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Anne-Helen Harding and coworkers presented mortality data from 98 117 workers followed-up for 1 779 580 person-years.1 They found an increased mortality due to ischaemic heart disease (IHD), standardised mortality ratio (SMR) 1.40 (95% CI 1.36 to 1.44). The total number of IHDs was 4183 and total number of deaths was 15 496. Many factors (eg, length of exposure, latency, smoking status, main job category) were taken into account when studying several cancers, asbestosis and cerebrovascular disease. However, IHD was not further analysed. There are some good arguments for further scrutinising this cause of death.
Today it is a rather established fact that exposure to particulate air pollutants is associated with increases in mortality and hospital admissions due to respiratory and cardiovascular disease.2 Short-term effects of air pollutants have been studied among 38 million persons in eight European cities. An increase of 10 μg/m3 in particulate matter ⩽10 μm (PM10) was associated with 0.5% (95% CI 0.2 to 0.8%) increase in hospital admissions for cardiac causes.3 A US cohort of approximately 500 000 persons was formed in 1982 and followed for 16 years. Each 10 μg/m3 elevation of fine particulate matter ⩽2.5 μm (PM2.5) was associated with a 6% increase of cardiopulmonary deaths.4 In an intervention study the cardiovascular death rate decreased by 10% in Dublin after the ban of coal sales in 1990, which decreased the average black smoke by 36 μg/m3 in the city.5 Thus effects have been observed at very low levels of exposure and it is unclear whether a threshold concentration exists for particulate matter under which no effects occur.2
Whether inhalation of asbestos fibres can cause IHD is today an unsolved question. Several studies show a relationship between asbestos exposure and IHD despite a biased comparison with the total population. Some studies also show a relationship between the occurrence of pleural plaques and IHD and one investigation shows a relation between asbestosis and IHD.
An increased mortality due to diseases of the circulatory system (ICD-7, 400–468) was found among white male textile workers exposed to chrysotile in the USA (SMR 1.25, p<0.05). The smoking habits were about the same as in the control group of US men.6 The cohort was expanded to contain altogether 3072 workers and followed through 2001. By this time an increased risk of IHD was observed (SMR 1.20, 95% CI 1.10 to 1.32).7
Enterline and coworkers reported the mortality experience of 1074 white men who retired from a US asbestos company during the period 1941–1967. The participants were exposed during production or maintenance and followed until 1980. An increased mortality due to coronary heart disease (ICD-7, 420) was observed (SMR 1.12, p<0.05) when the cohort was compared with US national death rates.8
A cohort of 3211 men first employed between 1933 and 1974 at a Rockdale asbestos textile factory, were followed until 1983. A small but not significantly increased mortality due to circulatory disease was observed when the cohort was compared with death rates for England and Wales (SMR 1.15) and death rates for Rockdale (SMR 1.18).9
A cohort of 952 workers first employed between 1930 and 1965 in a chrysotile asbestos mine in Northern Italy was followed until 1975. An increased mortality due to cardiovascular diseases (ICD-7, 400–468) was recorded (SMR 1.48, p<0.01) when the cohort was compared with Italian national death rates.10
A cohort of about 11 000 men born between 1891 and 1920 and employed for at least 1 month in the chrysotile mines and mills of Quebec was followed until 1988. IHD was more common among those exposed to ⩾300 million particles per cubic foot × years (SMR 1.24) compared with those exposed to <30 (SMR 0.92).11 One part of this large cohort comprising 4559 men was followed regarding radiological findings. Uncalcified pleural changes were associated with an increased mortality risk regarding diseases of the heart (ICD-7, 400–443) (relative risk (RR) 1.54, p<0.005). Pleural calcifications were also associated with a somewhat increased risk of the same disease (RR 1.34, p<0.10).12
A total of 1106 workers were selected from the workforce of the asbestos industry in Western Australia. These workers were exposed to crocidolite and pleural thickening was a risk factor for death from other causes (RR 1.5, 95% CI 1.3 to 1.8) and IHD formed the largest proportion of deaths from other causes.13
A case-referent study comprised 148 coronary patients and 100 lung cancer patients. Calcified pleural plaques were more common among the coronary patients (35%) than among the lung cancer patients (19%). The RR of calcified pleural plaques, adjusted for age and gender, was 2.2 (95% CI 1.4 to 3.3) for the coronary patients as compared with the lung cancer patients.14
IHD was studied in a cohort of 1725 Swedish male shipyard workers exposed to asbestos. Men with pleural plaques had a slightly increased risk of IHD compared with men without pleural plaques (RR 1.3, 95% CI 0.8 to 2.0) after stratification for age and smoking habits. However, men with asbestosis or suspected asbestosis had a significantly higher risk (RR 3.1, 95% CI 1.5 to 6.4) of dying from IHD than did men without asbestosis, after stratification for age and smoking habits.15
Non-smoking patients with asbestosis were compared with healthy controls. The asbestosis patients had significantly increased serum levels of the inflammatory markers C reactive protein and interleukin-6.16 During the last decade these markers of inflammation have emerged as risk factors for IHD.17 18 A general hypothesis about exposure to inhaled air pollutants and the occurrence of IHD can be expressed in the following way. Inhalation of particles and irritant gases in the lungs 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.19 20
I hope these arguments will encourage Anne-Helen Harding and coworkers to further explore the relationship between asbestos exposure and the occurrence of IHD in internal analysis.
Competing interests None declared.
Provenance and peer review Not commissioned; not externally peer reviewed.