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

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

Jet Fuel Toxins More Of A Problem To Airfield Workers Than To Travelers

If you are a frequent flier for business or pleasure, should you be worried about jet fuel exposure? People who are exposed to jet fuel vapors only occasionally typically have a chance to recover between flights. For them, problems from jet fuel are likely to be minimal.

But if you work at the airport, especially if you work in close proximity to planes, or you live under a flight path, the toxic effects of jet fuel pollution should be a concern for you. Here are seven facts airfield and airport workers and people who live close (within 1 mile/2 km) of airports need to know.

Read full article on Steady Health