Six year follow up of lung function in men occupationally exposed to formaldehyde.

The long term effects of formaldehyde on the respiratory tract have been investigated in a group of 164 workers exposed daily to the chemical during the production of urea formaldehyde resin, together with 129 workers not exposed to free formaldehyde. Exposure was classified as high (corresponding to an eight hour time weighted exposure of more than 2.0 ppm), medium (0.6 to 2.0 ppm), or low (0.1 to 0.5 ppm). Twenty five per cent of workers had had high exposure at some time and 17% moderate exposure. Both the exposed and unexposed groups had an annual assessment that included lung function. The proportion with self reported respiratory symptoms was similar in the two groups, 12% and 16% reporting breathlessness on hurrying and 26% and 20% wheezing. The initial forced expiratory volume in one second (FEV1) was within 0.5 l (approximately one standard deviation (SD)) of the predicted value (by age and height) in 65% of the exposed and 59% of unexposed workers and more than 0.5 l below the predicted value in 9% of exposed and 11% of unexposed workers. The mean decline in FEV1 was 42 ml a year (SD 45) in the exposed group and 41 ml a year in the unexposed group (SD 40 ml a year). The rate of decline showed the expected association with smoking in the unexposed group, but in the exposed group the mean rate of decline in the never smokers was similar to that in current smokers. There were, however, relatively few never smokers and considerable variation in the rates of decline. In the exposed group no association was found between the rate of decline and indices of exposure to formaldehyde. Thus there is no evidence from this study of an excess of respiratory symptoms or decline in lung function in the workers exposed to formaldehyde. The similar rate of decline of FEV1 however in never smokers and smokers of the exposed group is consistent with findings of other studies for workers exposed to formaldehyde and to toluene di-isocyanate.     

Six year follow up of lung function in men occupationally exposed to formaldehyde

The long term effects of formaldehyde on the respiratory tract have been investigated in a group of 164 workers exposed daily to the chemical during the production of urea formaldehyde resin, together with 129 workers not exposed to free formaldehyde. Exposure was classified as high (corresponding to an eight hour time weighted exposure of more than 2.0 ppm), medium (0.6 to 2.0 ppm), or low (0.1 to 0.5 ppm). Twenty five per cent of workers had had high exposure at some time and 17% moderate exposure. Both the exposed and unexposed groups had an annual assessment that included lung function. The proportion with self reported respiratory symptoms was similar in the two groups, 12% and 16% reporting breathlessness on hurrying and 26% and 20% wheezing. The initial forced expiratory volume in one second (FEV1) was within 0.5 l (approximately one standard deviation (SD)) of the predicted value (by age and height) in 65% of the exposed and 59% of unexposed workers and more than 0.5 l below the predicted value in 9% of exposed and 11% of unexposed workers. The mean decline in FEV1 was 42 ml a year (SD 45) in the exposed group and 41 ml a year in the unexposed group (SD 40 ml a year). The rate of decline showed the expected association with smoking in the unexposed group, but in the exposed group the mean rate of decline in the never smokers was similar to that in current smokers. There were, however, relatively few never smokers and considerable variation in the rates of decline. In the exposed group no association was found between the rate of decline and indices of exposure to formaldehyde. Thus there is no evidence from this study of an excess of respiratory symptoms or decline in lung function in the workers exposed to formaldehyde. The similar rate of decline of FEV1 however in never smokers and smokers of the exposed group is consistent with findings of other studies for workers exposed to formaldehyde and to toluene di-isocyanate.     

Workers exposed to ethylene oxide: a follow up study.

A cohort study has been carried out of 2876 men and women with potential exposure to ethylene oxide. Subjects were identified from employment records at four companies that have produced or used ethylene oxide since the 1950s and at eight hospitals which have had ethylene oxide sterilising units since the 1960s. The cohort represents a substantial proportion of the British workforce with a history of occupational exposure to ethylene oxide. Industrial hygiene data were not available before 1977, but since then time weighted average exposures have been less than 5 ppm in almost all jobs and less than 1 ppm in many. Past exposures were probably somewhat higher. In contrast to some previous studies, no clear excess of leukaemia (three deaths observed, 2.09 expected) and no increase in stomach cancer (five deaths observed, 5.95 expected) were found. This discrepancy with earlier reports may be due in part to differences in levels of exposure. Total cancer mortality was similar to that expected from national and local death rates. Some specific cancers showed small excesses but their relevance to ethylene oxide exposure is doubtful. Again, contrary to some earlier reports, no excess of cardiovascular disease was found. This study does not exclude the possibility that ethylene oxide is a human carcinogen but suggests that any risk of cancer from currently permitted occupational exposures is small.     

Ten year follow up of farmers with farmer''s lung.

Twenty-nine patients previously diagnosed as having suffered from farmer's lung in or before 1970 were asked whether the condition had recurred and what measures they had taken to avoid such recurrence. Those who had retired from farming had been least affected by recurrence, while those who continued to farm had been protected by making silage instead of hay or by wearing protective respirators. To be effective, a respirator should be worn on every occasion that farm dust is encountered and must be properly maintained.     

Workers exposed to ethylene oxide: a follow up study

A cohort study has been carried out of 2876 men and women with potential exposure to ethylene oxide. Subjects were identified from employment records at four companies that have produced or used ethylene oxide since the 1950s and at eight hospitals which have had ethylene oxide sterilising units since the 1960s. The cohort represents a substantial proportion of the British workforce with a history of occupational exposure to ethylene oxide. Industrial hygiene data were not available before 1977, but since then time weighted average exposures have been less than 5 ppm in almost all jobs and less than 1 ppm in many. Past exposures were probably somewhat higher. In contrast to some previous studies, no clear excess of leukaemia (three deaths observed, 2.09 expected) and no increase in stomach cancer (five deaths observed, 5.95 expected) were found. This discrepancy with earlier reports may be due in part to differences in levels of exposure. Total cancer mortality was similar to that expected from national and local death rates. Some specific cancers showed small excesses but their relevance to ethylene oxide exposure is doubtful. Again, contrary to some earlier reports, no excess of cardiovascular disease was found. This study does not exclude the possibility that ethylene oxide is a human carcinogen but suggests that any risk of cancer from currently permitted occupational exposures is small.     

Effects of intervention on the cardiovascular mortality of workers exposed to carbon disulphide: a 15 year follow up.

The cardiovascular mortality of a cohort of 343 Finnish men exposed for at least five years to carbon disulphide (CS2) in a viscose rayon plant has been monitored prospectively from 1967 to 1982. The results from the first five years of follow up in 1972 showed a 4.7-fold excess mortality for ischaemic and other heart diseases (ICD A83-A84) compared with a comparable reference cohort of paper mill workers. After 1972 a preventive intervention programme instituted at the rayon plant included removing all workers with coronary risk factors from exposure. Thus only 19% of the exposed cohort continued to be exposed in 1977 compared with 53% in 1972. Moreover, exposure levels were reduced after 1972 in compliance with the set hygienic standard of 10 ppm. These measures were reflected in a normalisation of the risk of cardiovascular death; the relative risk was 1.0 in the period after the intervention (1 July 1974 to 30 June 1982), whereas it had previously been 3.2 (from 1 July 1972 to 30 June 1974). The risk of a fatal heart attack remained at 11.6% throughout the 15 year follow up period (95% confidence limits 8.5%-15.4%) among the exposed compared with 7.8% (5.3%-11.2%) among the unexposed. The entire risk difference of 3.8% was accumulated during the first seven years of follow up. Thus we can estimate that 59 CS2-related cardiovascular deaths would have occurred during the next eight years (instead of the actual 19 deaths) had there been no preventive action. Calculations yielded a preventive fraction of 68%.     

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.     

A nine year follow up study of renal effects in workers exposed to cadmium in a zinc ore refinery.

Renal changes with time have been studied in 14 workers engaged in the production of cadmium (Cd) in a zinc ore refinery. These workers were examined once a year in the period 1980 to 1985 and 13 of them also in 1989. Four of the workers (group A) had been employed in an old Cd plant before 1973 and had received higher exposures to Cd than the other workers (group B). Average urinary Cd concentrations over the whole study period in workers of group A ranged from 6.9 to 9.2 micrograms/g creatinine (median 8.4 micrograms/g) and in workers of group B from 0.64 to 7.1 micrograms/g creatinine (median 1.9 micrograms/g). Renal effects were assessed by the determination of urinary N-acetyl-beta-D-glucosaminidase (NAG), beta 2-microglobulin (beta 2-M), retinol binding protein, albumin, total protein, and serum creatinine concentrations and activity. Urinary beta 2-M concentrations in three of four workers of group A were close to or marginally above the upper normal limit during the study period. The beta 2-microglobinuria was not, however, progressive. No values outside normal limits were detected for any of the other renal tests in workers of groups A and B, related to exposure to Cd. Dose-response relations showed that urinary Cd correlated significantly with urinary NAG activity and total protein and beta 2-M. The earliest change induced by Cd was seen for urinary NAG activity within normal limits of NAG excretion. The regression lines were similar in the surveys between 1981 and 1989, indicative of no progression to higher values for any of the renal tests. The current biological exposure index (BEI) of 10 micrograms/g creatinine for workers exposed to Cd, set by the American Conference of Governmental Industrial Hygienists (ACGIH), therefore seems justified, although the safety margin is small. The World Health Organisation recommended limit and ACGIH (1992-3) proposed limit of 5 micrograms/g creatinine would provide a much larger safety margin, and could be regarded as an action point for increased health surveillance.     

The Epping jaundice outbreak: a 24 year follow up.

STUDY OBJECTIVE--The aim was to trace 84 cases of jaundice that occurred following accidental ingestion of methylene dianiline (MDA) in Epping in 1965, and to look at long term health effects. DESIGN--The original case notes of the cases were used to identify the patients. Subsequent tracing procedures included local general practitioners, the Central NHS Registry, electoral rolls, and company records. SETTING--This was a community based survey. MAIN RESULTS--The health status of 68 (81%) of the group was established with 18 deaths. Of the 50 cases known to be alive, 58% completed a health questionnaire. The causes of death were unremarkable except for one case of carcinoma of the biliary tract. Two surviving cases had suffered retinal pathology. Four other surviving cases had had a further, perhaps unrelated, episode of jaundice. CONCLUSIONS--Although the dose and route of administration in the epidemic differed from occupational exposure, this follow up study a generation on provides little, if any, evidence of long term health sequelae. Nevertheless, in the absence of well documented exposure and health effects data, such accidental poisonings with proven animal carcinogens warrant long term follow up. The identified cohort will be the subject of further study.     

Effects of intervention on the cardiovascular mortality of workers exposed to carbon disulphide: a 15 year follow up

The cardiovascular mortality of a cohort of 343 Finnish men exposed for at least five years to carbon disulphide (CS2) in a viscose rayon plant has been monitored prospectively from 1967 to 1982. The results from the first five years of follow up in 1972 showed a 4.7-fold excess mortality for ischaemic and other heart diseases (ICD A83-A84) compared with a comparable reference cohort of paper mill workers. After 1972 a preventive intervention programme instituted at the rayon plant included removing all workers with coronary risk factors from exposure. Thus only 19% of the exposed cohort continued to be exposed in 1977 compared with 53% in 1972. Moreover, exposure levels were reduced after 1972 in compliance with the set hygienic standard of 10 ppm. These measures were reflected in a normalisation of the risk of cardiovascular death; the relative risk was 1.0 in the period after the intervention (1 July 1974 to 30 June 1982), whereas it had previously been 3.2 (from 1 July 1972 to 30 June 1974). The risk of a fatal heart attack remained at 11.6% throughout the 15 year follow up period (95% confidence limits 8.5%-15.4%) among the exposed compared with 7.8% (5.3%-11.2%) among the unexposed. The entire risk difference of 3.8% was accumulated during the first seven years of follow up. Thus we can estimate that 59 CS2-related cardiovascular deaths would have occurred during the next eight years (instead of the actual 19 deaths) had there been no preventive action. Calculations yielded a preventive fraction of 68%.     

Clinical reactions to Aspergillus niger in a biotechnology plant: an eight year follow up.

The manufacture of citric acid by fermentation of molasses with Aspergillus niger has previously been described as a cause of occupational asthma in a factory. A longitudinal survey of the workforce of this factory has been carried out from 1984 to 1991. Over this period 160 of the original 278 workers left the workforce, together with 39 of 76 new recruits. Partial enclosure of the process and exhaust ventilation, installed in 1984, was effective in preventing any new cases of occupational asthma over the eight year period, and no new skin sensitisation was detected. Spore counts of A niger averaged about 100 times those in the outside air. Health in the 1984 survey had a striking influence on subsequent retiral; only 11 of the 79 with respiratory symptoms remained in 1991, compared with 90 of the 182 with no symptoms. In conclusion A niger is a weak antigen and simple hygiene measures protect the workforce. Exclusion of recruits with positive skin tests is not necessary if such measures are taken. The survey provided evidence of the selection factors operating within a workforce over this period contributing to retiral of the less healthy.     

Ventilatory decrements in former asbestos cement workers: a four year follow up.

A four year follow up of the ventilatory function in former asbestos cement workers has been performed to determine whether any further decrease occurred after cessation of exposure. Seventy five of 125 subjects were eligible for re-examination and were compared with local referents. None showed signs of asbestosis but 32% had pleural plaques at the renewed examination. Cumulative asbestos exposure calculated as fibre x years had been estimated individually in the original examination. After adjustment for age, height, tracheal area, and smoking category the FVC and FEV1 for all exposed subjects were on average 7% v 6% less than predicted from the referents and twice as much for the subjects with the highest exposure. The four year declines in FVC and FEV1 were larger than in the referents, significantly so for FEV1. There were no significant correlations between pleural plaque and ventilatory function after adjustment for exposure. Thus the age adjusted reduction in ventilatory function had progressed during the follow up period despite the cessation of exposure and the lack of radiological signs of asbestosis.     

Health significance of cadmium induced renal dysfunction: a five year follow up.

To assess the health significance of the early renal changes after chronic exposure to cadmium, 23 workers removed from exposure because of the discovery of an increased urinary excretion of beta 2-microglobulin or retinol binding protein, or both, have been examined once a year for five years. Eight of these workers had also an increased albuminuria. These workers had been exposed to cadmium for six to 41.7 years (mean 25 years) and their first follow up examination took place when they had been removed from exposure for six years on average. At that time, their mean age was 58.6 years (range: 45.5-68.1). It has been confirmed that the proteinuria induced by cadmium is irreversible. The most important finding, however, is a significant increase of creatinine and beta 2-microglobulin concentrations in serum with time, indicating a progressive reduction of the glomerular filtration rate despite removal from exposure. It is estimated that on average this rate has decreased by 31 ml/min/1.73 m2 during the five year follow up study. This decrease is significantly greater (about five times) than that accounted for by aging and is not more pronounced in workers with impaired renal function at the start of the study than in those presenting only with subclinical signs of renal damage. Serum alkaline phosphatase activity also increases significantly with time. In conclusion, the present study indicates that the early renal changes induced by cadmium should be regarded as adverse effects; they are predictive of an exacerbation of the age related decline of the glomerular filtration rate.     

Two year follow up of pulmonary function values among welders in New Zealand

OBJECTIVES: To examine whether welding is a risk factor for an accelerated decline in pulmonary function. METHODS: 2 Year follow up of pulmonary function and respiratory symptoms among 54 welders and 38 non- welders in eight New Zealand welding sites. RESULTS: There were no significant differences in age, height, smoking habits, ethnicity, or total time in industrial work between welders and non-welders. No overall differences were noted in the changes of pulmonary function variables between the two study groups. However, when the comparison was restricted to smokers, welders had a significantly greater (p = 0.02) annual decline (88.8 ml) in FEV1 than non-welders, who had a slight non-significant annual increase (34.2 ml). Also, welders without respiratory protection or local exhaust ventilation while welding had a greater annual decline both in forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) than welders with protection (p = 0.001 and 0.04, respectively). Among welders a significant association was found between the acute across shift change and the annual decline in FEV1. Chronic bronchitis was more common among welders (24%) than non-welders (5%). Only one welder (2%) but eight non- welders (21%) reported having asthma. CONCLUSIONS: Welders who smoked and welders working without local exhaust ventilation or respiratory protection have an increased risk of accelerated decline in FEV1.

 

     

Lung function and radiographic signs of pulmonary fibrosis in oil exposed workers in a cable manufacturing company: a follow up study.

Thirty seven workers employed for at least three years in oil impregnation of cables during 1963-83 were followed up in 1990 to study the development of pulmonary fibrosis and consequences for lung function. They had been exposed to concentrations of mineral oil vapours of 50-100 mg/m3, and concentrations of oil mist of 0.5-1.5 mg/m3. All 29 living persons were traced. For each person one control matched for age, height, and smoking habits was selected. Among 25 workers followed up with radiographic studies, 10 cases of pulmonary fibrosis were found, by contrast with one case in the control group (p less than 0.01). Chest radiographs from 1979-80 and 1989-90 were reviewed. The profusion of small opacities increased in seven of 16 persons during 10 years without exposure. Seventeen workers had lung function tests. The bellows function (VC, FEV1, MVV) and lung volumes (TLC, RV) did not differ from those in the matched controls (p greater than 0.05), but the carbon monoxide transfer factor (TLCO) was decreased. The largest reduction of TLCO (1.5 mmol/kPa/min) was found among workers exposed for 10 years or more (p less than 0.05). Arterial blood gases were not affected at rest, but during maximum tread mill exercise, PO2 and HbO2 were reduced in exposed workers compared with controls, particularly among those exposed for at least 10 years (p less than 0.05). Exposure to low viscosity oil mist and vapour is the most plausible cause of the fibrosis. Unaffected bellows function, reduced TLCO, and decreased arterial blood oxygen during exercise is compatible with peribronchiolar fibrosis.     

Lung function and radiographic signs of pulmonary fibrosis in oil exposed workers in a cable manufacturing company: a follow up study.

Thirty seven workers employed for at least three years in oil impregnation of cables during 1963-83 were followed up in 1990 to study the development of pulmonary fibrosis and consequences for lung function. They had been exposed to concentrations of mineral oil vapours of 50-100 mg/m3, and concentrations of oil mist of 0.5-1.5 mg/m3. All 29 living persons were traced. For each person one control matched for age, height, and smoking habits was selected. Among 25 workers followed up with radiographic studies, 10 cases of pulmonary fibrosis were found, by contrast with one case in the control group (p less than 0.01). Chest radiographs from 1979-80 and 1989-90 were reviewed. The profusion of small opacities increased in seven of 16 persons during 10 years without exposure. Seventeen workers had lung function tests. The bellows function (VC, FEV1, MVV) and lung volumes (TLC, RV) did not differ from those in the matched controls (p greater than 0.05), but the carbon monoxide transfer factor (TLCO) was decreased. The largest reduction of TLCO (1.5 mmol/kPa/min) was found among workers exposed for 10 years or more (p less than 0.05). Arterial blood gases were not affected at rest, but during maximum tread mill exercise, PO2 and HbO2 were reduced in exposed workers compared with controls, particularly among those exposed for at least 10 years (p less than 0.05). Exposure to low viscosity oil mist and vapour is the most plausible cause of the fibrosis. Unaffected bellows function, reduced TLCO, and decreased arterial blood oxygen during exercise is compatible with peribronchiolar fibrosis.     

Mortality of workers exposed to ethylene oxide: extended follow up of a British cohort

Aims: To obtain further information about the risks of cancer associated with occupational exposure to ethylene oxide

Methods: Follow up was extended by 13 years for a cohort of 2876 men and women with definite or potential exposure to ethylene oxide in the chemical industry or in hospital sterilising units. Subjects were traced through National Health Service and social security records, and their mortality was compared with that expected from rates in the national population by the person-years method.

Results: Analysis was based on 565 deaths, of which 339 had occurred during the additional period of follow up. Mortality was close to or below expectation for all causes (565 deaths v 607.6 expected), all cancers (188 v 184.2), and for all specific categories of malignancy including stomach cancer (10 v 11.6), breast cancer (11 v 13.2), non-Hodgkin's lymphoma (7 v 4.8), and leukaemia (5 v 4.6). All five deaths from leukaemia occurred in the subset of subjects with greatest potential for exposure to ethylene oxide, but even in this group the excess of deaths was small (2.6 expected).

Conclusions: The balance of evidence from this and other epidemiological investigations indicates that any risk of human cancer from ethylene oxide is low, particularly at the levels of occupational exposure that have occurred in Britain over recent decades. This may reflect the capacity of human cells to repair DNA damage caused by the chemical, which is a potent genotoxin and animal carcinogen.

     

Health and re-employment in a two year follow up of long term unemployed.

STUDY OBJECTIVE--The aim was to examine re-employment and changes in health during a two year follow up of a representative sample of long term unemployed. DESIGN--This was a cross sectional study and a two year follow up. Health was measured by psychometric testing, Hopkins symptom checklist, General health questionnaire, and medical examination. Health related selection to continuous unemployment and recovery by re-employment was estimated by logistic regression with covariances deduced from the labour market theories of human capital and segmented labour market. SETTING--Four municipalities in Greenland, southern Norway. SUBJECTS--Participants were a random sample of 17 to 63 year old people registered as unemployed for more than 12 weeks. MAIN RESULTS--In the cross sectional study, the prevalence of depression, anxiety, and somatic illness was from four to 10 times higher than in a control group of employed people. In the follow up study, there was considerable health related selection to re-employment. A psychiatric diagnosis was associated with a 70% reduction in chances of obtaining a job. Normal performance on psychometric testing showed a two to three times increased chance of re-employment. Recovery of health following re-employment was less than expected from previous studies. CONCLUSIONS--Health related selection to long term unemployment seems to explain a substantial part of the excess mental morbidity among unemployed people. An increased proportion of the long term unemployed will be vocationally handicapped as years pass, putting a heavy burden on social services.     

Loss and representativeness in a 43 year follow up of a national birth cohort.

STUDY OBJECTIVE--The aim was to describe rates of loss and assessment of representativeness during 43 years of a national birth cohort study. DESIGN--The study population is a class stratified random sample of all single, legitimate births that occurred during one single week in 1946; it has been studied at regular intervals, so far to 1989. MAIN RESULTS--Losses through death and emigration were comparable to those in the national population of the same age. Response rates from the population resident in Britain have remained high, and the responding population is in most respects representative of the native population born in the early postwar years. Response rates within some serious physical illnesses did not differ from those of the healthy population. CONCLUSIONS--The continuing high response rate and representativeness of this national birth cohort is likely to be the result of home based data collections and of the regular contact to provide feedback of information and to check addresses of the study population.