Journal
ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
Volume 30, Issue 24, Pages 65204-65216Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s11356-023-26813-9
Keywords
Biomarker; Environmental health; Environmental exposure; Metals; Risk; Vulnerability
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Exposure to arsenic and its adverse health outcomes are poorly researched in South Africa. This study investigated the long-term exposure of residents in Limpopo province, finding significant differences in arsenic distribution among water, soil, and blood samples from exposed and control villages. The study highlights the need for potable water in areas with high environmental arsenic concentrations.
Exposure to arsenic even at low levels can lead to adverse health outcomes, however, there is a paucity of research from South Africa in relation to human exposure to arsenic. We investigated long-term exposure of residents in Limpopo province, South Africa, in a cross-sectional study by analysing water, soil and blood arsenic concentrations from two arsenic-exposed (high and medium-low exposure) villages and one non-exposed (control) village. There were statistically significant differences in the distribution of arsenic in water, soil and blood amongst the three sites. The median drinking water arsenic concentration in the high-exposure village was 1.75 mu g/L (range = 0.02 to 81.30 mu g/L), 0.45 mu g/L (range = 0.100 to 6.00 mu g/L) in the medium- / low-exposure village and 0.15 mu g/L (range = < limit of detection (LOD) to 29.30 mu g/L) in the control site. The median soil arsenic concentration in the high-exposure village was 23.91 mg/kg (range = < LOD to 92.10 mg/kg) whilst arsenic concentrations were below the limit of detection in all soil samples collected from the medium-/low-exposure and control villages. In the high-exposure village, the median blood arsenic concentration was 1.6 mu g/L (range = 0.7 to 4.2 mu g/L); 0.90 mu g/L (range = < LOD to 2.5 mu g/L) in the medium-/low-exposure village and 0.6 mu g/L (range = < LOD to 3.3 mu g/L) in the control village. Significant percentages of drinking water, soil and blood samples from the exposed sites were above the internationally recommended guidelines (namely, 10 mu g/ L, 20 mg/kg and 1 mu g/L, respectively). Majority of participants (86%) relied on borehole water for drinking and there was a significant positive correlation between arsenic in blood and borehole water (p-value = 0.031). There was also a statistically significant correlation between arsenic concentrations in participants' blood and soil samples collected from gardens (p-value = 0.051). Univariate quantile regression found that blood arsenic concentrations increased by 0.034 mu g/L (95% CI = 0.02-0.05) for each one unit increase in water arsenic concentrations (p < 0.001). After adjusting for age, water source and homegrown vegetable consumption in multivariate quantile regression, participants from the high-exposure site had significantly higher blood concentrations than those in the control site ( coefficient: 1.00; 95% CI = 0.25-1.74; p-value = 0.009) demonstrating that blood arsenic is a good biomarker of arsenic exposure. Our findings also provide new evidence for South Africa on the association between drinking water and arsenic exposure, emphasising the need for the provision of potable water for human consumption in areas with high environmental arsenic concentrations.
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