Send letter to journal:
Re: Exposure-response association between air pollutants and ischaemic heart disease mortality

To the Editor of Occupational and Environmental Medicine:

We agree with suggestion of Dr. Sjögren that examination of the exposure-response relationship between occupational exposures and ischaemic heart disease (IHD) is scientifically justified and is of great importance to public health. An important motive for exploring this research question in the work environment are repeated observations in outdoor pollution studies which show elevated risks for cardiovascular disease in association with exposure to (ultra-) fine particulate matter. Therefore, the readers may wish to learn that, while examining the association between occupational exposure to polycyclic aromatic hydrocarbons (PAH) in road paving and risk of death from IHD, we observed and reported positive exposure-response association at air concentrations that may well be typical of polluted urban air[1]. Specifically, there were 418 cases of fatal IHD in a cohort of 12,367 male asphalt paving workers from Denmark, Finland, France, Germany, Israel, The Netherlands and Norway. Both cumulative and average exposure indices for benzo(a)pyrene (chosen marker of exposure to PAH) were positively and strongly associated with mortality from IHD. The highest relative risk for fatal IHD was observed for average benzo(a)pyrene exposures of 273 ng/m3 or higher, for which the relative risk was 1.64 (95% confidence interval 1.13–2.38). External adjustment for potential confounding by smoking suggested that such confounding was an unlikely explanation for the result. In the same cohort, we also observed that there was a dose- response in the association between mortality from obstructive lung disease (chromic obstructive pulmonary disease and/or asthma combined) and exposure to PAH[2]. Thus, there may well be mounting evidence that occupational (and environmental) carcinogens and/or fine particles resulting from condensation of semi-volatile organic fumes, can cause certain non-malignant chronic conditions, which is not very surprising given that tobacco smoke is a recognized cause of a broad range for both malignant and non-malignant diseases.

Igor Burstyn, PhD

Associate Professor, Community and Occupational Medicine Program, Department of Medicine, Faculty of Medicine and Dentistry, The University of Alberta, Edmonton, Canada iburstyn@ualberta.ca

and

Dick Heederik, PhD

Professor of Health Risk Analysis and Head Division Environmental Epidemiology Institute for Risk Assessment Sciences, University Utrecht, Utrecht, The Netherlands d.heederik@uu.nl

References

1.Burstyn I, Kromhout H, Partanen T, et al. Polycyclic aromatic hydrocarbons and fatal ischemic heart disease. Epidemiology 2005;16 (6):744-50.

2. Burstyn I, Boffetta P, Heederik D, et al. Mortality from Obstructive Lung Diseases and Exposure to Polycyclic Aromatic Hydrocarbons among Asphalt Workers. Am J Epidemiol 2003;158 (5):468-78.

Send letter to journal:
Re: Chrysotile exposure and lung cancer

September 17, 2007

Editor Occupational and Environmental Medicine

Hein et al reported an excess of lung cancer in a cohort of South Carolina textile workers attributed to chrysotile asbestos exposure(1). Information on smoking, the predominant risk factor for lung cancer, was not known. Table 2 in the publication shows an excess mortality from ischemic heart disease (SMR 1.39) and chronic obstructive pulmonary disease (SMR 1.41) which are well recognized tobacco related diseases. The difference in actual tobacco use by these markers and the estimated tobacco use described by the authors likely explains the lung cancer excess. Most of the studies that have identified high risks of lung cancer from asbestos exposure were from cohort studies among workers whose exposure was mainly during the period 1940-1970. Studies conducted on more recently exposed workers and studies using case-control methods, have generally not found clear evidence of excess risks of lung cancer from exposure to asbestos(2).

Yours truly,

Stuart A. Levy, M.D.

1. 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

2. Henderson DW, Rodelsperger K, Woitowitz HJ, Leigh J. After Helsinki: a multidisciplinary review of the relationship between asbestos exposure and lung cancer, with special emphasis on studies published during 1997-2004. Pathology 2004; 36: 517-550

Send letter to journal:
Re: Ischaemic heart disease among chrysotile textile workers

Letter to the editor regarding Follow-up study of chrysotile textile workers: cohort mortality and exposure-response by Hein MJ, Stayner LT, Lehman E, Dement JM in Occup Environ Med 2007; 64: 616-625.

Bengt Sjögren MD, PhD, Work Environment Toxicology, Institute of Environmental Medicine, Karolinska Institutet, SE-177 77 Stockholm, Sweden, Phone +46 8 524 822 29, Fax +46 8 31 41 24, E-mail bengt.sjogren@ki.se

Hein and coworkers followed a cohort of 3072 chrysotile textile workers until 2001(1). One of the main messages was an excess mortality from ischaemic heart disease (IHD), SMR 1.20 (95% CI 1.10-1.32). There were altogether 469 deaths due to IHD which is higher than the total number of cancers being 463, but there were no calculations of dose- response regarding IHD.

Today health effects of general air pollutants have been studied intensively. Exposure to airborne particulate matter has been associated with increases in mortality and hospital admissions due to cardiovascular diseases. These effects have been found in short-term studies, which relate day-to-day variations in air pollution and health and in long-term studies, which have followed cohorts of exposed individuals over time(2,3). Short-term effects of air pollutants have been studied among 38 million persons in eight European cities. An increase of 10 µg/m3 in PM10 was associated with 0.5% (95%CI 0.2-0.8%) increase in hospital admissions for cardiac causes(4). A cohort of approximately 500 000 persons was formed in 1982 and followed for 16 years. Each 10 µg/m3 elevation of fine particulate (PM2.5) was associated with a 6% increase of cardiopulmonary deaths(5). 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(6). 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(3).

So far very few occupational studies have focused on the relation between air pollutants and IHD and to my knowledge none has investigated dose-response relations between air pollutants and IHD. It is urgent that Hein and her coworkers take this opportunity to investigate the dose- response relationship between chrysotile asbestos exposure and IHD.

References

1. 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.

2. Brook RD, Franklin B, Cascio W, et al. Air pollution and cardiovascular disease. A statement for healthcare professionals from the expert panel on population and prevention science of the American Heart Association. Circulation; 2004; 109: 2655-2671.

3. Brunekreef B, Holgate ST. Air pollution and health. Lancet 2002; 360: 1233-1242.

4. Le Tertre A, Medina S, Samoli E, et al. Short-term effects of particulate air pollution on cardiovascular diseases in eight European cities. J Epidemiol Community Health 2002; 56: 773-779.

5. Pope CA III, Burnett RT, Thun MJ, et al. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA 2002; 287: 1132-1141.

6. Clancy L, Goodman P, Sinclair H, Dockery DW. Effect of air- pollution control on death rates in Dublin, Ireland: an intervention study. Lancet 2002; 360: 1210-1214.