Laura Leyssens

Cobalt toxicity in humans—a review of the potential sources and systemic health effects

Cobalt (Co) and its compounds are widely distributed in nature and are part of numerous anthropogenic activities. Although cobalt has a biologically necessary role as metal constituent of vitamin B12, excessive exposure has been shown to induce various adverse health effects. This review provides an extended overview of the possible Co sources and related intake routes, the detection and quantification methods for Co intake and the interpretation thereof, and the reported health effects. The Co sources were allocated to four exposure settings: occupational, environmental, dietary and medical exposure. Oral intake of Co supplements and internal exposure through metal-on-metal (MoM) hip implants deliver the highest systemic Co concentrations. The systemic health effects are characterized by a complex clinical syndrome, mainly including neurological (e.g. hearing and visual impairment), cardiovascular and endocrine deficits. Recently, a biokinetic model has been proposed to characterize the dose-response relationship and effects of chronic exposure. According to the model, health effects are unlikely to occur at blood Co concentrations under 300μg/l (100μg/l respecting a safety factor of 3) in healthy individuals, hematological and endocrine dysfunctions are the primary health endpoints, and chronic exposure to acceptable doses is not expected to pose considerable health hazards. However, toxic reactions at lower doses have been described in several cases of malfunctioning MoM hip implants, which may be explained by certain underlying pathologies that increase the individual susceptibility for Co-induced systemic toxicity. This may be associated with a decrease in Co bound to serum proteins and an increase in free ionic Co2+. As the latter is believed to be the primary toxic form, monitoring of the free fraction of Co2+ might be advisable for future risk assessment. Furthermore, future research should focus on longitudinal studies in the clinical setting of MoM hip implant patients to further elucidate the dose-response discrepancies.

The test–retest reliability of questionnaires regarding attitudes and beliefs toward noise, hearing loss, and hearing protector devices in young adults

Context: Young people expose themselves to high noise levels during leisure activities, and might thus be at risk of acquiring hearing-related problems. Therefore, information regarding risk-taking behavior is necessary to prevent future hearing problems and to optimize future preventive campaigns. Aim: This study evaluated the test–retest reliability of the Youth Attitude to Noise Scale (YANS) and beliefs about hearing protection and hearing loss (BAHPHL) instrument. Settings and Design: Forty-three young adults between 18 and 29 years filled in a questionnaire at two test moments. Materials and Methods: The YANS and BAHPHL instrument were used to evaluate the attitudes toward noise, hearing loss, and hearing protection. Each participant completed the retest within 21–55 days after the first administration of the questionnaire. Results: Paired Student’s t-tests showed no significant differences in mean scores between test and retest for both the entire YANS and BAHPHL instrument as well as their factors. Furthermore, a good agreement between test and retest scores was seen by Bland–Altman analyses. Intraclass correlation coefficients were above 0.70 for the entire YANS and the factor related to youth culture as well as for the entire BAHPHL and all the factors of the BAHPHL instrument, except for the factor related to the severity of the consequences of hearing loss. Conclusion: Reliable test–retest measurements of the YANS and BAHPHL instrument can be performed. Hence, these questionnaires can be used in longitudinal studies to explore young adults’ changes in attitudes toward noise, hearing loss, and hearing protection, with or without an educational intervention.

Standard vs. nose electrode placement for measuring oVEMPs : test-retest reliability and preliminary patient results

Introduction: Loss of hypocretin (HCRT) neurons has been linked to narcolepsy. These neurons project widely throughout brain, but it is not known which projection to which target site produces what symptom. We showed that HCRT receptors are present in brainstem areas implicated in REM sleep Begin superscript 1 End superscript. Since abnormal REM sleep triggering characterizes narcolepsy, we used HCRT2-saporin (HCRT2SAP), a toxin that selectively lesions HCRT receptor bearing cells, to assess the effects of such lesions on sleep. We also used α-DBH-sap to specifically destroy NA-LC neurons, which are the major brainstem targets of HCRT neurons. Methods: Twenty-three male Sprague-Dawley rats (350-620 g) instrumented for sleep recordings were given a single bilateral microinjection of either saline (n=11), or α-DBH-sap (n=5; 100 ng), or HCRT2-SAP (n=6; 46 ng). All injections were stereotaxically aimed to dorsolateral pons (A=-0.7; L=±1.4-1.6;V=+3.0). Then 24 h sleep recordings were done on 3rd, 6th, 9th, 12th and 18th days post-injections (12:12h lights on/off). Scoring was made visually on a computer (Icelus software) in 12s epochs for waking, slow wave sleep (SWS) and REM sleep (REMS) by one technician blind to treatment. ANOVA and t-test were used to compare changes in sleep parameters. Then brain were fixed, removed and sectioned for immunohistochemistry against DBH (1:50K;Chemicon) TH (1:12K; Chemicon) and NeuN (1:1K;Chemicon) proteins. Histochemistry for NADPH was made as well. A technician blind to treatment counted DBH-ir and NADPH+ cells in a 1:5 sections across the mesopontine tegmentum. Results: α-DBH-sap lesioned DBH-ir cells in the locus coeruleus (LC) region but did not affect the number of NADPH+ cells (cholinergic) in the LDTg (Fig 1). In addition α-DBH-sap produced a major loss in DBH fibers-ir among several LC-projection sites. TH and NeuN-ir neurons were not evident in the LC after α-DBH-sap either. Despite all these major degenerative signs observed in the LC after α-DBHsap, sleep parameters over the long-term were not different from saline-injected rats. In contrast rats lesioned with HCRT2-SAP showed a significant increase in nighttime sleep time across three weeks after injections (Table 1). Nighttime SWS+REMS time percent increased by 44% in HCRT2-SAP lesioned rats (P<0.01). The nighttime increase in sleep was associated with a significant increase in SWS and REMS bouts (P<0.05) but not with any change in bout duration. Daytime sleep was not affected by HCRT2-SAP. This toxin lesioned NADPH+ neurons in LDTg as well as NeuN-ir neurons in the parabrachial nucleus although DBH-ir cells were spared in the LC. Figure 1