Reproductive after birth

Of 50 adult rats used in a reproductive/developmental study, 22% of those that received 6 mg/kg/day heptachlor in the diet developed lens cataracts 4.5-9.5 months following exposure. In addition, 6-8% of the pi offspring and 6% of the p2 offspring of these rats also developed cataracts 19-21 days after birth (Mestitzova 1967). The author of this study eliminated the possibility of a vitamin B deficiency or a recessive genetic trait as the cause of the cataracts. She could not rule out the possibility of altered vitamin B metabolism caused by heptachlor. 

Developmental toxicity, defined in its widest sense to include any adverse effect on normal development either before or after birth, has become of increasing concern in recent years. Developmental toxicity can result from exposure of either parent prior to conception, from exposure of the embryo or fetus in utero or from exposure of the progeny after birth. Adverse developmental effects may be detected at any point in the life span of the organism. In addition to stmcmral abnormalities, examples of manifestations of developmental toxicity include fetal loss, altered growth, functional defects, latent onset of adult disease, early reproductive senescence, and shortened life span (WHO/IPCS 2001b). 

Many of the effects of toxic exposure in utero are not manifested until after birth. Such effects include the onset of autism and reproductive problems. 

Toxic infertility as used here refers to adverse effects on the reproductive systems of human males and females that result from exposure to xenobiotic single chemicals and chemical mixtures. This infertility may be because of direct toxic effects on the male or female reproductive organs and endocrine systems, or on the developing fetus such that the fetus cannot be either conceived or carried to term after conception. Developmental toxicity, the onset of adverse effects on the developing fetus or child after birth are discussed in Chapter 24. 

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