Phototoxicity and the cornea. (73/289)

The cornea is sensitive to the effects of ultraviolet (UV) light and can suffer both acute and chronic toxicity. Ultraviolet keratitis is associated with relatively short exposures to light sources such as welding arcs or tanning lamps. The corneal effects are seen within a few hours following exposure and typically will resolve within 72 hours. Chronic exposure to environmental UV light may lead to a variety of ocular surface abnormalities that rarely resolve in the absence of therapy. Ultraviolet light, while potentially destructive, also can be used therapeutically. Recently, the photoablative properties of the excimer laser have been used in corneal refractive surgery. This laser uses UV light to break chemical bonds and remove tissue. Corneal phototoxicity is a reflection of the sensitivity of the ocular surface to photochemical injury. Fortunately, effective protection in the form of UV-blocking lenses is widely available.  (+info)

Metal fume fever presenting as aseptic meningitis with pericarditis, pleuritis and pneumonitis. (74/289)

BACKGROUND: Metal fume fever (MFF) is a well-known complication of zinc oxide fume inhalation. Prompt recognition of this condition is essential for the proper medical management of this self-limited disease. AIM: To present a unique and unusual case of MFF. RESULTS: Our patient is a 25-year-old male welder who had MFF and presented with aseptic meningitis with pericarditis, pleuritis and pneumonitis. To our knowledge, this is the first case of MMF presenting with these signs and symptoms. CONCLUSIONS: MFF can present with a systemic inflammatory response causing a multi-organ serositis. Our case highlights the utmost importance of obtaining an occupational history on all our patients, even if they are critically ill.  (+info)

Parkinson's disease and other basal ganglia or movement disorders in a large nationwide cohort of Swedish welders. (75/289)

INTRODUCTION: Although it has been hypothesised that metal welding and flame cutting are associated with an increased risk for Parkinson's disease due to manganese released in the welding fume, few rigorous cohort studies have evaluated this risk. METHODS: The authors examined the relation between employment as a welder and all basal ganglia and movement disorders (ICD-10, G20-26) in Sweden using nationwide and population based registers. All men recorded as welders or flame cutters (n = 49,488) in the 1960 or 1970 Swedish National Census were identified and their rates of specific basal ganglia and movement disorders between 1964 and 2003 were compared with those in an age and geographical area matched general population comparison cohort of gainfully employed men (n = 489,572). RESULTS: The overall rate for basal ganglia and movement disorders combined was similar for the welders and flame cutters compared with the general population (adjusted rate ratio (aRR) = 0.91 (95% CI 0.81 to 1.01). Similarly, the rate ratio for PD was 0.89 (95% CI 0.79 to 0.99). Adjusted rate ratios for other individual basal ganglia and movement disorders were also not significantly increased or decreased. Further analyses of Parkinson's disease by attained age, time period of follow up, geographical area of residency, and educational level revealed no significant differences between the welders and the general population. Rates for Parkinson's disease among welders in shipyards, where exposures to welding fumes are higher, were also similar to the general population (aRR = 0.95; 95% CI 0.70 to 1.28). CONCLUSION: This nationwide record linkage study offers no support for a relation between welding and Parkinson's disease or any other specific basal ganglia and movement disorders.  (+info)

Inflammatory responses to the occupational inhalation of metal fume. (76/289)

Occupational exposure to metal fume promotes a reversible increase in the risk of pneumonia, but by mechanisms which are unclear. To investigate, the current authors measured various markers of host defence function in welders and nonwelders. Induced sputum and venous blood samples were collected from 27 welders with regular long-term exposure to ferrous metal fume and 31 unexposed matched controls. In sputum, the present authors measured cell counts, the soluble and cellular iron concentration, and levels of interleukin-8, tumour necrosis factor-alpha, myeloperoxidase, matrix metalloproteinase-9, immunoglobulin (Ig)A, alpha(2)-macroglobulin and unsaturated iron-binding capacity. Blood samples were assayed for evidence of neutrophil activation and pneumococcal IgG antibodies. Welders had significantly higher iron levels and a substantially lower unsaturated iron-binding capacity in their sputum, but, despite a high iron challenge, there was a noteworthy absence of an inflammatory response. Only blood counts of eosinophils and basophils were significantly related to the extent of welding. Weak nonsignificant trends were observed for several other measures, consistent with low-grade priming of neutrophils. In conclusion, these data suggest that chronic exposure to metal fume blunts responsiveness to inhaled particulate matter. However, the mechanism behind the lack of detectable local inflammatory response requires further investigation.  (+info)

Update of a meta-analysis on lung cancer and welding. (77/289)

OBJECTIVES: This study is an update, over the period 1954-2004, of a previous meta-analysis completed in 1994. It was aimed at assessing lung cancer risk among welders, while addressing heterogeneity, publication bias, and confounding issues. METHODS: Combined relative risks (CRR) and their variances were calculated using fixed and random effects models. Heterogeneity was tested using the Q statistic. The publication bias was estimated using funnel plots, and Egger's regression and partially controlled by excluding studies with positive reporting bias. RESULTS: The literature provided 60 studies eligible for the meta-analysis. No heterogeneity was observed. The fixed effect CRR for all of the welders and all of the studies was 1.26 (95% CI 1.20-1.32) after partial control of publication bias. No difference was observed according to welding activities. Smoking did not appear to be a marked confounder in the relationship between lung cancer and welding, but the effect of asbestos could not be assessed. CONCLUSIONS: The meta-analysis showed a 26% excess of lung cancer for welders without any difference according to welding activities.  (+info)

A combined analysis of XRCC1, XRCC3, GSTM1 and GSTT1 polymorphisms and centromere content of micronuclei in welders. (78/289)

The aims of the present study were to assess clastogenic and aneugenic properties of welding fumes using fluorescent in situ hybridization (FISH) with a human pancentromeric DNA probe. The involvement of genetic polymorphisms in DNA repair genes (p.Arg399Gln of XRCC1 and p.Thr241Met of XRCC3) and in detoxification genes (GSTM1 and GSTT1) on the centromere content of micronuclei (MN) was also evaluated. This study included 27 male welders working without any collective protection device and a control group (n = 30). The welders showed significantly higher levels of chromosome/genome damage compared to the controls. The frequencies of MN and centromere-positive MN (C+MN) per 1,000 binucleated cells were significantly higher in the exposed group than in the control group (7.1 per thousand +/- 3.7 versus 4.9 per thousand +/- 1.8; P = 0.012 and 3.5 per thousand +/- 1.8 versus 2.4 per thousand +/- 1.2; P = 0.018, respectively, Mann-Whitney U-test). The centromere-negative MN (C-MN) frequency was higher in the exposed subjects than in the controls (3.6 per thousand +/- 3.4 versus 2.5 per thousand +/- 1.4), but the Mann-Whitney U-test did not yield a significant result. In the total population, the GSTM1 and GSTT1 polymorphisms significantly affected the frequencies of C-MN and C+MN defined by FISH. GSTM1 positive subjects showed an increased C-MN frequency and GSTT1 null subjects showed an elevated C+MN frequency. When GSTM1 and GSTT1 genotypes were included in multiple regression analysis, the effect of the occupational exposure could better be demonstrated; both C+MN and C-MN were significantly increased in the welders. Our results suggest that the combined analysis of genetic polymorphisms and centromeres in MN may improve the sensitivity of the micronucleus assay in detecting genotoxic effects.  (+info)

The effect of occupational exposure to metals on the nervous system function in welders. (79/289)

We explored the relationship between metals exposure and nervous impairment in welders. The metals exposure of 82 welders and 51 operators were evaluated for blood Pb, Cd and Mn by atomic absorption spectrometry, and the nervous system impairment was evaluated with the neurobehavioral core test battery and electromyography. Pb (geometric mean: 117.31 mug/L; range: 0.5-327.6 mug/L) and Cd (geometric mean: 3.54 mug/L; range: 0.2-12.5 mug/L) in welders were significantly higher than those in operators. Welders had higher prevalence of nervous system symptoms and worse standard scores of 8 items such as depression-dejection than operators. Significant difference of nervous performance in welders only existed in different concentration groups of Pb and Mn. The performances of fatigue-inertia and some others had negative correlations with Pb and digit span with Mn. Therefore, the nervous system impairment in welders could be attributed to occupational exposure of Pb and Mn, but not Cd, concomitantly.  (+info)

Welding fume exposure and associated inflammatory and hyperplastic changes in the lungs of tumor susceptible a/j mice. (80/289)

It has been suggested that welding fume (WF) exposure increases lung cancer risk in welders. Epidemiology studies have failed to conclude that WF alone causes lung cancer and animal studies are lacking. We examined the course of inflammation, damage, and repair in the lungs of A/J mice, a lung tumor susceptible strain, caused by stainless steel WF. Mice were exposed by pharyngeal aspiration to 40 mg/kg of WF, silica, or saline. Bronchoalveolar lavage (BAL) was performed 24 hours, 1 and 16 weeks to assess lung injury and inflammation and histopathology was done 1, 8, 16, 24, and 48 weeks postexposure. Both exposures increased inflammatory cells, lactate dehydrogenase and albumin at 24 hr and 1 week. At 16 weeks, these parameters remained elevated in silica-exposed but not WF-exposed mice. Histopathologic evaluation at 1 week indicated that WF induced bronchiolar epithelial hyperplasia with associated cellular atypia, alveolar bronchiolo-alveolar hyperplasia (BAH) in peribronchiolar alveoli, and peribronchiolar lymphogranulomatous inflammation. Persistent changes included foci of histiocytic inflammation, fibrosis, atypical bronchiolar epithelial cells, and bronchiolar BAH. The principle changes in silica-exposed mice were histiocytic and suppurative inflammation, fibrosis, and alveolar BAH. Our findings that WF causes persistent bronchiolar and peribronchiolar epithelial changes, suggest a need for studies of bronchiolar changes after WF exposure.  (+info)