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Biomedical subjects

J Liira

Publications and source records attributed to J Liira.

18 recordsLinked to original sources
PubMed1999

Predictors and consequences of unemployment among construction workers: prospective cohort study.

OBJECTIVE: To study predictors and consequences of unemployment. DESIGN: Prospective cohort study. SETTING: 11 construction companies in southern Finland. PARTICIPANTS: 586 male employees, aged 40-59 years at baseline in 1991 and not retired during a 4 year follow up. MAIN OUTCOME MEASURES: Long term unemployment, stress symptoms, disease, alcohol consumption, exercise activity, and body mass index. RESULTS: In a multiple logistic regression model, long term unemployment (>24 months v </=24 months) was predicted by age 50-54 years v 40-44 years (odds ratio 2.0, 95% confidence interval 1.1 to 3.7), </=3 years' employment in the present job (3.1, 1.9 to 5.1), previous unemployment (2.1, 1.2 to 3.8), being single (1.8, 1.1 to 3. 1), current smoking (2.6, 1.4 to 4.7), high alcohol consumption (2.1, 1.1 to 4.3), body mass index <23 kg/m(2 )v 23-29 kg/m(2 )(2.4, 1.3 to 4.4), frequent stress symptoms (2.0, 1.2 to 3.2), mental disorders (7.8, 1.5 to 40.0), and skin diseases (2.0, 1.0 to 3.9). Workers who were unemployed long term reported increased stress (2.1, 1.2 to 3.5) but fewer incident diseases (0.6, 0.4 to 0.9), decreased alcohol consumption (2.9, 1.6 to 5.2), increased exercise (1.9, 1.2 to 3.0), and increased body mass index (2.3, 1.3 to 4.0) compared with the rest of the cohort. CONCLUSIONS: The workers' perceptions of work did not predict unemployment. Health based selection to long term unemployment was shown. Smoking and high alcohol consumption predated unemployment, but favourable lifestyle changes were observed among the unemployed workers. Stress predicted unemployment, which further increased the stress.

Adult↗
PubMed1999

Predictors and consequences of unemployment in construction and forest work during a 5-year follow-up.

OBJECTIVES: The study investigated whether indicators of health, work conditions, or life-style predict subsequent unemployment and also the unemployment consequences related to health or life-style. METHODS: A questionnaire was administered to 781 male construction and 877 male forest workers (aged 20-49 years and working at the beginning of the study) in 1989 and 1994. Employment status during follow-up was ranked into the following 4 categories according to the employment status and unemployment time: continuously employed, re-employed, short-term (< or = 24 months) unemployed and long-term (> or =24 months) unemployed. RESULTS: The following base-line factors were associated with long-term unemployment during follow-up among the construction workers: age >40 years, poor subjective health, smoking, frequent heavy use of alcohol, low job satisfaction, marital status (single), and unemployment during the year preceding the initial survey. Among the forest workers, age >40 years, frequent stress symptoms, and preceding unemployment entered the model. In addition smoking predicted unemployment among the forest workers with no preceding unemployment. The proportion of regular smokers decreased among the long-term unemployed. Physical exercise was more frequent at the time of follow-up than it was initially, particularly among the unemployed. Stress symptoms increased among the construction workers, but musculoskeletal symptoms decreased significantly among the long-term unemployed. Among the forest workers stress symptoms decreased among the continuously employed and re-employed persons, but musculoskeletal symptoms decreased significantly for them all. CONCLUSIONS: Unemployment among construction workers is to some extent dependent on life-style, health, and job satisfaction in addition to age, marital status, and unemployment history. For forest workers, unemployment is less determined by individual factors. Changes in distress and musculoskeletal symptoms are dependent on employment, particularly among construction workers.

Adult↗
PubMed1991

Metabolic interaction and disposition of methyl ethyl ketone and m-xylene in rats at single and repeated inhalation exposures.

1. Rats were exposed to m-xylene (300 ppm) and methyl ethyl ketone (MEK, 600 ppm) vapour, separately and in combination. 2. Repeated exposures to m-xylene enhanced liver drug-metabolizing capacity, whereas MEK showed no effects. After mixed exposure the cytochrome P-450-dependent monooxygenase activities were additively or synergistically induced. 3. In the presence of MEK the overall metabolism of xylene was strongly inhibited both after single and repeated exposures, an effect accompanied by elevation of xylene concentration in blood (18-29%) and fat (25-32%). 4. The 24-h excretion of the urine metabolites of m-xylene was decreased by 22-24% in mixed exposures: the excretion of methylhippuric acid was decreased (29%), but that of 2,4-dimethylphenol increased (9-35%). 5. After repeated inhalation exposures the excretion of xylene metabolites in urine was consistently higher, whereas the concentrations of xylene in fat (but not the concentration of MEK) were lower than after a single treatment, conceivably due to accelerated metabolic clearance of xylene. 6. Thioether excretion in urine was enhanced in xylene-treated rats (7-13-fold), but was not influenced by the induced changes in the metabolism of xylene. Xylene inhalation caused liver GSH to decrease slightly (10%), as did inhalation of MEK, but the latter did not enhance the excretion of thioethers. 7. MEK is a potent inhibitor of the side-chain oxidation of m-xylene producing methylhippuric acid, but not of its ring oxidation to 2,4-dimethylphenol, and exhibits a synergistic inducing effect on liver enzymes responsible for the oxidation of m-xylene. The increased ring oxidation of m-xylene was not associated with increased production of reactive metabolites indicated by GSH-depletion or thioether formation.

Administration, Inhalation↗
PubMed1990

Cytochrome P450 isozyme induction by methyl ethyl ketone and m-xylene in rat liver.

The rat hepatic cytochrome P450 induction pattern caused by administration of a high peroral dose of methyl ethyl ketone (MEK, 1.4 ml/kg once daily for 3 consecutive days) and m-xylene (1.0 ml/kg X 3) was studied by catalytic activity and immunoblotting techniques. MEK caused a marked increase in the amount of P450 isozymes belonging to the phenobarbital- and ethanol-inducible P450 subfamilies P450IIB and P450IIE, respectively. Catalytic activities linked with these isozymes, pentoxyresorufin O-depentylase (P450IIB), aniline hydroxylase, and N-nitrosodimethylamine N-demethylase (P450IIE), were also increased (18.0-, 5.4-, and 2.4-fold, respectively). The activity of ethoxyresorufin O-deethylase, which is predominantly linked with the polycyclic aromatic hydrocarbon-inducible P450 isozymes, was also increased 2.3-fold without an apparent increase in the amount of the respective P450 protein (P450IA). m-Xylene caused a similar induction pattern with less effect on P450IIE. Simultaneous administration of MEK and m-xylene resulted in an additive or, in the case of pentoxyresorufin O-depentylase, a potentiating effect on P450-linked catalytic activities. These data indicate that MEK and m-xylene elicit a qualitatively similar induction of P450 isozymes, which may play a role in the metabolic interactions of these compounds.

Animals↗
PubMed1990

Dose-dependent kinetics of inhaled methylethylketone in man.

Physiologically based stimulation of earlier human inhalation exposure to methylethylketone (MEK) at a concentration of 200 ppm for 4 h suggested that the kinetics were dose-dependent. Two male volunteers were therefore exposed to MEK for 4 h at 3 exposure concentrations: 25, 200 and 400 ppm. Blood MEK concentrations were monitored during and after exposure. The results showed clearly that the kinetics of MEK were dose-dependent at higher exposure concentrations. Simulated exposure to MEK for 8 h suggests that saturation kinetics are reached at an exposure concentration of 50-100 ppm, depending on the physical work load.

Administration, Inhalation↗
PubMed1990

Effects of ethanol on the kinetics of methyl ethyl ketone in man.

The kinetics of inhaled methyl ethyl ketone (MEK) at a concentration of 200 ppm for four hours were studied in volunteers after swallowing ethanol at a dose of 0.8 g/kg. Ethanol was given either before or at the end of the exposure to MEK. The blood concentrations of MEK, 2-butanol, and 2,3-butanediol were monitored during and after the exposure. MEK concentrations in exhaled air and MEK and 2,3-butanediol concentrations in urine were also measured. Ethanol inhibited the primary oxidative metabolism of MEK and caused an increase in the blood concentrations of MEK and 2-butanol after ingestion. Ethanol ingestion, through higher blood MEK concentrations, also increased the elimination of MEK in the urine and exhaled air. Ethanol taken before exposure to MEK reduced the serum concentration of 2,3-butanediol initially but there was an increase about eight hours after the exposure. Urinary excretion of 2,3-butanediol followed the same pattern. Prior ingestion of ethanol thus seemed to interfere with the metabolism of 2,3-butanediol during and after exposure to MEK.

Adult↗
PubMed1988

Kinetics of methyl ethyl ketone in man: absorption, distribution and elimination in inhalation exposure.

The kinetics of inhaled methyl ethyl ketone (MEK) in human volunteers was studied in an exposure chamber. Relative pulmonary uptake was about 53% throughout a 4-h exposure period at 200 ppm. Blood MEK concentration rose steadily until the end of exposure. Repeated bicycle exercise increased the overall blood MEK level markedly in comparison to sedentary activity, with transient peaks in association with cycling; thus blood MEK concentration depended both on the rate of uptake and the amount taken up. Only 3% of the absorbed dose was excreted unchanged by exhalation. A well-known metabolite of MEK, 2,3-butanediol, was detected in the urine with maximum rates of excretion at about 6 to 12 h from the beginning of exposure. About 2% of the MEK dose taken up by the lungs was excreted in the urine as 2,3-butanediol. The main part of inhaled MEK is supposedly metabolized in the intermediary metabolism. Elimination of MEK in blood appeared to exhibit two phases: the initial alpha-phase (T1/2 = 30 min; kel alpha = 0.023) over the first post-exposure hour, followed by the terminal beta-phase (T1/2 = 81 min; kel beta = 0.009).

Administration, Inhalation↗
PubMed1988

Coexposure of man to m-xylene and methyl ethyl ketone. Kinetics and metabolism.

In a study of the kinetics and metabolic interaction of xylene and methyl ethyl ketone (MEK) eight male volunteers were exposed to m-xylene (100 ppm) and MEK (200 ppm). The exposures to the two compounds were carried out both separately and in combination. Respiratory uptake and blood concentration, as well as urinary metabolites (methyl hippuric acid and 2,3-butanediol), were monitored. Coexposure to xylene and MEK resulted in inhibited xylene metabolism. The xylene concentration in blood increased significantly, and the urinary excretion of methyl hippuric acid decreased. The combined exposure did not cause any change in the concentration of MEK in the blood or the excretion of 2,3-butanediol in the urine. Exposure to MEK 20 h before the m-xylene exposure had no detectable effect on the kinetics of m-xylene.

Adult↗
PubMed1987

Chip pile workers and mould exposure. A preliminary clinical and hygienic survey.

Chip pile workers are exposed to high concentrations of airborne mould spores. Few sporadic cases of allergic alveolitis have been reported in Finland. Eight non-smoking workers, six on chip piles and two on bark piles, were examined to study the immunological and clinical response to continuous mould spore exposure. The spore exposure ranged between 10(4) and 10(5) spores/m3. Three of the six chip pile workers had precipitating serum antibodies against Aspergillus fumigatus. The three antibody-positive workers had a tendency to decreased total pulmonary diffusion capacity and vital capacity. Significant respiratory symptoms were not noted. Long-term spore exposure may include an occupational health risk to chip pile workers.

Adult↗
PubMed1985

Occupational exposure to toluene: neurotoxic effects with special emphasis on drinking habits.

Neurotoxic effects of toluene were examined in 43 male rotogravure printers exposed to toluene (age 27-63, mean 41 years; duration of exposure 11-40, mean 22 years) and 31 male offset printers of the same age with slight exposure to aliphatic hydrocarbons. A neurological examination, tests for autonomic nervous function, electroencephalography, psychological tests and computerized tomography of the brain were carried out in addition to a standardized interview. Exposure levels were evaluated for each person separately on the basis of his work history and the results of an earlier study on exposure levels at the same printing shops. Besides a thorough history of alcohol consumption, information about the printers' drinking habits was obtained from the occupational health care centers of the printing shops. The examinations found only slight abnormalities, and there were no statistically significant group differences in the prevalences of abnormalities. No correlations between the abnormalities and the exposure indices were found either. One of the retired workers, however, who had been exposed to high toluene concentrations for over 40 years, had been diagnosed as having chronic organic solvent intoxication. Heavy drinkers of alcohol were clearly more common in the toluene-exposed group. This study detected no clinically significant abnormalities attributable to toluene alone among workers exposed to 68-185 ppm (mean 117) of toluene for over 10 years. The connection between alcohol consumption and toluene exposure is interesting and deserves further study.

Adult↗
PubMed1982

Relation between central cerebral atrophy, memory defects and prolactin secretion.

Concentrations of prolactin in cerebrospinal fluid (CSF) and in serum were determined from 26 neurological patients with or without minor central cerebral atrophy. Neuropsychological memory tests also were performed on these patients. Twenty-eight neurological patients with peripheral nervous lesions and without endocrine dysfunctions served as controls for prolactin levels. Patients with central cerebral atrophy had significant loss of recall capacity, though they did not differ significantly from the normal population in their intellectual performances. CSF and serum prolactin levels in the patients with central cerebral atrophy and/or memory defects did not differ from the values obtained in the patients without cerebral atrophy. Thus, prolactin levels do not appear to reflect either central cerebral atrophy or memory dysfunctions, most likely due to the minor degree of neuronal atrophy around the third ventricle that occurs in patients with these findings.

Adult↗
PubMed1981

Prolactin levels in cerebrospinal fluid of patients with chronic schizophrenia.

Baseline concentrations of prolactin (PRL) was determined in the CSF of 28 lobotomized and 28 non-lobotomized patients with chronic schizophrenia. The mean PRL level of the female patients was significantly higher than that of the male patients (p < 0.001). In addition, non-lobotomized patients had significantly higher concentrations of CSF PRL than patients of the lobotomized group (p < 0.05). On the other hand, patients belonging to the latter group exhibited significantly more central as well as cortical brain atrophy than the patients on whom no psychosurgery had been performed (0.05 > p < 0.001). The significance of cerebrospinal PRL as an index of central dopamine metabolism is discussed.

Adult↗
PubMed1979

Neuropeptide hormones in cerebrospinal fluid. Experimental and clinical aspects.

Neuroendocrinologists are now realising that the brain-pituitary relationships in man are more complex than they had previously thought. It seems that the brain is also a gland, whereas the pituitary produces neuropeptide hormones which work in the brain. Since most substances which carry information between those two neuroendocrine partners are present in cerebrospinal fluid, it is natural to assume that cerebrospinal fluid has an important role as a carrier of molecular signals between the brain and pituitary. Whether or not the analysis of cerebrospinal fluid neuropeptide hormones will give more information about the brain activity in neurological and psychiatric patients is not yet known exactly despite some promising new findings.

Brain Chemistry↗
PubMedDate not supplied

Low prolactin levels in cerebrospinal fluid: an after effect of lobotomy in chronic schizophrenia.

In order to elucidate the interplay of prolactin and dopamine in schizophrenia, base-line levels of prolactin were assayed in the cerebrospinal fluid (CSF) of chronic schizophrenic patients with or without lobotomy. Cental and cortical atrophy and significantly lowered CSF prolactin levels were found in lobotomized patients in comparison to equally neuroleptic-treated non-lobotomized patients. The mean CSF prolactin level in the female patients was significantly higher than in the male patients. This study did not support the 'dopamine hypothesis' of schizophrenia, since CSF prolactin levels did not correlate with schizophrenic symptoms. The brain atrophy blocked completely the expected elevation of CSF prolactin levels induced by neuroleptics.

Adult↗