Diesel emissions significantly influence composition and mutagenicity of ambient particles: a case study in São Paulo, Brazil.

In 2003, a bus strike paralyzed the fleet of buses in Sao Paulo, Brazil during 3 days, from 6 to 8 of April, the complete interruption of services being achieved on the 7th. We evaluated the effect of the absence of this source of pollution on the composition, mutagenicity, and toxicity of the fine particulate material collected during this period. Particles were sampled in glass fiber filters on days 7 and 15 of April of 2003 (strike and nonstrike days, respectively), using a high-volume sampler. Trace element determinations (As, Br, Co, Cl, Fe, La, Mn, Sb, Sc, and Th) of particulate material samples were carried out by neutron activation analysis. Sulfur determination was done by X-ray fluorescence analysis. The ratio between nonstrike/strike concentrations of hydrocarbons associated with automotive emissions (benzene, toluene, ethyl-benzene, and xylenes; BTEX) was determined by gas chromatography/mass spectrometry. Mutagenesis of testing solutions was determined by means of the Tradescantia micronucleus assay in early tetrads of Tradescantia pallida. The inhibition of mitosis of the cells of the primary meristema of the root tips of Allium cepa was used as an index of the toxicity. Fine particle trace element contents were lower during the strike. The concentrations of sulfur and BTEX were 50% and 39.3% lower, respectively, on the strike day. A significant (P=0.038) reduction of micronuclei induced by fine particles sampled during the strike was observed. No effect of the strike on toxicity was detected. These results indicate that a program aiming to reduce emissions of the bus fleet in our town may impact positively the air quality by reducing the mutagenic potential of ambient particles.

Morphometric differences in pulmonary lesions in primary and secondary ARDS. A preliminary study in autopsies.

The present study was undertaken in order to describe the morphological differences between pulmonary lesions in acute respiratory distress syndrome originating from direct pulmonary injury (ARDSp) and those originating from extrapulmonary injury (ARDSexp). We investigated a total of 38 ARDS-patients (27 males) ranging in age from 19 to 75 years, classified according to underlying disease in pulmonary (ARDSp) and extrapulmonary disease (ARDSexp). The extent of acute diffuse alveolar damage was assessed morphometrically on histologic gross sections in the upper and lower lobes of one lung. The lesions showed quantitative differences in extent and distribution according to underlying disease (primary pulmonary or secondary involvement). In pulmonary ARDS, a predominance of alveolar collapse (16.6%+/-12.3% versus 10.3%+/-11.9%, p = 0,03), fibrinous exudate (1.7%+/-3.2% versus 0.4%+/-1.1%, p = 0.01) and alveolar wall edema (11.2%+/-7.4% versus 6.6%+/-4.4%, p = 0,05) were found compared to extrapulmonary ARDS. We conclude that the morphology of acute diffuse alveolar damage (DAD) is mainly determined by underlying disease (pulmonary ARDS or extrapulmonary ARDS) differing in quantitative terms within the lung. Physiological, radiographic and respiratory system mechanics differences described in ARDSp and ARDSexp may therefore be due to morphometric differences in pulmonary lesions.

Urban levels of air pollution modifies the progression of urethane-induced lung tumours in mice.

This paper investigates the effects of air pollution in urethane-induced lung tumours in mice by means of histological, morphometrical, and DNA ploidy. The experimental exposure was done in locations with different air pollution profiles: a polluted area (downtown São Paulo) and a "clean" environment. Swiss mice were employed and urethane (3 g/kg) was used as a carcinogenic substance. All the animals, whether exposed or not to air pollution, were sacrificed after 6 months, and the lung lesions were analysed. The results showed a significant effect of air pollution on tumour progression, observed by changes in the phenotype of the tumour cells as demonstrated by morphometry and DNA ploidy. We observed more atypical adenomas in the air pollution-exposed group (p = 0.02). Coherently, morphometric differences were also detected between the two groups. Neoplasms of exposed mice exhibited an increase in the nuclear fraction (p = 0.002) and in the nucleus/cytoplasm ratio (p = 0.011), as a decrease in the stromal fraction (p < 0.001). There was a higher risk of aneuploidy in the 6-months-of-air-pollution-exposure group (relative risk: 1.58; 95% of confidence interval: 1.007 to 2.403). These results indicate that urban air pollution accelerates the process of progression towards malignancy.

Exploring the clastogenic effects of air pollutants in São Paulo (Brazil) using the Tradescantia micronuclei assay.

This study was designed to determine the clastogenicity of particulate matter (aerodynamic diameter smaller than 10 microm) in the urban polluted air in the city of São Paulo. The Tradescantia-micronucleus (Trad-MCN) assay was used throughout this study to evaluate the clastogenicity of the extracts of the particulate matter. Tradescantia pallida (Rose) Hunt. cv. purpurea, an indigenous cultivar, was used in the Trad-MCN assay. The efficacy of this plant material for the Trad-MCN assay was validated with dose-response studies using formaldehyde and beta radiation. Dose-response curves were established with these known mutagens. The extracts of the PM10 particles at concentrations between 5 and 50 ppm induced a dose-related increase in MCN frequencies. The results indicate that T. pallida is equally sensitive to mutagens as the standard Tradescantia clone 4430 or 03 and the particulate matter in the urban air are clastogenic to the chromosomes of this plant. Inhalation of these particles by urban dwellers may affect their health by inducing similar genetic damage.

Urban air pollution enhances the formation of urethane-induced lung tumors in mice.

This paper investigates the association between air pollution and lung neoplasia in an animal model. The experimental exposures were done in two locations with different air pollution profiles: a polluted area (downtown São Paulo) and a "clean" environment (Atibaia). Swiss mice were employed and urethane (3 g/kg) was used as carcinogenic substance. Two experiments were performed: Experiment I was designed to verify whether air pollution acts as initiator and/or promoter of lung cancer, using 300 mice; Experiment II employed 250 animals and aimed to verify if the effects of air pollution on the development of lung tumors was dose dependent. A significant effect of air pollution in augmenting lung carcinogenecity induced by urethane was observed. This effect was shown to be dose-dependent and reproducible on two different occasions. In addition, morphometric studies revealed that pollution may influence tumor phenotype. These results support the hypothesis that air pollution plays a significant role in the development of lung tumors.

Effects of water pollution on the gill apparatus of fish.

The study was designed to investigate the influence of water pollution on gill apparatus. Specimens of Nile tilapia were collected from a polluted site in the São Paulo metropolitan area (Billings reservoir) and from a "clean" area. Fish from the polluted site showed a chronic inflammatory process in the distal region of the gill filaments, with epithelial hyperplasia. The raker length was increased and hypersecretion occurred, with a considerable volume of alcian blue-positive mucin on the epithelium of the rakers and a smaller volume of periodic acid-Schiff-positive mucin on the epithelial surface of the filaments. The rigidity of mucus in fish from the polluted site was increased, but no abnormalities in the viscosity to elasticity ratio or in mucus "wettability" were observed.

Air pollution and mortality in elderly people: a time-series study in Sao Paulo, Brazil.

The relationship between daily mortality of elderly (65+ y) persons and air pollution in the metropolitan area of Sao Paulo, Brazil, for the period May 1990 to April 1991 was evaluated by time series regression, controlling for season, weather, and other factors. Mortality was associated with respirable particles (PM10), nitrogen oxides (NOx), sulfur dioxide (SO2), and carbon monoxide (CO). The association with PM10 was most statistically significant, robust, and independent of other air pollutants. An increase in PM10 equal to 100 micrograms/m3 was associated with an increase in overall mortality equal to approximately 13%. This association was consistent across various model specifications and estimation techniques. The dose-response relationship between mortality and respirable particulate pollution was almost linear, with no evidence of a "safe" threshold level. The results were similar to those observed in London and several U.S. cities. The results were also supportive of recent animal studies that have observed adverse health outcomes in experimental animals exposed to air pollution in Sao Paulo.

Quantitative pathology of nasal passages in rats exposed to urban levels of air pollution.

In order to assess the adverse effects of urban levels of air pollution, rats were used as biological indicators in a chronic exposure experiment. Animals were housed for 6 months in the center of São Paulo (the largest South American town) and compared to controls kept for the same period in a clean area. Pollution levels were obtained from a state air pollution monitoring station, 200 m distant from exposure location, which provided the levels of CO, SO2, particulates, and ozone. The nasal septum was submitted to quantitative analysis of morphological and histochemical parameters, comprising the measurement of volume of epithelium and lamina propria per unity of surface of basal lamina, the amount of mucus stored in the surface epithelium, the volume densities of neutral and acidic mucus in the lamina propria glands, and the densities of secretory and ciliated cells in the epithelium. The results obtained in the present investigation suggest that chronic exposure to urban levels of air pollution induces secretory hypertrophy, combined with a shift toward acidic mucus secretion and ciliary damage. The results are consistent with the idea that prolonged exposure to low levels of air pollution deteriorates respiratory defenses against infectious agents and may cause an increase in respiratory morbidity and perhaps mortality.

Association between air pollution and mortality due to respiratory diseases in children in São Paulo, Brazil: a preliminary report.

This work presents the results of a time series study relating air pollution and respiratory mortality in children under 5 years of age in the metropolitan area of São Paulo, Brazil. Daily records of mortality (excluding neonatal mortality) for the period May 1990 to April 1991 were collected along with daily records of relative humidity, temperature, SO2, CO, particulates (PM10), O3, and NOx concentrations. Using multiple regression methods we demonstrated a significant association between mortality due to respiratory diseases and the NOx levels. After controlling for weather and season effects, the odds of dying due to respiratory diseases, considering the mean levels of NOx in São Paulo, was estimated at 1.3 (+/- 0.13). This result is in accord with previous animal studies conducted by our group and indicates that air pollution in São Paulo has reached levels high enough to have adverse health effects on the exposed population.