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Rare occupational cause of nasal septum perforation: Nickel exposure

100%

Bolek E. C., Erden A., Kulekci C., Kalyoncu U., Karadag O.

International Journal of Occupational Medicine and Environmental Health

2017

vol. 30

issue 6

963-967

Many etiologies are held accountable for nasal septum perforations. Topical nasal drug usage, previous surgeries, trauma, nose picking, squamous cell carcinoma, some rheumatological disorders such as granulomatosis with polyangiitis (Wegener granulomatosis), some infectious diseases such as syphilis and leprosy are among the causes of the perforations. Occupational heavy metal exposures by inhalation rarely may also cause nasal septum perforation. Here, we present a 29-year-old patient without any known diseases, who is a worker at a metallic coating and nickel-plating factory, referred for investigation of his nasal cartilage septum perforation from an otorhinolaryngology clinic. The patient questioning, physical examination and laboratory assessment about rheumatic and infectious diseases were negative. There was a metallic smell in the breath during the physical examination. The analysis showed serum nickel level at 31 μg/l and urine nickel at 18 μg/l (84.11 μg/g creatinine). Other possible serum and urine heavy metal levels were within normal ranges. Nickel exposure is usually together with other heavy metals (chromium or cadmium), it is rarely alone. Nickel ingested by inhalation usually leads to respiratory problems such as reduced olfactory acuity, ulcers, septum perforation or tumors of the nasal sinuses. This case demonstrates the importance of occupational anamnesis and awareness of diagnosis. Int J Occup Med Environ Health 2017;30(6):963–967

Induction of hemolysis and eryptosis by occupational pollutant nickel chloride is mediated through calcium influx and p38 MAP kinase signaling

100%

Alfhili M. A., Alamri H. S., Alsughayyir J., Basudan A. M.

International Journal of Occupational Medicine and Environmental Health

2021

vol. 35

issue 1

1-11

ObjectivesNickel (Ni) is an abundant environmental hazard and an occupational pollutant. Exposure to Ni compounds is prevalent in electroplating workers and in the printing industry, among others. The toxicity of Ni manifests as dermatological, gastrointestinal, respiratory, allergic, and cardiovascular symptoms. In particular, hyperbilirubinemia and reticulocytosis have been detected in intoxicated subjects; an observation possibly implicating selective red blood cell (RBC) toxicity. Herein, the interaction of nickel chloride (NiCl2) with human RBCs and associated molecular mechanisms are described.Material and MethodsCells from healthy donors were incubated for 24 h at 37°C in the presence or absence of 0.5‒10 mM of NiCl2, and cytotoxicity was determined through hemoglobin leakage by colorimetry under different experimental conditions. Eryptotic markers were also identified by flow cytofluorometry using Annexin-V-FITC tagging for phosphatidylserine (PS) exposure, light scatter properties for cellular dimensions, Fluo4/AM labeling for intracellular calcium, and H2DCFDA staining for reactive oxygen species (ROS). Additionally, small molecule inhibitors were used to probe the signaling pathways involved.ResultsIt was found that NiCl2 at 10 mM caused profound intracellular calcium overload and significant calcium-dependent hemolysis. Also, NiCl2 reduced forward scatter and increased side scatter, Annexin-positive cells, and ROS levels. Importantly, NiCl2-induced hemolysis was significantly attenuated by the exclusion of extracellular calcium, and in the presence of p38 MAP kinase (MAPK) inhibitor SB203580.ConclusionsIt is concluded that NiCl2 induces p38 MAPK-dependent hemolysis, and stimulates the canonical features of premature eryptosis. This report presents the first description of the molecular mechanisms underlying the hemolytic and eryptotic potential of NiCl2 and, thus, may explain changes in hematological parameters observed in poisoning victims.

Evaluation of heavy metal levels in serum of Wistar rats exposed to engine oil

84%

Iyanda, A.A, Anetor, J.I, Anetor, G.O

Progress in Health Sciences

2018

vol. 8(2)

94-98

Purpose: Data are available that indicate there is an elaborate elemental constitution of petroleum products, with identified elements contained in the many products being additive (e.g. Ca, Zn and P) as well as wear metals (e.g. Ag, Al, Ba, Cd, Cr, Cu, Fe, Mg, Mo, Na, Ni, Pb and Sn). In addition, incessant deliberate exposure of engine oil to both human beings and farm animals for therapeutic reason has been reported. Therefore the objective of this study is to evaluate the levels of heavy metals in serum of engine oil-exposed rats. Materials & Methods: Thirty adult female rats were divided equally into 5 groups. The first and second groups were treated with engine oil by oral route (as contaminant of feed) at dosage levels of 0.5 and 1.0 mL/kg body weight respectively. The third and forth groups received the test agent through the dermal route at dosage levels of 0.5 and 1.0 mL/kg body weight while the fifth group served as the control. The duration of the study was 30 days, after which blood was obtained from each rat, centrifuged and the resultant serum used for the analysis of heavy metals by employing Atomic Absorption Spectrometry (AAS). Data were analyzed using analysis of variance (ANOVA), p≤0.05 was considered significant. Results: Data obtained showed that there were significant differences in the levels of aluminium, silicon, cadmium, lead, arsenic, vanadium, and nickel. Conclusions: These increases suggest that incessant exposure to engine oil may be dangerous and therefore constitute health hazard.

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2 International Journal of Occupational Medicine and Environmental Health

1 Progress in Health Sciences

1 Alamri H. S.

1 Alfhili M. A.

1 Alsughayyir J.

1 Anetor, G.O

1 Anetor, J.I

1 Basudan A. M.

1 Bolek E. C.

1 Erden A.

1 Iyanda, A.A

1 Kalyoncu U.

1 Karadag O.

1 Kulekci C.

1 2022

1 2019

1 2017

Search results

Rare occupational cause of nasal septum perforation: Nickel exposure

Induction of hemolysis and eryptosis by occupational pollutant nickel chloride is mediated through calcium influx and p38 MAP kinase signaling

Evaluation of heavy metal levels in serum of Wistar rats exposed to engine oil