Health Stream Literature Summary - Issue 56 - December 2009

A cross-sectional analysis of type II diabetes in a community with exposure to perfluorooctanoic acid (PFOA).
MacNeil J, Steenland NK, Shankar A and Ducatman A. (2009) Environmental Research, 109(8); 997-1003.

Perfluorooctanoic acid (PFOA, C8) is used in the manufacture of several types of fluoropolymers as a polymerisation aid. PFOA is considered a probable human carcinogen by the US Environmental Protection Agency however its human health effects are not well established. An increase in diabetes mellitus mortality has previously been reported in workers exposed to PFOA. Since 1951, PFOA has been used in manufacturing fluoropolymers at the DuPont's Washington Works plant in Washington, West Virginia. In 2001, a class-action lawsuit by local residents alleging contamination of drinking water supplies resulted in the implementation of a large cross-section health survey called the C8 Health Project. This paper describes a sub-study of the relationship between serum PFOA and type II diabetes in the community.

The C8 project began testing in August 2005 and completed testing in August 2006. Data were collected on 69,030 subjects with at least 1 year of exposure. Self-reported information on diabetes status was validated through examination of medical records, (referred to as 'validated type II diabetes'). PFOA was measured in the serum of participants and also fasting serum glucose level. The analysis was restricted to adults greater than or equal to 20 years of age (N = 54, 468). A prevalence case-control analysis was conducted to examine the relationship between exposure and type II diabetes. Cases were either those with self-reported type II diabetes or validated type II diabetes. Controls were those who did not report type II diabetes and were not found to have a diagnosis of type II diabetes after medical review. The primary analysis was restricted to long-term residents (N=13,922) of contaminated water districts (greater than or equal to 20 years, i.e. residence since 1985 or earlier). Type II diabetes cases for this analysis (N=1055) were restricted to those with medical record validation who had lived in a contaminated water district for at least 10 years prior to diagnosis. Risk factors in the final model included: age, gender, race, family history of type II diabetes and use of cholesterol- or blood-pressure lowering medication. An analysis was also conducted without the use of blood pressure or cholesterol medications. A linear regression analysis was also conducted for fasting serum glucose levels excluding those who reported eating in the 6 h prior to their blood draw and all subjects who self-reported or had validated type II diabetes (N=21,643). The final linear regression model included the risk factors of age, BMI, gender, diabetes family history and race.

There were 4278 cases of self-reported type II diabetes and 3539 cases of validated type II diabetes. Self-reported age-adjusted prevalence of diabetes in this population was 7.8% which is similar to that of Ohio (7.1%) and West Virginia (10.1%), based on 2005 data. Median serum PFOA was 28.1 ng/ml for all study subjects, 30.3 ng/ml for self-reported type II diabetes subjects, 32.6 ng/ml for validated type II diabetes and 48.5 for validated type II diabetes in long-term residents, diagnosed in the last 10 years. Odds ratios (ORs) for the primary analysis restricted to those who had lived in their contaminated water district for at least 20 years (mean duration = 31.7 years) with cases restricted to those medically validated with a least 10 years exposure before their diagnosis were calculated and after adjusting for covariates, there were no clear trends found for odds of diabetes with increasing decile of serum PFOA. Instead people with serum PFOA levels in the upper deciles showed lower risks of self-reported or validated Type II diabetes than the lowest (referent) decile, but without any consistent negative trend. The upper decile was also split into two for analysis but no increased risk of disease was found in the top 5%. ORs for PFOA decile without cholesterol- or blood-pressure-lowering medication showed little change. The ORs for final models with self-reported type II diabetes and validated type II diabetes with no restriction on length of residence showed no clear trend in the risk of diabetes with level of serum PFOA. The regression model for the log of fasting glucose level showed no consistent pattern between fasting serum glucose by decile and serum PFOA.

In this analysis there were no clear trends found between risk of type II diabetes or fasting serum glucose and serum PFOA level. The data here are limited by the cross-section nature of the study and the possibility of a causal relationship can not be ruled out on the basis of. Future analyses are planned using more detailed temporal exposure estimates. These analyses will be able to more accurately estimate exposure prior to disease development.

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