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Biomedical subjects

J M Samet

Publications and source records attributed to J M Samet.

At least 37 records · Page 2Linked to original sources
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↗
PubMed2000

Estimating particulate matter-mortality dose-response curves and threshold levels: an analysis of daily time-series for the 20 largest US cities.

Numerous studies have shown a positive association between daily mortality and particulate air pollution, even at concentrations below regulatory limits. These findings have motivated interest in the shape of the exposure-response relation. The authors have developed flexible modeling strategies for time-series data that include spline and threshold exposure-response models; they apply these models to daily time-series data for the 20 largest US cities for 1987-1994, using the concentration of particulate matter <10 microm in aerodynamic diameter (PM10) as the exposure measure. The spline model showed a linear relation without indication of threshold for PM10 and relative risk of death for all causes and cardiorespiratory causes; by contrast, for other causes, the risk did not increase until approximately 50 microg/m3 PM10. For all-cause mortality, a linear model without threshold was preferred to the threshold model and to the spline model, using the Akaike information criterion (AIC). The findings were similar for cardiovascular and respiratory deaths combined. By contrast, for causes other than cardiovascular and respiratory, a threshold model was more competitive with a threshold value estimated at 65 microg/m3. These findings indicate that linear models without a threshold are appropriate for assessing the effect of particulate air pollution on daily mortality even at current levels.

Air Pollutants↗
PubMed2000

Occupational and environmental risk factors for idiopathic pulmonary fibrosis: a multicenter case-control study. Collaborating Centers.

Occupational exposures were investigated in a multicenter case-control study of clinically and histologically diagnosed idiopathic pulmonary fibrosis (IPF), a chronic diffuse interstitial lung disease of unknown etiology. Results are based on 248 cases, aged 20-75 years, diagnosed at 16 referral centers between January 1989 and July 1993. There were 491 controls ascertained by random digit dialing and matched to cases on sex, age, and geographic region. Data were collected using a standard telephone questionnaire. Occupational factors were based on a detailed history of jobs lasting 6 months or more and job activity, hobby, and specific substance checklists. Several occupational factors, adjusted for age and smoking in conditional multivariate logistic regression analyses, were significantly associated with IPF: farming (odds ratio (OR) = 1.6, 95% confidence interval (CI): 1.0, 2.5); livestock (OR = 2.7, 95% CI: 1.3, 5.5); hairdressing (OR = 4.4, 95% CI: 1.2, 16.3); metal dust (OR = 2.0, 95% CI: 1.0, 4.0); raising birds (OR = 4.7, 95% CI: 1.6, 14.1); stone cutting/polishing (OR = 3.9, 95% CI: 1.2, 12.7); and vegetable dust/animal dust (OR = 4.7, 95% CI: 2.1, 10.4). Interaction was detected between smoking and exposure to livestock (p = 0.06) and farming (p = 0.08). Results confirm previous studies showing increased risk associated with dusty environments.

Adult↗
PubMed2000

Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study.

CONTEXT: Sleep-disordered breathing (SDB) and sleep apnea have been linked to hypertension in previous studies, but most of these studies used surrogate information to define SDB (eg, snoring) and were based on small clinic populations, or both. OBJECTIVE: To assess the association between SDB and hypertension in a large cohort of middle-aged and older persons. DESIGN AND SETTING: Cross-sectional analyses of participants in the Sleep Heart Health Study, a community-based multicenter study conducted between November 1995 and January 1998. PARTICIPANTS: A total of 6132 subjects recruited from ongoing population-based studies (aged > or = 40 years; 52.8% female). MAIN OUTCOME MEASURES: Apnea-hypopnea index (AHI, the average number of apneas plus hypopneas per hour of sleep, with apnea defined as a cessation of airflow and hypopnea defined as a > or = 30% reduction in airflow or thoracoabdominal excursion both of which are accompanied by a > or = 4% drop in oxyhemoglobin saturation) [corrected], obtained by unattended home polysomnography. Other measures include arousal index; percentage of sleep time below 90% oxygen saturation; history of snoring; and presence of hypertension, defined as resting blood pressure of at least 140/90 mm Hg or use of antihypertensive medication. RESULTS: Mean systolic and diastolic blood pressure and prevalence of hypertension increased significantly with increasing SDB measures, although some of this association was explained by body mass index (BMI). After adjusting for demographics and anthropometric variables (including BMI, neck circumference, and waist-to-hip ratio), as well as for alcohol intake and smoking, the odds ratio for hypertension, comparing the highest category of AHI (> or = 30 per hour) with the lowest category (< 1.5 per hour), was 1.37 (95% confidence interval [CI], 1.03-1.83; P for trend = .005). The corresponding estimate comparing the highest and lowest categories of percentage of sleep time below 90% oxygen saturation (> or = 12% vs < 0.05%) was 1.46 (95% CI, 1.12-1.88; P for trend <.001). In stratified analyses, associations of hypertension with either measure of SDB were seen in both sexes, older and younger ages, all ethnic groups, and among normal-weight and overweight individuals. Weaker and nonsignificant associations were observed for the arousal index or self-reported history of habitual snoring. CONCLUSION: Our findings from the largest cross-sectional study to date indicate that SDB is associated with systemic hypertension in middle-aged and older individuals of different sexes and ethnic backgrounds.

Adult↗
PubMed2000

Lung mucin production is stimulated by the air pollutant residual oil fly ash.

Human and animal exposure to particulate air pollution is correlated with airway mucus hypersecretion and increased susceptibility to infection. Seeking clues to the mechanisms underlying this pathology, we examined the effect of the particulate air pollutant residual oil fly ash (ROFA) on production of the major component of mucus, mucin, and the major antibacterial protein of the respiratory tract, lysozyme. We found that following in vitro exposure to ROFA, epithelial cells showed an increase in mucin (MUC5AC) and lysozyme (LYS) steady state mRNA. This upregulation was controlled at least partly at the level of transcription as shown by reporter assays. Experiments testing the ability of the major components of ROFA to mimic these effects showed that vanadium, a metal making up 18.8% by weight, accounted for the bulk of the response. A screen of signaling inhibitors showed that MUC5AC and LYS induction by ROFA are mediated by dissimilar signaling pathways, both of which are, however, phosphotyrosine dependent. Recognizing that the ROFA constituent vanadium is a potent tyrosine phosphatase inhibitor and that mucin induction by pathogens is phophotyrosine dependent, we suggest that vanadium-containing air pollutants trigger disease-like conditions by unmasking phosphorylation-dependent pathogen resistance pathways.

Air Pollutants↗
PubMed2000

Concepts of time in clinical research.

The study of events in time is fundamental to biomedical research and public health surveillance. Clinicians have an intuitive appreciation for the relevance of time to health and disease, and patients invariably ask questions relating to time for which clinicians need answers. An appreciation of the picture of health and disease over time is equally fundamental to public health. Research designs that incorporate time have long been in use; the cohort study, which involves follow-up of persons overtime, is the fundamental design. Analysis of longitudinal data, generated by cohort studies and related approaches, has been enhanced by new statistical methods that are appropriate to data collected over time from repeated observations. In the next millennium, new and increasingly complex questions will undoubtedly require investigation. The research designs and analytic methods used to address clinical questions in time will continue to evolve and will provide better, sharper answers.

Acquired Immunodeficiency Syndrome↗
PubMed2000

In vivo and in vitro correlation of pulmonary MAP kinase activation following metallic exposure.

Residual oil fly ash (ROFA) is a particulate pollutant produced in the combustion of fuel oil. Exposure to ROFA is associated with adverse respiratory effects in humans, induces lung inflammation in animals, and induces inflammatory mediator expression in cultured human airway epithelial cells (HAEC). ROFA has a high content of transition metals, including vanadium, a potent tyrosine phosphatase inhibitor that we have previously shown to disregulate phosphotyrosine metabolism and activate mitogen-activated protein kinase (MAPK) signaling cascades in HAEC. In order to study MAPK activation in response to in vivo metal exposure, we used immunohistochemical methods to detect levels of phosphorylated protein tyrosines (P-Tyr) and the MAPKs ERK1/2, JNK, and P38 in lung sections from rats intratracheally exposed to ROFA. After a 1-h exposure to 500 microg ROFA, rat lungs showed no histological changes and no significant increases in immunostaining for either P-Tyr or phospho-(P-) MAPKs compared to saline-instilled controls. At 4 h of exposure, there was mild and variable inflammation in the lung, which was accompanied by an increase in specific immunostaining for P-Tyr and P-MAPKs in airway and alveolar epithelial cells and resident macrophages. By 24 h of exposure, there was a pronounced inflammatory response to ROFA instillation and a marked increase in levels of P-Tyr and P-MAPKs present within the alveolar epithelium and in the inflammatory cells, while the airway epithelium showed a continued increase in the expression of P-ERK1/2. By comparison, HAEC cultures exposed to 100 microg/ml ROFA for 20 min resulted in marked increases in P-Tyr and P-MAPKs, which persisted after 24 h of exposure. P-Tyr levels continued to accumulate for up to 24 h in HAEC exposed to ROFA. These results demonstrate in vivo activation in cell signaling pathways in response to pulmonary exposure to particulate matter, and support the relevance of in vitro studies in the identification of mechanisms of lung injury induced by pollutant inhalation.

Air Pollutants↗
PubMed2000

A measurement error model for time-series studies of air pollution and mortality.

One barrier to interpreting the observational evidence concerning the adverse health effects of air pollution for public policy purposes is the measurement error inherent in estimates of exposure based on ambient pollutant monitors. Exposure assessment studies have shown that data from monitors at central sites may not adequately represent personal exposure. Thus, the exposure error resulting from using centrally measured data as a surrogate for personal exposure can potentially lead to a bias in estimates of the health effects of air pollution. This paper develops a multi-stage Poisson regression model for evaluating the effects of exposure measurement error on estimates of effects of particulate air pollution on mortality in time-series studies. To implement the model, we have used five validation data sets on personal exposure to PM10. Our goal is to combine data on the associations between ambient concentrations of particulate matter and mortality for a specific location, with the validation data on the association between ambient and personal concentrations of particulate matter at the locations where data have been collected. We use these data in a model to estimate the relative risk of mortality associated with estimated personal-exposure concentrations and make a comparison with the risk of mortality estimated with measurements of ambient concentration alone. We apply this method to data comprising daily mortality counts, ambient concentrations of PM10measured at a central site, and temperature for Baltimore, Maryland from 1987 to 1994. We have selected our home city of Baltimore to illustrate the method; the measurement error correction model is general and can be applied to other appropriate locations.Our approach uses a combination of: (1) a generalized additive model with log link and Poisson error for the mortality-personal-exposure association; (2) a multi-stage linear model to estimate the variability across the five validation data sets in the personal-ambient-exposure association; (3) data augmentation methods to address the uncertainty resulting from the missing personal exposure time series in Baltimore. In the Poisson regression model, we account for smooth seasonal and annual trends in mortality using smoothing splines. Taking into account the heterogeneity across locations in the personal-ambient-exposure relationship, we quantify the degree to which the exposure measurement error biases the results toward the null hypothesis of no effect, and estimate the loss of precision in the estimated health effects due to indirectly estimating personal exposures from ambient measurements.

Journal Article↗
PubMed2000

Indoor air pollution in developing countries and acute lower respiratory infections in children.

BACKGROUND: A critical review was conducted of the quantitative literature linking indoor air pollution from household use of biomass fuels with acute respiratory infections in young children, which is focused on, but not confined to, acute lower respiratory infection and pneumonia in children under two years in less developed countries. Biomass in the form of wood, crop residues, and animal dung is used in more than two fifths of the world's households as the principal fuel. METHODS: Medline and other electronic databases were used, but it was also necessary to secure literature from colleagues in less developed countries where not all publications are yet internationally indexed. RESULTS: The studies of indoor air pollution from household biomass fuels are reasonably consistent and, as a group, show a strong significant increase in risk for exposed young children compared with those living in households using cleaner fuels or being otherwise less exposed. Not all studies were able to adjust for confounders, but most of those that did so found that strong and significant risks remained. CONCLUSIONS: It seems that the relative risks are likely to be significant for the exposures considered here. Since acute lower respiratory infection is the chief cause of death in children in less developed countries, and exacts a larger burden of disease than any other disease category for the world population, even small additional risks due to such a ubiquitous exposure as air pollution have important public health implications. In the case of indoor air pollution in households using biomass fuels, the risks also seem to be fairly strong, presumably because of the high daily concentrations of pollutants found in such settings and the large amount of time young children spend with their mothers doing household cooking. Given the large vulnerable populations at risk, there is an urgent need to conduct randomised trials to increase confidence in the cause-effect relationship, to quantify the risk more precisely, to determine the degree of reduction in exposure required to significantly improve health, and to establish the effectiveness of interventions.

Acute Disease↗
PubMed2000

A parental history of asthma is a risk factor for wheezing and nonwheezing respiratory illnesses in infants younger than 18 months of age.

The relationship between respiratory infection and allergy as risk factors for the development of wheezing illnesses in infants has been in dispute. We hypothesized that a parental history of allergic diseases would be associated with an increased rate of respiratory infections as well as an increased rate of wheezing during infectious episodes. We prospectively evaluated 1,193 infants from birth to 18 mo of age, using bi-weekly telephone surveillance to document all respiratory events. The overall rate of respiratory illness (all RI) increased to a maximum of 10.6 illnesses/infant/year in the 7- to 9-mo age group and then leveled off in the older infants. Multivariable models adjusting for demographic variables, breast feeding, month of illness, number of siblings, and attendance at day care showed an increase in the rate of all RI in infants older than 7 mo of age who had a parental history of asthma (OR = 1.24, CI = 1.09 to 1.41) or a parental history of atopy (OR = 1.14, CI = 1.03 to 1.26). The rate of lower respiratory illnesses accompanied by wheezing was related only to a parental history of asthma (OR = 2.06, CI = 1.36 to 3.11). We conclude that all RI, most of which represent viral infections, are increased in otherwise normal infants with a parental history of asthma or atopy, whereas wheezing is related only to a parental history of asthma.

Asthma↗
PubMed2000

Vanadium-induced kappaB-dependent transcription depends upon peroxide-induced activation of the p38 mitogen-activated protein kinase.

Activation of nuclear factor (NF)-kappaB and subsequent proinflammatory gene expression in human airway epithelial cells can be evoked by oxidative stress. In this study we examined signal transduction pathways activated by vanadyl sulfate (V(IV))-induced oxidative stress in normal human bronchial epithelial cells. Both nuclear translocation of NF-kappaB and enhanced kappaB-dependent transcription induced by V(IV) were inhibited by overexpression of catalase, but not Cu,Zn superoxide dismutase (Cu,Zn-SOD), indicating that peroxides rather than superoxides initiated signaling. Catalase selectively blocked the response to V(IV) because it inhibited neither NF-kappaB translocation nor kappaB-dependent transcription evoked by the proinflammatory cytokine tumor necrosis factor (TNF)-alpha. The V(IV)-induced kappaB-dependent transcription was dependent upon activation of the p38 mitogen-activated protein kinase because overexpression of dominant-negative mutants of the p38 MAPK pathway inhibited V(IV)-induced kappaB-dependent transcription. This inhibition was not due to suppression of NF-kappaB nuclear translocation because NF-kappaB DNA binding was unaffected by the inhibition of p38 activity. Overexpression of catalase, but not Cu,Zn-SOD, inhibited p38 activation, indicating that peroxides activated p38. Catalase failed to block V(IV)- induced increases in phosphotyrosine levels, suggesting that the catalase-sensitive signaling components were independent of V(IV)-induced tyrosine phosphorylation. The data demonstrate that V(IV)-induced oxidative stress activates at least two distinct pathways, NF-kappaB nuclear translocation and p38-dependent transactivation of NF-kappaB, both of which are required to fully activate kappaB-dependent transcription. Moreover, V(IV)-induced oxidative stress activated these pathways in bronchial epithelial cells by upstream signaling cascades that were distinct at some level from those used by the proinflammatory cytokine TNF-alpha.

Bronchi↗
PubMed2000

The potential health impacts of climate variability and change for the United States: executive summary of the report of the health sector of the U.S. National Assessment.

We examined the potential impacts of climate variability and change on human health as part of a congressionally mandated study of climate change in the United States. Our author team, comprising experts from academia, government, and the private sector, was selected by the federal interagency U.S. Global Change Research Program, and this report stems from our first 18 months of work. For this assessment we used a set of assumptions and/or projections of future climates developed for all participants in the National Assessment of the Potential Consequences of Climate Variability and Change. We identified five categories of health outcomes that are most likely to be affected by climate change because they are associated with weather and/or climate variables: temperature-related morbidity and mortality; health effects of extreme weather events (storms, tornadoes, hurricanes, and precipitation extremes); air-pollution-related health effects; water- and foodborne diseases; and vector- and rodent-borne diseases. We concluded that the levels of uncertainty preclude any definitive statement on the direction of potential future change for each of these health outcomes, although we developed some hypotheses. Although we mainly addressed adverse health outcomes, we identified some positive health outcomes, notably reduced cold-weather mortality, which has not been extensively examined. We found that at present most of the U.S. population is protected against adverse health outcomes associated with weather and/or climate, although certain demographic and geographic populations are at increased risk. We concluded that vigilance in the maintenance and improvement of public health systems and their responsiveness to changing climate conditions and to identified vulnerable subpopulations should help to protect the U.S. population from any adverse health outcomes of projected climate change.

Adolescent↗