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Cadmium chronic effect

Air-poUutant effects on neural and sensory functions in humans vary widely. Odorous pollutants cause only minor annoyance yet, if persistent, they can lead to irritation, emotional upset, anorexia, and mental depression. Carbon monoxide can cause death secondary to the depression of the respiratory centers of the central nervous system. Short of death, repeated and prolonged exposure to carbon monoxide can alter sensory protection, temporal perception, and higher mental functions. Lipid-soluble aerosols can enter the body and be absorbed in the lipids of the central nervous system. Once there, their effects may persist long after the initial contact has been removed. Examples of agents of long-term chronic effects are organic phosphate pesticides and aerosols carrying the metals lead, mercury, and cadmium. [Pg.2179]

Bay, S.M., D.J. Greenstein, P. Szalay, and D.A. Brown. 1990. Exposure of scorpionfish Scorpaena guttata) to cadmium biochemical effects of chronic exposure. Aquat. Toxicol. 16 311-320. [Pg.69]

Gentile, S.M., J.H. Gentile, J. Walker, and J.F. Heltshe. 1982. Chronic effects of cadmium on 2 species of mysid shrimp Mysidopsis bahia and Mysidopsis bigelowi. Hydrobiologia 93 195-204. [Pg.72]

Chronic effects are of particular concern because cadmium is very slowly excreted from the body, with a half-life of about 30 years. Thus low levels of exposure can result in considerable accumulation of cadmium. The main organ of damage following long-term exposure is the kidney, with the proximal tubules being the primary site of... [Pg.52]

Mueller PW, Paschal PC, Hammel RR, Klincewitz SL, McNeil ML, Speirto B, Steinberg KK. Chronic effects in three studies of men and women occupationally exposed to cadmium. Arch Environ Contam Toxicol 1992 23 125-136. [Pg.782]

The objective of this chapter is to put into perspective some of the current knowledge with respect to trace metals and their health implications. Potential adverse health effects of occupational exposures to trace metals are dis cussed cancer (arsenic, beryllium chromium nickel, and perhaps cadmium) chronic lung disease (beryllium and cadmium) neurologic and reproductive disorders (lead and mercury) and kidney disorders (lead and cadmium). Also discussed are the National Institute for Occupational Safety and Health (NIOSH) recommended standards for occupational exposure to several trace metals, the difficulty of establishing safe levels of exposure (particularly for carcinogens), and problems involved in identifying toxic components of trade name products. Special attention is given to the role of chemists to help protect the public health. [Pg.27]

Chronic effects of exposure to elevated cadmium concentrations lead to lung emphysema, renal damage and softening of bones. The atomic diameter of cadmium is very similar to that of calcium which leads to the substitution of calcium by cadmium and its building into the bones which results in osteomyelitis and osteoporosis. Experiments carried out on animals showed cancerous effects of cadmium and its influence on zinc metabolism (Lehman and Poisner, 1984). [Pg.508]

W. J. Birge and J. A. Black (unpublished data) evaluated the chronic effects of cadmium on reproduction of the rainbow trout. Adult fish were exposed to cadmium at 0.2 fig/lilQi in moderately hard water (102 mg/liter as CaCOg) for 18... [Pg.75]

Reports on chronic effects of cadmium on human liver function are rare. In experimental animals, liver also accumulates substantial amounts of cadmium after both acute and chronic poisoning (Kotsonis and Klaassen 1977, 1978), which results in hepatic injury with both types of exposure (Dudley et al. 1982 Stowe et al. 1972 Faeder et al. 1977). Dudley et al. (1982) demonstrated that liver is a target organ after acute exposure and that the liver injury may play a role in the lethality of animals soon after exposure. The prominent morphological changes after an acute high dose of cadmium... [Pg.195]

Therefore, risk assessment for human health is limited by (i) the scarcity of analytical data and poor predictive power of cadmium distribution in the body in relation to health outcome, (ii) the lack of information about chronic effects of cadmium accumulating over decades in tissues, and (iii) the lack of suitable biomarkers other than for irreversible kidney damage. Thus, the epidemiological studies linking health effects and cadmium exposure suffer from a relative lack of consensus knowledge about the modes of action of cadmium in multi-cellular... [Pg.27]

Perry HM, Erlanger MW. 1978. Pressor effects of chronically feeding cadmium and lead together. In Hemphill DD, ed. Trace substances in environmental health. Vol. 12. Columbia, MO University of Missouri-Columbia, 268-275. [Pg.562]

Thorp, J.H., J.P. Giesy, and S.A. Wineriter. 1979. Effects of chronic cadmium exposure on crayfish survival, growth, and tolerance to elevated temperatures. Arch. Environ. Contam. Toxicol. 8 449-456. [Pg.77]

Visviki, L. and J.W. Rachlin. 1994a. Acute and chronic exposure of Dunaliella salina and Chlamydomonas bullosa to copper and cadmium effects on growth. Arch. Environ. Contam. Toxicol. 26 149-153. [Pg.233]

Proximity to the smokestacks of metal smelters is positively associated with increased levels of lead in the hair (manes) of horses and in tissues of small mammals, and is consistent with the results of soil and vegetation analyses (USEPA 1972). Lead concentrations were comparatively high in the hair of older or chronically impaired horses (USEPA 1972). However, tissues of white-tailed deer (Odocoileus virginianus) collected near a zinc smelter did not contain elevated levels of lead (Sileo and Beyer 1985). Among small mammals near a metal smelter, blood ALAD activity was reduced in the white-footed mouse but normal in others, e.g., the short-tailed shrew (Beyer et al. 1985). The interaction effects of lead components in smelter emissions with other components, such as zinc, cadmium, and arsenic, are unresolved (USEPA 1972) and warrant additional research. [Pg.257]

The most severe form of chronic cadmium (Cd) poisoning caused by prolonged oral Cd ingestion is Itai-itai disease, which developed in numerous inhabitants of the Jinzu River basin in Toyama Prefecture, Japan in the 1950s (Figure 20.7). For the first time, cadmium pollution was shown to have severe consequences on human health, particularly in women. The most important effects were softening of the bones and kidney failure. The name of the disease is derived from the painful screams (Japanese /to/) caused by the severe pain in the... [Pg.346]

Chronic exposure can result in obstructive lung disease, emphysema, and kidney disease. Cadmium may also be related to increases in blood pressure (hypertension) and is a possible lung carcinogen. Cadmium affects calcium metabolism and can result in bone loss. This condition has been referred to as Itai-Itai disease, which means Ouch-Ouch in Japanese and reflects the bone pain associated with cadmium effects on calcium. [Pg.127]


See other pages where Cadmium chronic effect is mentioned: [Pg.63]    [Pg.924]    [Pg.133]    [Pg.198]    [Pg.75]    [Pg.18]    [Pg.1009]    [Pg.195]    [Pg.204]    [Pg.18]    [Pg.388]    [Pg.50]    [Pg.43]    [Pg.70]    [Pg.68]    [Pg.196]    [Pg.347]    [Pg.243]    [Pg.257]    [Pg.143]    [Pg.68]    [Pg.196]   
See also in sourсe #XX -- [ Pg.690 ]




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Chronic effects

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