Lung environmental

Sulfur dioxide. The sources are burning coal and oil, especially high sulfur coal from Eastern US, and industrial processes (paper and metal industry). Health effects include breathing problems, which may cause permanent damage to lungs. Environmental effects are as follows S02 is an ingredient of acid rain (acid aerosols), which can damage trees and life in lakes. Acid aerosols can also reduce visibility. 

Beryllium, beryllium-containing aUoys, and beryUium oxide ceramic in soHd or massive form present no hazard whatsoever (31). SoHd shapes may be safely handled with bare hands (32) however, care must be taken in the fabrication and processing of beryUium products to avoid inhalation of airborne beryUium particulate matter such as dusts, mists, or fumes in excess of the prescribed workplace exposure limits. Inhalation of fine airborne beryUium may cause chronic beryUium disease, a serious lung disease in certain sensitive individuals. However, the vast majority of people, perhaps as many as 99%, do not react to beryUium exposure at any level (33). The biomedical and environmental aspects of beryUium have been summarized (34). 

Effects of indoor air pollutants on humans are essentially the same as those described in Chapter 7. However, there can be some additional pollutant exposures in the indoor environment that are not common in the ambient setting. From the listing in Table 23-1, radon exposures indoors present a radiation hazard for the development of lung cancer. Environmental tobacco smoke has been found to cause lung cancer and other respiratory diseases. Biological agents such as molds and other toxins may be a more likely exposure hazard indoors than outside. 

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). 

Utell, M. J. (1985). Effects of inhaled acid aerosols on lung mechanics an analysis of human exposure studies. Environmental Health Perspect. 63, 39-44. 

Increased morbidity and mortality is associated with increases in outdoor particle concentrations (U.S. Environmental Protection Agency 1995). Of particular concern are the particles smaller than 2.5 micrometers in diameter, which are more likely to deposit deep inside the lungs (U.S. Environmental Protection Agency 1995). Some particles, biological in origin, may cause allergic or inflammatory reactions or be a source of infectious disease. 

Beri-beri or clinically manifest thiamin deficiency exists in several subforms infantile beri-beri and adult beri-beri. Infantile beri-beri occurs in exclusively breastfed infants of thiamin-deficient mothers. Adults can develop different forms of the disease, depending on their constitution, environmental conditions, the relative contribution of other nutrients to the diet as well as the duration and severity of deficiency. First of all, there is a so called dry or atrophic (paralytic or nervous) form, including peripheral degenerative polyneuropathy, muscle weakness and paralysis. Second, a wet or exudative (cardiac) form exists. In this form, typical symptoms are lung and peripheral oedema as well as ascites. Finally, there is a cerebral form, that can occur as Wernicke encephalopathy or Korsakoff psychosis. Tli is latter form mostly affects chronic alcoholics with severe thiamin deficiency. 

During COPD, the following symptoms occur, usually in the order mucus hypersecretion, ciliary dysfunction, airflow limitation, pulmonary hyperinflation, gas exchange abnormalities, pulmonary hypertension and cor pulmonale. Acute exacerbations appear to be mainly triggered by bacteria, viruses or environmental pollutants. They lead to a worsening of lung functions, wasting and increased mortality their psychosocial impacts include depression and anxiety that may be associated with the will to die. 

NPIP induces esophageal and nasal cavity tumors in the rat, forestomach, liver and lung tumors in the mouse, and tracheal tumors in the Syrian golden hamster (43, 44, 45). Its potent carcinogenicity is indicated by the fact that a single dose of only 22 mg/kg was sufficient to induce tumors in 20% of Syrian golden hamsters (45). The environmental occurrence of NPIP appears to be less frequent than that of NPYR, but it has been detected in food (J, 44). 

By its intrinsic structure and function, the primary organ exposed to environmental dust is of course the lung. 

Phagocyte-derived ROMs have been implicated in the pathogenesis of a number of pulmonary diseases, including emphysema, acute respiratory distress syndrome, and various environmental diseases such as asbestos-related fibrosis and cancer (Mossman and Marsh, 1985). The relatively high oxygen tension in pulmonary tissue renders the lung prone to oxidative stress (Edwards and Lloyd, 1988). 

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. 

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,... 

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