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3.  Increase in neuropsychiatric symptoms after occupational exposure to low levels of styrene. 
The results of this study suggest that exposure to styrene below the current Swedish permissible exposure limit of 20 ppm induces neurotoxic effects expressed as an increased number of neuropsychiatric symptoms. Twenty men exposed to styrene at a plastics factory participated. The reference group included 20 non-exposed men matched for age, working schedule, and physical work load. Exposure to styrene during one workday was assessed by personal air monitoring and biological monitoring. To evaluate the physical work load the pulse(heart) rate was measured. One week before the study each man completed a neuropsychiatric symptom questionnaire containing 16 items. Also 17 questions regarding acute symptoms of local irritation and symptoms of the central nervous system were presented after the psychometric tests were performed. The tests were simple reaction time, colour word vigilance, and symbol digit. A follow up with regard to the symptoms among the exposed men was done after their summer vacation, about two to five weeks after their last exposure. The mean eight hour time weighted average (TWA) concentration of styrene in air, measured by passive dosimetry was 8.6 ppm (range 0.04-50.4 ppm). The exposed men had significantly more symptoms than the referents although there were no significant differences for the psychometric tests. At the follow up the exposed men reported fewer symptoms. This study indicates that symptoms are earlier indicators of adverse effects than complex tests and underlines the importance of regular follow up of people exposed to styrene (and probably organic solvents in general).
PMCID: PMC1061318  PMID: 8398879
4.  Mortality and incidence of cancer among sewage workers: a retrospective cohort study. 
To study the incidence of and mortality from cancer among sewage workers a retrospective analysis was performed on a cohort of 656 men employed for at least one year at any one of 17 Swedish sewage plants during the years 1965-86. Assessment of exposure was done by classification of work tasks. Lower than expected total mortality (standardised mortality ratio (SMR) = 0.75, 95% confidence interval (95% CI) 0.58-0.97) and cardiovascular mortality (SMR = 0.61, 95% CI 0.39-0.91) was found. This was interpreted as a result of the healthy worker effect. For all cancers combined the mortality (SMR = 1.08, 95% CI 0.68-1.67) and morbidity (SMR = 1.02, 95% CI 0.72-1.38) were comparable with those of the general population. There were increased incidences for brain tumours (SMR = 2.19, 95% CI 0.45-6.39), gastric cancers (SMR = 2.73, 95% CI, 1.00-5.94), and renal cancers (SMR = 1.68, 95% CI = 0.35-4.90). For lung cancer the risk was reduced (SMR = 0.70, 95% CI 0.15-2.05). Allowance for a latency period of 10 years from the start of exposure did not change the pattern. Logistic modelling was used to search for exposure-response relations. In a logistic model with the confounder age forced in, renal cancer had a significant positive relation with a weighted sum of employment times, where the weights describe the classification of exposure. No exposure-response relations were found for brain tumors or gastric cancers. The increased risks are based on small numbers of cases. A future follow up will add more conclusive power to the study. Specific exposures need to be identified to allow for a better dose-response analysis.
PMCID: PMC1035503  PMID: 8343427
5.  Exposure dependent increase in DNA single strand breaks in leucocytes from workers exposed to low concentrations of styrene. 
Single strand breaks in DNA were monitored in leucocytes from 17 men occupationally exposed to styrene. Personal air monitoring was carried out during one workday with two diffusion samplers and a portable photoionisation detector placed in the breathing zone. Exposure to styrene was also monitored by analysing styrene in blood and urine and mandelic acid in urine. Single strand breaks were measured in leucocytes by the alkaline elution technique. The biological samples were collected before a shift, at the end of a shift, and the next morning, before the next shift. An exposure dependent increase in single strand breaks was seen at the end of a shift but not before a shift or the next morning. Linear regression analysis indicated that the amount of DNA damage was roughly doubled after eight hours of exposure to 18 ppm styrene or at a urine concentration of 240 mg mandelic acid/g creatinine compared with the damage in non-exposed men. This study indicates that monitoring of single strand breaks with the alkaline elution technique may be a sensitive marker of genotoxic effects. To our knowledge, this is the first time that such a marker has been shown to correlate with exposure to less than 20 ppm styrene.
PMCID: PMC1035485  PMID: 8329323
6.  Occupational exposure to organic solvents as a cause of sleep apnoea. 
A high prevalence of sleep apnoea was found in a group of men occupationally exposed to organic solvents. Workers with long term exposure to organic solvents often report symptoms such as fatigue, forgetfulness, and concentration difficulties. These symptoms are strikingly similar to those reported by patients with obstructive sleep apnoea syndrome (OSAS). This is a frequently diagnosed disorder characterised by disturbed sleep causing psychic or somatic complications and daytime sleepiness. A study was undertaken to evaluate whether people with long term occupational exposure to organic solvents have a higher prevalence of sleep apnoea than the general population. Patients exposed to solvents (66 men) were invited to participate in a screening for sleep apnoea. A static charge sensitive bed was used for the monitoring of respiration movements and pulse oximetry during one night. A classical sleep apnoea was diagnosed if periodic respiration movement exceeded 45% of estimated sleep time and the oxygen desaturation index exceeded 6. The prevalence of sleep apnoea among the men exposed to solvents was compared with the prevalence in the general population (1.4%). The prevalence among the participating exposed men was 19.7% which gave a conservative relative risk estimate of 14.1 (95% confidence interval (95% CI) 7.5-24.2). The results indicate that exposure to organic solvents causes sleep apnoea. An alternative possibility is that people with sleep apnoea are misdiagnosed as cases of solvent induced toxic encephalopathy. The interpretation has importance for the caring of the patient.
PMCID: PMC1061276  PMID: 8457496
7.  Environmental, occupational, and personal factors related to the prevalence of sick building syndrome in the general population. 
Possible relations between prevalence of sick building syndrome (SBS) and environmental, occupational, and personal factors were studied in a random sample (0.1%) of the general population aged 20-65 in a three county region in middle Sweden. Childhood exposure to environmental tobacco smoke from smoking mothers and a childhood in urban areas was related to SBS symptoms. Current urban residency, fresh paint, and preschool children in the dwelling were also related to symptoms. Other residential factors such as age of building, type of building, degree of crowding, mechanical ventilation, or signs of moisture or mould growth were not related to symptoms. Other factors related to symptoms were history of atopy, allergy to nickel, proneness to infection, hyperreactivity, static electricity, work with video display units (VDU), work satisfaction, and climate of cooperation at work. Age, sex, marital state, education level, work stress, obesity, current or earlier smoking, regular physical exercise, or occupational exposure to chemicals did not correlate with symptoms. Women had a higher proportion of symptoms than men but these differences were not significant when adjusting for differences in allergy to nickel, hyperreactivity, and proneness to infection. Maternal smoking was related to a twofold increase of both atopy and allergy to nickel in the adult offspring. Eye symptoms were most common in administrative, managerial, and service work. Airway symptoms were most common in transport and communication work. Dermal symptoms were most common in professional and technical and related work. General symptoms were most common in service, health, hospital, and social work. The lowest prevalence of symptoms was found in agricultural, forestry, and sales work. Women and subjects allergic to nickel worked more often in occupations without exposure to chemicals, but no evidence was found for selection mechanisms causing sensitive persons to move from exposed to unexposed occupations. It was concluded that symptoms included in SBS are common in the general population, and of multifactorial origin related to both personal, occupational, and residential factors, and certain environmental exposures such as maternal smoking, the urban environment, VDU work, and volatile organic hydrocarbons from newly painted dwellings.
PMCID: PMC1035398  PMID: 1854648
8.  Volatile organic compounds, respirable dust, and personal factors related to prevalence and incidence of sick building syndrome in primary schools. 
Possible relations between incidence and prevalence of sick building syndrome (SBS), indoor exposures, and personal factors were studied in a four year longitudinal study among personnel (n = 129) in six primary schools. The mean concentration of carbon dioxide was above the recommended value of 0.08 microliter/l (800 ppm) in all schools, indicating a poor outdoor air supply. Indoor concentration of volatile hydrocarbon (VOC) was enhanced at high room temperatures. Respirable dust, but not concentration of VOC was enhanced at lower ventilation rates and high air humidity. Chronic SBS was related to VOC, previous wall to wall carpeting in the schools, hyper-reactivity, and psychosocial factors. Incidence of new SBS was related to concentration of respirable dust, current smoking, and the psychosocial climate. Remission of hyperreactivity, decrease in sick leave owing to airway illness, removal of carpeting in the schools, and moving from new to old dwellings resulted in a decrease in SBS score. It is concluded that SBS is of multifactorial origin, related to a variety of factors and exposures. The total concentration of hydrocarbons is a simple and convenient measure of exposure, which also seems to be a predictor of chronic symptoms. Further investigations on the effect of temperature, ventilation, and air humidity on SBS should consider how these factors may influence the chemical composition of the air. Because poor air quality in schools could also affect the children, it may have implications for the state of health of a large proportion of the population.
PMCID: PMC1035263  PMID: 2123116
9.  Cardiac arrhythmia in refrigerator repairmen exposed to fluorocarbons. 
A field study of 89 refrigerator repairmen was carried out to ascertain whether occupational exposure to fluorocarbons induces cardiac arrhythmia. The concentrations of fluorocarbons in the breathing zones and the heart activity were recorded simultaneously. Most cooling systems contained FC 12 or FC 22. The highest level recorded in one minute was 14,000 ppm and the highest time weighted level during eight hours was 280 ppm. Two types of arrhythmia were recorded, ectopic beats and sudden bradycardia. A within subject comparison design was applied and the main parameter was the difference in arrhythmia frequencies between exposed and unexposed periods. No appreciable differences between exposed and unexposed periods and no consistent dose effect relations were observed, although subjects in the medium exposure category showed a difference of borderline significance (Wilcoxon's test: p = 0.05, one tailed). The frequencies of arrhythmia when unexposed were somewhat higher than previously reported. Misclassification of the exposure and the possible confounding effect of physical workload and psychological strain may have obscured a causal relation and therefore a minor effect cannot be ruled out. The results do not support the notion that fluorocarbons induce cardiac arrhythmia in occupationally exposed refrigerator repairmen.
PMCID: PMC1035134  PMID: 2328227
10.  Long-term follow up of workers exposed to solvents. 
Long term occupational exposure to organic solvents may cause adverse effects to the central nervous system. This collaborative study between six Swedish departments of occupational medicine examines the overall prognosis in terms of working capacity, symptoms, and psychometric test performance for individuals occupationally exposed to organic solvents. After re-analyses of the data from an initial clinical investigation of 111 men, the subjects were divided into two subgroups: one group of 65 with symptoms but no impairment on the tests and one group of 46 with toxic encephalopathy (symptoms and test impairment). At least five years after the initial examination the subjects were asked to attend a re-examination that included a structured medical interview and a psychometric investigation. The results indicate that effects on the central nervous system persist even when exposure has ceased. In the group of 46 more men had stopped working and were receiving sickness or early retirement pensions. This group also had reduced activity levels with regard to everyday life, leisure activities, and education or training and more neuropsychiatric symptoms. There was no support for the view that a solvent induced toxic encephalopathy is a progressive disease comparable with presenile dementia such as Alzheimer's disease or Pick's disease. If a worker was removed from exposure when he presented symptoms without signs of impairment in intellectual function recovery was seen in most cases.
PMCID: PMC1035105  PMID: 2178676
12.  Occupational exposure to formaldehyde and histopathological changes in the nasal mucosa. 
To study the cytotoxic effect of formaldehyde on the human nasal mucosa 75 men with occupational exposure to formaldehyde or to formaldehyde and wood dust, were examined, looking particularly at early signs of irritative effects and histopathological changes in the nasal mucosa. All men underwent a medical examination and a nasal biopsy specimen was examined by a pathologist and graded from 0-8 according to the morphological changes. A high frequency of nasal symptoms, mostly a running nose and crusting, was related to exposure to formaldehyde. Only three men had a normal mucosa; the remainder had loss of cilia and goblet cell hyperplasia (11%) and squamous metaplasia (78%); in six cases (8%) there was a mild dysplasia. The histological grading showed a significantly higher score when compared with unexposed contents (2.9 v 1.8). There was no dose response relation, no malignancies, and no difference in the histological score between those exposed to formaldehyde or to formaldehyde and wood dust.
PMCID: PMC1009694  PMID: 3203081
13.  Mortality and cancer incidence among workers in an abrasive manufacturing industry. 
Earlier epidemiological studies have shown that exposure to aluminium oxide and silicon carbide might carry with it an increased risk of lymphomas, stomach cancer, and non-malignant respiratory disease. To elucidate further this possible hazard, the cancer morbidity and the total mortality pattern was studied among 521 men manufacturing abrasive materials who had been exposed to aluminium oxide, silicon carbide, and formaldehyde. Total dust levels were in the range of 0.1-1.0 mg/m3. The cohort was followed up from 1958 until December 1983. No significant increase was found in total mortality, cancer mortality, or incidence of non-malignant respiratory diseases.
PMCID: PMC1007779  PMID: 3814536
14.  Lung function in workers using cadmium containing solders. 
The lung function of 57 male workers previously exposed to cadmium in connection with the use of cadmium containing solders was examined by spirometry (FVC, FEV1, FEV%, and MMF) and single breath nitrogen washout (CV, CV%, and phase III). A reference group (n = 31) from a nearby industry was examined at the same time. Despite the fact that the exposure in previous years had been relatively high, in the order of 0.05-0.5 mg Cd/m3, and that 24 (42%) of the workers had cadmium induced renal damage in the form of beta 2-microglobulinuria there was no evidence of pulmonary damage. There were no significant differences in lung function data from the exposed and reference group and there was no dose-response relation within the exposed group. It thus appears that signs of kidney toxicity in the form of low molecular weight proteinuria precede those that may be identified in the lung with commonly used lung function tests.
PMCID: PMC1007733  PMID: 3778835
15.  Cancer mortality among leather tanners. 
Workers were studied at a tannery that operated from 1873 to 1960, once one of the biggest in Scandinavia. The results show a slight numerical increase of deaths from cancer of the stomach and a significant, threefold excess mortality from cancer of the pancreas. Even in view of critical questions about validity it seems likely that this excess might be related to exposure to chemicals in tannery work.
PMCID: PMC1007690  PMID: 3718898
16.  Assessment of renal function in workers previously exposed to cadmium. 
Cadmium induced renal effects were examined in 60 workers (58 men, 2 women) previously exposed to cadmium. Tubular damage in the form of beta 2-microglobulinuria was found in 40%, and urinary albumin and orosomucoid increased significantly with increasing urinary cadmium and increasing relative clearance of beta 2-microglobulin. It is suggested that increased albumin excretion is secondary to the tubular damage. In no case was typical glomerular proteinuria found that could be related to cadmium. Histories of renal stones were more common among the workers with high urinary cadmium concentrations. The glomerular filtration rate was measured in 17 of the workers who had pronounced tubular dysfunction. The average glomerular filtration rate for these men was less than the age adjusted predicted value (mean = 84%). Furthermore, there was a significant (p less than 0.05) correlation (r = -0.47) between tubular reabsorption loss and a decreased glomerular filtration rate.
PMCID: PMC1007572  PMID: 3904816
17.  Radon daughter exposure and lung cancer. 
PMCID: PMC1007566  PMID: 4063214
18.  No acute behavioural effects of exposure to styrene: a safe level of exposure? 
To determine whether exposure to low levels of styrene (below 110 mg/m3) causes acute behavioural effects and symptoms that may be related to concentrations of styrene in air or urinary mandelic acid or both, 12 men occupationally exposed to styrene were studied and compared with a reference group of 10 unexposed men. Simple reaction time was measured before and after work and information about symptoms was obtained by questionnaire. Active and passive sampling of airborne styrene was carried out and urinary mandelic acid concentrations were measured. Although the size of the study groups is small, the results indicate that exposure to styrene below 110 mg/m3 does not cause any acute adverse effects on the central nervous system.
PMCID: PMC1007476  PMID: 3986140
19.  Raised serum bile acid concentrations after occupational exposure to styrene: a possible sign of hepatotoxicity? 
Fasting serum concentrations of conjugated bile acids were investigated in 23 men who had been exposed to styrene and compared with the concentrations in 60 non-exposed individuals. Eleven of the exposed subjects had raised concentrations of either cholic acid or chenodeoxycholic acid or both. There were no indications of alcohol abuse, drug intake, or undiagnosed liver disease. It is possible, therefore, that the raised bile acid concentrations were due to exposure to styrene. This would support the concept that occupational exposure to styrene may affect the liver and point to the possibility that raised serum bile acid concentrations might be a sensitive and early indicator of hepatic injury in individuals exposed to organic solvents.
PMCID: PMC1009293  PMID: 6722052
20.  Quantitative aspects of radon daughter exposure and lung cancer in underground miners. 
Epidemiological studies have shown an excessive incidence of lung cancer in miners with exposure to radon daughters. The various risk estimates have ranged from six to 47 excess cases per 10(6) person years and working level month, but the effect of smoking has not been fully evaluated. The present study, among a group of iron ore miners, is an attempt to obtain quantitative information about the risk of lung cancer due to radon and its daughters among smoking and non-smoking miners. The results show a considerable risk for miners to develop lung cancer; even non-smoking miners seem to be at a rather high risk. An additive effect of smoking and exposure to radon daughters is indicated and an estimate of about 30-40 excess cases per 10(6) person years and working level month seems to apply on a life time basis to both smoking and non-smoking miners aged over 50.
PMCID: PMC1009169  PMID: 6830715

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