Abstract Introduction First-hand smoking is a major cause of global morbidity and mortality. Exposure to environmental tobacco smoke (ETS; “second-hand” or “passive smoking”) may also cause ill health but establishing ETS as the cause is challenging, in part due to confounding and reverse causation. Methods We applied Mendelian randomisation (MR) to investigate causal effects of ETS. We use four approaches to instrument ETS exposure: The first and second used an index individual’s parent’s genetically predicted smoking, independent of the index individual’s genetically predicted smoking to assess the effects of that parent’s smoking on the index individual. The third and fourth used one index individual’s parent’s genetically predicted smoking, independent of the other parent’s genetically predicted smoking to assess the effects of the first parent’s smoking on the second parent. We then meta-analyse the four MR approaches. Results Our findings suggest a causal effect of genetically predicted ETS exposure on lung cancer and chronic obstructive pulmonary disease (pFDR 0.001 for both). We did not find evidence supporting an effect on hypertension, depression, coronary heart disease, or stroke (pFDR = 1.000 for all four non-respiratory outcomes). Conclusion These results support existing public health measures to limit exposure to ETS.
Woolf et al. (Tue,) studied this question.