When designing a study considering the effects of lead on human health, it is important to consider potential routes of exposure that may contribute to any lead levels detected. This consideration is important both tor the purposes of designing interventions intended to limit exposure and for providing information on potential confounding variables (e.g., socioeconomic status). While lead exposure is declining in the United States, it remains present in the modern environment, creating potential exposure risks that carry significant health effects. Historically, lead exposure in the United States and in most developed countries originated from lead-based gasoline in automobiles and lead-based paint in home residences. Growing recognition of the health effects of lead in the 1970s ushered in governmental regulation. In 1973, the Environmental Protection Agency initiated regulations requiring reductions in the amount of lead content in gasoline (Lewis, 1985), while in 1990, revisions to the Clean Air Act resulted in a complete ban on lead-based gasoline. In addition, in 1978 a ban was issued on lead-based residential paint, followed in 1986 by a ban on lead products used in plumbing (Brown & Margolis, 2012). Collectively, these regulations—particularly the restrictions on lead-based gasoline—have produced a dramatic decline in BLLs in both children and adults (Pirkle, 1994).
While these regulations have been effective, they have not curbed occupational exposure, which remains the leading cause of lead exposure in adults. According to the most recent estimates from the Adult Blood Lead Epidemiology and Surveillance Program, 20.4 per 100,000 employed adults in the United States have a BLL of 10 pg/dL or higher (Alarcon, 2016). Elevated lead exposure is prevalent for individuals employed in manufacturing (e.g., storage battery manufacturing), construction (e.g., highway, street, and bridge construction), remediation services, or mining industries (e.g., copper, nickel, lead, zinc; reviewed in Shafter & Gilbert, 2018), as well as for workers in developing countries where regulations limiting worker lead exposure are absent (e.g., Gottesfeld & Pokhrel, 2011).
In contrast to adults, ingestion of lead present in soil, dust, and paint chips is the primary cause of exposure in children (Council on Environmental Health, 2016). Lead may be present in the soil surrounding a home due to its proximity to the street, deteriorating exterior paint, or renovations performed on the home's exterior (e.g., Mielke, Powell, Shah, Gonzales, & Mielke, 2001; Zahran, Laidlaw, McElmurry, Filippelli, & Taylor, 2013). Indoor household dust may contain lead particles from contaminated soil brought into the home from footwear worn outside (Clark, Menrath, Chen, Succop, Bornschein, Galke, et al., 2004). Aside from external sources of lead brought into the home, interior sources of lead may also be ingested. Most notably, paint chips from deteriorating indoor lead-based paint (Su, Barrueto, & Hoffman, 2002) and lead present in water from aging pipes can contribute to children’s lead exposure, most recently demonstrated by the Flint water crisis (Hanna-Attisha, LaChance, Sadler, & Champney Schnepp, 2016; Ngueta, Abdous, Tardif, St-Laurent, & Levalloi, 2016). The risk for exposure conveyed by these different routes varies depending upon a child’s age. Lead ingested from soil or household dust is the major lead exposure route in children from birth to six months, while lead ingested from water is the major route of exposure in children between one and two years old (Zartarian, Xue, Tornero-Velez, & Brown, 2017).
Well-designed research exploring lead exposure routes is essential, given the established effects of lead on various health outcomes (see “Health Outcome Selection" later for a review). A natural experiment conducted by Mielke, Gonzales, Powell, and Mielke (2017) provides an example of a creative research design that demonstrates the impact of lead-contaminated soil on children's BLLs. In the study, soil lead concentrations and BLLs in children under six years were compared before and after Hurricane Katrina. Following Katrina, the city of New Orleans razed and replaced all public housing using lead-free paint and amended landscapes on both public and private properties with fresh soil. These actions provided an unplanned opportunity for lead abatement. Soil samples were collected as part of an ongoing series of soil surveys performed in New Orleans (Mielke, Gonzales, Powell, & Mielke, 2005, 2016).
In total, 3314 pre-Katrina soil samples were collected from 1998 to 2001 and 3320 post-Katrina soil samples were collected from 2013 to 2015. Blood samples were obtained from the Louisiana Childhood Blood Lead Surveillance System, a local program conducted by the Louisiana State Department of Health to monitor the BLLs of children residing within the state. In total, 13,379 pre-Katrina and 4,820 post-Katrina blood samples were collected. Soil and blood samples were divided into four groups according to their geographical location within the city of New Orleans (i.e., public vs. private properties located within the core vs. outer regions of the city). Results demonstrated large reductions in the soil lead content and corresponding decreases in the BLLs of children residing in New Orleans in all groups. In particular, soil lead concentrations decreased 59% to 81% in the private and public core areas of the city—regions in which congested traffic patterns, deteriorating housing, and aging lead smelting plants are located. Likewise, in these regions of the city, the percentage of children with BLLs exceeding 5 pg/dL decreased by 70% to 88%. Collectively, these results highlight the profound impact that soil replacement can have on child BLLs and provide a compelling argument for the implementation of polices and soil replacement practices in the city of New Orleans.
Although relatively high BLLs are likely a consequence of these important exposure routes, low-level BLLs might occur as a result of more pervasive and repeated low-level exposure to sources such as airborne dust from contaminated soil (Laidlaw, Mielke, Filippelli, Johnson, & Gonzales, 2005) and food (Leroux, Ferreira, Silva, Bezerra, da Silva, Salles, et al., 2018). For example, in the Environmental Exposures and Child Health Outcomes (EECHO) cohort, we have found that African American (AA) children have significantly higher BLLs than European American (EA) children, and, furthermore, this difference in BLL is a result of AAs consuming more total fruit (based on total dietary records) than EAs (Gump, Hruska, Parsons, Palmer, MacKenzie, Bendinskas, et al., 2020). From a public health standpoint, these prevalent, low-level, persistent sources of lead exposure may be more important than isolated, high-level, acute sources of lead exposure (e.g., water pipes in Flint, Michigan; Ruckart, Ettinger, Hanna-Attisha, Jones, Davis, & Breysse, 2019). Moreover, such chronic low-level exposures might be particularly important in the etiology of slow-developing diseases such as CRD and hypertension.