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Manufacture of lead-containing products has long been associated with various health risks. To get an insight into the related genotoxic risks, we conducted a biomonitoring study in 50 exposed workers and 48 matched controls using a battery of endpoints that sensitively detect the extent of genome instability in peripheral blood lymphocytes. The levels of primary DNA damage were estimated with the alkaline comet assay, while cytogenetic abnormalities were determined with the cytokinesis-block micronucleus (CBMN) cytome assay. Additionally, CBMN slides of 20 exposed and 16 control participants were subjected to fluorescence in situ hybridisation (FISH), coupled with pancentromeric probes to establish the incidence of centromere-positive micronuclei, nuclear buds, and nucleoplasmic bridges. Blood lead levels (B-Pb) were measured with atomic absorption spectrometry. To further characterise cumulative effects of occupational exposure, we measured erythrocyte protoporphyrin (EP) concentrations and delta-aminolevulinic acid dehydratase (ALAD) activity in blood. We also assessed the influence of serum folate (S-folate) and vitamin B12 (S-B12) on genome stability. Compared to controls, occupationally exposed workers demonstrated significantly higher B-Pb (298.36±162.07 vs 41.58±23.02), MN frequency (18.71±11.06 vs 8.98±7.50), centromere positive MN (C+ MN) (8.15±1.8 vs 3.69±0.47), and centromere negative MN (C- MN) (14.55±1.80 vs 4.56±0.89). Exposed women had significantly higher comet tail intensity (TI) and length (TL) than control women. Furthermore, workers showed a positive correlation between age and nuclear buds and MN, between MN and years of exposure, and between S-B12 levels and TI and ALAD activity, while a negative correlation was found between TI and B-Pb. These findings suggest that occupational settings in the manufacture of lead-containing products pose significant genotoxic risks, which calls for developing more effective work safety programmes, including periodical monitoring of B-Pb and genetic endpoints.

A method has been developed for direct determination of lead in wine by graphite furnace atomic absorption spectrometry (GFAAS) with Zeeman-effect background correction. The thermal behaviour of Pb during pyrolysis and atomisation stages was investigated without matrix modifier and in the presence of Pd(NO(3))(2), Pd(NO(3))(2) + Mg(NO(3))(2) × 6H(2)O, and NH(4)H(2)PO(4) + Mg(NO(3))(2) × 6H(2)O as matrix modifiers. A simple 1:1 dilution of wine samples with Pd(NO3)2 as a matrix modifier proved optimal for accurate determination of Pb in wine. Mean recoveries were 106 % for red and 114 % for white wine, and the detection limit was 3 μg L(-1). Within-run precision of measurements for red and white wine was 2.1 % and 1.8 %, respectively. The proposed method was applied for analysis of 23 Croatian wines. Median Pb concentrations were 33 μg L(-1), range (16 to 49) μg L(-1) in commercially available wines and 46 μg L(-1), range (14 to 559) μg L(-1) in home-made wines. There were no statistically significant differences (P<0.05) in Pb concentration between commercial and home-made wines or between red and white wines.

The influence of exposure to lead on the frequency of micronuclei (MN), nuclear buds and nucleoplasmatic bridges was investigated in peripheral blood lymphocytes in 15 male battery-manufacturing workers and 15 controls matched for age and smoking habits. In addition to MN test, blood lead (B-Pb) and cadmium (B-Cd), delta aminolevulinic acid dehydratase (ALAD) activity, erythrocyte protoporphyrin (EP), serum vitamin B(12) (S-Vit B(12)) and folate (S-folate) were determined in all subjects. Lead-exposed subjects had significantly higher MN frequency and B-Pb concentrations than controls. In control smokers we found a significant negative correlation between B-Pb concentration and frequency of nucleoplasmatic bridges, and nuclear division index. In control non-smokers a significant positive correlation was observed only between age and nuclear buds frequency, and between S-folate and B-Pb level. In lead exposed smokers, significant positive correlations between MN frequency and S-Vit B(12), S-folate, and nuclear buds frequency were found. A positive correlation in exposed smokers was also found between nuclear buds frequency and S-Vit B(12) concentration. A negative correlation was found between ALAD and EP, and B-Pb in exposed smokers. Exposed non-smokers showed significant negative correlation between MN frequency and B-Cd, and ALAD and EP. The results indicate a genotoxicity of lead, pointing to a micronucleus assay as a relevant test for assessing genotoxic effects resulting from occupational exposure. The other indicators did not necessarily follow the results of THE MN test. Influence of smoking should be further investigated., (2009 John Wiley & Sons, Ltd.)

The combined influence of age, smoking, alcohol, blood lead and cadmium concentrations, and serum copper, zinc, and selenium concentrations on prostate-specific antigen (PSA) in serum was investigated in a group of 57 men aged 21 years to 40 years. The subjects had no occupational exposure to metals and no other known reasons suspected of influencing prostate function or metal metabolism. No significant correlation was found between PSA and any of the explanatory variables considered. Nevertheless, when taking into account all of the above-mentioned potentially explanatory variables, the results of stepwise multiple regression showed a significant increase in PSA with respect to an increase in blood lead, and a decrease in PSA with respect to an increase in intensity of alcohol consumption. The median and range values of blood lead concentration in the 57 men were 26.0 microg L(-1) and (10.1 to 108.0) microg L(-1), respectively. These results suggest that even a low-level environmental lead exposure, common for general populations worldwide, may contribute to the risk of prostate cancer in men. The influence of lead as well as cadmium, zinc, and selenium on prostate damage and PSA should be further investigated in relatively young men for the purpose of disease prevention.

Background: The effect of lead (Pb) and potential confounding variables on blood pressure was examined in healthy male industrial workers 20-43 years of age., Methods: In 100 Pb workers and 51 reference subjects, the following variables were measured: blood Pb (BPb), activity of delta-aminolevulinic acid dehydratase (ALAD), erythrocyte protoporphyrin (EP), blood cadmium (BCd), serum zinc (SZn), serum copper (SCu), hematocrit (Hct), body mass index (BMI), and blood pressure. The inter-relationship of biomarkers of Pb (BPb, ALAD, EP) and BCd, SZn, SCu, Hct, BMI, age, smoking, and alcohol to systolic and diastolic blood pressure was calculated by forward stepwise multiple regression., Results: There was no significant difference in blood pressure between the two groups, possibly because the reference subjects had relatively high BPb levels and significantly higher BMI (P < 0.05) as compared to the Pb workers. According to the multiple regression results in Pb workers, an increase in systolic blood pressure was significantly associated with increasing EP (P = 0.001) and BMI (P < 0.002), or alternatively with increasing BMI (P < 0.004) and decreasing ALAD (P < 0.04) and BCd (P < 0.05). An increase in diastolic blood pressure was significantly associated with increasing BMI (P < 0.009) and EP (P = 0.05) and decreasing BCd (P < 0.04). With respect to the EP range of 0.73-13.94 micromol/l erythrocytes in 100 Pb workers, an increase of 17 mm Hg in systolic and 6 mm Hg in diastolic blood pressure was found., Conclusions: Long-term cumulative Pb exposure, which is better reflected by EP than by ALAD or current BPb level, can significantly increase blood pressure in moderately Pb-exposed male workers (long-term average BPb <400 microg/l; exposure duration 2-21 years)., (Copyright 2004 Wiley-Liss, Inc.)

The influence of exposure to lead and cadmium on serum concentrations of calcium, zinc, and copper was examined in 299 healthy Croatian men 20-55 years of age, including 143 workers in a lead battery factory and 156 control subjects. The interrelationship of blood lead, activity of delta-aminolevulinic acid dehydratase, erythrocyte protoporphyrin, blood cadmium, age, smoking habits, and alcohol consumption with respect to serum calcium, zinc, and copper levels was calculated by forward stepwise multiple regression. The results showed that chronic moderate exposure to lead decreased serum zinc, calcium and, to a lesser extent, copper levels. Exposure to cadmium occurred mostly through smoking and seemed to contribute to a decrease of serum zinc. All changes in serum concentrations of these essential elements were significant but remained within the normal range. The results suggest possible mechanisms of lead- and/or cadmium-induced adverse health effects in humans.

This study evaluates the interaction of toxic elements cadmium (Cd) and lead (Pb) due to exposure from cigarette smoking, essential elements, and steroidogenesis in the maternal–placental–fetal unit. In a cohort of 155 healthy, postpartum women with vaginal term deliveries in clinical hospitals in Zagreb, Croatia, samples of maternal blood/serum and urine, placental tissue, and umbilical cord blood/serum were collected at childbirth. The biomarkers determined were concentrations of Cd, Pb, iron (Fe), zinc (Zn), copper (Cu), and selenium (Se), and steroid hormones progesterone and estradiol in maternal and umbilical cord blood and the placenta. Three study groups were designated based on self-reported data on cigarette smoking habits and confirmed by urine cotinine levels: never smokers (n = 71), former smokers (n = 48), and active smokers (n = 36). Metal(loid)s, steroid hormones, urine cotinine, and creatinine levels were analyzed by ICP–MS, ELISA, GC–MS, and spectrophotometry. Cigarette smoking during pregnancy was associated with increased Cd levels in maternal, placental, and fetal compartments, Pb in the placenta, and with decreased Fe in the placenta. In active smokers, decreased progesterone and estradiol concentrations in cord blood serum were found, while sex steroid hormones did not change in either maternal serum or placenta. This study provides further evidence regarding toxic and essential metal(loid) interactions during prenatal life, and new data on sex steroid disruption in cord serum related to cigarette smoking. The results indicate that umbilical cord sex steroid levels may be a putative early marker of developmental origins of the future burden of disease related to harmful prenatal exposure to cigarette smoke. [ABSTRACT FROM AUTHOR]

Toxic metals are extensively found in the environment, households, and workplaces and contaminate food and drinking water. The crosstalk between environmental exposure to toxic metals and human diseases has been frequently described. The toxic mechanism of action was classically viewed as the ability to dysregulate the redox status, production of inflammatory mediators and alteration of mitochondrial function. Recently, growing evidence showed that heavy metals might exert their toxicity through microRNAs (miRNA)—short, single-stranded, noncoding molecules that function as positive/negative regulators of gene expression. Aberrant alteration of the endogenous miRNA has been directly implicated in various pathophysiological conditions and signaling pathways, consequently leading to different types of cancer and human diseases. Additionally, the gene-regulatory capacity of miRNAs is particularly valuable in the brain—a complex organ with neurons demonstrating a significant ability to adapt following environmental stimuli. Accordingly, dysregulated miRNAs identified in patients suffering from neurological diseases might serve as biomarkers for the earlier diagnosis and monitoring of disease progression. This review will greatly emphasize the effect of the toxic metals on human miRNA activities and how this contributes to progression of diseases such as cancer and neurodegenerative disorders (NDDs). [ABSTRACT FROM AUTHOR]