The Dictionary of Substances and Their Effects (DOSE): Volume 03 D

The Dictionary
of Substances
and their Effects
Second Edition

The Dictionary
of Substances
and their Effects
Second Edition
EDITOR
SGangolli, Consultant, MRC ToxicologyUnit,UK
EDITORIALADVISORY BOARD
Dr D Anderson, BIBRA International, UK
Dr J Chadwick,Health and Safety Executive, UK
Professor t Ebdon, Universityof Plymouth, UK
Dr D Gammon, California EPA, USA
Professor L King, University of Surrey, UK
Dr R McClellan,ChemicalIndustry Institute of Toxicalugy,USA
Professor I Rowland, University of Ulster,UK
Dr J Solbe, Unilever,UK
Dr T Sugimura, National CancerCentre,Japan
Professor P van Bladeren, TNO Nutrition and Food Research Institute, The Netherlands
ROYAL SCCIRy OF CHEMISTRY

PRODUCTIONTEAM
Ken Wilkinson (Staff Editor)
Richard Ellis
Sally Faint
JulieHetherington
Alan Skull
The publishers make no representation,expressor implied, with regard to the accuracy of the
information contained in this book and cannot accept any legal responsibility or liability for
any errors or omissionsthat may be made.
Volume 3 ISBN 0-85404-818-9
Seven-volumeset ISBN 0-85404-803-0
A cataloguerecord for this book is availablefrom the British Library.
0The Royal Society of Chemistry 1999
All rights reserved
Apart j?om any fair dealing for the purpose of research or private study, or criticism or review as
permitted under the terms of the UK Copyright, Designs and Patents Act, 1988, this publication may
not be reproduced, stored or transmitted, in anyform or by any means, without the prior permission in
writing of The Royal Society of Chemistry, or in the case of reprographic reproduction only in
accordance with the terms of the licences issued by the Copyright Licensing Agency in the UK, or in
accordance with the terms of the licences issued by the appropriate Reproduction Rights Organisation
outside the UK. Enquiries concerning reproduction outside the terms stated here should be sent to The
Royal Society of Chemistry at the address printed on this page.
Published by The Royal Society of Chemistry, Thomas Graham House, Science Park, Milton
Road, Cambridge,CB4 OWF, UK
Typesetby Land & Unwin (DataSciences)Ltd, Bugbrooke, UK
Printed and bound by Bookcraft (Bath)Ltd., UK

Contents
Volume 1
Foreword
Introduction
Guide to Content
A-B Compounds
Abbreviations
Glossary of Medical and BiologicalTerms
Glossary of Organism Names
Volume 2
Guide to Content
C Compounds
Volume 3
Guide to Content
D Compounds
Volume 4
Guide to Content
E-J Compounds
Volume 5
Guide to Content
K-N Compounds
Volume 6
Guide to Content
0-S Compounds
Volume 7
Guide to Content
T-Z Compounds
Index of ChemicalNames and Synonyms
Index of CASRegistryNumbers
Index of Molecular Formulae
vii
ix
xi
863-865
1-862
867-881
882-889
vii
1-865
vii
1-832
vii
1-892
vii
1-953
vii
1-952
vii
713-914
1-712
915-956
957-998

Guide to Content
The data for each chemical in DOSE are organised as follows:
DOSE No.
Chemical name
Structure/ line formula
Molecular formula
Molecular weight
CAS Registry No.
Synonyms
EINECSNo.
RTECS No.
Uses
Occurrence
Physical properties
Melting point
Boiling point
Flash point
Specificgravity
Partition coefficient
Volatility
Solubility
Occupationalexposure
Limit values
UN number
HAZCHEM code
Conveyanceclassification
Supplp classification
Risk phrases
Safetyphrases
Ecotoxicity
Fish toxicity
Invertebrate toxicity
Toxicity to other species
Bioaccumulation
Environmentalfate
Nitrification inhibition
Carbonaceous inhibition
Anaerobic effects
Degradation studies
Abiotic removal
Adsorption and retention
Mammalian and avian toxicity
Acute data
Sub-acuteand sub-chronic data
Carcinogenicityand chronic effects
Teratogenicity and reproductive effects
Metabolism and toxicokinetics
Irritancy
Sensitisation
Genotoxicity
Other effects
Other adverse effects (human)
Any other adverse effects
LegisIation
0ther comment s
References
These headings only appear in an item when data have been identified for that heading. The
user can, therefore, assume that the absence of a heading means that no relevant data were
retrieved from the sources examined.
vii Guide to Content

Dose No.
Each of the 4123 compounds in DOSE is identified by a unique, sequential alphanumeric
DOSE No. For example,the first compound in DOSE, A-a-C, has DOSE No. A2;the last entry,
zoxazolarnine, has DOSE No. 225.
Chemical name
In general, the chemical name is the common name of the substance, for example
nitrobenzene. If it is not possible to allocate a precise chemical name (i.e.if the substanceis of
unknown or variable composition,or consists of biological materials),a short phrase appears
instead, for examplechlorinated paraffins (C12,60%).
Molecular formula
This is the elemental composition of the compound. The elements appear alphabeticallyfor
inorganic compounds, i.e. Ag2C03, C12Cr, etc, but for organic compounds, carbon and
hydrogen content are shown first followed by the other elements in alphabetical order, i.e.
C6HSBr.
Molecular weight
This is directly calculated from the molecular formula. No molecular weights are given for
polymers.
CAS Registry No.
The CAS Registry No. is a number sequence adopted by the Chemical Abstracts Service
(American Chemical Society, Columbus, Ohio, USA) to uniquely identify specific chemical
substances. The number contains no information relating to the chemical structure of a
substance and is, in effect, a catalogue number relating to one of the millions of unique
chemicalsubstancesrecorded in the CAS Registry.New numbers are assigned sequentiallyto
each new compound identified by Chemical Abstracts Service. This information is also
provided in the full index of CASRegistry Numbers availableat the end of Volume 7.
Synonyms
For common chemicals, several chemical names and numerous trade names may be applied
to describe the chemical in question. Many of these names are identified to aid users on the
range of names which have been used to describeeach substance.
EINECS No.
This number is assigned by the European Commission to each record in the EINECS
(European Inventory of Existing Commercial Chemical Substances)inventory. The numbers
are in the format XXX-XXX-X, for example,202-726-0 for hifrobenzene.
RTECS No.
The RTECS (Registry of Toxic Effects of Chemical Substances)number is a unique identifier
assigned by NIOSH (NationalInstitute of OccupationalSafetyand Health in the US) to every
substance in the RTECS database. The number is in the format of two alphabetic characters
followed by seven numeric characters,for example, DA 6475000 for nitrobenzene.
Guide to Content viii

Uses
Principal uses of the substances are given, with information on other significant uses in
industrial processes.
Occurrence
Natural occurrences, whether in plants, animals or fungi are reported.
Physical properties
Melting/Boiling point
These data are derived from various sources.
Flash point
The flash point is the lowest temperature at which the vapours of a volatile combustible
substance will sustain combustion in air when exposed to a flame. The flash point
information is derived from various sources. Where possible the method of determination of
the flash point is given.
Specific gravity (density)
The specific gravity of each substance has been derived from a variety of sources. Where
possible the data have been standardised.
Partition coefficient
Partition coefficients, important for structure-activity relationship considerations,
particularly in the aquatic environment, are indicated. Ideally the n-octanol/water partition
coefficient is quoted. The major data source for this measurement is:
Sangster,J J. Phys. Chem.Ref. Data 1989,18(3),1111-1229
Where no reference is quoted, it can be assumed that the information was derived from this
source.
VolatiIity
The vapour pressure and vapour density are quoted where available. Where possible, the
data have been standardised.
SolubiIity
Solubility data derived from several sources are quoted for both water and organic solvents
where available.
Occupational exposure
Limit values
This field contains the occupational exposure limit values (or threshold limit values) from
France,Germany,Japan, Sweden, UK and USA.
ix Guide to Content

The airborne limits of permitted concentrations of hazardous chemicals represent conditions
under which it is believed that nearly all workers may be repeatedly exposed day after day
without adverse effect. These limits are subject to periodic revision and vary between
different countries. The term threshold limit relates primarily to the USA, but equivalent terms
are available in most industrialised countries. The data relates to concentrations of substances
expressed in parts per million (ppm)and milligrams per cubic meter (rng m-3).
French exposure limits are published by the French Ministry in Charge of Labour and
presented in the report Valeurs limites d'exposition pvofessionnelleaux agents chimiques en France
(ND 1945-153-93).The values in DOSE have been taken from the 1998 edition. The FR-VLE
values are short-term limits (15minutes), and FR-VME values are long-term limits (8hours).
German data currently include the national MAK values where available. The MAK value
(Maximale Arbeitsplatz-Konzentration) is defined as the maximum permissible
concentration of a chemical compound present in the air within a working area which,
according to current knowledge, does not impair the health of the employee or cause undue
annoyance. Under those conditions, exposure can be repeated and of long duration over a
daily period of eight hours, constituting an average working week of 40 hours. MAK values
are published by the Geschaftsstelle der Deutschen Forschungsgemeinschaft, Bonn, in
"Maximum Concentrations at the Workplace and Biological Tolerance Values for Working
Materials." The values in DOSE have been taken from the 1998edition.
Japanese exposure limits are those recommended by the Japanese Society of Occupational
Health. Unless otherwise indicated, these values are long-term exposure limits (the mean
exposure concentration at or below which adverse health effects caused by the substance do
not appear in most workers, working 8 hours a day, 40 hours a week under a moderate
workload).The values in DOSE were published in 1997.
Swedish data can include short-term exposure limit, a level limit, or a ceiling limit. The
values in DOSE were adopted in 1996.
In the UK occupational limits relating to airborne substances hazardous to health are
published by the Health and Safety Executive annually in Guidance Note EH40. The values
in the DOSE items have been taken from the 1999edition.
There are Maximum Exposure Limits (MEL) in the UK which are subject to regulation and
which should not normally be exceeded. They derive from Regulations, Approved Codes of
Practice, European Community Directives, or from the Health and Safety Commission. In
addition, there are Occupational Exposure Standards (OES) which are considered to
represent good practice and realistic criteria for the control of exposure. In an analogous
fashion to the USA Threshold Limits, there are long-term limits, expressed as time-weighted
average concentrations over an 8-hour working day, designed to protect workers against the
effects of long-term exposure. The short-term exposure limit is for a time-weighted average
of 15minutes. For those substances for which no short-term limit is listed, it is recommended
that a figure of three times the long-term exposure limit averaged over a 15-minute period be
used as a guideline for controlling exposure to short-term excursions.
Guide to Content X

The threshold limit values for the USA have been taken from the Threshold Limit Values and
Biological Exposure Indices, 2999 produced by the American Conference of Governmental
Industrial Hygienists, Cincinnati, USA. The limits relate to Threshold Limit - Time Weighted
Average, Threshold Limit - Short Term Exposure Limit and Threshold Limit - Ceiling Limit. The
Threshold Limit Value -Time Weighted Average (TLV-TWA)allows a time-weighted average
concentrationfor a normal 8-hour working day and a 40-hour working week, to which nearly
all workers may be repeatedly exposed day after day, without adverse effect. The Threshold
Limit Value - Short Term Exposure Limit (TLV-STEL) is defined as a 15-minute, time-
weighted average which should not be exceeded at any time during a work day, even if the
8-hour time-weighted average is within the TLV. It is designed to protect workers from
chemicals which may cause irritancy, chronic or irreversible tissue damage, or narcosis of
sufficient degree to cause the likelihood of accidental injury. Many STELs have been deleted
pending further toxicological assessment. With Threshold Limit - Ceiling Values (TLV-C)the
concentration should not be exceeded during any part of the working day.
UN number
The United Nations Number is a four-figure code used to identify hazardous chemicals and
is used for identification of chemicals transported internationally by road, rail, sea and air. In
the UK this number is also called the “SubstanceIdentificationNumber” or “SI Number”.
HAZCHEM code
The Hazchem Code is used to instruct United Kingdom emergency services on equipment,
evacuation and other methods of dealing with transportation incidents. It is administered by
the Chemical Industries Association.
Conveyanceclassification
The information presented for the transportation of substances dangerous for conveyance by
road is derived from the UK’s Approved Carriage List, Health and Safety Commission, UK.
Supply classification
The information presented for the supply of substances is derived from the UK’s Approved
Supply List: information approved for the classification and labelling of substances and
preparations dangerous for supply [Chemicals (Hazard Information and Packaging)
Regulations 1999(CHIP99)*]Health and Safety Commission,UK.
Risk and safety phrases
Risk and safety phrases used in connection with DOSE items are approved phrases for
describing the risks involved in the use of hazardous chemicals and have validity in the
United Kingdom and throughout the countries of the European Community. The approved
texts have designated R (Risk) and S (Safety)numbers from which it is possible to provide
translations for all approved languages adopted by the European Community. The risk and
safety phrases quoted in DOSE relate to the UK’s Approved Supply List: information
*At the time of going to press the Health and Safety Commission, UK announced that an amendment (Amendment No. 2) to the
CHIP 99 regulations is intended to come into force on 1 January 2000. The supply classificationsand the risk and safety phrases
reported in this edition of DOSE do not include any changes which are proposed in Amendment No. 2 to CHIP 99. These changes are
incorporated in the updates to the electronicversions of DOSE released after 1January2000.
xi Guide to Content

approved for the classification and labelling of substances and preparations dangerous for
supply [Chemicals (Hazard Information and Packaging)Regulations, 1999(CHIP99)]Health
and Safety Commission, UK. The risk and safety phrases should be used to describe the
hazards of chemicals on data sheets for use and supply; for labelling of containers, storage
drums, tanks etc., and for labelling of articles specified as dangerous for conveyanceby road.
(Seealso footnote on page xi.)
Ecotoxicity
Information is presented on the effectsof chemicalson various ecosystems. Results of studies
carried out on aquatic species, primarily fish and invertebrates, but also fresh water and
marine microorganisms and plants are reported. Persistence and potential for accumulation
in the environment and any available information on the harmful effects to non-target
species, i.e. the unintentional exposure of terrestrial and/ or aquatic species to a toxic
substance is given. Ecotoxicology can be defined as that science involved in the study of the
production of harmful effects by substances entering the natural environment, especially
effects on populations, communities and ecosystems; or as the study of the effects of
chemicals on ecosystems and their non-human components. An essential part of the
ecotoxicology is the assessment of movement of potentially toxic imbalance through
environmental compartments and through food webs.
Ecotoxicology, unlike human toxicology, is more concerned with the effects to populations
than to individuals. Human toxicology is based on the extrapolation of data from many
species to one species man, whereas ecotoxicology necessitates the extrapolation from a few
speciesto many, or from limited field data to entire ecosystems.
Ecotoxicologymust not be confused with environmental toxicology which is the direct effects
of environmental chemicals to humans. The term environmental toxicology should only be
applied to the study of direct effects of environmental chemicals on human beings. Although
the main thrust of preventative toxicology is in the area of human health, it is becoming
increasinglyevident that human health is intimately connected with conditions in the natural
environment. Chemicals released into the environment far from human habitation may
become a health hazard for humans through food chain accumulation. Other chemicals may
adversely affect crop growth or kill economically important fish stocks or bird life.
Fish toxicity
LC50 values, with duration of exposure, are quoted for two species of freshwater and one
marine species if available. Any additional information on bioassay type (static or flow
through) and water condition (pH, temperature, hardness or oxygen content) is reported.
LC50 values with duration of exposure, are quoted for molluscs and crustaceans. EC50 values,
i.e. concentrations which will immobilise 50% of an exposed population, are given for
microbes, algae and bacteria. Values which will inhibit microbial or algal growth are
reported. Duration of exposure is given when available.
Guide to Content xii

Toxicityto other species
Toxicity to species other than mammals, birds, invertebrates and fish (e.g. reptiles,
amphibians, plants, seaweeds), is reported here. LD50, LC50 and EC50 values are given with
duration of exposure, concentration and as much supplementary information as possible.
Bioaccurnulation
Bioaccumulation, biomagnification and bioconcentration data are quoted primarily for fish,
invertebrates, bacteria and algae. Bioaccumulation is the progressive increase in the amount
of a chemical in an organism or part of an organism which occurs because the rate of intake
exceeds the organism’s ability to remove the substance from its body. Bioconcentration is a
process leading to a higher concentration of a chemical in an organism than in its
environment. Lastly, biomagnification is a sequence of processes in an ecosystem by which
higher concentrations are attained in organisms at higher trophic levels, i.e. at higher levels in
the food chain.
Environmental Fate
Degradation data are used to assess the persistence of a chemical substance in the
environment, in water, soil and air. If the substance does not persist, information on the
degradation products is also desirable. Intermediates may be either harmless or toxic
substances which will themselves persist. Degradation occursvia two major routes, microbial
degradation utilising microorganisms from a variety of habitats and decomposition by
chemical methods. Microbial degradation is associated with the production of elemental
carbon, nitrogen and sulfur from complex molecules.Standard biodegradation tests estimate
the importance of microbial biodegradation as a persistence factor. Most tests use relatively
dense microbial populations adapted to the compound being studied. Rapid degradation
results in these tests implies that the compound will degrade under most environmental
conditions, although specialised environments where degradation would not occur can exist.
Compounds which are not readily degradable are likely to persist over a wide range of
environmenta1situations.
Chemical degradation processes include photolysis, hydrolysis, oxidation and removal by
reversible/irreversible binding to sediment. Factors which influence degradation rates, such
as duration of exposure, temperature, pH, salinity,concentrations of test substance, microbial
populations, and other nutrients, must alsobe taken into account.
Due care must also be given when metabolism results in the production of substances that
are more toxic than their parents.
The nitrogen cycle is the major biogeochemical process in the production of nitrogen, an
essential element contained in amino acids and proteins. Nitrogen is an essential element in
microorganisms,higher plants and animals. Interference in the production of nitrogen from
more complex molecules can be determined by standard tests using nitrogen-fixing bacteria.
The degree of inhibition can be used to estimate the environmental impact of the test
chemical.
Guide to Content
...XI11

Carbonaceousinhibition
Another major biogeochemical process is the recycling of carbon via the decomposition of
complex organic matter by bacteria and fungi. In nature the process is important in the
cycling of elements and nutrients in ecosystems. The degradation sequence occurs in stages,
cellulose -+ cellobiose -+glucose -+ organic acids and carbon dioxide. Chemical inhibition of
microbial processes at all or any of these stages is reported here.
Anaerobic effects
Anaerobic microbial degradation of organic compounds occurs in the absence of oxygen and
is an important degradation process in both the natural environment and in waste treatment
plants. Data on the effects of chemicalson anaerobic systems are reported here. An important
method uses anaerobic digestion tests which compare the production of methane and carbon
dioxide by anaerobic microbes in a sludge sample with and without added test material.
Methane production is at the end of the food chain process used by a wide range of anaerobic
microorganisms.
Degradation studies
This section focuses on microbial degradation in both soil and water under anaerobic and
aerobic conditions. The half-life of the chemical substance in the environment is reported
with its degradation products where possible, giving an indication of the degree of its
persistence. Water pollution factors: BOD (biochemical/biological oxygen demand), COD
(chemical oxygen demand) and ThOD (theoretical oxygen demand) are stated, where
available. BOD estimates the extent of natural purification which would occur if a substance
were discharged into rivers, lakes or the sea. COD is a quicker chemical method for this
determination which uses potassium dichromate or permanganate to establish the extent of
oxidation likely to occur. ThOD measures the amount of oxygen needed to oxidise
hydrocarbons to carbon dioxide and water. When organic molecules contain other elements
nitrogen, sulfur or phosphorus, the ThOD depends on the final oxidation stage of these
elements.
Abiotic removal
Information on chemical decomposition processes is contained in this section. The energy
from the sun is able to break carbon-carbon, and carbon-hydrogen bonds, cause
photodissociation of nitrogen dioxide to nitric oxide and atomic oxygen and photolytically
produce significant amounts of hydroxyl radicals. Hydrolysis occurs when a substance
present in water is able to react with the hydrogen or hydroxyl ions of the water. Therefore
the extent of photolytic and oxidative reactions occurring in the atmosphere and hydrolysis
in water can be used as a measure of environmental pollution likely to arise from exposure to
a substance. Removal by activated carbon is also reported.
The environmental impact of a chemical substance is determined by its ability to move
through the environment. This movement depends on the affinity of the chemical toward
particulate matter: soil and sediment. Chemicalswhich have a high affinity for adsorption are
less readily transported in the gaseous phase or in solution, and therefore can accumulate in a
particular medium. Chemical substances which are not readily adsorbed are transported
through soil, air and aquatic systems.
Guide to Content xiv

Mammalian and avian toxicity
Studies on mammalian species are carried out to determine the potential toxicity of
substances to humans. Avian species are studied primarily to assess the environmental
impact on the ecosystem,however data from avian studies are also used for assessing human
toxicity.This is specifically applied to pesticides, with neurotoxicologystudies.
Procedures involve undertaking a series of established exposure studies on a particular
substance using specific routes, oral, inhalation, dermal or injection for variable durations.
Exposure durations include acute or single exposure to a given concentration of substance.
Sub-acuteor sub-chronic exposure, i.e. repeat doses over an intermediate time period, up to 4
weeks for sub-acute and 90 day/l3 week (in rodents) or 1 year (in dogs) for sub-chronic
studies. Chronic/long-term studies involve exposure to specific concentrations of chemical
for a duration of 18 month-2 years. A variety of species are used in toxicity testing, most
commonly rodents (rats, mice, hamsters) and rabbits, but tests can also be carried out on
monkeys, domestic animals and birds.
Acute data
Singleexposure studies quoting LD50, LCLO,LDLo, TCLOand TDLOdata.
Sub-acute and sub-chronicdata
Results of repeat doses, intermediate duration studies are quoted. Priority is given to
reporting the adverse effects on the gastro-intestinal, hepatic, circulatory, cardiopulmonary,
immune, renal and central nervous systems.
Carcinogenicity and chronic effects
Information on the carcinogenicity of substances unequivocally proven to cause cancer in
humans and laboratory animals, together with equivocal data from carcinogenicity assays in
laboratory animals are reported. Additionally, treatment-related chronic adverse effects are
reported. Criteria for inclusion required the study to report the species, duration of exposure,
concentration and target organ(s);sex is also given where available.
Teratogenicity and reproductiveeffects
The results of studies carried out in intact animal and in vitro systems to determine the
potential for teratogenic, foetotoxic and reproductive damage are reported here. Criteria for
inclusion required the species, duration of exposure, concentration and details of the effect in
relation to fertility to be stated. Adverse effects reported in this section include sexual organ
dysfunction, developmental changes (to embryos and foetuses), malformations, increases in
spontaneous abortions or stillbirths, impotence, menstrual disorders and neurotoxic effects
on offspring.
Data are quoted on the metabolic fate of the substance in mammals, and includes adsorption,
distribution, storage and excretion.Mechanisms of anabolic or catabolic metabolism, enzyme
activation and half-lives within the body are reported when available. Additionally findings
from in vitro studies are reported.
xv Guide to Content

lrritancy
Chemical substances which cause irritation (itching, inflammation) to skin, eye and mucous
membranes on immediate contact in either humans or experimental animals are reported
here. Exposure can be intentional in human or animal experiments, or unintentional via
exposure at work or accident to humans.
Sensitisation
Sensitisation occurs where an initial accidental or intentional exposure to a large or small
concentration of substance causes no reaction or irritant effects. However, repeat or
prolonged exposure to even minute amounts of a sensitising chemical causes increasingly
acute allergic reactions.
Genotoxicity
Genotoxicity testing is carried out to determine the mutagenic and/or carcinogenicpotential
of a chemical substance. A standard series of tests are carried out under controlled laboratory
conditions on an established set of test organisms. A hierarchical system using bacteria,
yeasts, cultured human and mammalian cells, in vivo cytogenetic tests in mammals and plant
genetics is used to assess the genotoxic potential of the substance under study. Bacteria,
unlike mammals, lack the necessary oxidative enzyme systems for metabolising foreign
compounds to the electrophilicmetabolites capable of reacting with DNA. Therefore,bacteria
are treated with the substance under study in the presence of a post-mitochondial
supernatant (S9) prepared from the livers of mammals (usually rats). This fraction is
supplemented with essential co-factors to form the S9 mix necessary for activation. DOSE
reports published studies: giving the test organisms, whether metabolic activation (S9)was
required, and the result, positive or negative.
Other effects
Adverse effects to humans from single or repeat exposures to a substance are given. The
section includes results of epidemiological studies, smaller less comprehensive studies of
people exposed through their work environment and accidental exposure of a single, few or
many individuals.
Adverse effects to organisms or animals other than man are reported here.
Guide to Content xvi

LegisIation
Any form of legislation, medical (food and drugs) or environmental from European,
American and worldwide sources is reported.
Other comments
All other relevant information, including chemical instability and incompatibility, reviews,
phytotoxicity and toxic effectsassociatedwith impurities, is contained in this section.
References
Contains references to data from above sections.
Indexes
The most convenient means of accessing a chemical in DOSE is via one of the indexes at the
back of Volume 7. DOSE contains three indexes:chemical name and synonyms, CAS Registry
Numbers and molecular formulae.
Index of chemical names and synonyms
Contains the name of the chemical used in DOSE together with a number of synonyms for
that chemical. All names are arranged alphabetically.
Index of CAS Registry Numbers
Contains a list of the CAS Registry Numbers of the chemicals in DOSE in ascending order.
This number is linked to the preferred DOSE name for that chemical and its DOSE number.
Index of molecular formulae
Contains a list of the molecular formulae of the chemicals in DOSE in alphabetical order for
inorganic compounds, i.e. Ag2C03, ClzCr, etc., but for organic compounds, carbon and
hydrogen content are shown first followed by the other elements in alphabetical order, i.e.
C6H5Br. This number is linked to the preferred DOSE name for that chemical and its DOSE
number.
xvii Guideto Content

Note
The Royal Society of Chemistry (RSC)has only assessed published information in compiling
The Dictionary of Substances and their Effects. However, the RSC would welcome any
relevant information on the chemicalsthat is not readily accessible,but in the public domain,
for inclusion when the items in DOSE are updated.
If you have any relevant information, please contact:
Chemical Databank Production
Royal Society of Chemistry
Thomas Graham House
SciencePark
Cambridge CB4 OWF
UK
Telephone: +44 (0)1223420066
Fax: +44 (0)1223423429
Document Delivery
The Library and Information Centre (LIC) of the RSC offers a Document Delivery Servicefor
items in chemistry and related subjects. Contact: Library and Information Centre, the Royal
Societyof Chemistry, Burlington House, Piccadilly, London W1V OBN, UK.
Telephone: +44 (0)207437 8656
Fax: +44 (0)207287 9798
Email: library@rsc.org
Guide to Content xviii

D1
CSH6C1203 Mol. Wt. 221.04 CAS Registry No. 94-75-7
Synonyms (2,4-dichlorophenoxy)aceticacid; 2,4dichlorophenoxyacetic acid
EINECS NO.202-361-1
Uses Systemicherbicide.
RTECS No. AG 6825000
Physical properties
M. Pt. 140.5"C
Partition coefficient log Po, 2.58-2.83(pH 1)(1) Volatility v.p. 0.34mmHg at 160°C
Solubility Water: 311mg 1-1 at pH 1,25"C.Organicsolvents:acetone, diethyl ether, dioxane, ethanol, heptane,
toluene, xylene, dimethyl sulfoxide
B. Pt. 160°Cat 0.4 mmHg Flash point >79.4"C Specific gravity 1.565at 30°C
DE-MAK 1mg m-3 (inhalablefraction of aerosol)
FR-VME 10mg m-3
UK-LTEL 10mg m-3
US-TWA 10mg m-3
Supply classification harmful
Risk phrases Harmful if swallowed-Irritating to eyes, respiratory system and skin (R22,R36/37/38)
Safety phrases Keep out of reach of children (if sold to general public)-Wear suitable protective clothingand
gloves (S2,S36/37)
UK-STEL 20 mg m-3
Ecotoxicity
Fish toxicity
LC50 (96hr) cut-throat trout 0.5-1.2mg 1-1 (2).
LC50 (48hr) rainbow trout, bluegill sunfish 0.9-1.1mg kg-1 (3).
LC50 (96hr) channel catfish, bluegill sunfish 181.2,266.3mg 1-1, respectively(4).
Caused 50% decreasein oxygen evolution and 50% decreasein growth rate in several species of algae at
concentrationsof between 5-9mg 1-1 (5).
In blue-greenalga Anabaenopsis ruciborskii growth and nitrogen fixationstimulated at 10mg 1-1, no growth
inhibition occurred at 100mg 1-1 and completegrowth inhibition occurred at 1000g1-1 (6).
Not toxic to bees (7).
LC50 (96hr) crawfish 750.1 mg 1-1 (4).
Environmentalfate
Very slight inhibition of nitrificationoccurred in soil incubated with 3 ppm (8).
Degradation studies
In soil tl/2 <7days (7).
Twentysix days for ring cleavagein soil suspension (9).
Biodegradable(10).
1

Mineralisationof [14C]2,4-Din soil amended with NH4O3 fertilizerwas markedly reduced and progressively
decreased with N application rate. The addition of Ca(H2P04)2did not generally affectmineralisation. Addition
of both N and P fertilizersto the soil either further reduced or did not affectmineralisation. NH4N03 may
increaseoverall soilmicrobial activity,especially nitrificationactivity,but as a result of cataboliterepression it
may inhibit 2,4-D degradation (11).
Abiotic removal
Rate of adsorption to activated carbon from 22 mg 1-1 solution 60.1% at pH 3.0; 18.8%at pH 7.0; 14.3%at pH 11.0
(12).
Mammalian & avian toxicity
Acute data
LD50 oral Japanese quail 668 mg kg-1(7).
LDN oral wild duck >lo00 mg kg-1(7).
LDw oral pigeon 668mg kg-1(7).
LD50 oral pheasant 472 mg kg-1 (7).
LD50 oral mouse, rat 347,375 mg kg-1, respectively(13J4).
Gavage cfand 9 Fischer 344 rats no-observed-advese-effectlevelfor acute neurotoxicity 15mg kg-1 (15).
LD50 dermal rabbit >1600 mg kg'(7).
LD50 intraperitoneal mouse, rat 375,666mg kg-1, respectively(16).
Sub-acuteand sub-chronicdata
Mice fed 1000mg kg-1 diet for 1month had increased mortality, depressed growth rate, slightly increased liver
weight and slightly cloudy swellingof the liver.Animals fed up to 10,000 mg kg-1 diet refused food with rapid
weight loss. Increasedliver and kidney weights and unstated pathological changes were noted in these organs
(13).
Cr and 9 Fischer 344 rats administered 2,4-Din feed for 52 wk. No-observed-adverse-effectlevel 75 mg kg-1 day-1
in diet (15).
No adverse effectswere reported in a man who took 500mg orally daily for 3 weeks (- 8 mg kg-1 day-1) (17).
Fatalityhas been reported followingingestion of 6 g, yet in another patient 7 g was not fatal. Estimated no effect
level (NOEL)36 mg kg-I(l8).
Long term oral administration and subcutaneous administration did not cause a significantincreasein tumours in
mice. In long term oral administration to rats an increased incidenceof randomly distributed malignant tumours
was observed. Results from a singlecohort study among exposed workers in Sweden was not sufficientto
evaluate carcinogenicityto man. No evaluation of carcinogenicitycould be made from available animal data (19).
In 2 yr dietary trials, rats receiving1250mg kg-1 diet and dogs receiving 500 mg kg-1 diet showed no ill-effects
(7).
Caused embryo-lethal and growth retarding effects,but no teratogenic effect following maximum tolerated dose
to pregnant rats (20).
Foetal anomalies were observed in some strains of mice. Results of various other studies were variable (19).
Metabolismand toxicokinetics
In rats, followingoral administration, eliminated rapidly mainly as the unchanged substance. Singledoses up to
10mg kg-1 eliminated almost completelyafter 24 hr. With higher doses, complete elimination takes longer (7).
Pregnant New Zealand rabbits were administered a single intravenous dose of carbon-14-labelled2,4-D with
unlabelled sodium 2,4-D (1,10or 40 mg kg-1) in saline on days 28-30 of gestation. Blood and tissue was collected
up to 2 h after dosing. Therewas rapid transfer of 2,4-D to the foetalplasma and brain, which peaked after 30 min
for plasma. The maternal kidney and uterus showed the highest extraplasma tissue levels of 2,4-D, and the foetal
brain had the lowest. The foetal tissue content was 120% of that in the dam, but the level in the brain was 7% of
that in foetalplasma compared with 2% of that in maternal plasma (21).
3

Irritancy
Dermal rabbit (24hr)500 mg caused mild irritation and 750 pg instilled into rabbit eye caused severe irritation
(22).
Genotoxicity
Salmonella typhimurium TA1535,TA1537with and without metabolic activationnegative (19).
Bacillus subtilis with and without metabolicactivationrec assay did not indicate DNA damage (23).
Saccharornyces cereuisiae D4, gene conversionincreased by concentrations>400 pg ml-1 (24).
Sacchuromyces cereuisiaeD5, mitotic recombinationincreasedat 300 pg ml-1 (25).
Did not increasedominant lethal mutations followingoral and intraperitoneal administration to mice (26).
No detectableincreasein micronucleiin erythrocytesof mouse bone marrow (27).
No increasein the number of recessivelethalsobserved in d'Drosophila rnelanogaster (28).
Induced chromosomeaberrations,including chromosomebridges, fragments, laggingchromosomes,C-mitosis
and chromatin bodies, in a number of plants (29,30).
Other effects
Chroniceffectsamong workers include fibrillarymovements,skeletalmuscle damage, peripheral neuropathy and
paralysis (19).
Caused moderate to severechloracnein 18%of 73employeesengaged in manufacture of 2,4D and 2,4,5-T. No
systemictoxicity was observed (31).
29% inhibition of testicular DNA synthesis at 200 mg kg-1 in mice (32).
150values (inhibitionof 50% of enzyme activity)for serum enzymes (speciesunspecified) alanine
aminotransferase,alkalinephosphatase, y-glutamyltransferase and lactatedehydrogenase (invitro)are 6.97x 10-2
M, 5.05x 10-2 M, 2.35 x 10-2 M and 1.07x 10-2 M, respectively (33).
Legislation
Limited under EC Directiveon DrinkingWater Quality 80/778/EEC. Pesticides:maximum admissible
concentration0.1 pg 1-1 (34).
UK DOEadvisory value for drinking water 1000pg 1-1 (35).
WHO ClassI1human tolerabledaily intake (TDI)0.3 mg kg-1 EEC maximum residual levelcitrus fruits 2 ppm (8).
Use of 2,4-D, its salts and esters prohibited in India and Colombia. Use restricted in USA and Guatemala (36).
Other comments
Persistence:degraded leachesinto water;some degradation occursin water (35).
Residuesfound on crops, soiland water (19).
In plants and micro-organisms, metabolisminvolveshydroxylation,decarboxylation,cleavageof the acid side
chain and ring opening (7).
Two submersed aquatic macrophytes,Potamogeton pectinatus L. and Myriophyllurnsibiricum Kornarov, were grown
in the presence of 0.01and 0.1mg 2,4-D 1-1. The lower concentrationsof 2,4-D stimulated floweringby
M.sibiricum and tuber production by P,pectinatus. Both specieswere injured by the higher concentration (37).
Reviewintegrating data from worker exposure studies, whole animals,metabolicand laboratory studies with
epidemiologicalfindings to assessthe increasedrisk of developing human cancer to exposure (38).
Saltsare readily absorbed by roots while esters are readily absorbed by foliage.Acts as growth inhibitor (7).
The toxicityof 2,4-D to Rhizobiurn sp. may be mediated by its abilityto combinewith cellular macromolecules,
interferingwith the normal functionsof the cell (39).
Odour threshold detection 3.13mg kg-1 (40).
Toxicity and hazards reviewed (41).
Metabolicpathways reviewed (42).
3

References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
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15.
16.
17.
18.
19.
20.
21.
22.
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24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42.
Verschueren, K. Handbook of Environmental Data on Organic ChemicaZs 2nd ed., 1983,495,Van Nostrand Reinhold,New York,
USA.
The PesticideManual 10th ed., 1994,British Crop ProtectionCouncil,Farnham/The Royal Society of Chemistry, Cambridge,
UK.
Edwards, C.A. Pesticidesin Aquatic Environments 1977,Plenum Press, New York, USA.
Abdelghani,A. A. et a1 Environ. Toxicol.WaterQual. 1997,12(3),237-243.
Ukeles, R. Appl. Microbiol. 1962,10(6),532-537.
Das, B.et a1Arch. Environ. Contam. Toxicol.1977,5,437-445.
TheAgrochemicals Handbook 3rd ed., 1991,The Royal Societyof Chemistry,London, UK.
Richardson,M. L. Nitrificntion Inhibition in the Treatment of Sewage 1985,The Royal Society of Chemistry,London,UK.
Alexander, M. Environmental Toxicologyof Pesticides 1972,AcademicPress, New York, USA.
Ministry of lnternational Tradeand Industry (MITI) 1984,Japan.
Mulroy, P. T. et a1J. Environ. Sci. Health, Part B 1997,B32(3),352-362.
Ward, T.M. et a1Environ. Sci. Toxicol.1970,4(1),64-67.
Rowe, V. K. et a1Am. I. Vet.Res. 1954,15,622-629.
Rocz. Panstw. Zakl. Hig. 1980,31,373.
Mattsson,J. L.et a1Fundam. Appl. Toxicol.1997,40(1),111-119.
Hill, D. et a11.Ind. Hyg. TOX.1947,29,85.
Mitchell, J.W.et all. Anim. Sci. 1946,5,226-232.
Martindale: The Extra Pharmacopoeia31st ed., 1996,TheRoyal PharmaceuticalSociety,London, UK.
IARC Monograph 1977,15,111-138.
Schwetz,B. A. et a1Food Cosmet. Toxicol. 1971,9,801-817.
Sandberg,J. A. et a11.Toxicol. Environ. Health 1996,49(5),497-509.
Lenga, R. E.The Sigma-Aldrich Libraryof ChemicalSafety Data 2nd ed., 1988,1,1152,Sigma-Aldrich,Milwaukee,WI,USA.
Shirasu,Y. Environ. Qual. Saf. 1975,4,226-231.
Siebert,D. et a1Mutat. Res. 1974,22,111-120.
Zetterberg,G. et a1Mutat. Res. 1977,44,3-18.
Epstein,S. S.et a1Toxicol. Appl. Pharmacol. 1972,23,288-325.
Jenssen,D. et a1Chem.-Bid. Interact. 1976,14,291-299.
Vogel, E.et a1Experientia 1974,30,621-623.
Ronchi, V. N.et a1Mutat. Res. 1976,36,67-72.
Mohandas, T. et a1Can.J. Genet. Cytol. 1972,14,773-783.
Poland, A. P. et a1Arch. Environ. Health 1971,22,316-327.
Seiler,J. P. Bull. Environ. Contam. Toxicol. 1979,2189-92.
Sekeroglu,M.R. et a1J. Environ. Sci. Health, Part A: Environ. Sci. Eng. ToxicHazard. Subst. Control 1997,A32(7), 1975-1980.
EC Directive Relating to the Quality of Water Intendedfor Human Consumption 1982,80/778/EEC,Office for Official
Publicationsof the EuropeanCommunities,2rue Mercier, L-2985Luxembourg.
S. I. 1989No. 2147 The WaterSupply (Water Quality)Regulations 1989,HMSO, London, UK.
Environmental Health Criteria29 1984,WHO,Geneva,Switzerland.
Forsyth, D. J. et a1Environ. Polluf.1997,95(2),259-268.
Munroe,I. C.et a1J. Am. Coll. Toxicol.1992,11(5),559-664.
Fabra, A.et a1Bull. Environ. Contam. Toxico1.1997,59(4),645-652.
Sigworth,E. A. J. Am. Water WorksAssoc. 1964,57,1016-1022.
Izmerov, N. F.Scientific Reviews of Soviet Literature on Toxicity and Hazards of Chemicals 1991,70,UNEP/IRPTC, Geneva,
Switzerland.
Roberts, T.R. et a1(Eds.)Metabolic Pathways of Agrochemicals. Part 1: Herbicidesand Plant Growth Regulators 1998,The Royal
Society of Chemistry, Cambridge,UK
4

D2 2,4-D, amine salt
cI<,-,kocH2C02NH2
%I
CsH7C12N03 Mol. Wt. 236.05 CAS Registry No. 1982-42-9;2307-55-3
Synonyms 2,4-dichlorophenoxyacetic acid, amine salt; (2,4-dichlorophenoxy)aceticacid, amino salt;
2-(2,4-dichlorophenoxy)acetamide; 2,4-D-ammoniumsalt
EINECS NO.217-842-1
RTECS No. AB 6945000;AG 7075000
Physical properties
M. Pt. 179-180°C
DE-MAK 1mg m-3 (total dust)
Risk phrases Harmful by inhalation, in contact with skin and if swallowed (R20/21/22)
Safety phrases Keep out of reach of children (if sold to general public) -Keep away from food, drink and animal
feeding stuffs (S2,S13)
Environmentalfate
Persists in soil for -1 month (1).
Acute data
LD50oral rat 1200mg kg-1 (2).
LD50 oral mouse 300 mg kg-1 (2).
Following oral administration to rats, rapidly absorbed giving peak plasma concentrations after 4-7 hr (1).
Legis1ation
Limited under EC Directiveon Drinking Water Quality 80/778/EEC. Pesticides:maximum admissible
concentration 0.1 pg 1-1 (3).
Included in Schedule 6 (Releaseinto Land: Prescribed Substances)Statutory Instrument No. 472,1991 (4).
Other comments
Residual of 1pg 1-1 detected in treated water supplies (5).
Approved for use on river banks (5).
References
1.
2.
Criteria (DoseEfect Re1afionship)forOrganochlorine Pesticides, 1981,223-239,C.E.C.
Izmerov,N. F. et a1ToxicornetricParametersof Industrial ToxicChemicals Under Single Exposure 1982,47, CIP, Moscow,USSR
5

3.
4.
5.
EC Directive Relating to the Qualifyof Water Intendedfor Human Consumption 1982,80/778/EEC, Officefor Official
Publications of the European Communities, 2 rue Mercier, L-2985Luxembourg,
S. 1. 1991No. 472 The Environmental Protection (PrescribedProcesses and Substances)Regulations 1991,HMSO,London, UK.
Guidelinesfor the Useof Herbicideson Weedsin or Near Water Courses and Lakes 1988, MAFF, London, UK
D3 2,4-D, butoxyethanol ester
C14H18C1204 Mol. Wt. 321.20 CAS Registry No. 1929-73-3
Synonyms 2,4-dichlorophenoxyaceticacid, butoxyethanol ester; (2,4-dichlorophenoxy)aceticacid,
butoxyethanol ester; 2,4-D(BEE); (2,4-dichlorophenoxy)aceticacid, 2-butoxyethylester; 2,4-D-butotyl
EINECSNO.217-680-1
RTECS No.AG 7700000
Physical properties
B. Pt. 156-162°Cat 1mmHg
Volatility v.p. 1.70 x 10-3 mmHg at 25OC
Solubility Water:12mg 1-1. Organicsolvents:oils
Specific gravity 1.225at 20°C with respect to water at 20°C
DE-MAK 1mg m-3 (totaldust)
Risk phrases Harmful by inhalation, in contactwith skin and if swallowed (R20/21/22)
feedingstuffs (S2,S13)
Ecotoxicity
Fish toxicity
LC50 fathead minnow (96hr) 56 mg 1-1; 1500pglethal to eggs in 48 hr exposure; 10months no effect level 300 pg
LC50 (96hr) Gammarus Iacustris 440 pg1-1 (2).
LC50 (96hr) Gamrnarusfusciutus 6 mg 1-1 (3).
LC50 (48hr) Daphnia magna 6 mg 1-1 (3).
LC50 (48hr) Cypridopsis vidua 2 mg 1-1 (3).
LC9 (48hr)Asellus brevicaudus 3 mg 1-1 (3).
LC50 (48hr) Palaernoneteskudiakensis 1mg 1-1 (3).
LCm (96hr) Pteronarcys californica 1mg 1-1 (4).
1-1 (1).
6

Mammalian& aviantoxicity
Acute data
LD50 oral Cr rat 940 mg kg-1(5).
LD50 dermal rabbit 4000 mg kg’(5).
LC508day dietary trial, bobwhite quail and Japanesequail >5000mg kg-1 (6).
LC508day dietary trial, ring-neckedpheasant and mallard >5000mg kg-1 (6).
TDL, oral rat (6-15day pregnant) 1500mg kgI(7).
Caused embryo-lethaland growth retarding effects, but no teratogeniceffectfollowingmaximum tolerated dose
to pregnant rats (8).
Irritancy
Acute eye and skin irritation reported in agricultural workers (9).
Legislation
concentration0.1 kg 1-1 (10).
Included in Schedule6 (Releaseinto Land:Prescribed Substances)Statutory Instrument No. 472,1991(11).
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
Mount, D. I. et a1Trans. Am. Fish. SOC.1967,96(2),185-193.
Sanders,H. 0.Toxicity ofPesticides to the Crustacean,Gammrus lacustris 1969,Bureau Sport Fisheries and Wildlife Tech.
Paper 25, Govt. Print. Off., Washington, DC,USA.
Sanders,H. 0.I. Water Pollut. Control Fed. 1970,42(8,Part l),1544-1550.
Sanders,H. 0.et a1Limnol. Oceanogr. 1968,13(1),112-117.
Matm’al Safety Manual Sheet 1978,Dow Chemical.
Hill, E. F. et a1Lethal Dietary Toxicities of Environmental Pollutants to Birds 1975,15, U.S.Fish and WildlifeService, Report
Wildlife No. 191,Washington, DC, USA.
Toxicol.Appl. Phurmacol. 1972,22,14.
Schwertz, B. A. et a1Food Cosmet. Toxicol.1971,9,801-817.
Environmental Health Criteria 1984,95,World HealthOrganisation,Geneva,Switzerland.
EC Directive Relating to the Quality of WaterIntendedfor Human Consumption 1982,80/778/EEC, Office for Official
Publicationsof the EuropeanCommunities, 2 rue Mercier,L-2985 Luxembourg.
S.1.1991No.472 The Environmental Protection (Prescribed Processes and Substances)Regulations 1991,HMSO,London,UK
D4 2,4-D, butyl ester
C,~,=,~OCH~COI(CH~~~CH~
CI
C12H14C1203 Mol. Wt. 277.15 CAS RegistryNo. 94-80-4
Synonyms 2,4-dichlorophenoxyaceticacid,butyl ester; (2,4-dichlorophenoxy)aceticacid,butyl ester; butyl
dichlorophenoxyacetate
EINECS NO.202-364-8
RTECSNo.AG 8050000
7

Physical properties
M. Pt. 9°C
Solubility Water: 1mg 1-1 at 25°C.Organicsolvents:ethanol
B. Pt. 146-147°C Flash point >79.4"C Volatility v.p. 3.9 x 10-4mm Hg at 25°C
Supplyclassificationharmful
Risk phrasesHarmful by inhalation, in contactwith skin and if swallowed (R20/21/22)
Safetyphrases Keep out of reach of children (if sold to general public)-Keep away from food, drink and animal
feeding stuffs (S2, S13)
Acute data
LD50 oral rat, mouse 380-920mg kg-1(1).
No adverse effectsnoted when 5ml of 3.13%solution administered 5 x wk-1 for 3 wk to intact and abraded rabbit
skin (2).
No increasein incidenceof tumours observed in mice treated with single injection of 21.5mg kgl(3).
No evaluation of carcinogenicitycould be made from subcutaneous and oral administration tests in mice (4).
Oral administration produced increased frequencyof foetal anomalies among BL6, AKR and/or C3H strains of
mice, but not among B6AK and A/Ha strains (4).
Genotoxicity
Not mutagenic in bacterial test systems (5).
LegisIation
Limited under the EC Directive on Drinking Water Quality 80/778/EEC. Pesticides:maximum admissible
Included in Schedule6 (Releaseinto Land: PrescribedSubstances)Statutory Instrument No. 472,1991 (7).
References
1.
2.
3. IARC Monograph 1977,15,111-138.
4.
5.
6.
7.
Konstantimova,T. K. Proceedings Conf. Problems Hygiene Toxicol. of Pesticides 1967,177-179, USSR.
Kay, J. H. et a1Arch. Environ. Health 1965,11,448-651.
Evaluation of CarcinogenicTeratogenicand Mutagenic Activities of Selected Pesticidesand Industrial Chemicals 1968,2, Natl.Tech.
Inf.Service,US DepartmentCommerce,Washington,DC, USA.
IARC Monograph 1987, Suppl. 6,233.
EC Directive Relating to the Quality of Water Intendedfor Human Consumption 1982,80/778/EEC, Officefor Official
Publicationsof the EuropeanCommunities,2 rue Mercier,L-2985Luxembourg.
S. I. 2992 No. 472 The Environmental Protection (PrescribedProcesses and Substances) Regulations 1991, HMSO, London,UK
8

~5 2,4-D, sec-butyl ester
C12H14C1203 Mol. Wt. 277.15 CAS Registry No.94-79-1
Synonyms 2,4-dichlorophenoxyaceticacid, sec-butylester; (2,4-dichlorophenoxy)aceticacid, sec-butylester
OccupationaI exposure
Safety phrases Keep out of reach of children (if sold to generalpublic)-Keep away from food, drink and animal
Acute data
LD50 oral rat, mouse 620-713mg kg-1 (1).
LD50 oral chicken 2000 mg kg-1(1).
Legislation
concentration0.1 pg1-1 (2).
Included in Schedule6 (Releaseinto Land:Prescribed Substances)Statutory Instrument No. 472,1991 (3).
References
1.
2.
3.
Rowe, V. K. et a1Am. J. Vet.Res. 1954,15,622-629.
EC Directive Relating to the Quality of WaterZntendedfor Human Consumption 1982,80/778/EEC, Officefor Official
Publicationsof the EuropeanCommunities,2 rue Mercier, L-2985 Luxembourg.
S. 1. 1991 No. 472 The Environmental Protection (Prescribed Processes and Substances) Regulations 1991,HMSO,London, UK
9

D6 2,4-D, 4-chloro-2-butenyl ester
C12HllC1303 Mol. Wt. 309.58 CAS RegistryNo. 2971-38-2
Synonyms 2,4-dichlorophenoxyaceticacid, 4-chloro-2-butenylester; (2,4-dichlorophenoxy)aceticacid,
Pchloro-Zbutenyl ester
Physical properties
Solubility Organicsolvents:oils
Occupationai exposure
DE-MAK 1 mg m-3 (totaldust)
Supply classificationharmful
Risk phrasesHarmful by inhalation, in contactwith skinand if swallowed (R20/21/22)
Safety phrasesKeep out of reach of children (if sold to general public) -Keep away from food, drink and animal
feeding stuffs(S2,S13)
Acute data
LDN oral rat, mouse 490-550mg kg-1 (1).
LDa (2hr) inhalation mouse 2190 mg m-3 (1).
Legis1ation
Included in Schedule6 (Releaseinto Land: Prescribed Substances)Statutory Instrument No. 472,1991(3).
References
1.
2.
3.
Imerov, N. F. et a1Toxicometric Parameters oflndustrial ToxicChemicals Under Single Exposure 1982,35,CIP, Moscow, USSR.
EC Directive Relating to the Quality of Water Intendedfor Human Consumption 1982,80/778/EEC, Officefor Official
Publicationsof the European Communities, 2 rue Mercier, L-2985Luxembourg.
S. I. 1991 No.472 The Environmental Protection (Prescribed Processes and Substances) Regulations 1991,HMSO,London,UK
10

~7 2,4-D, diethylamine salt
C12H17C12N03 Mol. Wt. 294.18 CAS RegistryNo. 20940-37-8
Synonyms 2,4-dichlorophenoxyacetic acid, diethylamine salt; (2,4-dichlorophenoxy)aceticacid, diethylamine
salt; 2,4-DE; (2,4-dichlorophenoxy)aceticacid, N-ethylethonamineester; 2,4-D, diethylammonium salt
EINECS NO.244-120-3
RiskphrasesHarmful by inhalation,in contactwith skin and if swallowed (R20/21/22)
SafetyphrasesKeep out of reach of children (ifsold to generalpublic)-Keep away from food, drink and animal
feedingstuffs(S2,S13)
Ecotoxicity
Invertebratetoxicity
LCw (48hr) Daphnia magnu 4 mg 1-1 (1).
LC9 (48hr) Cypridopsis vidua 8mg 1-1. No effect level (48hr) Gammrusfasciafus,Asellus cermicaudus,Orconecfes
nais and Palaemonetes kadiakensis 100mg 1-1 (1).
Acute data
LD50oral rat 405 mg kg-1 (2).
Legislation
Included in Schedule6 (Releaseinto Land:PrescribedSubstances)Statutory Instrument No. 472,1991 (4).
References
1.
2.
3.
4.
Sanders,H. 0.1.WaterPollut. Control Fed. 1970,42(8,part l),1544-1550.
Gig. Tr.Prof. Zabol. 1973,17(3),35.
Publicationsof the EuropeanCommunities, 2 rue Mercier,L-2985Luxembourg.
S.I. 1991No. 472 The Environmental Protection (Prescribed Processes and Substances) Regulations 1991,HMSO, London,UK
11

D8 2,4-D, dimethylamine salt
Cl---(=>OCH2CO2H / .HN(CH&

CI
C10H13C12N03 Mol. Wt. 266.12 CAS Registry No.2008-39-1
Synonyms 2,4-dichlorophenoxyaceticacid, dimethylamine salt; (2,4-dichlorophenoxy)aceticacid,
dimethylaminesalt; 2,4-D-DMA; 2,4-D, dimethylammonium salt
EINECS NO.217-915-8
Physical properties
M. Pt. 85-87°C
Solubility Water:3kg 1-1 at 20°C.Organicsolvents:acetone, ethanol, methanol, isopropanol
Flash point >88"C Volatility v.p. 8x 1o-SmmHg at 25°C
Safety phrases Keep out of reach of children (if sold to general public)-Keep away from food, drink and animal
feeding stuffs (S2, S13)
Ecotoxicity
Fish toxicity
Lowest observed avoidanceconcentration,rainbow trout 1.0mg 1-1 (1).
LC50 (48hr) rainbow trout 258 mg 1-1 (2).
LC50 (96hr) rainbow trout 100mg 1-1 (3).
LC50 (48hr) bluegillsunfish 382 mg 1-1 (2).
LC50 (48hr) fathead minnow 184mg 1-1 (2).
Lowest observed avoidance concentration,mayfly nymphs >10 mg 1-1 (1).
Environmentalfate
Degradation studies
The effect of pH, organics, metal reductants, fixed aerobic conditions versus cycling through aerobicand
anaerobicconditions on the degradation of 2,4-D dimethylamine salt was studied in model soilbeds (containing
loamy sand soil).Applied liming was effectivein reducing 2,4-D concentrationsin soils.Added organicmatter
decreased 2,4-D concentrationand zinc had little effect on aerobic degradation of 2,4D. 2,4-D degradation was
slower under anaerobicconditions;however, cycling through aerobicand anaerobicconditions promoted
degradation of 2,4-D. Upward movement of 2,4-D was observed (4).
Mammalian 8t avian toxicity
Acute data
LD50 oral mouse, rabbit,rat 338-960mg kg-1 (5).
LD50 oral rat, mouse 300-515mg kg-1 (6).
LD50 dermal rabbit 2115 mg kg-1 (6).
12

Sub-acute and sub-chronic data
No adverse effectsnoted when 15ml of 3.13% solution administered 5 x wkly for 3wk to intact and abraded
rabbit skin (7).
LC50 8day dietary trial, bobwhite quail,Japanese quail >5,000 mg kg-1 (8).
LCN 8 day dietary trial, ring-necked pheasant and mallard duck >5,000 mg kg-1 (8).
Oral administration of 10-100mg kg-1 for 60 days to cats decreased the number of B- and T-lymphocytesand
neutrophils in blood. In sheep, 100-200kgkg-1 for 20 days decreasedcellular and humoral immunity (5).
LDL, oral rat (6-15days gestation)3 gkg-1 (9).
LegisIation
Limited under EC Directive on DrinkingWater Quality 80/778/EEC. Pesticides:maximum admissible
Included in Schedule6 (Releaseinto Land: Prescribed Substances)Statutory Instrument No. 472,1991 (11).
WHO Class II; EPA ToxicityClass I (eyes),Class I11 (oral)(12).
Other comments
Experimentalconcentrationsof 0.5mg 1-1can significantlytaint the flesh of rainbow trouts to make them
unpalatable (13).
Regionaldermal deposition on farmers when handling, mixing and spraying the herbicide was determined
following30 separate exposures. Threedistinct levelsof dermal deposits could be clearly ascertained.These
densities were quite uniform and indicated a greatly reduced but nevertheless general permeation of the
herbicide through 2 layers of protective clothing.Somewhathigher median deposit densities were found on
exposedbody regionsless likely to be contaminated during the mixing process, such as the head, neck and
outside elbow regions.The highest median deposit densities occurred on regions of the body most likely to be
contaminated during the mixing process, i.e. the wrist and chest regions. The overall body deposits, minus the
hand regions, were 10-20%of the total body deposits and thus, when protective garments equivalent to those
used in this study are worn, hand protectionmust remain a major concern when spraying herbicides with
ground-rigs (14).
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
Folmer, F. C. Bull. Environ. Contam. Toxicol.1978,19(3),312-318.
Alexander, H. C. Bull. Environ. Contam. Toxicol.1985,35,314-321.
ThePesticideManual 11thed., 1997,BritishCrop Protection Council, Farnham, UK.
Hodapp, D. M.et a1Bull. Environ. Contam. Toxicol.1989,43(1), 36-44.
Loktionov,V.N. et al Veterinariya(Moscow) 1987,7,70-71 (Russ.) (Chem.Abstr. 107,192594~).
Farm ChemicalHandbook 1989,C95, Meister, Willoughby, OH, USA.
Hill, E. F. et a1Lethal Dietary ToxicitiesofEnuironmenta1Pollutantsto Birds 1975,15,U.S. Fish and WildlifeService,Report
Wildlife No. 191,Washington, DC,USA.
Toxicol.Appl. Pharmacol.1972,22,14.
EC DirectiveRelating to the Quality of WaterIntendedfor Human Consumption1982,80/778/EEC, Officefor Official
Publications of the European Communities, 2 rue Mercier, L-2985Luxembourg.
S. I. 1991 No. 472 The Environmental Protection (PrescribedProcessesand Substances)Regulations 1991,HMSO,London,UK.
ThePesticide Manual 9th ed., 1991,British Crop Protection Council, Farnham, UK.
Leroy, C. F. Bull. Environ.Contam.Toxicol.1980,24,217-224.
Grover, R. et a1ASTM Spec. Tech.Publ. 1988,989
13

2,4-D, isobutyl ester
C12H14C1203
Synonyms 2,
Mol.Wt. 277.15 CAS RegistryNo. 1713-15-1
.dichlorophenoxyaceticacid, isobutyl ester; (2,4-dichloro~,.enoxy)aceticacid, isobutyl ester;
(2,4-dichlorophenoxy)aceticacid, 2-methylpropylester; 2,4-D-2-methylpropylester
EINECS NO.216-992-5 RTECS No. AG 8550000
Physical properties
B.Pt. 133-134°C
Supplyclassificationharmful
Safetyphrases Keep out of reach of children (if sold to general public)-Keep away from food, drink and animal
Acute data
LD50 oral rat, rabbit 300-500mg kg-* (1,2).
Legislation
Limited under EC Directive on DrinkingWater Quality 80/778/EEC. Pesticidesmaximum permissible
References
1.
2.
3.
NTlS Report PB 85-143-766,Natl. Tech. Inf.Ser., Springfield,VA, USA.
Marhold,J. V. Prehled Prumyslove Toxikof.Org. Latky 1986,550,Prague,Czechoslovakia.
Publicationsof the EuropeanCommunities,2rue Mercier, L-2985 Luxembourg
14

DIO 2,4-D, isooctyl ester

CI
Synonyms 2,4-dichlorophenoxyaceticacid, isooctylester; (2,4-dichlorophenoxy)aceticacid, isooctyl ester;
2,4-D(IOE); 2,4-dichlorophenoxyaceticacid, 6-methylheptaneester; isooctyl2,4-dichlorophenoxyacetate
EINECS NO.246-704-3
Physical properties
M. Pt. 12°C
Volatility v.p. 2 x 10-6mmHg at 25°C
Solubility Water: 10mg 1-1. Organic solvents:acetone, dimethyl sulfoxide,ethanol, oils
B. Pt. 317°C Flash point 51.7"C Specificgravity 1.152at 20°C with respect to water at 4°C
Risk phrases Harmful by inhalation,in contactwith skin and if swallowed (R20/21/22)
Ecotoxicity
Fish toxicity
LC50 (48hr) bluegill sunfish 8.8-60mg 1-1 (1).
Not toxic to cutthroat trout and lake trout below 60 mg 1-1 (2).
LCm (96hr) Gammarus lacustris2.4 mg 1-1 (3).
Acute data
LD50oral rat, rabbit 300 mg kg-1 (4).
LD50percutaneous rabbit >4000mg kg-1 (5).
No adverse effectsnoted when 15ml of 3.13% solution administered 5 x wkly for 3 wk to intact and abraded
rabbit skin (6).
5/17 9 mice treated with 21.5 mg kg-1 developed reticulum-cell sarcomas(7).
No evaluation of carcinogenicitycould be made from oral administration tests in mice (8).
Oral administration produced increasedfrequency of foetal anomalies among BL6,AKR and/or C3H strains of
15

Irritancy
Skin and eye irritant (9).
Genotoxicity
Salmonella typhimuriumTA100,TA1357, TA98 with and without metabolicactivation negative (10).
Legislation
Limited under EC Directive on Drinking Water Quality 80/778/EEC. Pesticides:maximum admissible
concentration0.1pg 1-1 (11).
Included in Schedule6 (Releaseinto Land: PrescribedSubstances)Statutory Instrument No. 472,1991 (12).
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
Hughes, J. S.et a1Weeds 1963,11,50-53.
Woodward, D. E et a1Tech.Pap. U. S. Fish Wildl. Sew. 1978,97,1-6.
Sanders, H.O. Toxicity of Pesticidesto the Crustacean, Gammarus lacustris 1969,Bureau of Sport Fisheries and Wildlife Tech.
Paper 25, Govt. Print. Off., Washington,DC, USA.
Farm ChemicalsHandbook Meister, 1989,C309,Meister, Willoughby, OH, USA.
Verschueren,K. Handbookof Environmental Data on Organic Chemicals2nd ed., 1983,499-500,Van Nostrand Remhold,New
York, USA.
Evaluation of Carcinogenic,Teratogenic and Mutagenic Activities of Selected Pesticidesand Industrial Chemicals 1968,2, Natl. Tech.
Inf.Service,US Dept. of Commerce,Washington,DC,USA.
lARC Monograph 1977,15,111-138.
Keith, L. H. et a1Compendiumof Safety Data Sheetsfor Research and Industrial Chemicals 1987,52268, VCH, New York, USA.
IARC Monograph 1987,Suppl. 6,233.
EC Directive Relating to the Quality of Water Intendedfor Human Consumption 1982,80/778/EEC, Office for Official
Publicationsof the European Communities, 2 rue Mercier, L-2985Luxembourg.
S.I. 1991No. 472 The EnvironmenfalProtection(Prescribed Processes and Substances) Regulations 1991,HMSO, London, UK
D11 2,4-D, isopropyl ester
CllH12C1203 Mol. Wt. 263.12 CAS Registry No. 94-11-1
Synonyms 2,4-dichlorophenoxyaceticacid, isopropyl ester; (2,4-dichlorophenoxy)aceticacid, isopropyl ester;
(2,4-dichlorophenoxy)aceticacid, 1-methylethylester
EINECS NO.202-305-6
Physical properties
M. Pt. Crystallisesin 2 forms:5-10°Cand 20-25°C
25°C with respect to water at 25°C
Solubility Water:46 mg 1-1. Organicsolvents:alcohols,most oils
B. Pt. 130°Cat 1mmHg
Volatility v.p. 1.05x 10-2 mmHg at 25°C
Specific gravity 1.255-1.270at
16

Ecotoxicity
Fish toxicity
LC50 (48hr) bluegill sunfish 0.8 mg 1-1 (1).
Acute data
LD50oral rat, mouse 375-540mg kg-1 (2,3).
LD50 oral chicks 1420mg kg-1 (2).
No increasein incidenceof tumours observed in mice treated with singleinjection of 21.5 mg kg-1 (4).
No evaluation of carcinogenicitycould be made from subcutaneous and oral administration tests in mice (5).
Oral administration produced increased frequency of foetal anomaliesamong BL6, AKR and/or C3H strains of
Irritancy
Irritating to skin and eyes (6).
Legis1ation
concentration0.1pg1-1 (7).
Other comments
Hazardous properties reviewed (9).
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
Phenoxy Herbicides -Their efects on Environmental Quality 1978,1800-181, Natl. Res. Council, Canada, NRCC No. 16075.
Rowe, V. K. et a1Am. 1.Vet.Res. 1954,15,622-629.
Farm ChemicalsHandbook 1989,C166,Meister, Willoughby, OH,USA.
Evaluation of Carcinogenic,Teratogenicand Mutagenic Activities of Selected Pesticides and lndustrial Chemicals 1968,2, Natl. Tech.
Inf. Service,US Dept. Commerce, Washington, DC, USA.
IARC Monograph 1977,15,622-629.
Hazardous Chemical Data 1984-85,2,US Coast Guard, Dept. Transportation, Washington, DC, USA.
EC Directive Relating to the Quality of Water lntendedfor Human Consumption 1982,80/778/EEC, Officefor Official
Publications of the European Communities, 2 rue Mercier,L-2985Luxembourg.
S. I. 1991No. 472 The Environmental Protection (Prescribed Processes and Substances) Regulations 1991,HMSO, London, UK.
Dangerous Prop. Ind. Muter. Rep. 1987,7(5),56-62
17

~ 1 2 2,4-D, lithium salt
CsHSClzLi03 Mol. Wt. 226.97 CAS Registry No.3766-27-6
Synonyms 2,4-dichlorophenoxyaceticacid, lithium salt; (2,4-dichlorophenoxy)aceticacid, lithium salt
RTECS No.AG 8800000
feeding stuffs (S2,513)
Acute data
LD50 oral rat 850mg kg-1 (1).
Legis1ation
Included in Schedule 6 (Releaseinto Land: Prescribed Substances)Statutory Instrument No. 472,1991 (3).
References
1.
2.
3.
Farm ChemicalsHandbook 1989,C177,MeisterPublishing Co.,Willoughby, OH, USA.
EC Directive Relating to the Quality of WaterIntendedfor Human Consumption 1982,80/778/EEC,OfficeforOfficial
Publicationsof the European Communities, 2 rue Mercier, L-2985 Luxembourg.
S. 1. 2992 No. 472 The Environmental Protection (Prescribed Processes and Substances) Regulations 1991,HMSO, London, UK
18

D I ~ 2,4-D, methyl ester

CI
Synonyms 2,4-dichlorophenoxyaceticacid, methyl ester; (2,4-dichlorophenoxy)aceticacid, methyl ester
EINECS NO.217-670-7
Physical properties
B.Pt. 119°Cat 11mmHg
Risk phrases Harmful by inhalation,in contact with skin and if swallowed (R20/21/22)
Legislation
References
1.
2.
EC Directive Relating to the Quality of Water Intendedfor Human Consumption 1982,80/778/EEC,Office for Official
Publications of the European Communities,2 rue Mercier,L-2985Luxembourg.
S. I. 2991No. 472 The Environmental Protection (PrescribedProcesses and Substances) Regulafions1991,HMSO, London, UK
D I ~ 2,4-D, octyl ester

CI
Synonyms 2,4-dichlorophenoxyaceticacid, octyl ester; (2,4-dichlorophenoxy)aceticacid, octyl ester
EINECS NO.217-674-9
19

Physical properties
B. Pt. 173-174°Cat 1mmHg
Acute data
LD50 oral mouse 1200mg k g l (1).
LDL, dermal rabbit 2 g kg-1 (1).
Legislation
Limited under EC Directive on Drinking Water Quality 80/778/EEC. Pesticides: maximum admissible
concentration 0.1 pg 1-1 (2).
References
1.
2.
3.
Izmerov, N. F. et a1 ToxicornefricParameters oflndustrial Toxic ChemicalsUnder Single Exposure 1982,95, CIP, Moscow, USSR.
EC DirectiveRelating to the Qualifyof WaterIntended for Human Consumption 1982,80/778/EEC, Office for Official
S. 1. 1991No. 472 The Environmental Protection (PrescribedProcesses and Substances) Regulations 1991,HMSO, London, UK
~ ~ ~ _ _ _
DIS 2,4-D, propylene glycol butyl ether ester
Cl-$ /~~CHZCO~CHCH~O(CH,),CH,I
CI CH3
Synonyms (2,4-dichlorophenoxy)aceticacid, monoester with 1,2-propanediol,butyl ether ester;
2,4-dichlorophenoxyaceticacid, propylene glycolbutyl ether ester;
glycol butyl ether ester; 2,4-D PGBE
(2,4-dichlorophenoxy)aceticacid, propylene
Physical properties
Volatility v.p. 2.4 mmHg at 25°C
Solubility Organicsolvents:oils
20

OccupationaI exposure
Risk phrasesHarmful by inhalation,in contact with skin and if swallowed (R20/21/22)
SafetyphrasesKeep out of reach of children (if sold to generalpublic)-Keep away from food,drink and animal
Acute data
LD50 oral rat 500 mg kg-1 (1).
Teratogenicityand reproductiveeffects
Caused embryo-lethaland growth retarding effects, but no teratogeniceffect followingmaximum tolerated dose
to pregnant rat (2).
Legislation
Limited'under EC Directiveon DrinkingWater Quality 80/778/EEC. Pesticides: maximum admissible
References
1.
2.
3.
4.
NTIS Report PB 85-143-766, Natl.Tech.Inf.Ser.,Springfield,VA, USA.
Schwertz,8.A. et a1Food Cosmef.ToxicoI. 1971,9,801-817.
EC DirectiveRelating to the Quality of Water Intendedfor Human Consumption 1982,80/778/EEC,Officefor Official
Publicationsof the EuropeanCommunities,2 rue Mercier,L-2985Luxembourg.
S. 1.1991 No. 472 The Environmental Protection (PrescribedProcesses and Substances) Regulations 1991, HMSO,London, UK
CBH5C1203Na Mol. Wt. 243.02 CAS RegistryNo. 2702-72-9
Synonyms 2,4-dichlorophenoxyaceticacid, sodium salt; (2,4-dichlorophenoxy)aceticacid, sodium salt;
2,4-DNa
EINECS NO.220-290-4
Physical properties
Solubility Water:18 g 1-1 at 20°C
21

Safetyphrases Keep out of reach of children (if sold to general public) -Keep away from food, drink and animal
Acute data
LD50 oral wild duck ~ 2 0 2 5mg kg-1(1).
LDm oral mouse, rat, rabbit, guinea pig 375,550,800,1000mg kg-1, respectively (2).
LD50 intraperitoneal mouse, rat 375,424mg kg-1, respectively(1,3).
LD50 intravenous rabbit 400 mg kg-1(4).
Genotoxicity
Induced chromosomalaberrations in the meristems of Allium cepa and barley (5).
Legislation
Limited under EC Directive on DrinkingWater Quality 80/778/EEC.Pesticides:maximum admissible
Other comments
Adsorption on bentonite, illite,kaoliniteand translocation measured in brown forest soil was studied and
environmental fate reviewed (8).
References
1.
2.
3.
4.
5.
6.
7.
8.
TheAgrochemicalsHandbook 3rd ed., 1991,The Royal Society of Chemistry, London, UK.
Material Safety Data Sheet 1978,Dow Chemical.
Bromatol. Chem. Toksykol. 1981,14,17, Warsaw, Poland.
1.Znd. Hyg. 1947,29,83.
Grover, I. S. et a1Prog. Clin. Biol. Res. 1990,34OE,91-106.
EC DirectiveRelating to the Quality of Water Intendedfor Human Consumption 1982,80/778/EEC, Officefor Official
S. I. 1991No. 472 TheEnvironmental Protection (PrescribedProcesses and Substances) Regulations 1991,HMSO, London, UK.
Karoly, G. Novenyvedelem (Budapest)1986,22(10),438-444 (Hung.)(Chem.Abstr. 108,145360a)
D I ~ dacarbazine
HN,QCONH2
C6H10N60 Mol. Wt. 182.19 CAS RegistryNo.4342-03-4
Synonyms 5-(3,3-dimethyl-l-tririazenyl)-lH-imidazole-4-carboxamide;5-(3,3dimethyl-l-triazeno)-imidazole-4-
carboxamide; 5(or4)-(3,3-dimethyl-1-triazeno)-imidazole-4(or5)carboxamide; biocarbazineR; detricine; DTIC
EINECS NO.224-396-1
Uses Antineoplasticagent.
RTECS No. NI 3950000
22

PhysicaI properties
M. Pt. 250-255°C(decomp.)
Solubility Water: 1mg ml-1 at 20°C
Acute data
LD50 intraperitoneal mouse, was reported in one experiment to be 350 mg kg-1, but in another experiment,
tumour-bearing mice tolerated an intraperitoneal dose of 1200mg kg-1 (1).
LD50 oral mouse >lo60mg kg'(1).
LD50 intraperitoneal rat 350 mg k g l (2).
LD50 intraperitoneal mouse 567 mg kg-1 (3).
LD50 intravenous rat 411mg kg-1 (4).
Rats given a single intraperitoneal dose of 500 mg kg-1 showed weight loss, pallor and bloody nares, and those
given 1000mg kg-1 orally also had stilted gait,pulmonary congestion,pleural fluid, anaemia and leucopenia.In
dogs the maximum tolerated dose over 28 days was 2.5 mg kg-1 day1 when given intraperitoneally,and 5 mg
kg-1 day-1 orally.In monkeys the respective doses were 15-30and 10mg kg-1. In all animals studied major
toxicityinvolved damage to the gut, bone marrow and lymphoid tissue.Recovery from toxic effectswas reported
to be within 6 wk of cessationof treatment (1).
In humans leucopenia and thrombocytopeniaoccurred from 5 to 21 days after a dose of 4.5 mg kg-1 day1 for 10
days;blood counts recovered only after 2-3 wk. Nausea and vomiting have limited the therapeutic dose given
either intravenously or orally (5).
Threecases of hepatic vein thrombosisleading to fatal hepatic necrosishave been reported. In each, the patient
was treated for melanoma with 200-260 mg m-2 daily intravenously for one cycleof 5 days. All patients
experiencedmoderately severe gastrointestinaland bone marrow toxicityand also developed symptoms of liver
failurehalf-way through the secondcourse of therapy, which followed about 1month after the first course (6).
Sufficientevidencefor carcinogenicityin animals,inadequate data for evaluation of carcinogenicityin humans,
IARC classificationgroup 2B (7).
Ratswere fed dacarbazine in the diet for up to 14wk. Cumulative doses of various groups were 974 mg in a" rats,
and 740,608,570 or 346 mg in 9 rats. Of the a"rats 8/16 developed mammary adenocarcinomas, 15/16 thymic
lymphosarcomasand 5/16 splenic lymphosarcomasby 18wk; one haemangioma also occurred. No neoplasm
was found in a" controls at that time. Of the high dose 9/24/24 had mammary adenocarcinomas and thymic
lymphosarcomas,21/24 had spleniclymphosarcomas,10/24 had cerebral ependymomas and 4/24 had
pulmonary alveolar carcinomasby 18wk. In the group given 608 mg, 6/12 had mammary carcinomas,5/12
thymic lymphosarcomas and 3/12 spleniclymphosarcomasby 24 wk. With 570 mg 1/16 had a mammary
adenocarcinoma,12116had mammary adenofibromas,3116thymic lymphosarcomas,2116splenic
lymphosarcomas,uterine leiomyosarcomasand leiomyosarcomaselsewhere.Among the 1209 controlsa total of
4 mammary adenocarcinomasand 10mammary adenofibromasoccurred (8).
Mice were given intraperitoneal injectionsof 25 or 50 mg kg-13 x a wk for 6 months. The combined tumour
incidenceswith the 2 doses were 21/41 lung tumours, 15/41 lymphomas and 10/41 splenic haemangiomas in a"
mice, and 16/19 lung tumours and 5/19 uterine tumours in 9 mice. The tumour incidence in all controlswas 31%,
with 10lung tumours, 3 lymphomas and no haemangiomas in 101a", and 21 lung tumours and 3uterine tumours
in 1539 (9).
Groups of 169 rats were given singleintraperitoneal injectionsof 100,250or 400 mg per rat. Another group was
injected with 2.5 mg 3 x a wk for 12wk (total76.5mg).After 66 wk the treated rats displayed a dose-dependent
increase in mammary adenocarcinomaincidencewith 0/20 in the group that received multiple injections,1/16 in
those given 100mg, 5/16 in those given 250 mg and 11/16 in those given 400 mg. Other tumours that occurred
with increased frequencyincluded mammary adenofibromas,cerebralependymomas, ependymoblastoma,
embryonal adenosarcomas,adrenal cortical adenoma, bronchogenicadenocarcinomasand renal cortical
adenocarcinoma.No tumour was observed in the controlgroups (8).
23

In a large systematicfollow-upof patients with Hodgkin's disease treated with an intensive chemotherapeutic
combinationincluding dacarbazine,plus adriamycin,vinblastine and bleomycinbut no alkylating agent,
preliminary evidence suggested no excessof acute nonlymphocytic leukaemia in the first decade after therapy
(10).
Teratogenicityand reproductive effects
Adult 0" mice were administered singleintraperitoneal doses of 50 or 200 mg kg-1. Ultrastructural changes in
spermatogonia and spermatocytes indicative of cytotoxicitywere observed after the higher dose. Abnormalities
were also observed in early spermatids in the Golgi and cap phases, with defects in acrosomeformation and
disruptions of the acrosomalsac.Spermatids in stages of maturation exhibited normal ultrastructures (11).
When rats were injected on the 12thday of pregnancy with a single intraperitoneal dose of 100-1000mg kg-1,
urogenital anomalies,such as hydronephrosis, hydroureter and hypoplastic, ectopic testes were observed in the
foetuses.Embryotoxicitydid not exceed that in controlswith doses of 100-900mg kg-1, but 1000mg kg-1 induced
15%embryolethality.Dose-dependent foetal growth retardation was observed with all doses (12).
Foetusesof rabbits given intraperitoneal injectionsof 10mg kg-1 on days 6-18of gestation showed skeletal
abnormalities.Doses of 2.5 and 5.0 mg kg-1 were ineffective.Ratswere given intraperitoneal injectionsof 30,50 or
70 mg kg-1 on days 6-15of pregnancy. Teratogeniceffects,including abnormalities of the skeletalsystem,eyes,
cardiovascularsystem and abdominal wall, were seen with the 2 higher doses. The mean foetalweight was
reduced with all 3 doses, and the rate ofresorptions increased.Offspring of rats treated from day 15 of pregnancy
through day 21post parfumwith 7.5,15 or 30 mg kg-1 showed a dose-dependent increase in postnatal mortality
(13)-
Following a single intraperitoneal injectionof [14C]methyl-labelleddacarbazine to rats, exhalation of WO2
occurred with a tmaxof -2 hr (0.95mg kgl) and 2.5hr (95mg kg-1). Of the total radioactivity administered, 8.5%
was exhaled as 14CO2,54% was excreted via the urine, predominantly as the unchanged substance. In the liver,
kidney and lung formations of 7-[14C]methylguaninein DNA and RNA was directly proportional with dose.
DNA methylation with a single dose of 9.8 mg kg-1 was highest in the liver (35pmoles 7-methylguanine per mole
of guanine), followedby the kidney (25pmoles)and lung (20 pmoles).The remainder tissues showed 7-
methylguanine concentrations=50%of those in liver DNA, with the exceptionof the brain which had =1pmole
per mole of guanine. At the specificradioactivity used (48 mCi mmole-1) the promutagenic base 06-
methylguanine was only detectable in the liver,kidney, lung and stomach DNA (0.6-0.8pmoles mole-1 guanine).
Autoradiography studies revealed a diffusedistribution of reaction products in rat liver. In contrast, N-
nitrosodimethylamine known to be bioactivatedby the hepatic cytochromeP450system showed a predominantly
centrilobulardistribution. This differencemay be due to the greater stabilityof proximate carcinogensgenerated
by a-Chydroxylation at one of the methyl groups of dacarbazine (14).
Dacarbazineis poorly absorbed from the gastrointestinal tract (15).
Sensitisation
Dacarbazinetreatment has frequentlybeen reported to cause photosensitivity reactions (16).
Genotoxicity
Mutagenic in the tk+/tk- assay with mouse lymphoma cellsafter metabolicactivation (17).
Mutagenic to Drosophila melanogaster (18).
Induced mitoticcrossing-over in Sacchuromycescerevisiae(19).
Induced chromosome anomaliesand reduced the mitotic index in mouse bone marrow cells in vivo (20).
No sister chromatid exchange was observed in the peripheral lymphocytes of 6melanoma patients given
intravenous injectionsof 250 mg m-2 daily for 5 days (21).
Other effects
Leucopenia and thrombocytopeniamay be severe in patients and the maximum effectmay not be seen for 3-4 wk.
Anorexia, nausea and vomiting are common.Other side effectsinclude hepatotoxicity, skin reactions,alopecia, an
24

influenza-likesyndrome, and facialflushing and paraesthesia. Extravasion produces pain and tissue damage.
Anaphylaxishas occurred occasionally(15).
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
Goldsmith, M. A. et a15-~3,3-dimethyl-l-triazeno)imidazole-4-carboxamide(DTIC,DlC) NSC-45388, Clinical Brochure National
Cancer Institute, 1972.
Arch. Geschwulstforsch. 1980,50,3-6.
CancerTreat. Rep. 1978,62,721.
Yachuri to Chiryo. Pharmacologyand Therapeutics 1981,9,3105.
Skibba, J. L. et a1CancerRes. 1969,29,1944-1951.
ZARC Monograph 1981,26,203-215.
ZARC Monograph 1987, Suppl. 7,184-185.
Beal, D. D. et a1J. Natl. CancerInst. 1975,54,951-957.
Weisburger,E. K. Cancer 1977,40,1935-1951.
Valagussa, P. et a1Blood 1982,59,488-494.
Martinova, Y. et a1Z. Mikrosk-Anat. Forsch. 1990,104(6),969-974 (Chem.Abstr. 115,21738e).
Chaube, S. et a1Anat. Rec. 1976,186,461-469.
Thompson, D. J. et a1 Toxicol.Appl.Pharmacol. 1975,33,281-290.
Meer, L. et a1Biochem. Pharmacol. 1986,35(19),3243-3247.
Martindale: The Extra Pharmacopoeia31st ed., 1996,The Royal Pharmaceutical Society, London, UK.
Med. Lett. 1986,28,51.
Matheson, D. et a1Drug Chem. Toxicol. 1978,1,277-304.
Zijlstra,J. A. et a1Mutat. Res. 1988,202(1),251-267.
Ferguson, L. R. et a1Mutat. Res. 1988,204(2),239-249.
Al-Hawary, B. A. et a1Mutat. Res. 1989,223(2),259-266.
Lambert, B. et a1Mutat. Res. 1979,59,295-300
D I ~ daidzein
C15H1004 Mol. Wt.254.24 CAS RegistryNo.486-66-8
Synonyms 7-hydroxy-3-(4-hydroxyphenyl)-4H-1-benzopyran-4-one;isoflavone, 4’,7-dihydroxy-;
4’,7-dihydroxyisoflavone; 7,4’-dihydroxyisoflavone; daidzeol
EINECS NO.207-635-4
Uses Daidzein is the major activeprinciple in extractsof Radix pueruriae, a traditional Chinese medication.
OccurrenceIsoflavonephytoestrogen found in numerous plants eaten by humans and food-producing
animals.
Physical properties
M. Pt. 297-298°C(dendritic needles from ether; slight decomp.);315-323°Cdecomp.
SolubilityWater: practicallyinsolublein water.Organic solvents:ethanol, diethyl ether
25

Environmentalfate
Degradationstudies
Three metaboliteswere isolated from the anaerobicfermentation of daidzein by human faecalbacteria under
anaerobicconditions:dihydrodaidzein, benzo-4,7-diol,3-(4-hydroxyphenyl),and equol(1).
Metabolismand toxicokinetics
Significantglucuronidation of plant oestrogensoccursin the gastrointestinal tract of sheep and cattle,which
reduces the role of hepatic glucuronidation of ingested substances (2).
Genotoxicity
Salmonella typhimuriurnTA98, TA100, TA1538with and without metabolic activation negative (3).
Daidzein did not exhibit clastogenicitynor did it induce hypoxanthine guanine phosphoribosyltransferase
mutations in cultured Chinesehamster V79 cells (4).
The effect of daidzein in the single cell gel electrophoresisassay (Cometassay) in human sperm was compared
with its effect on human periphereal lymphocytesfrom the same donor. Daidzein caused a greater positive
response in sperm than in peripheral lymphocytes,which may have been due to the fact that damage induced in
the elongated spermatids and consequent spermatozoa cannot be repaired (5).
Other effects
Any other adverseeffects
Sixteensamples of soybean meal examined in the mouse uterine weight bioassay had oestrogenicactivity.EtOAc
extracts of the meals also had oestrogenicactivity.Genisteinand daidzein were present in the extracts;the former
may have been responsible for most of the oestrogenicactivity (6).
Daidzein and genistein in the diet of captive cheetahshave been suggested as a probable cause of infertilityand
liver disease in these animals (7).
Daidzein binds to rat a-fetoprotein with Kd c. 5x 10-6 M. The authors suggest that this is sufficientlyhigh that
daidzein may modulate estradiol and estrone binding to rat a-fetoprotein in viva when present at dietary levels
(8).
0ther comments
Culture broths of an unidentified speciesof Streptornyces,designated 85-88,showed toxicity to mosquito larvae
that was traced to three crystallinecompounds, identified as tangeritin, genistein,and daidzein. The acetatesof
these isoflavonesshowed greater activitythan the parent compounds (9).
Daidzein is a potent and selectiveinhibitor of human mitochondria1aldehyde dehydrogenase and suppresses the
ethanol intake of Syrian golden hamsters. The as yet undefined mechanism by which daidzein suppresses ethanol
intake differsfrom that proposed for the classicADH inhibitor disulfram (10).
Two potent, reversibleinhibitors of human alcoholdehydrogenase isoenzymes isolated from the Kudzu root
(Radix puerariae)were identified as daidzein and genistein.Rat and rabbit class I ADHs are also inhibited by these
isoflavones. The 7-0-glucosyl derivatives of daidzein and genistein do not inhibit ADH but are potent aldehyde
dehydrogenase inhibitors (11).
Phytochemical mimicry of reproductive hormones and modulation of herbivore fertilityby phytoestrogens
reviewed (12).
Endocrinedisrupting effectsdiscussed (13J4).
References
1.
2.
3.
4.
Chang,Y.-C. et a11.Naf. Prod. 1995,58(12),1892-1896.
Lundh,T. J. 0.1.Agric. Food Chem. 1990,38(4), 1012-1016.
Bartholomew, R. M. et a1Mufaat. Res. 1980,78(4),317-326
Kulling,S. E. et a1Food Chem. Toxicol. 1997,35(6), 605-613.
26

5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
Anderson, D. et a1Teratog. Carcinog.Mutagen. 1997,17(1),29-43.
Drane, H. M. et a1Food Cosmet Toxicol. 1980,18(4),425-427.
Setchell,K. D. R. et a1Gastroenterology1987,93,225-238.
Baker, M. E. et a1Proc. SOC.Exp. Med. 1998,217(3),317-321.
Rao, K. V. et a1J. Agric. Food. Chem. 1990,38(6), 1427-1430.
Keung, W.-M. Proc. Natl. Acad. Sci. USA 1997,94(5),1675-1679.
Keung, W.-M. Alcohol:Clin. Exp. Res., 1993,17(6), 1254-1260.
Hughes, C. L., Jr. Environ. Health Perspect.1988,78,171-175.
Mazur, W. M. in Proc. Con&EndocrineDisrupters in the Environment,20-21 May 1997 1997, IBC Conference, 57-61 Mortimer
Street, London W1N 8JX,UK.
IEH Assessment on Environmental Oestrogens:Consequencesto Human Health and Wildlife 1995, Institute for Environment and
Health, Leicester,UK
D I ~ dalapon
C3H4C1202
CH3CC12C02H
Mol. Wt. 142.97 CAS Registry No. 75-99-0
Synonyms 2,2-dichloropropionicacid; a,a-dichloropropionic acid
EINECS NO.200-923-0
Uses Herbicide.Intermediate in organicsynthesis.
RTECSNo. UF 0690000
PhysicaI properties
M. Pt. 20°C B. Pt. 190°C Flash point >llO"C Specific gravity 1.389at 20°C
Partition coefficient log Po, 0.76 (1)
Solubility Organic solvents:diethyl ether, ethanol
Volatility v.p. 0.12mmHg at 25°C
DE-MAKlppm(5.9 mgm-3)
FR-VME 1ppm (6 mg m-3)
US-TWA 1ppm (5.8mg m-3)
Risk phrases Harmful if swallowed -.;ritating to L e skin -Risk of serious camage to eyes (R2
Safety phrases Keep out of reach of children (if sold to general public)-In case of contact with eyes, rinse
immediately with plenty of water and seekmedicaladvice -Wear eye/face protection (S2,S26, S39)
R38, R41)
Ecotoxicity
Fish toxicity
LC50 (96hr) rainbow trout, goldfish, channel catfish >lo0mg 1-1 (2).
EC50 (48hr) Daphnia pulex 11mg 1-1 (3).
LC50 (48hr) SirnocephaIus serrulatus 16mg 1-1 (3).
Non-toxicto bees (2).
Bioaccumulation
Calculatedbioconcentrationfactor 2 indicated that environmental accumulation is unlikely (4).
27

Environmentalfate
Reported to be slightly inhibitory to nitrificationmicrobes in soil (5).
Degradation studies
Degraded by soilbacteriaAfcaligenesspp. (6).
Can be degraded by methanogenicbacteria (7).
Microbialdegradation involved dechlorinationand liberation of carbon dioxide (8).
Followingsoil application at a rate of 22 kg ha-1 duration of herbicide activity is =3-4hr (2).
Abiotic removal
Hydrolytic tl/2 =3-4month, degradation product pyruvic acid (1).
tl/Z for reaction with photochemicallyproduced hydroxy radicals 72 days (9).
Adsorption and'retention
Reported to be leached readily from soil (2).
Acute data
LD50 oral Japanese quail, chicken >5000-5660mg kg-1 (2).
LD50 oral rat 907 mg kg-1 (1).
LD50 oral rat 7570-9330mg kg-1 (10).
LD50 oral 9 mouse >4600mg kg-1 (2).
Rats were fed 50 mg k g l day-1 for 2 yr in diet. Evidence of slight average increasein kidney weight but no
adrenal effectsobserved at 15mg kg-1 day-1 (1).
Oral dog rapidly eliminated, following a single dose of 500 mg 65-70% was excreted within 2 hr (2).
Irritancy
Non-permanent irritant to skin and eyes of rabbit (concentrationand duration unspecified) (2).
Genotoxicity
Salmonella typhimurium TA1535, TA1536, TA1537, TA1538with and without metabolic activation negative (11).
Streptomyces caelicolor spot; plate testsbase substitution, frameshiftmutation negative (11).
Legislation
Other comments
Residueshave been isolated from drinking water supplies (14).
Environmentalfate reviewed (14).
References
1.
2.
3.
4.
5.
Kenaga, E. E. et a1Residue Rev. 1974,53,109-151.
The AgrochemicalsHandbook 3rd. ed., 1991,The Royal Society of Chemistry,London, UK.
Sanders,H. 0.et a1 Trans. Am. Fish. SOC.1966,95,165.
Lyman, W. J. et a1Handbook of Chemical Property Estimation Methods: Environmental Behaviour of Organic Compounds 1982,15,
McGraw-Hill, New York, USA.
Parr,J. F. Pestic. Soil Wafer1974,321-340.
28

6.
7.
8.
9.
10.
11.
12.
13.
14.
Brokamp,A. et a1DECHEMA Biotechnol.Conf. 1990,1211-1215(Chem.Abstr. 115,228197~).
Shanker,R. et a1Lett. Appl. Microbiol.1991,12(1),8-10.
Day, 8.E. et a1Soil Sci. 1963,95,326.
Atkinson, R. Int.1.Chem. Kinet 1987'19,799-828.
Gaines, T. 8.et a1Fundam. Appl. Toxicol. 1986,7,299.
Carere, A. et a1Mutat. Res. 1978,57,277-286.
EC Directive Relating to the QuaIity of Water Intendedfor Human Consumption 1982,80/778/EEC, Office for Official
S. I. 1991 No. 472 The Environmental Protection(Prescribed Processes and Substances) Regulations 1991,HMSO, London, UK.
Howard, P. H. Handbook of Environmental Fate and Exposure Datafor OrganicChemicals 1991,3,196-202,Lewis Publishers,
Chelsea, MI, USA
~ 2 0 dalapon-sodium
C3H3Cl~Na02 Mol. Wt. 164.95 CAS Registry No. 127-20-8
Synonyms 2,2-dichloropropanoicacid, sodium salt; 2,2-dichloropropionicacid, sodium salt;
sodium 2,2-dichloropropionate; dikopan
EINECS NO.204-828-5
RTECS No. UF 1225000
Physical properties
M. Pt. >191"C(decomp.)
Solubility Water: 900 g kg-1 at 25°C.Organic solvents:ethanol, methanol
Volatility v.p. 7.52 x 10-8mmHg at 20°C
DE-MAK lppm(5.9 mg m-3)
Ecotoxicity
Fish toxicity
LC50 (96hr) rainbow trout, goldfish,channel catfish>lo0 mg 1-1 (1).
LC50 (96hr) carp >500mg 1-1 (1).
LC50 (96hr-static)guppy 223 mg 1-1 (2).
LC50 (48hr) bluegill sunfish 115mg 1-1 (3).
LD50 (48hr) Duphniu pulex 11mg 1-1 (4).
Environmentalfate
Degradation studies
In soil, readily undergoes microbial degradation involvingdechlorinationand liberation of carbon dioxide (5).
Followingan application rate of 22 kg ha-1 duration of residual activity in soil is =3-4months (1).
Abiotic removal
Slowlyhydrolysed in aqueous solutions at 25°C (1).
29

Acute data
LD50 oral Japanese quail, 9 mouse >4600mg kg-1 (1).
LD50 oral chicken 5660 mg kg-1.
LD50 oral 9 rat 7570 mg kg-1 (1).
LD50 oral d rat 9330 mg kg-1 (1).
LD50 oral 9 guinea pig, rabbit 3860 mg kg-1 (1).
LDx dermal rabbit >2000 mg kg-1(1).
Sub-acuteand sub-chronic data
LC50mallard duck, Japanese quail, pheasant >5000 mg kg-18 day diet (6).
In 2 yr feeding trials, rats receiving 15mg kg-1 day1 showed no ill-effects,but at 50 mg kg day-1 there was a
slight increasein kidney weight (1).
Legis1ation
WHO ClassTable 5; EPA ToxicityClass I1 (1).
Other comments
Mode of action-by the precipitation of protein, which interfereswith the production of pantothenic acid (1).
Doesnot undergo significantdegradation in plants (1).
Toxicity and hazards reviewed (9).
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
The PesticideManual 11ed., 1997,British Crop ProtectionCouncil, Farnham, UK.
Kam-Wing, L. et a1Hydrobiologia 1977, 56,49.
Edwards, C. A. Pesticidesin Aquatic Environments 1977,Plenum Press, New York, USA.
Sanders, H. 0.et a1Trans.Am. Fish SOC.1966,95(2),165-169.
Day, B. E. et a1Soil Sci. 1963,95,326.
Hill, E. F. et a1Lethal Dietary ToxicitiesofEnvironmenta1 Pollutants to Birds 1975,US Fish and Wildlife Service, Report Wildlife
No. 191,Washington,DC, USA.
EC Directive Relating to the Quality of Water Intendedfor Human Consumption 1982,80/778/EEC, Office for Official
Publications of the European Communities, 2 rue Mercier, L-2985 Luxembourg.
S. I. 1991No. 472 The Environmental Protection (Prescribed Processesand Substances) Regulations 1991,HMSO, London, UK.
Izmerov, N. F. Scienf$c Reviews of Soviet Literature on Toxicity and Hazards of Chemicals 1991,95,UNEP/IRPTC, Geneva,
Switzerland
021 daminozide
C6H12N203 Mol. Wt. 160.17 CAS Registry No. 1596-84-5
Synonyms N-(dimethy1amino)succinamic acid; butanedioicacid, mono(2,2-dimethylhydrazide); succinic
acid, mono(2,2-dimethylhydrazide); SADH
EINECS NO.216-485-9
Uses Plant growth regulator.
RTECS No. WM 9625000
30

Physical properties
M. Pt. 154-155°C
Solubility Water:100g 1-1 at 25°C. Organic solvents:acetone, methanol
Partition coefficient log Po, -2.4914 at 2°C Volatility v.p. 1.71x 10-4mmHg at 23°C
Risk phrases Possible risk of irreversibleeffects (R40)
Safety phrases Keep out of reach of children (if sold to general public)-Wear suitable protective clothing and
gloves (S2, S36/37)
Ecotoxicity
Fish toxicity
LC50 (96hr) bluegill sunfish 423mg 1-1 (1).
LC50 (96hr) rainbow trout 149mg 1-1 (1).
EC50 (96hr) Daphnia sp. 76 mg 1-1 (1).
Not toxic to bees (2).
Environmentalfate
Degradation studies
tl/2 17.3hr, aerobiccondition in sandy loam at pH 5.6, containing 7.34% organic matter (3).
Abiotic removal
Slowlydecomposed by light, tl/Z 105days (3).
Mammalian 8t avian toxicity
Acute data
LD50 oral rat 8400mg kg-1 (2).
LD50 oral redwing blackbird >lo0mg kgI(4).
LC50 (1hr) inhalation rat >147mg 1-1 air (2).
LD50 dermal rabbit >5000mg kgl(2).
LD50 intraperitoneal mouse 1325mg kg-1 (5).
LC50 (8day) mallard duck, bobwhite quail >10,000mg kg-1 diet (3).
In 1yr feeding trials no ill-effect observed in dogs up to 70,000 mg kg-1 diet total dose (3).
Non-carcinogenicin 2 yr feeding trial in rats at 5000mg kg-1 diet and in mice at 3000mg kg-1 diet (2).
In a 3-generationstudy in rats no effect level (NOEL)1000mg kg-1 diet on reproduction. In rabbits NOEL 3000
mg kg-1 diet on teratogenicityand embryotoxicity(3).
Genotoxicity
Salmonella typhimurium TA98, TA100,TA1535,TA1537, TA97with and without metabolicactivation negative (6).
Legislation
31

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