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The arguably strongest evidence stems from prenatal studies (5, 6).
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The initial results from prenatal cohort studies are still preliminary, and the process they describe is still in its infancy.
The reasons vary, from no long-term human health studies and no synergistic toxicity studies (eating a pesticide sprayed with other weedkillers, anyone?) to no prenatal studies and concerns over everything from cancer to allergies.
For at least the prenatal studies, there is the loud ticking of the biological clock.
Our study uses more histological data than any previous study, and includes data from prenatal ovaries, allowing us to analyse complete models involving both population establishment and decline.
Study interviewers abstracted data from prenatal and delivery medical records that were completed by hospital/clinic personnel and provided to the study participants.
But in 2005, an expert panel suggested that there was "insufficient evidence" to demonstrate adverse outcomes from prenatal amphetamine use, since none of the studies could adjust for poor prenatal case in general.
There is also growing evidence from human studies of adverse developmental effects from prenatal exposure to PAHs (Naufal et al. 2010; Ren et al. 2011).
PBDEs and their metabolites cross the placenta and studies in rodents demonstrate neurodevelopmental toxicity from prenatal exposures.
Instead, we can engage in a combination of epidemiologic, rodent, primate, and human studies to identify the biological steps leading from prenatal SSRI exposure to depression in adolescence.
In preclinical studies, choline partially ameliorates memory and learning deficits from prenatal alcohol exposure.
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