Too loud? Do powered hand dryers violate federal noise exposure standards?

OBJECTIVE: The aim of this study was to determine if high-powered air hand dryers produce sufficient noise to warrant concern over acoustic trauma as determined by federally established standards. STUDY DESIGN: Prospective observational field data collection SETTING: Urban and suburban community SUBJECTS AND METHODS: Using a NIOSH developed and calibrated soundmeter app, powered hand dryers were measured throughout two metropolitan areas. Ear level measurements were performed while drying wet hands. Recorded variables included average LAeq, Time-Weighted Average, Max and Peak Levels, Noise Dose, and Projected Dose according to NIOSH and OSHA standards, and all three major weighting networks (A, C, and Z). RESULTS: Fifty-four trials were performed at 27 locations. Average dryer run time was 28.9 s (range 14-45 s). Average LAeq (dBA), average maximum level (dBA), and average TWA (dBA) were 90.46 ± 5.32, 94.86 ± 5.73, 59.90 ± 6.80, respectively. The noise generated exceeded published manufacturer specifications. However, even with estimated cumulative daily exposure, the noise generated by these dryers did not exceed federal safety standards. CONCLUSIONS: Air-powered hand dryers produce noise output at a level that many would find subjectively uncomfortable with some brands/models consistently producing noise in excess of 90 dBA. Nonetheless, these dryers do not produce sound exceeding NIOSH standards for noise exposure.

Brain Hyperglycemia Induced by Heroin: Association with Metabolic Neural Activation.

Glucose enters the brain extracellular space from arterial blood, and its proper delivery is essential for metabolic activity of brain cells. By using enzyme-based biosensors coupled with high-speed amperometry in freely moving rats, we previously showed that glucose levels in the nucleus accumbens (NAc) display high variability, increasing rapidly following exposure to various arousing stimuli. In this study, the same technology was used to assess NAc glucose fluctuations induced by intravenous heroin. Heroin passively injected at a low dose optimal for maintaining self-administration behavior (100 µg/kg) induces a rapid but moderate glucose rise (∼150-200 µM or ∼15-25% over resting baseline). When the heroin dose was doubled and tripled, the increase became progressively larger in magnitude and longer in duration. Heroin-induced glucose increases also occurred in other brain structures (medial thalamus, lateral striatum, hippocampus), suggesting that brain hyperglycemia is a whole-brain phenomenon but changes were notably distinct in each structure. While local vasodilation appears to be the possible mechanism underlying the rapid rise in extracellular glucose levels, the driving factor for this vasodilation (central vs peripheral) remains to be clarified. The heroin-induced NAc glucose increases positively correlated with increases in intracerebral heat production determined in separate experiments using multisite temperature recordings (NAc, temporal muscle and skin). However, glucose levels rise very rapidly, preceding much slower increases in brain heat production, a measure of metabolic activation associated with glucose consumption.