Chemical exposure

The number of new breast cancer cases among women is increasing in almost all western countries and evidence is emerging that environmental influences, including chemical exposure, are playing a role. Although an ageing population, better screening, late age at first childbirth and genetics are shown to contribute to the rising incidence, the sheer number of newly diagnosed cases cannot solely be explained by these factors. In my recent review of toxicological and epidemiological evidence entitled ‘Breast cancer and exposure to hormonally active chemicals’, some of the most important findings related to the causes of breast cancer are highlighted. It suggests a need to reappraise the dominant view that breast cancer is a genetic and lifestyle disease. Risk reduction will not be achievable without considering preventable causes, particularly exposure to certain environmental chemicals.

Analysis of the differences in cancer incidence between identical twins can be used to estimate the relative contribution of heritable and environmental factors to disease causation. Recent studies among Scandinavian twins found that hereditability accounted for 27 per cent of the variation, shared environmental factors explained 6 per cent and environmental factors not common to the pair contributed 67 per cent. Studies of families with a heritable predisposition to breast cancer suggest environmental factors make a significant contribution to disease causation. For example, women who carry a mutated form of the tumour suppressor genes BRCA1 and BRCA2 suffer from a significantly higher risk of developing breast and ovarian cancer. However, carriers of the altered genes who were born before 1940 face a 24 per cent risk of developing breast cancer by the age of 50, compared with a 67 per cent risk of being diagnosed with breast cancer at 50 years of age among women born after 1940. Together, these observations show that even where women have a genetic background that strongly predisposes them to breast cancer, non-genetic factors can dramatically modulate risk. This lends further urgency to the question: What are these non-genetic factors?

There is overwhelming evidence that oestrogens are strong determinants of breast cancer risks. This is not limited to natural oestrogens formed in a woman’s body, but extends to synthetic hormones used as pharmaceuticals, including those employed for the alleviation of menopausal symptoms. The demonstration of breast cancer risks from oestrogen-only and, more pronounced, from combined oestrogen-progesterone regimens is another case in point. Very recent, rapid decreases in breast cancer incidence in the USA, Canada, France, and in parts of Germany have followed a reduction in hormone therapy use.

Given that natural oestrogens and man-made oestrogens used as pharmaceuticals have a role in breast cancer, concerns arise about the potential contribution of industrial chemicals and pesticides with hormonal activity. Such chemicals include several that have been banned already, but can still be found in human tissues, such as polychlorinated biphenyls (PCBs) and compounds related to 1,1,1-trichloro-2,2-bis(4-chloro-phenyl)ethane (DDT). A large number of chemicals currently used in consumer products also fall into this category (phthalates, bisphenol A, UV-filter substances and many more).

To date, the few studies carried out to examine whether certain environmental chemicals are implicated in breast cancer leave much uncertainty about a possible link. But to avoid wrongly dismissing a role for chemicals in breast cancer, two issues must be addressed. First, the available studies have largely focused on single chemicals and have ignored the possibility that large numbers of agents may act in concert. Recent evidence from Spain suggests that cumulative exposure to oestrogenic chemicals is associated with breast cancer risks. A second reason why existing research may be leading us to wrongly dismiss a role for chemicals in breast cancer is that it has mainly addressed exposures later in a woman’s life when the breast tissue is perhaps less vulnerable. Critical periods of vulnerability during puberty and development in the womb must be considered. Very recent studies demonstrating breast cancer risks from exposure to the pesticide DDT before or during puberty, and from in-utero exposure to the oestrogenic anti-miscarriage drug diethylstilboestrol (DES) further underline the importance of early-life chemical exposure in breast cancer.

The report points to the need for targeted research strategies based on these recent findings. However, preventative action should not wait for human epidemiological studies that may take decades to complete. Preventative action should be based on evidence already available from experimental laboratory studies. Given the known role of oestrogens in breast cancer, it would be prudent to reduce exposures to chemicals that can mimic oestrogen. Consideration should therefore be given to amending current chemicals policy so that such chemicals are replaced with safer alternatives, where possible.

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