Table 4

Evaluation of Hill viewpoints for causal inference about the association between exposure to household biomass fuel use and lung cancer

1Strength of associationThe strength of association for all studies combined is weak, for men and women. When restricted to studies among women (the majority) with at least moderate adjustment and explicit clean fuel reference group, larger ORs are seen, in the range 1.6–>2, depending on the sub-analysis criteria. When restricted to studies in developing countries where exposure is expected to be higher, an effect >2 is also seen for studies with at least moderate adjustment and a clean fuel reference group.
2Consistency across populations, study designsAll studies used a case-control design, although control selection and exposure definitions varied substantially. Findings for studies overall are consistent for men (five estimates; I2=0), but not for women among whom high levels of statistical heterogeneity are seen overall and for most sub-analyses. Heterogeneity was, however, much reduced with analysis stratified by developed vs developing country settings, particularly with the latter restricted to studies with at least moderate adjustment and a clean fuel reference group.
3SpecificityBiomass smoke exposure is linked to a wide range of outcomes; specificity is a viewpoint that is no longer considered useful.26
4Temporality (exposure precedes outcome)Although studies were retrospective case-control designs, subjects exposed at the time of data collection would almost certainly have been exposed in the past for many years, and duration of exposure was assessed in some. Bias (towards the null) is also possible in reference groups reporting current use of clean fuel, as at least some of these subjects may well have had prior exposure to biomass fuel during the latent period for the development of lung cancer.
5Biological gradient (dose–response)A dose–response relationship was reported only from the re-analysis of European data in the Lissowska et al study5 and only statistically significant for men.
6Biological plausibilityStrong evidence is available on biological plausibility. Evidence on mutagenicity and other mechanisms was summarised in the International Agency for Research on Cancer (IARC) monograph review, and noted (1) the presence of polycyclic aromatic hydrocarbons and other established carcinogenic compounds at levels in wood smoke that are known to be carcinogenic, (2) evidence of mutagenicity of woodsmoke, and (3) multiple studies that show cytogenetic damage in humans who are exposed to wood smoke.3
7Coherence with natural history, animal studiesGlobally, rates of lung cancer incidence and mortality are driven primarily by smoking, and where studied within China for household fuel by the use and type of coal.27 This review has found evidence of higher risk in studies from parts of the world expected to have higher exposure to biomass smoke. Evidence from animal studies was summarised by the IARC monograph review, and described as limited for the carcinogenicity of emissions from combustion of wood, but sufficient for the carcinogenicity of wood smoke extracts.
8ExperimentNo experimental or intervention-based epidemiologic evidence for biomass and lung cancer is available.
9AnalogyEvidence from other combustion sources, including active and second-hand tobacco smoking, and ambient air pollution, is well established.