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PubMed1999

Synthesis and Characterization of Zinc and Cadmium Compounds with Arenephosphinothiol Ligands. Crystal and Molecular Structures of [Cd(2){2-(Ph(2)PO)C(6)H(4)S}(4)], [Zn{2-(Ph(2)P)-6-(Me(3)Si)C(6)H(3)S}(2)], [Cd{2-(Ph(2)PO)-6-(Me(3)Si)C(6)H(3)S}(2)(CH(3)OH)], and [Zn{PhPO(C(6)H(4)S-2)(2)}(bipy)].

The electrochemical oxidation of a metallic anode (zinc or cadmium) in an acetonitrile solution of a series of arenephosphinothiol ligands, 2-(Ph(2)P)C(6)H(4)SH, 2-(Ph(2)P)-6-(Me(3)Si)C(6)H(3)SH, 2-(Ph(2)PO)-6-(Me(3)Si)C(6)H(3)SH, and PhP(C(6)H(4)SH-2)(2) [abbreviated RP-(SH)(x)(), x = 1 or 2], affords [M(RP-S)(2)] and [M(RP-S(2))], M = Zn, Cd. Adducts of several of these compounds with 1,10-phenanthroline and 2,2'-bipyridine have also been obtained by addition of these coligands to the electrolysis phase. The compounds obtained have been characterized by microanalysis, IR, UV-visible, FAB spectrometry and (1)H, (31)P NMR spectroscopic studies. The compounds, [Cd(2){2-(Ph(2)PO)C(6)H(4)S}(4)]CH(3)CN (1), [Zn{2-(Ph(2)P)-6-(Me(3)Si)C(6)H(3)S}(2)] (2), [Cd{2-(Ph(2)PO)-6-(Me(3)Si)C(6)H(3)S}(2)(CH(3)OH)] (3), and [Zn{PhPO(C(6)H(4)S-2)(2)}(bipy)] (4), have been also characterized by single-crystal X-ray diffraction. Compound 1 is binuclear with a {Cd(2)S(2)} core and distorted trigonal bipyramidal {CdO(2)S(3)} geometry about the Cd sites. Compounds 2, 3, and 4 are mononuclear with distorted tetrahedral {ZnP(2)S(2)}, distorted square pyramidal {CdO(3)S(2)}, and distorted trigonal bipyramidal {ZnON(2)S(2)} geometries, respectively. Crystal data: 1, C(42)H(37)N(3)O(2)P(2)S(2)Cd, triclinic, P&onemacr;, a = 13.5780(2) Å, b = 13.8505(2) Å, c = 13.9526(2) Å, alpha = 106.622(1) degrees, beta = 109.693(1) degrees, gamma = 107.137(1) degrees, V = 2133.30(5) Å(3), Z = 2, 9560 reflections, R = 0.0483; 2, C(46)H(50)N(2)P(2)S(2)Si(2)Zn, monoclinic, C2/c, a = 21.332(4) Å, b = 9.391(2) Å, c = 25.938(5) Å, beta = 113.84(3) degrees, V = 4753(2) Å(3), Z = 4, 2564 reflections, R = 0.0377; 3, C(43)H(48)CdO(3)P(2)S(2)Si(2), triclinic, P&onemacr;, a = 12.1237(4) Å, b = 14.0568(4) Å, c = 15.0938(2) Å, alpha = 70.836(2) degrees, beta = 83.410(2) degrees, gamma = 65.397(2) degrees, V = 2208.7(1) Å(3), Z = 2, 4936 reflections, R = 0.0738; 4, C(29)H(22)Cl(3)N(2)OP(2)S(2)Zn, triclinic, P&onemacr;, a = 8.9556(3) Å, b = 12.7911(4) Å, c = 14.0598(5) Å, alpha = 82.671(1) degrees, beta = 73.140(1) degrees, gamma = 74.113(1) degrees, V = 1480.44(9)(1) Å(3), Z = 2, 3820 reflections, R = 0.0511.

Journal Article↗
PubMed1986

Acute inhalation study in the rat of comparative uptake, distribution and excretion for different cadmium containing materials.

Single 2-hr inhalation exposures were conducted at levels of approximately 100 mg/m3 (based on cadmium content) with the use of two cadmium pigments (cadmium red and cadmium yellow), a dust of cadmium carbonate, and a cadmium fume. An air exposed control group also was included. The rate of elimination of cadmium in the urine and feces, and the cadmium levels in selected tissues were measured at several intervals following the exposure. In addition, observations of the animals for clinical signs of toxicity and mortality and measurements of organ weights and body weight were performed. There was no mortality in the control, cadmium red or cadmium yellow exposed groups. In the cadmium carbonate exposed group, 3 out of 52 rats died, and in the cadmium fume exposed group, 25 out of 52 rats died. Cadmium blood levels indicated that cadmium from the cadmium carbonate and fume was absorbed to a greater degree than cadmium from the red and yellow pigments. The major route of elimination of cadmium following exposure to the two pigments was via the feces, with 80% being cleared within 24 hr. Elimination was slower following exposure to the carbonate. The levels of cadmium in the liver and kidneys were much higher following exposure to the carbonate than following exposure to the red and yellow pigments. It appeared that these cadmium compounds were not equivalent with respect to toxicity, absorption, distribution or excretion. Exposure to the two insoluble compounds, cadmium red and cadmium yellow, did not produce mortality and resulted in rapid elimination in the feces with lower tissue levels of cadmium than observed following exposure to the cadmium carbonate.

Animals↗
PubMed1993

Carcinogenicity of trace elements with reference to evaluations made by the International Agency for Research on Cancer.

The monograph program of the International Agency for Research of on Cancer has evaluated many trace elements for their carcinogenicity to humans. Five groups of compounds were considered human carcinogens: arsenic and arsenic compounds, beryllium and beryllium compounds, cadmium and cadmium compounds, hexavalent chromium compounds, and nickel compounds. Antimony trioxide, cobalt and cobalt compounds, lead and inorganic lead compounds, methylmercury compounds, and metallic nickel were considered possibly carcinogenic to humans. Antimony trisulfide, trivalent chromium compounds, metallic chromium, ferric oxide, organolead compounds, metallic mercury, inorganic mercury compounds, selenium and selenium compounds, and titanium dioxide were not classifiable. Trace elements studied to a limited extent include copper, manganese, tin, vanadium, and zinc. Among the problems are the lack of relevant data, the definition of active species, the extrapolation of the results of experimental studies to humans, the methodological problems of epidemiologic studies, and the possible anticarcinogenic activity of some trace elements.

Humans↗
PubMed2001

Effect of fetal calf serum on the cadmium clastogenicity.

Inconsistent results among reports on cadmium genotoxicity revealed that certain confounding factors might significantly influence the outcomes of assessment. In Chinese hamster ovary (CHO-W8) cells, chromosome aberration induced by six different cadmium compounds was found positively associated with intracellular cadmium concentration. A parallel association was also observed among different CHO strains treated with same cadmium compound, the cadmium acetate. Both the cadmium-induced chromosome aberration and cadmium uptake were influenced by the presence of fetal calf serum (FCS). The presence of 10% FCS during the 2h treatment period greatly retarded the cellular cadmium uptake, and concurrently reduced the chromosome aberration induction. Other factors such as specific cadmium anion involved and the duration of cadmium treatment period in the investigation also influenced the assessment results of cadmium-induced chromosome aberration. In the protocol with a 2h pulse treatment, cadmium acetate, chloride and sulfate induced more chromosome aberration than cadmium nitrate, carbonate and oxide. When cadmium was present in the culture of the entire treatment period for 18 h, the results went the opposite way. Cadmium nitrate, carbonate and oxide induced significant chromosome aberration, while other three cadmium compounds gave negative results. Cadmium compounds did not induce significant SCE at the same dose level that yielded significant chromosome aberration induction, either in the protocol with the short pulse or long treatment period.

Animals↗
PubMed2006

[Exposure to metal compounds in occupational galvanic processes].

BACKGROUND: Occupational galvanic processes are provided in more than 600 small and medium enterprises in Poland. Workers who deal with galvanic coating are exposed to heavy metal compounds: tin, silver, copper and zinc. Some of them are carcinogenic, for example, hexavalent chromium compounds, nickel and cadmium compounds. MATERIAL AND METHODS: Research covered several tens of workstations involved in chrome, nickel, zinc, tin, silver, copper and cadmium plating. Compounds of metals present in the air were determined: Cr, Ni, Cd, Sn, Ag--by atomic absorption spectrometry with electrothermal atomization (ET-AAS) and Zn--by atomic absorption spectrometry with flame atomization (F-AAS). RESULTS: The biggest metal concentrations--of silver and copper--were found at workstations of copper, brass, cadmium, nickel and chrome plating, conducted at the same time. Significant concentrations of copper were found at workstations of maintenance bathing and neutralizing of sewage. The concentrations of metals did not exceed Polish MAC values. MAC values were not exceeded for carcinogenic chromium(VI), nickel or cadmium, either. CONCLUSIONS: In galvanic processes there was no hazard related to single metals or their compounds, even carcinogenic ones. Combined exposure indicators for metals at each workstation did not exceed 1, either. However, if there are even small quantities of carcinogenic agents, health results should always be taken into consideration.

Air Pollutants, Occupational↗
PubMed1990

The search for chelate antagonists for chronic cadmium intoxication.

Cadmium is unique among the metals because of its combination of toxicity in low dosages, long biological half-life (of about 30 years in humans), its low rate of excretion from the body and the fact that it is stored predominantly in the soft tissues (liver and kidney). There has been an increase in exposure to cadmium because its presence in fertilizers and sewage sludge and also its increased industrial use in Cd-Ni batteries. Although there are a number of reports on occupational and environmental exposures to cadmium compounds, treatment of cadmium poisoning has been difficult because there is neither a safe practical means of evaluating bioavailable body burden nor is there a recommended therapeutic chelating agent for chronic cadmium intoxication. In this review, the various factors affecting the chelation of cadmium such as its binding to intracellular metallothionein, the structural requirements of compounds for effective removal of cadmium, the excretion pattern of cadmium after its mobilization from intracellular stores and the recent developments in the design and synthesis of new compounds for cadmium chelation are discussed. The importance of protecting sensitive organs such as kidney and brain during cadmium chelation is addressed. The progress made during the last decade on the synthesis of new compounds, especially derivatives of dithiocarbamates, is remarkable. Some of these compounds provide promise for development of a useful and safe therapeutic chelating agent which can be used for the assessment of cadmium body burden and for preventive removal of cadmium as well as for use in overt cadmium poisoning in humans.

Animals↗
PubMed1985

[Health effects of occupational exposure to cadmium and its compounds and proposed preventive measures].

The paper presents effects of cadmium compounds upon human organism. Special attention was paid to disturbances resulting from chronic occupational exposure to those compounds. In addition, the description of toxic effects was supplemented with suggestions to carry on pre-employment and periodic examinations that would enable undertaking appropriate preventive measures for the population occupationally exposed to cadmium compounds.

Cadmium↗
PubMed1989

Quantification of proliferative lesions in hamster lungs after chronic exposure to cadmium aerosols.

The development of proliferative areas in the lungs of Syrian golden hamsters was studied after chronic inhalation of cadmium oxide, cadmium sulfide, cadmium chloride or cadmium sulfate. Lung tissue from randomly selected animals in each group was evaluated by morphometric histopathologic techniques. Estimation of the volumetric ratio of proliferative areas within the lungs of exposed animals showed significantly different extents of these lesions in dependence on the respective cadmium compound administered. The most severe changes were observed after inhalation of cadmium oxide and cadmium sulfide. Lesions were mainly found in the peribronchial region of the lung. Electron microscopic analysis of these proliferative areas revealed that they were composed of ciliated and Clara cells. From its histophatologic appearance this of lesion was qualitatively comparable in all hamsters which had been treated with the different cadmium compounds.

Administration, Inhalation↗
PubMed1995

NTP Toxicity Studies of Cadmium Oxide (CAS No. 1306-19-0) Administered by Inhalation to F344/N Rats and B6C3F1 Mice.

Three thousand tons of cadmium are imported or produced annually in the United States, and approximately 90% of this is cadmium oxide. Cadmium oxide is used in batteries, electroplating baths, pigments, plastics, synthetic products, and a variety of other materials. Cadmium oxide was nominated for study by the National Cancer Institute because of its widespread use and to obtain toxicity and carcinogenicity information. This report describes toxicity studies of cadmium oxide aerosol in F344/N rats and B6C3F1 mice, including sperm motility and vaginal cytology evaluations, and developmental toxicity studies of cadmium oxide aerosol in Sprague-Dawley rats and Swiss (CD-1(R)) mice. Genetic toxicology studies were done in Salmonella typhimurium and B6C3F1 mice erythrocytes. Cadmium oxide has been evaluated by other investigators for long-term carcinogenic effects, and recently the International Agency for Research on Cancer (IARC) evaluated cadmium and cadmium compounds for carcinogenic risks to humans. IARC (1993) classified cadmium and cadmium compounds as human carcinogens (Group I chemicals). GENETIC TOXICITY: Cadmium oxide was not mutagenic in Salmonella typhimurium strains TA98, TA100, TA1535, or TA1537, with or without exogenous metabolic activation, and did not induce micronuclei in erythrocytes of mice exposed by inhalation for 13 weeks. DEVELOPMENTAL TOXICITY STUDIES: For these studies, sperm-positive Sprague-Dawley rats and Swiss (CD-1(R)) mice were exposed to 0, 0.05, 0.5, or 2 mg/m(3) cadmium oxide 6 hours per day, 7 days per week, on gestation Day 4 through 19 (rats) or gestation Day 4 through 17 (mice). Maternal toxicity was observed in Sprague-Dawley rats exposed to 2 mg/m(3) cadmium oxide for 16 days and included body weights lower than those of the controls and clinical signs of toxicity (dyspnea and hypoactivity). There was no evidence of embryolethality in rats at any exposure level. However, in rats exposed to 2 mg/m(3), developmental toxicity was evidenced by lower fetal weights and a significant increase in the incidence of reduced skeletal ossifications. Maternal toxicity was also observed in Swiss (CD-1(R)) mice exposed to 2 mg/m(3) cadmium oxide for 14 days. Clinical signs were dyspnea, hypoactivity, lower body weight, and a lower pregnancy rate (30% vs. 97% in the control group). The total number of resorptions per litter was increased at the 2 mg/m(3) level. Developmental toxicity was evidenced by lower fetal weights in the 0.5 and 2 mg/m(3) groups and an increase in the incidence of reduced sternebral ossification in the 2 mg/m(3) group. TOXICITY STUDIES: Male and female F344/N rats and B6C3F1 mice were exposed to cadmium oxide aerosol (MMAD=1.1-1.6 mm) for 6 hours per day, 5 days per week, for 2 or 13 weeks. Exposure levels were 0.1 to 10 mg/m(3) for the 2-week studies and 0.025 to 1 mg/m(3) for the 13-week studies. The current Occupational Safety and Health Administration (OSHA) standards for cadmium, based on the results of these and other studies, are 2.5 mg/m(3) for the action level (AL) and 5 mg/m(3) for the permissible exposure limit (PEL) (29 CFR &sec; 1910.1027). The AL and PEL are calculated as an 8-hour, time-weighted average exposure. In the 2-week studies, all rats and mice at the highest exposure level (10 mg/m(3)) died from respiratory toxicity characterized by inflammation, necrosis, and fibrosis of the lung. Toxicity to the nasal cavity and tracheobronchial lymph nodes was also observed in the 10 mg/m(3) groups. At the lower exposure levels, treatment-related toxic lesions were not life threatening, and all body weights were within 10% of controls. In the 13-week studies, all rats and mice (with the exception of one control mouse) survived to the end of the studies. The final mean body weight of rats in the highest exposure groups (1 mg/m(3)) was 93% of the control value. For all other exposed rat and mouse groups, final mean body weights corresponded to those of the respective controls. For rats and mice in the 13-week studies, the major toxicity was to the respiratory system. Treatment-related lesions were observed in the lung, tracheobronchial lymph node, larynx, and nose. The no-observed-adverse-effect level (NOAEL) in the lungs was 0.025 mg/m(3) for rats. A NOAEL was not found in the lungs or larynx of mice or in the larynx of rats. At the 0.025 and 0.05 mg/m(3) levels in mice, lung lesions were minimal and not considered life threatening. A NOAEL in the nasal cavity was 0.05 mg/m(3) for rats and mice. Reproductive toxicity was observed in the 1 mg/m(3) groups of rats and was evidenced by a reduced number of spermatids per testis and an increase in the length of the estrous cycle. Reproductive toxicity was not observed at any exposure level in mice.

Journal Article↗
PubMed1996

Inhibition of L-threonine intestinal absorption in rabbits by cadmium.

Cadmium compounds are widely spread in the environment. Animal exposure to cadmium compounds occurs mainly through foods or drinks contaminated by this metal. Cadmium has been shown to produce several negative effects on the gastrointestinal tract such as inhibition on sugars and amino acids absorption. The aim of the present work was to study the inhibitory characteristics of cadmium on L-threonine intestinal absorption in rabbits in order to understand about this malabsorption of nutrients. Our results show that L-threonine tissue accumulation as well as mucosal to serosal transepithelial fluxes are decreased in a dose-dependent manner in rabbit jejunum. Amino acid diffusion across the intestinal epithelium was not affected by cadmium. A noncompetitive mechanism and a partial reversion by dithioerythritol (thiol groups protector) is described for this inhibition.

Animals↗