Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most prominent potential marker of disease-related non-occupational exposure to mineral fibres is mesothelioma. Although many cases of mesothelioma have resulted from occupational exposure to asbestos, some have been associated with para-occupational domestic and/or neighbourhood exposure and have been reported in case series, case-control studies and a cohort study among non-occupationally exposed subjects. However, little information is available on mesothelioma as a direct consequence of general environmental asbestos exposure. Such cases of mesothelioma related to non-occupational exposure to asbestos as have occurred to date are likely to have resulted from past exposures much higher than those prevailing at the present time (in the developed countries); numbers will therefore probably decrease in the future. Very high rates of mesothelioma have been reported as a result of exposure to erionite. No studies are available on the effects of non-occupational exposure to man-made mineral fibres but, among occupationally exposed workers, a risk of mesothelioma is not apparent. There are suggestions of raised lung cancer rates among household contacts of asbestos workers and among individuals exposed to erionite. Non-malignant parenchymal and pleural abnormalities have been observed in subjects exposed non-occupationally to asbestos and erionite, but these are not necessarily associated with malignant lesions. Quantitative risk estimates of adverse effects on health have not been derived from these studies, essentially because of the absence of fibre exposure measurements.
 ...
PMID:Effects on health of non-occupational exposure to airborne mineral fibres. 266 17

The role of asbestos in the etiology of lung cancer and of mesothelioma of the pleura and peritoneum has been well documented. The evidence for a causal association between asbestos and other human cancers is not as extensive but suggests that asbestos may be carcinogenic at several different sites. This paper is concerned specifically with a possible causal association between asbestos and human kidney cancer. A review of the evidence to date indicates that only three human studies have sufficient statistical power to detect an excess mortality from kidney cancer among workers exposed to asbestos. All three were occupational cohort studies, and two of these gave strong direct evidence for such an excess; a study of U.S. insulators (kidney cancer SMR = 2.22, 90% CI 1.44-3.30), and a study of U.S. asbestos products company workers (kidney cancer SMR = 2.76, 90% CI 1.29-5.18). The third study, of Italian shipyard workers, reported excess mortality from "cancers of the kidney, urinary bladder, and other urinary organs" (SMR = 1.98, 90% CI 1.42-2.70). Further support for a causal association includes studies finding asbestos fibers in human kidneys and urine, as well as reports of kidney tumors in two animal bioassays. It is concluded that asbestos should be regarded as a probable cause of human kidney cancer.
 ...
PMID:Asbestos and kidney cancer: the evidence supports a causal association. 267 1

The mortality of workers from an Ontario factory manufacturing amosite asbestos insulation materials under poorly controlled environmental conditions is reported here. Seven (58%) of 12 deaths among exposed workers 10 or more years after first exposure were due to malignancies; four (25%) were from lung cancer, and there were two deaths from peritoneal mesothelioma. Those dying from mesothelioma were 47 and 49 years of age. Three (25%) of 12 deaths were from respiratory disease, two were attributed to asbestosis (in men 42 and 53 years of ages), and one to pneumonia in a 54-year-old male.
 ...
PMID:Mortality among employees of an Ontario factory manufacturing insulation materials from amosite asbestos. 272 89

Because very recent data on asbestos in the environment are available, some fairly firm conclusions can now be drawn regarding current exposure to asbestos fibres. If account is taken of occupational exposure data (where past exposure levels were very high indeed, leading to a very significant risk to workers at the time), it is possible to make some reasoned estimates of the risk from ambient air. In the past, there was considerable confusion regarding the degree of risk for both occupational and environmental conditions. In estimating the risk, account needs to be taken, in particular, of the fact that: (a) occupational exposures in the past were frequently higher than reported; (b) asbestosis (a disease only associated with very heavy occupational exposures) would seem to be mechanistically involved in the development of lung cancer associated with asbestos exposure; (c) chrysotile asbestos is now the commonest form of fibre used unlike in the past, when greater quantities of crocidolite and amosite were used, the latter types being much more closely associated with mesothelioma than chrysotile; (d) overall levels of asbestos in environmental ambient air are lower than they used to be; (e) ingested asbestos seems to be associated with a negligible degree of risk as indicated by animal and human studies. The estimated values of risk provided here are smaller than those published some years ago but are similar to those given in very recent key publications. The level of environmental lifetime risk from exposure to airborne asbestos would appear to be about 1 in 100,000 or even lower. Such a level of risk is exceedingly low, and bearing in mind the criteria of both WHO and the Royal Society of London, it would appear to represent an acceptable 'rare-event' extremely low-level risk, like the cancer risk from the cosmic radiation adsorbed when flying across the Atlantic or from eating charcoal broiled meat, or the risk of being killed by lightning.
 ...
PMID:Estimations of risk from environmental asbestos in perspective. 274 43

This paper describes mortality in a cohort of 324 men exposed to chrysotile asbestos and coal tar pitch used in the manufacture of electrical conduit pipe from a mixture of newsprint, bentonite, and asbestos. One death in a factory worker was attributed to pleural mesothelioma, and long-term employees experienced an increased risk of lung cancer (Standardized Mortality Ratio (SMR) 221; six deaths) and non-malignant respiratory disease (SMR 215; four deaths). In a case-control analysis, men whose jobs involved adding asbestos to the mix of raw materials were found to have a risk of lung cancer sevenfold higher (lower 95% confidence limit: 2.3) than men who had never worked at this job. Exposure to coal tar pitch is presumed to be responsible for the death of one worker from squamous cell carcinoma of the scrotum.
 ...
PMID:Mortality among employees of an Ontario factory that manufactured construction materials using chrysotile asbestos and coal tar pitch. 278 16

Although mesothelioma is generally considered to be caused by asbestos, epidemiologic studies indicate that some cases have another cause. In order to determine whether pulmonary asbestos burden can be used to define asbestos-related mesotheliomas, asbestos burden was quantified in 27 shipyard or construction workers with diffuse malignant mesothelioma of the pleura or peritoneum and a history of asbestos exposure. Their burden was significantly greater than the burden found in 19 unexposed men (P less than 0.001). The burdens were also compared to those of previously reported subjects with asbestosis or lung cancer. The median concentration for total amphibole fibers (2.7 million/g dry lung) in subjects with mesothelioma did not differ significantly from our previously reported median values for 14 subjects with asbestosis (1.3 million/g dry lung) or for 60 asbestos workers with lung cancer (1.3 million/g dry lung). Fiber size distribution for amosite, the most prevalent fiber type, was similar in all three subject groups. Fifteen of 25 (60%) subjects with mesothelioma had mild asbestosis. Asbestos body (AB) concentrations were greater than or equal to 1900/g dry lung, and total amphibole fiber concentrations were greater than or equal to 390,000/g dry lung. Counts of ABs greater than or equal to 0.5/cm2 in histologic sections always signified both of these concentrations in extracts. Thus, histologic sections showing greater than or equal to 0.5 ABs/cm2 or extracts containing asbestos body or amphibole fiber concentrations of at least 1900 or 390,000/g dry lung, respectively, will confirm an asbestos-related mesothelioma.
 ...
PMID:Lung asbestos burden in shipyard and construction workers with mesothelioma: comparison with burdens in subjects with asbestosis or lung cancer. 279 62

Sixteen patients with lung cancer or mesothelioma have been treated with escalating doses of carboplatin. Five patients (10 courses) were given 800 mg/m2, four patients (five courses) 1200 mg/m2 and seven patients (eight courses) 1600 mg/m2. Myelosuppression was the major toxicity encountered. The median duration of grade 4 neutropenia ranged from 1 day (800 mg/m2) to 11 days (1600 mg/m2) and the median duration of grade 4 thrombocytopenia ranged from 1 day (800 mg/m2) to 7 days (1600 mg/m2). The median fall in haemoglobin (Hb) ranged from 2.2 g/l (800 mg/m2) to 3.6 g/l (1600 mg/m2). Nephrotoxicity was encountered at all dosages and was in part, though not entirely, dose related. 2/9 patients receiving 800 mg/m2 and 4/6 of the patients receiving 1600 mg/m2 had a fall in glomerular filtration rate (GFR) greater than 25% but less than 50%. 800 mg/m2 of carboplatin was well tolerated, the performance status in 9/10 (90%) courses being 0-1 (ECOG scale). At 1600 mg/m2 in 6/8 (75%) courses the performance status was 2-4. There was one treatment-related death from neutropenia at this dose level. The severity of nausea and vomiting was not dose related but other toxicities including diarrhoea, alopecia, mild neuropathy and ototoxicity and possible CNS toxicity occurred at doses of 1200 mg/m2 and over. 5/7 patients with small cell lung cancer achieved a complete or partial response to treatment.
 ...
PMID:High dose carboplatin in the treatment of lung cancer and mesothelioma: a phase I dose escalation study. 282 9

Six new non-small-cell lung cancer (NSCLC) cell lines were established directly from human tissue or indirectly via nude mouse xenografts in serum-supplemented media with success rates of 8% and 13%, respectively. They comprised one adenocarcinoma (ADLC-5M2), two squamous cell carcinomas (EPLC-32M1, EPLC-65H), two large cell carcinomas (LCLC-97TM1, LCLC-103H), and one malignant biphasic mesothelioma (MSTO-211H). All cell lines grew adherent to culture vessels with population doubling times (PDT) of 16-40 h, formed colonies in soft agarose with efficiencies of 0.1%-5.1%, and all grew in athymic nude mice. Xenograft histologies appeared as follows: (a) undifferentiated carcinomas with feeble resemblance to the original tumors in the case of adenocarcinomas and squamous cell carcinomas; (b) large cell carcinoma with high resemblance to the original tumor; (c) an undifferentiated tumor with predominance of large epithelial cells and few fibrous cells in the case of mesothelioma. Human chorionic gonadotropin (HCG) was found by radioimmunoassay and high-affinity binding sites for epidermal growth factor (EGF) by radio-receptor assay in 4/4 cell lines. A very low activity of L-DOPA decarboxylase (DDC) was detectable only in the adenocarcinoma cell line. All cell lines overexpressed the c-myc protooncogene, and no gene rearrangement or amplification was observed. Chromosome analysis revealed modal chromosome numbers of 70-73 in ADLC-5M2, EPLC-32M1, EPLC-65H, and MSTO-211H. Cell lines derived from large cell carcinoma had modal values of 65 and 170 and a wider chromosome distribution than all other cell lines. A NSCLC specific chromosomal aberration has been undetectable until now. These cell lines may aid in elucidating the biology of NSCLC and its interrelationship to other lung tumors.
 ...
PMID:Characterization of the state of differentiation of six newly established human non-small-cell lung cancer cell lines. 284 Mar 15

A small cohort of 194 men with low exposure to fibrous tremolite (mean 0.75 f/ml y) in the mining and milling of vermiculite in South Carolina experienced 51 deaths 15 years or more from first employment. The SMR (all causes) was 1.17 reflecting excess deaths from circulatory disease. There were four deaths from lung cancer and 3.31 expected (SMR 1.21, 95% CI 0.33-3.09). Three of the four deaths were in the lowest exposure category (less than 1 f/ml y); no death was attributed to mesothelioma or pneumoconiosis. These findings contrast with those in Montana where the vermiculite ore was heavily contaminated with fibrous tremolite. A radiographic survey of 86 current and recent South Carolina employees found four with small parenchymal opacities (greater than or equal to 1/0) and seven with pleural thickening. These proportions were not higher than in a non-exposed group and much lower than had been observed in Montana. Examination of sputum from 76 current employees showed that only two specimens contained typical ferruginous bodies, confirming low cumulative fibre exposure. Any possible adverse effects of work with vermiculite, minimally contaminated with fibrous or non-fibrous tremolite, were thus beyond the limits of detection in this workforce.
 ...
PMID:Health of vermiculite miners exposed to trace amounts of fibrous tremolite. 284 33

A cohort of 820 men in a Paterson, New Jersey, amosite asbestos factory which began work during 1941-1945 was observed from 5 to 40 years after start of work. Most of the cohort had limited duration of work experience (days, weeks, months), though some men worked for several years until the factory closed in 1954. With white males of New Jersey as the control population, Standardized Mortality Ratios (SMRs) of 500 are evident for the cohort for lung cancer and for noninfectious pulmonary diseases (including asbestosis), while being almost 300 for total cancer and about 170 for all causes of death. A statistically significant SMR of almost 200 is seen for colon-rectum cancer. Mesothelioma incidence initially shows a strong relationship with advancing time since onset of exposure and then tails off. The main concern of the study is with dose-response patterns. Response is measured by the mortality for relevant causes of death, while the direct asbestos dosage was measured in two ways. One way was the length of time worked in the factory and the other was the individual's accumulated fiber exposure, calculated by multiplying the aforementioned length of time worked by the estimated fiber exposures associated with the particular job that the worker had in the factory. Whichever measure of dosage is used, it was found that, in general, the lower the dose, the longer it took for adverse mortality to become evident and, also, the smaller the magnitude of that adverse mortality.
 ...
PMID:Mortality experience of amosite asbestos factory workers: dose-response relationships 5 to 40 years after onset of short-term work exposure. 288 May 2


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>