adam

BACKGROUND:
Mercury (Hg) has been suspected of causing autism in the past, especially a suspected link with vaccinations containing thiomersal, but a review of the literature shows that has been largely repudiated. Of more significant burden is the total quantity of Hg in the environment. Here, we have used the Avon Longitudinal Study of Parents and Children (ALSPAC) to test whether prenatal exposure from total maternal blood Hg in the first half of pregnancy is associated with the risk of autism or of extreme levels of autistic traits. This is the largest longitudinal study to date to have tested this hypothesis and the only one to have considered early pregnancy.

METHODS:
We have used three strategies: (1) direct comparison of 45 pregnancies resulting in children with diagnosed autism from a population of 3840, (2) comparison of high scores on each of the four autistic traits within the population at risk (n~2800), and (3) indirect measures of association of these outcomes with proxies for increased Hg levels such as frequency of fish consumption and exposure to dental amalgam (n > 8000). Logistic regression adjusted for social conditions including maternal age, housing circumstances, maternal education, and parity. Interactions were tested between risks to offspring of fish and non-fish eaters.

RESULTS:
There was no suggestion of an adverse effect of total prenatal blood Hg levels on diagnosed autism (AOR 0.89; 95% CI 0.65, 1.22) per SD of Hg (P = 0.485). The only indication of adverse effects concerned a measure of poor social cognition when the mother ate no fish, where the AOR was 1.63 [95% CI 1.02, 2.62] per SD of Hg (P = 0.041), significantly different from the association among the offspring of fish-eaters (AOR = 0.74 [95% CI 0.41, 1.35]).

CONCLUSION:
In conclusion, our study identifies no adverse effect of prenatal total blood Hg on autism or autistic traits provided the mother ate fish. Although these results should be confirmed in other populations, accumulating evidence substantiates the recommendation to eat fish during pregnancy.

The German Environmental Specimen Bank (ESB) is a monitoring instrument of the German Federal Ministry for the Environment, Nature Conservation and Nuclear Safety. The permanent biobank facility is run since 1981 containing environmental and human samples from Germany. All samples are collected according to standard operating procedures (SOP). An standardized annual collection of human samples at four different regional sites of the country has been established since 1997. Routine sampling is done once a year, recruiting healthy non occupationally exposed students aged 20-29 years, in an equal gender distribution. The number of participants recruited is approximately 120 students per site and year. Directly after the annual sampling process, the human samples are analyzed for selected environmental chemicals. The time-trends of lead in blood, mercury and pentachlorophenol in 24 h-urine and polychlorinated biphenyls in plasma demonstrated a decrease of exposure during the last two decades by about 40-90 percent. In parallel retrospective studies using cryo-archived samples revealed increasing time trends of emerging chemicals used as substitutes for regulated toxicants. The data demonstrates the great relevance of the ESB for the health related environmental monitoring and shows the importance of human biomonitoring as a tool in information based policy making.

Neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and multiple sclerosis are characterized by a chronic and selective process of neuronal cell death. Although the causes of neurodegenerative diseases remain still unknown, it is now a well-established idea that more factors, such as genetic, endogenous, and environmental, are involved. Among environmental causes, the accumulation of mercury, a heavy metal considered a toxic agent, was largely studied as a probable factor involved in neurodegenerative disease course. Mercury exists in three main forms: elemental mercury, inorganic mercury, and organic mercury (methylmercury and ethylmercury). Sources of elemental mercury can be natural (volcanic emission) or anthropogenic (coal-fired electric utilities, waste combustion, hazardous-waste incinerators, and gold extraction). Moreover, mercury is still used as an antiseptic, as a medical preservative, and as a fungicide. Dental amalgam can emit mercury vapor. Mercury vapor, being highly volatile and lipid soluble, can cross the blood-brain barrier and the lipid cell membranes and can be accumulated into the cells in its inorganic forms. Also, methylmercury can pass through blood-brain and placental barriers, causing serious damage in the central nervous system. This review describes the toxic effects of mercury in cell cultures, in animal models, and in patients with neurodegenerative diseases. In vitro experiments showed that mercury exposure was principally involved in oxidative stress and apoptotic processes. Moreover, motor and cognitive impairment and neural loss have been confirmed in various studies performed in animal models. Finally, observational studies on patients with neurodegenerative diseases showed discordant data about a possible mercury involvement.

This paper assessed approximately 30 studies, mostly involving occupationally exposed subjects, concerning the extent to which those who developed elemental mercury (Hg)-induced central and/or peripheral neurotoxicities from chronic or acute exposures recover functionality and/or performance. While some recovery occurred in the vast majority of cases, the extent of such recoveries varied considerably by individual and endpoint. Factors accounting for the extensive inter-individual variation in toxicity and recovery were not specifically assessed such as age, gender, diet, environmental enrichment, chelation strategies and dose-rate. While the data indicate that psychomotor endpoints often show substantial and relatively rapid (i.e., 2-6 months) recovery and that neuropsychological endpoints display slower and less complete recovery, generalizations are difficult due to highly variable study designs, use of different endpoints measured between studies, different Hg exposures based on blood/urine concentrations and Hg dose-rates, the poor capacity for replicating findings due to the unpredictable/episodic nature of harmful exposures to elemental Hg, and the inconsistency of the initiation of studies after induced toxicities and the differing periods of follow up during recovery periods. Finally, there is strikingly limited animal model literature on the topic of recovery/reversibility of elemental Hg toxicity, a factor which significantly contributes to the overall marked uncertainties for predicting the rate and magnitude of recovery and the factors that affect it.

Investigators postulated that early-life exposure to organic mercury (Hg) significantly increases the risk of childhood neurodevelopmental disorders (NDs). The Vaccine Adverse Event Reporting System database was utilized to conduct a hypothesis testing case-control study by evaluating 3486 total adverse event reports reported following Haemophilus influenza type b (Hib) vaccination. Exposed subjects received a Thimerosal-containing formulation (HIBTITER™, Wyeth-Lederle), while unexposed subjects received a Thimerosal-free formulation (PEDVAXHIB™, Merck). Subjects were included if they received either of these two Hib vaccine formulations between 1995 and 1999. Cases were defined as adverse event reports with a reported outcome of autism, developmental delay, psychomotor delay, or NDs in general. Cases with reported outcomes of febrile convulsions, pyrexia, or injection site pain, all of which have no biologically plausible relation to Hg exposure, were also examined. Controls were defined as adverse event reports without any mention of the specific case outcome examined. Cases of reported autism (odds ratio (OR) = 2.75, p < 0.02), developmental delay (OR = 5.39, p < 0.01), psychomotor disorder (OR = 2.38, p < 0.03), and neurodevelopmental disorder in general (OR = 2.70, p < 0.001) were each significantly more likely than their respective controls to receive Thimerosal-containing Hib vaccine than Thimerosal-free Hib vaccine. Significant effects for neurodevelopmental disorder in general were observed for males (OR = 2.52, p < 0.005), but not females when separated by gender. For the outcomes that had no biologically plausible relation to Hg exposure, the cases were no more likely than their respective controls to receive Thimerosal-containing Hib vaccine than Thimerosal-free Hib vaccine. This study provides suggestive evidence of an association between Thimerosal and neurodevelopmental outcomes and provides support for carrying out additional well-designed studies examining the association between Thimerosal-containing vaccines and a wide range of neurodevelopmental outcomes.