Arsenic Exposure within the Korean Community (United States) Based on Dietary Behavior and Arsenic Levels in Hair,Urine, Air,and Water

Background

Determining arsenic exposure in groups based on geographic location, dietary behaviors, or lifestyles is important, as even moderate exposures may lead to health concerns.

Objectives/Methods

The Korean community in Washington State, represents a group warranting investigation, as they consume foods (e.g., shellfish, rice, finfish, and seaweed) known to contain arsenic. As part of the Arsenic Mercury Intake Biometric Study, we examined the arsenic levels in hair and urine along with the diets of 108 women of childbearing age from within this community. Arsenic levels in indoor air and drinking water were also investigated, and shellfish commonly consumed were collected and analyzed for total and speciated arsenic.

Results

The six shellfish species analyzed (n = 667) contain total arsenic (range, 1–5 μg/g) but are a small source of inorganic arsenic (range, 0.01–0.12 μg/g). Six percent of the individuals may have elevated urinary inorganic arsenic levels (> 10 μg/L) due to diet. Seaweed, rice, shellfish, and finfish are principal sources for total arsenic intake/excretion based on mass balance estimates. Rice consumption (163 g/person/day) may be a significant source of inorganic arsenic. Air and water are not significant sources of exposure. Hair is a poor biometric for examining arsenic levels at low to moderate exposures.

Conclusions

We conclude that a portion of this community may have dietary inorganic arsenic exposure resulting in urine levels exceeding 10 μg/L. Although their exposure is below that associated with populations exposed to high levels of arsenic from drinking water (> 100 μg/L), their exposure may be among the highest in the United States.     

Association between Lifetime Exposure to Inorganic Arsenic in Drinking Water and Coronary Heart Disease in Colorado Residents

Background: Chronic diseases, including coronary heart disease (CHD), have been associated with ingestion of drinking water with high levels of inorganic arsenic (> 1,000 μg/L). However, associations have been inconclusive in populations with lower levels (< 100 μg/L) of inorganic arsenic exposure.Objectives: We conducted a case-cohort study based on individual estimates of lifetime arsenic exposure to examine the relationship between chronic low-level arsenic exposure and risk of CHD.Methods: This study included 555 participants with 96 CHD events diagnosed between 1984 and 1998 for which individual lifetime arsenic exposure estimates were determined using data from structured interviews and secondary data sources to determine lifetime residence, which was linked to a geospatial model of arsenic concentrations in drinking water. These lifetime arsenic exposure estimates were correlated with historically collected urinary arsenic concentrations. A Cox proportional-hazards model with time-dependent CHD risk factors was used to assess the association between time-weighted average (TWA) lifetime exposure to low-level inorganic arsenic in drinking water and incident CHD.Results: We estimated a positive association between low-level inorganic arsenic exposure and CHD risk [hazard ratio (HR): = 1.38, 95% CI: 1.09, 1.78] per 15 μg/L while adjusting for age, sex, first-degree family history of CHD, and serum low-density lipoprotein levels. The risk of CHD increased monotonically with increasing TWAs for inorganic arsenic exposure in water relative to < 20 μg/L (HR = 1.2, 95% CI: 0.6, 2.2 for 20–30 μg/L; HR = 2.2; 95% CI: 1.2, 4.0 for 30–45 μg/L; and HR = 3, 95% CI: 1.1, 9.1 for 45–88 μg/L).Conclusions: Lifetime exposure to low-level inorganic arsenic in drinking water was associated with increased risk for CHD in this population.Citation: James KA, Byers T, Hokanson JE, Meliker JR, Zerbe GO, Marshall JA. 2015. Association between lifetime exposure to inorganic arsenic in drinking water and coronary heart disease in Colorado residents. Environ Health Perspect 123:128–134; http://dx.doi.org/10.1289/ehp.1307839     

Lung Cancer in a U.S. Population with Low to Moderate Arsenic Exposure

Background

Little is known about the carcinogenic potential of arsenic in areas with low to moderate concentrations of arsenic (< 100 μg/L) in drinking water.

Objectives

We examined associations between arsenic and lung cancer.

Methods

A population-based case–control study of primary incident lung cancer was conducted in 10 counties in two U.S. states, New Hampshire and Vermont. The study included 223 lung cancer cases and 238 controls, each of whom provided toenail clippings for arsenic exposure measurement by inductively coupled–plasma mass spectrometry. We estimated odds ratios (ORs) of the association between arsenic exposure and lung cancer using unconditional logistic regression with adjustment for potential confounders (age, sex, race/ethnicity, smoking pack-years, education, body mass index, fish servings per week, and toenail selenium level).

Results

Arsenic exposure was associated with small-cell and squamous-cell carcinoma of the lung [OR = 2.75; 95% confidence interval (CI), 1.00–7.57] for toenail arsenic concentration ≥ 0.114 μg/g, versus < 0.05 μg/g. A history of lung disease (bronchitis, chronic obstructive pulmonary disease, or fibrosis) was positively associated with lung cancer (OR = 2.86; 95% CI, 1.39–5.91). We also observed an elevated risk of lung cancer among participants with a history of lung disease and toenail arsenic ≥ 0.05 μg/g (OR = 4.78; 95% CI, 1.87–12.2) than among individuals with low toenail arsenic and no history of lung disease.

Conclusion

Although this study supports the possibility of an increased risk of specific lung cancer histologic types at lower levels of arsenic exposure, we recommend large-scale population-based studies.     

One-year follow-up of perfluorinated compounds in plasma of German residents from Arnsberg formerly exposed to PFOA-contaminated drinking water

In Arnsberg, Sauerland area Germany, 40 000 residents were exposed to PFOA-contaminated drinking water (500-640 ng PFOA/l; May 2006). In July 2006, the PFOA-concentrations in drinking water were lowered significantly by activated charcoal filtering in the waterworks, mostly below the limit of detection (10 ng/l). A first human biomonitoring study performed in autumn 2006 revealed that PFOA-concentrations in blood plasma of residents living in Arnsberg were 4.5–8.3 times higher than in the reference groups. One year after the first survey, all participants (2006: 164 mothers, 90 children, 101 men) were invited to take part in a follow-up study. It was the aim of the study to determine the decline of the PFOA-concentrations in blood plasma. 288 persons (81%) were included in the statistical analysis. The (geometric) mean PFOA-concentrations in blood plasma of Arnsberg's residents decreased from 22.1 to 17.4 μg/l in children, from 23.4 to 18.8 μg/l in mothers and from 25.3 to 23.4 μg/l in men within one year. The average (geometric mean) changes in each individual's PFOA-concentrations were approximately 10 (men), 17 (mothers) and 20 (children) percent/year. The observed decline in PFOA-concentrations indicates a slow elimination in humans. This finding in groups of the general population is in agreement with data on long elimination half-lives observed in occupationally exposed workers.     

Estimated Exposure to Arsenic in Breastfed and Formula-Fed Infants in a United States Cohort

Background: Previous studies indicate that concentrations of arsenic in breast milk are relatively low even in areas with high drinking-water arsenic. However, it is uncertain whether breastfeeding leads to reduced infant exposure to arsenic in regions with lower arsenic concentrations.Objective: We estimated the relative contributions of breast milk and formula to arsenic exposure during early infancy in a U.S. population.Methods: We measured arsenic in home tap water (n = 874), urine from 6-week-old infants (n = 72), and breast milk from mothers (n = 9) enrolled in the New Hampshire Birth Cohort Study (NHBCS) using inductively coupled plasma mass spectrometry. Using data from a 3-day food diary, we compared urinary arsenic across infant feeding types and developed predictive exposure models to estimate daily arsenic intake from breast milk and formula.Results: Urinary arsenic concentrations were generally low (median, 0.17 μg/L; maximum, 2.9 μg/L) but 7.5 times higher for infants fed exclusively with formula than for infants fed exclusively with breast milk (β = 2.02; 95% CI: 1.21, 2.83; p < 0.0001, adjusted for specific gravity). Similarly, the median estimated daily arsenic intake by NHBCS infants was 5.5 times higher for formula-fed infants (0.22 μg/kg/day) than for breastfed infants (0.04 μg/kg/day). Given median arsenic concentrations measured in NHBCS tap water and previously published for formula powder, formula powder was estimated to account for ~ 70% of median exposure among formula-fed NHBCS infants.Conclusions: Our findings suggest that breastfed infants have lower arsenic exposure than formula-fed infants, and that both formula powder and drinking water can be sources of exposure for U.S. infants.Citation: Carignan CC, Cottingham KL, Jackson BP, Farzan SF, Gandolfi AJ, Punshon T, Folt CL, Karagas MR. 2015. Estimated exposure to arsenic in breastfed and formula-fed infants in a United States cohort. Environ Health Perspect 123:500–506; http://dx.doi.org/10.1289/ehp.1408789     

No Association between Arsenic Exposure from Drinking Water and Diabetes Mellitus: A Cross-Sectional Study in Bangladesh

Background

The long-term effects of arsenic exposure from drinking water at levels < 300 μg/L and the risk of diabetes mellitus remains a controversial topic.

Method

We conducted a population-based cross-sectional study using baseline data from 11,319 participants in the Health Effects of Arsenic Longitudinal Study in Araihazar, Bangladesh, to evaluate the associations of well water arsenic and total urinary arsenic concentration and the prevalence of diabetes mellitus and glucosuria. We also assessed the concentrations of well water arsenic, total urinary arsenic, and urinary arsenic metabolites in relation to blood glycosylated hemoglobin (HbA1c) levels in subsets of the study population.

Results

More than 90% of the cohort members were exposed to drinking water with arsenic concentration < 300 μg/L. We found no association between arsenic exposure and the prevalence of diabetes. The adjusted odds ratios for diabetes were 1.00 (referent), 1.35 [95% confidence interval (CI), 0.90–2.02], 1.24 (0.82–1.87), 0.96 (0.62–1.49), and 1.11 (0.73–1.69) in relation to quintiles of time-weighted water arsenic concentrations of 0.1–8, 8–41, 41–91, 92–176, and ≥ 177 μg/L, respectively, and 1.00 (referent), 1.29 (0.87–1.91), 1.05 (0.69–1.59), 0.94 (0.61–1.44), and 0.93 (0.59–1.45) in relation to quintiles of urinary arsenic concentrations of 1–36, 37–66, 67–114, 115–204, and ≥ 205 μg/L, respectively. We observed no association between arsenic exposure and prevalence of glucosuria and no evidence of an association between well water arsenic, total urinary arsenic, or the composition of urinary arsenic metabolites and HbA1c level.

Conclusions

Our findings do not support an association of arsenic exposure from drinking water and a significantly increased risk of diabetes mellitus in the range of levels observed. Further prospective studies would be valuable in confirming the findings.     

Dietary Selenium Deficiency Partially Mimics the Metabolic Effects of Arsenic

Chronic arsenic exposure via drinking water is associated with diabetes in human pop-ulations throughout the world. Arsenic is believed to exert its diabetogenic effects via multiple mechanisms, including alterations to insulin secretion and insulin sensitivity. In the past, acute arsenicosis has been thought to be partially treatable with selenium supplementation, though a potential interaction between selenium and arsenic had not been evaluated under longer-term exposure models. The purpose of the present study was to explore whether selenium status may augment arsenic’s effects during chronic arsenic exposure. To test this possibility, mice were exposed to arsenic in their drinking water and provided ad libitum access to either a diet replete with selenium (Control) or deficient in selenium (SelD). Arsenic significantly improved glucose tolerance and decreased insulin secretion and β-cell function in vivo. Dietary selenium deficiency resulted in similar effects on glucose tolerance and insulin secretion, with significant interactions between arsenic and dietary conditions in select insulin-related parameters. The findings of this study highlight the complexity of arsenic’s metabolic effects and suggest that selenium deficiency may interact with arsenic exposure on β-cell-related physiological parameters.     

Influence d'une supplémentation en vitamine E sur le sélénium au cours d'une nutrition parentérale exclusive chez l'enfant

Double supplementation in selenium and vitamin E during total parenteral nutrition (TPN) now appears essential to avoid clinical manifestations of their deficiencies. We studied children of 1 month to 12 years of age deficient in selenium (plasmatic selenium : P-Se : 40–80 μg/L) and vitamin E (ratio vitamin E on total lipids : VE/LT = 1.10 − 1.80 mg/g). Prior to supplementation, the ratio VE/LT is negatively correlated to P-Se (r = −0.81) and positively to erythrocyte selenium (RBC-Se, r = +0.64). These results suggest a balance between both. The parenteral alimentation was then supplemented with sodium selenite (3 μg/kg/d) and weekly with IM vitamin E (Protocol 1 : P1 : 30 to 60 mg according to age; Protocol 2 : P2 : twice these doses). The ratio VE/LT returned to normal faster in P2 than in P1 (P2 : 15–30 days; P1 : about 120 days). Selenium supplementation restores P-Se quickly (45–60 days) contrary to RBC-Se which is a slow process (120 d). High vitamin E intakes do not seem to have an effect upon selenium stores : no statistical differences were found between P1 and P2 during the same period. Such intakes may however be indicated during the first month of TPN to balance the time course for repletion of RBC-Se which is long (120 days).     

Effects of nonylphenol on cholinesterase and carboxylesterase activities in male guppies (Poecilia reticulata)

Compared to the estrogenic effects of 4-nonylphenol (NP), there is little data available on other potential toxic effects of NP in aquatic animals. The effects of NP on cholinesterase (ChE) and carboxylesterase (CbE) activities of male guppies exposed to 10, 60, 150, or 300 μg L⁻¹ NP were examined after 1, 2, 4, and 7 days of treatment. A significant muscle ChE inhibition, that used acetylthiocholine iodide as a substrate, was noted in male guppies in all NP treatment groups after a 4-day exposure, and 60 and 150 μg L⁻¹ of NP treatment groups after a 7-day exposure. All guppies exposed to 300 μg L⁻¹ NP died during the 7-day treatment. However, there was no significant inhibition of muscle ChE that used butyrylthiocholine iodide as a substrate in male guppies for any NP treatments in different exposure times. There were no CbE activity differences in livers of male guppies among NP treatment groups after different exposure times. This is the first report showing the ChE activity inhibition by NP in fish. Further mechanistic studies are needed to define how NP directly or indirectly alters ChE activities at molecular level. The implication of ChE inhibition of NP on potential impacts of aquatic animals also warrants further research.     

Serum Selenium Concentrations and Diabetes in U.S. Adults: National Health and Nutrition Examination Survey (NHANES) 2003–2004

Background

Increasing evidence suggests that high selenium levels are associated with diabetes and other cardiometabolic risk factors.

Objectives

We evaluated the association of serum selenium concentrations with fasting plasma glucose, glycosylated hemoglobin levels, and diabetes in the most recently available representative sample of the U.S. population.

Methods

We used a cross-sectional analysis of 917 adults ≥ 40 years of age who had a fasting morning blood sample in the National Health and Nutrition Examination Survey 2003–2004. We evaluated the association of serum selenium, measured by inductively coupled plasma-dynamic reaction cell-mass spectrometry, and diabetes, defined as a self-report of current use of hypoglycemic agents or insulin or as fasting plasma glucose ≥ 126 mg/dL.

Results

Mean serum selenium was 137.1 μg/L. The multivariable adjusted odds ratio [95% confidence interval (CI)] for diabetes comparing the highest quartile of serum selenium (≥ 147 μg/L) with the lowest (< 124 μg/L) was 7.64 (3.34–17.46). The corresponding average differences (95% CI) in fasting plasma glucose and glycosylated hemoglobin were 9.5 mg/dL (3.4–15.6 mg/dL) and 0.30% (0.14–0.46%), respectively. In spline regression models, the prevalence of diabetes as well as glucose and glycosylated hemoglobin levels increased with increasing selenium concentrations up to 160 μg/L.

Conclusions

In U.S. adults, high serum selenium concentrations were associated with higher prevalence of diabetes and higher fasting plasma glucose and glycosylated hemoglobin levels. Given high selenium intake in the U.S. population, further research is needed to determine the role of excess selenium levels in the development or the progression of diabetes.     

Carotid Intima-Media Thickness and Plasma Asymmetric Dimethylarginine in Mexican Children Exposed to Inorganic Arsenic

Background: Arsenic exposure is a risk factor for atherosclerosis in adults, but there is little information on arsenic and early risk biomarkers for atherosclerosis in children. Carotid intima-media thickness (cIMT) is an indicator of subclinical atherosclerotic burden that has been associated with plasma asymmetric dimethylarginine (ADMA), a predictor of cardiovascular disease risk.Objectives: The aim of this study was to investigate associations of arsenic exposure with cIMT, ADMA, and endothelial adhesion molecules [soluble intercellular cell adhesion molecule-1 (sICAM-1); soluble vascular cell adhesion molecule-1 (sVCAM-1)] in children who had been exposed to environmental inorganic arsenic (iAs).Methods: We conducted a cross-sectional study in 199 children 3–14 years of age who were residents of Zimapan, México. We evaluated cIMT using ultrasonography, and plasma lipid profiles by standard methods. We analyzed ADMA, sICAM-1, and sVCAM-1 by ELISA, and measured the concentrations of total speciated arsenic (tAs) in urine using hydride generation cryotrapping atomic absorption spectrometry.Results: In the multiple linear regression model for cIMT, tAs categories were positively associated with cIMT increase. The estimated cIMT diameter was greater in 35- to 70-ng/mL and > 70-ng/mL groups (0.035 mm and 0.058 mm per 1-ng/mL increase in urinary tAs, respectively), compared with the < 35-ng/mL group. In addition to tAs level, plasma ADMA was a significant predictor of cIMT. In the adjusted regression model, cIMT, percent iAs, and plasma sVCAM-1 were significant predictors of ADMA levels (e.g., 0.419-μmol/L increase in ADMA per 1-mm increase in cIMT).Conclusions: Arsenic exposure and plasma ADMA levels were positively associated with cIMT in a population of Mexican children with environmental arsenic exposure through drinking water.Citation: Osorio-Yáñez C, Ayllon-Vergara JC, Aguilar-Madrid G, Arreola-Mendoza L, Hernández-Castellanos E, Barrera-Hernández A, De Vizcaya-Ruíz A, Del Razo LM. 2013. Carotid intima-media thickness and plasma asymmetric dimethylarginine in Mexican children exposed to inorganic arsenic. Environ Health Perspect 121:1090–1096; http://dx.doi.org/10.1289/ehp.1205994     

Effects of Dietary Selenomethionine on Larval Rainbow Trout (Oncorhynchus mykiss)

Increased selenium (Se) concentrations in water (>10 μg/L) have been measured in the San Diego Creek, which is a tributary of the Upper Newport Bay in Orange County, CA. The objective of this study was to develop tissue- and dietary-based thresholds for Se in resident fish species in San Diego Creek. A 90-day dietary experiment was conducted to determine the effects of seleno-L-methionine (SeMe) on the growth, survival, and whole-body Se accumulation in larval (24-day-old) rainbow trout. Decreased and oxidized glutathione (GSH-to-GSSG ratio) and thiobarbituric acid–reactive substances (TBARS) were also measured in livers of exposed animals to assess oxidative damage caused by Se. Fish food was spiked with SeMe to contain 4.6, 12, and 18 μg/g (dry weight) of Se. Fish exposed to SeMe for 90 days exhibited a significant decrease in body weight and fork length in the 4.6 and 12 μg/g Se treatments compared with controls. Whole-body total Se concentrations increased significantly in fish fed 12 and 18 μg/g SeMe after 90 days compared with controls. Lipid peroxidation (TBARS) and GSH-to-GSSG ratios were unchanged by SeMe treatment. Based on decreased growth after 90 days, a dietary Se lowest observed-effect concentration (LOEC) value of 4.6 μg/g and a Se body burden LOEC of 1.20 μg/g (wet weight) were estimated.     

Selenium supplements do not increase plasma total homocysteine concentrations in men and women

Studies in rats indicate that plasma total homocysteine (tHcy) is decreased in selenium deficiency and increases with selenium supplementation. The aim of this study was to determine the effect of selenium supplements on plasma tHcy concentrations in a population that has suboptimal selenium status. Subjects from Dunedin, New Zealand (n = 189) were randomly assigned to receive a supplement containing 200 micro g selenium or placebo for 20 wk. At baseline, 67% (n = 112) of the participants had plasma selenium concentrations < 1.2 micro mol/L, a concentration believed to be that necessary for full glutathione peroxidase (Gpx) activity. At 20 wk, plasma selenium concentration and Gpx activity increased in the selenium group by 1.2 micro mol/L [95% confidence interval (CI): 1.1, 1.3] and 5.1 nkat/g protein (3.7, 6.5), respectively, changes that were significantly greater than the changes in the placebo group (P < 0.001). At 20 wk, mean changes in plasma tHcy concentrations were 0.1 micro mol/L (95% CI: -0.4, 0.5) and -0.2 micro mol/L (-0.7, 0.3) in the supplemented and placebo groups, respectively, compared to baseline. There was no difference in the mean changes in plasma tHcy between the supplemented and placebo groups (P = 0.54). These results suggest that selenium supplementation does not influence plasma tHcy concentrations in healthy populations in developed countries, whose selenium status is characterized by lower plasma selenium concentrations.     

Total and individual carotenoid profiles in Solanum phureja of cultivated potatoes: I. Concentrations and relationships as determined by spectrophotometry and HPLC

Total and individual carotenoid concentrations were determined by spectrophotometry and HPLC, in raw tubers of a sample of 23 accessions of Solanum phureja potatoes taken at random from the world germplasm collection following its stratification on tuber flesh color. Lutein, zeaxanthin, violaxanthin, antheraxanthin and β-carotene were detected in all accessions and three distinct patterns of carotenoid accumulation were evidenced by cluster analysis. Accessions in group 1 showed the highest concentrations of total carotenoids (1258–1840 μg 100 g⁻¹ FW) comprised largely of zeaxanthin (658–1290 μg 100 g⁻¹ FW) with very low or no presence of β-carotene (below 5.4 μg 100 g⁻¹ FW). Accessions in group 2 presented moderate total carotenoid concentrations with violaxanthin, antheraxanthin, lutein and zeaxanthin as the major carotenoids. Accessions in group 3 showed low concentrations of total carotenoids (97–262 μg 100 g⁻¹ FW) and very low or no zeaxanthin, with lutein and violaxanthin as the predominant carotenoids and relatively high concentrations of β-carotene (up to 27 μg 100 g⁻¹ FW). Five accessions with significant concentrations of zeaxanthin were identified with the accession 703566 showing the highest concentration (1290 μg 100 g⁻¹ FW). This value is to our knowledge higher than any value previously reported for potatoes, including those achieved through genetic modification. For the 23 S. phureja accessions, total carotenoid concentration was positively and significantly correlated with antheraxanthin and zeaxanthin concentrations, and negatively and significantly correlated with β-carotene concentration.     

Transfer of nodularin to three-spined stickleback (Gasterosteus aculeatus L.), herring (Clupea harengus L.), and salmon (Salmo salar L.) in the northern Baltic Sea

Nodularin (NODLN) is a hepatotoxin produced by the cyanobacterium Nodularia spumigena, which occurs regularly in the Baltic Sea. The primary aim of this study was to study the transfer of NODLN to three-spined stickleback (Gasterosteus aculeatus L.), herring (Clupea harengus membras L.), and salmon (Salmo salar L.), which were caught from the northern Baltic Sea between August 2002 and August 2003. Liquid chromatography mass spectrometry (LC-MS) was used for NODLN analysis. NODLN was found in both herring (0–90 μg kg⁻¹ dw) and three-spined sticklebacks samples (2.8–700 μg kg⁻¹ dw). The recovery for the spiked stickleback samples in vitro was 28%. Only 1 salmon of a total of 10 contained a small amount of NODLN (10 μg kg⁻¹ dw). However, the high concentrations in individual stickleback suggest that possible transfer to higher trophic levels deserves more research.     

Urine Arsenic Concentrations and Species Excretion Patterns in American Indian Communities Over a 10-year Period: The Strong Heart Study

Background

Arsenic exposure in drinking water disproportionately affects small communities in some U.S. regions, including American Indian communities. In U.S. adults with no seafood intake, median total urine arsenic is 3.4 μg/L.

Objective

We evaluated arsenic exposure and excretion patterns using urine samples collected over 10 years in a random sample of American Indians from Arizona, Oklahoma, and North and South Dakota who participated in a cohort study from 1989 to 1999.

Methods

We measured total urine arsenic and arsenic species [inorganic arsenic (arsenite and arsenate), methylarsonate (MA), dimethylarsinate (DMA), and arsenobetaine] concentrations in 60 participants (three urine samples each, for a total of 180 urine samples) using inductively coupled plasma/mass spectrometry (ICPMS) and high-performance liquid chromatography/ICPMS, respectively.

Results

Median (10th, 90th percentiles) urine concentration for the sum of inorganic arsenic, MA, and DMA at baseline was 7.2 (3.1, 16.9) μg/g creatinine; the median was higher in Arizona (12.5 μg/g), intermediate in the Dakotas (9.1 μg/g), and lower in Oklahoma (4.4 μg/g). The mean percentage distribution of arsenic species over the sum of inorganic and methylated species was 10.6% for inorganic arsenic, 18.4% for MA, and 70.9% for DMA. The intraclass correlation coefficient for three repeated arsenic measurements over a 10-year period was 0.80 for the sum of inorganic and methylated species and 0.64, 0.80, and 0.77 for percent inorganic arsenic, percent MA, and percent DMA, respectively.

Conclusions

This study found low to moderate inorganic arsenic exposure and confirmed long-term constancy in arsenic exposure and urine excretion patterns in American Indians from three U.S. regions over a 10-year period. Our findings support the feasibility of analyzing arsenic species in large population-based studies with stored urine samples.     

The Effect on Selenium Concentrations of a Randomized Intervention with Fish and Mussels in a Population with Relatively Low Habitual Dietary Selenium Intake

Selenium status of the Danish population is below that assumed optimal for the suggested protective effects against chronic diseases, including certain cancers. Fish and shellfish are important dietary sources of selenium in Denmark. We investigated the effect of increased fish and mussel intake on selenium blood concentrations in a population with relatively low habitual dietary selenium intake. We randomly assigned 102 healthy men and women (all non-smokers) aged 48–76 years to an intervention group (n = 51) or a control group (n = 51). Intervention participants received 1000 g fish and mussels/week for 26 weeks (~50 μg selenium/day). Controls received no intervention. Non-fasting blood samples were taken and whole blood selenium was determined using inductively coupled plasma-mass spectrometry (ICP-MS), and plasma selenoprotein P (SelP) was determined by high performance liquid chromatography coupled to ICP-MS. All available observations were included in linear multiple regression analysis to evaluate the effect of the intervention. The difference in mean change for intervention compared with control persons was 14.9 ng/mL (95% CI: 10.2, 19.7) for whole blood selenium, and 7.0 ng/mL (95% CI: 3.1, 10.9) for plasma SelP (Weeks 0–26). Selenium concentrations were significantly increased after 26 weeks of intervention, albeit to a lower degree than expected.     

Pre-Antiretroviral Therapy Serum Selenium Concentrations Predict WHO Stages 3, 4 or Death but not Virologic Failure Post-Antiretroviral Therapy

A case-cohort study, within a multi-country trial of antiretroviral therapy (ART) efficacy (Prospective Evaluation of Antiretrovirals in Resource Limited Settings (PEARLS)), was conducted to determine if pre-ART serum selenium deficiency is independently associated with human immunodeficiency virus (HIV) disease progression after ART initiation. Cases were HIV-1 infected adults with either clinical failure (incident World Health Organization (WHO) stage 3, 4 or death by 96 weeks) or virologic failure by 24 months. Risk factors for serum selenium deficiency (<85 μg/L) pre-ART and its association with outcomes were examined. Median serum selenium concentration was 82.04 μg/L (Interquartile range (IQR): 57.28–99.89) and serum selenium deficiency was 53%, varying widely by country from 0% to 100%. In multivariable models, risk factors for serum selenium deficiency were country, previous tuberculosis, anemia, and elevated C-reactive protein. Serum selenium deficiency was not associated with either clinical failure or virologic failure in multivariable models. However, relative to people in the third quartile (74.86–95.10 μg/L) of serum selenium, we observed increased hazards (adjusted hazards ratio (HR): 3.50; 95% confidence intervals (CI): 1.30–9.42) of clinical failure but not virologic failure for people in the highest quartile. If future studies confirm this relationship of high serum selenium with increased clinical failure, a cautious approach to selenium supplementation might be needed, especially in HIV-infected populations with sufficient or unknown levels of selenium.     

Phylloquinone (vitamin K1) content of vegetables

Assessment of vitamin K (VK) dietary intakes has been limited by incomplete VK food composition data for the US food supply. The phylloquinone (VK-1 or vitamin K₁) concentrations of a variety of geographically representative vegetables (n=218) were determined by reversed-phase high performance liquid chromatography with fluorescent detection. Green leafy and flower vegetables including broccoli, broccoli raab, spinach, and certain lettuces, contained >100 μg phylloquinone/100 g vegetable. In contrast, raw tubers and roots contained <10 μg phylloquinone/100 g vegetable. Iceberg lettuce, a primary dietary source of phylloquinone, contained 24.1 μg phylloquinone/100 g vegetable, which is less than previously listed in nutrient databases. Potential factors affecting phylloquinone concentrations include processing and varietal type of leafy vegetables.     

Metallothionein Gene Expression in Liver of Rats Exposed to Cadmium and Supplemented with Zinc and Selenium

Cadmium (Cd), one of the most widely distributed heavy metals, is highly toxic to humans and animals. It is well known that zinc (Zn) and selenium (Se) administration reduce the Cd-induced toxicity and that metallothioneins can have a protective effect to mitigate Cd toxicity in biological systems. In this study we report the expression analysis of the two metallothioneines gene classes MT-1 and MT-2 as well as the total metalloprotein content in the liver of rats exposed to Cd (200 ppm), Cd + Zn (200 ppm + 500 ppm), Cd + Se (200 ppm + 0.1 ppm) or Cd + Zn + Se (200 ppm + 500 ppm + 0.1 ppm) in their drinking water for 35 days. Metals accumulation was quantified in rat liver. Cd decreased significantly the hepatic concentrations of Se and increased those of Zn. The treatment of Cd-exposed rats with Se alone or combined with Zn reversed the Cd-induced depletion of Se concentrations in the liver. However, Zn or Zn + Se administration significantly increased the liver Cd uptake and had no effect on the Cd-induced increase in hepatic concentrations of Zn. The molecular assay showed a decreasing trend of MT-1 relative gene expression levels in animals supplemented with Zn (6.87-fold), Se (3.58-fold), and their combination (1.69-fold) when compared to Cd-treated animals (16.22-fold). Upregulation of the MT-2 expression were recorded in all conditions, although fold induction levels were less pronounced than MT-1 expressions. Our data suggest that the well-established protective effect of Zn and Se against Cd-induced toxicity passes through non-MT gene expression mechanisms, being more dependent on the oxidative stress status of the cell.