The Pharmaceutical Journal
Vol 269 No 7206 p78
13 July 2002

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Poisoned waters [more]
Rainy day saint [more]
A mystery solved [more]

Poisoned waters

A highly disturbing state of affairs is revealed in a commentary in Science for 21 June from D. Kirk Nordstrom of the Water Resources Division of the US Geological Survey in Colorado. He points out that, with a world population exceeding six million, a fundamental resource for human survival, water, is shrinking. An estimate from the World Health Organization indicates that 43 per cent of the population lack adequate sanitation, while 22 per cent have no clean drinking water.

The failure of surface water supplies has led to increased dependence upon ground water in many parts of the world. In India and Bangladesh this move has resulted in 36 million people having to consume water dangerously contaminated with arsenic. In many other places, too, notably Taiwan, the threat is known to exist.

Arsenic is not abundant throughout the earth's continental crust. It is usually concentrated in sulphide-bearing mineral deposits, especially pyrite, and in deposits of hydrated iron oxides. The degree to which arsenic is solubilised so as to enter ground waters depends on pH, redox conditions and temperature. High arsenic concentrations occur in many geothermal waters, and concentrations exceeding the now accepted drinking water standard of not more than 10mcg per litre are not uncommon.

Significant contributors to arsenic in water supplies are organic-rich or black shales, alluvial sediments of Holocene date with slow flushing rates, mineralised and mined areas (particularly gold deposits), volcanic strata and thermal springs. The distribution is not simple. Waters with high levels of arsenic include the thermal sources of Kamchatka, New Zealand, Japan, Alaska, California and Wyoming, where black shales abound, whereas the waters of Hawaii and Iceland are low in the element. Arsenic concentrations may change over periods of a few years, which makes dealing with them difficult.

In another article in the same journal, public health scientists from the University of California discuss the possible effects of drinking water of high arsenic content. Arsenic was one of the first chemicals associated with cancer — high rates of lung cancer in miners in Saxony being noted in 1879. Then skin cancers were encountered in patients treated with arsenical medicines. It was much later, in the 1930s, that skin cancers were linked to drinking water containing arsenic in Argentina and other places. More evidence from Argentina in the 1960s associated drinking water with internal cancers, particularly of the lung and urinary tract.

Failure to deal with the situation promptly may have been due to the fact that most drinking water standards were set on the basis of animal studies, and that other factors such as smoking complicated the picture. Moreover, progress may have been impeded by discussion over the existence of a threshold for arsenic exposure, below which it would not have any toxic effect. "Prudent public health decisions should not wait until there is proof of serious cancer risks at low exposure" remark the commentators.

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Rainy day saint

With the approach of mid-July there are still plenty of people whose thoughts turn to the chance of a long period of rainy weather. They remember the l6th century pronouncement:

St Swithun's day, if thou dost rain,
For forty days it will remain;
St Swithun's day, if thou be fair,
For forty days 'twill rain na mair.

In view of the weeks of fairly constant rain we have enjoyed (or possibly deplored) during this spring and early summer, we ought by now to be accustomed to it.

Swithun, sometimes erroneously called Swithin, was of noble birth and was an adviser to King Egbert of Wessex. He is inextricably linked with Winchester, becoming bishop of that diocese.

He acquired a reputation for humility and his kindly attitude to humble folk, a rare quality in the leading clergy of his time. He made contributions to the Anglo-Saxon Chronicle and, according to the chronicler William of Malmesbury in his 'Gesta Pontificum Anglorum' of 1123, he requested on his death that he be buried outside his church, where his grave would be trodden by the feet of passers-by and receive the raindrops from the eaves. Accordingly, Swithun was buried between the north wall of the minster and the wooden belfry tower.

Swithun's death occurred on 2 July in the year 862, not on the day when he is celebrated by the church, which is 15 July. However, when Bishop Ethelwold, his successor, undertook rebuilding in the abbey he had Swithun's remains removed to a shrine at the east end of the building. This was on 15 July 971. Many miracles of healing were reported thereafter, according to William of Malmesbury.

In 1315 the saint was again moved into a prominent position inside the church, and one day later a great flood afflicted Winchester, the river submerging crops and destroying houses and people. His shrine was destroyed in 1538, as part of the suppression of the monasteries, to be given a complete restitution in 1962. It is sad to record that vandals attacked the new monument and stole special amethyst adornments that had been added to it. There are reported to be 43 churches in England dedicated to St Swithun.

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A mystery solved

According to a commentary published in The Lancet for 8 June, researchers in the United States have managed to throw light upon a mystery. They have explained how glyceryl trinitrate is able to relieve the symptoms of angina pectoris and cardiac failure, and also why it loses its efficacy after being used for prolonged periods.

The assumption has been that glyceryl trinitrate relieves such symptoms by producing nitric oxide, a compound known to relax smooth muscle, but the mechanism of the reaction was obscure. Now it is believed that the enzyme mitochondrial aldehyde dehydrogenase first converts glyceryl trinitrate into nitrite, which is in turn activated by the mitochondria to nitric oxide, thus producing vasodilation. However, the aldehyde dehydrogenase tends to become oxidised, and so inhibited, by more glyceryl trinitrate, so that the effect is diminished. Until the muscle mitochondria have had time to undergo reduction through rest the medication ceases to be effective.

Such findings are helpful since they explain the physiology behind the observation that patients who use trinitrate regularly tend to become tolerant to it. Moreover, the fact that aldehyde dehydrogenase is itself inhibited by nitric oxide renders the situation worse.

There is reason to question the value of long-term nitrate therapy in angina, and a need to consider possible hazards, since the appearance of tolerance is an indication of damage at the cellular level. Nevertheless, critics have commented that we should be reluctant to infer direct implications for therapeutics merely on the strength of biochemical studies performed in vitro.

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