Metal smelting requires heat and carbon from such sources as coke, coal, or wood to reduce mineral ores to smelted metals (42
). Dusts are released into the workplace during metal smelting. Johnsen and colleagues investigated the relationship between the annual change in lung function and occupational dust exposure among workers in 15 Norwegian smelting facilities (43
). They found that for all smelters, the annual decline in FEV1
was negatively associated with increasing dust exposure, suggesting that metal smelting may increase the risk of developing COPD.
Shi and colleagues performed a prospective cohort study in 447 cotton textile workers exposed to cotton dust and 472 unexposed silk textile workers (44
). Cessation of textile work was positively associated with an improvement in FEV1
that was greater in cotton (11.3 ml/yr) than silk (5.6 ml/yr) workers. Smoking seemed to exacerbate the spirometric changes, and the risk of symptoms of chronic bronchitis and byssinosis, associated with cotton work.
Tossa and colleagues examined the utility of exhaled nitric oxide (NO) measurements in predicting the development of AHR in apprentice bakers, pastry makers, and hairdressers during their 2 years of training (45
). They found that an increase in the fractional concentration of exhaled nitric oxide during the training was associated with an increased incidence of AHR in atopic and nonatopic subjects. The development of atopy in bakers/pastry makers and the sensitization of hairdressers to alkaline persulfates were also independently associated with the incidence of AHR.
Rodríguez-Trigo and colleagues compared lung function, respiratory symptoms, and a variety of biomarkers in local fisherman who were involved or uninvolved in the cleanup of oil resulting from the crash of the oil tanker Prestige
, which spilled more than 67,000 tons of bunker oil off the coast of northwestern Spain (46
). Whereas lung function was similar in the two groups, fisherman exposed to oil were at increased risk for lower respiratory tract symptoms; had higher exhaled breath levels of 8-isoprostane, vascular endothelial growth factor, and basic fibroblast growth factor; and had more structural chromosomal abnormalities. These findings indicate that even brief periods of exposure to oil sediments may have important health effects. Appropriate precautions should be taken to protect workers in oil clean-up activities.
Ameille and colleagues sought to determine whether occupational exposure to asbestos is associated with the development of airway obstruction (47
). They examined the association between asbestos exposure in 3,660 subjects and pulmonary function and high-resolution computed tomographic abnormalities. They were unable to find an association between the cumulative exposure to asbestos and pulmonary function parameters. Although this study may suggest that some individuals are resistant to the adverse consequences of asbestos, the difficulties in examining even these very large cohorts are discussed in an accompanying editorial (48
Cummings and colleagues reported two cases of pulmonary alveolar proteinosis, including one death, in workers at a facility producing indium-tin oxide (ITO), a compound used to make flat panel displays (49
). Both workers were exposed to airborne ITO dust and had indium in lung tissue specimens. One worker was tested for autoantibodies to granulocyte-macrophage colony-stimulating factor and was found to have an elevated level. These cases suggest that inhalational exposure to ITO causes pulmonary alveolar proteinosis, which may occur via an autoimmune mechanism. The mechanism of this toxicity was discussed in an accompanying editorial (50
Mack and colleagues evaluated the role of regulatory T cells in chronic beryllium disease, which is a CD4+
T cell–mediated disorder characterized by persistent lung inflammation (52
). The bronchoalveolar lavage fluid from patients with chronic beryllium disease showed a reduction in the number of regulatory T cells, which were also dysfunctional. Furthermore, the percentage of regulatory T cells in bronchoalveolar lavage fluid was inversely correlated with disease severity.
In a study that evaluated the mechanisms by which zinc oxide (ZnO) nanoparticles cause metal fume fever, Kim and colleagues found that ZnO nanoparticles caused dose- and time-dependent injury in lung epithelial cells via mitochondrial dysfunction, and increased intracellular reactive oxygen species (53