Changes in CO2 during ocean anoxic event 1d indicate similarities to other carbon cycle perturbationsTools Richey, Jon D., Upchurch, Garland, Montañez, Isabel P., Lomax, Barry H., Suarez, Marina B., Crout, Neil M.J., Joeckel, R.M., Ludvigson, Greg A. and Smith, Jon J. (2018) Changes in CO2 during ocean anoxic event 1d indicate similarities to other carbon cycle perturbations. Earth and Planetary Science Letters, 491 . pp. 172-182. ISSN 0012-821X Full text not available from this repository.AbstractPast greenhouse intervals of the Mesozoic were repeatedly punctuated by Ocean Anoxic Events (OAEs), major perturbations to the global carbon cycle and abrupt climate changes that may serve as relevant analogs for Earth’s greenhouse gas-forced climate future. The key to better understanding these transient climate disruptions and possible CO2 forced tipping-points resides in high-resolution, precise, and accurate estimates of atmospheric CO2 for individual OAEs. Here we present a high-temporal resolution, multi-proxy pCO2 reconstruction for the onset of mid-Cretaceous (Albian-Cenomanian Boundary) OAE1d. Coupling of pCO2 estimates with carbon isotopic compositions (δ13C) of charcoal, vitrain, and cuticle from the Rose Creek Pit (RCP), Nebraska, reveals complex phasing, including a lag between the well-documented negative δ13C excursion defining the onset of OAE1d and the CO2 increase. This lag indicates that increased CO2 or other C-based greenhouse gases may not have been the primary cause of the negative excursion. Our study reveals a pCO2 increase within the interval of the negative δ13C excursion, reaching a maximum of up to ~840 ppm (95% confidence interval -307 ppm/+167 ppm) toward its end. The reconstructed magnitude of CO2 increase (~357 ppm) is similar to that of Late Cretaceous OAE2 but of smaller magnitude than that of other major carbon cycle perturbations of the Mesozoic assessed via stomatal methods (e.g., the Toarcian OAE [TOAE], Triassic-Jurassic boundary event, Cretaceous-Paleogene Boundary event). Furthermore, our results indicate a possible shared causal or developmental mechanism with OAE1a and the TOAE.
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