| ORIGINAL ARTICLE |
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| Year : 2017 | Volume
: 19
| Issue : 90 | Page : 213--221 |
Chronic noise exposure in the spontaneously hypertensive rat
Anne T.M Konkle1, Stephen E Keith2, James P McNamee2, David Michaud2
1 Interdisciplinary School of Health Sciences, Faculty of Health Sciences, University of Ottawa, Ottawa, Ontario; School of Psychology, Faculty of Social Sciences, University of Ottawa, Ottawa, Ontario, Canada
2 Healthy Environments and Consumer Safety Branch, Environmental and Radiation Health Sciences Directorate, Consumer and Clinical Radiation Protection Bureau, Health , Ottawa, Ontario, Canada
Correspondence Address:
David Michaud
775 Brookfield Road, Postal Locator 6201B, Ottawa K1A1C1, Ontario
Canada
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/nah.NAH_15_17
Introduction: Epidemiological studies have suggested an association between the relative risk for developing cardiovascular disease (CVD) and long-term exposure to elevated levels of transportation noise. The contention is that this association is largely owing to an increase in stress-related biomarkers that are thought to be associated with CVD. Animal models have demonstrated that acute noise exposure is capable of triggering a stress response; however, similar studies using chronic noise models are less common. Materials and Methods: The current study assessed the effects of intermittent daily exposure to broadband 80 kHz bandwidth noise of 87.3 dBA for a period of 21 consecutive days in spontaneously hypertensive rats. Results: Twenty-one days of exposure to noise significantly reduced body weight relative to the sham and unhandled control groups; however, noise had no statistically significant impact on plasma adrenocorticotropic hormone (or adrenal gland weights). Noise was associated with a significant, albeit modest, increase in both corticosterone and aldosterone concentrations following the 21 days of exposure. Interleukin 1 and interleukin 6 levels were unchanged in the noise group, whereas both tumour necrosis factor alpha and C-reactive protein were significantly reduced in noise exposed rats. Tail blood sampling for corticosterone throughout the exposure period showed no appreciable difference between the noise and sham exposed animals, largely due to the sizeable variation for each group as well as the observed fluctuations over time. Discussion: The current pilot study provides only modest support that chronic noise may promote stress-related biological and/or developmental effects. More research is required to verify the current findings and resolve some of the unexpected observations.
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