Introduction
National Industrial Chemicals Notification and
Assessment Scheme
Alkyl Phosphate Anti-Valve Seat
Recession Additive
_________________________________________
Priority Existing Chemical
Assessment Report No. 25
July 2003
Chemical
i
Commonwealth of Australia 2003
ISBN 0-9750516-8-7
This work is copyright. Apart from any use as permitted under the Copyright Act 1968,
no part may be reproduced by any process without prior written permission from the
Commonwealth available from the Department of Communications, Information
Technology and the Arts. Requests and inquiries concerning reproduction and rights
should be addressed to the Commonwealth Copyright Administration, Intellectual
Property Branch, Department of Communications, Information Technology and the
Arts, GPO Box 2154, Canberra ACT 2601 or posted at http://www.dcita.gov.au/cca .
Priority Existing Chemical Assessment Report Number 25
ii
Preface
This assessment was carried out under the National Industrial Chemicals Notification and
Assessment Scheme (NICNAS). This Scheme was established by the Industrial Chemicals
(Notification and Assessment) Act 1989 (Cwlth) (the Act), which came into operation on
17 July 1990.
The principal aim of NICNAS is to aid in the protection of people at work, the public and the
environment from the harmful effects of industrial chemicals.
NICNAS assessments are carried out in conjunction with Environment Australia which carry
out the environmental assessments.
NICNAS has two major programs: the assessment of the health and environmental effects of
new industrial chemicals prior to importation or manufacture; and the other focussing on the
assessment of chemicals already in use in Australia in response to specific concerns about their
health/or environmental effects.
There is an established mechanism within NICNAS for prioritising and assessing the many
thousands of existing chemicals in use in Australia. Chemicals selected for assessment are
referred to as Priority Existing Chemicals.
This Priority Existing Chemical report has been prepared by the Director (Chemicals
Notification and Assessment) in accordance with the Act. Under the Act manufacturers and
importers of Priority Existing Chemicals are required to apply for assessment. Applicants for
assessment are given a draft copy of the report and 28 days to advise the Director of any errors.
Following the correction of any errors, the Director provides applicants and other interested
parties with a copy of the draft assessment report for consideration. This is a period of public
comment lasting for 28 days during which requests for variation of the report may be made.
Where variations are requested the Director's decision concerning each request is made
available to each respondent and to other interested parties (for a further period of 28 days).
Notices in relation to public comment and decisions made appear in the Commonwealth
Chemical Gazette.
In accordance with the Act, publication of this report revokes the declaration of this chemical as
a Priority Existing Chemical, therefore manufacturers and importers wishing to introduce this
chemical in the future need not apply for assessment. However, manufacturers and importers
need to be aware of their duty to provide any new information to NICNAS, as required under
section 64 of the Act.
For the purposes of Section 78(1) of the Act, copies of assessment reports for New and Existing
Chemical assessments may be inspected by the public at the library of the National
Occupational Health and Safety Commission (NOHSC). Summary Reports are published in the
Commonwealth Chemical Gazette, which are also available to the public at the NOHSC library.
Copies of this and other Priority Existing Chemical reports are available on the NICNAS
website. Hard copies are available free of charge from NICNAS either by using the prescribed
application form at the back of this report, or directly from the following address:
iii
Alkyl Phosphate AVSR Additive
GPO Box 58
Sydney
NSW 2001
AUSTRALIA
Tel: +61 (2) 8577 8800
Fax: +61 (2) 8577 8888
Freecall: 1800 638 528
Other information about NICNAS (also available on request and on the NICNAS web
site) includes:
? NICNAS Service Charter;
? information sheets on NICNAS Company Registration;
? information sheets on the Priority Existing Chemicals and New Chemical assessment
programs;
? safety information sheets on chemicals that have been assessed as Priority Existing
Chemicals;
? details for the NICNAS Handbook for Notifiers; and
? details for the Commonwealth Chemical Gazette.
More information on NICNAS can be found at the NICNAS web site:
http://www.nicnas.gov.au
Other information on the management of workplace chemicals can be found at the web
site of the National Occupational Health and Safety Commission:
http://www.nohsc.gov.au
Priority Existing Chemical Assessment Report Number 25
iv
Overview
Anti-valve seat recession (AVSR) fuel additives were declared as Priority Existing Chemicals
for full assessment under the Industrial Chemicals (Notification and Assessment) Act 1989 on
5 December 2000. They were nominated because of health and environmental concerns due to
their increasingly widespread use in automotive lead replacement petrol (LRP). This report
concerns the alkyl phosphate additive which is one of four AVSR additives which have been
notified for assessment: methylcyclopentadienyl manganese tricarbonyl-, phosphorus-, sodium-
and potassium-based AVSR additives.
AVSR fuel additives are available for both industrial and consumer use. They are delivered
either by oil companies pre-blending them into unleaded petrol (ULP) (known as bulk LRP
addition) or by the vehicle owner purchasing and adding them to ULP (known as aftermarket
addition).
The alkyl phosphate additive is manufactured in Australia for export and domestic bulk LRP
formulation and imported as two aftermarket alkyl phosphate additive products
(Valvemaster).
The scope of the alkyl phosphate additive assessment of toxicity in this report is limited to that
of the kerosene-based product DMA-4, which contains the alkyl phosphate additive in the range
70-90% and is synonymous with the alkyl phosphate additive product manufactured in
Australia. Environmental and health hazards addressed in this report also relate to phosphoric
acid, which is the postulated combustion by-product of the alkyl phosphate additive.
The natural attrition of older cars requiring AVSR additives means a decreasing AVSR additive
market and consequently, the use of AVSR additives including the alkyl phosphate additive is
likely to decline with time. The production of, and infrastructure support for, LRP will
eventually become economically unviable and aftermarket addition of AVSR additives will be
the sole method of providing valve seat protection through fuel. This report considered the
occupational health and safety, public health and environmental consequences of two separate
scenarios for the use of the alkyl phosphate additive ?a "Present Use" scenario assuming 100%
market share and present delivery modes and levels of demand and a "2004" scenario assuming
attrition of the AVSR additive vehicle fleet, with reduced demand and delivery of the alkyl
phosphate additive via aftermarket addition only.
Based on limited data, the alkyl phosphate formulation DMA-4 (synonymous with
Valvemaster Concentrate) has low acute aquatic toxicity. Spill incidents and leaks to water
bodies and land should be managed through existing Federal, State and Territory legislative
frameworks and protocols to mitigate adverse effects to the environment. Such accidental
incidents may potentially occur during shipment into and out of Australia, bulk transport,
handling and storage.
Use of the alkyl phosphate in internal combustion engines and subsequent degradation through
combustion indicate that aquatic and terrestrial organisms are unlikely to be exposed to the
active component (the alkyl phosphate additive) or the proposed exhaust emission of the
combustion derivative, phosphoric acid, at or above levels of concern. A low environmental
risk is, therefore, predicted.
Phosphorus, which is found in the alkyl phosphate additive products, is naturally occurring and
ubiquitous in the environment. It is an essential nutrient of plants and animals. Phosphorus
v
Alkyl Phosphate AVSR Additive
pollution, leading to eutrophication and nuisance algal blooms in aquatic ecosystems, is a major
environmental issue in Australia, and in general, phosphorus reduction in waterways is the
current Australian policy direction. Even so, the predicted incremental increase in phosphorus
in the environment from use of fuels containing the alkyl phosphate AVSR additive is unlikely
to develop to levels of concern to aquatic environments given the current use and declining
future use pattern of AVSR additives. The findings of this assessment have not identified any
significant risk to the environment given the current use pattern of fuels containing the alkyl
phosphate AVSR additive.
Mammalian toxicity studies of DMA-4 indicate low acute toxicity by oral or dermal exposure
and possible irritant effects. The inclusion of kerosene in the formulation can not be discounted
as a contributing factor to the irritancy effects. There are insufficient toxicology data for
classification of DMA-4 in accordance with the NOHSC Approved Criteria for Classifying
Hazardous Substances. The inclusion of kerosene in the alkyl phosphate additive presents
health hazards such as irritation and lung damage (if swallowed).
As the alkyl phosphate additive is combusted to phosphoric acid, the health hazards associated
with the use of the alkyl phosphate additive also include those associated with phosphoric acid.
The critical effects from exposure to phosphoric acid relate to its acidic nature and hence
corrosive/irritancy effects. The severity of the symptoms for the eye, skin or pulmonary
irritation depends, however, on the concentration and length of exposure to the acid.
Minimal occupational exposure to the alkyl phosphate additive is likely for workers involved in
the manufacture of the alkyl phosphate additive, manufacture and distribution of LRP or
aftermarket fuel additives, and automotive maintenance. Overall, the conclusion is that there is
a low occupational risk associated with the alkyl phosphate additive. While dermal exposure to
the aftermarket product may potentially cause irritation, such an effect is confounded by the
presence of kerosene, which is a known irritant. Occupational exposure is expected to be
infrequent, minor and of short duration.
Where automotive usage is ubiquitous, chronic inhalation of phosphoric acid may result, e.g.
service stations, car parks and workshops, and particularly in work spaces that are enclosed or
poorly ventilated. In the absence of Australian occupational exposure data, a worst-case
scenario was considered for phosphoric acid exposure of such workers. This exposure was
assessed as low and hence, of low risk.
The public risk of acute dermal reactions in consumers to the aftermarket products is considered
low given the small amounts of additive to which people are likely to be exposed and the fact
that any spill on the skin is unlikely to remain untreated for long periods.
The potential for acute health effects from the alkyl phosphate additive could occur as a result
of accidental ingestion of LRP by adults, e.g. when siphoning LRP, or by children. The health
risk following acute accidential ingestion of the alkyl phosphate additive in LRP was
considered low. This is because of the low level of the alkyl phosphate additive in LRP and
low acute oral toxicity of the alkyl phosphate additive. Accidental ingestion of the alkyl
phosphate additive via the aftermarket products similarly does not represent a significant acute
health risk for children by virtue of the alkyl phosphate additive content. Ingestion of other
constituents such as kerosene and solvent naptha, however, may represent specific heath effects.
Chronic inhalation scenarios were considered for phosphoric acid exposure by the public as a
result of the use of the alkyl phosphate additive in LRP. Overall, the public health risks
associated with phosphoric acid exposure from the alkyl phosphate additive's combustion in
LRP were assessed as low.
Priority Existing Chemical Assessment Report Number 25
vi
While there is insufficient toxicology data for classification of the alkyl phosphate additive and
its kerosene-based products, the data gaps are not regarded as significant impediments to an
adequate assessement of the risks associated with the current use of the alkyl phosphate additive
in LRP.
vii
Alkyl Phosphate AVSR Additive
Contents
PREFACE III
OVERVIEW V
CONTENTS VIII
ACRONYMS AND ABBREVIATIONS XIII
1. INTRODUCTION 1
1.1 Declaration 1
1.2 Objectives 1
1.3 Sources of information 1
1.4 Peer review 2
2. BACKGROUND 3
2.1 What is an anti-valve seat recession additive? 3
2.2 International perspectives 4
2.3 Australian perspective 4
2.4 Assessment by other national or international bodies 5
3. APPLICANTS 6
4. CHEMICAL IDENTITY AND COMPOSITION 7
4.1 Chemical identity 7
5. PHYSICAL AND CHEMICAL PROPERTIES 8
5.1 Physical state 8
5.2 Chemical properties 9
5.3 Physico-chemical hazards 9
6. METHODS OF DETECTION AND ANALYSIS 10
6.1 Identification 10
6.2 Atmospheric monitoring methods 10
6.3 Biological monitoring methods 10
7. MANUFACTURE, IMPORTATION AND USE 11
7.1 Manufacture and importation 11
7.2 Uses 12
Priority Existing Chemical Assessment Report Number 25
viii
7.3 Demand for anti-valve seat recession additives 12
7.4 AVSR use scenarios 14
7.5 Use scenarios for the alkyl phosphate additive 15
7.6 Methods of use 16
8. EXPECTED ALKYL PHOSPHATE ADDITIVE COMBUSTION EMISSIONS 18
8.1 Introduction 18
8.1.1 Equilibrium Computational Model 18
8.1.2 Predicted tailpipe emission levels of phosphoric acid 19
8.1.3 Further consideration of alkyl phosphate by-products in
tailpipe emissions 19
8.2 Summary of findings 22
9. EXPOSURE 23
9.1 Environmental exposure to the alkyl phosphate additive 23
9.2 Exhaust release from combustion of the alkyl phosphate additive 25
9.3 Fate 25
9.3.1 Phosphorus biogeochemical cycle 26
9.3.2 Environmental biodegradation and bioaccumulation 27
9.3.3 Landfill disposal and fate of the alkyl phosphate additive 28
9.3.4 Groundwater and fate of the alkyl phosphate additive 28
9.4 Potential environmental concentrations of phosphoric acid 28
9.4.1 Exposure from use 29
9.4.2 Potential release of phosphorus to water compartment 31
9.5 Occupational exposure to the alkyl phosphate additive 32
9.5.1 Manufacture 33
9.5.2 Bulk LRP blending 33
9.5.3 Petrol stations and maintenance workshops 35
9.5.4 Importation, transport and handling of the alkyl phosphate
products 36
9.6 Occupational exposure to phosphoric acid from the alkyl phosphate
additive use 36
9.7 Public exposure and level of exposure to the alkyl phosphate additive 37
9.7.1 Consumer exposure 37
9.7.2 Indirect exposure via environment 38
9.7.3 Public exposure and level of exposure to phosphoric acid via
air 39
10. ANIMAL AND HUMAN HEALTH EFFECTS OF THE ALKYL PHOSPHATE
ADDITIVE 41
10.1 Acute toxicity 41
ix
Alkyl Phosphate AVSR Additive
10.2 Irritation and corrosivity 42
10.3 Sensitisation 44
10.4 Neurotoxicity 44
11. PHARMACOKINETICS AND TOXICITY OF PHOSPHORIC ACID 46
11.1 Introduction 46
11.2 The phosphate body load 46
11.3 Toxicokinetics of phosphoric acid 47
11.4 Acute phosphoric acid toxicity in animals and humans 48
11.4.1 Acute toxicity 48
11.4.2 Irritation and corrosivity 49
11.4.3 Repeat exposure 50
11.5 Mutagenicity, genotoxicity and carcinogenicity 54
Reproductive toxicity
11.6 55
12. HAZARD CLASSIFICATION 56
12.1 Health hazards 56
12.2 Physico-chemical hazards 56
13. EFFECTS ON ORGANISMS IN THE ENVIRONMENT 57
13.1 Terrestrial organisms 57
13.1.1 Alkyl phosphate additive 57
13.1.2 Phosphoric acid 57
13.1.3 Phosphorus 58
13.2 Aquatic organisms 58
13.2.1 Alkyl phosphate additive 58
13.2.2 Phosphoric acid 58
13.2.3 Phosphorus and aquatic ecosystems 59
14. RISK CHARACTERISATION 62
14.1 Environmental risk 62
14.1.1 Terrestrial risk 62
14.1.2 Aquatic risk 63
14.2 Occupational risk 64
14.2.1 Critical health effects 65
14.2.2 Occupational health and safety risks 66
14.2.3 Uncertainties 68
14.3 Public health risk 69
14.3.1 Acute effects 69
14.3.2 Chronic effects 70
Priority Existing Chemical Assessment Report Number 25
x
14.3.3 Uncertainties 71
15. RISK MANAGEMENT 72
15.1 Assessment of current control measures 72
15.1.1 Elimination and substitution 72
15.1.2 Isolation and engineering controls 73
15.1.3 Safe work practices 74
15.1.4 Personal protective equipment 74
15.2 Hazard communication 75
15.2.1 Labels 75
15.2.2 MSDS 77
15.2.3 Education and training 78
15.3 Occupational monitoring and regulatory controls 78
15.3.1 Atmospheric monitoring 78
15.3.2 Occupational exposure standards 78
15.3.3 Health surveillance 79
15.3.4 National transportation regulation 79
15.3.5 Control of major hazard facilities 80
15.4 Public health regulatory controls 80
15.5 Environmental regulatory controls 80
15.5.1 Air quality management 81
15.5.2 Aquatic ecosystem management 82
15.5.3 Disposal and waste treatment 83
15.5.4 Emergency procedures 83
16. DISCUSSION AND CONCLUSIONS 85
16.1 Health hazards 86
16.1.1 Alkyl phosphate additive 86
16.1.2 Phosphoric acid 86
16.2 Environmental hazards and risks 87
16.3 Occupational health and safety risks 88
16.4 Public health risks 88
16.5 Data gaps 89
17. RECOMMENDATIONS 91
17.1 Recommendations for importers and manufacture of the alkyl phosphate
additive 91
17.1.1 Hazard communication ?MSDS 91
18. SECONDARY NOTIFICATION 92
xi
Alkyl Phosphate AVSR Additive
APPENDIX 1 CALCULATION OF LRP VOLUMES FOR 2004 93
APPENDIX 2 PHYSICO-CHEMICAL PROPERTIES OF PHOSPHORIC ACID 94
APPENDIX 3 MSDS ASSESSMENT SUMMARY 96
REFERENCES 98
Priority Existing Chemical Assessment Report Number 25
xii
Acronyms and Abbreviations
ABS Australian Bureau of Statistics
ACGIH American Conference of Governmental Industrial
Hygienists
ADG Code Australian Dangerous Goods Code
ADI acceptable daily intake
AF air/fuel ratio
ai active ingredient
AICS Australian Inventory of Chemical Substances (NICNAS)
AIP Australian Institute of Petroleum
ALD acute lethal dose
AMSA Australian Maritime Safety Authority
ANSI American National Standards Institute
ANZECC Australian and New Zealand Environment and
Conservation Council
ANZFA Australia New Zealand Food Authority
ARMCANZ Agriculture and Resource Management Council of
Australia and New Zealand
AS Australian Standard
AST above ground storage tank
ATSDR Agency for Toxic Substances and Disease Registry
AVE average exposure estimate
AVSR anti-valve seat recession
bar barometric pressure
BPP bioavailable particulate phosphorus
BP boiling point
bw bodyweight
C carbon
癈 Celsius
C0p standard heat capacity at constant pressure
xiii
Alkyl Phosphate AVSR Additive
CAA Clean Air Act
CAS Chemical Abstracts Service
CEPA Canadian Environmental Protection Act
CI confidence interval
CICAD Concise International Chemical Assessment Document
cm centimetre
Cmax maximum concentration
COWIPP Clean Our Waterways Industry Partnership Program
compression ratio
CR
CRCFE Co-operative Research Centre for Freshwater Ecology
DETR Department of Environment, Transport and Regions
(UK)
DNA deoxyribonucleic acid
DMMP dimethyl methylphosphonate
DP dissolved phosphorus
DSL Domestic Substances List (Canada)
EA Environment Australia
EC50 median effective concentration
EC European Community, or European Commission
ECB European Chemicals Bureau
ECETOC European Centre for Ecotoxicology and Toxicology of
Chemicals
EHD estimated human dose
EINECS European Inventory of Existing Commercial Chemical
Substances
ELINCS European List of Notified Chemical Substances
ERMA Environmental Risk Management Authority (New
Zealand)
EU European Union
FAO Food and Agriculture Organization (United Nations)
FCL full container load
FORS Federal Office of Road Safety
FTIR Fourier Transform InfraRed
Priority Existing Chemical Assessment Report Number 25
xiv
g gram
g/m3 gram per cubic metre
GC gas-chromatography
GC-MS gas-chromatography/mass spectrometry
GHS Globally Harmonised System (of Classification and
Labelling of Chemicals)
GLC gas liquid chromatography
GLP good laboratory practice
fH0 standard enthalpy of formation of the substance at 298 K
HAPs hazardous air pollutants
hr hour
H3PO4 orthophosphoric acid/phosphoric acid
H3PO3 phosphorous acid
HPLC high-performance liquid chromatography
HQ hazard quotient
IC(NA) Act Industrial Chemicals (Notification and Assessment) Act
1989 (Commonwealth)
IDLH immediately dangerous to life and health
IMO International Maritime Organisation
IP intraperitoneal
IPCS International Programme on Chemical Safety
IR infrared
IRIS Integrated Risk Information System (US EPA)
ISO International Standards Organisation
IUCLID International Uniform Chemical Information Database
IUPAC International Union of Pure and Applied Chemistry
iv intravenous
K Kelvin
kg kilogram
kg/ha/a kilogram per hectare per annum
kJ kiloJoule
xv
Alkyl Phosphate AVSR Additive
Koc organic carbon partition coefficient
Kow octanol/water partition coefficient
km kilometre
L litre
LC50 median lethal concentration
LD50 median lethal dose
LEL lower explosive limit
LEV local exhaust ventilation
LOAEL lowest-observed-adverse-effect level
LOEL lowest-observed-effect level
LRP lead replacement petrol
礸 microgram
m metre
m3 cubic metre
MegaL megalitre
mg milligram
mg/dL milligram per decalitre
mg/kg milligram per kilogram
mg/kg bw/d milligram per kilogram bodyweight per day
mg/L milligram per litre
mg/m3 milligram per cubic metre
min minute
MITI Ministry of International Trade and Industry (Japan)
mL millilitre
ML megalitre
mm millimetre
MMAD mass median aerodynamic diameter
mmol/L millimole per litre
MMT methylcyclopentadienyl manganese tricarbonyl
MOE margin of exposure
Priority Existing Chemical Assessment Report Number 25
xvi
MOE Ministry of Environment (Korea)
mol mole
MSDS Material Safety Data Sheet
MTDI maximum tolerable daily intake
N nitrogen
n number
NA not applicable
NAPS National Air Pollution Surveillance (Canada)
NDPSC National Drugs and Poisons Schedule Committee
NEPM National Environment Protection Measure
ng nanogram
ng/m3 nanogram per cubic metre
ng/mL nanogram per millilitre
ng/L nanogram per litre
NHMRC National Health and Medical Research Council
NICNAS National Industrial Chemicals Notification and
Assessment Scheme
NIOSH National Institute of Occupational Safety and Health
NOAEL no-observed-adverse-effect level
NOEC no-observed-effect concentration
NOEL no-observed-effect level
NOHSC National Occupational Health and Safety Commission
NOS not otherwise specified
NPI National Pollutant Inventory (NPI)
NSW EPA New South Wales Environment Protection Authority
O oxygen
OECD Organisation for Economic Cooperation and
Development
OH hydroxyl
OSHA Occupational Safety and Health Administration (USA)
pressure
P
xvii
Alkyl Phosphate AVSR Additive
P phosphorus
P4 white phosphorus
PH3 phosphine
P2O5 (or P4O10 in its most stable phosphorus pentoxide
form)
PEC predicted environmental concentration
PEL permissible exposure limit (US OSHA)
pressure (final)
Pfinal
pressure (initial)
Pinitial
pKa dissociation constant
PNEC predicted no-effect concentration
ppb parts per billion
PPE personal protective equipment
ppm parts per million
PULP premium unleaded petrol
PVC polyvinyl chloride
QA quality assurance
QSAR Quantitative Structure Activity Relationship
RDA Recommended Daily Allowance
Re Reynolds number
REM reasonable maximum exposure estimate
RfC reference concentration
RNA ribonucleic acid
RP/BR red phosphorus/butyl rubber
RTECS Registry of Toxic Effects of Chemical Substances (US)
s second
S0298 standard entropy of the substance at 298 K
sc subcutaneous
SEM Scanning Electron Microscope
STEL short-term exposure limit
Priority Existing Chemical Assessment Report Number 25
xviii
STP sewage treatment plant
SUSDP Standard for the Uniform Scheduling of Drugs and
Poisons
half life
t1/2
T temperature
TGA Therapeutic Goods Administration
TLV Threshold Limit Value (ACGIH)
TM Trademark
TMP trimethylphosphate
TOTP tri-o-tolyl phosphate
TP total phosphorus
TP/L total phosphorus per litre
TSCA Toxic Substances Control Act (US)
TWA time-weighted average (NOHSC)
ratio of specific heats
UK HSE United Kingdom Health and Safety Executive
UEL upper explosive limit
ULP unleaded petrol
UN Number United Nations (Identifications) Number
US EPA United States Environmental Protection Agency
USI Urban Stormwater Initiative
UST underground storage tank
VSR valve seat recession
WHO World Health Organization
xix
Alkyl Phosphate AVSR Additive
Priority Existing Chemical Assessment Report Number 25
xx
1. Introduction
1.1 Declaration
Anti-valve seat recession (AVSR) fuel additives were declared as Priority Existing
Chemicals for full assessment under the Industrial Chemicals (Notification and
Assessment) Act 1989 on the 5 December 2000. They were nominated because of
their increasingly widespread use in lead replacement petrol (LRP) and potential
adverse effects on the environment and human health.
NICNAS received applications for the following AVSR additives in use in
Australia:
? Methylcyclopentadienyl manganese tricarbonyl (MMT)-based;
? Phosphorus-based;
? Sodium-based; and
? Potassium-based.
Each AVSR fuel additive has been assessed individually and separate reports are
prepared for each. This present report addresses the use of an alkyl phosphate
additive as an AVSR additive.
1.2 Objectives
The objectives of this assessment are to:
? Characterise the chemical and physical properties of the alkyl phosphate
additive;
? Determine the current and potential occupational, public and
environmental exposure to the alkyl phosphate additive as an AVSR
additive;
? Characterise the intrinsic capacity of the alkyl phosphate additive to cause
adverse effects on persons or the environment;
? Characterise the risk to humans and the environment resulting from
exposure to the alkyl phosphate additive as an AVSR additive;
? Determine the extent to which any risk is capable of being reduced and
make recommendations for the management of these risks.
1.3 Sources of information
Consistent with these objectives, this report presents a summary and critical
evaluation of the relevant information relating to the potential health and
environmental hazards caused by exposure to the alkyl phosphate additive.
Relevant scientific data were submitted by the applicants listed in Section 3,
obtained from published papers identified in a comprehensive literature search of
1
Alkyl Phosphate AVSR Additive
several online databases up to 3 January 2003, and retrieved from other sources
such as reports and resource documents prepared by overseas regulatory bodies.
1.4 Peer review
This report has been subject to peer review by NICNAS and Environmental
Australia (EA) during all stages of the preparation. NICNAS sought expert advice
on postulated alkyl phosphate additive combustion by-products from Associate
Professor John C. Mackie, School of Chemistry, University of Sydney.
2 Priority Existing Chemical Assessment Report Number 25
2. Background
The phosphorus-based anti-valve seat recession additive, i.e. alkyl phosphate additive,
which is the subject of this Priority Existing Chemical assessment report, was originally
developed by DuPont in the USA during the 1960s and 1970s and known worldwide as
the carburettor detergent DMA-4 (Octel undated;a).
2.1 What is an anti-valve seat recession additive?
Anti-valve seat recession (AVSR) fuel additives are added to petrol to stop excessive
valve seat wear and recession of the valve seat into the automotive engine cylinder head
(Figure 1).
Figure 1. Exhaust valve recession into the cylinder head. From: Barlow (1999)
Although valve seat recession (VSR) occurs as part of the normal wear of an engine,
premature erosion of the valve seats are observed as excessive VSR when vehicles with
soft exhaust valve seats, normally designed to operate on leaded petrol, are operated on
unleaded petrol (ULP).
Valve seats in engines designed for leaded fuel are generally relatively soft. With
leaded fuels, lead oxide formed by the combustion of lead alkyls forms a thin layer of
lead oxide on the valve and valve seat, so acting as a solid lubricant and preventing
erosion of the valve seats in the cylinder head of the engine (Figure 1). VSR can cause
valve burning and loss of compression and, if allowed to progress, results in serious
loss of performance and ultimately engine failure. Lead replacement petrol (LRP) uses
AVSR additives to provide the lubricating qualities previously provided by lead.
During fuel combustion, the AVSR additive burns and forms a coating on the exhaust
valve seats, providing similar protective lubrication to lead oxide.
Since the early 1970s, increasing environmental and health concerns have resulted in
the reduction of lead levels in petrol and the complete removal of leaded petrol in
several countries (Lovei, 1998). In 2000, the World Bank reported that 36 countries
had already phased out the use of leaded petrol and this was expected to increase to
55 countries by 2005 (Benbarka, 2000). In addition, the use of catalytic converters in
3
Alkyl Phosphate AVSR Additive
automotive exhaust systems required the introduction of unleaded fuels since lead
destroys the capacity of catalytic converters to reduce other pollutants (Lovei, 1998).
A consequence of the removal of lead from petrol is that engine designers have been
required to use harder exhaust valve seat materials that maintain integrity without lead
lubrication. For existing cars with soft valve seats, the removal of lead has required
motorists to use LRP containing an AVSR additive or to modify their engine by fitting
hardened exhaust valve seats suitable for ULP with no AVSR fuel additive (Lovei,
1998).
The use of AVSR additives has risen with the demand for LRP petrol resulting from the
lead phase out worldwide. The demands for LRP and hence AVSR additives in
individual countries have been determined largely by policy decisions regarding the
import, sale and retirement of older vehicles, the encouragement of new technology and
environmentally cleaner engines and improved petrol standards. Consequently, the
population of VSR sensitive cars, and thus demand for AVSR additives in LRP, vary
from country to country.
2.2 International perspectives
A variety of petrol additives have been available worldwide to substitute for the
lubricating function of lead. These AVSR fuel additives are available for LRP at
distribution centres either via the service station pump (bulk supply) or sold in
bottles/devices for addition to the petrol tank to treat unleaded petrol (ULP) by the
motorist (aftermarket supply).
The gradual worldwide removal of lead from petrol from the early 1970s to the present
denotes a diminishing market for AVSR fuel additives - particularly in high-income
and middle-income countries (Lovei, 1998). This is based on the observation of older
technology petrol vehicles being encouraged to be removed from the world's vehicle
population, the gradual attrition/scrappage of vehicles requiring leaded petrol from
motor vehicle fleets and the use of increased hardness of exhaust valve seats by auto
manufacturers for new vehicles.
The alkyl phosphate additive described in this report has been used in the bulk
treatment of petrol in the USA since 1975 (A S Harrison & Co, 2001). Furthermore,
the alkyl phosphate additive has been used for bulk treatment of LRP in Argentina,
Macau/Hong Kong and the United Kingdom and Ireland since 1994, 1997 and 1999,
respectively, and as an aftermarket product in the USA, New Zealand (1996),
Singapore (1998), Philippines (1998) and Malaysia (1998) (Octel undated;b).
The chemical listings for the alkyl phosphate additive include the USA (TSCA),
Canada (DSL), Europe (EINECS), Japan (MITI) and Korea (MOE). Over 5 billion
litres of fuel worldwide is estimated to have been treated with the alkyl phosphate
additive (Octel undated;b).
2.3 Australian perspective
In Australia, under the Fuel Quality Standards Act 2000 (Cwlth), lead was removed
from automotive fuel from 1 January 2002, requiring the use of alternative additives for
valve seat protection. Under this Act, provision is made for the listing of prohibited
fuel additives. The alkyl phosphate additive is not listed.
4 Priority Existing Chemical Assessment Report Number 25
An Australian Standard, AS 4430.1 - 1996 (Standards Australia, 1996), exists for the
evaluation of devices and additives which claim to improve vehicle performance. Part 1
of AS 4430.1 ?1996 is noteworthy for the present report as it considers engines
designed for leaded fuel to operate on unleaded fuels and includes assessment of valve
seat recession.
2.4 Assessment by other national or international bodies
NICNAS has not identified any published hazard or risk assessment for the alkyl
phosphate additive although it has been used in LRP on a large scale worldwide for at
least the past decade and prior to that as a carburettor detergent known as DMA-4.
Preceding the introduction of the alkyl phosphate additive in New Zealand in 1996, it
was subject to assessment by the New Zealand Ministry of Health's Toxic Substance
Board and accepted as an AVSR additive at a treatment dose of 600 ppm (mg/kg) or
30 ppm (mg/kg) phosphorus of petrol. Approximately 350 000 vehicles were estimated
to require an AVSR additive when leaded petrol supples were withdrawn in New
Zealand in 1996 (A S Harrison & Co, 2000). The New Zealand assessment of the alkyl
phosphate additive is not publicly available.
5
Alkyl Phosphate AVSR Additive
3. Applicants
Following the declaration of anti-valve seat recession (AVSR) additives as a Priority
Existing Chemical, two organisations applied for assessment of the alkyl phosphate
additive. The applicants supplied information on the properties, import quantities and
uses of the alkyl phosphate additive. In accordance with the Industrial Chemicals
(Notification and Assessment) Act 1989, NICNAS provided the applicants with a draft
copy of the report for comment during the correction/variation phase of the assessment.
The applicants were as follows:
A S Harrison & Co Pty Limited
PO Box W2
Warringah Mall
NSW 2100
Asia Pacific Speciality Chemicals
Limited
15 Park Road
Seven Hills
NSW 2147
6 Priority Existing Chemical Assessment Report Number 25
4. Chemical Identity and Composition
4.1 Chemical identity
The chemical name, CAS number, molecular and structural formulae, molecular
weight, spectral data and details of the chemical composition of the alkyl phosphate
additive have been exempted from publication in this report.
The alkyl phosphate additive is not isolated per se but manufactured in situ with
varying amounts of kerosene used as a hydrocarbon diluent depending on the
proprietary product. The chemical composition of the alkyl phosphate additive
products described in this report is given in Table 1 (Asia Pacific Specialty Chemicals
2000a, 2000b).
Valvemaster Concentrate is synonymous with the carburettor detergent DMA-4
(Octel undated;a). The chemicals contained in the dye mixture used in the described
product are listed on the Australian Inventory of Chemical Substances (AICS) and are
typically used in hydrocarbon products.
Table 1 - Chemical composition of the alkyl phosphate additive products
Ingredients CAS No. Proportion Use
Valvemaster Concentrate
kerosene 8008-20-6 10-30% Bulk LRP (Valvemaster
Concentrate) & 10 mL single-
70-90%
alkyl phosphate confidential
use aftermarket product
additive
Valvemaster VM11
kerosene 8008-20-6 1-15% 250 mL multi-use aftermarket
product (Valvemaster
VM11)
64742-94-5 30-60%
solvent naptha
alkyl phosphate confidential 30-60%
additive
< 0.5% (total)
dye mixture Mixture
7
Alkyl Phosphate AVSR Additive
5. Physical and Chemical Properties
No physical or chemical properties are available for the alkyl phosphate additive
because it is manufactured in situ during the formulation of the proprietary products
and never isolated. The physical and chemical properties described below relate to the
proprietary products described in Section 4.
5.1 Physical state
ValvemasterTM Concentrate is a pale yellow to colourless liquid. ValvemasterTM VM11
is an orange liquid.
Physical properties of the alkyl phosphate additive products
Property Value
ValvemasterTM Concentrate a
220 癈
Autoignition temp.
> 149 癈
Boiling point
< -20 癈
Melting point
920 kg/m3
Density (15癈)
72 癈
Flash point (closed cup)
Very low (practically insoluble)
Water solubility
< 0.1 kPa
Vapour pressure
1% (kerosene)
LEL Flamm. Limit
6% (kerosene)
UEL Flamm. Limit
98
Viscosity (40癈; centi posie)
107 (cST)
5.1
Phosphorus % w
ValvemasterTM VM11 b
220 癈
Autoignition temp.
> 149 癈
Boiling point
920 kg/m3
Density (15癈)
63 癈
Flash point (closed cup)
Insoluble in water
Water solubility
unknown
Vapour pressure
1% (kerosene)
LEL Flamm. Limit
7% (kerosene)
UEL Flamm. Limit
4.5
Viscosity (40癈; centi poise)
a
Details are given in references (Octel, 1999b; Asia Pacific Specialty Chemicals, 2000a;
Octel, 2000). b Details are given in references (Octel, 1999a; Asia Pacific Specialty
Chemicals (2003).
8 Priority Existing Chemical Assessment Report Number 25
5.2 Chemical properties
Stability: The alkyl phosphate additive products are stable when exposed to light.
Hazardous decomposition: The alkyl phosphate additive products may decompose on
exposure to heat. Decomposition products may include toxic and irritant fumes
containing phosphorus compounds and oxides of carbon (Asia Pacific Specialty
Chemicals, 2000a).
Incompatibilities: The alkyl phosphate additive products are incompatible with strong
oxidising agents ( Asia Pacific Specialty Chemicals, 2000a).
5.3 Physico-chemical hazards
The products are flammable because the alkyl phosphate additive products contain
kerosene.
9
Alkyl Phosphate AVSR Additive
6. Methods of Detection and Analysis
6.1 Identification
No data are available on the detection and analysis of the alkyl phosphate additive other
than the determination of specific parameters for the proprietary products. These
parameters include the pH value, phosphorus content and infrared (IR) spectrum of
product. Specific characteristics such as the elemental composition of the alkyl
phosphate additive formulation are routinely determined for quality assurance purposes
during the manufacturing process by a wet chemical titration method and inductively
coupled plasma (ICP) instrumental techniques.
6.2 Atmospheric monitoring methods
None available.
6.3 Biological monitoring methods
None available.
10 Priority Existing Chemical Assessment Report Number 25
7. Manufacture, Importation and Use
7.1 Manufacture and importation
The alkyl phosphate additive is manufactured as Valvemaster Concentrate in situ in a
closed reaction vessel and diluted with kerosene to produce the final formulated
product as one process.
The manufacture is undertaken in a closed non-aerosol forming process with the alkyl
phosphate additive remaining within the reactor vessel. At the completion of the
manufacture, the alkyl phosphate additive formulation may be held in the
manufacturing vessel or transferred from the manufacturing vessel, through dedicated
flexible transfer lines via air pumps into either an on-site holding tank (200 kg closed
head steel drums) or 20-22 tonne nominal weight, bottom discharge ISO tanks for
distribution to oil companies for addition to LRP or export.
The alkyl phosphate manufacturing site is a licensed Dangerous Goods storage facility,
with the manufacture of alkyl phosphate additive undertaken in a Zone 1, Class 1 plant
by a single operator (with two operators per manufacturing cycle).
For synthesis, the reaction vessel is charged with the individual chemical components,
with the reaction vessel maintained during the procedure at no greater than 85癈.
Nitrogen sparging and the application of a vacuum are required during the process.
Also during the process, the operators undertake a number of quality assurance tests
that require the sampling of approximatly 250 mL of the alkyl phosphate additive
product.
Raw materials are loaded either manually through the reactor hatch (solids) or by
vacuum pumps (liquids). There is a dust extraction system located in proximity to the
hatch to collect dust particles during the loading of raw materials. The reactor is
connected to a scrubber system which treats vapours emitted during the manufacturing
process. The reaction vessel is located in a bunded building which would facilitate the
containment of spills. The reaction vessel is connected via a bursting disc to a catch
tank which would contain product in the event that control of the reaction was lost.
Drums of product are stored in appropriate undercover warehouses at the site of
manufacture until dispatched to the oil companies for bulk LRP blending. ISO tanks
are dispatched directly from the manufacturing site to the oil companies for bulk LRP
blending.
Washings and effluent from the drums and manufacturing plant are transferred to a
Trade Waste Treatment plant on the manufacturing site for processing prior to any
discharge of effluent off-site.
Manufacture of the alkyl phosphate additive aftermarket products does not occur in
Australia but the products are imported into Australia by either seafreight or air.
The imported aftermarket products are stored in warehouses located in state capital
cities and supplied directly to retail sites in carton quantities. The 10 mL single-use
aftermarket applicators are imported in cartons of 160 units while the multi-treat
250 mL bottles are imported in cartons of 24 units.
11
Alkyl Phosphate AVSR Additive
7.2 Uses
Bulk LRP
The alkyl phosphate additive is used in Australia by major and independent oil
companies for bulk LRP production. Bulk LRP is supplied by the oil companies to
service stations.
Addition (or treatment) rates in Australia of the alkyl phosphate for bulk LRP blending
vary between 180 to 600 ppm (mg/kg) or 9 to 30 ppm (mg/kg) phosphorus of petrol,
depending on the oil company. The typical treatment rate of the alkyl phosphate
additive in Australia for bulk LRP is 600 mg/kg of petrol.
Alkyl phosphate-based LRP is blended by oil companies by the addition of the alkyl
phosphate additive into the ULP while the ULP is being loaded into petrol tankers prior
to distibution to service stations. The methods of use and addition mechanisms are
described in Sections 7.6 and 9.5.2, respectively.
Aftermarket LRP
The alkyl phosphate 10 mL single-use applicator and 250 mL multi-treat device are
used by the vehicle owner for adding the alkyl phosphate additive directly into a
vehicle fuel tank containing ULP. This is decribed as aftermarket use of the alkyl
phosphate additive.
The 10 mL single-use applicators and 250 mL multi-treat plastic bottles are used to
treat 20 L and 250 L, respectively, of ULP.
The typical treatment rate of the alkyl phosphate additive for aftermarket AVSR
application in Australia is equivalent to the treatment rate for the bulk LRP market, i.e.
600 mg/kg of petrol.
The aftermarket products are sold by retail service stations across Australia. While the
single-use 10 mL applicators have been available for some time, the introduction of the
250 mL multi-treat bottles is recent and primarily for marine and farm users as well as
for VSR sensitive motor vehicles.
The composition of alkyl phosphate additive formulation supplied to the oil companies
for use in bulk LRP blending is identical to the formulation used in the 10 mL
aftermarket applicators (Section 4). The methods of use of the aftermarket products is
described in Section 7.6.2.
7.3 Demand for anti-valve seat recession additives
This section describes scenarios for generic AVSR additive use based on the current
and anticipated AVSR additive demand in Australia.
AVSR additive fuel additives are available for both oil refinery or terminal use and
consumer use. AVSR fuel additives may be delivered either by pre-blending to ULP at
the oil refinery or terminal or purchased separately and added to ULP by the vehicle
owner. The total Australian AVSR additive market will be referred to as the `LRP
market' in this report.
Following the declaration of AVSR fuel additives as a Priority Existing Chemical,
importers and manufacturers of various AVSR fuel additives provided information on
12 Priority Existing Chemical Assessment Report Number 25
the import and/or manufacturing quantities and uses of their chemicals for the years
2000 and 2001. This information was used to estimate a total LRP market for 2001 of
approximately 2500 ML (megalitre). This was calculated using AVSR additive
treatment doses for LRP and AVSR additive import/manufacturing volumes as
recommended by AVSR additive manufacturers. The calculated figure of 2500 ML is
slightly higher than the bulk LRP sales volumes for July 2000 to June 2001 of 1848 ML
(Department of Industry, Science and Resources, 2001).
The market share of individual AVSR fuel additives in Australia has not been disclosed
in this report due to commercial-in-confidence considerations. An analysis of the
import and manufacturing data demonstrated that the aftermarket application of AVSR
additives in Australia was less than 10% of the total LRP market in 2001.
In Australia, vehicles requiring leaded petrol are the major consumers of LRP. These
vehicles include passenger vehicles, light commercial trucks, rigid trucks, articulated
trucks, non-freight carrying trucks, buses and motorcycles (Australian Bureau of
Statistics (ABS, 2001). It is likely there are also other VSR sensitive vehicles requiring
AVSR additives, e.g. tractors and some plant and equipment engines, not included on
the Australian Motor Vehicle Census. These vehicles and engines are not expected,
however, to represent a significant component of the AVSR additive market.
There is a declining Australian market for LRP sales (Australian Institute of Petroleum,
1999) and hence AVSR additives. This is due to attrition from the Australian motor
fleet of vehicles designed to run on leaded petrol (Figure 2).
Figure 2 - The number of vehicles using leaded petrol 1995-2000 () and forecast
number (- - -) of vehicles using leaded petrol 2001-2004: Australian motor vehicle
fleet. Data are taken from the Motor Vehicle Census, Australian Bureau of Statistics
(Australian Bureau of Statistics (ABS), 1998, 2001).
Leaded Vehicle Population, Census Year
6
Leaded Vehicle Numbers
5
4
(million)
3
2
1
0
1994 1996 1998 2000 2002 2004
Motor Vehicle Census Year (ABS)
13
Alkyl Phosphate AVSR Additive
By 2004, bulk sales of LRP are expected to decline to less than 5% of total petrol sales
(Australian Petroleum Gazette, 1999). This may render the general provision and sale
of bulk LRP by the oil refineries and terminals uneconomical. The Australian
petroleum industry is yet to announce a phase-out by the oil refineries and terminals of
the provision of bulk LRP.
Aftermarket addition of AVSR fuel additives rather than bulk treatment by the oil
refineries and terminals is therefore likely to become eventually the only option for
motorists with vehicles designed to run on leaded petrol. This may occur as early as
2004 as the supply of LRP from the oil refineries and terminal diminishes significantly.
Implementation of any partial or total changeover from bulk to aftermarket supply of
LRP would, no doubt, require a broad consensus among stakeholders, entailing
consideration of the technical and practical needs of the program and understanding and
acceptance by the public.
7.4 AVSR use scenarios
Two use (exposure and emission) scenarios have been assessed in this report ?the
present state of the market and that likely to occur at 2004. Both scenarios are
considered because of anticipated changes in occupational health and safety, public
health or environmental exposure as a result of a decreasing supply of bulk LRP as well
as the consequent increased use of aftermarket AVSR products and the attrition from
the Australia motor vehicle fleet of VSR sensitive vehicles. Details of the AVSR
additive use scenarios are presented in Table 2.
Table 2 - A summary of the AVSR additive use scenarios.
Present
Present AVSR additive LRP market: 2500 ML (megalitres) for 2 500 000 vehicles.
10% service station forecourt: 90% bulk AVSR additive market.
2004
AVSR additive LRP market in 2004: 1000 ML (megalitres) for 1 000 000 vehicles.
100% service station forecourt AVSR additive market.
The present use scenario was based on AVSR additive import and manufacturing data
provided by industry for the 2001 calendar year. The calculation of 2 500 000 vehicles
is based on 2001 calendar year total AVSR additive import and manufacturing data and
a petrol fill-up rate of 19.4 L/week/leaded vehicle (Appendix 1).
The calculated figure of 2 500 000 vehicles for the present use scenario (Table 2) is
slightly lower than the 2 904 342 vehicles reported in the ABS Motor Vehicle Census
31 March 2001 (Australian Bureau of Statistics (ABS), 2001). This is attributed to the
inclusion in the ABS data of all leaded vehicles irrespective of the requirement for or
use of an AVSR additive. For example, not all vehicles requiring leaded petrol are VSR
susceptible and require an AVSR additive. In 2000, more than 30% of cars built before
1986 were estimated to run efficiently on normal unleaded petrol, with the remaining
14 Priority Existing Chemical Assessment Report Number 25
70% requiring an AVSR additive (Hill, 2000). The forecast of 1 000 000 vehicles was
derived from Australian Bureau Statistics motor vehicle census data (Australian Bureau
of Statistics (ABS, 1998, 2001). One million VSR susceptible vehicles equates to a
demand for LRP of approximately 1000 ML (megalitres) in 2004. A description of the
calculation for LRP demand in 2004 is also given in Appendix 1. The calculated LRP
demand of 1000 ML in 2004 is slightly higher than the Australian Institute of
Petroleum (AIP) sales forecast made in 1999 of nil to 800 ML (Australian Petroleum
Gazette, 1999).
In 2010, a niche market of VSR-sensitive older vehicles and engines requiring leaded
petrol is expected to remain (National Heritage Trust, 2000).
For the purposes of commercial-in-confidence and changes in market share, it has been
assumed that only one AVSR additive has 100% market share in each use scenario.
Across the assessments of all AVSR additives, the same bulk to aftermarket share is
assumed for each AVSR additive.
7.5 Use scenarios for the alkyl phosphate additive
Alkyl phosphate additive products currently sold in Australia include Valvemaster
Concentrate and Valvemaster VM11. The chemical composition and addition rates
for LRP of these products is described in Section 4 and and Section 7.2, respectively.
The two LRP use scenarios (`present' and `2004') developed in Table 2 have been used
to estimate the tonnage of Valvemaster Concentrate likely to be used in Australia in
these time periods (Table 3).
Due to the commercial-in-confidence nature of the information provided by the
Applicants, the calculated tonnage of the alkyl phosphate additive is not disclosed. The
estimated tonnage of phosphorus per annum for the two use scenarios is based on
5.1% wt phosphorus in Valvemaster Concentrate.
Table 3 - Estimated alkyl phosphate additive use (`present' and `2004')
Scenario 1: Present
Estimated LRP use per annum (present) 2500 ML (megalitres)
Estimated rate of use of Valvemaster 10 mL of Valvemaster Concentrate
Concentrate per annum per 20 L ULP (or 0.5 mL per L)
1 250 000 L (1.25 ML)
Estimated volume of Valvemaster
Concentrate per annum
Density of Valvemaster Concentrate 0.92 kg/L (at 15癈) (Octel, 1999b)
1150 tonnes per annum
Estimated tonnage of Valvemaster
Concentrate per annum
Estimated tonnage of phosphorus per annum 57.5 tonnes
15
Alkyl Phosphate AVSR Additive
Scenario 2: 2004
Estimated LRP use per annum (2004) 1000 ML (megalitres)
Estimated rate of Valvemaster Concentrate 10 mL of Valvemaster Concentrate per 20 L
per annum ULP (or 0.5 mL per L)
500 000 L (0.5 ML)
Estimated volume of Valvemaster
Concentrate per annum
0.92 kg/L
Density of Valvemaster Concentrate
460 tonnes per annum
Estimated tonnage of Valvemaster
Concentrate per annum
Estimated tonnage of phosphorus per annum 23 tonnes
7.6 Methods of use
Bulk LRP
The bulk LRP is distributed by oil companies to retail service stations in dedicated
petroleum road ISO tankers. The contents of the LRP road tanker are discharged either
by gravity or by pump into customer storage tanks. After delivery, the transport
contractor conducts an inspection of the interior of the road tankers to ensure the
complete discharge of the load into the service station tanks. The road tankers are
subsequently cleaned by cleaning contractors using effluent treatment facilities.
Forecourt LRP refueling is typically undertaken by vehicle owners and occurs via a
service station forecourt pump or bowser with a direct link to the service station's LRP
storage tank. At some service stations, forecourt staff may undertake the refueling
activity.
Aftermarket products
Two alkyl phosphate additive aftermarket products are available for consumer use. The
aftermarket products are 10 mL and 250 mL formulations that are presented as a single-
and multiple-use device, respectively, made from recyclable polyolefin plastic. The
alkyl phosphate aftermarket products are available throughout Australia. The chemical
composition of the formulations are described in Section 4.
The 10 mL applicators are intended for sale primarily through service station retail sites
as a forecourt LRP additive to treat 20 L of ULP. The syringe-like 10 mL plastic
applicators are designed to empty completely. As a safety feature, the 10 mL applicator
plunger locks in place after use thus preventing refilling with other products. After
fueling with ULP the motorist purchases one or more 10 mL applicators and 'injects'
the alkyl phosphate additive into the petrol via the fuel tank opening. The motorist
disposes of the empty applicator on the service station forecourt in a similar manner to
the disposal of empty plastic lubricant bottles.
16 Priority Existing Chemical Assessment Report Number 25
The 250 mL multi-treat product is designed for treating larger volumes of ULP, e.g.
boating or farm applications, as well as for multi-use as a forecourt additive at service
stations. The multi-treat bottle is fitted with a calibrated measuring chamber. To use
this device, the customer squeezes the bottle in order to fill the measuring chamber to
the level corresponding to the fuel volume to be treated. The contents of the measuring
chamber are then dispensed directly into the fuel tanks. The multi-treat bottle is
designed to drain completely.
While the 250 mL multi-treat bottles contain a less concentrated form of the alkyl
phosphate additive than the 10 mL single-use product, the calibrated measuring
chamber is designed to deliver an alkyl phosphate treatment dose equivalent to that of
the single-use applicator.
The 10% aftermarket share of the present LRP market (Scenario 1) equates to
approximately 13 million single-use alkyl phosphate additive aftermarket applicators
Australia-wide (Table 2), assuming all VSR sensitive cars use the single-use product.
This number increases in 2004 to 52 million single-use applicators Australia-wide
(Scenario 2) when bulk LRP is no longer available (Table 2).
17
Alkyl Phosphate AVSR Additive
8. Expected Alkyl Phosphate Additive
Combustion Emissions
8.1 Introduction
In the absence of consistent data, NICNAS commissioned expert advice on the
expected combustion and the final tailpipe emissions by-product(s) of the alkyl
phosphate additive as a consequence of the high temperature combustion environment
most likely to occur under engine operating conditions.
The advice was sought because of anticipated public and occupational exposure to the
combustion by-product(s) of the alkyl phosphate additive. The identification of the
thermal combustion products of the alkyl phosphate additive was considered a pre-
requisite for determining the risks associated with the use of the chemical.
Choice of the expert advice sought was based on eminence in the field of high
temperature kinetics and thermal decomposition studies. Relevant extracts from the
advice provided are included in the following sections.
8.1.1 Equilibrium Computational Model
The study on the expected tailpipe emissions from the alkyl phosphate additive is based
on an equilibrium computational model and the thermodynamics of the four-stroke
spark-ignition engine.
The thermodynamics of the four-stroke spark-ignition engine are well understood
(Heywood, 1988) and is described as follows. The intake gases ?vaporized fuel, fuel
additive and air ?enter the cylinder at atmospheric pressure and at a temperature near
to 373 K as the cylinder walls are maintained at a constant temperature by pressurised
water circulation.
Because the compression stroke is so rapid, there is insufficient time for heat exchange
between the air-fuel mixture and the cylinder walls. Hence the compression
approximates well to an adiabatic compression. The final pressure, pfinal after
compression is given by:
pfinal/pinitial = (CR) (1)
where CR is the compression ratio and is the ratio of specific heats. In the
computations used in the model, compression ratios of 8:1 and 11:1 have been
considered, representing the two extremes of compression ratios encountered in cars
using lead replacement petrol. The typical value of = 1.32 for the intake gases at
combustion temperatures has been adopted (Heywood, 1988).
The equilibrium calculations for a 4-stroke spark-ignition engine used in the
computational studies were made for adiabatic compressions from an initial
temperature of 373 K and initial pressure of 1 bar to a final pressure given by eqn (1),
i.e., pfinal = 15 bar (CR = 8:1) and pfinal = 23 bar (CR = 11:1). The final combustion
temperature was essentially independent of compression ratio but depended on the
18 Priority Existing Chemical Assessment Report Number 25
air/fuel ratio, AF, and computations were made for AF values ranging from 12.5:1 to
14:1, corresponding to full throttle and part throttle conditions, respectively.
Equilibrium computations were carried out using the CHEMKIN II (Kee, 1989) and
EQUIL (Lutz, 1990) suite of computer codes on UNIX workstations. The exhaust gas
temperature range was from 330 K to 1200 K.
The fuel used in the computational studies was iso-octane and the alkyl phosphate
additive added at the recommended level of 600 ppm or 600 mg/kg of petrol. The
percentage of phosphorus (P) was taken from manufacturers' specifications to be 5.0%
giving a level of 30 mg/kg iso-octane or 1.1 ?10-4 moles of phosphorus per mole of
iso-octane. Phosphorus-containing species considered at equilibrium were P, P4 (the
molecular formula of elemental phosphorus in its most stable form), PH3 (phosphine),
P2O5 (phosphorus pentoxide), PO, PO2, P(OH)2, P(OH)3, OP(OH)2, HOPO and HOPO2
together with H3PO4 (orthophosphoric acid) and H3PO3 (phosphorous acid).
Carbon-hydrogen-oxygen-nitrogen species included in the calculations were, in
addition to iso-octane, C, H, O, N2, O2, OH, CO, CO2, H2, H2O, CH4, HCO, HO2, CH3,
C2H6, C2H4, C2H2, NO, CH2O and H2O2. These comprise a comprehensive set of
product species known to be present following combustion of iso-octane.
The distribution of products was calculated for the combustion chamber and throughout
the exhaust system. The final data on tailpipe emissions is most relevant to the current
assessment and is reported here.
8.1.2 Predicted tailpipe emission levels of phosphoric acid
Equilibrium calculations performed for a temperature of 300 K and an air/fuel ratio of
12.5:1 yield a maximum mole fraction of H3PO4 (phosphoric acid) of 2.1 ?10-6 in 1 bar
of exhaust gases. Treating the exhaust gases as ideal, 1 bar of exhaust gases occupies
0.0249 m3 mol-1 at 300 K. Hence the maximum emission of H3PO4 at the tailpipe is
calculated to be 8.3 mg m-3. The vapour pressure of H3PO4 is stated (MSDS, 2000) to
be 0.03 Torr at 20癈 corresponding to 160 mg m-3 at this temperature. Hence the
phosphoric acid emitted from the tailpipe should remain in the vapour phase.
8.1.3 Further consideration of alkyl phosphate by-products in tailpipe emissions
Phosphoric acid tailpipe emission rates
Estimates of the level of phosphoric acid emission from the tailpipe have been made on
the basis that all of the phosphorus originally added to the fuel is emitted from the
exhaust system. No allowance in these estimates was made for possible heterogeneous
reaction between gas phase combustion products containing phosphorus with metal
components of the engine or exhaust system. Since the combustion gases reach
temperatures exceeding 2000 K in the engine and enter the exhaust system at
temperatures around 1200 K, heterogeneous reaction with metal surfaces might take
place. This will also depend on the residence time of the combustion gases.
The most likely sites for metal-phosphorus species reaction would appear to be the
exhaust valve seating and the top of the exhaust system. It is well known (Corbridge,
1990) that iron and steel and many other heavy metals react with orthophosphoric acid
to produce hydrogen phosphates and orthophosphates over a wide range of
temperatures. Surface reaction to produce iron phosphates would reduce the level of
phosphoric acid in the mainstream (exhaust) gases.
19
Alkyl Phosphate AVSR Additive
Estimation of the extent of reaction between phosphoric acid in the exhaust gases and
the walls of the exhaust system is very complex, depending on the extent of adsorption
on the surface, presence of engine oil or other deposits, turbulence of the exhausting
gases, rate of surface reaction and the temperatures of surface and gases. Most of the
gas will exhaust in the initial blowdown process when the exhaust valve opens
(Heywood, 1988). The flow will initially become sonic and hence choked. Pressure
pulses will be smoothed out subsequently in the exhaust system and become quasi-
steady. Using an average fuel consumption of 8 L/100 km there will be approximately
10 m3 of exhaust gases per litre of petrol consumed. At an average speed of 100 km hr-
1
the volumetric flow rate of exhaust gases from the tailpipe is approximately
0.020 m3 s-1. For a tailpipe of 50 mm internal diameter this corresponds to a linear
flow rate of about 10 m s-1. Thus the gases exhaust from the tailpipe significantly less
than 1 s after opening of the exhaust valve.
Under these conditions the flow in the exhaust pipe is turbulent (Kanury, 1975) with a
Reynolds number, Re 4000. It is possible to make a maximum estimate of the
phosphoric acid that might be able to react with the surface of the exhaust system by
assuming turbulent flow with diffusion to the walls of the pipe.
It would be expected that most reaction between phosphoric acid and the metal surfaces
of the exhaust would occur in the first 0.1 m when the temperature is high (~1000 K).
Approximating the exhaust gases as air and the diffusion coefficient of phosphoric acid
in air to be 8 ?10-5 m2 s-1 at 1000 K (a value typical of smaller condensible molecules
in air) (Kanury, 1975), using the standard formulation (Willeke, 1993) for turbulent
diffusional flow through a pipe, it is estimated that the percentage of phosphoric acid
molecules diffusing to the walls is 2.6%. If, instead, an average temperature of 700 K
is assumed, then the percentage of molecules diffusing to the walls in a distance of 1 m
from the exhaust valve is 28%.
If this latter figure is adopted as an upper limit for diffusional losses and if it is assumed
that all the phosphoric acid molecules that diffuse to the exhaust pipe walls were
capable of reacting and hence removal from the mainstream, this would reduce the
emission level of H3PO4 from the earlier estimate of 8.3 mg m-3 to 6.0 mg m-3.
Reaction between phosphoric acid and the metal surfaces of the exhaust system would
lead to the production of metal phosphates. From a cast iron exhaust system, iron
phosphates would be expected. Part of any metal phosphates produced might deposit
on the walls of the exhaust system. However, it is conceivable that some metal
phosphates might also be emitted as particulates from the exhaust system.
Reactivity of phosphoric acid
A final consideration concerns the possibility that the combustion process or
subsequent passage of the exhaust gases through the exhaust system might lead to the
production of the highly toxic gas phosphine, PH3.
Phosphine was, therefore, included in the phosphorus species considered in the
equilibrium computations after combustion of the air-fuel mixture. Its concentration in
the combustion products was found to be completely negligible as might be expected
owing to its facile oxidation (to H3PO4 and H2O) under combustion conditions.
Nevertheless, the possibility that the phosphorus-containing combustion products,
especially the oxyacids HOPO, HOPO2, H3PO3 or H3PO4, might form phosphine in the
exhaust system should be discussed. Certainly the equilibrium calculations for the
exhaust gases made at cooling temperatures indicate that there are negligible levels of
20 Priority Existing Chemical Assessment Report Number 25
PH3, however, the possibility of some catalytic reaction with metal walls leading to PH3
formation should be considered.
Phosphine is known (Corbridge, 1990) to form by heating dry phosphorous acid,
H3PO3, at 200癈. Phosphorous acid has the structure O=P(H)(OH)2. It is a tautomer of
P(OH)3. P(OH)3 is a species identified by Mackie, Bacskay and Haworth (Mackie,
2002) as having some stability at high temperatures. However, they showed that
P(OH)3 rapidly undergoes decomposition to form the more stable HOPO + H2O rather
than tautomerize to phosphorous acid. Hence it is unlikely that there would be any
H3PO3 (phosphorous acid) of sufficient quantity to make phosphine in the exhaust and
this is borne out by the equilibrium calculations which show that it is only present over
a limited temperature range and only attains a level of about 0.02 of the
orthophosphoric acid at most. The maximum computed mole fraction of phosphorous
acid was 1.2 ?10-8 or 0.012 ppm and this maximum is only achieved over a very
narrow range of exhaust gas temperatures around 1000 K (727癈). By the time the
gases have cooled to 700 K, the computed level of phosphorous acid is only 0.0006
ppm and hence, negligible.
The literature was searched for any reference to the possible formation of PH3 from
H3PO4. These were an early Japanese study (Kuwa, 1966) of gases evolved during
electrolytic condensation of phosphoric acid in which at high current densities some
PH3 was generated by the reduction of H3PO4 and the title only (no abstract) of a
Russian publication (Sul'kov, 1975) entitled, "Phosphine Evolution during Production
of Furnace-Process Phosphoric Acid". The electrolytic conditions of the first study are
irrelevant to a consideration of the exhaust gases; there are no details of the second
study available.
The formation of phosphine during phosphoric acid-based metal cleaning is reported in
the literature (Patty's 1993). Patty's Industrial Hygeine and Toxicology cites "With
regard to this, impurities in the metal may lead to the formation of phosphine". In
regard to this claim for phosphoric acid, no evidence to support this can be found in the
literature. However, there are several references to the formation of phosphine from
phosphorous acid when heated. The most likely explanation for the above claim is that
impure phosphoric acid containing phosphorous acid, when undergoing exothermic
reaction with metals can lead to overheating of the impurity phosphorous acid which
could decompose to phosphine.
Orthophosphoric acid is a moderately strong acid and can produce molecular hydrogen
when it reacts with many metals (Corbridge, 1990; ChemAlert, 2002). However, there
is already hydrogen in the exhaust gases arising from fuel-rich combustion and this
level of hydrogen would be significantly higher than any which might be produced
from reaction of phosphoric acid with the exhaust pipe.
Certainly conditions in the exhaust gases are reducing ?nominally all of the oxygen
from air has been burned. However, during the cycling operation there is a period of
valve overlap when both intake and exhaust valve are simultaneously open, allowing
some air-fuel mixture to flow directly into the exhaust (Heywood, 1988). Additionally
there will be some air-fuel mixture in the crevice volume around the edges of the
exhaust valve during compression and combustion (Heywood, 1988). Thus oxygen
will not be entirely excluded from the exhaust gases. Phosphine is so readily oxidized
(Corbridge, 1990) that even if traces were produced, they would most likely be
converted into H3PO4 and H2O by residual oxygen present in the exhaust gases.
21
Alkyl Phosphate AVSR Additive
8.2 Summary of findings
The final equilibrium computations indicate no P (phosphorus), P4 (white phosphorus)
or PH3 (phosphine) of any significance is expected in the tailpipe emission.
If no account is taken of any reaction between orthophosphoric (phosphoric) acid and
the metals of the exhaust valve seat or exhaust system, the level of emission of
phosphoric acid (H3PO4) at the tailpipe is estimated to be 8.3 mg/m3 of exhaust gas.
Using a model of turbulent flow of the exhaust gases through the exhaust system, an
upper limit of losses of H3PO4 through reaction with the metals of the exhaust system is
estimated to be 28%, leading to a lower limit of 6.0 mg/m3 emitted from the tailpipe.
The orthophosphoric (phosphoric) acid emitted from the tailpipe is expected to remain
in the vapour phase, with this level being lowered by atmospheric dilution as it leaves
the tailpipe.
NICNAS raised concerns over the hypothetical formulation of phosphine (PH3) because
phosphine forms from phosphorous acid. Maximum levels of phosphorous acid
(H3PO3) of 0.012 ppm were computed. This level was reached only over a very limited
range of exhaust gas temperatures around 1000 K (727癈). When the exhaust gases
have cooled to 700 K, the phosphorous acid is computed to drop to negligible levels.
Phosphine is readily oxidized so that even if traces were produced, they would most
likely be converted into orthophosphoric acid (H3PO4) and water (H2O) by residual
oxygen present in the exhaust gases.
22 Priority Existing Chemical Assessment Report Number 25
9. Exposure
9.1 Environmental exposure to the alkyl phosphate additive
The importation, manufacture, handling, storage, blending and transportation of alkyl
phosphate AVSR additives for use in LRP are unlikely to involve large releases into the
environment. Such accidental releases are likely to be at managed facilities, or to be of
a diffuse nature since LRP is used throughout Australia.
The active alkyl phosphorus-based component is manufactured in situ in a reaction
vessel and then diluted into the final formulated Valvemaster product as one process.
At the completion of manufacture, the manufacturer packs the product into ISO tanks
or 200 L closed head steel drums. Product stored in drums is kept in appropriate
undercover warehouses at the manufacturing site until dispatched to customers. The
manufacturing site is a licensed Dangerous Goods Storage facility and products and
raw materials are stored there in accordance with a licence. The full drums are
transported around the manufacturing site and loaded and unloaded from delivery
vehicles using fork lifts.
Bulk quantities of the alkyl phosphate additive (Valvemaster Concentrate) for the
production of LRP are supplied to oil companies in 20-22 tonne nominal weight,
bottom discharge ISO tanks or in 186 kg steel drums in truckloads of 10-12 drums per
load. Since the tanks and drums are transported as sealed containers, there is a low
likelihood of environmental release.
After use, empty drums are cleaned and recycled, any residue being removed by the
recycling process. A residual amount of Valvemaster Concentrate, e.g. 500 mL, may
be retained in each drum.
Bulk quantities of Valvemaster Concentrate are stored at the manufacturing facility at
oil company terminals. Bulk quantities of the alkyl phosphate additive are also
transported by road tankers and haul vehicles from storage facilities to customers and
retail outlets. Where the alkyl phosphate additive is exported, bulk quantities may be
present on ships in Australian waters and at port facilities in ISO tanks and 200 L
drums as full container loads (FCLs).
Spillage of Valvemaster Concentrate from road tankers may potentially occur during
incidents at ISO tank filling, transportation, and emptying operations, although filling
and emptying facilities are likely to be located within containment facilities.
Potentially, road transportation accidents may result in the loss of concentrated product
from ISO tank along transportation routes.
LRP containing diluted Valvemaster is not stored in bulk at oil terminals, but is
contained in road tankers during transport, at customer and retail service station outlet
underground (UST) and above ground (AST) storage tanks.
All pumping and metering at oil terminals during LRP blending is typically conducted
under automated control and it is expected that the ISO tanks and the pumping and
control equipment associated with the transfer of the alkyl phosphate additive would be
installed in bunded areas to contain all leaks or spills. Due to these engineering
controls, the release of Valvemaster Concentrate or LRP is not expected during
routine operations. Spillages resulting from transfer would likely be contained and
23
Alkyl Phosphate AVSR Additive
diverted to on-site waste treatment facilities and disposed of appropriately in
accordance with an approved waste management plan.
Spill incidents involving LRP containing diluted Valvemaster may potentially occur
from road tankers during transportation to customers and retail services stations and
during transfer activities. Minor spillage of LRP may also occur during customer usage
from bowsers. Spillage resulting from transfer activities is likely to be managed in
accordance with established safety procedures and diverted to site waste containment
facilities for collection and off-site waste disposal if present. Such incidents are rare
and typically involve small quantities of LRP.
A relatively smaller quantity of the alkyl phosphate additive is currently imported in
aftermarket products. Large environmental releases of the alkyl phosphate additive
from aftermarket products are unlikely. This may arise due to spillage or residual
quantities remaining in the containers following disposal. Most emptied bottles and
applicators are disposed of to landfills, although recycling of plastic bottles is also
possible. Due to the Australia-wide use of these additives, the associated release of the
alkyl phosphate additive from disposal facilities will be diffuse and at low levels.
Physico-chemical properties of the alkyl phosphate additive products are given in
Section 4. Valvemaster VM11 and Valvemaster Concentrate show persistent
qualities under typical environmental conditions. Atypical conditions, however, e.g.
landfill, increase the rate of degradation. Spills of Valvemaster may be persistent in
the environment and may enter water and be adsorbed into sediment and soil
compartments.
Like other fuels, LRP is typically stored in underground storage tanks (USTs). In
general, USTs have a tendency to begin leaking over time, resulting in release of fuel to
groundwater. USTs have been installed throughout Australia at terminals and
refineries, fuel depots, service stations, and many private facilities and organisations
have USTs for fuel storage.
Not all USTs leak. However, many have and have required decommissioning and land
remediation. The length of service of the tank is one of a number of factors increasing
the risk of UST leakage. Other factors include the type of construction materials,
presence of liners, fuel type, fittings/pipes and environmental conditions surrounding
the UST. Major fuel suppliers generally have tank decommissioning and replacement
programs and install leak detection equipment on their tanks to prevent leaks from
occurring and to trigger pollution abatement procedures to minimise risks to the
environment where leaks are detected.
Except in the cases of gross spillage of LRP containing the chemical, e.g. leakage from
USTs or aboveground spillages, very little release to the soil compartment is likely and
apart from areas in the vicinity of such spills and leaks no accumulation of the alkyl
phosphate additive is likely in soils.
In the immediate vicinity of leaking USTs, and at LRP spill sites, the alkyl phosphate
additive concentration may approximate that of the alkyl phosphate additive in LRP
(180-600 mg/L). Site-specific conditions will determine the fate and environmental
concentration of the alkyl phosphate additive in groundwater with distance away from
leaking UST sources.
24 Priority Existing Chemical Assessment Report Number 25
9.2 Exhaust release from combustion of the alkyl phosphate additive
The main fate of the alkyl phosphate additive products is likely to be destruction
through combustion in internal combustion engines. Most of the alkyl phosphate
component of the Valvemaster products is destroyed in the cylinders and exhaust
trains of motors with the main phosphorus-based compound emitted being phosphoric
acid (Section 8).
Based on the current LRP market and assuming an LRP content of 0.5 mL of
Valvemaster per litre of LRP, the amount of the alkyl phosphate additive in the
AVSR additive market in Australia is currently expected to be less than 1150 tonnes
per annum as Valvemaster Concentrate (Table 3). Corresponding to the expected
decline in demand for LRP over time as vehicles requiring AVSR additives are phased
out, the amount of alkyl phosphate additive in the AVSR additive market in Australia is
expected to decline to 460 tonnes as Valvemaster Concentrate in 2004 (Table 3).
Valvemaster Concentrate has a total phosphorus content of approximately 4.8% to
5.2%. (5.1%, Octel, 1999b). It is conservative to assume that all the phosphorus is
discharged in exhaust emissions. It is indicated that approximately 28% of the
phosphoric acid may become entrained in the exhaust system by reaction with metal
surfaces (Section 8). Some metal phosphate particulates might also be emitted from
exhaust systems (Section 8).
Based on conservative assumptions, i.e. no losses or entrainment of particulate matter
in the exhaust system and 5% total phosphorus content, the amount of phosphorus in
exhaust emissions may be approximately 57.5 tonnes at present and 23 tonnes in 2004,
declining further over time (Table 3). Assuming 28% exhaust entrainment (Section 8),
the current and 2004 Australia-wide emission tonnages of phosphorus are reduced to
42.5 and 16.6 tonnes, respectively.
Once emitted, these phosphoric acid vapours and metal phosphate particulates may be
transported in air, the fate of which depends on local and regional environmental and
climatic conditions. Eventually, precipitation to land or water, or both, is likely.
According to USEPA/USDA (1988), the average vehicle exhaust emissions of CO, HC
and NOx from combustion of LRP containing the alkyl phosphate additive were not
consistently nor significantly affected by additive use in most cases. Phosphorus
emissions will increase as a result of using the alkyl phosphate additive but lead
emissions will be less due to the lower lead content of the LRP.
9.3 Fate
This section provides a description of the potential environmental fate of phosphoric
acid vapours following exhaust gas emission after combustion of fuels containing the
alkyl phosphate additive.
In summary, phosphoric acid vapours are likely to eventually precipitate to land or
water, or both, and to integrate with the existing phosphorus biogeochemical cycle in
the environment.
This section also describes the fate of the alkyl phosphate addititive in ground water
and following disposal to landfill where it forms inorganic phosphate, which will
integrate with the existing phosphorus biogeochemical cycle in a similar manner to
phosphoric acid.
25
Alkyl Phosphate AVSR Additive
9.3.1 Phosphorus biogeochemical cycle
The earth's crust contains approximately 0.12% phosphorus, but it does not occur in
free form, being found in the form of phosphates in minerals such as chlorapatite,
fluorapatite, vivianlite, wavelite and phosphate rock or phosphorite (Merck, 2001).
Phosphorus compounds derived from the combustion of the alkyl phosphate additive
are likely to integrate into the existing phosphorus biogeochemical cycle. The
phosphorus biogeochemical cycle involves natural and pollutant sources of phosphorus,
including biological, organic and inorganic forms. ANZECC and ARMCANZ (2000)
indicate that phosphorus is constantly cycled from one form to another within aquatic
ecosystems although a fraction may be buried through the process of sedimentation in
water bodies or isolated through mineralisation in complexes of low solubility.
Not all phosphorus in the environment is in a bioavailable form. The most bioavailable
form of phosphorus is considered to be orthophosphate (PO43-). Bioavailable
phosphorus is comprised of dissolved phosphorus (DP) and bioavailable particulate
phosphorus (BPP). Particulate phosphorus is presumed to be less available, however,
for aquatic ecosystems this issue has not been fully resolved (ANZECC and
ARMCANZ, 2000).
Biological phosphorus is a key constituent of cellular DNA. The major inorganic
phosphorus species include soluble dihydrogen phosphate ion (H2PO4-) and
(HPO42-)
monohydrogen phosphate ion and insoluble hydroxyapatite
(Ca10(PO4)6(OH)2) (Manahan, 1993; ANZECC and ARMCANZ, 2000).
Soil and aquatic processes are very important in the phosphorus cycle. Phosphorus is a
common limiting factor in aquatic environments, particularly for the growth of algae.
Bacteria are even more effective than algae in taking up phosphate from water and
accumulating phosphorus as excess cellular phosphorus that can be released to support
additional growth, if the supply of phosphorus becomes limiting in the future
(Manahan, 1993).
Phosphorus occurs as organic or inorganic phosphates. Organic phosphates are derived
from living plants and animals. Inorganic phosphates may occur naturally and may
bond to soil particles. Phosphorus exists in water in both dissolved and particulate
forms. Particulate phosphorus includes phosphorus bound up in organic compounds,
such as proteins, and phosphorus adsorbed to suspended particulate matter such as clays
and detritus (dead and decaying organisms). Dissolved phosphorus includes inorganic
orthophosphate (H2PO4-, HPO42- and PO43-), polyphosphates, organic colloids and low
molecular weight phosphate esters.
Dead microorganisms release phosphorus that can support additional organisms
(Manahan, 1993). Biodegradation of phosphorus compounds is important in the
environment for mineralisation (release of inorganic phosphorus from the organic form,
thereby providing a source of nutrient orthophosphate) (Manahan, 1993).
Although the percentage of phosphorus in plants is low, it is an essential component.
Phosphorus must be present in a simple inorganic soluble form before it can be taken in
plants. Utilisable forms for plants include forms of the orthophosphate ion. In the pH
range present in most soils, these forms predominantly include H2PO4- and HPO42-,
with H2PO4- dominant in slightly acidic soils and HPO42- dominant in slightly alkaline
soils.
26 Priority Existing Chemical Assessment Report Number 25
In acidic soils, phosphate ions are precipitated or adsorbed by species of aluminium and
iron:
Al(OH)3 + H2PO4- (soluble) Al(OH)2HPO4 insoluble (1)
In alkaline soils, orthophosphate may react with calcium carbonate to form relatively
insoluble hydroxyapatite (Ca10(PO4)6(OH)2).
In agricultural systems, phosphorus compounds (including phosphoric acid) are applied
to enhance soil nutrition for crop and pasture growth. In general, because of sorption
and precipitation, little phosphorus applied as fertilizer leaches from the soil. However,
agricultural fertilizer runoff has led to phosphate pollution issues (Manahan, 1993).
In soil, the contribution of phosphorus from fallout from the combustion of the alkyl
phosphate additive is expected to be low but bioavailable and to be taken up by
opportunistic organisms. A fraction may also complex with metals, e.g., aluminium
and iron, and adsorb to soil particles. A portion may partition into runoff, leading to
discharge into aquatic receiving environments.
Phosphoric acid will also precipitate from air to water in a bioavailable form for uptake
by opportunistic aquatic organisms, e.g. phytoplankton. Sediments can accumulate
phosphorus compounds and recycling into the water column can occur through
resuspension and diffusion under certain environmental conditions. A fraction may be
isolated through the process of sedimentation.
Phosphoric acid is highly miscible in water. Water solubility is estimated at 750 to
850 g/L at 20癈. Phosphoric acid in water is likely to dilute due to mixing and
dispersion. The concentration depends on the quantity in the water and the
environmental conditions at the time. Natural water hardness minerals, e.g. calcium,
magnesium, iron and aluminium, in water bodies are likely to buffer against a reduction
in pH (Equation 1). The phosphorus component may persist in the biogeochemical
cycle (Environment Canada, 1981, as cited in ECB, 2000).
Sediments (both bottom and suspended) play a significant role in the cycling of
nutrients. Phosphorus exists as phosphates, both monomeric and polymeric. In
sediments, phosphorus is usually bound with iron (ANZECC and ARMCANZ, 2000).
Considerable phosphorus (and nitrogen) can also be bound by bacteria. Under
anaerobic conditions, phosphate can be released from sediments into the overlying
water, but the general understanding of the processes that drive the cycling of nutrients
through sediments is poor (CSIRO, 2000).
Davis et al (1974) introduced radiotracer phosphoric acid into water, which was rapidly
accumulated in the sediment, with most becoming bound to iron and aluminium.
Bioturbation by sediment-dwelling organisms increased the rate of accumulation and
depth of infiltration of phosphorus into the sediment, as did diffusion.
9.3.2 Environmental biodegradation and bioaccumulation
Phosphorus is an essential nutrient of microorganisms, plants and animals. Phosphoric
acid is readily utilisable by terrestrial and aquatic plants and microorganisms.
Phosphorus compounds are an important component of living matter and all organisms
contain a certain quantity; however, excessive bioaccumulation is unlikely due to
natural metabolic processes for essential nutrients (Frausto da Silva & Willimans,
1991).
27
Alkyl Phosphate AVSR Additive
9.3.3 Landfill disposal and fate of the alkyl phosphate additive
Woodward-Clyde (1996) has reviewed the potential likely effects of the disposal of
retained Valvemaster Concentrate in spent applicators in a typical landfill setting. In
summary, the alkyl phosphate additive is not expected to be highly mobile in landfills
and is expected to degrade. Cleavage of the phosphate alkyl bond will occur under the
mildly acidic conditions typically occurring in landfill and will result in the formation
of an aliphatic chain and the remaining alkyl phosphate. Such hydrolysis of the alkyl
group is likely to occur rapidly once the alkyl acid phosphate compounds are exposed
to water and progressive loss of the alkyl chains to form inorganic phosphate is likely.
Of these resulting products, orthophosphate is soluble in water and will exist in the di-
protonated form in the pH range of approximately 2.5 to 7. The severed aliphatic chain
will remain insoluble in water (Woodward-Clyde, 1996).
The Woodward-Clyde proposal for the biodegradation of the alkyl phosphate additive
in mildly acidic conditions is consistent with the general reactivity of
organophosphorus compounds. The rate of degradation or reactivity of the alkyl
phosphate additive will depend on the nature of the nucleophiles in the landfill and on
the leaving groups on the alkyl phosphate additive as well as the acidity of the landfill.
Under anaerobic landfill conditions, the aliphatic chains of the alkyl acid phosphate
compounds will have a maximum half life of approximately 16 to 20 weeks
(Woodward-Clyde, 1996). Aliphatic chains will be readily degraded by heterotrophic
bacteria. The presence of the amino group in the active component will assist the
microbial degradation of the alkyl phosphate. The more mobile orthophosphate
compound will be utilised by landfill microorganisms as a nutrient for growth.
Phosphate is also strongly adsorbed to soil particulates such as iron and aluminium
oxides and hydroxides and aluminosilicate minerals which will reduce the mobility of
this compound in the landfill (Woodward-Clyde, 1996).
The quantities of the alkyl phosphate additive sent to landfills for disposal are unlikely
to contribute significantly to the total phosphorus already in landfill leachates from a
range of other sources. The Woodward-Clyde (1996) study tries to quantify the amount
of Valvemaster in landfill for use patterns in New Zealand. A similar negligible
contribution to total phosphorus in landfill leachate is expected in Australia. Many
landfill systems have leachate collection and treatment systems to capture and treat
leachate wastes to prevent environmental contamination.
9.3.4 Groundwater and fate of the alkyl phosphate additive
The processes affecting the fate of the alkyl phosphate additive in groundwater are
expected to be similar to those in a landfill leachate environment (refer above). The
chemical is not expected to be highly mobile in groundwater and is expected to degrade
over time by hydrolysis and biodegradation processes.
9.4 Potential environmental concentrations of phosphoric acid
This section provides an estimation of the potential environmental concentrations of the
alkyl phosphate additive and phosphoric acid in the environment following the
combustion and exhaust emission of fuels containing the alkyl phosphate additive.
28 Priority Existing Chemical Assessment Report Number 25
9.4.1 Exposure from use
Following combustion and exhaust emission, the atmospheric concentration of
phosphoric acid is expected to be low due to the diffuse patterns of use and release
across Australia.
The level of atmospheric phosphorus resulting from the combustion of fuel containing
the alkyl phosphate additive is dependent on the amount of fuel used, the quantity
entrained in exhaust systems and meteorological conditions in the areas where the fuel
is used. There are uncertainties associated with each of these factors and in order to
make estimates of likely levels of atmospheric phosphoric acid resulting from use of the
alkyl phosphate additive in Australian fuel, it is necessary to make some assumptions
based on the following consideration.
All estimates are made for Sydney which, with a population of 3.8 million, comprises
20% of the total Australian population of 19 million and covers an area of
approximately 1550 km2. Since it is reasonable to assume that fuel use would
approximate population density, it is assumed that 20% of the petrol usage in Australia
would be used in Sydney.
Based on expected LRP demand, two AVSR additive use scenarios (Table 3) are
examined corresponding to:
? Scenario 1: where the total current Australian use of Valvemaster
Concentrate is constant at 1150 tonnes per annum for 90% bulk LRP
and 10% aftermarket use; and
? Scenario 2: where the total Australian use of Valvemaster
Concentrate is constant at 460 tonnes per annum in 2004 for 100%
aftermarket use with bulk LRP no longer available for sale.
An atmospheric box model approach has been used. Implicit in the box model
approach is that emissions are expected to behave as if they are released into a box with
horizontal dimensions of the urban area (selected so that there is no significant influx of
emissions into the box). Various assumptions can then be made about phosphoric acid
accumulation and dispersion of phosphoric acid from the atmospheric box.
Two predicted environmental exposure concentrations for phosphorus and phosphoric
acid in the air have been estimated resulting from the current and future use of the alkyl
phosphate additive in Australian fuel. These include an average (AVE) estimate and a
reasonable maximum exposure (RME) estimate.
For the calculation of the AVE, representing a long-term average exposure
concentration, total yearly alkyl phosphate additive use is used to calculate phosphorus
and phosphoric acid emissions over each day with assumed daily clearance of
accumulated air from the atmospheric box.
The RME calculation represents the phosphorus and phosphoric acid concentration that
may potentially accumulate in the air during weather periods of consecutive windless
days. This concentration is unlikely to be attained frequently. Information on
consecutive windless days in Australian cities is not readily available as this is not a
parameter normally monitored. As such, a conservative estimate of 3 consecutive
windless days has been used in this assessment.
29
Alkyl Phosphate AVSR Additive
Exposure Scenario 1: Present Use
RME concentration for phosphorus and phosphoric acid
The estimated LRP market for 2001 is described in Section 7.5 (Table 3). If 20% of
this market was to be used in Sydney, this is equivalent to approximately 500 ML
(mega litres) of LRP containing approximately 230 tonnes of Valvemaster
Concentrate. The phosphorus content of Valvemaster Concentrate is approximately
5% (Octel, 1999b). This quantity corresponds to approximately 11.5 tonnes of
phosphorus.
Phosphoric acid (H3PO4) has a molecular weight of approximately 97.994, and
phosphorus contributes about 31.61% of this molecular weight. Oxygen contributes
approximately 65.31%, and hydrogen 3.08%. As such, the 11.5 tonnes of phosphorus
per annum may equate to approximately 36.4 tonnes as phosphoric acid.
It is readily shown that the effective height of the air column over a particular area is
6.15 km (see for example Connell and Hawker, 1986), and so this 11.5 tonnes of
phosphorus (36.4 tonnes of phosphoric acid) would potentially be released into an
atmospheric volume of 1550 x 6.15 km3 or approximately 1013 m3. However, the
assumption that the phosphoric acid would be homogeneously distributed throughout a
6.15 km air column is unrealistic. A more realistic assumption is to assume that the
particles are only distributed in the lowest 615 metres (i.e. 1012 m3).
In order to go any further it is now necessary to make some simplifying assumptions,
and while these are not entirely realistic they nevertheless allow for a first
approximation to the atmospheric phosphorus level. If it is assumed that the air column
is perfectly static, that the particulate matter is homogeneously distributed through the
air volume and that none is precipitated with rain or through other mechanisms, then
after one year the atmospheric phosphorus level is estimated as 1.15 x 1016 ng/1012 m3 =
11 500 ng/m3. In terms of phosphoric acid concentration, this equates to 3.64 x 1016
ng/1012 m3 = 36 400 ng/m3 of phosphoric acid.
The assumptions made above are considered unrealistic in that no dispersion through
wind or by rain is considered. If it is assumed that all the phosphorus emitted each day
remains suspended for 3 days without removal, as may potentially occur occasionally
following 3 consecutive windless days, then the atmospheric RME concentration could
be as high as 95 ng/m3 phosphorus or 300 ng/m3 phosphoric acid.
AVE concentration for phosphorus and phosphoric acid
An AVE phosphorus and phosphoric acid concentration in air at ground-level may be
estimated taking into account losses due to wind dispersion out of the urban area. The
average concentration at any one time within the atmospheric box may be estimated as
the influx rate minus the emission rate from the atmosphere box.
An influx of 1.15 x 1016 nanograms P/year (3.15 x 1013 ng P/day) has been estimated
above. Emitted into an air volume of 1012 m3 each day, an average daily air
concentration of 31.5 ng/m3 has been estimated using this model. This equates to
100 ng/m3 of phosphoric acid (Table 4).
Exposure Scenario 2: 2004
This scenario assumes bulk sales of LRP have declined to 1000 ML as outlined in
Section 7.5 (Table 3) which equates to 460 tonnes of Valvemaster Concentrate.
30 Priority Existing Chemical Assessment Report Number 25
Assuming 20% (92 tonnes of Valvemaster Concentrate) is used in Sydney, the
calculations and assumptions for this scenario are identical to the above. Therefore,
with a 20% release rate, approximately 4.6 tonnes per annum of phosphorus
(14.6 tonnes of phosphoric acid per annum) may be emitted into the air column
(Table 4).
The estimated phosphorus and phosphoric acid atmospheric AVE and RME values for
the current and 2004 use scenarios are given in Table 4.
Table 4 - Estimated average and reasonable maximum potential atmospheric
levels in Sydney with the use of the Alkyl Phosphate Additive
Atmospheric Dispersion of Phosphorus Compounds (a)
AVE RME
Nil
Use Scenario
(ng/m3) (b) (ng/m3) (ng/m3) (d)
P H3PO4 P H3PO4 P H3PO
4
Scenario 1: Present 11 500 36 400 31.5 100 95 300
Scenario 2: 2004 4 600 14 560 12.6 40 38 120
a. Air column volume of 1012 m3 (615 m high x 1550x106 m2); b. Assumes no dispersion throughout year
(unrealistic); c. AVE (Long Term Average), assumes wind dispersion with daily clearance of atmospheric
box; d. RME (Reasonable Maximum Exposure) ?Quiescent conditions for 3 days.
Due to the complexities implied by uncertainties in the use rate of the alkyl phosphate
additive and the prevailing atmospheric conditions in particular areas, these estimates
of the atmospheric phosphoric acid should be treated as indicative only. The level of
phosphoric acid in the atmosphere would be dependent on factors such as rain and
wind, and it is likely that ambient and prior weather conditions would impact on any
particular daily measurement.
9.4.2 Potential release of phosphorus to water compartment
Based on Scenario 1, the annual use in Sydney of approximately 230 tonnes of
Valvemaster Concentrate would generate a worst case of 36.4 tonnes of phosphoric
acid (11.5 tonnes of phosphorus) emissions (Section 9.4.1).
Eventually, the phosphoric acid will precipitate to the earth's surface (land and water)
in rainfall or dust where the soluble nature of the compound means that it may leach
into soil and dissolve in water. Reactions forming stable compounds with particulate
matter, calcium carbonate or metals, e.g. aluminium, iron, are likely to occur in soils
and sediments. The bioavailability of the phosphoric acid means that a fraction may be
taken up by biota. Thus, a proportion of the phosphorus fallout will be associated with
soils and biota.
Atmospheric dispersion associated with weather patterns is also likely to result in
movement of phosphoric acid away from source areas.
If it is assumed that Sydney, with a land area of approximately 1550 km2 , receives an
average annual rain fall of one metre, then it is possible to estimate the concentration of
phosphorus in storm water (assuming no stabilization of phosphorus compounds in soil,
31
Alkyl Phosphate AVSR Additive
biological uptake, atmospheric dispersion from source areas) as
11.5 x 106 (grams)/(1550 x 106 (m2) x 1 m) = 0.0074 g/m3 or 7.4 礸/L in annual
stormwater runoff for the present use scenario, and approximately 2.96 礸/L in the year
2004, assuming lower future LRP use rates. By allowing for atmospheric dispersion
due to wind, the annual average phosphorus stormwater run-off concentration is likely
to be much lower for the present use and 2004 scenarios.
These concentrations are much less than the concentration range of total phosphorus in
estuarine and marine waters in southeast Australia, which is approximately 25 to
30 礸/L (ANZECC and ARMCANZ, 2000).
The assumption of discounting soil attenuation processes following atmospheric
precipitation of phosphoric acid is unrealistic because of the sorption and precipitation
processes that are likely to occur in both alkaline and acidic soils (Manahan, 1993).
Assuming 50% of the land surface is developed, i.e. pavement or hard surface other
than soil, the above stormwater concentration estimates could be halved. In addition,
some atmospheric dispersion is likely to occur, thus contributing to a reduction in the
phosphoric acid in the air column of the Sydney region.
Furthermore, the stormwater concentration estimates do not take into account the
dilution, mixing and sedimentation that is likely to occur in receiving waters within and
beyond stormwater outlet mixing zones or pollution control measures, e.g. sediment
traps, which may reduce stormwater concentrations discharged by several orders of
magnitude. As such, the concentration estimates above are unlikely to reflect ambient
water quality conditions.
9.5 Occupational exposure to the alkyl phosphate additive
Occupational exposure to the alkyl phosphate additive is possible during manufacture
of bulk Valvemaster Concentrate, transport and handling of bulk Valvemaster
Concentrate and aftermarket products and the blending, transport and handling of alkyl
phosphate additive-based LRP.
Ideally, the assessment of occupational exposure is based on workplace monitoring data
or, where such data is inadequate or unavailable, on knowledge-based models that
estimate exposure when the various patterns of use and the physical properties of the
substance under investigation are known.
Due to the lack of monitoring data and physico-chemical properties for the alkyl
phosphate additive itself, quantitative exposure estimates for the additive could not be
undertaken. Consequently, a qualitative description of the potential levels of
occupational exposure to the alkyl phophate additive are described in the following
section.
Furthermore, a quantitative estimate is made of the potential level of occupational
exposure to phosphoric acid, which is identified as the combustion and tailpipe
emission by-product of the the alkyl phosphate additive (Section 8).
The major routes for occupational exposure to the alkyl phosphate additive are skin and
eye contact with the alkyl phosphate additive products or LRP. Inhalation exposure to
the alkyl phosphate additive is not regarded as a major route of exposure due to the low
vapour pressure of the alkyl phosphate additive products (Section 5).
32 Priority Existing Chemical Assessment Report Number 25
9.5.1 Manufacture
Occupational exposure in Australia to the alkyl phosphate additive during formulation
is limited to the manufacture and formulation in situ of bulk Valvemaster
Concentrate.
Valvemaster Concentrate is manufactured at one plant in Australia and usually takes
place twice a month or a total of approximately four working weeks per year. The
number of workers involved in the process is typically two operators (8-hour day) per
batch, with one laboratory worker involved in the quality assurance testing of the batch.
The occupational exposure levels to the alkyl phosphate additive during the formulation
of Valvemaster Concentrate are predicted to be low given the fully enclosed
formulation process, low vapour pressue of the product and intermittent (twice
monthly) formulation schedule.
9.5.2 Bulk LRP blending
Several oil companies are blenders of bulk LRP and hence handlers of AVSR fuel
additives.
ISO tanks and drums transported to oil company terminals and depots by road (or rail)
will remain unopened prior to use in fuel blending. Consequently, provided these
containers are not accidentially punctured, exposure of transport workers to the alkyl
phosphate additive is not expected.
At the oil company terminals and depots, bulk Valvemaster Concentrate is typically
unloaded in the open air by manually connecting a flexible hose to the lower delivery
tank flange of the ISO tank via a closed gravity transfer/delivery system or decanted
from drums via a hand pump and a spear or a dedicated pumping system into a bulk
storage tank. Oil company terminals are characteristically larger operations than
depots.
During LRP blending at oil company terminals and depots, Valvemaster Concentrate
is typically pumped using an automated vapour recovery system from the storage tank
and injected directly (in-line dosing) into the petrol stream of the LRP road tanker. At
some depot(s), Valvemaster Concentrate is decanted manually into a receptacle for
addition to the LRP tanker compartment.
During bulk LRP blending and transfer activities workers wear pvc or rubber gloves,
safety goggles, shoes and protective clothing. In addition, a respirator with an organic
cartridge is used at depot(s) which decant the alkyl phosphate additive manually into
the trunk compartment. Typical exposure durations for workers engaged in bulk LRP
blending at terminal and depots decanting Valvemaster Concentrate from drums or
ISO tankers are shown in Table 5.
Exposure of terminal and depot staff to the alkyl phosphate additive may occur during
inadvertent spills and slops resulting from the manual handling of transfer lines
containing either LRP or Valvemaster Concentrate, the manual addition of the alkyl
phosphate additive to road tankers and handling of the final blended fuel in the
laboratory.
33
Alkyl Phosphate AVSR Additive
Table 5 - Handling of the alkyl phosphate additive during LRP blending at typical
terminals and depots
Category of No. of Description of Hours/day Days/year
worker workers Work
Terminal
Terminal 2 Decanting (dedicated 6 3
pump) of 200 L
staff
drums
Terminal 1 Assisting 1 12
staff maintenance staff
2 1
Facility Gravity discharge
operator ISO tanker contents
into underground
tank
Fitters 1 Connect ISO tanker 5 min/2 weeks 25
to additive pump
< 0.5
Tank 1 Stock reconcilation 52
dipping
operator
Maintenance 1 Maintain additive 4 2
worker pump injector
Transport 10 Transport of LRP 1 300
staff
Maintenance 2 Maintain despatch 2 12
worker systems
Depot
5 min 260
Depot 1 Decanting additive to
labourers receptacle and into
LRP truck
compartment
Yardmen 1 Decanting (dedicated 2 hr/month 12
pump) of 200 L
drums to storage tank
Depot staff 1 Automated addition 5 min variable
to LRP truck
compartment
34 Priority Existing Chemical Assessment Report Number 25
The exposure levels during bulk LRP blending are predicted to be low given the
typically automated and enclosed transfer activities and the use of personal protective
equipment (PPE). Non-automated additions of the alkyl phosphate additive at small
depots may potentially result in increased occupational exposure for short (5 min)
periods compared to automated enclosed additions of the alkyl phosphate additive to
the LRP truck compartment.
9.5.3 Petrol stations and maintenance workshops
Scenario 1: Present use
At petrol stations, bulk LRP, which constitutes 90% of the LRP market, will be
transferred from road tankers to underground storage tanks. Transfer requires that
tanker drivers manually connect and disconnect flexible tansfer lines between the
tanker and storage tank. During this process, skin and eye exposure to the diluted alkyl
phosphate additive in LRP is possible from slops and spills.
Potential exposure of transport drivers may occur frequently during the day in
metropolitan areas with numerous offloads and less frequently during tanker deliveries
to regional areas. There is the potential of mainly dermal exposure for petrol station
workers undertaking dip measurement of underground LRP tanks. Typically, dipping
occurs for up to 10 minutes once per week.
The potential occupational exposure profile to the aftermarket alkyl phosphate additive
products for Scenario 1 will be similar for Scenario 2 and is described below.
Scenario 2: 2004
As bulk LRP blending is replaced by forecourt addition by vehicle owners, no
occupational exposure to the alkyl phosphate additive by depot and terminal staff and
other personnel associated with bulk LRP blending and distribution will occur.
Service station forecourt workers may be exposed if they assist vehicle owners in filling
cars; however, this is likely to be infrequent as most service stations are self service and
the majority of cars do not use LRP. The extent of the occupational exposure during
this activity is likely to be variable, depending on vehicle throughput, average LRP fill
rate per vehicle, the customer's preferred choice for blending LRP, i.e. single- or multi-
treat applicators, and the amount of alkyl phosphate additive contaminating spent
aftermarket devices.
The potential exposure per vehicle fill-up is greater with the 250 mL multi-treat bottle
compared with the 10 mL single-use syringe-type aftermarket product. This is because
more contamination from spills and slops may occur when using the multi-treat
compared with the single-use applicator. The difference is that the treatment volume is
delivered from an open mouthed bottle versus direct injection from a syringe into the
fuel tank.
Furthermore, the more viscous alkyl phosphate additive formulation contained in the
single use applicators, as compared with the multi-treat bottles, would further limit
spills and slops. The more concentrated alkyl phosphate formulation in the 10 mL
applicators increases, however, the potential alkyl phosphate dose per exposure. In
most cases, exposure will be at most once a week (per fill) for short duration, e.g.
5 minutes, and will not be undertaken by workers.
35
Alkyl Phosphate AVSR Additive
As for both Scenario 1 and 2, automechanics at petrol stations and maintenance
workshops may be exposed to the diluted alkyl phosphate additive in LRP during
maintenance of automotive fuel systems. The extent of exposure during these activities
is likely to be highly variable and to decrease over time as VSR susceptible vehicles are
withdrawn from the Australian motor vehicle fleet.
9.5.4 Importation, transport and handling of the alkyl phosphate products
Aftermarket alkyl phosphate additive products are imported in cartons through a single
port of entry prior to central warehousing and dispatching by road (and rail) to
distribution centres and retail outlets within the states and territories.
The extent of exposure to the alkyl phosphate additive in the aftermarket devices during
these activities is expected to be unlikely except if accidental puncturing of the plastic
devices occurs.
9.6 Occupational exposure to phosphoric acid from the alkyl phosphate
additive use
The combustion of the alkyl phosphate additive produces phosphoric acid exhaust gas
emissions (Section 8). Several classes of workers are exposed potentially to phosphoric
acid in occupational settings due to emissions from automotive exhaust of vehicles
using fuel containing the alkyl phosphate additive. The extent of this exposure will
diminish as VSR susceptible cars are gradually removed via attrition from the
Australian motor vehicle fleet.
The exposure of petrol station attendants is likely to be highly variable depending on
the required duties (purely retail versus petrol pumping), the level of customer traffic,
the separation of retail from service areas and the vehicle fleet, i.e. cars using LRP
versus ULP.
Automechanics may be particularly exposed to phosphoric acid exhaust emissions
when servicing operating autoengines in poorly ventilated workshops. Attendants,
security and other personnel who work in enclosed car parks such as underground
parking stations, also have a potential for inhalation exposure to phosphoric acid
exhaust emissions during routine duties. Like service station workers, exposure during
the working day is likely to be highly variable and dependent on the level of, and
proximity to, customer traffic and the effectiveness of ventilation of the enclosed
parking station.
Professional drivers such as taxi and truck operators and road maintenance workers
may also be exposed to phosphoric acid from inhalation of automotive exhaust
emissions. Again, the level of exposure is likely to be highly variable and dependent on
traffic volume and, in the case of road workers, whether work is on new,
uncommissioned or light duty roads or on heavily trafficked arterial roads repaired
while in use.
The major routes for occupational exposure to phosphoric acid in exhaust emissions are
eye and inhalation. No quantitative data are available regarding personal exposure
levels to phosphoric acid as a result of the use of the alkyl phosphate additive based
LRP within workplaces.
36 Priority Existing Chemical Assessment Report Number 25
It is anticipated that occupational exposure of garage mechanics/autorepairers may
potentially be high depending on the degree of ventiliation and whether or not the
workshop doors are open or closed.
A tailpipe phosphoric acid exhaust emission concentration of 6.0 to 8.3 mg/m3 is
calculated (Section 8) dependent on reaction between phosphoric acid and the metals of
the exhaust valve seat or exhaust system.
Atmospheric dilution of tailpipe phosphoric acid exhaust emissions will occur. An
estimated atmospheric phosphoric concentration is calculated assuming an exhaust gas
dilution factor of 100 (Dolan et. al, 1979) which may occur within two metres of the
end of a tailpipe on an idling vehicle. This estimated atmospheric phosphoric
concentration of 0.06 to 0.083 mg/m3 is potentailly reduced by a factor of 3 to 5 as the
distance from the tailpipe increases to 4 metres (Dolan et. al, 1979) to give atmospheric
phosphoric acid concentrations of 0.02 mg/m3 to 0.028 mg/m3 (for a dilution factor of
300) and 0.012 mg/m3 to 0.017 mg/m3 (for a dilution factor of 500).
9.7 Public exposure and level of exposure to the alkyl phosphate additive
9.7.1 Consumer exposure
Consumer exposure to the alkyl phosphate additive is likely to occur as a result of
contact during refuelling vehicles with LRP, adding aftermarket product to petrol tanks,
using LRP as a solvent or cleaner, or substance abuse (petrol sniffing). Direct
exposure of skin and eyes to the additive is, therefore, probable.
Due to lack of information, it is difficult to quantify the level of exposure likely to be
encountered during consumer end-use of bulk LRP and the aftermarket alkyl phosphate
products. Nonetheless, it is expected that consumer exposure is likely to be a regular
occurrence for vehicle owners, e.g. weekly, take place under open conditions and
involve small quantities per event, as evidenced by the small size of the aftermarket
devices and low concentration of the alkyl phosphate additive in LRP.
The low vapour pressure of the concentrated alkyl phosphate additive product
(< 0.1 kPa) indicates that the extent of inhalation exposure to the alkyl phosphate
additive during filling with LRP is limited. Exposure to the petroleum constituents of
LRP is considered to be of greater potential concern than exposure to the alkyl
phosphate additive. Further, exposure to alkyl phosphate additive via the aftermarket
products is likely to be of greater potential concern than exposure via LRP. This is
because the aftermarket products contain higher concentrations of the alkyl phosphate
additive than LRP.
Accidental skin and possibly eye exposure to the alkyl phophate additive may occur
when refuelling vehicles with LRP and adding aftermarket products to fuel tanks.
Consumer dermal exposure to the alkyl phosphate additive will be highly variable yet
regular depending on a vehicle's or an engine's LRP use. Accidental ocular exposure
as a result of splashes of LRP and/or aftermarket products is likely to occur only
infrequently and involve very small amounts of the alkyl phosphate additive.
In young children, ingestion exposure is generally unlikely, although accidental
ingestion may occur if aftermarket products are stored in or around the home. Children
aged between one and a quarter and three and a half years can swallow approximately
4.5 mL of liquid (Gosselin et al., 1976). A child (10 kg) ingesting one mL of the
37
Alkyl Phosphate AVSR Additive
Valvemaster Concentrate (5.1% wt phosphorus) single use or multi-treat
Valvemaster VM11 (2.5% wt phosphorus) aftermarket product would receive an oral
dose of 4.7 mg/kg bw phosphorus (equivalent to 14.4 mg/kg bw PO43-) and
2.35 mg/kg bw phosphorus (equivalent to 7.2 mg/kg bw PO43-), respectively. The
ingestion by a child (10 kg) of 1 to 4.5 mL of Valvemaster Concentrate represents
9.4% to 42.2% of the recommended daily allowance (RDA) of phosphorus of 500 mg
(National Academies, 2003), for a child aged between 1 and 10 years of age
(Section 11). This ingested phosphate dose is halved if the alkyl phosphate additive is
obtained from the multi-treat aftermarket device. Aftermarket products are more likely
to be stored in garages than homes. Furthermore, the single-use applicator is primarily
purchased and immediately used as required at the service station forecourt by the
vehicle owner and the multi-treat aftermarket product is fitted with a child resistant
closure.
Accidental ingestion of the alkyl phosphate additive in LRP could occur when
syphoning petrol. Accidental ingestion by a child could occur also if LRP containing
the alkyl phosphate additive is stored in inappropriate containers in or around the home
environment. Australian National Hospital Morbidity Data shows approximately
133 hospital discharges annually between 1998 and 2000 were associated with the toxic
effects of petroleum products (AIHW, 2002). Victorian data show that there were
75 hospital admissions between 1987 to 1994 involving children below five years of
age who were poisoned by petroleum fuels and cleaners including kerosene. Data from
a selection of Victorian hospitals showed that there were 16 emergency department
presentations between 1989 and 1995 involving children below 5 years of age ingesting
petrol. Three of the 16 had syphoned petrol from a car or lawn mower and two had
drunk petrol from drink bottles (Ashby and Routely, 1996).
Although no data was available on the amounts of petrol ingested in these cases, it is
likely that only small amounts of LRP would be accidentally ingested. Data collected
by Watson et. al (1983) shows that the average volume of a swallow (of tap water) for a
child up to 5 years of age is between approximately 1 and 7 mL and for a person
between 5 and 18 years of age is between 2 and about 30 mL. Given these low
amounts of LRP and the low concentrations of the alkyl phosphate (600 mg/kg or
30 mg/kg phosphorus) in LRP, accidential ingestion would involve potentially only
very small amounts of the alkyl phosphate additive. With the solvent nature of
petroleum products, repeated ingestion or ingestion of larger amounts of LRP, e.g.
100 mL or more, is considered unlikely.
9.7.2 Indirect exposure via environment
As outlined in Section 9.1, exposure to the alkyl phosphate via the environment would
be due to incidental or accidental environmental release of the alkyl phosphate additive,
which will differ only slightly according to the nature of the application, e.g. bulk
application by the oil companies for the production of bulk LRP or aftermarket
applications by the general public.
The importation, manufacture, handling, storage and transportation of alkyl phosphate
AVSR additives for use in LRP are unlikely to involve large releases of the alkyl
phosphate additive into the environment (Section 9.1). Accidental releases are likely to
be at managed facilities or of a diffuse nature since LRP is used throughout Australia.
Therefore, it is likely that public exposure to the alkyl phosphate additive as a result of
atmospheric, soil, water or food contamination would be very low.
38 Priority Existing Chemical Assessment Report Number 25
9.7.3 Public exposure and level of exposure to phosphoric acid via air
The combustion by-product of the alkyl phosphate additive is phosphoric acid
(Section 8), which thus has the potential to increase public exposure to airborne
phosphoric acid.
Using atmospheric phosphoric acid concentrations from the most realistic atmospheric
dispersion model (Table 4) for Sydney, an estimate can be made for the potential public
inhalation exposure to phosphoric acid according to the two use scenarios described in
(Table 2). Scenario 1 assumes the LRP market share is maintained at present levels and
patterns of use. Scenario 2 assumes the LRP market is reduced in the year 2004 to an
aftermarket supply.
No data is currently available on ambient phosphoric acid levels in Australia. Given no
significant sources of airborne phosphoric acid can be identifed in Sydney, a negligible
mean air concentration of phosphoric acid is assumed as a background level for
Sydney. Furthermore, it is assumed that the total estimated phosphoric acid emissions
due to the combustion of the alkyl phosphate additive in LRP is respirable phosphoric
acid. The estimated atmospheric phosphoric acid levels given for Scenario 1 and 2
(Table 6) represent the estimated increase in air phosphoric acid concentrations and
exposures attributable to combustion of the alkyl phsophate additive in LRP.
As a worst case, it could be assumed that indoor and outdoor air concentrations of
respirable phosphoric acid are the same and individuals will be exposed to ambient air
phosphoric acid for 24 hours per day. The phosphoric acid exposure estimates also
assume an average respiration rate of 20 m3/day for a 70 kg adult and the calculation of
the human dose assumes 100% absorption of the respirable phosphoric acid.
Table 6 - Lifetime average estimated human exposure to phosphoric acid in
ambient air
Average ambient air Human
Human dose a
Scenario concentration exposure
(ng/kg bw/day)
(H3PO4 ng/m3) (ng/day)
Baseline negligible negligible negligible
Scenario 1: Increase due to
combustion of the alkyl phosphate 100 2000 28.6
additive
Scenario 2 : Increase due to
combustion of the alkyl phosphate 40 800 11.4
additive
a
Dose for a 70 kg person.
People living in rural areas would be expected to have lower exposure than people
living in cities. Thus, given that the estimated total phosphoric acid concentration in
Sydney due to the use of the alkyl phosphate-based LRP is 100 ng/m3 (Table 4),
exposures of Australians living in rural and remote regions are expected to be even
lower.
39
Alkyl Phosphate AVSR Additive
People living in areas that have industries emitting phosphoric acid could be expected
to have the highest levels of exposure. No Australian ambient air phosphoric acid
concentration data are available and no personal monitoring studies have been
completed in Australia.
It should be noted that ambient air concentrations may not always reflect the actual
exposure of individuals living in a given area. This is because typical human activity
patterns include time spent in microenvironments with higher or lower concentrations
of a pollutant and for which there is generally no monitoring data. Hence, a
measurement of personal exposure to a compound is preferable to ambient air data.
Furthermore, a measurement of personal exposure should be representative of the
population of interest throughout the time period of interest. The above worst case
estimate of public inhalation exposure to phosphoric acid as a result of the combustion
of the alkyl phosphate additive cannot be refined and can be considered only as a
general exposure level.
Exposure to phosphate via food, water and soil
It is conceivable that phosphorus levels in foodstuff may be increased as a result of
environmental contamination with the combustion products of the alkyl phosphate
additive. There are no Australian studies on the possible contribution of the alkyl
phosphate additive combustion product to phosphorus levels in food.
It is considered that the contribution of the combustion of the alkyl phosphate additive
to phosphorus intake from foodstuff in Australia is likely to be very low. This is
because of the expected low atmospheric (Table 4), water (Section 9.4.2), and soil
(Section 14.1.1) levels of phosphoric acid or phosphate due to the combustion of the
alkyl phosphate additive in LRP, especially in rural areas, compared with the
recommended dietary intake of phosphate (Section 11).
Other possible sources of phosphate exposure
Another possible source of phosphate exposure is soil ingestion. Phosphate exposure as
a result of soil ingestion is not expected to increase significantly from current exposure
levels (Section 14.1.1). This is because of the estimated low fallout value of
phosphoric acid as a result of the combustion of the alkyl phosphate additive in LRP.
40 Priority Existing Chemical Assessment Report Number 25
10. Animal and Human Health Effects
of the Alkyl Phosphate Additive
The aim of this section is to describe the health effects of the alkyl phosphate additive.
The scope of this section is limited to describing the health effects of the proprietary
product DMA-4 in animals (mammals and avian). This is because of the lack of data
for the alkyl phosphate additive itself and the equivalence of DMA-4 to Valvemaster
Concentrate (Section 4) (Octel, 1999b).
In the case of end-points studied in animals (mainly irritation and acute toxicity
studies), this assessment report is based on a limited number of individual animal
studies. Some of the animal studies do not comply with Good Laboratory Practices
(GLP) or international standards such as the Organisation for Economic Co-operation
and Development (OECD) Test Guidelines. In view of the small number of studies, all
existing studies are included in this section irrespective of their compliance with formal
quality criteria. Studies that provide insufficient scientific detail to permit a critical
appraisal of their conclusions are acknowledged.
There are no published case reports, epidemiology or other studies addressing the
human health effects of the alkyl phosphate additive or its proprietary products
Valvemaster Concentrate (including DMA-4) and Valvemaster VM11. No
subchronic, chronic, reproductive or developmental toxicity or genotoxicity studies
were available for DMA-4.
No work-related injuries or health conditions due to exposure to alkyl phosphate
additive were reported in industry submissions.
10.1 Acute toxicity
The acute oral toxicity study of DMA-4 in male rats is based on the OECD 401 "Acute
Oral Toxicity" Guideline (Haskell Laboratory, 1964). A single animal was dosed at
670, 2250, 3400, 5000, 7500, 11 000, 17 000 or 25 000 mg/kg bw by intragastric
intubation, with single doses undiluted, or as a solution in peanut oil. Survival was
recorded over a 14-day timeframe. Generalized clinical observations of weight loss,
digging motion, salivation after dosing, pallor and diarrhoea were observed at doses of
5000 mg/kg bw and above. Animals died at the top two doses (17 000 and
25 000 mg/kg bw) at Day 2. Under the conditions of the study, the oral acute lethal
dose (ALD) for DMA-4 in male rats was 17 000 mg/kg bw.
In an acute oral study in male rats of DMA-4 in rats, a single oral dose (1 animal per
dose ) of 710, 2300, 3400, 5100, 7500 or 11 000 mg/kg bw was administered in corn oil
by intragastric intubation (Haskell Laboratory, 1986). No deaths occurred over the 14-
day study period. The clinical signs of toxicity most commonly observed included
diarrhoea, discharge from the nose and mouth, wet perineum and weight losses (6-12%
of body weight) up to three days after dosing. Ruffled fur was observed in rats dosed at
7500 and 11 000 mg/kg bw. Weakness, yellow stained perineum, ocular discharge and
hunched posture were also observed in the rat dosed at 11 000 mg/kg bw. Under the
conditions of the study, the oral ALD was greater than 11 000 mg/kg bw.
41
Alkyl Phosphate AVSR Additive
In the acute dermal lethality study of DMA-4 in rabbits, a single dose was applied to
clipped, intact skin of male New Zealand White (Haskell Laboratory, 1987). The
treatment dose included one animal treated at 2250 mg/kg bw and 6 animals treated at
5000 mg/kg bw; under occlusion for 24 hours. The rabbits were observed for 14 days
post-application and no animals died. No details are given of the method used to
describe the symptoms of skin irritation nor observations given for the individual
animals. While the test parameters do not comply with a standard testing guideline,
they are considered to be scientifically reliable with regard to the measured endpoint,
i.e. mortality.
Approximately 5-7% weight loss occurred within 24-hours in all the rabbits dosed at
5000 mg/kg bw, with weight recovery by the end of the study. Superficial necrosis and
dry cracked skin were observed at the termination of the study in 5 out of the 6 animals
dosed at 5000 mg/kg bw. The single rabbit treated at 2250 mg/kg bw displayed only
mild erythema and oedema at Day 3 and no skin irritation was observed by the sixth
day. Under the conditions of the study, the ALD by skin absorption for DMA-4 was
greater than 5000 mg/kg bw in male White New Zealand Rabbits.
The results of a first phase study to investigate delayed neurotoxic response in mature
female white leghorn chickens (n = 4), reports a LD50 for DMA-4 to be in excess of
5000 mg/kg bw following a single oral dose of 5000 mg/kg bw administered to each
bird. Further details of this study are given in Section 10.4. Clinical signs of toxicity
noted in the four birds included slight lethargy and anorexia at Day 2 and Day 3,
respectively, which resolved at Day 3. There were no deaths associated with the doses
given (Du Pont De Nemours & Co., 1986) .
10.2 Irritation and corrosivity
Eye irritation
The effect of direct contact of DMA-4 with the eye was examined in New Zealand
white rabbits using the Draize scoring method. Study methodology was similar to
OECD Guideline for Acute Eye Irritation/Corrosion 405 (Haskell Laboratory for
Toxicilogy and Industrial Medicine, 1986a). The study involved two animals and the
instillation of 0.01 mL of DMA-4 (rather than 0.1 mL as recommended by OECD
Guideline for Acute Eye Irritation/Corrosion 405) into the lower conjunctival sac of the
right eye, with the left eye used as a control. The treatment and control eyes of one
animal remained unwashed while the eyes of the other animals were rinsed for one
minute with water approximately 20 seconds after the administration of the test
material. Approximately one and four hours and one, two and three days after
treatment, the rabbits were examined for evidence of eye irritation. No cornea/iris
irritation was observed in both washed and unwashed eyes in both animals. Slight
redness/chemosis of the conjuctiva (Score 1) was observed only at one hour in both
washed and unwashed eyes for both animals after exposure to DMA-4. No reactions of
the cornea or iris were observed in either animal.
Skin irritation
Skin irritation in 6 female rabbits was assessed using a Draize scale (Draize et. al,
1944) for scoring primary skin irritation in a modified OECD Guideline 404 for
assessing Acute Dermal Irritation/Corrosion (Haskell Laboratory for Toxicology and
Industrial Medicine, 1986b). The dermal application of 0.5 mL of DMA-4 was
administered at each test site, 4 test sites per animal for 24 hours under an occlusive
42 Priority Existing Chemical Assessment Report Number 25
(rubber) wrap Test sites were evaluated at 25, 48 and 72 hours after application. The
test material caused moderate to severe inflammation of the skin under the conditions
of the study (Table 7). Test results show delayed oedema following the initial observed
erythema. The peak oedema time point may be beyond the 72-hour end-point used in
the study.
Table 7 - Results of a skin irritation study in rabbits
Lesion Mean Score Maximum Value
Erythema/Eschar (25 hr) 2 3
Oedema (25 hr) 0.33 2
Erythema/Eschar (48 hr) 3 3
Oedema (48 hr) 2.7 4
Erythema/Eschar (72 hr) 3 3
Oedema (72 hr) 2.8 4
In an additional study of skin irritation, an unknown volume of 0.5, 1, 5, 10 and 25% of
DMA-4 was applied to intact and abraded skin for 24 hours to an unspecified number
of test sites per animal in 9 male guinea pigs (described non-specifically as young and
old) (Haskell Laboratory for Toxicology and Industrial Medicine, 1964). The study
method is non-standard and involved the application of the test material in a 1:1
solution of acetone:dioxan with 13% guinea pig fat. No grading scale is described
other than nil, mild, or strong erythema. No information is given as to whether or not
an occlusive dressing was used. The study gives only a limited narrative description of
the observed erythema (Table 8).
Table 8 - Results of a skin irritation study in guinea pigs
DMA-4 (%) Observation
25 Strong erythema on intact skin
10 Strong erythema on intact skin; moderate to mild erythema on
abraded skin
5 Mild erythema on intact and abraded skin (young guinea pig);
strong erythema and strong to mild erythema on intact and
abraded skin, respectively, in older guinea pigs.
1 Occasional mild erythema on intact skin
0.5 No erythema
Under the study conditions, the application of DMA-4 was reported to be irritating to
guinea pig skin in concentrations as low as 10%. No information is available from the
study of the resolution time for the induced erythema. The study authors noted that the
test material appears to be more irritating to older than younger guinea pigs. No data or
details are available or given for individual animals. There is insufficient
documentation and experimental detail to reliably accept the adequacy of the results
and conclusions.
43
Alkyl Phosphate AVSR Additive
10.3 Sensitisation
A single study is reported on the potential skin sensitisation of DMA-4 using an
unknown method in 9 male albino guinea pigs (Haskell Laboratory for Toxicology and
Industrial Medicine, 1964). The study was undertaken concurrently with the primary
irritation skin test in guinea pigs that is reported in Section 10.2. A 10% solution of
DMA-4 was applied topically to abraded skin in guinea pig fat 9 times over a three
week period. No further experimental details were reported.
None of the 9 treated animals are reported to show allergic skin sensitisation. The data
generated, however, is not in accordance with an acceptable methodology and there is
insufficient experimental detail and documentation for assessment.
10.4 Neurotoxicity
A 21-day neurotoxicity study of H-16,407 (also described as DMA-4 in the study) in
mature female white leghorn chickens (19-20 months) is reported (Du Pont De
Nemours & Co., 1986). While not stated, the study appears similar to the OECD
Delayed Neurotoxicity of Organophosphorous Substances Following Acute Exposure
Guideline 418 and involved a first phase (range finding) study to determine an LD50
value and a subsequent second phase 21-day neurotoxicity study. The objective of the
study was to establish whether or not the compound produces a delayed neurotoxic
response.
The first phase (range finding study) involved four birds orally dosed at 5000 mg/kg bw
administered as a single dose by gavage. All birds were observed on a daily basis for
seven days post-dosing and sacrificed at the end of the study period. No mortality nor
signs of delayed neuropathy were observed. Clinical signs of toxicity noted included
greasy cage droppings at Day 1 and Day 2; slight lethargy Day 2 and anorexia at Day 3.
All these observed clinical signs resolved after Day 3. The results of the first phase
showed the acute oral LD50 for H-16,407 to be in excess of 5000 mg/kg bw.
In the second phase of the investigation, 40 birds were selected for the 21-day
neurotoxicity study. The birds were divided into a treatment control group of 10 birds
(receiving a single oral dose of corn oil), a positive neurotoxicity control group of
10 birds (receiving a single oral dose of tri-o-tolyl phosphate (TOTP) 500 mg/kg bw at
0 hour on test Day 1), and a H-16,407 treatment group of 20 birds (receiving a single
oral dose of H-16,407 of 5000mg/kgbw at 0 hour on test Day 1 following an
approximate 19 hour fast with water permitted). The study contains no details as to
whether or not the positive or treatment control animals were also fasted. The
treatment control birds received corn oil in an amount equal to the largest dosage of test
material administered in the H-16,407 treatment group, i.e. 10.7 mL. The selected
dosage level for the H-16,407 treatment group in the 21-day neurotoxicity was derived
from the first phase of the study, i.e. 5000 mg/kg bw. All animals were sacrificed at the
end of the study on Day 21. Gross pathology investigations including a complete
necroscopic and microscopic examination of the brain, spinal cord and sciatic nerves, in
addition to a microscopic examination for neoplasms, were undertaken on the carcasses
at the end of the study period.
The birds were evaluated daily for signs of neurotoxicity and graded with a score of 0
to 5 according to criteria as follows: no neurological signs (Grade 0); generalised
weakness with or without slight intermittent ataxia (Grade 1); slight continuous ataxia
(Grade 2); moderate to severe ataxia (Grade 3); bird unable to stand, sits on haunches
44 Priority Existing Chemical Assessment Report Number 25
(Grade 4); bird unable to stand, paralysis of legs and wings (Grade 5). Individual body
weights were recorded at 0 hour Day 1 of the study and on test days Day 3, 6, 9, 12, 15,
18 and 21. Food consumption was determined at each weighing interval.
No clinical signs of delayed neurotoxicity or death were noted in either the treatment
control or H-16,407 treatment group over the 21-day study period. By comparison, the
positive control birds exhibited behavioural signs of neurotoxicity by Day 9 post-
treatment; with all animals showing signs of delayed neurotoxicity by Day 12 and
progressively worsening signs of neurotoxicity by Day 16. All positive control birds
were sacrificed at Day 16 post-treatment due to severe neurological signs.
Signs of lethargy, anorexia and abnormal cage droppings were present following dosing
with H-16,407, with recovery by Day 8. Greasy droppings were noted in the H-16,407
group within 21 hours post-dosing and were still evident 24 hours later along with
concomitant lethargy and anorexia (Day 2). A statistically significant reduction in body
weight was noted at Day 3 (9.7% reduction; 99% CI) and Day 5 (8.2% reduction; 95%
CI) that resolved by Day 9. All birds (including cage droppings) appeared normal on
Day 7-8 of the study.
No visible lesions or gross pathology were revealed in the 10 treatment control birds
sacrificed on Day 21 nor in 17 of the 20 birds treated with H-16,407. Of the remaining
three birds in the H-16,407 treatment group, one bird revealed a slightly emaciated
carcass, another displayed ruptured egg yolks in the oviduct and the third bird revealed
reabsorbed egg yolk material in the abdominal cavity in addition to a slightly emaciated
carcass. In the 10 positive control birds, no abnormal tissue alterations were noted in
seven birds. One displayed an enlarged caecum (or distension due to gas), another
emaciation and one bird revealed reabsorbed eggs in the visceral cavity.
The results of the above studies indicate H-16,407 to be of low toxicity in chickens via
the oral route; with no signs of delayed neurotoxicity noted under the conditions of the
study. Furthermore, gross pathological examinations of the sciatic nerves, brain and
vertebral column of all birds sacrificed on Day 21 revealed no abnormal tissue changes
in the H-16,407 treatment group.
45
Alkyl Phosphate AVSR Additive
11. Pharmacokinetics and Toxicity of
Phosphoric Acid
11.1 Introduction
The toxicology of phosphoric acid (orthophosphoric acid) is addressed in this section
because it is postulated to be the significant combustion by-product of the alkyl
phosphate additive in LRP (Section 8). A brief description of the physico-chemical
properties of phosphoric acid is given in Appendix 2.
The mammalian toxicity data and information presented in this section builds on the
review of phosphoric acid undertaken in 1993 by the Working Group on the
Assessment of Toxic Substances (WATCH Committee) of the UK Health and Safety
Commission's Advisory Committee on Toxic Substances (Payne et al., 1993) and the
U.S. EPA's Integrated Risk Information System (IRIS) summary of phosphoric acid
that was last updated on 8 January 2003 (IRIS, 2003). Any additional relevant data
identified in recent literature searches are also included.
The toxicity studies in this section do not represent a review of the complete toxicology
of phosphoric acid. The main focus is chronic inhalation and acute exposure to an
aqueous mist of phosphoric acid. Such exposures are likely to be the most relevant
scenarios as a result of the combustion of the alkyl phosphate additive in LRP.
The reported inhalation toxicity of phosphoric acid characteristically relate to the
effects of phosphorus pentoxide (P2O5), which is the anhydride form of phosphoric
acid. It is generated from the combustion of phosphorus under oxygen rich conditions.
This is because there is little or no data generated in humans or animals on the effect of
the inhalation of phosphoric acid which would allow a more accurate assessment of the
threshold level of irritation or evaluation of the effects of prolonged low-level
inhalation exposure. The treatment doses used in these inhalation studies may be
expressed as phosphorus pentoxide, phosphorus or phosphoric acid equivalents.
Phosphorus pentoxide is relevant because it hydrolyses with moisture in the air and
lungs to produce phosphoric acid. Phosphorus pentoxide is a powerful dehydrating
agent that, when combined with moisture in the atmosphere or in the respiratory tract,
produces phosphoric acid in an exothermic reaction. This reaction generates heat and is
likely to desiccate tissues with which phosphorus pentoxide comes into it contact,
thereby causing more tissue damage than pre-formed phosphoric acid. The application
of the results of inhalation toxicity studies on phosphorus pentoxide to an assessment of
the hazards of phosphoric acid will possibly overestimate the inhalation hazard of
phosphoric acid.
11.2 The phosphate body load
Most of the phosphorus in the human body exists as phosphates or esters, with
phosphate playing an important role in the maintenance of the body's acid-base balance
(Haslett et al., 1999).
Phosphoric acid dissociates in water to hydrogen and phosphate ions (Appendix 2).
Phosphoric acid, in the form of the phosphate anion, is an essential component (not
46 Priority Existing Chemical Assessment Report Number 25
synthesised by the body) of the normal body and skeleton of practically all life forms
and is a natural component of the diet (Fauci et al., 1998). The phosphate body
load/content is often expressed in terms of elemental phosphorus. Of the average 700 g
of phosphorus in the human body, 85% is in the skeleton (Fauci et al., 1998).
Dietary phosphate is found in highest concentrations (0.1-0.5% or more, in terms of
phosphorus) in such foods as milk, cheese, nuts, fish, meat, poultry, eggs (yolk) and
certain cereals (WHO, 1965). Phosphoric acid is also used in a range of foods as
additives (ANZFA, 2001). For example, phosphoric acid is added as an acidifier in soft
drinks, as a nutrient in the preparation of yeast and in the refining of cane sugar, oil and
fats (Commission of the European Communities, 1992). Dietary phosphorus occurs in
both inorganic and organic forms such as phospholipids, phospho-sugars and phospho-
proteins (Lee et al., 1981). Most organic phosphates are hydrolysed in the gut to
release the inorganic phosphate that is absorbed, although some phospholipids may be
absorbed in the organic form (Lee et al., 1981).
The daily human intake of phosphorus is estimated to range between 1 and 2 g ( Haslett
et al., 1999, WHO, 1965). The World Health Organization (WHO) states the value of
70 mg/kg bw as representing the maximum tolerable daily intake (MTDI) of
phosphates expressed as phosphorus when the diet contains adequate calcium (WHO,
1982). A daily phosphorus intake of 70 mg/kg bw equates to 4.2 g of phosphorus or
12.9 g of the phosphate anion (PO43-) for a 60 kg adult.
The US National Academies, Institute of Medicine has published Recommended
Dietary Allowance (RDA) values for phosphorus ranging from from 100 mg for infants
(0.0 to 0.5 years old), 500 mg for children (1 to 10 years of age) and up to 1250 mg
for adolescents (11 to 18 years of age) and adults (National Academies, 2003). A
maximum level of daily phosphorus intake of 4000 mg is specified by the US National
Academies, Institute of Medicine as a level that is likely to pose no risk in adults of
adverse effects (National Academies, 2003).
11.3 Toxicokinetics of phosphoric acid
There is no information on the toxicokinetics of phosphoric acid per se . However, the
mechanisms controlling the acid-base homeostasis in the body (including the
interrelationships of phosphate and calcium) and the potential of exogenous phosphorus
and hence, phosphate loads, to disrupt the body's acid-base balance and cause
hypocalcaemia and hyperphosphatemia, is well understood. These mechanisms are not
described here because they are well explained in publications on phosphorus and
phosphate metabolism and distribution (Lee et al., 1981; Fauci et al., 1998; Haslett et
al., 1999).
In humans, hyperphosphataemia is defined in adults as an elevation of serum
phosphorus above 1.67 mmol/L (5 mg/dL) with decreased renal excretion of
phosphorus the most common cause (Fauci et al., 1998). High phosphate loads may
lead to the deposition of calcium phosphate complexes in soft tissue and a range of
physiological disturbances such as kidney damage, extra-skeletal calcification and bone
demineralisation (Lee et al., 1981; Fauci et al., 1998) (Haslett et al., 1999).
In general, when dietary phosphate intake is increased or decreased, the body's
homeostatic mechanisms are activated to maintain the phosphate balance in the body;
with serum phosphate levels tending to remain within normal ranges (0.8 to 1.4 mmol/L
fasting (Haslett et al., 1999).
47
Alkyl Phosphate AVSR Additive
11.4 Acute phosphoric acid toxicity in animals and humans
11.4.1 Acute toxicity
Humans
The limited human inhalation exposure data on phosphoric acid relates to accidental
exposure. Weakness, dry cough, chest pain and shortness of breath/dyspnea were
reported as developing 7 to 8 hours after exposure to high concentrations of phosphoric
acid in a 37 year old mechanic aboard a ship transporting 4000 tonnes of phosphoric
acid. Investigating a leak, the mechanic developed symptoms following exposure to
phosphoric acid vapours on three occasions, each for approximately
20 minutes/exposure (Boutoux et al., 1995). The mechanic was a non-smoker with no
history of allergies or previous respiratory problems. Symptoms of reactive airways
dysfunction were reported in the worker one year after the incident. A colleague
similarly exposed to the phosphoric acid vapours was taken to hospital and died in a
state of severe respiratory distress. Medical staff initially suspected Legionella to be
the cause of the fatality, but blood tests for the organism proved negative.
In a poorly reported Russian study of 15 non-smoking healthy adults aged between 18
and 36 years, "momentary" inhalation of hydro-aerosols of phosphoric acid expressed
as 1.2, 5.2 or 8.0 mg P2O5/m3 (equivalent to 1.6, 7.2, or 11.0 mg H3PO4/m3) reportedly
produced irritation in 18% of the subjects at exposure level of 5.2 mg P2O5/m3 and 82%
at exposure level 8.0 mg P2O5/m3 (Sigova, 1983, as cited in Payne et al., 1993). The
lowest concentration reportedly did not provoke irritation in any of the volunteers. A
copy of the original reference was unavailable to NICNAS and the reliability of the
data is uncertain.
Animal
Oral and dermal
Phosphoric acid has low acute oral and dermal toxicity as demonstrated by an oral rat
LD50 of 1530 mg/kg bw and dermal rabbit LD50 of 2740 mg/kg, respectively (Payne
et. al, 1993).
A study of the administration to groups of 5 Sprague-Dawley rats of commercial
preparations of 85%, 80% and 75% phosphoric acid by oral gavage, report oral LD50
values of 3500, 4200 and 4400 mg of test material/kg bw, respectively (Randall &
Robinson, 1990).
Inhalation
A rat LC50 (1-hr) value of > 850 mg/m3 is reported for phosphoric acid (BIOFAX
Industrial Bio-Test Laboratories, as cited in RTECS, 1998) but the individual data is
unavailable to NICNAS and the reliability of the study cannot be validated. The
WATCH Committee report notes the availability of a phosphoric acid mouse inhalation
LD50 of 25.5 mg/m3 indicates serious doubts about the validity of the study (Payne et
al., 1993).
A range of LC50 (1-hr) values for phosphoric acid (and phosphorus equivalents) in
male rabbits, mice and guinea pigs was comprehensively reported by Ballantyne in
1998 (Ballantyne, 1998). This followed an earlier short communication on the study
48 Priority Existing Chemical Assessment Report Number 25
that was described as an acute inhalation toxicity study of phosphorus pentoxide smoke
(Ballantyne, 1981).
The LC50 (1-hr) values, expressed as phosphorus and phosphoric acid equivalents,
relate to inhalation toxicity following the complete oxidation of unformulated red
phosphorus and exposure to a range of phosphorus concentrations from 35 to
2000 mg/m3 (equivalent to 111 to 6327 mg/m3 phosphoric acid) (Ballantyne, 1998).
The use of unformulated red phosphorus under complete oxidation conditions was cited
by the investigator in order to result in phosphoric acid as the principal combustion
product and to avoid the presence of formulation by-products in the generated smoke.
Expressed as phosphorus, the LC50 (1-hr) values were 1689 mg/m3 (rabbit),
1217 mg/m3 (rat), 271 mg/m3 (mouse), and 61 mg/m3 (guinea pig); expressed by
Ballantyne as phosphoric acid equivalents, the values are 5337 (rabbit), 3846 (rat), 856
(mouse), and 193 (guinea pig) mg/m3, respectively (Ballantyne, 1981; Ballantyne,
1998). Most of the animals that died did so during exposure although a small
proportion survived a few hours or days post-exposure. Concentrations of phosphorus
pentoxide not associated with respiratory tract pathology in 14-day survivors were
450 mg/m3 (rat and rabbit), 111 mg/m3 (mouse) and 36 mg/m3 (guinea pig). This is
equivalent to phosphoric acid concentrations of 621 (rat and rabbit), 153 (mouse) and
50 (guinea pig) mg/m3.
11.4.2 Irritation and corrosivity
Human
Gastrointestinal
Widespread corrosion of the human gastrointestinal tract is reported in a fatal case
report of oral ingestion of phosphoric acid (unspecified quantity) (Hawkins et al.,
1980).
Eye
Phosphoric acid in concentrated solution is reported as corrosive to the human eye and
splashes have been reported to result in permanent injury in severe cases (Proctor &
Hughes, 1978, as cited by Payne et al., 1993). A single drop into the human eye of
approximately 1.5% phosphoric acid buffered at pH 2.5 (volume unspecified) is
reported as causing a moderate brief stinging but no injury, with the same solution at
pH 3.4 reportedly having no discomfort (Grant, 1974).
Dermal
Stinging sensations following the facial application to humans of phosphoric acid
during profuse sweating is reported (Frosch & Klingman, 1977). The study reports an
immediate yet transient stinging response within the first 10 seconds of exposure to
5% phosphoric acid; followed by a severe stinging sensation developing after 2-
8 minutes. The severe delayed response was also experienced on the application of
3.3% (pH 1.9) phosphoric acid solutions, whereas 1% (pH 2.1) phosphoric acid
solution produced only a slight response. The study (on several acids) did not find a
correlation between stinging and irritancy.
49
Alkyl Phosphate AVSR Additive
Animal
Eye
Based on an unknown scoring methodology in a rabbit test model, severe eye irritation
is reported with phosphoric acid at a dosage level of 119 mg (no further details are
available) (RTECS, 1998).
In a testing protocol equivalent to OECD Guideline 405: Acute Eye
Irritation/Corrosion, mild conjunctivitis, chemosis and opacity of the cornea is reported
following the instillation of a 100 礚 of a 17% solution (pH not given) into rabbit eye
(n = 6) (Jacobs, 1992). In the same study, a reduction in the mean Draize scores was
observed after the instillation of a 100 礚 of a 10% solution (pH not given). Mild
conjunctiviti was the only adverse effect observed at the study end-point at 96 hours.
Irrigation of a rabbit eye for 5 minutes with a solution of phosphoric acid at pH 3.8
(unspecified concentration) reportedly caused slight transient redness and swelling,
with the eye normal by the next day (Grant, 1974).
Instillation of an unspecified volume of 4% phosphoric acid (pH not given) into the
rabbit eye produced significant conjunctival swelling one hour later, as measured by a
50% increase in moisture content of the conjunctiva in comparison with the untreated
eye (Larson et al., 1956).
Dermal
Based on an unknown scoring methodology in a rabbit test model, severe skin irritation
is reported with phosphoric acid at a dosage level of 595 mg/24-hour (no further details
are available) (Payne et al., 1993).
A range of phosphoric acid solutions is reported to be skin irritants in animals; with the
length of exposure, degree of occlusion and concentration of the acid significant
factors. For example, phosphoric acid solutions (0.5 mL; 75- 85% applied to an
unspecified number of animals) are reported as corrosive in primary skin irritation tests
in rabbits following 24-hour exposure under semi-occlusion (Randall & Robinson,
1990). In the same study, 75% and 80% phosphoric acid solutions were non-corrosive
to rabbit skin after 4-hour exposure. In a modified test protocol involving only one
rabbit, 0.5 mL of a 75% phosphoric acid solution applied for 4 hours under occlusion
was not found to be irritating (Weiner et al., 1990). Phosphoric acid concentrations of
17.5% and above (pH 0.6-0.2) under occlusion for 4 hours, however, are reported to be
corrosive in rabbit skin as evidenced by the formation of scar tissue (Loden et al., 1985)
as cited by (Payne et al., 1993). One of three rabbits in the study reportedly developed
severe erythema of the skin with mild to moderate swelling 48-72-hours after exposure
to 2.5% phosphoric acid at pH 2.1.
A 5% phosphoric acid solution (pH < 2) is reported as moderately to severely corrosive
in rat and mice skin irritation tests following the application of 1mL/kg (50 mg/kg) for
7 days without occlusion (Sekizawa et al., 1994).
11.4.3 Repeat exposure
Oral
In a poorly described study, rats were fed a diet containing 0, 4000 or 7500 ppm
phosphoric acid from weaning up to 15 months of age. Offspring were similarly fed for
50 Priority Existing Chemical Assessment Report Number 25
up to 6 months of age (Bonting & Jansen, 1956, as cited by Payne et al., 1993). No
adverse effects on body weight, blood clinical chemistry or substance-related
macroscopic or microscopic abnormalitites of the liver, spleen, adrenals, testicles,
skeletal muscles or femur were observed.
It is suggested by the World Health Organization (WHO) that an important and
sensitive criterion of orally ingested phosphate overload is the appearance of metastatic
calcification in the soft tissues, especially the kidney, i.e. nephrocalcinosis, as well as in
the stomach and aorta (Joint FAO/WHO Expert Committee on Food Additives, 1974).
Phosphoric acid has been shown to cause nephrocalcinosis in rats when administered at
relatively high concentrations in the diet (FAO, 1970; USEPA, 1990) (Joint FAO/WHO
Expert Committee on Food Additives, 1974). The WHO has determined that the lowest
level that produces nephrocalcinosis in the rat is 1% phosphorus in the diet (Joint
FAO/WHO Expert Committe on Food Additives, 1974). This figure is the basis for an
extrapolation by the WHO to a dose of 6.6 g of phosphorus daily (based on a daily food
intake of 2800 calories) as an estimate of the lowest possible level that may cause
nephrocalcinosis in humans (Joint FAO/WHO Expert Committe on Food Additives,
1974). This is equivalent to 20.2 g of the phosphate anion (PO43-).
Inhalation
Phosphoric acid
Human
High prevalence of chronic bronchitis (45.7%) and a significant incidence of impaired
respiratory performance has been reported for workers at one plant producing
phosphoric acid (Fabbri et al., 1977). Concomittant exposure to volatile fluorides
(hydrofluoric acid, hexafluorosilicic acid and tetrafluoride) was considered to be very
significant, however, the direct contribution of phosphoric acid to the observed effects
is not known.
In another study, the health of workers was investigated in the phosphoric acid
production division (type of process unspecified) of a phosphate fertiliser plant (Renke
et al., 1987). The incidence of bronchial and peribronchial changes in the phosphoric
acid division was 13% compared to no greater than 11.8% for non-exposed office staff
at the same factory.
No conclusions can be drawn about the toxic effects of phosphoric acid from these
occupational studies because exposure to emissions other than phosphoric acid cannot
be discounted. In addition, in neither study was the exposure concentration or duration
reported.
Animal
Studies of the effects of chronic inhalation of phosphoric acid in animals (using pre-
prepared phosphoric acid treatments) could not be found in the literature.
51
Alkyl Phosphate AVSR Additive
Phosphorus Pentoxide
Human
An occupational study is reported on lung function in a cohort of 131 workers involved
in refining phosphorus rock for 3 to 46 years to obtain elementary phosphorus (Dutton
et al., 1993).
Typical exposures included phosphoric-acid, phosphorus oxides (including phosphorus
pentoxide), fluorides, and coal-tar-pitch volatiles. While protective equipment was
available to the workers, observation revealed they rarely made use of it. The
maximum concentrations of phosphorus-pentoxide, fluorides, and coal-tar-pitch
volatiles in the refinery air were 2.23, 4.21 and 1.04 mg/m3, respectively. Fifty-five
subjects were current smokers, 39 were former smoker and 37 were nonsmokers. The
mean duration of exposure was 11.4 years for all workers, 11.0 years for smokers, 15.1
years for former smokers and 7.8 years for nonsmokers.
Pulmonary function tests (forced vital capacity, forced expiratory volume in one second
and forced expiratory flow) were conducted annually over an 8-year period in all
workers to assess any effects of occupational exposure. These data were analysed
longitudinally over 3 to 7 years and cross-sectionally. Neither analysis revealed any
significant effect as measured by spirometry measures of pulmonary function after
adjusting for age and smoking. The authors concluded that occupational exposures in
the refinery did not contribute to annual changes in pulmonary function in the workers
as measured by spirometry measures. The observed decline in pulmonary function in
smoking workers was attributed to the effects of smoking.
Animal
In a poorly reported Russian study (a copy of which could not be sourced), rats were
exposed for an unspecified time, described as chronic, to a hydro-aerosol of phosphoric
acid expressed as phosphorus pentoxide 10.6 mg/m3 (which is equivalent of 14.6 mg/m3
phosphoric acid) (Sigova, 1983, as cited by Commission of the European Communities,
1992). At post mortem, increased relative weights of the lungs, kidneys and spleen
were reported. Inflammation of the bronchi, cell damage in the convoluted tubules and
enlargement of the glomeruli in the kidney, an increase in the amount of lymphatic
tissue in the spleen and liver damage is cited. A "threshold value" for these effects was
determined to be 2.5 mg/m3 for phosphorus pentoxide (which is equivalent to
3.45 mg/m3 phosphoric acid). Nevertheless, it is unclear from the report if this dose
represents the lowest dose at at which effects were seen or the highest dose at which
effects were not seen (Commission of the European Communities, 1992).
A chronic inhalation toxicity study reports pulmonary toxicity in rats, mice and guinea
pigs following exposure to phosphorus smoke generated by the combustion of 95%
amorphous oiled red phosphorus and 5% polyvinyl butyral BL18 at phosphorus
concentrations of 0, 16 or 128 mg/m3 for 1-hour/day, 5 days/week for 180 to 200 days
(Marrs et al., 1989). While the smoke is reported to contain mostly phosphoric acid
(derived from phosphorus pentoxide), phosphine (which is produced from phosphorus
trioxide), cyclotetraphosphoric and other polyphosphoric acids are proposed as
additional components of the smoke.
Marrs et al reports marked interspecies differences in tolerance to the smoke (Marrs et
al., 1989). Rats were more tolerant, guinea pigs least and mice intermediate. There
was a high death rate in all groups (including controls). With the exception of the high
52 Priority Existing Chemical Assessment Report Number 25
dose guinea pig group, decedents mostly failed to show statistically significant
pathological changes either in the respiratory tract or elsewhere. Pulmonary congestion
(accompanied in some cases by haemorrhage and collapse) was observed, however, in
the high dose guinea pig group and in all the animals that died during or just after the
first exposure. The investigators attributed these observations to exposure to the
smoke.
A study in male Sprague-Dawley rats (sample sizes unspecified) investigated the
effects of exposure to smoke generated by burning 95% of red phosphorus 5% butyl
rubber (RP/BR). Exposure was to a single inhalation of 1000 mg/m3 for 3.5 hours or
subchronic smoke concentrations ranging from 300 to 1200 mg/m3 for 2.25 h/day for 4
consecutive days and 4 and 13 weeks (Aranyi et al., 1988a; Aranyi et al., 1988b). Total
phosphoric acids levels were measured in the smoke and reported to contribute to
around 70% of the smoke.
The respiratory tract was identified as the target organ. Mild or moderate-to-severe
terminal bronchiolar fibrosis was reported in all rats after 4- and 13-week exposures to
750 mg/m3 of RP/BR. Of those animals exposed to 300 mg/m3 for 13 weeks, 13%
had terminal bronchiolar fibrosis. The severity of the lesions increased with the
severity of the exposure conditions. The investigators state that the incidence of
fibrosis in those rats sacrificed 8 weeks after the 13 week exposure to 750 or
1200 mg/m3 of the smoke, suggested that the severity of the lesion did not increase
following the cessation of exposure nor resolve with time. Decreased pulmonary
bactericidal activity was depressed after acute and 13-week exposures but not after 4-
week exposures.
The paper states that an additional subchronic study has identified the no-effect level of
the smoke for fibrosis of 50 mg/m3; however, no details are provided. This result is
also cited by the US EPA in a description of two parallel 13-week inhalation studies but
full copies of the studies were not available and could not be reviewed for this
assessment report.
The two parallel 13-week inhalation studies reported by the US EPA involve exposure
of Sprague-Dawley rats for 2.25 hours/day on 4 consecutive days/week to either filtered
air (controls) or an aerosol of combustion products from burning 95% red phosphorus
and 5% butyl rubber (Aranyi et al., 1988a; Aranyi et al., 1988b) as cited by (US EPA).
In the first study, male Sprague-Dawley rats were exposed to filtered air or 300, 750, or
1200 mg/m3 of combustion products (Aranyi et al., 1988a; Aranyi et al., 1988b). In the
second study, male Sprague-Dawley rats (40 per group) were exposed to either filtered
air or 50, 180, or 300 mg/m3 of these same combustion products.
The percentage of the aerosols that were phosphorous acids ranged from 71-79%
(apparently based on gravimetric analysis). The duration-adjusted values for the
second, lower concentration study were 2.7, 9.6, and 16.7 mg/m3.
In the first study, the number of rats in the control and high- and mid-exposure groups
was 176 and 84 rats were in the group exposed to 300 mg/m3. All major organs and
respiratory tract tissues were examined histologically in a portion of the animals
(n = 12) from each exposure group. Neurobehavioural studies also were performed in
the first of the study, although details are not reported by the US EPA.
The focus of the second, lower concentration study was the respiratory tract. Tissues
examined in this study included the turbinates (two sections), trachea and five lobes of
53
Alkyl Phosphate AVSR Additive
the lung from 20 animals in each exposure group and controls. Concentration-related
decreases in pulmonary bactericidal activity were observed for all exposure groups only
in the first study.
Agent-related mortality was observed among the animals exposed to the two highest
concentrations: 19/176 at 1200 mg/m3 and 1/176 at 750 mg/m3. Decreases in body
weight gain also were observed in these two groups. The number of deaths in the
controls is not reported by the US EPA. No deaths were noted in the second study.
The US EPA states that both studies indicated the target organ to be the respiratory
tract, specifically the terminal bronchioles. Pathological examination of a portion of
those animals that died revealed extensive involvement of bronchiolar and laryngeal
mucosa, the latter probably contributing to death. Terminal bronchiolar fibrosis
(minimal to severe) with no or minimal involvement of pulmonary tissues was the only
concentration-dependent lesion noted in the respiratory tract of animals surviving
repeated exposures. This lesion was present in all animals examined that had been
exposed to 750 or 1200 mg/m3, including those necropsied after an 8-week recovery
period, and was judged predominately as moderate and severe. In the second study, this
lesion was present with minimal severity in 9/20 animals exposed to 300 mg/m3,
4/20 animals exposed to 180 mg/m3 and 0/20 animals exposed to 50 mg/m3. Based on
the histologic lesions in the tracheobronchiolar region for smoke generated from
burning 95% red phosphorus and 5% butyl rubber, 180 mg/m3 is the LOAEL, and
50 mg/m3 is the NOAEL.
The smokes generated in the above studies are complex and uncertainty has been
expressed over the exact chemical identities generated (Payne et al., 1993). For
example, temperature and oxygen conditions can affect the type of phosphorus oxide
formed during combustion of the phosphorus. Phosphorus pentoxide is produced in an
oxygen-rich environment while phosphorus trioxide is produced if the oxygen levels
are limited (Corbridge, 1985). In an excess of cold or hot water, the hydrolysis product
of phosphorus trioxide is phosphorous acid or a mixture of products (phosphoric acid,
phosphine and phosphorus), respectively (Corbridge, 1985). Furthermore, a low
concentration of phosphine along with phosphorus pentoxide has been reported in
phosphorus smoke aerosols used in some animal inhalation studies (Burton et al., 1982;
Marrs et al., 1989).
11.5 Mutagenicity, genotoxicity and carcinogenicity
Phosphoric acid yields negative results in bacterial mutagenicity assays, the only
genotoxicity data available to date on phosphoric acid (Demerec et al., 1951; Cipollaro
et al., 1986; Al-ani & Al-Lami, 1988). No human data are available on phosphoric
acid's potential to cause genotoxicity.
There is no reliable information on the carcinogenic potential of phosphoric acid in
animals or humans. Workers in the phosphate industries such as mining and processing
or fertiliser production reportedly appear to have a slight increase in lung cancer
(Commission of the European Communities, 1992). The evidence for the slight
increase in lung cancer in such workers is regarded as weak due to the workers'
exposure to a wide variety of chemicals. These chemicals include sulphuric acid,
arsenic, chromium and soluble fluorine compounds, some of which are known to be
associated with lung cancer.
54 Priority Existing Chemical Assessment Report Number 25
In a population-based case-control study, an increased risk for renal cancer in relation
to occupational exposure to phosphoric acid is reported (Parent et al., 2000). The low
precision of the odds ratio estimates (3.4 (1.3-9.2; 95% CI)) and the lack of detail on
the industry environment to which the workers were exposed points to further
investigations being required to confirm any proposed correlation.
11.6 Reproductive toxicity
There are no adequate reproductive toxicity investigations of phosphoric acid in
humans and animals. In a poorly described animal oral toxicity study, the effect of a
prolonged intake of phosphoric acid is reported in rats fed diets containing nil or
4000 ppm phosphoric acid since weaning and mated at 32 weeks and again at 43 weeks
of age (with the offspring fed the same diet). (Bonting & Jansen, 1956). No adverse
effects on reproduction were reported in the study as judged by the weight of the
mothers and offspring at birth, the number of live and stillborn young and the survival
of young up to weaning.
No information is available on the teratogenicity, neurotoxicity, sensitisation or
immunotoxicity of phosphoric acid in mammals.
55
Alkyl Phosphate AVSR Additive
12. Hazard Classification
12.1 Health hazards
There is no or insufficient toxicity data to enable the alkyl phosphate additive to be
classified according to the NOHSC Approved Criteria for Classifying Hazardous
Substances (the Approved Criteria) (NOHSC, 1999a) or the OECD Globally
Harmonised System of Classification and Labelling of Chemicals (GHS) (OECD, 2002).
The Approved Criteria are cited in the NOHSC National Model Regulations for the
Control of Workplace Hazardous Substances (NOHSC, 1994a) and provide the
mandatory criteria for determining whether a workplace chemical is hazardous or not.
Classifications under the GHS will come into force when it is adopted by the Australian
Government and promulgated into Commonwealth legislation.
There are no data for the alkyl phosphate additive itself due to its manufacture and
formulation in situ. Toxicology data supplied by the Applicants relate to the alkyl
phosphate formulation DMA-4 which is equivalent to Valvemaster Concentrate.
Mammalian DMA-4 toxicology data indicate, low acute oral and dermal toxicity and
possibly skin irritant effects, most likely related to or confounded by the kerosene
content of DMA-4.
Kerosene, which is the hydrocarbon diluent used in the manufacture of the alkyl
phosphate formulations (Section 4), is contained in the Valvemaster products at and
above a concentration of 20% which can be considered a skin irritant according to the
NOHSC List of Designated Hazardous Substances (NOHSC, 1999b). The alkyl
phosphate additive is not listed in the NOHSC List of Designated Hazardous
Substances (NOHSC, 1999b). Solvent naptha at concentrations greater or equal to 10%
is classified according to the NOHSC List of Designated Hazardous Substances
(NOHSC, 1999b) as Harmful (Xn) and may cause lung damage if swallowed (R65).
12.2 Physico-chemical hazards
There are no physio-chemical data for the alkyl phosphate additive itself due to its
manufacture and formulation in situ. The data supplied by the Applicants relate to the
alkyl phosphate formulations Valvemaster Concentrate and Valvemaster VM11
described in Section 5.
Valvemaster Concentrate has a low volatility (vapour pressure < 0.1 kPa at 20癈), a
boiling point greater than 149癈, and a flash point of 72oC (open cup). The
autoignition temperature is 220癈. Valvemaster VM11 has an unknown vapour
pressure with a boiling point greater than 149 癈 and flash point of 63 oC (open cup).
The autoignition temperature is 220癈.
Regarding the ADG Code (FORS 1998), Valvemaster Concentrate and
Valvemaster VM11 meet the criterion for C1 combustible liquids based on their flash
points, which need to range between 60.5 and 150 癈 to meet this criterion. Regarding
the ADG Code (FORS 1998), the alkyl phosphate aftermarket products do not meet the
criteria for classification as a dangerous good on the basis of physicochemical hazards.
56 Priority Existing Chemical Assessment Report Number 25
13. Effects on Organisms in the
Environment
This section provides information on the effects of the alkyl phosphate additive on
animals and plants. In addition, information is provided on phosphoric acid (H3PO4),
the predicted main phosphorus-based combustion product (Section 8) and phosphorus.
Based on the alkyl phosphate additive use pattern and environmental fate, the review of
effects has included the potential effects to organisms typically inhabiting terrestrial
and aquatic environments.
Issues associated with the use of the alkyl phosphate additive to the environment
include:
? ecotoxicological issues associated with accidental spills and leaks to waters and
land of alkyl phosphate additive as a concentrate or diluted solution in LRP;
? ecotoxicological issues associated with exhaust emissions of phosphoric acid;
and
? contribution to nutrient pollution and eutrophication in aquatic environments
due to the emission of a nutrient, i.e. phosphorus, that is often limiting in the
environment.
13.1 Terrestrial organisms
13.1.1 Alkyl phosphate additive
No toxicity data were available on the effects of the alkyl phosphate additive on
terrestrial plants. Toxicity data for the alkyl phosphate additive product DMA-4 which
is synonymous with Valvemaster Concentrate in mammals is presented in Section 10.
These DMA-4 animal studies show that the alkyl phosphate additive formulation is not
acutely toxic by oral or dermal exposure. The oral ALD in male rats was cited as
17 000 mg/kg bw and ALD by skin absorption greater than 5000 mg/kg bw in male
white New Zealand rabbits. While the test guidelines were not standard, the DMA-4
animal toxicity studies indicate the potential for DMA-4 to cause skin and eye
irritation.
The results of a 21-day delayed neurotoxicty study using mature white leghorn
chickens, indicate DMA-4 to be of low toxicity in chickens via the oral route (LD50
greater than 5000 mg/kg body weight), with no signs of delayed neurotoxicity noted
under the conditions of the study.
13.1.2 Phosphoric acid
Animals
Kinetics, metabolism and toxicity of phosphoric acid to mammals is presented in
Section 11.
57
Alkyl Phosphate AVSR Additive
Plants
Environment Canada (1981), as cited by the European Chemicals Bureau (ECB, 2000),
describes phytotoxicity test data for concentrated phosphoric acid applied to foliage of
peas, beans, beets, rapeseed and weeds. A 15% to 20% solution of phosphoric acid
(estimated pH 0.8 to 0.9) applied to foliage-resulted in the death of the exposed plants.
Phosphoric acid, in low concentrations, is a natural component of many fruits and their
juices (Furia, 1972).
13.1.3 Phosphorus
Phosphorus is a macronutrient of plants and is also an essential element for
microorganisms and animals. It is a structural component of nucleic acids, which are
basic building blocks of DNA and RNA. Phosphorus is necessary for cell division and
the regulation of all cell processes (Ohio State University, 1996).
In plants, the addition of phosphorus stimulates early root formation, rapid and
vigorous growth, hastens maturity and blooming and gives winter hardiness.
Phosphorus deficiency symptoms in terrestrial plants include reddish-purple leaves with
the older leaves affected first, short thin leaves, stunted plant growth and defoliation
starting at the lower leaves.
Phosphorus toxicity in plants, such as that caused by the addition of excessive amounts
of fertilizer to crops, may result in zinc or iron deficiency (Rosen and Eliason, 2002)
and necrosis and death in extreme cases.
13.2 Aquatic organisms
13.2.1 Alkyl phosphate additive
Acute aquatic toxicity of DMA-4 was tested by Haskell (1986c) using juvenile fathead
minnows (Pimephales promelas), a warm freshwater fish, under static, unaerated test
conditions. DMA-4 contains the alkyl phosphate compound at similar concentrations to
Valvemaster Concentrate. Fish (2.1 cm length, 0.085 g weight) were laboratory
bred and acclimated for 141 days prior to testing. Nominal concentrations tested were
1000, 750, 562.5, 422, 316, 237, 178, 133, 100 and 0 mg/L. Fish were not fed 48 hours
prior to, or during, the tests. Test solutions were not aerated but dissolved oxygen was
monitored. Temperature was maintained between 21.8 and 22.1癈. Day/night
simulation was maintained at 16 hours light:8 hours dark. Mortality counts were made
each 24 hours during the 96-hour period and pH was monitored. The 96-hour LC50,
derived by probit analysis, was 230 mg/L (95% CI of 210 to 270 mg/L).
Based on this study, DMA-4 does not meet the classification criteria for acute aquatic
toxicity using the Globally Harmonised System of Classification and Labelling of
Chemicals (GHS; OECD, 2002).
13.2.2 Phosphoric acid
This section provides a brief description of toxicity data for phosphoric acid.
58 Priority Existing Chemical Assessment Report Number 25
Aquatic toxicity data for phosphoric acid has been obtained from an IUCLID dataset of the
European Chemicals Bureau (ECB, 2000). Environment Australia has not reviewed all of
the publications referenced (see citation for specific reference sources).
Although the pH of phosphoric acid is approximately pH 1 to 1.5 (ECB, 2000), it is
unlikely that pH changes to water bodies would result from the emission of phosphoric acid
from the combustion of LRP containing Valvemaster. Nevertheless, following is a brief
account of the potential adverse effects of low pH on aquatic organisms.
Low pH can cause direct adverse effects on fish and aquatic insects, and pH changes
(particularly reduced pH) can cause the toxicity of several pollutants (e.g. ammonia,
cyanide, aluminium) to significantly increase (ANZECC and ARMCANZ, 2000).
Following is a summary of aquatic toxicity data for aquatic animals exposed to
concentrated phosphoric acid. No toxicity data were available for aquatic plants.
Table 9 - Summary of aquatic toxicity data for phosphoric acid
Taxa Habitat Acute LC(EC)50
Reported as pH value
4.6
Invertebrates Freshwater
Marine ---
3.5
Fish Freshwater
Marine ---
--- = No data available.
ECB (2000) has summarised aquatic toxicity data for two species of freshwater
invertebrates (Daphnia magna and D. pulex waterfleas), with derived 12-hour LC50
values of pH 4.6 and 4.1, respectively. The survival rate was found to depend on the
pH value generated by the acid. In addition, a 12-hour LC50 for amphipods (Gammarus
pulex and G. fossarum) of pH 3.4 has been derived.
The acute (96-hour) toxicity of concentrated phosphoric acid has been studied in two
species of freshwater fish including Bluegill sunfish (Lepomis macrochirus) and mosquito
fish (Gambusia affinis) under static test conditions. ECB (2000) reported aquatic toxicity
data for phosphoric acid, with a 96-hour LC50s of pH 3.0 to 3.5 for both species. At
sublethal concentrations of acids, L. macrochirus become hypoactive with respect to their
swimming behavior (Ellgaard and Gilmore, 1984, as cited by ECB, 2000). The LC50 range
of pH 3.0 to 3.5 for fish is common to phosphoric acid and several other acids including
sulfuric acid, nitric acid and hydrochloric acid. The contribution of the anions of these
acids to fish toxicity is similar.
Most natural freshwaters have a pH in the range 6.5 to 8.0, while the pH of most marine
waters is close to 8.2. The pH in most waters is controlled by the carbonate-bicarbonate
buffer system, which is particularly strong in marine waters ANZECC/ARMCANZ (2000).
13.2.3 Phosphorus and aquatic ecosystems
Phosphorus occurs naturally in waters of aquatic ecosystems, typically at
concentrations that limit plant and algae growth (Cullen, 1986, Donnelly et al., 1992;
cited by NSW EPA, 2000). Nevertheless, excess phosphorus can lead to excessive
growth of algae (blooms) and other aquatic plants. Eutrophication is the over-
enrichment of a body of water with nutrients, primarily nitrogen and phosphorus,
59
Alkyl Phosphate AVSR Additive
resulting in excessive growth of organisms and depletion of the oxygen concentration,
often affecting other aquatic organisms. NSW EPA (2000) indicates that in most
instances, algal blooms are harmless; however, cyanobacteria can cause environmental
problems either by giving rise to odours and taints, or by producing toxins. A number
of cyanobacteria species may produce one or more potent toxins with up to four modes
of action including hepatotoxins (liver and internal organs), neurotoxins
(neuromuscular blocking agents), endotoxins (dermatitis and conjunctivitis) and
cytotoxins (internal organs) (Water Directorate, 2001). These toxins may potentially
pose risks to aquatic organisms, wildlife and people. Other negative effects of
excessive algal growth and decay include reduced light penetration into water,
unpleasant smells from decomposing algae, restriction of fish migration and
impairment of recreational use of water (e.g. boating, fishing, swimming).
In marine waters (including estuaries), blooms of diatoms and dinoflagellates may
occur. Many dinoflagellates, whose blooms are known as 'red tides', can produce toxins
that lead to skin irritations and illness in exposed humans. They can also enter the food
chain where they are particularly hazardous to human consumers of seafood, who may
contract an illness known as paralytic shellfish poisoning (NSW EPA, 2000).
Nutrient pollution of waters is a major environmental issue in Australia. The NSW EPA
highlighted important anthropogenic sources of nutrients in ground water, fresh surface
waters, estuarine waters and marine waters including:
? run-off from urban and rural residential areas (including road run-off);
? discharges from sewage treatment plants (STPs) and septic systems;
? erosion and run-off from grazing and cultivated land;
? run-off from intensive animal industries and forestry;
? tailwater from irrigation areas; and
? increasing riverbank and streambank erosion arising from the removal of
vegetation.
The significance of diffuse sources in any given situation depends on the yield of nutrient
generated by the particular land-use activity and the area or proportion of the catchment
devoted to that activity, i.e., kilograms of nutrient per hectare per annum. Generally, the
highest yields of nutrients are from urban areas, with lower yields from agricultural and
forested catchments (Campbell & Doeg, 1989, as cited in ANZECC and ARMCANZ,
2000).
In NSW in 2000, the NSW EPA indicated that most inland rivers had concentrations of
phosphorus that exceeded management objectives for the control of eutrophication.
Generally, phosphorus concentrations increased with distance downstream; however,
phosphorus concentrations in coastal rivers were generally low (NSW EPA, 2000). NSW
EPA (2000) phosphorus management objectives for phosphorus for the management of
eutrophication is a scale:
? <0.02 mg Total Phosphorus (TP)/Litre - Good
? 0.02 to 0.05 mg TP/Litre - Fair
? >0.05 mg TP/Litre - Poor
A value of >0.05 mg TP/Litre would exceed the phosphorus management objective. As
indicated later in Section 15.5.2, caution is advised when trying to correlate total
60 Priority Existing Chemical Assessment Report Number 25
phosphorus with prediction of eutrophication and algae bloom (type, magnitude or
duration), as phosphorus may not be linked due to other important factors.
Regarding coastal rivers, NSW EPA (2000) indicates that between 1997 and 1999 two
algal blooms potentially harmful to marine organisms and seven blooms potentially
toxic to humans were recorded. These bloom frequencies were similar to those
recorded between 1994 and 1996. The high nutrient (nitrogen and phosphorus) levels
in stormwater and sewer overflows affect many of the urban estuaries in Sydney.
Polluted stormwater in urban areas is a major non-point-source contributor to poor
water quality. During periods of high rainfall, significant volumes of water enter rivers
and streams, transporting nutrients into waterways. Stormwater in urban areas is a
particular problem because of the large area of paved surfaces and complex drainage
systems (NSW EPA, 2000).
Depending on the level of treatment, the hundreds of licensed sewage treatment plants in
NSW discharge effluent that can affect water quality, particularly during periods of little
rainfall and low river flow. Sewage treatment plants are a significant contributor of
nutrients in all NSW waterways (NSW EPA, 2000).
There are no definitive guidelines to assess the risks posed by marine and estuarine algal
blooms, primarily because of the number of species that are potentially toxic and the
variability in toxicity of algal blooms. The degree of toxicity depends on environmental and
physiological factors (NSW EPA, 2000).
The National Land and Water Resources Audit (AMU, 2002) has identified nutrients
(total phosphorus and total nitrogen) as a major surface water quality issue in Australia
affecting most of the more intensively developed basins in the North-East Coast,
Murray-Darling, South-East Coast and South-West Coast drainage divisions. Basins
assessed to have nutrient levels within acceptable levels include the relatively well
vegetated and less developed basins in areas such as north Queensland, north eastern
Victoria and south western Australia.
61
Alkyl Phosphate AVSR Additive
14. Risk Characterisation
The information on the biological effects of the alky phosphate additive and related
vehicle emissions presented in Section 10 is integrated in this section with the
environmental, public and occupational exposure estimates developed in Section 9. An
overall estimation is provided of the incidence and severity of the adverse effects the
chemical may have on people and the environment in Australia. This process provides
the basis for identifying areas of concern and evaluating risk management strategies.
14.1 Environmental risk
A hazard quotient (HQ) approach has been used to predict the hazard to terrestrial and
aquatic organisms. The HQ is the ratio of the predicted environmental concentration
(PEC) to the predicted no effect concentration (PNEC). To predict a low environmental
hazard, the HQ value needs to be 1 or less (i.e. HQ 1).
No PNECs for phosphorus in waters for eutrophication and algal bloom end-points are
available. ANZECC and ARMCANZ (2000) provide guidance levels only due to the
complexity of correlating phosphorus concentration to algal bloom occurrence (Harris,
1994).
Leakages of LRP containing the alkyl phosphate additive from underground storage
tanks (USTs) poses specific risks at local scales; however, the risk to the environment
will depend on site-specific environmental conditions and in most situations it is
expected to pose a negligible risk.
While emergency spill incidents and accidents and leakages from USTs may lead to the
alkyl phosphate additive in the environment, terrestrial and aquatic wildlife are unlikely
to be exposed at or above levels of concern under current use patterns.
14.1.1 Terrestrial risk
Animals
Most of the alkyl phosphate additive used each year will be destroyed during
combustion within internal combustion engine cylinders with the emission of
phosphoric acid and other exhaust gases. Animals may be exposed to phosphoric acid
in air through inhalation.
Section 11 describes a NOAEL (in rats) of 50 mg/m3 from two parallel 13-week
inhalation studies of an aerosol of 95% red phosphorus and 5% butyl rubber
combustion products containing 70% phsophoric acids. A phosphoric acid
PNECmammals of 0.5 mg/m3 is derived by dividing the NOAEL by an assessment factor
of 100. Conservative estimation of potential phosphoric acid levels in air indicates
PECs of 0.1 ng/L (current) and 0.040 ng/L (2004) (Table 4) These PECs are several
orders of magnitude lower than the estimated phosphoric acid PNECmammals of 500 ng/L.
Plants
No published phytotoxicity benchmark or data were available on the acceptable
concentration of phosphoric acid in air for terrestrial plants. No records of adverse
62 Priority Existing Chemical Assessment Report Number 25
effects on plants were identified in the literature in existing alkyl phosphate additive use
areas. Phosphorus is an essential nutrient for plants and of low toxicity, only becoming
a problem to terrestrial plants when exposed to excessive soil or foliar concentrations.
An estimate of the concentration of phosphoric acid deposition from air to land can be
made using the Sydney use pattern as an example and the alkyl phosphate additive use
scenarios developed in Section 9.3.1.
Research by Handreck (1997) suggests that Australian plants from a range of genre can
tolerate phosphate concentrations of 0.9 kg/m3 soil (at least 1400 mg PO43-/kg soil
assuming soil density of 1.6 kg/m3). Sydney land area is 1550 km2 or 1.55 x 109 m2.
With a biologically-active soil depth of approximately 0.1 m, this equates to
1.55 x 108 m3 soil. Assuming conservatively that 50% of the soil surface is exposed,
this equates to 7.75 x 107 m3 of soil in the biologically-active zone in the Sydney
region. Assuming soil density of 1.6 kg/m3, the soil volume equates to 1.24 x 108 t (or
1.24 x 1011 kg) soil.
For Sydney, the estimated worst case (Scenario 1) atmospheric fallout of phosphorus is
equivalent to about 11.5 tonnes of P or 35.3 tonnes when presented as PO43- per annum
(or 3.53 x 1010 mg)/annum. By assimilating the available soil mass (1.24 x 1011 kg)
with the estimated atmospheric fallout (3.53 x 1010 mg/annum), the incremental
amount of PO43- per kg surface soil is estimated to be approximately
0.28 mg PO43-/kg soil/annum.
Biological uptake by soil fauna and plants of an undefined portion of this phosphate
would likely occur resulting in soil concentrations being lowered simultaneously. The
proportion of land area is probably under-stated. It is doubtful whether soil phosphate
concentrations would ever exceed phytotoxicologically-significant levels, even in
Sydney soils.
14.1.2 Aquatic risk
The alkyl phosphate formulation DMA-4 (synonymous with Valvemaster
Concentrate) has a median lethal concentration (LC50) for fish of 230 mg/L (95% CI
210-270 mg/L).
Concentrated phosphoric acid is acutely toxic to terrestrial and aquatic organisms, with
LC50 values of pH 4.6 or less ; however, the likelihood of environmental pH values
reaching levels of concern is unlikely due to low input and natural buffering capacity.
Phosphorus is a nutrient of plants and animals, but typically limits growth in the
environment due to its low concentrations and/or low bioavailability. Excessive
amounts of phosphorus can increase the risk of eutrophication and nuisance plant and
algae growth in aquatic environments.
ANZECC and ARMCANZ (2000) indicate that a wide range of nutrient concentrations
have been reported for Australian rivers and streams. Total phosphorus concentrations
have been recorded in the range of 10 礸/L or less in near pristine mountain streams to
approximately 1000 礸/L in polluted rivers. There are few published surveys of
nutrient concentrations in estuarine waters of Australia and those available indicate
considerable spatial variation in the nutrient concentrations in Australian waters. While
no trigger values are available for phosphoric acid, ANZECC and ARMCANZ (2000)
provide guidance ranges for total phosphorus in Australian aquatic ecosystems for use
in preliminary assessment of risks of eutrophication and algal blooms to aquatic
63
Alkyl Phosphate AVSR Additive
ecosystems. Guidance levels for freshwater and marine ecosystems for total
phosphorus are 10-50 and 25-30 礸/L, respectively (ANZECC and ARMCANZ, 2000).
The basis of the default trigger values is that phosphorus may potentially promote
nuisance aquatic plant/algal growth in waterways. These indicative values are not
standards that should never be exceeded. This is because other environmental
conditions may enhance or limit aquatic plant or algal growth.
As indicated in Section 9.3.3, the predicted environment concentration (PEC) for total
phosphorus in Sydney's stormwater derived from urban runoff using conservative
assumptions may approximate only a fraction of the estimated background
concentrations.
In general, effects from multiple natural and anthropogenic sources of phosphorus in the
Australian aquatic environment will be cumulative. Together, they increase the risk to
the aquatic environment of eutrophication and nuisance algal blooms. Nevertheless,
comparison with typical background concentrations of total phosphorus in marine areas
supports a conclusion of a negligible contribution, or low expected incremental risk,
from use of LRP containing alkyl phosphate-based AVSR additives for the uses
prescribed and the volumetric use rates estimated.
The above-mentioned PEC values are based on conservative assumptions including
limited atmospheric dispersion, limited soil attenuation or other losses of phosphorus.
Furthermore, the effects of dilution, mixing and sedimentation that are likely to occur in
receiving waters have not been taken into account. No atmospheric data were available
to verify the PEC estimates made in this assessment.
The two use scenarios developed in this assessment report represent the worst case
examples for AVSR petrol additives. Elsewhere in Australia the amount of LRP used
would be less than the worst-case example calculated in this assessment.
14.2 Occupational risk
There is no documentation on adverse human health effects due to the alkyl phosphate
additive. Therefore, the risks characterisation to human health of the alkyl phosphate
additive is assessed with regard to the proprietary products Valvemaster Concentrate
and Valvemaster VM11 and the combustion by-product phosphoric acid.
The margin of exposure methodology is commonly adopted in international
assessments for determining risk to to human health from exposure to chemicals (EC,
1994; OECD, 1994). For health effects caused by repeated or prolonged exposure,
risk(s) have been characterised as follows:
? Identification of critical effect(s)
? Identification of the most appropriate/reliable NOAEL (if available) for the critical
effect(s)
? Where appropriate, comparison of the NOAEL with the estimated human dose
(EHD) or exposure, to provide a margin of exposure (MOE) that is defined as:
MOE = NOAEL/EHD
? Characterisation of risk by evaluating whether the MOE indicates a concern for the
human population under consideration.
64 Priority Existing Chemical Assessment Report Number 25
The MOE provides a measure of the likelihood that a particular adverse effect will
occur under the conditions of exposure. As the MOE increases, the risk of potential
adverse effects decreases. In deciding whether the MOE is of sufficient magnitude,
expert judgement is required. Such judgements are usually made on a case-by-case
basis and should take into account uncertainties arising in the risk assessment process,
such as the completeness and quality of the database, the nature and severity of effect(s)
and variability between and within species.
14.2.1 Critical health effects
The critical health effects described in this section are derived from toxicity studies of
the alkyl phosphate formulation DMA-4 (see Section 10) and it's predicted combustion
by-product, phosphoric acid, which is described in Section 8.
Alkyl phosphate additive
Animal (mammalian) studies of DMA-4 indicate the alkyl phosphate additive is not
acutely toxic by oral or dermal exposure, although irritant effects are possible. No
repeated dose data are available. While there are no toxicokinetic data available for the
alkyl phosphate additive, exposure has the potential to add to the total body
phosphate/phosphorus load.
In poorly reported studies, the acute lethal doses were reported as greater than 11 000
and as 17 000 mg/kg bw for oral exposure in male rats. The acute lethal dose via the
dermal route in rabbits was greater than 5000 mg/kg bw.
Animal (mammalian) studies indicate moderate to severe dermal irritation following
prolonged exposure (24-72 hours). The inclusion of kerosene in the alkyl phosphate
additive formulation can not be discounted as a contributing factor to the observed
irritant response observed in these animal studies.
Neither surrogate data nor Quantitative Structure Activity Relationships (QSAR) are
used in this assessment report to predict irritancy. This is because even with simple
inorganic phosphates, a wide range of eye and skin irritancy is reported (Weiner, 2001).
The inclusion of kerosene in the formulation presents additional adverse health effects
such as irritancy and lung damage (if swallowed) (NOHSC, 1999b).
Phosphoric acid
The present assessment also considers the health effects of phosphoric acid which is
identified as the combustion by-product of the alkyl posphate additive.
In animals (mammalian) and humans, the critical effects following acute exposure to
phosphoric acid relate to the acidic nature and hence the corrosive effects of the acid.
The corrosive effects of phosphoric acid include eye, skin, pulmonary and
gastrointestinal irritation with the severity of the symptoms depending on the
concentration and length of exposure to the acid.
Corrosion of the gastrointestinal tract and permanent eye damage are reported in
humans following accidental oral ingestion and splashes to the eye, respectively, of
phosphoric acid. Animal data confirm the eye and dermal irritancy of phosphoric acid
with concentration, occlusion and length of exposure determining the severity of the
adverse effect. A single drop into the human eye of 1.5% phosphoric acid reportedly
65
Alkyl Phosphate AVSR Additive
causes moderate stinging but no injury. Concentrations as low as 2.5-5% phosphoric
acid causes skin irritation in animals.
There are limited human inhalation exposure data for phosphoric acid. Weakness, dry
cough, chest pain and shortness of breath or dyspnea are reported following accidental
occupational inhalation of high (unspecified) concentrations of phosphoric acid vapour.
Symptoms of reactive airways dysfunction were evident one year after exposure.
In animals (mammalian), based on limited data, phosphoric acid has low acute oral,
dermal and inhalation toxicity. Phosphoric acid does not appear to have been well
studied with respect to repeated dose toxicity in animals or humans. No reports have
been found in the literature of systemic poisoning following repeated inhalation
exposure to phosphoric acid. Phosphorus pentoxide which hydrolyses to phosphoric
acid also has low acute inhalation toxicity although there appears to be differences
between species. Repeated dose toxicity data for phosphoric acid rely on phosphorus
smokes generating phosphorus pentoxide which is hydrolysed to phosphoric acid.
These studies show the nature of the effect is dependent on the concentration, duration
of exposure and the hydroscopic character of the acid with interspecies differences.
Concentration dependent terminal bronchiolar fibrosis in male Sprague-Dawley rats is
reported in two parallel 13-week inhalation studies. Both involved exposure to the
combustion products of 95% red phosphorus and 5% butyl rubber, with a reported
NOAEL of 50 mg/m3. The study proposed 71-79% phosphoric acid in the inhaled
aerosols.
Phosphorus
The WHO cites a maximum tolerable daily intake of phosphorus of 70 mg/kg bw,
which, if calcium intake is adequate, equates to 4.2 g of phosphorus or 12.9 g of
phosphate ( an ionic form of phosphoric acid) for a 60 kg person.
14.2.2 Occupational health and safety risks
Manufacture
Exposure during the manufacture of the alkyl phosphate additive is predicted to be low
given the fully enclosed manufacturing method, enclosed tranfer systems and use of
personal protective equipment.
Exposure during manufacture to the alkyl phosphate additive via dermal and ocular
routes is possible from spills and slops while manually connecting transfer lines, e.g.,
from the reaction vessels or on-site holding tanks to steel drums or ISO tanks.
Dermal and ocular expousure is also possible during manual sampling of the alkyl
phosphate additive formulation from the reaction vessel for quality assurance (QA)
testing and during laboratory testing of the QA sample.
The oral and dermal ALD values of 11 000-17 000 mg/kg bw and greater than
5000 mg/kg bw, respectively, for DMA-4 indicate the overall risk of acute health
effects is low given the small amounts to which workers are likely to be exposed.
Exposure to the alkyl phosphate additive is expected to be infrequent, minimal and of
short duration.
Oil company terminals and depots
66 Priority Existing Chemical Assessment Report Number 25
Exposure levels during bulk LRP blending are predicted to be low given the typically
automated and enclosed transfer activities and use of personal protective equipment
(PPE). Non-automated additions of the alkyl phosphate additive at some depots may
potentially result in increased occupational exposure for short (5 min) periods daily.
Exposure via the dermal and ocular routes is possible from slops, spills and residue
during decanting of Valvemaster Concentrate from either drums or ISO tanks into
storage tanks. Such exposure is expected to be infrequent, minimal and of short
duration, although staff decanting from drums via a hand pump and a spear or a
dedicated pumping system into a bulk tank may be exposed for a longer period of time,
e.g. six hours, but infrequently, e.g., three times per year at most.
In general, as for manufacturing workers, the risk to the terminal's workers from
handling the alkyl phosphate additive is assessed as low because direct handling of the
alkyl phosphate additive is miminal or infrequent, or both.
Occupations associated with vehicles
Petrol stations, maintenance workshops and car parks
Tanker drivers, petrol station attendants and auto mechanics may be exposed
occupationally to the alkyl phosphate additive through contact with LRP fuels and less
frequently with aftermarket products containing the the alkyl phosphate additive.
Although exposure to fuel vapours may be expected during a typical working day, the
low vapour pressure of the alkyl phosphate additive formulations and its high dilution
in fuel renders inhalation exposure to the alkyl phosphate additive unlikely.
Exposure to the alkyl phosphate additive via dermal and ocular routes is expected to be
infrequent, minor and of short duration and also limited due to its dilution with solvents
and other additives in the fuel and fuel additives. Therefore, the risk to petrol station
and maintenance workshop workers from handling the alkyl phosphate additive is
assessed as low. Car park personnel are not expected to handle the alkyl phosphate
additive.
Auto mechanics at petrol stations and at dedicated maintenance workshops and car park
personnel have the potential for repeated exposure to phosphoric acid associated with
auto exhaust. Such exposure is likely to be highly variable depending on the level of
separation from the exhaust sources and traffic densities. No personal exposure data
for such workers are reported.
The level of emission of phosphoric acid at the tailpipe of vehicles using alkyl
phosphate additive-based LRP is estimated in this assessment report to range from 6 to
8.3 mg/m3 (equivalent to 600 to 830 ng/L) of exhaust gas depending on whether or not
entrapment of phosphoric acid occurs in the exhaust system (Section 8).
Atmospheric dilution of the exhaust gas will occur. Dilution rates used in this report to
predict atmospheric phosphoric concentrations around vehicles using the alkyl
phosphate additive rely on the work of Dolan et al (Dolan et. al, 1979). The estimated
atmospheric phosphoric acid concentration at 2 metres from the exhaust tailpipe is 0.06
to 0.083 mg/m3 based on an exhaust gas dilution rate of 100. This is significantly lower
than the phosphoric acid LC50 values of 111 to 6327 mg/m3. There is the potential for
higher occupational exposures to atmospheric phosphoric concentrations found in
enclosed or poorly ventilated workshops or car parks and at busy petrol station
forecourts.
67
Alkyl Phosphate AVSR Additive
For repeated occupational exposure, margins of exposure can be calculated from
estimated atmospheric phosphoric acid concentration at 2 metres from the exhaust
tailpipe by applying the NOAEL of 50 mg/m3 for pulmonary fibrosis in rats
(Ballantyne, 1998).
Applying the NOAEL of 50 mg/m3, assuming 100% phosphoric acid in the smoke and
converting intermittent exposures (4 days/week, 2.25 hours/day) to a working week
(5 days/week, 8-hr day) exposure, the following margins of exposure are calculated:
At 2 m from the tailpipe, assuming no entrapment of exhaust phosphoric acid emissions
(8.3 mg/m3) and an exhaust gas dilution rate of 100:
Margin of Exposure = (50 mg/m3 x 4/5 x 2.25/8)/0.083 mg/m3 = 135 (3)
Using the same calculation above, the MOE at 2 metres is increased to 187 if
entrapment of exhaust phosphoric acid emissions (6.0 mg/m3) occurs.
The risk to petrol stations and maintenance workshops workers and car park personnel
from phosphoric acid associated with auto exhaust is, therefore, considered low.
Furthermore, the typical use of open workshops and limited forecourt service at service
stations in Australia will decrease the exposure of maintenance and petrol station
workers, respectively, to exhaust gas phosphoric acid. Exposure may be higher for car
park personnel if they are confined to enclosed or poorly ventilated car parks.
Professional drivers and road maintenance workers
Like petrol station, maintenance workshop and car park personnel, professional drivers
and road maintenance workers may be occupationally exposed to phosphoric acid
exhaust emissions. No personal exposure data for professional drivers and road
maintenance workers are reported.
Calculations based on Dolan's work (Dolan et. al, 1979) may be made of atmospheric
phosphoric acid concentrations from the tailpipes of moving vehicles. An exhaust gas
dilution rate is reported as typically 1000 in less than one second, with the dilution rates
ranging from approximately 630 at idle to 5000 at 80 km/hour vehicle speeds (Dolan et.
al, 1979). Consequently, the phosphoric acid exhaust gas levels of 68.3 mg/m3 will be
diluted to 9.52 x 10-3 mg/m3to 0.0132 mg/m3 (idle speed) and 1.2 x 10-3 mg/m3 to
1.66 x 10-3 mg/m3 (80 km/hr), respectively. These phosphoric acid concentrations are
several magnitudes lower than the LC50 values for acute exposure and the NOAEL for
repeated exposure.
Given that the exposure of professional drivers and road maintainence workers is lower
than for petrol station, maintenance workshop and car park personnel, the risk of this
group to phosphoric acid exhaust emissions in Australia is likewise considered to be
low.
14.2.3 Uncertainties
Uncertainties exist in the assessment of risk to local workers from the use of the
phosphorus AVSR additive. No Australian personal exposure data exist regarding
exposures to the alkyl phosphate additive or phosphoric acid in the workplace.
There are no data on the potential health effects of the alkyl phosphate additive because
it is never isolated; instead, it is manufactured in situ into a formulated proprietary
product at a concentation range of 70-90%.
68 Priority Existing Chemical Assessment Report Number 25
The limited number of toxicity studies relied on in this report relate to the kerosene-
based alkyl phosphate additive formulation DMA-4. The kerosene in DMA-4 will be a
confounding factor in determining the toxicology profile of the alkyl phosphate
additive.
There are limitations in the DMA-4 toxicological data. For example, few of the DMA-
4 studies meet standard test guidelines. No repeated dose toxicity, reproductive effects,
genotoxicity or carcinogenicity data in humans and animals are available for the alkyl
phosphate additive or DMA-4. Also, there is insufficient data to determine specifically
the irritancy potential of the alkyl phosphate additive.
There are limited data on the inhalation toxicity of the phosphoric acid. Animal
(mammalian) studies rely on smokes generated from the oxidation of phosphorus and
may contain combustion products other than phosphoric acid. Furthermore, there
appears to be interspecies differences in the toxic effects of phosphoric acid inhalation
that makes the extrapolation of such data to humans problematic.
There is also uncertainty associated with the estimation of potential doses that may be
received and the extrapolation from animal data to humans.
Uncertainities exist in estimating the atmospheric phosphoric acid concentrations
because exhaust gas dilution rates will vary depending on distance from the tailpipe,
wind speeds and ventilation rates, different volume flow rates and velocities of the
exhaust gases as well as the speed and type of vehicle.
Adding to these uncertainties in the assessment of occupational risk in this report are:
? climatic conditions (which may affect the extent or otherwise of the use of
enclosed workplaces and dissipation of the the AVSR additive and phosphoric
acid)
? lack of ambient alkyl phosphate additive and phosphoric acid levels and
exhaust gas analyses on the alkyl phosphate additive and
? differences in local use patterns for AVSR additives.
14.3 Public health risk
14.3.1 Acute effects
Direct public exposure to the alkyl phosphate additive is likely to occur primarily via
the skin as a result of spills and splashes of LRP and aftermarket products. The alkyl
phosphate additive is not expected to be a skin or eye irritant at the concentrations
present in LRP. There is a low risk of acute systemic health effects in the general
public as a result of skin exposure to the alkyl phosphate additive.
Skin irritation is possible following exposure to aftermarket products containing the
alkyl phosphate additive, due in part to the presence of kerosene.
Acute health effects could occur as a result of accidental ingestion by a child.
Accidental ingestion might occur in young children if aftermarket products are stored in
or around the home. Children between one and a quarter and three and a half years of
age can swallow approximately 4.5 mL of liquid (Gosselin et al., 1976).
Given the RDA of phosphorus for infants 1 to 8 years of age is approximately 500 mg
(equivalent to 50 mg/kg bw for a 10 kg child), ingestion of half the contents of a 10 mL
69
Alkyl Phosphate AVSR Additive
single use aftermarket product corresponds to 23.5 mg/kg bw phosphorus for a 10 kg
child or approximately half of the phosphorus RDA (Section 9.7.1). This ingested alkyl
phosphate additive dose corresponds to 368 mg/kg bw for a 10 kg child compared with
the DMA-4 oral acute lethal dose (in rats) of 11 000-17 000 mg/kg bw.
The multi-treat product contains a less concentrated alkyl phosphate additive
formulation compared with the single use product and, therefore, the risk is lower.
Small ingested volumes of the alkyl phosphate additive may potentially occur in
children, but will not significantly add to the phosphorus body load nor represent a
significant acute health risk. Ingestion of the kerosene contained in the product,
however, may present an additional risk due to in advertent inhalation and the potential
lung damage that can occur with kerosene.
In general, public exposure to the alkyl phosphate additive is expected to be minimal
and of short duration. Consequently, the risk to the public from handling the alkyl
phosphate additive is assessed as low.
The public's inhalation exposure to phosphoric acid from tailpipe emissions is likely to
be lower than for occupational exposure. This is because of the rapid dissipation of
phosphoric acid from the tailpipe of moving vehicles (Dolan et. al., 1979).
14.3.2 Chronic effects
Total phosphorus exposures from the combination of all sources is unlikely to be
changed significantly by the use of the alkyl phosphate additive. This is because the
ingestion of food represents by far the greatest proportion of the total daily phosphorus
dose (Section 11.2).
Data in Table 4 shows that the use of the alkyl phosphate additive according to the
present use scenario of maintained LRP market share and the 2004 scenario of
diminished LRP market share will increase the phosphoric acid dose inhaled to levels
above assumed negligible ambient air concentrations.
Applying the NOAEL of 50 mg/m3 (50 x106 ng/m3), assuming 100% phosphoric acid in
the smoke and converting intermittent exposures (4 days/week, 2.25 hours per
24 hours/day) to continuous exposures, the following margins of exposure are
calculated:
For Present Use scenario, where current LRP market share is maintained:
Margin of Exposure = (50 x106 ng/m3 x 4/7 x 2.25/24)/100 ng/m3 = 26 786
For 2004 scenario, where the LRP market share declines:
Margin of Exposure = (50 x106 ng/m3 x 4/7 x 2.25/24)/40 ng/m3 = 66 964
These margins of exposure are considered satisfactory and the risk is considered low.
The US EPA have derived a chronic inhalation reference concentration (RfC) that is
based on bronchiolar fibrosis of the respiratory tract in rats for phosphoric acid of
10 礸/m3 (IRIS, 2003). In general, the RfC is an estimate of a daily inhalation exposure
of the human population (including sensitive subgroups) which is proposed as likely to
be without an appreciable risk of deleterious effects during a lifetime. The RfC value
assumes that thresholds exist for certain toxic effects such as cellular necrosis.
70 Priority Existing Chemical Assessment Report Number 25
The RfC determined by the US EPA uses uncertainty factors to account for intraspecies
and interspecies variability. It is extrapolated from subchronic to chronic exposure,
specific data on bronchiolar fibrosis in the tracheobronchial region in Sprague-Dawley
rats, estimates of the diameter of the hydrated aerosol particles at the site of the
pulmonary lesions and an average weight of the rats.
There is currently no Australian ambient air standard for phosphoric acid. Comparing
the estimated ambient air concentrations in Table 4 (up to 100 ng/m3) with the RfC
value set in the US (10 礸/m3), it is apparent that the estimated phosphoric acid air
concentrations for Scenarios 1 and 2 are much lower than the US EPA RfC value.
14.3.3 Uncertainties
Like uncertainties associated with occupational risk assessment, uncertainties involved
in the chronic public health risk assessment are derived in part from significant
database limitations. There is a general lack of public exposure data and Australian
baseline ambient air phosphoric acid data on which to base a realistic exposure
assessment.
71
Alkyl Phosphate AVSR Additive
15. Risk Management
This section discusses measures currently employed in the management of human and
environmental risks from exposure to the alkyl phosphate additive.
The key elements on the management of risks discussed in this section are:
? Workplace control measures
? Hazard communication and
? Regulatory controls.
15.1 Assessment of current control measures
According to the NOHSC National Model Regulations for the Control of Workplace
Hazardous Substances (NOHSC 1994a), exposure to hazardous substances should be
prevented or, when this is not practicable, adequately controlled, so as to minimise risks
to health and safety. The NOHSC National Code of Practice for the Control of
Workplace Hazardous Substances (NOHSC 1994b) provides further guidance in the
form of a hierarchy of control strategies, namely, elimination, substitution, isolation,
engineering controls, safe work practices and personal protective equipment (PPE).
15.1.1 Elimination and substitution
Elimination is the removal of a chemical from a process and should be the first option
considered when minimising risks to health. In situations where it is not feasible or
practical to eliminate the use of a chemical, substitution should be considered.
Substitution includes replacing the chemical with a less hazardous substance or the
same substance in a less hazardous form.
As indicated in Section 7.3.1, there is a declining market for LRP sales and hence
AVSR additives due to attrition from the Australian motor fleet of vehicles designed to
run on leaded petrol.
By 2004, bulk sales of LRP are expected to decline to less than 5% of total petrol sales
(Australian Petroleum Gazette, 1999). The general provision and sale of bulk LRP by
the oil companies will become uneconomical at some point. This will eliminate the
requirement for the addition by oil companies of the alkyl phosphate additive to fuel.
When bulk LRP is phased out, aftermarket addition of AVSR fuel additives will
become the only option for those motorists with vehicles designed to run on leaded
petrol. Given the likelihood that mechanical alteration of engine components to run on
ULP may be prohibitive for some vehicles, e.g. vintage vehicles, the total elimination
of AVSR additives from the Australian fuel market is unlikely and the use of the alkyl
phosphate additive as an aftermarket additive may continue indefinitely.
Several AVSR additives that are potential substitutes for the alkyl phosphate additive
are available on the Australian market (Section 1.1). Users will need to consider the
efficacy, cost, health, safety and environmental effects of each as alternatives to the
alkyl phosphate additive.
72 Priority Existing Chemical Assessment Report Number 25
15.1.2 Isolation and engineering controls
Isolation as a control measure aims to separate employees, as far as practicable, from
the chemical hazard. This can be achieved by distance, use of barriers or enclosure.
Engineering controls are plant or processes which minimise the generation and release
of hazardous substances. They include total or partial enclosure, local exhaust
ventilation and automation of processes.
Manufacturing plant
At the manufacturing plant, the alkyl phosphate manufacturing vessel is isolated in a
bunded building. Engineering controls include a fully enclosed manufacturing process
with the reaction vessel connected to a scrubber system that treats any vapours emitted
during the manufacturing process. The finished manufactured product is transferred
from the reaction vessel to a storage tank, ISO tanks or drums using manually
controlled enclosed and dedicated transfer lines. The reaction vessel is connected via a
bursting disc to a catch tank which would contain product in the unlikely event that
control of the reaction was lost.
Oil company terminals and depots
Oil company terminals use a number of different control measures when receiving the
bulk alkyl phosphate additive from the manufacturing plant and when blending bulk
LRP for distribution to service stations. These control measures generally rely on
closed transfer systems with the nature of the control measure dependent on the type of
container received from the manufacturing plant, e.g. ISO tanks or drum lots of the
alkyl phosphate additive.
Decanting of drummed alkyl phosphate additive at the oil terminals is carried out using
a sealed and dedicated transfer system into the bulk storage tank. While full drums of
the alkyl phosphate additive are stored undercover prior to decanting (in an approved
flammable drum storage area), the decanting occurs on an open air concrete bunded bay
with workers manually transferring a suction pipe from drum to drum during the
process. Drum decanting is limited to three times per year. On occasions when it is
necessary to discharge drums of the alkyl phosphate additive, a hand pump and a spear
into the underground tank is reported to be used.
For bulk LRP blending, the terminals use an automated closed in-line dosing system for
adding the alkyl phosphate additive to road tankers. The alkyl phosphate additive is
pumped directly from the bulk storage tank and injected into the unleaded petrol stream
as the LRP road tanker is loaded with fuel.
During pipeline maintenance, drainage into containers for return to storage tanks is
used at terminals to limit accidential release of the alkyl phosphate additive.
Once of the ISO tankers of the alkyl phosphate additive are received at the terminal,
discharge by gravity feed into a closed underground tank via a manually controlled,
closed delivery hose system is used.
No engineering controls are reported at some oil company depots, i.e. small terminals,
which use manual addition by workers of the alkyl phosphate additive to road tankers.
The manual addition (undertaken by workers wearing PPE) involves decanting the
alkyl phosphate additive into a receptacle prior to pouring it into the road tanker
compartment.
73
Alkyl Phosphate AVSR Additive
Petrol stations
All oil companies report that transportation of the alkyl phosphate additive-based LRP
to service stations is carried out using dedicated petroleum road tankers. Isolation and
engineering controls are achieved at petrol stations by using enclosed transfer hoses for
transferring LRP containing the alkyl phosphate additive from the road tankers and
storage in underground tanks.
With regards to USTs, there are currently no existing leak prevention or detection
requirements for operators of underground fuel storage tanks in all states to detect and
control leakages from UST facilities. UST leak detection systems are implemented on
a voluntary basis by industry, particularly by major petroleum suppliers
Aftermarket product use
Engineering controls for public and occupational users of aftermarket products
containing the alkyl phosphate additive consist presently of single use injection devices,
which completely empty when the contents are injected into the petrol tank and multi-
treat bottles, which have childproof screw caps and measuring chambers designed to
drain completely into the petrol tank. The viscous nature of alkyl phosphate additive
formulation contained in the single use aftermarket product lends itself to minimisation
of any leakage or dripping of the formulation when the device is handled.
15.1.3 Safe work practices
Safe work practices are administrative practices that require people to work in ways
that are safe.
Manufacturing plant
At the alkyl phosphate additive manufacturing plant, all work procedures relating to the
manufacture and handling of the alkyl phosphate additive are documented. This
documentation includes instructions regarding temperature and vacuum controls as well
as PPE requirements, categories of exposure to be avoided and saftey precautions to be
taken due to the properties of the chemicals handled.
Oil company terminals and depots
At oil company terminals and depots, all work procedures relating to the handling and
storage of the the alkyl phosphate additive are documented as are the PPE requirements
for handling of the fuel additive. Procedures for maintenance and calibration of oil
terminal in-line dosing systems are reported. Terminals have written procedures for
decanting drums and transferring product containing the alkyl phosphate additive.
Areas are designated for this task and operators trained in the correct handling
procedures for the product and task, with full access to the Material Safety Data Sheet
(MSDS).
15.1.4 Personal protective equipment
Where other measures are not practicable or adequate to control exposure, personal
protective equipment (PPE) should be used. The PPE requirements recommended by
the manufacturers for the handling the alkyl phosphate additive are based on avoidance
of the potential irritant effect of the kerosene-based product and hence the prevention of
skin and eye contact.
74 Priority Existing Chemical Assessment Report Number 25
Manufacture
Specific safety requirements are provided to operators via the safety instructions on the
manufacturing batch sheet. During the manufacture of the alkyl phosphate additive,
operators wear protective overalls, impermeable gloves, safety footwear and safety
glasses at all times. In addition, the wearing of a face shield, a protective apron and
respiratory protection such as a particle filter respirator is recommended during the
handling of components during the manufacturing process. During analysis of the alkyl
phosphate additive samples for quality control tests, the analyst wears protective
clothing including a lab coat, safety footwear, and safety gloves and glasses.
Oil company terminals and depots
The practice at oil company terminals is to use gloves, protective clothing and safety
shoes and glasses during the discharge of the ISO tankers and the decanting of the
drums containing the alkyl phosphate additive. Similar PPE is also worn during in-line
dosing of the road tanker with the alkyl phosphate additive and during maintenance of
equipment used in the various processes.
Typically, protective clothing such as PVC gloves, safety glasses, wrist to ankle
clothing and safety boots are worn by the terminal workers during drum decanting.
Depots where the alkyl phosphate additive is added manually to the road tanker,
recommend that an organic vapour cartridge respirator be worn along with rubber
gloves and safety goggles.
Petrol stations and maintenance workshops
At petrol stations during the unloading of road tankers and the dipping of underground
tanks, workers typically wear protective clothing, footwear and gloves. Auto
mechanics with potential exposure to the alkyl phosphate additive in fuel also wear
protective clothing and footwear.
15.2 Hazard communication
15.2.1 Labels
Labels for two aftermarket alkyl phosphate additive products and one label for alkyl
phosphate additive used in bulk LRP blending were available for assessment.
Labels submitted for assessment were assessed for requirements under the NOHSC
National Code of Practice for the Labelling of Workplace Substances (NOHSC,
1994c). The assessment took the form of a qualitative appraisal of the following
categories of information:
Substance identification;
? hazard category/Signal word
? ADG Code classification/packaging group
? details of manufacturer or supplier
? risk information (or phrase)
? safety information (or phrase)
75
Alkyl Phosphate AVSR Additive
? information on spills, leaks or fires and
? reference to MSDS.
There are insufficient toxicity data for the alkyl phosphate additive to be classified in
accordance with the NOHSC Approved Criteria for Classifying Hazardous Substances
(NOHSC 1999a). The limited data for the alkyl phosphate additive products suggest
the alkyl phosphate additive has a low acute oral and dermal toxicity and may cause
dermal irritation.
Kerosene is a major ingredient of the Valvemaster products (Section 4) and is
classified as a hazardous substance (NOHSC 1999a). Given the kerosene content of the
alkyl phosphate additive products, the labels should contain the following hazard
classification, risk and safety phrases with regard to the NOHSC Approved Criteria for
Classifying Hazardous Substances (NOHSC 1999a):
Products containing kerosene 10% should be classified as Xn (Harmful) with the risk
phrase R65: Harmful: May cause lung damage if swallowed. The most appropriate
safety phrases are S2: Keep out of reach of children, S23: Do not breathe vapour, S24:
Avoid contact with skin and S62: If swallowed, do not induce vomiting; seek medical
advice immediately and show this container or label.
An additional classification for kerosene is Xi (Irritant) with the risk phrase R38:
Irritating to skin, in products where the kerosene content is 20%. This additional
classification for kerosene (unspecified nature) is sourced from the Australian Institute
of Petroleum AIP (NOHSC 1999a).
Solvent naptha at concentrations greater than or equal to 10% is classified as Xn
(Harmful) with the risk phrase R65: Harmful: May cause lung damage if swallowed.
The most appropriate safety phrases are S2: Keep out of reach of children, S23: Do not
breathe vapour, S24: Avoid contact with skin and S62: If swallowed, do not induce
vomiting; seek medical advice immediately and show this container or label (NOHSC
1999a).
Bulk alkyl phosphate additive
One label for the alkyl phosphate additive formulation (Valvemaster Concentrate)
used in bulk LRP blending was available for assessment.
The label contained identification information and the signal words and risk phrases
"Hazardous", "Harmful: may cause lung damage if swallowed", and "irritating to eyes,
respiratory tract and skin". The label contained appropriate signal words and safety
phrases, first aid and emergency procedures and included details of the Australian
manufacturer and references to the MSDS.
Aftermarket products
In the case of labelling of hazardous substances of 500 mL capacity or less and where
space on the containers is especially limited, the NOHSC Labelling Code describes the
required minimum information as:
? signal words
? product name and
? details of manufacturer or importer.
76 Priority Existing Chemical Assessment Report Number 25
Products sold to the public should meet the requirements of the Standard for the
Uniform Scheduling of Drugs and Poisons (SUSDP, 2002) which describe labelling
and packaging requirements.
10 mL aftermarket products
The 10 mL aftermarket consumer product does not need to meet the requirements of the
SUSDP (SUSDP, 2002). This is because the formulation's container has a nominal
capacity less than 15 mL (SUSDP, 2002).
The 10 mL label contains the product name and appropriate signal words, e.g.
`harmful', `irritating' and discloses the exact kerosene and phosphate additive content
(volume/volume concentration) of the product. The label contains details of the
overseas packaging company (but not the local distibutor), and describes the
recommended use and the directions for use, with advice to refer to the brochure for
full instructions.
The label contains the safety phrases S2: Keep out of reach of children, S23: Do not
breathe vapour and S24: Avoid contact with skin, but not S62: If swallowed, The label
notes the product may be harmful if swallowed and includes the phrase "Caution".
250mL aftermarket product
The 250 mL label contains the product name and the appropriate signal words, harmful
and irritating, details of the local distributor, and disclosure of the exact kerosene
content of the product but not the concentration (nor concentration range) of the alkyl
phosphate additive. The label identifies the product's recommended use and gives
directions for use. The label contains the safety phrase S2: Keep out of reach of
children, and the phrase "Caution".
The 250 mL aftermarket product contains the safety phrase S62: If swallowed, do not
induce vomiting; seek medical advice immediately and show this container or label.
The label includes advice that the product is "irritating to skin", "harmful, may cause
lung damage if swallowed". First aid advice is grouped together and prefaced by the
words "FIRST AID" and the contact number of the Poisons Information Centre is
included. The 250 mL plastic container is embossed with the word "POISON".
15.2.2 MSDS
Material Safety Data Sheets (MSDSs) are the primary source of information for
workers involved in the handling of chemicals. Under the NOHSC National Model
Regulations for the Control of Workplace Hazardous Substances (NOHSC 1994a) and
the corresponding state and territory legislation, suppliers of a hazardous chemical for
use at work are obliged to provide a current MSDS to their customers and employers
must ensure that an MSDS is readily accessible to those employees with potential for
exposure to the chemical.
A total of two MSDSs, one for the alkyl phosphate additive formulation used in bulk
LRP blending and the single-use aftermarket product, and one for the multi-treat
aftermarket product, were available for assessment against the NOHSC National Code
of Practice for the Preparation of Material Safety Data Sheets (NOHSC 1994e). The
results of the MSDS assessment are presented in Appendix 3.
77
Alkyl Phosphate AVSR Additive
In general, the MSDSs comply well with the NOHSC National Code of Practice for the
Preparation of Material Safety Data Sheets (NOHSC 1994e). The Valvemaster
Concentrate MSDS, however, did not identify the recommended use.
The MSDS for the multi-treat aftermarket product Valvemaster VM11 assigns a
Class 9 Dangerous Good classification (UN Number 3082 Environmentally Hazardous
Substance, Liquid, NOS) with regards the ADG Code (FORS, 1998). This is consistent
with the inclusion of Solvent Naptha in the formulation.
Although an assessment of the toxicology of kerosene and solvent naptha have not been
undertaken in this assessment report, the inclusion of such information in the MSDS is
regarded as pertinent.
15.2.3 Education and training
Guidelines for the induction and training of workers exposed to hazardous substances
are provided in the NOHSC National Model Regulations for the Control of Workplace
Hazardous Substances (NOHSC 1994a). Under these regulations, employers are
obliged to provide training and education to workers handling hazardous substances.
These regulations stipulate that training and induction should be appropriate for the
workers concerned.
Oil company terminals and depots that use the alkyl phosphate additive specify
procedures for handling the fuel additive including PPE requirements.
15.3 Occupational monitoring and regulatory controls
15.3.1 Atmospheric monitoring
Under the NOHSC Model Regulations (NOHSC, 1994a), employers are required to
carry out an assessment of the workplace for all hazardous substances. The NOHSC
Guidance Note for the Assessment of Health Risks Arising from the Use of Hazardous
Substances in the Workplace (NOHSC, 1994d) provides the methodology for this
assessment. When the assessment indicates that the risk of exposure via inhalation is
significant, atmospheric monitoring should be conducted to measure levels of the
hazardous substances in the workplace before the implementing of suitable control
measures to reduce exposure. Subsequent monitoring is also required to ensure that
such measures are effective.
No atmospheric monitoring programs for the alkyl phosphate additive in workplaces
have been identified and none is considered necessary.
15.3.2 Occupational exposure standards
While Australia as well as other countries have not set occupational exposure standards
for the alkyl phosphate additive, it has set occupational exposure limits for phosphoric
acid.
According to the NOHSC Exposure Standards for Atmospheric Contaminants in the
Occupational Environment, the current Australian national occupational exposure
standard for phosphoric acid is 1 mg/m3, expressed as an 8-hr time-weighted average
(TWA) airborne concentration (NOHSC, 1995). In Australia, the short-term exposure
limit (STEL) for phosphoric acid is 3 mg/m3. The Australian occupational exposure
limits for phosphoric acid are comparable to those set by the majority of overseas
78 Priority Existing Chemical Assessment Report Number 25
countries (ACGIH, 2000). Some countries, however, have set an 8-hr TWA but not a
STEL value or vise versa (ACGIH, 2000). Both Ireland and the Netherlands have set a
STEL value of 2 mg/m3 (ACGIH, 2000).
NIOSH cite a revised Immediately Dangerous to Life or Health (IDLH) concentration
for phosphoric acid of 1000 mg/m3 based on acute oral toxicity data in animals
(NIOSH, 1996). This IDHL concentration for phosphoric acid is cited by NIOSH as a
conservative value due to the lack of relevant acute toxicity data for workers.
According to the NOHSC Exposure Standards (NOHSC, 1995) a process is not
considered to be under reasonable control if short-term exposures exceed three times
the TWA exposure standard for more than 30 minutes per 8 h working day, or if a
single short-term value exceeds five times the TWA exposure standard.
15.3.3 Health surveillance
In accordance with NOHSC Model Regulations (NOHSC, 1994a), employers have a
responsibility to provide health surveillance in those workplaces where the workplace
assessment indicates that exposure to a hazardous substance may lead to an identifiable
substance-related disease or adverse health effect. The alkyl phosphate additive is not
listed in Schedule 3 (list of substances requiring health surveillance) and as such there
are no formal requirements for health surveillance programs for exposed workers.
No personal air monitoring or health surveillance programs for the alkyl phosphate
additive have been reported in Australia.
15.3.4 National transportation regulation
The alkyl phosphate additive is not listed in the Australian Code for the Transport of
Dangerous Goods by Road and Rail (ADG) Code, however Valvemaster and
Valvemaster VM11 meet the criteria for C1 combustible liquids (Section 12.2).
It is noted with respect to the ADG Code Section 2.1.10 (FORS 1988) sub-clause (1)
that combustible liquids are taken to be dangerous goods of Class 3 if:
(a) the combustible liquids are transported in a bulk container or a tank
which is part of a vehicle; and
(b) the combustible liquids are transported on the same vehicle with:
(i) dangerous goods of Class 3 in bulk; or
(ii) packaged dangerous goods of Class 3 in an aggregate quantity of
more than 1000 L.
Sub-clause (2) of the ADG Code Section 2.1.10 (FORS 1988) does not apply to the
transport of combustible liquids and dangerous goods of Class 3 on a rail wagon if the
combustible liquids and the dangerous goods are in different bulk or freight containers
which are separated by at least 12 metres. .
The National Standard for the Storage and Handling of Workplace Dangerous Goods
(NOHSC, 2001) and National Code of Practice for the Storage and Handling of
79
Alkyl Phosphate AVSR Additive
Dangerous Goods (NOHSC, 2001b) complement the National Model Regulations for
the Control of Workplace Hazardous Substances (NOHSC 1994a).
The National Standard for the Storage and Handling of Workplace Dangerous Goods
sets out requirements to ensure the effective control of the storage and handling of
dangerous goods in order to protect the safety and health of workers and the public and
to protect property and the environment (NOHSC 2001a). The accompanying National
Code of Practice for the Storage and Handling of Dangerous Goods (National Code)
provides practical advice on compliance for those who have duties under the National
Standard. In addition, the National Code provides information and guidance for storage
and handling of dangerous goods as minor quantities and as consumer packages
supplied by retailers.
The National Standard and National Code for the storage and handling of dangerous
goods apply only to hazardous substances in the workplace that meet the classification
requirements for dangerous goods. Where dangerous goods are stored or handled in
private residences or other premises which are not workplaces, the National Standard
and National Code may provide useful guidelines for ensuring health and safety.
The National Standard for the Storage and Handling of Workplace Dangerous Goods
specifies the trigger levels (based on the quantities in Schedule 1) for the following
requirements for C1 combustible liquids:
? Placarding Placard Level - Schedule 1
? Develop a manifest and
site plan for the premises Manifest Level - Schedule 1
? Develop of an Emergency Plan Manifest Level - Schedule 1
? Notify the Appropriate Authority Manifest Level - Schedule 1
For C1 combustible liquids, a placard as specified in Schedule 2 of the National
Standard is required for C1 combustible liquid in quantities exceeding 10 000 L in bulk
containers, 50 000 L in packages, and 50 000 L combined bulk and packaged (provided
the quantity of C1 combustible liquids in bulk does not exceed 10 000 L). Similarly, an
occupier of a premise must ensure that the above requirements triggered at the Manifest
Level of Schedule 1 are complied with in instances where the total quantity of a C1
combustible liquid exceeds 100 000 L bulk or packaged.
15.3.5 Control of major hazard facilities
According to the NOHSC National Standard for the Control of Major Hazard
Facilities (NOHSC, 1996), the alkyl phosphate additive is not one of the specifically
identified chemicals that must be considered when determining whether a site is a
major hazard facility.
15.4 Public health regulatory controls
The alkyl phosphate additive is not currently included in a Schedule of the Standard for
the Uniform Scheduling of Drugs and Poisons (SUSDP, 2002).
15.5 Environmental regulatory controls
This section provides information on the environmental regulatory controls governing
Valvemaster and phosphorus compounds in Australia with reference to international
80 Priority Existing Chemical Assessment Report Number 25
control initiatives. In brief, the management of environmental pollution and waste in
Australia is regulated through individual state and territory regulatory systems rather
than at a national level. All states and territories have general environment protection
legislation pertaining to pollution and contaminated land.
However, there are currently no existing leak prevention or leak detection requirements
for operators of underground fuel storage tanks in NSW, and probably other states and
territories, to detect and control leakages from UST facilities. Leakages from USTs
have historically resulted in contamination of the environment. In Australia, UST leak
detection systems are implemented on a voluntary basis by industry, particularly by
major petroleum suppliers.
15.5.1 Air quality management
Australia
Emissions of `air toxics' (defined below) in Australia are regulated through individual
state and territory regulatory systems rather than at a national level. Each state and
territory has established legislative frameworks and strategies for monitoring and
managing air quality. National strategies are or have been developed to allow
consistent management of ambient air quality throughout Australia (refer below).
Air toxics are gaseous, aerosol or particulate pollutants that are present in the air in low
concentrations. Characteristics such as toxicity or persistence make them hazardous to
human, plant or animal life. The terms `air toxics' and `hazardous air pollutants'
(HAPs) are used interchangeably. Air toxics include volatile and semi-volatile organic
compounds, polycyclic aromatic hydrocarbons, metals and aldehydes (NEPC, 2002).
Specific emission limitations and maximum ground level concentrations for individual
sources are used in some states to control emissions from industrial sources (NEPC,
2002).
Emissions of air toxics from new motor vehicles are controlled through Australian
Design Rules that set emission standards for a range of pollutants. These are set at a
national level rather than state or territory level. Recently the Australian Government
introduced National fuel quality standards that will reduce the level of some air toxics
in ambient air. Currently, no AVSR is listed in the register of prohibited fuel additives.
At a national level, at least two National Environment Protection Measures (NEPMs)
apply to air quality including the National Pollutant Inventory (NPI) NEPM (NEPC,
1998a) and the Ambient Air Quality NEPM (NEPC, 1998b). An additional NEPM
(Ambient Air Toxics) is also being developed (NEPC, 2002). The Ambient Air Quality
National Environment Protection Measure (NEPM) (NEPC, 1998b) sets national
standards for six air pollutants. Phosphorus compounds are not specifically included in
either of the two Ambient Air Toxics NEPMs being developed (refer NEPC, 2002) or
the Ambient Air Quality NEPM (NEPC, 1998b).
An inventory of emissions of phosphoric acid from facilities with significant emission
are included in the National Pollutant Inventory (NPI) NEPM (NEPC, 1998a). NPI
data are obtained from registered facilities. In 2000-2001, reportable emissions of
phosphoric acid into air were derived from three industry sources in Australia, with a
total emission of 3.7 tonnes to air (NPI, 2001). Use of Valvemaster in LRP (Scenario
1) is estimated to result in the emission of approximately 182 tonnes per annum of
phosphoric acid (57.6 tonnes of phosphorus per annum) Australia wide and 36.4 tonnes
phosphoric acid for the Sydney region, but to decline over time as demand for LRP
81
Alkyl Phosphate AVSR Additive
declines. The decline in emissions of phosphoric acid from vehicles reliant on LRP to
2004 (Scenario 2) is estimated to be 60%.
International air quality management
Several international organisations have introduced regulations or policies that aim to
limit the exposure of the general public to air toxics. The Organisation for Economic
Cooperation and Development (OECD, 1999) has implemented the Advanced Air
Quality Indicators and Reporting Project in OECD member countries, including
Australia. The project focuses on six major urban air pollutants. Phosphorus
compounds are not among them (Environment Australia, 2001).
In the United States, air quality is managed and regulated under the Clean Air Act
(CAA) 1970. The National Air Toxics Program: The Integrated Urban Air Strategy
(US EPA 1999) outlines the US EPA's plan for addressing cumulative health risks from
189 identified HAPs, including phosphorus compounds, in urban areas of the United
States. Phosphorus compounds in air are not of such concern in the United States as to
be listed as one of the 33 priority urban air toxics (Environment Australia, 2001).
In Canada, a range of air toxics is measured and analysed within the National Air
Pollution Surveillance (NAPS) Network, which was established in 1969 to monitor and
assess the quality of ambient air in Canadian urban areas. Canada does not identify
phosphorus compounds as priority air pollutants (Environment Australia, 2001).
Air quality in the United Kingdom (UK) is managed by the Department of
Environment, Transport and Regions (UK DETR). The UK also does not identify
phosphorus compounds in air as priority air pollutants (Environment Australia, 2001).
In 1994, the New Zealand (NZ) Ministry for the Environment published Ambient Air
Quality Guidelines. Guideline values were established for 8 common air pollutants.
Phosphorus compounds are not considered a priority air pollutants in New Zealand
(NZME, 1994).
15.5.2 Aquatic ecosystem management
Shipping safety and pollution from ships is managed at a national level by the
Australian Maritime Safety Authority (AMSA). Australia is a member of the
International Maritime Organisation (IMO) and is a signatory to the International
Convention for the Prevention of Pollution from Ships 1973/78 (MARPOL 73/78;
Commonwealth of Australia, 1988). This convention controls operational pollution and
introduces measures to mitigate the effects of marine pollution.
The Commonwealth Department of Transport and Regional Services manages chemical
transportation in Australia at a national level. The Australian Code for the Transport of
Dangerous Goods by Road and Rail and its supplements (ADG code) (FORS, 1998) is
designed to apply to all surface land transport in Australia.
Significant facility discharges of phosphoric acid to the Australian aquatic environment
are monitored by a National Pollutant Inventory (NEPC, 1998a), with one registered
facility discharging approximately 16 tonnes per annum to water.
The Australian water quality guidelines (ANZECC and ARMCANZ, 2000), established
under the National Water Quality Management Strategy, provide assessment guidance
and water and sediment quality assessment values for freshwater and marine
ecosystems throughout Australian states and territories.
82 Priority Existing Chemical Assessment Report Number 25
There has been considerable investment in the development and implementation of
catchment based nutrient reduction strategies across Australia in response to algal
management issues (CRCFE, 2000). These strategies involve national, state and
territory and local governments, environment protection agencies, catchment
management committees, industry and the community. Examples at the national level
include the National Water Quality Management Strategy, the Urban Stormwater
Initiative (USI), which aims to enhance water quality in the waterways of major coastal
cities by improving stormwater management, and the Cleaning Our Waterways
Industry Partnership Program (COWIPP), which encourages local government and
industry to enhance long-term economic performance with cleaner production
techniques that benefit the natural environment.
The NSW Algal Management Strategy has been established to address the immediate
management of bloom effects, short- to medium-term management measures (such as
biological control methods), and management of bloom causes (such as nutrient control
strategies and waterway management). Responses to the occurrence of blooms are
coordinated through regional algal coordinating committees. Each committee has
prepared an algal contingency plan. Algal bloom management is also being improved
by better environmental flows in rivers throughout NSW. In addition, the NSW Marine
Algal Biotoxin Group has been established. Sydney Water Corporation and Sydney
Catchment Authority each have nutrient pollution reduction programs underway or
planned. Similar nutrient reduction programs operate in other states and territories in
Australia through government and non-government stakeholders.
As indicated above, algal blooms can be a surrogate indicator of eutrophication or high
nutrient load. High nutrient concentrations in fresh waters in NSW have been linked to
algal blooms and poor water quality (ANZECC and ARMCANZ, 2000). Conversely,
ANZECC and ARMCANZ (2000) provide guidance levels for total phosphorus and
other nutrients throughout Australia, with the intention of providing preliminary water
quality assessment values for assessing risks of eutrophication and algal blooms.
Quantifying relationships of nutrient load, availability and algal growth is complex and
has rarely been achieved in Australia (Harris, 1994; CRCFE, 2000). This is a key data
gap for algal management strategies (CRCFE, 2000). Factors affecting the survival and
growth of algae do not only include phosphorus concentration, but also nutrient sources
(internal and external), transformation and bioavailability of nutrients for uptake by
algae, influences of light, temperature and mixing conditions, and processes such as
grazing by herbivores. The modelling of any or all of these components is complex,
even for a single species or in a single reservoir, and the availability of acceptable data
will be critical to the assessment (CRCFE, 2000).
15.5.3 Disposal and waste treatment
Each Australian state and territory provides statutory controls on waste generation and
management. In general, non-recyclable materials should be sent to licenced waste
disposal contractors in accordance with state and territory requirements. Care should
be exercised in disposing of contaminated wastes to avoid pollution of the environment.
15.5.4 Emergency procedures
The availability of an emergency response plan to deal with unexpected releases of the
aklyl phosphate additive products, such as large spills, is good practice. All employees
should be trained in accident and emergency procedures. All emergency plans and
83
Alkyl Phosphate AVSR Additive
procedures should be documented fully and made available to all workers. Local
emergency services should be consulted on the appropriateness of the emergency
procedures developed.
Emergency and first aid measures in place at oil company terminals are generally
comprehensive. They include access to safety showers and eye wash stations, staff
trained in first-aid and access to a trained emergency response team. Companies do not
have emergency plans specific to the alkyl phosphate additive products.
Fire and spill responses for products containing the alkyl phosphate additive are
included in MSDSs and are as follows:
Spills
For spills and leaks, wear suitable protective clothing, gloves and eye/face
protection. Shut off all ignition sources. Absorb spillage with suitable inert
material. Ventilate the area and the wash spill site after material pick-up is
complete. Do not allow the spill to enter public sewers and watercourses.
Disposal of the spilled material should be in accordance with local, state,
territory or national legislation.
Fire response
Wear a chemical protection suit and a positive-pressure breathing apparatus.
Use water, alcohol resistant foam, carbon dioxide or a dry agent to extinguish
the fire. Do not use water jets. In the advent of an adjacent fire, cool the
containers containing the alkyl phosphate additive with water spray.
84 Priority Existing Chemical Assessment Report Number 25
16. Discussion and Conclusions
Alkyl phosphate additive is used in Australia in lead replacement petrol (LRP) as an
anti-valve seat recession (AVSR) additive. As no data is available for the alkyl
phosophate chemical because it is manufactured in situ into a kerosene product, the
report relates to two alkyl phosphate AVSR additive formulations currently available
on the Australian market.
AVSR fuel additives are added to petrol to prevent excessive valve seat wear and
consequent recession of automotive engine valves into the engine head. Until its phase
out in lead petrol, tetraethyl lead was the most commonly used AVSR additive in
Australia.
There are currently four types of AVSR additives marketed in Australia.
Methylcyclopentadienyl manganese tricarbonyl (MMT)-, phosphorus- and sodium-
based AVSR additives are presently being assessed by NICNAS as Priority Existing
Chemicals. A potassium-based AVSR additive has been assessed by NICNAS as a
New Chemical. These four AVSR fuel additives are either pre-blended into bulk LRP
supplies by oil companies for distribution to service stations or sold as aftermarket
products for addition by consumers to unleaded petrol (ULP).
The exposure and risk assessments for the different types of AVSR additive assessed as
Priority Existing Chemicals assume a 100% LRP market share for the individual AVSR
additive. This is because of the commercial-in-confidence nature of the information
provided by companies on the market share for the individual AVSR additives.
Moreover, the risk assessments were conducted under two separate scenarios based on
generic AVSR additive use patterns. This is because the use of AVSR additives is
governed by a declining population of older vehicles requiring these fuel additives.
The first scenario (`present use') assumes a continuation of the current LRP market of
2500 ML per year with 90% of the AVSR additive delivered as bulk LRP by oil
companies and 10% as aftermarket products for consumer applications. The second
scenario (`2004') assumes a decline of the LRP market to 1000 ML with the AVSR
additive delivered completely as an aftermarket product for consumer applications.
These two use scenarios are based on motor vehicle statistics and forecasts from the
Australia Bureau of Statistics and the Australian Institute of Petroleum. The
occupational health and safety, public health and environmental consequences of these
volumes and modes of delivery of AVSR additives are considered in this assessment
report accordingly.
Bulk alkyl phosphate additive (Valvemaster Concentrate) which contains 5.1%
phosphorus is manufactured in Australia for the domestic and export market while the
alkyl phosphate 10 mL single-use (containing 5.1% phosphorus) and 250 mL multi-
treat (containing 2.5% phosphorus) Valvemaster aftermarket products are imported.
The `present use' and `2004-use' scenarios equate to approximately 1150 and
460 tonnes of Valvemaster Concentrate per annum, respectively. These estimates are
based on the typical treatment rate as recommended by the manufacturers for the alkyl
phosphate additive in LRP of 600 mg/kg or 30 mg phosphorus per kg fuel.
85
Alkyl Phosphate AVSR Additive
16.1 Health hazards
Health hazards addressed in this report relate not only to those associated with the alkyl
phosphate products but also with phosphoric acid, the postulated combustion by-
product.
16.1.1 Alkyl phosphate additive
The scope of the alkyl phosphate additive assessment of toxicity in this report is limited
to that of the kerosene-based product DMA-4 (which is synonymous with
Valvemaster Concentrate).
Animal (mammalian and avian) toxicity studies of DMA-4 indicate the alkyl phosphate
additive is not acutely toxic by oral or dermal exposure, although it has some possible
irritant effects. The inclusion of kerosene in DMA-4 can not be discounted as a
contributing factor to the irritancy effects observed in the animal studies. No repeated
dose DMA-4 toxicity data are available. While there are no toxicokinetic data available
for the alkyl phosphate additive, exposure has the potential to add to the total body
phosphate/phosphorus load.
There are no published case reports, epidemiology or other studies addressing the
human health effects of the alkyl phosphate additive or its proprietary products, e.g.
DMA-4. There is insufficient toxicology data for classification of the alkyl phosphate
additive products in accordance with the NOHSC Approved Criteria for Classifying
Hazardous Substances (NOHSC, 1999a).
16.1.2 Phosphoric acid
The critical effects from exposure to phosphoric acid relate to its acidic nature and
hence corrosive and irritancy effects. The severity of the symptoms for eye, skin or
pulmonary irritation depends, however, on the concentration and length of exposure to
the acid.
Based on limited animal (mammalian) data, phosphoric acid has low acute oral, dermal
and inhalation toxicity. Phosphoric acid does not appear to have been well studied with
respect to repeated dose toxicity in animals or humans. There are no adequate
reproductive toxicity investigations of phosphoric acid in humans or animals. No
information is available on the teratogenicity, neurotoxicity, sensitisation or
immunotoxicity of phosphoric acid, nor is there any reliable information on the
carcinogenicity potential of phosphoric acid in animals or humans.
The phosphate anion, PO43-, which is an ionic form of phosphoric acid, is an essential
component of the normal body and skeleton of practically all life forms and is a natural
component of diet. At low doses, inorganic phosphate is incorporated into the body's
homeostatic mechanisms which maintain the phosphate balance in the body. Assuming
an adequate calcium intake, 4.2 g of phosphorus or 12.9 g of phosphate (PO43-) equates
to the World Health Organization (WHO) calculation of a maximum tolerable daily
intake of phosphorus of 70 mg/kg bw for a person weighing 60 kg.
The most relevant route of phosphoric acid exposure due to the use of the alkyl
phosphate additive in LRP is inhalation. There is limited human inhalation exposure
data for phosphoric acid. No reports have been found in the literature of systemic
poisoning following repeated inhalation exposure to phosphoric acid. Weakness, dry
cough, chest pain and shortness of breath or dyspnea is reported following an accidental
86 Priority Existing Chemical Assessment Report Number 25
occupational inhalation exposure to high (unspecified) concentrations of phosphoric
acid vapour. Reports of occupational exposure to phosphoric acid are typically
complicated by exposure to other chemicals within the workplace.
All available animal (mammalian) inhalation studies relating to phosphoric acid are
based on studies which generate smokes based on phosphorus pentoxide. The smokes
typically generated in these animal inhalation studies are complex, with the use of
phosphorus pentoxide possibly overestimating the inhalation hazard of phosphoric acid
due to its strong dehydrating potential in the lungs.
A concentration-dependent bronchiolar fibrosis is reported from two parallel 13-week
inhalation studies in rats using an aerosol containing up to approximately 80%
phosphoric acids generated from burning 95% red phosphorus and 5% butyl rubber
report. The study reports a NOAEL of 50mg/m3 and LOAEL of 180mg/m3 for the
smoke.
16.2 Environmental hazards and risks
Use of the alkyl phosphate in internal combustion engines and subsequent degradation
through combustion indicate that aquatic and terrestrial organisms are unlikely to be
exposed to the active component (the alkyl phosphate additive) or proposed exhaust
emission, phosphoric acid, at or above levels of concern. A low environmental risk is,
therefore, predicted.
The alkyl phosphate formulation DMA-4 (synonymous with Valvemaster
Concentrate) has a median lethal toxicity (LC50) to fish of 230 mg/L. Based on this
limited data, the alkyl phosphate formulation DMA-4 (synonymous with
Valvemaster Concentrate) has low acute aquatic toxicity. Spill incidents and leaks to
water bodies and land should be managed through existing federal, state and territory
legislative frameworks and protocols to mitigate adverse effects to the environment.
Such accidental incidents may potentially occur during shipment into Australia, bulk
transport, handling and storage.
No toxicity data were available on the effects of DMA-4 nor the alkyl phosphate
additive chemical on plants. Whilst there are no biodegradation studies of the alkyl
phosphate additive, it is not expected to be highly mobile in landfills and is expected to
degrade to inorganic phosphate and aliphatic carbon chains which are further degraded
by bacteria.
Phosphorus, which is found in the alkyl phosphate additive products, is naturally
occurring and ubiquitous in the environment. It is an essential nutrient for plants and
animals. Phosphorus pollution, leading to eutrophication and nuisance algal blooms in
aquatic ecosystems, is a major environmental issue in Australia and in general,
phosphorus reduction in waterways is the current Australian policy. Cumulative effects
from an additional anthropogenic source of phosphorus together with existing natural
and anthropogenic catchment sources in the Australian environment increases the risk
to the aquatic environment of eutrophication and nuisance algal blooms. Nevertheless,
the predicted incremental increase in phosphorus in the environment from use of fuels
containing the phosphorus-based AVSR additive is unlikely to develop to levels of
concern to aquatic environments given the current use and declining future use pattern.
There is the potential for leakage from USTs to occur. Such leakages represent
localised, point source discharge. Although a large number of USTs in Australia have
been replaced or have had leak detection systems or other measures installed in recent
87
Alkyl Phosphate AVSR Additive
years due to increased awareness of environmental pollution from these sources, many
USTs do not have leak detection systems. Although there is potential for risk to the
environment from leakage of fuel (which may or may not contain the alkyl phosphate
additive) from USTs, the risk would be site specific.
The findings of this assessment have not identified any significant risk to the
environment given the current use pattern of fuels containing the alkyl phosphate
AVSR additive.
16.3 Occupational health and safety risks
Manufacture of the alkyl phosphate additive products and blending of bulk LRP are
typically enclosed processess and, therefore, exposure is expected to be low. Exposure
to the the alkyl phosphate additive is possible during handling of LRP, alkyl phosphate
additive aftermarket products and automotive fuel system components. This is
expected to be infrequent, minor and of short duration. Mild irritation is possible on
contact with fuels or fuel additives containing the alkyl phosphate additive but given
the significant dilution of the AVSR additive with petroleum distillates, irritation is
likely due to the irritant properties of the petroleum distillates more than the the alkyl
phosphate additive itself. Overall, the risks to workers posed by the alkyl phosphate
additive during manufacture and during handling of LRP, aftermarket alkyl phosphate
additive products and automotive fuel system components contaminated with the alkyl
phosphate additive is low. The current identified controls for occupational health and
safety are considered to be adequate for the hazard and risk profile for the alkyl
phosphate additive.
Exposure to phosphoric acid via inhalation may occur in occupations associated with
vehicles using LRP, e.g. service stations, car parks and workshops, and particularly in
work spaces which are enclosed or poorly ventilated. A worst-case scenario was
considered for phosphoric acid exposure of such workers. Using an estimated tailpipe
phosphoric acid emission concentration of 8.3 mg/m3 for a worker within 2 m of the
vehicle tailpipe and an exhaust gas dilution rate of 100, a Margin of Exposure of 135
was derived. This is considered a sufficient Margin of Exposure particulary given that
the conservative nature of the estimate assumes the alkyl phosphate additive has 100%
of the AVSR additive market. Therefore, the occupational health risks associated with
phosphoric acid exposure from the alkyl phosphate additive's combustion are assessed
as low.
The inclusion of kerosene and solvent naptha in the alkyl phosphate additive
formulations presents health hazards such as irritancy and lung damage (if swallowed).
Two MSDSs and three labels for the alkyl phosphate additive products were assessed
qualitatively against the NOHSC MSDS and Labelling Codes. In general, the MSDSs
and labels adequately reflected the required information, and relevant hazard warnings,
risks and safety phrases. The Valvemaster Concentrate MSDS did not identify the
recommended use.
16.4 Public health risks
Direct public exposure to the alkyl phosphate additive is likely to occur primarily via
the dermal route as a result of spills and splashes of LRP and aftermarket products.
88 Priority Existing Chemical Assessment Report Number 25
In LRP, the alkyl phosphate additive is not expected to be a skin irritant at present
concentrations. The risk of acute health effects for the general public as a result of
dermal exposure to the alkyl phosphate additive in LRP is considered low given the
likely small quantities of such spills and the low acute dermal toxicity for DMA-4.
While dermal exposure to the aftermarket product may potentially cause irritation, such
an effect is confounded by the presence of kerosene which is a known irritant. Overall,
the risk of acute dermal effects is considered low given the small amounts of additive to
which people are likely to be exposed, low dermal toxicity and the fact that any spill on
the skin is unlikely to reside untreated for long periods.
Acute health effects due to the alkyl phosphate additive could occur as a result of
accidental ingestion of LRP by adults when siphoning fuel or by a child. The health
risk to adults from accidental ingestion of LRP containing the alkyl phosphate additive
during siphoning or to children following ingestion of LRP stored inappropriately
around the home is considered low, given the low level of the alkyl phosphate additive
(600 mg/kg petrol) in LRP.
Ingestion of half the contents of the the 10 mL single use aftermarket product by a
10 kg child equates to approximately half of the recommended daily allowance of
phosphorus for a child aged 3 to 4 years. This ingested dose corresponds to
368 mg/kg bw for a 10 kg child compared with the oral ALD (rats) of 11 000-
17 000 mg/kg bw for the Valvemaster Concentrate. Therefore, the alkyl phosphate
aftermaket products are not considered a significant acute health risk for children by
virtue of the alkyl phosphate additive. The inclusion of kerosene, particularly in the
concentrations present in the multi-treat aftermarket product, represents specific health
effects relevant to the kerosene content, i.e. irritancy and lung damage (if swallowed).
Phosphate is an ubiquitous component of the human body and is contained in the
normal diet. Thus chronic phosphoric acid exposures (from all sources combined) are
unlikely to be significantly changed by the use of the alkyl phosphate additive in LRP.
Exposure via food represents by far the greatest proportion of the total human
phosphate dose.
A chronic inhalation scenario was considered for phosphoric acid exposure by the
public as a result of the use of the alkyl phosphate additive in LRP. The use of the
alkyl phosphate additive will increase the phosphoric acid dose received by inhalation
above assumed negligible ambient air concentrations of phosphoric acid. By
comparing a NOAEL with estimated continuous exposures, a Margin of Exposure of
26 786 and 66 964 is calcualted for the `present use' and `2004' scenarios, respectively.
These margins of exposure are considered satisfactory and the public risk to inhaled
phosphoric acid as result of the use of the alkyl phosphate additive in LRP is considered
low.
16.5 Data gaps
The data gaps identified in this assessment are not regarded as significant impediments
to an adequate assessement of the risks associated with the current use of the alkyl
phosphate additive in LRP.
There are no data pertaining to the alkyl phosphate additive chemical because it is
manufactured in situ and never isolated. While limited, all toxicity data relates to
DMA-4 which contains the alkyl phosphate additive in a range of 70-90% (Section 4)
89
Alkyl Phosphate AVSR Additive
and indicate low dermal and oral mammalian toxicty of DMA-4 and possible irritancy
effects.
Similarly, while phosphoric acid does not appear to have been well studied with respect
to all toxicity or genotoxicity end points, inorganic phosphate is an essential component
of practically all life forms and is a natural component of the diet.
Furthermore, while the studies of phosphoric acid inhalation toxicity are not without
weaknesses, they most likely overestimate the adverse pulmonary effects of inhaled
phosphoric acid. This is because the inhalation studies are based on phosphorus
smokes rather than pre-formed phosphoric acid, with the smokes possibly containing
entities other than phosphoric acid, which can likewise affect pulmonary function.
90 Priority Existing Chemical Assessment Report Number 25
17. Recommendations
This section provides recommendations arising from the Priority Existing Chemical
assessment of the alkyl phosphate additive to improve occupational and public health as
a results of its use as an AVSR additive.
Whilst there is insufficient toxicology data for classification of the alkyl phosphate
additive in accordance with the NOHSC Approved Criteria for Classifying Hazardous
Substances (NOHSC, 1999a) and OECD Globally Harmonised System of Classification
and Labelling of Chemicals (OECD, 2002), the data gaps are not regarded as significant
impediments to an adequate assessement of the risks associated with the current use of
the alkyl phosphate additive in LRP.
In general, the current identified controls for occupational health and safety and public
health are considered to be adequate for the hazard and risk profile for the alkyl
phosphate additive. One action is recommened.
17.1 Recommendations for importers and manufacture of the alkyl phosphate
additive
17.1.1 Hazard communication ?MSDS
This assessment finds the MSDSs for the two alkyl phosphate additive products
conform well with the requirements of the NOHSC National Code of Practice for the
Preparation of Material Safety Data Sheets (NOHSC 1994e). It is recommended that
the use for which the Valvemaster Concentrate is intended be included on the MSDS.
91
Alkyl Phosphate AVSR Additive
18. Secondary Notification
Under Section 64 of the Industrial Chemicals (Notification and Assessment) Act 1989,
the secondary notification of a chemical that has been assessed under the Act may be
required where an introducer (manufacturer or importer) of a chemical becomes aware
of any circumstances that may warrant a reassessment of its hazards and risks. In the
case of the alkyl phosphate additive, specific circumstances include:
? use of the alkyl phosphate additive in bulk transport fuels other than LRP and
? additional information has become available to the introducers as to adverse
health and or environmental effects of of the alkyl phosphate additive.
The Director (Chemicals Notification and Assessment) must be notified within 28 days
of the manufacturer or importer becoming aware of any of the above or other
circumstances prescribed under Section 64(2) of the Act.
92 Priority Existing Chemical Assessment Report Number 25
Appendix 1
Calculation of LRP Volumes for 2004
A. The weekly fill-up rate for vehicles using lead replacement petrol (LRP) was calculated
from:
? sales volumes of lead and lead replacement petrol (LRP) during the period
from July 2000 to June 2001, which totalled 2937.36 ML (Department of
Industry, Science and Resources, 2001) and
? the number of vehicles using leaded petrol as at 31 March 2001 which totalled
2 904 342 (Australian Bureau of Statistics Motor Vehicle Census, 2001)
with the result:
2937.36 x 106 litres/year ?2 904 342 vehicles = 1011 litres/year/vehicle
= 19.4 litres/week/vehicle
B. LRP volumes in 2004 for 1 000 000 VSR susceptible vehicles were calculated by using a
19.4 litre LRP fill-up rate per week per vehicle, i.e. 1011 litres/year:
1 000 000 vehicles x 1011 litres/year/vehicle = 1 011 000 000 litres/year
1000 ML/year of LRP in 2004
93
Alkyl Phosphate AVSR Additive
Appendix 2
Physico-chemical Properties of
Phosphoric Acid
Table A2.1 - Chemical Identity of phosphoric acid
IUPAC Name Phosphoric Acid
Chemical Name: Orthophosphoric acid
CAS No.: 7664-38-2
EINECS No.: 231-633-2
Synonyms: Phosphoric acid
Hydrogen phosphate
o-phosphoric acid
orthophosphoric acid
white phosphoric acid
Molecular Formula: H3PO4
Structural Formula:
O
P OH
OH
OH
Molecular Weight: 98.00
Phosphoric acid (orthophosphoric acid) is identified as the major combustion by-product of the
alkyl phosphate additive in LRP (Section 8).
The physico-chemical properties of phosphoric acid (H3PO4) are well described: (Corbridge, 1985;
Commission of the European Communities, 1992; and Environment Canada, 1985). Phosphoric
acid is a triphasic oxyacid of pentavalent phosphorus that dissociates in water (pKa1 = 2.15,
pKa2 = 7.1, pKa3 = 12.4 at 25癈) to hydrogen and phosphate anion (PO43-) as represented in the
following scheme (Corbridge, 1985):
94 Priority Existing Chemical Assessment Report Number 25
H3PO4 H+ + H2PO4- 2H+ + HPO42- 3H+ + PO43-
Phosphoric acid is odourless (Commission of the European Communities, 1992). Phosphoric acid
is stronger than acetic, oxalic and silicic acid but weaker than sulphuric, hydrochloric, nitric and
chromic acid (Commission of the European Communities, 1992).
Between pH 2 and 7, most of the phosphate ions in an aqueous phosphoric acid solution will exist
as H2PO4- and as HPO42- between pH 7 and 12. A 0.1N aqueous solution has a pH value 1.5 and a
1% solution has a pH value of 2.0 to 2.2 (Merck, 1983).
The vapour pressure of aqueous phosphoric acid solutions is highly dependent on temperature and
concentration (Health Directorate, 2000; Commission of the European Communities, 1992). For
example, the vapour pressure of a 10% aqueous phosphoric acid solution decreases from 2.31 K Pa
at 20癈 to nil for a 100% solution. (Commission of the European Communities, 1992) The boiling
point, freezing point and density of an aqueous phosphoric acid solution depend on the
concentration of phosphoric acid (Commission of the European Communities, 1992).
At room temperature, phosphoric acid is likely to occur predominantly in aerosol/droplet form,
although vapour may be appreciable at high temperatures (Health Directorate, 2000).
Phosphoric acid has essentially no oxidising properties below 350-400癈. At higher temperatures it
is fairly reactive to metal, being reduced by it. (Corbridge, 1985) Phosphoric acid is not explosive
or flammable, nor is it very corrosive. Phosphoric acid is described as corrosive to ferrous metals
and alloys. Any corrosive behaviour due to phosphoric acid is attributed to impurities, e.g.
sulphuric acid, chlorine, and is exacerbated by heat (Becker, 1989).
4.08 mg/m3 H3PO4 = 1 ppm (20癈, 101 kPa) (Health Directorate, 2000)
95
Alkyl Phosphate AVSR Additive
Appendix 3
MSDS Assessment Summary
Number of General Comments
Selected Core Information as per Code
MSDS
containing
correct
information
INTRODUCTORY AND COMPANY DETAILS
Date of issue (month/year) 2/2
Statement of hazardous nature 2/2
Name of Australian company and address 2/2
Telephone number 2/2
Emergency telephone number 2/2
IDENTIFICATION
Product name 2/2
Other name 2/2
UN Number 1/1 MSDS states UN Number 3082
for Valvemaster VM11.
Dangerous goods class 1/1 MSDS states Class 9 Packing
group 111 for Valvemaster
VM11.
HAZCHEM code NA MSDS states HAZCHEM code
2X for Valvemaster VM11.
Poisons Schedule number 1/1 MSDS states Schedule 5 for
ValvemasterVM11.
Use 1/2 No uses identified for
Valvemaster Concentrate.
Physical Description/Properties
Appearance 2/2
Boiling point/Melting point 2/2
Vapour pressure 2/2 Vapour pressure of
Valvemaster Concentrate stated
as not known
96 Priority Existing Chemical Assessment Report Number 25
Specific gravity 2/2
Flashpoint 2/2
Flammability limits 2/2
Solubility in water 2/2
Ingredients 2/2
Proportion details 2/2
HEALTH HAZARD INFORMATION
Eye irritation 2/2
Skin irritation 2/2
Damage to lungs if swallowed 2/2 Both MSDS state "risk of
aspiration into the lungs".
First Aid for ingestion, inhalation, skin and eye 2/2
exposure
Advice to doctor 2/2
PRECAUTIONS FOR USE
Exposure limits NA Both MSDS state no exposure
standard is established for the
products
2/2
Engineering controls
Personal protective equipment 2/2
Flammability information 2/2 MSDS describe both products as
C1 combustible liquids
SAFE HANDLING INFORMATION
Storage and transport 2/2
Spills and disposal 2/2
Fire/Explosion hazard 2/2
CONTACT POINT
Contact details (Australian) 2/2
NA = not applicable.
97
Alkyl Phosphate AVSR Additive
References
ACGIH (American Conference of Governmental Industrial Hygienists) (2000) 2000 TLV's and
BEI's: Threshold limit values for chemical substances and physical agents and biological exposure
indices. Cincinnatti, Ohio, ACGIH.
AIHW (Australian Institute of Health and Welfare) (2002) National Hospital Morbidity Database.
. Accessed 2002.
Al-ani FY & Al-Lami SK (1988) Absence of mutagenic activity of acidity regulators in the AMes
Salmonella/microsome test. Mutation Research, 206: 467-470.
AMU (Audit Management Unit) (2002) National land and water resources audit. Canberra,
Commonwealth Government.
ANZECC and ARMCANZ (2000) Australian and New Zealand guidelines for freshwater and
marine waters. Australian and New Zealand Environment and Conservation Council and the
Agriculture and Resource Management Council of Australia and New Zealand. National Water
Quality Management Strategy. ,
Accessed 2002.
ANZFA (Australia New Zealand Food Authority) (2001) Schedule 2 Miscellaneous additives
permitted in accordance with GMP in processed foods specified in Schedule 1, Australia New
Zealand Food Authority.
m>, Accessed 2002.
Aranyi C, Henry MC, Vana SC & Iverson WO (1988a) Effects of multiple intermittent inhalation
exposures to red phosphorus/butyl rubber obscurant smokes in Sprague-Dawley rats. Inhal.
Toxicol, 1: 65-78.
Aranyi C, Vana S, Bradof J & Sherwood R (1988b) Effects of inhalation of red phosphorus-butyl
rubber combustion products on alveolar macrophage responses in rats. J. Appl. Toxicol., 8: 393-
398.
AS Harrison and Co Pty Limited (2000) Valvemaster Information Dossier submitted to National
Industrial Chemicals Notification and Assessment Scheme (NICNAS), Sydney.
Ashby K & Routely V (1996) Childhood domestic chemical and plant poisonings. HAZARD, 28:1-
7. Victorian Injury Surveillance System, Monash University Accident Research Centre.
Asia Pacific Specialty Chemicals (2000a) Material Safety Data Sheet Valvemaster Concentrate.
Sydney.
Asia Pacific Specialty Chemicals (2003) Material Safety Data Sheet Valvemaster (VM11). No.
6ACDC. Sydney. March 2003.
Australian Bureau of Statistics (1998) 9309.0 Motor Vehicle Census 31 October 1997. Canberra,
ABS.
Australian Bureau of Statistics (2001) 9309.0 Motor vehicle census 31 March 2001. Canberra,
ABS.
Australian Institute of Petroleum Ltd (1999) Petroleum Gazette, 34(2).
98 Priority Existing Chemical Assessment Report Number 25
Ballantyne B (1981) Acute inhalation toxicity of phosphorus pentoxide smoke. Toxicologist,
1(140): Abstract No. 508.
Ballantyne B (1998) Acute inhalation toxicity of red phosphorus smoke. Toxic Substance
Mechanisms, 17(4): 251-266.
Barlow PL (1999) The lead ban, lead replacement petrol, and the potential for engine damage.
Anti-corrosion Methods and Materials, 46(6): 439-449.
Becker P (1989) Phosphates and phosphoric acid. Strasburg, Marcel Dekker, INC.
Benbarka A (2000) Lead phase-out in sub-saharan countries. The case of three gasoline-importing
countries: Benin, Burkina Faso and Senegal. Washington D.C., USA, The World Bank.
BIOFAX Industrial Bio-Test Laboratories I, Data Sheets. (1810 Frontage Rd., Northbrook, IL
60062) Data Sheets. Northbrook, BIOFAX Industrial Bio-Test Laboratories.
Bonting SL & Jansen BC, (1956) The effect of a prolonged intake of phosphoric acid and citric acid
in rats. Voeding, 17: 137-148.
Boutoux M, Leroyer C, Bernard R & Dewitte JD (1995) Reactive airways dysfunction syndrome
after exposure to phosphoric acid vapours. Archives des maladies professionnelles et de m鈋decine
du travail, 56(1): 45-47.
Burton FG, Clark ML, Miller RA & Schirmer RE (1982) Generation and characterisation of red
phosphorus smoke aerosols for inhalation exposure of laboratory animals. Am Ind Hyg Assoc J,
43(10): 767-772.
Campbell IC & Doeg TJ (1989). Impact of timber harvesting and production on streams: A review.
Australian Journal of Marine and Freshwater Research, 40, 519-539.
Caravati EM (1987) Metabolic abnormalities associated with phosphoric acid ingestion. Ann.
Emerg. Med, 16: 904-906.
ChemAlert Report: Phosphoric Acid (Orica), ?2002 RMT.
Cipollaro M, Corsale G, Zesposito A, Ragucci E, Staiano N, Giordano GG & Pagano G (1986)
Sub-lethal pH decreases may cause genetic damage to eukaryotic cell: a study on sea urchins and
Salmonella typhimurium. Teraogen. Carconogen. Mutagen, 6: 275-287.
Commission of the European Communities (1992) Occupational exposure limits. Criteria document
for phosphoric acid. London, Employment, Industrial Relations and Social Affairs, Health and
Safety Direcotrate (Report No. EUR 14178 EN).
Commonwealth of Australia (1988) Protocol of 1978 relating to the International Convention for
the Prevention of Pollution from Ships of 2 November 1978, as amended. London, 17 February
1978. Australian Treaty Series 1988 No. 29. Department of Foreign Affairs and Trade, Canberra.
Australian Government Publishing Service.
Connell DW & Hawker D (1986). Predicting the distribution of persistent organic chemicals in the
Environment. Chemistry in Australia. December 1986. pp. 428-431.
Corbridge DEC (1985) Phosphorus: An outline of its chemistry, Biochemistry and Technology.
Amsterdam, Elsevier.
Corbridge DEC (1990) Phosphorus. An outline of its chemistry, biochemistry and
technology", 4th Ed. Amsterdam, Elsevier.
99
Alkyl Phosphate AVSR Additive
CRCFE (Co-operative Research Centre for Freshwater Ecology) (2000) Quantifying nutrient ?br>
algae relationships in freshwater ecosystems. Outcomes from a Workshop held at Monash
University, 8th August 2000. Technical Report No. 8/2000.
CSIRO (Commonwealth Scientific & Industrial Research Organisation) (2000) Orthophosphoric
acid. CSIRO Atmospheric Research. AirWatch ?Safety Orthophosphoric Acid.
http://www.dar.csiro.au/airwatch
Cullen P (1986) Managing nutrients in aquatic ecosystems: the eutrophication problem. In Deckker
P & Williams WD (eds.), Limnology in Australia. Melbourne, CSIRO, pp. 539-54.
Davis RB, Thurlow DL & Brewster FE (1974) Effects of burrowing tubificid worms on the
exchange of phosphorus between lake sediment and overlying water. Winnipeg, Congress of
Canada 1974.
Demerec M, Bertami G & Flint J (1951) A survey of chemicals for mutagenic action on E. coli.
The Americal Naturalist, 85(821): 119-135.
Department Industry, Science and Resources (2001) Automotive gasoline sales in Australia.
Canberra., Department Industry, Science and Resources.
Dolan DF & Kittelson DB (1979) Roadway measurements of diesel exhaust aerosols, SAE (Society
of Automotive Engineers) Technical Paper No 790492.
Donnelly TH, Caitcheon GG & Wasson RJ (1992) Algal blooms in inland Australian water
systems: sourcing nutrients and turbidity. In CSIRO Division of Water Resources Divisional Report
92/4. Canberra, CSIRO, pp.74-81.
Draize JH, Woodard G & Calverz HO (1944) Methods for the study of irritation and toxicity of
substances applied topically to the skin and mucous membranes. J. Pharm. Exp. Ther., 82: 377-390
Du Pont De Nemours & Co. Inc. (1986) DMA-4 Report to E.I Du Pont De Nemours & Co., Inc.
21-day neurotoxicity study with H-16,407 in mature white leghorn chickens. E.I Du Pont De
Nemours & Co., Inc.
Dutton CB, Pigeon MJ, Renzi PM, Feustel PJ, Dutton RE & Renzi GD (1993) Lung function in
workers refining phosphorus rock to obtain elementary phosphorus. J. Occup. Med., 35: 1028-33.
ECB (European Chemicals Bureau) (2000) International Uniform Chemical Information Database
(IUCLID) Orthophosphoric Acid. Ispra, Italy, European Commission ?JRC, 69 pp.
Ellgaard EG & Gilmore JY Jnr (1984) J. Fish Biol. 25(2): 133-137.
Environment Australia (2000) Setting national fuel quality standards, Paper 2A. Canberra,
Department of Environment and Heritage, Commonwealth of Australia.
Environment Australia (2001) State of knowledge report: air toxics and indoor air quality in
Australia. Canberra, EA. Accessed 2002.
Environment Canada (1981) Technical information for problem spills: Phosphoric Acid (Draft).
Environment Canada (1985) Phosphoric Acid. Ottawa, Ontario, Technical Services Branch,
Environment Protection Programs Directorate.
Fabbri L, Mapp C, Rossi A, Cortese S & Saia B (1977) Chronic broncopneuomopathy and
pneumoniosis in workers employed in phosphoric acid production. Lavoro Umano, 28: 50-57.
FAO (Food and Agriculture Organization of the United Nations World Health Organization of the
United NationsNations) (1970) Fourteenth Report of the Joint FAO/WHO Expert Committe on
Food Aditives. Toxicological evaluation of some extraction solvents and certain other substances.
100 Priority Existing Chemical Assessment Report Number 25
Geneva, Food and Agriculture Organization of the United Nations World Health Organization of
the United Nations.
Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, Hauser SL & Longo
DL (eds) (1998) Harrison's principles of internal medicine. New York, McGraw-Hill.
FORS (Federal Office of Road Safety) (1998) Australian code for the transport of dangerous goods
by road and rail (6th ed). Canberra, AGPS.
Frausto da Silva JJR & Willimans RJP (1991) The biological chemistry of the elements. The
inorganic chemistry of life. Oxford, Clarendon Press.
Frosch PJ & Klingman AM (1977) A method for appraising the stinging capacity of topically
applied substances. J. Soc. Cosmet. Chem., 28: 197-209.
Furia TE (1972) CRC handbook of food additives (2nd ed). Cleveland: The Chemical Rubber Co.
(Cited in Hazardous Substances Database HSBD for Phosphoric Acid. National Library of
Medicine, Toxnet system. http://toxnet.nlm.nih.gov)
Gosselin RE, Hodge HC, Smith RP & Gleason MN (1976) Clinical toxicology of commercial
products. Acute Poisoning. Baltimore, USA, Williams and Wilkins Co.
Grant WM (1974) Toxicology of the eye. Springfield Illinois, Charles C Thomas.
Gungahlin Weather Centre. (2003). The Great Australian Weather Debate. 3 pp. Internet:
Handreck K (1997) Phosphorus needs of some Australia plants. Australian Plants Online.
Accessed 2002.
Harris GP (1994) Nutrient loading and algal blooms in Australian waters ?A discussion paper.
LWRRDC Occasional Paper No 12/94, Canberra.
Haskell Laboratory (1964) Report No. 19-64 Acute oral toxicity in rats.
Haskell Laboratory (1987) Du Pont Approximate lethal dose (ALD) by skin absorption of DMA-4
in rabbits: Haskell Laboratory Report No. 172-87. Haskell Laboratory,
Haskell Laboratory for Toxicology and Industrial Medicine (1964) Primary irritation and
sensitization test, Haskell Laboratory Report No. 19-64. E. I. Du Pont de Noumes and Company,
Haskell Laboratory for Toxicology and Industrial Medicine.
Haskell (Haskell Laboratory for Toxicology and Industrial Medicine) (1986) Approximate lethal
dose (ALD) of DMA-4 in rats. Report No. 409-86. Haskell Laboratory for Toxicology and
Industrial Medicine. Haskell Laboratory for Toxicology and Industrial Medicine.
Haskell Laboratory for Toxicology and Industrial Medicine (1986a) Eye irritation test in rabbits of
DMA-4, Haskell Laboratory Report No. 372-86, E. I. Du Pont de Nemours and Company,
Haskell Laboratory for Toxicology and Industrial Medicine. Haskell Laboratory for Toxicology and
Industrial Medicine.
Haskell Laboratory for Toxicology and Industrial Medicine (1986b) Skin irritation test in rabbits of
DMA-4, Haskell Laboratory Report No. 509-86. E. I. Du Pont de Noumes and Company, Haskell
Laboratory for Toxicology and Industrial Medicine.
Haskell (Haskell Laboratory for Toxicology and Industrial Medicine) (1986c). Static acute 96-hour
LC50 of DMA-4 to fathead minnows. Report No. 377-86. MR no. 7884-001.
Haslett C, Chilvers ER, Hunter JAA & Boon NA (Eds) (1999) Davidson's principles and practice of
medicine (18th ed). London, Churchill Livingstone.
101
Alkyl Phosphate AVSR Additive
Hawkins DB, Demeter MJ & Barnett TE (1980) Caustic ingestion: Controversies in management.
A Review of 214 cases. The Laryngoscope, 90: 98-109.
Health Directorate (2000) European Commission Directive 2000/39/EC establishing a first line
indicative occupational exposure limit values at European Community level in implementation of
council directive 98/24/EC on the protection of the health and safety of workers from the risks
related to chemical agents at work. London, Health and Safety Commission.
Heywood JB (1988) Internal combustion engine fundamentals. N.Y., McGraw-Hill.
Hill R (2000) Leaded petrol to be phased out by 2002, Media Release, Federal Minister for the
Environment and Heritage The Hon Robert Hill MP, 15 March 2001.
IRIS (Intergrated Risk Information System) Phosphoric acid. United States Environment Protection
Agency, Last update 8 January 2003.
Jacobs GA (1992) Two dilutions of phosphoric acid tested on eye. J Am Coll Toxicol, 11(6): 724.
Joint FAO/WHO Expert Committe on Food Additives (1976). 17th Report of the Joint FAO/WHO
Committe on Food Additives. Toxicological evaluation of some food additives including
anticacking agents, antimicrobials, antioxidants, emulsifiers and thickening agents (WHO Food
Additive Series No. 5). Geneva, World Health Organization.
Kee RJ, Miller JA & Jefferson TH (1989) CHEMKIN-II: FORTRAN Chemical kinetics code
package for the analysis of gas-phase chemical kinetics. Sandia National Laboratories Report
SAND89-8009. Albuquerque, Sandia Laboratorie s.
Larson PS, Finnegan JK & Haag HB (1956) Observations on the effect of chemical configuration
on the odema-producing potency of acids, aldehydes, ketones and alcohols. J. Pharmac.exp Ther.,
116: 119-122.
Lee DBN, Brautbar N & Kleeman CR (1981) Disorders of phosphorus metabolism. In Disorders of
mineral metobolism. New York, Academic Press.
Loden M, Larsson R, Haggqvist I & Karlsson N (1985) The dermal irritancy/corrosion of 20
compounds in aqueous solutions. FOA Report E 40023. Umea, Sweden, National Defence
Research Institute.
Lovei M (1998) Phasing out lead from gasoline worldwide experiences and policy implications.
World Bank Technical Paper No. 397. The World Bank , Washington D.C.
Accessed 2002.
Lutz AE, Rupley FM, Kee RJ & Reynolds WC (1990) EQUIL: Chemkin Interface for
Stanjan-III. Albuquerque, Sandia Laboratories.
Mackie JC, Bacskay GB & Haworth NL, J. Phys. Chem. A, 2002 (in press).
Manahan SE (1993) Fundamentals of environmental chemistry. Michigan, Lewis Publishers.
Marrs T, Colgrave H, Edginton J, Rice P & Cross N (1989) The toxicity of a red phosphorus smoke
after repeated inhalation. J. Haz. Mat, 22: 269-82.
Mensink BJWG, Montforts M, Wijkhuizen-Maslankiewicz L, Tibosch H & Linders JBHJ (1995)
Manual for summarizing and evaluating the environmental aspects of pesticides, Report No.
679101022. Bilthoven, The Netherlands, National Institute of Public Health and Environmental
Protection..
Merck (1983) The Merck Index (edited by M Windholz). Rahway, N.J. U.S.A., Merck & Co., Inc.
102 Priority Existing Chemical Assessment Report Number 25
Merck (Merck Research Laboratories) (2001) The Merck index. An encyclopedia of chemicals,
drugs and biologicals (13th Edition). NJ, USA, Merck & Co.
MSDS (2000) Accessed 2000.
National Academies (2003), Institute of Medicine, Food and Nutrition Board, Dietary Reference
Intakes: Elements.
Accessed 2002.
National Heritage Trust (2000) Setting national fuel quality standards. Review of fuel quality
requirements for Australian transport, Appendix 6B-10. Canberra, Commonwealth of Australia.
NEPC (National Environment Protection Council) (1998a) National Pollutant Inventory. National
Environment Protection Measure for the National Pollutant Inventory. 27 February 1998. Adelaide,
SA, NEPC.
NEPC (National Environment Protection Council) (1998b) Ambient Air Quality. National
Environment Protection Measure for Ambient Air Quality. Adelaide, SA, NEPC.
NEPC (National Environment Protection Council) (2002) Towards a National Environment
Protection (Ambient Air Toxics) Measure. Discussion Paper. 22 March 2002. Adelaide, SA, NEPC.
NIOSH (National Institute of Occupational Safety and Health) (1996) Phosphoric acid IDLH
documentation. . Last updated July 2000.
NLM (National Library of Medicine) (2002) Hazardous Substances Databank (HSDB) for
Phosphoric Acid. .
NPI (National Pollutant Inventory) (2001) National Pollutant Inventory: Emission report:
phosphoric acid. .
NSW EPA. (Environment Protection Authority) (2000) State of the Environment Report 2000.
Accessed 2003.
NOHSC (National Occupational Health and Safety Commission) (1994a) National model
regulations for the control of workplace hazardous substances [NOHSC:1005(1994)] (Updated for
Amendments), National Occupational Health and Safety Commission, 1994, Canberra, Australian
Government Publishing Service.
NOHSC (National Occupational Health and Safety Commission) (1994b) National code of practice
for the control of workplace hazardous substances [NOHSC: 2007(1994)]. Canberra, Australian
Government Publishing Service.
NOHSC (National Occupational Health and Safety Commission) (1994c) National code of practice
for the labelling of workplace substances [NOHSC: 2012(1994). Canberra, Australian Government
Publishing Service.
NOHSC (National Occupational Health and Safety Commission) (1994d) Guidance note for the
assessment of health risks arising from the use of hazardous substances in the workplace
[NOHSC:3017(1994)]. Canberra, Australian Government Publishing Service.
NOHSC (National Occupational Health and Safety Commission) (1994e) National code of practice
for the preparation of Material Safety Data Sheets. Canberra, ACT, Australian Government
Publishing Service.
NOHSC (National Occupational Health and Safety Commission) (1995) Exposure standards for
atmospheric contaminants in the occupational environment : Guidance note [NOHSC:3008(1995)]
103
Alkyl Phosphate AVSR Additive
and National exposure standards [NOHSC:1003(1995)]. Canberra, Australian Government
Publishing Service.
NOHSC (National Occupational Health and Safety Commission) (1996) National standard for the
control of major hazard facilities [NOHSC:1014(1996)]. Canberra, Australian Government
Publishing Service.
NOHSC (National Occupational Health and Safety Commission) (1999a) Approved criteria for
classifying hazardous substances [NOHSC:1008(1999)].Sydney, National Occupational Health and
Safety Commission.
NOHSC (National Occupational Health and Safety Commission) (1999b) List of designated
hazardous substances [NOHSC:10005(1999)]. Sydney, National Occupational Health and Safety
Commission.
NOHSC (National Occupational Health and Safety Commission) (2001a) National standard for the
storage and handling of workplace dangerous goods [NOHSC: 1015(2001)]. National Occupational
Health and Safety Commission,
2001_STANDARD.pdf>. Accessed 2002.
NOHSC (National Occupational Health and Safety Commission) (2001b) National code of practice
for the storage and handling of workplace dangerous goods [NOHSC:2017 (2001)].
. Accessed 2002.
NZME (New Zealand Ministry for the Environment) (1994) Ambient air quality guidelines for
New Zealand. Wellington, Ministry for the Environment.
Octel OIP 8.385 (1999) Safety Data Sheet ?Valvemaster Concentrate. OIP 8.114. 6./5/99.
Octel (undated;a) Octel Valvemaster Dossier ?Health, safety & environmental aspects of
Valvemaster and comparison with other Valve Seat Recession (VSR) Additives.
Octel. (undated;b). Octel Valvemaster Dossier ?Worldwide history of use summary.
Octel (1999a) Valvemaster VM11 Product information issued 13/07/99.
Octel (1999b) Valvemaster Product information. Issue 6 6/4/99. 1 pp.
Octel (1999c) Valvemaster in lead replacement gasoline: Technical review July 1999.
Octel (2000) Valvemaster Product Information issued 24/01/00.
Octel A (1999b) Valvemaster in Lead Replacement Gasoline Technical Review. Associated
Octel.
OECD (Organisation for Economic Cooperation and Development) (1999) Advanced air quality
indicators and reporting. Working Party on Pollution Prevention and Control. Environment
Directorate, Environment Policy Committee. ENV/EPOC/PPC(99)9/Final. 27 September 1999.
OECD (Organisation for Economic Co-Operation and Development). (2002). Amendment to the
GHS. Document No. UN/SCEGHS/3/INF.16. Annex 3 of Document ST/SG/AC.10/C.4/2001/26.
Sub-Committee of Experts on the Globally Harmonised System of Classification and Labelling of
Chemicals. Third Session, 10-12 July, 2002.
Ohio State University. (1996) Ohio Agronomy Guide. Bulletin 472 - Soil Fertility,
Accessed 2003.
Parent ME, Hua Y & Siemiatychi J (2000) Occupational risk factors for renal cell carcinoma in
Montreal. Am. J. Ind. Med., 38(6): 609-618.
104 Priority Existing Chemical Assessment Report Number 25
Patty's (1993), Vol. II, Part A, Patty's Industrial Hygiene and Toxicology, 4th Ed., 1993, Ed.,
George D. Clayton & Florence E Clayton. New York, John Wiley & Sons.
Payne MP, Shillaker RO & Wilson AJ (1993) Toxicity Review 30. London, Health and Safety
Executive, Working Group on the Assessment of Toxic Substances.
Proctor NH & Hughes JPW (1978) Chemical hazards in the work place. Philadelphia, Lippincott
Co.
Randall DJ & Robinson EC (1990) Acute toxicologic evaluation of various concentrations of
phosphoric acid. Journal of the American College of Toxicology, B: 69-70.
Renke DE, Winnicka A & Graczyk M (1987) Estimation of occupational hazards of the employees
of a phosphate fertiliser plant. Bull. Inst. Mar. Trop. Med. Gdynia, 38: 5-16.
Rosen CJ & Eliason R (2002) Nutrient management for commercial fruit & vegetable crops in
Minnesota. University of Minnesota Extension Service. Department of Soil, Water and Climate.
.
RTECS (1998) Registry of Toxic Effects of Chemical Substances. National Institute for
Occupational Safety and Health, United States. CHEM-BANKTM, Compact disc SP-018-031,
SilverPlatter Internationel N.V., November, 1998. Last update: October 1998.
Sekizawa J, Yasuhara K, Suyama Y, Yamanaka S, Tobe M & Nishimura M (1994) A simple
method for screening assessment if skin and eye irritation. Journal of Toxicological Sciences,
19(1): 25-35.
Sigova NV (1983) Toxicological characteristics of phosphoric acid and some of its chromium salts
used as a binder in refractory production. Gig. Truda i Prof. Patol. v Tsv i Cher. Metallurgii, M: 65-
69.
Standards Australia (1990) Australian Standards for Petrol (gasoline) for motor vehicles, AS
18760-1990. North Sydney, Standards Australia.
Standards Australia (1996) Australian Standard 4430.1-1996: Evaluation of devices and additives
which claim to improve vehicle performance. Part 1: Engines designed for leaded petrol to operate
on unleaded petrol. North Sydney, Standards Australia.
State of the Environment Advisory Council (1996) State of the Environment Australia 1996.
Canberra, Department of the Environment and Heritage, Environment Australia
Standard for the Uniform Scheduling of Drugs and Poisons (SUSDP) (2002). No. 17 Effective Date
2 June 2002. National Drugs and Poisons Schedule Committee (NDPSC). Canberra,
Commonwealth Department of Heath and Ageing.
Sul'kov, V.P., Miroshnikov, N.A., and Dovina, V.M., Tr. Nll po Udobr. i
Insektofungitsidam 1975, 226, 41-43. From Ref. Zh., Khim. 1976, Abstr. No. 11L159. From
Chem. Abstracts 1976:529745.
US EPA (United States Environment Protection Agency) (1990) Memorandum from Janette Houk,
Ph.D., Hazard Integrator, Chemical Review and Evaluation Branch, Health and Environmental
Review Division. Re: Petition to delist phosphoric acid (Febuary 14, 1990).
US EPA (United States Environment Protextion Agency) (1999). 64 Fed. Reg. (FR) 38705.
National Air Toxics Program: The Integrated Urban Strategy (Notice). July 19, 1999.
Water Directorate (2001). Blue-green algal bloom management protocols. New South Wales Water
Directorate. November 2001.
105
Alkyl Phosphate AVSR Additive
Watson WA, Bradford DC, & Veltri JC (1983) The volume of a swallow: correlation of deglutition
with patient and container parameters. Am. J. Emergency Med., 1, 3, 278-281.
Weiner M, Freeman C, McMCarty JD, Kotkoskie LA & Fletcher MJ (1990) Modified skin
irritation study on 75% phosphoric acid in a single rabbit. Acute Toxic Data, 1(2): 98-99.
Weiner M, Salminen WF, Larson PR, Barter RA, Kranetz JL, Simon GS (2001) Toxicological
review of inorganic phosphates. Food and Chem. Toxicol., 39, 8, 759-786.
Woodward-Clyde (1996). Disposal of Valvemaster applicators. Unpublished consultancy letter
report to Mr Chris Mulcare, Asia Pacific Specialty Chemicals. Ref: L004-D.DOC\24 APR 96.
WHO (World Health Organization) (1982) Toxicological evaluations of certain food additives:
WHO food additive series 17. Prepared by the Joint FAO/WHO Expert Committee on Food
Additives, Rome, 19-28 April 1982.
Accessed 2002.
WHO (World Health Organization) (1965) Specifications for identity and purity and toxicological
evaluation of some antimicrobials and antioxidants: Phosphoric acid. Joint FAO/WHO Expert
Committee on Food Additives, FAO Nutrition Meetings Report Series 38a. <
http://www.inchem.org/documents/jecfa/jecmono/v38aje10.htm> Accessed 2002.
106 Priority Existing Chemical Assessment Report Number 25
107
Alkyl Phosphate AVSR Additive
|