Exposure to vibration has detrimental effects on sensory nerve function and physiology. However, many of these changes are more prominent at 250-Hz exposure than at lower frequencies.

Objective-Occupational exposure to hand-transmitted vibration can result in damage to nerves and sensory loss. The goal of this study was to assess the frequency-dependent effects of repeated bouts of vibration on sensory nerve function and associated changes in nerves.Methods-The tails of rats were exposed to vibration at 62.5, 125, or 250 Hz (constant acceleration of 49m/s 2 ) for 10 days. The effects on sensory nerve function, nerve morphology, and transcript expression in ventral tail nerves were measured.Results-Vibration at all frequencies had effects on nerve function and physiology. However, the effects tended to be more prominent with exposure at 250 Hz.Conclusion-Exposure to vibration has detrimental effects on sensory nerve function and physiology. However, many of these changes are more prominent at 250-Hz exposure than at lower frequencies.Hand-arm vibration syndrome (HAVS) is caused by repeated exposure to vibration through the use of powered and pneumatic hand tools. 1 The hallmark symptom of HAVS is coldinduced vasospasms that result in finger blanching. However, sensorineural deficits in the fingers and hands are also prevalent in workers with HAVS. 2 These deficits include reductions in tactile and heat sensitivity and a loss of manual dexterity. In addition, workers with HAVS also develop hand and finger pain, particularly when exposed to cold. 3 Biopsy samples collected from the fingers of workers diagnosed with HAVS have demonstrated that these changes in sensorineural function are associated with a loss of peripheral nerves, nerve fibrosis, and demyelination. 4,5 Even though the morphologic and functional changes associated with sensory loss in workers with HAVS have been characterized, the mechanisms by which vibration causes these changes are still not well understood.One factor that is believed to affect the risk of injury is the vibration frequency or frequencies to which a worker is exposed. Currently, the International Standards Address correspondence to: Kristine Krajnak, PhD, NIOSH, 1095. None of the authors have any conflicts of interest with regards to this research. HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptOrganization (ISO) standard ISO 5349-1 6 presents a weighting curve that predicts the risk of developing a vibration-induced injury. One of the factors used to calculate the weighting factor is the dominant frequency to which a worker is exposed. This weighting curve assigns significantly greater weighting to low-frequency vibration (ie, ≤16 Hz), and the weighting dramatically decreases with exposures greater than 100 Hz. However, experimental and epidemiologic studies suggest that vibration-induced injuries to the fingers and hands may actually be more prevalent in workers using tools that emit a higher-frequency vibration. [7][8][9] It has been hypothesized that the increased risk of injury associated with exposure to higher frequencies may be because stress and strain to the soft tissues of the fingers and hands is grea...

Exposure to wet aerosols generated during use of spray products containing silver (Ag) has not been evaluated. The goal was to assess the potential for cardiopulmonary toxicity following an acute inhalation of wet silver colloid. Rats were exposed by inhalation to a low concentration (100 μg/m(3) ) using an undiluted commercial antimicrobial product (20 mg/L total silver; approximately 33 nm mean aerodynamic diameter [MAD]) or to a higher concentration (1000 μg/m(3)) using a suspension (200 mg/L total silver; approximately 39 nm MAD) synthesized to possess a similar size distribution of Ag nanoparticles for 5 h. Estimated lung burdens from deposition models were 0, 1.4, or 14 μg Ag/rat after exposure to control aerosol, low, and high doses, respectively. At 1 and 7 d postexposure, the following parameters were monitored: pulmonary inflammation, lung cell toxicity, alveolar air/blood barrier damage, alveolar macrophage activity, blood cell differentials, responsiveness of tail artery to vasoconstrictor or vasodilatory agents, and heart rate and blood pressure in response to isoproterenol or norepinephrine, respectively. Changes in pulmonary or cardiovascular parameters were absent or nonsignificant at 1 or 7 d postexposure with the exceptions of increased blood monocytes 1 d after high-dose Ag exposure and decreased dilation of tail artery after stimulation, as well as elevated heart rate in response to isoproterenol 1 d after low-dose Ag exposure, possibly due to bioavailable ionic Ag in the commercial product. In summary, short-term inhalation of nano-Ag did not produce apparent marked acute toxicity in this animal model.

Our laboratory has previously demonstrated that application of an antimicrobial spray product containing titanium dioxide (TiO 2 ) generates an aerosol of titanium dioxide in the breathing zone of the applicator. The present report describes the design of an automated spray system and the characterization of the aerosol delivered to a whole body inhalation chamber. This system produced stable airborne levels of TiO 2 particles with a median count size diameter of 110 nm. Rats were exposed to 314 mg/m 3 min (low dose), 826 mg/m 3 min (medium dose), and 3638 mg/m 3 min (high dose) of TiO 2 under the following conditions: 2.62 mg/m 3 for 2 h, 1.72 mg/m 3 4 h/day for 2 days, and 3.79 mg/m 3 4 h/day for 4 days, respectively. Pulmonary (breathing rate, specific airway resistance, inflammation, and lung damage) and cardiovascular (the responsiveness of the tail artery to constrictor or dilatory agents) endpoints were monitored 24 h post-exposure. No significant pulmonary or cardiovascular changes were noted at low and middle dose levels. However, the high dose caused significant increases in breathing rate, pulmonary inflammation, and lung cell injury. Results suggest that occasional consumer use of this antimicrobial spray product should not be a hazard. However, extended exposure of workers routinely applying this product to surfaces should be avoided. During application, care should be taken to minimize exposure by working under well ventilated conditions and by employing respiratory protection as needed. It would be prudent to avoid exposure to children or those with pre-existing respiratory disease.

Repeated exposure to hand-transmitted vibration through the use of powered hand tools may result in pain and progressive reductions in tactile sensitivity. The goal of the present study was to use an established animal model of vibration-induced injury to characterize changes in sensory nerve function and cellular mechanisms associated with these alterations. Sensory nerve function was assessed weekly using the current perception threshold test and tail-flick analgesia test in male Sprague-Dawley rats exposed to 28 d of tail vibration. After 28 d of exposure, Aβ fiber sensitivity was reduced. This reduction in sensitivity was partly attributed to structural disruption of myelin. In addition, the decrease in sensitivity was also associated with a reduction in myelin basic protein and 2',3'- cyclic nucleotide phosphodiasterase (CNPase) staining in tail nerves, and an increase in circulating calcitonin gene-related peptide (CGRP) concentrations. Changes in Aβ fiber sensitivity and CGRP concentrations may serve as early markers of vibration-induced injury in peripheral nerves. It is conceivable that these markers may be utilized to monitor sensorineural alterations in workers exposed to vibration to potentially prevent additional injury.