Hazardous Chemicals in Medical Devices: Bisphenol A (BPA)

“Due to the extensive presence of Bisphenol A (BPA) in the environment, the large amount of scientific data showing human exposure to BPA via different routes and the fact that safety thresholds of no effect cannot be set for endocrine disrupting chemicals like BPA, it is of paramount importance to try to avoid all possible sources of exposure to BPA, particularly for vulnerable groups. In the healthcare sector, this can be achieved by phasing out hazardous chemicals in medical devices and using products that do not contain BPA and other harmful chemicals, whilst keeping high quality medical care.

Bisphenol A can be polymerized to produce polycarbonate plastic and other plastic products, or used as an additive in polyvinyl chloride (PVC) plastic. Applications in medical devices include among others, medical tubing, hemodialysers, newborn incubators and dental composite resins [1], [2]. Several studies have shown that BPA is a strong endocrine disrupting chemical (EDC), able to interfere with the action of estrogen and the estradiol hormone. Relating high and low levels of BPA exposure with an increase in the rate of developmental cancers, reproductive impairments (lower sperm counts, hormonal changes, enlarged prostate glands, early onset of puberty), neurological and behavioural disorders, cardiovascular diseases, obesity and diabetes [3], [4], [5], [6], [7].

BPA has been shown to leach from medical devices containing PVC (similarly to phthalates), from polymerized plastics in devices by diffusion of residual BPA left behind after the manufacturing process and from dental sealants in normal conditions of use [8], [9], [10]. The scientific community has considered leaching from medical devices as an important source of exposure to BPA in humans [7]. BPA has been found in a variety of human tissues and fluids such as placental tissue, breast milk, urine, blood, and saliva [7]. Once in the body, most BPA is believed to be quickly transformed by the liver and intestines from ‘free BPA’ (active molecule) to ‘conjugated BPA’ (not active and less likely to have health effects) and eliminated in the urine. However, BPA transformation is not fully efficient, and different bio-monitoring studies have shown that the general human population is exposed to BPA, including significant internal body exposure to free BPA [7]. Moreover, free BPA can be stored in body fat and slowly released into the blood stream. Moreover, a recent study has also suggested that MBP, a metabolite of BPA, can actually interfere more strongly with estrogen than BPA [11].”

“Haemodialysis patients can be exposed to substantial amounts of BPA due to the use of polycarbonate in dialysers, polysulfones in haemodialysis membranes and PVC in tubing [9]. Impaired kidney functions have been associated with a decrease in excretion [12] of urinary BPA. Hence, the use of BPA containing haemodialysis equipment can put patients at higher risk and due to their renal disease, lead to an increase of BPA in their blood.

A recent study found that newborns receiving medical treatment using four or more devices had a level of BPA in their urine three times higher than babies treated with three or fewer medical devices [13]. Premature infants that receive intensive care treatment are both developmentally and physiologically immature and are therefore at a higher risk of exposure to BPA. Early life exposure is of high concern. Different studies have suggested that young animals have inefficient abilities to transform chemical substances.”

– Health Care Without Harm (HCWH) (PDF)

29 April 2013

Endnotes:

1 Advanced Medical Technology Association, 2008, Medical devices and articles used in product manufacturing containing

Bisphenol A related materials. 5pp

2 Geen et al., 2011, Are potential sources for human exposure to bisphenol-A overlooked? Int J Hyg Environ Health 214: 339-347.

3 Hugo et al., 2008, Bisphenol A at environmentally relevant doses inhibits adiponectin release from human adipose tissue explants and adipocytes. Environ Health Persp 116: 1642-1647.

4 Lang et al., 2008, Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults. J Amer Med Assoc 300:1303-1310.

5 Kortenkamp et al., 2010, Combined exposures to anti-androgenic chemicals: steps towards cumulative risk assessment. Int J Androl 33: 463-474.

6 Li et al., 2010, Relationship between urine bisphenol-A (bisphenol A) level and declining male sexual function. J Androl 31: 500-506.

7 Vandenberg et al., 2007, Human exposure to bisphenol A (BPA) Reprod Toxicol 24: 139–177

8 Vandentorren et al., 2011, Bisphenol-A and phthalates contamination of urine samples by catheters in the Elfe pilot study: implications for large-scale biomonitoring studies. Environ Res 111: 761-764.

9 Murakami et al., 2007, Accumulation of bisphenol A in hemodialysis patients. Blood Purif 25: 290-294.

10 Fleisch et al., 2010, Bisphenol A and related compounds in dental materials. Pediatrics 126: 780-788.

11 Baker et al., 2012, 3D Models of MBP, a biologically active metabolite of Bisphenol A, in human estrogen receptor α and estrogen receptor β. PLoS ONE 7: e46078.

12 You et al. 2011, Renal function, Bisphenol A, and alkylphenols: Results from the National Health and Nutrition Examination Survey (NHANES 2003–2006). Environ Health Persp 119: 527-533.

13 Duty et al., 2013, Potential sources of Bisphenol A in the neonatal intensive care unit. Pediatrics 131: 483-489.

14 Calafat et al., Exposure to Bisphenol A and other phenols in neonatal intensive care unit premature infants. Environ Health Persp 117: 639-644.

15 Braun et al., 2012, Variability of urinary phthalate metabolite and Bisphenol A concentrations before and during pregnancy. Environ Health Persp 120: 739-745.

16 Lischka et al., 2011, Substituting phthalates in plastic medical devices: the Austrian experience-PVC-free neonatal intensive care unit of Children's Hospital Glanzing in Vienna. J Environ Sci Eng 5: 1162-1166.