Effects Of Environmental Noise Exposure Research Articles

Sex/Gender-Differences in the Health Effects of Environmental Noise Exposure on Hypertension and Ischemic Heart Disease-A Systematic Review.

Previous studies have demonstrated cardiovascular health effects of environmental noise exposure, partly showing different effect estimates for males and females. This cannot be explained by biological differences between males and females alone. It is assumed that health outcomes and exposure patterns also depend on gender, determined by social, economic, and cultural factors in society. This systematic review evaluated the current state of how sex/gender is integrated in studies on environmental noise associated with hypertension, blood pressure, and ischemic heart diseases. A systematic literature search was conducted in three different databases, identifying thirty studies published between 1 January 2000 and 2 February 2020. Effects varied, with no consistent findings for both males and females. All studies used a binary operationalization of sex/gender, assuming static differences between males and females. The differentiation between biological and social dimensions of sex/gender was not present in any of the studies and the terms “sex” and “gender” were used interchangeably. However, biological and social dimensions of sex/gender were unconsciously taken up in the discussion of the results. Integrating sex/gender-theoretical concepts into future studies offers great potential to increase the validity of research findings, thus making them more useful for prevention efforts, health promotion, and health care.

Noise‐induced vascular dysfunction, oxidative stress and inflammationare improved by pharmacological heme oxygenase‐1 induction

Endothelial dysfunction, vascular oxidative stress and inflammation are consequences of traditional cardiovascular risk factors and triggers of cardiovascular disease. However, emerging environmental stressors such as traffic noise exposure may facilitate the development of cardiovascular and metabolic diseases.C57BL/6J mice were exposed to aircraft noise (maximum sound level of 85 dB(A), average sound pressure level of 72 dB(A)) applied for 1, 2 and 4 days caused an increase in systolic blood pressure, stress hormones and induced endothelial dysfunction, oxidative stress and inflammation (Eur Heart J 2017). We also observed reduced vascular NO levels due to eNOS uncoupling and increased levels of nitrotyrosine, interleukin‐6, NADPH oxidase isoform Nox2 and endothelin‐1 in the mice exposed to aircraft noise. More recently, we have shown that aircraft noise induces also cerebral oxidative stress and a neuroinflammatory phenotype that is up‐stream of the observed adverse cardiovascular effects, all of which was normalized by genetic deletion of NADPH oxidase isoform Nox2 (Eur Heart J 2018).The role of heme oxygenase‐1 (HO‐1) as an antioxidant response is currently being investigated. C57BL/6J mice were treated with the HO‐1 activator hemin (25 mg/kg i.p.). Our preliminary data show a protective effect of hemin infusion on aircraft noise exposure (4 days) induced increase of systolic blood pressure and vascular dysfunction. There was also a trend of normalization of noise‐triggered oxidative stress ny hemin infusion. Within the ongoing studies, we will address the impact of HO‐1 induction in noise‐exposed mice on expression of genes and proteins involved in pathways of oxidative stress and systemic inflammation. In a later stage of the study, we will also test whether genetic deficiency of HO‐1 (HO‐1+/− mice) aggravates and the Nrf2 activator dimethyl fumarate (DMF) ameliorates noise‐triggered cardiovascular complications. The present study aims at identifying new targets for mitigation strategies against adverse health effects of environmental noise exposure of the general population. Since HO‐1 and Nrf2 induction can be achieved by natural dietary constituents, these pathways represent promising targets for preventive measures.Support or Funding InformationOur experimental studies on noise effects in mice were supported by vascular biology research grants from the Else‐Kröner‐Fresenius Foundation for “Noise and arterial hypertension” (2017_A106) and the Boehringer Ingelheim Foundation for the collaborative research group „Novel and neglected cardiovascular risk factors: molecular mechanisms and therapeutic implications”.

Sex/gender differences in the association of environmental noise exposure and cardiovascular health - systematic review and meta-analysis

TPS 781: Health effects of noise, Exhibition Hall, Ground floor, August 27, 2019, 3:00 PM - 4:30 PM Epidemiological studies have demonstrated cardiovascular health effects of environmental noise exposure with some showing different effect estimates for males and females. However, results are far from being consistent. There is a need to disentangle the impact of biological sex and gender including social role or cultural norms and the interplay of both. Our objective is to evaluate the current state of integrating sex/gender into environmental noise epidemiology and to quantify the sex/gender specific effects of noise from different sources on cardiovascular health outcomes. We conducted a systematic literature search using the electronic databases PubMed and Web of Science (WoS). Publications in English or German between 2000 and 2019 which provide sex/gender specific effect estimates for short- and long-term associations between noise and ischemic heart disease (IHD) as well as blood pressure and hypertension were screened. We will review the studies concerning conceptualization and operationalization of sex/gender, report male and female specific baseline characteristics, exposure and health data as well as discuss the sex/gender specific results. After study quality rating sex/gender specific effects will be quantified by applying meta-analytic tools. Of 247 and 194 identified articles in Pubmed and WoS, respectively, 33 studies met our inclusion criteria, of which 12 studies deal with IHD, 19 studies with hypertension and 8 studies with blood pressure. The studies cover noise from road (N=24), aircraft (N=8) and railway traffic (N= 4) as well as community noise (N=6). Preliminary results show that studies generally used a dichotomous category “male/female”, did not contain information on a clear conceptualization and missed a gainful discussion of their sex-specific results. In the next steps we will continue with the extraction of necessary information and preparation of meta-analysis where possible.

The Adverse Effects of Environmental Noise Exposure on Oxidative Stress and Cardiovascular Risk.

Epidemiological studies have provided evidence that traffic noise exposure is linked to cardiovascular diseases such as arterial hypertension, myocardial infarction, and stroke. Noise is a nonspecific stressor that activates the autonomous nervous system and endocrine signaling. According to the noise reaction model introduced by Babisch and colleagues, chronic low levels of noise can cause so-called nonauditory effects, such as disturbances of activity, sleep, and communication, which can trigger a number of emotional responses, including annoyance and subsequent stress. Chronic stress in turn is associated with cardiovascular risk factors, comprising increased blood pressure and dyslipidemia, increased blood viscosity and blood glucose, and activation of blood clotting factors, in animal models and humans. Persistent chronic noise exposure increases the risk of cardiometabolic diseases, including arterial hypertension, coronary artery disease, diabetes mellitus type 2, and stroke. Recently, we demonstrated that aircraft noise exposure during nighttime can induce endothelial dysfunction in healthy subjects and is even more pronounced in coronary artery disease patients. Importantly, impaired endothelial function was ameliorated by acute oral treatment with the antioxidant vitamin C, suggesting that excessive production of reactive oxygen species contributes to this phenomenon. More recently, we introduced a novel animal model of aircraft noise exposure characterizing the underlying molecular mechanisms leading to noise-dependent adverse oxidative stress-related effects on the vasculature. With the present review, we want to provide an overview of epidemiological, translational clinical, and preclinical noise research addressing the nonauditory, adverse effects of noise exposure with focus on oxidative stress. Antioxid. Redox Signal. 28, 873–908.

WHO Environmental Noise Guidelines for the European Region: A Systematic Review on Environmental Noise and Effects on Sleep.

To evaluate the quality of available evidence on the effects of environmental noise exposure on sleep a systematic review was conducted. The databases PSYCINFO, PubMed, Science Direct, Scopus, Web of Science and the TNO Repository were searched for non-laboratory studies on the effects of environmental noise on sleep with measured or predicted noise levels and published in or after the year 2000. The quality of the evidence was assessed using GRADE criteria. Seventy four studies predominately conducted between 2000 and 2015 were included in the review. A meta-analysis of surveys linking road, rail, and aircraft noise exposure to self-reports of sleep disturbance was conducted. The odds ratio for the percent highly sleep disturbed for a 10 dB increase in Lnight was significant for aircraft (1.94; 95% CI 1.61–2.3), road (2.13; 95% CI 1.82–2.48), and rail (3.06; 95% CI 2.38–3.93) noise when the question referred to noise, but non-significant for aircraft (1.17; 95% CI 0.54–2.53), road (1.09; 95% CI 0.94–1.27), and rail (1.27; 95% CI 0.89–1.81) noise when the question did not refer to noise. A pooled analysis of polysomnographic studies on the acute effects of transportation noise on sleep was also conducted and the unadjusted odds ratio for the probability of awakening for a 10 dBA increase in the indoor Lmax was significant for aircraft (1.35; 95% CI 1.22–1.50), road (1.36; 95% CI 1.19–1.55), and rail (1.35; 95% CI 1.21–1.52) noise. Due to a limited number of studies and the use of different outcome measures, a narrative review only was conducted for motility, cardiac and blood pressure outcomes, and for children’s sleep. The effect of wind turbine and hospital noise on sleep was also assessed. Based on the available evidence, transportation noise affects objectively measured sleep physiology and subjectively assessed sleep disturbance in adults. For other outcome measures and noise sources the examined evidence was conflicting or only emerging. According to GRADE criteria, the quality of the evidence was moderate for cortical awakenings and self-reported sleep disturbance (for questions that referred to noise) induced by traffic noise, low for motility measures of traffic noise induced sleep disturbance, and very low for all other noise sources and investigated sleep outcomes.

WHO Environmental Noise Guidelines for the European Region: A Systematic Review on Environmental Noise and Cardiovascular and Metabolic Effects: A Summary.

To update the current state of evidence and assess its quality, we conducted a systematic review on the effects of environmental noise exposure on the cardio-metabolic systems as input for the new WHO environmental noise guidelines for the European Region. We identified 600 references relating to studies on effects of noise from road, rail and air traffic, and wind turbines on the cardio-metabolic system, published between January 2000 and August 2015. Only 61 studies, investigating different end points, included information enabling estimation of exposure response relationships. These studies were used for meta-analyses, and assessments of the quality of evidence using the Grading of Recommendations Assessment, Development and Evaluation (GRADE). A majority of the studies concerned traffic noise and hypertension, but most were cross-sectional and suffering from a high risk of bias. The most comprehensive evidence was available for road traffic noise and Ischeamic Heart Diseases (IHD). Combining the results of 7 longitudinal studies revealed a Relative Risk (RR) of 1.08 (95% CI: 1.01–1.15) per 10 dB (LDEN) for the association between road traffic noise and the incidence of IHD. We rated the quality of this evidence as high. Only a few studies reported on the association between transportation noise and stroke, diabetes, and/or obesity. The quality of evidence for these associations was rated from moderate to very low, depending on transportation noise source and outcome. For a comprehensive assessment of the impact of noise exposure on the cardiovascular and metabolic system, we need more and better quality evidence, primarily based on longitudinal studies.

Public health implications of environmental noise associated with unconventional oil and gas development.

Modern oil and gas development frequently occurs in close proximity to human populations and increased levels of ambient noise have been documented throughout some phases of development. Numerous studies have evaluated air and water quality degradation and human exposure pathways, but few have evaluated potential health risks and impacts from environmental noise exposure. We reviewed the scientific literature on environmental noise exposure to determine the potential concerns, if any, that noise from oil and gas development activities present to public health. Data on noise levels associated with oil and gas development are limited, but measurements can be evaluated amidst the large body of epidemiology assessing the non-auditory effects of environmental noise exposure and established public health guidelines for community noise. There are a large number of noise dependent and subjective factors that make the determination of a dose response relationship between noise and health outcomes difficult. However, the literature indicates that oil and gas activities produce noise at levels that may increase the risk of adverse health outcomes, including annoyance, sleep disturbance, and cardiovascular disease. More studies that investigate the relationships between noise exposure and human health risks from unconventional oil and gas development are warranted. Finally, policies and mitigation techniques that limit human exposure to noise from oil and gas operations should be considered to reduce health risks.

Effects of environmental noise exposure on DNA methylation in the brain and metabolic health

Environmental noise exposure is associated with adverse effects on human health including hearing loss, heart disease, and changes in stress-related hormone levels. Alteration in DNA methylation in response to environmental exposures is a well-known phenomenon and it is implicated in many human diseases. Understanding how environmental noise exposures affect DNA methylation patterns may help to elucidate the link between noise and adverse effects on health. In this pilot study we examined the effects of environmental noise exposure on DNA methylation of genes related to brain function and investigated whether these changes are related with metabolic health. We exposed four groups of male Wistar rats to moderate intensity noise (70–75dB with 20–4000Hz) at night for three days as short-term exposure, and for three weeks as long-term exposure. Noise exposure was limited to 45dB during the daytime. Control groups were exposed to only 45dB, day and night. We measured DNA methylation in the Bdnf, Comt, Crhr1, Mc2r, and Snca genes in tissue from four brain regions of the rats (hippocampus, frontal lobe, medulla oblongata, and inferior colliculus). Further, we measured blood pressure and body weight after long-term noise exposure. We found that environmental noise exposure is associated with gene-specific DNA methylation changes in specific regions of the brain. Changes in DNA methylation are significantly associated with changes in body weight (between Bdnf DNA methylation and Δ body weight: r=0.59, p=0.018; and between LINE-1 ORF DNA methylation and Δ body weight: =−0.80, p=0.0004). We also observed that noise exposure decreased blood pressure (p=0.038 for SBP, p=0.017 for DBP and p 0. 017 for MAP) and decreased body weight (β=−26g, p=0.008). In conclusion, environmental noise exposures can induce changes in DNA methylation in the brain, which may be associated with adverse effects upon metabolic health through modulation of response to stress-related hormones.

Auditory and non-auditory effects of noise on health: An ICBEN perspective

Noise is pervasive in everyday life and induces both auditory and non-auditory health effects. Noise-induced hearing loss remains the most common occupational disease in the United States, but is also increasingly caused by social noise exposure (e.g., through music players). Simultaneously, evidence on the public health impact of non-auditory effects of environmental noise exposure is growing. According to the World Health Organization (WHO), ca. 1.6 Million healthy life years (DALYs) are lost annually in the western member states of the European Union due to exposure to environmental noise. The majority (>90%) of these effects can be attributed to noise-induced sleep disturbance and community annoyance, but noise may also interfere with communication and lead to cognitive impairment of children. Epidemiological studies increasingly support an association of long-term noise exposure with the incidence of hypertension and cardiovascular disease. Up-to-date exposure-response relationships are needed for health impact assessments, to reassess the validity of current noise policy and to better mitigate the negative health consequences of noise. The International Commission on Biological Effects of Noise (ICBEN) is a non-profit organization constituted 1978 that promotes all aspects of noise effects research and its application through International Noise Teams and an International Congress every three years.

Cardiovascular effects of environmental noise exposure

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.

Impact of environmental noise on growth and neuropsychological development of newborn rats

We aimed to investigate the effects of environmental noise exposure on the growth and neuropsychological development in neonatal rats. Twenty-four postnatal 7-day-old Sprague-Dawley rats were randomly assigned into control, high-noise and reduced noise groups. The rats in the high-noise group were exposed to 90 dB white noise, and those in the control group were grown under standard condition, while those in the reduced noise group were exposed to standard condition with sound-absorbing cotton. Ten, 15, and 20 days post noise exposure, both the body weight and length of the rats in high-noise group were lower than those in the control and reduced noise groups, respectively. The secretion of growth hormone was significantly decreased in the rats exposed to high noise environment, compared to those exposed to standard condition and reduced noise. More interestingly, the swimming distance was apparently increased and the swimming speed was significantly decreased in high-noise group compared with those in control and reduced noise groups. Importantly, the mRNA and protein levels of SYP in the rats hippocampus were significantly decreased in high-noise group compare with those in control and reduced noise groups. Similarly, the positive expression of SYP in the CA1 region of hippocampus was also significantly decreased in the high noise group rats. In conclusion, our results demonstrated that high noise exposure could decrease the production of growth hormone and SYP in neonatal rats, which may retard the growth of weight and length and the capability of learning and memory.

Effects of environmental noise exposure on 24-h ambulatory vascular properties in adults

Exposure to environmental noise has been associated with hypertension, but the related mechanism of vascular structural changes is unclear. This repeated-measure study investigated the effects of noise exposure on the 24-h ambulatory vascular structural properties in 66 adults aged 18–32 years. Individual noise exposure and personal vascular parameters were measured simultaneously in all subjects. Linear mixed-effects regressions were used to estimate the effects. A 1-A-weighted decibel (dBA) increase was significantly associated with the transient effects of 1.39 (95% confidence interval: 1.07, 1.79) %mL/mmHg in arterial compliance at nighttime but −1.70 (−2.05, −1.10) kdynes·s/cm5 in arterial resistance during the daytime and −2.38 (−3.44, −1.64) kdynes·s/cm5 in arterial resistance at nighttime among all subjects. Such effects were observed in arterial distensibility only during the daytime after the 30-min (−1.84 [−2.61, −1.29] %/mmHg) and 60-min (−2.06 [−2.95, −1.44] %/mmHg) time-lagged noise exposures. For 24-h environmental noise, a 1-dBA increment was significantly associated with a sustained increase of 1.25 (1.10, 1.42) %mL/mmHg in arterial compliance but a decrease of 2.12 (−2.51, −1.80) kdynes·s/cm5 in arterial resistance. Environmental noise exposure may have transient and sustained effects on adult vascular properties.

Acute Effects of Environmental Noise Exposure on the Control of Cardiac Output in Healthy Adults

Acute Effects of Environmental Noise Exposure on the Control of Cardiac Output in Healthy Adults

Effects of environmental noise exposure on ambulatory blood pressure in young adults

Epidemiological studies have demonstrated that environmental noise exposure is associated with hypertension in middle-aged and older populations, but the relationship in the young subpopulation and between the genders is still unclear. This panel study investigated effects of environmental noise exposure on 24-h ambulatory blood pressure in 60 adults aged 18-32 years. Individual noise exposure and personal blood pressure were measured simultaneously for 30 males and 30 females. Linear mixed-effects regression models were applied to estimate effects. Total subjects (56.6+/-16.5A-weighted decibels (dBA)) had transient elevations of 1.15 (95% CI=0.86-1.43)mmHg SBP and 1.16 (0.93-1.38)mmHg DBP at daytime, as well as 0.74 (0.21-1.26)mmHg SBP and 0.77 (0.34-1.20)mmHg DBP at nighttime, significantly associated with a 5-dBA increase in noise exposure. Such effects on SBP and DBP still persisted at the 30- and 60-min time-lagged noise exposure. Per 5-dBA increase in 24-h average noise exposure was significantly associated with sustained increments of 1.15 (0.76-1.54)mmHg SBP and 1.27 (0.96-1.58)mmHg DBP in males (57.4+/-16.0dBA), as well as the higher levels of 1.65 (1.36-1.94)mmHg SBP and 1.51 (1.27-1.75)mmHg DBP in females (55.9+/-17.0dBA). We found that environmental noise exposure may have elevated effects on adults' blood pressure. Young females are more susceptible to noise exposure than males.

Effects of Environmental Noise Exposure on Ambulatory Blood Pressure in Healthy Adults

Effects of Environmental Noise Exposure on Ambulatory Blood Pressure in Healthy Adults

Contributions of Theodore Schultz to understanding community response to environmental noise exposure

This presentation reviews contributions made over 2 decades by Ted Schultz to the technical literature on community effects of environmental noise exposure. Two of his best‐known contributions to assessment of environmental impacts of noise exposure are: (1) a much‐cited reference book and (2) a well‐known (and initially highly controversial) empirical dosage‐response relationship for the prevalence of annoyance. Ted made a number of important, but less well known, contributions as well, however. At the time of his death, he was collaborating on development of another, theoretically based dosage‐response relationship for the U. S. Air Force NSBIT program, as well as on a handbook chapter on annoyance.