Neurobehavioral function and low-level metal exposure in adolescents

Kiciński, Michał; Vrijens, Jan; Vermier, G.; Hond, Elly Den; Schoeters, Greet; Nelen, Vera; Bruckers, Liesbeth; Sioen, Isabelle; Baeyens, Willy; Larebeke, N. Van; Viaene, Mineke; Nawrot, Tim S.

doi:10.1016/j.ijheh.2014.09.002

Cited by 30 publications

(19 citation statements)

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“…In Belgium, mean urinary cadmium mass concentrations in children and adolescents were 0.23-0.27 μg L −1 ; in adult never smokers 0.56 μg L −1 and in elderly never smokers 0.94 μg L −1 [87]. Similar values have been reported in other studies [88,95]. In the U.S., geometric mean urinary cadmium, measured in 2011-2012, was approximately 0.08 nmol mmol −1 creatinine in children and adolescents (6-19 years) and 0.22 nmol mmol −1 creatinine in adults [78].…”

Section: Cadmium In Urinesupporting

confidence: 87%

Risk assessment of effects of cadmium on human health (IUPAC Technical Report)

Nordberg

Bernard

Diamond³

et al. 2018

Pure and Applied Chemistry

176

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Chemistry and Human Health, Division VII of the International Union on Pure and Applied Chemistry (IUPAC), provides guidance on risk assessment methodology and, as appropriate, assessment of risks to human health from chemicals of exceptional toxicity. The aim of this document is to describe dose-response relationships for the health effects of low-level exposure to cadmium, in particular, with an emphasis on causation. The term “cadmium” in this document includes all chemical species of cadmium, as well as those in cadmium compounds. Diet is the main source of cadmium exposure in the general population. Smokers and workers in cadmium industries have additional exposure. Adverse effects have been shown in populations with high industrial or environmental exposures. Epidemiological studies in general populations have also reported statistically significant associations with a number of adverse health effects at low exposures. Cadmium is recognized as a human carcinogen, a classification mainly based on occupational studies of lung cancer. Other cancers have been reported, but dose-response relationships cannot be defined. Cardiovascular disease has been associated with cadmium exposure in recent epidemiological studies, but more evidence is needed in order to establish causality. Adequate evidence of dose-response relationships is available for kidney effects. There is a relationship between cadmium exposure and kidney effects in terms of low molecular mass (LMM) proteinuria. Long-term cadmium exposures with urine cadmium of 2 nmol mmol−1creatinine cause such effects in a susceptible part of the population. Higher exposures result in increases in the size of these effects. This assessment is supported by toxicokinetic and toxicodynamic (TKTD) modelling. Associations between urine cadmium lower than 2 nmol mmol−1creatinine and LMM proteinuria are influenced by confounding by co-excretion of cadmium with protein. A number of epidemiological studies, including some on low exposures, have reported statistically significant associations between cadmium exposure and bone demineralization and fracture risk. Exposures leading to urine cadmium of 5 nmol mmol−1creatinine and more increase the risk of bone effects. Similar associations at much lower urine cadmium levels have been reported. However, complexities in the cause and effect relationship mean that a no-effect level cannot be defined. LMM proteinuria was selected as the critical effect for cadmium, thus identifying the kidney cortex as the critical organ, although bone effects may occur at exposure levels similar to those giving rise to kidney effects. To avoid these effects, population exposures should not exceed that resulting in cadmium values in urine of more than 2 nmol mmol−1creatinine. As cadmium is carcinogenic, a ‘safe’ exposure level cannot be defined. We therefore recommend that cadmium exposures be kept as low as possible. Because the safety margin for toxic effects in kidney and bone is small, or non-existent, in many populations around the world, there is a need to reduce cadmium pollution globally.

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Section: Cadmium In Urinesupporting

confidence: 87%

Risk assessment of effects of cadmium on human health (IUPAC Technical Report)

Nordberg

Bernard

Diamond³

et al. 2018

Pure and Applied Chemistry

176

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“…The validity of this assumption has now been called into question by studies showing that low-level U-Cd is strongly, if not mainly, influenced by factors unrelated to Cd body burden. One of the most challenging findings is that adolescents and young children have U-Cd values similar to, if not higher than, those of adults despite a Cd body burden that is 5â€“10 times lower (median values of U-Cd for most age groups of the general population are in the range of 0.2â€“0.4 ÎĽg/g creatinine in nonsmoking subjects) ( Chaumont et al 2013 ; Hoet et al 2013 ; Kicinski et al 2015 ). Further calling into question the reliability of U-Cd as a marker of cumulative exposure, some studies found no differences in U-Cd between never-smokers and past smokers, an unexpected observation for a biomarker supposedly reflecting the body burden of the metal ( Chaumont et al 2013 ; Ikeda et al 2005 ; Paschal et al 2000 ).…”

Section: Discussionmentioning

confidence: 99%

Confusion about Cadmium Risks: The Unrecognized Limitations of an Extrapolated Paradigm

Bernard

2016

Environ Health Perspect

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BackgroundCadmium (Cd) risk assessment presently relies on tubular proteinuria as a critical effect and urinary Cd (U-Cd) as an index of the Cd body burden. Based on this paradigm, regulatory bodies have reached contradictory conclusions regarding the safety of Cd in food. Adding to the confusion, epidemiological studies implicate environmental Cd as a risk factor for bone, cardiovascular, and other degenerative diseases at exposure levels that are much lower than points of departure used for setting food standards.ObjectiveThe objective was to examine whether the present confusion over Cd risks is not related to conceptual or methodological problems.DiscussionThe cornerstone of Cd risk assessment is the assumption that U-Cd reflects the lifetime accumulation of the metal in the body. The validity of this assumption as applied to the general population has been questioned by recent studies revealing that low-level U-Cd varies widely within and between individuals depending on urinary flow, urine collection protocol, and recent exposure. There is also evidence that low-level U-Cd increases with proteinuria and essential element deficiencies, two potential confounders that might explain the multiple associations of U-Cd with common degenerative diseases. In essence, the present Cd confusion might arise from the fact that this heavy metal follows the same transport pathways as plasma proteins for its urinary excretion and the same transport pathways as essential elements for its intestinal absorption.ConclusionsThe Cd risk assessment paradigm needs to be rethought taking into consideration that low-level U-Cd is strongly influenced by renal physiology, recent exposure, and factors linked to studied outcomes.CitationBernard A. 2016. Confusion about cadmium risks: the unrecognized limitations of an extrapolated paradigm. Environ Health Perspect 124:1–5; http://dx.doi.org/10.1289/ehp.1509691

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“…Numerous studies of this age group show a positive relationship even between low concentrations of lead aerosols and damage to hemopoiesis, nervous tissue, hearing, changes in neurobehavioral functions, and intellectual [ 29 ] [ 30 ] [ 31 ] [ 32 ]. Reports of blocking the bioactivity of porphyrin synthesis enzymes, impaired haem- synthesis and the development of anemia by the action of lead is found in research by de Carvalho RP et al, 2006; Zimmermann M. B. et al, 2006; Muwakkit S. et al, 2008; Rondó P. K. et al, 2011, Park S. et al, 2014 [ 33 ] [ 34 ] [ 35 ] [ 36 ] [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Mathematical Model for Forecasting the Influence of Atmospheric Pollution on Population Morbidity in Stara Zagora Municipality (Bulgaria)

Platikanova¹,

Hristova²,

Milcheva³

2018

Open Access Maced J Med Sci

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AIM:This paper aims to create a mathematical model for forecasting the morbidity of the population in the Republic of Bulgaria and the Stara Zagora Municipality in particular as a consequence of the atmospheric pollution.SUBJECTS AND METHODS:This model is based on a formula which determines the correlation between the average annual concentrations of atmospheric pollutants SO2, PM10, Pb aerosols, NO2 and H2S) and the morbidity of the population based on the number of people who visited their GPs in a relation with a chronic health problem or emergency condition and the number of hospitalisations in two age groups (newborn to 17 years olds and 18 and older) as well as for the entire population in the period 2009-2013, making it possible to predict morbidity levels.RESULTS:The expected morbidity level predictions based on the number of people who visited their GPs in Municipality are lower, while hospitalisation level predictions are higher. This model has been created and tested and is applicable in all residential areas.CONCLUSIONS:A new, very sensitive, mathematical model has been created and tested (average margin of error from 0.61% to 2.59%) and is applicable in all residential areas.

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Neurobehavioral function and low-level metal exposure in adolescents

Cited by 30 publications

References 76 publications

Risk assessment of effects of cadmium on human health (IUPAC Technical Report)

Risk assessment of effects of cadmium on human health (IUPAC Technical Report)

Confusion about Cadmium Risks: The Unrecognized Limitations of an Extrapolated Paradigm

Mathematical Model for Forecasting the Influence of Atmospheric Pollution on Population Morbidity in Stara Zagora Municipality (Bulgaria)

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