Inverse association of intellectual function with very low blood lead but not with manganese exposure in Italian adolescents
(2012) In Environmental Research 118. p.65-71- Abstract
- Background: Pediatric lead (Pb) exposure impacts cognitive function and behavior and co-exposure to manganese (Mn) may enhance neurotoxicity. Objectives: To assess cognitive and behavioral function in adolescents with environmental exposure to Pb and Mn. Methods: In this cross sectional study, cognitive function and behavior were examined in healthy adolescents with environmental exposure to metals. The Wechsler Intelligence Scale for Children (WISC) and the Conners-Wells' Adolescent Self-Report Scale Long Form (CASS:L) were used to assess cognitive and behavioral function, respectively. ALAD polymorphisms rs1800435 and rs1139488 were measured as potential modifiers. Results: We examined 299 adolescents (49.2% females) aged 11-14 years.... (More)
- Background: Pediatric lead (Pb) exposure impacts cognitive function and behavior and co-exposure to manganese (Mn) may enhance neurotoxicity. Objectives: To assess cognitive and behavioral function in adolescents with environmental exposure to Pb and Mn. Methods: In this cross sectional study, cognitive function and behavior were examined in healthy adolescents with environmental exposure to metals. The Wechsler Intelligence Scale for Children (WISC) and the Conners-Wells' Adolescent Self-Report Scale Long Form (CASS:L) were used to assess cognitive and behavioral function, respectively. ALAD polymorphisms rs1800435 and rs1139488 were measured as potential modifiers. Results: We examined 299 adolescents (49.2% females) aged 11-14 years. Blood lead (BPb) averaged 1.71 mu g/dL (median 1.5, range 0.44-10.2), mean Blood Manganese (BMn) was 11.1 mu g/dL (median 10.9, range 4.00-24.1). Average total IQ was 106.3 (verbal IQ= 102, performance IQ= 109.3). According to a multiple regression model considering the effect of other covariates, a reduction of about 2.4 IQ points resulted from a two-fold increase of BPb. The Benchmark Level of BPb associated with a loss of 1 IQ-point (BML01) was 0.19 mu g/dL, with a lower 95% confidence limit (BMLL01) of 0.11 mu g/dL. A very weak correlation resulted between BPb and the ADHD-like behavior (Kendall's tau rank correlation=0.074, p=0.07). No influence of ALAD genotype was observed on any outcome. Manganese was not associated with cognitive and behavioral outcomes, nor was there any interaction with lead. Conclusions: These findings demonstrate that very low level of lead exposure has a significant negative impact on cognitive function in adolescent children. Being an essential micro-nutrient, manganese may not cause cognitive effects at these low exposure levels. (c) 2012 Elsevier Inc. All rights reserved. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/3187474
- author
- Lucchini, Roberto G. ; Zoni, Silvia ; Guazzetti, Stefano ; Bontempi, Elza ; Micheletti, Serena ; Broberg Palmgren, Karin LU ; Parrinello, Giovanni and Smith, Donald R.
- organization
- publishing date
- 2012
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Cognitive functions, Lead, Manganese, Children
- in
- Environmental Research
- volume
- 118
- pages
- 65 - 71
- publisher
- Elsevier
- external identifiers
-
- wos:000309303100009
- scopus:84866014309
- pmid:22925625
- ISSN
- 1096-0953
- DOI
- 10.1016/j.envres.2012.08.003
- language
- English
- LU publication?
- yes
- id
- 3588b61c-580a-46d6-95cb-3694cdfa500f (old id 3187474)
- date added to LUP
- 2016-04-01 10:25:50
- date last changed
- 2022-04-27 21:57:22
@article{3588b61c-580a-46d6-95cb-3694cdfa500f, abstract = {{Background: Pediatric lead (Pb) exposure impacts cognitive function and behavior and co-exposure to manganese (Mn) may enhance neurotoxicity. Objectives: To assess cognitive and behavioral function in adolescents with environmental exposure to Pb and Mn. Methods: In this cross sectional study, cognitive function and behavior were examined in healthy adolescents with environmental exposure to metals. The Wechsler Intelligence Scale for Children (WISC) and the Conners-Wells' Adolescent Self-Report Scale Long Form (CASS:L) were used to assess cognitive and behavioral function, respectively. ALAD polymorphisms rs1800435 and rs1139488 were measured as potential modifiers. Results: We examined 299 adolescents (49.2% females) aged 11-14 years. Blood lead (BPb) averaged 1.71 mu g/dL (median 1.5, range 0.44-10.2), mean Blood Manganese (BMn) was 11.1 mu g/dL (median 10.9, range 4.00-24.1). Average total IQ was 106.3 (verbal IQ= 102, performance IQ= 109.3). According to a multiple regression model considering the effect of other covariates, a reduction of about 2.4 IQ points resulted from a two-fold increase of BPb. The Benchmark Level of BPb associated with a loss of 1 IQ-point (BML01) was 0.19 mu g/dL, with a lower 95% confidence limit (BMLL01) of 0.11 mu g/dL. A very weak correlation resulted between BPb and the ADHD-like behavior (Kendall's tau rank correlation=0.074, p=0.07). No influence of ALAD genotype was observed on any outcome. Manganese was not associated with cognitive and behavioral outcomes, nor was there any interaction with lead. Conclusions: These findings demonstrate that very low level of lead exposure has a significant negative impact on cognitive function in adolescent children. Being an essential micro-nutrient, manganese may not cause cognitive effects at these low exposure levels. (c) 2012 Elsevier Inc. All rights reserved.}}, author = {{Lucchini, Roberto G. and Zoni, Silvia and Guazzetti, Stefano and Bontempi, Elza and Micheletti, Serena and Broberg Palmgren, Karin and Parrinello, Giovanni and Smith, Donald R.}}, issn = {{1096-0953}}, keywords = {{Cognitive functions; Lead; Manganese; Children}}, language = {{eng}}, pages = {{65--71}}, publisher = {{Elsevier}}, series = {{Environmental Research}}, title = {{Inverse association of intellectual function with very low blood lead but not with manganese exposure in Italian adolescents}}, url = {{http://dx.doi.org/10.1016/j.envres.2012.08.003}}, doi = {{10.1016/j.envres.2012.08.003}}, volume = {{118}}, year = {{2012}}, }