Injaian Allison S, Gonzalez-Gomez Paulina L, Taff Conor C, Bird Alicia K, Ziur Alexis D, Patricelli Gail L, Haussmann Mark F, Wingfield John C
Department of Ecology and Evolution, University of California Davis, One Shields Avenue, Davis, CA 95616, USA.
Department of Neurobiology, Physiology and Behavior, University of California Davis, One Shields Avenue, Davis, CA 95616, USA; Universidad Autónoma de Chile, Providencia 425, Santiago, Chile.
Gen Comp Endocrinol. 2019 May 15;276:14-21. doi: 10.1016/j.ygcen.2019.02.017. Epub 2019 Feb 20.
Anthropogenic impacts, such as noise pollution from transportation networks, can serve as stressors to some wildlife species. For example, increased exposure to traffic noise has been found to alter baseline and stress-induced corticosterone levels, reduce body condition and reproductive success, and increase telomere attrition in free-living birds. However, it remains unknown if alterations in nestling phenotype are due to direct or indirect effects of noise exposure. For example, indirect (maternal) effects of noise may occur if altered baseline and stress-induced corticosterone in mothers results in differential deposition of yolk steroids or other components in eggs. Noise exposure may also alter nestling corticosterone levels directly, given that nestlings cannot escape the nest during development. Here, we examined maternal versus direct effects of traffic noise exposure on baseline and stress-induced corticosterone levels, and body condition (as measured by size-corrected mass) in nestling tree swallows (Tachycineta bicolor). We used a two-way factorial design and partially cross-fostered eggs between nests exposed to differing levels (i.e. amplitudes) of traffic noise. For nestlings that were not cross-fostered, we also investigated the effects of traffic noise on telomere dynamics. Our results show a positive relationship between nestling baseline and stress-induced corticosterone and nestling noise exposure, but not maternal noise exposure. While we did not find a relationship between noise and body condition in nestlings, nestling baseline corticosterone was negatively associated with body condition. We also found greater telomere attrition for nestlings from nests with greater traffic noise amplitudes. These results suggest that direct, rather than maternal, effects result in potentially long-lasting consequences of noise exposure. Reduced nestling body condition and increased telomere attrition have been shown to reduce post-fledging survival in this species. Given that human transportation networks continue to expand, strategies to mitigate noise exposure on wildlife during critical periods (i.e. breeding) may be needed to maintain local population health in free-living passerines, such as tree swallows.
人为影响，比如交通网络产生的噪音污染，可能会对一些野生动物物种构成压力源。例如，研究发现，自由生活的鸟类接触交通噪音增加会改变其基础皮质酮水平和应激诱导的皮质酮水平，降低身体状况和繁殖成功率，并加速端粒磨损。然而，雏鸟表型的改变是由于噪音暴露的直接影响还是间接影响，目前尚不清楚。例如，如果母亲基础皮质酮水平和应激诱导的皮质酮水平发生改变，导致卵黄类固醇或其他成分在卵中的差异沉积，那么噪音可能会产生间接（母体）影响。鉴于雏鸟在发育过程中无法逃离巢穴，噪音暴露也可能直接改变雏鸟的皮质酮水平。在这里，我们研究了交通噪音暴露对雏鸟树燕（双色树燕）基础皮质酮水平和应激诱导的皮质酮水平以及身体状况（通过体型校正质量来衡量）的母体影响与直接影响。我们采用了双因素析因设计，并在暴露于不同水平（即振幅）交通噪音的巢穴之间部分交叉寄养鸟蛋。对于未交叉寄养的雏鸟，我们还研究了交通噪音对端粒动态的影响。我们的研究结果表明，雏鸟基础皮质酮水平和应激诱导的皮质酮水平与雏鸟噪音暴露呈正相关，但与母体噪音暴露无关。虽然我们没有发现噪音与雏鸟身体状况之间的关系，但雏鸟基础皮质酮水平与身体状况呈负相关。我们还发现，来自交通噪音振幅较大巢穴的雏鸟端粒磨损更严重。这些结果表明，直接影响而非母体影响会导致噪音暴露产生潜在的长期后果。研究表明，雏鸟身体状况下降和端粒磨损加剧会降低该物种出飞后的存活率。鉴于人类交通网络持续扩张，可能需要采取策略来减轻关键时期（即繁殖期）野生动物所受的噪音暴露，以维持自由生活的雀形目鸟类（如树燕）的当地种群健康。
