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Exposure assessment quality is a fundamental consideration in the design and evaluation of observational studies. High quality exposure assessment is particularly relevant for outcomes with long latency, such as cancer, where detailed information on past exposures are often missing and must therefore be estimated. For the IARC Monograph on welding, the exposure group provided an overview of assessment methods used in the key epidemiological studies. Strengths and weaknesses of each study were assessed, along with their potential effects on interpretation of risk estimates. For the association between lung cancer and welding fume exposure, 9 cohort and 10 case-control studies were reviewed. For ocular melanoma and ultraviolet radiation (UVR) from welding, 7 case-control studies were reviewed. Quality criteria were: full occupational histories, and standardized, blinded and quantitative exposure assessment. Additional criteria for lung cancer: specifically assessing welding fumes and using information on welding tasks. For ocular melanoma: assessing artificial and solar radiation separately, taking into account eye burns, eye protection and welding type. Exposure assessment of welding fumes by applying a 'welding-exposure matrix' (n=2) or welding-specific questionnaires (n=3) were considered highest quality, followed by case-by-case expert assessment (n=5) or general job-exposure matrices (JEMs, n=4). Job title alone was considered less informative (n=5). For exposure to UVR, JEMs were most informative (n=2), followed by self-reported eye burns and self-reported exposure from specific welding types (n=2), although caution is advised regarding recall bias. Assessing welding fume exposure or ever exposure to welding arcs as proxy for UVR was considered less informative. For both exposures, ever versus never welder, or assessments based on data collected from proxies, were considered least informative. The overall evaluation was that there is sufficient evidence in humans for the carcinogenicity of welding fumes and ultraviolet radiation from welding.

In a previous editorial in this journal1 we have argued that there are likely to be important occupational causes of neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) (also commonly known as motor neuron disease) which have not yet been discovered or established. However, for most neurodegenerative diseases, including ALS, the epidemiology has not been ‘done’, and there have been relatively few high-quality studies, in contrast to the situation with other non-communicable diseases (NCDs) such as cancer and respiratory disease. Nevertheless, a number of occupational exposures are suspected of contributing to the risk of ALS,2 including agricultural chemicals, metals, welding fume, electric shocks and extremely low-frequency electromagnetic fields (ELF-EMFs)3 and organic solvents (eg, formaldehyde), although the evidence to date is inconsistent. Recently, a cluster of motor neurone disease (MND) cases has been linked to exposure to the fumigant methyl bromide.4 Other putative risk factors include military service,5 rural or urban residence, and a history of head injury including sporting injuries.6 ,7 The paper by Peters …

Aims: To assess hazards associated with exposure to dust in the London Underground railway and to provide an informed opinion on the risks to workers and the travelling public of exposure to tunnel dust. Methods: Concentrations of dust, as mass (PM2.5) and particle number, were measured at different underground stations and in train cabs; its size and composition were analysed; likely maximal exposures of staff and passengers were estimated; and in vitro toxicological testing of sample dusts in comparison with other dusts was performed. Results: Concentrations on station platforms were 270–480 µg/m3 PM2.5 and 14 000–29 000 particles/cm3. Cab concentrations over a shift averaged 130–200 µg/m3 and 17 000–23 000 particles/cm3. The dust comprised by mass approximately 67% iron oxide, 1–2% quartz, and traces of other metals, the residue being volatile matter. The finest particles are drawn underground from the surface while the coarser dust is generated by interaction of brakes, wheels, and rails. Taking account of durations of exposure, drivers and station staff would have maximum exposures of about 200 µg/m3 over eight hours; the occupational exposure standard for welding fume, as iron oxide, is 5 mg/m3 over an eight hour shift. Toxicology showed the dust to have cytotoxic and inflammatory potential at high doses, consistent with its composition largely of iron oxide. Discussion: It is unjustifiable to compare PM2.5 exposure underground with that on the surface, since the adverse effects of iron oxide and combustion generated particles differ. Concentrations of ultrafine particles are lower and of coarser (PM2.5) particles higher underground than on the surface. The concentrations underground are well below allowable workplace concentrations for iron oxide and unlikely to represent a significant cumulative risk to the health of workers or commuters.

In a recent article, Offermans et al studied the agreement of three job-exposure matrices (JEM) in the Netherlands Cohort (NLCS) with respect to asbestos, polycyclic aromatic hydrocarbons (PAH) and welding fume exposure.1 The studied JEMs were quite different in their approach to assess exposure: one was based on prevalent mesothelioma cases in jobs highly exposed to asbestos (Asbestos-JEM), the second one (FINJEM) used time-dependent continuous values based on expert assessment and measurement data, and the third (DOMJEM) was a semi-quantitative expert-based JEM that assigned exposure scores (0, 1, 2) to job titles without consideration of change of exposure levels over time. Thus time-dependent exposure levels are not available for the DOMJEM. Using …

Aims: To investigate the acute systemic inflammatory response to welding fume exposure. Methods: Twenty four welders (42% smokers) and 13 non-exposed controls (23% smokers) were monitored at a welding school. Exposure to fine particulate matter (PM 2.5 ) was assessed using cyclone samplers. Markers of systemic inflammation, including C-reactive protein (CRP), fibrinogen, and white blood cell (WBC) levels, were determined in peripheral blood samples collected at baseline and after 5.3 (SD 1.0) hours of exposure. Results: The median PM 2.5 concentration for welders was 1.66 mg/m 3 , which was significantly greater than that for controls (0.04 mg/m 3 ). Compared to non-smokers, smokers had a significantly higher baseline WBC count, but comparable levels of CRP and fibrinogen. In non-smokers, welding fume exposure was associated with a significant increase in WBC and neutrophil counts immediately following exposure (+0.8×10 3 /μl, 95% CI 0.1 to 1.6, and +1.0×10 3 /μl, 95% CI 0.4 to 1.7, respectively). A significant decrease in fibrinogen levels was observed in non-smokers (−32 mg/dl, 95% CI −63 to −1). No significant changes in WBC, neutrophil, and fibrinogen levels were found in smokers. Sixteen hours after welding exposure, CRP levels were found to be significantly increased in both non-smokers and smokers (0.90 mg/l, 95% CI 0.17 to 1.64). PM 2.5 concentrations were found to be significantly associated with absolute neutrophil counts in non-smokers, and CRP levels in both non-smokers and smokers. Conclusions: High levels of welding fume exposure induce acute systemic inflammation in a relatively young, healthy working population. These results also suggest that smoking may modify the effect of welding fume exposure on specific inflammatory markers.

Objectives Siderosis due to excessive iron exposure is a rare disease in welders. Less is known about the effect of inhaled iron on systemic iron status in welders. Here we present the association between exposure to iron as major constituent of the welding fume and the iron status in German welders. Method In this analysis we included 192 welders from the German WELDOX study not wearing respirators. Respirable welding fume was measured during one shift and analysed for its metal content. Iron status was assessed with different measures, including serum iron, serum ferritin (SF), transferrin, and prohepcidin. High iron stores were classified according to international standards. The influence of exposure to iron and other factors on the iron status was analysed with multiple regression models. Results Median shift exposure to respirable iron was 88 µg/m³ (interquartile range 13–690 µg/m³). For the overall study population the prevalence of high iron stores (SF > 200 µg/L) was 31.3%. A lower prevalence was found for tungsten inert gas (TIG) welders (16.9%). For all other welders using welding techniques with higher emission rates it was 38.6%. The regression models revealed a significant association of respirable iron and prohepcidin (exp (β)=1.08, 95% CI 1.05; 1.11) and a weaker association between respirable iron and serum ferritin (exp (β)=1.06, 95% CI 1.00; 1.12). Conclusions Although the iron status is biologically well regulated we found positive associations of respirable iron in welding fumes on prohepcidin and ferritin. We observed more welders with high iron stores in comparison to male persons from the general population.

Objectives Welding fume is suspected to accelerate the decline of lung function and development of chronic obstructive pulmonary disease (COPD). The aim of this study was to examine the relationship between welding fume exposure and COPD in Korean shipyard welders. Method 240 male welders who were working at two shipyards and took the annual health examination including pulmonary function test in 2010 participated in this study. A questionnaire about smoking habits and occupational history was administered. PFT was carried out with strict quality control measures. Exposed fume concentrations were estimated using 884 welding fume measurements taken 2002–2009 in one of the shipyards. Linear multiple regression was employed to evaluate the association between cumulative fume exposure and lung function parameters. Logistic regression was employed to test the excess risk of COPD by cumulative fume exposure. Age, height, the smoking amount, and cumulative fume exposure were incorporated as independent variables in those models. Results Mean age was 48, and mean work duration was 18 years. The mean cumulative fume exposure was 7.7 mg/m 3 . The prevalence of COPD was 14.6%. FEV 1 and FVC showed negative correlations with cumulative fume exposure, but statistically non-significant. Odds ratios of COPD were significantly elevated for middle (5.02, 95% CI:1.27–33.55) and high exposure group (6.20, 95% CI:1.41–44.98) compared to the low fume exposure group. Conclusions Our findings suggest a potential association between metal fume exposure and COPD. Further study with a prospective design is needed to investigate the excessive decline of lung function by welding fume exposure.

Objectives The objective of this analysis was to investigate levels and determinants of exposure to respirable and urinary chromium (CrR, CrU), and chromium in whole blood and in erythrocytes (CrBl, CrEry) in welders. Methods Respirable welding fume was collected in 241 welders during a working shift. Blood samples and spot urine samples were collected after the working shift. The content of CrR in the welding fume was determined using inductively coupled plasma mass spectrometry. CrU, CrBl and CrEry were measured by means of graphite furnace atom absorption spectrometry. Linear regression models were applied to model exposure to chromium. A multiple imputation approach was chosen to account for values below the limit of quantitation (LOQ). Results Median concentrations of CrR were Conclusions CrR was mainly influenced by the chromium content in the materials and the welding process. Welding in confined space increased exposure to CrR. Efficient local exhaust ventilation and the use of respirators decreased exposure. Airborne Cr concentration was a good predictor of urinary Cr exposure.

Objectives The aim of this analysis was to explore exposure to welding fumes and potential influencing factors of the airborne concentrations. Methods Personal sampling of welding fumes was carried out in 241 welders. Ninety respirable dust measurements were below the limits of detection (LOD). Therefore, we applied Tobit regression and imputations of values below LOD according to the log-normal distributions of the data ≥LOD with maximum likelihood estimation. We estimated regression coefficients for the welding processes, protective measures, and other factors. Results Main determinant of the concentrations was the type of welding process. The use of flux-cored wire in gas metal arc welding was estimated to increase the concentration in comparison with gas metal arc welding with solid wire (GMAW) by a factor of 2.20 (95% CI 1.58 to 3.06) using Tobit regression and by 2.36 (95% CI 1.51 to 3.69) using imputation. Tungsten inert gas welding was associated with 0.15 fold lower levels than with GMAW in both models. Dust extraction reduced the concentrations, whereas welding in confined space increased exposure levels with significant effects in both approaches. Conclusions Exposure to respirable welding fumes was frequently found below LOD. Two different approaches to deal with data

OBJECTIVES: To study the airway response and its mechanism to welding fumes in six welders with respiratory symptoms. METHODS: Methacholine and welding challenge tests were carried out. The concentration of welding fumes during the exposure test was measured. On two subjects who developed bronchoconstricition to welding challenge, additional tests were carried out including prick, patch, and inhalation challenges with metal salt solutions. RESULTS: Three subjects developed immediate bronchial reaction to exposure to welding fume; one to mild steel and stainless steel welding, another to mild steel and galvanised welding, and one only to galvanised welding. They all had a moderate to pronounced degree of non-specific bronchial hyperresponsiveness. The concentration of fumes during welding tests, particularly to galvanised welding, was high. An inhalation challenge test with zinc chloride salt solution in two subjects who reacted to galvanised welding was negative. Prick and patch tests with zinc chloride were also negative. CONCLUSION: The airway response to welding in these subjects is non-specific and is due to irritation rather than to sensitisation.