Recovery from manual metal arc-stainless steel welding-fume exposure induced lung fibrosis in Sprague-Dawley rats.

Welders with radiographic pneumoconiosis abnormalities have exhibited a gradual clearing of the X-ray identified effects following removal from exposure. In some cases, the pulmonary fibrosis associated with welding fumes appears in a more severe form in welders. Accordingly, to investigate the disease and recovery process of pneumoconiosis induced by welding-fume exposure, rats were exposed to welding fumes with concentrations of 63.6+/-4.1 mg/m(3) (low dose) and 107.1+/-6.3 mg/m(3) (high dose) of total suspended particulate for 2 h per day in an inhalation chamber for a total of 2 h or 15, 30, 60 or 90 days. Thereafter, the rats were no longer exposed and allowed to recover from the welding fume-induced lung fibrosis for 90 days. When compared to the unexposed control group, the lung weights significantly increased in both the low- and high-dose rats from day 15 to 90. A histopathological examination combined with fibrosis-specific staining revealed that the lungs from the low-dose rats did not exhibit any significant progressive fibrotic changes. Whereas, the lungs from the high-dose rats exhibited early delicate fibrosis from day 15, which progressed into the perivascular and peribronchiolar regions by day 30. Interstitial fibrosis appeared at day 60 and became prominent by day 90, along with the additional appearance of pleural fibrosis. Recovery, evaluated based on the body and lung weights and a histopathological examination, was observed in both the high and low-dose rats that were exposed up to 30 days. The rats exposed for 60-90 days at the low dose also recovered from the fibrosis, yet the rats exposed for 60-90 days at the high dose did not fully recover. Consequently, recovery from pneumoconiosis induced by welding-fume exposure was observed when the degree of exposure was short-term and moderate.

Potential source of asbestos in non-asbestos textile manufacturing company.

Recently, a worker with lung carcinoma and a metastatic brain tumor was diagnosed as having a work-related disease. He had been employed in a non-asbestos textile company for 25 years. Consequently, to identify and explore possible causative agents for lung cancer in a non-asbestos textile manufacturing company and establish a causal relationship between exposure and lung cancer, an epidemiological investigative study was conducted and the work processes the worker was engaged in were examined. Air samples were taken from the workplace and during the drilling processes, and a suspected causative material was analyzed. The study revealed that the subject had been employed in the non-asbestos textile manufacturing company for 25 years from 1973 and his responsibilities included repairing spinning machines. In particular, the subject was involved in drilling B-bushings that were used to protect against gear abrasion in the spinning machines. An analysis of the B-bushings using a transmission electron microscope equipped with an energy dispersive X-ray analyzer indicated that they contained crocidolite asbestos fibers. Air samples obtained when drilling the B-bushings clearly indicated that the subject had most likely been exposed to crocidolite fibers when installing the B-bushings in the spinning machines. The frequency and duration of the work suggested that there would be a sufficient degree of exposure to crocidolite fibers to cause lung cancer. Except for smoking and asbestos exposure, no other chemical exposure was suspected for developing lung cancer in the workplace. Smoking appeared to be more of a potentiating risk factor in conjunction with the asbestos exposure. Accordingly, this case may provide significant evidence in identifying the cause of the mesothelioma or lung carcinoma found among workers in non-asbestos textile manufacturing companies elsewhere.

Evaluation of lead exposure in workers at secondary lead smelters in South Korea: with focus on activity of erythrocyte pyrimidine 5'-nucleotidase (P5N).

To evaluate lead exposure among secondary lead-smelting workers with a focus on erythrocyte pyrimidine 5'-nucleotidase (P5N) activity, blood lead concentration (PbB), activity of P5N and other biological variables were examined in 88 exposed workers in five secondary lead smelters and in 24 non-exposed workers in Korea. All of the mean values of air lead concentration (PbA) in the three processes, scrap pretreatment, blast furnace smelting, and refining and casting of the secondary lead smelters, markedly exceeded 0.05 mg/m3. In this survey, 29 (97%) of 30 air samples for lead exceeded 0.05 mg/m3. The highest mean PbA and PbB values were found in the section of blast furnace smelting. All of the mean PbB values in all the sections were higher than 30 microg/dl. PbB of 71 (81%) of the 88 exposed workers exceeded 30 microg/dl. In 31 (35%) of the exposed workers, PbB was above 60 microg/dl. Compared with the non-exposed group, zinc protoporphyrin (ZPP) in the exposed group was significantly increased, whereas erythrocyte P5N activity and activity of erythrocyte delta-aminolevulinic acid dehydratase (ALAD) were significantly inhibited. Erythrocyte P5N activity had valid biological correlation with PbB and with other biological variables, such as ALAD activity or ZPP. Lead exposure affected hemoglobin levels via inhibition of P5N activity, as well as the heme biosynthetic pathway, in the high-exposure state.