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Your Environment. Your Health.

Final Progress Reports: University of California-Berkeley: Exposomics and Arsenic Epidemiology

Superfund Research Program

Exposomics and Arsenic Epidemiology

Project Leader: Craig Murray Steinmaus
Co-Investigators: Martyn T. Smith, Allan H. Smith
Grant Number: P42ES004705
Funding Period: 1995-2022
View this project in the NIH Research Portfolio Online Reporting Tools (RePORT)

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Final Progress Reports

Year:   2016  2010  2005 

Using the unique exposure scenario in northern Chile, the research team recently published new findings linking arsenic to increases in both hypertension and non-malignant lung disease. The latter involved decrements in lung function of a similar magnitude to those seen with smoking. These findings are important since the current US Environmental Protection Agency (EPA) regulatory standard on arsenic only considers cancer. The research team’s findings suggest that other common illnesses like hypertension should also be considered in developing this standard. Previously the team published data showing that early-life arsenic exposures were associated with high rates of cancer. More recently, they published new data showing that obesity could be a major susceptibility factor for these effects. They found that the risks of both arsenic-related lung and bladder cancer were 3-4 times higher in people who were obese compared to those with lower BMIs. Recently, the team submitted a manuscript showing similar effects for non-malignant lung disease. They are also finalizing a manuscript in which they found that polymorphisms in two genes (AS3MT and N6AMT1) could confer important susceptibility to arsenic. Most US environmental regulatory standards do not specifically address susceptible groups. Research on susceptibility like this research could lead to new standards that help protect all major groups. Ongoing projects include analyses of DNA methylation, gene expression (mRNA), and immune function in adults who were exposed in early life. The goal is to see whether early life exposure can lead to epigenetic or immune function changes that persist into adulthood. New mechanistic information like this could lead to new ideas regarding prevention, disease screening, or treatment.

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