Fact sheet:

DDT

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 ddt
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: DDT

code: C11

Description: The sum of DDT, DDD (or TDE-) and DDE isomers, expressed in DDT. 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 and biocides (permitted in the EU)

C11 DDT (sum of DDT-, DDD- (or Feed materials and compound feed with the - 0.05 mg/kg Commission OZM Part 2; OSP-
TDE-) and DDE-isomers, exception of: Regulation (EU) No 11
expressed as DDT) 574/2011 amending
- fats en oils - 0.5 mg/kg Annex I to Directive
2002/32/EC

[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
DDT and its analogues referred to in this fact sheet comprises the sum of p,p-DDT, o,p-
DDT, p,p-DDE, o,p-DDE, p,p-DDD and o,p-DDD, expressed as DDT.

Chemical name
p,p-DDT = 1,1,1-trichloro-2,2-bis (p-chlorophenyl)ethane
o,p-DDT = 1,1,1-trichloro 2-(o-chlorophenyl) 2-(p-chlorophenyl)ethane
p,p-DDE = 1,1-dichloro 2,2-bis(p-chlorophenyl)ethylene
o,p-DDE = 1,1-dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)ethylene
p,p-DDD = 1,1-dichloro 2,2-bis(p-chlorophenyl)ethane
o,p-DDD = 1,1-dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)ethane

CAS-number
p,p-DDT = 50-29-3
o,p-DDT = 789-02-6
p,p-DDE = 72-55-9
o,p-DDE = 3424-82-6
p,p-DDD = 72-54-8
o,p-DDD = 53-19-0

Synonyms
See appendix III.

1. Nature, history and prevalence DDT compounds

DDT stands for DichloorDifenylTrichloorethaan and was commercially introduced as an
organochlorine insecticide in the 1940s and has found a broad range of agricultural and non-
agricultural applications. DDT is one of the pesticides listed in as Persistent Organic Pollutant
(POP) of the Stockholm Convention on POPs (Mrner et al., 2002) and the United Nations
Economic Commission for Europe (UNECE) Convention on long-range trans-boundary air
pollution protocol on POPs (CLRTAP-POP) (EFSA, 2006).
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.

Technical DDT contains 65 80 % p,p-DDT. Other important constituents in the technical

grade products are o,p-DDT, p,p-DDE and p,p-DDD. The latter two compounds (along with
their ortho, para analogues formed from o,p-DDT) are also the major breakdown products in
biological systems (EFSA, 2006). In figure 1, the chemical structure of p,p-DDT is shown.

Figure 1. Chemical structure of p,p-DDT.

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 The technical product is a white amorphous powder that is odourless or has a slight aromatic
odour. It melts over the range of 80 94C (EFSA, 2006), however the ATSDR(2002)
mentions melting points of individual DDT isomers, being lowest at 74.2C for o,p-DDT and
highest at 110C for p,p-DDD. Technical DDT has a solubility of < 0.15 mg/L in water at
25C. It is very soluble in lipids and most organic solvents. p,p-DDT is dehydrochlorinated to
form DDE at temperatures above the melting point, especially in the presence of catalysts or
light. Solutions in organic solvents are dehydrochlorinated by alkali or organic bases.
Otherwise, DDT formulations are highly stable (WHO1, 1979).

Technical grade DDT is synthesized by condensing chloral hydrate with chlorobenzene in

concentrated sulphuric acid. It was first synthesized in 1874 (ATSDR, 2002).

DDT was used during the Second World War to protect troops and civilians from the spread
of malaria, typhus and other vector borne diseases. DDT has been broadly applied in
agriculture to control insects on various kinds of crops and for the control of disease vectors.
In 1972, 67-90 % of the total United States use of DDT was on cotton; the remainder was
primarily used on peanuts and soybeans. DDT has been used extensively to eradicate forest
pests, such as the gypsy moth and spruce budworm. It was used in the home as a
mothproofing agent and to control lice (ATSDR, 2002). In some regions of the world where
malaria poses a problem, DDT is sprayed onto the interior surfaces of homes to decrease
the incidence and spread of the disease by controlling mosquitoes (Attaran et al., 2000;
Roberts et al., 2000). Not only is DDT a contact toxin for mosquitoes, it is also a contact
irritant and repellent. As such, DDT has been shown to be effective in controlling malaria by
not only limiting the survival of the mosquito, but also decreasing the odds of an individual
being bitten within the sprayed homes. p,p-DDD was also used as an insecticide. o,p'-DDD
(Mitotane) is used medically in the treatment of cancer of the adrenal gland (PDR 1999, as
cited by ATSDR, 2002). DDE has no commercial use (ATSDR, 2002).

DDT was banned in many European countries for most uses in the early 1970s, because of
its persistence in the environment and insecticide resistance (RIVM, 2009). The use of DDT
as a pesticide has been very restrictive since 1981 and banned since 1986 in the EU.
Although being banned in most countries worldwide, DDT is still used for vector control
especially in areas with endemic malaria, and extended use was recently recommended by
WHO for indoor residual spraying to control malaria. It is also still used as an intermediate in
the production of the pesticide dicofol (2,2,2-trichloro-1,1-bis(p-chlorophenyl)ethanol), where
it is handled in closed production systems (EFSA, 2006). Analytical studies have shown that
p,p-DDT, p,p-DDE as well as the intermediate p,p-Cl-DDT may be present in technical
grade dicofol (ATSDR, 2002). Dicofol is widely used as a pesticide in agriculture applications.
The European Community has forced Prohibition Directive 79/117/EEC to reduce DDT in
dicofol formulations. Specifically, DDT content in a dicofol formulation should not exceed
0.1%. (Turgut et al., 2009). However several surveys showed DDT levels higher than 0.1%.
In the EU the authorisations for plant protection products containing dicofol were withdrawn
at 30 March 2009 by Commission Decision 2008/764/EC. Any period of grace granted by
Member States has expired on 30 March 2010. However this might not go for its use in other
parts in the world.

2. Transmission and likelihood of occurrence

Environment
DDT does not occur naturally in the environment. Before its ban, DDT entered the air, water,
and soil during its production and use as an insecticide. DDT is present at many waste sites,
releases from these sites might continue to contaminate the environment. Most DDT in the
environment is a result of past use. DDD was also used as a pesticide to a limited extent in
the past. DDT still enters the environment because of its current use in some areas of the

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 world. DDE is only found in the environment as a result of contamination or breakdown of
DDT. DDD also enters the environment during the breakdown of DDT (ATSDR, 2002).

Large amounts of DDT were released into the air and on soil or water when it was sprayed
on crops and forests to control insects. DDT was also sprayed in the environment to control
mosquitoes. Although the use of DDT is no longer permitted in many parts of the world, DDT
may be released into the atmosphere in countries where it is still manufactured and used,
e.g. for vector control especially in areas with endemic malaria. DDT compounds may also
enter the air when they evaporate from contaminated water and soil. In the air they then will
be deposited on land or surface water. DDT compounds may occur in the atmosphere as a
vapour or be attached to solids in air. Vapour phase DDT compounds may break down in the
atmosphere due to reactions caused by the sun. The half-life of these chemicals in the
atmosphere as vapours has been calculated to be approximately 1.53 days. However, in
reality, this half-life estimate is too short to account for the ability of DDT compounds to be
carried long distances in the atmosphere (ATSDR, 2002).

Some DDT may have entered the soil from waste sites or from its former use as an
insecticide. DDT compounds last in the soil for a very long time, potentially for hundreds of
years. Most DDT breaks down slowly into DDE and DDD, generally by the action of micro-
organisms. These chemicals may also evaporate into the air and be deposited in other
places. They stick strongly to soil, and therefore generally remain in the surface layers of soil
(ATSDR, 2002). For this reasons crops containing adherent soil are possibly of risk to
contain DDT from its former use as insecticide. This also goes for free range and grazing
animals, ingesting soil.
Some soil particles with attached DDT compounds may get into rivers and lakes in runoff.
Only a very small amount, if any, will seep into the ground and get into groundwater. The
length of time that DDT will last in soil depends on many factors including temperature, type
of soil, and whether the soil is wet. DDT lasts for a much shorter time in the tropics where the
chemical evaporates faster and where micro-organisms degrade it faster. DDT disappears
faster when the soil is flooded or wet than when it is dry. DDT disappears faster when it
initially enters the soil. Later on, evaporation slows down and some DDT moves into spaces
in the soil that are so small that micro-organisms cannot reach the DDT to break it down
efficiently. In tropical areas, DDT compounds may disappear in much less than a year. In
temperate areas, half of the amount initially present usually disappears in about 5 years.
However, in some cases, half of the amount initially present will remain for 20, 30, or more
years (ATSDR, 2002).

In surface water, DDT will bind to particles in the water, settle, and be deposited in the
sediment. DDT is taken up by small organisms and fish in the water. It accumulates to high
levels in fish and marine mammals (such as seals and whales), reaching levels many
thousands of times higher than in water. In these animals, the highest levels of DDT are
found in their adipose tissue (ATSDR, 2002). Because of its strong tendency to be adsorbed
onto surfaces, most DDT that enters water is and remains firmly attached to soil particles. If it
does find its way into water, it is gradually lost by adsorption onto surfaces (WHO3, 2004).
However, Kumari et al. (1996) report DDT contamination of river and pond water in India,
used as drinking water for cattle. This contamination was related to the use of DDT on
agricultural crops at that time (1992-1994).

The cycle of evaporation and deposition may be repeated many times. As a result, DDT,
DDE, and DDD can be carried long distances in the atmosphere. These chemicals have
been found in bogs, snow, and animals in the Arctic and Antarctic regions, far from where
they were ever used (ATSDR, 2002)

DDT is used as an intermediate in the production of the pesticide dicofol and may occur as
a major impurity in the final product (EFSA, 2006). While in the EU, the amount of DDT and

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 related compounds in dicofol is limited to 0.1 %, (Directive 79/117/EEC16), the analysis of 23
commercial dicofol formulation from 7 producers in China revealed average concentrations
for o,p-DDT, p,p-Cl-DDT, o,p-DDE, and p,p-DDT of 11.4, 6.9, 4.4, and 1.7 %, respectively
(Qiu et al.,2005). In 1988 Di Muccio et al. conducted a survey of DDT-like compounds in
dicofol formulations commercially available in Italy. The total of DDT-like compounds,
calculated on a dicofol content basis, was in the range 0.6323.19%, with an average of
8.28%. Turgut et al. (2009) studied contents and sources of DDT impurities in dicofol
formulations in Turkey and found that all DDT concentrations in dicofol samples analyzed
were higher than the permitted 0.1% level of Prohibition Directive 79/117/EEC. The DDT
content as an impurity in analyzed dicofol formulations was as high as 14.3%. The authors
stated that dicofol has been identified as a contributor to continued DDT contamination in soil
and water.

Plants
Despite being strongly bound to soil, at least a portion of DDT, DDE, and DDD is bioavailable
to plants (ATSDR, 2002). Nash and Beall (1970) studied the DDT residues in soybeans.
They found that the major source of DDT contamination was due to sorption of volatilized
residues from surface-treated soil. In other experiments with oats and peas, root uptake of
DDT was low and there was little or no evidence of translocation of the insecticide
(Fuhremann and Lichtenstein 1980; Lichtenstein and Schultz 1960). Verma and Pillai (1991)
reported that maize, and rice plants accumulate DDT adsorbed to soil. Most of the residues
were found in the roots of the plant, and the lowest concentration of DDT residues was found
in the shoots, indicating low translocation of DDT.

As an insecticide, DDT is predominantly applied as a spray. Therefore, vegetables and crops

with large and waxy leaf surfaces grown in areas with ongoing or recent use of DDT are
more likely to contain elevated DDT levels. In contrast, uptake of DDT by roots is generally
low due to its low water solubility (EFSA, 2006).

Residual dicofol, containing DDT, might also contaminate crop. However no data were found.

In literature no specific crops are indicated as of risk to contain hazardous levels of DDT.
Products of risk are possibly crops containing adherent soil from DDT compounds
contaminated areas. No data was found concerning residual DDT in soil present as an
impurity in dicofol.

Marine algae are known to bioaccumulate DDT and its analogues (Rice and Sikka, 1973).
Consequently marine algae, and products derived from marine algae are of risk containing
DDT and its analogues.

DDT is stable under most of the conditions when present as a residue on food products.
Therefore, residues in food products will not normally diminish greatly from most food
products during shipping and storage. It is especially stable in a fatty medium (FAO/WHO1,
1967).
Washing and processing produced a marked reduction in residues. Since DDT does not
penetrate significantly into non-fatty food products, a large loss is shown when the surface is
removed such as in peeling, shelling, harsh brushing, milling, etc (FAO/WHO1, 1967).
Data presented by the FAO/WHO1 (1967) showed a very significant conversion of DDT to
DDD during certain heat processing. The extent to which DDT is converted to DDD depends
on the time and temperature of processing. After processing green beans for 12 minutes at
121C, DDT and DDD were found in the canned product, but after processing spinach for 50
minutes at 122C only DDD and DDE could be found. The DDD and DDE found in these
products account for less than half of the DDT.

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 In the DOS-database data can be found concerning DDT levels in feed materials of vegetal
origin.

Animals
Exposure:
Feed materials of animal origin, especially fish derived products, are in general more
contaminated than feed materials of plant origin (EFSA, 2006). The EFSA (2006) present
DDT data in fish meal and fish oil from several EU Member States, as shown in table 1.

Table 1. DDT compounds levels (g/kg) in fish meal and fish oil (EFSA, 2006).
EU member Product p,p-DDT o,p-DDT p,p-DDE o,p-DDE p,p-DDD o,p-DDD Range
state Sum DDT
Norway Meal 2.3-15
(2005)
Oil 27-201
(2005)
Meal 4-17
(2000-2004)
Oil 27-36.3
(2000-2004)
Czech Meal <0.5-1.7 <0.5-4.0 <0.5-11.9 <0.5 <0.5-4.6 <0.5-0.82 <0.5-23.02
Republic (2004)
Iceland Meal 2.1-30.8
Iceland Oil 20.4-370

In feed samples of animal origin the metabolite p,p-DDE normally represents more than 50
% of sum of DDT. A considerable lower contribution of p,p-DDE to the sum of DDT may
indicate recent use of DDT. Samples of plant origin are generally dominated by the parent
compound p,p-DDT. Feed commodities including fish derived products generally contain
levels in the low g/kg range and thus are far below those that have been found to cause
adverse effects in fish and domestic animals (EFSA, 2006).
The concentrations determined in feed commodities including fish derived products generally
are in the low g/kg range and thus well below those that have been found to cause adverse
effects in fish and domestic animals. However, it can not be excluded that elevated levels
may be found in feed commodities that originate from areas where DDT has recently been or
still is used (EFSA, 2006).

Despite being strongly bound to soil, at least a portion of DDT, DDE, and DDD is bioavailable
to soil invertebrates (ATSDR, 2002). In a study by Morrison et al (1999), cited by the EFSA
(2006) studying the bioavailability of DDT, DDE, and DDD to earthworms, it was shown that
the concentrations of DDT, DDE, DDD, and DDT were consistently lower in earthworms
exposed to these compounds that had persisted in soil for 49 years than in earthworms
expose to soil containing freshly added insecticides at the same concentration. The uptake
percentages of DDT and its metabolites by earthworms were in the range of 1.30-1.75% for
the 49-year-aged soil, but were 4.00-15.2% for the fresh soil. No data were found the
contribution of DDT contaminated earthworms to the dietary exposure of free-range chickens
and its carry over to eggs.
In 1999 the Veterinary Medicines Directorate (VMD) in the UK found high levels of DDT in
eggs produced on a free-range farm. The most likely source of contamination was from soil
on the farm, ingested by chickens (PAN, 2000). Several authors mention that consuming soil
by grazing animals, also attributes to dietary DDT exposure. However no data were found
concerning its bioavailability.

Absorption:
DDT is readily absorbed in animals and is dependent on the dose and on the vehicle (EFSA,
2006). Absorption occurs primarily through lymphatic channels, with only a minor portion
being absorbed into the portal circulation (Palin et al., 1982; Pocock and Vost, 1974).
Absorption of small doses, such as those found in the residues of food, is virtually complete

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 and is facilitated by the presence of fat in food (EFSA, 2006). Approximately 70 90 % of the
administered dose is absorbed by rats after oral exposure to DDT in an oil vehicle (Keller and
Yeary, 1980 as cited by the EFSA (2006); Rothe et al., 1957 as cited by the EFSA (2006)).
No data were found concerning the bioavailability of DDT and its analogues attached to
particles (e.g. soil).

Distribution:
Once absorbed, they are readily distributed via the lymph and blood to all body tissues and
are stored in these tissues generally in proportion of their lipid content (EFSA, 2006). The
distribution of p,p-DDT in newborn rats from dams administered p,p-DDT in the diet before
mating and throughout gestation was evaluated before and after suckling had occurred
(Woolley and Talens, 1971). In newborn rats sacrificed 01 hours after birth, before suckling
had occurred, levels of p,p-DDT were noted in the brain, liver, kidneys, and stomach. These
results demonstrate that DDT readily passes through the placental barrier to enter tissues of
the developing foetus. The EFSA (2006) also mention that in laboratory animals DDT
metabolites have been shown to cross the placenta. Kan and Meijer (2007) state that
accumulation of DDT and DDE is eggs (poultry) is considerable.

Excretion:
Studies with rats, mice and hamsters indicate that DDT and related metabolites are excreted
primarily in faeces. The bile appears to be the principal source of DDT metabolites in the
faeces. Milk has been reported as an important excretion route for DDT and related
metabolites. The half-life for DDT is one month in rats. In animals DDE is generally more
persistent than DDT (EFSA, 2006).

Metabolism:
The first step in the metabolism of DDT is the formation of DDD and DDE (EFSA, 2006).
Several authors found that 2,2-bis-chlorophenyl acetic acid (DDA) isomers are the major
urinary metabolites of p,p-DDT and o,p-DDT in all mammals (WHO1, 1979). The conversion
of DDT to DDD or to DDE are the first steps in the formation of DDA. The conversion of DDD
to DDA occurs primarily by hydroxylation, leading to acyl chloride DDA, which on hydrolysis,
gives DDA. This acyl chloride may also be formed from DDE via an epoxidation route.
Another possible intermediate in the formation of DDA from DDD is 1-chloro-2,2-bis(4-
chlorophenyl) ethane (DDMU) (Gold and Brunk, 1984; Fawcett et al., 1987).
In addition to the formation of DDA, several hydroxylated compounds can be formed from
DDE (EFSA, 2006).

Humans via animal products

DDT is a compound with high accumulation in the animal (Kan and Meijer, 2007) and
consequently in products of animal origin. Specifically products high in fat content might
contain high(er) levels of DDT.
In a study conducted by Pandit and Sahu (2002) butter and cheese samples showed higher
concentrations of these compounds, compared to other milk products such as curd (all Indian
origin). They reported an average p,p'-DDT level of 1.05 (g/ml), 1.2 (g/mg), 20.97 (g/mg)
and 9.53 (g/mg) in milk, curd, butter and cheese respectively.
In ruminants carry over of DDT and related compounds to milk, expressed as a percentage
of ingested dose, is about 5 %, 8 % and 26 % for p,p-DDT, p,p-DDD and p,p-DDE,
respectively (EFSA, 2006). Whereas Blthgen (2000) (as cited by Kan and Meijer, 2007)
reported very different carry over percentages from feed to milk for DDT (4%) and DDE
(80%). Nag and Raikwar (2008) report a DDT level of 0.1724 mg/kg in bovine milk (Indian
origin) (EFSA, 2006).
Retention of DDT in fish can vary from 20-95 % of the dose depending on the concentration
in the diet. The accumulation ratio calculated from the sum of p,p-DDT and p,p-DDE
residues in adipose tissue relative to the p,p-DDT levels in feed varied from 2.2 in sheep to

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 6-30 for broilers. The reported values for DDT only in beef cattle were in the 0.7-0.9 range
whereas they were in the 11-26 range for DDE (EFSA, 2006).
Concerning eggs, it was found that eggs from private owners were more contaminated than
eggs from commercial farms. The ratios of levels in eggs from private owners to the levels in
eggs from commercial farms ranged from 2 to 8 for the toxic contaminants lead, mercury,
thallium, dioxins, polychlorinated biphenyls and the group of DDT. DDT contamination was
marked by the substantial presence of p,p'-DDT in eggs from private owners in addition to
p,p-DDE and p,p'-DDD. It is postulated that environmental pollution is at the origin of the
higher contamination of eggs from private owners (Van Overmeire et al., 2006).
Aulakh et al. (2006) studied the carry over of DDT in poultry feed to the chicken muscle and
egg. The mean total DDT level in feed was 0.91 mg/kg, the respective value for chicken
muscle was 0.24 mg/kg. Higher residues were encountered in eggs as compared to muscle.
Kan and Meijer (2007) state that accumulation of DDT and DDE is eggs is considerable. The
EFSA (2006) reports that the transfer of p,p-DDT, o,p-DDT and p,p-DDE to the egg
contents were 34, 3.5 and 42 %, respectively.

Products of animal origin, originating from DDT contaminated area, or originating form
animals fed DDT contaminated feed, are possibly of risk, containing high(er) levels of DDT.

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

materials of animal origin.

Humans
Exposure:
Data from total diet studies, as well as from human milk monitoring programmes performed in
various EU Member States, show a considerable decline of up to 90 % in human exposure to
DDT and related compounds over the past three decades (EFSA, 2006).
Food of animal origin is the major source of human exposure to DDT and related
compounds (EFSA, 2006). As does the ATSDR (2002) state that the largest fraction of DDT
in a diet comes from meat, poultry, dairy products, and fish.
Recent studies performed in some EU Member States indicate a mean dietary intake for
adults and children of 5-30 g/kg bodyweight per day which is more than two orders of
magnitude below the provisional tolerable daily intake (PTDI) of 0.01 mg/kg bodyweight
(EFSA, 2006).
Recent exposure of breastfed infants was estimated to be around 0.001 mg/kg bodyweight
(EFSA, 2006). In addition to that the ATSDR (2002) reports that consumption of cows milk is
a route of potential exposure of DDT to children; however, the concentrations of DDT and its
metabolites are typically lower in cows milk than in human breast milk.
Extensive consumption of eggs from private owners is likely to result in toxic equivalent
quantity intake levels exceeding the tolerable weekly intake (Van Overmeire et al., 2006)

Absorption:
DDT is readily absorbed in humans (EFSA, 2006). The actual amounts of DDT, DDE, and
DDD absorbed from foods depends on both the concentration of chemical in the food and the
amount of food eaten (ATSDR, 2002). In humans, the absorption of DDT follows the same
pattern as the absorption of dietary fat. Absorption is slow, however absorption appears to be
complete after 24 hours (Morgan and Roan, 1977, cited by US EPA, 1984).

Distribution:
DDT, DDE, and DDD are stored most readily in fatty tissue, especially DDE. Some of these
stored amounts leave the body very slowly. Levels in fatty tissues may either remain
relatively the same over time or even increase with continued exposure. However, as
exposure decreases, the amount of DDT in the body also decreases. DDT metabolites leave
the body mostly in urine, but may also leave by breast milk and pass directly to nursing

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 infants (ATSDR, 2002). DDT and DDT metabolites have been shown to cross the placenta
(Waliszewki et al. 2000).

Excretion:
The major route of excretion of absorbed DDT in humans appears to be in the urine, but
some excretion also occurs by way of faeces (ATSDR, 2002) and breast milk (Takei et al.
1983). DDA is the main urinary metabolite of DDT (WHO1, 1979). The half-life for DDT in
humans is four years. In humans DDE is generally more persistent than DDT (EFSA, 2006).

Metabolism:
Metabolism of DDT in humans appears similar to that seen in rats, mice, and hamsters,
except that not all intermediate metabolites detected in animals have been identified in
humans (ATSDR, 2002).
DDT is converted to a slight extent to the much less toxic DDE by dehydrochlorination; DDE
apparently does not undergo further biotransformation, but it is stored for an indefinite period
of time in adipose tissues. Most of the p,p-DDE present in human fat represents preformed
dietary DDE rather than endogenously produced DDE. The major detoxification pathway of
DDT is via dechlorination to DDD, an active insecticide which readily degrades to DDA, a
water soluble, rapidly excreted detoxification product (Baselt, 1982 as cited by the WHO2,
1999).

3. Diagnose of poisoning

Animals
No specific biomarkers of exposure were found. However, in experiments DDT and its
analogues have been analysed in feed material, adipose tissue, eggs, milk, urine, faeces,
blood and plasma.

Humans
In general, biomarkers of exposure to DDT can be classified as specific, such as DDT itself
and its metabolites, and non-specific, such as changes in endogenous chemicals that might
indicate exposure to DDT, but also to other unrelated chemicals as well. DDT, DDE, and
DDD have been detected and measured in adipose tissue, blood, serum, urine, faeces,
semen, and breast milk using several analytical techniques. Metabolites of DDT have also
been measured in body fluids (ATSDR, 2002). The major urinary metabolite identified in
humans is DDA. p,p-DDE has also been detected in amniotic fluid (Foster et al. 2000).
Changes in plasma concentrations of endogenous chemicals that might be consistent with
DDT exposure (inhalation) include increased vitamin A plasma levels, which have been
shown to increase with increasing plasma levels of DDE in humans (Nhachi and Kasilo
1990).These authors state that that plasma vitamin A levels, can be used as an indice of
DDT exposure (inhalation). Increased levels of urinary 17-hydroxycortisone have also been
reported as indicators of DDT exposure in humans (Nhachi and Loewenson 1989). However,
none of these potential biomarkers are specific to DDT, DDE, or DDD exposure, and not all
the body compartments in which these changes occur are accessible for sampling in living
humans (ATSDR, 2002).
Food can also be analysed for DDT and its analogues.

4. Potential adverse effects

Environment
DDT and its analogues bioconcentrate in the food chain. Their lipophilic property, combined
with an extremely long half-life is responsible for their high bioconcentration in aquatic
organisms (i.e., levels in organisms exceed those levels occurring in the surrounding water).

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 Organisms also feed on other animals at lower trophic levels. The result is a progressive
biomagnification of DDT in organisms at the top of the food chain (ATSDR, 2002). Since
DDT is used in controlling malaria, it limits the survival of the mosquito carrying malaria.
It also causes inhibition of growth and photosynthesis in green algae (WHO4, 1989).

Animals
The sensitivity to DDT exposure varies with species, strain, age, gender, health status and
fat depot. Lean animals are more susceptible to intoxications than fat animals, since the
insecticide is deposited in fat (EFSA, 2006).

The signs of chronic toxicity are principally similar to those of acute intoxication. The main
target organs are the nervous system and the liver. It also affects hormonal tissues,
reproduction, foetal development and the immune system (EFSA, 2006). The FAO/WHO2
(2000) state that the effects on reproduction in animals include decreased fertility and
abortions, and stillbirths.

In many studies, particular the old ones, it was not specified whether technical grade or pure
p,p-DDT was used. In the following the chemical tested is specified. If not specified in the
reports only the term DDT is used.
Radeleff et al. (1955) fed a lactating cow DDT at 100 mg/kg bodyweight daily for 23 days. At
the first 16 days no evidence of toxic symptoms was observed, but then the cow started to
loose weight rapidly, and slight evidence of excitation was noted on the last three days of
administration. Welch (1948) (cited by the EFSA (2006)) found severe neurological
symptoms in sheep treated with DDT at 100 mg/kg bodyweight for 10 days.

In a study of Rosenberg and Adler, (1950, cited by the EFSA (2006)) in young chicks those
fed the higher concentration (5000 mg/kg) displayed marked tremors and hyperexcitability
before death between 36 and 114 hours. Chicks fed the lower concentration (2500 mg/kg)
died within a period of between 54 and 162 hours.
Srebocan and Pompe, (1970,cited by the EFSA(2006)) found inhibition of corticosterone
synthesis by that technical grade DDT and o,p-DDD in male chicks above five weeks of age
(technical grade DDT, or o,p-DDD at 100 mg/kg diet for 10-30 days).
In a 12 weeks study of Rubin et al. (1947, cited by the EFSA (2006)) egg production fell in
hens given the lowest DDT level diet (310 mg/kg), and in those fed the second lowest
concentration (620 mg/kg) in addition reduced hatchability was observed. Birds fed with the
two highest levels (1250 and 2500 mg/kg) exhibited strong toxic symptoms including
moulting, marked tremors, poor coordination, twisting of the neck with head held down, a
desire to rest on keel or side, loss of bodyweight and death.
For laying hens, reduced egg production and reduced egg shell thickness seem to be the
critical clinical effect (EFSA, 2006).

The International Agency for Research on Cancer (IARC, 1991) states hat DDT has been
tested adequately for carcinogenicity by oral administration in mice, rats and hamsters.
Following oral administration it caused liver-cell tumours, increased incidence of lung
carcinomas and malignant lymphomas.
p,p'-DDE, has been tested for carcinogenicity in mice and hamsters. DDD was also tested
and increased the incidence of liver tumours in male mice and of lung tumours in animals of
each sex in one of the two studies in mice. An increase in the number of thyroid tumours was
observed in one study in male rats. DDE produced a high incidence of liver tumours in mice.
The conclusion of the IARC (1991) was that there is sufficient evidence in experimental
animals for the carcinogenicity of DDT.

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

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 Humans
DDT has estrogenic potential, and the main metabolite, p,p'-DDE, is a potent antiandrogen
and results of the study conducted by Aneck-Hahn et al. (2007) implied that non-
occupational exposure to DDT is associated with impaired seminal parameters in men.
Several studies have been conducted to assess the relation between DDT and male
reproduction parameters. Overall, the available epidemiological evidence tends to suggest
that if such relation exists, it is found in populations exposed at high DDT concentrations
(ATSDR, 2002). Concerning women, the results of the study of Perry et al. (2006) support
the potential for DDT to be associated with decrements in oestrogen and progesterone levels
at times during the menstrual cycle that are critical for ovulation and early pregnancy
maintenance. Korrick et al. (2001) found a potential increased risk of spontaneous abortion
associated with maternal serum DDE levels. High prenatal exposure to p,p'-DDE has been
reported to decrease height in children (Ribas-Fit et al., 2006).
Concerning immunological effects, Sunyer et al. (2005) found that prenatal exposure to DDE
residues may contribute to development of asthma in children. Karmaus et al. (2003) studied
the adverse effect of DDE in breast milk against the onset of atopic manifestations during
childhood. The results of this study suggest that DDE may modify this protective effect of
breast milk.
Haematological effects were found by Dunstan et al. (1996). They found that the red blood
cell distribution width (variation in erythrocyte cell width change; often a sign of anemia) was
significantly greater in a high serum DDE group than in a low serum DDE Group.

The IARC (1991) classified DDT, based on inadequate evidence for carcinogenicity in
humans and sufficient evidence in experimental animals as possibly carcinogenic to humans.
Several studies have reported positive associations between DDT/DDE/DDD body burden,
measured in adipose tissue, and breast cancer (ATSDR, 2002).

In Appendix I the potential adverse effects of DDT and its analogues 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 DDT and its analogues is
based on the worst case scenario, as shown in table 2, and is based upon the potential
adverse effects stated in chapter 4 and Appendix I.

The severity of DDT and its analogues toxicosis in animals is classified as high because:
The IARC (1991) states that there is sufficient evidence in experimental animals for the
carcinogenicity of DDT;
Reproductive effects have been observed: it affects foetal development (EFSA, 2006) as
a decreased fertility and abortions, and stillbirths (FAO/WHO2 , 2000);
Several authors report deaths after chronic exposure to DDT.

The severity of DDT and its analogues toxicosis in humans is classified as high because:
The IARC (1991) classified DDT, based on inadequate evidence for carcinogenicity in
humans and sufficient evidence in experimental animals as possibly carcinogenic to
humans;
Haematological effects were found by Dunstan et al. (1996);
Reproductive effects on man and woman were found (Aneck-Hahn et al., 2007; Perry et
al., 2006; Korrick et al., 2001; Ribas-Fit et al., 2006);
Immunological effects were found concerning asthma by Sunyer et al. (2005) and
concerning atopic manifestations (Karmaus et al., 2003).

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 Table 2. Severity of DDT and its analogues
Severity
Low Medium High
Animals x
Humans x

6. Legislation and standards

The U.S. Food and Drugs Administration (FDA, 2000) has stated action levels of DDT, DDE
and DDD in animal feed.

7. Methods of analysis
During the synthesis of the active insecticide p,p-DDT considerable concentrations of o,p-
DDT may be formed. In addition, p,p-DDD, o,p-DDE and p,p-DDE are all impurities in
technical grade p,p-DDT as well as metabolites. Consequently, besides p,p-DDT the
analysis of feed and food samples should also cover these compounds (EFSA, 2006).
European standards are laid down and specify a gas chromatographic/mass spectrometric
method (GC/MS) (NEN1, 2009) or a gas chromatographic method with electron capture
detection (GC/ECD) (NEN2, 2009) for the determination of organochlorine pesticides (OC's),
among which DDT, in animal feeding stuffs and oil. The methods are applicable to animal
feeding stuffs with a water content up to about 20 % and oil/fatty samples (NEN1,2, 2009).

8. Possible control measures

Products with a higher risk to contain hazardous levels or exceeding maximum limits of DDT
and its analogues, are products:
Originating from an environment with a high DDT, and its analogues, burden. Mind that
DDT and its analogues are known for its worldwide, long-range atmospheric transport. In
some parts of the world DDT is used to eradicate malaria by spraying. Products from
these parts of the world are of higher risk, because of the presence of DDT production
sites and the actual presence of the compound DDT itself;
Products of mineral origin and products derived from these products, like soil
contaminated with DDT and its analogues;
Products of vegetal origin and products derived from these products, like crops
containing soil contaminated. Since marine algae are known to bioaccumulate DDT
and its analogues these and products derived from marine algae are also of risk;
Products of animal origin and products derived from these products, like fish meal
and fish oil or other products high in fat. Dairy products are also mentioned as are
eggs (specifically form contaminated area);
Where during cultivation, DDT and its analogues was / is were used. Mind that he use of
DDT and its analogues is now phased out in most of the world but that in some parts of
the world it still might be used.

Lean animals are more susceptible to poisoning than fat animals, since DDT and its
analogues are deposited and immobilized in fat depots.

Cultivation / husbandry:
Study if products originate from an environment with a high DDT and its analogues
burden. Also include dicofol in this study, because of the possible presence of residual
DDT and its analogues. The study should include investigating:
o Is the use of DDT and its analogues or dicofol authorized in the country of origin
and if yes: for which crops is its use authorized

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 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 DDT and its
analogues and dicofol (e.g. DDT and its analogues analyses of the soil and
water).

Storage and transport:

No use of DDT and its analogues and dicofol 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 DDT and its analogues 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 DDT and its analogues might occur in certain
(by) products during processing (e.g. products from animal origin high in fat);
o Determination if DDT and its analogues are destroyed or removed during
processing, and in which (by)-products DDT and its analogues might still be
present;
o Use of possible DDT and its analogues contaminated additives / processing aids
and its possible contamination of feed or food materials.
Implement a DDT and its analogues 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 a DDT and its analogues 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 DDT and its
analogues in the feed material(s) of risk.
Use the HACCP system to assess the risk of DDT and its analogues in the animal feed.
Besides others, the following items should be addressed:
o Use of possible DDT and its analogues contaminated additives / processing aids.
Implement a DDT and its analogues 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. Also include feed materials which might be
susceptible for adulteration in the monitoring program
Implement a DDT and its analogues 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 Aneck-Hahn et al., Impaired semen quality associated with environmental DDT

exposure in young men living in a malaria area in the Limpopo Province, South
Africa, Journal of Andrology, Volume 28(3), 2007, pages 423-434
2 ATSDR, Toxicological Profile for DDT, DDE and DDD, 2002
3 Attaran et al., Balancing risks on the backs of the poor, Nature Medicine, Volume 6,
No. 7, 2000, pages 729-731
4 Aulakh et al., Organochlorine pesticide residues in poultry feed, chicken muscle
and eggs at a poultry farm in Punjab, India, Journal of the Science of Food and

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 Agriculture, Volume 86, Issue 5, 2006, pages 741-744
5 Di Muccio et al., Survey of DDT-like compounds in dicofol formulations,
Ecotoxicology and Environmental Safety, Volume 16, Issue 2, 1988, pages 129-
132
6 Dunstan et al., Bioaccumulated chlorinated hydrocarbons and red/white blood cell
parameters, Biochemical and Molecular Medicine, Volume 58(1), 1996, pages 77-
84
7 EFSA, Opinion of the Scientific Panel on Contaminants in the Food Chain on a
Request from the Commission related to DDT as an Undesirable Substance in
Animal Feed, The EFSA Journal 433, 2006
8 FAO/WHO1, Evaluation of some pesticides in food: DDT, FAO/PL:1967/M/11/1,
WHO/Food Add./68.30, 1967
9 FAO/WHO2, Pesticides residues in food: DDT, Pesticide residues in food - 2000.
Evaluations. Part II Toxicology. Joint FAO/WHO Meeting on Pesticide Residues
(JMPR), 2000
10 Fawcett et al., The metabolism of 14C-DDT, 14C-DDD, 14C-DDE and 14C-DDMU
in rats and Japanese quail, Xenobiotica, Volume 17(5), 1987, pages 525-528
11 FDA, Action levels for poisonous or deleterious substances in human food and
animal feed, 2000
12 Foster et al., Detection of Endocrine-Disrupting Chemicals in Samples of Second
Trimester Human Amniotic Fluid, The Journal of Clinical Endocrinology &
Metabolism, Volume 85, No. 8, 2000, pages 2954-2957
13 Fuhreman and Lichtenstein, A comparative study of the persistence, movement,
and metabolism of six carbon-14 insecticides in soils and plants, Journal of
Agricultural and Food Chemistry, Volume 28(2), 1980, pages 446-452
14 Gold and Brunk, A mechanistic study of the metabolism of 1,1-dichloro-2,2-bis(p-
chlorophenyl)ethane (DDD) to 2,2-bis(p-chlorophenyl)acetic acid (DDA),
Biochemical Pharmacology, Volume 33(7), 1984, pages 979-982
15 IARC, DDT and Associated Compounds, Summaries & Evaluations, Volume 53,
1991, page 179
16 Kan and Meijer, The risk of contamination of food with toxic substances present in
animal feed, Animal Feed Science and Technology, Volume 133, No. 1-2, 2007,
pages 84-108.
17 Karmaus et al., Atopic manifestations, breast-feeding protection and the adverse
effect of DDE, Paediatric and Perinatal Epidemiology, Volume 17(2), 2003, pages
212-220
18 Korrick et al., Association of DDT with spontaneous abortion: a case-control study,
Annals of Epidemiology, Volume 11(7), 2001, pages 491-496
19 Kumari et al., DDT and HCH Compounds in Soils, Ponds, and Drinking Water of
Haryana, India, Bulletin of Environmental Contamination and Toxicology, Volume
57, 1996, pages 787-793
20 Lichtenstein and Schulz, Insecticide Movement in Plants, Translocation of Some
Chlorinated Hydrocarbon Insecticides into the Aerial Parts of Pea Plants, Journal of
Agricultural and Food Chemistry, Volume 8(6), 1960, pages 452-456
21 Mrner et al. (WHO/FAO/UNEP), Reducing and Eliminating the use of Persistent
Organic Pesticides: Guidance on alternative strategies for sustainable pest
and vector management, 2002
22 Nag and Raikwar, Organochlorine Pesticide Residues in Bovine Milk, Bulletin of
Environmental Contamination and Toxicology, Volume 80, 2008, pages 5-9
23 Nash and Beall, Chlorinated Hydrocarbon Insecticides: Root Uptake versus Vapor
Contamination of Soybean Foliage, Science, Volume 168, 1970, pages 1109-1111
24 NEN1, Animal feeding stuffs - Determination of OC-pesticides and PCB's by
GC/MS: NEN-EN 15741:2009, 2009
25 NEN2, Animal feeding stuffs - Determination of OC-pesticides and PCB's by
GC/ECD: NEN-EN 15742:2009, 2009

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 26 Nhachi and Kasilo, Occupational Exposure to DDT among Mosquito Control
Sprayers, Bulletin of Environmental Contamination and Toxicology, Volume 45,
1990, pages 189-192
27 Nhachi and Loewenson, Comparison Study of the Sensitivities of Some Indices of
DDT Exposure in Human Blood and Urine Bulletin of Environmental Contamination
and Toxicology, Volume 43, 1989, pages 493-498
28 Palin et al., The effect of oils on the lymphatic absorption of DDT, The Journal of
Pharmacy and Pharmacology, Volume 34(11), 1982, pages 707-710
29 PAN (Pesticide Action Network), High levels of DDT found in eggs, Pesticides
News, No. 49, 2000, page 22
30 Pandit and Sahu, Assessment of risk to public health posed by persistent
organochlorine pesticide residues in milk and milk products in Mumbai, India,
Journal of Environmental Monitoring, Volume 4, 2002, pages 182-185
31 Perry et al., A prospective study of serum DDT and progesterone and estrogen
levels across the menstrual cycle in nulliparous women of reproductive age,
American Journal of Epidemiology, Volume 164(11), 2006, pages 1056-1064
32 Pocock and Vost, DDT absorption and chylomicron transport in rat, Lipids, Volume
9, No. 6, 1974, pages 374-381
33 Qui et al., Contribution of Dicofol to the Current DDT Pollution in China,
Environmental Science and Technology, Volume 39, Issue 12, 2005, pages 4385-
4390
34 Radeleff et al., The acute toxicity of chlorinated hydrocarbons and organic
phosphorus insecticides to livestock, U.S. Department of Agriculture, Technical
Bulletin 1122, 1955, pages 1-46
35 Ribas-Fit et al., Prenatal exposure to 1,1-dichloro-2,2-bis (p-chlorophenyl)-
ethylene (p,p'-DDE) in relation to child growth, International Journal of
Epidemiology, Volume 35(4), 2006, pages 853-858
36 Rice and Sikka, Uptake and metabolism of DDT by six species of marine algae,
Journal of Agricultural and Food Chemistry, Volume 21(2), 1973, pages 148-152
37 RIVM, DDT en DDT-derivaten, Voortgangsrapportage Milieubeleid voor
Nederlandse Prioritaire Stoffen, 2009
38 Roberts et al., DDT house spraying and re-emerging Malaria, Lancet, Volume 356,
No. 9226, 2000, pages 330-332
39 Sunyer et al., Prenatal dichlorodiphenyldichloroethylene (DDE) and asthma in
children, Environmental Health Perspectives, Volume 113(12), 2005, pages 1787-
1790
40 Takei et al., Analyses of human milk samples collected in Hawaii for residues of
organochlorine pesticides and polychlorobiphenyls, Bulletin of Environmental
Contamination and Toxicology, Volume 30, No. 1, 1983, pages 606-613
41 Turgut et al., Contents and sources of DDT impurities in dicofol formulations in
Turkey, Environmental Science & Pollution Research, Volume 16, 2009, pages
214-217
42 US EPA, Health Effects Assessment for DDT, 1984
43 Van Overmeire et al., Chemical contamination of free-range eggs from Belgium,
Food Additives and Contaminants, Volume 23(11), 2006 pages 1109-1122
44 Verma and Pillai, Bioavailability of soil-bound residues of DDT and HCH to certain
plants, Soil Biology and Biochemistry, Volume 23, Issue 4, 1991, pages 347-351
45 Walizewki et al., Partitioning Coefficients of Organochlorine Pesticides Between
Mother Blood Serum and Umbilical Blood Serum, Bulletin of Environmental
Contamination and Toxicology, Volume 65, No. 3, 2000, pages 293-299
46 WHO1, DDT and its derivates, Environmental Health Criteria 9, 1979
47 WHO2, DDT, Poisons Information Monographs 127, 1999
48 WHO3, DDT and it Derivates in Drinking-water, 2004
49 WHO4, DDT and its derivates, Environmental Health Criteria 83, 1989

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 50 Woolley and Talens, Distribution of DDT, DDD, and DDE in tissues of neonatal rats
and in milk and other tissues of mother rats chronically exposed to DDT,
Toxicology and Applied Pharmacology, Volume 18, Issue 4, 1971, pages 907-916

10. Websites

1 http://www.gmpplus.org
2 http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1178620762040.htm
3 http://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=81&tid=20
4 http://www.inchem.org/documents/ehc/ehc/ehc009.htm
5 http://www.inchem.org/documents/pims/chemical/pim127.htm
6 http://www.inchem.org/documents/ehc/ehc/ehc83.htm
7 http://www.inchem.org/documents/jmpr/jmpmono/v00pr03.htm

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 APPENDIX I Potential adverse effect of DDT and its analogues

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

DDT and its Death Carcinogen Mutagen Reproductive Internal injury Neurological Immunological Organs
2
analogues (physical effect
contamination)
1,2

Animals x x x x x x

Humans x x x

2 2 2 2
DDT and its Dermal and Respiratory Musculo- Cardiovascular Gastrointestinal Hematological Endocrine Body weight
2 2
analogues ocular skeletal
Animals x x

Humans x

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 DDT and its analogues
If not specified in the reports or when summary statements are cited, only the term DDT is used
NOAEL (mg/kg BW) ADI (mg/kg BW) LD50 (mg/kg BW)
DDT 0.5 (laying hen)2 (Smith et al., 113-800 (rat) (ATSDR, 2002)
1970B)
0.3 (Japanese quail)5 237-300 (mouse) (ATSDR,
(shellenberger, 1978B) 2002)
1 (rat)6 (FAO/WHO2, 2000) 400 (guinea pig) (ATSDR,
2002)
300 (rabbit) (ATSDR, 2002)
Technical DDTA 30 (broiler)1 (Latimer and
Siegel, 1974B)
75% p,p-DDT, 25% o,p'- 18 (laying hen)3 (Britton,
DDT 1975B)
p,p-DDT 12 (Japanese quail)4 (Simth PTDIC 0.01 (FAO/WHO2,
et al., 1969B) 2000)
A
Technical DDT is a mixture of various isomers of which p,p-DDT is the most prevalent (ATSDR, 2002).
B
Cited by EFSA (2006)
C
PTDI = Provisional Tolerable Daily Intake
1
for four week, NOAEL for clinical symptoms DDT intoxication
2
for two months, NOAEL for reduced egg production and shell thickness
3
for 35 days, NOAEL for egg production and shell quality
4
for 60 days, NOAEL for mortality and reproductive performance
5
for four generations, NOAEL for reduced fertility and hatchability
6
duration not known, NOAEL for developmental toxicity

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 APPENDIX III Synonyms DDT and its analogues
Compound Synonym
p,p-DDT 4,4'-DDT
1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane; dichlorodiphenyltrichloroethane
DDT; 1,1'-(2,2,2-trichloroethylidene)bis(4-chlorobenzene)
- -bis(p-chlorophenyl)-, , -trichloroethane
o,p-DDT 4,4'-DDT
1,1,1-trichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)-ethane
o,p'-dichlorodiphenyltrichloroethane
p,p-DDE 4,4'-DDE; dichlorodiphenyldichloroethane
1,1-dichloro-2,2-bis(p-chlorophenyl) ethylene
1,1'-(2,2-dichloroethylidene)bis(4-chlorobenzene)
DDE
o,p-DDE 2,4'-DDE
1,1-dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)ethylene
1-chloro-2-(2,2-dichloro-1-(4-chlorophenyl)ethenylbenzene
p,p-DDD 4,4'-DDD
DDD
1,1-dichloro-2,2-bis(p-chlorophenyl)ethane
1,1-bis(4-chlorophenyl)-2,2-dichloroethane
TDE
tetrachlorodiphenylethane
o,p-DDD 2,4'-DDD
Mitotane
1,1-dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)ethane
o,p'-TDE
Choditane
2-(o-chlorophenyl)-2-(p-chlorophenyl)-1,1-dichloroethane

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