More information about text formats
Mortality among British asbestos workers undergoing regular medical examinations (1971-2005). Occup Environ Med 2009; 66: 487-95.
Bengt Sjögren, MD, PhD
Work Environment Toxicology
Institute of Environmental Medicine
P.O. Box 210
SE-171 77 Stockholm
Tel +46 8 524 822 29
Fax +46 8 31 41 24
Anne-Helen Harding and coworker...
Anne-Helen Harding and coworkers1 presented mortality data from 98117 asbestos-exposed workers and increased mortality due to ischaemic heart disease (IHD), SMR 1.40 (95% CI 1.36-1.44). There are good arguments for further scrutinizing this observation.
Today it is rather established that inhalation of urban air pollutants are associated with increases in mortality and morbidity due to cardiovascular disease. This was observed in short-term, cohort and intervention studies and effects were seen at low concentrations.2
Whether inhalation of asbestos fibers can cause IHD is today an unsolved question. Some studies show a relationship between asbestos exposure and IHD.
A cohort of 3072 white male textile workers exposed to chrysotile was followed through 2001. An increased risk of ischemic heart disease was observed (SMR 1.20, 95%CI 1.10 – 1.32).3
A cohort of about 11000 men employed in the chrysotile mines and mills of Quebec was followed until 1988. IHD was more common among those exposed to 300 or more million particles per cubic foot x years (SMR 1.24) compared with those exposed to less than 30 (SMR 0.92).4
Non-smoking patients with asbestosis were compared with healthy controls. The asbestosis patients had significantly increased serum levels of inflammatory markers.5 During the last decade these markers of inflammation have emerged as risk factors for IHD. A general hypothesis about exposure to inhaled air pollutants and the occurrence of IHD can be expressed in the following way. Inhalation of particles will create a low grade inflammation associated with an increase in plasma fibrinogen and other blood clotting agents. A higher concentration of these agents will increase the likelihood for blood clotting and thereby the risk for myocardial infarction and IHD. 2
I hope these arguments will encourage Harding and coworkers to further explore the relationship between asbestos exposure and the occurrence of IHD in internal analysis.
1. Harding A-H, Darnton A, Wegerdt J, McElvenny D. Mortality among British asbestos workers undergoing regular medical examinations (1971-2005). Occup Environ Med 2009; 66: 487-95.
2. Sjögren B. Occupational exposure to air pollutants, inflammation and ischemic heart disease, Editorial. Scand J Work Environ Health 2004;30:421-423.
3. Hein MJ, Stayner LT, Lehman E, Dement JM. Follow-up study of chrysotile textile workers: cohort mortality and exposure-response. Occup Environ Med 2007; 64: 616-625.
4. McDonald JC, Liddell FDK, Dufresne A, McDonald AC. The 1891-1920 birth cohort of Quebec chrysotile miners and millers: mortality 1976-88. Br J Ind Med 1993;50:1073-1081.
5. Lehtonen H, Oksa P, Lehtimäki L, et al. Increased alveolar nitric oxide concentration and high levels of leukotriene B4 and 8-isoprostane in exhaled breath condensate in patients with asbestosis. Thorax 2007; 62: 602-607.