Читать книгу Exposed Science - Sara Shostak - Страница 8

Introduction

In the spring of 2000, a two-year-old girl named Sunday Abek was treated at a New Hampshire hospital emergency room for a low-grade fever and vomiting. Because her throat culture was positive for strep, the doctors sent her home with a prescription for an antibiotic. Her condition worsened, and three weeks later Sunday was admitted to the hospital, where she fell into a coma. Two days later, she died. The cause of her death was lead poisoning.

Originally from Sudan, Sunday’s family had recently moved to the United States from an Egyptian refugee camp, where she had lived for most of her brief life. She was poisoned, however, by lead in her family’s home in an apartment building in Manchester, New Hampshire. Following her death, testing at the apartment revealed that the porch, where Sunday played, was covered with peeling, flaking paint.¹ Window wells in the apartment were contaminated with lead dust. At the time of her death, Sunday’s blood lead level was 391 μg/dL (micrograms of lead per deciliter of blood), nearly 40 times higher than the threshold at which a child is considered to have lead poisoning.²

Less than a century ago, severe lead poisoning of infants and children was a major public health challenge (Markowitz & Rosner 2002; Rabin 1989). Children are more susceptible to lead poisoning than adults for numerous reasons. Per kilogram of body weight, children drink more fluids, eat more food, breathe more air; they also have a larger skin surface in proportion to their body volume. Children absorb a larger fraction of ingested lead than do adults, and they are more greatly affected by absorbed lead. Children’s behaviors—crawling, putting things in their mouths, playing outdoors—also increase their risk of lead exposure.³ However, Sunday was the first child to die of lead poisoning in the United States in over a decade (Lord 2001).

Lead poisoning in children became a preventable disease as a result of decades of research and advocacy by environmental health scientists, progressive social reformers, and policy makers (Markowitz & Rosner 2002; Sellers 1997). In the United States, primary prevention—that is, preventing exposure—is at the center of efforts to protect children from the harmful effects of lead.⁴ Public policy has played an especially prominent role. In 1973, the Environmental Protection Agency (EPA) mandated the phaseout of lead in gasoline.⁵ In 1977, the Consumer Products Safety Commission (CPSC) limited the lead in most paints. Similarly, the United States has banned the use of lead in food containers, children’s toys, and municipal water systems. Together, these regulations resulted in a 78% reduction in human exposure to lead between 1976 and 1991 in the United States, as measured in blood lead levels (Pirkle et al. 1994; 1998). This is one of the major public health success stories of the last quarter century (Grosse et al. 2002).

Despite these successes, thousands of U.S. children, especially low-income and minority children, are exposed to harmful levels of lead each year.⁶ As blood lead levels have fallen nationally, disparities in lead exposure and lead poisoning have increased. According to the Centers for Disease Control and Prevention (CDC), lead-based paint in older housing, along with the contaminated dust and soil it generates, remains the most widespread and dangerous high-dose source of lead exposure for young children. From 1991 to 1994, 16% of low-income children living in older housing had elevated blood lead levels, compared to 4.4% of all children (CDC 1997). Likewise, low-income children living in older housing have more than a thirty-fold greater prevalence of elevated blood lead levels compared to middle-income children in newer housing (Pirkle et al. 1998). Between 1997 and 2001, of the children reported with confirmed elevated blood lead levels, approximately 60% were African American (CDC 2003). The apartment building where Sunday Abek’s family lived was built in 1910 and, at the time of her death, was home to families who had immigrated recently from Kosovo, Sudan, Rwanda, and Zimbabwe (Daniel 2001).⁷

Simply put, although children share biological susceptibility to lead, they are not equally at risk for lead poisoning. Rather, vulnerability to lead poisoning is socially determined. Because they are more likely to live in older houses, low-income and minority children are more likely to be exposed to lead and to suffer from lead poisoning (Lanphear et al. 1998). Recognizing the social factors that make low-income children more susceptible to lead poisoning, the President’s Task Force on Environmental Health Risks and Safety Risks to Children⁸ has called for targeting federal grants to control and remediate lead hazards in low-income housing and expanding blood lead screening and follow-up services for at-risk children, especially Medicaid-eligible children.

At the same time that the environmental health scientists on the President’s Task Force were calling for programs and policies that would address the social factors that make children susceptible to the harmful effects of lead exposure, their colleagues had begun to develop a very different way of conceptualizing how we become vulnerable to lead. In October of 2000, researchers at the Johns Hopkins School of Public Health published the results of a study on lead conducted in Korea⁹ that focused on variations in a person’s genetic makeup, which, in part, determine how lead is handled by the body (Schwartz et al. 2000). The study found that people who carry specific variants of two genes had significantly higher blood, bone, and chelatable¹⁰ lead levels. This project was funded by the National Institute of Environmental Health Sciences’ (NIEHS) Environmental Genome Project, a high-profile research initiative that sought to identify genetic variations that modify the body’s response to environmental exposures, thereby making some people more vulnerable to the harmful effects of toxic substances. The scientists who worked on this study are world-renowned experts in environmental and occupational health. The lead author is particularly well-known for his research on the health effects of cumulative lead exposure. As a result of this work, he has suggested that the measures currently used to regulate occupational exposure to lead (e.g., blood lead levels) are an insufficient basis for assessing risk because they reflect only recent—rather than lifetime—lead exposures; such research has clear and important policy implications. And, these respected environmental health scientists—and public policy advocates—were among many whose research, in the early 1990s, turned to the question of genetic susceptibility to environmental exposures. This book asks what motivated scientists to study gene-environment interaction and explores the consequences of environmental health research that focuses inside the human body and at the molecular level.

LEAD INSIDE THE HUMAN BODY?

At the center of this book are the interlinked puzzles of why and how environmental health scientists rallied around research on gene-environment interaction. To frame these puzzles narrowly—again by focusing on the case of lead—we might ask:

 Given that so much is known about the harmful effects of lead, the social factors that put children at risk of lead poisoning, and the demonstrated though partial successes of policy approaches to reducing lead exposure in the U.S. population, why would the NIEHS prioritize research on the genetics of lead absorption?

 What do scientists believe can be learned about how to prevent lead poisoning by looking deep inside the human body, at the molecular level?

 Given the lead industry’s history of calling into question children’s genetic susceptibilities and behaviors as a means of denying the harmful health effects of lead,11 why would scientists committed to public health study gene-lead interactions?

 Is there any reason to think that knowledge about gene-environment interaction can help to protect low-income and minority children, who are most at risk of lead poisoning?

 Conversely, by focusing attention at the molecular level, might research on gene-environment interaction obscure, however unintentionally, the social, political, and economic factors that make low-income and minority children particularly susceptible to lead poisoning?

To answer these questions, I conducted interviews with more than eighty environmental health scientists, policy makers, and environmental justice activists. I was a participant-observer in research laboratories, at scientific symposia, and at meetings of activists. I undertook a comprehensive review of scientists’ publications.¹² In brief, I found that environmental health scientists offer three broad types of answers, not only in regard to research on lead in particular, but, more generally, on research on gene-environment interaction.

First, environmental health scientists emphasize the ongoing challenges posed to environmental health research insofar as it is used as a basis for regulating industries that produce toxic substances.¹³ For example, one environmental health scientist noted that, although “we have known about the health effects of lead for two thousand years” and clearly can reduce these effects without knowledge of gene-lead interactions, given how “politicized” environmental regulation is, having data about molecular genetic mechanisms “does help make the point” (Interview S50). Related, scientists frame research on gene-environment interaction as a solution to a variety of sources of uncertainty in their research. For regulators who are “constantly fighting an uphill battle with economic forces that would rather preserve the status quo” (Interview S50), any source of perceived scientific uncertainty makes the regulations based on environmental health research vulnerable to legal challenge.¹⁴ Indeed, as documented both by historians and by regulatory scientists, “manufacturing uncertainty” has itself become a “big business” as companies seek to prevent, delay, and overturn regulation (Michaels 2008: 46). Challenging the relevance and/or reliability of the science supporting regulatory decisions is a key strategy of “merchants of doubt” (Oreskes and Conway 2010).¹⁵ According to a prominent environmental health scientist, the contentious dynamics between “industry” and “environmental protection” have become the “drumbeat” to which the field works (Interview S27). Scientists express hope, therefore, that molecular genetic and genomic technologies will make their research findings more robust, especially in the context of risk assessment and regulation (Olden & Wilson 2000).

In a second set of answers, environmental health scientists point to the rising power of the idea that all human disease is a genetic phenomenon. To the extent that scientists, policy makers, and the general public assume that genes are primary determinants of human health and illness,¹⁶ even when research seeks to evaluate disparities in lead poisoning that are most likely “explained by socioeconomic differences, social differences, and exposure differences that vary by the neighborhoods in which people live,” it must also assess genetic influences: “[I]f you want to . . . convince people that it’s not genes, you’ve got to measure genes” (Interview S11). Thus, scientists believe that research on gene-environment interaction may play a role in protecting the jurisdiction (Abbott 1988) of the environmental health sciences, that is, investigation into how the environment affects human health.

Scientists’ third set of answers also centers on jurisdictional concerns, highlighting the possibility that research on gene-environment interaction might generate not only a more robust basis for regulation, but also new biomedical markets for their research. Traditionally, environmental health science has contributed to environmental health risk assessment and regulation; it serves as the empirical basis for public policies that seek to reduce environmentally associated disease at the population level. In regard to its potential to improve public policy, scientists suggest that research on individual genetic variation in susceptibility to environmental hazards demonstrates that existing regulations provide insufficient protection and require revision: “[W]hat it does in that situation is it allows you to say, if we’re going to protect children . . . then it’s not enough to protect the average kid. You’ve got to protect this more [genetically] vulnerable group” (Interview S06). At the same time, research on gene-environment interaction has the potential to foster a “a more biomedical environmental health” (Interview S20), in which environmental health science would inform behavioral and clinical interventions for reducing the harmful health effects of environmental exposures; thus, scientists envision going beyond the “status quo” of “we tell the EPA and FDA and OSHA [that a substance is harmful] and they regulate” (Olden, Oral History Interview July 2004). For example, identifying high-risk individuals might contribute to the development of so-called “lifestyle prescriptions” to minimize the risks of exposure or to new pharmaceutical interventions to prevent harmful consequences of exposure (Olden, Guthrie, & Newton 2001). The NIEHS leadership sees new behavioral and biomedical strategies as especially important for substances like lead because “it’s going to be a long time before we get many of these things out of our environment” (Olden, Oral History Interview July 2004). Further, such an individualized, biomedical approach is well aligned with neoliberal public health policy regimes (Peterson & Lupton 1996).

TOWARD A SOCIOLOGY OF THE ENVIRONMENTAL HEALTH SCIENCES

Each of these answers points to a part of the story told in this book. However, these explanations make sense only within a broader analysis of the field of the environmental health sciences. As such, this book takes the ascendance of gene-environment interaction within the environmental health sciences as an analytic lever¹⁷ that reveals important dimensions of the structure of the field of environmental health science; its central institutions; the commitments, practices, and strategies of those working within it; and how this shapes what we know about—and how we seek to govern—the relationships between the environment and human health. The central argument is that scientists’ perceptions of and responses to the structural vulnerabilities of the field of environmental health sciences have both intended and unintended consequences for what we know about the somatic vulnerabilities of our bodies to environmental exposures.

In crafting this analysis, I draw on several different theoretical frameworks, each of which supports inquiry into a different aspect of environmental health research and its consequences. This theoretical tool kit enables me to ask questions about the structure of the environmental health sciences as a field, to examine the relationships between key institutions, to conceptualize environmental health scientists as skilled social actors, and to investigate the biopolitical effects of their recent strategies.¹⁸ To be clear, my goal in this book is not to extend a given theoretical framework (see Burawoy 1999), but rather to solve an empirical puzzle. Consequently, I use these perspectives to help me identify, describe, and fit together a variety of puzzle pieces. In the following chapters, these theoretical tools appear as “points of departure” and as “a means for generating new questions” (Lamont 2012).

Fields Theory

To begin, I draw on fields theory, an analytic approach (Martin 2003: 24) that highlights the importance of analyzing the forces and struggles within fields (Bourdieu 1996, 1998, 2004).¹⁹ Recent writing on strategic action fields directs analytic attention to four aspects of a field: (1) a diffuse understanding of what is going on in the field, that is, what is at stake (Bourdieu & Wacquant 1992); (2) sets of actors in the field who possess more or less power; (3) a set of shared understandings about the rules of the field, or how “the game” is legitimately played; (4) an interpretive frame that individual and collective actors use to make sense of activity within the field (Fligstein & McAdam 2011: 4).

In this particular case, a big part of what is at stake is the ability to make legitimate and robust claims about the causes of environmental health and illness.²⁰ As such, among the questions explored in the following analysis are:

 What are the rules of the field? Who has the technical capacity and the social power to speak and act legitimately in this domain (Bourdieu 1975: 19)? What kinds of capital govern status within the field?

 What hierarchies exist among actors in the field? Who are the dominant players? That is, which actors have managed to impose a definition of science that says that its highest realization “consists in having, being, doing, what they have, are, and do . . . ” (Bourdieu 2004: 63)? What options are available to scientists whose research is seen as inferior? How might actors endeavor to define good science in ways that will benefit them by increasing the value of the kind of science they do?

 What is the subjective structure, or habitus, that social actors within the field acquire through participation in it (Bourdieu 1996)?21 What “possibilities and impossibilities” are thereby “offered to their dispositions” (Bourdieu 2004: 36)?

Recent writing on strategic action fields has emphasized also the importance of the broader field environment, or what I call an arena.²² As noted by Fligstein and McAdam, “virtually all of the work on fields focuses only on the internal workings of these orders, depicting them as largely self-contained, autonomous worlds.” However, fields do not exist in a vacuum; relationships and boundaries with other fields are often powerful parts of a field’s developmental history (Fligstein & McAdam 2012: 59). Insofar as we fail to attend to the ties that link fields to each other—and to the arenas (or broader field environment) in which they are located—we constrain our ability to understand field dynamics, “including the potential for conflict and change in any given field” (Fligstein & McAdam 2011:8). It is especially important to understand the relationships between a given field and that subset of state and nonstate fields on which it routinely is exposed.²³

A central consideration is the extent to which the field is independent from demands—or shocks—from actors and/or events outside the field. Against the assumption that scientific fields are always “autonomous and isolated,” with changes in science driven primarily by dynamics internal to the field (Albert & Kleinman 2011; 267; Mialet 2003; see also Bourdieu 1975: 29), I seek to investigate empirically conflicts regarding the autonomy and legitimacy of specific forms of knowledge production.²⁴ In so doing, I demonstrate that in the environmental health arena, scientific claims, the struggle for scientific authority, and ongoing political and economic concerns have become deeply intertwined.

Second, my work draws on the insights of institutional theory regarding how fields are constituted and may be reconstituted through patterns of institutional interactions and relations.²⁵ Neoinstitutional theory also focuses on fields but conceives of them more broadly as “those organizations that, in the aggregate, constitute a recognized area of institutional life: key suppliers, resource and product consumers, regulatory agencies, and other agencies that produce similar services and products” (DiMaggio & Powell 1983: 148). Neoinstitutional theory posits that the structure of fields is a consequence of the requirements and demands of the state, the structure of the professions, and competition for resources, political power, and institutional legitimacy. Most broadly, an institutional approach to the sociology of science attends to the “rules and routines, organizations, and resource distributions that shape knowledge production systems” (Frickel & Moore 2006: 7).

Historically, scholars in this tradition also have asked questions about two different, if often interrelated, forms of institutional change. First, scholars have investigated the processes through which institutions come to resemble each other, identifying mechanisms of isomorphic change such as coercion (a consequence of political influence and problems of legitimacy), mimesis (by which institutions copy each other in an effort to manage uncertainty), and norms that are established and transmitted through professional networks (Schneiberg & Clemens 2006). Second, and related, they have asked questions about the diffusion of innovations, behavioral strategies and organizational structures, and their adoption (Strang & Soule 1998: 268). Research on diffusion points to the importance of structural mechanisms, such as social networks and reference groups (Burt 1987; Granovetter 1973; Simmons, Dobbin, & Garrett 2008; Strang & Soule 1998). At the same time, sociologists describe diffusion as a deeply cultural process; for example, the cultural understanding that organizations or institutions belong to a common social category may provide the basis for a tie between them (Strang & Meyer 1993: 490–492). As we will see, both the competition and the connections between NIH institutes, such as the National Cancer Institute (NCI) and NIEHS, and between regulatory agencies, especially the Food and Drug Administration (FDA) and EPA, have motivated, constrained, enabled, and been reshaped by the diffusion of molecular genetic and genomic techniques.²⁶

Viewed through these theoretical lenses—and, as highlighted by the scientists whom I interviewed—the environmental health sciences faced myriad challenges in the waning decades of the twentieth century. I detail these challenges in the following chapters. In brief, they include the relative lack of autonomy of the environmental health sciences as a field,²⁷ ongoing challenges to and critiques of environmental epidemiology and toxicology in controversies over risk assessment and regulation, the rising power of genetic (versus all other) explanations for human health and illness, and growing concern that specific institutions of environmental health research—including the NIEHS and the National Toxicology Program (NTP)—were losing status, funding, and political support. My argument in this book is that research on gene-environment interaction, with its focus inside the human body and at the molecular level, has been compelling to environmental health scientists precisely insofar as it offers a diverse array of strategies for meeting these challenges.²⁸

Strategies and Consequences

Environmental health scientists had choices about how they responded to these challenges, and the decision to take up research on gene-environment interaction was not without risks. I ask ”How did environmental health scientists, as “skilled social actors” (Fligstein 2001), perceive, evaluate, and pursue this particular strategy for strengthening their field, garnering resources for their institutions, protecting their professional jurisdiction, and doing important and meaningful scientific research, as they understand it?²⁹ To answer this question, the subsequent chapters take up also the following topics:

 What motivated environmental health scientists to make gene-environment interaction a defining focus of their research?

 How did environmental health scientists build a coalition around the idea that understanding gene-environment interaction is integral to disease prevention and public health? What identities or stories were at play in constructing this coalition?

 How have environmental health scientists articulated the relevance of gene-environment interactions in the context of a field that historically has oriented primarily on public policy rather than on biomedical interventions?

 In what ways have scientists adapted molecular genetic and genomic technologies, developed originally to study the health of individuals, to answer questions about how environmental exposures affect population health?

 How did advocates for research on gene-environment interaction in the environmental health sciences mobilize support for this view of the future of the environmental health sciences?

Answering these questions requires a careful consideration of the history of the environmental health sciences, especially environmental epidemiology and toxicology, and the relationships among biomedicine, public health, and public policy.³⁰ Therefore, although the phenomena that I seek to explain are decidedly contemporary, my analysis is and must be deeply historical.³¹ The historical accounts highlighted in this book come from archival data, scientists’ written and oral reflections on the trajectories of research in their individual laboratories and/or field, and the work of historians of science and medicine. History is important to understanding actor’s strategies, which vary under different conditions of power and uncertainty; moreover, as will be seen, such strategies have drawn extensively on existing rules, resources, understandings and controversies regarding the warrants of particular fields, institutions, and professions (Fligstein 2001: 106). In crafting this aspect of the analysis, I draw on a relatively loose understanding of path dependence, that is, the insight that key decisions at earlier points in time produce outcomes that set history on a course from which it is often is difficult to return (Katznelson 2003: 290).³² At the same time, I am interested in how the past can be a source of creativity as well as constraint; history may not only foreclose options but “may also lead to and shape the switch points confronted by later generations, drawing fault-lines along which later crises erupt and creating options for new solutions” (Haydu 1998: 357).

Lastly, I consider the consequences of these transformations for how we understand and intervene in the relationships among human bodies, the environment, and health and illness. Specifically, I argue that examining how environmental health scientists and policy makers have taken up, modified, and advocated for research on gene-environment interaction provides an important means of understanding what we know and don’t know about relationships about our bodies, the environment, and human health and illness.

In making this argument, I draw on contemporary writings on biopolitics and coproduction. Biopolitics refers broadly to “all the specific strategies and contestations over problematizations of collective human vitality, morbidity and mortality” (Rabinow & Rosee 2006: 195–217; see also Foucault 1978/1990). Today, three elements constitute biopolitics: “[k]nowledge of vital life processes, power relations that take humans as living beings as their object, and the modes of subjectivation through which subjects work on themselves qua living beings” (Rabinow & Rose 2006). The central insight of coproduction is that our ways of knowing the world are inextricable from controversies regarding how to best live in it (Jasanoff 2004). To understand biopolitics, then, one must examine not only knowledge production, but also the politics of institutions, the making of identities, and their relationships to each other (Epstein 2007). In the context of environmental health, these perspectives highlight the importance of tracing the relationships among knowledge production in the environmental health sciences, the governance of environmental risks to human health, the identification of individual and groups at risk, and the development of notions of the ethics and responsibilities of such persons. When stabilized in relationship to each other, these elements produce a biopolitical paradigm, that is, a “framework of ideas, standards, formal procedures, and unarticulated understandings that specify how concerns about health, medicine, and the body are made the simultaneous focus of biomedicine and state policy” (Epstein 2007: 17). Although we may not be aware of it, the biopolitical paradigm of the environmental health sciences profoundly shapes how we live today.

Chicago Bans Bottles with BPA plastic.³³ San Francisco Passes Cellphone Radiation Law.³⁴ Bottle Maker to Stop Using Plastic Linked to Health Concerns.³⁵ Ground Zero Workers Reach Deal over Claims.³⁶ Current newspaper headlines highlight the many ways that the environmental health sciences enter into our daily lives, determining not only what technologies and products we use, but also what we know about their effects on our health.³⁷ Federal regulatory agencies, such as the EPA and FDA, and their counterparts at the state and local levels, use the results of environmental health research to determine the methods and extent to which they will regulate the emission of industrial chemicals into our communities and whether products containing specific chemicals should remain on the shelves of grocery and drug stores. Industries use data from environmental health research to decide what combinations of chemicals they will use to produce consumer products, as well as to justify their decisions when they are challenged by regulators or activists. In the courts, environmental health science contributes to decisions about whether people who have been exposed to an environmental contaminant should receive compensation for its effects on their bodies or on the bodies of their children. At the same time, as consumers, we increasingly are called upon to use information from environmental health research to make personal choices about the potential risks of the water we drink (“That Tap Water Is Legal but May Be Unhealthy”³⁸), the food we eat (“High Mercury Levels Are Found in Tuna Sushi”³⁹), and the products we use on our bodies and in our homes (“Should You Worry About the Chemicals in Your Makeup?”⁴⁰) (Szasz 2007).

Given the critical role of environmental health research in modern life, social scientists have paid remarkably little attention to the fields, institutions, social actors, and practices most central to the production of contemporary environmental health science.⁴¹ To date, research has tended to focus on the social life of the products of environmental health science, as when specific research on the health effects of a chemical are challenged by environmental health activists (Allen 2003; Brown 2007; Corburn 2005), denied by industry (Brandt 2007; Markowitz & Rosner 2002; Oreskes & Conway 2010; Proctor 1995), or (re)interpreted by legislators (Jasanoff 1990; Keller 2009), rather than examining the scientific research practices and institutional contexts through which such claims come into being. These studies of community-based environmental health controversies and challenges to environmental regulation provide rich analyses of the contentious politics of the environmental health arena. What remains understudied is how contemporary environmental health scientists make choices about the foci and methods of their research, seek to transform processes of risk assessment and regulation, and protect the legitimacy of their field, all in the context of these ongoing political and legal challenges.

GENE-ENVIRONMENT INTERACTION: FROM AN “ANNOYING DETAIL” TO “OUR MANTRA”

The ascendance of gene-environment interaction as a way of understanding how the environment affects human health, its institutionalization⁴² in environmental health research and policy making, and the responses and critiques of environmental justice activists provide the substantive foci of this book.

In the past three decades, environmental health scientists have redefined human genetic variation from an “annoying detail” to a “central determinant of risk” in research on environmental illness (Hattis 1996; see also Puga et al. 1996). By the early 1990s, the NIEHS had made gene-environment interaction its “mantra” (Olden, Oral History Interview July 2004). The NIEHS’s investment in research on gene-environment interaction was instantiated in “flag raising initiatives” (Interview S27), such as the Environmental Genome Project, the National Center for Toxicogenomics, and the Toxicogenomics Research Consortium, and in increased extramural funding for university-based efforts to develop the subfield of molecular epidemiology. Gene-environment interaction is now at the center of collaborations between the NIEHS and the National Human Genome Research Institute (NHGRI), such as the Genes, Environment, and Health Initiative (GEI), a multimillion-dollar project launched in 2006 to identify genetic predispositions and improve the measurement of environmental exposures associated with common diseases, such as asthma, autism, and diabetes (NIEHS 2006).⁴³ NIEHS administrators contend that these initiatives have transformed the standing of their institute:

So, we started [the genomics initiatives] . . . and the National Institute of Environmental Health Sciences has become a major player at the National Institutes of Health. It used to be, quite frankly, that they didn’t see us as important to the mission of the National Institutes of Health, to protecting public health. But now we are a major part of the Institutes—we are integrated with the National Cancer Institute, the National Human Genome Research Institute—and they see how important our work is for public health (Field Notes, NIH December 2001).

As described in the following pages, the genomics initiatives have also transformed profoundly the research practices of many environmental health scientists.

To date, environmental health scientists have established two broad ways of studying gene-environment interaction. First, scientists seek to identify genetic susceptibilities that make some people more vulnerable to being harmed by environmental exposures. In this framing of gene-environment interaction, scientists acknowledge the harmful effects of environmental contaminants, but genetic variations in individuals’ responses to them are the crucial problem to be explained. Second, scientists examine how environmental chemicals affect human genetic material, whether by causing DNA damage (e.g., mutations) or by altering gene expression (e.g., epigenetics). In this framing of gene-environment interaction, scientists acknowledge human genetic variability, but the effects of environmental exposures are the crucial problem to be explained. Although environmental health scientists have long been interested in how environmental pollutants damage DNA (Frickel 2004), they describe the broad integration of molecular genetic and genomic techniques as a “revolution” in their field (Field Notes, NIEHS 2002).

In recent years, this molecular revolution has redefined what it means to do environmental health research in the United States. As a leading molecular epidemiologist⁴⁴ recalled, in the early 1990s, when he first arrived in the department of environmental health sciences at a prestigious school of public health, his colleagues challenged the molecular biological focus of his work:

There was a lot of reluctance to accept the concept that molecular biology had something to say in environmental health. There were many, many older faculty people who weren’t even willing to accept that. [They said] . . . “This is not right. This is bullshit. You are not studying environmental health.”

However, he continued, over time “those people started losing their funding and we started getting our funding. And then the emphasis shifted . . . now we really have created a large group of [scientists studying] molecular biology in the department” (Interview S20). Departments of environmental health science across the country now teach and conduct molecular genetic and genetic research as part of their standard coursework and in the context of interdepartmental programs.⁴⁵ Environmental health scientists advocate for research on gene-environment interaction by claiming that protecting population health requires investigation of “how the environment operates at the molecular level.”⁴⁶

The development of molecular genetic and genomic technologies and practices within the environmental health sciences has not gone unnoticed by other key actors in the arena of environmental health politics. The EPA and FDA have launched partnerships with the NIH and NTP to explore the application of molecular techniques in risk assessment and regulation. One such initiative, Tox21, endeavors to create a system of environmental risk assessment and regulation that replaces whole animal bioassays with in vitro methods that will evaluate the effects of chemicals by examining changes in cell lines (NRC 2007b: 1).⁴⁷ The chemical industry has taken a keen interest in these developments; in 2001, the International Council of Chemical Associations held a workshop and subsequently promulgated their recommendations for “best practices” for emerging “-omics” technologies⁴⁸ (Henry et al. 2002). Environmental health and justice activists have responded to the emergence of molecular genetic and genomic techniques both with curiosity about their potential for enhancing advocacy efforts and with intense criticism of what they see as the limitations and dangers of looking for the causes of human health and illness through a molecular genetic lens.

The critiques of EJ activists highlight the population health implications of environmental health research. A critical issue is whether environmental inequalities are an underlying cause of pervasive health disparities in the United States (Brulle & Pellow 2006; Evans and Kantrowitz 2002). There is evidence that income is often directly related to environmental quality; likewise, there is evidence that poor environmental quality is related to multiple physical and psychological health outcomes (Evans & Kantrowitz 2002: 324). These associations hold for exposure to a wide range of suboptimal environmental conditions (e.g., hazardous wastes and other toxins, ambient and indoor air pollutants, water quality, ambient noise, residential crowding, housing quality, educational facilities, work environments, and neighborhood conditions). Thus, it is possible that “the accumulation of exposure to multiple, suboptimal physical conditions rather than any singular environmental exposure” may accounts for the inverse relationship between income and a wide variety of health outcomes (Evans & Kantrowitz 2002: 304; see also Williams et al. 2010). Consequently, researchers have suggested that integrating data on environmental inequality and its health impacts into the existing research on health disparities is critical to efforts to understand the causes and identify solutions to the ongoing problem of health disparities between demographic groups in the United States (Brulle & Pellow 2006). These concerns about health inequalities have shaped the meanings of research on gene-environment interaction in the environmental health sciences, as well as the efforts of scientists and regulators to build consensus around the potential applications of genomic knowledge in risk assessment.

NOT JUST GENETICIZATION

In its analysis of the ascendance of research on gene-environment interaction in the environmental health sciences, this book contributes also to recent efforts to push social scientific analysis of molecular genetics and genomics beyond the geneticization thesis. Geneticization refers to “an ongoing process by which differences between individuals are reduced to their DNA codes” (Lippmann 1991: 19). Fundamentally, this approach asks us to consider whether and how genes are understood to be the primary cause of health, illness, and other forms of human variation. The concept of geneticization has been at the center of much social scientific analysis, where it often serves as connotative shorthand for a number of interlocking concerns about the myriad potential negative social implications of genetics; however, research suggests that the consequences of molecular genetics and genomics are more complex and contingent (Freese & Shostak 2009). Moreover, I contend that if, following the lead of the geneticization thesis, our analyses focus primarily on the extent to which scientists continue to study environmental causes of variation in human health and social outcomes, we miss the opportunity to observe profound changes in how genes, environments, and human bodies are conceptualized and operationalized in scientific research.

Therefore, in contrast to the geneticization thesis, I draw on the work of social theorists and historians of science to conceptualize the ascendance of research on gene-environment interaction as the molecularization of the environmental health sciences (de Chadarevian & Kamminga 1998; Kay 1993; Rose 2007). The molecular vision of life visualizes, operationalizes, and seeks to act upon life itself—including genes, environments, bodily variations and behaviors—at the submicroscopic level (Kay 1993). The molecularization of biology and medicine began in the 1910s, bringing profound changes in understandings of the causes and appropriate treatment of disease. Broadly speaking, contemporary uses of pharmaceuticals, vitamins, and hormones in biomedicine have their origin in the molecular vision of human health and illness (de Chadarevian and Kamminga 1998: 4; Sturdy 1998). However, even as some disciplines, such as biology, have been extensively molecularized, others, including the environmental health sciences, continued to conduct many of their operations well above the molecular level. For example, while specific domains of toxicology have made use of molecular biological technologies and concepts (Frickel 2004), many of the most important indices of toxicity used in toxicological risk assessments exist at what scientists describe as the “phenomenological” level: body weight, organ weight, level of activity, tumors, and death.⁴⁹ In environmental epidemiology, researchers historically focused on the relationships between exposures, disease, and death at the population level, without looking inside the “black box of the human body” (Interview S04).

Molecularization has met with myriad challenges in the context of environmental health research. Analytically, these challenges make the environmental health sciences an advantageous case for observing the social processes through which molecularization is accomplished. First, molecularizing environmental health research has required that scientists find ways to operationalize gene-environment interaction in work objects (Casper 1998), technologies, and experimental systems relevant to environmental health research. As belied by their names—e.g., environmental response genes, molecular biomarkers—most often, these new objects and practices are hybrid forms that combine more traditional objects with new materials or techniques. The following chapters describe the development of these new ways of doing environmental health research. At the same time, this is a deeply historical analysis, attending particularly to how new techniques extend previous research practices, are shaped by institutional concerns, and seek to address the structural vulnerabilities of the field.

Second, and related, much research in the environmental health sciences is directed toward applications in environmental health risk assessment, regulation, and policy making. Assessing whether a chemical causes mutations in DNA has been a required part of the registration of new chemicals since the passage of the Toxic Substances Control Act in 1976 (Frickel 2004). However, the regulation of the ambient environment depends rather on measurements of chemicals in the air, water, and soil; historically, it has not taken gene-environment interaction into account. Related, the gold standard of toxicological testing relies on the thirteen-week and two-year rodent bioassays and other whole animal studies (NTP 2002). Consequently, even as environmental health scientists argue that molecular genetic and genomic techniques will improve their contributions to environmental regulation, they have had to develop what I call technologies of translation as a means of articulating new modes of knowledge production within established regulatory processes.

Third, and again in contrast to many other domains of research in the life sciences, molecularization requires that environmental health scientists develop strategies for conceptualizing and measuring not just the human body, but the environment at the molecular level. Such strategies have emerged as a site of contention between scientists and environmental justice activists. In particular, activists question the appropriateness of molecular measures, given the extensive evidence of race- and class-based inequalities in environmental exposures (Brulle & Pellow 2006; Evans& Kantrowitz 2002). Many activists are concerned that social structural factors that put poor people and people of color at increased risk of environmental exposure will be obfuscated, however inadvertently, as research on molecular genetic research recasts the environment as something best understood and measured at the molecular level.

Simply put, the environmental health sciences provide an intriguing vantage point for studying the consequences of genetics precisely because the environment is their jurisdictional focus. In fact, some environmental health scientists position their research on gene-environment interaction as a corrective to the Human Genome Project’s genocentric view of human health and illness: “[G]enocentric views reflect a fundamental misunderstanding of the disease process, and have led to unrealistic expectations and disappointment” (Olden & White 2005: 721). In contrast to genocentrism, environmental health scientists contend that research on gene-environment interaction is the key to explaining when and how genetic variations shape human health and illness: “Differences in our genetic makeup certainly influence our risks of developing various illnesses. . . . We only have to look at family medical histories to know that is true. But whether a genetic predisposition actually makes a person sick depends on the interaction between genes and the environment” (NIEHS 2006; see also Schwartz & Collins 2007).

Sociologists have expressed skepticism about the extent to which scientific research on gene-environment interaction actually represents an alternative to geneticization. Some have suggested that research on gene-environment interaction generates merely a narrative of “enlightened geneticization,” which privileges genetic explanations and minimizes the effect of environmental factors, even while acknowledging that they play a role in human health and illness (Hedgecoe 2001). Others note that media coverage of research on gene-environment interaction selectively emphasizes genes and largely ignores environmental causes (Horwitz 2005).

My analysis shifts the focus, however, to the question of how different kinds of research on gene-environment interaction conceptualize and measure genes, environments, and their effects on human bodies. This allows us to see that at stake in this research is not only the question of whether genes or the environment cause human health and illness. Rather, I demonstrate that, by conceptualizing and measuring the environment at the molecular level, research on gene-environment interaction has profound consequences for how we understand the environment and how it affects our health.