British Journal of Industrial Medicine最新文献

It has previously been shown that granite workers with heavy exposure to silica had glomerular and proximal tubular dysfunction evidenced by increased urinary excretions of albumin, alpha-1-microglobulin (AMG), and beta-N-acetyl-glucosaminidase (NAG). The investigation was replicated in another group of granite workers to further elucidate the exposure effect relation. The urinary excretion of albumin, alpha-1-microglobulin (AMG), beta-2-microglobulin (BMG), and beta-N-acetyl-glucosaminidase (NAG) was determined in two groups of granite workers with low and high exposure to silica. Low molecular weight proteinuria and enzymuria were significantly correlated with duration of exposure in the high but not the low exposure group. These increases were most pronounced in those with 10 or more years of heavy exposure, and in those with radiological evidence of pulmonary fibrosis, particularly those with rounded small opacities denoting classical silicosis. These results provide further evidence that prolonged and heavy exposure to silica is associated with nephrotoxic effects in granite workers.

The association between exposure to dust and pulmonary function was studied by longitudinal and cross sectional analyses in a group of United States underground coal miners beginning work in or after 1970. Quantitative estimates of exposure to respirable coal mine dust were derived from air samples taken periodically over the entire study period. The cohort included 977 miners examined both in round 2 (R2) (1972-5) and round 4 (R4) (1985-8) of the National Study of Coal Workers' Pneumoconiosis. Multiple linear regression models were developed for both cross sectional (pulmonary function at R2 and R4) and longitudinal (change in pulmonary function between R2 and R4) analyses with exposure partitioned into pre-R2 and post-R2 periods and controlled for covariates including smoking history. The results indicate a rapid initial (at R2) loss of FVC and FEV1 in association with cumulative exposure of the order of 30 ml per mg/m3-years. Between R2 and R4 (about 13 years) no additional loss of function related to dust exposure was detected although the percentage of predicted FVC and FEV1 did decline over the period. After some 15 years since first exposure (at R4), a statistically significant association of cumulative exposure with FEV1 of about -5.9 ml per mg/m3-years was found. These results indicate a significant non-linear effect of exposure to dust on pulmonary function at dust concentrations present after regulations took effect. The initial responses in both the FVC and FEV1 are consistent with inflammation of the small airways in response to exposure to dust.

Incidence of cancer and mortality were studied among 674 men exposed to mercury vapour for more than one year at two chloralkali plants. Mercury excretion in urine had been monitored among the workers at the two plants since 1948 and 1949. An individual cumulative urinary mercury dose was calculated, based on about 20,000 urinary mercury measurements. The incidence of cancer and the mortality were followed up from 1953 to 1989 and 1953 to 1988 respectively. The general Norwegian male population served as a reference population. There was a lung cancer excess of borderline significance (standardised incidence ratio = 1.66, 95% confidence interval = 1.00-2.59). The introduction of a 10 year latent period before developing lung cancer did not increase the incidence ratio. The excess may be partly explained by the smoking habits in the cohort or possibly by exposure to asbestos. No excess of cancer was found in the target organs for mercury toxicity--namely, the kidney and the nervous system. No significant excess mortality was found for nephritis and nephrosis or nonmalignant diseases of the nervous system.

Mortality trends for 1059 production workers at a rubber chemicals plant in Nitro, West Virginia were examined to find whether they had increased mortality from cancer associated with exposure to 2-mercaptobenzothiazole (MBT). This chemical and its derivatives are vulcanising agents that have been manufactured at the plant since 1935. Analyses were conducted on MBT exposed employees by cumulative exposure and time since first exposure, and were also stratified by past assignment to p-aminobiphenyl (PAB) related departments; PAB is a potent bladder carcinogen that was used at the plant between 1935 and 1955. There was an excess of bladder cancer in MBT workers who had PAB related assignments (standardised mortality ratio (SMR) = 3200, 95% confidence interval (95% CI) 1286-6593). In employees without a job assignment with exposure to PAB, there were no associations between exposure to MBT and increased rates of most malignant neoplasms. The SMR for bladder cancer was increased based on three deaths (SMR = 455, 95% CI 94-1328), although these results were too few to evaluate trends by cumulative exposure category. The possibility of confounding by PAB for exposures for jobs that covered all areas of the plant for these three cases must be considered in the light of the potency of PAB as a bladder carcinogen. There were no deaths from bladder cancer among MBT workers hired after the end of manufacture and use of PAB, but the expected number of deaths was only 0.03.

Mortality from lung cancer was greater in Ontario uranium miners than in the general male population of Ontario (observed = 152, expected = 67.6, standardised mortality ratio 225, 95% confidence interval 191-264). Part of the excess of lung cancer may be because the proportion of men who are smokers or have smoked is greater in uranium miners than in Ontario men. Smoking does not explain the whole excess. Mortality from lung cancer in Ontario uranium miners is clearly related to exposure to short lived radon progeny. The excess relative risk of lung cancer from the same degree of exposure to short lived radon progeny is greatest five to 14 years after exposure and less subsequently. It is greater in men under the age of 55 years and less in older men. Part of the excess of lung cancer mortality in Ontario uranium miners is probably also due to exposure to arsenic that occurred earlier in gold mines. In Ontario uranium miners, the lung cancer mortality from exposure to arsenic increases as the intensity of exposure to short lived radon progeny increases. This finding is consistent with the hypothesis that the risk of lung cancer from exposure to arsenic is enhanced by exposure to other carcinogens. In Ontario uranium miners, the proportion of lung cancers that are small cell carcinomas is greater than in the general population. The proportion of small cell carcinomas is especially great five to 14 years after exposure to short lived radon progeny and in men who die from lung cancer at younger ages.

The objective of this study was to evaluate the combined effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor (TNF) by alveolar macrophages. Rats were exposed to cigarette smoke in vivo, and production of TNF by alveolar macrophages was measured in the presence of mineral fibres in vitro. For smoke exposure, rats were divided into two groups. Five were exposed to a daily concentration of 10 mg/m3 of cigarette smoke for an eight hour period, and five rats (controls) were not exposed to smoke. Bronchoalveolar lavage was performed after exposure to smoke and the recovered alveolar macrophages were incubated with either chrysotile or ceramic fibres on a microplate for 24 hours. Activity of TNF in the supernatant was determined by the L-929 fibroblast cell bioassay. When alveolar macrophages were not stimulated by mineral fibres, production of TNF by rats exposed to smoke and unexposed rats was essentially the same. When alveolar macrophages were stimulated in vitro by chrysotile or ceramic fibres, production of TNF by alveolar macrophages from rats exposed to smoke was higher than that by alveolar macrophages from unexposed rats. The findings suggest that cigarette smoke and mineral fibres have a synergistic effect on TNF production by alveolar macrophages.

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).

The study investigates mortality from cancer and other diseases in a cohort of wives of asbestos cement workers in Casale Monferrato (northwest Italy). After the exclusion of women with an occupational record in the asbestos cement industry, the cohort comprised 1964 women. Their domestic exposure was estimated according to their husbands' periods of employment in the plant: 1740 had a period of domestic exposure whereas the remaining 224 married an asbestos cement worker only after he definitely stopped his activity in the asbestos cement plant; these have, therefore, been considered as unexposed. The cohort of wives was constructed entirely through official records in the town offices and is both exhaustive and unaffected by recall bias. At the end of follow up (1988) 1669 women were alive, 270 were dead and 25 (1.2%) were untraced. Main mortality analyses were only up to age 79 to reduce the misclassification of causes of death. Expected mortality was based on local rates. Mortality analyses were limited to the period 1965-88 due to the availability of local rates: in that period 210 deaths occurred among women with domestic exposure v 229.1 expected. There were four deaths from pleural tumours (one diagnosed as mesothelioma at necropsis) and six from lung cancer v. 0.5 and 4.0 expected respectively. Two further cases of mesothelioma were diagnosed by histological examination after the end of follow up. None of the three wives with histologically diagnosed mesothelioma had been engaged in industrial activities. Corresponding information for the other three cases could not be traced.