Auditory and non-auditory effects of noise on health

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Abstract

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. Copyright © 2014 Elsevier Ltd. All rights reserved.

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Most cited references 67

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Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010

Theo Vos, Abraham D. Flaxman, Mohsen Naghavi … (2013)

Non-fatal health outcomes from diseases and injuries are a crucial consideration in the promotion and monitoring of individual and population health. The Global Burden of Disease (GBD) studies done in 1990 and 2000 have been the only studies to quantify non-fatal health outcomes across an exhaustive set of disorders at the global and regional level. Neither effort quantified uncertainty in prevalence or years lived with disability (YLDs). Of the 291 diseases and injuries in the GBD cause list, 289 cause disability. For 1160 sequelae of the 289 diseases and injuries, we undertook a systematic analysis of prevalence, incidence, remission, duration, and excess mortality. Sources included published studies, case notification, population-based cancer registries, other disease registries, antenatal clinic serosurveillance, hospital discharge data, ambulatory care data, household surveys, other surveys, and cohort studies. For most sequelae, we used a Bayesian meta-regression method, DisMod-MR, designed to address key limitations in descriptive epidemiological data, including missing data, inconsistency, and large methodological variation between data sources. For some disorders, we used natural history models, geospatial models, back-calculation models (models calculating incidence from population mortality rates and case fatality), or registration completeness models (models adjusting for incomplete registration with health-system access and other covariates). Disability weights for 220 unique health states were used to capture the severity of health loss. YLDs by cause at age, sex, country, and year levels were adjusted for comorbidity with simulation methods. We included uncertainty estimates at all stages of the analysis. Global prevalence for all ages combined in 2010 across the 1160 sequelae ranged from fewer than one case per 1 million people to 350,000 cases per 1 million people. Prevalence and severity of health loss were weakly correlated (correlation coefficient -0·37). In 2010, there were 777 million YLDs from all causes, up from 583 million in 1990. The main contributors to global YLDs were mental and behavioural disorders, musculoskeletal disorders, and diabetes or endocrine diseases. The leading specific causes of YLDs were much the same in 2010 as they were in 1990: low back pain, major depressive disorder, iron-deficiency anaemia, neck pain, chronic obstructive pulmonary disease, anxiety disorders, migraine, diabetes, and falls. Age-specific prevalence of YLDs increased with age in all regions and has decreased slightly from 1990 to 2010. Regional patterns of the leading causes of YLDs were more similar compared with years of life lost due to premature mortality. Neglected tropical diseases, HIV/AIDS, tuberculosis, malaria, and anaemia were important causes of YLDs in sub-Saharan Africa. Rates of YLDs per 100,000 people have remained largely constant over time but rise steadily with age. Population growth and ageing have increased YLD numbers and crude rates over the past two decades. Prevalences of the most common causes of YLDs, such as mental and behavioural disorders and musculoskeletal disorders, have not decreased. Health systems will need to address the needs of the rising numbers of individuals with a range of disorders that largely cause disability but not mortality. Quantification of the burden of non-fatal health outcomes will be crucial to understand how well health systems are responding to these challenges. Effective and affordable strategies to deal with this rising burden are an urgent priority for health systems in most parts of the world. Bill & Melinda Gates Foundation. Copyright © 2012 Elsevier Ltd. All rights reserved.

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Acceleration of age-related hearing loss by early noise exposure: evidence of a misspent youth.

Sharon G Kujawa, M Charles Liberman (2006)

Age-related and noise-induced hearing losses in humans are multifactorial, with contributions from, and potential interactions among, numerous variables that can shape final outcome. A recent retrospective clinical study suggests an age-noise interaction that exacerbates age-related hearing loss in previously noise-damaged ears (Gates et al., 2000). Here, we address the issue in an animal model by comparing noise-induced and age-related hearing loss (NIHL; AHL) in groups of CBA/CaJ mice exposed identically (8-16 kHz noise band at 100 dB sound pressure level for 2 h) but at different ages (4-124 weeks) and held with unexposed cohorts for different postexposure times (2-96 weeks). When evaluated 2 weeks after exposure, maximum threshold shifts in young-exposed animals (4-8 weeks) were 40-50 dB; older-exposed animals (> or =16 weeks) showed essentially no shift at the same postexposure time. However, when held for long postexposure times, animals with previous exposure demonstrated AHL and histopathology fundamentally unlike unexposed, aging animals or old-exposed animals held for 2 weeks only. Specifically, they showed substantial, ongoing deterioration of cochlear neural responses, without additional change in preneural responses, and corresponding histologic evidence of primary neural degeneration throughout the cochlea. This was true particularly for young-exposed animals; however, delayed neuropathy was observed in all noise-exposed animals held 96 weeks after exposure, even those that showed no NIHL 2 weeks after exposure. Data suggest that pathologic but sublethal changes initiated by early noise exposure render the inner ears significantly more vulnerable to aging.

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Annoyance from transportation noise: relationships with exposure metrics DNL and DENL and their confidence intervals.

H M Miedema, C Oudshoorn (2001)

We present a model of the distribution of noise annoyance with the mean varying as a function of the noise exposure. Day-night level (DNL) and day-evening-night level (DENL) were used as noise descriptors. Because the entire annoyance distribution has been modeled, any annoyance measure that summarizes this distribution can be calculated from the model. We fitted the model to data from noise annoyance studies for aircraft, road traffic, and railways separately. Polynomial approximations of relationships implied by the model for the combinations of the following exposure and annoyance measures are presented: DNL or DENL, and percentage "highly annoyed" (cutoff at 72 on a scale of 0-100), percentage "annoyed" (cutoff at 50 on a scale of 0-100), or percentage (at least) "a little annoyed" (cutoff at 28 on a scale of 0-100). These approximations are very good, and they are easier to use for practical calculations than the model itself, because the model involves a normal distribution. Our results are based on the same data set that was used earlier to establish relationships between DNL and percentage highly annoyed. In this paper we provide better estimates of the confidence intervals due to the improved model of the relationship between annoyance and noise exposure. Moreover, relationships using descriptors other than DNL and percentage highly annoyed, which are presented here, have not been established earlier on the basis of a large dataset.

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Author and article information

Journal

Title: The Lancet

Abbreviated Title: The Lancet

Publisher: Elsevier BV

ISSN (Print): 01406736

Publication date Created: April 2014

Publication date (Print): April 2014

Volume: 383

Issue: 9925

Pages: 1325-1332

Article

DOI: 10.1016/S0140-6736(13)61613-X

PMC ID: 3988259

PubMed ID: 24183105

SO-VID: 3188b315-003f-4b57-9419-a6c2c77de670

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https://www.elsevier.com/tdm/userlicense/1.0/

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