• 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2020-03
  • 2020-07
  • 2020-08
  • 2021-03
  • We opted to estimate the


    We opted to estimate the preventability of cancer using the most recent exposure data in Brazil, which may not have properly accounted for the latency between exposures and cancer. This approach has been used in the literature due to uncertainty and variation in regard to latency of lifestyle exposures to cancer occurrence and deaths [29]. We used data from POF 2008/09 and PNS 2013 in order to estimate the prevalence of lifestyle risk factors, although cancer cases and deaths were estimated for 2012. Depending on trends of cancer incidence and risk factors over time, this Paxilline may have underestimated or overestimated our estimates. We limited our estimates to associations supported by convincing evidence according to the IARC and the WCRF, and results from recent meta-analyses [[7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17],21,22]. Our results might be underestimated, especially for lifestyle exposures with recent promise findings in regard to cancer prevention [42]. For instance, a recent pooled analysis found that physical activity was associated with lower risk of 13 types of cancer [42]. If these associations are causal, our estimates preventability of cancer due to physical activity are underestimated. Regarding the dietary factors, calcium was the only nutrient considered in our analysis. The WCRF report assessed the association between consumption of dairy products as well as calcium supplements as probable protective against colorectal cancer [12]. One potential interpretation is that both results on dairy products and calcium supplements supports calcium as the key protective component. In fact, a meta-analysis of prospective studies found that calcium supplements and non-dairy products fortified with calcium may play a role in colorectal cancer prevention [43]. In our study, we considered exposure as total dietary calcium consumption only. PAF estimates did not either account for interaction between lifestyle risk factors nor exposures at earlier stages of life, which may also have underestimated the actual preventability of cancer in Brazil. Finally, this study focused on lifestyle risk factors, but reductions in other modifiable risk factors (e.g., infections) may certainly play an important role in cancer prevention. These modifiable risk factors were considered in a previous study in Brazil [20], but since then its prevalences have not been updated.
    Funding Leandro Fórnias Machado de Rezende receives a doctoral scholarship from São Paulo Research Foundation (FAPESP), grants #2014/25614-4 and #2016/21390-0.
    Conflict of interest
    Authorship contribution statement
    Introduction Although involuntary smoking is an established risk factor for lung cancer [1], the association with other tobacco-related cancers, and in particular head and neck cancer, is not established. In an International Head and Neck Cancer Epidemiology (INHANCE) Consortium study, 6 studies from North America, South America and Central Europe were pooled on 542 head and neck cancer cases oils were never tobacco users to investigate involuntary smoking. Involuntary smoking for more than 15 years in the home (OR = 1.60, 95%CI = 1.12, 2.28) and for more than 15 years at work (OR = 1.55, 95%CI = 1.04, 2.30) were both associated with increased risks of head and neck cancer among never tobacco users [2]. In a multicenter case-control study in Western Europe, oral cavity and oropharyngeal cancer risk (n = 111) among never tobacco users were increased for involuntary smoking exposure for more than 15 years at work (OR = 1.92, 95%CI = 1.12, 3.28) [3]. A US based study of 184 never smoking head and neck cancer patients reported no association between childhood passive smoking and head and neck cancer risk but a two-fold increase in the risk of oropharyngeal cancer (OR = 2.02, 95%CI = 1.02, 4.06) [4]. Finally, a case-control study of 238 female oral cavity cancer patients in China reported more than two-fold increases in risk due to passive smoking with dose-response relations for both frequency and duration of exposure [5]. On the other hand, several studies reported either null associations with involuntary smoking or positive associations with wide confidence intervals [[6], [7], [8], [9], [10]].