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Biomedical subjects

K H Kilburn

Publications and source records attributed to K H Kilburn.

At least 55 records · Page 3Linked to original sources
PubMed1989

An examination of factors that could affect choice reaction time in histology technicians.

Histology technicians exposed to formaldehyde and solvents have symptoms and objective evidence of neurobehavioral impairment of memory, judgment, and equilibrium. Because reaction time has been prolonged in many groups of workers exposed to toxicants, choice reaction time was measured in 385 female formaldehyde and solvent-exposed histology technicians, and 79 unexposed female laboratory workers. Choice reaction time to a visual stimulus (CRT) is defined, for the purpose of this study, as the time required for discriminated cancellation of two different letters on a microcomputer screen by pressing the matching keys. Initial analysis showed that increases in age, years of cigarette smoking, and hours per day of formaldehyde exposure significantly lengthened CRT, but xylene-toluene exposure had no effect. Since duration of smoking and length of daily formaldehyde exposure were age related, multiple linear regression analysis of CRT was performed using them as independent variables. Increasing age was the only significant factor in lengthening CRT. However, in these female histology technicians, the second measurement one year later was 44 msec faster (p less than .04). The reason for improved performance is unclear, but it may be an effect of training encompassing familiarity, improved attention, or learning.

Environmental Exposure↗
PubMed1989

Choice (CRT) and simple reaction times (SRT) compared in laboratory technicians: factors influencing reaction times and a predictive model.

Choice reaction time (CRT) and simple reaction time (SRT) tests were administered to 151 female histology laboratory technicians to determine if occupational exposure to organic solvents and formaldehyde delayed either or both. The relationships between CRT and SRT latencies were evaluated using different testers, sequences of administration, and microcomputers. Formaldehyde exposure, cigarette smoking history, ethnicity, and alveolar CO levels did not significantly influence CRT and SRT. However, slightly different protocols did significantly affect SRT. A linear model demonstrated that logSRT (LSRT) and LogCRT (LCRT) were longer with increasing age, promising further clinical applications. It is concluded that both CRT and SRT measure some overlapping and some different neurologic pathways. Reaction times in large "normal" populations are needed to compare with groups exposed to potential neurotoxins.

Adult↗
PubMed1989

Pulmonary functional impairment from years of arc welding.

PURPOSE: The adverse effects of arc welding on pulmonary function have been previously documented. However, in many of these studies, the effects of welding exposure and smoking were not separated. Also, some studies did not adjust for or ignored the effects of asbestosis on pulmonary function. We assessed the long-term effects of welding on pulmonary function in welders who had no evidence of asbestosis on chest radiographs, and adjusted each individual value for height, age, and years of cigarette smoking. PATIENTS AND METHODS: The study consisted of 226 male construction welders who had never worked in shipyards. Forced vital capacity (FVC) and flows were measured by spirometry, chest radiographs were obtained and examined for evidence of asbestosis using International Labor Office (ILO) criteria, and thoracic gas volume (TGV) was determined by planimetry. The subjects were also administered an occupational and respiratory questionnaire. Data on workers with asbestosis (ILO profusion 1/0 or greater) and pleural abnormalities were excluded. The mean age for the 226 subjects without asbestosis was 45 years, mean height was 175.7 cm, and mean duration of welding was 21.3 years. Pulmonary function measurements are presented as mean percentage of predicted (pop) and adjusted for height, age, and years of smoking. RESULTS: In 151 current cigarette smokers, mean midflows and terminal flows were decreased, FEF25-75 to 93.2 pop and FEF75-85 to 91.2 pop, but FVC, forced expiratory volume in one second (FEV1) and TGV were normal. The 43 nonsmokers also had reductions in flows but normal FVC and TGV. Flows in both groups were significantly (p less than 0.05) below those of the referent group. The regression coefficient was -0.0031 for years of welding and FVC pop, -0.0035 for FEV1 pop, and -0.0080 for midflow pop (FEF25-75) (all significant at p less than 0.05), but the coefficient for FEF75-85 pop was not significant. As calculated from regression equations, 40 years of welding would reduce FVC to 95.2 pop, FEV1 to 92.2 pop, midflow to 79.2 pop, and FEF75-85 to 81.7 pop. CONCLUSION: Long-term exposure to welding gases and fumes reduced flows in small airways of welders without asbestosis.

Adult↗
PubMed1989

Respiratory symptoms and functional impairment from acute (cross-shift) exposure to welding gases and fumes.

One hundred forty-five male welders from a West Coast shipyard were studied cross-sectionally and across a Monday work shift by pulmonary function tests and a questionnaire. Ten years of welding was associated with chronic bronchitis in 23.3% of nonsmokers compared to 3.3% in male controls, shortness of breath in 31.5% of nonsmokers compared to 1.5% in controls, and chest pain or heaviness in 38.4% compared to 4.4% in controls. Men who welded aluminum but had never smoked had more frequent wheezing, chest tightness, phlegm, feverishness and fatigue than those welding mild (black) or stainless steel. There were no significant cross-shift effects from welding exposure on measurements of pulmonary function. Although baseline expiratory flows were reduced slightly when compared to Caucasian-predicted values, ethnic specific comparisons for the largest subgroup showed only that FEF25-75 was reduced to 92.9 percentage of predicted values. Diffusing capacities for carbon monoxide were significantly reduced as compared to referents. The pulmonary function values of 25 current smokers were indistinguishable from the 41 who had never smoked, which probably reflects their low consumption of cigarettes.

Acute Disease↗
PubMed1989

Pulmonary function in histology technicians compared with women from Michigan: effects of chronic low dose formaldehyde on a national sample of women.

Chronic workplace exposure to formaldehyde and solvents at low doses reduced pulmonary function in 280 non-smoker white women working as histology technicians. They were studied during national workshops at four United States cities for four years. Height and age adjusted comparisons of pulmonary function were made with women in a stratified random population sample of Michigan and with a selected subset of the population that was used to model predictive pulmonary equations for function. The major functional change in histology technicians was a steeper decrement in vital capacity and flows from age 20 to 60 by regression analysis than occurred in the modelled Michigan population. Furthermore non-smoking and currently smoking women studied at two sites had significantly lower flows than were found in the sample of Michigan women. There was no consistent effect of an aerosol bronchodilator on flows of women at the four sites. Diffusing capacity for carbon monoxide single breath and alveolar volume were below the comparison group of Michigan women only when tested at Washington DC.

Adult↗
PubMed1986

Interaction of asbestos, age, and cigarette smoking in producing radiographic evidence of diffuse pulmonary fibrosis.

The study of 3,472 chest x-rays from four populations with different levels of exposure to asbestos and with different cigarette smoking histories shows that smoking in the general population does not produce pulmonary fibrosis recognizable on chest radiography. In the general population of Michigan, the prevalence of a radiographic pattern of fibrosis was 0.5 percent in men and 0.0 percent in women. In a Long Beach, California census tract population, the prevalences were 3.7 percent for men and 0.6 percent for women. Similarly, cigarette smoking does not enhance fibrosis when the exposure to asbestos has been as light as that in households of shipyard workers. Asbestosis was recognized in 6.6 percent of 137 shipyard workers' wives who have never smoked and 7.6 percent of 132 who had ever smoked. Cigarette smoking and asbestos appear to be synergistic in those occupationally exposed to asbestos (as insulators), since 7.2 percent of 97 nonsmokers and 20.5 percent of 316 ever-smokers showed fibrosis. This apparent synergy was also found in shipyard workers up to age 70 with 31 percent of nonsmokers and 43.3 percent of ever-smokers having fibrosis. There were increases of approximately 10 percent in the prevalence of fibrosis in cigarette smokers and nonsmokers for each decade after age 40.

Adult↗
PubMed1986

Medical screening for lung cancer: perspective and strategy.

Strategies to prevent or reverse cancer promotion are described. One strategy, involving the screening and prompt treatment of small lung cancers, is proposed as a study to be tested in occupational groups with very high risk, specifically asbestos-exposed shipyard workers who smoke cigarettes. The relative risk can be assigned on the basis of (1) age, (2) years since first asbestos exposure, and (3) cigarette smoking amount, recency of cessation and age at onset. Proposed surveillance would be chest x-ray films at 4-month intervals and sputum cytology in current smokers and those within 10 years of cessation. Means of detection, such as monoclonal antibody tests for adenocarcinoma and other marker molecules, would be explored. Prompt conventional treatment would be assured. Other inquiries would be directed at new treatment, such as using targeted molecules directed at surface antigens.

Asbestosis↗
PubMed1986

Asbestos diseases and pulmonary symptoms and signs in shipyard workers and their families in Los Angeles.

Families of 338 male and 81 female shipyard workers (SYW), including 280 wives, 144 daughters, and 81 sons, were examined for diseases resulting from asbestos. The workers were initially exposed to asbestos at least 20 years prior to the study date. Radiographic signs of asbestosis (using standard criteria international Labor Office 1980) were found in 64% of 288 male SYW and 21% of 71 female SYW. After excluding those with any occupational exposure to asbestos, asbestosis prevalence was 11% in wives, 8% in sons, and 2% in daughters. Asbestos disease prevalence in workers and in wives increased with the number of years from initial exposure. Male SYW who had smoked had airway obstruction without volume loss. Nonsmokers had normal pulmonary functions. In SYW households prevalences of respiratory diseases, wheezing on physical examination, and symptoms of asthma and chronic bronchitis, exceeded those in the comparison (Michigan) population, even for the younger daughters and sons. These differences, and airway obstruction and distribution defects reported earlier were not explained by cigarette smoking or by asbestos exposure. Instead, they are tentatively ascribed to long-term exposure to ambient air pollution in Los Angeles.

Age Factors↗
PubMed1985

Signs of asbestosis and impaired pulmonary function in women who worked in shipyards.

Fifteen of 71 women (21.1%) who had worked in shipyards before May, 1961 had radiographic signs of asbestos disease. There were irregular opacities in the lung parenchyma in seven and pleural disease in eight, two of whom had pleural calcifications. The 71 women who volunteered to be studied had a mean age of 61.5 years. Chronic bronchitis was diagnosed in 21%, 71% had dyspnea on climbing two flights of stairs, and 42% had wheezing. These prevalences were 50% higher than in wives of shipyard workers. In 50 white women, mean values for expiratory flow rates, log (FEF25-75) and log (FEF75-85), were decreased for non-, ex- and current smokers as compared to normal nonsmokers. Ex-smokers and current smokers showed the greater effects. Diffusing capacity (DLCOsb) and alveolar volume (ALV) were also reduced in all three smoking categories. Comparison to a reference population without asbestos exposure showed that for current, ex- and nonsmoking subgroups, there were significant reductions in log (FEF25-75), DLCOsb, and ALV for nonsmokers, reductions in FEV1, log (FEV25-75), and log (FEF75-85) in ex-smokers, and reduced ALV in current smokers. These decreases may reflect a locality effect. Further studies are recommended.

Age Factors↗
PubMed1985

Pulmonary functional impairment and symptoms in women in the Los Angeles Harbor area.

Spirometric measurements of vital capacity and flow rates, thoracic gas volume, and single-breath diffusing capacity for carbon monoxide were obtained in 360 white women, 238 wives age 58 years and 122 daughters age 32 years of shipyard workers from the Long Beach area of southern California. The values for nonsmokers, exsmokers, and current smokers were compared with smoking-specific mean values, age- and height-adjusted, from a reference population in Michigan. The wives from Long Beach had significantly lower mid and terminal flows, single-breath diffusing capacity for carbon monoxide, and alveolar volume, except that single-breath diffusing capacity for carbon monoxide was not significantly lower in current smokers. Nonsmokers and ex-smokers showed significantly different values for one-second forced expiratory volume in addition to flow rates and single-breath diffusing capacity for carbon monoxide. Daughters showed significant reductions in single-breath diffusing capacity for carbon monoxide and alveolar volume, which are attributable to maldistribution of inspired gas. These data showed that a powerful factor has affected expiratory air flow and distribution of gas, resulting in altered single-breath diffusing capacity for carbon monoxide and alveolar volume in this population. The factor is additive with and resembles the effect of cigarette smoking, and it is postulated that this factor is oxidant air pollution.

Adult↗
PubMed1985

Asbestosis, pulmonary symptoms and functional impairment in shipyard workers.

A group of 339 male shipyard workers responded to an invitation via shipyards, unions, and news media to be studied for the presence of asbestosis and its functional effects. Of these, 288 were white or black, had begun working in shipyards at least 20 years earlier, and had satisfactory chest x-ray film findings; 257 underwent spirometric testing, and 199 had single-breath diffusing capacities for carbon monoxide (Dsb) determined. There were radiographic signs of asbestosis in 64 percent. Of these, 28 percent had parenchymal disease only, 37 percent had pleural disease only, and 35 percent had both. There was pleural calcification in 9 percent. In only 14 (8 percent) was the profusion of opacities greater than 1/1 by the International Labour Organization's criteria. Age was closely related to the duration of exposure to asbestos. Thus, 87 percent of the workers who had asbestosis were born from before 1900 to 1910, 70 percent of those born in 1911 to 1920 had asbestosis, 62 percent of those born in 1921 to 1930 had the disease, and 31 percent of those born in 1931 to 1940 had signs of asbestosis. Function in nonsmokers was not significantly different from the reference population except for alveolar volume; ex-smokers had significantly reduced forced expiratory volume in one second, flow rates, Dsb, and alveolar volume. The forced vital capacity and thoracic gas volume were normal. Shipyard workers who smoked resembled reference smokers except for significantly reduced alveolar volume. These shipyard workers had minimal to moderate asbestosis with much pleural disease and little functional impairment when compared to a smoking-specific reference population.

Adolescent↗
PubMed1985

Asbestos disease in family contacts of shipyard workers.

Radiologic signs of pulmonary asbestos disease were found in 11.3 per cent of 274 wives of shipyard workers who were 20 or more years from initial hiring-on in shipyards in Los Angeles County. Asbestosis was also found in 7.6 per cent of 79 sons and 2.1 per cent of 140 daughters of these workers. The wives, sons, and daughters were without occupational exposure. Comparable radiographic signs were not found in comparison groups. It is probable that asbestos exposure in the household places these family members at risk for mesothelioma and lung cancer.

Adolescent↗
PubMed1984

Particles causing lung disease.

The lung has a limited number of patterns of reaction to inhaled particles. The disease observed depends upon the location: conducting airways, terminal bronchioles and alveoli, and upon the nature of inflammation induced: acute, subacute or chronic. Many different agents cause narrowing of conducting airways (asthma) and some of these cause permanent distortion or obliteration of airways as well. Terminal bronchioles appear to be particularly susceptible to particles which cause goblet cell metaplasia, mucous plugging and ultimately peribronchiolar fibrosis. Cancer is the last outcome at the bronchial level and appears to depend upon continuous exposure to or retention of an agent in the airway and failure of the affected cells to be exfoliated which may be due to squamous metaplasia. Alveoli are populated by endothelial cells, Type I or pavement epithelial cells and metabolically active cuboidal Type II cells that produce the lungs specific surfactant, dipalmytol lecithin. Disturbances of surfactant lead to edema in distal lung while laryngeal edema due to anaphylaxis or fumes may produce asphyxia. Physical retention of indigestible particles or retention by immune memory responses may provoke hyaline membranes, stimulate alveolar lipoproteinosis and finally fibrosis. This later exuberant deposition of connective tissue has been best studied in the occupational pneumoconioses especially silicosis and asbestosis. In contrast emphysema a catabolic response, appears frequently to result from leakage or release of lysosomal proteases into the lung during processing of cigarette smoke particles. The insidious and probably most important human lung disease due to particles is bronchiolar obstruction and obliteration, producing progressive impairment of air flow. The responsible particle is the complex combination of poorly digestive lipids and complex carbohydrates with active chemicals which we call cigarette smoke. More research is needed to perfect, correct and quantify our preliminary picture of the pathogenesis of lung disease by particles, but a useful start has been made.

Animals↗
PubMed1983

Cadmium induced metal fume fever: results of inhalation challenge.

Inhalation challenges were performed on a patient who had developed symptoms of metal fume fever, after six years of welding. Vital signs, white blood cell count and differential, nasal smears, chest X-ray, and pulmonary function tests were monitored during each inhalation challenge. There was no significant reaction to methylcholine, or to fumes of zinc, copper, and mild steel. Significant restrictive ventilatory impairment, leucocytosis, fever, and symptoms of metal fume fever were noticed after exposure to fumes of silver solder containing twenty four percent cadmium.

Adult↗
PubMed1983

Chemically induced congenital thymic dysgenesis in the rat: a model of the DiGeorge syndrome.

The DiGeorge syndrome, a variable complex of thymic aplasia, congenital heart disease, hypoparathyroidism, and anomalies of the face and neck, is thought to result from exposure to teratogenic agents. A group of congenital defects closely resembling this syndrome can be produced in newborn rats by the administration of the fat-soluble zinc chelating agent WIN 18,446, a bis-dichloroacetylamine. This drug, nontoxic to adult animals, is a powerful teratogen when administered to pregnant rats during days 9-12 of the 21-day gestation period. Our animal data suggest that the human syndrome results from exposure in utero to agents like WIN 18,446, which damage the fetus during a critical period of organogenesis.

Animals↗
PubMed1983

Cathepsin B and prolyl endopeptidase activity in rat peritoneal and alveolar macrophages. Stimulation of peritoneal macrophages by saline lavage.

Cathepsin B and prolyl endopeptidase activity was determined in purified rat pulmonary and peritoneal macrophages and cathepsin B was determined in blood monocytes. The activity of cathepsin B in pulmonary macrophages was more than two times higher than in resident peritoneal macrophages and about eight times higher than in circulating monocytes. The simple process of peritoneal lavage with PBS induced an increase in cathepsin B activity in peritoneal macrophages that by 96 and 144 hr reached those levels observed in pulmonary macrophages. Both pulmonary and peritoneal macrophages contain prolyl endopeptidase activity. Repeated peritoneal lavage induced a significant increase in the activity of the enzyme, but not of the magnitude observed for cathepsin B. The data suggest that the transformation of monocytes into macrophages is associated with a significant increase in cathepsin B activity and that this increase is much greater in pulmonary than in peritoneal macrophages.

Animals↗