55 research outputs found

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

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    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

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    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

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    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

    An Overview on Mycotoxin Contamination of Foods in Africa

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    Metal extent in blood of livestock from Dandora dumping site, Kenya: source identification of Pb exposure by stable isotope analysis

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    Nairobi city in Kenya produces 2000 tons/day of garbage, and most of it is dumped onto the Dandora dumping site, home to a quarter-million residents. This study was conducted (1) to assess the contamination levels of nine metals and a metalloid (arsenic) in the blood of pigs, goats, sheep and cattle from Dandora, and (2) to identify a possible source of lead (Pb) pollution. Cadmium (Cd, 0.17–4.35 μg/kg, dry-wt) and Pb (90–2710 μg/kg) levels in blood were generally high, suggesting human exposure to Cd through livestock consumption and Pb poisoning among pigs (2600 μg/kg) and cattle (354 μg/kg). Results of Pb isotope ratios indicated that the major exposure route might differ among species. Our results also suggested a possibility that the residents in Dandora have been exposed to the metals through livestock consumptio

    Accumulation properties of inorganic mercury and organic mercuryin the red-crownedcrane Grus japonensis in east Hokkaido, Japan

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    The red-crowned (Japanese) crane Grus japonensis is native to east Hokkaido, Japan, in contrast to the East Asia mainland. Previously, we reported that red-crowned cranes in Hokkaido were highly contaminated with mercury in the 1990s and that the contamination rapidly decreased to a moderate level in the 2000s. In the present study, we determined levels of organic mercury (O–Hg) in the liver and kidney of cranes in east Hokkaido in comparison with levels of total mercury (T–Hg). T–Hg levels in the kidneys were higher than those in the livers in adults but not in subadults and juveniles; however, the reverse was the case for O–Hg even for adults. The ratio of O–Hg to T–Hg in both the liver and kidney decreased as T–Hg increased in the three developmental stages. While the ratios of O–Hg to T–Hg in the liver and kidney of adults were significantly lower than those of juveniles, the ratios were similar for adults and juveniles in a lower range of T–Hg. The ratio of selenium (Se) to T–Hg decreased as T–Hg increased in both the liver and kidney, irrespective of stages. Mercury burdens in feathers were about 59% and 67% of the total body burdens for juveniles and adults, respectively. Furthermore, ratios of carbon and nitrogen stable isotopes to T–Hg varied greatly, with no relation to mercury level in the liver. The results suggest slow accumulation of inorganic mercury in the kidney of red-crowned cranes in east Hokkaido, Japa

    LC-ESI/MS/MS analysis of neonicotinoids in urine of very low birth weight infants at birth

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    Objectives Neonicotinoid insecticides are widely used systemic pesticides with nicotinic acetylcholine receptor agonist activity that are a concern as environmental pollutants. Neonicotinoids in humans and the environment have been widely reported, but few studies have examined their presence in fetuses and newborns. The objective of this study is to determine exposure to neonicotinoids and metabolites in very low birth weight (VLBW) infants. Methods An analytical method for seven neonicotinoids and one neonicotinoid metabolite, N-desmethylacetamiprid (DMAP), in human urine using LC-ESI/MS/MS was developed. This method was used for analysis of 57 urine samples collected within 48 hours after birth from VLBW infants of gestational age 23–34 weeks (male/female = 36/21, small for gestational age (SGA)/appropriate gestational age (AGA) = 6/51) who were admitted to the neonatal intensive care unit of Dokkyo Hospital from January 2009 to December 2010. Sixty-five samples collected on postnatal day 14 (M/F = 37/22, SGA/AGA = 7/52) were also analyzed. Results DMAP, a metabolite of acetamiprid, was detected in 14 urine samples collected at birth (24.6%, median level 0.048 ppb) and in 7 samples collected on postnatal day 14 (11.9%, median level 0.09 ppb). The urinary DMAP detection rate and level were higher in SGA than in AGA infants (both p<0.05). There were no correlations between the DMAP level and infant physique indexes (length, height, and head circumference SD scores). Conclusion These results provide the first evidence worldwide of neonicotinoid exposure in newborn babies in the early phase after birth. The findings suggest a need to examine potential neurodevelopmental toxicity of neonicotinoids and metabolites in human fetuse
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