Fact sheet:

Aldrin or Dieldrin

Version: 09/01/2015

GMP+ International B.V.

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 Content

General Summary

Summary of GMP+ products standards for the animal feed sector

More Facts
1. Nature, history and prevalence of aldrin or dieldrin
2. Transmission to the environment, plants, animals and humans
3. Diagnose of poisoning
4. Potential hazards and adverse effects
5. Severity of the hazard
6. Standards
7. Analysis methods
8. Control measures
9. References
10. Websites

APPENDIX / APPENDICES

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 General Summary

Name: Aldrin or Dieldrin

code: C02

Description: Separately or jointly expressed in Dieldrin. Aldrin can actually convert to Dieldrin.
Pesticide which may still be used outside the EU. Can occur in all (imported) feed
materials.
Type: chemical

Severity: high

Control measures: - Analyse intermediate product(s)

- Crop registration
- Distance between sections of land
- Establish purchasing requirements
- Establish purchasing requirements for pesticides
- Finished product analysis
- Monitor cultivation area (certified)
- Monitor fish catch area
- Received product/raw material analysis
- Refinery

The control measures specified in this fact sheet are all control measures which can be used depending on the
product and/or process step.

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 SUMMARY OF GMP+ SPECIFIC FEED SAFETY LIMITS FOR THE ANIMAL FEED SECTOR
Contaminant Product Action limit(1) Rejection limit(1) Source Supplementary Analysis method7
requirements
Chemical: Crop protection agents (Pesticides which are not permitted in the EU)

C2 Aldrin Feed materials and compound feed, with the - 0.01 mg/kg Commission Maximum level for aldrin OZM Part 2; OSP-
exception of: Regulation (EU) No and dieldrin, singly or 11
Dieldrin 574/2011 amending combined, expressed as
Annex I to Directive dieldrin.
(Singly or combined expressed as 2002/32/EC
dieldrin)
- fats and oils, 0,1 mg/kg
- compound feed for fish 0.2 mg/kg

[1 ] Action limit: A feasible limit agreed in consultation with the sector, supplier or customer. If this limit is exceeded then an investigation into the cause should be undertaken and corrective measures should be
taken to remove or control that cause. Maximum levels in mg/kg (ppm) of the feed materials or compound feeds, derived to a moisture content of 12% unless mentioned differently.
Rejection limit: A feasible limit agreed in consultation with the sector, supplier or customer. If this limit is exceeded then the product is not suitable for use as feed material or animal feed. Maximum levels in mg/kg
(ppm) of the feed materials or compound feeds, derived to a moisture content of 12% unless mentioned differently.
[7] The research methods (OZM) can be found via the PDV website (www.pdv.nl ; quality; research methods)

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 More facts

Chemical name
Aldrin:
1,2,3,4,10,10-hexachloro-1,4,4,5,8,8-hexahydro-exo-1,4-endo-5,8-dimethanonaphthalene.
Dieldrin:
1,2,3,4,10,10-hexachloro-6,7-epoxy-1,4,4,5,6,7,8,8-octahydro-endo-1,4-exo-5,8,-
dimethanonaphthalene.

CAS-number
Aldrin = 309-00-2
Dieldrin = 60-57-1

Synonyms
Aldrin = Aldrine; HHDN.
Dieldrin = Dieldrine; HEOD.

1. Nature, history and prevalence aldrin and dieldrin

Aldrin and dieldrin are organochlorine insecticides with similar structures. Dieldrin is a
metabolite of aldrin as well as a marketed insecticide. They have previously been widely
used, but are now banned in most countries worldwide and are included in the Stockholm
convention on persistent organic pollutants (POPs) and the United Nation Economic
Commission for Europe (UNECE) Convention on long-range trans-boundary air pollution
protocol on POPs (CLRTAP-POP). These compounds can be transported over long
distances via the atmosphere. There are still residues of dieldrin in the environment and in
human tissues, but the levels have been declining over the last 30 years. (EFSA, 2005)
Persistent Organic Pollutants (POPs) are chemicals that (Mrner et al., 2002):
are extremely stable and persist in the environment;
bio-accumulate in organisms and food chains;
are toxic to humans and animals and have chronic effects such as disruption of
reproductive, immune and endocrine systems, as well as being carcinogenic, and are
transported in the environment over long distances to places far from the points of
release.

While technical grade aldrin is a tan to dark brown solid with a melting point of 49 - 60C,
pure aldrin is a colourless crystalline solid with an odourless to mild chemical odour. It has a
melting point of 104C. While the solubility in water is only 0.011 mg/L, aldrin is readily
soluble in most organic solvents (ATSDR, 2002). Aldrin is a fat soluble (EFSA, 2005). The
molecular formula of aldrin is C12H8Cl6. Its chemical structure is shown in figure 1.

Figure 1. Chemical structure aldrin.

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 Technical grade dieldrin consists of light brown tan flakes, with a melting point of 95C, pure
dieldrin is a white crystalline solid with a mild chemical odour. Its melting point is 175 -
176C. The solubility of dieldrin in water is reported between 0.11 and 0.19 mg/L and thus
practically insoluble, it is moderately soluble in most common organic solvents (ATSDR,
2002). Dieldrin is fat soluble (EFSA, 2005). The molecular formula of dieldrin is C12H8Cl6O.
Its chemical structure is shown in figure 2.

Figure 2. Chemical structure dieldrin.

Aldrin and dieldrin were first synthesized in 1948 in the United States. Commercial
manufacture began in 1950, first in the United States and later on in The Netherlands
(WHO1, 1989). Aldrin is synthesized by the Diels-Alder reaction of
hexachlorocyclopentadiene (HCCP) with an excess of bicycloheptadiene followed by a
condensation reaction at approximately 120C and atmospheric pressure. Excess
bicycloheptadiene is then removed by distillation, and the final product is further purified by
recrystallization (Sittig, 1980 as cited by EFSA (2008)).
Dieldrin may be synthesized by the epoxidation of aldrin with a peracid such as peracetic
acid, but may also be synthesized through the condensation of hexachlorocyclopentadiene
with the epoxide of bicycloheptadiene (WHO1, 1989).

In 2003 aldrin was still formally allowed for use in a few African, Austral-Asian and South
American countries, but the use is generally restricted (UNEP, 2003). It was/is used as a
broad-spectrum soil insecticide (generally at 0.5 to 5 kg/hectare) for the protection of corn,
potato, citrus, and other crops against termites, corn rootworms, seed corn beetles and
maggots, wireworms, rice water weevil, grasshoppers, Japanese beetles, etc., as well as a
seed dressing for rice and to combat ant and termite infestations of wooden structures
(ATSDR, 2002; WHO1,2, 1989).
In 2003 dieldrin was still registered in a few African, Asian and South American countries
similarly to aldrin in agriculture, but the use is restricted (UNEP, 2003). It was/is often used
principally to protect wooden structures against ant and termite attack, in industry for
protection against termites, wood borers and textile pests, and as a residual spray and
larvacide for the control of several insect vectors of disease (ATSDR, 2002; WHO1,2, 1989;
US-EPA, 2003).

2. Transmission and likelihood of occurrence

Environment
Aldrin and dieldrin production and use has been cancelled in several countries. Because of
the persistent nature of these compounds, however, these compounds are still present in the
environment. Aldrin and dieldrin may be volatilized from sediment and redistributed by air
currents, contaminating areas far from their sources. They have been identified in a variety of
environmental media (air, surface water, groundwater, soil, and sediment) (ATSDR, 2002).

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 Past application of aldrin and dieldrin for termite control is a continuing source of
contamination of indoor air. In addition, these compounds may be released to the
atmosphere from previously treated soil and contaminated surface waters. Release of aldrin
and dieldrin into the air may also occur as a result of atmospheric dispersal of contaminated
soils (ATSDR, 2002).
Aldrin and dieldrin may be released to surface waters as a result of runoff from contaminated
croplands and other contaminated sites. Although aldrin and dieldrin are no longer permitted
for general use in many countries, dieldrin, in particular, has been detected in many
waterways and cropping soils. Due to the persistence of these compounds, especially
dieldrin, they have been detected in a wide variety of aquatic systems. The chemical
characteristics of aldrin and dieldrin suggest movement through soil and contamination of
groundwater will be minimal. The only reports of aldrin or dieldrin contamination of
groundwater occurred at sites with high concentrations of these compounds (ATSDR, 2002).
Possible releases of aldrin and dieldrin to soil may come from the improper disposal of old
stocks. Wet and dry deposition of particulate phase aldrin and dieldrin from the atmosphere
is another potential source of soil contamination. As aldrin and dieldrin take decades to break
down in the environment, past agricultural uses of aldrin and dieldrin have resulted in
persisting soil residues and uptake in a wide range of crops (ATSDR, 2002). Water has been
found to compete with aldrin for adsorption sites in clay minerals, and thus aldrin binds to a
greater extent when the soil is dry; in dry soils, mineral components play the largest role in
adsorption, whereas in moist soils, organic materials are predominant; and other factors
being equal, adsorption is expected to be the lowest in sandy soils having minimal organic
content (WHO1, 1989).

In biological systems of soils, plants, and animals, aldrin converts rapidly to dieldrin by a
microsomal oxidation reaction (epoxidation). The transformation of aldrin to aldrin acid also
occurs in soils. The half-life of aldrin in soil is estimated to be 53 days. Dieldrin is much more
resistant to biodegradation than aldrin. The half-life of dieldrin in temperate soils is about 5
years, while it disappears more quickly (up to 90% in 1 month) from tropical soils (ATSDR,
2002).

No data were found concerning aldrin and dieldrin levels in products of mineral origin.

Plants
Aldrin and dieldrin uptake by plants has been reported to be substantially higher in root
crops than in grain crops; root crops are much more likely to take up residues from treated
soils, whereas it is rare in grain crops for residues to reach detectable levels in the grain
(WHO1, 1989). In one model ecosystem study of Cole et al. (1976, as cited by ATSDR,
2002), maize was planted in vermiculite soil to which 2.09 ppm radiolabeled aldrin had been
applied; after 14 days, the maize contained 2.83 ppm radiolabeled residue, of which 0.762
ppm was aldrin and 1.538 ppm dieldrin. About 78% of the residues were found in the roots,
with the remainder in the shoots. The mechanism of uptake into plants for these compounds
is not clear. It may vary considerably with species and the nature of the soils in which they
are grown, and apparently involves both absorption through roots and absorption of vapours
through leaves (ATSDR, 2002; WHO1, 1989).
Marine algae accumulate dieldrin. Results of a study by Rose and McIntire (1970) indicated
that increases in concentration up to 30,000 times that of the water had occurred.

Chaudry et al. (1976) studied the aldrin and dieldrin distribution in soybeans, oil and by-
products during processing. Soybean samples acquired from aldrin-treated and non-treated
fields were analysed for aldrin and dieldrin content. In general, dieldrin levels in soybeans, or
fractions thereof, had a clear positive relationship with the aldrin applications. Deodorization
of oil was noted to be the most effective in the removal of pesticides, and deodorizer
distillate had high concentrations of aldrin and dieldrin, although pesticide levels in the oil
decreased somewhat after each processing step. Refined oil was found to be free of aldrin

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 and dieldrin residues up to instrumental detection limits. No data were found concerning
aldrin and dieldrin levels in vegetable oils and their by-products, however looking at the
hydrophobic character of aldrin and dieldrin, residues in these products cannot be excluded.
Specifically when they originate from contaminated fields.

The EFSA (2005) reports levels of aldrin and dieldrin in products of vegetal origin, analysed
by EU Member States. In general levels were below limits of detection. Denmark reported a
number of samples containing aldrin at levels between 2 and 19 g/kg and dieldrin at levels
between 1 and 13 g/kg, however no information was given concerning the origin (vegetal or
animal) of the samples. Norway reported a level of 0.4 g/kg dieldrin in one sample of
vegetable oil. Feed products of plant origin only occasionally showed levels of aldrin and
dieldrin near the limit of determination of 2 - 10 g/kg (EFSA, 2005).
No data were found concerning levels of aldrin and dieldrin in crops containing adherent soil
originating from contaminated soil (e.g. grass and beet products) or contaminated soil
ingested by grazing animals.

In the DOS-database data can be found concerning aldrin and dieldrin in feed materials of
vegetal origin.

Animals
Exposure:
Dieldrin rather than aldrin predominates in feed materials of animal origin. It seems that fish
oil is by far the most important source of dieldrin contamination of the feed chain. However,
depending on species and geographical origin, the range of contamination may differ
considerably. On average, fishmeal samples are less contaminated by at least one order of
magnitude. With some exceptions, fish derived feeding stuffs from the Southern hemisphere
seem to contain somewhat lower dieldrin levels than the corresponding samples from the
Northern hemisphere (EFSA, 2005).

Important foods in dieldrin exposure of humans are products of animal origin with a high
fat content i.e. milk, and meat. Possibly feed materials originating form milk and meat are
also of importance for animal exposure. An incident of dieldrin contaminated potatoes being
fed to steers was reported by Harr et al. (1974), resulting in residues in the rendered fat of
these animals (0.1 to 0.2 ppm dieldrin (dry weight basis) in potatoes vs. 0.76 ppm in
rendered fat).

No data were found concerning aldrin and dieldrin exposure originating from soil. However
based on US-EPA (2003) human exposure data, as shown in tables 1 and 2, it can be
assumed that animals are exposed to dieldrin via the intake of soil. Additionally free-range
poultry might be exposed to dieldrin via eating earthworms. Earthworms take up dieldrin
from the soil and concentrate it to a maximum of about 170 times (WHO1, 1989). In a Kenyan
study by Mugambi et al. (1989) it was shown that free-rang eggs contained significant higher
dieldrin levels than eggs from enclosed hens. Indicating a higher level of dieldrin exposure
for free-range hens. Similar results were found during a Belgian study by Windal et al. (2009)
who also found higher concentrations of dieldrin in free-range eggs compared to battery
eggs. These authors stated that these higher dieldrin levels are a consequence of contact
with the environment and especially the soil.

No data were found concerning the level of exposure to aldrin and dieldrin. However the
EFSA (2005) states that based on the available data on animal exposure via feed produced
according to good agricultural practice, it is not likely that terrestrial animals will be exposed
to levels that cause toxic effects.

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 Absorption:
Although data are limited regarding absorption of aldrin and dieldrin following oral exposure,
several metabolic studies carried out in rats demonstrated that these compounds are
absorbed via the gastrointestinal tract. Based on the analysis of radioactivity excreted or
remaining in the carcass of rats, Ludwig et al. (1964) estimated the absorption of aldrin to
approximately 10 % of the administered dose. Absorption of dieldrin in rats was shown by
Hayes (1974).

Distribution:
Given their hydrophobic nature and high solubilitys in fat, the largest concentrations of aldrin,
dieldrin, and their metabolites are generally found in adipose tissue (ATSDR, 2002; WHO1,
1989; US-EPA, 2003).
When dairy cows, steers, hogs, and lambs were fed dieldrin for 12 weeks at levels between
0.1 and 2.25 mg/kg feed (Gannon et al., 1959 as cited by EFSA, 2005), the compound was
detectable in the adipose tissue of all animals at all dose levels (LOQ = 0.01 mg/kg). In all
species, the concentrations in the main tissues were in the following order: adipose tissue >
meat > liver > kidney. Concentrations in the various tissues are roughly proportional to their
fat content, explaining the relatively high levels found in samples of muscle containing also
surrounding fat. Average dieldrin in fat from animals, which had been fed the highest dose,
was 8.7, 4.3, 5.5 and 1.7 mg/kg for steers, dairy cows, pigs and lambs respectively.
In hens, dietary exposed to dieldrin (0.75 mg/kg of feed) (Gannon et al., 1959, as cited by
EFSA, 2005), residues in fat after 12 weeks of exposure were above 35 mg/kg.
Studies show that trans-placental transfer of aldrin and dieldrin occurs (ATSDR, 2002).

Excretion:
In rats dosed with 14C-aldrin at 0.012 mg/kg bodyweight/day for three months, both aldrin and
dieldrin were found in the faeces, with lower concentrations of both compounds also found in
the urine (Ludwig et al., 1964). In a study of sheep dosed with 14C-dieldrin, excretion of
radioactivity was higher in the faeces than in the urine: 3-14% of the radioactive dose was
recovered in the urine over periods of 3-6 days (Hedde et al., 1970).
The 9-hydroxy dieldrin derivative is the major excreted metabolite in rats, mice, sheep and
monkey, whereas in rabbit dieldrin is mainly eliminated as the 6,7-trans- dihydroxy
biotransformation product. In addition to these metabolites, pentachloroketone and aldrin
dicarboxylic acid may be present in excreta (EFSA, 2005).
The excretion of dieldrin via milk has been reported by several authors (US-EPA, 2003;
ATSDR, 2002; EFSA, 2005).

Metabolism:
The first step in the biotransformation of aldrin is the formation of dieldrin. In rats liver
microsomes are responsible for the epoxidation (Ghiasuddin and Menzer, 1976). Two major
metabolic pathways of dieldrin are predominant in mammals: (1) oxidation of carbon 9,
resulting in 9-hydroxydieldrin, and (2) hydrolysis of epoxide, resulting in 6,7-trans-
dihydroxydihydroaldrin. Both 6,7-trans-dihydroxydihydroaldrin and 9-hydroxydieldrin can be
conjugated to glucuronic acid before being excreted. In addition to these metabolites,
pentachloroketone (produced from skeletal rearrangement of dieldrin) and aldrin dicarboxylic
acid (formed from 6,7-trans-dihydroxydihydroaldrin) may be present in excreta (EFSA, 2005).

Humans via animal products

Due to the progressive decline of aldrin/dieldrin concentrations in food and levels in human
tissues, the availability of new intake studies is limited. The ATSDR (2002) gives a good
overview on intake of these components based on literature published up to the 1990s.
Because of its rapid conversion to dieldrin in the environment, aldrin is not considered to be
an important human dietary contaminant. The average aldrin intake is nowadays estimated
to be less than 1 g/kg body weight/day. Food is considered the most important source of
human dieldrin exposure. Important foods are those with a high fat content i.e. fish, milk,

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 and meat (EFSA, 2005). Residues levels of aldrin and dieldrin in dairy products are reported
by several authors. For example, residue levels were reported in Argentinian butter
(Lenardn et al., 1994) and in Mexican cheese (Albert et al., 1990).
During the period of 1965 - 1970, total US dietary intake was reported to be 50 - 80 g
dieldrin/kg body weight/day and 0.1 - 40 g aldrin/kg body weight/day (ATSDR, 2002). Since
the late 1970s, the use of aldrin and dieldrin declined and dietary intake has decreased
(EFSA, 2005).

The transfer rates from feed to milk, eggs and adipose tissue are among the highest found
for chlorinated pesticides, making aldrin, and especially dieldrin, highly accumulative
compounds. Due to a high level of bioaccumulation in the aquatic food chain, fish derived
products, particularly fish oil, were identified to contain the highest levels of dieldrin (EFSA,
2005).
Concerning eggs, in a Kenyan study by Mugambi et al. (1989) and in a Belgian study by
Windal et al. (2009) it was shown that free-range eggs contained significant higher dieldrin
levels than eggs from enclosed hens.

Biotransfer factors (BTFs) for beef and milk, defined as the ratio of a compound in beef or
milk (mg/kg) to its daily intake by the animal (mg/day), have been estimated for aldrin to be
0.085 and 0.023, respectively (ATSDR, 2002).
Noble (1990, as cited by EFSA, 2005) derived transfer ratios (concentration in milk or eggs
relative to the concentration in the diet) from trials which have involved feeding aldrin/dieldrin
to dairy cattle and laying hens. The ratio of dieldrin calculated for whole milk was 0.15 - 0.39,
whereas the values reported on a milk fat basis were within a 4.5 - 8.2 range. No aldrin data
were available from this study. The transfer ratio determined in whole eggs was about 1.2 for
aldrin and 0.7 - 2.5 for dieldrin.

In the DOS-database data can be found concerning undesirable substances in feed

materials of animal origin.

Humans
Exposure:
Because of its rapid conversion to dieldrin in the environment, aldrin is not considered to be
an important human dietary contaminant. The average aldrin intake is nowadays estimated
to be less than 1 g/kg bodyweight/day. Food is considered the most important source of
human dieldrin exposure. Important foods are those with a high fat content i.e. fish, milk, and
meat (EFSA, 2005). Breastfed babies are exposed to aldrin and dieldrin via breast milk
(ATSDR, 2002).
Besides food, soil, when ingested, might be a route of exposure. Based on its cancellation
and its rapid conversion to dieldrin in the environment (ATSDR, 2002), it is assumed that the
general population is more likely to be exposed to dieldrin than aldrin in soils (US-EPA,
2003). Dieldrin has been detected in residential soils samples (Lewis et al., 1994).
The US-EPA (2003) collected aldrin and dieldrin data and calculated general population
exposures in media other than water, as shown in tables 1 and 2.

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 Table 1. General population exposures to aldrin in media other than water (US-EPA, 2003).
Parameter Medium
Food Air Soil
Adult Child Adult Child Adult Child
-7 3 1
Concentration Non-Fish Food (NF): 4.5 x 10 mg/m NA
in medium 0.0016 mg/kg

Fish and Shellfish (F):

0.01 to 0.12 mg/kg
-7 -7 2
Estimated NF: NF: 1.3 x 10 6.8 x 10 -- --
-5 -4
daily intake 3.0 x 10 1.3 x 10
(mg/kg/day)
F: F:
-6 -6
2.9 x 10 4.0 x 10
to to
-5 -5
3.5 x 10 4.8 x 10
1
NA = No data found
2
-- = Unable to estimate from available information

Table 2. General population exposures to dieldrin in media other than water (US-EPA, 2003).
Parameter Medium
Food Air Soil
Adult Child Adult Child Adult Child
-6 3
Concentration Non-Fish Food (NF): 1.6 x 10 mg/m 0.03 to 1.1 mg/kg
in medium 0.0015 mg/kg

Fish and Shellfish (F):

0.028 mg/kg
-7 -6 -8 -7
Estimated NF: NF: 4.6 x 10 2.4 x 10 2.1 x 10 3.0 x 10
-5 -4
daily intake 2.8 x 10 1.3 x 10 to to
-7 -5
(mg/kg/day) 7.9 x 10 1.1 x 10
F: F:
-6 -5
8.0 x 10 1.1 x 10

The daily intake from food for adults and children seems to be in the range of 1 - 10 g /kg
body weight, and approximately 22 g /kg body weight for breast-fed babies (EFSA, 2005).

Absorption:
Aldrin and dieldrin are absorbed when ingested (WHO3, 2003). No quantitative data
specifically describing human absorption of aldrin and dieldrin following oral exposure were
found.

Distribution:
As a result of its relatively rapid conversion to dieldrin, aldrin is seldom observed in human
tissues, and very little information is available concerning its distribution within the human
body following absorption into the circulating blood (ATSDR, 2002; WHO1, 1989). Given their
hydrophobic nature and high solubilitys in fat, it is not surprising that the largest
concentrations of aldrin, dieldrin, and their metabolites are generally found in adipose tissue
(ATSDR, 2002; WHO1, 1989; US-EPA, 2003).
Studies show that trans-placental transfer of aldrin and dieldrin occurs (ATSDR, 2002).

Excretion:
Excretion in humans following exposure to aldrin or dieldrin appears to occur largely through
the bile and faeces (US-EPA, 2003).
Nursing mother excrete dieldrin via breast milk (ATSDR, 2002; EFSA, 2005; US-EPA, 2003).
Nair et al. (1992) also found aldrin in breast milk (from Delhi residents), however at lower
levels than dieldrin.

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 Metabolism:
Following absorption, aldrin is quickly metabolized to dieldrin (Health Canada, 1995). No
other human data were found concerning metabolism.

3. Diagnose of poisoning

Animals
The EFSA (2005) reports that in several studies, dieldrin was analysed in blood of animals.
Dieldrin was also reported to be found in adipose fat of animals (Falandysz and Kannan,
1992).

Humans
Exposure to aldrin and dieldrin is measured almost exclusively by determining the level of
dieldrin in the blood. Because aldrin is rapidly converted to dieldrin in the body, the detection
of aldrin in body tissues is rare. Detection of dieldrin in the blood may indicate either recent
or past exposure to aldrin or dieldrin. Dieldrin would be detected in the blood either
immediately after inhalation, oral, or dermal absorption or as stores of dieldrin are slowly
released from adipose tissue (ATSDR, 2002).
Because dieldrin rapidly redistributes to adipose tissue, the highest levels of dieldrin are
found in fat (except immediately after exposure). Thus, fat levels of dieldrin are also a good
source for identifying exposure to aldrin or dieldrin. However, obtaining fat samples requires
at least minor surgery; therefore, this method is not commonly used (ATSDR, 2002).

4. Potential adverse effects

Environment
Aldrin is readily converted to dieldrin, which is ubiquitous in the environment. Dieldrin persists
because it is more resistant to biotransformation and abiotic degradation than aldrin. As a
result, it is found in all environmental media, even at a distance from the site of
concentration. Dieldrin bioconcentrates and biomagnifies through the terrestrial and aquatic
food chains (ATSDR, 2002).
Aldrin and dieldrin have only minor effects on soil bacteria, even at levels far exceeding
those normally encountered. Concerning plants, the toxicity of dieldrin for higher plants is
low, crops only being affected at application rates greater than 22 kg/ha. Aldrin is more
phytotoxic, to tomatoes and cucumbers particularly, but only at application rates many times
greater than those recommended. Cabbage is the most sensitive crop to aldrin (WHO1,
1989).

Animals
Sensitivity to aldrin and dieldrin exposure varies with species, strain, age, gender, health
status and fat depot. Since both insecticides are deposited in fat depots and toxic effects
occur in the central nervous system, animals with relative small fat depots are generally
more susceptible to poisoning (EFSA, 2005).
Free-range animals might be exposed to higher levels of dieldrin than enclosed animals
(e.g. via ingestion of soil (Windal et al., 2009) and earthworms). These free-range animals
are not necessarily more sensitive to dieldrin than enclosed animals, however are exposed to
higher levels, which might consequently result in toxic effects.

The dominant toxic effects in animals are observed in the nervous system and in the liver.
Aldrin and dieldrin are approximately equally potent. Genotoxicity or teratogenicity have not
been observed (EFSA, 2005).
Oral data in animals, as summarized by the ATSDR (2002), also show that the nervous
system is an important target of toxicity as is the liver, but also other effects may be

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 associated with exposure to aldrin or dieldrin, including kidney toxicity, immunosuppression,
fetal toxicity and increased postnatal mortality, neurodevelopmental effects, and decreased
reproductive function. Conflicting results exist regarding developmental effects in animals
(ATSDR, 2002).
Other reported effects are reduced weight gain and death of lambs at the highest level of
exposure of 4 mg/kg bodyweight (Davison, 1970), death of hens and reduced chick survival
(Brown et al., 1974).

The International Agency for Research on Cancer (IARC) states that there is limited
evidence for the carcinogenicity of dieldrin (IARC1, 1987) and aldrin (IARC2, 1987) to
animals. In mice hepatocarcinogenicity, caused by dieldrin, was demonstrated.

In Appendix I the potential adverse effects of aldrin and dieldrin in animals are shown. For
toxicity data, see Appendix II.

Humans
Limited data are available concerning oral human studies, other than acute exposure, which
is not addressed to in this fact sheet.

The available literature included almost no direct evidence for any human subpopulations
that would be particularly sensitive to the toxic effects of aldrin/dieldrin, or for which relevant
toxicokinetics are known to differ significantly from those for the general population.
Speculatively, the fetus and very young children might be at increased risk from exposures
to aldrin/dieldrin as a result of immature hepatic detoxification and excretion functions, as
well as developing target organ systems (US-EPA, 2003).

Both aldrin and dieldrin are highly toxic to humans, the target organs being the central
nervous system and the liver (WHO3, 2003).
The IARC1,2 (1987) state that aldrin and dieldrin are not classifiable as to their carcinogenicity
to humans, due to inadequate evidence. However in a more recent study of Hyer1 et al.
(1998) dieldrin was associated with a significantly increased dose-related risk of
breast cancer. The findings in a later study of Hyer2 et al. (2000) also suggests that
past exposure to estrogenic organochlorines such as dieldrin may not only affect the risk of
developing breast cancer but also the survival of breast cancer.

In Appendix I the potential adverse effects of aldrin and dieldrin in humans are shown. For
toxicity data, see Appendix II.

5. Severity of the potential adverse effects

The severity of contamination of food and / or feed materials with aldrin and dieldrin is based
on the worst case scenario, as shown in table 3, and is based upon the potential adverse
effects stated in chapter 4 and Appendix I.

The severity of aldrin and dieldrin toxicosis in animals is classified as high because:
Deaths have been reported in lambs (Davison, 1970) and poultry (Brown et al., 1974);
There is limited evidence for the carcinogenicity of dieldrin (IARC1, 1987) and aldrin
(IARC2, 1987);
Reproductive effects have been observed in animals (ATSDR, 2002).

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 The severity of aldrin and dieldrin toxicosis in humans is classified as high because:
Dieldrin is associated with a significantly increased dose-related risk of breast
cancer (Hyer1 et al., 1998).
Table 3. Severity of aldrin and dieldrin toxicosis
Severity
Low Medium High
Animals x
Humans x

6. Legislation and standards

Mind that in some countries aldrin and dieldrin might still be approved.

7. Methods of analysis
Prerequisites for a reliable analytical determination of aldrin and dieldrin are an exhaustive
extraction combined with a meticulous clean up, efficient separation and a sensitive
detection. A number of well-proven, validated methods for the quantitative determination of
aldrin, dieldrin are available. Care has to be taken in order to avoid losses due to aggressive
clean up methods, such as treatment with concentrated sulphuric acid (EFSA, 2005). Several
studies have shown that this kind of sample clean up may result in complete loss of dieldrin
(Saxena and Siddiqui, 1981; Hernandez Hernandez et al., 1987; Pan et al., 2004).
Due to the high electro negativity caused by the six chlorine atoms of both compounds,
capillary gas chromatography with electron capture detection (GC/ECD) is the analytical
method of choice, not only to differentiate between dieldrin and its stereoisomer endrin, but
also to separate them from possible interfering co-extractants. An efficient separation of
aldrin and dieldrin from other interfering compounds, such as other organochlorine pesticides
and polychlorinated biphenyls (PCBs) is especially important when using GC/ECD. The use
of gas chromatographic separation on two capillary columns of different polarity in routine
monitoring programs is therefore mandatory. Potential co-elution problems (= also emerging
other chemicals from the column) can also be overcome by applying combined capillary gas
chromatography/mass spectrometry (GC/MS) either with electron impact (EI) or negative
chemical ionization (NCI) mode as an alternative method. Although being more selective and
providing the opportunity to use isotope labelled compounds as ideal internal standards,
GC/MS methods do not necessarily offer a higher sensitivity compared to GC/ECD (EFSA,
2005).

8. Possible control measures

Products with a higher risk to contain hazardous levels or exceeding maximum limits of aldrin
and dieldrin, are:
Products originating from an environment with a high aldrin or dieldrin burden.
Mind that aldrin or dieldrin are known for their long-range atmospheric transport. In some
parts of the world aldrin or dieldrin are still used for several applications. Products from
these parts of the world are of higher risk, because of the presence of aldrin or dieldrin
production sites and the actual presence of the compound aldrin or dieldrin themselves;
Products of mineral origin and products derived from these products, like soil
contaminated with aldrin or dieldrin;
Products of vegetal origin or products derived from these products, like crops
containing adherent contaminated soil, root products, vegetable oils and their by-
products (e.g. distillates). Marine algae are known to accumulate dieldrin up to high
levels;

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 Products of animal origin or products derived from these products, like fishmeal
and fish oil (especially when originating from the Northern hemisphere), or other
products high in fat. Meat and dairy products (e.g. cheese, butter) are also
mentioned, as are eggs (especially free-range eggs). Earthworms should also be
mentioned because of their bioaccumulation of dieldrin and the exposure of free-range
poultry.

Lean animals are more susceptible to poisoning than fat animals, since aldrin and dieldrin
are deposited and immobilized in fat depots. As to higher levels of exposure free-range
animals are of risk.

Cultivation / husbandry:
Study if products originate from an environment with a high aldrin or dieldrin burden. The
study should include investigating:
o Is the use of aldrin or dieldrin authorized in the country of origin and if yes: for
which crops is its use authorized;
o The history and the present situation in the area and focus on industries present
or that were present and what the activities are or were of these industries;
o Possible contamination of soil and water by present or former use of aldrin or
dieldrin (e.g. aldrin and dieldrin analyses of the soil and water).

Storage and transport:

No use of aldrin or dieldrin during storage or transport;
Feed and food materials should be stored and transported in a clean storage area and
means of transport without residual storage material and cargo.

Processing feed or food material:

Use the HACCP system to assess the risk of aldrin or dieldrin in the feed or food
material. Include processes starting from cultivation or husbandry. Besides others, the
following items should be addressed:
o Determination if concentration of aldrin or dieldrin might occur in certain (by)
products during processing (e.g. products from animal or vegetal origin high in
fat);
o Determination if aldrin or dieldrin are destroyed or removed during processing,
and in which (by)-products aldrin or dieldrin might still be present;
o Use of possible aldrin or dieldrin contaminated additives / processing aids and its
possible contamination of feed and food products;
Implement an aldrin and dieldrin monitoring program on the following products, which
were determined of risk by the HACCP study: raw materials, additives, processing aids
and water and possibly other products of risk.
Implement an aldrin and dieldrin monitoring program on end products produced, with a
higher frequency of analysis in end products of high(er) risk (based on the HACCP
study).

Processing animal feed:

Verify if the supplier / producer has assessed the hazard and risk of aldrin and dieldrin in
the feed material(s) of risk.
Use the HACCP system to assess the risk of aldrin and dieldrin in the animal feed.
Besides others, the following items should be addressed:
o Use of possible aldrin and dieldrin contaminated additives / processing aids.
Implement an aldrin and dieldrin monitoring program on the following products, which
were determined of risk by the HACCP study: raw materials, additives, processing aids
and water and possibly other products of risk.

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 Implement an aldrin and dieldrin monitoring program on animal feed produced, with a
higher frequency of analysis in end products for animals of risk or containing high levels
of feed materials of risk (based on the HACCP study).

9. References

1 Albert et al., A survey of organochlorine pesticide residues in cheese samples from

three Mexican regions, Environmental Pollution, Volume 65(2), 1990, pages 119-
126
2 ATSDR, Toxicological Profile for Aldrin and Dieldrin, 2002
3 Brown et al, The toxicity of dieldrin (HEOD) to domestic fowl, Pesticide Science,
Volume 5(5), 1974, pages 567-586
4 Davison, Growth, hemoglobin, body composition and vitamin A of sheep fed
dieldrin, Journal of Animals Science, Volume 31, 1970, pages 567-575
5 EFSA, Opinion of the Scientific Panel on Contaminants in the Food Chain on a
request from the Commission related to aldrin and dieldrin as undesirable
substance in animal feed, The EFSA Journal 285, 2005
6 Ely et al., Studies of feeding aldrin to dairy cows, Journal of Animal Science,
Volume 37(3), 1954, pages 294-298
7 Falandysz and Kannan, Organochlorine pesticide and polychlorinated biphenyl
residues in slaughtered and game animal fats from the northern part of Poland,
Zeitschrift fr Lebensmitteluntersuchung und forschung A, Volume 195(1), 1992,
pages 17-21
8 Ghiasuddin and Menzer, Microsomal epoxidation of aldrin to dieldrin in rats,
Bulletin of Environmental Contamination and Toxicology, Volume 15(3), 1976,
pages 324-329
9 Harr et al., A therapeutic regimen for purging dieldrin from adulterated individuals,
Bulletin of Environmental Contamination and Toxicology, Volume 12(4), 1974,
pages 433-441
10 Hayes, Distribution of dieldrin following a single oral dose, Toxicology and Applied
Pharmacology, Volume 28(3), 1974, pages 485-492
11 Health Canada, Aldrin and Dieldrin, 1995
12 Hedde et al., Dieldrin-14C metabolism in sheep: distribution and isolation of urinary
metabolites, Journal of Agricultural and Food Chemistry, Volume 18(1), 1970,
pages 116-119
13 Hernndez Hernndez et al., Sulfuric acid cleanup and KOH-ethanol treatment for
confirmation of organochlorine pesticides and polychlorinated biphenyls:
application to wastewater samples, Association off Analytical Chemistry, Volume
70(4), 1987, pages 727-733
14 Hyer1 et al., Organochlorine exposure and risk of breast cancer, Lancet, Volume
352(9143), 1998, pages 1816-1820
15 Hyer2 et al., Organochlorine exposure and breast cancer survival, Journal of
Clinical Epidemiology, Volume 53(3), 2000, pages 323-330
16 IARC1, Dieldrin, Summaries & Evaluations, Supplement 7, 1987, page 196
17 IARC2, Aldrin, Summaries & Evaluations, Supplement 7, 1987, page 88
18 Lenardn et al., Organochlorine pesticides in Argentinian butter, Science of The
Total Environment, Volume 144(1-3), 1994, pages 273-277
19 Lewis et al., Evaluation of methods for monitoring the potential exposure of small
children to pesticides in the residential environment, Archives of Environmental
Contamination and Toxicology, volume 26(1), 1994, pages 37-46
20 Ludwig et al., Excretion and distribution of aldrin-14C and its metabolites after oral
administration for a long period of time, Life Sciences, Volume 3(2), 1964, pages
123-130
21 Mrner et al. (WHO/FAO/UNEP), Reducing and Eliminating the use of Persistent

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 Organic Pesticides: Guidance on alternative strategies for sustainable pest and
vector management, 2002
22 Mugambi et al., Organochlorine pesticide residues in domestic fowl (Gallus
domesticus) eggs from Kenya, Journal of the Science of Food and Agriculture,
Volume 49(2), 1989, pages 165-176
23 Nair et al., Aldrin and dieldrin residues in human fat, milk and blood serum
collected from Delhi, Human Experimental Toxicology, Volume 11(1), 1992, pages
43-45
24 Pan et al., Sample purification for analysis of organochlorine pesticides in sediment
and fish muscle, Journal of Environmental Science and Health, Part B, Volume
39(3), 2004, pages 353-365
25 Saxena and Siddiqui, Reduced recovery of dieldrin residues-a shortcoming of
sulfuric cleanup of biological samples, Journal of Analytical Toxicology, Volume
5(3), 1981, pages 150-152
26 UNEP (United Nations Environment Programme), Master list of actions. On the
Reduction and/or Elimination of the Releases of Persistent Organic Pollutants, Fifth
Edition, 2003
27 US-EPA, Health Effects Support Document for Aldrin/Dieldrin, 2003
28 WHO1, Aldrin and dieldrin, Environmental Health Criteria 91, 1989
29 WHO2, Aldrin and dieldrin, Health and Safety Guide 21, 1989
30 WHO3, Aldrin and dieldrin in drinking-water: Background document for
development of WHO Guidelines for drinking-water quality, 2003
31 WHO4, Inventory of IPCS and other WHO pesticide evaluations and summary of
toxicological evaluations performed by the Joint Meeting on Pesticide Residues
(JMPR) through 2002, 7th edition, 2002
32 Windal et al., PCB and organochlorine pesticides in home-produced eggs in
Belgium, Science of The Total Environment, Volume 407(15), 2009, pages 4430-
4437

10. Websites

1 http://www.gmpplus.org
2 http://www.efsa.europa.eu/en/efsajournal/doc/285.pdf
3 http://www.who.int/ipcs/publications/jmpr/jmpr_pesticide/en/print.html
4 http://www.inchem.org/documents/ehc/ehc/ehc91.htm
5 http://www.inchem.org/documents/hsg/hsg/hsg021.htm
6 http://www.pops.int/documents/meetings/inc7/mastlist5/ml5.pdf

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 APPENDIX I Potential adverse effect of aldrin and dieldrin

1,2 1,2 1,2 1,2 2 2

Aldrin and Death Carcinogen Mutagen Reproductive Internal injury Neurological Immunological Organs
2
dieldrin (physical effect
contamination)
1,2

Animals x x x x x x

Humans x

2 2 2 2
Aldrin and Dermal and Respiratory Musculo- Cardiovascular Gastrointestinal Hematological Endocrine Body weight
2 2
dieldrin ocular skeletal

Animals x

Humans

1
This potential adverse effect is classified as high severity for animals
2
This potential adverse effect is classified as high severity for humans

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 APPENDIX II Toxicity data of aldrin and dieldrin

NOAEL (mg/kg BW) ADI (mg/kg BW) LD50 (mg/kg BW)

Aldrin 1.5 (cow)1 (Ely et al., 1954)
0.12 (turkey)2 (Anderson et
al., 1952 as cited by EFSA,
2005)
0.06 (domestic bird)3 (EFSA,
2005)
Dieldrin 1 (lamb)4 (Davison, 1970)
0.06 (domestic bird)3 (EFSA,
2005)
0.6 (domestic hen)5 (EFSA,
2005)
Aldrin + dieldrin
40-70 (mouse, rat) (WHO1,
1989)
50-80 (rabbit) (Borgmann,et
al., 1952 as cited by WHO1,
1989)
10 (3 wks chicken) (Brown et
al., 1965 as cited by EFSA,
2005)
40-70 (mouse, rat) (WHO1,
1989)
45-50 (rabbit) (Borgmann,
1952 as cited by WHO1,
1989)
20 (3 wks chicken) (Brown et
al., 1965 as cited by EFSA,
2005)
0.0001 (PTDI*) (WHO4, 2002)

1
During 43-44 days, NOAEL for neurological effects.
2
During 6 weeks, NOAEL for clinical signs of toxicity.
3
During 2 years, NOAEL for clinical effects
4
During 32 weeks, NOAEL for reduced weight gain, body fat and vitamin A content of plasma.
5
During 13 months, NOAEL for clinical effects
*
PTDI = Provisional Tolerable Daily Intake

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