The Dictionary of Substances and Their Effects (DOSE): Volume 01 A-B

The Dictionary
of Substances
and their Effects
Second Edition

The Dictionary
of Substances
and their Effects
Second Edition
EDITOR
S Gangolli,Consultant,MRC Toxicology Unit,UK
EDITORIAL ADVISORY BOARD
Dr D Anderson, BIBRA International, UK
Dr J Chadwick, Health and Safety Executive, UK
Professor L Ebdon, University of Plymouth, UK
Dr D Gammon, California €PA,USA
Professor L King, University of Surrey, UK
Dr R McClellan, ChemicalIndustry Institute of Toxicology,USA
Professor I Rowland, Universityof Ulster,UK
Dr J Solbk, Unilever,UK
Dr T Sugimura, National CancerCentre,Japan
Professor P van Bladeren, 7"Nutrition and Food Research Institute, TheNetherlands
RSeCROYAL SOClEN OF CHEMISTRY

PRODUCTIONTEAM
Ken Wilkinson (Staff Editor)
Richard Ellis
Sally Faint
JulieHetherington
Alan Skull
The publishers make no representation, express or 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 omissions that may be made.
Volume 1 ISBN 0-85404-808-1
Seven-volume set ISBN 0-85404-803-0
A catalogue record for this book is available from the British Library.
0The Royal Society of Chemistry 1999
All rights reserved
Apart from 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 anyformor by any means, without the prior permission in
writing of The Royal Society of Chemistry, or in the case uf 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
Typeset by Land & Unwin (Data Sciences)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 Cornpounds
Volume 6
Guide to Content
0-SCompounds
Volume 7
Guide to Content
T-Z Compounds
Index of ChemicalNames and Synonyms
Index of CASRegistry Numbers
Index of Molecular Formulae
vii
ix
xi
863-865
1-862
867-88 1
882-889
vii
1-865
vii
1-832
vii
1-892
vii
1-953
vii
1-952
vii
1-712
713-91 4
915-956
957-998

Foreword
The lifestyle of the modern world can only be sustained by the effective utilisation of
chemicals in the protection of our health, production of our food, manufacture and
commerce. Yet these same chemicalsin the wrong place can have potentially harmful effects.
To understand the quantitative risks to human health and ecosystems,reliable information is
required about the substances and their biological effects.The Dictionary of Substances and their
Efiects (DOSE)seeks to provide such information comprehensively yet in an easily accessible
format.
As our understanding of the complexity of life and the intricate interactions which sustain
ecosystems has grown, so has our requirement for information. The toxicologist,
ecotoxicologist,and users and suppliers of chemicals need to know the properties, chemistry,
biological effects and likely use of substances. Yet too often comprehensive data are difficult
to obtain. The first edition of DOSE was hailed as an important breakthrough for those who
needed a comprehensive and reliable compilation of data on chemicals with environmental
impact. This second edition significantly updates the toxicological data and extends the
number of chemicalsto 4123.
While regulators might argue that the provision of toxicological data should be the
responsibility of chemicalsuppliers, the reality is that often when such data are supplied they
are overly brief or ridiculously over-cautious. I recently received a sample labelled "tap
water" with the warning that it contained "hydrogen, which is a flammable substance". To
have a single compilation of data, collected only from the peer-reviewed literature, and
published under the authoritative imprimatur of the Royal Society of Chemistry, is surely the
most effectiveanswer to this problem.
The editorial team which has brought together this excellent second edition is to be
congratulated on its achievement. DOSE will allow users to identify the hazards pertaining to
given substances readily. Professor Lord Lewis in his introduction to the first edition
emphasised the difference between hazard identification and risk assessment. Lord Lewis
stressed the need for training to evaluate risks quantitatively and, in particular, the risks
posed by combinations of chemicals.He quoted Paracelsus, the father of toxicology, and his
famous dictum often translated as "the dose maketh the poison". In a world reliant on
chemicals, but with an environment seriously threatened by anthropological damage, DOSE
will enable scientists and regulators to ensure that the dose received by the organism will be
far less than poison, indeed below that which has an effect.
Professor Les Ebdon
Deputy Vice-Chancellor(Academic)
University of Plymouth
vii Foreword

Introduction
The risk evaluation of the potential adverse effects of a chemical on human health and the
ecosystem, widely recognised by regulatory agencies as being of vital importance for the
protection of man and his environment, requires the assessment of a broad range of
information on the chemistry and biological properties of that chemical. Except for certain
special human and veterinary medicine and some agrochemicals,relevant data for the vast
majority of chemicals traded commercially are either not available or sparsely dispersed in
the scientific literature. Thus, the assessment of the health and environmental risks of a
chemical would be an onerous task without access to a single comprehensive compilation of
relevant information.
In the publication of the first edition of The Dictionary of Substances and their €fiects (DOSE),
the Royal Society of Chemistry addressed the formidable logistical problems faced by
scientists in obtaining the relevant data for the risk assessment of chemicals due to the
paucity of publications containing compilations of appropriate data. The aim of this
acclaimed publication was to collect and collate relevant chemical and biological data from
peer-reviewed scientific literature to provide information for the quantitative risk evaluation
of a chemical at its various levels of usage and conditions of exposure. The chemicals in the
first edition were selected mainly from sources such as the Authorised and Approved List
from the EC’s Classification, Packaging and Labelling Regulations; the EC’s “Black” and
“Grey” lists of dangerous substances; the ”Red” list prepared by the UK Department of the
Environment; and the Priority Pollutant Lists from the USA and Canada, and the German
Pollutant List. Data considered to be of relevance for each of the 4003 chemicals in the first
edition included physico-chemical properties; toxic effects on various species in the
ecosystem; persistence and degradability in the environment; and toxicity data,
encompassing genotoxicity, reproductive effects and toxicokinetic studies in avian and
mammalian species,including man. Relevant legislativeinformation was also included.
The success of the first edition of DOSE as a unique reference source of essential information
for the risk evaluation of chemicals was clearly reflected by sales, encouraging reviews and,
most importantly, the favourable comments received from users. Since the publication of the
first edition there has been a year on year increase in the numbers of research papers on
topics relevant for the risk assessment of chemicals in the literature. These considerations,
together with the burgeoning literature on the toxicology of chemicals subsequent to the
publication of the first edition, were persuasive factors in influencing the Royal Society of
Chemistry to embark on the preparation of the present second edition of DOSE. Relevant
information is reported in DOSE if it has been published in the scientific literature, and it is
interesting to note that toxicity data on many industrial chemicals are still not available. A
recent US Environmental Protection Agency study1 has shown that, of the estimated 3000
high production volume chemicals (i.e. in excess of 1million pounds/annum) produced or
imported in the USA, only 7%had a full set of basic toxicity data, and 43% had no toxicity
data at all.
1.Pesticide and Toxic Chemical News 1998, 26 (28), 7-8.
ix Introduction

A number of important additions have been incorporated in this second edition. Apart from
updating the toxicological data for the original compounds in the first edition, the number of
compounds has increased to 4123. Special classes of chemicals have been added, including
several endocrine disrupting chemicals, a number of pesticides, a few of the high production
volume chemicalsfor which data have recently been collected by the OECD, and compounds
tested for carcinogenicityby IARC and/or NTP. Risk and safety phrases have been updated,
and some headings have been changed to conform with current practice and convention. A
new field, Toxicity to other species, has been included, occupational exposure data have been
expanded to include values for France, Germany, Sweden and Japan as well as for the UK
and USA. RTECS and EINECSnumbers have also been included in the entries.
It is my fervent hope that the second edition of DOSE will constitute a scientifically sound
foundation and a paradigm for future publications that will be required to satisfy the need
for accurate and timely data in this important field.
I am grateful to members of the Editorial Advisory Board for their helpful suggestions and
advice. I must also place on record my sincere thanks to the staff members of the Royal
Society of Chemistry for their invaluable support and cooperation in the preparation of this
edition of DOSE.
Sharat Gangolli
Editor
Introduction X

Guide to Content
The data for each chemicalin DOSE are organised as follows:
DOSE No.
Chemical name
Structure/line formula
Molecular formula
Molecular weight
CAS Registry No.
Synonyms
EINECS No.
RTECS No.
Uses
Occurrence
Physical properties
Melting point
Boiling point
Flash point
Specific gravity
Partition coefficient
Volatility
Solubility
Occupational exposure
Limit values
UN number
HAZCHEM code
Conveyanceclassification
Supply classification
Risk phrases
Safety phrases
Ecotoxicity
Fish toxicity
Invertebrate toxicity
Toxicity to other species
Bioaccumulation
Environmental fate
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
Legislation
Other comments
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.
xi 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,
zoxazolamine,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 substance is of
unknown or variable composition,or consistsof biological materials),a short phrase appears
instead, for examplechlorinated parafins (C12, 60%).
Molecular formula
This is the elemental composition of the compound. The elements appear alphabetically for
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.
CbHSBr.
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
chemical substances recorded in the CASRegistry.New numbers are assigned sequentiallyto
each new compound identified by Chemical Abstracts Service. This information is also
provided in the full index of CAS Registry Numbers available at 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 describe each substance.
EINECS No.
This number is assigned by the European Commission to each record in the EINECS
(EuropeanInventory of Existing Commercial Chemical Substances)inventory. The numbers
are in the format XXX-XXX-X, for example, 202-726-0 for nitrobenzene.
RTECS No.
The RTECS (Registry of Toxic Effectsof Chemical Substances)number is a unique identifier
assigned by NIOSH (NationalInstitute of OccupationalSafetyand Health in the US) to every
substancein the RTECS database. The number is in the format of two alphabetic characters
followed by seven numeric characters,forexample, D A 6475000for nitrobenzene.
Guide to Content xii

Uses
Principal uses of the substances are given, with information on other sign
industrial processes.
ficant uses n
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-octanollwater 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.
Solubility
Solubility data derived from several sources are quoted for both water and organic solvents
where available.
Limit values
This field contains the occupational exposure limit values (or threshold limit values) from
France, Germany,Japan, Sweden, UK and USA.
Guideto Content
...
Xlll

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
differentcountries. 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 (mgvi3).
French exposure limits are published by the French Ministry in Charge of Labour and
presented in the report Valeurs limites d’exposition professionnelle aux 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 xiv

The threshold limit values for the USA have been taken from the Threshold Limit Values and
Biological Exposure Indices, 1999 produced by the American Conference of Governmelital
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
concentration for a normal %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
&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.
Conveyance classification
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 1January 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 CHIP99. Thesechanges are
incorporated in the updates to the electronicversions of DOSE released after 1January2000.
xv Guideto 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 xv.)
Ecotoxicity
Information is presented on the effectsof chemicals on 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. Ecotoxicologycan 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
species to 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 affectcrop 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.
Invertebratetoxicity
LC50values 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.
Guideto Content xvi

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.
Bioaccumulation
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.
EnvironmentalFate
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
environmental situations.
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 also be 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.
xvii Guideto Content

Carbonaceous inhibition
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. Chemicalinhibition 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 effectsof 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.
Adsorption and retention
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 xviii

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.
Carcinogenicityand chroniceffects
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 vitvo studies are reported.
xix 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 accidentto 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 allergicreactions.
Genotoxicity
Genotoxicity testing is carried out to determine the mutagenic and/ or carcinogenic potential
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 cytogenetictests 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 capableof reactingwith 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 effectsto organisms or animalsother than man are reported here.
Guide to Content xx

Legislation
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 effects associated with impurities, is contained in this section.
References
Contains referencesto 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, Cl,Cr, etc., but for organic compounds, carbon and
hydrogen content are shown first followed by the other elements in alphabetical order, i.e.
CbH5Br. This number is linked to the preferred DOSE name for that chemical and its DOSE
number.
xxi 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 chemicals that 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
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Email: library@rsc.org
Guide to Content xxii

A-a-C
H
c33YNH2 /
CllH9N3 Mol. Wt. 183.21 CAS Registry No. 26148-68-5
Synonyms 2-amino-a-carboline; 2-amino-9H-pyrido[2,3-b]indole;lH-pyrido[2,3-b]indole-2-amine;
2-amino-lH-pyrido[2,3-b]indole
Uses Not used commercially.
OccurrenceNot known to occur in nature.
Physical properties
M.Pt. 202°C
Solubility Organicsolvents:dimethyl sulfoxide, methanol
Mammalian & avian toxicity
Carcinogenicity and chronic effects
No data for carcinogenicityto humans, sufficientevidencefor carcinogenicity4oanimals, IARC classification
Group 2B (1).
Oral mice (685days) 800mg kg-1 in diet. Tumourswere observed in the livers and blood vessels of treated
animals.No such tumours were seen in controls(2).
NADPH-dependent oxidation of A-a-C to form six products was catalysedby human, rat, and mouse hepatic
microsomes.3-Hydroxy-A-a-C and 6-hydroxy-A-a-Cwere the two major metabolites (c. 85%of total).N-
Hydroxy-A-a-Cand its oxidation products comprised the rest (3).
Genotoxicity
Salmonella typhimuriurn TA98 and TA98/1,8-DNP6 with metabolic activationpositive (4).
Hepatocyte/DNA repair test (cf rats, a*and 9 mice, cf hamsters) positive (5).
Sister-chromatid exchangesin human lymphoblastoidcellswith metabolicactivation positive (6).
In transgenicmice fed A-a-C (800ppm) in diet for 30,60, or 90 days lac1mutations were induced in the colon (7).
Other effects
Rats fed A-a-C suffered no atrophy of the salivaryglands and pancreas whereas rats fed 3-Me-A-a-C suffered
severelyin most casesfrom one or the other, or both (8).
Other comments
Heterocyclicamine product formedby the cooking and pyrolysis of meat.
The most common heterocyclicamine found in all types of satay (chicken,mutton, pork) cooked accordingto
Chinese and Malay styles (1.3-12ppb) (9).
1

References
1.
2.
3.
4.
5.
6.
7.
8.
9.
IARCMonograph 1986,40,250.
Ohgaki,H. et a1Carcinogenesisfbndon) 1984,5,815-819.
Ram, H. et a1Drug Metab. Dispos.1996,24(4),395-400.
Nago,M. et a1Biochem.Biophys. Res. Commun.1983,114(2),626-631
Yoshimi, N. et a1Environ.Mol.Mutagen.1988,12(1), 53-64.
Toda,H. et a1Mufat. Res. 1980,77(1), 65-69.
Zhang,X. 8.et a1Carcinogenesis 1996,17(10),2259-2265.
Takayama,S.et a1Proc. Ipn. Acad.,Ser. B 1985,61(6), 277-280.
Wu,J. et a1Environ. Monit.Assess. 1997,44(1-3),405-412
A2 abietic acid
C20H3002 Mol. Wt. 302.46 CAS Regis- No. 514-10-3
Synonyms podocarpa-7,13-dien-15-oic acid, 13-isopropyl-; (-)-abietic acid; 7,13-abietadien-l8-oicacid;
sylvicacid
EINECS No.208-178-3 (technical)
Uses In the manufacture of ester gums and of “metalresinates”,soaps, plastics, and paper sizes.
Physical properties
M. Pt. 172-175°C(monoclinicplates fromalcoholplus water), commercialabieticacid may be glassyor partly
crystalline and may melt as low as 85°C
Solubility Water: insoluble. Organic solvents: acetone,alcohol,benzene, carbon disulfide, chloroform,ether
Ecotoxicity
Fish toxicity
LC50 (96hr) cohosalmon 0.56mg 1-1 (1).
LC50 (96hr) rainbow trout 0.7mg 1-1 (2).
An abieticacid mixture (37%abietic acid, 6% dehydroabieticacid, and a remainder of unknown compounds)
showed slight oestrogenicactivity in trout when administered in feed, but was completelyinactivewhen given
intraperitoneallyin implant. Theoestrogeniccomponentof the mixture was not identified (3).
LCm (96hr) shrimp 6.2mg 1-1 (4).
2

Acute data
LD50 intravenous mouse 180mg kg-1(5).
Teratogenicityand reproductive effects
Ingestionof hexane extract of Pinus ponderosu needles causesreproductive failure in mice during the early stages
of gestation. The activecomponents of the hexaneextract were identified as a mixture of diterpene resin acids,
including abieticacid (6).
Abietic acid is metabolisedin the rabbit to primary, secondary,and tertiary alcohols, with the primary alcohol
predominating (7).
Other effects
Abietic acid was oestrogenicin breast cancer cell lines MCF-7and T-47D (3).
Abieticacid (225pg ml-1 inhibited (Na,K)-and (H,K)-ATPases,both of which are typical membrane-bound
enzymes.Abietic acid also inhibited gastricacid secretioncaused by (H,K)-ATPase.Non-specific inhibitionby
abieticacid suggests that it acts primarily by inducing disorganisationof the cell membrane constitution (8).
Abieticacid (micromolarconcentrations)depolarised mammalian synaptosomal membrane and caused
acetylcholinerelease. These responseswere not inhibited by tetradotoxin.Abietic acid caused weak inhibitionof
mammalian synaptosomal ATPase activity.Two actionsof abieticacid which may contribute to neurotoxicityare
membrane depolarisation and neurotransmitter release (9).
Other comments
Prepared by the isomerisationof rosin.
Abieticacid was detected only in the shell and not in the soft tissue of the gastropod mollusk Ausfrocochleu
consfricfa.It is suggested that the shellmay act as a "toxic waste sink" to facilitatethe removal of potentially
harmful compounds from the more metabolicallyactivesoft tissue (10).
Abieticacid was identified as a major toxicant to juvenilecohosalmon in softwood debarking effluentsand
pulping waste streams (11).
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
Leach,J, M. et a1J.Fish. Res. Board Can. 1973,30,479-484.
Leach,J.M. et a1J. Fish. Res. Board Can. 1975,32,1249-1257.
Mellanen,P. et a1Toxicol.Appf.Phurmacol. 1996,136(2),381-388.
Linden, E.et a1Chemosphere 1979,ll-12,843-851.
Report No.N X 02819USArmy Armament Research andDevelopment Command,ChemicalSystemsLaboratory,NIOSH
ExchangeChemicals,AberdeenProvingGround,MD 21010,USA.
Kubick, Y.M.et a1Cornell Vet.1981,71(1),34-42.
Asakawa, Y. et a1Xenobiotica 1986,16(8),753-767.
Sekido,H.et a1Agfic. Biol. Chem. 1990,54(2),287-290.
Nicholson,R. A. Biochem. SOC.Trans. 1994,22(2),226s.
Walsh, K. et a1Arch. Environ. Confam.Toxicol. 1994,26(3),367-373.
Leach,J. M. et a1Prog. Water Technol.1978,9(4),787-798
3

A3 acenaphthene
C12H10 Mol. Wt. 154.21 CAS Registry No. 83-32-9
Synonyms 1,2-dihydroacenaphthylene; 1,8-ethylenenaphthalene; periethylenenaphthalene
EINECSNO.201-469-6
Uses A dyestuff intermediate,insecticideand fungicide.In the manufactureof plastics.
OccurrenceA product of coal combustion,in coal tar and diesel fuel emissions.Volatile componentof cassava
and nectarines.
RTECSNo. AB 1000000
PhysicaI properties
M.Pt. 93-95°C B.Pt. 279°C Specificgravity 1.0242at 90°Cwith respect to water at 4°C
Partition coefficient log Po, 3.92 Volatility v.p. 10mmHg at 131°C
Solubility Organicsolvents:benzene,ethanol
Ecotoxicity
Fish toxicity
LC50 (96hr) fathead minnow,channelcatfish,rainbow trout,brown trout 600-1700pg 1-1 flow throughbioassay,
LC50(exposureunspecified)himedaka killifish 6.3mg 1-1 (2).
LC50 (96hr) bluegillsunfish1700pg 1-1 staticbioassay (3).
LCm (96hr) snail2040pg 1-1 flow throughbioassay (1).
LCa (96hr) mysid shrimp 970pg1-1 staticbioassay (3).
Bioaccumulation
Mussels, scallopsand snailshave no detectablearyl-hydrocarbonhydroxylaseenzymesystemand therefore
accumulateacenaphthene(4).
Bluegillsunfishbioconcentrationfactor387-389(5,6).
pH 7.5-7.6(1).
Environmentalfate
The microbialdegradationof acenaphtheneunder denitrificationconditionsat soil-to-waterratios of 1.25with
soilcontaining lo5 denitrifyingorganismsg-1 was investigated.Under excessnitrite conditions,acenaphthene
was degraded to undetectablelevelsin <9wk. Acclimation periods of 12-38days were observed in testswith soil
not previously exposed to polycyclic aromatichydrocarbon (PAH)compounds.The acclimationperiod resulted
from the time required for a smallpopulationof organismscapableof PAH degradation to attain sufficient
densitiesto exhibit detectablePAH reduction.Under nitrite limitingconditionsthe PAH compoundswere stable
(7).
Anaerobiceffects
Under anaerobicconditionsno significantdegradationwas observed over a period of 70days (7).
4

Degradation studies
Microbialdegradation from initial aqueous phase concentrationof 1mg 1-1 to non-detectable levelsoccurred
within 10days under aerobicconditions (7).
Concentrationsof 25-150 pg 1-1 were degraded at ambient temperatures within 3 days in groundwater (8).
In flooded soil contaminated with acenaphthene, biodegradation occurredunder aerobic and denitrifying
environments at rates of 0.39 and 0.30-0.32 ppm day-1, respectively.No significantbiodegradation was seen under
sulfate-reducingor methanogenicenvironments (9).
Abiotic removal
Acenaphthene, in commonwith other polycyclicaromatichydrocarbons and cyclic alkanes, resists environmental
hydrolysis (10).
The photolytic tl/2 of acenaphthene in water at 20°C exposed to 100W Hg lamp is reported to be 3 hr (11).
Acenaphthene adsorbed on coal fly ash resistsphoto-oxidation (12).
Mammalian studies have yielded equivocalfindings (13).
Acenaphthene, in common with other PAHs, accumulatesin adipose tissue,but its transport into cellsand
between intracellular membranes is not well understood. Molecular volume is considered to be a rate-
determining factor (14).
In mammals, PAHs are oxidisedby aryl hydrocarbon hydroxylaseactivityand excretedas glucuronide conjugates
(15).
Genotoxicity
Salmonella typhimuriumTA97, TA98, TA100, TA1535, TA1537with and without metabolic activationnegative (16).
Resistanceto 8-azaguaninewas induced in Salmonella typhimurium with metabolicactivation (17).
Salmonella typhimurium TA1537, TA1538 with and without metabolic activationnegative. Although non-
mutagenic, all the 1,Zring fused acenaphthenes were found to be indirect frameshiftmutagens in strain TA1537
(18).
Escherichiaculi PQ37 SOS chromotestwith metabolic activationnegative (19).
Other effects
A case-control study was undertaken in Montrealto investigate the possible associationsbetween occupational
exposures and cancersof oesophagus, stomach,colorectum, liver,pancreas, lung, prostate, bladder, kidney, skin
and lymphoid tissue. In total, 3726 cancerpatients were interviewedbetween 1979-1985,to obtain detailed
lifetimejob histories, which were translated into a history of occupationalexposures to PAHs (20).
Legislation
Limited under EC Directiveon DrinkingWater Quality 80/778/EEC. Polycyclicaromatic hydrocarbons:
maximum admissibleconcentration0.2 pg1-1 (21).
Other comments
In a survey of UK drinking water treatment facilitiesacenaphthene was detected in treated samples at 2 of 14
facilities(22).
Detected in water bottom sediments and fish in Japan (23).
Experimentaltoxicology, human health effectsand environmental effectsreviewed (13,24).
5

References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
31.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
Holcombe, G. W. et al Ecotoxicol.Enuiron. Safety 1983,7(4),400-409.
Niinomi, J. et a1Mie-ken Kugaku Senta Kenkyu Hokoku 1989,9,53-60Gap.) (Chem.Abstr. 111,189142~).
Ambient WaterQuality Criteria Document 1980,EPA B-4Draft.
Malins,D. C.Ann. N.Y.Acad. Sci. 1977,298,482-496.
Sittig, M. (Ed.)PriorityToxicPollutants1980,46-47.
Veith, G.D. et a1ASTM STP707Aquatic Toxicology1980,116-129,Easton, J. G. (Ed.),Am. SOC. Test Materials,USA.
Mihelcic,J. R. et a1Appl. Environ. Microbiol. 1988, 54(5),1182-1198.
Owaga, I. et a1Talanta 1981,28(10),725-729.
Leduc,R. et a1WaterSci.Tech. 1992,26(1-2),51-60.
Lyman, W. J. et a1Handbookof ChemicalProperty EstimationMethods 1982,7-14,McGraw-Hill, New York, NY, USA.
Fukuda, K. et a1Chemosphere1988,17,651-659.
Korfmacher, W.A. et a1Science 1980,207,763-765.
Health Efects Assessmentfor Acenaphthene 1987,EPA 600/8-88/010.
Plant, A. L. et a1Chem-Biol.Interact. 1983,44(3),237-246.
Sittig,M. Handbookof Toxicand HazardousChemicalsand Carcinogens2nd ed., 1985,741,Noyes Data Corp.,Park Ridge,NJ, USA.
Zeiger, E. et a1Environ.Mol. Mutagen. l992,197(Suppl.21),2-141.
Krishnan,S. et a1Environ.Sci. Technol.1979,13(12),1532.
Gatehouse, D. Mutat. Res. 1980,78,121-135.
Mersch-Sundermann,V. et a1Mutugenesis1994,9(2),205-224.
Krewski, D. et a1Environ. Sci. Res. 1990,39,343-352.
EC Directive Relating to the Quality of WaterIntendedfor Human Consumption 1982,80/778/EEC, Officefor Official
Publicationsof the European Communities,2 rue Mercier,L-2985Luxembourg.
Fielding,M. et a1Organic Pollutantsin Drinking Water1984,49, TR-159,Water Res. Centre, UK.
JETOCNewsletters1988,6,20.
ECETOC TechnicalReport No. 72 1996,European Centre for Ecotoxicology and Toxicologyof Chemicals,4 AvenueE. Van
Nieuwenhuyse (Bte6), 8-1160Brussels, Belgium
A4 acenaphthylene
C12H8 Mol.Wt. 152.20 CAS Regis- No. 208-96-8
Synonyms cyclopenta[de]naphthalene
EINECS NO.205-917-1
OccurrenceIn cigarettesmokeand in sootsgeneratedby the combustionof aromatichydrocarbonfuels
containingpyridine (1).
PhysicaI properties
M. Pt. 92-93°C B. Pt. 265-275°C Specificgravity 0.899 at 16°C with respect to water at 2°C
Volatility v.p. 9.12 x 10-4 mmHg at 25°C
Solubility Water: 16mg 1-1 at 25°C. Organicsolvents:ethanol,diethylether,benzene
6

UN No.2570
Ecotoxicity
Bioaccumulation
Bullhead catfish(BlackRiver, Ohio)and stripedbass (PotomacRiver,Maryland)contained270 and 43ppb
acenaphthylene,respectively. Oystersand clamscontained36 and 130ppb, respectively(2,3).
Environmentalfate
Degradation studies
Concentrationsof 25-150 pg 1-1 were almosttotallydegraded within 3 days at ambienttemperatures in
groundwater(4).
Microbialdegradationof acenaphthylenein water sampleswas low (5).
In floodedsoilcontaminatedwith acenaphthylene,biodegradationoccurredunder aerobicand denitrifying
environmentsat rates of 0.53and 0.35-0.37ppm day-1. No significantbiodegradationwas seen under sulfate-
reducing or methanogenicenvironments(6).
Abiotic removal
Acenaphthylene,in commonwith otherpolycyclicaromatichydrocarbons(PAHs),is unlikely to undergo
environmentalhydrolysis(7).
Aqueousphotolysis data for acenaphthyleneindicate it is likelyto undergodirectphotolysisin the environment (8,9).
Acenaphthylenewas completelydegraded after 16monthsincubationin the dark at 20°C, which suggests
volatilisationis more important thanbiodegradationin the removalof this compound (10).
Mammalian 81avian toxicity
Metabolismand toxicokinetics
In mammals,acenaphthyleneand other PAHs are oxidisedby arylhydrocarbonhydroxylase activityand excreted
as glucuronideconjugates(11).
Genotoxicity
Salmonella typhimuriuin TA1537,TA1538with and without metabolic activationnegative.Althoughnon-
mutagenic,all 1,Zring fused acenaphtheneswere found to be indirectframeshiftmutagens in strain TA1537(12).
Other effects
Other adverse effects(human)
A case-controlstudy was undertakenin Montrealto investigatethe possibleassociationsbetweenoccupational
exposuresand cancersof oesophagus,stomach,coloredum,liver, pancreas,lung, prostate,bladder, kidney, skin
and lymphoidtissue. In total, 3726cancer patientswere interviewed between 1979-1985to obtaindetailedlifetime
job histories,whichwere translated into a history of occupationalexposuresto PA& (13).
Legislation
Limited under EC Directiveon DrinkingWater Quality 80/778/EEC. Polycyclicaromatichydrocarbons:
maximumadmissibleconcentration0.2pg 1-1 (14).
Other comments
Found in Canadiandrinking water 0.1-20ng 1-1 (15).
Seafoodsand agriculturalproducecan containtracesof acenaphthyleneand other PAHs absorbed from the
atmosphereand fromcontaminatedwater supplies(16).
Toxicityand hazards reviewed (17).
Reviewson human healtheffects,experimentaltoxicology,environmentaleffects and exposurelevelslisted (18).
7

References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
Health Eflects Assessmentfor Acenaphthylene 1987,EPA 600/8-88/011.
Vassilaros, D. L. et a1Anal. Chem. 1982,54,106-112.
McFall,J. A. et a1Chemosphere1985,14,1561-1569.
Ogawa, I. et a1Talanta 1981,28(10),725-729.
Niinomi, J. et a1Mie-ken Kankugu Senta Kenkyu Hokoku 1989,9,53-60 Oap.) (Chem.Abstr. 111 189142~).
Leduc, R. et a1Water Sci. Tech. 1992,26(1-2),51-60.
Lyman, W. J. et a1Handbook of ChemicalProperty Estimation Methods 1982,7-14, McGraw Hill, New York, NY, USA.
Fukuada, K. et a1Chemosphere1988,17,651-659.
Behymer, T.D. et a1Environ. Sci. Technol. 1985,19,1004-1006.
Bossert, I. D. et a1Bull. Environ. Contam. Toxicol. 198637,490-495.
Sittig,M. Handbook ojToxic and Hazardous Chemicalsand Carcinogens2nd ed., 1985,741,Noyes Data Corp., Park Ridge,NJ,USA.
Donnelly,K. C. et a1Mutat. Res. 1987,180(1),31-42.
Krewski,D. et a1Environ. Sci. Res. 1990,39,343-352.
EC Directive Relating to the Quality of WaterIntendedfor Human Consumption 1982,80/778/EEC, Office for Official
Publications of the European Communities, 2 rue Mercier, L-2985Luxembourg.
Benoit, F. M. et a1Bull. Environ. Contam. Toxicol. 1979,23,774.
Ellenham,M.J. et a1Medical Toxicology-Diagnosisand Treatmentof Human Poisoning 1988,953,Elsevier,New York, NY, USA.
Izmerov,N.F. Scientific Reviews of Soviet Literature on Toxicity and Hazards of Chemicals 1991, Eng. Trans.Richardson, M. L.
(Ed.), UNEP/IRPTC, Geneva, Switzerland.
ECETOC Technical Report No. 71 1996,European Centre for Ecotoxicology and Toxicology of Chemicals,4 Avenue E. Van
Nieuwenhuyse (Bte6), 8-1160 Brussels,Belgium
AS acephate
0
CH3CONHP,“-0CH3
SCH3
C4HloN03PS Mol. Wt. 183.17 CAS Registry No. 30560-19-1
Synonyms acetylphosphoramidothioicacid 0,s-dimethyl ester; 0,s-dimethyl acetylphosphoramidothioate;
Orthene
EINECS NO.250-241-2
Uses Contactand systemicinsecticide.
RTECS No. TB 4760000
Physical properties
M. Pt. 88-90°C;82-93°C(technicalgrade) Specific gravity 1.35(temperatureunspecified)
Volatility v.p.1.72x 10-6mmHg
SolubilityWater:790 g 1-1 at 20°C.Organicsolvents:acetone,benzene,ethanol,ethyl acetate,hexane
Occupationalexposure
Supplyclassificationharmful
Risk phrases Harmful if swallowed (R22)
Safetyphrases Keep out of reach of children(ifsold to generalpublic)-Wear suitableprotectiveclothing (S2,
S36)
8

Ecotoxicity
Fish toxicity
LC50 (96hr) rainbow trout, largemouth black bass >1000,1725 mg 1-1, respectively(1).
LC50 (96hr) bluegill sunfish, channel cat fish 2050,2230 mg 1-1, respectively (1).
Exposure (24hr) to 400 mg 1-1 depressed brain cholinesteraselevels in rainbow trout for 15days (2).
LC50 (96hr) pink shrimp, mysid shrimp 3.8-7.3 mg 1-1 (3).
LD50 topicallyChoristoneura uccidenfalisand Anugustu kuehniellu larvae 23-48pg g-1 (4).
Administration of 0.25,0.5, and 1ppm acephate to bees for 14days, caused a dose-dependent decreasein their
numbers (5).
LD50oral bee 1.2pg adult bee-1. Acephateclassifiedas a poison without amorphogenic effects(6).
Environmentalfate
Studies on the effectof acephate on growth and nitrogen fixationby Wesfiellopsinprolifica and Anabuena sp.
showed that low concentrationsof 1.0-50pg ml-1 enhanced growth, while higher concentrations were lethal to
organisms.Concentrations>5pg ml-1 decreased total nitrogen content (7).
Degradation studies
tl/2 in soil 7-10 days, methamidophos was identified as a metabolite.In plants residual activitylasted for 10-15
days (1).
Abiotic removal
50% hydrolysis occurred in 60 hr at pH 9 and 40°C and in 710 hr at pH 3 and 40°C (1).
Hydrolytic products formed at 37°Cand varying pH, included methamidophos, 0,s-dimethyl phosphorothiolate,
and 0-methyl acetylphosphoramidothiolate(8).
Acute data
LD50 oral mallard duck, ringneck pheasant 140-350mg kg-1 (1).
LD50 (24hr) oral littlebrown bats 197-1500mg kgl, prevented 9 of30 surviving bats from righting themselves
when placed on their backs 24 hr after dosing, initialsample size50. From this information the calculatedtoxicity
was ED50 687mg kg-1(9).
LD50 oral dog >681mg kg-1 (1).
LD50oral rat 866-945mg kg-1 (1).
LD50oral mouse 361mg kg-1 (1).
LD50percutaneous rabbit >2000mg kg-l(l).
Sub-acute and sub-chronic data
Mouse and meadow voles were fed 0-400 ppm acephate for 5 days. Brain and plasma cholinesteraseactivities
were reduced in a dose-dependent manner. Body, liver weight, plasma enzyme activitiesand cytochromecontent
were not affected (10).
The exposure of rats to 1or 10mg kg-1 ofacephate for 15wk, caused altered activity of the noncholinergicsystem
without altering the cholinergicactivity.The authors suggest that low level chronic exposure to
organophosphones cannot be predicted by measuring cholinesteraseor acetylcholinesteraseenzyme activities
(11).
In a 2-yr feeding trial, rats receiving30 mg kg-1 diet and dogsreceiving 100mg kg-1 diet showed depression of
cholinesterasebut no other significantside effects(1).
50 and 100mg kg-1 acephate administered orally to white-footedmice inhibited brain acetylcholinesterase
activity45% and 56% and reduced basal luteinisinghormone concentration29% and 25°/~,respectively,after 4 hr.
9

Dietary exposure to 25,100 and 400ppm inhibited brain acetylcholinesteraseactivitybut did not affectplasma
basal luteinising hormone. Reproductivefunction effectscould be possible (10).
Following an oral dose of acephate to mice, metabolicproducts detected in the liver up to 30 hr were
methamidophos, 0,s-dimethyl phosphoramidothiolate and S-methylacetylphosphoramidothiolate.Acephate
and methamidophos had inhibitory cholinesteraseeffectson mouse erythrocyte enzyme (8).
[W-acetyllacephate (40mg kg-1) was administered orally to pregnant rats on day 18 of gestation. The rats were
then killed after 10min and at 0.5,1,3,6,12,24 and 48 hr. At the end of48 hr, 22.83%of the dose was exhaledas
CO2with 1.25 and 0.6%being eliminated in the urine and faeces, respectively.Acephate was rapidly absorbed
and distributed in the tissues with the highest concentrationof radioactivitybeing found in the maternal stomach
followed by the liver. A total of 0.72%of the dose was recovered from the foetus (12).
Genotoxicity
Acephate produced gene conversionand mitotic recombinationin Saccharornyces cerevisiae and unscheduled DNA
synthesis in human fibroblastsin culture (13).
In vivo tests in the mouse showed significantenhancement in chromosomalaberrations, differencesin micronuclei
and sperm abnormalities in acephate-treated animals. In a dominant lethal assay in mice, dead implants were
significantlyhigher at wk 3 in treated animals (14).
The clastogenicpotential of acephate was evaluated in a chick in vivo test system using the chromosome
aberration assay in bone marrow cellsand the micronucleustest in bone marrow cellsand peripheral blood
erythrocytes.25,50 and 100mg kg-1 induced significantincreasesin micronucleiin both bone marrow and
peripheral blood erythrocytesfollowingintraperitoneal injection,but only 50mg kg-1 induced significantbone
marrow chromosomeaberrations after a 24 hr exposure (15).
At dose levelslimited by toxicity, negative results were observed for induction of sex-linked,recessive lethalityin
Drosophila melanogaster (16).
Acephate was positive in an assay for clastogenicity in Viciufuba (17).
Other effects
Inhalation and skin exposure to acephate was evaluated in four workers engaged in the formulation of 97%pure
technicalproduct. Urine content, erythrocyteand plasma cholinesteraselevelswere monitored. High correlation
was found between skin exposure level and urine elimination.One subjectwith urinary excretionlevelsbetween
3-8 mg 1-1 had slightly decreased values of plasma and erythrocytescholinesteraseactivities(18).
Field application of acephate did not have any adverse effect on a population of meadow vole, although brain
acetylcholinesteraseand plasma cholinesteraseactivitieswere depressed (19,20).
Investigationof inhibition in vitro of human erythrocyte,rat brain and insect acetylcholinesteraselevelsindicated
that acephate inhibits acetylcholinesterasein vitro in proportion to its toxicity in vivu (9,21).
Legislation
Limited under EC Directiveon Drinking Water Quality 80/778/EEC. Pesticidesand related products: maximum
admissibleconcentration 0.1pg 1-l' (22).
Included in Schedule6 (Releaseinto Land: Prescribed Substances)of Statutory Instrument No. 472,1991 (23).
Other cornments
Anticholinesteraseproperties of methamidophos and acephate in insects and mammals reviewed (14).
Acephate showed toxiceffectson carbohydrate metabolismin rats and inhibited electrontransfer in the
respiration of isolated mitochondria. The activityof cytochromec oxidase was severely inhibited at alkalinepH
(24).
10

References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
The PesticideManual 11th ed., 1997, BritishCrop Protection Council.
Zmkl, J. G. et a1 Bull Environ. Contam. Toxicol. 1987,38(1),22-28.
Rosli bin Mohamad,et a1Pertanika 1987,10(1),75-80.
Fiedler,L. Bull. Environ. Contam.Toxicol.1987,38(4), 594-601.
Atkins,E. L. et a11.Apic. Res. 1986,25(4),242-255.
Maharana,R. K. et a1 Geobios 1986,13(5), 185-188.
Chukwudebe,A. C. et a11.Environ. Sci. Health Part B 1984,198(6),501-522.
Clark,D. R. et a1Environ. Toxicol. Chem. 1987,6(9), 705-708.
Rattner, 8.A. et a1Toxicol. Lett. 1985,24(1),65-69.
Singh,A. K. et a1 Environ. Res. 1987,43(2),342-349.
Salama,A. K. et a11.Occup. Med. Toxicol. 1992,1(3), 265-274.
NTlS Report 1980, PB 80-133226,NationalTechnicalInformationService, Springfield,VA, USA.
Behera, 8.C.et a1Mutat. Res. 1989,223(3),287-293.
Jena,G. B. et a1Mutagenesis 1994,9(4), 319-324.
Carver,J. H. et a1 Toxicol. 1985,35(2), 125-142.
De Kergommeaux, J. et a1Mutat. Res. 1983,124(1),69-84.
Maroni,M.et a1Arch. Environ. Contam. Toxicol. 1990,19(5), 782-788.
Jett,D. A. Environ. Toxicol. Chem. 1986,5(3), 255-260.
Sykes,P.W. Jr.Condor 1985,87(3),438.
Hussain,M. A. Bull. Environ. Contam. Toxicol. 1987,38(1), 131-138.
EC Directive Relating to the Quality of Water Intendedfor Human Consumption 1982,80/778/EEC, Office for Official
Publicationsof the EuropeanCommunities,2 rue Mercier,L-2985Luxembourg.
S.1. 7991 No. 472 The Environmental Protection(Prescribed Processesand Substances) Regulations 1991, HMSO, London, UK.
Ando, M.Arch. Environ. Contam. Toxicol.1985,14(5),535-540
USEPA Report 1981, EPA 600/4-81-041.
A6 acetal
C6H1402 Mol. Wt. 118.18 CAS RegistryNo. 105-57-7
Synonyms acetaldehyde diethylacetal; 1,l-diethoxyethane; diethyl acetal; ethylidenediethylether
EINECS NO.203-310-6
Uses Solvent in synthetic perfumessuch asjasmine.Used in organicsynthesis,flavours.Formerly used as a
hypnotic.
RTECSNo. AB 2800000
Physical properties
M. Pt. -100°C B. Pt. 102.7"C Flash point -20.5"C Specific gravity 0.8254at20°Cwith respect to water at
4°C Volatility v.p.10mmHg at 8°C;v.den.4.10
Solubility Water:50 g 1-1. Organic solvents:diethylether, ethanol, ethyl acetate,heptane
UN No. 1088 HAZCHEMCode 3P1E Conveyanceclassificationflammable liquid
Supply classificationhighly flammable,irritant
Risk phrasesHighly flammable-Irritating to eyes and skin (R11,R36/38)
SafetyphrasesKeep out of reachof children(if sold to general public)-Keep containerin a well ventilated place
-Keep away from sourcesof ignition-No smoking-Take precautionarymeasures against static discharges (S2,
S9, S16,S33)
11

Acute data
LDm oral rat, rabbit, mouse 3500-4600mg kg-1 (1-3).
LC5o (4 hr) inhalation rat 4000 ppm (4).
Irritancy
Dermal rabbit (24hr) 10mg caused irritation and 500 mg instilled into rabbit eye caused irritation (4).
Other effects
Central nervous system narcotic in high doses (3).
Other comments
Reviewson physico-chemicalproperties, experimental toxicology and human health effectslisted (5).
References
1.
2. Med. u. Ernaehrung 1967,8,244.
3.
4.
5.
Proc. SOC.Exp. Biol. Med. 1903/ 1904,1,AcademicPress, New York, NY,USA.
Bhzina, A. Z. et a1 Gig.Sanit. 1977,3,12-15 (ChernAbstr. 88,32649b).
Smyth,H. F. et a1J. Ind. Hyg. Toxicol. 1949,31,60.
ECETOC Technical Report No. 71 1996,EuropeanCentre for Ecotoxicologyand Toxicologyof Chemicals,4 Avenue E. Van
Nieuwenhuyse (Bte6),B-1160 Brussels, Belgium
A7
PhysicaI
acetatdehyde
CH3CHO
C2H40 Mol. Wt. 44.05 CAS Registry No.75-07-0
Synonyms aceticaldehyde; ethanal; ethylaldehyde
EINECS NO.200-836-8
Uses In the manufacture of aniline dyestuffs, perfumes, flavours,plastics, synthetic rubbers and for silvering
mirrors and hardening gelatin fibres.
RTECS No. AB 1925000
properties
M. Pt. -123.5"C B. Pt. 20.2"C Flash point -27°C Specific gravity 0.783 at 20°C
Partition coefficient log Po, -0.40 (calc.)(1) Volatility v.p. 740 mmHg ;v.den. 1.52
Solubility Water:miscible. Organicsolvents: diethyl ether, ethanol
DE-MAK50ppm (91mg m-3)
FR-VME 100ppm (180mg m-3)
JP-OEL ceilinglimit 50 ppm (90mg m-3)
SE-LEVL25 ppm (45mg m-3)
UK-LTEL 20 pprn (37mg m-1)
US-STEL ceilinglimit 25 pprn (45mg m-3)
UN No. 1089 HAZCHEM Code 2YE Conveyance classification flammable liquid
SE-STEL50 ppm (90mg m-3)
UK-STEL 50 ppm (92mg m-1)
12

Supply classification extremelyflammable, harmful
Risk phrases Extremely flammable-Irritating to eyes and respiratory system-Possiblerisk of irreversibleeffects
(R12, R36/37, R40)
Safety phrases Keep out of reach of children (if sold to general public)-Keep away from sources of ignition-No
smoking -Take precautionary measures against static discharges-Wear suitable protective clothing and gloves
(S2,S16,S33,S36/37)
Ecotoxicity
Fish toxicity
LC50 (24hr) pinperch 70 mg 1-1 (2).
LC50 (96hr) bluegill sunfish 53mg 1-1 (3).
Cell multiplication inhibition test Uronernaparduczi 57mg 1-1 (4).
EC50 (48hr) Daphnia magna 9-14g 1-1 (5).
IC5*Saccharomycescerevisiae 230 mg 1-1 (6).
Environmentalfate
Degradation studies
67-97% degradation occurred in an anaerobicsystem (7,8).
Biodegradable(9).
A number of studies confirm the degradability of acetaldehydeby acclimated sludge. Someloss may be
attributed to volatilisation (10-14).
Abiotic removal
Photolytictl/2 8-16hr (calc.)(15).
Acute data
LD50 oral rat 1930mg kg-1 (6,16).
LD50 subcutaneous mouse 560mg kg'(6).
LD50 intravenous mouse 212 mg kg-l(l7).
Inadequate evidence for carcinogenicityto humans, sufficientevidence for carcinogenicityto animals, IARC
classificationgroup 2B (18).
Inhalation d,9 rat ( 9 8month) 0,1500 or 3000 pprn (6hr day-l,5 day wk-1) gradually reduced to 1000ppm
during the first 52 wk. Major compound-related effectsinclude increased mortality, growth retardation, nasal
tumours, and non-neoplasticnasal changesin each of the test groups. The treatment-related nasal changes
comprised: degeneration, hyperplasia, metaplasia,and adenocarcinomasof the olfactoryepithelium at all
exposure levels;squamous metaplasia accompaniedby slight to severekeratinisation and squamous cell
carcinomasof the respiratory epithelium at the two highest exposure levels; and slight to severe rhinitis and
sinusitis in the highest concentrationgroup of rats (19,20).
Long-terminhalation and intratracheal instillationstudies of acetaldehyde were carried out in Syrian hamsters.
Exposureto acetaldehyde vapour at a concentrationof 1500pprn resulted in epithelial hyperplasia and
metaplasia accompanied by inflammationin the nasal cavity and trachea.Extensive peribronchiolar adenomatoid
lesionsoften accompanied by inflammatorychanges occurred in the lungs after intratracheal instillationof
acetaldhyde. Therewas no evidenceof acetaldehyde possessing carcinogenicactivity (21).
Teratogenicity and reproductive effects
In mice caused decreased weight and abnormal closureof neural tube (17).
Rat malformations included microcephaly,micromelia and digital anomalies(22).
Rat embryos were explanted on days 9.5 or 10of gestation and cultured for30-48 hours in rat serum containing0,
10or 20 pgml-1 of acetaldehyde. Exposureof 9.5-day embryos to 20 pgml-1 resulted in looo%embryolethality
13

whereas 10pg ml-1 induced growth retardation and teratogenic effects.No effectswere seen when 10-day
embryos were exposed to 10pg ml-1(23).
Genotoxicity
Salmonella typhimuriurn TA98, TA100, TA1535, TA1537 with and without metabolicactivation negative (24).
Escherichiacoli PQ37 SOSchromotestwith and without metabolicactivation negative (25).
Escherichia coli K-12/343/113 DNA repair test without metabolicactivation negative (26).
Acetaldehyde produced chromosomalaberrations including chromosomal fragments, achromaticlesionsand
chromatid breaks in metaphases at 12hr and 24 hr in primary cultures of rat skin fibroblasts.Dose-related
increasesin aneuploidy were also observed (27).
Other effects
Human foetalhepatic cell line (WRL-68)cells (which do not express alcoholdehydrogenase or cytochromeP450
activity)were exposed for 120minutes to 10mM acetaldehyde. No celldeaths or morphological alterations were
observed by light microscopy.Lipid peroxidation values, measured as malondialdehyde production, were 60%
compared to control values and studies on cell proliferation,cell adhesion capacity,neutral red incorporation into
lysosomes,glutathione content, protein sulfhydryl compounds, lipid peroxidation, inner mitochondria1
membrane integrity,lactatedehydrogenase activityand ultrastructural alterations indicated that acetaldehyde
produced damage at the cellular level (28).
General narcotic. In humans large doses cause death by respiratory paralysis (29).
No health risks were found for workers exposed to acetaldehyde during the processing of heat shrinkable tubings
on telephone cables (30).
Other comments
Toxicity and hazards reviewed (31,32).
Reviews on exposure data, experimental toxicologyand human health effectslisted (33).
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
Hansch, C. et a1Med. Chem. Proj. 1981,No. 19,Pomona College,Claremont, CA, USA.
Garrett,J. T. et a1TexasI.Sci. 1951,3,391.
McKee,J. E. et a1Water Quality Criteria 1963,California State Water Quality Board.
Bringmann,G. et a1Z. WasserlAbwasserForsch. 1980,1,26.
Takahashi,I. T. et a1Bull. Environ. Contam. Toxicol. 1987,39,229-236.
Koch, H. P. et a1Meth. Find. Exp. Clin. Phurmacol. 1993,15(3),141-152.
Chou, W. L. et a1Biotech.Bioeng. Symp. 1979,8,391-414.
Selected BiodegradationTechniquesfor TreatmentAIltirnate Disposal of Organic Materials 1979,EPA 600/2-79-006.
MITI Report 1984, Ministry of International Trade and Industry, Tokyo,Japan.
Gerhold, R. M. et a11.WaterPollut. Control Fed. 1966,38,562-579.
Hatfield, R. Ind. Eng. Chem. 1957,49 192-196.
Heukelekian, H. et a11.WaterPollut. Control Fed. 1955,29,1040-1053.
Rogovskaya,T.et a1Inst. Vodosnakzh Kunaliz Gidrotekhn Sooruzhenii Inzh Gidrogeol1962,178-213 (Russ.)(Chem.Abstr. 57,
11659b).
Ludzach, J. R. et all. WaterPollut. Control Fed. 1960,32,1173-2000.
Weaver,J.Diss. Abstr. Int.B 1977,1976,37,3427.
Arch. Ind. Hyg. Occup.Med. 1951,4,199.
OShea, K. S. et all. Anat. 1979,128(1),65.
IARC Monograph 1987,Suppl. 7,77.
Wouterson,R. A. et a1Toxicology1986,41(2),213-231.
Eur.1.CancerClin. Oncol.1982,18,13.
Feron, V. J. Prog. Exp. Tumour Res. 1977,162.
Padmanabhan, R. et a1lndiun 1.Pharrnacol. 1982,14(3),247.
14

23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
Giavini, E. et a1In VitroCell. Dev.Biol.:Anim. 1992,28A(3,Part l),205-210.
Mortelmans, K. et a1Environ. Mof.Mutagen. 1986,8(Suppl.7), 1-119.
Mersch-Sundermann, V.et a1Mutagenesis 1994,9(3),205-224.
Hellmer,L. et a1Mutat. Res. 1992,272(2),145-160.
Bird, R. P. et a1Mutat. Res. 1982,101(3),237-246.
Olivares,I. P.et a1Toxicology1997,120(2),133-144.
TheMerck Index 12thed., 1996,Merck & Co., Inc., Whitehouse Station,NJ, USA.
Hoogesteger,J.J. Spec. Publ. -R. Soc. Chem. 1992,10B(CleanAir Work),73-76.
Izmerov, N. F. Scientific Reviews ofSoviet Literatureof Toxicity 6 Hazards of Chemicals1991,111, Eng. Trans.Richardson,M. L.
(Ed.),UNEP/IRPTC, Geneva, Switzerland.
BIBRA Toxicity Profile 1989,BritishIndustrial BiologicalResearch Asociation,Carshalton, UK.
ECETOC Technical Report No. 71 1996, European Centre for Ecotoxicology and Toxicologyof Chemicals,4 Avenue E. Van
Nieuwenhuyse(Bte6), 8-1160Brussels, Belgium
acetaldehyde formylmethylhydrazone
C4HSN20 Mol. Wt. 100.12 CAS Registry No. 16568-02-8
Synonyms acetaldehyde N-methyl-N-formylhydrazone;ethylidene gyromitrin; ethylidene methyl hydrazine
carboxaldehyde; gyromitrin
RTECS No. LQ 8500000
Occurrence Fungal toxin from falsemorels, Gyromitruspp.
PhysicaI properties
M.Pt. 5°C
Acute data
LD50oral rat, mouse 320-340 mg kg-1 (1,2).
LD50 oral rabbit 50 mg kg-1 (3).
LDL, (unspecifiedroute) human 10-20mg kg-1 (4).
TDL, (90 day) oral rabbit 5 mg kg-1 day-1 degeneration of liver observed (5).
TDL, (90 day)oral chicken0.5 mg kg-1 day1degeneration of liver, kidneys and heart observed (5).
No adequate evidence for carcinogenicity to humans, limited evidence for carcinogenicityto animals, IARC
classificationgroup 3 (6).
Acetaldehyde methylformylhydrazone administered 100pgg-1 wk-1 by intragastric instillations for 52wk in
mice, induced tumours of the lungs, preputial glands, forestomachand clitoral glands (6,7).
Target organs of carcinogenicity:mouse clitoralgland and stomach (8).
After oral administration of acetaldehyde formylmethylhydrazone to rabbits, rats and chickens,some of the
compound was excreted unchanged in the urine of rabbits (2).
At 37°Cunder acidicconditions (pH 1to 3), acetaldehyde formylmethylhydrazone is converted into
methylhydrazine a known tumour inducer in mice and hamsters via an intermediate, N-methyl-N-
formylhydrazine (9).
15

Other effects
Otheradverseeffects (human)
Poisoning of a family of four at an unspecifiedexposure level has been reported, toxic effects included liver injury,
seizures and haemolysis. Recoveryoccurred within 4-8 days (10).
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Mutat. Res. 1978,54, 167.
Makinen, S. M. et a1Food Cosmet. Toxicol. 1977,15(6), 575-578.
Pyysalo, H. Naturwissenschaften 1975,62,395.
Schmidlin-Meszaros, J. Mitt. Geb. Lebensmittelunters. Hyg. 1974,65,453.
Niskanen, A. et a1Food Cosmet. Toxicol. 1976,14(5), 409-415.
ZARC Monograph 1987, Suppl. 7,64,391.
Toth, B. et a11.Natl. Cancer Inst. 1981,67(4), 881-887.
Gold, L. S. et a1Mutat. Res. 1993,286(1), 75-100.
Nagel, D. et a1Cancer Res. 1977,37(9), 3458-3460.
Gamier, R. et a1 Toxicol.Eur. Res. 1978,1(6), 359-364
A9 acetaldoxime
CH3CH=NOH
CzHsNO Mol. Wt. 59.07 CAS RegistryNo. 107-29-9
Synonyms acetaldehyde oxime; aldoxime; ethanal oxime; ethylidine hydroxylamine
EINECSNO.203-479-6
Uses Chemicalintermediate. Corrosion inhibitor.
RTECSNo. AB 2975000
Physical properties
M. Pt. 47°C B. Pt. 115°C Volatility v.p. 18.9mmHg at 25°C
Solubility Water: 185g 1-1 at 25°C. Organic solvents:diethyl ether, ethanol
UN No. 2332 HAZCHEMCode 2Y Conveyanceclassification flammableliquid
Ecotoxicity
Bioaccumulation
The calculatedbioconcentrationfactor of 0.5 indicates that environmental accumulation is unlikely (1).
Environmentalfate
Carbonaceousinhibition
Acetaldoximewas utilised as a sole carbon sourceby one bacterium isolate and one fungus isolate obtained from
a silty clay soil (2).
Degradationstudies
Reduced to NOz- by Pseudornonas aeruginosa (3).
Soilmobility and leaching potential was predicted to be high (4,5).
16

Abiotic removal
The photolytic t1/2 of acetaldoximewas calculated to be 7.3days (5).
Acute data
LD50 interperitoneal mouse 100 mg kg-1 (6).
LD50 unspecified route mouse 115mg mg-1 (7).
References
1.
2.
3.
4.
5.
6.
7.
Lyman,W. J. et a1Handbook of ChemicalProperty Estimation Methods 1982,5-14, McGraw-Hill,New York, NY,USA.
Doxtader,K. G. et a1 Soil Sci. SOC.Am. Proc. 1966,30,351-355.
Amarger,N. et a1I.Bacteriol. 1968,95(5),1651-1657.
Swarm,R. L. et a1Res. Rev. 1983,85,16-28.
Hansch,C.et a1Medchem Project No. 26 1985, PomonaCollege,Claremont,CA,USA.
NTIS Report AD 277-689, Natl.Tech.Inf.Ser.,Springfield,VA, USA.
Freidman,A. L. Khim.-Farm. Zh. 1978,12(2), 88-92 (Russ.)(Chem.Abstr. 88,182874k)
AIO acetamide
CH3CONH2
C~HSNO Mol. Wt. 59.07 CAS RegistryNo. 60-35-5
Synonyms acetic acid amide; amide C2; ethanamide; methane carboxamide
EINECS NO.200-473-5
Uses Solvent,plasticiser and stabiliser.Alcohol denaturant.
PhysicaI properties
M. Pt. 79-81°C
Partitioncoefficient log Po, -1.26
Solubility Water: 2 kg 1-1. Organicsolvents:hot benzene, chloroform,ethanol, glycerol, pyridine
B. Pt. 222°C Specific gravity 1.159at 20°Cwith respect to water at 4°C
SE-LEVL 10ppm (25mg m-3)
Supply classification harmful
Risk phrasesPossiblerisk of irreversibleeffects (R40)
SafetyphrasesKeep out of reach of children (if sold to general public)- Wear suitable protective clothing and
gloves (S2, S36/37)
SE-STEL25 ppm (60mg m-3)
Ecotoxicity
Fish toxicity
LC50 (24-96hr) mosquito fish 26-13 g 1-1 (1).
Cell multiplication inhibition test,Microcystis aeruginosa 6200mg 1-1, Entosiphonsulcaturn 99 mg 1-1, Pseudornonas
putida >10,000mg kg-1 (2).
17

Environmentalfate
At 100mg 1-1 no inhibition of NH3 oxidation by Nifrosomonasspp. (3).
Mammalian& avian toxicity
Acute data
LD50intraperitoneal and subcutaneous rat 10g kgl(4).
No adequate data for evidence of carcinogenicityto humans, sufficientevidence for carcinogenicityto animals,
IARC classificationgroup 2B (5).
Administration of 2.5%acetamide (1yr) diet rats induced malignant liver tumours, hyperplastic nodules and
precancerouslesions (6).
Oral administration of acetamide induced benign and malignant liver tumours in rats and an increased incidence
of malignant lymphomas in a"mice (7-9).
Target organ of carcinogenicity:rat liver (10).
Genotoxicity
Salmonella fyphimurium TA98, TA100, TA1535, TA1537 with metabolicactivation negative (4).
EscherichiacoliK-12/343/113 DNA repair test with and without metabolicactivation negative (11).
Drosophila melanogasterwhite-ivory somaticmutation assay.Acetamide did not increasethe frequency of mutant
clones (12).
Drosophila melanogaster in vim (white/white+)eye mosaic assay inactive (13).
Acetamidewas inactive in morphologicaltransformation assays in mouse embryo cells (14).
Other comments
Acetamide, a known animal carcinogen, is discussed in relation to humans receivingmetronidazole therapy (15).
Human health effects, epidemiology, workplace experience,physico-chemical properties and experimental
toxicityreviewed (16J7).
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
Meinck, F. et a1Les Eaux ResiduairesIndustrielles 1970.
Bringmann,G. et a1Water Res. 1980,14,231-241.
Hockenbury,M. R.et a11.WaterPollut. Control Fed. 1977,49(5),768-777.
McCann, J. et a1Proc. Nut. Acad. Sci. USA 1975,72(12),5135-5139.
IARC Monograph 1987,Suppl. 7,56,389-390.
Weisburger, J.H.et a1Toxicol.Appl. Pharmacoll969,14,163-175.
IARC Monograph 1974,7,197-202.
Flaks,B. et a1Carcinogenesis1983,4,1117-1125.
Fleischman,R.W.et a11.Enuiron. Path. Toxicol.1980,3(5-6),149-170.
Gold, L.S.et a1Mutat. Res. 1993,286(1),75-100.
Hellmer,L.et a1Mutat. Res. 1992,272(2),145-160.
Batiste-Alentom,M. et a1Enuiron. Mol. Mutagen. 1994,24(2),143-147.
Vogel,E.W.et a1Mutagenesis 1993,8(1),57-81.
Patierno, S.R.et a1CancerRes. 1989,49(4),1038-1044.
Koch, R.L.et a1Science 1981,211(4488),398-400.
BIBRA Toxicity Profile 1989,British IndustrialBiologicalResearchAssociation,Carshalton, UK.
ECETOC Technical Report No. 72 1996,European Centre for Ecotoxicology and Toxicology of Chemicals,4AvenueE. Van
Nieuwenhuyse (Bte6))1160-Brussels,Belgium
18

AII acetanilide
NHCOCH3
I
Physical
CsHgNO Mol. Wt. 135.17 CAS RegistryNo. 103-84-4
Synonyms acetylaminobenzene; acetylaniline; N-phenylacetamide
EINECS NO.203-150-7
Uses Manufacture of medicinals and dyestuffs.An antipyretic and analgesic.Used as a stabiliser for peroxide
solutions and as an additive to celluloseester varnishes.
RTECS No. AD 7350000
properties
M. Pt. 114-115°C B. Pt. 304-305°C Flash point 173°C(open cup) Specificgravity 1.2105at 4°C with respect
to water at 4°C Partition coefficient log Po, 1.16 Volatility v.p. 1mmHg at 114°C;v.den.4.65
Solubility Water: 5 g1-1. Organicsolvents:benzene, chloroform,diethyl ether, ethanol
Ecotoxicity
Fish toxicity
LCg (96hr) bluegill sunfish 100mg 1-1 (40%survival in staticbioassay at 23°C) (1).
LC50 (96 hr) inland silverside 115mg 1-1 (100-20% survival in staticbioassy at 23°C) (1).
IC50 Saccharornyces cerevisiae 109mg 1-1 (2).
Bioaccumulation
Bioconcentrationfactorin goldfish 1.2 (3).
Environmentalfate
Degradationstudies
Confirmed biodegradable (4).
BOD10 1.20mg 1-1 oxygen using standard dilute sewage (5).
94% COD at 14.7mg CODg dry inoculum-1hrl at 20°C in an activated sludge system using the substance as sole
carbon source.With influent of 50 mg 1-1 and 365+days acclimation50% COD at 20°C was recorded in a
observation period of 10days, at a concentrationof 600-1000 mg 1-1 and under similar conditions inhibitionwas
reported (6).
Aryl acylamineamidohydrolase (EC3.5.1),isolated from Aspergillus nidulans shows activity to acetanilide.Enzyme
activity occurs over a range of pH values between 7.8 and 10.2(7).
Acute data
LD50 oral rat 800mg kg-1 (2,8).
LD50oral dog 500 mg kg-f (9).
LD50oral mouse 1210mg kg-1 (2).
LD50 oral d,9 rat 594-4350mg kgl(l0).
19

LD50 intraperitoneal mouse 500 mg kg-1 (11).
Classifiedas harmful using the acute-toxic-classmethod, an alternative to the LD50 test (10).
LDL, (1hr intermittently) oral human 56mg kg-1 central nervous system and gastrointestinal effects(12).
Acetanilideis readily excreted in the urine as sulfate and glucuronide conjugates (13).
>99.9%of acetanilideremains un-ionised at body pH, facilitatingabsorption from blood to cerebrospinalfluid
(14).
Readily absorbed from the gastrointestinal tract (15).
In healthy subjectsgiven acetanilide orally at concentrations of 50 mg kg-1, plasma clearancevalues varied from
12-25ml h r l (16).
Other comments
Acetanilidehas been replaced by safer analgesics(17).
Reviews on human health effects, experimental toxicology, environmental effects,ecotoxicologyand exposure
levelslisted (18).
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
Dawson, G. et a1J.Hazardous Materials 1975/77,1,303-318.
Koch, H. I? et a1Meth. Find. Exp. Clin. Pharrnacol.1993,15(3), 141-152.
Nakatsugawa, T. et a1Environ. Toxicol. Pesticides 1972,Matsumura, F. (Ed.),Academic Press.
MlTl Report 1984, Ministry of International Tradeand Industry, Tokyo, Japan.
Mills, E. J. et a1Proc. 8th Purdue Ind. WasteCon$ 1953,492.
Ludzack, F. J. et a1J. Hazardous Materials 1975/77,1.
Pelsy, F. et a1Pestic. Biochem.Physiol. 1987,27(2), 182-188.
J. Pharm. Exp. Ther. 1935,54,159.
Abdernelden’s Handbuch der Biologischen Arbeitsmethoden 1935,4,1290.
Schlede,E. et a1Arch. Toxicol.1992,66(7), 455-470.
NTIS Report AD 277-689, National TechnicalInformation Service,Springfield, VA, USA.
Am. J.Med. Sci. 1901,122,770.
Patty,F.A. Industrial Hygiene and Toxicology2nd ed., 1963,1835, IntersciencePublishers, New York, NY, USA.
LaDu, B. N. et a1Fundamentals of Drug Metabolism and Disposition 1971,82, Williams& Wilkins,Baltimore, MD, USA.
Thienes C. et a1Clinical Toxicology5th ed., 1972, Lea & Febiger, Philadelphia, PA, USA.
Cunningham, J. L. et a1Eur. 1.Clin. Pharmacol.1974,7(6), 461.
Martindale: The Extra Pharmacopoeia 31st ed., 1996,The Royal Pharmaceutical Society,London, UK.
ECETOC Technical Report No. 72 1996, European Centre for Ecotoxicology and Toxicology of Chemicals,4 Avenue E. Van
Nieuwenhuyse (Bte6), 8-1160 Brussels, Belgium
~ 1 2 acetic acid
C2H402 Mol. Wt. 60.05 CAS Registry No. 64-19-7
Synonyms ethanoic acid; ethylic acid; glacial acetic acid; methanecarboxylicacid; vinegar acid
EINECS NO.200-580-7
Uses In the manufacture of various acetates and acetyl compounds. In plastics, rubber, tanning, printing and
dyeing silks.An acidulant and preservative in foods and a solvent for gums, resins, volatile oils.
RTECS No. AF 1225000
20

PhysicaI properties
M. Pt. 17°C B. Pt. 118°C Flashpoint 39°C (closedcup) Specific gravity 1.049at 25°C with respect to water
at 25°C
Solubility Water:miscible.Organicsolvents:acetone, benzene, diethyl ether, ethanol
Volatility v.p. 11.4mmHg at 20°C ;v.den. 2.07
DE-MAK 10pprn (25mg m-3)
FR-VLE10pprn (25 mg m-3)
JP-OEL10ppm (25 mg m-3)
SE-LEVL5 ppm (13mg m-3)
UK-LTEL10ppm (25mg m-3)
US-TWA10ppm (25mg m-3)
UN No. 2789 (glacialor solutions SOYO)
UN No. 2790 (solutions >lo%580%)
(solutions>lo%580%) Conveyanceclassificationcorrosivesubstance
Supply classification corrosive
Risk phrasesFlammable-Causes severeburns (R10, R35)
SafetyphrasesKeep locked up and out of the reach of children (if sold to general public) -Do not breathe vapour
-In case of contactwith eyes,rinse immediatelywith plenty of water and seek medical advice -In case of
accident or if you feel unwell, seek medical advice immediately (show label where possible) (S1/2, S23,S26,S45)
SE-STEL10pprn (25mg m-3)
UK-STEL 15ppm (37mg m-3)
US-STEL15pprn (37mg m-3)
HAZCHEM Code 2P (glacialor solutions 230%) HAZCHEM Code2R
Ecotoxicity
Fish toxicity
LC50 (96hr) bluegill sunfish 75mg 1-1 (1).
LC50 (96hr) fathead minnow 88mg 1-1 staticbioassay 18-22°C(2).
LC50 (24 hr) goldfish 423 mg 1-1. Period of survival (48-96hr) 100mg 1-1 at pH 6.8; period of survival (96hr) 10mg
1-1 at pH 7.3 (3).
EC50 (24-48hr) Daphnia magna, brine shrimp 47-32mg 1-1 (1,4).
Cell multiplication inhibition test Microcystisaeruginosa 90 mg 1-1, Scenedesmus quadricauda4000 mg 1-1, Entusiphon
sulcatum 78 mg 1-1, Urunemaparduczi 1350mg 1-1 (2,5).
Bioaccumulation
Acetic acid shows no potential for biologicalaccumulationor food chain contamination (6).
EnvironmentaI fate
Nitrificationinhibition
The effect of aceticacid on the nitrification activityof activated sludge was studied in laboratory batch
experiments. The critical concentrationat which activityceased was 115mM-aCetiC acid (7).
Carbonaceousinhibition
Cell multiplication inhibition test, Pseudurnonas putida 2850 mg 1-1 (8)
Degradationstudies
Biodegradable(9).
BOD10 82% reduction dissolved oxygen in fresh water and 88%reduction dissolved oxygen in seawater at 20°C
ThOD540% 24 hr incubation activated sludge (4).
BOD values:0.556 using a BOD biosensor; 0.34-0.88using a conventional5-day method (10).
(1).
21

Acute data
LD50 oral rat 3310mg kg-1 (11).
LC50 (1hr) inhalation guinea pig 5000ppm (12).
LD50 dermal rabbit 1060mg kgl(l3).
A single 50 p1 intratesticular injectionof 36% aceticacid produced sterility in male rats (14).
Sucklingrats were given 0.3 g 1-1 aceticacid in drinking water from parturition until the pups were 18days old.
Offspringexposed to acetic acid were less activeand showed significantweight gain compared to controls(15).
Acetic acid applied repeatedly to the skin of papilloma-bearing mice resulted in an increased incidenceof skin
cancer (16).
Irritancy
Exposurecan causebums to skin and eye irritation (17).
The irritancy of acetic acid was evaluated using the chickenenucleated eye test. The compound had a moderate
effect on corneal swelling and a severe effect on comeal opacity and fluoresceinretention (18).
Genotoxicity
Salmonella typhimuriumTA97, TA98, TA100, TA1535, TA1537with and without metabolic activation negative
(19,20).
Escherichia coIi PQ37 SOS chromotestwith and without metabolicactivation negative (21).
A single application of acetic acid to mouse epidermis induced a sustained stimulation of DNA, RNA and protein
synthesis, indicating that aceticacid acted as a promoting agent (22).
Other effects
Chronicexposure may cause erosionof dental enamel and bronchitis. Ingestion may cause severe corrosion of
mouth and gastrointestinal tract with vomiting, haematemesis, diarrhoea, circulatorycollapse,uremia and death
(speciesunspecified) (17).
0ther comments
The toxicity of aceticacid has been reviewed (23).
Reviews on human health effects,experimental toxicology, physico-chemicalproperties, epidemiology,workplace
experience,ecotoxicologyand environmental effectslisted (24).
Incompatiblewith carbonates,,hydroxides, oxides, phosphates. Corrosive.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
Price,K. S.I. WaterPollut. Control Fed. 1974,46,1.
Mattson, V. R. et a1Acute Toxicity of Selected Organic Compounds to Fathead Minnows 1976, EPA 600/3-76-097.
Ellis,M. M. Detection and Measurement of Stream Pollution 1937,US Dept of Commerce,Bureauof Fisheries.
Elkins,H. F. et a1Sewage Ind. Wastes 1956,28(12), 1475.
Bringmann, G.et a1 WaferRes. 1980,14,231-241.
Environment Canada,Tech.Info.for Problem Spills on Acetic Acid Draft 1981,1,76.
Eilersen,A. M. et a1 Water Res. 1994,28(6), 1329-1336.
Bringmann,G. et a1Z. Wasser/Abwasser Forsch. 1980, (l),26-31.
MITl Report 1984,Ministry of International Trade and Industry, Tokyo,Japan.
Li, Y.-R.et a1Appl. Biochem.Biotechnol.1991,28-29,855-863.
UnionCarbideData Sheet 1963, UnionCarbide Corp.,New York, NY,USA.
Verschuern,K. Handbook of Environmental Data on Organic Chemicals 1983, Van Nostrand Reinhold,New York, NY, USA.
Am. lnd. Hyg. Assoc. J. 1972,33,624.
22

14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
Freeman,C. et a1Fertility Sterility 1973,24,884-890.
Barrett, J.et a1Neurobehuviord Toxicol. Terutol. 1982,4,105-108.
Rotstein,J.B. et a1CancerLett. 1988,42(1-2),87-90.
The Merck lndex 12thed., 1996,Merck & Co. Inc., WhitehouseStation,NJ,USA.
Prinsen, M. K. et a1Food Chem. Toxicol.1993,31(1),69-76.
Zeiger, E. et a1Environ. Mol. Mutagen. 1992,19(Suppl. 21), 2-141.
McCann, J. et a1Proc. Nut. Acud. Sci. 1975,72(12),5135-5139.
Mersch-Sundermann,V. et a1Mutugenesis 1994,9(3),205-224.
Slaga, T.J. et a1J. Natl. CancerInstit. 1975,55(4),983-987.
BlBRA Toxicity ProFle 1990,British Industrial Biological Research Association, Carshalton, UK.
ECETOC Technical Report No. 72 1996,European Centre for Ecotoxicologyand Toxicology of Chemicals,4 Avenue E. Van
Nieuwenhuyse (Bte6), B-1160 Brussels, Belgium
A I ~ acetic anhydride
C4H603 Mol. Wt. 102.09 CAS RegistryNo. 108-24-7
Synonyms acetic acid, anhydride; aceticoxide; acetyl anhydride; acetylether; acetyl oxide; ethanoic
anhydrate
EINECS NO.203-564-8
Uses Manufacture of acetylcompounds and celluloseacetate fibres and plastics.An acetylating agent and solvent
in examining wool, fat, glycerol,fatty and volatileoils, resins. Widely used in organic synthesis. A dehydrating
agent and acetylatingagent in the production of pharmaceuticals,dyestuffs,perfumes and explosives.
RTECS No. AK 1925000
Physical properties
M. Pt. -73°C B. Pt. 139°C Flashpoint 49°C (closedcup) Specific gravity 1.082at 20°C with respect to
water at 4°C Volatility v.p. 3.5mmHg at 20°C ;v.den. 3.52
Solubility Organicsolvents:misciblewith acetone, diethyl ether, ethanol;soluble in benzene, chloroform,
dimethyl sulfoxide
OccupationaI exposure
DE-MAK 5ppm (21mg m-3)
JP-OELceilinglimit 5ppm (21mg m-3) UK-STEL5 ppm (21mg m-3)
US-TWA5 pprn (21mg m-3)
UN No. 1715 HAZCHEMCode 2W Conveyanceclassification corrosivesubstance, danger of fire (flammable
liquid)
Supply classification corrosive
Risk phrasesFlammable-Causesburns (R10, R34)
SafetyphrasesKeep locked up and out of the reach of children (ifsold to general public) -In case of contactwith
eyes, rinse immediately with plenty of water and seek medicaladvice-In case of accident or if you feel unwell,
seek medical advice immediately (showlabel where possible) (S1/2, S26, S45)
FR-VLE5 pprn (20mg m-3)
SE-CEIL5 ppm (20mg m-3)
Ecotoxicity
Fish toxicity
Aquatic toxicityrating, designated non-toxic to trout, bluegill sunfish and goldfish (1).
23

Cell multiplication inhibition test, Pseudomonas putidu 1150mg 1-1, Scenedesmus quadricuuda 3400 mg 1-1, Chlorella
pyrenoidosa 360 mg 1-1, Entosiphon sulcatum 30 mg 1-1 (2,3).
Acute data
LD50 oral rat 1780mg k g 1 (4).
LD50 dermal rabbit 4000 mg kg-1 (5).
LC50 (4hr) inhalation rat 1000ppm (6).
Imtancy
10mg applied to rabbit skin for 24 hr caused mild irritation, 250 pg instilled in rabbit eye caused severeirritation
(4).
Skin, eye and upper respiratory tract irritant (7).
May cause dermatitis and occasionalsensitisation (8).
Genotoxicity
Salmonella typhimurium TA98, TA100, TA1535, TA1537with and without metabolic activation negative (9).
Other effects
Other adverseeffects (human)
Workersexposed to (undetermined) high vapour concentrationsreported burning sensations in nose and throat
and dyspnoea (10).
Can cause bronchial and lung injury (11).
Lachrymatorand may cause conjunctivaloedema and corneal burns. Temporary or permanent interstitial
keratitis with corneal opacity and loss of vision have been reported (12).
Other comments
Physical and chemical properties, hazards and current French legislation on aceticanhyride reviewed (13).
Reviews on experimental toxicologyand human health effectslisted (14).
Reacts with water to form aceticacid (9.v.).Explosion risk.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
Wood, E. M. Toxicity of 3400 Chemicals to Fish 1987,EPA 560/6-87-002, PB 87-200-275.
Bringmann,G.et a1 Water Res. 1980,14,231-241.
Jones,H. R. Environmental Control in the Organic and Petrochemical Industries 1971,Noyes Data Corporation, New York, NY,
USA.
Arch. lnd. Hyg. Occup. Med. 1951,4,119.
Union Carbide Data Sheet 1963,Union Carbide Corp., New York, NY, USA.
Deichmann, W. B. Toxicologyof Drugs and Chemicals 1969,AcademicPress, New York, NY, USA.
ChemicalSafety Data Sheets 1990,3,11-15,The RoyalSocietyof Chemistry,London, UK.
Fassett,D. W. et a1Toxicology1963,2,Wdey-Interscience,New York, NY, USA.
Mortelmans, K. et a1Environ. Mutagen. 1986,8(7),1-119.
Am. Ind. Hyg.Assoc. I. 1971,32,64.
Henderson, Y. et a1Noxious Gases 1943,129,Van Nostrand Reinhold,New York, NY, USA.
Colman,J. P. et a1Inorg. Synth. 1963,7,205-207.
Cah.Notes Doc. 1986,125,593-596.
ECETOC Technical Report No. 72 1996,European Centre for Ecotoxicology and Toxicology of Chemicals, 4 Avenue E. Van
Nieuwenhuyse (Bte6),8-1160 Brussels,Belgium
24

AM acetochlor
COCH2CI
"'
CH3CH20CH2
C14H20C1N02 Mol. Wt. 269.77 CAS Registry No. 34256-82-1
Synonyms 2-chloro-N-(ethoxymethyl)-N-(2-ethyl-6-methylphenyl)acetamide;2-chloro-N-ethoxymethyl-6'-
ethylacet-o-toluidide
EINECS NO.251-899-3
Uses Herbicide.
Physical properties
M. Pt. 0°C
Solubility Water:223mg 1-1 at 25°C. Organicsolvents:acetone, benzene,diethylether,ethanol,ethylacetate,toluene
Ecotoxicity
Fish toxicity
LC50 (96hr) rainbow trout, bluegill sunfish 0.5,1.3mg 1-1, respectively (1).
EC50 (48hr) Daphnia 16mg 1-1 (1).
LD50,1.715mg bee-1 (1).
Environmentalfate
Degradation studies
Microbialdegradation accounts for most loss from soil (2).
Abiotic removal
Stronglyabsorbed by soil (1).
Acute data
LD50 oral bobwhite quail 1590mg kg-1 (1).
LD50 oral rat 1063-2183mg kg-1 (2,3).
LD50 percutaneous rabbit 4166 mg kg-1(2).
Oral rat (42day) 10-50mg kg-1 administered 5 day wk-1 caused changesin enzyme activity, including
cytochromeoxidase, lactate dehydrogenase and glucose-6-phosphatedehydrogenase, suggesting adverse effects
on mitochondria1metabolicfunction (3).
Oral rabbit (12 month) 0.3-30mg kg-1 induced atheroscleroticchanges in aorta. Simultaneous administration of
cholesterol and acetochlorinduced more severechanges than single administration of either compound (4).
Rats were given 2000 mg kg-1 of acetochlor (route unspecified).Severebody weight loss and some deaths
occurred. In addition reduced implantation and pregnancy rates were observed at 18-25days post-dosing. The
ova of 9 rats mated with a"rats exposed to acetochlor revealed a lack of fertilisation at 18-25days (5).
25

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