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Upper airway cancer, myeloid leukemia, and other cancers in a cohort of British chemical workers exposed to formaldehyde.

ABSTRACT: The International Agency for Research on Cancer controversially has classified formaldehyde as causing nasopharyngeal carcinoma and myeloid leukemia. To provide further information on this question, we extended follow-up of a cohort of 14,008 chemical workers at 6 factories in England and Wales, covering the period 1941-2012. Mortality was compared with national death rates for England and Wales, and associations with incident upper airway cancer and leukemia were explored in nested case-control analyses. We observed excess deaths from cancers of the esophagus (100 observed vs. 93.1 expected), stomach (182 vs. 141.4), rectum (107 vs. 86.8), liver (35 vs. 26.9), and lung (813 vs. 645.8), but none of these tumors exhibited a clear exposure-response relationship. Nested case-control analyses of 115 men with upper airway cancer (including 1 nasopharyngeal cancer), 92 men with leukemia, and 45 men with myeloid leukemia indicated no elevations of risk in the highest exposure category (high exposure for ?1 year). When the 2 highest exposure categories were combined, the odds ratio for myeloid leukemia was 1.26 (95% confidence interval: 0.39, 4.08). Our results provide no support for an increased hazard of myeloid leukemia, nasopharyngeal carcinoma, or other upper airway tumors from formaldehyde exposure. These results indicate that any excess risk of these cancers, even from relatively high exposures, is at most small.

SUBMITTER: Coggon D

PROVIDER: S-EPMC4189094 | biostudies-literature | 2014 Jun

REPOSITORIES: biostudies-literature

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Upper airway cancer, myeloid leukemia, and other cancers in a cohort of British chemical workers exposed to formaldehyde.

Coggon David D Ntani Georgia G Harris E Clare EC Palmer Keith T KT

American journal of epidemiology 20140408 11

The International Agency for Research on Cancer controversially has classified formaldehyde as causing nasopharyngeal carcinoma and myeloid leukemia. To provide further information on this question, we extended follow-up of a cohort of 14,008 chemical workers at 6 factories in England and Wales, covering the period 1941-2012. Mortality was compared with national death rates for England and Wales, and associations with incident upper airway cancer and leukemia were explored in nested case-control ...[more]

PMID: 24714728

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Project description:Formaldehyde, a common indoor air pollutant, exacerbates asthma and synergizes with allergen to induce airway hyperresponsiveness (AHR) in animal models. The mechanisms mediating formaldehyde-induced AHR remain poorly understood. We posit that formaldehyde modulates agonist-induced contractile response of human airway smooth muscle (HASM) cells to elicit AHR. HASM cells were exposed to formaldehyde or vehicle and agonist-induced intracellular Ca2+ ([Ca2+]i) and myosin light-chain phosphatase (MYPT1) phosphorylation were determined. Air-liquid interface-differentiated human bronchial epithelial (HBE) cells were exposed to formaldehyde or vehicle and cocultured with HASM cells. Agonist-induced [Ca2+]i and MYPT1 phosphorylation were determined in the cocultured HASM cells. Precision-cut human lung slices were exposed to PBS or varying concentrations of formaldehyde, and then carbachol-induced airway narrowing was determined 24 hours after exposure. HASM cells were transfected with nontargeting or nuclear factor erythroid-derived 2, like 2 (Nrf-2)-targeting small interfering RNA and exposed to formaldehyde or vehicle, followed by determination of antioxidant response (quinone oxido-reductase 1 and thioredoxin 1) and basal and agonist-induced MYPT1 phosphorylation. Formaldehyde enhanced the basal Rho-kinase activity and MYPT1 phosphorylation with little effect on agonist-induced [Ca2+]i in HASM cells. Formaldehyde induced Nrf-2-dependent antioxidant response in HASM cells, although the MYPT1 phosphorylation was independent of Nrf-2 induction. Although HBE cells exposed to formaldehyde had little effect on agonist-induced [Ca2+]i or MYPT1 phosphorylation in cocultured HASM cells, formaldehyde enhanced carbachol-induced airway responsiveness in precision-cut human lung slices. In conclusion, formaldehyde induces phosphorylation of the regulatory subunit of MYPT1, independent of formaldehyde-induced Nrf-2 activation in HASM cells. The findings suggest that the Rho kinase-dependent Ca2+ sensitization pathway plays a role in formaldehyde-induced AHR.

Dataset Information

Upper airway cancer, myeloid leukemia, and other cancers in a cohort of British chemical workers exposed to formaldehyde.

Publications

Upper airway cancer, myeloid leukemia, and other cancers in a cohort of British chemical workers exposed to formaldehyde.

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