The increase in the incidence of various cancers in the 20th century led scientists to investigate potential environmental causes such as asbestos, silica, particulate matter, benzene, and formaldehyde. The signature health trends of today include declining IQ; rising rates of autism, obesity, diabetes, and testicular cancer; and worrisome indications of declining male and female fertility. A leading hypothesis for these 21st century ailments is the profusion of chemicals in our environment that disrupt the normal functioning of the endocrine system.
The origins of the endocrine disruption hypothesis can be traced back to the landmark study of the so-called “DES daughters” published in the New England Journal of Medicine in 1971. Women given the synthetic estrogen diethylstilbestrol during pregnancy gave birth to girls with a much higher likelihood of developing clear cell adenocarcinoma, a rare form of vaginal and cervical cancer. Later study has shown that DES children and grandchildren have higher rates of breast cancer, pregnancy complications, and, for girls and boys alike, obesity and cardiovascular disease.
The complex network of glands and organs known as the endocrine system synthesize, secrete, and respond to hormones (e.g., sex steroids, stress hormones, thyroid hormone), which in turn regulate a host of critical biological functions and processes including metabolism, growth, reproduction, and mood. “Endocrine disruption,” a term first coined in 1991, hypothesizes that chemical exposures can profoundly disrupt this finely-tuned system by directly or indirectly interfering with normal hormonal signaling.
CoMeta’s endocrine disruption theme captures 71 Litagion agents that are under investigation for their potential to cause human harm via endocrine disruption. These potentially endocrine disrupting chemicals (EDCs) represent more than a quarter of the current Litagion agent library reflecting just how central the endocrine disruption hypothesis has become in the biomedical literature. The degree of scientific support for whether these specific EDCs negatively impact human health varies significantly, but it is fair to say that there is widespread consensus that EDCs in general pose a serious threat to human health. One study estimates that the annual social cost of EDCs in terms of diminished IQ and increased incidence of obesity, diabetes, and other chronic disease totals more than 2% of U.S. gross domestic product.
With EDCs exacting such high social costs, it is natural to wonder whether the companies that have profited from their widespread use might ultimately be held accountable. As is often the case, the trouble for would-be plaintiffs is the ubiquity of the exposure and non-specificity of the harm. In the case of DES, injured plaintiffs recovered damages from DES manufacturers because both the exposure and harm were highly specific. Today, virtually everyone is exposed to multiple EDCs through the widespread use of pesticides, flame retardants, per- and polyfluoroalkyl substances, bisphenols, phthalates, and other compounds and a high percentage of the population suffers one or more chronic diseases associated with such exposure.
But scientific understanding of the specific mechanisms by which EDCs disrupt the normal functioning of the endocrine system is advancing rapidly. For example, while scientists have long known that some EDCs mimic hormones (e.g., oganotins) resulting in hormone overproduction and others block hormone receptors (e.g., bisphenols) causing too little hormone production, scientists are now investigating how EDCs affect the metabolic processes within a cell that affect endocrine signaling. So-called “mitochondrial dysfunction” is yet another means by which EDCs can lead to chronic disease. It is not far-fetched to think that such detailed mechanistic study will one day reveal one or more signature EDC exposure-disease pathways that could open the door to a range of new EDC-related litigation events.
Casualty insurers are arguably in a better position than consumers to manage the risk of endocrine disruption. EDCs are everywhere and so difficult to avoid entirely as a consumer. Casualty insurers also cannot avoid EDCs entirely, at least not if they hope to remain relevant to a wide swath of the U.S. economy. Instead they should seek to hold a portfolio of EDCs that diversifies against the risk that scientists discover signature EDC exposure-disease pathways that support litigation. Like any well-diversified asset portfolio, its composition should then evolve as new information (i.e., biomedical discovery) becomes available.
But, wait: How can casualty insurers manage such a portfolio when there are so many EDCs and with commercial exposures and scientific literature constantly shifting? Well, you wouldn’t be reading this blog if you didn’t know the answer to that question… [Answer: CoMeta and Oortfolio!]