This study addresses integrating atmospheric lead (Pb), soil Pb, and blood Pb for understanding spatiotemporal dynamics of Pb poisoning, especially in urban settings. The 1925 Yandell Henderson warning about the effects of inhaled air Pb on physiology and human organ systems suggested that Pb aerosols are especially important and underrecognized [1]. Current studies relating air Pb and blood Pb support Professor Henderson’s early concerns.

A major issue for the research community was the inability to measure clinically, environmentally, and appropriately small quantities of Pb. This capability only became widely available in the late 1960s and early 1970s [2]. A major application was the measurement of blood Pb and conducting clinical studies. The combination of blood Pb and human clinical studies revealed that Pb exposure was excessive, and the public health response was to lower the blood Pb guidelines [2].

The use of leaded petrol was approved despite Henderson’s concerns about inhalation. The lead industry promoted leaded petrol and within a few decades, Pb contamination became an international public health disaster [3]. The blood Pb of children and adults fluctuates depending on the culture and regulations in each country regarding the use of leaded petrol. Children are the most susceptible group to Pb exposure. The consequences of children’s Pb exposure includes damaging effects on intelligence and behavior and negative effects on personality traits of the adult population [4,5]. By 30 August 2021, nearly a century after Henderson’s statements, leaded petrol for highway use was banned throughout the world [6].

Lead-based paints, with high Pb content, have often been assumed to be the major source of lead poisoning. The Lead Industry Association (LIA) actively dissuaded any notion that sources of Pb beyond lead-based paint have been involved in lead poisoning. On 14 April 1969, the board of directors of the LIA stated, “It should be a primary objective of any LIA program, or LIA participation in other programs, aimed at resolving the childhood lead poisoning problem to keep attention focused on old, leaded paint as its primary source and to make clear that other sources of lead are not significantly involved [7].” The critical issue is the failure to include Pb aerosols from Pb additives in petrol as a major source of Pb exposure, a bias that continues [8]. As Figure 1 illustrates, the amount of Pb used in the U.S. as Pb additives in petrol (gasoline) was about equal to the amount of Pb in lead-based paint [9].

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Overall, these studies from around the world show that leaded gasoline emissions created high levels of air Pb, which resulted in high levels of children’s blood Pb, as well as high levels of soil Pb. Results from the UK, New Zealand, Mexico, Durban SA, Korea, NW Europe, and the US show that the decline in leaded petrol air emissions was also a driver of reductions in blood Pb levels. US agencies generally focused on lead-based paint and associated Pb dust as the primary source of lead poisoning and followed a “soil Pb is due to old leaded paint” mantra promoted by the lead industry [7]. Most European countries agreed to ban the use of lead-based paint for household use in the 1920s; the US did not agree to the ban until 1978. Pb in household paint was then regulated to 600 µg/g, still a significant amount of Pb [29]. While leaded paint is undeniably a local exposure source, we call attention to the rapid decline in blood Pb following the cessation of leaded petrol as shown by Figure 2, Figure 3, Figure 4 and Figure 5 and backed by U.S. blood Pb reports [30,31], demonstrating the importance of atmospheric Pb from leaded petrol as a major source of exposure. However, despite the sharp decreases in air Pb, the blood Pb responses were not as steep. Furthermore, as illustrated globally by Figure 2, Figure 3, Figure 4 and Figure 5, population blood Pb stabilizes at concentrations above zero, levels which clinicians regard as unsafe [5,29].

Studies conducted in Korea and NW Europe provide insights into the causes of the continued above zero µg/dL Pb exposure of the population. Korea observed that further regulation of other sources of Pb such as industrial, food, and baby products are required to reduce exposure [24]. Studies in NW Europe and the discrepancy between air Pb and blood Pb suggests alternative Pb sources continue to present exposure. These include exogenous (outside the body) and endogenous (inside the body) Pb sources [25].

Exogenous sources of Pb include inhaled air Pb [1]. Even though air Pb has declined, it persists as a legacy source of Pb. As described in Section 3.2.1, the findings in London show that current atmospheric Pb isotopes match the soil and dust Pb, originally emitted to the environment from vehicles using leaded petrol [26]. Studies from New Orleans, described in Section 3.2.2, illustrate that Pb contaminated soil is strongly associated with blood Pb [27]. The atmospheric Pb becomes settled Pb dust in the environment. Lead dust in soil is a reservoir of Pb and consequently, a source for further Pb exposure via inhalation and dust ingestion. As demonstrated in London, air Pb, driven by remobilization from the past accumulation of soil Pb, appears to have become an important contributor to the Pb baseline in urban environments. The amount of soil Pb depends on the size of an urban area; the larger the city, the more highly contaminated the soils will be [32]. Here, we place the research from London into global context, connecting the available data on air Pb, soil Pb, and blood Pb, to show how ubiquitous and harmful these legacy Pb sources are.

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