Long-term exposure to ambient air pollution and mortality due to cardiovascular disease and cerebrovascular disease in Shenyang, China

Background

The relationship between ambient air pollution exposure and mortality of cardiovascular and cerebrovascular diseases in human is controversial, and there is little information about how exposures to ambient air pollution contribution to the mortality of cardiovascular and cerebrovascular diseases among Chinese. The aim of the present study was to examine whether exposure to ambient-air pollution increases the risk for cardiovascular and cerebrovascular disease.

Methodology/Principal Findings

We conducted a retrospective cohort study among humans to examine the association between compound-air pollutants [particulate matter <10 µm in aerodynamic diameter (PM₁₀), sulfur dioxide (SO₂) and nitrogen dioxide (NO₂)] and mortality in Shenyang, China, using 12 years of data (1998–2009). Also, stratified analysis by sex, age, education, and income was conducted for cardiovascular and cerebrovascular mortality. The results showed that an increase of 10 µg/m³ in a year average concentration of PM₁₀ corresponds to 55% increase in the risk of a death cardiovascular disease (hazard ratio [HR], 1.55; 95% confidence interval [CI], 1.51 to 1.60) and 49% increase in cerebrovascular disease (HR, 1.49; 95% CI, 1.45 to 1.53), respectively. The corresponding figures of adjusted HR (95%CI) for a 10 µg/m³ increase in NO₂ was 2.46 (2.31 to 2.63) for cardiovascular mortality and 2.44 (2.27 to 2.62) for cerebrovascular mortality, respectively. The effects of air pollution were more evident in female that in male, and nonsmokers and residents with BMI<18.5 were more vulnerable to outdoor air pollution.

Conclusion/Significance

Long-term exposure to ambient air pollution is associated with the death of cardiovascular and cerebrovascular diseases among Chinese populations.     

Dental disease and risk of coronary heart disease and mortality.

OBJECTIVE--To investigate a reported association between dental disease and risk of coronary heart disease. SETTING--National sample of American adults who participated in a health examination survey in the early 1970s. DESIGN--Prospective cohort study in which participants underwent a standard dental examination at baseline and were followed up to 1987. Proportional hazards analysis was used to estimate relative risks adjusted for several covariates. MAIN OUTCOME MEASURES--Incidence of mortality or admission to hospital because of coronary heart disease; total mortality. RESULTS--Among all 9760 subjects included in the analysis those with periodontitis had a 25% increased risk of coronary heart disease relative to those with minimal periodontal disease. Poor oral hygiene, determined by the extent of dental debris and calculus, was also associated with an increased incidence of coronary heart disease. In men younger than 50 years at baseline periodontal disease was a stronger risk factor for coronary heart disease; men with periodontitis had a relative risk of 1.72. Both periodontal disease and poor oral hygiene showed stronger associations with total mortality than with coronary heart disease. CONCLUSION--Dental disease is associated with an increased risk of coronary heart disease, particularly in young men. Whether this is a causal association is unclear. Dental health may be a more general indicator of personal hygiene and possibly health care practices.     

Decline in mortality from coronary heart disease in Finland from 1969 to 1979.

The trends in mortality from coronary heart disease in the 1970s and the differences in trends between counties within Finland were calculated from official mortality statistics among the population aged 35 to 64 years. During this period coronary mortality declined by a mean of 1.1% for men and 2.3% for women annually in the whole of Finland. A community based cardiovascular control programme was started in 1972 in North Karelia, a county in the east of Finland. The decline in coronary mortality in this county between 1969 and 1979 was 24% in men and 51% in women. The decline in the rest of Finland over the same period was 12% in men and 24% in women. The decline in North Karelia was greater than that in other counties of Finland for both men and women and that difference exceeded random variation, with over 95% likelihood for both sexes. Even with adjustment for rates before 1974 with cross-county multiple regression analyses the difference persisted. Although further studies are needed, the changes in coronary mortality in North Karelia suggest that the preventive programme has been effective.     

Dietary factors in the fall in coronary heart disease mortality.

The role of dietary change in the fall in heart disease mortality has been hotly debated. Three countries, Australia, USA and UK with equal 'care' and sophistication of surgical techniques have shown different timing in the beginning of the decline of this 'epidemic'; around the mid 1960s in the first two countries, but not until the late 1970s for the UK. The cause of this difference may be the changing food habits of their populations. Using food disappearance data, apparent consumption of butter and margarine show opposite trends (butter down and margarine up) predating the decline in mortality in both the USA and Australia by at least 7 years and also in the UK, but at a later time, (about 1970). Changes in adipose tissue linoleate, a marker for polyunsaturated fat intake, support this indirect evidence, with depot levels rising in the USA from the 1960s and 10 years later in the UK. Other evidence support the view of decreasing saturated fat intake and increasing polyunsaturated intake prior to 1960 in the USA. Although many factors must contribute to the decline in mortality from CHD, change in dietary P/S ratio would seem to be the major dietary contributor.     

Contribution of SELP and PSGL-1 genotypes and haplotypes to the presence of coronary heart disease in Tunisians

P-selectin (SELP) and its counter-receptor, P-selectin glycoprotein ligand-1 (PSGL-1), play key role in the transient attachment of leukocytes to endothelial cells predisposing to coronary heart disease (CHD). In the current report, 293 angiographically proven CHD patients and 327 age, gender, and race-matched controls were included. Our aim was to evaluate the contribution to CHD of the following SNPs: C-2123G, G-1969A and T715P in SELP, Met62Ile and the VNTR variants in PSGL-1 gene in a North African population from Tunisia. While there were no significant differences in the distribution of SELP or PSGL-1 alleles or genotypes between patients and controls, a trend for a significant association of the C-2123G genotypes distribution with incident CHD was observed (P = 0.06). Assuming an additive model of transmission, the risk was 74% higher among subjects carrying the GG genotypes in comparison to those carrying the CC genotype (OR = 1.74 [1.01–2.98], P = 0.04) and 80% higher in the recessive model (OR = 1.80 [1.08–3.01], P = 0.02). Haplotype analysis did not identify any specific SELP or PSGL-1 haplotypes to be associated with CHD. The present study demonstrated no evidence of association between individual SELP or PSGL-1 SNPs or haplotypes with incident CHD. However, this study replicates absence of association of the mostly studied SNP, T715P, previously reported in individuals with African origin.     

Common genetic variation in multiple metabolic pathways influences susceptibility to low HDL-cholesterol and coronary heart disease

A low level of HDL-C is the most common plasma lipid abnormality observed in men with established coronary heart disease (CHD). To identify allelic variants associated with susceptibility to low HDL-C and CHD, we examined 60 candidate genes with key roles in HDL metabolism, insulin resistance, and inflammation using samples from the Veterans Affairs HDL Intervention Trial (VA-HIT; cases, n = 699) and the Framingham Offspring Study (FOS; controls, n = 705). VA-HIT was designed to examine the benefits of HDL-raising with gemfibrozil in men with low HDL-C (≤40 mg/dl) and established CHD. After adjustment for multiple testing within each gene, single-nucleotide polymorphisms (SNP) significantly associated with case status were identified in the genes encoding LIPC (rs4775065, P < 0.0001); CETP (rs5882, P = 0.0002); RXRA (rs11185660, P = 0.0021); ABCA1 (rs2249891, P = 0.0126); ABCC6 (rs150468, P = 0.0206; rs212077, P = 0.0443); CUBN (rs7893395, P = 0.0246); APOA2 (rs3813627, P = 0.0324); SELP (rs732314, P = 0.0376); and APOC4 (rs10413089, P = 0.0425). Included among the novel findings of this study are the identification of susceptibility alleles for low HDL-C/CHD risk in the genes encoding CUBN and RXRA, and the observation that genetic variation in SELP may influence CHD risk through its effects on HDL.     

The potential effects of climate change on winter mortality in England and Wales

In Britain death rates from several important causes, particularly circulatory and respiratory diseases, rise markedly during the colder winter months. This close association between temperature and mortality suggests that climate change as a result of global warming may lead to a future reduction in excess winter deaths. This paper gives a brief introductory review of the literature on the links between cold conditions and health, and statistical models are subsequently developed of the associations between temperature and monthly mortality rates for the years 1968 to 1988 for England and Wales. Other factors, particularly the occurrence of influenza epidemics, are also taken into account. Highly significant negative associations were found between temperature and death rates from all causes and from chronic bronchitis, pneumonia, ischaemic heart disease and cerebrovascular disease. The statistical models developed from this analysis were used to compare death rates for current conditions with those that might be expected to occur in a future warmer climate. The results indicate that the higher temperatures predicted for 2050 might result in nearly 9000 fewer winter deaths each year with the largest contribution being from mortality from ischaemic heart disease. However, these preliminary estimates might change when further research is able to make into account a number of additional factors affecting the relationship between mortality and climate.     

Parallelism of atmospheric electrical potential and mortality in London air pollution episodes

Atmospheric electrical potential (E) was evaluated statistically with smoke and sulfur dioxide as a predictor of excess mortality during the London air pollution episodes of the 1950s. E, as a surrogate of respirable aerosols, in combination with SO₂ proved to be a better predictor of excess episode mortality than smoke.     

What contribution has cardiac surgery made to the decline in mortality from coronary heart disease?

The number of deaths from coronary artery disease is declining in New Zealand as in some other Western countries. It has been estimated that in 1981 in the Auckland metropolitan area there were 126 fewer deaths than would have been expected from the data in 1974. The contribution made by cardiac surgery to this decline was assessed from the known numbers of patients who were operated on, from their survival rate, and from the predicted mortality of the surgical cohort had they not undergone operation. Such mortality was predicted from past studies of patients with similar symptoms, exercise data, studies of unstable angina, and the coronary artery surgical study registry. From this method it was estimated that coronary surgery accounted for 26% to 42% of the reduction in coronary deaths. Two previous studies estimated, from calculations based on the European study of patients with modest symptoms, that the contribution of cardiac surgery was much lower. Extrapolating data from one subset of patients to a second subset with quite different characteristics is a conceptual fallacy.     

Worldwide variation in life-span sexual dimorphism and sex-specific environmental mortality rates

In all human populations mean life span of women generally exceeds that of men, but the extent of this sexual dimorphism varies across different regions of the world. Our purpose here is to study, using global demographic and environmental data, the general tendency of this variation and local deviations from it. We used data on male and female life history traits and environmental conditions for 227 countries and autonomous territories; for each country or territory the life-span dimorphism was defined as the difference between mean life spans of women and men. The general tendency is an increase of life-span dimorphism with increasing average male-female life span; this tendency can be explained using a demographic model based on the Makeham-Gompertz equation. Roughly, the life-span dimorphism increases with the average life span because of an increase in the duration of expressing sex- and age-dependent mortality described by the second (exponential) term of the Makeham-Gompertz equation. Thus we investigated the differences in male and female environmental mortality described by the first term of the Makeham-Gompertz equation fitted to the data. The general pattern that resulted was an increase in male mortality at the highest and lowest latitudes. One plausible explanation is that specific factors tied to extreme latitudes influence males more strongly than females. In particular, alcohol consumption increases with increasing latitude and, on the contrary, infection pressures increase with decreasing latitude. This finding agrees with other observations, such as an increase in male mortality excess in Europe and Christian countries and an increase in female mortality excess in Asia and Muslim countries. An increase in the excess of female mortality may also be due to increased maternal mortality caused by an increase in fertility. However, this relation is not linear: In regions with the highest fertility (e.g., in Africa) the excess of female mortality is smaller than in regions with relatively lower fertility (e.g., in Asia). A possible explanation of this phenomenon is an evolutionary adaptation of women to the pressures of extremely high fertility by means of some reduction of their maternal mortality.     

Sex matters: secular and geographical trends in sex differences in coronary heart disease mortality

ObjectiveTo examine secular trends and geographical variations in sex differences in mortality from coronary heart disease and investigate how these relate to distributions in risk factors.Design National and international data were used to examine secular trends and geographical variations in sex differences in mortality from coronary heart disease and risk factors.SettingEngland and Wales, 1921-98; Australia, France, Japan, Sweden, and the United States, 1947-97; 50 countries, 1992-6.ResultsThe 20th century epidemic of coronary heart disease affected only men in most industrialised countries and had a very rapid onset in England and Wales, which has been examined in detail. If this male only epidemic had not occurred there would have been 1.2 million fewer deaths from coronary heart disease in men in England and Wales over the past 50 years. Secular trends in mean per capita fat consumption show a similar pattern to secular trends in coronary heart disease mortality in men. Fat consumption is positively correlated with coronary heart disease mortality in men (r_s=0.79; 95% confidence interval 0.70 to 0.86) and inversely associated with coronary heart disease mortality in women (−0.30; −0.49 to −0.08) over this time. Although sex ratios for mortality from coronary heart disease show a clear period effect, those for lung cancer show a cohort effect. Sex ratios for stroke mortality were constant and close to unity for the entire period. Geographical variations in the sex ratio for coronary heart disease were associated with mean per capita fat consumption (0.64; 0.44 to 0.78) but were not associated with the sex ratio for smoking.ConclusionSex differences are largely the result of environmental factors and hence not inevitable. Understanding the factors that determine sex differences has important implications for public health, particularly for countries and parts of countries where the death rates for coronary heart disease are currently increasing.

What is already known on this topic

Mortality for coronary heart disease is greater in men than women in most industrialised countriesThe most widely accepted explanation for this difference is that women are protected by oestrogen

What this study adds

The sex difference in mortality from coronary heart disease varies over time and between countries in a way that cannot be explained by endogenous oestrogenThese trends indicate that sex differences in mortality from coronary heart disease are driven primarily by environmental factorsSex differences in coronary heart disease are not inevitableUnderstanding more about the factors that cause the sex differences in mortality from coronary heart disease has important public health implications     

Impacts of air pollution and climate change on forest ecosystems--emerging research needs

Outcomes from the 22nd meeting for Specialists in Air Pollution Effects on Forest Ecosystems "Forests under Anthropogenic Pressure--Effects of Air Pollution, Climate Change and Urban Development", September 10-16, 2006, Riverside, CA, are summarized. Tropospheric or ground-level ozone (O3) is still the phytotoxic air pollutant of major interest. Challenging issues are how to make O3 standards or critical levels more biologically based and at the same time practical for wide use; quantification of plant detoxification processes in flux modeling; inclusion of multiple environmental stresses in critical load determinations; new concept development for nitrogen saturation; interactions between air pollution, climate, and forest pests; effects of forest fire on air quality; the capacity of forests to sequester carbon under changing climatic conditions and coexposure to elevated levels of air pollutants; enhanced linkage between molecular biology, biochemistry, physiology, and morphological traits.