Introduction: Lead is one of the oldest widely used industrial metals. Throughout the ages, its significant toxicity caused poisoning of exposed people. Even today occupational exposure remains a significant hazard.

Aim: The aim of the study is to depict the risk associated with lead exposure on the base of the case report.

Methods: Patient’s medical history analysis and the review of available literature.

Results: Two patients with history of occupational lead exposure were admitted to hospital. Their symptoms suggested chronic lead poisoning. Blood lead level was excessive in both cases. The patients were treated with antioxidants and advised to reduce their exposure to lead, with continuing ambulatory therapy. 

Conclusions: All known effects of  Pb are extremely harmful to humans. 

Lead poisoning still appears to be a problem in some jobs and environments, particularly in cases of chronic low level exposure. Proper monitoring of  workplace conditions and regular medical checkups for those at risk should be practiced to avoid cases of chronic poisoning  in the future

Andrzej Kościuk

Justyna Drankowska

Michał Kos

Michał Tchórz

Journal of Education Health and Sport

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185Kościuk Andrzej, Kos Michał, Drankowska Justyna, Tchórz Michal. Lead poisoning linked to occupational exposure - case reports.Journal of Education, Health and Sport. 2019;9(1):185-190. eISNN 2391-8306. DOI http://dx.doi.org/10.5281/zenodo.2546071http://ojs.ukw.edu.pl/index.php/johs/article/view/6497The journal has had 7 points in Ministry of Science and Higher Education parametric evaluation. Part B item 1223 (26/01/2017).1223 Journal of Education, Health and Sport eISSN 2391-8306 7© The Authors 2019;This article is published with open access at Licensee Open Journal Systems of Kazimierz Wielki University in Bydgoszcz, PolandOpen Access. This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium,provided the original author (s) and source are credited. This is an open access article licensed under the terms of the Creative Commons Attribution Non commercial license Share alike.(http://creativecommons.org/licenses/by-nc-sa/4.0/) which permits unrestricted, non commercial use, distribution and reproduction in any medium, provided the work is properly cited.The authors declare that there is no conflict of interests regarding the publication of this paper.Received: 03.01.2019. Revised: 11.01.2019. Accepted: 23.01.2019.Lead poisoning linked to occupational exposure - case reportsName Andrzej KościukAffiliation Research Group in the Department of Toxicology, Medical University of LublinCountry PolandBio Statement —Principal contact for editorial correspondence.Name Michał KosAffiliation Research Group in the Department of Toxicology, Medical University of LublinCountry PolandBio Statement —Name Justyna DrankowskaAffiliation Research Group in the Department of Toxicology, Medical University of LublinCountry PolandBio Statement —Name Michal TchórzAffiliation Department of Toxicology, Medical University of LublinCountry PolandBio Statement —IntroductionLead is one of the first metals widely used by human cultures, with documented usefrom antiquity [1,2]. Its attributes- ductility, low melting point, and corrosion resistancecontributed to its prominent role in various industries and products, including paints, pipes,plastics [1,3] .The first symptoms of lead poisoning have been described as early as second century B.C.,with cases of colic and paralysis following lead intake mentioned by physician from Greece,Nikander. Lead-sweetened wine was a crucial part of Roman elites’ diet [4]. Along withwater contamination from lead pipes, it caused significant exposure to lead toxicity amongRomans [2]. Lead poisoning is, somewhat controversially, posited as an important factor inthe decline of Roman Empire [4].186In XIX century, cases of lead poisoning became more recurrent due to rapid industrialisation.In the latter half of the century, this induced some governments, e.g. United Kingdom, to passfirst occupational safety laws [5].At high levels of exposure practically all tissues and organs are damaged, with functions ofcentral nervous system, blood and kidneys especially impaired. Serious poisoning can bedeadly. At low levels we observe a range of effects, from disturbance of biochemicalprocesses, the most important being haeme synthesis, to psychological and neurobehaviouraldysfunctions [6].While acute poisoning became relatively rare, at least in countries with appropriate workingconditions, low level exposure remains an intensively studied problem, especially in children,in which it can cause neurodevelopmental disorders [7].Keywords: Lead poisoning, occupational exposureCase reportsWe hereby describe two patients with chronic lead poisoning related to occupationalexposure.A 57-year-old male, exposed to zinc and lead due to his job in zinc industry, was admitted tothe hospital for evaluation of suspected lead poisoning. He had the following symptomsduring past 12 months: vertigo and dizziness, hot flashes, paresthesia, red skin lesions onforearms. He was also reported to become more aggressive and nervous during this period.Physical examination did not reveal much, except for paresthesia in lower extremities. TheMR of the head showed nonspecific demyelination in frontal and parietal lobes of the brain. Acomprehensive blood testing was undertaken as well, including complete blood count, anelectrolyte panel and glucose level; all results remained within reference range. The lead levelin patient’s blood was slightly elevated at 5,2 ug/dL. His relatively benign condition onadmission precluded the staff from using chelation therapy, and he was treated with 5%glucose solution with an ascorbic acid. After scheduling lead level check- up, the therapy wascontinued in outpatient clinic.Another patient, a 30-year-old male, was admitted to the Department of Toxicology andCardiology due to suspected chronic lead poisoning. He had significant occupational exposureto lead as he repaired lead- acid batteries. For the last 8 months, he experienced recurrentepisodes of intensive retrosternal pain, often coupled with painful sensations in epigastricregion. He also mentioned nausea, vision impairment, headaches, paresthesia in the left armand aching knee joints. The blood tests showed a few discrepancies, including slightlyelevated level of liver enzymes, heightened CRP, a decreased amount of limphocytes and anincreased number of neutrophiles. Blood lead level was elevated at 23,2 ug/dL. Subsequently,the patient underwent multifaceted examination, including neurological and ophthalmologiccheckup, gastroscopy, and echocardiography. The investigation revealed slight left ventricularhypertrophy, probably related to hypertension or hypertrophic cardiomiopathy. Meanwhile,the lead level in blood has fallen to 15,52 ug/dL. The patient was discharged from hospitaland advised to continue therapy in an outpatient clinic and decrease his lead exposure.DiscussionLead toxicity affects nearly every major organ and system of human body, withparticularly visible influence on nervous tissue, hematopoiesis, kidneys, cardiovascular andreproductive systems. [1]( Table 1) The adults with lead poisoning often present neurologicalsymptoms ranging from lethargy to serious motor neuropathy [8]. Loss of myelin sheath in187peripheral neurons can impair nerve impulses’ transmission, which leads to reduced motoractivity, resulting in muscle weakness, fatigue and lack of muscles’ coordination [9].Table 1. Symptoms of lead poisoning [1]length of exposure typical symptomsacute poisoning fatigue, headaches, muscle pain,stomachache, vomiting, seizures, comachronic poisoningpersistent emesis, lethargy,encephalopathy, convulsions andcoma, deliriumBoth of our patients reported to experience moderate neurological symptoms, includingheadaches and numbness in upper or lower extremities since about a year. The older patienthas also developed behavioral issues- he had outbursts of aggression. MRI scan of his headshowed demyelination in the brain. The characteristic sign of severe lead poisoning in adultsis bilateral wrist drop [8]. This symptom was observed in neither patient as it is usually visibleonly with much higher blood lead levels than those measured.On the other hand, children with chronic, low level exposure suffer from central nervoussystem damage, including developmental disorders leading to intelligence impairment andother CNS dysfunctions [8]. In comparison to healthy children, kids exposed to lead toxicityoften show aberrant behaviors, including depressive disorders, social withdrawal and oddbody movements, aggressions and propensity to destruction [10].High level exposure can lead to encephalopathy, with symptomatic irritability, attentiondeficits, dreariness, headaches, convulsions, memory disorders and hallucinations [3].Anemia is another important symptom of lead poisoning, caused by restricted hemoglobinsynthesis and increased rate of hemolysis. Lead suppresses hematopoiesis by hinderingessential enzymes needed for haeme synthesis, and reduces erythrocytes’ lifespan byweakening cell membranes. [1] The affected enzymes include δ-aminolevulinic aciddehydratase (ALAD), aminolevulinic acid synthetase (ALAS) and ferrochelatase [11].Renal dysfunction includes both acute and chronic nephropathies. In acute form, one observesproximal tubular dysfunction giving rise to glycosuria, hyperphosphaturia, aminoaciduria(Fanconi’s syndrome) . Long-term exposure to high levels of lead causes irreversible changesin the kidney such as interstitial fibrosis, glomerular sclerosis, tubular atrophy. The final resultis renal failure, and every patient with lead level >60 ug/dL is at risk of developing suchcondition. Recent research proves that renal abnormalities can ensue even at blood lead levelapproaching 10 ug/dL, previously considered to be safe [3].Lead poisoning can have a number of undesirable effects on cardiovascular system. Leadintoxication was demonstrated to stimulate atherosclerosis in animal experiments.Furthermore, chronic exposure was connected with atherosclerosis and cardiovascularmortality in humans as well [12]. One of our patients was diagnosed with mild cardiachypertrophy. However, while it could be related to lead exposure, the presence of188cardiomiopathy in family history may suggest genetic predisposition to such diseases in thiscase. Some studies claim that low- level lead exposure is correlated with diseases such ashypertension and peripheral artery disease [12]. Other important disorders are ischemiccoronary heart disease and cerebrovascular accidents [1].Reproductive system is also susceptible to lead toxicity. Symptoms in men include infertility,abnormal spermatogenesis and prostatic function, chromosomal impairment, changes in libidoand testosterone levels. Affected women are more vulnerable to miscarriage, infertility,preeclampsia, premature delivery and pregnancy hypertension [13]. Prenatal lead exposurewas linked to toxic harm to the fetus’ tissues [3].Lead is absorbed primarily through inhalation and, to a lesser degree, through gastrointestinaltract. It is stored in three major tissue groups: blood, muscle and bones. Over 90% of all leadis deposited in bones, with biological t1/2 =20-30 years; hence it is nearly impossible toremove it completely after significant exposure [8]. Pb2+ is principally eliminated with feces,with some smaller amount removed via urinary tract. Trace amounts of lead can also beeliminated through sweat, hair, nails and breast milk [14]. Children have higher total leadabsorption compared to adults and higher percentage of all bodily lead deposited in softtissues- two of the reasons for their increased susceptibility for lead poisoning [1,8].Lead appears to have two primary mechanisms of toxicity, i.e. inducing oxidative stress andsubstituting other bivalent cations in diverse metabolic processes [1]. The first processconsists of simultaneous production of reactive oxygen species and disabling cellularantioxidant mechanisms [15]. Lead has the ability to bond with sulfhydryl groups inantioxidants (e.g. glutathione), which inactivate them [1]. In analogous way, lead can interruptenzymes like ALAD (blocking haeme synthesis) and gluthatione reductase, glutathioneperoxidase and glutathione-S- transferase (contributing to reduction in glutathione activity)[16]. Lead can also supplant some bivalent cations, including Ca2+, Fe2+, Mg2+ and somemonovalent ions e.g. Na+. This can have a profound effect on cell functioning [17]. Thisprocess is most damaging in central nervous system, where Pb cations replace Ca2+ ions andcross blood-brain barrier. Afterwards they accrete in CNS in astroglial cells. The damagecaused by lead accumulation is especially apparent in immature nervous system, where itimpedes myelin sheath development. Lead can also influence some neurotransmitters, e.g.protein kinase C. [1]Figure 1. Blood lead level considered excessive according to CDC [18]Diagnosis is usually made on the basis of typical symptoms and blood lead level [8]. Theevidence for negative effects of lead exposure even at very low thresholds prompted arevision of safe BLL guidelines.( Figure 1) The upper value for children reference range is189now 5 ug/dL. Current CDC/NIOSH reference BLL for adults is also 5 µg/dL [18]. Both of ourpatients exceeded this level and were eligible for therapy. It is important to note that eventhough one of our patients outstripped the threshold only minimally, he nevertheless showedsome serious symptoms, like behavioral problems and CNS demyelination. Another usefuldiagnostic tool is zinc protoporphyrin (ZPP) level, which allows to asses lead exposure up to3 months before patient’s admission. ALA (aminolevulinic acid) elimination with urine andALAD activity are also sensitive lead exposure indicators, but are not used very often.Treatment involves primarily removing the source of exposure and using chelation therapy toisolate lead from cell components and remove them from the body [8].ConclusionsNo biological function of lead in human body is known. All known effects of Pb areextremely harmful to humans, especially exposure in childhood which can culminate inserious behavioral and cognitive deficits in children. Even after Pb exposure ended, theseoutcomes persist well into adulthood [14].Lead poisoning still appears to be a problem in some jobs and environments, particularly incases of chronic low level exposure. Proper monitoring of workplace conditions and regularmedical checkups for those at risk should be practiced to avoid cases of chronic poisoning inthe future.References:1. Flora G, Gupta D, Tiwari A. Toxicity of lead: A review with recent updates.Interdiscip Toxicol. 2012; Vol. 5(2): 47–58. doi: 10.2478/v10102-012-0009-22. Gilbert S, Weiss B. A rationale for lowering the blood lead action level from 10 to 2mg/dL. NeuroToxicology. 2006; 27: 693–701. doi: 10.1016/j.neuro.2006.06.0083. Flora S, Flora G, Saxena G. Environmental Occurrence, Health Effects andManagement of Lead Poisoning. In Lead. 2006; p. 158–228. Elsevier.https://doi.org/10.1016/B978-044452945-9/50004-X (accessed: 2018.12.27)4. Needleman H. Lead poisoning. Annu Rev Med. 2004; 55: 209-222. doi:10.1146/annurev.med.55.091902.1036535. Tong S, Schirnding Y, Prapamontol T. Environmental lead exposure: a public healthproblem of global dimensions. Bulletin of the World Health Organization. 2000; 78(9): 1068- 1077. https://www.who.int/bulletin/archives/78(9)1068.pdf (accessed:2018.12.27)6. WHO World Health Organization. Inorganic Lead. Environmental Health CriteriaNumber 165, Geneva. 1995. http://www.inchem.org/documents/ehc/ehc/ehc165.htm(accessed: 2018.12.28)7. Tong S. Lead exposure and cognitive development: persistence and a dynamic pattern.Journal of Paediatrics and Child Health. 1998; 34: 114–118.https://doi.org/10.1046/j.1440-1754.1998.00187.x (accessed: 2018.12.29)8. Gordon J, Taylor A, Bennett P. Lead poisoning: case studies. Blackwell Science LtdBr J Clin Pharmacol. 2002; 53: 451- 458. https://doi.org/10.1046/j.1365-2125.2002.01580.x (accessed: 2018.12.29)9. Sanders T, Liu Y, Buchner V, Tchounwou P. Neurotoxic effects and biomarkers oflead exposure: A Review. Res Environ Health. 2009; 24: 15–45.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2858639/ (accessed: 2018.12.29)10. Hou S, Yuan L, Jin P, Ding B, Qin N, Li L et al.: A clinical study of the effects of leadpoisoning on the intelligence and neurobehavioral abilities of children. Theoretical190Biology and Medical Modelling. 2013; 10:13.http://www.tbiomed.com/content/10/1/13 (accessed: 2018.12.29)11. Piomelli S. Childhood lead poisoning. Pediatr Clin North Am. 2002; 49: 1285- 1304.DOI: 10.1016/S0031-3955(02)00097-412. Alissa E, Ferns G. Heavy Metal Poisoning and Cardiovascular Disease. HindawiPublishing Corporation Journal of Toxicology Volume 2011, Article ID 870125, 21pages. doi:10.1155/2011/87012513. Flora S. Arsenic induced oxidative stress and its reversibility. Free Rad Biol Med.2011; 51: 257–281. DOI: 10.1016/j.freeradbiomed.2011.04.00814. Neal A, Guilarte T. Mechanisms of Lead and Manganese Neurotoxicity.http://pubs.rsc.org | doi:10.1039/C2TX20064C (accessed: 2018.12.23)15. Flora S. Nutritional components modify metal absorption, toxic response and chelationtherapy. J Nut Environ Med. 2002; 12: 53–67.https://doi.org/10.1080/13590840220123361 (accessed: 2018.12.28)16. Ahamed M, Siddiqui M. Low level lead exposure and oxidative stress: Currentopinions. Clin Chim Acta. 2007; 383: 57–64.https://doi.org/10.1016/j.cca.2007.04.024 (accessed: 2018.12.29)17. Garza A, Vega R, Soto E. Cellular mechanisms of lead neurotoxicity. Med Sci Monit.2006; 12: RA57–65. PMID: 1650143518. ATSDR CASE STUDIES IN ENVIRONMENTAL MEDICINE (CSEM). LeadToxicity. https://www.atsdr.cdc.gov/csem/csem.asp?csem=34&po=8#table4 (accessed:2018.12.27)

Lead poisoning linked to occupational exposure - case reports

Introduction: Lead is one of the oldest widely used industrial metals. Throughout the ages, its significant toxicity caused poisoning of exposed people. Even today occupational exposure remains a significant hazard.
Aim: The aim of the study is to depict the risk associated with lead exposure on the base of the case report.
Methods: Patient’s medical history analysis and the review of available literature.
Results: Two patients with history of occupational lead exposure were admitted to hospital. Their symptoms suggested chronic lead poisoning. Blood lead level was excessive in both cases. The patients were treated with antioxidants and advised to reduce their exposure to lead, with continuing ambulatory therapy. 
Conclusions: All known effects of  Pb are extremely harmful to humans. 
Lead poisoning still appears to be a problem in some jobs and environments, particularly in cases of chronic low level exposure. Proper monitoring of  workplace conditions and regular medical checkups for those at risk should be practiced to avoid cases of chronic poisoning  in the future

Lead poisoning linked to occupational exposure - case reports

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