Absence of multiplicative interactions between occupational lung carcinogens and tobacco smoking: a systematic review involving asbestos, crystalline silica and diesel engine exhaust emissions.
Tobacco smoking is the main cause of lung cancer, but it is not the sole causal factor. Significant proportions of workers are smokers and exposed to occupational lung carcinogens. This study aims to systematically review the statistical interaction between occupational lung carcinogens and tobacco smoking, in particular asbestos, crystalline silica and diesel engine exhaust emissions.



Articles were identified using Scopus, PubMed, and Web of Science, and were limited to those published in English or French, without limitation of time. The reference list of selected studies was reviewed to identify other relevant papers. One reviewer selected the articles based on the inclusion and exclusion criteria. Two reviewers checked the eligibility of articles to be included in the systematic review. Data were extracted by one reviewer and revised by two other reviewers. Cohorts and case-control studies were analyzed separately. The risk of bias was evaluated for each study based on the outcome. The results of the interaction between the tobacco smoking and each carcinogen was evaluated and reported separately.



Fifteen original studies were included for asbestos-smoking interaction, seven for silica-smoking interaction and two for diesel-smoking interaction. The results suggested the absence of multiplicative interaction between the three occupational lung carcinogens and smoking. There is no enough evidence from the literature to conclude for the additive interaction. We believe there is a limited risk of publication bias as several studies reporting negative results were published.



There are no multiplicative interactions between tobacco smoking and occupational lung carcinogens, in particular asbestos, crystalline silica and diesel engine exhaust emissions. Even though, specific programs should be developed and promoted to reduce concomitantly the exposure to occupational lung carcinogens and tobacco smoking.
Univ. Bordeaux, Inserm, Bordeaux Population Health Research Center, team EPICENE, UMR 1219, Bordeaux, F-33000, France.
Mohamad
M
El Zoghbi
School of Pharmacy, Lebanese American University, Byblos, Lebanon.|Epidemiological & Clinical Laboratory Research, Faculty of Pharmacy, Lebanese University, Beirut, Lebanon.
Pascale
P
Salameh
Université Paris Saclay, University of Paris-Sud, UVSQ, CESP, INSERM, Villejuif, France.
Isabelle
I
Stücker
Univ. Bordeaux, Inserm, Bordeaux Population Health Research Center, team EPICENE, UMR 1219, Bordeaux, F-33000, France.|CHU de Bordeaux, Pole de sante publique, Service de médecine du travail et de pathologie professionnelle, Bordeaux, F-33000, France.
Patrick
P
Brochard
Univ. Bordeaux, Inserm, Bordeaux Population Health Research Center, team EPICENE, UMR 1219, Bordeaux, F-33000, France.|CHU de Bordeaux, Pole de sante publique, Service de médecine du travail et de pathologie professionnelle, Bordeaux, F-33000, France.
Fleur
F
Delva
Univ. Bordeaux, Inserm, Bordeaux Population Health Research Center, team EPICENE, UMR 1219, Bordeaux, F-33000, France. aude.lacourt@isped.u-bordeaux2.fr.
Aude
A
Lacourt
D001194:Asbestos / Q000009:adverse effects*; D016022:Case-Control Studies; D006801:Humans; D008175:Lung Neoplasms / Q000209:etiology*; D016273:Occupational Exposure / Q000706:statistics & numerical data*; D012306:Risk; D012822:Silicon Dioxide / Q000009:adverse effects*; D012907:Smoking / Q000009:adverse effects*; D001335:Vehicle Emissions / Q000506:poisoning*
D001335:Vehicle Emissions; D001194:Asbestos; D012822:Silicon Dioxide
Interaction; Lung cancer; Occupational exposures; Smoking