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Biomedical subjects

Jonathan M Samet

Publications and source records attributed to Jonathan M Samet.

At least 19 recordsLinked to original sources
PubMed2006

Cotinine concentration in smokers from different countries: relationship with amount smoked and cigarette type.

This four-country study examined salivary cotinine as a marker for nicotine intake and addiction among smokers in relation to numbers and types of cigarettes smoked. Smoking characteristics of cigarette smokers in Brazil, China, Mexico, and Poland were identified using a standard questionnaire. Cotinine concentration was measured using a saliva sample from each participant; its relationship with numbers and types of cigarettes smoked was quantified by applying regression techniques. The main outcome measure was salivary cotinine level measured by gas chromatography. In all four countries, cotinine concentration increased linearly with cigarettes smoked up to 20 per day [11.3 ng/mL (95% confidence interval, 10.5-12.2)] and then stabilized as the number of cigarettes exceeded 20 [6.8 ng/mL per cigarette (95% confidence interval, 6.3-7.4) for up to 40 cigarettes]. On average, smokers of regular cigarettes consumed more cigarettes and had higher cotinine levels than light cigarette smokers. Cotinine concentration per cigarette smoked did not differ between regular and light cigarette smokers. Results suggest a saturation point for daily nicotine intake and minimal or no reduction in nicotine intake by smoking light cigarettes.

Adolescent↗
PubMed2006

Body-mass index and mortality in Korean men and women.

BACKGROUND: Obesity is associated with diverse health risks, but the role of body weight as a risk factor for death remains controversial. METHODS: We examined the association between body weight and the risk of death in a 12-year prospective cohort study of 1,213,829 Koreans between the ages of 30 and 95 years. We examined 82,372 deaths from any cause and 48,731 deaths from specific diseases (including 29,123 from cancer, 16,426 from atherosclerotic cardiovascular disease, and 3362 from respiratory disease) in relation to the body-mass index (BMI) (the weight in kilograms divided by the square of the height in meters). RESULTS: In both sexes, the average baseline BMI was 23.2, and the rate of death from any cause had a J-shaped association with the BMI, regardless of cigarette-smoking history. The risk of death from any cause was lowest among patients with a BMI of 23.0 to 24.9. In all groups, the risk of death from respiratory causes was higher among subjects with a lower BMI, and the risk of death from atherosclerotic cardiovascular disease or cancer was higher among subjects with a higher BMI. The relative risk of death associated with BMI declined with increasing age. CONCLUSIONS: Underweight, overweight, and obese men and women had higher rates of death than men and women of normal weight. The association of BMI with death varied according to the cause of death and was modified by age, sex, and smoking history.

Adult↗
PubMed2006

Fine particulate air pollution and hospital admission for cardiovascular and respiratory diseases.

CONTEXT: Evidence on the health risks associated with short-term exposure to fine particles (particulate matter < or =2.5 microm in aerodynamic diameter [PM2.5]) is limited. Results from the new national monitoring network for PM2.5 make possible systematic research on health risks at national and regional scales. OBJECTIVES: To estimate risks of cardiovascular and respiratory hospital admissions associated with short-term exposure to PM2.5 for Medicare enrollees and to explore heterogeneity of the variation of risks across regions. DESIGN, SETTING, AND PARTICIPANTS: A national database comprising daily time-series data daily for 1999 through 2002 on hospital admission rates (constructed from the Medicare National Claims History Files) for cardiovascular and respiratory outcomes and injuries, ambient PM2.5 levels, and temperature and dew-point temperature for 204 US urban counties (population >200,000) with 11.5 million Medicare enrollees (aged >65 years) living an average of 5.9 miles from a PM2.5 monitor. MAIN OUTCOME MEASURES: Daily counts of county-wide hospital admissions for primary diagnosis of cerebrovascular, peripheral, and ischemic heart diseases, heart rhythm, heart failure, chronic obstructive pulmonary disease, and respiratory infection, and injuries as a control outcome. RESULTS: There was a short-term increase in hospital admission rates associated with PM2.5 for all of the health outcomes except injuries. The largest association was for heart failure, which had a 1.28% (95% confidence interval, 0.78%-1.78%) increase in risk per 10-microg/m3 increase in same-day PM2.5. Cardiovascular risks tended to be higher in counties located in the Eastern region of the United States, which included the Northeast, the Southeast, the Midwest, and the South. CONCLUSION: Short-term exposure to PM2.5 increases the risk for hospital admission for cardiovascular and respiratory diseases.

Aged↗
PubMed2006

Residential radon and lung cancer: end of the story?

The earliest evidence of increased lung cancer risk associated with radon came largely from studies of highly exposed underground miners. In the United States, concerns about residential exposures became prominent in the early 1980s with the identification of the Watras home, which had remarkably elevated radon concentrations. By then, the problem of indoor radon was already recognized in Europe and the first epidemiological studies on indoor radon had been reported. The concern about the risk of indoor radon motivated a series of case-control studies of residential radon and lung cancer in the United States, Canada, China, and a number of European countries. In 1999, the U.S. National Research Council Committee on the Biological Effects of Ionizing Radiation (BEIR VI) weighed the scientific evidence available at that time on this issue and concluded that residential radon was an important contributor to the lung cancer burden and that risks were appropriately estimated by a linear nonthreshold model. Since individual case-control studies have not provided consistent direct evidence of excess lung cancer risk at residential exposure levels, combined analyses of residential radon studies have been undertaken in both North America and Europe. These combined analyses, including the North American pooled analysis described in this issue, represent an important complement to the findings of the miner studies and further support the linear no-threshold model for cancer risk adopted by the BEIR VI Committee and other groups.

Air Pollutants, Radioactive↗
PubMed2006

Improving performance of HVAC systems to reduce exposure to aerosolized infectious agents in buildings; recommendations to reduce risks posed by biological attacks.

The prospect of biological attacks is a growing strategic threat. Covert aerosol attacks inside a building are of particular concern. In the summer of 2005, the Center for Biosecurity of the University of Pittsburgh Medical Center convened a Working Group to determine what steps could be taken to reduce the risk of exposure of building occupants after an aerosol release of a biological weapon. The Working Group was composed of subject matter experts in air filtration, building ventilation and pressurization, air conditioning and air distribution, biosecurity, building design and operation, building decontamination and restoration, economics, medicine, public health, and public policy. The group focused on functions of the heating, ventilation, and air conditioning systems in commercial or public buildings that could reduce the risk of exposure to deleterious aerosols following biological attacks. The Working Group's recommendations for building owners are based on the use of currently available, off-the-shelf technologies. These recommendations are modest in expense and could be implemented immediately. It is also the Working Group's judgment that the commitment and stewardship of a lead government agency is essential to secure the necessary financial and human resources and to plan and build a comprehensive, effective program to reduce exposure to aerosolized infectious agents in buildings.

Advisory Committees↗
PubMed2006

Challenging the epidemiologic evidence on passive smoking: tactics of tobacco industry expert witnesses.

OBJECTIVE: To analyse the statements given by tobacco industry defence witnesses during trial testimonies and depositions in second-hand smoke cases and in parallel, to review criticisms of epidemiology in industry-funded publications in order to identify strategies for discrediting epidemiologic evidence on passive smoking health effects. METHODS: A collection of depositions and trial testimony transcripts from tobacco industry-related lawsuits filed in the United States during the 1990s, was compiled and indexed by the Tobacco Deposition and Trial Testimony Archive (DATTA). Statements in DATTA made by expert witnesses representing the tobacco industry relating to the health effects of passive smoking were identified and reviewed. Industry-supported publications within the peer-reviewed literature were also examined for statements on exposure misclassification, meta-analysis, and confounding. RESULTS: The witnesses challenged causation of adverse health effects of passive smoking by citing limitations of epidemiologic research, raising methodological and statistical issues, and disputing biological plausibility. Though not often cited directly by the witnesses, the defence tactics mirrored the strategies used in industry-funded reports in the peer-reviewed literature. CONCLUSION: The tobacco industry attempted to redirect the focus and dialogue related to the epidemiologic evidence on passive smoking. This approach, used by industry experts in trial testimony and depositions, placed bias as a certain alternative to causation of diseases related to passive smoking and proposed an unachievable standard for establishing the mechanism of disease.

Animals↗
PubMed2006

Lead, genetic susceptibility, and risk of adult brain tumors.

BACKGROUND: Although few etiologic factors for brain tumors have been identified, limited data suggest that lead may increase the risk of brain tumors, particularly meningioma. The ALAD G177C polymorphism affects the toxicokinetics of lead and may confer genetic susceptibility to adverse effects of lead exposure. METHODS: We examined occupational exposure to lead and risk of brain tumors in a multisite, hospital-based, case-control study of 489 patients with glioma, 197 with meningioma, and 799 non-cancer controls frequency matched on hospital, age, sex, race/ethnicity, and residential proximity to hospital. ALAD genotype was assessed by a Taqman assay for 355 glioma patients, 151 meningioma patients, and 505 controls. Exposure to lead was estimated using a rigorous questionnaire-based exposure assessment strategy incorporating lead measurement and other occupational data abstracted from published articles and reports. RESULTS: Increased risk of meningioma with occupational lead exposure (estimated by odds ratios and 95% confidence intervals) was most apparent in individuals with the ALAD2 variant allele, for whom risk increased from 1.1 (0.3-4.5) to 5.6 (0.7-45.5) and 12.8 (1.4-120.8) for estimated cumulative lead exposures of 1 to 49 microg/m3-y, 50 to 99 microg/m3-y, and >or=100 microg/m3-y, respectively, compared with unexposed individuals (two-sided P trend = 0.06). This relationship became stronger after excluding occupational lead exposures characterized by a low confidence level or occurring in the 10 years before meningioma diagnosis. Occupational lead exposure was not associated with glioma risk. CONCLUSIONS: Although our results indicate that lead may be implicated in meningioma risk in genetically susceptible individuals, these results need to be interpreted with caution given the small numbers of exposed cases with a variant genotype.

Adolescent↗
PubMed2005

White blood cell count and risk for all-cause, cardiovascular, and cancer mortality in a cohort of Koreans.

The authors conducted a 10-year prospective cohort study of mortality in relation to white blood cell counts of 437,454 Koreans, aged 40-95 years, who received health insurance from the National Health Insurance Corporation and were medically evaluated in 1993 or 1995, with white blood cell measurement. The main outcome measures were mortality from all causes, all cancers, and all atherosclerotic cardiovascular diseases (ASCVD). Hazard ratios and 95% confidence intervals were calculated using Cox proportional hazards models with adjustment for age and potential confounders. During follow-up, 48,757 deaths occurred, with 15,507 deaths from cancer and 11,676 from ASCVD. For men and women, white blood cell count was associated with all-cause mortality and ASCVD mortality but not with cancer mortality. In healthy nonsmokers, a graded association between a higher white blood cell count and a higher risk of ASCVD was observed in men (highest vs. lowest quintile: hazard ratio = 2.10, 95% confidence interval: 1.50, 2.94) and in women (hazard ratio = 1.35, 95% confidence interval: 1.17, 1.56). In healthy smokers, a graded association between a higher white blood cell count and a higher risk of ASCVD was also observed in men (highest vs. lowest quintile: hazard ratio = 1.46, 95% confidence interval: 1.25, 1.72). These findings indicate that the white blood cell count is an independent risk factor for all-cause mortality and for ASCVD mortality.

Adult↗
PubMed2005

Epidemiology of lung cancer: looking to the future.

In the United States, the 20th century witnessed the emergence of a lung cancer epidemic that peaked and began to decline by the century's end, a decline that continues today. However, lung cancer continues to be an unabating pandemic. In research carried out over the last half of the 20th century, many factors were causally associated with lung cancer and studies were implemented to identify determinants of susceptibility to these factors. Cigarette smoking was identified as the single most predominant cause of the lung cancer epidemic, but other causes were found, including workplace agents (eg, asbestos, arsenic, chromium, nickel, and radon) and other environmental factors (passive smoking, indoor radon, and air pollution). Contemporary epidemiologic research on lung cancer now focuses on a new set of issues, primarily related to susceptibility to the well-identified causal factors, particularly smoking, and on the consequences of changes in tobacco products for risks to smokers. Diet and the possibility of reducing risk through chemoprevention remain a focus of research emphasis through experimental and observational approaches. Questions have also been raised about possible differences in susceptibility to lung cancer by sex and race. Population patterns in smoking prevalence will continue to be the most powerful predictor of the future occurrence of lung cancer. Evaluation of recent US patterns in smoking prevalence indicates that for the next approximately 10 to 15 years, lung cancer rates will decrease, but will then level off starting in approximately 2030. Unless further reductions in the prevalence of cigarette smoking are achieved over the next decade, lung cancer will remain as an all too common, but avoidable, disease.

Global Health↗
PubMed2005

Seasonal analyses of air pollution and mortality in 100 US cities.

Time series models relating short-term changes in air pollution levels to daily mortality counts typically assume that the effects of air pollution on the log relative rate of mortality do not vary with time. However, these short-term effects might plausibly vary by season. Changes in the sources of air pollution and meteorology can result in changes in characteristics of the air pollution mixture across seasons. The authors developed Bayesian semiparametric hierarchical models for estimating time-varying effects of pollution on mortality in multisite time series studies. The methods were applied to the database of the National Morbidity and Mortality Air Pollution Study, which includes data for 100 US cities, for the period 1987-2000. At the national level, a 10-microg/m(3) increase in particulate matter less than 10 microm in aerodynamic diameter at a 1-day lag was associated with 0.15% (95% posterior interval (PI): -0.08, 0.39), 0.14% (95% PI: -0.14, 0.42), 0.36% (95% PI: 0.11, 0.61), and 0.14% (95% PI: -0.06, 0.34) increases in mortality for winter, spring, summer, and fall, respectively. An analysis by geographic region found a strong seasonal pattern in the Northeast (with a peak in summer) and little seasonal variation in the southern regions of the country. These results provide useful information for understanding particle toxicity and guiding future analyses of particle constituent data.

Air Pollution↗
PubMed2005

Fasting serum glucose level and cancer risk in Korean men and women.

CONTEXT: Diabetes is a serious and costly disease that is becoming increasingly common in many countries. The role of diabetes as a cancer risk factor remains unclear. OBJECTIVE: To examine the relationship between fasting serum glucose and diabetes and risk of all cancers and specific cancers in men and women in Korea. DESIGN, SETTING, AND PARTICIPANTS: Ten-year prospective cohort study of 1,298,385 Koreans (829,770 men and 468,615 women) aged 30 to 95 years who received health insurance from the National Health Insurance Corp and had a biennial medical evaluation in 1992-1995 (with follow-up for up to 10 years). MAIN OUTCOME MEASURES: Death from cancer and registry-documented incident cancer or hospital admission for cancer. RESULTS: During the 10 years of follow-up, there were 20,566 cancer deaths in men and 5907 cancer deaths in women. Using Cox proportional hazards models and controlling for smoking and alcohol use, the stratum with the highest fasting serum glucose (> or =140 mg/dL [> or =7.8 mmol/L]) had higher death rates from all cancers combined (hazard ratio [HR], 1.29; 95% confidence interval [CI], 1.22-1.37 in men and HR, 1.23; 95% CI, 1.09-1.39 in women) compared with the stratum with the lowest level (<90 mg/dL [<5.0 mmol/L]). By cancer site, the association was strongest for pancreatic cancer, comparing the highest and lowest strata in men (HR, 1.91; 95% CI, 1.52-2.41) and in women (HR, 2.05; 95% CI, 1.43-2.93). Significant associations were also found for cancers of the esophagus, liver, and colon/rectum in men and of the liver and cervix in women, and there were significant trends with glucose level for cancers of the esophagus, colon/rectum, liver, pancreas, and bile duct in men and of the liver and pancreas in women. Of the 26,473 total cancer deaths in men and women, 848 were estimated as attributable to having a fasting serum glucose level of less than 90 mg/dL. For cancer incidence, the general patterns reflected those found for mortality. For persons with a diagnosis of diabetes or a fasting serum glucose level greater than 125 mg/dL (6.9 mmol/L), risks for cancer incidence and mortality were generally elevated compared with those without diabetes. CONCLUSION: In Korea, elevated fasting serum glucose levels and a diagnosis of diabetes are independent risk factors for several major cancers, and the risk tends to increase with an increased level of fasting serum glucose.

Adult↗