Lead

The HBM4EU Scoping document on lead provides background information on these substances, identifies relevant policy questions on the group of substances and outlines research activities under HBM4EU.

The lead author of the scoping document was former Chemical Group Leader Peter Rudnai of National Public Health Institute (NPHI) .The document was published in March 2019. New Chemical Group Leader is Tamás Szigeti (NPHI).

This page was last updated in January 2020.

 

Uses of Lead

Lead is manufactured and/or imported in the European Economic Area in 1,000,000 – 10,000,000 tons per year (ECHA, 2018). About 50 nations mine lead in quantities ranging from a few hundred tons to more than half a million tons (U.S. Bureau of Mines, 1993). Roughly 20 nations produce only secondary (i.e., recycled) lead. Secondary smelting (recycling) of lead from lead-acid batteries from vehicles and industries has become increasingly important and by the end of the 20th century accounted for almost half of world refined lead production. Other uses of lead include pigments and other compounds, rust inhibitors, rolled and extruded products, cable sheathing, alloys, radiation shielding, ceramic glazes, plastic stabilizers, jewellery making, soldering, crystal products, fishing weights, shot and ammunition, electronic waste, use in water pipes, and fuel additives (The Global Dimensions of Lead Poisoning: An Initial Analysis, 1994). Due to regulation in Europe on the use of lead in dyes and ceramics it is expected that exposure through these applications is decreasing.Global consumption of lead is increasing today, because of increasing demand for energy-efficient vehicles. The largest current use of lead is in storage batteries for cars and other vehicles. (WHO, 2010).

 

Hazardous properties of Lead

Lead is a soft, silvery grey metal. It is highly resistant to corrosion, but is soluble in nitric and hot sulphate acids. Solubility in water varies: lead sulphide and lead oxides are purely soluble while nitrate, chlorate and chloride salts are reasonably soluble in cold water. Lead also forms salts with organic acids as lactic and acetic acids, and stable organic compounds such as tetraethyl lead and tetramethyl lead.

Although lead and its organic compounds occur (or used to occur) in various man-made substances like petrol additives (tetraethyl- and tetramethyl lead), or lead-based paints (lead(II) chromate – „chrome yellow”, lead (II,IV) oxide – „red lead”, lead carbonate – „white lead”), a considerable proportion of human exposure is also resulted from inorganic lead or lead salts (lead pipes and solder in plumbing systems, lead-soldered food cans, batteries, etc.). Independently of their original form the toxicity of lead compounds is determined by their ionic lead content (IARC, 2006), therefore human biomonitoring of lead exposure concentrates on measuring inorganic lead in human biological materials.

Absorption and distribution

Gastrointestinal absorption of ingested lead is influenced by physiological factors (e.g. age, fasting, nutritional calcium and iron status, pregnancy) and the physicochemical characteristics of particles (size, solubility, and lead species). (Jakubowski, 2012).

Deposition and absorption of inhaled lead-containing particles are influenced by their size and solubility. Large particles are transferred by mucociliary transport into the pharynx and then swallowed, with possible absorption from the gastrointestinal tract. Smaller particles can be deposited in the alveolar part of the lungs and almost completely absorbed (Jakubowski, 2012).

Lead in blood is found primarily in the red blood cells (96-99%). The half-life of lead in blood is approximately 30 days in adult male humans but it varies depending on the level of exposure, sex and age. (Jakubowski, 2012). Half life of lead in bones is approximately 10-30 years (EFSA, 2010), but it can be mobilized by certain physiological processes like pregnancy or other factors.

General overview of health effects

Lead has been classified by the German Research Foundation (MAK Commission) in category 2, to be regarded as human carcinogen. IARC classified lead (in general) as possibly carcinogenic to humans (Group 2B) (IARC, 1987), inorganic lead compounds as probably carcinogenic to humans (Group 2A) (IARC, 2006) and organic lead compounds were not classifiable as to their carcinogenicity to humans (Group 3) (IARC, 2006).

Epidemiological evidence indicated cancers of the stomach, lung, kidney, and brain in workers exposed to inorganic lead, but not in all studies.

Genetic susceptibility to lead exposure related to ALAD gene polymorphism has been indicated by some but not all studies (IARC, 2014).

Lead exposure may damage fertility, may damage the unborn child (reduced foetal growth and disturbed maturation, pre-term delivery) and may cause harm to breast-fed children.

Lead can easily cross the placental barrier, therefore can readily enter the bloodstream of the foetus. Since Pb can also pass the blood brain barrier, neurological development is of great concern when prenatal exposure to lead occurs (Baeyens et al., 2014). There is also a potential link between blood lead level and increase of blood pressure in pregnant women at low level exposure (Wells et al., 2011)

A systematic review evaluating the evidence on the associations between lead exposure and cardiovascular endpoints in human populations concluded that the evidence is sufficient to infer a causal relationship of lead exposure with hypertension (Navas-Acien et al., 2007).

Lead is known to affect several enzymatic reactions critical in haem synthesis resulting in anaemia. (EHC, 1995)

Lead is associated with a wide range of toxicity in children These toxic effects extend from acute, clinically obvious, symptomatic poisoning at high levels of exposure down to subclinical (but still very damaging) effects at lower levels. Lead poisoning can affect virtually every organ system in the body. The principal organs affected are the central and peripheral nervous system and the cardiovascular, gastrointestinal, renal, endocrine, immune and haematological systems. (WHO, 2010).

Acute clinical toxicity

Intense, acute, high-dose exposure to lead can cause symptomatic poisoning in children. It is characterized by colic, constipation, fatigue, anaemia and neurological features that can vary from poor concentration to stupor. In the most severe cases, a potentially fatal acute encephalopathy with ataxia, coma and convulsions can occur. In many instances, children who survive acute lead poisoning go on to have permanent and clinically apparent deficits in their neurodevelopmental function (Byers & Lord, 1943, cit in WHO, 2010).

Subclinical (chronic) toxicity

The subclinical toxic effects of lead can be very damaging. The premise underlying the concept of subclinical toxicity is that there is a dose-related continuum of toxic effects in which clinically apparent effects have their asymptomatic (but still very real) counterparts (Landrigan, 1989).

Haematological toxicity

Anaemia is the classic clinical manifestation of lead toxicity in erythrocytes. The severity and prevalence of lead-induced anaemia correlate directly with the blood lead concentration. Younger and iron deficient children are at higher risk of lead-induced clinical anaemia. The anaemia induced by lead is caused primarily by impairment of the haem biosynthesis, but an increased rate of erythrocyte destruction may also occur (Schwartz et al., 1990).

Neurotoxicity

Neurodevelopmental effect of lead is the most important hazard of chronic lead exposure from public health point of view. In the central nervous system, lead causes asymptomatic impairment of neurobehavioural function in children at doses insufficient to produce clinical encephalopathy. The dose–response relationship between blood lead levels and loss of IQ was found to be stronger at blood lead levels lower than 10 µg/dl than at higher levels (Lanphear et al., 2000). An international pooled analysis of data from seven cohorts has confirmed these findings (Lanphear et al., 2005)

An increase in blood lead level from less than 1 µg/dl to 10 µg/dl was associated with a six IQ point decrement, which is considerably greater than the decrement associated with an increase in blood lead level from 10 µg/dl to 20 µg/dl. The findings of this pooled analysis – that there are adverse effects below 10 µg/dl and that the effects are steepest at the lowest levels of exposure – have been confirmed by numerous investigators (Emory et al., 1999, 2003; Bellinger & Needleman, 2003; Wasserman et al., 2003; Chiodo, Jacobson & Jacobson, 2004; Despres et al., 2005; Fraser, Muckle & Despres, 2006; Hu et al., 2006; Kordas et al., 2006; Schnaas et al., 2006; Tellez-Rojo et al., 2006; Chiodo et al., 2007; Surkan et al., 2007, all cit. in WHO, 2010).

When a population’s exposure to lead is sufficiently widespread to cause a decrease in its mean IQ, there results a substantial increase in the number of children with diminished intelligence and mental retardation. At the same time, there is a substantial reduction in the number of children with truly superior intelligence. The consequences are: (a) a substantial increase in the number of children who do poorly in school, who may require special education and other remedial programmes, and who may not contribute fully to society when they become adults; (b) a reduction in a country’s future leadership; and (c) a widening gap in socioeconomic attainment between countries with high and low levels of population exposed to lead (Needleman et al., 1979).

However, adverse effects of chronic lead exposure on cognitive function were observed not only in children. Sufficient evidence exists to conclude that there is an association between lead dose and decrements in cognitive function in adults, too. Overall, while the association between blood lead levels and cognitive function is more pronounced in occupational groups with high current lead exposures, associations between bone lead levels and cognitive function are more evident in studies of older subjects with lower current blood lead levels, particularly in longitudinal studies of cognitive decline. (Shih RA et al., 2007).

 

Substances included in the Lead group

Please see the link to the scoping document on Lead at the top of the page for this information

 

Human exposure to Lead

Although some exposure to lead results from direct contact with lead containing products, human exposure more frequently occurs via environmental media such as air, water, and soil. Based on worldwide collection of results of airborne lead concentrations measured before 1994, it was concluded that lead levels in both air and soil were generally higher in urban areas and near industrial sources than in other areas (median values in urban areas were 1.075 µg/m3, in suburban ones 0.33 µg/m3 and in rural areas 0.1 µg/m3). In urban areas, air and soil levels were associated with use of leaded petrol. Lead concentrations in both air and soil increased with traffic density and proximity to roads, as well as with higher lead concentrations in petrol. (The Global Dimensions of Lead Poisoning: An Initial Analysis, 1994).

The ECHA (2018) is mentioning that releases of lead to the environment is likely to occur from:

  • outdoor use in long-life materials with low release rate (e.g. metal, wooden and plastic construction and building materials)
  • indoor use in long-life materials with low release rate (e.g. flooring, furniture, toys, construction materials, paints, curtains, foot-wear, leather products, paper and cardboard products, electronic equipments)
  • indoor use in close systems with minimal release (e.g. cooling liquids in refrigerators, oil-based electric heaters)
  • outdoor use in close systems with minimal release (e.g. hydraulic liquids in automotive suspension, lubricants in motor oil and break fluids)

Human exposure to lead from drinking water results primarily from lead leaching from leaded plumbing components, rather than contamination of source waters (i.e., lakes, rivers, and aquifers).

The following sources and products account for most cases of childhood exposure to lead and lead poisoning (WHO, 2010):

  • lead from an active industry, such as mining (especially in soils)
  • lead-based paints and pigments,
  • lead solder in food cans
  • ceramic glazes
  • drinking-water systems with lead solder and lead pipes
  • lead in products, such as herbal and traditional medicines, folk remedies, cosmetics and toys
  • lead released by incineration of lead-containing waste
  • lead in electronic waste (e-waste)
  • lead in the food chain, via contaminated soil
  • lead contamination as a legacy of historical contamination from former industrial sites

Human exposure routes:

  • Inhalation: inhalation of lead particles generated by burning materials containing lead (e.g. during smelting, recycling, stripping leaded paint, and using leaded petrol or leaded aviation fuel)
  • Oral: ingestion of lead-contaminated dust, water (from leaded pipes), food from lead-glazed or lead-soldered containers, highly consumed food with low/medium lead content (e.g. grains) or food with known elevated lead content (e.g. mussels and lead-shot game meat).
  • Trans placental: Lead in bone is released into blood during pregnancy and becomes a source of exposure to the developing fetus. Moreover, lead is transmitted by maternal milk to infants.

Availability of HBM data:

Surveys measuring blood lead levels in the general population have been conducted in several countries since the early 1980-ies. After phasing out lead from petrol in most of the European countries interest in blood lead levels has been faded for a while. Results of blood lead level surveys conducted during the past two decades among the general population were found to be available in sixteen European countries (see Table 1), most of them covered children population, too. Decreasing trend in blood lead level of children could be observed with lowering lead content of petrol and finally phasing out leaded petrol in various countries. However, e.g. in Sweden it was found that after 2009 the decrease in the blood lead level discontinued (Wennberg et al., 2017) which means that there are still other existing lead exposure sources to be detected and eliminated.

Unfortunately, there are very few data on the present blood lead levels among the general population in the European countries. In an intensive literature search only 7 countries (Belgium, Germany, Denmark, Kosovo, Poland, Slovenia and Sweden) were found from where blood lead levels measured during the past 5 years were available.

 

Technical challenges in biomonitoring Lead in humans

To prevent false-positive results, stringent procedures are necessary to reduce environmental contamination of blood collection devices and supplies. Consequently, venous blood collected using evacuated tubes and needles certified as “lead-free” is considered the most appropriate specimen for blood lead measurements. However, collection of venous blood from paediatric subjects is sometimes difficult; thus, capillary blood from a finger puncture is used widely for screening purposes. Published studies have compared the quality of blood lead results for capillary and venous specimens drawn simultaneously (Schlenker et al., 1994; Schonfeld et al., 1994; Parsons et al., 1997). With stringent precautions, particularly rigorous hand washing, contamination errors can be held to <4% (Parsons et al. 1997). Therefore, although venous blood is preferable for epidemiologic studies of environmental lead exposure, use of capillary blood is acceptable if collected by staff specially trained in the technique using devices certified as “lead-free.” Data should be provided showing an acceptably low rate of contamination errors and low mean bias in the capillary BLLs as collected using the study protocol. (CDC, 2005)

Acceptable analytic methods include graphite furnace AAS (GFAAS, also known as electrothermal AAS), ASV, and ICP-MS. Information on laboratory performance (i.e., accuracy and precision) from external and internal quality control data should be provided.

Societal concern

Blood lead levels vary widely from country to country and region to region. The highest blood lead levels and the largest burden of disease from exposures to lead are seen in low-income countries – in particular, in areas where there are industrial uses of lead (such as smelters, mines and refineries) and/or where leaded petrol is still used heavily.

Although lead can affect children from every socioeconomic stratum, socially and economically deprived children and children in low-income countries carry the greatest burden of disease due to lead. Poor people are more likely to be exposed to lead and to be at risk of exposure to multiple sources. They are more likely to dwell on marginal land (near landfills and polluted sites), to live in substandard housing with ageing and deteriorating lead-based paint, and to live near industry, sites where waste is burned and heavy traffic. Also, lead smelting is used by marginalized populations to generate resources (WHO,2010).

The economic costs associated with childhood exposure to lead are substantial (Landrigan et al., 2002). The costs of childhood lead poisoning may be divided into direct and indirect costs. The direct or medical costs include those costs associated with the provision of medical care to children with acute lead poisoning, as well as the costs of treating cardiovascular disease in adults who have developed hypertension following exposure to lead.

Analyses of the indirect (non-medical) costs of lead poisoning have focused mainly on the loss of intelligence that is caused by lead and on the lifelong decrements in economic productivity that result from this loss of intelligence. These costs are sometimes referred to as lost opportunity costs. Using a conservative estimate, the decrease in intelligence attributable to each 1 μg/dl increase in blood lead level is 0.25 IQ points, and the decrement in lifetime economic productivity associated with each lost IQ point is 2.4%. (WHO, 2010)

 

Legislative status in the European Union

The EU’s Drinking Water Directive (98/83/EC) aims at protection of human health from adverse effects of any contamination of water intended for human consumption. It defines the health limit value of lead in drinking water as 10 μg/L.

According to the „Proposal for a DIRECTIVE OF THE EUROPEAN PARLIAMENT AND OF THE COUNCIL on the quality of water intended for human consumption” the Commission proposes lowering the value to 5 μg/l 10 years after the entry into force of the Directive. During this transitional 10-year period, the current value of 10 μg/l will be maintained.(EU, 2017)

The 2013/39/EU Directive amending directives 2000/60/EC and 2008/1056EC as regards priority substances in the field of water policy, suggests to have lead concentration lowered to a limit of 1.2 μg/L in inland surface water, and 1.3 μg/L in outland surface water.

Directive 2008/50/EC of the European Parliament and of the Council sets a regulatory limit value for lead in air as 0.5 μg/m3 per calendar year.

Regulatory limit value of lead in soil: 50 – 300 mg/kg, in sludge for agriculture: 750 – 1200 mg/kg (“EUR-Lex (86/278/EEC)”

1881/2006/EC set maximum levels for certain contaminants, including lead in foodstuffs.

However, the Panel on Contaminants in the Food Chain (CONTAM Panel) of the European Food Safety Authority (EFSA) concluded that the present PTWI of 25 μg/kg b.w. is no longer appropriate and noted that there was no evidence for a threshold for a number of critical endpoints including developmental neurotoxicity and renal effects in adults. Therefore, a margin of exposure approach was applied to risk characterisation. (EFSA, 2010)

 

Occupational exposure limit

Is regulated by the Chemical Agents Directive 98/24/EC containing both a binding OEL and a Biological Limit Value for inorganic lead and its compounds, this latter being 70 μg/dL.

Blood lead levels vary widely from country to country and region to region. The highest blood lead levels and the largest burden of disease from exposures to lead are seen in low-income countries – in particular, in areas where there are industrial uses of lead (such as smelters, mines and refineries) and/or where leaded petrol is still used heavily.

Although lead can affect children from every socioeconomic stratum, socially and economically deprived children and children in low-income countries carry the greatest burden of disease due to lead. Poor people are more likely to be exposed to lead and to be at risk of exposure to multiple sources. They are more likely to dwell on marginal land (near landfills and polluted sites), to live in substandard housing with ageing and deteriorating lead-based paint, and to live near industry, sites where waste is burned and heavy traffic. Also, lead smelting is used by marginalized populations to generate resources (WHO,2010).

The economic costs associated with childhood exposure to lead are substantial (Landrigan et al., 2002). The costs of childhood lead poisoning may be divided into direct and indirect costs. The direct or medical costs include those costs associated with the provision of medical care to children with acute lead poisoning, as well as the costs of treating cardiovascular disease in adults who have developed hypertension following exposure to lead.

Analyses of the indirect (non-medical) costs of lead poisoning have focused mainly on the loss of intelligence that is caused by lead and on the lifelong decrements in economic productivity that result from this loss of intelligence. These costs are sometimes referred to as lost opportunity costs. Using a conservative estimate, the decrease in intelligence attributable to each 1 μg/dl increase in blood lead level is 0.25 IQ points, and the decrement in lifetime economic productivity associated with each lost IQ point is 2.4%. (WHO, 2010)

 

Policy questions on Lead

  1. What is the concentration of lead in the human blood nowadays (after phasing out leaded petrol) in the countries of Europe?
  2. Do blood lead levels of both adults and children still indicate permanent existence of lead exposure?
  3. What are the sources of still existing lead exposure in different countries of Europe?
  4. What kind of exposure sources are the most important for the children of various age groups and the younger or older adult population?
  5. Taking the hazard from transplacental lead exposure of the unborn child into consideration, what are the blood lead levels of pregnant women?
  6. Taking the presumably low concentration of lead in blood, is it feasible to measure blood lead levels in children from as small amount of blood as it can be gained from capillary samples? What criteria should be applied in order to avoid contamination from outside sources?

Please find answers to the updated (2020) Policy-related questions on Lead here 

 

Stakeholder comments on the scoping document

In the interest of transparency and accountability, HBM4EU invites interested stakeholders to submit comments on the scoping document on acrylamide.

All submitted comments will be made available for download on this webpage and will be taken into consideration by the HBM4EU consortium, where possible.

Please click here to submit your comments.

 

References

  1. Abass K et al (2017): Arsenic, cadmium, lead and mercury levels in blood of Finnish adults and their relation to diet, lifestyle habits and sociodemographic variables. Environ Sci Pollut Res 24:1347–1362
  2. Baeyens W. et al. (2014). Trace metals in blood and urine of newborn/mother pairs, adolescents and adults of the Flemish population (2007-2011). Int J Hyg Environ Health 217(8):878-90
  3. Bocca B. et al (2013). Metals as biomarkers of the environmental human exposure. E3S Web of Conferences DOI: 10.1051/ C
  4. Canas, A.I. et al (2014) Blood lead levels in a representative sample of the Spanish population: the BIOAMBIENT.ES Projet. International Journal of Hygiene and Environmental Health 217(4): 452-459
  5. CDC (1991). Preventing Lead Poisoning in Young Children. U.S. Department of Health and Human Services, Public Health service, Centers for Disease Control.
  6. CDC (2012): CDC Response to Advisory Committee on Childhood Lead Poisoning Prevention Recommendations in “Low Level Lead Exposure Harms Children: A Renewed Call of Primary Prevention”) http://www.cdc.gov/nceh/lead/ACCLPP/CDC_Response_Lead_Exposure_Recs.pdf
  7. Cerna M. et al. (2012). Human biomonitoring in the Czech Republic. An overview. Int J Hyg Environ Health 215(2), 109-119
  8. ECHA (2018). Brief profile on lead, https://echa.europa.eu/brief-profile/-/briefprofile/100.028.273)
  9. EFSA (2010) Panel on Contaminants in the Food Chain (CONTAM). Scientific Opinion on Lead in Food. EFSA Journal 2010; 8(4):1570 [151 pp.], doi: 10.2903 /j.efsa.2010.1570. Available online: www.efsa.europa.eu
  10. EHC (1995) Environmental Health Criteria vol. 165: Inorganic Lead, WHO, Geneva.
  11. Etchevers A. et al (2014). Blood lead levels and risk factors in young children in France, 2008-2009. Int J Hyg Environ Health. 2014 Apr-May;217(4-5):528-37. doi: 10.1016/j.ijheh.2013.10.002.
  12. EU (2017) http://ec.europa.eu/environment/water/water-drink/pdf/revised_drinking_water_directive.pdf
  13. Falq, G et al. (2008). Exposition de la population adulte au plomb en France – Valeurs de référence. (étude nationale nutrition santé, ENNS 2006-2007), available at: http://invs.santepubliquefrance.fr/publications/2008/jvs_2008/47_poster_falq.pdf
  14. Fierens S. et al. (2016). Human biomonitoring of heavy metals in the vicinity of non-ferrous metal   plants in Ath, Belgium. Archives of Public Health 74:42
  15. Garcia-Esquinas, E. et al. (2013). Lead, mercury and cadmium in umbilical cord blood and its association with parental epidemiological variables and birth factors. BMC Public Health 13:841. http://www.biomedcentral.com/1471-2458/13/841
  16. Grigiryan, R. et al (2016) Risk factors for children’s blood lead levels in metal mining and smelting communities in Armenia: a cross-sectional study. BMC Public Health 16:945
  17. Hruba F. et al. (2012). Blood cadmium, mercury, and lead in children: an international comparison of cities in six European countries, and China, Ecuador, and Morocco. Environ Int. 2012 May;41:29-34. doi: 10.1016/j.envint.2011.12.001.
  18. IARC (1987) IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Supplement 7: Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42, IARC Lyon, France
  19. IARC (2006). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Vol. 87: Inorganic and Organic Lead Compounds, IARC Lyon, France.
  20. IARC (2014) https://monographs.iarc.fr/wp-content/uploads/2018/08/14-002.pdf)
  21. Jakubowski, M (2012). Lead In: Issues in Toxicology No.9. Biomarkers and Human Biomonitoring, Vol.1.: Ongoing Programs and Exposures, Eds: Knudsen L.E. and Merlo F., Royal Society of Chemistry.
  22. Kutllovci-Zogaj, D et al (2014). Correlation between blood lead level and hemoglobin level in Mitrovica children. Med Arh. 2014 Oct; 68(5): 324-328
  23. Landrigan, P.J. (1989). Toxicity of lead at low dose. Brit J Ind Med 46(9):593-596
  24. Landrigan, P.J. et al (2002). Environmental pollutants and disease in American children: estimates of morbidity, mortality, and costs for lead poisoning, asthma, cancer, and developmental disabilities. Environ Health Perspect, 110(7):721-728
  25. Lanphear BP et al. (2000). Cognitive deficits associated with blood lead concentrations <10µ/dL n US children and adolescents. Public Health Reports 115:521-529
  26. Lanphear BP et al. (2005).Low-level environmental lead exposure and children’s intellectual function: an international pooled analysis. Environ Health Perspect. 113(7):894-899
  27. Navas-Acien A. et al. (2007). Lead exposure and cardiovascular disease – a systematic review. Environ Health Perspect. 115(3):472-482
  28. Needleman H.L. et al. (1979). Deficit in psychologic and classroom performance of children with elevated dentine lead levels. New England J Med, 300(13):689-695
  29. Oulhote, Y et al. (2013). Implications of different residential lead standards on children’s blood lead levels in France: predictions based on a national cross-sectional survey. Int J Hyg Environ Health. 2013 Nov;216(6):743-50. doi: 10.1016/j.ijheh.2013.02.007.
  30. Parsons, P.J., Reilly, A.A., Esernio-Jenssen, D.(1997) Screening children exposed to lead: an assessment of the capillary blood lead fingerstick test. Clin Chem. 43:302–311
  31. Pelc W. et al. (2016). Environmental and socioeconomic factors contributing to elevated blood lead levels in children from an industrial area of Upper Silesia. Environ Toxicol Chem 2016;35:2597–2603.
  32. Polanska K. et al (2014). Predictors of environmental lead exposure among pregnant women – a prospective cohort study in Poland. Ann Agric Environ Med. 21(1): 49–54.
  33. Rosofsky A. et al (2017). Exposure to multiple chemicals in a cohort of reproductive –aged Danish women. Environmental Research 154 (Supplement C): 73-85 https://doi.org/10.1016/envres.2016.12.011.
  34. Rudnai P, Varró M.J, Rudnai T, Náray M, Schoket B, Anna L, Györffy E, Kovács K, Ürömi J, Herczegh T, Bodnár J (2009). Associations between the children’s blood lead level and their health status. Epidemiology 20(6):S260
  35. Schlenker, T.L., Fritz, C.J., Mark, D., Layde, M., Linke, G., Murphy, A., et al.(1994) Screening for pediatric lead poisoning. Comparability of simultaeously drawn capillary and venous blood samples. JAMA.271:1346–1348.
  36. Schonfeld, D.J., Cullen, M.R., Rainey, P.M., Berg, A.T., Brown, D.R., Hogan Jr., J.C., et al. (1994) Screening for lead poisoning in an urban pediatric clinic using samples obtained by fingerstick. Pediatrics. 94:174–179.
  37. Schultz, C. et al. (2017). German Environmental Survey for Children and Adolescents 2014-2017 (GerES V) – the environmental module of KiGGS Wave 2. Journal of Health Monitoring ·2017 2(S3)DOI 10.17886/RKI-GBE-2017-108
  38. Schwartz J et al. (1990). Lead-induced anemia: dose-response relationships and evidence for a threshold. Amer J Publ Health, 80(2):165-168
  39. Shih RA et al.(2007). Cumulative Lead Dose and Cognitive Function in Adults: A Review of Studies That Measured Both Blood Lead and Bone Lead. Environ Health Perspect. 115:483–492
  40. Szkup-Jabłońska, M et al. (2012). Effects of blood lead and cadmium levels on the functioning of children with behaviour disorders in the family environment. Annals of Agricultural and Environmental Medicine 2012, Vol 19, No 2, 241-246
  41. The Global Dimensions of Lead Poisoning: An Initial Analysis.(1994), Alliance to End Childhood Lead Poisoning, Environmental Defense Fund
  42. Tratnik J.S. et al. (2013). Biomonitoring of selected trace elements in women, men and children from Slovenia. E35 Web of conferences 1: 26001. https://doi.org/10.1051/e3sconf/20130126001
  43. U.S. Bureau of Mines (1993). Lead. Annual Report – 1991. US Department of the Interior, Washington, D.C.
  44. UBA (2018). https://www.umweltbundesamt.de/sites/default/files/medien/355/dokumente/tabelle-ref-werte_-_metalle_mai_2018_aktualisiert.pdf
  45. Wells, E.M. et al. (2011). Low level lead exposure and elevations in blood pressure during pregnancy. Environ Health Perspect. 119(5):664-669
  46. Wennberg M. et al (2017). Time trends and exposure determinants of lead and cadmium int he adult population of Northern Sweden 1990-2014. Environmental Research 159 (Supplement C): 111-117. https://doi.org/10.1016/j.envres.2017.07.029
  47. WHO (2010). Childhood lead poisoning, WHO, Geneva
  48. Wilhelm, M. et al. (2010) Reassessment of critical lead effects by the German Human Biomonitoring Commission results in suspension of the Human Biomonitoring values (HBM I and HBM II) for lead in blood of children and adults. Int J Hyg Environ Health 213(4):265-69