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Residence in urban areas with much traffic has been associated with various negative health effects. However, the contribution of traffic emissions to these adverse health effects has not been fully determined. Therefore, the objective of this in vivo study is to compare the pulmonary and systemic responses of rats exposed to particulate matter (PM) obtained from various locations with contrasting traffic profiles. Samples of coarse (2.5 microm-10 microm) and fine (0.1 microm-2.5 microm) PM were simultaneously collected at nine sites across Europe with a high-volume cascade impactor. Six PM samples from various locations were selected on the basis of contrast in in vitro analysis, chemical composition, and traffic profiles. We exposed spontaneously hypertensive (SH) rats to a single dose (3 mg PM/kg body weight or 10 mg PM/kg body weight) of either coarse or fine PM by intratracheal instillation. We assessed changes in biochemical markers, cell differentials, and histopathological changes in the lungs and blood 24 h postexposure. The dose-related adverse effects that both coarse and fine PM induced in the lungs and vascular system were mainly related to cytotoxicity, inflammation, and blood viscosity. We observed clear differences in the extent of these responses to PM from the various locations at equivalent dose levels. There was a trend that suggests that samples from high-traffic sites were the most toxic. It is likely that the toxicological responses of SH rats were associated with specific PM components derived from brake wear (copper and barium), tire wear (zinc), and wood smoke (potassium).

We investigated the cytotoxic and inflammatory activities of size-segregated particulate samples (particulate matter, PM) from contrasting air pollution situations in Europe. Coarse (PM10-2.5), fine (PM2.5-0.2), and ultrafine (PM0.2) particulate samples were collected with a modified Harvard high-volume cascade impactor (HVCI). Mouse RAW 264.7 macrophages were exposed to the samples for 24 h. Selected inflammatory mediators, nitric oxide (NO) and cytokines (tumor necrosis factor alpha [TNFalpha], interleukin 6 [IL-6], macrophage inflammatory protein-2 [MIP-2]), were measured together with cytotoxicity (MTT test), and analysis of apoptosis and cell cycle (propidium iodide staining). The PM10-2.5 samples had a much higher inflammatory activity than the PM2.5-0.2 and PM0.2 samples, but the PM2.5-0.2 samples showed the largest differences in inflammatory activity, and the PM0.2 samples in cytotoxicity, between the sampling campaigns. The PM2.5-0.2 samples from traffic environments in springtime Barcelona and summertime Athens had the highest inflammatory activities, which may be related to the high photochemical activity in the atmosphere during the sampling campaigns. The PM0.2 sample from wintertime Prague with proven impacts from local coal and biomass combustion had very high cytotoxic and apoptotic activities and caused a distinct cell cycle arrest. Thus, particulate size, sources, and atmospheric transformation processes affect the toxicity profile of urban air particulate matter. These factors may explain some of the heterogeneity observed in particulate exposure-response relationships of human health effects in epidemiological studies.

This article provides an overview of recent U.S. cohort studies on air pollution and health and discusses design issues related to the study hypothesis, exposure assessment, confounder assessment, and effect modification. The article argues that, given the potential long-term effects of air pollution on survival and the enormous costs of achieving further air pollution reductions, it would be shortsighted not to invest in new cohort studies to address unresolved scientific questions. In addition, following the examples of Sweden, the Netherlands, and Germany, the use of geographical information systems is recommended to assess exposure to air pollutants at the address rather than the community level.

Epidemiologic work conducted over several decades has suggested that long-term residence in cities with elevated ambient levels of air pollution from combustion sources is associated with increased mortality. Subsequently, two prospective cohort studies, the Six Cities Study (as reported in Dockery et al., 1993) and the American Cancer Society (ACS) Study (as reported in Pope et al., 1995), estimated that annual average all-cause mortality increased in association with an increase in fine particles (all particles less than 2.5 µm in median aerodynamic diameter [PM2.5]). As part of the Six Cities Study, Dockery and colleagues (1993) had prospectively followed a cohort of 8111 adult subjects in the northeastern and midwestern United States for 14 to 16 years beginning in the mid-1970s. The authors found that higher ambient levels of fine particles and sulfate (SO ) were associated with a 26% increase in mortality from all causes when comparing the most polluted to the least polluted city and that an increase in fine particles was also associated with increased mortality from cardiopulmonary disease. The relative risks in all-cause mortality were associated with a difference (or range) in ambient fine particle concentrations of 18.6 µg/m 3 and a difference of ambient sulfate concentrations of 8.0 µg/m 3 , comparing the least polluted city to the most polluted city.

We studied the association of daily mortality with short-term variations in the ambient concentrations of major gaseous pollutants and PM in the Netherlands. The magnitude of the association in the four major urban areas was compared with that in the remainder of the country. Daily cause-specific mortality counts, air quality, temperature, relative humidity, and influenza data were obtained from 1986 to 1994. The relationship between daily mortality and air pollution was modeled using Poisson regression analysis. We adjusted for potential confounding due to long-term and seasonal trends, influenza epidemics, ambient temperature and relative humidity, day of the week, and holidays, using generalized additive models. Influenza episodes were associated with increased mortality up to 3 weeks later. Daily mortality was significantly associated with the concentration of all air pollutants. An increase in the PM10 concentration by 100 micrograms/m3 was associated with a relative risk (RR) of 1.02 for total mortality. The largest RRs were found for pneumonia deaths. Ozone had the most consistent, independent association with mortality. Particulate air pollution (e.g., PM10, black smoke [BS]) was not more consistently associated with mortality than were the gaseous pollutants SO2 and NO2. Aerosol SO4(-2), NO3-, and BS were more consistently associated with total mortality than was PM10. The RRs for all pollutants were substantially larger in the summer months than in the winter months. The RR of total mortality for PM10 was 1.10 for the summer and 1.03 for the winter. There was no consistent difference between RRs in the four major urban areas and the more rural areas.

(2000). Session 2: What Properties of Particulate Matter are Responsible for Health Effects? Inhalation Toxicology: Vol. 12, No. sup1, pp. 15-18.

To investigate the validity of ambient fine-particle concentrations as a measure of exposure in epidemiological time-series studies, we established the association between personal and ambient concentrations, within subjects, over time. We conducted repeated measurements of personal and ambient fine-particle concentrations in 13 children who lived in Wageningen, The Netherlands. For each child separately, we related personal exposures to ambient concentrations in a regression analysis. The median Pearson's correlation coefficient was 0.86. Personal fine-particle concentrations were also highly correlated with ambient particulate matter (i.e., < or = 10-microm) concentrations (median Pearson's correlation coefficient = .75). Personal fine-particle concentrations were typically approximately 11 microg/m3 higher than ambient concentrations. We excluded measurements of children who were exposed to environmental tobacco smoke, and the difference was only 5 microg/m3. The findings of high correlations between personal fine-particle concentrations and both ambient fine-particle concentrations and particulate matter (i.e., < or = 10-microm) found in this group of children provide support for investigators to use ambient particulate matter concentrations to measure exposure to fine-particle concentrations in epidemiological time-series studies.

Elevated concentrations of nitrogen dioxide (NO{sub 2}) are produced in the home by the use of unvented gas appliances. In studies on potential health effects of indoor exposure to NO{sub 2}, exposure has mostly been estimated from the presence or absence of sources like gas cookers in the home. This leads to misclassification of exposure, as NO{sub 2} concentrations in the home depend also on source use, ventilation habits, time budgets, etc. The availability of cheap, passive monitoring devices has made it possible to measure indoor concentrations of NO{sub 2} directly in health effects studies, albeit with averaging times of one to several days. So far, it has not been evaluated whether this increases the sensitivity of a study to detect health effects of NO{sub 2}. In this paper, a comparison is made between NO{sub 2} sources and weekly average indoor NO{sub 2} measurements, as predictors of pulmonary function in a study among children aged 6-12 years. The relationship between exposure and lung functions was found to be generally non-significant in this study. The results further suggested that in this study, measuring indoor NO{sub 2} concentrations with passive monitors offered no advantage over the simple use of source presence asmore » exposure variable.« less