mal births), use of a chemical hair straightener (relaxer) or chemical curl products by African American women just before or during pregnancy had no effect on the risk for preterm birth (Blackmore-Prince et al., 1999).
More research is needed obtain an improved understanding of environmental pollution with respect to race-ethnicity and preterm birth. Because exposure to environmental chemicals may be codependent with race-ethnicity, examination of racial-ethnic differences in environmental exposures during pregnancy may provide new insight into the racial-ethnic disparities in the rates of preterm birth.
There has been little research on mechanisms by which pollutants may stimulate preterm birth. Conceivably, pollutants could increase risk for preterm birth by prematurely activating physiologic mechanisms of parturition or by activating pathologic mechanisms that prematurely initiate parturition. Consequently, biological mechanisms by which pollutants may stimulate preterm birth could include disruption of the endocrine systems that regulate parturition, activation of cell signaling pathways that stimulate uterine muscle contraction, and activation of the inflammatory pathway, among others (see Chapters 6 for discussion of these mechanisms in preterm birth). Moreover, toxicants may be considered as potential tools to uncover previously unknown aspects of parturition, as has been the case for the nervous system.
Mechanisms of direct stimulation of uterine contraction frequency have been studied in rat uteri exposed to DDT isomers and polychlorinated biphenyls (PCBs). These studies suggest that stimulation of uterine contraction frequency by a DDT isomer and a commercial PCB mixture (Aroclor 1254) involves increased intracellular calcium due to activation of voltagesensitive calcium channels in the uterine smooth muscle cells (Bae et al., 1999b; Juberg and Loch-Caruso, 1992; Juberg et al, 1995). Moreover, stimulation of uterine contraction by the PCB mixture is dependent on activation of a calcium-independent phospholipase A2 and increased release of arachidonic acid (Bae et al., 1999a). A PCB congener (PCB 50) was shown to stimulate rat uterine contractions by activating an endometrial calcium-independent phospholipase A2 that was differentially expressed in late gestation (Brant et al., 2006a). Furthermore, Brant and colleagues showed that PCB 50 activation of phospholipase A2 is mediated by p38 mitogen activated protein kinase (MAPK) (Brant and Caruso, 2005). Although increased intracellular calcium of uterine muscle cells, arachidonic acid release, prostaglandin release, and increased uterine contraction frequency are characteristics of parturition, it is not known if these responses measured in rat cells and tissues in vitro have relevance for human preterm birth.