A review of health effects associated with exposure to jet engine emissions in and around airports

Background

Airport personnel are at risk of occupational exposure to jet engine emissions, which similarly to diesel exhaust emissions include volatile organic compounds and particulate matter consisting of an inorganic carbon core with associated polycyclic aromatic hydrocarbons, and metals. Diesel exhaust is classified as carcinogenic and the particulate fraction has in itself been linked to several adverse health effects including cancer.

Photo of Alouette III No 196 showing soiling of the tail boom with soot from exhaust gasses.
Method

In this review, we summarize the available scientific literature covering human health effects of exposure to airport emissions, both in occupational settings and for residents living close to airports. We also report the findings from the limited scientific mechanistic studies of jet engine emissions in animal and cell models.

Beechcraft 200 Super King Air No 240 showing soiling of the engine panels with soot from exhaust gasses.
Results

Jet engine emissions contain large amounts of nano-sized particles, which are particularly prone to reach the lower airways upon inhalation. Size of particles and emission levels depend on type of aircraft, engine conditions, and fuel type, as well as on operation modes. Exposure to jet engine emissions is reported to be associated with biomarkers of exposure as well as biomarkers of effect among airport personnel, especially in ground-support functions. Proximity to running jet engines or to the airport as such for residential areas is associated with increased exposure and with increased risk of disease, increased hospital admissions and self-reported lung symptoms.

Conclusion

We conclude that though the literature is scarce and with low consistency in methods and measured biomarkers, there is evidence that jet engine emissions have physicochemical properties similar to diesel exhaust particles, and that exposure to jet engine emissions is associated with similar adverse health effects as exposure to diesel exhaust particles and other traffic emissions.

Read full article journal at BMC

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The layout of the Irish Air Corps base at Casement Aerodrome ensures that aircraft exhaust gasses are blown over populated sections of the airbase when winds are from the south, south east or south west. This includes hangars, offices, workshops and living in accommodation such as the apprentice hostel and married quarters. Calm weather also creates conditions where exhaust gasses linger in higher concentrations.

This results in all Irish Air Corps personnel (commissioned, enlisted, civilian & living-in family) being exposed to emissions from idling aircraft engines, emissions that are known to cause harm.

In the mid 1990s a study of air pollution adjacent to the ramp area at Baldonnel was commissioned. This report relating to this study has gone missing. 

  • Anecdotal evidence suggests increased prevalence of occupational asthma & adult onset asthma amongst serving & former personnel who served in Baldonnel or Gormanston aerodromes. 
  • Older gas turbine engines produce dirtier exhaust gasses.
  • Idling gas turbine engines produce dirtier exhaust gasses.
Below are some of the gas turbine powered Air Corps aircraft that were powered by elderly engine designs.
AircraftRetiredEngine FamilyFirst Run
Alouette III2007Turbomeca Artouste1947
Fouga Magister1999Turbomeca Marboré1951
Gazelle2005Turbomeca Astazou1957
King Air 2002009Pratt & Whitney Canada PT61960
Dauphin II2005Turbomeca Arriel1974

DELAY – DENY – DIE

‘IT’S A SCANDAL’ RAF airman who flew with Prince William proves rare cancer was caused by the Sea King chopper

AN airman who flew choppers with Prince William has proved his rare form of bone marrow cancer was caused by the RAF Sea King.

Flight Sergeant Zach Stubbings was diagnosed with multiple myeloma after years of inhaling toxic exhaust fumes spewed from the powerful twin engines of the now retired aircraft.

Flight Sergeant Zach Stubbings, who flew choppers with Prince William, has proved his rare form of bone marrow cancer was caused by the RAF Sea King

And last month, the winch operator won a settlement from the Ministry of Defence after a six-year legal battle. Zach has been paid an undisclosed sum and the MoD had to admit in writing his 15 years of service in the RAF caused his life-threatening condition.

It will likely spark concern for the royals. Wills flew the Sea King in 150 search-and-rescue operations over a three-year period.  It is not known if he was affected by the fumes. Prince Andrew also flew the aircraft in the Falklands in 1982.

And The Sun can lift the lid on an apparent government cover-up of the issue.  Bombshell documents uncovered by Zach during his legal fight prove experts warned the MoD of the dangers of the Sea King exhaust as far back as 1999 but nothing was done.

Zach, 42, of Cardiff, said: “The Government chose to ignore it. It’s a scandal.”

Read more on the The sun

Particulate matter from aircraft engines affects airways

According to the World Health Organization (WHO), seven million people worldwide die as a consequence of air pollution every year. For around 20 years, studies have shown that air-borne particulate matter negatively affects human health. Now, in addition to already investigated particle sources like emissions from heating systems, industry and road traffic, aircraft turbine engine particle emissions have also become more important.

Photo of Alouette III No 196 showing soiling of the tail boom with soot from exhaust gasses.

In a unique, innovative experiment, researchers have investigated the effect of exhaust particles from aircraft turbine engines on human lung cells.

The cells reacted most strongly to particles emitted during ground idling.

It was also shown that the cytotoxic effect is only to some extent comparable to that of particles from gasoline and diesel engines.The primary solid particles, i.e. those emitted directly from the source, have the strongest effect on people in its immediate vicinity. 

Now a multidisciplinary team, led by lung researcher Marianne Geiser of the Institute of Anatomy at the University of Bern, together with colleagues from Empa Dübendorf and the University of Applied Sciences and Arts Northwestern Switzerland (FHNW), has shown that primary soot particles from kerosene combustion in aircraft turbine engines also cause direct damage to lung cells and can trigger an inflammatory reaction if the solid particles are inhaled in the direct vicinity of the engine.

The researchers demonstrated for the first time that the damaging effects also depend on the operating conditions of the turbine engine, the composition of the fuel, and the structure of the generated particles.

Beechcraft 200 Super King Air No 240 showing soiling of the engine panels with soot from exhaust gasses.

Extremely small particles in the nanoscale range

Particles emitted from aircraft turbine engines are generally ultrafine, i.e. smaller than 100 nm. By way of comparison, a human hair has a diameter of about 80,000 nm. When inhaled, these nanoparticles — like those from other combustion sources -efficiently deposit in the airways. In healthy people, the well-developed defense mechanisms in the lungs normally take care of rendering the deposited particles ineffective and removing them from the lungs as quickly as possible.

However, if the inhaled particles manage to overcome these defense mechanisms, due to their structure or physico-chemical properties, there is a danger for irreparable damage to the lung tissue. This process, already known to researchers from earlier experiments with particle emissions from gasoline and diesel engines, has now also been observed for particle emissions from aircraft engines.

Toxicity depends on the operating conditions of the turbines and the type of fuel

Evidence of increased cell membrane damage and oxidative stress in the cell cultures was identified. Oxidative stress accelerates ageing of cells and can be a trigger for cancer or immune system diseases.

Overall, according to the researchers, it has been demonstrated that the cell-damaging effect caused by exposure to particles generated by the combustion of gasoline, diesel and kerosene fuel are comparable for similar doses and exposure times.

Additionally, a similar pattern was found in the secretion of inflammatory cytokines after exposure to gasoline and kerosene fuel particles.

Aerosols: distance from the source is crucial

Aerosols are the finest solid or fluid substance suspended in the air. In combustion processes, the composition of ultrafine particles is highly variable. In addition, aerosols are unstable, and they are modified after their formation. Primary ultrafine solid particles have a high diffusion velocity. As a result, at high concentrations such particles either stick together or attach to other particles. Therefore, the effect of primary ultrafine particles depends on the distance from the source, implying that there is a difference depending on whether a person is close to the source (such as people at the roadside ) or at a greater distance (aircraft taxiing or taking off). Further research is needed to clarify how strong the impact would be at a greater distance from an aircraft engine

Read full article in ScienceDaily

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The layout of the Irish Air Corps base at Casement Aerodrome ensures that aircraft exhaust gasses are blown over populated sections of the airbase when winds are from the south, south east or south west. This includes hangars, offices, workshops and living in accommodation such as the apprentice hostel and married quarters. Calm weather also creates conditions where exhaust gasses linger in higher concentrations.

This results in all Irish Air Corps personnel (commissioned, enlisted, civilian & family) being exposed to emissions from idling aircraft engines, emissions that are known to cause harm.

In the mid 1990s a study of air pollution adjacent to the ramp area at Baldonnel was commissioned. This report relating to this study has gone missing. 

  • Anecdotal evidence suggests increased prevalence of occupational asthma & adult onset asthma amongst serving & former personnel who served in Baldonnel or Gormanston aerodromes. 
  • Older gas turbine engines produce dirtier exhaust gasses.
  • Idling gas turbine engines produce dirtier exhaust gasses.
Below are some of the gas turbine powered Air Corps aircraft that were powered by elderly engine designs.
AircraftRetiredEngine FamilyFirst Run
Alouette III2007Turbomeca Artouste1947
Fouga Magister1999Turbomeca Marboré1951
Gazelle2005Turbomeca Astazou1957
King Air 2002009Pratt & Whitney Canada PT61960
Dauphin II2005Turbomeca Arriel1974

DELAY – DENY – DIE

RAAF jet fuel damaged ground crews’ body cells; long-term consequences unknown, says groundbreaking research

Royal Australian Air Force (RAAF) personnel who worked with widely used jet fuel suffered damage to their body’s cells with unknown long-term consequences, according to groundbreaking research released after a Freedom of Information laws request.

Defence’s senior physician in occupational and environmental medicine, Dr Ian Gardner, described the findings as a “part of the puzzle” and a hypothesis-making study”, and pointed it out that it was one of a series of pieces of research currently underway.

“What it shows is there is evidence of small but persistent cellular damage,” Dr Gardner told the ABC. He said it was not yet clear what the long-term effects of that damage might be.

“For the future though there are a lot of other aircraft maintenance workers who have done similar jobs on other aircraft types, and now Defence and DVA and Air Force are considering what additional work should be done in relation to those other people who are not actually on the F-111 programs but have done essentially similar work,” Dr Gardner said.

The Jet Fuel Syndrome Study also shows that the fuel is more toxic to the body’s cells than the two solvents initially blamed for the sickness suffered by the deseal/reseal workers, and that the toxicity is even higher when those solvents and the fuel were mixed.

The results of the research project, headed by Professor Francis Bowling of Brisbane’s Mater Hospital, were handed to Defence last September, and have been the subject of significant scrutiny and review due to the potential significance of the findings.

They will give heart to former and serving Defence personnel who believe they have been left out in the cold by Defence after developing serious health complaints while working with fuel and other substances.

Read full article on ABC Australia from 2015

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Junior Minister with responsibility for Defence said in the Dáil that he was assured by the Irish Air Corps that the RAAF F1-11 deseal/reseal exposure tragedy is completely different to any exposures at the Irish Air Corps.

Was the minister suggesting that Irish Air Corps gas turbine engines don’t run on jet fuel?

DELAY – DENY – DIE

Irish Air Corps whistle-blower claims death toll from chemical-linked illnesses surpasses 72

A MAN WHO is taking the State to court over his time in the Air Corps believes 72 of his colleagues died prematurely, linking their deaths to alleged chemical exposure at work.

The recent death of a former airman has brought the alleged death toll to 72, according to the whistle-blower.

He also alleges that:

  • 72 verified deaths have occurred in total since 1980
  • 59 of these deaths have occurred since 2000
  • 36 of these deaths have occurred since 2010

The whistle-blower is claiming that the State neglected health and safety rules and exposed himself and his fellow workers to seriously harmful levels of toxic chemicals. This continues to be strongly contested by the State.

The whistle-blowers in this case alleges there was a disregard for the safety of young Air Corps members. According to an online resource created for those who believe they were affected by the chemical exposure, there was:

  • No meaningful chemical risk assessments.
  • No risk specific health surveillance
  • No Personal Protective Equipment (PPE) issued
  • No chemical health and safety training whatsoever
  • No reporting of health and safety incidents
  • No follow up of unusual illnesses by medical personnel
  • Ignoring dangerous air quality reports
  • Personnel doused in toxic chemicals as pranks (hazing) incidents
  • Highly toxic chemicals disposed of onsite in an unsafe manner

Read full article on The Journal website below…

Bilateral Vestibular Dysfunction Associated With Chronic Exposure to Military Jet Fuel

Abstract

We describe three patients diagnosed with bilateral vestibular dysfunction associated with the jet propellant type-eight (JP-8) fuel exposure. Chronic exposure to aromatic and aliphatic hydrocarbons, which are the main constituents of JP-8 military aircraft jet fuel, occurred over 3–5 years’ duration while working on or near the flight line.

Exposure to toxic hydrocarbons was substantiated by the presence of JP-8 metabolite n-hexane in the blood of one of the cases. The presenting symptoms were dizziness, headache, fatigue, and imbalance. Rotational chair testing confirmed bilateral vestibular dysfunction in all the three patients. Vestibular function improved over time once the exposure was removed.

Bilateral vestibular dysfunction has been associated with hydrocarbon exposure in humans, but only recently has emphasis been placed specifically on the detrimental effects of JP-8 jet fuel and its numerous hydrocarbon constituents. Data are limited on the mechanism of JP-8-induced vestibular dysfunction or ototoxicity.

Early recognition of JP-8 toxicity risk, cessation of exposure, and customized vestibular therapy offer the best chance for improved balance. Bilateral vestibular impairment is under-recognized in those chronically exposed to all forms of jet fuel.

CASE REPORTS

Case 1: Military Flight Refueler

A37-year-old woman presented with several years of progressively worsening continuous dizziness, headache, and fatigue. The dizziness consisted of sensations of spinning, tilting, disequilibrium, and head fullness. She did not report tinnitus or hearing loss. She was employed as a military flight refueler and exposed to JP-8 vapors and exhaust while working full-time on and around a KC-135E tanker aircraft, a plane used for performing in-flight refueling missions. She worked in a large enclosed hangar that housed all but the tail section of the tanker aircraft. During inspection and maintenance of the aircraft, up to 9,750 gallons of fuel would be loaded. Jet fuel vapors were always present in the hangar due to venting, small leaks, and fuel residue. Fuel vapor concentrations were even greater when engine maintenance necessitated removal of fuel filters and fuel components, draining of fuel into buckets, and opening of fuel lines. She worked in engine maintenance with over 4 years of inhalational and dermal exposure to JP-4 and JP-8.

Her examination showed moderately impaired equilibrium to walk only three steps in tandem before taking a sidestep. Romberg testing revealed more sway during eye closure but no falling. Her medical and neurological examinations were normal. There was no spontaneous, gaze, or positional nystagmus. Qualitative head impulse test was not performed at that time.
Cases 2 and 3

The following two patients were employees in a small purchasing warehouse, located 75 feet south of the fight path, which was separated from the blast and heat emissions from jet aircraft engines by a metal-coated and chain-link fence. Neither air conditioning vents nor carpet had not been cleaned or replaced for over a decade. On inspection, the vents were found to be mal-functioning such that air was able to enter the building but unable to escape. Subsequent inspection by the U. S. Occupational Safety and Health Administration (OSHA) confirmed poor ventilation evidenced by carbon dioxide concentrations >1,500ppm (nor-mal <1,000 ppm according to the U.S. Department of Labor). Hydrocarbons discovered in the carpet via an independent analysis using gas chromatography/mass spectrometry included undecane (C11), dodecane (C12), tridecane (C13), tetradecane (C14), and toluene (C8)—all known JP-8 constituents (2). The chemicals present in the office carpet likely reflected poor indoor air quality. Vapor, aerosol, dermal, and eye absorption of JP-8 are presumed.

Case 2: Warehouse Employe 1

A 45-year-old female contracting officer for the National Guard reported several years of imbalance, headache, fatigue, eye and skin irritation, coughing, sinus congestion, recurrent urinary tract infections, chest tightness, irritability, depression, shortness of breath, palpitations, and numbness. She described her dizziness as an intermittent floating and a rightward tilting sensation with imbalance lasting minutes to hours without any particular pattern. She had a history of asthma and allergies including reaction to aspirin causing urticaria and airway obstruction. In 1998, she developed syncope and dizziness though no specific cause was found. She started working in the building in 1994 and worked there full-time for 5 years.

Case 3: Warehouse Employe 2

A 54-year-old female National Guard contract specialist presented with 2 years of intermittent dizziness, blurred vision, and occasional palpitations. Dizziness was experienced at least 3 days a week. She reported intermittent problems with erratic heart beats, cough, sneezing, headaches, fatigue, recurrent sinus infections, upper respiratory tract, and bladder infections. She worked in the purchasing warehouse full-time for 3 years. When away from the workplace her symptoms were improved. After moving with her colleagues into a new building, the frequency of dizziness was lessened.

Human Exposure and Absorption of Jet Fuel

Military duties such as fuel transportation, aircraft fueling and defueling, aircraft maintenance, cold aircraft engine starts, maintenance of equipment and machinery, use of tent heaters, and cleaning or degreasing with fuel may result in jet fuel exposure. Fuel handlers, mechanics, flight line personnel, especially crew chiefs, and even incidental workers remain at risk for developing illness secondary to chronic JP-8 fuel exposure in aerosol, vapor or liquid form. JP-8 is one of the most common occupational chemical exposures in the US military (1).

The Air Force has set recommended exposure limits for JP-8 at 63ppm (447mg/m3 as an 8-h time-weighted average) (22).In addition to exposure by JP-8 vapor inhalation, toxicity may also occur by absorption through the skin, which is proportional to the amount of skin exposed and the duration of exposure (23, 24). In addition to the standard operating procedure and safety guidelines, double gloving, immediate onsite laundering of contaminated/soiled jumpsuits, regular washing of safety goggles and masks, reduced foam handling time, smoking cessation, adequate cross ventilation, and frequent shift breaks may reduce the overall risk of JP-8 induced illness

At this time, OSHA has not determined a legal limit for jet fuels in workroom air. The U.S. National Institute of Occupational Safety and Health set a recommended limit of 100mg/m3 for kerosene in air averaged over a 10-h work day. Multi-organ toxicity has been documented from JP-8 exposure in animal experiments over the past 15 years. More recently, toxicology researchers are investigating the adverse tissue effects of JP-8 jet fuel in concentrations well below permissible exposure limits.

Ultimately, the new data may help us to better understand the emerging genetic, metabolic and inflammatory mechanisms underpinning JP-8 cellular toxicity—including auditory and vestibular toxicity—and lead to a reassessment of the safe JP-8 exposure limits (25, 26).

CONCLUSION

Bilateral vestibular dysfunction in these three patients with prolonged vapor and dermal JP-8 fuel exposure should raise awareness in people with occupations that expose them to jet fuels, liquid hydrocarbons, or organic solvents. Dizziness and mild imbalance may be the main initial symptoms. Early recognition and limiting further exposure as well as treatment with vestibular therapy (32) may improve their function and quality of life


Bilateral Vestibular Dysfunction… (PDF Download Available)
. Available from: https://www.researchgate.net/publication/325175906_Bilateral_Vestibular_Dysfunction_Associated_With_Chronic_Exposure_to_Military_Jet_Propellant_Type-Eight_Jet_Fuel

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Difference between Jet A1 & JP-8

Jet fuel, aviation turbine fuel (ATF), or avtur, is a type of aviation fuel designed for use in aircraft powered by gas-turbine engines. It is colorless to straw-colored in appearance. The most commonly used fuels for commercial aviation are Jet A and Jet A-1, which are produced to a standardized international specification. The only other jet fuel commonly used in civilian turbine-engine powered aviation is Jet B, which is used for its enhanced cold-weather performance.

Jet fuel is a mixture of a large number of different hydrocarbons. The range of their sizes (molecular weights or carbon numbers) is defined by the requirements for the product, such as the freezing or smoke point. Kerosene-type jet fuel (including Jet A and Jet A-1) has a carbon number distribution between about 8 and 16 (carbon atoms per molecule); wide-cut or naphtha-type jet fuel (including Jet B), between about 5 and 15.[1]

Additives

The DEF STAN 91-91 (UK) and ASTM D1655 (international) specifications allow for certain additives to be added to jet fuel, including:[13][14]

  • Antioxidants to prevent gumming, usually based on alkylated phenols, e.g., AO-30, AO-31, or AO-37; 
  • Antistatic agents, to dissipate static electricity and prevent sparking; Stadis 450, with dinonylnaphthylsulfonic acid (DINNSA) as a component, is an example
  • Corrosion inhibitors, e.g., DCI-4A used for civilian and military fuels, and DCI-6A used for military fuels;
  • Fuel system icing inhibitor (FSII) agents, e.g., Di-EGME; FSII is often mixed at the point-of-sale so that users with heated fuel lines do not have to pay the extra expense.
  • Biocides are to remediate microbial (i.e., bacterial and fungal) growth present in aircraft fuel systems. Currently, two biocides are approved for use by most aircraft and turbine engine original equipment manufacturers (OEMs); Kathon FP1.5 Microbiocide and Biobor JF.[15]
  • Metal deactivator can be added to remediate the deleterious effects of trace metals on the thermal stability of the fuel. The one allowable additive is N,N’-disalicylidene 1,2-propanediamine.

As the aviation industry’s jet kerosene demands have increased to more than 5% of all refined products derived from crude, it has been necessary for the refiner to optimize the yield of jet kerosene, a high value product, by varying process techniques. New processes have allowed flexibility in the choice of crudes, the use of coal tar sands as a source of molecules and the manufacture of synthetic blend stocks. Due to the number and severity of the processes used, it is often necessary and sometimes mandatory to use additives. These additives may, for example, prevent the formation of harmful chemical species or improve a property of a fuel to prevent further engine wear.

https://en.wikipedia.org/wiki/Jet_fuel

JP-8, or JP8 (for “Jet Propellant 8”) is a jet fuel, specified and used widely by the US military. It is specified by MIL-DTL-83133 and British Defence Standard 91-87, and similar to commercial aviation’s Jet A-1, but with the addition of corrosion inhibitor and anti-icing additives.

A kerosene-based fuel, JP-8 is projected to remain in use at least until 2025. It was first introduced at NATO bases in 1978. Its NATO code is F-34.

https://en.wikipedia.org/wiki/JP-8

Ototoxicity – Ototoxicants in the environment and workplace

Ototoxicity is the property of being toxic to the ear (oto-), specifically the cochlea or auditory nerve and sometimes the vestibular system, for example, as a side effect of a drug.

The effects of ototoxicity can be reversible and temporary, or irreversible and permanent. It has been recognized since the 19th century.[1] There are many well-known ototoxic drugs used in clinical situations, and they are prescribed, despite the risk of hearing disorders, to very serious health conditions.[2]

Ototoxic drugs include antibiotics such as gentamicin, loop diuretics such as furosemide and platinum-based chemotherapy agents such as cisplatin. A number of nonsteroidal anti-inflammatory drugs (NSAIDS) have also been shown to be ototoxic.[3][citation needed]

This can result in sensorineural hearing loss, dysequilibrium, or both. Some environmental and occupational chemicals have also been shown to affect the auditory system and interact with noise.[4]

Signs and symptoms

Symptoms of ototoxicity include partial or profound hearing loss, vertigo, and tinnitus.[5]

The cochlea is primarily a hearing structure situated in the inner ear. It is the snail-shaped shell containing several nerve endings that makes hearing possible.[6] Ototoxicity typically results when the inner ear is poisoned by medication that damages the cochlea, vestibule, semi-circular canals, or the auditory/ vestibulocochlear nerve. The damaged structure then produces the symptoms the patient presents with. Ototoxicity in the cochlea may cause hearing loss of the high-frequency pitch ranges or complete deafness, or losses at points between.[7] It may present with bilaterally symmetrical symptoms, or asymmetrically, with one ear developing the condition after the other or not at all.[7] The time frames for progress of the disease vary greatly and symptoms of hearing loss may be temporary or permanent.[6]

The vestibule and semi-circular canal are inner-ear components that comprise the vestibular system. Together they detect all directions of head movement. Two types of otolith organs are housed in the vestibule: the saccule, which points vertically and detects vertical acceleration, and the utricle, which points horizontally and detects horizontal acceleration. The otolith organs together sense the head’s position with respect to gravity when the body is static; then the head’s movement when it tilts; and pitch changes during any linear motion of the head. The saccule and utricle detect different motions, which information the brain receives and integrates to determine where the head is and how and where it is moving.

The semi-circular canals are three bony structures filled with fluid. As with the vestibule, the primary purpose of the canals is to detect movement. Each canal is oriented at right angles to the others, enabling detection of movement in any plane. The posterior canal detects rolling motion, or motion about the X axis; the anterior canal detects pitch, or motion about the Y axis; the horizontal canal detects yaw motion, or motion about the Z axis. When a medication is toxic in the vestibule or the semi-circular canals, the patient senses loss of balance or orientation rather than losses in hearing. Symptoms in these organs present as vertigo, difficulties walking in low light and darkness, disequilibrium, oscillopsia among others.[7] Each of these problems is related to balance and the mind is confused with the direction of motion or lack of motion. Both the vestibule and semi-circular canals transmit information to the brain about movement; when these are poisoned, they are unable to function properly which results in miscommunication with the brain.

When the vestibule and/or semi-circular canals are affected by ototoxicity, the eye can also be affected. Nystagmus and oscillopsia are two conditions that overlap the vestibular and ocular systems. These symptoms cause the patient to have difficulties with seeing and processing images. The body subconsciously tries to compensate for the imbalance signals being sent to the brain by trying to obtain visual cues to support the information it is receiving. This results in that dizziness and “woozy” feeling patients use to describe conditions such as oscillopsia and vertigo.[7]

Cranial nerve VIII, is the least affected component of the ear when ototoxicity arises, but if the nerve is affected, the damage is most often permanent. Symptoms present similar to those resulting from vestibular and cochlear damage, including tinnitus, ringing of the ears, difficulty walking, deafness, and balance and orientation issues.

Ototoxicants in the environment and workplace

Ototoxic effects are also seen with quinine, pesticides, solvents, asphyxiants (such as carbon monoxide) and heavy metals such as mercury and lead.[4][5][36] When combining multiple ototoxicants, the risk of hearing loss becomes greater.[37] As these exposures are common, this hearing impairment can affects many occupations and industries.[38]

Ototoxic chemicals in the environment (from contaminated air or water) or in the workplace interact with mechanical stresses on the hair cells of the cochlea in different ways. For organic solvents such as toluene, styrene or xylene, the combined exposure with noise increases the risk of occupational hearing loss in a synergistic manner.[4][39] The risk is greatest when the co-exposure is with impulse noise.[40][41] Carbon monoxide has been shown to increase the severity of the hearing loss from noise.[39] Given the potential for enhanced risk of hearing loss, exposures and contact with products such as paint thinners, degreasers, white spirits, exhaust, should be kept to a minimum. Noise exposures should be kept below 85 decibels, and the chemical exposures should be below the recommended exposure limits given by regulatory agencies.

Drug exposures mixed with noise potentially lead to increased risk of ototoxic hearing loss. Noise exposure combined with the chemotherapeutic cisplatin puts individuals at increased risk of ototoxic hearing loss.[33] Noise at 85 dB SPL or above added to the amount of hair cell death in the high frequency region of the cochlea In chinchillas.[42]

The hearing loss caused by chemicals can be very similar to a hearing loss caused by excessive noise. A 2018 informational bulletin by the US Occupational Safety and Health Administration (OSHA) and the National Institute for Occupational Safety and Health (NIOSH) introduces the issue, provides examples of ototoxic chemicals, lists the industries and occupations at risk and provides prevention information.[43]

Treatment

No specific treatment may be available, but withdrawal of the ototoxic drug may be warranted when the consequences of doing so are less severe than those of the ototoxicity.[5] Co-administration of anti-oxidants may limit the ototoxic effects.[33]

Ototoxic monitoring during exposure is recommended by the American Academy of Audiology to allow for proper detection and possible prevention or rehabilitation of the hearing loss through a cochlear implant or hearing aid. Monitoring can be completed through performing otoacoustic emissions testing or high frequency audiometry. Successful monitoring includes a baseline test before, or soon after, exposure to the ototoxicant. Follow-up testing is completed in increments after the first exposure, throughout the cessation of treatment. Shifts in hearing status are monitored and relayed to the prescribing physician to make treatment decisions.[44]

It is difficult to distinguish between nerve damage and structural damage due to similarity of the symptoms. Diagnosis of ototoxicity typically results from ruling out all other possible sources of hearing loss and is often the catchall explanation for the symptoms. Treatment options vary depending on the patient and the diagnosis. Some patients experience only temporary symptoms that do not require drastic treatment while others can be treated with medication. Physical therapy may prove useful for regaining balance and walking abilities. Cochlear implants are sometimes an option to restore hearing. Such treatments are typically taken to comfort the patient, not to cure the disease or damage caused by ototoxicity. There is no cure or restoration capability if the damage becomes permanent,[45][46] although cochlear nerve terminal regeneration has been observed in chickens,[47] which suggests that there may be a way to accomplish this in humans.

See full Wikipedia article below

Article from US National Library of Medicine National Institutes of Health

Bilateral Vestibular Dysfunction Associated With Chronic Exposure to Military Jet Propellant Type-Eight Jet Fuel

Self help for those exposed to chemical immuno sensitisers at Irish Air Corps

Evidence is mounting that many of the illnesses Air Corps Chemical Abuse Survivors are suffering may have an immunological origin whereby personnel were immunologically sensitised by unprotected exposure to chemicals in use by the Irish Army Air Corps that are recognised skin & respiratory sensitisers.

Whist the sensitising effects on skin & respiratory system are well known we suspect that harm continues after the sensitising chemicals penetrate further than than the skin & lungs and are likely having an effect upon the central nervous system, and digestive tract.

We have added a page with some sensible precautions that affected serving and former personnel can take to avoid or reduce the possibility of triggering an immune response.

We would also like to take this opportunity to say hello to fellow military service personnel from the Australia, UK and the USA who are suffering similar problems.

Please visit the page below and share it using the Facebook, Twitter & What’s App links.

Precautions

Report on the Molecular Investigations into the Jet Fuel and solvent exposure in the DeSeal/ReSeal programme conducted at the Mater Research Institute (UQ), Brisbane.

Executive Summary

Overview

The main objective of this project was to investigate the toxicity of JP-8 fuel and the solvents used in the Deseal/Reseal programme using a systems biology approach. In the exposure environment (fuel tanks, aircraft hangers etc), workers were typically exposed either by inhalation of vapours or by absorption through the skin. There were occasionally reports of direct ingestion through the mouth. Health studies of exposed workers and other research reports show premature death for some individuals, an increased risk of unusual malignancies in internal organs such as small bowel, erectile dysfunction, and behavioural disturbances. These findings may manifest years after exposure suggesting changes to the cells and tissues not directly exposed to the fuel and solvents. Changes to the systems biology was investigated by proteomic and genomic studies.

Laboratory cell studies of DeSeal/ReSeal compounds

Development of Cell exposure model

Previous methods for studying cellular responses to JP8 and solvents involved direct addition of these compounds to cells in laboratory growth plates using other solvents such as Ethanol. These methods were considered to be inadequate because they did not recognise the role of circulating blood plasma in distributing these compounds to internal organs. The JFES project team developed a method of studying cells by exposing them to blood plasma, which they believe is a better model of the inhalation and skin exposure routes for distributing solvents to internal organs. This method has been published in a peer reviewed journal. (See Appendix 1)

Distribution of JP8 and DeSeal/ReSeal solvents

The studies of plasma exposed to JP8 and solvents showed that the compounds are not distributed by plasma in the same proportions as found in the fuel and solvent mixtures. This means that higher levels of some compounds are actually presented to cells and organs than those proportions in the fuel solvent mixtures. The study showed that the majority of the compounds are distributed by binding to plasma lipids rather than simply dissolved in the plasma water. This raises the possibility that individuals with higher bloods lipids may distribute more of the compounds to internal organs.

The effects of the JP8 and solvents on cells

The study then tested the effects of the JP8 and solvents on cells. The JP8
and solvents were tested as a mixture and individually. The key findings
were:-

  • Plasma exposed to JP8 alone is directly toxic to cells
  • Plasma exposed to a mixture of JP8 combined with solvents has greater
    toxicity to cells with 40% cells showing changes before 4 hours, and 90%
    cells affected at 12 hours.

The following individual components were found to have the highest cellular toxicity:-

  • Kerosene
  • Benzene and butylbenzene
  • All Alkanes including iso-octane, decane, dodecane, tetradecane and
    hexadecane
  • Diegme
  • N, N Dimethyl acetimide
  • Naptha
  • Thiophenol

The solvents used in the Deseal/Reseal programme demonstrated either low cell toxicity or manifest toxicity to a lesser extent than the JP8 fuel components.

Effects on gene expression

Gene expression in cells was altered following exposure. Changes greater then 5 fold were considered significant. The genes altered are shown in table (3). The function of these genes involved mostly cell survival/death, metabolism, cell cycle, DNA maintenance (housekeeping), and cell regulation. These genes have been implicated in pathological processes including cancer, neurodegeneration, and immune suppression.

Effects on proteins

Cellular proteins were altered after exposure. The changes to cellular proteins reflected the changes in gene expression involving cell survival/death, metabolism, cell division, and roles in cellular gene transcription/translation.

Cell Death

Cell death occurred by two mechanisms. A number of cells appeared more vulnerable with death occurring by disruption of cellular membranes and by lysis (bursting) of the cells. The more common mechanism of cell death was by apoptosis, which is a programmed response of cells to injury. Not all injured cells undergo complete apoptosis indicating persistence of injured cells. This may suggest a survival of injured cells with malignant potential. The cell culture methods could not determine the long term effects.

Study of exposed workers

The study of exposed workers showed differences from the matched control group in health indices, and in some genomic studies. The changes were not as significant as those seen in the acute cell exposure model in the laboratory.

Rating of exposure

Because of the unavailability of accurate exposure data (degree and duration), a problem also encountered in other studies, the workers were classified into 3 groups.

  1. Definite high exposure who worked inside the fuel tanks
  2. Significant contact such as by dosing of skin or accidental ingestion
  3. Minimal contact in the general area such as collection of rags or
    cleaning of the area.
Health Assessment Scores

The Health assessment scores showed exposed workers to have a lower health rating than controls. There did not appear to be a decrease in the health scores (dose response) related to the degree of exposure. Workers with mild exposure had the same decrease in their health scores as those with high exposure. This suggests that other factors beyond the Deseal/ Reseal contact have decreased the health scores.

Genetic studies of blood cells from exposed workers

All studies were undertaken on plasma and white blood cells as these were
the only tissues for which it was possible to obtain samples. The genetic studies of blood cells examined two types of changes in gene expression, the presence of chromosomal changes, and for appearance of mutations in
the mitochondrial DNA. There were no chromosomal changes detected at a
level of 50Kb using a high resolution SNP ARRAY.

There were no changes in the mitochondrial DNA mutation load between exposed workers and age matched controls (Mitochondrial DNA changes can accumulate with age).

There were no changes in the amount or type of protein coding mRNA expression, which is an index of cell activity. In disease states , these are usually tissue specific and may not appear in blood cells unless they are directly involved in the disease process.

There were small but significant and consistent changes in the expression of regulatory microRNAs that control activity of other genes. The regulatory functions of the altered genes have been linked to neurological changes and neurodegenerative disorders. It must be emphasised that interpretation of the function of regulatory genes is an evolving science with much uncertainty at present. The regulatory genes, which compose 98% of our genome, have a major role in human development, adaptation and response to disease. The function is only known for ~40% of these at present. Disease causing associations, with some early exceptions, are still unmapped.

Protein studies of plasma and blood cells

No significant changes were seen in the levels and types of protein expressed in the plasma and blood cells of exposed workers. A few small changes were seen consistently, but these did not reach a level that the researchers considered significant.

Discussion and Conclusions

Confounders and sensitivity
Dose response not detected

A dose response would have been expected but was not observed in the workers with different exposure histories. The unexpected similarity in the health scores and genomic studies within the exposed groups (low, medium, high) raises several hypotheses:-

Confounders

There are other factors independent of Deseal/Reseal exposure which could produce the changes seen. Confounders could include:-

  • An ascertainment bias whereby only those workers affected by any exposure volunteered to participate in the study.
  • An ascertainment bias whereby only those workers NOT affected by the exposure (i.e. Survivors) volunteered to participate in the study.
  • The workers were stratified by their exposure to Deseal/Reseal materials. The effects seen may NOT be due to the Deseal/Reseal materials but to some other experience of the workers. The cellular studies suggest that exposure to fuel alone could be responsible.
  • It was not possible to examine other possible shared confounding events in the work careers or in the lifestyle of the personnel. (e.g. other occupational exposure not related to Deseal/Reseal such as medications, substance abuse, nutrition)
  • This study was conducted on individuals between 10 and 30 years after their exposure. If significant changes occurred at the time of exposure, normal cellular repair and selection mechanisms may have lessened the biological signal that could be observed in this study. The small but consistent changes observed suggest this possibility. Either the effect at the time was minimal but has persisted, or the effect was larger but has diminished over-time.
  • The cellular studies show that the compounds are mostly distributed by plasma lipids. The exposure to organs within the body would likely depend on the concentration of plasma lipids at the time of fuel exposure. Plasma lipids vary genetically between individuals, with lifestyle and alcohol intake, with composition of their diet, as well as the time after meals when the exposure occurred. The lack of a dose effect could be explained if workers in the lower exposure group had higher plasma lipids at the time of exposure. Individuals in the high exposure group worked within the fuel tanks and were selected because they were leaner and smaller, possibly protected to some extent by lower plasma lipids.

Significance of findings

The cellular findings, supported by other recently published genomic studies, indicate a definite toxicity from JP8 to exposed cells. The components of JP8 tested are commonly found in most (aviation) fuels. The results indicate that there is a need for concern about exposure to fuels in general. The study was not designed to determine the degree of occupational exposure necessary to produce cellular changes. However, the results show that cells grown in a nutrient containing as little as 5% exposed plasma are affected. In the body, blood cells have 100% exposure to plasma while other organs will have less exposure depending on the net blood flow and cellular membrane barriers. Organs such as brain, liver and bowel have very high blood flow. Cellular membranes generally have greater permeability to substances dissolved in lipids.

The study was also not designed to determine the most toxic routes of exposure (inhalation, ingestion, skin contact), but did demonstrate that fuel components can be distributed to organs through blood plasma, i.e. organs such as brain or liver, not directly exposed in the contact, may undergo secondary exposure. The implication is that all body systems must be considered in assessing/monitoring the health of exposed workers.

While the changes seen many years after exposure were small, they were consistent. The changes are most apparent in gene regulation and had some association to the health problems (e.g., malignancy) identified in other studies.

There were no chromosomal changes or mutations linked to the exposure. The genes changes seen can be described as Epigenetic, which is a mechanism of cellular adaptation to some environmental influence. Epigenetic changes are less clearly linked (at the present knowledge) to disease. Epigenetic changes occur through a variety of cellular mechanisms and these were not investigated in this study. Some epigenetic changes can be transferred down through successive generations but currently have not been shown to cause birth defects or mutation in off-spring.

Recommendations

The cell results show a definite cellular toxicity from JP8 fuel. The components of the fuel exhibiting toxicity are common to most fuels. Consideration should be given to further studies of workers exposed to fuel of any type.

Newer genomic and bioinformatic technologies have been developed during the time of this study and have been employed in other studies of occupational fuel exposure. These technologies can be applied to other exposure risks (including PTSD) in defence (veteran) health risk assessment. An expert committee should be constituted to advise on research and clinical application of these technologies.

Plasma free DNA sequencing can now be used to assess (from blood samples), the cellular death associated with tumours, transplant rejection, miscarriage and infections. Targeted RNA expression studies can reveal immediate changes in gene activity following fuel exposure. A study of workers with recent or past fuel exposure is recommended.

The best time to study cellular changes would be immediately after direct exposure. A protocol should be established for assessment of an exposed individual to include sample collection immediately after the exposure for quantification of plasma lipids, plasma fuel components, free DNA sequencing, and targeted RNA expression.

Exposed veterans should be reassured that while small and consistent changes were observed in this study, there were no changes detected known to have immediate or severe health consequences. The changes support the findings from other studies that there is a possible increased risk of developing health problems. As the changes observed are in gene regulation, it is also possible that healthy lifestyle changes may ameliorate the risk.

31st JULY 2014

Download the full report on the Royal Australian Air Force website below.

***

Difference between Jet A1 & JP8

Jet fuel, aviation turbine fuel (ATF), or avtur, is a type of aviation fuel designed for use in aircraft powered by gas-turbine engines. It is colorless to straw-colored in appearance. The most commonly used fuels for commercial aviation are Jet A and Jet A-1, which are produced to a standardized international specification. The only other jet fuel commonly used in civilian turbine-engine powered aviation is Jet B, which is used for its enhanced cold-weather performance.

Jet fuel is a mixture of a large number of different hydrocarbons. The range of their sizes (molecular weights or carbon numbers) is defined by the requirements for the product, such as the freezing or smoke point. Kerosene-type jet fuel (including Jet A and Jet A-1) has a carbon number distribution between about 8 and 16 (carbon atoms per molecule); wide-cut or naphtha-type jet fuel (including Jet B), between about 5 and 15.[1]

Additives

The DEF STAN 91-91 (UK) and ASTM D1655 (international) specifications allow for certain additives to be added to jet fuel, including:[13][14]

  • Antioxidants to prevent gumming, usually based on alkylated phenols, e.g., AO-30, AO-31, or AO-37;
  • Antistatic agents, to dissipate static electricity and prevent sparking; Stadis 450, with dinonylnaphthylsulfonic acid (DINNSA) as a component, is an example
  • Corrosion inhibitors, e.g., DCI-4A used for civilian and military fuels, and DCI-6A used for military fuels;
  • Fuel system icing inhibitor (FSII) agents, e.g., Di-EGME; FSII is often mixed at the point-of-sale so that users with heated fuel lines do not have to pay the extra expense.
  • Biocides are to remediate microbial (i.e., bacterial and fungal) growth present in aircraft fuel systems. Currently, two biocides are approved for use by most aircraft and turbine engine original equipment manufacturers (OEMs); Kathon FP1.5 Microbiocide and Biobor JF.[15]
  • Metal deactivator can be added to remediate the deleterious effects of trace metals on the thermal stability of the fuel. The one allowable additive is N,N’-disalicylidene 1,2-propanediamine.

As the aviation industry’s jet kerosene demands have increased to more than 5% of all refined products derived from crude, it has been necessary for the refiner to optimize the yield of jet kerosene, a high value product, by varying process techniques. New processes have allowed flexibility in the choice of crudes, the use of coal tar sands as a source of molecules and the manufacture of synthetic blend stocks. Due to the number and severity of the processes used, it is often necessary and sometimes mandatory to use additives. These additives may, for example, prevent the formation of harmful chemical species or improve a property of a fuel to prevent further engine wear.

JP-8, or JP8 (for “Jet Propellant 8”) is a jet fuel, specified and used widely by the US military. It is specified by MIL-DTL-83133 and British Defence Standard 91-87, and similar to commercial aviation’s Jet A-1, but with the addition of corrosion inhibitor and anti-icing additives.

A kerosene-based fuel, JP-8 is projected to remain in use at least until 2025. It was first introduced at NATO bases in 1978. Its NATO code is F-34.

Biological monitoring for Isocyanates

Organic diisocyanates are a significant occupational health problem.

They are respiratory and skin sensitizers and a major cause of occupational asthma in the UK. The most common are hexamethylene diisocyanate (HDI), toluene diisocyanate (TDI), isopherone diisocyanate (IPDI) and methylene-diphenyl diisocyanate (MDI) in decreasing order of volatility. HDI and IPDI are used for varnishes, coatings and two-pack spray paints used in motor vehicle repair. TDI and MDI are used for flexible and rigid polyurethane foams, floor coverings and adhesives. This wide range of uses means that there are thousands of workers potentially exposed to isocyanates.

In the UK, a management control system is required for workers exposed to isocyanates and for this to be successful workers should not become sensitized. Apart from occupational asthma, airway irritation and asthma-like symptoms such as cough, wheezing and dyspnoea are commonly reported. Other respiratory effects are hypersensitivity pneumonitis, rhinitis and accelerated rate of decline in lung function. Diisocyanates can also cause both irritant and allergic contact dermatitis as well as skin and conjunctival irritation.

Health surveillance that detects occupational asthma is recording failure – there needs to be intervention earlier in the exposure-to-disease paradigm. Although there is evidence that detecting respiratory symptoms early and removing workers from exposure improves prognosis, the goal should be to control exposure to prevent any symptoms.

Please read more on the Society of Occupational Medicine website from September 2007.


This is a long article but a very informative read and is especially relevant for those on post 1995 contracts who were dismissed from the Irish Army Air Corps due to occupational asthma.