A Schutz

Markers of high fish intake are associated with decreased risk of a first myocardial infarction

High intake of fish has been associated with reduced risk of CHD. The high content of n-3 polyunsaturated fatty acids (PUFA) in fish has been suggested to be a protective factor. In addition, fish is the entirely dominating source of methylmercury for the general population, and the concentration of Hg in erythrocytes (Ery-Hg) is often used as an index of fish consumption. Our aim was to study the relationships between a first-ever myocardial infarction, Ery-Hg, activity of gluthathione peroxidase in erythrocytes (Ery-GSH-Px) and plasma concentration of the n-3 PUFA eicosapentaenoic and docosahexaenoic acids (P-PUFA). In a population-based prospective nested case-control study within Northern Sweden seventy-eight cases of a first-ever myocardial infarction were compared with 156 controls with respect to Ery-Hg, P-PUFA and Ery-GSH-Px. Both Ery-Hg and P-PUFA, but not Ery-GSH-Px, were significantly higher in subjects reporting high fish intake (at least one meal per week) than in those with lower intake. This finding suggests that Ery-Hg and P-PUFA reflect previous long-term fish intake. Low risk of myocardial infarction was associated with high Ery-Hg or high P-PUFA. In a multivariate model the risk of myocardial infarction was further reduced in subjects with both high Ery-Hg and high P-PUFA (odds ratio 0.16, 95 % CI 0.04, 0.65). In conclusion, there is a strong inverse association between the risk of a first myocardial infarction and the biomarkers of fish intake, Ery-Hg and P-PUFA, and this association is independent of traditional risk factors.

Yearly measurements of blood lead in Swedish children since 1978: an update focusing on the petrol lead free period 1995-2001.

Background and Aims: To assess blood lead concentrations (B-Pb) in children not exposed to petrol lead. In a previous paper we reported the results for the period 1978–94 (2441 children measured). A substantial decrease of B-Pb was found, which reflected a beneficial effect of gradual banning of petrol lead. Since 1994, petrol sold in Sweden has not contained lead. Methods: In the south of Sweden, each year from 1995 to 2001, B-Pb was measured in 329 boys and 345 girls, aged 7–11 years. Results: The geometric mean (GM) of B-Pb was 21 (range 6–80) μg/l. There was no consistent change of B-Pb from 1995 to 2001. Children living near a lead smelter had raised B-Pb (GM 24 μg/l, range 11–80). Passive smoking, but not age and sex, influenced B-Pb significantly. Conclusions: B-Pb in Swedish children, no longer exposed to petrol lead, seems to have stabilised at an average level close to 20 μg/l (provided there is no nearby industrial lead emission).

Environmental exposure to lead and arsenic among children living near a glassworks

Concentrations of lead (Pb) in blood (B-Pb, geometric mean 34.6 micrograms l-1, n = 127) and inorganic arsenic (As) and its metabolites in urine (U-As, mean 5.1 micrograms/g creatinine, n = 35) did not differ between children living in a village close to a glassworks emitting both Pb and As and children living in a reference area. There was no significant effect on B-Pb and U-As related to parents working at the glassworks or consumption of domestically grown vegetables. Neither was there any significant effect upon B-Pb of sex, age, potentially lead-exposing hobbies, or consumption of canned foods. Boys had higher U-As than girls (5.8 vs 4.2 micrograms/g creatinine, p = 0.005), and there was a decrease with age (range 8.4-10.4 years, 27% per year, p = 0.01). Further, parental smoking habits had a significant effect on both B-Pb and U-As. In children of non-smoking parents the B-Pb was 30 micrograms l-1, in children with one parent who smoked 39 micrograms l-1 (smoking father 37, smoking mother 41 micrograms l-1) and in children with two parents who smoked 47 micrograms l-1 (p less than 0.001). The corresponding values for U-As were 4.2, 5.5, and 13 micrograms/g creatinine, respectively (p = 0.01).

Chelatable lead versus lead in human trabecular and compact bone

In active and retired lead workers there was a close correlation between urinary excretion of lead during 6 h after intake of a single oral dose of 0.5 g penicillamine, and the excretion during 24 h. In chelation tests it is thus sufficient to collect urine for only a few hours. There was a close correlation between the amount of chelatable lead and the blood-lead level, as well as the lead level in biopsies of trabecular bone from vertebrae, but there was no association with lead in compact bone, as measured in finger-bone by in vivo X-ray fluorescence. The chelatable lead probably mainly reflects the soft tissue lead pool and a fraction of the trabecular bone lead pool, which has a relatively rapid turnover. It is not a valid indicator of the pool of lead which has slowly accumulated in the compact bone, and it is thus not useful as a time-integrated index of the exposure over a long period of time.