<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Fang F</submitter><funding>NIDA NIH HHS</funding><funding>NIEHS NIH HHS</funding><funding>Jonsson Comprehensive Cancer Center</funding><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIH HHS</funding><pagination>1579-1586</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10932807</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>154(9)</volume><pubmed_abstract>Fine particulate matter (PM&lt;sub>2.5&lt;/sub> ) contains carcinogens similar to those generated by tobacco smoking, which may increase the risks of developing smoking-related cancers, such as upper aerodigestive track (UADT) cancers, for both smokers and never-smokers. Therefore, it is imperative to understand the relation between ambient PM&lt;sub>2.5&lt;/sub> exposure and risk of UADT cancers. A population-based case-control study involving 565 incident UADT cancer cases and 983 controls was conducted in Los Angeles County from 1999 to 2004. The average residential PM&lt;sub>2.5&lt;/sub> concentration 1 year before the diagnosis date for cases and the reference date for controls was assessed using a chemical transport model. The association between ambient PM&lt;sub>2.5&lt;/sub> and the UADT cancers was estimated by unconditional logistic regression, adjusting for confounders at the individual and block-group level. Stratified analyses were conducted by sex, tobacco smoking status and UADT subsites. We also assessed the interaction between PM&lt;sub>2.5&lt;/sub> and tobacco smoking on UADT cancers. PM&lt;sub>2.5&lt;/sub> concentrations were associated with an elevated odds of UADT cancers (adjusted odds ratio = 1.21 per interquartile range [4.5 μg/m&lt;sup>3&lt;/sup> ] increase; 95% confidence interval: 1.02, 1.44). The association between PM&lt;sub>2.5&lt;/sub> and UADT cancers was similar across UADT subsites, sex and tobacco smoking status. The interaction between PM&lt;sub>2.5&lt;/sub> and tobacco smoking on UADT cancers was approximately additive on the odds scale. The effect estimate for PM&lt;sub>2.5&lt;/sub> and UADT cancers was similar among never smokers. Our findings support the hypothesis that exposure to PM&lt;sub>2.5&lt;/sub> increases the risk of UADT cancers. Improvements in air quality may reduce the risk of UADT cancers.</pubmed_abstract><journal>International journal of cancer</journal><pubmed_title>Association between ambient exposure to PM&amp;lt;sub&amp;gt;2.5&amp;lt;/sub&amp;gt; and upper aerodigestive tract cancer in Los Angeles.</pubmed_title><pmcid>PMC10932807</pmcid><funding_grant_id>CA90833</funding_grant_id><funding_grant_id>ES06718</funding_grant_id><funding_grant_id>DA11386</funding_grant_id><funding_grant_id>T32 CA009142</funding_grant_id><funding_grant_id>CA077954</funding_grant_id><funding_grant_id>U01 CA096134</funding_grant_id><funding_grant_id>R21 ES011667</funding_grant_id><funding_grant_id>R03 CA077954</funding_grant_id><funding_grant_id>R01 CA090833</funding_grant_id><funding_grant_id>R01 DA011386</funding_grant_id><funding_grant_id>ES011667</funding_grant_id><funding_grant_id>CA96134</funding_grant_id><funding_grant_id>CA009142</funding_grant_id><pubmed_authors>Morgenstern H</pubmed_authors><pubmed_authors>Ritz B</pubmed_authors><pubmed_authors>Zhu Y</pubmed_authors><pubmed_authors>Zhang ZF</pubmed_authors><pubmed_authors>Fang F</pubmed_authors><pubmed_authors>Tashkin DP</pubmed_authors><pubmed_authors>Rao J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Association between ambient exposure to PM&amp;lt;sub&amp;gt;2.5&amp;lt;/sub&amp;gt; and upper aerodigestive tract cancer in Los Angeles.</name><description>Fine particulate matter (PM&lt;sub>2.5&lt;/sub> ) contains carcinogens similar to those generated by tobacco smoking, which may increase the risks of developing smoking-related cancers, such as upper aerodigestive track (UADT) cancers, for both smokers and never-smokers. Therefore, it is imperative to understand the relation between ambient PM&lt;sub>2.5&lt;/sub> exposure and risk of UADT cancers. A population-based case-control study involving 565 incident UADT cancer cases and 983 controls was conducted in Los Angeles County from 1999 to 2004. The average residential PM&lt;sub>2.5&lt;/sub> concentration 1 year before the diagnosis date for cases and the reference date for controls was assessed using a chemical transport model. The association between ambient PM&lt;sub>2.5&lt;/sub> and the UADT cancers was estimated by unconditional logistic regression, adjusting for confounders at the individual and block-group level. Stratified analyses were conducted by sex, tobacco smoking status and UADT subsites. We also assessed the interaction between PM&lt;sub>2.5&lt;/sub> and tobacco smoking on UADT cancers. PM&lt;sub>2.5&lt;/sub> concentrations were associated with an elevated odds of UADT cancers (adjusted odds ratio = 1.21 per interquartile range [4.5 μg/m&lt;sup>3&lt;/sup> ] increase; 95% confidence interval: 1.02, 1.44). The association between PM&lt;sub>2.5&lt;/sub> and UADT cancers was similar across UADT subsites, sex and tobacco smoking status. The interaction between PM&lt;sub>2.5&lt;/sub> and tobacco smoking on UADT cancers was approximately additive on the odds scale. The effect estimate for PM&lt;sub>2.5&lt;/sub> and UADT cancers was similar among never smokers. Our findings support the hypothesis that exposure to PM&lt;sub>2.5&lt;/sub> increases the risk of UADT cancers. Improvements in air quality may reduce the risk of UADT cancers.</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 May</publication><modification>2025-06-27T03:05:32.069Z</modification><creation>2025-06-27T03:05:32.069Z</creation></dates><accession>S-EPMC10932807</accession><cross_references><pubmed>38180239</pubmed><doi>10.1002/ijc.34835</doi></cross_references></HashMap>