Tag: disease Air Corps

Human Health Effects of Trichloroethylene: Key Findings and Scientific Issues

Abstract

Background

Background: In support of the Integrated Risk Information System (IRIS), the U.S. Environmental Protection Agency (EPA) completed a toxicological review of trichloroethylene (TCE) in September 2011, which was the result of an effort spanning > 20 years.

Objective

We summarized the key findings and scientific issues regarding the human health effects of TCE in the U.S. EPA’s toxicological review.

Methods

In this assessment we synthesized and characterized thousands of epidemiologic, experimental animal, and mechanistic studies, and addressed several key scientific issues through modelling of TCE toxicokinetics, meta-analyses of epidemiologic studies, and analyses of mechanistic data.

Discussion

Toxicokinetic modelling aided in characterizing the toxicological role of the complex metabolism and multiple metabolites of TCE. Meta-analyses of the epidemiologic data strongly supported the conclusions that TCE causes kidney cancer in humans and that TCE may also cause liver cancer and non-Hodgkin lymphoma. Mechanistic analyses support a key role for mutagenicity in TCE-induced kidney carcinogenicity.

Recent evidence from studies in both humans and experimental animals point to the involvement of TCE exposure in autoimmune disease and hypersensitivity.

Recent avian and in vitro mechanistic studies provided biological plausibility that TCE plays a role in developmental cardiac toxicity, the subject of substantial debate due to mixed results from epidemiologic and rodent studies.

Conclusion

TCE is carcinogenic to humans by all routes of exposure and poses a potential human health hazard for noncancer toxicity to the central nervous system, kidney, liver, immune system, male reproductive system, and the developing embryo/fetus.

Read full study below

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Persons working with or working in areas using trichloroethylene in Baldonnel have suffered the following illnesses. 

Untimely deaths are marked thus *

      • Brain Tumour*
      • Colorectal Cancer*
      • Crohn’s Disease*
      • Lung Cancer*
      • Multiple Sclerosis
      • Non-Hodgkin’s Lymphoma*
      • Oesophageal Cancer*
      • Pancreatic Cancer*
      • Parkinson’s Disease
      • Renal Cancer*

Impact of Firefighting Aqueous Film-Forming Foams on Human Cell Proliferation and Cellular Mortality

Abstract

Objective

Evaluate the toxic effects of Aqueous Film-Forming Foams used by firefighters for Class B fire suppression in human-derived kidney cells (HEK-293).

Methods

Three widely used AFFFs were collected from fire departments and were added to HEK-293 cells in various concentrations. Seventy-two hours post-treatment, cellular proliferation and toxicity were examined using commercially available kits.

Results

All AFFFs evaluated induced cellular toxicity and significantly decreased cell proliferation, even when cells were treated with concentrations 10-fold lower than the working concentration used for fire suppression.

Conclusion

Despite the reduced usage of PFAS-containing AFFFs in the firefighter work environment, the evaluated AFFFs demonstrated significantly altered cellular proliferation, while also inducing toxicity, indicating the presence of toxic compounds. Both stronger implementation of PFAS-containing AFFFs restrictions and robust evaluation of fluorine-free and next-generation AFFFs are warranted.

In Brief

Firefighters are routinely exposed to per- and polyfluoroalkyl substances (PFAS) through the use of Aqueous Film-Forming Foams (AFFFs) for the suppression of Class B fire, which derive from flammable and combustible liquids, such as gasoline and alcohol. The addition of surfactants and PFAS in the AFFFs allows them to form an aqueous film that can extinguish the fire, while also coating the fuel. As such, AFFFs are often used for fire extinction in airports and military bases.

Exposure to PFAS in the general population may arise from ingestion of contaminated food or water, usage of consumer products containing PFAS, such as non-stick cookware or stain resistant carpets and textiles, and inhalation of PFAS-containing particulate matter. Detection of increased serum PFAS concentrations has been linked to an elevated risk for kidney cancer in humans, and firefighters are known to have increased serum concentrations of certain PFAS after attending training exercises. In the same study it was also observed that the average urinary excretions of 2-butoxyacetic acid (2-BAA) a surfactant often added in AFFFs exceeded the reference limit of the occupationally unexposed population, ranging from 0.5 to 1.4 mmol/mol creatinine.

Furthermore, an increased risk of mortality from kidney cancer has been observed in firefighters compared to the U.S. population. The detrimental health effects of PFAS are exacerbated by their increased half-lives in humans. A recently published study examined the half-lives of short- and long- chained PFAS in the serum of 26 airport employees and observed a wide range of half-lives which was dependent on the length and chemical structure of each substance that was examined. Indicatively, the shortest half-life was described for perfluorobutanesulfonic acid (PFBS), while the linear isomer of perfluorooctanesulfonic acid (PFOS) had the longest half-life (average of 44 days and 2.93 years, respectively), findings which are in agreement with other sources in the literature.

One aspect of this phenomenon could be attributed to renal reabsorption, as humans actively transport PFAS in the proximal tubules. A recently published scoping review of 74 epidemiologic, pharmacokinetic, and toxicological studies examined the relationship between PFAS exposure and kidney-related health outcomes. It was observed that exposure to PFAS was associated with lower kidney function, including chronic kidney disease (CKD), and histological abnormalities in the kidneys, as well as alterations in key mechanistic pathways, that can induce oxidative stress, and metabolic changes leading to kidney disease.

The alarming number of studies showcasing the harmful health effects pertaining to PFAS exposure has led to the banning of the production of AFFFs containing highly toxic, long chain PFAS, such as perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) since 2015. However, this regulation is gradually being implemented across states and little is known about the toxicity of the next generation AFFFs. Based on the above, in the present study we evaluate cellular proliferation and toxicity in kidney-derived cells (HEK-293) that were exposed to three widely used AFFFs.

Read full study below

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Organic solvents and Multiple Sclerosis susceptibility

Abstract

Photo of dichloromethane (DCM) as stored by Irish Air Corps in 2015. DCM was banned in the EU in 2012.
Objective

We hypothesize that different sources of lung irritation may contribute to elicit an immune reaction in the lungs and subsequently lead to multiple sclerosis (MS) in people with a genetic susceptibility to the disease. We aimed to investigate the influence of exposure to organic solvents on MS risk, and a potential interaction between organic solvents and MS risk human leukocyte antigen (HLA) genes.

Methods

Using a Swedish population-based case-control study (2,042 incident cases of MS and 2,947 controls), participants with different genotypes, smoking habits, and exposures to organic solvents were compared regarding occurrence of MS, by calculating odds ratios with 95% confidence intervals using logistic regression. A potential interaction between exposure to organic solvents and MS risk HLA genes was evaluated by calculating the attributable proportion due to interaction.

Results

Overall, exposure to organic solvents increased the risk of MS (odds ratio 1.5, 95% confidence interval 1.2–1.8, p = 0.0004). Among both ever and never smokers, an interaction between organic solvents, carriage of HLA-DRB1*15, and absence of HLA-A*02 was observed with regard to MS risk, similar to the previously reported gene-environment interaction involving the same MS risk HLA genes and smoke exposure.

Conclusion

The mechanism linking both smoking and exposure to organic solvents to MS risk may involve lung inflammation with a proinflammatory profile. Their interaction with MS risk HLA genes argues for an action of these environmental factors on adaptive immunity, perhaps through activation of autoaggressive cells resident in the lungs subsequently attacking the CNS.

Read full study below

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Anecdotal evidence has been emerging for some time of potential illness clusters at Casement Aerodrome to which Multiple Sclerosis has now been added. We are calling for these potential clusters to be investigated by competent authorities.

Suspected illness clusters currently include.

Illnesses linked to #Trichloroethylene aka TCE aka TRIKE

Illnesses linked to trichloroethylene aka TCE aka TRIKE

CAS number: 79-01-6

Diseases linked to this toxicant grouped by strength of evidence.

Strong Evidence

  • Acute hepatocellular injury (hepatitis)*

Good Evidence

  • Acute tubular necrosis
  • Arrhythmias
  • Autoimmune antibodies (positive ANA, anti-DNA, RF, etc.)*
  • Cardiac congenital malformations*
  • Childhood leukemias
  • Cirrhosis*
  • Cognitive impairment (includes impaired learning, impaired memory, and decreased attention span) / mental retardation / developmental delay*
  • Decreased coordination / dysequilibrium
  • Fetotoxicity (miscarriage / spontaneous abortion, stillbirth)*
  • Hearing loss*
  • Hepatocellular cancer (liver cancer)*
  • Lymphoma (non-Hodgkin’s)*
  • Psychiatric disturbances (disorientation, hallucinations, psychosis, delirium, paranoias, anxiety/depression, emotional lability, mood changes, euphoria)*
  • Renal (kidney) cancer*
  • Scleroderma
  • Trigeminal neuropathy

Limited Evidence

  • ADD/ADHD, hyperactivity*
  • Adult-onset leukemias*
  • Brain cancer – adult*
  • Breast cancer*
  • Cervical cancer
  • Choanal atresia
  • Genito-urinary malformations (includes male and female)
  • Hodgkin’s disease (lymphoma)*
  • Immune suppression
  • Low birth weight / small for gestational age / intra-uterine growth retardation
  • Lung cancer*
  • Multiple myeloma*
  • Nephrotic syndrome
  • Neural tube defects / CNS malformations
  • Oral clefts (cleft lip and palate)
  • Pancreatic cancer*
  • Pancreatitis
  • Peripheral neuropathy*
  • Prostate cancer*
  • Raynaud’s phenomenon
  • Systemic lupus erythematosus*
  • Testicular cancer*

Illnesses marked thus * have been suffered by Irish Air Corps personnel or their offspring.

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.

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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