Urinary n-acetyl- glucosaminidase excretion and environmental lead exposure

Ja Liang Lin, Kuan Hung Yeh, Hsun Chih Tseng, Wei Yu Chen, Hsien Hung Lai, Yu Ching Lin, Ping Hong Chen, Chien Jen Chen

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

To understand the relationship between chronic low-level lead exposure and renal function, residents living nearby a lead battery factory for more than 10 years were selected and entered in this cross-section study. The residents living in the 1st village, within 500 m from the factory, were rouped in group 1; those in the 2nd village, within 1,000-1,500 m, in group 2, and those in the 3rd village, far from any lead-contaminated sources, in group 3. Twenty-four-hour urinary N-acetyl-glucosaminidase (NAG) was detected as early indicator of renal damage, and an ethylenediamine-tetraacetic acid mobilization test was performed to estimate total body lead burden of lead-exposed persons. Blood lead level (BLL) showed a significant difference among the three study groups. The further the distance between the group and the factory, the higher BLL. The results showed a significant high prevalence of abnormal urine NAG exretion in the chronic lead-exposed group, although BLL and body lead burden of these persons were within the ‘normal’ range. A significant correlation between body lead burden less than 200 pg and 24-hour urine NAG excretion and a dose- response relationship between them were found. These observations suggested that lead was the possible cause of abnormal renal tubular function in persons with chronic low-level lead exposure, but this effect became blunt when body lead burden was more than 200 pg. The possible explanation may be that high body lead burden from long-term exposure will deplete the kidney of NAG or render it insensitive to the effects of lead exposure. Whether urine NAG is an early indicator of lead nephropathy is still unconclusive, and long-term follow- up in our study is needed to detail these relations.

Original languageEnglish
Pages (from-to)442-447
Number of pages6
JournalAmerican Journal of Nephrology
Volume13
Issue number6
DOIs
Publication statusPublished - 1993

Fingerprint

Hexosaminidases
Environmental Exposure
Body Burden
Kidney
ethylenediamine
Urine
Lead
Blood Group Antigens
Reference Values

Keywords

  • Environmental lead exposure
  • Ethylenediaminetetraacetic acid mobilization test
  • N-acetyl-glucosaminidase
  • Renal damage

ASJC Scopus subject areas

  • Nephrology

Cite this

Lin, J. L., Yeh, K. H., Tseng, H. C., Chen, W. Y., Lai, H. H., Lin, Y. C., ... Chen, C. J. (1993). Urinary n-acetyl- glucosaminidase excretion and environmental lead exposure. American Journal of Nephrology, 13(6), 442-447. https://doi.org/10.1159/000168661

Urinary n-acetyl- glucosaminidase excretion and environmental lead exposure. / Lin, Ja Liang; Yeh, Kuan Hung; Tseng, Hsun Chih; Chen, Wei Yu; Lai, Hsien Hung; Lin, Yu Ching; Chen, Ping Hong; Chen, Chien Jen.

In: American Journal of Nephrology, Vol. 13, No. 6, 1993, p. 442-447.

Research output: Contribution to journalArticle

Lin, JL, Yeh, KH, Tseng, HC, Chen, WY, Lai, HH, Lin, YC, Chen, PH & Chen, CJ 1993, 'Urinary n-acetyl- glucosaminidase excretion and environmental lead exposure', American Journal of Nephrology, vol. 13, no. 6, pp. 442-447. https://doi.org/10.1159/000168661
Lin, Ja Liang ; Yeh, Kuan Hung ; Tseng, Hsun Chih ; Chen, Wei Yu ; Lai, Hsien Hung ; Lin, Yu Ching ; Chen, Ping Hong ; Chen, Chien Jen. / Urinary n-acetyl- glucosaminidase excretion and environmental lead exposure. In: American Journal of Nephrology. 1993 ; Vol. 13, No. 6. pp. 442-447.
@article{254a2cc4353840a7960647fd0eb83244,
title = "Urinary n-acetyl- glucosaminidase excretion and environmental lead exposure",
abstract = "To understand the relationship between chronic low-level lead exposure and renal function, residents living nearby a lead battery factory for more than 10 years were selected and entered in this cross-section study. The residents living in the 1st village, within 500 m from the factory, were rouped in group 1; those in the 2nd village, within 1,000-1,500 m, in group 2, and those in the 3rd village, far from any lead-contaminated sources, in group 3. Twenty-four-hour urinary N-acetyl-glucosaminidase (NAG) was detected as early indicator of renal damage, and an ethylenediamine-tetraacetic acid mobilization test was performed to estimate total body lead burden of lead-exposed persons. Blood lead level (BLL) showed a significant difference among the three study groups. The further the distance between the group and the factory, the higher BLL. The results showed a significant high prevalence of abnormal urine NAG exretion in the chronic lead-exposed group, although BLL and body lead burden of these persons were within the ‘normal’ range. A significant correlation between body lead burden less than 200 pg and 24-hour urine NAG excretion and a dose- response relationship between them were found. These observations suggested that lead was the possible cause of abnormal renal tubular function in persons with chronic low-level lead exposure, but this effect became blunt when body lead burden was more than 200 pg. The possible explanation may be that high body lead burden from long-term exposure will deplete the kidney of NAG or render it insensitive to the effects of lead exposure. Whether urine NAG is an early indicator of lead nephropathy is still unconclusive, and long-term follow- up in our study is needed to detail these relations.",
keywords = "Environmental lead exposure, Ethylenediaminetetraacetic acid mobilization test, N-acetyl-glucosaminidase, Renal damage",
author = "Lin, {Ja Liang} and Yeh, {Kuan Hung} and Tseng, {Hsun Chih} and Chen, {Wei Yu} and Lai, {Hsien Hung} and Lin, {Yu Ching} and Chen, {Ping Hong} and Chen, {Chien Jen}",
year = "1993",
doi = "10.1159/000168661",
language = "English",
volume = "13",
pages = "442--447",
journal = "American Journal of Nephrology",
issn = "0250-8095",
publisher = "S. Karger AG",
number = "6",

}

TY - JOUR

T1 - Urinary n-acetyl- glucosaminidase excretion and environmental lead exposure

AU - Lin, Ja Liang

AU - Yeh, Kuan Hung

AU - Tseng, Hsun Chih

AU - Chen, Wei Yu

AU - Lai, Hsien Hung

AU - Lin, Yu Ching

AU - Chen, Ping Hong

AU - Chen, Chien Jen

PY - 1993

Y1 - 1993

N2 - To understand the relationship between chronic low-level lead exposure and renal function, residents living nearby a lead battery factory for more than 10 years were selected and entered in this cross-section study. The residents living in the 1st village, within 500 m from the factory, were rouped in group 1; those in the 2nd village, within 1,000-1,500 m, in group 2, and those in the 3rd village, far from any lead-contaminated sources, in group 3. Twenty-four-hour urinary N-acetyl-glucosaminidase (NAG) was detected as early indicator of renal damage, and an ethylenediamine-tetraacetic acid mobilization test was performed to estimate total body lead burden of lead-exposed persons. Blood lead level (BLL) showed a significant difference among the three study groups. The further the distance between the group and the factory, the higher BLL. The results showed a significant high prevalence of abnormal urine NAG exretion in the chronic lead-exposed group, although BLL and body lead burden of these persons were within the ‘normal’ range. A significant correlation between body lead burden less than 200 pg and 24-hour urine NAG excretion and a dose- response relationship between them were found. These observations suggested that lead was the possible cause of abnormal renal tubular function in persons with chronic low-level lead exposure, but this effect became blunt when body lead burden was more than 200 pg. The possible explanation may be that high body lead burden from long-term exposure will deplete the kidney of NAG or render it insensitive to the effects of lead exposure. Whether urine NAG is an early indicator of lead nephropathy is still unconclusive, and long-term follow- up in our study is needed to detail these relations.

AB - To understand the relationship between chronic low-level lead exposure and renal function, residents living nearby a lead battery factory for more than 10 years were selected and entered in this cross-section study. The residents living in the 1st village, within 500 m from the factory, were rouped in group 1; those in the 2nd village, within 1,000-1,500 m, in group 2, and those in the 3rd village, far from any lead-contaminated sources, in group 3. Twenty-four-hour urinary N-acetyl-glucosaminidase (NAG) was detected as early indicator of renal damage, and an ethylenediamine-tetraacetic acid mobilization test was performed to estimate total body lead burden of lead-exposed persons. Blood lead level (BLL) showed a significant difference among the three study groups. The further the distance between the group and the factory, the higher BLL. The results showed a significant high prevalence of abnormal urine NAG exretion in the chronic lead-exposed group, although BLL and body lead burden of these persons were within the ‘normal’ range. A significant correlation between body lead burden less than 200 pg and 24-hour urine NAG excretion and a dose- response relationship between them were found. These observations suggested that lead was the possible cause of abnormal renal tubular function in persons with chronic low-level lead exposure, but this effect became blunt when body lead burden was more than 200 pg. The possible explanation may be that high body lead burden from long-term exposure will deplete the kidney of NAG or render it insensitive to the effects of lead exposure. Whether urine NAG is an early indicator of lead nephropathy is still unconclusive, and long-term follow- up in our study is needed to detail these relations.

KW - Environmental lead exposure

KW - Ethylenediaminetetraacetic acid mobilization test

KW - N-acetyl-glucosaminidase

KW - Renal damage

UR - http://www.scopus.com/inward/record.url?scp=0027744081&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027744081&partnerID=8YFLogxK

U2 - 10.1159/000168661

DO - 10.1159/000168661

M3 - Article

C2 - 8141178

AN - SCOPUS:0027744081

VL - 13

SP - 442

EP - 447

JO - American Journal of Nephrology

JF - American Journal of Nephrology

SN - 0250-8095

IS - 6

ER -