ERA14FA417

The pilot’s failure to ensure the airplane maintained adequate airspeed during the initial climb and the subsequent exceedance of its critical angle of attack, which resulted in an aerodynamic stall. Contributing to the accident were the pilot’s impairment due to a sedating antihistamine, which led to his decision to possibly allow the passenger to attempt the takeoff, and his delayed remedial action to lower the nose when the airplane began to pitch up too much.

Witnesses reported observing the commercial pilot and passenger departing from the turf runway. After a normal takeoff, the airplane's angle of attack (AOA) began to increase, and it continued to increase until the airplane's critical AOA was exceeded. The airplane then experienced an aerodynamic stall and entered an uncontrolled descent. Postaccident examination of the airplane, including the flight controls and stall warning system, and the engine revealed no evidence of any preaccident mechanical failures or malfunctions that would have precluded normal operation. The pilot had reported that he had hypertension, gastro-esophageal reflux disease (GERD), and high cholesterol and that he was using lisinopril, pantoprazole, and simvastatin to treat those conditions to the Federal Aviation Administration. However, given that high blood pressure and high cholesterol cause no direct symptoms and that no evidence of a stroke, heart attack, or significant natural disease were identified on autopsy, it is unlikely that either of these conditions or the medications the pilot was taking to treat them contributed to the accident. Further, although GERD can cause heartburn, it is unlikely to have been acute or severe enough to have contributed to the accident. Postaccident toxicology testing of the pilot's specimens identified significant levels of diphenhydramine, which is a sedating antihistamine, in the femoral and cavity blood, indicating that it is likely that the pilot's diphenhydramine level was near the middle of the therapeutic window at the time of the accident. Even at therapeutic levels, diphenhydramine is quite impairing. In fact, in a driving simulator study, a single dose of diphenhydramine impaired driving ability more than a blood alcohol concentration of 0.100%. Thus, it is very likely that the pilot was impaired by diphenhydramine at the time of the accident. Toxicology testing of the passenger's specimens detected a level of zolpidem, which is a short-acting sedative hypnotic used as a sleep aid, in the heart blood that was at the lower end of the therapeutic window and would likely have been significantly lower at the time of the accident. Although it could not be determined with certainty, it is not likely that the passenger was significantly impaired by zolpidem at the time of the accident. The pilot was seated in the left seat; one witness reported seeing his left hand on the glareshield as the AOA began to increase whereas another witness reported seeing his hand reach for the glareshield as the AOA began to increase. Based on the pilot's reported hand position at takeoff, it is possible that he had decided to let the unrated passenger attempt the takeoff; however, this could not be definitively determined. In either case (with the passenger or the pilot flying), the pilot failed to ensure that the airplane maintained adequate airspeed, which led to the airplane exceeding its critical angle of attack. It is likely that the pilot's impairment by diphenhydramine contributed to the accident and led to his poor decision-making or affected his ability to respond to the stall quickly.

Hampton Airfield was privately-owned, and was located 2 miles north of Hampton, New Hampshire. It was classified by the FAA as a non-towered public use airport. The airport elevation was 93 feet above mean sea level and there was one runway oriented in a 02/20 configuration. Runway 02 was turf, and in good condition. The total length was 2,100 foot long by 170 foot wide. Pitot Static System The airspeed indicator, was operated by the pitot static system. This system consisted of a pitot tube, mounted under the leading edge of the left wing and two pressure ports (static ports) mounted on opposite sides of the fuselage just aft of the firewall. Examination of the pitot tube and static pressure ports during the wreckage examination revealed that they were clear of obstructions. Stall Warning System According to the Cessna 180 Owner's Manual, the aerodynamic stall characteristics were conventional for flaps up and flaps down conditions and slight buffeting could occur just before the stall with flaps down. The airplane when at aft center of gravity and full gross weight at sea level would stall with the wing flaps set at 20-degrees at a true indicated airspeed (TIAS) of: 55 mph at 0-degrees angle of bank 59 mph at 30-degrees angle of bank 78 mph at 60-degrees angle of bank To help avoid aerodynamic stalls, the airplane was equipped with a stall warning system. The stall warning system was comprised of a stall warning indicator (stall warning horn) which was mounted on the back of the glove compartment box, next to the firewall, and an actuating switch (stall vane) which was mounted on the leading edge of the left wing and was actuated by airflow over the surface of the wing. The switch would close as approximately 5 to 10 mph above the airplane stall speed. According to the Cessna 180 Owner's Manual, the stall warning indicator would provide protection from inadvertent stalls. It would give a warning whenever an aerodynamic stall was approached, regardless of speed, attitude, altitude, acceleration, or other factors, which could change the stalling speed. Examination of the stall warning system did not reveal any anomalies, and testing of the actuating switch with a multimeter, indicated that it was functional. Use of Wing Flaps According to the Cessna 180 Owner's Manual, the wing flap control handle was operated by depressing the thumb button and moving the handle to the desired flap setting. By releasing the thumb button, the handle could be locked to provide 0, 20, 30, and 40-degree flap positions. The flaps could be lowered or raised during normal flying whenever the airspeed was less than 100 mph. The wing flaps could supply considerable lift and drag. For takeoff, the flaps could be selected to the 0-degree (flaps up), or 20-degree (first notch), positions. During the wreckage examination, the wing flap handle was found to be in the 20-degree (first notch) position, which according to the Cessna 180 Owner's Manual, would shorten the takeoff distance to clear a 50 foot obstacle as a result of slower forward speeds, even though the use of wing flaps would lessen the rate of climb. The use of 30 or 40 degrees of wing flaps was not recommended at any time for takeoff. The manual also stated to "REMEMBER" that you "Don't under marginal conditions, leave wing flaps on long enough that you are losing both climb and airspeed. Don't raise wing flaps with airspeed below "Flaps Up stalling speed" and "Do slowly release the wing flaps as soon as you reasonably can after take-off, preferably 50 feet or more over terrain or obstacles." Pilot An autopsy was performed on the pilot by the State of New Hampshire, Office of the Chief Medical Examiner. The reported cause of death was blunt impact injuries. Toxicological testing of the pilot was conducted at the FAA Bioaeronautical Sciences Research Laboratory, Oklahoma City, Oklahoma. The specimens from the pilot were negative for ethanol, and basic, acidic, and neutral drugs, with the exception of Diphenhydramine, which was detected in urine and blood, and Ibuprofen, which was detected in urine. Testing for Carbon Monoxide and Cyanide were not performed. On April 11, 2013, during his last aviation medical examination, the 77-year old male pilot reported a new diagnosis of hypertension as well as long standing gastro-esophageal reflux disease (GERD) and high cholesterol. He reported using the medications Lisinopril, Pantoprazole, and Simvastatin. He was issued a third class medical certificate limited by a requirement to wear corrective lenses for distance vision and possess glasses for near vision. At the time, he was 66 inches tall, and weighed 152 pounds. Lisinopril is a prescription blood pressure medication commonly sold with the name Vasotec. Pantoprazole is a proton pump inhibitor used to treat GERD and other sources of heartburn. It is available over the counter with the name Prilosec. Simvastatin is a prescription cholesterol lowering agent commonly sold with the name Lipitor. According to the autopsy report, the examination identified atherosclerotic disease in the aorta and some calcification of the coronary arteries without coronary artery stenosis. The remainder of the examination was unremarkable. Toxicology testing performed by the NMS Labs at the request of the Chief Medical Examiner identified 0.077 ug/ml of Diphenhydramine in femoral blood and caffeine in chest blood. Toxicology testing performed by the FAA's Bioaeronautical Research Laboratory identified Diphenhydramine and Ibuprofen in urine; 0.432 ug/ml of Diphenhydramine was quantified in cavity blood. Ibuprofen is a non-steroidal anti-inflammatory medication used as an analgesic and fever reliever; it is available over the counter marketed as Motrin and Advil. Diphenhydramine is a sedating antihistamine used to treat cold and allergy symptoms and as a sleep aid. It is available over the counter under the trade names Benadryl and Unisom. Diphenhydramine's therapeutic window is between 0.0250 ug/ml and 0.1120 ug/ml. It carries the following FDA warning: may impair mental and/or physical ability required for the performance of potentially hazardous tasks (e.g., driving, operating heavy machinery). Compared to other antihistamines, diphenhydramine causes marked sedation; it is also classed as a Central Nervous System (CNS) depressant and this is the rationale for its use as a sleep aid. Altered mood and impaired cognitive and psychomotor performance may also be observed. In fact, in a driving simulator study, a single dose of Diphenhydramine impaired driving ability more than a blood alcohol concentration of 0.100%. Diphenhydramine undergoes postmortem redistribution; after death it can move back into pooled blood from storage sites. For diphenhydramine, postmortem central or cavity blood levels may increase by three times or more. Passenger An autopsy was performed on the passenger by the State of New Hampshire, Office of the Chief Medical Examiner. The reported cause of death was blunt impact injuries. Toxicological testing of the passenger was conducted at the FAA Bioaeronautical Sciences Research Laboratory, Oklahoma City, Oklahoma. The specimens from the pilot were negative for ethanol, and basic, acidic, and neutral drugs, with the exception of Zolpidem, which was detected in liver and blood, and Ibuprofen, which was detected in blood. Testing for Carbon Monoxide and Cyanide were not performed. Toxicology testing performed by the FAA's Bioaeronautical Research Laboratory identified Ibuprofen and 0.0250 ug/ml of Zolpidem in heart blood as well as of 0.068 ug/ml of Zolpidem in liver. Zolpidem is a short acting sedative hypnotic used as a sleep aid and available by prescription; it is commonly called Ambien. Zolpidem's therapeutic window is between 0.0250 and 0.300 ug/ml and it carries the following warning: may impair mental and/or physical ability required for th