Biogenic carbon pool production maintains the Southern Ocean carbon sink.

Through biological activity, marine dissolved inorganic carbon (DIC) is transformed into different types of biogenic carbon available for export to the ocean interior, including particulate organic carbon (POC), dissolved organic carbon (DOC), and particulate inorganic carbon (PIC). Each biogenic carbon pool has a different export efficiency that impacts the vertical ocean carbon gradient and drives natural air-sea carbon dioxide gas (CO2) exchange. In the Southern Ocean (SO), which presently accounts for ~40% of the anthropogenic ocean carbon sink, it is unclear how the production of each biogenic carbon pool contributes to the contemporary air-sea CO2 exchange. Based on 107 independent observations of the seasonal cycle from 63 biogeochemical profiling floats, we provide the basin-scale estimate of distinct biogenic carbon pool production. We find significant meridional variability with enhanced POC production in the subantarctic and polar Antarctic sectors and enhanced DOC production in the subtropical and sea-ice-dominated sectors. PIC production peaks between 47°S and 57°S near the "great calcite belt." Relative to an abiotic SO, organic carbon production enhances CO2 uptake by 2.80 ± 0.28 Pg C y-1, while PIC production diminishes CO2 uptake by 0.27 ± 0.21 Pg C y-1. Without organic carbon production, the SO would be a CO2 source to the atmosphere. Our findings emphasize the importance of DOC and PIC production, in addition to the well-recognized role of POC production, in shaping the influence of carbon export on air-sea CO2 exchange.

Observing Changes in Ocean Carbonate Chemistry: Our Autonomous Future.

PURPOSE OF REVIEW: We summarize recent progress on autonomous observations of ocean carbonate chemistry and the development of a network of sensors capable of observing carbonate processes at multiple temporal and spatial scales. RECENT FINDINGS: The development of versatile pH sensors suitable for both deployment on autonomous vehicles and in compact, fixed ecosystem observatories has been a major development in the field. The initial large-scale deployment of profiling floats equipped with these new pH sensors in the Southern Ocean has demonstrated the feasibility of a global autonomous open-ocean carbonate observing system. SUMMARY: Our developing network of autonomous carbonate observations is currently targeted at surface ocean CO2 fluxes and compact ecosystem observatories. New integration of developed sensors on gliders and surface vehicles will increase our coastal and regional observational capability. Most autonomous platforms observe a single carbonate parameter, which leaves us reliant on the use of empirical relationships to constrain the rest of the carbonate system. Sensors now in development promise the ability to observe multiple carbonate system parameters from a range of vehicles in the near future.

Reassessing Southern Ocean Air-Sea CO2 Flux Estimates With the Addition of Biogeochemical Float Observations.

New estimates of pCO2 from profiling floats deployed by the Southern Ocean Carbon and Climate Observations and Modeling (SOCCOM) project have demonstrated the importance of wintertime outgassing south of the Polar Front, challenging the accepted magnitude of Southern Ocean carbon uptake (Gray et al., 2018, https://doi:10.1029/2018GL078013). Here, we put 3.5 years of SOCCOM observations into broader context with the global surface carbon dioxide database (Surface Ocean CO2 Atlas, SOCAT) by using the two interpolation methods currently used to assess the ocean models in the Global Carbon Budget (Le Quéré et al., 2018, https://doi:10.5194/essd-10-2141-2018) to create a ship-only, a float-weighted, and a combined estimate of Southern Ocean carbon fluxes (<35°S). In our ship-only estimate, we calculate a mean uptake of -1.14 ± 0.19 Pg C/yr for 2015-2017, consistent with prior studies. The float-weighted estimate yields a significantly lower Southern Ocean uptake of -0.35 ± 0.19 Pg C/yr. Subsampling of high-resolution ocean biogeochemical process models indicates that some of the differences between float and ship-only estimates of the Southern Ocean carbon flux can be explained by spatial and temporal sampling differences. The combined ship and float estimate minimizes the root-mean-square pCO2 difference between the mapped product and both data sets, giving a new Southern Ocean uptake of -0.75 ± 0.22 Pg C/yr, though with uncertainties that overlap the ship-only estimate. An atmospheric inversion reveals that a shift of this magnitude in the contemporary Southern Ocean carbon flux must be compensated for by ocean or land sinks within the Southern Hemisphere.

Differential induction of apoptosis by cigarette smoke extract in primary human lung fibroblast strains: implications for emphysema.

Cigarette smoke is the principal cause of emphysema. Recent attention has focused on the loss of alveolar fibroblasts in the development of emphysema. Fibroblasts may become damaged by oxidative stress and undergo apoptosis as a result of cigarette smoke exposure. Not all smokers develop lung diseases associated with tobacco smoke, a fact that may reflect individual variation among human fibroblast strains. We hypothesize that fibroblasts from different human beings vary in their ability to undergo apoptosis after cigarette smoke exposure. This could account for emphysematous changes that occur in the lungs of some but not all smokers. Primary human lung fibroblast strains were exposed to cigarette smoke extract (CSE) and assessed for viability, morphological changes, and mitochondrial transmembrane potential as indicators of apoptosis. We also examined the generation of intracellular reactive oxygen species (ROS), 4-hydroxy-2-nonenal, and changes in glutathione (GSH) and glutathione disulfide (GSSG) levels. Each human lung fibroblast strain exhibited a differential sensitivity to CSE as judged by changes in mitochondrial membrane potential, viability, ROS generation, and glutathione production. Interestingly, the thiol antioxidants N-acetyl-L-cysteine and GSH eliminated CSE-induced changes in fibroblast morphology such as membrane blebbing, nuclear condensation, and cell size and prevented alterations in mitochondrial membrane potential and the generation of ROS. These findings support the concept that oxidative stress and apoptosis are responsible for fibroblast death associated with exposure to tobacco smoke. Variations in the sensitivity of fibroblasts to cigarette smoke may account for the fact that only some smokers develop emphysema.