Contextualizing racial disparities in preterm delivery: a rhetorical analysis of U.S. epidemiological research at the turn of the 21st century.

Social Science & Medicine 115 (2014) 82e93

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Social Science & Medicine journal homepage: www.elsevier.com/locate/socscimed

Review

Contextualizing racial disparities in preterm delivery: A rhetorical analysis of U.S. epidemiological research at the turn of the 21st century Erica Prussing a, b, * a b

Department of Anthropology, University of Iowa, 114 Macbride Hall, Iowa City, IA 52242, USA Department of Community & Behavioral Health, University of Iowa, 100 CPHB, Iowa City, IA 52242, USA

a r t i c l e i n f o

a b s t r a c t

Article history: Received 3 February 2014 Received in revised form 1 June 2014 Accepted 12 June 2014 Available online 13 June 2014

Preterm delivery (PTD), defined as delivery prior to 37 weeks gestation, is a key contributor to persistent racial disparities in infant mortality in the United States. Five major funding initiatives were devoted to advancing PTD epidemiology during the 1990s and 2000s. By examining content and rhetorical features of 94 studies conducted under these initiatives, and published between 1993 and 2011, this paper considers how calls for more “contextual” approaches (focusing on social and environmental contexts) interacted with more “conventional” approaches (focusing on individual-level risk factors) to PTD epidemiology during this period. Contextual advocates initially emphasized complex biosocial reasoning to better connect social adversity with embodied outcomes. Yet responses by researchers invested in conventional approaches, as well as in studies published under new initiatives that explicitly claimed to incorporate contextual insights, often reframed this complex reasoning in biologically reductionist terms. Subsequent contextual advocates then focused on developing statistical methods to support research about social and environmental causes of PTD, and this strategy appears to have gained some traction with conventional researchers. These findings call for closer attention to language and power in both social scientific studies of epidemiological knowledge production, as well as among epidemiologists themselves. © 2014 Elsevier Ltd. All rights reserved.

Keywords: Epidemiology Preterm delivery Race Medical anthropology Science & technology studies Rhetoric

1. Introduction Calls for change in epidemiological research in the United States by the late 20th century sparked intense debates that some called the “epidemiology wars” (Poole and Rothman, 1998). Conventional approaches in the profession by this era focused on assessing risk factors at the individual level, and identifying statistical links between risk/exposure variables and disease outcomes in populations (Susser and Stein, 2009). Advocates for change called for a more contextual approach that clearly conceptualized the social, cultural and environmental settings in which adverse exposures emerge and interact to produce population patterns in health outcomes (e.g., Krieger, 2011). By the 1990s, research about racial disparities in health offered key support for contextual research, examining race as a cultural

* Department of Anthropology, University of Iowa, 114 Macbride Hall, Iowa City, IA 52242, USA. E-mail address: [email protected]. http://dx.doi.org/10.1016/j.socscimed.2014.06.023 0277-9536/© 2014 Elsevier Ltd. All rights reserved.

construction linked with socially patterned experiences of inequality (e.g., economic deprivation, environmental hazards, psychosocial stress, targeted marketing of unhealthy foods and substances, inaccessible and/or inadequate health care) that demote health (James, 1993; Geronimus, 2000; Jones, 2001; Kaufman and Cooper, 2001; Krieger, 2005; Williams, 1997). These efforts supported a new focus on health disparities by U.S. public health agencies, advanced by President Clinton's 1998 Presidential Initiative on Race. Social epidemiologists like Krieger (2005, 2011) and those in allied fields like Dressler et al. (2005) and Gravlee and Sweet (2008) in medical anthropology, have argued compellingly that research linking bodily outcomes to social experience can productively destabilize popular American cultural assumptions that racial differences are innate and immutable. Yet tracing the shifting course of epidemiological research about preterm delivery (PTD) the 1990s and 2000s poses new questions about how the persuasive power of this important strategy may vary across different research topics. In this paper, I examine the interplay between “conventional” and “contextual” approaches in studies produced under five major

E. Prussing / Social Science & Medicine 115 (2014) 82e93

research initiatives for PTD epidemiology in the 1990s and 2000s. Initial efforts to promote contextual approaches emphasized connecting social environments with biological outcomes. Yet close readings of how these calls for change were made, and responded to, indicate that this biosocial reasoning was often reinterpreted in ways that moved to reassert the primacy of conventional perspectives and agendas in the field. This reformulation occurred not only in PTD research initiatives that were expressly committed to conventional approaches, but within new initiatives in the early 2000s that explicitly claimed to integrate contextual with conventional approaches. This rather ambivalent engagement of contextual approaches in these sectors of PTD epidemiology contrasted markedly with how policies in major U.S. public health institutions, like the American Public Health Association, had fully endorsed contextual research about PTD by the mid-2000s. By the later 2000s, contextual advocacy in PTD epidemiology no longer explicitly focused on linking biological factors with social determinants, but instead on developing and publicizing statistical methods to better measure social and environmental exposures. Shortly afterwards, researchers who had previously worked in either contextual or conventional research streams entered into new collaborations (e.g., Culhane and Goldenberg, 2011). While both conceptual and methodological tools are needed to support change in any field of scientific research, attending to how different advocacy strategies figured within these transformations in PTD epidemiology poses key questions for social scientific studies of how epidemiologists produce knowledge (Janes et al., 1986; Shim and Thomson, 2010; Trostle, 2005). Tracing the interplay of contextual and conventional approaches through a series of successive research initiatives foregrounds the significance of rhetoric in epidemiological research, and asks how we can better comprehend the ways in which rhetorical strategies may reflect the distinctive networks of resources and researchers that coalesce around particular topics at given points in time. As I suggest here, for example, the prominence of clinical biomedical practitioners and perspectives in epidemiological research about pregnancy outcomes may help to account for the apparent resistance to biosocial reasoning within conventional PTD research, and seemingly greater responsiveness to new technical developments in statistical methods there. How might the specific social worlds of research that develop around a given topic shape how the cultural and political authority of conventional approaches are enacted, perpetuated, and contested when advocates propose alternative approaches? When and how do biomedical perspectives wield particular cultural and institutional authority in U.S. epidemiology? How do these social, cultural and political processes in turn shape the impact of specific strategies for change that advocates employ? I approach these questions here through analysis of the content and rhetorical features of studies from five PTD epidemiology research initiatives that unfolded through the 1990s and 2000s. This analysis extends recent social scientific studies of U.S. epidemiology at the turn of the 21st century. Shim and Thomson (2010) describe how distinctive “inductive” and “deductive” approaches to epidemiology (equivalent to what I designate as “contextual” and “conventional” here) had become embroiled in open conflict by the 1990s. As they conclude, the cultivation of a “flexible but robust” (2010:175) concept of multi-factorial causation in the 2000s superficially smoothed over this divide, but major tensions remained such that the profession continues to be in a state of “tremendous flux” (2010:176). I argue here that social scientific understandings of these dynamic tensions are enriched by examining a series of studies about a specific topic, not only for their explicit causal reasoning but also for their more implicit rhetorical strategies for articulating and legitimating knowledge claims.

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Change in any research field clearly involves a broad array of cultural, technological, structural and institutional factors. In epidemiology these range from the availability of concepts, measures, and methods to the institutional pressures that shape epidemiological training and research funding. It is beyond my scope here to provide a full analysis of how all have contributed to the evolving course of PTD research, and I do not claim that any particular advocacy strategy has single-handedly shaped its trajectory. My goal instead is to highlight how close attention to rhetorical strategies can help to illustrate the cultural and political dimensions of interactions among distinct approaches to epidemiological research. 2. Understanding PTD epidemiology: social scientific perspectives Research initiatives throughout the 1990s and 2000s supported new epidemiological studies about PTD, as researchers and policymakers responded to PTD's connection to infant mortality. Infant mortality first emerged during the 19th century as a key indicator of population well-being (Brosco, 1999; McElhinny, 2005; Meckel, 1990), and the U.S.'s poor international ranking on this measure (MacDorman and Mathews, 2008; National Research Council and Institute of Medicine, 2013) has provoked recurrent concern. This ranking is widely attributed to the disproportionate prevalence of infant mortality among racial and ethnic minority populations. Although national infant mortality rates steadily declined throughout the 20th century, racial disparities have persisted (Wise, 2003) and even increased in recent decades (David and Collins, 2007), despite recurrent efforts to define and address their causes. Concern with low birthweight organized many epidemiologic studies of infant mortality, but by the 1970s researchers focused increasingly on PTD as a key cause of low birthweight and more accurate indicator of infant mortality (see also Basso et al., 2006). Studies consistently report PTD rates at least 2e3 times higher among African Americans than white Americans (Reagan and Salsberry, 2005). Yet efforts to understand the causes of PTD and the reasons for its unequal social distribution have not yet yielded effective interventions. PTD researchers recurrently use terms such as “stubborn challenge” (Johnston et al., 2001: 3) and “enigma” (Muglia and Katz, 2010:529) to highlight these challenges. The puzzles and prospects of PTD research generated five major funding initiatives for epidemiological research through the 1990s and 2000s. Here I analyze 94 of the resulting studies published between 1993 and 2011, focusing on both content themes and rhetorical strategies. Previous social scientific studies have constructively examined the cultural and political dimensions of epidemiological knowledge (e.g., Fujimura and Chou, 1994; Janes et al., 1986; Shim and Thomson, 2010; Trostle, 2005), considering epidemiology's role in the emergence and elaboration of new diagnostic categories (Armstrong, 1998; Treichler, 1999), medical therapies (Kahn, 2009), academic disciplines (Clarke, 1998), and national research policies (Epstein, 2007). Analyses of the controversies that arise around specific hypotheses about the causes of health conditions (e.g., Garrety, 1997) also help to document how cultural influences shape the conceptualization, measurement, and interpretation of epidemiological variables. Analyses of causal hypotheses that enjoy popular legitimacy, despite limited and questionable evidence (e.g., Kaufman and Hall, 2003), similarly highlight how political processes influence the legitimacy, authority, and circulation of epidemiological knowledge claims. In explicitly examining the politics of legitimation that accompany advocacy for change in health research, Shim (2005) and

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Epstein (1996, 2007) emphasize how lay activists have maneuvered for recognition and inclusion in health research, but how in practice, this strategy sometimes perpetuates rather than transforms the political and institutional authority of researchers. Yet both authors focus on lay activists as compared to professional researchers. A similar analysis of power/knowledge can be applied to relationships among professional researchers themselves. Since publishing studies is essential to circulating research findings, attending to use of language in journal articles offers a means of analyzing these relationships. Briggs (2005) and Treichler (1999) both emphasize how terms circulate in public health, and how they may be imbued with multiple meanings by authors from different social positions with access to distinctive cultural resources. Within PTD research, I will describe how key terms such as “race” and those referring to factors in hypothesized causal pathways (e.g., “stress,” “infection,” etc.) are variably used in ways that highlight not only the contrasting causal reasoning across conventional and contextual approaches, but also differences in how study authors undertake the rhetorical tasks of legitimating their concepts, measures and findings. 3. Study design & methods Assessing content themes and rhetorical features in PTD epidemiology first requires defining a manageable focus. A basic search in PubMed using the MeSH term “premature birth” (introduced in 2005 to add more distinctions within the term “labor, premature”), yields thousands of works, even when qualified by successively applying the keywords “epidemiology,” “etiology” and “prevention.” Possible strategies include selecting works from journals with high impact factors (e.g., Shim and Thomson, 2010), and examining themes in studies sampled from regular federal funding streams (e.g., Lee, 2009). Yet attending to well-defined research initiatives undertaken by federal or private agencies offers similar advantages and additional strengths. By definition, peer-reviewed articles' use of language, images, and organization of ideas have also been deemed persuasive by a community of scientists within a particular arena (e.g., Brenneis, 1994). Since new research initiatives explicitly characterize the current state of knowledge and chart future research directions, they are especially useful for analyzing the encounters and debates among different perspectives. The 1990s and 2000s featured five major U.S. initiatives for PTD research. Starting in 1990, the Centers for Disease Control and Prevention launched a major effort to study PTD with the agenda of better accounting for how poverty, racism, and sexism intersect to shape the reproductive experiences of African American women (Rowley et al., 1993). Discussions of these potential causal pathways toward PTD were disseminated in a 1993 special issue of American Journal of Preventive Medicine that set forth research agendas (9 articles, 6 of which specifically concern PTD and/or measures for use in PTD research), a 2001 special issue of Maternal and Child Health Journal that reported study findings (9 articles, 7 of which address PTD), and an ethnographic monograph about one of the initiative's central projects (Mullings and Wali, 2001). A second major initiative, the Preterm Prediction Study, began in 1992 within a network of academic medical centers that the National Institute of Child Health and Human Development had constructed in 1986 to cultivate evidence-based practices in maternal and fetal medicine (Meis et al., 2003). This initiative's agenda focused on conducting randomized controlled trials to ascertain biomarkers predicting PTD that could support preventive screening and new clinical interventions. Major publications appeared in medical and public health journals between 1995 and 2005 (28 articles). A special issue of Seminars in Perinatology in

2003 also featured broad overviews of the initiative's findings (10 articles, 6 of which concern PTD). In 1998, the March of Dimes (MOD) foundation then launched a Perinatal Epidemiological Research Initiative. Its agenda was to promote new epidemiological research about what MOD leaders viewed as three of the most promising hypothesized pathways towards PTD: infection, genetics, and stress (Johnston et al., 2001). Descriptions of the initiative and its six newly funded studies appeared in a 2001 special issue of Paediatric and Perinatal Epidemiology (14 articles). Four of these studies subsequently published findings in epidemiological and medical journals, between 2003 and 2010 (20 articles). Shortly afterward, the National Institute of Nursing Research (NINR) highlighted epidemiological studies in a special supplemental issue of the American Journal of Obstetrics and Gynecology in 2005, “Optimizing Pregnancy Outcomes in Minority Populations” (9 articles, 6 of which centrally concerned PTD). Finally, in the early 2000s the Maternal and Child Bureau in the Health Resources and Services Administration of the Department of Health & Human Services (MCHB-HRSA) funded a 5-year “Multilevel Modeling of Disparities Explaining Preterm Delivery” project. With an explicit agenda of examining the impact of neighborhood environments on PTD through multi-level analysis, this initiative supported new methods for statistically modeling racial disparities in PTD by university-based researchers in collaboration with state and local health departments in eight geographic areas across four states. Resulting publications appeared in a variety of public health and social science journals from 2006 through 2011 (10 articles). All studies were identified through searches in PubMed. Publications from the CDC and MOD initiatives were tracked based on key authors and works citing articles from the 1993 (CDC) or 2001 (MOD) special journal issue that launched each. For the CDC and MOD as well as MCHB-HRSA initiatives, searches with key terms (and authors, once identified) also pinpointed potential studies that were then confirmed through authors' acknowledgements of funding sources. The NINR produced one special journal issue, so was readily identifiable. The NIH initiative's publications either featured “preterm prediction study” in their titles or appeared in a 2003 special journal issue. This process yielded a total of 97 journal articles. After review, three were excluded since they focused exclusively on special circumstances of pregnancy (e.g., twin gestation) or dealt with outcomes other than PTD, bringing the total number of articles analyzed to 94. Including the monograph by Mullings and Wali (2001) brought the grand total of studies consulted to 95. A full list of the articles reviewed is available as an online Appendix. I used MAXQDA qualitative data analysis software to code article content themes. I first examined forms of causal reasoning that authors employed and/or referenced. I categorized a focus on individual-level risk factors and proximate causal pathways as evidence of a more “conventional” approach to epidemiological research; while work to more explicitly conceptualize how social experiences impact health, and/or to identify and include ecological-level measures, constituted a more “contextual” approach. I then assessed rhetorical strategies through detailed comparisons of how authors using different approaches employed the same key terms in distinctive ways. Examining how authors situated their work relative to other studies, characterized key problems with PTD epidemiology to date, and charted future directions for the field also provided evidence of authors' rhetorical strategies for legitimating their claims. 4. PTD research initiatives: close readings Studies across the five research initiatives constructed the causes of PTD in markedly different ways. Table 1 shows the frequency


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Table 1 Causal reasoning in PTD research initiatives: frequency of references.a Elements in causal reasoning

CDC (13 articles)b

Individual factors 70 Social/environmental context 186 Chi-square ¼ 253.390, df ¼ 4, p-value < 0.0001

NIH-PPS (31 articles)

MOD (34 articles)

NINR (6 articles)

MCHB-HRSA (10 articles)

154 17

229 185

40 109

7 77

Chi-square from k-proportions test (conducted with XLSTAT software) indicates that proportions of references to individual vs. contextual factors are significantly different across the five initiatives. Results for each pair of studies (not shown) were also statistically significant except for CDC vs. NINR. a Frequences reflect# of coded segments (coded using MAXQDA qualitative data analysis software). b Given that Mullings & Wali's (2001) ethnographic monograph was substantially longer than other sources, it was not included in this frequency table.

of references to individual-level as opposed to social or environmental factors across studies produced through each initiative. The CDC's investment in contextual and NIH-PPS's investment in conventional approaches are both clearly visible here. The MOD that followed then appears to achieve the greatest balance of contextual and conventional features, while the smaller NINR offered a greater contextual focus more similar to the CDC's. The MCHB-HRSA initiative then heavily emphasized contextual approaches. Examining the rhetorical strategies used by study authors across these five initiatives extends this basic content analysis, offering a richer portrait of how CDC authors advocated for contextual approaches through biosocial reasoning and how authors using conventional approaches in the NIH-PPS responded. Rowley et al. explicitly positioned biosocial reasoning as central to the CDC initiative, through statements such as: “We view the high rate of preterm delivery [among African American women] as a sociobiological problem. Different social environments can account for different health states” (1993:2) by impacting host susceptibility. In contrast, NIH-PPS researchers characterized their agenda as assessing “many potential predictors of spontaneous preterm birth to determine their relative strengths and to evaluate whether several of the tests could be used together (as a multiple marker test) to predict spontaneous preterm birth more effectively” (Goldenberg et al., 2001: 644). While acknowledging demographic factors and occasionally examining social and psychosocial factors, this initiative focused overwhelmingly on evaluating “28 potential biologic markers for spontaneous preterm birth in asymptomatic women” (Goldenberg et al., 2001: 643). At first glance, the agenda of the MOD initiative that followed seemed to bridge the gap between the CDC's and NIH-PPS's agendas, by supporting close attention to both biological mechanisms and the connections of these biological manifestations to social and environmental causes. Howse characterized the MOD's central aim here as “the collection and analysis of data on medical, genetic, psychological and social factors, in combination with data on maternal and fetal biochemical variables, in order to look for clues to the causes of preterm birth” (2001:1). Yet close readings of MOD studies highlight that despite their explicit acknowledgment of contextual insights, they continued to rely heavily on individual-level conceptualizations of PTD. These conceptualizations recurrently materialized through an emphasis on biological plausibility in causal reasoning, for example, such that needed attention to pathophysiological mechanisms all too often stopped short of fully considering their social and environmental antecedents. By 2005, the continuing challenges posed to contextual by conventional approaches to PTD epidemiology were evident in the NINR initiative, which collected works from each perspective in a special journal issue. While not characterizing the problem in these exact terms, NINR authors expressed concern that PTD researchers with different approaches to epidemiology were still “working in parallel rather than in partnership” (Patrick and Bryan, 2005:S70) at this point in time.

Studies within the final MCHB-HRSA initiative illustrate how by the late 2000s, investment in developing and demonstrating appropriate statistical methods had emerged as a new strategy for promoting contextual perspectives in PTD epidemiology. Study authors framed this initiative's agenda as identifying “policy-relevant contextual factors associated with infant and child health disparities to inform state and city Maternal and Child Health officials of potentially modifiable environmental risk factors relevant for policy and program planning” (Messer et al., 2006: 1043). Authors focused on developing and publicizing accessible methods for statistical modeling of ecological-level variables as a measure of risk factors that stem from adverse social environments. While attention to ecological-level measures is fully compatible with biosocial reasoning, MCHB-HRSA authors rarely referenced biological mechanisms and thereby employed a distinctively different rhetoric. 4.1. Promoting “a new research paradigm” for contextual research The subtitle of the 1993 journal volume introducing the CDC's research initiative called for “developing a new research paradigm,” framing current approaches as fundamentally insufficient for understanding race as a social experience that impacts PTD. Authors here emphasized understanding racial disparities in PTD as a primary agenda for the field, and noted how doing so requires looking beyond well-publicized risk factors like poverty, teenage pregnancy, maternal substance abuse, and limited prenatal care (Rowley et al., 1993; Wise, 1993). Krieger et al. (1993) emphasized how African American women of high socioeconomic status still experience disproportionate rates of PTD, while Wise (1993) stressed how most African American women who experience PTD have avoided all known behavioral risks. The initiative focused on how racism-related psychosocial stress (Jackson et al., 2001) figured in the etiology of PTD, a line of inquiry that developed from the 1990s onward across numerous studies working to improve the conceptualization and measurement of race in health research (e.g., Dressler et al., 2005; Sternthal et al., 2011). CDC authors coupled this agenda with explicit criticism of current PTD research. Given how racialized experiences of stress are chronic, for example, authors pointed out that short-term psychosocial interventions during pregnancy are unlikely to demonstrate significant reductions in PTD among African American women (e.g., McLean et al., 1993). Instead, they supported broader social and structural rather than individual and often clinicallybased interventions. Based on one of the initiative's major studies, the ethnographic Harlem Birth Right study (Mullings and Wali, 2001), Mullings et al. (2001) emphasized how stress may intensify for African American women during pregnancy, as women become more cognizant of limits in resources (e.g., housing) and take steps to resolve these. In so doing, they engage family and peer networks of both women and men, and interventions to improve pregnancy outcomes need to recognize both the significance and limitations of both. Study authors also highlighted needs to conduct

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participatory research, describing how qualitative research guided by community advisory groups allows for richer understandings which can then inform subsequent epidemiological studies, as well as support more effective interventions. In addition to new etiologies and research practices, CDC authors emphasized needs to operationalize race more coherently and clearly in epidemiological studies, noting how being African American is more than the “absence of whiteness” (Rowley, 2001:73), and directly challenging the validity of the very common practice of measuring race as a dichotomous variable (see also Kaufman, 2008; Kaufman and Cooper, 1995, 2008) in studies of PTD. Instead, many CDC studies focused exclusively on African American women, in an effort to better understand how their everyday experiences emerge through the social hierarchy of race, including its intersections with hierarchies of class and gender. Rowley summarized how the CDC's research stream “moves beyond the traditional epidemiologic reductionist framework and takes on a distinctly black feminist approach” (2001:73), connecting an explicit critique of reductionistic causal reasoning with a well-developed body of social theory. While all CDC authors positioned the initiative as a critical response to conventional approaches, not all referenced social theory or framed problems with current concepts and measures in such explicit terms. Some instead positioned contextual research as a means of improving science through generating clearer evidence about the complexities of PTD. Hogan et al., for example, noted needs to expand understanding of psychosocial and ecological risks for PTD through multiple methods, “synthesizing the findings across biologic, epidemiologic, and ethnographic research and … attempting more complex multilevel studies to measure these factors simultaneously” (2001: 138). To position social exposures in the daily life experiences of African American women as causes of biological outcomes, they constructed a linear sequence: Defining what those exposures are and determining how best to measure them using qualitative research and community participation had to come first. Later steps will include measuring whether biologic phenomena are affected by such social stresses or not, and determining these stresses' contribution to the racial disparity (2001:67e8). In these ways, CDC authors defined a contextual approach to PTD research that positioned biological dimensions of PTD as outcomes of prior social experiences. They did not call for the exclusion of individual-level concepts and measures, but rather the integration and incorporation of these features of conventional PTD research into a fuller contextual paradigm. Different CDC authors variably framed the initiative's research agenda as a morally and politically compelling response to racial disparities, grounded in social theory; and in terms of the progressive improvement of science. 4.2. Conventional approaches unfold: the preterm prediction study (PPS) The major agendas of the PPS initiative, along with its large numbers of publications (see Table 1), illustrate how conventional approaches to PTD epidemiology remained prominent through the 1990s and 2000s. The PPS focused on understanding PTD etiology more broadly, recognizing the contributions of race but offering limited theorization of how race impacts health. PPS studies heavily emphasized individual-level measures and clinical interventions, and demonstrate limited incorporation of contextual insights through the 1990s and 2000s.

PPS studies worked to identify new risk factors and clarify relationships between known and new factors (Goldenberg et al., 1998), with the specific aims of developing a more effective, multi-marker screening test for PTD. Primarily designed as a prospective study, the PPS followed a large and sociodemographically diverse sample of women through pregnancy and birth. It also included numerous nested case-control studies focused on specific risk factors (see Andrews and Goldenberg, 2003). Here researchers focused on clinically measurable, maternal serum or vaginal biomarkers for PTD. Etiologically, PPS authors hypothesized that subclinical infection or inflammation leads to membrane disruption and then cervical shortening, which then precipitates PTD (Goldenberg et al., 2000, 1997). This detailed attention to the pathophysiology of PTD contrasts markedly with the CDC's efforts to connect biologic phenomena to social and environmental antecedents. Recognition of calls for clearer theorization of race in epidemiologic study designs, made by researchers studying race and health in general as well as by CDC authors, was limited in PPS studies. Some did not mention race (e.g., Andrews et al., 1999; Goepfert et al., 2000; Goldenberg et al., 1997; Iams, 2003; Owen and Iams, 2003), yet most included race as a significant, known risk factor for PTD. Strategic sampling resulted in many PPS studies including 60e65% African American women (e.g., Meis et al., 1995; Mercer et al., 1999). Most commonly, PPS authors then treated race as a dichotomous variable (e.g., “Black vs. nonBlack”) in their statistical models. Shifting terminology in PPS studies seems to reflect some awareness of critiques of these approaches, with later PPS studies tending to substitute “African American” ethnicity for “black race,” or to include more than two racial/ethnic categories (e.g., Andrews and Goldenberg, 2003; Newman et al., 2008). Yet these acts of substitution were not accompanied by conceptual discussions of the impact of race on health, or discussions of distinctions between race and ethnicity (indeed, some PPS authors awkwardly conflated the two in constructing new terms like “black ethnicity” [Goldenberg et al., 2003; Meis et al., 1998]). Although reducing racial disparities was not the initiative's central aim, some PPS authors specifically addressed them. Efforts to comprehend race and PTD emerged most explicitly in PPS studies of subclinical infection. These built upon previous studies (Carey et al., 1993), which yielded promising new findings about PTD and bacterial vaginosis (BV), a “potentially treatable” (Goldenberg et al., 1998: 237) condition that features patterned alterations in vaginal flora and that is more prevalent among African American women. Most PPS studies included BV and race as dichotomous covariates, with little discussion. But one did examine how socioeconomic status might interact with race to produce BV (Meis et al., 2000), assessing SES by individual-level measures of marital status, income, use of public insurance, household composition, residential stability, and select amenities (e.g., home telephone, access to a car). Meis and colleagues also included use of tobacco, alcohol and drugs and reproductive history as factors, and found that none of the variables studied helped to explain racial disparities in BV. The sole reliance on individual-level measures here reflects the initiative's general commitment to a conventional approach, and working to explain the influence of race in terms of the pathophysiologic biomarker of BV reflects an individual-level conceptualization of the impact of race on health. Such efforts contrast with CDC studies, some of which also addressed BV. Culhane et al. (2001), for example, reported that chronic maternal stress predicted BV during pregnancy independently of race, other sociodemographic, and behavioral variables. While relying on individual-level measures, their focus on chronic stress supports


contextual approaches by foregrounding complex psychosocial experiences rather than only bodily processes. By 2000 clinical trials of treatment for BV during pregnancy produced disappointing results (Andrews and Goldenberg, 2003; Carey et al., 2000). More than a decade later, clinical guidelines do not recommend general screening for/treatment of BV to prevent PTD (Brocklehurst et al., 2013). Yet the initiative did provide significant new information about PTD's pathophysiology, documenting that vaginal fetal fibronectin and short cervical length mark significant disruption of the chorioamniotic membranes and significantly predict PTD, and that several serum biomarkers may improve the accuracy of these predictions (Goldenberg et al., 2003). In their focus on pathophysiology, PPS authors continually positioned biological measures as legitimating knowledge claims about PTD. While epidemiologists in general employ numerous criteria to support claims of causation (e.g., Thygesen et al., 2005), PPS studies focused heavily on biological plausibility in their causal reasoning about PTD. As Goldenberg et al. explained, “as the study progressed, additional analyses were proposed on the various fluids. These were encouraged, as long as there was reasonable biologic plausibility for an association with spontaneous preterm birth” (emphasis added; 2003: 644). The central if not exclusive role of biological factors in legitimating research questions and findings here contrasts sharply with the CDC's efforts to position biological factors as outcomes of social and environmental exposures. PPS authors' discussions of the state of PTD research reveal additional contrasts between conventional and contextual approaches in this era. PPS authors attributed their study limitations to the complex nature of PTD itself, highlighting the multifactorial nature of PTD and the difficulty of detecting physiological processes that may variously shift, resolve, or intensify at different points during pregnancy (Meis et al., 1998; Mercer et al., 1996). This positivistic focus on the materiality of PTD contrasted markedly with the CDC's more reflexive focus on epistemology, which attributed the field's limitations not to PTD itself but to the ways in which researchers had been conceptualizing and approaching it. These contrasts in causal reasoning, as well as in rhetorical strategies for legitimating claims and explaining limitations, indicate that contextual and conventional approaches to epidemiology were active in largely separate streams of PTD research in the 1990s. Yet overlap and interaction between the two approaches is also evident in the studies described above. Additional analysis of how authors from each examined the same factors differently demonstrates how the primacy placed on biological factors in conventional PTD epidemiology posed serious challenges for advocates using biosocial reasoning to promote contextual approaches. 4.3. Shared terms with disparate meanings: biology and legitimacy Some PPS authors examined the relationships among stress, race and PTD, yet did so in ways that foreclosed consideration of the CDC's complex biosocial reasoning. Copper et al. (1996) checked for independent contributions and interactions among key individuallevel measures of race and other demographic factors, socioeconomic factors, substance use, and several psychological variables. While this study did not produce evidence of a specific interaction between stress and race, its findings partially supported the CDC's hypothesis that stress is an important contributor to PTD. Rather than considering how stress might be linked to social experiences, however, Copper and colleagues described how stress can produce adverse health impacts through “maladaptive health behaviors” (1996: 1286) and noted the disappointing results from psychosocial intervention studiesdboth characterizations that had been explicitly criticized earlier by CDC authors. Copper et al. also emphasized that direct mechanisms for stress influencing PTD

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include how “periods of stress can precipitate the release of catecholamines, resulting in vasoconstriction and subsequently oxygen and calorie reduction to the fetus” (1996:1289), By offering this pathophysiological interpretation without explicit connection to demographic, socioeconomic, or ecological factors, this statement moves to legitimate the impact of stress on PTD in purely biological rather than fully biosocial terms. In these ways, conventional approaches posed continuing political challenges to advocates' efforts to position pathophysiological mechanisms not as ends in themselves, but as outcomes of contextual factors. Instances of contradiction and ambivalence further highlight these challenges. In introducing a special journal issue devoted to study findings eight years after the CDC's research initiative was framed efforts to connect social context introduced, Hogan and Ferre to pathophysiologies of PTD as tentative and in progress: The research papers presented in this issue are a first step in a long scientific process to determine the contribution of social stress to the racial/ethnic disparity in PTD. These original studies are not intended to prove that black women's social exposures are directly linked to biologic phenomena causing PTD (2001:67). Yet in concluding the same volume, Hogan, et al. seemed to offer a fuller endorsement of biological plausibility in the hypothesized connections of psychosocial stress and PTD, in what can again be read as reflecting the rhetorical power of pathophysiology and biological plausibility in PTD epidemiology in this era: “These papers also establish a plausible conceptual basis for the effects of social stressors on physiologic function” (2001:136). In addition, two other articles in this special issue offered highly detailed portraits of the pathophysiology of PTD accompanied by very limited discussions of racial/ethnic disparities or racialized social experiences (Culhane et al., 2001; Wadhwa et al., 2001a). Wadhwa et al. listed “social adversity” as an ultimate cause of PTD in their abstract (2001a:119) and noted needs to better understand “determinants of social disparities” (2001a:124) in PTD in their conclusion, but otherwise only addressed such contextual perspectives briefly in the text, through statements like “… stress may not entirely be an individual-level phenomenon, but may also be linked to the individual's social-structural context (e.g., see recent studies in pregnancy by Collins et al. and O'Campo et al.)” (2001a:123). These citations refer to works on ecological/environmental sources of stress in African American communities, and while their inclusion here affirms this contextual approach, the rest of the article relies heavily on the rhetorical power of references to pathophysiologydwith authors explicitly noting that establishing biological plausibility is “perhaps one of the most important questions” (2001:119) for efforts to explain how psychosocial stress may translate into PTD. These 2001 examples indicate that references to biological mechanisms of PTD continued to powerfully arbitrate the scientific legitimacy of claims about its etiology in this era. The MOD and NINR initiatives that immediately followed explicitly called for more coordinated attention to both social determinants and pathophysiological pathways. Yet close readings of studies from both initiatives further document how references to pathophysiology continued to be heavily developed, and continually positioned as essential grounds for legitimating knowledge claims. 4.4. Calls to integrate social with biological: close readings of the MOD and NINR The MOD and NINR initiatives both called for integrating social and biological levels of analysis in PTD research, and further

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examined etiological hypotheses drawn from the preceding CDC and PPS efforts. Both featured a variety of new authors as well as some who had participated in these previous initiatives. The MOD initiative explicitly called for integrating social context with biological levels of analysis, and more specifically, for capitalizing upon the discovery of a key new biomarker for stress in the late 1990s, corticotropin releasing hormone, to advance the field of study about how stress contributes to PTD (e.g., Howse, 2001; Johnston et al., 2001; Mattison et al., 2001). In the special journal issue introducing the initiative, Wadhwa et al. (2001b) offered a review of biological mechanisms similar to one by the same first four authors from the CDC stream (discussed above), but that here focused on how stress and infection connect. While noting the relevance of these perspectives for understanding racial disparities in PTD, and stating their goal as helping to define “mechanisms that may translate social adversity during pregnancy into pathophysiology” (2001b: 17), the authors offer little discussion or conceptual development of what this social adversity might entail, and do not specify their work's significance for understanding or resolving social disparities in PTD. In the same special issue, a four-tiered heuristic diagram developed by Holzman et al. (2001) similarly includes contextual elements with limited elaboration. In this diagram, three of the four tiers concern individual-level factors and the conceptual emphasis is on distinguishing different physiological pathways between stress and PTD (infection, vascular, and a non-specific pathway) that play out in placental and fetal membrane histology. Poverty and racism are included here, but accorded far less attention, development, and cited references than the pathophysiological details. The authors further describe seven areas of data collection, six of which concern measures of the material body (including placental analysis, biomarkers) while one (the last discussed) describes measures of mind and society: Mind in the form of individual-level psychosocial and behavioral data, and ecological in the form of census tract data of neighborhoods of study subjects. This pattern of devoting markedly greater attention to biological pathways alongside more limited attention to possible social antecedents was maintained as MOD study findings were published through the 2000s. A number of MOD authors examined genetic contributions to PTD (Kramer et al., 2009a; Jones et al., 2010; Pearce et al., 2008; Scheid et al., 2007). Contextual perspectives, efforts to address social disparities, and explicit discussions of race were limited in these works: Scheid et al. explicitly described geneeenvironment interactions in assessing vulnerability to stress from abuse, but only analyzed data from Euro-American subjects; while Jones et al. described previous evidence of a racially-specific polymorphism influencing vaginal flora, but their own findings did not confirm this association. Outside of the MOD initiative at this same time, David and Collins (2007) were highlighting contextual alternatives to such work with a compelling argument in the American Journal of Public Health that focusing on socioeconomic contexts helps to explain social disparities in infant mortality far more than genetic polymorphisms. Only a handful of MOD's published findings used ecological measures, or offered extended conceptual discussions of how proximate phenomena are linked with social context. Kramer et al. (2009b), for example, used one individual-level measure and one ecological measure of neighborhood income. Tiedje et al. (2008) considered how psychological factors like hostility and anomie take shape in social environments to explain social disparities in PTD along both race and class lines: Differing distributions of anomie and hostility by racial/ethnic group and by social class suggest both a different reaction to the larger social environment and an environment not equally

inclusive across groups. Macro-level factors such as economic instability, institutional racism, and neighborhood violence shape perspectives and may induce unhealthy physiologic responses creating an escalating spiral among groups most affected (2008: 1318). While acknowledging the macro-level variables noted here, the authors did not directly measure them in this study, instead offering more diffuse support for contextual approaches by citing key works in social epidemiology regarding racism/“effortful coping” and income inequality (e.g., Colen et al., 2006; Grady, 2006; Kahn et al., 2000; Thompson et al., 2006). Holzman et al. (2006) employed a contextual approach more fully, reporting findings that race and class are linked with greater vulnerability to depression across the life course, especially when women experience abuse in both childhood and adulthood. These authors also specifically recommended structural changes to prevent abuse and other forms of stress that interact with abuse to produce PTD: We might begin by designing sound public health strategies that reduce the risk of violence and abuse and that provide widely available substance use prevention and treatment services. We might also develop government policies that guard against experiences with economic problems throughout a life course (2006:137). Overall, however, MOD studies prominently featured findings justified in terms of pathophysiology, and in some cases also, through explicit reference to biological plausibility (e.g., Jones et al., 2010; Kramer et al., 2001, 2010). A number offered limited or no connection to social context (e.g., Cauci et al., 2003; Hvilsom et al., 2002; Vogel et al., 2004). Researcher discussions of the field's current state and future needs also emphasized pathophysiology, with some again noting how the physiological complexities of pregnancy pose challenges for PTD research (e.g., Chen et al., 2010; Curry et al., 2007). By emphasizing the limitations imposed by the nature of PTD rather than by the process of epidemiological knowledge production, such perspectives echoed earlier NIH/PPS authors and overlooked the wider-ranging critiques articulated by contextual advocates through the preceding decade. Race figured prominently but unevenly in MOD study designs and methods. Most used sampling strategies to include both African American and Euro-American participants. Some emphasized self-reported race (Scheid et al., 2007), and others (Holzman et al., 2006) first checked for differences among multiple racial groups before deciding to collapse these data into dichotomous categories. Other studies did not emphasize sociodemographic diversity in sampling, however (e.g., Pearce et al., 2008). Some presented such “homogeneity” (Hvilsom et al., 2002:427) as a helpful in assessing biomarkers for PTD, a logic that actively decouples biological from social factors. The MOD initiative's central concern with corticotropin releasing hormone (CRH) may well have helped to foster the pathophysiological focus of many of its studies. Their examinations of CRH's role in PTD produced mixed findings. Chen et al. (2010) examined stressors, psychological responses, sociodemographic factors, and physiological factors for their associations with maternal CRH, and concluded that CRH is not a cause of PTD so much as a marker for the effects of known sociodemographic and behavioral risk factors. Overall, while MOD studies frequently acknowledged contextual perspectives and some actively included them in their study designs, authors in this initiative still frequently positioned biological forms of reasoning and individual levels of analysis as


primary and necessary, rather than more fully supporting contextual efforts to link biological manifestations to social determinants. During the same time period, the NINR coordinated a special journal issue in 2005 focused on “Optimizing Pregnancy Outcomes in Minority Populations” that brought together researchers from both the preceding NIH/PPS and CDC initiatives in a new collection of studies about racial disparities in PTD (Grady, 2006). Like the MOD, this collection explicitly called for greater integration of social and biological levels of analysis, yet its studies underscore how a limited integration of contextual with conventional approaches in PTD epidemiology, and the continuing rhetorical importance of references to pathophysiology in legitimating claims about PTD's causes, continued through the mid-2000s. Two of the six NINR articles about PTD focused solely on biological mechanisms. The rest worked to connect biological and social factors by including biomarkers in their discussions of how neighborhood context and psychosocial stress may influence PTD in minority communities. Representing the CDC stream, Hogue and Bremner's conceptual model of racism-related stress and PTD clearly positioned biological factors as proximate rather than ultimate causesdwith “stress reactivity” and “gene/environment interactions” appearing in the middle ring of their heuristic, labeled “host susceptibility” (2005:S50). But Goldenberg and colleagues in the same volume represented the PPS stream with an exclusive focus on “biologic fluid tests” (2005: S42) as risk markers for PTD, including over twenty measures here. These examples demonstrate how major conventional approaches continued to overlook insights from contextual approaches, while contextual advocates continued to argue for the significance of social antecedents in terms of their more proximate, biological manifestations. The continuing rhetorical authority and political power of conventional, individual-level, pathophysiologic references in PTD epidemiology is evident in both approaches. While not characterizing the interplay between conventional and contextual approaches in these exact terms, some NINR authors expressed concern that different approaches to PTD epidemiology were still not as integrated as they could or should be (Patrick and Bryan, 2005). The close readings of content themes and rhetorical features above document how contextual perspectives had clearly gained a foothold in PTD epidemiology by the early 2000s. Yet reductionistic biological reasoning still remained a prominent and authoritative reference point in the field, posing continual challenges to advocates who were calling for more complex biosocial conceptualizations of PTD. Rather than continuing the strategy of explicitly linking social determinants with biological pathways, studies conducted under final major PTD research initiative of the 2000s, the MCHB-HRSA, rarely mentioned biological mechanisms and instead focused intensively on developing and publicizing statistical methodologies to better support contextual research about PTD. 4.5. Shifting strategy: intensive methodological development Studies conducted through the MCHB-HRSA initiative examined a range of ecological factors for their impact on PTD, specifically focusing on neighborhood characteristics. The initiative piloted a strategy of using existing data from public records to study neighborhood-level impacts on PTD, including individual-level data from birth certificates as well as ecological data about education, employment, poverty, housing quality, and residential stability within U.S. census tracts (O'Campo et al., 2008). Some also included additional neighborhood features such as availability of outlets for alcohol, tobacco, fast-food, or groceries (e.g., Farley et al., 2006). MCHB-HRSA studies examined how ecological factors impacted PTD, while controlling for key individual-level variables (e.g., Farley et al., 2006; O'Campo et al., 2008). Key authors

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developed a neighborhood deprivation index that can be linked with pregnancy outcomes for women living in a given community (Messer et al., 2006; Messer et al., 2008a). Others compared different statistical approaches (e.g., hybrid fixed-effects modeling) to using this index, in order to document the extent to which data from public records may not fully account for neighborhood-level impacts on PTD and other pregnancy outcomes (Schempf et al., 2011). In contrast to CDC studies, MCHB-HRSA works offered little discussion of individual-level measures and rarely mentioned biological mechanisms (see Table 1). Yet in concert with the CDC, this initiative heavily prioritized explaining racial disparities in PTD (e.g., Messer et al., 2008a,b), and referenced bodies of scholarship that offered clear conceptualizations of links between social experiences of discrimination and embodied outcomes. In an MCHBHRSA study published in the American Journal of Public Health, for example, Holzman et al. (2009) linked study findings to the “weathering hypothesis” set forth by Geronimus, which connects experiences of racial discrimination and social adversity to accelerated aging and infant mortality. The authors found that race, high-risk behaviors such as smoking, and living in neighborhoods meeting high deprivation index placed women at increased risk for PTD in ways consonant with the concept of weathering. MCHB-HRSA authors also publicized their findings and especially their methodological developments through the agency's “Dataspeak” online workshops. Authors led workshop participants through examples of using the methods and working through associated questions in three sessions from May through July 2007, which continue to be available through transcripts posted on the agency's website. The initiative therefore used technological resources not only to develop new statistical methods, but also to disseminate these methods. These efforts seem to have gained some traction among key conventional PTD researchers, resulting in a recent publication by one author who had co-authored studies in the CDC, NINR, and MCHBHRSA initiatives and another who was one of the leading figures in the PPS stream (Culhane and Goldenberg, 2011). Possible reasons for the apparent persuasive power of these new technical and methodological developments are numerous. It is possible that researchers using conventional approaches had been persuaded of the importance of contextual approaches for some time, but placed a premium value on methodological rigor and were awaiting appropriate statistical tools to better measure contextual variables. Alternatively, it is possible that by the time these statistical tools were developed and disseminated, resistance from and by conventional researchers had been tempered by pressures not only within PTD epidemiology, but also from the visible acceptance of contextual approaches within other sectors of epidemiology and/or U.S. public health as a whole. Whatever the case, it is striking that the heavy focus on biological mechanisms within PTD epidemiology from both conventional and contextual approaches to date is nearly absent in studies published under the MHCB-HRSA initiative. While fully compatible with biosocial approaches in theory, this initiative in practice focused centrally on providing access to key technical and methodological tools for contextual research. It's assertion that environmental risk factors are sites of potential public health intervention accompanied this focus, and seems to have been accepted by at least one prominent researcher with long-standing commitments to conventional approaches. 5. PTD epidemiology: tracking the politics of knowledge production This close reading of PTD epidemiology across five major research initiatives demonstrates how responses to calls for

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contextual approaches to PTD epidemiology in the 1990s and 2000s often reframed contextual agendas in conventional terms. Such reframing appeared in efforts that explicitly aimed to integrate contextual and conventional approaches, in a process that seems better characterized as co-optation and appropriation rather than substantive engagement (see also Epstein, 2007). The heavily institutionalized focus on biological mechanisms to legitimate claims about PTD's etiology, while clearly presenting opportunities for contextual advocacy based on biosocial reasoning, also moved to constrain such advocacy's impact. Appropriations that underplay social and environmental causes are especially concerning in research about race and health, given the common tendency of U.S. health researchers to default to colloquial conceptualizations of race as an immutable and essentially biological characteristic (e.g., Chapman and Berggren, 2005; Dressler et al., 2005; Hunt and Megyesi, 2008). Shim (2002) has documented the prevalence of reductionistic biological reasoning in U.S. epidemiological approaches to race, and it may be especially significant in clinically-oriented sectors of the profession. Many epidemiologists distinguish public health from biomedicine by positioning biological plausibility as only one factor to consider in causation, for example, focusing instead on assessing statistical relationships since these can help to reveal connections between factors and outcomes (and provide possibilities for effective intervention) whose biological mechanisms are not yet understood (Bhopal, 1999; Parascandola and Weed, 2001; Thygesen et al., 2005). The greater significance of biological plausibility in PTD epidemiology may reflect the general medicalization of pregnancy by the late 20th century U.S., and associated prominence of biomedical physicians and clinical interventions in research about pregnancy outcomes. This configuration of the social world of PTD research by the 1990s seems to have promoted a narrow conceptualization of health in terms of individual bodies (Scheper-Hughes and Lock, 1987), and oriented searches for technical rather than social or environmental solutions (Syme, 1994). Such clinical sensibilities contrast with the population-based and preventive goals that are more characteristic of epidemiology as a whole, and that are especially emphasized within contextual approaches. While pressures toward biological reductionism may be especially marked in PTD epidemiology, Lilienfeld (2007) notes that biomedical institutions remain highly prominent in both the training of epidemiological researchers and the funding of epidemiological research in the U.S. The example of PTD research therefore highlights ongoing needs for social scientists to examine how biomedical interests shape the social worlds of epidemiology researchers that coalesce around particular topics at given points in time, shaping the promises and pitfalls of particular efforts toward change in research approaches there. My findings specifically suggest that under these conditions, advocacy to improve the quality of epidemiological research may gain the most traction when expressed in an idiom of access to technical and methodological developments, rather than relying on biosocial reasoning alone. This suggestive evidence poses new questions for social scientific studies of how U.S. epidemiological research changes: What conceptual, methodological, and political resources are needed in order to more effectively integrate contextual and conventional approaches in epidemiology, for example; and how might the persuasive power of calls for change vary by the topics and institutions involved at a given point in time? When might calls for change that connect with experienced needs for new methodological tools, and/or with the positive connotations of technological progress, engage broader or different audiences than calls that move to capitalize on the cultural authority that is so often linked with biological claims?

5.1. Limitations This analysis focuses on a short period of time, so is not able to draw definitive conclusions about why PTD epidemiology shifted to include more contextual approaches by the mid- to late 2000s. Focusing on published research is also clearly limited, only telling part of the story of the interests, agendas, alliances, competitions that shape the unfolding course of any field of research. Archival analysis (e.g., of requests for proposals, meetings and conference proceedings), ethnographic observations, and ethnohistorical interviews (e.g., DiGiacomo, 1999) would offer a richer portrait of how interactions between conventional and contextual approaches unfolded in PTD epidemiology, and took shape in the context of broader shifts in U.S. public health. Comparison with how conventional and contextual approaches interacted in other areas of epidemiologic inquiry would also offer richer answers to these questions, as would examining how contextual epidemiologies of PTD research developed outside of the specific initiatives discussed here (e.g., Ahern et al., 2003; Collins et al., 1997). More recent PTD research features the continuing development of biosocial approaches by researchers formerly involved in these 1990s-2000s initiatives (e.g., Kramer and Hogue, 2009), as well studies by newer researchers using explicitly sociomedical approaches (e.g., Misra et al., 2010). It is clear that space has been successfully claimed for contextual research in PTD epidemiology, reflecting the impacts of strategic advocacy initiated by the CDC initiative and undertaken by others over the course of two decades now. What remains to be seen is how these integrations will make use of the methodological developments provided through the MCHB-HRSA studies, and how they will be received within the clinically-oriented sectors of in PTD epidemiology that also remain active (e.g., Dodd et al., 2013). 5.2. Future directions Documenting the initially partial and ambivalent incorporation of contextual approaches into PTD research, and the fuller integration of these approaches nearly 20 years after initial calls for change, underscores how U.S. epidemiology at the turn of the 21st century features competing approaches and professional commitments. This unfolding story highlights the analytical power of biosocial reasoning but also conditions that can work to constrain its persuasive power, such that multiple advocacy tactics may be needed to promote contextual approaches and interventions– especially in clinically-oriented sectors of the profession. The shifting course of PTD research described here specifically highlights how the influence of biomedical perspectives in epidemiology warrants continued scrutiny, including discussions of what role such work does and should play in the profession's response to major public health problems like infant mortality, which provoke recurrent national interest and concern. Examining the relationship of epidemiological knowledge to public health as a whole also poses broader questions for social scientific study. Krieger (2011) notes that while attention to social determinants has gained a foothold, studies of the political determinants of health, such as racial discrimination, have faced more resistance. Problems that call for reconsidering fundamental ways in which a society is structured inevitably encounter more and stronger layers of resistance. Examining the rhetorical features of responses that variously support, appropriate, or resist advocacy for change in epidemiological knowledge production offers one means to enrich social scientific understanding of how this resistance works. Focusing on funding initiatives, with all of the cultural capital as well as economic resources that these represent, offers one strategy for examining how institutional pressures help to


constitute the social worlds of researchers that coalesce around particular topics at given points in time, and that become linked in turn with specific rhetorical strategies for making and legitimating knowledge claims that can in turn work to promote or resist change. Epidemiology itself could also benefit from more fully examining how both advocacy for and resistance to change can play out in and through its research, and how these processes may vary by topic. Considering these cultural and political dimensions as essential to epidemiological knowledge production stands to enhance the profession's capacities to react more responsively when significant new developments, like efforts to better comprehend and address racial disparities in health, gain traction at key historical moments in U.S. public health. Acknowledgments This project began, innocently enough, as a paper reviewing a small set of epidemiologic studies of preterm delivery for my M.P.H degree. Many thanks are due to faculty and students at the University of California at Berkeley for feedback on that early work. The current paper is much elaborated, reflecting my own professional development in medical anthropology and science & technology studies in the years since. Very special thanks are due to the anonymous reviewers for Social Science & Medicine, whose detailed and thought-provoking feedback has substantially improved the paper. Appendix A. Supplementary data Supplementary data related to this article can be found at http:// dx.doi.org/10.1016/j.socscimed.2014.06.023. References Ahern, J., Pickett, K.E., Selvin, S., Abrams, B., 2003. Preterm birth among African American and white women: a multilevel analysis of socioeconomic characteristics and cigarette smoking. J. Epidemiol. Community Health 57 (8), 606e611. Andrews, W.W., Goldenberg, R.L., National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network, 2003. What we have learned from an antibiotic trial in fetal fibronectin positive women. Semin. Perinatol. 27 (3), 231e238. Andrews, W.W., Tsao, J., Goldenberg, R.L., Hauth, J.C., Mercer, B., Iams, J., McNellis, D., 1999. The preterm prediction study: failure of midtrimester cervical sialidase level elevation to predict subsequent spontaneous preterm birth. Am. J. Obstet. Gynecol. 180 (5), 1151e1154. Armstrong, E.M., 1998. Diagnosing moral disorder: the discovery and evolution of fetal alcohol syndrome. Soc. Sci. Med. 47 (12), 2025e2042. Basso, O., Wilcox, A.J., Weinberg, C.R., 2006. Birth weight and mortality: causality or confounding? Am. J. Epidemiol. 164 (4), 303e311. Bhopal, R., 1999. Paradigms in epidemiology textbooks: in the footsteps of Thomas Kuhn. Am. J. Public Health 89 (8), 1162e1165. Brenneis, D., 1994. Discourse and discipline at the national research council: a bureaucratic bildungsroman. Cult. Anthropol. 9 (1), 23e36. Briggs, C.L., 2005. Communicability, racial discourse, and disease. Annu. Rev. Anthropol. 34, 269e291. Brocklehurst, P., Gordon, A., Heatley, E., Milan, S.J., 2013. Antibiotics for treating bacterial vaginosis in pregnancy. Cochrane Database Syst. Rev. 1, CD000262. Brosco, J.P., 1999. The early history of the infant mortality rate in america: “a reflection upon the past and a prophecy of the future”. Pediatrics 103 (2), 478e485. Carey, J.C., Klebanoff, M.A., Hauth, J.C., Hillier, S.L., Thom, E.A., Ernest, J.M., Varner, M., 2000. Metronidazole to prevent preterm delivery in pregnant women with asymptomatic bacterial vaginosis. N. Engl. J. Med. 342 (8), 534e540. Carey, J.C., Yaffe, S.J., Catz, C., 1993. The vaginal infections and prematurity study: an overview. Clin. Obstet. Gynecol. 36 (4), 809e820. Cauci, S., Thorsen, P., Schendel, D.E., Bremmelgaard, A., Quadrifoglio, F., Guaschino, S., 2003. Determination of immunoglobulin A against gardnerella vaginalis hemolysin, sialidase, and prolidase activities in vaginal fluid: implications for adverse pregnancy outcomes. J. Clin. Microbiol. 41 (1), 435e438.

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