The most interesting part of this to me is that, even though this evidence is extremely weak, it is actually stronger than the evidence from animal studies that tobacco smoke can cause lung cancer. It is nearly impossible to devise a study in which breathing in the smoke increases lung cancer rates.

Actually it took researchers half a century to figure out a way despite easily causing lung cancer with radioactive dust, etc. Eventually they discovered you need to expose a special strain of mice starting within hours of birth, and then simulate quitting smoking by stopping the exposure as adults. It is actually the healing from the smoke-induced damage that seems to cause cancer, which makes sense if you believe cancer is a disease caused by too many cell divisions.

>"Strain A mice were exposed first to a comparatively high concentration of ETS, generated from the sidestream (89%) and mainstream (11%) smoke from burning Kentucky 1R4F cigarettes, as described before in detail [9]. After a 5-month exposure, the animals were allowed to recover in air for another 4 months before evaluation of the lung tumor response. The same protocol was eventually adopted by three other laboratories [10–12]. [...] The flat dose-response suggests that tobacco smoke is a comparatively weak carcinogen. A previous study in which a dose-response was conducted in one single experiment came to the same conclusion [13]. It may to some extent explain why most inhalation studies done with tobacco smoke in mice failed to give a positive tumor response [14, 15]. The fact that ‘‘only’’ 10% to 25% of all smokers develop lung cancer [16] might also be construed to indicate that tobacco smoke is not a very potent carcinogen in man." https://www.ncbi.nlm.nih.gov/pubmed/15765916

>"In spite of the dominant role of cigarette smoke (CS) in the epidemiology of lung tumors, tumors at other sites, and other chronic degenerative diseases [1, 2], it is very difficult to reproduce the noxious effects of this complex mixture in animal models. [...] During the last decade, we developed a novel murine model that convincingly reproduces the carcinogenicity of MCS [6] and its modulation under conditions mimicking interventions either in current smokers and/or ex-smokers. [...] Our model involves exposure of mice for 4 months, starting at birth, followed by a period of 3-4 months in filtered air in order to give enough time for the growth of histopathological lesions." https://www.ncbi.nlm.nih.gov/pubmed/29370344