Arsenic exposure routes

Carcinogenicity. Neoplasia in man has been implicated as a consequence of arsenic exposure both by the oral (skin cancer) (104) and inhalation routes (lung cancer) (105) with the latter association being... 

Figure 4 Relative contribution by exposure route to predicted dose Estimated population lifetime average daily dose of arsenic for children exposed to chromated copper arsenate (CCA)-treated wood playsets and decks in warm climate regions (from Zartarian et al., 2006).

Conclusive evidence of skin cancer from topical exposure to metal compounds alone is not available (Chap. 29). Arsenic exposure has caused skin cancer, but the route has mainly been oral. 

The importance of toxic elements in environmental chemistry is rarely questioned, but a relatively small number of elements (mercury, lead, and cadmium) have received a large share of researchers attention. The environmental chemistry of the transition metals, e.g., chromium, nickel, manganese, cobalt, copper, etc., has also been investigated principally because of their roles in metabolism, especially enzymatic processes. However, two non-metals, arsenic and selenium, and two metals, beryllium and vanadium, are elements which will become more significant in the future from environmental and toxicological points of view. Arsenic and selenium have been investigated, but much more work is needed because of the importance of these two elements in the environment. The author considers beryllium and vanadium to be problem metals of the future . The primary exposure route for both beryllium and vanadium is via the atmosphere and as lower environmental standards are imposed, more uses are found for each element, and more fossil fuels (source of V) are burned, the amounts added to the atmosphere will have more significance. 

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. 

Cancer. The information available on the carcinogenicity of lead in occupationally exposed humans is limited in its usefulness because the lead compound(s), the route(s) of exposure, and the levels of exposure were not always reported. Furthermore, concurrent exposure to other chemical (including arsenic, particularly in lead smelters) and confounding variables, such as smoking, were often not evaluated. Therefore, the data currently available do not support an assessment of the potential carcinogenic risk of lead in humans. 

Chronic exposure to arsenicals by way of the air, diet, and other routes has been associated with liver, kidney, and heart damage, hearing loss, brain-wave abnormalities, and impaired resistance to viral infections. 

When appropriately validated and understood, biomarkers present unique advantages as tools for exposure assessment (Gundert-Remy et al, 2003). Biomarkers provide indices of absorbed dose that account for all routes and integrate over a variety of sources of exposure (IPCS, 1993, 2001a). Certain biomarkers can be used to represent past exposure (e.g. lead in bone), recent exposure (e.g. arsenic in urine), and even future target tissue doses (e.g. pesticides in adipose tissue). Once absorbed dose is determined using biomarkers, the line has been crossed between external exposure and the dose metrics that reflect the pharmacokinetics and toxicokinetics of an agent (see section 5.3.3). 

Levvy (1947) reported that an average of 64% of inhaled arsine was absorbed in mice exposed by inhalation route at concentrations of 25-2500 mg/m for periods ranging from 0.40 min to 24 h. Blair et al (1990b) measured the arsenic content in liver after exposure of rats to variable arsine concentrations (0.08, 1.6, and 8.1 mg/m for 6 h/day for 90 days). Arsenic concentration in liver increased with airborne arsine concentration and was higher in females than in males. The arsenic level in 3-4 days after a 90 day exposure at a concentration of 8.1 mgW was 6-8 pg/g (compared with approximately 1.5 pg/g in controls). 

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. 

HUMAN TOXICITY DATA no LD50/LC50 information found related to normal routes of occupational exposure Toxicity data, as referred to metallic arsenic, is as follows oral-man TDLo 76mg/kg/12Y-intermittent toxic effect carcinogenic oral-man TDLo 7857 mg/kg/55Y toxic effect skin oral-man TDLo 7857 mg/kg/55Y toxic effect gastrointestinal tract. 

Arsenic is absorbed into the body through a G1 route and inhalation. The acute symptoms include fever, G1 disturbances, irritation of the respiratory tract, ulceration of the nasal septum, and dermatitis. Chronic exposure can produce pigmentation of the skin, peripheral neuropathy, and degeneration of liver and kidneys. 

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