Mobil Jet Oil II
Overview of
Available
Scientific
Background Information
Prepared by:
Date:
9 September 1999
Index
|
1. |
About NICNAS |
2 |
|||
|
2. |
Background |
2 |
|||
|
3. |
Composition of Mobil Jet
Oil II |
3 |
|||
|
4. |
Chemical ingredient
profile |
4 |
|||
|
4.1 |
Tricresyl phosphate (TCP) |
4 |
||
|
4.2 |
4,4’-Dioctyldiphenylamine
(DODPA) |
6 |
||
|
4.3 |
Phenyl-alpha-naphthylamine
(PAN) |
7 |
||
|
4.4 |
Phenyl-beta-naphthylamine
(PBN) |
7 |
||
|
4.5 |
Alpha-naphthylamine (ANA) |
9 |
||
|
4.6 |
Beta-naphthylamine (BNA) |
9 |
||
|
4.7 |
Discussion and conclusions |
10 |
||
|
5. |
Products of combustion |
11 |
|||
|
6. |
Hazard of product as a
whole |
11 |
|||
|
7. |
References |
13 |
|||
1.
About NICNAS
The
National Industrial Chemicals Notification and Assessment Scheme (NICNAS) was
established with the enactment of the Industrial Chemicals (Notification and
Assessment) Act 1989 (Cwlth) on 18 July 1990. Its goal is to aid in the
protection of the Australian people and the environment by identifying the
risks to occupational health, public health and the environment from industrial
chemicals. NICNAS disseminates information about industrial chemicals through
the release of public assessment reports, the Chemical Gazette and its Internet
site.
NICNAS
is a Commonwealth Government scheme administered within the Chemical Assessment
Division of the National Occupational Health and Safety Commission (NOHSC). The
Minister responsible is the Minister for Employment, Workplace Relations and
Small Business.
NICNAS
ensures that all new industrial chemicals introduced into Australia are
assessed to determine the potential risk to human health and the environment
prior to their importation and/or manufacture (New Chemicals Program). NICNAS
also identifies and assesses the risks from industrial chemicals which are
already in use in Australia on a priority basis under the Existing Chemicals
Program.
2. Background
On
22 July 1999 NICNAS received a letter from the Australian Federation of Air
Pilots requesting a review of the hazardous properties of the lubricant Mobil
Jet Oil II. The lubricant was alleged to leak into the air-conditioning system
of BAe-146 aircraft causing odours and having adverse health effects on
crewmembers. NICNAS has also received letters from several airline crew
requesting a review of Mobil Jet Oil II.
NICNAS
has been informed that the Senate Rural and Regional Affairs and Transport
Committee will conduct an inquiry into various matters relating to domestic air
services, including an examination of air safety, with particular reference to
cabin air quality in BAe-146 aircraft.
NICNAS assesses individual chemicals rather than
products, although two or more chemicals of the same chemical group can be
assessed together. As with a number of other chemicals recently recommended for
review, NICNAS is in the process of collecting health and environmental
exposure information for the chemicals that make up Mobil Jet Oil II. Even if
one or more of these chemicals are selected for review, an assessment could not
be completed in time for the Senate inquiry as public reports issued by NICNAS
have a statutory comment/appeal phase totalling 5 months.
However, NICNAS also has an information provision
role and from time to time makes available to the public, or others,
collections of published information on the hazardous properties of chemicals
and overviews of published background/scientific information.
As
such, this paper is not an assessment of Mobil Jet Oil II, but an overview of
reliable, published information on relevant properties of the chemical
ingredients of the lubricant.
3. Composition of Mobil Jet Oil II
A
label for Mobil Synthetic Jet Engine Oil provided by the Australian Federation
of Air Pilots contains the following information about the composition of the
product:
“This product
contains one or more of the following base oils:
·
synthetic
esters NJTS
003066009-5088P
·
synthetic
esters NJTS
003066009-5234P
·
phosphoric
acid, tris(methylphenyl)ester 1330-78-5
·
benzenamine,
4-octyl-N-(4-octylphenyl) 101-67-7
·
1-naphthaleneamine,
N-phenyl 90-30-2
·
1-naphthaleneamine 134-32-7
·
2-naphthaleneamine 91-59-8
·
contents
partially unknown.”
The
synthetic esters are apparently characterised by a proprietary code number.
According to the importer, the base liquid of Mobil Jet Oil II is a
pentaerythritol ester made with mixed organic acids containing 5-10 carbon
atoms (Mobil, 1999).
The
declared additives are uniquely identified by their Chemical Abstracts Services
number (CAS No.). The chemical name, CAS No., common name and acronym of each
of the additives are listed below:
|
Chemical name |
CAS No. |
Common name |
Acronym |
|
Phosphoric acid,
tris(methylphenyl)ester |
1330-78-5 |
Tricresyl phosphate |
TCP |
|
Benzeneamine,
4-octyl-N(4-octylphenyl) |
201-67-7 |
4,4’-Dioctyldiphenylamine |
DODPA |
|
1-Naphthaleneamine, N-phenyl |
90-30-2 |
Phenyl-alpha-naphthylamine |
PAN |
|
1-Naphthaleneamine |
134-32-7 |
Alpha-naphthylamine |
ANA |
|
2-Naphthaleneamine |
91-59-8 |
Beta-naphthylamine |
BNA |
The
above chemicals are listed in the Australian Inventory of Chemical Substances,
except BNA which is a prohibited carcinogenic substance (NOHSC, 1995b). A
chemical listed in the Inventory is in use in Australia, but has not
necessarily been assessed by NICNAS.
According to Material Safety Data Sheets (MSDS) provided
by the Australian Federation of Air Pilots and Mobil Oil Australia Ltd, Mobil
Jet Oil II contains >90% synthetic esters and <10% additives and/or other
ingredients, including 3% (or 1-5%) TCP and 1% (or 1-5%) PAN. A MSDS from 1992
also lists 2-naphthalenamine, N-phenyl (CAS No. 135-88-6) as an ingredient.
This chemical, also known as phenyl-beta-naphthylamine (PBN) is listed in the Australian
Inventory of Chemical Substances, too.
4.
Chemical ingredient profile
Published
information is available on the physico-chemical and hazardous properties of
each of the above-mentioned individual additives and is summarised below. In
interpreting the data, it should be noted that toxicity tests generally use
doses which are high compared to likely human exposures. The use of high doses
increases the likelihood that potentially significant toxic effects will be
identified.
4.1 Tricresyl phosphate (TCP)
TCP (CAS No. 1330-78-5) is a complex mixture of isomeric
esters between phosphate and ortho-, meta- and para-cresol and excludes the
toxic ortho-isomers as much as possible (HSDB, 1999). Phosphate esters of other
substituted phenolic compounds may be present in varying proportions (IPCS,
1990).
Unless otherwise indicated, the properties of TCP and
its isomers described below are summarised from the peer-reviewed international
assessment of TCP published by the International Programme on Chemical Safety
(IPCS, 1990). The isomer tri-ortho-cresyl phosphate will be referred to as
TOCP.
Physico-chemical properties
TCP
is a non-flammable, non-explosive, practically colourless, odourless liquid
with a low vapour pressure (0.133 Pa at 20ºC) which boils at 420ºC (HSDB,
1999). When heated to decomposition, it can emit highly toxic fumes of
phosphorous oxides (HSDB, 1999). TCP is widely used in fire-resistant,
extreme-pressure lubricants as an anti-wear agent.
The
TOCP isomer has a vapour pressure of 1.33 kPa at 265ºC and boils at 410ºC. A
method exists for the determination of TOCP in air at levels between 0.002-2
mg/m3 (NIOSH, 1994).
Kinetics and metabolism
TOCP
is absorbed from the gastro-intestinal tract and through the skin. There are no
reliable data on absorption via inhalation. TOCP is metabolised to a variety of
smaller molecules, one of which is a relatively unstable neurotoxin known as
saligenin cyclic ortho-tolyl phosphate. TOCP and its metabolites are eliminated
via the urine and faeces.
Toxicity in laboratory animals
The
critical effects of TCP include delayed neuropathy ascribed to the TOCP isomer,
and reproductive toxicity.
Neuropathy may occur after both single and repeated
exposure to TOCP and is similar in its mechanisms of action and manifestations
to the delayed nerve damage induced by other organophosphates. Clinical signs
of paralysis typically appear after a latency period of 1-4 weeks.
Histologically, there are degenerative changes in the axons which gradually
spread towards the cell body. The lesions are attributed to the metabolite
saligenin cyclic ortho-tolyl phosphate, which irreversibly inhibits a subset of
nervous system esterases called neuropathy target esterases (NTE). Chickens and
cats are considerably more sensitive to TOCP neurotoxicity than rodents.
However, factors other than metabolism such as route of exposure, age, sex and
strain of the animals also influence variability in response to TOCP
neurotoxicity and a clear no observed effect level has not been established.
In a 10-week study in hens, aviation engine oil
formulations containing 1% or 3% TCP were administered by oral gavage at a dose
2 g/kg/day. Hens receiving oil with 3% TCP showed significant neurotoxicity in
the form of ataxia, 77% inhibition of NTE activity, and microscopic lesions of
the nervous system, whereas axonal degeneration was minimal in hens given oil
with 1% TCP (Freudenthal et al., 1993). In another study, 1 g/kg/day of jet
engine lubricant containing 3% TCP was administered to adult hens by gavage for
up to 13 weeks, with a dose of 7.5 mg/kg TOCP used as a positive control. After
6 and 13 weeks, there were no clinical or histopathological signs of
neurotoxicity in the lubricant-treated animals, although NTE activity was
decreased by 32% at week 13 (Daughtrey et al., 1996).
The
neurotoxicity of jet engine oil containing TCP has been reviewed in a recent
paper from Mobil Business Resources Corporation and Mobil Technology Company
(Mackerer et al., 1999). The paper states that although it has been known for
many years that TCP contains neurotoxic components, lubricant formulators have
been reluctant to replace the additive because of its excellent performance in
critical applications. However, manufacturers have taken steps to lower the
level of ortho-cresyl isomers in TCP. When current standard grades of TCP were
hydrolysed and analysed for content of phenolic compounds they were found to
contain 0.36-1.7% of ortho-substituted phenolic compounds and 0.08-0.27%
ortho-cresol. By comparison, a so-called low-toxicity grade TCP now used in
certain jet oils contained 0.15-0.61% of ortho-substituted phenolic compounds
and 0-0.04% ortho-cresol. In oral bioassays for NTE inhibition, the potency of
low-toxicity grade TCP was about 1/10 of the average potency of standard grades
of TCP.
In reproductive toxicity studies in rats and mice,
TOCP has been shown to cause histopathological damage to the testes and
ovaries, morphological changes in sperm, decreased fertility in both sexes, and
decreased litter size and viability, again without a clearcut no observed
effect level. In a continuous breeding study in rats, oral administration of
TCP free of any detectable TOCP at a dose of 400 mg/kg/day caused a significant
decrease in fertility index, number of litters born and number of pups per
litter, reaching 100% infertility after 41 days of exposure (Latendresse et
al., 1994). A cross-over mating experiment showed that this was due to an
effect on male rather than female fertility. At necropsy after 63 days of
exposure, both sexes had a significant decrease in body weight and an increase
in adrenal gland and liver weights. Testicular and epididymal weights were
significantly decreased in male rats, whereas female rats had increased ovarian
weights.
There is no record of developmental toxicity. No
evidence of genetic toxicity in vitro
or of carcinogenicity in rats and mice was found in studies conducted by the US
National Toxicology Program (NTP, 1994).
Human health effects
There
are numerous case reports of human poisoning with TCP as a result of ingestion
of adulterated or contaminated beverages, foods or drugs (IPCS, 1990). In some
cases, transient gastro-intestinal symptoms such as nausea, vomiting and
diarrhoea have occurred shortly after the ingestion, whereas the neurological
symptoms are characteristically delayed and persistent. Initially, there are
pain and paraesthesia in the lower extremities, with a mild impairment of
cutaneous sensations and, at times, of vibratory sense. Muscle weakness may
progress to paralysis of the lower extremities, with or without an involvement
of the upper extremities. Recovery can be extremely slow and extend over a
number of months or years.
Nerve
biopsies show axonal degeneration. Erythrocyte cholinesterase activity is
reduced by about 50% shortly after the onset of the neurological symptoms,
whereas plasma cholinesterase activity is increased.
There
is a marked inter-individual variability in the susceptibility to TCP
poisoning, with severe symptoms reported after the ingestion of 0.15 g in one
person while other individuals were not affected after ingesting 1-2 g.
Neurological
symptoms have also been reported in a limited number of workers exposed to TCP
or TOCP by skin contact or inhalation.
Hazard classification
In the NOHSC Designated
List of Hazardous Substances (NOHSC, 1999b), TCP isomers containing at
least one ortho-cresyl moiety are classified as toxic and assigned risk phrases
R23/24/25 (Toxic by inhalation, in contact with skin and if swallowed) and R39
(Danger of very serious irreversible effects). TOCP is also listed in the NOHSC
Exposure Standards for Atmospheric
Contaminants in the Occupational Environment (NOHSC, 1995a) with an
exposure standard of 0.1 mg/m3 (8-h time-weighted average) and a
‘skin notation’.
4.2 4,4’-Dioctyldiphenylamine (DODPA)
Physico-chemical properties
DODPA
is a light tan powder with a melting point of 80-90ºC which is used as an
antioxidant for lubricants, plastics and rubbers (HSDB, 1999).
Kinetics and metabolism
There
are no studies on kinetics and metabolism.
Toxicity in laboratory animals
According
to an industry review (Anon., 1990), DODPA is of low acute toxicity and no skin
irritation or sensitisation has been reported, although the chemical is
slightly irritating to the eye. A number of in
vitro and in vivo tests for
genetic toxicity have been inconclusive. There are no studies on subchronic or
chronic toxicity, carcinogenicity or reproductive toxicity.
Human health effects
There
are no reports of adverse health effects in humans.
Hazard classification
DODPA is not on the NOHSC Designated List of Hazardous Substances (NOHSC, 1999b).
4.3 Phenyl-alpha-naphtylamine (PAN)
Physico-chemical properties
PAN
is a slightly yellowish crystalline material, which melts at 62-63ºC and boils
at 335ºC (at 528 mm Hg) (CRC, 1985). The chemical is combustible and decomposes
on burning producing toxic fumes including nitrogen oxides (IPCS, 1993). It is
used as an antioxidant.
Kinetics and metabolism
In the rat, orally administered PAN is absorbed,
extensively metabolised and excreted primarily with faeces within 48 h (German
Chemical Society, 1993). According to its International Chemical Safety Card
(IPCS, 1993), PAN can also be absorbed by inhalation of aerosols and through
the skin. Hydroxylated metabolites may be excreted in the urine as glucuronides
or sulfates.
Toxicity in laboratory animals
According to a review by the German Chemical Society
(1993), the acute toxicity of PAN is low, with a slight methaemoglobinaemia
being a characteristic sign of intoxication. In standard tests, PAN is slightly
irritating to the skin and eye and has the potential to sensitise the skin.
There are no adequately conducted chronic or reproduction toxicity or
carcinogenicity studies. It was positive in one in vitro test for mutagenicity, but this has not been confirmed in vivo.
Human health effects
PAN
is not a skin irritant in humans, but has been associated with cases of
allergic contact dermatitis (German Chemical Society, 1993).
Hazard classification
PAN
is not on the NOHSC Designated List of
Hazardous Substances (NOHSC, 1999b).
4.4 Phenyl-beta-naphtylamine (PBN)
PBN
is declared as an ingredient in Mobile Jet Oil II in a MSDS from 1992, whereas
in MSDS from 1998-99 the only
phenyl-naphtylamine listed is PAN. Given the properties of PBN described below,
it is conceivable that the manufacturer has replaced PBN with PAN some time
between 1992 and 1998.
Unless otherwise indicated, the properties of PBN
described below are summarised from the peer-reviewed international assessments
published by the International Agency for Research on Cancer (IARC, 1978, 1987).
Physico-chemical properties
PBN
is a gray to tan flaky or powdery solid, which melts at 185ºC and boils at
395ºC. Commercial grades contain BNA as an impurity in an amount which nowadays
is in the order of 1 ppm (1 mg/kg) (NTP, 1988). It was formerly used
extensively as an antioxidant in rubber processing, greases and lubricating and
transformer oils.
Kinetics and metabolism
Rats do not metabolise PBN to BNA (NTP, 1988). In
dogs administered labelled PBN, more than 90% of the radioactivity was excreted
over 3 days, mainly in the faeces. Only 2.8% of the radioactivity was excreted
in the urine, which was found to contain small amounts of BNA, indicating the
transformation of PBN to BNA by removal of the N-phenyl group. There is some
evidence from a study in human volunteers that up to 0.03% of a single 10 mg
dose of PBN is converted to BNA.
Toxicity in laboratory animals
The
acute toxicity of PBN is low. In rats, chronic oral administration causes
weight loss, CNS depression, disturbances of liver function, nephropathy and
impairment of reproductive function. In a 2-week inhalation study in rats,
there was weight loss and emphysema. Reproductive toxicity studies are not
available. PBN is not mutagenic in bacterial test systems. The chemical has
been tested for carcinogenicity by oral administration in mice, rats, hamsters
and dogs. Most experiments were negative, although tumours were found in the
liver, kidney or lung in some studies.
Human health effects
There
are some epidemiological studies of the occurrence of bladder cancer in workers
exposed to PBN. The evidence is inconclusive and according to the IARC there is
inadequate evidence for carcinogenicity of PBN in humans (IARC, 1987). The chemical
has been associated with cases of both irritant and allergic contact dermatitis
in humans (HSDB, 1999).
Hazard classification
In the NOHSC Designated
List of Hazardous Substances (NOHSC, 1999b), PBN is classified as a
carcinogen in Category 3[1]
and as an irritant and assigned risk phrases R36/38 (Irritating to eyes and
skin), R40 (Possible risks of irreversible effects) and R43 (May cause
sensitisation by skin contact). The chemical is listed in the NOHSC Exposure Standards for Atmospheric
Contaminants in the Occupational Environment (NOHSC, 1995a) as a carcinogen
in Category 2 (probably carcinogenic in humans) without an exposure limit but
with a recommendation to control exposure to the lowest practicable level.
4.5 Alpha-naphtylamine (ANA)
Unless otherwise indicated, the data summarised
below were obtained from the peer-reviewed
international assessments published by the International Agency for
Research on Cancer (IARC, 1978, 1987).
Physico-chemical properties
ANA is a colourless crystalline material which
darkens in air to a purple red colour. It has a weak ammonia-like odour. It has
a melting point of 50ºC and boils at 301ºC. It is used as a chemical
intermediate in the preparation of a large number of compounds, including PAN.
Commercial preparations of ANA contain small amounts of BNA as an impurity.
Kinetics and metabolism
In
rats and humans, ANA is metabolised by ring hydroxylation followed by excretion
in the urine as glucuronide and sulfate conjugates (HSDB, 1999). Contrary to
BNA, ANA does not undergo N-oxidation.
Toxicity in laboratory animals
The acute toxicity of ANA is
low, with a slight methaemoglobinaemia being a characteristic sign of
intoxication (HSDB, 1999). ANA is mutagenic in bacteria, whereas findings in
mammalian in vitro systems and in Drosophila have been inconclusive. No
carcinogenic effect was observed following oral administration to hamsters or
dogs, whereas results were inconclusive after oral administration to adult mice
and after subcutaneous injection of newborn mice.
Human health effects
There
are some epidemiological studies of the occurrence of bladder cancer in workers
exposed to PBN. However, in view of the contamination of the commercial product
with BNA and the mixed nature of the exposures concerned, the evidence is
inconclusive and according to the IARC there is inadequate evidence for
carcinogenicity of PBN in humans (IARC, 1987).
Hazard classification
In the NOHSC Designated
List of Hazardous Substances (NOHSC, 1999b), ANA is classified as harmful
and assigned risk phrase R22 (Harmful if swallowed).
4.6 Beta-naphtylamine (BNA)
Unless
otherwise indicated, the data summarised below were obtained from the peer-reviewed international assessments
published by the International Agency for Research on Cancer (IARC, 1978,
1987).
Physico-chemical properties
BNA
is a colourless crystalline material with a faint aromatic odour. In air it
darkens to a reddish-purple colour. It has a melting point of 111-113ºC and
boils at 306ºC. In the past, BNA was used as an intermediate in the manufacture
of dyes and antioxidants. It is now a prohibited carcinogenic substance, but is
present in small amounts as an impurity in a number of other chemicals,
including but not limited to PNA and ANA.
Kinetics and metabolism
Numerous
hydroxylated metabolites of BNA have been identified in the urine of rats,
rabbits, dogs and monkeys, including N-hydroxy and nitroso metabolites which
have been demonstrated to be the direct carcinogens of BNA.
Toxicity in laboratory animals
The acute toxicity of BNA is low, with a slight
methaemoglobinaemia being a characteristic sign of intoxication (HSDB, 1999).
BNA forms adducts with DNA in bladder and liver cells of dogs in vivo and is mutagenic in bacteria and
genotoxic in a number of mammalian in
vitro and in vivo test systems.
Following oral administration, BNA consistently induces bladder cancer in
hamsters, dogs and non-human primates, and liver tumours in mice.
Human health effects
A
number of human case reports and epidemiological studies have shown that
occupational exposure to BNA, either alone or as an impurity in other
compounds, is causally associated with the occurrence of bladder cancer. As
such, BNA is classified by IARC as a confirmed human carcinogen (IARC, 1987).
Hazard classification
In the NOHSC Designated
List of Hazardous Substances (NOHSC, 1999b), BNA is classified as a
Category 1[2]
carcinogen and assigned risk phrases R45 (May cause cancer) and R22 (Harmful if
swallowed). Under the NOHSC National
Model Regulations for the Control of Scheduled Carcinogenic Substances
(NOHSC, 1995b), BNA is a prohibited carcinogenic substance which shall not be
used for any purpose other than for bona fide research or analysis or where an
exemption to use the substance has been granted by the relevant public
authority.
4.7 Discussion and conclusions
In
the NOHSC Designated List of Hazardous
Substances (NOHSC, 1999b), TCP containing at least one ortho-cresyl moiety
is classified as toxic, PBN as possibly carcinogenic, ANA as harmful, and BNA
as a carcinogen in Category 1. Since PBN is a possible carcinogen because of
its content of BNA as an impurity, it can be concluded that according to the
Designated List the most hazardous additives listed as ingredients in Mobil Jet
Oil II are TCP and BNA.
The
toxicity of TCP is due to the presence of small amounts of isomers containing
the ortho-cresyl moiety such as tri-ortho-cresyl phosphate; ortho, ortho,
meta-tricresyl phosphate; ortho, ortho, para-tricresyl phosphate; ortho, meta,
meta-tricresyl phosphate; ortho, meta, para-tricresyl phosphate; and ortho,
para, para-tricresyl phosphate. The exact quantity of these toxic isomers in
Mobil Jet Oil II is not known, but levels of 0.36-2% have been reported for
some commercial grades of TCP (HSDB, 1999; IPCS, 1990; Mackerer, 1999). Since
Mobil Jet Oil II contains about 3% TCP, the maximum content of TOCP is unlikely
to exceed 0.06%. In humans, short-term exposure to toxic isomers of TCP may
cause acute gastrointestinal symptoms and signs of delayed neurotoxicity.
BNA
may be present as an impurity of PBN, usually at levels below 1 ppm. From the
MSDS provided to NICNAS, it appears that Mobile Jet Oil II no longer contains
PBN which seems to have been replaced by PAN. PAN may contain small quantities
of ANA (which is declared on the label) which in turn may be contaminated with
BNA. BNA may cause bladder cancer in humans upon repeated exposure for
substantial lengths of time.
5. Products of combustion
Investigations
conducted by the US Air Force and Navy have shown that some synthetic gas
turbine and jet engine lubricants have the potential to form a potent
neurotoxin under extreme conditions of thermal degradation (Centers, 1992;
Wyman et al., 1993). The toxin, trimethylolpropane phosphate (TMPP), is formed
by the reaction of TCP with trimethylolpropane esters in the lubricant
basestock at temperatures between 250-750°C, with a maximum 15% theoretical
yield in air at 550°C (Wright, 1996). These conditions do not occur under
normal or excessive use conditions, but TMPP formation has been demonstrated
from combustion or incineration of lubricants formulated with
trimethylolpropane esters and TCP (Rubey, 1996; Wyman, 1993).
In
mice and rats, TMPP has been shown to bind at the GABA-receptor and induce
clonic convulsions and death in 50% of the animals when injected
intra-peritoneally at dose levels of 1 mg/kg and from 50-100 mg/kg when applied
dermally (Centers, 1992). In laboratory animals, short-term exposure to TMPP at
doses that do not induce convulsions (for example, 0.1 mg/kg intra-peritoneally
once daily for 3-4 days) has been shown to induce acute anxiety and long-term
reductions of seizure thresholds as well as long-lasting changes in behaviour
(Bekkedal et al., 1998).
6. Hazard of the product as a whole
In
the available MSDS, it is stated that the “Worksafe classification” of Mobil
Jet Oil II is “not hazardous by Worksafe criteria”.
According
to the NOHSC Approved Criteria for
Classifying Hazardous Substances (NOHSC, 1999a), mixtures of chemicals can
be classified by one of two methods: the mixture can be tested and classified
as a whole, or it can be classified by consideration of the health effects of
each of its ingredients. By the latter method, based on the inclusion of some
of the additives of Mobil Jet Oil II in the NOHSC Designated List of Hazardous Substances (NOHSC, 1999b), the product
is not hazardous by the NOHSC Approved Criteria if the content of TOCP is lower
than 0.2%, the content of PBN is lower than 1%, the content of ANA is lower
than 25%, and the content of BNA is lower than 0.1%. Even if these
concentration limits are exceeded, the product could still be classified as
non-hazardous if this is the outcome of tests of the product as a whole
covering all of the end-points that determined the listing of its components in
the first place.
In
this context it should be noted that the toxicological profile of a product
containing two or more chemical ingredients is not necessarily the sum of the
toxicological profiles of the individual ingredients. The ingredients may interact
in the body, or, under certain circumstances, react with one another outside of
the body to form new chemicals that are more or less toxic than their
precursors. For example, synthetic lubricants containing TCP and
trimethylolpropane esters may form the potent neurotoxin TMPP when heated to
temperatures above 250°C. However, according to the importer, Mobil Jet Oil II
does not contain esters of trimethylolpropane (Mobil, 1999).
7. References[3]
*Anon. (1990) Dioctyldiphenylamin (abstract).
Heidelberg, Berufsgenossenschaft der chemischen Industrie.
*Bekkedal MYV, Panksepp J, Rossi J III (1998)
Long-term changes in rat social behavior following treatment with
trimethylolpropane phosphate. Neurotoxicology and Teratology, 20:307-316.
*Centers PW (1992) Potential neurotoxin formation in
thermally degraded synthetic ester turbine lubricants. Archives of Toxicology, 66:679-680.
*Daughtrey W, Biles R, Jortner B, Ehrich M (1996)
Subchronic delayed neurotoxicity evaluation of jet engine lubricants containing
phosphorous additives. Fundamental and Applied Toxicology, 32:244-249.
*Freudenthal
RI, Rausch L, Gerhart JM, Barth ML, Mackerer CR, Bisinger EC (1993) Subchronic
neurotoxicity of oil formulations containing either tricresyl phosphate or
tri-orthocresyl phosphate. Journal of the American College of Toxicology, 12:409-416.
*German
Chemical Society (1993) N-phenyl-1-naphtylamine (abstract). Stuttgart, S.
Hirzel Verlag.
HSDB
(1999) Hazardous substances data bank. Bethesda, MD, National Library of
Medicine.
IARC (1978) Some aromatic amines and related nitro
compounds – hair dyes, colouring agents and miscellaneous industrial chemicals.
IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man,
volume 16. Lyon, International Agency for Research on Cancer.
IARC (1987) Overall evaluations of carcinogenicity:
an updating of IARC Monographs volumes 1 to 42. IARC Monographs on the
Evaluation of the Carcinogenic Risk of Chemicals to Man, supplement 7. Lyon,
International Agency for Research on Cancer.
IPCS (1990) Tricresyl phosphate. Environmental
Health Criteria 110. Geneva, World Health Organization.
*IPCS (1993) International chemical safety card:
N-phenyl-1-naphtylamine. Http://www.cdc.gov/niosh/ipcs/
ipcs1113.html.
*Latendresse JR, Brooks CL, Flemming CD, Capen CC
(1994) Reproductive toxicity of butylated triphenyl phosphate and tricresyl
phosphate fluids in F3444 rats. Fundamental and Applied Toxicology, 22:392-399.
*Mackerer
CR, Barth ML, Krueger AJ, Chawla B, Roy TA (1999) Comparison of neurotoxic
effects and potential risks from oral administration or ingestion of tricresyl
phosphate and jet engine oil containing tricresyl phosphate. Journal of
Toxicology and Environmental Health, 56:293-328.
*Mobil (1999) Letter dated 3 September 1999 from JC
Plummer, Manager, Aviation Lubricant Sales, Mobil Oil Australia Ltd.
*NIOSH
(1994) NIOSH manual of analytical methods, 4th ed. Cincinnati, OH, National
Institute of Occupational Safety and Health.
NOHSC
(1995a) Exposure standards for atmospheric contaminants in the occupational
environment. Canberra, ACT, Australian Government Publishing Service.
NOHSC
(1995b) National model regulations for the control of scheduled carcinogenic
substances. Canberra, ACT, Australian Government Publishing Service.
NOHSC
(1999a) Approved criteria for classifying hazardous substances. Sydney,
National Occupational Health and Safety Commission.
NOHSC
(1999b) List of designated hazardous substances. Sydney, National Occupational
Health and Safety Commission.
*NTP (1988) Toxicology and carcinogenesis studies of
N-phenyl-2-naphtylamine (CAS No. 135-88-6) in F344/N rats and B6C3F1 mice
(feed studies). Http://ntp-server.niehs.nih.gov/htdocs/LT-studies/tr333.html.
*NTP (1994) Toxicology and carcinogenesis studies of
tricresyl phosphate(CAS No. 1330-78-5) in F344/N rats and B6C3F1 mice
(gavage and feed studies).
Http://ntp-server.niehs.nih.gov/htdocs/LT-studies/tr433.html.
*Rubey WA, Stribich RC, Bush J, Centers PW, Wright
RL (1996) Neurotoxin formation from pilot-scale incineration of synthetic ester
turbine lubricants with a triaryl phosphate additive. Archives of Toxicology, 70:508-509.
*Wright RL (1996) Formation of the neurotoxin TMPP
from TMPE-phosphate formulations. Tribology Transactions, 39:827-834.
*Wyman J, Pitzer E, Williams F, Rivera J, Durkin A,
Gehringer J, Servé P, von Minden D, Macys D (1993) Evaluation of shipboard
formation of a neurotoxin (trimethylolpropane phosphate) from thermal
decomposition of synthetic aircraft engine lubricant. American Industrial
Hygiene Association Journal, 54:584-592.