LETTERS: Letters to the Editor
Institute and Policlinic for Occupational and Social Medicine School of Medicine and Dentistry University of Cologne Cologne, Germany email@example.com
To the Editor:
With interest we read Dr. Stayner's commentary1 on the large European study by Cassidy and colleagues2 into occupational exposures to crystalline silica and the risk of lung cancer. On the basis of this study and numerous previous investigations, Dr. Stayner gave a personal “yes” to the following question: “Have we reached a point at which there is enough evidence to conclude that, at least under some circumstances, exposure to silica is causally associated with an increased risk of lung cancer?”
We agree. And yet, there is a critical “but.” Importantly, we think that such judgment is not enough in terms of prevention. We don't want to fall into the trap of an inevitable call for further research. However, in order to make sound public health decisions concerning silica at the low end of the exposure scale we need to answer the following causal question posed earlier by, among others, Checkoway and Franzblau3: Is silicosis required for silica-associated lung cancer?
Indeed, silicosis could be part of the pathogenetic chain that leads to silica-associated cancer. Alternatively, or additionally, it could be a complex biomarker of exposures to silica and of susceptibility to lung carcinogens, including silica, or susceptibility to lung alterations and disease, including cancer. Following this rationale leads to 2 public health consequences. If silicosis is necessary to increase the risk of lung cancer, then the public health goal should be to prevent silicosis. But if it is not a necessary exposure, then lung cancer risks may be increased at much lower doses of silica not known to cause silicosis, implying that current exposure standards may not be appropriate to prevent lung cancer.
Unfortunately, the studies to date, including the one by Cassidy et al,2 do not allow unambiguous answers to the questions regarding the causal path(s) that may lead to lung cancer in silica-exposed workers nor do they provide the much-needed insights into possible effects at the low ends of exposure. (The cumulative exposure distribution presented by Cassidy et al differs considerably from distributions found in other studies, including the cited investigation by Hughes et al.4)
Future studies should consider the entire exposure-response range between silica dust exposure, silicosis development and lung cancer occurrence, and researchers should analyze data in terms of processes, taking intermediate confounding5 and possible threshold effects into account.6
Thomas C. Erren
Christine B. Glende
Institute and Policlinic for Occupational and Social Medicine, School of Medicine and Dentistry, University of Cologne, Cologne, Germany firstname.lastname@example.org
1. Stayner L. Silica and lung cancer: when is enough evidence enough? Epidemiology. 2007;18:23–24.
2. Cassidy A, ′t Mannetje A, van Tongeren M, et al. Occupational exposure to crystalline silica and risk of lung cancer: a multicenter case-control study in Europe. Epidemiology. 2007;18:36–43.
3. Checkoway H, Franzblau A. Is silicosis required for silica-associated lung cancer? Am J Ind Med. 2000;37:252–259.
4. Hughes JM, Weill H, Rando RJ, et al. Cohort mortality study of North American industrial sand workers. II. Case-referent analysis of lung cancer and silicosis deaths. Ann Occup Hyg. 2001;45:201–207.
5. Witteman JCM, D'Agostino RB, Stijnen T, et al. G-estimation of causal effects: isolated systolic hypertension and cardiovascular death in the Framingham Heart Study. Am J Epidemiol. 1998;148:390–401.
6. Morfeld P, Albrecht C, Drommer W, et al. Dose-response and threshold analysis of tumour prevalence after intratracheal instillation of six types of low and high surface area particles in a chronic rat experiment. Inhal Toxicol. 2006;18:215–225.
© 2007 Lippincott Williams & Wilkins, Inc.