Animal and human studies have suggested that phthalate alters thyroid hormone concentrations.
Our analysis suggested that phthalate exposure during the first trimester disrupts maternal thyroid hormone levels.
Shifts in the infrared absorption structure of the phthalate complexed with the surface compared to the solute species indicate that phthalate forms a seven-membered ring chelate complex.
Although it is well known that phthalate esters induce testicular dysfunction in both adult and immature rats, there have been few reports on the long-term effect of phthalate esters on the testicular function of male rats exposed to phthalate esters in utero.
There is evidence that phthalate plasticizers are endocrine active.
To the extent that phthalate exposures were misclassified, our results would be biased toward the null.
Background: Studies suggest that phthalate exposures may adversely affect child respiratory health.
Our results demonstrate that phthalate metabolites are unlikely to be detectable in milk and saliva.
These findings support our hypothesis that phthalate exposure may affect TNFα methylation.
In this study, we provide evidence that phthalate promotes hepatocellular carcinoma progression through a nongenomic AhR pathway.
Furthermore, this study cannot confirm that phthalate exposure caused these problems via altered thyroid function or any other mechanism.
