We aim to assess the risks of renal dysfunction and osteoporosis that is attributed to the seawater acidification caused cadmium (Cd) level increase in human consumed shellfish. A physiology-based pharmacokinetic model was used to estimate Cd concentrations in urine and blood among shellfish-only consumers and among the general population. We used the benchmark dose (BMD) method to determine the threshold limits of Cd in urine for renal dysfunction and in blood for osteoporosis for assessing the human health risk. Our results revealed that seawater acidification could increase the Cd accumulation in shellfish by 10-13% compared to the situations under current pH levels. Under the lower seawater pH level, the daily intake of Cd could increase by 21%-67% among shellfish-only consumers, and by 13%-17% among the general population. Our findings indicated that seawater acidification would lead to a marginal increase in Cd intake among humans in shellfish-only consumers. The results of BMDs of urinary Cd showed that the threshold limits for renal dysfunction at 5% were 3.00 mu g g(-1) in males and 12.35 mu g g(-1) in females. For osteoporosis, the estimated BMDs of blood Cd were 7.95 mu g L-1 in males and 1.23 mu g L-1 in females. These results of the risk of Cd intake showed that the consumption of Cd-contaminated shellfish in the general population is largely unaffected by changes in seawater pH levels. Notably, the potential impact of seawater acidification on renal dysfunction for males in shellfish-only consumers face a 14% increase of risk.
