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Endocrine disrupting compounds (EDCs) are an emerging environmental concern and commonly occur as a mixture of compounds. The EDC mixture can be more toxic than any single compound. The present study analyses EDCs in surface water in the case of an urban tropical river, the Langat River, using the multiresidue analytical method of solid phase extraction and liquid chromatography-tandem mass spectrometry (SPE-LC-MS/MS). The Langat River is used as a drinking water source and is treated for Malaysian drinking water supply. A total of 14 EDCs i.e. five hormones, seven pharmaceuticals, one pesticide, and one plasticizer were detected. Caffeine was observed to be highest at 19.33 ng/L, followed by bisphenol A and diclofenac at 8.24 ng/L and 6.15 ng/L, respectively. Using a conservative risk quotient (RQ) method, EDCs were estimated for having negligible risks under acute and chronic exposure (RQ < 0.002 and RQ < 0.003; RQ < 0.01), suggesting that there is currently an insignificant ecological risk related to these compounds in the Langat River riverine ecosystem. However, the presence of EDCs in surface water raises concerns about potential human exposure to EDCs via dietary intake i.e. food and drinking water supply. Although the ecological risks are considered negligible, these risks should not be neglected in terms of future prioritization and risk management. Improvements in water quality monitoring and risk assessment in water source protection are required to support a multibarrier approach to managing drinking water supply systems for safe water supply. The present study proposes a risk management and monitoring framework for EDCs to support the aforementioned multibarrier approach.
This article was published in the following journal.
Name: The Science of the total environment
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A group of autosomal dominant diseases characterized by the combined occurrence of tumors involving two or more ENDOCRINE GLANDS that secrete PEPTIDE HORMONES or AMINES. These neoplasias are often benign but can be malignant. They are classified by the endocrine glands involved and the degree of aggressiveness. The two major forms are MEN1 and MEN2 with gene mutations on CHROMOSOME 11 and CHROMOSOME 10, respectively.
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A form of multiple endocrine neoplasia that is characterized by the combined occurrence of tumors in the PARATHYROID GLANDS, the PITUITARY GLAND, and the PANCREATIC ISLETS. The resulting clinical signs include HYPERPARATHYROIDISM; HYPERCALCEMIA; HYPERPROLACTINEMIA; CUSHING DISEASE; GASTRINOMA; and ZOLLINGER-ELLISON SYNDROME. This disease is due to loss-of-function of the MEN1 gene, a tumor suppressor gene (GENES, TUMOR SUPPRESSOR) on CHROMOSOME 11 (Locus: 11q13).
A form of multiple endocrine neoplasia characterized by the presence of medullary carcinoma (CARCINOMA, MEDULLARY) of the THYROID GLAND, and usually with the co-occurrence of PHEOCHROMOCYTOMA, producing CALCITONIN and ADRENALINE, respectively. Less frequently, it can occur with hyperplasia or adenoma of the PARATHYROID GLANDS. This disease is due to gain-of-function mutations of the MEN2 gene on CHROMOSOME 10 (Locus: 10q11.2), also known as the RET proto-oncogene that encodes a RECEPTOR PROTEIN-TYROSINE KINASE. It is an autosomal dominant inherited disease.
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