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Ninety-five (63%) mothers qualified as having heavy traffic exposure and 55 (37%) as light traffic exposure. Among the exposed group, 11.6% had lead poisoning compared with 7.3% of unexposed group. A positive association was found, between living near heavy traffic and lead poisoning, OR ¼ 1.6, however, this association was not statistically significant with a P-value of 0.3. Likewise other exposure risk factors, e.g. use of tap water for cooking and drinking, and living in a painted house also showed a positive association with OR ¼ 1.4 and 1.4, respectively, but this association was not statistically significant (P-value 0.4 and 0.5, respectively). Cosmetics (black eye liner) was used by 58.7% of all mothers, however, there was no association between lead poisoning and use of cosmetics, OR ¼ 1. Discussion It is well recognized that cord blood lead levels correlate closely with maternal blood lead levels and that this can be used as a community-screening procedure [7]. This study found that the overall prevalence of lead poisoning (defined as blood lead level 10mg/dl) in cord blood among newborns is 10%. Given that, there is no naturally occurring level of lead in the human body, and that lead is unsafe at any level, therefore, a prevalence of 10% is of public health importance. Evidence is now emerging that, levels even below 10 mg/dl can cause neurological damage; although a level of 10 mg/dl is still an acceptable level of safety [8]. The correlation of cord blood lead level has been previously reported to be 70% of maternal level [7]. Thus, the 10% prevalence of lead poisoning in the cord blood would reflect about the same level of prevalence among mothers; and be considered to represent the prevalence of lead poisoning in the general population of Dar es Salaam where these mothers come from. In this study, confounding factors such as severe anaemia, EPH gestosis, severe malnutrition and multiple pregnancies were considered. The effects of these potential confounders as effect modifiers were carefully studied. There was no correlation between these potential confounders and low birth weight or prematurity. Although this study did not find significant correlations with recognized risk factors, it clearly indicates that there is about 10% prevalence. This report therefore augments the available reports in Tanzania, giving evidence that lead poisoning is indeed a problem [9]. Funding Ministry of Health and Social Welfare.
MARY M. AZAYO, KARIM MANJI, and FESTUS KALOKOLA Department of Paediatrics and Child Health, Muhimbili University of Health and Allied Sciences (MUHAS), Dar-es-Salaam, Tanzania doi:10.1093/tropej/fmn085 Advance Access Published on 4 October 2008
References 1. Nriagu JO, Blackson M, Ocran K. Childhood lead poisoning in Africa, a growing public health problem. Sci Total Environ 1996;181:100. 2. Mathee A, Von Schirrnding YE, Levin J, Ismail A. A survey of blood level among Johannesburg school children. Environ Res 2002;90:181–4. 3. Statement—World Bank Regional Conference on the phase out of leaded gasoline in sub-Saharan Africa, Dakar, Senegal, 26–28 June 2001. 4. Yen C, Shen X, Ao L. Lead exposure in umbilical cord blood and its related factors. Zhonghua Yu Fang Yi Xue Za Zhi 1997;31:9–12. 5. Lead Toxicity on reproductive health, fetal development, and breast milk, chapter 13, 2002: The Wisconsin childhood lead poisoning prevention and control. http:// dhs.wisconsin.gov/lead/doc/chapter13Preg&Breast.pdf (8 July 2008, date last accessed) 6. Furman A, Laleli M. Maternal and umbilical cord blood lead levels: an Istambul study. Arch Environ Health 2001;56:26–8. 7. Bughurst PA, Robertson RK, Oldfield BM, et al. Lead in placentae, membranes and umbilical cord in relation to pregnancy outcome. Environ Health Persp 1991;90:315–20. 8. Carbone R, Laforgia N, Crollo E, et al. Blood lead levels during pregnancy in the newborn period. Study of the population of Bari. Ann Ist Supper Sanita 1998;34:117–9. 9. Mashimba ENM, Kalima J, Mtega S. The use of laboratory analytical data for health and safety. A paper presented at the 5th environmental and theoretical chemistry workshop in Africa, University of Dar es Salaam, December 2003. Correspondence: Prof. Karim Manji, Department of Pediatrics and Child Health, MUHAS, P.O. Box 65001, Dar-es-Salaam, Tanzania. Tel: þ255 754 350 630, Fax: þ255 222153114. E-mail .
Acquired Methemoglobinemia Due to Contaminated Colours: A Preventable Disaster To celebrate the beginning of spring in India, a traditional Hindu colour festival called ‘Holi’ is celebrated by people by throwing coloured powders or spraying coloured water on each other. On 7
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March 2004 on ‘Holi’ day, 10 children were admitted to our ward in quick succession, over a 4–5 h period, with complaints of breathlessness and drowsiness which had developed within 1–2 h of playing with colours bought from a local vendor. The age of the children (five were boys) ranged from 4 to13 years (mean age 9.2 years). The first patient to be admitted was a 4-year-old boy. On clinical examination, he had shallow and irregular respiration, central cyanosis and was deeply unconscious. He was intubated and ventilated. His blood appeared chocolate brown in colour. His arterial blood gas analysis revealed an increased level of methemoglobin (60.9%) with normal partial pressure of oxygen (PaO2) and oxygen saturation levels. A diagnosis of acquired methemoglobinemia due to contaminated colours was made. He was given a thorough stomach and skin wash, nasal oxygen, supportive intravenous fluids and intravenous methylene blue (1 mg/kg over 10 min) [1, 2] As cyanosis persisted the methylene blue dose was repeated after half an hour. After another 3 h, the patient regained consciousness, had normal respiration and was extubated. His methemoglobin level had normalized to 0.9%. The other nine children were also breathless, drowsy and had central cyanosis. However, they did not require ventilatory support. Methemoglobin level was raised in all of them ranging from 18% to 48% with normal PaO2 and oxygen saturation levels. All of them were treated similarly. All 10 children recovered fully and were discharged the next day. This year, also during the festival of Holi (March 2008), two children aged 8 years were admitted to our hospital with breathlessness and drowsiness after exposure to contaminated colours. Investigations confirmed the diagnosis of acquired methemoglobinemia and both children were successfully managed by us. Methemoglobin is an altered state of hemoglobin whereby the ferrous form of iron is oxidized to the ferric state, making the heme moiety incapable of carrying oxygen [2]. Methemoglobinemia causes serious tissue hypoxia when the amount of reduced hemoglobin exceeds 5 g/dl [2]. Nitrites are potent oxidant agents of ferrohemoglobin [2]. Acquired
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methemoglobinemia has been reported to develop in children after exposure to oxidant drugs such as dapsone, local anesthetic agents; high-nitrate foods such as spinach, carrots, silver beets consumed as homemade purees; as well as acute nitrite toxicity resulting from accidental exposure to aniline dyes, colouring compounds or cleaning solutions [2]. However, an extensive PubMed search did not reveal a single case report of acquired methemoglobinemia due to exposure to contaminated colours used during ‘Holi’ festival. We suspect that the colours used in the Holi festival were contaminated with aniline dyes which are known to cause acquired methemoglobinemia in Indian industrial workers as an occupational hazard [3]. In bringing the attention of pediatricians to this rare cause of acquired methemoglobinemia, we hope that it will result in its prompt treatment and possible prevention. ANUPAMA MAUSKAR, SUNIL KARANDE, and MADHURI KULKARNI Department of Paediatrics, Lokmanya Tilak Municipal Medical College and General Hospital, Sion, Mumbai (Bombay) 400 022, Maharashtra, India doi:10.1093/tropej/fmn119 Advance Access Published on 21 January 2009
References 1. Clifton J 2nd, Leikin JB. Methylene blue. Am J Ther 2003;10:289–91. 2. Dahshan A, Donovan GK. Severe methemoglobinemia complicating topical benzocaine use during endoscopy in a toddler: a case report and review of the literature. Pediatrics 2006;117:e806–9. 3. Dewan A, Patel A, Saiyed H. Acute methemoglobinemia – a common occupational hazard in an industrial city in western India. J Occup Health 2001;43:168–71. Correspondence: Dr Anupama Mauskar, Associate Professor of Paediatrics, Department of Paediatrics, Lokmanya Tilak Municipal Medical College and General Hospital, Sion, Mumbai (Bombay) 400 022, India. Email .
Journal of Tropical Pediatrics
Vol. 55, No. 2
