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Increased risk for lead exposure in children through consumption of produce grown in urban soils.

ABSTRACT: Childhood Pb exposure is associated with a multitude of poor health outcomes. In food-insecure areas, growing fresh produce in backyard gardens or on vacant industrial properties is seen as an option for parents. The question arises, could Pb accumulate in consumable tissues of common produce when grown in metals-rich soils at concentrations that would pose a risk to children. This study investigated factors contributing to the accumulation of Pb in consumable tissues of nine common produce crops grown in metals-rich soils from backyard gardens and a former industrial property. Pb in consumable tissues was directly quantified at concentrations less than 1 μg g^-1 via X-ray fluorescence (XRF) using protocols specifically developed for use in plant matrices. The accumulation of Pb in prepared raw consumable tissues in three Pb-rich soils was the greatest in modified taproot crops (mean Pb of 11.8 ± 14.6 μg g^-1; turnip, beetroot, radish, carrot), with lesser concentrations in fruits (mean Pb of 2.0 ± 3.0 μg g^-1; tomato, pepper), and potatoes (mean Pb of 0.7 ± 1.1 μg g^-1). An exposure risk evaluation using the USFDA IRL for Pb indicates that consumption of less than 1 g of certain produce grown in this study, including produce grown in garden soils from residential properties, drastically increases the risk of Pb exposure in children. This study further indicates that the proportion of Pb contributed to the daily body burden in children from food is far greater than previously understood, and in all modeled cases, the contribution of Pb from food on a daily basis far outweighs the contribution of Pb from drinking water. For an average child, after addressing over-riding soil/dust impacts, addressing food quality is critical to minimizing Pb exposure.

SUBMITTER: Byers HL

PROVIDER: S-EPMC7492482 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description: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??g/g (SD: 0.18). Egg lead concentrations ranged from below the limit of detection (0.0014??g/g) to 1.798??g/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??g/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??g/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.

Project description:BackgroundHigh blood pressure (BP) in childhood is frequently renal in origin and a risk factor for adult hypertension and cardiovascular disease. Shorter gestations are a known risk factor for increased BP in adults and children, due in part to a nephron deficit in children born preterm. As nephrogenesis is incomplete until 36 weeks gestation, prenatal lead exposure occurring during a susceptible period of renal development may contribute to programming for later life renal disease. The relationship between shorter gestation and children's BP has not yet been explored to identify i) critical windows using nonlinear piecewise models or ii) combined with other early life risk factors such as prenatal lead exposure.Objectives(1) To evaluate the nonlinear relationship between lower gestational age and childhood BP measured at 4-6 years of age, and (2) to investigate modification by prenatal lead exposure.MethodsIn a prospective longitudinal birth cohort, we assessed 565 children between 4 and 6 years of age (mean: 4.8 years) in the PROGRESS cohort in Mexico City, Mexico. Gestational age at delivery was calculated using maternal report of last menstrual period (LMP) and confirmed with Capurro physical examination at birth. We measured pregnant women's blood lead levels (BLLs) in the second trimester via inductively coupled plasma-mass spectrometry and children's BP using an automated device. We performed both linear and nonlinear piecewise regression analyses to examine associations of gestational age with children's BP adjusting for children's age, sex, height, prenatal exposure to smoke, and maternal socioeconomic status. We stratified to assess modification by prenatal lead exposure, and used a data-adaptive approach to identify a lead cutpoint.ResultsMaternal second trimester BLLs ranged from 0.7 to 17.8 μg/dL with 112 (20%) women above the CDC guideline level of 5 μg/dL. In adjusted linear regression models, a one week reduction in gestational age was associated with a 0.5 mm Hg (95%CI: 0.2, 0.8) increase in SBP and a 0.4 mm Hg (95%CI 0.1, 0.6) increase in DBP. Our nonlinear models suggested evidence for different magnitude estimates on either side of an estimated join-point at 35.9 weeks' gestation, but did not reach statistical significance. However, when stratified by prenatal lead exposure, we identified a cutpoint lead level of concern of 2.5 μg/dL that suggested an interaction between gestational age and blood lead. Specifically, for BLLs ≥ 2.5 μg/dL, SBP was 1.6 (95%CI: 0.3, 2.9) mm Hg higher per each week reduction in gestational age among children born before 37.0 weeks; and among children born after 37.0 weeks, this relationship was attenuated yet remained significant [β: 0.9, 95%CI (0.2, 1.6)]. At BLLs below 2.5 μg/dL, there was no appreciable association between lower gestational age and SBP.ConclusionsOur findings suggest that shorter gestation combined with higher prenatal lead exposure contributes to a higher risk of increased SBP at 4-6 years of age, particularly among infants born <37 weeks gestation. Our results underscore the importance of preventing prenatal lead exposure - even levels as low as 2.5 μg/dL - especially among pregnant women at risk for preterm birth. Given that high BP in childhood is a risk factor for adult hypertension and cardiovascular disease later in life, these results may have implications that extend across the life span.

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Increased risk for lead exposure in children through consumption of produce grown in urban soils.

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