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Welders are exposed to high concentrations of nanoparticles. Compared to larger particles, nanoparticles have been associated with more toxic effects at the cellular level, including the generation of more reactive oxygen species activity. Current methods for welding-fume aerosol exposures do not differentiate between the nano-fraction and the larger particles. The objectives of this work are to establish a method to estimate the respiratory deposition of the nano-fraction of selected metals in welding fumes and test this method in a laboratory setting. Manganese (Mn), Nickel (Ni), Chromium (Cr), and hexavalent chromium (Cr(VI)) are commonly found in welding fume aerosols and have been linked with severe adverse health outcomes. Inductively coupled plasma mass spectrometry (ICP-MS) and ion chromatography (IC) were evaluated as methods for analyzing the content of Mn, Ni, Cr, and Cr(VI) nanoparticles in welding fumes collected with nanoparticle respiratory deposition (NRD) samplers. NRD samplers collect nanoparticles at deposition efficiencies that closely resemble physiological deposition in the respiratory tract. The limits of detection (LODs) and quantitation (LOQs) for ICP-MS and IC were determined analytically. Mild and stainless steel welding fumes generated with a robotic welder were collected with NRD samplers inside a chamber. LODs (LOQs) for Mn, Ni, Cr, and Cr(VI) were 1.3 μg (4.43 μg), 0.4 μg (1.14 μg), 1.1 μg (3.33 μg), and 0.4 μg (1.42 μg), respectively. Recovery of spiked samples and certified welding fume reference material was greater than 95%. When testing the method, the average percentage of total mass concentrations collected by the NRD samplers was ~30% for Mn, ~50% for Cr, and ~60% for Ni, indicating that a large fraction of the metals may lie in the nanoparticle fraction. This knowledge is critical to the development of toxicological studies aimed at finding links between exposure to welding fume nanoparticles and adverse health effects. Future work will involve the validation of the method in workplace settings. [Supplementary materials are available for this article. Go to the publisher's online edition of Journal of Occupational and Environmental Hygiene for the following free supplemental resource: Digestion, extraction, and analysis procedures for nylon mesh screens.].

Sodium fluoroacetate (1080) is a highly toxic metabolic poison that has the potential because of its lack of defined color, odor, and taste and its high water solubility to be intentionally or unintentionally ingested through food adulteration. Although the mechanism of action for 1080 has been known since the 1950s, no known antidote exists. In an effort to better understand the cardiopulmonary impacts of 1080, we utilized whole-body plethysmography and telemeterized Sprague-Dawley rats which allowed for the real-time measurement of respiratory and cardiac parameters following exposure using a non-invasive assisted-drinking method. Overall, the animals showed marked depression of respiratory parameters over the course of 24 h post-exposure and the development of hemorrhage in the lung tissue. Tidal volume was reduced by 30% in males and 60% in females at 24 h post-exposure, and respiratory frequency was significantly depressed as well. In telemeterized female rats, we observed severe cardiac abnormalities, highlighted by a 50% reduction in heart rate, 75% reduction in systolic blood pressure, and a 3.5-fold lengthening of the QRS interval over the course of 24 h. We also observed a reduction in core body temperature of nearly 15°C. Our study was able to describe the severe and pronounced effects of sodium fluoroacetate poisoning on cardiopulmonary function, the results of which indicate that both tissue specific and systemic deficits contribute to the toxicological progression of 1080 intoxication and will need to be accounted for when developing any potential countermeasure for 1080 poisoning.

Debate exists as to whether welding fume is carcinogenic, but epidemiological evidence suggests that welders are an at-risk population for development of lung cancer. Our objective was to expose, by inhalation, lung tumor susceptible (A/J) and resistant C57BL/6J (B6) mice to stainless steel (SS) welding fume containing carcinogenic metals and characterize the lung-inflammatory and tumorigenic response. Male mice were exposed to air or gas metal arc (GMA)-SS welding fume at 40 mg/m(3)×3 h/day for 6 and 10 days. At 1, 4, 7, 10, 14, and 28 days after 10 days of exposure, bronchoalveolar lavage (BAL) was done. Lung cytotoxicity, permeability, inflammatory cytokines, and cell differentials were analyzed. For the lung tumor study, gross tumor counts and histopathological changes were assessed in A/J mice at 78 weeks after 6 and 10 days of exposure. Inhalation of GMA-SS fume caused an early, sustained macrophage and lymphocyte response followed by a gradual neutrophil influx and the magnitudes of these differed between the mouse strains. Monocyte chemotactic protein-1 (MCP-1), macrophage inflammatory protein-2 (MIP-2), and tumor necrosis factor-α (TNF-α) were increased in both strains while the B6 also had increased interleukin-6 (IL-6) protein. BAL measures of cytotoxicity and damage were similar between the strains and significantly increased at all time points. Histopathology and tumorigenesis were unremarkable at 78 weeks. In conclusion, GMA-SS welding fume induced a significant and sustained inflammatory response in both mouse strains with no recovery by 28 days. Under our exposure conditions, GMA-SS exposure resulted in no significant tumor development in A/J mice.

Prolonged, extensive exposure to asphalt fume has been associated with several adverse health effects. Inhaled polycyclic aromatic hydrocarbons (PAHs) from asphalt fume exposure are of concern. The objective of this study was to characterize both qualitative and quantitative differences between fumes generated at 150 degrees C and 180 degrees C using a well-controlled laboratory road paving fume generation system. Fumes were characterized by total volatile and particulate concentration, simulated boiling point profile, and specific PAH content. The mean concentrations of the volatile fractions generated at 180 degrees C and 150 degrees C were 23.3 mg/m3 and 11.2 mg/m3, respectively, demonstrating a statistically significant shift in concentration. The mean concentrations of the particulate fractions generated at 180 degrees C and 150 degrees C were 42.4 mg/m3 and 28.0 mg/m3, respectively. The simulated boiling point profile did not show a significant qualitative difference between the fumes generated at the two temperatures. Naphthalene, acenaphthene, fluorene, phenanthrene, fluoranthene, pyrene, and chrysene were identified and quantified from the fumes.

Asphalt fume inhalation has been suspected of affecting immune function in exposed workers. The objective of this study was to evaluate the effect of asphalt exposure on lung immune responses in rats using a bacterial infectivity model. Pathogen-free male Sprague-Dawley rats were exposed by inhalation to asphalt fumes (72.6 +/- 4.95 mg/m3) or filtered air for 6 h/day for 5 days. One day after the final asphalt exposure, rats were intratracheally inoculated with 5 x 10(5) Listeria monocytogenes. At 0 (prior to bacterial inoculation), 3, and 7 days after L. monocytogenes instillation, the lungs of each animal were divided. Bronchoalveolar lavage (BAL) was performed on right lungs. The recovered BAL cells were then differentiated and counted, and alveolar macrophage (AM) function was determined. Albumin and lactate dehydrogenase (LDH), two indices of lung injury, were measured in the acellular BAL fluid. To assess bacterial clearance, the left lungs were removed, homogenized, and bacterial colony-forming units (CFUs) were counted. In addition, lung-draining lymph nodes were removed, and lymphocyte phenotype and lymphocyte-induced cytokine production were examined. Asphalt fume exposure did not cause lung injury or inflammation in rats in the absence of infection. Infection induced elevations in AMs, neutrophils (PMNs), albumin, and LDH. Importantly, no significant differences were seen when comparing the asphalt group with the air and nonexposed naive groups at any time before or after infection. Also, asphalt fume inhalation exposure did not affect the rate of pulmonary clearance of L. monocytogenes or AM production of reactive oxygen and nitrogen species. However, asphalt-related increases in lymphocyte secretion of interferon (IFN)-gamma, interleukin (IL)-6, and IL-10 were observed at different times after bacterial infection, whereas the total number of lymph-node cells and the percentage of CD4+ and CD8+ cells were not significantly different among the treatment groups. Despite the asphalt-induced changes observed in lymphokine secretion, adaptive immune function seemed to function properly in lung defense against bacterial infection. Because innate nonspecific lung responses and pulmonary clearance of L. monocytogenes were unaffected by asphalt fume exposure, lung defenses were sufficient to control the infection. It was concluded that acute inhalation of asphalt fumes at a high concentration had a minimal effect on lung immune responses to infection in rats.

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