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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/short/oem.2008.042788v1?rss=1">
<title><![CDATA[APPLICATION OF OMICS TECHNOLOGIES IN OCCUPATIONAL AND ENVIRONMENTAL HEALTH RESEARCH; CURRENT STATUS AND PROJECTIONS]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.042788v1?rss=1</link>
<description><![CDATA[
<p>OMICS technologies are relatively new biomarker discovery tools that can be applied to study large sets of biological molecules. Their application in human observational studies (HOS) has become feasible in recent years due to a spectacular increase in the sensitivity, resolution and throughput of OMICS based assays. Although, the number of OMIC techniques is ever expanding, the five most developed OMICS technologies are genotyping, transcriptomics, epigenomics, proteomics and metabolomics. These techniques have been applied in HOS to various extents. However, their application in Occupational Environmental Health (OEH) research has been limited. Here, we will discuss the opportunities these new techniques provide for OEH research. In addition we will address difficulties and limitations to the interpretation of the data that is generated by OMICS technologies. To illustrate the current status of the application of OMICS in OEH research, we will provide examples of studies that used OMICS technologies to investigate human health effects of two well known toxicants, benzene and arsenic.</p>
]]></description>
<dc:creator><![CDATA[Vlaanderen, J., Moore, L. E, Smith, M. T, Lan, Q., Zhang, L., Skibola, C. F, Rothman, N., Vermeulen, R.]]></dc:creator>
<dc:date>Fri, 20 Nov 2009 03:58:59 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.042788</dc:identifier>
<dc:title><![CDATA[APPLICATION OF OMICS TECHNOLOGIES IN OCCUPATIONAL AND ENVIRONMENTAL HEALTH RESEARCH; CURRENT STATUS AND PROJECTIONS]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-20</prism:publicationDate>
<prism:section>Education</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.051219v1?rss=1">
<title><![CDATA[OMICS technologies: an opportunity for "two-way" translation from basic science to both clinical and population-based research]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.051219v1?rss=1</link>
<description><![CDATA[
<p>Vlaanderen and colleagues<sup>1</sup> provide a timely summary of how OMICS technologies can be applied to research into the health effects of occupational and environmental exposures. The type of exciting advances being made in understanding pathogenesis at the molecular level is well-illustrated by recent discoveries concerning epigenetic mechanisms of carcinogenesis<sup>2</sup>. This accumulation of mechanistic knowledge is, in part at least, based on the technological advances of the various OMICS platforms summarised in the accompanying article.</p>
]]></description>
<dc:creator><![CDATA[Wild, C. P.]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 22:07:16 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.051219</dc:identifier>
<dc:title><![CDATA[OMICS technologies: an opportunity for "two-way" translation from basic science to both clinical and population-based research]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Editorial</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.050344v1?rss=1">
<title><![CDATA[Dermal exposure to polycyclic aromatic hydrocarbons in asphalt workers]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.050344v1?rss=1</link>
<description><![CDATA[
<p><b>Objectives:</b> To assess dermal exposure to 16 polycyclic aromatic hydrocarbons (PAHs) in asphalt workers by applying polypropylene pads to six body sites (neck, shoulder, upper arm, wrist, groin, ankle), to identify the compounds and exposure sites most representative of total PAH exposure, and to integrate dermal exposure results with environmental and biological data.</p>
<p> <b>Methods:</b> Twenty-four asphalt workers were recruited. Dermal exposure was assessed during a single work shift. Sixteen PAHs (from naphthalene to indeno[1,2,3-cd]pyrene) were quantified via large-injection-volume gas chromatography-mass spectrometry (limit of quantification from 0.010 to 0.044 ng/cm<sup>2</sup>). Personal airborne exposure, urinary PAHs and monohydroxy metabolites were also investigated.</p>
<p> <b>Results:</b> Phenanthrene (PHE),  present in 100% of the samples, was the most abundant compound (median 0.805-1.825 ng/cm<sup>2</sup>). High-molecular weight analytes were present in a smaller fraction of the samples, i.e. benzo[a]pyrene (BaP) was present in 75% of the samples (0.046-0.101 ng/cm2).  Wrist had the highest total PAH contamination, with median PHE, pyrene (PYR), and BaP concentrations of 1.825, 0.527, and 0.063 ng/cm<sup>2</sup>. PHE and PYR in wrist samples correlated with almost all 3- to 4-ring PAHs (0.405&le;0.856), but not with BaP; BaP correlated with almost all 4- to 6- ring PAHs (0.584&le;0.633). Significant correlations were observed between PHE level, airborne exposure, and the corresponding urinary PHE and monohydroxy metabolites. In the case of PYR, significant correlations existed only between urinary PYR and monohydroxy metabolites. Multiple linear regression analysis revealed that 42% of the end-of-shift monohydroxy metabolites were the result of airborne exposure, dermal exposure, and baseline levels of biomarkers.</p>
<p> <b>Conclusions:</b> Dermal exposure to PAHs was in the low ng/cm2 range. PHE or PYR and BaP were the most representative compounds and the wrist was the best location to perform dermal exposure assessments. Both dermal and airborne exposure contributed to the total body burden of PAHs, though the relative contribution was analyte-dependent.</p>
]]></description>
<dc:creator><![CDATA[Fustinoni, S., Campo, L., Cirla, P. E., Martinotti, I., Buratti, M., Longhi, O., Foa, V., Bertazzi, P.]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 22:02:01 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.050344</dc:identifier>
<dc:title><![CDATA[Dermal exposure to polycyclic aromatic hydrocarbons in asphalt workers]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.050583v1?rss=1">
<title><![CDATA[Selecting an appropriate biomonitoring strategy to evaluate dermal exposure to opioid narcotic analgesics in pharmaceutical production workers]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.050583v1?rss=1</link>
<description><![CDATA[
<p><b>Objectives:</b> In follow-up of a previous study, in which exposure pathways for opioid narcotic analgesics were identified in pharmaceutical workers involved in drug synthesis, the current study focused on the selection of an appropriate biomonitoring strategy.</p>
<p><b>Methods:</b> Six opioid narcotic production workers were intensively monitored during a (one week) fentanyl production campaign. A systematic sampling scheme was followed that provided information about hand contamination and biomarker levels at multiple points in time.</p>
<p><b>Results:</b> Linear mixed-effects models, incorporating half-shift and end-of-shift hand contamination levels, showed a positive and significant correlation with fentanyl urinary excretion occurring at numerous of the different 4h period investigated time lags (4 to 28h). Optimum model characteristics, including both minimal between- and within-worker variability were obtained at a lag time of 24h and 20h respectively, implicating a pre-shift urine sampling strategy on the following working day. For these lag-times also the portion of the variability explained by the model was maximal. Furthermore, using a distributed lag model, it was demonstrated that urinary fentanyl levels were positively correlated with hand contamination levels of the preceding four 8h-period time lags (8 to 32h), although statistical significance was only shown for a lag time of 24h.</p>
<p><b>Conclusion:</b> Fentanyl levels in pre-shift urine samples reflect the compound&rsquo;s dermal exposure during the previous day. Thus, in the specific working environment investigated, a biological monitoring protocol evaluating pre-shift urinary fentanyl levels could provide an adequate risk estimate in individual workers.</p>
]]></description>
<dc:creator><![CDATA[Van Nimmen, N. F J, Poels, K. L C, Severi, M., Godderis, L., Veulemans, H. A F]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 22:00:52 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.050583</dc:identifier>
<dc:title><![CDATA[Selecting an appropriate biomonitoring strategy to evaluate dermal exposure to opioid narcotic analgesics in pharmaceutical production workers]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.048702v1?rss=1">
<title><![CDATA[An approach for estimating the health effects of changes over time in air pollution: an illustration using cardio-respiratory hospital admissions in London]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.048702v1?rss=1</link>
<description><![CDATA[
<p><b>Objectives:</b> First, we present a general analytical approach to estimating the association between medium-term changes in air pollution and health across small areas.  As a specific illustration, we then applied the approach to data on London residents from a four-year period to test whether reductions in traffic-related air pollution were associated with reductions in cardio-respiratory hospital admissions. </p>
<p><b>Methods:</b> A binomial distribution was used to model change in admissions over time in each small area, which was measured as the proportion of admissions in 2003-04 out of admissions over all study years (2001-04). Annual average concentrations of nitrogen oxides (NOx) were modelled using an emissions-dispersion model.  The association between change in NOx and change in hospital admissions was estimated using logistic regression and an instrumental variable approach. </p>
<p><b>Results:</b> For some diagnostic groups, suggestive associations between reductions in NOx and reductions in admissions were observed, for example, OR=0.97(0.96-0.99) for an IQR decrease in NOx (3 &micro;g/m3) and all respiratory admissions.  Accounting for spatial dependence attenuated several of the associations, for respiratory admissions, the OR was 1.00(0.98-1.02), leaving only that for bronchiolitis significant (OR=0.91(0.84-0.99)).  In this particular illustration, the instrumental variable approach did not appear to add information.</p>
<p><b>Conclusions:</b> In this illustration, there was relatively limited power to detect an association between changes in air pollution and hospital admissions over time. However, the analytical approach could deliver more robust estimates of the health effects of changes in air pollution in settings with greater spatial contrast in changes in air pollution over time.</p>
]]></description>
<dc:creator><![CDATA[Tonne, C., Beevers, S., Kelly, F., Jarup, L., Wilkinson, P., Armstrong, B. G]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 22:08:38 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.048702</dc:identifier>
<dc:title><![CDATA[An approach for estimating the health effects of changes over time in air pollution: an illustration using cardio-respiratory hospital admissions in London]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.045096v1?rss=1">
<title><![CDATA[Employee control over working times and risk of cause-specific disability pension: the Finnish Public Sector Study]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.045096v1?rss=1</link>
<description><![CDATA[
<p><b>Objective:</b> To examine the association between worktime control and subsequent retirement on health ground (disability pension) among employees. </p>
<p><b>Methods:</b> A prospective cohort study of 30 700 public sector employees (78% women) aged 18 to 64 at baseline. Two scores of worktime control (self-assessed and co-worker assessed), were obtained from responses to the baseline survey in 2000-2001 (score range 1 to 5). Information on cause-specific disability pension during follow-up was collected from national registers.</p>
<p><b>Results:</b> During a mean follow-up of 4.4 years, 1178 employees were granted disability pension (incidence per 1000 person-years 9.2 in women and 8.7 in men). The most common causes of a disability pension were musculoskeletal disorders (43% of all pensions), mental disorders (25%), tumours (8%), and diseases of the circulatory system (6%) and the nervous system (6%). A 1 unit increase in self-assessed and co-worker assessed worktime control score was associated with a 41-48% lowering of the risk of disabling musculoskeletal disorders in men and 33-35% lowering in women. This association was robust to adjustment for all 17 baseline covariates (in men and women combined, adjusted hazard ratio 0.76, 95% CI 0.67-0.87 and 0.64, 95% CI 0.51-0.79 per 1 unit increase in self-assessed and co-worker assessed worktime control, respectively).Self-assessed worktime control was also associated with the risk of disability retirement due to mental disorders in women, but this association was not replicated using co-workers' assessment. Disability pensions from other disease categories were not related to control over working times.</p>
<p><b>Conclusions:</b> In this cohort of public sector employees, high worktime control was associated with reduced risk of early retirement caused by musculoskeletal disorders independent of baseline characteristics.</p>
]]></description>
<dc:creator><![CDATA[Vahtera, J., Laine, S., Virtanen, M., Oksanen, T., Koskinen, A., Pentti, J., Kivimaki, M.]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 22:05:36 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.045096</dc:identifier>
<dc:title><![CDATA[Employee control over working times and risk of cause-specific disability pension: the Finnish Public Sector Study]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.044560v1?rss=1">
<title><![CDATA[Agreement in diagnosing occupational asthma by occupational and respiratory physicians who report to surveillance schemes for work-related ill-health]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.044560v1?rss=1</link>
<description><![CDATA[
<p><b>Objectives:</b> To assess diagnostic agreement for occupational asthma (OA) by physicians within and between clinical disciplines, and to identify case and rater characteristics associated with making an OA diagnosis. </p>
<p><b>Methods:</b> Anonymised summaries for 19 possible OA cases were sent to 51 occupational physicians (OPs) and 53 respiratory physicians (RPs). In phase 1, raters were asked to assign a likelihood score (0-100%) of OA for 4 case histories; in phase 2, raters were asked again after seeing investigative procedures/results for 2 of their cases. Interclass correlation coefficients were calculated as statistical measures of reliability for OA scores. Comparisons between mean scores for OPs and RPs were assessed for statistical significance using tests based on multilevel models.  Relative risks were calculated to summarise  effects of raters' demographics on OA diagnosis, and of supplying investigative procedures/results.  </p>
<p><b>Results:</b> OA scores from OPs and RPs were not systematically different. Mean overall OA scores from phase 1 were 52.1% (OPs) and 50.0% (RPs), the difference (OPs'-RPs'mean) was 2.1% (95%CI: -2.6,6.8 p=0.37). In phase 2, mean overall OA scores for OPs and RPs were 46.1% and 41.5%; the difference (OPs'-RPs'mean) was 4.6% (95%CI: -3.5,12.5 p=0.27). Raters with GMC registration &ge;1986 were more likely to give a positive OA diagnosis, and in phase 2 males were much more likely to label a case as OA than females RR=4.5 (95%CI;3.3-6.0).  </p>
<p><b>Conclusions:</b> The RR of a positive OA diagnosis was not affected by clinical specialty (OP/RP), however there was only limited agreement between physicians within each group. Further work on what triggers physicians to consider a case as OA will assist better diagnosis and prevention of this disease.</p>
]]></description>
<dc:creator><![CDATA[Turner, S., McNamee, R., Roberts, C., Bradshaw, L., Curran, A., Francis, M., Fishwick, D., Agius, R.]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 22:04:19 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.044560</dc:identifier>
<dc:title><![CDATA[Agreement in diagnosing occupational asthma by occupational and respiratory physicians who report to surveillance schemes for work-related ill-health]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.050096v1?rss=1">
<title><![CDATA[Is silicosis becoming more frequent in coal miners?-Cohen]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.050096v1?rss=1</link>
<description><![CDATA[
<p>Commissioned commentary for Laney, Petsonk, and Attfield article.</p>
]]></description>
<dc:creator><![CDATA[Cohen, R. A]]></dc:creator>
<dc:date>Wed, 11 Nov 2009 21:37:29 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.050096</dc:identifier>
<dc:title><![CDATA[Is silicosis becoming more frequent in coal miners?-Cohen]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-11</prism:publicationDate>
<prism:section>Commentaries (Commission Only)</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.047977v1?rss=1">
<title><![CDATA[Solvent Exposure and Cognitive Ability at Age 67: A Follow-Up Study of the 1947 Scottish Mental Survey.]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.047977v1?rss=1</link>
<description><![CDATA[
<p><b>Objectives:</b> Organic solvent exposure may be associated with cognitive impairment in later life although the evidence for this association is inconsistent. This study sought to examine the association between organic solvent exposure and cognitive function in later life. </p>
<p><b>Methods:</b> A prospective longitudinal study set in Aberdeen, Scotland involved 336 men and women born in 1936 who participated in the 1947 Scottish Mental Survey. Cognitive function, aged 67 years, was measured using Trail Making Test B (TMT B), digit symbol (DS), and auditory verbal learning test (AVLT). Occupational hygienists reviewed occupational histories, blind to cognitive function, and estimated lifetime solvent exposures.  Multiple regression analyses were employed to explore the association between solvent exposure and cognitive performance after adjustment for confounders. </p>
<p><b>Results:</b> After adjusting for childhood IQ, smoking, alcohol and sex, the solvent-exposed group took on average almost 10 seconds longer than the unexposed to complete TMT B, a highly significant difference. For DS, after adjusting for childhood IQ, smoking and gender, the exposed group scored on average two points lower than the unexposed, again highly significant. There was no evidence of an effect for cumulative solvent exposure on TMT B or DS. For AVLT there were no significant differences associated with exposure. </p>
<p><b>Conclusions:</b> This study, of subjects with generally low exposures, found no clear evidence of an association between solvent exposure and cognitive function.</p>
]]></description>
<dc:creator><![CDATA[Dick, F. D, Bourne, V. J, Semple, S., Fox, H. C, Miller, B. G, Deary, I. J, Whalley, L. J]]></dc:creator>
<dc:date>Wed, 11 Nov 2009 21:38:37 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.047977</dc:identifier>
<dc:title><![CDATA[Solvent Exposure and Cognitive Ability at Age 67: A Follow-Up Study of the 1947 Scottish Mental Survey.]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-11</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.052860v1?rss=1">
<title><![CDATA[Mesothelioma Risk From Chrysotile]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.052860v1?rss=1</link>
<description><![CDATA[
<p>E-letter on 'Lung cancer mortality and fibre exposures among North Carolina asbestos textile workers' titled 'Mesothelioma risk from chrysotile'</p>
]]></description>
<dc:creator><![CDATA[Hodgson, J. T., Darnton, A.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 21:41:16 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.052860</dc:identifier>
<dc:title><![CDATA[Mesothelioma Risk From Chrysotile]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-10</prism:publicationDate>
<prism:section>Letters</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.050120v1?rss=1">
<title><![CDATA[Asbestos fiber dimensions and lung cancer mortality among workers exposed to chrysotile]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.050120v1?rss=1</link>
<description><![CDATA[
<p><b>Objectives:</b> To estimate exposures to asbestos fibers of specific sizes among asbestos textile manufacturing workers exposed to chrysotile using data from transmission electron microscopy (TEM) and to evaluate the extent to which the risk of lung cancer varies with fiber length and diameter.  </p>
<p><b>Methods:</b> 3803 workers employed for at least 1 day between 1 January 1950 and 31 December 1973 in any of 3 plants in North Carolina, USA that produced asbestos textile products and followed for vital status through 31 December 2003 were included.  Historical exposures to asbestos fibers were estimated from work histories and 3578 industrial hygiene measurements taken 1935-1986.  Exposure-response relations for lung cancer were examined within the cohort using Poisson regression. </p>
<p><b>Results:</b> Indicators of fiber length and diameter obtained by TEM were positively and significantly associated with increasing risk of lung cancer.  Exposures to longer and thinner fibers tended to be most strongly associated with lung cancer, and models for these fibers fit the data best.  Simultaneously modeling indicators of cumulative mean fiber length and diameter yielded a positive coefficient for fiber length and a negative one for fiber diameter.</p>
<p><b>Conclusions:</b> The results support the hypothesis that the risk of lung cancer among workers exposed to chrysotile asbestos increases with exposure to longer fibers.  More research is needed to improve the characterization of exposures by fiber size and number and to analyze the associated risks in a variety of industries and populations.</p>
]]></description>
<dc:creator><![CDATA[Loomis, D., Dement, J., Richardson, D., Wolf, S.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 20:29:43 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.050120</dc:identifier>
<dc:title><![CDATA[Asbestos fiber dimensions and lung cancer mortality among workers exposed to chrysotile]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-05</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.048785v3?rss=1">
<title><![CDATA[Ambient particulate pollution and the world-wide prevalence of asthma, rhinoconjunctivitis and eczema in children: Phase One of the International Study of Asthma and Allergies in Childhood (ISAAC)]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.048785v3?rss=1</link>
<description><![CDATA[
<p><b>Objectives:</b> To investigate the role of ambient particulate matter in explaining international variations in the prevalence of asthma, rhinoconjunctivitis and eczema in children.</p>
<p><b>Methods:</b> The prevalence of symptoms and diagnoses of asthma, rhinoconjunctivitis and eczema obtained in Phase One of the International Study of Asthma and Allergies in Childhood (ISAAC) were matched with city-level estimates of particulate matter with aerodynamic diameter &lt; 10&micro;m (PM10) obtained from a World Bank model.  Associations were investigated using a binomial regression model which adjusted for Gross National Product per capita and for clustering within country.  For countries with more than one centre a two stage meta-analysis was done.  The results were compared with a meta-analysis of published multi-centre studies.</p>
<p><b>Results:</b> Annual concentrations of PM10 at city level were obtained for 105 ISAAC centres in 51 countries.  After controlling for GNP per capita, there was a weak negative association between PM10 and the various outcomes.  For severe wheeze in the 13-14 year age group, the odds ratio for a 10 &micro;g/m3 increase in PM10 was 0.92 (95% CI 0.84,1.00).  In 24 countries with more than one centre, most of the summary estimates for within-country associations were weakly positive.  For severe wheeze in the 13-14 year age group, the summary odds ratio for a 10 &micro;g/m3 increase in PM10 was 1.01 (0.92,1.10).  This result was close to a summary odds ratio of 0.99 (0.91,1.06) obtained from published multi centre studies.</p>
<p><b>Conclusions:</b> Modelled estimates of PM at city level will necessarily be imprecise and incomplete estimates of personal exposure to ambient air pollutants.  Nevertheless, the results of this world-wide ecological analysis, together with those of previous multicentre studies, suggest that urban background PM10 has little or no association with the prevalence of childhood asthma, rhinoconjunctivitis or eczema either within or between countries.</p>
]]></description>
<dc:creator><![CDATA[Anderson, H. R., Ruggles, R., Pandey, K. D, Kapetenakis, V., Brunekreef, B., Lai, C. K W, Strachan, D. P, Weiland, S. K]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 01:46:26 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.048785</dc:identifier>
<dc:title><![CDATA[Ambient particulate pollution and the world-wide prevalence of asthma, rhinoconjunctivitis and eczema in children: Phase One of the International Study of Asthma and Allergies in Childhood (ISAAC)]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-05</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046227v3?rss=1">
<title><![CDATA[The work-related burden of injury in a rapidly industrializing commune in Viet Nam]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046227v3?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Health and injury surveillance data of the highest achievable quality is needed in order to appropriately allocate scarce resources at the local and national levels.</p>
<p><b>Methods:</b> This study is the first reported surveillance study of injury using a complete community sample in Viet Nam.  The workplaces in Xuan Tien commune most likely to benefit from intervention were identified and ranked by the magnitude of the problem (or highest injury count workplaces or jobs), the risk (or highest incidence rates) and the burden (or the effect of injuries on the livelihoods of the workers).</p>
<p> <b>Results:</b> Five hundred ninety-one injuries were recalled in the one month prior to survey administration, which satisfied the injury case criteria of this study (the annualized incidence rate (IR) was 681 per 1000 residents).  Four hundred eighty-two were attributed to work activities (82%), yielding an annualized IR of 1001/1000 Full Time Equivalent workers (FTEs)).  The highest number of injuries occurred in the manufacturing sector (n = 299) followed by agriculture, second in rank with many fewer injuries (n = 70).  The highest rate of injury was in the transport, storage and communications sector (annualized IR = 1,583/1000 FTE) followed by manufacturing (1,235/1000 FTE); agriculture ranked third (844/1000 FTE).</p>
<p> <b>Conclusion:</b> This study identified patterns of risk which, because of the consideration of work culture and resultant data collection methods, are believed to be more reliable than those from previous studies.  Interventions in the manufacture of machinery and equipment sector (the largest industry in the commune) would have the most impact on reducing occupational injuries.  Despite the trend towards manufacturing, agriculture is still a high priority, and its impact will likely be substantial for many years.</p>
]]></description>
<dc:creator><![CDATA[Marucci-Wellman, H., Leamon, T. B, Binh, T. T. T., Diep, N. B., Willetts, J. L, Wegman, D. H, Kriebel, D.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 01:45:17 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046227</dc:identifier>
<dc:title><![CDATA[The work-related burden of injury in a rapidly industrializing commune in Viet Nam]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-05</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.048249v1?rss=1">
<title><![CDATA[Musculoskeletal pain at multiple sites and its effects on work ability in a general working population]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.048249v1?rss=1</link>
<description><![CDATA[
<p><b>Objectives:</b> Musculoskeletal pain often occurs at multiple sites concurrently. The aim of this study was to examine the associations between multi-site pain and self-rated work ability and retirement plans among actively working people. </p>
<p><b>Methods:</b> A comprehensive health examination survey (The Health 2000 Survey) was carried out in 2000-2001 among a representative sample of the Finnish adults. Musculoskeletal pain during the preceding month in the low back, neck or shoulders, upper extremities, hips and lower extremities, as well as work ability and intentions to retire early were assessed with a face-to-face interview. The subjects were also clinically examined by a physician using standardized diagnostic criteria. Analyses were restricted to 30-64-year-old subjects actively working during the preceding 12 months and who provided information on the work ability outcomes (population-weighted number of subjects 4087). Log-binomial regression was used to estimate prevalence ratios of reduced work ability. </p>
<p><b>Results:</b> Single-site pain was reported by 33% of the subjects, whereas 20%, 9% and 4% reported pain in 2, 3 and 4 sites, respectively. The prevalence of poor work ability varied from 8 to 15%. Every fifth had thought about retiring early. Age- and gender-adjusted risks of poor physical work ability and own prognosis of poor future work ability increased from 2 for single-site pain to 8 for pain at 4 sites. Risks remained considerably elevated after adjustment for various covariates, even for clinical musculoskeletal disorders and functional capacity. Poor current work ability was most affected by multi-site pain at older age (50-64 years), and intentions to retire early at age 40-49 years. </p>
<p><b>Conclusions:</b> Co-occurring pain per se poses a considerable threat to work ability. Workers with multi-site pain may benefit from targeted preventive measures to sustain their work ability. Future studies should also consider multi-site pain as an important risk factor for reduced work ability.</p>
]]></description>
<dc:creator><![CDATA[Miranda, H., Kaila-Kangas, L., Heliovaara, M., Leino-Arjas, P., Haukka, E., Liira, J., Viikari-Juntura, E.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 21:51:03 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.048249</dc:identifier>
<dc:title><![CDATA[Musculoskeletal pain at multiple sites and its effects on work ability in a general working population]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-03</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.051136v1?rss=1">
<title><![CDATA[Increased bladder cancer risk among workers exposed to o-toluidine and aniline: A reanalysis]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.051136v1?rss=1</link>
<description><![CDATA[
<p><b>Introduction:</b> In 1991, the U.S. National Institute for Occupational Safety and Health (NIOSH) reported an increased bladder cancer risk in a cohort of 1749 workers potentially exposed to <I>o</I>-toluidine and aniline at a chemical manufacturing plant. Additional information showed that workers in certain departments had been misclassified regarding <I>o</I>-toluidine exposure; therefore, we conducted a reanalysis of the data using updated exposure categories. </p>
<p><b>Methods:</b> We updated exposure categories based on information ascertained during a plant walkthrough, documents on file at the plant, interviews with current and former employees, and answers provided by company and union officials on specific questions. Bladder cancer incidence was determined through 31 December 1988 and mortality through 31 December 1994. </p>
<p><b>Results:</b> Thirteen cases of bladder cancer were observed, versus 3.57 expected (New York State rates excluding New York City) [standardized incidence ratio (SIR) 3.64, 95% confidence interval (CI) 1.94-6.23]. Among workers classified as definitely exposed, increasing risks were observed for longer duration of employment [for &ge;10 years, standardized rate ratio (SRR) 6.07, 95% CI 0.77-48.17] and time since first employment in the exposed departments (for &ge;20 years, SRR 3.39, 95% CI 0.40-29.03). One bladder cancer death was observed among those definitely exposed. </p>
<p><b>Conclusions:</b> These findings are comparable to the results reported earlier by NIOSH, and confirm that workers in this plant have an increased risk of bladder cancer.</p>
]]></description>
<dc:creator><![CDATA[Carreon, T., Hein, M. J, Viet, S. M, Hanley, K. W, Ruder, A. M, Ward, E. M]]></dc:creator>
<dc:date>Mon, 02 Nov 2009 15:24:47 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.051136</dc:identifier>
<dc:title><![CDATA[Increased bladder cancer risk among workers exposed to o-toluidine and aniline: A reanalysis]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-02</prism:publicationDate>
<prism:section>Short Report</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.051201v1?rss=1">
<title><![CDATA[Air-pollution and congenital anomalies]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.051201v1?rss=1</link>
<description><![CDATA[
<p>Congenital anomalies, a leading cause of fetal loss, contribute significantly to preterm birth and childhood and adult morbidity. Serious structural defects are present in 3-8% of newborns worldwide and, while some can readily be attributed to chromosomal or syndromic disorders or known teratogenic or fetotoxic agents, a recent commentary maintained that causes for most anomalies remain a mystery.<sup>1</sup>  Maternal smoking during pregnancy has long been associated with birth defects<sup>2</sup> and numerous biologic pathways have been identified whereby particulate air pollutants might impact the placenta and fetus (reviewed in Kannan<sup>3</sup>) providing biologic rationale to the assessment of air pollution&rsquo;s influence on fetal development.  Although quantitatively lower than exposure from maternal smoking, exposure to ambient air toxics affects large populations and, importantly, is not modifiable by the individual; and thus of great public health and policy relevance.</p>
]]></description>
<dc:creator><![CDATA[Ritz, B.]]></dc:creator>
<dc:date>Mon, 02 Nov 2009 15:21:51 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.051201</dc:identifier>
<dc:title><![CDATA[Air-pollution and congenital anomalies]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-02</prism:publicationDate>
<prism:section>Editorial</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046193v1?rss=1">
<title><![CDATA[Air Pollution, Obesity, Genes, and Cellular Adhesion Molecules]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046193v1?rss=1</link>
<description><![CDATA[
<p><b>Objectives:</b> Particulate matter (PM) has been associated with acute cardiovascular outcomes, but our understanding of the mechanism is incomplete.  We examined the association between PM and cell adhesion molecules. We also investigated the modifying effect of genotype and phenotype variation to gain insight into the relevant biological pathways for this association.  </p>
<p><b>Methods:</b> We used mixed regression models to examine the association of PM2.5 and black carbon (BC) with serum concentrations of soluble Intercellular Adhesion Molecule (sICAM-1) and soluble Vascular Cell Adhesion Molecule (sVCAM-1), markers of endothelial function and inflammation, in a longitudinal study of 809 participants in the Normative Aging Study (1819 total observations).   We also examined whether this association was modified by genotype, obesity, or diabetes status. Genes selected for analyses were either related to oxidative stress, endothelial function, lipid metabolism or metal processing.  </p>
<p><b>Results:</b> BC during the 2 days prior to blood draw was significantly associated with increased sVCAM-1 (4.5% increase per 1&micro;g/m3 95% CI 1.1, 8.0).  Neither pollutant was associated with sICAM-1.  Larger effects of BC on sVCAM were seen in subjects with obesity (p=0.007) and who were GSTM1 null (p=0.02). </p>
<p><b>Conclusions:</b> BC is associated with markers of endothelial function and inflammation.  Genes related to oxidative defense may modify this association.</p>
]]></description>
<dc:creator><![CDATA[Madrigano, J., Baccarelli, A., Wright, R., Suh, H., Sparrow, D., Vokonas, P., Schwartz, J.]]></dc:creator>
<dc:date>Mon, 02 Nov 2009 15:23:17 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046193</dc:identifier>
<dc:title><![CDATA[Air Pollution, Obesity, Genes, and Cellular Adhesion Molecules]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-02</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.048660v1?rss=1">
<title><![CDATA[Air temperature and inflammatory and coagulation responses in men with coronary or pulmonary diseases during the winter season]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.048660v1?rss=1</link>
<description><![CDATA[
<p><b>Background and objective:</b> Air temperature changes have been associated with increased cardiovascular and respiratory risk, but the role of inflammation and coagulation markers in these relationships is not well understood. We investigated the associations between temperature and several blood markers in individuals with coronary heart disease (CHD) and pulmonary disease (PD). </p>
<p><b>Methods:</b> Two panel studies were conducted in Erfurt, Germany, in two subsequent winters. In total, 578 and 381 repeated blood measurements from 57 CHD and 38 PD patients were collected, respectively. Data on patient characteristics and disease history were gathered at the baseline visit. Meteorological data were collected from existing networks. Associations were analyzed using additive mixed models with random patient effects. Effect modification by diabetes status was investigated only in CHD patients, as only two diabetic individuals were part of the PD panel. </p>
<p><b>Results:</b> Mean daily air temperature varied between -13&deg;C and 16&deg;C in both study periods. A 10&deg;C decrease in the 5-day-average of temperature before the blood withdrawal led to an increase in platelet counts (%-change from the mean: 3.0%; 95%-confidence interval: [0.6%; 5.5%]) and fibrinogen (5.5%[1.3%; 9.7%]), and to no change in C-reactive protein in PD patients, whereas for CHD patients a decrease was observed. A two day delayed increase in factor VII in association with a temperature decrease was seen in CHD patients (4.9%[0.7%; 9.2%]), while PD patients showed no effect. The effects in CHD patients without diabetes were similar to those of the PD patients, whereas diabetic CHD patients showed a strong effect (12.1%[5.8%;18.9%]).</p>
<p><b>Conclusions:</b> The present study suggests that a temperature decrease is associated with a change in several blood parameters. The complex interplay of blood markers at low temperature may contribute to the observed association between cold and cardiovascular mortality and morbidity.</p>
]]></description>
<dc:creator><![CDATA[Hampel, R., Breitner, S., Ruckerl, R., Frampton, M. W, Koenig, W., Phipps, R. P, Wichmann, H E., Peters, A., Schneider, A.]]></dc:creator>
<dc:date>Mon, 02 Nov 2009 15:20:28 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.048660</dc:identifier>
<dc:title><![CDATA[Air temperature and inflammatory and coagulation responses in men with coronary or pulmonary diseases during the winter season]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-02</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.048231v1?rss=1">
<title><![CDATA[Perspectives on Research and Practice in Occupational and Environmental Health: The Case of Benzene]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.048231v1?rss=1</link>
<description><![CDATA[
<p>Readers of Occupational and Environmental Medicine (OEM) are quite familiar with reports that highlight clinical cases or workplace incidents that may represent sentinel events or exposures. There is a storied history of these in the field and there are countless examples of their utility and importance to physicians and researchers. Recently, when I was reviewing the Archives of OEM online ([http://oem.bmj.com/contents-by-date.0.dtl] - browsing this archive is an activity I highly recommend to all) I was struck by the considerable evidence of the active evolution of medicine and science. The archive is replete with published descriptions of occupational disease that, in retrospect, offer striking evidence of the incremental advance in the understanding of mechanism, diagnosis and prognosis in a large number of complex medical conditions. I was particularly attracted to two descriptions of the potential adverse effects of benzene exposure; the first presented in 1966 by the then 32 year old Finnish occupational physician and epidemiologist Sven Hernberg (1) and the second, a paper authored in 1971 by a group of Turkish hematologists headed by Muzaffer Aksoy (2). In 1966 benzene was suspected to be acutely quite toxic to the blood forming tissues and the American Conference of Governmental Hygienists threshold limit value for benzene exposure in the workplace was 25 ppm, having been lowered from35ppm in 1963.</p>
]]></description>
<dc:creator><![CDATA[Kelsey, K. T]]></dc:creator>
<dc:date>Mon, 02 Nov 2009 15:19:03 PST</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.048231</dc:identifier>
<dc:title><![CDATA[Perspectives on Research and Practice in Occupational and Environmental Health: The Case of Benzene]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-11-02</prism:publicationDate>
<prism:section>Editorial</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046953v1?rss=1">
<title><![CDATA[Increased risk of oesophageal adenocarcinoma among upstream petroleum workers]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046953v1?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p> To investigate the risk of major cancer types with a particular focus on oesophageal cancer among male upstream petroleum workers offshore potentially exposed to various carcinogenic agents.</p>
</sec>
<sec><st>Methods:</st>
<p> Using the Norwegian Registry of Employers and Employees, we included 24,765 male offshore workers registered from 1981 to 2003 and 283,002 male referents from the general working population matched by age and community of residence. The historical cohort was linked to the Cancer Registry of Norway and the Norwegian Cause of Death Registry.</p>
</sec>
<sec><st>Results:</st>
<p> Male offshore workers had excess risk of oesophageal cancer (rate ratio (RR) = 2.6;95% confidence interval (CI) 1.4&ndash;4.8) compared with the general male working population. Only the adenocarcinoma type was significantly increased (RR 2.7;95% CI 1.0&ndash;7.0), and the increased risk was mainly ascribed to an increased risk among "upstream operators" (RR 4.3;95% CI 1.3&ndash;14.5). "Upstream operators" did not have significant excess of cancer of the respiratory system or colon or mortality from any of the lifestyle-related diseases investigated.</p>
</sec>
<sec><st>Conclusion:</st>
<p> We found a four-fold excess risk of oesophageal adenocarcinoma among male workers assumed to have had the most extensive contact with different phases of crude oil. Due to the small number of cases, and a lack of detailed data on occupational exposure and lifestyle factors found to be associated with esophageal adenocarcinoma, the results must be interpreted with caution. Nevertheless, given the low risk of lifestyle-related cancers and causes of death in this working group, the results add to the observations in other low-powered studies on oesophageal cancer further suggesting that factors related to the petroleum stream or carcinogenic agents used in the production process might be associated with the risk of oesophageal adenocarcinoma.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Kirkeleit, J., Riise, T., Bjorge, T., Moen, B. E., Bratveit, M., Christiani, D. C]]></dc:creator>
<dc:date>Mon, 26 Oct 2009 17:52:48 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046953</dc:identifier>
<dc:title><![CDATA[Increased risk of oesophageal adenocarcinoma among upstream petroleum workers]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-26</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.049205v1?rss=1">
<title><![CDATA[Polymorphisms within the putative micro-RNA binding sites of mesothelin gene are associated with the serum levels of the mesothelin-related protein.]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.049205v1?rss=1</link>
<description><![CDATA[
<p>Serum mesothelin, also known as soluble mesothelin-related protein (SMRP), reportedly shows increased levels in epithelial-type Malignant Pleural Mesothelioma (MPM), but sometimes also arrives at high values in healthy asbestos-exposed subjects. This study is aimed to investigate whether single nucleotide polymorphisms in the 3'untranslated region (3'UTR) of the mesothelin-encoded gene (MSLN) are associated with the SMRP levels measured in serum. The 3'UTR of the mesothelin gene  was genotyped in 59 healthy asbestos-exposed subjects, selected on the basis of their SMRP levels. Direct sequencing did not show any new polymorphism, but enabled us to genotype two known SNPs (rs1057147, rs57272256). Differences in the mean values of SMRP in wild-type and variant heterozygote groups were calculated. High levels of SMRP in healthy asbestos-exposed subjects were significantly associated with polymorphism rs1057147 (G &lt; A). Regarding rs57272256, there was no statistically significant difference between wild-type and heterozygote groups. Our study suggests that rs1057147 polymorphism can affect mesothelin expression. Although these data need to be confirmed with a larger number of cases, this study warrants further research in order to better understand the relationship between mesothelin polymorphisms and SMRP.</p>
]]></description>
<dc:creator><![CDATA[Cristaudo, A., Foddis, R., Bonotti, A., Simonini, S., Vivaldi, A., Guglielmi, G., Bruno, R., Landi, D., Gemignani, F., Landi, S.]]></dc:creator>
<dc:date>Mon, 26 Oct 2009 17:50:00 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.049205</dc:identifier>
<dc:title><![CDATA[Polymorphisms within the putative micro-RNA binding sites of mesothelin gene are associated with the serum levels of the mesothelin-related protein.]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-26</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.043893v1?rss=1">
<title><![CDATA[High frequency of fumigants and other toxic gases in imported freight containers - an underestimated occupational and community health risk]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.043893v1?rss=1</link>
<description><![CDATA[
<p>Residues of pesticide fumigants and toxic industrial chemicals in freight containers represent a health hazard to employees and consumers, especially since freight containers are sealed for transport and distributed widely throughout the importing countries before being opened for unloading.</p>
<p>We investigated 2113 freight containers arriving at the second largest container terminal in Europe, Hamburg, Germany, over a 10-week period in 2006. The countries of origin, type of contents and the pesticide fumigation history declared on labels attached to the container were recorded.</p>
<p>We determined that 1478 (70%) containers were contaminated with toxic chemicals above chronic reference exposure levels (RELs), 761 (36%) even exceeded the higher acute REL thresholds. Benzene and/or formaldehyde contamination was 4-times greater than for fumigants.</p>
<p>Our findings indicate a health risk for dockworkers, container unloaders and even end-consumers, especially as many of the cancerogenic or toxic gases elude subjective detection.</p>
]]></description>
<dc:creator><![CDATA[Baur, X., Poschadel, B., Budnik, L. T.]]></dc:creator>
<dc:date>Mon, 26 Oct 2009 17:51:26 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.043893</dc:identifier>
<dc:title><![CDATA[High frequency of fumigants and other toxic gases in imported freight containers - an underestimated occupational and community health risk]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-26</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.047852v1?rss=1">
<title><![CDATA[Airway Inflammation in Cement Production Workers]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.047852v1?rss=1</link>
<description><![CDATA[
<sec><st>Objective:</st>
<p> Cement aerosol exposure is associated with increased morbidity of airway disease among exposed workers. The aim of this study was to compare the levels of inflammatory cells and soluble inflammatory markers in induced sputum samples of cement production workers between exposed and unexposed periods, and to compare these variables between cement workers and references.</p>
</sec>
<sec><st>Methods:</st>
<p> A total of 35 healthy, non-smoking aerosol-exposed production workers from a cement plant in Norway provided a blood sample and performed induced sputum and spirometry after 5 days without exposure and again during a period of exposure during regular work. We compared these values with those obtained from an internal low-exposed reference group of 15 office workers from the plant and an external reference group (ERG) comprising 39 non-exposed workers. Differential cell counts and inflammatory markers were assessed.</p>
</sec>
<sec><st>Results:</st>
<p> The median thoracic aerosol concentration over one work shift (8 hours) was 0.6 mg/m3 (range, 0.2 to 8.1) in maintenance workers and 1.75 mg/m3 (0.2 to 15.5) in furnace department workers. In the cement production workers (from the maintenance and furnace department), the median percentage of airway neutrophils was 51% (32 to 66) in the exposed period, which was significantly higher than in the unexposed period (median, 38%; range, 23 to 55) (p=0.04) and than in the external reference group (30%; 19 to 44) (p=0.001). The median interleukin-1&beta; concentration was elevated compared with the office workers (p=0.05), and compared with the external reference group (p=0.006).</p>
</sec>
<sec><st>Conclusions:</st>
<p> A significantly higher percentage of neutrophils was observed in cement production workers during the exposed period compared with the non-exposed period and with the external reference group. This elevated percentage corresponded with an elevated IL-1&beta; concentration. These data indicate that cement aerosol exposure in concentrations below the Norwegian occupational limits (respirable dust, 5 mg/m3; total dust, 10 mg/m3) may cause airway inflammation.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Fell, A. K. M., Sikkeland, L. I. B., Svendsen, M. V., Kongerud, J.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 22:13:00 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.047852</dc:identifier>
<dc:title><![CDATA[Airway Inflammation in Cement Production Workers]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.047969v1?rss=1">
<title><![CDATA[B[a]P-induced neurobehavioral function and neurotransmitter alterations in coke oven workers]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.047969v1?rss=1</link>
<description><![CDATA[
<sec><st>Objective:</st>
<p> To study the alterations of neurobehavioral function and neurotransmitters in coke oven workers occupationally exposed to B[a]P and explore the possible biomarkers of B[a]P&rsquo;s neurotoxicity.</p>
</sec>
<sec><st>Methods:</st>
<p> One hundred seventy-six coke oven workers occupationally exposed to B[a]P and 48 warehouse workers (controls) in the raw material plant were investigated by questionnaire. Their neurobehavioral functions were determined using WHO/NCTB involving emotional and cognitive function. B[a]P&rsquo;s concentrations in the working environments and levels of urinary 1-OH-Py of workers were assayed by HPLC with a fluorescence detector. HPLC was also used to detect the contents of monoamine and amino acid neurotransmitters, and spectrophotometry was used to determine the contents of choline neurotransmitters. And then correlation between the neurobehavioral changes and the neurotransmitters' contents were analyzed.</p>
</sec>
<sec><st>Results:</st>
<p> The concentrations of airborne B[a]P were higher in the coke oven plant than that in the controls' working place, and the levels of 1-OH-Py increased significantly compared to the controls (p=0.000). The scores of digital span and order digital span reflecting learning and memory decreased significantly in the coke oven workers (p=0.006), and which decreased with 1-OH-Py level increasing. The contents of NE, DA, 5-HT and HVA decreased, while the levels of 5-HIAA increased in the exposed group compared to the controls, and the difference in NE was significant (p=0.000). Compared to the control group, the contents of Asp and GABA decreased significantly (p=0.004 and p=0.004). The Ach contents increased to 4-5 times of that in the controls, and the activities of AchE decreased significantly (p=0.000 and p =0.012). Statistical analysis showed that the scores of digital span and order digital span negatively correlated to Ach and positively correlated to AchE.</p>
</sec>
<sec><st>Conclusion:</st>
<p> Occupational B[a]P exposure could reduce both the coke oven workers' neurobehavioral function and the contents of monoamine, amino acid and choline neurotransmitters. Moreover, Ach and AchE correlated with the neurobehavioral function, AchE has a poor specificity, so Ach may be the potential biomarker of B[a]P&rsquo;s neurotoxicity.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Niu, Q., Zhang, H., Li, X., Li, M.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 22:09:27 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.047969</dc:identifier>
<dc:title><![CDATA[B[a]P-induced neurobehavioral function and neurotransmitter alterations in coke oven workers]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.047431v1?rss=1">
<title><![CDATA[Physical Examination is Minimally Useful in Defining Carpal Tunnel Syndrome in Population Based Studies]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.047431v1?rss=1</link>
<description><![CDATA[
<sec><st>Objective:</st>
<p> We evaluated the utility of physical examination maneuvers in the prediction of carpal tunnel syndrome (CTS) in a population-based research study.</p>
</sec>
<sec><st>Methods:</st>
<p> We studied a cohort of 1108 newly employed workers in several industries. Each worker completed a symptom questionnaire, a structured physical examination, and nerve conduction study. For each hand, our CTS case definition required both median nerve conduction abnormality and symptoms classified as "classic" or "probable" on a hand diagram. We calculated the positive predictive values and likelihood ratios for physical examination maneuvers, in subjects with and without symptoms.</p>
</sec>
<sec><st>Results:</st>
<p> The prevalence of CTS in our cohort was 1.2% for the right hand and 1.0% for the left hand. The likelihood ratios of a positive test for physical provocative tests ranged from 2.0 to 3.3, and those of a negative test from 0.3 to 0.9. The post-test probability of positive testing was less than 50% for all strategies tested.</p>
</sec>
<sec><st>Conclusion:</st>
<p> Our study found that physical examination, alone or in combination with symptoms, was not predictive of CTS in a working population. We suggest using specific symptoms as a first level screening tool, and nerve conduction study as a confirmatory test, as a case definition strategy in research settings.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Descatha, A., Dale, A.-m., Franzblau, A., Coomes, J., Evanoff, B.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.047431</dc:identifier>
<dc:title><![CDATA[Physical Examination is Minimally Useful in Defining Carpal Tunnel Syndrome in Population Based Studies]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-22</prism:publicationDate>
<prism:section>Short Report</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.047175v1?rss=1">
<title><![CDATA[Identifying Pesticide Use Patterns among Flower Growers to Assess Occupational Exposure to Mixtures]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.047175v1?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p> Exposure assessment to a single pesticide does not capture the complexity of the occupational exposure. Recently, pesticide use patterns analysis has emerged as an alternative to study these exposures. The aim of this study is to identify the pesticide use pattern among flower growers in Mexico participating in the study on the endocrine and reproductive effects associated with pesticide exposure.</p>
</sec>
<sec><st>Methods:</st>
<p> A cross-sectional study was carried out to gather retrospective information on pesticide use applying a questionnaire to the person in charge of the participating flower growing farms. Information about seasonal frequency of pesticide use (rains and dry) for the years 2004 and 2005 was obtained. Principal components analysis was performed.</p>
</sec>
<sec><st>Results:</st>
<p> Complete information was obtained for 88 farms and 23 pesticides were included in the analysis. Six principal components were selected, which explained more than 70% of the data variability. The identified pesticide use patterns during both years were: 1) fungicides benomyl, carbendazim, thiophanate and metalaxyl (both seasons), including triadimephon during the rainy season, chlorotalonyl and insecticide permethrin during the dry season; 2) insecticides oxamyl, biphenthrin and fungicide iprodione (both seasons), including insecticide methomyl during the dry season; 3) fungicide mancozeb and herbicide glyphosate (only during the rainy season); 4) insecticides metamidophos and parathion (both seasons); 5) insecticides omethoate and methomyl (only rainy season); and 6) insecticides abamectin and carbofuran (only dry season). Some pesticides do not show a clear pattern of seasonal use during the studied years.</p>
</sec>
<sec><st>Conclusions:</st>
<p> The principal component analysis is useful to summarize a large set of exposure variables into smaller groups of exposure patterns, identifying the mixtures of pesticides in the occupational environment that may have an interactive effect on a particular health effect.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Schilmann, A., Lacasana, M., Blanco-Munoz, J., Aguilar-Garduno, C., Salinas-Rodriguez, A., Flores-Aldana, M., Cebrian, M. E.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 22:01:55 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.047175</dc:identifier>
<dc:title><![CDATA[Identifying Pesticide Use Patterns among Flower Growers to Assess Occupational Exposure to Mixtures]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.047092v2?rss=1">
<title><![CDATA[Could mining be protective against prostate cancer? A study and literature review.]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.047092v2?rss=1</link>
<description><![CDATA[
<p>Prostate cancer is one of the most commonly diagnosed cancers in Western men and one in three Australian men develop the cancer before the age of 75.  Currently, only increasing age and family history have been well established as risk factors.  A growing number of studies have investigated occupation in relation to prostate cancer but, like other risk factors, no associations have been confirmed.  Mining employs a significant proportion of the work force in Western Australia.  The aims of this study were: to describe the characteristics of miners in the Western Australian Prostate Health Study and investigate mining as a risk factor for prostate cancer and; to conduct a systematic search of the literature for studies that have investigated mining as an occupational risk factor for prostate cancer and to compare and contrast their methodologies and results.</p>
<p>Data was obtained from a population-based case control study conducted from January 1 2001 to August 20 2002 at The University of Western Australia. After controlling for age, family history and military service in Vietnam, miners had a statistically significantly reduced risk of prostate cancer (AOR 0.35 95% CI 0.16-0.75).  The systematic literature search of studies examining mining and prostate found a reasonably consistent trend of a decreased risk of prostate cancer amongst miners.  None of the published articles discussed their results regarding mining and prostate cancer in detail, and a biological mechanism to support these results has not previously been suggested.  The relationship between mining and prostate cancer deserves further investigation.</p>
]]></description>
<dc:creator><![CDATA[Girschik, J., Glass, D., Ambrosini, G. L, Fritschi, L.]]></dc:creator>
<dc:date>Tue, 20 Oct 2009 03:42:41 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.047092</dc:identifier>
<dc:title><![CDATA[Could mining be protective against prostate cancer? A study and literature review.]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-20</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.050054v1?rss=1">
<title><![CDATA[Integrated health impact assessment of cycling]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.050054v1?rss=1</link>
<description><![CDATA[
<p>After years of decline in usage and image in the Western world from the 1950s on, the bicycle is now emerging as a centre of interest for many researchers, policy-makers, practitioners and advocacy groups in the health and environmental fields. The proportion of journeys taken by bicycle still varies greatly, from around 1-2% in the US up to 30% in the Netherlands. In the past decade, bicycle-promotion policies have begun to flourish in Europe and North America, with in particular the highly popular city bike sharing programs as in Paris, London or Barcelona.</p>
]]></description>
<dc:creator><![CDATA[de Nazelle, A., Nieuwenhuijsen, M.]]></dc:creator>
<dc:date>Fri, 09 Oct 2009 00:18:36 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.050054</dc:identifier>
<dc:title><![CDATA[Integrated health impact assessment of cycling]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-09</prism:publicationDate>
<prism:section>Commentaries (Commission Only)</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.048470v1?rss=1">
<title><![CDATA[Do pre-employment influences explain the association between psychosocial factors at work and coronary heart disease? The Whitehall II study.]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.048470v1?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p> To examine whether the association between psychosocial factors at work and incident coronary heart disease (CHD) is explained by pre-employment factors, such as family history of CHD, education, paternal education and social class, number of siblings, and height.</p>
</sec>
<sec><st>Methods:</st>
<p> A prospective cohort study of 6435 British men aged 35-55 years at phase 1 (1985-1988) and free from prevalent CHD at phase 2 (1989-1990). Psychosocial factors at work were assessed at phases 1 and 2 and mean scores across the two phases were used to determine long-term exposure. Selected pre-employment factors were assessed at phase 1. Follow-up for coronary death, first non-fatal myocardial infarction or definite angina between phase 2 and 1999 was based on clinical records (250 events, follow-up 8.7 years).</p>
</sec>
<sec><st>Results:</st>
<p> The selected pre-employment factors were associated with risk for CHD: hazard ratios (CI 95%) were 1.33 (1.03-1.73) for family history of CHD, 1.18 (1.05-1.32) for each quartile decrease in height, and 1.16 (0.99-1.35) for each category increase in number of siblings. Psychosocial work factors also predicted CHD: 1.72 (1.08-2.74) for low job control and 1.72 (1.10-2.67) for low organisational justice. Adjustment for pre-employment factors changed these associations by 4.1% or less.</p>
</sec>
<sec><st>Conclusions:</st>
<p> In this well-characterised occupational cohort of British men, the association between psychosocial factors at work and CHD was largely independent of family history of CHD, education, paternal educational attainment and social class, number of siblings, and height.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Hintsa, T., Shipley, M., Gimeno, D., Elovainio, M., Chandola, T., Jokela, M., Keltikangas-Jarvinen, L., Vahtera, J., Marmot, M. G, Kivimaki, M.]]></dc:creator>
<dc:date>Fri, 09 Oct 2009 00:17:10 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.048470</dc:identifier>
<dc:title><![CDATA[Do pre-employment influences explain the association between psychosocial factors at work and coronary heart disease? The Whitehall II study.]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-09</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.047407v1?rss=1">
<title><![CDATA[Fatal Occupational injuries in Taiwan: 1994-2005]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.047407v1?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p> This study examines the trends in rates of fatal occupational injuries by demographic groups and occupations for the period from 1994-2005 in Taiwan.</p>
</sec>
<sec><st>Methods:</st>
<p> Data on deaths due to injuries on worksites that occurred from 1994 through 2005 were obtained from Department of Health which is responsible for the death registration system in Taiwan. Employment data, which were used as the denominators of fatality rates in this study, were retrieved from the Directorate-General of Budget and Accounting Statistics "Employment and Earnings" database. A Poisson regression model was used to examine the trends in rates of fatal occupational injuries in various occupations while controlling for demographic characteristics.</p>
</sec>
<sec><st>Results:</st>
<p> Overall fatal occupational injury rates declined during the study periods among all demographic groups and occupations. Adjusted annual changes in rates of fatal injuries ranged from a decline of 13.6% a year in machine operators/related workers to a decline of 35.9% in clerks. The annual decrement was faster for males than for females and for older workers compared to young workers.</p>
</sec>
<sec><st>Conclusions:</st>
<p> Despite declining rates, the number of fatal occupational injuries in Taiwan remains significant because of its growing workforce. Disparities in fatal injury trends provide prime targets for further attention.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Ho, S.-C., Wang, L.-Y., Ho, C.-K., Yang, C.-Y.]]></dc:creator>
<dc:date>Fri, 09 Oct 2009 00:15:49 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.047407</dc:identifier>
<dc:title><![CDATA[Fatal Occupational injuries in Taiwan: 1994-2005]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-09</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.047324v1?rss=1">
<title><![CDATA[Justice at Work and Metabolic Syndrome: the Whitehall II Study]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.047324v1?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p> Growing evidence shows that high levels of justice are beneficial for employee health, although biological mechanisms underlying this association are yet to be clarified. We aim to test whether high justice at work protects against metabolic syndrome.</p>
</sec>
<sec><st>Methods:</st>
<p> A prospective cohort study of 20 civil service departments in London (the Whitehall II study) including 6123 male and female British civil servants aged 35 to 55 years without prevalent CHD at baseline (1985-1990). Perceived justice at work was determined by means of questionnaire on two occasions between 1985 and 1990. Follow-up for metabolic syndrome and its components occurring from 1990 through 2004 was based on clinical assessments on three occasions over more than 18 years.</p>
</sec>
<sec><st>Results:</st>
<p> Cox proportional hazard models adjusted for age, ethnicity and employment grade showed that men who experienced a high level of justice at work had a lower risk of incident metabolic syndrome than employees with a low level of justice (hazard ratio 0.75; 95% confidence interval: 0.63-0.89). There was little evidence of an association between organizational justice and metabolic syndrome or its components in women (hazard ratio 0.88; 95%CI: 0.67-1.17).</p>
</sec>
<sec><st>Conclusions:</st>
<p> Our prospective findings provide evidence of an association between high levels of justice at work and the development of metabolic syndrome in men.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Gimeno, D., Tabak, A. G, Ferrie, J. E, Shipley, M. J, De Vogli, R., Elovainio, M., Vahtera, J., Marmot, M. G, Kivimaki, M.]]></dc:creator>
<dc:date>Fri, 09 Oct 2009 00:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.047324</dc:identifier>
<dc:title><![CDATA[Justice at Work and Metabolic Syndrome: the Whitehall II Study]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-09</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046557v1?rss=1">
<title><![CDATA[Occupational exposure to organic solvents and breast cancer in women]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046557v1?rss=1</link>
<description><![CDATA[
<sec><st>Background:</st>
<p> Although studies in rodents suggest possible associations between exposure to organic solvents and breast cancer, the evidence in humans is limited.</p>
</sec>
<sec><st>Methods:</st>
<p> We evaluated job histories of 2383 incident breast cancer cases, and 2502 controls who participated in a large population-based case-control study in Poland and were diagnosed during 2000-2003. Industrial hygienists reviewed occupational histories and developed   exposure metrices for total organic solvents and benzene. Unconditional logistic regression analyses estimated odds ratios (ORs) and 95% confidence intervals (CIs) as the measure of association with breast cancer risk, controlling for breast cancer risk factors. Stratified analyses examined the potential modification by known breast cancer risk factors. Associations were also evaluated by estrogen (ER) and progesterone receptor (PR) status and by other clinical characteristics of the tumours using polytomous regression analyses.</p>
</sec>
<sec><st>Results:</st>
<p> Women who ever worked at jobs with organic solvents exposure had a small but  nonsignificantly increased breast cancer risk (OR=1.16; 95%CI 0.99 to 1.4), A significant association was present for ER and PR negative tumors (OR 1.40; 95% CI 1.1 to 1.8, but not for tumors with both positive receptors (OR 0.97; 95% CI 0.8 to 1.2,(p-heterogeneity: 0.008)). However, we did not observe trends with increasing level of exposure. Known breast cancer risk factors did not modify the association with organic solvents and breast cancer risk. No significant association with risk was found for benzene exposure (OR 1.00; 95% CI  0.8 to 1.3).</p>
</sec>
<sec><st>Conclusion:</st>
<p> Our study provides weak evidence for a possible association between occupational exposure to organic solvents as a class and breast cancer risk.  The association might be limited to hormone receptor negative tumors.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Peplonska, B., Stewart, P., Szeszenia-Dabrowska, N., Lissowska, J., Brinton, L. A, Gromiec, J. P, Brzeznicki, S., Yang, R., Sherman, M., Garcia-Closas, M., Blair, A.]]></dc:creator>
<dc:date>Fri, 09 Oct 2009 00:13:05 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046557</dc:identifier>
<dc:title><![CDATA[Occupational exposure to organic solvents and breast cancer in women]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-09</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046425v1?rss=1">
<title><![CDATA[The bibliographic impact of epidemiologic studies: what can be learnt from citations?]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046425v1?rss=1</link>
<description><![CDATA[
<sec><st>Objective:</st>
<p> To document one dimension of the impact of an epidemiologic study, the impact through citations in scientific journals.</p>
</sec>
<sec><st>Methods:</st>
<p> Two sets of articles from studies performed in France were considered. They presented original results on occupational risk factors for low back pain (LBP) and upper limb disorders (ULD). Citations of these articles were retrieved through the Web of Science and Google scholar, and described according to several criterias.</p>
</sec>
<sec><st>Results:</st>
<p> Most citations present in the Web of Science were also retrieved by Google Scholar, except for the most recent ones.</p>
</sec>
<sec>
<p>In the Web of Science, after exclusion of self-citations and duplicates, the total number of citations was 109, from 23 different countries, for the LBP articles; the corresponding numbers were 96 and 18 for ULD. A relatively large number of the citations belonged to clinical journals outside the fields of occupational health, ergonomics, and public health.</p>
</sec>
<sec><st>Conclusion:</st>
<p> This example suggests that results dealing with occupational health disseminate into various fields of clinical research. However, this is only one dimension of the impact of a study.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Leclerc, A., Chastang, J.-F., Kaniewski, N., Cyr, D., Ozguler, A., Descatha, A.]]></dc:creator>
<dc:date>Fri, 09 Oct 2009 00:11:43 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046425</dc:identifier>
<dc:title><![CDATA[The bibliographic impact of epidemiologic studies: what can be learnt from citations?]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-09</prism:publicationDate>
<prism:section>Short Report</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046151v1?rss=1">
<title><![CDATA[Cause-specific mortality in British coal workers and exposure to respirable dust and quartz]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046151v1?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p> In the 1950&rsquo;s the Pneumoconiosis Field Research (PFR) programme was set up to study the health of British coalworkers.  Studies included regular health surveys, an intensive characterisation of workers&rsquo; individual exposures, and entry to a cohort followed up to the present for cause-specific mortality. This study reports on analyses of cause-specific mortality in a cohort of almost 18,000 men from 10 British collieries.</p>
</sec>
<sec><st>Methods:</st>
<p> External analyses used standardised mortality ratios, comparing observed mortality with reference rates from the regions in which the collieries were situated. Causes investigated include lung and stomach cancers, COPD, and cardiovascular endpoints.  Internal analyses used Cox regression models with time-dependent exposures adjusting for the confounding effects of age, smoking, cohort entry date and regional differences in population mortality rates.</p>
</sec>
<sec><st>Results:</st>
<p> Several causes showed evidence of a healthy worker effect early in the follow-up, with a deficit in the SMR diminishing over time. For most of the causes there was a significant excess in the latter part of follow-up.</p>
</sec>
<sec>
<p>Internal analyses found evidence of an association between increased risks of lung cancer and increased quartz exposure, particularly at a lag of 15 years.</p>
</sec>
<sec>
<p>Risks of mortality from non-malignant respiratory disease showed increases with increased exposure to respirable dust.</p>
</sec>
<sec><st>Conclusions:</st>
<p> This paper adds to the evidence on the long-term effects of exposure to coalmine dust on mortality from respiratory diseases.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Miller, B. G, MacCalman, L.]]></dc:creator>
<dc:date>Fri, 09 Oct 2009 00:07:32 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046151</dc:identifier>
<dc:title><![CDATA[Cause-specific mortality in British coal workers and exposure to respirable dust and quartz]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-09</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046391v1?rss=1">
<title><![CDATA[Occupational determinants of serum cholinesterase inhibition among organophosphate-exposed agricultural pesticide handlers in Washington State]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046391v1?rss=1</link>
<description><![CDATA[
<sec><st>Objective:</st>
<p> To identify potential risk factors for serum cholinesterase (BuChE) inhibition among agricultural pesticide handlers exposed to organophosphate (OP) and N-methyl-carbamate (CB) insecticides.</p>
</sec>
<sec><st>Methods:</st>
<p> We conducted a longitudinal study among 154 agricultural pesticide handlers who participated in the Washington State cholinesterase monitoring program in 2006 and 2007.  BuChE inhibition was analyzed in relation to reported exposures before and after adjustment for potential confounders using linear regression.  Odds ratios estimating the risk of &lsquo;BuChE depression&rsquo; (&gt;20% from baseline) were also calculated for selected exposures based on unconditional logistic regression analyses.</p>
</sec>
<sec><st>Results:</st>
<p> An overall decrease in mean BuChE activity was observed among study participants at the time of follow-up testing during the OP/CB spray season relative to pre-season baseline levels (mean decrease of 5.6%, P &lt; 0.001).  Score for estimated cumulative exposure to OP/CB insecticides in the past 30 days was a significant predictor of BuChE inhibition (coefficient = -1.74, P &lt; 0.001).  Several specific work practices and workplace conditions were associated with greater BuChE inhibition, including mixing/loading pesticides and cleaning spray equipment.  Factors that were protective against BuChE inhibition included full-face respirator use, wearing chemical-resistant boots, and storing personal protective equipment in a locker at work.</p>
</sec>
<sec><st>Conclusions:</st>
<p> Despite existing regulations, agricultural pesticide handlers continue to be exposed to OP/CB insecticides at levels resulting in BuChE inhibition.  These findings suggest that modifying certain work practices could potentially reduce BuChE inhibition.  Replication from other studies will be valuable.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Hofmann, J. N, Keifer, M. C, De Roos, A. J, Fenske, R. A, Furlong, C. E, van Belle, G., Checkoway, H.]]></dc:creator>
<dc:date>Fri, 09 Oct 2009 00:06:04 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046391</dc:identifier>
<dc:title><![CDATA[Occupational determinants of serum cholinesterase inhibition among organophosphate-exposed agricultural pesticide handlers in Washington State]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-09</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.045997v1?rss=1">
<title><![CDATA[Ambient Air Pollution and Risk of Congenital Anomalies in England, 1991-99]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.045997v1?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p> To investigate whether there is an association between risk of congenital anomaly and annual ward level exposure to air pollution in England during the 1990s.</p>
</sec>
<sec><st>Methods:</st>
<p> A geographical study was conducted across four regions of England with population-based congenital anomaly registers, 1991-99. Exposure was measured as 1996 annual mean background SO2, PM10 and NO2 concentrations at census ward level (n=1474). Poisson regression, controlling for maternal age, area socioeconomic deprivation, and hospital catchment area was used to estimate relative risk for an increase in pollution from the 10th to the 90th centile.</p>
</sec>
<sec><st>Results:</st>
<p> For non-chromosomal anomalies combined, relative risks were 0.99 (95%CI 0.93-1.05) for SO2, 0.97 (95%CI 0.84-1.11) for NO2, 0.89(95%CI 0.75-1.07) for PM10.  For chromosomal anomalies, relative risks were 1.06 (95%CI 0.98-1.15) for SO2, 1.11 (95%CI 0.95-1.30) for NO2, 1.18 (0.97-1.42) for PM10. Raised risks were found for Tetralogy of Fallot and SO2 (RR=1.38, 95%CI 1.07-1.79), NO2 (RR=1.44, 95%CI 0.71-2.93) and PM10 (RR=1.48, 95%CI 0.57-3.84), of interest in the light of previously reported associations between this cardiac anomaly and other air pollutants.</p>
</sec>
<sec><st>Conclusions:</st>
<p> While air pollution in the 1990s did not lead to sustained geographical differences in overall congenital anomaly rate in England, further research regarding specific anomalies is indicated.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Dolk, H., Armstrong, B., Lachowycz, K., Vrijheid, M, Rankin, J., Abramsky, L, Boyd, P., Wellesley, D.]]></dc:creator>
<dc:date>Fri, 09 Oct 2009 00:04:40 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.045997</dc:identifier>
<dc:title><![CDATA[Ambient Air Pollution and Risk of Congenital Anomalies in England, 1991-99]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-09</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.044966v1?rss=1">
<title><![CDATA[Dengue fever and El Nino-Southern Oscillation in Queensland, Australia: a time series predictive model]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.044966v1?rss=1</link>
<description><![CDATA[
<sec><st>Background:</st>
<p> It remains unclear over whether it is possible to develop an epidemic forecasting model for transmission of Dengue fever in Queensland, Australia.</p>
</sec>
<sec><st>Objectives:</st>
<p> To examine the potential impact of El Ni&ntilde;o/Southern Oscillation (ENSO) on the transmission of dengue fever in Queensland, Australia and explore the possibility of developing a forecast model of dengue fever.</p>
</sec>
<sec><st>Methods:</st>
<p> Data on the Southern Oscillation Index (SOI), an indicator of ENSO activity, were obtained from the Australian Bureau of Meteorology. Numbers of dengue fever cases notified and the numbers of postcode areas (PA) with dengue fever cases between January 1993 and December 2005 were obtained from the Queensland Health and relevant population data were obtained from the Australia Bureau of Statistics. A multivariate Seasonal Auto-regressive Integrated Moving Average (SARIMA) model was developed and validated by dividing the data file into two datasets: the data from January 1993 - December 2003 were used to construct a model and those from January 2004 - December 2005 were used to validate it.</p>
</sec>
<sec><st>Results:</st>
<p> A decrease in the average SOI (i.e., warmer conditions) during the preceding 3 &ndash; 12 months was significantly associated with an increase in the monthly numbers of PA with dengue fever cases (&beta; = &ndash; 0.038; p = 0.019). Predicted values from the SARIMA model were consistent with the observed values in the validation dataset (root-mean-square percentage error: 1.93%).</p>
</sec>
<sec><st>Conclusions:</st>
<p> Climate variability is directly and/or indirectly associated with dengue transmission and the development of a SOI-based epidemic forecasting system is possible for dengue fever in Queensland, Australia.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Hu, W., Clements, A., Williams, G., Tong, S.]]></dc:creator>
<dc:date>Fri, 09 Oct 2009 00:10:18 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.044966</dc:identifier>
<dc:title><![CDATA[Dengue fever and El Nino-Southern Oscillation in Queensland, Australia: a time series predictive model]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-09</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.044727v1?rss=1">
<title><![CDATA[Search strings for study of putative occupational determinants of disease]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.044727v1?rss=1</link>
<description><![CDATA[
<sec><st>Objective:</st>
<p> To identify efficient PubMed search strategies to retrieve articles regarding putative occupational determinants of conditions not generally considered to be work-related.</p>
</sec>
<sec><st>Methods:</st>
<p> Based on Medical Subject Heading (MeSH) definitions and expert knowledge, we selected as candidate search terms the four MeSH terms describing "occupational disease", "occupational exposure", "occupational health" and "occupational medicine" (DEHM) alongside 22 other promising terms. We first explored overlaps between the candidate terms in PubMed. Using random samples of abstracts retrieved by each term, we estimated proportions of articles containing potentially pertinent information regarding occupational aetiology in order to formulate two search strategies (one more "specific", one more "sensitive"). We applied these strategies to retrieve information on possible occupational aetiology of meningioma, pancreatitis, and atrial fibrillation.</p>
</sec>
<sec><st>Results:</st>
<p> Only 20.3% abstracts were retrieved by more than one DEHM term. The more "specific" search string was based on the combination of terms that yielded the highest proportion (40%) of potentially pertinent abstracts. The more "sensitive" string was based on use of broader search fields and additional coverage provided by other search terms under study. Using the specific string, the numbers of abstracts needed to read to find one potentially pertinent article were: 1.2 for meningioma; 1.9 for pancreatitis; 1.8 for atrial fibrillation. Using the sensitive strategy, the numbers needed to read were 4.4 for meningioma; 8.9 for pancreatitis; 10.5 for atrial fibrillation.</p>
</sec>
<sec><st>Conclusions:</st>
<p> The proposed strings could help health care professionals explore putative occupational aetiology for diseases that are not generally thought to be work-related.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Mattioli, S., Zanardi, F., Baldasseroni, A., Schaafsma, F., Cooke, R. M., Mancini, G., Fierro, M., Santangelo, C., Farioli, A., Fucksia, S., Curti, S., Violante, F. S, Verbeek, J.]]></dc:creator>
<dc:date>Fri, 09 Oct 2009 00:08:57 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.044727</dc:identifier>
<dc:title><![CDATA[Search strings for study of putative occupational determinants of disease]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-09</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046359v1?rss=1">
<title><![CDATA[Particulate matter and out-of-hospital coronary deaths in eight Italian cities]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046359v1?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p> We evaluated the association between concentration of particulate matter below 10 microns (PM10) and out-of-hospital coronary deaths in eight Italian cities during 1997-2004, investigating the role of individual effect-modifiers.</p>
</sec>
<sec><st>Methods:</st>
<p> A total of 16,989 subjects over 35 years who died out-of-hospital from coronary causes (ICD-9: 410-414) were studied; for each individual, hospital admissions in the previous two years were identified using record-linkage procedures. Daily PM10 values from urban monitoring stations were available and we studied the effect of the mean of current and previous day levels (lag 0-1). A city-specific case-crossover analysis was applied using a time-stratified approach while considering as confounders weather, holidays, influenza epidemics, and the summer decrease in the population. The pooled percentage increase (and 95% CI) in mortality per 10 &micro;g/m3 of PM10 was estimated.</p>
</sec>
<sec><st>Results:</st>
<p> A significant increase in out-of-hospital coronary deaths in relation to a 10 &micro;g/m3 increase in PM10: 1.46% (95% CI: 0.50; 2.43). Although no statistically significant effect modification by age was found, the effect was stronger among subjects  65 years (1.60%, 0.59; 2.63), in particular among those aged 65-74 (3.01%, 0.74; 5.34). People in the lowest socio-economic status category (3.34%, 1.28; 5.45) had a stronger effect than those in the highest category. No clear effect modification was seen for gender, season, or any specific comorbidity. An indication of negative effect modification was seen for persons with previous admission for cardiac dysrhythmias. Subjects without hospital admissions in the previous two years were slightly more affected by PM10 effects (1.91%, 0.28; 3.47) than those with at least one previous hospital admission (1.44%, 0.09; 2.82).</p>
</sec>
<sec><st>Conclusions:</st>
<p> Our results show that short-term exposure to PM10 has a strong effect on coronary mortality, greater among the elderly and socio-economically disadvantaged people. No clear effect modification by previous hospitalizations was detected, except for cardiac dysrhythmias possibly due to a protective treatment.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Serinelli, M., Vigotti, M. A., Stafoggia, M., Berti, G., Bisanti, L., Mallone, S., Pacelli, B., Tessari, R., Forastiere, F.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 20:33:19 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046359</dc:identifier>
<dc:title><![CDATA[Particulate matter and out-of-hospital coronary deaths in eight Italian cities]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-08</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046599v1?rss=1">
<title><![CDATA[Mortality from myocardial infarction in relation to exposure to vibration and dust among a cohort of iron-ore miners in Sweden]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046599v1?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p> The aim of this study was to investigate myocardial infarction mortality in relation to exposure to hand-arm vibration (HAV) and whole-body vibration (WBW) as well as exposure to dust among men employed in two Swedish iron-ore mines.</p>
</sec>
<sec><st>Methods:</st>
<p> This study comprised employed men at two iron-ore mines in Sweden who had been employed for at least one year from 1923 up to 1996. The causes of death were obtained from the national cause of death register from 1952 to 2001. Myocardial infarction mortality was obtained by linking personal identification numbers to the national cause of death register. Poisson regression was used for risk estimations on exposure-response relation, and analyses were made on the two age groups &le;60 years and &gt;60 years.</p>
</sec>
<sec><st>Results:</st>
<p> Relative risks for myocardial infarction mortality in relation to exposure were significantly increased for exposure (0/&gt;0) to WBV (RR: 1.18, 95% CI 1.06-1.31) and dust (RR: 1.15, 95% CI 1.02-1.31), and the results indicated an exposure-response relation for WBV and dust separately. For 60 years and younger, exposure to HAV (0/&gt;0) (RR: 1.34, 95% CI 1.03-1.74) and WBV (0/&gt;0) (RR: 1.39, 95% CI 1.13-1.72) increased the risk of MI mortality. An exposure-response was found for HAV and WBV, as the medium and high exposed categories showed significantly increased risk estimates. None of the exposures significantly increased the risk in the group above 60 years. The increased risk estimates for exposure to WBV remained when adjusting for exposure to dust.</p>
</sec>
<sec><st>Conclusions:</st>
<p> The results for the working-age (&le;60 years) group showed significantly increased myocardial infarction mortality for univariate exposure to hand-arm vibration, whole-body vibration, and dust. We found an association between increased mortality from myocardial infarction and occupational exposure to whole-body vibration, and the risk remained after adjustment for dust exposure.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Bjor, B. M, Burstrom, L., Eriksson, K., Jonsson, H., Nathanaelsson, L., Nilsson, T. K F]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 19:30:22 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046599</dc:identifier>
<dc:title><![CDATA[Mortality from myocardial infarction in relation to exposure to vibration and dust among a cohort of iron-ore miners in Sweden]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-10-08</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046318v1?rss=1">
<title><![CDATA[Smoking habits and disability pension - a cohort study of 14 483 construction workers.]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046318v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> Although smoking causes a variety of diseases and both, a high smoking prevalence and permanent disability pension  are a great burden on the population level, data about the impact of smoking habits on occupational disability are sparse. The objective of this study was to examine the influence of smoking habits on disability pension among construction workers, an occupational group with particularly high smoking prevalence.</P>
<P>
<B>Methods:</B> The association between smoking and disability pension was examined during a mean follow-up of 10.8 years in a cohort of 14 483 male construction workers in W&uuml;rttemberg, Germany. The cohort was linked to the regional pension register of the German pension fund to identify workers who were granted a disability pension during the follow-up. Hazard ratios were calculated with non smokers as reference by the Cox proportional hazards model adjusting for potential confounding factors such as age, nationality, type of occupation, alcohol consumption and body mass index (BMI).</P>
<P>
<B>Results:</B> Overall, 2643 cases of disability pension were observed, with dorsopathy (21%) being the most common cause. Clear dose-response relationships were seen between smoking and disability pension due to all causes, as well as disability pension due to respiratory, cardiovascular and mental diseases, cancer and dorsopathy. Particularly strong associations were seen between heavy smoking (&gt;= 20 cigarettes/day) and disability pension due to mental and respiratory diseases (hazard ratios with 95% confidence intervals: 3.25; 1.93-5.46 3.23; 1.92-5.43 and 3.26; 1.69-6.27 3.31; 1.73-6.36respectively).</P>
<P> 
<B>Conclusion:</B> Smoking is associated with increased risk of disability pension among construction workers, in particular disability pension due to respiratory, cardiovascular and mental diseases, cancer and dorsopathy.</P>
]]></description>
<dc:creator><![CDATA[Claessen, H., Arndt, V., Drath, C., Brenner, H.]]></dc:creator>
<dc:date>Tue, 22 Sep 2009 02:07:42 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046318</dc:identifier>
<dc:title><![CDATA[Smoking habits and disability pension - a cohort study of 14 483 construction workers.]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.047126v1?rss=1">
<title><![CDATA[Pneumoconiosis among underground bituminous coal miners in the United States: is silicosis becoming more frequent?]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.047126v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> Epidemiologic reports since 2000 have documented increased prevalence and rapid progression of pneumoconiosis among underground coal miners in the United States. To investigate a possible role of silica exposure in the increase, we examined chest x-rays (CXRs) for specific abnormalities (r-type small opacities) known to be associated with silicosis lung pathology.</P>
<P>
<B>Methods:</B> Underground coal miners are offered CXRs every 5 years. Abnormalities consistent with pneumoconiosis are recorded by National Institute for Occupational Safety and Health (NIOSH) B Readers using the International Labour Office Classification of Radiographs of Pneumoconioses.  CXRs from 1980&ndash;2008 of 90,973 participating miners were studied, focusing on reporting of r-type opacities (small rounded opacities 3&ndash;10 mm in diameter). Log binomial regression was used to calculate prevalence ratios adjusted for miner age and profusion category.</P>
<P>
<B>Results:</B> Among miners from Kentucky, Virginia, and West Virginia, the proportion of radiographs showing r-type opacities increased in the 1990s (PR=2.5; 95% CI=1.7&ndash;3.7) and after 1999 (PR=4.1; 95% CI=3.0&ndash;5.6), compared to the 1980s (adjusted for profusion category and miner age).  The prevalence of progressive massive fibrosis in 2000-2008 was also elevated compared to the 1980&rsquo;s (PR=4.4; 95% CI=3.1&ndash;6.3) and 1990&rsquo;s (PR=3.8; 95% CI=2.1&ndash;6.8) in miners from Kentucky, Virginia, and West Virginia.</P>
<P>
<B>Conclusions:</B> The increasing prevalence of pneumoconiosis over the past decade and the change in the epidemiology and disease profile documented in this and other recent studies imply that U.S. coal miners are being exposed to excessive amounts of respirable crystalline silica.</P>
]]></description>
<dc:creator><![CDATA[Laney, A S., Petsonk, E. L, Attfield, M. D]]></dc:creator>
<dc:date>Tue, 22 Sep 2009 01:59:45 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.047126</dc:identifier>
<dc:title><![CDATA[Pneumoconiosis among underground bituminous coal miners in the United States: is silicosis becoming more frequent?]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046680v1?rss=1">
<title><![CDATA[Occupational Exposure to Polycyclic Aromatic Hydrocarbons and Lung Cancer Risk: a Multicenter Study in Europe]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046680v1?rss=1</link>
<description><![CDATA[
<p><P><B>Background:</B> Lung cancer incidence in Central and Eastern Europe (CEE) is among the highest in the world, and the role of occupational exposures has not been adequately studied in these countries.</P>
<P>
<B>Objectives:</B> To investigate the contribution of occupational exposure to polycyclic aromatic hydrocarbons (PAH) to lung cancer in CEE.</P>
<P>
<B>Methods:</B> A case-control study was conducted in Czech Republic, Hungary, Poland, Romania, Russia, and Slovakia, as well as the United Kingdom (UK) between 1998 and 2002. Occupational and socio-demographic information was collected through interviews from 2861 newly diagnosed lung cancer cases and 2936 population or hospital controls. Industrial hygiene experts in each country evaluated exposure to 70 occupational agents, whereof 15 mixtures containing PAH. Odds ratios (OR) of lung cancer were calculated after adjusting for other occupational exposures and tobacco smoking.</P>
<P>
<B>Results:</B> The OR for ever-exposure to PAH in the CEE countries was 0.93 (95% CI 0.77-1.14). The OR for the highest category of cumulative exposure, duration of exposure and intensity of exposure were 1.13 (95% CI 0.80-1.58), 1.02 (95% CI 0.66-1.57) and 1.11 (95% CI 0.60-2.05), respectively. The OR for ever PAH exposure in the UK was 1.97 (95% CI 1.16-3.35).</P>
<P> 
<B>Conclusion:</B> Occupational PAH exposure does not appear to substantially contribute to the burden of lung cancer in CEE. The apparently stronger effect observed in the UK may be due to high exposure levels and a joint effect with asbestos.</P>
]]></description>
<dc:creator><![CDATA[Olsson, A. C, Fevotte, J., Fletcher, T., Cassidy, A., 't Mannetje, A., Zaridze, D., Szeszenia-Dabrowska, N., Rudnai, P., Lissowska, J., Fabianova, E., Mates, D., Bencko, V., Foretova, L., Janout, V., Brennan, P., Boffetta, P.]]></dc:creator>
<dc:date>Tue, 22 Sep 2009 01:58:36 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046680</dc:identifier>
<dc:title><![CDATA[Occupational Exposure to Polycyclic Aromatic Hydrocarbons and Lung Cancer Risk: a Multicenter Study in Europe]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.047316v1?rss=1">
<title><![CDATA[Occupational coke oven emissions exposure and risk of abnormal liver function: modifications of body mass index and hepatitis virus infection]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.047316v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> Occupational coke oven emissions (COE) have been considered an important health issue. However, there is no conclusive data on human hepatic injury due to COE exposure. We explored the association of COE exposure with liver function and assessed the effects of modification of potential non-occupational factors.</P>
<P>
<B>Methods:</B> We investigated 705 coke oven workers and 247 referents. Individual cumulative COE exposure was quantitatively estimated. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), -glutamyl transferase(GGT), alkaline phosphatase (ALP), hepatitis B surface antigen (HBsAg), and anti-hepatitis C antibody were measured.</P>
<P> 
<B>Results:</B> Among those with high COE exposure, the adjusted odd ratios of abnormal ALT and AST were 5.23 (95% CI 2.66 to10.27) and 1.95 (95% CI 1.18 to 3.52), respectively. Overweight individuals (BMI &ge;25 kg/m<SUP>2</SUP>) with high COE exposure had elevated risks of abnormal ALT (adjusted OR 23.93; 95% CI 8.73 to 65.62) and AST (adjusted OR 5.18; 95% CI 2.32 to11.58). Risk of liver damage in HBV or HCV positive individuals with COE exposure was also elevated.</P>
<P> 
<B>Conclusions:</B> Long-term exposure to COE increases the risk of liver dysfunction, which is more prominent among those with higher BMI and hepatitis virus infection. The risk assessment of liver damage associated with COE exposure should take BMI and hepatitis virus infection into consideration.</P>
]]></description>
<dc:creator><![CDATA[Hu, Y., Chen, B., Qian, J., Jin, L., Jin, T., Lu, D.]]></dc:creator>
<dc:date>Tue, 22 Sep 2009 01:56:25 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.047316</dc:identifier>
<dc:title><![CDATA[Occupational coke oven emissions exposure and risk of abnormal liver function: modifications of body mass index and hepatitis virus infection]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046326v1?rss=1">
<title><![CDATA[Occupational Exposure to Silica and Lung Cancer Risk in the Netherlands]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046326v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> Lung cancer carcinogenicity of crystalline silica dust remains subject of discussion. Epidemiological evidence is based on occupational cohort studies and population-based case-control studies. The aim of the study was to assess associations between male lung cancer risk and silica exposure, in a population-based cohort study.</P>
<P>  
<B>Methods:</B> The study was conducted among men aged 55&ndash;69 years (n=58 279) from the Netherlands Cohort Study, which included self-reported, life time job histories. Job titles were linked to the occupational groups of the external Finnish Job Exposure Matrix (FINJEM), including probability and level of silica exposure, each for specific time periods. 1667 incident lung cancer cases with known silica exposure status (210 exposed) were available after 11.3 years of follow-up. Risks were estimated based on a case-cohort design, and using Cox proportional hazards models.</P>
<P> 
<B>Results:</B> Adjusted for smoking and other confounders, elevated risks were observed for exposure duration (RR 1.65, 95% CI 1.14-2.41 for 26-51 yrs versus no exposure) and cumulative exposure (RR 1.47, 95%CI 0.93-2.33 for &ge; 3 versus &lt; 3 mg/m&sup3;.yr). Associations with average exposure levels were weaker. Associations were stronger for occupations with an exposure probability of  &ge; 90%. Adjustment for asbestos exposure slightly increased the risk.</P>
<P> 
<B>Conclusions:</B> Results from this prospective population-based cohort study corroborates the classification of crystalline silica as lung carcinogen. Associations could not be explained by smoking or by asbestos exposure.</P>
]]></description>
<dc:creator><![CDATA[Preller, L., Van den Bosch, L., Van den Brandt, P., Kauppinen, T., goldbohm, a.]]></dc:creator>
<dc:date>Tue, 22 Sep 2009 01:51:09 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046326</dc:identifier>
<dc:title><![CDATA[Occupational Exposure to Silica and Lung Cancer Risk in the Netherlands]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046847v1?rss=1">
<title><![CDATA[Respiratory health effects of ultrafine and fine particle exposure in cyclists]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046847v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> Monitoring studies have shown that commuters are exposed to high air pollution concentrations, but there is limited evidence of health effects related to these short exposures. We performed a study to investigate acute respiratory health effects of air pollution related to commuting by bicycle.</P>
<P>
<B>Methods:</B> Twelve healthy adults cycled a low and a high traffic intensity route during morning rush hour in Utrecht, The Netherlands. Exposure to traffic-related air pollution was characterized by measurements of PM10, soot and particle number. Before, directly after and six hours after cycling we measured lung function (FEV1, FVC, PEF), exhaled NO (FENO), and respiratory symptoms. The association between post minus pre-exposure difference in health effects and exposure during cycling was evaluated with linear regression models.</P>
<P>
<B>Results:</B> The average particle number concentration was 59% higher, while the average soot concentration was 39% higher on the high-traffic route than on the low-traffic route. There was no difference for PM10. Contrary to our hypothesis, associations between air pollution during cycling and lung function changes immediately after cycling were mostly positive. Six hours after cycling, associations between air pollution exposure and health were mostly negative for lung function changes and positive for changes in exhaled NO, though non-significant.</P>
<P>
<B>Conclusions:</B> We found a substantial contrast in ultrafine particle number and soot exposure between two urban cycling routes. Exposure to ultrafine particles and soot during cycling was weakly associated with an increase in exhaled NO, indicative of airway inflammation, and decrements in lung function six hours after exposure. A limitation of the study was a relatively small sample size.</P>
]]></description>
<dc:creator><![CDATA[Strak, M., Boogaard, H., Meliefste, K., Oldenwening, M., Zuurbier, M., Brunekreef, B., Hoek, G.]]></dc:creator>
<dc:date>Tue, 22 Sep 2009 01:49:55 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046847</dc:identifier>
<dc:title><![CDATA[Respiratory health effects of ultrafine and fine particle exposure in cyclists]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.044610v1?rss=1">
<title><![CDATA[Programmed health surveillance and detection of emerging diseases in occupational health: contribution of the French national occupational disease surveillance and prevention network (RNV3P).]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.044610v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objective:</B> The French national occupational disease surveillance and prevention network (RNV3P) includes the 30 occupational disease consultation centres in university hospitals, where patients are referred for a potentially work-related disease, and an occupational health service (OHS). The aim of this work is to demonstrate the contribution of this network to national health surveillance.</P>
<P> 
<B>Methods:</B> Data from consultations are recorded in standardised occupational health reports  and coded using international or national classifications. Programmed health surveillance is carried out through annual follow-up of annual referrals to experts for pre-selected disease-exposure associations, as well as incidence estimations for the well characterized working population followed by the OHS. Hypotheses on new emerging diseases are generated using statistical methods employed in pharmacosurveillance and by modelisation as an exposome to analyse multiple exposures.</P>
<P>
<B>Results:</B> 58 777 occupational health reports were collected and analysed from 2001 to 2007. Referrals to the 30 university hospital centres increased significantly for asbestos-related diseases, mood disorders and adjustment disorders related to psychological and organisational demands, and for elbow and shoulder disorders related to manual handling. Referrals significantly decreased for asthma, rhinitis related to exposure to organic dusts (vegetable or animal) or to chemicals, except for cosmetics and cleaning products. Estimation of incidences by the occupational health services showed a different pattern in different sectors of activity. The methods for detecting emerging diseases are presented and illustrated by the example of systemic sclerosis, identifying new exposures and new sectors of activity to be investigated.</P>
<P> 
<B>Conclusion:</B> The RNV3P collects data from two complementary samples: 30 university hospital centres (workers or former workers) and an occupational health service (current workers). This dual approach is useful for surveillance and for hypothesis generation on new emerging disease-exposure associations.</P>
]]></description>
<dc:creator><![CDATA[Bonneterre, V., Faisandier, L., Bicout, D., Bernardet, C., Ameille, J., De Claviere, C., Aptel, M., Lasfargues, G., de Gaudemaris, R.]]></dc:creator>
<dc:date>Tue, 22 Sep 2009 21:08:49 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.044610</dc:identifier>
<dc:title><![CDATA[Programmed health surveillance and detection of emerging diseases in occupational health: contribution of the French national occupational disease surveillance and prevention network (RNV3P).]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.045542v1?rss=1">
<title><![CDATA[Long-term exposure to traffic-related air pollution and mortality in Shizuoka, Japan]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.045542v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> The number of studies investigating the health effects of long-term exposure to air pollution is increasing, however, most studies have been conducted in Western countries. The health status of Asian populations may be different to that of Western populations and may, therefore, respond differently to air pollution exposure. Thus, we evaluated the health effects of long-term exposure to traffic-related air pollution in Shizuoka, Japan.</P>
<P> 
<B>Methods:</B> Individual data were extracted from participants of an ongoing cohort study. A total of 14,001 elderly residents, who were randomly chosen from all 74 municipalities of Shizuoka, completed questionnaires and were followed from December 1999 to March 2006. Individual nitrogen dioxide exposure data, as an index for traffic-related exposure, were modeled using a Land Use Regression model. We assigned participants an estimated concentration of nitrogen dioxide exposure during 2000-2006. We then estimated the adjusted hazard ratios and their confidence intervals for a 10 &micro;g/m<SUP>3</SUP> increase in exposure to nitrogen dioxide for all-cause or cause-specific mortality.</P>
<P>
<B>Results:</B> The adjusted hazard ratio for all-cause mortality was 1.02 (95% confidence interval: 0.96-1.08). Regarding cause-specific mortality, the adjusted hazard ratio for cardiopulmonary mortality was 1.16 (95% confidence interval: 1.06-1.26); in particular the adjusted hazard ratio for ischemic heart disease mortality was 1.27 (95% confidence interval: 1.02-1.58) and for pulmonary disease mortality it was 1.19 (95% confidence interval: 1.02-1.38). Furthermore, among non-smokers, a 10 &micro;g/m<SUP>3</SUP> increase in NO<SUB>2</SUB> was associated with a higher risk for lung cancer mortality (hazard ratio =1.30, 95% confidence interval: 0.85-1.93).</P>
<P> 
<B>Conclusion:</B> Long-term exposure to traffic-related air pollution, indexed by NO<SUB>2</SUB> concentration, increases the risk of cardiopulmonary mortality, even in a population with a relatively low BMI and increases the risk of lung cancer mortality in non-smokers.</P>
]]></description>
<dc:creator><![CDATA[Yorifuji, T., Kashima, S., Tsuda, T., Takao, S., Suzuki, E., Doi, H., Sugiyama, M., Ishikawa-Takata, K., Ohta, T.]]></dc:creator>
<dc:date>Tue, 22 Sep 2009 01:57:29 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.045542</dc:identifier>
<dc:title><![CDATA[Long-term exposure to traffic-related air pollution and mortality in Shizuoka, Japan]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.044024v1?rss=1">
<title><![CDATA[Association between genetic variants in VEGF, ERCC3 and occupational benzene hematotoxicity]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.044024v1?rss=1</link>
<description><![CDATA[
<p><P>Benzene is an established human hematotoxin, with substantial interindividual variation in benzene-induced toxicity.  To further examine if genetic variation contributes to benzene hematotoxicity, we analyzed 1,023 tagSNPs in 121 gene regions important for benzene metabolism, hematopoiesis, leukemia, and lymphoma among 250 benzene-exposed workers and 140 unexposed controls in a cross-sectional study carried out in China. Linear regression was used to analyze the relationship between genetic polymorphisms and total white blood cell (WBC) count and its subtypes, adjusting for potential confounders and occupational exposure to benzene and toluene among exposed workers.  The minP test assessed the association on the gene region level. The False Discovery Rate method controlled for multiple comparisons. VEGF (minP = 0.0030) and ERCC3 (minP = 0.0042) were the most significantly associated gene regions with altered WBC counts among benzene-exposed workers, after accounting for multiple comparisons.  Highly significant changes were also found for WBC subtype counts, including granulocytes, CD4+ T cells, and lymphocytes for VEGF and granulocytes and NK cells for ERCC3.  In workers exposed to &lt;1ppm, a SNP in VEGF was associated with changes in WBC and granulocyte counts, and SNPs in ERCC3 were associated with changes in WBC, NK cell, and granulocyte counts.  Our findings suggest that genetic variation in VEGF, which is critical to blood vessel growth, and ERCC3, which is a member of the DNA repair pathway and is responsible for repairing bulky DNA damage formed by chemicals, may contribute to individual susceptibility to benzene-induced hematotoxicity at relatively low levels of benzene exposure.</P>
]]></description>
<dc:creator><![CDATA[Hosgood, H D., Zhang, L., Shen, M., Berndt, S. I, Vermeulen, R., Li, G., Yin, S., Yeager, M., Yuenger, J., Rothman, N., Chanock, S., Smith, M., Lan, Q.]]></dc:creator>
<dc:date>Tue, 22 Sep 2009 01:55:05 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.044024</dc:identifier>
<dc:title><![CDATA[Association between genetic variants in VEGF, ERCC3 and occupational benzene hematotoxicity]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.045500v1?rss=1">
<title><![CDATA[Cross-validation and refinement of the Stoffenmanager as a first tier exposure assessment tool for REACH]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.045500v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> For regulatory risk assessment under REACH a tiered approach is proposed in which the first tier models should provide a conservative exposure estimate that can discriminate between scenarios of concern and those which are not. The Stoffenmanager is mentioned as first tier approach in the REACH guidance. In an attempt to investigate the validity of the Stoffenmanager algorithms a cross-validation study was performed.</P>
<P>
<B>Methods:</B> Exposure estimates using the Stoffenmanager algorithms were compared with exposure measurement results (n=254). Correlations between observed and predicted exposures, bias and precision were calculated. Stratified analyses were performed for the scenarios "handling of powders and granules" (n=82), "handling solids resulting in comminuting" (n=60), "handling of low-volatile liquids" (n=40) and for "handling of volatile liquids" (n=72).</P>
<P> 
<B>Results:</B> The relative bias of the 4 algorithms ranged between -9% and -77% with a precision of approximately 1.7. The 90-percentile estimate of 1 out of 4 algorithms was not conservative enough. Based on these statistics and analyses of residual plots the underlying algorithm was adapted. Subsequently, the calibration and the cross-validation dataset were merged to one dataset (n=952) used for calibrating the adapted Stoffenmanager algorithms. This new calibration resulted in new exposure algorithms for the 4 scenarios.</P>
<P> 
<B>Conclusions:</B> The Stoffenmanager is capable of discriminating among exposure levels mainly between scenarios in different companies. The 90-percentile estimates of the Stoffenmanager are verified to be sufficiently conservative. Therefore, the Stoffenmanager could be a useful Tier 1 exposure assessment tool for REACH.</P>
]]></description>
<dc:creator><![CDATA[Schinkel, J., Fransman, W., Heussen, H., Kromhout, H., Marquart, H., Tielemans, E.]]></dc:creator>
<dc:date>Tue, 22 Sep 2009 01:53:46 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.045500</dc:identifier>
<dc:title><![CDATA[Cross-validation and refinement of the Stoffenmanager as a first tier exposure assessment tool for REACH]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.044602v1?rss=1">
<title><![CDATA[Does socio-economic status modify the effect of particulate air pollution on cardiorespiratory mortality?]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.044602v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> To investigate whether deprivation index modifies the acute effect of black smoke on cardiorespiratory mortality.</P>
<P> 
<B>Methods:</B> Generalised linear Poisson regression models were used to investigate whether deprivation index (as measured by the Carstairs deprivation index) modified the acute effect of black smoke on mortality in the two largest Scottish cities (Glasgow and Edinburgh) between January 1981 and December 2001. Lag periods of up to one month were assumed for the effects of black smoke.</P>
<P> 
<B>Results:</B> Deprivation index significantly modified the effect of black smoke on mortality with black smoke effects generally increasing as level of deprivation increased. The interaction coefficient from a parametric model assuming a linear interaction between black smoke (&micro;gm-3) and deprivation in their effect on mortality &ndash; equivalent to a test of &lsquo;linear trend&rsquo; across Carstairs Categories &ndash; was significant for all mortality outcomes. In a model where black smoke effects were estimated independently for each deprivation category, the estimated increase in respiratory mortality over the ensuing one-month period associated with a 10&micro;gm-3 increase in the mean black smoke concentration was 8.0 percent (95% CI: 5.1, 10.9) for subjects residing in the &lsquo;most&rsquo; deprived category (Carstairs category 7) compared to 3.7 percent (95% CI: -0.7, 8.4) for subjects residing in the &lsquo;least&rsquo; deprived category (Carstairs category 1).</P>
<P> 
<B>Conclusions:</B> The results suggest a stronger effect of black smoke on mortality among people living in more deprived areas. The effect was greatest for respiratory mortality although significant trends were also seen for other groups. If corroborated, these findings could have important public health implications.</P>
]]></description>
<dc:creator><![CDATA[Carder, M., McNamee, R., Beverland, I., Elton, R. A, Cohen, G., Boyd, J., van Tongeren, M. v., Agius, R. M]]></dc:creator>
<dc:date>Tue, 22 Sep 2009 01:52:27 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.044602</dc:identifier>
<dc:title><![CDATA[Does socio-economic status modify the effect of particulate air pollution on cardiorespiratory mortality?]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.045260v1?rss=1">
<title><![CDATA[Prolonged time to pregnancy in residents exposed to ionising radiation in Co-60 contaminated buildings]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.045260v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> Radiation-induced cytogenetic damage in somatic cells has raised concern that low-dose ionising radiation could also damage germ cells and influence gamete production and/or function, resulting in decreased fertility. We used time to pregnancy (TTP) to investigate whether exposure to -radiation affected fertility among the residents of Co-60 contaminated buildings in Taiwan.</P>
<P>
<B>Methods:</B> This was a retrospective pregnancy-based study of 357 pregnancies born to 124 exposed couples. We estimated both the cumulative dose and dose rate for each pregnancy based on a physical dose reconstruction program. The comparison population consisted of 612 pregnancies born to 225 couples randomly sampled from the Taiwan general population. Information on TTP was collected by personal interviews. Fecundability ratios (FRs) were calculated with a discrete proportional hazards model.</P>
<P>
<B>Results:</B> For exposed mothers, fertility decreased significantly when unprotected intercourse began during the period of living in the radiation-contaminated buildings (FR 0.75, 95% CI 0.61 to 0.92). The effect was borderline significant for fathers (FR 0.83, 95% CI 0.68 to 1.02). There was evidence that prolonged TTP was associated with the rate of exposure for both mothers and fathers (tests for trend: female, p = 0.0006; male, p = 0.03), especially evident for dose rates &ge; 10 mSv/year (female, FR 0.60, 95% CI 0.43 to 0.84; male, FR 0.68, 95% CI 0.49 to 0.96).</P>
<P>
<B>Conclusions:</B> Our findings suggest that exposure to low-dose ionising radiation of Co-60 contaminated buildings may decrease fertility, especially in females. Fertility declined with increasing concurrent dose but not with cumulative dose.</P>
]]></description>
<dc:creator><![CDATA[Lin, C.-M., Chang, W. P, Doyle, P., Wang, J.-D., Lee, L.-T., Lee, C. L, Chen, P.-C.]]></dc:creator>
<dc:date>Tue, 22 Sep 2009 01:48:41 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.045260</dc:identifier>
<dc:title><![CDATA[Prolonged time to pregnancy in residents exposed to ionising radiation in Co-60 contaminated buildings]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.044917v1?rss=1">
<title><![CDATA[Organizational justice and markers of inflammation: The Whitehall II study]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.044917v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> Low organizational justice has been shown to be associated with increased risk of various health problems, but the underlying mechanisms remain unclear. We tested whether organisational injustice contributes to chronic inflammation in a population of middle-aged men and women.</P>
<P>  
<B>Methods:</B> This prospective cohort study uses data from 3205 men and 1204 women aged 35&ndash;55 years at entry into the Whitehall II study (Phase 1, 1985-1988). Organisational justice perceptions were assessed at Phase 1 and Phase 2 (1989-1990) and circulating inflammatory markers C-reactive protein and interleukin-6 at Phase 3 (1991-1993) and Phase 7 (2003-2004).</P>
<P> 
<B>Results:</B> In men, low organisational justice was associated with increased C-reactive protein levels at both follow-ups (Phase 3 and 7) and increased interleukin-6 at the second follow-up (Phase 7). The long term (Phase 7) associations were largely independent of covariates, such as age, employment grade, body mass index and depressive symptoms.  In women, no relationship was found between organisational justice and C-reactive protein or interleukin-6.</P>
<P>
<B>Conclusions:</B> This study suggests that organisational injustice is associated with increased long-term levels of inflammatory markers among men.</P>
]]></description>
<dc:creator><![CDATA[Elovainio, M., Ferrie, J. E, Gimeno, D., DeVogli, R., Shipley, M., Vahtera, J., Brunner, E., Marmot, M. G, Kivimaki, M.]]></dc:creator>
<dc:date>Tue, 22 Sep 2009 01:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.044917</dc:identifier>
<dc:title><![CDATA[Organizational justice and markers of inflammation: The Whitehall II study]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-22</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.043034v1?rss=1">
<title><![CDATA[A dynamic population-based model for the development of work related respiratory health effects amongst bakery workers]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.043034v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> This paper presents a dynamic population-based model for the development of sensitisation and respiratory symptoms in bakery workers. The model simulates a population of individual workers longitudinally and tracks the development of work-related sensitisation and respiratory symptoms in each worker.</P>
<P>  
<B>Methods:</B> The model has three components: a multi-stage disease model describing the development of sensitisation and respiratory symptoms in each worker over time; an exposure model describing occupational exposure to flour dust and allergens; and a basic population model describing the length of a worker&rsquo;s career in the bakery sector and the influx of new workers. Each worker&rsquo;s disease state is modelled independently using a discrete time Markov Chain, updated yearly using each individual&rsquo;s simulated exposure. A Bayesian analysis of data from a recent epidemiological study provided estimates of the yearly transition probabilities between disease states.</P>
<P>  
<B>Results:</B> For non-atopic/non-sensitised workers the estimated probabilities of developing moderate (upper respiratory) symptoms and progression to severe (lower respiratory) symptoms are 0.4% (95% C.I. 0.3%-0.5%)  and 1.1% (95% C.I. 0.6%-1.9%)  per mg/m3/year flour dust respectively and approximately twice these for atopic workers. The model predicts that 36% (95% C.I. 26%-46%) of workers with severe symptoms are sensitised to wheat and 22% (95% C.I. 12%-37%) to amylase. The predicted mean latency period for respiratory symptoms was 10.3 years (95% C.I. 8.3-12.3).</P>
<P>
<B>Conclusions:</B> Whilst the model provides a valuable population level representation of the mechanisms contributing to respiratory diseases in bakers, it was primarily developed for use in quantitative Health Impact Assessment. Future research will use the model to evaluate a range of workplace interventions, including achievable reductions in exposure and health surveillance. The general methodology is applicable to other diseases such as Chronic Obstructive Pulmonary Disease (COPD), Silicosis and Musculoskeletal Disorders and could be particularly valuable for forecasting changes in long latency diseases.</P>
]]></description>
<dc:creator><![CDATA[Warren, N., Meijster, T., Heederik, D., Tielemans, E.]]></dc:creator>
<dc:date>Tue, 08 Sep 2009 23:37:59 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.043034</dc:identifier>
<dc:title><![CDATA[A dynamic population-based model for the development of work related respiratory health effects amongst bakery workers]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-08</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046797v1?rss=1">
<title><![CDATA[Incidence of metabolic syndrome among night shift health care workers]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046797v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objective:</B> Night shift work is associated with ischemic cardiovascular disorders. It is not currently known whether it may be causally linked to the metabolic syndrome (MS), a risk condition for ischemic cardiovascular disorders. The syndrome is given by  the presence, in the same individual, of visceral obesity associated with even mild alterations in glucidic and lipidic homeostasis, and in blood pressure. Aim of this study was to assess whether a causal relationship exists between night shift work and the development of MS.</P>
<P>
<B>Methods:</B> Male and female nurses performing night shifts, free from any component of MS at baseline, were evaluated annually for the development of the disorder during a four-year follow-up. Male and female nurses performing daytime work only, visited during the same time period, represented the control group.</P>
<P>
<B>Results:</B> The cumulative incidence of MS was 9.0% (36 out of 402) among  night shift workers, and 1.8% (6 out of 336) among day-time workers (Relative Risk-R.R.-: 5.0, 95% Confidence Intervals-C.I.- 2.1 to 14.6). The annual rate of incidence of MS was 2.9% in night-shift workers and 0.5%  in day-time workers. Kaplan-Meier survival curves of the two groups were significantly different (Log Rank test; p&lt;0.001). Multiple Cox regression analysis (forward selection method based on likelihood ratio) showed that among selected variables (age, gender, smoking, alcohol intake, familiar history, physical activity, and work schedule) the only predictors of occurrence of MS were sedentariness (Hazard Ratio-HR-=2.92; 95% CI=1.64 to 5.18; p=0.017),  and night shift work (HR=5.10; 95% CI=2.15 to 12.11; p&lt;0.001).</P>
<P>
<B>Conclusions:</B> the risk of developing MS is strongly associated with night shift work in nurses. Medical counseling should be promptly instituted in night shift workers with the syndrome, and in case of persistance or progression, a change in work schedule should be considered.</P>
]]></description>
<dc:creator><![CDATA[Pietroiusti, A., Neri, A., Somma, G., Coppeta, L., Iavicoli, I., Bergamaschi, A., Magrini, A.]]></dc:creator>
<dc:date>Mon, 07 Sep 2009 20:11:24 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046797</dc:identifier>
<dc:title><![CDATA[Incidence of metabolic syndrome among night shift health care workers]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-07</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046250v1?rss=1">
<title><![CDATA[Occupation and renal cell cancer in Central and Eastern Europe]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046250v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objective:</B> Central and Eastern Europe has among the highest rates of renal cell cancer worldwide. Few studies have been conducted in these areas to investigate the possible role of occupational exposures in renal cell cancer etiology.  The purpose of this study was to examine the association of renal cell cancer with employment in specific occupations and industries.</P>
<P>
<B>Methods:</B> From 1999-2003, we conducted a hospital-based case-control study in seven areas of the Czech Republic, Poland, Romania and Russia. A detailed occupational history was collected from renal cell cancer cases and controls, together with information on potential confounders. Odds ratios (OR) and 95% confidence intervals (CI) of cancer risk were calculated for having ever been employed in selected jobs and industries, with follow-up analyses examining duration of employment.</P>
<P>
<B>Results:</B> A total of 992 histologically confirmed incident renal cell cancer cases and 1,465 controls were included in the analysis. An increased risk of renal cell cancer was observed for workers in agricultural labor and animal husbandry (OR=1.43, 95% CI 1.05, 1.93), particularly among women employed as general farm workers (OR=2.73, 95% CI 1.05, 7.13). Risk gradients for agricultural work increased with longer employment.  An overall increased risk of renal cell cancer was seen among architects and engineers (OR=1.89, 95% CI 1.35, 2.65), and mechanical engineers (OR=1.71, 95% CI 1.03, 2.84).</P>
<P>  
<B>Conclusions:</B> Our data suggest an association between renal cell cancer and agricultural work, particularly among female workers.</P>
]]></description>
<dc:creator><![CDATA[Heck, J. E, Charbotel, B., Moore, L. E, Karami, S., Zaridze, D. G, Matveev, V., Janout, V., Kollarova, H., Foretova, L., Bencko, V., Szeszenia-Dabrowska, N., Lissowska, J., Mates, D., Ferro, G., Chow, W.-H., Rothman, N., Stewart, P., Brennan, P., Boffetta, P.]]></dc:creator>
<dc:date>Mon, 07 Sep 2009 20:10:41 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046250</dc:identifier>
<dc:title><![CDATA[Occupation and renal cell cancer in Central and Eastern Europe]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-07</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.044743v1?rss=1">
<title><![CDATA[Parental occupational exposure to organic solvents and the risk of anencephaly in Mexico]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.044743v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objective:</B> To assess the relationship between parental occupational exposure to organic solvents, and the risk of anencephaly in Mexico.</P>
<P>  
<B>Methods:</B> A case control study was conducted based on the registers of the Epidemiological Surveillance System for Neural Tube Defects in Mexico, 151 cases of anencephaly of 20 weeks or more gestation were included. A control, born alive and without any apparent congenital malformations at birth, was selected for each case in the same maternity service in which the case was born. Information on occupational exposures, lifestyle habits, reproductive history, use of medicines, supplementation with multivitamins and folic acid, was obtained by a general questionnaire; a food frequency questionnaire was also applied to obtain information of daily intake of folate and other vitamins of the group B.  Occupational exposure to organic solvents was based on job title as a proxy for exposure and analyzed considering two critical periods around conception.</P>
<P> 
<B>Results:</B> In logistic regression analysis, the risk of having a child with anencephaly was higher if the mother or the father was occupationally exposed to organic solvents during the periconceptional period, or when  both parents or at least one of them were occupationally exposed during this period with an adjusted odds ratio (OR)  of 2.97 [ 95% confidence interval (CI)= 1.36-6.52].</P>
<P>
<B>Conclusions:</B> The results support the hypothesis that both maternal and  paternal  occupational exposure to organic solvents can increase the risk of having a child with anencephaly.</P>
]]></description>
<dc:creator><![CDATA[Aguilar-Garduno, C., Lacasana, M., Blanco-Munoz, J., Borja-Aburto, V. H., Garcia, A. M]]></dc:creator>
<dc:date>Mon, 07 Sep 2009 20:09:55 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.044743</dc:identifier>
<dc:title><![CDATA[Parental occupational exposure to organic solvents and the risk of anencephaly in Mexico]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-07</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.043281v1?rss=1">
<title><![CDATA[Roles of Age, Length of Service and Job in Work-related Injury: A Prospective Study of 446,120 Person-Years in Railway Workers]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.043281v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> Because work-related injuries are common and yet the mechanisms through which various types of injuries relate to age, length of service and job remain unknown, this study assessed the role of age, length of service and job in work-related injury.</P>
<P>
<B>Methods:</B> Prospective study of all 164,814 permanently employed male workers at the French national railway company during 1998-2000, based on the company&rsquo;s injury database: 446,120 person-years, 15,195 injuries with working days lost, coded using the company&rsquo;s injury classification which is derived from that of the French health insurance scheme. We investigated the incidence of ten types of injury: fall on same level, fall to lower level, handling materials/machine parts during assembly, handling objects, lifting/handling equipment, collision with/by moving objects, collision with/by vehicles, operating machines/equipment, using hand-tools, other injuries. Data were analyzed using negative binomial regression.</P>
<P>
<B>Results:</B> Workers aged &lt;25 were subject to a higher injury risk from handling materials/machine parts during assembly, collision with/by moving objects or vehicles. Older workers, especially those aged 50-55, were subject to a higher risk of fall and injury resulting from lifting/handling materials/equipment/objects or from collision with/by moving objects/vehicles. Using hand-tools was a risky task for workers aged &lt;30 or &ge;40. The relative risk decreased steadily with increasing length of service with the company, from 2.6 for one year to 1.0 for &ge;30 years, and the slope of the trend is stronger for fall to lower level, lifting/handling materials/equipment, and collision with/by moving objects.</P>
<P> 
<B>Conclusion:</B> Younger and older ages and shorter length of service are at risk for various types of injuries. Preventive measures should improve working conditions, especially for younger/older ages, provide knowledge through specific training during the first years in a job and help workers to be more aware of risks associated with their age, years of employment and job.</P>
]]></description>
<dc:creator><![CDATA[Chau, N., Wild, P., Dehaene, D., Benamghar, L., Mur, J.-M., Touron, C.]]></dc:creator>
<dc:date>Mon, 07 Sep 2009 20:09:12 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.043281</dc:identifier>
<dc:title><![CDATA[Roles of Age, Length of Service and Job in Work-related Injury: A Prospective Study of 446,120 Person-Years in Railway Workers]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-07</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.043786v1?rss=1">
<title><![CDATA[Effect of a participatory ergonomics intervention on psychosocial factors at work in a randomized controlled trial]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.043786v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> To study the effect of a participatory ergonomics intervention on psychosocial factors at work among kitchen workers.</P>
<P> 
<B>Design:</B> A cluster randomized controlled trial.</P>
<P> 
<B>Setting:</B> Four cities in Finland in 2002-2005.</P>
<P>
<B>Participants:</B> 504 workers of 119 municipal kitchens.</P>
<P>
<B>Intervention:</B> Kitchens were randomized to intervention (n = 59) and control (n = 60) groups. The intervention lasted 11 to 14 months. It was based on the workers' active participation in work analysis, planning, and implementing the ergonomic changes aimed to decrease physical and mental workload.</P>
<P>
<B>Main outcome measures:</B>  Mental stress, mental strenuousness of work, hurry, job satisfaction, job control, skill discretion, co-worker relationships, supervisor support. Data were collected by questionnaire at baseline, at the end of the intervention, and at a 12- month follow-up (PI12).</P>
<P>
<B>Results:</B> At the end of the intervention, the odds ratio (OR) of job dissatisfaction for the intervention group as compared with the control group was 3.0 (95% CI 1.1-8.5), of mental stress 2.3 (1.2-4.7) and of poor co-worker relationships 2.3 (1.0-5.2). At the PI12, the respective OR of job dissatisfaction was 3.0 (1.2-7.8). Analysis of the independent and joint effects of the intervention and extraneous organizational reforms showed that adverse changes were accentuated among those with exposure to both.</P>
<P> 
<B>Conclusions:</B>  No favourable effects on psychosocial factors at work were found. The adverse changes were due to a joint effect of the intervention and the extraneous organizational reforms. The findings do not support the usefulness of this kind of intervention in changing unsatisfactory psychosocial working conditions.</P>
]]></description>
<dc:creator><![CDATA[Haukka, E., Pehkonen, I., Leino-Arjas, P., Viikari-Juntura, E., Takala, E.-P., Malmivaara, A., Hopsu, L., Mutanen, P., Ketola, R., Virtanen, T., Holtari-Leino, M., Nykanen, J., Stenholm, S., Ojajarvi, A., Riihimaki, H.]]></dc:creator>
<dc:date>Mon, 07 Sep 2009 20:08:30 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.043786</dc:identifier>
<dc:title><![CDATA[Effect of a participatory ergonomics intervention on psychosocial factors at work in a randomized controlled trial]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-07</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.040857v1?rss=1">
<title><![CDATA[Indoor and outdoor fine and ultrafine particles in relation to lung function in asthma / COPD patients in four European cities]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.040857v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> Misclassification of exposure related to the use of central sites may be larger for ultrafine particles than for PM2.5 and PM10 and may result in underestimation of health effects This paper describes the relative strength of the association between outdoor and indoor exposure to ultrafine particles, PM2.5 and PM10 and lung function.</P>
<P>
<B>Methods:</B> In four European cities (Helsinki, Athens, Amsterdam and Birmingham), lung function (FVC, FEV1 and PEF) was measured with three times a day for one week in 135 patients with asthma or COPD, covering study periods of more than one year. Daily concentrations of particle number, PM2.5 and PM10 were measured at a central site in each city and both inside and outside the subjects&rsquo; homes.</P>
<P>
<B>Results:</B> Daily average particle number concentrations ranged between 2,100 and 66,100 particles/cm3.  We found no association between 24-hour average particle number or particle mass concentrations and FVC, FEV1 and PEF. Substituting home outdoor or home indoor concentrations of particulate air pollution instead of the central site measurements did not change the observed associations. Analyses restricted to asthmatics also showed no associations.</P>
<P> 
<B>Conclusions:</B> No consistent associations between lung function and 24-hour average particle number or particle mass concentrations were found in panels of patients with mild to moderate COPD or asthma. More detailed exposure assessment did not change the observed associations. The lack of association could be due to the high prevalence of medication use, limited ability to assess lagged effects over several days or absence of an effect.</P>
]]></description>
<dc:creator><![CDATA[de Hartog, J. J, Ayres, J. G, Karakatsani, A., Analitis, A., ten Brink, H., Hameri, K., Harrison, R. M, Katsouyanni, K., Kotronarou, A., Kavouras, I., Meddings, C., Pekkanen, J., Hoek, G.]]></dc:creator>
<dc:date>Sun, 06 Sep 2009 20:33:30 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.040857</dc:identifier>
<dc:title><![CDATA[Indoor and outdoor fine and ultrafine particles in relation to lung function in asthma / COPD patients in four European cities]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-06</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.044222v1?rss=1">
<title><![CDATA[Third follow-up of a Dutch cohort occupationally exposed to chlorophenoxy herbicides, chlorophenols and dioxins]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.044222v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objective:</B> A retrospective cohort study was conducted in two chlorophenoxy herbicide manufacturing factories, producing mainly 2,4,5-T (factory A) and MCPA, MCPP, and 2,4-D (factory B). Previously, we have shown elevated risks for mortality and cancer mortality in this cohort. The purpose of the current, third follow-up, is to provide an updated assessment of cause-specific mortality for both factories.</P>
<P>
<B>Methods:</B> The study population was defined as all persons working in one of the two factories during 1955-1985 for factory A, or during 1965-1986 for factory B. Analyses were done using Cox proportional hazard models, using attained age as the time-scale. Exposure to phenoxy herbicides and dioxins was expected to be different for factory A and B and the factories were therefore analyzed separately.</P>
<P> 
<B>Results:</B> Previously reported increased risks for respiratory cancer, non-Hodgkin&rsquo;s lymphoma and ischemic heart disease in factory A could not be confirmed in the present analysis. However, increased risks were observed for all cancers in both factory A (HR=1.31; 95% CI 0.86-2.01) and factory B (HR=1.54; 95% CI 1.00-2.37). Increased risks for urinary cancers (HR=4.2; 95% CI 0.99-17.89) and genital cancers (HR=2.93; 95% CI 0.61-14.15) were observed in factory A, consistent with earlier reported results in this population. More detailed analyses showed that this increased risk for urinary and genital cancers in exposed workers was not due to selection of healthy controls and could not be attributed to specific products or departments.</P>
<P>  
<B>Conclusion:</B> The results of this study showed only slight increases in cancer mortality risk. The increased risk for urinary cancers is noteworthy, but could not be linked to a specific exposure and needs to be confirmed in similar cohorts.</P>
]]></description>
<dc:creator><![CDATA[Boers, D., Portengen, L., Bueno-de-Mesquita, H B., Heederik, D. J J, Vermeulen, R.]]></dc:creator>
<dc:date>Sun, 06 Sep 2009 20:32:19 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.044222</dc:identifier>
<dc:title><![CDATA[Third follow-up of a Dutch cohort occupationally exposed to chlorophenoxy herbicides, chlorophenols and dioxins]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-06</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.043794v1?rss=1">
<title><![CDATA[Circulating adhesion molecules after short-term exposure to particulate matter among welders]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.043794v1?rss=1</link>
<description><![CDATA[
<p><P><B>Background:</B>  Studies from several countries indicate that welders experience increased risk of mortality and morbidity from ischemic heart disease. Although the underlying mechanisms are unclear, vascular responses to particulate matter contained in welding fumes may play a role. To investigate this, we studied the acute effects of welding fume exposure on the endothelial component of vascular function, as measured by circulating adhesion molecules involved in leukocyte adhesion (sICAM-1 and sVCAM-1) and coagulation (vWF).</P>
<P> 
<B>Methods:</B> A panel of twenty-six male welders was studied repeatedly across a six-hour work-shift on a high exposure welding day and/or a low exposure non-welding day. Personal PM<SUP>2.5</SUP> exposure was measured throughout the work-shift. Blood samples were collected in the morning (baseline) prior to the exposure period, immediately after the exposure period, and the following morning. To account for the repeated measurements, we used linear mixed models to evaluate the effects of welding (binary) and PM<SUP>2.5</SUP> (continuous) exposure on each blood marker, adjusting for baseline blood marker concentration, smoking, age, and time of day.</P>
<P> 
<B>Results:</B> Welding and PM<SUP>2.5</SUP> exposure were associated with a statistically significant decrease in sVCAM-1 in the afternoon and the next morning and increase in vWF in the afternoon.</P>
<P> 
<B>Conclusions:</B> The data suggest that welding and short-term occupational exposures to PM<SUP>2.5</SUP> may acutely affect the endothelial component of vascular function.</P>
]]></description>
<dc:creator><![CDATA[Fang, S. C, Eisen, E. A, Cavallari, J. M, Mittleman, M. A, Christiani, D. C]]></dc:creator>
<dc:date>Sun, 06 Sep 2009 20:31:28 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.043794</dc:identifier>
<dc:title><![CDATA[Circulating adhesion molecules after short-term exposure to particulate matter among welders]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-06</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.039578v1?rss=1">
<title><![CDATA[Occupational Asthma & Allergy in Snow Crab Processing in Newfoundland and Labrador]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.039578v1?rss=1</link>
<description><![CDATA[
<p><P><B>Background:</B> Risk factors and prevalence of occupational asthma (OA) and allergy (OAl) in the snow crab processing industry have been poorly studied.</P>
<P> 
<B>Aim:</B> Estimate the prevalence of OA and OAl in snow crab processing workers and determine their relationship with exposure to snow crab allergens and other potential risk factors.</P>
<P>
<B>Methods:</B> A total of 215 workers (120 F/95 M) were recruited from four plants in Newfoundland and Labrador, Canada in 2001-02.  Results from questionnaires, skin-prick tests to snow crab meat and cooking water, specific IgE against the latter, spirometry and peak flow monitoring were used to develop a diagnostic algorithm. An index based on work history and exposure measurements of snow crab aeroallergens was developed to estimate the cumulative exposure for each worker.</P>
<P>
<B>Results:</B> The prevalence of almost certain or highly probable OA and OAl were 15.8% and 14.9%, respectively. A high cumulative exposure to crab allergens, in jobs mostly held by women, was associated with OA (OR=14.0; 95% confidence intervals 3.0-65.8) (highest vs. lowest cumulative exposure index) and with OAl (OR=7.1, 1.9-29.0); job held when symptoms started (cleaning, packing, freezing) also predicted OA (OR=3.9, 1.6-8.7) and OAl (OR=3.2, 1.4-7.5). Atopy (OR=2.8; 1.2-6.8), female gender (OR=10.7; 3.6-32.1) and smoking were significant determinants for OA (OR=3.1, 1.3-7.4).</P>
<P>
<B>Conclusions:</B> The prevalence of OA and OAl is high in snow crab processing workers of the Canada's East Coast. Cumulative exposure to snow crab allergens was related to the prevalence of OA and OAl in a dose-response manner taking into account atopy, gender and smoking.</P>
]]></description>
<dc:creator><![CDATA[Gautrin, D., Cartier, A., Howse, D., Horth-Susin, L., Jong, M., Swanson, M., Lehrer, S., Fox, G., Neis, B.]]></dc:creator>
<dc:date>Sun, 06 Sep 2009 20:30:04 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.039578</dc:identifier>
<dc:title><![CDATA[Occupational Asthma & Allergy in Snow Crab Processing in Newfoundland and Labrador]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-09-06</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.042663v1?rss=1">
<title><![CDATA[Early Changes in Respiratory Health in Trades' Apprentices and Physician Visits for Respiratory Illnesses Later in Life]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.042663v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> An inception cohort of trades' apprentices had rapid declines in lung function (FEV1) and rapid increases in bronchial responsiveness (BR) over the first 2 years of employment. We used physician visit data to assess respiratory health over the following 13 years.</P>
<P>
<B>Methods:</B> Construction painter, electrician, insulator and machinist apprentices beginning at a British Columbia trade school in 1988 were invited to participate and were followed-up 2 years later. Subjects were linked to provincial medical databases to examine physician visits for asthma and other respiratory illnesses for the 13 years following. Multivariable models with rapid decline in FEV1 and rapid increase in BR from year 1-3 were constructed. Respiratory symptoms were also examined as predictors of visit rates and meeting a case definition (for asthma or other respiratory illness).</P>
<P>
<B>Results:</B> The cohort included 281 apprentices (97% male). Sixteen subjects met the asthma case definition (&ge;2 visits coded as asthma in 1 year) and 20 met the other respiratory illness case definition (&ge;3 visits for bronchitis, emphysema, respiratory symptoms in 1 year). In models controlling for demographic factors and smoking, subjects with bronchitis symptoms at baseline were more likely to develop other respiratory illness during follow-up (RR 4.4 95%CI 1.6 -11.9). Apprentices who developed asthma symptoms over the first 2 years were approximately six times more likely to become asthma cases (95%CI 1.9 - 18.8). Those with a rapid increase in BR were at increased risk of becoming asthma cases (RR 5.5, 95%CI 1.9 - 16.1)), as well as having higher asthma visit rates (RR 6.5). Subjects with rapid decline in FEV<SUB>1</SUB> were 3.2 times more likely to become asthma cases (95%CI 0.8 - 12.1)).</P>
<P>
<B>Conclusions:</B> Changes in respiratory health early in adulthood, especially increased BR, are associated with respiratory physician visits. These findings are important for workplace screening and prevention, and also suggest that physician visit databases are promising research tools in respiratory epidemiology.</P>
]]></description>
<dc:creator><![CDATA[Peters, C E, Demers, P A, Sehmer, J, Karlen, B, Kennedy, S M]]></dc:creator>
<dc:date>Sun, 09 Aug 2009 23:05:15 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.042663</dc:identifier>
<dc:title><![CDATA[Early Changes in Respiratory Health in Trades' Apprentices and Physician Visits for Respiratory Illnesses Later in Life]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-08-09</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.045393v1?rss=1">
<title><![CDATA[Coarse Particles and Mortality:  Evidence from a Multi-City Study in California]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.045393v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objective:</B> To examine the risk of all-cause and cardiovascular mortality associated with short-term coarse particle exposure in California while addressing issues of exposure misclassification by limiting the study to those residing near a pollution monitor.</P>
<P>  
<B>Methods:</B> Deaths in 15 California counties from 1999-2005 were linked to coarse particulate monitoring data.  Case deaths were limited to those residing in a zip code within 20 km of a pollution monitor.  We used conditional logistic regression with a case-crossover design to estimate county-specific effects of coarse particles.  County estimates were then pooled using random-effects meta-analysis to create overall study estimates.  Effects specific to race and educational status were also analyzed.</P>
<P> 
<B>Results:</B> We observed an increased excess risk (ER) of both all-cause mortality (ER per 10 &micro;g/m<SUP>3</SUP> = 0.7%, 95% CI: -0.1, 1.5) and cardiovascular mortality (ER per 10 &micro;g/m<SUP>3</SUP> = 1.3%, 95% CI: 0.1, 2.5) from a two-day lag in coarse particles.  Greater effects were observed among Hispanics and non-high school graduates.  Adjustment for fine particles and decreasing the inclusion buffer to 10 km did not substantively alter the results.</P>
<P>  
<B>Conclusions:</B> Our study provides further evidence of an association between acute exposure to coarse particles and mortality, and supports the hypothesis that lower socioeconomic status groups may be more susceptible to its effects.</P>
]]></description>
<dc:creator><![CDATA[Malig, B. J, Ostro, B. D]]></dc:creator>
<dc:date>Thu, 30 Jul 2009 22:31:02 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.045393</dc:identifier>
<dc:title><![CDATA[Coarse Particles and Mortality:  Evidence from a Multi-City Study in California]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-07-30</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.044693v1?rss=1">
<title><![CDATA[Mortality from cancer and other causes in the balangero cohort of chrysotile asbestos miners]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.044693v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> To provide further information on mortality from cancer and other causes among chrysotile asbestos miners several years after stopping exposure, we updated the analyses from the cohort of Balangero mine workers with follow-up to the end of 2003.</P>
<P>
<B>Methods:</B> The cohort included 1056 males, for a total of 34,432 man-years of observation. We obtained employment data from personnel records at the factory, and ascertained vital status and causes of death through population registers and death certificates from municipal registration offices. We computed expected numbers of death and standardized mortality ratios (SMR) for relevant causes using the province of Turin and national death rates, for each 5-year calendar period and age group.</P>
<P>
<B>Results:</B> We found a significant excess mortality from pleural cancer only (4 deaths, SMR=4.67) and pleural and peritoneal cancers combined (5 deaths, SMR=3.16). All pleural and peritoneal cancer deaths occurred 30 or more years after first exposure. The SMRs were 1.27 for lung cancer (45 deaths), 1.82 for laryngeal cancer (8 deaths) and 1.12 for all cancers (142 deaths). Cumulative dust exposure and various time factors considered did not show a clear pattern of risk with mortality from lung cancer. There were 57 deaths from cirrhosis (SMR=2.94) and 54 from accidents and violence (SMR=1.88). Overall, we observed a total of 590 deaths as compared to 412.9 expected (SMR=1.43).</P>
<P> 
<B>Conclusions:</B> This updated analysis, with almost 60% of workers of the cohort who had died, confirmed the excess mortality from pleural and peritoneal cancers and from several alcohol-related causes.</P>
]]></description>
<dc:creator><![CDATA[Pira, E., Pelucchi, C., Piolatto, P. G., Negri, E., Bilei, T., La Vecchia, C.]]></dc:creator>
<dc:date>Wed, 29 Jul 2009 22:47:24 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.044693</dc:identifier>
<dc:title><![CDATA[Mortality from cancer and other causes in the balangero cohort of chrysotile asbestos miners]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-07-29</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.043265v1?rss=1">
<title><![CDATA[Cancer risk of radiation workers larger than expected?]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.043265v1?rss=1</link>
<description><![CDATA[
<p><P><B>Background:</B> Occupational exposures to ionizing radiation mainly occur at low dose rates and may accumulate effective doses of up to several hundred milligray. It is presently assumed that the cancer risk per dose after such exposures is smaller than for acute, high-dose exposures.</P>
<P>
<B>Objective:</B> To evaluate the evidence of cancer risks from low-dose-rate, moderate-dose (LDRMD) exposures to ionizing radiation.</P>
<P>
<B>Methods:</B> A literature search for primary epidemiological studies on cancer incidence and mortality risks from LDRMD exposures included publications from 2002 to 2007, and an update of the UK National Registry for Radiation Workers study. The analysis was restricted to studies reporting excess relative risk (ERR) estimates per dose for all or large groups of cancers. For each study we calculated the risk for the same types of cancer among the atomic bomb survivors with the same gender proportion and matched quantities for dose, mean age-attained and mean age-at-exposure. A combined estimator of the ratio of the ERR per dose from the LDRMD to the corresponding value for the atomic bomb survivors was calculated.</P>
<P>
<B>Results:</B> Generally, the ERR per dose was larger than or similar to the corresponding estimate for the atomic bomb survivors. Overall, the ratio of the ERR per dose in the LDRMD studies to the corresponding quantity in the atomic bomb survivors was 1.21 (90% CI: 0.51; 1.90).</P>
<P>
<B>Conclusions:</B> The present analysis does not confirm that the cancer risk per dose for LDRMD exposures is lower than for acute, high-dose exposures. Although the individual epidemiological studies all have methodological and statistical limitations, the results of the present analysis challenge the cancer risk values currently assumed for occupational exposures. This particularly applies to the use of a dose and dose-rate effectiveness factor (DDREF) for low-dose-rate exposures.</P>
]]></description>
<dc:creator><![CDATA[Jacob, P, Ruhm, W, Walsh, L, Blettner, M, Hammer, G, Zeeb, H]]></dc:creator>
<dc:date>Tue, 30 Jun 2009 22:59:05 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.043265</dc:identifier>
<dc:title><![CDATA[Cancer risk of radiation workers larger than expected?]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-06-30</prism:publicationDate>
<prism:section>Review</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.045047v1?rss=1">
<title><![CDATA[Traffic Particles and Occurrence of Acute Myocardial Infarction: a case-control analysis]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.045047v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> We modeled exposure to traffic particles using a latent variable approach and investigated whether long-term exposure to traffic particles is associated with an increase in the occurrence of acute myocardial infarction (AMI) using data from a population-based coronary disease registry.</P>
<P>  
<B>Methods:</B> Cases of individually validated AMI were identified between 1995 and 2003 as part of the Worcester Heart Attack Study. Population controls were selected from Massachusetts, USA, resident lists. NO2 and PM2.5 filter absorbance were measured at 36 locations throughout the study area. The air pollution data were used to estimate exposure to traffic particles using a semiparametric latent variable regression model. Conditional logistic models were used to estimate the association between exposure to traffic particles and occurrence of AMI.</P>
<P> 
<B>Results:</B> Modeled exposure to traffic particles was highest near the city of Worcester. Cases of AMI were more exposed to traffic and traffic particles compared to controls. An interquartile range increase in modeled traffic particles was associated with a 10% (95% CI 4%, 16%) increase in the odds of AMI.  Accounting for spatial dependence at the census tract, but not block group, scale substantially attenuated this association.</P>
<P> 
<B>Conclusions:</B> These results provide some support for an association between long-term exposure to traffic particles and risk of AMI.  The results were sensitive to the scale selected for the analysis of spatial dependence, an issue that requires further investigation.  The latent variable model captured variation in exposure, though on a relatively large spatial scale.</P>
]]></description>
<dc:creator><![CDATA[Tonne, C., Yanosky, J., Gryparis, A., Melly, S., Mittleman, M., Goldberg, R., von Klot, S., Schwartz, J.]]></dc:creator>
<dc:date>Tue, 23 Jun 2009 22:32:45 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.045047</dc:identifier>
<dc:title><![CDATA[Traffic Particles and Occurrence of Acute Myocardial Infarction: a case-control analysis]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-06-23</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.045427v1?rss=1">
<title><![CDATA[Cancer incidence and mortality in a historical cohort of Australian pest control workers]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.045427v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B>  To determine the rates of mortality and incident cancer in a historical cohort of pest control operators.</P>
<P>
<B>Methods:</B>  A retrospective cohort was assembled from former state government occupational health surveillance programs.  This cohort was linked to the Australian national registries of cancer and mortality and the results were compared with the general Australian population rates.</P>
<P>
<B>Results:</B> 125 deaths and 89 incident cancers were found during the periods of observation (mortality 1983-2004 and cancer 1983-2002). Overall cancer incidence and mortality rates were not found to be significantly different from the general population.  Among the specific causes of death, suicide and unintentional falls were significantly in excess, although the latter was based on only 4 deaths.  Melanoma was the only specific incident cancer found significantly in excess.</P>
<P>  
<B>Conclusions:</B>  Pest control workers have overall mortality and cancer rates similar to the general population.  Excess rates of incident melanoma and intentional self-poisoning mortality are of concern and warrant further investigation.  Follow up of this cohort as its members age will provide more insight into these possible associations.</P>
]]></description>
<dc:creator><![CDATA[MacFarlane, E, Benke, G, Del Monaco, A, Sim, M R]]></dc:creator>
<dc:date>Tue, 23 Jun 2009 22:32:09 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.045427</dc:identifier>
<dc:title><![CDATA[Cancer incidence and mortality in a historical cohort of Australian pest control workers]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-06-23</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2009.046128v1?rss=1">
<title><![CDATA[A prospective cohort study of exposure-response relationship for  vibration induced white finger]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2009.046128v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> To investigate prospectively the relation between vibration-induced white finger (VWF) and measures of cumulative (lifetime) exposure to hand-transmitted vibration (HTV).</P>
<P>
<B>Methods:</B> Two hundred and forty-nine HTV workers and 138 control men of the same companies participated in a three-year follow up study. The diagnosis of VWF (Raynaud&rsquo;s phenomenon in the controls) was based on the medical history, the administration of color charts and the results of a cold test. Tool vibration magnitudes were expressed as r.m.s acceleration, frequency weighted according to international standard ISO 5349-1 and also unweighted over the frequency range 6.3 to 1250 Hz. From the vibration magnitudes and exposure durations, alternative measures of cumulative vibration dose were calculated for each HTV worker, according to the expression: dose = <I>a</I><SUB><I>i</I></SUB><SUP><I>m</I></SUP>t<SUB><I>i</I></SUB>, where a<SUB><I>i</I></SUB> is the acceleration magnitude on tool i, ti is the lifetime exposure duration (hours) for tool i, and m = 0, 1, 2 or 4.</P>
<P> 
<B>Results:</B> The incidence of VWF varied from 5 to 6% in the HTV workers vs 0 to 1.5% for Raynaud&rsquo;s phenomenon in the controls. After adjusting for potential confounders, measures of cumulative vibration dose derived from total operating hours and high powers of unweighted acceleration (i.e. <I>a</I><SUP><I>m</I></SUP><SUB><I>uwi</I></SUB>t<SUB><I>i</I></SUB>, with <I>m</I>&gt;1) gave better predictions of the occurrence of VWF than dose measures calculated from frequency-weighted acceleration (i.e. <I>a</I><SUP><I>m</I></SUP><SUB><I>wi</I></SUB>t<SUB><I>i</I></SUB>). These findings were observed in the entire sample of HTV workers, in those with no VWF at the initial investigation, and in those with normal cold test results at baseline.</P>
<P>
<B>Conclusions:</B> This prospective cohort study suggests that measures of cumulative vibration doses constructed from unweighted r.m.s. acceleration perform better for the prediction of VWF than dose measures calculated according to the recommendations of current standards. These findings should contribute to the improvement of the ISO frequency weighting for evaluating the severity of hand-transmitted vibration.</P>
]]></description>
<dc:creator><![CDATA[Bovenzi, M.]]></dc:creator>
<dc:date>Sun, 14 Jun 2009 19:17:26 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046128</dc:identifier>
<dc:title><![CDATA[A prospective cohort study of exposure-response relationship for  vibration induced white finger]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-06-14</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2008.044396v1?rss=1">
<title><![CDATA[Night-work, long working hours, job control and cortisol secretion in mid-life: evidence from a British birth cohort]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2008.044396v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> To examine the relationships between exposure to workplace factors (night-work, extended working hours, psychosocial work stress) and cortisol secretion, and to test whether workplace factors interact, resulting in combined effects.</P>
<P>
<B>Methods:</B> Multiple linear and logistic regression was used to test relationships between workplace factors and cortisol secretion in the 1958 British birth cohort at 45y.  Salivary cortisol was measured twice on the same day to capture the post-waking decline, facilitating the analysis of different cortisol patterns: (i) Time 1 (T1, 45min post-waking) (ii) Time 2 (T2, 3hrs after T1) (iii) average 3h exposure from T1 to T2 cortisol (iv) T1 to T2 change. To identify altered diurnal cortisol patterns we calculated (i) flat T1-T2 change in cortisol (ii) top 5% T1 (iii) bottom 5% T1 (iv) T1 hypo- or hyper-secretion. Models were adjusted for socio-economic position at birth and in adulthood, qualifications, marital status, dependent children, and smoking status.</P>
<P>
<B>Results:</B> 25% of men and 8% of women were exposed to &gt;1 workplace factor (night-work, extended work-hours, job-strain). Night-work was associated with a 4.28% (95%CI=1.21, 7.45) increase in average 3h cortisol secretion independently of job strain or work hours. Night workers not exposed to job strain had elevated T1 cortisol (5.81%, 1.61, 10.19), although for T2 cortisol it was night-workers exposed to low job control who had elevated levels (11.72%, 4.40, 19.55). Men (but not women) working &gt;48 hrs/week had lower average 3h cortisol secretion (4.55%, -8.43, -0.50). There were no main effects for psychosocial work stress. All associations for T2 and average 3h cortisol secretion weakened slightly after adjustment for confounding factors, but associations for T1 cortisol were unaffected by adjustment.</P>
<P>
<B>Conclusions:</B> Our study suggests that night-work in particular is associated with elevated cortisol secretion and that cortisol dysregulation may exist in subgroups with specific combinations of stressors.</P>
]]></description>
<dc:creator><![CDATA[Thomas, C., Hertzman, C., Power, C.]]></dc:creator>
<dc:date>Sun, 14 Jun 2009 19:16:10 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.044396</dc:identifier>
<dc:title><![CDATA[Night-work, long working hours, job control and cortisol secretion in mid-life: evidence from a British birth cohort]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2009-06-14</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/oem.2005.025213v1?rss=1">
<title><![CDATA[NO2 and children{inverted exclamation}|s respiratory symptoms in the PATY study]]></title>
<link>http://oem.bmj.com/cgi/content/short/oem.2005.025213v1?rss=1</link>
<description><![CDATA[
<p><P><B>Objectives:</B> 
NO2 is a major urban air pollutant. Previously reported associations between ambient NO2 and children&iexcl;&brvbar;s respiratory health have been inconsistent, and independent effects of correlated pollutants hard to assess.  We examine effects of NO2 on a spectrum of  11 respiratory symptoms, controlling for PM10 and SO2, using a large pooled dataset.
</P>
<P>
<B>Methods:</B>  Cross-sectional studies were conducted in Russia, Austria, Italy, Switzerland and The Netherlands, during 1993-1999, contributing in total 23,955 children.  Study-specific odds ratios for associations with ambient NO2 are estimated using logistic regressions with area-level random effects. Heterogeneity between study-specific results, and mean estimates (allowing for heterogeneity) are calculated. 
</P>
<P>
<B>Results:</B> Long-term average NO2 concentrations were unrelated to prevalences of bronchitis or asthma.  Associations were found for sensitivity to inhaled allergens and allergy to pets, with mean odds ratios around 1.14 per 10 &igrave;g/m3 NO2.  SO2 had little confounding effect, but an initial association between NO2 and morning cough was reduced after controlling for PM10.   Associations with reported allergy were not reduced by adjustment for the other pollutants. Odds ratios for allergic symptoms tended to be higher for the 9-12 year old children compared to the 6-8 year old children. 
</P>
<P>
<B>Conclusions:</B> Evidence for associations between NO2 and respiratory symptoms was robust only for inhalation allergies.  NO2 most likely is acting as an indicator of traffic-related air pollutants, though its direct effect cannot be ruled out. This remains important, as policies to reduce traffic-related air pollution will not result in rapid reductions.</P>
]]></description>
<dc:creator><![CDATA[Pattenden, S., Hoek, G., Braun-Fahrlander, C., Forastiere, F., Kosheleva, A., Neuberger, M., Fletcher, A C]]></dc:creator>
<dc:date>Mon, 17 Jul 2006 04:47:24 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2005.025213</dc:identifier>
<dc:title><![CDATA[NO2 and children{inverted exclamation}|s respiratory symptoms in the PATY study]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:publicationDate>2006-07-17</prism:publicationDate>
<prism:section>Original Article</prism:section>
</item>

</rdf:RDF>