scholarly journals Long-term Neurotoxic Effects of Early-life Exposure to Tetrachloroethylene-contaminated Drinking Water

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.


2016 ◽  
Vol 58 (10) ◽  
pp. 1040-1045 ◽  
Author(s):  
Ann Aschengrau ◽  
Lisa G. Gallagher ◽  
Michael R. Winter ◽  
Veronica M. Vieira ◽  
Patricia A. Janulewicz ◽  
...  

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Ann Aschengrau ◽  
Alexandra Grippo ◽  
Michael R. Winter ◽  
Margaret G. Shea ◽  
Roberta F. White ◽  
...  

Abstract Background Many studies of adults with occupational exposure to solvents such as tetrachloroethylene (PCE) have shown adverse effects on cognition, mood and behavioral problems. Much less is known about neurotoxic effects in early life at lower exposure levels seen in community settings. We recently reported that illicit drug use was more frequent among adults from Cape Cod, Massachusetts who were exposed to PCE-contaminated drinking water during gestation and early childhood than their unexposed counterparts. Using newly collected data from this population-based retrospective cohort study, the current analysis examines whether early life PCE exposure is also associated with drug use disorder over the life course. Methods Three-hundred and sixty-three subjects with prenatal and early childhood PCE exposure and 255 unexposed subjects were studied. These individuals (median age: 40–41 years) completed self-administered questionnaires on the eleven established diagnostic criteria for drug use disorder and confounding variables. A validated leaching and transport model was used to estimate exposure to PCE-contaminated water. Results Overall, 23.3% of subjects reported having at least one criterion for drug use disorder over their lifetime. Early life PCE exposure was associated with a modest increase in the lifetime presence of one or more diagnostic criteria for drug use disorder (adjusted RR: 1.4, 95% CI: 1.0–1.8). Compared to unexposed subjects, PCE-exposed subjects were more likely to report having most diagnostic criteria of drug use disorder, including neglecting major roles due to drug use, physical and psychological problems related to drug use, and giving up activities due to drug use. No dose-response relationships were observed with increasing levels of PCE exposure. Conclusions These results suggest that exposure to PCE-contaminated drinking water during early life modestly increases the risk of developing diagnostic criteria for drug use disorder later in life. Because this study has several limitations, these findings should be confirmed in follow-up investigations of other exposed populations with more diverse racial and socioeconomic characteristics.


2012 ◽  
Vol 34 (4) ◽  
pp. 552-560 ◽  
Author(s):  
Florencia Harari ◽  
Ana María Ronco ◽  
Gabriela Concha ◽  
Miguel Llanos ◽  
Margaretha Grandér ◽  
...  

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

2014 ◽  
Vol 26 (9) ◽  
pp. 613-624 ◽  
Author(s):  
G. Cruz ◽  
W. Foster ◽  
A. Paredes ◽  
K. D. Yi ◽  
M. Uzumcu

Blood ◽  
2008 ◽  
Vol 112 (4) ◽  
pp. 1530-1538 ◽  
Author(s):  
Shannon J. Opiela ◽  
Robert B. Levy ◽  
Becky Adkins

AbstractEarly life exposure to noninherited maternal antigens (NIMAs) may occur via transplacental transfer and/or breast milk. There are indications that early life exposure to NIMAs may lead to lifelong tolerance. However, there is mounting evidence that exposure to NIMAs may also lead to immunologic priming. Understanding how these different responses arise could be critical in transplantation with donor cells expressing NIMAs. We recently reported that murine neonates that received a transplant of low doses of NIMA-like alloantigens develop vigorous memory cytotoxic responses, as assessed by in vitro assays. Here, we demonstrate that robust allospecific cytotoxicity is also manifest in vivo. Importantly, at low doses, NIMA-expressing cells induced the development of in vivo cytotoxicity during the neonatal period. NIMA-exposed neonates also developed vigorous primary and memory allospecific Th1/Th2 responses that exceeded the responses of adults. Overall, we conclude that exposure to low doses of NIMA-like alloantigens induces robust in vivo cytotoxic and Th1/Th2 responses in neonates. These findings suggest that early exposure to low levels of NIMA may lead to long-term immunologic priming of all arms of T-cell adaptive immunity, rather than tolerance.


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