conflicting negative and positive results making it difficult to form
a definite conclusion relating to mutagenicity. Two papers show that benomyl
causes an increased incidence of chromosomal aberrations. In a range of in
vitro assays there was evidence that benomyl caused aneuploidy (a chromosome
abnormality). Other results show it is not mutagenic(22).
Benomyl binds strongly to soil and does not dissolve in water to any great
extent. When applied to turf, it has a half-life of three to six months, and
when applied to bare soil the half-life is six to 12 months(23).
Resistance to benzimidazole fungicides in general has reduced the market share
of benomyl in recent years. Benomyl was the first truly systemic fungicide and
originally showed a wide range of activity against pathogens in many different
Crop damage claims in Florida
In 1991, many US growers blamed Benlate DF for destroying millions of dollars
worth of crops. Growers placed as many as 1,900 damage claims against the
manufacturers Du Pont, mostly involving ornamental crops in Florida. The reason
for the crop damage is not clear. The Florida Department of Agriculture
suggested Benlate was contaminated with dibutylurea and sulfonylurea herbicides.
A non-pesticide theory suggested that unusual weather was also a contributory
After many years of legal wrangling Du
Pont paid out about US$750 million in damages and out-of-court settlements. By
1993, a coalition of farm worker and environmental groups came together to form
Benlate Victims Against Du Pont that called for a nation-wide boycott of Du Pont
After carrying out tests, Du Pont
denied that Benlate was contaminated with dibutylurea and sulfonylureas and
stopped compensation pay-outs. In 1995, a Florida judge rejected a complaint
from the Florida Department of Agriculture that had alleged such a link(25). The
affair continues to inflict financial repercussions on Du Pont. The third
quarter results in 1996 included a US$47 million charge relating to the Benlate
The main area of concern with benomyl involves its chronic effects. At high
doses, adverse effects such as eye birth defects occur after exposing
experimental animals to the fungicide. MAFF says people are unlikely to receive
such doses and therefore conclude it is safe. This issue raises two questions:
is there a safe level of exposure, and is the timing of the exposure during
As yet, national regulatory authorities
have not taken a precautionary approach and banned benomyl on health grounds. An
alternative, Azoxystrobin, may be coming onto the market. It is based on a
natural fungicide and may prove to be safer than benomyl. However, it will
probably be more expensive, and follows a chemical-for-chemical replacement
strategy that may not be successful.
1. Tomlin, C., (Ed.) The Pesticide Manual, 10th Edition, British Crop
Protection Council/Royal Society of Medicine, 1994.
2. Benomyl, Extoxnet, Pesticide Management Education Program, Cornell
University, NY, May 1994.
3. World Health Organisation, WHO/PCS/94.87 Data sheet on benomyl, Geneva,
4. Whitehead, R (Ed) The UK Pesticide Guide, British Crop Protection
Council/CAB International, 1996.
5. Thomas, M.R. and Garthwaite, D.G., Orchards and Fruit Stores in Great
Britain 1992, Pesticide Usage Survey Report 115, Central Science Laboratory,
6. Thomas, M.R. and Garthwaite, D.G., Outdoor Bulbs and Flowers in Great
Britain 1993, Pesticide Usage Survey Report 121, Central Science Laboratory,
7. Garthwaite, D.G., Thomas, M.R., Hart, M.J, and Wild, S, Outdoor vegetable
crops in Great Britain 1995, Pesticide Usage Survey Report 134, Central
Science Laboratory, 1997.
8. Thomas, M.R. and Garthwaite, D.G., Hardy Nursery Stock in Great Britain
1993, Pesticide Usage Survey Report 120, Central Science Laboratory, 1995.
9. Op. cit. 2.
10. Benomyl evaluation No. 57, MAFF, July 1992, pp109-111.
11. More problems for Benlate? Agrow, 13 March 1992, p13.
12. Op. cit. 2.
13. List of Chemicals Evaluated for Carcinogenic Potential, US EPA Office of
Pesticide Programs, Washington, US, 1996.
14. Op. cit. 10, p91.
15. Benomyl, Environmental Health Criteria No 148, World Health
Organisation, Geneva, Switzerland, 1993.
16. Op. cit. 10, p110.
17. Op. cit. 14.
18. Mystery of babies with no eyes, 'clusters' raise fears of link with
pesticide, 17 January 1991.
19. Press statement on benomyl, MAFF, 1 March 1993.
20. OP. cit. 10, p110.
21. US$4 million for Benlate eye victim, Pesticides News No 33, p8.
22. Op. cit. 3.
23. Op. cit. 2.
24. Copping, L.G., Agrow's Top Twenty Five, PJB Publications, 1996, p105.
25. Various Agrow reports from March 1992 to June 1996.
26. Op. cit. 24.
[This article first
appeared in Pesticides News No.35, March 1997, p20-21]