Lung occupational

Kilbum KH, Warshaw RH. 1992. Irregular opacities in the lung, occupational asthma, and airways dysfunction in aluminum workers. Am J Ind Med 21 845-853. 

The biological half-time of uranium dioxide in human lungs (occupational exposure) at German fuel fabrication facilities was estimated to be 109 days. Body burden measurements of uranium taken from 12 people who handled uranium oxides for 5-15 years were used for this determination. Twice a year for 6 years, a urinalysis was conducted on workers exposed to uranium. In vivo lung counting was performed on the last day before and the first day after a holiday period. Levels of uranium in feces were measured during the first 3 days and the last 3 days of a holiday period and the first 3 days after the restart of work. For some employees, the levels of uranium in feces was measured during 3 days one-half year after the holiday period (Schieferdecker et al. 1985). 

EXPOSURE ROUTES home burning of wood, coal, and certain plastics chlorinated swimming pools drinking water at low levels cigarette smoke polystyrene insulation aerosol propellants forest and brush fire volcanoes adsorption through skin and lungs occupational exposure car dealers, metal industries, building contractors... 

Roussel S, Reboux G, Dalphin JC, Bardonnet K, Millon L, Piarroux R (2004) Microbiological evolution of hay and relapse in patients with farmer s lung. Occup Environ Med 61 e3... 

Magnesium vanadates, as vanadium compounds in general, are known irritants of the respiratory tract and conjunctiva. The threshold limit value (TLV) for vanadium compounds in air recommended by the National Institute of Occupational Safety and Health is 0.05 mg/m based on a typical 8-h workday and 40-h workweek (7,147). Chronic inhalation can lead to lung diseases such as bronchitis, bronchopneumonia, and lobar pneumonia. These dust-related effects can be avoided by use of individual respirators in areas where exposure is likely. 

MS(Bjl6 Save your breath occupational lung disease. (A guide for employers)... 

Polycyclic aromatic hydrocarbons have been classified as human carcinogens because they induce cancers in experimental animals and because smoking and exposure to mixtures of chemicals containing polycyclic aromatic hydrocarbons in the workplace increase the risk of lung cancer in exposed individuals. In experimental animals, benzo(a)pyrene induces cancer in different organs depending on the route of administration.Furthermore, exposure to polycyclic aromatic hydrocarbons commonly occurs in occupations related to traffic (use of diesel engines in transportation and railways). 

Coggoii, D., Pannett, B., and Ache.son, E. D. (1984). Use of job-exposure matrix in an occupational analysis of lung and bladder cancers on the basis of death certificates. /. Natl. Cancer Inst. 72, 61-65. 

At typical indoor concentrations, COj is not thought to be a direct cause of adverse health effects however, COj is an easily-measured surrogate for other occupant-generated pollutants. Eye, nose, and throat irritation headaches lung cancer may contribute to heart disease buildup of fluid in the middle ear increased severity and frequency of asthma episodes decreased lung function. ETS is also a source of odor and irritation complaints. 

The a-tocopherol, P-carotene (ATBC) Cancer Prevention study was a randomised-controlled trial that tested the effects of daily doses of either 50 mg (50 lU) vitamin E (all-racemic a-tocopherol acetate), or 20 mg of P-carotene, or both with that of a placebo, in a population of more than 29,000 male smokers for 5-8 years. No reduction in lung cancer or major coronary events was observed with any of the treatments. What was more startling was the unexpected increases in risk of death from lung cancer and ischemic heart disease with P-carotene supplementation (ATBC Cancer Prevention Study Group, 1994). Increases in the risk of both lung cancer and cardiovascular disease mortality were also observed in the P-carotene and Retinol Efficacy Trial (CARET), which tested the effects of combined treatment with 30 mg/d P-carotene and retinyl pahnitate (25,000 lU/d) in 18,000 men and women with a history of cigarette smoking or occupational exposure to asbestos (Hennekens et al, 1996). 

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. 

The majority of people who smoke never develop lung cancer. Genetic risk factors may predispose certain smokers to lung cancer. After adjustments for age, smoke exposure, occupation, and gender, relatives of a lung cancer patient have approximately a twofold risk of developing lung cancer. The... 

Lefuma J, Chameaud J, Perraud R, et al. 1976. [An experimental study on a comparison between the toxic effects of radon-222 and its daughters on the lungs, and those exerted by alpha-emitters of the actinium series.] Occup Saf Health Ser 32 43-53. (French). 

Pulmonary hbrosis is a potentially fatal condition that is the end result of persistent lung inflammation and can occur in a variety of clinical settings (1,8,65). It can be a manifestation of environmental or occupational exposure,... 

Diquat and paraquat are quaternary ammonium compounds largely used as contact herbicides and crop desiccants. When systemic absorption occurs, paraquat and diquat are rapidly distributed into the body. Paraquat primarily accumulates in the lungs and kidneys, while the highest diquat concentrations have been found in the gastrointestinal tract, liver, and kidneys (WHO, 1984). Urine is the principal route of excretion for both diquat and paraquat, which are primarily eliminated as unmodified compounds. Occupationally exposed workers can be monitored by measuring paraquat and diquat concentrations in urine samples (Table 6). Blood concentrations are useful to monitor acute poisoning cases. 

Witzmann FA et al. Proteomic analysis of simulated occupational jet fuel exposure in the lung. Electrophoresis 1999 20 3659-3669. 

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