Thursday, September 29, 2022

Environmental Factor – August 2019: Outer 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 lead to the development of prostate cancer 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 World Trade Center disaster and later developed prostate cancer. The team compared the expression of some immune system and inflammation genes in these tumors with that of prostate cancer patients who were not exposed to WTC dust. They also exposed mice to WTC dust and measured changes in gene expression to study the immediate effects of WTC dust on a healthy prostate. 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-associated prostate cancer showed a distinct pattern of gene expression and an increase in cells that signal inflammation, specifically immune cells called helper T cells. The scientists found that some immune system and inflammatory genes overexpressed in mice after exposure to WTC dust were also overexpressed in human prostate cancer tissues, suggesting a link between exposure, local immune dysregulation, and prostate cancer development. In mice, acute exposure to dust resulted in long-lasting changes in gene expression in the prostate. According to the authors, these findings collectively suggest that respiratory exposure to WTC dust can trigger inflammatory and immune responses in prostate tissue.

the quote: Gong 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 WTC responders shows evidence of an inflammatory cascade. Res Mall Cancer. doi: 10.1158/1541-7786.MCR-19-0115 [Online 16 July 2019].

Continuing medical education as a tool to communicate research

A new study by NIEHS grant recipients describes how health communication research can identify gaps in knowledge and lead to better communication between health care providers and patients about breast cancer and the environment. They have developed Continuing Medical Education (CME) training to communicate research findings to health practitioners and bridge the gap between research and practice.

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

The team used these findings to create an online continuing medical education training that describes the links between the environment and breast cancer, why girls are more likely to be exposed during critical windows of sensitivity such as puberty, how to minimize exposure, and the best communication strategies for healthcare providers. Share relevant information with patients.

the quote: Silk KJ, Walling B, Totzkay D, Mulroy M, Smith SW, Quaderer T, Boumis J, Thomas B. 2019. Continuing Medical Education as a Translated Scholarly Opportunity for Researchers in Health Communication: The BCERP Model. Community Health doi: 10.1080/10410236.2019.1625003 [Online 5 June 2019].

E-cigarettes destroy brain stem cells

A NIEHS-funded study found that exposure to electronic cigarettes (e-cigarettes) can produce a stress response in brain cells called neural stem cells (NSCs). Beneficiaries reported that nicotine, and not the other components of e-cigarettes, was responsible for the cellular damage.

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

The team noted that nicotine binds to special receptors in the nerve cell’s membrane, causing it to open. This resulted in an overload of calcium entering the cell. Too much calcium in mitochondria can change its shape and function. Exposed cells showed activation of stress-induced mitochondrial hyperfusion (SIMH), a rescue mechanism that renders mitochondria less susceptible to degradation. However, chronic exposure to nicotine overshadowed the protection of SIMH and increased mitochondrial damage.

The study provides evidence that nicotine and nicotine-containing products such as e-cigarettes trigger a chain of cellular events that damage the mitochondria of the NSC, 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.

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

Nutrition-related metabolites may play a role in childhood leukemia risk

NIEHS recipients have revealed associations between the presence of certain metabolites soon after birth and a pediatric diagnosis of acute lymphoblastic leukemia (ALL). Notably, all late-onset patients showed more metabolites associated with artificial feeding rather than breast milk, suggesting a possible role of nutrition in the risk of late-onset ALL.

Using archived newborn blood spots, researchers compared 332 children who later developed ALL with 324 healthy children. Newborn blood spots were usually obtained between 24 and 48 hours after birth, 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 old.

The researchers identified the exclusive metabolic features of each of the two groups of cases compared to controls. Nine metabolites predicted early diagnosis of ALL and 19 different metabolites predicted late diagnosis. In the late diagnosis group, they found a group of metabolites indicating that linoleic acid, an essential nutrient, was more abundant in these children than in the early cases or the control group. Linoleic acid metabolites were also greater in infants who were fed formula milk instead of breast milk, in the form of colostrum, in the first few days of life. Levels of metabolites increased with increasing maternal BMI before pregnancy, suggesting that maternal weight may also be involved in the late all-risk diagnosis.

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

the quote: Petrick 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. Neonatal blood spot metabolism reveals distinct phenotypes of pediatric acute lymphoblastic leukemia and potential effects of early-life nutrition. Cancer 452: 71-78.

(Sarah Amuligbe is a research and communications specialist for MDB Inc., a contractor with the Research and Training Outside the Walls of NIEHS.)



from San Jose News Bulletin https://sjnewsbulletin.com/environmental-factor-august-2019-outer-papers-of-the-month/

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