Global spread of hypoxia in freshwater ecosystems during the last three centuries is caused by rising local human pressure

© 2015 John Wiley & Sons Ltd.

Détails bibliographiques
Publié dans:Global change biology. - 1999. - 22(2016), 4 vom: 15. Apr., Seite 1481-9
Auteur principal: Jenny, Jean-Philippe (Auteur)
Autres auteurs: Francus, Pierre, Normandeau, Alexandre, Lapointe, François, Perga, Marie-Elodie, Ojala, Antti, Schimmelmann, Arndt, Zolitschka, Bernd
Format: Article en ligne
Langue:English
Publié: 2016
Accès à la collection:Global change biology
Sujets:Journal Article Research Support, Non-U.S. Gov't anoxic conditions aquatic transition global change lake ecosystem local human pressure varved sediment Oxygen S88TT14065
Description
Résumé:© 2015 John Wiley & Sons Ltd.
The spread of hypoxia is a threat to aquatic ecosystem functions and services as well as to biodiversity. However, sparse long-term monitoring of lake ecosystems has prevented reconstruction of global hypoxia dynamics while inhibiting investigations into its causes and assessing the resilience capacity of these systems. This study compiles the onset and duration of hypoxia recorded in sediments of 365 lakes worldwide since AD 1700, showing that lacustrine hypoxia started spreading before AD 1900, 70 years prior to hypoxia in coastal zones. This study also shows that the increase of human activities and nutrient release is leading to hypoxia onset. No correlations were found with changes in precipitation or temperature. There is no evidence for a post-1980s return to well-oxygenated lacustrine conditions in industrialized countries despite the implementation of restoration programs. The apparent establishment of stable hypoxic conditions prior to AD 1900 highlights the challenges of a growing nutrient demand, accompanied by increasing global nutrient emissions of our industrialized societies, and climate change
Description:Date Completed 13.12.2016
Date Revised 30.12.2016
published: Print-Electronic
Citation Status MEDLINE
ISSN:1365-2486
DOI:10.1111/gcb.13193