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Biomedical subjects

J M Samet

Publications and source records attributed to J M Samet.

At least 19 recordsLinked to original sources
PubMed2001

Comorbidity and survival of elderly head and neck carcinoma patients.

BACKGROUND: Alcohol and tobacco, the primary etiologic agents for head and neck carcinoma (HNCA), cause other chronic diseases and may contribute to the high prevalence of comorbid conditions and generally poor survival of persons with HNCA. METHODS: The authors explored the prognostic role of comorbidity in persons with HNCA using Health Care Finance Administration Medicare (HCFA) files linked with the appropriate files of the Surveillance, Epidemiology, and End Results (SEER) Program. The Charlson comorbidity index was applied to in-patient data from the HCFA files. The SEER data were used to ascertain survival and identify persons with HNCA diagnosed from 1985 to 1993 (n = 9386). RESULTS: In a proportional hazards regression model adjusted for age and historic stage at diagnosis, race, gender, marital status, socioeconomic status, histologic grade, anatomic site, treatment, and pre-1991 diagnosis, Charlson index scores of 0, 1, and 2+ had estimated relative hazards (RHs) with 95 confidence intervals (CIs) of 1.00, 1.33 (95% CI, 1.21-1.47), and 1.83 (95% CI, 1.64-2.05), respectively (P value for trend < 0.0001). The adjusted RH for a Charlson index score of 1 or more compared with 0, using stratified models, was found to be greater in whites (RH, 1.55; 95% CI, 1.43-1.67) than blacks (RH, 1.24; 95% CI, 0.96-1.60), local (RH, 1.72; 95% CI, 1.50-1.96) versus distant stage (RH, 1.25; 95% CI, 1.00-1.56), and age 65-74 years (RH, 1.53; 95% CI, 1.38-1.69) versus age 85+ years (RH, 1.42; 95% CI, 1.09-1.84). CONCLUSIONS: This study establishes comorbidity as a predictor of survival in an elderly HNCA population and lends support to the inclusion of comorbidity assessment in prognostic staging of patients with HNCA diagnosed after 65 years of age.

Aged↗
PubMed2001

Enhancement of mast cell survival: a novel function of some secretory phospholipase A(2) isotypes.

This study tested the hypothesis that certain secretory phospholipase A(2) (sPLA(2)) isotypes act in a cytokine-like fashion through cell surface receptors to influence mast cell survival. Initial experiments revealed that sPLA(2) activity and sPLA(2) receptor expression are increased, and mast cells lost their capacity to maintain membrane asymmetry upon cytokine depletion. Groups IB and III, but not group IIA PLA(2), prevented the loss of membrane asymmetry. Similarly, group IB prevented nucleosomal DNA fragmentation in mast cells. Providing putative products of sPLA(2) hydrolysis to cytokine-depleted mast cells did not influence survival. Furthermore, catalytic inactivation of sPLA(2) did not alter its capacity to prevent apoptosis. Inhibition of protein synthesis using cycloheximide or actinomycin reversed the antiapoptotic effect of sPLA(2). Additionally, both wild-type and catalytically inactive group IB PLA(2) induced IL-3 synthesis in mast cells. However, adding IL-3-neutralizing Ab did not change Annexin V(FITC) binding and only partially inhibited thymidine incorporation in sPLA(2)-supplemented mast cells. In contrast, IL-3-neutralizing Ab inhibited both Annexin V(FITC) binding and thymidine incorporation in mast cells maintained with IL-3. sPLA(2) enhanced phosphoinositide 3'-kinase activity, and a specific inhibitor of phosphoinositide 3'-kinase reversed the antiapoptotic effects of sPLA(2). Likewise, sPLA(2) increased the degradation of I-kappaBalpha, and specific inhibitors of nuclear factor kappa activation (NF-kappaB) reversed the antiapoptotic effects of sPLA(2). Together, these experiments reveal that certain isotypes of sPLA(2) enhance the survival of mast cells in a cytokine-like fashion by activating antiapoptotic signaling pathways independent of IL-3 and probably via sPLA(2) receptors rather than sPLA(2) catalytic products.

Animals↗
PubMed2001

Physical activity and breast cancer risk in hispanic and non-hispanic white women.

To investigate breast cancer risk in Hispanic and non-Hispanic White women, the authors conducted a population-based case-control study of New Mexican women during 1992-1994 using incident breast cancer cases aged 35-74 years and frequency-matched controls selected using random digit dialing. Activity type and weekly duration of usual nonoccupational physical activity were used to calculate weekly metabolic equivalent (MET)-hours of total and vigorous physical activity (> or =5 METs). Conditional logistic regression models were fitted to estimate the relative risk of breast cancer for levels of physical activity and to assess the difference in effects by ethnicity, body mass index, energy intake, and menopausal status. Vigorous physical activity was associated with reduced breast cancer risk in both Hispanic and non-Hispanic White women. Women in the highest category of vigorous activity had lower risk of breast cancer (adjusted odds ratio = 0.34, 95% confidence interval: 0.22, 0.51 for Hispanic; adjusted odds ratio = 0.60, 95% confidence interval: 0.41, 0.89 for non-Hispanic White women) compared with women reporting no vigorous physical activity. Both pre- and postmenopausal Hispanic women showed decreasing risk with increasing level of activity. Physical activity was protective only among postmenopausal non-Hispanic White women. The effects of physical activity were independent from reproductive factors, usual body mass index, body mass index at age 18, adult weight gain, and total energy intake.

Adult↗
PubMed2001

Effect of antioxidant supplementation on ozone-induced lung injury in human subjects.

To determine whether antioxidants can influence human susceptibility to ozone (O(3))-induced changes in lung function and airway inflammation, we placed 31 healthy nonsmoking adults (18 to 35 yr old) on a diet low in ascorbate for 3 wk. At 1 wk, subjects were exposed to filtered air for 2 h while exercising (20 L/min/m(2)), and then underwent bronchoalveolar lavage (BAL) and were randomly assigned to receive either a placebo or 250 mg of vitamin C, 50 IU of alpha-tocopherol, and 12 oz of vegetable cocktail daily for 2 wk. Subjects were then exposed to 0.4 ppm O(3) for 2 h and underwent a second BAL. On the day of the O(3) exposure, supplemented subjects were found to have significantly increased levels of plasma ascorbate, tocopherols, and carotenoids as compared with those of the placebo group. Pulmonary function testing showed that O(3)-induced reductions in FEV(1) and FVC were 30% and 24% smaller, respectively, in the supplemented cohort. In contrast, the inflammatory response to O(3) inhalation, as represented by the percent neutrophils and the concentration of interleukin-6 recovered in the BAL fluid at 1 h after O(3) exposure was not different for the two groups. These data suggest that dietary antioxidants protect against O(3)-induced pulmonary function decrements in humans.

Adult↗
PubMed2001

The American Society of Anesthesiologists' class as a comorbidity index in a cohort of head and neck cancer surgical patients.

BACKGROUND: We assessed the American Society of Anesthesiologists' (ASA) class, as a measure of comorbidity in comparison to the commonly used Charlson index for prognostic ability in a HNCA population. METHODS: Proportional hazards methods were applied to head and neck cancer patients whose treatment included surgery by the Johns Hopkins Otolaryngology service (n = 388). RESULTS: The Charlson index and ASA class were modestly correlated (Spearman 0.36, p <.001). Compared with patients with ASA class 1 or 2, those with ASA class 3 or 4 had a two-fold elevated mortality rate (Relative Hazard (RH) = 2.00, 95% CI, 1.38-2.89). This association was stronger than observed for a Charlson index score of 1 or more compared with 0 (RH = 1.59, 95% CI, 1.17-2.17). Both the Charlson index and ASA class adjusted RHs displayed dose-response patterns (p value for trend <.001). CONCLUSIONS: Compared with the Charlson index, the ASA class had comparable if not greater prognostic ability for mortality in this elderly HNCA population.

Aged↗
PubMed2001

Ethnic differences in asthma and associated phenotypes: collaborative study on the genetics of asthma.

BACKGROUND: In the Collaborative Study on the Genetics of Asthma, 314 families with 2584 subjects were characterized for asthma and allergy. OBJECTIVE: The purpose of this investigation was to examine clinical heterogeneity observed in asthma and allergic characteristics among 3 ethnic groups (African American, white, and Hispanic family members). METHODS: Pulmonary function parameters and asthma associated phenotypes were compared among the ethnic groups. RESULTS: In comparison with the other groups, African American sibling pairs had a significantly lower baseline FEV(1) percent of predicted (P =.0001) and a higher rate of skin test reactivity to cockroach allergen (P =.0001); Hispanic sibling pairs had significantly more skin reactivity overall (P =.001); and white sibling pairs had significantly lower total serum IgE (P <.05). In addition, there were significantly more relatives with asthma among the African American families than among the white and the Hispanic families (P =.001). CONCLUSION: Although different environmental backgrounds should be considered, these clinical differences could be due to differences in genetic susceptibility among the ethnic groups, such as those suggested by our previous genome screen.

Adolescent↗
PubMed2001

Smoking cessation in China: findings from the 1996 national prevalence survey.

OBJECTIVES: To describe patterns of smoking and smoking cessation in China within the context of the stages of change model, using data from the 1996 national prevalence survey. DESIGN: A cross sectional survey was carried out using the 145 preselected disease surveillance points, which provide a representative sample for the entire country. A standardised questionnaire on smoking was interviewer administered. SETTING: The country of China. SUBJECTS: 122,220 people aged 15-69 years. MAINTENANCE MEASURES: Smoking cessation patterns, as defined by smoking status (current or former) and stage of change (precontemplation, contemplation, and action). RESULTS: The sample included 45,995 ever smokers of whom 4336 had quit. About 72% of current smokers reported not intending to give up their smoking behaviour, and about 16% of current smokers said they intended to do so, but have not taken any action. Of all ever smokers, the percentage of former smokers was 9.5%, and 12% of current smokers had quit at least once, but relapsed by the time of the survey. The patterns were similar in men and women with regard to the stated intent to quit. Among males, the percentage of former smokers increased with age but the percentage intending to quit was constant at about 15% across age strata. The most common reason for quitting was illness. Participants with a university education were more likely to have made an attempt to quit. CONCLUSIONS: The percentage of smokers contemplating quitting was low in China in 1996. The study shows that smokers in China must be mobilised to contemplate quitting and then to take action.

Adolescent↗
PubMed2001

Activation of the EGF receptor signaling pathway in airway epithelial cells exposed to Utah Valley PM.

Exposure to ambient particulate matter (PM) in the Utah Valley has previously been associated with a variety of adverse health effects. To investigate intracellular signaling mechanisms for pulmonary responses to Utah Valley PM inhalation, human primary airway epithelial cells were exposed to aqueous extracts of PM collected from the year before (Y1), during (Y2), and after (Y3) the closure of a local steel mill located in the Utah Valley in this study. Transfection with kinase-deficient extracellular signal-regulated kinase (ERK) 1 constructs partially blocked Utah Valley PM-induced interleukin (IL)-8 promoter reporter activity. The mitogen-activated protein kinase/ERK kinase (MEK) activity inhibitor PD-98059 significantly abolished IL-8 released in response to Utah Valley PM, as did the epidermal growth factor (EGF) receptor kinase inhibitor AG-1478. Western blotting showed that Utah Valley PM induced phosphorylation of EGF receptor tyrosine, MEK1/2, and ERK1/2, which could be ablated with AG-1478 or PD-98059. For all findings, the potency of Utah Valley PM collected during Y2 was found to be lower relative to that of Y1 and Y3. These data demonstrate that Utah Valley PM can induce IL-8 expression partially through the activation of the EGF receptor signaling.

Air Pollutants, Occupational↗
PubMed2001

Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study.

Disordered breathing during sleep is associated with acute, unfavorable effects on cardiovascular physiology, but few studies have examined its postulated association with cardiovascular disease (CVD). We examined the cross-sectional association between sleep- disordered breathing and self-reported CVD in 6,424 free-living individuals who underwent overnight, unattended polysomnography at home. Sleep-disordered breathing was quantified by the apnea-hypopnea index (AHI)-the average number of apneas and hypopneas per hour of sleep. Mild to moderate disordered breathing during sleep was highly prevalent in the sample (median AHI: 4.4; interquartile range: 1.3 to 11.0). A total of 1,023 participants (16%) reported at least one manifestation of CVD (myocardial infarction, angina, coronary revascularization procedure, heart failure, or stroke). The multivariable-adjusted relative odds (95% CI) of prevalent CVD for the second, third, and fourth quartiles of the AHI (versus the first) were 0.98 (0.77-1.24), 1.28 (1.02-1.61), and 1.42 (1.13-1.78), respectively. Sleep-disordered breathing was associated more strongly with self-reported heart failure and stroke than with self-reported coronary heart disease: the relative odds (95% CI) of heart failure, stroke, and coronary heart disease (upper versus lower AHI quartile) were 2.38 (1.22-4.62), 1.58 (1.02- 2.46), and 1.27 (0.99-1.62), respectively. These findings are compatible with modest to moderate effects of sleep-disordered breathing on heterogeneous manifestations of CVD within a range of AHI values that are considered normal or only mildly elevated.

Aged↗
PubMed2001

Hydrogen peroxide has opposing effects on IKK activity and IkappaBalpha breakdown in airway epithelial cells.

Recent studies have advanced our knowledge about the signal transduction cascade involved in the activation of nuclear factor (NF) kappaB, including the identification and characterization of IkappaB kinases (IKKs). Although exposure to hydrogen peroxide (H2O2) in vitro can activate NF-kappaB, this response is not universal and depends on the cell type and transformation state. In this study, we examined the effects of H2O2 on IKKs and activation of NF-kappaB in primary normal human bronchial epithelial (NHBE) cells. Our results demonstrate that treatment with H2O2 increased IKK activity, phosphorylation, and ubiquitination of IkappaBalpha in NHBE cells. However, there was no significant proteolytic degradation of IkappaBalpha, nuclear translocation of p65, or NF-kappaB DNA binding activity in cells treated with H2O2. Treatment with H2O2 also inhibited tumor necrosis factor (TNF)-alpha-induced IkappaBalpha breakdown, NF-kappaB DNA binding activity, and NF-kappaB-dependent transcription but had no effect on TNF-alpha-induced IkappaBalpha phosphorylation or ubiquitination. Furthermore, treatment with H2O2 alone or in combination with TNF-alpha increased the levels of other ubiquitinated proteins in NHBE cells, suggesting general inhibition of proteasomal activity by H2O2. Taken together, these results demonstrate that in airway epithelial cells treatment with H2O2 has opposing effects on IKK activity and proteasomal degradation of IkappaBalpha, and suggest that H2O2 may suppress TNF-alpha-induced NF-kappaB- dependent gene expression.

Bronchi↗
PubMed2001

The potential impacts of climate variability and change on air pollution-related health effects in the United States.

Climate change may affect exposures to air pollutants by affecting weather, anthropogenic emissions, and biogenic emissions and by changing the distribution and types of airborne allergens. Local temperature, precipitation, clouds, atmospheric water vapor, wind speed, and wind direction influence atmospheric chemical processes, and interactions occur between local and global-scale environments. If the climate becomes warmer and more variable, air quality is likely to be affected. However, the specific types of change (i.e., local, regional, or global), the direction of change in a particular location (i.e., positive or negative), and the magnitude of change in air quality that may be attributable to climate change are a matter of speculation, based on extrapolating present understanding to future scenarios. There is already extensive evidence on the health effects of air pollution. Ground-level ozone can exacerbate chronic respiratory diseases and cause short-term reductions in lung function. Exposure to particulate matter can aggravate chronic respiratory and cardiovascular diseases, alter host defenses, damage lung tissue, lead to premature death, and possibly contribute to cancer. Health effects of exposures to carbon monoxide, sulfur dioxide, and nitrogen dioxide can include reduced work capacity, aggravation of existing cardiovascular diseases, effects on pulmonary function, respiratory illnesses, lung irritation, and alterations in the lung's defense systems. Adaptations to climate change should include ensuring responsiveness of air quality protection programs to changing pollution levels. Research needs include basic atmospheric science work on the association between weather and air pollutants; improving air pollution models and their linkage with climate change scenarios; and closing gaps in the understanding of exposure patterns and health effects.

Aerosols↗
PubMed2001

Turning science into junk: the tobacco industry and passive smoking.

In this issue, Glantz and Ong offer a powerful analysis of the tobacco industry's attempt to discredit the scientific evidence on passive smoking, particularly the industry's use of the label "junk science." Environmental epidemiologic studies in other arenas have also been targets for the "junk science" label. Lessons for researchers involved in high-stakes issues in the public policy arena include a need for awareness of competing interests, for transparency concerning funding, and for adherence to rigorous quality assurance and peer review practices. The goal of "sound science" seems an admirable one; it should not, however, be used to dismiss available but uncertain evidence in order to delay action.

Carcinogens↗
PubMed2000

Fine particulate air pollution and mortality in 20 U.S. cities, 1987-1994.

BACKGROUND: Air pollution in cities has been linked to increased rates of mortality and morbidity in developed and developing countries. Although these findings have helped lead to a tightening of air-quality standards, their validity with respect to public health has been questioned. METHODS: We assessed the effects of five major outdoor-air pollutants on daily mortality rates in 20 of the largest cities and metropolitan areas in the United States from 1987 to 1994. The pollutants were particulate matter that is less than 10 microm in aerodynamic diameter (PM10), ozone, carbon monoxide, sulfur dioxide, and nitrogen dioxide. We used a two-stage analytic approach that pooled data from multiple locations. RESULTS: After taking into account potential confounding by other pollutants, we found consistent evidence that the level of PM10 is associated with the rate of death from all causes and from cardiovascular and respiratory illnesses. The estimated increase in the relative rate of death from all causes was 0.51 percent (95 percent posterior interval, 0.07 to 0.93 percent) for each increase in the PM10 level of 10 microg per cubic meter. The estimated increase in the relative rate of death from cardiovascular and respiratory causes was 0.68 percent (95 percent posterior interval, 0.20 to 1.16 percent) for each increase in the PM10 level of 10 microg per cubic meter. There was weaker evidence that increases in ozone levels increased the relative rates of death during the summer, when ozone levels are highest, but not during the winter. Levels of the other pollutants were not significantly related to the mortality rate. CONCLUSIONS: There is consistent evidence that the levels of fine particulate matter in the air are associated with the risk of death from all causes and from cardiovascular and respiratory illnesses. These findings strengthen the rationale for controlling the levels of respirable particles in outdoor air.

Air Pollutants↗