Societal shifts due to COVID-19 reveal large-scale complexities and feedbacks between atmospheric chemistry and climate change.

The COVID-19 global pandemic and associated government lockdowns dramatically altered human activity, providing a window into how changes in individual behavior, enacted en masse, impact atmospheric composition. The resulting reductions in anthropogenic activity represent an unprecedented event that yields a glimpse into a future where emissions to the atmosphere are reduced. Furthermore, the abrupt reduction in emissions during the lockdown periods led to clearly observable changes in atmospheric composition, which provide direct insight into feedbacks between the Earth system and human activity. While air pollutants and greenhouse gases share many common anthropogenic sources, there is a sharp difference in the response of their atmospheric concentrations to COVID-19 emissions changes, due in large part to their different lifetimes. Here, we discuss several key takeaways from modeling and observational studies. First, despite dramatic declines in mobility and associated vehicular emissions, the atmospheric growth rates of greenhouse gases were not slowed, in part due to decreased ocean uptake of CO2 and a likely increase in CH4 lifetime from reduced NO x emissions. Second, the response of O3 to decreased NO x emissions showed significant spatial and temporal variability, due to differing chemical regimes around the world. Finally, the overall response of atmospheric composition to emissions changes is heavily modulated by factors including carbon-cycle feedbacks to CH4 and CO2, background pollutant levels, the timing and location of emissions changes, and climate feedbacks on air quality, such as wildfires and the ozone climate penalty.

Observing Annual Trends in Vehicular CO2 Emissions.

Transportation emissions are the largest individual sector of greenhouse gas (GHG) emissions. As such, reducing transportation-related emissions is a primary element of every policy plan to reduce GHG emissions. The Berkeley Environmental Air-quality and CO2 Observation Network (BEACO2N) was designed and deployed with the goal of tracking changes in urban CO2 emissions with high spatial (∼1 km) and temporal (∼1 hr) resolutions while allowing the identification of trends in individual emission sectors. Here, we describe an approach to inferring vehicular CO2 emissions with sufficient precision to constrain annual trends. Measurements from 26 individual BEACO2N sites are combined and synthesized within the framework of a Gaussian plume model. After removing signals from biogenic emissions, we are able to report normalized annual emissions for 2018-2020. A reduction of 7.6 ± 3.5% in vehicular CO2 emissions is inferred for the San Francisco Bay Area over this 2 year period. This result overlaps with, but is slightly larger than, estimates from the 2017 version of the California Air Resources Board EMFAC emissions model, which predicts a 4.7% decrease over these 2 years. This demonstrates the feasibility of independently and rapidly verifying policy-driven reductions in GHG emissions from transportation with atmospheric observations in cities.

Npas4 regulates a transcriptional program in CA3 required for contextual memory formation.

The rapid encoding of contextual memory requires the CA3 region of the hippocampus, but the necessary genetic pathways remain unclear. We found that the activity-dependent transcription factor Npas4 regulates a transcriptional program in CA3 that is required for contextual memory formation. Npas4 was specifically expressed in CA3 after contextual learning. Global knockout or selective deletion of Npas4 in CA3 both resulted in impaired contextual memory, and restoration of Npas4 in CA3 was sufficient to reverse the deficit in global knockout mice. By recruiting RNA polymerase II to promoters and enhancers of target genes, Npas4 regulates a learning-specific transcriptional program in CA3 that includes many well-known activity-regulated genes, which suggests that Npas4 is a master regulator of activity-regulated gene programs and is central to memory formation.