Case-specific colleague guidance for general practitioners' management of sickness absence.

BACKGROUND: General practitioners (GPs) report sickness absence certification as challenging. They express need for support with functional assessment beyond guidelines and reforms. Case-specific collegial one-to-one guidance for other clinical topics has proved popular with GPs and may be an acceptable and effective way to improve GPs skills and competence in sickness absence certification. AIMS: To present a new model of case-specific colleague guidance focusing on the management of long-term sickness absence and to describe its feasibility in terms of application and reception among GPs, and also GPs' self-reports of effects on their practice. METHODS: Randomly selected GPs received case-specific collegial guidance over a 12-month period, in two Norwegian trials, delivered by former GPs employed by the social security administration. We measured reception and perceived effects by GPs' self-report and registered participation and withdrawal rates. RESULTS: The participation rate (n = 165) was 94%, and no GPs withdrew during training. Among the 116 GPs responding to the survey (70%), 112 (97%; 95% CI 92-99) stated they would recommend it to their colleagues. Considerable benefit from the guidance was reported by 68 (59%; 95% CI 50-68). The GPs self-reported other effects on their sickness absence certification, specifically an increased use of part-time sickness absence (Fit-Note equivalent). CONCLUSIONS: This model of case-specific colleague guidance to aid GPs' management of long-term sickness absence is feasible and was popular. This type of guidance was perceived by GPs to be somewhat beneficial and to alter their sickness absence certification behaviour, though the true impact requires further testing in controlled trials.

Urinary selenium excretion in workers with low exposure to mercury vapour.

Urinary selenium excretion was studied in 21 mercury vapour (Hgo)-exposed workers involved in the demolition of a chloralkali plant. The subjects had no known previous occupational exposure to mercury. Their mean pre-exposure urinary mercury concentration, determined on average 1.2 days prior to the exposure, was 0.8 nmol mmol-1 creatinine (range 0.3-1.9). Their last mean urinary mercury concentration, determined on average after 51.4 days (range 19-103) of exposure, was 4.8 nmol mmol-1 creatinine (range 1.2-10.0). The exposure ceased on average 4.1 days after the last determined urinary mercury concentration. The corresponding concentrations of urinary selenium decreased from an average of 39.1 nmol mmol-1 creatinine (range 13.9-89.5) to 29.0 nmol mmol-1 creatinine (range 10.1-52.9) (P = 0.002). This finding may indicate that even a low to moderate work-related exposure to Hgo may reduce the urinary selenium concentration in humans in a manner that is not yet fully known.

Production and surveillance of mercury exposure over 40 years at a chloralkali plant.

Mercury vapour exposure was studied for 40 years in 419 chloralkali workers. The concentration of mercury was measured in the work room (stationary) from 1953 and in urine from 1948. There were major differences in the mean urinary concentrations between different types of job. The mean urinary mercury concentration, uncorrected for urinary dilution, for all subjects varied between 30 and 250 micrograms 1.(-1) during the study period. For workers in the cell-room the correlation (r) between urinary mercury and mercury in the work room was r = 0.74 (P < 0.001), and for repair men/mechanics it was r = 0.70 (P < 0.001). The introduction of new cells and stabilizing the volume of production may have been important for reducing air-Hg and U-Hg, whereas other changes in the production process, or actions to reduce the release of mercury to the work environment, had no detectable effect. The urinary mercury concentration among all workers was related to the relative energy consumption (r = 0.83, P < 0.001).

Incidence of cancer and mortality among workers exposed to mercury vapour in the Norwegian chloralkali industry.

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.