Absence of corneal endothelium injury in non-human primates treated with and without ophthalmologic drugs and exposed to 2.8 GHz pulsed microwaves.

Microwave-induced corneal endothelial damage was reported to have a low threshold (2.6 W/kg), and vasoactive ophthalmologic medications lowered the threshold by a factor of 10-0.26 W/kg. In an attempt to confirm these observations, four adult male Rhesus monkeys (Macaca mulatta) under propofol anesthesia were exposed to pulsed microwaves in the far field of a 2.8 GHz signal (1.43 +/- 0.06 micros pulse width, 34 Hz pulse repetition frequency, 13.0 mW/cm(2) spatial and temporal average, and 464 W/cm(2) spatial and temporal peak (291 W/cm(2) square wave equivalent) power densities). Corneal-specific absorption rate was 5.07 W/kg (0.39 W/kg/mW/cm(2)). The exposure resulted in a 1.0-1.2 degrees C increase in eyelid temperature. In Experiment I, exposures were 4 h/day, 3 days/week for 3 weeks (nine exposures and 36 h total). In Experiment II, these subjects were pretreated with 0.5% Timolol maleate and 0.005% Xalatan(R) followed by 3 or 7 4-h pulsed microwave exposures. Under ketamine-xylazine anesthesia, a non-contact specular microscope was used to obtain corneal endothelium images, corneal endothelial cell density, and pachymetry at the center and four peripheral areas of the cornea. Ophthalmologic measurements were done before and 7, 30, 90, and 180 days after exposures. Pulsed microwave exposure did not cause alterations in corneal endothelial cell density and corneal thickness with or without ophthalmologic drugs. Therefore, previously reported changes in the cornea exposed to pulsed microwaves were not confirmed at exposure levels that are more than an order of magnitude higher.

Thermal modeling of millimeter wave damage to the primate cornea at 35 GHz and 94 GHz.

Recent data on damage to the primate cornea from exposure to millimeter wave radiation are interpreted in terms of a simple thermal model. The measured temperature increases during the exposures (duration 1-5 s, 35 or 94 GHz, 2-7 W cm(-2)) agree with the model within the variability of the data. The thresholds for damage to the cornea (staining of the corneal epithelium by fluorescein and corneal edema) correspond to temperature increases of about 20 degrees C at both irradiation frequencies. Within the limits of the one-dimensional model, thresholds for thermal damage to the cornea can be predicted for a range of exposure conditions.

Millimeter wave absorption in the nonhuman primate eye at 35 GHz and 94 GHz.

The purpose of this study was to evaluate anterior segment bioeffects of pulsed 35 GHz and 94 GHz microwave exposure in the nonhuman primate eye. Five juvenile rhesus monkeys (Macaca mulatta) underwent baseline anterior segment ocular assessment consisting of slit lamp examination, corneal topography, specular microscopy, and pachymetry. These studies were repeated after exposure of one eye to pulsed 35 GHz or 94 GHz microwaves at varied fluences, with the other eye serving as a control. The mean fluence required to produce a threshold corneal lesion (faint epithelial edema and fluorescein staining) was 7.5 J cm(-2) at 35 GHz and 5 J cm(-2) at 94 GHz. Transient changes in corneal topography and pachymetry were noted at these fluences. Endothelial cell counts remained unchanged. Threshold corneal injury from 35 GHz and 94 GHz microwave exposure is produced at fluences below those previously reported for CO2 laser radiation. These data may help elucidate the mechanism of thermal injury to the cornea, and resolve discrepancies between IEEE C95.1 (1999), NCRP (1986), and ICNIRP (1998) safety standards for exposure to non-ionizing radiation at millimeter wavelengths.