Arsenic exposure alters lung function and airway inflammation in children: A cohort study in rural Bangladesh.
Exposure to arsenic has been associated with increased risk of reduced lung function in adults, but the adverse impacts in early life are unclear. We aim to examine whether prenatal and childhood arsenic exposure is associated with reduced lung function and increased airway inflammation in school-aged children. Children born in the MINIMat cohort in rural Bangladesh were evaluated at 9years of age (n=540). Arsenic exposure was assessed in urine (U-As) that was collected from mothers during early pregnancy and their children aged 4.5 and 9years. In the 9-year-old children, lung function was assessed using spirometry and airway inflammation was assessed by the NIOX MINO system. C-reactive protein (CRP) and Clara cell secretory protein (CC16) concentrations were measured in plasma by immunoassays. The U-As concentrations in 9-year-old children were lower (median 53μg/l) compared to their mothers (median 76μg/l). Maternal U-As (log2transformed) was inversely associated with forced vital capacity (FVC) and forced expiratory volume at 1s (FEV1) (β=-12; 95% CI: -22, -1.5; p=0.031 and β=-12; 95% CI: -22, -1.9; p=0.023, respectively) in all children, and the associations were stronger in boys and among children with adequate height and weight, as well as among those whose mothers had higher percentages of methylarsonic acid (MMA) and lower percentages of dimethylarsinic acid (DMA). U-As (log2transformed) at 4.5 and 9years was positively associated with fractional exhaled nitric oxide (FENO) concentrations in boys (β=0.89; 95% CI: 0.13, 1.66; p=0.022 and β=0.88; 95% CI: 0.16, 1.61; p=0.017, respectively) but not in girls. Increased CC16 concentrations were associated with higher lung function indices. In conclusion, our findings suggest that prenatal arsenic exposure is related to impaired lung function, while childhood exposure may increase airway inflammation, particularly in boys.
Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.
Sultan
S
Ahmed
Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.
Evana
E
Akhtar
Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh.
Adity
A
Roy
Departments of Community Health Sciences and Epidemiology, Fielding School of Public Health, University of California Los Angeles, CA 90095, USA.
Ondine S
OS
von Ehrenstein
Institute of Environmental Medicine, Karolinska Institutet, SE-171 77 Stockholm, Sweden.
Marie
M
Vahter
Department of Clinical Trial and Clinical Epidemiology, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan.
Yukiko
Y
Wagatsuma
Infectious Diseases Division, icddr,b, Dhaka 1212, Bangladesh. Electronic address: rubhana@icddrb.org.
Rubhana
R
Raqib
D000328:Adult; D001151:Arsenic / Q000633:toxicity* / Q000652:urine; D001459:Bangladesh; D002097:C-Reactive Protein / Q000378:metabolism*; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D004781:Environmental Exposure; D004785:Environmental Pollutants / Q000633:toxicity* / Q000652:urine; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012424:Rural Population; D012737:Sex Factors; D014797:Vital Capacity
D004785:Environmental Pollutants; D002097:C-Reactive Protein; D001151:Arsenic
Airway inflammation; Arsenic exposure; Cohort study; Lung function; Niox Mino; Spirometry