Classroom acoustics and hearing ability as determinants for perceived social climate and intentions to stay at work.

Background noise and room acoustics may impede social interactions by interfering with oral communication and other cognitive processes. Accordingly, recent research in school environments has showed that social relationships with peers and teachers are described more negatively in rooms with long reverberation times (RT). The purpose of this study was to investigate how RT and hearing ability (i.e., hearing thresholds [HT] and distortion product oto-acoustic emissions) were associated with school teachers' perceptions of the social climate at work and their intentions to stay on the job. School teachers (n = 107) from 10 schools that worked in classrooms classified by acoustical experts as "short RT" (3 schools, mean RT 0.41-0.47 s), "medium RT" (3 schools, mean RT 0.50-0.53 s), and "long RT" (4 schools, mean RT 0.59-0.73 s) were examined. Teachers who worked in classrooms with long RT perceived their social climate to be more competitive, conflict laden, and less relaxed and comfortable. They were more doubtful about staying on the job. Even if the teachers were generally satisfied with their work the results suggest that the comfort at work may have been further improved by acoustical interventions that focus on reducing sound reflections in the classrooms. Yet, due the study design and the novelty of the findings the potential practical significance of our observations remains to be evaluated.

An experimental protocol for maternal pulmonary exposure in developmental toxicology.

To establish a protocol for studying effects of pulmonary exposure in developmental toxicity studies, the effects of intratracheal sham instillation under short-term isoflurane anaesthesia were evaluated with a protocol including multiple instillations during gestation. Twelve time-mated mice (C57BL/6BomTac) were anaesthetized with isoflurane and intratracheally instilled with saline containing 10% bronchoalveolar lavage (BAL) on gestation days 8, 11, 15 and 18. In addition, the early effects of the procedure were assessed in naive female mice. Control animals were not handled. Dams were followed until weaning, and the offspring were observed from birth to sexual maturation. The cell composition of BAL was examined in the females early after treatment (3 days) and in the dams at weaning (25 days). DNA damage in BAL and liver cells was determined by the comet assay. The procedure did not affect gestation or viability, growth and sexual maturation of the offspring. Lung markers of inflammation and DNA damage were comparable in control and treated dams. Livers of the anaesthetized and instilled females, dams and their offspring displayed no induction of DNA damage. Intratracheal instillation under isoflurane anaesthesia did not induce observable effects in pregnant mice or their offspring. We suggest that this procedure can be used as a means of exposure through the airways in studies of developmental toxicity.

Hazards to hearing from combined exposure to toluene and noise in rats.

INTRODUCTION: The main risk of hearing impairment from workplace exposure to organic solvents may stem from the potentiation of effects caused by concomitant noise exposure. The aim of the present study was to identify the main hazards from combined long-term, low-level exposure to noise and aromatic organic solvents, like toluene, in rats. MATERIAL AND METHODS: The rats were exposed to steady-state, wide-band noise (WBN) and 0 ppm, 100 ppm, 200 ppm and 500 ppm toluene for 90 days. Hearing was assessed using Auditory Brain Stem Responses (ABR) and Distortion Product Oto-Acoustic Emissions (DPOAE) eight weeks after exposure. The impact of noise composition on the interaction between solvent and noise exposure was investigated in rats exposed for 10 days either to 0 ppm, 500 ppm, 1000 ppm or 1500 ppm toluene and either WBN or impulse noise. ABR and DPOAE tests were performed before and two weeks after exposure. RESULTS: Long-term exposure of rats to WBN and toluene at 500 ppm or less did not show any increase in hearing impairment, compared to the rats exposed to noise only. Synergistic interaction was demonstrated in short-term exposure to 1500 ppm toluene and both to WBN and impulse noise, but hearing impairment was much larger when following exposure to impulse noise. CONCLUSION: In combined exposure to low-levels of noise and toluene, even a long-term exposure did not reveal a potential hazard of hearing impairment. Synergistic interaction in combined short-term exposure to toluene and noise was noted both with respect to WBN and impulse noise, but the impulse noise was much more disruptive than WBN at the same level of noise exposure. The ototoxicity of organic solvents may primarily be a hazard also to human hearing due to the exacerbation of hearing loss by a possible co-exposure to especially harmful noise, such as impulse noise.

No evidence for enhanced noise induced hearing loss after prenatal stress or dexamethasone.

It was recently implied that prenatal stress and fetal exposure to glucocorticoids may interfere with hearing ability and noise induced hearing loss in adulthood. In the present study pregnant Wistar rats were stressed during gestation by Chronic Mild Stress (CMS, a variable schedule of different stressors) or by dexamethasone (a synthetic glucocorticoid, i.e. a pharmacological stressor). At birth, but not at weaning, the dexamethasone offspring exhibited significantly decreased body weight compared to both control offspring and progeny from dams exposed to CMS during pregnancy. As adults, male offspring were exposed to 105 dB sound pressure level (SPL) wide band noise either continuously for eight hours or for two hours per day on three consecutive days. Oto-acoustic emissions and auditory brainstem responses were recorded before and after exposure to noise. Neither prenatal chronic stress nor prenatal dexamethasone exposure was associated with significantly enhanced noise induced hearing loss compared to controls, and these results were consistent in both subsets of animals. Our data do not support previous reports that prenatal exposure to mild stress nor to dexamethasone is detrimental to the hearing organ per se. However, hearing may be modulated by prenatal stressors under certain circumstances, of which the timing and degree are probably the most important.

Smoking and height as risk factors for prevalence and 5-year incidence of hearing loss. A questionnaire-based follow-up study of employees in Denmark aged 18-59 years exposed and unexposed to noise.

This paper investigated whether smoking and short stature in adulthood were independent risk factors for hearing loss. We reanalyzed data from the Danish Work Environment Cohort Study (an existing cohort study), on prevalence of self-reported hearing loss among 7,221 employees and on five-year incidence among 4,610 employees. We found that smoking predicted hearing loss incidence and prevalence. Smoking did not predict incidence at noise exposure during half or more of a worker's hours. Very short stature predicted prevalence in the total adult population only weakly, but strongly among employees born before 1951. These prospective findings indicate that smoking is an independent risk factor for incidence of hearing loss. Very short stature predicted prevalence of hearing loss only in a subpopulation.

Prenatal stress may increase vulnerability to life events: comparison with the effects of prenatal dexamethasone.

Prenatal stress has been associated with a variety of alterations in the offspring. The presented observations suggest that rather than causing changes in the offspring per se, prenatal stress may increase the organism's vulnerability to aversive life events. Offspring of rat dams stressed gestationally by chronic mild stress (CMS, a variable schedule of different stressors) or dexamethasone (DEX, a synthetic glucocorticoid, i.e., a pharmacological stressor) was tested for reactivity by testing their acoustic startle response (ASR). Two subsets of offspring were tested. One was experimentally naïve at the time of ASR testing, whereas the other had been through blood sampling for assessment of the hormonal stress response to restraint, 3 months previously. Both prenatal CMS and dexamethasone increased ASR in the offspring compared to controls, but only in prenatally stressed offspring that had been blood sampled 3 months previously. In conclusion, similarity of the effects of maternal gestational exposure to a regular stress schedule and of exposure to a synthetic glucocorticoid suggests that maternal glucocorticoids may be a determining factor for changes in the regulatory mechanisms of the acoustic startle response. Further, a single aversive life event showed capable of changing the reactivity of prenatally stressed offspring, whereas offspring of dams going through a less stressful gestation was largely unaffected by this event. This suggests that circumstances dating back to the very beginning of life affect the individual's sensitivity towards experiences in life after birth. The prenatal environment may thus form part of the explanation of the considerable individual variation in the development of psychopathology.

Effects of prenatal exposure to chronic mild stress and toluene in rats.

The aim of the present study was to elucidate whether prenatal chronic stress, in combination with exposure to a developmental neurotoxicant, would increase effects in the offspring compared with the effects of either exposure alone. Development and neurobehavioral effects were investigated in female offspring of pregnant rats (Mol:WIST) exposed to chronic mild stress (CMS) during gestational days (GD) 9-20, or 1500 ppm toluene, 6 h/day during gestational days 7-20, or a combination of the two. Prenatal CMS was associated with decreased thymic weight and increased auditory startle response. The corticosterone response to restraint seemed modified by prenatal exposure to toluene. Lactational body weight was decreased in offsprings subjected to CMS, primarily due to effects in the combined exposure group. Cognitive function was investigated in the Morris water maze, and some indications of improved function due to CMS were observed. In the present experimental setting, there was no indication of the two exposures potentiating each other with respect to adverse effects on the nervous system. However, the effects of prenatal CMS indicate that stress during fetal life may interfere with the development of the thymus and increase the reactivity (startle reflex) of the offspring.

Toluene depresses plasma corticosterone in pregnant rats.

Combined exposure to stressors and chemicals may result in synergistic effects. The effects of prenatal exposure to the organic solvent toluene resemble those observed in offspring of gestationally stressed dams, a possible common mechanism being transfer of stress-/toluene-induced increments of corticosteroids from the maternal to the foetal compartment. Pregnant rats were subjected to either 1500 ppm toluene 6 hr/day and/or a schedule of "Chronic mild stress" during the last two weeks of gestation. Exposure to toluene was associated with reduced birth weight and lower maternal weight gain, the latter being enhanced by maternal stress. A depressant effect of toluene on maternal corticosterone was observed, hence the study does not provide immediate evidence that transfer of elevated levels of corticosterone from the maternal to the foetal compartment mediates the effects of prenatal exposure to toluene.

Effect of long-term, low-level noise exposure on hearing thresholds, DPOAE and suppression of DPOAE in rats.

Loss of adaptability rather than loss of sensitivity may be one of the initial signs of auditory impairment following exposure to noise. One way to examine the adaptability of hearing in experimental investigation is to measure the magnitude of the suppression, exerted by the medial olivocochlear efferent system, on the ipsilateral otoacoustic emissions in response to contralateral sound stimulation. Thus, in order to test the hypothesis it was decided to measure hearing thresholds (HT), the cubic DPOAE and suppression of cubic DPOAE by contralateral wide band noise in rats exposed to long-term, low level noise (90 days of 90 dBlin 4-20 kHz wide band noise 4 hours/day, 5 days/week). Measurements of HT were performed by assessment of the ABR, elicited by tone-pips from the same probe assembly used in the measurements of DPOAE. The suppression of the cubic distortion product (CDP) was determined in ketamine/xylazine anaesthesia, allowing a stable response for a minimum of 20 min. Of the frequencies tested, the rats exposed to noise had an increase in HT at 12.8 kHz only (6.8 dB, P<0.05), while a reduction on the CDP was evident with f2 going from 9.2 kHz to the upper limit at 17.4 kHz. Further, the rats exposed to noise had little suppression of the CDP at low levels of contralateral noise (CN), but no difference from the control animals was seen as the CN noise level was increased. The measurement of DPOAE suppression did not reveal any effects of the low level noise exposure that was not paralleled also by shifts in hearing thresholds. The most sensitive assessment of the auditory changes in the study was the measurements of DPOAE, and further elaboration on the bandwidth and frequency distribution of the CN is necessary, before auditory changes in the high frequency range can be probably assessed.

Rats exposed to Toluene and Noise may develop Loss of Auditory Sensitivity due to Synergistic Interaction.

Hearing loss in workers exposed to organic solvents has been shown to be the effect of interaction between the exposure to solvents and noise. Synergistic interaction has been demonstrated in rats following simultaneous exposure to toluene and noise, but only at high-level toluene exposure. The present study was initiated to investigate the potential interaction of exposure to noise and toluene on the auditory system of the rat, covering a dose-range of toluene exposure (0, 500, 1000, 1500, and 2000 ppm, 6 h/d, 10 d). Exposed to toluene only, the rats exposed at the 1500 and 2000 ppm level developed a mid-frequency ABR threshold shift, whereas rats exposed to 0, 500, and 1000 ppm did not exhibit signs of auditory impairment. Rats exposed to 500 ppm toluene and noise (96 dB SPL, 2h following the daily toluene exposure, 10 d) developed a small, but statistically significant threshold shift, equal to the hearing loss in rats exposed to noise only (0 ppm). Synergistic interaction was evident at the 1000, 1500, and 2000 ppm toluene exposure levels. There was no further hearing loss at the 2000 ppm than at the 1500 ppm level, indicating that a saturation of the auditory impairment had been reached. When acute noise exposure (105 dB SPL, 4 h) followed the toluene exposure by 30 days, interaction was noted at the 1500 ppm toluene exposure level, but not at the 1000 ppm level. However, the latter type of interaction is of indirect nature and should be distinguished from the direct interaction, taking place when toluene is physically present in the cochlea during exposure to noise. Further investigations in animal models should preferentially be carried out as long-term, low-level exposure studies, showing the possible interaction at low exposure levels, where exposure to each factor alone is without any effect.