PFAS Health Study Component four: Data linkage study of health outcomes associated with living in PFAS exposure areas December 2021
Creators: name: Law, Hsei Di
name: Armstrong, Bruce
name: D'Este, Catherine
name: Randall, Deborah
name: Hosking, Rose
name: Lazarevic, Nina
name: Trevenar, Susan
name: Smurthwaite, Kayla
name: Lal, Aparna
name: Lucas, Robyn
name: Mueller, Jochen
name: Clements, Archie
name: Kirk, Martyn
name: Korda, Rosemary
Publisher: name: National Centre for Epidemiology and Population Health, The Australian National University
Year: 2021

description: Per- and polyfluoroalkyl substances (PFAS) are man-made chemicals that may have adverse effects on the environment and human health. The primary aim of the PFAS Data Linkage Study was to examine whether adverse health outcomes were more common in people who had lived in towns with known PFAS contamination—Katherine in Northern Territory (NT), Oakey in Queensland (Qld) and Williamtown in New South Wales (NSW) (the ‘exposure towns’). To do this, we compared rates of selected health outcomes in these towns, to rates in other separate but similar areas in Australia not known to have PFAS contamination (the ‘comparison areas’). We conducted three separate studies that investigated four groups of health outcomes. Study 1 investigated maternal and infant (perinatal) health (15 outcomes); Study 2 examined childhood development (6); and Study 3 investigated cancer (23) and deaths due to specific causes (4)—a total of 48 outcomes. All studies used multiple data sources with records collected over many years, which were linked to create richer datasets for analyses. All data used were originally collected for administrative purposes. We only used data that did not identify individual people and no direct contact was made with anyone whose data were included in the studies. Over the three separate studies, for most of the health outcomes studied we did not conclude that rates were higher in the towns than the comparison areas. For several health outcomes studied, we observed higher rates in one but not the other two towns. These were: in Katherine, prostate cancer; in Oakey, stillbirth, developmental vulnerability in two domains (physical health and wellbeing, and communication skills and general knowledge) and laryngeal cancer; and in Williamtown, postpartum haemorrhage (heavy blood loss following pregnancy), pregnancy-induced hypertension (high blood pressure), kidney cancer and lung cancer. Rates of death from coronary heart disease were higher in both Oakey and Williamtown. For most of these health outcomes, we estimated the differences between the towns and comparison areas to be relatively small. For others, the differences were of modest size, but our estimates were imprecise, meaning the likely size of each difference could be anywhere between quite small to quite large. Even though our studies included almost everyone who had ever lived in the towns in the years we had available data (in some cases dating back to 1983), some of the conditions studied are uncommon and we observed only a few cases. For these outcomes, we could not precisely estimate the differences between the towns and comparison areas, and there is very little we can say about whether a difference really exists. Due to the nature of our studies, there were certain design limitations. We were unable to fully account for certain risk factors (e.g. smoking) that could have led to observed differences in rates (or lack of them) between the towns and comparison areas (‘confounding’). In particular, we were not able to account for socioeconomic factors as well as we would have liked. This is important, as socioeconomic conditions are strongly linked to health. In addition, some findings could have arisen just by chance alone and not because an association truly exists. In light of the above, while there were higher rates of some adverse outcomes in individual towns, the evidence suggesting that this was due to living in these areas was limited. We did not have direct measurements of PFAS exposure and we cannot rule out that the higher rates were due to chance or confounding. Further, there was low consistency in our observations across the three towns (something we would not expect if PFAS caused an outcome), and there is limited evidence from other studies observing similar results or explaining how potential biological processes can result in PFAS causing these effects in humans. Overall, our findings are consistent with previous studies, which have not conclusively identified causative links between PFAS and these health outcomes.