Epigenetic Harm and the Irish Army Air Corps

Epigenetics is the study of heritable phenotype changes that do not involve alterations in the DNA sequence. The Greek prefix epi- (ἐπι- “over, outside of, around”) in epigenetics implies features that are “on top of” or “in addition to” the traditional genetic basis for inheritance. Epigenetics most often denotes changes that affect gene activity and expression, but can also be used to describe any heritable phenotypic change. Such effects on cellular and physiological phenotypic traits may result from external or environmental factors, or be part of normal developmental program. The standard definition of epigenetics requires these alterations to be heritable, either in the progeny of cells or of organisms.

The term also refers to the changes themselves: functionally relevant changes to the genome that do not involve a change in the nucleotide sequence. Examples of mechanisms that produce such changes are DNA methylation and histone modification, each of which alters how genes are expressed without altering the underlying DNA sequence. Gene expression can be controlled through the action of repressor proteins that attach to silencer regions of the DNA.

These epigenetic changes may last through cell divisions for the duration of the cell’s life, and may also last for multiple generations even though they do not involve changes in the underlying DNA sequence of the organism; instead, non-genetic factors cause the organism’s genes to behave (or “express themselves”) differently.

Read the full article on Wikipedia

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.

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

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

Methylene Chloride (Dichloromethane)

Above is a photgraph taken in Irish Air Corps in 2015 of a drum of Dichloromethane. This was in use by the spray paint shop in Baldonnel for stripping paint but was handed out to staff from any other unit that wanted some in containers like soft drinks bottles or milk cartons.

Note : The European Union had banned this chemical 3 years earlier in 2015. The current Health & Safety officer in Baldonnel didn’t know Dichlorometheane had been banned and in fact didn’t even know Dichlorometheane was actually in use as no chemical register was in existance at the time despite being mandatory since 1989.

This was prior to the Irish Air Corps becoming LEADERS in workplace chemical Healh & Safety as “self-declared” recently to the Oireachtas Joint Committee on Foreign Affairs and Trade, and Defence.

CAS  75-09-2

Hazard Summary

Methylene chloride is predominantly used as a solvent. The acute (short-term) effects of methylene chloride inhalation in humans consist mainly of nervous system effects including decreased visual, auditory, and motor functions, but these effects are reversible once exposure ceases.

The effects of chronic (long-term) exposure to methylene chloride suggest that the central nervous system (CNS) is a potential target in humans and animals.

Human data are inconclusive regarding methylene chloride and cancer. Animal studies have shown increases in liver and lung cancer and benign mammary gland tumors following the inhalation of methylene chloride.

Please Note: The main sources of information for this fact sheet are the Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological Profile for Methylene Chloride and EPA's Integrated Risk Information System (IRIS), which contains information on oral chronic toxicity and the RfD, and the carcinogenic effects of methylene chloride including the unit cancer risk for inhalation exposure

Uses

  • Methylene chloride is predominantly used as a solvent in paint strippers and removers; as a process solvent in the manufacture of drugs, pharmaceuticals, and film coatings; as a metal cleaning and finishing solvent in electronics manufacturing; and as an agent in urethane foam blowing. (1)
  • Methylene chloride is also used as a propellant in aerosols for products such as paints, automotive products, and insect sprays. (1)
  • It is used as an extraction solvent for spice oleoresins, hops, and for the removal of caffeine from coffee. However, due to concern over residual solvent, most decaffeinators no longer use methylene chloride. (1)
  • Methylene chloride is also approved for use as a postharvest fumigant for grains and strawberries and as a degreening agent for citrus fruit. (1)

Sources and Potential Exposure

  • The principal route of human exposure to methylene chloride is inhalation of ambient air. (1)
  • Occupational and consumer exposure to methylene chloride in indoor air may be much higher, especially from spray painting or other aerosol uses. People who work in these places can breathe in the chemical or it may come in contact with the skin. (1)
  • Methylene chloride has been detected in both surface water and groundwater samples taken at hazardous waste sites and in drinking water at very low concentrations. (1)

Assessing Personal Exposure

  • Several tests exist for determining exposure to methylene chloride. These tests include measurement of methylene chloride in the breath, blood, and urine. It is noted that smoking and exposure to other chemicals may affect the results of these tests. (1)

Health Hazard Information

Acute Effects:

  • Case studies of methylene chloride poisoning during paint stripping operations have demonstrated that inhalation exposure to extremely high levels can be fatal to humans. (1,2)
  • Acute inhalation exposure to high levels of methylene chloride in humans has resulted in effects on the central nervous system (CNS) including decreased visual, auditory, and psychomotor functions, but these effects are reversible once exposure ceases. Methylene chloride also irritates the nose and throat at high concentrations. (1,2)
  • Tests involving acute exposure of animals have shown methylene chloride to have moderate acute toxicity from oral and inhalation exposure. (3)

Chronic Effects (Noncancer):

  • The major effects from chronic inhalation exposure to methylene chloride in humans are effects on the CNS, such as headaches, dizziness, nausea, and memory loss. (1,2)
  • Animal studies indicate that the inhalation of methylene chloride causes effects on the liver, kidney, CNS, and cardiovascular system. (1,2)
  • EPA has calculated a provisional Reference Concentration (RfC) of 3 milligrams per cubic meter (mg/m3) based on liver effects in rats. The RfC is an estimate (with uncertainty spanning perhaps 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. (5)
  • The Reference Dose (RfD) for methylene chloride is 0.06 milligrams per kilogram body weight per day (mg/kg/d) based on liver toxicity in rats. (4)
  • EPA has medium confidence in the RfD based on: high confidence in the study on which the RfD is based because a large number of animals of both sexes were tested in four dose groups, with a large number of controls, many effects were monitored, and a dose-related increase in severity was observed; and medium to low confidence in the database because only a few studies support the no-observed-adverse-effect level (NOAEL). (4)

Reproductive/Developmental Effects:

  • No studies were located regarding developmental or reproductive effects in humans from inhalation or oral exposure. (1,2)
  • Animal studies have demonstrated that methylene chloride crosses the placental barrier, and minor skeletal variations and lowered fetal body weights have been noted. (1,2)

Cancer Risk:

  • Several studies did not report a statistically significant increase in deaths from cancer among workers exposed to methylene chloride. (1,2)
  • Animal studies have shown an increase in liver and lung cancer and benign mammary gland tumors following inhalation exposure to methylene chloride. (1,2,4)
  • EPA considers methylene chloride to be a probable human carcinogen and has ranked it in EPA’s Group B2.(4)
  • EPA uses mathematical models, based on 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 4.7 × 10-7 (µg/m3)-1. EPA estimates that, if an individual were to continuously breathe air containing methylene chloride at an average of 2.0 µg/m3 (0.002 mg/m3) over his or her entire lifetime, that person would theoretically have no more than a one-in-a-million increased chance of developing cancer as a direct result of breathing air containing this chemical. Similarly, EPA estimates that breathing air containing 20 µg/m3 (0.02 mg/m3 ) would result in not greater than a one-in-a-hundred
    breathing air containing 20 µg/m3 (0.02 mg/m3) would result in not greater than a one-in-a-hundred thousand increased chance of developing cancer, and air containing 200 µg/m3(0.2 mg/m3) would result in not greater than a one-in-ten thousand increased chance of developing cancer. For a detailed discussionof confidence in the potency estimates, please see IRIS. (4)
  • Note the MAX mathamatical/theoretical EPA level above of 200 µg/m3(0.2 mg/m3) equates to 0.05758ppm (parts per million). Dichloromethane was measured in ERF on Wednesday 12th & Thursday 13th July, 1995 at 175ppm. This equates to 607,880 µg/m3(607.88 mg/m3). So the level the EPA use to calculate a one-in-a hundred thousand increased chance of developing cancer were exceeded by the Irish Air Corps by a factor of 3,039. So statistically if a person inhalled the levels that many Irish Air Corps were exposed to 24/7 for a lifetime they would have a 1 in 33 chance of developing cancer as a result.
  • EPA calculated an oral cancer slope factor of 7.5 x 10-3 (mg/kg/d)-1. (4)

Physical Properties

  • A common synonym for methylene chloride is dichloromethane. (1,4)
    Methylene chloride is a colorless liquid with a sweetish odor. (1,6)
    The chemical formula for methylene chloride is CH2Cl2, and the molecular weight is 84.93 g/mol. (1)
  • The vapor pressure for methylene chloride is 349 mm Hg at 20 °C, and it has an octanol/water coefficient (log Kow) of 1.30. (1)
  • Methylene chloride has an odor threshold of 250 parts per million (ppm). (7)
  • Methylene chloride is slightly soluble in water and is nonflammable. (1,6)

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

*****

Relavance to personnel who served in the Air Corps

  1. Dichloromethane was a  component of Ardrox 666 used in ERF.
  2. Dichloromethane was a component of the Paint Remover 82510 used by the Spray Paint Shop but also by technicians in No3 Sp Wing, BFTS & possibly elsewhere.

There are possibly more chemicals used by the Air Corps that contain Dichloromethane. If you know of some let us know in the comments section. We are not statisticians and our interpretation of the cancer statistics are open to correction.

Cresol / Cresylic Acid – Guide to Hazardous Air Pollutants used by the Irish Air Corps

Cresol / Cresylic Acid

o-CRESOL, m-CRESOL, p-CRESOL

Cresylic Acid spilled all over the floor of the NDT shop of ERF and indeed dribbling down the wall from the extractor fan.

CAS  1319-77-3 , 95-48-7, 108-39-4, 106-44-5

Hazard Summary

Ambient air contains low levels of cresols from automobile exhaust, power plants, and oil refineries. Acute (short-term) inhalation exposure by humans to mixed cresols results in respiratory tract irritation, with symptoms such as dryness, nasal constriction, and throat irritation.  Mixed cresols are also strong dermal irritants.

No information is available on the chronic (long-term) effects of mixed cresols in humans, while animal studies have reported effects on the blood, liver, kidney, and central nervous system (CNS), and reduced body weight, from oral and inhalation exposure to mixed cresols.

Several animal studies suggest that o-cresol, m-cresol, and p-cresol may act as tumor promotors.  EPA has classified o-cresol, m-cresol, and p-cresol as Group C, possible human carcinogens.

Please Note: The main sources of information for this fact sheet are EPA's IRIS (4), which contains information on oral chronic toxicity and the RfD, and the carcinogenic effects of cresols, and the Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological Profile for Cresols. (1)

Uses

  • Mixed cresols are used as disinfectants, preservatives, and wood preservatives. (1)
  • o-Cresol is used as a solvent, disinfectant, and chemical intermediate. (1)
  • m-Cresol is used to produce certain herbicides, as a precursor to the pyrethroid insecticides, to produce antioxidants, and to manufacture the explosive, 2,4,6-nitro-m-cresol. (1)
  • p-Cresol is used largely in the formulation of antioxidants and in the fragrance and dye industries. (1)

Sources and Potential Exposure

  • Mixed cresols may be found in ambient air; sources are car exhaust, electrical power plants, municipal solid waste incinerators, oil refineries, and cigarettes. (1)
  • People in residential areas where homes are heated with coal, oil, or wood may be exposed to mixed cresols in the air. (1)
  • Some foods, such as tomatoes, ketchup, asparagus, cheeses, butter, bacon, and smoked foods, as well as beverages, such as red wine, raw and roasted coffee and black tea, contain mixed cresols. (1)
  • Occupational exposure to mixed cresols may also occur at workplaces where mixed cresols and/or cresol containing products are produced or used. (1)

Assessing Personal Exposure

  • Mixed cresols can be measured in the urine of exposed individuals.

Health Hazard Information

Acute Effects:

  • Acute inhalation exposure by humans to mixed cresols results in respiratory tract irritation, with symptoms such as dryness, nasal constriction, and throat irritation.  Mixed cresols are also strong dermal irritants. Ingestion of high levels of mixed cresols by humans has resulted in effects on the respiratory system, gastrointestinal system, blood, liver, kidney, and CNS. (1,2)
  • Animal studies have reported respiratory tract and eye irritation, and effects on the liver, kidney, and CNS from acute inhalation exposure to mixed cresols. (1)
  • Acute animal tests in rats have shown mixed cresols to have moderate acute toxicity, while o-cresol, m-cresol, and p-cresol have been shown to have high acute toxicity from oral exposure. (3)

Chronic Effects (Noncancer):

  • No information is available on the chronic effects of mixed cresols in humans. (1)
  • Animal studies have reported effects on the blood, liver, kidney, and CNS, as well as reduced body weight, from oral and inhalation exposure to mixed cresols. (1,5)
  • EPA has not established a Reference Concentration (RfC) or a Reference Dose (RfD) for mixed cresols. (4)
  • The California Environmental Protection Agency 3  (CalEPA) has established a chronic reference exposure level of 0.004 milligrams per cubic meter (mg/m ) for mixed cresols based on bone marrow effects in rats. The CalEPA reference exposure level is a concentration at or below which adverse health effects are not likely to occur. It is not a direct estimator of risk, but rather a reference point to gauge the potential effects. At lifetime exposures increasingly greater than the reference exposure level, the potential for adverse health effects increases. (5)
  • EPA has not established an RfC for o-, m-, or p-cresol.  (5-7)
  • The RfD for o-cresol and m-cresol is 0.05 milligrams per kilogram body weight per day (mg/kg/d) based on decreased body weights and neurotoxicity in rats. The RfD is an estimate (with uncertainty spanning
    perhaps an order of magnitude) of a daily oral exposure to the human population (including sensitive subgroups) that is likely to be without appreciable risk of deleterious noncancer effects during a lifetime. (5,6)
  • EPA has high confidence in the studies on which the RfDs are based because they provided adequate toxicological endpoints that included both general toxicity and neurotoxicity; medium confidence in the database because there are adequate supporting subchronic studies but lacking chronic toxicity and reproductive studies; and, consequently, medium confidence in the RfD. (5,6)
  • The provisional RfD for p-cresol is 0.005 mg/kg/d based on neurological and respiratory effects in rabbits. The provisional RfD is a value that has had some form of Agency review, but it does not appear on IRIS. (8)

Reproductive/Developmental Effects:

  • No information is available on the reproductive or developmental effects of mixed cresols in humans. (1)
  • Animal studies have reported developmental effects, but only at maternally toxic doses, and no reproductive effects from oral exposure to mixed cresols. (1)

Cancer Risk:

  • Only anecdotal information is available on the carcinogenic effects of mixed cresols in humans. (4-7)
  • The only available oral animal study is a 13-week study that suggested that p-cresol may act as a promotor for tumors of the forestomach. (1)
  • Several dermal animal studies have suggested that o-cresol, m-cresol, and p-cresol may act as tumor promotors. (1,4-7)
  • EPA has classified o-cresol, m-cresol, and p-cresol as Group C, possible human carcinogens. (5-7)

Physical Properties

  • Mixed cresols are colorless solids, but usually they occur as a brown liquid mixture. (1)
  • Mixed cresols have a medicinal odor; the odor thresold for m-cresol is 0.00028 parts per million (ppm). (1,9)
  • The chemical formula for cresol is C 7 H 8 O, and the molecular weight is 108.14 g/mol. (1)
  • The primary synonym for o-cresol is 2-methylphenol; m-cresol is 3-methylphenol, and p-cresol is 4-methylphenol. (5-7)
  • The vapor pressures, at 25 °C, for o-cresol, m-cresol, and p-cresol are 0.299 mm Hg, 0.138 mm Hg, and 0.11 mm Hg, respectively. (1)
  • The octanol/water partition coefficients (log K ow) for o-cresol, m-cresol, and p-cresol are 1.95, 1.96, and 1.94, respectively. (1)

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

*****

Relavance to personnel who served in the Air Corps

  1. Cresylic Acid is  component of Ardrox 666
  2. Cresols are consitituent chemicals of turbine engine oils. e.g. Tri-cresyl phosphate which is an organophosphate.

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

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

Benzene

CAS  71-43.2

Hazard Summary

Benzene is found in the air from emissions from burning coal and oil, gasoline service stations, and motor vehicle exhaust. Acute (short-term) inhalation exposure of humans to benzene may cause drowsiness,  dizziness, headaches, as well as eye, skin, and respiratory tract irritation, and, at high levels, unconsciousness. Chronic (long-term) inhalation exposure has caused various disorders in the blood, including reduced numbers of red blood cells and aplastic anemia, in occupational settings.   Reproductive effects have been reported for women exposed by inhalation to high levels, and adverse effects on the developing fetus have been observed in animal tests. Increased incidence of leukemia (cancer of the tissues that form white blood cells) have been observed in humans occupationally exposed to benzene. EPA has classified benzene as known human carcinogen for all routes of exposure.

Please Note: The main sources of information for this fact sheet are the Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological Profile for Benzene (1) and EPA's Integrated Risk Information System (IRIS) (4),which contains information on the health effects of benzene including the unit cancer risk for inhalation
exposure.

Uses

  • Benzene is used as a constituent in motor fuels; as a solvent for fats, waxes, resins, oils, inks, paints, plastics, and rubber; in the extraction of oils from seeds and nuts; and in photogravure printing. It is also used as a chemical intermediate. Benzene is also used in the manufacture of detergents, explosives, pharmaceuticals, and dyestuffs. (1,2,6)

Sources and Potential Exposure

  • Individuals employed in industries that manufacture or use benzene may be exposed to the highest levels of benzene. (1)
  • Benzene is found in emissions from burning coal and oil, motor vehicle exhaust, and evaporation from gasoline service stations and in industrial solvents. These sources contribute to elevated levels of benzene in the ambient air, which may subsequently be breathed by the public. (1)
  • Tobacco smoke contains benzene and accounts for nearly half the national exposure to benzene. (1)
  • Individuals may also be exposed to benzene by consuming contaminated water. (1)

Assessing Personal Exposure

Measurement of benzene in an individual’s breath or blood or the measurement of breakdown products in the urine (phenol) can estimate personal exposure. However, the tests must be done shortly after exposure
and are not helpful for measuring low levels of benzene. (1)

Health Hazard Information

Acute Effects:

  • Coexposure to benzene with ethanol (e.g., alcoholic beverages) can increase benzene toxicity in humans. (1)
  • Neurological symptoms of inhalation exposure to benzene include drowsiness, dizziness, headaches, and Neurological symptoms of inhalation exposure to benzene include drowsiness, dizziness, headaches, and unconsciousness in humans.  Ingestion of large amounts of benzene may result in vomiting, dizziness, and convulsions in humans. (1)
  • Exposure to liquid and vapor may irritate the skin, eyes, and upper respiratory tract in humans.  Redness and blisters may result from dermal exposure to benzene. (1,2)
  • Animal studies show neurologic, immunologic, and hematologic effects from inhalation and oral exposure to benzene. (1)
  • Tests involving acute exposure of rats, mice, rabbits, and guinea pigs have demonstrated benzene to have low acute toxicity from inhalation, moderate acute toxicity from ingestion, and low or moderate acute toxicity from dermal exposure. (3)
  • The reference concentration for benzene is 0.03 mg/m3 based on hematological effects in humans. The RfC is an estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation
    exposure to the human population (including sensitive groups) that is likely to be without appreciable risk deleterious noncancer effects over a lifetime. (4)

Chronic Effects (Noncancer):

  • Chronic inhalation of certain levels of benzene causes disorders in the blood in humans. Benzene specifically affects bone marrow (the tissues that produce blood cells). Aplastic anemia (a risk factor for acute nonlymphocytic leukemia), excessive bleeding, and damage to the immune system (by changes in blood levels of antibodies and loss of white blood cells) may develop. (1)
  • In animals, chronic inhalation and oral exposure to benzene produces the same effects as seen in humans. (1)
  • Benzene causes both structural and numerical chromosomal aberrations in humans. (1)
  • EPA has established an oral Reference Dose (RfD) for benzene of 0.004 milligrams per kilogram per day (mg/kg/d) based on hematological effects in humans. The RfD is an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral 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 for effects. At exposures increasingly greater than the RfD, the potential for adverse health effects increases. Lifetime exposure above the RfD does not imply that an adverse health effect would necessarily occur. (4)
  • EPA has established a Reference Concentration (RfC) of 0.03 milligrams per cubic meter (0.03 mg/m3) for benzene based on hematological effects in humans. The RfC is an inhalation exposure concentration at or below which adverse health effects are not likely to occur. It is not a direct estimator of risk, but rather a reference point to gauge the potential for effects. At lifetime exposures increasingly greater than the reference exposure level, the potential for adverse health effects increases. (4)

Reproductive/Developmental Effects:

  • There is some evidence from human epidemiological studies of reproductive and developmental toxicity of benzene, however the data do not provide conclusive evidence of a link between exposure and effect. (4)
    Animal studies have provided limited evidence that exposure to benzene may affect reproductive organs, however these effects were only observed at exposure levels over the maximum tolerated dose. (4)
  • Adverse effects on the fetus, including low birth weight, delayed bone formation, and bone marrow damage, have been observed where pregnant animals were exposed to benzene by inhalation.(4)

Cancer Risk:

  • Increased incidence of leukemia (cancer of the tissues that form white blood cells) has been observed in humans occupationally exposed to benzene. (1,4)
  • EPA has classified benzene as a Group A, known human carcinogen. (4)
  • 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 a range of 2.2 x 10 -6  to 7.8 x 10 -6  as the increase in the lifetime risk of an individual who is continuously exposed to 1 µg/m3 of benzene in the air over their lifetime.
  • EPA estimates that, if an individual were to continuously breathe the air containing benzene at an average of 0.13 to 0.45 µg/m 3  (1.3×10 -4  to 4.5x -4mg/m 3 ) over his or her entire lifetime, that person would theoretically have no more than a one-in-a-million increased chance of developing cancer as a direct result of continuously breathing air containing this chemical. Similarly, EPA estimates that continuously breathing air containing 1.3 to 4.5 µg/m 3 (1.3×10 -3  to 4.5×10 -3  mg/m 3 ) would result in not greater than a one-in-ahundred thousand increased chance of developing cancer, and air containing 13 to 45 µg/m3  (1.3 x 10 – 2  to 4.5 x 10-2 mg/m3) would result in not greater than a one-in-ten thousand increased chance of developing cancer. For a detailed discussion of confidence in the potency estimates, please see IRIS.(4)
  • EPA has calculated an oral cancer slope factor ranging from 1.5 x 10-2  to 5.5 x 10 -2 (mg/kg/d)-1  that is an extrapolation from inhalation dose-response data. (4)

Physical Properties

  • The chemical formula for benzene is C6H6, and it has a molecular weight of 78.11 g/mol. 4) Benzene occurs as a volatile, colorless, highly flammable liquid that dissolves easily in water. (1,7)
  • Benzene has a sweet odor with an ASTDR reported odor threshold of 1.5 ppm (5 mg/m3).
  • The vapor pressure for benzene is 95.2 mm Hg at 25 °C, and it has a log octanol/water partition coefficient (log Kow) of 2.13. (1)

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

*****

Relavance to personnel who served in the Air Corps

  1. Benzene is a component of Jet A1 (AVTUR) and/or Jet A1 exhaust 
  2. Benzene is a component of 100LL (AVGAS) and/or 100LL exhaust
  3. Cellulose Thinners used in spray painting contain Benzene
  4. Akzo Nobel Hardner S66/22R contains <25% Benzene
  5. Mastinox 6856k contains 1-3% Benzene

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

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

Asbestos

CAS  1332-21-4

Hazard Summary

Asbestos production and use has decreased dramatically over the years in the United States. Exposure to asbestos may occur from ambient air, indoor air, or water. Effects on the lung are a major health concern from asbestos, as chronic (long-term) exposure to asbestos in humans via inhalation can result in a lung disease termed asbestosis. Asbestosis is characterized by shortness of breath and cough and may lead to severe impairment of respiratory function. Cancer is also a major concern associated with asbestos exposure, as inhalation exposure causes lung cancer and mesothelioma (a rare cancer of the thin membranes lining the abdominal cavity and surrounding internal organs), and possibly stomach, laryngeal, and colorectal cancer. EPA has classified asbestos as a Group A, known human carcinogen.

Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System (IRIS) (2), which contains information on the carcinogenic effects of asbestos including the unit cancer risk for inhalation exposure, and the Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological Profile for Asbestos. (1)

Uses

  • Asbestos production and use in the U.S. has decreased dramatically over the years due to healthconcerns and regulations banning its use. (1)
  • U.S. production of asbestos decreased from 300 million pounds in 1973 to 6 million pounds in 2002. (3)
  • In 2010, there were two U.S. suppliers of asbestos and most of the asbestos used in the U.S. is imported from Canada. (3)
  • Asbestos has been used in building materials, paper products, asbestos-cement products, friction products, textiles, packings and gaskets, and asbestos-reinforced plastics. (1,4)
  • Many uses have been prohibited, including the spraying of asbestos-containing material on buildings and structures for fireproofing, insulation and decorative purposes, asbestos inclusion in patching compounds and asbestos heat shields in hair dryers. Asbestos substitutes continue to be developed. For example, nonasbestos friction materials are currently being used in disc brake pads, and substitutes have been developed for drum brake linings. (1)

Sources and Potential Exposure

  • Airborne exposure to asbestos may occur through the erosion of natural deposits in asbestos bearing rocks, from a variety of asbestos-related industries, or from clutches and brakes on cars and trucks. The concentrations in outdoor air are highly variable. (1,4)
  • Asbestos has been detected in indoor air, where it is released from a variety of building materials such as insulation and ceiling and floor tiles. It is only released, however, when these building materials are damaged or disintegrate. (1)
  • Asbestos may be released into water from a number of sources, including erosion of natural deposits, corrosion from asbestos-cement pipes, and disintegration of asbestos roofing materials with subsequent transport into sewers. (1,4)

Health Hazard Information

Acute Effects:

  • No studies were located on the acute (short-term) toxicity of asbestos in animals or humans. (1)

Chronic Effects (Noncancer):

  • Chronic inhalation exposure to asbestos in humans can lead to a lung disease called asbestosis, which consists of a diffuse fibrous scarring of the lungs. Symptoms of asbestosis include shortness of breath, difficulty in breathing, and coughing. Asbestosis is a progressive disease, i.e., the severity of symptoms tends to increase with time, even after the exposure has stopped. In severe cases, this disease can lead to death, due to impairment of respiratory function. (1,2)
  • Other effects from asbestos exposure via inhalation in humans include pulmonary hypertension and immunological effects. (1,2)
  • Feeding studies in animals exposed to high doses of asbestos have not detected any evidence of adverse toxic effects. (1,2)
  • EPA has not established a Reference Concentration (RfC) or a Reference Dose (RfD) for asbestos. (2)

Reproductive/Developmental Effects:

  • No studies were located on the developmental or reproductive effects of asbestos in animals or humans via inhalation. (1)
  • Birth defects were not noted in the offspring of animals exposed to asbestos in the diet during pregnancy. (1)
  • No effects on fertility were observed in animals exposed to asbestos in the diet during breeding, pregnancy, and lactation. (1)

Cancer Risk:

  • A large number of occupational studies have reported that exposure to asbestos via inhalationcauses lung cancer and mesothelioma (a rare cancer of the membranes lining the abdominal cavity and surrounding internal organs). (1,2,3)
  • Individuals who smoke and are also exposed to asbestos have a greater than additive increased risk of developing lung cancer. (1,2,3)
  •  Long and intermediate-range asbestos fibers (>5 micrometers (µm)) appear to be more carcinogenic than short fibers (<5 µm). (1)
  • Some occupational studies have reported an increased risk of stomach, laryngeal, or colorectal cancer from asbestos exposure. However, the data are not as strong as that for lung cancer and mesothelioma. (1)
  • Epidemiological studies have not found a clear association between asbestos exposure in drinking water and an increased risk of stomach cancer. (1,2,3)
  • A series of large-scale lifetime feeding studies in animals reported that exposure to intermediate-range asbestos fibers increased the incidence of a benign tumor of the large intestine in male rats, while short-range asbestos fibers showed no significant increase in tumor incidence. (1)
  • EPA has classified asbestos as Group A, human carcinogen. (2)
  • 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 2.3 × 10-1 (fibers/cm3)-1. EPA eestimates that, if an individual were to continuously breathe air containing asbestos at an average of 0.000004 fibers/cm3 over his or her entire lifetime, that person would theoretically have no more than a one-in-a-million  increased chance of developing cancer as a direct result of breathing air containing this chemical. Similarly, EPA estimates that breathing air containing 0.00004 fibers/cm3 would result in not greater than a one-in-a-hundred thousand increased chance of developing cancer, and air containing 0.0004 fibers/cm3 would result in not greater than a one-in-ten-thousand increased chance of developing cancer. (2)

Physical Properties

  • Asbestos is the name applied to a group of six different fibrous silicate minerals that occur naturally in the environment. (1)
  • There are two groups of asbestos minerals: serpentine and amphibole. There are also nonfibrous forms of serpentine and amphibole which are not asbestos. (1)
  • Serpentine asbestos are relatively long and flexible crystalline fibers that may be woven, and includes the mineral chrysotile, and amphibole asbestos are more brittle than serpentine asbestos and includes the minerals amosite, crocidolite, tremolite, anthophyllite, and actinolite. (1)
  • Asbestos is neither volatile nor soluble; however, small fibers may occur in suspension in both air and water. (1)

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

*****

Relavance to personnel who served in the Air Corps

  1. Pipework in a number of Air Corps buildings was lagged with Asbestos most notably the Apprentice hostel was lagged with badly damaged Asbestos until the early 1990s. So every apprentice who served from approximately the 55th Apprentice Class and before was exposed to asbestos in their sleeping environment.
  2. The apprentice hangar roof was made from asbestos.
  3. Parts of engine shop ceiling was discovered to be made from asbestos when it partially collapsed and dislocated the shoulder of a machinist working beneath it.
  4. The fire crew wore special fire suits made from asbestos. 

It is likely that we have missed many areas of asbestos usage  in both Baldonnel and Gormanston aerodromes so please help us by listing usage locations in comments section below.