Progress in understanding the biological basis for associations between exposures to environmental pollutants and preterm birth have been limited, in part, by the significant limitations of current laboratory animal models (see Chapter 6). Additionally, few studies have examined mechanisms by which pollutants may stimulate preterm birth. Because pollutants may increase risk for preterm birth by prematurely activating physiologic mechanisms of parturition or by activating pathologic mechanisms that prematurely initiate parturition, toxicant mechanisms need to consider. 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. Clearly, there is need for improved understanding of toxicant modification of mechanisms of normal and preterm birth.

Understanding the potential impact of exposure to environmental pollutants on preterm birth is inherently a complex proposition. However, the challenge posed by its complexity should not negate the importance of the task. By and large, women’s exposures to environmental pollutants are unavoidable and unintended. Furthermore, there is the potential for very large numbers of women to be exposed to particular pollutants, such that an increased risk presented by such exposures could have a significant impact on the population as a whole. Public health therefore plays an important role in regulating such exposures. However, regulatory actions to protect the health of pregnant women and their unborn children cannot be made in a vacuum of information.

As the discussion in this chapter indicates, there is a need to increase and improve research in this area to provide the knowledge foundation needed to design effective public health preventive strategies to minimize the risk of preterm birth as a result of environmental exposures.