The aim of this study was to evaluate hexachlorocyclohexane (HCH) exposure in children living in nine hot spots in four Mexican states. We analyzed HCH (a, ß, and ?-isomers) in blood using gas chromatography/mass spectrometry. HCH exposure level in 261 children was assessed and approximately 75 % of the children studied had detectable levels of HCH. These levels ranged from 188 to 40,096.7 ng/g lipid. The highest mean levels were found in Lacanja (5,446.9 ng/g lipid), an indigenous community in Chiapas, Mexico. Our data indicate high exposure to HCH in children living in these communities.
The role of environmental exposure to lead as a risk factor for chronic kidney disease (CKD) and its progression remains controversial, and most studies have been limited by a lack of direct glomerular filtration rate (GFR) measurement.
We evaluated the association between lead exposure and GFR in children with CKD.
In this cross-sectional study, we examined the association between blood lead levels (BLLs) and GFR measured by the plasma disappearance of iohexol among 391 participants in the Chronic Kidney Disease in Children (CKiD) prospective cohort study.
Median BLL and GFR were 1.2 µg/dL and 44.4 mL/min per 1.73 m2, respectively. The average percent change in GFR for each 1-µg/dL increase in BLL was -2.1 (95% CI: -6.0, 1.8). In analyses stratified by CKD diagnosis, the association between BLL and GFR was stronger among children with glomerular disease underlying CKD; in this group, each 1-µg/dL increase in BLL was associated with a -12.1 (95% CI: -22.2, -1.9) percent change in GFR. In analyses stratified by anemia status, each 1-µg/dL increase in BLL among those with and without anemia was associated with a -0.3 (95% CI: -7.2, 6.6) and -4.6 (95% CI: -8.9, -0.3) percent change in GFR, respectively.
There was no significant association between BLL and directly measured GFR in this relatively large cohort of children with CKD, although associations were observed in some subgroups. Longitudinal analyses are needed to examine the temporal relationship between lead and GFR decline, and to further examine the impact of underlying cause of CKD and anemia/hemoglobin status among patients with CKD.
Cites: Environ Health Perspect. 2008 Oct;116(10):1285-9318941567
Cites: J Am Soc Nephrol. 2009 Mar;20(3):629-3719158356
Knowledge about changes in exposure to toxic metals over time remains very sparse, in particular for children, the most vulnerable group. Here, we assessed whether a reduction in environmental pollution with cadmium (Cd) and mercury (Hg) caused a change in exposure over time. In total, 1257 children (age 4-9) in two towns in Sweden were sampled once in 1986-2013. Blood concentrations of Cd (b-Cd; n=1120) and Hg (b-Hg; n=560) were determined.
The median b-Cd was 0.10 (geometric mean 0.10; range 0.010-0.61) ?g/L and b-Hg was 0.91 (geometric mean 0.83; range 0.021-8.2) ?g/L. Children living close to a smelter had higher b-Cd and b-Hg than those in urban and rural areas. There was no sex difference in b-Cd or b-Hg, and b-Cd and b-Hg showed no significant accumulation by age. b-Cd decreased only slightly (0.7% per year, p
Studies conducted in the Faeroe Islands and Japan suggest a negative impact of mercury on heart rate variability (HRV) among children while the results regarding blood pressure (BP) are less consistent.
To assess the impact of mercury on HRV and BP among Nunavik Inuit children.
A cohort of 226 children was followed from birth to 11 years old. Mercury concentration in cord blood and in blood and hair at 11 years old were used as markers of prenatal and childhood exposure, respectively. HRV was measured using ambulatory 2 h-Holter monitoring while BP was measured through a standardized protocol. Simple regression was used to assess the relationship of mercury to BP and HRV parameters. Multiple linear regressions were performed adjusting for covariates such as age, sex, birth weight, body mass index (BMI), height, total n-3 fatty acids, polychlorinated biphenyls (PCB 153), lead, selenium and maternal smoking during pregnancy.
Median cord blood mercury and blood mercury levels at 11 years old were 81.5 nmoL/L (IQR:45.0?140.0) and 14.5 nmol/L (IQR: 7.5?28.0), respectively. After adjusting for the covariates, child blood mercury was associated with low frequency (LF) (b = 0.21, p = 0.05), the standard deviation of R?R intervals (SDNN) (b = 0.26, p = 0.02), the standard deviation of R?R intervals measured over 5 min periods (SDANN) (b = 0.31, p = 0.01) and the coefficient of variation of R?R intervals (CVRR) (b = 0.06,p = 0.02). No significant association was observed with BP.
Mercury exposure during childhood seems to affect HRV among Nunavik Inuit children at school age.
Some evidence suggests that various diet components and nutrients, including vegetables, fruit and food-derived antioxidants, could mitigate contaminant exposure and/or adverse health effects of contaminants. To examine the effect of the consumption of tomato products on blood mercury levels in Inuit preschool children, 155 Inuit children (25.0±9.1months) were recruited from 2006-2008 in Nunavik childcare centers (northern Québec, Canada). Food frequency questionnaires were completed at home and at the childcare center, and total blood mercury concentration was measured by inductively coupled plasma-mass spectrometry. Multivariate regression analysis was performed after multiple imputation. The median blood concentration of mercury was 9.5nmol/L. Age, duration of breastfeeding, annual consumption frequency of seal meat, and monthly consumption frequency of tomato products were significant predictors of blood mercury levels, whereas annual consumption frequencies of beluga muktuk, walrus, Arctic char, and caribou meat were not. Each time a participant consumed tomato products during the month before the interview was associated with a 4.6% lower blood mercury level (p=0.0005). All other significant predictors in the model were positively associated with blood mercury levels. Further studies should explore interactions between consumption of healthy store-bought foods available in Arctic regions and contaminant exposure.
Exposure to persistent organic pollutants (POPs) during prenatal and postnatal life has been extensively studied in relation to adverse health effects in children.
The aim was to identify determinants of the concentrations of polychlorinated biphenyls (PCBs), brominated flame retardants (polybrominated diphenyl ethers, PBDEs; polybrominated biphenyl, PBB), and organochlorine pesticides (OCPs) in blood samples from pregnant women and children in The Norwegian Mother and Child Cohort Study (MoBa).
Blood samples were collected from two independent subsamples within MoBa; a group of women (n=96) enrolled in mid-pregnancy during the years 2002-2008 and a group of 3 year old children (n=99) participating during 2010-2011. PCB congeners (74, 99, 138, 153, 180, 170, 194, 209, 105, 114, 118, 156, 157, 167, and 189), brominated flame retardants (PBDE-28, 47, 99, 100, 153, 154, and PBB-153), as well as the OCPs hexachlorobenzene (HCB), oxychlordane, 4,4'dichlorodiphenyltrichloroethane (DDT), and 4,4'dichlorodiphenyldichloroethylene (DDE) were measured in both pregnant women and children.
Age, low parity, and low pre-pregnant BMI were the most important determinants of increased plasma concentrations of POPs in pregnant women. In 3 year old children, prolonged breastfeeding duration was a major determinant of increased POP concentrations. Estimated dietary exposure to PCBs during pregnancy was positively associated with plasma concentrations in 3 year old children, but not in pregnant women. Plasma concentrations were approximately 40% higher in children compared to pregnant women.
Several factors associated with exposure and toxicokinetics, i.e. accumulation, excretion and transfer via breastmilk of POPs were the main predictors of POP levels in pregnant women and children. Diet, which is the main exposure source for these compounds in the general population, was found to predict PCB levels only among children. For the PBDEs, for which non-dietary sources are more important, toxicokinetic factors appeared to have less predictive impact.
High blood lead levels (BLLs) can be found in Inuit from Nunavik. At the same time, various nutrients such as calcium could lower lead absorption and toxicity. We examined the effect of dietary calcium intakes on BLLs in 245 preschool Inuit children attending childcare centres in Nunavik. Calcium intake was assessed with one 24-h dietary recall and BLLs were determined by inductively coupled plasma mass spectrometry in whole blood samples. Multiple imputation was performed to deal with missing data. Median blood lead concentration was 0.08 µmol/L. A high proportion of children did not meet the Estimated Average Requirement for vitamin D intake (73 %) and, to a lower extent, for calcium (20 %). Calcium intake was negatively associated with BLLs (p = 0.0001) while child's age and energy intake were positively associated with BLLs (p = 0.015 and p = 0.024, respectively). Consuming traditional foods rich in calcium as well as milk and alternatives may protect against lead exposure.
Arctic populations are exposed to substantial levels of environmental contaminants that can negatively affect children's health and development. Moreover, emerging contaminants have never been assessed in Inuit children. In this study, we document the biological exposure to toxic metals and legacy and emerging persistent organic pollutants (POPs) of 155 Inuit children (mean age 25.2 months) attending childcare centers in Nunavik. Blood samples were analyzed to determine concentrations of mercury, lead, polychlorinated biphenyls (PCBs), pesticides, brominated flame retardants [e.g., polybrominated diphenyl ethers (PBDEs)] and perfluoroalkyl and polyfluoroalkyl substances [PFASs; e.g. perfluorooctanesulfonate (PFOS) and perfluorooctane (PFOA)]. Lead [geometric mean (GM) 0.08 µmol/L], PCB-153 (GM 22.2 ng/g of lipid), BDE-47 (GM 184 ng/g of lipid), PFOS (GM 3369 ng/L), and PFOA (GM 1617 ng/L) were detected in all samples. Mercury (GM 9.8 nmol/L) was detected in nearly all blood samples (97%). Levels of metals and legacy POPs are consistent with the decreasing trend observed in Nunavik and in the Arctic. PBDE levels were higher than those observed in many children and adolescents around the world but lower than those reported in some U.S. cities. PFOS were present in lower concentrations than in Nunavimmiut adults. There is a clear need for continued biomonitoring of blood contaminant levels in this population, particularly for PBDEs and PFASs.
Erratum In: Environ Sci Technol. 2012 Jul 17;46(14):7926
Immune suppression may be a critical effect associated with exposure to perfluorinated compounds (PFCs), as indicated by recent data on vaccine antibody responses in children. Therefore, this information may be crucial when deciding on exposure limits.
Results obtained from follow-up of a Faroese birth cohort were used. Serum-PFC concentrations were measured at age 5 years, and serum antibody concentrations against tetanus and diphtheria toxoids were obtained at age 7 years. Benchmark dose results were calculated in terms of serum concentrations for 431 children with complete data using linear and logarithmic curves, and sensitivity analyses were included to explore the impact of the low-dose curve shape.
Under different linear assumptions regarding dose-dependence of the effects, benchmark dose levels were about 1.3 ng/mL serum for perfluorooctane sulfonic acid and 0.3 ng/mL serum for perfluorooctanoic acid at a benchmark response of 5%. These results are below average serum concentrations reported in recent population studies. Even lower results were obtained using logarithmic dose-response curves. Assumption of no effect below the lowest observed dose resulted in higher benchmark dose results, as did a benchmark response of 10%.
The benchmark dose results obtained are in accordance with recent data on toxicity in experimental models. When the results are converted to approximate exposure limits for drinking water, current limits appear to be several hundred fold too high. Current drinking water limits therefore need to be reconsidered.
In 1999, the Government of Canada regulated the use of lead shot for hunting. Concurrently, the Nunavik Regional Board of Health and Social Services (NRBHSS) was informed of the results of an isotope study that pointed to lead ammunition as a likely source of lead exposure in Nunavik. Rapidly thereafter, a coalition for the banning of lead shot was implemented by the NRBHSS as well as by regional/local partners and by Inuit hunters in order to disseminate this information to the public.
The purpose of this article is to describe the intervention conducted in the winter of 1999 by the NRBHSS and to assess the combined impact of national legislation and an awareness campaign on blood lead levels in Nunavik.
Impact assessment of the intervention for the banning of lead shot conducted in 1999 in Nunavik using blood lead levels data before and after the intervention.
Data on blood lead levels in Nunavik describing foetal exposure as well as during childhood and in adults published between 1992 and 2009 were compiled. Blood lead levels in Nunavik prior to and after the interventions were compared. To assess the current situation, the most recent blood lead levels were compared with those from surveys conducted during the same period in North America.
Analysis of blood samples collected from umbilical cord and from adults show that blood lead levels in Nunavik significantly declined between 1992 and 2004. Nevertheless, lead exposure in Nunavik still remains higher in comparison to that observed in other North American surveys.
The current situation regarding lead exposure in Nunavik has significantly improved as a result of the implemented intervention. However, according to recent data, a gap still subsists relative to other North American populations.