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

A case-control study of residents who lived in the vicinity of a primary zinc smelter and a large steel manufacturing plant in eastern Pennsylvania was undertaken to investigate the role of environmental pollutants in the etiology of lung cancer. Lifetime residential, occupational, and smoking histories were obtained from the next of kin of 335 white male lung cancer cases and 332 white male controls. Soil samples were collected and analyzed for content in ppm of arsenic, copper, lead, manganese, zinc, and cadmium. Relative risks were determined according to distance of residence from the zinc smelter and the steel plant, and according to residence in areas with heavy and light levels of various pollutants. Two-fold risks for lung cancer were associated with residence near the zinc smelter and with residence in areas with heavy levels of arsenic and cadmium, although the number of individuals living in these higher risk areas was small. These increases were not explained by the effects of cigarette smoking or by employment in the zinc or steel industry. No excess risk was associated with living near the steel plant. The limited size of the study precludes causal interpretation, but the findings suggest the need for further investigation of metallic air pollution and lung cancer.
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PMID:Lung cancer in relation to environmental pollutants emitted from industrial sources. 674 27

A review of the health effects of cadmium is presented. Overexposure to cadmium produces numerous acute and chronic effects. Cases of acute poisoning resemble metal-fume poisoning. The first and most distinctive indication of chronic effects is renal tubular dysfunction characterized by proteinuria. Other chronic effects include liver damage, emphysema, osteomalacia, neurological impairment, testicular, pancreatic, and adrenal damage, and anemia. Tumorigenic effects have been observed in animals, and excessive prostatic and lung cancer has been observed in worker studies. In vitro and in vivo mutagenic effects have been noted. Cadmium has been shown to cause hypertension in animals; however, it is unclear whether it is capable of causing similar effects in exposed human populations. Normal urinary excretion is less than 2 micrograms/day and correlates with exposure. Normal blood concentration is below 10 ng/gm of whole blood, and although levels are elevated in exposed groups, there is no apparent direct correlation. Hair values correlate well with exposure. Occupational and environmental standards are discussed.
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PMID:A review of the health effects of cadmium. 704 11

Analysis of cancer mortality in whites has revealed a significant excess in both males and females in an old lead/zinc mining and smelting area. This area consists of three rural contiguous counties: Cherokee County, Kansas, Jasper County, Missouri, and Ottawa County, Oklahoma. The lung cancer excess has persisted for at least 28 years for males and 5 years for females. A pilot case/control study is underway in Cherokee County to assess the influence of cigarette smoking, occupation, and residence on the lung cancer excess. Analysis will incorporate the histologic findings. From an environmental perspective, there are numerous mine tailings containing lead, zinc, cadmium, sulfur, germanium, and other chemicals. Considerable dust is airborne. Numerous openings (sink holes and bore holes) connect the old mines with the surface. Radium 226 has been detected in the untreated groundwater.
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PMID:Lung cancer excess in an abandoned lead-zinc mining and smelting area. 715 73

Lead, cadmium, mercury and arsenic are widely dispersed in the environment. Adults are primarily exposed to these contaminants in the workplace. Children may be exposed to toxic metals from numerous sources, including contaminated air, water, soil and food. The chronic toxic effects of lead include anemia, neuropathy, chronic renal disease and reproductive impairment. Lead is a carcinogen in three animal species. Cadmium causes emphysema, chronic renal disease, cancer of the prostate and possibly of the lung. Inorganic mercury causes gingivitis, stomatitis, neurologic impairment and nephrosis, while organic mercurials cause sensory neuropathy, ataxia, dysarthria and blindness. Arsenic causes dermatitis, skin cancer, sensory neuropathy, cirrhosis, angiosarcoma of the liver, lung cancer and possibly lymphatic cancer.
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PMID:Occupational and community exposures to toxic metals: lead, cadmium, mercury and arsenic. 716 33

Concentrations of arsenic and selenium in lung, liver, and kidney tissue from dead smelter workers and from a control group have been determined with the aid of neutron activation analysis. A sevenfold increase of arsenic was found in lung tissue from the exposed workers compared with the control group. The median value of arsenic in lung tissue from workers dead from respiratory cancer was not higher than corresponding values from workers dead from other malignancies or from cardiovascular or other diseases. With increasing period of retirement the malignancies or from cardiovascular or other diseases. With increasing period of retirement the arsenic content diminished in liver tissue but not in lung tissue, indicating a long biological half life of arsenic in lung tissue. The workers dead from malignancies had a higher As/Se quotient than workers dead from other diseases, which does not contradict the protective theory of selenium. Accumulation of antimony, cadmium, lead and lanthanum was observed in lung tissue from the exposed workers. Six of the workers died from lung cancer and the highest concentrations of any of the elements were always observed in the lung tissue from these six cases. This observation speaks in favour of a multifactorial cause behind the excess mortality from lung cancer in smelter workers.
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PMID:Arsenic and selenium in lung, liver, and kidney tissue from dead smelter workers. 723 43

In view of the historic importance of smelter workers in the field of occupational medicine, it is surprising that until very recently little data was available on the mortality experience of these workers. The problem in most studies lies in identifying the smelter workers, because smelting, strictly speaking, refers to the melting of ores for the purposes of recovering metals, whereas smelters sometimes perform the operations of roasting, calcining, sintering, converting, and refining. These distinctions are not made in most mortality studies. Most mortality studies of smelter workers conducted to date have shown some excess in lung cancer. For lead, copper, cadmium, and nickel smelters a different etiologic agent has been proposed for each. These different explanations arise partly from different initial perspectives in conducting the studies. In this paper, data are presented on a current historical-prospective study of males who worked a year or more during the period January 1, 1940 to December 31, 1964 at a copper smelter in Tacoma, Washington. This smelter (and refinery) handled a copper ore with a relatively high arsenic content and produced arsenic trioxide as a by-product. Overall 97.2% of the original study population was traced through 1976. Of the 1,061 who were found to have died, death certificates were obtained for 1,018, or 96%. For all causes of death, the mortality rates in this cohort, expressed as a Standardized Mortality Ratio (SMR), were 3.5% higher than that expected based on the United States white male mortality experience. A total of 104 respiratory system cancers were observed compared to 54.6 expected (SMR = 190.5, p less than .05). Respiratory cancer rates were found to be elevated in both smokers and nonsmokers. Overall, a gradual rise in SMR's for respiratory cancer was observed with increasing duration of exposure but not with an increasing interval from onset of exposure. This observation is consistent with the notion that the effects of arsenic on cancer incidence disappear with time. This phenomenon has also been observed for cigarette smokers and chromate workers. Additional analyses are planned for the Tacoma cohort, which will examine mortality according to process as well as by exposure to arsenic and other contaminants. The importance of studies of workers at other kinds of smelters and refineries is stressed.
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PMID:Mortality studies of smelter workers. 734 69

Epidemiologic studies of occupational cohorts have played a major role in the quantitative assessment of risks associated with several carcinogenic hazards and are likely to play an increasingly important role in this area. Relatively little attention has been given in either the epidemiologic or the risk assessment literature to the development of appropriate methods for modeling epidemiologic data for quantitative risk assessment (QRA). The purpose of this paper is to review currently available methods for modeling epidemiologic data for risk assessment. The focus of this paper is on methods for use with retrospective cohort mortality studies of occupational groups for estimating cancer risk, since these are the data most commonly used when epidemiologic information is used for QRA. Both empirical (e.g., Poisson regression and Cox proportionate hazards model) and biologic (e.g., two-stage models) models are considered. Analyses of a study of lung cancer among workers exposed to cadmium are used to illustrate these modeling methods. Based on this example it is demonstrated that the selection of a particular model may have a large influence on the resulting estimates of risk.
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PMID:Modeling epidemiologic studies of occupational cohorts for the quantitative assessment of carcinogenic hazards. 775 7

Since 1988, the National Institute for Occupational Safety and Health (NIOSH) has notified workers who were subjects in occupational epidemiology studies of the study findings ("worker notification"). This paper describes seven notifications and the worker's reactions to them. The chemicals of interest in the studies were: carbon monoxide, o-toluidine, bis-chloromethyl ether, polychlorinated biphenyls, cadmium, acid mist, and dioxin. Materials describing the study results were sent to 15,958 subjects who were notified of their increased risk of arteriosclerotic heart disease, bladder cancer, lung cancer, melanoma, kidney dysfunction, laryngeal cancer, all cancers combined, or soft tissue sarcoma. Workers provided feedback via telephone calls, and for three notifications, by postcards containing workers' comments and ratings of the notification materials. The percentage of telephone calls received from notified workers ranged from 0.3% to 3.8%, and the percentage returning postcards ranged from 8.8% to 17.6%. The two largest categories of callers were those with questions about their disease risk (30%) or who reported on their health status (25%). Most of the comments on postcards (26%) were complimentary or expressed appreciation for receiving the letters; reports of ill health were second (20%). A majority (66%) rated the notification materials well done. Few of the callers (5%) requested information on legal issues. Most (85%) did not find the materials, which ranged in reading level from sixth to ninth grade, too hard to read, although 15% reported difficulty reading them. Although this response system was effective in producing some input from workers, its limitation is that respondents may not be representative of all notified workers. However, such information is useful because there are few data on the effects of notifications on workers.
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PMID:Workers' response to risk notification. 779 20

Occupational exposures to cadmium are associated with increased risk of lung cancer and renal disease. The Occupational Safety and Health Administration (OSHA) published two standards for cadmium on September 14, 1992 that reduced the permissible occupational exposure limit. In the cadmium industry, women were less likely to be exposed to high levels of cadmium and more likely to hold job titles containing the word "hand" than were men. Only small numbers of female workers were exposed to any level of cadmium. OSHA's risk assessment relied, in part, on morbidity and mortality data from male workers and in part on rodent (animal) data from both sexes. OSHA did not evaluate illness rates specific to female workers. Several factors may alter the risk of these illnesses and their sequelae among workers, including differences in smoking, route of exposures, ability to wear personal protective equipment, and lifestyle.
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PMID:High-risk occupations for women exposed to cadmium. 780 73

This investigation concerned the use of quantitative risk assessment for estimating cancer mortality at low-level exposures. We empirically tested whether extrapolating by linear no-threshold models predicted implausible risks at low-level exposures. Cadmium in cigarette smoke was the low-level exposure, and extrapolation was based on potencies estimated from an occupational study and a rodent cancer bioassay. Inhaled cadmium in mainstream and sidestream smoke was estimated from published laboratory experiments. Smoking-specific lung cancer and all-cause mortality rates were estimated from large population-based studies. The mortality rates, amount of inhaled cadmium, and potency values were used to construct life tables for calculating lifetime lung cancer risk with and without a contribution from cadmium in cigarette smoke. The epidemiologic data predicted that 1 to 18 lung cancer deaths per 10,000 smokers may be attributable to inhaled cadmium in cigarette smoke, or approximately 0.2% to 1.6% of smoking-induced lung cancer deaths. Upper 95% bounds on these figures are 7 to 95 lung cancer deaths or 1.6% to 8.8% of smoking-related deaths. The rodent data predicted that 80 to 416 lung cancer deaths per 10,000 smokers (95% upper bounds: 136-707) or 13% to 47% (23-81%) of smoking-induced lung cancer mortality may be attributable to cadmium in cigarette smoke. Linear extrapolation from human data appears to provide plausible estimates of risk at low doses. Considering the large number of carcinogens present in cigarette smoke, the extrapolation from rodents appears to overestimate human risks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of cadmium in cigarettes to lung cancer: an evaluation of risk assessment methodologies. 803 Nov 88


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