Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
Association of Blood Levels of Forever Plastics with Lung Cancer Mortality among Ever Smokers in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cohort Study.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Irajizad Ehsan, Fahrmann Johannes F, Wu Ranran, Rudsari Hamid, Dennison Jennifer B, Ostrin Edwin, Ajani Jaffer, Hanash Samir
Аннотация
PURPOSE: Recent evidence suggests a significant association between microplastic (MP), forever chemicals, and plasticizers and various diseases, including cancer. In this study, we evaluated circulating levels of plastic-associated chemicals in relation to lung cancer incidence and mortality among smokers in the Prostate, Lung, Colorectal, and Ovarian (PLCO) study.
EXPERIMENTAL DESIGN: Using mass spectrometry, we screened for 29 known MP, forever plastics [per- and polyfluoroalkyl substances (PFAS)], and plasticizer chemicals in 245 sera collected preceding a lung cancer diagnosis and 1,200 noncase sera from participants in the PLCO study who had a history of smoking. Five PFAS and three plasticizers were detected and quantified in sera. A PFAP model, consisting of perfluorooctane sulfonate (PFOS) + perfluorohexanesulfonic acid (PFHA) + mono-iso-nonyl phthalate, was developed for predicting lung cancer mortality and risk strata based on quantiles established.
RESULTS: Higher circulating levels of PFOS, PFHA, and mono-iso-nonyl phthalate were associated with increased risk of lung cancer death (P < 0.05) but not incidence. Compared with the lowest quantile (reference), individuals with PFAP scores in the highest quantile were at markedly higher risk of death from lung cancer (P < 0.0001), with respective cause-specific and subdistributional HR of 1.86 [95% confidence interval (CI), 1.18-2.93] and 1.82 (95% CI, 1.15-2.88). Substratified analyses confirmed that the PFAP model remained an independent predictor of lung cancer-specific mortality (P < 0.05) across strata defined by age, sex, smoking history, histologic subtype, and stage at diagnosis.
CONCLUSIONS: In the PLCO cohort, elevated levels of PFOS, PFHA, and mono-iso-nonyl phthalate were associated with increased lung cancer mortality among ever smokers across disease subgroups.
EXPERIMENTAL DESIGN: Using mass spectrometry, we screened for 29 known MP, forever plastics [per- and polyfluoroalkyl substances (PFAS)], and plasticizer chemicals in 245 sera collected preceding a lung cancer diagnosis and 1,200 noncase sera from participants in the PLCO study who had a history of smoking. Five PFAS and three plasticizers were detected and quantified in sera. A PFAP model, consisting of perfluorooctane sulfonate (PFOS) + perfluorohexanesulfonic acid (PFHA) + mono-iso-nonyl phthalate, was developed for predicting lung cancer mortality and risk strata based on quantiles established.
RESULTS: Higher circulating levels of PFOS, PFHA, and mono-iso-nonyl phthalate were associated with increased risk of lung cancer death (P < 0.05) but not incidence. Compared with the lowest quantile (reference), individuals with PFAP scores in the highest quantile were at markedly higher risk of death from lung cancer (P < 0.0001), with respective cause-specific and subdistributional HR of 1.86 [95% confidence interval (CI), 1.18-2.93] and 1.82 (95% CI, 1.15-2.88). Substratified analyses confirmed that the PFAP model remained an independent predictor of lung cancer-specific mortality (P < 0.05) across strata defined by age, sex, smoking history, histologic subtype, and stage at diagnosis.
CONCLUSIONS: In the PLCO cohort, elevated levels of PFOS, PFHA, and mono-iso-nonyl phthalate were associated with increased lung cancer mortality among ever smokers across disease subgroups.