Dataset Information

Geographical Variability in Mortality in Urban Areas: A Joint Analysis of 16 Causes of Death.

ABSTRACT: The geographical distribution of mortality has frequently been studied. Nevertheless, those studies often consider isolated causes of death. In this work, we aim to study the geographical distribution of mortality in urban areas, in particular, in 26 Spanish cities. We perform an overall study of 16 causes of death, considering that their geographical patterns could be dependent and estimating the dependence between the causes of death. We study the deaths in these 26 cities during the period 1996-2015 at the census tract level. A multivariate disease mapping model is used in order to solve the potential small area estimation problems that these data could show. We find that most of the geographical patterns found show positive correlations. This suggests the existence of a transversal geographical pattern, common to most causes of deaths, which determines those patterns to a higher/lower extent depending on each disease. The causes of death that exhibit that underlying pattern in a more prominent manner are chronic obstructive pulmonary disease (COPD), lung cancer, and cirrhosis for men and cardiovascular diseases and dementias for women. Such findings are quite consistent for most of the cities in the study. The high positive correlation found between geographical patterns reflects the existence of both high and low-risk areas in urban settings, in general terms for nearly all the causes of death. Moreover, the high-risk areas found often coincide with neighborhoods known for their high deprivation. Our results suggest that dependence among causes of death is a key aspect to be taken into account when mapping mortality, at least in urban contexts.

SUBMITTER: Martinez-Beneito MA

PROVIDER: S-EPMC8197960 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Geographical Variability in Mortality in Urban Areas: A Joint Analysis of 16 Causes of Death.

Martinez-Beneito Miguel A MA Vergara-Hernández Carlos C Botella-Rocamora Paloma P Corpas-Burgos Francisca F Pérez-Panadés Jordi J Zurriaga Óscar Ó Aldasoro Elena E Borrell Carme C Cabeza Elena E Cirera Lluís L Delfrade Osinaga Josu J Fernández-Somoano Ana A Gandarillas Ana A Lorenzo Ruano Pedro L PL Marí-Dell'Olmo Marc M Nolasco Andreu A Prieto-Salceda M Dolores MD Ramis Rebeca R Rodríguez-Sanz Maica M Sánchez-Villegas Pablo P The Medea Project Group

International journal of environmental research and public health 20210525 11

The geographical distribution of mortality has frequently been studied. Nevertheless, those studies often consider isolated causes of death. In this work, we aim to study the geographical distribution of mortality in urban areas, in particular, in 26 Spanish cities. We perform an overall study of 16 causes of death, considering that their geographical patterns could be dependent and estimating the dependence between the causes of death. We study the deaths in these 26 cities during the period 19 ...[more]

PMID: 34070635

Similar Datasets

Project description:Introduction: Several polymorphisms altering the NAT2 activity have already been identified. The geographical distribution of NAT2 variants has been extensively studied and has been demonstrated to vary significantly among different ethnic population. Here, we describe the genetic variability of human N-acetyltransferase 2 (NAT2) gene and the predominant genotype-deduced acetylation profiles of Brazilians. Methods: A total of 964 individuals, from five geographical different regions, were genotyped for NAT2 by sequencing the entire coding exon. Results: Twenty-three previously described NAT2 single nucleotide polymorphisms (SNPs) were identified, including the seven most common ones globally (c.191G>A, c.282C>T, c.341T>C, c.481C>T, c.590G>A, c.803A>G and c.857G>A). The main allelic groups were NAT2*5 (36%) and NAT2*6 (18.2%), followed to the reference allele NAT2*4 (20.4%). Combined into genotypes, the most prevalent allelic groups were NAT2*5/*5 (14.6%), NAT2*5/*6 (11.9%) and NAT2*6/*6 (6.2%). The genotype deduced NAT2 slow acetylation phenotype was predominant but showed significant variability between geographical regions. The prevalence of slow acetylation phenotype was higher in the Northeast, North and Midwest (51.3%, 45.5% and 41.5%, respectively) of the country. In the Southeast, the intermediate acetylation phenotype was the most prevalent (40.3%) and, in the South, the prevalence of rapid acetylation phenotype was significantly higher (36.7%), when compared to other Brazilian states (p < 0.0001). Comparison of the predicted acetylation profile among regions showed homogeneity among the North and Northeast but was significantly different when compared to the Southeast (p = 0.0396). The Southern region was significantly different from all other regions (p < 0.0001). Discussion: This study contributes not only to current knowledge of the NAT2 population genetic diversity in different geographical regions of Brazil, but also to the reconstruction of a more accurate phenotypic picture of NAT2 acetylator profiles in those regions.

Project description:BackgroundDeath adders (Acanthophis spp) are found in Australia, Papua New Guinea and parts of eastern Indonesia. This study aimed to investigate the clinical syndrome of death adder envenoming and response to antivenom treatment.Methodology/principal findingsDefinite death adder bites were recruited from the Australian Snakebite Project (ASP) as defined by expert identification or detection of death adder venom in blood. Clinical effects and laboratory results were collected prospectively, including the time course of neurotoxicity and response to treatment. Enzyme immunoassay was used to measure venom concentrations. Twenty nine patients had definite death adder bites; median age 45 yr (5-74 yr); 25 were male. Envenoming occurred in 14 patients. Two further patients had allergic reactions without envenoming, both snake handlers with previous death adder bites. Of 14 envenomed patients, 12 developed neurotoxicity characterised by ptosis (12), diplopia (9), bulbar weakness (7), intercostal muscle weakness (2) and limb weakness (2). Intubation and mechanical ventilation were required for two patients for 17 and 83 hours. The median time to onset of neurotoxicity was 4 hours (0.5-15.5 hr). One patient bitten by a northern death adder developed myotoxicity and one patient only developed systemic symptoms without neurotoxicity. No patient developed venom induced consumption coagulopathy. Antivenom was administered to 13 patients, all receiving one vial initially. The median time for resolution of neurotoxicity post-antivenom was 21 hours (5-168). The median peak venom concentration in 13 envenomed patients with blood samples was 22 ng/mL (4.4-245 ng/mL). In eight patients where post-antivenom bloods were available, no venom was detected after one vial of antivenom.Conclusions/significanceDeath adder envenoming is characterised by neurotoxicity, which is mild in most cases. One vial of death adder antivenom was sufficient to bind all circulating venom. The persistent neurological effects despite antivenom, suggests that neurotoxicity is not reversed by antivenom.

Dataset Information

Geographical Variability in Mortality in Urban Areas: A Joint Analysis of 16 Causes of Death.

Publications

Geographical Variability in Mortality in Urban Areas: A Joint Analysis of 16 Causes of Death.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets