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<title>Occupational and Environmental Medicine recent issues</title>
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<title>Occupational and Environmental Medicine</title>
<url>http://hwmaint.oem.bmj.com/homepage/OEM_95x60.gif</url>
<link>http://oem.bmj.com</link>
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<item rdf:about="http://oem.bmj.com/cgi/content/short/69/3/157?rss=1">
<title><![CDATA[2011: the year in review]]></title>
<link>http://oem.bmj.com/cgi/content/short/69/3/157?rss=1</link>
<description><![CDATA[ <p>The Journal continued its tradition of service to the research community in 2011. Contributions to OEM continued to increase, and although final statistics are not in as of this writing, we expect to have received more than 700 papers by the end of the year. The journal is increasingly international, with the largest numbers of contributions coming from the USA, the Netherlands, the UK, Spain, Australia, Canada, Italy, Taiwan, Germany and France, in that order. These rankings are broadly reminiscent of worldwide trends in scientific publication, but with some notable exceptions. OEM receives relatively more contributions from the Netherlands, Spain and Australia, and we still have not seen substantial growth in submissions from emerging scientific nations like China, India and Brazil, whose overall scientific output is increasing rapidly.<cross-ref type="bib" refid="b1">1</cross-ref> We are interested in receiving contributions from these countries, whose growing economies account for a large proportion of the...]]></description>
<dc:creator><![CDATA[Loomis, D.]]></dc:creator>
<dc:date>2012-02-10T05:30:20-08:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2012-100680</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2012-100680</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[2011: the year in review]]></dc:title>
<prism:publicationDate>2012-03-01</prism:publicationDate>
<prism:section>Editorial</prism:section>
<prism:volume>69</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>157</prism:startingPage>
<prism:endingPage>157</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/69/3/158?rss=1">
<title><![CDATA[Forest fires are associated with elevated mortality in a dense urban setting]]></title>
<link>http://oem.bmj.com/cgi/content/short/69/3/158?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>The climate and vegetation of the greater Athens area (population over three million) make forest fires a real threat to the environment during the summer. A few studies have reported the adverse health effects of forest fires, mainly using morbidity outcomes. The authors investigated the short-term effects of forest fires on non-accidental mortality in the population of Athens, Greece, during 1998&ndash;2004.</p>
</sec>
<sec><st>Methods</st>
<p>The authors used generalised additive models to investigate the effect of forest fires on daily mortality, adjusting for time trend and meteorological variables, taking into account air pollution as measured from fixed monitors. Forest fires were classified by size according to the area burnt.</p>
</sec>
<sec><st>Results</st>
<p>Small fires do not have an effect on mortality. Medium sized fires are associated with an increase of 4.9% (95% CI 0.3% to 9.6%) in the daily total number of deaths, 6.0% (95% CI &ndash;0.3% to 12.6%) in the number of cardiovascular deaths and 16.2% (95% CI 1.3% to 33.4%) in the number of respiratory deaths. Cardiovascular effects are larger in those aged &lt;75&nbsp;years, while respiratory effects are larger in older people. The corresponding effects of the one large fire are: 49.7% (95% CI 37.2% to 63.4%), 60.6% (95% CI 43.1% to 80.3%) and 92.0% (95% CI 47.5% to 150.0%). These effects cannot be completely explained by an increase in ambient particle concentrations.</p>
</sec>
<sec><st>Conclusion</st>
<p>Forest fires have an immediate effect on mortality, not associated with accidental deaths, which is a significant public health problem, especially if the fire occurs near a densely populated area.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Analitis, A., Georgiadis, I., Katsouyanni, K.]]></dc:creator>
<dc:date>2012-02-10T05:30:20-08:00</dc:date>
<dc:identifier>info:doi/10.1136/oem.2010.064238</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oem.2010.064238</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Air pollution, air quality, Other exposures]]></dc:subject>
<dc:title><![CDATA[Forest fires are associated with elevated mortality in a dense urban setting]]></dc:title>
<prism:publicationDate>2012-03-01</prism:publicationDate>
<prism:section>Environment</prism:section>
<prism:volume>69</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>158</prism:startingPage>
<prism:endingPage>162</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/69/3/163?rss=1">
<title><![CDATA[The impact of heatwaves on mortality and emergency hospital admissions from non-external causes in Brisbane, Australia]]></title>
<link>http://oem.bmj.com/cgi/content/short/69/3/163?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>Heatwaves can have significant health consequences resulting in increased mortality and morbidity. However, their impact on people living in tropical/subtropical regions remains largely unknown. This study assessed the impact of heatwaves on mortality and emergency hospital admissions (EHAs) from non-external causes (NEC) in Brisbane, a subtropical city in Australia.</p>
</sec>
<sec><st>Methods</st>
<p>We acquired daily data on weather, air pollution and EHAs for patients aged 15 years and over in Brisbane between January 1996 and December 2005, and on mortality between January 1996 and November 2004. A locally derived definition of heatwave (daily maximum &ge;37&deg;C for 2 or more consecutive days) was adopted. Case&ndash;crossover analyses were used to assess the impact of heatwaves on cause-specific mortality and EHAs.</p>
</sec>
<sec><st>Results</st>
<p>During heatwaves, there was a statistically significant increase in NEC mortality (OR 1.46; 95% CI 1.21 to 1.77), cardiovascular mortality (OR 1.89; 95% CI 1.44 to 2.48), diabetes mortality in those aged 75+ (OR 9.96; 95% CI 1.02 to 96.85), NEC EHAs (OR 1.15; 95% CI 1.07 to 1.23) and EHAs from renal diseases (OR 1.41; 95% CI 1.09 to 1.83). The elderly were found to be particularly vulnerable to heatwaves (eg, for NEC EHAs, OR 1.24 for 65&ndash;74-year-olds and 1.39 for those aged 75+).</p>
</sec>
<sec><st>Conclusions</st>
<p>Significant increases in NEC mortality and EHAs were observed during heatwaves in Brisbane where people are well accustomed to hot summer weather. The most vulnerable were the elderly and people with cardiovascular, renal or diabetic disease.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Wang, X. Y., Barnett, A. G., Yu, W., FitzGerald, G., Tippett, V., Aitken, P., Neville, G., McRae, D., Verrall, K., Tong, S.]]></dc:creator>
<dc:date>2012-02-10T05:30:20-08:00</dc:date>
<dc:identifier>info:doi/10.1136/oem.2010.062141</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oem.2010.062141</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Air pollution, air quality, Other exposures]]></dc:subject>
<dc:title><![CDATA[The impact of heatwaves on mortality and emergency hospital admissions from non-external causes in Brisbane, Australia]]></dc:title>
<prism:publicationDate>2012-03-01</prism:publicationDate>
<prism:section>Environment</prism:section>
<prism:volume>69</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>163</prism:startingPage>
<prism:endingPage>169</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/69/3/170?rss=1">
<title><![CDATA[Exposure to wood smoke particles produces inflammation in healthy volunteers]]></title>
<link>http://oem.bmj.com/cgi/content/short/69/3/170?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>Human exposure to wood smoke particles (WSP) impacts on human health through changes in indoor air quality, exposures from wild fires, burning of biomass and air pollution. This investigation tested the postulate that healthy volunteers exposed to WSP would demonstrate evidence of both pulmonary and systemic inflammation.</p>
</sec>
<sec><st>Methods</st>
<p>Ten volunteers were exposed to filtered air and, 3&nbsp;weeks or more later, WSP. Each exposure included alternating 15&nbsp;min of exercise and 15&nbsp;min of rest for a total duration of 2&nbsp;h. Wood smoke was generated by heating an oak log on an electric element and then delivered to the exposure chamber. Endpoints measured in the volunteers included symptoms, pulmonary function tests, measures of heart rate variability and repolarisation, blood indices and analysis of cells and fluid obtained during bronchoalveolar lavage.</p>
</sec>
<sec><st>Results</st>
<p>Mean particle mass for the 10 exposures to air and WSP was measured using the mass of particles collected on filters and found to be below the detectable limit and 485&plusmn;84&nbsp;&mu;g/m<sup>3</sup>, respectively (mean&plusmn;SD). There was no change in either symptom prevalence or pulmonary function with exposure to WSP. At 20&nbsp;h after wood smoke exposure, blood tests demonstrated an increased percentage of neutrophils, and bronchial and bronchoalveolar lavage revealed a neutrophilic influx.</p>
</sec>
<sec><st>Conclusions</st>
<p>We conclude that exposure of healthy volunteers to WSP may be associated with evidence of both systemic and pulmonary inflammation.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Ghio, A. J., Soukup, J. M., Case, M., Dailey, L. A., Richards, J., Berntsen, J., Devlin, R. B., Stone, S., Rappold, A.]]></dc:creator>
<dc:date>2012-02-10T05:30:20-08:00</dc:date>
<dc:identifier>info:doi/10.1136/oem.2011.065276</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oem.2011.065276</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Air pollution, air quality, Other exposures]]></dc:subject>
<dc:title><![CDATA[Exposure to wood smoke particles produces inflammation in healthy volunteers]]></dc:title>
<prism:publicationDate>2012-03-01</prism:publicationDate>
<prism:section>Environment</prism:section>
<prism:volume>69</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>170</prism:startingPage>
<prism:endingPage>175</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/69/3/176?rss=1">
<title><![CDATA[Occupational noise exposure assessment using O*NET and its application to a study of hearing loss in the US general population]]></title>
<link>http://oem.bmj.com/cgi/content/short/69/3/176?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>Although occupational noise is a well known risk factor for hearing loss, little epidemiological evidence has been reported on its association with hearing loss in the general population, in part, because of the difficulty in exposure assessment. This study introduced a quantitative occupational noise exposure assessment tool using the Occupational Information Network (O*NET) database and evaluated its applicability for epidemiological research using data from the National Health and Nutrition Examination Survey (NHANES) 1999&ndash;2004.</p>
</sec>
<sec><st>Methods</st>
<p>The O*NET noise exposure data were assessed by questionnaires across numerous occupations, asking the frequency of exposure to sounds and noise levels that are distracting and uncomfortable (with five possible responses from &lsquo;never&rsquo; to &lsquo;every day&rsquo;). Means of the O*NET noise scores were computed to correspond to NHANES occupational categories and assigned to 3828 adults aged 20&ndash;69&nbsp;years, who participated in the 1999&ndash;2004 NHANES. Pure-tone averages (PTA) of hearing thresholds at 0.5, 1, 2 and 4&nbsp;kHz were computed, and hearing loss was defined as a PTA &gt;25&nbsp;dB in either ear. Linear and logistic regression models with either continuous or quintiles of the O*NET noise scores were fitted on log-transformed PTA and binary hearing loss, respectively.</p>
</sec>
<sec><st>Results</st>
<p>Noise scores ranged from 1.80 to 4.37 with mean&plusmn;SE of 3.06&plusmn;0.02. After controlling for potential confounders, the highest (vs lowest) noise score quintile had a 22.5% (95% CI 11.0% to 35.2%) increase in PTA, and there was a linear dose-dependent trend across the quintiles of noise scores (p trend&lt;0.0001). The adjusted OR for hearing loss comparing the highest with the lowest noise score quintiles was 2.1 (95% CI 1.2 to 3.6).</p>
</sec>
<sec><st>Conclusion</st>
<p>This study suggests that the O*NET noise score is a useful tool for examining occupational noise-induced health effects in the general population in the absence of actual occupational noise exposure assessment data.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Choi, Y.-H., Hu, H., Tak, S., Mukherjee, B., Park, S. K.]]></dc:creator>
<dc:date>2012-02-10T05:30:21-08:00</dc:date>
<dc:identifier>info:doi/10.1136/oem.2011.064758</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oem.2011.064758</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Unlocked]]></dc:subject>
<dc:title><![CDATA[Occupational noise exposure assessment using O*NET and its application to a study of hearing loss in the US general population]]></dc:title>
<prism:publicationDate>2012-03-01</prism:publicationDate>
<prism:section>Exposure assessment</prism:section>
<prism:volume>69</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>176</prism:startingPage>
<prism:endingPage>183</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/69/3/184?rss=1">
<title><![CDATA[Structural equation models in occupational health: an application to exposure modelling]]></title>
<link>http://oem.bmj.com/cgi/content/short/69/3/184?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>Many occupational hygiene surveys are designed to collect pollutant monitoring data from multiple locations simultaneously to better reflect the reality of work-related exposure. The exposure model must account for the complexity inherent in this study design, as well as be flexible to extrapolating exposures across an occupational cohort for dose&ndash;response modelling and risk assessment. This paper explores the structural equation model (SEM) as a tool to analyse pollutant monitoring data from occupational studies with multiple concurrent sampling across exposure locations.</p>
</sec>
<sec><st>Methods</st>
<p>This study uses exposure data from a comprehensive assessment of diesel exhaust in the US trucking industry to test the strength of SEMs over more standard analytical approaches such as ordinary least squares (OLS). The exposure data consist of concurrent sampling of elemental carbon from multiple co-located monitors on individual workers, work area and background levels at 36 different trucking terminals across the USA.</p>
</sec>
<sec><st>Results</st>
<p>The SEM is compared with two separate OLS specifications&mdash;one that focuses only on predicting personal exposure and excludes data from the additional monitoring sites, and a second that estimates three separate OLS specifications. When compared with the OLS specifications, the SEM provided a better fit to these layered exposure data. The OLS specifications suffered from bias in the coefficients, including downward bias in the work area and background exposure levels and overstatement of the smoking effect. Additionally, many theoretically valid covariates were significant only in the SEM.</p>
</sec>
<sec><st>Conclusions</st>
<p>This study provides evidence in favour of more widespread use of SEMs in occupational health. SEMs represent a more robust and realistic framework for modelling multiple exposure pathways and have the potential to reduce exposure misclassification bias and strengthen the linkages between studies of exposure and disease outcomes.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Davis, M. E.]]></dc:creator>
<dc:date>2012-02-10T05:30:21-08:00</dc:date>
<dc:identifier>info:doi/10.1136/oem.2010.063032</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oem.2010.063032</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Other exposures]]></dc:subject>
<dc:title><![CDATA[Structural equation models in occupational health: an application to exposure modelling]]></dc:title>
<prism:publicationDate>2012-03-01</prism:publicationDate>
<prism:section>Methodology</prism:section>
<prism:volume>69</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>184</prism:startingPage>
<prism:endingPage>190</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/69/3/191?rss=1">
<title><![CDATA[A case-cohort study of lung cancer in poultry and control workers: occupational findings]]></title>
<link>http://oem.bmj.com/cgi/content/short/69/3/191?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>We conducted a mortality study of members of the United Food and Commercial Workers International Union who worked in poultry slaughtering/processing plants, and controls. Excess deaths from cancer at 11 different cancer sites including lung cancer were observed in the poultry workers. The study described here is a pilot case&ndash;cohort study of lung cancer nested within the cohort to examine if it is possible, in a larger study to be conducted later, to identify specific potentially carcinogenic occupational exposures in poultry workers.</p>
</sec>
<sec><st>Methods</st>
<p>Subjects or the next of kin of deceased subjects were interviewed by phone. Logistic regression ORs and Cox proportional HRs were estimated.</p>
</sec>
<sec><st>Results</st>
<p>Elevated risks for poultry exposure were recorded for subjects who (1) killed chickens at work (OR 4.2, 95% CI 1.2 to 14.7; HR 1.8, 95% CI 1.0 to 3.3) and (2) ever had direct contact with chicken blood at work (OR 1.9, 95% CI 1.0 to 3.8; HR 1.3, 95% CI 0.9 to 2.0). These activities are associated with high exposure to oncogenic viruses.</p>
</sec>
<sec><st>Conclusion</st>
<p>These results may have important public health implications, since the general population is also exposed to these viruses. Elevated risks were observed for non-poultry-related occupational exposures such as working in a stockyard, working in a chemical plant, use of chemicals to kill moulds, and working in plants where plastic products were manufactured. These preliminary findings indicate that full scale epidemiological studies of adequate statistical power are needed to examine the role of occupational exposures in cancer occurrence in poultry workers.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Felini, M., Preacely, N., Shah, N., Christopher, A., Sarda, V., Elfaramawi, M., Sall, M., Bangara, S., Gandhi, S., Johnson, E. S.]]></dc:creator>
<dc:date>2012-02-10T05:30:21-08:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2011-100310</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2011-100310</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[A case-cohort study of lung cancer in poultry and control workers: occupational findings]]></dc:title>
<prism:publicationDate>2012-03-01</prism:publicationDate>
<prism:section>Workplace</prism:section>
<prism:volume>69</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>191</prism:startingPage>
<prism:endingPage>197</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/69/3/198?rss=1">
<title><![CDATA[Risk factors for musculoskeletal symptoms of the neck or shoulder alone or neck and shoulder among hospital nurses]]></title>
<link>http://oem.bmj.com/cgi/content/short/69/3/198?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>To investigate the relationship between sociodemographic, individual and work place factors, and neck pain alone, shoulder pain alone, and neck and shoulder pain among nurses working across three public hospitals in Melbourne, Australia.</p>
</sec>
<sec><st>Methods</st>
<p>Information on participant demographics, somatisation tendency, health beliefs, mental and physical health status, workplace physical and psychosocial factors, and musculoskeletal symptoms and pain at several body sites was collected.</p>
</sec>
<sec><st>Results</st>
<p>1111 participants (response rate 38.6%) were included in the study: 17.2% reported neck pain alone, 11.6% shoulder pain alone and 15.8% both neck and shoulder pain in the past month. Self-reported neck and shoulder pain were independently associated with poorer mental (OR 0.96, 95% CI 0.94 to 0.98) and physical (0.92, 0.90 to 0.95) health and well-being, somatisation (1.77, 1.03 to 3.04) and negative work-causation beliefs (2.51, 1.57 to 3.99). Neck pain alone was more consistently associated with sociodemographic factors, mental (0.97, 0.96 to 0.99) and physical (0.97, 0.94 to 0.99) health and well-being, and shoulder pain alone was associated with physical health and well-being (0.95, 0.92 to 0.98) and fear-avoidance beliefs (0.45, 0.24 to 0.86).</p>
</sec>
<sec><st>Conclusion</st>
<p>Risk factors for self-reported pain between regions of the neck and shoulder alone, and neck and shoulder differed. While neck and shoulder pain was consistently associated with several risk factors, neck and shoulder pain in isolation were both associated with physical health and well-being and individually associated with sociodemographic and health beliefs, respectively. These findings suggest that different factors may be associated with a single pain region versus pain in two regions.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Hoe, V. C. W., Kelsall, H. L., Urquhart, D. M., Sim, M. R.]]></dc:creator>
<dc:date>2012-02-10T05:30:21-08:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2011-100302</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2011-100302</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Risk factors for musculoskeletal symptoms of the neck or shoulder alone or neck and shoulder among hospital nurses]]></dc:title>
<prism:publicationDate>2012-03-01</prism:publicationDate>
<prism:section>Workplace</prism:section>
<prism:volume>69</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>198</prism:startingPage>
<prism:endingPage>204</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/69/3/205?rss=1">
<title><![CDATA[Occupational health impact of the 2009 H1N1 flu pandemic: surveillance of sickness absence]]></title>
<link>http://oem.bmj.com/cgi/content/short/69/3/205?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>Workplace absences due to illness can disrupt usual operations and increase costs for businesses. This study of sickness absence due to influenza and influenza-related illness presents a unique opportunity to characterise and measure the impact of the 2009 (H1N1) pandemic, by comparing trends during the pandemic to those of previous years, and adding this information to that obtained by traditional epidemiological surveillance systems.</p>
</sec>
<sec><st>Methods</st>
<p>We compared the numbers of cases of sickness absence due to illness caused by influenza and influenza-related illness in 2007&ndash;2009, and in the first 3&nbsp;months of 2010 in Catalonia (n=811 940) using a time series approach. Trends were examined by economic activity, age and gender. The weekly endemic-epidemic index (EEI) was calculated and its 95% CI obtained with the delta method, with observed and expected cases considered as independent random variables.</p>
</sec>
<sec><st>Results</st>
<p>Influenza activity peaked earlier in 2009 and yielded more cases than in previous years. Week 46 (in November 2009) had the highest number of new cases resulting in sickness absence (EEI 20.99; 95% CI 9.44 to 46.69). Women and the &lsquo;education, health and other social activities&rsquo; sector were the most affected.</p>
</sec>
<sec><st>Conclusions</st>
<p>Results indicate that the new H1N1 pandemic had a significant impact on business, with shifts in the timing of peak incidence, a doubling in the number of cases, and changes in the distribution of cases by economic activity sector and gender. Traditional epidemiological surveillance systems could benefit from the addition of information based on sickness absence data.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Tora-Rocamora, I., Delclos, G. L., Martinez, J. M., Jardi, J., Alberti, C., Manzanera, R., Yasui, Y., Cleries, R., Tobias, A., Benavides, F. G.]]></dc:creator>
<dc:date>2012-02-10T05:30:21-08:00</dc:date>
<dc:identifier>info:doi/10.1136/oem.2011.065003</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oem.2011.065003</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Editor's choice]]></dc:subject>
<dc:title><![CDATA[Occupational health impact of the 2009 H1N1 flu pandemic: surveillance of sickness absence]]></dc:title>
<prism:publicationDate>2012-03-01</prism:publicationDate>
<prism:section>Workplace</prism:section>
<prism:volume>69</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>205</prism:startingPage>
<prism:endingPage>210</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/69/3/211?rss=1">
<title><![CDATA[Noise exposure and serious injury to active sawmill workers in British Columbia]]></title>
<link>http://oem.bmj.com/cgi/content/short/69/3/211?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Occupational noise might increase the risk of workplace injury through a variety of mechanisms, including interference with communication and increased stress.</p>
</sec>
<sec><st>Objectives</st>
<p>The purpose of this study was to assess the effect of chronic noise exposure on serious workplace injury, and how the timing of exposure influenced risk.</p>
</sec>
<sec><st>Methods</st>
<p>The authors examined a cohort of 26 000 workers, who worked between 1950 and 1989. Cases were those hospitalised for a work-related injury (ICD-9 codes 800&ndash;999, and E codes E800&ndash;E999), from April 1989 to December 1998. Cumulative exposure levels were estimated for subjects based on a quantitative retrospective exposure assessment. An internal comparison of cumulative noise exposure and subchronic durations of noise exposure and injury was conducted using Poisson regression. There were 163 cases for the cumulative and 161 cases for the subchronic analysis.</p>
</sec>
<sec><st>Results</st>
<p>Cumulative noise exposure were associated with a decreased risk for injuries, with the risk generally decreasing as cumulative noise levels increased, while most durations of subchronic exposure were associated with an increased risk for injury. An inverse U-shaped trend was observed with the time period of 90&nbsp;days to 1&nbsp;year demonstrating the most elevated RR compared with 0&ndash;1&nbsp;days of exposure.</p>
</sec>
<sec><st>Conclusions</st>
<p>Workers highly exposed to noise, or exposed for long periods of time, might develop effective methods of communicating the risk and preventing injuries when exposed to noise.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Kling, R. N., Demers, P. A., Alamgir, H., Davies, H. W.]]></dc:creator>
<dc:date>2012-02-10T05:30:21-08:00</dc:date>
<dc:identifier>info:doi/10.1136/oem.2010.058107</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oem.2010.058107</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Noise exposure and serious injury to active sawmill workers in British Columbia]]></dc:title>
<prism:publicationDate>2012-03-01</prism:publicationDate>
<prism:section>Workplace</prism:section>
<prism:volume>69</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>211</prism:startingPage>
<prism:endingPage>216</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/69/3/217?rss=1">
<title><![CDATA[Occupational dust and radiation exposure and mortality from stomach cancer among German uranium miners, 1946-2003]]></title>
<link>http://oem.bmj.com/cgi/content/short/69/3/217?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>&lsquo;Dusty occupations&rsquo; and exposure to low-dose radiation have been suggested as potential risk factors for stomach cancer. Data from the German uranium miner cohort study are used to further evaluate this topic.</p>
</sec>
<sec><st>Methods</st>
<p>The cohort includes 58 677 miners with complete information on occupational exposure to dust, arsenic and radiation dose based on a detailed job-exposure matrix. A total of 592 stomach cancer deaths occurred in the follow-up period from 1946 to 2003. A Poisson regression model stratified by age and calendar year was used to calculate the excess relative risk (ERR) per unit of cumulative exposure to fine dust or from cumulative absorbed dose to stomach from &alpha; or low-LET (low linear energy transfer) radiation. For arsenic exposure, a binary quadratic model was applied.</p>
</sec>
<sec><st>Results</st>
<p>After adjustment for each of the three other variables, a statistically non-significant linear relationship was observed for absorbed dose from low-LET radiation (ERR/Gy=0.30, 95% CI &ndash;1.26 to 1.87), &alpha; radiation (ERR/Gy=22.5, 95% CI &ndash;26.5 to 71.5) and fine dust (ERR/dust-year=0.0012, 95% CI &ndash;0.0020 to 0.0043). The relationship between stomach cancer and arsenic exposure was non-linear with a 2.1-fold higher RR (95% CI 0.9 to 3.3) in the exposure category above 500 compared with 0 dust-years.</p>
</sec>
<sec><st>Conclusion</st>
<p>Positive statistically non-significant relationships between stomach cancer and arsenic dust, fine dust and absorbed dose from &alpha; and low-LET radiation were found. Overall, low statistical power due to low doses from radiation and dust are of concern.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Kreuzer, M., Straif, K., Marsh, J. W., Dufey, F., Grosche, B., Nosske, D., Sogl, M.]]></dc:creator>
<dc:date>2012-02-10T05:30:21-08:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2011-100051</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2011-100051</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Metals, Other exposures]]></dc:subject>
<dc:title><![CDATA[Occupational dust and radiation exposure and mortality from stomach cancer among German uranium miners, 1946-2003]]></dc:title>
<prism:publicationDate>2012-03-01</prism:publicationDate>
<prism:section>Workplace</prism:section>
<prism:volume>69</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>217</prism:startingPage>
<prism:endingPage>223</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/69/3/224?rss=1">
<title><![CDATA[Exposure to metal-working fluids in the automobile industry and the risk of male germ cell tumours]]></title>
<link>http://oem.bmj.com/cgi/content/short/69/3/224?rss=1</link>
<description><![CDATA[
<sec><st>Introduction</st>
<p>In a previous analysis of a case&ndash;control study of testicular cancer nested in a cohort of automobile workers, we observed an increased risk for testicular cancer among workers who had ever been involved in occupational metal-cutting tasks. We investigated whether this risk increase was due to exposure to metal-working fluids (MWF).</p>
</sec>
<sec><st>Methods</st>
<p>Occupational exposure to MWF was assessed in detail using a job-specific questionnaire for metal-cutting work. We calculated ORs and associated 95% CIs individually matched for age (&plusmn;2&nbsp;years) and adjusted for a history of cryptorchidism by conditional logistic regression.</p>
</sec>
<sec><st>Results</st>
<p>The prevalence of exposure to MWF was 39.8% among cases and 40.1% among controls. For total germ cell tumours and seminomas we did not observe risk increases for metal-cutting tasks or occupational exposure to MWF (OR 0.95; 95% CI 0.69 to 1.32 and OR 0.88; 95% CI 0.58 to 1.35, respectively). However, dermal exposure to oil-based MWF was associated with an increased risk for non-seminomatous testicular cancer. Dermal exposure to oil-based MWF for more than 5000&nbsp;h showed particularly high risk estimates (OR 4.72; 95% CI 1.48 to 15.09).</p>
</sec>
<sec><st>Discussion</st>
<p>Long-term dermal exposure to oil-based MWF was a risk factor for the development of non-seminomatous testicular germ cell cancer. Possible measures to reduce exposure include the introduction of engineering control measures such as venting or enclosing of machines, and enforcing the use of personal protective equipment during metal cutting.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Behrens, T., Pohlabeln, H., Mester, B., Langner, I., Schmeisser, N., Ahrens, W.]]></dc:creator>
<dc:date>2012-02-10T05:30:21-08:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2011-100070</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2011-100070</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Exposure to metal-working fluids in the automobile industry and the risk of male germ cell tumours]]></dc:title>
<prism:publicationDate>2012-03-01</prism:publicationDate>
<prism:section>Short report</prism:section>
<prism:volume>69</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>224</prism:startingPage>
<prism:endingPage>226</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/69/3/227?rss=1">
<title><![CDATA[A proposed threshold exposure for airborne asbestos]]></title>
<link>http://oem.bmj.com/cgi/content/short/69/3/227?rss=1</link>
<description><![CDATA[ <p>The article by Clin <I>et al</I><cross-ref type="bib" refid="b1">1</cross-ref> provides additional information for a dose&ndash;response relationship between asbestos and cancer. Information where a response curve changes the effect as observed from the background is critical in establishing a safe exposure limit (threshold-exposure/concentration-dose). Some investigators have reported that this threshold is around 25&nbsp;fibre/ml-years, although for some members of an exposed group this may be lower. However, a cumulative no-effect value does not provide information applicable for practical everyday use when monitoring worker exposure. Recent studies<cross-ref type="bib" refid="b2">2&ndash;4</cross-ref><cross-ref type="bib" refid="b3"></cross-ref><cross-ref type="bib" refid="b4"></cross-ref> have suggested levels of exposure where there was no excess increase in cancer, notably lung cancer and mesothelioma. This is especially noted for non-smokers where the risk does not exceed unity (lung cancer), even for high asbestos exposure, while there is a significant increased risk for smokers and former smokers.<cross-ref type="bib" refid="b4">4</cross-ref> Thus, it appears that smoking is the primary...]]></description>
<dc:creator><![CDATA[Lange, J. H., Mastrangelo, G., Cegolon, L.]]></dc:creator>
<dc:date>2012-02-10T05:30:21-08:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2011-100225</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2011-100225</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[A proposed threshold exposure for airborne asbestos]]></dc:title>
<prism:publicationDate>2012-03-01</prism:publicationDate>
<prism:section>PostScript</prism:section>
<prism:volume>69</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>227</prism:startingPage>
<prism:endingPage>228</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/69/3/227-a?rss=1">
<title><![CDATA[Fixed FEV1/FVC ratio <0.7 for identifying airflow limitation: not a good idea in occupational settings]]></title>
<link>http://oem.bmj.com/cgi/content/short/69/3/227-a?rss=1</link>
<description><![CDATA[ <p>Dr S&oslash;yseth and colleagues recently reported an increased prevalence of airflow limitation in workers employed in the Norwegian smelting industry and significant associations with workplace dust exposures.<cross-ref type="bib" refid="b1">1</cross-ref> The prevalence of airflow limitation was assessed using prebronchodilator spirometry and two measures of airflow limitation: FEV<SUB>1</SUB>/FVC ratio &lt;0.7 and FEV<SUB>1</SUB>/FVC ratio &lt;lower limit of normal (LLN). When compared across age categories (&lt;35, 35&ndash;44, &ge;45&nbsp;years), the prevalence of airflow limitation based on the ratio &lt;0.7 versus LLN was approximately doubled in the &ge;45&nbsp;years age categories across all levels of exposure duration (overall 17.6 vs 8.8%). The rate of FEV<SUB>1</SUB> decline was increased for prevalent and incident cases of airflow limitation defined by both criteria, but it would be of interest to see the rates of decline for workers with FEV<SUB>1</SUB>/FVC &lt;0.7 compared with those where the ratio is &lt;LLN and &ge;LLN.</p> <p>The authors recommended that &lsquo;in occupational healthcare settings, FEV<SUB>1</SUB>/FVC...]]></description>
<dc:creator><![CDATA[Hnizdo, E., Petsonk, E. L.]]></dc:creator>
<dc:date>2012-02-10T05:30:21-08:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2011-100365</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2011-100365</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Fixed FEV1/FVC ratio <0.7 for identifying airflow limitation: not a good idea in occupational settings]]></dc:title>
<prism:publicationDate>2012-03-01</prism:publicationDate>
<prism:section>PostScript</prism:section>
<prism:volume>69</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>227</prism:startingPage>
<prism:endingPage>227</prism:endingPage>
</item>
</rdf:RDF>
