%0 Journal Article
%T Betel quid chewing as a source of manganese exposure: total daily intake of manganese in a Bangladeshi population
%A Shaban W Al-Rmalli
%A Richard O Jenkins
%A Parvez I Haris
%J BMC Public Health
%D 2011
%I BioMed Central
%R 10.1186/1471-2458-11-85
%X Inductively coupled plasma mass spectrometry (ICP-MS) was used to determine (1) urinary Mn levels for 15 chewers and 22 non-chewers from the ethnic Bangladeshi community in the United Kingdom, and (2) Mn levels in betel quids, its individual components and other Bangladeshi foods.Betel quid chewers displayed a significantly higher (P = 0.009) mean Mn concentration in urine (1.93 ¦Ìg L-1) compared to non-chewers (0.62 ¦Ìg L-1). High levels of Mn were detected in Piper betel leaves with an overall average of 135 mg kg-1 (range 26 -518 mg kg-1). The mean concentration of Mn in betel quid was 41 mg kg-1 (SD 27) and the daily intake of Mn in the Bangladeshi population was estimated to be 20.3 mg/day. Chewing six betel quids could contribute up to 18% of the maximum recommended daily intake of Mn.We have demonstrated that Mn in betel quids is an overlooked source of exposure to Mn in humans. Chewers display a 3.1 fold increased urinary Mn concentration compared to non-chewers. The practice of betel quid chewing contributes a high proportion of the maximum recommended daily intake of Mn, which could make chewers in Bangladesh more vulnerable to Mn neurotoxicity.The problem of As exposure in the Bangladeshi population through drinking contaminated groundwater has been well documented. Recently Mn has been identified as another element that may pose health risks in Bangladeshi populations through drinking Mn contaminated groundwater. Mn levels higher than the World Health Organisation standard (0.400 mg L-1) have been detected in Bangladeshi groundwater [1-3]. Although Mn is an essential element for human health, exposure to high levels of Mn can induce neurological effects such as manganism which is characterised by movement disturbances similar to that observed in Parkinson's disease [4]. Mn can accumulate at the cellular level in mitochondria, where it disrupts oxidative phosphorylation and increases the generation of reactive oxygen species (ROS) [5]. Unlike arsenic, the s
%U http://www.biomedcentral.com/1471-2458/11/85