Social inequalities in male mortality, and in male mortality from smoking: indirect estimation from national death rates in England and Wales, Poland, and North America

Background There are substantial social inequalities in adult male mortality in many countries. Smoking is often more prevalent among men of lower social class, education, or income. The contribution of smoking to these social inequalities in mortality remains uncertain. Methods The contribution of smoking to adult mortality in a population can be estimated indirectly from disease-specific death rates in that population (using absolute lung cancer rates to indicate proportions due to smoking of mortality from certain other diseases). We applied these methods to 1996 death rates at ages 35-69 years in men in three different social strata in four countries, based on a total of 0.6 million deaths. The highest and lowest social strata were based on social class (professional vs unskilled manual) in England and Wales, neighbourhood income (top vs bottom quintile) in urban Canada, and completed years of education (more than vs less than 12 years) in the USA and Poland. Results In each country, there was about a two-fold difference between the highest and the lowest social strata in overall risks of dying among men aged 35-69 years (England and Wales 21% vs 43%, USA 20% vs 37%, Canada 21% vs 34%, Poland 26% vs 50%: four-country mean 22% vs 41%, four-country mean absolute difference 19%). More than half of this difference in mortality between the top and bottom social strata involved differences in risks of being killed at age 35-69 years by smoking (England and Wales 4% vs 19%, USA 4% vs 15%, Canada 6% vs 13%, Poland 5% vs 22%: four-country mean 5% vs 17%, four-country mean absolute difference 12%). Smoking-attributed mortality accounted for nearly half of total male mortality in the lowest social stratum of each country. Conclusion In these populations, most, but not all, of the substantial social inequalities in adult male mortality during the 1990s were due to the effects of smoking. Widespread cessation of smoking could eventually halve the absolute differences between these social strata in the risk of premature death.

Rising longevity, education, savings, and growth

This paper examines the impact of declines in adult mortality on growth in an overlapping generations model. With public education and imperfect annuity markets, a decline in mortality affects growth through three channels. First, it raises the saving rate and thereby increases the rate of physical capital accumulation. Second, it reduces accidental bequests, lowers investment, and thereby lowers the rate of physical capital accumulation. Third, it may lead the median voter to increase the tax rate for public education initially but lower the tax rate in a later stage. Starting from a high mortality rate as found in many Third World populations, the net effect of a decline in mortality is to raise the growth rate. However, starting from a low mortality rate such as is found in most industrial populations, the net effect of a further decline in mortality is to reduce the growth rate. The findings appear consistent with recent empirical evidence. (C) 2002 Elsevier Science B.V All rights reserved.

Global and regional burden of disease and risk factors, 2001: systematic analysis of population health data

Background Our aim was to calculate the global burden of disease and risk factors for 2001, to examine regional trends from 1990 to 2001, and to provide a starting point for the analysis of the Disease Control Priorities Project (DCPP). Methods We calculated mortality, incidence, prevalence, and disability adjusted life years (DALYs) for 136 diseases and injuries, for seven income/geographic country groups. To assess trends, we re-estimated all-cause mortality for 1990 with the same methods as for 2001. We estimated mortality and disease burden attributable to 19 risk factors. Findings About 56 million people died in 2001. Of these, 10.6 million were children, 99% of whom lived in low-and-middle-income countries. More than half of child deaths in 2001 were attributable to acute respiratory infections, measles, diarrhoea, malaria, and HIV/AIDS. The ten leading diseases for global disease burden were perinatal conditions, lower respiratory infections, ischaemic heart disease, cerebrovascular disease, HIV/AIDS, diarrhoeal diseases, unipolar major depression, malaria, chronic obstructive pulmonary disease, and tuberculosis. There was a 20% reduction in global disease burden per head due to communicable, maternal, perinatal, and nutritional conditions between 1990 and 2001. Almost half the disease burden in low-and-middle-income countries is now from non-communicable diseases (disease burden per head in Sub-Saharan Africa and the low-and-middle-income countries of Europe and Central Asia increased between 1990 and 2001). Undernutrition remains the leading risk factor for health loss. An estimated 45% of global mortality and 36% of global disease burden are attributable to the joint hazardous effects of the 19 risk factors studied. Uncertainty in all-cause mortality estimates ranged from around 1% in high-income countries to 15-20% in Sub-Saharan Africa. Uncertainty was larger for mortality from specific diseases, and for incidence and prevalence of non-fatal outcomes. Interpretation Despite uncertainties about mortality and burden of disease estimates, our findings suggest that substantial gains in health have been achieved in most populations, countered by the HIV/AIDS epidemic in Sub-Saharan Africa and setbacks in adult mortality in countries of the former Soviet Union. our results on major disease, injury, and risk factor causes of loss of health, together with information on the cost-effectiveness of interventions, can assist in accelerating progress towards better health and reducing the persistent differentials in health between poor and rich countries.

Effect of soil burial depth and wetting on mortality of diapausing larvae and patterns of post-diapause adult emergence of sorghum midge, Stenodiplosis sorghicola (Coquillett) (Diptera : Cecidomyiidae)

In south-eastern Queensland, Australia, sorghum planted in early spring usually escapes sorghum midge, Stenodiplosis sorghicola, attack. Experiments were conducted to better understand the role of winter diapause in the population dynamics of this pest. Emergence patterns of adult midge from diapausing larvae on the soil surface and at various depths were investigated during spring to autumn of 1987/88-1989/90. From 1987/88 to 1989/90, 89%, 65% and 98% of adult emergence, respectively, occurred during November and December. Adult emergence from larvae diapausing on the soil surface was severely reduced due to high mortality attributed to surface soil temperatures in excess of 40 degrees C, with much of this mortality occurring between mid-September and mid-October. Emergence of adults from the soil surface was considerably delayed in the 1988/89 season compared with larvae buried at 5 or 10 cm which had similar emergence patterns for all three seasons. In 1989/90, when a 1-cm-deep treatment was included, there was a 392% increase in adult emergence from this treatment compared with deeper treatments. Some diapausing larvae on the surface did not emerge at the end of summer in only 1 year (1989/90), when 28.0% of the larvae on the surface remained in diapause, whereas only 0.8% of the buried larvae remained in diapause. We conclude that the pattern of emergence explains why spring plantings of sorghum in south-eastern Queensland usually escape sorghum midge attack.

Adult-population incidence of severe sepsis in Australian and New Zealand intensive care units

Objective. To determine the population incidence and outcome of severe sepsis occurring in adult patients treated in Australian and New Zealand intensive care units (ICUs), and compare with recent retrospective estimates from the USA and UK. Design. Inception cohort study. Setting. Twenty-three closed multi-disciplinary ICUs of 21 hospitals (16 tertiary and 5 university affiliated) in Australia and New Zealand. Patients. A total of 5878 consecutive ICU admission episodes. Measurements and results. Main outcome measures were population-based incidence of severe sepsis, mortality at ICU discharge, mortality at 28 days after onset of severe sepsis, and mortality at hospital discharge. A total of 691 patients, 11.8 (95% confidence intervals 10.9-12.6) per 100 ICU admissions, were diagnosed with 752 episodes of severe sepsis. Site of infection was pulmonary in 50.3% of episodes and abdominal in 19.3% of episodes. The calculated incidence of severe sepsis in adults treated in Australian and New Zealand ICUs is 0.77 (0.76-0.79) per 1000 of population. 26.5% of patients with severe sepsis died in ICU, 32.4% died within 28 days of the diagnosis of severe sepsis and 37.5% died in hospital. Conclusion. In this prospective study, 11.8 patients per 100 ICU admissions were diagnosed with severe sepsis and the calculated annual incidence of severe sepsis in adult patients treated in Australian and New Zealand ICUs is 0.77 per 1000 of population. This figure for the population incidence falls in the lower range of recent estimates from retrospective studies in the U.S. and the U.K.

Regional, disease specific patterns of smoking-attributable mortality in 2000

Background: Smoking has been causally associated with increased mortality from several diseases, and has increased considerably in many developing countries in the past few decades. Mortality attributable to smoking in the year 2000 was estimated for adult males and females, including estimates by age and for specific diseases in 14 epidemiological subregions of the world. Methods: Lung cancer mortality was used as an indirect marker of the accumulated hazard of smoking. Never-smoker lung cancer mortality was estimated based on the household use of coal with poor ventilation. Estimates of mortality caused by smoking were made for lung cancer, upper aerodigestive cancer, all other cancers, chronic obstructive pulmonary disease ( COPD), other respiratory diseases, cardiovascular diseases, and selected other medical causes. Estimates were limited to ages 30 years and above. Results: In 2000, an estimated 4.83 million premature deaths in the world were attributable to smoking, 2.41 million in developing countries and 2.43 million in industrialised countries. There were 3.84 million male deaths and 1.00 million female deaths attributable to smoking. 2.69 million smoking attributable deaths were between the ages of 30 - 69 years, and 2.14 million were 70 years of age and above. The leading causes of death from smoking in industrialised regions were cardiovascular diseases ( 1.02 million deaths), lung cancer (0.52 million deaths), and COPD (0.31 million deaths), and in the developing world cardiovascular diseases (0.67 million deaths), COPD (0.65 million deaths), and lung cancer (0.33 million deaths). The share of male and female deaths and younger and older adult deaths, and of various diseases in total smoking attributable deaths exhibited large inter-regional heterogeneity, especially in the developing world. Conclusions: Smoking was an important cause of global mortality in 2000, affecting a large number of diseases. Age, sex, and disease patterns of smoking-caused mortality varied greatly across regions, due to both historical and current smoking patterns, and the presence of other risk factors that affect background mortality from specific diseases.

Statistical modeling and projections of lung cancer mortality in 4 industrialized countries

The purpose of this work was to model lung cancer mortality as a function of past exposure to tobacco and to forecast age-sex-specific lung cancer mortality rates. A 3-factor age-period-cohort (APC) model, in which the period variable is replaced by the product of average tar content and adult tobacco consumption per capita, was estimated for the US, UK, Canada and Australia by the maximum likelihood method. Age- and sex-specific tobacco consumption was estimated from historical data on smoking prevalence and total tobacco consumption. Lung cancer mortality was derived from vital registration records. Future tobacco consumption, tar content and the cohort parameter were projected by autoregressive moving average (ARIMA) estimation. The optimal exposure variable was found to be the product of average tar content and adult cigarette consumption per capita, lagged for 2530 years for both males and females in all 4 countries. The coefficient of the product of average tar content and tobacco consumption per capita differs by age and sex. In all models, there was a statistically significant difference in the coefficient of the period variable by sex. In all countries, male age-standardized lung cancer mortality rates peaked in the 1980s and declined thereafter. Female mortality rates are projected to peak in the first decade of this century. The multiplicative models of age, tobacco exposure and cohort fit the observed data between 1950 and 1999 reasonably well, and time-series models yield plausible past trends of relevant variables. Despite a significant reduction in tobacco consumption and average tar content of cigarettes sold over the past few decades, the effect on lung cancer mortality is affected by the time lag between exposure and established disease. As a result, the burden of lung cancer among females is only just reaching, or soon will reach, its peak but has been declining for I to 2 decades in men. Future sex differences in lung cancer mortality are likely to be greater in North America than Australia and the UK due to differences in exposure patterns between the sexes. (c) 2005 Wiley-Liss, Inc.

Design options for sample-based mortality surveillance

Background Reliable information on causes of death is a fundamental component of health development strategies, yet globally only about one-third of countries have access to such information. For countries currently without adequate mortality reporting systems there are useful models other than resource-intensive population-wide medical certification. Sample-based mortality surveillance is one such approach. This paper provides methods for addressing appropriate sample size considerations in relation to mortality surveillance, with particular reference to situations in which prior information on mortality is lacking. Methods The feasibility of model-based approaches for predicting the expected mortality structure and cause composition is demonstrated for populations in which only limited empirical data is available. An algorithm approach is then provided to derive the minimum person-years of observation needed to generate robust estimates for the rarest cause of interest in three hypothetical populations, each representing different levels of health development. Results Modelled life expectancies at birth and cause of death structures were within expected ranges based on published estimates for countries at comparable levels of health development. Total person-years of observation required in each population could be more than halved by limiting the set of age, sex, and cause groups regarded as 'of interest'. Discussion The methods proposed are consistent with the philosophy of establishing priorities across broad clusters of causes for which the public health response implications are similar. The examples provided illustrate the options available when considering the design of mortality surveillance for population health monitoring purposes.

Adult obesity and number of years lived with and without cardiovascular disease

Objective: To determine the differences in number of years lived free of cardiovascular disease (CVD) and number of years lived with CVD between men and women who were obese, pre-obese, or normal weight at 45 years of age. Research Methods and Procedures: We constructed multistate life tables for CVD, myocardial infarction, and stroke, using data from 2551 enrollees (1130 men) in the Framingham Heart Study who were 45 years of age. Results: Obesity and pre-obesity were associated with fewer number of years free of CVD, myocardial infarction, and stroke and an increase in the number of years lived with these diseases. Forty-five-year-old obese men with no CVD survived 6.0 years [95% confidence interval (CI), 4.1; 8.1] fewer than their normal weight counterparts, whereas, for women, the difference between obese and normal weight subjects was 8.4 years (95% CI: 6.2; 10.8). Obese men and women lived with CVD 2.7 (95% CI: 1.0; 4.4) and 1.4 years (95% CI: -0.3; 3.2) longer, respectively, than normal weight individuals. Discussion: In addition to reducing life expectancy, obesity before middle age is associated with a reduction in the number of years lived free of CVD and an increase in the number of years lived with CVD. Such information is paramount for preventive and therapeutic decision-making by individuals and practitioners alike.

Contribution of changes in risk factors to the decline of coronary heart disease mortality in Australia over three decades

BACKGROUND: Coronary heart disease has been a major cause of mortality in Australian adults, but the rate has declined by 83% from the 1968 peak by the year 2000. The study objective is to determine the contribution of changes in population risk factors - mean serum cholesterol and diastolic blood pressure and tobacco smoking prevalence - to the decline in coronary heart disease mortality in Australia over three decades. METHODS: Coronary heart disease deaths (International Classification of Disease-9, 410-414) and population by year, age group and sex were obtained from the Australian Bureau of Statistics. Risk factor levels were obtained from population surveys and estimated average annual changes by period were used to calculate average annual 'attributable' proportional declines in CHD mortality by period (age 35-64 years). RESULTS: Over the period 1968-2000, 74% of male decline and 81% of the female decline in coronary heart disease mortality rate was accounted for by the combined effect of reductions in the three risk factors. In males 36% of the decline was contributed by reductions in diastolic blood pressure, 22% by cholesterol and 16% by smoking. For females 56% was from diastolic blood pressure reduction, 20% from cholesterol and 5% from smoking. Effects of reductions in serum cholesterol on coronary heart disease mortality occurred mainly in the 1970s. Declines in diastolic blood pressure had effects on coronary heart disease mortality over the three decades, and declines in tobacco smoking had a significant effect in males in the 1980s. CONCLUSION: Most of the spectacular decline in coronary heart disease mortality over the last three decades in Australia can be ascribed to reductions in population risk factors from primary and secondary prevention.