Cadmium and Lead Exposure, Nephrotoxicity, and Mortality

Soisungwan Satarug, Glenda C Gobe, David A Vesey, Kenneth R Phelps, Soisungwan Satarug, Glenda C Gobe, David A Vesey, Kenneth R Phelps

Abstract

The present review aims to provide an update on health risks associated with the low-to-moderate levels of environmental cadmium (Cd) and lead (Pb) to which most populations are exposed. Epidemiological studies examining the adverse effects of coexposure to Cd and Pb have shown that Pb may enhance the nephrotoxicity of Cd and vice versa. Herein, the existing tolerable intake levels of Cd and Pb are discussed together with the conventional urinary Cd threshold limit of 5.24 μg/g creatinine. Dietary sources of Cd and Pb and the intake levels reported for average consumers in the U.S., Spain, Korea, Germany and China are summarized. The utility of urine, whole blood, plasma/serum, and erythrocytes to quantify exposure levels of Cd and Pb are discussed. Epidemiological studies that linked one of these measurements to risks of chronic kidney disease (CKD) and mortality from common ailments are reviewed. A Cd intake level of 23.2 μg/day, which is less than half the safe intake stated by the guidelines, may increase the risk of CKD by 73%, and urinary Cd levels one-tenth of the threshold limit, defined by excessive ß2-microglobulin excretion, were associated with increased risk of CKD, mortality from heart disease, cancer of any site and Alzheimer's disease. These findings indicate that the current tolerable intake of Cd and the conventional urinary Cd threshold limit do not provide adequate health protection. Any excessive Cd excretion is probably indicative of tubular injury. In light of the evolving realization of the interaction between Cd and Pb, actions to minimize environmental exposure to these toxic metals are imperative.

Keywords: cadmium; chronic kidney disease; lead; mortality; nephrotoxicity; threshold limit; tolerable intake level.

Conflict of interest statement

The authors have no potential conflict of interest to declare.

Figures

Figure 2
Figure 2
Cadmium and lead accumulation levels in kidneys and their levels in urine.
Figure 1
Figure 1
Entry routes, distribution, storage and urinary excretion of cadmium and lead.

References

    1. Satarug S., Vesey D.A., Gobe G.C. Health risk assessment of dietary cadmium intake: Do current guidelines indicate how much is safe? Environ. Health Perspect. 2017;125:284–288. doi: 10.1289/EHP108.
    1. Satarug S., Vesey D.A., Gobe G.C. Current health risk assessment practice for dietary cadmium: Data from different countries. Food Chem. Toxicol. 2017;106:430–445. doi: 10.1016/j.fct.2017.06.013.
    1. Shefa S.T., Héroux P. Both physiology and epidemiology support zero tolerable blood lead levels. Toxicol. Lett. 2017;280:232–237. doi: 10.1016/j.toxlet.2017.08.015.
    1. Daley G.M., Pretorius C.J., Ungerer J.P. Lead toxicity: An Australian perspective. Clin. Biochem. Rev. 2018;39:61–98.
    1. World Health Organization (WHO) Preventing Disease through Healthy Environments: Ten Chemicals of Major Public Health Concern; Public Environment WHO: Geneva, Switzerland. [(accessed on 12 August 2020)]; Available online: .
    1. Satarug S., Haswell-Elkins M.R., Moore M.R. Safe levels of cadmium intake to prevent renal toxicity in human subjects. Br. J. Nutr. 2000;84:791–802. doi: 10.1017/S0007114500002403.
    1. Satarug S., Baker J.R., Urbenjapol S., Haswell-Elkins M., Reilly P.E., Williams D.J., Moore M.R. A global perspective on cadmium pollution and toxicity in non-occupationally exposed population. Toxicol. Lett. 2003;137:65–83. doi: 10.1016/S0378-4274(02)00381-8.
    1. Satarug S. Dietary cadmium intake and its effects on kidneys. Toxics. 2018;6:15. doi: 10.3390/toxics6010015.
    1. Satarug S. Long-term exposure to cadmium in food and cigarette smoke, liver effects and hepatocellular carcinoma. Curr. Drug Metab. 2012;13:257–271. doi: 10.2174/138920012799320446.
    1. Satarug S., Moore M.R. Emerging roles of cadmium and heme oxygenase in type-2 diabetes and cancer susceptibility. Tohoku J. Exp. Med. 2012;228:267–288. doi: 10.1620/tjem.228.267.
    1. Gibb H.J., Barchowsky A., Bellinger D., Bolger P.M., Carrington C., Havelaar A.H., Oberoi S., Zang Y., O’Leary K., Devleesschauwer B. Estimates of the 2015 global and regional disease burden from four foodborne metals-arsenic, cadmium, lead and methylmercury. Environ. Res. 2019;174:188–194. doi: 10.1016/j.envres.2018.12.062.
    1. Satarug S., Gobe G.C., Ujjin P., Vesey D.A. A comparison of the nephrotoxicity of low doses of cadmium and lead. Toxics. 2020;8:18. doi: 10.3390/toxics8010018.
    1. Wang X., Ding N., Tucker K.L., Weisskopf M.G., Sparrow D., Hu H., Park S.K. A Western diet pattern is associated with higher concentrations of blood and bone lead among middle-aged and elderly men. J. Nutr. 2017;147:1374–1383. doi: 10.3945/jn.117.249060.
    1. Ding N., Wang X., Tucker K.L., Weisskopf M.G., Sparrow D., Hu H., Park S.K. Dietary patterns, bone lead and incident coronary heart disease among middle-aged to elderly men. Environ. Res. 2019;168:222–229. doi: 10.1016/j.envres.2018.09.035.
    1. Shi Z., Taylor A.W., Riley. M., Byles. J., Liu J., Noakes M. Association between dietary patterns, cadmium intake and chronic kidney disease among adults. Clin. Nutr. 2018;37:276–284. doi: 10.1016/j.clnu.2016.12.025.
    1. Shi Z., Zhen S., Orsini N., Zhou Y., Zhou Y., Liu J., Taylor A.W. Association between dietary lead intake and 10-year mortality among Chinese adults. Environ. Sci. Pollut. Res. 2017;24:12273–12280. doi: 10.1007/s11356-017-8871-2.
    1. Gobe G., Crane D. Mitochondria, reactive oxygen species and cadmium toxicity in the kidney. Toxicol. Lett. 2010;198:49–55. doi: 10.1016/j.toxlet.2010.04.013.
    1. Nair A.R., Lee W.K., Smeets K., Swennen Q., Sanchez A., Thévenod F., Cuypers A. Glutathione and mitochondria determine acute defense responses and adaptive processes in cadmium-induced oxidative stress and toxicity of the kidney. Arch. Toxicol. 2015;89:2273–2289. doi: 10.1007/s00204-014-1401-9.
    1. Matović V., Buha A., Ðukić-Ćosić D., Bulat Z. Insight into the oxidative stress induced by lead and/or cadmium in blood, liver and kidneys. Food Chem. Toxicol. 2015;78:130–140. doi: 10.1016/j.fct.2015.02.011.
    1. Satarug S., Vesey D.A., Gobe G.C. Kidney cadmium toxicity, diabetes and high blood pressure: The perfect storm. Tohoku J. Exp. Med. 2017;241:65–87. doi: 10.1620/tjem.241.65.
    1. Garza-Lombó C., Posadas Y., Quintanar L., Gonsebatt M.E., Franco R. Neurotoxicity linked to dysfunctional metal ion homeostasis and xenobiotic metal exposure: Redox signaling and oxidative stress. Antioxid. Redox Signal. 2018;28:1669–1703. doi: 10.1089/ars.2017.7272.
    1. Valko M., Jomova K., Rhodes C.J., Kuča K., Musílek K. Redox- and non-redox-metal-induced formation of free radicals and their role in human disease. Arch. Toxicol. 2016;90:1–37. doi: 10.1007/s00204-015-1579-5.
    1. Moulis J.M., Bourguinon J., Catty P. Chapter 23 Cadmium. In: Wolfgang M., Anthony W., editors. RSC Metallobiology Series No. 2, Binding, Transport. and Storage of Metal. Ions in Biological Cells. The Royal Society of Chemistry; London, UK: 2014. pp. 695–746.
    1. Cangelosi V., Pecoraro V. Chapter 28 Lead. In: Wolfgang M., Anthony W., editors. RSC Metallobiology Series No. 2, Binding, Transport. and Storage of Metal. Ions in Biological Cells. The Royal Society of Chemistry; London, UK: 2014. pp. 843–882.
    1. Sanders T., Liu Y., Buchner V., Tchounwou P.B. Neurotoxic effects and biomarkers of lead exposure: A review. Rev. Environ. Health. 2009;24:15–45. doi: 10.1515/REVEH.2009.24.1.15.
    1. Carpenter M.C., Shami Shah A., DeSilva S., Gleaton A., Su A., Goundie B., Croteau M.L., Stevenson M.J., Wilcox D.E., Austin R.N. Thermodynamics of Pb(ii) and Zn(ii) binding to MT-3, a neurologically important metallothionein. Metallomics. 2016;8:605–617. doi: 10.1039/C5MT00209E.
    1. Satarug S., Baker J.R., Reilly P.E., Esumi H., Moore M.R. Evidence for a synergistic interaction between cadmium and endotoxin toxicity and for nitric oxide and cadmium displacement of metals in the kidney. Nitric Oxide. 2000;4:431–440. doi: 10.1006/niox.2000.0295.
    1. Satarug S., Baker J.R., Reilly P.E., Moore M.R., Williams D.J. Changes in zinc and copper homeostasis in human livers and kidneys associated with exposure to environmental cadmium. Hum. Exp. Toxicol. 2001;20:205–213. doi: 10.1191/096032701678766787.
    1. Satarug S., Nishijo M., Ujjin P., Moore M.R. Chronic exposure to low-level cadmium induced zinc-copper dysregulation. J. Trace Elem. Med. Biol. 2018;46:32–38. doi: 10.1016/j.jtemb.2017.11.008.
    1. Prozialeck W.C., Lamar P.C., Edwards J.R. Effects of sub-chronic Cd exposure on levels of copper, selenium, zinc, iron and other essential metals in rat renal cortex. Toxicol. Rep. 2016;3:740–746. doi: 10.1016/j.toxrep.2016.09.005.
    1. Thevenod F. Nephrotoxicity and the proximal tubule. Insights from cadmium. Nephron Physiol. 2003;93:87–93. doi: 10.1159/000070241.
    1. Moulis J.M. Cellular mechanisms of cadmium toxicity related to the homeostasis of essential metals. Biometals. 2010;23:877–896. doi: 10.1007/s10534-010-9336-y.
    1. Nzengue Y., Candéias S.M., Sauvaigo S., Douki T., Favier A., Rachidi W., Guiraud P. The toxicity redox mechanisms of cadmium alone or together with copper and zinc homeostasis alteration: Its redox biomarkers. J. Trace Elem. Med. Biol. 2011;25:171–180. doi: 10.1016/j.jtemb.2011.06.002.
    1. Nzengue Y., Steiman R., Rachidi W., Favier A., Guiraud P. Oxidative stress induced by cadmium in the C6 cell line: Role of copper and zinc. Biol. Trace Elem. Res. 2012;146:410–419. doi: 10.1007/s12011-011-9265-9.
    1. Eom S.Y., Yim D.H., Huang M., Park C.H., Kim G.B., Yu S.D., Choi B.S., Park J.D., Kim Y.D., Kim H. Copper-zinc imbalance induces kidney tubule damage and oxidative stress in a population exposed to chronic environmental cadmium. Int. Arch. Occup. Environ. Health. 2020;93:337–344. doi: 10.1007/s00420-019-01490-9.
    1. Rubino F.M. Toxicity of glutathione-binding metals: A review of targets and mechanisms. Toxics. 2015;3:20–62. doi: 10.3390/toxics3010020.
    1. Phillips J.D. Heme biosynthesis and the porphyrias. Mol. Genet. Metab. 2019;128:164–177. doi: 10.1016/j.ymgme.2019.04.008.
    1. Tobwala S., Wang H.-J., Carey J.W., Banks W.A., Ercal N. Effects of lead and cadmium on brain endothelial cell survival, monolayer permeability, and crucial oxidative stress markers in an in vitro model of the blood-brain barrier. Toxics. 2014;2:258–275. doi: 10.3390/toxics2020258.
    1. Wang W., Duan B., Xu H., Xu L., Xu T.L. Calcium-permeable acid-sensing ion channel is a molecular target of the neurotoxic metal ion lead. J. Biol. Chem. 2006;281:2497–2505. doi: 10.1074/jbc.M507123200.
    1. FAO/WHO . Evaluation of Certain Food Additives and Contaminants (Forty-First Report of the Joint FAO/WHO Expert Committee on Food Additives) World Health Organization; Geneva, Switzerland: 1993. (WHO Technical Report Series No. 837).
    1. Food and Agriculture Organization of the United Nations (FAO) World Health Organization (WHO) Summary and Conclusions; Proceedings of the Joint FAO/WHO Expert Committee on Food Additives Seventy-Third Meeting; Geneva, Switzerland. 8–17 June 2010; [(accessed on 12 August 2020)]. Available online: .
    1. Flannery B.M., Dolan L.C., Hoffman-Pennesi D., Gavelek A., Jones O.E., Kanwal R., Wolpert B., Gensheimer K., Dennis S., Fitzpatrick S.U.S. Food and Drug Administration’s interim reference levels for dietary lead exposure in children and women of childbearing age. Regul. Toxicol. Pharmacol. 2020;110:104516. doi: 10.1016/j.yrtph.2019.104516.
    1. Dolan L.C., Flannery B.M., Hoffman-Pennesi D., Gavelek A., Jones O.E., Kanwal R., Wolpert B., Gensheimer K., Dennis S., Fitzpatrick S. A review of the evidence to support interim reference level for dietary lead exposure in adults. Regul. Toxicol. Pharmacol. 2020;111:104579. doi: 10.1016/j.yrtph.2020.104579.
    1. Ferraro P.M., Costanzi S., Naticchia A., Sturniolo A., Gambaro G. Low level exposure to cadmium increases the risk of chronic kidney disease: Analysis of the NHANES 1999–2006. BMC Public Health. 2010;10:304. doi: 10.1186/1471-2458-10-304.
    1. Lin Y.S., Ho W.C., Caffrey J.L., Sonawane B. Low serum zinc is associated with elevated risk of cadmium nephrotoxicity. Environ. Res. 2014;134:33–38. doi: 10.1016/j.envres.2014.06.013.
    1. Madrigal J.M., Ricardo A.C., Persky V., Turyk M. Associations between blood cadmium concentration and kidney function in the U.S. population: Impact of sex, diabetes and hypertension. Environ. Res. 2018;169:180–188. doi: 10.1016/j.envres.2018.11.009.
    1. Crinnion W.J. The CDC fourth national report on human exposure to environmental chemicals: What it tells us about our toxic burden and how it assists environmental medicine physicians. Altern. Med. Rev. 2010;15:101–108.
    1. Levey A.S., Stevens L.A., Schmid C.H., Zhang Y., Castro A.F., III, Feldman H.I., Kusek J.W., Eggers P., Van Lente F., Greene T., et al. A new equation to estimate glomerular filtration rate. Ann. Intern. Med. 2009;150:604–612. doi: 10.7326/0003-4819-150-9-200905050-00006.
    1. Levey A.S., Inker L.A., Coresh J. GFR estimation: From physiology to public health. Am. J. Kidney Dis. 2014;63:820–834. doi: 10.1053/j.ajkd.2013.12.006.
    1. Levey A.S., Becker C., Inker L.A. Glomerular filtration rate and albuminuria for detection and staging of acute and chronic kidney disease in adults: A systematic review. JAMA. 2015;313:837–846. doi: 10.1001/jama.2015.0602.
    1. Satarug S., Ruangyuttikarn W., Nishijo M., Ruiz P. Urinary cadmium threshold to prevent kidney disease development. Toxics. 2018;6:26.
    1. Satarug S., Boonprasert K., Gobe G.C., Ruenweerayut R., Johnson D.W., Na-Bangchang K., Vesey D.A. Chronic exposure to cadmium is associated with a marked reduction in glomerular filtration rate. Clin. Kidney J. 2018;12:468–475. doi: 10.1093/ckj/sfy113.
    1. Satarug S., Vesey D.A., Nishijo M., Ruangyuttikarnm W., Gobe G.C. The inverse association of glomerular function and urinary β2-MG excretion and its implications for cadmium health risk assessment. Environ. Res. 2019;173:40–47. doi: 10.1016/j.envres.2019.03.026.
    1. Satarug S., Vesey D.A., Ruangyuttikarn W., Nishijo M., Gobe G.C., Phelps K.R. The source and pathophysiologic significance of excreted cadmium. Toxics. 2019;7:55. doi: 10.3390/toxics7040055.
    1. Järup L. Hazards of heavy metal contamination. Br. Med. Bull. 2003;68:167–182. doi: 10.1093/bmb/ldg032.
    1. Wu S., Deng F., Hao Y., Shima M., Wang X., Zheng C., Wei H., Lv H., Lu X., Huang J., et al. Chemical constituents of fine particulate air pollution and pulmonary function in healthy adults: The Healthy Volunteer Natural Relocation study. J. Hazard. Mater. 2013;260:183–191. doi: 10.1016/j.jhazmat.2013.05.018.
    1. Jung M.S., Kim J.Y., Lee H.S., Lee C.G., Song H.S. Air pollution and urinary N-acetyl-β-glucosaminidase levels in residents living near a cement plant. Ann. Occup. Environ. Med. 2016;28:52. doi: 10.1186/s40557-016-0138-8.
    1. Jin Y., Lu Y., Li Y., Zhao H., Wang X., Shen Y., Kuang X. Correlation between environmental low-dose cadmium exposure and early kidney damage: A comparative study in an industrial zone vs. a living quarter in Shanghai, China. Environ.Toxicol. Pharmacol. 2020;79:103381. doi: 10.1016/j.etap.2020.103381.
    1. Repić A., Bulat P., Antonijević B., Antunović M., Džudović J., Buha A., Bulat Z. The influence of smoking habits on cadmium and lead blood levels in the Serbian adult people. Environ. Sci. Pollut. Res. Int. 2020;27:751–760. doi: 10.1007/s11356-019-06840-1.
    1. Dumkova J., Vrlikova L., Vecera Z., Putnova B., Docekal B., Mikuska P., Fictum P., Hampl A., Buchtova M. Inhaled cadmium oxide nanoparticles: Their in vivo fate and effect on target organs. Int. J. Mol. Sci. 2016;17:874. doi: 10.3390/ijms17060874.
    1. Dumková J., Smutná T., Vrlíková L., Le Coustumer P., Večeřa Z., Dočekal B., Mikuška P., Čapka L., Fictum P., Hampl A., et al. Sub-chronic inhalation of lead oxide nanoparticles revealed their broad distribution and tissue-specific subcellular localization in target organs. Part. Fibre Toxicol. 2017;14:55. doi: 10.1186/s12989-017-0236-y.
    1. Tulinska J., Masanova V., Liskova A., Mikusova M.L., Rollerova E., Krivosikova Z., Stefikova K., Uhnakova I., Ursinyova M., Babickova J., et al. Six-week inhalation of CdO nanoparticles in mice: The effects on immune response, oxidative stress, antioxidative defense, fibrotic response, and bones. Food Chem. Toxicol. 2020;136:110954. doi: 10.1016/j.fct.2019.110954.
    1. Sutunkova M.P., Solovyeva S.N., Chernyshov I.N., Klinova S.V., Gurvich V.B., Shur V.Y., Shishkina E.V., Zubarev I.V., Privalova L.I., Katsnelson B.A. Manifestation of systemic toxicity in rats after a short-time inhalation of lead oxide nanoparticles. Int. J. Mol. Sci. 2020;21:690. doi: 10.3390/ijms21030690.
    1. Zahran S., McElmurry S.P., Sadler R.C. Four phases of the Flint qater crisis: Evidence from blood lead levels in children. Environ. Res. 2017;157:160–172. doi: 10.1016/j.envres.2017.05.028.
    1. Roy S., Tang M., Edwards M.A. Lead release to potable water during the Flint, Michigan water crisis as revealed by routine biosolids monitoring data. Water Res. 2019;160:475–483. doi: 10.1016/j.watres.2019.05.091.
    1. Bandara J.M., Wijewardena H.V., Liyanege J., Upul M.A., Bandara J.M. Chronic renal failure in Sri Lanka caused by elevated dietary cadmium: Trojan horse of the green revolution. Toxicol. Lett. 2010;198:33–39. doi: 10.1016/j.toxlet.2010.04.016.
    1. Kader M., Lamb D.T., Mahbub K.R., Megharaj M., Naidu R. Predicting plant uptake and toxicity of lead (Pb) in long-term contaminated soils from derived transfer functions. Environ. Sci. Pollut. Res. Int. 2016;23:15460–15470. doi: 10.1007/s11356-016-6696-z.
    1. Lamb D.T., Kader M., Ming H., Wang L., Abbasi S., Megharaj M., Naidu R. Predicting plant uptake of cadmium: Validated with long-term contaminated soils. Ecotoxicology. 2016;25:1563–1574. doi: 10.1007/s10646-016-1712-0.
    1. Wilkinson J.M., Hill J., Phillips C.J. The accumulation of potentially-toxic metals by grazing ruminants. Proc. Nutr. Soc. 2003;62:267–277. doi: 10.1079/PNS2003209.
    1. Bischoff K., Hillebrandt J., Erb H.N., Thompson B., Johns S. Comparison of blood and tissue lead concentrations from cattle with known lead exposure. Food Addit. Contam. Part A Chem. Anal. Control. Expo. Risk Assess. 2016;33:1563–1569. doi: 10.1080/19440049.2016.1230277.
    1. Centers for Disease Control and Prevention CDC Response to Advisory Committee on Childhood Lead Poisoning Prevention Recommendations in “Low Level Lead Exposure Harms Children: A Renewed Call of Primary Prevention”. [(accessed on 12 August 2020)];2012 Available online: .
    1. Feng C.X., Cao. J., Bendell L. Exploring spatial and temporal variations of cadmium concentrations in pacific oysters from British Columbia. Biometrics. 2011;67:1142–1152. doi: 10.1111/j.1541-0420.2010.01534.x.
    1. Losasso C., Bille L., Patuzzi I., Lorenzetto M., Binato G., Pozza M.D., Ferrè N., Ricci N. Possible influence of natural events on heavy metals exposure from shellfish consumption: A case study in the north-east of Italy. Front. Public Health. 2015;3:21. doi: 10.3389/fpubh.2015.00021.
    1. Guéguen M., Amiard J.-C., Arnich N., Badot P.-M., Claisse D., Guérin T., Vernoux J.-P. Shellfish and residual chemical contaminants: Hazards, monitoring, and health risk assessment along French coasts. Rev. Environ. Contam. Toxicol. 2011;213:55–111.
    1. Burioli E.A.V., Squadrone S., Stella C., Foglini C., Abete M.C., Prearo M. Trace element occurrence in the Pacific oyster Crassostrea gigas from coastal marine ecosystems in Italy. Chemosphere. 2017;187:248–260. doi: 10.1016/j.chemosphere.2017.08.102.
    1. Renieri E.A., Alegakis A.K., Kiriakakis M., Vinceti M., Ozcagli E., Wilks M.F., Tsatsakis A.M. Cd, Pb and Hg biomonitoring in fish of the Mediterranean region and risk estimations on fish consumption. Toxics. 2014;2:417–442. doi: 10.3390/toxics2030417.
    1. Cobbett C.S. Phytochelatins and their roles in heavy metal detoxification. Plant. Physiol. 2000;123:825–832. doi: 10.1104/pp.123.3.825.
    1. Cobbett C., Goldsbrough P. Phytochelatins and metallothioneins: Roles in heavy metal detoxification and homeostasis. Annu. Rev. Plant Biol. 2002;53:159–182. doi: 10.1146/annurev.arplant.53.100301.135154.
    1. Pivato M., Fabrega-Prats M., Masi A. Low-molecular-weight thiols in plants: Functional and analytical implications. Arch. Biochem. Biophys. 2014;560:83–99. doi: 10.1016/j.abb.2014.07.018.
    1. Klaassen C.D., Liu J., Diwan B.A. Metallothionein protection of cadmium toxicity. Toxicol. Appl. Pharmacol. 2009;238:215–220. doi: 10.1016/j.taap.2009.03.026.
    1. Scott S.R., Smith K.E., Dahman C., Gorski P.R., Adams S.V., Shafer M.M. Cd isotope fractionation during tobacco combustion produces isotopic variation outside the range measured in dietary sources. Sci. Total Environ. 2019;688:600–608. doi: 10.1016/j.scitotenv.2019.06.269.
    1. Aoshima K. Epidemiology and tubular dysfunction in the inhabitants of a cadmium-polluted area in the Jinzu River basin in Toyama Prefecture. Tohoku J. Exp. Med. 1987;152:151–172. doi: 10.1620/tjem.152.151.
    1. Spungen J.H. Children’s exposures to lead and cadmium: FDA total diet study 2014–2016. Food Addit. Contam. Part A Chem. Anal. Control. Expo. Risk Assess. 2019;36:893–903. doi: 10.1080/19440049.2019.1595170.
    1. Gavelek A., Spungen J., Hoffman-Pennesi D., Flannery B., Dolan L., Dennis S., Fitzpatrick S. Lead exposures in older children (males and females 7–17 years), women of childbearing age (females 16–49 years) and adults (males and females 18+ years): FDA total diet study 2014-16. Food Addit. Contam. Part A Chem. Anal. Control. Expo. Risk Assess. 2020;37:104–109. doi: 10.1080/19440049.2019.1681595.
    1. European Food Safety Agency (EFSA) Statement on tolerable weekly intake for cadmium. EFSA J. 2011;9:1975.
    1. European Food Safety Agency (EFSA) Cadmium dietary exposure in the European population. EFSA J. 2012;10:2551. doi: 10.2903/j.efsa.2012.2551.
    1. Callan A., Hinwood A., Devine A. Metals in commonly eaten groceries in Western Australia: A market basket survey and dietary assessment. Food Addit. Contam. Part A Chem. Anal. Control. Expo. Risk Assess. 2014;31:1968–1981. doi: 10.1080/19440049.2014.973457.
    1. Sand S., Becker W. Assessment of dietary cadmium exposure in Sweden and population health concern including scenario analysis. Food Chem. Toxicol. 2012;50:536–544. doi: 10.1016/j.fct.2011.12.034.
    1. Wei J., Gao J., Cen K. Levels of eight heavy metals and health risk assessment considering food consumption by China’s residents based on the 5th China total diet study. Sci. Total Environ. 2019;689:1141–1148. doi: 10.1016/j.scitotenv.2019.06.502.
    1. Xiao G., Liu Y., Dong K.F., Lu J. Regional characteristics of cadmium intake in adult residents from the 4th and 5th Chinese total diet study. Environ. Sci. Pollut. Res. Int. 2020;27:3850–3857. doi: 10.1007/s11356-019-06923-z.
    1. Jin Y., Liu P., Sun J., Wang C., Min J., Zhang Y., Wang S., Wu Y. Dietary exposure and risk assessment to lead of the population of Jiangsu province, China. Food Addit. Contam. Part A Chem. Anal. Control. Expo. Risk Assess. 2014;31:1187–1195.
    1. Lim J.A., Kwon H.J., Ha M., Kim H., Oh S.Y., Kim J.S., Lee S.A., Park J.D., Hong Y.S., Sohn S.J., et al. Korean research project on the integrated exposure assessment of hazardous substances for food safety. Environ. Health Toxicol. 2015;30:e2015004. doi: 10.5620/eht.e2015004.
    1. Kim H., Lee J., Woo H.D., Kim D.W., Choi I.J., Kim Y.I., Kim J. Association between dietary cadmium intake and early gastric cancer risk in a Korean population: A case-control study. Eur. J. Nutr. 2019;58:3255–3266. doi: 10.1007/s00394-018-1868-x.
    1. Schwarz M.A., Lindtner O., Blume K., Heinemeyer G., Schneider K. Cadmium exposure from food: The German LExUKon project. Food Addit. Contam. Part A Chem. Anal. Control. Expo. Risk Assess. 2014;31:1038–1051. doi: 10.1080/19440049.2014.905711.
    1. Marín S., Pardo O., Báguena R., Font G., Yusà V. Dietary exposure to trace elements and health risk assessment in the region of Valencia, Spain: A total diet study. Food Addit. Contam. Part A Chem. Anal. Control. Expo. Risk Assess. 2017;34:228–240. doi: 10.1080/19440049.2016.1268273.
    1. Puerto-Parejo L.M., Aliaga I., Canal-Macias M.L., Leal-Hernandez O., Roncero-Martín R., Rico-Martín S., Moran J.M. Evaluation of the dietary intake of cadmium, lead and mercury and its relationship with bone health among postmenopausal women in Spain. Int. J. Environ. Res. Public Health. 2017;14:564. doi: 10.3390/ijerph14060564.
    1. Kim K., Melough M.M., Vance T.M., Noh H., Koo S.I., Chun O.K. Dietary cadmium intake and sources in the US. Nutrients. 2018;11:2. doi: 10.3390/nu11010002.
    1. Adams S.V., Quraishi S.M., Shafer M.M., Passarelli M.N., Freney E.P., Chlebowski R.T., Luo J., Meliker J.R., Mu L., Neuhouser M.L., et al. Dietary cadmium exposure and risk of breast, endometrial, and ovarian cancer in the Women’s Health Initiative. Environ. Health Perspect. 2014;122:594–600. doi: 10.1289/ehp.1307054.
    1. Filippini T., Cilloni S., Malavolti M., Violi F., Malagoli C., Tesauro M., Bottecchi I., Ferrari A., Vescovi L., Vinceti M. Dietary intake of cadmium, chromium, copper, manganese, selenium and zinc in a Northern Italy community. J. Trace Elem. Med. Biol. 2018;50:508–517. doi: 10.1016/j.jtemb.2018.03.001.
    1. Schneider K., Schwarz M.A., Lindtner O., Blume K., Heinemeyer G. Lead exposure from food: The German LExUKon. Food Addit. Contam. Part A Chem. Anal. Control. Expo. Risk Assess. 2014;31:1052–1063. doi: 10.1080/19440049.2014.905875.
    1. Arnich N., Sirot V., Rivière G., Jean J., Noël L., Guérin T., Leblanc J.-C. Dietary exposure to trace elements and health risk assessment in the 2nd French Total Diet Study. Food Chem. Toxicol. 2012;50:2432–2449. doi: 10.1016/j.fct.2012.04.016.
    1. Vromman V., Waegeneers N., Cornelis C., De Boosere I., Van Holderbeke M., Vinkx C., Smolders E., Huyghebaert A., Pussemier L. Dietary cadmium intake by the Belgian adult population. Food Addit. Contam. Part A Chem. Anal. Control. Expo. Risk Assess. 2010;27:1665–1673. doi: 10.1080/19440049.2010.525752.
    1. Horiguchi H., Oguma E., Sasaki S., Miyamoto K., Hosoi Y., Ono A., Kayama F. Exposure assessment of cadmium in female farmers in cadmium-polluted areas in Northern Japan. Toxics. 2020;8:44. doi: 10.3390/toxics8020044.
    1. Nishito Y., Kambe T. Absorption mechanisms of iron, copper, and zinc: An overview. J. Nutr. Sci. Vitaminol. 2018;64:1–7. doi: 10.3177/jnsv.64.1.
    1. Vesey D.A. Transport pathways for cadmium in the intestine and kidney proximal tubule: Focus on the interaction with essential metals. Toxicol. Lett. 2010;198:13–19. doi: 10.1016/j.toxlet.2010.05.004.
    1. Thévenod F., Lee W.-K., Garrick M.D. Iron and cadmium entry into renal mitochondria: Physiological and toxicological implications. Front. Cell Develop. Biol. 2020;8:848. doi: 10.3389/fcell.2020.00848.
    1. Kovacs G., Danko T., Bergeron M.J., Balazs B., Suzuki Y., Zsembery A., Hediger M.A. Heavy metal cations permeate the TRPV6 epithelial cation channel. Cell Calcium. 2011;49:43–55. doi: 10.1016/j.ceca.2010.11.007.
    1. Kovacs G., Montalbetti N., Franz M.C., Graeter S., Simonin A., Hediger M.A. Human TRPV5 and TRPV6: Key players in cadmium and zinc toxicity. Cell Calcium. 2013;54:276–286. doi: 10.1016/j.ceca.2013.07.003.
    1. Fujishiro H., Hamao S., Tanaka R., Kambe T., Himeno S. Concentration-dependent roles of DMT1 and ZIP14 in cadmium absorption in Caco-2 cells. J. Toxicol. Sci. 2017;42:559–567. doi: 10.2131/jts.42.559.
    1. Thevenod F., Fels J., Lee W.-K., Zarbock R. Channels, transporters and receptors for cadmium and cadmium complexes in eukaryotic cells: Myths and facts. Biometals. 2019;32:469–489. doi: 10.1007/s10534-019-00176-6.
    1. Mackenzie B., Takanaga H., Hubert N., Rolfs A., Hediger M.A. Functional properties of multiple isoforms of human divalent metal-ion transporter 1 (DMT1) Biochem. J. 2007;403:59–69. doi: 10.1042/BJ20061290.
    1. Illing A.C., Shawki A., Cunningham C.L., Mackenzie B. Substrate profile and metal-ion selectivity of human divalent metal-ion transporter-1. J. Biol. Chem. 2012;287:30485–30496. doi: 10.1074/jbc.M112.364208.
    1. Bannon D.I., Abounader R., Lees P.S., Bressler J.P. Effect of DMT1 knockdown on iron, cadmium, and lead uptake in Caco-2 cells. Am. J. Physiol. Cell Physiol. 2003;284:C44–C50. doi: 10.1152/ajpcell.00184.2002.
    1. Aduayom I., Jumarie C. Reciprocal inhibition of Cd and Pb sulfocomplexes for uptake in Caco-2 cells. J. Biochem. Mol. Toxicol. 2005;19:256–265. doi: 10.1002/jbt.20085.
    1. Mitchell C.J., Shawki A., Ganz T., Nemeth E., Mackenzie B. Functional properties of human ferroportin, a cellular iron exporter reactive also with cobalt and zinc. Am. J. Physiol. Cell Physiol. 2014;306:C450–C459. doi: 10.1152/ajpcell.00348.2013.
    1. Jeon H.-K., Jin H.-S., Lee D.-H., Choi W.-S., Moon C.-K., Oh Y.J., Lee T.H. Proteome analysis associated with cadmium adaptation in U937 cells: Identification of calbindin-D28k as a secondary cadmium-responsive protein that confers resistance to cadmium-induced apoptosis. J. Biol. Chem. 2004;279:31575–31583. doi: 10.1074/jbc.M400823200.
    1. Fujita Y., ElBelbasi H.I., Min K.-S., Onosaka S., Okada Y., Matsumoto Y., Mutoh N., Tanaka K. Fate of cadmium bound to phytochelatin in rats. Res. Commun. Chem. Pathol. Pharmacol. 1993;82:357–365.
    1. Langelueddecke C., Roussa E., Fenton R.A., Thévenod F. Expression and function of the lipocalin-2 (24p3/NGAL) receptor in rodent and human intestinal epithelia. PLoS ONE. 2013;8:e71586. doi: 10.1371/journal.pone.0071586.
    1. Langelueddecke C., Lee W.-K., Thevenod F. Differential transcytosis and toxicity of the hNGAL receptor ligands cadmium-metallothionein and cadmium-phytochelatin in colon-like Caco-2 cells: Implications for cadmium toxicity. Toxicol. Lett. 2014;226:228–235. doi: 10.1016/j.toxlet.2014.01.049.
    1. Jorge-Nebert L.F., Gálvez-Peralta M., Figueroa J.L., Somarathna M., Hojyo S., Fukada T., Nebert D.W. Comparing gene expression during cadmium uptake and distribution: Untreated versus oral Cd-treated wild-type and ZIP14 knockout mice. Toxicol. Sci. 2015;143:26–35. doi: 10.1093/toxsci/kfu204.
    1. McKenna I.M., Gordon T., Chen L.C., Anver M.R., Waalkes M.P. Expression of metallothionein protein in the lungs of Wistar rats and C57 and DBA mice exposed to cadmium oxide fumes. Toxicol. Appl. Pharmacol. 1998;153:169–178. doi: 10.1006/taap.1998.8399.
    1. Takeda K., Fujita H., Shibahara S. Differential control of the metal-mediated activation of the human heme oxygenase-1 and metallothionein IIA genes. Biochem. Biophys. Res. Commun. 1995;207:160–167. doi: 10.1006/bbrc.1995.1167.
    1. Hart B.A. Cellular and biochemical response of the rat lung to repeated inhalation of cadmium. Toxicol. Appl. Pharmacol. 1986;82:281–291. doi: 10.1016/0041-008X(86)90203-6.
    1. Hart B.A., Gong Q., Eneman J.D. Pulmonary metallothionein expression in rats following single and repeated exposure to cadmium aerosols. Toxicology. 1996;112:205–218. doi: 10.1016/0300-483X(96)03397-5.
    1. Chandler J.D., Wongtrakool C., Banton S.A., Li S., Orr M.L., Barr D.B., Neujahr D.C., Sutliff R.L., Go Y.M., Jones D.P. Low-dose oral cadmium increases airway reactivity and lung neuronal gene expression in mice. Physiol. Rep. 2016;4:e12821. doi: 10.14814/phy2.12821.
    1. Sabolić I., Breljak D., Skarica M., Herak-Kramberger C.M. Role of metallothionein in cadmium traffic and toxicity in kidneys and other mammalian organs. Biometals. 2010;23:897–926. doi: 10.1007/s10534-010-9351-z.
    1. Yu J., Fujishiro H., Miyataka H., Oyama T.M., Hasegawa T., Seko Y., Miura N., Himeno S. Dichotomous effects of lead acetate on the expression of metallothionein in the liver and kidney of mice. Biol. Pharm. Bull. 2009;32:1037–1042.
    1. Dai S., Yin Z., Yuan G., Lu H., Jia R., Xu J., Song X., Li L., Shu Y., Liang X., et al. Quantification of metallothionein on the liver and kidney of rats by subchronic lead and cadmium in combination. Environ. Toxicol. Pharmacol. 2013;36:1207–1216. doi: 10.1016/j.etap.2013.10.003.
    1. Kikuchi Y., Nomiyama T., Kumagai N., Dekio F., Uemura T., Takebayashi T., Nishiwaki Y., Matsumoto Y., Sano Y., Hosoda K., et al. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. J. Occup. Health. 2003;45:43–52. doi: 10.1539/joh.45.43.
    1. Wang X., Kim D., Tucker K.L., Weisskopf M.G., Sparrow D., Hu H., Park S.K. Effect of dietary sodium and potassium on the mobilization of bone lead among middle-aged and older men: The Veterans Affairs Normative Aging Study. Nutrients. 2019;11:2750.
    1. Nielsen R., Christensen E.I., Birn H. Megalin and cubilin in proximal tubule protein reabsorption: From experimental models to human disease. Kidney Int. 2016;89:58–67.
    1. Onodera A., Tani M., Michigami T., Yamagata M., Min K.S., Tanaka K., Nakanishi T., Kimura T., Itoh N. Role of megalin and the soluble form of its ligand RAP in Cd-metallothionein endocytosis and Cd-metallothionein-induced nephrotoxicity in vivo. Toxicol. Lett. 2012;212:91–96.
    1. Langelueddecke C., Roussa E., Fenton R.A., Wolff N.A., Lee W.K., Thévenod F. Lipocalin-2 (24p3/neutrophil gelatinase-associated lipocalin (NGAL)) receptor is expressed in distal nephron and mediates protein endocytosis. J. Biol. Chem. 2012;287:159–169.
    1. Fels J., Scharner B., Zarbock R., Zavala Guevara I.P., Lee W.K., Barbier O.C., Thévenod F. Cadmium complexed with β2-microglubulin, albumin and lipocalin-2 rather than metallothionein cause megalin:cubilin dependent toxicity of the renal proximal tubule. Int. J. Mol. Sci. 2019;20:2379.
    1. Nascimento C.R.B., Risso W.E., Martinez C.B.D.R. Lead accumulation and metallothionein content in female rats of different ages and generations after daily intake of Pb-contaminated food. Environ. Toxicol. Pharmacol. 2016;48:272–277.
    1. Satarug S., Baker J.R., Reilly P.E., Moore M.R., Williams D.J. Cadmium levels in the lung, liver, kidney cortex, and urine samples from Australians without occupational exposure to metals. Arch. Environ. Health. 2002;57:69–77.
    1. Baker J.R., Edwards R.J., Lasker J.M., Moore M.R., Satarug S. Renal and hepatic accumulation of cadmium and lead in the expression of CYP4F2 and CYP2E1. Toxicol. Lett. 2005;159:182–191.
    1. Barregard L., Fabricius-Lagging E., Lundh T., Mölne J., Wallin M., Olausson M., Modigh C., Sallstenm G. Cadmium, mercury, and lead in kidney cortex of living kidney donors: Impact of different exposure sources. Environ. Res. 2010;110:47–54.
    1. Järup L., Rogenfelt A., Elinder C.G., Nogawa K., Kjellström T. Biological half-time of cadmium in the blood of workers after cessation of exposure. Scand. J. Work Environ. Health. 1983;9:327–331.
    1. Börjesson J., Bellander T., Järup L., Elinder C.G., Mattsson S. In vivo analysis of cadmium in battery workers versus measurements of blood, urine, and workplace air. Occup. Environ. Med. 1997;54:424–531.
    1. Suwazono Y., Kido T., Nakagawa H., Nishijo M., Honda R., Kobayashi E., Dochi M., Nogawa K. Biological half-life of cadmium in the urine of inhabitants after cessation of cadmium exposure. Biomarkers. 2009;14:77–81. doi: 10.1080/13547500902730698.
    1. Ishizaki M., Suwazono Y., Kido T., Nishijo M., Honda R., Kobayashi E., Nogawa K., Nakagawa H. Estimation of biological half-life of urinary cadmium in inhabitants after cessation of environmental cadmium pollution using a mixed linear model. Food Addit. Contam. Part A Chem. Anal. Control. Expo. Risk Assess. 2015;32:1273–1276.
    1. Fransson M.N., Barregard L., Sallsten G., Akerstrom M., Johanson G. Physiologically-based toxicokinetic model for cadmium using Markov-chain Monte Carlo analysis of concentrations in blood, urine, and kidney cortex from living kidney donors. Toxicol. Sci. 2014;141:365–376.
    1. Specht A.J., Lin Y., Weisskopf M., Yan C., Hu H., Xu J., Nie L.H. XRF-measured bone lead (Pb) as a biomarker for Pb exposure and toxicity among children diagnosed with Pb poisoning. Biomarkers. 2016;21:347–352.
    1. Orlowski C., Piotrowski J.K., Subdys J.K., Gross A. Urinary cadmium as indicator of renal cadmium in humans: An autopsy study. Hum. Exp. Toxicol. 1998;17:302–306.
    1. Akerstrom M., Barregard L., Lundh T., Sallsten G. The relationship between cadmium in kidney and cadmium in urine and blood in an environmentally exposed population. Toxicol. Appl. Pharmacol. 2013;268:286–293.
    1. Wallin M., Sallsten G., Lundh T., Barregard L. Low-level cadmium exposure and effects on kidney function. Occup. Environ. Med. 2014;71:848–854. doi: 10.1136/oemed-2014-102279.
    1. Gerhardsson L., Englyst V., Lundström N.G., Sandberg S., Nordberg G. Cadmium, copper and zinc in tissues of deceased copper smelter workers. J. Trace Elem. Med. Biol. 2002;16:261–266. doi: 10.1016/S0946-672X(02)80055-4.
    1. Lou M., Garay R., Alda. J.O. Cadmium uptake through the anion exchanger in human red blood cells. J. Physiol. 1991;443:123–136. doi: 10.1113/jphysiol.1991.sp018826.
    1. Wu F., Satchwell T.J., Toye A.M. Anion exchanger 1 in red blood cells and kidney: Band 3’s in a pod. Biochem. Cell Biol. 2011;89:106–114.
    1. Parker M.D., Boron W.F. The divergence, actions, roles, and relatives of sodium-coupled bicarbonate transporters. Physiol. Rev. 2013;93:803–959. doi: 10.1152/physrev.00023.2012.
    1. Savigni D.L., Morgan E.H. Transport mechanisms for iron and other transition metals in rat and rabbit erythroid cells. J. Physiol. 1998;508:837–850. doi: 10.1111/j.1469-7793.1998.837bp.x.
    1. Simons T.J. The role of anion transport in the passive movement of lead across the human red cell membrane. J. Physiol. 1986;378:287–312. doi: 10.1113/jphysiol.1986.sp016220.
    1. Simons T.J. Lead transport and binding by human erythrocytes in vitro. Pflugers Arch. 1993;423:307–313. doi: 10.1007/BF00374410.
    1. Lang F., Abed M., Lang E., Föller M. Oxidative stress and suicidal erythrocyte death. Antioxid. Redox Signal. 2014;21:138–153. doi: 10.1089/ars.2013.5747.
    1. Lang E., Lang F. Mechanisms and pathophysiological significance of eryptosis, the suicidal erythrocyte death. Semin. Cell Dev. Biol. 2015;39:35–42. doi: 10.1016/j.semcdb.2015.01.009.
    1. Attanzio A., Frazzitta A., Vasto S., Tesoriere L., Pintaudi A.M., Livrea M.A., Cilla A., Allegra M. Increased eryptosis in smokers is associated with the antioxidant status and C-reactive protein levels. Toxicology. 2019;411:43–48. doi: 10.1016/j.tox.2018.10.019.
    1. Scott B.J., Bradwell A.R. Identification of the serum binding proteins for iron, zinc, cadmium, nickel, and calcium. Clin. Chem. 1983;29:629–633. doi: 10.1093/clinchem/29.4.629.
    1. Horn N.M., Thomas A.L. Interactions between the histidine stimulation of cadmium and zinc influx into human erythrocytes. J. Physiol. 1996;496:711–718. doi: 10.1113/jphysiol.1996.sp021721.
    1. Turell L., Radi R., Alvarez B. The thiol pool in human plasma: The central contribution of albumin to redox processes. Free Radic. Biol. Med. 2013;65:244–253. doi: 10.1016/j.freeradbiomed.2013.05.050.
    1. Morris T.T., Keir J.L., Boshart S.J., Lobanov V.P., Ruhland A.M., Bahl N., Gailer J. Mobilization of Cd from human serum albumin by small molecular weight thiols. J. Chromatogr. B Anal. Technol. Biomed. Life Sci. 2014;958:16–21. doi: 10.1016/j.jchromb.2014.03.012.
    1. Sagmeister P., Gibson M.A., McDade K.H., Gailer J. Physiologically relevant plasma d,l-homocysteine concentrations mobilize Cd from human serum albumin. J. Chromatogr. B Anal. Technol. Biomed. Life Sci. 2016;1027:181–186. doi: 10.1016/j.jchromb.2016.05.014.
    1. Gaudet M.M., Deubler E.L., Kelly R.S., Diver W.R., Teras L.R., Hodge J.M., Levine K.E., Haines L.G., Lundh T., Lenner P., et al. Blood levels of cadmium and lead in relation to breast cancer risk in three prospective cohorts. Int. J. Cancer. 2019;144:1010–1016. doi: 10.1002/ijc.31805.
    1. Lin J., Zhang F., Lei Y. Dietary intake and urinary level of cadmium and breast cancer risk: A meta-analysis. Cancer Epidemiol. 2016;42:101–107. doi: 10.1016/j.canep.2016.04.002.
    1. Rokadia H.K., Agarwal S. Serum heavy metals and obstructive lung disease: Results from the National Health and Nutrition Examination Survey. Chest. 2013;143:388–397. doi: 10.1378/chest.12-0595.
    1. Yang G., Sun T., Han Y.Y., Rosser F., Forno E., Chen W., Celedón J.C. Serum cadmium and lead, current wheeze, and lung function in a nationwide study of adults in the United States. J. Allergy Clin. Immunol. Pract. 2019;7:2653–2660.e3. doi: 10.1016/j.jaip.2019.05.029.
    1. Bergdahl I.A., Schütz A., Gerhardsson L., Jensen A., Skerfving S. Lead concentrations in human plasma, urine and whole blood. Scand. J. Work Environ. Health. 1997;23:359–363. doi: 10.5271/sjweh.232.
    1. Manton W.I., Rothenberg S.J., Manalo M. The lead content of blood serum. Environ. Res. 2001;86:263–273. doi: 10.1006/enrs.2001.4271.
    1. Smith D., Hernandez-Avila M., Téllez-Rojo M.M., Mercado A., Hu H. The relationship between lead in plasma and whole blood in women. Environ. Health Perspect. 2002;110:263–268. doi: 10.1289/ehp.02110263.
    1. Barbosa F., Jr., Tanus-Santos J.E., Gerlach R.F., Parsons P.J. A critical review of biomarkers used for monitoring human exposure to lead: Advantages, limitations, and future needs. Environ. Health Perspect. 2005;113:1669–1674. doi: 10.1289/ehp.7917.
    1. Gulson B.L., Mizon K.J., Korsch M.J., Horwarth D., Phillips A., Hall J. Impact on blood lead in children and adults following relocation from their source of exposure and contribution of skeletal tissue to blood lead. Bull. Environ. Contam. Toxicol. 1996;56:543–550.
    1. Gulson B.L., Mahaffey K.R., Mizon K.F., Korsch M.J., Cameron M.A., Vimpani G. Contribution of tissue lead to bone lead in adult female subjects based on stable lead-isotope methods. J. Lab. Clin. Med. 1995;125:703–712.
    1. Gwiazda R., Campbell C., Smith D. A noninvasive isotopic approach to estimate the bone lead contribution to blood in children: Implications for assessing the efficacy of lead abatement. Environ. Health Perspect. 2005;113:104–110. doi: 10.1289/ehp.7241.
    1. Manton W.I., Angle C.R., Stanek K.L., Reese Y.R., Kuehnemann T.J. Acquisition and retention of lead by young children. Environ. Res. 2000;82:60–80. doi: 10.1006/enrs.1999.4003.
    1. Roberts J.R., Reigart. J.R., Ebeling. M., Hulsey T.C. Time required for blood lead levels to decline in nonchelated children. Clin. Toxicol. 2001;39:153–160. doi: 10.1081/CLT-100103831.
    1. Landrigan P.J., Todd A.C. Direct measurement of lead in bone-a promising biomarker. JAMA. 1994;271:239–240. doi: 10.1001/jama.1994.03510270085045.
    1. O’Flaherty E.J. Physiologically based models for bone-seeking elements V: Lead absorption and disposition in childhood. Toxicol. Appl. Pharmacol. 1995;131:297–308. doi: 10.1006/taap.1995.1072.
    1. Hu H., Rabinowitz M., Smith. D. Bone lead as a biological marker in epidemiologic studies of chronic toxicity: Conceptual paradigms. Environ. Health Perspect. 1998;106:1–8. doi: 10.1289/ehp.981061.
    1. Nilsson U., Attewell R., Christoffersson J.O., Schütz A., Ahlgren L., Skerfving S., Mattsson S. Kinetics of lead in bone and blood after end of occupational exposure. Pharmacol. Toxicol. 1991;68:477–484. doi: 10.1111/j.1600-0773.1991.tb01273.x.
    1. Price J., Grudzinski A.W., Craswell P.W., Thomas B.J. Repeated bone lead levels in Queensland, Australia—Previously a high lead environment. Arch. Environ. Health. 1992;47:256–262. doi: 10.1080/00039896.1992.9938358.
    1. Brito J.A., McNeill F.E., Stronach I., Webber C.E., Wells S., Richard N., Chettle D.R. Longitudinal changes in bone lead concentration: Implications for modelling of human bone lead metabolism. J. Environ. Monit. 2001;3:343–351. doi: 10.1039/b101493p.
    1. Wilker E., Korrick S., Nie L.H., Sparrow D., Vokonas P., Coull B., Wright R.O., Schwartz. J., Hu H. Longitudinal changes in bone lead levels: The VA normative aging study. J. Occup. Environ. Med. 2011;53:850–855. doi: 10.1097/JOM.0b013e31822589a9.
    1. Gerhardsson L., Akantis A., Lundström N.G., Nordberg G.F., Schütz A., Skerfving S. Lead concentrations in cortical and trabecular bones in deceased smelter workers. J. Trace Elem. Med. Biol. 2005;19:209–215. doi: 10.1016/j.jtemb.2005.06.004.
    1. Gerhardsson L., Englyst V., Lundström N.G., Nordberg G., Sandberg S., Steinvall F. Lead in tissues of deceased lead smelter workers. J. Trace Elem. Med. Biol. 1995;9:136–143. doi: 10.1016/S0946-672X(11)80037-4.
    1. Hernandez-Avila M., Smith D., Meneses F., Sanin L.H., Hu H. The influence of bone and blood lead on plasma lead levels in environmentally exposed adults. Environ. Health Perspect. 1998;106:473–477. doi: 10.1289/ehp.106-1533211.
    1. Hu H., Shih R., Rothenberg S., Schwartz B.S. The epidemiology of lead toxicity in adults: Measuring dose and consideration of other methodologic issues. Environ. Health Perspect. 2007;115:455–462. doi: 10.1289/ehp.9783.
    1. Shih R.A., Hu H., Weisskopf M.G., Schwartz B.S. Cumulative lead dose and cognitive function in adults: A review of studies that measured both blood lead and bone lead. Environ. Health Perspect. 2007;115:483–492. doi: 10.1289/ehp.9786.
    1. Farooqui Z., Bakulski K.M., Power M.C., Weisskopf M.G., Sparrow D., Spiro A., III, Vokonas P.S., Nie L.H., Hu H., Park S.K. Associations of cumulative Pb exposure and longitudinal changes in mini-mental status exam scores, global cognition and domains of cognition: The VA normative aging study. Environ. Res. 2017;152:102–108. doi: 10.1016/j.envres.2016.10.007.
    1. Wright R.O., Tsaih S.W., Schwartz J., Spiro A., III, McDonald K., Weiss S.T., Hu H. Lead exposure biomarkers and mini-mental status exam scores in older men. Epidemiology. 2003;14:713–718. doi: 10.1097/01.EDE.0000081988.85964.db.
    1. Zheutlin A.R., Hu H., Weisskopf M.G., Sparrow D., Vokonas P.S., Park S.K. Low-level cumulative lead and resistant hypertension: A prospective study of men participating in the Veterans Affairs normative aging study. J. Am. Heart Assoc. 2018;7:e010014. doi: 10.1161/JAHA.118.010014.
    1. Hirata M., Yoshida T., Miyajima K., Kosaka H., Tabuchi T. Correlation between lead in plasma and other indicators of lead exposure among lead-exposed workers. Int. Arch. Occup. Environ. Health. 1995;68:58–63. doi: 10.1007/BF01831634.
    1. Schütz A., Olsson M., Jensen A., Gerhardsson L., Börjesson J., Mattsson S., Skerfving S. Lead in finger bone, whole blood, plasma and urine in lead-smelter workers: Extended exposure range. Int. Arch. Occup. Environ. Health. 2005;78:35–43. doi: 10.1007/s00420-004-0559-5.
    1. Fukui Y., Miki M., Ukai H., Okamoto S., Takada S., Higashikawa K., Ikeda M. Urinary lead as a possible surrogate of blood lead among workers occupationally exposed to lead. Int. Arch. Occup. Environ. Health. 1999;72:516–520. doi: 10.1007/s004200050409.
    1. Bai Y., Laenen A., Haufroid V., Nawrot T.S., Nemery B. Urinary lead in relation to combustion-derived air pollution in urban environments. A longitudinal study of an international panel. Environ. Int. 2019;125:75–81. doi: 10.1016/j.envint.2019.01.044.
    1. Wang X., Jin P., Zhou Q., Liu S., Wang F., Xi S. Metal biomonitoring and comparative assessment in urine of workers in lead-zinc and steel-iron mining and smelting. Biol. Trace Elem. Res. 2019;189:1–9. doi: 10.1007/s12011-018-1449-0.
    1. Li S., Wang J., Zhang B., Liu Y., Lu T., Shi Y., Shan G., Dong L. Urinary lead concentration is an independent predictor of cancer mortality in the U.S. general population. Front. Oncol. 2018;8:242. doi: 10.3389/fonc.2018.00242.
    1. Dudley R.E., Gammal L.M., Klaassen C.D. Cadmium-induced hepatic and renal injury in chronically exposed rats: Likely role of hepatic cadmium-metallothionein in nephrotoxicity. Toxicol. Appl. Pharmacol. 1985;77:414–426. doi: 10.1016/0041-008X(85)90181-4.
    1. Chan H.M., Zhu L.F., Zhong R., Grant D., Goyer R.A., Cherian M.G. Nephrotoxicity in rats following liver transplantation from cadmium-exposed rats. Toxicol. Appl. Pharmacol. 1993;123:89–96. doi: 10.1006/taap.1993.1225.
    1. Shaikh Z.A., Vu T.T., Zaman K. Oxidative stress as a mechanism of chronic cadmium-induced hepatoxicity and renal toxicity and protection by antioxidants. Toxicol. Appl. Pharmacol. 1999;154:256–263. doi: 10.1006/taap.1998.8586.
    1. Goyer R.A., Miller C.R., Zhu S.-Y., Victery W. Non-metallothionein-bound cadmium in the pathogenesis of cadmium nephrotoxicity in the rat. Toxicol. Appl. Pharmacol. 1989;101:232–244. doi: 10.1016/0041-008X(89)90272-X.
    1. Liu Y., Liu J., Habeebu S.S.M., Klaasen C.D. Metallothionein protects against the nephrotoxicity produced by chronic CdMT exposure. Toxicol. Sci. 1999;50:221–227. doi: 10.1093/toxsci/50.2.221.
    1. Vestergaard P., Shaikh Z.A. The nephrotoxicity of intravenously administered cadmium-metallothionein: Effect of dose, mode of administration, and preexisting renal cadmium burden. Toxicol. Appl. Pharmacol. 1994;126:240–247. doi: 10.1006/taap.1994.1113.
    1. Min K.S., Onosaka S., Tanaka K. Renal accumulation of cadmium and nephropathy following long-term administration of cadmium-metallothionein. Toxicol. Appl. Pharmacol. 1996;141:102–109. doi: 10.1016/S0041-008X(96)80014-7.
    1. Price R.G. The role of NAG (N-acetyl-β-D-glucosaminidase) in the diagnosis of kidney disease including the monitoring of nephrotoxicity. Clin. Nephrol. 1992;38:S14–S19.
    1. Bernard A., Thielemans N., Roels H., Lauwerys R. Association between NAG-B and cadmium in urine with no evidence of a threshold. Occup. Environ. Med. 1995;52:177–180. doi: 10.1136/oem.52.3.177.
    1. Jin T., Nordberg G., Wu X., Kong Q., Wang Z., Zhuang F., Cai S. Urinary N-acetyl-beta-D-glucosaminidase isoenzymes as biomarker of renal dysfunction caused by cadmium in a general population. Environ. Res. 1999;81:167–173. doi: 10.1006/enrs.1999.3959.
    1. Tassi C., Abbritti G., Mancuso F., Morucci P., Feligioni L., Muzi G. Activity and isoenzyme profile of N-acetyl-beta-D-glucosaminidase in urine from workers exposed to cadmium. Clin. Chim. Acta. 2000;299:55–64. doi: 10.1016/S0009-8981(00)00276-X.
    1. Prozialeck W.C., Edwards J.R. Early biomarkers of cadmium exposure and nephrotoxicity. Biometals. 2010;23:793–809. doi: 10.1007/s10534-010-9288-2.
    1. Prozialeck W.C., Vaidya V.S., Liu J., Waalkes M.P., Edwards J.R., Lamar P.C., Bernard A.M., Dumont X., Bonventre J.V. Kidney injury molecule-1 is an early biomarker of cadmium nephrotoxicity. Kidney Int. 2007;72:985–993. doi: 10.1038/sj.ki.5002467.
    1. Prozialeck W.C., Edwards J.R., Vaidya V.S., Bonventre J.V. Preclinical evaluation of novel urinary biomarkers of cadmium nephrotoxicity. Toxicol. Appl. Pharmacol. 2009;238:301–305. doi: 10.1016/j.taap.2009.01.012.
    1. Prozialeck W.C., Edwards J.R., Lamar P.C., Liu J., Vaidya V.S., Bonventre J.V. Expression of kidney injury molecule-1 (Kim-1) in relation to necrosis and apoptosis during the early stages of Cd-induced proximal tubular injury. Toxicol. Appl. Pharmacol. 2009;238:306–314. doi: 10.1016/j.taap.2009.01.016.
    1. Pennemans V., De Winter L.M., Munters E., Nawrot T.S., Van Kerhove E., Rigo J.-M., Reynders C., Dewitte H., Carleer R., Penders J., et al. The association between urinary kidney injury molecule 1 and urinary cadmium in elderly during long-term, low-dose cadmium exposure: A pilot study. Environ. Health. 2011;10:77. doi: 10.1186/1476-069X-10-77.
    1. Ruangyuttikarn W., Panyamoon A., Nambunmee K., Honda R., Swaddiwudhipong W., Nishijo M. Use of the kidney injury molecule-1 as a biomarker for early detection of renal tubular dysfunction in a population chronically exposed to cadmium in the environment. Springerplus. 2013;2:533. doi: 10.1186/2193-1801-2-533.
    1. Zhang Y., Wang P., Liang X., Chuen S., Tan J., Wang J., Huang Q., Huang R., Li Z., Chen W., et al. Associations between urinary excretion of cadmium and renal biomarkers in nonsmoking females: A cross-sectional study in rural areas of South China. Int. J. Environ. Res. Public Health. 2015;12:11988–12001. doi: 10.3390/ijerph121011988.
    1. Chaumont A., Voisin C., Deumer G., Haufroid V., Annesi-Maesano I., Roels H., Thijs L., Staessen J., Bernard A. Associations of urinary cadmium with age and urinary proteins: Further evidence of physiological variations unrelated to metal accumulation and toxicity. Environ. Health Perspect. 2013;121:1047–1053. doi: 10.1289/ehp.1306607.
    1. Nomiyama K., Foulkes E.C. Reabsorption of filtered cadmium-metallothionein in the rabbit kidney. Proc. Soc. Exp. Biol. Med. 1977;156:97–99. doi: 10.3181/00379727-156-39883.
    1. Tanimoto A., Hamada T., Koide O. Cell death and regeneration of renal proximal tubular cells in rats with subchronic cadmium intoxication. Toxicol. Pathol. 1993;21:341–352. doi: 10.1177/019262339302100401.
    1. Roels H.A., Lauwerys R.R., Buchyet J.-P., Bernard A., Chettle D.R., Harvey T.C., Al-Haddad I.K. In vivo measurement of liver and kidney cadmium in workers exposed to this metal: Its significance with respect to cadmium in blood and urine. Environ. Res. 1981;26:217–240. doi: 10.1016/0013-9351(81)90199-7.
    1. Weaver V.M., Kim N.-S., Jaar B.G., Schwartz B.S., Parsons P.J., Steuerwald A.J., Todd A.C., Simon D., Lee B.-K. Associations of low-level urine cadmium with kidney function in lead workers. Occup. Environ. Med. 2011;68:250–256. doi: 10.1136/oem.2010.056077.
    1. Buser M.C., Ingber S.Z., Raines N., Fowler D.A., Scinicariello F. Urinary and blood cadmium and lead and kidney function: NHANES 2007–2012. Int. J. Hyg. Environ. Health. 2016;219:261–267. doi: 10.1016/j.ijheh.2016.01.005.
    1. Jin R., Zhu X., Shrubsole M.J., Yu C., Xia Z., Dai Q. Associations of renal function with urinary excretion of metals: Evidence from NHANES 2003–2012. Environ. Int. 2018;121:1355–1362. doi: 10.1016/j.envint.2018.11.002.
    1. Kawada T., Koyama H., Suzuki S. Cadmium, NAG activity, and β2-microglobulin in the urine of cadmium pigment workers. Br. J. Ind. Med. 1989;46:52–55.
    1. Kawada T., Shinmyo R.R., Suzuki S. Urinary cadmium and N-acetyl-β-D-glucosaminidase excretion of inhabitants living in a cadmium-polluted area. Int. Arch. Occup. Environ. Health. 1992;63:541–546. doi: 10.1007/BF00386343.
    1. Koyama H., Satoh H., Suzuki S., Tohyama C. Increased cadmium excretion and its relationship to urinary N-acetyl-β-D-glucosaminidase activity in smokers. Arch. Toxicol. 1992;66:598–601. doi: 10.1007/BF01973392.
    1. Thomas L.D., Hodgson S., Nieuwenhuijsen M., Jarup L. Early kidney damage in a population exposed to cadmium and other heavy metals. Environ. Health Perspect. 2009;117:181–184. doi: 10.1289/ehp.11641.
    1. Wang D., Sun H., Wu Y., Zhou Z., Ding Z., Chen X., Xu Y. Tubular and glomerular kidney effects in the Chinese general population with low environmental cadmium exposure. Chemosphere. 2016;147:3–8. doi: 10.1016/j.chemosphere.2015.11.069.
    1. Akesson A., Lundh T., Vahter M., Bjellerup P., Lidfeldt J., Nerbrand C., Samsioe G., Strömberg U., Skerfving S. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Environ. Health Perspect. 2005;113:1627–1631. doi: 10.1289/ehp.8033.
    1. Eom S.-Y., Seo M.-N., Lee Y.-S., Park K.-S., Hong Y.-S., Sohn S.-J., Kim Y.-D., Choi B.-S., Lim J.-A., Kwon H.-J., et al. Low-level environmental cadmium exposure induces kidney tubule damage in the general population of Korean adults. Arch. Environ. Contam. Toxicol. 2017;73:401–409. doi: 10.1007/s00244-017-0443-4.
    1. Swaddiwudhipong W., Limpatanachote P., Mahasakpan P., Krintratun S., Punta B., Funkhiew T. Progress in cadmium-related health effects in persons with high environmental exposure in northwestern Thailand: A five-year follow-up. Environ. Res. 2012;112:194–198. doi: 10.1016/j.envres.2011.10.004.
    1. Piscator M. Long-term observations on tubular and glomerular function in cadmium-exposed persons. Environ. Health Perspect. 1984;54:175–179. doi: 10.1289/ehp.8454175.
    1. Roels H.A., Lauwerys R.R., Buchyet J.P., Bernard A.M., Vos A., Oversteyns M. Health significance of cadmium induced renal dysfunction: A five year follow up. Br. J. Ind. Med. 1989;46:755–764. doi: 10.1136/oem.46.11.755.
    1. Jarup L., Persson B., Elinder C.G. Decreased glomerular filtration rate in solderers exposed to cadmium. Occup. Environ. Med. 1995;52:818–822. doi: 10.1136/oem.52.12.818.
    1. Mason H.J., Davison A.G., Wright A.L., Guthrie C.J.G., Fayers P.M., Venables K.M., Smith N.J., Chettle D.R., Franklin D.M., Scott M.C., et al. Relations between liver cadmium, cumulative exposure, and renal function in cadmium alloy workers. Br. J. Ind. Med. 1988;45:793–802. doi: 10.1136/oem.45.12.793.
    1. Satarug S., Moore M.R. Adverse health effects of chronic exposure to low-level cadmium in foodstuffs and cigarette smoke. Environ. Health Perspect. 2004;112:1099–1103. doi: 10.1289/ehp.6751.
    1. Schnaper H.W. The tubulointerstitial pathophysiology of progressive kidney disease. Adv. Chronic Kidney Dis. 2017;24:107–116. doi: 10.1053/j.ackd.2016.11.011.
    1. Schardijn G.H.C., Statius van Eps L.W. β2-microglobulin: Its significance in the evaluation of renal function. Kidney Int. 1987;32:635–641. doi: 10.1038/ki.1987.255.
    1. Hall P.W., III, Chung-Park M., Vacca C.V., London M., Crowley A.Q. The renal handling of beta2-microglobulin in the dog. Kidney Int. 1982;22:156–161. doi: 10.1038/ki.1982.147.
    1. Gauthier C., Nguyen-Simonnet H., Vincent C., Revillard J.-P., Pellet M.V. Renal tubular absorption of β2-microglobulin. Kidney Int. 1984;26:170–175. doi: 10.1038/ki.1984.151.
    1. Norden A.G.W., Lapsley M., Lee P.J., Pusey C.D., Scheinman S.J., Tam F.W.K., Thakker R.V., Unwin R.J., Wrong O. Glomerular protein sieving and implications for renal failure in Fanconi syndrome. Kidney Int. 2001;60:1885–1892. doi: 10.1046/j.1523-1755.2001.00016.x.
    1. Wibell L., Evrin P.-E., Berggard J. Serum β2-microglobulin in renal disease. Nephron. 1973;10:320–331. doi: 10.1159/000180203.
    1. Wibell L.B. Studies on β2-microglobulin in patients and normal subjects. Acta Clin. Belg. 1976;31:14–26.
    1. Wibell L. The serum level and urinary excretion of β2-microglobulin in health and renal disease. Pathol. Biol. (Paris) 1978;26:295–301.
    1. Hall P.W., III, Ricanati E.S. Renal handling of β2-microglobulin in renal disorders with special reference to hepatorenal syndrome. Nephron. 1981;27:62–66. doi: 10.1159/000182026.
    1. Portman R.J., Kissane J.M., Robson A.M. Use of β2-microglobulin to diagnose tubulo-interstitial renal lesions in children. Kidney Int. 1986;30:91–98. doi: 10.1038/ki.1986.156.
    1. Bernard A. Renal dysfunction induced by cadmium: Biomarkers of critical effects. Biometals. 2004;17:519–523. doi: 10.1023/B:BIOM.0000045731.75602.b9.
    1. Nogawa K., Kobayashi E., Honda R. A study of the relationship between cadmium concentrations in urine and renal effects of cadmium. Environ. Health Perspect. 1979;28:161–168. doi: 10.1289/ehp.7928161.
    1. Ikeda M., Ezaki T., Moriguchi J., Fukui Y., Ukai H., Okamoto S., Sakurai H. The threshold cadmium level that causes a substantial increase in β2-microglobulin in urine of general populations. Tohoku J. Exp. Med. 2005;205:247–261. doi: 10.1620/tjem.205.247.
    1. Peterson P.A., Evrin P.-E., Berggard I. Differentiation of glomerular, tubular, and normal proteinuria: Determinations of urinary excretion of β2-microglobulin, albumin, and total protein. J. Clin. Investig. 1969;48:1189–1198. doi: 10.1172/JCI106083.
    1. Elinder C.G., Edling C., Lindberg E., Agedal B.K., Vesterberg A. Assessment of renal function in workers previously exposed to cadmium. Br. J. Ind. Med. 1985;42:754–760. doi: 10.1136/oem.42.11.754.
    1. Norden A.G.W., Lapsley M., Unwin R.J. Urine retinol-binding protein 4: A functional biomarker of the proximal renal tubule. Adv. Clin. Chem. 2014;63:85–122.
    1. Blaner W.S. Retinol-binding protein: The serum transport protein for vitamin A. Endocri. Rev. 1989;10:308–316. doi: 10.1210/edrv-10-3-308.
    1. Pallet N., Chauvet S., Chasse J.-F., Vincent M., Avilloach P., Levi C., Meas-Yedid V., Olivo-Marin J.-C., Nga-Matsogo D., Beaune P., et al. Urinary retinol binding protein is a marker of the extent of interstitial kidney fibrosis. PLoS ONE. 2014;9:e84708. doi: 10.1371/journal.pone.0084708.
    1. Bernard A., Vyskocyl A., Mahieu P., Lauwerys R. Effect of renal insufficiency on the concentration of free retinol-binding protein in urine and serum. Clin. Chim. Acta. 1988;171:85–94. doi: 10.1016/0009-8981(88)90293-8.
    1. Jarup L., Akesson A. Current status of cadmium as an environmental health problem. Toxicol. Appl. Pharmacol. 2009;238:201–208. doi: 10.1016/j.taap.2009.04.020.
    1. Heymsfield S.B., Arteaga C., McManus C., Smith J., Moffitt S. Measurement of muscle mass in humans: Validity of the 24-hour urinary creatinine method. Am. J. Clin. Nutr. 1983;37:478–494. doi: 10.1093/ajcn/37.3.478.
    1. Jenny-Burri J., Haldimann M., Bruschweiler B.J., Bochuyd M., Burnier M., Paccaud F., Dudler V. Cadmium body burden of the Swiss population. Food Addit. Contam. Part A Chem. Anal. Control. Expo. Risk Assess. 2015;32:1265–1272. doi: 10.1080/19440049.2015.1051137.
    1. Chevalier R.L., Forbes M.S. Generation and evolution of atubular glomeruli in the progression of renal disorders. J. Am. Soc. Nephrol. 2008;19:197–206. doi: 10.1681/ASN.2007080862.
    1. Ferenbach D.A., Bonventre J.V. Acute kidney injury and chronic kidney disease: From the laboratory to the clinic. Nephrol. Ther. 2016;12(Suppl. 1):S41–S48. doi: 10.1016/j.nephro.2016.02.005.
    1. Zammouri A., Barbouch S., Najjar M., Aoudia R., Jaziri F., Kaaroud H., Hedri H., Abderrahim E., Goucha R., Hamida F.B., et al. Tubulointerstitial nephritis due to sarcoidosis: Clinical, laboratory, and histological features and outcome in a cohort of 24 patients. Saudi J. Kidney Dis. Transpl. 2019;30:1276–1284. doi: 10.4103/1319-2442.275471.
    1. Goules A., Geetha D., Arend L.J., Baer A.N. Renal involvement in primary Sjogren’s syndrome: Natural history and treatment outcome. Clin. Exp. Rheumatol. 2019;37(Suppl. 118):S123–S132.
    1. Jasiek M., Karras A., Le Guern V., Krastinova E., Mesbah R., Faguer S., Jourde-Chiche N., Fauchais A.-L., Chiche L., Dernis E., et al. A multicentre study of 95 biopsy-proven cases of renal disease in primary Sjogren’s syndrome. Rheumatology. 2017;56:362–370. doi: 10.1093/rheumatology/kew376.
    1. Kelly C.J., Neilson E.G. Tubulointerstitial diseases. In: Taal M.W., Chertow G.M., Marsden P.A., Skorecki K., Alan S.L., Brenner B.M., editors. Brenner & Rector’s The Kidney. 10th ed. Elsevier; Philadelphia, PA, USA: 2011. pp. 1209–1230.
    1. Nath K.A. Tubulointerstitial changes as a major determinant in the progression of renal damage. Am. J. Kidney Dis. 1992;20:1–17. doi: 10.1016/S0272-6386(12)80312-X.
    1. Risdon R.A., Sloper J.C., De Wardener H.E. Relationship between renal function and histological changes found in renal-biopsy specimens from patients with persistent glomerular nephritis. Lancet. 1968;292:363–366. doi: 10.1016/S0140-6736(68)90589-8.
    1. Schainuck L.I., Striker G.E., Cutler R.E., Benditt E.P. Structural-functional correlations in renal disease: Part II: The correlations. Human Pathol. 1970;1:631–641. doi: 10.1016/S0046-8177(70)80061-2.
    1. Bohle A., von Gise H., Mackensen-Haen S., Stark-Jakob B. The obliteration of the postglomerular capillaries and its influence upon the function of both glomeruli and tubuli. Functional interpretation of morphologic findings. Klin. Wochenschr. 1981;59:1043–1051. doi: 10.1007/BF01747747.
    1. Baba H., Tsuneyama K., Kumada T., Aoshima K., Imura J. Histopathological analysis for osteomalacia and tubulopathy in itai-itai disease. J. Toxicol. Sci. 2014;39:91–96. doi: 10.2131/jts.39.91.
    1. Yasuda M., Miwa A., Kitagawa M. Morphometric studies of renal lesions in itai-itai disease: Chronic cadmium nephropathy. Nephron. 1995;69:14–19. doi: 10.1159/000188354.
    1. Saito H., Shioji R., Hurukawa Y., Nagai K., Arikawa T. Cadmium-induced proximal tubular dysfunction in a cadmium-polluted area. Contrib. Nephrol. 1977;6:1–12.
    1. Nogawa K., Ishizaki A., Fukushima M., Shibata I., Hagino N. Studies on the women with acquired Fanconi syndrome observed in the Ichi River basin polluted by cadmium. Environ. Res. 1975;10:280–307. doi: 10.1016/0013-9351(75)90090-0.
    1. Rappaport S.M., Smith M.T. Environment and disease risks. Science. 2010;330:460–461. doi: 10.1126/science.1192603.
    1. Lee J., Oh S., Kang H., Kim S., Lee G., Li L., Kim C.T., An J.N., Oh Y.K., Lim C.S., et al. Environment-wide association study of CKD. Clin. J. Am. Soc. Nephrol. 2020;15:766–775. doi: 10.2215/CJN.06780619.
    1. Soderland P., Lovekar S., Weiner D.E., Brooks D.R., Kaufman J.S. Chronic kidney disease associated with environmental toxins and exposures. Adv. Chronic Kidney Dis. 2010;17:254–264. doi: 10.1053/j.ackd.2010.03.011.
    1. Chevalier R.L. The proximal tubule is the primary target of injury and progression of kidney disease: Role of the glomerulotubular junction. Am. J. Physiol. Renal. Physiol. 2016;311:F145–F161. doi: 10.1152/ajprenal.00164.2016.
    1. Crowley S.D., Coffman T.M. The inextricable role of the kidney in hypertension. J. Clin. Investig. 2014;124:2341–2347.
    1. Nakhoul N., Batuman V. Role of proximal tubules in the pathogenesis of kidney disease. Contrib. Nephrol. 2011;169:37–50.
    1. De Nicola L., Zoccali C. Chronic kidney disease prevalence in the general population: Heterogeneity and concerns. Nephrol. Dial. Transplant. 2016;31:331–335. doi: 10.1093/ndt/gfv427.
    1. Glassock R.J., David G., Warnock D.G., Delanaye P. The global burden of chronic kidney disease: Estimates, variability and pitfalls. Nat. Rev. Nephrol. 2017;13:104–114. doi: 10.1038/nrneph.2016.163.
    1. Chen T.K., Knicely D.H., Grams M.E. Chronic kidney disease diagnosis and management: A review. JAMA. 2019;322:1294–1304. doi: 10.1001/jama.2019.14745.
    1. Lees J.S., Welsh C.E., Celis-Morales C.A., Mackay D., Lewsey J., Gray S.R., Lyall D.M., Cleland J.G., Gill J.M.R., Jhund P.S., et al. Glomerular filtration rate by differing measures, albuminuria and prediction of cardiovascular disease, mortality and end-stage kidney disease. Nat. Med. 2019;25:1753–1760. doi: 10.1038/s41591-019-0627-8.
    1. Sarnak M.J., Amann K., Bangalore S., Cavalcante J.L., Charytan D.M., Craig J.C., Gill J.S., Hlatky M.A., Jardine A.G., Landmesser U., et al. Chronic kidney disease and coronary artery disease: JACC state-of-the-art review. J. Am. Coll. Cardiol. 2019;74:1823–1838. doi: 10.1016/j.jacc.2019.08.1017.
    1. Liu Y., Lv P., Jin H., Cui W., Niu C., Zhao M., Fan C., Teng Y., Pan B., Peng Q., et al. Association between low estimated glomerular filtration rate and risk of cerebral small-vessel diseases: A meta-analysis. J. Stroke Cerebrovasc. Dis. 2016;25:710–716. doi: 10.1016/j.jstrokecerebrovasdis.2015.11.016.
    1. Kelly D.M., Rothwell P.M. Does chronic kidney disease predict stroke risk independent of blood pressure? A systematic review and meta-regression. Stroke. 2019;50:3085–3092. doi: 10.1161/STROKEAHA.119.025442.
    1. Akoudad S., Sedaghat S., Hofman A., Koudstaal P.J., van der Lugt A., Ikram M.A., Vernooij M.W. Kidney function and cerebral small vessel disease in the general population. Int. J. Stroke. 2015;10:603–608. doi: 10.1111/ijs.12465.
    1. Sedaghat S., Ding J., Eiriksdottir G., van Buchem M.A., Sigurdsson S., Ikram M.A., Meirelles O., Gudnason V., Levey A.S., Launer L.J. The AGES-Reykjavik study suggests that change in kidney measures is associated with subclinical brain pathology in older community-dwelling persons. Kidney Int. 2018;94:608–615. doi: 10.1016/j.kint.2018.04.022.
    1. White C.A., Allen C.M., Akbari A., Collier C.P., Holland D.C., Day A.G., Knoll G.A. Comparison of the new and traditional CKD-EPI GFR estimation equations with urinary inulin clearance: A study of equation performance. Clin. Chim. Acta. 2019;488:189–195. doi: 10.1016/j.cca.2018.11.019.
    1. George C., Mogueo A., Okpechi I., Echouffo-Tcheugui J.B., Kengne A.P. Chronic kidney disease in low-income to middle-income countries: The case for increased screening. BMJ Glob. Health. 2017;2:e000256. doi: 10.1136/bmjgh-2016-000256.
    1. Payton M., Hu H., Sparrow D., Weiss S.T. Low-level lead exposure and renal function in the Normative Aging Study. Am. J. Epidemiol. 1994;140:821–829. doi: 10.1093/oxfordjournals.aje.a117330.
    1. Navas-Acien A., Tellez-Plaza M., Guallar E., Muntner P., Silbergeld E., Jaar B., Weaver V. Blood cadmium and lead and chronic kidney disease in US adults: A joint analysis. Am. J. Epidemiol. 2009;170:1156–1164. doi: 10.1093/aje/kwp248.
    1. Zhu X.J., Wang J.J., Mao J.H., Shu Q., Du L.Z. Relationships between cadmium, lead and mercury levels and albuminuria: Results from the National Health and Nutrition Examination Survey Database 2009−2012. Am. J. Epidemiol. 2019;188:1281–1287. doi: 10.1093/aje/kwz070.
    1. Harari F., Sallsten G., Christensson A., Petkovic M., Hedblad B., Forsgard N., Melander O., Nilsson P.M., Borné Y., Engström G., et al. Blood lead levels and decreased kidney function in a population-based cohort. Am. J. Kidney Dis. 2018;72:381–389. doi: 10.1053/j.ajkd.2018.02.358.
    1. Sommar J.N., Svensson M.K., Björ B.M., Elmståhl S.I., Hallmans G., Lundh T., Schön S.M., Skerfving S., Bergdahl I.A. End-stage renal disease and low level exposure to lead, cadmium and mercury; a population-based, prospective nested case-referent study in Sweden. Environ. Health. 2013;12:9. doi: 10.1186/1476-069X-12-9.
    1. Satarug S., Swaddiwudhipong W., Ruangyuttikarn W., Nishijo M., Ruiz P. Modeling cadmium exposures in low- and high-exposure areas in Thailand. Environ. Health Perspect. 2013;121:531–536. doi: 10.1289/ehp.1104769.
    1. Swaddiwudhipong W., Nguntra P., Kaewnate Y., Mahasakpan P., Limpatanachote P., Aunjai T., Jeekeeree W., Punta B., Funkhiew T., Phopueng I. Human health effects from cadmium exposure: Comparison between persons living in cadmium-contaminated and non-contaminated areas in northwestern Thailand. Southeast Asian J. Trop. Med. Public Health. 2015;46:133–142.
    1. Sun Y., Sun D., Zhou Z., Zhu G., Lei L., Zhang H., Chang X., Jin T. Estimation of benchmark dose for bone damage and renal dysfunction in a Chinese male population occupationally exposed to lead. Ann. Occup. Hyg. 2008;52:527–533.
    1. Chen X., Zhu G., Wang Z., Zhou H., He P., Liu Y., Jin T. The association between lead and cadmium co-exposure and renal dysfunction. Ecotoxicol. Environ. Saf. 2019;173:429–435. doi: 10.1016/j.ecoenv.2019.01.121.
    1. Kim N.H., Hyun Y.Y., Lee K.B., Chang Y., Ryu S., Oh K.H., Ahn C. Environmental heavy metal exposure and chronic kidney disease in the general population. J. Korean Med. Sci. 2015;30:272–277. doi: 10.3346/jkms.2015.30.3.272.
    1. Myong J.P., Kim H.R., Baker D., Choi B. Blood cadmium and moderate-to-severe glomerular dysfunction in Korean adults: Analysis of KNHANES 2005−2008 data. Int. Arch. Occup. Environ. Health. 2012;85:885–893. doi: 10.1007/s00420-012-0737-9.
    1. Chung S., Chung J.H., Kim S.J., Koh E.S., Yoon H.E., Park C.W., Chang Y.S., Shin S.J. Blood lead and cadmium levels and renal function in Korean adults. Clin. Exp. Nephrol. 2014;18:726–734. doi: 10.1007/s10157-013-0913-6.
    1. Lim H., Lim J.A., Choi J.H., Kwon H.J., Ha M., Kim H., Park J.D. Associations of low environmental exposure to multiple metals with renal tubular impairment in Korean adults. Toxicol. Res. 2016;32:57–64. doi: 10.5487/TR.2016.32.1.057.
    1. Hambach R., Lison D., D’Haese P.C., Weyler J., De Graef E., De Schryver A., Lamberts L.V., van Sprundel M. Co-exposure to lead increases the renal response to low levels of cadmium in metallurgy workers. Toxicol. Lett. 2013;222:233–238. doi: 10.1016/j.toxlet.2013.06.218.
    1. Ferraro P.M., Sturniolo A., Naticchia A., D’Alonzo S., Gambaro G. Temporal trend of cadmium exposure in the United States population suggests gender specificities. Intern. Med. J. 2012;42:691–697. doi: 10.1111/j.1445-5994.2011.02627.x.
    1. Agarwal S., Zaman T., Tuzcu E.M., Kapadia S.R. Heavy metals and cardiovascular disease: Results from the National Health and Nutrition Examination Survey (NHANES) 1999–2006. Angiology. 2011;62:422–429. doi: 10.1177/0003319710395562.
    1. Hecht E.M., Arheart K.L., Lee D.J., Hennekens C.H., Hlaing W.M. Interrelation of cadmium, smoking, and cardiovascular disease (from the National Health and Nutrition Examination Survey) Am. J. Cardiol. 2016;118:204–209. doi: 10.1016/j.amjcard.2016.04.038.
    1. Hecht E.M., Arheart K.L., Lee D.J., Hennekens C.H., Hlaing W.M. Interrelationships of cadmium, smoking, and angina in the National Health and Nutrition Examination Survey, a cross-sectional study. Cardiology. 2018;141:177–182. doi: 10.1159/000496016.
    1. Chen C., Xun P., Tsinovoi C., McClure L.A., Brockman J., MacDonald L., Cushman M., Cai J., Kamendulis L., Mackey J., et al. Urinary cadmium concentration and the risk of ischemic stroke. Neurology. 2018;91:e382–e391. doi: 10.1212/WNL.0000000000005856.
    1. Gallagher C.M., Chen J.J., Kovach J.S. Environmental cadmium and breast cancer risk. Aging (Albany NY) 2010;2:804–814. doi: 10.18632/aging.100226.
    1. Tellez-Plaza M., Navas-Acien A., Menke A., Crainiceanu C.M., Pastor-Barriuso R., Guallar E. Cadmium exposure and all-cause and cardiovascular mortality in the U.S. general population. Environ. Health Perspect. 2012;120:1017–1022. doi: 10.1289/ehp.1104352.
    1. Menke A., Muntner P., Silbergeld E.K., Platz E.A., Guallar E. Cadmium levels in urine and mortality among U.S. adults. Environ. Health Perspect. 2009;117:190–196. doi: 10.1289/ehp.11236.
    1. Adams S.V., Passarelli M.N., Newcomb P.A. Cadmium exposure and cancer mortality in the Third National Health and Nutrition Examination Survey cohort. Occup. Environ. Med. 2012;69:153–156. doi: 10.1136/oemed-2011-100111.
    1. Hyder O., Chung M., Cosgrove D., Herman J.M., Li Z., Firoozmand A., Gurakar A., Koteish A., Pawlik T.M. Cadmium exposure and liver disease among US adults. J. Gastrointest. Surg. 2013;17:1265–1273. doi: 10.1007/s11605-013-2210-9.
    1. Min J.Y., Min K.B. Blood cadmium levels and Alzheimer’s disease mortality risk in older US adults. Environ. Health. 2016;15:69. doi: 10.1186/s12940-016-0155-7.
    1. Peng Q., Bakulski K.M., Nan B., Park S.K. Cadmium and Alzheimer’s disease mortality in U.S. adults: Updated evidence with a urinary biomarker and extended follow-up time. Environ. Res. 2017;157:44–51. doi: 10.1016/j.envres.2017.05.011.
    1. Moberg L., Nilsson P.M., Samsioe G., Sallsten G., Barregard L., Engström G., Borgfeldt C. Increased blood cadmium levels were not associated with increased fracture risk but with increased total mortality in women: The Malmö Diet and Cancer Study. Osteoporos Int. 2017;28:2401–2408. doi: 10.1007/s00198-017-4047-7.
    1. Deering K.E., Callan A.C., Prince R.L., Lim W.H., Thompson P.L., Lewis J.R., Hinwood A.L., Devine A. Low-level cadmium exposure and cardiovascular outcomes in elderly Australian women: A cohort study. Int. J. Hyg. Environ. Health. 2018;221:347–354. doi: 10.1016/j.ijheh.2017.12.007.
    1. Suwazono Y., Nogawa K., Morikawa Y., Nishijo M., Kobayashi E., Kido T., Nakagawa H., Nogawa K. All-cause mortality increased by environmental cadmium exposure in the Japanese general population in cadmium non-polluted areas. J. Appl. Toxicol. 2015;35:817–823. doi: 10.1002/jat.3077.
    1. Watanabe Y., Nogawa K., Nishijo M., Sakurai M., Ishizaki M., Morikawa Y., Kido T., Nakagawa H., Suwazono Y. Relationship between cancer mortality and environmental cadmium exposure in the general Japanese population in cadmium non-polluted areas. Int. J. Hyg. Environ. Health. 2020;223:65–70. doi: 10.1016/j.ijheh.2019.10.005.
    1. Maruzeni S., Nishijo M., Nakamura K., Morikawa Y., Sakurai M., Nakashima M., Kido T., Okamoto R., Nogawa K., Suwazono Y., et al. Mortality and causes of deaths of inhabitants with renal dysfunction induced by cadmium exposure of the polluted Jinzu River basin, Toyama, Japan; a 26-year follow-up. Environ. Health. 2014;13:18. doi: 10.1186/1476-069X-13-18.
    1. Nishijo M., Nakagawa H., Suwazono Y., Nogawa K., Sakurai M., Ishizaki M., Kido T. Cancer mortality in residents of the cadmium-polluted Jinzu River basin in Toyama, Japan. Toxics. 2018;6:23. doi: 10.3390/toxics6020023.
    1. van Bemmel D.M., Li Y., McLean J., Chang M.H., Dowling N.F., Graubard B., Rajaraman P. Blood lead levels, ALAD gene polymorphisms, and mortality. Epidemiology. 2011;22:273–278. doi: 10.1097/EDE.0b013e3182093f75.
    1. Lanphear B.P., Rauch S., Auinger P., Allen R.W., Hornung R.W. Low-level lead exposure and mortality in US adults: A population-based cohort study. Lancet Public Health. 2018;3:e177–e184. doi: 10.1016/S2468-2667(18)30025-2.
    1. Aoki Y., Brody D.J., Flegal K.M. Blood lead and other metal biomarkers as risk factors for cardiovascular disease mortality. Medicine. 2016;95:e2223. doi: 10.1097/MD.0000000000002223.
    1. Kim M.G., Ryoo J.H., Chang S.J., Kim C.B., Park J.K., Koh S.B., Ahn Y.S. Blood lead levels and cause-specific mortality of inorganic lead-exposed workers in South Korea. PLoS ONE. 2015;10:e0140360. doi: 10.1371/journal.pone.0140360.
    1. Min Y.S., Ahn Y.S. The association between blood lead levels and cardiovascular diseases among lead-exposed male workers. Scand. J. Work Environ. Health. 2017;43:385–390. doi: 10.5271/sjweh.3631.

Source: PubMed

Szponzorok és közreműködők

Egészségi állapot

Kábítószer-beavatkozások

3
Iratkozz fel