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Exposure to Cadmium

Exposure of humans to cadmium occurs both through the environment and occupational settings. Atmospheric emissions from man-made sources exceed those from natural sources by about one order of magnitude (Kazantzis 1986). [Pg.190]

Food and cigarettes constitute the two major sources of cadmium exposure for the general population. Cadmium is present in most foods, with highest concentrations found in kidney, liver, and shellfish (Lauwerys 1978). The concentration of cadmium in lungs of smokers is approximately twice that of nonsmokers (Lewis et al. 1972). The cadmium intake from the atmosphere is negligible compared with that from food for the general population. Much higher concentrations of cadmium are found in industrialized urban areas. In workplaces associated with cadmium use, exposure is mainly due to inhalation of fumes and dusts. [Pg.190]

In humans, intestinal absorption of cadmium is estimated at 5% (McLellan et al. 1978 Friberg et al. 1986). Both human and animal data demonstrate that cadmium absorption from the lungs is 25%-50% (Friberg et al. 1986). Others report that up to 90% of cadmium deposited deep in the lung can be absorbed and distributed to other critical organs such as liver, kidney, and testis (Oberdorster 1986 Waalkes and Oberdorster 1990). [Pg.190]

The major route of excretion of cadmium is via feces and bile. Approximately 95% of oral cadmium dose is excreted in the feces due to the poor absorption of cadmium from the GI tract. Urinary excretion of cadmium may become significant after the onset of renal damage. [Pg.191]


Acute exposure to cadmium may lead to chemical pneumonitis and edema, but is rare nowadays (Herber 1994b). Chronic exposure to Cd affects mostly the renal tubules and the lung. Exposure to Cd can take place both in the occupational and environmental area. [Pg.204]

A negative correlation was found between PbB and systolic pressure in Belgian men in the Cadmibel study (a cross-sectional population study of the health effects of environmental exposure to cadmium) (Staessen et al. 1991). In this study, blood pressure and urinary cation (positive ions found in the urine, such as sodium, potassium, and calcium) concentration data were obtained from 963 men and 1,019 women multiple stepwise regression analyses were conducted adjusting for age, body mass index, pulse... [Pg.55]

In a historical cohort mortality study of 1,990 primary lead smelter workers, an SMR of 2.04 for mortality from renal cancer was calculated (Selevan et al. 1985). The cohort consisted of workers who had worked at least 1 year, with at least 1 day of employment at the smelter between 1940 and 1965. The cohort had been heavily exposed to lead and in 1976 the PbB levels averaged 56.3 pg/dL. Exposures to cadmium and arsenic were generally minor. A follow-up study of this cohort was conducted from 1977 through 1988 (Steenland et al. 1992). Analysis of the follow-up study revealed an excess of kidney cancer, particularly in the high-lead group (SMR 2.39). Although, as the authors indicate, the study is... [Pg.129]

Iannaccone A. Carmignani M, Boscolo P. 1981. [Cardiovascular reactivity in the rat following chronic exposure to cadmium and lead.] Ann 1st Super Sanita 17 655-660. (Italian)... [Pg.535]

Auslander M, Yudkovski Y, Chalifa-Caspi V, Herat B, Ophir R, Reinhardt R, Neumann PM, Tom M (2008) Pollution-affected fish hepatic transcriptome and its expression patterns on exposure to cadmium. Mar Biotechnol (NY) 10(3) 250-261... [Pg.292]

Canli, M. and R.M. Stagg. 1996. The effects of in vivo exposure to cadmium, copper and zinc on the activities of gill ATPases in the Norway lobster, Nephmps norvegicus.Arch. Environ. Contam. Toxicol. 31 494-501. [Pg.70]

Miliou, H., N. Zaboukas, and M. Moraitou-Apostolopoulou. 1998. Biochemical composition, growth, and survival of the guppy, Poecilia reticulata, during chronic sublethal exposure to cadmium. Arch, Environ. Contam. Toxicol. 35 58-63. [Pg.74]

Ricard, A.C., C. Daniel, P. Anderson, and A. Hontela. 1998. Effects of subchronic exposure to cadmium chloride on endocrine and metabolic functions in rainbow trout Oncorhynchus mykiss. Arch. Environ. Contam. Toxicol. 34 377-381. [Pg.75]

Saxena, D.K., R.C. Murthy, C. Singh, and S.V. Chandra. 1989a. Zinc protects testicular injury induced by concurrent exposure to cadmium and lead in rats. Res. Commun. Chem. Pathol. Pharmacol. 64 317-329. [Pg.740]

Cadmium is a widely distributed metal used in manufacturing and is present in a number of consumer products. Dietary exposure to cadmium is possible from shellfish and plants grown on cadmium-contaminated soils. Absorption is increased when associated with low levels of iron or calcium in the diet. Some plants, such as tobacco, can concentrate cadmium from even low levels in the soil. The lung readily absorbs cadmium, thus cigarette smokers have elevated cadmium exposure. Cadmium is also used as a metal alloy, in paint, and in batteries (Ni-Cad, nickel-cadmium). Workplace exposure can occur in welding and battery manufacture. [Pg.127]

Srivastava RC, Husain MM, Srivastava SK, et al. 1995. Effect of pre-exposure to cadmium and silver on nickel induced toxic manifestations in mice possible role of ceruloplasmin and metallothionein. Bull Environ Contam Toxicol 54 751-759. [Pg.252]

The toxic effects of chronic exposure to cadmium differ somewhat with the route of exposure. The kidney is affected following either pulmonary or gastrointestinal exposure marked effects are observed in the lungs only after exposure by inhalation. [Pg.1000]

Cadmium is a cumulative toxicant with a biologic half-life of up to 30 years in humans. More than 70% of the cadmium in the blood is bound to red blood cells accumulation occurs mainly in the kidney and the liver, where cadmium is bound to metallothionein. In humans the critical target organ after long-term exposure to cadmium is the kidney, with the first detectable symptom of kidney toxicity being an increased excretion of specific proteins. [Pg.46]

Acute effects of exposure to cadmium result primarily from local irritation. After ingestion, the main effects are nausea, vomiting, and abdominal pain. Inhalation exposure may result in pulmonary edema and chemical pneumonitis. [Pg.52]


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Cadmium exposure

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