Cadmium concentrations in blood and seminal plasma: correlations with sperm number and motility in three male populations (infertility patients, artificial insemination donors, and unselected volunteers)

Abstract

To investigate a possible common environmental exposure that may partially explain the observed decrease in human semen quality, we correlated seminal plasma and blood cadmium levels with sperm concentration and sperm motility. We studied three separate human populations: group 1, infertility patients (Long Island, NY, USA); group 2, artificial insemination donors (AID) (Rochester, NY, USA); and group 3, general population volunteers (Rochester, NY, USA). Information about confounding factors was collected by questionnaire. Seminal plasma cadmium did not correlate with blood cadmium (Spearman correlation, n = 91, r = -0.092, P = 0.386, NS). Both blood and seminal plasma cadmium were significantly higher among infertility patients than the other subjects studied (for example, median seminal plasma cadmium was 0.282 microg/L in infertility patients versus 0.091 microg/L in AID and 0.092 microg/L in general population volunteers; Kruskal-Wallis test, P < 0.001). The percentage of motile sperm and sperm concentration correlated inversely with seminal plasma cadmium among the infertility patients (r = -0.201, P < 0.036 and r = -0.189, P < 0.05, respectively), but not in the other two groups. Age (among infertility patients) was the only positive confounder correlating with seminal plasma cadmium. To validate our human findings in an animal model, we chronically exposed adolescent male Wistar rats to low-moderate cadmium in drinking water. Though otherwise healthy, the rats exhibited decreases in epididymal sperm count and sperm motility associated with cadmium dose and time of exposure. Our human and rat study results are consistent with the hypothesis that environmental cadmium exposures may contribute significantly to reduced human male sperm concentration and sperm motility.

Figure 1

Cadmium exposure results in a time and dose-dependent reduction in sperm count. The control and each cadmium-exposure group (5 mg/L, 50 mg/L, and 100 mg/L) were composed of five Wistar rats. Sperm count was determined individually for the left and right cauda epididymes of each rat and then totaled. Sperm counts (in term of millions of sperm) are presented as means with standard errors. An inverse relationship between cadmium dose and sperm concentration was detected after 4 wks of exposure (ANOVA, P < 0.018). Post hoc pairwise comparisons indicated that sperm counts of control animals and those exposed to 5 mg/L cadmium were indistinguishable (H-S, P = 0.252, not significant). At exposures of 50 mg/L and 100 mg/L, however, there was a dose-dependent decrease in sperm counts as compared with controls (H-S, respectively, P < 0.028 and P < 0.003).

Figure 2

Cadmium in water given ad libitum reduces sperm motility. Sperm motility was determined individually for the left and right cauda epididymes of each rat in the control group (n = 5) and the cadmium-exposed groups (5 mg/L, n = 5; 50 mg/L, n = 5; and 100 mg/L, n = 5). Data are presented as sperm motility of cadmium-treated rats as a percentage of that of control animals. A dose-dependent decrease in sperm motility was observed after exposure to cadmium for 4 wks (ANOVA, P < 0.007; H-S, P < 0.025 to P < 0.001). Sperm motility at 8 wks of cadmium treatment was lower than at 4 wks, and the effect of dose was no longer apparent (ANOVA, P = .239, not significant).