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Fibrogenic potential of welding fumes.

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TLDR
Although insoluble Cr(VI) is probably the active fibrogen in stainless steel fumes, an etiological factor common to all fibrogenic welding exposures must be sought and it is tentatively proposed to be NO2, a potent experimental in vivo fibrogen copiously produced by certain welding processes and ubiquitous at low concentrations in the welding environment.
Abstract
A search of 3600 indexed pathology cases has disclosed pulmonary fibrosis in 29 welders. Scanning electron microscopy of biopsy material revealed macrophages laden with inorganic particulates which have characteristics compatible with welding aerosols. In order to establish a possible relationship between fibrotic reaction and welding-fume exposure, the fibrogenic potential fo some 11 different welding fumes and metallic aerosols, considered to be reference standard surrogates for the commonly used welding technologies and applications responsible for 70% of welders exposure, were screened using the Rat Peritoneal Macrophage in vitro bioassay. Only one class of fumes, that from the manual metal arc welding of stainless steel, showed distinct fibrogenic potential. This fume is, however, not common to more than four or five of the heretofore 90 cases of pulmonary fibrosis reported among welders. Thus, although insoluble Cr(VI) is probably the active fibrogen in stainless steel fumes, an etiological factor common to all fibrogenic welding exposures must be sought. It is tentatively proposed to be NO2, a potential experimental in vivo fibrogen copiously produced by certain welding processes and ubiquitous at low concentrations in the welding environment.

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Journal ArticleDOI

Interstitial pulmonary fibrosis after severe exposure to welding fumes

TL;DR: It is reasonable to conclude that a causal relationship exists between IPF in welders with long term exposure to high concentrations of welding fumes, and the pattern of restriction or combined restriction-obstruction, lower diffusion capacity, and reduced blood oxygen tension at exercise is found.
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Aluminum welding fume-induced pneumoconiosis.

TL;DR: Scanning electron microscopy and energy dispersive x-ray analysis of the exogenous particle content in the lung tissue of 2 coworkers, employed by the same aluminum shipbuilding facility, who died of complications from this disease revealed the highest concentrations of aluminum particles among the 812 similar analyses in the pneumoconiosis database.
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Assessment of risk of lung cancer for welders.

TL;DR: If welders of stainless steels suffer an "equivalent lung cancer risk" to that of chromate workers because of their equivalent chromium (VI) exposure, then a resulting three-fold risk ratio for 10% of all welders engaged in stainless steel welding would account for the total over-incidence experienced by the entire occupational group.
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Pulmonary function abnormalities and airway irritation symptoms of metal fumes exposure on automobile spot welders.

TL;DR: It is suggested that restrictive and obstructive lung abnormalities, and airway irritation symptoms are associated with spot and arc welding exposures.
References
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Journal ArticleDOI

Pulmonary alveolar proteinosis.

TL;DR: A remarkable disease of the lung that consists of the filling of the alveoli by a PAS-positive proteinaceous material, rich in lipid, appears to be produced by the lining cells, which slough into the lumen, ultimately becoming necrotic and yielding granules and variable laminated bodies to theAlveolar content.
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Experimental determination of the regional deposition of aerosol particles in the human respiratory tract.

TL;DR: The retention of the radioactive particles present in the body after aerosol administration is measured with a body counter designed and constructed for these experiments, and the elimination of material from the chest is found to be much slower for the material deposited in the alveolar region than for the amount deposit in the tracheobronchial tree.
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Cigarette smoking induces functional antiprotease deficiency in the lower respiratory tract of humans.

TL;DR: Determination of the antielastase activity of alpha 1-antitrypsin revealed a nearly twofold reduction in the functional activity of this elastase inhibitor in the lungs of cigarette smokers, suggesting that cigarette smokers may lose some of the normal antiElastase protective screen of the lower respiratory tract, making them more vulnerable to destructive lung disease.
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