Level IIb or IV involvement is rare. Superselective neck dissection (IIa, III) seems to be indicated in T1T2 N0 tumor. In case of advanced tumor or pre-epiglottic space or cartilage invasion, functional neck dissection is mandatory.

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The human health impact of the historic and current mining and industrial activities in Tunisia is not known. This study assessed the exposure to metals in the population of Southern Tunisia, using biomonitoring. The aim of this pilot study was to evaluate metal exposure on 350 participants living near mining and active industrial areas in the South of Tunisia. Blood specimens were analyzed for metals (Cd, Cr, As, and Ni) by Atomic Absorption Spectrometer equipped with Zeeman background correction and AS-800 auto sampler by graphite furnace and graphite tubes with integrated L'vov platform. The sample population was classified according to different age groups, sex, smoking habit, sea food and water drinking consumption, occupational exposure, amalgam fillings and place of residence. The blood As, Cd, Cr and Ni values expressed as mean ± SD were 1.56 ± 2.49, 0.74 ± 1.15, 35.04 ± 26.02 and 30.56 ± 29.96 μg/l, respectively. Blood Cd and Ni levels in smokers were 2 and 1.2 times, respectively, higher than in non-smokers. Blood Cd levels increase significantly with age (p = 0.002). As, Cd and Ni were significantly correlated with gender and age (p < 0.05). Cd level in blood samples of subjects occupationally exposed was 1.3 times higher than that of non-exposed. Blood metals were not significantly affected by amalgam fillings, place of living and sea food and drinking water consumption. This first biomonitoring study of metal exposure in the South of Tunisia reveals a substantial exposure to several metals. The pathways of exposure and health significance of these findings need to be further investigated.

Chronic exposure to heavy metals has long been recognized as being capable of increasing head and neck cancer (HNC) incidence, such as laryngeal (LC) and nasopharyngeal (NPC), among exposed human populations. The aim of the present study was to evaluate the concentrations of arsenic (As) and cadmium (Cd) in the blood of 145 patients (LC and NPC) and 351 controls in order to establish a potential relationship between these factors and the occurrence of LC and NPC. Mean blood levels of As and Cd in patients (5.67 and 3.51 μg/L, respectively) were significantly higher than those of controls (1.57 and 0.74 μg/L, respectively). The blood levels of As and Cd were mostly significantly higher than those of controls (p<0.05) after controlling the other risk factors of HNC including tobacco smoking and chewing, and alcohol drinking. Cd levels in blood increase significantly with the number of occupational exposure years for patients (p<0.05). However, seafood was not found to be contributing as an exposure source. Among these risk factors, smoking (>30 pack years) and occupational exposure (>20 years) presented the most significant association with HNC (OR=10.22 and 10.38, respectively, p<0.001). Cd level in blood sample of cases that are occupationally exposed/tobacco users (smokers and chewers) were higher than that of non-occupationally exposed/nontobacco users (p<0.001). The logistic regression model illustrated that HNC (LC+NPC) was significantly associated with blood levels of As (OR=2.41, p<0.001) and Cd (OR=4.95, p<0.001).

The high prevalence/incidence of hearing loss (HL) in humans makes it the most common sensory defect. The majority of the cases are of genetic origin. Non-syndromic hereditary HL is extremely heterogeneous. Genetic approaches have been instrumental in deciphering genes that are crucial for auditory function. In this study, we first used NADf chip to exclude the implication of known North-African mutations in HL in a large consanguineous Tunisian family (FT13) affected by autosomal recessive non-syndromic HL (ARNSHL). We then performed genome-wide linkage analysis and assigned the deafness gene locus to ch:5q23.2-31.1, corresponding to DFNB60 ARNSHL locus. Moreover, we performed whole-exome sequencing on FT13 patient DNA and uncovered aminoacid substitution p.Cys113Tyr in SLC22A4, a transporter of organic cations, cosegregating with HL in FT13 and therefore the cause of ARNSHL DFNB60. We also screened a cohort of small Tunisian HL families and uncovered an additional deaf proband of consanguineous parents that is homozygous for p.Cys113Tyr carried by the same microsatellite marker haplotype as in FT13, indicating that this mutation is ancestral. Using immunofluorescence, we found that Slc22a4 is expressed in stria vascularis (SV) endothelial cells of rodent cochlea and targets their apical plasma membrane. We also found Slc22a4 transcripts in our RNA-seq library from purified primary culture of mouse SV endothelial cells. Interestingly, p.Cys113Tyr mutation affects the trafficking of the transporter and severely alters Ergothioneine uptake. We conclude that SLC22A4 is an organic cation transporter of the SV endothelium that is essential for hearing, and its mutation causes DFNB60 form of HL.