US EPA

2192691 

Technical Report 

Developmental effects of dioxins and other endocrine disrupting chemicals 

Birnbaum, LS 

1995 

1 

NeuroToxicology
ISSN: 0161-813X
EISSN: 1872-9711 

DART/TER/95001518 

7 

1 

748 

English 

BCI:BCI199698755285 

is also published as 150745 Developmental effects of dioxins and related endocrine disrupting chemicals

Alteration of hormonal systems has long been known to cause developmental problems. TCDD and other structurally related PHAHs modulate the levels of many different hormones and their receptors. These effects are all mediated through binding to the Ah receptor. Dioxin and related compounds are developmental toxicants, causing a spectrum of morphological and functional deficits. At doses below those where maternal toxicity is observed, dioxins cause fetotoxicity. In the mouse, exposure of the dam results in hydronephrosis and cleft palate in the pups. Thymic atrophy and hemorrhage are observed in many species at doses which are not maternally toxic. Prenatal exposure to both rats and hamsters results in alterations to the genitourinary tract of the offspring, which is not detectable until puberty. Delays in puberty, permanent reduction in sperm counts, and long-term alterations in immune functions have also been observed. Prenatal exposure to PCBs has been shown to cause similar effects in rats and guinea pigs, as well as decrements in the auditory threshold. Children exposed prenatally to complex mixtures of PCBs and PCDFs are smaller and have problems at puberty, hearing deficits, increased respiratory disease, and IQ and behavioral deficits. Many of these effects are similar to those observed with known hormone modulators. The complex alteration of multiple endocrine systems is likely associated with the spectrum of adverse developmental effects caused by dioxin and related compounds.