Radon Exposure, Clonal Hematopoiesis, and Stroke Susceptibility in the Women's Health Initiative
Studies suggest that clonal hematopoiesis of indeterminate potential (CHIP) may increase risk of hematologic malignancy and cardiovascular disease, including stroke. However, few studies have investigated plausible environmental risk factors for CHIP such as radon, despite the climate-related increa...
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| Veröffentlicht in: | Neurology 2024-01, Vol.102 (2), p.e208055 |
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| creator | Anthony, Kurtis M Collins, Jason M Love, Shelly-Ann M Stewart, James D Buchheit, Sophie F Gondalia, Rahul Schwartz, Gary G Huang, David Y Meliker, Jaymie R Zhang, Zhenzhen Barac, Ana Desai, Pinkal Hayden, Kathleen M Honigberg, Michael C Jaiswal, Siddhartha Natarajan, Pradeep Bick, Alexander G Kooperberg, Charles Manson, JoAnn E Reiner, Alexander P Whitsel, Eric A |
| description | Studies suggest that clonal hematopoiesis of indeterminate potential (CHIP) may increase risk of hematologic malignancy and cardiovascular disease, including stroke. However, few studies have investigated plausible environmental risk factors for CHIP such as radon, despite the climate-related increases in and documented infrequency of testing for this common indoor air pollutant.The purpose of this study was to estimate the risk of CHIP related to radon, an established environmental mutagen.
We linked geocoded addresses of 10,799 Women's Health Initiative Trans-Omics for Precision Medicine (WHI TOPMed) participants to US Environmental Protection Agency-predicted, county-level, indoor average screening radon concentrations, categorized as follows: Zone 1 (>4 pCi/L), Zone 2 (2-4 pCi/L), and Zone 3 (0.02. We identified prevalent and incident ischemic and hemorrhagic strokes; subtyped ischemic stroke using Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria; and then estimated radon-related risk of CHIP as an odds ratio (OR) and 95% CI using multivariable-adjusted, design-weighted logistic regression stratified by age, race/ethnicity, smoking status, and stroke type/subtype.
The percentages of participants with CHIP in Zones 1, 2, and 3 were 9.0%, 8.4%, and 7.7%, respectively (
= 0.06). Among participants with ischemic stroke, Zones 2 and 1 were associated with higher estimated risks of CHIP relative to Zone 3: 1.39 (1.15-1.68) and 1.46 (1.15-1.87), but not among participants with hemorrhagic stroke: 0.98 (0.68-1.40) and 1.03 (0.70-1.52), or without stroke: 1.04 (0.74-1.46) and 0.95 (0.63-1.42), respectively (
= 0.03). Corresponding estimates were particularly high among TOAST-subtyped cardioembolism: 1.78 (1.30-2.47) and 1.88 (1.31-2.72), or other ischemic etiologies: 1.37 (1.06-1.78) and 1.50 (1.11-2.04), but not small vessel occlusion: 1.05 (0.74-1.49) and 1.00 (0.68-1.47), respectively (
= 0.10). Observed patterns of association among strata were insensitive to attrition weighting, ancestry adjustment, prevalent stroke exclusion, separate analysis of
driver mutations, and substitution with 3 alternative estimates of radon exposure.
The robust elevation of radon-related risk of CHIP among postmenopausal women who develop incident cardioembolic stroke is consistent with a potential role of somatic genomic mutation in this societall |
| doi_str_mv | 10.1212/WNL.0000000000208055 |
| format | Article |
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We linked geocoded addresses of 10,799 Women's Health Initiative Trans-Omics for Precision Medicine (WHI TOPMed) participants to US Environmental Protection Agency-predicted, county-level, indoor average screening radon concentrations, categorized as follows: Zone 1 (>4 pCi/L), Zone 2 (2-4 pCi/L), and Zone 3 (<2 pCi/L). We defined CHIP as the presence of one or more leukemogenic driver mutations with variant allele frequency >0.02. We identified prevalent and incident ischemic and hemorrhagic strokes; subtyped ischemic stroke using Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria; and then estimated radon-related risk of CHIP as an odds ratio (OR) and 95% CI using multivariable-adjusted, design-weighted logistic regression stratified by age, race/ethnicity, smoking status, and stroke type/subtype.
The percentages of participants with CHIP in Zones 1, 2, and 3 were 9.0%, 8.4%, and 7.7%, respectively (
= 0.06). Among participants with ischemic stroke, Zones 2 and 1 were associated with higher estimated risks of CHIP relative to Zone 3: 1.39 (1.15-1.68) and 1.46 (1.15-1.87), but not among participants with hemorrhagic stroke: 0.98 (0.68-1.40) and 1.03 (0.70-1.52), or without stroke: 1.04 (0.74-1.46) and 0.95 (0.63-1.42), respectively (
= 0.03). Corresponding estimates were particularly high among TOAST-subtyped cardioembolism: 1.78 (1.30-2.47) and 1.88 (1.31-2.72), or other ischemic etiologies: 1.37 (1.06-1.78) and 1.50 (1.11-2.04), but not small vessel occlusion: 1.05 (0.74-1.49) and 1.00 (0.68-1.47), respectively (
= 0.10). Observed patterns of association among strata were insensitive to attrition weighting, ancestry adjustment, prevalent stroke exclusion, separate analysis of
driver mutations, and substitution with 3 alternative estimates of radon exposure.
The robust elevation of radon-related risk of CHIP among postmenopausal women who develop incident cardioembolic stroke is consistent with a potential role of somatic genomic mutation in this societally burdensome form of cerebrovascular disease, although the mechanism has yet to be confirmed.</description><identifier>ISSN: 0028-3878</identifier><identifier>ISSN: 1526-632X</identifier><identifier>EISSN: 1526-632X</identifier><identifier>DOI: 10.1212/WNL.0000000000208055</identifier><identifier>PMID: 38170948</identifier><language>eng</language><publisher>United States: Lippincott Williams & Wilkins</publisher><subject>Clonal Hematopoiesis ; Female ; Humans ; Ischemic Stroke ; Radon - adverse effects ; Radon - analysis ; Risk Factors ; Stroke - chemically induced ; Stroke - epidemiology ; Stroke - genetics ; Women's Health</subject><ispartof>Neurology, 2024-01, Vol.102 (2), p.e208055</ispartof><rights>2024 American Academy of Neurology 2024 American Academy of Neurology</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c363t-d55cd31a9945c32b2e063711b038d0558154c37b98e5f5287107966990b35f23</citedby><cites>FETCH-LOGICAL-c363t-d55cd31a9945c32b2e063711b038d0558154c37b98e5f5287107966990b35f23</cites><orcidid>0000-0001-7029-2203 ; 0000-0002-0658-8752 ; 0000-0002-9440-3892 ; 0000-0002-7986-8560 ; 0000-0003-4843-3641</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38170948$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Anthony, Kurtis M</creatorcontrib><creatorcontrib>Collins, Jason M</creatorcontrib><creatorcontrib>Love, Shelly-Ann M</creatorcontrib><creatorcontrib>Stewart, James D</creatorcontrib><creatorcontrib>Buchheit, Sophie F</creatorcontrib><creatorcontrib>Gondalia, Rahul</creatorcontrib><creatorcontrib>Schwartz, Gary G</creatorcontrib><creatorcontrib>Huang, David Y</creatorcontrib><creatorcontrib>Meliker, Jaymie R</creatorcontrib><creatorcontrib>Zhang, Zhenzhen</creatorcontrib><creatorcontrib>Barac, Ana</creatorcontrib><creatorcontrib>Desai, Pinkal</creatorcontrib><creatorcontrib>Hayden, Kathleen M</creatorcontrib><creatorcontrib>Honigberg, Michael C</creatorcontrib><creatorcontrib>Jaiswal, Siddhartha</creatorcontrib><creatorcontrib>Natarajan, Pradeep</creatorcontrib><creatorcontrib>Bick, Alexander G</creatorcontrib><creatorcontrib>Kooperberg, Charles</creatorcontrib><creatorcontrib>Manson, JoAnn E</creatorcontrib><creatorcontrib>Reiner, Alexander P</creatorcontrib><creatorcontrib>Whitsel, Eric A</creatorcontrib><title>Radon Exposure, Clonal Hematopoiesis, and Stroke Susceptibility in the Women's Health Initiative</title><title>Neurology</title><addtitle>Neurology</addtitle><description>Studies suggest that clonal hematopoiesis of indeterminate potential (CHIP) may increase risk of hematologic malignancy and cardiovascular disease, including stroke. However, few studies have investigated plausible environmental risk factors for CHIP such as radon, despite the climate-related increases in and documented infrequency of testing for this common indoor air pollutant.The purpose of this study was to estimate the risk of CHIP related to radon, an established environmental mutagen.
We linked geocoded addresses of 10,799 Women's Health Initiative Trans-Omics for Precision Medicine (WHI TOPMed) participants to US Environmental Protection Agency-predicted, county-level, indoor average screening radon concentrations, categorized as follows: Zone 1 (>4 pCi/L), Zone 2 (2-4 pCi/L), and Zone 3 (<2 pCi/L). We defined CHIP as the presence of one or more leukemogenic driver mutations with variant allele frequency >0.02. We identified prevalent and incident ischemic and hemorrhagic strokes; subtyped ischemic stroke using Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria; and then estimated radon-related risk of CHIP as an odds ratio (OR) and 95% CI using multivariable-adjusted, design-weighted logistic regression stratified by age, race/ethnicity, smoking status, and stroke type/subtype.
The percentages of participants with CHIP in Zones 1, 2, and 3 were 9.0%, 8.4%, and 7.7%, respectively (
= 0.06). Among participants with ischemic stroke, Zones 2 and 1 were associated with higher estimated risks of CHIP relative to Zone 3: 1.39 (1.15-1.68) and 1.46 (1.15-1.87), but not among participants with hemorrhagic stroke: 0.98 (0.68-1.40) and 1.03 (0.70-1.52), or without stroke: 1.04 (0.74-1.46) and 0.95 (0.63-1.42), respectively (
= 0.03). Corresponding estimates were particularly high among TOAST-subtyped cardioembolism: 1.78 (1.30-2.47) and 1.88 (1.31-2.72), or other ischemic etiologies: 1.37 (1.06-1.78) and 1.50 (1.11-2.04), but not small vessel occlusion: 1.05 (0.74-1.49) and 1.00 (0.68-1.47), respectively (
= 0.10). Observed patterns of association among strata were insensitive to attrition weighting, ancestry adjustment, prevalent stroke exclusion, separate analysis of
driver mutations, and substitution with 3 alternative estimates of radon exposure.
The robust elevation of radon-related risk of CHIP among postmenopausal women who develop incident cardioembolic stroke is consistent with a potential role of somatic genomic mutation in this societally burdensome form of cerebrovascular disease, although the mechanism has yet to be confirmed.</description><subject>Clonal Hematopoiesis</subject><subject>Female</subject><subject>Humans</subject><subject>Ischemic Stroke</subject><subject>Radon - adverse effects</subject><subject>Radon - analysis</subject><subject>Risk Factors</subject><subject>Stroke - chemically induced</subject><subject>Stroke - epidemiology</subject><subject>Stroke - genetics</subject><subject>Women's Health</subject><issn>0028-3878</issn><issn>1526-632X</issn><issn>1526-632X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdUV1LwzAUDaK4Of0HInnTBzvz0TTJk8hQNxgKKuhbTNvMRdukNqnov7cyHep9uXDvOefewwFgH6MxJpic3F_Nx2hdBAnE2AYYYkayJKPkYRMM-7FIqOBiAHZCeEaoX3K5DQZUYI5kKobg8UaX3sHz98aHrjXHcFJ5pys4NbWOvvHWBBuOoXYlvI2tfzHwtguFaaLNbWXjB7QOxqWB97427jD0PF3FJZw5G62O9s3sgq2FroLZ--4jcHdxfjeZJvPry9nkbJ4UNKMxKRkrSoq1lCkrKMmJQRnlGOeIirJ3JjBLC8pzKQxbMCI4RlxmmZQop2xB6AicrmSbLq9NWRgXW12pprW1bj-U11b93Ti7VE_-TWEkOOLpl8LRt0LrXzsToqpt77SqtDO-C4pIjLDMsMh6aLqCFq0PoTWL9R2M1Fc4qg9H_Q-npx38_nFN-kmDfgLFJopi</recordid><startdate>20240123</startdate><enddate>20240123</enddate><creator>Anthony, Kurtis M</creator><creator>Collins, Jason M</creator><creator>Love, Shelly-Ann M</creator><creator>Stewart, James D</creator><creator>Buchheit, Sophie F</creator><creator>Gondalia, Rahul</creator><creator>Schwartz, Gary G</creator><creator>Huang, David Y</creator><creator>Meliker, Jaymie R</creator><creator>Zhang, Zhenzhen</creator><creator>Barac, Ana</creator><creator>Desai, Pinkal</creator><creator>Hayden, Kathleen M</creator><creator>Honigberg, Michael C</creator><creator>Jaiswal, Siddhartha</creator><creator>Natarajan, Pradeep</creator><creator>Bick, Alexander G</creator><creator>Kooperberg, Charles</creator><creator>Manson, JoAnn E</creator><creator>Reiner, Alexander P</creator><creator>Whitsel, Eric A</creator><general>Lippincott Williams & Wilkins</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7029-2203</orcidid><orcidid>https://orcid.org/0000-0002-0658-8752</orcidid><orcidid>https://orcid.org/0000-0002-9440-3892</orcidid><orcidid>https://orcid.org/0000-0002-7986-8560</orcidid><orcidid>https://orcid.org/0000-0003-4843-3641</orcidid></search><sort><creationdate>20240123</creationdate><title>Radon Exposure, Clonal Hematopoiesis, and Stroke Susceptibility in the Women's Health Initiative</title><author>Anthony, Kurtis M ; Collins, Jason M ; Love, Shelly-Ann M ; Stewart, James D ; Buchheit, Sophie F ; Gondalia, Rahul ; Schwartz, Gary G ; Huang, David Y ; Meliker, Jaymie R ; Zhang, Zhenzhen ; Barac, Ana ; Desai, Pinkal ; Hayden, Kathleen M ; Honigberg, Michael C ; Jaiswal, Siddhartha ; Natarajan, Pradeep ; Bick, Alexander G ; Kooperberg, Charles ; Manson, JoAnn E ; Reiner, Alexander P ; Whitsel, Eric A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c363t-d55cd31a9945c32b2e063711b038d0558154c37b98e5f5287107966990b35f23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Clonal Hematopoiesis</topic><topic>Female</topic><topic>Humans</topic><topic>Ischemic Stroke</topic><topic>Radon - adverse effects</topic><topic>Radon - analysis</topic><topic>Risk Factors</topic><topic>Stroke - chemically induced</topic><topic>Stroke - epidemiology</topic><topic>Stroke - genetics</topic><topic>Women's Health</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Anthony, Kurtis M</creatorcontrib><creatorcontrib>Collins, Jason M</creatorcontrib><creatorcontrib>Love, Shelly-Ann M</creatorcontrib><creatorcontrib>Stewart, James D</creatorcontrib><creatorcontrib>Buchheit, Sophie F</creatorcontrib><creatorcontrib>Gondalia, Rahul</creatorcontrib><creatorcontrib>Schwartz, Gary G</creatorcontrib><creatorcontrib>Huang, David Y</creatorcontrib><creatorcontrib>Meliker, Jaymie R</creatorcontrib><creatorcontrib>Zhang, Zhenzhen</creatorcontrib><creatorcontrib>Barac, Ana</creatorcontrib><creatorcontrib>Desai, Pinkal</creatorcontrib><creatorcontrib>Hayden, Kathleen M</creatorcontrib><creatorcontrib>Honigberg, Michael C</creatorcontrib><creatorcontrib>Jaiswal, Siddhartha</creatorcontrib><creatorcontrib>Natarajan, Pradeep</creatorcontrib><creatorcontrib>Bick, Alexander G</creatorcontrib><creatorcontrib>Kooperberg, Charles</creatorcontrib><creatorcontrib>Manson, JoAnn E</creatorcontrib><creatorcontrib>Reiner, Alexander P</creatorcontrib><creatorcontrib>Whitsel, Eric A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Anthony, Kurtis M</au><au>Collins, Jason M</au><au>Love, Shelly-Ann M</au><au>Stewart, James D</au><au>Buchheit, Sophie F</au><au>Gondalia, Rahul</au><au>Schwartz, Gary G</au><au>Huang, David Y</au><au>Meliker, Jaymie R</au><au>Zhang, Zhenzhen</au><au>Barac, Ana</au><au>Desai, Pinkal</au><au>Hayden, Kathleen M</au><au>Honigberg, Michael C</au><au>Jaiswal, Siddhartha</au><au>Natarajan, Pradeep</au><au>Bick, Alexander G</au><au>Kooperberg, Charles</au><au>Manson, JoAnn E</au><au>Reiner, Alexander P</au><au>Whitsel, Eric A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Radon Exposure, Clonal Hematopoiesis, and Stroke Susceptibility in the Women's Health Initiative</atitle><jtitle>Neurology</jtitle><addtitle>Neurology</addtitle><date>2024-01-23</date><risdate>2024</risdate><volume>102</volume><issue>2</issue><spage>e208055</spage><pages>e208055-</pages><issn>0028-3878</issn><issn>1526-632X</issn><eissn>1526-632X</eissn><abstract>Studies suggest that clonal hematopoiesis of indeterminate potential (CHIP) may increase risk of hematologic malignancy and cardiovascular disease, including stroke. However, few studies have investigated plausible environmental risk factors for CHIP such as radon, despite the climate-related increases in and documented infrequency of testing for this common indoor air pollutant.The purpose of this study was to estimate the risk of CHIP related to radon, an established environmental mutagen.
We linked geocoded addresses of 10,799 Women's Health Initiative Trans-Omics for Precision Medicine (WHI TOPMed) participants to US Environmental Protection Agency-predicted, county-level, indoor average screening radon concentrations, categorized as follows: Zone 1 (>4 pCi/L), Zone 2 (2-4 pCi/L), and Zone 3 (<2 pCi/L). We defined CHIP as the presence of one or more leukemogenic driver mutations with variant allele frequency >0.02. We identified prevalent and incident ischemic and hemorrhagic strokes; subtyped ischemic stroke using Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria; and then estimated radon-related risk of CHIP as an odds ratio (OR) and 95% CI using multivariable-adjusted, design-weighted logistic regression stratified by age, race/ethnicity, smoking status, and stroke type/subtype.
The percentages of participants with CHIP in Zones 1, 2, and 3 were 9.0%, 8.4%, and 7.7%, respectively (
= 0.06). Among participants with ischemic stroke, Zones 2 and 1 were associated with higher estimated risks of CHIP relative to Zone 3: 1.39 (1.15-1.68) and 1.46 (1.15-1.87), but not among participants with hemorrhagic stroke: 0.98 (0.68-1.40) and 1.03 (0.70-1.52), or without stroke: 1.04 (0.74-1.46) and 0.95 (0.63-1.42), respectively (
= 0.03). Corresponding estimates were particularly high among TOAST-subtyped cardioembolism: 1.78 (1.30-2.47) and 1.88 (1.31-2.72), or other ischemic etiologies: 1.37 (1.06-1.78) and 1.50 (1.11-2.04), but not small vessel occlusion: 1.05 (0.74-1.49) and 1.00 (0.68-1.47), respectively (
= 0.10). Observed patterns of association among strata were insensitive to attrition weighting, ancestry adjustment, prevalent stroke exclusion, separate analysis of
driver mutations, and substitution with 3 alternative estimates of radon exposure.
The robust elevation of radon-related risk of CHIP among postmenopausal women who develop incident cardioembolic stroke is consistent with a potential role of somatic genomic mutation in this societally burdensome form of cerebrovascular disease, although the mechanism has yet to be confirmed.</abstract><cop>United States</cop><pub>Lippincott Williams & Wilkins</pub><pmid>38170948</pmid><doi>10.1212/WNL.0000000000208055</doi><orcidid>https://orcid.org/0000-0001-7029-2203</orcidid><orcidid>https://orcid.org/0000-0002-0658-8752</orcidid><orcidid>https://orcid.org/0000-0002-9440-3892</orcidid><orcidid>https://orcid.org/0000-0002-7986-8560</orcidid><orcidid>https://orcid.org/0000-0003-4843-3641</orcidid></addata></record> |
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| ispartof | Neurology, 2024-01, Vol.102 (2), p.e208055 |
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| language | eng |
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| source | MEDLINE; Alma/SFX Local Collection; Journals@Ovid Complete |
| subjects | Clonal Hematopoiesis Female Humans Ischemic Stroke Radon - adverse effects Radon - analysis Risk Factors Stroke - chemically induced Stroke - epidemiology Stroke - genetics Women's Health |
| title | Radon Exposure, Clonal Hematopoiesis, and Stroke Susceptibility in the Women's Health Initiative |
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