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Crew Effects from Toxic Exposures on Aircraft


Abstract and Figures

The cabin of an airplane is aspecialised working environment and should be considered as such. The oils and hydraulics used in airplane engines are toxic, and specific ingredients of such materials are irritating, sensitising and neurotoxic. If oil or hydraulic fluids leak out of engines, this contamination may be in the form of unchanged oil/fluid, degraded oil/fluid from long use in the engine, combusted oil/fluid or pyrolised oil/fluid, in the form of gases, vapours, mists and particulate matter. If leak incidents occur and the oil/fluid is ingested into bleed air and is passed to the flight deck and passenger cabins of airplanes in flight, aircrew and passengers may be exposed to contaminants that can affect their health and safety. Where contamination of air in the flight deck and passenger cabin occurs that is sufficient to cause symptoms of discomfort, fatigue, irritation or toxicity, this contravenes the air quality provisions of Federal Aviation Regulations, most notably FAR 25.831. Symptoms of immediate or short-term nature and reported by exposed staff in single or few leak incidents are consistent with the development of irritation and discomfort. Symptoms of along-term nature (that is, sustained symptoms for at least six months) reported by some exposed staff following small to moderate numbers of leak incidents are consistent with the development of an irreversible discrete occupational health condition, termed aerotoxic syndrome. Features of this syndrome are that it is associated with air crew exposure at altitude to atmospheric contaminants from engine oil or other aircraft fluids, temporarily juxtaposed by the development of aconsistent symptomology including short-term skin, gastro-intestinal, respiratory and nervous system effects, and long-term central nervous and immunological effects.
Content may be subject to copyright.
Hdb Env Chem Vol. 4, Part H (2005): 223–x
DOI 10.1007/b107246
©Springer-Verlag Berlin Heidelberg 2005
Published online:
Crew Effects from Toxic Exposures on Aircraft
C. Winder (u)·S.Michaelis
School of Safety Science, The University of New South Wales, NSW 2052 Sydney,
Austral ia,
1Introduction................................... 224
2 Toxic Ingredients of Jet Oils .......................... 225
2.1 TheSubstitutedDiphenylamine ........................ 226
2.2 N-Phenyl-alpha-naphthylamine ........................ 227
2.3 TricresylPhosphate ............................... 228
3 Effects of Aircraft Oil Leaks on Crew ..................... 231
4 Other Factors of Importance to the Aviation Industry ........... 234
5Conclusions................................... 236
References ....................................... 239
Abstract The cabin of an airplane is a specialised working environment and should be
considered as such. The oils and hydraulics used in airplane engines are toxic, and spe-
cific ingredients of such materials are irritating, sensitising and neurotoxic. If oil or
hydraulic fluids leak out of engines, this contamination may be in the form of unchanged
oil/fluid, degraded oil/fluid from long use in the engine, combusted oil/fluid or pyrolised
oil/fluid, in the form of gases, vapours, mists and particulate matter. If leak incidents
occur and the oil/fluid is ingested into bleed air and is passed to the flight deck and
passenger cabins of airplanes in flight, aircrew and passengers may be exposed to con-
taminants that can affect their health and safety. Where contamination of air in the
flight deck and passenger cabin occurs that is sufficient to cause symptoms of discom-
fort, fatigue, irritation or toxicity, this contravenes the air quality provisions of Federal
Aviation Regulations, most notably FAR 25.831. Symptoms of immediate or short-term
nature and reported by exposed staff in single or few leak incidents are consistent with
the development of irritation and discomfort. Symptoms of a long-term nature (that is,
sustained symptoms for at least six months) reported by some exposed staff following
small to moderate numbers of leak incidents are consistent with the development of an
irreversible discrete occupational health condition, termed aerotoxic syndrome. Features
of this syndrome are that it is associated with air crew exposure at altitude to atmo-
spheric contaminants from engine oil or other aircraft fluids, temporarily juxtaposed
by the development of a consistent symptomology including short-term skin, gastro-
intestinal, respiratory and nervous system effects, and long-term central nervous and
immunological effects.
Keywords Aircraft air contamination ·Substituted diphenylamine ·
Phenyl-alpha-naphthylamine ·Tricresyl phosphate ·Triorthocresyl phopshate ·
Organophosphate induced chronic neurotoxicity (OPICN) ·Aerotoxic syndrome
224 C. Winder · S. Michaelis
CAS Chemical Abstracts Service
COPIND Chronic organophosphate-induced neuropsychological disorder
DOCP Di-ortho cresyl phosphate
FAR U.S. Federal Aviation Regulation
JAR Joint Aviation Regulation
MOCP Mono-ortho cresyl phosphate
MSDB Material Safety Data Bulletin
NTE Neurotoxic esterases
OHS Occupational Health and Safety
OP Organophosphorus
OPICN Organophosphorus ester-induced chronic neurotoxicity
OPIDN Organophosphorus ester-induced delayed neurotoxicity
PAN Phenyl-alpha naphthylamine
TCP Tricresyl phosphate
TOCP Tri-ortho cresyl phosphatekp
As already noted in Chapters 10 and 11, the oils and hydraulics used in
aircraft engines can be toxic, and specific ingredients of oils can be irri-
tating, sensitising (such as phenyl-alpha-naphthylamine) or neurotoxic (for
example, ortho-containing triaryl phosphates such as tri-orthocresyl phos-
phate) [1, 2]. If oil or hydraulic fluid leaks occur, this contamination may be in
the form of unchanged material, degraded material from long use, combusted
or pyrolised materials. These materials can contaminate aircraft cabin air in
the form of gases, vapours, mists and aerosols.
Notwithstanding emergency situations, a range of other situations can
arise whereby aircraft cabin air can be contaminated [3]. These include:
uptake of exhaust from other aircraft or on ground contamination sources,
application of de-icing fluids,
hydraulic fluid leaks from landing gear and other hydraulic systems,
excessive use of lubricants and preservative compounds in the cargo hold,
preservatives on the inside of aircraft skin,
large accumulations of dirt and brake dust may build up on inlet ducts
where auxilliary power units extract air from near the aircraft belly,
ingestion of oil and hydraulic fluid at sealing interfaces, around oil cooling
fan gaskets and in worn transmissions,
oil contamination from synthetic turbine oil,
engine combustion products (for example, defective fuel manifolds, seal
failures, engine leaks).
Significant contaminants include: aldehydes; aromatic hydrocarbons; aliphatic
hydrocarbons; chlorinated, fluorinated, methylated, phosphate or nitrogen
Crew Effects from Toxic Exposures on Aircraft 225
compounds; esters; and oxides [4–6]. One additional problem is the lower
partial pressure of oxygen that is present in the cabins of planes flying at
altitude [7].
To date, most studies that have been carried out to measure atmospheric
contamination in aircraft by engine oil leaks or hydraulic fluids are suffi-
ciently flawed on procedural and methodological grounds as to render their
conclusions invalid. Further, no monitoring has occurred during an oil leak.
International aviation legislation such as the US Federal Aviation Regula-
tions (FAR) and airworthiness standards for aircraft air quality state “crew
and passenger compartment air must be free from harmful and hazardous
concentrations of gases or vapors” [8]. Where contamination of air in the
flight deck and passenger cabin occurs that is sufficient to cause symptoms of
discomfort, fatigue, irritation or toxicity, this contravenes such standards and
Inhalation is an important route of exposure, with exposure to uncovered
skin being a second, less significant route (for example, following exposure to
oil mists or vapours). Ingestion is unlikely.
Occasionally, such exposures may be of a magnitude to induce symptoms
of toxicity. In terms of toxicity a growing number of aircrew are developing
symptoms following both short-term and long-term repeated exposures, in-
cluding dizziness, fatigue respiratory problems, nausea, disorientation, con-
fusion, blurred vision and tremors [9–11]. Neurotoxicity is a major flight
safety concern especially where exposures are intense [12].
Toxic Ingredients of Jet Oils
The engine oils that are used in jet engines are precision oils that need to op-
erate in extreme conditions. Some commercial jet oils have been in use as
engine oils in aviation for decades. For example, Mobil USA note that Mobil
Jet Oil II (a jet oil with close to half the market share) “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” [13].
Chemical exposures in aircraft are not unheard of. In 1953, the US
Aeromedical Association first expressed their concerns about the toxicity
risks of cabin air contamination by hydraulics and lubricants [14]. Other
risks have been identified more recently, either as part of the chemicals rou-
tinely used in maintaining aircraft [15], or as toxicological factors in aviation
accidents [16, 17].
A complex approval process exists for ensuring that materials used in
aviation are manufactured to relevant standards, and the jet engine oil spe-
cification of the US Navy MIL-PRF-23699 is used for jet oils. This process of
226 C. Winder · S. Michaelis
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 substi-
tuting toxic TCP additives that perform well in critical applications. This has
meant that potentially toxic products have continued to be available and used
long after their toxicity was recognised [18].
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%remainsun-
changed. However, as Mobil indicate, only the base stock esters have been
modified over the past thirty or so years, suggesting that the mixture of iso-
mers in TCP stock has not been changed.
as the supplier’s label on the cardboard box the cans are shipped in, the
product Material Safety Data Bulletin (MSDB), and information from the
manufacturer, list the following ingredients [6]:
synthetic esters based in a mixture of 95%C
5-C10 fatty acid esters of pen-
taerythritol and dipentaerythritol;
3% tricresyl phosphate (Phoshoric acid, tris(methylphenyl) ester, CAS No
1% phenyl-alpha-naphthylamine (PAN) (1-Naphthalenamine, N-phenyl,
CAS No 90-30-2);
a substituted diphenylamine;
a last entry “ingredients partially unknown” is also noted on some docu-
Of these ingredients, the most toxicologically significant components are the
substituted diphenylamine, phenyl-alpha-naphthylamine (PAN) and tricresyl
phosphate (TCP).
The Substituted Diphenylamine
The substituted diphenylamine is variously reported as benzamine, 4-octyl-
N-(4-octylphenyl), (CAS No 101-67-7) or 0.11%N-phenyl-benzeneamine,
reaction product with 2,4,4-trimethylpentene (CAS No 68411-46-1), and used
as an antioxidant, in concentrations not greater than 1%(seeFig.1).
There is little toxicity data available for this ingredient, although it is not
believed to be toxic by single exposure (no data on long-term exposure). The
disclosure of this ingredient in hazard communication by identity probably
Crew Effects from Toxic Exposures on Aircraft 227
Fig. 1 Substituted diphenylamines
relates to its environmental effects, such as poor biodegradability and toxicity
to aquatic invertebrates [19].
N-Phenyl-alpha-naphthylamine, (CAS No 90-30-2), also known as phenyl-
alpha-naphthylamine (PAN), is a lipophilic solid as an antioxidant in lubri-
cation oils and as a protective agent in rubber products (see Fig. 2). In these
products, the chemical acts as a radical scavenger in the auto-oxidation of
polymers or lubricants. It is generally used in these products at a concen-
tration of about 1% (its concentration in jet oils). The commercial prod-
uct 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 100500 ppm) and 2-naphthylamine (below 3 to 50 ppm), aniline (be-
low 100 to 2500 ppm), 1-naphthol (below 5000 ppm), 1,1-dinaphthylamine
(below 1000 ppm).
PAN is readily absorbed by mammalian systems and rapidly biotrans-
formed [20]. Both urine and faeces appear to be the main routes of excre-
tion [21].
By single dosing, PAN has a short-term low toxicity, with LD50 sabove
1g/kg. The chemical has a similar mechanism of toxicity to 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 [22]. This result is supported by case
studies in exposed workers [23, 24]. At the concentration used (1%), Mobil Jet
Fig. 2 N-Phenyl-1-naphthylamine
228 C. Winder · S. Michaelis
Oil II meets cut off criteria (1%) for classification as a hazardous substance in
Australia for sensitisation properties.
Most genotoxicity studies report negative results, suggesting little genotox-
icity potential [21].
Most repeated dose toxicological studies focus on its potential carcino-
genicity. 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 [25]. While the method-
ology 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 in-
cidence of various forms of cancer was also found among workers exposed
to antirust oil containing 0.5% PAN [26]. While these animal and human re-
sults 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 Pro-
gram 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 [27].
Tricresyl Phosphate
Tricresyl phosphate (CAS No 1330-78-5), is also known as phosphoric acid,
tris(methylphenyl) ester or tritolyl phosphate. TCP is a blend of ten tricre-
syl phosphate isomer molecules, plus other structurally similar compounds,
including phenolic and xylenolic compounds. TCP is a molecule comprised
of three cresyl (methylphenyl) groups linked to a phosphate group. The lo-
cation of the methyl group in the cresyl group is critical for the expression
of neurotoxicity, with ortho-, meta- or para- prefixes that denote how far
apart the hydroxyl and methyl groups are on the cresol molecule. Techni-
cally, there are 27 (33) different combinations of meta, ortho and para cresyl
groups in TCP (see Fig. 3). Since the apparently different three-dimensional
structures of the molecule are not chemically locked in place, they are not
optical isomers. Therefore, structures with similar numbers of cresyl groups
(such as ppm, pmp and mpp) are considered the same molecules. This gets
the apparent 27 structures down to the real ten isomers conventionally de-
CAS number descriptors for tricresyl phosphate chemicals have been in-
troduced to differentiate between ortho-cresyl and non-ortho-cresyl isomers:
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);
Crew Effects from Toxic Exposures on Aircraft 229
Fig. 3 Structure of Tricresyl phosphate
CAS No 78-32-0 tricresyl phosphate (containing m-m-m, m-m-p, m-p-p,
p-p-p isomers).
TCP is a compound with a toxicity typical of the organophosphorus com-
pounds. Human toxicity to organophosphorus (OP) compounds has been
known since at least 1899, when neurotoxicity to phosphocreosole (then used
in the treatment of tuberculosis) was reported [28]. The study of OP toxic-
ity is extensive, and generally characterised by a toxicity of inhibition of the
esterase enzymes, most particularly cholinesterases [29] and neurotoxic es-
terases [30]. The mechanism of effect is phosphorylation [31].
Signs of low level intoxication include headache, vertigo, general weakness,
drowsiness, lethargy, difficulty in concentration, slurred speech, confusion,
emotional lability and hypothermia [32]. The reversibility of such effects has
been questioned [33].
Signs of poisoning are usually foreshadowed by the development of early
symptoms related to acetylcholine overflow and include salivation, lacrima-
tion, conjunctivitis, visual impairment, nausea and vomiting, abdominal
pains and cramps, diarrhoea, parasympathomimetic effects on heart and cir-
culation, fasciculations and muscle twitches [34]. This is the basic site of
inhibition for all OP molecules [35, 36].
A second reaction with certain OPs (including TCP) leads to further
neurotoxic and neuropathological changes. This is inhibition of neurotoxic
esterases (NTE) which produces a progressive distal symmetrical sensori-
motor mixed peripheral neuropathy, called organophosphorus-induced de-
layed neurotoxicity (OPIDN) [36, 37]. The mechanism of toxicity is now fairly
well understood, as indeed are the organophosphorus structures which are
predicted to cause OPIDN [38].
OPIDN has a severe pathology. It is quite likely that such a severe condition
would be presaged with a range of clinical and pre-clinical signs and symp-
toms. These have been reported extensively, and an “intermediate syndrome”
was defined in 1987 [39].
More recently, chronic exposure to organophosphates has been associated
with a range of neurological and neuropsychological effects [4044]. Such
230 C. Winder · S. Michaelis
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-induced neuropsycholog-
ical disorder (COPIND) has been described, of neurological and neuropsy-
chological symptoms [45]. These include:
diffuse neuropsychological symptoms (headaches, mental fatigue, depres-
sion, 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 [46], or long-term low level
repeated exposure with (often) no apparent signs of exposure [43]. 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.
In addition, since the introduction and extensive use of synthetic organo-
phosphorus compounds in agriculture and industry half a century ago, many
studies have reported long-term, persistent, chronic neurotoxicity symptoms
in individuals as a result of acute exposure to high doses that cause acute
cholinergic toxicity, or from long-term, low-level, subclinical doses of these
chemicals [4749]. The neuronal disorder that results from organophospho-
rus ester-induced chronic neurotoxicity (OPICN), which leads to long-term
neurological and neurobehavioral deficits and has recently been linked to
the effects being seen in aircrew despite OP levels being too low to cause
OPIDN [50].
Furthermore, OPICN induced by low-level inhalation of organophosphates
present in jet engine lubricating oils and the hydraulic fluids of aircraft
could explain the long-term neurological deficits consistently reported by
crewmembers and passengers, although organophosphate levels may have
been too low to produce OPIDN [50].
While the description above relate to the general toxicity of OPs, they
are characteristic of exposure to tricresyl phosphate. The ten isomers that
make up TCP are toxicologically different, and it is well established that the
ortho-containing isomers are the most toxic [51–53]. Of the ten isomers of
TCP, six contain at least one ortho-cresyl group: three mono-ortho (MOCP)
isomers, two di-ortho (DOCP) isomers and one tri-ortho (TOCP) isomer, tri-
orthocresyl phosphate (TOCP). Other, similar ortho- containing chemicals,
such as the xylenols and phenolics, are also present in commercial TCP for-
mulations in small amounts. Manufacturers of TCP have reduced the levels of
ortho-cresyl and ortho-ethylphenyl isomers to reduce the potential for neu-
Crew Effects from Toxic Exposures on Aircraft 231
rotoxicity of products containing TCP [18]. How much these refinements had
removed the toxic impurities outlined above is not known. Indeed, toxic-
ity was still being detected in commercially available products in 1988 [18],
and questions have been raised about the lack of consistency between stated
ingredient data and actual amounts of toxic isomers present in commercial
formulations, and their impact on exposed individuals [6].
Effects of Aircraft Oil Leaks on Crew
Where exposure may be to high levels of airborne contaminants, it is not un-
reasonable for signs of irritancy and discomfort to be observed. Similarly,
it is not unreasonable to consider that a person exposed to a chemical that
contains 1% of a sensitiser and 3% of a neurotoxicant might show signs of ir-
ritancy and neurotoxicity.These symptoms are often reported in air crew who
may be exposed to aircraft fluids.
The earliest case found in the literature of toxicity following jet oil expo-
sure and adverse health problems in air crew was reported in 1977 [55]. A pre-
viously healthy member of an aircraft flight crew was acutely incapacitated
during flight with neurological impairment and gastrointestinal distress. His
clinical status returned to normal within a day. The aetiology of his symptoms
was related to an inhalation exposure to aerosolised or vapourised synthetic
lubricating oil arising from a jet engine of his aircraft.
Other studies of exposures in aircraft exist in the literature, including
a 1983 study of eighty nine cases of smoke/fumes in the cockpit in the US Air
Force [56], a 1983 study of Boeing 747 flight attendants in the USA (this paper
linked symptoms to ozone) [57], a 1990 study of aerospace workers [58], and
a 1998 study of BAe 146 flight crews in Canada over a four-month period [9].
A recent report of seven case studies considered representative of the com-
mon symptoms of irritancy and toxicity described similar symptoms [10],
and a follow up survey by the same research group reported similar findings
in a larger group of fifty crew respondents [59]. Two union-based studies in
pilots provide additional data [60, 61].
These studies investigated different exposures and situations, and the
range of symptoms in these studies was quite broad, affecting many body
systems. However, there are common themes in symptom clusters in these
studies, as shown in Table 1 overleaf.
While this Table shows a longlist of symptoms, it is possible to characterise
many symptoms more consistently. For example, different papers report
dizziness or loss of balance or light-headededness or feeling faint or feeling
intoxicated or disorientation. It would be incorrect to regard such symptoms
as being entirely different from each other – they point to a basic neuropsy-
chological dysfunction affecting balance. But rather than dismissing such
232 C. Winder · S. Michaelis
Table 1 Studies reporting signs and symptoms in aircrew
Symptom cluster Sign or symptom Reference [56] [57] [58] [9] [10] [59] [60] [61]
Number of cases/reports 89 248 53 112 7 50 21 106
Loss of consciousness/Fainting/loss of consciousness/grey out 4%4%3/714%
Inability to function Respiratory distress, shortness of breath, 73%2%4/762%26%4%
respiration requiring oxygen
Symptoms of direct irritation Irritation of eyes, nose and throat 7/732%37%
to eye, airways or skin Eye irritation, eye pain 35%74%57%24%4/776%
Respiratory symptoms secondary Sinus congestion 35%54%5%2/7
to irritation Nose bleed 17%1/74%
Throat irritation, burning throat, gagging and coughing 2%64%57%43%2/776%
Cough 69%2/712%
Difficulty in breathing, chest tightness 68%3/762%
Loss of voice 35%1/7
Skin symptoms secondary Rashes, blisters (on uncovered body parts) 36%4/748%16%8%
to irritation
Gastrointestinal symptoms Nausea, vomiting, gastrointestinal symptoms 26%23%15%8%6/758%5%15%
Abdominal spasms/cramps/diarrhoea 26%3/720%5%16%
Neurotoxic symptoms Blurred vision, loss of visual acuity 11%13%1%4/750%5%4%
Shaking/tremors/tingling 9%3%3/740%
Numbness (fingers, lips, limbs), loss of sensation 8%2%4/710%12%
Crew Effects from Toxic Exposures on Aircraft 233
Table 1 (continued)
Symptom cluster Sign or symptom Reference [56] [57] [58] [9] [10] [59] [60] [61]
Number of cases/reports 89 248 53 112 7 50 21 106
Neurological symptoms related Trouble thinking or counting, word blindness, confusion, 26%39%42%6/758%21%22%
to basal nervous system function coordination problems
Memory loss, memory impairment, forgetfulness 42%7/766%26%11%
Cognitive/neuropsychological Disorientation 26%15%4/716%8%
symptoms related to higher Dizziness/loss of balance 47%6%4/772%16%3%
nervous system function Light-headed, feeling faint or intoxicated 35%54%32%7/721%33%
Nonspecific general symptoms Chest pains 7%81%6%2/722%
Severe headache, head pressure 25%52%26%7/786%21%33%
Fatigue, exhaustion 7/762%21%30%
Chemical sensitivity 32%4/772%26%10%
Immune system effects 21%3%
General increase in feeling unwell 21%27%
Behaviour modified, depression, irritability 26%20%60%4/740%
Change in urine 3%6%4%
Joint pain, muscle weakness, muscle cramps 29%2/738%5%30%
234 C. Winder · S. Michaelis
symptoms as being multitudinous and variable [62], it may be more appro-
priate to re-categorise symptoms with clearer definitions, so that the artificial
distinctions between symptom reporting can be clarified, and a shorter list of
“symptom clusters” be developed (as shown in the first column of Table 1).
Other Factors of Importance to the Aviation Industry
The cockpit or cabin of an aircraft is a unique environment. It is a spe-
cialised working environment for the air crew that cannot (indeed, must not)
be equated with workplaces at sea level, or workplaces where specialised ven-
tilation and escape are possible [63].
The process of aircraft pressurisation means that the working environment
is hypoxic. Flying crew are required to conduct complex operations requiring
high order cognitive skills and coordination expertise. Flight attendants may
be required to direct emergency procedures requiring composure and confi-
dence. Anything that may have an impact on the delivery of these tasks can
have serious consequences.
A lowered level of oxygen may in turn have an impact on the emergence of
adverse health problems to toxic exposures.
For these reasons, the application of conventional occupational health and
safety procedures to this specialised environment are inappropriate. Exam-
ples of these include:
permissible exposure standards for occupational exposures to airborne
contaminants – extenuating circumstances on board aircraft (including
humidity and cabin pressure) have not been studied to the extent that
a suitable exposure standard can be identified that incorporates these fac-
tors or identifies interactions between factors [64];
There is “not agreement on a toxicological standard among aviation tox-
icologists to apply to aircraft”. Exposure standards were developed by
the American Conference of Industrial Hygienists (ACGIH) for the aver-
age worker at or near sea level pressure in relatively good health. Flight
crew work in conditions where atmospheric pressure is reduced. [67] Most
chemicals do not have exposure standards and of those that do exist most
“are still regulated by voluntary standards set before 1971”, when adopted
uncritically and unchanged with new science having had no impact on
them. [68];
it is incorrect to assume the exposure standard for TOCP as being “ade-
quately protective” for a TCP containing mixture of TCP isomers as other
ortho isomers (MOCPs, DOCPs) are more toxic than TOCP [65];
procedures for assessing the risks of exposures to more than one chemical,
that may act in synergy to produce toxicity (for example, carbon monox-
ide and lowered oxygen);
Crew Effects from Toxic Exposures on Aircraft 235
under circumstances of exposure to mixtures of contaminants, levels may
be well below recommended levels in currently accepted exposure stan-
dards – yet still generate complaints or signs and symptoms, because they
act in synergy with other contaminants or because some standards may
be outdated and have not incorporated more recent scientific and medical
evidence [64];
ventilation rates for buildings.
Occupational exposure standards may be inadequate to protect nonworkers,
for example passengers.
Further, an oil leak from an engine at high pressure and temperature may
burn or pyrolise before it enters the cabin. This produces carbon-containing
materials which, in the presence of energy and oxygen, produce the two
oxides of carbon: carbon dioxide (CO2) and carbon monoxide (CO). The
first of these (CO2) 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 quite toxic 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 [66].
Many combustion and pyrolysis products are toxic. The toxic asphyxiants,
such as carbon monoxide, have already been introduced above. Some thermal
degradation products, such as acrolein and formaldehyde are highly irritat-
ing. 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.
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 tempera-
ture 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 trans-
formed, it is possible to speculate in only general terms about the cocktail of
chemicals that could form. Presumably it would include carbon dioxide, car-
bon monoxide, partially burnt hydrocarbons (including irritating and toxic
by-products, such as acrolein and other aldehydes, and TCP (which is sta-
ble at high temperatures). These contaminants will be in gas, vapour, mist
and particulate forms. These contaminants could not be classified as being of
low toxicity. The possible problems that might arise from exposure to such
a cocktail cannot be dismissed without proper consideration.
236 C. Winder · S. Michaelis
What emerges in the analysis of this data is a pattern of symptoms related to
local effects to exposure to an irritant, overlaid by development of systemic
symptoms in a number of body systems, including the nervous system, res-
piratory system, gastro-intestinal system, and possibly the immune system
and cardiovascular system. These symptoms may be expressed specifically to
these systems, or may be seen more generally, such as headache, behavioural
change or chronic fatigue.
The symptoms reported by exposed individuals as shown in Table 1 are
sufficiently consistent to indicate the development of a discrete occupational
health condition, and the term aerotoxic syndrome is introduced to describe
it (Etymology: aero refers to aviation, toxic to toxicity of exposure and as-
sociated symptoms). Features of this syndrome are that it is associated with
air crew exposure at altitude to atmospheric contaminants from engine oil or
other aircraft fluids, temporarily juxtaposed by the development of a consis-
tent symptomology including short-term skin, gastro-intestinal, respiratory
and nervous system effects, and long-term central nervous, respiratory and
immunological effects (see Table 2). This syndrome may be reversible fol-
lowing brief exposures, but features are emerging of a chronic syndrome
following significant exposures [10, 11, 59].
The presence of contaminants in flight decks and passenger cabins of com-
mercial jet aircraft should be considered an air safety, occupational health
and passenger health problem:
As shown in the section on leaks, incidents involving leaks or engine oil
and other aircraft materials into the passenger cabin of aircraft occur
frequently and are “unofficially” recognised through service bulletins, de-
fect statistics reports and other sources. From the analysis in Chapter 11,
the rates of occurrence of incidents are higher than the aviation industry
admits, and for some models of aircraft are significant. These need ap-
propriate reporting, follow up investigations and health investigations for
those exposed.
The oils used in aircraft engines contain toxic ingredients which can cause
irritation, sensitisation and neurotoxicity. This does not present a risk to
crew or passengers as long as the oil stays in the engine. However, if the oil
leaks out of the engine, it may enter the air conditioning system and cabin
air. Where these leaks cause crew or passenger discomfort, irritation or
toxicity, this is a direct contravention of the US Federal Aviation Author-
ity’s and the European Joint Aviation Authorities’ airworthiness standards
for aircraft ventilation (FAR/JAR 25.831).
As indicated by manufacturer information and industry documentation,
aviation materials such as jet oils and hydraulic fluids are hazardous and
Crew Effects from Toxic Exposures on Aircraft 237
Table 2 Aerotoxic syndrome: short- and long-term symptoms
Short term exposure Long term exposure
Neurotoxic symptoms: blurred or tunnel Neurotoxic symptoms:numbness(ngers,
vision, nystagmus, disorientation, shaking lips, limbs), parathesias;
and tremors, loss of balance and vertigo,
seizures, loss of consciousness, parathesias;
Neuropsychological or Psychotoxic Neuropsychological or Psychotoxic
symptoms: memory impairment, headache, symptoms: memory impairment
light-headedness, dizziness, confusion and forgetfulness, lack of coordination, severe
feeling intoxicated; headaches, dizziness balance, sleep
Gastro-intestinal symptoms:nausea, Gastro-intestinal symptoms:salivation,
vomiting; nausea, vomiting, diarrhoea;
Respiratory symptoms:cough,breathing Respiratory symptoms:breathing
difficulties (shortness of breath), tightness difficulties (shortness of breath), tightness
in chest, respiratory failure requiring in chest, respiratory failure, susceptibility
oxygen; to upper respiratory tract infections;
Cardiovascular symptoms: increased heart Cardiovascular symptoms:chestpain,
rate and palpitations; increased heart rate and palpitations;
Skin symptoms: skin itching and rashes,
skin blisters (on uncovered body parts),
hair loss;
Irritation of eyes, nose and upper airways. Irritation of eyes, nose and upper airways;
Sensitivity: signs of immunosuppression,
chemical sensitivity leading to acquired
or multiple chemical sensitivity
General: weakness and fatigue (leading to
chronic fatigue), exhaustion, hot
flashes, joint pain, muscle weakness and
contain toxic ingredients. If such fluids leak into the air supply, cabin
and flight deck, toxic exposures are possible. Presently, the aircraft man-
ufacturers, airline operators and the aviation regulators deny that this is
Leaks of oil and other fluids into aircraft may be considered of a nuisance
type, but where they affect the health and performance of crew, or the
health of passengers, this is to be considered a flight safety and health
issue and must be given appropriate priority.
Pilots continue to fly when experiencing discomfort or symptoms. There
is a lack of understanding by pilots regarding the toxicity of the oil leaks,
occupational health and safety (OHS) implications and the necessity to
use oxygen. This is further compounded by the airline health professionals
238 C. Winder · S. Michaelis
who, when confronted with a pilot who has been exposed in a fume event
and who is concerned about its consequences, have a poor understanding
of the short and long-term medical issues that may arise and tend to be
dismissive about their implications.
Attempts by the industry to minimise this issue, such as acceptance of
under-reporting of incidents, inadequate recognition of the extent of the
problem, inadequate adherence/interpretation of the regulations, inade-
quate monitoring, inappropriate use of exposure standards and care pro-
vided to crew reporting problems, have perpetuated this problem.
The health implications, both short and long-term, following exposure to
contaminants being reported by crew and passengers must be properly
addressed. A syndrome of symptoms is emerging, called aerotoxic syn-
drome, suggesting these exposures are common and a substantial group of
affected individuals exists.
Where contaminants impair the performance or affect the ability of pi-
lots to fly planes, as has been reported for a number of incidents, this is
a major safety problem. Where contaminants cause undue discomfort or
even transient health effects in staff and passengers, this is a breach of FAR
25.831 and other regulations.
Contaminants in the air of an occupational environment should, under nor-
mal circumstances, alert management to a potential problem [63]. Proper
medical and scientific research needs to be undertaken in order to help airline
management and crew to better understand both the short-term and long-
term medical effects of being subjected to air contamination.
Over the past fifty years, the concept of duty of care has emerged as one of
the most important legal responsibilities for employers. In the workplace, the
duty of care of an employer to its workers has been crystallised into OHS leg-
islation. Aviation safety is something that a person outside the industry would
understand to cover all aspects of safety, including the health and safety of
its workers. However, this does not seem to be how all industry insiders see
it. Many in the industry see aviation safety as being about making sure the
planes keep flying. Both the aviation regulators and the airlines themselves
think that OHS is not their business – which is strange, because if they do not
look after the health and safety of workers in the industry, then who will?
More scientific and medical research is needed on the short and long-
term effects of exposure to contaminated air and, until this is completed, all
areas of the aviation industry should take fume exposure events seriously;
they should be seen as an important part of educating crew and the aviation
industry, thereby addressing the problem.
Many of the world’s leading experts who have seen aircrew from around
the globe or were familiar with the issue spoke at a recent conference held in
London by the British Airline Pilot Association (BALPA) looking at the issues
of contaminated air by engine oils and concluded:
Crew Effects from Toxic Exposures on Aircraft 239
There is a workplace problem resulting in chronic and acute illness
amongst flight crew (both pilots and cabin crew).
The workplace in wich these illnesses are being induced is the aircraft
cabin environment. This is the resulting in significant flight safety issues, in
addition to unacceptable flight crew personnel healt implications.
Further, we are concerned the passengers may also be suffering from simi-
lar symptoms to those exhibited by flight crew.
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... Adverse effects being reported by aircrew in relation to exposures to aircraft supply air contamination include a range of both acute and chronic effects that is being labelled primarily as a discrete occupational health condition increasingly termed ' Aerotoxic Syndrome' [4][5][6][7][8][9]. The diffuse pattern of acute and chronic effects include the following areas: neurological, neurobehavioural, respiratory, cardiovascular, gastrointestinal, general (fatigue, Open Access *Correspondence: 1 Occupational and Environmental Health Research Group, University of Stirling, Stirling, UK Full list of author information is available at the end of the article rheumatological, chemical sensitivity, performance decrement, soft tissue), irritant and skin [6]. ...
... The pattern of symptoms reported included a diffuse range of acute and chronic effects include the following areas: neurological, neurobehavioural, respiratory, cardiovascular, gastrointestinal, general (fatigue, rheumatological, chemical sensitivity, performance decrement, soft tissue) irritant and skin [6]. Similar patterns have been increasingly reported elsewhere [4,5,9,[57][58][59][60][61][62][63][64][65][66][67][68]. The FAA reported a range of similar adverse effects as well as delayed effects could be expected following exposure to the complex mixtures associated with pyrolysed jet oils [53]. ...
... Michaelis et al. found a clear cause and effect relationship when taking into account symptoms, diagnoses and findings in relation to the occupational environment [6]. This was described as a new occupational disease in a similar manner to the 2005 reporting of the "development of an irreversible discrete occupational health condition" [4,6]. A clear cause and effect relationship between exposures and acute and chronic adverse effects and inadequate medical management has been reported elsewhere [7,67,69]. ...
Full-text available
Background Airline crew members report adverse health effects during and after inhalation exposure to engine oil fumes sourced to the air supply system onboard commercial and military aircraft. Most investigations into the causal factors of their reported symptoms focus on specific chemical contaminants in the fumes. The adverse health effects reported in aircrew exposed to the aircraft air supply, bled unfiltered off the engine or Auxiliary Power Unit (APU) may be related to particulate exposures, which are widely known to effect health. While oil contaminates the aircraft air supply, some suggest that this will only occur when there is a bearing seal failure, others document that there is low level oil contamination of the air supply during normal engine operation. This brief pilot study explores whether particulate exposure may be associated with the normal engine/APU and air supply operation and to therefore increase the understanding that UFP exposures may have on crew and passengers. Methods An ultrafine particle counter was utilised by an experienced airline captain in the passenger cabin of four short-haul commercial passenger aircraft. All flights were under 90 min on aircraft from two different carriers ranging from 7 months to 14 years old. Results UFP concentrations showed maximum concentrations ranging from 31,300 to 97,800 particles/cm ³ when APU was selected on as a source of air on the ground and with engine bleed air and the air conditioning packs selected on during the climb. In 2 of the 4 flights the peaks were associated with an engine oil smell. Increases in UFP particle concentrations occurred with changes in engine/APU power and air supply configuration changes. Conclusions This study identified increases in UFP concentrations associated with engine and APU power changes and changes in air supply configuration. These results correlated with times when engine and APU oil seals are known to be less effective, enabling oil leakage to occur. The concentrations reached in the passenger cabins exceeded those taken in other ground-based environments. UFP exposures in aircraft cabins during normal flight indicates there will be health consequences for long serving aircrew and some passengers.
... Thus, raising awareness, firstly among physicians, of the physical health effects of exposure to lubricating oilrelated atmospheric contamination is in itself important [28,29]. There is also the aspect of physical differences in the aircraft cabin environment compared with the normal terrestrial situation. ...
... In the absence of chemical meters continuously monitoring organophosphate levels one cannot "prove" that organophosphates (notably, TCPs) were present in the atmosphere on a particular flight. 28 Similarly, in the absence of reliable blood (or other biofluid) test convenient enough to be carried out shortly after landing one cannot "prove" that a given individual was exposed to TCPs and absorbed them. But it can be confidently anticipated that a suitable blood test will soon be available [60]. ...
Full-text available
It is known that organophosphates (tricresyl phosphates) are present in jet engine lubricating oil. Oil may leak into the aircraft cabin if its air supply is bled off the engine. Depending on the type of oil seal, this may always occur to a small degree. The amount of leakage may increase due to faulty maintenance (including during the interval immediately preceding a scheduled maintenance intervention). If there is actual failure of a component of the seal, leakage may be considerable. In any case, leakage tends to be greater when the engine is cold and when the engine is working hard. Furthermore, some oil is pyrolysed in the engine, and the complex mixture of pyrolysis products may also be present in the bleed air. Tricresyl phosphates are potent neurotoxins. This has been most extensively established through animal testing (mainly cats, chickens and rabbits). The effects of human exposure have mainly been deduced by extrapolation from animal exposure and from observing cases of accidental human exposure. Any agent that damages the nervous system is prima facie expected to have a very broad spectrum of effects, given the pervasive nature of the nervous system in the control of any large multicellular organism. The proposition examined in this paper is that certain substances, namely tricresyl phosphates and their derivatives, if present in aircraft cabin air and hence inhaled, cause neural degeneration. Sufficient evidence would appear to have accumulated to make this a definite aviation hazard. The frequency of occurrence of acute “fume events”, in which a high concentration of neurotoxins is likely to be released into the cabin, cannot be estimated with a high degree of certainty but would appear to be around one in a thousand commercial flights. These constitute a safety hazard. Evidence for almost omnipresent low concentrations of neurotoxins suggests an occupational health hazard for aircrew and frequently flying business passengers, since the tricresyl phosphates accumulate in the body. Priority actions are needed to ensure that especially vulnerable people do not travel in jet aircraft that use bleed air to pressurize the cabin and to develop an appropriate sensor for continuously monitoring cabin air quality.
... TCP has been detected widely-distributed in water, soil and air due to its release of production and use [20][21][22]. The presence of TCP and ToCP was reported in cockpits and cabin air [23][24][25], which was likely to cause the symptom clusters of the crew [26]. The conventional methods for detection of TCP in various samples are gas or liquid chromatography coupled to mass spectrometry [27][28][29][30]. ...
Full-text available
Tricresyl phosphate (TCP) is an organophosphorous neurotoxin that has been detected in water, soil and air. Exposure to TCP in cockpit and cabin air poses a severe threat to flight safety and the health of the aircraft cabin occupants. Conventional methods for the detection of TCP in various samples are gas or liquid chromatography coupled to mass spectrometry, which are complex and expensive. To develop a simple low-cost methodology for the real-time monitoring of TCP in the environment, an effective catalyst is demanded for the hydrolysis of TCP under neutral condition. In this study, Ruthenium (III) hydroxide and Iron (III) hydroxide are found to facilitate the production of the alcoholysis and hydrolysis products of TCP, suggesting their role as a catalyst. With this finding, these metal hydroxides provide new potential to realize not only simple colorimetric or electrochemical detection of TCP, but also a simple detoxication strategy for TCP in environment. In addition, the catalytic capability of Ru (III) or Fe (III) hydroxide for TCP gives a hint that they can potentially serve as catalysts for the hydrolysis of alcolyolysis of many other organophosphate compounds.
... [22] CBDP inhibits carboxylesterases, neurotoxic esterase, acetylcholinesterase and butyrylcholinesterase (BChE). [23,24] CBDP forms a covalent adduct to the active serine site (Ser198) of BChE. A study of the kinetics of adduct formation showed that CBDP was a potent BChE inhibitor (k i = 1.6 × 10 8 M À1 min À1 ). ...
Tri-ortho-cresyl phosphate (ToCP) is an anti-wear, flame retardant additive used in industrial lubricants, hydraulic fluids and gasoline. The neurotoxic effects of ToCP arise from the liver-activated metabolite 2-(o-cresyl)-4H-1,3,2-benzodioxaphosphoran-2-one (cresyl saligenin phosphate or CBDP), which inhibits esterase enzymes including butyrylcholinesterase (BChE). Following BChE adduction, CBDP undergoes hydrolysis to form the aged adduct ortho-cresyl phosphoserine (oCP-BChE), thus providing a biomarker of CBDP exposure. Previous studies have identified ToCP in aircraft cabin and cockpit air, but assessing human exposure has been hampered by the lack of a laboratory assay to confirm exposure. This work presents the development of an immunomagnetic-UHPLC-MS/MS method for the quantitation of unadducted BChE and the long-term CBDP biomarker, oCP-BChE, in human serum. The method has a reportable range from 2.0 ng/ml to 150 ng/ml, which is consistent with the sensitivity of methods used to detect organophosphorus nerve agent protein adducts. The assay demonstrated high intraday and interday accuracy (≥85%) and precision (RSD ≤ 15%) across the calibration range. The method was developed for future analyses of potential human exposure to CBDP. Analysis of human serum inhibited in vitro with CBDP demonstrated that the oCP-BChE adduct was stable for at least 72 h at 4, 22 and 37 °C. Compared to a previously reported assay, this method requires 75% less sample volume, reduces analysis time by a factor of 20 and demonstrates a threefold improvement in sensitivity. Published 2015. This article is a U.S. Government work and is in the public domain in the USA. Published 2015. This article is a U.S. Government work and is in the public domain in the USA.
Contamination of aircraft cabin air can result from leakage of engine oils and hydraulic fluids into bleed air. This may cause adverse health effects in cabin crews and passengers. To realistically mimic inhalation exposure to aircraft cabin bleed-air contaminants, a mini bleed-air contaminants simulator (Mini-BACS) was constructed and connected to an air-liquid interface (ALI) aerosol exposure system (AES). This unique “Mini-BACS + AES” setup provides steady conditions to perform ALI exposure of the mono- and co-culture lung models to fumes from pyrolysis of aircraft engine oils and hydraulic fluids at respectively 200 °C and 350 °C. Meanwhile, physicochemical characteristics of test atmospheres were continuously monitored during the entire ALI exposure, including chemical composition, particle number concentration (PNC) and particles size distribution (PSD). Additional off-line chemical characterization was also performed for the generated fume. We started with submerged exposure to fumes generated from 4 types of engine oil (Fume A, B, C, and D) and 2 types of hydraulic fluid (Fume E and F). Following submerged exposures, Fume E and F as well as Fume A and B exerted the highest toxicity, which were therefore further tested under ALI exposure conditions. ALI exposures reveal that these selected engine oil (0–100 mg/m³) and hydraulic fluid (0–90 mg/m³) fumes at tested dose-ranges can impair epithelial barrier functions, induce cytotoxicity, produce pro-inflammatory responses, and reduce cell viability. Hydraulic fluid fumes are more toxic than engine oil fumes on the mass concentration basis. This may be related to higher abundance of organophosphates (OPs, ≈2800 µg/m³) and smaller particle size (≈50 nm) of hydraulic fluid fumes. Our results suggest that exposure to engine oil and hydraulic fluid fumes can induce considerable lung toxicity, clearly reflecting the potential health risks of contaminated aircraft cabin air.
We reviewed 47 documents published 1967–2019 that reported measurements of volatile organic compounds (VOCs) on commercial aircraft. We compared the measurements with the air quality standards and guidelines for aircraft cabins and in some cases buildings. Average levels of VOCs for which limits exist were lower than the permissible levels except for benzene with average concentration at 5.9 ± 5.5 μg/m3. Toluene, benzene, ethylbenzene, formaldehyde, acetaldehyde, limonene, nonanal, hexanal, decanal, octanal, acetic acid, acetone, ethanol, butanal, acrolein, isoprene and menthol were the most frequently measured compounds. The concentrations of semi‐volatile organic compounds (SVOCs) and other contaminants did not exceed standards and guidelines in buildings except for the average NO2 concentration at 12 ppb. Although the focus was on VOCs, we also retrieved the data on other parameters characterizing cabin environment. Ozone concentration averaged 38 ppb below the upper limit recommended for aircraft. The outdoor air supply rate ranged from 1.7 to 39.5 L/s per person and averaged 6.0 ± 0.8 L/s/p (median 5.8 L/s/p), higher than the minimum level recommended for commercial aircraft. Carbon dioxide concentration averaged 1315 ± 232 ppm, lower than what is permitted in aircraft and close to what is permitted in buildings. Measured temperatures averaged 23.5 ± 0.8°C and were generally within the ranges recommended for avoiding thermal discomfort. Relative humidity averaged 16% ± 5%, lower than what is recommended in buildings.
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Organophosphorus flame retardants (OPFRs) are used as additives in plasticizers, foams, hydraulic fluids, anti-foam agents, and coatings for electronic components/devices to inhibit flames. These chemicals were developed and used as flame retardants because of environmental and health concerns of previously used brominated and chlorinated flame retardants (FRs). OPCFRs are divided into five main groups: organophosphates, organophosphonates, organophosphinates, organoposphine oxide, and organophosphites. Most of OPFRs are organophosphate esters that are further classified into the following five groups: 1. Aliphatic, 2. Brominated aliphatic, 3. Chlorinated aliphatic, 4. Aromatic-aliphatic, and 5. Aromatic phosphates. These OPFRs have the following neurotoxic actions: 1. Cholinergic Neurotoxicity, 2. Organophosphate-Induced Delayed Neurotoxicity (OPIDN), and 3. Organophosphate-Induced Chronic Neurotoxicity (OPICN) in addition to being endocrine disruptors. OPFRs have very low cholinergic neurotoxicity and this effect does not pose significant health hazards to adults or children. On the other hand, some OPFRs have shown to cause OPIDN that is a delayed central-peripheral axonopathy, characterized by neuronal cell death of the lower brain regions, spinal cord and peripheral nervous systems, leading to long-term neuronal injury. OPICN is characterized by neuronal cell death in the cortex, hippocampus campus and cerebellum and spinal cord. Finally, OPCFRs act as endocrine disrupters, that affect many functions of the body such thyroid glands and reproductive functions, and may be involved in the development of diabetes and cancer. Residues of these OPCFRs are widespread in the environment, home and workplaces. These chemicals adversely affect human health, especially for vulnerable population such as the elderly, pregnant women, fetuses, and children. Because some OPFRs cause neuronal cell death in the brain and spinal cord that do not repair as well as act as endocrine disrupters they may lead to permanent functional deficits such obesity, memory impairment, decreased motor skill and even more serious diseases such as diabetes and cancer. Because recent reports have accredited FRs for significant decrease in building fires, it is important to balance the risk and benefits of FRs and to use only the safest available FRs including OPFRs.
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Aircraft cabin air can possibly be contaminated by tricresyl phosphates (TCP) from jet engine oils during fume events. o-TCP, a known neurotoxin, has been addressed to be an agent that might cause the symptoms reported by cabin crews after fume events. A total of 332 urine samples of pilots and cabin crew members in common passenger airplanes, who reported fume/odour during their last flight, were analysed for three isomers of tricresyl phosphate metabolites as well as dialkyl and diaryl phosphate metabolites of four flame retardants. None of the samples contained o-TCP metabolites above the limit of detection (LOD 0.5 μg/l). Only one sample contained metabolites of m- and p-tricresyl phosphates with levels near the LOD. Median metabolite levels of tributyl phosphate (TBP), tris-(2-chloroethyl) phosphate (TCEP) and triphenyl phosphate (TPP) (DBP 0.28 μg/l; BCEP 0.33 μg/l; DPP 1.1 μg/l) were found to be significantly higher than in unexposed persons from the general population. Median tris-(2-chloropropyl) phosphate (TCPP) metabolite levels were significantly not higher in air crews than in controls. Health complaints reported by air crews can hardly be addressed to o-TCP exposure in cabin air. Elevated metabolite levels for TBP, TCEP and TPP in air crews might occur due to traces of hydraulic fluid in cabin air (TBP, TPP) or due to release of commonly used flame retardants from the highly flame protected environment in the airplane. A slight occupational exposure of air crews to organophosphates was shown.
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The concerns that were brought to the Australian Federation of Air Pilots regarding air quality problems revealed a number of operational and OHS issues. This prompted the design and conduct of a survey of symptoms in members who fly BAe 146 aircraft in Australia. A total of 19 pilots and two flight attendants responded. Survey respondents showed high rates of symptoms which included headaches, eye, skin and upper airway irritation, neuropsychological impairment, respiratory problems, food/alcohol intolerances, muscle/joint pain, diarrhoea, and so on. While the results of this survey cannot be considered representative, they do provide self-reported data from a small number of pilots about health problems on the BAe 146, and suggest that the denials by the airlines should be re-examined.
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A survey of health symptoms was undertaken in pilots who were members of the British Airline Pilots Association flying the Boeing 737, Boeing 757 and Airbus A320. Six hundred questionnaires were sent out to members, and 106 pilots responded. Survey respondents were predominantly male (104/106) and many had extensive flying experience. With regard to leak events (that is, leaks of engine oil and hydraulic fluids into the aircraft), 93/106 reported that they had been involved in at least one. The total number of incidents reported was estimated to be 1,674+, with all but seven occurring on the B757. Following exposure to the contaminated air, high rates of symptoms were reported by the pilots, including: irritation of the eyes, nose and throat; headaches, light-headedness and dizziness; fatigue, weakness and a decrease in performance; a general increase in feeling unwell; concentration difficulties and confusion; diarrhoea; nausea, vomiting and gastrointestinal problems; numbness (head, limbs, lips, fingers); short-term memory impairment; and joint pain/muscle weakness. These symptoms are a direct breach of US Federal Aviation Regulation 25.831, which includes a specific requirement that cabin air should not cause symptoms of discomfort, fatigue, irritation or toxicity.
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The term "aerotoxic syndrome" was proposed in 1999 to describe the association of symptoms observed among flight crew and cabin crew who have been exposed to hydraulic fluid or engine oil vapours or mists. A descriptive epidemiological study was conducted to investigate the health effects of aircrew through a questionnaire mail-out. Most of the respondents (88%) reported that symptoms occurred after exposure to engine oil or hydraulic fluid leaks which caused odours and/ or visible contamination in the cabin. Invariably, aircrew directly attributed their symptoms to exposure to in-cabin airborne contaminants. A comparison between 18 respondents from the United States and the 50 Australian respondents shows significant similarities in reported symptoms. There was sufficient commonality in reported symptoms to conclude a symptom basis for aerotoxic syndrome.
AlliedSignal Aerospace, the manufacturer of the propulsion engines and auxiliary power unit of the BAe146 airframe performed air quality testing in cooperation with the airframe manufacturer, British Aerospace and the customer, Ansett Airlines to identify possible air contaminants entering the aircraft and to evaluate other factors that could affect the comfort of the aircraft occupants. Parameters measured include: volatile and semivolatile organic compounds, aldehydes, carbon dioxide, carbon monoxide, oxygen, relative humidity, temperature, and airflow. The airline evaluated the test results and recommendations and implemented changes in the aircraft air handling system based on these results. Measurement of carbon dioxide levels in the galleys was performed by the airline after modification to verify the effectiveness of the changes. Integrated carbon dioxide levels ranged from 780 to 4700 ppm during flight in the aft galley. Carbon monoxide was not detected by on-line measurement methods, and was at the method detection limit of the integrated sampling techniques. No tri-ortho-cresylphospahte, trimeta-and-para-cresylphosphate, or trimethylolpropane phosphate were detected on charcoal filters used in the air supply systems to the cabin and cockpit. These filters had been in use for over 1000 hours. Tri-butyl-phosphate was detected, however. Volatile organic contaminants in the supply air and aft galley ranged from 0.11 to 4.43 mg/M3. Summation of odor thresholds ranged from 0.28 to 5.35 for mixtures in air and 9.63 to 88.9 for mixtures in water, indicating that some odors could potentially be detected.
Neurological damage from exposures to organophosphate (OP) chemicals has been reported since 1899, including acute fatal poisoning from nerve warfare agents and agricultural insecticides. Chlorpyrifos is the most commonly used insecticide in the United States. Sensitive testing to evaluate effects of chronic low-level exposures to OPs has not been applied until recently. Methods: Twenty-two patients exposed to assumed low levels of chlorpyrifos were studied for neurobehavioral impairments. Impairment was detected by testing balance, simple and choice reaction time, blink reflex latency, visual field performance, hearing, color discrimination and grip strength and compared to unexposed referents after adjusting for age, sex, height and other test determinants. Cognitive, recall, perceptual motor speed and embedded memory functions and moods were also compared, adjusted for age, educational attainment and other determinants. Results: Exposed subjects had significantly impaired balance, visual fields, color discrimination, simple and choice reaction time, grip strength, hearing, cognitive, recall, embedded memory and perceptual motor performance. No confounding factors nor other diagnoses explained the abnormalities. Exposure to chlorpyrifos, sprayed indoors, impaired brains, probably irreversibly.
Poor air quality and health complaints from flight crews operating BAe-146 aircraft, requiring admission to emergency departments on several occasions, led to an investigation into the source of these problems. Health complaints could be classified as those consistent with exposure to carbon monoxide, respiratory irritants, and possible neurological agents. Cabin air is bled off from the engine's combustion air, passes through a catalytic converter to clean the air from oil contaminants, is cooled from 550° to 50°C, and enters the cabin after it passes through an airpack unit which conditions the air as appropriate. Excessive oil leakage from oil seals overloaded the catalytic converter, allowing smoke and lubricating oil components to enter the cabin. A complaint aircraft air, during a test flight, was found to contain oil contaminants including siloxane lubricating oils, as well as methylated propane and butane ester derivatives. Tricresyl phosphates, known to be neurotoxic, were identified in bulk oil samples, but could not be demonstrated in the cabin air. Air quality measurements in a problem aircraft tested on the tarmac indicated carbon monoxide at 3 ppm and carbon dioxide at 900 ppm. Air quality measurements during normal commercial flights of three noncomplaint aircraft (two BAe-146s and one de Haviland Dash 8-100) showed no detectable levels of carbon monoxide, 800 to 2700 ppm for carbon dioxide, and 19.6 to 21.9 percent for oxygen. Carbon dioxide and oxygen levels would change predictably during takeoff and landing for the former and pressurization and depressurization for the latter. Carboxyhemoglobin levels in four individuals admitted to emergency departments ranged from 0.7 to 2.0 percent. Since no direct carbon monoxide measurements were available during these incidents, it was recommended that potential problem aircraft be equipped with datalogging carbon monoxide monitors to identify or eliminate carbon monoxide exposure as a problem.
Acute organophosphate pesticide poisonings cause substantial morbidity and mortality world wide; however, whether organophosphates cause chronic neurological sequelae has not been established. To see whether single episodes of acute unintentional organophosphate intoxication lead to chronic neuropsychological dysfunction, we carried out a retrospective study of agricultural workers in Nicaragua who had been admitted to hospital between July 1, 1986, and July 31, 1988, for occupationally related organophosphate intoxication. This "poisoned" group (36 men) was tested on average about two years after the episode of pesticide poisoning and compared with a matched control group. The poisoned group did much worse than the control group on all neuropsychological subtests, with significantly worse performance on five of six subtests of a World Health Organisation neuropsychological test battery and on 3 of 6 additional tests that assessed verbal and visual attention, visual memory, visuomotor speed, sequencing and problem solving, and motor steadiness and dexterity. Differences in neuropsychological performance could not be explained by other factors. The findings of a persistent decrease in neuropsychological performance among individuals with previous intoxication emphasise the importance of prevention of even single episodes of organophosphate poisoning.