Medical Effects of Smoke on the Pancreas

Smoking Tobacco is a Known Link to the Development of Pancreatic Inflammation and Disease. Many of the same chemicals are in other kinds of smoke, such as barbecue and wood smoke. Here are 2 new research reports: March 2007

Dioxin Induced Pancreatic Inflammation

Research Strengthens Link Between Smoking, Pancreatic Cancer

Science Daily: - Source: Michigan State University
Date: March 11, 2007 Researchers at Michigan State University have added yet another piece to the puzzle that links cigarette smoking with cancer of the pancreas, one of the deadliest forms of cancer.

In research published in the recent issue of the International Journal of Cancer, MSU’s James Trosko and colleagues zeroed in on the mechanism by which a healthy cell turns cancerous.

Specifically, they found that the chemicals produced by the burning of tobacco products – polycyclic aromatic hydrocarbons, or PAHs – interfere with communication between the body’s cells. More importantly, the work showed that some of these chemicals don’t necessarily initiate the cancer, but rather contribute to the promotion of it.

“These PAH chemicals are related to the multistage, multimechanism process of carcinogenesis, not by mutating the stem cell, but by triggering the stem cell that’s been previously mutated to proliferate,” said Trosko, a professor of pediatrics and human development. “This finding has major implications, including the possibility that dietary intervention might interrupt or even reverse the promotion of pancreatic cancers.”

Until now, most scientists thought that specific PAHs produced by burning tobacco mutated genes which, in turn, triggered the cancer mechanism.

“We take issue with this interpretation,” Trosko said. “We don’t believe that the PAH chemicals cause mutations which then lead to cancer.”

Pancreatic cancer is one of the more deadly forms of cancer, with an average survival rate of only about a year. It’s projected that more than 37,000 Americans will be diagnosed with pancreatic cancer in 2007.

Trosko noted that PAHs are formed when any substance containing certain proteins is burned, including foods.

“PAHs are all over,” he said. “When you grill a steak or a hamburger, for example, you get exactly the same class of chemicals.”

This research is the culmination of nearly 30 years of work in Trosko’s lab. It was in 1979 that Trosko, colleagues and students demonstrated that tumor-promoting chemicals interfered with a cell’s ability to communicate with other cells. Later, this group isolated adult human pancreatic stem cells from human pancreatic tissue.

Subsequent published findings indicated that these stem cells appeared to be targets for cancer.

“Since we had the system here in our lab, we decided to see if PAHs would act as a tumor promoter,” he said. “And sure enough they did.”

The good news is that people who quit smoking can dramatically improve their chances of avoiding cancers.

“If these chemicals act like cancer promoters and not initiators,” Trosko said, “then quitting smoking can assist in interrupting the process.”

Note: This story has been adapted from a news release issued by Michigan State University.
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Dioxin Induced Pancreatic Inflammation

Exocrine pancreatic pathology in female Harlan Sprague-Dawley rats after chronic treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin and dioxin-like compounds
Environmental Health Perspectives, June, 2004 by Abraham Nyska, Michael P. Jokinen, Amy E. Brix, Donald M. Sells, Michael E. Wyde, Denise Orzech, Joseph K. Haseman, Gordon Flake, Nigel J. Walker
Key words: carcinogenesis, dioxin, furans, inflammation, pancreas, polychlorinated biphenyls. doi:10.1289/ehp.6869 available via [Online 4 March 2004]

We evaluated the effect of chronic exposure to dioxin and dioxin-like compounds on the pancreas in female Harlan Sprague-Dawley rats. This investigation represents part of an ongoing National Toxicology Program initiative to determine the relative potency of chronic toxicity and carcinogenicity of polychlotinated dioxins, furans, and biphenyls. Animals were treated by gavage for up to 2 years with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3,3',4,4',5-pentachlorobiphenyl (PCB-126), 2,3,4,7,8-pentachlorodibenzofuran (PeCDF), or a toxic-equivalency-factor (TEF) mixture of these agents; control animals received corn oil-acetone vehicle alone. A complete necropsy was performed on all animals, and a full complement of tissues was collected and examined microscopically. Administration of each of the four compounds was associated with increased incidences of several nonneoplastic changes in the exocrine pancreas, including cytoplasmic vacuolation, chronic active inflammation, atrophy, and arteritis. Low incidences, but higher than those in the historical database, of pancreatic acinar adenoma and carcinoma were seen in the TCDD, PeCDF, and TEF-mixture groups. These results indicate that the pancreatic acini are target tissues for dioxin and certain dioxin-like compounds. Key words: carcinogenesis, dioxin, furans, inflammation, pancreas, polychlorinated biphenyls. doi:10.1289/ehp.6869 available via [Online 4 March 2004]

In the United States, pancreatic cancer ranks as the fifth most common cause of cancer death in humans of both sexes (American Cancer Society 2003). Risk factors for pancreatic cancer include heritable, germline mutations in genes such as p16 (Hruban et al. 1999) and BRCA2 (Risch et al. 2001); cigarette smoking [International Agency for Research on Cancer (IARC) 1986]; and a diet consisting of an increased intake of meat or cholesterol (Howg and Burch 1996). Recently, Risch (2003) proposed that the risk of pancreatic cancer is also increased by prolonged excessive gastric/ duodenal acidity and frequent or repeated exposure to N-nitroso compounds or their precursors. Of particular concern are observations suggesting that chronic pancreatitis may predispose individuals to cancer of the pancreas.

Chronic pancreatitis, an irreversible process with permanent loss of pancreatic function due to fibroinflammatory changes originating from various factors (Malsonneuve and Lowenfels 2002), often precedes the development of pancreatic malignancies. This chronic condition occurs in tropical regions or it may result from metabolic or hereditary disorders. Patients suffering from tropical calcifying pancreatitis (a form of nonalcoholic calcific pancreatitis in adolescents or young adults with no proven etiologic factor) have a significantly increased risk of developing pancreatic cancer (Chari et al. 1994), suggesting that chronic pancreatitis is a premalignant disease. Two independent epidemiologic studies calculated a 7- to 50-fold increased risk of pancreatic cancer in patients with hereditary pancreatitis (Lowenfels et al. 1997). Chronic pancreatic inflammation may also be induced by alcohol, congenital defects such as cystic fibrosis, some infectious diseases, drugs, and radiation therapy. Epidemiologic studies support the concept that inflammation associated with glandular destruction is a risk factor for exocrine pancreatic cancer. Lowenfels et al. (1993) studied 2,015 subjects with chronic pancreatitis and concluded that the risk of pancreatic cancer is significantly increased in this population and appears to be independent of sex, country, and type of pancreatitis. In addition, several environmental agents have been proposed as causal for chronic pancreatitis and pancreatic carcinomas and are associated with the wood and pulp industry, the dry cleaning business, and gasoline production and use (Foster et al. 1993; Lin and Kessler 1981; Milham and Demers 1984).

Polyhalogenated aromatic hydrocarbons (PHAHs) comprise a large class of compounds including polychlorinated dibenzodioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), polychlorinated biphenyls (PCBs), polychlorinated naphthalenes, and polybrominated diphenyl ethers. Certain PCDDs, PCDFs, and coplanar PCBs have the ability to bind to the aryl hydrocarbon receptor (AhR) and exhibit biologic actions similar to those of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); they are commonly referred to as dioxin-like compounds (DLCs). Exposure of humans to high levels of TCDD has been implicated in the development of diabetes. According to one study (Bertazzi et al. 2001), an increase of diabetes mellitus was suggestively time related among females in all exposure groups. Exposure of female Sprague-Dawley rats of the Spartan strain to 100 ng/kg TCDD for 2 years was associated with atrophy, fibrosis, and periarteritis of the pancreas (Kociba et al. 1978), whereas TCDD administered intraperitoneally to hamsters at the dose of 100 [micro]m/kg induced hepatocytic transdifferentiation of the acinar pancreatic cells (Rao et al. 1988). Others, however, have observed little or no correlation between diabetes and dioxin exposure (Steenland et al. 1999).

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