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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The two-stage system introduced by the Veterans' Affairs Lung Study Group continues to be widely utilized in small-cell lung cancer (SCLC), mainly because of its simplicity and clinical utility. Approximately one third of patients with SCLC present with limited-stage disease, which is defined as disease that can be encompassed in a tolerable radiation field. However, this definition is controversial when it is applied to the staging classification of patients with locoregionally advanced disease manifested as the presence of an ipsilateral pleural effusion, contralateral supraclavicular lymphadenopathy, or contralateral mediastinal lymphadenopathy. The more descriptive TNM system is useful for patients with disease limited to the lung, when surgical resection may be feasible; this occurs in far less than 10% of cases. As shown by clinical studies and autopsy data, metastatic disease frequently involves the liver, adrenals, bone, bone marrow, and brain. History and physical examination, complete blood count and chemistry studies, chest x-ray studies, computed tomography of the chest or upper abdomen, computed tomographic scanning or magnetic resonance imaging of the brain, and bone scans are recommended for the pretreatment evaluation of patients with SCLC. A bone marrow biopsy may be omitted for patients with normal blood counts, normal lactate dehydrogenase level, and negative result on bone scan. The use of new imaging modalities, such as magnetic resonance imaging of the bone marrow and positron emission tomographic scanning, may optimize staging evaluation. Multiple prognostic parameters have been identified for patients with SCLC, the most important of which are the stage or extent of disease, performance status, serum lactate dehydrogenase level, and male gender. Identification of risk factors for treatment-related mortality is important for the management of patients with SCLC.
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PMID:Staging and clinical prognostic factors for small-cell lung cancer. 1169 3

Strategies for identifying patients at high risk of chemotherapy-induced neutropenia are reviewed. Among lung cancer patients, a 24% rate of neutropenia has been reported. This rate is below the 40% threshold recommended by the American Society of Clinical Oncology (ASCO) for the prophylactic use of colony-stimulating factors. Risk factors for febrile neutropenia in patients receiving adjuvant chemotherapy for breast cancer include older age, fluorouracil-containing regimens, bone marrow involvement or prior myelosuppressive therapy, and concomitant or prior radiation therapy. According to the Silber predictive model, factors suggesting a high risk of hospitalization for febrile neutropenia include the absolute neutrophil count during the neutrophil nadir in cycle 1 of chemotherapy. Patients with non-Hodgkin's lymphoma (NHL) are at risk of febrile neutropenia and fall on the edge of the ASCO guidelines. Risk factors in NHL patients include certain combination chemotherapy regimens, an albumin concentration of > 3.5 g/dL, an above-normal lactate dehydrogenase concentration, bone marrow involvement, age of > 65 years, and renal disease. Patients can be stratified into low-risk and high-risk categories for febrile neutropenia. High risk is associated with a duration of neutropenia of more than seven days and concomitant medical conditions, such as hypotension and diarrhea. A majority of low-risk patients can be managed as outpatients. Prophylactic use of colony-stimulating factors is currently believed not to be cost-effective if the frequency of febrile neutropenia is less than about 20% for a given treatment regimen. Patients at higher risk of febrile neutropenia in association with cancer chemotherapy may include the elderly and those with specific malignancies and prior neutropenic events, as well as those receiving combination chemotherapy and radiation therapy.
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PMID:Identification of cancer patients at high risk of febrile neutropenia. 1216 33

Proinflammatory cytokines Interleukin-1 beta (IL-1 beta) and Interleukin-6 (IL-6) play a significant role in the pathogenetic processes related to various malignant and inflammatory conditions. Leukocytosis, thrombocytosis and increased acute phase protein levels are part of a systemic inflammatory response. In this study, we measured the concentrations of IL-1 beta, IL-6 and ferritin as well as hemoglobin, lactate dehydrogenase (LDH), C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) in 23 patients (male 15, female 8, median age 68 years) with lung cancer and reactive thrombocytosis (LCRT), in 27 (male 18, female 9, median age 64 years) with benign inflammatory lung disorder (BILD) and 18 (male 10, female 8, median age 62 years) lung cancer patients with a normal platelet count (LCNP). IL-1 beta levels were significantly higher in the three patient groups in comparison with control subjects (P < 0.001) but without significant difference among the three patient groups. IL-6 was higher in all three patients groups but only in the BILD group it was significantly higher than the control group (P < 0.05). However, no significant difference in IL-6 serum levels was found between the two lung cancer groups. CRP and LDH were significantly higher in the LCRT group in comparison with the other two patient groups (P < 0.01 and 0.001, respectively), while ferritin was higher in both lung cancer groups in comparison with the BILD group (P < 0.001). Our data suggest that in lung cancer patients, reactive thrombocytosis is part of the systemic inflammatory reaction for which IL-1 beta and IL-6 may be intermediate but not independent mediators.
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PMID:Serum proinflammatory cytokines and its relationship to clinical parameters in lung cancer patients with reactive thrombocytosis. 1219 34

The objective of this study was to evaluate the clinical value of an elevated platelet count and other routine laboratory tests for predicting malignancy in patients with radiologically suspected lung cancer. Platelet count, haemoglobin, total leukocyte count, erythrocyte sedimentation rate (ESR) and serum lactate dehydrogenase (LDH) were analysed in 126 prospectively admitted patients with suspected lung cancer. The patients were divided by pathologic diagnosis into those with benign disorders (n=65) and with malignancies (n=61). Patients with lung cancer were staged (TNM) and the tumours were classified according to histological types (WHO). Thrombocytosis (platelet count >400x10(9)/l) was present in 8% (5/65) of patients with benign disease and in 57% (35/61) of patients with malignant disease (p<0.00001). The prevalence of thrombocytosis in patients with primary lung cancer was 53% (27/51). Elevated platelet count was more common in advanced disease (stage III and IV). No difference was observed between histological types. The sensitivity of thrombocytosis for predicting malignancy was 0.57 and the specificity 0.92. When elevated platelet counts, LDH and ESR were combined, a sensitivity of 0.71 and a specificity of 1.00 was achieved. The positive and negative predictive values were 1.00 and 0.89, respectively. Elevated platelet count is frequently observed in patients with lung cancer. When test results of platelet count and other routine blood analyses are combined, a high sensitivity and specificity for predicting malignancy can be achieved. These tests are clinically useful in the evaluation of patients with radiologically suspected lung cancer.
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PMID:Diagnostic significance of platelet count and other blood analyses in patients with lung cancer. 1246 71

Talc ore may contain several other minerals including calcite, dolomite, magnesite, tremolite, anthophyllite, antigorite, quartz, pyrophyllite, micas, or chlorites. Talc products are sold in a multitude of grades which have physical or functional characteristics especially suited for particular applications, so occupational and consumer exposures to talc are complex. Epidemiology studies have suggested an association between non-fibrous talc and lung cancer risk. Talc was nominated by the National Institute of Occupational Safety and Health (NIOSH) for study by the NTP because of widespread human exposure and because of the lack of adequate information on its chronic toxicity and potential carcinogenicity. Toxicology and carcinogenicity studies of talc (non-asbestiform, cosmetic grade), a finely powdered hydrous magnesium silicate, were conducted by exposing groups of F344/N rats to aerosols for 6 hours per day, 5 days per week for up to 113 weeks (males) or 122 weeks (females). Groups of B6C3F1 mice were exposed similarly for up to 104 weeks. LIFETIME STUDY IN RATS: Groups of 49 or 50 male and 50 female rats were exposed to aerosols of 0, 6, or 18 mg/m(3) talc until mortality in any exposure group reached 80% (113 weeks for males and 122 weeks for females). These exposures were selected based on 4-week inhalation studies of the terminal lung talc burden in F344/N rats; concentrations greater than 18 mg/m(3) were expected to overwhelm lung clearance mechanisms and impair lung function. These exposure concentrations provided a dose equivalent of 0, 2.8, or 8.4 mg/kg per day for male rats and 0, 3.2, or 9.6 mg/kg per day for female rats. In a special study, additional groups of 22 male and 22 female rats were similarly exposed and examined for interim pathology evaluations or pulmonary function tests after 6, 11, 18, and 24 months and lung biochemistry and cytology studies after 24 months. The talc aerosols had a median mass aerodynamic diameter of 2.7 mm in the 6 mg/m(3) chamber and a median diameter of 3.2 mm in the 18 mg/m(3) chamber, with geometric standard deviations of 1.9 mm. However, there was a 7-week period beginning at study week 11 during which the chamber concentration for the 18 mg/m(3) rats varied from approximately 30 to 40 mg/m(3) because of difficulties with the aerosol concentration monitoring system. Further, there was a 12-week period beginning at approximately week 70 during which there were difficulties in generating the talc aerosol, and the chamber concentrations for rats and mice were substantially lower than the target concentrations. Survival, Body Weights, and Clinical Findings: The survival of male and female rats exposed to talc was similar to that of the controls. Mean body weights of rats exposed to 18 mg/m(3) were slightly lower than those of controls after week 65. No clinical findings were attributed to talc exposure. Pathology Findings: Absolute and relative lung weights of male rats exposed to 18 mg/m(3) were significantly greater than those of controls at the 6-, 11-, and 18-month interim evaluations and at the end of the lifetime study, while those of female rats exposed to 18 mg/m(3) were significantly greater at the 11-, 18-, and 24-month interim evaluations and at the end of the lifetime study. Inhalation exposure of rats to talc produced a spectrum of inflammatory, reparative, and proliferative processes in the lungs. Granulomatous inflammation occurred in nearly all exposed rats and the severity increased with exposure duration and concentration. Hyperplasia of the alveolar epithelium and interstitial fibrosis occurred in or near foci of inflammation in many exposed rats, while squamous metaplasia of the alveolar epithelium and squamous cysts were also occasionally seen. Accumulations of macrophages (histiocytes), most containing talc particles, were found in the peribronchial lymphoid tissue of the lung and in the bronchial and mediastinal Iymph nodes. In female rats, the incidences of alveolar/bronchiolar adenoma, carcinoma, and adenoma or carcinoma (combined) in the 18 mg/m(8 mg/m(3) group were significantly greater than those of controls. The incidences of pulmonary neoplasms in exposed male rats were similar to those in controls. Minor alterations attributed to talc exposure were also observed in the upper respiratory tract. Hyperplasia of the respiratory epithelium of the nasal mucosa in males and accumulation of cytoplasmic, eosinophilic droplets in the nasal mucosal epithelium in male and female rats occurred with a concentration-related increased incidence in the exposed groups. Adrenal medulla pheochromocytomas [benign, malignant, or complex (combined)] occurred with a significant positive trend in male and female rats, and the incidences in the 18 mg/m(3) groups were significantly greater than those of controls. Although adrenal medulla hyperplasia occurred with similar frequency among exposed and control females, the incidences of hyperplasia in exposed males were significantly lower than in controls. Lung Talc Burden: Lung talc burdens of male and female rats exposed to 6 mg/m(3) were similar and increased progressively from 6 to 24 months. Lung talc burdens of females exposed to 18 mg/m(3) also increased progressively from 6 to 24 months, while those of males exposed to 18 mg/m(3) remained about the same after 18 months. Lung burdens were generally proportional to exposure concentration at each interim evaluation. Pulmonary Function, Bronchoalveolar Lavage, and Lung Biochemistry: In exposed male and female rats there was a concentration-related impairment of respiratory function which increased in severity with increasing exposure duration. The impairment was characterized by reductions in lung volume (total lung capacity, vital capacity, and forced vital capacity), lung compliance, gas exchange efficiency (carbon monoxide diffusing capacity), and nonuniform intrapulmonary gas distribution. After 24 months, males exposed to 6 mg/m(3) talc had a significant increase in beta-glucuronidase and polymorphonuclear leukocytes; males exposed 18 mg/m(3) had significant increases in b -glucuronidase, lactate dehydrogenase, alkaline phosphatase, and total protein in bronchoalveolar lavage fluid. All exposed females had significantly increased a-glucuronidase, lactate dehydrogenase, alkaline phosphatase, total protein, and polymorphonuclear leukocytes; 18 mg/m(3) females also had significantly increased glutathione reductase. Viability and phagocytic activity of macrophages recovered from lavage fluid were not affected by talc exposure. Total lung collagen was significantly increased in rats at both exposure concentrations after 24 months, while collagenous peptides in lavage fluid and the percentages of newly synthesized protein from females, but not males, were also significantly increased at the 6 or 18 mg/m(3) levels. In addition, lung proteinase activity, primarily cathepsin D-like activity, was significantly greater in exposed males and females. Rats exposed to talc also had significant increases in collagenous peptides and acid proteinase in lung homogenates. 2-YEAR STUDY IN MICE: Groups of 47 to 49 male and 48 to 50 female mice were exposed to aerosols containing 0, 6, or 18 mg/m(3) talc for up to 104 weeks. These exposures were selected based on 4-week inhalation studies of the terminal lung talc burden in B6C3F1 mice; concentrations greater than 18 mg/m(3) were expected to overwhelm lung clearance mechanisms and impair lung function. These exposure concentrations provide a dose equivalent of 0, 2, or 6 mg/kg per day for male mice and 0, 1.3, or 3.9 mg/kg per day for female mice. In a special study, additional groups of 39 or 40 male and 39 or 40 female mice similarly exposed were examined for interim pathology evaluations, lung biochemistry, and cytology studies after 6, 12, and 18 months of exposure. The talc aerosols had a median mass aerodynamic diameter of 3.3 mm with a geometric standard deviation of 1.9 mm in the 6 mg/m(3) chamber, and a median diameter of 3.6 mm with a geometric standard deviation of 2.0 mm in the 18 mg/m(3) chamber. Further, there was a 12-week period beginning at approximately week 70 during which there were difficulties in generating the talc aerosol, and the chamber concentrations for rats and mice were substantially lower than the target concentrations. Survival, Body Weights, and Clinical Findings: Survival and final mean body weights of male and female mice exposed to talc were similar to those of the controls. There were no clinical findings attributed to talc exposure. Pathology Findings: Inhalation exposure of mice to talc was associated with chronic active inflammation and the accumulation of macrophages in the lung. In contrast to rats, hyperplasia of the alveolar epithelium, squamous metaplasia, or interstitial fibrosis were not associated with the inflammatory response in mice, and the incidences of pulmonary neoplasms in exposed and control groups of mice were similar. Accumulations of macrophages (histiocytes) containing talc particles were also present in the bronchial Iymph node. In the upper respiratory tract, cytoplasmic alteration, consisting of the accumulation of cytoplasmic eosinophilic droplets in the nasal mucosal epithelium, occurred with a concentration-related increased incidence in exposed male and female mice. Lung Talc Burden: Lung talc burdens of mice exposed to 6 mg/m(3) were similar between males and females and increased progressively from 6 to 24 months, except for males at 18 months. The lung talc burdens of mice exposed to 18 mg/m(3) were also similar between the sexes at each interim evaluation. Although the talc burdens of males and females increased substantially from 6 to 24 months, the values at 12 and 18 months were similar. Generally, lung burdens of mice exposed to 18 mg/m(3) were disproportionately greater than those of mice exposed to 6 mg/m(3), suggesting that clearance of talc from the lung was impaired, or impaired to a greater extent, in mice exposed to 18 mg/m(3) than in mice exposed to 6 mg/m(3). Bronchoalveolar Lavage and Lung Biochemistry: Increases in total protein, beta-glucuronidase, lactate dehydrogenase, glutathione reductase, total nucleated cells, and polymorphonuclear leukocytes in bronchoalveolar lavage fluid were observed primarily in mice exposed to 18 mg/m(3), although some parameters were also increased in mice exposed to 6 mg/m(3). The amount of collagenous peptides in lavage fluid and total lung collagen were increased in male and female mice exposed to 18 mg/m(3). Acid proteinase activity, principally cathepsin D-like activity, of lung homogenate supernatant fluid was also significantly increased in mice at the 18 mg/m(3) exposure concentration. CONCLUSIONS: Under the conditions of these inhalation studies, there was some evidence of carcinogenic activity of talc in male F344/N rats based on an increased incidence of benign or malignant pheochromocytomas of the adrenal gland. There was clear evidence of carcinogenic activity of talc in female F344/N rats based on increased incidences of alveolar/bronchiolar adenomas and carcinomas of the lung and benign or malignant pheochromocytomas of the adrenal gland. There was no evidence of carcinogenic activity of talc in male or female B6C3F1 mice exposed to 6 or 18 mg/m(3). The principal toxic lesions associated with inhalation exposure to the same concentrations of talc in rats included chronic granulomatous inflammation, alveolar epithelial hyperplasia, squamous metaplasia and squamous cysts, and interstitial fibrosis of the lung. These lesions were accompanied by impaired pulmonary function characterized primarily by reduced lung volumes, reduced dynamic and/or quasistatic lung compliance, reduced gas exchange efficiency, and nonuniform intrapulmonary gas distribution. In mice, inhalation exposure to talc produced chronic inflammation of the lung with the accumulation of alveolar macrophages. Synonyms: talcum; agalite; emtal 596; non-asbestiform talc; non-fibrous talc; steatite; hydrous magnesium silicate
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PMID:NTP Toxicology and Carcinogenesis Studies of Talc (CAS No. 14807-96-6)(Non-Asbestiform) in F344/N Rats and B6C3F1 Mice (Inhalation Studies). 1261 90

Syndecan-1 is a multifunctional transmembrane heparan sulphate proteoglycan (HSPG) that is present on a variety of cell types. The extracellular syndecan domains can be shed from the cell surface in a highly regulated process called ectodomain shedding. We studied the influence of soluble syndecan-1 on outcome in 88 small cell lung cancer (SCLC) patients treated within the context of two randomised clinical trials with platinum-based therapy. Serum syndecan-1 concentrations were determined using enzyme-linked immunosorbent assay (ELISA) from sera taken prior to initiation of chemotherapy. Patients with the serum syndecan-1 level within the highest tertile (>212 microg/l) had only 38% 1-year and 3% 2-year survival, whereas 58% of those with a lower serum level survived for 1 year and 25% for 2 years following the diagnosis (P=0.0034). A high serum syndecan-1 level (>212 microg/l) was associated with a high pretreatment lactate dehydrogenase (LDH) level (P=0.0024) and a poor Karnofsky's performance status (P=0.021), but not with the clinical stage or the presence of distant metastases at diagnosis. A high serum syndecan-1 level had independent influence on survival also in a multivariate analysis (the relative risk, RR, 1.68; 95% CI, 1.02-2.77; P=0.044) together with the clinical stage (RR, 1.72; 95% CI, 1.05-2.82; P=0.032). We conclude that high pretreatment serum syndecan-1 level is associated with poor prognosis in SCLC treated with platinum-based chemotherapy.
Lung Cancer 2003 Aug
PMID:Pretreatment serum syndecan-1 levels and outcome in small cell lung cancer patients treated with platinum-based chemotherapy. 1287 80

Inhalation of hard metal dust (WC-Co particles) has been associated with an increased risk for lung cancer in occupational settings. In vitro, WC-Co was genotoxic in human lymphocytes producing DNA strand breaks and micronuclei. The aim of the present study was to evaluate the in vivo genotoxic effects of WC-Co dust in rat type II pneumocytes. DNA breaks/alkali-labile sites (alkaline comet assay) and chromosome/genome mutations (micronucleus test) were assessed after a single intra-tracheal (i.t.) instillation of WC-Co, including dose-effect and time trend relationships. In addition, the alkaline comet assay was performed on cells obtained after broncho-alveolar lavage (BAL) and on peripheral blood mononucleated cells (PBMC). As pulmonary toxicity parameters, protein content, lactate dehydrogenase activity, total and differential cell count in BAL fluid were evaluated in parallel. In type II pneumocytes, WC-Co induced a statistically significant increase in tail DNA (12 h time point) and in micronuclei (72 h) after a single treatment with 16.6 mg WC-Co/kg body wt, a dose that produced mild pulmonary toxicity. This observation provides the first evidence of the in vivo mutagenic potential of hard metal dust. In PBMC, no increase in DNA damage or micronuclei was observed. This study indicates the potential to detect chromosome/genome mutations (micronuclei) in relevant target cells (type II pneumocytes) after i.t. instillation of a particle mixture.
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PMID:In vivo genotoxicity of hard metal dust: induction of micronuclei in rat type II epithelial lung cells. 1294 52

The aim of this phase II trial was to assess the efficacy and tolerability of docetaxel/vinorelbine as second-line therapy. Thirty-two patients with a performance status (PS) of <or= 2 (5 with locally advanced and 27 with metastatic non-small-cell lung cancer [NSCLC]) who were previously treated with platinum-based chemotherapy, were recruited. Docetaxel 75 mg/m2 on day 1 and vinorelbine 20 mg/m2 on days 1 and 5 were administered every 3 weeks with dexamethasone premedication but without prophylactic granulocyte colony-stimulating factor and antibiotics. The overall response rate (intent-to-treat analysis) was 9.5%, including 3 patients with a partial response, 15 (47%) with stable disease, and 9 (28%) with progressive disease. Myelosupression was the limiting toxicity, with 8 episodes of febrile neutropenia and 3 deaths due to sepsis. Median overall survival and progression-free survival were 25 weeks and 13 weeks, respectively. Patients with a PS of 2 (P < 0.02) and elevated lactate dehydrogenase (P < 0.01) had a worse prognosis. Histology of adenocarcinoma appeared to positively influence survival (P = 0.09). Our study confirms that the docetaxel/vinorelbine schedule has activity in NSCLC patients pretreated with platinum-based therapies.
Clin Lung Cancer 2002 Nov
PMID:Phase II study of docetaxel/vinorelbine in patients with non-small-cell-lung cancer previously treated with platinum-based chemotherapy. 1470 66

To determine the usefulness of serum KL-6 levels for predicting the occurrence of radiation pneumonitis (RP) after the application of single high-dose stereotactic radiation therapy for lung tumors, the serum KL-6 levels were measured in 16 patients before irradiation and every 1 or 2 months thereafter. Three of the 16 patients experienced RP of grade 3 severity according to the European Organization for Research and Treatment of Cancer/Radiation Therapy Oncology Group toxicity criteria. RP occurred 3 months after the completion of radiation therapy in two patients, and 4 months after completion in one patient. RP occurred at significantly increased frequencies in patients with primary lung cancer (p = 0.01) and adenocarcinoma (p = 0.01), and in those undergoing the concurrent irinotecan therapy (p = 0.02). In all 16 patients, the lactate dehydrogenase level remained normal during the follow-up period. In all three of the patients with RP, KL-6 levels increased by > 1.5-fold compared to the pretreatment value and over the cutoff level of 500 IU. The ratio of the increase in serum KL-6 values 2 months after the patient had undergone irradiation showed a significant correlation with the occurrence of RP (p = 0.04). In conclusion, KL-6 is a useful marker for prediction of the occurrence of RP after single, fractional, high-dose stereotactic irradiation of lung tumors.
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PMID:Serum levels of KL-6 for predicting the occurrence of radiation pneumonitis after stereotactic radiotherapy for lung tumors. 1471 65

Epidemiological research has demonstrated the relationship between exposure to quartz dust and an elevated risk of pneumoconiosis and possible elevated risk of cancer. The current study was designed to evaluate the biological responses of workplace particles containing crystalline silica using an in vitro cell test. Respirable particle samples were sampled from four tin mines, where the standardized mortality ratio (SMR) for pneumoconiosis was 51.6 and SMR for lung cancer was 2.2 in dust-exposed miners. Alveolar macrophages (AM) are considered as the target cells for primary dust effects. The samples were then measured at 15, 30, 60 and 120 microg particle per 10(6) AM for cytoxicity with the release of glucuronidase, lactate dehydrogenase, for reactive oxygen damage with H(2)O(2) release, and for ability to induce fibrosis using the secretion of tumor necrosis factor-alpha (TNF-alpha). Pure quartz (DQ12) and corundum were used as controls. The results showed the samples from tin mines caused a higher cytoxicity when compared to corundum, yet lower when compared to quartz. However, reactive oxygen species release (148-177 nmol/3 x 10(5) AM in high concentration of 120 microg/10(6) AM) induced by the samples were significantly higher than that induced by quartz (57 nmol/3 x 10(5) AM) and corundum (62 nmol/3 x 10(5) AM). Furthermore, particle samples induced higher TNF-alpha secretion than corundum, the samples from Limu tin mine induced much higher TNF-alpha levels than that induced by DQ12 quartz. The results from the in vitro tests help elucidate the degree of hazard of dust particles in tin mines. The in vitro reaction patterns of AM also constitute a powerful tool to monitor biological and pathogenic responses of humans following dust particle exposure.
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PMID:Biological responses of workplace particles and their association with adverse health effects on miners. 1556 45


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