The long-term effect of COVID-19 infection on olfaction and taste; a prospective analysis.

PURPOSE: To estimate long-term prognosis of chemosensory dysfunctions among patients recovering from COVID-19 disease. METHODS: Between April 2020 and July 2022, we conducted a prospective, observational study enrolling 48 patients who experienced smell and/or taste dysfunction during the acute-phase of COVID-19. Patients were evaluated for chemosensory function up to 24 months after disease onset. RESULTS: During the acute-phase of COVID-19, 80% of patients reported anosmia, 15% hyposmia, 63% ageusia, and 33% hypogeusia. At two years' follow-up, 53% still experienced smell impairment, and 42% suffered from taste impairment. Moreover, 63% of patients who reported parosmia remained with olfactory disturbance. Interestingly, we found a negative correlation between visual analogue scale scores for smell and taste impairments during the acute-phase of COVID-19 and the likelihood of long-term recovery. CONCLUSION: Our study sheds light on the natural history and long-term follow-up of chemosensory dysfunction in patients recovering from COVID-19 disease. Most patients who initially suffered from smell and/or taste disturbance did not reach full recovery after 2 years follow-up. The severity of impairment may serve as a prognostic indicator for full recovery.

Chemosensory function and food perception is affected in COPD, but unrelated to sarcopenia risk.

BACKGROUND & AIMS: Patients with advanced COPD often have difficulty maintaining sufficient dietary intake. Chemosensory function influences food choice and intake but is often overlooked in dietary assessment and intervention strategies. This study aimed to assess differences in chemosensory function and hedonic evaluation of food between patients with COPD and age- and gender-matched healthy controls. Additionally, a possible association between increased risk of sarcopenia or frailty and chemosensory impairments was explored. METHODS: We recruited 53 COPD patients (34 males, mean age 66.6 ± 7.6 years) and 53 controls (25 males, mean age 68.4 ± 5.7 years). Chemosensory function was assessed using a smell threshold, smell identification (Sniffin' Sticks, Burghart) and taste recognition test (Taste Strips, Burghart) and through self-report. Sensory properties (appearance, smell, taste, mouthfeel) of four standardized food products were evaluated on 9-point hedonic rating scales. Sarcopenia risk was assessed with the SARC-F. RESULTS: The COPD group scored lower on both the smell (p = 0.026 for threshold, p = 0.001 for identification) and taste recognition tests (p < 0.001) and also reported more smell and taste impairments (p < 0.001) compared to controls. Hedonic evaluation of food items' appearance (p = 0.009) and smell (p = 0.033) was lower in COPD patients. Within the COPD group, risk of sarcopenia was not associated with chemosensory function. CONCLUSION: This study demonstrates that COPD patients have poorer chemosensory function and experience more impairments compared to controls. COPD patients also tend to evaluate foods less positive than do their controls but within COPD patients, sarcopenia risk is not associated with chemosensory function.

Human odor exploration behavior is influenced by olfactory function and interest in the sense of smell.

Olfaction plays an important role in social interaction. This study examined the influence of chemosensory and cognitive abilities on conscious odor sniffing behaviors in humans. Participants (N = 349) were surveyed using a questionnaire for the frequency of behaviors in terms of odor exploration from intrinsic and external sources. Chemosensory functions (e.g., odor identification, trigeminal sensitivity, taste functions, and nasal patency), self-reported olfactory function, and the subjective importance of olfaction were assessed. Hierarchical regression analyses demonstrate a strong impact of olfactory importance on odor exploration behavior. Both female gender and chemosensory function (odor identification ability and trigeminal sensitivity) had a positive impact on odor exploration behavior from individuals' own body and from external sources. Moreover, participants with dysosmia compared to those with normosmia showed less frequent odor exploration behaviors, while their behaviors were partly predicted by nasal patency. In conclusion, conscious olfactory exploration behaviors reflect the interest in the sense of smell and is strongly modulated by chemosensory function. In turn, individuals with lower olfactory sensitivity invest less in olfactory explorations.

Olfaction in patients with Parkinson's disease: a new threshold test analysis through turning points trajectories.

Olfactory deficit is a widely documented non-motor symptom in Parkinson's disease (PD). Abnormal turning points trajectories through olfactory threshold testing have been recently reported in patients with olfactory dysfunction, who seem to adapt faster to olfactory stimuli, but data on PD patients are lacking. The aim of this study is to perform olfactory threshold test and explore the turning points trajectories in PD patients in comparison to normal controls. We recruited 59 PD patients without dementia, and no conditions that could influence evaluation of olfaction and cognition. Sixty healthy subjects served as controls. Patients and controls underwent a comprehensive olfactory evaluation with the Sniffin' Sticks extended test assessing threshold, discrimination and identification and a full neuropsychological evaluation. Besides, threshold test data were analyzed examining all the turning points trajectories. PD patients showed a different olfactory threshold test pattern, i.e., faster olfactory adaptation, than controls with no effect of age. Normosmic PD patients showed different olfactory threshold test pattern, i.e., better threshold score, than normosmic controls. Visuospatial dysfunction was the only factor that significantly influenced this pattern. Olfactory threshold trajectories suggested a possible adaptation phenomenon in PD patients. Our data offered some new insights on normosmic PD patients, which appear to be a subset with a specific psychophysical profile. The analysis of the turning points trajectories, through an olfactory threshold test, could offer additional information on olfactory function in PD patients. Future larger studies should confirm these preliminary findings.

Multiple Chemosensory Neurons Mediate Avoidance Behavior to Rare Earth Ions in Caenorhabditis elegans.

As rare earth (RE) metals are abundantly present in the soil, in spite of their name, it is conceivable that organisms may encounter and interact with RE ions. In the present study, we demonstrated that the soil nematode Caenorhabditis elegans avoids RE ions, such as yttrium and all examined lanthanide ions, which exhibit toxic effects on nematodes. We also demonstrated that the chemosensory system of this animal mediates avoidance behavior toward RE ions similar to heavy metal (HM) ion avoidance. The C. elegans dyf-11(pe554) mutant is unable to respond to chemosensory cues because it lacks all ciliated endings of the chemosensory neurons required for the detection of environmental chemicals. Cell-specific rescue of the dyf-11 mutant and cell-specific genetic ablation studies revealed that the avoidance behavior toward HM and RE ions was mediated by a partially overlapping but distinct subset of chemosensory neurons (ASH, ADL, ASE, ADF, and ASK). With the help of multiple chemosensory neurons, worms may improve the fidelity of avoidance behavior to evade RE ions. Among the chemosensory neurons in C. elegans, ADF and ASK neurons were involved in RE avoidance, but not in HM avoidance. These results suggested that ADF and ASK neurons in C. elegans have RE-selective mechanisms to mediate the avoidance response.

Olfaction and taste in Parkinson's disease: the association with mild cognitive impairment and the single cognitive domain dysfunction.

Mild cognitive impairment (MCI) and chemosensory dysfunction are non-motor symptoms of Parkinson's disease (PD), but their association is unclear. We explored if MCI and the involvement of single cognitive domains influence olfaction and taste in PD. The role of demographic, clinical and neuropsychiatric variables was tested. We recruited 50 PD patients without dementia, no other reasons for cognitive impairment, no condition that could influence evaluation of cognition, olfaction and taste. They underwent a full neuropsychological and chemosensory (i.e., olfaction and taste) test with the Sniffin' Sticks Extended test (SSET), Whole Mouth test (WMT) and Taste Strips test (TST). Fifty age- and sex-matched healthy subjects served as controls. Olfactory function and sweet identification were worse in PD than controls. MCI negatively influenced odor identification. Factors associated with poor olfactory function were age, overall cognition, apathy, and visuospatial dysfunction. Sour identification was affected by MCI and executive dysfunction, and salty identification by executive dysfunction. MCI, age and executive dysfunction worsened TST score. Awareness of olfactory dysfunction was impaired in PD with MCI. Education positively influenced SSET and TST scores. Our data confirmed that olfaction is abnormal in PD, while taste was only slightly impaired. Olfaction was worse in PD patients with visuospatial dysfunction, while sour and salty identification was worse in those with MCI and executive dysfunction, suggesting different underlying anatomical abnormalities. Future studies should incorporate neuroimaging and cerebrospinal fluid data to confirm this hypothesis. SSET odor identification and TST sour identification could be explored as quick screening tests for PD-MCI.

A longitudinal study of altered taste and smell perception and change in blood pressure.

BACKGROUND AND AIMS: Previous studies suggest that olfactory receptors, which mediate smell chemosensation, are located in the kidney and involved in blood pressure regulation. Mammalian epithelial sodium channels located in taste receptor cells are also found to participate in blood pressure regulation. However, there is currently no human study that has examined the association between taste and smell function and blood pressure. We thus conducted a longitudinal study to examine whether participants with altered taste and smell perception had larger increases in blood pressure compared with those without altered perception in a community-based cohort. METHODS AND RESULTS: The study included 5190 Chinese adults (4058 men and 1132 women) who were normotensive at baseline. Taste and smell perception were assessed via questionnaire in 2012 (baseline). Blood pressure was measured in 2012 and 2014 to determine relative change in blood pressure. Mean differences of 2-year blood pressure change and 95% confidence intervals (CIs) across four categories of taste and smell perception were calculated after adjusting for known risk factors for hypertension. After adjusting for potential confounders, individuals with altered taste and smell perception had larger increases in systolic blood pressure (adjusted mean difference = 5.1 mmHg, 95% CI: 0.1-10.0, p-value: 0.04) and mean arterial pressure (adjusted mean difference = 3.8 mmHg, 95% CI: 0.4-7.1, p-value: 0.03) after two years of follow-up compared with those having neither altered taste nor altered smell perception. No significant association was observed in individuals with altered taste or smell perception only. CONCLUSION: Our results suggest an association between chemosensory function and blood pressure.

Low-dose oral cadmium increases airway reactivity and lung neuronal gene expression in mice.

Inhalation of cadmium (Cd) is associated with lung diseases, but less is known concerning pulmonary effects of Cd found in the diet. Cd has a decades-long half-life in humans and significant bioaccumulation occurs with chronic dietary intake. We exposed mice to low-dose CdCl2 (10 mg/L in drinking water) for 20 weeks, which increased lung Cd to a level similar to that of nonoccupationally exposed adult humans. Cd-treated mice had increased airway hyperresponsiveness to methacholine challenge, and gene expression array showed that Cd altered the abundance of 443 mRNA transcripts in mouse lung. In contrast to higher doses, low-dose Cd did not elicit increased metallothionein transcripts in lung. To identify pathways most affected by Cd, gene set enrichment of transcripts was analyzed. Results showed that major inducible targets of low-dose Cd were neuronal receptors represented by enriched olfactory, glutamatergic, cholinergic, and serotonergic gene sets. Olfactory receptors regulate chemosensory function and airway hypersensitivity, and these gene sets were the most enriched. Targeted metabolomics analysis showed that Cd treatment also increased metabolites in pathways of glutamatergic (glutamate), serotonergic (tryptophan), cholinergic (choline), and catecholaminergic (tyrosine) receptors in the lung tissue. Protein abundance measurements showed that the glutamate receptor GRIN2A was increased in mouse lung tissue. Together, these results show that in mice, oral low-dose Cd increased lung Cd to levels comparable to humans, increased airway hyperresponsiveness and disrupted neuronal pathways regulating bronchial tone. Therefore, dietary Cd may promote or worsen airway hyperresponsiveness in multiple lung diseases including asthma.