Effects of fossil fuel and total anthropogenic emission removal on public health and climate.

Anthropogenic greenhouse gases and aerosols are associated with climate change and human health risks. We used a global model to estimate the climate and public health outcomes attributable to fossil fuel use, indicating the potential benefits of a phaseout. We show that it can avoid an excess mortality rate of 3.61 (2.96-4.21) million per year from outdoor air pollution worldwide. This could be up to 5.55 (4.52-6.52) million per year by additionally controlling nonfossil anthropogenic sources. Globally, fossil-fuel-related emissions account for about 65% of the excess mortality, and 70% of the climate cooling by anthropogenic aerosols. The chemical influence of air pollution on aeolian dust contributes to the aerosol cooling. Because aerosols affect the hydrologic cycle, removing the anthropogenic emissions in the model increases rainfall by 10-70% over densely populated regions in India and 10-30% over northern China, and by 10-40% over Central America, West Africa, and the drought-prone Sahel, thus contributing to water and food security. Since aerosols mask the anthropogenic rise in global temperature, removing fossil-fuel-generated particles liberates 0.51(±0.03) °C and all pollution particles 0.73(±0.03) °C warming, reaching around 2 °C over North America and Northeast Asia. The steep temperature increase from removing aerosols can be moderated to about 0.36(±0.06) °C globally by the simultaneous reduction of tropospheric ozone and methane. We conclude that a rapid phaseout of fossil-fuel-related emissions and major reductions of other anthropogenic sources are needed to save millions of lives, restore aerosol-perturbed rainfall patterns, and limit global warming to 2 °C.

Mortality-Air Pollution Associations in Low Exposure Environments (MAPLE): Phase 2.

INTRODUCTION: Mortality is associated with long-term exposure to fine particulate matter (particulate matter ≤2.5 µm in aerodynamic diameter; PM2.5), although the magnitude and form of these associations remain poorly understood at lower concentrations. Knowledge gaps include the shape of concentration-response curves and the lowest levels of exposure at which increased risks are evident and the occurrence and extent of associations with specific causes of death. Here, we applied improved estimates of exposure to ambient PM2.5 to national population-based cohorts in Canada, including a stacked cohort of 7.1 million people who responded to census year 1991, 1996, or 2001. The characterization of the shape of the concentration-response relationship for nonaccidental mortality and several specific causes of death at low levels of exposure was the focus of the Mortality-Air Pollution Associations in Low Exposure Environments (MAPLE) Phase 1 report. In the Phase 1 report we reported that associations between outdoor PM2.5 concentrations and nonaccidental mortality were attenuated with the addition of ozone (O3) or a measure of gaseous pollutant oxidant capacity (Ox), which was estimated from O3 and nitrogen dioxide (NO2) concentrations. This was motivated by our interests in understanding both the effects air pollutant mixtures may have on mortality and also the role of O3 as a copollutant that shares common sources and precursor emissions with those of PM2.5. In this Phase 2 report, we further explore the sensitivity of these associations with O3 and Ox, evaluate sensitivity to other factors, such as regional variation, and present ambient PM2.5 concentration-response relationships for specific causes of death. METHODS: PM2.5 concentrations were estimated at 1 km2 spatial resolution across North America using remote sensing of aerosol optical depth (AOD) combined with chemical transport model (GEOS-Chem) simulations of the AOD:surface PM2.5 mass concentration relationship, land use information, and ground monitoring. These estimates were informed and further refined with collocated measurements of PM2.5 and AOD, including targeted measurements in areas of low PM2.5 concentrations collected at five locations across Canada. Ground measurements of PM2.5 and total suspended particulate matter (TSP) mass concentrations from 1981 to 1999 were used to backcast remote-sensing-based estimates over that same time period, resulting in modeled annual surfaces from 1981 to 2016.Annual exposures to PM2.5 were then estimated for subjects in several national population-based Canadian cohorts using residential histories derived from annual postal code entries in income tax files. These cohorts included three census-based cohorts: the 1991 Canadian Census Health and Environment Cohort (CanCHEC; 2.5 million respondents), the 1996 CanCHEC (3 million respondents), the 2001 CanCHEC (3 million respondents), and a Stacked CanCHEC where duplicate records of respondents were excluded (Stacked CanCHEC; 7.1 million respondents). The Canadian Community Health Survey (CCHS) mortality cohort (mCCHS), derived from several pooled cycles of the CCHS (540,900 respondents), included additional individual information about health behaviors. Follow-up periods were completed to the end of 2016 for all cohorts. Cox proportional hazard ratios (HRs) were estimated for nonaccidental and other major causes of death using a 10-year moving average exposure and 1-year lag. All models were stratified by age, sex, immigrant status, and where appropriate, census year or survey cycle. Models were further adjusted for income adequacy quintile, visible minority status, Indigenous identity, educational attainment, labor-force status, marital status, occupation, and ecological covariates of community size, airshed, urban form, and four dimensions of the Canadian Marginalization Index (Can-Marg; instability, deprivation, dependency, and ethnic concentration). The mCCHS analyses were also adjusted for individual-level measures of smoking, alcohol consumption, fruit and vegetable consumption, body mass index (BMI), and exercise behavior.In addition to linear models, the shape of the concentration-response function was investigated using restricted cubic splines (RCS). The number of knots were selected by minimizing the Bayesian Information Criterion (BIC). Two additional models were used to examine the association between nonaccidental mortality and PM2.5. The first is the standard threshold model defined by a transformation of concentration equaling zero if the concentration was less than a specific threshold value and concentration minus the threshold value for concentrations above the threshold. The second additional model was an extension of the Shape Constrained Health Impact Function (SCHIF), the eSCHIF, which converts RCS predictions into functions potentially more suitable for use in health impact assessments. Given the RCS parameter estimates and their covariance matrix, 1,000 realizations of the RCS were simulated at concentrations from the minimum to the maximum concentration, by increments of 0.1 µg/m3. An eSCHIF was then fit to each of these RCS realizations. Thus, 1,000 eSCHIF predictions and uncertainty intervals were determined at each concentration within the total range.Sensitivity analyses were conducted to examine associations between PM2.5 and mortality when in the presence of, or stratified by tertile of, O3 or Ox. Additionally, associations between PM2.5 and mortality were assessed for sensitivity to lower concentration thresholds, where person-years below a threshold value were assigned the mean exposure within that group. We also examined the sensitivity of the shape of the nonaccidental mortality-PM2.5 association to removal of person-years at or above 12 µg/m3 (the current U.S. National Ambient Air Quality Standard) and 10 µg/m3 (the current Canadian and former [2005] World Health Organization [WHO] guideline, and current WHO Interim Target-4). Finally, differences in the shapes of PM2.5-mortality associations were assessed across broad geographic regions (airsheds) within Canada. RESULTS: The refined PM2.5 exposure estimates demonstrated improved performance relative to estimates applied previously and in the MAPLE Phase 1 report, with slightly reduced errors, including at lower ranges of concentrations (e.g., for PM2.5 <10 µg/m3).Positive associations between outdoor PM2.5 concentrations and nonaccidental mortality were consistently observed in all cohorts. In the Stacked CanCHEC analyses (1.3 million deaths), each 10-µg/m3 increase in outdoor PM2.5 concentration corresponded to an HR of 1.084 (95% confidence interval [CI]: 1.073 to 1.096) for nonaccidental mortality. For an interquartile range (IQR) increase in PM2.5 mass concentration of 4.16 µg/m3 and for a mean annual nonaccidental death rate of 92.8 per 10,000 persons (over the 1991-2016 period for cohort participants ages 25-90), this HR corresponds to an additional 31.62 deaths per 100,000 people, which is equivalent to an additional 7,848 deaths per year in Canada, based on the 2016 population. In RCS models, mean HR predictions increased from the minimum concentration of 2.5 µg/m3 to 4.5 µg/m3, flattened from 4.5 µg/m3 to 8.0 µg/m3, then increased for concentrations above 8.0 µg/m3. The threshold model results reflected this pattern with -2 log-likelihood values being equal at 2.5 µg/m3 and 8.0 µg/m3. However, mean threshold model predictions monotonically increased over the concentration range with the lower 95% CI equal to one from 2.5 µg/m3 to 8.0 µg/m3. The RCS model was a superior predictor compared with any of the threshold models, including the linear model.In the mCCHS cohort analyses inclusion of behavioral covariates did not substantially change the results for both linear and nonlinear models. We examined the sensitivity of the shape of the nonaccidental mortality-PM2.5 association to removal of person-years at or above the current U.S. and Canadian standards of 12 µg/m3 and 10 µg/m3, respectively. In the full cohort and in both restricted cohorts, a steep increase was observed from the minimum concentration of 2.5 µg/m3 to 5 µg/m3. For the full cohort and the <12 µg/m3 cohort the relationship flattened over the 5 to 9 µg/m3 range and then increased above 9 µg/m3. A similar increase was observed for the <10 µg/m3 cohort followed by a clear decline in the magnitude of predictions over the 5 to 9 µg/m3 range and an increase above 9 µg/m3. Together these results suggest that a positive association exists for concentrations >9 µg/m3 with indications of adverse effects on mortality at concentrations as low as 2.5 µg/m3.Among the other causes of death examined, PM2.5 exposures were consistently associated with an increased hazard of mortality due to ischemic heart disease, respiratory disease, cardiovascular disease, and diabetes across all cohorts. Associations were observed in the Stacked CanCHEC but not in all other cohorts for cerebrovascular disease, pneumonia, and chronic obstructive pulmonary disease (COPD) mortality. No significant associations were observed between mortality and exposure to PM2.5 for heart failure, lung cancer, and kidney failure.In sensitivity analyses, the addition of O3 and Ox attenuated associations between PM2.5 and mortality. When analyses were stratified by tertiles of copollutants, associations between PM2.5 and mortality were only observed in the highest tertile of O3 or Ox. Across broad regions of Canada, linear HR estimates and the shape of the eSCHIF varied substantially, possibly reflecting underlying differences in air pollutant mixtures not characterized by PM2.5 mass concentrations or the included gaseous pollutants. Sensitivity analyses to assess regional variation in population characteristics and access to healthcare indicated that the observed regional differences inconcentration-mortality relationships, specifically the flattening of the concentration-mortality relationship over the 5 to 9 µg/m3 range, was not likely related to variation in the makeup of the cohort or its access to healthcare, lending support to the potential role of spatially varying air pollutant mixtures not sufficiently characterized by PM2.5 mass concentrations. CONCLUSIONS: In several large, national Canadian cohorts, including a cohort of 7.1 million unique census respondents, associations were observed between exposure to PM2.5 with nonaccidental mortality and several specific causes of death. Associations with nonaccidental mortality were observed using the eSCHIF methodology at concentrations as low as 2.5 µg/m3, and there was no clear evidence in the observed data of a lower threshold, below which PM2.5 was not associated with nonaccidental mortality.

Mortality-Air Pollution Associations in Low-Exposure Environments (MAPLE): Phase 1.

INTRODUCTION: Fine particulate matter (particulate matter ≤2.5 µm in aerodynamic diameter, or PM2.5) is associated with mortality, but the lower range of relevant concentrations is unknown. Novel satellite-derived estimates of outdoor PM2.5 concentrations were applied to several large population-based cohorts, and the shape of the relationship with nonaccidental mortality was characterized, with emphasis on the low concentrations (<12 µg/m3) observed throughout Canada. METHODS: Annual satellite-derived estimates of outdoor PM2.5 concentrations were developed at 1-km2 spatial resolution across Canada for 2000-2016 and backcasted to 1981 using remote sensing, chemical transport models, and ground monitoring data. Targeted ground-based measurements were conducted to measure the relationship between columnar aerosol optical depth (AOD) and ground-level PM2.5. Both existing and targeted ground-based measurements were analyzed to develop improved exposure data sets for subsequent epidemiological analyses.Residential histories derived from annual tax records were used to estimate PM2.5 exposures for subjects whose ages ranged from 25 to 90 years. About 8.5 million were from three Canadian Census Health and Environment Cohort (CanCHEC) analytic files and another 540,900 were Canadian Community Health Survey (CCHS) participants. Mortality was linked through the year 2016. Hazard ratios (HR) were estimated with Cox Proportional Hazard models using a 3-year moving average exposure with a 1-year lag, with the year of follow-up as the time axis. All models were stratified by 5-year age groups, sex, and immigrant status. Covariates were based on directed acyclical graphs (DAG), and included contextual variables (airshed, community size, neighborhood dependence, neighborhood deprivation, ethnic concentration, neighborhood instability, and urban form). A second model was examined including the DAG-based covariates as well as all subject-level risk factors (income, education, marital status, indigenous identity, employment status, occupational class, and visible minority status) available in each cohort. Additional subject-level behavioral covariates (fruit and vegetable consumption, leisure exercise frequency, alcohol consumption, smoking, and body mass index [BMI]) were included in the CCHS analysis.Sensitivity analyses evaluated adjustment for covariates and gaseous copollutants (nitrogen dioxide [NO2] and ozone [O3]), as well as exposure time windows and spatial scales. Estimates were evaluated across strata of age, sex, and immigrant status. The shape of the PM2.5-mortality association was examined by first fitting restricted cubic splines (RCS) with a large number of knots and then fitting the shape-constrained health impact function (SCHIF) to the RCS predictions and their standard errors (SE). This method provides graphical results indicating the RCS predictions, as a nonparametric means of characterizing the concentration-response relationship in detail and the resulting mean SCHIF and accompanying uncertainty as a parametric summary.Sensitivity analyses were conducted in the CCHS cohort to evaluate the potential influence of unmeasured covariates on air pollution risk estimates. Specifically, survival models with all available risk factors were fit and compared with models that omitted covariates not available in the CanCHEC cohorts. In addition, the PM2.5 risk estimate in the CanCHEC cohort was indirectly adjusted for multiple individual-level risk factors by estimating the association between PM2.5 and these covariates within the CCHS. RESULTS: Satellite-derived PM2.5 estimates were low and highly correlated with ground monitors. HR estimates (per 10-µg/m3 increase in PM2.5) were similar for the 1991 (1.041, 95% confidence interval [CI]: 1.016-1.066) and 1996 (1.041, 1.024-1.059) CanCHEC cohorts with a larger estimate observed for the 2001 cohort (1.084, 1.060-1.108). The pooled cohort HR estimate was 1.053 (1.041-1.065). In the CCHS an analogous model indicated a HR of 1.13 (95% CI: 1.06-1.21), which was reduced slightly with the addition of behavioral covariates (1.11, 1.04-1.18). In each of the CanCHEC cohorts, the RCS increased rapidly over lower concentrations, slightly declining between the 25th and 75th percentiles and then increasing beyond the 75th percentile. The steepness of the increase in the RCS over lower concentrations diminished as the cohort start date increased. The SCHIFs displayed a supralinear association in each of the three CanCHEC cohorts and in the CCHS cohort.In sensitivity analyses conducted with the 2001 CanCHEC, longer moving averages (1, 3, and 8 years) and smaller spatial scales (1 km2 vs. 10 km2) of exposure assignment resulted in larger associations between PM2.5 and mortality. In both the CCHS and CanCHEC analyses, the relationship between nonaccidental mortality and PM2.5 was attenuated when O3 or a weighted measure of oxidant gases was included in models. In the CCHS analysis, but not in CanCHEC, PM2.5 HRs were also attenuated by the inclusion of NO2. Application of the indirect adjustment and comparisons within the CCHS analysis suggests that missing data on behavioral risk factors for mortality had little impact on the magnitude of PM2.5-mortality associations. While immigrants displayed improved overall survival compared with those born in Canada, their sensitivity to PM2.5 was similar to or larger than that for nonimmigrants, with differences between immigrants and nonimmigrants decreasing in the more recent cohorts. CONCLUSIONS: In several large population-based cohorts exposed to low levels of air pollution, consistent associations were observed between PM2.5 and nonaccidental mortality for concentrations as low as 5 µg/m3. This relationship was supralinear with no apparent threshold or sublinear association.

A panel study in congestive heart failure to estimate the short-term effects from personal factors and environmental conditions on oxygen saturation and pulse rate.

OBJECTIVES: Recent studies suggest that persons with congestive heart failure (CHF) may be at higher risk for short-term effects of air pollution. This daily diary panel study in Montreal, Quebec, was carried out to determine whether oxygen saturation and pulse rate were associated with selected personal factors, weather conditions and air pollution. METHODS: Thirty-one subjects with CHF participated in this study in 2002 and 2003. Over a 2-month period, the investigators measured their oxygen saturation, pulse rate, weight and temperature each morning and recorded these and other data in a daily diary. Air pollution and weather conditions were obtained from fixed-site monitoring stations. The study made use of mixed regression models, adjusting for within-subject serial correlation and temporal trends, to determine the association between oxygen saturation and pulse rate and personal and environmental variables. Depending on the model, we accounted for the effects of a variety of personal variables (eg, body temperature, salt consumption) as well as nitrogen dioxide (NO2), ozone, maximum temperature and change in barometric pressure at 8:00 from the previous day. RESULTS: In multivariable analyses, the study found that oxygen saturation was reduced when subjects reported that they were ill, consumed salt, or drank liquids on the previous day and had higher body temperatures on the concurrent day (only the latter was statistically significant). Relative humidity and decreased atmospheric pressure from the previous day were associated with oxygen saturation. In univariate analyses, there was negative associations with concentrations of fine particulates, ozone, and sulphur dioxide (SO2), but only SO2 was significant after adjustment for the effects of weather. For pulse rate, no associations were found for the personal variables and in univariate analyses the study found positive associations with NO(2), fine particulates (aerodynamic diameter of 2.5 microm or under, PM(2.5)), SO2, and maximum temperature, although only the latter two were significant after adjustment for environmental effects. CONCLUSIONS: The findings from the present investigation suggest that personal and environmental conditions affect intermediate physiological parameters that may affect the health of CHF patients.

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.

The role of particulate size and chemistry in the association between summertime ambient air pollution and hospitalization for cardiorespiratory diseases.

In order to address the role that the ambient air pollution mix, comprised of gaseous pollutants and various physical and chemical measures of particulate matter, plays in exacerbating cardiorespiratory disease, daily measures of fine and coarse particulate mass, aerosol chemistry (sulfates and acidity), and gaseous pollution (ozone, nitrogen dioxide, sulfur dioxide, and carbon monoxide) were collected in Toronto, Ontario, Canada, in the summers of 1992, 1993, and 1994. These time series were then compared with concurrent data on the number of daily admissions to hospitals for either cardiac diseases (ischemic heart disease, heart failure, and dysthymias) or respiratory diseases (tracheobronchitis, chronic obstructive long disease, asthma, and pneumonia). After adjusting the admission time series for long-term temporal trends, seasonal variations, the effects of short-term epidemics, day of the week effects, and ambient temperature and dew point temperature, positive associations were observed for all ambient air pollutants for both respiratory and cardiac diseases. Ozone was least sensitive to adjustment for the gaseous and particulate pollution measures. However, the association between the health outcomes and carbon monoxide, fine and coarse mass, sulfate levels and aerosol acidity could be explained by adjustment for exposure to gaseous pollutants. Increases in ozone, nitrogen dioxide, and sulfur dioxide equivalent to their interquartile ranges corresponded to an 11% and 13% increase in daily hospitalizations for respiratory and cardiac diseases, respectively. The inclusion of any one of the particulate air pollutants in multiple regression models did not increase these percentages. Particle mass and chemistry could not be identified as an independent risk factor for the exacerbation of cardiorespiratory diseases in this study beyond that attributable to climate and gaseous air pollution. We recommend that effects of particulate matter on health be assessed in conjunction with temporally covarying gaseous air pollutants.

Acute lung function responses to ambient acid aerosol exposures in children.

We examined the relationship between lung function changes and ambient acid aerosol episodes in children attending a residential summer camp. Young females (112) performed daily spirometry, and 96 were assessed on one occasion for airway hyperresponsiveness using a methacholine bronchoprovocation test. Air quality measurements were performed on site and four distinct acid aerosol episodes were observed during the 41-day study. The maximum values observed during the 41-day study were: O3 at 143 ppb; H2SO4 at 47.7 micrograms/m3; and [H+] at 550 nmole/m3. Maximum decrements of 3.5 and 7% for FEV1 and PEF, respectively, were observed to be associated with the air pollution episodes. There was some evidence of a differential lung function response to the episodes where children with a positive response to a methacholine challenge had larger decrements compared to their nonresponsive counterparts.

Association between ozone and asthma emergency department visits in Saint John, New Brunswick, Canada.

This study examines the relationship of asthma emergency department (ED) visits to daily concentrations of ozone and other air pollutants in Saint John, New Brunswick, Canada. Data on ED visits with a presenting complaint of asthma (n = 1987) were abstracted for the period 1984-1992 (May-September). Air pollution variables included ozone, sulfur dioxide, nitrogen dioxide, sulfate, and total suspended particulate (TSP); weather variables included temperature, humidex, dewpoint, and relative humidity. Daily ED visit frequencies were filtered to remove day of the week and long wave trends, and filtered values were regressed on air pollution and weather variables for the same day and the 3 previous days. The mean daily 1-hr maximum ozone concentration during the study period was 41.6 ppb. A positive, statistically significant (p < 0.05) association was observed between ozone and asthma ED visits 2 days later, and the strength of the association was greater in nonlinear models. The frequency of asthma ED visits was 33% higher (95% CI, 10-56%) when the daily 1-hr maximum ozone concentration exceeded 75 ppb (the 95th percentile). The ozone effect was not significantly influenced by the addition of weather or other pollutant variables into the model or by the exclusion of repeat ED visits. However, given the limited number of sampling days for sulfate and TSP, a particulate effect could not be ruled out. We detected a significant association between ozone and asthma ED visits, despite the vast majority of sampling days being below current U.S. and Canadian standards.

Health risks from acid rain: a Canadian perspective.

Acidic deposition, commonly referred to as acid rain, is causing serious environmental damage in eastern Canada. The revenues from forest products, tourism and sport fishing are estimated to account for about 8% of the gross national product. The impact on human health is not as clearcut and a multi-department program on the Long-Range Transport of Airborne Pollutants (LRTAP) was approved by the federal government in June 1980. The objectives of the LRTAP program are to reduce wet sulfate deposition to less than 20 kg/ha per year in order to protect moderately sensitive areas. This will require a 50% reduction in Canadian SO2 emissions east of the Saskatchewan/Manitoba border and concomitant reductions in the eastern U.S.A. The objectives of the health sector of the program are to assess the risk to health posed by airborne pollutants which are subjected to long-range transport and to monitor the influence of abatement programs. Two major epidemiology studies were undertaken in 1983, one in which the health effects related to acute exposure to transported air pollutants were studied in asthmatic and nonasthmatic children, and another in which the effects of chronic exposure to these pollutants were studied in school children living in towns with high and low levels of pollutants. Preliminary analysis of the data do not indicate major health effects, but definitive conclusions must await final analysis. Studies on the indirect effects of acid deposition on water quality have shown that acidified lake water left standing in the plumbing system can adversely affect water quality and that federally set guidelines for copper and lead are exceeded. Flushing of the system before using the water rectifies the situation. Additional studies are planned to further delineate the magnitude of the health effects of acidified lake water.

Identification of persons with cardiorespiratory conditions who are at risk of dying from the acute effects of ambient air particles.

This study was undertaken to identify subgroups of the population susceptible to the effects of ambient air particles. Fixed-site air pollution monitors in Montreal, Quebec, Canada, provided daily mean levels of various measures of particulates and gaseous pollutants. Total sulfates were also measured daily (1986-1993) at a monitoring station 150 km southeast of the city (Sutton, Quebec, Canada). We used coefficient of haze (COH), extinction coefficient, and Sutton sulfates to predict fine particles and sulfates from a fine particles model for days that were missing. We used the universal Quebec medicare system to obtain billings and prescriptions for each Montreal resident who died in the city from 1984 to 1993. These data were then used to define cardiovascular and respiratory conditions that subjects had before death. Using standard Poisson regression time-series analyses, we estimated the association between daily nonaccidental mortality and daily concentrations of particles in the ambient air among persons with cardiovascular and respiratory conditions diagnosed before death. We found no persuasive evidence that daily mortality increased when ambient air particles were elevated for subgroups of persons with chronic upper respiratory diseases, airways disease, cerebrovascular diseases, acute coronary artery disease, and hypertension. However, we found that daily mortality increased linearly as concentrations of particles increased for persons who had acute lower respiratory diseases, chronic coronary artery diseases (especially in the elderly), and congestive heart failure. For this latter set of conditions, the mean percent increase in daily mortality (MPC) for an increase in the COH across its interquartile range (18.5 COH units per 327.8 linear meters), averaged over the day of death and the 2 preceding days, was MPC = 5.09% [95% confidence interval (CI) 2.47-7.79%], MPC = 2.62 (95% CI 0.53-4.75%), and MPC = 4.99 (95% CI 2.44-7.60%), respectively. Adjustments for gaseous pollutants generally attenuated these associations, although the general pattern of increased daily mortality remained. In addition, there appeared to be a stronger association in the summer season. The positive associations found for persons who had acute lower respiratory diseases and congestive heart failure are consistent with some prevailing hypotheses and may also be consistent with recent toxicologic data implicating endothelins. Further epidemiologic studies are required to confirm these findings.

Do socioeconomic characteristics modify the short term association between air pollution and mortality? Evidence from a zonal time series in Hamilton, Canada.

STUDY OBJECTIVE: To assess the short term association between air pollution and mortality in different zones of an industrial city. An intra-urban study design is used to test the hypothesis that socioeconomic characteristics modify the acute health effects of ambient air pollution exposure. DESIGN: The City of Hamilton, Canada, was divided into five zones based on proximity to fixed site air pollution monitors. Within each zone, daily counts of non-trauma mortality and air pollution estimates were combined. Generalised linear models (GLMs) were used to test mortality associations with sulphur dioxide (SO(2)) and with particulate air pollution measured by the coefficient of haze (CoH). MAIN RESULTS: Increased mortality was associated with air pollution exposure in a citywide model and in intra-urban zones with lower socioeconomic characteristics. Low educational attainment and high manufacturing employment in the zones significantly and positively modified the acute mortality effects of air pollution exposure. DISCUSSION: Three possible explanations are proposed for the observed effect modification by education and manufacturing: (1) those in manufacturing receive higher workplace exposures that combine with ambient exposures to produce larger health effects; (2) persons with lower education are less mobile and experience less exposure measurement error, which reduces bias toward the null; or (3) manufacturing and education proxy for many social variables representing material deprivation, and poor material conditions increase susceptibility to health risks from air pollution.

Effect of short-term exposure to gaseous pollution on asthma hospitalisation in children: a bi-directional case-crossover analysis.

STUDY OBJECTIVE: Assess associations between short-term exposure to gaseous pollutants and asthma hospitalisation among boys and girls 6 to12 years of age. DESIGN: A bi-directional case-crossover analysis was used. Conditional logistic regression models were fitted to the data for boys and girls separately. Exposures averaged over periods ranging from one to seven days were used to assess the effects of gaseous pollutants on asthma hospitalisation. Estimated relative risks for asthma hospitalisation were calculated for an incremental exposure corresponding to the interquartile range in pollutant levels, adjusted for daily weather conditions and concomitant exposure to particulate matter. SETTING: Toronto, Ontario, Canada. PARTICIPANTS: A total of 7319 asthma hospitalisations for children 6 to 12 years of age (4629 for boys and 2690 for girls) in Toronto between 1981 and 1993. MAIN RESULTS: A significant acute effect of carbon monoxide on asthma hospitalisation was found in boys, and sulphur dioxide showed significant effects of prolonged exposure in girls. Nitrogen dioxide was positively associated with asthma admissions in both sexes. The lag time for certain gaseous pollutant effects seemed to be shorter in boys (around two to three days for carbon monoxide and nitrogen dioxide), as compared with girls (about six to seven days for sulphur dioxide and nitrogen dioxide). The effects of gaseous pollutants on asthma hospitalisation remained after adjustment of particulate matter. The data showed no association between ozone and asthma hospitalisation in children. CONCLUSIONS: The study showed positive relations between gaseous pollutants (carbon monoxide, sulphur dioxide, and nitrogen dioxide) at comparatively low levels and asthma hospitalisation in children, using bi-directional case-crossover analyses. Though, the effects of certain specific gaseous pollutants were found to vary in boys and girls.

Air pollution, aeroallergens and cardiorespiratory emergency department visits in Saint John, Canada.

Existing studies of the association between air pollution, aeroallergens and emergency department (ED) visits have generally examined the effects of a few pollutants or aeroallergens on individual conditions such as asthma or chronic obstructive pulmonary disease. In this study, we considered a wide variety of respiratory and cardiac conditions and an extensive set of pollutants and aeroallergens, and utilized prospectively collected information on possible effect modifiers which would not normally be available from purely administrative data. The association between air pollution, aeroallergens and cardiorespiratory ED visits (n = 19,821) was examined for the period 1992 to 1996 using generalized additive models. ED visit, air pollution and aeroallergen time series were prefiltered using LOESS smoothers to minimize temporal confounding, and a parsimonious model was constructed to control for confounding by weather and day of week. Multipollutant and multi-aeroallergen models were constructed using stepwise procedures and sensitivity analyses were conducted by season, diagnosis, and selected individual characteristics or effect modifiers. In single-pollutant models, positive effects of all pollutants but NO2 and COH were observed on asthma visits, and positive effects on all respiratory diagnosis groups were observed for O3, SO2, PM10, PM2.5, and SO4(2-). Among cardiac conditions, only dysrhythmia visits were positively associated with all measures of particulate matter. In the final year-round multipollutant models, a 20.9% increase in cardiac ED visits was attributed to the combination of O3 (16.0%, 95% CI 2.8-30.9) and SO2 (4.9%, 95%CI 1.7-8.2) at the mean concentration of each pollutant. In the final multipollutant model for respiratory visits, O3 accounted for 3.9% of visits (95% CI 0.8-7.2), and SO2 for 3.7% (95% CI 1.5-6.0), whereas a weak, negative association was observed with NO2. In multi-aeroallergen models of warm season asthma ED visits, Ascomycetes, Alternaria and small round fungal spores accounted for 4.5% (95% CI 1.8-7.4), 4.7% (95% CI 1.0-8.6) and 3.0% (95% CI 0.8-5.1), respectively, of visits at their mean concentrations, and these effects were not sensitive to adjustment for air pollution effects. In conclusion, we observed a significant influence of the air pollution mix on cardiac and respiratory ED visits. Although in single-pollutant models, positive associations were noted between ED visits and some measures of particulate matter, in multipollutant models, pollutant gases, particularly ozone, exhibited more consistent effects. Aeroallergens were also significantly associated with warm season asthma ED visits.

Kidney and liver levels of some major, minor and trace elements in two Ontario communities.

The contents of Ag, As, Ba, Be, Ca, Cd, Co, Cr, Cu, Fe, Hg, K, Mg, Mn, Mo, Na, Ni, P, Pb, Se, Sr, Th, Ti and Zn in 143 autopsied liver and kidney specimens from two Ontario communities (Kingston and Ottawa) were determined using the techniques of inductively-coupled plasma--atomic emission spectrometry, and electrothermal atomization--atomic absorption spectrometry coupled with hydride evolution (As, Se), reduction--aeration (Hg), or solvent extraction (Pb). The majority of samples came from individuals older than 50 y. In general, the data for the various elements were independent of age or sex but showed some dependence on location for elements such as Cu, Fe, K, Mg, Mn, Na, P, Se and Zn. Despite these differences the elemental values of the liver and kidney samples from both the communities were within the normal range.

Association of particulate matter components with daily mortality and morbidity in urban populations.

Indices of atmospheric particulate matter (PM) have been reported to be associated with daily mortality and morbidity in a large number of recent time-series studies. However, the question remains as to which components of PM are responsible for the reported associations. Multiple PM components rarely are measured simultaneously. To investigate PM effects on mortality and morbidity, we used the multiple PM components measured in Windsor, Ontario, at a site only a few miles from downtown Detroit, Michigan. This study focused primarily on two study periods in which multiple PM components were measured in Windsor: 1985 to 1990, when levels of total suspended particles (TSP), sulfate from TSP (TSP-SO4(2-)), PM less than 10 microns in diameter (PM10), and nonthoracic TSP (TSP-PM10) were measured throughout the year; and 1992 to 1994, when data on PM10, PM2.5 (PM less than 2.5 microns in diameter), PM10-2.5 (PM10 minus PM2.5), particle acidity (H+), and artifact-free sulfates (SO4(2-)) were available for mostly summer months. Mortality data were analyzed for the 1985 to 1990 study period, and data on both mortality and hospital admissions of elderly patients were analyzed for the 1992 through 1994 period. Poisson regressions were used to estimate the effects of these PM components and gaseous criteria pollutants on mortality (nonaccidental, circulatory, respiratory, and nonaccidental without circulatory and respiratory) and on hospital admissions of elderly patients (for pneumonia, chronic obstructive pulmonary disease [COPD], ischemic heart disease, dysrhythmias, heart failure, and stroke), adjusting for temperature and humidity, trends and seasonal cycles, and day of the week. Both PM10 and TSP were associated significantly with respiratory mortality for the 1985 to 1990 period, with similar relative risk (RR) estimates for PM10 (RR = 1.123; 95% confidence interval [CI] 1.0361-1.218) and TSP (RR = 1.109; 95% CI 1.028-1.197), per 5th to 95th percentile increment. The effect-size estimates for TSP-SO4(2-) and TSP-PM10 were smaller and less significant. In two-pollutant models, simultaneous inclusion of gaseous pollutants with PM10 or TSP reduced PM coefficients by 0 to 34%. The effect-size estimates for total mortality, circulatory mortality, and total minus circulatory and respiratory mortality were less than those for respiratory mortality. Ozone (O3) and nitrogen dioxide (NO2) also were associated significantly with total and circulatory mortality, but a simultaneous consideration of these pollutants with PM10 reduced PM10 coefficients only slightly, or even increased them. In these results, pollution coefficients often were positive at multiple lag days (0-day through 3-day lags were examined), but for PM indices, 1-day lag coefficients were most significant. However, when all combinations of multiple-day average exposures were examined, for cases in which multiple lag days were positive, the choice of single-day or multiple-day average exposure did not appreciably change the estimated effect sizes. An examination of temporal correlation showed that the order of spatial uniformity as expressed by the median site-to-site correlation was O3 (0.83), PM10 (0.78), TSP (0.71), NO2 (0.70), carbon monoxide (CO) (0.50), and sulfur dioxide (SO2) (0.49), which suggests less exposure error for O3 and PM10 than for the other measured pollutants. Thus, these results suggest that spatially homogeneous pollution indices show higher associations with measured health outcomes.

Identifying subgroups of the general population that may be susceptible to short-term increases in particulate air pollution: a time-series study in Montreal, Quebec.

This study was undertaken in order to shed light on which groups of the general population may be susceptible to the effects of ambient particles. The objectives of the study were (1) to determine whether concentrations of particles in the ambient air of Montreal, Quebec, were associated with daily all-cause and cause-specific mortality in the period 1984 to 1993, and (2) to determine whether groups of the population had higher than average risks of death from exposure to particles. From the network of fixed-site air pollution monitors in Montreal we obtained daily mean levels of various measures of particles, gaseous pollutants, and weather variables measured at Dorval International Airport. We also used measurements of sulfate from an acid rain monitoring station 150 km southeast of the city (Sutton, Quebec). We estimated associations for particulate matter (PM) with an aerodynamic diameter of 10 microns or smaller (PM10), or 2.5 microns or smaller (PM2.5), total suspended particles (TSP), coefficient of haze (COH), an extinction coefficient, and sulfate. Because substantial data for fine particles were missing, we developed a regression model to predict PM2.5 and to predict sulfate from PM2.5. In the main body of the report, we present results for COH, predicted PM2.5, and sulfate. Detailed results for all pollutants are included in Appendices H through O, which are available on request from Health Effects Institute and from the HEI web site at www.healtheffects.org. To address the first objective, we made use of the underlying causes of death among all 140,939 residents of Montreal who died between 1984 and 1993. We regressed the logarithm of daily counts of cause-specific mortality on the daily mean levels for a variety of measures of particles, accounting for seasonal and subseasonal fluctuations in the mortality time series, overdispersion, and weather factors. To address the second objective, we developed algorithms to define conditions that subjects had prior to death, with the focus on cardiopulmonary diseases. These algorithms were based on information retained on the databases of the universal Quebec Health Insurance Plan (QHIP). The databases include records of all procedures (e.g., type of surgery), physician visits, and consultations carried out by all physicians in Quebec. For persons > or = 65 years and for all recipients of social assistance the prescription database contains records of all pharmaceuticals dispensed (type of medication, dose, quantity). For each group of conditions defined, we used the same statistical model that was used in the analyses of all nonaccidental causes of death. In the analyses of cause-specific mortality, we found evidence of associations for all nonaccidental causes of death and specific causes of death--cancer, coronary artery disease, respiratory diseases, and diabetes--that were consistent across most metrics of ambient air particle concentrations, evaluated as the 3-day mean of particle concentrations measured on the day of death (lag 0) and on each of the two days before death (lag 1, lag 2). Associations for all cardiovascular diseases combined were found only with sulfate. As well, we generally found increased daily mortality for persons 65 years of age and over. The results for all nonaccidental causes of death are similar to findings from other studies; the mean percent increase in mortality for a 100 micrograms/m3 increase in daily TSP at lag 0 was 6.7%. In the analyses of the groups defined from the QHIP data, there was little evidence of associations with air pollutants among persons who before death were classified as having acute or chronic upper respiratory diseases, airways diseases, hypertension, acute coronary artery diseases, and cerebrovascular diseases. On the other hand, we found consistent increases across most types of ambient particles for persons who had cancer, acute lower respiratory diseases, any form of cardiovascular disease, chronic coronary artery diseases, and congestive heart failure. As well, we found an association for individuals who did not have any cardiovascular disease, lower respiratory diseases, and cancer. This latter group consisted of persons who had no interactions with the health care system one year before death (12%) and individuals with a wide variety of potentially fatal diseases (52%), including neurological conditions (12%), diabetes (8%), cardiac dysrhythmias (8%), dementia (6%), organic psychotic disorders (6%), and anemias (4%). As statistical power was reduced in the analyses presented above, differences between groups (e.g., < 65 and > or = 65 year age groups) were not usually statistically significant. The association with diabetes has not been reported previously, and this needs to be replicated in other studies. (ABSTRACT TRUNCATED)

Inhalation toxicology of urban ambient particulate matter: acute cardiovascular effects in rats.

Wistar rats were exposed for 4 hours by nose-only inhalation to clean air, resuspended Ottawa ambient particles (EHC-93*, 48 mg/m3), the water-leached particles (EHC-93L, 49 mg/m3), diesel soot (5 mg/m3), or carbon black (5 mg/m3). Continuous data for physiologic endpoints (heart rate, blood pressure, body temperature, animal's activity) were captured by telemetry before and after exposure. Blood was sampled from jugular cannulas 1 to 3 days before exposure and at 2 and 24 hours after exposure, and by heart puncture on termination at 32 hours (histology group) or 48 hours (telemetry group) after exposure. Lung injury was assessed by 3H-thymidine autoradiography after the rats were killed. We measured endothelins (plasma ET-1, big ET-1, ET-2, ET-3) to assess the vasopressor components; nitric oxide (NO)-related metabolites (blood nitrate, nitrite, nitrosyl compounds, and plasma 3-nitrotyrosine) to assess the vasodilator components; and catecholamines (epinephrine, norepinephrine, L-DOPA, dopamine) and oxidative stressors (m- and o-tyrosine) for additional insight into possible stress components. Lung cell labeling was uniformly low in all treatment groups, which indicates an absence of acute lung injury. Inhalation of EHC-93 caused statistically significant elevations (P < 0.05) of blood pressure on day 2 after exposure, plasma ET-1 at 32 hours after exposure, and ET-3 at 2, 32, and 48 hours after exposure. In contrast, the modified EHC-93L particles, from which soluble components had been extracted, did not affect blood pressure. The EHC-93L particles caused early elevation (P < 0.05) of the plasma levels of ET-1, ET-2, and ET-3 at 2 hours after exposure, but the endothelins returned to basal levels 32 hours after exposure. Exposure to diesel soot, but not carbon black, caused an elevation (P < 0.05) of plasma ET-3 at 36 hours after exposure; blood pressure was not affected by diesel soot. Our results indicate that inhalation of the urban particles EHC-93 can affect blood levels of ET-1 and ET-3 and cause a vasopressor response in Wistar rats without causing acute lung injury. Furthermore, the potency of the particles to influence hemodynamic changes appears to be modified by removing polar organic compounds and soluble elements. Because the pathophysiologic significance of elevated endothelins has been clinically established in humans, our observations suggest a novel mechanism by which inhaled particles may cause cardiovascular effects. These findings in rats contribute to the weight of evidence in favor of a biologically plausible epidemiologic association between ambient particulate matter and cardiovascular morbidity and mortality in human populations.

The effect of the urban ambient air pollution mix on daily mortality rates in 11 Canadian cities.

OBJECTIVE: Determine the risk of premature mortality due to the urban ambient air pollution mix in Canada. METHODS: The number of daily deaths for non-accidental causes were obtained in 11 cities from 1980 to 1991 and linked to concentrations of ambient gaseous air pollutants using relative risk regression models for longitudinal count data. RESULTS: Nitrogen dioxide had the largest effect on mortality with a 4.1% increased risk (p < 0.01), followed by ozone at 1.8% (p < 0.01), sulphur dioxide at 1.4% (p < 0.01), and carbon monoxide at 0.9% (p = 0.04) in multiple pollutant regression models. A 0.4% reduction in premature mortality was attributed to achieving a sulphur content of gasoline of 30 ppm in five Canadian cities, a risk reduction 12 times greater than previously reported. CONCLUSIONS: Ambient air pollution generated from the burning of fossil fuels is a risk factor for premature mortality in 11 Canadian cities.

PIP: The authors investigate "the risk of premature mortality due to the urban ambient air pollution mix in Canada.... Nitrogen dioxide had the largest effect on mortality with a 4.1% increased risk (p0.01), followed by ozone at 1.8% (p0.01), sulphur dioxide at 1.4% (p0.01), and carbon monoxide at 0.9% (p=0.04) in multiple pollutant regression models. A 0.4% reduction in premature mortality was attributed to achieving a sulphur content of gasoline of 30 ppm in five Canadian cities, a risk reduction 12 times greater than previously reported." (EXCERPT)

The costs of cardiorespiratory disease episodes in a study of emergency department use.

OBJECTIVE: The average per person direct cost of illness of cardiorespiratory disease episodes was estimated based on a prospective study of emergency department visits. METHODS: Economic modelling of health care costs using prospectively collected resource utilization data (9/1/94 to 8/31/95) from hospital emergency department visitors assigned a diagnosis of asthma, chronic obstructive pulmonary disease (COPD), respiratory infections or cardiac conditions. RESULTS: The total direct costs (1997 CDN$) [95% C.I.] per patient were $1,043.55 [$922.65, $1,164.47] for asthma, $1,690.11 [$1,276.92, $2,103.30] for COPD, $676.50 [$574.46, $778.54] for respiratory infections, and $3,318.74 [$2,937.72, $3,699.76] for cardiac conditions. CONCLUSIONS: This study showed that on average, patients diagnosed with a cardiac condition had the highest total direct cost. Hospitalization cost was the largest component of costs for all diagnoses except asthma, for which medications were the single largest component of direct costs.

Beyond administrative data: characterizing cardiorespiratory disease episodes among patients visiting the emergency department.

We attempted to address deficiencies in administrative health service data during a study of cardiorespiratory emergency department visits. From 1994-1996, we obtained data on 9,264 visits and conducted 1,772 follow-up interviews. The median interval between symptoms and visit ranged from 0.8 days (95% CI 0-1.7) for cardiac conditions to 4.0 days for chronic obstructive pulmonary disease (COPD) (95% CI 2.7-5.3) and respiratory infections (95% CI 3.5-4.5). Infection was the most common trigger of respiratory visits. Although most had improved at follow-up, symptoms persisted following the visit for a mean of 4.5 days (95% CI 3.8-5.4) for cardiac conditions to 8.4 days (95% CI 7.2-9.5) for COPD. Among adults aged < 70, the mean number of reduced activity days per episode ranged from 4.7 (95% CI 3.9-5.4) for asthma to 6.6 (95% CI 5.9-7.4) for respiratory infections. Our data assist in interpreting epidemiological studies based on administrative data, and illustrate the broad impacts of cardiorespiratory disease episodes.