Collaboration reveals in utero and early life exposure to arsenic in drinking water decreases lung function in children

July 8, 2016

Over the last ten years, it has become increasingly evident that early life exposures to arsenic in mice and humans can lead to alterations in lung function and chronic lung disease in adults.  Research conducted by Dr. Clark Lantz, Associate Director of the University of Arizona Superfund Research Program (UA SRP) has shown that in utero and early postnatal exposure of mice to arsenic in drinking water alters airway structure, increases inflammation and alters adult pulmonary function.1,2 Similar alterations have also been observed in human populations. However, very few studies have examined the effects of these early life arsenic exposures on pulmonary function and disease in children. 

Also during this last decade, Dr. Lantz has formed a strong collaboration with Dr. Rogelio Recio-Vega from the Universidad Autonoma de Coahuila, Torreon, Mexico. The collaboration has resulted in numerous exchanges of faculty and students between the UA SRP and Universidad Autonoma de Coahuila, and in the development of research studies into the effects of arsenic on children living in and around Torreon, Mexico. The UA SRP has played a key role in this collaborative research by providing intellectual input from investigators and by analyzing samples from the study. This collaborative research has resulted in a series of three publications with the most recent one appearing this month in Environmental and Molecular Mutagenesis.3,4,5

These publications show that exposure to arsenic through drinking water during in utero and early life is associated with a decrease in lung function in children. Further they demonstrate that this decline in lung function is negatively correlated with anti-inflammatory proteins and positively correlated with pro-inflammatory biomarkers and that polymorphisms in arsenic metabolizing genes negatively influence arsenic metabolism. These results indicate that arsenic-induced alterations in inflammatory biomarkers may contribute to the development of restrictive lung diseases in children and that carriers of arsenic metabolizing gene variants may be at increased risk for arsenic-related diseases.

The on-going collaboration between the UA SRP and Universidad Autonoma de Coahuila exemplifies the NIEHS Superfund Research Program mandate to encourage investigator-initiated research translation and to identify and respond to emerging environmental threats to human health, on both a local and global scale.


1Lantz, R. Clark, Binh Chau, Priyanka Sarihan, Mark L. Witten, Vadim I. Pivniouk, Guan Jie Chen. In utero and postnatal exposure to arsenic alters pulmonary structure and function.  Toxicol Appl Pharmacol. 235:105-113, 2009. 

2Petrick, Jay S., Francoise M. Blachere, Ornella Selmin and R. Clark Lantz.  Inorganic arsenic as a developmental toxicant: in utero exposure and alterations in developing lung.  Mol. Nut. Food Res.  53:583-591, 2009.

3Recio-Vega Rogelio, Tania Gonzalez-Cortes, Edgar Olivas-Calderon, R. Clark Lantz, A. Jay Gandolfi, Cesar Gonzalez-De Alba. In utero and early childhood exposure to arsenic decreases lung function in children. J Appl Toxicol, 35:358-366, 2015. 

4Olivas-Calderón E, Recio-Vega R, Gandolfi AJ, Lantz RC, González-Cortes T, Gonzalez-De Alba C, Froines JR, Espinosa-Fematt JA, Lung inflammation biomarkers and lung function in children chronically exposed to arsenic Toxicol Appl Pharmacol  287:161-167, 2015.

5Recio-Vega, Rogelio, Tania González-Cortes, Edgar Olivas-Calderón, R. Clark Lantz, A. Jay Gandolfi, Gladis Michel-Ramirez.  Association between polymorphisms in arsenic metabolism genes with urinary arsenic methylation profile in girls and boys chronically exposed to arsenic.  2016,  Environment Mol Mutagenesis. DOI: 10.1002/em.22026