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A systematic search of the peer-reviewed scientific literature that examines the relationship between environmental noise and non-aural health effects identified 35 relevant studies published since 2001. Twenty-five of these report unique findings on long term exposure to transportation noise from road, rail or air traffic; three others report on acute exposures, two in the sleep laboratory and another in an occupational setting. The remaining seven are literature reviews – two of these reviews (Babisch, 2008; Kaltenbach, et al., 2008) quantify the evidence linking chronic noise to adverse health impacts in a dose-effect relationship. Overall, the evidence from these studies supports the hypothesis of certain adverse health effects from environmental noise. The strongest evidence links exposure to noise above 60 dB(A) in the daytime and above 45 dB(A) at night to an increased incidence of arterial hypertension. Results also link noise above 60 dB(A) to an increased risk of myocardial infarction; at 70 dB(A) the risk is over 20% higher than in the unexposed population. Daytime exposure above 55 dB(A) is linked to learning difficulties in school children. The chief mediating mechanisms for these effects are sleep disturbance and physiological stress responses. A more detailed description of these findings appears below. Appendix 1 includes details on the design, measurement and methods of 16 key studies. The World Health Organization in 2009 released their recommendations on night-time exposure thresholds. We concur with their assessment of the strength of the research evidence. Their summary tables appear in Appendix 2. Cardiovascular Effects Noise-induced cardiovascular effects have been extensively studied in occupational settings as well as at community levels. It has been concluded that prolonged exposure to occupational and/or environmental noise (at sound levels of 60-85 dB(A)) can contribute to increased risk for cardiovascular disease (Babisch, Beule, Schust, Kersten, & Ising, 2005; Babisch, 2008; Kaltenbach, Maschke, & Klinke, 2008; Stansfeld & Matheson, 2003). Noise-induced cardiovascular effects include: elevated blood pressure level, prevalence of hypertension, myocardial infarction (MI), abnormalities in the electrocardiogram, more heartbeat irregularities, faster pulse rate, total cholesterol, total triglycerides, blood viscosity, slower recovery of vascular constriction, and increased consumption of cardiovascular medications (Babisch et al., 2005; Jarup et al., 2008; Kaltenbach et al., 2008; Stansfeld & Matheson, 2003) Arterial Hypertension In a major retrospective cohort study examining hypertension (HT), Sbihi followed 10,842 sawmill workers for eight years, identifying 828 cases from physician-billing and hospital discharge records (Sbihi, Davies, & Demers, 2008). Noise exposure was estimated from predictive models based on 1,900 personal dosimetry measurements. The study reported a statistically significant exposure response for noise and HT reaching a relative risk (RR), after adjustment for potential confounders, of 1.5 after 30 years of exposure over 85 dB(A). Lusk et al. also examined ambulatory blood pressure (BP) and heart rate (HR) in 46 automobile engine assembly plant workers. The study used mixed-effect modeling because of the repeated blood pressure (BP) measures (taken at 10 minute intervals). Logged noise dosimetry allowed the calculation of short-term exposure metrics over the same intervals. After controlling for a large number of personal cardiovascular disease (CVD) risk factors, they found noise associated with three physiological measures (systolic and 3 diastolic blood pressure and heart rate) and showed a possible difference in mechanisms between BP (that they showed was correlated to average acute noise) and HR (which was correlated to peaks)(Lusk, Gillespie, Hagerty, & Ziemba, 2004). Several recent studies examined the effect of noise (from a range of sources) on hypertension in community settings. Leon Bluhm, et al. (Bluhm, Berglind, Nordling, & Rosenlund, 2007) studied self-reported HT for 667 adults in a municipality near Stockholm, Sweden. Road noise was modeled for major roads (55-65 dB) and the rest (n=513) estimated by expert judgment. Thirteen percent of subjects were diagnosed with HT. There was a linear exposure response relation between traffic noise and prevalence of HT with an adjusted odds ratio (ORADJ) of 1.38 per 5 dB(A). The authors also showed interactions for time in residence, bedroom orientation, glazing and older homes. Another Swedish study carried out around Stockholm’s major airport assessed the prevalence of (self-reported doctor-diagnosed) high blood pressure by postal questionnaire. An exposure response association between aircraft noise and high blood pressure was found with relative risks ranging between 1.1 and 2.1 for noise levels between approximately energy-averaged levels (FBN) = 53 to 63 dB(A)(Rosenlund, Berglind, Pershagen, Järup, & Bluhm, 2001). When noise categories were combined, the effect was significant for FBN > 55 dB(A). The trend analysis resulted in a 

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