Anthropogenic emission inventory and spatial analysis of greenhouse gases and primary pollutants for the Galapagos Islands.

Climate change and air pollution are critical challenges that humanity is currently facing. Understanding the sources of emissions released into the atmosphere is of great importance to evaluate the local footprint, the impacts of human activities, and the opportunities to develop and implement solutions to mitigate emissions and adapt to climate change particularly in vulnerable places like the Galapagos Islands. In this study, we present an anthropogenic emissions inventory for Santa Cruz, San Cristobal, and Isabela Islands in which emissions were spatially mapped for greenhouse gasses (GHGs) and primary pollutants (PP). Emissions were estimated for the energy stationary sources, energy mobile sources, waste, and other sectors, and emissions for 2019 were spatially distributed along with an uncertainty assessment. Results demonstrated that energy mobile sources which are aerial, terrestrial, and maritime transportation generated the most significant emissions in the Galapagos Islands in terms of PP and GHGs. In fact, maritime transportation was the highest one in 2019, at 41% of total CO2 emissions for Galapagos, with the most predominant PP being NOx and CO. The aerial transportation made up 36% of emissions, and the electricity generation contributed 15%. Emissions from waste and other sectors comprise a smaller percentage relative to the rest of the emission sectors. These results highlight the strong dependency of the islands on fossil fuels for transportation and electricity generation. Alternatives to mitigate and reduce emissions from the islands are discussed. This spatially mapped emissions inventory for the Galapagos Islands represents a powerful tool to make informed decisions to contribute to the long-term sustainability of the archipelago.

Mucinous Adenocarcinoma With Intrapulmonary Metastasis Harboring KRAS and GNAS Mutations Arising in Congenital Pulmonary Airway Malformation.

OBJECTIVES: Mucinous adenocarcinoma arising in unresected congenital pulmonary airway malformation (CPAM) is rare. Underlying driver mutations in addition to KRAS gain-of-function mutations in this setting and the long-term outcomes of these patients are unknown. METHODS: We report a case of metastatic mucinous adenocarcinoma harboring both KRAS and GNAS mutations arising in a type 1 CPAM of a 14-year-old male. A literature review was performed. RESULTS: Next-generation sequencing revealed identical KRAS (G12V) mutations in both the CPAM and metastatic adenocarcinoma and a missense mutation in the GNAS (R201C) gene in the metastatic adenocarcinoma only. Median survival was 23 and 4 years for patients with localized (no or limited spread within the same lobe of CPAM) and distant involvement (spread to any different lobe of CPAM) of mucinous cells, respectively (95% confidence interval, 23-23 and 1.5-22 years, respectively; P = .017). CONCLUSIONS: Mucinous cell proliferation associated with type 1 CPAM has exceptionally good long-term outcomes if confined within the same lobe of CPAM. A second oncogenic mutation in the GNAS gene may be necessary for progression to malignancy and distant spread.