Persistent adverse effects on health and reproduction caused by exposure of zebrafish to 2,3,7,8-tetrachlorodibenzo-p-dioxin during early development and gonad differentiation.

Little is understood regarding the impacts of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure during early development on the health, survival, and reproductive capability of adults. Here we use zebrafish to determine whether early life stage exposure to TCDD induces toxicity in adult zebrafish and their offspring. Zebrafish were exposed to graded concentrations of TCDD (0-400 pg/ml) via waterborne exposure for 1 h/week from 0 to 7 weeks of age. The heart and swim bladder were identified as being most sensitive to TCDD exposure during early development. Subtle developmental toxic responses collectively impaired survival, and only zebrafish in the 0, 25, and 50 pg TCDD/ml groups survived to adulthood. Surviving fish exhibited TCDD toxicity in craniofacial structures (i.e., operculum and jaw), heart, swim bladder, and ovary. Exposure to 25 pg TCDD/ml impaired egg production (40% of control), fertility (90% of control), and gamete quality. TCDD-treated males contributed more than females to impaired reproductive capacity. Transgenerational effects were also discovered in that offspring from parents exposed to TCDD during early life stages showed a 25% increase in mortality compared with the F1 of dimethyl sulfoxide fish, reduced egg production (30-50% of control) and fertility (96% of control). Thus, adverse effects resulting from TCDD exposure during early life stages for one generation of zebrafish were sufficient to cause adverse health and reproductive effects on a second generation of zebrafish. In the environment, transgenerational effects such as these may contribute to population declines for the most TCDD sensitive fish species.