PubMed · 15915692
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Rudolph S Caparros. 2005. Safe & secure storage.. https://pubmed.ncbi.nlm.nih.gov/15915692/
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Beryllium exposure can cause a granulomatous lung disease in workers who develop a lymphocyte-mediated sensitization to the metal. Workers in diverse industries are at risk because beryllium's properties are critical to nuclear, aerospace, telecommunications, electronic, metal alloy, biomedical, and semiconductor industries. The occupational air concentration standard's failure to protect beryllium workers is driving many scientific and occupational health advances. These developments include study of bioavailability of different physicochemical forms of beryllium, medical surveillance to show effectiveness of skin protection in preventing sensitization in high-risk processes, gene-environment interaction, transgenic mice for use in experimental research, and risk-based management of industrial exposures in the absence of effective exposure-response information. Beryllium sensitization and disease prevention are paradigms for much broader public health action in both occupational and general population settings.
Exposure data on biocides are relatively rare in published literature, especially for secondary exposure. This is also the case for antifouling exposure. Therefore, a field study was carried out measuring exposure to antifouling paints. Both primary exposure (rolling and spraying) and secondary exposure (during sand blasting) were studied. Exposure during rolling was measured in boatyards where paints containing dichlofluanid (DCF) were applied. Spraying was measured in dockyards (larger than boatyards) where paints containing copper were applied. Furthermore, during sand blasting the removal of old paint layers containing copper was measured. A total of 54 datasets was collected, both for inhalation and dermal exposure data. For paint and stripped paint bulk analyses were performed. The following values are all arithmetic means of the datasets. Inhalation of copper amounted to 3 mg m-3 during spraying and to 0.8 mg m-3 during sand blasting. Potential body exposure loading amounted to 272 mg h-1 copper during spraying and 33 mg h-1 during sand blasting. For dichlofluanid the inhalation exposure loading was 0.14 mg m-3 during rolling, whereas the potential body exposure loading was 267 mg h-1 and potential hand exposure loading 277 mg h-1. The results for primary exposure compare well to the very few public data available. For the secondary exposure (sand blasting) no comparable data were available. The present study shows that the exposure loading should be considered more extensively, including applicable protective gear. In this light the findings for the potmen during sand blasting suggest that personal protective equipment should be (re)considered carefully.
OBJECTIVES: To investigate the interaction between welding fumes and noise in causation of hearing impairment. METHODS: Groups of rabbits (n=6) were exposed to noise, welding fumes or combination of both prior to Distortion Product Otoacoustic-Emissions (DPOAEs) analysis. The function of outer hair cells (OHCs) was examined by DPOAE assessment over a broad range of frequencies. Variations in DPOAE amplitude were compared between control (n=6) and exposed (n=18) groups. RESULTS: The DPOAEs levels measured at different frequencies (1379-6299 Hz) were found to decrease significantly (P<0.05) in rabbits exposed to 110 dB sound pressure level (SPL) broadband noise (8h/day, 12 days). In rabbits, exposed to carbon-steel welding fumes alone (157 mg/m(3)), the threshold shift was limited to the high frequencies (2759-6299 Hz), whereas, mixed exposure to noise and fumes resulted in reduction of DPOAEs at all the frequencies. Changes in DPOAEs were associated with increased susceptibility of erythrocytes to oxidation (P<0.05). Exposure to noise or fumes alone or simultaneously, suppressed total antioxidant ability of plasma as measured by ferric reducing ability of plasma (FRAP). Noise alone or in combination with fumes resulted in depletion of blood glutathione (GSH). Despite suppression of FRAP in the exposed groups, GSH was found to remain unchanged due to welding fumes suggesting that antioxidants other than GSH are affected by toxicants present in metal welding fumes. CONCLUSION: Exposure to very high levels of welding fumes can increase noise-related effects on OHC function by extending hearing threshold shift to wide band frequencies.