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Evaluation of the mutagenic potential of urban air pollution in São Paulo, Southeastern Brazil, using the Tradescantia stamen‐hair assay

2004; Wiley; Volume: 19; Issue: 6 Linguagem: Inglês

10.1002/tox.20065

1522-7278

Eliane Tigre Guimarães, Mariângela Macchione, D.J.A. Lobo, Marisa Domingos, Paulo Hilário Nascimento Saldiva,

Noise Effects and Management

Abstract We used a short‐term bioassay—the Tradescantia stamen‐hair assay (TSH)—to evaluate the toxicity of ambient particles with an aerodynamic diameter less than 10 μm sampled in the metropolitan region of São Paulo, Brazil. Two exposure locations were selected: downtown São Paulo and Caucaia do Alto (mean PM 10 levels of 64 and 14 μg/m 3 , respectively). The experiment was conducted July 11–August 15, 2002, and toxicity was assessed with the Tradescantia stamen‐hair assay (TSH) employing clone KU‐20 of Tradescantia . Four experimental groups were defined: inflorescences collected from plants cultivated in Caucaia, inflorescences collected from plants cultivated in São Paulo (to establish the baseline level of mutations in stamen hairs at both sites), inflorescences collected from plants cultivated in Caucaia and brought to São Paulo and maintained in chambers that received ambient air, and inflorescences collected from plants cultivated in Caucaia and brought to São Paulo and maintained in chambers that received air passed through a particle filter. The frequency of mutations observed in Caucaia was significantly lower than that in the remaining groups. Flower cuttings brought from Caucaia and receiving ambient air of São Paulo showed a rate of mutations similar to that of plants cultivated in São Paulo. Filtering particles from the air reduced the rate of mutation but not sufficiently to reach the level of that in Caucaia. The frequency of mutations observed in São Paulo was significantly associated with PM 10 levels on the fifth day before the opening of the flowers ( r = 0.47, p = 0.025). Our results indicate that urban particles play a significant role in the development of pollution‐dependent mutations. © 2004 Wiley Periodicals, Inc. Environ Toxicol 19: 578–584, 2004.