Years Of Mortality Data Research Articles

Population reconstruction as an informative tool for monitoring chamois populations

Knowledge of population trends is of key importance for sustainable management of wildlife and finding reliable and cost–effective monitoring methods is therefore of great interest. In two populations of Alpine chamois Rupicapra rupicapra, we collected data on mortality from 12 424 individuals hunted or found dead and population size data based on ground counts over a period of 28 years. Our study had three aims: 1) we investigated if changes in population size obtained with a simple deterministic population reconstruction (DPR) approach using hunting and natural mortality covary with population size estimates obtained from ground count data. 2) We investigated if the performance of DPR is affected by the removal of natural mortality data. 3) We assessed how many years of mortality data are needed to obtain consistent population trends using DPR. Our results suggested that 1) population abundance from mortality data using DPR significantly and positively correlated with population abundance obtained with ground counts. 2) DPR without natural mortality data performed similarly as compared to DPR using full data (hunting and natural mortality). 3) Consistent estimates of population trends can be obtained with ≥10 years of mortality data, however, this time span was influenced by the mean age at death, which in turn was affected by the local hunting regime. Our results suggest that DPR and ground counts perform similarly for the estimation of temporal trends in Alpine chamois abundance. The consistence of ground counts and DPR supports the use of these methods as reliable tools for tracking abundance of chamois populations over time. However, the reliability of abundance estimates using DPR may vary between populations and the influence of different hunting regimes must be considered for the correct interpretation of results.

Recent Trends in Heat-Related Mortality in the United States: An Update through 2018

AbstractMuch research has shown a general decrease in the negative health response to extreme heat events in recent decades. With a society that is growing older, and a climate that is warming, whether this trend can continue is an open question. Using eight additional years of mortality data, we extend our previous research to explore trends in heat-related mortality across the United States. For the period 1975–2018, we examined the mortality associated with extreme-heat-event days across the 107 largest metropolitan areas. Mortality response was assessed over a cumulative 10-day lag period following events that were defined using thresholds of the excess heat factor, using a distributed-lag nonlinear model. We analyzed total mortality and subsets of age and sex. Our results show that in the past decade there is heterogeneity in the trends of heat-related human mortality. The decrease in heat vulnerability continues among those 65 and older across most of the country, which may be associated with improved messaging and increased awareness. These decreases are offset in many locations by an increase in mortality among men 45–64 (+1.3 deaths per year), particularly across parts of the southern and southwestern United States. As heat-warning messaging broadly identifies the elderly as the most vulnerable group, the results here suggest that differences in risk perception may play a role. Further, an increase in the number of heat events over the past decade across the United States may have contributed to the end of a decades-long downward trend in the estimated number of heat-related fatalities.

Forecasting mortality rates using hybrid Lee\u2013Carter model, artificial neural network and random forest

Inaccurate prediction would cause the insurance company encounter catastrophic losses and may lead to overpriced premiums where low-earning consumers cannot afford to insure themselves. The ability to forecast mortality rates accurately can allow the insurance company to take preventive measures to introduce new policies with reasonable prices. In this paper, several Lee–Carter (LC) based models are used to forecast the mortality rates in a case study of the Malaysian population. The LC-ARIMA model and also a combination of the LC model with two machine learning (ML) methods, namely the random forest (RF) and artificial neural network (ANN) methods are utilized on the prediction of mortality rates for males and females in Malaysia, whereby the LC-Random Forest (LC-RF) hybrid model is a new model that is introduced in this paper. Seventeen years of mortality data in Malaysia are selected as the dataset for this research. To analyze how the forecasting models perform for other countries, we have determined the model that has the best fit and produced the best forecasted mortality rates for all the other countries that are studied. This research has showed that LC-ANN and LC-ARIMA are the best model in predicting the mortality rates of males and females in Malaysia, respectively. This study has also found that the LC-ARIMA model is the best performing model in forecasting the mortality rates in countries that have longer life expectancy and a good healthcare system such as Sweden, Ireland, Japan, Hong Kong, Norway, Switzerland and Czechia. In contrast, the LC-ANN model is the best performing model in forecasting the mortality rates in countries that have a less efficiency, less accessibility healthcare system, and bad personal behavior such as Malaysia, Canada and Latvia.

Synthetic Opioids Should Be Excluded When Examining the Association Between Cannabis Laws and Opioid Overdose Mortality

We read with great interest the recent work in PNAS by Shover et al. revisiting the relationship between medical cannabis laws and opioid overdose mortality. They expand the 2014 Bachhuber et al. by adding 7 recent years of mortality data to cover a longer study period 1999-2017. They suggest that the reduction in opioid overdose mortality following medical cannabis laws became statistically indistinguishable from 0 when data in 2013-2016 are added and reversed after data in 2017 are added. The authors interpret the sensitivity of the results to the study endpoint to suggest that the association is spurious. We agree that the associations found in ecological studies should not be interpreted as causal relationships. However, we argue that the sensitivity of the results could be likely attributable to the recent spike in overdose mortality related to synthetic opioids.

1,3-Butadiene, styrene and lymphohematopoietic cancer among male synthetic rubber industry workers – Preliminary exposure-response analyses

We updated the mortality experience of North American synthetic rubber industry workers to include follow-up from 1944 through 2009, adding 11 years of mortality data to previous investigations. The present analysis used Cox regression to examine the exposure-response relationship between 1,3-butadiene (BD) and styrene (STY) parts per million (ppm)-years and leukemia (N = 114 deaths), non-Hodgkin lymphoma (NHL) (N = 89) and multiple myeloma (MM) (N = 48). A pattern of largely monotonically increasing rate ratios across deciles of BD ppm-years and a positive, statistically significant exposure-response trend were observed for BD ppm-years and leukemia. Using continuous, untransformed BD ppm-years the regression coefficient (β) adjusted only for age was 2.6 × 10−4 (p < 0.01); the regression coefficient adjusted for age, year of birth, race and plant was 2.9 × 10−4 (p < 0.01). STY ppm-years also displayed a positive exposure-response association with leukemia. STY and BD were strongly correlated, and the separate effects of these two agents could not be estimated. For NHL, a pattern of approximately monotonically increasing rate ratios across deciles of exposure was seen for STY but not for BD; the test of trend was statistically significant in one of five models that used different STY exposure metrics and adjusted for age and other covariates. BD ppm-years and STY ppm-years were not associated with MM. The present analyses indicated a positive exposure-response relationship between BD cumulative exposure and leukemia. This result along with other research and biological information support an interpretation that BD causes leukemia in humans. STY exposure also was positively associated with leukemia, but its independent effect could not be delineated because of its strong correlation with BD, and there is no external support for a STY-leukemia association. STY, but not BD, was associated positively with NHL. The interpretation of this result is uncertain because the exposure-response data were statistically imprecise and because consistent support for causality from other studies is lacking. The current study provides no support for an association between BD or STY and MM.

Paths to health equity: Local area variation in progress toward eliminating breast cancer mortality disparities, 1990-2009.

US breast cancer deaths have been declining since 1989, but African American women are still more likely than white women to die of breast cancer. Black/white disparities in breast cancer mortality rate ratios have actually been increasing. Across 762 US counties with enough deaths to generate reliable rates, county-level, age-adjusted breast cancer mortality rates were examined for women who were 35 to 74 years old during the period of 1989-2010. Twenty-two years of mortality data generated twenty 3-year rolling average data points, each centered on a specific year from 1990 to 2009. Mixed linear models were used to group each county into 1 of 4 mutually exclusive trend patterns. The most recent 3-year average black breast cancer mortality rate for each county was also categorized as being worse or not worse than the breast cancer mortality rate for the total US population. More than half of the counties (54%) showed persistent, unchanging disparities. Roughly 1 in 4 (24%) had a divergent pattern of worsening black/white disparities. However, 10.5% of the counties sustained racial equality over the 20-year period, and 11.7% of the counties actually showed a converging pattern from high disparities to greater equality. Twenty-three counties had 2008-2010 black mortality rates better than the US average mortality rate. Disparities are not inevitable. Four US counties have sustained both optimal and equitable black outcomes as measured by both absolute (better than the US average) and relative benchmarks (equality in the local black/white rate ratio) for decades, and 6 counties have shown a path from disparities to health equity.

Racial and ethnic disparities in fatal unintentional drowning among persons less than 30 years of age — United States, 1999–2010

BackgroundIn the U.S., almost 4,000 persons die from drowning annually. Among those 0–29years, drowning is in the top three causes of unintentional injury death. MethodsTo describe racial/ethnic differences in drowning rates by age of decedent and drowning setting, CDC analyzed 12years of mortality data from 1999 through 2010 for those ≤29years. ResultsCompared to whites, American Indians/Alaska Natives were twice, and blacks were 1.4 times, as likely to drown. Disparities were greatest in swimming pool settings, with drowning rates among blacks aged 5–19years 5.5 times higher than those among whites. ConclusionsDrowning rates for black children and teens are higher than those of other race/ethnicities, especially in swimming pools. Practical applicationThe practicality and effectiveness of current drowning prevention strategies varies by setting; however, basic swimming skills can be beneficial across all settings and may help reduce racial disparities.

Unintentional drowning mortality, by age and body of water: an analysis of 60 countries

BackgroundTo examine unintentional drowning mortality by age and body of water across 60 countries, to provide a starting point for further in-depth investigations within individual countries.MethodsThe latest available three years...

A double-exponential GARCH model for stochastic mortality

In this paper, a generalized GARCH-based stochastic mortality model is developed, which incorporates conditional heteroskedasticity and conditional non-normality. First, a detailed empirical analysis of the UK mortality rates from 1922 to 2009 is provided, where it was found that both the conditional heteroskedasticity and conditional non-normality are important empirical long-term structures of mortality. To describe conditional non-normality, a double-exponential distribution that allows conditional skewness and the heavy-tailed features found in the datasets was selected. For the practical implementation of the proposed model, a two-stage scheme was introduced to estimate the unknown parameters. First, the Quasi-Maximum Likelihood Estimation (QMLE) method was employed to estimate the GARCH structure. Next, the MLE was adopted to estimate the unknown parameters of the double-exponential distribution using residuals as input data. The model was then back-tested against the previous 10 years of mortality data to assess its forecasting ability, before Monte Carlo simulation was carried out to simulate and produce a table of forecast mortality rates from the optimal distribution.

Cause-specific mortality by occupational skill level in Canada: a 16-year follow-up study

Mortality data by occupation are not routinely available in Canada, so we analyzed census-linked data to examine cause-specific mortality rates across groups of occupations ranked by skill level. A 15% sample of 1991 Canadian Census respondents aged 25 years or older was previously linked to 16 years of mortality data (1991-2006). The current analysis is based on 2.3 million people aged 25 to 64 years at cohort inception, among whom there were 164 332 deaths during the follow-up period. Occupations coded according to the National Occupation Classification were grouped into five skill levels. Age-standardized mortality rates (ASMRs), rate ratios (RRs), rate differences (RDs) and excess mortality were calculated by occupational skill level for various causes of death. ASMRs were clearly graded by skill level: they were highest among those employed in unskilled jobs (and those without an occupation) and lowest for those in professional occupations. All-cause RRs for men were 1.16, 1.40, 1.63 and 1.83 with decreasing occupational skill level compared with professionals. For women the gradient was less steep: 1.23, 1.24, 1.32 and 1.53. This gradient was present for most causes of death. Rate ratios comparing lowest to highest skill levels were greater than 2 for HIV/AIDS, diabetes mellitus, suicide and cancer of the cervix as well as for causes of death associated with tobacco use and excessive alcohol consumption. Mortality gradients by occupational skill level were evident for most causes of death. These results provide detailed cause-specific baseline indicators not previously available for Canada.

Cardiovascular disease mortality among First Nations people in Canada, 1991–2001

To compare cardiovascular disease mortality patterns between First Nations people and non-Aboriginal adults by sex and by income adequacy quintile and level of educational attainment. A 15% sample of 1991 Canadian census respondents aged 25 years or older was previously linked to 11 years of mortality data. In this study, First Nations people were defined by North American Indian ethnic origin (ancestry), registration under the Indian Act, and/or membership in an Indian band or First Nation. The cohort included 62 400 First Nations people and 2 624 300 non-Aboriginal people. Compared to non-Aboriginal cohort members, the age-standardized cardiovascular disease mortality rate was 30% higher for First Nations men and 76% higher for First Nations women. This represented an excess of 58 deaths and 71 deaths per 100 000 person-years at risk, for First Nations men and women, respectively. Within each income adequacy quintile (adjusted for family size and region of residence) and level of educational attainment, the risk of dying from cardiovascular disease was higher for First Nations people compared to their non-Aboriginal counterparts. First Nations people had higher rates of death from cardiovascular disease than non-Aboriginal Canadians within each income quintile and level of education. Income and education accounted for 67% and 25% of the excess mortality of First Nations men and women respectively.

Daily Mortality and Air Pollution in Atlanta: August 1998–December 2006

ISEE-0879 Background and Objective: Authors have previously published using two years of mortality data for the two largest counties in Atlanta, GA (Inhalation Toxicology 16, 2004). In response to questions regarding limiting the geographic area to only two counties, the authors investigate whether the estimated effects remain consistent in terms of magnitude and/or statistical significance with the addition of an extended mortality data series and/or larger geographic area of decedents. Methods: The authors estimate the effects of pollution on human mortality for various AQI among decedents at least 65 years of age during 8/1/1998–12/31/2006. The authors also compare the effects for a four-county geographic area (Fulton, DeKalb, Gwinnett and Cobb counties) to the two-county area (Fulton and DeKalb counties) investigated previously. Results: The estimated effects differ depending on the time series and geographic area. The estimated effect of PM2.5 is lower in both magnitude and significance when estimated over the extended time series. Specifically, the published estimated effect for PM2.5 was .0054 (2.96 t-value) for the period 8/1/1998–7/31/2000 compared to .0016 (1.83 t-value) for 8/1/1998–12/31/2006. The estimated effect declined further when estimated using mortality within the four-county geographic area. Results for other AQI are similar in that the estimated effects using the larger geographic area are generally lower, although t-values are higher in some instances. Conclusion: Since it is difficult to define the “best” or most appropriate geographic area related to a specific measurement site, a comparison of various geographic definitions can illustrate the affect of different opinions on the estimated effects. The authors have shown the impact for a particular study location which should be replicated in other locations. It is likely, however, that no general pattern exists.

Pandemic Human Viruses Cause Decline of Endangered Great Apes

Commercial hunting and habitat loss are major drivers of the rapid decline of great apes [1]. Ecotourism and research have been widely promoted as a means of providing alternative value for apes and their habitats [2]. However, close contact between humans and habituated apes during ape tourism and research has raised concerns that disease transmission risks might outweigh benefits [3-7]. To date only bacterial and parasitic infections of typically low virulence have been shown to move from humans to wild apes [8, 9]. Here, we present the first direct evidence of virus transmission from humans to wild apes. Tissue samples from habituated chimpanzees that died during three respiratory-disease outbreaks at our research site, Côte d'Ivoire, contained two common human paramyxoviruses. Viral strains sampled from chimpanzees were closely related to strains circulating in contemporaneous, worldwide human epidemics. Twenty-four years of mortality data from observed chimpanzees reveal that such respiratory outbreaks could have a long history. In contrast, survey data show that research presence has had a strong positive effect in suppressing poaching around the research site. These observations illustrate the challenge of maximizing the benefit of research and tourism to great apes while minimizing the negative side effects.

An Examination of Urban Versus Rural Mortality in China Using Community and Individual Data

Urban/rural residence is a critical health determinant and one researchers have historically found to distinguish health experiences. In this study, we investigated variations in older adult mortality across urban and rural areas of China and assessed mechanisms driving an urban advantage through a series of socioeconomic and health service covariates measured at individual and community levels. We employed 15 years of mortality data from the China Health and Nutrition Survey. We calculated average annual age-specific death rates and used combinations of covariates to examine Cox proportional hazards models. We employed the 2000 Chinese Census and the 2002 Demographic Yearbook descriptively to assess reliability and provide an alternative source for mortality variation. Hazard ratios and standardized death rates showed rural mortality to be about 30% higher than urban mortality. Cadre status, amenities within the community, and average wage within the community are important determinants of mortality, and adjusting for these covariates reduced the urban advantage. There is great differentiation in economic and social life between urban and rural China, and this appears to be negatively influencing survival chances of older adults in rural areas. The policy implications are fairly clear: Investment in rural China is needed to reduce health inequalities.

Inorganic Arsenic in Drinking Water: An Evolving Public Health Concern

In recent years, ingestion of inorganic arsenic from drinking water has emerged as an important scientific issue and public health concern. The International Agency for Research on Cancer has identified sufficient evidence in humans that inorganic arsenic causes lung, bladder, and nonmelanoma skin cancers ( 1 ) (summary at http://monographs.iarc.fr/ ). Reports by expert committees have suggested associations with several other cancer and noncancer outcomes ( 2 – 4 ). As a result, the US Environmental Protection Agency lowered the maximum contaminant level for arsenic in drinking water supplied by community water systems from 50 µ g/L, a level set in 1942, to 10 µ g/L, effective from January 2006. The reduction will necessitate changes to water systems serving approximately 13 million people ( http://www.epa.gov/safewater/arsenic/compliance. html ). The World Health Organization has similarly recommended 10 µ g/L for arsenic in water as a “guideline value” for setting national standards ( http://www.who.int/mediacentre/factsheets/fs210/en/ index.html ). Substantial numbers of people worldwide are exposed to elevated concentrations of arsenic. An estimated 25 million people in Bangladesh (19% of the population) and 6 million people in West Bengal, India (8% of the population), consume water with arsenic exceeding 50 µ g/L ( 5 ), with perhaps twice these numbers in these countries consuming water with arsenic levels exceeding 10 µ g/L. High levels of inorganic arsenic levels are found in drinking water in many other parts of the world, including areas of Argentina (county means ranged to 178 µ g/L) ( 6 ), the Inner Mongolia and Xinjiang autonomous regions in China (levels in excess of 600 µ g/L) ( 7 ), Finland (levels were generally low but ranged to 64 µ g/L) ( 8 ), northern Mexico (ranges in exposed areas to 160 – 740 µ g/L) ( 9 ), and the United States (with some areas in California, Nevada, Alaska, Michigan, New England, New Mexico, and Utah exceeding 50 µ g/L) (see US Geological Survey map of 31 350 ground water measurements at http://co.water.usgs.gov/trace/ pubs/arsenic_fi g1.html ). Drinking water arsenic levels in excess of 150 µ g/L also occur in Nepal ( 10 ), Thailand ( 11 ), Vietnam ( 12 ), Hungary ( 13 ), Ghana ( 14 ), and elsewhere ( 15 ). Although arsenic contamination of water supplies arises mainly from natural sources, human activities such as mining and ore processing may also contribute to elevated arsenic levels in some areas. Although ingestion of high levels of inorganic arsenic is most strongly linked to lung, bladder, and nonmelanoma skin cancers, there is evidence for associations with cancers of the kidney, liver, and possibly prostate ( 16 ). In addition, high levels of drinking water arsenic have been linked to cutaneous effects (hyperpigmentation, hypopigmentation, palmar – plantar hyperkeratoses, and leucomelanosis), gastrointestinal effects (gastrointestinal distress and liver cirrhosis), vascular effects (peripheral vascular diseases, such as blackfoot disease and Raynaud’s syndrome; arterial occlusions; cardiovascular disease; cerebrovascular disease; and hypertension), diabetes mellitus, and peripheral neuropathy ( 2 ), as well as to chronic cough, shortness of breath, and other respiratory effects ( 17 ). Arsenic can cross the placental barrier, and ingestion of high levels by pregnant women may cause adverse reproductive and developmental effects and increase rates of stillbirths, spontaneous abortions, low – birth weight deliveries, and neonatal and postneonatal mortality ( 18 , 19 ). Many of these associations were identifi ed from ecologic studies conducted in a limited number of populations; there have been relatively few analytic studies. Thus, many of the associations between arsenic ingestion and cancers other than lung, bladder, and nonmelanoma skin cancers and noncancer outcomes have not been conclusively demonstrated, and additional studies are needed. In this issue of the Journal, Marshall et al. ( 20 ) analyzed 50 years of mortality data for lung and bladder cancers, substantially extending a previous analysis ( 21 ). Data are ecologic and come from the climatologically and geologically unique setting of Region II in northern Chile. The climate is extremely arid, and the population lives primarily in cities and towns and relies almost exclusively on municipally supplied drinking water. Based on arsenic measurements made since the 1950s, arsenic levels within Region II have varied spatially and temporally, from highs of

Natural mortality amoung four common ungulate species on Letaba Ranch, Limpopo Province, South Africa

Five years of mortality data of impala Aepyceros melampus, blue wildebeest Connochaetes taurinus, buffalo Syncerus caffer and kudu Tragelaphus strepsiceros have been used to describe the minimum mortality profiles of the respective species in an open savanna system with the full compliment of predators. Predation is the principle cause of natural mortalities on the study site, Letaba Ranch, which is adjacent to the Kruger National Park. The principle cause of impala mortality are leopards Panthera pardus and wild dogs Lycaon pictus. Lion Panthera leo were major contributors to the mortality of wildebeest and buffalo. Anthrax Bacillus anthracis was the main cause of kudu mortality.

Healthy volunteer effect in a cohort study: Temporal resolution in the adventist health study

The healthy volunteer effect was studied by comparing 6 years of mortality data for 31,124 participants from the Adventist Health Study (AHS) who responded to both a relatively brief census questionnaire (CQ) in 1974 and a detailed life-style questionnaire (LQ) in 1976 (responders), to mortality data for 8,762 individuals who did not respond to the second questionnaire. The rate ratio (RR) comparing LQ nonresponders to responders for all cause mortality decreased from 2.5 (2.2-2.9) in 1977 to 1.4 (1.2-1.7) in 1982 (p for trend = 0.02); for ischemic heart disease mortality from 2.3 (1.8-3.0) to 1.3 (1.0-1.7); and for all sites cancer mortality from 1.8 (1.3-2.5) to 1.5 (1.1-2.0). The death rate decreased markedly among nonresponders and increased slightly among responders during the study. Similar results were seen for age and gender subgroups. Multivariate analysis controlling for confounding variables confirms these results, except that the apparent effect of education is probably due to effect modification by age. The RR decreased to about one after 3 years of follow-up in young subjects but remained elevated (> 2) in older subjects. Available sociodemographic information reveals that a higher proportion of responders are married, have college education, are SDA church members, and use medical services less than nonresponders during the previous year. Because the risk remains elevated at the end of the study in some but not all subgroups, it seems reasonable that the elevated risk in nonresponders may be due in part to a less healthy life style and in part to exclusion of individuals who did not feel well during enrollment. The results suggest that for internal comparisons no bias is likely to occur; but descriptive statistics for certain subgroup comparisons, and external comparisons, may be biased by the healthy volunteer effect.

Stand development in a 130-year-old spruce-hemlock forest based on age structure and 50 years of mortality data

Influences on forest stand development were assessed using tree age and long-term mortality data in ten 0.4 ha permanent plots established in 1935. The stand originated following a major fire in the 1840s with a period of rapid invasion (1851–1870). This was followed by slower filling to full stand closure (1871–1900), recruitment suppression (1901–1930), reinitiation of hemlock recruitment (1931–1950), and continued slow recruitment (1951-present). Recruitment re-initiation was apparently associated with natural stand thinning and not with major disturbance. Large blowdown patches occurred in two plots in the 1960s, but the primary effect was release of hemlock advance regeneration rather than recruitment of new individuals. From 1935 to 1983 annual mortality (calculated from 5–10-years remeasurements) was 0.5–1.2% for both species. At this rate, continued thinning will likely allow a gradual transition to an all-aged forest, as population turnover time is short relative to frequency of intermediate or major disturbance.