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<title>Occupational and Environmental Medicine current issue</title>
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<prism:coverDisplayDate>Nov  1 2009 12:00:00:000AM</prism:coverDisplayDate>
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<title>Occupational and Environmental Medicine</title>
<url>http://oem.bmj.com/homepage/OEM_95x60.gif</url>
<link>http://oem.bmj.com</link>
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<item rdf:about="http://oem.bmj.com/cgi/content/short/66/11/713?rss=1">
<title><![CDATA[Predicting occupational diseases]]></title>
<link>http://oem.bmj.com/cgi/content/short/66/11/713?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Suarthana, E., Meijer, E., Grobbee, D. E, Heederik, D.]]></dc:creator>
<dc:date>Fri, 16 Oct 2009 10:01:41 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.045609</dc:identifier>
<dc:title><![CDATA[Predicting occupational diseases]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>66</prism:volume>
<prism:endingPage>714</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>713</prism:startingPage>
<prism:section>Editorial</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/66/11/715?rss=1">
<title><![CDATA[Deciphering the clinical spectrum of occupational rhinitis]]></title>
<link>http://oem.bmj.com/cgi/content/short/66/11/715?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Gautrin, D., Castano, R.]]></dc:creator>
<dc:date>Fri, 16 Oct 2009 10:01:41 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.043190</dc:identifier>
<dc:title><![CDATA[Deciphering the clinical spectrum of occupational rhinitis]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>66</prism:volume>
<prism:endingPage>716</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>715</prism:startingPage>
<prism:section>Commentaries</prism:section>
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<item rdf:about="http://oem.bmj.com/cgi/content/short/66/11/716?rss=1">
<title><![CDATA[An improved estimate of the quantitative relationship between polycyclic hydrocarbons and lung cancer]]></title>
<link>http://oem.bmj.com/cgi/content/short/66/11/716?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mirabelli, D.]]></dc:creator>
<dc:date>Fri, 16 Oct 2009 10:01:41 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.047720</dc:identifier>
<dc:title><![CDATA[An improved estimate of the quantitative relationship between polycyclic hydrocarbons and lung cancer]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>66</prism:volume>
<prism:endingPage>717</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>716</prism:startingPage>
<prism:section>Commentaries</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/66/11/718?rss=1">
<title><![CDATA[Rhinitis associated with pesticide exposure among commercial pesticide applicators in the Agricultural Health Study]]></title>
<link>http://oem.bmj.com/cgi/content/short/66/11/718?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>Rhinitis is common, but the risk factors are not well described. To investigate the association between current rhinitis and pesticide use, we used data from 2245 Iowa commercial pesticide applicators in the Agricultural Health Study.</p>
</sec>
<sec><st>Methods:</st>
<p>Using logistic regression models adjusted for age, education and growing up on a farm, we evaluated the association between current rhinitis and 34 pesticides used in the past year.</p>
</sec>
<sec><st>Results:</st>
<p>74% of commercial pesticide applicators reported at least one episode of rhinitis in the past year (current rhinitis). Five pesticides used in the past year were significantly positively associated with current rhinitis: the herbicides 2,4-D, glyphosate and petroleum oil, the insecticide diazinon and the fungicide benomyl. The association for 2,4-D and glyphosate was limited to individuals who used both in the past year (OR 1.42, 95% CI 1.14 to 1.77). Both petroleum oil and diazinon showed consistent evidence of an association with rhinitis, based on both current use and exposure&ndash;response models. We saw no evidence of confounding by common agricultural rhinitis triggers such as handling grain or hay.</p>
</sec>
<sec><st>Conclusions:</st>
<p>Exposure to pesticides may increase the risk of rhinitis.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Slager, R E, Poole, J A, LeVan, T D, Sandler, D P, Alavanja, M C R, Hoppin, J A]]></dc:creator>
<dc:date>Fri, 16 Oct 2009 10:01:41 PDT</dc:date>
<dc:subject><![CDATA[Agriculture and farming, Other]]></dc:subject>
<dc:identifier>info:doi/10.1136/oem.2008.041798</dc:identifier>
<dc:title><![CDATA[Rhinitis associated with pesticide exposure among commercial pesticide applicators in the Agricultural Health Study]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>66</prism:volume>
<prism:endingPage>724</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>718</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/66/11/725?rss=1">
<title><![CDATA[Cancer mortality and congenital anomalies in a region of Italy with intense environmental pressure due to waste]]></title>
<link>http://oem.bmj.com/cgi/content/short/66/11/725?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>Waste management in the Campania region has been characterised, since the 1980s, by widespread uncontrolled and illegal practices of waste dumping, generating concerns over the health implications. The objective of this study was to evaluate possible adverse health effects of such environmental pressure.</p>
</sec>
<sec><st>Methods:</st>
<p>The health effects of waste-related environmental exposures in Campania were assessed in a correlation study on nine causes of death (for the years 1994&ndash;2001) and 12 types of congenital anomaly (CA) (1996&ndash;2002) in 196 municipalities of the provinces of Naples and Caserta. Poisson regression was used to analyse the association between health outcomes and environmental contamination due to waste, as measured through a composite index, adjusting for deprivation.</p>
</sec>
<sec><st>Results:</st>
<p>Statistically significant excess relative risks (ERR, %) in high-index compared with low-index (unexposed) municipalities were found for all-cause mortality (9.2 (95% CI 6.5 to 11.9) in men and 12.4 (9.5 to 15.4) in women and liver cancer (19.3 (1.4 to 40.3) in men and 29.1 (7.6 to 54.8) in women). Increased risks were also found for all cancer mortality (both sexes), stomach and lung cancer (in men). Statistically significant ERRs were found for CAs of the internal urogenital system (82.7 (25.6 to 155.7)) and of the central nervous system (83.5 (24.7 to 169.9)).</p>
</sec>
<sec><st>Conclusion:</st>
<p>Although the causal nature of the association is uncertain, findings support the hypothesis that waste-related environmental exposures in Campania produce increased risks of mortality and, to a lesser extent, CAs.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Martuzzi, M, Mitis, F, Bianchi, F, Minichilli, F, Comba, P, Fazzo, L]]></dc:creator>
<dc:date>Fri, 16 Oct 2009 10:01:41 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.044115</dc:identifier>
<dc:title><![CDATA[Cancer mortality and congenital anomalies in a region of Italy with intense environmental pressure due to waste]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>66</prism:volume>
<prism:endingPage>732</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>725</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/66/11/733?rss=1">
<title><![CDATA[Regression models for public health surveillance data: a simulation study]]></title>
<link>http://oem.bmj.com/cgi/content/short/66/11/733?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>Poisson regression is now widely used in epidemiology, but researchers do not always evaluate the potential for bias in this method when the data are overdispersed. This study used simulated data to evaluate sources of overdispersion in public health surveillance data and compare alternative statistical models for analysing such data. If count data are overdispersed, Poisson regression will not correctly estimate the variance. A model called negative binomial 2 (NB2) can correct for overdispersion, and may be preferred for analysis of count data. This paper compared the performance of Poisson and NB2 regression with simulated overdispersed injury surveillance data.</p>
</sec>
<sec><st>Methods:</st>
<p>Monte Carlo simulation was used to assess the utility of the NB2 regression model as an alternative to Poisson regression for data which had several different sources of overdispersion. Simulated injury surveillance datasets were created in which an important predictor variable was omitted, as well as with an incorrect offset (denominator). The simulations evaluated the ability of Poisson regression and NB2 to correctly estimate the true determinants of injury and their confidence intervals.</p>
</sec>
<sec><st>Results:</st>
<p>The NB2 model was effective in reducing overdispersion, but it could not reduce bias in point estimates which resulted from omitting a covariate which was a confounder, nor could it reduce bias from using an incorrect offset. One advantage of NB2 over Poisson for overdispersed data was that the confidence interval for a covariate was considerably wider with the former, providing an indication that the Poisson model did not fit well.</p>
</sec>
<sec><st>Conclusion:</st>
<p>When overdispersion is detected in a Poisson regression model, the NB2 model should be fit as an alternative. If there is no longer overdispersion, then the NB2 results may be preferred. However, it is important to remember that NB2 cannot correct for bias from omitted covariates or from using an incorrect offset.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Kim, H, Kriebel, D]]></dc:creator>
<dc:date>Fri, 16 Oct 2009 10:01:41 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.042887</dc:identifier>
<dc:title><![CDATA[Regression models for public health surveillance data: a simulation study]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>66</prism:volume>
<prism:endingPage>739</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>733</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/66/11/740?rss=1">
<title><![CDATA[Exposure-response relationship between lung cancer and polycyclic aromatic hydrocarbons (PAHs)]]></title>
<link>http://oem.bmj.com/cgi/content/short/66/11/740?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>To estimate the exposure&ndash;response function associating polycyclic aromatic hydrocarbon (PAH) exposure and lung cancer, with consideration of smoking.</p>
</sec>
<sec><st>Methods:</st>
<p>Mortality, occupational exposure and smoking histories were ascertained for a cohort of 16 431 persons (15 703 men and 728 women) who had worked in one of four aluminium smelters in Quebec from 1950 to 1999. A variety of exposure&ndash;response functions were fitted to the cohort data using generalised relative risk models.</p>
</sec>
<sec><st>Results:</st>
<p>In 677 lung cancer cases there was a clear trend of increasing risk with increasing cumulative exposure to PAH measured as benzo(a)pyrene (BaP). A linear model predicted a relative risk of 1.35 (95% CI 1.22 to 1.51) at 100 &micro;g/m<sup>&ndash;3</sup> BaP years, but there was a significant departure from linearity in the direction of decreasing slope with increasing exposures. Among the models tried, the best fitting were a two-knot cubic spline and a power curve (RR = (1+bx)<sup>p</sup>), the latter predicting a relative risk of 2.68 at 100 &micro;g/m<sup>&ndash;3</sup> BaP years. Additive models and multiplicative models for combining risks from occupational PAH and smoking fitted almost equally well, with a slight advantage to the additive.</p>
</sec>
<sec><st>Conclusion:</st>
<p>Despite the large cohort with long follow-up, the shape of the exposure&ndash;response function and the mode of combination of risks due to occupational PAH and smoking remains uncertain. If a linear exposure&ndash;response function is assumed, the estimated slope is broadly in line with the estimate from a previous follow-up of the same cohort, and somewhat higher than the average found in a recent meta-analysis of lung cancer studies.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Armstrong, B G, Gibbs, G]]></dc:creator>
<dc:date>Fri, 16 Oct 2009 10:01:41 PDT</dc:date>
<dc:subject><![CDATA[Other exposures]]></dc:subject>
<dc:identifier>info:doi/10.1136/oem.2008.043711</dc:identifier>
<dc:title><![CDATA[Exposure-response relationship between lung cancer and polycyclic aromatic hydrocarbons (PAHs)]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>66</prism:volume>
<prism:endingPage>746</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>740</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/66/11/747?rss=1">
<title><![CDATA[Associations of long- and short-term air pollution exposure with markers of inflammation and coagulation in a population sample]]></title>
<link>http://oem.bmj.com/cgi/content/short/66/11/747?rss=1</link>
<description><![CDATA[
<sec><st>Background:</st>
<p>Exposure to elevated levels of ambient air pollutants can lead to adverse cardiovascular effects. Potential mechanisms include systemic inflammation and perturbation of the coagulation balance.</p>
</sec>
<sec><st>Objectives:</st>
<p>To investigate long- and short-term effects of air pollution exposure on serum levels of inflammatory (IL-6, TNF- and CRP) and coagulation (fibrinogen and PAI-1) markers relevant for cardiovascular pathology.</p>
</sec>
<sec><st>Methods:</st>
<p>The study group consisted of a population sample of 1028 men and 508 women aged 45&ndash;70 years from Stockholm. Long-term air pollution exposure was assessed using spatial modelling of traffic-related NO<SUB>2</SUB> and heating-related SO<SUB>2</SUB> emissions at each subject&rsquo;s residential addresses over retrospective periods of 1, 5 and 30 years. Short-term exposure was assessed as averages of rooftop measurements over 12&ndash;120 h before blood sampling.</p>
</sec>
<sec><st>Results:</st>
<p>Long-term exposures to both traffic-NO<SUB>2</SUB> and heating-SO<SUB>2</SUB> emissions showed consistent associations with IL-6 levels. 30-year average traffic-NO<SUB>2</SUB> exposure was associated with a 64.5% (95% CI 6.7% to 153.8%) increase in serum IL-6 per 28.8 &micro;g/m<sup>3</sup> (corresponding to the difference between the 5th and 95th percentile exposure value), and 30-year exposure to heating-SO<SUB>2</SUB> with a 67.6% (95% CI 7.1% to 162.2%) increase per 39.4 &micro;g/m<sup>3</sup> (5th&ndash;95th percentile value difference). The association appeared stronger in non-smokers, physically active people and hypertensive subjects. We observed positive non-significant associations of inflammatory markers with NO<SUB>2</SUB> and PM<SUB>10</SUB> during 24 h before blood sampling. Short-term exposure to O<SUB>3</SUB> was associated with increased, and SO<SUB>2</SUB> with decreased, fibrinogen levels.</p>
</sec>
<sec><st>Conclusions:</st>
<p>Our results suggest that exposure to moderate levels of air pollution may influence serum levels of inflammatory markers.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Panasevich, S, Leander, K, Rosenlund, M, Ljungman, P, Bellander, T, de Faire, U, Pershagen, G, Nyberg, F]]></dc:creator>
<dc:date>Fri, 16 Oct 2009 10:01:41 PDT</dc:date>
<dc:subject><![CDATA[Air pollution, air quality, Other exposures]]></dc:subject>
<dc:identifier>info:doi/10.1136/oem.2008.043471</dc:identifier>
<dc:title><![CDATA[Associations of long- and short-term air pollution exposure with markers of inflammation and coagulation in a population sample]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>66</prism:volume>
<prism:endingPage>753</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>747</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/66/11/754?rss=1">
<title><![CDATA[Detergent protease exposure and respiratory disease: case-referent analysis of a retrospective cohort]]></title>
<link>http://oem.bmj.com/cgi/content/short/66/11/754?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>To examine the relationship between protease exposure and respiratory disease in a cohort of detergent enzyme manufacturers.</p>
</sec>
<sec><st>Methods:</st>
<p>Case&ndash;referent analysis of a cohort of employees working in a European detergent factory between 1989 and 2002. Cases with new lower or upper respiratory disease were ascertained by examination of occupational health records and matched to referents on date of first employment. Personal exposures to airborne detergent protease were estimated, using a job exposure matrix, from &gt;12 000 measurements taken in the factory during the period of study.</p>
</sec>
<sec><st>Results:</st>
<p>We found clear, monotonic relationships between estimated protease exposure and both lower and upper respiratory disease. After control for age, sex and smoking, the odds ratio of lower respiratory disease was significantly elevated (1.98, 95% CI 1.04 to 3.79) in those employees working in jobs in the highest quartile of protease exposure (geometric mean 7.9 ng.m<sup>&ndash;3</sup>). For employees with upper respiratory disease, the risk was significantly elevated at a lower level of estimated protease exposure (geometric mean 2.3 ng.m<sup>&ndash;3</sup>).</p>
</sec>
<sec><st>Conclusions:</st>
<p>These findings provide strong evidence of an association between detergent enzyme exposure and the development of respiratory disease in an occupational setting. Using the routinely collected information on specific sensitisation and the close attention to workplace exposures that are characteristic of this industry, it should be possible to derive meaningful occupational exposure standards for most detergent enzymes.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Brant, A, Upchurch, S, van Tongeren, M, Zekveld, C, Helm, J, Barnes, F, Newman Taylor, A J, Cullinan, P]]></dc:creator>
<dc:date>Fri, 16 Oct 2009 10:01:41 PDT</dc:date>
<dc:subject><![CDATA[Other exposures]]></dc:subject>
<dc:identifier>info:doi/10.1136/oem.2008.043851</dc:identifier>
<dc:title><![CDATA[Detergent protease exposure and respiratory disease: case-referent analysis of a retrospective cohort]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>66</prism:volume>
<prism:endingPage>758</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>754</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/66/11/759?rss=1">
<title><![CDATA[A cross-sectional study among detergent workers exposed to liquid detergent enzymes]]></title>
<link>http://oem.bmj.com/cgi/content/short/66/11/759?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>To investigate sensitisation and respiratory health among workers who produce liquid detergent products and handle liquid detergent enzymes.</p>
</sec>
<sec><st>Methods:</st>
<p>We performed a cross-sectional study among 109 eligible workers of a detergent products plant. 108 were interviewed for respiratory and allergic symptoms and 106 blood samples were taken from them to examine sensitisation to enzymes. Those sensitised to &gt;=1 enzymes were referred for clinical evaluation. Workers and representatives were interviewed to characterise exposure qualitatively and estimate exposure semi-quantitatively. Workers were classified into three exposure groups with varying exposure profiles to enzymes, based on frequency, duration, and level of exposure.</p>
</sec>
<sec><st>Results:</st>
<p>Workers were exposed to proteases, -amylase, lipase and cellulase. The highest exposures occurred in the mixing area. Liquid spills with concentrated enzyme preparations and leakage of enzymes during weighing, transportation and filling were causing workplace contaminations and subsequently leading to both dermal and inhalation exposure for workers.</p>
<p>Workers with the highest exposures reported significantly more work-related symptoms of itching nose (prevalence ratio (PR) = 4.2, 95% CI 1.5 to 12.0) and sneezing (PR = 4.0, 95% CI 1.5 to 10.8) and marginally significant more symptoms of wheezing (PR = 2.9, 95% CI 0.9 to 8.7) compared with the least exposed group.</p>
<p>Fifteen workers (14.2%) were sensitised to &gt;=1 enzymes. A marginally statistically significant gradient in sensitisation across the exposure categories was found (p = 0.09). There was a clinical case of occupational asthma and two others with probable occupational rhinitis.</p>
</sec>
<sec><st>Conclusions:</st>
<p>Workers exposed to liquid detergent enzymes are at risk of developing sensitisation (14%) and respiratory allergy.</p>
</sec>
]]></description>
<dc:creator><![CDATA[van Rooy, F G B G J, Houba, R, Palmen, N, Zengeni, M M, Sander, I, Spithoven, J, Rooyackers, J M, Heederik, D J J]]></dc:creator>
<dc:date>Fri, 16 Oct 2009 10:01:41 PDT</dc:date>
<dc:subject><![CDATA[Allergy, asthma, Respiratory]]></dc:subject>
<dc:identifier>info:doi/10.1136/oem.2008.045245</dc:identifier>
<dc:title><![CDATA[A cross-sectional study among detergent workers exposed to liquid detergent enzymes]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>66</prism:volume>
<prism:endingPage>765</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>759</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/66/11/766?rss=1">
<title><![CDATA[Population-based asbestosis surveillance in British Columbia]]></title>
<link>http://oem.bmj.com/cgi/content/short/66/11/766?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>To investigate the use of multiple health data sources for population-based asbestosis surveillance in British Columbia, Canada.</p>
</sec>
<sec><st>Methods:</st>
<p>Provincial health insurance registration records, workers&rsquo; compensation records, hospitalisation records, and outpatient medical service records were linked using individual-specific study identifiers. The study population was restricted to individuals &gt;=15 years of age living in the province during 1992&ndash;2004.</p>
</sec>
<sec><st>Results:</st>
<p>1170 new asbestosis cases were identified from 1992 to 2004 for an overall incidence rate of 2.82 (men: 5.48, women: 0.23) per 100 000 population; 96% of cases were male and average (SD) age was 69 (10) years. Although the annual number of new cases increased by 30% during the surveillance period (&beta; = 2.36, p = 0.019), the observed increase in annual incidence rates was not significant (&beta; = 0.02, p = 0.398). Workers&rsquo; compensation, hospitalisation and outpatient databases identified 23%, 48% and 50% of the total new cases, respectively. Of the new cases, 82% were identified through single data sources, 10% were only recorded in the workers&rsquo; compensation records, and 36% only in each of the hospitalisation and outpatient records. 84% of hospitalisation cases and 83% of outpatient cases were not included in the workers&rsquo; compensation records. The three data sources showed different temporal trends in the annual number of new cases and annual incidence rates.</p>
</sec>
<sec><st>Conclusions:</st>
<p>Single data sources were not sufficient to identify all new cases, thus leading to serious underestimations of the true burden of asbestosis. Integrating multiple health data sources could provide a more complete picture in population-based surveillance of asbestosis and other occupational diseases.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Gan, W Q, Demers, P A, McLeod, C B, Koehoorn, M]]></dc:creator>
<dc:date>Fri, 16 Oct 2009 10:01:41 PDT</dc:date>
<dc:subject><![CDATA[Respiratory]]></dc:subject>
<dc:identifier>info:doi/10.1136/oem.2008.045211</dc:identifier>
<dc:title><![CDATA[Population-based asbestosis surveillance in British Columbia]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>66</prism:volume>
<prism:endingPage>771</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>766</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/66/11/772?rss=1">
<title><![CDATA[Association between passive jobs and low levels of leisure-time physical activity: the Whitehall II cohort study]]></title>
<link>http://oem.bmj.com/cgi/content/short/66/11/772?rss=1</link>
<description><![CDATA[
<sec><st>Background:</st>
<p>There is mixed evidence on the association between psychosocial work exposures (ie, passive jobs) and physical activity, but previous studies did not take into account the effect of cumulative exposures nor did they examine different trajectories in exposure. We investigated whether exposure to passive jobs, measured three times over an average of 5 years, is associated with leisure-time physical activity (LTPA).</p>
</sec>
<sec><st>Methods:</st>
<p>Data were from working men (n = 4291) and women (n = 1794) aged 35&ndash;55 years who participated in the first three phases of the Whitehall II prospective cohort. Exposure to passive jobs was measured at each phase and LTPA at phases 1 and 3. Participants were categorised according to whether or not they worked in a passive job at each phase, leading to a scale ranging from 0 (non-passive job at all three phases) to 3 (passive job at all three phases). Poisson regression with robust variance estimates were used to assess the prevalence ratios of low LTPA.</p>
</sec>
<sec><st>Results:</st>
<p>An association was found in men between exposure to passive jobs over 5 years and low LTPA at follow-up, independently of other relevant risk factors. The prevalence ratio for low LTPA in men was 1.16 (95% CI 1.01 to 1.33) times greater for employees with three reports of passive job than for those who had never worked in passive jobs. No association was observed in women.</p>
</sec>
<sec><st>Conclusion:</st>
<p>This study provides evidence that working in passive jobs may encourage a passive lifestyle in men.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Gimeno, D, Elovainio, M, Jokela, M, De Vogli, R, Marmot, M G, Kivimaki, M]]></dc:creator>
<dc:date>Fri, 16 Oct 2009 10:01:41 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2008.045104</dc:identifier>
<dc:title><![CDATA[Association between passive jobs and low levels of leisure-time physical activity: the Whitehall II cohort study]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>66</prism:volume>
<prism:endingPage>776</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>772</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/66/11/777?rss=1">
<title><![CDATA[Biomass fuel use and indoor air pollution in homes in Malawi]]></title>
<link>http://oem.bmj.com/cgi/content/short/66/11/777?rss=1</link>
<description><![CDATA[
<sec><st>Background:</st>
<p>Air pollution from biomass fuels in Africa is a significant cause of mortality and morbidity both in adults and children. The work describes the nature and quantity of smoke exposure from biomass fuel in Malawian homes.</p>
</sec>
<sec><st>Methods:</st>
<p>Markers of indoor air quality were measured in 62 homes (31 rural and 31 urban) over a typical 24 h period. Four different devices were used (one gravimetric device, two photometric devices and a carbon monoxide (HOBO) monitor. Gravimetric samples were analysed for transition metal content. Data on cooking and lighting fuel type together with information on indicators of socioeconomic status were collected by questionnaire.</p>
</sec>
<sec><st>Results:</st>
<p>Respirable dust levels in both the urban and rural environment were high with the mean (SD) 24 h average levels being 226 &micro;g/m<sup>3</sup> (206 &micro;g/m<sup>3</sup>). Data from real-time instruments indicated respirable dust concentrations were &gt;250 &micro;g/m<sup>3</sup> for &gt;1 h per day in 52% of rural homes and 17% of urban homes. Average carbon monoxide levels were significantly higher in urban compared with rural homes (6.14 ppm vs 1.87 ppm; p&lt;0.001). The transition metal content of the smoke was low, with no significant difference found between urban and rural homes.</p>
</sec>
<sec><st>Conclusions:</st>
<p>Indoor air pollution levels in Malawian homes are high. Further investigation is justified because the levels that we have demonstrated are hazardous and are likely to be damaging to health. Interventions should be sought to reduce exposure to concentrations less harmful to health.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Fullerton, D G, Semple, S, Kalambo, F, Suseno, A, Malamba, R, Henderson, G, Ayres, J G, Gordon, S B]]></dc:creator>
<dc:date>Fri, 16 Oct 2009 10:01:41 PDT</dc:date>
<dc:subject><![CDATA[Air pollution, air quality, Other exposures]]></dc:subject>
<dc:identifier>info:doi/10.1136/oem.2008.045013</dc:identifier>
<dc:title><![CDATA[Biomass fuel use and indoor air pollution in homes in Malawi]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>66</prism:volume>
<prism:endingPage>783</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>777</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://oem.bmj.com/cgi/content/short/66/11/784?rss=1">
<title><![CDATA[Environmental epidemiology study methods and application]]></title>
<link>http://oem.bmj.com/cgi/content/short/66/11/784?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mills, I C]]></dc:creator>
<dc:date>Fri, 16 Oct 2009 10:01:42 PDT</dc:date>
<dc:identifier>info:doi/10.1136/oem.2009.046573</dc:identifier>
<dc:title><![CDATA[Environmental epidemiology study methods and application]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>66</prism:volume>
<prism:endingPage>784</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>784</prism:startingPage>
<prism:section>PostScript</prism:section>
</item>

</rdf:RDF>