Science of The Total Environment – 2017
•We explored the associations between blood mercury levels and autistic behaviors.
•This study involved an ongoing multi-center prospective birth cohort.
•Blood mercury levels were repeatedly measured from early pregnancy to 3 years.
•Autistic behaviors were assessed at 5 years with the Social Responsiveness Scale.
•Prenatal and early childhood mercury levels were associated with autistic behaviors.
Although mercury is an established neurotoxin, only few longitudinal studies have investigated the association between prenatal and early childhood mercury exposure and autistic behaviors.
We conducted a longitudinal cohort study using an ongoing prospective birth cohort initiated in 2006, wherein blood mercury levels were measured at early and late pregnancy; in cord blood; and at 2 and 3 years of age. We analyzed 458 mother-child pairs. Autistic behaviors were assessed using the Social Responsiveness Scale (SRS) at 5 years of age. Both continuous SRS T-scores and T-scores dichotomized by a score of ≥ 60 or < 60 were used as outcomes.
The geometric mean of mercury concentrations in cord blood was 5.52 μg/L. In adjusted models, a doubling of blood mercury levels at late pregnancy (β = 1.84, 95% confidence interval [CI]: 0.39, 3.29), in cord blood (β = 2.24, 95% CI: 0.22, 4.27), and at 2 years (β = 2.12, 95% CI: 0.54, 3.70) and 3 years (β = 2.80, 95% CI: 0.89, 4.72) of age was positively associated with the SRS T-scores. When the SRS T-scores were dichotomized, we observed positive associations with mercury levels at late pregnancy (relative risk [RR] = 1.31, 95% CI: 1.08, 1.60) and in cord blood (RR = 1.28, 95% CI: 1.01, 1.63).
We found that blood mercury levels at late pregnancy and early childhood were associated with more autistic behaviors in children at 5 years of age. Further study on the long-term effects of mercury exposure is recommended.
Molecular Neurobiology – 22 July 2017
Exposure to organic forms of mercury has the theoretical capacity to generate a range of immune abnormalities coupled with chronic nitro-oxidative stress seen in children with autism spectrum disorder (ASD). The paper discusses possible mechanisms explaining the neurotoxic effects of mercury and possible associations between mercury exposure and ASD subtypes. Environmental mercury is neurotoxic at doses well below the current reference levels considered to be safe, with evidence of neurotoxicity in children exposed to environmental sources including fish consumption and ethylmercury-containing vaccines. Possible neurotoxic mechanisms of mercury include direct effects on sulfhydryl groups, pericytes and cerebral endothelial cells, accumulation within astrocytes, microglial activation, induction of chronic oxidative stress, activation of immune-inflammatory pathways and impairment of mitochondrial functioning. (Epi-)genetic factors which may increase susceptibility to the toxic effects of mercury in ASD include the following: a greater propensity of males to the long-term neurotoxic effects of postnatal exposure and genetic polymorphisms in glutathione transferases and other glutathione-related genes and in selenoproteins. Furthermore, immune and inflammatory responses to immunisations with mercury-containing adjuvants are strongly influenced by polymorphisms in the human leukocyte antigen (HLA) region and by genes encoding effector proteins such as cytokines and pattern recognition receptors. Some epidemiological studies investigating a possible relationship between high environmental exposure to methylmercury and impaired neurodevelopment have reported a positive dose-dependent effect. Retrospective studies, on the other hand, reported no relationship between a range of ethylmercury-containing vaccines and chronic neuropathology or ASD. On the basis of these results, we would argue that more clinically relevant research is required to examine whether environmental mercury is associated with ASD or subtypes. Specific recommendations for future research are discussed.
PubMed.gov – 8 May 2017
Environmental factors have been implicated in the etiology of autism spectrum disorder (ASD); however, the role of heavy metals has not been fully defined. This study investigated whether blood levels of mercury, arsenic, cadmium, and lead of children with ASD significantly differ from those of age- and sex-matched controls. One hundred eighty unrelated children with ASD and 184 healthy controls were recruited. Data showed that the children with ASD had significantly (p < 0.001) higher levels of mercury and arsenic and a lower level of cadmium. The levels of lead did not differ significantly between the groups. The results of this study are consistent with numerous previous studies, supporting an important role for heavy metal exposure, particularly mercury, in the etiology of ASD. It is desirable to continue future research into the relationship between ASD and heavy metal exposure