Exposure to toxic environmental chemicals during pregnancy and breastfeeding is ubiquitous and is a threat to healthy human reproduction. There are tens of thousands of chemicals in global commerce, and even small exposures to toxic chemicals during pregnancy can trigger adverse health consequences. Exposure to toxic environmental chemicals and related health outcomes are inequitably distributed within and between countries; universally, the consequences of exposure are disproportionately borne by people with low incomes. Discrimination, other social factors, economic factors, and occupation impact risk of exposure and harm. Documented links between prenatal exposure to environmental chemicals and adverse health outcomes span the life course and include impacts on fertility and pregnancy, neurodevelopment, and cancer. The global health and economic burden related to toxic environmental chemicals is in excess of millions of deaths and billions of dollars every year. On the basis of accumulating robust evidence of exposures and adverse health impacts related to toxic environmental chemicals, the International Federation of Gynecology and Obstetrics (FIGO) joins other leading reproductive health professional societies in calling for timely action to prevent harm. FIGO recommends that reproductive and other health professionals advocate for policies to prevent exposure to toxic environmental chemicals, work to ensure a healthy food system for all, make environmental health part of health care, and champion environmental justice.

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Abstract-Agonistic autoantibodies to the angiotensin II type I receptor (AT1-AA) and endothelin -1 (ET-1) are suggested to be important links between placental ischemia and hypertension during preeclampsia. Activation of the angiotensin II type 1 receptor (AT1R) increases endothelial cell production of ET-1; however, the importance of ET-1 in response to AT1-AA-mediated AT1 R activation during preeclampsia is unknown. Furthermore, the role of AT1-AA-mediated increases in blood pressure during pregnancy remains unclear. The objective of this study was to test the hypothesis that AT1-AA, increased to levels observed in preeclamptic women and placental ischemic rats, increases mean arterial pressure (MAP) by activation of the ET-1 system. Chronic infusion of purified rat AT1-AA into normal pregnant (NP) rats for 7 days increased AT1-AA from 0.68Ϯ0.5 to 10.88Ϯ1.1 chronotropic units (PϽ0.001). The increased AT1-AA increased MAP from 99Ϯ1 to 119Ϯ2 mm Hg (PϽ0.001). The hypertension was associated with significant increases in renal cortices (11-fold) and placental (4-fold) ET-1. To determine whether ET-1 mediates AT1-AA-induced hypertension, pregnant rats infused with AT1-AA and NP rats were treated with an ET A receptor antagonist. MAP was 100Ϯ1 mm Hg in AT1-AAϩET A antagonist-treated rats versus 98Ϯ2 mm Hg in ET A antagonist-treated rats. Collectively, these data support the hypothesis that one potential pathway whereby AT1-AAs increase blood pressure during pregnancy is by an ET-1-dependent mechanism. Key Words: preeclampsia Ⅲ hypertension Ⅲ kidney Ⅲ placenta Ⅲ inflammation T he initiating event in early onset preeclampsia is postulated to involve inadequate vascularization of the subplacental decidua with reduced placental perfusion that leads to hypertension during pregnancy by mechanisms not yet elucidated. 1,2 Recent studies have suggested that the production of agonistic autoantibodies to the angiotensin II (Ang II) type I receptor (AT1-AA) may be an important link between placental ischemia and hypertension in preeclamptic women. 3-8 The AT1-AA induces signaling in vascular cells that are blocked by an AT1 receptor antagonist including activating protein-1, calcineurin, and nuclear factor kappa B activation. 3,4,7 Recent studies by Zhou et al demonstrate that immunoglobulin isolated from preeclamptic women increases systolic blood pressure 4 days after retro-orbital injection into pregnant mice. 7,8 This hypertensive response was attenuated by administration of an AT1 receptor antagonist. Although these findings suggest that AT1-AAs from preeclamptic women increases blood pressure in pregnant mice, possibly by activation of the AT1 receptor, it remains unclear by what mechanism purified AT1-AA mediates hypertension during pregnancy.We recently reported that hypertension in response to reductions in uterine perfusion pressure in pregnant rats (RUPP) is associated with increased circulating levels of the AT1-AA. 9,10 Moreover, we found that the increased blood pressure response in RUPP pregnant rats decreased ma...