Invited Perspective: An Argument for Changing the Reporting Units for Lead in Blood.

OBJECTIVEThis study investigated determinants of bone and blood lead concentrations in 430 lactating Mexican women during the early postpartum period and the contribution of bone lead to blood lead.METHODSMaternal venous...

Heavy metals causing chronic nephrotoxicity may play a key role in the pathogenesis of chronic kidney disease (CKD). This study hypothesized that plasma folate and vitamin B12 would modify the association of CKD with total urinary arsenic and blood lead and cadmium levels. We recruited 220 patients with CKD who had an estimated glomerular filtration rate of <60 mL/min/1.73 m2 for ≥3 consecutive months and 438 sex- and age-matched controls. We performed inductively coupled plasma mass spectrometry to measure blood cadmium and lead levels. The urinary arsenic level was determined using a high-performance liquid chromatography–hydride generator–atomic absorption spectrometry. Plasma vitamin B12 and folate levels were measured through the SimulTRAC-SNB radioassay. Compared with patients with plasma vitamin B12 ≤ 6.27 pg/mL, the odds ratio (OR) and 95% confidence interval of CKD for patients with plasma vitamin B12 > 9.54 pg/mL was 2.02 (1.15–3.55). However, no association was observed between plasma folate concentration and CKD. A high level of plasma vitamin B12 combined with high levels of blood lead and cadmium level and total urinary arsenic tended to increase the OR of CKD in a dose-response manner, but the interactions were nonsignificant. This is the first study to demonstrate that patients with high plasma vitamin B12 level exhibit increased OR of CKD related to high levels of blood cadmium and lead and total urinary arsenic.

Relationship between low-level lead, cadmium and mercury exposures and blood pressure in children and adolescents aged 8–17 years: An exposure-response analysis of NHANES 2007–2016

To investigate the risk of lead poisoning among household members exposed to 'backyard' battery repair shops (BBRS) in Kingston, Jamaica, environmental and blood lead (PbB) were measured at 24 households (112 individuals) with a BBRS worker or located at a BBRS premises and at 18 neighbourhood control households (74 individuals). Elevated PbB (greater than or equal to 25 micrograms per decilitre [micrograms/dl]) was common among subjects of all ages living at BBRS premises, especially among children less than age 12, 43% of whom had PbB greater than 70 micrograms/dl. Potentially hazardous soil and house dust lead levels were also common at BBRS premises, where 84% of yards had soil lead levels above 500 parts per million (geometric mean 3388 parts per million [ppm] at BBRS premises households with a BBRS worker). Geometric mean blood and environmental lead levels were significantly lower at control households, where less than 10% of subjects in all age groups had elevated PbB (maximum 33 micrograms/dl). Sharing a premises with a BBRS was a stronger determinant of household blood lead and environmental contamination than was the presence of a BBRS worker in a household. Blood lead levels were associated with soil and house dust lead levels in all age groups. We conclude that small battery repair shops, which have also been described in other developing countries, create a high lead poisoning risk for nearby residents.

This study aimed to evaluate the relationship between blood lead and serum creatinine and blood lead and serum urea nitrogen levels as biomarkers of lead exposure from subjects living in a historic polymetallic mining area in China. Elevated levels were found for blood lead, serum creatinine, and serum urea nitrogen in the mining area with mean values at 245.65μg/l, 74.16μmol/l, and 12.79mmol/l, which were significantly higher than those in the control area, respectively. Moreover, the coefficients between paired results for blood lead and serum creatinine and blood lead and serum urea nitrogen were positively statistically significant (serum creatinine vs. blood lead, r = 0.35, p < 0.05; serum urea nitrogen vs. blood lead, r = 0.48, p < 0.05). With respect to the effects of sex and age on the blood lead, serum creatinine, and serum urea nitrogen levels, data analysis revealed there was a tendency for higher blood lead, serum creatinine, and serum urea nitrogen levels in females than in males, and the levels of blood lead, serum creatinine, and serum urea nitrogen increased among older residents. We conclude that females and the older population in the mining area are more susceptible to lead exposure. Blood lead, serum creatinine, and serum urea nitrogen can be useful biomarkers of lead exposure among populations under environmental stress.

BackgroundWhile the relationship between blood pressure and blood lead has been studied more extensively, the effect of high-density lipoprotein (HDL) concentration on this relationship remains uncertain. Therefore, this study aimed to determine the effect of HDL concentration on the relationship between blood lead and blood pressure.MethodsThe research used cross-sectional data from the 2005 to 2014 National Health and Nutrition Examination Survey (NHANES), which included 16,451 participants aged 20–60 years. Multivariable linear regression was used to evaluate the correlation among blood lead, systolic blood pressure (SBP), and diastolic blood pressure (DBP). HDL concentration was determined by low HDL concentration (≤ 49 mg/dl) and high HDL concentration (>49 mg/dl) stratified. The effect of HDL concentration was assessed by an interaction test between blood lead and SBP in multivariable linear regression.ResultsIn this cross-sectional research, we identified a positive correlation between blood lead and SBP, but not DBP. The relationship between blood lead and SBP was different in the group with low and high HDL concentrations (β: 0.21 95% Cl:−0.05-0.46 vs. β:0.47 95% Cl: 0.15-0.79). In addition, high HDL significantly altered the positive correlation between blood lead and SBP (P-value of interaction < 0.001).ConclusionThe study suggests an interaction between HDL and blood lead in elevating SBP, which may have important clinical implications.

Childhood lead poisoning in China: challenges and opportunities.

Data (N = 2552) from National Health and Nutrition Examination Survey for US adults aged ≥ 20 years for 2011-2016 were analyzed to estimate the associations between the concentrations of blood cadmium, lead, and total mercury and the concentrations of seven perfluoroalkyl acids (PFAA), namely, 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (MPAH), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluoroundecanoic acid (PFUnDA), perfluorohexane sulfonic acid (PFHxS), and perfluorooctane sulfonic acid (PFOS). Concentrations of blood cadmium were negatively associated with the concentrations of PFHxS (β = - 0.05428, p < 0.01) and PFOS (β = - 0.0212, p = 0.02). Concentrations of blood lead were positively associated with the concentrations of MPAH (β = 0.03301, p < 0.01), PFOA (β = 0.04783, p = 0.01), PFNA (β = 0.11761, p < 0.01), PFDA (β = 0.08007, p < 0.01), PFUA (β = 0.11382, p < 0.01), and PFOS (β = 0.04996, p = 0.02). Percent increases in the concentration of blood lead were 0.32%, 0.46%, 1.13%, 0.77%, 1.09%, and 0.48% for 10% increases in the concentrations of MPAH, PFOA, PFNA, PFDA, PFUA, and PFOS, respectively. Concentrations of blood total mercury were positively associated with the concentrations of PFNA (β = 0.37105, p < 0.01), PFDA (β = 0.46875, p < 0.01), PFUA (β = 0.56934, p < 0.01), and PFOS (β = 0.17557, p < 0.01). Percent increases in the concentration of blood total mercury were 3.6%, 4.57%, 5.58%, and 1.69% for 10% increases in the concentrations of PFNA, PFDA, PFUA, and PFOS, respectively. Associations between the concentrations of PFAAs with blood total mercury were substantially stronger than the concentrations with blood lead. Higher the carbon chain length for PFAAs, stronger were the associations between PFAAs with lead and mercury.

In an analysis of blood lead and haemoglobin estimations from 655 lead workers, there was no indication of any change in the haemoglobin until the blood lead exceeded 110 μg./100 ml.; the slight fall at higher levels of blood lead was not significant at the 5% level of confidence. Sixty-seven men who had blood leads greater than 90 μg./100 ml. were examined clinically. One had a low haemoglobin but none had symptoms or signs that were likely to be due to lead absorption. A further 18 men had haemoglobins of 89% (13 g./100 ml.) or less. None was thought to be low due to lead absorption. The absence of symptoms, signs, and low haemoglobins in association with relatively high blood leads is unlikely to be due to errors in blood lead or haemoglobin estimation. Alternative possibilities are that there were no susceptible workers among those studied; or that the stable conditions of exposure in this population allowed the development of relatively high blood leads without other evidence of high lead absorption. When the haemoglobin is abnormal, blood lead observations may be more meaningful if a correction factor, approximately equal to [Formula: see text] is used. It is concluded that in a population where sophisticated lead control is practised no purpose is served by estimating haemoglobins in all lead workers every three months, but only in those whose blood lead is likely to be in excess of 110 μg./100 ml. It may also be of value in the first year of exposure to detect susceptible workers.

Measurement of lead in whole blood by use of the carbon rod atomizer and atomic absorption spectrophotometry was investigated for three methods: (a) a simple dilution (one volume of whole blood to two volumes of surfactant solution; (b) direct analysis of whole blood (no sample preparation); and (c) a standard chelation extraction procedure in which sodium diethyldithiocarbamate and methyl isobutyl ketone (isopropylacetone) are used. Within-run precision data for normal and above-normal pools favored the Triton dilution method, for which coefficients of variation were less than 5%. Recoveries of added lead ranged from 94-107% for all three methods. We saw no change in the standard curves for any of the procedures on addition of ethylenediaminetetraacetate to samples. The method of additions was necessary to prepare standards of a matrix composition identical to that of the unknowns.

Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine

Blood lead and lead-210 analyses were performed on blood samples from non-smoking residents of Toulouse (city of 400,000 inhabitants). Simultaneous surface soil lead content determinations were carried out by the same procedure on rural zone samples of southwestern France. The observed isotopic ratios were compared in order to evaluate food chain contamination. For an average of 19.7 ± 5.8 μg 100 cc−1 of lead in blood, atmospheric contamination amounts to 20%, estimated as follows: 6% from direct inhalation and 14% from dry deposits on vegetation absorbed as food. The natural levels carried over by the food chain reach 14.9 μg 100 cc−1 and have a 210Pb/Pb concentration ratio of 0.055 dpmμg−1. These results lead to a maximum value of 15 μg 100 cc−1 for natural lead in human blood according to the ICRP model.

This study was conducted to find out the concentration of heavy metals (lead, cadmium, and mercury) in human and sheep blood along the Tigris River (Mosul, Salahuddin, Baghdad, Wasit, and Misan). Blood samples were taken from different regions to study the effect of heavy metal pollutants on human and sheep health. Lead and cadmium concentrations in the blood of humans and sheep in Baghdad, Mousel, and Misan governorates were significantly (P&lt; 0.05) higher compared with their concentrations in other governorates; on the other hand, the concentration of lead in the blood of humans and sheep was lowest in Wasit governorate. Mercury were significantly higher (P&lt;0.05) only in blood of the human and sheep in Misan governorate.

Back to table of contents Previous article Next article Clinical & Research NewsFull AccessLead in Children's Blood May Contribute to ADHD's Hyperactivity ComponentJoan Arehart-TreichelJoan Arehart-TreichelSearch for more papers by this authorPublished Online:2 Nov 2007https://doi.org/10.1176/pn.42.21.0020aThanks to government regulation, lead poisoning in children is no longer common in the United States. However, American youngsters are still widely exposed to low levels of lead in water, soil, and other venues.But even these lower levels of lead in turn may contribute to attention-deficit/hyperactivity disorder (ADHD) in some American children, a new study suggests.The study was headed by Joel Nigg, Ph.D., a professor of clinical psychology at Michigan State University. Results are in press with Biological Psychiatry.Studies done in the 1980s have already linked the amount of lead in children's blood with ADHD. But the levels—10-20 ug/dl—were higher than the levels usually found in American children today, which average 1-2 ug/dl. So Nigg and his colleagues wanted to see whether these lower blood levels could also be associated with ADHD.The researchers recruited subjects for the study from schools, clinics, and advertisements. To obtain the broadest and most representative sample possible, the investigators advertised for both healthy children and children suspected of having or diagnosed with ADHD. A total of 845 families expressed interest in participating in the study.The children in these families were then screened extensively with various instruments—say, the Child Behavior Checklist and the Kiddie Schedule for Affective Disorders and Schizophrenia—to determine whether they had ADHD or other psychiatric disorders.One hundred-and-fifty children aged 8 to 17 were finally selected to participate in the study. A third had ADHD, combined type; a third had ADHD, predominantly inattentive type; and the remainder did not have ADHD and could thus serve as controls. Moreover, the levels of lead in the blood of all the subjects closely matched the American average of 1-2 ug/dl, with a maximum level of 3.4 ug/dl.Blood lead levels were significantly higher in the children with ADHD, combined type, than in the control children, but this was not the case in children who had ADHD, predominantly inattentive type. So Nigg and his group believe that low lead levels in the blood might play a role in the hyperactivity component of ADHD, but not in the inattention component of it.How lead might contribute to hyperactivity is not clear. It does not seem to be mediated by lead's negative impact on intelligence, because while the researchers found that blood lead levels in their subjects were correlated with IQ, they also found that IQ could not explain the link between lead and hyperactivity. Low-level lead exposure is known to disrupt mid-brain dopamine circuitry, and this circuitry, however, is involved in ADHD.Although the researchers suspect that low blood levels of lead may play a role in a number of cases of ADHD-related hyperactivity, they do not believe that this is so in all cases, because some of their subjects with mildly elevated blood levels did not have ADHD-related hyperactivity, while some of their subjects with ADHD-related hyperactivity did not have elevated blood levels of lead.The study's results have public health policy implications, Nigg told Psychiatric News, emphasizing that “prevention of lead exposure may be important at even lower levels than we thought.”The study was financed by Michigan State University and the Centers for Disease Control and Prevention.An abstract of “Low Blood Lead Levels Associated With Clinically Diagnosed Attention-Deficit/Hyperactivity Disorder and Mediated by Weak Cognitive Control” is posted at<www.journals.elsevierhealth.com//periodicals/bps> under “Articles in Press.” ▪ ISSUES NewArchived

Revised and new reference values for arsenic, cadmium, lead and mercury in blood or urine of children. Basis for validation of human biomonitoring data in environmental medicine