For their time and consideration in reading drafts of chapters—and, in some instances, the entire manuscript—I offer my heartfelt thanks to Rene Almeling, Peter Bearman, Debbie Becher, Jason Beckfield, Ruha Benjamin, Catherine Bliss, Phil Brown, Wendy Cadge, Monica Casper, Peter Conrad, David Cunningham, Scott Frickel, Micah Kleit, Sabrina McCormick, Alondra Nelson, Aaron Panofsky, David Pellow, Jenny Reardon, Sarah Richardson, David Rosner, Natasha Schull, Janet Shim, Stefan Timmermans, Jocelyn Viterna, and Peter Wissoker. For helping me navigate my way through the writings of Pierre Bourdieu, I thank Aaron Panofsky, Rebecca Lave, and Catherine Bliss. I am grateful to Phil Brown for suggesting that I write what became the Afterword, and for being a role model for scholars interested in the intersections between sociology, health, and the environment. I really could not ask for better colleagues and am happy to count so many of these scholars as my friends.
I am indebted to Phil Brown and David Rosner for directing me to Hannah Love, the editor for health at the University of California Press. Hannah guided the manuscript through the review process with a mix of intelligence and grace that was a true blessing for a new author. I was privileged, then, to work with Naomi Schneider during the process of revising and bringing the manuscript to press. I thank Chris Lura and Francisco Reinking for their skillful project management.
No words are adequate to express my appreciation to my friends for the love, cheerleading, solace, and great company that they have provided in the decade it took me to complete this project. I trust that you know who you are when I say thank you for taking long walks with me, inviting me to stay with you (in California each winter, in New York year-round), indulging my need for adventures (especially by the ocean), showing up (sometimes across great distances) without my even asking, offering your home as a writing retreat (and writing there with me), sharing summer veggies (thank you to Waltham Fields Community Farm for the veggies themselves), sitting with me in silence (even for a week at a time), going out with me to hear music (as well as being the source of that music), encouraging me to bike and to read and to garden and to cook, and, in so many ways, reminding me of all that is beautiful in the world. Two very young people brought especial gifts: Jackson and Arabella. Thank you for singing to my Mom—and me—during difficult moments.
Finally, I humbly offer boundless love and gratitude to my family. To my father, Peter, whose unwavering faith in me and my abilities set me on the right path and, when needed, helped me keep moving forward. To Eli and Erin, whom I would choose to have by my side in any situation, and to Delia Jane, whose presence brings such joy. To Matt, who gave me safe harbor when I needed it most and seems to be able to make me laugh in any situation. A Kauany, minha linda enteada. And to my mother, Myra, whose unending strength, ability to love, capacity for amazement, and commitment to “turn toward gratitude” made me who I am and continue to inspire me every day.
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