title: Gender-specific protective effect of hemoglobin on arsenic-induced skin lesions.
abstract: Chronic arsenic poisoning remains a public health crisis in Bangladesh. As arsenic has been shown to bind to human hemoglobin (Hb), hematologic mechanisms may play a role in the pathway through which arsenic exerts its toxicity. Two separate studies, a case-control and a cohort, were conducted to investigate the role of Hb in the development of arsenic-induced skin lesions. In the first, conditional logistic regression was used to investigate the effect of Hb on skin lesions among 900 case-control pairs from Pabna, Bangladesh, in which individuals were matched on gender, age, and location. In the second, mixed linear regression models were used to examine the association between toenail arsenic, urinary arsenic, and Hb within a cohort of 184 individuals from 50 families in the same region who did not have arsenic-induced skin lesions. Hb was significantly associated with skin lesions but this association was gender specific. In males, a 40% reduction in the odds of skin lesions occurred for every 1 g/dL increase in Hb (odds ratio, 0.60; 95% confidence interval, 0.49-0.73). No effect was observed for females (odds ratio, 1.16; 95% confidence interval, 0.92-1.46). In the cohort of 184 individuals, no associations between toenail arsenic or urinary arsenic species and Hb levels were observed. Low Hb levels may exacerbate the detrimental health effects of chronic arsenic poisoning. Whereas providing clean water remains the optimal solution to Bangladesh's problem of arsenic poisoning, improving nutrition and reducing iron-deficiency anemia may ameliorate negative health effects, such as skin lesions in individuals who have been exposed.
authors.affiliation: Department of Environmental Health, Harvard School of Public Health, Room 1420, Building I, 665 Huntington Avenue, Boston, MA 02115, USA. cbreton@hsph.harvard.edu
authors.forename: Carrie V
authors.initials: CV
authors.lastname: Breton
authors.forename: E Andres
authors.initials: EA
authors.lastname: Houseman
authors.forename: Molly L
authors.initials: ML
authors.lastname: Kile
authors.forename: Quazi
authors.initials: Q
authors.lastname: Quamruzzaman
authors.forename: Mahmuder
authors.initials: M
authors.lastname: Rahman
authors.forename: Golam
authors.initials: G
authors.lastname: Mahiuddin
authors.forename: David C
authors.initials: DC
authors.lastname: Christiani
mesh_terms: D001151:Arsenic / Q000032:analysis; D020261:Arsenic Poisoning / Q000150:complications* / Q000453:epidemiology; D001459:Bangladesh / Q000453:epidemiology; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D015331:Cohort Studies; D015986:Confounding Factors, Epidemiologic; D004198:Disease Susceptibility; D004781:Environmental Exposure; D005260:Female; D005838:Genotype; D051549:Glutathione S-Transferase pi / Q000235:genetics; D005982:Glutathione Transferase / Q000235:genetics; D006454:Hemoglobins / Q000032:analysis*; D006801:Humans; D016014:Linear Models; D016015:Logistic Models; D008297:Male; D016133:Polymerase Chain Reaction; D012307:Risk Factors; D012878:Skin Neoplasms / Q000139:chemically induced* / Q000453:epidemiology / Q000235:genetics; D014874:Water Pollutants, Chemical / Q000032:analysis / Q000506:poisoning; D014881:Water Supply
chemical_list: D001151:Arsenic; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase; D006454:Hemoglobins; D014874:Water Pollutants, Chemical; C413545:glutathione S-transferase T1; C496556:GSTP1 protein, human