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Biomedical subjects

J M Dement

Publications and source records attributed to J M Dement.

At least 37 records · Page 2Linked to original sources
PubMed1989

Design and conduct of occupational epidemiology studies: I. Design aspects of cohort studies.

Cohort and case-control studies are two standard approaches for investigating the etiology of occupational diseases. This paper, which is the first of a four-part series, contains a review of the design features of occupational cohort studies. Topics discussed include the basic features of prospective and historical cohort studies, options for defining the cohort, disease incidence ascertainment, and considerations involved in planning an occupational cohort study. Subsequent papers in this series will focus on data analysis of occupational cohort studies and the design and analysis of occupational case-control studies.

Cohort Studies↗
PubMed1989

Design and conduct of occupational epidemiology studies: II. Analysis of cohort data.

This paper reviews strategies and statistical methods for analyzing data from occupational cohort studies. Emphasis is placed on the common methods for grouped data analysis involving external and internal comparison populations. Analysis procedures reviewed are standardized mortality ratio, standardized rate ratio, and Mantel-Haenszel techniques for estimating relative risks. Methods for control of confounding, assessment of effect modification, and allowance for disease latency are discussed. These concepts and procedures are illustrated with data from an historical cohort mortality study of workers from an asbestos textile plant.

Biometry↗
PubMed1987

Inhalation exposure system used for acute and repeated-dose methyl isocyanate exposures of laboratory animals.

Laboratory animals were exposed by inhalation for 2 hr/day (acute) or 6 hr/day (four consecutive days, repeated dose) to methyl isocyanate (MIC). Exposures were conducted in stainless steel and glass inhalation exposure chambers placed in stainless steel, wire mesh cages. MIC was delivered with nitrogen via stainless steel and Teflon supply lines. Chamber concentrations ranged from 0 to 60 ppm and were monitored continuously with infrared spectrophotometers to 1 ppm and at 2-hr intervals to 20 ppb with a high performance liquid chromatograph equipped with a fluorescence detector. Other operational parameters monitored on a continuous basis included chamber temperature (20-27 degrees C), relative humidity (31-64%), static (transmural) pressure (-0.3 in.), and flow (300-500 L/min). The computer-assistance system interfaced with the inhalation exposure laboratory is described in detail, including the analytical instrumentation calibration system used throughout this investigation.

Animals↗
PubMed1986

An evaluation of the effectiveness of a recirculating laboratory hood.

Ductless, benchtop hoods have become a popular tool for use in the control of toxic substances in the laboratory. Low price and ease of installation are major factors contributing to their increased utilization. Little objective performance data exist for these devices. One such hood was evaluated for efficacy as an engineering control in typical laboratory applications. Face velocity, flow profile, ability to retain vapors, sorptive capacity of the filter media and overall worker protection were evaluated. The manufacturer's report of an average face velocity of 30.6 cm/s (60 fpm) proved to be accurate; however, this value was found to be substandard when compared with the hood and room design criteria which must be met for this rate to provide adequate control. The hood was designed in a manner which prevented smooth flow through the hood and increased observed turbulence and rolling. The sorptive capacity of the carbon filter proved to be comparable to that reported for organic vapor respirator cartridges. Design deficiencies are discussed to improve protection offered to the worker in an as-used situation. Further work is needed to provide a quantitative measure of the protection offered by these hoods.

Air Pollution↗
PubMed1986

Contribution of environmental fibers to respiratory cancer.

This article reviews studies of the carcinogenicity of mineral fibers, notably asbestos, and presents seven major recommendations for further research. Mineral fibers represent the greatest cause--after cigarette smoke--of respiratory cancer due to air pollutants. Past asbestos exposure may currently account for 2000 mesothelioma deaths per year and 4000 to 6000 lung cancer deaths per year. All major commercial types of asbestos (crocidolite, amosite, and chrysotile) can cause each of the major asbestos-related respiratory diseases. Lung cancers in asbestos-exposed individuals probably do not have a different distribution of histological types from that of non-asbestos-related lung cancers. Nonoccupational exposures are likely to be associated with malignant disease outcomes qualitatively similar to those associated with occupational exposures. Further investigations of fibers are needed to characterize the relationships among physicochemical properties, patterns of migration and clearance, dose, and adverse health effects. Transmission electron microscopy has been found to be the preferred method of analysis of environmental fibers. Relations among time factors (e.g., age at first exposure), dose, and risk for adverse health effects require analyses of existing and new epidemiologic studies of exposed cohorts. Concomitant exposure, behavioral factors, and host factors affecting susceptibility to asbestos should be identified.

Air Pollutants↗
PubMed1983

Exposures and mortality among chrysotile asbestos workers. Part I: exposure estimates.

A detailed study of plant processes and dust control methods over the period 1930-1975 was conducted in an asbestos textile plant processing chrysotile. Linear statistical models for reconstructing historic dust exposure levels, taking into account textile processes, dust control measures, and job assignments, were developed. Parameters of these statistical models were estimated using 5,952 industrial hygiene sampling measurements covering the period 1930-1975. For most textile operations, exposure levels were significantly reduced by about 1940, when most engineering dust control measures were in place. Results of the exposure estimates indicated "precontrol" exposure levels to range from 3 to 78 fibers/cc with typical levels well above 10 fibers/cc. After textile operations were provided with dust control measures, estimated exposure levels ranged from 3 to 17 fibers/cc and were usually in the range of 5 to 10 fibers/cc. These exposure estimates were combined with an assessment of mortality among workers at this plant to investigate exposure-response relationships. Exposure-response results are presented in the companion manuscript in this volume.

Asbestos↗
PubMed1983

Exposures and mortality among chrysotile asbestos workers. Part II: mortality.

A retrospective cohort mortality study was conducted among a cohort of 1,261 white males employed one or more months in chrysotile asbestos textile operations and followed between 1940 and 1975. Statistically significant excess mortality was observed for all causes combined (standardized mortality ratio [SMR] = 150), lung cancer (SMR = 135), diseases of the circulatory system (SMR = 125), nonmalignant respiratory diseases (SMR = 294), and accidents (SMR = 134). Using estimated fiber exposure levels in conjunction with detailed worker job histories, exposure-response relationships were investigated. Strong exposure-response relationships for lung cancer and asbestos related non-malignant respiratory diseases were observed. Compared with data for chrysotile miners and millers, chrysotile textile workers were found to experience significantly greater lung cancer mortality at lower lifetime cumulative exposure levels. Factors such as differences in airborne fiber characteristics may partially account for the large differences in exposure response between textile workers and miners and millers.

Asbestos↗
PubMed1982

Mortality patterns of rock and slag mineral wool production workers: an epidemiological and environmental study.

An epidemiological and environmental study of rock and slag mineral wool production workers was undertaken at a plant that has been in operation since the early 1900s. Size characteristics of fibres produced by each process at the plant and data from industrial hygiene surveys were used to evaluate current and past exposures. These data suggest that the average historical airborne fibre concentration probably did not exceed 2.5 fibres/cc before 1935 and 1.0 fibre/cc after 1935. A retrospective cohort mortality study was designed to assess mortality patterns. Detailed occupational histories were compiled on all plant employees. All jobs in the plant were assigned to one of eight potential exposure categories to assess the extent and severity of mineral wool exposure and the effect of other significant exposures on employee mortality. Findings included an increase in the number of deaths due to cancer of the digestive system and non-malignant respiratory disease among workers who had over 20 years' exposure to mineral wool or who had survived 20 years since their first exposure to mineral wool. These findings are not inconsistent with those of Enterline's (Symposium on Biological Effects of Mineral Fibres, Lyon, France, September 1979) in the Thermal Insulation Manufacturers' Association's mortality study of men employed in four mineral wool plants.

Adult↗
PubMed1980

Epidemiology of asbestos-related diseases.

This paper is intended to give the reader an overview of the epidemiology of asbestos-related diseases and is restricted to primarily occupational exposure studies. However, some mention of nonoccupational exposures are made because of their direct relationship to a worker or to a secondary occupational source. Over 100 epidemiological studies are reviewed, dating back to the first case of asbestos-associated disease reported by Montague Murray in 1906. The studies are divided by specific fiber type and by specific disease outcomes and the interaction of asbestos and cigarette smoking is discussed in great detail.

Asbestos↗