ObjectivesMany studies have shown consistent associations between evident indoor dampness or mold and respiratory or allergic health effects, but causal links remain unclear. Findings on measured microbiologic factors have received little review. We conducted an updated, comprehensive review on these topics.Data sourcesWe reviewed eligible peer-reviewed epidemiologic studies or quantitative meta-analyses, up to late 2009, on dampness, mold, or other microbiologic agents and respiratory or allergic effects.Data extractionWe evaluated evidence for causation or association between qualitative/subjective assessments of dampness or mold (considered together) and specific health outcomes. We separately considered evidence for associations between specific quantitative measurements of microbiologic factors and each health outcome.Data synthesisEvidence from epidemiologic studies and meta-analyses showed indoor dampness or mold to be associated consistently with increased asthma development and exacerbation, current and ever diagnosis of asthma, dyspnea, wheeze, cough, respiratory infections, bronchitis, allergic rhinitis, eczema, and upper respiratory tract symptoms. Associations were found in allergic and nonallergic individuals. Evidence strongly suggested causation of asthma exacerbation in children. Suggestive evidence was available for only a few specific measured microbiologic factors and was in part equivocal, suggesting both adverse and protective associations with health.ConclusionsEvident dampness or mold had consistent positive associations with multiple allergic and respiratory effects. Measured microbiologic agents in dust had limited suggestive associations, including both positive and negative associations for some agents. Thus, prevention and remediation of indoor dampness and mold are likely to reduce health risks, but current evidence does not support measuring specific indoor microbiologic factors to guide health-protective actions.

Wood dust exposure is high in joinery workers and (to a lesser extent) furniture makers with frequent use of hand tools and cleaning being key drivers of exposure. Vacuum extraction on hand tools and alternative cleaning methods reduced workplace exposures substantially, but may be insufficient to achieve compliance with current occupational exposure limits.

generally saw a stronger effect for squamous-and small cell lung carcinomas than for adenocarcinomas. Smoking and simultaneous exposure to other occupational exposures exerted a minor confounding effect on the risk estimates. The effect modifications with smoking tended to be supra-additive. Conclusions SYNERGY adds valuable knowledge to the field of occupational cancer epidemiology, and underlines the importance to collect data on histology, and lifelong information on occupational exposures and smoking. Objectives To derive a meta-exposure-response curve (ERC) for DEE and lung cancer mortality and estimate lifetime excess risks (ELRs) of lung cancer mortality based on assumed occupational and environmental exposure scenarios. Method We conducted a meta-regression of lung cancer mortality and cumulative exposure to elemental carbon (EC), a proxy measure of DEE, based on relative risk (RR) estimates reported by three large occupational cohort studies. Based on the derived risk function, we calculated ELRs for several lifetime occupational and environmental exposure scenarios, and also calculated the fractions of annual lung cancer deaths attributable to DEE. Results We estimated a lnRR of 0.00098 (95% CI: 0.00055, 0.0014) for lung cancer mortality with each 1-µg/m 3-year increase in cumulative EC. Estimated numbers of excess lung cancer deaths through age 80 for lifetime occupational exposures of 1, 10, and 25 µg/m 3 EC were 17, 200, and 689 per 10 000, respectively. For lifetime environmental exposure to 0.8 µg/m 3 EC, we estimated 21 excess lung cancer deaths per 10 000. Based on broad assumptions regarding past exposures we estimate that approximately 6% of annual lung cancer deaths may be due to DEE exposure. Conclusions Combined data from three US occupational cohort studies suggest that DEE at levels common in the workplace and in outdoor air appear to pose substantial excess lifetime risks of lung cancer, above usually acceptable limits in the US and Europe, which are generally set at 1/1000 and 1/100 000 based on lifetime exposure for the occupational and general population, respectively. Objectives We report on the first ever analysis of a UK cohort of workers with blood lead level measurements that was assembled in the late 1970s. 0374 0375 MORTALITY OF A COHORT OF WORKERS IN GREAT BRITAIN WITH BLOOD LEAD MEASUREMENTSMethod As an alternative to mean and maximum blood lead levels, we carried out an exposure assessment that assigned workers to high, medium or low exposure to lead. We additionally assessed whether workers would be exposed to an important level of relevant co-carcinogens.Results 3466 deaths were observed among 7770 men and 1352 women. The SMRs for all causes (109, 95% CI 105-112) and all malignant neoplasms (113,107-120) were significantly raised. SMRs for oesophageal, stomach, bladder, brain and kidney cancer and non-malignant kidney disease were not raised, but were raised for lung cancer (142,. The SMR for circulatory diseases (105,99-100) was of borderline significance. No trends were ...