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Objectives: Occupational exposure to respirable crystalline silica (RCS) is common. The study aimed to assess the risk for acute myocardial infarction (AMI) after long-term exposure to RCS and to explore differences in risk between men and women., Methods: The cohort included all manual workers identified from the Swedish National Census in 1980 using data on job titles and demography altogether from five censuses from 1960 to 1990, in total 605 246 men and 480 607 women. Information on AMI was obtained from nationwide registers from 1992 to 2006. Exposure to RCS was assessed with a job-exposure matrix. HRs and 95% CIs were estimated by Cox regression, adjusted for age, socioeconomic status and urbanisation index., Results: Among manual workers ever exposed to RCS, the adjusted risk of AMI was HR 1.29 (95% CI 1.15 to 1.46) in women, and HR 1.02 (95% CI 1.00 to 1.04) in men. In the highest quartile of cumulative exposure, the risk of AMI was HR 1.66 (95% CI 1.27 to 2.18) for women, and HR 1.06 (95% CI 1.03 to 1.10) for men, respectively. The risk of AMI increased with cumulative exposure to RCS both in women (p=0.001) and in men (p=0.016). An interaction analysis showed that the relative risk from exposure to RCS was statistically significantly lower in men than in women at similar exposure levels., Conclusions: Occupational exposure to RCS was related to the risk of AMI. Women were more sensitive to exposure to RCS than men., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Objective: To investigate the relation between signs and symptoms of irritation and biomarkers of inflammatory markers in blood in healthy volunteers exposed to different chemical vapours for 2 or 4 hours in an exposure chamber., Methods: The investigated chemicals were: acetic acid (5 and 10 ppm), acrolein (0.05 and 0.1 ppm), 1,4-dioxane (20 ppm), n-hexanal (2 and 10 ppm), hydrogen peroxide (0.5 and 2.2 ppm), 2-propanol (150 ppm), m-xylene (50 ppm), standard and dearomatised white spirit (100 and 300 mg/m 3 ). C reactive protein (CRP), serum amyloid A protein and interleukin 6 were measured in plasma immediately before and 2 or 4 hours after the exposures. Symptoms were rated from 0 to 100 mm in Visual Analogue Scales and covered 10 questions whereof four related to irritation: discomfort in the eyes, nose and throat and dyspnoea. The effect measurements included blink frequency by electromyography, nasal swelling by acoustic rhinometry and lung function by spirometry., Results: Logistic quantile regression analyses revealed no significant associations except a negative relation between ratings of irritation and CRP., Conclusion: The results suggest a down-regulation of CRP after short-term exposure to low levels of vapours of irritating chemicals. This response might be mediated by the cholinergic anti-inflammatory pathway and further studies are recommended in order to refute or confirm this hypothesis., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Ambient particulate air pollution has been linked to cardiovascular disease. Occupational particle exposure levels may be several times higher than ambient levels but has been less studied., Objectives: The authors investigated the association between occupational exposure to particles and the incidence of ischaemic heart disease (IHD)., Methods: The cohort included all manual workers in the Swedish national census of 1980 with information on demographic data and occupation. Information on hospital admissions for acute myocardial infarction or other IHDs and cause of death were obtained from nation-wide registers. A job-exposure matrix for exposure to small (<1 μm) and large (>1 μm) particles was developed. HRs were calculated with Cox regression with adjustment for sex, age, socioeconomic group and urban/rural residential area., Results: Exposure to small particles was associated with an increased HR for acute myocardial infarction of 1.12 (95% CI 1.09 to 1.15), and HR for exposure to large particles was 1.14 (95% CI 1.10 to 1.18). The association was somewhat stronger for workers exposed to small particles for more than 5 years, 1.21 (95% CI 1.11 to 1.31), but no trend with exposure intensity was found. The risk associated with exposure to small particles was higher among women than among men, 1.30 (95% CI 1.12 to 1.51) and 1.10 (95% CI 1.07 to 1.14), respectively. Findings were essentially similar for other IHDs., Conclusions: This explorative study gives some support to the hypothesis that occupational exposure to particles increases the risk of acute myocardial infarction and other IHD. The findings must be interpreted cautiously due to lack of smoking data.

Objectives: To review the possible association between occupational exposure to dust and ischaemic heart disease (IHD)., Methods: A literature search was performed of relevant studies regarding IHD in specific exposures to dust. The chosen exposures were arsenic, asbestos, beryllium, lead, polycyclic aromatic hydrocarbons, and quartz. The chosen occupations were farmers, paper and paper pulp workers, sawyers, and welders., Discussion: A theory was launched in 1995 that urban particulate air pollution may provoke alveolar inflammation, with release of mediators capable of increasing blood coagulability in susceptible people and cause cardiovascular deaths. The present review expands this hypothesis and links occupational exposure to inhaled particles with the occurrence of ischaemic heart disease., Conclusion: This hypothesis should be tested by comparing the concentrations of fibrinogen in workers exposed and nonexposed to particles with control for other possible confounders such as smoking habits.

Objectives: The purpose was to study the effects on the nervous system in welders exposed to aluminium and manganese., Methods: The investigation included questionnaires on symptoms, psychological methods (simple reaction time, finger tapping speed and endurance, digit span, vocabulary, tracking, symbol digit, cylinders, olfactory threshold, Luria-Nebraska motor scale), neurophysiological methods (electroencephalography, event related auditory evoked potential (P-300), brainstem auditory evoked potential, and diadochokinesometry) and assessments of blood and urine concentrations of metals (aluminium, lead, and manganese)., Results: The welders exposed to aluminium (n = 38) reported more symptoms from the central nervous system than the control group (n = 39). They also had a decreased motor function in five tests. The effect was dose related in two of these five tests. The median exposure of aluminium welders was 7065 hours and they had about seven times higher concentrations of aluminium in urine than the controls. The welders exposed to manganese (n = 12) had a decreased motor function in five tests. An increased latency of event related auditory evoked potential was also found in this group. The median manganese exposure was 270 hours. These welders did not have higher concentrations of manganese in blood than the controls., Conclusions: The neurotoxic effects found in the groups of welders exposed to aluminium and manganese are probably caused by the aluminium and manganese exposure, respectively. These effects indicate a need for improvements in the work environments of these welders.

Stainless steel welding is associated with exposure to metals including hexavalent chromium and nickel. This study is a meta-analysis of five studies of stainless steel welders and the occurrence of lung cancer. Asbestos exposure and smoking habits have been taken into account. The calculated pooled relative risk estimate was 1.94 with a 95% confidence interval of 1.28-2.93. This result suggests a causal relation between exposure to stainless steel welding and lung cancer.