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Centuries of human activities, particularly housing and transportation practices from the late 19(th) century through the 1980’s, dispersed hundreds of millions of tons of lead into our urban areas. The urban lead burden is evident among humans, wild and domesticated animals, and plants. Animal lead exposures closely mirror and often exceed the lead exposure patterns of their human partners. Some examples: Pigeons in New York City neighborhoods mimicked the lead exposures of neighborhood children, with more contaminated areas associated with higher exposures in both species. Also, immediately following the lead in drinking water crisis in Flint MI in 2015, blood lead levels in pet dogs in Flint were 4 times higher than in surrounding towns. And combining lead’s neurotoxicity with urban stress results in well-characterized aggressive behaviors across multiple species. Lead pollution is not distributed evenly across urban areas. Although average US pediatric lead exposures have declined by 90% since the 1970s, there remain well defined neighborhoods where children continue to have toxic lead exposures; animals are poisoned there, too. Those neighborhoods tend to have disproportionate commercial and industrial lead activity; a history of dense traffic; older and deteriorating housing; past and operating landfills, dumps and hazardous waste sites; and often lead contaminated drinking water. The population there tends to be low income and minority. Urban wild and domesticated animals bear that same lead burden. Soil, buildings, dust and even trees constitute huge lead repositories throughout urban areas. Until and unless we begin to address the lead repositories in our cities, the urban lead burden will continue to impose enormous costs distributed disproportionately across the domains of the natural environment. Evidence-based research has shown the efficacy and cost-effectiveness of some US public policies to prevent or reduce these exposures. We end with a series of recommendations to manage lead-safe urban environments.

Lead adversely impacts the health of humans, animals, and the natural environment. Higher lead burdens in warm weather occur in humans, domesticated and wild animals; land and water species; urban and rural, developed and pristine environments. The array of evidence suggests that lead seasonality is multifactorial within the natural world, including humans. Seasonally higher temperatures, solar radiation, humidity and anthropogenic pollution result in lower pH (acidification) in air, water and soil. Environmental acidification increases lead's bioavailability and mobility thus intensifying human, animal and plant exposures. In addition, lead seasonality in the biosphere is influenced by higher growth rates, slightly increased exposures, and more Vitamin D metabolism. Methodologically, we applied a One Health perspective to EPA's Integrated Science Assessments of Lead to review the published literature, supplemented with subsequent and related publications to assess data on the seasonality of lead exposure across species and through the earth's systems. Our integrated assessment suggests that: 1) 'Seasonality' is a multifactorial, terrestrial phenomenon affecting the natural world; human activities have exacerbated natural cyclicities that impact lead exposures across species. 2) To be sustainable, human lead remediation strategies must consider the total environment. 3) Global warming and climate change events may increase lead exposures and toxicity to all species throughout the natural environment.

Backyard chicken ownership is rapidly increasing in urban areas in the United States, largely as a way to provide eggs for household consumption. Despite elevated levels of environmental lead contamination in many US cities, the role of backyard chicken eggs as a pathway for lead exposure, particularly for children, has received limited scrutiny. To characterize lead exposure from consumption of backyard chicken eggs for children and predict related effects on blood lead level (BLL), we conducted a cross-sectional study of backyard chicken owners in the Greater Boston area (n = 51). We interviewed participants regarding egg consumption by household members and collected backyard eggs (n = 201) and coop soil samples (n = 48) for analysis. Inductively coupled plasma mass spectrometry (ICP-MS) was used to evaluate lead concentration in homogenized eggs and an X-ray fluorescence (XRF) portable device was used to assess soil lead levels in the laboratory. We used the USEPA's Integrated Exposure Uptake Biokinetic Model for Lead in Children (IEUBK) to assess the relative contribution of backyard egg consumption to aggregate BLL in children. Four scenarios were developed in the IEUBK model to address variability in egg consumption rates and egg lead contamination. Lead was detected in egg samples from 98% of the households that provided egg samples. Mean household lead concentration was 0.10 μg/g (SD: 0.18). Egg lead concentrations ranged from below the limit of detection (0.0014 μg/g) to 1.798 μg/g (1.4-1198 ppb). Egg lead levels were strongly positively correlated with lead concentration in coop soil (r = 0.64; p 0.001). In modeled scenarios where a child 7 years frequently ate eggs highly contaminated with lead, BLLs are predicted to increase by 0.9-1.5 μg/dL. In three other scenarios reflecting more moderate egg lead contamination and consumption rates, BLLs were predicted to increase from 0.1 to 0.8 μg/dL. Consumption of backyard chicken eggs can contribute to lead exposure in children. Soil lead remediation prior to chicken ownership may reduce lead exposure from backyard eggs.