Endometriosis

 What we know
 Incidence and costs
 Environmental risk factors

What we know

Endometriosis is a chronic disorder that develops when endometrial cells successfully implant and grow in locations in the body outside the uterus, such as on the surface of the ovaries or outside the intestine, for example. Endometrial cells form the tissue that lines the womb. During the menstrual cycle, they respond to hormonal signals and grow and break down. In endometriosis these cells located outside the uterus continue to grow and break down once a month, leading to internal bleeding. This causes pain and internal scarring. Symptoms of endometriosis include lower abdominal pain, infertility, pain with intercourse, fatigue, allergic diseases and bowel and bladder problems.

Incidence and costs

It is estimated that endometriosis affects 14 million women and girls in Europe alone, and costs the EU an estimated 30 billion euros a year in days taken off work [1]. There are suggestions that prevalence of the disease is on the rise, but this is difficult to confirm due to the inconsistent records and the fact that endometriosis is a disease difficult to diagnose.

Several theories propose mechanisms of development for endometriosis. One suggestion is that the disease occurs as a result of retrograde menstruation, whereby a certain amount of endometrial cells escape the uterus via the fallopian tubes instead of exiting via the vagina during menstruation. Another theory is that the cells lining the peritoneal cavity (a membrane that lines the abdominal cavity) transform themselves into endometrial cells.

Both the endocrine (hormone) and immune systems are involved in the survival and implantation of endometrial tissue. Endometriosis requires oestrogen to aid the survival and promote implantation. The immune system in turn, fails to “clean up” endometrial implants.

The causes of endometriosis are still unknown. It is thought to result from the complex interaction between hereditary factors and the environment. Close relatives of someone with endometriosis have a 5-8% increased risk of developing the condition. However, genetic factors cannot explain all cases of endometriosis or the suggested increased disease incidence.

Environmental risk factors

Therefore, it is suggested that environmental factors have a significant role to play. Environmental agents implicated in endometriosis include dioxins and polychlorinated biphenyls (PCBs), which have dioxin-like qualities. For example, studies of a colony of Rhesus monkeys fed a diet containing dioxin found that ten years after exposure was discontinued, 70% of the animals receiving the low dose, and over 80% of those receiving the high dose had endometriosis, compared with 33% of the control animals not fed dioxin [2]. Furthermore, in Seveso, Italy, the site of an industrial accident that led to the release of high levels of a toxic form of dioxin, a group of exposed women have been reported to have a doubled risk of endometriosis [3], [4], [5].

Other environmental chemical culprits with endocrine-disrupting properties likely to affect the hormone system include: pesticides such as methoxychlor, which is weakly estrogenic; bisphenol A, a chemical used in many food and drink containers; alkylphenols, used in detergents; and plasticisers such as phthalates, used in many every-day products to make plastics more pliable. Although most of these chemicals are weakly estrogenic, in combination they may have a significant impact, particularly in susceptible individuals.

Further research into the role of environmental agents is clearly needed. However, the potentially important role of certain chemicals in the development endometriosis supports a precautionary approach, and the implementation of preventive measures aimed at reducing and preventing exposure to certain potentially hazardous chemicals.