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


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

  • 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
  • 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:-


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.


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]


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.

Developments in laboratory diagnostics for Isocyanate Asthma

Purpose of review

Isocyanates, reactive chemicals used to generate polyurethane, are a leading cause of occupational asthma worldwide. Workplace exposure is the best-recognized risk factor for disease development, but is challenging to monitor. Clinical diagnosis and differentiation of isocyanates as the cause of asthma can be difficult. The gold-standard test, specific inhalation challenge, is technically and economically demanding, and is thus only available in a few specialized centers in the world. With the increasing use of isocyanates, efficient laboratory tests for isocyanate asthma and exposure are urgently needed.

Recent findings

The review focuses on literature published in 2005 and 2006. Over 150 articles, identified by searching PubMed using keywords ‘diphenylmethane’, ‘toluene’ or ‘hexamethylene diisocyanate’, were screened for relevance to isocyanate asthma diagnostics. New advances in understanding isocyanate asthma pathogenesis are described, which help improve conventional radioallergosorbent and enzyme-linked immunosorbent assay approaches for measuring isocyanate-specific IgE and IgG. Newer immunoassays, based on cellular responses and discovery science readouts are also in development.


Contemporary laboratory tests that measure isocyanate-specific human IgE and IgG are of utility in diagnosing a subset of workers with isocyanate asthma, and may serve as a biomarker of exposure in a larger proportion of occupationally exposed workers.



Diisocyanates (toluene diisocyanate, TDI; hexamethylene diisocyanate, HDI; and diphenylmethane diisocyanate, MDI) or functionally similar polymeric isocyanates are the obligate cross-linking agent for the commercial production of polyurethane, a polymer upon which modern society has become dependent. Millions of tons of isocyanate are produced and consumed annually throughout the world in a wide variety of end-use work environments [1,2–5,6•,7•]. Workplace exposure remains the best-recognized risk factor for isocyanate asthma, but is complicated to quantitate, involving mixtures of isomers and ‘prepolymers’ diluted in solvents, in aerosol and vapor phases. In certain occupational settings, exposure can cause isocyanate asthma and long-lasting bronchial hyperreactivity [1,8,9,10•,11•]. Early recognition of isocyanate asthma and prompt removal from isocyanate exposure improves the long-term prognosis for sensitive individuals [9]. There thus exists the need for practical screening/diagnostic tests for isocyanate asthma as well as tests that can monitor personal exposure.

The clinical presentation of isocyanate asthma is strikingly similar to common environmental asthma, prompting the hypothesis that the disease has an immunological basis, although subtle differences have been noted [9,10•,12•]. Animal models support this hypothesis, and are beginning to dissect the potential role of individual genes with transgenic strains [13••,14••,15,16••,17,18]. Allergists and immunologists have overcome substantial challenges working with reactive isocyanates to develop serology assays for isocyanate-specific antibodies [19–21]. Such assays have provided evidence to support allergic asthma to isocyanate in a small percentage of workers, but cannot detect isocyanate-specific IgE in the majority of sensitive individuals. These results have left great uncertainty in the field. Does isocyanate asthma involve mechanisms of pathogenesis (e.g. non-IgE) distinct from those in common atopic asthma or are specific IgE antibodies present, but our detection assay for them is flawed? Are we using the wrong antigenic form of isocyanate in our serology tests, or testing workers at the wrong time (after removal from exposure)? Does isocyanate asthma, as presently defined, possibly represent a spectrum of diseases, which only in some cases is associated with an antibody response [3,9,10•]?

The present review summarizes the rationale and use of clinical laboratory tests for immune responses that reflect isocyanate exposure and asthma, with emphasis on data generated within the past year. The potential utility of ‘isocyanate-specific’ serum IgE and IgG as biomarkers and the isocyanate antigen recognized by these immunoglobulins are described [22••,23]. Clinical usage and limits of contemporary assays for isocyanate asthma and exposure are discussed along with promising future assays [20,24,25••].

Read more on the US National Center for Biotechnology Information


The Irish Army Air Corps has dismissed a number of previously fit personnel as suffering from asthma. It has never carried out a health study of personnel exposed long term and without protection to Isocyanates and has never carried out adequate risk specific health surveillance. Neither has the Air Corps ever carried out risk specific health surveillance for personnel who suffered long term exposure to jet fuel & jet exhaust gasses. 

Bizarrely serving and former Air Corps personnel have been “reassured” by Air Corps medical personnel that their asthma does not have a workplace related cause despite no evidence of any testing for them to form a conclusion either way.

Considering what is now known about the extremely poor chemical health & safety environment in the Irish Air Corps any doctor, dismissing without appropriate testing, any possibility of a workplace casual link is surely opening himself or herself up to accusations of professional misconduct.

The tiniest trickle of blood – Another human cost of the Irish Air Corps Toxic Chemical Health & Safety scandal

The tiniest trickle of blood

My father was an aircraft technician in the Air Corps at Casement Aerodrome in Baldonnel for 21 years. During his time there he worked on a variety of aircraft and worked with an assortment of chemicals and sprays often without, as he said himself, even glove protection.

Over that time he developed severe psoriasis on his body, but in particular his hands and legs. This resulted in intense itch and pain and a daily routine of medication and treatment of the various lesions on his legs and also a stay in St. Bricin’s Hospital. It was not until a combination of appointments with a renowned Traditional Medical Herbalist, coupled with his retirement from the Air Corps that improvements began. This psoriasis, while appearing at a much slighter level during his life, never appeared to the same extent after leaving Baldonnel.

My mother passed away in 2009, and since then Dad lived with my wife and I, and subsequently, our two daughters. He adored his family and his granddaughters. He also really enjoyed an active and healthy life, learning to swim, regularly walking, going dancing, and eating very healthily. He liked his few social pints but gave up smoking before his first granddaughter was born eight years ago. He also had regular full check-ups with his GP.

In December 2013, while Dad was feeling very well, in great form, he spotted the tiniest trickle of blood in his urine. After attending his GP and a urologist, it was confirmed that he had renal cancer, which had completely taken over one of his kidneys and indeed had also spread to his lungs. Treatment was possible but immediate: he would need to have his kidney removed and a tablet form of chemotherapy would need to be taken for the rest of his life. Thankfully medical advances had developed this treatment, otherwise he would not have survived.

Almost two years passed and Dad had little or no side-effects to his treatment other than his dark hair turning grey overnight. He maintained his life as it was, keeping up his hobbies and his active lifestyle, as well as continuing his breaks to Lanzarote. Unfortunately in November 2015, things began to change and his body rejected the tablet. He became very ill with a litany of mystery illnesses that befuddled doctors but, miraculously, he managed to survive and came home. However, he spent his New Year’s Day in A&E, complaining of intense pain in his back. On examination and scanning, it was found that he had a broken vertebrae due to cancer spreading to his back. Again, thankfully it was in the position that it was, as it was treatable and would not end up with him in a wheelchair. Inserting rods either side of his spine meant that he would walk again.

The last months of his life were a mix of regular check-ups, consultant appointments, progress and setbacks. It was a roller-coaster of emotions where his unyielding positivity was tested repeatedly but never left him. 

It would have been interesting to see if his background in Baldonnel could have informed his treatment, or if indeed anything could have been done to prevent his disease. However such thoughts are merely conjecture and would distract from the magnificent memories we hold of a man who touched so many hearts and leaves behind a legacy fitting for such a character.

Irish Air Corps Chemical List Update – Mastinox 6856k

We have just added some links to information on the constituent chemicals for Mastinox 6856k from PubChem the Open Chemistry Database. Please have a look at green links on our chemical info page here. We will add more on a regular basis.

Mastinox 6856k is a corrosion inhibitor and contains the following

  • Strontium Chromate
  • Barium Chromate
  • Xylene
  • Toluene
  • Ethylbenzene
  • N-Octane
  • Naptha
  • Heptane
  • Methylcyclohexane

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.

Skin Cancer in Irish Air Corps personnel – Basal Cell Carcinoma

Photo of BCC on the leg of a former Air Corps employee who worked daily with Ardrox 666. This person also has cancerous growths on his arm & scalp.

Basal Cell Carcinoma’s are abnormal, uncontrolled growths or lesions that arise in the skin’s basal cells, which line the deepest layer of the epidermis (the outermost layer of the skin). BCCs often look like open sores, red patches, pink growths, shiny bumps, or scars and are usually caused by a combination of cumulative and intense, occasional sun exposure.

Both long-term sun exposure over your lifetime and occasional extended, intense exposure (typically leading to sunburn) combine to cause damage that can lead to BCC. Almost all BCCs occur on parts of the body excessively exposed to the sun — especially the face, ears, neck, scalp, shoulders, and back.

On rare occasions, however, tumors develop on unexposed areas. In a few cases, contact with arsenic, exposure to radiation, open sores that resist healing, chronic inflammatory skin conditions, and complications of burns, scars, infections, vaccinations, or even tattoos are contributing factors.

It is not possible to pinpoint a precise, single cause for a specific tumor, especially one found on a sun-protected area of the body or in an extremely young individual.

Skin cancer (non-melanoma)
Causes grouped by strength of evidence
Strong  Good  Limited 
arsenic aromatic amines acrylamide
benzo(a)pyrene arsenical pesticides vinyl chloride
coal tars benz(a)anthracene
ionizing radiation creosotes
mineral oils dibenz(a,h)anthracene
shale oils dimethyl benzanthracene
UV radiation ethylene oxide

We are aware of a number of current & former Air Corps technicians who have developed Basal Cell Carcinoma. It is interesting to note that there is good evidence to link creosotes with Basal Cell Carcinoma. Creosotes are a component chemical of Ardrox 666.

However, Basal Cell Carcinoma is a very common cancer and so the occurrence may not be unusual.

Key point as with almost all of the illnesses suffered by Air Corps Chemical Abuse Survivors is of course vigilance. Don’t delay going to your doctor.

Irish Army Air Corps Toxic Chemical Exposure – Survivors List of Demands

The priorities of the Air Corps Chemical Abuse Survivors is firstly to prevent further unnecessary loss of life amongst survivors and secondly to improve the quality of life of survivors by reducing unnecessary suffering.

Both the Royal Australian Air Force & the Armed forces of the Netherlands have offered templates as to how to approach unfortunate workplace chemical exposure issues with competence, fairness, justice & urgency.

We urge that all responsible organisations in the state such as political parties, government departments and the Defence Forces to work together to commit the state to provide the following for survivors as an ex. gratia scheme with no admission of liability by the state.

Current & future legal cases should be allowed to take their natural course unhindered whilst all survivors are cared for equally by the state.

Read more about our demands below.

Dáil Éireann Written Answers 17/05/17 – Department of Defence – Protected Disclosures

Aengus Ó Snodaigh (Dublin South Central, Sinn Fein)

To ask the Taoiseach and Minister for Defence if he has received and read a recent protected disclosure on serious breaches of health and safety procedures at Casement Aerodrome, including claims that personnel have died prematurely as a result of handling hazardous chemicals without adequate protection from retired Air Corps personnel who worked on the base; and his plans to deal with these latest revelations. [23196/17]

Paul Kehoe (Wexford, Fine Gael)

There are a number of elements to the correspondence to which the Deputy refers. I am arranging for the elements of the correspondence which relate to previous protected disclosures concerning health and safety issues in the Air Corps to be sent to the independent third party I appointed last year to review those allegations. Legal advice has recently been received in respect of the correspondence referred to by the Deputy and is being considered.

Once a final review is to hand, I will determine any further steps required and ensure that all recommendations will be acted upon to ensure the safety of the men and women of the Air Corps.

Dáil Éireann Written Answers 04/04/17 – Department of Defence – Airfield Harvesting

Aengus Ó Snodaigh (Dublin South Central, Sinn Fein)

698. To ask the Taoiseach and Minister for Defence if the Air Corps at Casement Aerodrome, Baldonnel receives moneys from the annual harvesting of silage on the airbase; and if he will make a statement on the matter. [16654/17]

Paul Kehoe (Wexford, Fine Gael)

I have been advised by the Military Authorities that the Air Corps operate a ‘safe grass’ policy in order to reduce the hazards posed on the airfield in Baldonnel by bird populations. This policy is an integral part of the wider bird control management program, which is line with best international practices and seeks to reduce the risk of bird strikes during critical phases of flight.

The airfield at Baldonnel is cultivated with FESCUE grass which was specifically sown and grown to prevent birds landing and nesting in the grass and thereby being a hazard to the aircraft. A contractor is hired to top the grass at a height of 9 inches throughout the growing season. The clippings are returned. The frequent topping of the grass and the return of clippings are required to produce an appropriate level of soil fertility to support adequate grass growth. The crop type does not have the nutrient needs for grazed cattle silage and the clippings are required to maintain nutrient levels in the soil.

Accordingly, the Air Corps receive no funding from the annual harvesting of silage on the airbase. As there is no harvesting of silage, the issue of income from harvesting does not arise.

Minister Paul Kehoe T.D. again misrepresents the truth. Is Minister Kehoe misleading in his answers to parliamentary questions or are the Irish Army Air Corps misleading the Minister? Someone is giving misleading answers that is for sure.

Photos below taken in the past week and posted on an Air Corps related Facebook page.

This last photo taken 13th May 2017

Dáil Éireann Written Answers 04/04/17 – Department of Defence – Air Corps Equipment

Lisa Chambers (Mayo, Fianna Fail)

688. To ask the Taoiseach and Minister for Defence the detail of the 2017 opening stock figure, current stock figure, cumulative new stock figure to date in 2017 and cumulative issued stock figure in 2017 for chemical hazard PPE respirators for technical personnel at Casement Aerodrome, Baldonnel; and if he will exclude military grade respirators used for military training purposes. [16143/17]

689. To ask the Taoiseach and Minister for Defence the detail of the 2016 opening stock figure, closing stock figure, cumulative new stock figure and cumulative issued stock figure for disposable coveralls at Casement Aerodrome, Baldonnel. [16144/17]

691. To ask the Taoiseach and Minister for Defence the testing and selection criteria for disposable overalls in use by the Air Corps to insure they offer personnel adequate protection from the toxic chemicals in use. [16146/17]

Paul Kehoe (Wexford, Fine Gael)

I propose to take Questions Nos. 688, 689 and 691 together.

Unfortunately, it has not been possible to compile the information requested in the time available. My officials are working with the military authorities to obtain the information which will be forwarded to the Deputy as soon as it is available.

Again Minister Paul Kehoe T.D. demonstrates that he is incapable of supplying simple answers to basic questions about the Irish Army Air Corps.  The answers to questions 688 & 689 are available at the touch of a button from the AMMS computer system.

It appears that either the Minister for Defence, the Department of Defence or the Defence Forces may have something to hide.