Cancer risks among iron and steel workers in Anshan, China, part I: Proportional mortality ratio analysis

Abstract

A standardized proportional mortality ratio (SPMR) study of 8,887 deaths during 1980–1989 among male workers in a large integrated iron‐steel complex in Anshan, China, was conducted to provide clues to occupational risk factors. Accidents and cancer accounted for a higher proportion of deaths among the iron‐steel workers than among the general male population (SPMR = 1.21; 95% CI = 1.12–1.31 and 1.14; 95% CI = 1.10–1.18, respectively). Among all workers, SPMRs were significantly elevated for stomach, lung, and colorectal cancers (SPMR = 1.37, 1.37, 1.38, respectively), but not other cancers. Risks of stomach cancer appeared to be highest among workers employed in jobs with exposure to iron and coal dust, whereas significant increases in colorectal cancer were seen for loading and other dusty jobs and for administrative and sedentary jobs without dust exposure. Risks of lung cancer appeared increased for a variety of jobs throughout the complex, especially those with probable high levels of exposure to polycyclic hydrocarbons and asbestos. Risk of esophageal cancer was significantly elevated for fire‐resistant brick makers, and risk of nonmalignant respiratory disease was significantly elevated for those employed as furnace workers, foundry workers, and fire‐resistant brick makers. (This article is a US Government work and, as such, is in the public domain in the United States of America.) © 1996 Wiley‐Liss, Inc.

Further evidence for a link between silica dust and esophageal cancer

“…As a follow-up to the earlier proportional mortality ratio (PMR) study that showed an increased standardized PMR of 2.2 among refractory brick makers in China, 17 Pan et al conducted a nested case-control study to specifically look into the relationship between esophageal cancer deaths and occupational exposure to silica dust, 6 using deaths from other causes as controls. After adjusting for confounding factors (including alcohol drinking, cigarette smoking and meat and fruit consumption), occupational exposure to silica dust had an odds ratio of 2.8, and a clear dose-response relationship by length of exposed years was present.…”

Summary of Notifiable Noninfectious Conditions and Disease Outbreaks: Surveillance for Silicosis — Michigan and New Jersey, 2003–2010

“…For workers who may have been exposed to crystalline silica, there have been infrequent reports of statistically significant excesses of deaths or cases of other cancers such as nasopharyngeal or pharyngeal cancer [Chen et al 1992;Carta et al 1991], salivary gland cancer [Zheng et al 1996], liver cancer [Chen et al 1992;Hua et al 1992], bone cancer [Forastiere et al 1989;Steenland and Beaumont 1986], pancreatic cancer [Kauppinen et al 1995], skin cancer [Partanen et al 1994;Rafnsson and Gunnarsdóttir 1997], esophageal cancer [Pan et al 1999;Xu et al 1996;Belli et al 1989], cancers of the digestive system [Decoufle and Wood 1979], intestinal or peritoneal cancer [Amandus et al 1991;Goldsmith et al 1995;Costello et al 1995], lymphopoietic or hematopoietic cancers [Redmond et al 1981;Silverstein et al 1986;Steenland and Brown 1995b], brain cancer [Rafnsson and Gunnarsdóttir 1997], and bladder cancer [Bravo et al 1987]. Again, an association has not been established between these cancers and exposure to crystalline silica.…”

“…Liu et al [1996,1998] challenged Chinese hamster lung fibroblasts with dusts pretreated with a phospholipid surfactant to simulate the condition of particles immediately after deposition on the pulmonary alveolar surface. Results of the experiments showed that untreated Min-U-Sil 5, Min-U-Sil 10, and noncrystalline silica induced micronucleus formation in a dose-dependent manner, but surfactant pretreatment suppressed that activity [Liu et al 1996]. A subsequent experiment found that surfactant pretreatment suppressed quartzinduced DNA damage in lavaged rat pulmonary macrophages, but DNA-damaging activity was restored with time as the phospholipid surfactant was removed by intracellular digestion [Liu et al 1998].…”

Iron Metabolism and Leukemia

“…[26][27][28]. In humans, hepatocellular carcinoma, malignant mesothelioma (iron in asbestos fibers), colorectal cancer, stomach cancer, lung cancer and ovarian endometriosis have been associated with iron overload [10,24,29]. Possible mechanisms of iron carcinogenesis include ironmediated ROS damage, iron-induced oxidative responsive transcription factors like Activator Protein-1 (AP-1), and Nuclear Factor Kappa B (NFkB), affecting signal-regulate kinases (ERKs) such as StressActivated Protein Kinases/c-Jun NH2 terminal Kinases (SAPK/JNK), and p38 Mitogen-Activated Protein Kinase (MAPK) , cell cycle growth and immune system [30][31][32][33][34][35][36].…”