So many people here have pointed at various environmental exposures to substances, etc. that this second statement is likely to be of widespread interest.
Endocr Rev. 2015 Nov 6:er20151010. [Epub ahead of print]
EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals.
Gore AC1, Chappell VA1, Fenton SE1, Flaws JA1, Nadal A1, Prins GS1, Toppari J1, Zoeller RT1.
Author information
Abstract
The Endocrine Society's first Scientific Statement in 2009 provided a wake-up call to the scientific community about how environmental endocrine-disrupting chemicals (EDCs) affect health and disease. Five years later, a substantially larger body of literature has solidified our understanding of plausible mechanisms underlying EDC actions and how exposures in animals and humans-especially during development-may lay the foundations for disease later in life. At this point in history, we have much stronger knowledge about how EDCs alter gene-environment interactions via physiological, cellular, molecular, and epigenetic changes, thereby producing effects in exposed individuals as well as their descendants. Causal links between exposure and manifestation of disease are substantiated by experimental animal models and are consistent with correlative epidemiological data in humans. There are several caveats because differences in how experimental animal work is conducted can lead to difficulties in drawing broad conclusions, and we must continue to be cautious about inferring causality in humans. In this second Scientific Statement, we reviewed the literature on a subset of topics for which the translational evidence is strongest: 1) obesity and diabetes; 2) female reproduction; 3) male reproduction; 4) hormone-sensitive cancers in females; 5) prostate; 6) thyroid; and 7) neurodevelopment and neuroendocrine systems. Our inclusion criteria for studies were those conducted predominantly in the past 5 years deemed to be of high quality based on appropriate negative and positive control groups or populations, adequate sample size and experimental design, and mammalian animal studies with exposure levels in a range that was relevant to humans. We also focused on studies using the developmental origins of health and disease model. No report was excluded based on a positive or negative effect of the EDC exposure. The bulk of the results across the board strengthen the evidence for endocrine health-related actions of EDCs. Based on this much more complete understanding of the endocrine principles by which EDCs act, including nonmonotonic dose-responses, low-dose effects, and developmental vulnerability, these findings can be much better translated to human health. Armed with this information, researchers, physicians, and other healthcare providers can guide regulators and policymakers as they make responsible decisions.
• A large number of chemicals and chemical classes are known to affect the thyroid system.
• Animal studies have also demonstrated that a number of chemicals, including but not limited to PCBs, PBDEs, some phthalates, and perchlorate, can reduce circulating levels of thyroid hormone.
Interestingly, not all of these chemicals also cause an increase in serum TSH.
• Some chemicals that affect the thyroid system in animals have been shown to be associated with cognitive deficits in humans. However, exposure is not always correlated with reductions in thyroid hormone in humans.
• Thyroid hormone produces different effects at different developmental stages—in humans as well as in animals—and the consequences of disruption are stage-specific.
• Some chemicals clearly exert actions on the thyroid system in humans and animals at environmentally relevant concentrations. The mechanism(s) by which chemicals can produce this effect varies.
• Three key areas of research are urgently needed:
1) identify biomarkers of thyroid hormone action in tissues to test the ability of chemicals to interfere with hormone action in the absence of effects on serum hormone concentrations;
2) determine whether chemicals with different mechanisms of action on the thyroid system can synergize to cause adverse effects; and
3) identify high throughput assays that predict thyroid “disruption.”
Thyroid hormone is essential for normal development and for the control of many aspects of adult physiology in vertebrates. There is a growing list of synthetic chemicals
that can interfere with thyroid function or thyroid hormone action. There are several important conclusions to be drawn from the recent data on thyroid disruption.
First, there is good evidence from animal, biochemical, and human studies that specific chemicals can interfere with thyroid hormone action and cause adverse effects at the population level.
Second, the current biomarker of thyroid “disruption”—circulating levels of thyroid hormone— may not be faithfully reflecting EDC effects on thyroid
hormone action in tissues.
Specific EDCs have beenshownto interfere with a number of the pathways involved in thyroid hormone biosynthesis, metabolism, receptor activation, and function. Recent
publications have demonstrated effects of EDCs on iodide uptake and organification, thyroid hormone interactions with its distributor proteins in the blood, and metabolism and cellular transport of thyroid hormone. Developmental exposure is particularly pertinent to the thyroid axis because neural development is impaired by
thyroid perturbations. Evidence from rodents supports cognitive and other behavioral impairments caused by prenatal EDC exposures that interfere with thyroid hormone
action. Epidemiological data in humans support cognitive deficits in children and diminished IQ in children exposed to certain thyroid disruptors prenatally.
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