Cd Body Burden Research Articles

Urinary N-acetylglucosaminidase in People Environmentally Exposed to Cadmium Is Minimally Related to Cadmium-Induced Nephron Destruction

Exposure to even low levels of the environmental pollutant cadmium (Cd) increases the risk of kidney damage and malfunction. The body burden of Cd at which these outcomes occur is not, however, reliably defined. Here, multiple-regression and mediation analyses were applied to data from 737 non-diabetic Thai nationals, of which 9.1% had an estimated glomerular filtration rate (eGFR) ≤ 60 mL/min/1.73 m2 (a low eGFR). The excretion of Cd (ECd), and renal-effect biomarkers, namely β2-microglobulin (Eβ2M), albumin (Ealb), and N-acetylglucosaminidase (ENAG), were normalized to creatinine clearance (Ccr) as ECd/Ccr Eβ2M/Ccr, Ealb/Ccr, and ENAG/Ccr. After adjustment for potential confounders, the risks of having a low eGFR and albuminuria rose twofold per doubling ECd/Ccr rates and they both varied directly with the severity of β2-microglobulinuria. Doubling ECd/Ccr rates also increased the risk of having a severe tubular injury, evident from ENAG/Ccr increments [POR = 4.80, p = 0.015]. ENAG/Ccr was strongly associated with ECd/Ccr in both men (β = 0.447) and women (β = 0.394), while showing a moderate inverse association with eGFR only in women (β = −0.178). A moderate association of ENAG/Ccr and ECd/Ccr was found in the low- (β = 0.287), and the high-Cd body burden groups (β = 0.145), but ENAG/Ccr was inversely associated with eGFR only in the high-Cd body burden group (β = −0.223). These discrepancies together with mediation analysis suggest that Cd-induced nephron destruction, which reduces GFR and the tubular release of NAG by Cd, involves different mechanisms and kinetics.

Intake and excretion of cadmium of Japanese adult

ObjectiveIt is the aim of this study if the recent Cd intake and excretion is consistent with the regression equation proposed by Ikeda et al. (Environ. Health Prev. Med. 20 (2015) 455–459) which utilized intake/excretion data of 3 decades ago MethodMatched duplicate diet and spot urine samples were collected in 2017–2019 from 150 Japanese adults (85 females and 65 males, mean age being 44.9) for the estimation of daily Cd intake and urinary excretion. Cd concentration in diet and urine was measured by ICP mass spectrometry. ResultGeometric mean (geometric standard deviation) of Cd intake was 12.1 (1.67) μg/person/day or 0.206 (1.66) μg/kg body wt./day. Urinary Cd concentration was 0.54 (2.6) μg/g creatinine or 0.67 μg/L (2.3) (gravimetric correction). These were lower than those reported previously for Japanese populations. Urinary concentration was significantly higher in females than in males for both creatinine and gravimetric corrections. Dietary intake was higher in males than in females but this difference diminished after body weight correction. There was no significant correlation between Cd intake and urinary concentration on individual basis, which was expected because urinary Cd concentration reflects Cd body burden but not recent intake level. Meanwhile, the geometric mean intake and urine concentration was consistent with the regression equation proposed by Ikeda et al., which was based on intake and excretion surveys for 30 non-exposed Japanese female populations. ConclusionThis result supported that the regression equation of Ikeda et al. could be used for conversion of urinary Cd excretion level of a population to intake level.

Environmental Cadmium Exposure Induces an Increase in Systolic Blood Pressure by Its Effect on GFR

Chronic exposure to the nephrotoxic metal pollutant, cadmium (Cd), has been associated with hypertension, but the mechanism by which it raises blood pressure is not understood. We hypothesize that exposure to Cd reduces the glomerular filtration rate (GFR), which in turn causes a rise in blood pressure. Data were collected from 447 Thai subjects with a mean age of 51.1 years, of which 48.8% had hypertension, 15.4% had diabetes, and 6.9% had an estimated GFR (eGFR) below 60 mL/min/1.73 m2 (low eGFR). More than half (58.8%) and 23.9% had moderate and severe tubular proteinuria, respectively. The mean blood and urinary Cd concentrations were 2.75 and 4.23 µg/L, respectively. Doubling of body burden of Cd increased the prevalence odds ratios (POR) for low eGFR and severe tubular proteinuria 41% and 48%, respectively. The POR for hypertension rose twofold in those with blood Cd levels of 0.61–1.69 µg/L or urinary Cd excretion levels ≥ 0.98 µg/g creatinine. In the hypertensive group, the eGFR was inversely associated with age (β = −0.517), the Cd excretion rate (β = −0.177), and diabetes (β = −0.175). By mediation analysis, an increase in SBP was attributable totally to the effect of Cd on GFR. Thus, blood pressure appeared to rise as GFR fell. This finding is consistent with the well-known role of the kidney in long-term blood pressure regulation, and explains a universally high prevalence of hypertension among patients with low eGFR.

Is Chronic Kidney Disease Due to Cadmium Exposure Inevitable and Can It Be Reversed?

Cadmium (Cd) is a metal with no nutritional value or physiological role. However, it is found in the body of most people because it is a contaminant of nearly all food types and is readily absorbed. The body burden of Cd is determined principally by its intestinal absorption rate as there is no mechanism for its elimination. Most acquired Cd accumulates within the kidney tubular cells, where its levels increase through to the age of 50 years but decline thereafter due to its release into the urine as the injured tubular cells die. This is associated with progressive kidney disease, which is signified by a sustained decline in the estimated glomerular filtration rate (eGFR) and albuminuria. Generally, reductions in eGFR after Cd exposure are irreversible, and are likely to decline further towards kidney failure if exposure persists. There is no evidence that the elimination of current environmental exposure can reverse these effects and no theoretical reason to believe that such a reversal is possible. This review aims to provide an update on urinary and blood Cd levels that were found to be associated with GFR loss and albuminuria in the general populations. A special emphasis is placed on the mechanisms underlying albumin excretion in Cd-exposed persons, and for an accurate measure of the doses-response relationships between Cd exposure and eGFR, its excretion rate must be normalised to creatinine clearance. The difficult challenge of establishing realistic Cd exposure guidelines such that human health is protected, is discussed.

Toxicity Tolerance in the Carcinogenesis of Environmental Cadmium.

Cadmium (Cd) is an environmental toxicant of worldwide public health significance. Diet is the main non-workplace Cd exposure source other than passive and active smoking. The intestinal absorption of Cd involves transporters for essential metals, notably iron and zinc. These transporters determine the Cd body burden because only a minuscule amount of Cd can be excreted each day. The International Agency for Research on Cancer listed Cd as a human lung carcinogen, but the current evidence suggests that the effects of Cd on cancer risk extend beyond the lung. A two-year bioassay demonstrated that Cd caused neoplasms in multiple tissues of mice. Also, several non-tumorigenic human cells transformed to malignant cells when they were exposed to a sublethal dose of Cd for a prolonged time. Cd does not directly damage DNA, but it influences gene expression through interactions with essential metals and various proteins. The present review highlights the epidemiological studies that connect an enhanced risk of various neoplastic diseases to chronic exposure to environmental Cd. Special emphasis is given to the impact of body iron stores on the absorption of Cd, and its implications for breast cancer prevention in highly susceptible groups of women. Resistance to cell death and other cancer phenotypes acquired during Cd-induced cancer cell transformation, under in vitro conditions, are briefly discussed. The potential role for the ZnT1 efflux transporter in the cellular acquisition of tolerance to Cd cytotoxicity is highlighted.

Role Of Selenium and Vitamins E And C In Combating Cadmium Bioaccumulation in The Selected Tissues of Rats: A Therapeutic Approach

The aim of the present investigation is to check the therapeutic role of selenium (Se) and vitaminE and C on cadmium (Cd) induced bioaccumulation in liver, kidney and testis of Cd treated rats. Wistar strain male albino rats were treated with cadmium chloride at a dose of 1/10th of LD50 /48h i.e. 22.5 mg/Kg body weight for 7, 15 and 30 days (d) time intervals. Then 15d Cd treated rats were divided into two groups. Group I supplemented with Se (1mg/kg body weight) and II group received combination of Se, vitamins E (300mg/kg) and C (200mg/kg) and observed for 7, 15 and 30days. After specific time intervals, rats were decapitated and tissues such as liver, kidney and testis were isolated and used for the estimation of Cd bioaccumulation levels by using Atomic Absorption Spectrophotometer (AAS – Schimadzu AA6300). There was a significant elevation in Cd concentrations in the test tissues with increased period of Cd treatment. Maximum Cd accumulation was found in 30d Cd treated rat kidney (42.80±0.30μg / gm). However, there was a significant reduction in Cd bioaccumulation with Se and vitamin E and C supplementation. Maximum decrease in Cd accumulation was found in 30d rat kidney (5.04 ±0.08μg / gm) supplemented with the combination of Se andvitamin E and C. Our findings clearly envisage that combined supplementation of Se and vitamin E and C is more effective in reducing the Cd body burden when compared to the individual mode of supplementation.

Gender Differences in the Severity of Cadmium Nephropathy.

The excretion of β2-microglobulin (β2M) above 300 µg/g creatinine, termed tubulopathy, was regarded as the critical effect of chronic exposure to the metal pollutant cadmium (Cd). However, current evidence suggests that Cd may induce nephron atrophy, resulting in a reduction in the estimated glomerular filtration rate (eGFR) below 60 mL/min/1.73 m2. Herein, these pathologies were investigated in relation to Cd exposure, smoking, diabetes, and hypertension. The data were collected from 448 residents of Cd-polluted and non-polluted regions of Thailand. The body burden of Cd, indicated by the mean Cd excretion (ECd), normalized to creatinine clearance (Ccr) as (ECd/Ccr) × 100 in women and men did not differ (3.21 vs. 3.12 µg/L filtrate). After adjustment of the confounding factors, the prevalence odds ratio (POR) for tubulopathy and a reduced eGFR were increased by 1.9-fold and 3.2-fold for every 10-fold rise in the Cd body burden. In women only, a dose-effect relationship was seen between β2M excretion (Eβ2M/Ccr) and ECd/Ccr (F = 3.431, η2 0.021). In men, Eβ2M/Ccr was associated with diabetes (β = 0.279). In both genders, the eGFR was inversely associated with Eβ2M/Ccr. The respective covariate-adjusted mean eGFR values were 16.5 and 12.3 mL/min/1.73 m2 lower in women and men who had severe tubulopathy ((Eβ2M/Ccr) × 100 ≥ 1000 µg/L filtrate). These findings indicate that women were particularly susceptible to the nephrotoxicity of Cd, and that the increment of Eβ2M/Ccr could be attributable mostly to Cd-induced impairment in the tubular reabsorption of the protein together with Cd-induced nephron loss, which is evident from an inverse relationship between Eβ2M/Ccr and the eGFR.

Chronic Kidney Disease Induced by Cadmium and Diabetes: A Quantitative Case-Control Study.

Kidney disease associated with chronic cadmium (Cd) exposure is primarily due to proximal tubule cell damage. This results in a sustained decline in glomerular filtration rate (GFR) and tubular proteinuria. Similarly, diabetic kidney disease (DKD) is marked by albuminuria and a declining GFR and both may eventually lead to kidney failure. The progression to kidney disease in diabetics exposed to Cd has rarely been reported. Herein, we assessed Cd exposure and the severity of tubular proteinuria and albuminuria in 88 diabetics and 88 controls, matched by age, gender and locality. The overall mean blood and Cd excretion normalized to creatinine clearance (Ccr) as ECd/Ccr were 0.59 µg/L and 0.0084 µg/L filtrate (0.96 µg/g creatinine), respectively. Tubular dysfunction, assessed by β2-microglobulin excretion rate normalized to Ccr(Eβ2M/Ccr) was associated with both diabetes and Cd exposure. Doubling of Cd body burden, hypertension and a reduced estimated GFR (eGFR) increased the risks for a severe tubular dysfunction by 1.3-fold, 2.6-fold, and 84-fold, respectively. Albuminuria did not show a significant association with ECd/Ccr, but hypertension and eGFR did. Hypertension and a reduced eGFR were associated with a 3-fold and 4-fold increases in risk of albuminuria. These findings suggest that even low levels of Cd exposure exacerbate progression of kidney disease in diabetics.

Cadmium-Induced Tubular Dysfunction in Type 2 Diabetes: A Population-Based Cross-Sectional Study.

The global prevalence of diabetes, and its major complication, diabetic nephropathy, have reached epidemic proportions. The toxic metal cadmium (Cd) also induces nephropathy, indicated by a sustained reduction in the estimated glomerular filtration rate (eGFR) and the excretion of β2-microglobulin (β2M) above 300 µg/day, which reflects kidney tubular dysfunction. However, little is known about the nephrotoxicity of Cd in the diabetic population. Here, we compared Cd exposure, eGFR, and tubular dysfunction in both diabetics (n = 81) and non-diabetics (n = 593) who were residents in low- and high-Cd exposure areas of Thailand. We normalized the Cd and β2M excretion rates (ECd and Eβ2M) to creatinine clearance (Ccr) as ECd/Ccr and Eβ2M/Ccr. Tubular dysfunction and a reduced eGFR were, respectively, 8.7-fold (p < 0.001) and 3-fold (p = 0.012) more prevalent in the diabetic than the non-diabetic groups. The doubling of ECd/Ccr increased the prevalence odds ratios for a reduced eGFR and tubular dysfunction by 50% (p < 0.001) and 15% (p = 0.002), respectively. In a regression model analysis of diabetics from the low-exposure locality, Eβ2M/Ccr was associated with ECd/Ccr (β = 0.375, p = 0.001) and obesity (β = 0.273, p = 0.015). In the non-diabetic group, Eβ2M/Ccr was associated with age (β = 0.458, p < 0.001) and ECd/Ccr (β = 0.269, p < 0.001). However, after adjustment for age, and body mass index (BMI), Eβ2M/Ccr was higher in the diabetics than non-diabetics of similar ECd/Ccr ranges. Thus, tubular dysfunction was more severe in diabetics than non-diabetics of similar age, BMI, and Cd body burden.

Source-soil-rice-human multi-objective optimization to minimize the cadmium intake risk to consumers of field planting rice

Cadmium (Cd) exposure risks to consumers of locally grown rice are often estimated without considering the sources and bioavailability of Cd. Here, we present the first comprehensive and quantitative analysis on the sources and transport of Cd in paddy ecosystems by combining a regional investigation in southern China, a positive matrix factorization algorithm, and a classification and regression tree approach. Results showed that local atmospheric emission regulations failed to mitigate Cd contamination as the Cd inputs from industrial effluent irrigation were largely overlooked. Leaching loss of soil Mn is an invisible threat to grain safety as Mn can exhibit a significant facilitation effect on rice Cd uptake under acidic pH. A probability-based toxicokinetic model is proposed to optimize the strategies for minimizing the Cd body burden through the source-soil-rice-human pathway. Urinary Cd exceeded its safety threshold in 61.7% of local female adults (6.14±4.42 µg g -1 creatinine) who consumed less rice grain but with a low Zn bioavailability. To protect 85% of local rice production from causing excessive Cd exposure risk, irrigation channel needs to be effectively cleaned up, and the pH and amorphous Mn content of rice soils need to be raised to 5.50 and 179 mg kg -1 , respectively. • Contamination sources should not be confused with the causative factors of Cd exposure risks. • Manganese exhibited significant facilitation effect with acidic pH on rice Cd uptake. • Urinary Cd from local adults can be better predicted with probability-based toxicokinetic model. • Optimum scenarios help protect 85% of rice production from causing excessive kidney burden.

Polystyrene microplastics alter bioaccumulation, and physiological and histopathological toxicities of cadmium in the polychaete Perinereis aibuhitensis

Heavy metal (HM) pollution in the marine environment has been of concern for decades. The potential impact of HMs carried by emerging marine pollutants such as microplastics (MPs) has attracted attention only in recent years. In this study, we investigated the single and combined chronic toxic effects (growth, burrowing behavior, and histopathology) of cadmium (Cd, three concentrations of low, medium, and high) and polystyrene (PS) microspheres (1 μm, 10 μg/L) on the coastal polychaete Perinereis aibuhitensis. Cd bioaccumulation under two exposure scenarios was also explored. Our results showed that Cd and PS did not affect worm growth for single or combined exposure, while 13.08 μg/L of Cd (CdL) alone significantly decreased the burrowing time of P. aibuhitensis in sediment. The presence of PS mitigated the hormetic effect of Cd on worm burrowing behavior, and this influence was Cd concentration-related. Cd body burdens in worms exposed to the medium and high Cd concentrations (CdM and CdH) were significantly greater than those of control worms with or without the presence of PS. In addition, Cd bioaccumulation was significantly higher with the coexistence of PS than those of Cd alone at the CdL and CdM groups. Histopathological analyses demonstrated a trend of epidermal and intestinal damages for single Cd/PS and their combined groups, and the contribution of PS-MPs should not be ignored. Our results indicate that the toxic effects and bioaccumulation pattern of Cd could be altered with the presence of PS-MPs for P. aibuhitensis, especially at environmentally relevant concentrations.

Low-level exposure to lead, cadmium and mercury, and histopathological findings in kidney biopsies

BackgroundLead (Pb), cadmium (Cd) and mercury (Hg) are all nephrotoxic metals, and a large part of the body burden of Cd and Hg is found in the kidneys. There are, however, few studies on associations between exposure to these toxic metals and renal biopsy findings, and none at low-level exposure. AimTo examine the hypothesis that low-level concentration of Pb, Cd or Hg in the kidneys is associated with histopathological changes in the kidneys. MethodsWe determined concentrations of Pb, Cd and Hg in kidney, blood and urine in 109 healthy kidney donors, aged 24–70 years. The renal biopsies were scored according to the Banff classification regarding tubular atrophy, interstitial fibrosis, glomerulosclerosis, arteriosclerosis, and arteriolohyalinosis. Kidney function was assessed based on glomerular filtration rate (GFR) as well as urinary excretion of albumin, low molecular weight proteins, kidney injury molecule 1 and N-acetylglucose aminidase. Associations between metal concentrations and histopathological changes, were assessed in models also including age, sex and smoking. ResultsThe median kidney concentrations of Pb, Cd and Hg were 0.08, 13 and 0.21 μg/g, respectively. There were signs of tubular atrophy in 63%, interstitial fibrosis in 21%, glomerulosclerosis in 71%, arteriosclerosis in 47%, and arteriolohyalinosis in 36% of the donors, but, as could be expected, the histopathological findings were limited, mostly Banff grade 1. In models adjusted for age, sex and smoking, kidney Cd was positively associated with tubular atrophy (p = 0.03) and possibly with arteriolohyalinosis (p = 0.06). Kidney Hg was associated with arteriosclerosis (p = 0.004). Discussion and conclusionsThe results suggest that even low levels of Cd in the kidney can induce a mild degree of tubular atrophy. This is in line with previous findings at high-level Cd exposure. The association between kidney Hg and renal arteriosclerosis was unexpected, and may be a chance finding.

Tobacco Smoke Exposure and Urinary Cadmium in Women from Northern Mexico.

Cadmium (Cd), a carcinogenic metal also related to reproductive and cardiovascular diseases, is contained in tobacco and elevated concentrations of it in humans have been consistently associated with first-hand tobacco smoke; however, there is scarce and inconclusive evidence of the relationship between Cd and secondhand smoke (SHS) exposure. Our aim was to evaluate the association between exposure to tobacco, both active and SHS, with urinary Cd concentrations in Mexican women. In a cross-sectional analysis that included 998 women living in northern Mexico, we measured the concentration of creatinine-adjusted urinary Cd (µg-cadmium/g-creatinine) using inductively coupled plasma triple quadrupole (ICP-QQQ) in tandem mass spectrometry mode (MS/MS). We gathered tobacco smoking information through an in-person interview and formed seven groups: non-smokers without SHS exposure; non-smokers with SHS exposure; ex-smokers without SHS exposure <1 year of quitting; ex-smokers without SHS exposure ≥1 year of quitting, ex-smokers with SHS exposure <1 year of quitting; ex-smokers with SHS exposure ≥1 year of quitting and current smokers. The interview also yielded sociodemographic characteristics. We used linear multivariable regression models to estimate the association between Cd concentrations and tobacco smoke exposure. Compared to non-smokers without SHS exposure, we found higher Cd concentrations in ex-smokers with SHS exposure <1 year of quitting and current smokers (adjusted geometric means 0.51 vs. 1.01 and 0.69 µg-cadmium/g-creatinine, respectively). Our results do not support a conclusion that SHS exposure is a source of Cd body burden.

Plant food intake is associated with lower cadmium body burden in middle-aged adults.

Dietary intake is a primary source of cadmium (Cd) exposure in the non-smoking population. Plant foods containing metal-binding plant compounds such as polyphenols, phytates, and phytochelatins may reduce Cd bioavailability and result in lower Cd body burden. In this study, we investigated the association between plant food intake and urinary creatinine-adjusted Cd (uCd), a well-established marker of Cd body burden. Participants were from a cross-sectional sample of 1901 adults in the REasons for Geographic and Racial Differences in Stroke (REGARDS) cohort. Dietary intake was assessed with a food frequency questionnaire. We created a 12-point plant food score (PFS) based on reported intake across seven categories (fruits, vegetables, legumes, nuts/seeds, whole grains, tea, and wine). Higher scores indicated higher consumption and diversity of plant food intake. Multivariable linear regression models were used to estimate the association between PFS and uCd. Due to the influence of age and smoking on Cd status, stratified analyses were conducted. Mean PFS was 5.4 (SD 2.2) and mean uCd was 0.53µg/g creatinine (SD 0.39). In adjusted models, PFS was not associated with uCd (p > 0.05). In stratified analyses, PFS was inversely associated with uCd (p = 0.047) with a 1-point higher PFS associated with 0.018µg/g lower uCd among middle-aged (45-59) adults. No significant association was observed between PFS and uCd in older (≥ 60) adults. The association of PFS and uCd did not differ by smoking status. Our findings suggest higher plant food intake is associated with lower Cd body burden in middle-aged but not older adults.

Effect of short-term dietary exposure on metal assimilation and metallothionein induction in the estuarine fish Pseudogobius sp.

Metals introduced into the urban aquatic environment through anthropogenic activities have the potential to accumulate in organisms via multiple uptake routes. Understanding the impact different routes have on metal accumulation is important for the continued management of these ecosystems, where current water quality guidelines (WQGs) tend to be derived from aqueous metal exposure tests. In this study, the estuarine fish Pseudogobius sp. was exposed to a mixture of cadmium (Cd) and zinc (Zn) radiotracers dissolved in water or present in experimental food. Metal-spiked food was presented to fish as a single ‘pulse-chase’ feed or as three consecutive feeds, where the cumulative metal dose provided by both treatments was equal. Fish did not accumulate either metal from water, even after the length of exposure was increased from 12 h to 36 h. Fish did accumulate metals from diet and the assimilation efficiency (AE) was low following a single feed (12% for both Cd and Zn). Following multiple feeds fish displayed a significantly higher AE for zinc only, suggesting that fish are susceptible to retention of dietary Zn over an extended time period albeit at lower daily loadings. The final body burden and efflux rate did not differ between feeding regimes. Tissue accumulation of Cd and Zn indicated metal specific distribution. The gastro-intestinal (GI) tract contained >90% of total Cd body burden, whilst the carcass accounted for the majority (70–88%) of Zn body burden. There was significant induction of the biomarker metallothionein (MT) in the GI tract. These results demonstrate the differences in Cd and Zn metal uptake characteristics in this estuarine fish species, and how feeding frequency and metal loading of food may influence assimilation. This study highlights the importance of considering the inclusion of dietary exposures in WQG frameworks.

Influence of environmentally relevant concentrations of Zn, Cd and Ni and their binary mixtures on metal uptake, bioaccumulation and development in larvae of the purple sea urchin Strongylocentrotus purpuratus

Metal accumulation, disturbance of Ca2+ homeostasis, and occurrence of abnormalities are well-established consequences of single metal exposure during early development stages of sea urchins. However, the effects caused by low concentrations of metals and metal mixtures need to be better understood in marine invertebrates. Therefore, the present study investigated the effects of environmentally relevant concentrations of Zn (9 μg/L), Cd (30 μg/L) and Ni (5 μg/L) in single and binary exposures (Zn + Cd, Cd + Ni and Ni + Zn) to the early life stages of the purple sea urchin Strongylocentrotus purpuratus. Endpoints checked in all treatments after 48-h exposure were unidirectional metal influx rates, bioaccumulation, and Ca2+ influx rates. Additionally, the presence of abnormal larvae and developmental delay was evaluated at 24 h, 48 h and 72 h of exposure. Unidirectional influx rates of all three metals were significantly higher than control background rates in all single exposures and binary mixtures, and were generally not different between them. Net accumulation (body burden) of both Zn and Cd increased significantly as a result of their respective single exposures, while Ni accumulation decreased considerably. When Zn or Cd were presented in binary exposures with other metals, the net accumulations of Zn or Cd were reduced relative to single exposures to these metals, whereas this did not occur for Ni accumulation. Thus, bioaccumulation proved to be a better metric than influx rate measurements to analyze metal competition at a whole organism level at these low metal concentrations. Short-term Ca2+ influx also did not appear to be a sensitive metric, as the measured rates did not vary among all single and binary exposures, with the exception of a lower rate in Ni + Zn binary exposure. A critical aspect observed was the relationship between bioaccumulation versus influx measurements, which proved positive for Cd, but negative for Zn and Ni, demonstrating possible capacities for both Zn and Ni regulation by sea urchin larvae. Increases in larval abnormalities relative to controls occurred only after binary mixtures, starting at 48 h exposure and maintained until 72 h. However, delay of the sea urchin development by the presence of gastrula stage at 72 h exposure occurred in Zn and Ni single exposures and all metal mixtures, with very high abnormal development when Ni was present.

Spatial and temporal trends in physiological biomarkers of adult eastern oysters, Crassostrea virginica, within an urban estuary

Heavy metal contamination and water quality may alter reproductive capacity of oysters in highly urbanized, eutrophic ecosystems. This study assessed physiological biomarkers and heavy metal body burdens in adult oysters, Crassostrea virginica, placed at a highly urban and reference site. Condition index and Vitellogenin-like proteins were significantly different between sites, but protein concentration and activity of the electron transport system were not. Accumulation of Cd and Hg occurred at both sites, and Cd body burden was greater at the urban site. There was a negative relationship between condition index and Cd body burden at the urban site, while no relationship was found between physiological biomarkers and metal burden at the reference site. The results suggest that oyster condition and reproductive potential may be negatively influenced by the biotic and abiotic factors typically found within urban, eutrophic ecosystems.

Facing the threat: common yellowjacket wasps as indicators of heavy metal pollution

We investigated the common wasp, Vespula vulgaris as a bioindicator and biomonitor of metals in the industrial area. Using traps, we collected 257 yellowjackets along a pollution gradient in the Harjavalta Cu-Ni smelter in Southwest Finland. Our method detected metal elements such as arsenic (As), cobalt (Co), copper (Cu), iron (Fe), nickel (Ni), lead (Pb), zinc (Zn), and mercury (Hg) in wasps. The data analyses revealed V. vulgaris can be a proper indicator for As, Cd, Co, Cu, Ni, and Pb, rather than for Fe and Zn contamination. Body burdens of As, Cd, Co, Cu, Ni, and Pb decreased with an increase in distance from smelter. Enrichment factor (EF) followed the pattern Pb ˃ Cd ˃ As ˃ Co ˃ Cu ˃ Ni. The highest bioaccumulation (BAF) values were revealed for Cd (5.9) and the lowest for Pb (0.1). Specially designed software (WaspFacer) allowed revealing body burdens of As, Cd, Co, Cu, Ni, and Pb to be associated with rather smaller than more asymmetric facial colour markings in yellowjackets. These results add to the body of literature on how heavy metal contaminants can have tangible phenotypic effects on insects and open future opportunities for using wasps as indicators of metal pollution.

Urinary cadmium and timing of menarche and pubertal development in girls

BackgroundCadmium (Cd) is a developmental toxicant that is released into the environment during industrial processes. Previous animal studies suggest that Cd may impact the onset of puberty. ObjectivesTo determine whether Cd exposure, measured as urinary Cd concentration, was associated with ages at menarche and pubertal development. MethodsA cohort of 211 girls, ages 10–13 years at baseline, was followed for up to two years. Girls completed an interview and self-assessment of Tanner stages of breast development and pubic hair growth. They were followed monthly until menarche. Urinary Cd concentrations were measured in overnight urine specimens. Multivariable Cox regression was used to evaluate the association between urinary Cd and age at menarche and cumulative logit regression was used to evaluate the associations between urinary Cd and breast development and pubic hair growth. ResultsThe baseline geometric mean creatinine-adjusted Cd concentration was 0.22 μg/g creatinine (geometric standard deviation = 1.6) and decreased with increasing age (p-trend = 0.04). Cd levels were higher among Asian than White girls or girls of other/mixed race/ethnicity (p = 0.04). In multivariable analyses, girls with urinary Cd ≥ 0.4 μg/L were less likely to have attained menarche than girls with urinary Cd < 0.2 μg/L (hazard ratio = 0.42; 95% confidence interval, 0.23–0.78). Urinary Cd was negatively associated with pubic hair growth (p-trend = 0.01) but not with breast development (p-trend = 0.72) at baseline. ConclusionsThese findings suggest that a higher Cd body burden may delay some aspects of pubertal development among girls.

Spatial and temporal variations of trace metal body burdens of live mussels Mytilus galloprovincialis and field validation of the Artificial Mussels in Australian inshore marine environment

The body burdens of eight trace metals: Cd, Pb, Cu, Zn, Cr, Se, Hg, and As, were measured in live mussels (LMs) Mytilus galloprovincialis at 14 coastal sites in Port Phillip Bay, Victoria, Australia in winter and summer between 2017 and 2018. The spatial and temporal variations of body burdens were evaluated. The results revealed significantly higher body burdens of Cd, Pb, Cu, Zn, Cr, and Hg in summer at the sites where the city centre and industries are located. Elevated levels of most trace metals including 3 toxic, non-essential metals (Cd, Pb, and Hg) were detected in LMs from the site of Geelong. The body burdens of Zn, Cr, Se, and As appeared higher at the sites from the Bellarine Peninsula and the mouth of Port Phillip Bay.Besides, the “Artificial Mussels” (AMs) were deployed at the same sites in summer for 28 d and retrieved when the LMs were collected. The accumulations of the eight metals were compared between AMs and LMs summer results. It indicated significant correlations for Pb, Cu, and Cr, lower correlations in Zn and Hg, and irregular correlations for Se and As. The AM results of Cd were below the detection limit of the analytical method. This study demonstrates that AMs are excellent replacement of LMs for the biomonitoring of multiple kinds of trace metals.