connective tissue diseases is not likely to be greatly elevated in children of women with implants (Kjoller et al., 1998).
Since study participants were drawn from a nationwide register of patients and children were traced through population registers, sample selection bias was unlikely. However, using hospital record data, rather than clinical data collected prospectively, may limit the interpretation of study results. Episodic symptoms of dysphagia, feeding problems, abdominal pain, or vomiting are probably evaluated outside the hospital setting and escape recognition by the national registry. The average time of five years between the date of implantation and the birth of a child may be too short to appropriately evaluate the effect of implant gel fluid diffusion or rupture. Few data were available on breast-feeding history, and the type of breast implant was not specified in 16% of the sample. Nevertheless this study has moderately large numbers of women and children and is well designed.
The committee concludes on the basis of the studies reviewed in this chapter that evidence for an association of maternal silicone breast implants and children's health effects is insufficient or flawed. No biologically plausible causation has been suggested. Convincing evidence is available that silicon concentrations in breast milk are the same in mothers with and without breast implants, and thus there are no data to support transmission of silicone to infants in breast milk of mothers with implants. A modest number of normal mothers are positive for ANAs. Except for rare instances, as noted, evidence that this or similar situations in mothers with silicone breast implants have deleterious effects on children is lacking. Evidence for children's esophageal disease caused by maternal breast implants is insufficient or flawed.