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Vera Go,¹ Joan Garey,² Mary S. Wolff,² and Beatriz G.T. Pogo³

¹Molecular Basis of Diseases Program; ²Department of Community and Preventive Medicine; and ³Department of Medicine, Division of Neoplastic Diseases, Mount Sinai School of Medicine, New York, NY 10029 USA

Abstract

Estrogens, whether natural or synthetic, clearly influence reproductive development, senescence, and carcinogenesis. Pyrethroid insecticides are now the most widely used agents for indoor pest control, providing potential for human exposure. Using the MCF-7 human breast carcinoma cell line, we studied the estrogenic potential of several synthetic pyrethroid compounds in vitro using pS2 mRNA levels as the end point. We tested sumithrin, fenvalerate, d-trans allethrin, and permethrin. Nanomolar concentrations of either sumithrin or fenvalerate were sufficient to increase pS2 expression slightly above basal levels. At micromolar concentrations, these two pyrethroid compounds induced pS2 expression to levels comparable to those elicited by 10 nM 17ß-estradiol (fivefold) . The estrogenic activity of sumithrin was abolished with co-treatment with an antiestrogen (ICI 164,384) , whereas estrogenic activity of fenvalerate was not significantly diminished with antiestrogen co-treatment. In addition, both sumithrin and fenvalerate were able to induce cell proliferation of MCF-7 cells in a dose-response fashion. Neither permethrin nor d-trans allethrin affected pS2 expression. Permethrin had a noticeable effect on cell proliferation at 100 µM, whereas d-trans allethrin slightly induced MCF-7 cell proliferation at 10 µM, but was toxic at higher concentrations. Overall, our studies imply that each pyrethroid compound is unique in its ability to influence several cellular pathways. These findings suggest that pyrethroids should be considered to be hormone disruptors, and their potential to affect endocrine function in humans and wildlife should be investigated. Key words: 17ß-estradiol, MCF-7 human breast carcinoma cells, pS2, pyrethroid, RNA. Environ Health Perspect 107:173-177 (1999) . [Online 21 January 1999]

http://ehpnet1.niehs.nih.gov/docs/1999/107p173-177go/ abstract.html

Address correspondence to B.G.T. Pogo, Department of Medicine, Division of Neoplastic Diseases, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1131, New York, NY 10029 USA.

We thank Rachel Hazan for her assistance with the Coulter Counter and Noah Roy for his help with statistical analyses.

Supported by funds from the T.J. Martell Foundation for Leukemia, Cancer and AIDS Research ; the Chemotherapy Foundation ; and NIEHS Superfund Basic Research grant P42ES07384.

Received 28 July 1998 ; accepted 19 October 1998.