Biomedical subjects

M E Knafelc

Publications and source records attributed to M E Knafelc.

5 recordsLinked to original sources

PubMed2000

Hearing function in a hyperbaric environment.

Navy divers' hearing function was assessed as part of three saturation deep dives to 1,000 feet of sea water (fsw) to determine explanations for threshold shifts observed under hyperbaric conditions. Across the three deep dives, different aspects of the ear were evaluated, including air- and bone-conduction pure-tone thresholds, real ear probe microphone measurements, auditory evoked potentials, and central auditory processing assessments. Attempts to measure middle ear function and cochlear function (through otoacoustic emissions) were unsuccessful. Baseline measurements were obtained at 0 fsw in air before and after the saturation deep dives. Results showed that some aspects of hearing function remained unchanged with increases in depth. In general, audiometric thresholds at depth were similar to those measured on the surface at 500, 1,000, 2,000, 3,000, and 4,000 Hz. However, hearing sensitivity actually improved at depth at 6,000 and 8,000 Hz. The use of a specially designed sound booth for a pressurized heliox environment yielded significantly lower ambient noise levels and improved the accuracy of threshold measurement. Auditory evoked potential measurements and central auditory processing function were relatively unaffected by changes in depth. Significant changes at depth were seen in ear canal resonance which shifted up in frequency; this finding was attributed to the effect of helium on the hearing mechanism. Because objective measurement of middle ear and inner ear function were not methodologically possible, questions still remain regarding the interpretation of middle and inner ear function at depth. Nonetheless, our overall findings suggest that most aspects of hearing functioning are similar under high atmospheric pressures and in heliox as they are on the surface, with the exception of shifts in ear canal resonance and improvements in audiometric thresholds at high frequencies.

Acoustic Impedance Tests↗

PubMed1999

Noise-induced neurologic disturbances in divers exposed to intense water-borne sound: two case reports.

Divers may be exposed to intense noise underwater. Two cases of neurologic disturbances during experimental exposures to 15 min of continuous underwater sound are described. Sound exposure in the first case consisted of a warble tone with center frequency of 240 Hz and a sound pressure level of 160 dB re 1 microPa. Symptoms during exposure consisted of somnolence, lightheadedness, and an inability to concentrate. No apparent effect on hearing was noted. In the second case, a center frequency of 1,000 Hz at 181 dB was used. Lightheadedness, inability to concentrate, agitation, and head vibrations were noted during the exposure. The diver also exhibited a temporary auditory threshold shift of 19.2 dB. In both cases, overt symptoms resolved within 30 min after exposure, but both divers reported recurrent symptoms days to weeks after the exposures. Medical histories and examinations, assessment of dive profiles, and breathing gas analysis failed to support a source other than the sound exposures to account for the symptoms observed. Potential mechanisms for the described symptoms are discussed.

Adult↗

PubMed1987

Evaluation of noise within the MK 12 SSDS helmet and its effect on divers' hearing.

The noise inside the U.S. Navy MK 12 SSDS helmet was measured and its effect on the hearing of divers assessed. Seven male divers completed 20 dives while breathing air at simulated depths ranging from 1.8 to 30.5 msw with dive durations ranging from 40 to 120 min. Microphones recorded sound pressure levels inside the helmet while the diver was in the water and exercising. Average corrected sound intensity levels in the helmet ranged from 90.5 dB(A) at 1.8 msw to 97.3 dB(A) at 30.5 msw. Diver hearing threshold level shifts were recorded as a function of helmet noise exposure; moderate threshold shifts were observed at depths of 9.1 msw or deeper after 120-min dives. The hearing of all divers completing dives up to 120 min returned to predive levels within 24 h after noise exposure. However, dive durations in excess of 120 min at 9.1 and 20.1 msw resulted in substantial auditory shifts in 1 diver, which required 2-3 d to recover to predive levels. These results suggest that the impact of helmet noise on diver hearing should be included in planning operations using the MK 12 SSDS.

Adult↗

PubMed1986

Screening for oxygen intolerance in U.S. Navy divers.

All U.S. Navy diving candidates are screened for their tolerance to hyperbaric oxygen by taking an oxygen tolerance test (OTT). During a recent experimental oxygen dive series at the U.S. Navy Experimental Diving Unit, three divers were noted to be reproducibly oxygen sensitive. These three divers were then given additional OTTs to see if any evidence of central nervous system oxygen toxicity would be detected by these multiple tests. The additional OTTs did not produce any signs or symptoms of oxygen toxicity in these already proven susceptible divers. A subsequent review of the records of the Naval Safety Center yielded a total of 1347 OTTs from 1 January 1972 to 31 December 1981. A review of diving accidents reported during this period revealed that 26 episodes of oxygen toxicity were noted during OTTs for a derived failure rate of 1.9%. Analysis of oxygen toxicity episodes encountered during operational Navy diving for this period found that 9 episodes of nonconvulsive oxygen toxicity were seen in mixed gas diving and 3 episodes of nonconvulsive oxygen toxicity were noted in closed circuit oxygen diving. Conclusions from this paper are: Screening for oxygen intolerance is complicated by intraindividual variation in oxygen tolerance; U.S. Navy diving using 100% oxygen during the period studied has had an acceptable safety record according to the data on record at the Naval Safety Center; the OTT as currently administered by the U.S. Navy does not identify all individuals who are relatively susceptible to oxygen toxicity; those individuals who do fail the OTT are unusually susceptible to oxygen toxicity; and because of the need to continue to identify these unusually susceptible individuals, the OTT should continue to be administered to U.S. Navy diver candidates.

Adult↗

PubMed1980

Dissociation of intracellular lysosomal rupture from the cell death caused by silica.

The relationship between intracellular lysosomal rupture and cell death caused by silica was studied in P388d(1) macrophages. After 3 h of exposure to 150 mug silica in medium containing 1.8 mM Ca(2+), 60 percent of the cells were unable to exclude trypan blue. In the absence of extracellular Ca(2+), however, all of the cells remained viable. Phagocytosis of silica particles occurred to the same extent in the presence or absence of Ca(2+). The percentage of P388D(1) cells killed by silica depended on the dose and the concentration of Ca(2+) in the medium. Intracellular lyosomal rupture after exposure to silica was measured by acridine orange fluorescence or histochemical assay of horseradish peroxidase. With either assay, 60 percent of the cells exposed to 150 mug silica for 3 h in the presence of Ca(2+) showed intracellular lysosomal rupture, was not associated with measureable degradation of total DNA, RNA, protein, or phospholipids or accelerated turnover of exogenous horseradish peroxidase. Pretreatment with promethazine (20 mug/ml) protected 80 percent of P388D(1) macrophages against silica toxicity although lysosomal rupture occurred in 60-70 percent of the cells. Intracellular lysosomal rupture was prevented in 80 percent of the cells by pretreatment with indomethacin (5 x 10(-5)M), yet 40-50 percent of the cells died after 3 h of exposure to 150 mug silica in 1.8 mM extracellular Ca(2+). The calcium ionophore A23187 also caused intracellular lysosomal rupture in 90-98 percent of the cells treated for 1 h in either the presence or absence of extracellular Ca(2+). With the addition of 1.8 mM Ca(2+), 80 percent of the cells was killed after 3 h, whereas all of the cells remained viable in the absence of Ca(2+). These experiments suggest that intracellular lysosomal rupture is not causally related to the cell death cause by silica or A23187. Cell death is dependent on extracellular Ca(2+) and may be mediated by an influx of these ions across the plasma membrane permeability barrier damaged directly by exposure to these toxins.

Animals↗