Smoking and air pollution are risk factors for cataract

Like in previous years, this winter saw heated debates in the TV and print media over the poor air quality in most regions of North India. A common refrain among the commentators was that breathing the polluted Delhi air was like smoking two packs of cigarettes daily. Lung cancer and chronic obstructive pulmonary disease (COPD) are well-known hazards of smoking. So is inhaling poor quality air for the children, elderly and those who already have diseased lungs and hearts. While awareness is high, there is little we can do individually except cease smoking.

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In the late 1970s, my chief, Prof IS Jain, noticed that the surgically removed cataracts of people who smoked heavily were black in colour. It was a mystery. He approached Prof R Nath, the then head of biochemistry at the PGI, Chandigarh, to solve the mystery. It was known even then that the crystalline lens of nocturnal animals is colourless, and that of humans and other diurnal animals, is shades of yellow and amber.

Based on lab experiments, Prof Zigman from Rochester University had speculated that the yellow colouration of the lens was due to the oxidation of specific amino acids (building blocks of proteins) by ultraviolet light. He suggested that three major small molecules, viz peptides, reduced glutathione and ascorbic acid (Vitamin C) were the key antioxidants in preventing damage to the cell proteins. Most biological reactions that use oxygen for energy production, generate highly reactive oxygen species (ROS), quenched by the abundant antioxidants that nature has provided.

The human crystalline lens is constantly exposed to light; notably, the lens and the fluid surrounding it carries very high ascorbic acid concentrations to maintain transparency.

If you wished to, there were ample opportunities in those times to study intact cataracts as these were removed in surgical eye camps that were commonplace in that era. Each camp saw several hundred patients operated upon for their cataracts.

Dr Rajendra Prasad, now a retired professor of biochemistry and research scholar then, was duly asked to collect the surgically removed intact cataractous lenses in liquid nitrogen for analysis in Dr Nath’s lab. The surgeries were performed by Dr Jain, me and Dr Jagat Ram. The smoking habits of patients were duly noted. To our profound surprise, the ascorbic acid content of the black-coloured cataracts was substantially lower than the white-coloured ones.

Until that time, it was not known that smoking was a risk factor for developing cataracts. The mystery of the black colouration of cataracts was solved.

Soon after, Professor Jain was invited to deliver a lecture at Yale University Medical School, where he, for the first time in the world, presented evidence of smoking as a risk factor. The young doctors laughed off his arguments as most of them were smoking in the lecture hall and claimed that they did not have a cataract!

In the subsequent decades, data generated by Dr Sheila West from Johns Hopkins and several others, have established smoking as the most significant risk factor for cataracts.

Beedi/cigarette smoke carries more than 4,000 toxic chemicals, including cadmium, a heavy metal, which tobacco plants actively absorb from the subsoil-contaminated water. Research by Prof Nath, Rajendra Prasad, Rajat Sandhir and others has shown cadmium accumulation in the peripheral cortex of cataracts and other body tissues, including kidneys, liver and brain.

Unlike several organs and body cavities, including the skin, lungs and gastrointestinal tracts, wherein actively dividing epithelial cells replace the damaged lining, the slowly dividing epithelial cells in the periphery of the crystalline lens are not shed and keep accumulating.

Thus, surgically extracted cataracts, if available, could have been an index of lifetime cadmium exposure. In the last four decades, cataracts are no longer being extracted intact but piecemeal to replace them with artificial implants, a case of a missed opportunity to monitor cadmium accumulation!

Evidence shows that cadmium inhibits the detoxifying enzymes, setting the stage for lung inflammation and cancer. Notably, cadmium and organic compounds, with special reference to the carcinogens, co-exist in cigarette smoke and polluted air.

Augmented cadmium levels interfere with ascorbic acid absorption and essential trace elements like calcium, zinc and copper. There is evidence that smokers who consume alcohol have enhanced accumulation of heavy metals, viz cadmium, lead and mercury. Interestingly, ascorbic acid and selenium supplements in laboratory animals are helpful in inhibiting cadmium absorption.

While the technology to measure inhalational pollutants has been available since the late 1960s, air monitoring has become a regular feature only in the last 15-20 years. The air quality index (AQI) is now reported regularly. It is graded, based on measuring many air pollutants, solids and gases. Tools like atomic absorption spectrometry and inductive coupled plasma mass spectrometry required for measuring water and soil contamination with heavy metals are not readily available outside sophisticated laboratories. I am sure the Pollution Control Boards regularly monitor these carcinogens. However, the data remains buried in less readily available reports than the AQI data.

The common man blissfully remains unaware of the daily exposure to these hazardous elements, and the elephant in the room does not figure in the media reports.

A wake-up call was given recently in a Lancet study, which shows that, increasingly, non-smokers are developing a deadly lung cancer arising from the Type-II pneumocytes. The good news is that ascorbic acid (Vitamin C) has been noted to ameliorate heavy metals like cadmium, lead and mercury toxicity. However, beware of consuming Vitamin E supplements, as these were shown in some studies to increase the risk of lung cancer in smokers.

However, more research is needed to understand how Vitamin E, Vitamin C and other anti-oxidant supplements may affect human cancer cell activity.