Cancer Prevention

There’s a valuable book out there on cancer prevention written by Richard Beliveau, a biochemist who specializes in cancer prevention and by Denis Gingras, an oncology researcher, both of whom work at UQAM. They start with the following tantalizing question:

Why do many spontaneously formed cancerous lesions remain latent in one person and yet develop into cancer in another? Factors beyond our control, like aging and heredity are often cited as the main agents determining cancer risk, but their influence is in fact much weaker than might be thought.

To back this thesis they cite evidence that in every age group, including in people over 75, esophageal cancer rates have jumped 3 to 12 times between the 1975-79 period and between 2000-2004.

But there are a couple of things that irk me about the book.

(1) If there isn’t strong evidence that age plays a major role in cancer development, why aren’t the authors criticizing organizations like the American Cancer Society and Center for Disease Control for consistently presenting age-adjusted cancer data to the public?

SmokeCancer
from CDH

Given that heredity and age are not the most fundamental variables in cancer formation, why then will the number of new cases possibly rise by about 70% over the next 2 decades according to the World Health Organization?  The authors focus on individual lifestyle choices, and in their defense, tobacco smoke is indeed one of the main causes of cancer, accounting for 30% of worldwide cases. In the same manner that production of goods has shifted overseas where standards are lower and therefore inexpensive, tobacco companies have found new nicotine users in a global market. Consequently, tobacco consumption is still increasing worldwide even though the number of smokers has gone down in several Western countries. Of the 4000 compounds and elements in tobacco smoke that include radioactive polonium 210, 70 are known carcinogens, and those in group I  include benzene, benzopyrene, NNK, arsenic, chromium and four others.  As a result of this, smoking increases the risk of lung cancer by a factor of 25 and also plays a role in other cancers.

Also central to the authors’ thesis is that along with tobacco smoke, other lifestyle-roles including exposure to UV, poor diet, obesity, alcohol and physical activity supposedly account for 75% of cancers.

(2) This brings us to a second flaw in the book: “Chance” accounts for the rest of the causes, where “pollution” is clumped with inflammatory diseases, infections, defective genes, cell division and spontaneous DNA damage, factors that are beyond the individual’s control. Beliveau and Gingras make no mention of the 2010 President’s Cancer Panel report which stated that :

  • There’s a growing body of evidence linking environmental exposures to cancer.
  • There’s much work ahead to identify the many existing but unrecognized environmental carcinogens and eliminate those that are known from our workplaces, schools, and homes.
  • The true burden of environmentally induced cancer has been grossly underestimated. With nearly 80,000 chemicals on the market in the United States, many of which are used by millions of Americans in their daily lives and are understudied and largely unregulated, exposure to potential environmental carcinogens is widespread.
  • The public remains unaware of many common environmental carcinogens such as naturally occurring radon and manufacturing and combustion by-products such as formaldehyde and benzene.

In fact benzene, the group I carcinogen in tobacco smoke, is not only a combustion byproduct, but we expose ourselves to benzene each time we gas up at the fuel pump. At best, 0.62% of the volume of gasoline is benzene.

What I do like about the UQAM researchers’work is that they not only present epidemiological statistics, but they provide the chemical basis of cancer-preventative strategies. For instance:

  • Depending on the amount of consumption, red meat and processed meat increase the colon cancer rate by 10 to 50 % due to PhIp, a heterocyclic amine formed during cooking and due to nitrosamines formed from the addition of nitrites, respectively.
  • curcumin
    Curcumin,C21H20O6, an anti-cancer compound in an Indian spice.

    Although other  variables are involved, India’s cancer rate is only about 1/4 of that of Europe and the U.S. partly because of their six to 12 times rate of spice consumption. Turmeric has over 200 polyphenolic compounds, including curcumin, which inhibits cancer cell growth and blocks angiogenesis. Angiogenesis, the process where new blood vessels form from old ones, is used by some cancer growths. Curcumin also has anti inflammatory properties and it induces apoptosis, in this context, the death of cancer cells in a tumor. Although curcumin on its own is poorly absorbed in the intestine due to conversion by the enzyme UDP glucorryl transferase, the latter is inhibited by a component of another common spice used by Indians, piperidine in pepper.

In a nutshell then, many cancers can be prevented but not only from making lifestyle changes but by pressuring our governments to further limit our exposure to industrial carcinogens.

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Lessons Learned From The Sandoz Disaster

Circled in red is the site of the 1986 Sandoz disaster.
Circled in red is the site of the 1986 Sandoz disaster.

In 1986, on the border of Switzerland and Germany, 1350 tonnes of highly toxic compounds suddenly went up in flames at a warehouse belonging to Sandoz (now part of Novartis). The fire brigade responded promptly and put out the fire in about five hours. But to do so they used millions of liters of water. Due to inadequate catch basins at the factory, 20 tonnes of a pesticide-brew tagged along and flowed into the Rhine. Eventually within a couple of weeks, along a 400 km path, fish and birds were killed, and so were most of the eels in the river. The Ijssel River as far as the Netherlands was affected, even though they closed floodgates. Initially a Sandoz spokesperson had dismissed the 70-km long red slick as “a harmless dyestuff” Understandably the safety director of the company was later pelted with dead eels by protestors.

The most problematic compounds in the mixture released into the river were dinitro-orthocresol, propetamphos and parathion. Until 1991, the first compound was used as a pesticide. It’s toxic to aquatic organisms at low concentrations(0.07 to 5.7 ppm). The latter two are organophosphate pesticides, which are cholinesterase inhibitors and which are also moderately to highly toxic to fish. Parathion, specifically, is lethal after 96 hours of exposure to 50% of fish at concentrations ranging from 0.02 to 2.7 ppm, depending on the species.

As a result of the public outcry from the disaster, the Rhine Action Program came into effect in the following year. It set goals to cut 1985 discharge levels by half. It increased safety regulations for industries. Adequate catch basins had to be set up to prevent leaks into the river. Spawning grounds for salmon had to be restored in the Rhine’s tributaries with the hope of having salmon again in the river by the year 2000. Finally, shoreline ecosystems had to be revived with indigenous species. Fourteen years later, three years ahead of schedule, salmon returned to the Rhine. Nitrates and phosphate levels were cut by 50% and there was a 80 to 100% reduction in some other forms of water pollution.

A second program came into effect in 2001 when the ministers in charge of the Rhine adopted “Rhine 2020“. Here’s an outline of its main goals.

(1)The presence of salmon in the Rhine is still dependent on human intervention. One aim of the new program is to get wild salmon from the ocean to return and to increase population to self-sustaining levels.

(2) A second commendable goal is to keep improving water quality. A number of target values have been set, and currently the elements and compounds whose concentrations are still above desired levels are copper, cadmium, zinc, diurone and benzopyrene. Diurone was a mercury-based diuretic Benzopyrene is a group 1 carcinogen formed from the combustion of oil, wood and tobacco.

(3) Since lowered groundwater tables  pose a problem in parts of Moselle/Saar, the Lower Rhine and the Delta Rhine, in particular in mining zones, Rhine 2020 also aims to protect drinking water in those areas.

Here in Quebec, we have something comparable to the Rhine 2020 program known as the St. Lawrence Action Plan, but unfortunately it does not include specific goals with regard to reducing contaminants. And yet the sediments of the St.Lawrence are moderately contaminated as revealed by this 2012 map:

from http://planstlaurent.qc.ca/en/state_monitoring/overview_of_the_state_of_the_st_lawrence_2014.html#c2747
from http://planstlaurent.qc.ca/en/state_monitoring/overview_of_the_state_of_the_st_lawrence_2014.html#c2747

beluga-whale_458_600x450We also have a serious problem with belugas, whose population in the gulf of the St. Lawrence River has declined from 8000 individuals in 1920 to 886 in 2012,  Hunting of belugas was banned in 1979, yet the species continued to suffer. Although the concentration of many contaminants declined, there was a doubling of PBDE levels in male belugas between 1985 and the 2000s. PBDEs are polybrominated diphenyl ethers, compounds used as flame retardants in many household goods. A number of toxicological studies have demonstrated that exposure to PBDEs may have critical endocrine disrupting effects during fetal development of belugas. Biologists realize that a number of other stress factors are involved, many of which are, however, also caused by mismanagement of the river. For instance, toxins released by some algal blooms could very well be involved. There were also 334 spills involving ships in the St. Lawrence River between February 2002 and November 2012. Meanwhile Environment Canada is at least currently considering prohibition of PBDE compounds.

Enlist Duo: Dow Walks Into Monsanto’s Footsteps

In October of 2014, the U.S. Environmental Protection agency announced that they would register Dow Chemical’s Enlist Duo, a herbicide treatment system consisting of 2,4-D and glyphosate along with seeds of crops that were genetically modified to resist the pair of herbicides. It was a controversial decision which prompted a lawsuit. Slipping under the radar is that a year earlier, Health Canada also gave the product its approval without any of EPA’s restrictions. Adding more nuance to the issue is that since the EPA decision, of one of Enlist’s ingredients has been reclassified by the International Organization for Research on Cancer.

1. What is Glyphosate?

CRO_Health_USGS_Glyphosate_barplot_11-14
Roundup’s use soared after introduction of foods genetically modified to resist glyphosate

Although it had been made 20 years earlier, glyphosate was rediscovered by Monsanto in 1970.

620px-Glyphosate.svg
glyphosate

The compound kills plants because it interferes with a plant enzyme and prevents the synthesis of certain amino acids. Its use skyrocketed after Monsanto, the manufacturer of Roundup (commercial name of glyphosate), also genetically engineered corn to be  resistant to the herbicide. In fact, mostly due to its application in corn and soy fields, its use went up by more than a factor of 10 in about 2 decades (see graph).

In a current example of natural selection, by the mid 2000s, morning glory, amaranthus species, lambs quarters, giant and common ragweeds, horseweed, and velvet leaf all developed resistance against glyphosate. The natural variants or perhaps mutants that were not killed by Roundup went on to reproduce, and eventually their genes became those of the majority. The resistant ” superweeds” are now spread over 70 million acres in the US alone. To combat the resistance, Dow Agrosciences used genetic modification to protect crops against both glyphosate and 2, 4-D, which they include in their new Enlist Duo weed-killing mix.

2. What is 2,4-D and How Has Glyphosate Been Classified?

2,4-D, short for 2,4-Dichlorophenoxyacetic acid, is a synthetic auxin, a plant hormone which overstimulates and especially kills broadleaf plants. Critics of Dow point out that 2,4-D was an ingredient in the health hazard known as Agent Orange, a notorious defoliant used in the Vietnam War. Dow defends itself by pointing out that Agent Orange also had 2, 4, 5-T, which at the time was contaminated with dioxins. Certain dioxins are in the same class as tobacco smoke and benzene; they are proven human carcinogens. However, 2,4-D is not in that category of compounds. It is a possible carcinogen, classified as 2B, safer than class 2A, which includes probable carcinogens. But  as reported  in the Lancet in March, 2015, the problem is that Enlist‘s other ingredient, glyphosate, has just been placed in class 2A by WHO’s cancer research division.

lancet_carcinogens

3. EPA’s Restrictions and is the Duo Approach Ecological?

The EPA correctly points out that the variety of 2,4-D is an ester of lower volatility (it’s a quaternary ammonium salt called 2,4-D choline),

Choline quaternary ammonium salt  of 2,4-D, formed easily by mixing choline  hydroxide with 2,4-D in water
Choline quaternary ammonium salt of 2,4-D, formed easily by mixing choline hydroxide with 2,4-D in water

lowering the amount that will end up in groundwater. They ordered  a 30-foot in-field “no spray” buffer zone around application areas. It has also banned use when wind speeds are over 15 miles per hour.  EPA will also apparently monitor the herbicide for resistance and reevaluate the product after 6 years, instead of granting the usual 15-year time frame. But since their decision was made before the WHO’s reclassification of glyphosate, they have given Dow the authority to toss more of a questionable compound into an already stressed ecological stew. The whole idea of having the same company market a package of herbicide and GMO-compatible seeds seems to be more about short-term economic gains and less about using science to feed the world in an ecological manner.

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