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Noise-induced hearing loss (NIHL) is one of the major occupational disease that has influence on the quality of life of mining workers. Several reports suggest NIHL is attributed to noise exposure at workplace and approximately 16% of hearing loss is due to it. NIHL occurs as a result of exposure to high-level noise (>85 dB) in the workplace. Noise disrupts proteins present in the micromachinery of the ear that is required for mechano-electric transduction of sound waves. High-level noise exposure can lead to hearing impairment owing to mechanical and metabolic exhaustion in cochlea, the major organ responsible for resilience of sound. Several key proteins of cochlea include tectorial membrane, inner hair cells, outer hair cells, and stereocilia are damaged due to high-level noise exposure. Numerous studies conducted in animals have shown cochlear proteins involvement in NIHL, but the pertinent literature remains limited in humans. Detection of proteins and pathways perturbed within the micromachinery of the ear after excessive sound induction leads toward the early identification of hearing loss. The situation insisted to present this review as an update on cochlear proteins associated with NIHL after an extensive literature search using several electronic databases which help to understand the pathophysiology of NIHL.

Noise Induced Hearing Loss (NIHL) is caused by excessive noise exposure due to occupational activities thus affects communication and quality of life. Prolonged occupational and environmental exposure to loud noise damages key molecules present in the micro-machinery of the ear which are required for the mechano-electrical transduction of sound waves in cochlea. Specific proteins are known to be associated with hearing loss and related structural and functional disabilities in the human inner, outer hair cells and cochlea. Rationale of this study was to identify the cochlear proteins associated with the pathophysiology of NIHL using proteomic approaches in mining based industrial workers. Total (n = 210) samples were collected from mining based industrial workers of central India. Subjects were categorized based on audiometric analysis. Proteome changes of the host serum were investigated using one and two-dimensional electrophoresis in combination with LC-MS/MS and MALDI-TOF-MS. Up-regulated 46 cochlear proteins among confirmed NIHL cases were identified by MASCOT. Shrinkage discriminant analysis provided top 25 discriminating feature proteins namely myosin, transthyretin, SERPIN, CCDC50, enkurin, transferin etc. The identified potential proteins may be used as biomarkers for early detection and to understand the pathogenic mechanism of NIHL. Evaluation of these biomarkers in follow-up cases may further aid in improving NIHL diagnosis. Significance Human proteome study in Noise Induced Hearing Loss (NIHL) cases has not been published till date. This study represents most comprehensive proteomic analysis in NIHL cases taken from Indian mine workers. The identified key twenty-five discriminating feature proteins which are upregulated when an individual develops (or is in stage of development of) NIHL, provides insights into the potential roles of these varied proteins in disease progression. The proteins thus identified by proteomic approach may be used as early diagnostic biomarker to predict the occurrence of disease at very early stage.

Background: Manifestation of certain health morbidity in copper dust–exposed subjects impels us to obtain a cogent view regarding the implicate relationship of immunoglobulin on health risk assessment in them. We present here immunological profile of copper pit worker and office employees residing in the vicinity. Rationale of this study is to delineate the risk factors involved for copper toxicity. Materials and Methods: Copper mine workers (n = 87) were selected from a copper mine at Malanjkhand. Blood metal concentration and immunological profile such as IgG, IgM, IgA, and IgE were analyzed from these subjects. Data analysis was carried out using proper statistical tools. Results: Chronically copper dust–exposed miners (N = 71) and office employees (N = 47) exhibited significantly higher contents of copper (P < 0.0001) when compared with normal control. Serum IgG and IgA were found to be elevated significantly (P < 0.0001) in them when compared with both office employees and normal control. Contrarily, significant decrease in serum IgM was observed in both the groups when compared with normal control (P < 0.0001). Serum IgE was found to be elevated more significantly only in miner when compared with normal control. Copper exhibited significant positive Pearson's correlation coefficient with IgE, IgG, and IgA (r = 0.39; r = 0.28; r = 0.21) but negative correlation (r = −0.39) with IgM. Odds ratio analysis validated that elevated levels of IgE in miner and decrease in levels of IgM in both groups were truly affected by increase in copper levels from normal to abnormal. Conclusion: Miners are prone to morbidity such as type 2 diabetes and respiratory discomfort (asthma and hypersensitivity) since imbalance in both IgM and IgE is known to be associated with such morbidity. Immunopathy observed in chronically exposed miners could be attributed to copper toxicity in them.

Introduction: Age related hearing impairment (ARHI) is the most common sensory deficit in the elderly population and has become a severe social health problem. Several mechanisms have been described for hearing impairment in elderly people. Probable cause of hearing impairment may result from damage in the inner and outer hair cell, loss of stria vascularis, thickening of basilar membrane, or loss of sensory elements in the basal end of the cochlea. The aim of present study is to identify the protein biomarkers associated with ARHI using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Materials and Methods: Total 96 study subjects (48 experimental and 48 controls) were selected for this study. Serum samples were used for biochemical analysis and one-dimensional electrophoresis. Statistical analysis was done by GraphPad software. Results: Glucose, serum creatinine, and urea levels were in normal range and mean urea and creatinine levels are insignificantly associated with ARHI while mean glucose level is significantly associated with ARHI. Smoking/alcohol consumption did not show any significant association with ARHI. The molecular weight of the differentially expressed protein was 16.2 kDa as calculated by gel image analyzer software. The differentially expressed protein may be cochlin tomoprotein (CTP) of 16 kDa which is an isomer of cochlin protein. CTP contains all the known mutation sites associated with deafness. Conclusion: The expression of differentially expressed protein was consistently observed among experimental subjects as compared to control. This protein may help in the prediagnosis of ARHI due to added advantage of enhanced expression in subjects of ARHI. Results revealed males were more prone to ARHI than female.

Introduction: Bauxite ore is a major source of aluminum (Al) which contains approximately 35–60% Al by weight. Occupational and environmental bauxite dust exposure may cause toxicity by interaction with human biological systems resulting in oxidative stress (OS) and cell death. A neopterin derivative as an antioxidant is able to modulate cytotoxicity by the induction of OS. Materials and Methods: A total of 273 subjects were selected for blood collection from three different major Al producing bauxite mines and were categorized into three groups as experimental (Exp) (n = 150), experimental controls (ExC) (n = 73) and control (Con) (n = 50). Whole blood and serum samples were used for measurement of Al, neopterin, urea and creatinine values. Statistical analysis was performed using R-2.15.1 programming language. Results and Discussion: The result showed that age, body mass index and the behavioral habits, that is, smoking, tobacco and alcohol consumption have possible effects on neopterin level. Serum neopterin levels were found to be significantly higher (P

Silicosis is a chronic lung disease characterized by granulomatous and fibrotic lesions, which occurs due to accumulation of respirable silica mineral particles. Apoptosis is an important phenomenon of cell death in silicosis. The relationship between silica dust and its exposure is well established. But, the complex chain of cellular responses, which leads to caspase activation in silicosis, has not been fully discovered. Caspase activation plays a central role in the execution of apoptosis. Silica-induced apoptosis of the alveolar macrophages could potentially favor a proinflammatory state, occurring in the lungs of silicotic patients, resulting in the activation of caspase prior to induction of the intrinsic and extrinsic apoptosis pathways. Recent studies indicated that apoptosis may involve in pulmonary disorders. This review summarizes the current knowledge about the underling mechanism of biochemical pathways in caspase activation that have been ignored so far in silicosis. In addition, caspase could be a key apoptotic protein that can be used as an effective biomarker for the study of occupational diseases. It may provide an important link in understanding the molecular mechanisms of silica-induced lung pathogenesis.