DDT
| 1. DDT |
| 1.1 Substance |
| 1.2 Group |
| 1.3 Synonyms |
| 1.4 Identification numbers |
| 1.4.1 CAS |
| 1.4.2 Other numbers |
| 1.5 Brand names/Trade names |
| 1.6 Manufacturers, importers |
| 2. SUMMARY |
| 2.1 Main risks and target organs |
| 2.2 Summary of clinical effects |
| 2.3 Diagnosis |
| 2.4 First-aid measures and management principles |
| 3. PHYSICO-CHEMICAL PROPERTIES |
| 3.1 Origin of the substance |
| 3.2 Chemical Structure |
| 3.3 Physical properties |
| 3.3.1 Colour |
| 3.3.2 State/Form |
| 3.3.3 Description |
| 3.4 Hazardous characteristics |
| 4. USES |
| 4.1 Uses |
| 4.1.1 Uses |
| 4.1.2 Description |
| 4.2 High risk circumstances of poisoning |
| 4.3 Occupationally Exposed Population |
| 5. ROUTES OF EXPOSURE |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Others |
| 6. KINETICS |
| 6.1 Absorption by route of exposure |
| 6.2 Distribution by route of exposure |
| 6.3 Biological half-life by route of exposure |
| 6.4 Metabolism |
| 6.5 Elimination and excretion |
| 7. TOXICOLOGY |
| 7.1 Mode of action |
| 7.2 Toxicity |
| 7.2.1 Human data |
| 7.2.1.1 Adults |
| 7.2.1.2 Children |
| 7.2.2 Relevant animal data |
| 7.2.3 Relevant in vitro data |
| 7.2.4 Workplace standards |
| 7.2.5 Acceptable daily intake (ADI) |
| 7.3 Carcinogenicity |
| 7.4 Teratogenicity |
| 7.5 Mutagenicity |
| 7.6 Interactions |
| 8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS |
| 8.1 Material sampling plan |
| 8.1.1 Sampling and specimen collection |
| 8.1.1.1 Toxicological analyses |
| 8.1.1.2 Biomedical analyses |
| 8.1.1.3 Arterial blood gas analysis |
| 8.1.1.4 Haematological analyses |
| 8.1.1.5 Other (unspecified) analyses |
| 8.1.2 Storage of laboratory samples and specimens |
| 8.1.2.1 Toxicological analyses |
| 8.1.2.2 Biomedical analyses |
| 8.1.2.3 Arterial blood gas analysis |
| 8.1.2.4 Haematological analyses |
| 8.1.2.5 Other (unspecified) analyses |
| 8.1.3 Transport of laboratory samples and specimens |
| 8.1.3.1 Toxicological analyses |
| 8.1.3.2 Biomedical analyses |
| 8.1.3.3 Arterial blood gas analysis |
| 8.1.3.4 Haematological analyses |
| 8.1.3.5 Other (unspecified) analyses |
| 8.2 Toxicological Analyses and Their Interpretation |
| 8.2.1 Tests on toxic ingredient(s) of material |
| 8.2.1.1 Simple Qualitative Test(s) |
| 8.2.1.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.1.3 Simple Quantitative Method(s) |
| 8.2.1.4 Advanced Quantitative Method(s) |
| 8.2.2 Tests for biological specimens |
| 8.2.2.1 Simple Qualitative Test(s) |
| 8.2.2.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.2.3 Simple Quantitative Method(s) |
| 8.2.2.3 Advanced Quantitative Method(s) |
| 8.2.2.5 Other Dedicated Method(s) |
| 8.2.3 Interpretation of toxicological analyses |
| 8.3 Biomedical investigations and their interpretation |
| 8.3.1 Biochemical analysis |
| 8.3.1.1 Blood, plasma or serum |
| 8.3.1.2 Urine |
| 8.3.1.3 Other fluids |
| 8.3.2 Arterial blood gas analyses |
| 8.3.3 Haematological analyses |
| 8.3.4 Interpretation of biomedical investigations |
| 8.4 Other biomedical (diagnostic) investigations and their interpretation |
| 8.5 Overall interpretation of all toxicological analyses and toxicological investigations |
| 8.6 References |
| 9. CLINICAL EFFECTS |
| 9.1 Acute poisoning |
| 9.1.1 Ingestion |
| 9.1.2 Inhalation |
| 9.1.3 Skin exposure |
| 9.1.4 Eye contact |
| 9.1.5 Parenteral exposure |
| 9.1.6 Other |
| 9.2 Chronic poisoning |
| 9.2.1 Ingestion |
| 9.2.2 Inhalation |
| 9.2.3 Skin exposure |
| 9.2.4 Eye contact |
| 9.2.5 Parenteral exposure |
| 9.2.6 Other |
| 9.3 Course, prognosis, cause of death |
| 9.4 Systemic description of clinical effects |
| 9.4.1 Cardiovascular |
| 9.4.2 Respiratory |
| 9.4.3 Neurological |
| 9.4.3.1 Central nervous system |
| 9.4.3.2 Peripheral nervous system |
| 9.4.3.3 Autonomic nervous system |
| 9.4.3.4 Skeletal and smooth muscle |
| 9.4.4 Gastrointestinal |
| 9.4.5 Hepatic |
| 9.4.6 Urinary |
| 9.4.6.1 Renal |
| 9.4.6.2 Others |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatologic |
| 9.4.9 Eye, ears, nose, throat: local effects |
| 9.4.10 Haematological |
| 9.4.11 Immunological |
| 9.4.12 Metabolic |
| 9.4.12.1 Acid base disturbances |
| 9.4.12.2 Fluid and electrolyte disturbances |
| 9.4.12.3 Others |
| 9.4.13 Allergic reactions |
| 9.4.14 Other clinical effects |
| 9.4.15 Special risks |
| 9.5 Others |
| 9.6 Summary |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Life supportive procedures and symptomatic treatment |
| 10.3 Decontamination |
| 10.4 Enhanced Elimination |
| 10.5 Antidote treatment |
| 10.5.1 Adults |
| 10.5.2 Children |
| 10.6 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from the literature |
| 12. ADDITIONAL INFORMATION |
| 12.1 Specific preventive measures |
| 12.2 Other |
| 13. REFERENCES |
| 14. AUTHOR(S), REVIEWER(S), DATE (INCLUDING EACH UP-DATE), COMPLETE ADDRESSES |
DDT
International Programme on Chemical Safety
Poisons Information Monograph 127
Chemical
1. DDT
1.1 Substance
Dichlorodiphenyltrichloroethane (DDT)
1.2 Group
1.3 Synonyms
Alpha,alpha-bis(p-chlorophenyl)beta, beta,
beta-Trichlorethane;
2,2-Bis(p-chlorophenyl)-1,1,1-Trichloroethane;
Clofenotane (INN);
Chlorinated diphenyloxide;
Chlorophenothane (USP);
p,p'-DDT;
Dicophane (BP);
ENT - 1506;
Klorfenoton (Swedish);
1,1,1,Trichloor2,2-bis(4-chloor-fenyl)-Ethaan(Dutch);
1,1,1,Trichlor-2,2 bis(4-chlor-phenyl)aethan(German);
1,1,1,Trichloro,2,2-Di(4-chlorophenyl)ethane;
1,1-(2,2,2-trichloroethylidene)-bis (4-chlorobenzene) (CAS);
1,1,1-trichloro-2,2-bis (4-chlorophenyl) ethane (IUPAC);
OMS-16;
1.4 Identification numbers
1.4.1 CAS
50-29-3
1.4.2 Other numbers
UN transportation number 2761
RTECS KJ 3325000
NCI C 00464
1.5 Brand names/Trade names
Anofax;
Cezarex;
DinozideGesarol;
Guesapan;
Guesarol;
Gyron;
Ixodex;
Neocide;
Neocidol;
Zerdane;
1.6 Manufacturers, importers
To be added by the poison control centre.
2. SUMMARY
2.1 Main risks and target organs
DDT has a wide margin of safety when used
judiciously, and few if any adequately documented cases of
DDT poisoning in man have been fatal. It appears that the
main toxicity to humans is related more to the solvent
vehicle rather than the DDT itself.
DDT is a central nervous system stimulant, acting chiefly
on the cerebellum and motor cortex. The liver is the only
other organ significantly affected by DDT.
2.2 Summary of clinical effects
The earliest symptom of poisoning by DDT is
hyperaesthesia of the mouth and lower part of the face.
This is followed by paraesthesia of the same area and of
the tongue and then by dizziness, an objective disturbance
of equilibrium, paraesthesia and tremor of the
extremities, confusion, malaise, headache, fatigue, and
delayed vomiting (probably centrally mediated).
Convulsions only occur in severe poisoning. It is not
clear whether cardiac arrhythmia might be a possible cause
of death in acute poisoning. In most instances of
fatalities following ingestion of DDT solutions, the signs
and symptoms were predominantly or exclusively those of
poisoning by the solvent vehicle.
2.3 Diagnosis
Clinical diagnosis may be difficult as symptoms are
not specific and are dose related. The clinical effects of
DDT may be modified by the vehicle or co -ingredients. A
single dose of DDT at the rate of 10 mg/kg may produce
illness in some but not all subjects; smaller doses
generally produce no illness.
Blood levels are not clinically useful.
There are both simple qualitative and recommended
qualitative (involving thin layer chromatography) tests
for biological samples (stomach contents or suspect
fluids). Gas liquid chromatography can be performed on
blood and urine within 72 hours. The urine can be
examined for the presence of DDA when the diagnosis is
uncertain.
Hyperlipoproteinaemia can be tested for if chronic
exposure is suspected.
2.4 First-aid measures and management principles
In the event of exposure to DDT, contaminated
clothing and contact lenses should be removed to prevent
further absorption. In the case of skin contact, the
affected area should be washed carefully with soap and
water. Wash eyes for 10 to 15 minutes with clean running
water. First aid personnel should wear rubber or plastic
gloves and avoid contamination.
Ingestions of small amounts of DDT do not constitute a
significant risk, and may be managed by dilution with
water.
The management of large quantities of ingested DDT should
be primarily directed towards decontamination and
supportive care, as there is no specific antidote. The
use of gastric lavage for recent large ingestions and
activated charcoal are indicated.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
A synthetic product, DDT can be manufactured by the
condensation of chlorobenzene with trichloroacetaldehyde
(Worthing & Walker, 1987).
3.2 Chemical Structure
The chemical name for DDT is:
1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane
The empirical formula is C14H9Cl5
The relative molecular mass is 354.50
3.3 Physical properties
3.3.1 Colour
White
3.3.2 State/Form
Solid-crystals
3.3.3 Description
At room temperature DDT is a white,
tasteless, almost odourless crystalline solid
(Hayes & Laws, 1991).
Solubility: Practically insoluble in water
2g/100mL ethanol
28g/100mL ether
Highly soluble in apolar
organic solvents
Boiling point: 185°C
Melting point: 108.5°C to 109.0°C
Flash point: 162-171 °F
Density (20°C): 1.016 kg/L
Specific gravity: 1.55
Vapour pressure (20°C) 2.53 × 10-5 Pa
3.4 Hazardous characteristics
The term DDT is generally understood to refer to para
para'-DDT. However, the compound's structure permits
several different isomeric forms including ortho para-DDT
and meta para-DDT. Technical DDT consists predominantly
of para para'-DDT with smaller amounts of other compounds
such as ortho para-DDT, para para'-TDE, ortho para-DDE
(WHO, 1989). These other isomeric forms may add to the
action of DDT as it is known that ortho para-DDT is of
insecticidal value (Worthing & Walker, 1987).
DDT is resistant to destruction by light and oxidation
(Budavari et al., 1989).
para para'-DDT is dehydrochlorinated, at temperatures
above its melting point, to DDE which has no insecticidal
properties. This reaction is catalysed by iron(III) or
aluminium chlorides, UV light and in solution by alkalis
(Worthing & Walker, 1987). As such, DDT should not be
stored in iron containers and should not be mixed with
iron and aluminium salts or with alkaline solutions.
High temperatures should also be avoided (Budavari et al.,
1989).
The environmental distribution and effects of DDT arise
from its unusual chemical stability and hence its
persistence. DDT and some of the breakdown products of
DDT, principally DDE, are highly persistent in soil,
sediment and biota as they are relatively resistant to
breakdown by the enzymes and higher organisms found in the
soil (WHO, 1979). Thus, contamination by materials can
last long after cessation of DDT use.
DDT and its metabolites are highly toxic to fish and,
besides their lethal effects, they affect development,
behaviour and biochemical processes. DDT and its
metabolites, should be regarded as hazardous to fish
productivity and distribution and, hence, to human food
supplies. Accumulated DDT and its metabolites are further
transferred from aquatic organisms to consumers, including
birds, mammals, and, ultimately, humans (WHO, 1979).
When exposed to simulated atmospheric conditions DDT
decomposes to carbon dioxide and hydrochloric acid (WHO,
1979).
Fires involving DDT may produce irritating or poisonous
gases. Fire fighters should wear self contained breathing
apparatus and chemical protective clothing. For small
fires, use dry chemical, CO2, halon, water spray or
standard foam extinguishment. For larger fires, water
spray, fog or standard foam is recommended. For spills,
take up with sand or other non-combustible absorbent
material and place into containers for later disposal
(DOT, 1987).
4. USES
4.1 Uses
4.1.1 Uses
Pesticide For Use Against Invertebrate Animals
Insecticide
4.1.2 Description
DDT is a potent non-systemic stomach and
contact insecticide. It is persistent on solid
surfaces, in soil, sediment and biota (Worthing &
Walker, 1987).
DDT has had a wide usage, particularly in
agriculture and vector control, and as such has
been formulated in almost every conceivable form.
These include solutions in xylene and petroleum
distillates, emulsifiable concentrates, water-
wettable powders, granules, aerosols, smoke
candles, and charges for vaporisers (Hayes & Laws,
1991).
For its use as a topical medication it has also
been formulated as lotions, dusting powders and
shampoos (Reynolds, 1989).
The use of DDT is restricted or banned in some
countries except when it is needed for the
protection of health.
4.2 High risk circumstances of poisoning
Accidental poisoning of children by DDT present in
the home or garage (mostly a problem when in non aqueous
solution, and the vehicle is often more of a problem than
the DDT).
Accidental exposure among adult farm workers and secondary
exposure to their children.
Suicide attempts.
Exposure of the general population may occur through the
consumption of foodstuffs treated incorrectly with DDT or
harvested prematurely before residues have declined to
acceptable levels, from contact with treated areas or from
domestic use.
Use and contact with DDT formulated with oils, fats and
lipid solvents.
4.3 Occupationally Exposed Population
Factory workers involved in synthesising DDT.
Workers involved in formulating and dispensing DDT.
Agricultural spray workers.
Crop harvesters during disease vector control periods.
Public health workers involved in vector control.
5. ROUTES OF EXPOSURE
5.1 Oral
Ingestion occurs through accidental or deliberate
ingestion and ingestion via contaminated foodstuffs.
5.2 Inhalation
DDT is relatively non volatile and, although
inhalation of spray drift may occur during occupational
use, respiratory exposure is a less significant
route.
5.3 Dermal
DDT is poorly absorbed via the dermal route and as
such is a less important route of entry. Dermal
absorption increases when DDT is formulated in oily
solutions.
5.4 Eye
Exposure to vapours, dust and aerosols.
5.5 Parenteral
Accidental or intentional.
5.6 Others
No data available
6. KINETICS
6.1 Absorption by route of exposure
In inhalation, most DDT dust is of such large
particle size that any that is inhaled is deposited in the
upper respiratory tract and eventually is swallowed (Hayes
& Laws, 1991).
Absorption of DDT from the gastrointestinal tract is slow.
Studies based on toxicity indicate that DDT dissolved in
animal or vegetable fats is absorbed from the
gastrointestinal tract about 1.5- to times more
effectively than is undissolved DDT. Convulsions occur
only after 2 hours when DDT is administered orally at a
rate of 2 or more times the oral LD50 value (Hayes &
Laws, 1991).
Intravenous injection at the rate of 50 mg/kg produces
convulsions in rats in 20 minutes (Hayes & Laws,
1991).
Dermal absorption of DDT is very limited (Hayes & Laws,
1991).
6.2 Distribution by route of exposure
DDT is stored in all tissues. Storage of the
compound in blood, liver, kidney, heart and the central
nervous system (CNS) has been reported. Higher
concentrations of DDT are usually found in adipose tissue
than in other tissues (Hayes & Laws, 1991).
In the general population DDT and some of its metabolic
derivatives can be stored in the tissues and excreted in
urine and milk (Hayes & Laws, 1991).
DDT and one of its major metabolic products, DDE, have
high fat: water partition coefficients and, therefore,
tend to accumulate in adipose tissue. Studies in both
humans and laboratory animals indicate that there is a
log-log relationship between the daily intake and the
residues of both DDT and DDT-derived material in adipose
tissue. At a constant rate of intake, however, the
concentration of insecticide in adipose tissue reaches an
equilibrium and remains relatively constant (Klaassen et
al., 1986).
6.3 Biological half-life by route of exposure
In a study of volunteer adult males who ingested
between 3.5 and 35 mg DDT/person/day, the storage of DDT
was proportional to dosage. DDT was slowly lost from
storage in fat after dosing was stopped. The
concentration remaining following 25.5 months of recovery
was from 32 to 35% of the maximum stored for those who had
received 35 mg DDT/person/day but was 66% for those who
received only 3.5 mg DDT/person/day. This indicated that
a slower loss occurred at lower storage levels (Hayes &
Laws, 1991).
6.4 Metabolism
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
para, para-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).
6.5 Elimination and excretion
DDT is slowly eliminated from the body. Elimination
has been estimated at a rate of approximately 1% of stored
DDT per day (Klaassen et al., 1986).
Urinary DDA presents about 47% of ingested precursor
material during low exposure, but DDA excretion becomes
quantitatively less important as DDT intake increases.
Urinary DDA concentrations correlate reasonably well with
DDT storage levels in body fat. DDA was undetectable in
the urine of members of the general population and ranged
from 0.01 to 2.67 mg/L in workers with low to high
exposure to DDT. By contrast, urine concentrations of
DDT, DDE and DDD in healthy unexposed persons averaged
0.007, 0.016 and 0.003 mg/L respectively, and 0.011, 0.021
and 0.006 mg/L respectively in occupationally exposed
workers (Baselt, 1982).
DDT is also excreted in human milk and transferred through
the placenta (Hayes & Laws, 1991).
7. TOXICOLOGY
7.1 Mode of action
DDT is a central nervous system stimulant acting
chiefly on the cerebellum and motor cortex. Its action
produces hyperexcitability, tremor and muscular weakness.
Convulsions and myocardial sensitivity may occur
(Dreisbach & Robertson, 1987).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
DDT has a wide margin of safety
when used judiciously, and few if any
adequately documented cases of DDT
poisoning in man have been fatal
(Gosselin et al., 1984). It appears that
the main toxicity to humans is related
more to the solvent vehicle rather than
the DDT itself.
10 mg/kg is the single oral dose of DDT
necessary to produce illness in some but
not all subjects even though no vomiting
may occur (Hayes & Laws, 1991).
Convulsions have occurred in cases when
the dosage level was 16 mg/kg or greater
and no effective treatment was undertaken
(Hseih, 1954).
Amounts at least as high as 285 mg/kg
have been ingested without fatalities.
However, the amount retained is unknown
as these doses lead promptly to vomiting
(Hayes & Laws, 1991).
Considerable individual variation is
recognized with DDT toxicity. Woodward
et al. (1944) described the generally
accepted acute mean lethal dose (LD50) in
rats as 250 mg/kg and Gosselin et al.
(1984) suggest that this is a reasonable
estimate for man. Baselt (1982) states
that in general, DDT is relatively safe
with an estimated lethal dose of 30 g in
an adult.
Fats and oils enhance the toxicity of DDT
by promoting absorption. In many
instances of alleged poisoning with DDT
the principal symptoms have been due to
the commercial vehicle that the DDT is
formulated with. This vehicle has often
been kerosene (Reingold & Lasky,
1947).
7.2.1.2 Children
From studies in the young of
animal species it has been suggested
(Hayes & Laws, 1991) that the young are
at no greater risk than an
adult.
7.2.2 Relevant animal data
Animal Formulation Oral Dermal IV
LD50 LD50 LD50
mg/kg mg/kg mg/kg
Rat Water 500 1000 -
suspension to 2500
or powder
Oil solution 113 250 to 47
to 450 3000
Mouse Water 300 to 375 -
suspension 1600
or powder
Oil solution 100 to 250 to -
800 500
(Hayes & Laws, 1991)
7.2.3 Relevant in vitro data
No data available.
7.2.4 Workplace standards
STEL ACGIH 3 milligram per cubic metre
(Parmeggiani, 1983)
TLV-TWA 1 milligram per cubic metre
(ACGIH, 1989)
OSHA PEL-TWA 1 milligram per cubic metre
(skin designation) (OSHA,
1989)
Odour threshold not pertinent as is odourless
(CHRIS, 1985)
7.2.5 Acceptable daily intake (ADI)
0.02 mg/kg body weight (provisional tolerable
daily intake, WHO 1995) [sum of p,p'DDT, o,p'DDT,
p,p'DDE and p,p'TFE(DDD)]
Other Guideline Levels:
WHO guideline value for drinking water:
1 microgram/L (total isomers) (WHO, 1984)
7.3 Carcinogenicity
DDT has been evaluated by the International Agency for
Research on Cancer (IARC, 1987,1991). It was concluded that
the human evidence from several epidemiological studies was
not adequate to indicate that DDT was carcinogenic.
Many experiments have been conducted in rodents. Liver
tumours were introduced in most of the mouse and in two of
the rat experiments (IARC, 1991).
Some risk of lymphoma, leukemia, pancreatic cancer, and
breast cancer was found in humans exposed to DDT. Animal
studies showed a significant association between DDT
administration and lymphoma, respiratory cancer, liver
cancer, and estrogenic effects on mammary tissue. On the
basis of epidemiological principles, human studies were
deficient in adequate sample sizes and were not exempt from
such confounding factors as multiple chemical exposure,
lifestyle factors, genetic, and other environmental
influences (Jaga and Brosius, 1999).
7.4 Teratogenicity
The effects of DDT on reproduction parameters have been
summarised by IARC (1991). One human study has suggested
that there may be a weak relationship between DDT levels in
cord blood and low birth weight. Studies in rodents and
rabbits have not demonstrated any teratogenic potential, but
exposure of rodents to DDT impaired reproductive function
(e.g., spermatogenesis, neonatal survival) in some
studies.
7.5 Mutagenicity
IARC (1991) reported one study in which chromosomal
aberrations were observed in the peripheral lymphocytes of
workers with increased plasma DDT levels. This finding is not
supported by studies on bone-marrow cells of rodents. In
most studies, DDT did not induce genetoxic effects in
cultured rodent or human cell systems and was not mutagenic
to fungi or bacteria.
7.6 Interactions
DDT is known to interfere with the metabolism and
function of steroid hormones. One such mechanism is by the
induction of hepatic microsomal enzymes which results in an
increased conversion of oestrogens, androgens, and
glucocorticoids to more polar metabolites. Increased urinary
excretion of the more polar metabolites is usually
compensated for by increased steroid biosynthesis (Gosselin
et al., 1984).
Individuals on chronic drug therapy with phenobarbitol and/or
phenytoin have increased hepatic microsomal enzymes activity.
Watson et al. (1972) suggest that this increased activity
accelerates the metabolism of some DDT to DDA by the slow
series of dehydrohalogenation reactions.
Fat and oils increase the absorption of DDT from the
intestine.
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
Sample should be drawn into a vial
or tube filter with a teflon or foil lined
screw cap. Polyethylene or rubber caps must
be used. Sample size: 7 to 10 mL. Use
whole blood without added anticoagulant
(EPA, 1982).
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
If an analysis cannot be run
immediately, place in refrigerator at 2 to
5°C for periods of up to 24 hours before
analysis. If time interval to analysis
exceeds 24 hours, sample (serum) should be
stored in a deep-freeze at -15 to -25°C.
Stored in this manner, analysis may be
delayed up to a month. (EPA, 1982).
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
Nitric-sulphuric acid colour test:
The reagent:
Mix 1 mL nitric acid with 30 mL sulphuric
acid
Method:
Dissolve the sample in 1 mL Ethanol, and add
a pellet of potassium hydroxide. Evaporate
to dryness at 100°C in a waterbath. To the
residue, add 0.5 mL water and 1 mL carbon
tetrachloride. Shake, allow to separate,
decant the lower carbon tetrachloride layer
and shake it with 1 mL reagent.
Indications:
A RED colour in the acid layer suggests the
presence of DDT or its metabolite DDE. The
red colour changes to ORANGE then to GREEN.
A RED colour is also given by DDD but the
colour does not change (Moffat, 1986).
8.2.2.2 Advanced Qualitative Confirmation Test(s)
Thin Layer chromatography:
Recommended qualitative for biological sample
(stomach contents or suspect fluids).
Sampling:
10 to 20 mL stomach content
Chemical and reagents:
*Petroleum ether (40 to 60°C boiling
fraction)
*Aqueous sodium hydroxide (20 g/L)
*Sodium sulphate (anhydrous)
*Organochlorine standards (DDT, HCH, Lindane,
HCB, heptachlor, aldrin, endrine) (all in 1
g/L) in methanol, Silica gel.
Equipment:
TLC plates (20 × 20 cm), pipettes, spray
bottle.
Method:
10 mL of sample is extracted twice with 5 mL
portions of petroleum ether. Extracts are
combined and washed with 5 mL portions of
purified water and sodium hydroxide solution.
The extract is dried over sodium sulphate and
evaporated to dryness under stream of
compressed air.
The extract is reconstituted in 100 mg
methanol and 20 mg is spotted on TLC plate.
Standard mixture is spotted on a second
column. The chromatogram is developed using
petroleum ether (saturated tank) and allowed
to dry. The plate is sprayed with silver
nitrate solution and after drying in ambient
temperature, is exposed to UV light (254 nm,
15 min).
Organochlorine compounds give a BROWN-GREY
reaction and identification is made by
comparison with the standard
chromatogram.
8.2.2.3 Simple Quantitative Method(s)
8.2.2.3 Advanced Quantitative Method(s)
Recommended quantitative test for
biological sample (blood).
Principle of test:
A 2 mL aliquot of serum is extracted with 6
mL of hexane in a round bottom tube. The
extraction is conducted for 2 hours on a slow
speed rotating mixer. If emulsion forms,
centrifugation may be used to effect
separation. A 5 mL aliquot of the hexane
layer is quantitatively transferred to an
evaporative concentrator tube to which a
micro-snider column is affixed. The extract
is concentrated in a water bath, and the
final volume is adjusted to correspond to the
expected concentration of the pesticide
residue. A suitable aliquot is analysed by
electron capture gas chromatography.
Sampling:
7 to 10 mL blood drawn, is transferred to a
vial or tube fitted with a teflon or foil
lined screw. Whole blood sample is placed in
the refrigerator for about 30 minutes for
setting and centrifuged for 10 minutes for
the separation of at least 3 mL of clear
serum 2 mL of serum is used for
extraction.
Chemicals and reagents:
Hexane, distilled in glass, pesticide grade.
Equipment:
1. A rotatory mixer, designed to accommodate
the 16 mm culture tubes and which may be
operated at a rotary speed of 50 rpm.
2. Gas chromatograph, fitted with electron
capture detector.
3. Tubes, culture, 16 125 mm, fitted with
screw caps with teflon-faced rubber
liners.
4. Micro-snider column.
5. Concentrator tube.
6. Syringe, 100 mL, Hamilton.
7. Vortex mixer.
8. Pipette, Mohr type, 1 mL grad in 0.01 mL
increments.
9. Pipettes, transfer, 2,5 and 6 mL.
10. Beads solid, glass, 3 mm.
11. Water bath capable of holding temperature
of 95 to 100°C.
12. Centrifuge, capable of speed of 2000 rpm.
Specimen preparation:
No special preparation required.
Procedure:
Mix blood serum sample thoroughly and, with a
volumetric pipette, transfer 2 mL to a 15 mL
round bottom culture tube. In case of the
presence of any flocculent or sedimentary
material, centrifuge in 5 min 2000 rpm before
pipetting, in order to avoid poor
reproducibility of replicated analyses of the
same sample.
Add 6 mL hexane from a volumetric pipette.
Tightly stopper the culture tube. Place on
rotator for 2 hours of 50 rpm speed. In the
case of emulsion formation centrifuge at 2000
rpm 4 to 5 minutes. Transfer 5 mL of the
hexane extract to a 10 mL grad. concentrator
tube, add one 3 mm glass bead and attach a
modified micro - Snider column. Evaporate the
extract in a steam or hot bath at 100°C.
(When working with blood from high exposure
donors, the 5 mL aliquot may require dilution
rather than concentration) allow the tube to
cool 3 to 5 minutes, remove the micro -
Snider column an rinse down the sides of the
tube and the column joint with hexane.
Stopper the concentrator tube and hold on the
Vortex mixer, set for high speed for 30
seconds for volumes of 6 mL or less. For
larger volumes mix for 1 minute. Proceed with
electron capture GLC.
p.p.b = \f(a b x, c y) × 0.6
Where:
a = nanograms of pesticide in standard peak
b = height of sample peak
c = height of standard peak
x = total volume of final extract in
microlitres
y = microliters of extract injected
e.g.: nanograms in standard peak = 0.3
height of sample peak = 80 mm
height of standard peak = 90 mm
total volume of final extract = 1000
microlitre
volume of final extract injected = 5
microlitre
p.p.b = \f(0.3 × 80 × 1000,90 × 5) × 0.6 = 32
ppb
Quality Control:
Composition of standard mixture:
a HCH 20 pg/mL HCB 20 pg/mL pp DDT 80 pg/mL
b HCH 40 pg/mL Heptachlor 20 pg/mL pp DDE 60 pg/mL
g HCH 20 pg/mL op DDT 50 pg/mL pp DDD 50 pg/mL
Specificity:
It is group specific
Detection Limit:
b-HCH, lindane, heptachlor, heptachlor
epoxide, o,p-DDE, dieldrin:-1 ppb
endrin, op-DDT,pp-DDD,pp-DDT:-2 ppb
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
Blood levels are not clinically useful.
Biochemical tests to detect liver and kidney
dysfunction should be performed although the
results are expected to be negative (Gosselin
et al., 1984).
Determination of blood sugar and sugar
tolerance levels are desirable (Gosselin et
al., 1984).
8.3.1.2 Urine
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
interpretation
8.5 Overall interpretation of all toxicological analyses and
toxicological investigations
Relevant laboratory analyses and other investigations:
Laboratory analysis may indicate prolonged exposure to DDT
but has little relation to acute exposure management as
decontamination needs to be undertaken before laboratory
results are available.
Sample collection:
Analysis of blood and urine is required within 72 hours to
detect high DDT levels.
Biomedical analysis:
Blood levels are not clinically useful.
Biochemical tests to detect liver and kidney dysfunction
should be performed although the results are expected to be
negative (Gosselin et al., 1984).
Determination of blood sugar tolerance levels are desirable
(Gosselin et al., 1984).
Toxicological analysis:
Gas liquid chromatography can be performed on blood and urine
within 72 hours.
The urine can be examined for the presence of DDA when the
diagnosis is uncertain (Gosselin et al., 1984).
Other investigations:
Hyperlipoproteinaemia can be tested for if chronic exposure
is suspected (Gosselin et al., 1984).
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Onset of signs and symptoms depends on the
dose. Onset may be as soon as 30 minutes after
ingestion of a large dose or as late as 6 hours after
smaller but still toxic doses.
Large doses are followed promptly by vomiting due to
local gastric irritation. Delayed emesis and/or
diarrhoea may occur.
Onset of signs and symptoms are characterised by
paraesthesia of the tongue, lips and face. In more
severe poisonings paraesthesia may also involve the
extremities. The patient suffers from a sense of
apprehension, dizziness, an objective disturbance of
equilibrium, and ataxia. Confusion may develop,
malaise, headache, fatigue and sore throat may also be
present. Tremor is a characteristic manifestation,
usually involving first the neck and head and
particularly the eyelids. Convulsions both clonic and
tonic may develop and alternate with periods of coma
and paresis. In the absence of convulsions, the vital
signs are essentially normal, but in severe poisoning
the pulse may be irregular and abnormally slow.
Because DDT sensitises the heart to endogenous
adrenaline, ventricular fibrillation and sudden death
may occur at any time during the acute phase of
poisoning. Complicating pulmonary signs suggesting a
pulmonary oedema are probably due to concomitant
solvent intoxication. Death, if it occurs, is usually
due to respiratory failure from medullary paralysis
(Gosselin et al., 1984; Dreisbach & Robertson, 1987;
Hayes & Laws, 1991).
9.1.2 Inhalation
Inhalation of fine DDT aerosol or dust into the
lung produces moderate irritation of nose, throat and
eyes with no other detectable ill effects (Hayes &
Laws, 1991).
9.1.3 Skin exposure
Dermal exposure to DDT is usually associated
with no illness and usually no irritation.
Formulations of DDT involving solvents have been shown
to cause a slight transient dermatitis. These effects
have usually been shown to be related to the solvent
(Hayes & Laws, 1991).
9.1.4 Eye contact
Contact with the eyes may cause ocular irritation.
Further effects may be due to the solvent present.
9.1.5 Parenteral exposure
Intravenous administration in animals has
resulted in ventricular fibrillation and death. This
could be extrapolated to mean something similar in
humans.
9.1.6 Other
No data available.
9.2 Chronic poisoning
9.2.1 Ingestion
No data available.
9.2.2 Inhalation
No data available.
9.2.3 Skin exposure
No data available.
9.2.4 Eye contact
No data available.
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
There have been no accidents or suicides involving
respiratory or dermal exposure leading to recognised signs
and symptoms of DDT poisoning.
Onset of acute poisoning may be as soon as 30 minutes after
ingestion of a large dose or as late as 6 hours after smaller
but still toxic doses. Recovery from mild poisoning is
essentially complete in 24 hours, but recovery from severe
poisoning requires several days.
The earliest symptom of poisoning by DDT is hyperaesthesia of
the mouth and lower part of the face. This is followed by
paraesthesia of the same area and of the tongue and then by
dizziness, an objective disturbance of equilibrium,
paraesthesia and tremor of the extremities, confusion,
malaise, headache, fatigue, and delayed vomiting (probably
centrally mediated). Convulsions only occur in severe
poisoning. It is not clear whether cardiac arrhythmia might
be a possible cause of death in acute poisoning. In most
instances of fatalities following ingestion of DDT solutions,
the signs and symptoms were predominantly or exclusively
those of poisoning by the solvent vehicle (Hayes & Laws,
1991).
9.4 Systemic description of clinical effects
9.4.1 Cardiovascular
Cardiac arrhythmias have been associated with
death following DDT poisoning in some species of
laboratory animals, but this may not be the case in
acute human poisonings. Palpitations, tachycardia and
irregular heart action have been noted in some cases
of acute poisonings (Hayes & Laws, 1991).
9.4.2 Respiratory
The effects of DDT on the respiratory system
are secondary to the effects on the nervous system
(Hayes & Laws, 1991).
9.4.3 Neurological
9.4.3.1 Central nervous system
Dizziness, an objective disturbance
of equilibrium, confusion, malaise, headache,
fatigue, and delayed vomiting (probably
centrally mediated) may occur following
ingestion of DDT. Convulsions only occur in
severe poisoning (Hayes & Laws,
1991).
9.4.3.2 Peripheral nervous system
The earliest symptom of poisoning by
DDT is hyperaesthesia of the mouth and lower
part of the face. This is followed by
paraesthesia of the same area and of the
tongue, then paraesthesia of the extremities
(Hayes & Laws, 1991).
9.4.3.3 Autonomic nervous system
Increased salivation has been
reported in persons who ingested
DDT-contaminated food (Hayes & Laws,
1991).
9.4.3.4 Skeletal and smooth muscle
Tremor of the extremities has been
reported in persons who ingested
DDT-contaminated food (Hayes & Laws,
1991).
9.4.4 Gastrointestinal
Except for vomiting, which is probably
centrally mediated, the gastrointestinal system has
not been affected in acute poisoning (Hayes & Laws,
1991).
9.4.5 Hepatic
DDT is a hepatic enzyme inducer. Involvement of
the liver has been mentioned in only a small
proportion of cases of accidental DDT poisoning (Hayes
& Laws, 1991).
9.4.6 Urinary
9.4.6.1 Renal
There is no indication of renal damage
in people accidentally poisoned by DDT or
in workers heavily exposed to it (Hayes &
Laws, 1991).
9.4.6.2 Others
9.4.7 Endocrine and reproductive systems
The effects of DDT on reproduction parameters
have been summarised by IARC (1991). One human study
has suggested that there may be a weak relationship
between DDT levels in cord blood and low birth weight.
Studies in rodents and rabbits have not demonstrated
any teratogenic potential, but exposure of rodents to
DDT impaired reproductive functions (e.g.,
spermatogenesis, neonatal survival) in some
studies.
DDT is known to interfere with the metabolism and
function of steroid hormones. One such mechanism is
by the induction of hepatic microsomal enzymes which
results in an increased conversion of oestrogens,
androgens, and glucocorticoids to more polar
metabolites. Increased urinary excretion of the more
polar metabolites is usually compensated for by
increased steroid biosynthesis (Gosselin et al.,
1984).
9.4.8 Dermatologic
Skin irritation results from extensive contact
with organochlorine pesticides or with the white
petroleum distillate vehicles.
9.4.9 Eye, ears, nose, throat: local effects
Eyes-Acute
DDT has not been demonstrated to have a selective
effect on the eyes. Pure DDT dissolved in purified
kerosene was tested in a concentration of 0.01% on a
human eye and caused no discomfort or irritation; it
also proved non-irritating at 4% concentration on
rabbit eyes. Rare instances have been reported of
ocular irritation following contamination of the eye
by powders containing DDT (Grant, 1986).
Eyes - Chronic
In one instance chronic superficial punctate keratitis
was associated with fatal poisoning from long exposure
to DDT dust, but it was possible that constituents
other than DDT were responsible, or that there was
hypersensitivity (Grant, 1986).
Nose and throat-acute
Volunteers exposed to DDT dispersed into the air
either by volatilising units or by continuously or by
intermittently operated aerosol dispensers in some
instances reported some dryness of the throat, but
otherwise the results were negative (Hayes & Laws,
1991).
9.4.10 Haematological
In acute poisoning a slight decrease in
haemoglobin and a moderate leukocytosis without any
constant deviation in the differential white count
have been observed in volunteers. These findings are
considered secondary to the neurological
effects.
9.4.11 Immunological
DDT appears to have a depressant effect on the
immune system although the evidence is by no means
conclusive (Hayes & Laws, 1991).
9.4.12 Metabolic
9.4.12.1 Acid base disturbances
No data available
9.4.12.2 Fluid and electrolyte disturbances
No data available
9.4.12.3 Others
No data available
9.4.13 Allergic reactions
No data available
9.4.14 Other clinical effects
No data available
9.4.15 Special risks
Pregnancy
The effect of DDT on reproduction parameters have been
summarised by IARC (1991). One human study has
suggested that there may be a weak relationship
between DDT levels in cord blood and low birth weight.
Studies in rodents and rabbits have not demonstrated
any teratogenic potential, but exposure of rodents to
DDT impaired reproductive function (e.g.,
spermatogenesis, neonatal survival) in some
studies.
Breast feeding
Concentrations of DDT in the milk of women in various
populations have been reported. Values reported from
Guatemala (0.48 to 4.07 ppm total DDT, 1970-1974) and
early values from the USSR (1.22 to 4.88 ppm total
DDT, 1964) were much higher than those of other
countries, and yet there was no indication of illness
among babies fed such milk (Hayes & Laws, 1991).
Enzyme deficiencies
DDT is known to interfere with the metabolism and
function of steroid hormones. One such mechanism is
by the induction of hepatic microsomal enzymes which
results in an increased conversion of oestrogens,
androgens, and glucocorticoids to more polar
metabolites. Increased urinary excretion of the more
polar metabolites is usually compensated for by
increased steroid biosynthesis (Gosselin et al.,
1984).
Individuals on chronic drug therapy with phenobarbitol
and/or phenytoin have increased hepatic microsomal
enzyme activity. Watson et al. (1972) suggest that
this increased activity accelerates the metabolism of
some DDT to DDA by the slow series of
dehydrohalogenation reactions.
9.5 Others
No data available
9.6 Summary
10. MANAGEMENT
10.1 General principles
Management should be directed towards decontamination
of the patient especially where hydrocarbon solvents are
involved. Care must be taken to minimise further problems,
due to aspiration of solvents that may follow spontaneous
emesis or treatment. Other solvent effects should also be
monitored. The patient should be observed carefully
especially for central nervous system effects such as
convulsions. Convulsions, hypoxaemia and resultant acidosis
are the immediate life-threatening emergencies. Diazepam is
the anticonvulsant of choice. Moderate to severely poisoned
patients should have intravenous lines and a cardiac monitor
in place as DDT also sensitises myocardial tissue.
Affected skin must also be decontaminated. Wash the area
well with soap and water.
Oils and fats should not be given. Do not administer
adrenaline, other adrenergic amines or stimulants, because of
the enhanced myocardial sensitivity induced by DDT these may
induce ventricular fibrillation.
10.2 Life supportive procedures and symptomatic treatment
Make a proper assessment of airway, breathing,
circulation and neurological status of the patient.
Control convulsions with appropriate drug regimen.
Monitor blood pressure and ECG.
Control cardiac dysrhythmias with proper drug regimen (proper
means).
Monitor acid-base balance.
Where spontaneous emesis has occurred monitor respiratory
functions and watch for signs of pulmonary aspiration.
10.3 Decontamination
Oral exposure:
Emesis is contra indicated.
Perform gastric lavage for recent large ingestions.
Administer activated charcoal. If an oro- or naso-gastric tube
is in place, administer after lavage through the tube.
If the patient is obtunded, convulsing or comatose, or if the
poison involved may induce these conditions rapidly, insert
an oro- or naso-gastric tube and lavage after endotracheal
intubation.
Inhalation:
Move patient to fresh air and monitor respiratory function.
Eye exposure:
Irrigate exposed eyes with copious amount of water.
Remove contact lenses.
Dermal exposure:
Remove and discard contaminated clothing.
Wash skin with soap and copious amounts of water.
10.4 Enhanced Elimination
Elimination techniques such as dialysis, diuresis and
haemoperfusion have not been shown to be effective due to
extensive tissue binding and large volume of distribution.
10.5 Antidote treatment
10.5.1 Adults
No specific antidote is available.
10.5.2 Children
No specific antidote is available.
10.6 Management discussion
As body stores diminish, the elimination half-life of
DDT for the remaining store increases dramatically. This is
probably due to complex lipoprotein binding, wherein
different bound forms exhibit different association
characteristics. This requires further research and
clarification in order to understand the mechanism
sufficiently to be able to successfully mobilise DDT from
adipose tissue.
11. ILLUSTRATIVE CASES
11.1 Case reports from the literature
Oral (food contamination), male, adults
In three men who ate pancakes made with DDT and who ingested
5 to 6 g each, slight jaundice appeared after 4 to 5 days and
lasted 3 to 4 days (Hayes & Laws, 1991).
Oral, child
A 2-year-old child drank an unknown quantity of flyspray,
which 5% was DDT, but the nature of the other active
ingredients or the solvent was unknown. About one hour after
taking the material, the child became unconscious and had a
generalised, sustained convulsion. Convulsions were present
when the child was hospitalised 2 hours post-ingestion, and
these were controlled by barbiturates and other sedatives.
Convulsions re-occurred on Day 4, and again on Day 21, but
responded to treatment. On day 12, it was noted that the
patient was deaf. Hearing began to improve about Day 24 and
was normal, as were other neurological findings, when the
patient was seen at 2.5 months after the accident (Hayes &
Laws, 1991).
12. ADDITIONAL INFORMATION
12.1 Specific preventive measures
It is essential that persons intending to use DDT be
provided with adequate health precautions and other safety
instructions prior to usage. This information should be
provided by the manufacturer in the form of either an
information leaflet or on a label attached to the DDT
container.
Protective clothing is important. Protective measures may
include wearing a long-sleeved shirt, long trousers or
overalls, and a hat of some sort. Respiratory protection
should be considered. The label should give these
details.
Clothing worn during spraying should be washed daily after
use. Contaminated clothing should be washed separately from
the general wash to avoid cross-contamination. When working
with liquids, there is often a danger of a splash in the
eyes. This may damage the eyes. Simple goggles or a face
shield will protect against this. Eye protection is most
important if wearing contact lenses, because DDT may get in
behind the lenses. They must be removed before the eyes are
washed.
Greater precautions are necessary when mixing the
concentrated material than when spraying. Measurements should
be accurate and spillages should be cleaned up promptly. Mix
the chemical carefully using a stick or paddle. Ensure there
is minimal skin exposure by he use of gloves. If any
concentrate is spilled on the skin, wash it off as soon as
possible.
The hazards of spraying increase dramatically on a windy day,
as there is an increased risk of inhaling spray drift or
contaminating the skin.
Always wash hands before eating, drinking, or smoking. After
spraying, shower and change clothing.
By preference, DDT should be stored in a locked shed, safely
out of reach of children and animals. DDT should also be kept
away from work areas and separate from other stored materials
such as animal foods. Always leave DDT in its original
containers, or if it must be transferred to another container
ensure that this is one not normally used for food or drink.
This secondary container should be well labelled and of a
variety that is not likely to leak.
Empty containers must be disposed of carefully, so as to
ensure that rivers, streams, and other water sources are not
polluted, and that unsuspecting people or animals are not
exposed to residues of concentrate. Crushing or burning,
followed by burial, is generally the best method.
12.2 Other
No data available
13. REFERENCES
ACGIH (1981) Documentation of the Threshold limit value, 4th
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Cincinnati, Ohio.
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Budavari S, O'Neil MJ, Smith A & Heckleman PE (1989) The Merck
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Chris (1985) Chris hazardous chemical data. US Department of
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Dreisbach RH & Robertson WO (1987) Handbook of Poisoning:
Prevention, Diagnosis & Treatment. Appleton & Lange, Connecticut,
99-100 pp.
EPA (1982) Manual of analytical methods for the analysis of
pesticide residues in human and environmental samples.
EPA (1982) Management of Pesticide Poisoning.
Gosselin RE, Smith RP & Hodge HC (1984) Clinical toxicology of
commercial products, Williams & Wilkins, Baltimore 134-136 pp.
Grant WM (ed) (1986) Toxicology of the eye, pp. 305-306, 3rd
edition. Charles C Thomas, Springfield, Illinois, USA.
Hayes WJ (Jr) & Laws ER (Jr) (eds) (1991) Handbook of pesticide
toxicology, Academic Press, Inc. 743-780 pp.
Hsieh HC (1954) DDT intoxication in a family of southern Taiwan.
Arch. Ind. Hyg. Occup. Med. 10:3 44-346.
IARC (1991) IARC Monograph: Occupational Exposures in Insecticide
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IARC (1987) IARC Monographs: An updating of IARC Monographs Vol. 2
to 42 Supplement 7 440 pp.
Jaga K & Brosius D (1999) Pesticide exposure: human cancers on
the horizon. Reviews on Environmental Health. 14(1):39-50
Klaassen CC, Amdur MO & Doull J (eds) (1986) Casarett & Doull's
Toxicology: The basic science of poisons. 3rd ed. Macmillan
Publishing Co., New York, pp. 543-549.
Moffat AC (ed) (1986) Clarke's Isolation and Identification of
Drugs. 2nd Edition The Pharmaceutical Press, London, pp. 143.
OSHA (1989) Department of Labour, Occupational Safety and Health
Administration: 29 CFR Part 1910; Air contaminants; final rule.
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Safety. 592-593 pp Vol. 1, 3rd (revised) edition. International
Labour Office, Geneva.
Reingold I & Lasky II (1947) Acute fatal poisoning following
ingestion of a solution of DDT. Ann. Intern. Med. 26:945-947.
Reynolds JEF (ed) (1989) Martindale: The Extra Pharmacopoeia 29th
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Watson M, Gabica J & Benson WW (1972) Serum organochlorine
pesticides in mentally retarded patients on differing drug
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WHO (1979) DDT and its derivatives. Environmental Health Criteria
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WHO (1989) DDT and its derivatives - environmental aspects.
Environmental Health Criteria 83. WHO, Geneva 12 pp.
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14. AUTHOR(S), REVIEWER(S), DATE (INCLUDING EACH UP-DATE), COMPLETE
ADDRESSES
Author:
Dr Nida Besbelli
Poison Centre
Refik Saydam Hygiene Institute
Cemal Gürsel Cad. No. 18 Sihhiye
06100 Ankara
Turkey
Prepared: February 1990
Reviewers:
Dr Wayne A. Temple
National Toxicology Group
University of Otago Medical School
Dr Nerida A. Smith
Pharmacy School
University of Otago Medical School
P.O. Box 913
Dunedin, New Zealand
Telephone 64 3 4797244
Facsimile 64 3 4770509
Reviewed: August 1992
Updated and Peer Reviewed, Sao Paulo INTOX-11, October 21,1999.
Drs W. Temple, New Zealand- co-ordinator; B. Groszek, Poland; J.
de Kom, Surinam; J.C. Rios Bustamante, Chile; J.C. Piola,
Argentina.