Air pollution and daily mortality in Inchon, Korea.

The association between total daily mortality and air pollution was investigated for a 1-year period (January 1995 to December 1995) in Inchon, Korea. The purpose of this study was to evaluate the relative importance of particulate and gaseous air pollution as predictors of daily mortality. Concentration of total suspended particulates (TSP), inhalable particles (PM10), and gaseous pollutants, such as sulfur dioxide, nitrogen dioxide, ozone, carbon monoxide, were measured daily during the study period. A generalized additive model was used to regress daily death counts on each air pollutant, controlling for time trend and meteorologic influences such as temperature or relative humidity. Total mortality was found to increase 1.2% (95% CI: 0.2 to 2.2%) for each 10 microg/m3 increase in 6-day moving average of TSP, and 1.2% (95% CI 0.2 to 2.1%) for each 10 microg/m3 increase in 5-day moving average of PM10. The association is similar in magnitude to associations between particulate air pollution and mortality found in several other communities in America and Europe. Associations with gaseous pollutants were all statistically insignificant in the generalized additive model. The relative risk of death increased at particulate levels that were well below the current Korean Ambient Air Quality Standard.     

Mortality over a period of 10 years in patients with peripheral arterial disease.

BACKGROUND. Previous investigators have observed a doubling of the mortality rate among patients with intermittent claudication, and we have reported a fourfold increase in the overall mortality rate among subjects with large-vessel peripheral arterial disease, as diagnosed by noninvasive testing. In this study, we investigated the association of large-vessel peripheral arterial disease with rates of mortality from all cardiovascular diseases and from coronary heart disease. METHODS. We examined 565 men and women (average age, 66 years) for the presence of large-vessel peripheral arterial disease by means of two noninvasive techniques--measurement of segmental blood pressure and determination of flow velocity by Doppler ultrasound. We identified 67 subjects with the disease (11.9 percent), whom we followed prospectively for 10 years. RESULTS. Twenty-one of the 34 men (61.8 percent) and 11 of the 33 women (33.3 percent) with large-vessel peripheral arterial disease died during follow-up, as compared with 31 of the 183 men (16.9 percent) and 26 of the 225 women (11.6 percent) without evidence of peripheral arterial disease. After multivariate adjustment for age, sex, and other risk factors for cardiovascular disease, the relative risk of dying among subjects with large-vessel peripheral arterial disease as compared with those with no evidence of such disease was 3.1 (95 percent confidence interval, 1.9 to 4.9) for deaths from all causes, 5.9 (95 percent confidence interval, 3.0 to 11.4) for all deaths from cardiovascular disease, and 6.6 (95 percent confidence interval, 2.9 to 14.9) for deaths from coronary heart disease. The relative risk of death from causes other than cardiovascular disease was not significantly increased among the subjects with large-vessel peripheral arterial disease. After the exclusion of subjects who had a history of cardiovascular disease at base line, the relative risks among those with large-vessel peripheral arterial disease remained significantly elevated. Additional analyses revealed a 15-fold increase in rates of mortality due to cardiovascular disease and coronary heart disease among subjects with large-vessel peripheral arterial disease that was both severe and symptomatic. CONCLUSIONS. Patients with large-vessel peripheral arterial disease have a high risk of death from cardiovascular causes.     

Effects of air pollution on asthma hospitalization rates in different age groups in Hong Kong

AIMS: To assess the relationship between levels of ambient air pollutants and hospitalization rates for asthma in Hong Kong (HK). METHODS: This is a retrospective ecological study. Data of daily emergency hospital admissions to 15 major hospitals in HK for asthma and indices of air pollutants [sulphur dioxide (SO(2)), nitrogen dioxide (NO(2)), ozone (O(3)), particulates with an aerodynamic diameter of <10 microm particulate matter (PM(10)) and 2.5 microm (PM(2.5))] and meteorological variables from January 2000 to December 2005 were obtained from several government departments. Analysis was performed by the generalized additive models with Poisson distribution. The effects of time trend, season, other cyclical factors, temperature and humidity were adjusted. Autocorrelation and overdispersion were corrected. RESULTS: Altogether, 69 716 admissions were assessed. Significant associations were found between hospital admissions for asthma and levels of NO(2), O(3), PM(10) and PM(2.5). The relative risks (RR) for hospitalization for every 10 microg/m(3) increase in NO(2), O(3), PM(10) and PM(2.5) were 1.028, 1.034, 1.019 and 1.021, respectively, at a lag day that ranged from cumulative lag 0-4 to 0-5. In a multi-pollutant model, O(3) was significantly associated with increased admissions for asthma. The younger age group (0-14 years) tended to have a higher RR for each 10 microg/m(3) increase in pollutants than those aged 15-65 years. The elderly (aged >/=65 years) had a shorter 'best' lag time to develop asthma exacerbation following exposure to pollutants than those aged <65 years. CONCLUSION: Adverse effects of ambient concentrations of air pollutants on hospitalization rates for asthma are evident. Measures to improve air quality in HK are urgently needed.     

Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study

A pattern of left ventricular hypertrophy evident on the electrocardiogram is a harbinger of morbidity and mortality from cardiovascular disease. Echocardiography permits the noninvasive determination of left ventricular mass and the examination of its role as a precursor of morbidity and mortality. We examined the relation of left ventricular mass to the incidence of cardiovascular disease, mortality from cardiovascular disease, and mortality from all causes in 3220 subjects enrolled in the Framingham Heart Study who were 40 years of age or older and free of clinically apparent cardiovascular disease, in whom left ventricular mass was determined echocardiographically. During a four-year follow-up period, there were 208 incident cardiovascular events, 37 deaths from cardiovascular disease, and 124 deaths from all causes. Left ventricular mass, determined echocardiographically, was associated with all outcome events. This relation persisted after we adjusted for age, diastolic blood pressure, pulse pressure, treatment for hypertension, cigarette smoking, diabetes, obesity, the ratio of total cholesterol to high-density lipoprotein cholesterol, and electrocardiographic evidence of left ventricular hypertrophy. In men, the risk factor-adjusted relative risk of cardiovascular disease was 1.49 for each increment of 50 g per meter in left ventricular mass corrected for the subject's height (95 percent confidence interval, 1.20 to 1.85); in women, it was 1.57 (95 percent confidence interval, 1.20 to 2.04). Left ventricular mass (corrected for height) was also associated with the incidence of death from cardiovascular disease (relative risk, 1.73 [95 percent confidence interval, 1.19 to 2.52] in men and 2.12 [95 percent confidence interval, 1.28 to 3.49] in women). Left ventricular mass (corrected for height) was associated with death from all causes (relative risk, 1.49 [95 percent confidence interval, 1.14 to 1.94] in men and 2.01 [95 percent confidence interval, 1.44 to 2.81] in women). We conclude that the estimation of left ventricular mass by echocardiography offers prognostic information beyond that provided by the evaluation of traditional cardiovascular risk factors. An increase in left ventricular mass predicts a higher incidence of clinical events, including death, attributable to cardiovascular disease.     

Respiratory tract pathology and cytokine imbalance in clinically healthy children chronically and sequentially exposed to air pollutants

Chronic exposure of children to a complex mixture of air pollutants leads to recurrent episodes of upper and lower respiratory tract injury. An altered nasal mucociliary apparatus leaves the distal acinar airways more vulnerable to reactive gases and particulate matter (PM). The heterogeneity of structure in the human lung can impart significant variability in the distribution of ozone dose and particle deposition; this, in turn, influences the extent of epithelial injury and repair in chronically exposed children. Cytokines are low-molecular-weight proteins that act as intercellular mediators of inflammatory reactions, including lung injury of various etiologies. Cytokines are involved in generating inflammatory responses that contribute to injury at the lung epithelial and endothelial barriers. Mexico City is a 20-million-person megacity with severe air pollution problems. Southwest Metropolitan Mexico City (SWMMC) atmosphere is characterized by a complex mixture of air pollutants, including ozone, PM, and aldehydes. There is radiological evidence that significant lower respiratory tract damage is taking place in clinically healthy children chronically and sequentially exposed to air pollutants while growing up in SWMMC. We hypothesize that there is an imbalanced and dysregulated cytokine network in SWMMC children with overproduction of proinflammatory cytokines and cytokines involved in lung tissue repair and fibrosis. The nature of the sustained imbalance among the different cytokines ultimately determines the final lung histopathology, which would include subchronic inflammation, emphysema, and fibrosis. Cytokines likely would reach the systemic circulation and produce systemic effects. Individuals with an underlying respiratory or cardiovascular disease are less able to maintain equilibrium of the precarious cytokine networks.     

Effects of physiologic pacing versus ventricular pacing on the risk of stroke and death due to cardiovascular causes. Canadian Trial of Physiologic Pacing Investigators

BACKGROUND: Evidence suggests that physiologic pacing (dual-chamber or atrial) may be superior to single-chamber (ventricular) pacing because it is associated with lower risks of atrial fibrillation, stroke, and death. These benefits have not been evaluated in a large, randomized, controlled trial. METHODS: At 32 Canadian centers, patients without chronic atrial fibrillation who were scheduled for a first implantation of a pacemaker to treat symptomatic bradycardia were eligible for enrollment. We randomly assigned patients to receive either a ventricular pacemaker or a physiologic pacemaker and followed them for an average of three years. The primary outcome was stroke or death due to cardiovascular causes. Secondary outcomes were death from any cause, atrial fibrillation, and hospitalization for heart failure. RESULTS: A total of 1474 patients were randomly assigned to receive a ventricular pacemaker and 1094 to receive a physiologic pacemaker. The annual rate of stroke or death due to cardiovascular causes was 5.5 percent with ventricular pacing, as compared with 4.9 percent with physiologic pacing (reduction in relative risk, 9.4 percent; 95 percent confidence interval, -10.5 to 25.7 percent [the negative value indicates an increase in risk]; P=0.33). The annual rate of atrial fibrillation was significantly lower among the patients in the physiologic-pacing group (5.3 percent) than among those in the ventricular-pacing group (6.6 percent), for a reduction in relative risk of 18.0 percent (95 percent confidence interval, 0.3 to 32.6 percent; P=0.05). The effect on the rate of atrial fibrillation was not apparent until two years after implantation. The observed annual rates of death from all causes and of hospitalization for heart failure were lower among the patients with a physiologic pacemaker than among those with a ventricular pacemaker, but not significantly so (annual rates of death, 6.6 percent with ventricular pacing and 6.3 percent with physiologic pacing; annual rates of hospitalization for heart failure, 3.5 percent and 3.1 percent, respectively). There were significantly more perioperative complications with physiologic pacing than with ventricular pacing (9.0 percent vs. 3.8 percent, P<0.001). CONCLUSIONS: Physiologic pacing provides little benefit over ventricular pacing for the prevention of stroke or death due to cardiovascular causes.     

Air pollution and airway disease

Epidemiological and toxicological research continues to support a link between urban air pollution and an increased incidence and/or severity of airway disease. Detrimental effects of ozone (O₃), nitrogen dioxide (NO₂) and particulate matter (PM), as well as traffic‐related pollution as a whole, on respiratory symptoms and function are well documented. Not only do we have strong epidemiological evidence of a relationship between air pollution and exacerbation of asthma and respiratory morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD), but recent studies, particularly in urban areas, have suggested a role for pollutants in the development of both asthma and COPD. Similarly, while prevalence and severity of atopic conditions appear to be more common in urban compared with rural communities, evidence is emerging that traffic‐related pollutants may contribute to the development of allergy. Furthermore, numerous epidemiological and experimental studies suggest an association between exposure to NO₂, O₃, PM and combustion products of biomass fuels and an increased susceptibility to and morbidity from respiratory infection. Given the considerable contribution that traffic emissions make to urban air pollution researchers have sought to characterize the relative toxicity of traffic‐related PM pollutants. Recent advances in mechanisms implicated in the association of air pollutants and airway disease include epigenetic alteration of genes by combustion‐related pollutants and how polymorphisms in genes involved in antioxidant pathways and airway inflammation can modify responses to air pollution exposures. Other interesting epidemiological observations related to increased host susceptibility include a possible link between chronic PM exposure during childhood and vulnerability to COPD in adulthood, and that infants subjected to higher prenatal levels of air pollution may be at greater risk of developing respiratory conditions. While the characterization of pollutant components and sources promise to guide pollution control strategies, the identification of susceptible subpopulations will be necessary if targeted therapy/prevention of pollution‐induced respiratory diseases is to be developed. Cite this as: F. J. Kelly and J. C. Fussell, Clinical & Experimental Allergy, 2011 (41) 1059–1071.     

A prospective study of dehydroepiandrosterone sulfate, mortality, and cardiovascular disease

It has been postulated that dehydroepiandrosterone (DHEA) and its sulfate ester, dehydroepiandrosterone sulfate (DHEAS), the major secretory products of the human adrenal gland, may be discriminators of life expectancy and aging. We examined the relation of base-line circulating DHEAS levels to subsequent 12-year mortality from any cause, from cardiovascular disease, and from ischemic heart disease in a population-based cohort of 242 men aged 50 to 79 years at the start of the study. Mean DHEAS levels decreased with age and were also significantly lower in men with a history of heart disease than in those without such a history. In men with no history of heart disease at base line, the age-adjusted relative risk associated with a DHEAS level below 140 micrograms per deciliter was 1.5 (P not significant) for death from any causes, 3.3 (P less than 0.05) for death from cardiovascular disease, and 3.2 (P less than 0.05) for death from ischemic heart disease. In multivariate analyses, an increase in DHEAS level of 100 micrograms per deciliter was associated with a 36 percent reduction in mortality from any causes (P less than 0.05) and a 48 percent reduction in mortality from cardiovascular disease (P less than 0.05), after adjustment for age, systolic blood pressure, serum cholesterol level, obesity, fasting plasma glucose level, cigarette smoking status, and personal history of heart disease. Our conclusions are limited by the single determination of DHEAS levels, but the data suggest that the DHEAS concentration is independently and inversely related to death from any cause and death from cardiovascular disease in men over age 50.     

A long-term study of mortality in men who have undergone vasectomy.

BACKGROUND. Vasectomy is a reliable and widely accepted method of contraception, but there is some uncertainty and few data about a possible long-term adverse effect on health. METHODS. We examined the relation between vasectomy and mortality rates from cardiovascular disease, cancer, and all causes in a retrospective cohort of husbands of members of the Nurses' Health Study. In 1989 we obtained data by questionnaire on 14,607 men who had undergone vasectomy as of 1976 and 14,607 men who had not. RESULTS. Among the men who were free of cancer at the start of the study, 1052 died: 446 of cardiovascular disease, 341 of cancer, and 265 of other causes. Vasectomy was associated with reductions in mortality from all causes (age-adjusted relative risk, 0.85; 95 percent confidence interval, 0.76 to 0.96) and mortality from cardiovascular disease (relative risk, 0.76; 95 percent confidence interval, 0.63 to 0.92). Vasectomy was unrelated to mortality from all forms of cancer (relative risk, 1.01; 95 percent confidence interval, 0.82 to 1.25). Among men who had a vasectomy at least 20 years earlier, the procedure had no relation to mortality from all causes (relative risk, 1.11; 95 percent confidence interval, 0.92 to 1.33) or that from cardiovascular disease (relative risk, 0.85; 95 percent confidence interval, 0.63 to 1.16). However, mortality from cancer was increased in men who had a vasectomy at least 20 years earlier (relative risk, 1.44; 95 percent confidence interval, 1.07 to 1.92). The excess risk of cancer in these men was due primarily to lung cancer. None of the observed associations were confounded by smoking habits, body-mass index, alcohol consumption, or educational level. CONCLUSIONS. Vasectomy is not associated with an increase in overall mortality or mortality from cardiovascular disease. Our study also found no increase in overall mortality from cancer after vasectomy, but there was an apparent increase in the risk of cancer 20 or more years after vasectomy that requires further study.     

Association of aortic-valve sclerosis with cardiovascular mortality and morbidity in the elderly.

BACKGROUND: Although aortic-valve stenosis is clearly associated with adverse cardiovascular outcomes, it is unclear whether valve sclerosis increases the risk of cardiovascular events. METHODS: We assessed echocardiograms obtained at base line from 5621 men and women 65 years of age or older who were enrolled in a population-based prospective study. On echocardiography, the aortic valve was normal in 70 percent (3919 subjects), sclerotic without outflow obstruction in 29 percent (1610), and stenotic in 2 percent (92). The subjects were followed for a mean of 5.0 years to assess the risk of death from any cause and of death from cardiovascular causes. Cardiovascular morbidity was defined as new episodes of myocardial infarction, angina pectoris, congestive heart failure, or stroke. RESULTS: There was a stepwise increase in deaths from any cause (P for trend, <0.001) and deaths from cardiovascular causes (P for trend, <0.001) with increasing aortic-valve abnormality; the respective rates were 14.9 and 6.1 percent in the group with normal aortic valves, 21.9 and 10.1 percent in the group with aortic sclerosis, and 41.3 and 19.6 percent in the group with aortic stenosis. The relative risk of death from cardiovascular causes among subjects without coronary heart disease at base line was 1.66 (95 percent confidence interval, 1.23 to 2.23) for those with sclerotic valves as compared with those with normal valves, after adjustment for age and sex. The relative risk remained elevated after further adjustment for clinical factors associated with sclerosis (relative risk, 1.52; 95 percent confidence interval, 1.12 to 2.05). The relative risk of myocardial infarction was 1.40 (95 percent confidence interval, 1.07 to 1.83) among subjects with aortic sclerosis, as compared with those with normal aortic valves. CONCLUSIONS: Aortic sclerosis is common in the elderly and is associated with an increase of approximately 50 percent in the risk of death from cardiovascular causes and the risk of myocardial infarction, even in the absence of hemodynamically significant obstruction of left ventricular outflow.     

Transmission electron microscopy findings in the respiratory epithelium of guinea pigs exposed to the polluted air of southwest Mexico City.

We evaluated the nature and the extent of the damage to the respiratory epithelium of guinea pigs after a 4-month exposure to the mixture of air pollutants in southwest Mexico City. Guinea pigs were placed outdoors on the roof of our facility, 8 hours daily, from February to May 1995. At the same time, control guinea pigs were kept indoors breathing filtered air. Air pollutants, temperature, and humidity data were obtained from the nearest station of the Environmental Monitoring Net. The airways and lung parenchyma were analyzed after 120 days using transmission electron microscopy (TEM). During the 4-month exposure period, ozone (O3) exceeded the norm during 511 hours, and suspended particles less than 10 microm in diameter (PM10) during 52 hours. Both pollutants reached peak levels of more than twice the norm. TEM revealed no important abnormalities in the control group. In the exposed group, there was loss of cilia, detachment of epithelial cells, and eosinophil and macrophage migration toward alveolar spaces through type I pneumocytes with destruction of their basal membranes. In six guinea pigs in the exposed group, we noted bacteria along the airways, with associated inflammatory response. We explain the colonization of the respiratory epithelium by bacteria as the result of the impairment on the defense mechanism caused by the exposure to environmental O3 and PM10.     

Maternal mortality in Massachusetts. Trends and prevention

To identify ways in which the safety of childbirth might be increased, we investigated the causes of death among the 886 women who died during pregnancy or within 90 days post partum ("maternal deaths") in Massachusetts from 1954 through 1985. The maternal mortality rate declined from 50 per 100,000 live births in the early 1950s to the current rate of 10 per 100,000 live births. Between one third and one half of the maternal deaths were considered to have been preventable. The leading causes of maternal death from 1954 through 1957 were infection, cardiac disease, pregnancy-induced hypertension, and hemorrhage. In contrast, from 1982 through 1985 the leading causes of death were trauma (suicide, homicide, and motor vehicle accidents) and pulmonary embolus. We observed a rapid increase in the frequency of death among women who received little or no antenatal care. From 1980 through 1984 the maternal mortality rate for white women was 9.6 per 100,000 live births, whereas for nonwhites it was 35 per 100,000 live births (relative risk, 2.9; 95 percent confidence limits, 2.5 and 3.2). Fifty percent of the nonwhite women who died during pregnancy or within 90 days post partum received little or no antenatal care, in contrast to only 15 percent of the white women. These data show that the leading causes of maternal death have changed markedly in Massachusetts during the past 30 years. Although the overall maternal mortality rate has declined sharply, further improvement may occur with better antenatal care and specific efforts to prevent trauma and pulmonary embolus.     

Air pollutants enhance rhinoconjunctivitis symptoms in pollen-allergic individuals.

BACKGROUND: Little is know about the relation of airborne pollen allergens to nasal and ocular symptoms in combination with air pollutants. OBJECTIVE: The hypothesis was that air pollutants exacerbate allergic symptoms of the nose and eyes during the pollen season. In addition, the use of allergen measurements instead of pollen counts should be tested. METHODS: Fifteen pollen-allergic, nonsmoking subjects with weak reactivity of the airways recorded rhinoconjunctival symptoms and medication every morning and evening throughout the pollen season. Symptoms were compared with air pollutants (nitrogen oxide [NOx], particulate matter smaller than 10 microm, and ozone) and birch and grass pollen counts or, alternatively, to airborne birch and grass allergens determined using ELISA-techniques. A multiple linear regression model was used which controlled for autocorrelation of the residuals of the time series (Cochrane-Orcutt approach). This model was applied to each subject individually, followed by calculations of summary scores for the group. RESULTS: Air pollution levels were moderate, often meeting air quality standards. Effect estimates (increase of score with 10-fold increase of concentration) were NOx = 1.06, P < 0.01; ozone = 1.59, P < 0.01; and pollen = 0.48, P < 0.001. Using allergen concentrations instead of pollen counts resulted in similar effect estimates. Using particulate matter smaller than 10 microm instead of NOx gave comparable but less consistent results. CONCLUSIONS: Symptoms were related to moderate levels of pollutants, suggesting that rhinoconjunctival tissue is very sensitive to irritant stimuli during an ongoing allergic inflammation, and that susceptibility toward allergens might be increased in areas with increased levels of air pollutants. Allergen measurements seem equally usable as pollen counts to investigate rhinoconjunctivitis.     

Excess mortality in Harlem

In recent decades mortality rates have declined for both white and nonwhite Americans, but national averages obscure the extremely high mortality rates in many inner-city communities. Using data from the 1980 census and from death certificates in 1979, 1980, and 1981, we examined mortality rates in New York City's Central Harlem health district, where 96 percent of the inhabitants are black and 41 percent live below the poverty line. For Harlem, the age-adjusted rate of mortality from all causes was the highest in New York City, more than double that of U.S. whites and 50 percent higher than that of U.S. blacks. Almost all the excess mortality was among those less than 65 years old. With rates for the white population as the basis for comparison, the standardized (adjusted for age) mortality ratios (SMRs) for deaths under the age of 65 in Harlem were 2.91 for male residents and 2.70 for female residents. The highest ratios were for women 25 to 34 years old (SMR, 6.13) and men 35 to 44 years old (SMR, 5.98). The chief causes of this excess mortality were cardiovascular disease (23.5 percent of the excess deaths; SMR, 2.23), cirrhosis (17.9 percent; SMR, 10.5), homicide (14.9 percent; SMR, 14.2), and neoplasms (12.6 percent; SMR, 1.77). Survival analysis showed that black men in Harlem were less likely to reach the age of 65 than men in Bangladesh. Of the 353 health areas in New York, 54 (with a total population of 650,000) had mortality rates for persons under 65 years old that were at lest twice the expected rate. All but one of these areas of high mortality were predominantly black or Hispanic. We conclude that Harlem and probably other inner-city areas with largely black populations have extremely high mortality rates that justify special consideration analogous to that given to natural-disaster areas.     

Physical fitness as a predictor of cardiovascular mortality in asymptomatic North American men. The Lipid Research Clinics Mortality Follow-up Study

Limited data are available on the relation between physical fitness and mortality from cardiovascular disease. We examined this question in a study of 4276 men, 30 to 69 years of age, whom we followed for an average of 8.5 years. Examinations at base line included assessment of conventional coronary risk factors and treadmill exercise testing. The heart rate during submaximal exercise (stage 2 of the exercise test) and the duration of exercise were used as measures of physical fitness. Men with incomplete data (n = 308) or who were using cardiovascular drugs (n = 213) were excluded from the analysis. Men who had clinical evidence of cardiovascular disease at base line (n = 649) were analyzed separately. Forty-five deaths from cardiovascular causes occurred among the remaining 3106 men. A lower level of physical fitness was associated with a higher risk of death from cardiovascular and coronary heart disease, after adjustment for age and cardiovascular risk factors. The relative risk of death from cardiovascular causes was 2.7 (95 percent confidence interval, 1.4 to 5.1; P = 0.003) for healthy men with an increment of 35 beats per minute in the heart rate during stage 2, and 3.0 (95 percent confidence interval, 1.6 to 5.5; P = 0.0004) for those with a decrement of 4.4 minutes in the exercise time spent on the treadmill. The corresponding values for death from coronary heart disease were 3.2 (95 percent confidence interval, 1.5 to 6.7; P = 0.003) and 2.8 (95 percent confidence interval, 1.3 to 6.1; P = 0.007), respectively. We conclude that a lower level of physical fitness is associated with a higher risk of death from coronary heart disease and cardiovascular disease in clinically healthy men, independent of conventional coronary risk factors.     

Ten-year mortality from cardiovascular disease in relation to cholesterol level among men with and without preexisting cardiovascular disease

To determine the associations of total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol with mortality from coronary heart disease and cardiovascular disease, we studied 2541 white men who were 40 to 69 years old at base line and followed them for an average of 10.1 years. Seventeen percent had some manifestation of cardiovascular disease at base line, whereas the others did not. Among the men who had cardiovascular disease at base line, we found, after multivariate adjustment, that those with "high" blood cholesterol levels (above 6.19 mmol per liter) had a risk of death from cardiovascular disease, including coronary heart disease, that was 3.45 times higher (95 percent confidence interval, 1.63 to 7.33) than that for men with "desirable" blood cholesterol levels (below 5.16 mmol per liter). The corresponding hazard ratios were 5.92 (95 percent confidence interval, 2.59 to 13.51) for LDL cholesterol levels above 4.13 mmol per liter as compared with those below 3.35 mmol per liter, and 6.02 (95 percent confidence interval, 2.73 to 13.28) for HDL cholesterol levels below 0.90 mmol per liter as compared with those above 1.16 mmol per liter. All three lipid levels were also significant predictors of death from coronary heart disease alone (P less than 0.005). Total cholesterol and LDL cholesterol levels were also significant predictors of death from cardiovascular and coronary heart disease in men without preexisting cardiovascular disease, although at a lower level of absolute risk of death. Thus, the 10-year risk of death from cardiovascular disease for a man with preexisting cardiovascular disease increased from 3.8 percent to almost 19.6 percent with increasing levels of total cholesterol from "desirable" to "high," whereas the corresponding risk for a man who was free of cardiovascular disease at base line increased from 1.7 percent to 4.9 percent. Our findings suggest that total, LDL, and HDL cholesterol levels predict subsequent mortality in men 40 to 69 years of age, especially those with preexisting cardiovascular disease.     

Smoking and mortality among older men and women in three communities

BACKGROUND. Although cigarette smoking is the leading avoidable cause of premature death in middle age, some have claimed that no association is present among older persons. METHODS. We prospectively examined the relation of cigarette-smoking habits with mortality from all causes, cardiovascular causes, and cancer among 7178 persons 65 years of age or older without a history of myocardial infarction, stroke, or cancer who lived in one of three communities: East Boston, Massachusetts; Iowa and Washington counties, Iowa; and New Haven, Connecticut. At the time of the initial interview, prevalence rates of smoking in the three communities ranged from 5.2 to 17.8 percent among women and from 14.2 to 25.8 percent among men. During five years of follow-up there were 1442 deaths, 729 due to cardiovascular disease and 316 due to cancer. RESULTS. In both sexes, rates of total mortality among current smokers were twice what they were among participants who had never smoked. Relative risks, as adjusted for age and community, were 2.1 among the men (95 percent confidence interval, 1.7 to 2.7) and 1.8 among the women (95 percent confidence interval, 1.4 to 2.4). Current smokers had higher rates of cardiovascular mortality than those who had never smoked (as adjusted for age and community, the relative risk was 2.0 [95 percent confidence interval, 1.4 to 2.9] among the men and 1.6 [95 percent confidence interval, 1.1 to 2.3] among the women), as well as increased rates of cancer mortality (relative risk, 2.4 [95 percent confidence interval, 1.4 to 4.1] among the men and 2.4 [95 percent confidence interval, 1.4 to 3.9] among the women). In both sexes, former smokers had rates of cardiovascular mortality similar to those of the participants who had never smoked, regardless of age at cessation, whereas the rates for all cancers, as well as smoking-related cancers, remained elevated among men who had once smoked. CONCLUSIONS. Our prospective findings indicate that the mortality hazards of smoking extend well into later life, and suggest that cessation will continue to improve life expectancy in older people.     

Effect of short-term exposure to air pollution and pollen on medical emergency calls: a case-crossover study in Spain

Background:  A symmetric case-crossover design was used to analyse the short-term relationship between air pollution, pollen and emergency calls to medical services.
Methods:  This study covered patients who made medical emergency calls in the City of Vigo (Spain) during the period 1996–1999. Morbidity data were obtained from the records of the 061 Medical Emergency Control Center, in its capacity as the body officially coordinating all medical emergencies by telephone. Air pollution data were furnished by the Vigo Municipal Air Pollution Surveillance Grid. Pollen levels were provided by the staff of the Spanish Aerobiology Network in Vigo.
Results:  A rise of 10μg/m³ in ambient particulate levels led to the risk of medical emergency calls requesting attention increasing by: (i) 1.97% [95% confidence interval (95% CI): 1.83–2.11%] for circulatory causes on the same day; (ii) 1.95% (95% CI: 1.76–2.14%) for respiratory causes at 2 days and (iii) 1.34% (95% CI: 1.23–1.45%) for combined circulatory and respiratory causes on the same day. A number of pollens displayed a statistically significant relationship with emergency calls. No interaction was in evidence between pollens and air pollutants.
Conclusions:  While elevations in particulate air pollution increase medical emergency calls because of cardiac or respiratory causes or both combined, elevations in pollen levels increase medical emergency calls because of respiratory causes.     

Association between air pollution and asthma admission among children in Hong Kong

OBJECTIVE: To examine the association of air pollutants with hospital admission for childhood asthma in Hong Kong. METHODS: Data on hospital admissions for asthma, influenza and total hospital admissions in children aged < or =18 years at all Hospital Authority hospitals during 1997-2002 were obtained. Data on daily mean concentrations of particles with aerodynamic diameter <10 microm (i. e. PM10) and <2.5 microm (i. e. PM2.5), nitrogen dioxide (NO2), sulphur dioxide (SO2), and ozone (O3) and data on meteorological variables were associated with asthma hospital admissions using Poisson's regression with generalized additive models for correction of yearly trend, temperature, humidity, day-of-week effect, holiday, influenza admissions and total hospital admission. The possibility of a lag effect of each pollutant and the interaction of different pollutants were also examined. RESULTS: The association between asthma admission with change of NO2, PM10, PM2.5 and O3 levels remained significant after adjustment for multi-pollutants effect and confounding variables, with increase in asthma admission rate of 5.64% (3.21-8.14) at lag 3 for NO2, 3.67% (1.52-5.86) at lag 4 for PM10, 3.24% (0.93-5.60) at lag 4 for PM2.5 and 2.63% (0.64-4.67) at lag 2 for O3. Effect of SO2 was lost after adjustment. CONCLUSION: Ambient levels of PM10, PM2.5) NO2 and O3 are associated with childhood asthma hospital admission in Hong Kong.     

Association between NOx exposure and deaths caused by respiratory diseases in a medium-sized Brazilian city

Exposure to nitrogen oxides (NOx) emitted by burning fossil fuels has been associated with respiratory diseases. We aimed to estimate the effects of NOx exposure on mortality owing to respiratory diseases in residents of Taubaté, São Paulo, Brazil, of all ages and both sexes. This time-series ecological study from August 1, 2011 to July 31, 2012 used information on deaths caused by respiratory diseases obtained from the Health Department of Taubaté. Estimated daily levels of pollutants (NOx, particulate matter, ozone, carbon monoxide) were obtained from the Centro de Previsão de Tempo e Estudos Climáticos Coupled Aerosol and Tracer Transport model to the Brazilian developments on the Regional Atmospheric Modeling System. These environmental variables were used to adjust the multipollutant model for apparent temperature. To estimate association between hospitalizations owing to asthma and air pollutants, generalized additive Poisson regression models were developed, with lags as much as 5 days. There were 385 deaths with a daily mean (±SD) of 1.05±1.03 (range: 0-5). Exposure to NOx was significantly associated with mortality owing to respiratory diseases: relative risk (RR)=1.035 (95% confidence interval [CI]: 1.008-1.063) for lag 2, RR=1.064 (95%CI: 1.017-1.112) lag 3, RR=1.055 (95%CI: 1.025-1.085) lag 4, and RR=1.042 (95%CI: 1.010-1.076) lag 5. A 3 µg/m³ reduction in NOx concentration resulted in a decrease of 10-18 percentage points in risk of death caused by respiratory diseases. Even at NOx concentrations below the acceptable standard, there is association with deaths caused by respiratory diseases.