Lung, Bladder, and Kidney Cancer Mortality 40 Years After Arsenic Exposure Reduction

Smith, Allan H.; Marshall, Guillermo; Roh, Taehyun; Ferreccio, Catterina; Liaw, Jane; Steinmaus, Craig

doi:10.1093/jnci/djx201

Cited by 128 publications

(56 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…One thing is certain however: studying environmental exposures solely at the time of symptom onset is unlikely to reveal all that needs to be known, since the neurodegenerative disease process probably began years prior to the onset of clinical symptoms. We have no empirical evidence regarding the "incubation period" of ALS, but work in cancer may be relevant, where, for instance, arsenic has been reported to increase the incidence of bladder cancer only after 10 years of exposure and the incidence continued to rise for 20 years after termination of exposure [10].…”

Section: Temporal Considerations In Exposures To Chronic Environmentamentioning

confidence: 99%

Gene-Environment-Time Interactions in Neurodegenerative Diseases: Hypotheses and Research Approaches

et al. 2018

View full text Add to dashboard Cite

Background: Amyotrophic lateral sclerosis (ALS), Alzheimer’s, and Parkinson’s diseases are age-related neurodegenerative diseases. ALS is not a single entity but a syndrome with many different causes. In all 3 diseases, gene mutations account for only 10–15% of cases. Many environmental and lifestyle factors have been implicated as risk factors for ALS, though none have been proven to cause the disease. It is generally believed that ALS results from interactions between environmental risk factors and genetic predisposing factors. The advent of next-generation sequencing and recent advances in research into environmental risk factors offer the opportunity to investigate these interactions. Summary: We propose a hypothesis to explain the syndrome of ALS based on the interaction of many individual environmental risk factors with many individual genetic predisposing factors. We hypothesize that there are many such combinations of individual, specific, genetic, and environmental factors, and that each combination can lead to the development of the syndrome of ALS. We also propose a hypothesis that explains the overlap between the age-related neurodegenerations and their genetic underpinnings. Age and duration of exposure are crucial factors in these age-related neurodegenerative diseases, and we consider how these may relate to gene-environment interactions. Key Messages: To date, genetic studies and environmental studies have investigated the causes of ALS separately. We argue that this univariate approach will not lead to discoveries of important gene-environment interactions. We propose new research approaches to investigating gene-environment interactions based on these hypotheses.

show abstract

Section: Temporal Considerations In Exposures To Chronic Environmentamentioning

confidence: 99%

Gene-Environment-Time Interactions in Neurodegenerative Diseases: Hypotheses and Research Approaches

et al. 2018

View full text Add to dashboard Cite

show abstract

“…The other major source is As‐contaminated air and food caused by combustion high As‐containing coal in unventilated indoor stoves for cooking, which has been exclusively reported in Guizhou province in China in 2002 year 8 . Epidemiological studies have shown that there is high prevalence of arsenicosis such as skin, 9,10 liver, 11 kidney, 12 lung, 13 and bladder damage 14 . Liver, as one of the important target organs of arsenic toxicity, exhibits an increase of hepatocyte apoptosis in hepatic tissues and primary hepatocytes 15,16 .…”

Section: Introductionmentioning

confidence: 99%

ROS‐mediated PERK‐eIF2α‐ATF4 pathway plays an important role in arsenite‐induced L‐02 cells apoptosis via regulating CHOP‐DR5 signaling

Liu

Zhang

2020

Environmental Toxicology

View full text Add to dashboard Cite

Chronic exposure to arsenic remains a worldwide environmental health issue, affecting hundreds of millions of people. Although, arsenic‐induced oxidative stress and apoptosis have been determined, the underlying apoptosis mechanism has not been fully elucidated yet. Oxidative stress integrated‐ER stress plays an important role in Life‐and‐Death decision of cells. The current study was to investigate whether NaAsO2 utilizes oxidative stress integrated‐ER stress signaling to exert pro‐apoptotic activity in L‐02 cells. Results showed that death receptor 5 (DR5) was a mediator of NaAsO2‐induced apoptosis by enhancing construction of the death‐inducing signaling complex (DISC). NaAsO2‐sensitized DR5 elevation required maintainable transcription and its transcription factor C/EBP homologous protein (CHOP). Further results showed that NaAsO2 increased expression in biomarker of endoplasmic reticulum (ER) stress and activated the protein kinase R‐like ER kinase (PERK)‐eukaryotic translation initiation 2α (eIF2α)‐activating transcription factor 4 (ATF4) pathway. PERK inhibitor and ATF4 siRNA significantly attenuated NaAsO2‐induced CHOP and DR5 expressions. In addition, the antioxidant N‐acetyl‐l‐cysteine (NAC) treatment led to amelioration of NaAsO2‐induced production of reactive oxygen species (ROS) and some ER stress‐ and apoptosis‐ related protein levels and cell viability. Taken together, the results indicate that ROS‐mediated PERK‐eIF2α‐ATF4 pathway activated by NaAsO2 is the critical upstream event for subsequent apoptosis induction via regulating CHOP‐DR5 signaling in L‐02 cells when chronic exposure to arsenic, and support that antioxidants might be potential therapeutic agents for preventing or delaying the onset and progress of arsenic‐induced hepatotoxicity.

show abstract

“…Chronic exposure to inorganic arsenic via drinking water is associated with increased risk for various human cancers, as well as diseases of myriad body systems that include cardiovascular, neurologic, endocrine, integumentary and respiratory (García-Esquinas et al, 2013;Hong, Song, & Chung, 2014;Martinez, Vucic, Becker-Santos, Gil, & Lam, 2011;Putila & Guo, 2011;Smith et al, 1992;Smith et al, 2006;Tyler & Allan, 2014). Focusing on the respiratory system, studies in arsenic-exposed populations in northern Chile documented increased risk for early death from lung cancer and obstructive pulmonary disease (Smith et al, 2018;Smith, Goycolea, Haque, & Biggs, 1998). Furthermore, arsenic exposure from drinking water in Bangladesh has been linked to dyspnea and pneumonia (George et al, 2015;Pesola et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Chronic exposure to arsenite enhances influenza virus infection in cultured cells

Amouzougan

Lira

Klimecki

2020

J of Applied Toxicology

View full text Add to dashboard Cite

Arsenic is a ubiquitous environmental toxicant that has been associated with human respiratory diseases. In humans, arsenic exposure has been associated with increased risk of respiratory infection. Considering the existing epidemiological evidence and the well‐established impact of arsenic on epithelial cell biology, we posited that the effect of arsenic exposure in epithelial cells could enhance viral infection. In this study, we characterized influenza virus A/WSN/33 (H1N1) infection in Madin‐Darby Canine Kidney (MDCK) cells chronically exposed to low levels of sodium arsenite (75 ppb). We observed a 27.3‐fold increase in viral matrix (M2) protein (24 hours postinfection [p.i.]), a 1.35‐fold increase in viral mRNA levels, and a 126% increase in plaque area in arsenite‐exposed MDCK cells (48 hours p.i.). Arsenite exposure resulted in 114% increase in virus attachment‐positive cells (2 hours p.i.) and 224% increase in α‐2,3 sialic acid‐positive cells. Interestingly, chronic exposure to arsenite reduced the effect of the antiviral drug, oseltamivir in MDCK cells. We also found that exposure to sodium arsenite resulted in a 4.4‐fold increase in viral mRNA levels and significantly increased cytotoxicity in influenza A/Udorn/72 (H3N2) infected BEAS‐2B cells. This study suggests that chronic arsenite exposure could result in enhanced influenza infection in epithelial cells, and that this may be mediated through increased sialic acid binding. Finally, the decreased effectiveness of the anti‐influenza drug, oseltamivir, in arsenite‐exposed cells raises substantial public health concerns if this effect translates to arsenic‐exposed, influenza‐infected people.

show abstract

Lung, Bladder, and Kidney Cancer Mortality 40 Years After Arsenic Exposure Reduction

Abstract: Lung, bladder, and kidney cancer mortality due to arsenic exposure have very long latencies, with increased risks manifesting 40 years after exposure reduction. Our findings suggest that arsenic in drinking water may involve one of the longest cancer latencies for a human carcinogen.

Cited by 128 publications

References 38 publications

Gene-Environment-Time Interactions in Neurodegenerative Diseases: Hypotheses and Research Approaches

Gene-Environment-Time Interactions in Neurodegenerative Diseases: Hypotheses and Research Approaches

ROS‐mediated PERK‐eIF2α‐ATF4 pathway plays an important role in arsenite‐induced L‐02 cells apoptosis via regulating CHOP‐DR5 signaling

Chronic exposure to arsenite enhances influenza virus infection in cultured cells

Contact Info

Product

Resources

About