Epidemiological studies of acute ozone exposures and mortality.

Many, but not all, observational epidemiological studies of ozone (O(3)) air pollution have yielded significant associations between variations in daily ambient concentrations of this pollutant and a wide range of adverse health outcomes. We evaluate some past epidemiological studies that have assessed the short-term association of O(3) with mortality, and investigate one possible reason for variations in their O(3) effect estimate, i.e., differences in their approaches to the modeling of weather influences on mortality. For all of the total mortality-air pollution time-series studies considered, the combined analysis yielded a relative risk, RR=1.036 per 100-ppb increase in daily 1-h maximum O(3) (95% CI: 1.023-1.050). However, the subset of studies that specified the nonlinear nature of the temperature-mortality association yielded a combined estimate of RR=1.056 per 100 ppb (95% CI: 1.032-1.081). This indicates that past time-series studies using linear temperature-mortality specifications have underpredicted the premature mortality effects of O(3) air pollution. For Detroit, MI, an illustrative analysis of daily total mortality during 1985-1990 also indicated that the model weather specification choice can influence the O(3) health effects estimate. Results were intercompared for alternative weather specifications. Nonlinear specifications of temperature and relative humidity (RH) yielded lower intercorrelations with the O(3) coefficient, and larger O(3) RR estimates, than a base model employing a simple linear spline of hot and cold temperature. We conclude that, unlike for particulate matter (PM) mass, the mortality effect estimates derived by time-series analyses for O(3) can be sensitive to the way that weather is addressed in the model. The same may well also be true for other pollutants with largely temperature-dependent formation mechanisms, such as secondary aerosols. Generally, we find that the O(3)-mortality effect estimate increases in size and statistical significance when the nonlinearity and the humidity interaction of the temperature-health effect association are incorporated into the model weather specification. We recommend that a minimization of the intercorrelations of model coefficients be considered (along with other critical factors such as goodness of fit, autocorrelation, and overdispersion) when specifying such a model, especially when individual coefficients are to be interpreted for risk estimation.

The burden of air pollution: impacts among racial minorities.

Various epidemiologic investigations have shown that ambient air pollution levels are associated with acute increases in hospital admissions and mortality in the United States and abroad. The objectives of this investigation were a) to determine if racial minorities are more adversely affected by ambient air pollution than their white counterparts and b) to assess the contribution of socioeconomic status to any observed racial differences in pollution effect. Time-series regression methods were conducted to investigate these hypotheses for daily respiratory hospital admissions in New York City, New York. Pollutants considered included mean daily levels of particulate matter with a mass median aerodynamic diameter less than 10 microm (PM(10), ozone (O3), strong aerosol acidity (H+), and sulfates (SO4(2). The relative risk for respiratory hospital admission was calculated for each pollutant for a maximum minus mean increment in mean daily pollutant concentration. The greatest difference between the white and nonwhite subgroups was observed for O(3), where the white relative risk (RR) was 1.032 [95% confidence interval (CI): 0.977-1.089] and the nonwhite RR was 1.122 (95%CI: 1.074-1.172). Although not statistically different from each other, the various pollutants' RR estimates for the Hispanic nonwhite category in New York City were generally larger in magnitude than those for the non-Hispanic white group. When these analyses incorporated differences in the underlying respiratory hospitalization rates across races (that for nonwhites, was roughly twice that for whites), the disparities in attributable risks from pollution (in terms of excess admissions per day per million persons) were even larger for nonwhites versus whites. However, when insurance status was used as an indicator of socioeconomic/health coverage status, higher RRs were indicated for the poor/working poor (i.e., those on Medicaid and the uninsured) than for those who were economically better off (i.e., the privately insured), even among non-Hispanic whites. Thus, although potential racial differences in pollution exposures could not be explored as a factor, within-race analyses suggested that most of the apparent differences in air pollutant effects found across races were explained by socioeconomic and/or health care disparities.

Monitor-to-monitor temporal correlation of air pollution and weather variables in the North-Central U.S.

Numerous time series studies have reported associations between daily ambient concentrations of air pollution and morbidity or mortality. Recent personal exposure studies have also reported relatively high longitudinal correlation between personal exposures to particulate matter (PM) and home outdoor PM concentrations, lending support to the health effects reported in time series studies. However, the question remains as to how well the temporal fluctuations in the air pollution levels observed at an outdoor monitor represent the temporal fluctuations in the population exposures to pollution of outdoor origins in a city, and how such representativeness affects the size and significance of risk estimates. Also, such spatio-temporal correlations would vary from pollutant to pollutant, likely influencing their relative significance of statistical associations with health outcomes. In this study, we characterized the extent of monitor-to-monitor correlation over time among multiple monitoring sites for PM less than 10 microm (PM10), gaseous criteria pollutants, and several weather variables in seven central and eastern contiguous states (IL, IN, MI, OH, PA, WI, and WV) during the study period of 1988-1990. After removing seasonal trends, the monitor-to-monitor temporal correlation among the air pollution/weather variables within 100-mile separation distance in these areas could be generally ranked into three groups: (1 ) temperature, dew point, relative humidity (r>0.9); (2) O3, PM10, NO2 (r: 0.8-0.6); and (3) CO, SO2 (r<0.5). Using the subsets for separation distance less than 100 miles, regression analyses of these monitor-to-monitor correlation coefficients were also conducted with explanatory variables including separation distance, qualitative (land use, location setting, and monitoring objectives) and quantitative (large and small variance) site characteristics, and region indicators for Air Quality Control Region (AQCR). The separation distance was a significant predictor of monitorto-monitor correlation decline especially for PM10 and NO2 (approximately 0.2 drop over 30 miles). Site characteristic variables were, in some cases, significant predictors of monitor-to-monitor correlation, but the magnitude of their impacts was not substantial. Regional differences, as examined by AQCR, were in some cases (e.g., in Metropolitan Philadelphia) substantial. In these areas, the pollutants that had generally poor monitor-to-monitor correlation in the overall seven states data (i.e., for SO2 and CO) showed higher monitor-to-monitor correlations, comparable with PM10 and O3, within the AQCR. These results are useful in interpreting some of the past time series epidemiological results. The differences in monitor-to-monitor correlations found across pollutants in this work (i.e., r approximately 0.8 vs. r approximately 0.4) are sufficiently large that they could be a factor in the different pollutant significance levels reported in the epidemiologic literature. It is recommended that future epidemiological studies collect and incorporate information on spatial variability among air pollutants in the analysis and interpretation of their results.

A time-series analysis of acidic particulate matter and daily mortality and morbidity in the Buffalo, New York, region.

A component of particulate matter (PM) air pollution that may provide one biologically plausible pathway for the observed PM air pollution-health effect associations is aerosol acidity (H(+)). An increasing number of observational studies have demonstrated associations between H(+) and increased adverse health effects in the United States and abroad. Although studies have shown significant H(+) associations with increased morbidity in the United States, similar associations have yet to be shown with daily mortality. We considered a 2.5-year record of daily H(+) and sulfate measurements (May 1988-October 1990) collected in the Buffalo, New York, region in a time-series analysis of respiratory, circulatory, and total daily mortality and hospital admissions. Other copollutants considered included particulate matter [less than/equal to] 10 microm in aerodynamic diameter, coefficient of haze, ozone, carbon monoxide, sulfur dioxide, and nitrogen dioxide. Various modeling techniques were applied to control for confounding of effect estimates due to seasonality, weather, and day-of-week effects. We found multiple significant pollutant-health effect associations--most strongly between SO(4)(2-) and respiratory hospital admissions (as indicated by its t-statistic). Additionally, H(+) and SO(4)(2-) demonstrated the most coherent associations with both respiratory hospital admissions [H(+): relative risk (RR) = 1. 31; 95% confidence interval (CI), 1.14-1.51; and SO(4)(2-): RR = 1. 18, CI, 1.09-1.28] and respiratory mortality (H(+): RR = 1.55, CI, 1. 09-2.20; and SO(4)(2-): RR = 1.24, CI, 1.01-1.52). Thus, acidic sulfate aerosols represent a component of PM air pollution that may contribute to the previously noted adverse effects of PM mass on human health, and the associations demonstrated in this study support the need for further investigations into the potential health effects of acidic aerosols.

Summertime haze air pollution and children with asthma.

In order to investigate associations between summertime haze air pollution and asthma at an individual level, 52, 58, and 56 children (ages 7 to 13) attending a summer "asthma camp" were followed during the last week of June in 1991, 1992, and 1993, respectively. Most of the subjects had moderate to severe asthma. Daily records were kept of the environmental conditions, as well as of subject medication use, lung function, and medical symptoms. Air pollution was found to be significantly and consistently correlated with acute asthma exacerbations, chest symptoms, and lung function decrements. The pollutant most consistently associated with adverse health consequences was ozone (O3), although associations with sulfates and hydrogen ion suggest a possible role by fine particles as well. Effects were found to be roughly monotonic as a function of O3 concentration. Regression of morning (8:00 A.M.) to afternoon (5:00 P.M.) peak flow change on O3 indicated pulmonary function reductions similar to those previously reported for more active children without asthma. Moreover, analyses also indicated an increased risk of an asthma exacerbation and of experiencing chest symptoms of approximately 40% on the highest pollution day, relative to the mean. Based on these relative risk estimates, a rise in the 1-h daily maximal O3 from 84 ppb to 160 ppb was associated in this group with an increase from 20 to 28 (+/- 2) in the expected number of unscheduled medications administered/day, and from 29 to 41 (+/- 3) in the expected total number of chest symptoms/day. Thus, air pollution can be a major contributor to the respiratory problems experienced by children with asthma during the summer months.

Sulfate concentrations as an indicator of ambient particulate matter air pollution for health risk evaluations.

Retrospective population studies that have compared regression coefficients for mortality and morbidity for sulfate (SO4(2-), fine particles (PM2.5; aerodynamic diameter < 2.5 microns), thoracic particles (PM10; aerodynamic diameter < 10 microns), and total suspended particulates (TSP; undefined and variable upper cut-size) generally have found SO4(2-) concentrations to be correlated with effects as well as or better than PM2.5. In addition, both SO4(2-) and PM2.5 have yielded somewhat stronger associations with adverse health effects than PM10, and much stronger associations than TSP. Sulfate has advantages over PM2.5 for retrospective epidemiology, at least in the United States, because considerably more data on sulfate have been collected in recent decades, and there is a broader epidemiological database in the literature for comparison to other studies. While SO4(2-), per se, is an unlikely causal factor for mortality or morbidity, it often is correlated closely with variations in the strong acid component of ambient particulate matter (H+) and PM2.5 concentrations (especially in summer), which are more likely causal factors. A detailed analysis of the SO4(2-) epidemiological database is presented in this paper. In addition, drawing on our substantial archives of SO4(2-) and H+ data, we show that SO4(2-) and H+ correlate, both spatially and over time, in the eastern United States. We demonstrate the utility of SO4(2-) as a useful surrogate for ambient PM2.5 and H+ in epidemiological studies and as an index of PM exposure in ambient air quality guidelines and standards.

The effects of ambient ozone on lung function in children: a reanalysis of six summer camp studies.

Studies of children attending summer camps often have observed relationships between daily outdoor ozone (O3) concentrations and decreased lung function that are qualitatively similar to results seen in human chamber studies. The former studies, focusing on the pulmonary effects of O3 and associated pollutants on children under natural conditions of exposure, are potentially of great importance to understanding the public health impact of ambient O3. However, a thorough assessment of the results of these studies has been hampered by differences in the analysis and reporting of data across the various studies. We obtained data sets from six summer camp studies carried out by three separate investigative groups, including two New Jersey studies performed by New York University, two studies in Ontario carried out by Health and Welfare Canada, and two studies in southern California. The data consisted of sequential, daily measurements of forced expiratory volume in 1 sec (FEV1), peak expiratory flow rate (PEFR), and 1-hr O3 concentration in the hour preceding lung function measurements for each child. We analyzed the relationships between lung function and O3 using linear regression models that fit subject-specific intercepts and a single, pooled O3 slope. These models were fit for each of the six studies separately and for all studies combined. All of the study-specific slopes of FEV1 on O3 were negative (i.e., increased O3 associated with decreased FEV1); five of six were statistically significant. Analysis of the combined six-study data set yielded a slope of -0.50 ml FEV1/ppb O3 (p<0.0001). Addition of time-trend variables to the combined-data analysis diminished, but did not eliminate, the FEV1-O3 relationship. Study-specific slopes for PEFR on O3 were more variable. Combined over studies, no significant relationship was observed between PEFR and O3. However, this negative finding appeared to be partially confounded by time trends in PEFR. The results of this reanalysis provide strong evidence that children exposed to O3 under natural conditions experience decreases in FEV1 of the kind demonstrated in laboratory studies, and raise concern that other acute respiratory effects observed in those studies (e.g., pulmonary inflammation) may also occur in young people exposed to ambient O3.

A critical review of PM10-mortality time-series studies.

While the mortality effects of particulate matter (PM) have been obvious during extreme historical pollution episodes (e.g., the London Fog of 1952), evaluating effects at more routine pollution levels has required the use of complex statistical modeling approaches. This paper critically reviews available time-series studies on PM10 mortality to provide a common basis for an evaluation of the PM10-mortality association. These PM10 studies confirm that an acute pollution-mortality association can occur at routine ambient levels, and suggest that such effects extend below the present United States air quality standards, especially for susceptible subpopulations. Furthermore, these new PM10 studies are consistent with the hypothesis noted in past studies that PM is a causal agent in the mortality impacts of air pollution. The relative risks (RRs) for PM10 mortality, however, were found to vary across studies. Variation probably was caused by differences in PM10 composition and in the PM10 averaging period employed in the analysis, as well as differences in whether other pollutants were considered simultaneously in the mortality-PM10 model. Overall, the RR estimates derived from available PM10-total mortality studies suggest a 24-h average, 100 micrograms/m3 PM10 acute exposure effect on the order of RR approximately 1.05-1.10 in the general population. Higher PM10 RRs were indicated for the elderly and for those with preexisting respiratory conditions, both of which represent subpopulations who appear to be especially at risk for the mortality implications of acute exposures to air pollution. A key research question remaining involves a determination of the component or components of PM10 (e.g., fine particles, sulfates, acid aerosols, or ultrafine particles) that are most important to the noted acute PM-mortality associations.

Intercommunity differences in acid aerosol (H+)/sulfate (SO4(2-) ratios.

Exposures to acid aerosols have been associated with acute and chronic health effects. Beginning in 1988, extensive monitoring of acid aerosols (H+), sulfates (SO4(2-)), and ammonia (NH3) was conducted in 24 communities in the United States and Canada in order to characterize the seasonal and daily variations of these pollutants. More recently, in 1992 and 1993, summer monitoring of the same pollutants was conducted by Harvard researchers at multiple locations in Philadelphia, Pennsylvania to examine the factors causing spatial variation in the acidity levels in the greater metropolitan Philadelphia area. Earlier, a similar study also was conducted by Harvard in a more rural community, State College, Ohio, providing data on acidity, sulfate, and ammonia levels. In addition to these studies, New York University researchers have gathered substantial data on aerosol acidity, sulfates, and NH3 levels from sites in the New York City metropolitan region, Albany, Buffalo, and the Toronto metropolitan region between 1988 and 1992. This paper examines the relationships among H+, SO4(2-), ozone, and population density using summer measurements from sites in 24 cities across the United States and Canada, as well as Philadelphia, State College, the New York City region, Buffalo, and Albany. While past studies have consistently shown that H+ and SO4(2-) are correlated over time at sites in eastern North America, the results of our analysis show that spatial variations in the ratios of mean acid-to-sulfate levels also can be predicted satisfactorily with the use of either a linear or a quadratic model, once variations in population density are addressed (R2 = 0.6). These models may be useful in retrospective epidemiological investigations of acid aerosol exposures and health effects, using widely available sulfate measurements and data on local population size.

Daily PM10/mortality associations: an investigations of at-risk subpopulations.

Recent time-series epidemiological studies have reported significant associations between daily air pollution and mortality. These studies typically report a short-term excess increase in deaths as the fractional increase of total (nonaccidental) deaths per unit of air pollutant. The relative risk (RR) calculated for the total population in these studies, however, may underestimate the risk for the most sensitive subpopulation(s) at risk. In this study, race, gender, and cause-specific counts of daily mortality in Cook County, Illinois (which encompasses the city of Chicago) during 1985-1990 were analyzed to determine if there was any heterogeneity in air pollution/weather/mortality associations across these various population subcategories. Seasonal cross-correlations between mortality and environmental variables first were examined to identify appropriate lag structures. Of the pollution variables considered-particulate matter less than 10 microns (PM10), ozone, carbon monoxide, sulfur dioxide, and visual range-derived extinction coefficient-both PM10 and ozone showed significant associations with same-day and next-day mortality. The Poisson regression models employed included seasonal cycles (sine/cosine series), square and linear terms of lagged temperature, trend line, day-of-week dummy variables, and the average of the same day's and previous day's PM10 or ozone. The RR for total nonaccidental mortality per 100 micrograms/m3 increase in PM10 was 1.05 (95% CI: 1.03-1.08). The respiratory (RR = 1.14; 95% CI: 1.04-1.25) and cancer (RR = 1.12; 95% CI: 1.06-1.18) categories showed higher estimates than the circulatory category (RR = 1.03; 95% CI: 0.98-1.07), while the residual of the total from these three categories showed no association with PM10 (RR = 1.01; 95% CI: 0.95-1.08). Among the race- and gender-specific categories, black (African-American) females showed the higher RRs for the total (RR = 1.11; 95% CI: 1.03-1.21), respiratory (RR = 1.31; 95% CI: 0.98-1.75), and cancer (RR = 1.25; 95% CI: 1.07-1.46) mortality categories. Neither ozone nor hot temperature showed such cause-specificity in mortality associations. Cold temperature lagged by two days was a significant predictor of circulatory and respiratory mortality. This study suggests the importance of race- and gender-specific analysis. The greater mortality risk to Chicago's black women from exposure to urban air pollution indicated by this finding should be tested in other metropolitan areas.

The nature and origins of acid summer haze air pollution in metropolitan Toronto, Ontario.

During July and August of 1986, 1987, and 1988, a field study was conducted of ambient acidic aerosol levels in Toronto, Ontario. Fine particle mass (da < 2.5 microns) samples were collected twice daily at a central-city site for the determination of particulate-phase strong acidity (H+) and sulfate (SO4 =). Two additional H(+)-monitoring sites were concurrently operated during the summers of 1986 and 1987 to examine the spatial variability of H+ within the metropolitan area. During the summer of 1986, a quasi-continuous total sulfate/sulfuric acid analyzer was also deployed to allow a determination of the chemical form of H+. Results indicate that acid aerosol episodes (H+ > or = 100 nmole/m3) did occur in this city during the summer months, and that H+ peaks were well correlated with sulfate peaks. Virtually all of the H+ was found to be present as ammonium bisulfate (NH4HSO4). While H+ concentrations were highly correlated among the three monitoring sites (r = 0.9), the highest H+/SO4 = ratios prevailed during SO4 = episode periods and at the least urbanized site. This latter trend was apparently due to greater neutralization of H+ by local ammonia at the more urbanized sites. Comparisons of day vs night H+/SO4 = ratios, an examination of air mass back-trajectories, and contemporaneous H+ measurements at surrounding sites collectively indicated that transported regional haze air pollution from the United States is a major contributor to the H+ events recorded within Toronto.

Respiratory hospital admissions and summertime haze air pollution in Toronto, Ontario: consideration of the role of acid aerosols.

A study of air pollution and daily hospital admissions for respiratory causes was conducted in Toronto, Ontario. Fine aerosol (da < 2.5 microns) samples were collected daily at a central city site during July and August 1986, 1987, and 1988 and were subsequently extracted and analyzed for daily particulate phase aerosol strong acidity (H+) and sulfates (SO4 =). Daily counts of respiratory admissions to 22 acute care hospitals and daily meteorological and environmental data (e.g. ozone [O3], total suspended particulate matter [TSP], and thoracic particle mass [PM10] were also obtained. Regression analyses indicated that only the O3, H+, and SO4 = associations with respiratory and asthma admissions remained consistently significant after controlling for temperature. Even after excluding days with maximum 1-hr O3 > 120 ppb, O3 was still strongly significant. In the various model specifications considered, the relative particle metric strengths of association with admissions were generally H+ > SO4 = > FP > PM10 > TSP, indicating that particle size and composition are of central importance in defining the adverse human health effects of particulate matter. On average, summertime haze air pollution was associated with 24% of all respiratory admissions (21% with O3, 3% with H+). On peak pollution days, however, aerosol acidity yielded the highest relative risk estimates (e.g., RR = 1.5 at 391 nmole/m3 H+), and summertime haze was associated with roughly half of all respiratory admissions.

Associations of London, England, daily mortality with particulate matter, sulfur dioxide, and acidic aerosol pollution.

During the extreme pollution episodes of 1952 and 1962 in London, England, excesses in daily mortality were clearly evident. In this study, we examined daily British Smoke, sulfur dioxide, acid aerosols, and weather variables for their short-term associations with daily mortality in the more typical (nonepisodic) winters of 1965-1972. Consideration of the acid aerosol data was of special interest because this chemical component has been suspected as a causal agent in past episodes. Temporal lag structures between the variables were examined after removal of long-term components from each series in order to obtain "rational" cross-correlations. Significant associations between same-day and lagged pollution variables and mortality were found. Alternative regression models with pollution and weather variables were also developed. The coefficients obtained were applied to the 1962 pollution episode to examine the continuity of the estimated slopes. The pollution-predicted deaths fit the observed deaths well, which supports the applicability of such deviation-derived coefficients to the absolute scale. These models were also employed to estimate mean excess daily deaths attributed hypothetically to air pollution. On average, mean effect ranged from 2-7% of all deaths during the nonepisodic winters in Greater London, but the 95% confidence intervals of these estimates overlapped for all model specifications examined. This estimated pollutant mixture "effect" cannot be attributed to a particular pollutant because of a lack of quantitative information on the relative downward biases caused by both analytical errors and errors in the spatial representativeness of each respective pollution index.

An automated sequential sampling system for particulate acid aerosols: description, characterization, and field sampling results.

An automated sequential sampling system for the measurement of particulate acid aerosols was developed in order to allow the routine collection of daily samples with only once-per-week site visits. The system's design, operation, and associated quality assurance (QA), quality control (QC), and data validation procedures are described. Results from a multi-year field application of this system in the Buffalo, Albany, and New York City metropolitan areas are reported, as well as from external audits and interlab analytical intercomparisons. It is found that the system successfully collected 94% of all possible samples in these three cities between May 1988 and December 1989. Weekly QA field blanks and positive control filters indicate that these data were collected with negligible acid contamination or neutralization. Peak aerosol acidity levels at these sites were found to be highest during the summer months, with peak 24-hr average levels in the 300-400 nmol/m3 range. It is concluded that this system represents a more convenient means of collecting extended daily records of valid particulate acid aerosol concentrations than has been possible in the past.

A multi-year study of air pollution and respiratory hospital admissions in three New York State metropolitan areas: results for 1988 and 1989 summers.

As part of a multi-year study of air pollution and respiratory hospital admissions in the Buffalo, Albany, and New York City, New York, metropolitan areas, filter samples were collected daily at suburban air monitoring sites and analyzed for their content of particulate phase aerosol strong acidity (i.e., hydrogen ion, H+) and sulfate (SO4 = ). In addition, daily hospital admissions for respiratory causes, other community air pollutant measurements (e.g., ozone, O3), and meteorological data (e.g., temperature) were also obtained for these metropolitan areas. The summer months (June-August) were selected for analysis because that is when the highest H+ (and O3) are usually experienced at these sites, and because these months are rarely complicated by other major influences (e.g., high pollen counts). Thus, any pollution-admissions relationships were expected to be most clearly discernible in this season. Prior to the health effects analysis, the summer admissions and environmental data were first detrended to eliminate long-wave autocorrelations, and day-of-week effects were removed via regression. Cross-correlations of the filtered 1988 and 1989 admissions and environmental data revealed strong associations between elevated summer haze pollution (i.e., H+, SO4 =, and O3) and increased total respiratory and asthma admissions on the same day and/or on subsequent days in Buffalo and New York City, especially during the summer of 1988 (when pollution levels were more extreme). Regression analyses indicated that the pollution-admissions associations remained significant (p < 0.05) even after the simultaneous inclusion of lagged daily maximum temperature. Mean effects calculations for these cities indicated that summertime haze can play a significant role in the occurrence of respiratory admissions in that season: accounting for an average 6 to 24% of 1988 Buffalo and NYC asthma admissions (depending on the pollutant index employed). O3 consistently had the highest mean effects estimates. Relative risk (RR) calculations indicated that the risk of admission for asthma was increased by a factor of 1.19 to 1.43 in these cities on maximum 1988 summertime pollution days, with H+ consistently having the highest RR estimates. These results are consistent with the hypothesis that ambient acid aerosol peaks (e.g., H+ > or = 100 nmol/m3) can potentiate the respiratory disease effects of O3. Associations were weaker in the less urbanized Albany metropolitan area and in the New York City (NYC) suburbs, even though the NYC suburban O3 exposures were similar to (and the H+ concentrations may even be somewhat higher than) those in the center city.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of heavy industrial pollution on respiratory function in the children of Cubatao, Brazil: a preliminary report.

Under a cooperative agreement between New York University and the Environmental Protection Agency, and in collaboration with the University of Sao Paulo (USP), a study is ongoing in Cubatao, Brazil, to try to establish exposure-response relationships on the impact of specific industrial effluents on respiratory function in school-age children. Cubatao, located on the coast about 44 km from the city of Sao Paulo, is surrounded by U-shaped mountains (approximately 800 m) covered with subtropical forests. Its area is approximately 160 km2, and it has a population of approximately 90,000. The geography is such that it causes a consistent diurnal land-sea breeze pattern and the opposite during the night, with low dispersion of the air pollutants. In a small area (approximately 40 km2) against the mountains there is a concentration of over 20 large plants: oil refinery; iron and steel mill; fertilizer, cement, and gypsum production; coke kilns; and chemical, paint, and many other ancillary plants. During the 1988 school year, March through June, August through November, 600 six-year-old children, attending six different kindergarten schools, underwent monthly spirometry tests. Because the children live within a 500 m radius of their school, pollution monitors were located on each of the six schools. Particles were collected using dichotomous stacked filter units placed on 20 m towers to reduce the influence of dust from unpaved roads. The units use different pore size filters for coarse, 2 to 10 microns, and fine particles, (dp) less than 2 microns, and took separate samples for day and nighttime.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of single- and multiday ozone exposures on respiratory function in active normal children.

Ventilatory function was measured twice daily on 46 healthy children aged 8-14 years on at least 7 days for each child during a 4-week period at a northwestern New Jersey residential summer camp in 1988. The highest 1-hr O3 concentration was 150 ppb, while the highest 12-hr H+ concentration (as H2SO4) was 18.6 micrograms/m3. The highest temperature-humidity index was 81 degrees F. The regressions of FVC, FEV1, FEF25-75, and PEFR on O3 in the hour preceding the afternoon function measurements yielded slopes essentially the same as those measured on other children at the same camp in 1984. Regressions of the changes in function between the late morning and late afternoon function measurements on average O3 concentration between them produced significant, but somewhat smaller effects, while regressions of morning function on O3 during the previous day indicated small but still significant effects. There were no significant correlations with other measured environmental variables including H+. Based on the results of this study and similar previous studies, we conclude that O3 exposures in ambient air produce greater lung function deficits in active young people in natural settings then does pure O3 in controlled chamber exposure studies because of: (1) longer exposures; (2) potentiation by other factors in the ambient exposures; (3) the persistence of effects from prior day's exposures; and (4) the persistence of a transient response associated with the daily peak of exposure. It follows that projections of likely effects in the real world from controlled chamber exposure studies should either have a large margin of safety, or the judgment of the extent of effects likely to occur among populations should be based directly on the effects observed in field studies.

Reexamination of London, England, mortality in relation to exposure to acidic aerosols during 1963-1972 winters.

Air pollution epidemiology since the 1950s has been able to demonstrate that increases in daily mortality in London, England, were associated with elevated concentrations of index air pollutants, i.e., British Smoke (BS) and sulfur dioxide (SO2). In this work, we reanalyze that portion of the 1958-1972 winter mortality-pollution record for which daily direct acid aerosol measurements were made at a central site in London (St. Bartholomew's Medical College). The purposes of these exploratory analyses are to examine the dataset for indications of a relationship between acid aerosol pollution and human mortality and to compare any noted associations with those for other pollution variables. It is found that the log of acid aerosol concentrations is more strongly associated with raw total mortality in bivariate analyses than is BS or SO2, despite the fact that acid data are available from only one central site (versus seven disperse sites for BS and SO2). The logarithmic nature of the exposure side of the H2SO4-mortality relationship implies a saturation model of pollution effects, possibly due to multiday pollution harvesting influences on a susceptible subpopulation. Moreover, mortality-pollution cross-correlation analyses indicate that mortality effects usually follow pollution in time, supporting a causal relationship between the two. The apparent advantage of H2SO4 over BS in predicting total raw mortality is consistent with the hypothesis that it is the portion of particulate mass of greater health significance and may also allow the development of London mortality results which are more easily transferable to other environments than is the case for existing BS results.

Characterization and reconstruction of historical London, England, acidic aerosol concentrations.

Several past studies of the historical London air pollution record have reported an association between daily mortality and British Smoke levels. However, this pollution index does not give direct information on particulate mass or its chemical composition. A more specific particulate matter index, aerosol acidity, was measured at a site in central London, and daily data are available for the period 1963-1972. British Smoke and SO2 were also measured at the same site. Also, meteorological parameters were routinely measured at a nearby British Meteorological Office. Thus, daily fluctuation of the acidic aerosols was characterized in terms of other environmental parameters. Each of the other parameters analyzed seems necessary, but not sufficient to explain a high level of acidic aerosol. Overall, about half of the variance of log-transformed daily fluctuations of acidic aerosols can be explained by a combination of parameters including SO2 and British Smoke concentrations, temperature, ventilation by wind, and humidity. The rest of the variance cannot be explained by the parameters included in this analysis. Potential factors responsible for this unique variance would be variations in the availability of basic gases to cause neutralization and variation in the availability of catalytic metal salts. Because the acidic aerosol has a unique component of variation, it may be possible to distinguish health effects due to this specific pollutant from other available pollution indices or environmental factors.