The effects of chelating drugs used clinically as antidotes to metal toxicity are reviewed. Human exposure to a number of metals such as lead, cadmium, mercury, manganese, aluminum, iron, copper, thallium, arsenic, chromium, nickel and platinum may lead to toxic effects, which are different for each metal. Similarly the pharmacokinetic data, clinical use and adverse effects of most of the chelating drugs used in human metal poisoning are also different for each chelating drug. The chelating drugs with worldwide application are dimercaprol (BAL), succimer (meso-DMSA), unithiol (DMPS), D-penicillamine (DPA), N-acetyl-D-penicillamine (NAPA), calcium disodium ethylenediaminetetraacetate (CaNa(2)EDTA), calcium trisodium or zinc trisodium diethylenetriaminepentaacetate (CaNa(3)DTPA, ZnNa(3)DTPA), deferoxamine (DFO), deferiprone (L1), triethylenetetraamine (trientine), N-acetylcysteine (NAC), and Prussian blue (PB). Several new synthetic homologues and experimental chelating agents have been designed and tested in vivo for their metal binding effects. These include three groups of synthetic chelators, namely the polyaminopolycarboxylic acids (EDTA and DTPA), the derivatives of BAL (DMPS, DMSA and mono- and dialkylesters of DMSA) and the carbodithioates. Many factors have been shown to affect the efficacy of the chelation treatment in metal poisoning. Within this context it has been shown in experiments using young and adult animals that metal toxicity and chelation effects could be influenced by age. These findings may have a bearing in the design of new therapeutic chelation protocols for metal toxicity.

Cadmium and other metallic ions can act as metalloestrogens and endocrine disruptors of reproductive tissues and fetal development in mammals, including humans. The detrimental effects occur with respect to the synthesis of both steroid and polypeptide hormones in the placenta. Leptin is produced by the trophoblast and may regulate fetal organogenesis and development. In human term placentas, concentrations of toxic metals and their effects on steroidogenesis were assessed in healthy parturients (109 non-smokers and 99 smokers) in relation to tobacco smoking. Trace elements (cadmium, lead, iron, zinc and copper) were analyzed in placentas using atomic absorption spectroscopy, and steroid hormones (progesterone and estradiol) were assayed in placental samples by an enzyme-immunometric method. Cadmium concentrations were doubled in placentas of smokers as compared with non-smokers, and placental lead and zinc concentrations increased significantly. Placental concentrations of iron, copper, progesterone and estradiol did not differ. In addition, human trophoblast cells were co-cultured with 0, 5, 10 or 20 microm CdCl(2) for 96 h and leptin mRNA assessed by quantitative polymerase chain reaction. Leptin mRNA declined dose-responsively as a result of CdCl(2) exposure. Collectively, the results confirm that human placental tissue offers a unique opportunity to biomonitor cadmium exposure in both the maternal and the internal fetal environments. In addition, the results strongly suggest that cadmium may cause a decline in placental leptin synthesis, as we have previously shown for placental progesterone production. This may constitute further evidence of the endocrine-disrupting effects of cadmium, as a constituent of tobacco smoke, on reproduction in women.

Hazardous levels of Der p 1, endotoxin and moulds were determined in poultry houses. High prevalence of work-related symptoms and IgG antibodies to moulds was found in PW. Healthy worker effect is proposed as an explanation of low atopy markers prevalence among PW.

The results indicate the need for the continuation of efforts to establish effective primary preventive programmes for OSDs at national and EU levels.

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The authors aimed to examine potential relationships between work-related symptoms attributed to sick building syndrome (SBS) and certain psychological, somatic, and environmental factors. The multidisciplinary, cross-sectional study comprised 171 female subjects working in air-conditioned and naturally ventilated nonindustrial office buildings. The authors collected information concerning symptoms related to SBS and made assessments of quality of life by using appropriate questionnaires. They assessed the women's levels of emotional stability or neuroticism using the Cornell Index. They determined skin and airway reactivity markers and indoor microclimate data by using standardized methods. The study showed that the subjects had a high prevalence of fatigue (60.2%), sore and dry eyes (57.9%), and headache (44.4%), as well as a generally high score according to the SBS Index. Neuroticism and subjectively estimated physical health as well as the type of building ventilation significantly contributed to the prediction of the SBS Index, explaining 15% of the variance.

Acute effects of food and cigarette consumption on exhaled breath condensate (EBC) acidity are insufficiently explored. The study aimed to evaluate potential changes in EBC pH within 2 hours following cigarette or food consumption. In 15 healthy smokers, samples were obtained after 10 hours of abstinence from smoking and then 15, 30, 60, and 120 minutes after smoking 1 cigarette. In 19 healthy nonsmoking adults, EBC samples were obtained in the morning after an overnight fast, and then 30, 60, and 120 minutes following standardized breakfast. Smoking of 1 cigarette after overnight tobacco abstinence induced significant increase in EBC pH during the 2-hour observation period, for approximately 0.60 logarithmic units (repeated-measures analysis of variance [ANOVA], P < .0001). The average presmoking pH value in smokers (7.00 ± 0.50) was significantly lower than average value in nonsmokers (7.62 ± 0.31; P = .0001). No effect of food consumption was found. These results show that cigarette smoking acutely increases EBC pH in healthy smokers. Smoking status and abstinence from smoking before EBC sampling seems to be important in studies evaluating EBC pH and should be standardized or at least stated in the methodology. Acute effects of food were not found under described study conditions in healthy adults.

The effect of calcium supplementation on tissue lead was evaluated in suckling Wistar rats. Such data are not yet available in the literature. The following artificial feeding regimen was used for calcium supplementation: cow's milk by addition of 1%, 3% or 6% Ca as CaHPO 4 ¿2H 2 O suspension to increase the daily calcium intake about 1.4, 2 or 3 times above control values. Artificial feeding was applied during 7 hr each day for nine consecutive days (from day 6 through 15 after birth). The effect of such treatment on lead absorption and elimination was evaluated in two separate experiments: calcium supplementation during oral lead exposure (as acetate; daily dose 2 mg Pb/kg body wt.; total Pb dose 18 mg/kg body wt.) or after a single intraperitoneal lead administration (5 mg/kg body wt.). At the end of experiments, lead in tissues (liver, kidneys, brain and carcass), and essential elements (Ca, Fe, Zn, Cu) were analysed by atomic absorption spectrometry. Calcium supplementation caused a statistically significant decrease of lead in all tissues of sucklings orally exposed to lead. This decrease was dose-related being about 1.3, 1.5 and 2 times lower in groups supplemented with 1%, 3%, or 6% calcium compared to controls, respectively. Increased calcium intake had no effect on incorporated lead after parenteral lead exposure. Calcium supplementation increased carcass calcium and had no effect on trace elements in tissues, pups' general appearance and body weight gain. It is concluded that higher calcium intake might be a way of efficient reduction of lead absorption during the suckling period.