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Year : 2020  |  Volume : 11  |  Issue : 4  |  Page : 169-173

Hematological, antioxidant, and trace elements status in healthy mechanical welders: A pilot study

1 Department of Community Medicine, Father Muller Medical College, Mangalore, Karnataka, India
2 Father Muller Research Centre, Mangalore, Karnataka, India
3 Department of Biochemistry, Father Muller Medical College, Mangalore, Karnataka, India

Date of Submission06-Apr-2020
Date of Decision15-Apr-2020
Date of Acceptance08-May-2020
Date of Web Publication17-Nov-2020

Correspondence Address:
Dr. Manjeshwar Shrinath Baliga
Mangalore Institute of Oncology, Pumpwell, Mangalore, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/joah.joah_37_20

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BACKGROUND: Welding work is considered to be an occupational hazard and welders are exposed to a range of metal fumes that are toxic to the blood system. Regular inhalation of the welding toxic fumes alters the hematological, antioxidant, and trace element levels and therefore an attempt is made at understanding these changes in the welders.
AIM OF THE WORK: In this case–control study, an attempt is made at understanding the general health, hematological, antioxidant, and trace elements status of welders by comparing with age-matched office workers from the same area.
MATERIALS AND METHODS: This was a purposive, case–control prospective study and was carried out in healthy volunteers devoid of any chronic or acute systemic ailments in Mangalore, India. The sociodemographic details were collected in a structured questionnaire, while a detailed clinical examination was carried out by the senior clinicians. The blood collected as per the standard laboratory procedure was analyzed for hematological parameters, antioxidant, and trace elements status. The data were subjected to frequency, percentage, and analyzed using the unpaired ttest. P < 0.05 was considered statistically significant.
RESULTS: The results suggest that when compared to the controls, the welders showed significantly lower neutrophil count (53.45 ± 6.11 vs. 46.68 ± 6.12; P = 0.0003) and platelet count (267409.1 ± 42329.4 vs. 199142.9 ± 73735.1; P = 0.0002), and significantly higher counts of eosinophils (5.86 ± 4.12 vs. 9.86 ± 2.76; P = 0.0004) and monocytes (2.45 ± 1.63 vs. 4.89 ± 1.17; P < 0.0001). The levels of lipid peroxidation were high (225.73 ± 56.88 vs. 255.82 ± 30.26; P = 0.04), whereas total antioxidant capacity was less (3.00 ± 0.91 vs. 2.16 ± 1.04; P = 0.004) in the welders. When compared to controls, the serum iron (84.09 ± 6.18 vs. 94.46 ± 8.44; P ≤ 0.0001), copper (104.68 ± 40.63 vs. 148.93 ± 34.18; P = 0.0002), and lead (8.53 ± 5.49 vs. 14.18 ± 8.05; P = 0.005) were all significantly high in welders. There was no significant difference in the serum zinc and glutathione levels between the controls and welders.
CONCLUSIONS: The results of the study indicate that occupational exposure to welding fumes among welders disturbs the homeostasis of trace elements in systemic circulation and induces oxidative stress.

Keywords: Copper, hematological status, iron, lead, total antioxidant, welders, zinc

How to cite this article:
Prabhu HS, Kalekhan F, Simon P, D'silva P, Shivashankara AR, Baliga MS. Hematological, antioxidant, and trace elements status in healthy mechanical welders: A pilot study. J Appl Hematol 2020;11:169-73

How to cite this URL:
Prabhu HS, Kalekhan F, Simon P, D'silva P, Shivashankara AR, Baliga MS. Hematological, antioxidant, and trace elements status in healthy mechanical welders: A pilot study. J Appl Hematol [serial online] 2020 [cited 2021 Apr 11];11:169-73. Available from: https://www.jahjournal.org/text.asp?2020/11/4/169/300765

  Introduction Top

From an occupational perceptiveness, welders who do the job of joining metals are exposed to fumes consisting of acetylene, carbon monoxide, oxides of nitrogen, ozone, phosgene, tungsten, arsenic, beryllium, cadmium, chromium, cobalt, copper, iron, lead, manganese, nickel, silver, and tin.[1],[2] Excessive exposure to welding fumes is reported to reduce the lung function capacity, increase incidence of respiratory ailments, (especially bronchitis) and lung infections.[3],[4] Epidemiological studies indicate that the welding fumes may actually be a direct cause of asthma.[5] Welding fumes can trigger and increase the chances of development of lung cancers, and reports from the International Agency for Research on Cancer suggest that the overall mortality in welders was found to be more than age-matched controls.[6]

Welding is a common indispensable procedure in engineering works and is associated with varied health hazards apart from the injuries. Welders are part of informal occupational sector in India. Hence, they do not have any organized occupational health services. Further, very limited attempts have been made to study occupational exposure and health profile of this population in India. Therefore, the present study was conducted to assess the duration of occupational-related exposure to various hazards and health of the workers. The objective of this study is to assess the effects of the toxins welders are exposed to on the general health and changes in the hematological parameters as a result of occupational exposure to hazardous material.

  Materials and Methods Top

This was a purposive, case–control prospective study and was done with welders working in Mangalore, Karnataka, India. The study was approved by the Institutional Ethics Committee and was done in as suggested in the Helsinki declarations and Indian Council of Medical Research Guidelines for research involving humans.[7] The inclusion criteria for the study included healthy men who worked fulltime as welders, were above the age of 18, did not have any comorbidities, were nonsmokers, nonalcoholics, and were residents of Mangalore for more than 10 years. The exclusion criteria included people from other professions, suffering from a mental health disorder, tuberculosis, diabetes, hypertension, cancer, HIV, who have had acute illness (such as malaria, dengue, leptospirosis, and scrub typhus), substance abusers, were on any medication, and from other parts of the country. For controls, the inclusion and exclusion criteria were the same other than the fact that they were office workers from adjoining area to avoid area bias in the study. In addition, the whole study was done in a span of 10 days to avoid possible seasonal variation.

Sample size selection

The sample size was selected using the following formula:

Where P1 = 0.2; P2 = 0.5; α = 0.05; β = 0.2 and ratio of Group 1 by Group 2 is 1, to give a sample size of 39 in each group. Considering possible attrition, we rounded up the number to 46 in each cohort.


A camp-based approach was done and garage workers included were from various places in Mangalore. During the health-care program, the volunteers were informed about the research objective and that it was not mandatory to participate in the study. Written informed consent was taken from all the willing volunteers. A self-structured questionnaire, validated by a group of community medicine physicians experienced in occupational health and medicine was filled along with the clinical examination of each of the garage and office workers in the study group. The questionnaire was filled by personally interviewing each garage worker by the student investigators. Clinical examination included history taking and general physical and systemic examination was carried by senior clinicians.

Blood analysis

From all willing volunteers, 5 ml of the blood was collected from each volunteer by trained phlebotomists in premarked in Ethylene diamine tetraacetic acid (EDTA) vacutainer. The blood collected was transported to the research laboratory and analyzed for hematological parameters such as red blood cells (RBCs), hemoglobin (Hb), white blood cells, neutrophils, lymphocytes, eosinophil, monocytes, using Beckhman Coulter LH 750. A senior pathologist unaware of the origin of the blood sample scored for hematological changes.

Levels of trace elements copper, iron, zinc, and lead in serum were estimated by spectrophotometric methods. The estimation of copper was based on the reaction of copper with dithiocarbamate;[8] iron assay was based on the formation of a colored product on the reaction of iron with ferrozine reagent;[8] zinc level was assayed based on the formation of colored product with 7-(4-Nitrophenylazo)-8-Hydroxyquinoline-5-Sulfonic Acid.[8] Level of lead was assayed using lead care II kit, and the lead quantification was done using an Anodic Stripping Voltameter (ASV, ESA, Inc., Chelmsford, MA, USA) as described earlier.[9]

Malondialdehyde (MDA) is the product of lipid peroxidation and is the sensitive and convenient marker of lipid peroxidation. Level of MDA in serum was estimated by the method of Ohkawa et al., which was based on the formation of thiobarbituric acid-reactive substances on reaction of MDA with thiobarbituric acid.[10] The MDA level was expressed in nmoles/L from the standard graph plotted with different concentrations of MDA standard (1, 1, 3, 3-tetramethoxypropane procured from Sigma-Aldrich). Assay of iron was done using ferrozine reagent.[8] The level of glutathione (GSH) was estimated by the method described by Beutler et al. 1963;[11] GSH reduces 5, 5/dithio, bis-nitrobenzoic acid to yellow color 5-thionitrobenzoic acid. Absorbance measured at 412 nm is directly proportional to the concentration of GSH. GSH standards ranging in concentration from 25 to 100 mg/dl were run simultaneously, and the GSH level was calculated from the standard curve and expressed as μmoles/L. The total antioxidant capacity (TAC) was estimated by using the method of Koracevic et al., which is based on the suppression of the formation of thiobarbituric acid-reactive substances by the antioxidants in blood or saliva.[12]

Statistical analysis

The accrued data were entered into Microsoft excel and categorized as demographic details, clinical and investigative data. The data were then transferred to SPSS (IBM version 22; Chicago, IL, USA) and calculated. The demographic and clinical details were subjected to frequency and percentage, χ2 analysis, whereas the hematological values were subjected to paired t-test. A statistical value of P < 0.05 was considered to be significant.

  Results Top

The hematological details of the welders (Group-2) did not show any significant difference with controls with regard to Hb, total count, lymphocyte count, RBC count packed cell volume, mean corpuscular volume, mean corpuscular Hb (MCH), MCH concentration, GSH level, and zinc level [Table 1]. There was a statistically significant difference between the two study groups with regard to counts of neutrophils, basophils, eosinophils, platelets, monocyte lymphocyte ratio, neutrophil lymphocyte ratio, and platelet lymphocyte ratio. There was also a significant difference with respect to MDA, TAC, and serum levels of iron, copper, and lead. The welders showed significantly lower neutrophil count and platelet count, and significantly higher counts of eosinophils and monocytes. The monocyte lymphocyte ratio was significantly higher, and platelets lymphocyte ratio and neutrophil ratio were significantly higher in welders, in comparison to the controls [Table 1]. Assessment oxidative stress revealed significantly higher lipid peroxidation evident by MDA level, and lower TAC in welders. The metals iron, copper, and lead were all significantly higher in welders when compared to the controls [Table 1]. There was no significant difference in the serum zinc levels between controls and welders [Table 1].
Table 1: Changes in the hematological, antioxidant (glutathione and total antioxidant capacity), malondialdehyde and heavy metal levels (iron, copper, zinc and lead) between control (office workers) and welders

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  Discussion Top

The results from our study showed significantly higher serum concentrations of lead in welders than in controls. The elevated serum concentrations of lead may be a direct result of the overexposure to this metal in the fume. Lead poisoning causes a variety of symptoms, including abnormal behavior which varies from person to person, while the time of exposure plays an important role.[13] Blood lead levels from 25 to 60 μg/dL give rise to neuropsychiatric effects such as delayed reaction times, irritability, and difficulty in concentrating, as well as slowed down motor nerve conduction and headache.[14] Anemia may appear at blood lead levels higher than 50 μg/dL.[15

In adults, abdominal colic, involving paroxysms of pain, may appear at blood lead levels higher than 80 μg/dL.[13] High blood lead levels which exceed 100 μg/dL cause very severe manifestations, such as signs of encephalopathy (a condition characterized by brain swelling) accompanied by increased pressure within the skull, delirium, coma, seizures, and headache.[15] However, such manifestations appear in children at lead levels of 70 μg/dL and more. Central nervous system and neuromuscular manifestations usually result from intense exposure, whereas gastrointestinal features usually result from the exposure over longer periods.[16] Signs and symptoms of chronic exposure include loss of short-term memory or concentration, depression, nausea, abdominal pain, loss of coordination, and numbness and tingling in the extremities.[17] Fatigue, problems with sleep, headaches, stupor, slurred speech, and anemia are also found in chronic lead poisoning.[18]

In our study, the average lead level among the welders was 14.18 ± 8.05 which requires discussion of the health risks of chronic lead exposure with those welders and possibly implementing practices that generate less lead dust, using engineering controls or personal protection (appropriate respirators and work clothes), and appropriate hand decontamination (washing with soap and water is not as effective in removing lead compared with using wipes containing iso stearamido propyl morpholine lactate and citric acid).[19]

We observed significantly elevated serum levels of iron among welders. Both these elements are considered to be prooxidants, and excess of these metals is known to cause damaging effects of vital tissues of the body. Iron is the major metal found in welding fumes, and although it is an essential trace element, its overload causes toxicity due to Fenton reactions. Previously, Casjens et al. assessed the iron status and quantitative associations between airborne iron, body iron stores, and iron homeostasis in 192 welders not wearing dust masks.[20]

Welders showed significantly higher levels of serum copper but nonsignificant change in serum zinc in comparison to controls. Wang et al. observed significantly higher levels of copper and lower levels of zinc in the saliva of welders when compared to controls, and a significant correlation between serum and saliva with respect to zinc levels in welders.[21] In a study on automobile workers, Luo et al. reported significant positive correlation of urinary zinc and copper with blood GSH, and significant positive correlation of urinary zinc with blood interleukin-6. However, there was no association between the urinary levels of metals and welding hours.[22]

In the present study, we observed significantly higher serum MDA and lower TAC in welders when compared to controls.Increased MDA level indicates increased lipid peroxidation and decreased TAC suggests depleted or impaired antioxidant defense, tilting the balance in favor of oxidants. There was no significant difference in erythrocyte GSH level among the controls and welders'. Oxidative stress is implicated in the pathogenesis of clinical problems of welding. The metals commonly present in the welding fumes include lead, cadmium, nickel, copper, chromium, iron, and manganese. These metals are capable of generating reactive oxygen species which further mediate the disease development. Workers occupationally exposed to welding fumes in an iron and steel factory showed significantly high blood levels of lead, cadmium, chromium, and iron and significantly low activity of the antioxidant enzyme superoxide dismutase (SOD) in blood.[23]

The present study observed no change in serum GSH in welding workers. Previous studies observed lower levels of serum total protein sulfhydryls and erythrocyte GSH in welding workers, in comparison to controls.[24] In nonsmoking welding apprentices exposed to tungsten inert gas welding fumes for 60 min under controlled, well-ventilated settings, significant changes in oxidant-status was evident 3 h postexposure. There was a significant increase in plasma and urinary hydrogen peroxide and 8-hydroxyguanosine.[25] In chromium exposed to welding workers, lymphocyte GSH level was significantly low and urine MDA was significantly high.[26] In welders working in a vehicle manufacturing unit, the serum levels of iron, lead, and MDA were significantly higher and erythrocyte SOD activity and serum zinc level were significantly lower in comparison to controls.[27] These findings suggest that occupational exposure to welding fumes among welders disturbs the homeostasis of trace elements in systemic circulation and induces oxidative stress.

  Conclusions Top

The case–control study indicated that the welders had significantly lower neutrophil and platelet and a concomitant higher eosinophil and monocyte counts. The levels of lipid peroxidation were high, iron, lead, and copper were high, whereas TAC was less. Together all these results indicate that occupational exposure to welding fumes disturbs the homeostasis of trace elements in systemic circulation and induces oxidative stress in welders. During the study, on enquiry, it was noted that some of the volunteers had expressed that they had experienced certain dermatological changes which might have been skin rashes, atopic dermatitis, contact dermatitis, or urticaria and respiratory features which possibly could be bronchitis or pneumonitis. In addition to this, chronic exposure to lead and metal is also known to cause neuropathies and cognitive impairments. Studies are being planned to understand the prevalence of these manifestation as the outcomes of these studies will be very useful for both society and medical fraternity.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Ataro Z, Geremew A, Urgessa F. Occupational health risk of working in garages: Comparative study on blood pressure and hematological parameters between garage workers and Haramaya University community, Harar, Eastern Ethiopia. Risk Manag Healthc Policy 2018;11:35-44.  Back to cited text no. 1
Meo SA, Al-Drees AM, Rasheed S, Meo IM, Khan MM, Al-Saadi MM, et al. Effect of duration of exposure to polluted air environment on lung function in subjects exposed to crude oil spill into sea water. Int J Occup Med Environ Health 2009;22:35-41.  Back to cited text no. 2
Wilson MP, Hammond KS, Nicas M, Hubbard AE. Worker exposure to volatile organic compounds in the vehicle repair industry. J Occup Environ Hyg 2007;4:5301-10.  Back to cited text no. 3
Dennison JE, Bigelow PL, Mumtaz Moiz M, Andersen Melvin E, Dobrev ID, Yang RS. Evaluation of potential toxicity from co-exposure to three CNS depressants (Toluene, Ethylbenzene, and Xylene) Under Resting and Working Conditions Using PBPK Modeling. J Occup Environ Hyg 2005;3:127-35.  Back to cited text no. 4
Moitra S, Ghosh J, Firdous J, Bandyopadhyay A, Mondal M, Biswas JK, et al. Exposure to heavy metals alters the surface topology of alveolar macrophages and induces respiratory dysfunction among Indian metal arc-welders. ToxicolInd Health 2018. pii: 748233718804426.  Back to cited text no. 5
International Hazard Datasheets on Occupation. Mechanic, Automobile, ILO/CIS; 1999.  Back to cited text no. 6
ICMR. Ethical Guidelines for Biomedical Research on Human Participants; 2006. Available from: http://icmr.nic.in/ethical_guidelines.pdf. [Last accessed on 2019 Feb 20].  Back to cited text no. 7
Burtis CA, Ashwood ER, Bruns DE, editors. Tietz Text book of Clinical Chemistry and Moelcular Diagnostics. 4th ed. Missouri: Elsevier Saunders; 2006.  Back to cited text no. 8
Pai V, Prabhu HS, Khalekhan F, Mathai RT, Shivashankara AR, Jakribettu RP, et al. Audit of toxic effects of body paint in the tiger dancers (Hulivesha) of Mangalore, India: An investigational study. Cutan Ocul Toxicol 2019;38:118-24.  Back to cited text no. 9
Ohkawa H, Ohishi N, Yagi K. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal Biochem 1979;95:351-8.  Back to cited text no. 10
Beutler E, Duron O, Kelly BM. Improved method for the determination of blood glutathione. J Lab Clin Med 1963;61:882-8.  Back to cited text no. 11
Koracevic D, Koracevic G, Djordjevic V, Andrejevic S, Cosic V. Method for the measurement of antioxidant activity in human fluids. J Clin Pathol 2001;54:356-61.  Back to cited text no. 12
Coyle P, Kosnett MJ, Hipkins K. Severe lead poisoning in the plastics industry: A report of three cases. Am J Ind Med 2005;47:172-5.  Back to cited text no. 13
Merill JC, Morton JJ, Soileau SD. Metals. In: Hayes AW, editor. Principal and Methods of Toxicology. 5th ed. New York, USA: CRC Press; 2007.  Back to cited text no. 14
Henretig FM. Lead. In: Goldfrank LR, editor. Goldfrank's Toxicologic Emergencies. 8th ed. New York, NY, USA: McGraw-Hill Professional; 2006.  Back to cited text no. 15
Brunton LL, Goodman LS, Blumenthal D, Buxton I, Parker KL, editors. Principles of Toxicology Goodman and Gilman's Manual of Pharmacology and Therapeutics. New York, NY, USA: McGraw-Hill Professional; 2007.  Back to cited text no. 16
Patrick L. Lead toxicity, a review of the literature. Part 1: Exposure, evaluation, and treatment. Altern Med Rev 2006;11:2.  Back to cited text no. 17
Pearce JM. Burton's line in lead poisoning. Eur Neurol 2007;57:118-9.  Back to cited text no. 18
National Research Council. Potential Health Risks to DOD Firing-Range Personnel from Recurrent Lead Exposure. Washington, DC: The National Academies Press; 2013.  Back to cited text no. 19
Casjens S, Henry J, Rihs HP, Lehnert M, Raulf-Heimsoth M, Welge P, et al. Influence of welding fume on systemic iron status. Ann Occup Hyg 2014;58:1143-54.  Back to cited text no. 20
Wang D, Du X, Zheng W. Alteration of saliva and serum concentrations of manganese, copper, zinc, cadmium and lead among career welders. Toxicol Lett 2008;176:40-7.  Back to cited text no. 21
Luo JC, Hsu KH, Shen WS. Inflammatory responses and oxidative stress from metal fume exposure in automobile welders. J Occup Environ Med 2009;51:95-103.  Back to cited text no. 22
Ananian FB, Helal SF, Rashed LA, Shehata RA. Oxidative stress status due to metal exposure in welding. Egypt J Occup Med 2013;37:19-31.  Back to cited text no. 23
Fidan F, Unlü M, Köken T, Tetik L, Akgün S, Demirel R, et al. Oxidant-antioxidant status and pulmonary function in welding workers. J Occup Health 2005;47:286-92.  Back to cited text no. 24
Graczyk H, Lewinski N, Zhao J, Sauvain JJ, Suarez G, Wild P, et al. Increase in oxidative stress levels following welding fume inhalation: A controlled human exposure study. Part Fibre Toxicol 2016;13:31.  Back to cited text no. 25
Goulart M, Batoréu MC, Rodrigues AS, Laires A, Rueff J. Lipoperoxidation products and thiol antioxidants in chromium exposed workers. Mutagenesis 2005;20:311-5.  Back to cited text no. 26
Li GJ, Zhang LL, Lu L, Wu P, Zheng W. Occupational exposure to welding fume among welders: Alterations of manganese, iron, zinc, copper, and lead in body fluids and the oxidative stress status. J Occup Environ Med 2004;46:241-8.  Back to cited text no. 27


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