Akita prefecture is located in the northern part of Japan and has many cadmium-polluted areas. We herein performed an exposure assessment of cadmium in 712 and 432 female farmers in two adjacent cadmium-polluted areas (A and B, respectively), who underwent local health examinations from 2001–2004. We measured cadmium concentrations in 100 food items collected from local markets in 2003. We then multiplied the intake of each food item by its cadmium concentration in each subject to assess cadmium intake from food and summed cadmium intake from all food items to obtain the total cadmium intake. Median cadmium intake levels in areas A and B were 55.7 and 47.8 µg/day, respectively, which were both higher than that of the general population and were attributed to local agricultural products, particularly rice. We also calculated weekly cadmium intake per body weight and compared it to the previous provisional tolerable weekly intake reported by the Joint FAO (Food and Agriculture Organization)/WHO (World Health Organization) expert committee on food additives or current tolerable weekly intake in Japan of 7 µg/kg BW/week. Medians in areas A and B were 7.2 and 6.0 µg/kg BW/week, respectively. Similar estimated values were also obtained by the Monte Carlo simulation. These results demonstrated that the cadmium exposure levels among the farmers were high enough to be approximately the tolerable weekly intake.

Objectives We investigated the relationship between lead in air (Pb‐A) measured by personal sampling and blood lead (Pb‐B) in workers with relatively low lead exposure to estimate the permissible air concentration of lead corresponding to the biological tolerance value of Pb‐B of 15 µg/dL. Methods We collected air samples at a lead‐acid battery factory in Japan by personal sampling devices attached to 32 workers (19 males and 13 females) and measured Pb‐A by a graphite furnace atomic absorption spectrophotometer in 2017‐2020. In addition, we collected information on age, smoking habits, Pb‐B, and urinary δ‐aminolevulinic acid from the records of medical examinations for lead poisoning. Samples were collected two times from four workers, resulting in 36 data sets. Results Before analyses, we excluded four inappropriate data sets. The levels of Pb‐A in the factory and Pb‐B in the workers were almost under the current permissible limits. Multiple regression models showed significant correlations between Pb‐B and Pb‐A, and sex, and borderline significance between Pb‐B and age. Based on them, we calculated Pb‐A corresponding to Pb‐B 15 μg/dL, and obtained similar values to the current occupational exposure limit (OEL) of 30 μg/m 3 , with slight variation between sex and age. Conclusion These results validate OEL, although supplementary conditions in terms of sex and age may be necessary.

Objectives The present study investigated the quantitative relationship between blood lead (Pb‐B) and urinary δ⁻aminolevulinic acid (ALA‐U) in lead workers, and examined the Pb‐B level that induces increases in ALA‐U and the corresponding ALA‐U. Methods We collected 10 562 data sets on Pb‐B, ALA‐U, age, and smoking habits from 808 workers (771 males and 37 females) who underwent multiple lead poisoning medical examinations at a lead‐acid battery and lead smelting plant in Japan between 1995 and 2018. Females were excluded, and data collected in 169 subjects prior to engaging in lead work were used as the control. Pb‐B and ALA‐U levels were measured by graphite furnace atomic absorption spectrophotometry and high‐performance liquid chromatography respectively. Results A significant dose‐response relationship was observed between Pb‐B and ALA‐U based on Pb‐B‐classified observations of increases in ALA‐U values and the prevalence of over‐reference ALA‐U as well as regression analyses independent of smoking habits. The results obtained revealed that the threshold of Pb‐B to increase ALA‐U was 25.1‐35.0 µg/dL based on the significant elevation point of the prevalence of over‐reference ALA‐U and 16.2‐22.3 µg/dL from a 3rd degree regression equation. Conclusions We proposed a threshold of Pb‐B to increase ALA‐U of 20 µg/dL and a biologically acceptable value of ALA‐U of 1 mg/L, corresponding to the threshold.