Journal Article The case for counting multiple causes of death in the COVID-19 era Get access Marie-Pier Petit, Marie-Pier Petit Department of Demography, Université de Montréal, Montreal, QC, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar Nadine Ouellette, Nadine Ouellette Department of Demography, Université de Montréal, Montreal, QC, Canada Corresponding author. Department of Demography, Université de Montréal, Lionel-Groulx Building, PO Box 6128 Centre-Ville STN, Montreal, QC H3C 3J7, Canada. E-mail: nadine.ouellette@umontreal.ca Search for other works by this author on: Oxford Academic PubMed Google Scholar Robert Bourbeau Robert Bourbeau Department of Demography, Université de Montréal, Montreal, QC, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar International Journal of Epidemiology, Volume 53, Issue 1, February 2024, dyad149, https://doi.org/10.1093/ije/dyad149 Published: 31 October 2023 Article history Received: 21 May 2023 Editorial decision: 19 September 2023 Published: 31 October 2023

Le contact visuel est un des signes de l’interaction entre un piéton et un automobiliste. C’est une fonction importante de l’attention lorsque le piéton se prépare à traverser la voie publique à une intersection. Cette recherche présente les résultats d’une enquête menée au printemps 2001 sur le comportement des piétons à Montréal et à Toronto. Les résultats montrent que le contact visuel est plus fréquent à Montréal par rapport à Toronto selon le genre et les groupes d’âge et il y a aussi des différences significatives, entre les deux villes, du comportement du piéton au départ et durant la traversée d’une intersection. La variable dépendante, dans les modèles de régression logistique, est contact/non contact visuel. Au regard du modèle comportemental, il y a 1,63 fois plus de chance à Montréal et 2,12 fois plus à Toronto d’observer un contact visuel lorsque le piéton a un comportement non respectueux des règles de sécurité routière. De plus, la probabilité est plus faible d’observer un contact visuel lorsque le piéton montréalais ne traverse pas à un passage piétonnier. Par contre, la probabilité d’un contact visuel est plus élevée lorsque le piéton torontois n’observe pas un respect strict des règles pour traverser à une intersection. Pour le modèle environnemental, les résultats indiquent que le piéton montréalais a plus de chance d’effectuer un contact visuel lorsqu’il traverse une intersection dans une zone résidentielle, dans une rue de trois voies et plus, en présence d’un feu standard et à une intersection située à la périphérie du centre-ville. À Toronto, le modèle extrait les deux dernières variables du modèle montréalais et, en plus, les flux de véhicules. La discussion souligne l’importance du concept d’attention pour expliquer le contact visuel du piéton dans un contexte environnemental.

The U.S. elderly experience shorter lifespans and greater variability in age at death than their Canadian peers. In order to gain insight on the underlying factors responsible for the Canada-U.S. old-age mortality disparities, we propose a cause-of-death analysis. Accordingly, the objective of this paper is to compare levels and trends in cause-specific modal age at death ( M ) and standard deviation above the mode ( SD ( M +)) between Canada and the U.S. since the 1970s. We focus on six broad leading causes of death, namely cerebrovascular diseases, heart diseases, and four types of cancers. Country-specific M and SD ( M +) estimates for each leading cause of death are calculated from P -spline smooth age-at-death distributions obtained from detailed population and cause-specific mortality data. Our results reveal similar levels and trends in M and SD ( M +) for most causes in the two countries, except for breast cancer (females) and lung cancer (males), where differences are the most noticeable. In both of these instances, modal lifespans are shorter in the U.S. than in Canada and U.S. old-age mortality inequalities are greater. These differences are explained in part by the higher stratification along socioeconomic lines in the U.S. than in Canada regarding the adoption of health risk behaviours and access to medical services.

AbstractThe recent decrease in adult and late-life mortality led to a very rapid increase in the number of centenarians within low mortality countries. This chapter examines the increase in the number of centenarians in Quebec (Canada) across birth cohorts (1871–1901), and outlines some of the underlying demographic mechanisms involved. We study the demographic situation of centenarians from Quebec (Canada) using all aggregated data available since 1871 (census data, vital statistics, and population estimations). Census data and population estimates are taken from Statistics Canada, while vital statistics come from the Canadian Human Mortality Database (CHMD, 2014 www.bdlc.umontreal.ca) and the Institut de la statistique du Québec.With demographic indicators such as the centenarian ratio, the survival probabilities and the maximal age at death, we try to demonstrate the remarkable progress realised in old age mortality. We also analyze the determinants of the increase in the number of centenarians in Quebec: increase in the size of birth cohorts, increase in the probabilities of surviving from birth to age 80 and from age 80 to 100 for specific cohorts, change in the number of persons aged 100 and over relative to the number of persons reaching exact age 100 and net change due to migration and other factors (errors). This decomposition shows that, among the factors identified, the improvement in late-life mortality (from age 80 to 100) is the main determinant of the increase of the number of centenarians.This study stresses the importance of monitoring the number as well as the quality of life of this emerging population of centenarians. It also helps us gain greater perspective on what should be expected in the coming years among low mortality countries such as Canada.

First, we use Lexis surfaces based on Serfling models to highlight influenza mortality patterns as well as to identify lingering effects of early-life exposure to specific influenza virus subtypes (e.g., H1N1, H3N2).

Plusieurs études démontrent l’existence d’une association entre la mortalité et le statut socioéconomique : les personnes appartenant aux catégories sociales les plus favorisées ont une mortalité plus faible que celles appartenant aux catégories défavorisées. Les données nécessaires à ce type d’analyse ne sont pas toujours disponibles et des études sont parfois menées auprès des groupes professionnels spécifiques. Cet article fournit une estimation de la mortalité des hommes médecins au Québec faite à partir des données d’un fichier administratif du Collège des médecins du Québec. Les résultats obtenus montrent une diminution de la mortalité des hommes médecins au cours de la période étudiée (1993 à 2010), mais les différences ne sont significatives que pour les groupes d’âge à partir d’environ 60 ans. Lorsqu’on compare la mortalité des médecins à celle de l’ensemble de la population masculine québécoise, nous constatons une mortalité plus faible chez les hommes médecins inscrits au tableau des membres du Collège des médecins. Finalement, cette étude ne montre pas de différence significative entre la mortalité des hommes médecins omnipraticiens et celle des hommes médecins spécialistes.

Recent outbreaks of H5, H7, and H9 influenza A viruses in humans have served as a vivid reminder of the potentially devastating effects that a novel pandemic could exert on the modern world. Those who have survived infections with influenza viruses in the past have been protected from subsequent antigenically similar pandemics through adaptive immunity. For example, during the 2009 H1N1 "swine flu" pandemic, those exposed to H1N1 viruses that circulated between 1918 and the 1940s were at a decreased risk for mortality as a result of their previous immunity. It is also generally thought that past exposures to antigenically dissimilar strains of influenza virus may also be beneficial due to cross-reactive cellular immunity. However, cohorts born during prior heterosubtypic pandemics have previously experienced elevated risk of death relative to surrounding cohorts of the same population. Indeed, individuals born during the 1890 H3Nx pandemic experienced the highest levels of excess mortality during the 1918 "Spanish flu." Applying Serfling models to monthly mortality and influenza circulation data between October 1997 and July 2014 in the United States and Mexico, we show corresponding peaks in excess mortality during the 2009 H1N1 "swine flu" pandemic and during the resurgent 2013-2014 H1N1 outbreak for those born at the time of the 1957 H2N2 "Asian flu" pandemic. We suggest that the phenomenon observed in 1918 is not unique and points to exposure to pandemic influenza early in life as a risk factor for mortality during subsequent heterosubtypic pandemics.IMPORTANCE The relatively low mortality experienced by older individuals during the 2009 H1N1 influenza virus pandemic has been well documented. However, reported situations in which previous influenza virus exposures have enhanced susceptibility are rare and poorly understood. One such instance occurred in 1918-when those born during the heterosubtypic 1890 H3Nx influenza virus pandemic experienced the highest levels of excess mortality. Here, we demonstrate that this phenomenon was not unique to the 1918 H1N1 pandemic but that it also occurred during the contemporary 2009 H1N1 pandemic and 2013-2014 H1N1-dominated season for those born during the heterosubtypic 1957 H2N2 "Asian flu" pandemic. These data highlight the heretofore underappreciated phenomenon that, in certain instances, prior exposure to pandemic influenza virus strains can enhance susceptibility during subsequent pandemics. These results have important implications for pandemic risk assessment and should inform laboratory studies aimed at uncovering the mechanism responsible for this effect.

Many studies have shown the existence of an association between mortality and socio-economic status. People belonging to the more privileged social categories have lower mortality than those in disadvantaged categories. The data required for this kind of analysis are not always available, and studies are sometimes conducted among specific professional groups. This article provides an estimation of mortality among male doctors in Quebec, based on data from an administrative database of the College des medecins du Quebec. The results show a lowering of mortality among male doctors over the study period (1993 to 2010), but the differences are not significant except for age groups above about 60 years. When we compare the mortality of doctors with that of the male population of Quebec as a whole, we find lower mortality among male doctors registered as members of the College des medecins. Finally, this study shows no significant difference between the mortality of male general practice doctors and that of male medical specialists.

The structure of causes of death in Canada has been changing since the onset of the “cardiovascular revolution.” While mortality due to cardiovascular diseases has been declining, mortality due to other causes of death, such as cancers and Alzheimer’s disease has been increasing. Our research investigates how these changes have re-modeled life expectancy at age 65 and age 85, and what specific causes of death are involved. We distinguish between premature and senescent deaths in Canada, using a cause-specific age structure. Our results suggest that although a decline in premature deaths has contributed to increasing life expectancy in recent years, most of the gains in life expectancy at age 65 and 85 have resulted from a decline in senescent deaths. We also find a decline in mortality due to the main causes of death, leading to a greater diversification of causes.Depuis le début de la révolution cardiovasculaire, le Canada a connu d’importants changements dans la distribution des décès selon la cause. La mortalité par maladies cardiovasculaires a connu une importante diminution alors que les taux de mortalité pour les cancers et pour la maladie d’Alzheimer ont augmenté. Cet article examine comment ces changements ont influencé les tendances de l’espérance de vie à 65 et à 85 ans et quelles causes de décès spécifiques furent impliquées. Une distinction entre les décès prématurés et les décès liés à un processus de sénescence est réalisée, se basant sur deux indicateurs de variations par âge des causes de décès. Nos résultats suggèrent que la majorité des gains en espérance de vie à 65 et 85 ans proviennent d’une plus faible mortalité par cause de décès sénescente. De plus, une diminution des principales causes de décès chez les personnes âgées de 65 ans et plus laisse place à une plus grande diversification de causes aux grands âges.

In the past 90 years, remarkable progress was made in substantially improving survival and longevity in Canada, establishing it as a member of today’s group of very low mortality countries. We use several demographic indicators of all-cause and cause-specific mortality to illustrate the nature of these major advances throughout the life span. Reviewing the literature on trends in Canadian mortality, we also uncover various challenges for the next decades. Reducing or even eliminating important disparities in mortality that persist with regards to geography and several socioeconomic factors is one of the greatest challenges ahead. Keywords: Mortality, longevity, health, trends, Canada

BACKGROUNDThe longevity gains recorded in high-income countries since the 1960s are mainly due to a reduction in mortality from chronic degenerative diseases, which particularly affect older individuals. In recent years the adult modal age at death (M) gained increasing recognition as a lifespan indicator for monitoring improvements in old-age survival. However, studies of M by cause of death are lacking.OBJECTIVEThis work investigates trends in M by leading causes of death in Canada over the 19742011 period and identifies the causes of death that have been more responsive to improvements in lifestyle behaviors and medical progress.METHODSWe extend a recent method for estimating the all-cause M using a flexible P-spline approach to the context of cause-of-death analysis. Using data from the Canadian Vital Statistics Database for the 1974. 2011 period, we derive cause-specific modal age-atdeath estimates and compare them in terms of levels and time-trends.RESULTSAlthough modal age-at-death estimates for heart diseases, cerebrovascular diseases, and the three types of cancers studied (breast/prostate, colorectal, and trachea, bronchus, and lung) differ greatly in terms of levels, they have all followed a steady upward trend since the mid-1970s in Canada. Moreover, the increase in cause-specific modal age estimates occurred at a strikingly similar pace for most causes, except for breast cancer females) and heart diseases (males), whose modal ages rose at a substantially faster pace.CONTRIBUTIONOur study introduces an innovative method for estimating cause-specific modal ages at death and provides the first available estimates of time-trends in M by leading causes of death.

Background: The Chiang method is the most widely accepted standard for estimating life expectancy (LE) at subnational scales; it is the only method that provides an equation for the LE variance. However, the Chiang variance formula incorrectly omits the contribution of the last age interval. This error is largely unknown to practitioners, and its impact has not been rigorously assessed. Objective: We aim to demonstrate the potentially substantial role of the last age interval on LE variance. We further aim to provide formulae and tools for corrected variance estimation. Methods: The delta method is used to derive variance formulae for a range of variance models of the last age interval. Corrected variances are tested on 291 empirical, abridged life tables drawn from Canadian data (2004-2008) spanning provincial, regional, and intra-regional scales. Results: The last age interval death count can contribute substantially to the LE variance, leading to overestimates of precision and false positives in statistical tests when using the uncorrected Chiang variance. Overdispersion amplifies the contribution while error in population counts has minimal impact. Conclusions: Use of corrected variance formulae is essential for studies that use the Chiang LE. The important role of the last age interval , and hence the life table closure method, on LE variance is demonstrated. These findings extend to other LE-derived metrics such as health expectancy. Contribution: We demonstrate that the last age interval death count can contribute substantially to the LE variance, thus resolving an ambiguity in the scientific literature. We provide heretofore-unavailable formulae for correcting the Chiang LE variance equation.

In the last decades, a lot of attention has been paid to the influence of socioeconomic features during childhood on adult health and mortality. Most studies have shown that an adverse environment in childhood leads to levels of morbidity (Blackwell et al., 2001; Hass, 2008; Moody-Ayers et al., 2004) and mortality (Elo and Preston, 1996; Galobardes et al., 2004; Osler et al., 2005) higher than the average. In this perspective, life course studies examine a range of potential processes through which biologic, social or physical exposures acting at different stages of life can have long-term effects on disease risks in later life and lead to inequalities in mortality. There is thus, without a doubt, multiple mechanisms through which conditions in early life may affect one’s health and mortality as an adult (Hertzman, 1999).

The Omran’s epidemiological transition theory has put forward a framework to interpret and accounts for the replacement of infectious diseases by chronic diseases due to expanded public health and sanitation. In this framework, mortality declines from infectious diseases are mainly driven by period factors in the short term, such as environmental changes, medical innovations and public policies. In contrast, chronic and degenerative disease mortality changes are mainly driven by long term cohort factors resulting from both the cumulative risks and cumulative advantages over the life-course (Omran 1971; Olshansky and Ault 1986).