Search

There is evidence that changes of the autonomic control of the heart are among the potential mechanisms responsible for pollution-related cardiac mortality. The objective of this work is to assess the acute effects of urban particulate matter of 2.5 microm (PM(2.5)) particles on heart rate (HR) and HR variability. Forty-seven healthy Wistar rats were anesthetized, submitted to tracheal intubation, and instilled with 1 mL of four different solutions: saline, blank filter, and 50 or 100 microg of PM(2.5). PM(2.5) was collected in glass fiber filters using a high-volume sampler. Electrodes for obtaining electrocardiograms were implanted subcutaneously in a Lead II configuration. HR and the standard deviation of the intervals between normal beats (SDNN) were assessed immediately before and 30 and 60 min after instillation. HR decreased significantly (P<0.001) with time, but no significant effect of treatment or interaction between time and treatment was observed. In contrast, there was a significant SDNN interaction between time and treatment (P=0.025). The SDNN decreased 60 min after instillation with a PM(2.5) of 50 and 100 microg. In conclusion, the injection of an aqueous suspension of PM(2.5) induced a reduction of SDNN in healthy rats. The effect was observed 1h after instillation and in a concentration of <100 microg.

Several epidemiological studies have consistently demonstrated significant associations between ambient levels of particulate matter and lung injury and cardiovascular events with increased morbidity and mortality. Particle surrogates (PS), such as residual oil fly ash (ROFA), have been widely used in experimental studies aimed at characterizing the mechanisms of particle toxicity. Since PS composition varies depending on its source, studies with different types of PS may provide clues about the relative toxicity of the components generated by high-temperature combustion process. In this work, we have studied the effects of nasal instillation of increasing doses of different PS in mice: saline, carbon, and two types of particle surrogates. PS type A (PSA) was the ROFA collected from the waste incinerator of our university hospital; PS type B (PSB) was collected from the electrostatic precipitator of a large steel company and thus had an elevated metal content. After 24h, we analyzed hematological parameters, fibrinogen, bronchoalveolar lavage, bone marrow, and pulmonary histology. Nasal instillation of the two types of PS-induced leucopenia. PSB elicited a greater elevation of plasma fibrinogen levels. Bone marrow and pulmonary inflammatory changes were more intense for PSA. We concluded that the PS composition modulates acute inflammatory changes more significantly than the mass for these two types of PS.

In this study, we explored the role of chronic exposure to urban air pollution in causing DNA damage (micronuclei frequency in peripheral erythrocytes) in rodents in vivo. Mice (n=20) were exposed to the urban atmosphere of São Paulo for 120 days (February to June 1999) and compared to animals (n=20) maintained in the countryside (Atibaia) for the same period. Daily levels of inhalable particles (PM10), CO, NO(2), and SO(2), were available for São Paulo. Occasional measurements of CO and O(3) were made in Atibaia, showing negligible levels of pollution in the area. The frequency of micronuclei (repeated-measures ANOVA) increased with aging, the highest values obtained for the 90th day of experiment (P<0.001). The exposure to urban air pollution elicited a significant (P=0.016) increase of micronuclei frequency, with no significant interaction with time of study. Associations (Spearman's correlation) between pollution levels of the week that precede blood sampling and micronuclei counts were observed in São Paulo. The associations between micronuclei counts and air pollution were particularly strong for pollutants associated with automotive emissions, such as CO (P=0.037), NO(2) (P<0.001), and PM10 (P<0.001). Our results support the concept that urban levels of air pollution may cause somatic mutations.