Environmental Carcinogens and Cancer Risk

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Causes, Screening and Diagnosis".

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 22834

Special Issue Editor


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Guest Editor
School of Community and Global Health, Claremont Graduate University, 675 W. Foothill Blvd, Claremont, CA 91711, USA
Interests: pesticides; ultraviolet radiation; air pollution; passive smoking; breast cancer; cognitive impairment; Parkinson’s disease

Special Issue Information

Dear colleagues,

Environmental carcinogens encompass a broad range of chemical, biological, and physical agents as well as some lifestyle factors. A unifying characteristic of these agents is the involuntary nature of their exposure from environmental and occupational settings. Both the National Toxicology Program (NTP) of the United States Department of Health and Human Services through their Report on Carcinogens and the International Agency for Research on Cancer (IARC) of the World Health Organization (WHO) through their Monographs have extensively evaluated potential environmental carcinogens and together have identified several hundred. Simply considering the tens of thousands of chemicals in use across the world, substantial work remains to understand the potential cancer risk to humans and mechanisms of action.

Certain populations are at higher risk of being exposed to environmental carcinogens by virtue of occupations involving use of cancer-causing agents or residences in proximity to sources of environmental contaminants. Pregnant women, infants, and children comprise vulnerable populations to effects of environmental carcinogens, and disparities exist by socioeconomic status, as persons of low income may be less able to modify their environmental circumstances.  

This Special Issue focuses on recent research addressing the association between environmental carcinogens and cancer risk as well as the biological mechanisms. Topics of interest to this issue are:

  • Environmental carcinogen exposure sources and susceptible populations;
  • Biomarkers of exposure, effect, and susceptibility;
  • Epidemiologic researches or large dataset analyses;
  • Mixture effects of multiple carcinogens;
  • Risk assessment and analytical methods;
  • Epigenetics and cancer risk assessment;
  • Molecular mechanisms assessment;
  • Exposure–response relationship;
  • Gene–environment interactions;
  • Cancer health disparities.

Submissions of original research, systematic reviews, meta-analyses, short communications, and commentaries covering the aforementioned topics and other related topics will be welcome.

Prof. Dr. Nicole M. Gatto
Guest Editor

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • route of exposure
  • pollution
  • radiation
  • occupational hazards
  • genotoxicity
  • teratogen
  • air
  • soil
  • water
  • pesticides
  • biomagnification
  • synergism
  • susceptibility
  • contamination
  • waste management
  • geographical
  • spatial

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Published Papers (5 papers)

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Editorial

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2 pages, 162 KiB  
Editorial
Environmental Carcinogens and Cancer Risk
by Nicole M. Gatto
Cancers 2021, 13(4), 622; https://doi.org/10.3390/cancers13040622 - 4 Feb 2021
Cited by 6 | Viewed by 1923
Abstract
The year 2022 will mark the 60th anniversary of the 1962 publication of Rachel Carson’s seminar work Silent Spring  [...] Full article
(This article belongs to the Special Issue Environmental Carcinogens and Cancer Risk)

Research

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18 pages, 2812 KiB  
Article
Low-Dose Pesticides Alter Primary Human Bone Marrow Mesenchymal Stem/Stromal Cells through ALDH2 Inhibition
by Amélie Foucault, Noémie Ravalet, Joevin Besombes, Frédéric Picou, Nathalie Gallay, Laetitia Babin, Jérôme Bourgeais, Sophie Hamard, Jorge Domenech, Pascal Loyer, Nicolas Vallet, Julien Lejeune, Emmanuel Gyan, Marie C. Béné, François Vallette, Christophe Olivier and Olivier Hérault
Cancers 2021, 13(22), 5699; https://doi.org/10.3390/cancers13225699 - 14 Nov 2021
Cited by 5 | Viewed by 3656
Abstract
(1) Background: The impact of occupational exposure to high doses of pesticides on hematologic disorders is widely studied. Yet, lifelong exposure to low doses of pesticides, and more particularly their cocktail effect, although poorly known, could also participate to the development of such [...] Read more.
(1) Background: The impact of occupational exposure to high doses of pesticides on hematologic disorders is widely studied. Yet, lifelong exposure to low doses of pesticides, and more particularly their cocktail effect, although poorly known, could also participate to the development of such hematological diseases as myelodysplastic syndrome (MDS) in elderly patients. (2) Methods: In this study, a cocktail of seven pesticides frequently present in water and food (maneb, mancozeb, iprodione, imazalil, chlorpyrifos ethyl, diazinon and dimethoate), as determined by the European Food Safety Authority, were selected. Their in vitro effects at low-doses on primary BM-MSCs from healthy volunteers were examined. (3) Results: Exposure of normal BM-MSCs to pesticides for 21 days inhibited cell proliferation and promoted DNA damage and senescence. Concomitantly, these cells presented a decrease in aldehyde dehydrogenase 2 (ALDH2: mRNA, protein and enzymatic activity) and an increase in acetaldehyde levels. Pharmacological inhibition of ALDH2 with disulfiram recapitulated the alterations induced by exposure to low doses of pesticides. Moreover, BM-MSCs capacity to support primitive hematopoiesis was significantly altered. Similar biological abnormalities were found in primary BM-MSCs derived from MDS patients. (4) Conclusions: these results suggest that ALDH2 could participate in the pathophysiology of MDS in elderly people long exposed to low doses of pesticides. Full article
(This article belongs to the Special Issue Environmental Carcinogens and Cancer Risk)
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22 pages, 22504 KiB  
Article
Short-Term and Long-Term Carcinogenic Effects of Food Contaminants (4-Hydroxynonenal and Pesticides) on Colorectal Human Cells: Involvement of Genotoxic and Non-Genomic Mechanisms
by Liana C. Arnaud, Thierry Gauthier, Augustin Le Naour, Saleha Hashim, Nathalie Naud, Jerry W. Shay, Fabrice H. Pierre, Elisa Boutet-Robinet and Laurence Huc
Cancers 2021, 13(17), 4337; https://doi.org/10.3390/cancers13174337 - 27 Aug 2021
Cited by 1 | Viewed by 2762
Abstract
To investigate environmental impacts upon colorectal carcinogenesis (CRC) by diet, we assessed two western diet food contaminants: 4-hydroxynonenal (HNE), a major lipid peroxidation product neoformed during digestion, and a mixture of pesticides. We used human colonic cell lines ectopically eliciting varied genetic susceptibilities [...] Read more.
To investigate environmental impacts upon colorectal carcinogenesis (CRC) by diet, we assessed two western diet food contaminants: 4-hydroxynonenal (HNE), a major lipid peroxidation product neoformed during digestion, and a mixture of pesticides. We used human colonic cell lines ectopically eliciting varied genetic susceptibilities to CRC: the non-transformed human epithelial colonic cells (HCECs) and their five isogenic cell lines with the loss of APC (Adenomatous polyposis coli) and TP53 (Tumor protein 53) and/or ectopic expression of mutated KRAS (Kristen-ras). These cell lines have been exposed for either for a short time (2–24 h) or for a long period (3 weeks) to 1 µM HNE and/or 10 µM pesticides. After acute exposure, we did not observe any cytotoxicity or major DNA damage. However, long-term exposure to pesticides alone and in mixture with HNE induced clonogenic transformation in normal HCECs, as well as in cells representing later stages of carcinogenesis. It was associated with genotoxic and non-genomic mechanisms (cell growth, metabolic reprogramming, cell mobility and epithelial-mesenchymal transition) depending on genetic susceptibility. This study demonstrated a potential initiating and promoting effect of food contaminants on CRC after long-term exposure. It supports that these contaminants can accelerate carcinogenesis when mutations in oncogenes or tumor suppressor genes occur. Full article
(This article belongs to the Special Issue Environmental Carcinogens and Cancer Risk)
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19 pages, 998 KiB  
Article
Night Work and Breast Cancer Risk in Nurses: Multifactorial Risk Analysis
by Juan Gómez-Salgado, Javier Fagundo-Rivera, Mónica Ortega-Moreno, Regina Allande-Cussó, Diego Ayuso-Murillo and Carlos Ruiz-Frutos
Cancers 2021, 13(6), 1470; https://doi.org/10.3390/cancers13061470 - 23 Mar 2021
Cited by 12 | Viewed by 4940
Abstract
Night work has been highlighted by the International Agency for Research on Cancer (IARC) as a likely carcinogenic factor for humans, associated with breast cancer and professions that require continuity of work. Knowing the impact that short and long-term night work has on [...] Read more.
Night work has been highlighted by the International Agency for Research on Cancer (IARC) as a likely carcinogenic factor for humans, associated with breast cancer and professions that require continuity of work. Knowing the impact that short and long-term night work has on the nurses’ collective seems a priority, therefore, this study aims to analyse the relationship between night work and the development of breast cancer risk factors in nurses. For this, a cross-sectional study through an online questionnaire on breast cancer risk variables and working life was designed. The study was conducted in Spain and the sample consisted of 966 nurses, of whom 502 were healthy participants and 56 were breast cancer patients. These two groups were compared in the analyses. A descriptive analysis was performed, and the relationship was tested using χ2 independence test and OR calculation. The CHAID (Chi Square Automatic Interaction Detection) data mining method allowed for the creation of a segmentation tree for the main risk variables. The most significant risk variables related to working life have been the number of years worked, nights worked throughout life, and years working more than 3 nights per month. Exceeding 16 years of work has been significant for women and men. When the time worked is less than 16 years, the number of cases increases if there is a family history of cancer and if there have been more than 500 nights of work. High-intensity night work seems more harmful at an early age. The accumulation of years and nights worked increase the risk of breast cancer when factors such as sleep disturbance, physical stress, or family responsibilities come together. Full article
(This article belongs to the Special Issue Environmental Carcinogens and Cancer Risk)
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Other

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24 pages, 632 KiB  
Systematic Review
Farming, Pesticides, and Brain Cancer: A 20-Year Updated Systematic Literature Review and Meta-Analysis
by Nicole M. Gatto, Pamela Ogata and Brittany Lytle
Cancers 2021, 13(17), 4477; https://doi.org/10.3390/cancers13174477 - 5 Sep 2021
Cited by 16 | Viewed by 7529
Abstract
Twenty additional years of epidemiologic literature have become available since the publication of two meta-analyses on farming and brain cancer in 1998. The current systematic literature review and meta-analysis extends previous research and harmonizes findings. A random effects model was used to calculate [...] Read more.
Twenty additional years of epidemiologic literature have become available since the publication of two meta-analyses on farming and brain cancer in 1998. The current systematic literature review and meta-analysis extends previous research and harmonizes findings. A random effects model was used to calculate meta-effect estimates from 52 studies (51 articles or reports), including 11 additional studies since 1998. Forty of the 52 studies reported positive associations between farming and brain cancer with effect estimates ranging from 1.03 to 6.53. The overall meta-risk estimate was 1.13 (95% CI = 1.06, 1.21), suggesting that farming is associated with a 13% increase in risk of brain cancer morbidity or mortality. Farming among white populations was associated with a higher risk of brain cancer than among non-white populations. Livestock farming (meta-RR = 1.34; 95% CI = 1.18, 1.53) was associated with a greater risk compared with crop farming (meta-RR = 1.13; 95% CI = 0.97, 1.30). Farmers with documented exposure to pesticides had greater than a 20% elevated risk of brain cancer. Despite heterogeneity among studies, we conclude that the synthesis of evidence from 40 years of epidemiologic literature supports an association between brain cancer and farming with its potential for exposure to chemical pesticides. Full article
(This article belongs to the Special Issue Environmental Carcinogens and Cancer Risk)
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