XXXX incidence decreases with elevation: evidence for @entity26 as an inhaled carcinogen.

@entity1 @entity5 @entity26 @entity16 @entity2 @entity105
The level of atmospheric @entity26 , a driver of free @entity16 and tumorigenesis, decreases sharply with rising elevation. To understand whether ambient @entity26 plays a role in @entity1 @entity105 , we characterized age-adjusted @entity5 incidence (compiled by the National @entity5 Institute from 2005 to 2009) across counties of the elevation-varying Western United States and compared trends displayed by @entity5 (lung) and @entity5 (breast, colorectal, and prostate). To adjust for important demographic and @entity5 -risk factors, 8-12 covariates were considered for each @entity5 . We produced regression models that captured known risks. Models demonstrated that elevation is strongly, negatively associated with @entity2 incidence (p < 10(-16)), but not with the incidence of @entity5 . For every 1,000 m rise in elevation, @entity2 incidence decreased by 7.23 99% CI [5.18-9.29] cases per 100,000 individuals, equivalent to 12.7% of the mean incidence, 56.8. As a predictor of @entity2 incidence, elevation was second only to smoking prevalence in terms of significance and effect size. Furthermore, no evidence of ecological fallacy or of confounding arising from evaluated factors was detected: the @entity2 association was robust to varying regression models, county stratification, and population subgrouping; additionally seven environmental correlates of elevation, such as exposure to sunlight and fine particulate matter, could not capture the association. Overall, our findings suggest the presence of an inhaled carcinogen inherently and inversely tied to elevation, offering epidemiological support for @entity26 -driven tumorigenesis. Finally, highlighting the need to consider elevation in studies of @entity2 , we demonstrated that previously reported inverse @entity2 associations with radon and UVB became insignificant after accounting for elevation.
