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Background: Both physical and psychological health outcomes have been associated with exposure to environmental noise. It is not known whether all individuals are equally susceptible to these effects. Noise sensitivity has chiefly been examined in studies of annoyance where it has been shown to moderate the annoyance responses to transport-related noise. Noise sensitivity could have the same moderating effect on physical and psychological health outcomes related to environmental noise exposure but this has been little tested. Noise sensitivity which is also associated with sensitivity to chemicals, light and odours could be an indicator of a more pervasive susceptibility to ill-health related to environmental sources. Methods: A cohort of 2398 men between 45 and 59 years, the longitudinal Caerphilly Collaborative Heart Disease study, was established in 1984/88 and followed into the mid-1990s. Road traffic noise maps were assessed at baseline. Baseline psychological ill-health measures were measured in phase 2 in 1984/88, at phase 3 follow up 1989/93 and phase 4 follow up in 1993/6.Ischaemic heart disease and risk factors were measured in clinic and by questionnaire at baseline and through hospital records and administrative records of deaths during follow up. This study aimed to test if noise sensitivity and noise annoyance have moderating effects on road traffic noise and psychological ill-health and secondly if noise sensitivity and noise annoyance predict physical and psychological ill-health and mortality, irrespective of exposure to road traffic noise. Results: Road traffic noise was associated with Phase 4 psychological ill-health but only among those exposed to 56-60dBA (OR= 1.98 95%CI 1.21, 3.24). High noise sensitivity was associated with lower mortality risk (HR=0.71, 95%CI 0.54-0.94). High noise sensitivity was associated longitudinally with psychological ill-health at phase 3 (OR=1.82 95%CI1.30, 2.56) and phase 4 (OR=1.78 95%CI 1.26, 2.52). There was weak evidence that noise sensitivity moderated the association of road traffic noise exposure with psychological ill-health. Noise annoyance predicted psychological ill-health at phase 4 in the sample in which baseline cases of psychological ill-health were included (OR= 2.08 95%CI 1.00, 4.31). Neither noise sensitivity nor noise annoyance moderated the effects of road traffic noise on ischaemic heart disease morbidity or mortality. Noise annoyance did not moderate the effects of road traffic noise on psychological ill-health.Conclusions: Noise sensitivity is a specific predictor of psychological ill-health and may be an indicator of current psychological ill-health as part of a wider construct of environmental susceptibility. It may increase the risk of psychological ill-health when exposed to road traffic noise.

Background Few studies have considered aircraft noise annoyance and noise sensitivity in analyses of the health effects of aircraft noise, especially in relation to medication use. This study aims to investigate the moderating and mediating role of these two factors in the relationship between aircraft noise levels and medication use among 5860 residents of ten European airports included in the HYENA and DEBATS studies. Methods Information on aircraft noise annoyance, noise sensitivity, medication use, and demographic, socio-economic and lifestyle factors was collected during a face-to-face interview at home. Medication was coded according to the Anatomical Therapeutic Chemical (ATC) classification. Outdoor aircraft noise exposure was estimated by linking the participant’s home address to noise contours using Geographical Information Systems (GIS) methods. Logistic regressions with adjustment for potential confounding factors were used. In addition, Baron and Kenny’s recommendations were followed to investigate the moderating and mediating effects of aircraft noise annoyance and noise sensitivity. Results A significant association was found between aircraft noise levels at night and antihypertensive medication only in the UK (OR = 1.43, 95%CI 1.19–1.73 for a 10 dB(A)-increase in Lnight). No association was found with other medications. Aircraft noise annoyance was significantly associated with the use of antihypertensive medication (OR = 1.33, 95%CI 1.14–1.56), anxiolytics (OR = 1.48, 95%CI 1.08–2.05), hypnotics and sedatives (OR = 1.60, 95%CI 1.07–2.39), and antasthmatics (OR = 1.44, 95%CI 1.07–1.96), with no difference between countries. Noise sensitivity was significantly associated with almost all medications, with the exception of the use of antasthmatics, showing an increase in ORs with the level of noise sensitivity, with differences in ORs among countries only for the use of antihypertensive medication. The results also suggested a mediating role of aircraft noise annoyance and a modifying role of both aircraft noise annoyance and noise sensitivity in the association between aircraft noise levels and medication use. Conclusions The present study is consistent with the results of the small number of studies available to date suggesting that both aircraft noise annoyance and noise sensitivity should be taken into account in analyses of the health effects of exposure to aircraft noise.

Background: Both physical and psychological health outcomes have been associated with exposure to environmental noise. It is not known whether all individuals are equally susceptible to these effects. Noise sensitivity has chiefly been examined in studies of annoyance where it has been shown to moderate the annoyance responses to transport-related noise. Noise sensitivity could have the same moderating effect on physical and psychological health outcomes related to environmental noise exposure but this has been little tested. Noise sensitivity which is also associated with sensitivity to chemicals, light and odours could be an indicator of a more pervasive susceptibility to ill-health related to environmental sources. Methods: A cohort of 2398 men between 45 and 59 years, the longitudinal Caerphilly Collaborative Heart Disease study, was established in 1984/88 and followed into the mid-1990 s. Road traffic noise maps were assessed at baseline. Baseline psychological ill-health measures were measured in phase 2 in 1984/88, at phase 3 follow up 1989/93 and phase 4 follow up in 1993/6.Ischaemic heart disease and risk factors were measured in clinic and by questionnaire at baseline and through hospital records and administrative records of deaths during follow up. This study aimed to test if noise sensitivity has a moderating effect on road traffic noise and psychological ill-health and secondly if noise sensitivity predicted physical and psychological ill- health and mortality, irrespective of exposure to road traffic noise. Results: Road traffic noise was associated with Phase 4 psychological ill-health but only among those exposed to 56-60dBA (OR = 1.98 95%CI 1.21, 3.24). High noise sensitivity was associated with lower mortality risk (HR = 0.71, 95%CI 0.54–0.94). High noise sensitivity was associated longitudinally with psychological ill-health at phase 3 (OR = 1.82 95%CI1.30, 2.56). There was also weak evidence that noise sensitivity moderated the association of road traffic noise exposure with psychological ill-health. Conclusions: Noise sensitivity is a specific predictor of psychological ill-health and may be an indicator of current psychological ill-health as part of a wider construct of environmental susceptibility. It may increase the risk of psychological ill-health when exposed to road traffic noise.

Air pollution, traffic noise and noise annoyance are suggested to be associated with hypertension and blood pressure (BP); however, the evidence remains inconsistent. Our study examined the long-term associations of modeled and self-reported measures of air pollution and traffic noise on prevalent hypertension and BP. We analyzed cross-sectional data from 2552 participants aged 31-72years from the KORA F4 (2006-2008) study conducted in the region of Augsburg, Germany. Land-use regression models were used to estimate residential long-term exposure to particulate matter

Background: Studies on the association between traffic noise and cardiovascular diseases have rarely considered air pollution as a covariate in the analyses. Isolated systolic hypertension has not yet been in the focus of epidemiological noise research. Methods: The association between traffic noise (road and rail) and the prevalence of hypertension was assessed in two study populations with a total of 4,166 participants 25–74 years of age. Traffic noise (weighted day–night average noise level; LDN) at the facade of the dwellings was derived from noise maps. Annual average PM2.5 mass concentrations at residential addresses were estimated by land-use regression. Hypertension was assessed by blood pressure readings, self-reported doctor-diagnosed hypertension, and antihypertensive drug intake. Results: In the Greater Augsburg, Germany, study population, traffic noise and air pollution were not associated with hypertension. In the City of Augsburg population (n = 1,893), where the exposure assessment was more detailed, the adjusted odds ratio (OR) for a 10-dB(A) increase in noise was 1.16 (95% CI: 1.00, 1.35), and 1.11 (95% CI: 0.94, 1.30) after additional adjustment for PM2.5. The adjusted OR for a 1-μg/m3 increase in PM2.5 was 1.15 (95% CI: 1.02, 1.30), and 1.11 (95% CI: 0.98, 1.27) after additional adjustment for noise. For isolated systolic hypertension, the fully adjusted OR for noise was 1.43 (95% CI: 1.10, 1.86) and for PM2.5 was 1.08 (95% CI: 0.87, 1.34). Conclusions: Traffic noise and PM2.5 were both associated with a higher prevalence of hypertension. Mutually adjusted associations with hypertension were positive but no longer statistically significant. Citation: Babisch W, Wolf K, Petz M, Heinrich J, Cyrys J, Peters A. 2014. Associations between traffic noise, particulate air pollution, hypertension, and isolated systolic hypertension in adults: the KORA Study. Environ Health Perspect 122:492–498; http://dx.doi.org/10.1289/ehp.1306981

Although traffic emits both air pollution and noise, studies jointly examining the effects of both of these exposures on blood pressure (BP) in children are scarce. We investigated associations between land-use regression modeled long-term traffic-related air pollution and BP in 2368 children aged 10 years from Germany (1454 from Munich and 914 from Wesel). We also studied this association with adjustment of long-term noise exposure (defined as day-evening-night noise indicator "Lden" and night noise indicator "Lnight") in a subgroup of 605 children from Munich inner city. In the overall analysis including 2368 children, NO2, PM2.5 mass (particles with aerodynamic diameters below 2.5μm), PM10 mass (particles with aerodynamic diameters below 10μm) and PM2.5 absorbance were not associated with BP. When restricting the analysis to the subgroup of children with noise information (N=605), a significant association between NO2 and diastolic BP was observed (-0.88 (95% confidence interval: -1.67, -0.08)). However, upon adjusting the models for noise exposure, only noise remained independently and significantly positively associated with diastolic BP. Diastolic BP increased by 0.50 (-0.03, 1.02), 0.59 (0.05, 1.13), 0.55 (0.03, 1.07), and 0.58 (0.05, 1.11)mmHg for every five decibel increase in Lden and by 0.59 (-0.05, 1.22), 0.69 (0.04, 1.33), 0.64 (0.02, 1.27), and 0.68 (0.05, 1.32)mmHg for every five decibel increase in Lnight, in different models of NO2, PM2.5 mass, PM10 mass and PM2.5 absorbance as the main exposure, respectively. In conclusion, air pollution was not consistently associated with BP with adjustment for noise, noise was independently and positively associated with BP in children.

The role of noise as an environmental pollutant and its impact on health are being increasingly recognized. Beyond its effects on the auditory system, noise causes annoyance and disturbs sleep, and it impairs cognitive performance. Furthermore, evidence from epidemiologic studies demonstrates that environmental noise is associated with an increased incidence of arterial hypertension, myocardial infarction, and stroke. Both observational and experimental studies indicate that in particular night-time noise can cause disruptions of sleep structure, vegetative arousals (e.g. increases of blood pressure and heart rate) and increases in stress hormone levels and oxidative stress, which in turn may result in endothelial dysfunction and arterial hypertension. This review focuses on the cardiovascular consequences of environmental noise exposure and stresses the importance of noise mitigation strategies for public health.

Background: Exposure to transportation noise showed negative health effects in children and adults. Studies in children mainly focussed on aircraft noise at school. Objectives: We aimed to investigate road traffic noise exposure at home and children’s behavioural problems and sleeping problems. Methods: 872 10-year-old children from Munich from two German population-based, birth-cohort studies with data on modelled fac - ade noise levels at home and behavioural problems were included. Noise was assessed by the day–evening–night noise indicator Lden and the night noise indicator Lnight. Behavioural problems were assessed by the Strengths and Difficulties Questionnaire (SDQ). A subgroup (N ¼ 287) had information on sleeping problems. Continuation ratio models (logistic regression models) adjusted for various covariates were applied to investigate the association between interquartile range increases in noise and SDQ scales (sleeping problems). Results: Noise measured by Lden at the most exposed fac - ade of the building was related to more hyperactivity/inattention (continuation odds ratio (cOR)¼ 1.28(95%-confidence interval(CI):1.03–1.58). Noise at the least exposed fac - ade increased the relative odds for having borderline or abnormal values on the emotional symptoms scale, especially the relative odds to have abnormal values for a subject with at least borderline values (Lden:cOR¼ 2.19(95% CI:1.32–3.64). Results for Lnight were similar. Nocturnal noise at the least exposed fac -ade was associated with any sleeping problems (odds ratio (OR) ¼ 1.79(95% CI ¼ 1.10–2.92)). Conclusions: Road traffic noise exposure at home may be related to increased hyperactivity and more emotional symptoms in children. Future longitudinal studies are required to explore noise exposure and behavioural problems in more detail, especially the role of sleep disturbances.

In the cross-sectional hypertension and exposure to noise near airports study the relationship between road traffic noise, aircraft noise and hypertension and annoyance was investigated. The data collection comprised a variety of potentially exposure modifying factors, including type of housing, location of rooms, window opening habits, use of noise-reducing remedies, shielding due to obstacles, lengths of exposure. In the present paper the quantitative role of these factors on the relationship between road and aircraft noise exposure and outcomes was analyzed. Multiple logistic and linear regression models were calculated including these co-factors and related interaction terms with noise indicators, as well as stratified analyses. Type of housing, length of residence, location of rooms and the use of noise reducing remedies modified the relationship between noise and hypertension. However, the effects were not always in the direction of a stronger association in higher exposed subjects. Regarding annoyance, type of housing, location of rooms, noise barriers, window opening habits, noise insulation, the use of noise reducing remedies, hours spent at home during daytime were significant effect modifiers. The use of noise-reducing remedies turned out to be indicators of perceived noise disturbance rather than modifiers reducing the annoyance.

Relationships between transportation noise and the level of annoyance attributed to a certain noise source are well established in adults. Little is known about the noise annoyance in children. The authors assessed the reported annoyance due to different noise sources of 8- to 14-year-old children in a representative population and compared the results with existing data on adults. The primary focus was on road traffic noise because of its pervasiveness. From all over Germany, 1,048 children were randomly selected. They completed a questionnaire regarding living conditions, including noise annoyance from different noise sources such as road traffic noise. The percentage of children’s homes located on busy roads was 16.5%, and approximately half of the children (47.7%) had their bedroom facing the street. Among the 8- to 10-year-olds, 7.3% were annoyed by road traffic noise during daytime (“yes” on a dichotomous annoyance scale). Among the 11- to 14-year-olds, 16.4% were at least “slightly” annoyed by road traffic noise during daytime (sum of the upper four categories of a 5-point annoyance scale). Compared with regularly reported representative data on adults, the relative frequency of children annoyed by road traffic noise at home was considerably lower.

In the HYENA study (HYpertension and Exposure to Noise near Airports) noise annoyances due to aircraft and road traffic noise were assessed in subjects that lived in the vicinity of 6 major European airports using the 11-point ICBEN scale (International Commission on Biological Effects of Noise). A distinction was made between the annoyance during the day and during the night. Lden and Lnight were considered as indicators of noise exposure. Pooled data analyses showed clear exposure–response relationships between the noise level and the noise annoyance for both exposures. The exposure–response curves for road noise were congruent with the EU standard curves used for predicting the number of highly noise annoyed subjects in European communities. Annoyance ratings due to aircraft noise, however, were higher than predicted by the EU standard curves. The data supports other findings suggesting that the people's attitude towards aircraft noise has changed over the years, and that the EU standard curve for aircraft noise should be modified. Keywords: Aircraft noise, Road traffic noise, Annoyance, Exposure–response curve, Change of annoyance

The biologic plausibility for noise stress-related cardiovascular responses is well established. Epidemiologic studies on the relationship between transportation noise and ischemic heart disease suggest a higher risk of myocardial infarction in subjects exposed to high levels of traffic noise.To determine the risk of road traffic noise for the incidence of myocardial infarction (MI), we carried out a hospital-based case-control study in the city of Berlin. We enrolled consecutive patients (n=1881), age 20-69 years, with confirmed diagnosis of MI from 1998 through 2001. Controls (n=2234) were matched according to sex, age, and hospital. Outdoor traffic noise level was determined for each study subject based on noise maps of the city. Standardized interviews were conducted to assess possible confounding factors and the annoyance from various noise sources.The adjusted odds ratio for men exposed to sound levels of more than 70 dB(A) during the day was 1.3 (95% confidence interval=0.88-1.8) compared with those where the sound level did not exceed 60 dBA. In the subsample of men who lived for at least 10 years at their present address, the odds ratio was 1.8 (1.0-3.2). Noise-exposed women were not at higher risk.The results support the hypothesis that chronic exposure to high levels of traffic noise increases the risk for cardiovascular diseases.

Aims: Traffic noise is a psychosocial stressor. Epidemiological studies suggest chronic noise stress to be a risk factor for cardiovascular disorders. Methods: In a prospective cohort study, the association between annoyance and disturbances due to road traffic noise and the incidence of ischaemic heart disease (IHD) was studied in 3950 middle aged men. Results: Depending on the questionnaire item, non-significant odds ratios for IHD incidence ranging from 0.9 to 1.4 were found for the highly noise annoyed/disturbed subjects when compared with the less annoyed/disturbed subjects, over the six year follow up period. However, this relation was strongly modified by the prevalence of pre-existing chronic diseases. In subjects free of any chronic disease at the beginning of the follow up, significant odds ratios between 1.7 and 3.0 were seen. In the subgroup with chronic diseases no such noise effects were seen. This surprising result of no effect in the group of people with a potential risk, due to pre-existing health problems, may be because of the dilution of the true effect due to recall bias. Conclusions: Annoyance and disturbance due to road traffic noise is associated with a higher incidence of IHD. Prevalence of disease can be an important effect modifier of the relation between noise annoyance and health outcomes.

Objective The association between the exposure to road traffic noise and the prevalence of hypertension was assessed accounting for background air pollution and the location of rooms with respect to the road. Methods A cross-sectional study was carried out inviting all subjects aged 35–74 years for participation that lived on 7 major trunk roads in 3–4 storey terraced apartment buildings and in parallel side streets that were completely shielded from noise due to the rows of houses along the major roads. The study was performed on 1770 subjects that did not have a self-reported medical doctor diagnosis of hypertension before they moved into their current residence. Noise levels at the facade of the front and the rear side of the houses were drawn from available noise maps of the area. A large set of covariates were considered to adjust the results for confounding. Results Significant increases between road traffic noise and hypertension were found with respect to the 24 h A-weighted average noise indicator LDEN. The adjusted odds ratio (OR) per noise level increment of 10 dB(A) was 1.11 (95% confidence interval (CI): 1.00–1.23). Stronger significant estimates of the noise effect were found in subjects with long residence time (OR=1.20, CI=1.05–1.37), and with respect to the exposure of the living room during daytime (OR=1.24, CI=1.08–1.41) compared with the exposure of the bedroom during night-time (OR=0.91, CI=0.78–1.06). Conclusion Chronic exposure to road traffic noise is associated with an increased risk of high blood pressure. Daytime noise exposure of the living room had a stronger impact on the association than night-time exposure of the bedroom.

We compared the prevalence of hypertension in subjects that lived on main roads with those that lived in side streets. An odds ratio of 1.310 (95% CI = 1.052-1.631) was found for those who lived on the main roads. In this traffic-exposed subgroup, subjects that had the living and the bedroom facing the road an odds ratio of 1.736 (CI = 0.673-1.882) was found in comparison with those who had both rooms on the rear side of the house. In subjects that lived on side streets the location of the rooms was meaningless (OR = 1.102, CI = 0.648-1.874).

The nocturnal excretion of catecholamines in urine was studied in 30–45-year-old women whose bedroom and/or living room were facing streets of varying traffic volume. The traffic volume of the streets was used as an indicator of noise exposure; adrenaline and noradrenaline concentrations were assessed as indicators of the outcome of the physiological stress. Significant associations between traffic volume and noradrenaline concentrations in urine were found with regard to the exposure of the bedroom (not the living room), indicating a higher chronic physiological arousal in noise-exposed subjects as compared to less exposed. Subjective measures of disturbance due to traffic noise were positively correlated with the noradrenaline level. However, this was only found in subjects where closing the window could not reduce the perceived disturbance, which points to the effectiveness of individual coping mechanisms. Stress hormones are useful indicators to study associations, mechanisms, and interactions between noise, health outcomes, and effect modifiers in epidemiological noise research. Keywords: Road traffic noise, Stress hormones, Coping, Epidemiological study

The relationship between subjective work noise exposure and the risk of myocardial infarction (MI) was assessed in a population based case-control study. 395 MI patients (31-65 years) were compared to 2148 controls from a random population sample with the same agelsex distribution. The relative risk (RR) for MI-adjusted for control variables (smoking, age, social status, etc.)-was found to increase significantly and steadily with noise category. Subjective work noise exposure was the second greatest risk factor for MI after smoking. Possible bias due to overreporting of subjective noise exposure is discussed. Interdisciplinary studies on the relationship between cardiovascular diseases and work-related stressors including subjective and objective noise assessment are needed to quantify the risk of MI due to work noise.

Summary Noise is pervasive in everyday life and can cause both auditory and non-auditory health effects. Noise-induced hearing loss remains highly prevalent in occupational settings, and is increasingly caused by social noise exposure (eg, through personal music players). Our understanding of molecular mechanisms involved in noise-induced hair-cell and nerve damage has substantially increased, and preventive and therapeutic drugs will probably become available within 10 years. Evidence of the non-auditory effects of environmental noise exposure on public health is growing. Observational and experimental studies have shown that noise exposure leads to annoyance, disturbs sleep and causes daytime sleepiness, affects patient outcomes and staff performance in hospitals, increases the occurrence of hypertension and cardiovascular disease, and impairs cognitive performance in schoolchildren. In this Review, we stress the importance of adequate noise prevention and mitigation strategies for public health.

Studies examining the association between road traffic noise and blood pressure in children are scarce. Nighttime noise levels and window orientations have not been considered in most previous studies. Investigate the association between road traffic noise exposure and blood pressure among children, and investigate the impact of bedroom window direction on this association. We measured blood pressure in 605 children aged 10 years from two Munich cohorts. Demographic and health information was collected by parent completed questionnaires. Road traffic noise levels were assessed by day-evening-night noise indicator "Lden" and night noise indicator "Lnight". Minimum and maximum levels within a 50 m buffer around childs home address were derived. Generalized additive models were applied to explore effect of noise levels on systolic and diastolic blood pressure (SBP and DBP). The orientation of childs bedroom window was considered in sensitivity analyses. DBP was significantly associated with the minimum level of noise during 24 h (Lden_min) and nightime (Lnight_min). Specifically, DBP increased by 0.67 and 0.89 mmHg for every 5 A-weighted decibels increase in Lden_min and Lnight_min. After adjusting for Lden_min (Lnight_min), DBP of children whose bedroom window faced the street was 1.37 (1.28) mmHg higher than those whose bedroom window did not, these children showed statistically significant increased SBP for Lden_min (3.05 mmHg) and Lnight_min (3.27 mmHg) compared to children whose bedroom window did not face the street. Higher minimum levels of weighted day-evening-night noise and nighttime noise around the home residence may increase a childs blood pressure.

Objectives The effect modifying impact of annoyance due to aircraft noise and road traffic noise on the relationships between the aircraft noise level and road traffic noise level on the prevalence of hypertension was investigated in 4861 subjects of the HYENA study (HYpertension and Exposure to Noise near Airports). Methods Different models were investigated either including the noise level and noise annoyance variables separately, or simultaneously, or together with an interaction term referring to the same noise source for the noise level and the noise annoyance. Results Significant effect modification was found with respect to the association between aircraft noise and hypertension. The association was stronger in more annoyed subjects. No clear interaction was found with respect to road traffic noise. The comparison of the magnitude of the main effects (per standard deviation or inter-quartile range) of noise level and noise annoyance variables revealed stronger associations with hypertension for the noise levels. Conclusion There is some indication that the noise level has a stronger predictive meaning for the relationship between noise exposure and hypertension than the reported noise annoyance (main effects). The results from the Hyena study support the hypothesis that noise annoyance acts as an effect modifier of the relationship between the noise level and hypertension.

Reviews have suggested that road noise exposure is associated with high blood pressure (hypertension). No reliable exposure-response relationship is as yet available. A meta-analysis was carried out in order to derive a quantitative exposure-response relationship between the exposure to road traffic noise and the prevalence of hypertension, and to gain some insight into the sources of heterogeneity among study results.Twenty-seven observational studies published between 1970 and 2010 in English, German or Dutch, were evaluated. Finally, the results of 24 studies were included into the data aggregation.Road traffic noise was positively and significantly associated with hypertension: Data aggregation revealed an odds ratio (OR) of 1.034 [95% confidence interval (CI) 1.011-1.056] per 5 dB(A) increase of the 16 h average road traffic noise level (LAeq16hr) [range 45-75 dB(A)]. Important sources of heterogeneity were the age and sex of the population under study, the way exposure was ascertained, and the noise reference level used. Also the way noise was treated in the statistical model and the minimum years of residence of the population under study, gave an explanation of the observed heterogeneity. No definite conclusions can be drawn about the threshold value for the relationship between road traffic noise and the prevalence of hypertension.Based on the meta-analysis, a quantitative relationship is derived that can be used for health impact assessment. The results of this meta-analysis are consistent with a slight increase of cardiovascular disease risk in populations exposed to transportation noise.

The hypothesis that prolonged exposure to road traffic noise causes ischaemic heart disease (IHD) was tested in two case-control studies including a cross-sectional study of middle-aged men. In the Berlin traffic noise studies, comprising a prestudy and a main study, interviews were conducted with 109 and 645 male patients (survivers) with acute myocardial infarction (MI) and 134 and 3390 controls, respectively, residing in Berlin for at least 15 y. The subjects were aged from 41–70 y. The odds ratio (95% confidence interval) of IHD incidence was 1.3 (0.5–3.8) in the pre- and 1.2 (0.8–1.7) in the main study for men in the highest noise category (71–80 dB (A)) as compared to the lowest noise category (51–60 dB (A)) after adjustment for potentially confounding factors. In a subsample of men who had not moved within the past 15 y, the odds ratio was 1.2 (0.3–4.1) in the pre- and 1.3 (0.9–2.0) in the main study, the latter borderline significant (p < 0.10). Cross-sectional analyses among the random sample of controls who had not moved within the past 15 y revealed for men in the highest noise category a relative prevalence of 1.2 (0.7–2.1) for self-reported MI and 1.4 (0.9–2.0) for the relative prevalence of gastro-intestinal ulcers.

Background and Aims: Laboratory experiments on humans and animals, occupational noise studies with high noise levels and transportation noise studies with lower noise levels support the evidence th...

As part of the Caerphilly and the Speedwell collaborative heart disease studies, associations between outdoor traffic noise level, risk factors for ischemic heart disease, and prevalence and incidence of ischemic heart disease were studied in two samples of 2,512 and 2,348 men, respectively, who were 45-63 y of age. Compared with the lowest noise category [Leq,6-22 h = 51-55 dB(A)], the subjects in the highest noise category [Leq,6-22 = 66-70 dB(A)] showed a slightly worse risk factor profile with respect to 9 identified endogenous risk factors. Logistic regression analysis suggested a marginal increase in risk (relative risk = 1.1) for ischemic heart disease incidence for these men based on risk factors. The prevalence of ischemic heart disease was slightly higher (relative risk = 1.2) in this noise group. The observed incidence of major ischemic heart disease within an observation period of approximately 4 y was slightly lower (relative risk = 0.8) for men in the highest noise group.

Objective To study the association between exposure to transportation noise and blood pressure (BP) reduction during nighttime sleep. Methods 24-h ambulatory BP measurements at 15-min intervals were carried out on 149 persons living near four major European airports. Noise indicators included total and source-specific equivalent indoor noise, total number of noise events, annoyance scores for aircraft and road traffic nighttime noise. Long-term noise exposure was also determined. Multivariate linear regression analysis was applied. Results The pooled estimates show that the only noise indicator associated consistently with a decrease in BP dipping is road traffic noise. The effect shows that a 5 dB increase in measured road traffic noise during the study night is associated with 0.8% (−1.55, −0.05) less dipping in diastolic BP. Noise from aircraft was not associated with a decrease in dipping, except for a non-significant decrease noted in Athens, where the aircraft noise was higher. Noise from indoor sources did not affect BP dipping. Conclusions Road traffic noise exposure may be associated with a decrease in dipping. Noise from aircraft was not found to affect dipping in a consistent way across centres and indoor noise was not associated with dipping.

The German Federal Environment Agency carried out its fourth German Environmental Survey (GerES IV), which is the first survey on children only and the environment-related module of the German Health Interview and Examination Survey for Children and Adolescents (German acronym: KiGGS), conducted by the Robert Koch Institute (RKI). The German Environmental Surveys are nationwide population studies conducted to determine the exposure to environmental pollutants, to explore exposure pathways and to identify sub-groups with higher exposure. GerES IV was conducted on randomly selected 1790 children aged 3–14 years from the cross-sectional sample of KiGGS. The participants of GerES IV lived in 150 sampling locations all over Germany. Field work was carried out from May 2003 to May 2006. The response rate in GerES IV was 77.3%. Due to the fact that participation in GerES IV was limited to children that had previously participated in the KiGGS study, the total response rate in GerES IV resulted in 52.6%. Response rates did neither differ significantly between West and East Germany, nor between different community sizes, age groups and gender. The basic study programme included blood samples, morning urine, tap water and house dust as well as comprehensive questionnaire-based interviews. In addition, subgroups were studied with regard to “noise, hearing capacity and stress hormones”, “chemical contamination of indoor air” and “biogenic indoor contamination”. A key element of the field work in GerES IV was a home visit to carry out interviews, conduct measurements and collect samples. An exception was blood sampling which was carried out within KiGGS. The quality of field work, data collection, evaluation, and chemical, biological and physical analyses was successfully evaluated by internal and external quality assurance. This comprehensive overview aims at giving other research groups the opportunity to compare different study designs or to adapt their own design to get comparable results.

Noise is a stressor that affects the autonomic nervous system and the endocrine system. Under conditions of chronic noise stress the cardiovascular system may adversely be affected. Epidemiological noise studies regarding the relationship between aircraft noise and cardiovascular effects have been carried out on adults and on children focussing on mean blood pressure, hypertension and ischemic heart diseases as cardiovascular endpoints. While there is evidence that road traffic noise increases the risk of ischemic heart disease, including myocardial infarction, there is less such evidence for such an association with aircraft noise. This is partly due to the fact that large scale clinical studies are missing. There is sufficient qualitative evidence, however, that aircraft noise increases the risk of hypertension in adults. Regarding aircraft noise and children's blood pressure the results are still inconsistent. The available literature was evaluated for the WHO working group on "Aircraft Noise and Health" based on the experts' comprehensive knowledge in this field. With respect to the needs of a quantitative risk assessment for burden of disease calculations an attempt was made to derive an exposure-response relationship based on a meta-analysis. This association must be viewed as preliminary due to limitations which are concerned with the pooling of studies due to methodological differences in the assessment of exposure and outcome between studies. More studies are needed to establish better estimates of the risk.

Objectives The German Environment Agency carried out its fourth German Environmental Survey (GerES IV) from 2003 to 2006, which was especially for children. 1048 children, 8–14 years of age, were randomly selected from all over Germany. The sample is representative of children in this age group living in Germany with respect to gender, community size, and region. Methods Blood pressure was measured under standardized conditions at clinical study centers. During home visits the children and their parents were asked about leisure activities, housing conditions and environmental factors, including traffic exposure of their homes. Orientating short-term noise measurements were carried out in front of the children's (bed-) room to validate the subjective ratings of the traffic volume (categories: no street, low, moderately, high/extremely high). Results With respect to the subjective rating of “type of street” (traffic volume) the lowest blood pressure readings were found in children whose room was facing a street with ‘low traffic’. The highest readings were found in the group where the children's rooms were facing a street with a ‘high or extremely high traffic’ volume. The difference between the two groups was 1.8 mm Hg (95% CI: 0.1 to 3.5, p = 0.036) for systolic and 1.0 mm Hg (95% CI: − 0.4 to 2.4, p = 0.148) for diastolic blood pressure. With respect to the short-term noise measurements, significant blood pressure increases of 1.0 mm Hg (95% CI: 0.3 to 1.6, p = 0.004) and 0.6 mm Hg (95% CI: 0.1 to 1.2, p = 0.025), respectively, were found per 10 dB(A) increment of the noise level. Conclusions The results show that road traffic noise at home is a stressor that could affect children's blood pressure.

Studies on the association between community noise and cardiovascular risk were subjected to a meta-analysis for deriving a common dose-effect curve. Peer-reviewed articles, objective assessment of exposure and outcome as well as control for confounding and multiple exposure categories were all necessary inclusion criteria. A distinction was made between descriptive (cross-sectional) and analytical (case-control, cohort) studies. Meta-analyses were carried out for two descriptive and five analytical studies for calculating a pooled dose-effect curve for the association between road traffic noise levels and the risk of myocardial infarction. No increase in risk was found below 60 dB(A) for the average A-weighted sound pressure levels during the day. An increase in risk was found with increasing noise levels above 60 dB(A) thus showing a dose-response relationship. A risk curve was estimated for the association using a polynomial fit of the data that can be used for risk assessment and the environmental burden of disease calculations.

Within the framework of the HYENA (hypertension and exposure to noise near airports) project we investigated the effect of short-term changes of transportation or indoor noise levels on blood pressure (BP) and heart rate (HR) during night-time sleep in 140 subjects living near four major European airports.Non-invasive ambulatory BP measurements at 15 min intervals were performed. Noise was measured during the night sleeping period and recorded digitally for the identification of the source of a noise event. Exposure variables included equivalent noise level over 1 and 15 min and presence/absence of event (with LAmax35 dB) before each BP measurement. Random effects models for repeated measurements were applied. An increase in BP (6.2 mmHg (0.63-12) for systolic and 7.4 mmHg (3.1, 12) for diastolic) was observed over 15 min intervals in which an aircraft event occurred. A non-significant increase in HR was also observed (by 5.4 b.p.m.). Less consistent effects were observed on HR. When the actual maximum noise level of an event was assessed there were no systematic differences in the effects according to the noise source.Effects of noise exposure on elevated subsequent BP measurements were clearly shown. The effect size of the noise level appears to be independent of the noise source.

Laboratory experiments and field measurements were carried out to determine relevant acute and long term effects of noise from low-flying military aircraft. Acute effects on the cardiovascular system were established under simulation conditions. Blood pressure, heart rate, and biochemical stress parameters (cortisol and catecholamines, renin and free fatty acids in blood) were measured as a function of time. Long-term effects of noise from low-flying aircraft were analyzed in 10 to 13-year-old children by comparative studies including a 75 m low-altitude flight area and a neighbouring area with flight altitudes of 150–450 m. Significantly higher blood pressure values were found in girls in the 75 m area. The hearing thresholds were significantly increased in boys and girls in the 75 m area. Altogether, acute effects of noise from low-flying aircraft on cardiovascular functions and hearing ability could be proved, and potential risks of long-term exposure to low-altitude flight noise are discussed.

As part of two large heart surveys, associations between traffic noise exposure and cardiovascular risk factors were studied. The Caerphilly sample (small town, total sample) consisted of 2512 men aged 45 to 59 years and the Speedwell sample (suburb of a major city, random sample) of 2030 men of same age group. Both studies have a prospective design; cross-sectional results are presented here. Acoustic measurements were carried out in both areas. Among the possible risk factors for ischaemic heart disease studied were blood pressure, blood coagulation, blood lipids and other biochemical factors. Statistically significant noise effects were detected for systolic blood pressure, total cholesterol, HDL cholesterol, total triglycerides, blood viscosity, platelet count and glucose level, although not all of these were consistent with noise being a risk factor for heart disease. In a subsample, the additional influence of work noise as determined by noise dosimetry was studied in 255 men, taking the use of ear protection into account. The associations between traffic noise and risk factors were more pronounced in men who also were exposed to high work noise levels.

Objectives: To evaluate existing research on the environmental health of children and provide a prioritised list of risk factors and policy recommendations for action, the Policy Interpretation Network on Children's Health and Environment (PINCHE) was set up within EU FP5 (QLK4-2002-02395). The project focused on air pollutants, carcinogens, neurotoxicants and noise. PINCHE was a multidisciplinary and multinational network of representatives from science, industry, NGOs, and consumer and patient organisations in Europe. Materials and methods: A literature search was performed using the Pubmed, Embase and Toxline databases. The quality of the gathered articles was assessed and their information and relevance was interpreted within a systematic framework. Information related to exposure, epidemiology, and toxicology was analysed separately and then a risk evaluation of particular environmental factors was made. Socioeconomic factors were specifically taken into account. The results were compiled, and considering the present regulatory situation, policy recommendations for action were made. Finally, the risk factors and policy recommendations were prioritised through a process of discussion between all the partners. Results and conclusions: PINCHE concluded that outdoor air pollutants (especially traffic-related), environmental tobacco smoke, allergens, and mercury were high priorities with an urgent need for action. Brominated flame retardants, lead, PCBs and dioxins, ionising and solar radiation, and some noise sources were classified as being of medium priority. Some toxins were given low priority, based on few exposed children, relatively mild health effects or an improving situation due to past policy measures. We recognise the shortcomings of such a prioritisation and, though some measures are more urgent than others, emphasise that ideally all policy measures should be carried out without delay for all toxins. This priority list must be continuously revised, the precautionary principle should be central to all decisions, and the focus should be on safe exposure levels for children.

Noise is pervasive in everyday life and induces both auditory and non-auditory health effects. Systematic research of the effects of noise on the cardiovascular system has been carried out for more than 50 decades. Noise is a stressor that affects the autonomic nervous system and the endocrine system. Animal experiments, laboratory and field studies carried out on humans provide evidence that persistent exposure to environmental noise affects physiological endpoints, which in turn are adversely associated with cardiovascular diseases. These include hypertension, coronary heart disease, and stroke. New endpoints have been studied, including clinical states of metabolic syndrome such as diabetes mellitus. Chronic sleep disturbance is considered as an important mediator of the effects. Public health policies rely on quantitative risk assessment to set environmental quality standards and to regulate the noise exposure that is generated by environmental noise sources in the communities. Meta-analyses were carried out to derive exposure-response relationships between noise and cardiovascular health. Most of the epidemiological studies refer to road traffic and aircraft noise. No biologically determined threshold values can be determined. Cardiovascular effects due to noise and traffic-related air pollutants are largely independent of one another due to different biological mechanisms.

Background: Noise can have auditory and non-auditory effects on children. Very few noise episodes affect children's hearing instantaneously; most effects are long-term and cumulative. Describing the risks of noise on children's health and well-being in a life-course perspective can illustrate the prospects of cumulative effects. Conclusion: The policy recommendations the Policy Interpretation Network on Children's Health and Environment (PINCHE) prepared for each age group or setting are described here.

Summary Traffic noise causes a lot of concern in the population. It annoys, disturbs sleep and can cause cardiovascular problems in chronically noise-exposed subjects. Approximately 50 million people in the European community are exposed to sound levels from road traffic at home, that are suspected of increasing the risk of cardiovascular disorders. The noise effects hypothesis is based on the general stress model. The mechanism includes arousal of the sympathetic and endocrine system. Heart rate, blood pressure, stress hormones and classical biological risk factors of ischaemic heart disease (IHD) are affected by the noise. In epidemiological studies, subjects who live in noise exposed areas show a higher prevalence of high blood pressure and IHD (including myocardial infarction). It is estimated that approximately 3 per cent of IHD cases in the general population may be attributed to traffic noise.

Compared to other environmental issues, only a limited number of epidemiological studies is available on the relationship between traffic noise and cardiovascular diseases. The available literature provides no epidemiological evidence of a relationship between noise exposure and mean blood pressure readings in adults. However, noise-related increases in blood pressure are consistently seen in children. As far as hypertension as a clinical outcome is concerned, there is little evidence that exposure to high traffic noise levels is associated with an increased risk. With regard to ischaemic heart disease there is some evidence in the literature of an increased risk in subjects who live in noisy areas with outdoor noise levels of greater than 65-70 dBA.

Reviews of epidemiological studies of cardiovascular effects of occupational noise have been published regularly in the literature. The first part of this paper summarises the conclusions which have been drawn. The second part focuses in more detail on the results of studies in which noise exposure was not assessed by objective measurements, but on the basis of subjective ratings as given by the study subjects in a questionnaire. Finally, the paper addresses some issues of occupational noise studies which deserve special attention from the methodological and conceptual point of view. These are concerned with study design, statistical inference, selection and confounding bias, overcontrolling, effect modification and exposure misclassification.

Noise has the potential to cause stress reactions. Chronic noise-induced stress accelerates the ageing of the myocardium and thus increase the risk of myocardial infarction. The involved pathomechanisms include acute increase of catecholamines or cortisol under acute noise exposure and an interaction between endocrine reactions and intracellular Ca/Mg shifts. Chronic noise exposure of animals on a diet with suboptimal magnesium content led to increase of connective tissue and calcium, and decrease of magnesium in the myocardium. These changes were correlated to noradrenaline and normal ageing. Post mortem studies of hearts from victims of ischemic heart diseases confirmed the importance of Ca/Mg shifts in humans. Recent epidemiological studies support the importance of noise as a risk factor in circulatory and heart diseases, especially in myocardial infarction.

In principle, the noise/stress hypothesis is well understood: Noise activates the pituitary-adrenal-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 cost-effectiveness, 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 effect-modifying factors, and the role of annoyance as a mediator of effect are issues for future research in this field.

The authors tested the hypothesis that prolonged exposure to road traffic noise causes ischemic heart disease in a 10-y follow-up cohort study of middle-aged men. In the Caerphilly and Speedwell studies, 2512 and 2348 men, respectively, who were 45-59 y of age were seen in the initial cross-sectional phase and at follow-up intervals of 10 y. Adjusted odds ratios of 1.1 (95% confidence interval = 0.6, 1.9) and 0.9 (95% confidence interval = 0.6, 1.4) were found in the total cohorts. However, the relative risk was 1.3 (95% confidence interval = 0.8, 2.2) in the pooled reconstructed cohort of men who were followed for 6 y (i.e., from phase 2 to phase 3) and for whom room orientation and window-opening habits could be considered. Furthermore, the relative risk increased to 1.6 (95% confidence interval = 0.9, 3.0) in the subsample of men who had lived at least 15 y in their present homes at the time of recruitment. Living adjacent to streets with high traffic noise levels was associated with an adjusted (for covariates) increase in relative risk of 1.01-1.02/y in residence--a result that was only borderline significant (p < .10).