Author: Collie

University of Limerick students exposed to Irish Air Corp toxic chemicals over decades

The University of Limerick sent 3 engineering students a year, from about 1990 to 2008, for work experience at the Irish Air Corps at Casement Aerodrome, Baldonnel.

During their work experience all the UL students were  exposed to a range of CMR chemicals in an unprotected manner and at levels known by the Air Corps to be over airborne health and safety limits.

To date the University of Limerick have refused to alert their former students to the fact that they were overexposed to toxic chemicals including Trichloroethylene, Trichloroethane, Dichloromethane, Hexamethylene Diisocyanate, Toluene, Xylene, Benzene, Hexavalent Chromium and many more.

Like their military counterparts that served during the same time period some of the UL students have been injured by their time serving in the Irish Air Corps. They all need to be informed of their exposure so that those suffering can receive appropriate medical help.

The actions of the University of Limerick on this issue to date have been shameful.

http://www.thejournal.ie/college-guide-ul-4181613-Aug2018/

Dáil Éireann Written Answers 12/07/18 – Department of Defence – Departmental Legal Costs

Aengus Ó Snodaigh (Dublin South Central, Sinn Fein)

QUESTION NO: 66

To ask the Taoiseach and Minister for Defence the estimated costs of defending litigation on Lariam and Air Corps toxic chemical exposure in each year over the past ten years, excluding settlements; and if he will make a statement on the matter. [32063/18]

Paul Kehoe (Wexford, Fine Gael)

The State Claims Agency manages and provides legal representation in relation to personal injury claims taken against the Minister including claims in respect of current or former members of the Defence Forces in relation to alleged personal injuries that are referred to in the Deputy’s question.

The Department reimburses the State Claims Agency in respect of any external legal costs. This Department does not hold details of the breakdown of the legal costs incurred in respect of the different categories of personal injuries claims managed by the State Claims Agency on behalf of my Department.

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  • The state claims agency were aware from 2013/2014 that the Irish Air Corps toxic chemical exposure problem was still a LIVE issue and not just a LEGACY issue. They had an opportunity at this time to inform the HSA and to start to have the ongoing exposure problems rectified but they chose not to do so.
  • The state claims agency are therefore directly responsible for personnel enduring a further 2 years (approx) of unprotected exposure.
  • The State Claims Agency are in charge of their own cover up and have unlimited taxpayer funds to carry out this task.

DELAY – DENY – DIE

Department of Defence coy on probe of bullying claims

An air corps whistleblower has been told that it is “difficult to envisage” how the Department of Defence would investigate complaints of bullying made in a protected disclosure about chemical exposure within the force.

The protected disclosure, seen by the Irish Examiner, contains allegations that the whistle-blower was doused in chemicals used to service aircraft as an initiation, and was frequently exposed to chemicals without protective equipment as he carried out his duties in the Engine Shop at Casement Aerodrome, Baldonnel.

He alleges that he became ill while still serving in the air corps, but was targeted by superiors for his frequent absences due to sickness.

His complaints match those of a number of other whistleblowers, and the State is currently facing at least seven separate legal actions from former air corps staff who claim they are chronically ill due to their exposure to chemicals at Casement Aerodrome.

A Government-commissioned report by former civil servant Christopher O’Toole into earlier whistleblower disclosures found there was no documentation available to demonstrate that the air corps met its health and safety obligations.

The latest whistleblower called on the Government to launch a fresh review into the complaints about conditions in Casement Aerodrome, and asked that his allegations of bullying be considered as part of this probe.

“My allegations need to be investigated in full as part of a wider investigation into the air corps chemical exposure scandal and the subsequent bullying and mistreatment of personnel injured by the same chemical exposure,” states the whistle blower.

Read full article on Irish Examiner website below…

Delay – Deny – Die

No response to latest Air Corps whistleblower claim

The Government has not responded to a new protected disclosure on chemical exposures within the Air Corps.

The disclosure was made by a whistleblower, who says he is chronically ill, due to his experiences at Casement Aerodrome, the Irish Examiner can reveal.

The protected disclosure, seen by this newspaper, was submitted to the Department of Defence last December, but the whistleblower has not been contacted since, bar an acknowledgement that his disclosure was received.

In the December 2017 disclosure, the former member of staff echoes previous submissions to the Government. He says he was doused in chemicals by other recruits colleagues, as an initiation, and was frequently exposed to various chemicals as part of his duties in the engine shop at Casement Aerodrome, Baldonnel.

He alleges that he became ill while still serving in the Air Corps, but was bullied and mistreated by superiors for his frequent absences, due to illnesses he believes were caused by his working environment.

Read full article on Irish Examiner website below…

Delay – Deny – Die

Dáil Éireann – Oral Question 38 – 26th June 2018 – Irish Air Corps Protected Disclosure

Mr. Aengus Ó Snodaigh (Dublin South-Central )

Question No. 38

To ask the Taoiseach and Minister for Defence if he has received a protected disclosure from a member of the  Defence Forces (details supplied); if he has responded to the disclosure; and the action that has been taken on foot of the disclosure. — Aengus Ó Snodaigh. [27762/18]

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To be clear Minister Paul Kehoe & Taoiseach Leo Varadkar received this Protected Disclosure in December 2017, issued a receipt and have ignored since. 

Study of Health Outcomes in Aircraft Maintenance Personnel (SHOAMP)

A research team from the University of Newcastle (Australia) has completed an investigation into whether there is an association between adverse health and an involvement in F-111 fuel tank deseal/reseal activities and, if so, the nature and strength of that association.

The current health status of those workers was compared with the health of groups of workers with similar backgrounds from Amberley and Richmond air bases.

Yield of literature review

Associations between exposure and health outcomes
  • Cancer
  • Multiple Sclerosis, Motor Neurone Disease and Other Neurological Examinations
  • Other Neurological Outcomes
  • Neuropsychology
  • Reproductive Health Effects
  • Other health effects
  • Health and the Manufacture and Maintenance of Aircraft
Measurement of exposure and outcomes
  • Bio-markers
  • Measurement of Neuropsychological Deficits
Summary of Results and Implications for General Health and Medical Study
  • Cancer
  • Multiple Sclerosis, Motor Neurone Disease and other Neurological Effects
  • Birth Defects
  • Neuropsychology
  • Other Health Effects
  • Biomarkers

http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.468.8401&rep=rep1&type=pdf

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When the RAAF and the Australian Government discovered there was a chemical exposure problem and associated health problems amongst aircraft maintenance personnel they initiated some health studies one of which became known as SHOAMP. These studies are ongoing and report every 4 years to the best of our knowledge.

Australia does have a Department of Veteran Affairs and operates schemes whereby medical & financial support are in place to support RAAF personnel affected by the F1-11 Deseal / Reseal program.

These schemes are far from perfect and are a cause of ongoing stress amongst Australian survivors but obviously preferable to Ireland where Irish Air Corps sick personnel have to risk their home to take the the state to court while our compassionate medically qualified Taoiseach (Prime Minister) Leo Varadkar recently refused medical help for Air Corps personnel in the Irish parliament and goaded sick survivors to sue.

Any person who served in the Irish Army Air Corps needs to read the above document which is the 2003 SHOAMP report. Unfortunately many links on the Australian DVA website are down. As we find newer SHOAMP reports we will make them available. 

Epichlorohydrin – Guide to Hazardous Air Pollutants used by the Irish Air Corps

Epichlorohydrin
(1-Chloro-2,3-Epoxypropane)

CAS  106-89-8

Hazard Summary

Epichlorohydrin is mainly used in the production of epoxy resins.  Acute (short-term) inhalation exposure to epichlorohydrin in the workplace has caused irritation to the eyes, respiratory tract, and skin of workers.

At high levels of exposure, nausea, vomiting, cough, labored breathing, inflammation of the lung, pulmonary edema, and renal lesions may be observed in humans.

Chronic (long-term) occupational exposure of humans to epichlorohydrin in air is associated with high levels of respiratory tract illness and hematological effects.

Damage to the nasal passages, respiratory tract and kidneys have been observed in rodents exposed to epichlorohydrin by inhalation for acute or chronic duration.  An increased incidence of tumors of the nasal cavity has been observed in rats exposed by inhalation. EPA has classified epichlorohydrin as a Group B2, probable human carcinogen.

Please Note: The main sources of information for this fact sheet are EPA's IRIS (2), which contains information on inhalation chronic toxicity and carcinogenic effects of epichlorohydrin and the RfC, and unit cancer risk estimate for inhalation exposure, and the Health and Environmental Effects Profile for Epichlorohydrin. (1)

Uses

  • The primary use of epichlorohydrin is in the production of epoxy resins used in coatings, adhesives, and plastics. (1,5)
  • Epichlorohydrin is also used in the manufacture of synthetic glycerine, textiles, paper, inks and dyes, solvents, surfactants, and pharmaceuticals. (1)
  • Epichlorohydrin is also listed as an inert ingredient in commercial pesticides. (1)

Sources and Potential Exposure

  • Individuals are most likely to be exposed to epichlorohydrin in the workplace. (1)
  • Epichlorohydrin may be released to the ambient air during its production and use. (1)
  • Accidental releases to waterways may expose the general public to epichlorohydrin. (1)

Assessing Personal Exposure

  • No information was located concerning the measurement of personal exposure to epichlorohydrin.

Health Hazard Information

Acute Effects:

  • Acute inhalation exposure to epichlorohydrin in the workplace has caused irritation to the eyes, respiratory tract, and skin of workers.  At high levels of exposure, nausea, vomiting, cough, labored breathing, chemical pneumonitis (inflammation of the lung), pulmonary edema, and renal lesions may be observed in humans. (1,2)
  • Dermal contact with epichlorohydrin may result in irritation and burns of the skin in humans and animals.(1)
  • In rats and mice acutely exposed to epichlorohydrin by inhalation, nasal and lower respiratory tract irritation and lesions, hemorrhage, and severe edema have been observed.  Renal degeneration and CNS depression with paralysis of respiration and cardiac arrest have also resulted from acute inhalation exposure in animals. (1-3)
  • Tests involving acute exposure of rats, mice and rabbits have demonstrated epichlorohydrin to have high acute toxicity from inhalation, oral, and dermal exposure. (4)

Chronic Effects (Noncancer):

  • Chronic occupational exposure of humans to epichlorohydrin in air is associated with high levels of respiratory tract illness and hematological effects (decreased hemoglobin concentration and decreased erythrocyte and leukocyte counts). (1,5)
  • Chronic inhalation exposure has been observed to cause pulmonary effects including inflammation and degenerative changes in the nasal epithelia, severe lung congestion, and pneumonia in rats and mice. Effects to the kidneys were also observed. (1,2)
  • Hepatic damage, hematological effects, myocardial changes, and damage to the CNS have been reported in chronically exposed rats. (1,5)
  • The Reference Concentration (RfC) for epichlorohydrin is 0.001 milligrams per cubic meter (mg/m3) basedon changes in the nasal turbinates in rats and mice. The RfC is an estimate (with uncertainty spanningperhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups), that is likely to be without appreciable risk of deleterious noncancer effects during a lifetime. It is not a direct estimator of risk but rather a reference point to gauge the potential effects. At exposures increasingly greater than the RfC, the potential for adverse health effects increases. Lifetime exposure above the RfC does not imply that an adverse health effect would necessarily occur. (2)
  • EPA has medium confidence in the study on which the RfC was based because of the inflammation in the respiratory tract of control and exposed animals although it was well conducted and contained detailed histopathological examinations of numerous tissues including the respiratory tract; medium confidence in the database because chronic studies that adequately address the respiratory system and a two-generation reproductive study are lacking and the only chronic inhalation study is confounded by severe nasal inflammation in the controls; and, consequently, medium confidence in the RfC. (2)
  • The provisional Reference Dose (RfD) for epichlorohydrin is 0.002 milligrams per kilogram body weight per day (mg/kg/d) based on kidney effects in rats. The provisional RfD is a value that has had some form of Agency review, but it does not appear on IRIS (6)

Reproductive/Developmental Effects:

  • In humans occupationally exposed to epichlorohydrin, effects on sperm counts, hormone levels, and fertility have been not detected. (1,2)
  • Epichlorohydrin has been demonstrated to reduce fertility in male rats when inhaled or administered orally.(1-3)
  • Teratogenic effects (birth defects) have not been observed in studies of rodents exposed by inhalation or ingestion. (1,2,5)

Cancer Risk:

  • An increased incidence of lung cancer mortality (not statistically significant) was reported in one study of workers exposed to epichlorohydrin. (1,2)
  • An increased incidence of tumors of the nasal cavity has been observed in rats exposed to epichlorohydrin by inhalation. (1,2,5)
  • An increased incidence of forestomach tumors has been reported in rats exposed via gavage (experimentally placing the chemical in the stomach) and in drinking water.  Mice have exhibited local tumors when exposed by subcutaneous injection. (1-3,5)
  • EPA has classified epichlorohydrin as a Group B2, probable human carcinogen. (2)
  • EPA uses mathematical models, based on human and animal studies, to estimate the probability of a EPA uses mathematical models, based on human and animal studies, to estimate the probability of a person developing cancer from breathing air containing a specified concentration of a chemical. EPA calculated an inhalation unit risk estimate of 1.2 × 10-6  (µg/m3)-1. EPA estimates that, if an individual were to continuously breathe air containing epichlorohydrin at an average of 0.8 µg/m3 (0.0008 mg/m3) over hisor her entire lifetime, that person would theoretically have no more than a one-in-a-million increasedchance of developing cancer as a direct result of breathing air containing this chemical. Similarly, EPA estimates that breathing air containing 8.0 µg/m3 (0.008 mg/m3) would result in not greater than a one in-a-hundred thousand increased chance of developing cancer, and air containing 80.0 µg/m3 (0.08mg/m3) would result in not greater than a one-in-ten thousand increased chance of developing cancer. Fora detailed discussion of confidence in the potency estimates, please see IRIS. (2)
  • EPA has calculated an oral cancer slope factor of 9.9 x 10-3 (mg/kg/d)-1. (2)

Physical Properties

  • The chemical formula for epichlorohydrin is C3H5OCl, and its molecular weight is 92.53 g/mol. (1,7)
  • Epichlorohydrin is a volatile and flammable clear liquid at room temperature and is insoluble in water.(1,2,7)
  • The threshold for odor perception of epichlorohydrin is 0.93 parts per million (ppm). Epichlorohydrin has a pungent, garlicky, sweet odor. (2,8) The vapor pressure for epichlorohydrin is 22 mm Hg at 30 °C. (1)

Read the full EPA (USA) PDF on the above Hazardous Air Pollutant with references below.

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Relavance to personnel who served in the Air Corps

  • Epichlorohydrin is a component of PR1829b windshield canopy sealant.

There are possibly more chemicals used by the Air Corps that contain Epichlorohydrin. If you know of some let us know in the comments section. 

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.

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Article from US National Library of Medicine National Institutes of Health

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