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Biomedical subjects

J T Carter

Publications and source records attributed to J T Carter.

At least 37 records · Page 2Linked to original sources
PubMed1988

Occupational toxicology.

1. Toxicology plays an important part in the prevention of work related disease. 2. The toxic effects of substances used at work are similar to those of other types of chemical, hence similar methods of investigation are used. 3. A very wide range of substances is used at work. The conditions of use determine the degree of exposure and the likelihood of adverse effects. 4. The scope for control of risks depends on a knowledge of likely adverse effects and the availability of technical and managerial means for reducing exposure. 5. The relationships between the employee, his employer, suppliers, expert advisers and the regulatory authorities determine the effectiveness with which toxic risks are identified and control measures implemented.

Environmental Exposure↗
PubMed1984

Genotoxicity studies on di-(2-ethylhexyl) phthalate and adipate and toxicity studies on di-(2-ethylhexyl) phthalate in the rat and marmoset.

These studies have provided evidence that DEHP and DEHA do not bind covalently to DNA and do not therefore possess the characteristics of a genotoxic agent (Lutz, 1982). This suggests that the tumours induced in the rodent liver may result from some non-genotoxic mechanism and supports the view that the weakly positive dominant lethal test seen on administration of DEHP by the ip (but not the oral) route (Singh et al. 1974) is unlikely to have resulted from a direct effect on the genome of the sperm cells. Although the mechanism responsible for the induction of tumours by high doses of DEHP in rodents is not clear, it would appear both from these studies and from work on hypolipidaemic agents, that peroxisomal proliferation and the induction of enzymes associated with this organelle are in some way implicated (Cohen & Grasso, 1981). Other studies have shown that changes of this type are produced by doses of hypolipidaemic agents that induce liver cancer in rodents (Cohen & Grasso, 1981) and our investigations have indicated that they were also prominent at dose levels of DEHP similar to those that induced liver cancer in the NCI study (National Toxicology Program, 1982). No cancer induction would be expected to occur in the absence of these changes. In our dose-response study in rats it was shown that at the lowest dose (50 mg/kg body weight/day, approximately equivalent to a dietary level of 1000 ppm) several effects seen with higher doses were not apparent and others differed only slightly from normal control values. This is particularly relevant to assessments of the risk posed by DEHP and DEHA present as contaminants in foods, since human exposure via the food chain has been estimated by Shiota, Chou & Nishimura (1980) as 30 micrograms/kg body weight/day, several orders of magnitude less than the lowest exposure level used in these experiments. In addition, our studies indicate that none of the changes found in the rat were observed in the marmoset, suggesting that rodents and primates differ fundamentally in their hepatic and testicular response to DEHP. Previous studies by other authors (reviewed by Cohen & Grasso, 1981) indicated that morphological changes in the endoplasmic reticulum and the proliferation of peroxisomes are not features of the response of monkeys and man to high doses of hypolipidaemic agents.(ABSTRACT TRUNCATED AT 400 WORDS)

Adipates↗
PubMed1981

Mortality of United Kingdom acrylonitrile polymerisation workers.

The mortality of 1111 men who worked on the polymerisation of acrylonitrile and the spinning of acrylic fibre from 1950 to 1968 was surveyed up to the end of 1978. Seventy-nine deaths were identified. The population was drawn from six factories, where polymerisation started before 1968, in England, Wales, Scotland, and Northern Ireland. In the group of men exposed to acrylonitrile for at least one year the total number of deaths was smaller than expected. An excess of deaths from all cancers was found, arising mainly from cancers of the lung, stomach, colon, and brain, but the excess was not statistically significant. Significant excesses of stomach cancer overall and in those aged 55-64, and of lung cancer in those aged 15-44 were found. Consideration of deaths according to factory indicated that the excesses of stomach cancer may have been due to regional factors. The excess of lung cancer was investigated further in view of the fact that, unusually, it occurred in relatively young men, but no consistent difference between the duration of exposure to acrylonitrile of the three young patients with lung cancer and matched controls was found. The study is limited and further analysis in the future is needed. The results are not conclusive and neither add to nor detract from existing suspicions that acrylonitrile is a human carcinogen but, taken together with evidence from other studies, indicate the necessity for the continuing surveillance of the exposed population in the United Kingdom.

Acrylonitrile↗
PubMed1976

Absence attributed to sickness in oil tanker crews.

Absences attributed to sickness were investigated in 1410 deck and engine-room crew members during a period of two years and five months. The mean frequency of absences was 0-23 per man year, with a mean duration per absence of 41 days. The absence frequency varied with both rank and place of work. Altogether 23% of deck officers serving throughout the study and 43% of engine-room ratings had one or more absences. Spells of absence in young officers were five times more frequent when they were on leave than at sea. In the younger officers more than half of all spells that were initiated while on leave occurred at the end of the leave period. The contrasting environments of ship and shore allow the relative importance of effects on absence frequency of the work and home environment and of medical and social factors to be considered separately.

Absenteeism↗
PubMed1975

Mortality study of workers in a polyvinyl-chloride production plant.

Age-standardised mortality-rates for a population of 2100 male workers exposed to vinyl chloride for periods of up to 27 years do not show any excess of total or cause-specific mortality. 1 case of angiosarcoma of the liver was identified just outside the study period. There was no suggestion of an increased frequency of deaths from the more common malignant diseases.

Adult↗