BrooklynDodger(s) comment: The review notes that human exposures - mostly through food - are close to recommended limits. Although studies in people are recommended, the Dodger(s) doubt(s) these are feasible - the limit of direct observation is too high, imposed by the population rate of adverse reproductive outcomes, and the high prevalence of exposure. The highest exposed population is kidney dialysis patients, not an optimistic group to compare outcomes in the general population. Public health authorities are going to have to make this call by the extrapolation of laboratory studies to people. While emphasis is on the phthalate moiety, attention should also be paid to 2-ethyl hexanol.
Reproductive and Developmental Toxicity of Phthalates
Authors: Jan L. Lyche a; Arno C. Gutleb bc; ke Bergman d; Gunnar S. Eriksen c; AlberTinka J. Murk ef; Erik Ropstad a; Margaret Saunders g; Janneche U. Skaare ac
Affiliations: | a Department of Production Animal Clinical Science, Norwegian School of Veterinary Science, Oslo, Norway |
b Dpartement Environnement et Agro-biotechnologies (EVA), Centre de Recherche Public Gabriel Lippmann, Belvaux, Grand-duchy of Luxembourg | |
c National Veterinary Institute, Oslo, Norway | |
d Department of Environmental Chemistry, Stockholm University, Stockholm, Sweden | |
e Wageningen University, Wageningen, The Netherlands | |
f Wageningen Imares, IJmuiden, The Netherlands | |
g Biophysics Research Unit, University Hospital Bristol, NHS Foundation Trust, Bristol, United Kingdom |
Journal of Toxicology and Environmental Health, Part B, Volume 12, Issue 4 April 2009 , pages 225 - 249
The purposes of this review are to (1) evaluate human and experimental evidence for adverse effects on reproduction and development in humans, produced by exposure to phthalates, and (2) identify knowledge gaps as for future studies. The widespread use of phthalates in consumer products leads to ubiquitous and constant exposure of humans to these chemicals. Phthalates were postulated to produce endocrine-disrupting effects in rodents, where fetal exposure to these compounds was found to induce developmental and reproductive toxicity. The adverse effects observed in rodent models raised concerns as to whether exposure to phthalates represents a potential health risk to humans. At present, di(2-ethylhexyl) phthalate (DEHP), di-n-butyl phthalate (DBP), and butyl benzyl phthalate (BBP) have been demonstrated to produce reproductive and developmental toxicity; thus, this review focuses on these chemicals. For the general population, DEHP exposure is predominantly via food. The average concentrations of phthalates are highest in children and decrease with age. At present, DEHP exposures in the general population appear to be close to the tolerable daily intake (TDI), suggesting that at least some individuals exceed the TDI. In addition, specific high-risk groups exist with internal levels that are several orders of magnitude above average. Urinary metabolites used as biomarkers for the internal levels provide additional means to determine more specifically phthalate exposure levels in both general and high-risk populations. However, exposure data are not consistent and there are indications that secondary metabolites may be more accurate indicators of the internal exposure compared to primary metabolites. The present human toxicity data are not sufficient for evaluating the occurrence of reproductive effects following phthalate exposure in humans, based on existing relevant animal data. This is especially the case for data on female reproductive toxicity, which are scarce. Therefore, future research needs to focus on developmental and reproductive endpoints in humans. It should be noted that phthalates occur in mixtures but most toxicological information is based on single compounds. Thus, it is concluded that it is important to improve the knowledge of toxic interactions among the different chemicals and to develop measures for combined exposure to various groups of phthalates.
No comments:
Post a Comment