## 4 Discussion  
Elemental analysis of clam tissues revealed that the following elements were readily (\(\geq\)2-fold) increased in clam tissues over the time survey at the polluted and BSM sites compared to the reference site MAB: V, Mn, Ce, Hg, Ag, Ni, Sm and Ga. The absence of a positive correlation between these eight elements with K suggests that these elements behaved as particles. However, K (as with sodium, Ca and Mg) is physiologically regulated and could have contributed, in part at least, to the lack of correlation. Despite this, K tissue levels were significantly lower in clams at the polluted and BSM sites, suggesting a decreased capacity to retain K in tissues. Loss of K could indicate electrolyte loss, perhaps by reduced respiration (metabolic activity) and Na/K-pump activity [16]. In a previous study with snails and mussels, exposure to mercury decreased K levels in tissues at both lethal and sublethal concentrations, providing some insights into the toxic effects of this contaminant in invertebrates [17]. It is noteworthy that nitrogen elimination (NH4\({}^{+}\)) follows Na\({}^{+}\)/K\({}^{+}\)-ATPase activity in membrane pores in gills [18], suggesting that low K\({}^{+}\) in tissues could be associated to altered nitrogen turnover. The highest increase in elements in clam tissues was V with a 20-fold increase at BS compared to the reference site. This element is a natural contaminant of crude oil, which is transported by commercial ships in the Saguenay Fjord or unknown sources of crude oil are inadvertently released in this area. This suggests that clams at the polluted and BSM sites are exposed to crude oil or diesel fuel contamination. Indeed, high levels of V were found in ashes from heavy fuel oil (diesel) combustion in marine engines [19]. Although V from fuel combustion would be V oxides, V\({}^{2+}\) was shown to induce oxidative stress and metallothioneein levels in _Mytilus_ sp. tissues [20]. This is consistent with a previous study showing increased levels of metallothioneeins in the digestive gland of clams located near a wharf compared to outside the harbor area [21]. This study also revealed that V in tissues (0.43-0.91 \(\mu\)g/g) were in the same range as those found in the present survey and negatively impacted the CF based on correlation analysis. Although the CF was not significantly correlated with V in tissues in the present study, V levels were negatively correlated with the air survival time of clams, which was in turn related to CF, age and the GI. It is interesting that the increase in V tissues in the 2006 study was 2.4-fold compared to 6.3-fold at the same sites in the present study; hence, V contamination in clams has been increasing over the last decades. In clams,  
Figure 5: Trend analysis of biomarker data. The 5 years of biomarker data were filtered by Fourier analysis (12 principal frequencies) to observe the global trends in time for CF (**A**), growth index (**B**) and lethal time (**C**). Each year (40 observations) of collection is separated by dotted lines. The reference site (MAB), polluted sites (BSC and TAD) and SLE beluga area (BSM) are marked in different colors. _Radiatapes philipipinarum_, chronically exposed to Cd, a threshold tissue concentration of 7 mg/g was associated to Cd-induced toxicity [22]. This concentration was about 50 higher than the 95 th percentile value of Cd concentration in tissues in this study. This suggests that Cd on its own is unlikely to be a major player of the observed effects. With respect to V, the levels of V in tissues at roughly 0.1 mg/g was related to metallothioneen levels in blue mussels, suggesting effects at the biochemical level [20]. Tissue mean concentrations of V in clams was circa 2.5 and 20 times higher than the reference site, suggesting that V could have contributed to toxicity based on the physiological health indicators CF, GI and LT.