Background

Temporal and regional trends of malignant and reproductive disorders have renewed interest in environmental pollutants. Although it is still a matter of conjecture whether human fertility has changed, there is evidence indicating increasing frequency of male reproductive disorders. The suggestive evidence on a decline in sperm count have been attributed to pesticides and several other chemicals mimicking human reproductive hormones but also air pollution, tobacco smoking, sexual behaviour and changing family size have been suggested as possible explanations. We have witnessed a tremendous increase in experimental research on effects of xenobiotic weak hormones in the environment but it is striking that very few resources have been allocated epidemiologic research in this field.
Biopersistent organochlorines in food are an important source of environmental exposure to xenohormones. This group of chemicals include organochlorine pesticides and several industrial chemicals. Regulations at the European and the national level have reduced tissue levels in humans from the sixties to the eighties but temporal trends during past 15 years are less obvious. Biopersistent organochlorine contamination are ubiquitous in European populations but in humans a high intake of seafood is associated with high exposure, which in the Arctic exceeds recommended thresholds.
Animal experiments indicate reproductive toxicity for a low level exposure to biopersistent organochlorines, in wildlife the reproductive function of seals of the Baltic and other areas has been impaired by PCBs in the food chain but epidemiologic data are limited and major gaps in knowledge continues to preclude evidence based risk assessment and management.
From occupational surveys there are several examples of substances causing suppression of spermatogenesis at exposure levels not associated with other known adverse health effects.
This project was initiated by a recognition of the major need to provide epidemiological evidence in support of or against the environmental hormone hypothesis and to increase our limited knowledge on human health impact of dietary persistent organochlorines.