Cadmium exposure pathways in a population living near a battery plant.

OBJECTIVES: The objectives of the present study were to assess the relative impact of different pathways of environmental cadmium (Cd) exposure and to evaluate the contribution from locally produced vegetables and root crops to the total dietary intake of Cd. METHODS: Cadmium in urine was determined for 492 individuals living near a closed down battery factory in Sweden. For each individual we created an environmental exposure-index based on Cd emissions to ambient air and number of years living at various distances from the plant. This information as well as dietary data were collected via questionnaires. Samples of soil, carrots and/or potatoes were collected from 37 gardens and analysed for Cd concentration. RESULTS: Eating home grown vegetables/potatoes, environmental Cd-exposure-index, female gender, age above 30 years and smoking more than one pack of cigarettes daily for at least 10 years were found to be significantly associated with increased urine concentrations of Cd (UCd>1.0 nmol/mmol creatinine). We found a statistically significant relation between Cd in urine and environmental Cd-exposure-index in persons eating home grown vegetables/potatoes regularly. Cd concentrations in home grown carrots, potatoes and in garden soil were highest in the area closest to the factory. Daily consumption of potatoes and vegetables cultivated in the vicinity of the closed battery factory was estimated to increase Cd intake by 18-38%. CONCLUSION: The present study shows that consumption of locally grown vegetables and root crops was an important exposure pathway, in subjects living near a nickel-cadmium battery plant, whereas direct exposure via ambient air was less important.

Methyl mercury exposure in Swedish women with high fish consumption.

We studied the exposure to methyl mercury (MeHg) in 127 Swedish women of childbearing age with high consumption of various types of fish, using total mercury (T-Hg) in hair and MeHg in blood as biomarkers. Fish consumption was assessed using a food frequency questionnaire (FFQ), including detailed information about consumption of different fish species, reflecting average intake during 1 year. We also determined inorganic mercury (I-Hg) in blood, and selenium (Se) in serum. The average total fish consumption, as reported in the food frequency questionnaire, was approximately 4 times/week (range 1.6-19 times/week). Fish species potentially high in MeHg, included in the Swedish dietary advisories, was consumed by 79% of the women. About 10% consumed such species more than once a week, i.e., more than what is recommended. Other fish species potentially high in MeHg, not included in the Swedish dietary advisories, was consumed by 54% of the women. Eleven percent never consumed fish species potentially high in MeHg. T-Hg in hair (median 0.70 mg/kg; range 0.08-6.6 mg/kg) was associated with MeHg in blood (median 1.7 microg/L; range 0.30-14 microg/L; rs = 0.78; p < 0.001). Hair T-Hg, blood MeHg and serum Se (median 70 microg/L; range 46-154 microg/L) increased with increasing total fish consumption (rs = 0.32; p < 0.001, rs = 0.37; p < 0.001 and rs = 0.35; p = 0.002, respectively). I-Hg in blood (median 0.24 microg/L; range 0.01-1.6 microg/L) increased with increasing number of dental amalgam fillings. We found no statistical significant associations between the various mercury species measured and the Se concentration in serum. Hair mercury levels exceeded the levels corresponding to the EPA reference dose (RfD) of 0.1 microg MeHg/kg b.w. per day in 20% of the women. Thus, there seems to be no margin of safety for neurodevelopmental effects in fetus, for women with high fish consumption unless they decrease their intake of certain fish species.

Fatty acid alterations in liver and milk of cadmium exposed rats and in brain of their suckling offspring.

Fatty acid composition was studied in milk at day 14 and in liver at day 24 after parturition of lactating rats exposed to 0 ppm, 5 ppm or 25 ppm cadmium (Cd) via drinking water for 17 days during lactation, and in the brain of their offspring at day 19 after birth. In the liver phospholipid fraction, 22:5(n-3) was significantly higher, while in the triacylglycerol fraction 22:6(n-3)/20:5(n-3) ratio was significantly lower in the 25 ppm group compared to the controls. Significantly higher proportions of 16:0 and lower proportions of medium-chain fatty acids, 8:0-14:0, were observed in milk of dams in the 25 ppm group, indicating decreased enzymatic activity of thiotransferase II in the mammary gland. Slightly increased levels of 20:3(n-6) were observed in brains of pups in the 25 ppm group compared to control. The results indicate that Cd exposure influences fatty acid metabolism in lactating rats.

Cadmium in food chain and health effects in sensitive population groups.

Even at the low exposure level of cadmium found in this study population living on farms in southern Sweden, there was an indication of effect on biochemical markers of renal function. Women had higher blood cadmium (BCd) and urinary cadmium (UCd) than men, which can be explained by higher absorption of Cd due to low iron status. In the present study, Cd in pig kidneys could not be used to predict human BCd or UCd even though cereals are a substantial part of both the human and the pig diet. The contribution of Cd from locally produced food to the total dietary intake in humans was relatively low and varied and the intake of Cd did not correlate with BCd or UCd. In contrast, Cd levels in pig kidney were significantly related to Cd levels in feed. However, there was no relationship between the locally produced cereals, constituting the main part of the feed, and Cd in pig kidneys. In pig feed, other non-locally produced ingredients contributed to a large part of the Cd in feed. The Cd in non-locally produced feed ingredients reaches the local circulation via excretion in faeces and application of manure to arable soils and will lead to increased levels in the crops. As indicated by experimental data from animals, neurochemical and neurobehavioral effects during development need to be further explored as sensitive endpoints for cadmium toxicity.