Brown Lung

Total frequencies of environmental illness are difficult to measure. When causes can be identified, however, scientists observe that frequencies of occurrence of a particular illness vary directly with the severity and extent of exposure. Particularly frequent in the workplace are skin lesions from many different causes and pulmonary diseases related to the inhalation of various dusts, such as coal dust (black lung), cotton dust (brown lung), asbestos fibers (asbestosis), and silica dust (silicosis). Environmental agents can also cause biological effects without overt clinical illness (for example, chromosome damage from irradiation). 

Individuals whose jobs expose them to unusually high particulate concentrations are especially susceptible to health problems from the pollutant. For example, men and women who work with the mineral asbestos are very prone to development of a serious and usually fatal condition known as asbestosis, in which fibers of the mineral become embedded in the interstices (the empty spaces within tissue) of the lung. Similar conditions are observed among coal workers who inhale coal dust (pneumoconiosis, or black lung disease) textile workers (byssinosis, or brown lung disease) those who work with clay, brick, silica, glass, and other ceramic materials (silicosis) and workers exposed to high levels of beryllium fumes (berylliosis). 

PNEUMOKONIOSES. Diseases of the lungs produced by inhalation of dusts, particularly those containing silica, asbestos and other inorganic material, or certain vegetable substances, notably sugar cane waste and raw cotton dust (brown lung). 

There are several major types of chronic lung disorders that can be caused by exposure to toxicants. A common symptom of chronic lung damage is chronic bronchitis. Among the toxicants that cause this condition are ammonia, arsenic, cotton dust (brown lung disease), and iron oxide from exposure to welding fumes. 

S.H. Moolgavkar, E.G. Luebeck, J. Turim, and R.C. Brown, Lung cancer risk associated with exposure to man-made fibers. Drug Chem. Toxicol. 23 223-242, 2000. 

Hazard Toxic by inhalation. TLV (dust) 0.2 mg/m3. Moderately flammable in the form of dust or linters fiber ignites readily. In the form of dust or linters, exposure of workers in textile mills may cause brown lung. ... 

The OSHA Cotton Dust Standard, 1910.1043, contains sign requirements specifically warning employees of the possibility of contracting brown lung disease from overexposure to cotton dust. The employer must post the following sign in each work area where the OSHA PEL for cotton dust is exceeded ... 

The promulgation of the OSHA Act of 1970 has resulted in positive results for safety the overall workplace death rate has been cut in half, brown lung disease has been virtually eliminated in the textile industry, and deaths from trench cave-ins have declined by 35%. 

Cotton dust standard promulgated to protect 600,000 workers from byssinosis cases of brown lung have declined to 0.1 cases per 10,000 workers. 

For example, brown lung, associated with the textile industry, does not show up on X-rays and remains questioned Judkins, We Offer Ourselves as Evidence. 

Botsch, Robert. Organizing the Breathless Cotton Dust, Southern Politics and the Brown Lung Association. Lexington University Press of Kentucky, 1993-... 

Brown G. Acetaminophen-induced hypotension. Heart Lung 1996 25(2) 137-140. 

Schanker, L. S., Mitchell, E. W., Brown, R. A., Jr., Species comparison of drug absorption from the lung after aerosol inhalation or intratrachael injection, Drug Metab. Dispos. 1986,... 

Michielsen, C.P., Bloksma, N., Ultee, A., van Mil, F., and Vos, J.G. (1997) Hexachlorobenzene-induced immunomodulation and skin and lung lesions A comparison between brown Norway, Lewis, and Wistar rats. Toxicol. Appl. Pharmacol., 144, 12, 1997. 

A number of studies of the toxicity of zinc oxide/hexachloroethane smoke have been conducted (Brown et al. 1990 Karlsson et al. 1986 Marrs et al. 1983). These studies demonstrate that smoke exposure results in pulmonary inflammation and irritation. When male Porton Wistar rats were exposed to hexachloroethane/zinc oxide smoke for 60 minutes, the lungs showed pulmonary edema, alveolitis, and areas of macrophage infiltration 3 days later. At 14 days, there was interstitial fibrosis and macrophage infiltration. At 28 days, increased fibrosis and macrophage infiltration were noted. However, these same symptoms occurred when the animals inhaled zinc chloride there was no apparent synergism between the zinc chloride and residual hexachloroethane (Brown et al. 1990 Richard et al. 1989). This is consistent with the fact that smoke contains little hexachloroethane and the observation that acute exposure to 260 ppm hexachloroethane had no effects on the lungs of rats (Weeks et al. 1979). 

Brown RF, Marrs TC, Rice P, et al. 1990. The histopathology of rat lung following exposure to zinc oxide/hexachloroethane smoke or instillation with zinc chloride followed by treatment with 70% oxygen. Environ Health Perspect 85 81-87. 

Table 5. The ratios of relative concentration of heavy metals in brown rice and the leaves of vegetable species growing in Lung-tang area (affected by acidic rains) and Lung-luan-tang area (non-affected by acidic rains) from 1996 to 1997 in Taiwan (Chen et al., 1998).

Kaposi s Sarcoma. These are tumors of the blood vessels. In non-AIDS patients, Kaposi s sarcoma (KS) is typically only seen in older men of Mediterranean or Jewish ancestry. In homosexual men with AIDS, as many as 69% may develop Kaposi s sarcoma. Initially, only few tumors appear as pink, purple, or brown skin lesions, usually located on the arms or legs. These tumors will spread and become widely distributed, eventually involving most of the linings of the body. If they spread to the lungs, they are difficult to control. 

Brown RA, Schanker LS (1983) Absorption of aerosolized drugs from the rat lung. Drug Metab Dispos 11 355-360. 

The final product of the aerobic metabolic pathway of chloroform is carbon dioxide (Brown et al. 1974a Fry et al. 1972). This carbon dioxide is mostly eliminated through the lungs, but some is incorporated into... 

Absorption, Distribution, Metabolism, and Excretion. Human data indicate that chloroform absorption from the lungs is rapid and fairly complete (Smith et al. 1973). The data also indicate that absorption after oral exposure is fairly complete for both animals and humans (Brown et al. 1974a Fry et al. 1972 Taylor et al. 1974). Although there are no experimental data regarding dermal absorption in humans, some data have been extrapolated from mouse studies (Tsumta 1975). The rate of absorption following oral or inhalation exposure is rapid (within 1-2 hours). Additional animal studies investigating the rate of dermal absorption would be useful to quantitate dermal absorption and to compare information from oral and inhalation studies. 

Mononuclear and polymorphonuclear cell infiltration and unspecified pathological lesions were noted in the lungs of guinea pigs after gavage administration of 3,200-8,000 mg/kg kerosene (Brown et al. 1974). 

Schneider et al. (2002) also examined the use of the TEF approach on the data from the Culp et al. (1998) study, and from several other studies using dermal or lung application of PAH mixtures of known composition. They used the TEF derived by Brown and Mittehnan (1993) (Table 10.4) and concluded that the benzo[a]pyrene equivalency factors do not adequately describe the potency of PAH mixtures and lead to underestimation of the carcinogenic potencies in most cases. 

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