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<title>Occupational and Environmental Medicine current issue</title>
<link>http://oem.bmj.com</link>
<description>Occupational and Environmental Medicine RSS feed -- current issue</description>
<prism:coverDisplayDate>May  1 2026 12:00:00:000AM</prism:coverDisplayDate>
<prism:publicationName>Occupational and Environmental Medicine</prism:publicationName>
<prism:issn>1351-0711</prism:issn>
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<title>Occupational and Environmental Medicine</title>
<url>http://hwmaint.oem.bmj.com/homepage/OEM_95x60.gif</url>
<link>http://oem.bmj.com</link>
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<item rdf:about="http://oem.bmj.com/cgi/content/short/83/3/121?rss=1">
<title><![CDATA[Prevalent occupational carcinogenic exposure under the microscope]]></title>
<link>http://oem.bmj.com/cgi/content/short/83/3/121?rss=1</link>
<description><![CDATA[ <p>Formaldehyde is a known respiratory and skin sensitiser and carcinogen. The International Agency for Research on Cancer (IARC) first classified formaldehyde as a Group 1 carcinogen more than two decades ago in 2004 and reaffirmed its classification in 2009.<cross-ref type="bib" refid="R1">1 2</cross-ref><cross-ref type="bib" refid="R2"></cross-ref> IARC determined that there was sufficient evidence from human and animal studies that chronic exposure to formaldehyde causes nasopharyngeal cancer and leukaemia. Formaldehyde (in aqueous solution, known as formalin) is used as a disinfectant and preservative in healthcare and other sectors (eg, dairy production).<cross-ref type="bib" refid="R3">3</cross-ref> Occupational exposures to formaldehyde also occur in the production of plastics, resins, metals and building materials. A recent review of exposure measurements showed how widespread occupational exposure to formaldehyde is.<cross-ref type="bib" refid="R4">4</cross-ref></p> <p>The Workplace Exposure Limit (WEL) for formaldehyde in the UK is currently 2 ppm (short-term and long-term) compared with the EU long-term binding limit of 0.3 ppm.<cross-ref...]]></description>
<dc:creator><![CDATA[Kromhout, H., van Tongeren, M.]]></dc:creator>
<dc:date>2026-06-25T00:06:28-07:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2026-111043</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2026-111043</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Press releases]]></dc:subject>
<dc:title><![CDATA[Prevalent occupational carcinogenic exposure under the microscope]]></dc:title>
<prism:publicationDate>2026-05-01</prism:publicationDate>
<prism:section>Commentary</prism:section>
<prism:volume>83</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>121</prism:startingPage>
<prism:endingPage>122</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/83/3/123?rss=1">
<title><![CDATA[Under the microscope: formaldehyde exposure in National Health Service pathology departments in the United Kingdom]]></title>
<link>http://oem.bmj.com/cgi/content/short/83/3/123?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>The US Environmental Protection Agency has determined that formaldehyde presents an &lsquo;unreasonable risk of injury to human health&rsquo;. Occupational inhalation exposure is associated with short- and long-term damage to the respiratory, female reproductive and nervous systems, and is also carcinogenic. The European Union (EU) has recently introduced formaldehyde work exposure limits (WELs) lower (long-term 0.3 ppm; short-term 0.6 ppm) than those currently applied in the UK (long-term 2 ppm; short-term 2 ppm). UK regulation additionally requires exposure to carcinogens to be reduced to <I>as low as is reasonably practicable</I>. We evaluated formaldehyde airborne concentrations in National Health Service (NHS) cell pathology departments to assess the adequacy of exposure controls.</p>
</sec>
<sec><st>Methods</st>
<p>Using the UK Freedom of Information Act (2000), we requested 12 months (2024&ndash;2025) of formaldehyde airborne monitoring data collected by cell pathology departments across 122 NHS Trusts in England (n=102), Scotland (n=10), Wales (n=6) and Northern Ireland (n=4). Results were evaluated empirically and using EN 689:2018 statistical methods to assess exposure variability, estimate upper-bound concentrations and determine the likelihood of adequate exposure control when benchmarked against EU WELs.</p>
</sec>
<sec><st>Results</st>
<p>A total of 1 715 516 formaldehyde airborne monitoring results were disclosed by 117 NHS cell pathology departments. Monitoring was infrequent, with 73% of sites measuring formaldehyde airborne concentrations once weekly or less. The EU long-term WEL was exceeded regularly at 70% of sites (95th percentile &gt;0.3 ppm), and the EU short-term WEL was exceeded regularly at 43% of sites (95th percentile &gt;0.6 ppm). The 95th percentile upper tolerance limit (UTL<SUB>95,70</SUB>) exceeded the EU short-term WEL at 68% of sites. Only 11% and 17% of departments demonstrated frequent (once daily or more) formaldehyde airborne monitoring with 95th percentiles below the EU long- and short-term WELs, respectively.</p>
</sec>
<sec><st>Conclusions</st>
<p>Formaldehyde exposure is infrequently monitored and inadequately controlled in NHS cell pathology departments.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Plesa, M., Yates, R. L.]]></dc:creator>
<dc:date>2026-06-25T00:06:28-07:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2025-110545</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2025-110545</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Press releases]]></dc:subject>
<dc:title><![CDATA[Under the microscope: formaldehyde exposure in National Health Service pathology departments in the United Kingdom]]></dc:title>
<prism:publicationDate>2026-05-01</prism:publicationDate>
<prism:section>Exposure assessment</prism:section>
<prism:volume>83</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>123</prism:startingPage>
<prism:endingPage>129</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/83/3/130?rss=1">
<title><![CDATA[Associations between maternal occupational history and autism spectrum disorder diagnosis in offspring in Denmark]]></title>
<link>http://oem.bmj.com/cgi/content/short/83/3/130?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>We investigated associations between maternal occupations and a diagnosis of autism spectrum disorder (ASD) in offspring.</p>
</sec>
<sec><st>Methods</st>
<p>We obtained data for 1702 ASD cases born between 1973 and 2012 from the Danish National Patient Registry and matched each case to up to 100 population based controls based on sex and birth year (n=110 234). Mothers&rsquo; employment histories were obtained from the Danish Pension Fund Registry. Conditional logistic regression models were used to test associations between occupations held ever, 1 year before conception, during pregnancy and during infancy, adjusting for the mother&rsquo;s age and history of neuropsychiatric disorders, parity and residential location.</p>
</sec>
<sec><st>Results</st>
<p>There were increased odds of having a child with ASD for mothers who were employed before conception up to infancy in ground transportation (adjusted OR (aOR) 1.24, 95% CI 1.08 to 1.42; <I>q</I>=0.036), public administration (aOR 1.20, 95% CI 1.07 to 1.35; <I>q</I>=0.018) and military/defence occupations (aOR 1.59, 95% CI 1.39 to 1.82; <I>q</I>&lt;0.001). Associations for judicial occupations and military/defence service were also apparent 1 year before conception and during pregnancy. We observed sex differences, with significant associations in male children for employment in ground transportation and defence occupations.</p>
</sec>
<sec><st>Conclusions</st>
<p>Associations between certain maternal employment categories with high toxicant or psychosocial stress exposure suggest future studies should focus on examining specific toxicant exposures common in those occupations and neurodevelopment in offspring. This is of particular concern for associations seen for occupations held several years before conception.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Dickerson, A. S., Liu, Y., Ladd-Acosta, C., Wang, J., Schendel, D., Weisskopf, M. G., Fallin, M. D., Hansen, J.]]></dc:creator>
<dc:date>2026-06-25T00:06:28-07:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2026-110912</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2026-110912</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Editor's choice, Press releases]]></dc:subject>
<dc:title><![CDATA[Associations between maternal occupational history and autism spectrum disorder diagnosis in offspring in Denmark]]></dc:title>
<prism:publicationDate>2026-05-01</prism:publicationDate>
<prism:section>Workplace</prism:section>
<prism:volume>83</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>130</prism:startingPage>
<prism:endingPage>137</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/83/3/138?rss=1">
<title><![CDATA[Health Watch: cancer and mortality update in a 40-year prospective cohort study of Australian petroleum workers]]></title>
<link>http://oem.bmj.com/cgi/content/short/83/3/138?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>To report estimates of cancer incidence (1982&ndash;2016) and mortality (1980&ndash;2020) in the Health Watch cohort after four decades of follow-up.</p>
</sec>
<sec><st>Methods</st>
<p>Health Watch is a prospective cohort study of 18 040 (16 666 men, 1374 women) employees recruited between 1981 and 2000.</p>
<p>Personal data were linked to national and state cancer and death registries. Standardised mortality ratios (SMRs) and standardised incidence ratios were calculated using national population rates adjusted for age, sex and calendar period.</p>
</sec>
<sec><st>Results</st>
<p>All-cause mortality was reduced compared with Australian population rates (men: SMR 0.79, 95% CI 0.77 to 0.82; women: SMR 0.70, 95% CI 0.59 to 0.83).</p>
</sec>
<sec><st>Conclusions</st>
<p>Lower mortality likely reflects the healthy worker effect. Persistent excesses of mesothelioma, melanoma and prostate cancer may reflect ongoing occupational risks warranting targeted prevention and surveillance. In particular, melanoma risk underscores the need to minimise both occupational and recreational ultraviolet exposure.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Wood, E., Glass, D. C., Gwini, S. M., Sim, M. R., Vander Hoorn, S., Del Monaco, A., Walker-Bone, K.]]></dc:creator>
<dc:date>2026-06-25T00:06:28-07:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2025-110739</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2025-110739</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Health Watch: cancer and mortality update in a 40-year prospective cohort study of Australian petroleum workers]]></dc:title>
<prism:publicationDate>2026-05-01</prism:publicationDate>
<prism:section>Workplace</prism:section>
<prism:volume>83</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>138</prism:startingPage>
<prism:endingPage>145</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/83/3/146?rss=1">
<title><![CDATA[Associations between sick leave during pregnancy and after childbirth and future labour force participation: a Dutch cohort study]]></title>
<link>http://oem.bmj.com/cgi/content/short/83/3/146?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>Women&rsquo;s labour force participation often declines after childbirth, but the role of sick leave during pregnancy and after childbirth in sustained employment remains unclear. This study examined: (1) the association between sick leave during pregnancy and/or within 2 years after childbirth and sustained labour force participation, (2) whether sick leave during pregnancy predicts sick leave within 2 years after childbirth, (3) demographic and employment-related factors associated with sick leave length and labour force participation.</p>
</sec>
<sec><st>Methods</st>
<p>Prospective cohort study including 261 171 women in the Netherlands who applied for maternity benefits in 2020 or 2021. A subset also received sick leave benefits during pregnancy or after childbirth. Logistic regression assessed associations between sick leave timing and sustained labour participation. General linear models examined determinants of the total length of sick leave during pregnancy and within 2 years after childbirth.</p>
</sec>
<sec><st>Results</st>
<p>Sick leave during pregnancy was associated with higher odds of sustained labour force participation (OR 1.20, 95% CI 1.17 to 1.23), whereas sick leave within 2 years after childbirth was associated with lower odds (OR 0.65, 95% CI 0.62 to 0.67). Sick leave during pregnancy strongly predicted sick leave within 2 years after childbirth (OR 3.63, 95% CI 3.53 to 3.74). Employment sector, contract type, residential area and age were associated with sick leave length and labour participation.</p>
</sec>
<sec><st>Conclusion</st>
<p>Sick leave within 2 years after childbirth was associated with reduced sustained labour force participation, whereas sick leave during pregnancy was not negatively associated. Employment characteristics were strongly associated with both sick leave patterns and sustained labour force participation.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Frijmersum, Z. Z., Van Der Meij, E., Huirne, J. A., Bakker, P. C., Anema, J.]]></dc:creator>
<dc:date>2026-06-25T00:06:28-07:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2025-110638</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2025-110638</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access]]></dc:subject>
<dc:title><![CDATA[Associations between sick leave during pregnancy and after childbirth and future labour force participation: a Dutch cohort study]]></dc:title>
<prism:publicationDate>2026-05-01</prism:publicationDate>
<prism:section>Workplace</prism:section>
<prism:volume>83</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>146</prism:startingPage>
<prism:endingPage>153</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/83/3/154?rss=1">
<title><![CDATA[Lung cancer risk prediction models and asbestos exposure: a validation study on the Western Australia Asbestos Review Program]]></title>
<link>http://oem.bmj.com/cgi/content/short/83/3/154?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>Asbestos exposure raises the lung cancer risk and has supra-additive synergy alongside tobacco exposure. Lung cancer screening (LCS) is effective when high-risk populations are targeted. This study examined the utility of various LCS eligibility and risk prediction models in an asbestos-exposed population.</p>
</sec>
<sec><st>Methods</st>
<p>The Western Australia Asbestos Review Program (ARP) consists of individuals with known exposure to asbestos. All participants underwent annual review with low-dose CT screening. The performance of the Prostate, Lung, Colorectal and Ovarian (PLCO)<SUB>m2012</SUB>, PLCO<SUB>m2014</SUB> and PLCO<SUB>occ</SUB> models, Liverpool Lung Project V.2 (LLP<SUB>v2</SUB>) and Bach models, together with the United States Preventive Services Task Force (USPSTF)<SUB>2021</SUB> and Australian LCS eligibility criteria were validated on the ARP.</p>
</sec>
<sec><st>Results</st>
<p>The cohort consisted of 2126 participants of which 85.4% were male with a median (IQR) age of 70 (63&ndash;75) years old. Former smokers comprised 55.1% (n=1172) and never smokers 36.2% (n=769) of the cohort. Median smoking and cessation duration were 24 years (IQR: 13&ndash;72) and 32 years (IQR: 22&ndash;41), respectively. Lung cancer was diagnosed in 51 (2.4%) participants.</p>
<p>When applying the risk models to the ARP cohort, the area under the curve for all models was modest, ranging from 0.602 to 0.675. All models underestimated risk in this cohort during calibration assessment, with the exception of the LLP V.2, which overestimated risk.</p>
</sec>
<sec><st>Conclusions</st>
<p>In an asbestos exposed population, current LCS eligibility criteria and risk models mostly underestimate the risk of lung cancer, reflecting the need for improved risk prediction models that adequately account for asbestos exposure.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Kumarasamy, C., Betts, K., Norman, R., Bennett, K., Franklin, P., Tammema&#x0308;gi, M., Brims, F.]]></dc:creator>
<dc:date>2026-06-25T00:06:28-07:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2025-110249</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2025-110249</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access]]></dc:subject>
<dc:title><![CDATA[Lung cancer risk prediction models and asbestos exposure: a validation study on the Western Australia Asbestos Review Program]]></dc:title>
<prism:publicationDate>2026-05-01</prism:publicationDate>
<prism:section>Methodology</prism:section>
<prism:volume>83</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>154</prism:startingPage>
<prism:endingPage>161</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/83/3/162?rss=1">
<title><![CDATA[Associations between occupational exposure to chromium (VI) and cancers of the oral cavity, small intestine, pancreas, prostate and urinary bladder: systematic review and meta-analyses]]></title>
<link>http://oem.bmj.com/cgi/content/short/83/3/162?rss=1</link>
<description><![CDATA[
<p>Hexavalent chromium (Cr(VI)) is a human carcinogen. It is unclear whether Cr(VI) can cause cancer of the small intestine, oral cavity, pancreas, prostate and urinary bladder. We performed a systematic review and meta-analyses of epidemiological studies on occupational exposure to Cr(VI) and incidence and mortality of these cancer sites.</p>
<p>A comprehensive review of human studies on Cr(VI) and cancer was performed in Embase and Scopus. 131 potentially relevant epidemiological studies were identified. Study quality was assessed using the Newcastle-Ottawa Scale. 29 publications including 81 observations for meta-analyses were based on cohort or case&ndash;control studies with exposure assessment of sufficient quality. Site-specific random-effects meta-analyses were done separately for incidence and mortality. Sensitivity analyses focused on the studies with the highest quality scores.</p>
<p>No indications for an association between Cr(VI) exposure and oral or small intestine cancer were found. Incidence of pancreatic cancer was not associated with Cr(VI) exposure (meta-relative risk (RR) 1.04; 95% CI 0.85 to 1.28) while for specific mortality RR was 1.41 (95% CI 0.96 to 2.08) with moderate heterogeneity (I<sup>2</sup>=41%) and an asymmetric funnel plot (Egger&rsquo;s test; p=0.002). For incidence of prostate cancer meta RR was 1.16 (95% CI 0.99 to 1.37) while the RR for mortality was 1.03 (95% CI 0.84 to 1.25). For bladder cancer, RR was 1.04 (95% CI 0.91 to 1.20) for incidence and 1.76 (95% CI 1.20 to 2.60) for mortality.</p>
<p>This comprehensive meta-analysis of epidemiological studies did not provide sufficient evidence that occupational Cr(VI) exposure may cause cancer of the oral cavity, small intestine, pancreas, prostate or the urinary bladder in humans.</p>
]]></description>
<dc:creator><![CDATA[Zock, J.-P., Rijs, K. J., Peters, S., Vlaanderen, J. J.]]></dc:creator>
<dc:date>2026-06-25T00:06:28-07:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2025-110733</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2025-110733</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Associations between occupational exposure to chromium (VI) and cancers of the oral cavity, small intestine, pancreas, prostate and urinary bladder: systematic review and meta-analyses]]></dc:title>
<prism:publicationDate>2026-05-01</prism:publicationDate>
<prism:section>Systematic review</prism:section>
<prism:volume>83</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>162</prism:startingPage>
<prism:endingPage>169</prism:endingPage>
</item>
<item rdf:about="http://oem.bmj.com/cgi/content/short/83/3/170?rss=1">
<title><![CDATA[Occupational and environmental risk factors for salivary gland cancer: a systematic literature review]]></title>
<link>http://oem.bmj.com/cgi/content/short/83/3/170?rss=1</link>
<description><![CDATA[
<p>Occupational and environmental risk factors for salivary gland cancer (SGC) are largely unrecognised. This systematic review is the first to characterise the relationship between employment in specific industries or occupations and risk of SGC, as well as exposure to key occupational and environmental hazards.</p>
<p>Studies published up to September 2023 were collected from three electronic databases and systematically screened. The Health Assessment Workplace Collaborative programme was used to tag studies based on pre-established inclusion and exclusion criteria. Studies eligible for inclusion (n=24) underwent an in-depth review to extract key study characteristics and findings, including effect estimates and 95% CIs. Studies were evaluated for influence of key biases. To identify priority sectors and hazards for intervention, effect direction plots were created to analyse the number and quality of studies reporting elevated rates of SGC across industry, occupation and exposure groups.</p>
<p>24 articles were included for analysis. Exposure misclassification and confounding bias were a common concern across studies. Industry and occupation groups with the strongest relationship to SGC included cleaning services, material handling, food services, rubber/plastics production, engineering and construction/painting. Exposures with the strongest relationship to SGC included silica dust, cement dust, chlorinated solvents, formaldehyde and white spirits.</p>
<p>Several occupational exposures were associated with an elevated risk of SGC, whereas environmental evidence was more limited. Additional research involving larger cohorts with quantitative exposure data is needed to further establish relationships between occupational and environmental exposures and often-overlooked rare cancers like SGC.</p>
<p>PROSPERO registration number: CRD42023468037.</p>
]]></description>
<dc:creator><![CDATA[Choi, D., Patel, K., Zarnke, A., Boyce-Fappiano, D., Cole, D., Rhodes, S. M.]]></dc:creator>
<dc:date>2026-06-25T00:06:28-07:00</dc:date>
<dc:identifier>info:doi/10.1136/oemed-2025-110485</dc:identifier>
<dc:identifier>hwp:master-id:oemed;oemed-2025-110485</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access]]></dc:subject>
<dc:title><![CDATA[Occupational and environmental risk factors for salivary gland cancer: a systematic literature review]]></dc:title>
<prism:publicationDate>2026-05-01</prism:publicationDate>
<prism:section>Systematic review</prism:section>
<prism:volume>83</prism:volume>
<prism:number>3</prism:number>
<prism:startingPage>170</prism:startingPage>
<prism:endingPage>180</prism:endingPage>
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