Fine particulate matter and polycyclic aromatic hydrocarbon concentration patterns in Roxbury, Massachusetts: a community-based GIS analysis.
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Given an elevated prevalence of respiratory disease and density of pollution sources, residents of Roxbury, Massachusetts, have been interested in better understanding their exposures to air pollution. To determine whether local transportation sources contribute significantly to exposures, we conducted a community-based pilot investigation to measure concentrations of fine particulate matter (particulate matter < 2.5 microm; PM(2.5)) and particle-bound polycyclic aromatic hydrocarbons (PAHs) in Roxbury in the summer of 1999. Community members carried portable monitors on the streets in a 1-mile radius around a large bus terminal to create a geographic information system (GIS) map of concentrations and gathered data on site characteristics that could predict ambient concentrations. Both PM(2.5) and PAH concentrations were greater during morning rush hours and on weekdays. In linear mixed-effects regressions controlling for temporal autocorrelation, PAH concentrations were significantly higher with closer proximity to the bus terminal (p < 0.05), and both pollutants were elevated, but not statistically significantly so, on bus routes. Regressions on a subset of measurements for which detailed site characteristics were gathered showed higher concentrations of both pollutants on roads reported to have heavy bus traffic. Although a more comprehensive monitoring protocol would be needed to develop robust predictive functions for air pollution, our study demonstrates that pollution patterns in an urban area can be characterized with limited monitoring equipment and that university-community partnerships can yield relevant exposure information. (+info)
Environmental and biological monitoring of traffic wardens from the city of Rome.
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A molecular epidemiological study on Roman policemen is ongoing. The results of a first assessment of the occupational exposure to aromatic compounds of 66 subjects engaged in traffic control and of 33 office workers are presented in this paper. Passive personal samplers and urinary biomarkers were used to assess exposure to benzene and polycyclic hydrocarbons during work shifts. The results obtained indicate that benzene exposure in outdoor workers is about twice as high as in office workers (geometric mean 7.5 and 3.4 micrograms/m3, respectively). The distribution of individual exposure values was asymmetrical and skewed toward higher values, especially among traffic wardens. Environmental benzene levels recorded by municipal monitoring stations during work shifts (geometric mean 11.2 micrograms/m3) were in the first instance comparable to or greater than individual exposure values. However, several outlier values were observed among personal data that greatly exceeded average environmental benzene concentrations. Among the exposure biomarkers investigated, only blood benzene correlated to some extent with previous exposure to benzene, while a seasonal variation in the excretion of 1-hydroxypyrene and trans-muconic acid was observed in both study groups. In conclusion, these results suggest that outdoor work gives a greater contribution than indoor activities to benzene exposure of Roman citizens. Moreover, relatively high-level exposures can be experienced by outdoor workers, even in the absence of large-scale pollution episodes. (+info)
Diesel emissions: is more health research still needed?
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It can legitimately be asked whether we need any more research on the health effects of diesel emissions. However, despite a research effort spanning at least 5 decades and the generation of a huge literature, there are still key uncertainties about the health impacts of present and future diesel emissions. This article briefly characterizes current knowledge and information gaps, and then proposes some key issues requiring further research. These issues include the adjuvant effect, the bioactivity of inhaled emissions at realistic doses, the toxicity of aged diesel exhaust particles, the importance of ultrafine particulate emissions, the need to improve our ability to predict the impacts of changes in emissions, and the placement of diesel health risks in context regarding other exposures. (+info)
Health effects of diesel exhaust emissions.
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Epidemiological studies have demonstrated an association between different levels of air pollution and various health outcomes including mortality, exacerbation of asthma, chronic bronchitis, respiratory tract infections, ischaemic heart disease and stroke. Of the motor vehicle generated air pollutants, diesel exhaust particles account for a highly significant percentage of the particles emitted in many towns and cities. This review is therefore focused on the health effects of diesel exhaust, and especially the particular matter components. Acute effects of diesel exhaust exposure include irritation of the nose and eyes, lung function changes, respiratory changes, headache, fatigue and nausea. Chronic exposures are associated with cough, sputum production and lung function decrements. In addition to symptoms, exposure studies in healthy humans have documented a number of profound inflammatory changes in the airways, notably, before changes in pulmonary function can be detected. It is likely that such effects may be even more detrimental in asthmatics and other subjects with compromised pulmonary function. There are also observations supporting the hypothesis that diesel exhaust is one important factor contributing to the allergy pandemic. For example, in many experimental systems, diesel exhaust particles can be shown to act as adjuvants to allergen and hence increase the sensitization response. Much of the research on adverse effects of diesel exhaust, both in vivo and in vitro, has however been conducted in animals. Questions remain concerning the relevance of exposure levels and whether findings in such models can be extrapolated into humans. It is therefore imperative to further assess acute and chronic effects of diesel exhaust in mechanistic studies with careful consideration of exposure levels. Whenever possible and ethically justified, studies should be carried out in humans. (+info)
Diesel exhaust particles suppress macrophage function and slow the pulmonary clearance of Listeria monocytogenes in rats.
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In this study, we tested the hypothesis that exposure to diesel exhaust particles (DEP) may increase susceptibility of the host to pulmonary infection. Male Sprague-Dawley rats received a single dose of DEP (5 mg/kg), carbon black (CB, 5 mg/kg), or saline intratracheally. Three days later, the rats were inoculated intratracheally with approximately 5,000 Listeria monocytogenes and sacrificed at 3, 5, and 7 days postinfection, and we determined the number of viable Listeria in the left lobe of lungs. The remaining lungs underwent bronchoalveolar lavage (BAL) and the retrieved BAL cells were identified and counted. Luminol-dependent chemiluminescence, a measure of reactive oxygen species (ROS) formation, generated by BAL cells was monitored and the levels of nitric oxide and tumor necrosis factor (TNF)-[alpha] produced by macrophages in culture were determined. At 7 days postinfection, we excised the lung-draining lymph nodes and phenotyped the lymphocyte subpopulations. Exposure of rats to DEP, but not to CB, decreased the clearance of Listeria from the lungs. Listeria-induced generation of luminol-dependent chemiluminescence by pulmonary phagocytes decreased by exposure to DEP but not CB. Similarly, Listeria-induced production of NO by alveolar macrophages was negated at 3, 5, and 7 days after inoculation in DEP-exposed rats. In contrast, CB exposure had no effect on Listeria-induced NO production at 3 days after infection and had a substantially smaller effect than DEP at later days. Exposure to DEP or CB resulted in enlarged lung-draining lymph nodes and increased the number and percentage of CD4(+) and CD8(+) T cells. These results showed that exposure to DEP decreased the ability of macrophages to produce antimicrobial oxidants in response to Listeria, which may play a role in the increased susceptibility of rats to pulmonary infection. This DEP-induced suppression is caused partially by chemicals adsorbed onto the carbon core of DEP, because impaired macrophage function and decreased Listeria clearance were not observed following exposure to CB. (+info)
Personal and outdoor nitrogen dioxide concentrations in relation to degree of urbanization and traffic density.
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To assess differences in exposure to air pollution from traffic in relation to degree of urbanization and traffic density, we measured personal and home outdoor nitrogen dioxide (NO(2)) concentrations for 241 children from six different primary schools in the Netherlands. Three schools were situated in areas with varying degrees of urbanization (very urban, fairly urban, and nonurban) and three other schools were located near highways with varying traffic density (very busy, fairly busy, and not busy). Weekly averaged measurements were conducted during four different seasons. Simultaneously, indoor and outdoor measurements were conducted at the schools. Personal and outdoor NO(2) concentrations differed significantly among children attending schools in areas with different degrees of urbanization and among children attending schools in areas close to highways with different traffic densities. For the children living near highways, personal and outdoor NO(2) concentrations also significantly decreased with increasing distance of the home address to the highway. Differences in personal exposures between children from the different schools remained present and significant after adjusting for indoor sources of NO(2). This study has shown that personal and outdoor NO(2) concentrations are influenced significantly by the degree of urbanization of the city district and by the traffic density of and distance to a nearby highway. Because NO(2) can be considered a marker for air pollution from traffic, the more easily measured variables degree of urbanization, traffic density, and distance to a nearby highway can all be used to estimate exposure to traffic-related air pollution. (+info)
Blood lead levels of primary school children in Dhaka, Bangladesh.
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Dhaka, Bangladesh, has one of the highest air lead levels in the world. In February 2000, we evaluated children at five primary schools in Dhaka to determine blood lead (BPb) levels, sources of environmental exposure, and potential risk factors for lead poisoning. Selected schools represented a range of geographic and socioeconomic strata. A total of 779 students 4-12 years of age participated. The mean BPb level was 15.0 microg/dL (range 4.2-63.1 microg/dL). Most students (87.4%) had BPb levels above the Centers for Disease Control and Prevention's level of concern (10 microg/dL). Elevated BPb levels correlated with soil eating [odds ratio (OR) = 3.31; 95% confidence interval (CI), 1.30-8.39], low parental education (OR = 2.72; 95% CI, 1.97-3.75), living close to major roads (OR = 2.30; 95% CI, 1.23-4.29), and increasing age (OR = 1.11; 95% CI, 1.06-1.16). BPb levels measured were similar to those in other countries that use leaded gasoline. No other potential sources of lead exposure were consistently identified. Combustion of leaded gasoline is the main source of lead exposure in Dhaka, resulting in ubiquitous contamination of the environment. The increase in BPb levels with age, a finding contrary to observations in the United States and Australia, may be related to increased outdoor activities. The Bangladeshi government recently announced a plan to eliminate leaded gasoline. Baseline BPb surveys are critical to develop and evaluate intervention policies. Strategies to reduce BPb levels need to address variations in socioeconomic status, construction type and location of housing, and levels of hygiene. (+info)
Particulate matter and daily mortality and hospital admissions in the west midlands conurbation of the United Kingdom: associations with fine and coarse particles, black smoke and sulphate.
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OBJECTIVES: There is considerable evidence linking ambient particles measured as particulate matter with aerodynamic diameter <10 microm (PM(10)) to daily mortality and hospital admissions but it is not clear which physical or chemical components of the particle mixture are responsible. The relative effects of fine particles (PM(2.5)), coarse particles (PM(2.5-10)), black smoke (mainly fine particles of primary origin) and sulphate (mainly fine particles of secondary origin) were investigated, together with ozone, SO(2), NO(2), and CO, on daily mortality and hospital admissions in the west Midlands conurbation of the United Kingdom. METHODS: Time series of health outcome and environmental data were obtained for the period 1994-6. The relative risk of death or hospital admission was estimated with regression techniques, controlling for long term time trends, seasonal patterns, influenza epidemics, effects of day of the week, and temperature and humidity. Models were adjusted for any remaining residual serial correlation and overdispersion. The sensitivities of the estimates for the effects of pollution to the inclusion of a second pollutant and seasonal interactions (warm or cool) were also examined. RESULTS: Daily all cause mortality was not associated with any gaseous or particulate air pollutant in the all year analysis, although all measures of particles apart from PM(2.5-10) showed significant positive effects of the warm season. Neither respiratory nor cardiovascular admissions (all ages) were associated with any air pollutant, and there were no important seasonal interactions. However, analysis of admissions by age found evidence for various associations-notably between PM(10), PM(2.5), black smoke, SO(2,) and ozone (negative) and respiratory admissions in the 0-14 age group. The coarse fraction, PM(2.5-10) differed from PM(2.5) in having smaller and less consistent associations (including several large significant negative associations) and a different lag distribution. The results for black smoke, an indicator of fine primary carbonaceous particles, were very similar to those for PM(2.5), and tended to be more robust in two pollutant models. The effects of sulphate, an indicator of secondary particles, also showed some similarities to those of PM(2.5). CONCLUSIONS: Clear effects of air pollution on mortality and hospital admissions were difficult to discern except in certain age or diagnostic subgroups and seasonal analyses. It was also difficult to distinguish between different measures of particles. Within these limitations the results suggest that the active component of PM(10) resides mostly in the fine fraction and that this is due mainly to primary particles from combustion (mainly vehicle) sources with a contribution from secondary particles. Effects of the coarse fraction cannot be excluded. (+info)