1 The relationship between the intake of methylmercury in fish and mercury in blood has been investigated in man. 2 The intakes of methylmercury were carefully controlled and lay in the range 40 - 230 μg/day, the Provisional Tolerable Weekly Intake is equivalent to about 30 μg/day. 3 The results indicate that a daily intake of 1 μg methylmercury would, at equilibrium, produce a blood mercury concentration of 0.8 μg/kg. 4 There is a good close-to-linear correlation between methylmercury intake and blood mercury concentrations within the wide range of intakes employed.

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Hair samples were analyzed for mercury in 942 persons living in either one of two coastal areas of the United Kingdom who reported above average fish consumption. A duplicate diet study group was selected from the 942 individual's who had elevated concentrations of mercury in their hair. The study group's fish consumption averaged 0.36 kg/person . wk during the duplicate diet. Concentration of total mercury in the blood of the study group ranged from 1.1 to 42.3 micrograms/L with an arithmetic mean of 8.8 micrograms/L. The linear curve fitted to the data on the concentration of total mercury in blood vs. mercury intake was similar to that observed in a previous study made in the United Kingdom, but different from that observed in other studies. The results from the present study indicate that people in the United Kingdom are unlikely to be adversely affected by the presence of methylmercury in the fish they consume.

1 Six volunteers ingested 74As-labelled arsenobetaine with a fish meal. The retention and distribution of the tracer were studied by body radioactivity measurements. 2 The tracer became rapidly dispersed in soft tissues, with no major concentration in any localized organ or region. 3 In all subjects < 1% of the ingested activity remained in the body after 24 days. 4 Any losses from the skin were minor in relation to those by other routes of excretion.

This paper considers whether the Department of the Environment's water lead concentration criterion for lead pipe replacement and action in individual cases, i.e. 50 micrograms/l in any sample, is too high when set against the Department of Health's advisory action limit for blood lead concentration of 25 micrograms/100 ml. The relationships between blood lead and water lead concentrations found in the Glasgow and Ayr duplicate diet studies, together with unpublished data from Glasgow and Liverpool, indicate that over 10% of people exposed to an average water lead concentration of 100 micrograms/l (the earlier action level) would have blood lead concentrations above 25 micrograms/100 ml, as would about 4% of those exposed to 50 micrograms/l (the Maximum Admissible Concentration in an EEC Directive). For adults, average water lead concentrations should not exceed 30 micrograms/l to ensure compliance with the limit for blood lead, i.e. so that not more than 2% exceed 25 micrograms/100 ml. However, for one of the critical groups, bottle-fed infants (whose diet is 90% water), average water lead concentrations should not exceed 10-15 micrograms/l. The WHO's Provisional Tolerable Weekly Intake (PTWI) for children (25 micrograms/kg body weight) also implies that their water lead concentrations should not exceed 10-15 micrograms/l.

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Following the finding that blood lead concentrations in middle-aged men were positively associated with alcohol consumption, the Royal Commission on Environmental Pollution recommended that information on lead in alcoholic beverages be obtained. The results reported here were obtained in response to the Royal Commission's request. About 90% of canned and bottled beers contained less than or equal to 10 micrograms/l of lead, whereas nearly half the draught beers sampled contained greater than 10 micrograms/l and 4% contained greater than 100 micrograms/l. Opening the cans and bottles and pouring the contents into a glass had no significant effect on the lead concentration in the beer. All wines sampled directly from the bottle, that is without pouring, contained less than 250 micrograms/l of lead. However the lead concentration in some wines contained in lead-capped bottles increased significantly when the wine was poured from the bottle, in one instance the increment was 1890 micrograms/l. It is concluded that consumption of beer containing 50 micrograms/l of lead could make a substantial contribution to blood lead concentrations in man. Consumption of 1 l/day of wine containing 150 micrograms/l of lead could also make a major contribution to blood lead concentrations. Lead contamination of wine when it is poured from a bottle, which had been lead-capped, can sometimes greatly increase lead concentrations in the wine.

Food has been found to be the main source of nickel intake by man. Nickel was fairly evenly distributed throughout the various food groups examined but highest concentrations of nickel were found in the canned vegetables, sugars and preserves, and bread and cereals food groups, suggesting a contribution from food processing equipment and, possibly, food cans. Mean dietary nickel intakes in the UK (1981-4) were between 0.14 and 0.15 mg/day. The contribution made to dietary nickel intakes by nickel from food utensils and cookware is discussed.