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Of lead toxicity

When in industrial use, lead is released to the atmosphere, and not only its stable isotope, but also radioactive isotopes, such as Pb-210, Pb-212 and Pb-214 are released. Their sources are radioactive gases (including radon). [Pg.60]

Lead is highly toxic substance, it is accumulated in the human body and expelled slowly together with the living activity products. Introduced in a human body it attacks the nervous system, marrow, blood and vascular, disturbing albumen synthesis and genetic structure of cells [7.12, 7.13, 7.14], [Pg.60]

Maximum permissible concentrations of lead in air and in water are respectively 10 mg/L and 0.03-0.1 mg/L. In normal reactor operation lead is kept within gas-tight circuit. Enhancement of lead concentration in working rooms is possible as a result of accidents causing leaks in the reactor upper plate, or its disassembly. [Pg.60]

TABLE 7.2. HUMAN DISRUPTION INDEX (ENERGY SUPPLY INPUT) [Pg.60]

Flow items Natural baseline flow Human Disruption Index Major causes [Pg.60]


Because of the toxicity of lead, special care must be taken when working with lead ahoys. Lead and its inorganic compounds are neurotoxias which may produce peripheral neuropathy. Eor an overview of the effects of lead exposure, see Occupational Exposure to Lead, Appendix A (29 CRE 1910.1025) (see... [Pg.62]

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). [Pg.78]

See pubhcations of R. LiUs for additional studies related to the toxicity of lead following occupational exposure. These pubHcations have been compiled into a volume entitied Studies on Eead Exposed Occupational Groups 1967—1989 and ate available from the Dept, of Community Medicine, Mount Sinai School of Medicine, New York, 1991. [Pg.79]

Soldered joints present their own characteristic corrosion problems usually in the form of dissimilar metal attack often aided by inadequate flux removal after soldering. Such joints have always been a source of concern to the electrical industry. Lead-containing solders must be used with caution for some types of electrical connection since PbfOHjj.PbCOj may be found as a corrosion product and can interrupt current flow. Indium has been found to be a useful addition to Sn-Pb solders to improve their corrosion resistanceHowever, in view of the toxicity of lead and its alloys, the use of lead solders, particularly in contact with potable waters and foodstuff s, is likely to decline. [Pg.102]

Tin-lead can be substituted for tin for other purposes, although the toxicity of lead limits the field of application. The corrosion resistance is usually no better than that of unalloyed tin, but there may be some saving of cost in applications such as wash-boilers and other vessels for non-potable liquids and light engineering components formed from sheet metal. Heavily coated terne-plates may be used for the fuel tanks of stoves and vehicles. [Pg.510]

The toxicity of lead-containing greases has led to alternative products being used for the protection of components where the product is likely to come in contact with rubber. Of those products considered silicone-based greases have been found to be particularly suitable and their application to hydraulic equipment components such as brake cylinders, where they can provide internal protection against corrosion both during transit and use, has been found particularly beneficial. [Pg.763]

Some elements come in and out of fashion, so to speak. Sixty years ago, elemental silicon was a chemical curiosity. Today, ultrapure silicon has become the basis for the multibillion-dollar semiconductor industry. Lead, on the other hand, is an element moving in the other direction. A generation ago it was widely used to make paint pigments, plumbing connections, and gasoline additives. Today, because of the toxicity of lead compounds, all of these applications have been banned in the United States. [Pg.3]

Toxicology Many companies are known to use gene expression profiling to assess the potential toxicity of lead compounds. This approach may require a database of reference compounds with known pharmacological and toxicological properties. Lead compounds can be compared to the database to predict compound-related or mechanism-related toxicity [5]. [Pg.769]

Route Dependent Toxicity. The toxicity of lead does not appear to be dependent on the route of exposure, but the time course may be affected. [Pg.260]

A high calcium diet was also shown to influence the toxicity of lead. Dam and pup hemoglobin... [Pg.325]

Iron Rat Tissue levels and relative toxicity of lead Iron deficiency increases lead absorption and toxicity Six and Goyer 1972... [Pg.326]

Cadmium also affects the toxicity of lead. A synergistic effect of these metals was found on prostatic cytology and testicular damage in male rats following intraperitoneal injection (Fahim and Khare 1980). Rats fed lead and cadmium or zinc had a marked reduction of reticulocytosis compared with rats fed lead alone (Thawley et al. 1977). Mice exposed simultaneously to lead and cadmium for 10 weeks had higher mortality rates than mice exposed to either metal alone (Exon et al. 1979). In addition, interactions between cadmium and lead have been reported at the behavioral effects level (Nation et al. 1990). [Pg.328]

Nutritional surveys indicate that children of low-income groups consume less than recommended dietary allowances of calcium and iron. Dietary deficiencies of these two minerals have been shown to potentiate the toxicity of lead (Johnson and Tenuta 1979 Yip et al. 1981 Ziegler et al. 1978). Thus, nutrient deficiencies in conjunction with a developmental predisposition to absorb lead makes this subset of children at a substantially elevated risk. More information on children s susceptibility to lead is presented in Section 2.6. [Pg.332]

University of Rochester, Behavioral toxicity of lead role of the Rochester, NY NMDA receptor... [Pg.359]

Cory-Slechta DA, Weiss B, Cox C. 1983. Delayed behavioral toxicity of lead with increasing exposure concentrations. Toxicol Appl Pharmacol 71 342-352. [Pg.505]

Grandjean P, Andersen O. 1982. Toxicity of lead additives. Lancet 2 333-334. [Pg.527]

Pounds JG, Long GJ, Rosen JF. 1991. Cellular and molecular toxicity of lead in bone. Environ Health Perspect 91 17-32. [Pg.564]

Smith CM, Wang X, Hu H, et al. 1995. A polymorphism in the delta-aminolevulinic acid dehydratase gene may modify the pharmacokinetics and toxicity of lead. Environ Health Perspect 103 248-253. [Pg.576]

Todd AC, Wetmur JG, Moline JM, et al. 1996. Unraveling the chronic toxicity of lead An essential priority for environmental health. Environ Health Perspect 104(1) 141-146. [Pg.580]

Denneman, C.A.J. and N.M. van Straalen. 1991. The toxicity of lead and copper in reproduction tests using the oribatid mite Platynothrus peltifer. Pedobiol. 35 305-311. [Pg.219]

The effect of diet on vulnerability to lead makes interpretation of published information on experimental lead poisoning in waterfowl extremely difficult (Chasko et al. 1984). For example, many mallards on a diet of com die within 10 to 14 days after ingesting a single lead shot, whereas similar birds on a balanced commercial duck ration appear outwardly normal after ingesting as many as 32 pellets of the same size (Wobeser 1981). Also, multiple nutritional deficiencies may have additional effects in potentiating the toxicity of lead in mallards (Carlson and Nielsen 1985). Under conditions of reduced dietary calcium availability, such as can occur in acid-impacted environments, birds risk increased uptake of lead (and other metals) and may accumulate toxic concentrations more rapidly (Scheuhammer 1996). Enhanced accumulation of lead was accompanied by an increased synthesis of metallothioneins and a greater inhibition of ALAD activity (Scheuhammer 1996). [Pg.299]

Chasko, G.G., T.R. Hoehn, and P. Howell-Heller. 1984. Toxicity of lead shot to wild black ducks and mallards fed natural foods. Bull. Environ. Contam. Toxicol. 32 417 428. [Pg.327]

Coughlan, D.J., S.P. Gloss, and J. Kubota. 1986 Acute and sub-chronic toxicity of lead to the early life stages of smallmouth bass (Micropterus dolomieui). Water Air Soil Pollut. 28 265-275. [Pg.328]

Davies, P.H., J.P. Goettl, Jr., J.R. Sinley, and N.F. Smith. 1976. Acute and chronic toxicity of lead to rainbow trout Salmo gairdneri, in hard and soft water. Water Res. 10 199-206. [Pg.328]

Heinz, G.H., D.J. Hoffman, L. Sileo, and L.J. LeCaptain. 1999. Toxicity of lead-contaminated sediments to mallards. Arch. Environ. Contam. Toxicol. 36 323-333. [Pg.332]

Kaplan, H.M., T.J. Anrholt, and J.E. Payne. 1967. Toxicity of lead nitrate solutions for frogs (Rana pipiens). Lab. Animal Care 17 240-246. [Pg.334]

Longcore, J.R., R. Andrews, L.N. Locke, G.E. Bagley, and L.T. Young. 1974b. Toxicity of lead and proposed substitute shot to mallards. U.S. Fish Wildl. Serv. Spec. Sci. Rep. —Wildl. 183. 23 pp. [Pg.336]

Oladimeji, A.A. and B.A. Offem. 1989. Toxicity of lead to Clarias lazera, Oreochromis niloticus, Chironomus tentans and Benacus sp. Water Air Soil Pollut. 44 191-201. [Pg.338]

Rattner, B.A., W.J. Fleming, and C.M. Bunck. 1989. Comparative toxicity of lead shot in black ducks (Anas rubripes) and mallards (Anas platyrhynchos). Jour. Wildl. Dis. 25 175-183. [Pg.339]

Grandy, J.W., IV, L.N. Locke, and G.E. Bagley. 1968. Relative toxicity of lead and five proposed substitute shot types to pen-reared mallards. Jour. Wildl. Manage. 32 483-488. [Pg.732]

A Division of Pharmacology had been formally set up in the Food and Drug Administration in 1935, composed mostly—as one of its members, Edwin P. Laug, remembered—of "biochemists who then changed sails and became pharmacologists" (7] ). To study the toxicity of lead and arsenic pesticide residues formed the division s initial purpose, but the Elixir Sulfanilamide crisis brought an almost total shift of effort to diethylene glycol. [Pg.129]

The corrosion rate of Pb02 - often enhanced by mechanical erosion - is relatively high and may be a problem due to the toxicity of lead. Pb02 can be stabilized by modification with, for example, silver, antimony, tin, cobalt oxides (or by alloying of the lead base metal with these metals, respectively) [29]. [Pg.42]

Marcus Vitruvius, architect and engineer under the Emperor Augustus, was familiar with the toxicity of lead and observed that the laborers in the smelters have pale complexions because of their prolonged exposure to lead dust and vapor (209). [Pg.42]


See other pages where Of lead toxicity is mentioned: [Pg.77]    [Pg.157]    [Pg.257]    [Pg.272]    [Pg.338]    [Pg.612]    [Pg.370]    [Pg.223]    [Pg.1]    [Pg.14]    [Pg.128]    [Pg.132]   
See also in sourсe #XX -- [ Pg.1379 , Pg.1379 , Pg.1380 , Pg.1380 ]

See also in sourсe #XX -- [ Pg.101 , Pg.245 ]

See also in sourсe #XX -- [ Pg.21 ]




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