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1.
Article in English | MEDLINE | ID: mdl-24827247

ABSTRACT

Close to a planar surface, lamellar structures are imposed upon otherwise bulk bicontinuous microemulsions. Thermally induced membrane undulations are modified by the presence of the rigid interface. While it has been shown that a pure membrane's dynamics are accelerated close to the interface, we observed nearly unchanged relaxation rates for membranes spiked with large amphiphilic diblock copolymers. An increase of the polymer concentration by a factor of 2-3 for the first and second surfactant membrane layers was observed. We interpret the reduced relaxation times as the result of an interplay between the bending rigidity and the characteristic distance of the first surfactant membrane to the rigid interface, which causes the hydrodynamic and steric interface effects described in Seifert's theory. The influence of these effects on decorated membranes yields a reduction of the frequencies and an amplification of the amplitudes of long-wavelength undulations, which are in accordance to our experimental findings.

2.
Inhal Toxicol ; 20(10): 949-60, 2008 Aug.
Article in English | MEDLINE | ID: mdl-18686108

ABSTRACT

We analyzed survival patterns among approximately 70,000 U.S. male military veterans relative to vehicular traffic density in their counties of residence, by mortality period and type of exposure model. Previous analyses show traffic density to be a better predictor than concentrations of criteria air pollutants. We considered all subjects and also the subset defined by availability of air quality monitoring data from the U.S. EPA PM(2.5) Speciation Trends Network (STN). Traffic density is a robust predictor of mortality in this cohort; statistically significant estimates of deaths associated with traffic range from 1.3% to 4.4%, depending on the method of analysis. This range of uncertainty is larger than the traditional 95% confidence intervals for each estimate (1-2%). Our best estimate of the relative risk for the entire follow-up period is 1.03. These deaths occurred mainly before 1997 in counties with STN air quality data, which tend to be more urban. We identified a threshold in mortality responses to traffic density, corresponding to county-average traffic flow rates of about 4000 vehicles/day. Relative risks were significantly higher in the more urban (STN) counties in the early subperiods, but this gradient appears to have diminished over time. We found larger risks by pooling results from separate portions of the overall follow-up period, relative to considering the entire period at once, which suggests temporal changes in confounding risk factors such as smoking cessation, for example. These results imply that the true uncertainties in cohort studies may exceed those indicated by the confidence intervals from a single modeling approach.


Subject(s)
Air Pollutants/toxicity , Mortality/trends , Vehicle Emissions/toxicity , Air Pollution/adverse effects , Cohort Studies , Databases, Factual , Humans , Male , Models, Biological , Regression Analysis , Risk Factors , Veterans
3.
Inhal Toxicol ; 18(9): 645-57, 2006 Aug.
Article in English | MEDLINE | ID: mdl-16864555

ABSTRACT

Air quality data on trace metals, other constituents of PM2.5, and criteria air pollutants were used to examine relationships with long-term mortality in a cohort of male U.S. military veterans, along with data on vehicular traffic density (annual vehicle-miles traveled per unit of land area). The analysis used county-level environmental data for the period 1997-2002 and cohort mortality for 1997-2001. The proportional hazards model included individual data on age, race, smoking, body mass index, height, blood pressure, and selected interactions; contextual variables also controlled for climate, education, and income. In single-pollutant models, traffic density appears to be the most important predictor of survival, but potential contributions are also seen for NO2, NO3-, elemental carbon, nickel, and vanadium. The effects of the other main constituents of PM2.5, of crustal particles, and of peak levels of CO, O3, or SO2 appear to be less important. Traffic density is also consistently the most important environmental predictor in multiple-pollutant models, with combined relative risks up to about 1.2. However, from these findings it is not possible to discern which aspects of traffic (pollution, noise, stress) may be the most relevant to public health or whether an area-based predictor such as traffic density may have an inherent advantage over localized measures of ambient air quality. It is also possible that traffic density could be a marker for unmeasured pollutants or for geographic gradients per se. Pending resolution of these issues, including replication in other cohorts, it will be difficult to formulate additional cost-effective pollution control strategies that are likely to benefit public health.


Subject(s)
Air Pollutants/adverse effects , Environmental Illness/mortality , Mortality/trends , Vehicle Emissions/adverse effects , Veterans/statistics & numerical data , Air Pollutants/analysis , Cohort Studies , Humans , Longevity , Male , Middle Aged , Survival Rate , Trace Elements/analysis , United States/epidemiology , Vehicle Emissions/analysis
4.
Inhal Toxicol ; 16 Suppl 1: 131-41, 2004.
Article in English | MEDLINE | ID: mdl-15204801

ABSTRACT

Associations between daily mortality and air pollution were investigated in Fulton and DeKalb Counties, Georgia, for the 2-yr period beginning in August 1998, as part of the Aerosol Research and Inhalation Epidemiological Study (ARIES). Mortality data were obtained directly from county offices of vital records. Air quality data were obtained from a dedicated research site in central Atlanta; 15 separate air quality indicators (AQIs) were selected from the 70 particulate and gaseous air quality parameters archived in the ARIES ambient air quality database. Daily meteorological parameters, comprising 24-h average temperatures and dewpoints, were obtained from Atlanta's Hartsfield International Airport. Effects were estimated using Poisson regression with daily deaths as the response variable and time, meteorology, AQI, and days of the week as predictor variables. AQI variables entered the model in a linear fashion, while all other continuous predictor variables were smoothed via natural cubic splines using the generalized linear model (GLM) framework in S-PLUS. Knots were spaced either quarterly, monthly, or biweekly for temporal smoothing. A default model using monthly knots and AQIs averaged for lags 0 and 1 was postulated, with other models considered in sensitivity analyses. Lags up to 5 days were considered, and multipollutant models were evaluated, taking care to avoid overlapping (and thus collinear) AQIs. For this reason, PM(2.5) was partitioned into its three major constituents: SO(2-)(4), carbon (EC + 1.4 OC), and the remainder; sulfate was assumed to be (NH(4))(2)SO(4) for this purpose. Initial AQI screening was based on all-cause (ICD-9 codes <800) mortality for those aged 65 and over. For the (apparently) most important pollutants--PM(2.5) and its 3 major constituents, coarse PM mass [CM], 1-h maximum CO, 8-h maximum O(3)--we investigated 15 mortality categories in detail. (The 15 categories result from three age groups [all ages, <65, 65+] and five cause-of-death groups [all disease causes, cardiovascular, respiratory, cancer, and other "remainder" disease causes]). The GLM model outputs that were considered included mean AQI effects and their standard errors, and two indicators of relative model performance (deviance and deviance adjusted for the number of observations and model parameters). The latter indicator was considered to account for variations in the number of observations created by varying amounts of missing AQI data, which were not imputed. The single-AQI screening regressions on all-cause 65+ mortality show that CO, NO(2), PM(2.5), CM, SO(2), and O(3), followed by EC and OC, consistently have the best model fits, after adjusting for the number of observations. Their relative rankings, however, vary according to the smoothing knots used, and there is no correspondence between mean AQI effect and overall model fit.(Other regression runs often show that the best model fits are obtained with no AQI in the model.) There is no correspondence between mean AQI effect and statistical significance or between mean effect and serial correlation. There is a highly significant (.001 level) relationship between overall model fit and serial correlation; the best fitting models have the most frequent knot spacing and the most negative serial correlation. The regression analyses by cause of death find elderly circulatory deaths to be consistently associated with CO for all models.


Subject(s)
Air Pollution/statistics & numerical data , Cause of Death , Mortality/trends , Urban Health/statistics & numerical data , Adult , Age Factors , Aged , Environmental Monitoring , Epidemiological Monitoring , Georgia/epidemiology , Humans , Linear Models , Middle Aged , Particle Size , Regression Analysis , Time Factors
6.
Occup Environ Med ; 59(3): 156-74, 2002 Mar.
Article in English | MEDLINE | ID: mdl-11886947

ABSTRACT

OBJECTIVE: To investigate longitudinal and spatial relations between air pollution and age specific mortality for United States counties (except Alaska) from 1960 to the end of 1997. METHODS: Cross sectional regressions for five specific periods using published data on mortality, air quality, demography, climate, socioeconomic status, lifestyle, and diet. Outcome measures are statistical relations between air quality and county mortalities by age group for all causes of death, other than AIDS and trauma. RESULTS: A specific regression model was developed for each period and age group, using variables that were significant (p<0.05), not substantially collinear (variance inflation factor <2), and had the expected algebraic sign. Models were initially developed without the air pollution variables, which varied in spatial coverage. Residuals were then regressed in turn against current and previous air quality, and dose-response plots were constructed. The validity of this two stage procedure was shown by comparing a subset of results with those obtained with single stage models that included air quality (correlation=0.88). On the basis of attributable risks computed for overall mean concentrations, the strongest associations were found in the earlier periods, with attributable risks usually less than 5%. Stronger relations were found when mortality and air quality were measured in the same period and when the locations considered were limited to those of previous cohort studies (for PM(2.5) and SO(4)(2-)). Thresholds were suggested at 100-130 microg/m(3) for mean total suspended particulate (TSP), 7-10 microg/m(3) for mean sulfate, 10-15 ppm for peak (95th percentile) CO, 20-40 ppb for mean SO(2.) Contrary to expectations, associations were often stronger for the younger age groups (<65 y). Responses to PM, CO, and SO(2) declined over time; responses in elderly people to peak O(3) increased over time as did responses to NO(2) for the younger age groups. These results generally agreed with previous prospective cohort and ecological studies for comparable periods, age groups, and pollutants, but they also suggest that the results of those previous studies may no longer be applicable. CONCLUSIONS: Spatially derived relations between air quality and mortality vary significantly by age group and period and may be sensitive to the locations included in the analysis.


Subject(s)
Air Pollution/adverse effects , Environmental Exposure/adverse effects , Mortality/trends , Adolescent , Adult , Age Factors , Aged , Aged, 80 and over , Cause of Death , Cross-Sectional Studies , Humans , Longitudinal Studies , Middle Aged , Particle Size , Regression Analysis , Residence Characteristics , Risk Factors , United States/epidemiology
7.
J Air Waste Manag Assoc ; 50(8): 1350-66, 2000 Aug.
Article in English | MEDLINE | ID: mdl-11002598

ABSTRACT

This paper uses U.S. linked birth and death records to explore associations between infant mortality and environmental factors, based on spatial relationships. The analysis considers a range of infant mortality end points, regression models, and environmental and socioeconomic variables. The basic analysis involves logistic regression modeling of individuals; the cohort comprises all infants born in the United States in 1990 for whom the required data are available from the matched birth and death records. These individual data include sex, race, month of birth, and birth weight of the infant, and personal data on the mother, including age, adequacy of prenatal care, and smoking and education in most instances. Ecological variables from Census and other sources are matched on the county of usual residence and include ambient air quality, elevation above sea level, climate, number of physicians per capita, median income, racial and ethnic distribution, unemployment, and population density. The air quality variables considered were 1990 annual averages of PM10, CO, SO2, SO4(2-), and "non-sulfate PM10" (NSPM10--obtained by subtracting the estimated SO4(2-) mass from PM10). Because all variables were not available for all counties (especially maternal smoking), it was necessary to consider various subsets of the total cohort. We examined all infant deaths and deaths by age (neonatal and postneonatal), by birth weight (normal and low [< 2500 g]), and by specific causes within these categories. Special attention was given to sudden infant death syndrome (SIDS). For comparable modeling assumptions, the results for PM10 agreed with previously published estimates; however, the associations with PM10 were not specific to probable exposures or causes of death and were not robust to changes in the model and/or the locations considered. Significant negative mortality associations were found for SO4(2-). There was no indication of a role for outdoor PM2.5, but possible contributions from indoor air pollution sources cannot be ruled out, given higher SIDS rates in winter, in the north and west, and outside of large cities.


Subject(s)
Air Pollution/adverse effects , Infant Mortality , Sudden Infant Death/etiology , Epidemiologic Studies , Female , Geography , Humans , Infant , Infant, Newborn , Male , Particle Size , Regression Analysis , Reproducibility of Results , Research Design , Sudden Infant Death/epidemiology , Sulfuric Acids/adverse effects , United States/epidemiology
8.
J Air Waste Manag Assoc ; 50(8): 1501-13, 2000 Aug.
Article in English | MEDLINE | ID: mdl-11002610

ABSTRACT

Time-series of daily mortality data from May 1992 to September 1995 for various portions of the seven-county Philadelphia, PA, metropolitan area were analyzed in relation to weather and a variety of ambient air quality parameters. The air quality data included measurements of size-classified PM, SO4(2-), and H+ that had been collected by the Harvard School of Public Health, as well as routine air pollution monitoring data. Because the various pollutants of interest were measured at different locations within the metropolitan area, it was necessary to test for spatial sensitivity by comparing results for different combinations of locations. Estimates are presented for single pollutants and for multiple-pollutant models, including gaseous pollutants and mutually exclusive components of PM (PM2.5 and coarse particles, SO4(2-) and non-SO4(2-) portions of total suspended particulate [TSP] and PM10), measured on the day of death and the previous day. We concluded that associations between air quality and mortality were not limited to data collected in the same part of the metropolitan area; that is, mortality for one part may be associated with air quality data from another, not necessarily neighboring, part. Significant associations were found for a wide variety of gaseous and particulate pollutants, especially for peak O3. Using joint regressions on peak O3 with various other pollutants, we found that the combined responses were insensitive to the specific other pollutant selected. We saw no systematic differences according to particle size or chemistry. In general, the associations between daily mortality and air pollution depended on the pollutant or the PM metric, the type of collection filter used, and the location of sampling. Although peak O3 seemed to exhibit the most consistent mortality responses, this finding should be confirmed by analyzing separate seasons and other time periods.


Subject(s)
Air Pollution/adverse effects , Mortality/trends , Adolescent , Adult , Aged , Child , Child, Preschool , Climate , Environmental Exposure , Epidemiologic Studies , Female , Humans , Infant , Infant, Newborn , Male , Middle Aged , Models, Theoretical , Oxidants, Photochemical/adverse effects , Ozone/adverse effects , Particle Size , Pennsylvania/epidemiology , Public Health , Urban Population
9.
Inhal Toxicol ; 12 Suppl 2: 1-2, 2000 Jan.
Article in English | MEDLINE | ID: mdl-26368516
10.
Inhal Toxicol ; 12 Suppl 4: 41-73, 2000.
Article in English | MEDLINE | ID: mdl-12881886

ABSTRACT

This article presents the design of and some results from a new prospective mortality study of a national cohort of about 50,000 U.S. veterans who were diagnosed as hypertensive in the mid 1970s, based on approximately 21 yr of follow-up. This national cohort is male with an average age at recruitment of 51 +/- 12 yr; 35% were black and 81% had been smokers at one time. Because the subjects have been receiving care at various U.S. Veterans Administration (VA) hospitals, access to and quality of medical care are relatively homogeneous. The health endpoints available for analysis include all-cause mortality and specific diagnoses for morbidity during VA hospitalizations; only the mortality results are discussed here. Nonpollution predictor variables in the baseline model include race, smoking (ever or at recruitment), age, systolic and diastolic blood pressure (BP), and body mass index (BMI). Interactions of BP and BMI with age were also considered. Although this study essentially controls for socioeconomic status by design because of the homogeneity of the cohort, selected ecological variables were also considered at the ZIP code and county levels, some of which were found to be significant predictors. Pollutants were averaged by year and county for TSP, PM10, CO, O3, and NO2; SO2 and Pb were considered less thoroughly. Both mean and peak levels were considered for gases. SO(4)2- data from the AIRS database and PM2.5, coarse particles, PM15, and SO(4)2- from the U.S. EPA Inhalable Particulate (IP) Network were also considered. Four relevant exposure periods were defined: 1974 and earlier (back to 1953 for TSP), 1975-1981, 1982-1988, and 1989-1996. Deaths during each of the three most recent exposure periods were considered separately, yielding up to 12 combinations of exposure and mortality periods for each pollutant. Associations between concurrent air quality and mortality periods were considered to relate to acute responses; delayed associations with prior exposures were considered to be emblematic of initiation of chronic disease. Preexposure mortality associations were considered to be indirect (noncausal). The implied mortality risks of long-term exposure to air pollution were found to be sensitive to the details of the regression model, the time period of exposure, the locations included, and the inclusion of ecological as well as personal variables. Both positive and negative statistically significant mortality responses were found. Fine particles as measured in the 1979-1984 U.S. EPA Inhalable Particulate Network indicated no significant (positive) excess mortality risk for this cohort in any of the models considered. Among the positive responses, indications of concurrent mortality risks were seen for NO2 and peak O3, with a similar indication of delayed risks only for NO2. The mean levels of these excess risks were in the range of 5-9%. Peak O3 was dominant in two-pollutant models and there was some indication of a threshold in response. However, it is likely that standard errors of the regression coefficients may have been underestimated because of spatial autocorrelation among the model residuals. The significant variability of responses by period of death cohort suggests that aggregation over the entire period of follow-up obscures important aspects of the implied pollution-mortality relationships, such as early depletion of the available pool of those subjects who may be most susceptible to air pollution effects.


Subject(s)
Air Pollutants/adverse effects , Mortality/trends , Veterans/statistics & numerical data , Aged , Air Pollution/adverse effects , Cohort Studies , Humans , Male , Regression Analysis , Risk Factors
11.
J Air Waste Manag Assoc ; 49(9): 182-91, 1999 09.
Article in English | MEDLINE | ID: mdl-11002835

ABSTRACT

Because of the U.S. Environmental Protection Agency's (EPA) new ambient air quality standard for fine particles, the need is likely to continue for more detailed scientific investigation of various types of particles and their effects on human health. Epidemiology studies have become the method of choice for investigating health responses to such particles and to other air pollutants in community settings. Health effects have been associated with virtually all of the gaseous criteria pollutants and with the major constituents of airborne particulate matter (PM), including all size fractions less than about 20 microns, inorganic ions, carbonaceous particles, metals, crustal material, and biological aerosols. In many of the more recent studies, multiple pollutants or agents (including weather variables) have been significantly associated with health responses, and various methods have been used to suggest which ones might be the most important. In an ideal situation, classical least-squares regression methods are capable of performing this task. However, in the real world, where most of the pollutants are correlated with one another and have varying degrees of measurement precision and accuracy, such regression results can be misleading. This paper presents some guidelines for dealing with such collinearity and model comparison problems in both single- and multiple-pollutant regressions. These techniques rely on mean effect (attributable risk) rather than statistical significance per se as the preferred indicator of importance for the pollution variables.


Subject(s)
Air Pollution/adverse effects , Air Pollution/statistics & numerical data , Health , Humans , United States/epidemiology , United States Environmental Protection Agency
12.
Science ; 278(5335): 19-20, 1997 Oct 03.
Article in English | MEDLINE | ID: mdl-9340746
13.
Risk Anal ; 17(3): 273-8, 1997 Jun.
Article in English | MEDLINE | ID: mdl-9232012

ABSTRACT

Studies using regression techniques report their results using a variety of statistics. Evaluation of the consistency of findings, such as in a metaanalysis, requires calculating the statistical estimates of the effect reported in each study in a comparable manner. In this paper, we consider multiple linear regression, multiple Poisson regression, and logistic regression estimates. We present results that are needed to calculate, on a common basis, the slope of the regression function at a specified value, the elasticity function of the regression function at a specified value, the relative risk at a specified value, and the odds ratio at a specified value. We apply these results to studies of the association of daily mortality in an area to the daily air pollution level of ozone and PM10. We calculate the estimated slope of the number of deaths per billion population associated with an increase of 1 ppb of ozone level in studies of daily mortality in three urban areas. These studies, in Los Angeles, New York, and St. Louis, produced very comparable results on a common basis, especially when compared to the coefficients as reported. We also calculated the estimated elasticity function of the daily mortality and daily PM10 level for eight areas and found that the elasticities varied within a factor of roughly two, much less than the variability in the coefficients as reported.


Subject(s)
Air Pollution/adverse effects , Mortality , Regression Analysis , Air Pollutants/adverse effects , Biometry , Humans , Linear Models , Logistic Models , Ozone/adverse effects , Poisson Distribution , Risk Factors , United States/epidemiology
14.
Risk Anal ; 17(2): 137-46, 1997 Apr.
Article in English | MEDLINE | ID: mdl-9202486

ABSTRACT

This paper considers the health effects of air pollution from three perspectives: historical, statistical, and public policy, and also as depicted by the recent epidemiology, primarily mortality studies. The historical perspectives establish the reality of population-based health effects, and they provide data with which to evaluate more recent evidence. Statistical perspectives imply that, while there is strong evidence that associations between air quality and health persist, many details of these relationships remain obscure, especially as to the existence of concentration thresholds that might define safe exposure levels. Additional major questions include the effects of uncertainties in actual pollution exposures, the degree of prematurity of "excess" deaths, and whether the development of new cases of chronic disease is associated with air pollution. Public policy issues center around interpreting the new epidemiological studies in the light of these uncertainties and the analysis and management of the concomitant health risks.


Subject(s)
Air Pollution/adverse effects , Health , Air Pollutants/adverse effects , Air Pollutants/analysis , Air Pollution/analysis , Air Pollution/history , Air Pollution/statistics & numerical data , Chronic Disease , Environmental Exposure , Epidemiology , Health Priorities , History, 20th Century , Humans , Maximum Allowable Concentration , Mortality , Public Policy , Risk Assessment , Risk Factors
15.
J Air Waste Manag Assoc ; 47(4): 517-23, 1997 Apr.
Article in English | MEDLINE | ID: mdl-9130440

ABSTRACT

In a previous paper, we showed that the mean effects on daily mortality associated with air pollution are essentially the same for gases and particulate matter (PM) and are invariant with respect to particle size and composition, based on 27 statistical studies that had been published at that time. Since then, a new analysis reported stronger mortality associations for the fine fractions of PM obtained from dichotomous samplers, relative to the coarse fractions. In this paper, we show that differential measurement errors known to be present in dichotomous sampler data preclude reliable determination of such statistical relationships by particle size. Further, it is necessary to consider gaseous pollutants simultaneously with particles to provide robust estimates of the responsibilities for the implied daily mortality gradients. Finally, certain regression model specifications may be sensitive to differences in frequency distribution characteristics according to particle size.


Subject(s)
Air Pollution/adverse effects , Environmental Exposure , Humans , Models, Statistical , Mortality , Particle Size , Regression Analysis
16.
Neurotoxicology ; 17(1): 197-211, 1996.
Article in English | MEDLINE | ID: mdl-8784831

ABSTRACT

This paper describes a probabilistic assessment of neurological risks incurred from consuming fish containing methylmercury (MeHg), focusing on the incremental effects of Hg deposited from local coal combustion. A Monte Carlo model is used to simulate a "worst case" scenario in which a population of 5000 fish eaters in the upper midwestern United States derive the freshwater fish portion of their diet from local waters near a hypothetical large coal-fired power plant. This population is characterized by distributions of body mass, half-life of MeHg, and the ratios of blood to body burden and hair to blood MeHg. Each person's diet consists of varying amounts of tuna fish, freshwater sportfish, and marine fish and shellfish, the MeHg contents of which are characterized by national distribution statistics, as are the consumption rates for marine fish. The consumption rates for freshwater fish are specific to the region. The fish portion size is linked to body mass by a variable correlation. Each meal is assumed to be an independent sample; thus, as metabolic equilibrium is approached, each person's body burden of MeHg tends to approach the value corresponding to the mean MeHg intake for the population. Predictions of MeHg levels in hair by this model compared well with an observed distribution of 1437 women. Two neurological endpoints were examined: adult paresthesia, as related to MeHg body burden, and congenital neurological effects, as associated with average concentrations of MeHg in maternal hair during pregnancy. Two exposure scenarios are considered: a "baseline" in which the source of the mercury in fish is from background atmospheric deposition, and an "impact" scenario, in which local Hg deposition and concentrations in fish are roughly doubled to represent additional deposition from the hypothetical nearby power plant. For both scenarios, the 99th percentile of MeHg body burden was more than an order of magnitude below the lowest level at which increased transient adult paresthesia was experienced in an acute MeHg poisoning incident in Iraq. We thus conclude that neurological risks to adults from MeHg resulting from atmospheric Hg deposition are trivial. Based on three epidemiological studies of congenital neurological risks, we find that fetal effects appear to be more critical and that there is a smaller margin of safety for pregnant consumers of freshwater sportfish. However, the margin of safety is still considerable and may have been diminished by uncertainties in the relationships between maternal hair Hg and the actual fetal exposures.


Subject(s)
Coal , Environmental Pollutants/adverse effects , Methylmercury Compounds/adverse effects , Power Plants , Prenatal Exposure Delayed Effects , Adult , Animals , Central Nervous System Diseases/chemically induced , Female , Fishes , Food Contamination , Humans , Midwestern United States , Monte Carlo Method , No-Observed-Adverse-Effect Level , Paresthesia/chemically induced , Pregnancy , Risk Assessment
17.
J Air Waste Manag Assoc ; 45(12): 949-66, 1995 Dec.
Article in English | MEDLINE | ID: mdl-8542379

ABSTRACT

Results from 31 epidemiology studies linking air pollution with premature mortality are compared and synthesized. Consistent positive associations between mortality and various measures of air pollution have been shown within each of two fundamentally different types of regression studies and in many variations within these basic types; this is extremely unlikely to have occurred by chance. In this paper, the measure of risk used is the elasticity, which is a dimensionless regression coefficient defined as the percentage change in the dependent variable associated with a 1% change in an independent variable, evaluated at the means. This metric has the advantage of independence from measurement units and averaging times, and is thus suitable for comparisons within and between studies involving different pollutants. Two basic types of studies are considered: time-series studies involving daily perturbations, and cross-sectional studies involving longer-term spatial gradients. The latter include prospective studies of differences in individual survival rates in different locations and studies of the differences in annual mortality rates for various communities. For a given data set, time-series regression results will vary according to the seasonal adjustment method used, the covariates included, and the lag structure assumed. The results from both types of cross-sectional regressions are highly dependent on the methods used to control for socioeconomic and personal lifestyle factors and on data quality. A major issue for all of these studies is that of partitioning the response among collinear pollution and weather variables. Previous studies showed that the variable with the least exposure measurement error may be favored in multiple regressions; assigning precise numerical results to a single pollutant is not possible under these circumstances. We found that the mean overall elasticity as obtained from time-series studies for mortality with respect to various air pollutants entered jointly was about 0.048, with a range from 0.01 to 0.12. This implies that about 5% of daily mortality is associated with air pollution, on average. The corresponding values from population-based cross-sectional studies were similar in magnitude, but the results from the three recent prospective studies varied from zero to about five times as much. Long-term responses in excess of short-term responses might be interpreted as showing the existence of chronic effects, but the uncertainties inherent in both types of studies make such an interpretation problematic.


Subject(s)
Air Pollution/adverse effects , Epidemiologic Methods , Mortality , Humans , United States/epidemiology
18.
Environ Health Perspect ; 101 Suppl 2: 229-68, 1993 Jul.
Article in English | MEDLINE | ID: mdl-8243395

ABSTRACT

Studies of the associations between air pollution and hospital admissions and emergency room use are reviewed, including studies of air pollution episodes, time-series analyses, and cross-sectional analyses. These studies encompass a variety of methods of analysis and levels of air quality. Findings from all three types of studies were generally consistent in that almost all of the studies reviewed found statistically significant associations between hospital use and air pollution; this unanimity may have resulted in part from publication bias. These associations were characterized by elasticities of the order of 0.20; i.e., a 100% change in air pollution was associated with a change in hospital use of about 20%, for specific diagnoses. Respiratory diagnoses were emphasized by most studies; cardiac diagnoses were included in five of them. The air pollutants most often associated with changes in hospital use were particulate matter, sulfur oxides, and oxidants. Apart from the major air pollution episodes, there was no obvious link between air pollution level and the significance or magnitudes of the associations. Long-term indicators of hospitalization appeared to also be influenced by medical care supply factors, including the numbers of beds and physicians per capita. These nonpathological causal factors could also have influenced the findings of the time-series studies by introducing extraneous factors in the patterns of admissions. Although consistent associations have been shown between hospital use and air pollution, further research is required to distinguish among potentially responsible pollutants and to deduce specific dose-response relationships of general utility.


Subject(s)
Air Pollution/statistics & numerical data , Environmental Monitoring/methods , Health Services Needs and Demand/statistics & numerical data , Hospitalization/statistics & numerical data , Lung Diseases/epidemiology , Air Pollution/adverse effects , Canada/epidemiology , Cross-Sectional Studies , Disasters/statistics & numerical data , Epidemiological Monitoring , Europe/epidemiology , Humans , Lung Diseases/etiology , Retrospective Studies , Time Factors , United States/epidemiology
19.
Environ Res ; 59(2): 374-99, 1992 Dec.
Article in English | MEDLINE | ID: mdl-1464290

ABSTRACT

A 6-year data set of daily counts of admissions to 79 acute care hospitals in Southern Ontario was analyzed in relation to concurrent measurements of air pollution and weather pooled over the same regions, using progressively more sophisticated statistical techniques. The diagnoses studied included a group of respiratory causes and two control diagnoses: accidents and gastrointestinal causes. The 6-year period (1979-1985) was subdivided into six 2-month "seasons" and the area of study was divided into three subregions. Bivariate correlations were found to be significant more often than expected due to chance for all three admissions variables, but accounting for the temporal variation within the 60-day seasons greatly reduced the significance of the control diagnoses. Twenty-four-hour averages for air quality were found to yield more significant associations than peak hourly concentrations. July-August was the only period not having important within-season temporal trends and also had the lowest daily counts for respiratory admissions. Based on a model which accounted for serial correlation, SO2, ozone, and sulfate aerosol were found to be significant predictors of respiratory admissions during July-August. Using cumulative lags increased the magnitude of the estimated response to about 20% of summer respiratory admissions, but no consistent relationships were found which could identify the "responsible" pollutant(s) with certainty. Average pollutant concentrations were generally within U.S. ambient standards.


Subject(s)
Air Pollution , Environmental Exposure , Hospitalization , Respiratory Tract Diseases/epidemiology , Accidents/statistics & numerical data , Adolescent , Adult , Analysis of Variance , Child , Child, Preschool , Gastrointestinal Diseases/epidemiology , Humans , Infant , Infant, Newborn , Middle Aged , Ontario/epidemiology , Regression Analysis , Seasons , Time Factors , Weather
20.
Science ; 256(5058): 722, 1992 May 08.
Article in English | MEDLINE | ID: mdl-1589747
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