Fetal deaths are linked to exposure to pesticides during the most sensitive period of fetal growth, pregnancy weeks 3-8. This is the time period when major organ systems are forming. Mothers living within a few miles of agricultural pesticide use are vulnerable.

Hypospadias--a birth defect of the penis--is occuring with increasing frequency in the United States and other countries. This defect is caused by developmental errors in the womb. It can be easily and reliably produced in laboratory experiments with rodents using endocrine disrupting chemicals.

Background levels of PCBs accumulated by eating fish and other contaminated food available in grocery markets can be sufficient to undermine immune system protections against childhood diseases.

Sperm counts may be holding steady in some places, but in others they are declining.

IQ and reading ability of children exposed to modestly elevated PCB levels in the womb are beneath their less-exposed peers.

Children exposed to high levels of agricultural pesticides have difficulty performing simple motor tasks.

Important broad trends in the emerging science emphasize the ubiquity of exposure, the extremely low levels at which impacts occur, the diversity of hormonal systems affected, the ever expanding list of chemicals involved, and the importance of focusing on life long impacts of fetal exposure.

Girls in the United States are reaching puberty at an increasingly early age. Animal studies show that the age of sexual maturity is affected by exposure to endocrine disruptors in the womb.

The evidence linking endocrine disruption and human cancer remains highly plausible but uncertain. For the most part, as affirmed by the National Academy of Sciences report released in August 1999, the necessary studies haven't been done.

• Human epidemiological studies testing for associations between endocrine disruptors and cancers typically focus on only a handful of endocrine disruptors (usually DDT or its metabolites, dioxin, and PCBs).
• For the most part, they measure contamination in adults and ask whether these are associated with cancer risks in adulthood.

Negative results from such studies tell you nothing about all the other endocrine disruptors, hundreds if not thousands of them, to which people are exposed daily. Nor do they reveal anything about the role that developmental exposure may play in increasing risk to adult cancers.

This approach--adult exposures, adult risks---has only limited merit for asking about cancers induced in adulthood, specifically for the contaminants tested. Interactions among contaminants may render the epidemiological studies virtually impossible to interpret. And now there is evidence for interactions among contaminants and infectious disease agents. Only a handful of studies have considered possibilities like this in relation to the origens of cancer. The difficulty of these epidemiological hurdles means that the likelihood of false negatives (statistical analysis indicating there is no relationship when in fact there is) is very high.

Some strong evidence, however, is accumulating as studies become more sophisticated and broaden the universe beyond the few highly studied contaminants. More...