Research report (Health Effects Institute)
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Res Rep Health Eff Inst · Dec 2003
Comparative StudyPeroxides and macrophages in the toxicity of fine particulate matter in rats.
Epidemiologists have observed a positive association between human morbidity and mortality and the atmospheric concentrations of fine particulate matter (PM), but the mechanisms underlying the toxic effects of PM have not been elucidated. Various components of ambient PM have been implicated in toxicity (including ultrafine particles, transition metals, organics and oxidants). Our research focused on hydrogen peroxide (H2O2). ⋯ Taken together, the results of our studies demonstrate that biological effects of inhaled H2O2 are augmented by fine PM. Moreover, tissue injury induced by (NH4)2SO4 + H2O2 may be related to altered production of cytotoxic mediators by alveolar macrophages. Determining the relevance of these toxicologic results to human health will be important in future studies for evaluating the risk of exposure.
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Res Rep Health Eff Inst · Dec 2003
Comparative Study Clinical Trial Controlled Clinical TrialHealth effects of acute exposure to air pollution. Part I: Healthy and asthmatic subjects exposed to diesel exhaust.
The purpose of this study was to assess the impact of short-term exposure to diluted diesel exhaust on inflammatory parameters in human airways. We previously exposed control subjects for 1 hour to a high ambient concentration of diesel exhaust (particle concentration 300 pg/m3--a level comparable with that found in North Sea ferries, highway underpasses, etc). Although these exposures did not have any measurable effect on standard indices of lung function, there was a marked neutrophilic inflammatory response in the airways accompanied by increases in blood neutrophil and platelet counts. ⋯ The increased level of IL-10 after diesel exhaust exposure in airways of subjects with asthma suggests that this pollutant may induce subtle changes in airway immunobiology. This is an important topic for further investigation. Other possible explanations for the apparent lack of response to diesel exhaust among subjects with asthma include (1) the time course of the response to diesel may differ from the response to allergens, which peaks 6 to 8 hours after exposure; (2) a different type of inflammation may occur that was not detectable by the standard methods used in this study; and (3) the increased sensitivity of patients with asthma to particulate air pollution may reflect the underlying bronchial hyperresponsiveness found in asthma rather than any specific increase in inflammatory responses.
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Res Rep Health Eff Inst · Jan 2002
Real-world particulate matter and gaseous emissions from motor vehicles in a highway tunnel.
Recent studies have linked atmospheric particulate matter with human health problems. In many urban areas, mobile sources are a major source of particulate matter (PM) and the dominant source of fine particles or PM2.5 (PM smaller than 2.5 pm in aerodynamic diameter). Dynamometer studies have implicated diesel engines as being a significant source of ultrafine particles (< 0.1 microm), which may also exhibit deleterious health impacts. ⋯ These particles appear to be primarily composed of sulfur, indicative of sulfuric acid emission and nucleation. Comparing the 1992 and 1999 HD emission rates, we observed a 48% increase in the NOx/CO2 emissions ratio. This finding supports the assumption that many new-technology diesel engines conserve fuel but increase NOx emissions.
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Res Rep Health Eff Inst · Nov 2000
Daily mortality and fine and ultrafine particles in Erfurt, Germany part I: role of particle number and particle mass.
Increases in morbidity and mortality have been observed consistently and coherently in association with ambient air pollution. A number of studies on short-term effects have identified ambient particles as a major pollutant in urban air. This study, conducted in Erfurt, Germany, investigated the association of mortality not only with ambient particles but also with gaseous pollutants and indicators of sources. ⋯ Furthermore, the results for SO2 were inconsistent with those from earlier studies conducted in Erfurt. We conclude that both fine particles (represented by particle mass) and ultrafine particles (represented by particle number) showed independent effects on mortality at ambient concentrations. Comparable associations for gaseous pollutants were interpreted as artifacts of collinearity with particles from the same sources.
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Res Rep Health Eff Inst · Mar 2000
1,3-butadiene: cancer, mutations, and adducts. Part II: Roles of two metabolites of 1,3-butadiene in mediating its in vivo genotoxicity.
1,3-Butadiene (BD) is carcinogenic in mice and rats, with mice being more susceptible than rats to its carcinogenic effects. 1,3-Butadiene is mutagenic in the bone marrow and spleen cells of B6C3F1 lacI transgenic mice. The goal of this research was to assess the roles of two BD metabolites, 1,2-epoxy-3-butene (BDO) and 1,2,3,4-diepoxybutane (BDO2), in the mutagenicity and mutational spectrum of the parent compound BD by determining the mutagenicity and mutational spectra of BDO and BDO2 in human and rodent cells in vitro and in vivo. In human TK6 lymphoblastoid cells (TK6 cells), BDO exposure increased the frequency of G. ⋯ Therefore, it is apparent that in mice exposed to BD at carcinogenic levels, BDO and BDO2 act in concert to mediate the range of genotoxic responses. These data demonstrate that certain DNA adducts (guanine or adenine) may be useful biomarkers for BD genetic effects. However, other DNA lesions that can account for BDO2-induced deletions and chromosomal alterations also need to be considered as biomarkers for BD-induced genotoxicity.