Behaviour and Climate Change: Consumer Perceptions of Responsibility

This paper explores the under-researched notion of consumer responsibility, a potentially significant influence on consumer behaviour that marketers and policymakers may be able to harness as they attempt to respond to environmental challenges such as climate change. The paper uses data derived from a commercially motivated survey (n = 1513) to explore domestic consumption behaviours most closely associated with the issue of disruptive climate change. A measure of 'General Environmental Responsiveness' (GER) is used to test: (1) the effects of consumers both taking responsibility for their actions and placing responsibility on others for the consequences of their consumption behaviour; and (2) whether sociodemographic variables can aid the targeting of consumers by the level and type of responsibility and pro-environmental behavioural intentions expressed. The study's findings demonstrate clear, if not strong, relationships between consumer conceptions of responsibilities for causing and tackling climate change and environment-related consumer behaviour. The study's implications both challenge accepted wisdom about environment-related consumer behaviour and suggest avenues for future research

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease