Social cost of mining-related lead (Pb) pollution in Kabwe, Zambia, and potential remediation measures

Lead (Pb) pollution has been one of the major environmental problems of worldwide significance. It is a latent factor for several fatal illnesses, whereas the exposure to lead in early childhood causes a lifetime IQ loss. The social cost is the concept to aggregate various adverse effects in a single monetary unit, which is useful in describing the pollution problem and provides foundation for the design of interventions. However, the assessment of the social cost is scarce for developing countries. In this study, we focus on the lead pollution problem of a former mining town, Kabwe, Zambia, where mining wastes abandoned near residential areas has caused a critical pollution problem. We first investigated the social cost of lead pollution that future generations born in 2025–2049 would incur in their lifetime. As the channels of the social cost, we considered the lost income from the IQ loss and the lost lives from lead-related mortality. The results showed that the social cost would amount to 224–593 million USD (discounted to the present value). Our results can be considered conservative, lower bound estimates because we focused only on well-identified effects of lead, but the social cost was still substantial. Then we examined several engineering remediation measures. The results showed that the social cost can be reduced (the benefits of remediations) more than the costs of implementing remediation measures. This study is the first to investigate the social cost of mining-related lead pollution problem in developing countries. Our interdisciplinary approach utilises the micro-level economic, health and pollution data and integrates the techniques in economics, toxicology and engineering.publishedVersio

Urinary neonicotinoids profiles in adults from Aveiro district, NW Portugal

Neonicotinoid insecticides (Neonics - NNs) are systemic insecticides widely used in agriculture to control insects. Due to their broad-spectrum insecticide activity, they are also used in the domestic environment and on animals, including household pets. Owing to their toxicity towards non-target organisms, particu-larly honeybees, the agricultural outdoor use of some neonics was already banned. Nevertheless, they can still be used in indoor activities. Neonics’ residues have been detected in food, water and indoor dust and, consequently, humans are exposed to these insecticides. However, human biomonitoring data is limited to a few studies worldwide, with no data for Portugal. In this study, levels of neonicotinoids namely ace-tamiprid (and its metabolite dm-acetamiprid), clothianidin, dinotefuran, imidacloprid, nitenpyran, thi-acloprid and thiamethoxan, were quantified in spot urine samples provided by 46 volunteers from Aveiro district. The volunteers were recruited from RESPIRA project, an ongoing study that aims to evaluate the role of environmental contaminants in the progression of respiratory diseases. Overall, the obtained re-sults disclose that 81.4% of the individuals were exposed to at least one neonicotinoid. Dinotefuran and dm-acetamiprid showed the highest detection frequencies (46.5%), followed by imidacloprid (41.9%), whereas nitenpyran and thiacloprid were never detected (bellow detection limit). The neonics with the highest concentrations were dm-acetamiprid (max: 1443 ug/g creatinine, average: 39.1 ug/g creatinine) and thiamethoxan (max: 152 ug/g creatinine, average: 6.9 ug/g creatinine). These results are in general accordance with previous reports that disclosed dm-acetamiprid as one of the most frequently detected NN in human urine samples.publishe

TCDD-induced chick cardiotoxicity is abolished by a selective cyclooxygenase-2 (COX-2) inhibitor NS398

Halogenated aromatic hydrocarbons, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), are known to cause severe heart defects in avian species. However, the mechanism of TCDD-induced chick cardiovascular toxicity is unclear. In this study, we investigated cyclooxygenase-2 (COX-2) as a possible mechanism of TCDD-induced cardiotoxicity. Fertile chicken eggs were injected with TCDD and a COX-2 selective inhibitor, NS398, and we investigated chick heart failure on day 10. We found that the chick heart to body weight ratio and atrial natriuretic factor mRNA expression were increased, but this increase was abolished with treatment of NS398. In addition, the morphological abnormality of an enlarged ventricle resulting from TCDD exposure was also abolished with co-treatment of TCDD and NS398. Our results suggested that TCDD-induced chick heart defects are mediated via the nongenomic pathway and that they do not require the genomic pathway

Metal and metalloid contamination in roadside soil and wild rats around a Pb-Zn mine in Kabwe, Zambia

Metal (Cr, Co, Cu, Zn, Cd, Pb, Ni) and metalloid (As) accumulation was studied in roadside soil and wild rat (Rattus sp.) samples from near a Pb–Zn mine (Kabwe, Zambia) and the capital city of Zambia (Lusaka). The concentrations of the seven metals and As in the soil samples and Pb in the rat tissue samples were quantified using atomic absorption spectroscopy. The concentrations of Pb, Zn, Cu, Cd, and As in Kabwe soil were much higher than benchmark values. Geographic Information System analysis indicated the source of metal pollution was mining and smelting activity. Interestingly, the area south of the mine was more highly contaminated even though the prevailing wind flow was westward. Wild rats from Kabwe had much higher tissue concentrations of Pb than those from Lusaka. Their body weight and renal Pb levels were negatively correlated, which suggests that mining activity might affect terrestrial animals in Kabwe. The area around Kabwe, Zambia is highly polluted with metals and As. Wild rats from this area had high tissue concentrations of Pb and decreased body weight