Cabin Crew Syndrome
by J. Wright BSN/Cabin Crew, and D. Clarke/Cabin Crew
Aircraft cabin air quality, has had a history of complaints of illness from cabin crewmembers. Symptoms are neurologic and respiratory, and acute or chronic( 2, 5, 9,12,13,18,19,37,42,43 ). Outcomes can be devastating. Complaints seem to be increasing. Lubricating oils/hydraulics(Skydrol), well known to be irritating to skin and mucous membranes, are of great concern due to the neurotoxicity of phosphate ester components and organophosphate additives such as tri cresyl phosphate, and thermal degradation products (1,6,15,21,34,35,38,39,41,44).
These chemicals, their fumes and aerosols, potentially contaminate aircraft ventilation systems and the cabin through seal leaks within engines and auxiliary power units (APU’s), system failures, design and maintenance problems, and operations issues (4,5,14,15,20,11).
Illness and symptom presentation with reports of odors/or not, ventilation restrictions and contamination, could be the varying facets of organophosphate poisoning, which can mimic many disorders (49).
Today we would like to share with you a history of the studies done to date, that mention contaminants as a probable contributor to illnesses in cabin crew. The case study will be presented in 12 overheads, with progression of symptoms to an incomplete recovery. Following the case study, 12 overheads will describe the pathophysiology of these chemicals, how they impact the nervous system, the symptoms of a “Cholinergic Crisis,” and expected outcomes.
Historical
This overhead shows some studies to date that refer to contamination. Studies in the mid-1980’s, with participation of a large carrier and union, suggested a cause and effect relationship between hydraulic/oil contamination and byproducts, and the report of symptoms (12,13). Among other things, tri cresyl phosphate, and phosphate esters were discussed. Actions taken at that time included increasing air flow capability, changing oil product, burnout of contaminants, cleaning the APU door and inlet duct and more frequent changing of water bags(12, 13).
Regulatory
There is no federal/state agency specifically assigned and involved with cabin crew safety and health. Regulatory approaches with the agriculture industry for organophosphate pesticides, have involved the Department of Agriculture, Environmental Protection Agency, and Occupational Safety and Health Administration. OSHA, in 1973, set Reentry Interval Levels as Standards for organophosphate insecticides. Responsibility was transferred to the EPA, which set 24 and 48 hour reentry times for the most toxic organophosphates. The term changed to “restricted entry interval” ( REI’s). In 1984, the EPA set guidelines with goal to avoid acute poisoning in workers (17). In 1992, the EPA “published new worker protection standard for agriculture to provide guidance in areas like reentry, hazard communication, and protective clothing” (48,17).
Lack of reporting, data collection, and epidemiological studies of cabin crew illness, it seems, must be due to this absence of regulatory involvement and guidance. Quality recordkeeping on the extent and character of illness is nonexistent. The magnitude of the illness is therefore difficult to estimate. Current record keeping, of which I am aware, is limited to local labor unions staffed by non-medical personnel with limited budgets.
Case Study
This case study was chosen because of the medical records available, and notes taken by the individual which allows a clinical picture to be seen. This incident does not include all of the myriad
of outcomes/diagnosis that have been witnessed, and anecdotally reported. These outcomes would however be consistent with a neurotoxic exposure(22): thyroid dysfunction, endocrine disorders, myoclonic tremors, parkinsons, multiple sclerosis signs and symptoms, liver damage, heart damage, environmental sensitivities, migraines, sciatica, back pain/weakness/injuries, immune disorders, convulsions/seizures, and paralysis.
This incident involved a 727 that had a hydraulic pressure light illuminated in flight. Maintenance and repair occurred on the ground. The engines were run 4-5 minutes, and thrust reverser cycled twice with APU on. The doors were open as fleet service was servicing on the ground.
A long taxi, and one hour flight followed. Ten minutes after takeoff, the notes describe headache, dizziness, nausea, sweating, shaking, labored painful breathing, requiring concentration and forcing self to breath. Shock like pain to the head, sensation of spiders crawling all over, anesthesia, fighting to stay awake, substernal chest pain and cramping, blue hands, metallic taste, tight and painful chest, incoherence, weakness and stumbling. She remembers a haze in the cabin and a sweet smell, but the flight attendants had been cooking cinnamon rolls. All four cabin crew were involved with the two in the back most severely ill. Passengers had headaches and nausea.
5 Hours
At five hours, the ER physician’s notes state “ probable inhalation injury.” The notes further describe - “vibrating eyelids, shaking and chills, like anesthesia.” Personal notes document tremendous muscle involvement- cramps, spasms, shakes, calf pain, neck pain, abdominal pain and cramps, leg weakness, parasthsias - tingling, needles, spiders, burning of skin, face, and chest, nausea, headache, hot flashes, ear ringing, brightness going in and out, sensation of slowly being anesthetized, and unsteadiness like a boat rocking.
16
Hours
At 16 hours, the second emergency room records carbon monoxide at 2.5, cognitive problems, memory and concentration problems, slurred speech, stammering, headache, nausea, dizziness, blurred vision , and disorientation. The same day an Internist documented ataxia, wobbly, inability to coordinate thumb and finger, inability to subtract 7 serially from 100, and inability to remember 3 digits. The diagnosis was toxic encephalopathy.
Day 2
Day 2 she writes, “ lost sense of humor, personality is gone,” can’t match socks, feels retarded, spasm of foot muscles, agitated, forgetful, no balance, falling up and down stairs, and diarrhea with a chemical odor.
Day 3
Day 3, a Neurologist documents toxic encephalopathy, with significant cognitive dysfunction, and a white macular rash. No psychosis, neurosis or personality disorder. A Neuropsychologist documents organic brain syndrome beyond acute anxiety, tremulous, weak right lower extremity, mild ataxia, memory loss, speech disorder, can’t set a clock, can’t draw a cube, doesn’t know the weeks in a year, cannot subtract serial 7s, cannot remember 4 words, and has confusion learning new information. The personal journal describes deterioration of handwriting and control of pen, a white rash on the face and neck, and a sore on her lower lip like a burn, that hurt and went away very fast.
Day 5/ 8-9
Day 5, she reads the paper but doesn’t remember what she read. There is increasing weakness and involvement of the neck muscles, and eye muscles. She cannot track words and has to go over sentences many times. Sitting quietly her head falls to the right.
Day 8-9, which could be the time frame for OPIDN (delayed motor neuropathy), she writes of increased weakness of arms and legs and spoke of how discouraging it was because everything seemed to be getting worse. Stumbling and weaving when walking, muscle twitches, neck pain, decreased manual dexterity of lift, place and grasp, repetitious movement, exaggerated startle, light sensitive, fuzzy vision, eye pain, hair loss and cognitive disorientation. She was not aware of time passing.
Day 10
Day 10,
the Neuropsychologist indicated
cognitive problems consistent with toxic
encephalopathy, and recommends specific cognitive remediation strategies to increase attention, and learning ability.
Day 14
Day 14, personal notes describe stumbling and weaving when walking, unstable, confusion, visual problems, headaches, joint pain, using words wrong. Internist documents, less stumbling, dizziness, lightheaded, modest confusion, generalized weakness, difficulty reading words because tend to jump on the page, intermittent drift of right arm and leg, symmetrical reflexes.
One
month
At one month, personal notes describe aching pain in the back and neck, visual floaters, and cognitive problems. The Internist documents unable to subtract serial sevens, unable to remember three digits (forgets one or more), wobbly, and ataxia. The Magnetic Resonance Imaging (MRI) of the brain finds- white matter high signal intensity spots, on the frontal lobe of the brain. Tissue damage.
Week 5, 7/8
Week 5, 7, and 8 show gradual improvement yet remaining fatigue, diarrhea and skin involvement.
6 months
At 6 months, the neuropsychologist notes moderate improvement in complex attention, short term memory, speed and accuracy of information processing, spatial motor skills, abstract conceptual and reasoning skills. Variabilities were noted in immediate attention, distractibility, verbal learning inefficiencies, weakness in arithmetic reasoning, and no menses for 6 months. Personal notes are of remaining cognitive impairment, short term memory, retention, learning, lowered immune, visual, some confusion.
Action of
Organophosphates and Phosphate esters
Understanding
nervous system physiology and mechanism of action of neurotoxins like organophosphates
and phosphate esters, is necessary to
recognize signs and symptoms of neurotoxic exposure. The nervous system’s ability to transmit signals throughout the
body is dependent on acetylcholine(ACh), a chemical neurotransmitter. The enzyme acetylcholinesterase(AChE)
continually degrades acetylcholine thereby regulating its levels/activity and
controlling vital parts of the central and peripheral nervous system, the
computer that runs the body.
The primary mechanism of organophosphate neurotoxicity is inhibition of the enzyme acetylcholinesterase at the synaptic sites of the central and peripheral nervous system. The subsequent accumulation of acetylcholine at these sites leads to massive overstimulation, and eventual paralysis of neurochemical transmission. “In the brain this causes sensory and behavioral disturbances, incoordination, depressed cognition, and respiratory failure”(8). The bonds forming the organophosphate-enzyme complex, initially weak and reversible, become irreversible after 24-48 hours and will not respond to antidote. Therefor the importance of accurate diagnosis and treatment, if indicated. Levels of AChE at nerve junctions in the central and peripheral nervous require 2 weeks to return to baseline, the body as a whole requires 1-3 months to return to baseline (8). The time frame required for return of acetylcholinesterase levels to baseline, is the rational behind monitoring and removal from work in agriculture, preventing a critical threshold of acute poisoning from being reached (48).
Organophosphates and phosphate esters may also inhibit neuropathic target esterase (NTE) similar to acetylcholinesterase. Its action is thought to effect the lipid metabolism of neurons. NTE has been associated with the development of organophosphate induced distal neuropathy (OPIDN) and delayed polyneuropathies. Historically this syndrome was seen in the 1930’s when thousands of people in the US acquired ginger jake paralysis a condition caused by drinking an alcoholic extract of Jamaican ginger contaminated with TOTP(triorthotolyl phosphate)( 8). The “Jake Walk” was the result of this contamination.
This is a diagram of the cholinergic synapse, showing the vesicles that release ACh, and the receptors on the organ or tissue to which they bond - enabling the biochemical transmission of nerve impulses. Phosphate esters and organophosphates rapidly pass the blood brain barrier. They act as anesthetics, effect the myelin, neurons, neurotransmitters, and structures of the nervous system (1). Employed in industry and useful as insecticides, they are also used as chemical weapons.
Agency for Toxic
Substances and Disease Registry
This chart (8) shows manifestation of acetylcholinesterase by site of effects. It provides a context by which to understand presenting symptoms of toxicity. All body systems, organs, glands, muscles, and vessels are innervated by nerves. Action initiated varies by receptor type on the tissue/organ, either muscarinic or nicotinic. Glands(muscarinic) secrete, muscles contract and become weak or paralysed. Eye muscles(muscarinic) contract with blurred vision, iris contracts with pinpoint pupils or dilation with paralysis. Tears glands secrete, salivary glands secrete, gut glands contract with causing nausea/vomiting/diarrhea. Sweat glands lead to profuse sweating. Respiratory glands secrete, with smooth muscle (muscarinic) contraction of the bronchi, and the diaphragm becomes weak causing acute respiratory symptoms. The heart rate and rhythm can react with slowing , irregularities , with heart block, and tachycardia. Skeletal muscle (nicotinic) contracts with spasms, fasciculations, cramping and eventual weakness and paralysis ( 8 ). The CNS becomes excited demonstrating headache, malaise, dizziness, confusion, delirium, psychosis, emotional liability. Late signs of depression of brain stem are loss of consciousness, respiratory depression, and diaphragm paralysis. Symptoms shown here are categorized as muscarinic or nicotinic (8). Of great concern, are involvement of cardiopulmonary system- the heart and muscles of respiration.
ACUTE CLASSIC SIGNS
Some acute and classic signs are headache, dizziness, nausea, abdominal pain, muscle involvement, excess secretions, and hyperactive bowels ( 8 ). Organophosphates absorbed dermally, show more nicotinic effects than muscarinic(8). SLUDGE is the acronym for muscarinic effects- Salivation, Lacrimation, Urination, Defecation, Gastrointestinal distress, and Emesis(8).
EXPECTED
OUTCOMES
Expected outcomes of organophosphate acute overexposure are muscle weakness, personality changes, persistent abnormalities in thought processes, problem solving, and organizational ability. Other persistent abnormalities are seen in attention, language, visuomotor, EEG, and anxiety/depression (8).
COGNITIVE PATHOLOGY
Dr. Linda Rosenstock, in 1990 studied a group of Nicaraguan farm workers, who had been hospitalized for organophosphate poisoning due to pesticide exposure. Two years later deficits were found in “verbal and visual attention, visual memory, visuomotor speed, sequencing and problem solving, motor steadiness, and dexterity.” “The findings of a persistent decrease in neuropsycological performance among individuals with previous intoxication emphasizes the importance of prevention of even a single episode of OP poisoning”(39).
peripheral nervous
system and musculature
Three disorders of peripheral nervous system and musculature are the intermediate syndrome, organophosphate induced distal neuropathy (OPIDN), and acetylcholine myopathy (8). The intermediate syndrome (“paralytic condition”) appears 24-96 hours after the cholinergic crisis. Cranial nerve palsies can occur, weakness of proximal limb, neck flexors, and respiratory muscles (8). OPIDN (primarily motor neuropathy), mentioned earlier, involves the dying back of axons and myelinic sheaths of the long nerve fibers of the legs and sometimes the arms. This leads to weakness, flaccidity, spasticity, parasthesias of the lower extremities, and sometimes the arms (8). Acetylcholine myopathy refers to persistent muscle pain and weakness, as well as necrotizing tissue due to effects of excess acetylcholine at motor end plates, the junction of nerve to muscle fiber (3).
Chronic Repeat Adsorption Subacute Level
Chronic repeat adsorption to organophosphates, can cause “orange pickers flu,” with persistent non-specific complaints of anorexia, weakness and malaise -symptoms resembling influenza, heat exhaustion, alcohol toxicity or simple fatigue”(8 ). Tolerance to cholinergic overstimulation develops and contributes to supersensitivity to subsequent exposures, vulnerability to poisoning, and cellular mechanisms leading to cognitive dysfunction (22). Symptoms of the cholinergic crisis may become obscured.
EPA - Guidelines for
Neurotoxicity Risk Assessment
The EPA in April 1998 completed Guidelines for Neurotoxicity Risk Assessment. In a Hazard Characterization of a toxicant this document states: “case studies assist in identifying common risk factors, especially when the association between the exposure and the disease is strong, the mode of action of the agent biologically plausible, and the clusters occur in a limited period of time.” “...case reports of acute high level exposures to a toxicant can be useful for identifying signs and symptoms that may apply to lower exposures”(22).
Occupational
Exposures
These exposure events are not rare, and have become all too familiar(19). It is difficult/impossible to get appropriate medical care and support for these people without recognition of occupational exposure. Minimal compensation becomes long-term demands for repayment of funds. The National Institutes of Occupational Safety and Health (NIOSH), and the World Health Organization (WHO), recognize routine cholinesterase monitoring, as an important tool, to prevent poisoning in workers exposed to cholinesterase inhibiting pesticide compounds. Some Physicians who have measured acetylcholinesterase in cabin crew, and have found increases two or three weeks after the incident - possibly indicative of an exposure to a cholinesterase- inhibiting compound. Perhaps this tool could be useful in aviation.
Canadian Perspectives
The Canadian Flight Attendants reported symptoms, that as we look through them start to look familiar. Symptoms among others include : headache, nausea, vomiting, stomach pain, tiredness, weakness, sudden fatigue, exhaustion, sweating, blurred vision, odors, ear ringing, and coincidentally, oil/lubricant contamination found on investigation (36). Ear ringing is also a sign of neurotoxicity(22 ).
Worldwide Exposures
A paper entitled Trace Contaminants and Crew Health, was presented in 1998, at the Aerospace Medical Association (AsMA). Reported symptoms worldwide in cabin crew are of central nervous system(CNS) effects: headache , nausea, memory loss, visual impairment, tremors, respiratory impairment, and CNS impairment from months to years. Odors reported were consistent throughout the industry. Statistics included some aircraft are more prone to leaks than others by virtue of design; incident types and contamination route, which is aircraft specific: engine oil leaks, APU oil leaks, hydraulic ingestion & engine/APU oil leaks, hydraulics sucked by rear engine, location of air inlet. Maintenance/operations questions arise because some aircraft represent a high percentage of the fleet, and repeated incident occur on the same aircraft within a short period of time.(5)
Summary and
Recommendations
To review, the Material Safety Data Sheets and research literature document the potential neurotoxicity of oils, hydraulics, and lubricants, their ability to inhibit acetylcholinesterase, neuropathic target esterase, and induce organophosphate phosphate induced distal neuropathy-OPIDN(1, 33, 34, 43, 44, 46). Crew members appear to be exhibiting classic symptoms of chronic and acute exposures, and expected reversible, and irreversible neurotoxic outcomes from some poison(2, 5, 9, 13, 18, 19, 36, 42). The Aviation Safety Reporting System, managed by NASA, documents the continuing occurrence of system failures, cabin crewmember exposures, and evacuations(31). This is a safety and health issue. The criteria for an intact Aviation System must include quality standards to control operations that have the potential to become unsafe, or health hazards.
Epidemiological studies must be carried out to assess occupational exposure and outcome(7). Medical community must be provided with complete information of exposure so if indicated treatment given might prevent permanent impairment, and allow return to health (33,34,47). Cabin crew must be informed of their risk, so in the event of an exposure they might recognize symptoms, seek medical care, and somehow make choices to manage their risk (16, 32, 44). Federal/State legislation must be enacted to allow compensation for chemical disability/injury.
International systems are needed with appropriate follow-up to determine the magnitude of aviation illnesses, to verify the identity of the chemicals associated with illness, to determine the circumstances that lead to the exposure, to document the exposure and its effects, and to evaluate the causal relationship. New procedures for maintenance and operations are needed to avoid repetition of these events. Regulatory authority must be assigned to enable recordkeeping/data collection. This Standards committee must address the urgency of this problem and include current scientific knowledge, on all neurotoxic chemicals and health hazards (1, 10, 14, 33, 34, 43, 49) as part of the Standards. The committee must set Standards with adequate ventilation to prevent the potentially devastating consequences of exposure to the chemicals used in aviation.
1. ACGIH. Documentation of Threshold Limit Values. Tributyl Phosphate. Triorthocresyl Phosphate. Dibutyl Phenyl Phosphate. 1986.
2. Air Quality Injured Flight Attendants Fact Sheet, AFA, Oct. 1998.
3. Algrene J., Myopathy of Chonic Organophosphate Poisoning: A Clinical Entity? Southern Medical Journal. May 1997, Vol. 72, No. 5.
4. Appendix Equipment and Controls. Draft, ASHRAE. 6/26/97.
5. Balouet C., In Cabin Trace Contaminants and Crew Health. Aerospace Medical Association Paper. Seattle, Washington. 1998.
6. Bleecher Jan et al., Neurological Aspects of Organophosphate poisoning. Clinical Neurology and Neurosurgery, 94(1992) 93-103.
7. Blondell J., Epidemiology of Pesticide Poisonings in the United States, with Special Reference to Occupational Cases. Occupational Medicine State of the Art Reviews- Vol. 12, No. 2, April- June 1997. Philadelphia, Hanley & Belfus Inc.
8. Case Studies in Environmental Medicine- Cholinesterase-Inhibiting Pesticide Toxicity. US Department Health and Human Services. Agency for Toxic Substances and Disease Registry. September 1993.
9. CBS News, Dan Rather, June 16, 1998. Unlocking an Airborne Mystery. Transcript
10. Centers P.W., [Aero Propulsion and Power Directorate, Wright Laboratories, WL/POSL, Wright-Patterson Air Force Base, Ohio 45433-6563, USA]. Letter to the Editors: Potential neurotoxin formation in thermally degraded synthetic ester turbine lubricants. Arch Toxicology (1992) 66:679-680.
11. Conceptual Exposure Model for MD-80 Aircraft, AFA, Union Presentation 1998.
12. Cone J., and J. Jones, Final Report. Association of Professional Flight Attendants Health Survey, San Francisco General Hospital, Occupational Health Clinic, 1984.
13. Cone J., Cabin Air Quality Casualties, A Flight Attendant Health Survey. Presented at Third Annual International Aircraft Cabin Safety Symposium. Jan 27, 1985. Anaheim, Calif.
14. Crane C., et al, Inhalation Toxicology: III. Evaluation of Thermal Degradation Products from Aircraft and Automobile Engine Oils, Aircraft Hydraulic Fluid, and Mineral Oil. CAMI Oklahoma City, Oklahoma. April 1983.
15. Daughtrey W., et al, Subchronic Delayed Neurotoxicity Evaluation of Jet Engine Lubricants Containing Phosphorus Additives, Fundamentals and Applied Toxicology 32, 244-249(1996) Article No. 0127.
16. EPA Worker Protection Standard for Agricultural Pesticides: Unit 1 : Quick Reference Guide. NASD.
17. Fenske R. A., Pesticide Exposure Assessment of Workers and their Families. Occupational State of the Art Reviews - Vol. 12, No. 2, April- June 1997. Philadelphia, Hanley & Belfus, Inc.
18. “Five fall ill from hydraulic fumes”, Seattle Post-Intelligencer, Saturday, Feb 21, 1998.
19. Flight Log . Association of Flight Attendants. AFL-CIO Summer 1998. Vol. 36 No.4.
20. Fox R., Aircraft Cabin Air Supply Contaminants and their Mitigation. ASHRAE, Aviation Subcommittee, 1/19/98.
21. Greenburg MD, MPh, Hamilton MD, Phillips MD; Occupational , Industrial and Environmental Toxicology; Mosby 1997. 1st Edition , Chapter 4: Aviation Personnel; Chapter 13: Exterminators.
22. Guidelines for Neurotoxicity Risk Assessment. US EPA, April 30, 1998.NTIS-PB-No PB 98-117831
http:wwwepa.gov/ncea.
23. H.R. 2985 Aug 6, 1993.
24. H.R. 3626 June 12, 1996.
25. Halfpenny P., Aircraft Ventilation A Presentation at International Health Conference. Flight Attendant Occupational Health Issues. Nov 14, 1990.
26. Healy C.E., et al, Subchronic Rat Inhalation Study with Skydrol 500B-4 Fire Resistant Hydraulic Fluid Am. Ind. Hyg. Assoc. J. 53(3):175-180(1992).
27. Hunt E., D. Space, The Airplane Cabin Environment, Issues Pertaining to Flight Attendants.
28. Lamb J., et al, Tricresyl Phosphate : Animal Reproductive and Fertility Research. .Research Triangle Institute. Environmental Health Perspectives, Vol. 105, Supplement 1, Feb. 1997.
29. Mautz W, et al, Effects of Exercise Exposure on Toxic Interactions between Inhaled Oxidant and Aldehyde Air Pollutants. J of Toxicology and Environmental Health, 25:165-177,1988.
30. McConnell R., et al, Monitoring Organophosphate Insecticide-Exposed Workers for Cholinesterase Depression. JOM , Jan. 1992.
31. MD-80 Hydraulic or Oil System Incidents. Search Request No. 5290. May 6, 1998. Aviation Reporting System.
32. Miller M., M. Keifer, Cholinesterase Monitoring in Washington State: Report from the Technical Advisory Group; August, 1995 Washington State Department of Labor and Industries, Safety and Health Assessment and Research for Prevention (SHARP).
33. MSDS, Mobile Oil Co. Mobile Jet Oil 254 430306.
34. MSDS, Monsanto Skydrol 500B-4-Fire Resistant Hydraulic Fluid.
35. NIOSH Report No. HETA 90- 226.
36. Pelletier F., “The Perspective of Canadian Flight Attendants on Cabin Air Issues”. A Presentation to the ASHRAE Aviation Subcommittee of TC 9.3 (Transportation) June 23, 1998.
37. Raymond R., Smoke/ Fumes in the Cockpit. Technical Note. Aviation, Space and Environmental Medicine Aug. 1983.
38. Rosenstock L., et al, Chronic Central Nervous System Effects of Acute Organophosphate Pesticide Intoxication. The Lancet Vol. 338; July 27, 1991 223-227.
39. Savage E. P., et al, Chronic Neurological Sequelae of Acute Organophosphate Poisoning. Archives of Environmental Health, Jan/Feb 1988 [Vol.43(No. 1)].
40. Spengler J., Harvard University school of Public Health; Aircraft Cabin Environmental Survey -Executive Summary, May 17, 1994.
41. Summary Results of Cabin Air Quality Survey January 1994; Division Health and Safety Committee and CUPE Research Department. Jan 1995.
42. Sussell. Correspondence. NIOSH 6/14/91. Summary Hazard Evaluation.
43. Toxicological Profile for Hydraulic Fluids. Draft for Public Comment. Dec 12, 1994. US Department of Health and Human Services.
44. WAC 296-62-05405 Part C, Hazard Communication. P6 Health Hazard-definition.
45. Wagner S., [Guest Editor] Case Studies in Environmental Medicine. Cholinesterase-Inhibiting Pesticide Toxicity. Agency for Toxic Substances and Disease Registry . Sept 1993
46. Wagner S., Diagnosis and Treatment of Organophosphate and Carbamate Intoxication.in OCCUPATIONAL MEDICINE: State of the Art Reviews. Vol. 12. No. 2, April- June 1997; Philadelphia, Hanley & Belfus Inc. pp. 239-249.
47. Walkinshaw D., Gasper Air Volatile Organic Compounds in a B737: June 1998.
48. Wilson B., et al.[ Department of Environmental Toxicology, Employee Health Services, Department of Pesticide Regulation-U of Calif. Davis & California EPA] Monitoring the Pesticide-Exposed Worker in OCCUPATIONAL MEDICINE : State of the Art Reviews- Vol. 12. No. 2. April-June 1997. Philadelphia, Hanely & Belfus, Inc.pp.347-363.
49. Wyman J. Evaluation of Shipboard Formation of a Neurotoxicant (Trimethylopropane Phosphate) from Thermal Decomposition of Synthetic Aircraft Engine Lubricant. Am. Ind. Hyg. Assoc. J. (54)/ Oct 1993.