Neurocognitive impact of metal exposure and social stressors among schoolchildren in Taranto, Italy.
Intellectual quotient
Metals
Neurocognitive functions
Neurotoxicity
Schoolchildren
Social stressors
Journal
Environmental health : a global access science source
ISSN: 1476-069X
Titre abrégé: Environ Health
Pays: England
ID NLM: 101147645
Informations de publication
Date de publication:
19 07 2019
19 07 2019
Historique:
received:
08
02
2019
accepted:
10
07
2019
entrez:
21
7
2019
pubmed:
22
7
2019
medline:
17
3
2020
Statut:
epublish
Résumé
Metal exposure is a public health hazard due to neurocognitive effects starting in early life. Poor socio-economic status, adverse home and family environment can enhance the neurodevelopmental toxicity due to chemical exposure. Disadvantaged socio-economic conditions are generally higher in environmentally impacted areas although the combined effect of these two factors has not been sufficiently studied. The effect of co-exposure to neurotoxic metals including arsenic, cadmium, manganese, mercury, lead, selenium, and to socio-economic stressors was assessed in a group of 299 children aged 6-12 years, residing at incremental distance from industrial emissions in Taranto, Italy. Exposure was assessed with biological monitoring and the distance between the home address and the exposure point source. Children's cognitive functions were examined using the Wechsler Intelligence Scale for Children (WISC) and the Cambridge Neuropsychological Test Automated Battery (CANTAB). Linear mixed models were chosen to assess the association between metal exposure, socio-economic status and neurocognitive outcomes. Urinary arsenic, cadmium and hair manganese resulted inversely related to the distance from the industrial emission source (β - 0.04; 95% CI -0.06, - 0.01; β - 0.02; 95% CI -0.05, - 0.001; β - 0.02 95% CI -0.05, - 0.003) while the WISC intellectual quotient and its sub-scores (except processing speed index) showed a positive association with distance. Blood lead and urinary cadmium were negatively associated with the IQ total score and all sub-scores, although not reaching the significance level. Hair manganese and blood lead was positively associated with the CANTAB between errors of spatial working memory (β 2.2; 95% CI 0.3, 3.9) and the reaction time of stop signal task (β 0.05; 95% CI 0.02, 0.1) respectively. All the other CANTAB neurocognitive tests did not show to be significantly influenced by metal exposure. The highest socio-economic status showed about five points intellectual quotient more than the lowest level on average (β 4.8; 95% CI 0.3, 9.6); the interaction term between blood lead and the socio-economic status showed a significant negative impact of lead on working memory at the lowest socio-economic status level (β - 4.0; 95% CI -6.9, - 1.1). Metal exposure and the distance from industrial emission was associated with negative cognitive impacts in these children. Lead exposure had neurocognitive effect even at very low levels of blood lead concentration when socio-economic status is low, and this should further address the importance and prioritize preventive and regulatory interventions.
Sections du résumé
BACKGROUND
Metal exposure is a public health hazard due to neurocognitive effects starting in early life. Poor socio-economic status, adverse home and family environment can enhance the neurodevelopmental toxicity due to chemical exposure. Disadvantaged socio-economic conditions are generally higher in environmentally impacted areas although the combined effect of these two factors has not been sufficiently studied.
METHODS
The effect of co-exposure to neurotoxic metals including arsenic, cadmium, manganese, mercury, lead, selenium, and to socio-economic stressors was assessed in a group of 299 children aged 6-12 years, residing at incremental distance from industrial emissions in Taranto, Italy. Exposure was assessed with biological monitoring and the distance between the home address and the exposure point source. Children's cognitive functions were examined using the Wechsler Intelligence Scale for Children (WISC) and the Cambridge Neuropsychological Test Automated Battery (CANTAB). Linear mixed models were chosen to assess the association between metal exposure, socio-economic status and neurocognitive outcomes.
RESULTS
Urinary arsenic, cadmium and hair manganese resulted inversely related to the distance from the industrial emission source (β - 0.04; 95% CI -0.06, - 0.01; β - 0.02; 95% CI -0.05, - 0.001; β - 0.02 95% CI -0.05, - 0.003) while the WISC intellectual quotient and its sub-scores (except processing speed index) showed a positive association with distance. Blood lead and urinary cadmium were negatively associated with the IQ total score and all sub-scores, although not reaching the significance level. Hair manganese and blood lead was positively associated with the CANTAB between errors of spatial working memory (β 2.2; 95% CI 0.3, 3.9) and the reaction time of stop signal task (β 0.05; 95% CI 0.02, 0.1) respectively. All the other CANTAB neurocognitive tests did not show to be significantly influenced by metal exposure. The highest socio-economic status showed about five points intellectual quotient more than the lowest level on average (β 4.8; 95% CI 0.3, 9.6); the interaction term between blood lead and the socio-economic status showed a significant negative impact of lead on working memory at the lowest socio-economic status level (β - 4.0; 95% CI -6.9, - 1.1).
CONCLUSIONS
Metal exposure and the distance from industrial emission was associated with negative cognitive impacts in these children. Lead exposure had neurocognitive effect even at very low levels of blood lead concentration when socio-economic status is low, and this should further address the importance and prioritize preventive and regulatory interventions.
Identifiants
pubmed: 31324194
doi: 10.1186/s12940-019-0505-3
pii: 10.1186/s12940-019-0505-3
pmc: PMC6642538
doi:
Substances chimiques
Air Pollutants
0
Metals, Heavy
0
Arsenic
N712M78A8G
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
67Subventions
Organisme : NIEHS NIH HHS
ID : R01 ES019222
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01ES019222, R56ES019222
Pays : United States
Références
Environ Health Perspect. 2008 Feb;116(2):243-8
pubmed: 18288325
Eur J Epidemiol. 1995 Jun;11(3):251-8
pubmed: 7493656
Environ Res. 2012 Oct;118:65-71
pubmed: 22925625
Toxicol Lett. 2014 Oct 15;230(2):295-303
pubmed: 24269718
Neurotoxicology. 2012 Aug;33(4):687-96
pubmed: 22322213
Environ Sci Process Impacts. 2013 Mar;15(3):677-89
pubmed: 23738367
Environ Res. 2017 Nov;159:344-354
pubmed: 28841522
Environ Sci Technol. 2013 Jan 15;47(2):1137-47
pubmed: 23253114
Environ Monit Assess. 2016 Dec;188(12):673
pubmed: 27853965
Neurotoxicology. 2011 Aug;32(4):450-7
pubmed: 21453724
PLoS One. 2013 May 29;8(5):e65230
pubmed: 23734241
Neurotoxicology. 2012 Jan;33(1):91-7
pubmed: 22182530
Sci Total Environ. 2017 Oct 15;596-597:207-211
pubmed: 28432910
Environ Int. 2018 Mar;112:49-58
pubmed: 29248865
Neurotoxicol Teratol. 2007 Mar-Apr;29(2):181-7
pubmed: 17079114
Neurotoxicology. 2006 Mar;27(2):210-6
pubmed: 16310252
Environ Health Perspect. 2014 Mar;122(3):310-6
pubmed: 24441767
Cent Eur J Public Health. 2003 Dec;11(4):184-6
pubmed: 14768779
Int J Hyg Environ Health. 2012 Feb;215(2):127-32
pubmed: 21940210
Int J Occup Med Environ Health. 2011 Mar;24(1):1-7
pubmed: 21468897
Int J Environ Res Public Health. 2017 Dec 05;14(12):
pubmed: 29206191
Biol Trace Elem Res. 2011 Nov;143(2):815-24
pubmed: 21225477
Environ Health Perspect. 2012 Jan;120(1):126-31
pubmed: 21885384
Environ Health Perspect. 2011 Jan;119(1):138-43
pubmed: 20855239
Epidemiol Prev. 2014 Mar-Apr;38(2 Suppl 1):125-33
pubmed: 24986501
Antioxid Redox Signal. 2003 Apr;5(2):205-15
pubmed: 12716480
Int J Hyg Environ Health. 2012 Feb;215(2):185-90
pubmed: 21964309
Epidemiology. 2007 Nov;18(6):686-94
pubmed: 18049185
Neurotoxicol Teratol. 2015 Nov-Dec;52(Pt A):25-35
pubmed: 26476195
Int J Environ Res Public Health. 2018 Jun 10;15(6):
pubmed: 29890770
Chemosphere. 2015 Apr;124:83-91
pubmed: 25434277
Neurotoxicology. 2015 Jul;49:114-20
pubmed: 26026402
Neurotoxicology. 2008 Sep;29(5):828-32
pubmed: 18501967
Environ Sci Pollut Res Int. 2017 Apr;24(12):11528-11535
pubmed: 28321698
Environ Res. 2011 Jan;111(1):156-63
pubmed: 20943219
Curr Opin Pediatr. 2009 Apr;21(2):222-9
pubmed: 19300262
J Environ Monit. 2010 Apr;12(4):832-7
pubmed: 20383363
Environ Health Perspect. 2006 Jan;114(1):124-9
pubmed: 16393669
Neurotoxicology. 2007 Nov;28(6):1170-7
pubmed: 17868887
Pediatr Res. 2017 Jan;81(1-2):214-226
pubmed: 27673421
J Pediatr. 2008 Feb;152(2):237-43
pubmed: 18206696
Sci Total Environ. 2018 Jan 1;610-611:741-749
pubmed: 28822941
J Trace Elem Med Biol. 2017 Sep;43:3-8
pubmed: 27769745
Environ Health Perspect. 2012 Jul;120(7):a258-60
pubmed: 22543002
Dan Med J. 2013 Jul;60(7):B4685
pubmed: 23809980
Environ Res. 2013 Oct;126:9-16
pubmed: 23790803
Environ Res. 2015 Aug;141:86-95
pubmed: 25440294
N Engl J Med. 2003 Apr 17;348(16):1517-26
pubmed: 12700371
Environ Sci Technol. 2013 Feb 5;47(3):1629-37
pubmed: 23259818
Neurotoxicology. 2014 Dec;45:301-8
pubmed: 24308913
Int J Environ Res Public Health. 2017 May 12;14(5):
pubmed: 28498344
Neurotoxicology. 2009 Jul;30(4):564-71
pubmed: 19635390
Environ Health Perspect. 2010 Oct;118(10):1465-70
pubmed: 20936744
Int J Mol Sci. 2017 Jan 24;18(2):
pubmed: 28125025
J Appl Toxicol. 2001 Jul-Aug;21(4):245-55
pubmed: 11481655
Int J Hyg Environ Health. 2009 Nov;212(6):637-47
pubmed: 19589725
Int J Hyg Environ Health. 2011 Dec;215(1):26-35
pubmed: 21820957
Environ Health Perspect. 2012 Oct;120(10):1418-24
pubmed: 23008276
Environ Health Perspect. 2005 Jul;113(7):894-9
pubmed: 16002379