Helena Sandoval-Insausti1, Yu-Han Chiu2, Dong Hoon Lee3, Siwen Wang3, Jaime E Hart4, Lidia Mínguez-Alarcón5, Francine Laden6, Andres V Ardisson Korat7, Brenda Birmann7, A Heather Eliassen2, Walter C Willett8, Jorge E Chavarro9. 1. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. Electronic address: hsandov@hsph.harvard.edu. 2. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 3. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 4. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. 5. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 6. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. 7. Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. 8. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. 9. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. Electronic address: jchavarr@hsph.harvard.edu.
Abstract
BACKGROUND: Conventionally grown fruits and vegetables (FVs) are the main source of general population exposure to pesticide residues. OBJECTIVE: To evaluate the relation of intake of high- and low-pesticide-residue FVs with cancer risk. METHODS: We followed 150,830 women (Nurses' Health Study, 1998-2016, and Nurses' Health Study II, 1999-2017) and 29,486 men (Health Professionals Follow-up Study, 1998-2016) without a history of cancer. We ascertained FV intake via validated food frequency questionnaires and categorized FVs as having high or low pesticide residue levels based on USDA surveillance data. We used Cox proportional hazards models to estimate hazard ratios (HR) and 95% confidence intervals (CI) of total and site-specific cancer related to quintiles of high- and low-pesticide-residue FV intake. RESULTS: We documented 23,678 incident cancer cases during 2,862,118 person-years of follow-up. In the pooled multivariable analysis, neither high- nor low-pesticide-residue FV intake was associated with cancer. The HRs (95% CI) per 1 serving/day increase in intake were 0.99 (0.97-1.01) for high- and 1.01 (0.99-1.02) for low-pesticide-residue FVs. Additionally, we found no association between high-pesticide-residue FV intake and risk of specific sites, including malignancies previously linked to occupational pesticide exposure ([HR, 95% CI comparing extreme quintiles of intake] lung [1.17 (0.95-1.43)], non-Hodgkin lymphoma [0.89 (0.72-1.09)], prostate [1.31 (0.88-1.93)]) or inversely related to intake of organic foods (breasts [1.03 (0.94-1.31)]). CONCLUSIONS: These findings suggest that overall exposure to pesticides through FV intake is not related to cancer risk, although they do not rule out associations with specific chemicals or sub-types of specific cancers.
BACKGROUND: Conventionally grown fruits and vegetables (FVs) are the main source of general population exposure to pesticide residues. OBJECTIVE: To evaluate the relation of intake of high- and low-pesticide-residue FVs with cancer risk. METHODS: We followed 150,830 women (Nurses' Health Study, 1998-2016, and Nurses' Health Study II, 1999-2017) and 29,486 men (Health Professionals Follow-up Study, 1998-2016) without a history of cancer. We ascertained FV intake via validated food frequency questionnaires and categorized FVs as having high or low pesticide residue levels based on USDA surveillance data. We used Cox proportional hazards models to estimate hazard ratios (HR) and 95% confidence intervals (CI) of total and site-specific cancer related to quintiles of high- and low-pesticide-residue FV intake. RESULTS: We documented 23,678 incident cancer cases during 2,862,118 person-years of follow-up. In the pooled multivariable analysis, neither high- nor low-pesticide-residue FV intake was associated with cancer. The HRs (95% CI) per 1 serving/day increase in intake were 0.99 (0.97-1.01) for high- and 1.01 (0.99-1.02) for low-pesticide-residue FVs. Additionally, we found no association between high-pesticide-residue FV intake and risk of specific sites, including malignancies previously linked to occupational pesticide exposure ([HR, 95% CI comparing extreme quintiles of intake] lung [1.17 (0.95-1.43)], non-Hodgkin lymphoma [0.89 (0.72-1.09)], prostate [1.31 (0.88-1.93)]) or inversely related to intake of organic foods (breasts [1.03 (0.94-1.31)]). CONCLUSIONS: These findings suggest that overall exposure to pesticides through FV intake is not related to cancer risk, although they do not rule out associations with specific chemicals or sub-types of specific cancers.
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