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<title>Occupational and Environmental Medicine current issue</title>
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<prism:coverDisplayDate>Jun  1 2008 12:00:00:000AM</prism:coverDisplayDate>
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<title>Occupational and Environmental Medicine</title>
<url>http://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/full/65/6/1?rss=1">
<title><![CDATA[[Work in Brief] Work in Brief]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Palmer, K.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:title><![CDATA[[Work in Brief] Work in Brief]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>1</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>1</prism:startingPage>
<prism:section>Work in Brief</prism:section>
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<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/367?rss=1">
<title><![CDATA[[Editorials] Occupational medicine, public health and disasters: a shared agenda?]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/367?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Morgan, O., Murray, V., Snashall, D.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1136/oem.2007.035295</dc:identifier>
<dc:title><![CDATA[[Editorials] Occupational medicine, public health and disasters: a shared agenda?]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>368</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>367</prism:startingPage>
<prism:section>Editorials</prism:section>
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<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/368?rss=1">
<title><![CDATA[[Editorials] Reanalysis: lessons great and small]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/368?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kriebel, D.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1136/oem.2007.034884</dc:identifier>
<dc:title><![CDATA[[Editorials] Reanalysis: lessons great and small]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>370</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>368</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/371?rss=1">
<title><![CDATA[[Review] Meta-analysis of benzene exposure and non-Hodgkin lymphoma: biases could mask an important association]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/371?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>Benzene is a widely recognised cause of leukaemia but its association with non-Hodgkin&rsquo;s lymphoma (NHL) is less well established. The goal of this project is to review the current published literature on this association.</p>
</sec>
<sec><st>Methods:</st>
<p>We performed a meta-analysis of cohort and case-control studies of benzene exposure and NHL and a meta-analysis of NHL and refinery work, a potential source of benzene exposure.</p>
</sec>
<sec><st>Results:</st>
<p>In 22 studies of benzene exposure, the summary relative risk for NHL was 1.22 (95% CI 1.02 to 1.47; one-sided p value = 0.01). When studies that likely included unexposed subjects in the "exposed" group were excluded, the summary relative risk increased to 1.49 (95% CI 1.12 to 1.97, n = 13), and when studies based solely on self-reported work history were excluded, the relative risk rose to 2.12 (95% CI 1.11 to 4.02, n = 6). In refinery workers, the summary relative risk for NHL in all 21 studies was 1.21 (95% CI 1.00 to 1.46; p = 0.02). When adjusted for the healthy worker effect, this relative risk estimate increased to 1.42 (95% CI 1.19 to 1.69).</p>
</sec>
<sec><st>Conclusions:</st>
<p>The finding of elevated relative risks in studies of both benzene exposure and refinery work provides further evidence that benzene exposure causes NHL. In addition, the finding of increased relative risks after removing studies that included unexposed or lesser exposed workers in "exposed" cohorts, and increased relative risk estimates after adjusting for the healthy worker effect, suggest that effects of benzene on NHL might be missed in occupational studies if these biases are not accounted for.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Steinmaus, C, Smith, A H, Jones, R M, Smith, M T]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1136/oem.2007.036913</dc:identifier>
<dc:title><![CDATA[[Review] Meta-analysis of benzene exposure and non-Hodgkin lymphoma: biases could mask an important association]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>378</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>371</prism:startingPage>
<prism:section>Review</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/379?rss=1">
<title><![CDATA[[Original articles] Adjustment for temporal confounders in a reanalysis of a case-control study of beryllium and lung cancer]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/379?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>To evaluate potential confounding of the association between beryllium and lung cancer in a reanalysis of data from a published case&ndash;control study of workers at a beryllium processing facility.</p>
</sec>
<sec><st>Methods:</st>
<p>The association of cumulative and average beryllium exposure with lung cancer among 142 cases and five age-match controls per case was reanalysed using conditional logistic regression. Adjustment was made independently for potential confounders of hire age and birth year. Alternative adjustments to avoid taking the logarithm of zero were explored.</p>
</sec>
<sec><st>Results:</st>
<p>Adjustment for either birth cohort or hire age (two highly correlated factors) attenuated lung cancer risk associated with cumulative exposure; however, lung cancer risk was significantly associated with average exposure using a 10-year lag following adjustment. Stratification of analyses by birth cohort found greater lung cancer risk from cumulative and average exposure for workers born before 1900 than for workers born later. The magnitude of the association between lung cancer and average exposure was not reduced by modifying the method used to take the log of exposure.</p>
</sec>
<sec><st>Conclusion:</st>
<p>In this reanalysis, average, but not cumulative, beryllium exposure was related to lung cancer risk after adjustment for birth cohort. Confounding by birth cohort is likely related to differences in smoking patterns for workers born before 1900 and the tendency for workers hired during the World War II era to have been older at hire.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Schubauer-Berigan, M K, Deddens, J A, Steenland, K, Sanderson, W T, Petersen, M R]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1136/oem.2007.033654</dc:identifier>
<dc:title><![CDATA[[Original articles] Adjustment for temporal confounders in a reanalysis of a case-control study of beryllium and lung cancer]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>383</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>379</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/384?rss=1">
<title><![CDATA[[Original articles] Exposure to inhalable dust and its cyclohexane soluble fraction since the 1970s in the rubber manufacturing industry in the European Union]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/384?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>As exposures to airborne particulates in the European rubber industry might still be causing genotoxic risks, it is important to assess trends in levels of inhalable dust and its cyclohexane soluble fraction (CSF) between the 1970s and 2003.</p>
</sec>
<sec><st>Methods:</st>
<p>13 380 inhalable and 816 respirable dust and 5657 CSF measurements, collected within the framework of the European Union Concerted Action EXASRUB, were analysed. Hierarchical mixed effects models were applied to assess exposure trends, taking into account between-factory, between-worker/location and day-to-day variances.</p>
</sec>
<sec><st>Results:</st>
<p>Geometric mean levels of inhalable dust and CSF exposure changed by &ndash;4% (range &ndash;5.8 to +2.9%) and &ndash;3% (range &ndash;8.6 to 0%) per year, respectively. Significant reductions in inhalable dust concentrations were found in all countries for handling of crude materials and mixing and milling (&ndash;7% to &ndash;4% per year), as well as for miscellaneous workers (&ndash;11% to &ndash;5% per year), while significant CSF exposure reductions were found in curing (&ndash;8.6% per year) and maintenance and engineering departments (&ndash;5.4% per year).</p>
</sec>
<sec><st>Conclusion:</st>
<p>These analyses suggest that on average exposure levels of inhalable dust and its CSF in the European rubber manufacturing industry have steadily declined. Most likely genotoxic risks have also lessened over time since exposure levels have decreased and the most toxic chemicals have been replaced. In addition to differences in exposure reductions and levels among various stages of the production process, large differences across countries were noted. These patterns should be taken into account in retrospective assessment of exposure for epidemiological studies assessing cancer risk in the rubber industry.</p>
</sec>
]]></description>
<dc:creator><![CDATA[de Vocht, F, Vermeulen, R, Burstyn, I, Sobala, W, Dost, A, Taeger, D, Bergendorf, U, Straif, K, Swuste, P, Kromhout, H, on behalf of the EU-EXASRUB consortium]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1136/oem.2007.034470</dc:identifier>
<dc:title><![CDATA[[Original articles] Exposure to inhalable dust and its cyclohexane soluble fraction since the 1970s in the rubber manufacturing industry in the European Union]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>391</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>384</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/392?rss=1">
<title><![CDATA[[Original articles] Inequities in reporting asbestos-related lung cancer: influence of smoking stigma and physician's specialty, workload and role perception]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/392?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>To study physician barriers to workers&rsquo; compensation claims for asbestos-related cancers, focusing on smokers&rsquo; stigma and physicians&rsquo; speciality and role perception.</p>
</sec>
<sec><st>Methods:</st>
<p>Cross-sectional telephone study of 486 randomly-selected general practitioners (GPs) and pulmonologists in south-eastern France. Standardised questionnaires explored their behaviour, attitudes and practices in the field of occupational health and their responses to a case vignette of a lung cancer patient with long-term occupational asbestos exposure. Randomised subgroups of GPs and pulmonologists heard alternative versions varying only as regards the worker&rsquo;s smoking status. We studied factors associated with the recommendation that the case vignette patient file a compensation claim with simple and multiple logistic regressions.</p>
</sec>
<sec><st>Results:</st>
<p>The response rate was 64.4% among GPs and 62.5% among pulmonologists. Recommending the filing of an occupational disease claim was significantly associated in multiple logistic regressions with speciality (OR 4.46; 95% CI 2.38 to 8.37, for pulmonologists vs GPs), patient&rsquo;s smoking status (OR 3.15; 95% CI 2.11 to 4.70, for non-smokers vs smokers), physician&rsquo;s workload (OR 1.83; 95% CI 1.17 to 2.88, for &lt;=25 consultations per day vs &gt;25) and role perception (OR 2.00; 95% CI 1.22 to 3.27, for those who considered completing occupational disease medical certificates to be part of their role vs those who did not).</p>
</sec>
<sec><st>Conclusions:</st>
<p>The results of this French study appear applicable to various countries and contexts. To make physicians and especially GPs more aware of occupational health and smoking stigma, officials and educators must give these topics higher priority during initial training and continuing medical education. Tools and equipment that take time constraints into account should be developed and disseminated to help physicians manage occupational diseases.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Verger, P, Arnaud, S, Ferrer, S, Iarmarcovai, G, Saliba, M-L, Viau, A, Souville, M]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1136/oem.2007.035808</dc:identifier>
<dc:title><![CDATA[[Original articles] Inequities in reporting asbestos-related lung cancer: influence of smoking stigma and physician's specialty, workload and role perception]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>397</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>392</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/397?rss=1">
<title><![CDATA[[Education] Answers to the questions on Genetic susceptibility to occupational exposures by D C Christiani, A J Mehta and C-L Yu, on pages 430-6.]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/397?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:title><![CDATA[[Education] Answers to the questions on Genetic susceptibility to occupational exposures by D C Christiani, A J Mehta and C-L Yu, on pages 430-6.]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>397</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>397</prism:startingPage>
<prism:section>Education</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/398?rss=1">
<title><![CDATA[[Original articles] A normative study of levels of uranium in the urine of British Forces personnel]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/398?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>The UK Ministry of Defence (MoD) controls a biological monitoring programme that includes testing for uranium in personnel who served in the conflict in Iraq in 2003. To help interpret the results, the MoD commissioned this study to quantify a normative reference distribution of urinary uranium concentrations in military personnel who had not served in that conflict.</p>
</sec>
<sec><st>Methods:</st>
<p>The study selected and visited various military establishments to recruit a representative mix of ranks, genders and occupational groups (combat, support and auxiliary). A standardised protocol and recruitment questionnaire were used. The 125 ml spot urine samples collected were analysed for uranium and creatinine concentrations and (where possible) for uranium isotope <sup>238</sup>U/<sup>235</sup>U ratio.</p>
</sec>
<sec><st>Results:</st>
<p>Samples from 732 eligible subjects were analysed. Adjusted uranium concentrations ranged up to 556 ng.g<sup>&ndash;1</sup> creatinine, somewhat higher than reference values quoted for the USA but much lower than recorded in granite areas such as Finland. Isotope ratio measurements were available for 125 samples (17%) with the highest concentrations; these all had a natural isotope signature and no evidence of depleted uranium (DU). On average, urinary uranium concentrations were somewhat lower in officers than in other ranks; they differed also across the services, the Navy being lowest and the Army highest. The levels give no concern regarding health risks in the personnel studied.</p>
</sec>
<sec><st>Conclusion:</st>
<p>Since even the highest values were from natural sources, we assume the differences represent differences in ingestion of natural uranium. Definition of a reference distribution or normal values will depend on the subpopulation of interest.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Miller, B G, Colvin, A P, Hutchison, P A, Tait, H, Dempsey, S, Lewis, D, Soutar, C A]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1136/oem.2007.033381</dc:identifier>
<dc:title><![CDATA[[Original articles] A normative study of levels of uranium in the urine of British Forces personnel]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>403</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>398</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/404?rss=1">
<title><![CDATA[[Original articles] Exposures and reported symptoms associated with occupational deployment to the Buncefield fuel depot fire, England 2005]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/404?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>An explosion at the Buncefield fuel depot outside London occurred on 11 December 2005. We conducted a retrospective cohort study of airborne exposures and health status for workers deployed.</p>
</sec>
<sec><st>Methods:</st>
<p>Deployed individuals were identified through their occupational health departments. We sent a self-completion questionnaire asking about health symptoms during the burn and post-burn phases. The prevalence of health symptoms in workers was compared to symptoms in local residents not under the smoke plume.</p>
</sec>
<sec><st>Results:</st>
<p>Of 1949 eligible individuals, 815 returned questionnaires (response rate 44%). Respiratory protection was used by 39%. Symptoms were reported by 41% of individuals during the burn phase compared with 26% in the post-burn phase. In a final multivariable model, reporting of any symptoms was associated with deployment inside the inner fire cordon during the burn phase (OR 2.07, 95% CI 1.24 to 3.47) and wearing a face mask (OR 2.33, 95% CI 1.67 to 3.26). Compared with the general public, eye irritation (prevalence ratio (PR) 2.1, 95% CI 1.5 to 3.0), coughing (PR 1.3, 95% CI 1.0 to 1.8) and headaches (PR 1.7, 95% CI 1.2 to 2.5) were more common in workers deployed during the burn phase but not the post-burn phase.</p>
</sec>
<sec><st>Conclusions:</st>
<p>Increased reporting of symptoms close to the fire during the burn phase was consistent with increased exposure to products of combustion, although no major acute illness was reported. That only a minority of individuals used face masks, which were not protective for symptoms, raises questions about the availability of adequate respiratory protection for such incidents.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Morgan, O, Verlander, N Q, Kennedy, F, Moore, M, Birch, S, Kearney, J, Lewthwaite, P, Lewis, R, O'Brian, S, Osman, J, Reacher, M]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1136/oem.2007.035303</dc:identifier>
<dc:title><![CDATA[[Original articles] Exposures and reported symptoms associated with occupational deployment to the Buncefield fuel depot fire, England 2005]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>411</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>404</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/412?rss=1">
<title><![CDATA[[Original articles] Arterial structure and function and environmental exposure to cadmium]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/412?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>Few studies have addressed the effect of cadmium toxicity on arterial properties.</p>
</sec>
<sec><st>Methods:</st>
<p>We investigated the possible association of 24 h urinary cadmium excretion (an index of lifetime exposure) with measures of arterial function in a randomly selected population sample (n = 557) from two rural areas with low and high environmental exposure to cadmium.</p>
</sec>
<sec><st>Results:</st>
<p>24 h urinary cadmium excretion was significantly higher in the high compared with the low exposure group (p&lt;0.001). Even though systolic (p = 0.42), diastolic (p = 0.14) and mean arterial pressure (p = 0.68) did not differ between the high and low exposure groups, aortic pulse wave velocity (p = 0.008), brachial pulse pressure (p = 0.026) and femoral pulse pressure (p = 0.008) were significantly lower in the high exposure group. Additionally, femoral distensibility (p&lt;0.001) and compliance (p = 0.001) were significantly higher with high exposure. Across quartiles of 24 h urinary cadmium excretion (adjusted for sex and age), brachial (p for trend = 0.015) and femoral (p for trend = 0.018) pulse pressure significantly decreased and femoral distensibility (p for trend = 0.008) and compliance (p for trend = 0.007) significantly increased with higher cadmium excretion. After full adjustment, the partial regression coefficients confirmed these associations. Pulse wave velocity (&beta; = &ndash;0.79&plusmn;0.27; p = 0.004) and carotid (&beta; = &ndash;4.20&plusmn;1.51; p = 0.006), brachial (&beta; = &ndash;5.43&plusmn;1.41; p = 0.001) and femoral (&beta; = &ndash;4.72&plusmn;1.74; p = 0.007) pulse pressures correlated negatively, whereas femoral compliance (&beta; = 0.11&plusmn;0.05; p = 0.016) and distensibility (&beta; = 1.70&plusmn;0.70; p = 0.014) correlated positively with cadmium excretion.</p>
</sec>
<sec><st>Conclusion:</st>
<p>Increased cadmium body burden is associated with lower aortic pulse wave velocity, lower pulse pressure throughout the arterial system, and higher femoral distensibility.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Schutte, R, Nawrot, T, Richart, T, Thijs, L, Roels, H A, Van Bortel, L M, Struijker-Boudier, H, Staessen, J A]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1136/oem.2007.035576</dc:identifier>
<dc:title><![CDATA[[Original articles] Arterial structure and function and environmental exposure to cadmium]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>419</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>412</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/419?rss=1">
<title><![CDATA[[Miscellanea] New test discloses inflammation in asbestosis non-invasively]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/419?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:title><![CDATA[[Miscellanea] New test discloses inflammation in asbestosis non-invasively]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>419</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>419</prism:startingPage>
<prism:section>Miscellanea</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/420?rss=1">
<title><![CDATA[[Original articles] Maternal exposure to water disinfection by-products during gestation and risk of hypospadias]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/420?rss=1</link>
<description><![CDATA[
<sec><st>Background:</st>
<p>The use of chlorine for water disinfection results in the formation of numerous contaminants called disinfection by-products (DBPs), which may be associated with birth defects, including urinary tract defects.</p>
</sec>
<sec><st>Methods:</st>
<p>We used Arkansas birth records (1998&ndash;2002) to conduct a population-based case-control study investigating the relationship between hypospadias and two classes of DBPs, trihalomethanes (THM) and haloacetic acids (HAA). We utilised monitoring data, spline regression and geographical information systems (GIS) to link daily concentrations of these DBPs from 263 water utilities to 320 cases and 614 controls. We calculated ORs for hypospadias and exposure to DBPs between 6 and 16 weeks&rsquo; gestation, and conducted subset analyses for exposure from ingestion, and metrics incorporating consumption, showering and bathing.</p>
</sec>
<sec><st>Results:</st>
<p>We found no increase in risk when women in the highest tertiles of exposure were compared to those in the lowest for any DBP. When ingestion alone was used to assess exposure among a subset of 40 cases and 243 controls, the intermediate tertiles of exposure to total THM and the five most common HAA had ORs of 2.11 (95% CI 0.89 to 5.00) and 2.45 (95% CI 1.06 to 5.67), respectively, compared to women with no exposure. When exposure to total THM from consumption, showering and bathing exposures was evaluated, we found an OR of 1.96 (95% CI 0.65 to 6.42) for the highest tertile of exposure and weak evidence of a dose&ndash;response relationship.</p>
</sec>
<sec><st>Conclusions:</st>
<p>Our results provide little evidence for a positive relationship between DBP exposure during gestation and an increased risk of hypospadias but emphasise the necessity of including individual-level data when assessing exposure to DBPs.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Luben, T J, Nuckols, J R, Mosley, B S, Hobbs, C, Reif, J S]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1136/oem.2007.034256</dc:identifier>
<dc:title><![CDATA[[Original articles] Maternal exposure to water disinfection by-products during gestation and risk of hypospadias]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>429</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>420</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/428?rss=1">
<title><![CDATA[[PostScript] What can be learned from the Japanese study of mobile phone use and acoustic neuroma?]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/428?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kundi, M]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:title><![CDATA[[PostScript] What can be learned from the Japanese study of mobile phone use and acoustic neuroma?]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>428</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>428</prism:startingPage>
<prism:section>PostScript</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/428-a?rss=1">
<title><![CDATA[[PostScript] Authors' reply]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/428-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Takebayashi, T, Akiba, S, Kikuchi, Y, Taki, M, Wake, K, Watanabe, S, Yamaguchi, N]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:title><![CDATA[[PostScript] Authors' reply]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>428</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>428</prism:startingPage>
<prism:section>PostScript</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/428-b?rss=1">
<title><![CDATA[[PostScript] New occupational threats to Japanese physicians: karoshi (death due to overwork) and karojisatsu (suicide due to overwork)]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/428-b?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Hiyama, T, Yoshihara, M]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1136/oem.2007.037473</dc:identifier>
<dc:title><![CDATA[[PostScript] New occupational threats to Japanese physicians: karoshi (death due to overwork) and karojisatsu (suicide due to overwork)]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>429</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>428</prism:startingPage>
<prism:section>PostScript</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/full/65/6/430?rss=1">
<title><![CDATA[[Education] Genetic susceptibility to occupational exposures]]></title>
<link>http://oem.bmj.com/cgi/content/full/65/6/430?rss=1</link>
<description><![CDATA[
<p>Because of their high prevalence in the general population, genetic variants that determine susceptibility to environmental exposures may contribute greatly to the development of occupational diseases in the setting of specific exposures occurring in the workplace. Studies investigating genetic susceptibilities in the workplace may: (1) provide mechanistic insight into the aetiology of disease, in particular the determination of environmentally responsive genes; (2) identify susceptible subpopulations with respect to exposure; and (3) provide valuable input in setting occupational exposure limits by taking genetic susceptibility into account. Polymorphisms in the <I>NAT2</I> and the <I>HLA-DPB1<sup>G</sup><sup>lu69</sup> </I>genes provide classic examples of how genetic susceptibility markers have a clear role in identifying disease risk in bladder cancer and chronic beryllium disease, respectively. For diseases with more complex and multifactorial aetiology such as occupational asthma and chronic airways disease, susceptibility studies for selected genetic polymorphisms provide additional insight into the biological mechanisms of disease. Even when polymorphisms for genetic susceptibility have a clear role in identifying disease risk, the value of wide scale genetic screening in occupational settings remains limited due to primarily ethical and social concerns. Thus, large scale genetic screening in the workplace is not currently recommended.</p>
]]></description>
<dc:creator><![CDATA[Christiani, D C, Mehta, A J, Yu, C-L]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1136/oem.2007.033977</dc:identifier>
<dc:title><![CDATA[[Education] Genetic susceptibility to occupational exposures]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>65</prism:volume>
<prism:endingPage>436</prism:endingPage>
<prism:publicationDate>2008-06-01</prism:publicationDate>
<prism:startingPage>430</prism:startingPage>
<prism:section>Education</prism:section>
</item>

</rdf:RDF>