Summary
The strengths of this analysis include the conservative assumptions used in calculating the
estimated exposures from Swedish snus as well as for the comparator exposures. The
component concentrations that were below the laboratory limits of detection (LOD) were
assumed to have a distribution below the LOD and used to generate estimated exposures for
several of the HPHCs. The upper range of extractions was also used so as not to
underestimate the amount of an HPHC that might be extracted in the mouth during snus use.
As discussed in the report, the comparisons with intakes from food assume similar extraction
and uptake of the HPHCs from food and snus, which is likely not the case, as absorption (and
thus exposure) from foods is likely to be more complete because of swallowing and digestion in
the gastrointestinal tract.
Sources of variability that contribute to uncertainty in the estimates include use of a single
(recent) year of annual mean HPHC concentrations in the eight Swedish Match snus products.
Variability within the year, and concentrations from previous years were not considered. The
worst case calculations, however, which used the highest reported HPHC concentration from
additional Swedish Match data, and the reported upper bound daily snus consumption, would
be expected to capture some of the variability in the laboratory measurements such that
estimated exposures from use of Swedish snus for most contemporary users would not likely be
higher than calculated in this report. Actual internal/systemic exposures can be measured by
use of appropriate exposure biomarkers.
Because the amounts of HPHCs in foods are also highly variable, estimates of human
exposures, which reflect not only the amounts in foods, but factors such as use patterns,
extraction and absorption, are also variable. The dietary estimates are not intended to apply to
any one individual but are population averages where these data were available and are meant
to represent usual intakes.
Though the exposure estimates and cancer risks presented in this report support the
epidemiological research on Swedish snus, in which no increased cancer risk has been
observed for cancers at sites observed in animals exposed to TSNAs, such as oral and lung
cancers, there are some inconsistencies in the epidemiology for other cancer sites, such as
pancreatic cancer, which remain to be confirmed by further research.
Clearly, however, the HPHC exposures to users of Swedish snus are generally no more than
that from foods, and for HPHC components unique to tobacco, namely nicotine and TSNAs,
exposures from Swedish snus are no more than that from smoking.
Citation
Environ. "Estimated HPHC Intakes from Snus Consumption – Comparison with Dietary Intakes or Smoking" 2014.