A genome-wide SNP investigation of chemical intolerance
Background: Chemical Intolerance (CI) also known as Multiple Chemical Sensitivity (MCS) is characterized by multi-system symptoms initiated by exposures to environmental toxins. Symptoms include fatigue, headache, mood changes, musculoskeletal pain, gastro-intestinal issues, and difficulties with me...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2023-07-01
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| Series: | Environmental Advances |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2666765723000406 |
| _version_ | 1827926411728388096 |
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| author | Raymond F. Palmer Marcio Almeida Roger B. Perales Rudy Rincon |
| author_facet | Raymond F. Palmer Marcio Almeida Roger B. Perales Rudy Rincon |
| author_sort | Raymond F. Palmer |
| collection | DOAJ |
| description | Background: Chemical Intolerance (CI) also known as Multiple Chemical Sensitivity (MCS) is characterized by multi-system symptoms initiated by exposures to environmental toxins. Symptoms include fatigue, headache, mood changes, musculoskeletal pain, gastro-intestinal issues, and difficulties with memory/concentration. With mixed results, researchers have targeted specific genes to understand the genetic pathways associated with CI. This study is the first to apply a genome-wide, untargeted exploratory method. Methods: A high-density genotyping platform was used to perform a hypothesis-free search for genetic variants associated with CI in a set of 200 participants. Each CI patient was verified using a validated survey. The association between CI and single nucleotide polymorphisms (SNPs) was obtained using SOLAR (Sequential Oligogenic Linkage Analysis Routines). Gene-Chemical-Disease interactions were determined using the DisGeNET Database. Results: Several SNPs were identified which either increase or decrease the associated risk of CI. These SNPs include markers close to genes involved in mast cell activation pathways. Four chemicals were found to most alter the gene expressions of the identified SNPs (bisphenol A, valproic acid, aflatoxin B, and benzo(a)pyrene). There were common adverse health effects associated with the genes and the chemicals that influence them, Discussion: This study supports evidence of novel genetic components associated with CI that may interact with common ubiquitous chemical and drug exposures affecting gene expression. There is evidence of immunological function and mast cell activation. The identified health consequences of the genes and associated chemicals are common to individuals with CI and implies gene/chemical exposure interactions that may influence the development or exacerbation of symptoms associated with CI. However, conclusions drawn from this data should not underestimate the complexity of gene/environment. The identified chemicals affecting these genes are ubiquitous environmental exposures, entering the body through air, food, and water, suggesting the need for greater public health policy efforts in an effort to protect vulnerable individuals. Future studies of CI would benefit from a systems biology approach. |
| first_indexed | 2024-03-13T05:38:47Z |
| format | Article |
| id | doaj.art-a1b7479e6d364352982808b99659fa1f |
| institution | Directory Open Access Journal |
| issn | 2666-7657 |
| language | English |
| last_indexed | 2024-03-13T05:38:47Z |
| publishDate | 2023-07-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Environmental Advances |
| spelling | doaj.art-a1b7479e6d364352982808b99659fa1f2023-06-14T04:34:27ZengElsevierEnvironmental Advances2666-76572023-07-0112100380A genome-wide SNP investigation of chemical intoleranceRaymond F. Palmer0Marcio Almeida1Roger B. Perales2Rudy Rincon3Department of Family and Community Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229-3900, USA; Corresponding author.Department of Human Genetics, South Texas Diabetes and Obesity Institute, School of Medicine, University of Texas Rio Grande Valley Brownsville, TX 78520, USADepartment of Family and Community Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229-3900, USADepartment of Family and Community Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229-3900, USABackground: Chemical Intolerance (CI) also known as Multiple Chemical Sensitivity (MCS) is characterized by multi-system symptoms initiated by exposures to environmental toxins. Symptoms include fatigue, headache, mood changes, musculoskeletal pain, gastro-intestinal issues, and difficulties with memory/concentration. With mixed results, researchers have targeted specific genes to understand the genetic pathways associated with CI. This study is the first to apply a genome-wide, untargeted exploratory method. Methods: A high-density genotyping platform was used to perform a hypothesis-free search for genetic variants associated with CI in a set of 200 participants. Each CI patient was verified using a validated survey. The association between CI and single nucleotide polymorphisms (SNPs) was obtained using SOLAR (Sequential Oligogenic Linkage Analysis Routines). Gene-Chemical-Disease interactions were determined using the DisGeNET Database. Results: Several SNPs were identified which either increase or decrease the associated risk of CI. These SNPs include markers close to genes involved in mast cell activation pathways. Four chemicals were found to most alter the gene expressions of the identified SNPs (bisphenol A, valproic acid, aflatoxin B, and benzo(a)pyrene). There were common adverse health effects associated with the genes and the chemicals that influence them, Discussion: This study supports evidence of novel genetic components associated with CI that may interact with common ubiquitous chemical and drug exposures affecting gene expression. There is evidence of immunological function and mast cell activation. The identified health consequences of the genes and associated chemicals are common to individuals with CI and implies gene/chemical exposure interactions that may influence the development or exacerbation of symptoms associated with CI. However, conclusions drawn from this data should not underestimate the complexity of gene/environment. The identified chemicals affecting these genes are ubiquitous environmental exposures, entering the body through air, food, and water, suggesting the need for greater public health policy efforts in an effort to protect vulnerable individuals. Future studies of CI would benefit from a systems biology approach.http://www.sciencedirect.com/science/article/pii/S2666765723000406Chemical intoleranceGenesChemical exposureHealth effects |
| spellingShingle | Raymond F. Palmer Marcio Almeida Roger B. Perales Rudy Rincon A genome-wide SNP investigation of chemical intolerance Environmental Advances Chemical intolerance Genes Chemical exposure Health effects |
| title | A genome-wide SNP investigation of chemical intolerance |
| title_full | A genome-wide SNP investigation of chemical intolerance |
| title_fullStr | A genome-wide SNP investigation of chemical intolerance |
| title_full_unstemmed | A genome-wide SNP investigation of chemical intolerance |
| title_short | A genome-wide SNP investigation of chemical intolerance |
| title_sort | genome wide snp investigation of chemical intolerance |
| topic | Chemical intolerance Genes Chemical exposure Health effects |
| url | http://www.sciencedirect.com/science/article/pii/S2666765723000406 |
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