This work was accomplished under the approved task AM-B-98-TOX-202. AbstractThe use of drugs and alcohol in aviation is closely monitored by the FAA Office of Aviation Medicine's (OAM's) Civil Aeromedical Institute (CAMI) through the toxicological analysis of specimens from pilots who have died in aviation accidents. This information on the use of drugs in aviation is helpful to the FAA in developing programs to reduce the usage of dangerous drugs and identify potentially incapacitating medical conditions that may cause an accident. Data collected from this research can be used to evaluate the effectiveness of the FAA drug testing program. The toxicology reports prepared by the CAMI Forensic Toxicology Research Section are used by the FAA and the National Transportation Safety Board to determine the cause of aviation accidents. Specimens (blood, urine, liver, kidney, vitreous fluid, and other bodily specimens) were collected by pathologists near the accident and placed in evidence containers provided by CAMI. These samples were refrigerated and shipped by overnight air. Upon receipt, the specimens were inventoried and accessioned for the analysis of drugs, alcohol, carbon monoxide, and cyanide. All data collected by the laboratory were entered into a computer database for future analysis. The database was searched using a Microsoft Access TM program developed by a local contractor. The database was sorted based on the class of drug, controlled dangerous substance schedules I and II, controlled dangerous substance schedules III-V, prescription drugs, over-the-counter drugs, and alcohol. The Toxicology and Accident Research Laboratory received specimens from 1683 pilots for postmortem toxicology analysis between 1994 to 1998. Controlled dangerous substances, CDS, (schedules I and II) were found in 89 of the pilots analyzed. Controlled dangerous substances (schedules III -V) were found in 49 of the pilots tested. Prescription drugs were found in 240 of the pilots analyzed. Over-the-counter drugs were found in 301 of the pilots analyzed. Alcohol at or above the legal limit of 0.04% was found in 124 pilots. The number of positive drug cases has doubled over the past 5 years. Over-the-counter medications are the most frequendy found drugs in fatal aviation accidents and many of these drugs, or the medical conditions for which they are being used, could impair a pilot's ability to safely fly an aircraft. The increased number of positive cases found in this research is most likely the result of improved methods of analysis, rather than an increase in the use of drugs. The low incidence of CDS III-V drugs found in fatal aviation accidents may be a result of the difficulty in finding and identifying the new benzodiazepines commonly prescribed in this class.

Carbon monoxide (CO) and hydrogen cyanide (HCN) are generated during aircraft interior fires in sufficient amounts to incapacitate cabin occupants. For typical post-crash and in-flight fires, minimum protection periods of 5 and 35 min, respectively, have been suggested for breathing devices to protect the occupants from smoke. Relationships of blood carboxyhemoglobin (COHb) and cyanide (CN-) levels to incapacitation have not been well defined for these gases. Therefore, time to incapacitation (ti) and blood COHb and CN- at incapacitation were examined in rats exposed to CO (5706 ppm for 5-min ti; 1902 ppm for 35-min ti), HCN (184 ppm for 5-min ti; 64 ppm for 35-min ti) and their mixtures (equipotent concentrations of each gas that produced 5- and 35-min ti). Blood CO and HCN uptakes were evaluated at the two concentrations of each gas. With either gas, variation in ti was higher for the 35-min ti than the 5-min ti The COHb level reached a plateau prior to incapacitation at both CO concentrations, and COHb levels at the 5- and 35-min ti were different from each other. Blood CN- increased as a function of both HCN concentration and exposure time, but CN- at the 5-min ti was half of the 35-min ti CN- level. The HCN uptake at the high concentration was about three times that at the low concentration. In the high concentration CO-HCN mixture, ti was shortened from 5 to 2.6 min; COHb dropped from 81 to 55% and blood CN- from 2.3 to 1.1 microgram ml(-1). At the low-concentration CO-HCN mixture, where ti was reduced from 35 to 11.1 min, COHb decreased from 71 to 61% and blood CN- from 4.2 to 1.1 microgram ml(-1). Any alteration in the uptake of either gas by the presence of the other was minimal. Our findings suggest that specific levels of blood COHb and CN- cannot be correlated directly with the incapacitation onset and that postmortem blood COHb and CN- levels should be evaluated carefully in fire victims.

The measurement of combustion gases produced by burning aircraft cabin materials poses a continuing limitation for smoke toxicity research. Because toxic effects of gases depend on both their concentrations and the duration of exposure, frequent atmosphere sampling is necessary to define the gas concentration-exposure time curve. A gas chromatographic (GC) method was developed for the simultaneous analyses of carbon monoxide (CO), hydrogen sulfide (H2S), sulfur dioxide (SO2), and hydrogen cyanide (HCN). The method used an MTI M200 dual-column gas chromatograph equipped with 4-m molecular sieve-5A and 8-m PoraPlot-U wall-coated capillary columns and two low-volume, high-sensitivity thermal conductivity detectors. Detectability (in parts per million [ppm]) and retention times (in seconds) for the gases were as follows: CO, 100 ppm, 28 s; H2S, 50 ppm, 26 s; SO2, 125 ppm, 76 s; and HCN, 60 ppm, 108 s. The method was effective for determining these gases in mixtures and in the combustion atmospheres generated by burning wool (CO, HCN, and H2S) and modacrylic fabrics (CO and HCN). Common atmospheric gaseous or combustion products (oxygen, carbon dioxide, nitrogen, water vapor, and other volatiles) did not interfere with the analyses. However, filtration of the combustion atmospheres was necessary to prevent restriction of the GC sampling inlet by smoke particulates. The speed, sensitivity, and selectivity of this method make it suitable for smoke toxicity research and for evaluating performance of passenger protective breathing equipment. Also, this method can potentially be modified to analyze these gases when they are liberated from biosamples.

335cated that the increase in alpha amino nitrogen was due to a generalized failure of the reabsorptive mechanisms rather than inhi bition of a specific transport system for groups of amino acids as described by Beyer( lo).The finding af variable potassium excretion appears to differ from the report by Robin, et aZ.( 11) that hypokalemia occurs during salicylate poisoning. However, this hypokalemia was thought to be a manifestation af the respiratory alkalosis caused by salicylate rather than a specific function of salicylate.Summary. 1. Both small and large amounts of acetylsalicylic acid have a marked inhibitory effect on renal excretion of sodium and chloride. 2. Uricosuric amounts of acetylsalicylic acid block the renal reabsorptive mechanisms for amino acids. 3. The findings of Yu and Gutman concerning the paradoxical effects of salicylate on uric acid excretion are confirmed.

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