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Lead (Pb) poisoning is estimated to account for 1 % of the global disease burden. The gold standard for diagnosing lead poisoning in human body relies on blood lead level (BLL), which is always performed in hospitals using expensive instruments. However, there are still many countries and regions with a lack of medical resources (without enough professional medical staff and analytical instruments). To achieve a facile diagnosis of lead poisoning by ordinary residents (without any expertise), this study conducted a research study on 810 participants to discover and validate a new lead poisoning indicator (creatinine-corrected urinary lead level, cULL) beyond BLL in non-invasive samples. A point-of-care testing (POCT) device to measure cULL was developed, equipped with liquid-phase microextraction and electromembrane extraction on a paper-based analytical device for on-site separation of lead and creatinine in the urine, using a smartphone for the quantification of analytes. The cULL as a novel indicator and the POCT device developed could be effective in reducing the risk of damage from lead contamination.

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BACKGROUND: Cadmium (Cd) and lead (Pb) exhibit nephrotoxic activity and may accelerate kidney disease complications in diabetic patients, but studies investigating the relation to diabetic kidney disease (DKD) have been limited. We aimed to examine the associations of Cd and Pb with DKD in diabetic patients. METHODS: 3763 adults with blood metal measurements and 1604 adults with urinary ones who were diabetic from National Health and Nutrition Examination Survey (NHANES) 2007-2016 were involved. Multivariate logistic regression models were used to analyze the associations of blood Cd (BCd), blood Pb (BPb), urinary Cd (UCd), and urinary Pb (UPb) with DKD. RESULTS: BPb, BCd, and UCd levels were higher among participants with DKD than diabetics without nephropathy, but UPb performed the opposite result. BPb and UCd were significantly associated with DKD in the adjusted models (aOR, 1.17 (1.06, 1.29);1.52 (1.06, 2.02)). Participants in the 2nd and 3rd tertiles of BPb and BCd levels had higher odds of DKD, with a significant trend across tertiles, respectively (all P-trend < 0.005). Multiplication interaction was also identified for BPb and BCd (P for interaction = 0.044). CONCLUSION: BPb, BCd, and UCd were positively associated with the risk of DKD among diabetic patients. Furthermore, there were the dose-response relationship and multiplication interaction in the associations of BPb, BCd with DKD.

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Background Occupational exposure to lead, cadmium, or arsenic is a potential risk factor for blood pressure elevation. Current studies mainly focus on the relationship between a single metal and blood pressure. However, mixed metal exposure often exists in the actual working environment, and the interactive effects of polymetallic interactions on blood pressure and the dose-effect relationship remain unclear yet. Objective To explore the influence proportion of occupational exposure to lead, cadmium, or arsenic on blood pressure and their interactive effects. Methods From January to December 2021, workers from a smelter in southern China were selected. Demographic characteristics, height, weight, and blood pressure of workers were collected through questionnaire and physical examination. At the same time, their urine samples were collected and the levels of urinary lead, urinary cadmium, and urinary arsenic were detected by inductively coupled plasma mass spectrometry, and corrected by urinary creatinine (Cr). Linear regression and logistic regression were used to analyze the relationship between urinary lead, cadmium, and arsenic and blood pressure. Weighted quantile sum (WQS) regression was applied to evaluate the dose-effect relationship between urinary lead, cadmium, and arsenic exposures and blood pressure and the effect weight of each metal on blood pressure. Generalized linear regression and additive/multiplicative scaling were used to identify interactive effects of the three metals on blood pressure. Results A total of 1075 workers were included in this study, with a mean age of (44.68±5.11) years and mean working seniority of (24.66±5.23) years. There were 891 males (88.9%) and 184 were females (17.1%); 24.7% workers were drinkers and 45.7% workers were smokers; 302 workers (28.1%) reported hypertension and 37 of them were taking antihypertensive drugs. The P50 (P25, P75) levels of urinary lead, urinary cadmium, and urinary arsenic were 6.11 (3.71, 11.08), 3.88 (2.68, 5.44), and 26.04 (19.99, 35.11) μg·g−1, respectively. After adjusting for gender, age, working seniority, body mass index, smoking, drinking, and the usage of antihypertensive drugs, systolic and diastolic blood pressure increased by 0.772 and 0.418 mmHg respectively for 10% increase in lead, cadmium, and arsenic mixed exposure. Urinary cadmium, among the three single exposures, had the greatest effect on systolic and diastolic blood pressure, weight (w)=0.523 and 0.551 respectively. The interaction of urinary lead and urinary cadmium was positively correlated with the occurrence of hypertension, multiplicative interaction OR (ORint)=1.88 (95%CI: 1.09, 3.63), attributable proportion due to interaction (AP)=1.19 (95%CI: 0.40, 8.18). Conclusion This study shows that mixed exposure to lead, cadmium, and arsenic has a positive relationship with blood pressure, in which cadmium plays a major role. Co-exposure to lead and cadmium has a positive interactive effect on hypertension development and systolic blood pressure elevation.

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Background Exposure to environmental lead can cause kidney damage and telomere wear. However, the relationship among lead, peripheral blood telomere length, and glomerular filtration rate (eGFR) are unclear. Objective This study is conducted to investigate the relationships of urinary lead level with peripheral blood telomere length and renal function index eGFR, and further explore whether peripheral blood telomere length plays an intermediary role in the relationship between urinary lead level and eGFR. Methods A case-control study was conducted to select 497 residents from two communities in a city, including 230 in the control group (eGFR≥80 mL·min−1) and 267 in the abnormal eGFR group (eGFR<80 mL·min−1). Basic information and health information of the subjects were collected through a face-to-face questionnaire survey. Fasting morning urine was collected, and urinary lead and urinary creatinine (UCr) were detected. Fasting peripheral venous blood was collected to detect telomere length and serum creatinine (SCr) in peripheral blood leukocytes. eGFR was estimated by the Levey formula. After further adjusting for age, gender, education level, family per capita monthly income, smoking, and drinking the relationship among urinary lead level, peripheral blood telomere length, and renal function index eGFR was evaluated by mediating effect analysis. Results The overall level of creatinine-adjusted urinary lead [M (P25, P75)] in the abnormal eGFR group was 3.85 (1.56, 7.34) μg·g−1 which was higher than that in the control group, 1.57 (0.60, 3.62) μg·g−1(P<0.001). In addition, the overall level of peripheral blood telomere length in the abnormal eGFR group was 2.42 (1.89, 3.10) Kb, lower than that in the control group, 2.69 (2.09, 3.64) Kb (P<0.001). The results of mediating effect analysis showed that the magnitude of mediating effect by peripheral blood telomere length was −0.276 (95%CI: −0.708-−0.001) and it contributed 3.35% to the relationship between urinary lead level and eGFR. In women, the magnitude of mediating effect by peripheral blood telomere length was −0.484 (95%CI: −1.160-−0.023) between urinary lead level and eGFR, and the proportion of the mediating effect was 5.34%. In men, no mediating role of peripheral blood telomere length was found between urinary lead and eGFR. Conclusion Urinary lead level is closely related to renal function index eGFR and telomere length in peripheral blood. Peripheral blood telomere length plays a mediating role in the relationship between female urinary lead and eGFR in women.

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The objective of this study is to highlight the effectiveness of urinary lead as an index of recent lead exposure. In the past scientific literature urinary lead has been studied as a parameter for recent lead exposure. It is a reliable indicator for occupational lead exposure. But, strangely enough, nowadays is scarcely used in the Netherlands and worldwide. We performed six field biological monitoring studies of preshift and postshift urinary lead tests during tank maintenance and bridge repair work. Highest values occurred during bridge repair. Mean urinary values were postshift 1,6-5 times higher than preshift values, indicating clearly recent lead exposure and failing protective measures. This is so far we know the first study combining preshift and postshift sampling of urinary lead. We compared our studies with crossectional and follow-up studies in occupational medicine. Our conclusion is that preshift and postshift urinary lead testing is a worker friendly test, ideally for detecting recent lead exposures in the field. It signals the need to review or possibly improve controls at work. There are no safe lead levels, so we recommend to use a target value for urinary lead of <3 µg/g creatinine for all lead workers in the Netherlands.

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Exposure to lead (Pb) and cadmium (Cd) were related to lung function impairment, and this association may be modified by genetic variants in oxidative stress response. Here we enrolled 1243 coke-oven workers in a prospective cohort who were followed up from 2010 to 2014, assessed the associations of Pb and Cd exposure with 4-year lung function impairment, and further explored the interaction effects of Pb with 2664 single nucleotide polymorphisms (SNPs) in 345 oxidative stress related genes. Urinary levels of Pb, Cd, and two oxidative stress biomarkers [8-iso-prostaglandin F2α (8-iso-PGF2α) for lipid peroxidation and 8-hydroxy-2'-deoxyguanosine (8-OHdG) for oxidative DNA damage] were measured at baseline only and their lung function levels were measured both at baseline and at the end of follow-up. Each 10-fold increase in urinary Pb was associated with -159 (95%CI: -254, -64.2) mL and -3.63% (95%CI: -6.48%, -0.78%) changes in FEV1 and percent predicted FEV1 (ppFEV1), respectively. But none significant associations were observed for Cd. NQO1 rs2917670 showed significant interaction with Pb on elevated FEV1 decline after multiple comparison (Pint=1.54 × 10-5). In addition, urinary Pb increased with 8-iso-PGF2α and the rs2917670-C could significantly decrease NQO1 expression in normal lung tissues. These findings suggested the gene-environmental interaction of NQO1 rs2917670 and Pb exposure on the reduction of FEV1. The effect of Pb exposure on elevated oxidative stress and the decreased expression of antioxidant enzyme NQO1 caused by rs2917670-C allele may partly explain the underlying biological mechanism.

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Bone is a major storage site as well as an endogenous source of lead in the human body. Dietary sodium and potassium intake may play a role in the mobilization of lead from bone to the circulation. We examined whether association between bone lead and urinary lead, a marker of mobilized lead in plasma, was modified by dietary intake of sodium and potassium among 318 men, aged 48-93 years, in the Veterans Affairs (VA) Normative Aging Study. Dietary sodium and potassium were assessed by flame photometry using 24-h urine samples, and a sodium-to-potassium ratio was calculated from the resulting measures. Patella and tibia bone lead concentrations were measured by K-shell-x-ray fluorescence. Urinary lead was measured by inductively coupled plasma mass spectroscopy in 24-h urine samples. Linear regression models were used to regress creatinine clearance-corrected urinary lead on bone lead, testing multiplicative interactions with tertiles of sodium, potassium, and sodium-to-potassium ratio, separately. After adjustment for age, body mass index, smoking, vitamin C intake, calcium, and total energy intake, participants in the highest tertile of sodium-to-potassium ratio showed 28.1% (95% CI: 12.5%, 45.9%) greater urinary lead per doubling increase in patella lead, whereas those in the second and lowest tertiles had 13.8% (95% CI: -1.7%, 31.7%) and 5.5% (95% CI: -8.0%, 21.0%) greater urinary lead, respectively (p-for-interaction = 0.04). No statistically significant effect modification by either sodium or potassium intake alone was observed. These findings suggest that relatively high intake of sodium relative to potassium may play an important role in the mobilization of lead from bone into the circulation.

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BACKGROUND: Urinary lead (Pb) is generally considered to have limited use in biomonitoring environmental exposure to lead. Carbon load in airway macrophages (AM BC) is an internal marker to assess long-term exposure to combustion-derived aerosol particles. In urban environments, atmospheric Pb and black carbon may have common sources. We aimed to study the temporal change of urinary Pb (U-Pb) when exposure to outdoor air pollution changes, and the relationship between U-Pb and AM BC. METHODS: A panel of 50 young healthy adults [mean (SD) 26.7 (5.2) years], including 17 long-term (>1 year) residents in Leuven, Belgium (BE), 15 and 18 newcomers (arrived <3 weeks) from low- and middle-income countries (LMIC) and high-income countries (HIC), respectively, underwent 8 repeated measurements at 6 weeks intervals. In urine spot samples obtained at 5 time points (T1, T2, T4, T6, T8), 24 trace elements were quantified by inductively coupled plasma-mass spectrometry. At each time point, AM BC was quantified as the median surface of black inclusions (in µm2) by means of image analysis of 25 macrophages obtained by induced sputum. Changes in urinary metal concentrations (with and without creatinine correction) and the relationship between U-Pb and AM BC were estimated using linear mixed models adjusted for covariates and potential confounders. RESULTS: Only U-Pb differed between groups and exhibited significant time trends. Participants from the LMIC group had significantly higher initial U-Pb (1.18 µg/g creat) than the HIC group (0.44 µg/g creat) and BE group (0.45 µg/g creat). In the LMIC group, U-Pb decreased significantly with time by 0.061 µg/g creatinine per 30 days [95% confidence interval (CI): 0.034, 0.088]. U-Pb remained unchanged in the other two groups. An increase in AM BC of 1 µm2 was associated with an increase in U-Pb of 0.369 µg/g creat (95% CI: 0.145, 0.593). CONCLUSION: This panel study demonstrates that U-Pb may be a valid alternative to blood Pb for biomonitoring changes in exposure to lead, at least at group level. In addition, we identified a positive association between U-Pb and AM BC, a biomarker of exposure to traffic-related air pollution, suggesting the existence of common sources of Pb and black carbon in urban environments.

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Lead is a ubiquitous pollutant that constitutes an environmental hazard worldwide. Although lead has been known as a carcinogenic factor in animal models, its role in human carcinogenesis is still a topic of debate with limited epidemiological evidence. Moreover, the association between urinary lead, as the most non-invasive and accessible way for lead measurement in human, and cancer mortality in general population has never been explored. We addressed this subject using continuous National Health and Nutrition Examination Survey 1999-2010 data and its Mortality Follow-Up Study. Of 5,316 subjects in study population, 161 participants died due to cancer. Cancer-specific mortality was associated with urinary lead levels after multivariable adjustment. Kaplan-Meier survival curve and cubic regression spline analyses indicated that high concentration of urinary lead exhibited significant association with raised death rate of cancer. Despite the marked decrease in environmental lead levels over the past three decades, lead exposure is still the significant determinant of cancer mortality in general population in U.S., and quantification of urinary lead may serve as a non-invasive approach to facilitate biomarker discovery and clinical translational research.

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Lead exposure remains an important public health problem. Contaminated foods may act as a source of lead exposure, while certain nutrients may reduce lead absorption. We examined the cross-sectional associations of dietary patterns and the intake of several nutrients and foods with blood (Pb-B) and urinary (Pb-U) lead concentrations in children (5-8y) from Montevideo, Uruguay. From two 24-hour recalls completed by caregivers, we derived the mean daily intake of select nutrients and food groups (dairy, milk, fruit, root vegetables, foods rich in heme and non-heme iron), as well as "nutrient dense" and "processed" food patterns. Pb-B (n=315) was measured using atomic absorption spectrometry; Pb-U (n=321) using ICP-MS. Pb-U was adjusted for specific gravity and log-transformed to approximate a normal distribution. Iron deficiency (ID) and dietary variables were tested as predictors of Pb-B and log-Pb-U in covariate-adjusted regressions. Median [5%, 95%] Pb-B and Pb-U were 3.8 [0.8-7.8] µg/dL and 1.9 [0.6-5.1] µg/L, respectively; ~25% of Pb-B above current U.S. CDC reference concentration of 5µg/dL. ID was associated with 0.75µg/dL higher Pb-B, compared to non-ID (p<0.05). Consumption of root vegetables was not associated with Pb-B or log-Pb-U. Higher scores on the nutrient-dense pattern were related with higher Pb-Bs, possibly due to consumption of green leafy vegetables. Dietary intake of iron or iron-rich foods was not associated with biomarkers of lead. Conversely, children consuming more calcium, dairy, milk and yogurt had lower Pb-B and log-Pb-U. Our findings appear consistent with existing recommendations on including calcium-rich, but not iron- or vitamin-C-rich foods in the diets of lead-exposed children, especially where the consumption of these foods is low.

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BACKGROUND: Cadmium (Cd) and lead (Pb) are widespread environmental contaminants that are known nephrotoxins. However, their nephrotoxic effects at low-environmental exposure levels are debated. OBJECTIVE: We examined the association of blood Pb (B-Pb), blood Cd (B-Cd), urinary Pb (U-Pb) and urinary Cd (U-Cd) with estimated glomerular filtration rate (eGFR) and urinary albumin (ALB). METHODS: We used multivariate linear regression to analyze the association between B-Pb, B-Cd, U-Pb, and U-Cd with eGFR and ALB in adult participants (≥20 years of age) in NHANES 2007-2012. The dataset was limited to NHANES individuals with both blood and urinary metal measurements. RESULTS: We found a statistically significant inverse association between eGFR and B-Cd and statistically significant positive associations between eGFR and both U-Cd and U-Pb, as well as statistically significant associations between ALB and the 3rd and 4th quartiles of U-Cd. CONCLUSIONS: The inverse association between eGFR and B-Cd, in conjunction with positive associations between eGFR and ALB with U-Cd, suggest that U-Cd measurement at low levels of exposure may result from changes in renal excretion of Cd due to kidney function and protein excretion. However, renal effects such as hyperfiltration from Cd-mediated kidney damage or creatinine-specific Cd effects cannot be excluded with this cross-sectional design.

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BACKGROUND: Urinary metallomics is presented here as a new "omics" approach that aims to facilitate personalized cancer screening and prevention by improving our understanding of urinary metals in disease. METHODS: Twenty-two urinary metals were examined with inductively-coupled plasma-mass spectrometry in 138 women newly diagnosed with breast cancer and benign conditions. Urinary metals from spot urine samples were adjusted to renal dilution using urine specific gravity. RESULTS: Two urinary metals, copper (P-value=0.036) and lead (P-value=0.003), were significantly increased in the urine of breast cancer patients. A multivariate model that comprised copper, lead, and patient age afforded encouraging discriminatory power (AUC: 0.728, P-value<0.0005), while univariate models of copper (61.7% sensitivity, 50.0% specificity) and lead (76.6% sensitivity, 51.2% specificity) at optimized cutoff thresholds compared favorably with other breast cancer diagnostic modalities such as mammography. Correlations found among various metals suggested potential geographic and dietary influences on the urine metallome that warrant further investigation. CONCLUSIONS: This proof-of-concept work introduces urinary metallomics as a noninvasive, potentially transformative "omics" approach to early cancer detection. Urinary copper and lead have also been preliminarily identified as potential breast cancer biomarkers.

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As a highly toxic heavy metal, the pollution and exposure risks of lead are of widespread concern for human health. However, the collection of blood samples for use as an indicator of lead pollution is not always feasible in most cohort or longitudinal studies, especially those involving children health. To evaluate the potential use of urinary lead as an indicator of exposure levels and source apportionment, accompanying with environmental media samples, lead concentrations and isotopic measurements (expressed as (207)Pb/(206)Pb, (208)Pb/(206)Pb and (204)Pb/(206)Pb) were investigated and compared between blood and urine from children living in the vicinities of a typical coking plant and lead-acid battery factory. The results showed urinary lead might not be a preferable proxy for estimating blood lead levels. Fortunately, urinary lead isotopic measurements could be used as an alternative for identifying the sources of children's lead exposure, which coincided well with the blood lead isotope ratio analysis.

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Lead is one of the most widely scattered toxic metals in the environment and used by mankind for over 9,000 years. Lead in the environment may be derived from natural or anthropogenic sources. In humans, lead can cause a wide range of biological effects depending upon the level and duration of exposure. The purpose of this study was to find out the effect of lead exposure on systolic and diastolic blood pressure, serum calcium, ionized calcium, phosphorus, parathyroid hormone and vitamin D and examine the overall effect of all these parameters on the bone mineral density of battery manufacture workers. For this study ninety battery manufacture workers were selected and divided in three groups depending upon duration of lead exposure. Group I-workers with duration of lead exposure 1-5 years, Group II-workers with duration of lead exposure 6-10 years and Group III-workers with duration of lead exposure more than 10 years. Each group consisted of thirty workers. Thirty age matched healthy control subjects were taken for comparison. Demographic, occupational and clinical data were collected by using questionnaire and interview. The venous blood samples were collected from the study groups and normal healthy control group. At the time of blood collection random urine samples were collected in amber coloured bottles. The biochemical parameters were estimated by using standard assay procedures. Statistical analysis of the data was done using independent student't' test for parametric variables. Values were expressed as mean ± standard deviation (SD). P values of 0.05 or less were considered to be statistically significant. The blood lead levels and urinary lead levels of all workers were significantly increased (P < 0.001) in proportion to the duration of lead exposure as compared to controls. Systolic and diastolic blood pressure were significantly raised (P < 0.001) in all three study groups of battery manufacture workers as compared to controls. Serum Calcium, Ionized calcium, phosphorus were significantly decreased (P < 0.001) in all the three study groups. Serum vitamin D levels were lowered (P < 0.01) and serum PTH was increased (P < 0.01) in workers as compared to controls. The results of this study clearly indicate that the absorption of lead is more in these workers which adversely affects blood pressure, disturbs calcium and phosphorus metabolism which further impairs mineralization of bone resulting in decreased bone mineral density observed in these workers. Lead toxicity is still persistent in battery manufacture workers though they are using sophisticated techniques in these industries. There is a need to protect the workers from the health hazards of occupational lead exposure.

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The purpose of this study was to find out the effect of lead exposure on systolic and diastolic blood pressure, heme biosynthesis related and hematological parameters of automobile workers. For this study 30 automobile workers were selected and compared with 30 age matched healthy control subjects. Significantly increased blood lead (364%, P < 0.001) and urinary lead (176%, P < 0.001) levels were observed in automobile workers (study group) as compared to controls. Systolic blood pressure (5.32%, P < 0.05) and diastolic blood pressure (5.87%, P < 0.05) were significantly increased in the automobile workers as compared to controls. The significantly decreased non-activated erythrocyte δ-aminolevulinic acid dehydratase (δ-ALAD) (-18.51%, P < 0.01) and activated δ-ALAD (-13.29%, P < 0.05) levels were observed in automobile workers as compared to normal healthy control subjects. But the ratio of activated/non-activated δ-ALAD was significantly increased (43.83%, P < 0.001) in automobile workers as compared to controls. Excretions of δ-aminolevulinic acid (83.78%, P < 0.001) and porphobilinogen (37%, P < 0.001) in urine were significantly increased in the study group as compared to the controls. In automobile workers heamoglobin (-11.51%, P < 0.001), hematocrit (-4.06%, P < 0.05), mean corpuscle volume (-3.34%, P < 0.05), mean corpuscle hemoglobin (-5.66%, P < 0.01), mean corpuscle hemoglobin concentration (-7.67%, P < 0.001), red blood cell count (-14.6%, P < 0.001) were significantly decreased and total white blood cell count (11.44%, P < 0.05) increased as compared to the controls. The results of this study clearly indicate that the absorption of lead is more in automobile workers and it affects on blood pressure, heme biosynthesis and hematological parameters observed in this study group.