Tobacco Smoking Using Midwakh Is an Emerging Health Problem – Evidence from a Large Cross-Sectional Survey in the United Arab Emirates

INTRODUCTION: Accurate information about the prevalence and types of tobacco use is essential to deliver effective public health policy. We aimed to study the prevalence and modes of tobacco consumption in the United Arab Emirates (UAE), particularly focusing on the use of Midwakh (Arabic traditional pipe). METHODS: We studied 170,430 UAE nationals aged ≥ 18 years (44% males and 56% females) in the Weqaya population-based screening program in Abu Dhabi residents during the period April 2008-June 2010. Self-reported smoking status, type, quantity and duration of tobacco smoked were recorded. Descriptive statistics were used to describe the study findings; prevalence rates used the screened sample as the denominator. RESULT: The prevalence of smoking overall was 24.3% in males and 0.8% in females and highest in males aged 20-39. Mean age (SD) of smokers was 32.8 (11.1) years, 32.7 (11.1) in males and 35.7 (12.1) in females. Cigarette smoking was the commonest form of tobacco use (77.4% of smokers), followed by Midwakh (15.0%), shisha (waterpipe) (6.8%), and cigar (0.66%). The mean durations of smoking for cigarettes, Midwakh, shisha and cigars were 11.4, 9.3, 7.6 and 11.0 years, respectively. CONCLUSIONS: Smoking is most common among younger UAE national men. The use of Midwakh and the relatively young age of onset of Midwakh smokers is of particular concern as is the possibility of the habit spreading to other countries. Comprehensive tobacco control laws targeting the young and the use of Midwakh are needed

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 hospitalization2–4 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

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