| Abstract|| |
Background: The risk of occupational lead exposure exists in lead smelting plants and battery industries, which may give rise to the issues related to lead poisoning among battery workers and low-exposed workers. Aims: To investigate the relationship between biochemical and hematological markers of lead effects and occupational exposure in battery workers and determine the role of work-related lead poisoning with emphasis on hemopetic system in exposed workers. Materials and Methods: Present study was carried out from July to October 2015, which collected demographic data, nonwork, and work-related symptoms from lead exposure nonexposed workers (N = 33) and battery wokers (N = 30), Nakhon Pathom, Thailand. Each blood sample was collected and analyzed for lead biomarkers, blood lead level (BLL)and δ-aminolevolinic dehydratase (ALAD) and hematological markers, such as complete blood count and recticulocyte count. Results and Discussion: Major non-work-related symptoms were droopiness and muscle pain among nonexposed groups. Major work-related symptoms in battery workers were occurred in lungs and nose. There was a significant increase in BLL, and a significant decrease activity of ALAD was observed in battery workers. Strong positive correlation between years of exposure and employment with BLL was observed and respiratorytract symptoms were also presented.Inverse correlation between the activity of ALAD and hemoglobin and a strong positive correlation between hemoglobin and BLL were found. Conclusion: The lead level and ALAD were good markers for screening lead exposures by significant related to hematological values, duration of work, and exposure and hypertension.
Keywords: δ-aminolevulinic dehydratase, battery workers, blood lead, complete blood count, lead exposure
|How to cite this article:|
Sudjaroen Y, Suwannahong K. Biomarker related lead exposure of industrial battery's workers. Ann Trop Med Public Health 2017;10:194-8
|How to cite this URL:|
Sudjaroen Y, Suwannahong K. Biomarker related lead exposure of industrial battery's workers. Ann Trop Med Public Health [serial online] 2017 [cited 2019 Sep 21];10:194-8. Available from: http://www.atmph.org/text.asp?2017/10/1/194/196523
| Introduction|| |
Lead is a ubiquitous environmental toxin that has been detected in almost all phases of biological systems. Even small quantities of lead are harmful to humans and other organisms because they induce a broad range of physiological, biochemical, and behavioral dysfunctions in many parts of the body, including the central and peripheral nervous systems, hematopoietic system, cardiovascular system, kidneys, liver, and reproductive systems. As a result, a safe level of lead exposure hasnot yet been defined., It has been proposed that the main mechanism involved in lead toxicity is the induction of oxidative stress. It is believed that lead is able to generate reactive oxygen species and alter the function of antioxidant defense system components, including antioxidant enzymes.,,,
Occupational lead poisoning has been a recognized health hazard for more than 2000 years. Lead toxicities were characterized by symptom feature including anemia, colic, neuropathy, nephropathy, sterility, and coma. Physicians have gained an extensive understanding of the causes, the clinical presentations, and the means of preventing lead poisoning. However, it remains one of the most important occupational and environmental health problems. Lead serves no useful biologic function in the human body. Over the past several years, concern has increased over the health effects of low-level lead exposure and the “normal” body burden of lead. In the occupational setting, the present “no-effect” level for lead exposure is currently being re-evaluated as more sensitive measures of the physiologic effects of lead are made available through clinical investigations.
Leadin human specimens is a biomarker for lead body burden, actual and previous or recent lead exposure. The biological markers of lead include increased levels of coproporphyrin and aminolevulinic acid in urine; pirimidine-5-nucleotidase, protoporphyrin and activity δ-aminolevulinic acid dehydratase (ALAD) in erythrocytes., The lowest observed adverse effect level of lead is 10 μg/dL in children and 30 μg/dL in adult. Lead exposure inhibits ALAD, ferrochelatase, and coporphyrinogenoxidase in heme synthesis; but its most significant effects are observed on ALAD. As the threshold for erythrocytes ALAD inhibition lays below10 μg/dL, the levels of δ-aminolevulinic acid in the blood and urine increased significantly. Similarly, the elevated levels of coproporphyrine in blood where the lead levels were 40 μg/dL have been reported by Jaffeet al.
Blood lead level (BLL) in the general population has decreased since the use of lead in paints and petroleum products and food containers have been curtailed. Nevertheless, other sources of lead continue to make lead an issue to public health. The exposure to environmental lead is an issue of great importance in lead battery repair and recycling industries and certain aspects of lead toxicity are yet to be elucidated.The risk of occupational lead exposure exists where workers are exposed to lead and its compounds in the form of lead dust, lead fumes especially in lead smelting plants, battery repairs, and recycling units. The presence of industrial battery at Nakhon Chaisri district, Nakhon Pathom may gave rise to the issues related to lead poisoning among battery workers and low-exposed workers.
The aim of present study was to investigate the relationship between biochemical and hematological markers oflead effects and occupational lead exposure in battery repair and recycling workers in industrial batteries' workers at Nakhon Chaisri district, Nakhon Pathom province, also to determine the roleof work-related lead poisoning in the progression oflead-related health hazards with particular emphasis onhemopoetic system in lead-exposed workers.
| Materials and Methods|| |
Subjects, demographic data, and lead exposure-related history
Present study was carried out from July to October 2015, to assess lead exposure and its toxic effects, which aimed to detect health impact caused by lead poisoning among non-exposed (N = 33), including human resource staffs, transport drivers, stock checkers and QC staffs, and battery workers (moderate to high exposed, N = 30) who working with smelting lead, repaired batteries, and recycled lead for new batteries production at Nakhon Chaisri district, Nakhon Pathom, Thailand. Data about demography, work history, hours of daily lead exposure, duration of employments, smoking status, prevailing disease, work-related symptoms, and preventive measures were obtained by using a structured questionnaire filled in by the subjects. The subjects with poor literacy were assisted to fill the questionnaire. An informed consent of each subject was obtained and study protocol was approved by the ethical review committee.The demographic characteristics, smoking habits duration of employment, and environmental lead exposure was not significantly different in the two groups studied.After taking a brief history, height and weight of each subject were recorded. Height was measured by using a fix stadia rod and an electronic scale was used to recordthe weight of each subject. Height and weight were used to calculate the body mass index of each subject. General and work-related symptoms of each subject were noted prior to the blood sampling.
Specimen preparation and laboratory assay
The 2 mL of whole blood was drawn from each subject a large antecubital vein using needle attached to EDTA vacutainer tube (containing K2EDTA 1.5 mg/mL of blood sample) and blood sample was stored at 4°C until tested for BLL on the same day with lead biochemical parameters, completed blood count, and other lead biomarkers. BLL was determined an Agilent SpectrAA-400Z with Zeeman background correction and an Agilent SpectrAA-400P with deuterium background correction. Both spectrometers were equipped with an Agilent GTA-96/96Z graphite tube atomizer and PSD-96 programmable sample dispenser. Inert gas was high purity argon (Agilent Technologies, USA). ALADwasanalyzed by spectroscopic method, which modified from previous study. All hematologic parameters of complete blood count (CBC) were analyzed by Celltac E MEK-7222 (Nihon Kohden, Tomioka, Japan) and reticulocyte and erythrocyte counts with basophilic stippling were determined by the method of Tasevski et al.The repeat ability of the analysis was assessed based on trip licateanalysis of three blood samples. In each case, the coefficient of variation calculated was 10% or less. All analyses were performed in certified clinical laboratories. Biochemical and hematological parameters were interpreted by reference values according by Clinical and Laboratory Standards Institute.
Descriptive and inferential statistical methods were used to analyze the data using Statistical Statistical Package for Social Sciences (SPSS) 12.0. The values of continuous variables were presented as mean ± SD, while nominal variables were expressed as percentages and numbers. The difference of parameters between battery workers and controls was tested by independent t-test and Pearson's correlation were tested for relation between the parameters and BLL and ALAD activity in battery workers and controls, which was present as correlation coefficient(r). Statistical significant was considered by P< 0.05.
A total of 63 industrial workers who participated in this study were divided into non-exposure as control group (N = 33), including human resource staffs, transport drivers, stock checkers and QC staffs, and battery workers or lead exposure group (moderate to high lead exposed, N = 30) who working with smelting lead, repaired batteries, and recycled lead for new battery production. The demographic characteristics of study subjects are shown in [Table 1]. There was no significant difference in the smoking habits, years of employment duration of exposure in the two groups studied, and more than 80% of battery works used protective equipments.
[Table 2] shows the history of nonwork-related symptoms during previous 1 year among the study subjects. Except for the higher prevalence of droopiness and muscle pain among nonexposed groups, there was no significant difference in the nonwork- related symptoms of battery workers when compared with controls.The occurrence of work-related symptoms and signs during last 1 year among battery workers and controls are depicted in [Table 3]. Among battery workers, the work-related symptoms in skin, lungs, eyes and nose were reported as 10%, 30%, 26.7%, and 36.7%, respectively. The work-related symptoms in skin and eyes were not significantly different in the two groups studied.Among battery workers, the work-related signs included tremor, hypertension, and impaired short-term memory, which were 10%, 20%, and 6.7%, respectively. However, all signs were not significantly different and no present of decreased proximal extremity force and lead line in the two groups studied.
|Table 2: History of non-work related symptoms during previous one year among the study subjects|
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|Table 3: Work related symptoms/signs in study subjects during the last one year|
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The mean and standard deviation values of biochemical and hematological markers of lead exposure among study groups are depicted in [Table 4]. There was a significant increase in the BLL, and a significant decrease activity of ALAD was observed in battery workers when compared with controls. However, only hematocrit, hemoglobin (Hb), mean corpuscular volume(MCV) of battery worker group, such as, RBC count and MCHC were lower than control, however, there were no statistical significance at p <0.05 and mean corpuscular Hb(MCH) of red blood cells were lower percentages in lead battery workers with statistically significant, when compared with nonlead-exposed workers.Other hematological values of battery worker group were also lower than control, but there were no statistical significance.
|Table 4: Biochemical and hematological markers in the blood of occupational exposed and non-exposed workers|
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[Table 5] shows the results of correlation analysis between the studied parameters and BLL and ALAD activity in battery workers and controls. BLL and ALAD showed a significant inverse correlation (r = −0.575, P< 0.01), while BLL was positively correlated with years of exposure (r = 0.355, P< 0.01) and years of employment (r = 0.321, P< 0.01). The activity of ALAD was found to be inversely correlated years of exposure (r = −0.251, P< 0.05) and years of employment (r = −0.425, P< 0.01) and blood pressure (r = −0.261, P< 0.05), while smoking duration was not significantly correlated either with BLL or the activity of ALAD. BLL was positivelycorrelated with Hb(r = 0.356, P< 0.01), MCV (r = 0.215, P< 0.05) and MCH (r = 0.341, P< 0.01), while the activity ofALAD was inversely correlated with Hb(r= −0.315, P< 0.05), MCV (r = −0.201, P< 0.05) and MCH (r = −0.245, P< 0.05), respectively.
|Table 5: Correlation coefficients (r) for the relationships between BLL and ALAD in study subjects|
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| Discussion|| |
In the present study, the lead battery workers had significantly decreased ALAD activity which was also significantly correlated with BLLs.Previous study reportedthat the activity of ALAD is highly sensitive to BLL and it is comparatively highly specific to BLL than the other biological markers of lead exposure. The results of present study showed no correlation between smoking characteristics and the activity of ALAD, while a strong positive correlation between years of exposure and yearsof employment with the BLL was observed. On the contrary, a negative correlation between these parameters and the activity of ALAD was also observed.
In consistence with other studies, our data showed the effects of lead exposure on the prevalence of respiratorytract symptoms. In agreement with the previous reports, the results of this study showed the prevalence of anemia accompanied by reticulocytosis among lead exposed subjects. In consistence with the results from previous study, present study also showed an inverse correlation between the activity of ALAD and Hband a strong positive correlation between Hband BLLs.
In the present study, age and BLL showed a positive correlation, age andthe activity of ALAD showed an inverse correlation,while body mass index showed no correlation with the markers of lead exposure, which is in consistencewith the previous findings. Present data showed that the activity of ALAD was inversely correlated with systolic blood pressure, while systolic blood pressure was not correlated with BLLs.In contrast, previous study reported a correlation of increased diastolic blood pressure with BLL in lead exposed workers.
BLL was significantly correlated with duration of work and exposure and some of Hbindices, which corresponded to previous study.
In our results, we suggested that combining of laboratory tests, such as lead exposed markers, including BLL and ALAD with routine hematological test or CBC may be useful for increase in sensitivity of screening the risk for lead exposure in industrial workers.
| Conclusion|| |
The comparison of lead and nonlead-exposed workers on demographic characteristics, nonwork and work-related symptoms, and lead-exposed biomarkers hasbeen done on this study.
Demographic data of both groups including age, BMI, duration of work, and duration of smoking were similar and no statistical difference and majority of exposed groups were used protective equipments. Nonrelated symptoms of controls were muscular pain and droopiness, which were more frequent than exposed group.Exposed-related symptoms were respiratory tract symptoms (lung and nose), which were significantly higher occur than other specific symptoms/signs. The lead biochemical markers (including BLL and ALAD) were good markers for screening lead exposures by significantly related to hematological values (Hb, MCV, and MCH), duration of work and exposure and hypertension.
Routine hematological laboratory (CBC) may be helpful for screening subclinical lead exposure, which was significantly different in levels between nonexpose and exposed groups, and this routine laboratory canalso improve sensitivity of BLL and ALAD, when used and interpreted together.
The authors are grateful to Department of Occupational Health, Safety and Environmental, Faculty Of Public Health, Western University, Kanchanaburi for interviewing subjects and collecting blood samples. They also like to thank the Research and Development Institute, Suan Sunandha Rajabhat University for partial funding support and Faculty of Science and Technology, Suan Sunandha Rajabhat University for instruments supports.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Hsu PC, Guo YL. Antioxidant nutrients and lead toxicity. Toxicol 2002;180:33-44.
Massó-González EL, Antonio-García MT. Natural antioxidants protect against lead-induced damage during pregnancy and lactation in rat's pups. Ecotoxicol EnvironSaf 2009;72:2137-42.
Casado MF, Cecchini AL, Simão AN, Oliveira RD, Cecchini R. Free radicalmediated pre-hemolytic injury in human red blood cells subjected to lead acetate as evaluated by chemiluminescence. Food ChemToxicol 2007;45:945-52.
Kasperczyk A, Machnik G, Dobrakowski M, Sypniewski D, Birkner E, Kasperczyk S. Gene expression and activity of antioxidant enzymes in the blood cells of workers who were occupationally exposed to lead. Toxicology 2012;30:79-84.
Kasperczyk S, Dobrakowski M, Kasperczyk J, Ostalowska A, Zalejska-Fiolka J, Birkner E. Beta-carotene reduces oxidative stress, improves glutathione metabolism and modifies antioxidant defense systems in lead-exposed workers. ToxicolApplPharmacol 2014;280:36-41.
Kasperczyk S, Dobrakowski M, Kasperczyk A, Nogaj E, Boron M, Szlacheta Z, Birkner E. et al
. Alpha-tocopherol supplementation and the oxidative stress, homocysteine, and antioxidants in lead exposure. Arch Environ Occup Health 2016 [Epub ahead of print]
Staudinger KC, Roth VS. Occupational Lead Poisoning. Am Fam Physician 1998;57:719-26.
Mahaffey K, McKinney J, Reigart JR. Lead and compounds. In: Lippmann M, editor. Environmental toxicants, human exposures and their health effects 2000; 2nd ed New York (NY) John Wiley and Sons, Inc., p.418-21.
McElvaine MD, Orbach HG, Binder S, Blanksma LA, Maes EF. Krieg RM, Evaluation of the erythrocyte protoporphyrin test as a screen for elevated blood lead levels. J Pediatr 1991;119:548-50.
Hernandez-Avila M, Cortez-Lugo M, Munoz I, Tellez MM, Rojo S. Lead exposure in developing countries. Studies and findings 1999 Available at http://www.leadpoison.net/general
. [Last Accessed 2011 Nov 10].
Kappas A, Sassa S, Galbraith RA, Scriver CR, Beaudet AL, Sly WS. The porphyrias. Tocopherol supplementation and editors. The metabolic and molecular basis of inherited disease 1995;7th edNew York (NY)McGraw-Hill Book Company 2103-59.
Jaffe EK, Bagla S, Michini PA. Reevaluation of a sensitive indicator of early lead exposure: measurement of porphobilinogen synthase in blood. Biol Trace Elem Res 1991;28:223-31.
Kocubovski M. Influence of lead from ambient air and evaluation of health condition in school children, in Macedonian. [Ph.D. Thesis]. Skopje: Medical faculty, University Sts 2004;Cyril and Methodius
Haider MJ, Qureshi N. Studies on battery repair and recycling workers occupationally exposed to lead in Karachi. RoczPanstwZaklHig 2013;64:37-42.
Tasevski S, Velkov S, Kostoski D. Determination of basophil punctuated erythrocytes count as a diagnostic method for occupational saturnism. Laboratory 2002;4:13.
Telisman S, PrpiMaji D, Ke S. In vivo
study on lead and alcohol interaction and the inhibition of erythrocyte delta-aminolevulinic acid dehydratase in man. Scand J Work Environ Health 1984;10:239-44.
Rastogi SK, Gupta BN, Husain T, Mathur N, Srivastava S. Spirometric abnormalities among welders. Environ Res 1991;56:15-24.
Goyer RA, Clarkson TW. Toxic effects of metals.CasarettandDoull's Toxicology. 2001;6th edNew York McGraw-Hill 811-67.
Kelada NS, Shelton E, Kaufmann RB, Khoury JM. ?-Aminolevulinic acid dehydratase genotype and lead toxicity: A huge review. Am J Epidemiol 2001;154:1-13.
Apostoli P, Baj A, Bavazzano P, Ganzi A, Neri G, Ronchi A. Blood lead reference values: the results of an Italian polycentric study. Sci Total Environ 2002;287:1-11.
Pocock SJ, Shaper AG, Ashby DT, Whitehead TP. Blood lead concentration, blood pressure, and renal function. Br Med J 1984;289:872-4.
Kianoush S, Balali-Mood M, Mousavi SR, Shakeri MT, Dadpour B, Moradi V. Clinical, toxicological, biochemical, and hematologic parameters in lead exposed workers of a car battery industry. Iran J Med Sci 2013;38:30-7.
Dr. Yuttana Sudjaroen
Department of Applied Science, Faculty of Science and Technology, Suan Sunandha Rajabhat University, 1 U-Thong Nok Rd., Bangkok
Source of Support: None, Conflict of Interest: None
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]