London School of Hygiene & Tropical Medicine

An association has been found between exposure to the chemical commonly known as C8, and delay in the onset of puberty. Dr Tony Fletcher, Senior Lecturer at the London School of Hygiene & Tropical Medicine, and a member of the C8 Science Panel, will present a summary of the study results at a press conference in the US today.

The C8 panel was established to determine whether a probably link exists between C8 and any human disease as part of a class action settlement of a lawsuit involving releases of a chemical known as C8 from DuPont's Washington Works in Wood County, West Virginia, United States. Dr Fletcher, and his two fellow panel members, all epidemiologists, were chosen jointly by the parties to the legal settlement.

It has been suggested that some polyfluoroalkyl compounds (PFCs) may alter animal sexual maturation. This study examines the relationship between levels of Perflurorooctaine Sulfonate (PFOA) and Perfluorooctanoic Acid (C8) measured in the blood serum of child participants in the C8 Health Project (3,076 boys and 2,931 girls), and estimates the chance of developing puberty and the number of days' delay in the average age of puberty. All participants had been resident for at least a year in the six water districts contaminated with C8 in the Mid-Ohio Valley.

Determinations were made as to whether a young person had reached puberty using the test results of male and female hormones which change due to puberty having occurred and, for the girls, asking whether menstrual periods had commenced. Dr Fletcher found that the association with pubertal delay was stronger for PFOS, or C8, and that there was a delay of about 5 to 6 months for boys and girls when higher exposure groups were compared with lower exposure groups. For PFOA there was a delay of about four months in puberty for girls.

Dr Fletcher comments: 'We did find an association between an exposure to PFCs, and in particular to C8, but these results need to be interpreted with caution. Other explanations need to be considered, in particular that the bodily changes associated with puberty could have led to changes in C8 levels in the children's blood serum. If puberty was causing a change in C8 concentrations in the body, rather than the other way around, this would still show up as an association between puberty and exposure. Another possibility is that some other factor might be leading to both changes in the age of puberty and difference in PFC uptake. We looked at other potential risks where we had the data, including reported smoking, alcohol intake, obesity and household income, and in no case did their inclusion make any difference to the findings. But there may be other such causes, and further research is needed'.