There is significant public concern about the potential health effects of exposure to mercury vapour (Hg(0)) released from dental amalgam restorations. The purpose of this article is to provide information about the toxicokinetics of Hg(0), evaluate the findings from the recent scientific and medical literature, and identify research gaps that when filled may definitively support or refute the hypothesis that dental amalgam causes adverse health effects. Dental amalgam is a widely used restorative dental material that was introduced over 150 years ago. Most standard dental amalgam formulations contain approximately 50% elemental mercury. Experimental evidence consistently demonstrates that Hg(0) is released from dental amalgam restorations and is absorbed by the human body. Numerous studies report positive correlations between the number of dental amalgam restorations or surfaces and urine mercury concentrations in non-occupationally exposed individuals. Although of public concern, it is currently unclear what adverse health effects are caused by the levels of Hg(0) released from this restoration material. Historically, studies of occupationally exposed individuals have provided consistent information about the relationship between exposure to Hg(0) and adverse effects reflecting both nervous system and renal dysfunction. Workers are usually exposed to substantially higher Hg(0) levels than individuals with dental amalgam restorations and are typically exposed 8 hours per day for 20-30 years, whereas persons with dental amalgam restorations are exposed 24 hours per day over some portion of a lifetime. This review has uncovered no convincing evidence pointing to any adverse health effects that are attributable to dental amalgam restorations besides hypersensitivity in some individuals.

High maternal oral exposures to chromium picolinate can cause morphological defects in developing offspring of mice.

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The issue of environmental tobacco smoke (ETS) exposure of children and respiratory health effects remains a matter of considerable controversy. We undertook to conduct a comprehensive and updated critical review and objective analysis of the epidemiological literature relevant to possible associations between ETS exposure and respiratory health of children. There appears to be a consistent association between parental (primarily maternal) smoking and respiratory symptoms and certain diseases in preschool children (44 reports). On the other hand, there is no consistent association between parental smoking and ( 1 ) respiratory symptoms or disease (46 reports); (2) middle ear disease (17 reports), (3) pulmonary function (38 reports), or (4) lung growth and development (5 reports) in school-age or older children. Possible explanations for these data and the age-related differences noted include (1) an ETS effect, with age-dependent variations in susceptibility and/or exposure to ETS; (2) pregnancy and/or lactational effects of maternal active smoking; (3) inaccuracies related to unvalidated clinical data and smoking status misclassification, and (4) variable treatment of socioeconomic status-related and other confounding factors. The available data relative to these issues is inconclusive, and which of these explanations pertain remains to be determined by further research.

Pregnant golden hamsters were injected ip with 2.5-20 mg/kg ochratoxin A on one of gestation days 7-10. The largest dosages when given on day 7,8, or 9 increased prenatal mortality and on day 9 diminished fetal growth. Malformations, such as micrognathia, hydrocephalus, short tail, oligodactyly, syndactyly, cleft lip, micromelia, and heart defects occurred, but no skeletal malformations were noted. These results add to the prenatal effects of ochratoxin A previously reported in mouse, rat, and chicken embryos.