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