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Accepted for publication, Environmental Research, 2001
THE TOXICITY OF COMMERCIAL JET
OILS
Chris Winder
1
and Jean-Christophe Balouet
2
1 Contact: Assoc Prof Chris Winder, School of Safety Science, University of New South Wales,
Sydney NSW 2052.
2 Jean-Christophe Balouet, Managing Director, Environment International, 31 Rue du General
Chanzy, 94130 Nogent sur Marne, France
Keywords: Jet Oils, Tricresyl phosphate, N-phenyl-1-naphthylamine, synthetic oils, oil exposure.
-2
-
Abstract
Jet oils are specialised synthetic oils used in high performance jet engines. The have
an appreciable hazard based on toxic ingredients, but are safe in use provided that
maintenance personnel follow appropriate safety precautions, and the oil stays in the
engine. Aircraft engines that leak oil may expose others to the oils through
uncontrolled exposure. Airplanes that use engines as a source of bleed air for cabin
pressurisation may have this source contaminated by the oil if an engine leaks.
Examination of the ingredients of the oil indicates that at least two ingredients are
hazardous: N-phenyl-1-naphthylamine (a skin sensitiser) and Tricresyl phosphate (a
neurotoxicant, if ortho-cresyl isomers are present). Publicly available information
such as labels and MSDS understates the hazards of such ingredients, and in the case
of ortho-cresyl phosphates, by several orders of magnitude.
-3
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Introduction
Some commercial jet oils have been in use as engine oils in aviation for decades. For
example, Mobil USA note that one of their products “Mobil Jet Oil II has been
essentially unchanged since its development in the early 1960s” and “most changes
have involved slight revisions of the ester base stock due to changes in raw material
availability”.
1
A complex approval process exists for ensuring that materials used in aviation are
manufactured to relevant standards, and the jet engine oil specification of the US Navy
MIL-PRF-23699 is used for jet oils. This process of approval and re-approval for new
product formulations has meant that there is some resistance to modifying
formulations (for example, for health and safety reasons).
Consequently, changing approved formulations is not conducted without significant
justification. In the case of the additive tricresyl phosphate (TCP), manufacturers have
been reluctant to modify product formulations by substituting toxic TCP additives that
perform well in critical applications. This has meant that potentially toxic products
have continued to be available long after their toxicity was recognised.
2
It is not known if an approved formulation containing, for example 3% tricresyl
phosphate, is considered a change in formulation if the proportion of individual
isomers in the TCP mixture is altered, but the 3% remains unchanged. However, as
Mobil indicate, only the base stock esters have been modified over the past thirty or so
years, suggesting that the mixture of isomers in TCP stock has not been changed.
3
Mobil USA notes that one of their jet oil products (Mobil Jet Oil II) has a market share
of 49%. With such a large market share, and the potential for significant exposure, it
would be appropriate to investigate this material in some detail.
Mobil Jet Oil II
Mobil Jet Oil II is a synthetic oil product imported into Australia. All product
worldwide is manufactured by one manufacturing facility in the USA. The product is
not labeled in accordance with Australian requirements under the Hazardous
Substances Regulation, but is assumed to comply by default.
4
This product is normally marketed in 0.946 L (1 US Quart) cans.
Ingredients
Various sources, such as the supplier's label on the cardboard box the cans are shipped
in, the product Material Safety Data Bulletin (MSDB), and information from Mobil
USA, lists the following ingredients:
synthetic esters based in a mixture of 95% C
5
-C
10
fatty acid esters of
pentaerythritol and dipentaerythritol;
3% tricresyl phosphate (Phosphoric acid, tris(methylphenyl) ester, CAS No
1330-78-5);
-4
-
1% phenyl-alpha-naphthylamine (PAN) (1-Naphthalenamine, N-phenyl, CAS
No 90-30-2);
Benzamine, 4-Octyl-N-(4-Octylphenyl), (CAS No 101-67-7);
a last entry "ingredients partially unknown" is also noted on some
documentation.
In Australia, classification of materials as being hazardous substances under the
Hazardous Substances Regulation use a list of hazardous substances
5
and approved
criteria,
6
with reference to the list being the primary step. Of the ingredients in Mobil
Jet Oil II, the most toxicologically significant ingredients are:
N-phenyl-alpha-naphthylamine, which can contains a number of contaminants
in trace amounts, including N-phenyl-beta–naphthylamine (135-88-6), 1-
Naphthylamine (CAS No 134-32-7) and 2-Naphthylamine (CAS No 91-59-8);
and
Tricresyl phosphate, a blend of ten tricresyl phosphate isomer molecules
(including tri-ortho-cresyl phosphate), plus other structurally similar
compounds, including phenolic and xylenolic compounds.
There are a number of issues relevant to these ingredients, outlined below.
N-Phenyl-1-naphthalenamine
Chemistry
N-Phenyl-1-naphthylamine, (CAS No 90-30-2), also known as Phenyl-alpha-
naphthylamine (PAN), is a lipophilic solid used as an antioxidant used in lubrication
oils and as a protective agent in rubber products. In these products, the chemical acts
as a radical scavenger in the auto-oxidation of polymers or lubricants. It is usually
used in these products at a concentration of about 1%.
The commercial product has a typical purity of about 99%. Named impurities are: N-
Phenyl-2-naphthylamine (CAS No 135-88-6, 500 to below 5000 ppm), 1-
Naphthylamine (below 100-500 ppm) and 2-Naphthylamine (below 3 to 50 ppm),
aniline (below 100 to 2500 ppm), 1-naphthol (below 5000 ppm), 1,1-dinaphthylamine
(below 1000 ppm) (see Figure below).
7
-5
-
Figure -1: Possible Contaminants in N-Phenyl-1-naphthylamine
NH
NH
2
OH
N
H
2
NH
2
NH
NH
N-Phenyl-2-naphthylamine2-Naphthylamine1-Naphthylamine
1-Naphthol
Aniline
1,1-Dinaphthylamine
2-Naphthylamine (CAS No 91-59-8) is also known as the established carcinogen β-
Naphthylamine.
8
Similarly 1-Naphthylamine is also known as α-Naphthylamine.
The formulation concentration of N-Phenyl-1-naphthalenamine in Mobil Jet Oil II is
about 1%. As ingredients such as the naphthylamines have been deleted from product
documentation such as the MSDB, the level of contamination of naphthylamines is
presumed to be below the concentration cut off values for disclosure of Category 1
carcinogens specified in the Approved Criteria for Classifying a Hazardous Substance
of 0.1% (1000 ppm).
6
Indeed, information from Mobil Australia notes that the level of contamination of
some of the contaminants in this material is partially known (50 ppm for N-Phenyl-2-
naphthylamine; 0.5 ppm for 2-Naphthylamine), and that they stopped listing such
ingredients in about 1992 “solely to a reassessment of what was considered meaningful
information from a hazard communication perspective”.
9
2-Naphthlyamine is not listed on the 1992 Australian inventory of Chemical
Substances (AICS),
10
and dependent on the amount present in the formulated product
(0.2%), could technically breach the requirements of the Commonwealth Industrial
Chemicals (Notification and Assessment) Act 1989. However, the probable
concentration of this contaminant in Mobil Jet Oil II is too low to exceed requirements
of this legislation. Further, this chemical is listed as a prohibited substance under the
Australian Hazardous Substances Regulation.
Toxicology
PAN is readily absorbed by mammalian systems and rapidly converted to
metabolites.
11
Both urine and feces appear to be the main routes of excretion.
12
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-
By single dosing, PAN does not seem particularly toxic, with LD
50
s above 1 g/kg. The
chemical has a similar mechanism of toxicity of many aromatic amines, of
methaemoglobin production. PAN is not irritating in primary skin and eye irritation
studies. However, in a guinea pig maximisation test, PAN was shown to be a strong
skin sensitiser.
13
This result is supported by case studies in exposed workers.
14,15
At
the concentration used (1%), Mobil Jet Oil II is classified as a hazardous substance in
Australia for its sensitisation properties.
6
Most genotoxicity studies report negative results, suggested little genotoxicity
potential.
12
Most repeated dose toxicological studies focus on its potential carcinogenicity. An
experimental study, using both PAN and the related compound N-phenyl-2-
naphthalenamine administered subcutaneously to mice found a heightened incidence
of lung and kidney cancers.
16
While the methodology used in this study makes
evaluation of the results problematic (use of one gender, small sample sizes, limited
number of dose groups, subcutaneous administration as an inappropriate route of
exposure, and so on). A high incidence of various forms of cancer was also found
among workers exposed to antirust oil containing 0.5% PAN.
17
While these animal
and human results offer only limited information, they are at least supportive of a mild
carcinogenic effect.
This must be contrasted with the results of long term carcinogenicity bioassays in rats
and mice conducted by the US National Toxicology Program with the structurally
related N-phenyl-2-naphthylamine (studies were not carried out on PAN), which have
not reported any carcinogenic potential for this chemical.
18
Regulatory Classification
PAN is not listed on the NOHSC Designated List of Hazardous Substances.
However, the NOHSC Approved Criteria for Classifying Hazardous Substances
6
note
that mixtures containing sensitisers should be classified as an “Irritant” hazardous
substance if included in the product at a concentration at or greater than 1%. Further, a
product containing a skin sensitiser at or above this value should carry risk statement
R43 – May cause skin sensitisation by skin contact.
The data on carcinogenicity of PAN is too limited to make a determination sufficient
to allow classification for regulatory purposes.
Nevertheless, based on established sensitisation properties and possible carcinogenic
properties, exposure to materials containing N-phenyl-1-naphthylamine should be
avoided.
Tricresyl phosphate
Phosphoric acid, tris(methylphenyl) ester (CAS No 1330-78-5) is better known as
Tricresyl phosphate (TCP) or Tri-tolyl phosphate.
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Chemistry of the Cresols and Tricresyl phosphate
Industrial manufacture
TCP is a molecule comprised of three cresyl (methylphenyl) groups linked to a
phosphate group. Cresol is an aryl structure comprising a hydroxyl (-OH) and methyl
(CH
3
) group attached to a benzene molecule. Industrial cresol is a mixture of three
isomers, ortho- para- and meta-cresol molecules in varying concentrations. The ortho-,
meta- or para- prefixes denote how far apart the hydroxyl and methyl groups are on the
cresol molecule (see Figure below).
Figure-2: Structure of Tricresyl Phosphate
O P O
O
O
CH
3
CH
3
CH
3
para
meta
ortho
TCP molecule showing designation of o, m and p cresyl groups
OH
CH
3
OH
CH
3
OH
CH
3
-
OPO
-
O
-
O
O P O
O
O
CH
3
CH
3
CH
3
o-Cresol m-Cresol p-Cresol Phosphate Tricresyl phosphate
Industrially, the chemical is made by reaction of phosphorus oxychloride (POCl
3
) with
industrial cresol.
Commercial grade TCP is a complex mixture of structurally related compounds, some
of which are known to have neurotoxic properties. These are produced from the ortho-
alkyl substituted phenols or xylenol present in the manufacturing process. ortho-
methyl phenols (cresol) or ortho-ethyl phenols lead to toxic components, whereas
ortho-substituted xylenols do not.
19
Initially, TCP contained high levels of all isomers. The neurotoxic potential of the
ortho-cresyl isomers, most notably tri-ortho-cresyl phosphate (TOCP), was recognised
quite early.
20
Indeed much research has been carried out on the toxicity of TOCP,
presumably on the basis that as it had three cresyl groups, it must be more toxic than
molecules with less.
There have been substantial modifications of TCP containing materials. Earlier TCP
products, such as “torpedo oil” used in World War II, were highly toxic, containing
perhaps 25-40% ortho-cresol. Notably, this product was more toxic than TOCP
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-
itself.
21
This is a critical finding, because it meant that the conventional view that the
toxicity of TCPs was correlated to their tri-ortho-cresyl content was incorrect. The
presence of other ortho-cresyl containing molecules (not just TOCP) needs
consideration in evaluating the overall toxicity of TCP.
Manufacturers reduced the levels of ortho-cresyl and ortho-ethylphenyl isomers to
reduce the potential for neurotoxicity. Changes to the phenolic mixture used to
manufacture TCP, introduction of processing alternatives and improved purification
methods all assisted in reducing ortho-cresol content. By the 1950s, commercially
available TCP contained about 3% ortho-cresol isomers. Further refinements in the
1980s to 1990s have decreased the ortho-cresol content further. How much these
refinements had removed the toxic impurities outlined above is not known. Indeed,
toxicity was still being detected in commercially available products in 1988.
2
It is difficult to obtain data on the amount of TOCP contamination in commercially
available materials now being marketed world-wide containing TCP. However,
conservative estimates of about 0.1-1% (1,000-10,000 ppm) seem realistic. This
suggests that a product containing 3% TCP would contain about 0.003-0.03% TOCP
(30-300 ppm). The “new generation” materials are claimed to have an even lower
TOCP content, although data on content is sparse.
2
Importantly however, is that the
focus of attention on the toxicity of TOCP has masked the study of the toxic potential
of other orthocresyl isomers. Further, work by Henschler and colleagues in the 1950s
(published, but published in German) was not reconsidered until the 1990s.
Typically, jet turbine engine oils are formulated with about 3% TCP. This includes
Mobil Jet Oil - 3% TCP is stated on MSDB, and is supported by data published in
elemental analyses,
22
where a Mobil Jet Oil was shown to contain 0.29% Phosphorus,
which extrapolates to about 3.5% organophosphate.
Uses of TCP
TCP has been a commercially useful material, and has been used as a plasticiser,
lubricant, hydraulic fluid, paint additive, oil additive, dust suppressant and so on.
23,24
Most commercial uses have now ceased.
In jet oil, TCP is used in the formulation of lubricants as an anti-wear additive to
enhance load bearing properties and improve tolerance to increasing speed of rotating
or sliding motion. It also has flame retardant properties. While some other triaryl
phosphates have similar properties and may also be used as oil additives, the anti-wear
properties of TCP are considered unique. For example, pure tri-para-cresyl phosphate
is considered to have poorer lubricating properties than commercial TCP.
2
Isomers of TCP
Generally, the chemical known as TCP comprises a mixture of unspecified ortho-
para- and meta-cresol molecules (as cresyl groups, see above), which can be formed
into a number of separate structures with similar chemical formulas (isomers).
Technically, there are ten possible tri-cresyl phosphate structures (see below).
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-
Figure-3: Possible Isomers of Tricresyl phosphate
o,m,p
o,o,o
o,o,p
o,o,m
o,m,m
m,m,m m,m,p
m,p,p
p,p,p
o,p,p
o ortho-cresyl group
m meta-cresyl group
p para-cresyl group
ortho-cresyl group containing molecules
are highlighted in bold
The structures of the ten different
isomers are shown below.
Figure -4: Possible Tricresyl phosphate Structures
ortho- ortho- Ortho- ortho- ortho- meta-
O P O
O
O
CH
3
H
3
C
CH
3
O P O
O
O
CH
3
CH
3
CH
3
tri-ortho-cresyl phosphate di-ortho-meta-cresyl phosphate
ortho- para- ortho- ortho- para- meta- ortho- meta- meta-
O P O
O
O
CH
3
CH
3
CH
3
O P O
O
O
CH
3
CH
3
CH
3
O P O
O
O
CH
3
CH
3
CH
3
di-ortho-para-cresyl phosphate ortho-para-meta-cresyl phosphate ortho-di-meta-cresyl phosphate
ortho- para- para- meta- para- para- para- para- para-
O P O
O
O
CH
3
CH
3
CH
3
O P O
O
O
CH
3
CH
3
C
H
3
O P O
O
O
CH
3
CH
3
C
H
3
ortho-di-para-cresyl phosphate meta-di-para-cresyl phosphate tri-para-cresyl phosphate
meta- meta- meta- meta- meta- para-
O P O
O
O
C
H
3
CH
3
CH
3
O P O
O
O
CH
3
C
H
3
CH
3
tri-meta-cresyl phosphate Para-di-meta-cresyl phosphate
The different isomers of TCP have different properties, and indeed, different toxicities.
Most notably, tri-orthocresyl phosphate (TOCP) is a well established neurotoxicant
(see below).
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-
TCP Nomenclature
Describing Tricresyl phosphate isomers chemically can be a complicated task.
However, the Chemical Abstracts Service (CAS) has simplified this process by
allocating four unique identifying CAS registry numbers to Tricresyl phosphate
mixtures. These are listed on the Australian Inventory of Chemical substances:
10
CAS No 1330-78-5 Phosphoric acid, tris(methylphenyl) ester (C
21
H
21
O
4
P),
which denotes Tricresyl phosphate (unspecified cresyl groups);
CAS No 78-30-8 Phosphoric acid, tris(2-methylphenyl) ester (C
21
H
21
O
4
P),
which denotes Tricresyl phosphate (containing ortho-cresyl groups);
CAS No 563-04-2 Phosphoric acid, tris(3-methylphenyl) ester (C
21
H
21
O
4
P),
which denotes Tricresyl phosphate (containing para-cresyl groups);
CAS No 78-32-0 Phosphoric acid, tris(4-methylphenyl) ester (C
21
H
21
O
4
P),
which denotes Tricresyl phosphate (containing meta-cresyl groups).
In the past, disclosure of tricresyl phosphate ingredients in products containing this
chemical invariably used the nonspecific 1330-78-5 CAS number. Unfortunately, this
provides no information about the various isomers in the mixture.
In its classification systems for hazardous substances, the European Union (EU) has
introduced modifications of two of the CAS descriptions for tricresyl phosphate
chemicals, being:
CAS No 78-30-8 Tricresyl phosphate (containing o-o-o, o-o-m, o-o-p,
o-m-m, o-m-p, o-p-p isomers);
CAS No 78-32-0 Tricresyl phosphate (containing m-m-m, m-m-p,
m-p-p, p-p-p isomers).
The reason for this change was to discourage use of the general TCP mixture CAS
Number 1330-78-5 (which is proposed to be deleted), and encourage better disclosure
of ortho-cresyl containing mixtures. Newer documentation by jet oil manufacturers
suggests this has not yet happened, with the older 1330-78-5 CAS Number still in use
on product information. It can be argued that the continued use of the older 1330-78-5
number by industry indicates that they are ignorant of the changes at the EU level and
the implications of these changes for disclosure on labels and material safety data
sheets.
The new CAS numbers will assist in identifying those products that contain the toxic
ortho-cresyl ingredients. At the moment, it may be presumed that from a marketing
perspective, disclosure of the new CAS number that indicates the presence of ortho-
cresyl containing TCP in commercial products is undesirable, and therefore companies
are persisting with the older generic CAS number. From this, it may be assumed that
the absence of the non-ortho-cresyl containing TCP CAS number indicates that ortho-
cresyl groups are present in the mixture. This is further supported by the absence of
positive statements about the absence of ortho-cresyl containing isomers in TCP
products.
-11
-
The EU chemical names and numbers are listed in the Australian List of Designated
Hazardous Substances, which forms a major part of the classification of hazardous
substances under the hazardous substances regulations.
5
Suppliers of tricresyl
containing materials should be referring to the new CAS numbers and chemical
descriptions as soon as practicable. Further, a requirement to “state on the label
whether the substance is a specific isomer or a mixture of isomers” is included in the
List.
Toxicity of Tricresyl phosphates
Toxicology of the Organophosphates
Human toxicity to organophosphorus compound has been known at least since 1899,
when neurotoxicity to phosphocreosole (then used in the treatment of tuberculosis)
was reported.
25
The study of the toxicity is extensive, with two very well established mechanisms on
esterases and on neurotoxic esterases (NTE).
Poisoning with Organophosphates
The organophosphorus compounds are generally characterised by a toxicity of
inhibition of the esterase enzymes, most particularly cholinesterases
26
and neurotoxic
esterases.
27
The mechanism of effect is phosphorylation.
28
The effect is a specific
mechanism of organophosphate toxicity.
An organophosphorus molecule can be represented by the general structure:
R
3
P
O
R
1
R
2
Where P is the Phosphorus atom, O is an oxygen atom and R
1
-R
3
represents organic
structures that can give the molecule a wide range of properties.
Because cholinesterases break down endogenous choline esters, inhibition of these
enzymes produces an accumulation of levels of choline esters. Most critical of these
esters is acetylcholine, a neurotransmitter molecule released throughout the cholinergic
nervous system. Any organ or tissue that receives a cholinergic input will become
more active or excited if cholinesterases are not available to catalyse the breakdown of
acetylcholine. Indeed, cholinergic overstimulation produces most, if not all, of the
symptoms of poisoning from single and short term exposure to organophosphates.
Signs of low level intoxication include headache, vertigo, general weakness,
drowsiness, lethargy, difficulty in concentration, slurred speech, confusion,
emotional lability and hypothermia.
29
The reversibility of such effects has been
questioned.
30
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-
Signs of poisoning are usually foreshadowed by the development of early symptoms
related to acetylcholine overflow and include salivation, lacrimation, conjunctivitis,
visual impairment, nausea and vomiting, abdominal pains and cramps, diarrhoea,
parasympathomimetic effects on heart and circulation, fasciculations and muscle
twitches.
31
This is the basic site of inhibition for all OP molecules.
32,33
Organophosphate Induced Delayed Neuropathy (OPDIN)
There is a second reaction that leads to further neurotoxic and neuropathological
changes.
Inhibition of neurotoxic esterases (NTE) can lead to a neuropathological condition of
progressive neuronal damage, called organophosphorus induced delayed neuropathy
(OPIDN).
34,33
The mechanism of toxicity is now fairly well understood, as indeed are
the organophosphorus structures which are predicted to cause OPIDN.
35
Basically, all
OP molecules react with any -OH groups on the active site of the enzyme:
Enzyme-OH +
R
3
P
O
R
1
R
2
=
Enzyme-O P
O
R
1
R
2
The basic process is the initial phosphorylation of a group of esterases called the
neurotoxic esterases (NTE). This is followed by a second reaction of enzyme “aging”,
where the enzyme structure (or its microenvironment) was modified so that it can no
longer function properly. The basic mechanism is a break in the P-O-R bond, resulting
in a negatively charged P–O
-
group, and a free -R group. A determinant of toxicity is
the extent of inhibition of these enzymes, in that marked toxicity occurs after
inhibition of over 50%.
36
Several theories about the significance of these events in the development of OPIDN,
37
and a pathway of events have been proposed.
38
The likelihood of this reaction occurring is dependent on the molecular structure of the
OP molecule. Where either or both of the R
1
or R
2
groups are linked to the
phosphorus with a P-O-R bond (instead of a P-R bond), OPIDN can develop. These
OP structures are:
Enzyme-O P
O
O
R
2
R
1
E n zym e -O P
O
R
1
O
R
2
Enzyme-O P
O
O
O
R
1
R
2
The main classes of organophosphorus molecules that have the potential to cause
OPIDN are phosphates (two P-O-R bonds) and phosphonates (one P-O-R bond). A
further group known to cause OPIDN are the phosphoroamidates, where the oxygen in
the P-O-R bond is replaced by nitrogen (R-N-R).
-13
-
Where the OP molecule only contains P-R bonds, aging (and therefore delayed
neuropathy) will not occur. The main classes of organophosphorus molecules that
have these structures are the phosphinates.
39
Not all animal species are susceptible to developing OPIDN: for example, rodents are
not particularly sensitive
40
(although neurological damage can be produced in the
rat
41
). However, along with the cat
42
and chicken,
43,44
humans are considered to be
among the most sensitive species.
45
OPIDN is caused when the organophosphate molecule binds with NTE in the long
processes of the nerves (the axons). The enzymes have functions related to transport
of nutrients and energy molecules from the cell body to the end of the nerves.
Phosphorylation of such proteins results in localised disruption of axoplasmic
transport. If prolonged, these effects are followed by swelling of the axon, followed by
degeneration from the site of the damage to the end of the axon. If exposure continues,
this process can continue up the axon by the phosphorylation of more proteins.
Lesions are characterised by degeneration of axons followed by degeneration of the
cells that surround (and contribute to the insulation of the fibres) the myelin containing
support cells.
45
This effect can occur in sensory or motor nerves in either the central or
peripheral nervous systems.
46
Initially, the condition arises as a distal symmetrical
sensori-motor mixed peripheral neuropathy mainly affecting the lower limbs with
tingling sensations, burning sensations, numbness and weakness. In severe cases
paralysis may develop.
47
Longer nerves are affected more, probably because or their
requirements for active nutrient supply (shorter nerves may continue to get supplied
through passive mechanisms, such as diffusion). Regeneration is possible if exposure
ceases and damage is not too extensive.
48,37
The Intermediate Syndrome
OPIDN is severe. It is quite likely that such a severe condition would be presaged with
a range of clinical and pre-clinical signs and symptoms. These have been reported
extensively, and an “intermediate syndrome” was defined in 1987.
49
Symptoms of the
intermediate syndrome include: proximal limb paralysis, weakness of neck muscles,
inhibition of respiratory muscles and cranial nerve involvement. The mechanism of
effect is different from poisoning or OPIDN effects, and is considered to be due to the
effect of the organophosphate at the level of the neuromuscular synapses.
50
Chronic Organophosphate Neuropsychological Disorder (COPIND)
More recently, chronic exposure to organophosphates has been associated with a range
of neurological and neuropsychological effects.
51,52,53,54,55
Such symptoms (mainly
neurological and neurobehavioural symptoms) may also be seen in exposed individuals
who have been sufficiently fortunate in not having exposures that were excessive
enough in intensity or duration to lead to clinical disease.
A distinct condition - chronic organophosphate neuropsychological disorder
(COPIND) has been described, of neurological and neuropsychological symptoms.
56
These include:
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-
diffuse neuropsychological symptoms (headaches, mental fatigue, depression,
anxiety, irritability);
reduced concentration and impaired vigilance;
reduced information processing and psychomotor speed;
memory deficit and linguistic disturbances;
COPIND may be seen in exposed individuals either following single or short term
exposures leading to signs of toxicity,
52
or long term low level repeated exposure with
(often) no apparent signs of exposure.
54
The basic mechanism of effect is not known,
although it is not believed to be related to the esterase inhibition properties of
organophosphorus compounds. It is also not known if these symptoms are permanent.
Toxicology of TCP and TOCP
Much of the early study of OPIDN was investigated not just with organophosphorus
compounds, but with the tricresyl phosphates
57,58
following outbreaks of poisoning
after accidental or criminal adulteration of food or beverages with TCP containing
products. A large literature is now available on the toxicity of the tricresyl phosphates
(most particularly, TOCP) and the basic mechanisms are well established.
59
TCP
produces acute poisoning based on cholinesterase inhibition, and a well defined
syndrome of neurological degeneration (either from short term or long term repeated
dose exposure). As well as affecting the nervous system, TCP also has toxic effects in
the adrenal glands, ovaries and testes.
60
TCP is also known to be a skin irritant and to
cause allergic dermatitis.
59
Neurotoxicity has been reported in TCP manufacture.
61
The toxic effects of oils
containing TCP have also been long recognised.
62
The toxic properties of tri-ortho-cresyl phosphate have been recognised for decades,
and the presence of this isomer in products containing TCP presents a significant
occupational health problem. Further, as noted above, there are five other orthocresyl
phosphate isomers:
two di-ortho-cresyl phosphates (di-ortho-mono-meta-cresyl phosphate or o-o-m
and di-ortho-mono-para-cresyl phosphate or o-o-p); and
three mono-ortho-cresyl phosphates that contain only one ortho-cresyl group
but various combinations of meta-cresyl and para-cresyl groups
(o-p-p, o-p-m, o-m-m).
These mono- and di- ortho-tricresyl phosphates are reported to have measurable
toxicities similar to the neurotoxicity produced by TOCP.
Other ortho-cresyl containing ingredients
Tricresyl phosphate will also contain mixed esters of orthophosphoric acid with
different cresyl radicals, of the mono- and di-cresyl types.
-15
-
Other contaminants, such as ortho containing di-cresyl phosphates may also be toxic.
Further, mono-ortho-cresyl-diphenyl phosphate (that is, an organophosphate molecule
with one cresyl group only (see below) appears to be the most toxic molecule of all.
21
O P O
O
O
C
H
3
Mono-ortho-di-phenyl phosphate
Further, other ortho-containing molecules, such as 2,3-Tri-xylenyl phosphate and 2,4-
Tri-xylenyl phosphate, are weakly neurotoxic (this is a cresyl molecule with an extra
methyl group, the 2- indicates the ortho- position, see below).
19
Possible Tri-xylenyl phosphate Structures
O P O
O
O
C
H
3
H
3
C
CH
3
C
H
3
CH
3
C
H
3
O P O
O
O
CH
3
CH
3
C
H
3
CH
3
CH
3
CH
3
2,3-Tri-xylenyl phosphate 2,4-Tri-xylenyl phosphate
Other trixylenyl phosphates, such as 2,5, 2,6, 3,4 and 3,5 were not neurotoxic.
Still other impurities, such as triphenyl phosphate, di-phenyl-mono-cresyl- phosphate,
di-phenyl-mono-xylenyl phosphate and tri-xylenyl phosphate may also be neurotoxic.
The presence of structures with methyl groups adjacent to the ester –O-P bond, needs
consideration in evaluating the overall toxicity of TCP.
Recent research has focused on identifying a dose response relationship for TOCP.
Results of a short term repeated dose study in hens of aviation engine oil containing
various amounts of commercial TCP suggest that oil containing 1% TCP (a TCP
equivalent of 20 mg/kg/day) was considered a no observable effect level.
63
Similar
findings were reported in a later study.
64
Finally, it is generally assumed that most exposure to TOCP is by the inhalational
route (ingestion is unlikely for persons not directly handling this material). However,
absorption through skin exposure should not be discarded, as significant exposure
(maximally estimated at a transdermal flux rate of 0.01 mg/cm
2
/hr) through this route
is possible.
65
Relative Toxicity of the ortho-Cresyl Containing Tricresyl phosphate Isomers
The ten isomers that make up TCP are toxicologically different, and it is well
established that the ortho containing isomers are the most toxic. Much research in the
past has concentrated on the tri-orthocresyl phosphate isomer (TOCP), which has
-16
-
shown to be associated with organophosphate induced delayed neuropathy (OPIDN).
TCP manufacturers have expended considerable energy in reducing levels of TOCP in
commercial grades of TCP.
However, what is less well known is that there are other ortho containing isomers
in TCP, three mono-ortho (MOCP) isomers and two di-ortho (DOCP) isomers.
These are not specified in mandated lists of hazardous chemicals, and this may be
one reason why they are not disclosed on labels and MSDS.
All these compounds are neurotoxic in the same way as TOCP - however they are
known to be more neurotoxic. For instance the DOCPs are five times more toxic,
and the MOCPs ten time more toxic, than TOCP.
19,21
The total toxicity of a
particular mixture is therefore dependent on consideration of the proportion of each
ingredient, their relative toxicities, and the effect of any interaction between mixtures
of chemicals.
In evidence to the Australian Senate Aviation Inquiry, Mobil USA noted that Mobil Jet
Oil II contains less than 5 ppb (0.005 ppm) TOCP.
3
This is an impressively low
amount, and suggests that the neurotoxic potential from a chemical containing such a
low level of tri-ortho-cresyl isomer be vanishingly small.
Concentrations of other neurotoxic ingredients were not so readily available. In
evidence to the Australian Senate Aviation Inquiry, it became apparent that DOCPs
were present in TCP at a concentration of 6 ppm, and MOCPs were present at a
concentration of 3070 ppm.
3
As these ingredients are present in higher concentrations
than TOCP, and have a significantly higher toxicity than TOCP, it is suggested that a
statement of low TOCP content is misleading as it underestimates the toxicity of the –
OCP ingredients by a factor of 30,730 (see the Table below).
Table 1: Tricresyl Phosphate: Toxicity of Isomers
Isomer Concentration (ppm) Relative Toxicity Equivalent Toxicity
TOCP 0.005 1 1 ×
DOCP 6 5 30 ×
MOCP 3070 10 30700 ×
Total
30731 ×
Further, the chemically similar organophosphates such as xylenols and phenolics are
also present in as contaminants in tricresyl phosphate. These also have a similar
neurotoxicity to the cresyl isomers, which would add to the relative toxicity listed
above.
New products are being introduced into the market. Claims that they are
organophosphate clear are untrue. Mobil 291, one such replacement oil contains less
than 1 ppb TOCP, 1.1 ppm DOCP and 1760 ppm MOCP.
3
This gives an equivalent
toxicity of 17606, which is about half that of the previously used product, Mobil Jet
Oil II. While this is a significant decrease in -OCP containing monomers, it is not
phosphate free.
-17
-
Regulatory Classification
Tricresyl phosphate is listed on the NOHSC Designated List of Hazardous Substances.
The first edition of the Designated List was current from 1994 to 1999.
66
This edition
contains three entries for Tricresyl phosphate.
The first entry for Tricresyl phosphate (as Tri-tolyl phosphate) uses the CAS No 1330-
78-5. This entry notes that mixtures this ingredient should be classified as “Harmful”
hazardous substances if included in the product at a concentration at or greater than
0.2% and “Toxic” hazardous substances if included in the product at a concentration at
or greater than 1%. Further, a product containing a this ingredient at or above 0.2%
should carry risk statement R23/24/25 – Toxic by inhalation, in contact with skin and
if swallowed and R39 – Danger of very serious irreversible effects.
There are two other entries in the 1994 edition of the Designated List, based on two
other chemical descriptions. Tricresyl phosphates (<1% o-cresol) and Tricresyl
phosphates (>1% o-cresol). Regulatory requirements for the former are classified as
Harmful if present in a mixture above 5% with risk phrases R21/22 – Harmful in
contact with skin and if swallowed. Regulatory requirements for the latter are the same
for Tri-tolyl phosphate (CAS No 1330-78-5).
A final entry also is listed for Triorthocresyl phosphate under the CAS No 78-30-8, but
no classification cut-off values are listed or risk phrases suggested.
Entries on product documentation have invariably used the 1330-78-5 description,
perhaps because of the problem of obtaining a true estimate of all the various
structures containing the “o-cresol” groups.
The second edition of the designated list has been current since 1999.
5
All entries for
TCP have been deleted, with two new entries:
CAS No 78-30-8 Tricresyl phosphate (o-o-o, o-o-m, o-o-p, o-m-m, o-m-p, o-p-
p);
†
Classified as “Harmful” at concentrations above 0.2%, with the risk
phrases R21/22 – Harmful in contact with skin and if swallowed.
Classified as “Toxic” at concentrations above 1%, with the risk
statements R23/24/25 – Toxic by inhalation, in contact with skin and if
swallowed and R39 – Danger of very serious irreversible effects.
CAS No 78-32-0 Tricresyl phosphate (m-m-m, m-m-p, m-p-p, p-p-p)
Classified as “Harmful” at concentrations above 5% with the risk
phrases R21/22 – Harmful in contact with skin and if swallowed.
†
This CAS No is also used to describe the entry for Tri-ortho-cresyl phosphate (TOCP),
suggesting that any Tricresyl phosphate containing ortho-cresyl containing isomers, can now be
loosely called TOCP.
-18
-
While these two new entries have attempted to clear up the confusion apparent in the
earlier entries, it is not known at which point that contamination of a non-ortho-cresyl-
TCP with ortho-cresyl containing monomers converts a low hazard “non-o-TCP” to an
o-TCP.
Use of these two new entries is not widespread, with the 1330-78-5 CAS number
remaining in common use. Unless an accurate measure of the ortho-cresyl (and
probably the “ortho”-xenyl isomers) can be made, it is prudent to continue to assume
that the TCP mixture contains significant levels of ortho-containing isomers.
Non-Organic Contaminants
One additional point that should be made is that these materials do not just contain
organic molecules. They also contain low levels of other contaminants. The elemental
analysis conducted by van Netten
22
investigated elemental concentrations of a range of
elements in three commercially available jet oils (see Figure below).
Figure -5: Toxic Metal Contaminants in Commercial Jet Oils
0.01
0.1
1
10
100
Cobalt Magnesium Manganese Vanadium Chromium
Toxic Metal Contaminant
Concentration (ppm)
Exxon 2380
Castrol 5000
Mobil Jet Oil 254
While concentrations of some metals are in ppm and even ppb concentrations, it is
misleading to ignore the possible effects of these and other exposures either singly, or
in combination.
Issues that can Impact on Exposure to Jet Oils
The Impact of Altitude
The concentration of oxygen at increasing altitude remains constant, at 20.9%. This
suggests that oxygen levels are unchanged. This is not true. Basically, as altitude
-19
-
increases, the atmospheric pressure declines. While the proportion of oxygen in air
remains unchanged, the actual amount of oxygen in air decreases.
Atmospheric pressure at sea level is 760 mm Hg, with the corresponding partial
pressure of oxygen in air is 159 mm Hg (20.9% or 760 mm Hg). The minimum O
2
concentration for work is considered to be about 136 mm Hg (18 kPa or 18%) O
2
in air
at sea level.
67
A minimum oxygen partial pressure of 118 mm Hg (equivalent to an
altitude of 2438 m/8000 ft) is required to prevent hypoxic cabin air in commercial
aircraft during normal operations. This partial pressure is maintained by the cabin
pressure system (a second requirement for release of oxygen dispensing units at 4572
m/15,000 ft is recommended).
68
The altitude at which the partial pressure of 136 mm Hg is reached is also quite close
to the pressure at which airplane cabins are pressurised (118 mm Hg). There is little
margin of safety in people working at altitude, and in many cases, such workers may
be beginning to become hypoxic.
69
This shown in the Figure below, where the area
bounded by the dashed partial pressure of Oxygen in Air curve, and the dotted line
representing the minimum physiological demand line represents the margin of safety at
which workers can be considered to have sufficient oxygen to work safely). Further,
the position of the cabin pressurisation line shows that in some cases, workers at
altitude may not be obtaining enough oxygen for their physiological requirements.
Figure -6: Pressures and Oxygen Concentrations at Altitude
0
100
200
300
400
500
600
700
800
0 2000 4000 6000 80 00 10 000 120 00 14000 16000 18000 20000
Altitude (metres)
Pressure (mm Hg)
0
20
40
60
80
100
Pressure (kPa)
Mount Everest
Cabin Pressure Altitude
Oxygen concentration
in air (159 mm Hg O
2
)
First signs of hypoxia
(118 mm Hg O
2
)
Margin of
safety
Atmospheric pressure (mm Hg)
Partial pressure of
Oxygen (mm Hg)
Assumptions:
Atmospheric pressure: 101 kPa (760 mm Hg) at sea level
Proportional concentration of O
2
in air: 20.9% (21 kPa or 159 mm Hg) at sea level)
Aircraft Pressurisation Pressure: Equivalent to an altitude of 2500 m (about 8000 ft).
Other problems with lowered oxygen concentrations include changes in sensitivity to
toxic exposures (for example, the toxicity of carbon monoxide is 50% higher at 8000 ft
than at sea level), and the possibility that incipient hypoxia may lead to higher
respiratory rates and therefore increased exposure.
-20
-
Other factors due to the manner in which air is circulated in planes, may also have an
effect, such as humidity, temperature, or contaminants such as carbon dioxide, carbon
monoxide, ozone and particulates.
70
The effects of hypoxia/low humidity have not been studied adequately,
71
but are
unlikely to be insignificant.
Issues Related to Vapours and Particulates
Airborne contaminants are generally divided into two types: gas/vapour and
particulates.
Gases/Vapours: A gas is those molecules of a chemical that exist in a gaseous phase.
Where all the molecules of a chemical are in the gaseous phase, the chemical is
considered a gas. A vapour is the gas phase of a liquid at room temperature.
Therefore, a vapour is that amount of liquid that evaporates into air (or dissolves into
air). Gases and vapours form true solutions in air. The amount of evaporation is
dependent on the individual vapour pressure of the contaminant. Where vapour
pressure is low, only a small amount of the contaminant will evaporate. Generally,
vapour pressure increases with temperature.
Where volatile organic chemicals (VOCs) have high vapour pressures, they will be
present in air in high concentrations, are more likely to reach toxic concentrations and
are amenable to sample collection and analysis using sorbent or gas collection
methods. Where semi-volatile or poorly volatile chemicals have low vapour pressures,
they are less likely to reach toxic concentrations unless they are highly toxic, and
sorbent or gas collection methods are less useful for sample collection.
Particulates: These are materials that are suspended, not dissolved, in air, and include
fumes, smoke, mists, aerosols, dusts, fibres and so on. Particulates may be in liquid
phase (such as mists), solid phase (smokes, fumes and dusts) or mixed phases
(aerosols). Precise criteria for these terms exist based on particle size and phase, but
are unnecessary for the present discussion.
72
Where a particulate is present in air and contains a volatile component, the volatile
components will evaporate at a rate dependent on individual vapour pressures.
However, depending on the amount of particulate present in air, it is possible to exceed
the vapour pressure of an individual contaminant. Where a contaminant has a low
vapour pressure, particulate exposure is more important than exposure to vapour.
Therefore, particulates containing a large proportion of volatile components will
evaporate quickly (sometimes even before settling), indicating that the vapour phase of
the contaminant is more important. Particulates containing poorly volatile components
will stay in particulate form for a long time, until gravity or turbulence causes them to
settle. Once settled, particles coalesce onto or adhere to surfaces, and any remaining
volatile components become subject to evaporation through their vapour pressures.
Where evaporative pressures are low, long term, low-level contamination leading to
residual exposures will occur.
-21
-
Further, because particulates can settle on exposed skin and be subject to absorption
through skin, sometimes after airborne exposure has ceased, it is important to consider
both the inhalational and skin routes when estimating exposure.
Particulates are not amenable to the same sampling and collection methods that are
required for gases and vapours. They require specialised sampling, usually by
filtration or gravimetric methods. Further, because particulates can exist in different
sizes and diameters, an estimate of that fraction of the particulate that is taken into the
respiratory system may be more critical than an estimation of the total concentration of
particulate. Consideration of the type of airborne contaminants, whether in vapour,
particulate or mixed phases is quite critical for the success and relevance of a
monitoring program.
Issues Related to Combustion and Pyrolysis
Any chemical or chemical mixture is subject to degradation processes, such as
oxidation or reduction. Over time, these can cause substantial loss of original
chemical structures and properties. This process occurs more rapidly at higher
temperatures and pressures, in accordance with the laws of thermodynamics.
However, for most commercial purposes (except perhaps in the production of food),
the processes of breakdown in chemical materials are slow, and can be disregarded.
However other breakdown processes are also possible, such as, a material subject to a
source of heat energy can burn. This is called thermal degradation or thermolysis. The
process of thermal degradation is a chemical process in which oxygen and energy are
used to transform the original chemical into its oxidised form. For example, carbon
containing materials will, in the presence of energy and oxygen, produce the two
oxides of carbon: Carbon dioxide (CO
2
) and Carbon monoxide (CO). The first of
these (CO
2
) is produced in the presence of an abundance of oxygen, the second (CO),
where stoichiometric concentrations of oxygen are lacking (usually in conditions of
incomplete combustion). Both of these oxides are gases, one (Carbon monoxide) is
indeed toxic, even at low concentrations, causing toxic asphyxiation. Single or short
term exposure to CO insufficient to cause asphyxiation produces headache, dizziness,
and nausea; long term exposure can cause memory defects and central nervous system
damage, among other effects.
73
Where oxygen is completely lacking, the process of thermal degradation can still
proceed, but this time, any carbon in a material, will be reduced from the chemical
form it is located, to molecules containing proportionally more carbon (and
proportionally less volatile components) and ultimately, carbon atoms. This process is
called pyrolysis. Both oxides of carbon are gases, but elemental carbon is a solid
(usually seen as smoke or soot). Further, the process of reducing carbon containing
materials to carbon depends on the chemical nature of the source material, and will
produce different pyrolysis products as the reaction process proceeds. Pyrolysis
products may be fairly pure in carbon content, but are more usually found with other
organic or inorganic breakdown products. The processes inherent in pyrolytic
degradation are very complex, and vary depending on the source materials, the
temperature and duration of combustion, and the progressive combustion of pyrolysis
products that occur in the thermal degradation process.
-22
-
Many combustion and pyrolysis products are toxic. The toxic asphyxiants, such as
carbon monoxide or hydrogen cyanide were discussed above. Some thermal
degradation products, such as acreolin and formaldehyde are highly irritating. Others,
such as oxides of nitrogen and phosgene, can produce delayed effects. Still others,
such as particulate matter (for example, soot) can carry adsorbed gases deep into the
respiratory tract where they may provoke a local reaction or be absorbed to produce
systemic effects.
74
Of course, in a situation where a fire occurs, all three processes can occur. Where
there is no oxygen, pyrolysis products (such as smoke) will be formed, where there is
incomplete combustion carbon monoxide will form, and where there is complete
combustion, carbon dioxide is formed. Further, these processes may proceed
sequentially, as oxygen becomes available to the burning material.
Therefore, as well as particulate and gas/vapour phases, consideration of the type of
airborne contaminants, whether in unchanged, degraded, combusted or pyrolised forms
is also critical for the success and relevance of a monitoring program.
Exposure to Jet Oils in the Occupational Environment
Exposure standard
The only ingredient in Mobil Jet Oil II with an exposure standard is TOCP, with a 40
hr/week time weighted average concentration of 0.1 mg/m
3
.
67
There is no exposure
standard for other isomers, although at least some are known to be more toxic.
Therefore estimating “acceptable” exposures based on monitoring for TOCP alone will
severely underestimate exposure.
This is critical in the interpretation of the results of experimental and exposure studies.
For example, chickens exposed to TCP mixtures containing about 1.5% TOCP (then
the US Navy specification) developed OPIDN within five days of oral dosage, and
sixty days of inhalational exposure at 23 mg/m
3
or more.
75
While this provides a
measure of comparison of oral to inhalational exposure, it can not provide a true
picture of the toxicity of TCP, as the concentrations of other orthocresyl containing
TCP isomers in the mixture used were not known. If, as shown above, the proportion
of such isomers is 30,000 times the concentration of TOCP, then using an exposure
standard for one isomer as an estimate of exposure is virtually meaningless.
Exposure situations
On ground Engineering operations
Exposure to jet oil is possible during maintenance operations on airplane engines
where the engine contains the oil. Personnel at risk in such operations are ground crew
involved in engineering and maintenance. These operatives get relevant information
(for example through engineering handbooks and maintenance), training, and are
warned about the toxicity of Mobil Jet Oil II by warnings on the label. For example:
Engine maintenance manuals note: Do not keep the oil on the skin for a long
time. If you do not clean the oil off, the oil can cause injury and Do not let the
-23
-
oil stay on your skin. You can absorb poisonous materials from the oil through
your skin. This suggests that oil is not harmless. This information is obviously
aimed at maintenance personnel, and presumably envisages that no one else
will come into contact with the oil. Further, new notices warning against the
inhalation of mists were added in 1997-8. Further, the exposure in maintenance
operations is probably mainly by skin contact, as the oil does not have an
appreciable vapour pressure in ambient conditions. Such operational
conditions can be seen to keep the risk of exposure to the oil under control.
The label for the pre-1998 container contained the following risk and safety
phrases:
Caution: Avoid spilling on insulation, plastic, rubber or paint
Warning! Contains Tricresyl Phosphate.
Produces paralysis if taken internally.
Do not use as medicine or food product.
Wash thoroughly after handling.
The label for the post-1998 container contained the following warnings, risks
and safety phrases:
Avoid spilling on insulation, plastic, rubber or paint
WARNING!
Contains Tricresyl Phosphate.
Swallowing this product can cause nervous system disorders, including paralysis.
Prolonged or repeated breathing of oil mist, or prolonged or repeated skin contact can
cause nervous system defects.
PRECAUTIONS:
Never swallow. Wash hands after handling and before eating. Never use in or around
food. Avoid prolonged or repeated overexposure to skin or lungs.
FIRST AID:
If swallowed, seek immediate medical attention. If medical attention is delayed, induce
vomiting. In case of contact, wash skin with soap and water. Remove contaminated
clothing.
FOR INDUSTRIAL USE ONLY
Not intended or suitable for use in or around a household or dwelling. Never use empty
container to carry water or food. Do not cut or weld on empty container.
(In thirteen languages) When using do not eat, drink or smoke. After contact with skin,
was immediately with plenty of soap and water.
The change in warning information in the two labels is quite significant (see Figure
below).
-24
-
Figure -7: Warnings: Mobil Jet Oil II
Warning
(pre-1992)
Warning
(post-1992)
No reason was given to maintenance workers handling Mobil Jet II for the new label
when it was introduced in 1998, although in evidence to the Senate Aviation Inquiry,
Mobil note:
Additional joint toxicology studies by Mobil and a major manufacturer of TCP confirmed that
an oil with 3% TCP could produce toxic effects in animals administered very high doses. This
led Mobil to adopt a very conservative labeling approach for its jet oils by including language
recommending minimizing exposure by all routes and by emphasising the importance of good
personal hygiene practices. The decision was made in 1997 and labeling was phased in during
the year.
3
In flight exposure
There is one other potential exposure to engine oils. This is when the engine leaks in
flight, and leaking engine oils contaminate air flowing to the flight deck or passenger
cabin. There are a number of possible exposure scenarios:
exposure to the oil;
exposure to a thermally degraded oil and its by-products;
exposure to engine components, such as seals or bearings, that have worn down
or have broken down into respirable particulates containing toxic elements such
as nickel, beryllium and copper, entering the bleed air system.
In such circumstances, exposed crew and passengers are exposed to airborne
contaminants that are leaking directly into air, and they are unaware of the toxicity of
the contaminants they are inhaling. There is little control of exposure. Mobil “do not
believe that Mobil Jet turbine oils pose any significant toxicological risk to individuals
accidentally exposed to aerosols or vapours in aircraft cabins. Such exposures are
not what we would refer to as ‘normal use’ but the cabin levels that can be reached
during such exposures … are considered safe”.
3
However, numerous leak incidents
indicate that such exposures will produce symptoms of toxicity.
If exposure is to oil, it will be at least partially in a particulate (mist) form, where it can
attain higher airborne concentrations than might be predicted from vapour pressures
-25
-
(even at elevated, but rapidly cooling, temperatures). Further, the potential for skin
exposure is greatly increased, as the mist can settle onto exposed skin, where it will
then be available for dermal absorption. Further, the emission of oil
vapours/smoke/mists into the passenger cabin would produce contamination of the
cabin. Particulates would settle out onto surfaces (such as ducting, cabin walls,
furniture and equipment), which would thereafter slowly vapourise, the rate of
evaporation being dependent on individual contaminant vapour pressures. This
residual contamination would continue until cleaned off or until it had evaporated.
While the toxicity of the oil has been established, little is known about the possible
transformations that may have occurred in the oil while in operation. A leak of such
an oil from an engine operating at altitude would see most of the oil pyrolise once it
leaves the confined conditions of temperature and pressure operating in the engine.
While it seems reasonable that any ingredients with suitable autoignition or
degradation properties that allow such a transformation after release from the engine
could be radically transformed, it is possible to speculate in only general terms about
the cocktail of chemicals that could form.
Presumably this would include:
combustion gases such as carbon dioxide and carbon monoxide;
other irritating gases, such as oxides of nitrogen;
partially burnt hydrocarbons (including irritating and toxic by-products, such as
acreolein and other aldehydes); and
TCP (which is fairly stable at high temperatures) or TCP thermal degradation
products, such as highly toxic phosphorus oxides (TCP boils at 420ºC; TOCP
boils at 410ºC); and
Materials formed from worn or broken engine components that are present in
the oil in particulate form.
These contaminants will be in gas, vapour, mist and particulate forms.
If the exposure is to a thermally degraded oil then as well any exposure to the oil mist
(as outlined above), exposure can also include particulates such as soots; thermally
degraded chemicals such as acreolin, and combustion gases such as carbon monoxide.
One final issue that should be given consideration on potential contaminants within a
thermally decomposed jet oil. A number of papers discuss the possibility of formation
of the strong neurotoxicant Trimethylolpropane phosphate (TMPP) in tricresyl
phosphate containing aircraft lubricating oils.
76,77,78,79,80
This chemical has an
organophosphate structure (see below).
-26
-
Figure -8: Structure of Trimethylolpropane phosphate
O
P
OO
O
CH
2
CH
2
CH
2
C
CH
2
CH
3
Operational temperature conditions for the maximal formation of TMPP (15%) is
550ºC.
80
Aircraft engines operate at such temperatures, although other conditions
(presence of suitable reaction intermediates) may not be present. Investigation by the
Naval Medical Research Institute Laboratory positively concluded that the thermal
decomposition of aircraft lubricating oil produces TMPP,
81
although evidence for this
synthesis is equivocal.
82
However, the toxic potency of TMPP is such that only a
small amount formed in thermal degradation could provoke signs of toxicity, as
“mechanistically, TMPP is thought to irreversibly inhibit the GABA-mediated
inhibitory response and thereby produce epileptiform clonic/tonic seizures with
convulsions followed by death”.
81
Conclusions
The jet oils are a commercially useful product. They are known to contain toxic
ingredients. While the continued use of toxic materials is always a matter requiring
caution and forethought, a full deliberation of risks and benefits may overcome such
considerations.
This has occurred with the jet oils. Known to contain toxic ingredients, they have been
used relatively unchanged for decades. The conservatism inherent in a complicated
approval process, the reluctance to change toxic ingredients known to perform well in
circumscribed situations, and the apparent lack of exposure scenarios where the
toxicity could become apparent have all produced a conclusion that everything was
within acceptable limits. Even the apparent toxicity of a jet oil reported from animal
experiments in 1988 was not viewed as a significant problem.
However, an increasing number of oil leaks in the 1990’s around the world and the
increase in a number of flight attendants and flight crew reporting signs of toxicity
after such events suggests the toxicity of the jet oils should be reconsidered:
Publicly available information such as labels and MSDS appear to underplay
the hazards of some toxic ingredients in Jet Oils. For PAN, no information is
available regarding the presence of a skin sensitiser. For TCP, the almost
complete reliance on expressing TCP toxicity in terms of how much TOCP is
present is misleadingly deceptive and ignores the possible contribution of other
ingredients, some present in higher amounts and with appreciably higher
toxicities.
-27
-
The exposure scenario at altitude is utterly different from conventional
exposures to the oils while using them in maintenance situations. Exposed
individuals do not know to what they are being exposed, exposure by
inhalational and dermal exposures can occur, the possibility of escape is absent,
the possibility of cleaning or decontamination is absent).
Options for the control of exposure are all but absent. Switching off an engine
or bleed air system may offer some assistance, but is less useful if an entire
ventilation system is contaminated.
The exposure may be not only to gases and vapours, but also to particulates
(such as oil mists or soots) that can be in proportionally greater concentrations
than they would be for vapours.
The exposure may to unchanged oil mists, or to combusted or pyrolised
contaminants, or particulates arising from worn or broken engine components.
The chemical make up of such a mixture would be difficult to deduce; the
toxicity of exposure to such a mixture would be difficult to predict.
However, these contaminants could not be classified as being of low toxicity. The
interactions of such effects with a specific toxic exposure is not known, but not
presumed to be benign. The possible problems that might arise from exposure to such
a cocktail cannot be dismissed without proper consideration.
Many of the signs and symptoms of exposure being reported by exposed flight crew
83
(and to a lesser extent, passengers). Symptoms arise from single, short term or long
term exposures include:
Symptoms from single or short term exposures include: blurred or tunnel
vision, disorientation, memory impairment, shaking and tremors,
nausea/vomiting, parasthesias, loss of balance and vertigo, seizures, loss of
consciousness, headache, lightheadedness, dizziness, confusion and feeling
intoxicated, breathing difficulties (shortness of breath, tightness in chest,
respiratory failure), increased heart rate and palpitations, nystagmus, irritation
(eyes, nose and upper airways).
Symptoms from long term low level exposure or residual symptoms from short
term exposures include: memory impairment, forgetfulness, lack of
coordination, nausea/vomiting, diarrhoea, respiratory problems, chest pain,
severe headaches, dizziness and feeling intoxicated, weakness and fatigue
(leading to chronic fatigue), exhaustion, increased heart rate and palpitations,
numbness (fingers, lips, limbs), hot flashes, joint pain, muscle weakness and
pain, salivation, irritation (eyes, nose and upper airways), skin itching and
rashes, skin blisters (on uncovered body parts), signs of immunosupression,
hair loss, chemical sensitivity leading to multiple chemical sensitivity.
It is also apparent that some symptoms occur immediately or soon after exposure, for
example, many of the irritant, gastric, nervous and respiratory effects. However,
others, such as nervous system impairment, immunodepression and chemical
sensitivity, develop later, perhaps months after exposures may have ceased. Further,
while some of these symptoms are fully reversible, others appear to persist for longer.
Debate is also continuing about the links between exposure and some of longer term
-28
-
symptoms (such as chemical sensitivity).
Symptom severity depends on a number of factors, including the range of
contaminants present, the intensity, duration and frequency of exposure, toxicity of
compounds (expectedly influenced by cabin environment factors such as humidity,
decreased oxygen concentration and contaminants such as carbon monoxide), and
individual susceptibility.
These appear consistent with the toxicity of some of the ingredients of the oils. These
include hydrocarbon neurotoxicity from exposure to organic chemicals, sensitivity
from exposure to a sensitiser, COPIND from organophosphate exposure, or long term
low level toxicity from exposure to carbon monoxide. These health problems need to
be evaluated with more care than is apparent in the aviation industry at present.
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