British Journal of Industrial Medicine最新文献

A cohort study of workers exposed to formaldehyde in the British chemical industry in any one of six factories has been extended after the earlier published report in 1984. A further eight years of follow up to the end of 1989 have been included for the originally reported 7660 workers first employed before 1965, and a first follow up to the same date has been carried out for 6357 workers first employed since 1964. Extensive checking of the database has taken place including records at the factories, the MRC Environmental Epidemiology Unit, and the National Health Service Central Register. The updated findings include one death from nasal cancer compared with 1.7 expected in this number of men during the follow up period--which gives no support to the original hypothesis based on animal experimental data that formaldehyde may be a nasal carcinogen in humans. There have been no cases of nasopharyngeal cancer in the cohort compared with an estimated 1.3 expected--which gives no support to the findings in a similarly designed study in the United States of an excess of cancers of the nasopharynx associated with exposure to formaldehyde. There has been a slight excess of about 12% for lung cancer with 402 deaths compared with about 359 expected. This is similar to that found in the United States study, but higher than we reported earlier before the checking procedures and extended follow up. Further analysis gives no definitive indication of this excess of lung cancer being clearly related to formaldehyde exposure, and the increase is within that generally thought consistent with possible confounding effects of cigarette smoking (although no data are available on this point).

Several organs (lung, skin, thyroid, heart, bone marrow) are potential targets of cobalt (Co). Whereas there is no doubt that inhalation of Co alone may cause bronchial asthma, its role in the occurrence of hard metal disease is still controversial because most cases were reported in workers exposed not only to Co but also to other substances such as tungsten carbide, titanium carbide, iron, silica and diamond. To assess whether exposure to pure Co dust (metal, oxides, or salts) may lead to adverse health effects a cross sectional study was carried out among 82 workers in a Co refinery. The results were compared with those in a sex and age matched control group. The Co group had been exposed for 8.0 years on average (range 0.3-39.4). The geometric mean time weighted average exposure assessed with personal samplers (n = 82) was about 125 micrograms/m3 and 25% of the values were higher than 500 micrograms/m3. The concentrations of Co in blood and in urine after the shift were significantly correlated with those in air. Concentration of Co in urine increased during the workweek. A slight interference with thyroid metabolism (decreased T3, T4, and increased TSH), a slight reduction of some erythropoietic variables (red blood cells, haemoglobin, packed cell volume) and increased white cell count were found in the exposed workers. The exposed workers complained more often of dyspnoea and wheezing and had significantly more skin lesions (eczema, erythema) than control workers. Within the exposed group a dose-effect relation was found between the reduction of the forced expiratory volume in one second/vital capacity and the intensity of current exposure to Co assessed by the measurement of Co in air or in urine. The prevalence of dyspnoea was related to the dustiness of the workplace as reflected by statistically significant logistic regression between this symptom and the current levels of Co in air and in urine. No difference between lung volumes, ventilatory performances, carbon monoxide diffusing capacity, and serum myocardial creatine kinase and procollagen III peptide was found between the Co and control groups and no lung abnormalities were detected on the chest radiographs in both groups. The results suggest that exposure to high airborne concentrations of Co alone is not sufficient to cause pulmonary fibrosis. This finding is compatible with experimental studies indicating that interaction of other airborne pollutants with Co particles play a part in the pathogenesis of parenchymal lung lesions.

The relations between osteoarticular disorders and occupational exposure to heavy physical work factors were studied in a random sample of retired subjects living in the Paris area, all of whom had contributed to the same retirement pension fund. 627 subjects were originally seen in 1982-3 and 464 of them were seen again five years later. On both occasions, the same questionnaire was completed during a home interview. Osteoarticular disorders were evaluated by the presence of pain, with or without restricted joint movement, for at least six months before interview. The heavy physical work factors were those reported by the subject at the first interview, and only subjects who stated that they had been exposed to these factors for more than 10 years were considered as exposed persons. For those who were seen twice, the frequency of osteoarticular pain increased during the five years between the two interviews, from 52% to 65% in the men and 72% to 82% in the women. Among both sexes, these frequencies were significantly higher in those who stated that in the past they had to carry heavy weights and work in tiring positions. The increases in frequency of pain during the five year study period were also related to these occupational factors. In general, the frequencies for subjects not exposed to occupational factors caught up with those found for the exposed group. This interaction of age with the relation between exposure to heavy physical work factors and osteoarticular disorders does not seem to be explained by confounding factors, including age at the first interview, the fact of living alone, of being a former manual worker, of having a cardiorespiratory disorder, and smoking habits. The results of the survey suggest that working conditions are an important cause of osteoarticular disorders that last well beyond the end of working life.

A case-control study of malignant and non-malignant respiratory disease among employees of the Owens-Corning Fiberglas Corporation's Newark, Ohio plant was undertaken. The aim was to determine the extent to which exposures to substances in the Newark plant environment, to non-workplace factors, or to a combination may play a part in the risk of mortality from respiratory disease among workers in this plant. A historical environmental reconstruction of the plant was undertaken to characterise the exposure profile for workers in this plant from its beginnings in 1934 to the end of 1987. The exposure profile provided estimates of cumulative exposure to respirable fibres, fine fibres, asbestos, talc, formaldehyde, silica, and asphalt fumes. Employment histories from Owens-Corning Fiberglas provided information on employment characteristics (duration of employment, year of hire, age at first hire) and an interview survey obtained information on demographic characteristics (birthdate, race, education, marital state, parent's ethnic background, and place of birth), lifetime residence, occupational and smoking histories, hobbies, and personal and family medical history. Matched, unadjusted odds ratios (ORs) were used to assess the association between lung cancer or non-malignant respiratory disease and the cumulative exposure history, demographic characteristics, and employment variables. Only the smoking variables and employment characteristics (year of hire and age at first hire) were statistically significant for lung cancer. For non-malignant respiratory disease, only the smoking variables were statistically significant in the univariate analysis. Of the variables entered into a conditional logistic regression model for lung cancer, only smoking (smoked for six months or more v never smoked: OR = 26.17, 95% confidence interval (95% CI) 3.316-206.5) and age at first hire (35 and over v less than 35: OR = 0.244, 95% CI 0.083-0.717) were statistically significant. There were, however, increased ORs for year of employment (first hired before 1945 v first hire after 1945: OR = 1.944, 95% CI 0.850-4.445), talc (cumulative exposure >1000 fibres/ml days v never exposed: OR = 1.355, 95% CI 0.407-5.515), and asphalt fumes (cumulative exposure >0.01 mg/m(3) days v never exposed: OR 1.131, 95% CI 0.468-2.730). For non-malignant respiratory disease, only the smoking variable was significant in the conditional logistic regression analysis (OR = 2.637, 95% CI 1.146-6.069). There were raised ORs for the higher cumulative exposure categories for respirable fibres, asbestos, silica, and asphalt fumes. For both silica and asphalt fumes, ORs were more than double the reference groups for all exposure categories. A limited number of subjects were exposed to fine fibres. The scarcity of cases and controls limits the extent to which analyses for fine fibre may be carried out. Within those limitations, among those who had worked with fine fibre, the unadjusted, unmatc

Measurements of the concentrations of smoke, lead, and five polycyclic hydrocarbons in the air have been made in the City of London in the middle of a busy street and at two control sites. Samples were taken only throughout the daytime hours on weekdays to enable us to assess the maximum contribution made by traffic to the pollution in the street. The results showed that during these periods the air in the middle of the street contained three times as much smoke, four times as much lead, and 1.7 times as much 3:4-benzpyrene as were present in the general atmosphere as the City of London as estimated from samples taken at the control sites. One of these sites was chosen because it was only 150 feet away from the street; analyses yielded no evidence that the traffic contributed to the pollution sampled there. Sulphur dioxide concentrations were determined in the early part of the study and the results showed that traffic appeared to add little to the background level. The concentrations of lead found were below those held to be safe by many authorities. Carbon monoxide concentrations, reported in greater detail elsewhere, sometimes reached the accepted industrial maximum allowable concentration of 100 p.p.m.

Computed tomography (CT; both conventional (CCT) and high resolution (HRCT)) scans of the thorax were evaluated to detect early asbestosis in 61 subjects exposed to asbestos dust in Québec for an average of 22(3) years and in five controls. The study was limited to consecutive cases with chest radiographs of the International Labour Organisation categories 0 or 1 determined independently. All subjects had a standard high kilovoltage posteroanterior and lateral chest radiograph, a set of 10-15 1 cm collimation CCT scans and a set of three to five 2 mm collimation HRCT scans in the upper, middle, and lower lung fields. Five experienced readers independently read each chest radiograph and sets of CT scans. On the basis of three to five readers agreeing for small opacities of the lung parenchyma, 12/46 (26%) negative chest radiographs were positive on CT scans, but 6/18 (33%) positive chest radiographs were negative on CT scan. On the basis of four to five readers agreeing on a chest radiograph, 36/66 (54%) subjects were normal (group A), 17/66 (26%) were indeterminate (group B), and 13/66 (20%) were abnormal (group C). By the combined readings of CCT and HRCT, 4/31 (13%) asbestos exposed subjects of group A were abnormal (p < 0.001), 6/17 (35%) of group B were abnormal, and in group C, 1/13 (8%) was normal, 2/13 were indeterminate, and 10/13 (77%) were abnormal. Separate readings of CCT and HRCT on distinct films in 14 subjects showed that all cases of asbestosis were abnormal on both CCT and HRCT. Inter-reader analyses by kappa statistics showed significantly better agreement for the readings of CT than the chest radiographs (p < 0.001), and for the reading of CCT than HRCT (p < 0.01). Thus CT scans of the thorax identifies significantly more irregular opacities consistent with the diagnosis of asbestosis than the chest radiograph (20 cases on CT scans v 13 on chest radiographs when four to five readers agreed, 13% of asbestos exposed subjects with normal chest radiographs or 21% of asbestos exposed subjects with normal or near normal chest radiographs. It decreased the number of indeterminate cases significantly from 17 on chest radiographs to 13 on CT scans. All cases of asbestosis detected only on CT scans were similarly seen on CCT and HRCT and did not have significant changes in lung function. The CT scans significantly reduced the inter-reader variability, despite the absence of ILO type reference films for these scans.

Two groups, each of six guinea pigs, were sensitised by the application of cobalt chloride (CoCl2) on the skin on day 0, 2, 7, and 9 and the establishment of contact allergy was confirmed by patch testing on day 21. A further six animals were not sensitised. Starting on day 42 one sensitised group and the non-sensitised group were exposed by inhalation to 2.4 (0.8) mg (mean (SD)) Co in the form of CoCl2 for six hours a day for two weeks. After exposure the lungs were lavaged and the cells obtained were studied by light and electron microscopy. In the sensitised exposed group much more lavage liquid was retained in the lungs than in the other two groups; although more liquid was instilled in the lungs of this group, on average only 5 (range 2.5-10) ml were recovered compared with 10 ml in all animals in the other two groups. In the sensitised exposed group, the percentage of neutrophils and eosinophils tended to be higher than in the non-sensitised exposed group. The results indicate that the lungs of guinea pigs allergic to contact with Co react differently to inhaled Co compared with those of non-sensitised ones.