Occupational exposure cadmium

The information available regarding the association of occupational exposure to lead with increased cancer risk is generally limited in its usefulness because the actual compound(s) of lead, the route(s) of exposure, and level(s) of lead to which the workers were exposed were often not reported. Furthermore, potential for exposure to other chemicals including arsenic, cadmium, and antimony occurred, particularly in lead smelters, and smoking was a possible confounder (Cooper 1976 IARC 1987). These studies, therefore, are not sufficient to determine the carcinogenicity of lead in humans, and the following discussion is restricted to the most comprehensive of these studies. 

Recommendations for cadmium in air and human health protection under the worst scenario (Table 1.8) assume that total daily air intake is 27.14 m3 for an adult human who spends about 6.3 h in occupational exposure to air containing 100 pg Cd/m3 (USEPA 1980). Under these conditions, a 70-kg adult would retain about 361 pg Cd/day, based on an absorption factor of 0.5 (USEPA 1980), and most of this cadmium would probably be translocated to the kidney a critical threshold level of 200 mg Cd/kg in the kidney would be reached in about 1.52 years. It is not now known... 

Occupational and environmental poisoning with metals, metalloids, and metal compounds is a major health problem. Exposure in the workplace is found in many industries, and exposure in the home and elsewhere in the nonoccupational environment is widespread. The classic metal poisons (arsenic, lead, and mercury) continue to be widely used. (Treatment of their toxicities is discussed in Chapter 57.) Occupational exposure and poisoning due to beryllium, cadmium, manganese, and uranium are relatively new occupational problems, which present new and previously unaddressed problems. 

Renal Effects. Occupational exposure to silver metal dust has been associated with increased excretion of a particular renal enzyme (N-acetyl-p-D glucosaminidase), and with decreased creatinine clearance (Rosenman et al. 1987). Both of these effects are diagnostic of marginally impaired renal function. However, the workers in this study were also exposed to cadmium, which was detected in the urine of 5 of the 27 workers studied. Cadmium is known to be nephrotoxic differentiation of the effects of the two metals in the kidney is not possible with the data presented. Therefore, no conclusion can be drawn regarding renal effects of silver based on this study. 

Cadmium Standard (29 CFR 1910.1027). Colorant and additive production also involves the use of cadmium compounds, thus, the cadmium standard (29 CFR 1910.1027) also becomes important. This standard applies to all occupational exposures to cadmium and cadmium compounds and requires respiratory protection when workplace exposure levels for lead reaches or exceeds 5pg/m3 (200pg/m3 for dry color formulators). 

Vlaene MK, Masschelein R, Leenders J, De GroofM, Swerts LJVC, Roels HA. Neuro behavioral effects of occupational exposure to cadmium a cross sectional epidemiological study. Occup Environ Med 2000 57 19-27. 

Effects of non-occupational exposure to cadmium [51], itai-itai disease in particular [52, 53], were occasionally compared with kidney damage seen in Balkan nephropathy patients. In spite of some resembhng features, the idea of a common etiology between cadmium nephropathy (including itai-itai disease) and Balkan nephropathy was refuted [52, 54]. 

It should be noted that in the majority of the above mentioned studies, metal-induced renal injury was considered as if exposure occurred to only one metal at a time. In reality it is clear that environmental and occupational exposure may involve several metals at the same time and in varying concentrations [34]. It has been shown that with combined exposure various metals may interact with each other and that one metal may alter the potential toxicity of another in either a beneficial or deleterious way. As an example, whilst arsenic has been shown to worsen cadmium-induced nephrotoxicity, data from experimental studies have shown that selenium may protect against the renal effects induced by cadmium [52]. Other studies have shown that the iron status may alter the toxic effects of aluminium at the level of the bone and the parathyroid gland [53,54], whilst in a recent increased lead accumulation was associated with disturbances in the concentration of a number of essential trace elements [55]. 

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. 

The primary routes of potential human exposure to coke oven emissions are inhalation and dermal contact. Occupational exposure to coke oven emissions may occur for those workers in the aluminum, steel, graphite, electrical, and construction industries. Coke oven emissions can have a deleterious effect on human health. Coke oven emissions contain literally several thousand compounds, several of which are known carcinogens and/or cocarcinogens including polycyclic organic matter from coal tar pitch volatiles, jS-naphthylamine, benzene, arsenic, beryllium, cadmium, chromate, lead, nickel subsulfide, nitric oxide, and sulfur dioxide. Most regulatory attention has been paid to coal tar pitch volatiles. 

Occupational exposures Acrylate and derivatives Cadmium dust Carbon disulfide Formaldehyde Hydrogen sulfide Solvents (volatile hydrocarbons)... 

S. Satarug, J. R. Baker, P. E. B. Reilly, M. R. Moore and D. J. Williams, Cadmium Levels in the Lung, Liver, Kidney Cortex, and Urine Samples from Australians without Occupational Exposure to Metals, Archives of Environmental Health, 57(1), 69-77 (2002). 

The human health and environmental issues associated with nickel-cadmium batteries arise mainly from the ultimate disposal of the spent batteries. In general, occupational exposures to and manufacturing wastes and emissions from nickel, cadmium, cobalt and other materials in NiCd battery production are well regulated and controlled. There is virtually no danger of nickel or cadmium exposure during normal use of NiCd batteries. Even when NiCd batteries are disposed of in landfills, there is little danger of risk or exposure, at least in the short to mid-term, to nickel or cadmium from the battery s electrodes since they are always encased in at least two layers of steel or plastic or both. 

Bauchinger M, Schmid E, Einbrodt HJ, et al. 1976. Chromosome abemations in lymphocytes after occupational exposure to lead and cadmium. Mutat Res 40 57-62. 

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