NORA Symposium 2006: Research Makes a Difference! April 18-26, 2006, Washington, DC. Washington, DC: National Institute for Occupational Safety and Health, 2006 Apr; :280-281
According to the Bureau of Labor Statistics, over 1 million U.S. workers in the manufacturing sector use vibrating hand tools, such as grinders, polishers, and power cutters; and NIOSH estimated that 50% of workers exposed to vibration will develop symptoms such as cold-induced vasospasms, loss of tactile sensory function, or loss of strength in fingers and hand, collectively known as vibration white finger (VWF) or hand-arm vibration syndrome (HAVS). Hand-transmitted vibration is also a major factor associated with carpal tunnel syndrome (CTS). Despite numerous studies of the pathological symptoms associated with prolonged vibration exposure, there is little understanding of the underlying physiological mechanisms that lead to injury. The purpose of this study was to examine gene expression in muscles exposed to prolonged vibration exposure and determine if changes are associated with vascular constriction and subsequent depletion of oxygen (hypoxia) in peripheral soft tissues. Manual dexterity was also assessed intermittently to determine if repeated disruption in blood flow and oxygen availability was accompanied by deficits in muscle function. A physiologically representative animal model was developed to experimentally investigate vibration-induced biological and functional changes. In this model, the right forelimb and paw of intact rats were exposed to a platform vibrated at a frequency of 250 Hz and amplitude of 49 ms-1, similar to the vibration caused by hand-held grinders and sanders commonly used in the manufacturing and construction sectors. Three groups of 8 rats each were studied: a vibration-exposed group, an exposure-control group, and a home-cage control group. Exposures were conducted 4 hr/day, 5 days/week for 5 weeks. After the exposure, gene-transcript levels for factors associated with vasoconstriction and hypoxia were determined from dissected flexor muscles of the rat forelimb. Manual dexterity was assessed intermittently during the exposure period with the Montoya stair-case test, which assessed the rat's ability to grasp and retrieve small food pellets. Compared with control the control groups, results for the vibration-exposed group showed significant 50% and 29% increases in the expression of a2c and a1a/d receptor transcripts, respectively, which are known to increase vascular sensitivity to norepinephrine-induced vasoconstriction. There also was a significant 63% increase in the level of hypoxia-induced factor-1 (HIF-1), a transcription factor associated with reductions in oxygen availability. The staircase test showed an average 57% improvement in manual dexterity for the control groups, but only a 9% change for the vibration-exposed group. Results are consistent with the notions that vibration causes increased vasoconstriction in the microvasculature, and subsequent tissue damage or loss of function may be associated with hypoxia. Follow-up investigations of these mechanisms can lead to the discovery of biomarkers for early detection and advancements in diagnostic methods or treatment options. In addition to advancing our understanding of the underlying physiological mechanisms of HAVS, the experimental findings generated by the use of the present model can support the development of exposure guidelines by determining the biological plausibility of various associations between exposure risk factors and HAVS.
Biological-effects; Vibration; Vibration-exposure; Vibration-effects; Muscle-tissue; Hand-tools; Hand-injuries; Arm-injuries; Injuries; Occupational-exposure; Muscle-function; Animals; Animal-studies; Models; Laboratory-animals; Exposure-levels; Exposure-assessment; Hypoxia; Risk-factors; Vibration-disease; Vibration-control; Carpal-tunnel-syndrome
NORA Symposium 2006: Research Makes a Difference! April 18-26, 2006, Washington, DC.