Inbred Fisher and Buffalo rats were exposed to nicotine and alcohol. Fertility was greatly reduced in both strains with nicotine treatments being much more deleterious than alcohol use. Fisher rats tolerated both toxins better than Buffalo rats. Both strains became 'extinct' after one generation of fetal and postnatal exposure to nicotine, but alcohol-ingesting Fisher rats had 3 or more generations of offspring. The total reproductive period was significantly shortened in both strains under the effect of both toxins, as was the total life span. The causes of the teratological effects of both toxins are inflammatory processes as evidenced by the presence of numerous lymphocytes and/or polymorphonuclear leukocytes. Their presence occurs earlier in nicotine than in alcohol use and earlier in Buffalo than in Fisher rats, but the damage done during nicotine treatment is reversible when the procedure is terminated. Inflammation is not transmitted to the newborn offspring of nicotine- or alcohol-treated mothers, but occurs in neonates during the nursing period or later. There is considerable individual variation in the tolerance to both toxins. Experimental results and clinical observations show a sufficient number of similarities to justify the use of experimental data as a model for further studies on human subjects.