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Lead concentration in plasma as a biomarker of exposure and risk, and modification of toxicity by delta-aminolevulinic acid dehydratase gene polymorphism

Tian, Liting ; Zheng, Guang ; Sommar, Johan Nilsson ; Liang, Yihuai ; Lundh, Tomas ; Broberg Palmgren, Karin LU orcid ; Lei, Lijian ; Guo, Weijun ; Li, Yulan and Tan, Mingguang , et al. (2013) In Toxicology Letters 221(2). p.102-109
Abstract
Blood lead concentration (B-Pb), the main biomarker of lead exposure and risk, is curvi-linearily related to exposure. We assessed plasma lead (P-Pb) as a marker for both lead exposure and toxic effects. We examined claims that delta-aminolevulinic acid dehydratase genotype (ALAD) can modify lead toxicity. In 290 lead-exposed and 91 unexposed Chinese workers, we determined P-Pb, B-Pb, urinary lead (U-Pb), AMD polymorphism (rs1800435, ALAD112; TaqMan assay), and also toxic effects on heme synthesis (blood zinc protoporphyrin and hemoglobin, urinary delta-aminolevulic acid), on the kidneys (urinary albumin, beta(2)microglobulin and N-acetyl-beta-D-glucosaminidase) and on the peripheral nervous system (sensory and motor conduction... (More)
Blood lead concentration (B-Pb), the main biomarker of lead exposure and risk, is curvi-linearily related to exposure. We assessed plasma lead (P-Pb) as a marker for both lead exposure and toxic effects. We examined claims that delta-aminolevulinic acid dehydratase genotype (ALAD) can modify lead toxicity. In 290 lead-exposed and 91 unexposed Chinese workers, we determined P-Pb, B-Pb, urinary lead (U-Pb), AMD polymorphism (rs1800435, ALAD112; TaqMan assay), and also toxic effects on heme synthesis (blood zinc protoporphyrin and hemoglobin, urinary delta-aminolevulic acid), on the kidneys (urinary albumin, beta(2)microglobulin and N-acetyl-beta-D-glucosaminidase) and on the peripheral nervous system (sensory and motor conduction velocities). In exposed workers, median P-Pb was 4.10 (range 0.35-27) mu g/L, B-Pb 401 (110-950) mu g/L, and U-Pb 188 (22-590) mu g/g creatinine. P-Pb had a higher ratio between exposed and unexposed workers (median 39, range 18-110) than B-Pb (19, 15-36; p<0.001) and U-Pb (28, 15-36; p<0.001). All three biomarkers were associated with all toxic effects (P-Pb: r(s)= -0.10 to 0.79; B-Pb: r(s) = -0.08 to 0.75; all p <0.05). In the exposed workers, B-Pb and U-Pb were significantly higher (p = 0.04) in AIAD2 carriers (7% in the exposed population) than in ALAD1 homozygotes. P-Pb values were similar; ALAD1 homozygotes suffered higher kidney toxicity at the same P-Pb. Conclusions: (i) P-Pb has advantages over B-Pb as a biomarker of high Pb exposure, but it was not significantly better as an index of risk of toxicity. (ii) The ALAD genotype modifies toxicokinetics and toxicodynamics. (C) 2013 Elsevier Ireland Ltd. All rights reserved. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Lead, Occupational exposure, Plasma, delta-Aminolevulinic acid, dehydratase gene, Gene-environment interaction
in
Toxicology Letters
volume
221
issue
2
pages
102 - 109
publisher
Elsevier
external identifiers
  • wos:000323087000004
  • scopus:84880380273
  • pmid:23792432
ISSN
1879-3169
DOI
10.1016/j.toxlet.2013.06.214
language
English
LU publication?
yes
id
54156a5c-7829-465c-a04a-26a7c41be0ea (old id 4027316)
date added to LUP
2016-04-01 14:00:37
date last changed
2022-03-29 18:39:36
@article{54156a5c-7829-465c-a04a-26a7c41be0ea,
  abstract     = {{Blood lead concentration (B-Pb), the main biomarker of lead exposure and risk, is curvi-linearily related to exposure. We assessed plasma lead (P-Pb) as a marker for both lead exposure and toxic effects. We examined claims that delta-aminolevulinic acid dehydratase genotype (ALAD) can modify lead toxicity. In 290 lead-exposed and 91 unexposed Chinese workers, we determined P-Pb, B-Pb, urinary lead (U-Pb), AMD polymorphism (rs1800435, ALAD112; TaqMan assay), and also toxic effects on heme synthesis (blood zinc protoporphyrin and hemoglobin, urinary delta-aminolevulic acid), on the kidneys (urinary albumin, beta(2)microglobulin and N-acetyl-beta-D-glucosaminidase) and on the peripheral nervous system (sensory and motor conduction velocities). In exposed workers, median P-Pb was 4.10 (range 0.35-27) mu g/L, B-Pb 401 (110-950) mu g/L, and U-Pb 188 (22-590) mu g/g creatinine. P-Pb had a higher ratio between exposed and unexposed workers (median 39, range 18-110) than B-Pb (19, 15-36; p&lt;0.001) and U-Pb (28, 15-36; p&lt;0.001). All three biomarkers were associated with all toxic effects (P-Pb: r(s)= -0.10 to 0.79; B-Pb: r(s) = -0.08 to 0.75; all p &lt;0.05). In the exposed workers, B-Pb and U-Pb were significantly higher (p = 0.04) in AIAD2 carriers (7% in the exposed population) than in ALAD1 homozygotes. P-Pb values were similar; ALAD1 homozygotes suffered higher kidney toxicity at the same P-Pb. Conclusions: (i) P-Pb has advantages over B-Pb as a biomarker of high Pb exposure, but it was not significantly better as an index of risk of toxicity. (ii) The ALAD genotype modifies toxicokinetics and toxicodynamics. (C) 2013 Elsevier Ireland Ltd. All rights reserved.}},
  author       = {{Tian, Liting and Zheng, Guang and Sommar, Johan Nilsson and Liang, Yihuai and Lundh, Tomas and Broberg Palmgren, Karin and Lei, Lijian and Guo, Weijun and Li, Yulan and Tan, Mingguang and Skerfving, Staffan and Jin, Taiyi and Bergdahl, Ingvar A.}},
  issn         = {{1879-3169}},
  keywords     = {{Lead; Occupational exposure; Plasma; delta-Aminolevulinic acid; dehydratase gene; Gene-environment interaction}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{102--109}},
  publisher    = {{Elsevier}},
  series       = {{Toxicology Letters}},
  title        = {{Lead concentration in plasma as a biomarker of exposure and risk, and modification of toxicity by delta-aminolevulinic acid dehydratase gene polymorphism}},
  url          = {{http://dx.doi.org/10.1016/j.toxlet.2013.06.214}},
  doi          = {{10.1016/j.toxlet.2013.06.214}},
  volume       = {{221}},
  year         = {{2013}},
}