In principle, the noise/stress hypothesis is well understood: Noise activates the pituitary­adrenal-cortical axis and the sympathetic-adrenal-medullary axis. Changes in stress hormones including epinephrine, norepinephrine and cortisol are frequently found in acute and chronic noise experiments. The catecholamines and steroid hormones affect the organism's metabolism. Cardiovascular disorders are especially in focus for epidemiological studies on adverse noise effects. However, not all biologically notifiable effects are of clinical relevance. The relative importance and significance of health outcomes to be assessed in epidemiological noise studies follow a hierarchical order, i.e. changes in physiological stress indicators, increase in biological risk factors, increase of the prevalence or incidence of diseases, premature death. Decision-making and risk management rely on quantitative risk assessment. Epidemiological methods are the primary tool for providing the necessary information. However, the statistical evidence of findings from individual studies is often weak. Magnitude of effect, dose-response relationship, biological plausibility and consistency of findings among studies are issues of epidemiological reasoning. Noise policy largely depends on considerations about cost­effectiveness, which may vary between populations. Limit or guideline values have to be set within the range between social and physical well-being - between nuisance and health. The cardiovascular risk is a key-outcome in non-auditory noise effects' research because of the high prevalence of related diseases in our communities. Specific studies regarding critical groups, different noise-sources, day/evening/night comparisons, coping styles and other effect­modifying factors, and the role of annoyance as a mediator of effect are issues for future research in this field.

56 children age 7 - 10 had a medical check-up and they and their mothers completed questionnaires. Additionally the children's excretion of free cortisol was measured by HPLC in two urine samples collected at 1 p.m. and in the morning. The children lived either at a busy road with 24 h lorry traffic or in quiet areas. At the side of the road the noise level was registered during five nights. In the bedrooms representative measurements of the short-term maximal sound level (L _Amax and L _Cmax ) and of the frequency spectrum were taken. During the night on average every 2 minutes a lorry with L _max > 80 dB(A) passed by the houses. The indoor levels of the higher exposed half of the children were L _max = 33-52 dB(A) resp. 55­-78dB(C)). The frequency spectrum had its maximum below 100 Hz. 74% of the higher exposed never opened their windows as compared to 25% in the lower exposed half group. The excretion of free cortisol and its metabolites in the first half of the night was significantly correlated to L _Cmax (co-variables: age, sex, and the day of the week) as well as to impaired sleep, memory and ability to concentrate. The cortisol excretion in the second half of the night was not correlated to the noise level. Disturbances of the normal circadian rhythm of cortisol can be quantified by the quotient of the cortisol excretion in the first half of the night in relation to that in the second half. Children under long-term road traffic noise exposure during the night had an increased risk of chronic stress hormone regulation disturbances. These disturbances were significantly correlated to L _Cmax and findings of allergy and/or asthma bronchial. Long-term low frequency noise exposure with Lmax < 55 dB(A) during the night resulted in chronic increases of children's excretion of free cortisol in the first half of the night and in serious disturbances of the circadian rhythm of cortisol. Indications of increased risks of asthma bronchial and allergies in noise exposed children with stress hormone regulation disturbances need further clarification

In a previous follow-up study of industrial workers (the CORDIS study, Melamed et al., 1999a) we demonstrated a dose-response relationship between occupational noise exposure levels and all-cause mortality. In that study the type of jobs that workers were engaged in was not taken into account. However, in further analyses of CORDIS data we have found that noise exposure is particularly detrimental to health for workers engaged in complex jobs. Therefore in this 12­year study we attempted to determine the combined effect of job complexity and noise exposure on all-cause mortality in 2606 industrial workers. We divided the workers into four groups based on a combination of either high or low noise exposure, and whether they performed simple or complex jobs. There was an increased risk for all-cause mortality (OR = 1.86, 95% CI = 1.04-3.32), in workers who performed complex jobs under high noise exposure levels compared to those who performed simple jobs under low noise exposure. This remained significant even after adjusting for possible confounding variables. There was a trend for a more pronounced effect among less educated workers, among blue-collar workers, and in those with higher tenure. We conclude that occupational noise exposure is associated with excess mortality risk among workers performing complex jobs.

A cross-sectional study was performed on a 5% sample of the adult population of the city of Pancevo (3622 residents). The response rate was 79 % (2874), with 1243 interviewed males (43%) and 1631 females (57%). Noise annoyance was assessed on a five- grade verbal scale (Not at all; Slightly; Moderately; Very; Extremely). Arterial hypertension was defined by antihypertensive treatment, information on which was obtained from questionnaire. Myocardial infarction was also subjectively confirmed. Prevalence and odds ratios of arterial hypertension and myocardial infarction were computed for subjects who were very much and extremely annoyed by noise, or moderately annoyed, using residents who were slightly annoyed or not annoyed at all as a referent category. Significant odds ratios (adjusted for age, body mass index and smoking habits) were found for self-reported arterial hypertension [1,8 (1,0-2,4 - 95% confidence interval) , P < 0,01] and myocardial infarction [1,7 (1,0 - 2,9), P < 0,05] in very much or extremely noise disturbed male subjects, compared to those who were not annoyed at all, or were slightly annoyed by noise. The respective odds ratios for females were lower and not statistically significant 1,1 (0,8-1,7) and 1 (0,4 - 2,0).

Noise induces cortisol excretion even below the awakening threshold. This is based upon the existence of very close subcortical central nervous connections between parts of the auditory system (e. g. amygdala) showing typical plasticity effects and the hypothalmic-pituitary­adrenal (HPA)-axis. Repeated noise events (e.g. over-flights during nigh-time) will lead to accumulation of the cortisol concentration in blood. This happens because its time constant of exponential decrease is about 50 to 10 times larger than that one for adrenaline and noradrenaline. A twofold attempt has been made to calculate the cortisol accumulation using an initial value of noise induced small cortisol increase (rounded value 14 ng/ml) at the nightly threshold of beginning vegetative overreaction around 53 dB(A). A mean time-constant of 64 min has been applied based upon experimental studies. Using in a first step the range of minimal and maximal normal cortisol values as border line and taking into account a relation between peak sound pressure level and cortical excitation given by a power function (exponent 0.32, based on evoked potential studies in man) results in a formula to estimate tolerable events during night-time periods (over-flights in a given time range). Examples of results for 8 hours in the night are for instance values of 11 events with 55 dB(A) indoor peak level or 5 events with 75 dB(A) indoor peak level respectively. Those values of tolerable nightly noise events estimated on the basis of physiological processes and peak levels cannot be recalculated as or compared with equivalent sound levels.

Listening to loud music has been associated, in a number of studies, with hearing loss and tinnitus among young people. However an unanswered question is whether or not these same young people want to have their music so loud. In our study 533 young men and 167 young women, in the age group 16 to 25, who were attending a vocational training centre, responded to a questionnaire and volunteered to have their hearing assessed. The questionnaire sought information on listening habits, on the kinds of events attended, on whether the music at these events was too loud or not, and if the respondents considered their hearing had been impaired. Analysis of this data indicated that 79% of the subjects attend discotheques, 52% pop and rock concerts, and 35% techno parties (e.g. raves). A significant number considered the music at these venues was too loud. Some 42% considered this was the case at discos, 35% thought pop and rock concerts too loud, and 39% held a similar view of techno parties. Conversely, fewer than 3% considered sound levels at these events to be too low. On the basis of the response to the questionnaire we estimate that over half the respondents (56.6%) have a sound exposure (L _eq ) from music of over 87 dB(A). It is not surprising therefore that 71% reported that they had suffered tinnitus following attendance at a music event. The hearing capacity of the sample was measured by audiometry. These measurements detected hearing loss in 11% of the 700 individuals tested. However it was not possible to show that the risk of hearing loss increased with increasing exposure to loud music. We conclude that young people neither demand nor require the excessive sound levels typical of most music events.

Objectives. To estimate the sound pressure levels in areas with heavy and with local traffic in the city of Sao Paulo and compare the data obtained with the thresholds established by the local law. Methods. Twenty-eight points in roads with heavy and local traffic were chosen. The measurements were done Monday to Friday, 8 am to 5 pm, using a 2236 Mediator (Briiel & Kjaer) following the International Standard (ref. no. 1996/1982 1,2,3). Each point was measured a number of times to produce a standard error lower than 1 dB. Results. The equivalent continuous A-weighted sound pressure level (Leq) for the roads with heavy traffic ranged from 70.88 to 80.18 dB(A), mean 75.88 dB(A) (95% CI: 74.49; 77.27) and the maximum peak (MaxP) ranged from 102.47 to 108.37 dB(C), mean 105.63 dB(C) (95% CI: 104.59; 106.68). For the roads with local traffic we observed: Leq from 50.82 to 66.88 dB(A), mean 61.11 dB(A) (95% CI: 57.97; 64.26) and MaxP 83.13 to 97.33 dB(C), mean 92.81 dB(C) (95% CI: 89.80; 95.82). There was a strong evidence, p < 0,001, in favour of the difference between the two types of traffic roads regarding the sound pressure levels. Conclusions. The Brazilian Standards establishes 50dB(A) and 70dB(A) as the maximum limits for environmental noise in residential and industrial areas, respectively. The results of this study indicate that the problem of urban noise in the city of Sao Paulo needs to be tackled urgently due to its important public health impact.

In order to find out the attitude of the community towards environmental noise, community surveys were conducted over the territory of Hong Kong through telephone sampling. Specific surveys were also carried out for areas previously affected by severe aircraft noise. Main observations on the community's response towards noise are that noise pollution was ranked the third among five selected social concerns (after "air pollution" and "security", and higher than "traffic jam" and "cleanliness"); about 60% of the respondents found the territory "noisy"; the most annoying noise source was "traffic noise"; 40% of people found the most annoying noise not tolerable and that most people affected by noise suffered from "distraction". Nonetheless, many did nothing (e.g. did not complain) against the noise and still preferred an open-window life style.

The purpose of this study was to examine the effects of industrial exposure to mercury and chlorinated hydrocarbons (CH) on the auditory pathway. To this effect, auditory brainstem responses (ABR) were recorded from 40 workers exposed to mercury, 37 workers exposed to CH and from a control group of 36 subjects that were never exposed to neurotoxic substances. The interpeak latency (IPL) of waves I-III, III-V and I-V were measured. The mean duration of exposure to mercury and CH was 15.5 (+6.4) and 15.8 (+7.2) years respectively. The air sample monitoring of mercury was 0.008 mg/m³ (0.32 of the Threshold Limit Value - TLV® as published by ACGIH 2000). The mean average air sample monitoring was found to be 98 ppm for TCE, 12.7 ppm for PCE and 14.4 ppm for TCA which is respectively between 0.28 - 0.51 of the TLV® of CH. The mean blood mercury (B-Hg) levels were found to be 0.5mgr% (+0.3mgr%), which is 0.13 of the upper range of the permitted biologic exposure index (BEI) published by the ACGIH 2000. The mean urine samples levels of trichloroacetic acid were between 0.11-0.2 of the permitted BEI for the CH workers. The percent of workers exposed to mercury and CH workers with abnormal prolongation of IPL I-III was higher than the control group (42.5% and 33.8% vs. 18.0% respectively p<0.02). These results are consistent with other studies and show that ABR may provide a sensitive tool for detecting subclinical central neurotoxicity caused by CH and mercury