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

The Formaldehyde Institute (FI) sponsored additional Poisson regression analysis of lung cancer mortality data from the joint National Cancer Institute (NCI)/FI cohort study of workers exposed to formaldehyde to investigate the previously reported effects of plant and latency period and to assess the impact of short-term workers (under 1 yr employment) on the results. There were 242 lung cancer deaths in this cohort of 20,067 white male workers. With OCMAP software, lung cancer death rates for the white males in this cohort were computed by plant, age, calendar time, and job type for several time-dependent formaldehyde exposures, including formaldehyde exposure in the presence of 12 selected co-exposures: ammonia (AM), antioxidants (AN), asbestos (AS), carbon black (CB), dyes/inks/pigments (DY), hexamethylenetetramine (HX), melamine (ME), particulates (PT), phenol (PH), plasticizers (PL), urea/urea compounds (UR), wood dust (WD), and a composite co-exposure (X5) involving AN, HX, ME, PH, and UR.A 1.6-fold increase in lung cancer risk was found, beginning approximately 16-20 yr after first employment in the study plants with no evidence of a differential effect of latency between hourly and salaried workers or among the various categories of formaldehyde exposure as measured by cumulative average intensity or length of exposure. The statistically significant heterogeneity in lung cancer risk among the 10 plants could not be explained by interplant differences in cumulative or average intensity of exposure to formaldehyde, either without regard to co-exposures or in the presence of any of the 12 co-exposures considered individually. Plant was not a statistically significant predictor of lung cancer risk when cumulative exposure to the composite X5 was included in the model, suggesting that some component of X5, or a correlate, could at least partly account for the overall heterogeneity. No significant associations were found for cumulative, average, or length of exposure to formaldehyde without regard to co-exposure, but positive associations were found for cumulative exposure to formaldehyde in the presence of several co-exposures (AN, HX, ME, PH, and UR). For workers who were never exposed to any of 10 co-exposures associated with an increased lung cancer risk, there was a decreasing pattern of estimated lung cancer risk ratios relative to cumulative formaldehyde exposure. Similar patterns were seen when the analysis was restricted to the long-term workers. Analysis of the internal cohort rates corroborates previous analyses of NCI/FI cohort data in that significant positive associations were found between the risk of lung cancer and cumulative exposure to formaldehyde in the presence of several of the same co-exposures. No such associations were found in the absence of these co-exposures.
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PMID:Lung cancer mortality among industrial workers exposed to formaldehyde: a Poisson regression analysis of the National Cancer Institute Study. 144 59

We conducted a follow-up study to evaluate mortality among 14,861 workers employed in five facilities producing or using phenol and formaldehyde. More than 360,000 person-years of follow-up accrued. Mortality rates from all causes of death combined were similar to those in the general U.S. population. We observed excesses of cancer of the esophagus, cancer of the kidney, and Hodgkin's disease among workers exposed to phenol, but none of these excesses showed a dose-response relation with exposure to phenol. Excess lung cancer mortality (SMR = 1.2) showed no consistent pattern by any exposure index. Workers exposed to phenol had lower mortality ratios for cancer of the buccal cavity and pharynx, cancer of the stomach, cancer of the brain, arteriosclerotic heart disease, emphysema, disease of the digestive system, and cirrhosis of the liver. Of these, arteriosclerotic heart disease, emphysema, and cirrhosis of the liver were inversely related to duration of phenol exposure and to cumulative phenol exposure levels. Although these inverse associations may be due to chance or uncontrolled confounders, the ability of phenol to interfere with the generation of oxidants in experimental systems suggests that the pattern may have biologic plausibility.
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PMID:Mortality among industrial workers exposed to phenol. 205

Although much of the evidence in environmental lung disease remains equivocal, some environmental exposures are known to be clinically relevant. Ambient air pollution remains of concern as a source of morbidity, particularly for susceptible populations such as persons with asthma, chronic obstructive pulmonary disease, or cardiac disease and the elderly. The adverse effects of several components of indoor air pollution have been established. Environmental tobacco smoke contributes to lower-respiratory illness in infants; office workers exposed to thermophilic actinomycetes contaminating ventilation systems have developed hypersensitivity pneumonitis; and in the home, components of house dust and fungus spores may provoke asthma via immediate hypersensitivity. The evidence is less compelling for a link between other exposures and disorders of the respiratory tract. For example, formaldehyde may be responsible for provoking vague respiratory symptoms and even nasal cancers; however, the associations are unproved. Likewise, the relation between low-level exposure to asbestos and the development of lung cancer, although a concern, is not conclusively established. The clinician should be aware of practical measures for patients who inquire about air cleaning. Often, relatively simple solutions are effective. A knowledge of sources and exposures as well as an understanding of the principles of inhalation lung injury should prove useful in directing patient care.
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PMID:Environmentally mediated disorders of the respiratory tract. 218 Dec 9

Epidemiological studies-especially data from smog episodes-indicate that antropogenous outdoor air pollution exercises a deleterious effect on health and particularly on the respiratory organs. Controlled exposure test in animals and man confirm this. The main pollutants are SO2, suspended dust particles (dust aerosols or solid atmospheric condensation nuclei) as well as NO2 (NOx) and O3. The adverse influence of quite a number of meteorological factors such as low temperature and inversion cannot be denied. During smog conditions in January 1985 in the Federal Republic of Germany there was a highly significant negative correlation between atmospheric temperature and the rate of exacerbations of bronchitis. Indoor air pollution is gaining in importance. Airtight sealing of buildings associated with reduced indoor ventilation results in novel health upsets ("sick building syndrome"). Interiors are characterised by an accumulation of CO2, CO, NO2, dust aerosols and various organic substances such as benzene, benzypyrene, formaldehyde, nitrosamines etc. Cigarette smoke is a frequent cause of indoor air pollution. The possible unhealthy effects of passive smoking (mainly the inhalation of sidestream smoke) have been frequently studied. Infants of smoking parents are more often affected by respiratory diseases than non-exposed children. The same applies to schoolchildren: the incidence of bronchial signs and symptoms increases with increasing smoke consumptions of the parents. However, no definitely established effect on lung function has been seen in children, adults and asthmatics. The important question as to whether passive smoking increases lung cancer risk is still a subject of controversial discussion among experts.
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PMID:[General environmental pollutants and passive smoking]. 219 21

Human health risk assessment has been the object of systematic study in recent years, with formal models of risk assessment and risk management having been proposed by several national and international health agencies. The particular model developed by the Environmental Health Directorate of Health and Welfare Canada was examined in some detail and used to focus on the role of epidemiology in the overall process of risk assessment. In addition to providing information fundamental to the identification of environmental carcinogens and the estimation of carcinogenic risks, epidemiology may also play a role in shaping risk perception and in improving risk communication practices. Taken collectively, epidemiologic data on health risks provide a basis for improved disease surveillance and prioritization of public health concerns. Both descriptive and analytic epidemiologic protocols may be used to gather information on disease etiology. Because of the potential for bias and confounding in observational studies of human populations, epidemiological data should be subjected to careful evaluation in accordance with established criteria before a causal relationship between exposure and disease is inferred. Toxicological studies using nonhuman test systems may be used to avoid these problems, but at the expense of obtaining indirect information on human health risks. Nonetheless, toxicological data provide an important complement to epidemiological data, providing information on potential health risks in advance of human exposure and offering a means of indirectly assessing risks in situations where human studies fail to provide informative results. The complementary roles of epidemiology and toxicology in health risk assessment were examined using four case studies. While the epidemiological evidence linking tobacco consumption to lung cancer is now unequivocal, the corresponding data on involuntary smoking, although strongly suggestive of increasing the relative risk of lung cancer, requires further confirmation before providing the same degree of evidence as now exists for active smoking. At present, the best estimates suggest that overall mortality attributable to active smoking may exceed that due to passive smoking by roughly 100-fold. Despite this large difference in health impact, passive smoking continues to be the focus of much public concern, in part because of the involuntary nature of the risk involved. Because of the abundance of good epidemiological data on tobacco, toxicology has assumed a secondary role in defining the health risks associated with smoking. In contrast, while epidemiological studies with saccharin and formaldehyde have provided unequivocal evidence of carcinogenic effects in animals exposed to high doses, thereby raising concerns over potential human carcinogenicity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of epidemiology in health risk assessment. 223 69

Over 30 epidemiologic studies have evaluated cancer risks associated with formaldehyde exposure. Excesses were reported for several sites, leukemia and cancers of the nasal cavities, nasopharynx, lung, and brain generating the greatest interest. The excesses of leukemia and brain and colon cancer found among professionals may not be related to formaldehyde exposure, since similar excesses were not observed among industrial workers. Inconsistencies among and within studies impede assigning formaldehyde a convincing causal role for the excesses of lung cancer found among industrial workers. A causal role for formaldehyde is the most probable for cancers of the nasopharynx and, to a less extent, the nasal cavities. Evidence of exposure-response relationships, the fact that direct contact with formaldehyde may occur at these upper respiratory sites, and the consistency of these findings with experimental studies make this assumption highly probable.
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PMID:Epidemiologic evidence on the relationship between formaldehyde exposure and cancer. 228 88

Respiratory cancer was examined in relation to occupational formaldehyde exposure in a case-referent study (136 cases, 408 referents) nested in a woodworker cohort. Plant- and time-specific job-exposure matrices were constructed for formaldehyde exposure. Over 3 ppm-months of formaldehyde exposure was associated with an odds ratio of 1.4 [90% confidence interval (90% CI) 0.5-4.1]. The odds ratios for lung cancer were near unity, the excess risk concentrating on the upper respiratory tract. That for combined exposure to formaldehyde-phenol exposure (all respiratory cancers) was 1.6 (90% CI 0.6-4.4) but 1.0 for formaldehyde only. No consistent exposure-response patterns emerged for the level, duration, or cumulative exposure. The results are hardly more than debatable support for the hypothesis concerning formaldehyde as a carcinogen in humans, the possible risk seemingly concentrating on the upper respiratory tract rather than the lung.
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PMID:Formaldehyde exposure and respiratory cancer among woodworkers--an update. 228 89

A historical cohort of 26,561 workers employed in ten facilities was assembled to evaluate cancer risks associated with exposure to formaldehyde. Historical exposures to formaldehyde by job, work area, plant, and calendar time were estimated using monitoring data available from participating plants, comments from long-term workers and company officials, exposure evaluations from walk-through surveys conducted by project industrial hygienists, and results from monitoring specifically performed for this project. A previous report of findings from this study noted a 30% excess mortality from lung cancer among wage workers. The relative risk for lung cancer (whether estimated by SMRs or SRRs) 20 or more years after first exposure did not generally rise with increasing exposure to formaldehyde. Various estimates of exposure were investigated including duration, intensity, peak, cumulative, and average, and by exposures lagged by 5, 10, 20, and 30 years. The excess did not appear to arise gradually, but emerged suddenly among workers whose total cumulative exposure was less than 0.1 ppm-years. Slightly positive, but nonsignificant, exposure-response associations between lung cancer and level of formaldehyde occurred in only a few out of a large number of comparisons (e.g., for persons hired before the start dates for the study and for workers also exposed to particulates). There was a lack of consistency among the various plants for risk of lung cancer, with six plants having elevated SMRs and four plants having deficits. Mortality from lung cancer was more strongly associated with exposure to other substances including phenol, melamine, urea, and wood dust than with exposure to formaldehyde. Workers exposed to formaldehyde without exposure to these substances did not experience an elevated mortality from lung cancer. The risk did not increase with cumulative levels of formaldehyde among those exposed to other substances and there was a slightly negative trend for those exposed to formaldehyde alone. Although some role for formaldehyde, particularly in association with other substances, in the excess of lung cancer seen among these workers cannot be ruled out, these findings suggest that exposure to phenol, melamine, urea, wood dust or other exposures also occurring in the area where these substances were used (i.e., production of resin and molding compounds) may play a more primary role. This association should be further evaluated in other studies that include workers from resin and molding compound operations.
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PMID:Mortality from lung cancer among workers employed in formaldehyde industries. 234 74

The expression of vimentin in pulmonary carcinomas was studied in 285 cases of surgically resected lung cancer from our hospital files. Formalin fixed, paraffin-embedded sections were studied by immunoreactive staining techniques using two monoclonal antibodies against vimentin. Cases demonstrating vimentin positivity by the avidin-biotin-peroxidase method included 11 of 129 adenocarcinomas studied (8.5%), and 15 of 61 large cell carcinomas studied (24.6%). Vimentin expression was not seen in any of the 51 squamous cell carcinomas or 35 small cell carcinomas in our series. The positive cases of adenocarcinoma were in moderately and poorly differentiated cancers. Four of the eight giant cell carcinomas (50%) demonstrated vimentin expression. All cases that exhibited vimentin positivity were studied for cytokeratin expression. Coexpression of vimentin and cytokeratin was demonstrated not only within the same tumor but also within the same cells in some cases stained by double antibody technique, including both adenocarcinomas and large cell carcinomas. Similar immunoreactive methods were also applied to sections from human lung cancer transplants grown in the nude mouse. Of 28 tumors studied, four of 11 adenocarcinomas (36%) and all 4 large cell carcinomas demonstrated coexpression of vimentin and cytokeratin, while none of the five squamous cell carcinomas or eight small cell carcinomas expressed vimentin.
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PMID:Expression of vimentin in surgically resected adenocarcinomas and large cell carcinomas of lung. 242 81

The analysis of an historical cohort study of mortality among individuals occupationally exposed to formaldehyde by Blair et al. (2) in 1986 failed to allow properly for the Healthy Worker Effect and to evaluate time integrated exposure and length of exposure simultaneously. In our reanalysis of the same data we find a risk for lung cancer, increasing with increasing cumulative exposure to formaldehyde.
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PMID:Reanalysis of lung cancer mortality in a National Cancer Institute Study on "Mortality among industrial workers exposed to formaldehyde". 263 42


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