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ABSTRACT The ability of organisms to effectively respond to challenges is critical for survival. We investigated how an acute stressor affected corticosterone, mitochondrial function, and DNA oxidative damage in a wild population of Leach's storm‐petrels (Hydrobates leucorhous). We conducted a standardized 20‐min handling procedure on storm‐petrel chicks and collected baseline and post‐handling blood samples. We measured plasma corticosterone and red blood cell DNA oxidative damage levels through the detection of a mutated DNA base 8‐Hydroxy‐2'‐deoxyguanosine (8‐OHdG). In addition, we quantified six measures of mitochondrial aerobic metabolism from red blood cells. Overall, the handling stressor increased plasma corticosterone levels and decreased mitochondrial efficiency to produce ATP. Although the increase in corticosterone was inversely related to the change in DNA oxidative damage, the decrease in mitochondrial efficiency was positively correlated with the change in DNA oxidative damage. Thus, over an acute stress response, individuals who had the largest increase in corticosterone also had the least amount of oxidative damage. In addition, individuals who prioritized ATP production during the acute stress also showed higher levels of oxidative damage. This work highlights the complex pathways by which corticosterone and mitochondrial efficiency affect oxidative damage during acute stress, providing new insights into the trade‐offs underlying physiological responses in wild animals. 

Abstract Children (<5 years) are highly vulnerable during hot weather due to their reduced ability to thermoregulate. There has been limited quantification of the burden of climate change on health in sub-Saharan Africa, in part due to a lack of evidence on the impacts of weather extremes on mortality and morbidity. Using a linear threshold model of the relationship between daily temperature and child mortality, we estimated the impact of climate change on annual heat-related child deaths for the current (1995–2020) and future time periods (2020–2050). By 2009, heat-related child mortality was double what it would have been without climate change; this outweighed reductions in heat mortality from improvements associated with development. We estimated future burdens of child mortality for three emission scenarios (SSP119, SSP245 and SSP585), and a single scenario of population growth. Under the high emission scenario (SSP585), including changes to population and mortality rates, heat-related child mortality is projected to double by 2049 compared to 2005–2014. If 2050 temperature increases were kept within the Paris target of 1.5 °C (SSP119 scenario), approximately 4000–6000 child deaths per year could be avoided in Africa. The estimates of future heat-related mortality include the assumption of the significant population growth projected for Africa, and declines in child mortality consistent with Global Burden of Disease estimates of health improvement. Our findings support the need for urgent mitigation and adaptation measures that are focussed on the health of children.