Early-life exposure to lithium and boron from drinking water

2012 ◽  
Vol 34 (4) ◽  
pp. 552-560 ◽  
Author(s):  
Florencia Harari ◽  
Ana María Ronco ◽  
Gabriela Concha ◽  
Miguel Llanos ◽  
Margaretha Grandér ◽  
...  
2016 ◽  
Vol 58 (10) ◽  
pp. 1040-1045 ◽  
Author(s):  
Ann Aschengrau ◽  
Lisa G. Gallagher ◽  
Michael R. Winter ◽  
Veronica M. Vieira ◽  
Patricia A. Janulewicz ◽  
...  

2016 ◽  
Vol 2016 (1) ◽  
Author(s):  
Florencia Harari* ◽  
Anna Karin Bernhardsson ◽  
Brita Palm ◽  
Esperanza Casimiro ◽  
Ying Lu ◽  
...  

2020 ◽  
Vol 4 (2) ◽  
pp. e089
Author(s):  
Md Alfazal Khan ◽  
Meera Hira-Smith ◽  
Syed Imran Ahmed ◽  
Mohammad Yunus ◽  
S. M. Tafsir Hasan ◽  
...  

2016 ◽  
Vol 82 (1) ◽  
pp. 169 ◽  
Author(s):  
Ann Aschengrau ◽  
Patricia A. Janulewicz ◽  
Roberta F. White ◽  
Veronica M. Vieira ◽  
Lisa G. Gallagher ◽  
...  

2022 ◽  
Vol 21 (1) ◽  
Author(s):  
Charlotte R. Doran ◽  
Ann Aschengrau

Abstract Background Communities in Cape Cod, Massachusetts were exposed to tetrachloroethylene (PCE) through contaminated drinking water from 1969 to 1983. PCE exposure during adulthood has well-established neurotoxic effects; however, long-term impacts stemming from early life exposure, especially adverse effects on sleep quality, are not well understood. Methods The present analysis was based on data from the Cape Cod Health Study, a retrospective cohort study of the long-term neurotoxic impacts of early-life exposure to PCE-contaminated drinking water. Exposure to PCE-contaminated water was estimated using a validated leaching and transport model. Measures of sleep quality were obtained from self-administered questionnaires. Generalized estimating equations were used to generate risk ratios and 95% confidence intervals to estimate the association between early-life PCE exposure and sleep quality among 604 participants. Results Compared to unexposed participants, any PCE exposure during early life was associated with 1.57 times the risk of reporting breathing pauses during sleep (95% CI 0.92–2.68). Low-level exposure to PCE was associated with 1.50 times the risk of reporting sleep apnea or other sleep disorders (95% CI 0.78–2.89), while high levels of exposure had comparable risk compared to no exposure (RR = 0.94, 95% CI 0.50–1.79). Weak or no associations were observed for other sleep quality outcomes. In stratified analyses participants with mental illness and/or substance use disorder had increased risk ratios for short sleep duration associated with PCE exposure. Conclusion These findings suggest that early-life exposure to PCE may be associated with a moderate increase in the risk of reporting breathing pauses during sleep in adulthood and that a history of mental illness and/or substance use disorder may exacerbate the risk of short sleep duration.


2013 ◽  
Vol 42 (4) ◽  
pp. 1077-1086 ◽  
Author(s):  
A. H. Smith ◽  
M. Yunus ◽  
A. F. Khan ◽  
A. Ercumen ◽  
Y. Yuan ◽  
...  

2012 ◽  
Vol 211 ◽  
pp. S140-S141
Author(s):  
Florencia Harari Freire ◽  
Ana María Ronco ◽  
Gabriela Concha ◽  
Miguel Llanos ◽  
Francisca Castro ◽  
...  

2016 ◽  
Vol 86 (1-2) ◽  
pp. 36-47 ◽  
Author(s):  
Imen Dridi ◽  
Nidhal Soualeh ◽  
Torsten Bohn ◽  
Rachid Soulimani ◽  
Jaouad Bouayed

Abstract.This study examined whether perinatal exposure to polluted eels (Anguilla anguilla L.) induces changes in the locomotor activity of offspring mice across lifespan (post-natal days (PNDs) 47 – 329), using the open field and the home cage activity tests. Dams were exposed during gestation and lactation, through diets enriched in eels naturally contaminated with pollutants including PCBs. Analysis of the eel muscle focused on the six non-dioxin-like (NDL) indicator PCBs (Σ6 NDL-PCBs: 28, 52, 101, 138, 153 and 180). Four groups of dams (n = 10 per group) received either a standard diet without eels or eels (0.8 mg/kg/day) containing 85, 216, or 400 ng/kg/day of ϵ6 NDL-PCBs. The open field test showed that early-life exposure to polluted eels increased locomotion in female offspring of exposed dams but not in males, compared to controls. This hyperlocomotion appeared later in life, at PNDs 195 and 329 (up to 32 % increase, p < 0.05). In addition, overactivity was observed in the home cage test at PND 305: exposed offspring females showed a faster overall locomotion speed (3.6 – 4.2 cm/s) than controls (2.9 cm/s, p <0.05); again, males remained unaffected. Covered distances in the home cage test were only elevated significantly in offspring females exposed to highest PCB concentrations (3411 ± 590 cm vs. 1377 ± 114 cm, p < 0.001). These results suggest that early-life exposure to polluted eels containing dietary contaminants including PCBs caused late, persistent and gender-dependent neurobehavioral hyperactive effects in offspring mice. Furthermore, female hyperactivity was associated with a significant inhibition of acetylcholinesterase activity in the hippocampus and the prefrontal cortex.


PEDIATRICS ◽  
2020 ◽  
Vol 146 (Supplement 4) ◽  
pp. S332.2-S333
Author(s):  
Suzanne R. Kochis ◽  
Jennifer Dantzer

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