APA

Kodavanti U. P., Schladweiler M. C., Ledbetter A. D., Watkinson W. P., Campen M. J., Winsett D. W., Richards J. R., Crissman K. M., Hatch G. E. & Costa D. L. (20000607). The spontaneously hypertensive rat as a model of human cardiovascular disease: evidence of exacerbated cardiopulmonary injury and oxidative stress from inhaled emission particulate matter. : Toxicology and applied pharmacology.

Chicago

Kodavanti U P, Schladweiler M C, Ledbetter A D, Watkinson W P, Campen M J, Winsett D W, Richards J R, Crissman K M, Hatch G E and Costa D L. 20000607. The spontaneously hypertensive rat as a model of human cardiovascular disease: evidence of exacerbated cardiopulmonary injury and oxidative stress from inhaled emission particulate matter. : Toxicology and applied pharmacology.

Harvard

Kodavanti U. P., Schladweiler M. C., Ledbetter A. D., Watkinson W. P., Campen M. J., Winsett D. W., Richards J. R., Crissman K. M., Hatch G. E. and Costa D. L. (20000607). The spontaneously hypertensive rat as a model of human cardiovascular disease: evidence of exacerbated cardiopulmonary injury and oxidative stress from inhaled emission particulate matter. : Toxicology and applied pharmacology.

MLA

Kodavanti U P, Schladweiler M C, Ledbetter A D, Watkinson W P, Campen M J, Winsett D W, Richards J R, Crissman K M, Hatch G E and Costa D L. The spontaneously hypertensive rat as a model of human cardiovascular disease: evidence of exacerbated cardiopulmonary injury and oxidative stress from inhaled emission particulate matter. : Toxicology and applied pharmacology. 20000607.