Production
Dicofol first appeared
in the scientific literature in 1956(1), and was
introduced onto the market by the US-based
multinational Rohm & Haas in 1957(2). Other
current manufacturers include Hindustan (India),
Lainco (Spain) and Makhteshim-Agan (Israel)(3).
It is sold under a number of trade names,
including Kelthane and Acarin.
DDT is one of the intermediate
products produced during dicofol manufacture. In
1986, the US Environmental Protection Agency
(EPA) temporarily cancelled the use of dicofol
because relatively high levels of DDT
contamination were ending up in the final
product. Modern processes can produce technical
grade dicofol that contains less than 0.1% DDT(4).
Uses
Dicofol is used to
kill crop-feeding mite pests such as the red
spider mite. It is a contact poison which kills
the pest after being ingested and picked up from
the surface of the crop. In many countries,
dicofol is also used in combination with other
pesticides such as the organophosphates
parathion-methyl, and dimethoate(5).
Application figures are not
generally available as most countries do not
record usage data according to particular active
ingredients. The UK data show the average amount
of dicofol active ingredient used between 1994
and 1997 was 1,143 kg per year(6). It is
approved for use on apples, pears, blackcurrants,
hops, strawberries, and protected crops of
cucumbers, tomatoes and ornamentals(7).
In the US dicofol is mostly
used on cotton, apples and citrus crops. Other
crops include strawberries, mint, beans, peppers,
tomatoes, pecans, walnuts, stonefruit, cucurbits,
and non-residential lawns/ornaments(8). During 1998
the manufacturers voluntarily cancelled all
residential turf uses(9). Based on available US data from 1987
to 1996, total annual domestic agricultural usage
of dicofol averaged 390,000 kg of active
ingredient for 290,000 hectares treated. The
largest markets for dicofol in the US are cotton
(over 50%) and citrus (almost 30%). Most of the
usage is in California and Florida(10).
Acute toxicity
The acute oral LD50
(the dose required to kill half a population of
laboratory test animals) for dicofol is 595-690
mg/kg for rats. It is classified by the World
Health Organisation as a Class III, 'slightly
hazardous' pesticide(11).
Like many insecticides and
acaricides, dicofol is a nerve poison. The exact
mode of action is not known, although in mammals
it causes hyperstimulation of nerve transmission
along nerve axons (cells). This effect is thought
to be related to the inhibition of certain
enzymes in the central nervous system(12).
Symptoms of ingestion and/or
respiratory exposure include nausea, dizziness,
weakness and vomiting; dermal exposure may cause
skin irritation or a rash; and eye contact may
cause conjuctivitis. Poisoning may affect the
liver, kidneys or the central nervous system.
Very severe cases may result in convulsions,
coma, or death from respiratory failure(13).
Dicofol can be stored in fatty
tissue. Intense activity or starvation may
mobilise the chemical, resulting in the
reappearance of toxic symptoms long after actual
exposure(14).
Occupational exposure
The US EPA reviewed
dicofol under its reregistration eligibility
decision (RED) programme in 1998 which raised
some strong concerns over hormonal and
development toxicity for mixers, loaders,
applicators, and field workers(15). In particular
the EPA is concerned about exposures to handlers
during the treatment of crops by ground and
aerial equipment, and during treatment of
ornamentals using hand-held equipment(16).
There are very few accurate
estimates of occupational ill health from
exposure to pesticides. Some figures are
available from the US and the UK.
The California Department of
Food and Agriculture has one of the world's most
extensive incident reporting systems. Between
1982 and 1992, 38 incidents involving dicofol
alone were reported: systemic 19 (50%); skin 10
(26%); eye 8 (21%); and eye/skin 1 (3%). The
number of incidents per 1,000 applications for
all illnesses ranged from 0.11 to 0.21.
The US National Pesticides
Telecommunications Network database collected
reports from 1984 to 1991 showing 91 human, 9
animal and 31 other poisoning incidents for a
total of 131 incidents involving dicofol from 571
phone calls made to the hotline(17).
In the UK two cases in recent
years were confirmed by the Pesticides Incident
Appraisal Panel, although this does not
necessarily reflect the true number of incidents
involving dicofol. In one incident, a woman
suffered inflammation and irritation to the skin
around her left eye after exposure to dicofol and
tetradifon. In another case, a four-year-old boy
developed a cough after the field of hops
adjacent to his garden was sprayed with a number
of pesticides, including dicofol(18).
Neurotoxicity
Dicofol produced
neurotoxic effects in adult rats in neurotoxicity
tests. The US EPA has also identified that a
postnatal development neurotoxicity study in rats
is required in order to fill current data
gaps(19).
Chronic effects
Tests on laboratory
animals show that the primary effects after long
term exposure to dicofol include increases in
liver weight and enzyme induction in the rat,
mouse and dog. There are also effects relating to
altered adrenocorticoid metabolism (part of the
hormonal system). In the rat hormonal changes
were accompanied by the histological observation
of vacuolation (empty cavities) of the cells of
the adrenal cortex(20).
The US EPA has classified
dicofol as a Group C, possible human carcinogen.
There is limited evidence that it may cause
cancer in laboratory animals, but there is no
evidence that it causes cancer in humans. This
classification was based on animal test data that
showed an increase in the incidence of liver
adenomas (benign tumour) and combined liver
adenomas and carcinomas in male mice(21).
Residues in food and water
An assessment of
dicofol by the UK Pesticides Safety Directorate
in 1996 found that residues in apples, pears,
blackcurrants and strawberries were higher than
expected. The assessors considered it likely that
the acceptable daily intake may be breached under
normal conditions of use. Because of data gaps,
they also found that implications are not clear
for data on the transfer of residues from hops
into beer, from blackcurrants into blackcurrant
juice and apples into apple puree(22).
There is no established US
maximum contaminant level (MCL) or health
advisory levels for residues of dicofol in
drinking water(23). In the European Union, the maximum
level is the same for all active ingredients 0.1
mg/litre (parts per billion [ppb])(24).
Cumulative effects
As part of the RED
review, US regulators have to assess all
available information concerning the cumulative
effects of pesticide residues and other
substances that have a common mechanism of
toxicity.
Dicofol is classed as an
organochlorine pesticide. Other members of this
class include DDT, methoxychlor, chlorbenzilate
and ethylan. Less closely related members include
lindane, dieldrin, endrin, chlordane, heptachlor,
aldrin, endosulfan, kepone and toxaphene(25). Currently
the US EPA does not have available data to
determine whether dicofol has a common mechanism
of toxicity with other substances or how to
include this pesticide in a cumulative risk
assessment(26).
Endocrine disruption
The US RED review
concludes that evidence for dicofol to cause
endocrine disruption is suggestive, but not
definitive. It has reproductive effects in some
species (see below), although they appear to
differ somewhat from its close analogues DDT
and/or DDE. Whether the difference is due to the
ability of dicofol to be metabolised to less
toxic chemicals, its relatively short half-life
(compared to DDT/DDE), or the reduced potency of
the parent compound, is not currently known(27).
In 1980, an accident at the US
Tower Chemical Company led to a release of
dicofol into Lake Apopka in Florida. Ten years
later Dr Guillette of Florida University linked
this incident to a subsequent decline in the
fertility of alligators in the lake. The US EPA
is still not clear whether dicofol is involved in
the reproductive failure of the alligator
population following the accidental spill(28).
In 1993, US scientists reported
the presence of dicofol in water samples from the
western San Joaquin Valley in California. The
highest concentration 2,500 ng/litre (2.5 ppb)
was found at Orestimba Creak following
agricultural spraying in the area. The
researchers were concerned about these levels and
called for further research into the
endocrine-disruption toxicology of chemicals
dissolved in water at low concentrations(29).
Environmental fate
According to the US
Department of Agriculture, dicofol has a
half-life in the environment of 60 days(30).
Other US EPA laboratory and field studies show
that dicofol has a half-life ranging from days to
months. In ecological monitoring studies
conducted in New York, Florida and California,
dicofol dissipated from the soil surface with a
half-life ranging from two to four months. The
chemical is likely to be more persistent in
acidic than neutral or alkaline soils or
waters(31).
Dicofol and DDT are similar
chemical structures, and the US EPA considers
that dicofol has to a lesser degree some ability
to accumulate in the environment(32).
Wildlife
Analytical screening
of wildlife tissue samples for organochlorine
chemicals rarely includes dicofol, and this may
explain why, compared with other organochlorines,
the relative hazard of dicofol to wildlife
populations is poorly known(33).
Dicofol is 'highly' to 'very
highly' toxic to a range of aquatic organisms,
including fish, invertebrates and
estuarine/marine organisms(34). The 96 hour LC50 for Channel catfish is 0.30 mg/litre
(parts per million [ppm]), 0.51 mg/l for
bluegill, 0.183 mg/l for fathead minnow, and 0.12
mg/l for rainbow trout(35). It also causes early life stage
toxicity at levels of 19 ppb for fathead minnow
and 1 ppb for rainbow trout(36). Little information is available on
bioaccumulation in fish species(37).
Estuarine/marine organisms are
particularly susceptible to dicofol. The 96 hour
LC50
for the eastern oyster embryo larvae is 15.1 mg/l
ppb, 0.14 mg/l (ppm) for mysid shrimp, and 0.37
ppm for sheepshead minnow(38).
In birds, dietary
concentrations of dicofol between one and 10 mg/g
(wet weight) fed to captive adult females caused
eggshell thinning, reduced hatching success, or
reduced fertility in American kestrels (Falco
spar-veruis) and eastern screech-owls
(Otus asio)(39). Similar effects have also been noted
in the mallard duck and ring dove(40). Researchers
in the US are concerned that there have been no
intensive field investigations of possible
reproductive effects, despite the results from
these laboratory findings(41). Because of its potential to
bioaccumulate in the environment, the US EPA has
requested that chronic reproduction testing is
required(42).
Regulation
In 1990, the use of
dicofol was suspended in Sweden for environmental
reasons(43). In Switzerland its use is permitted
for research purposes only(44). Throughout the
European Union dicofol containing less than 78%
pp'-dicofol or more than lg/kg (0.1%) of DDT or
DDT related compounds cannot be used(45).
The 1998 US EPA review of
dicofol recommended a number of changes in order
to protect the environment and wildlife. Dicofol
applications are limited to no more than one per
year. In the UK, the maximum number of treatments
permitted is two per year for apples and hops,
and two per crop for strawberries, protected
crops and tomatoes(46).
When the UK Advisory Committee
on Pesticides reviewed dicofol in 1995, it was
also concerned about occupational exposure, and
made some recommendations:
Conclusion
Environmental concerns
have prompted progressive countries like Sweden
to ban dicofol, and other countries are following
suit by imposing severe restrictions on its use.
Nevertheless dicofol is one of
the world's last organochlorines still in
widespread use. It has perhaps survived because
its environmental persistence is low relative to
DDT, although this is not the case when compared
with the vast majority of other pesticides on the
market. DDT is after all one of the lowest of all
common denominators.
References
1. WHO/Food and Agriculture Organisation, Fact Sheet on dicofol, No 81, 1996, 14pp.
2. US EPA RED FACTS, Dicofol, Office of Pesticide Programs, US EPA, Washington, 1998, 7pp.
3. Tomlin, CDS, The Pesticide Manual, BCPC, 1997, p380-382.
4. Extension Toxicology Network, (EXTOXNET), Dicofol, Cornell University, US, 1992, 5pp.
5. Op. cit. 3.
6. Pers. Comm. Miles Thomas, Pesticide Usage Survey Group, Central Science Laboratory, 1999.
7. Evaluation on: Review of dicofol, Ministry of Agriculture, Fisheries and Food, York, 1996, 105pp. p. 8.
8. Op. cit. 2.
9. Dicofol, Reregistration Eligibility Decision, Environmental Protection Agency, Office of Pesticides Programs, 1998, 238pp.
10. Op. cit. 9.
11. WHO Classification of Pesticides by Hazard 1996-1997, International Programme on Chemical Safety, WHO/IPCS/96.3.
12. Op. cit. 1.
13. Op. cit. 4.
14. OP cit. 4.
15. Op. cit. 2.
16. Op. cit. 9.
17. Op. cit. 9.
18. Review of Dicofol, Ministry of Agriculture Fisheries and Food, September 1996, 105pp.
19. Op. cit. 9.
20. Op. cit. 18.
21. OP cit. 4.
22. Op. cit. 18.
23. Op. cit. 9.
24. EU Drinking Water Directive, 80/778/EEC.
25. Ware, G.W., Fundamentals of Pesticides, Thomson Publications, 1982.
26. Op. cit. 9.
27. Op. cit. 9.
28. Op. cit. 9.
29. Domagalski, J., Occurrence of dicofol in the San Joaquin River, California, Bulletin of Environmental Contamination and Toxicology, 1996, 57:284-291.
30. Op. cit. 4.
31. Op. cit. 9.
32. Op. cit. 9.
33. Clark, D.R., and Flickinger, Dicofol and DDT residues in lizard carcasses and bird eggs from Texas, Florida and California, Bulletin of Environmental Contamination and Toxicology, 1995, 54:817-824.
34. Op. cit. 2.
35. Op. cit. 9.
36. Op. cit. 9.
37. Op. cit. 9.
38. Op. cit. 9.
39. Op. cit. 33.
40. Rohm and Haas, Material Safety Data Sheet, 1999.
41. Op. cit. 33.
42. Op. cit. 9.
43. Emmerman, Anders, Pesticides News No. 34, December 1996.
44. Dicofol, Decision Guidance Document, FAO/UNEP, 1993.
45. EC Prohibition Directive of 21 December 1978.
46. R. Whitehead (Ed.), UK Pesticide Guide 1999, BCPC, Farnham, Surrey, UK.
47. Op. cit. 18.
[This article first
appeared in Pesticides News No.43, March 1999, p20-21]