However, RA is part of a continuum from undifferentiated inflammatory polyarthritis (IP) to classical RA and evolution of disease may take up to 5 years .
The Nurses' Health Study and the Nurses' Health Study II are two large US-based cohorts following a total of 238 308 female nurses aged 25–42 years since 19, respectively.
Data from these cohorts suggest a dose-dependent effect of pack-years of smoking, and a threshold dose of 10 pack-years before an elevated risk becomes evident [RR 1.35 (1.04, 1.74) for 11–20 pack-years compared with never-smokers].
Diet and lifestyle factors are of particular interest as they are, at least in theory, modifiable.
The aim of this review is to summarize current knowledge of lifestyle factors implicated in the aetiology of RA and consider how these can contribute to disease prevention strategies.
A North American case-only analysis did not support the smoking–SE interaction  and studies among Korean and African American subjects have argued against its specificity for ACPA RA [35, 36].
It has also been suggested that smoking specifically increases the risk in subjects without the SE , that the risk may differ with different SE alleles  and that there may be other mechanisms of pathogenesis .
Case–control and cohort studies and systematic reviews published from 1948 through February 2011 and studying modifiable risk factors for RA were retrieved.
The risk is dose related, stronger in males and especially strong for anti-citrullinated peptide antibody positive (ACPA) RA through an interaction with the shared epitope.
We conducted a MEDLINE literature search in February 2011 with the Me SH search terms in Fig. Search headings were pre-defined from previous knowledge of the literature.