Letters to the Editor 1149 REFERENCES

Stephen P. Juraschek and Elizabeth Selvin (e-mail: [email protected]) Department of Epidemiology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD

DOI: 10.1093/aje/kwu057; Advance Access publication: March 26, 2014

Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health 2014. This work is written by (a) US Government employee(s) and is in the public domain in the US.

RE: “NEONATAL BILIRUBIN LEVELS AND CHILDHOOD ASTHMA IN THE US COLLABORATIVE PERINATAL PROJECT, 1959–1965” We read with interest the paper by Huang et al. (1) suggesting that neonatal jaundice is associated with childhood asthma. Using data from the Collaborative Perinatal Project (CPP), Huang et al. examined whether the associations between neonatal jaundice and childhood asthma could be due to phototherapy (which was unavailable at the time of the CPP) or a high bilirubin level itself, but the accompanying commentary (2) raised the issue of a potential common cause for both childhood asthma and hyperbilirubinemia, among other possible explanations. We suggest that such a common cause is likely to be maternal asthma, based on our recent findings on the neonatal health of infants born to mothers with asthma (3). We found an increased risk of hyperbilirubinemia (odds ratio = 1.09, 95% confidence interval: 1.04, 1.14) associated with maternal asthma after adjustment for detailed demographic Am J Epidemiol. 2014;179(9):1145–1150

and clinical information from a large US cohort study of electronic medical records. Given that maternal asthma is known to increase the risk of asthma among offspring (4), maternal asthma is a plausible common cause that has not (to our knowledge) been considered in the literature. These relationships are bound to be complex, and careful attention is needed to properly model the potential confounders and mediators of maternal-infant-childhood associations (5). In this case, Huang et al. adjusted their results for maternal allergic conditions (1), but this is a poor proxy for maternal asthma, since about half of current asthma is nonallergic and perhaps 30% of nonasthmatics have a common allergy response. On the other hand, we recognize that the differences between asthma diagnosis and treatment in the 1960s and in the present day add further complexity to the interpretation of these findings. This is an intriguing area of research,

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1. Knowles JW, Reaven G. RE: “Temporal relationship between uric acid concentration and risk of diabetes in a community-based study population” [letter]. Am J Epidemiol. 2014;179(9):1147–1148. 2. Pfister R, Barnes D, Luben R, et al. No evidence for a causal link between uric acid and type 2 diabetes: a Mendelian randomisation approach. Diabetologia. 2011;54(10): 2561–2569. 3. Howell RR. The interrelationship of glycogen storage disease and gout. Arthritis Rheum. 1965;8(5):780–785. 4. Stirpe F, Della Corte E, Bonetti E, et al. Fructose-induced hyperuricaemia. Lancet. 1970;2(7686):1310–1311. 5. Kodama S, Saito K, Yachi Y, et al. Association between serum uric acid and development of type 2 diabetes. Diabetes Care. 2009;32(9):1737–1742. 6. Bhole V, Choi JWJ, Kim SW, et al. Serum uric acid levels and the risk of type 2 diabetes: a prospective study. Am J Med. 2010; 123(10):957–961. 7. Herman JB, Goldbourt U. Uric acid and diabetes: observations in a population study. Lancet. 1982;2(8292):240–243. 8. Juraschek SP, McAdams-Demarco M, Miller ER, et al. Temporal relationship between uric acid concentration and risk of diabetes in a community-based study population. Am J Epidemiol. 2014;179(6):684–691. 9. Yang Q, Köttgen A, Dehghan A, et al. Multiple genetic loci influence serum urate levels and their relationship with gout and cardiovascular disease risk factors. Circ Cardiovasc Genet. 2010;3(6):523–530. 10. Mazzali M, Hughes J, Kim YG, et al. Elevated uric acid increases blood pressure in the rat by a novel crystalindependent mechanism. Hypertension. 2001;38(5):1101–1106. 11. Gonick HC, Rubini ME, Gleason IO, et al. The renal lesion in gout. Ann Intern Med. 1965;62:667–674. 12. Mazzali M, Kanellis J, Han L, et al. Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressureindependent mechanism. Am J Physiol Renal Physiol. 2002; 282(6):F991–F997.

13. Nakagawa T, Mazzali M, Kang DH, et al. Hyperuricemia causes glomerular hypertrophy in the rat. Am J Nephrol. 2003; 23(1):2–7. 14. Feig DI, Soletsky B, Johnson RJ. Effect of allopurinol on blood pressure of adolescents with newly diagnosed essential hypertension: a randomized trial. JAMA. 2008;300(8): 924–932. 15. Assadi F. Allopurinol enhances the blood pressure lowering effect of enalapril in children with hyperuricemic essential hypertension. J Nephrol. 2014;27(1):51–56. 16. Siu Y-P, Leung K-T, Tong MK-H, et al. Use of allopurinol in slowing the progression of renal disease through its ability to lower serum uric acid level. Am J Kidney Dis. 2006;47(1): 51–59. 17. Goicoechea M, de Vinuesa SG, Verdalles U, et al. Effect of allopurinol in chronic kidney disease progression and cardiovascular risk. Clin J Am Soc Nephrol. 2010;5(8): 1388–1393. 18. Momeni A, Shahidi S, Seirafian S, et al. Effect of allopurinol in decreasing proteinuria in type 2 diabetic patients. Iran J Kidney Dis. 2010;4(2):128–132. 19. Gibson T, Rodgers V, Potter C, et al. Allopurinol treatment and its effect on renal function in gout: a controlled study. Ann Rheum Dis. 1982;41(1):59–65. 20. Parascandola M, Weed DL. Causation in epidemiology. J Epidemiol Community Health. 2001;55(12): 905–912.

1150 Letters to the Editor

and given the high prevalence of asthma in contemporary pregnancy cohorts, it merits further attention. ACKNOWLEDGMENTS Conflict of interest: none declared. REFERENCES

Pauline Mendola1, S. Katherine Laughon1, and Tuija I. Männistö2 (e-mail: [email protected]) 1 Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892 2 Kastelli Research Centre, National Institute for Health and Welfare, FIN-90014 Oulu, Finland

DOI: 10.1093/aje/kwu064; Advance Access publication: March 31, 2014

© The Author 2014. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: [email protected].

THE AUTHORS REPLY We thank Mendola et al. (1) for their interest in our work (2). In the invited commentary accompanying our article, Kuzniewicz et al. (3) questioned whether the association between neonatal hyperbilirubinemia and asthma was due to confounding by breastfeeding or Rh isoimmunization. Likewise, Mendola et al. are concerned about confounding by maternal asthma (1). We created the model of the association between bilirubin level and asthma by putting each potential confounder into the model one at a time (2). However, the β coefficient of the exposure changed very slightly for breastfeeding, probably because of the small difference in the prevalence of breastfeeding between asthma (16.1%) and nonasthma (17.1%) groups in this study. Consequently, breastfeeding was not included in the final model. Similarly, only 0.70% and 0.81% of subjects in the asthma and nonasthma groups had Rh isoimmunization. When we excluded them from the analysis, the association remained unchanged. Finally, although the prevalence of child asthma was much higher among those whose mothers had asthma (14.3%) than among those whose mothers did not have asthma (4.5%), the prevalence of maternal asthma did not vary by bilirubin level (2.31%, 2.36%, 2.34%, 2.29%, and 2.33% in children with bilirubin levels of ≤3, 3.1–6, 6.1–9, 9.1–15, and >15 mg/ dL, respectively). As a result, the β coefficient did not change when we controlled for maternal asthma in the model. We agree that the diagnosis of asthma has changed over time. However, the misclassification of asthma may not necessarily differ in high- and low-bilirubin groups. This nondifferential misclassification in terms of bilirubin level may have biased the results toward the null. On the other hand, considering that the prevalence of childhood asthma in this study

was 5.26% in the 1960s and 1970s (2), the misclassification might not have been substantial. ACKNOWLEDGMENTS Conflict of interest: none declared. REFERENCES 1. Mendola P, Laughon SK, Männistö TI. Re: “Neonatal bilirubin levels and childhood asthma in the US Collaborative Perinatal Project, 1959–1965” [letter]. Am J Epidemiol. 2014;179(9): 1149–1150. 2. Huang L, Bao Y, Xu Z, et al. Neonatal bilirubin levels and childhood asthma in the US Collaborative Perinatal Project, 1959–1965. Am J Epidemiol. 2013;178(12):1691–1697. 3. Kuzniewicz MW, Wickremasinghe AC, Newman TB. Invited commentary: does neonatal hyperbilirubinemia cause asthma? Am J Epidemiol. 2013;178(12):1698–1701.

Lisu Huang1,2, Yixiao Bao2, and Jun Zhang1 (e-mail: [email protected]) 1 MOE-Shanghai Key Laboratory of Children’s Environmental Health, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200092, People’s Republic of China 2 Pediatrics Department, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200092, People’s Republic of China

DOI: 10.1093/aje/kwu065; Advance Access publication: March 31, 2014

Am J Epidemiol. 2014;179(9):1145–1150

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1. Huang L, Bao Y, Xu Z, et al. Neonatal bilirubin levels and childhood asthma in the US Collaborative Perinatal Project, 1959–1965. Am J Epidemiol. 2013;178(12):1691–1697. 2. Kuzniewicz MW, Wickremasinghe AC, Newman TB. Invited commentary: does neonatal hyperbilirubinemia cause asthma? Am J Epidemiol. 2013;178(12):1698–1701. 3. Mendola P, Männistö TI, Leishear K, et al. Neonatal health of infants born to mothers with asthma. J Allergy Clin Immunol. 2014;133(1):85–90.e1–4.

4. Martinez FD. Maternal risk factors in asthma. Ciba Found Symp. 1997;206:233–239. 5. VanderWeele TJ, Mumford SL, Schisterman EF. Conditioning on intermediates in perinatal epidemiology. Epidemiology. 2012; 23(1):1–9.

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