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PubMed2002

Personal exposure monitoring of particulate matter, nitrogen dioxide, and carbon monoxide, including susceptible groups.

AIMS: To investigate the relation between personal exposures to nitrogen dioxide, carbon monoxide, and PM(10), and exposures estimated from static concentrations of these pollutants measured within the same microenvironments, for healthy individuals and members of susceptible groups. METHODS: Eleven healthy adult subjects and 18 members of groups more susceptible to adverse health changes in response to a given level of exposure to nitrogen dioxide, carbon monoxide, and/or PM(10) than the general population (six schoolchildren, six elderly subjects, and six with pre-existing disease-two with chronic obstructive pulmonary disease (COPD), two with left ventricular failure (LVF), and two with severe asthma) were recruited. Daytime personal exposures were determined either directly or through shadowing. Relations between personal exposures and simultaneously measured microenvironment concentrations were examined. RESULTS: Correlations between personal exposures and microenvironment concentration were frequently weak for individual subjects because of the small range in measured concentrations. However, when all subjects were pooled, excellent relations between measured personal exposure and microenvironment concentration were found for both carbon monoxide and nitrogen dioxide, with slopes of close to one and near zero intercepts. For PM(10), a good correlation was also found with an intercept of personal exposure (personal cloud) of 16.7 (SD 10.4) micro g/m(3). Modelled and measured personal exposures were generally in reasonably good agreement, but modelling with generic mean microenvironment data was unable to represent the full range of measured concentrations. CONCLUSIONS: Microenvironment measurements of carbon monoxide and nitrogen dioxide can well represent the personal exposures of individuals within that microenvironment. The same is true for PM(10) with the addition of a personal cloud increment. Elderly subjects and those with pre-existing disease received generally lower PM(10) exposures than the healthy adult subjects and schoolchildren by virtue of their less active lifestyles.

Adult↗
PubMedDate not supplied

Ontario Medical Association position paper on health effects of ground-level ozone, acid aerosols and particulate matter.

This review of the evidence of the health effects of air pollutants focuses on research conducted in Ontario. Seven key Ontario studies are cited. These findings are highly significant for people living in the Great Lakes basin (and particularly the Windsor-Quebec corridor), where high levels of certain air pollutants (eg, ground-level ozone and ultra-fine particles) occur more frequently than in other parts of Canada. The issue is a serious one, requiring an integrated and comprehensive approach by many stakeholders, including the active involvement of organized medicine. It is important that the health effects of these air pollutants are understood. Governments must act to reduce emission levels through statue and regulation bolstered by noncompliance penalties. The findings of research have included the following: in a Toronto study, a 2% to 4% excess of respiratory deaths were attributable to pollutant levels; children living in rural Ontario communities with the highest levels of airborne acids were significantly more likely to report at least one episode of bronchitis, as well as to show decreases in lung function; and have been linked to increases in pollutants, emergency room visits and hospitalizations in Ontario. Every Ontarian is affected by air pollutants, although he or she may be unaware of the asymptomatic effects such as lung and bronchial inflammation. This health problem is preventable; while physicians know of the adverse health impacts of air pollution and they are concerned, individually they now focus on the treatment of symptoms. The major recommendations of the report are as follows: Enactment of more stringent sulphur and nitrogen oxide emission limits, including a provincewide sulphur dioxide reduction of 75% from current cap levels, and the maximum allowable nitrogen oxides emission limits of 6000 tonnes annually from Ontario Hydro. New transportation sector emission limits that should include California-level standards for light and heavy duty vehicles, reductions from off-road engines, an expanded vehicle inspection and maintenance program, and tougher standards for sulphur-in-fuel content. Petitioning the United States Environmental Protection Agency administrator under Section 115 of the United States Clear Air Act to require reductions in the American emission of sulphur dioxide and nitrogen oxides, which damage the health of Canadian residents and their environment. Physician advice to patients about the risks of smog exposure, physician support for more health effects research on air pollution, and physician promotion of the development of air pollution-related health education materials. The recommendations discussed in this paper will, if acted upon, lead to a significant reduction in the overall burden of illness from air pollutants, especially in children and the elderly. These recommendations have been selected from a review of recommendations made by various authorities, and are those that the OMA feels a particular responsibility to support.

Aerosols↗
PubMed2002

Interaction of alveolar macrophages and airway epithelial cells following exposure to particulate matter produces mediators that stimulate the bone marrow.

Exposure to ambient air pollution particles with a diameter of < 10 microm (PM(10)) has been associated with increased cardiopulmonary morbidity and mortality. We postulate that these adverse health effects are related to proinflammatory mediators produced in the lung and released into the circulation where they initiate a systemic inflammatory response. The present study was designed to determine if alveolar macrophages (AMs) and primary human bronchial epithelial cells (HBECs) interact to amplify the production of certain cytokines when exposed to ambient PM(10) (EHC-93). Candidate cytokines were measured at the mRNA level using a RNase protection assay and at the protein level by enzyme-linked immunosorbent assay (ELISA). When AM/HBEC cocultures were exposed to 100 microg/ml of PM(10), levels of tumor necrosis factor (TNF)-alpha, granulocyte macrophage colony stimulating factor (GM-CSF), interleukin (IL)-1beta, IL-6, leukemia inhibitory factor (LIF), oncostatin M (OSM), and IL-8 mRNA increased within 2 h (P < 0.05) and 8 h following exposure compared with control cells. GM-CSF mRNA expression was more rapidly induced in cocultured cells compared with HBECs or AMs alone. The concentrations of TNF-alpha, GM-CSF, IL-1beta, IL-6, and IL-8 in the cocultured supernatants collected after 24 h PM(10) exposure increased significantly compared with control cells. There was a significant synergistic effect between AMs and HBECs in the production of GM-CSF and of IL-6 (P < 0.05). Instillation of supernatants from HBECs cultured with PM(10) into lungs of rabbits failed to increase circulating band cell counts or stimulate the bone marrow. However, those from AM/HBEC cocultures exposed to PM(10) increased circulating band cell counts (P < 0.05) and shortened the transit time of polymorphonuclear leukocytes (PMNs) through the bone marrow compared with control co-cultures (P < 0.01). These results suggest that the interaction between AMs and HBECs during PM(10) exposure contributes to the production of mediators that induce a systemic inflammatory response.

Air Pollutants↗
PubMed2003

Particulate matter, sulfur dioxide, and daily mortality in Chongqing, China.

In 1995, daily mortality in a district of Chongqing, China, was analyzed from January through December for associations with daily ambient sulfur dioxide and fine particles (airborne particles with diameters less than or equal to 2.5 microm; PM2.5. The mean concentration of PM2.5 was 147 microg/m3 (maximum, 666 microg/m3), and that of SO2 was 213 microg/m3 (maximum, 571 microg/m3). On average, 9.6 persons died each day. We used a generalized additive model using robust Poisson regression to estimate the associations of mean daily SO2 and PM2.5 with daily mortality (on the same day and at lags up to 5 days) adjusted for trend, season, temperature, humidity, and day of the week. The relative risk of mortality associated with a 100 microg/m3 increase in mean daily SO2 was highest on the second lag day [1.04; 95% confidence interval (CI), 1.00-1.09] and the third lag day (1.04; 95% CI, 0.99-1.08). The associations between daily mortality and mean daily PM2.5 were negative and statistically insignificant on all days. The relative risk of respiratory mortality on the second day after a 100 microg/m3 increase in mean daily SO2 was 1.11 (95% CI, 1.02-1.22), and that for cardiovascular mortality was 1.10 (95% CI, 1.02-1.20). The relative risk of cardiovascular mortality on the third day after a 100 microg/m3 increase in mean daily SO2 was 1.20 (95% CI, 1.11-1.30). The relative risks of mortality due to cancer and other causes were insignificant on both days. The estimated effects of mean daily SO2 on cardiovascular and respiratory mortality risk remained after controlling for PM2.5.

Adolescent↗
PubMed2005

Estimating the exposure-response relationships between particulate matter and mortality within the APHEA multicity project.

Several studies have reported significant health effects of air pollution even at low levels of air pollutants, but in most of theses studies linear nonthreshold relations were assumed. We investigated the exposure-response association between ambient particles and mortality in the 22 European cities participating in the APHEA (Air Pollution and Health--A European Approach) project, which is the largest available European database. We estimated the exposure-response curves using regression spline models with two knots and then combined the individual city estimates of the spline to get an overall exposure-response relationship. To further explore the heterogeneity in the observed city-specific exposure-response associations, we investigated several city descriptive variables as potential effect modifiers that could alter the shape of the curve. We conclude that the association between ambient particles and mortality in the cities included in the present analysis, and in the range of the pollutant common in all analyzed cities, could be adequately estimated using the linear model. Our results confirm those previously reported in Europe and the United States. The heterogeneity found in the different city-specific relations reflects real effect modification, which can be explained partly by factors characterizing the air pollution mix, climate, and the health of the population.

Air Pollutants↗
PubMed2005

GIS-based estimation of exposure to particulate matter and NO2 in an urban area: stochastic versus dispersion modeling.

Stochastic modeling was used to predict nitrogen dioxide and fine particles [particles collected with an upper 50% cut point of 2.5 microm aerodynamic diameter (PM2.5)] levels at 1,669 addresses of the participants of two ongoing birth cohort studies conducted in Munich, Germany. Alternatively, the Gaussian multisource dispersion model IMMIS(net/em) was used to estimate the annual mean values for NO2 and total suspended particles (TSP) for the 40 measurement sites and for all study subjects. The aim of this study was to compare the measured NO2 and PM2.5 levels with the levels predicted by the two modeling approaches (for the 40 measurement sites) and to compare the results of the stochastic and dispersion modeling for all study infants (1,669 sites). NO2 and PM2.5 concentrations obtained by the stochastic models were in the same range as the measured concentrations, whereas the NO2 and TSP levels estimated by dispersion modeling were higher than the measured values. However, the correlation between stochastic- and dispersion-modeled concentrations was strong for both pollutants: At the 40 measurement sites, for NO2, r = 0.83, and for PM, r = 0.79; at the 1,669 cohort sites, for NO2, r = 0.83 and for PM, r = 0.79. Both models yield similar results regarding exposure estimate of the study cohort to traffic-related air pollution, when classified into tertiles; that is, 70% of the study subjects were classified into the same category. In conclusion, despite different assumptions and procedures used for the stochastic and dispersion modeling, both models yield similar results regarding exposure estimation of the study cohort to traffic-related air pollutants.

Air Pollutants↗
PubMed2006

Policy implications of genetic information on regulation under the Clean Air Act: the case of particulate matter and asthmatics.

The U.S. Clean Air Act (CAA) explicitly guarantees the protection of sensitive human subpopulations from adverse health effects associated with air pollution exposure. Identified subpopulations, such as asthmatics, may carry multiple genetic susceptibilities to disease onset and progression and thus qualify for special protection under the CAA. Scientific advances accelerated as a result of the groundbreaking Human Genome Project enable the quantification of genetic information that underlies such human variability in susceptibility and the cellular mechanisms of disease. In epidemiology and regulatory toxicology, genetic information can more clearly elucidate human susceptibility essential to risk assessment, such as in support of air quality regulation. In an effort to encourage the incorporation of genomic information in regulation, the U.S. Environmental Protection Agency (EPA) has issued an Interim Policy on Genomics. Additional research strategy and policy documents from the National Academy of Science, the U.S. EPA, and the U.S. Department of Health and Human Services further promote the expansion of asthma genetics research for human health risk assessment. Through a review of these government documents, we find opportunities for the inclusion of genetic information in the regulation of air pollutants. In addition, we identify sources of information in recent scientific research on asthma genetics relevant to regulatory standard setting. We conclude with recommendations on how to integrate these approaches for the improvement of regulatory health science and the prerequisites for inclusion of genetic information in decision making.

Air Pollutants↗