The quite recent policy statement from the American Academy of Pediatrics (AAP) drafted by Rogan and colleagues [1] is the source for today's short(ish) post. Highlighting a growing concern on the issue of iodine deficiency in women of reproductive age, the policy document also raises awareness of "commonly encountered environmental chemicals" potentially exacerbating such deficiency, and in particular "thiocyanate, nitrate and perchlorate". These chemicals are specifically mentioned because of their competition "for transport by the sodium iodide symporter (NIS)" involved in thyroid hormone biosynthesis. The paper by De Groef and colleagues [2] (open-access here) provides quite a good overview of the hows and whys of this chemical inhibition.
With my autism research hat on and hopefully without trying to make mountains out of molehills, I was interested in this latest policy statement in light of some interesting work talked about on this blog before. The Stine Andersen paper [3] covered in a previous post (see here) kinda sums up where we seem to be with regards to the 'association' between maternal hypothyroidism and subsequent heightened offspring risk of autism or an autism spectrum disorder (ASD). I did, on that post, also talk about iodine and the importance of iodine when it comes to making thyroid hormones. That iodine deficiency has also itself been linked to risk of offspring autism (see here) is another potentially important point to make.
The slightly more contentious area of 'chemical' (yes, that word again) involvement affecting iodine transport also seems to overlap with at least some work/speculation in the autism research arena. The paper by Gustavo Román [4] talking about environmental antithyroid agents and "transient in utero hypothyroxinemia" with autism in mind might be relevant. Román has already done some work in the area of thyroid hormones and offspring autism risk (see here) based on analyses from the Generation R cohort [5] (open-access). In that review article [4] there is talk about thiocyanate for example, and it being found in both food and other environmental sources as well as quite a few more other agents which have the ability to interfere with thyroid manufacture or function.
Perchlorate and autism is a slightly less well researched area. The paper by Chang and colleagues [6] is a good first effort when it came to assessing whether perchlorate-contaminated water might have any population-wide connection to rates of autism based on an ecological study design. On that occasion, no link was reported. That being said, measuring autism rates from a social healthcare program and perchlorate levels in drinking water from local water authority data might not necessarily provide the most accurate data as per the implications from the data from Mandell and colleagues [7] for example and the question of individual exposure patterns (something which might also be relevant to the recent pesticide-autism work too).
Given what is already known about maternal iodine deficiency and offspring outcome [8] the AAP policy document should be a welcome addition to the recommendations to US healthcare professionals in terms of ensuring iodine sufficiency particularly during pregnancy and early nursing periods. The addition of environmental variables also potentially affecting iodine levels whilst not shared by everyone [9] is something which requires further investigation. The more specific discussion about thiocyanate exposure from tobacco smoke in particular, taps into more generalised guidance for women to avoid smoking and second-hand smoke during pregnancy.
Music to close, and a bit of a favourite of mine... Fireflies (best listened to loud).
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[1] Iodine Deficiency, Pollutant Chemicals, and the Thyroid: New Information on an Old Problem. Council on Environmental Health. Pediatrics. 2014. 26 May.
[2] De Groef B. et al. Perchlorate versus other environmental sodium/iodide symporter inhibitors: potential thyroid-related health effects. Eur J Endocrinol. 2006 Jul;155(1):17-25.
[3] Andersen S. et al. Attention deficit hyperactivity disorder and autism spectrum disorder in children born to mothers with thyroid dysfunction: a Danish nationwide cohort study. BJOG. 2014 Mar 10.
[4] Román GC. Autism: transient in utero hypothyroxinemia related to maternal flavonoid ingestion during pregnancy and to other environmental antithyroid agents. J Neurol Sci. 2007 Nov 15;262(1-2):15-26.
[5] Román GC. et al. Association of gestational maternal hypothyroxinemia and increased autism risk. Ann Neurol. 2013 Nov;74(5):733-42.
[6] Chang S. et al. Pediatric neurobehavioral diseases in Nevada counties with respect to perchlorate in drinking water: an ecological inquiry. Birth Defects Res A Clin Mol Teratol. 2003 Oct;67(10):886-92.
[7] Mandell DS. et al. Age of diagnosis among Medicaid-enrolled children with autism, 2001-2004. Psychiatr Serv. 2010 Aug;61(8):822-9.
[8] Zimmerman MB. The effects of iodine deficiency in pregnancy and infancy. Paediatr Perinat Epidemiol. 2012 Jul;26 Suppl 1:108-17.
[9] Leung AM. et al. Environmental perchlorate and thiocyanate exposures and infant serum thyroid function. Thyroid. 2012 Sep;22(9):938-43.
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(2014). Iodine Deficiency, Pollutant Chemicals, and the Thyroid: New Information on an Old Problem PEDIATRICS, 133 (6), 1163-1166 DOI: 10.1542/peds.2014-0900
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