Indian Journal of Occupational and Environmental Medicine   Official publication of Indian Association of  0ccupational  Health  
 Print this page Email this page   Small font sizeDefault font sizeIncrease font size
 Users Online:164

  IAOH | Subscription | e-Alerts | Feedback | Login 

Home About us Current Issue Archives Search Instructions
  Search
 
   Next article
   Previous article 
   Table of Contents
  
 
    Similar in PUBMED
     Search Pubmed for
     Search in Google Scholar for
    Article in PDF (166 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  


   Environmental Le...
   Occupational Lea...
   Biomarkers of Ne...
   Glomerular Filtr...
   References
   Article Tables

 Article Access Statistics
    Viewed6364    
    Printed290    
    Emailed0    
    PDF Downloaded454    
    Comments [Add]    
    Cited by others 44    

Recommend this journal

 


 
EDITORIAL
Year : 2008  |  Volume : 12  |  Issue : 3  |  Page : 103-106
 

Renal effects of environmental and occupational lead exposure


CSIR Emeritus Scientist (Former Deputy Director and Head Epidemiological Section), Indian Institute of Toxicology Research, Post Box No. 80, Mahatma Gandhi Marg, Lucknow - 226 001, India

Correspondence Address:
S K Rastogi
CSIR Emeritus Scientist (Former Deputy Director and Head Epidemiological Section), Indian Institute of Toxicology Research, Post Box No. 80, Mahatma Gandhi Marg, Lucknow - 226 001
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5278.44689

Rights and Permissions

 



How to cite this article:
Rastogi S K. Renal effects of environmental and occupational lead exposure. Indian J Occup Environ Med 2008;12:103-6

How to cite this URL:
Rastogi S K. Renal effects of environmental and occupational lead exposure. Indian J Occup Environ Med [serial online] 2008 [cited 2022 Jan 22];12:103-6. Available from: https://www.ijoem.com/text.asp?2008/12/3/103/44689


Lead is one of the most useful elements in industry, but serves no useful function in the human body. Environmental and industrial lead exposures continue to pose major public health problems in the exposed population. [1] Over the years, it has become increasingly evident that low-level lead exposure resulting in blood lead levels between 10 and 15 µg/dL can lead to deleterious effects like cognitive impairment and behavioral deficits, high blood pressure (BP) and impaired renal function. [2],[3] Lancereaux [4] provided the first description of kidney disease and interstitial nephritis by postmortem examination of a lead-poisoned artist. It was not until the late 1920s when an epidemic of chronic nephritis in Queensland, Australia, was linked to childhood lead poisoning that the full spectrum of lead-induced nephropathy became apparent. [5],[6] This was followed by cases of renal diseases from the US in individuals consuming lead-contaminated illegally distilled moonshine whisky. [7]


  Environmental Lead Exposure Top


Environmental lead exposure continues to be a public health problem. In the past, lead-based paint was a major source of lead poisoning among children. The painted surfaces of old houses contained significant amounts of lead. Direct ingestion of lead paint, lead-contaminated house dust and water by children has been identified as a major contributor to lead poisoning among the children. Many studies have confirmed that lead-contaminated dust is a major determinant of lead concentrations in blood. [8] Similarly, a highly significant correlation between lead concentration in drinking water and blood lead concentrations has been reported. [9] Children are more susceptible to the effects of environmental lead than adults because of the increased gastrointestinal absorption of lead in children. Children are more vulnerable because they absorb lead 5-10 times more effectively than adults and have a greater exposure because of their exploratory behavior and frequent hand to mouth activity. [10] Adults at the highest risk are those exposed to lead fumes or dust in the industry. [11],[12]


  Occupational Lead Nephropathy Top


An association between lead poisoning and renal diseases in humans has been recognized and documented by several studies. [8],[12],[13] Elemental lead and inorganic lead compounds are absorbed by ingestion or inhalation, but organic lead compounds, e.g. tetraethyl lead, may also be absorbed by skin contact. Organic lead compounds are the most toxic. Absorption of lead from the lungs is very efficient, especially if the particles are less than 1 µm in diameter. The gastrointestinal absorption of lead varies with the age of the individual; children absorb around 50% of what they ingest but adults only absorb 10-20% of what they ingest. Lead is very similar to calcium chemically. Thus, once in the body, it is handled as if it were calcium. Lead serves no useful purpose in the human body and its presence in the body can lead to toxic effects, regardless of the exposure pathway.

The kidney is the critical organ after long-term occupational or environmental exposure to lead. Excessive exposure to lead may cause acute or chronic nephrotoxic effects. Two types of nephropathy, acute and chronic nephropathy, have been observed in humans. Acute Pb nephropathy is characterized functionally by a generalized deficit of tubular transport mechanisms (Fanconi syndrome) and morphologically by the appearance of degenerative changes in the tubular epithelium and the nuclear inclusion bodies containing Pb protein complexes. [15],[16] These effects, which are usually reversible with chelation therapy, have been reported mainly in children manifested by glycosuria and aminoaciduria. Chronic occupational exposure to lead has also been linked to a high incidence of renal dysfunction, which is characterized by glomerular and tubulointerstitial changes, resulting in chronic renal failure, hypertension and hyperuricemia. Chronic lead nephropathy is an irreversible renal disease that develops over months or years of excessive exposure. [17],[18] This has been reported in adults who had ingested leaded paint during childhood and those who consumed illicitly distilled alcohol (moonshine whisky). [14],[15] In the chronically exposed adults, Pb nephropathy occurs as a progressive tubulointerstitial nephritis that is difficult to diagnose at the early stage. Incipient Pb nephropathy is not associated with urine abnormalities easily detected by dipsticks. The tests evaluating the glomerular filtration rate (GFR) (creatinine clearance, blood urea nitrogen, serum creatinine) are the only ones that can be used to detect the renal effect caused by the occupational exposure to Pb. [14],[19],[20] But, when these tests are abnormal, the nephropathy has already reached the irreversible phase that may lead to renal sufficiency. [19] Chronic low-level exposure to lead is also associated with an increased urinary excretion of low molecular weight proteins and lysosomal enzymes. [21] Epidemiologic studies have shown an association between blood lead levels and BP, and hypertension is a cardinal feature of lead nephropathy. [13],[20],[22],[24]

Most lead-associated renal effects or toxicity are a result of the ongoing chronic or current high acute exposure. They can also be attributable to a previous chronic lead exposure. The lowest level at which Pb has an adverse effect on the kidney remains unknown. Both glomerular and tubular effects have been reported. [20] The glomerular effects range from an increased prevalence of high molecular weight proteinuria to a nephrotic syndrome. [18],[23] The reported tubular changes consist of an enhanced urinary excretion of enzymes.


  Biomarkers of Nephrotoxicity Top


The prevention of renal diseases induced by exposure to industrial or environmental Pb largely relies on the capability to detect nephrotoxic effects at a stage when they are still reversible or at least not yet compromising the renal function. During the past decade, various tests have been proposed for the early detection of the toxic effects at different sites on the nephron. Some of these tests have been validated and some need epidemiological validation.

Currently, there are some early and sensitive indicators available that are considered predictive or indicative of renal toxicity from lead exposure. Recent studies have shown more than 20 potential markers of renal effects that can be arbitrarily classified into three broad categories. [25],[26],[27],[28] [Table 1] shows the different biomarkers used in Pb-induced nephrotoxicity.

Functional markers

  1. Creatinine in serum (crt-S).


  2. Creatinine in urine (crt-U).


  3. Urinary proteins of low or high molecular weight.

    3.1. High molecular weight proteins - albumin, transferrin, immunoglobulin G.

    3.2. Low molecular weight proteins - retinol-binding protein (URBP), β2 -microglobulin (β2 -m), urinary α-1-microglobin (Uα1m).


  4. Urinary enzymes - N-acetylglucosaminidase (NAG).


  5. Alkaline phosphatase (ALP).


  6. γ-glutamyl transferase (γ-GT).


These are the biological markers of tubular damage, which are characterized by enhanced urinary excretion of α-1-microglobulin, β2- m, RBP, NAG, APL and γ-GT.

Cytotoxicity markers

These include:

  1. The brush border tubular antigens (BBA, BB 50 and HF 5 ).
  2. Enzymes - B-galactosidase.


Exposed Pb workers show an increased leakage of tubular antigens and several enzymes as a sign of renal toxicity. This is in all likelihood a reflection of the damage to the proximal tubular cells.

Biochemical markers

These include:

  1. Eicosanoids - 6-keto-prostaglandin F 1α (6-keto-PGF 1α), prostaglandin F 2α (PGF 2α), prostaglandin E 2 (PGE 2 ).
  2. Thromboxane (TxB 2 ).
  3. Fibronactin.
  4. Urinary sialic acid activity, sialic acid in plasma or in RBCs.
  5. Urinary kallikrein activity.
  6. Urinary glycosaminoglycans (GAG).
  7. Intestinal alkaline phosphate (IAP).


The most outstanding effect found in the workers exposed to Pb is an interference with the renal synthesis of eicosanoids, resulting in a lower urinary excretion of 6-keto-PGFα and an enhanced excretion of TXB 2 . It is generally accepted that the urinary 6-keto-PGF 1α and TXB 2 primarily reflect the glomerular synthesis of prostacyclin and TXA 2 , whereas urinary PGE 2 and PGF 2α are largely contributed by the renal medulla. The decrease in PGE 2 , PGF 2α and enhanced excretion of TXB 2 resulting from biochemical or cytotoxic effects in the medulla and glomeruli represent the earliest renal changes associated with exposure to Pb. [29],[30]

The early effects on urinary excretion of 6-keto-PGFα and TXB 2 suggest that the initial insult in Pb nephropathy might also involve the vasculature and glomeruli and is not exclusively localized in the tubulointerstitial compartment. The changes in the renal synthesis of eicosanoids raises the question of their relevance to health and are indicative of the degenerative process that may lead to a loss of renal function. [32]

Together with the changes in the urinary excretion of eicosanoids, the increased excretion of Tamm-Horsfall glycoprotein (THG) appears as an early renal effect induced by exposure to Pb. This increase could reflect an injury to the epithelial cells of the ascending limb of the Loop of Henle and the most proximal part of the distal convoluted tubules where this glycoprotein is localized. The physiological function of THG is still obverse . It might have several important functions, such as rendering the ascending limb of Henley's loop impermeable to water, transport to sodium, defense against infection or the immuneregulation of several cytokines. [22],[32]

Urinary kallikrein is a serine proteases synthesized by the distal tubular cells, which might serve as an index of distal nephrotoxicity. As most of the kallikreine is associated with the membranes that face the urinary compartment, an increased urinary excretion of kallikrein could result from toxic damage in the distal tubular cells.

The increased urinary excretion of sialic acids appears as a rather early effect of exposure to lead. The GAGs are polysacchrides composed of repetitive disaccharide units. They are found in the glomeruli and the tubules and their leakage into the urine has been suggested to be a marker of injury to the nephron. An increased excretion of GAG has also been suggested to be an indicator of damage to the renal papilla, which is rich in GAG. [24]


  Glomerular Filtration Rate Top


Creatinine clearance, blood urea nitrogen (BUN) and serum creatinine are some of the parameters that can be used to detect the renal effects caused by occupational exposure to Pb. But, when these tests are found abnormal, the nephropathy has already reached the irreversible phase that may lead to renal insufficiency. [17] The renal effects of Pb, consisting mainly in a decline of the GFR without proteinuria, have been reported in workers with a longstanding exposure to Pb, with a Pb-B of 600 µg/L or more. [20] So far, studies conducted on populations of workers with a lower level of exposure to Pb have disclosed no renal effect or only infraclinical changes of marginal significance. [12],[13] In humans, a reduced GFR (i.e. indicated by decreases in the creatinine clearance or increases in the serum creatinine concentration) has been observed in association with exposures resulting in average PbBs < 20ug/dL. However, some studies have shown an increased GFR with Pb exposure. This may represent hyperfiltration, which may contribute to adverse renal effects. Decrements in GFR may contribute to an elevation in the BP, and an elevated BP may predispose people to glomerular disease. These effects may be mechanistically related and, furthermore, can be confounders and covariables in epidemiological studies. [28],[29],[30],[41]

 
  References Top

1.Ekong EB, Jaar BG, Weaver VM. Lead-related nephrotoxicity: A review of the epidemiologic evidence. Kidney Int 2006;70:2074-84.  Back to cited text no. 1    
2.Goyer RA. Lead toxicity: Current concerns. Environ Health Perspect 1993;100:177-87.  Back to cited text no. 2    
3.Muntner P, He J, Vupputuri S, Coresh J, Batuman V. Blood lead and chronic kidney disease in the general United States population: Results from NHANES III. Kidney Int 2003;63:1044-50.  Back to cited text no. 3    
4.Lanceraux E. Arthritis and nephritis lead contamination: Co incidence of these diseases: Paeallele with nephritis and arthritis gouteusses al. Arch Gen Med 1981;6:641-7.  Back to cited text no. 4    
5.Nye L JJ. An investigation of the extraordinary incidence of chronic nephritis in young people in Queensland. Med J Aust 1929;2:145-59.  Back to cited text no. 5    
6.Benett WM. Lead nephropathy. Kidney Int 1985;28:212-20.  Back to cited text no. 6    
7.Morgan JM, Hartley MW, Miller RE. Nephropathy in chronic lead poisoning. Arch Intern Med 1966;118:17-29.   Back to cited text no. 7    
8.Bernard AM, Vyskocil A, Roels H, Kriz J, Kode M, lauwerys R. Renal effects in children living in the vicinity of a lead smelter. Environ Res 1995;68:91-5.  Back to cited text no. 8    
9.Campbell BC, Beattie AD, Moore MR, Goldberg A, Reid AG. Renal insufficiency associated with excessive lead exposure. Br Med J 1977;1:482-85.  Back to cited text no. 9    
10.Goyer RA, Mahaffey KR. Susceptibility to lead toxicity. Environ Health Perspect 1972;2:73-80.  Back to cited text no. 10    
11.Pollock CA, Ibels LS. Lead nephropathy: A preventable cause of renal failure. Int J Artif Organs 1988;11:75-8.  Back to cited text no. 11    
12.Pollock CA, Ibels LS. Lead intoxication in industry. Med J Aust 1986;145:635-9.  Back to cited text no. 12    
13.Adham ML. Renal effects of environmental and occupational lead exposure. Environ Health Perspect 1997;105:928-38.  Back to cited text no. 13    
14.Bennet WM. Lead Nephropathy. Kidney Int 1985;28:212-20.  Back to cited text no. 14    
15.Ritz E, Mann J, Stoeppler M. Lead and the kidney. Adv Nephrol 1988;17:241-74.  Back to cited text no. 15    
16.Goyer RA. Mechanism of lead and cadmium nephrotoxicity. Toxicol Lett 1989;46:153-62.  Back to cited text no. 16    
17.Odigie IP, Ladipo CO, Ettarh RR, Izegbu MC. Effect of chronic exposure to low levels of lead on renal function and renal ultrastructure in SD rats. Niger J Physiol Sci 2004;19:27-32.  Back to cited text no. 17    
18.Lin JL, Tan DT, Hsu KH, Yu CC. Environmental lead exposure and progressive renal insufficiency. Arch Intern Med 2001;161:264-71.  Back to cited text no. 18    
19.Muller PW, Smith AJ, Steinberg KK, Thun M. Chronic renal tubular effects in relation to urine cadmium levels. Nephron 1989;52:45-54.  Back to cited text no. 19    
20.Hommond PB, Lerner SJ, Gartside PS. The relationships of biological indices lead exposure to the health status of worker in a secondary lead smelter. J Occup Med 1980;22:475-84.  Back to cited text no. 20    
21.Yu CC, Lin JL, Lin Tan DT. Environmental exposure to lead and progression of chronic renal diseases: A four-year prospective longitudinal study. J Am Soc Nephrol 2004;15:1016-22.  Back to cited text no. 21    
22.Cardenas A, Roels H, Bernard AM, Barbon R, Buchet JP, Lauwerys RR, et al. Markers of early renal changes induced by industrial pollutants: II, Application to worker exposed to lead. Br J Ind Med 1993;50:28-36.  Back to cited text no. 22    
23.Nikolas CP, Eleftheria GH, Stamatis B, George NT, Aristidis MT. Lead toxicity update: A brief review. Med Sci Monit 2005;11:RA329-36.  Back to cited text no. 23    
24.Goyer RA, Weinberg CR, Victery WM, Miller CR. Lead induced nephrotoxicity: Kideny calcium as an indicator of tubular injury. In: Bach PH, Lock EA, editors. Nephrotoxicity: Invitro to invivo Animals to man. New York: Plenum Press; 1989. p. 11-20.  Back to cited text no. 24    
25.Lilis R, Gavrilescu N, Nestorescu B, Dumitriu C, Roventa A. Nephropathy in chronic lead poisoning. Br J Ind Med 1968;25:196-202.  Back to cited text no. 25    
26.Cramer K, Goyer RA, Jangenburg R, Wilson MH. Renal ultrastructure, renal function, and parameters of lead toxicity in workers with different period of lead exposure. Br J Ind Med 1974;31:113-27.  Back to cited text no. 26    
27.Wedeen RP, Maesaka JK, Weiner B, Lipat GA, Lyons MM, Vitale LF, et al. Occupational lead nephropathy. Am J Med 1975;59:630-41.  Back to cited text no. 27    
28.Wedeen RP, Mallik DK, Batuman V. Detection and treatment of occupational lead nephropathy. Arch Intern Med 1979;139:53-7.  Back to cited text no. 28    
29.Hong CD, Hanenson IB, Lerner S, Hammond PB, Pesce AJ, Pollak VE. Occupational exposure to lead: Effects on renal function. Kidney Int 1980;18:489-94.  Back to cited text no. 29    
30.Lilis R, Fischlrin A, Valciukas JA, Blumberg W, Selikoff IJ. Kidney function and lead: Relationships in several occupational groups with different levels of exposure. Am J Ind Med 1980;1:405-12.  Back to cited text no. 30    
31.de Kort WL, Ver Schoor MA, Wibowo AA, van Hemmen JJ. Occupational exposure to lead and blood pressure: A study of 105 workers. Am J Ind Med 1987;11:145-56.  Back to cited text no. 31    
32.Cardenas A, Roels H, Bernard AM, Barbon R, Buchet JP, Lauwerys RR, et al. Markers of early renal changes induced by industrial pollutants: I application to worker exposed to mercury vapors. Br J Ind Med 1993;50:17-27.  Back to cited text no. 32    
33.Verschoor M, Wibowo A, Herber R, van Hemmen J, Zielhuis R. Influence of occupational low-level lead exposure on renal parameters. Am J Ind Med 1987;12:341-51.  Back to cited text no. 33    
34.Staeseen JA, Yeoman WB, Fletcher AE, Markowe HL, Marmot MG, Rose G, et al. Blood lead concentration, renal function, and blood pressure in London civil servants. Br J Ind Med 1990;47:442-7.  Back to cited text no. 34    
35.Omae K, Sakurai H, Higashi T, Muto T, Ichikawa M, Sasaki N. No adverse effects of lead on renal function in lead exposed workers. Ind Health 1990;28:77-83.  Back to cited text no. 35    
36.Hu H. Knowledge of diagnosis and reproductive history among survivors of childhood plumbism. Am J Public Health 1991;81:1070-2.  Back to cited text no. 36    
37.Kim R, Rotnitzky A, Sparrow D, Weiss S, Wager C, Hu H. A longitudinal study of low-level lead exposure and impairment of renal function: The normative aging study. JAMA 1996;275:1177-81.  Back to cited text no. 37    
38.Fels LM, Wunsch M, Baranowski J, Norska-Borówka I, Price RG, Taylor SA, et al. Adverse effects of chronic low level lead exposure on kidney function: A risk group study in children. Nephrol Dial Transplant 1998;13:2248-56.  Back to cited text no. 38    
39.Hsiao CY, Wu H DI, Lai JS, Kuo HW. A longitudinal study of the effects of long term exposure to lead among lead battery factory workers in Taiwan (1989-1999). Sci Total Environ 2001;279:151-8.  Back to cited text no. 39    
40.Sonmez F, Donmez O, Sonmez HM, Keskinoπlu A, Kabasakal C, Mir S. lead exposure and urinary N-acetyl BD glucosaminidase activity in adolescent workers in auto repair workshops. J Adolesc Health 2002;30:213-6.  Back to cited text no. 40    
41.Muntner P, He J, Vupputuri S, Coresh J, Batuman V. Blood lead and chronic kidney disease in the general United States populations: Results from NHANES III. Kidney Int 2003;63:1044-50.  Back to cited text no. 41    



 
 
    Tables

  [Table 1]


This article has been cited by
1 A preliminary study on health impacts of Mexican mercury mining workers in a context of precarious employment
K. Saldańa-Villanueva, Francisco J. Pérez-Vázquez, Ivette P. Ávila-García, Karen B. Méndez-Rodríguez, Leticia Carrizalez-Yáńez, Arturo Gavilán-García, Juan M. Vargas-Morales, Evelyn Van-Brussel, Fernando Diaz-Barriga
Journal of Trace Elements in Medicine and Biology. 2022; : 126925
[Pubmed] | [DOI]
2 Ionic liquids in biological monitoring for exposure assessments
Arezoo Damokhi, Saeed Yousefinejad, Reza Yarmohammadi, Saeed Jafari
Journal of Molecular Liquids. 2021; 344: 117732
[Pubmed] | [DOI]
3 Clinical biochemical parameters associated with the exposure to multiple environmental metals in residents from Kabwe, Zambia
Hokuto Nakata, Shouta M.M. Nakayama, John Yabe, Kaampwe Muzandu, Haruya Toyomaki, Yared Beyene Yohannes, Andrew Kataba, Golden Zyambo, Yoshinori Ikenaka, Kennedy Choongo, Mayumi Ishizuka
Chemosphere. 2021; 262: 127788
[Pubmed] | [DOI]
4 Association of albumin to creatinine ratio with urinary arsenic and metal exposure: evidence from NHANES 2015–2016
Humairat H. Rahman, Danielle Niemann, Stuart H. Munson-McGee
International Urology and Nephrology. 2021;
[Pubmed] | [DOI]
5 Ameliorative effect of ZnO-NPs against bioaggregation and systemic toxicity of lead oxide in some organs of albino rats
Eman I. Hassanen, Abdel-Azem A. Khalaf, Amr R. Zaki, Marwa A. Ibrahim, Mona K. Galal, Khaled Y. Farroh, Rehab A. Azouz
Environmental Science and Pollution Research. 2021; 28(28): 37940
[Pubmed] | [DOI]
6 Low-level Eexposure to lead dust in unusual work schedules and hematologic, renal, and hepatic parameters
Fateme Kooshki, Masoud Neghab, Esmaeel Soleimani, Jafar Hasanzadeh
Toxicology and Applied Pharmacology. 2021; 415: 115448
[Pubmed] | [DOI]
7 Association of blood lead level with vitamin D binding protein, total and free 25-hydroxyvitamin D levels in middle-school children
Abdur Rahman, Reem Al-Sabah, Reem Jallad, Muddanna S. Rao
British Journal of Nutrition. 2021; : 1
[Pubmed] | [DOI]
8 Effect of chelation therapy on arrhythmogenic and basal ECG parameters of lead exposed workers
Mustafa Karanfil, Meside Gündüzöz, Murat Karakurt, Emre Arugaslan, Mustafa Bilal Özbay, Sefa Ünal, Kürsat Akbuga, Ahmet Akdi, Mehmet Akif Erdöl, Ahmet Göktug Ertem, Çagri Yayla, Özcan Özeke
Archives of Environmental & Occupational Health. 2021; : 1
[Pubmed] | [DOI]
9 Blood Lead Levels of Pregnant Women in Agricultural and Coastal Area: A SDG’s Indicator for Health and Pollution in Brebes District
N A Sakina
IOP Conference Series: Earth and Environmental Science. 2021; 940(1): 012072
[Pubmed] | [DOI]
10 Evaluation of the Role of KIM-1 in Detecting Early Nephrotoxicity in Lead-Exposed Workers
Abo-Bakr Abbas Hussein, Manal Hassan Ahmed, Manal Mohamed Kamal, Narges Abd-El-Atey Ayesh, Marwa Mohammed Fouad
Journal of Occupational & Environmental Medicine. 2021; 63(9): e605
[Pubmed] | [DOI]
11 Evaluation of blood lead among painters of buildings and cars
Ali Ghaffarian-Bahraman, Alireza Taherifard, Abbas Esmaeili, Hassan Ahmadinia, Mohsen Rezaeian
Toxicology and Industrial Health. 2021; : 0748233721
[Pubmed] | [DOI]
12 Issues and Challenges in the Application of the IEUBK Model in the Health Risk Assessment of Lead: A Case Study from Blantyre Malawi
Wells Utembe, Mary Gulumian
International Journal of Environmental Research and Public Health. 2021; 18(15): 8207
[Pubmed] | [DOI]
13 Disrupted Sleep Homeostasis and Altered Expressions of Clock Genes in Rats with Chronic Lead Exposure
Chung-Yao Hsu, Yao-Chung Chuang, Fang-Chia Chang, Hung-Yi Chuang, Terry Ting-Yu Chiou, Chien-Te Lee
Toxics. 2021; 9(9): 217
[Pubmed] | [DOI]
14 Hepatotoxic and neurotoxic effects of combined lead and di-(2-ethylhexyl) phthalate exposure: Activation of total -, Ca2+- and Na+K+- ATPases in the liver of male rats
Omugha Abam Esther, Elizabeth Kuyooro Seun, Abubakar Shawai, Chineyenwa Dim Esther
Journal of Toxicology and Environmental Health Sciences. 2021; 13(1): 18
[Pubmed] | [DOI]
15 Metal Levels, Genetic Instability, and Renal Markers in Electronic Waste Workers in Thailand
Richard L Neitzel, Stephanie K Sayler, Aubrey L Arain, Kowit Nambunmee
The International Journal of Occupational and Environmental Medicine. 2020; 11(2): 72
[Pubmed] | [DOI]
16 Nephrotoxicity Effect in Inhabitants of a Lead-zinc Mining Community, Ebonyi State, Nigeria
Bello H. Tilako, Sylvester O. Ogbodo, Innocent N. Okonkwo, Irene L. Shuneba, Ogbonna Enyinna, Saidi Odoma, Elvis N. Shu
Journal of Biological Sciences. 2020; 20(2): 80
[Pubmed] | [DOI]
17 Lead exposure induces metabolic reprogramming in rat models
Monica Shirley Mani, Manjunath B. Joshi, Rashmi R. Shetty, Venzil Lavie DSouza, M Swathi, Shama Prasada Kabekkodu, Herman Sunil Dsouza
Toxicology Letters. 2020; 335: 11
[Pubmed] | [DOI]
18 Environment-Wide Association Study of CKD
Jeonghwan Lee, Sohee Oh, Habyeong Kang, Sunmi Kim, Gowoon Lee, Lilin Li, Clara Tammy Kim, Jung Nam An, Yun Kyu Oh, Chun Soo Lim, Dong Ki Kim, Yon Su Kim, Kyungho Choi, Jung Pyo Lee
Clinical Journal of the American Society of Nephrology. 2020; 15(6): 766
[Pubmed] | [DOI]
19 Protective effects of spirulina against hemato-biochemical alterations, nephrotoxicity, and DNA damage upon lead exposition
M Gargouri, A Akrouti, C Magné, A El Feki, A Soussi
Human & Experimental Toxicology. 2020; 39(6): 855
[Pubmed] | [DOI]
20 Zinc ameliorates lead toxicity by reducing body Pb burden and restoring Pb-induced haematological and biochemical derangements
Emmanuel Ike Ugwuja, Nweze Vincent, Ikechukwu C Ikaraoha, Samuel R Ohayi
Toxicology Research and Application. 2020; 4: 2397847320
[Pubmed] | [DOI]
21 Herb-Derived Products: Natural Tools to Delay and Counteract Stem Cell Senescence
Provvidenza M. Abruzzo, Silvia Canaider, Valeria Pizzuti, Luca Pampanella, Raffaella Casadei, Federica Facchin, Carlo Ventura
Stem Cells International. 2020; 2020: 1
[Pubmed] | [DOI]
22 Metabolic adaptability in liver and gastrocnemius muscle of mice following subacute lead toxicity
Pritha Das, Sudipta Pal, Surochita Basu
Toxicology and Industrial Health. 2020; 36(7): 487
[Pubmed] | [DOI]
23 Persistent Effects on Cardiorespiratory and Nervous Systems Induced by Long-Term Lead Exposure: Results from a Longitudinal Study
Liana Shvachiy, Vera Geraldes, Ângela Amaro-Leal, Isabel Rocha
Neurotoxicity Research. 2020; 37(4): 857
[Pubmed] | [DOI]
24 Protective effects of andrographolide on lead-induced kidney injury through inhibiting inflammatory and oxidative responses in common carp
Yue Zhang, Peijun Zhang, Peng Yu, Xinchi Shang, Yunhe Fu, Yuting Lu, Yuehong Li
Aquaculture Reports. 2020; 17: 100395
[Pubmed] | [DOI]
25 Halide Perovskite Solar Cells with Biocompatibility
Trishna Debnath, Eun-Kyung Kim, Kwang-Geun Lee, Narayan Chandra Deb Nath
Advanced Energy and Sustainability Research. 2020; 1(1): 2000028
[Pubmed] | [DOI]
26 Evaluation of lead-induced cardiac toxicity in mice by measurement of selected biochemical as well as oxidative indices
Hasan Baghshani, Maryam LotfiGhahramanloo
Comparative Clinical Pathology. 2020; 29(6): 1165
[Pubmed] | [DOI]
27 Chronic kidney disease in the context of toxic effects the working chemical factors (literature review)
L. A Strizhakov, V. V Fomin, R. V Garipova, S. A Babanov, E. V Arkhipov, M. V Lebedeva
Terapevticheskii arkhiv. 2019; 91(6): 110
[Pubmed] | [DOI]
28 Biochemical and Molecular Bases of Lead-Induced Toxicity in Mammalian Systems and Possible Mitigations
Nitika Singh, Abhishek Kumar, Vivek Kumar Gupta, Bechan Sharma
Chemical Research in Toxicology. 2018; 31(10): 1009
[Pubmed] | [DOI]
29 Simultaneous Electrochemical Speciation of Oxidized and Reduced Glutathione. Redox Profiling of Oxidative Stress in Biological Fluids with a Modified Carbon Electrode
Patricia M. Olmos Moya, Minerva Martínez Alfaro, Rezvan Kazemi, Mario A. Alpuche-Avilés, Sophie Griveau, Fethi Bedioui, Silvia Gutiérrez Granados
Analytical Chemistry. 2017; 89(20): 10726
[Pubmed] | [DOI]
30 Orginal Article. Nephritic cell damage and antioxidant status in rats exposed to leachate from battery recycling industry
Jacob K. Akintunde, Ganiyu Oboh
Interdisciplinary Toxicology. 2016; 9(1): 1
[Pubmed] | [DOI]
31 Mitochondria defects are involved in lead-acetate-induced adult hematopoietic stem cell decline
Jun Liu,Dao-Yong Jia,Shi-Zhong Cai,Cheng-Peng Li,Meng-Si Zhang,Yan-Yan Zhang,Chong-Huai Yan,Ya-Ping Wang
Toxicology Letters. 2015; 235(1): 37
[Pubmed] | [DOI]
32 Glioprotective Effects of Ashwagandha Leaf Extract against Lead Induced Toxicity
Praveen Kumar,Raghavendra Singh,Arshed Nazmi,Dinesh Lakhanpal,Hardeep Kataria,Gurcharan Kaur
BioMed Research International. 2014; 2014: 1
[Pubmed] | [DOI]
33 A protocol for a systematic review of the effectiveness of interventions to reduce exposure to lead through consumer products and drinking water
Lisa Pfadenhauer,Jacob Burns,Anke Rohwer,Eva Rehfuess
Systematic Reviews. 2014; 3(1): 36
[Pubmed] | [DOI]
34 Lack of reversal of oxidative damage in renal tissues of lead acetate-treated rats
Ademola Adetokunbo Oyagbemi,Temidayo Olutayo Omobowale,Akinleye Stephen Akinrinde,Adebowale Bernard Saba,Blessing Seun Ogunpolu,Oluwabusola Daramola
Environmental Toxicology. 2014; : n/a
[Pubmed] | [DOI]
35 Biochemical evidence for lead and mercury induced transbilayer movement of phospholipids mediated by human phospholipid scramblase 1
Shettihalli, A.K. and Gummadi, S.N.
Chemical Research in Toxicology. 2013; 26(6): 918-925
[Pubmed]
36 Lead poisoning: Why wonćt this problem go away?
Wick, J.Y.
Pharmacy Times. 2013; 79(3)
[Pubmed]
37 Age related changes in aminergic system and behavior following lead exposure: Protection with essential metal supplements
D. Chand Basha,N. Saya Reddy,M. Usha Rani,G. Rajarami Reddy
Neuroscience Research. 2013;
[Pubmed] | [DOI]
38 Toxic effects of lead exposure in Wistar rats: Involvement of oxidative stress and the beneficial role of edible jute (Corchorus olitorius) leaves
Saikat Dewanjee, Ranabir Sahu, Sarmila Karmakar, Moumita Gangopadhyay
Food and Chemical Toxicology. 2013; 55: 78
[VIEW] | [DOI]
39 Safety and toxicity issues associated with lead-based traditional herbo-metallic preparations
Surya Nagarajan,Kalaiarasi Sivaji,Sridharan Krishnaswamy,Brindha Pemiah,Kalpoondi Sekar Rajan,Uma Maheswari Krishnan,Swaminathan Sethuraman
Journal of Ethnopharmacology. 2013;
[Pubmed] | [DOI]
40 Biochemical Evidence for Lead and Mercury Induced Transbilayer Movement of Phospholipids Mediated by Human Phospholipid Scramblase 1
Ashok Kumar Shettihalli,Sathyanarayana N. Gummadi
Chemical Research in Toxicology. 2013; 26(6): 918
[Pubmed] | [DOI]
41 Toxicity of lead: A review with recent updates
Flora, G. and Gupta, D. and Tiwari, A.
Interdisciplinary Toxicology. 2012; 5(2): 47-58
[Pubmed]
42 The protective effect of flaxseed oil on lead acetate-induced renal toxicity in rats
Ahmed E. Abdel Moneim, Mohamed A. Dkhil, Saleh Al-Quraishy
Journal of Hazardous Materials. 2011;
[VIEW] | [DOI]
43 The effect of oral administration of Allium sativum extracts on lead nitrate induced toxicity in male mice
Sharma, V., Sharma, A., Kansal, L.
Food and Chemical Toxicology. 2010; 48(3): 928-936
[Pubmed]
44 The effect of oral administration of Allium sativum extracts on lead nitrate induced toxicity in male mice
Veena Sharma,Arti Sharma,Leena Kansal
Food and Chemical Toxicology. 2010; 48(3): 928
[Pubmed] | [DOI]



 

Top
Print this article  Email this article
Previous article Next article