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Environmental Factor

Environmental Factor

Your Online Source for NIEHS News

August 2019

Papers of the Month

World Trade Center dust linked to prostate cancer

Changes in inflammation and immune regulation from exposure to World Trade Center (WTC) dust may drive prostate cancer progression among WTC first responders, according to a new NIEHS-funded study.

Researchers examined archived prostate tumors from rescue and recovery workers who responded to the WTC disaster and later developed prostate cancer. The team compared expression of certain immune system and inflammation genes in these tumors with tumors from prostate cancer patients who were not exposed to WTC dust. They also exposed rats to WTC dust and measured changes in gene expression to study the immediate effects of WTC dust on a healthy prostate. The dust samples, which contain metals and organic compounds such as polycyclic aromatic hydrocarbons and polychlorinated biphenyls, were collected on the day of the disaster, September 11, 2001.

In human tumors, WTC-related prostate cancer displayed a distinct gene expression pattern and an increase in cells that indicate inflammation, specifically immune cells called T helper cells. The scientists found that some of the immune system and inflammation genes overexpressed in the rat following WTC dust exposure were also overexpressed in human prostate cancer tissues, suggesting a link between exposure, local immune dysregulation, and prostate cancer development. In rats, the acute dust exposure led to long-lasting gene-expression changes in the prostate. According to the authors, these results taken together suggest that respiratory exposure to WTC dust can induce inflammatory and immune responses in prostate tissue.

CitationGong Y, Wang L, Yu H, Alpert N, Cohen MD, Prophete C, Horton L, Sisco M, Park SH, Lee HW, Zelikoff J, Chen LC, Suarez-Farinas M, Donovan MJ, Aaronson SA, Galsky M, Zhu J, Taioli E, Oh WK. 2019. Prostate cancer in World Trade Center responders demonstrates evidence of an inflammatory cascade. Mol Cancer Res; doi: 10.1158/1541-7786.MCR-19-0115 [Online 16 July 2019].

Continuing medical education as tool to communicate research

A new study by NIEHS grantees described how health communication research can identify gaps in knowledge and lead to better communication between healthcare providers and patients about breast cancer and the environment. They developed a continuing medical education (CME) training to communicate research results to health practitioners and bridge the gap between research and practice.

Health communication researchers worked with grantees in the NIEHS Breast Cancer and the Environment Research Program (BCERP) to design a CME training for healthcare providers that will help them integrate into everyday practice findings about environmental factors and breast cancer risk. The healthcare providers studied did not routinely discuss breast cancer risk factors with patients. However, when these providers learned that puberty can be a vulnerable time for breast cells that are exposed to certain chemicals, they acknowledged that it is important to address breast cancer with their patients. The team learned more about what the CME training should address by working with caregivers of young children regarding gaps in understanding about breast cancer and the environment and how the caregivers would prefer to receive this information.

The team used these findings to create an online CME training that describes links between the environment and breast cancer, why girls are more vulnerable to exposures during critical windows of susceptibility such as puberty, how to reduce exposures, and communication strategies for healthcare providers to best share the relevant information with patients.

CitationSilk KJ, Walling B, Totzkay D, Mulroy M, Smith SW, Quaderer T, Boumis J, Thomas B. 2019. Continuing medical education as a translational science opportunity for health communication researchers: the BCERP model. Health Commun; doi: 10.1080/10410236.2019.1625003 [Online 5 June 2019].

Electronic cigarettes damage brain stem cells

An NIEHS-funded study found that exposure to electronic cigarettes (e-cigarettes) can produce a stress response in brain cells called neural stem cells (NSCs). The grantees reported that nicotine, rather than other components of e-cigarettes, was responsible for the cellular damage.

The researchers exposed mouse NSCs to either refill fluids from a leading brand of e-cigarettes, e-cigarette aerosols, or nicotine alone. They found that exposure to e-liquids, aerosols, and nicotine produced a stress response and increased oxidative stress in the mitochondria, which are the energy-producing component of cells.

The team observed that nicotine bound to special receptors in the neural cell membrane, causing it to open up. This led to an overload of calcium entering the cell. Too much calcium in the mitochondria can alter its shape and function. The exposed cells showed activation of stress-induced mitochondrial hyperfusion (SIMH), which is a rescue mechanism that makes mitochondria less vulnerable to degradation. However, chronic exposure to nicotine overwhelmed SIMH protection and increased mitochondrial damage.

The study provides evidence that nicotine and nicotine-containing products like e-cigarettes trigger a series of cellular events that damage NSC mitochondria, which can accelerate aging and lead to neurodegenerative diseases. According to the authors, this may have long-term repercussions for both e-cigarette users and individuals passively exposed to nicotine-containing aerosols.

CitationZahedi A, Phandthong R, Chaili A, Leung S, Omaiye E, Talbot P. 2019. Mitochondrial stress response in neural stem cells exposed to electronic cigarettes. iScience 16:250-269.

Metabolites linked to nutrition may play a role in childhood leukemia risk

NIEHS grantees revealed associations between the presence of certain metabolites shortly after birth and childhood diagnosis of acute lymphoblastic leukemia (ALL). Notably, late-onset ALL patients exhibited more abundant metabolites linked to formula feeding rather than breast milk, indicating a possible role of nutrition in late-onset ALL risk.

Using archived neonatal blood spots, the researchers compared 332 children who later developed ALL with 324 healthy children. The newborn blood spots were typically obtained between 24 and 48 hours post-delivery, generally after infants had received multiple feedings. Children diagnosed with ALL were separated by age at diagnosis into two groups: early, 1-5 years; and late, 6-14 years.

The researchers identified metabolic features exclusive to each of the two groups of cases compared with controls. Nine metabolites predicted early ALL diagnosis and 19 different metabolites predicted late diagnosis. In the late-diagnosis group, they found a cluster of metabolites that indicated linoleic acid, an essential nutrient, was more abundant in these children than in either the early-onset cases or controls. Linoleic acid metabolites were also greater in infants fed formula rather than breast milk, in the form of colostrum, in the first few days of life. Levels of the metabolites increased with the mother’s pre-pregnancy body mass index, suggesting that mother’s weight may also be involved in late-diagnosis ALL risk.

According to the authors, this untargeted approach to measuring metabolites in neonatal blood spots may link early-life exposures with later health effects and also point to biological pathways involved in disease risk.

CitationPetrick LM, Schiffman C, Edmands WMB, Yano Y, Perttula K, Whitehead T, Metayer C, Wheelock CE, Arora M, Grigoryan H, Carlsson H, Dudoit S, Rappaport SM. 2019. Metabolomics of neonatal blood spots reveal distinct phenotypes of pediatric acute lymphoblastic leukemia and potential effects of early-life nutrition. Cancer Lett 452:71–78.

(Sara Amolegbe is a research and communication specialist for MDB Inc., a contractor for the NIEHS Division of Extramural Research and Training.)

Read the current Superfund Research Program Research Brief. New issues are published on the first Wednesday of every month.

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