Hearing Profile of Brazilian Forestry Workers' Noise Exposure

Introduction Researchers studying the hearing health of forestry workers have revealed the presence of a noise-induced hearing loss (NIHL) in this population and have concluded that the vibration of the equipment, the carbon monoxide released by motors, and pesticides might also contribute to NIHL. Objective To analyze the noise exposure in the Brazilian forestry industry workers and the effects on hearing. Methods The study sample comprised 109 employees of a company that specialized in reforestation. Their participants' mean age was 35.5 years (21 to 54 years), mean tenure at the company was 3.9 years (1 to 13 years), and mean total duration of noise exposure was 12.3 years (1 to 30 years). The existing documentation reporting on the jobs risk analysis was examined, noise level was measured, and pure tone audiometry was performed in all participants. Participants were divided into three groups according to their noise exposure levels in their current job. Results Of the participants who were exposed to noise levels less than 85 dBA (decibels with A-weighting filter), 23.8% had hearing loss, and 5.5% of the participants who were exposed to noise ranging from 85 to 89.9 dBA and 11% of the participants who were exposed to noise greater than 90 dBA had audiogram results suggestive of NIHL. Conclusion The implementation of a hearing loss prevention program tailored to forestry workers is needed. .

Neural mechanism of rapid eye movement sleep generation with reference to REM-OFF neurons in locus coeruleus.

The noradrenergic (NA-ergic) rapid eye movement (REM)-OFF neurons in locus coeruleus (LC) and cholinergic REM-ON neurons in laterodorsal/pedunculopontine tegmentum show a reciprocal firing pattern. The REM-ON neurons fire during REM sleep whereas REM-OFF neurons stop firing during REM sleep. The cessation of firing of REM-OFF neurons is a pre-requisite for the generation of REM sleep and non-cessation of those neurons result in REM sleep loss that is characterized by symptoms like loss of memory retention, irritation, hypersexuality, etc. There is an intricate interplay between the REM-OFF and REM-ON neurons for REM sleep regulation. Acetylcholine from REM-ON neurons excites the GABA-ergic interneurons in the LC that in turn inhibit the REM-OFF neurons. The cessation of firing of REM-OFF neurons withdraws the inhibition from the REM-ON neurons, and facilitates the excitation of these neurons resulting in the initiation of REM sleep. GABA modulates the generation of REM sleep in pedunculopontine tegmentum (PPT) by acting pre-synaptically on the NA-ergic terminals that synapse on the REM-ON neurons whereas in LC it modulates the maintenance of REM sleep by acting post-synaptically on REM-OFF neurons. The activity of REM sleep related neurons is modulated by wakefulness (midbrain reticular formation/ascending reticular activating system) and sleep inducing (caudal brainstem/medullary reticular formation) areas. Thus, during wakefulness the wake-active neurons keep on firing that excites the REM-OFF neurons, which in turn keeps the REMON neurons inhibited; therefore, during wakefulness REM sleep episodes are not expressed. Additionally, the wakefulness inducing area keeps the REM-ON neurons inhibited. In contrast, the sleep inducing area excites the REM-ON neurons. Thus, the wakefulness inducing area excites and inhibits the REM-OFF and REM-ON neurons, respectively, while the sleep inducing area excites the REM-ON neurons that facilitate the generation of REM sleep.