Spatial analysis of air pollution and mortality in California.

RATIONALE: Although substantial scientific evidence suggests that chronic exposure to ambient air pollution contributes to premature mortality, uncertainties exist in the size and consistency of this association. Uncertainty may arise from inaccurate exposure assessment. OBJECTIVES: To assess the associations of three types of air pollutants (fine particulate matter, ozone [O3], and nitrogen dioxide [NO2]) with the risk of mortality in a large cohort of California adults using individualized exposure assessments. METHODS: For fine particulate matter and NO2, we used land use regression models to derive predicted individualized exposure at the home address. For O3, we estimated exposure with an inverse distance weighting interpolation. Standard and multilevel Cox survival models were used to assess the association between air pollution and mortality. MEASUREMENTS AND MAIN RESULTS: Data for 73,711 subjects who resided in California were abstracted from the American Cancer Society Cancer Prevention II Study cohort, with baseline ascertainment of individual characteristics in 1982 and follow-up of vital status through to 2000. Exposure data were derived from government monitors. Exposure to fine particulate matter, O3, and NO2 was positively associated with ischemic heart disease mortality. NO2 (a marker for traffic pollution) and fine particulate matter were also associated with mortality from all causes combined. Only NO2 had significant positive association with lung cancer mortality. CONCLUSIONS: Using the first individualized exposure assignments in this important cohort, we found positive associations of fine particulate matter, O3, and NO2 with mortality. The positive associations of NO2 suggest that traffic pollution relates to premature death.

Long-term ozone exposure and mortality.

BACKGROUND: Although many studies have linked elevations in tropospheric ozone to adverse health outcomes, the effect of long-term exposure to ozone on air pollution-related mortality remains uncertain. We examined the potential contribution of exposure to ozone to the risk of death from cardiopulmonary causes and specifically to death from respiratory causes. METHODS: Data from the study cohort of the American Cancer Society Cancer Prevention Study II were correlated with air-pollution data from 96 metropolitan statistical areas in the United States. Data were analyzed from 448,850 subjects, with 118,777 deaths in an 18-year follow-up period. Data on daily maximum ozone concentrations were obtained from April 1 to September 30 for the years 1977 through 2000. Data on concentrations of fine particulate matter (particles that are < or = 2.5 microm in aerodynamic diameter [PM(2.5)]) were obtained for the years 1999 and 2000. Associations between ozone concentrations and the risk of death were evaluated with the use of standard and multilevel Cox regression models. RESULTS: In single-pollutant models, increased concentrations of either PM(2.5) or ozone were significantly associated with an increased risk of death from cardiopulmonary causes. In two-pollutant models, PM(2.5) was associated with the risk of death from cardiovascular causes, whereas ozone was associated with the risk of death from respiratory causes. The estimated relative risk of death from respiratory causes that was associated with an increment in ozone concentration of 10 ppb was 1.040 (95% confidence interval, 1.010 to 1.067). The association of ozone with the risk of death from respiratory causes was insensitive to adjustment for confounders and to the type of statistical model used. CONCLUSIONS: In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration of PM(2.5) was taken into account. We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration.

Cardiovascular mortality and exposure to airborne fine particulate matter and cigarette smoke: shape of the exposure-response relationship.

BACKGROUND: Fine particulate matter exposure from both ambient air pollution and secondhand cigarette smoke has been associated with larger risks of cardiovascular mortality than would be expected on the basis of linear extrapolations of the relative risks from active smoking. This study directly assessed the shape of the exposure-response relationship between cardiovascular mortality and fine particulates from cigarette smoke and ambient air pollution. METHODS AND RESULTS: Prospective cohort data for >1 million adults were collected by the American Cancer Society as part of the Cancer Prevention Study II in 1982. Cox proportional hazards regression models that included variables for increments of cigarette smoking and variables to control for education, marital status, body mass, alcohol consumption, occupational exposures, and diet were used to describe the mortality experience of the cohort. Adjusted relative risks of mortality were plotted against estimated average daily dose of fine particulate matter from cigarette smoke along with comparison estimates for secondhand cigarette smoke and air pollution. There were substantially increased cardiovascular mortality risks at very low levels of active cigarette smoking and smaller but significant excess risks even at the much lower exposure levels associated with secondhand cigarette smoke and ambient air pollution. CONCLUSIONS: Relatively low levels of fine particulate exposure from either air pollution or secondhand cigarette smoke are sufficient to induce adverse biological responses increasing the risk of cardiovascular disease mortality. The exposure-response relationship between cardiovascular disease mortality and fine particulate matter is relatively steep at low levels of exposure and flattens out at higher exposures.

Extended follow-up and spatial analysis of the American Cancer Society study linking particulate air pollution and mortality.

We conducted an extended follow-up and spatial analysis of the American Cancer Society (ACS) Cancer Prevention Study II (CPS-II) cohort in order to further examine associations between long-term exposure to particulate air pollution and mortality in large U.S. cities. The current study sought to clarify outstanding scientific issues that arose from our earlier HEI-sponsored Reanalysis of the original ACS study data (the Particle Epidemiology Reanalysis Project). Specifically, we examined (1) how ecologic covariates at the community and neighborhood levels might confound and modify the air pollution-mortality association; (2) how spatial autocorrelation and multiple levels of data (e.g., individual and neighborhood) can be taken into account within the random effects Cox model; (3) how using land-use regression to refine measurements of air pollution exposure to the within-city (or intra-urban) scale might affect the size and significance of health effects in the Los Angeles and New York City regions; and (4) what exposure time windows may be most critical to the air pollution-mortality association. The 18 years of follow-up (extended from 7 years in the original study [Pope et al. 1995]) included vital status data for the CPS-II cohort (approximately 1.2 million participants) with multiple cause-of-death codes through December 31, 2000 and more recent exposure data from air pollution monitoring sites for the metropolitan areas. In the Nationwide Analysis, the influence of ecologic covariate data (such as education attainment, housing characteristics, and level of income; data obtained from the 1980 U.S. Census; see Ecologic Covariates sidebar on page 14) on the air pollution-mortality association were examined at the Zip Code area (ZCA) scale, the metropolitan statistical area (MSA) scale, and by the difference between each ZCA value and the MSA value (DIFF). In contrast to previous analyses that did not directly include ecologic covariates at the ZCA scale, risk estimates increased when ecologic covariates were included at all scales. The ecologic covariates exerted their greatest effect on mortality from ischemic heart disease (IHD), which was also the health outcome most strongly related with exposure to PM2.5 (particles 2.5 microm or smaller in aerodynamic diameter), sulfate (SO4(2-)), and sulfur dioxide (SO2), and the only outcome significantly associated with exposure to nitrogen dioxide (NO2). When ecologic covariates were simultaneously included at both the MSA and DIFF levels, the hazard ratio (HR) for mortality from IHD associated with PM2.5 exposure (average concentration for 1999-2000) increased by 7.5% and that associated with SO4(2-) exposure (average concentration for 1990) increased by 12.8%. The two covariates found to exert the greatest confounding influence on the PM2.5-mortality association were the percentage of the population with a grade 12 education and the median household income. Also in the Nationwide Analysis, complex spatial patterns in the CPS-II data were explored with an extended random effects Cox model (see Glossary of Statistical Terms at end of report) that is capable of clustering up to two geographic levels of data. Using this model tended to increase the HR estimate for exposure to air pollution and also to inflate the uncertainty in the estimates. Including ecologic covariates decreased the variance of the results at both the MSA and ZCA scales; the largest decrease was in residual variation based on models in which the MSA and DIFF levels of data were included together, which suggests that partitioning the ecologic covariates into between-MSA and within-MSA values more completely captures the sources of variation in the relationship between air pollution, ecologic covariates, and mortality. Intra-Urban Analyses were conducted for the New York City and Los Angeles regions. The results of the Los Angeles spatial analysis, where we found high exposure contrasts within the Los Angeles region, showed that air pollution-mortality risks were nearly 3 times greater than those reported from earlier analyses. This suggests that chronic health effects associated with intra-urban gradients in exposure to PM2.5 may be even larger between ZCAs within an MSA than the associations between MSAs that have been previously reported. However, in the New York City spatial analysis, where we found very little exposure contrast between ZCAs within the New York region, mortality from all causes, cardiopulmonary disease (CPD), and lung cancer was not elevated. A positive association was seen for PM2.5 exposure and IHD, which provides evidence of a specific association with a cause of death that has high biologic plausibility. These results were robust when analyses controlled (1) the 44 individual-level covariates (from the ACS enrollment questionnaire in 1982; see 44 Individual-Level Covariates sidebar on page 22) and (2) spatial clustering using the random effects Cox model. Effects were mildly lower when unemployment at the ZCA scale was included. To examine whether there is a critical exposure time window that is primarily responsible for the increased mortality associated with ambient air pollution, we constructed individual time-dependent exposure profiles for particulate and gaseous air pollutants (PM2.5 and SO2) for a subset of the ACS CPS-II participants for whom residence histories were available. The relevance of the three exposure time windows we considered was gauged using the magnitude of the relative risk (HR) of mortality as well as the Akaike information criterion (AIC), which measures the goodness of fit of the model to the data. For PM2.5, no one exposure time window stood out as demonstrating the greatest HR; nor was there any clear pattern of a trend in HR going from recent to more distant windows or vice versa. Differences in AIC values among the three exposure time windows were also small. The HRs for mortality associated with exposure to SO2 were highest in the most recent time window (1 to 5 years), although none of these HRs were significantly elevated. Identifying critical exposure time windows remains a challenge that warrants further work with other relevant data sets. This study provides additional support toward developing cost-effective air quality management policies and strategies. The epidemiologic results reported here are consistent with those from other population-based studies, which collectively have strongly supported the hypothesis that long-term exposure to PM2.5 increases mortality in the general population. Future research using the extended Cox-Poisson random effects methods, advanced geostatistical modeling techniques, and newer exposure assessment techniques will provide additional insight.

Syndromic surveillance for influenzalike illness.

Emergency department data are currently being used by several syndromic surveillance systems to identify outbreaks of natural or man-made illnesses, and preliminary results suggest that regular outbreaks might be detected earlier with such data than with traditional reporting. This article summarizes a retrospective study of 5 influenza seasons in Ottawa,Canada; time-series analysis was used to look for an association between consultation to the emergency department for influenzalike illness and the isolation of influenza virus in the community. The population studied included both children and adults consulting to 3 local hospitals. In 4 seasons, visits to the emergency department involving children younger than 5 years consulting mainly for fever and for respiratory symptoms peaked 1 to 4 weeks before the isolation of influenza virus in the community. If monitored regularly for the presence of key symptoms, pediatric hospitals might be efficient and cost-effective sentinels of influenza and of other infectious diseases.

Ischemic Heart Disease Mortality and Long-Term Exposure to Source-Related Components of U.S. Fine Particle Air Pollution.

BACKGROUND: Fine particulate matter (PM2.5) air pollution exposure has been identified as a global health threat. However, the types and sources of particles most responsible are not yet known. OBJECTIVES: We sought to identify the causal characteristics and sources of air pollution underlying past associations between long-term PM2.5 exposure and ischemic heart disease (IHD) mortality, as established in the American Cancer Society's Cancer Prevention Study-II cohort. METHODS: Individual risk factor data were evaluated for 445,860 adults in 100 U.S. metropolitan areas followed from 1982 through 2004 for vital status and cause of death. Using Cox proportional hazard models, we estimated IHD mortality hazard ratios (HRs) for PM2.5, trace constituents, and pollution source-associated PM2.5, as derived from air monitoring at central stations throughout the nation during 2000-2005. RESULTS: Associations with IHD mortality varied by PM2.5 mass constituent and source. A coal combustion PM2.5 IHD HR = 1.05 (95% CI: 1.02, 1.08) per microgram/cubic meter, versus an IHD HR = 1.01 (95% CI: 1.00, 1.02) per microgram/cubic meter PM2.5 mass, indicated a risk roughly five times higher for coal combustion PM2.5 than for PM2.5 mass in general, on a per microgram/cubic meter PM2.5 basis. Diesel traffic-related elemental carbon (EC) soot was also associated with IHD mortality (HR = 1.03; 95% CI: 1.00, 1.06 per 0.26-µg/m3 EC increase). However, PM2.5 from both wind-blown soil and biomass combustion was not associated with IHD mortality. CONCLUSIONS: Long-term PM2.5 exposures from fossil fuel combustion, especially coal burning but also from diesel traffic, were associated with increases in IHD mortality in this nationwide population. Results suggest that PM2.5-mortality associations can vary greatly by source, and that the largest IHD health benefits per microgram/cubic meter from PM2.5 air pollution control may be achieved via reductions of fossil fuel combustion exposures, especially from coal-burning sources. CITATION: Thurston GD, Burnett RT, Turner MC, Shi Y, Krewski D, Lall R, Ito K, Jerrett M, Gapstur SM, Diver WR, Pope CA III. 2016. Ischemic heart disease mortality and long-term exposure to source-related components of U.S. fine particle air pollution. Environ Health Perspect 124:785-794; http://dx.doi.org/10.1289/ehp.1509777.

Association between gaseous ambient air pollutants and adverse pregnancy outcomes in Vancouver, Canada.

The association between ambient air pollution and adverse health effects, such as emergency room visits, hospitalizations, and mortality from respiratory and cardiovascular diseases, has been studied extensively in many countries, including Canada. Recently, studies conducted in China, the Czech Republic, and the United States have related ambient air pollution to adverse pregnancy outcomes. In this study, we examined association between preterm birth, low birth weight, and intrauterine growth retardation (IUGR) among singleton live births and ambient concentrations of sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone in Vancouver, Canada, for 1985-1998. Multiple logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for such effects. Low birth weight was associated with exposure to SO2 during the first month of pregnancy (OR = 1.11, 95% CI, 1.01-1.22, for a 5.0 ppb increase). Preterm birth was associated with exposure to SO2 (OR = 1.09, 95% CI, 1.01-1.19, for a 5.0 ppb increase) and to CO (OR = 1.08, 95% CI, 1.01-1.15, for a 1.0 ppm increase) during the last month of pregnancy. IUGR was associated with exposure to SO2 (OR = 1.07, 95% CI, 1.01-1.13, for a 5.0 ppb increase), to NO2 (OR = 1.05, 95% CI, 1.01-1.10, for a 10.0 ppb increase), and to CO (OR = 1.06, 95% CI, 1.01-1.10, for a 1.0 ppm increase) during the first month of pregnancy. In conclusion, relatively low concentrations of gaseous air pollutants are associated with adverse effects on birth outcomes in populations experiencing diverse air pollution profiles.

A time-series study of air pollution, socioeconomic status, and mortality in Vancouver, Canada.

We evaluated the relationship between daily levels of particulate and gaseous phase pollutants and mortality within a dynamic cohort of approximately 550,000 individuals whose vital status was ascertained between 1986 and 1999. Time-series methods were applied to evaluate whether there were differential pollutant effects on daily aggregated numbers of deaths in the cohort that was stratified into quintiles of income as defined by the 1991 and 1996 Canadian censuses. The percent change in all-cause, cardiovascular, respiratory, and cancer daily mortality was calculated in relation to short-term changes in levels of a number of particulate (PM(2.5), PM(10-2.5), total suspended particle co-efficient of haze PM(10), SO(4)) and gaseous (O(3), CO, SO(2), NO(2)) pollutants. The estimated effects of air pollution on mortality were adjusted for day of week effects, and several meteorologic variables including temperature, change in barometric pressure, and relative humidity. Several gaseous pollutants were associated with an increased risk of mortality. Specifically for an increase equivalent to the difference between the 90th and 10th percentiles, the estimated percent change in daily mortality based on the 3-day average of NO(2), and SO(2) was 4.0% and 1.3%, respectively. The corresponding changes in mortality associated with SO(2) were much higher when analyses were restricted to death from respiratory disease. Specifically, a difference between the 90th and 10th percentiles was associated with a 5.6% (95% CI= -0.7% to 12.3%). The daily mean coarse fraction (PM(10-2.5)) was associated with increased cardiovascular mortality (estimated change=5.9%, 95% CI=1.1-10.8%). PM(2.5) was not found to be an important predictor of mortality. For NO(2), CO, and SO(2), there was some suggestion of increased risk of all-cause and cardiovascular mortality at lower levels of socioeconomic status. However, these results should be interpreted cautiously due to the small number of deaths observed within each stratum of socioeconomic status.

Controlling for potential confounding by occupational exposures.

Occupational exposure is an important potential confounder in air pollution studies because it is plausible that individuals who live in highly polluted areas also work in more polluted environments. While the original investigators made some efforts to control for possible confounding by occupational variables, it was felt that these could be improved upon. The reanalysis team attempted to control for occupational confounding by supplementing the original data sets with two new variables, an indicator of the "dirtiness" of a subject's job and an indicator of possible exposure to occupational lung carcinogens. The attribution of these variables was based on the job title recorded by the original investigators and on the judgment of our experts concerning typical exposure patterns in different occupations. We fitted Cox proportional-hazards models identical to those that had been used by the original investigators while also including one or both of the new occupational covariates in the models. In none of the analyses did the inclusion of the occupational variables materially change the results. It would therefore appear that, in general, the results reported by the original investigators were not distorted by inadequate control of occupational variables. We also carried out some analyses using the dirtiness index as a stratification variable to assess effect modification. There was some indication, albeit inconsistent, that the effect of air pollution on mortality was greater among subjects with dirty jobs than among those with clean jobs.

Association between particulate air pollution and first hospital admission for childhood respiratory illness in Vancouver, Canada.

In this study, the authors assessed the impact of particulate air pollution on first respiratory hospitalization. Study subjects were children less than 3 years of age living in Vancouver, British Columbia, who had their first hospitalization as a result of any respiratory disease (ICD-9 codes 460-519) during the period from June 1, 1995, to March 31, 1999. The authors used logistic regression to estimate the associations between ambient concentrations of particulate matter (PM) and first hospitalization. The adjusted odds ratios for first respiratory hospitalization associated with mean and maximal PM10-2.5 with a lag of 3 days were 1.12 (95% confidence interval: 0.98, 1.28) and 1.13 (1.00, 1.27). After adjustment for gaseous pollutants, the corresponding odds ratios were 1.22 (1.02, 1.48) and 1.14 (0.99, 1.32). The data indicated the possibility of harmful effects from coarse PM on first hospitalization for respiratory disease in early childhood.

Association between maternal exposure to ambient air pollutants during pregnancy and fetal growth restriction.

Previous research demonstrated consistent associations between ambient air pollution and emergency room visits, hospitalizations, and mortality. Effect of air pollution on perinatal outcomes has recently drawn more attention. We examined the association between intrauterine growth restriction (IUGR) among singleton term live births and sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), ozone (O3), and fine particles (PM2.5) present in ambient air in the Canadian cities of Calgary, Edmonton, and Montreal for the period 1985-2000. Multiple logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for IUGR, based on average daily levels of individual pollutants over each month and trimester of pregnancy after adjustment for maternal age, parity, infant gender, season, and city of residence. A 1 ppm increase in CO was associated with an increased risk of IUGR in the first (OR=1.18; 95% CI 1.14-1.23), second (OR=1.15; 95% CI 1.10-1.19) and third (OR=1.19; 95% CI 1.14-1.24) trimesters of pregnancy, respectively. A 20 ppb increase in NO2 (OR=1.16; 95% CI 1.09-1.24; OR=1.14; 95% CI 1.06--1.21; and OR=1.16; 95% CI 1.09-1.24 in the first, second, and third trimesters) and a 10 mug/m3 increase in PM2.5 (OR=1.07; 95% CI 1.03-1.10; OR=1.06; 95% CI 1.03-1.10; and OR=1.06; 95% CI 1.03-1.10) were also associated with an increased risk of IUGR. Consistent results were found when ORs were calculated by month rather than trimester of pregnancy. Our findings add to the emerging body of evidence that exposure to relatively low levels of ambient air pollutants in urban areas during pregnancy is associated with adverse effects on fetal growth.

Effect of short-term exposure to low levels of gaseous pollutants on chronic obstructive pulmonary disease hospitalizations.

We examined the associations between gaseous pollutants and hospitalization for chronic obstructive pulmonary diseases (COPD) among elderly people living in Vancouver, British Columbia, Canada, a city in which ambient air pollution levels are relatively low. We regressed the logarithm of daily counts of acute COPD hospitalization during the 5-year period from 1994 to 1998 on the daily mean levels of each pollutant, after accounting for seasonal and subseasonal fluctuations, non-Poisson dispersion, and weather variables. Nitrogen dioxide and carbon monoxide were significantly associated with hospitalization for COPD, and the magnitude of effects was increased slightly with increasing days of exposure averaging, with the relative risk for a 7-day average being 1.11 (95%CI: 1.04, 1.20) and 1.08 (1.02, 1.13) for nitrogen dioxide and carbon monoxide, respectively. There was no significant association between either sulfur dioxide or ozone and COPD hospitalization. The combined relative risk for all four gaseous pollutants on COPD hospitalization was 1.21. The effects of gaseous pollutants on COPD hospitalization were not significant after adjustment for PM(10), although its inclusion did not have a marked effect on the point estimates for relative risks. Nitrogen dioxide has a significant impact on COPD hospitalization. Further studies are needed to separate the effects of single pollutants from the combined effects of the complex mixture of air pollutants in urban atmospheres.

The effect of coarse ambient particulate matter on first, second, and overall hospital admissions for respiratory disease among the elderly.

The objective of this article is to examine differences in the effect of ambient particulate matter on first, second, and overall hospital admissions for respiratory disease among the elderly. We studied 8989 adults 65 yr of age or older living in the greater Vancouver area who were admitted to hospital for any acute respiratory disease (ICD-9 codes 460-519) between June 1, 1995, and March 31, 1999. Time-series analysis was used to evaluate the association between respiratory admissions and daily measures of particulate matter (PM10, PM2.5, and PM10 - 2.5) in urban air, after adjustment for gaseous copollutants (CO, O3, NO2, and SO2) and meteorological variables. Repeated admissions for respiratory disease were common among the elderly. Approximately 30% of the subjects were readmitted to hospital after the first admission; 9% had more than 2 admissions for respiratory disease during the 4-yr study period. PM10 - 2.5 was significantly associated with the second and overall admissions for respiratory disease, but not with the first admission. The adjusted relative risks for an increment of 4.2 microg/m(3) in -day average PM10 - 2.5 concentrations were 1.03 (95% confidence interval: 0.98-1.09) for the first admission, 1.22 (1.10-1.36) for the second admission, and 1.06 (1.02, 1.11) for overall admissions. There was no significant association between PM2.5 and hospital admissions for respiratory disease among the elderly. Our data suggest that (1) people with a history of respiratory admissions are at a higher risk of respiratory disease in relation to particulate air pollution in urban areas, (2) analyses based on overall rather than repeated hospital admissions lead to lower estimates of the risk of respiratory disease associated with particulate air pollution, and (3) PM10 - 2.5 has a larger effect on respiratory admissions than PM2.5.

Spatial analysis of air pollution and mortality in Los Angeles.

BACKGROUND: The assessment of air pollution exposure using only community average concentrations may lead to measurement error that lowers estimates of the health burden attributable to poor air quality. To test this hypothesis, we modeled the association between air pollution and mortality using small-area exposure measures in Los Angeles, California. METHODS: Data on 22,905 subjects were extracted from the American Cancer Society cohort for the period 1982-2000 (5,856 deaths). Pollution exposures were interpolated from 23 fine particle (PM2.5) and 42 ozone (O3) fixed-site monitors. Proximity to expressways was tested as a measure of traffic pollution. We assessed associations in standard and spatial multilevel Cox regression models. RESULTS: After controlling for 44 individual covariates, all-cause mortality had a relative risk (RR) of 1.17 (95% confidence interval=1.05-1.30) for an increase of 10 mug/m PM2.5 and a RR of 1.11 (0.99-1.25) with maximal control for both individual and contextual confounders. The RRs for mortality resulting from ischemic heart disease and lung cancer deaths were elevated, in the range of 1.24-1.6, depending on the model used. These PM results were robust to adjustments for O3 and expressway exposure. CONCLUSION: Our results suggest the chronic health effects associated with within-city gradients in exposure to PM2.5 may be even larger than previously reported across metropolitan areas. We observed effects nearly 3 times greater than in models relying on comparisons between communities. We also found specificity in cause of death, with PM2.5 associated more strongly with ischemic heart disease than with cardiopulmonary or all-cause mortality.

Influence of relatively low level of particulate ar pollution on hospitalization for COPD in elderly people.

To assess the association between relatively low levels of size-fractioned particulate matter (PM) and hospitalization for chronic obstructive pulmonary disease (COPD), we conducted a time-series analysis among elderly people 65 yr of age or more living in Vancouver between June 1995 and March 1999. Measures of thoracic PM (PM(10)), fine PM (PM(2.5)), coarse PM (PM(10-2.5)), and coefficient of haze (COH) were examined over periods varying from 1 to 7 days prior to hospital admissions. Generalized additive models (GAMs; general linear models, GLMs) were used, and temporal trends and seasonal and subseasonal cycles in COPD hospitalizations were removed by using GLM with parametric natural cubic splines. The relative risks were calculated based on an incremental exposure corresponding to the interquartile range of these measures, and were adjusted for daily weather conditions and gaseous pollutants. PM measures had a positive effect on COPD hospitalization, especially 0 to 2 days prior to the admissions, before copollutants were accounted for. For 3-day average levels of exposure the relative risk estimates were 1.13 (95% confidence interval: 1.05-1.21) for PM(10), 1.08 (1.02-1.15) for PM(2.5), 1.09 (1.03-1.16) for PM(10-2.5), and 1.05 (1.01-1.09) for COH. The associations were no longer significant when NO(2) was included in the models. We concluded that the particle-related measures were significantly associated with COPD hospitalization in the Vancouver area, where the level of air pollution is relatively low, but the effects were not independent of other air pollutants.

Association between ozone and respiratory admissions among children and the elderly in Vancouver, Canada.

In this study, we examine the impact of ozone on daily respiratory admissions in both young children and the elderly in greater Vancouver, British Columbia. Study subjects included children less than 3 yr of age and adults 65 yr of age or over living in greater Vancouver who had acute hospital admissions for any respiratory diseases (ICD-9 codes 460-519) during the 13-yr period 1986-1998. Bidirectional case-crossover analysis was used to investigate associations between ambient ozone and respiratory hospitalizations after adjustment for other pollutants, including carbon monoxide, nitrogen dioxide, sulfur dioxide, and coefficient of haze. Potential effect modification by socioeconomic status as measured by household income was also examined. Respiratory admissions were associated with ozone levels 2, 3, 4, and 5 days prior to admission in both children and the elderly, with the strongest association observed at a lag of 4 days. Odds ratios for hospital admission of 1.22 (95% CI: 1.15-1.30) for children and 1.13 (1.09-1.18) for the elderly, respectively, were found, based on an increment in exposure corresponding to the interquartile range for ozone. Adjusting for other pollutants did not attenuate the ozone effect on respiratory admissions. Nor did socioeconomic status appear to modify the association between ozone and respiratory admissions in either children or the elderly. We concluded that ambient ozone is positively associated with respiratory hospital admission among young children and the elderly in Vancouver, British Columbia. These associations persisted after adjustment for both copollutant exposures and socioeconomic status.