Changes in ambient air quality and atmospheric composition and reactivity in the South East of the UK as a result of the COVID-19 lockdown.

The COVID-19 pandemic forced governments around the world to impose restrictions on daily life to prevent the spread of the virus. This resulted in unprecedented reductions in anthropogenic activity, and reduced emissions of certain air pollutants, namely oxides of nitrogen. The UK 'lockdown' was enforced on 23/03/2020, which led to restrictions on movement, social interaction, and 'non-essential' businesses and services. This study employed an ensemble of measurement and modelling techniques to investigate changes in air quality, atmospheric composition and boundary layer reactivity in the South East of the UK post-lockdown. The techniques employed included in-situ gas- and particle-phase monitoring within central and local authority air quality monitoring networks, remote sensing by long path Differential Optical Absorption Spectroscopy and Sentinel-5P's TROPOMI, and detailed 0-D chemical box modelling. Findings showed that de-trended NO2 concentrations decreased by an average of 14-38% when compared to the mean of the same period over the preceding 5-years. We found that de-trended particulate matter concentrations had been influenced by interregional pollution episodes, and de-trended ozone concentrations had increased across most sites, by up to 15%, such that total Ox levels were roughly preserved. 0-D chemical box model simulations showed the observed increases in ozone concentrations during lockdown under the hydrocarbon-limited ozone production regime, where total NOx decreased proportionally greater than total non-methane hydrocarbons, which led to an increase in total hydroxyl, peroxy and organic peroxy radicals. These findings suggest a more complex scenario in terms of changes in air quality owing to the COVID-19 lockdown than originally reported and provide a window into the future to illustrate potential outcomes of policy interventions seeking large-scale NOx emissions reductions without due consideration of other reactive trace species.

Effects of adenosine on human coronary arterial circulation.

Adenosine is a potent vasodilator used extensively to study the coronary circulation of animals. Its use in humans, however, has been hampered by lack of knowledge about its effects on the human coronary circulation and by concern about its safety. We investigated in humans the effects of adenosine, administered by intracoronary bolus (2-16 micrograms), intracoronary infusion (10-240 micrograms/min), or intravenous infusion (35-140 micrograms/kg/min) on coronary and systemic hemodynamics and the electrocardiogram. Coronary blood flow velocity (CBFV) was measured with a 3F coronary Doppler catheter. The maximal CBFV was determined with intracoronary papaverine (4.5 +/- 0.2.resting CBFV). In normal left coronary arteries (n = 20), 16-micrograms boluses of adenosine caused coronary hyperemia similar to that caused by papaverine (4.6 +/- 0.7.resting CBFV). In the right coronary artery (n = 5), 12-micrograms boluses caused maximal hyperemia (4.4 +/- 1.0.resting CBFV). Intracoronary boluses caused a small, brief decrease in arterial pressure (similar to that caused by papaverine) and no changes in heart rate or in the electrocardiogram. The duration of hyperemia was much shorter after adenosine than after papaverine administration. Intracoronary infusions of 80 micrograms/min or more into the left coronary artery (n = 6) also caused maximal hyperemia (4.4 +/- 0.1.resting CBFV), and doses up to 240 micrograms/min caused a minimal decrease in arterial pressure (-6 +/- 2 mm Hg) and no significant change in heart rate or in electrocardiographic variables. Intravenous infusions in normal patients (n = 25) at 140 micrograms/kg/min caused coronary vasodilation similar to that caused by papaverine in 84% of patients (4.4 +/- 0.9.resting CBFV). At submaximal infusion rates, however, CBFV often fluctuated widely. During the 140-micrograms/kg/min infusion, arterial pressure decreased 6 +/- 7 mm Hg, and heart rate increased 24 +/- 14 beats/min. One patient developed 1 cycle of 2:1 atrioventricular block, but otherwise, the electrocardiogram did not change. In eight patients with microvascular vasodilator dysfunction (delta CBFV, less than 3.5 peak/resting velocity after a maximally vasodilating dose of intracoronary papaverine), the dose-response characteristics to intracoronary boluses and intravenous infusions of adenosine were similar to those found in normal patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Experimental atrial septal defect closure with a new, transcatheter, self-centering device.

BACKGROUND: Despite two decades of research, a transcatheter atrial septal defect closure device is not available for clinical use. We have designed a new superelastic Nitinol-Dacron, double-disk, self-centering, atrial septal defect closure device and studied its efficacy in a canine model of atrial septal defects. METHODS AND RESULTS: Atrial septal defects were created surgically in 20 adult dogs using either a 7.5-mm or 10-mm punch. Percutaneous transcatheter closures were attempted using a new device. The device sizes used were 20 mm in 6 dogs, 22 mm in 9, and 25 mm in 5 (22.1 +/- 1.9 mm, mean +/- SD). The stretched atrial septal defect diameter was 10.5 +/- 1.3 mm, and the device to stretched atrial septal defect diameter ratio was 2.1 +/- 0.3. Closures were successful in 19 studies and unsuccessful in 1. Angiography showed a left-to-right shunt in all 20 dogs before closure. Immediately after closure (n = 19), there were no shunts in 17 and trivial shunts in 2. Six dogs were followed for a period of 4.7 +/- 3.0 months (range, 2 to 8 months). The trivial shunt present in 1 animal immediately after closure had closed by the time of the repeat study. Spontaneous embolization of the device was not seen during follow-up. A solitary wire fracture was found 8 months after closure in 1 device. Light microscopy at 8 weeks in 3 dogs showed the devices to be covered by smooth endocardium, enmeshed in mature collagen tissue, with a minimal mononuclear cell infiltration. Retrievability was assessed by deliberately embolizing 4 devices in 2 dogs into the right atrium (n = 1) and pulmonary artery (n = 3). All devices were successfully retrieved with a snare. CONCLUSIONS: This feasibility study demonstrates that this new self-centering atrial septal defect closure device has a number of design features that permit effective and safe closures in a canine model. These results support the investigation of this device in human clinical trials.