BACKGROUND: Exposure to compounds used in ceramic industries appears to be associated with induction of oxidative toxic stress. Objective: This cross sectional study was undertaken to assess the oxidative toxic stress parameters associated with occupational exposure to ceramic dust.
METHODS: Forty ceramic-exposed workers from a ceramic manufacturing industry and 40 unexposed referent subjects were studied. A questionnaire containing information regarding demographic variables, occupational history, history of any chronic disease, antioxidant consumption, and use of therapeutic drugs was administrated to them. Oxidative toxic stress biomarkers including lipid peroxidation (LPO), total antioxidant power (TAP), levels of total Thiol groups (TTG) and catalase (CAT) activity were measured.
RESULTS: Significant increments in blood LPO levels, CAT activity and concomitant lower TAP were observed in ceramic exposed workers in comparison to referent group. No statistically significant difference was noted between the means of TTG levels between the groups.
CONCLUSIONS: Findings of the study indicate that occupational exposure to ceramic dust induces oxidative toxic stress. Supplementation of workers with antioxidants may have beneficial effects on oxidative damages in ceramic industries.
HalvaniG, ZareM, HalvaniA, BarkhordariA.
Evaluation and comparison of respiratory symptoms and lung capacities in tile and ceramic factory workers of Yazd. Archives of Industrial Hygiene and Toxicology2008;59(3):197–204.
2.
SteenlandK, WardE.
Silica: A lung carcinogen. CA: A Cancer Journal for Clinicians2014;64(1):63–9.
3.
RapitiE, SperatiA, MiceliM, ForastiereF, Di LalloD, CavarianiF, et al.
End stage renal disease among ceramic workers exposed to silica. Occupational and Environmental Medicine1999;56(8):559–61.
4.
ForastiereF, GoldsmithDF, SperatiA, RapitiE, MiceliM, CavarianiF, et al.
Silicosis and lung function decrements among female ceramic workers in Italy. American Journal of Epidemiology2002;156(9):851–6.
5.
CheckowayH, FranzblauA.
Is silicosis required for silica-associated lung cancer?American Journal of Industrial Medicine2000;37(3):252–9.
6.
RanjbarA, GhasemiH, RostampourF.
The role of oxidative stress in metals toxicity; mitochondrial dysfunction as a key player. Galen Medical Journal2014;3(1):2–13.
FubiniB, HubbardA.
Reactive oxygen species (ROS) and reactive nitrogen species (RNS) generation by silica in inflammation and fibrosis. Free Radical Biology and Medicine2003;34(12):1507–16.
9.
SoleimaniE, MoghadamRH, RanjbarA.
Occupational exposure to chemicals and oxidative toxic stress. Toxicology and Environmental Health Sciences7(1):1–24.
10.
OhkawaH, OhishiN, YagiK.
Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Analytical Biochemistry1979;95(2):351–8.
11.
BenzieIF, StrainJ.
The ferric reducing ability of plasma (FRAP) as a measure of “antioxidant power”: The FRAP assay. Analytical Biochemistry1996;239(1):70–6.
12.
HuM-L.
Measurement of protein thiol groups and glutathione in plasma. Methods in Enzymology1994;233:380–5.
13.
ShangariN, O’BrienPJ.
Catalase activity assays. Current Protocols in Toxicology2006;7(1-7):16–.
14.
ValkoM, MorrisH, CroninM.
Metals, toxicity and oxidative stress. Current Medicinal Chemistry2005;12(10):1161–208.
15.
GreenbergMI, WaksmanJ, CurtisJ.
Silicosis: A review. Disease-a-Month2007;53(8):394–416.
16.
ZhangZ, ShenH-M, ZhangQ-F, OngC-N.
Critical role of GSH in silica-induced oxidative stress, cytotoxicity, and genotoxicity in alveolar macrophages. American Journal of Physiology-Lung Cellular and Molecular Physiology1999;277(4):L743–8.
17.
HalliwellB.
Free radicals, antioxidants, and human disease: Curiosity, cause, or consequence?Lancet1994;344(8924):721–4.
18.
HalliwellB.
Biochemistry of oxidative stress. Biochemical Society Transactions2007;35(5):1147–50.
19.
ErcalN, Gurer-OrhanH, Aykin-BurnsN.
Toxic metals and oxidative stress part I: Mechanisms involved in metal-induced oxidative damage. Current Topics in Medicinal Chemistry2001;1(6):529–39.
20.
KhanMHA, ParvezS.
Hesperidin ameliorates heavy metal induced toxicity mediated by oxidative stress in brain of wistar rats. Journal of Trace Elements in Medicine and Biology2015.
21.
BarnhamKJ, MastersCL, BushAI.
Neurodegenerative diseases and oxidative stress. Nature Reviews Drug Discovery2004;3(3):205–14.
22.
GhahramaniN.
Silica nephropathy. The International Journal of Occupational and Environmental Medicine2010;1(3 July).
23.
HamiltonRF, ThakurSA, HolianA.
Silica binding and toxicity in alveolar macrophages. Free Radical Biology and Medicine2008;44(7):1246–58.
24.
CastranovaV.
Signaling pathways controlling the production of inflammatory mediators in response to crystalline silica exposure: Role of reactive oxygen/nitrogen species. Free Radical Biology and Medicine2004;37(7):916–25.
25.
IyerR, HamiltonRF, LiL, HolianA.
Silica-induced apoptosis mediated via scavenger receptor in human alveolar macrophages. Toxicology and Applied Pharmacology1996;141(1):84–92.
26.
LiuH, ZhangH, FormanHJ.
Silica induces macrophage cytokines through phosphatidylcholine-specific phospholipase C with hydrogen peroxide. American Journal of Respiratory Cell and Molecular Biology2007;36(5):594–9.
27.
ZhangZ, ShenH-M, ZhangQ-F, OngC-N.
Involvement of oxidative stress in crystalline silica-induced cytotoxicity and genotoxicity in rat alveolar macrophages. Environmental Research2000;82(3):245–52.
28.
RojanasakulY, YeJ, ChenF, WangL, ChengN, CastranovaV, et al.
Dependence of NF-κB activation and free radical generation on silica-induced TNF-α production in macrophages. Molecular and Cellular Biochemistry1999;200(1-2):119–25.
