The evidence regarding lung cancer and occupational exposure to cement is controversial. However, there is some evidence that it is biologically plausible that cement dust could have the potential to cause cancers at sites of contact. As a highly alkaline substance, cement can cause irritation at sites of contact, such as the mouth, throat, and lungs. Persistent chronic irritation will cause repeated cycles of cell death, cell proliferation and other inflammatory responses. It is recognized that this process can be a step on the pathway to cancer [2
]. The present study suggests that cement workers (cement production and maintenance) present significantly elevated all respiratory and lung cancer mortality. On the contrary our study failed to suggest a significant increase of proportionate mortality from laryngeal cancer; however both PMRs were elevated based on small numbers. There is conflicting evidence on the association between occupation exposure to cement dust and risk of respiratory (lung and laryngeal) cancer. Jakobson et al, in a Swedish retrospective cohort study, did not find an increased mortality from respiratory cancer [8
]. Dab and colleagues, in a French cohort study with a follow up period of 15
years, also failed to demonstrate an elevated mortality from respiratory cancer among workers of a cement industrial plant [9
]. Giordano et al, in an Italian cohort study, found a significantly elevated mortality for respiratory cancer, exclusively in a group of cement workers with previous exposure to asbestos [10
]. On the other hand, Smailyte and coworkers in a cohort study among workers of the Lithuanian cement industry plan, found an excess in Standardised Mortality Ratio (SMR) for lung cancer [7
]. Rafnsson et al, in an Icelandic cohort study, found an increased risk of lung cancer among masons [6
]. Moreover, a case-control study commissioned by the International Agency Research Cancer (IARC) in Central and Eastern Europe, found that occupational exposure to cement dust was associated with an increased risk of lung cancer (Odds Ratio
3.62; 95%CI 1.11 to 12)[12
]. Compared to the previous studies, the present study has the considerable advantage to rely on data from the insurance scheme of cement workers. Therefore, our results may have the potential for a satisfactory level of generalizability.
Our study presents several limitations which need to be discussed. A first limitation is related to the PMR analysis employed in this study. Proportionate mortality analysis is used when the total population at risk is not known and only death information on the cohort under study is available. Consequently, proportionate mortality analysis does not provide a true estimate of the risk. Another limitation of our study is related to the exposure assessment. Since historical exposure data (industrial hygiene measurements) were not available, the job title was used as surrogate indicator of exposure to cement dust. In fact, despite of the presence of detailed information on employment of the workers in the cement industry, we cannot rule out that information bias in terms of exposure misclassification may have occurred. Another possible limitation of the present study is related to the confounding role of smoking. Our study lacks longitudinal information on smoking habit of the workers in the cement industry. This is also the case with almost all studies reporting mortality data from cement workers. However, we believe that is unlikely that our finding of the significantly elevated proportionate mortality from lung cancer could be due to the confounding effect of smoking. If that was the case, then the smoking habit would largely differ between production, maintenance and office workers. However, there are data suggesting that blue and white collar workers in Greece have comparable rates of smoking [13
]. Therefore we believe that there is no obvious reason that smoking habit should differ substantially between these categories of blue collar workers. Moreover, Axelson suggested that confounding from smoking would rarely explain risk ratios of more than about 1.5 for lung cancer [14
]. Based on the aforementioned data, it is likely that the confounding effect of smoking could be considered as minimal in the present study. This argument is supported by our finding regarding the comparable levels of bladder cancer proportionate mortality across the three categories of cement workers. Regarding the possible confounding effect of asbestos exposure the fact that no death from mesothelioma was found among cement workers suggests that asbestos does not represent a considerable confounding factor in the present study.
Moreover, an additional limitation of the proportionate mortality methodology is that the magnitude of each cause of death is dependent upon the magnitude of the proportionate mortality for other causes of death. If the PMR for the common cause of death is high, the PMRs for the other causes are artificially deflated, and vice versa [15
]. It is well known that in a working population the risk for diseases of the circulatory system is lower due to the ‘’healthy worker effect”, and therefore, in a proportionate mortality study the other causes could be artificially increased. However, this is not the case in the present study where diseases of the circulatory system were the prevalent cause of death. Moreover, the PMRs for two major causes of death ischemic heart disease and cerebro-vascular diseases (cement production workers only) were 1.37 and 1.11, respectively. Thus, it seems unlikely that the elevated PMR for lung cancer could be attributed to an under-representation of major causes of death like CHD, and CVD.
Last, an interesting finding of our study which deserves further future investigation was the elevated proportionate mortality from pneumonia among cement production workers. There is some evidence that exposure to inorganic dust increases the mortality from infectious pneumonia. It has been suggested that this biological effect could be mediated through induced airways inflammation [16