Occupational exposure arsenic

Occupational Exposure to Inofganic Arsenic, E.S. Dept, of HEW National Institute of Safety and Health, Washington, D.C., 1973. 

Non-arsenical insecticides (occupational exposures in spraying and application of) (Vol. 53 1991) Polychlorinated biphenyls [1336-36-3] (Vol. 18, Suppl. 7 1987)... 

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. 

The occupational exposure of five workers to arsine was reported by Phoon et al. (1984). All cases involved hematuria and, except for one patient, abdominal pain and jaundice. One worker was exposed for approximately 1 3/4 h, while the others were exposed for approximately 2 1/4 h. The latency in appearance of toxic effects was unusually short U-3 h). The following day, the arsine level in the workers breathing zone was 0.055 mg/m3 (0.017 ppm), although no processing of arsenic-containing material was taking place at the time of measurement. It was hypothesized by the report authors that the arsine... 

Landrigan et al. (1982) conducted an epidemiologic survey to evaluate occupational exposure to arsine in a lead-acid battery manufacturing plant. Arsine concentrations ranged from nondetectable to 49 /breathing zone samples. A high correlation was found between urinary arsenic concentration and arsine exposure (r=0.84 p=0.0001 for an n of 47). Additionally, arsine levels above 15.6 /ig/m3 (=0.005 ppm) were associated with urinary arsenic concentrations in excess of 50 //g/L. The investigators concluded that exposure to a 200 /ig/m3 arsine exposure standard would not prevent chronic increased absorption of trivalent arsenic. 

Landrigan, P.J., R.J.Castello, and W.T.Stringer. 1982. Occupational exposure to arsine. An epidemiologic reappraisal of current standards. Scand. J. Work Environ. Health. 8 169-177. Legge, T.M. 1916. Arsenic poisoning. In Diseases of Occupations and Vocational Hygiene, G.M.Kober and W.Hanson, eds. Philadelphia, PA Blakiston. 

This chapter presents specific information with regard to the effects of environmental and occupational exposure to arsenic on inflammatory processes, the immune system, and host defense. While the focus is on the in vivo and in vitro effects of arsenic on host immune responses (e.g., immunotoxicity and hypersensitivity) and their relationship to clinically observed manifestations of arsenic toxicity (e.g., inflammation and skin cancer), information on the potential mechanisms through which arsenic may exert its biological effects is also provided. 

Acute inhalation exposures have resulted in irritation of the upper respiratory tract, even leading to nasal perforations. Occupational exposure to arsenic compounds results in hyperpigmentation of the skin and hyperkeratoses of palmar and plantar surfaces, as well as dermatitis of both primary irritation and sensitization types. Impairment of peripheral circulation and Raynaud phenomenon have been reported with long-term exposure. ... 

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. 

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. 

Hair has been used in the biomonitoring of various elements, for example, arsenic, thallium, and zinc, and has been used in the monitoring of drugs and biological substances. The level of mercury in hair is widely used as a biological indicator for exposure to methyl mercury (MeHg). In addition, hair samples have been utilized to evaluate environmental exposure to pollutants such as lead, and occupational exposures to metals such as nickel and chromium. However, the ATSDR has stated ... 

The potential for unusual health effects of chemical mixtures due to the interaction of chemicals or their metabolites (e.g., metabolites of trichloroethylene and benzene) in or with the biosystem constitutes a real issue in the public health arena. However, toxicity testing to predict effects on humans has traditionally studied one chemical at a time for various reasons convenient to handle, physiochemical properties readily defined, dosage could easily be controlled, biologic fate could easily be measured, and relevant data were often available from human occupational exposures. Chemicals are known to cause disease for example, arsenic and skin cancer, asbestos and lung cancer, lead and decrements of IQ, and hepatitis B predisposes to aflatoxin-induced liver cancer but the link between the extent of human exposure to even well-defined chemical mixtures and disease formation remains relatively unexplored, but of paramount importance to public health. 

OSHA has in the past decade completed a number of rulemakings on occupational carcinogens, including arsenic, benzene, asbestos, ethylene oxide and acrylonitrile. The agency conducted risk assessments and concluded that occupational exposure standards - so-called Permissible Exposure Levels, PELs - were too high and had to be reduced. 

The World War I chemical arsenal included cyanide. Other potential cyanide exposures in the twentieth century came from medicinal and industrial sources. Thiocyanate, a medicine in the early twentieth century prescribed for hypertension, caused severe psychosis (Barnett et al. 1951). Hamilton and Hardy (1974) reviewed two cases of chronic occupational exposure to cyanide that caused intellectual impairment in one case and nervousness in the other. 

Beckett WS, Moore JL, Keogh JP, et al Acute encephalopathy due to occupational exposure to arsenic. British Journal of Industrial Medicine 43 66-67, 1986 Calderon J, Navarro ME, Jimenz-Capdeville ME, et al Exposure to arsenic and neuropsychological development in Mexican children. Environ Res 85 69-76, 2001 DePalma AE Arsine intoxication in a chemical plant. J Occup Med 11 582-587,1969 Eagle H, Magnuson HJ The systemic treatment of 227 cases of arsenic poisoning (encephalitis, dermatitis, blood dyscrasias, jaundice, fever) with 2,3-dimercapto-propanol (BAL). American Journal of Syphilis, Gonorrhea, and Venereal Diseases 30 420-441, 1946... 

Arsenic is one of the most important global environmental toxicants (Gebel 2000). Inorganic arsenic is a potent human carcinogen, and it has long been known that occupational exposure (e.g., in copper smelters) increases the risk for lung cancer (lARC... 

Arsenic exposure or intoxication is commonly assessed by determining the inorganic arsenic content in urine. In environmental exposure through drinking water (e.g.. Concha et al. 1998, Vahter 1999), urinary levels as high as several mg have been found. Levels below or around 100 xg L still may occur in occupational exposure (Ng et al. 1998, Dang et al. 1999). In drastic intoxication or suicidal cases, urine values for inorganic arsenic may attain > 100 mg L (see Section 6.4.2). 

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