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      Association between Six Environmental Chemicals and Lung Cancer Incidence in the United States

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          Abstract

          Background. An increased risk of lung cancer has been observed at exposure to certain industrial chemicals in occupational settings; however, less is known about their carcinogenic potential to the general population when those agents are released into the environment. Methods. We used the Toxics Release Inventory (TRI) database and Surveillance, Epidemiology, and End Results (SEER) data to conduct an ecological study at the county level. We used multiple linear regression to assess the association of age-adjusted lung cancer incidence with the quantities of on-site air and water releases of six selected industrial chemicals including arsenic, 1,3 butadiene, cadmium, chromium, formaldehyde, and nickel after controlling for other risk variables. Results. Overall, we observed a significantly increased risk of lung cancer incidence associated with releases of chromium, formaldehyde, and nickel. The links were present for both males and females. Significant effects were present in nonmetropolitan but not metropolitan counties. Releases of arsenic, 1,3 butadiene, and cadmium were reported by small numbers of facilities, and no relationships to lung cancer incidence were detected. Conclusions. Our results suggest that environmental exposure to chromium, formaldehyde, and nickel from TRI sites may increase population risk of lung cancer. These findings need to be confirmed in individual-level studies, but in congruence with the precautionary principle in environmental science, support prudent efforts to limit release of these agents into the environment.

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          Most cited references52

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          Lung cancer in never smokers: a review.

          Lung cancer is the leading cause of cancer-related death in the United States. Although tobacco smoking accounts for the majority of lung cancer, approximately 10% of patients with lung cancer in the United States are lifelong never smokers. Lung cancer in the never smokers (LCINS) affects women disproportionately more often than men. Only limited data are available on the etiopathogenesis, molecular abnormalities, and prognosis of LCINS. Several etiologic factors have been proposed for the development of LCINS, including exposure to radon, cooking fumes, asbestos, heavy metals, and environmental tobacco smoke, human papillomavirus infection, and inherited genetic susceptibility. However, the relative significance of these individual factors among different ethnic populations in the development of LCINS has not been well-characterized. Adenocarcinoma is the predominant histologic subtype reported with LCINS. Striking differences in response rates and outcomes are seen when patients with advanced non-small-cell lung cancer (NSCLC) who are lifelong never smokers are treated with epidermal growth factor receptor tyrosine kinase (EGFR-TK) inhibitors such as gefitinib or erlotinib compared with the outcomes with these agents in patients with tobacco-associated lung cancer. Interestingly, the activating mutations in the EGFR-TK inhibitors have been reported significantly more frequently in LCINS than in patients with tobacco-related NSCLC. This review will summarize available data on the epidemiology, risk factors, molecular genetics, management options, and outcomes of LCINS.
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            Environmental exposure to cadmium and risk of cancer: a prospective population-based study.

            Cadmium is a ubiquitous environmental pollutant, which accumulates in the human body such that 24-h urinary excretion is a biomarker of lifetime exposure. We aimed to assess the association between environmental exposure to cadmium and cancer. We recruited a random population sample (n=994) from an area close to three zinc smelters and a reference population from an area with low exposure to cadmium. At baseline (1985-89), we measured cadmium in urine samples obtained over 24 h and in the soil of participants' gardens, and followed the incidence of cancer until June 30, 2004. We used Cox regression to calculate hazard ratios for cancer in relation to internal (ie, urinary) and external (ie, soil) exposure to cadmium, while adjusting for covariables. Cadmium concentration in soil ranged from 0.8 mg/kg to 17.0 mg/kg. At baseline, geometric mean urinary cadmium excretion was 12.3 nmol/day for people in the high-exposure area, compared with 7.7 nmol/day for those in the reference (ie, low-exposure) area (p<0.0001). During follow-up (median 17.2 years [range 0.6-18.8]), 50 fatal cancers and 20 non-fatal cancers occurred, of which 18 and one, respectively, were lung cancers. Overall cancer risk was significantly associated with a doubling of 24-h cadmium excretion (hazard ratio 1.31 [95% CI 1.03-1.65], p=0.026. Population-attributable risk of lung cancer was 67% (95% CI 33-101) in the high-exposure area, compared with that of 73% (38-108) for smoking. For lung cancer, adjusted hazard ratio was 1.70 (1.13-2.57, p=0.011) for a doubling of 24-h urinary cadmium excretion, 4.17 (1.21-14.4, p=0.024) for residence in the high-exposure area versus the low-exposure area, and 1.57 (1.11-2.24, p=0.012) for a doubling of cadmium concentration in soil. Historical pollution from non-ferrous smelters continues to present a serious health hazard, necessitating targeted preventive measures.
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              Lung cancer and arsenic concentrations in drinking water in Chile.

              Cities in northern Chile had arsenic concentrations of 860 microg/liter in drinking water in the period 1958-1970. Concentrations have since been reduced to 40 microg/liter. We investigated the relation between lung cancer and arsenic in drinking water in northern Chile in a case-control study involving patients diagnosed with lung cancer between 1994 and 1996 and frequency-matched hospital controls. The study identified 152 lung cancer cases and 419 controls. Participants were interviewed regarding drinking water sources, cigarette smoking, and other variables. Logistic regression analysis revealed a clear trend in lung cancer odds ratios and 95% confidence intervals (CIs) with increasing concentration of arsenic in drinking water, as follows: 1, 1.6 (95% CI = 0.5-5.3), 3.9 (95% CI = 1.2-12.3), 5.2 (95% CI = 2.3-11.7), and 8.9 (95% CI = 4.0-19.6), for arsenic concentrations ranging from less than 10 microg/liter to a 65-year average concentration of 200-400 microg/liter. There was evidence of synergy between cigarette smoking and ingestion of arsenic in drinking water; the odds ratio for lung cancer was 32.0 (95% CI = 7.2-198.0) among smokers exposed to more than 200 microg/liter of arsenic in drinking water (lifetime average) compared with nonsmokers exposed to less than 50 microg/liter. This study provides strong evidence that ingestion of inorganic arsenic is associated with human lung cancer.
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                Author and article information

                Journal
                J Environ Public Health
                JEPH
                Journal of Environmental and Public Health
                Hindawi Publishing Corporation
                1687-9805
                1687-9813
                2011
                10 July 2011
                : 2011
                : 463701
                Affiliations
                1Department of Community Medicine, School of Medicine, West Virginia University, P.O. Box 9190, Morgantown, WV 26506, USA
                2West Virginia Rural Health Research Center, West Virginia University, P.O. Box 9190, Morgantown, WV 26506, USA
                3Mary Babb Randolph Cancer Center, West Virginia University, P.O. Box 9190, Morgantown, WV 26506, USA
                Author notes

                Academic Editor: Michael Bates

                Article
                10.1155/2011/463701
                3136160
                21776439
                0606ea69-375d-4a9e-af1c-b5d28f351c04
                Copyright © 2011 Juhua Luo et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 20 October 2010
                : 8 March 2011
                : 3 May 2011
                Categories
                Research Article

                Public health
                Public health

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