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Lead (Pb) is extremely toxic and a major cause of chronic diseases worldwide. Pb is associated with health disparities, particularly within low-income populations. In biological systems, Pb mimics calcium and, among other effects, interrupts cell signaling. Furthermore, Pb exposure results in epigenetic changes that affect multi-generational gene expression. Exposure to Pb has decreased through primary prevention, including removal of Pb solder from canned food, regulating lead-based paint, and especially eliminating Pb additives in gasoline. While researchers observe a continuous decline in children’s blood lead (BPb), reservoirs of exposure persist in topsoil, which stores the legacy dust from leaded gasoline and other sources. Our surveys of metropolitan New Orleans reveal that median topsoil Pb in communities (n = 274) decreased 44% from 99 mg/kg to 54 mg/kg (P value of 2.09 × 10−08), with a median depletion rate of ∼2.4 mg·kg·y−1 over 15 y. From 2000 through 2005 to 2011 through 2016, children’s BPb declined from 3.6 μg/dL to 1.2 μg/dL or 64%(P value of 2.02 × 10−85), a decrease of ∼0.2 μg·dL·y−1 during a median of 12 y. Here, we explore the decline of children’s BPb by examining a metabolism of cities framework of inputs, transformations, storages, and outputs. Our findings indicate that decreasing Pb in topsoil is an important factor in the continuous decline of children’s BPb. Similar reductions are expected in other major US cities. The most contaminated urban communities, usually inhabited by vulnerable populations, require further reductions of topsoil Pb to fulfill primary prevention for the nation’s children.

During the past 45 years, exposure to lead has declined dramatically in the United States. This sustained decline is measured by blood and environmental lead levels and achieved through control of lead sources, emission reductions, federal regulations, and applied public health efforts. Explore regulatory factors that contributed to the decrease in exposure to lead among the US population since 1970. We present historical information about the control of lead sources and the reduction of emissions through regulatory and selected applied public health efforts, which have contributed to decreases in lead exposure in the United States. Sources of lead exposure, exposure pathways, blood lead measurements, and special populations at risk are described. From 1976-1980 to 2015-2016, the geometric mean blood lead level (BLL) of the US population aged 1 to 74 years dropped from 12.8 to 0.82 μg/dL, a decline of 93.6%. Yet, an estimated 500 000 children aged 1 to 5 years have BLLs at or above the blood lead reference value of 5 μg/dL established by the Centers for Disease Control and Prevention. Low levels of exposure can lead to adverse health effects. There is no safe level of lead exposure, and child BLLs less than 10 μg/dL are known to adversely affect IQ and behavior. When the exposure source is known, approximately 95% of BLLs of 25 μg/dL or higher are work-related among US adults. Despite much progress in reducing exposure to lead in the United States, there are challenges to eliminating exposure. There are future challenges, particularly from the inequitable distribution of lead hazards among some communities. Maintaining federal, state, and local capacity to identify and respond to populations at high risk can help eliminate lead exposure as a public health problem. The results of this review show that the use of strong evidence-based programs and practices, as well as regulatory authority, can help control or eliminate lead hazards before children and adults are exposed.

In our study, blood concentrations of lead (Pb), arsenic (As), and cadmium (Cd) and urine concentrations of thallium (Tl) were measured together with related symptoms of heavy metal poisoning in cigarette smoking volunteers diagnosed with schizophrenia, in cigarette smokers not diagnosed with schizophrenia, and in the control group of non-smokers and not diagnosed with schizophrenia volunteers. Our study was performed on 171 volunteers divided into the following subgroups: patients diagnosed with schizophrenia with at least 1 year of continuous cigarette smoking experience (56 participants), cigarette smokers not diagnosed with schizophrenia with at least one year of continuous smoking experience (58), and control group (not diagnosed with schizophrenia and non-smoking volunteers) (57). Smoking durations of cigarette smokers diagnosed with schizophrenia and cigarette smokers not diagnosed with schizophrenia are not similar (p = 0.431). Blood Pb, As, and Cd concentrations and urine Tl concentrations were the highest in the subgroup of cigarette smokers not diagnosed with schizophrenia, followed by the subgroup of cigarette smokers diagnosed with schizophrenia, and the control group. Only blood Pb concentrations were significantly higher (probability value p < 0.05) in the group of cigarette smokers not diagnosed with schizophrenia (5.16 μg/dL), comparing to the group of cigarette smokers diagnosed with schizophrenia (3.83 μg/dL) and to the control group (3.43 μg/dL). Blood Cd and As concentrations and urine Tl concentrations were significantly higher (p < 0.05) in cigarette smokers not diagnosed with schizophrenia than in the control group. The results revealed a statistically significant positive correlation (p < 0.001) in the cigarette smokers in the schizophrenia diagnosed group between blood Pb, blood As, and urine Tl concentrations and the duration of cigarette smoking.

Traditional and alternative medicines are widely used around the world and include for example herbal medicine, Ayurveda, traditional Chinese medicine, and indigenous therapies. Due to the long history and the mostly natural origin of traditional remedies, it is often assumed that they are harmless, but in recent decades more and more case reports have been published in which traditional medicine has caused metal poisoning. This paper provides an analysis of published cases in which patients have suffered metal poisoning due to traditional or alternative medicines. A systematic literature search was performed on PubMed, whereby 210 patient cases from a total of 102 case reports and 30 case series were identified and then analyzed about various aspects. Most of the traditional medicines involved come from Asia and are mainly contaminated with lead and arsenic. The analyzed patient cases show a high degree of heterogeneity with regard to age, sex, intake reason, symptoms, and severity of intoxication. The metal intoxication itself and the cause of the poisoning often remained unrecognized for a long time, which resulted in many patients undergoing unnecessary diagnostic methods and ineffective therapeutic approaches before the correct diagnosis was made. The evaluation of the available patient cases revealed a higher sensitivity to metal poisoning in children compared to adults and a higher sensitivity in men compared to women. Anemia and basophilic stippling were frequently observed and became more common as the metal content in the blood increased. Hopefully, this paper raises awareness of the potential dangers of traditional and alternative medicines, both from the patient’s and the doctor’s perspective, so that in case of intoxication, treatment can be initiated quickly using the correct diagnostic methods. As ingested metals do not only circulate in the blood but also accumulate in soft tissues and bones, long-term monitoring is necessary to ensure that patients make a full recovery. Doctors should be aware that, in contrast to common belief, men are more sensitive to this type of intoxication than women, necessitating particular attention for diagnosis and treatment.

The reduction in cardiovascular disease (CVD) events with edetate disodium (EDTA) in the Trial to Assess Chelation Therapy (TACT) suggested that chelation of toxic metals might provide novel opportunities to reduce CVD in patients with diabetes. Lead and cadmium are vasculotoxic metals chelated by EDTA. We present baseline characteristics for participants in TACT2, a randomized, double-masked, placebo-controlled trial designed as a replication of the TACT trial limited to patients with diabetes. TACT2 enrolled 1,000 participants with diabetes and prior myocardial infarction, age 50 years or older between September 2016 and December 2020. Among 959 participants with at least one infusion, 933 had blood and/or urine metals measured at the Centers for Diseases Control and Prevention using the same methodology as in the National Health and Nutrition Examination Survey (NHANES). We compared metal levels in TACT2 to a contemporaneous subset of NHANES participants with CVD, diabetes and other inclusion criteria similar to TACT2’s participants. At baseline, the median (interquartile range, IQR) age was 67 (60, 72) years, 27% were women, 78% reported white race, mean (SD) BMI was 32.7 (6.6) kg/m2, 4% reported type 1 diabetes, 46.8% were treated with insulin, 22.3% with GLP1-receptor agonists or SGLT-2 inhibitors, 90.2% with aspirin, warfarin or P2Y12 inhibitors, and 86.5% with statins. Blood lead was detectable in all participants; median (IQR) was 9.19 (6.30, 13.9) µg/L. Blood and urine cadmium were detectable in 97% and median (IQR) levels were 0.28 (0.18, 0.43) µg/L and 0.30 (0.18, 0.51) µg/g creatinine, respectively. Metal levels were largely similar to those in the contemporaneous NHANES subset. TACT2 participants were characterized by high use of medication to treat CVD and diabetes and similar baseline metal levels as in the general US population. TACT2 will determine whether chelation therapy reduces the occurrence of subsequent CVD events in this high-risk population. ClinicalTrials.gov. Identifier: NCT02733185. https://clinicaltrials.gov/study/NCT02733185

Environmental lead exposure leads to various deleterious effects on multiple organs and systems, including the hematopoietic system. To explore the effects of lead exposure on platelet indices in preschool children from an informal, lead-contaminated electronic waste (e-waste) recycling area, we collected venous blood samples from 466 preschool children (331 from an e-waste area (Guiyu) and 135 from a non-e-waste area (Haojiang)). Child blood lead levels (BLLs) were determined by graphite furnace atomic absorption spectrophotometry, while platelet indices were quantified using a Sysmex XT-1800i hematology analyzer. Higher blood lead levels are observed in e-waste lead-exposed preschool children. Significant relationships between high blood lead levels (exceeding current health limits) and elevated platelet count (PLT), plateletcrit (PCT), mean platelet volume (MPV), and platelet large cell ratio (P-LCR) were also uncovered. Furthermore, the median PLT and PCT levels of children from the exposed group both exceeded the respective recommended maximum reference range value, whereas the reference group did not. Location of child residence in Guiyu and BLLs were both risk factors related to platelet indices. These results suggest that high blood lead exposure from e-waste recycling may increase the risk of an amplified coagulation process through the activation of platelets in preschool children.

Hypertension remains a major global public health crisis due to various contributing factors, such as age and environmental exposures. This study delves into exploring the intricate association between biological aging, blood lead levels, and hypertension, along with examining the mediating role of blood lead levels in the relationship between biological aging and hypertension. We analyzed data from two cycles of the NHANES, encompassing 4473 individuals aged 18 years and older. Our findings indicate that biological aging potentially escalates the risk of hypertension and the incidences of systolic blood pressure (SBP) and diastolic blood pressure (DBP) abnormalities. Utilizing weighted quantile sum (WQS) and quantile g-computation (QGC) model analyses, we observed that exposure to heavy metal mixtures, particularly lead, may elevate the likelihood of hypertension, SBP, and DBP abnormalities. Further mediation analysis revealed that lead significantly mediated the relationship between biological aging and hypertension and between biological aging and SBP abnormalities, accounting for 64% (95% CI, 49% to 89%) and 64% (95% CI, 44% to 88%) of the effects, respectively. These outcomes emphasize the criticality of implementing environmental health measures.

Epidemiological evidence on the relationship between lead exposure and mortality in specific chronic kidney disease (CKD) populations is limited. We aimed to examine the relationship between urinary lead and blood lead concentrations and all-cause mortality in US patients with CKD. This cohort study included 2320 participants with CKD from the National Health and Nutrition Examination Survey (2005–2018), with follow-up until December 31, 2019. All-cause mortality was ascertained by matching US National Death Index records. Hazard ratios (HRs) and 95% confidence intervals (CI) for urinary lead and blood lead concentrations in relation to all-cause mortality were estimated using a weighted Cox regression model. During a median follow-up period of 79 months, a total of 625 participants with CKD succumbed to mortality. Compared to the lowest quartile, the highest quartile of urine and blood lead concentrations was associated with an increased risk of all-cause mortality, with HRs and corresponding 95% CIs of 1.77 (1.05–2.99) and 2.65 (1.38–5.10), respectively. Furthermore, each additional unit increase in urinary and blood lead concentrations was associated with HRs for all-cause mortality of 1.21 (95% CI 1.06–1.38) and 1.09 (95% CI 1.01–1.19), respectively. Kaplan–Meier survival curve analysis and restricted cubic regression spline curve analysis demonstrated significant positive associations between elevated blood lead levels, elevated urinary lead levels, and all-cause mortality risk ( P  < 0.05). A nonlinear concentration–response relationship was observed between blood lead level and all-cause mortality risk ( P Nonlinear  < 0.05), with an inflection point at a concentration of 1.613 µg/dL. Subgroup analysis as well as sensitivity analysis yielded consistent findings. Our findings demonstrate that elevated levels of lead in urine and blood are associated with a significantly increased mortality risk among patients with CKD, underscoring the importance of reducing lead exposure to mitigate mortality risk in individuals at high risk for CKD.

ObjectivesBone lead and past blood lead levels may be more strongly associated with current health effects than current blood lead, representing recent exposure. We examined whether current bone lead was correlated with maximum past blood lead and compared how three lead measures predicted current blood pressure (BP) and kidney function among workers with past occupational lead exposure.MethodsAdult men in a lead surveillance programme residing near New York City were enrolled. Current bone and blood lead, BP and estimated glomerular filtration rate (eGFR) were measured. Maximum past blood lead was obtained from surveillance data. Regression models were used to determine associations of health with different lead measures.ResultsAmong 211 participants, median (IQR) bone, maximum past blood and current blood leads were 13.8 (9.4–19.5) µg lead per bone mineral gram, 29.0 (14.0–38.0) µg/dL and 2.5 (1.5–4.4) µg/dL, respectively. Maximum past and current blood lead were significantly associated with current bone lead in adjusted analyses (both p<0.0001), with associations driven by high blood lead. Bone lead was associated with increased continuous systolic BP (coefficient=0.36; 95% CI 0.05 to 0.67; p=0.02); categorical analyses indicated this was driven by the top two bone lead quartiles. Bone lead was non-significantly associated with decreased (worse) eGFR (coefficient=−0.15; 95% CI −0.36 to 0.07; p=0.18).ConclusionsBone lead was significantly associated with past maximum and current blood lead. The association between bone and current blood lead was possibly driven by bone lead resorption into blood. Bone lead, but not past or current blood lead, was associated with elevated systolic BP.

Lead is a confirmed neurotoxin, but questions remain about lead-associated intellectual deficits at blood lead levels < 10 μg/dL and whether lower exposures are, for a given change in exposure, associated with greater deficits. The objective of this study was to examine the association of intelligence test scores and blood lead concentration, especially for children who had maximal measured blood lead levels < 10 μg/dL. We examined data collected from 1,333 children who participated in seven international population-based longitudinal cohort studies, followed from birth or infancy until 5-10 years of age. The full-scale IQ score was the primary outcome measure. The geometric mean blood lead concentration of the children peaked at 17.8 μg/dL and declined to 9.4 μg/dL by 5-7 years of age; 244 (18%) children had a maximal blood lead concentration < 10 μg/dL, and 103 (8%) had a maximal blood lead concentration < 7.5 μg/dL. After adjustment for covariates, we found an inverse relationship between blood lead concentration and IQ score. Using a log-linear model, we found a 6.9 IQ point decrement [95% confidence interval (CI), 4.2-9.4] associated with an increase in concurrent blood lead levels from 2.4 to 30 μg/dL. The estimated IQ point decrements associated with an increase in blood lead from 2.4 to 10 μg/dL, 10 to 20 μg/dL, and 20 to 30 μg/dL were 3.9 (95% CI, 2.4-5.3), 1.9 (95% CI, 1.2-2.6), and 1.1 (95% CI, 0.7-1.5), respectively. For a given increase in blood lead, the lead-associated intellectual decrement for children with a maximal blood lead level < 7.5 μg/dL was significantly greater than that observed for those with a maximal blood lead level ≥ 7.5 μg/dL (p = 0.015). We conclude that environmental lead exposure in children who have maximal blood lead levels < 7.5 μg/dL is associated with intellectual deficits.