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.

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Reflections On “Breaking Bad”

Sep 18, 2012.  Updated August 10, 2013 and August 15, 2014 and July 17, 2018.

The Alcohol-Cancer Connection

Alcohol is categorized as a class 1 cancer-causing substance. Does that make it as dangerous as other proven human carcinogens such as benzene and heavy cigarette smoking? Generally, no. However, it doesn’t mean that the findings should be overlooked, especially with regard to certain types of cancers. Not surprisingly, the risk tends to increase with the overall amount of ethanol consumed and, with certain cancer types, females are more at risk. How small amounts affect anything, however, has not been quantified.

Dr. Rachel Thompson, Science Programme Manager at the WCRF (World Cancer Research Fund) said not too long ago,  “If you are drinking a pint of lager or a large glass of wine everyday, then this might not seem like a lot.” She further added, “But the science shows you are increasing your risk of bowel cancer by 18 percent and your risk of liver cancer by 20 percent.”

In contrast here are the risks of lung cancer ( just one of the many cancers that can arise from smoking ):

It was found that 172/1,000 of male current smokers will eventually develop lung cancer; the similar probability among female current smokers was 116/1,000. For those who never smoked on a regular basis the lifetime risk was substantially reduced. Only 13/1,000 males and 14/1,000 females in this category will develop lung cancer.

116/14 = 8  or 172/13 = 13 times more likely, depending on gender. That’s a lot more than the 20% added risk for liver cancer from a pint of beer!

Let’s look closer. One drink is considered 12 fluid oz of beer or 5 fluid oz of wine, or 1.5 fluid oz of 80-proof distilled spirits. There are 28.3 grams in an ounce. At 5%, 12% and 40 % alcohol content, respectively, that corresponds to 17 g of ethanol, regardless of type. From the data of a meta study, the pooled relative risk with a 95 % confidence interval is only available for an average consumption of 25, 50 and 100 g/day, which amounts to approximately 1.5, 3 and 6 drinks a day, respectively, with the latter being in alcoholic territory.

At the lowest end of consumption, the range of relative risk (RR) for all cancers is from 0.90 to 1.05, with an average of 1.01, which is not exactly alarming. But the overall average can lead to false security. For females drinking 25 g /day,the risk of liver cancer doubles, and if they consume 100 g/day the risk jumps to 9 times, surpassing the lung cancer risk associated with cigarettes in women. Males experience much lower rates of alcohol-induced liver cancers: the RRs range from 1.28 to 1.62, depending on amounts ingested. For 25 g /d-drinkers of both sexes,  there are elevated risks in the 1.4 to 1.7 zone for oral, larynx and esophageal cancers. Dr. Rachel Thompson was quoted as saying 1.18 for colon cancer. The other datum that stands out is the 1.31 for breast cancer which soars to an almost triple-risk for very heavy drinkers.

Statistics aside, how does ethanol induce cancers? No clear mechanism has been elucidated but there are many plausible scenarios, according to a 2006 review paper in the Lancet. Acetaldehyde, which is alcohol’s main metabolite, is genotoxic, especially in genetically susceptible individuals where the acetaldehyde is not as quickly oxidized to the innocuous acetate. There is at least in vitro evidence that acetaldehyde and not alcohol itself does genetic damage in the liver, head, neck and breast. Ethanol also increases estrogen concentration, and it acts as a solvent for tobacco’s carcinogens.

Sources:

Meta Study: http://pubs.niaaa.nih.gov/publications/arh25-4/263-270.htm

Review Paper of Possible Mechanisms
 http://www.omniameeting.com/filereviews/Cortese%20Review.pdf

http://www.ncbi.nlm.nih.gov/pubmed/7895211

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1646951/

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