Workplace interventions to reduce the risk of SARS-CoV-2 infection outside of healthcare settings

This is a protocol for a Cochrane Review (intervention). The objectives are as follows: To assess the benefits and harms of interventions in non‐healthcare‐related workplaces to reduce the risk of SARS‐CoV‐2 infection relative to other interventions or no intervention

Mortality among British asbestos workers undergoing regular medical examinations (1971-2005)

2 Objectives The Great Britain Asbestos Survey was established to monitor mortality among workers covered by regulations to control occupational exposure to asbestos. This study updates the estimated burden of asbestos-related mortality in the cohort, and identifies risk factors associated with mortality. Methods From 1971, workers were recruited during initially voluntary and later statutory medical examinations. A brief questionnaire was completed during the medical, and participants were flagged for death registrations. Standardised Mortality Ratios (SMRs) and Proportional Mortality Ratios (PMRs) were calculated for deaths occurring before 2006. Poisson regression analyses were undertaken for diseases with significant excess mortality. Results There were 15,496 deaths among 98,117 workers followed-up for 1,779,580 person-years. The SMR for all cause mortality was 141 (95 % CI 139-143) and for all malignant neoplasms 163 (95 % CI 159-167). The SMRs for cancers of th

Job-exposure matrix for historical exposures to rubber dust, rubber fumes and n-Nitrosamines in the British rubber industry

Objectives: To develop a quantitative historical job-exposure matrix (JEM) for rubber dust, rubber fumes and n-Nitrosamines in the British rubber industry for 1915-2002 to estimate lifetime cumulative exposure (LCE) for a cohort of workers with 49 years follow-up. Methods: Data from the EU-EXASRUB database - rubber dust (n=4157), rubber fumes (n=3803) and n-Nitrosamines (n=10 115) collected between 1977 and 2002 - were modelled using linear mixed-effects models. Sample year, stationary/personal measurement, industry sector and measurement source were included as fixed explanatory variables and factory as random intercept. Model estimates and extrapolations were used to construct a JEM covering all departments in both sectors of the rubber manufacturing industries for the years 1915-2002. JEM-estimates were linked to all cohort members to calculate LCE. Sensitivity analyses related to assumptions about extrapolation of time trends were also conducted. Results: Changes in rubber dust exposures ranged from -6.3 %/year (crude materials/mixing) to -1.0 %/year (curing) and -6.5 %/year (crude materials/mixing) to +0.5 %/year (finishing, assembly and miscellaneous) for rubber fumes. Declines in n-Nitrosamines ranged from -17.9 %/year (curing) to -1.3 %/year (crude materials and mixing). Mean LCEs were 61 mg/m 3 -years (rubber dust), 15.6 mg/ m 3 -years (rubber fumes), 2483.2 μg/m 3 -years (n-Nitrosamines sum score), 18.6 μg/m 3 -years (N-nitrosodimethylamine) and 15.0 μg/m 3 -years (N-itrosomorpholine). Conclusions: All exposures declined over time. Greatest declines in rubber dust and fumes were found in crude materials and mixing and for n-Nitrosamines in curing/vulcanising and preprocessing. This JEM and estimated LCEs will allow for evaluation of exposure-specific excess cancer risks in the British rubber industry

Cancer mortality in an international cohort of reinforced plastics workers exposed to styrene: a reanalysis

OBJECTIVE: To investigate the carcinogenicity of styrene by reanalysing data from a previous international cohort study of workers in the reinforced plastics industry. METHODS: Mortality from cancers of prior interest was analysed with more detailed consideration of exposure-response relations and an updated classification of leukaemias and lymphomas in data from a previous international cohort study of 37 021 reinforced plastics workers exposed to airborne styrene. RESULTS: Increased mortality from non-Hodgkin's lymphoma (NHL) was associated with the mean level of exposure to styrene in air (relative risk (RR) 2.31, 95% CI 1.29 to 4.12 per 100 ppm), but not with cumulative styrene exposure. Similar associations with mean exposure were observed for the oesophagus (RR 2.44, 95% CI 1.11 to 5.36 per 100 ppm) and pancreas (RR 1.89, 95% CI 1.17 to 3.09). Oesophageal cancer mortality was also associated with cumulative styrene exposure lagged 20 years (RR 1.16, 95% CI 1.03 to 1.31). No other cancer, including lung cancer, was associated with any indicator of styrene exposure. CONCLUSION: This reanalysis does not substantially change the conclusions of the original study with respect to NHL or lung cancer but new evidence concerning cancers of the oesophagus and pancreas merits further investigation

Job-exposure matrix for historical exposures to rubber dust, rubber fumes and n-Nitrosamines in the British rubber industry

Objectives: To develop a quantitative historical job-exposure matrix (JEM) for rubber dust, rubber fumes and n-Nitrosamines in the British rubber industry for 1915-2002 to estimate lifetime cumulative exposure (LCE) for a cohort of workers with 49 years follow-up. Methods: Data from the EU-EXASRUB database - rubber dust (n=4157), rubber fumes (n=3803) and n-Nitrosamines (n=10 115) collected between 1977 and 2002 - were modelled using linear mixed-effects models. Sample year, stationary/personal measurement, industry sector and measurement source were included as fixed explanatory variables and factory as random intercept. Model estimates and extrapolations were used to construct a JEM covering all departments in both sectors of the rubber manufacturing industries for the years 1915-2002. JEM-estimates were linked to all cohort members to calculate LCE. Sensitivity analyses related to assumptions about extrapolation of time trends were also conducted. Results: Changes in rubber dust exposures ranged from -6.3 %/year (crude materials/mixing) to -1.0 %/year (curing) and -6.5 %/year (crude materials/mixing) to +0.5 %/year (finishing, assembly and miscellaneous) for rubber fumes. Declines in n-Nitrosamines ranged from -17.9 %/year (curing) to -1.3 %/year (crude materials and mixing). Mean LCEs were 61 mg/m 3 -years (rubber dust), 15.6 mg/ m 3 -years (rubber fumes), 2483.2 μg/m 3 -years (n-Nitrosamines sum score), 18.6 μg/m 3 -years (N-nitrosodimethylamine) and 15.0 μg/m 3 -years (N-itrosomorpholine). Conclusions: All exposures declined over time. Greatest declines in rubber dust and fumes were found in crude materials and mixing and for n-Nitrosamines in curing/vulcanising and preprocessing. This JEM and estimated LCEs will allow for evaluation of exposure-specific excess cancer risks in the British rubber industry

Lung cancer mortality in the European cohort of titanium dioxide workers: a reanalysis of the exposure–response relationship

International audienceObjectives Animal bioassays have demonstrated convincing evidence of the potential carcinogenicity to humans of titanium dioxide (TiO 2 ), but limitations in cohort studies have been identified, among which is the healthy worker survivor effect (HWSE). We aimed to address this bias in a pooled study of four cohorts of TiO 2 workers. Methods We reanalysed data on respirable TiO 2 dust exposure and lung cancer mortality among 7341 male workers employed in TiO 2 production in Finland, France, UK and Italy using the parametric g-formula, considering three hypothetical interventions: setting annual exposures at 2.4 (U.S. occupational exposure limit), 0.3 (German limit) and 0 mg/m 3 for 25 and 35 years. Results The HWSE was evidenced. Taking this into account, we observed a positive association between lagged cumulative exposure to TiO 2 and lung cancer mortality. The estimated number of lung cancer deaths at each age group decreased across increasingly stringent intervention levels. At age 70 years, the estimated number of lung cancer deaths expected in the cohort after 35-year exposure was 293 for exposure set at 2.4 mg/m 3 , 235 for exposure set at 0.3 mg/m 3 , and 211 for exposure set at 0 mg/m 3 . Conclusion This analysis shows that HWSE can hide an exposure–response relationship. It also shows that TiO 2 epidemiological data could demonstrate an exposure–effects relationship if analysed appropriately. More epidemiological studies and similar reanalyses of existing cohort studies are warranted to corroborate the human carcinogenicity of TiO 2 . This human evidence, when combined with the animal evidence, strengthens the overall evidence of carcinogenicity of TiO 2