Relationships between non-occupational cadmium exposure and expression of nine cytochrome P450 forms in human liver and kidney cortex samples

This study was undertaken to assess associations between age, gender, cigarette smoke and non-workplace cadmium exposure, and liver pathology and inter-individual variation in cytochrome P450 (CYP) expression in human tissues. Autopsy specimens of twenty-eight Queensland residents whose ages ranged from 3 to 89 years were analyzed for the presence of nine CYP protein isoforms by immunoblotting. All subjects were Caucasians and their liver cadmium contents ranged from 0.11 to 3.95 kg/g wet weight, while their kidney cadmium contents were in the range of 2 to 63 mug/g wet weight. CYP1A2, CYP2A6, CYP2D6, CYP3A4, and CYP3A5 were detected in liver but not in kidney, and CYP1A1 and CYP1B1 were not found in liver or kidney. Lowered liver CYP2C8/19 protein contents were found to be associated with liver pathology. Importantly, we show elevated levels of CYP2C9 protein to be associated with cadmium accumulation in liver. No mechanism that explains this association is apparent, but there are two possibilities that require further study. One is that variation in CYP2C9 protein levels may be, in part, attributed to an individual's non-workplace exposure to cadmium, or an individual's CYP2C9 genotype may be a risk factor for cadmium accumulation. A positive correlation was found between liver CYP3A4 protein and subject age. Levels of liver CYPIA2 protein, but not other CYP forms, were increased in people more exposed to cigarette smoke, but there was no association between CYPIA2 protein and cadmium. CYP2A6 protein was found in all liver samples and CYP2A6 gene typing indicated the absence of CYP2A6 null allele (CYP2A6(D)) in this sample group, confirming very low prevalence of homozygous CYP2A6(D) in Caucasians. CYP2A6 gene types W/W, WIC, and CIC were not associated with variations in liver microsomal CYP2A6 protein. CYP2D6 protein was absent in all twenty-five kidney samples tested but was detectable in liver samples of all but two subjects, indicating the prevalence of the CYP2D6 null allele (CYP2D6(D)) in this sample group to be about 7%, typical of Caucasian populations. (C) 2001 Elsevier Science Inc. All rights reserved.

Intervention Trial to Assess Arsenic Exposure from Food Crops in Bangladesh

The authors assessed the contribution of food irrigated with arsenic-contaminated water to human exposure to arsenic in Bangladesh. An intervention trial was conducted in a village in the Jessore District of Bangladesh, where irrigation water had been field-tested in March 2000 and was found to contain arsenic with concentrations ranging from 100 to 500 mu g/l. In May 2000, a random sample of 63 households was selected from the village, and I eligible person from each household was recruited to the study and randomized to an intervention or control group. The intervention group received food purchased from a village where irrigation water was found to contain 100 mu g/l arsenic. Pre- and postintervention urine samples were collected for urinary arsenic speciation assays. Preintervention, the mean urinary total arsenic concentrations were 139.25 mu g/l and 129.15 mu g/l for the intervention and control groups, respectively. These concentrations did not change significantly following intervention. Arsenic concentrations in samples of selected raw and cooked foods from the low-contamination area did not contain less arsenic than samples from the high-contamination area. Further studies to investigate the arsenic content of food grown in areas with high and low arsenic contamination of irrigation water are recommended.

Speciation of arsenic metabolites in the urine of occupational workers and experimental rats using an optimised hydride cold-trapping method

A hydride cold-trapping technique was developed and optimised for the measurement of urinary arsenic metabolites. The analytical precision of the method was found to be 6.1, 4.0 and 4.8% (n = 5) for inorganic arsenic (As-i), monomethylarsonate (MMA) and dimethylarsinate (DMA), respectively, with recoveries close to 100%, The detection limits were 1.0, 1.3 and 3 ng for As-i, MMA and DMA, respectively. The method was then used to analyse urine samples obtained from three groups of workers for occupational exposure in three companies where copper chrome arsenate was used for timber treatment. The results were compared with those for a normal control group of laboratory workers. Arsenic and its metabolites were also measured in experimental rats given 5 mg As kg(-1) body mass by oral gavage in the form of sodium arsenite, calcium arsenite or sodium arsenate. Occupational workers showed a significantly higher excretion of As-i, Up to two fold increases of urinary As-i excretion in rats compared with control rats were also observed in animals dosed with various forms of arsenicals. The method is suitable for the measurement of arsenic metabolites in urine of both humans and experimental animals.

Exposure of rats to a high but not low dose of ethanol during early postnatal life increases the rate of loss of optic nerve axons and decreases the rate of myelination

Visual system abnormalities are commonly encountered in the fetal alcohol syndrome although the level of exposure at which they become manifest is uncertain. In this study we have examined the effects of either low (ETLD) or high dose (ETHD) ethanol, given between postnatal days 4-9, on the axons of the rat optic nerve. Rats were exposed to ethanol vapour in a special chamber for a period of 3 h per day during the treatment period. The blood alcohol concentration in the ETLD animals averaged similar to 171 mg/dl and in the ETHD animals similar to 430 mg/dl at the end of the treatment on any given day. Groups of 10 and 30-d-old mother-reared control (MRC), separation control (SC), ETLD and ETHD rats were anaesthetised with an intraperitoneal injection or ketamine and xylazine, and killed by intracardiac perfusion with phosphate-buffered glutaraldehyde. In the 10-d-old rat optic nerves there was a total of similar to 145000-165000 axons in MRC, SC and ETLD animals. About 4 % of these fibres were myelinated. The differences between these groups were not statistically significant. However, the 10-d-old ETHD animals had only about 75000 optic nerve axone (P < 0.05) of which about 2.8 % were myelinated. By 30 d of age there was a total of between 75000 90000 optic nerve axons, irrespective of the group examined. The proportion of axons which were myelinated at this age was still significantly lower (P < 0.001) in the ETHD animals (similar to 77 %) than in the other groups (about 98 %). It is concluded that the normal stages of development and maturation of the rat optic nerve axons, as assessed in this study, can be severely compromised by exposure to a relatively high (but not low) dose of ethanol between postnatal d 4 and 9.

Work-related stress and occupational therapy

Occupational stress and burnout have been studied extensively in the human services. It has been suggested that healthcare professionals in particular are at risk of stress owing to the caring nature of their work. Articles related to occupational therapy and work-related stress were reviewed in regard to practice in Australia, Canada, the United Kingdom, the United States and Sweden. Although the empirical literature is relatively weak for occupational therapy, it has been argued that occupational therapists in health care share risk factors with other healthcare professionals. These risk factors include repeated exposure to distress and difficult behaviour, prolonged interventions and uncertain outcome. Issues such as professional status, staffing issues and the nature of the profession have been identified as additional risk factors for occupational therapists. However, empirical studies that enable burnout rates of occupational therapists to be compared with those of related occupational groups suggest that this may not be the case. Occupational therapists may in fact be protected from some stress and burnout factors. Further research is recommended to clarify the nature of stress experienced by occupational therapists and to identify both risk and protective factors characteristic of the profession. Copyright © 2001 Whurr Publishers Ltd.