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Inside VP News EDITORIAL ... think scientifically, act scientifically... think scientifically, act scientifically... think scientifically, act... Published and Printed by Dr. Subodh Mahanti on behalf of Vigyan Prasar, C-24, Qutab Institutional Area, New Delhi - 110 016 & Printed at Saurabh Printers Pvt. Ltd., B-280, Okhla Industrial Area, Phase - I, New Delhi - 110 020 Editor : Dr. V.B. Kamble ISSN : 0972-169X Registered with the Registrar of Newspapers of India: R.N. 70269/98 Postal Registration No. : DL-11360/2004 April 2004 Vol. 6 No. 7 Price: Rs. 5.00 Venus Transit – Training Programmes V igyan Prasar, in association with NCSTC, has launched a country-wide programme on popularization of science and technology with activities built around the on-coming transit of Venus on June 08, 2004. The first of a series of training programmes for Master Resource Persons for the Southern Zone was organized at Hyderabad on March 18-19, 2004. Some 45 participants from Andhra Pradesh, Tamil Nadu, Kerala, Karnataka, Andaman & Nicobar Islands and Pondicherry participated in the programme. A.P. Council for Science & Technology were the local host. Professor Naidu, Member Secretary, APCOST, also participated in the programme. Similar programme for the Western Zone was organized at Mumbai during April 1-2, 2004. Some 42 participants from Gujarat, Maharashtra, Rajasthan, Madhya Pradesh, Silvassa, and Dadar & Nagar Haveli participated in the pgoramme. The programme was organized at Nehru Science Centre, Mumbai, jointly with S&T Cell, Government of Maharashtra. The programme was inaugurated by Shri M.V. Kamath, President, Vigyan Prasar. The inaugural talk was delivered by Prof. S.M. Chitre, well-known Astrophysicist. Shri Khullar, Secretary (S&T), Government of Maharashtra, Shri Routella, Director, Nehru Science Centre, and Dr. A.V. Sapre of S&T Council, Government of Maharashtra, were present during the inaugural session. Shri Anuj Sinha, Head, NCSTC, was present in the valedictory session. In both the programme the participants were given five resource articles, Venus transit activity kit and a CD containing six slide shows on different aspects of Venus Transit as resource material. Eye, Vision and Venus Transit (P. 42) The Global Effort To Eradicate Polio (P. 32) Vacation Health and Safety (P. 25) 1874 Transit of Venus Observations of Pathani Samanta Chandrasekhar (P.24) Vigyan Rail on the Move D uring the month of March 2004, Vigyan Rail travelled to Patna, Durgapur, Ranchi (instead to Hatia), Howrah, Bhubaneswar, Cuttack (additional stop), Vishakhapatnam, Durg, Nagpur, Secunderabad, and Tirupati. As usual, Vigyan Rail has continued to secure a huge response. In particular, Patna, Durgapur, Bhubaneswar, Vishakhapatnam, and Durg witnessed huge crowds to visit the Vigyan Rail – Science Exhibition on Wheels. Vigyan Rail has by now completed its run in the North, the North- East, the East and has entered the South. Vigyan Rail at Vishakhapatnam
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Inside�������

EDITORIAL

... think scientifically, act scientifically... think scientifically, act scientifically... think scientifically, act...

Published and Printed by Dr. Subodh Mahanti on behalf of Vigyan Prasar, C-24, Qutab Institutional Area, New Delhi - 110 016 & Printed at Saurabh PrintersPvt. Ltd., B-280, Okhla Industrial Area, Phase - I, New Delhi - 110 020 Editor : Dr. V.B. Kamble

ISSN : 0972-169XRegistered with the Registrar of Newspapers of India: R.N. 70269/98 Postal Registration No. : DL-11360/2004

April 2004 Vol. 6 No. 7 Price: Rs. 5.00

Venus Transit – Training Programmes

Vigyan Prasar, in association with NCSTC, has launched a country-wideprogramme on popularization of science and technology with activities built

around the on-coming transit of Venus on June 08, 2004. The first of a series oftraining programmes for Master Resource Persons for the Southern Zone wasorganized at Hyderabad on March 18-19, 2004. Some 45 participants from AndhraPradesh, Tamil Nadu, Kerala, Karnataka, Andaman & Nicobar Islands andPondicherry participated in the programme. A.P. Council for Science & Technologywere the local host. Professor Naidu, Member Secretary, APCOST, also participatedin the programme.

Similar programme for the Western Zone was organized at Mumbai duringApril 1-2, 2004. Some 42 participants from Gujarat, Maharashtra, Rajasthan,Madhya Pradesh, Silvassa, and Dadar & Nagar Haveli participated in the pgoramme.The programme was organized at Nehru Science Centre, Mumbai, jointly with S&TCell, Government of Maharashtra. The programme was inaugurated by Shri M.V.Kamath, President, Vigyan Prasar. The inaugural talk was delivered by Prof. S.M.Chitre, well-known Astrophysicist. Shri Khullar, Secretary (S&T), Government of Maharashtra, Shri Routella, Director, NehruScience Centre, and Dr. A.V. Sapre of S&T Council, Government of Maharashtra, were present during the inaugural session.Shri Anuj Sinha, Head, NCSTC, was present in the valedictory session.

In both the programme the participants were given five resource articles, Venus transit activity kit and a CD containingsix slide shows on different aspects of Venus Transit as resource material.

Eye, Vision and VenusTransit (P. 42)

The Global Effort ToEradicate Polio (P. 32)

Vacation Health andSafety (P. 25)

1874 Transit of VenusObservations of PathaniSamanta Chandrasekhar (P.24)

Vigyan Rail on the Move

During the month of March 2004, Vigyan Rail travelled to Patna,Durgapur, Ranchi (instead to Hatia), Howrah, Bhubaneswar, Cuttack

(additional stop), Vishakhapatnam, Durg, Nagpur, Secunderabad, andTirupati. As usual, Vigyan Rail has continued to secure a huge response.In particular, Patna, Durgapur, Bhubaneswar, Vishakhapatnam, and Durgwitnessed huge crowds to visit the Vigyan Rail – Science Exhibition onWheels. Vigyan Rail has by now completed its run in the North, the North-East, the East and has entered the South.

○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○

Vigyan Rail at Vishakhapatnam

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Editor : V.B. Kamble

Address for Vigyan Prasar, C-24, Qutab Institutional Area,correspondence : New Delhi-110 016; Tel : 26967532; Fax : 26965986

e-mail : [email protected] : http://www.vigyanprasar.com

Vigyan Prasar is not responsible for the statements and opinionsexpressed by the authors in their articles/write-ups published in“Dream 2047”

Articles, excerpts from articles published in “Dream 2047” maybe freely reproduced with due acknowledgement/credit.

The Sixth Wave

Contd. on page... 26

Over the last 600 million years of the geological history,the mass extinction has been witnessed five times

though separated by millions of years. The Palaeozoic era(590 to 248 million years ago) witnessed the massextinction thrice - during the period 505 to 438 million yearsago (Ordovician period), during the period 408 to 360 millionyears ago (Devonian period), and during the period 286 to248 million years ago (the Permian period). It was duringthese periods that several invertebrate and vertebrate groupsof animals, fish and amphibians evolved and died. The firstforests also appeared in this period. In particular, duringthe Permian period, the climate was dry and hot causingextinction of many marine animals and proliferation ofreptiles. The next two waves of extinction were in theMesozoic era (248-65 million years ago) – during the period248 to 213 million years ago (Triassic period) and duringthe period 144 to 65 million years ago (Cretaceous period– between Jurassic and Tertiary periods). It was duringthis era that dinosaurs became numerous. The climate waswarm and sea level rose. First flowering plants emerged.Domination of dinosaurs continued, but they died outtowards the end of the Cretaceous period. This is said tobe due to the catastrophic impact of one or more meteorites.A drastic climate change is also attributed to the extinctionof dinosaurs and many other organisms at this time.Indeed, the possible causes of the five waves of massextinction were natural - global warmings and coolings,devastating meteorite showers, volcanic activities and soon.

However, disappearance of some species or what isalso called extinction, and appearance of others is a naturalprocess that forms the basis of organic evolution. Accordingto the fossil records, no species has yet proved immortal.What is interesting is the fact that as few as only 2 to 4 percent of the species that have ever lived are believed to havesurvived till date. The remainder are extinct - the vast majorityhaving disappeared long before the arrival of human beings!

In a recent issue of the journal Science, an extensivestudy on the extinction of birds, butterflies and vascularplants in Britain has been presented. The study is basedon large sets of data collected over the past 20 to 40 yearsin England, Wales and Scotland and analysed at theNatural Environment Research Council Centre for Ecologyand Hydrology in Dorchester, UK. If the results are to bebelieved, then, a sixth massive extinction event in the

history of life is upon us yet again. The study shows a 28per cent decline of native plants, a 54 per cent decrease inabundance of native birds and a 71 per cent decline ofbutterflies! There appears to be a concrete evidence thatinsects which account for more than half the describedspecies on Earth are disappearing faster than the birds!This supports the view that the world is indeed on the vergeof another great species wipeout.

The rapid loss of species of flora and fauna on theEarth that we are witnessing today is estimated to bebetween 1,000 and 10,000 times higher than thebackground or expected natural extinction rate - estimatedat one species every four years. Why is it so? What couldbe the reason for the unusual rate of extinction of birds,butterflies and plants? Something as subtle but widespreadas habitat loss and degradation because of the humanactivity could be the plausible reason, compounded bydepletion of the ozone layer and greenhouse effect,deforestation and toxic pollution of the soil and water. Over-exploitation of resources like water and forests, agriculturalactivities, extraction (mining, fishing, logging, harvestingetc) and development (human settlements, industry andassociated infrastructure) – all have an adverse impact.Habitat loss and fragmentation leads to the formation ofisolated, small, scattered populations. These smallpopulations are increasingly vulnerable to inbreedingdepression, high infant mortality and consequently, in theend, possible extinction. Unlike the mass-extinction eventsof geological history that snuffed out innumerable speciesfrom the Earth five times earlier, the current extinctionphenomenon is one for which a single species – humanbeings - appears to be almost wholly responsible for thesixth extinction crisis.

India’s animal species account for 7.31 per cent of thefaunal species in the world and the flora account for 10.78per cent of the global total. About 33 per cent of thecountry’s recorded flora are concentrated mainly in theNorth-East, Western Ghats, North-West Himalayas andthe Andaman and Nicobar islands. However, this richbiodiversity of India is under severe threat owing to habitatdestruction, degradation, fragmentation and over-exploitation of resources. According to the Red List ofThreatened Animals published in 2000 by International Unionfor Conservation of Nature, India’s 44 plant species are

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��������� ��e-mail: [email protected]

Eye, Vision and Venus Transit

Figure 1: Structure of the eye

The transit of Venus will take place on 08 June 2004and will be seen throughout the country. Transits of

Mercury are relatively frequent occurring 13-14 time acentury. However, transits of Venus are extremely rare. Theoncoming transit of Venus will occur after a gap of nearly121 years. Surely, it would bea great occasion to witnessit. True, several websiteswould webcast the entiretransit live, and sitting in frontof the monitor of yourcomputer would be the"safest " way to observe thetransit! However, watching theVenus transit directlyrequires sufficient safetymeasures so as not todamage our eyes -temporarily or permanently.Smoked glass or sunglassesare not at all safe. It is not atall safe to look at the Sunwithout safe filters. It is onlyduring a total solar eclipsethat too only during the totalityphase that it is safe to lookat the Sun directly.

In this article, we shallreview the important factorsleading to injury to the eyesby naked viewing of the Sun and the means for theirprevention. We shall need to have a look at the structure ofthe eyes and the light radiations affecting it. We shall thenconsider the injuries caused to the eye especially by viewingat the Sun either with naked eye or through unsafe deviceslike smoked glass, sun glasses etc., methods of viewingthe Sun safely; and the measures to prevent injury to theeye.

Structure of the EyeThe eye does not actually see objects. Instead, it sees

the light they reflect or give off. The eye can see in brightlight and in dim light, but it cannot see in no light at all.Light rays enter the eye through transparent tissues. Theeye changes the rays into electrical signals. The signalsare then sent to the brain, which interprets them as visualimages.

The visible parts of the eyeball are the white sclera andthe coloured iris, shown in Figure 1. A membrane called

the conjunctiva covers the sclera. The sclera is the whitepart of the eye. The clear cornea lies in front of the iris.The lens is connected to the ciliary body. Inside the eyeballis a clear substance called vitreous humour. The retina,which underlies the choroid, changes light rays into

electrical signals. Theoptic nerve carries thesignals to the brain. Thefovea centralis, a pit in themacula lutea (explainedlater), is the area ofsharpest vision.

The iris is thecoloured disk that liesbehind the cornea. At thecenter of the iris is a roundopening called the pupil,which looks like a blackcircle, shown in Figure 2.The pupil regulates theamount of light that entersthe eye. Two muscles inthe iris automaticallyadjust the size of the pupilto the level of light. In dimlight, the dilator muscleenlarges the pupil. Asmuch light as possiblecan then enter the eye. Inbright light, the sphincter

muscle makes the pupil smaller, which prevents too muchlight from entering the eye. The pupil also becomes smallerwhen the eye looks at a nearby object, thus bringing theimage into sharp focus.

The ciliary body encircles the iris. It is connected bystrong fibres to the crystalline lens, which lies directlybehind the iris. The lens is a flexible structure about thesize and the shape of a aspirin tablet. Like the cornea,the lens is transparent because it has no blood vesselsand is relatively dehydrated. The muscles of the ciliarybody make constant adjustments in the shape of the lens.These adjustments produce a sharp visual image at alltimes as the eye shifts foci between nearby and distantobjects. The ciliary body also produces a clear wateryfluid called aqueous humour. This fluid nourishes andlubricates the cornea and the lens, and it fills the areabetween them. The ciliary body produces aqeous humourcontinuously. The old fluid is drained out as the new fluidtakes its place.

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The retina has cells called rods and cones, which absorb light rays and change them into electrical signals. There are more cones thanrods in the central area of the retina. The cones are concentrated in the fovea centralis. Nerve fibres attached to the rods and cones join toform the opticss nerve. Figure 3: Retina

The iris has a round opening called the pupil, whichregulates the amount of light that enters the eye. Indim light, the dilator muscle pulls the pupil openwider. In bright light, the, sphincter muscle tightensaround the pupil and makes it smaller.

Figure 2: The Iris

The choroid forms the back of theuveal tract (the iris, the ciliary body andthe choroid considered as onestructure). It looks and feels like ablotting paper soaked with black ink.The choroid has many blood vessels.Blood from the choroid nourishes theouter part of the retina.

The retina makes up the innermostlayer of the wall of the eyeball. It isabout as fragile as a piece of wet tissuepaper. the retina is made up of twotypes of light-sensitive cells - rods andcones. The cells are named for theirshape. The retina has about 120million rods and about 6 million cones,which absorb light rays and changethem into electrical signals (Figure 3).

Near the center of the retina is around area called the macula lutea ormacula. The macula consists chiefly of cones. It producesa sharp image of scenes at which the eyes are directlyaimed, especially in bright light. The rest of the retinaprovides peripheral vision - that is, it enables the eyes tosee objects to the side while looking straight ahead. Mostof the rods lie in this part of the retina. Because rods aremore sensitive in the dark than cones, faint objects oftencan be seen more clearly if the eyes are not aimed directlyat them. For example, looking to the side of a dim starmakes its image fall on the part of the retina that has themost rods and provides the best vision in dim light.

Nerve fibres attached to the rods and cones join at thecenter of the retina and form the optic nerve. This nerveconsists of about a million fibres. It serves as a flexiblecable that connects the eyeball to the brain. In act, theoptic nerve and the retina are actually extensions of the

brain. The optic nerve carries theelectrical signals produced in theretina to the brain, which interpretsthem as visual images.

How we seeLight rays that enter the eye

must come to a point on the retinafor a clear visual image to form.However, the light-rays that objectsreflect or give off do not naturallymove toward one another. Instead,they either spread out or travelalmost parallel. The focusing partsof the eye - the cornea and the lens- bend the rays toward one another.The cornea provides most of therefracting (bending) power of the eye.After light rays pass through thecornea, they travel through the

aqueous humor and the pupil to the lens. The lens bendsthe rays even closer together before they go through thevitreous humour and strike the retina. Light rays fromobjects at which the eyes are aimed come togetherat the fovea centralis, a tiny pit in the center of themacula (Figure 3). This is the area of sharpest vision.Light rays from objects to the sides strike other areas ofthe retina.

Adaptation to light and dark is partly controlled bythe pupil. In strong light, the pupil may become as smallas a pinhead and so prevent the eye from being damagedor dazzled by too much light. In the dark, it can get almostas large as the entire iris, thus letting in as much light aspossible. However, the most important part of adaptationto light and dark occurs in the retina.

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Figure 4 : The Electromagnetic Spectrum

WAVE-LENGTH (λλλλλ)in nm

COSMIC RAYS

γγγγγ-RAYS (-0.01nm)

X-RAYS (-100 nm)

1×10-1

0.005

1.04

14

400

800

1×103

4×105

1×109

3×1012

3×1013

Long-wave diathermy (300-600 m.)

HERTZIAN WAVES(100,000 nm-)

Short-wave diathermy (6-30 m.)Wireless (30 cm.-2 km.)

Television

Radar (cosmic radio emitters)Micro-wave diathermy (1-15 cm.)

Violet 397-424 nmIndigo 424-455Blue 455-492Green 492-575Yellow 575-585Orange 585-647Red 647-723

ULTRA-VIOLET(14-397)

VISIBLE

Solar Spectrum atEarth’s Surface(300-6,500)INFRA-RED(723-400,000)

{

Figure 5 : Optically Important Regions of theElectromagnetic Spectrum

X-Rays, γγγγγ-RaysTRANSMITTED BY CORNEA

SOFT X-RaysUV - ABSORBED BY CORNEA

SHORT IR + VISIBLE + LONG UVTRANSMITTED BY CORNEA

FOR INFRA - RED ABSORBED BYOUTER LAYERS OF CORNEA

CORNEA TRANSPARENT TO RADIOWAVES

100,000 nm

3000 nm

393 nm397 nmvisible723 nm

1 nm

Optically important regions in theelectromagnetic spectrum

Different sources of radiation emit electromagnetic energyin different parts of the electromagnetic spectrum, say, radiofrequency, infra-red, visible, ultra-violet, X-rays or gamma-rays.The wavelength of light is measured in the units of nanometres(nm), where 1nm = 10-9 metre. The electromagnetic spectrumis shown schematically in Figure 4.

The solar spectrum at Earth chiefly comprises of infra-red rays (say from 6500 nm - 723 nm), visible light (from723 nm - 399 nm), and ultra-violet rays (from 397 nm - 100nm). It would be interesting to note that the sunlightcontains about 58% infra-red radiation, 40% visible and2% ultraviolet.

The optically important regions are middle (i.e., from3000 nm - 393 nm) which includes infrared, visible and longultra-violet rays and the shortest wavelength in theelectromagnetic spectrum (i.e., less than 1 nm). These areschematically shown in the Figure 5.

Light transmitted through different parts ofthe eye

The ocular tissues, like the other tissues of the body,are transparent to the longest waves in the electromagnetic

spectrum: like other tissues they are opaque to the longerinfra-red radiations which are readily absorbed by water andare thus absorbed by the outer layers of the cornea. Below

3,000 nm, however, in the shorter infra-red, transparencyagain begins and throughout the middle regions of thespectrum the limits of absorption and transmissibility varyconsiderably until, in the long ultra-violet, all radiations below393 nm are again cut off by the cornea. Another band ofopacity exists throughout the short and extreme ultra-violet,a region wherein much of the radiation is absorbed by waterand some by air; but at the level of 1.0 nm, through thebands of soft and hard x-rays and y-rays. The two regionsof the spectrum, i.e., the middle and the shortest, are ofbiological significance.

Different parts of the eye, i.e., aqueous (i.e. throughaqueous humour between cornea and iris), lens, vitreousand retina transmit light of different wavelength in differentproportions. This is shown in Figure 6.

Below 3,000 nm an increasing proportion of infra-redradiation is transmitted through the cornea; there are bandsof relatively high absorption in the neighbourhood of 2,000and 1,400 nm to which this tissue is relatively opaque, but25% of the incident radiation is transmitted through it at2,300 nm, 65% at 1,650 nm, 80% at 1,200 nm, and almost100% at 1,000 nm. To this wavelength in the short infra-red,the cornea is more transparent than to visible red rays (750

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Wavelength in nmFigure 6: How direct and scattered light is transmitted

through the entire eye.

PE

RC

EN

T T

RA

NS

MIT

TAN

CE

TOTAL TRANSMITTANCE AT THEVARIOUS ANTERIOR SURFACES

1. AQUEOUS 3. VITREOUS

2. LENS 4. RETINA

100

80

60

40

20

300 400 500 600 800 1000 1200 1600 2000

1

2

3

4

Figure 7: The permeability of the eye to theelectromagnetic spectrum

Hertzian Long infra-red Short infra-red

Visible Short-ultra-violet X-rays

nm). Most of the visible radiation, however, is transmitteduntil absorption becomes apparent and increases steeply

in the long ultra-violet: at 370 nm 90%, at 330 nm 80%, at305 nm 50%, at 300 nm 25%, and at 290 nm only 2% ofthe radiation incident on the cornea is transmitted into theinner eye to be largely absorbed by the aqueous humour.Of the remaining 98% of this spectral band, half is absorbedby the corneal epithelium and half by the stroma; and at230 nm practically all (97.3%) of the incident energy is cutoff by the epithelium.

The radiation that traverses the cornea is absorbed inpart by the ocular tissues while some 10% of the incidentenergy is dissipated by diffusion. Most radiation which fallsupon the pigmentary layers of the iris and the retina,whether infra-red, visible or long ultra-violet, isabsorbed and converted into heat. Of the long-waveradiation which traverses the transparent media, the aqueoushumour absorbs all the infra-red above 2700 nm and partly atlower wavelengths. The lens absorbs all radiations longerthan 2300 nm, but, below it, it shows two bands of selectiveabsorption near 1900 nm and 1500 nm.

At the lower limits of the visible spectrum, the mostactively absorbent tissue is the lens. The lower limit oftransmissibility varies considerable proportion of ultra-violetrays down to 305.5 nm may pass through this tissue, inthe adult the effective zone of partial absorption is from 400-350 nm, although a feeble transmissibility down to 320 nmmay exist, and in the aged all rays below 450 nm in theviolet may be absorbed.

The concentration of radiant energyin the eye

The concentration of radiant energy within the eye isobviously of considerable importance in the study of its

effects upon the ocular tissues. The longest (radiowaves)and shortest (X- and Y-rays) radiations traverse the ocular

tissues without deflection, but radiations belonging to theinfra-red, visible and ultra-violet regions of the spectrum areretarded in their passage through the media and thus sufferrefraction to a degree depending on the optical density ofthe tissue and the wavelength in question; and shorter violetwaves are the most refrangible, while refraction becomesprogressively less towards the red end of the visible spectrumand the infra-red. This is schematically shown in Figure 7.

With a small source emitting radiations of middlespectral distribution, the density of energy is approximatelyuniform through the anterior half of the globe, sinceabsorption and dispersion in the media counterbalance fairlyexactly the concentrating effect of refraction; but in theposterior part of the globe where the beam is brought to afocus, the latter effect becomes the more prominent. Itfollows that with a small source (a point source or withsmall angular diameter) of energy damage may be causedat the retina while the anterior structures are left unaffected.This occurs, for example, in sun-blindness owing to therefraction of the infra-red and visible rays as shown in Figure(8). The effect of concentration, however, is limited by theimperfections of the optical system of the eye.

Hazards from UV RadiationUV radiation refers to the part of the electromagnetic

spectrum subdivided into ultraviolet (UV) rays withwavelengths of λ = 100-380 nm. UV radiation is furthersubdivided into UV-C (λ = 100-280nm), UV-B (λ = 280-315nm), and UV-A (λ = 315-380nm).

In general, the shorter the wavelength the moreenergetic the radiation making it damaging the plants andanimals. UV-C can do great damage but fortunately poses

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Figure 8: The concentration of radiant energy in the eye

BOX 1 WHY LOOKING AT THE SUN DIRECTLY IS

DANGEROUS?

The size of the image of the Sun at the retina is of theorder of 0.2 mm. Hence the energy available at retina isconcentrated approximately in an area of circle within radius0.1 mm.

Solar Energy incidenceon Earth = 1.36 Kw/m2

= 1.36 X 10-4Kw/cm2

Area of pupil = 0.03 cm2

(radius 1mm)Thus power incidenton the pupil = 1.36 X 10-4 X 0.03 kw

= 0.040 X 10-4 kw= 4 X 10-6 kw

70% of this energy isavailable at retina, i.e.,power incident at retina = 4 X 0.70 X 10-6 kw/cm2

= 3 X 10-6 kwThe size of the image being of diameter 0.2 mm, the energyabsorbed in the retina is concentrated in area = 0.03 mm2 =0.03 X 10-2 cm2 = 3 X 10-4 cm2.

Hence the concentration of solar power in area in whichimage is formed = 3 X 10-6/3 X 10-4 = 10-2 kw/cm2

= 100 kw/m2

Which is about 100 times more than the solar energyincident on Earth and quite powerful to cause retinal burnseven if viewed for only a few seconds!

Figure 9 : Depth of penetration of UV into the eye

Retina CorneaAqueous

Lens

Vitreous

Iris %Absorption λ λ λ λ λ nm

<280300320340360

100

92

45

37

34

6

16

14

12

2

36

48

522

I

I

no risk to life on Earth. It is completely filtered out by oxygenand ozone in the stratosphere. Ozone also plays a vitalrole in filtering UV-B, the ultra violet radiation i.e. the greatestthreat to life on Earth. But even a fully functioning ozonelayer does not absorb all the UV-B rays. UV-A surpassesthe stratosphere virtually unfiltered. But compared to theshorter wavelengths, UV-A causes little harm and even playsan important role synthesizing Vitamin D in humans. So, indiscussing the harmful effect of ultra violet radiation we aremainly talking about UV-B. Too much exposure to thistype of radiation can lead to skin cancer, cataract andsuppressed immune system. UV radiation accounts for20% of cataract cases, and 90% of all skin cancer.Cumulative exposure over a person's life exacerbateswrinkling and discolours the skin. The penetration of UVradiation in the eye is shown in Figure 9.

Radiation can have the greatest effect on the parts of theeye that absorb them. How deep the rays can penetrate intothe eye depends on their wavelength. Yet the dividing lines arenot quite so distinct. A more accurate distinction is made byconsidering how easily the different wavelengths pass throughthe components of the eye. The eye's translucence alsodepends on a person's age. In early life, the frontal part of theeye is more translucent than it is in old age.

Damage can also occur in places where the eyes aresubjected to high intensity UV radiation, say during electricarc welding or in snowy zones under clear skies. One longterm effect of UV radiation is a certain clouding of lens orformation of cataract. Certain proteins, so-called crystalline,

are altered in the lens cells by photochemical reaction inconnection with other factors, such as diabetes. This cancause a pigmentation of the cells and clouding of the lens.This process progresses over time until vision is sharplyimpaired or even blindness occurs. Since the lens tissue incontrast to other tissues in the body - does not grow the newcells, the damage is irreversible. Yet, modern surgicaltechnology does allow the clouding the lenses to be replacedby artificial lenses. The radiation responsible for this conditionis UV-A and UV-B which cause the damage. The intensity ofthe radiation that causes this disease is well below theintensity that can cause an acute inflammation of the corneaor conjunctiva. What is most important is the cumulativelength of exposure, mostly extending over severaldecades. Indeed, the disease can also be caused by artificialUV radiation sources. Plain sunlight can also cause thecataract but this often effect people who work a lot outdoors,such as farmers or seamen. Disease can effect practicallyanyone. The common form occur in people nearing the endof their seventies. The rate of cataract disease in the populationincreases with the age.

Retinal BurnsChorioretinal (i.e., involving choroid and retina) burns

are most usually produced after looking at the Sun;

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Figure 10 : This photograph is the back of the eye of a man whoviewed the partial solar eclipse of 1966 without eye protection.The arc-shaped scars are typical of an eclipse burn, and thevision in this eye has been reduced to 20/30 (6/9).Source : BBC News http://news.bbc.co.uk/1/hi/sci/tech/1376184.stm

Figure11: This picture shows a more extreme form of solarretinopathy in the left eye of a young man who staredunprotected at a partial eclipse of the Sun. Severalcrescent-shaped burns can be seen in the central retina, andthese have resulted in blindness in this eye, with his visionreduced to below 20/400 (6/120).Source : BBC News http://news.bbc.co.uk/1/hi/sci/tech/1376184.stm

occasionally they occur after accidental exposure tolightening, or the short-curcuit of a high-tension current or,more rarely, after gazing into a strong artificial source oflight such as a carbon arc. Sometimes, following subliminalexposures, only temporary subjective symptoms appear.Following severe exposures, a destructive burn causespermanent damage - a serious matter when, as is usuallythe case, the macula is involved. A solar choriorentinal burn(sun blindness or photoretinitis) is an injury of this type.

Let us consider the Sun as black body at temperature60000 K. The energy available in its radiation will be about1.36 kilowatt/m2 at the Earth's surface. If the pupil is stronglycontracted to about 2 mm, as is the case when the Sun isobserved directly, about 3% of this energy will enter the eye.Slightly over 30% of the energy that enters is lost in itspassage through different inner parts of the eye. We makeuse of this information to estimate the concentration of energyon the retina while observing objects like the Sun (Box1).

Symptoms - In case of an accidentThe subjective symptoms (after looking at the Sun without

adequate protection) are characteristic; and their severitybears little relation to the retinal appearances. In most casesnothing abnormal is noticed immediately except thedazzling sensation; but shortly thereafter a diffuse cloudfloats with irregular undulations before the eyes,associated usually with irritating after-images,photophobia (fear of light), and occasionally photopsia(flashes of light) and chromatopsia (disturbance in colourvision). After 24 hours, this diffuse cloud contracts intoa dense scotoma (a blind spot or area of depressedvision) which may last for weeks or months or evenpermanently. The scotoma is typically central and reducesthe visual acuity to an average of 6/12 (what a person withnormal eyesight may see from 12 feet would be seen by theaffected persons from 6 feet) but not infrequently to 6/60(what a person with normal eyesight may see from 60 feetwould be seen by the affected person from 6 feet) or less; itis discovered by the blurring or disappearance of small objectsor test letters and in the early weeks, it often undergoesflickering or rotatory movements. Metamorphosia (larger orsmaller images of objects rather than their normal sizes)may appear in the central field due initially to displacementof the retinal elements with oedema and eventually todegenerative changes. Do not take chances! Rush to anophthalmologist in case of any symptoms mentionedabove! To avoid this situation, follow the guidelines forviewing the Sun safely given later in this article.

The objective signs are typical, but even when thesubjective symptoms are marked, the fundus mayoccasionally appear normal. Initially in the slighter cases,the macula seems somewhat darker than usual, a changedoubtless due to choroidal congestion; in the more severecases the central area may be raised and oedematous,

showing perhaps a grey appearance and minutehaemorrhages or a dark central spot surrounded by anoedematous retinal detachment. The typical appearancewhich rapidly develops at the fovea is that of one or moreyellowish-white spots, oval in shape or sometimescrescentic, surrounded by an irregular zone of mottledpigmentation fading gradually into the background of thefundus (Figure 10 and 11). This appearance corresponds tothe lesions seen experimentally: careful ophthalmoscopicfocusing suggets that the central spot is a burnt-out hole inthe pigmentary epithelium, while the surrounding stippledring represents an aggregation of pigment. In the worstcases a typical macular hole may develop.

Vision after retinal burnsIn the majority of cases the vision improves within the

first month or two and the scotoma, if it persists, tends to

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BOX 2SOLAR BLINDNESS : A CASE STUDYLooking at the Sun directly without safe filters can be

quite dangerous. Even during a solar eclipse, it is equallydangerous to observe the Sun directly. It is safe to look atthe Sun directly only during the total phase of a total solareclipse. We give below a case study of eclipse blindnessfollowing a partial eclipse that was visible in the island ofHawaii in 1962.

On February 4, 1962, a partial eclipse of the Sun wasvisible from the islands of Hawaii. It was a cloud free day - aSunday afternoon- and the news media had directedattention at the impending eclipse. These factors combinedto produce an incidence of solar retinitis of epidemicproportions. This day was almost cloudless with unlimitedvisibility, though the eclipse was incomplete, sufficientsurface of Sun was obscured to effect a decrease in theamount of measurable incident radiant energy. The studyrevealed that, time of the year, height of Sun, degree of eclipseand amount of cloud cover, combined with leisure timeavailable to watch the eclipse were the factors primarilyassociated with the cases reported of solar retinitis.

A study involving Hawaii military personnel and theirdependents stated that the day following the eclipse, thefirst patient with solar retinitis presented at United StatesArmy Trippler General Hospital. Shortly thereafter, the outlyingdispensaries began to report a progressively increasingnumber of patients who had complaints of sudden onset ofunilateral and bilateral visual disturbance. Patients variedin the description of their complaints, but most patients notedan initial blur of vision which resolved by the followingmorning into a central scotoma. In unilateral cases, thepresence of the central scotoma was not immediatelyappreciated. New patients reported months after the eclipse.Three of the four personnel who registered no initialcomplaint had their lesions detected when they could notfire accurately on the rifle range.

Characteristic of solar retinitis epidemics is thesimultaneous onset of ocular injury in all patients. Stage 1of retinal burns could be described as a central yellow spotthat occupied the foveal area of the involved eye. Stage 2shows a redness of the macula. Its centre contains theyellow point of stage 1 with greatest intensity of rednessconcentric to this point. Gradual fading of the redness occursand after about 3-4 weeks, a central pigmentation isobserved as beginning of the third stage. Stage 3 may involvea macular hole or a pigmented area located in the deepestretinal layers, which may impair the vision permanently.

Patients examined immediately following the eclipsehad diminished visual acuity of varied degree. Thesepatients had not used any mode of protection; or the type ofprotection used included use of fingers as a pin-hole,photographic films of uncertain density or sun glass,smoked glass or cameral viewfinders. In a total of 52 eyesexamined, 27 regained the normal visual acuity while theremainder had visual losses with varying degree and thechance of recovery was approximately 50 per cent. In caseof persons with prior existing muscle imbalance in one eyeor with ambliopia (i.e., with very poor vision in one eye),solar retinitic lesion was generated in the dominant eye.

become relative sufficiently small; correspondingly the redzone with its yellow spots at the macula may become greyerand also disappear. Few records are available of patientswho have been injured for more than a year and fewer andfewer after several years. Improvement may occur overseveral months but in the majority of cases some disabilitypersists.

The return of the visual acuity to 6/6 does not necessarilymean recovery of normal vision because in some casessmall residual central or paracentral scotomata may persistand particularly if these are bilateral, they may lead topermanent impairment of reading or the ability to performfine work. In most cases with a permanent macular lesion,particularly a hole, a small area of central vision may bepermanently lost. After a few years, however, the visualcapacity may increase considerably and the resultantscotoma becomes small. Indeed the vision may appear tobe unaffected and the minimal disability is unnoticed by thepatient - a happy result which unfortunately is by no meansinvariable. The moral is - Never look at the Sun directly,even during partial solar eclipse. To illustrate the point, acase study of eclipse blindness following a partial eclipsethat was visible in the island of Hawaii in 1962 is given inBox 2.

Viewing the SunNever view the Sun directly, eclipse or no eclipse,

without safe, tested filters, otherwise temporary orpermanent damage could be caused to your eyes. TheSun can be viewed safely with the naked eye only duringthe few brief seconds or minutes of a total solar eclipse. Itis emphasised that even when 99% of the sun's surface isobscured during the partial phases, the remainingphotospheric crescent is intensely bright and cannot beviewed safely without sufficient eye protection. Hence, Donot attempt to observe the Sun directly, even duringthe partial (or annular) phases of any eclipse withnaked eye. Unless appropriate filters are used, it mayresult in permanent eye damage or even blindness! Itis, therefore, necessary to follow certain guidelines for safeviewing of the (partial or annular) solar eclipse. The factthat the Sun appears dark in a filter such as smokedglass, sun glasses, coloured film, phtographic neutraldensity filters etc. does not guarantee that your eyeswould be safe. Damage to the eyes comespredominantly from invisible infra-red wavelenghts.Avoid all unnecessary risks.

Observing a transit is like observing the Sun on anyday. It is necessary to reduce the intensity of Sunlight atleast by a factor of 100,000 or more for safe viewing. Anyfilter which reduces the intensity of a standard 60 Wattincandescent frosted electric bulb such that the printed codeis no longer readable would be safe enough. To prepare aneffective filter, put together two or more thicknesses of over-

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BOX 3DOs AND DON'Ts FOR OBSERVING THE

VENUS TRANSITDOs� Project the image of the Sun on a shaded wall through

a pin hole.� A small telescope or binoculars can be used to project

the image of the Sun on a white card / screen / wall. Ifbinoculars or telescope has any plastic parts, takenecessary precautions to protect them from heatingand melting by sunlight.

� Direct viewing of the partially eclipsed Sun should bedone only using a scientifically tested filter certified tobe safe. A dark welder's glass (No.14) is ideal. Thefilter provided in the Vigyan Prasar kit can also beused. Always, use only one of your eyes to view theeclipse. In all cases, please examine the filter beforeuse. A filter with pin holes / scratches must not beused. Don't touch, fold or wipe the film with yourfingers, under any circumstances. Any scratch or foldon the film would render it unsafe for viewing theeclipsed Sun.

� Look at the Sun only intermittently.

DON'Ts� Don't attempt to observe the Sun with naked eyes.� Never look at the Sun through a telescope or binocular

without a proper filter.� Don't use any filter that simply reduces the visible

intensity of the Sun. Fifty-two per cent of the Sun'srays are in the infra-red region of the spectrum.Damage to the eye is predominantly caused by thisinvisible infrared energy.

� Don't use smoked glass, colour film, sunglasses,non silvered black & white film, photographic neutraldensity filters and polarizing filters. They are not safe.

� Don't use solar filters designed to thread into eyepieces and often sold with inexpensive telescopes.

� Don't look at a reflection of the Sun from colouredwater.

SPECTRAL RESPONSE OF SOME COMMONLYAVAILABLE SOLAR FILTERS

(Reprinted from Total Solar Eclipse of 1999 August 11, Espenakand Anderson, 1997)

Note: In addition to the term transmittance t (which describes thelight transmitted through a filter in per cent), the energy transmissionof a filter can also be described by the term density (unitless) wheredensity "d" = log 10 (1/t). A density of "o" corresponds to atransmittance of 100%; a density of 1 corresponds to a transmittanceof 10%, a density of 2 corresponds to a transmittance of 1%, etc.

Figure 12

0 500 1000 1500 2000 2500

SOLARSKREEN

SN 14 WELDER’S FILTER

THOUSAND OAKS MYLAR

THOUSAND OAKS T2 GLASS

CD-ROM

FLOPPY DISK

EXPOSED &DEVELOPED FILM

PLUS X NEGATIVECOLOR NEGATIVE (UNSAFE!)

Wavelength (nm) B.R. Chou and F. Espenak, 1997 JanVISIBLE

0 500 1000 1500 2000 2500

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exposed black and white photographic or X-ray film (slowerfilms are best) until a density is obtained which just abolishesthe readability of print on a 60-watt bulb (Ref. Archieves ofOphthalmology, 70 (1964) 138). The light of the bulb in adark room will then appear as a glow similar to that of fullmoon on a moderately bright night. The metallic silvercontained in the film emulsion is the protective filter. However,black and white film even if fully exposed to light is likely tobe unsafe, since they often use dyes instead of silver. Apopular inexpensive alternative is aluminized mylar sheet(without any microholes) manufactured specifically for solarobservation. Ordinary mylar sheet may not be safe. DarkWelder's glasses (shade No. 14) could also be safely used.As a further precaution, do not view the Sun eventhrough these filters continuously beyond a fewseconds. Figure 12 gives spectral response for a selectionof safe solar filters as given in the NASA Reference

Publication 1398 on Total Solar Eclipse of August 11, 1999.It is however, emphasised that no legal liability forthese recommendations could be accepted since evenwith best of precautionary warnings, there is everylikelihood that accidents will occur with direct viewingof the Sun. Smoked glass, colour film or sunglasses arenot safe. Safest ways are viewing Sun's projected imagethrough a pin-hole on a card-board held at a distance ofabout 1 metre in a shaded room. DOs and DON'Ts to observethe Sun safely are given in Box 3.

ACKNOWLEDGEMENTSThe author wishes to thank Dr. Manisha Gupta, a

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No TransitVisible

Transit inprogressat sunrise

EntireTransitvisible

Transit inprogressat Sunset

08 June 2004 Transit of Venus

World Visibility Map of the Transit of Venus — Fred Espenak, NASA/GSFC

1800 w 1200 w 600 w 00 600 E 1200 E 1800 E

600N

300N

00

300S

600S

Lat

itu

de

Latitude

Path of the Venus across the Sun’s disk on 08 June 2004 and 06 June 2012 — Fred Espenak, NASA/GSFC

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Transit of Venus - 08 June 2004Circumstances for some important Indian Cities

Venus will pass across the disk of the Sun during a rare transit on 2004 June 08. This uncommonevent will be visible from the entire Indian subcontinent. The following table presents detailedpredictions for a number of Indian cities. The start and end times are given in Indian StandardTime. We are grateful to Dr. Fred Espenak, NASA/GSFC for providing us with the data oncircumstances for important Indian Cities.

Transit ContactsContact IV

ExternalEgress

H m s

16:50:2016:50:4816:51:2216:50:4216:50:3216:51:4616:51:0416:50:4816:50:4016:51:3616:51:5816:50:4616:50:3416:51:4916:50:1116:51:2416:50:1016:51:1216:50:0316:50:5616:50:5716:50:4316:52:1616:50:3216:50:4016:51:5816:51:3816:51:0716:50:4616:50:3116:51:0416:51:3616:50:1316:50:3716:51:2916:52:1016:50:3916:51:06

Contact III

InternalEgress

H m s

16:31:0616:31:3716:32:1516:31:3016:31:2016:32:4416:31:5616:31:3816:31:2716:32:3316:32:5716:31:3416:31:2116:32:4616:30:5516:32:1916:30:5416:32:0416:30:4616:31:4716:31:4616:31:3116:33:1716:31:2016:31:2816:32:5816:32:3316:31:5916:31:3416:31:1816:31:5616:32:3116:30:5716:31:2216:32:2316:33:1016:31:2716:31:59

GreatestTransit

H m s

13:46:4313:48:0113:48:3713:47:3913:47:0813:48:1413:48:0713:47:1613:48:0613:47:5613:48:1913:48:0513:47:1213:48:3613:46:4113:48:0413:46:2813:48:1713:46:3013:47:5113:48:1513:47:4813:48:4913:47:0013:47:4413:48:1313:48:3913:47:5813:48:0613:47:1913:46:3813:48:3313:46:4013:48:1713:48:3813:48:2213:47:3213:47:33

Contact II

InternalIngress

H m s

11:03:3211:05:0411:05:2511:04:3511:03:5811:04:2411:04:5611:03:5411:05:2011:04:0711:04:2211:05:1311:04:0211:04:5611:03:3711:04:3211:03:1911:05:0511:03:2911:04:4011:05:1611:04:4811:04:4911:03:4611:04:4511:04:1111:05:1311:04:4011:05:1211:04:1611:02:4011:05:0511:03:3411:05:4011:05:1911:04:1411:04:2811:04:02

Contact I

ExternalIngress

H m s

10:44:3410:46:0110:46:2410:45:3510:45:0010:45:3110:45:5710:44:5810:46:1410:45:1510:45:3010:46:0910:45:0410:44:5910:44:3810:45:3710:44:2110:46:0510:44:2910:45:4110:46:1310:45:4610:45:5610:44:4910:45:4410:45:2010:46:1510:45:4210:46:0910:45:1610:43:5110:46:0810:44:3610:46:3210:46:1910:46:2410:45:2810:45:08

LocationName

IndiaAgartalaAgraAhmedabadAllahabadAsansolBangaloreBhopalBhubaneswarChandigarhChennaiCoimbatoreDelhiDhanbadGangtokGuwahatiHyderabadImphalIndoreItanagarJabalpurJaipurKanpurKavarattiKolkataLucknowMaduraiMumbaiNagpurNew DelhiPatnaPort BlairPuneShillongSrinagarSuratThiruvananthapuramVaranasiVishakhapatnam

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The Global Effort To Eradicate PolioThe Crippler Disease

� Shivaprasad M Khenede-mail : [email protected]

The year 2004 might be the year of the last case ofpolio. If so, by 2007, polio could be certified as the

second disease ever to be eradicated. If this landmarkachievement is to be realized then Afghanistan, Pakistan,Egypt, Ethiopia, Sudan, Somalia, Angola, Niger, Nigeriaand specially India (countries wherePolio is still endemic) need to continuetheir relentless crusade against polio.India bears a dubious distinction ofharbouring 83 percent of worlds polioburden. Notwithstanding the adverseincrease and outbreak of polio cases in2002, reduction from 1,600 reportedcases of polio in 2002 to 230 in 2003 isa proper reassuring step in the directionof the polio free world. We mustremember, however, that theachievement of broad mass publichealth objectives depends to a greatextent on human cooperation—nomatter how smart or advanced thetechnology is, therefore the thrustshould be in this direction.

This article will focus on the historyand development of the polio vaccine andchronicle the drama and strugglesbehind the largest public health initiativein history — the global eradication of polio. It will also givean insight into the fascinating story of the pursuit to defeatpolio against great odds.

What is Polio?Poliomyelitis meaning inflammation of the grey matter

of the spinal cord — is a unique, fearsome potent diseasethat has demanded, and continues to demand, a distinctiveresponse and a significant financial investment to controlits spread manage its physical effects and ensure its finaleradication from the globe. The word “poliomyelitis” wasformed by putting together two Greek words for the site ofthe disease - polios, meaning gray, myelos, meaningmarrow, and adding the English suffix, itis, meaninginflammation. Polio has been referred by many namesincluding infantile paralysis, Heine-Medin’s Disease, debilityof the lower extremities, and spinal paralytic paralysis. Incommon usage, the term poliomyelitis is abbreviated topolio. Polio is a highly infectious disease caused by a virus,of which humans are the only natural host. Highlycontagious, the poliovirus spreads by contact with

contaminated feces or oral secretions. Children are mostvulnerable to the virus. The virus enters the body by noseor mouth and travels to the intestines, where it incubates.A few days later, most patients are either asymptomaticor they experience flu-like symptoms, such as headache,

nausea, vomiting, and fever. Whetherthey are symptomatic or not, people atthis stage can pass on the disease toothers.

Polio enters the host body throughcontact with infected feces or throughinfected droplets traveling through theair, in food, or in water. The virus nextenters the bloodstream, and thepatient’s immune system developsantibodies against the virus. In mostcases, the immune system stops theprogression of the virus and a lifelongimmunity against the disease isacquired. However 10% of infectedpeople develop symptoms and 1%develops the paralytic form of polio. Inserious cases the poliovirus destroysthe nerves in the brain and spinal cord,causing paralysis of the muscles in thechest, leg or arms. Once infested thepoliovirus invades the nervous system,

specifically damaging the anterior horn of the spinal cordresulting in muscle paralysis, usually affecting voluntarymuscles in the arms and/or legs. Five to ten percent of thepatients die because of paralysis of breathing and/orswallowing.

Fear of PolioParalytic poliomyelitis was perhaps the most feared

disease known in the first half of the twentieth century.Polio struck fast, there was no cure, and it crippled itsvictims for life. Hobbling on crutches, rolling in wheelchairs,or lying immobile in giant iron lungs, the legions of sufferersaccumulated from year to year. Even the exact mechanismof polio’s transmission was a hotly debated subject formany years; so many areas were placed under strictquarantine when cases of the disease began to manifestthemselves. Only the fear surrounding AIDS can rival thefeelings people had about polio in the first half of this century.

Only once in human history have we witnessed thetotal eradication of a dreaded disease, and that wassmallpox more than two decades ago. Now humanity stands

Dr. Jonas Salk, is seen working on poliovaccine in the laboratory at the University of

Pittsburgh

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Portrait of Dr. Albert BruceSabin

Franklin D Roosevelt the President ofUSA was also the victim of Polio. Hebegan the crusade for Polio eradication

on the brink of a second triumph: the globaleradication of polio — a scourge that at onetime killed or crippled half a million people ayear, many of them children. We cannot affordto falter, not when we are so close. As weinch towards that ultimate goal it is time tolook back on the developments that have ledus to this remarkable human endeavor.

President Roosevelt the crusaderof Polio eradication

Franklin D Roosevelt, President of theUnited States from 1932 to 1945, declared aWar on Polio during his presidency tenure.He constructively used the tremendousresources of postwar America to combat thepolio menace and aided the scientific community to developa vaccine that could help prevent polio.

Roosevelt was a polio victim. He wore heavy steelbraces on his legs and walking was difficult for him. Mostof his time was spent in a wheelchair. Roosevelt was affectedwith poliomyelitis, or infantile paralysis in1921, while vacationing at his Canadiansummerhouse on Campobello Island.Roosevelt’s legs were left permanentlyparalyzed. In cases such as his, the virusreaches the brain and spinal cord where itmultiplies and destroys the nerve tissue.At this point the disease becomes spinalor bulbar (involving the last four or fivecranial nerves), depending on which nervesare affected. Both forms are characterizedby muscle pain, stiff neck and back, andpossible paralysis. The spinal form affectsthe limbs. The bulbar form affects the lungsand the patients cannot breathe. After asevere attack of polio in its paralytic form,there is no treatment for the disease itself,although symptoms such as muscularparalysis can be helped with physical therapy. How mucha person will recover varies from individual to individual.

A few years after he was paralyzed by polio, Rooseveltheard about a young man, also a polio victim, who hadshowed great improvement after swimming for severalsummers in a warm-water pool. The pool belonged to anold summer resort, the Meriwether Inn, in the small townof Warm Springs, Georgia. Intrigued, Roosevelt visited theinn. Although the pool held no magical properties, swimmingin its warm water helped his weakened legs. Other victimsof polio were attracted to the pool and Roosevelt decidedto turn the old inn into a centre for the treatment of polio.He founded the Georgia Warm Springs Foundation, withhimself as president and his law partner, Basil O’Connoras treasurer. Most of those who came to the centre were

unable to pay for their treatment. So, Rooseveltand a small circle of friends provided the moneyto keep the centre in operation.

Roosevelt was determined not to let polioillness get the best of him. He not onlycontinued his illustrious political career,resulting in his well-documented and longterm Presidency of the United States, but hewent on to spearhead the fight against polio,increasing public awareness of the deadlydisease and promoting research. Althoughpolio never devastated large numbers of thepopulation like the plague or influenza, it wasa frightening, highly contagious disease thatattacked both the poor and rich and arose interrifying outbreaks which seemed impossible

to stop in spite of advances in medicine.

March of DimesIn 1932, Roosevelt was elected President. The fact

that the disease had affected a man in the White Houseseemed to awake the public’s interest. The trustees of the

Georgia Warm Springs Foundation decidedmoney could be raised for the foundationby holding dances in cities across thenation on the President’s birthday, January30. More money was raised than wasneeded for Warm Springs, so it was usedfor scientific research. In January 1938,alarmed by decades of worsening polioepidemics and the terrible toll the virus wastaking on America’s young, PresidentRoosevelt established the NationalFoundation for Infantile Paralysis. TheFoundation emphasized the nationwidesignificance and non-partisan character ofthe polio crusade. Roosevelt believed thatpeople could solve any problem if theyworked together. Comedian Eddie Cantor

coined the phrase “March of Dimes” (playing on the popularnewsreel feature “The March of Time”), appealing to radiolisteners all over the country to send their dimes directly tothe White House. The campaign to start with receivedlukewarm response but within weeks of launching thecampaign it became immensely popular and White Housewas flooded with loads of Dimes thus proving to be hugelysuccessful. The National Foundation officially changed itsname to the March of Dimes in 1979.The money collectedfrom this campaign was put to proper use by financingmedical research in the leading universities and medicalschools to develop a polio vaccine. This research has led,step by step, to the ultimate victory over polio. We are nowon the verge of wiping out polio from our planet. The Marchof Dimes occupies a unique place in American history. Its

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Georgia Warm springs was known for its therapeutictreatment of polio in its warm waters

efforts to provide care for thevictims of polio whileaggressively working to developvaccines against it, representsthe first large-scale, nationwidebiomedical initiative, led by acharitable organization. It alsohelped make the volunteermovement an integral part of thefabric of American life. Marchof Dimes investment has alsobeen made in other researchfields in science, which includesupport to 11 Nobel laureatescientists whose original workwas supported by grants fromMarch of Dimes.

The early yearsThe earliest modern clinical descriptions of poliovirus

were made in England in 1795, Italy in 1813, and India in1823, the first documented polio outbreaks occurred innorthern Europe, specifically in Norway in 1868 and Swedenin the 1880s. Early Studies suggested that the diseasemight be contagious, with an initial, infectious pre-paralyticphase with general ‘flu like symptoms.

During the 1905 polio epidemic in Sweden, IvarWickman was the first to clearly show the infectious natureof polio. This was soon followed by the isolation of thepoliovirus in laboratory monkeys in 1908 by Karl Landsteinerin Vienna. The nature of the disease spread by the polioviruswas termed as infantile paralysis. Landsteiner and hisassistant E. Popper experimented by injectingsuspensions from the spinal cord of a diseased 9-year-oldboy into rabbits, guinea pigs, mice and monkeys. Onlythe monkeys showed signs of disease. They also observedthat no bacteria were found in the monkeys and theirnervous system changes resembled those of rabies. Basedon their findings, Landsteiner suggested that the diseasehas a viral etiology. He then sent fragments of a spinalcord from a 13-year-old child afflicted with poliomyelitis tothe Pasteur Institute in Paris. Poliovirus was shown to bea filterable virus that could spread along nerves and betransferred between monkeys.

The discovery of the virus-causing poliomyelitis wasimmediately accepted. By 1909-10, the main focus of polioresearch had shifted to the Rockefeller Institute for MedicalResearch in New York City. The polio research at theinstitute was lead by Dr. Simon Flexner and his team. 1910was a landmark year for polio; the Congress of AmericanPhysicians and Surgeons devoted more attention to poliothat year than to any other subject. In Flexner’s lab thepoliovirus seemed to only infect the nervous system, butwas also present in a small number of non-neural sites,

particularly the upper nasalarea after direct inoculation.Polio thus seemed to be arespiratory infection with thevirus spread by infecteddroplets followed by directnervous system invasion viathe nerves in the nose. Thisnasal-nervous system modeldominated how polio wasapproached until the late1930s,

During the next coarse ofthe research one of the firstquestions to be answered waswhether just one particularvirus caused polio or if therewas more than one kind ofvirus. Research on this

question took several years. But it was finally proved thatthere are just three strains or types of virus that cause theailment. This gave hope that a vaccine could be producedto prevent polio.

Early efforts in the development PolioVaccines

The first great hope of developing polio vaccine emergedin 1934-35. Dr. Marice Brodie developed an inactivated poliovaccine and the rival group headed by Dr. John Kolmerwho developed an attenuated version of the polio vaccinesoon followed it. The success though was short-lived. Theirhasty use of vaccines in parts of US proved ineffective andin several cases fatal. This experience left polio researchershesitant to attempt another polio vaccine for the next 20years.

An important new era in the history of polio vaccinesbegan when a short paper was published in the journalScience. J.F. Enders, T.H. Weller and F.C. Robbins, ofBoston Children’s Hospital and Harvard Medical School,published this Nobel Prize winning report. They wereawarded the Nobel Prize for Physiology or Medicine in 1954for their discovery of the ability of poliomyelitis viruses togrow in cultures of various types of tissues. This paperdescribed the means of solving the long-standing problemof culturing the poliovirus in test tubes using non-nervoustissues. This discovery finally provided a method todemonstrate the presence of the poliovirus free from theexpensive process of inoculating monkeys, or even mice.This landmark discovery finally opened the door for thedevelopment of a practical polio vaccine.

In 1951 a method of providing passive immunity to poliowas first tried in North America. During the coarse of thisexperimentation it was discovered that the small amounts

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Inactivated Salk polio vaccine produced by ConnughtMedical Research Laboratory, Canada

of virus that entered the bloodstreamcould be overcome by a smallamount of poliovirus antibodies.Poliovirus antibodies contained ingamma globulin could thus be usedto neutralize poliovirus infection overa limited period of time. Furtherstudies showed antibodies againstpolio are formed in the blood of thevictim. That’s why a person who hassuffered an attack by one strain ofvirus is immune to that strainthereafter. After more work it becameapparent that a practical vaccine forthe prevention of polio could beproduced.

The Salk vaccine StoryDr. Jonas Salk while working at the University of

Pittsburgh undertook a major effort to sort out 196 knownstrains of poliovirus into three immunologically distincttypes. After a series of experiments he categorized thepoliovirus in to three strains namely, Type I (Brunhide), (161strains), Type II (Lansing), (20 strains) and Type III (Leon),(15 strains). Jonas Edward Salk, (1914-95) was anAmerican physician and a microbiologist. He did researchon the influenza virus at the Univ. of Michigan. In 1946 hebecame assistant professor of epidemiology at Michigan.By 1951, based on his earlier work of developing aninactivated influenza vaccine, and his experience with thepoliovirus typing project, coupled with the work of othersstudying poliovirus immunity in monkeys, Salk suggestedthat an inactivated polio vaccine might stimulate activeimmunity in humans. He developed the polio vaccine bycultivating three strains of the poliovirus separately inmonkey tissue. The virus was separated from the tissue,stored for a week, and killed with formaldehyde. He thenconducted tests to make sure that the virus was dead. Heproved that a series of three or four injections with the killedvirus vaccine were required to confer polio immunity. Theworks of Dr. Andrew J. Rhodes, a leading virologist fromEngland with a special interest in polio, were of specialsignificance to Salk in the development of his vaccine. By1951, Rhodes’ research team was able to grow all threetypes of poliovirus in a variety of tissues. Salk used themethod of growing poliovirus in different tissues in thedevelopment of a polio vaccine. This vaccine came to beknown as the Salk vaccine. Salk tried his vaccine by firstinjecting himself and his family including his son to infusea sense of confidence among the public. He thenproceeded to administer the vaccine to residents of aninstitution for disabled children near Pittsburgh. Theencouraging results of the trial were published in March1953. It was around this time that Dr. Leone Farrell

developed the “Toronto technique” toproduce bulk quantities of poliovirusfluids in large bottles. Thisdevelopment paved the way for massproduction of Salk vaccines.

Encouraged by Salk’s results,in July 1953, the NationalFoundation for Infantile Paralysisasked Connaught Medical ResearchLaboratories (now Aventis PasteurLimited), to provide all the poliovirusfluids required for an unprecedentedpolio vaccine field trial in the US.Some 3,000 litres of bulk poliovirusfluids produced by Connaught were

shipped to two major pharmaceutical companies, ParkeDavis and Eli Lilly in the US to be inactivated and processedinto a finished vaccine. Before being released for the fieldtrial, each batch of vaccine had to pass a battery of tests,first by Connaught, then each company, Salk’s lab andthe US government. Amidst intense publicity, the firstchildren were given the new vaccine on April 26, 1954. Thefield trial was one of the largest medical experiments inhistory and involved an elaborate tracking of some 1,800,000children in the age group of 5-8 years. They were eithergiven the vaccine, or were simply observed to see if theycontracted polio or not. The results were dramatic. Casesof polio fell spectacularly in the vaccinated test groups. In1955, the government quickly granted permission for thevaccine to be distributed to the children of US. On April 12,1955, the highly anticipated clinical trial results turned intoa major media event, perhaps the biggest in medical history.“SALK’S VACCINE WORKS!” screamed the headlines. Dr.Thomas Francis, director of the trial, reported that thevaccine was 60 to 80 per cent effective against paralyticpolio. He and Salk stressed that the vaccine was good,but it was not perfect.

The success though was not too long lived. Suddenly,on April 25, 1955, the Salk vaccine euphoria was shatteredwhen the first of a total of 205 cases of polio associatedwith vaccine made by Cutter Laboratories in California werereported; The problem was traced to incomplete inactivationof some virus particles, which was soon corrected. Sincethen the vaccine has been highly effective, with a 70 - 90%protection rate. The Salk vaccine is given in twointramuscular injections spaced one month apart and is tobe followed by boosters every 5 years.

Developing a Live Oral Polio VaccineIn 1957, in an effort to improve upon the killed Salk

vaccine, Albert Bruce Sabin began testing a live, oral formof vaccine in which the infectious part of the virus wasinactivated (attenuated) and not killed. Sabin (1906-93) anAmerican physician and a microbiologist, was born in

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Russia. He immigrated to the United States in 1921 andwas naturalized in 1930. Sabin completed his graduation(B.S) in 1928 and his M.S in 1931 from New York University.He conducted medical research for several organizationsbefore joining the faculty at the University of CincinnatiCollege of medicine in 1939. He then went on to become aprofessor of research pediatrics in 1946. He conductedresearch on viral and other infectious diseases anddeveloped a live oral polio vaccine (OPV) for immunizationagainst poliomyelitis in 1959. Sabin used a trivalent OPV,which contains live attenuated strains of all three serotypesof poliovirus in a 10:1:3 ratios. The viruses were attenuatedby serial passage in monkey kidney, Vero, or human diploidfibroblast cell cultures, allowing it to accumulate mutations.Ultimately, this resulted in an attenuated virus that couldbe given to a patient orally. The weaker virus replicatesnormally in the intestine, but cannot grow well enough toinvade the central nervous system. The vaccine is suppliedas a single 0.5 ml dose in a plastic dispenser. The vaccinecontains trace amounts of streptomycin andneomycin. The vaccine potency isstabilized with molar magnesium chlorideor sucrose. OPV replicates in thegastrointestinal tract and also in lymphnodes that drain the intestine. OPV inducestwo separate immune responses. First itactivates the humoral immune response,prompting the production of serum-neutralizing antibodies in the blood to allthree polio serotypes. This systemicresponse is long lasting and helps to preventthe spread of poliovirus to the nervoussystem. OPV also produces a mucosalimmune response consisting of interferonand virus-specific Immunoglobulin A (IgA)antibody in the epithelial lining of thegastrointestinal tract. Only primates aresusceptible to all three serotypes ofpoliovirus, so the safety of oral poliovirusvaccine (OPV) and its consistency have been tested inthe monkey neurovirulence test (MNVT).

Sabin’s vaccine could be taken orally and it providedlonger immunity than the killed-virus vaccine. The killed-virus vaccine could protect only against paralysis, whereasSabin’s live vaccine could guard against both paralysis andinfection. This vaccine became available for use in 1963.The Sabin oral vaccine is given in 3 doses in the first twoyears of life, and a booster is given when the child startsschool. Further boosters are not given unless the patientis exposed to polio or will be traveling to an endemic region.OPV is given orally rather than by injection. Itsadministration does not require a trained health worker andsterile injection equipment. This vaccine is relativelyinexpensive, facilitating mass purchasing of the vaccine

during National Immunization Days. The other advantagesof a live, oral vaccine are its long-lasting immunity, theprevention of reinfection of the digestive tract. A single doseof OPV produces immunity to all three-vaccine viruses inabout 50% of recipients. Three doses produce immunityto all 3 poliovirus types in more than 95% of recipients.Immunity from oral poliovirus vaccine is probably life long.OPV’s ability to stimulate mucosal immunity is responsiblefor the success of OPV mass campaigns in interruptingwild poliovirus transmission. Therefore, OPV remains thevaccine of choice for the eradication of polio. OPV intestinalimmunity reduces the chance that a vaccinated personwill become infected with wild virus if he or she is exposedwhile visiting a polio endemic country. Sabin’s oral poliovaccines are now used in India during the NationalImmunisation Day campaigns.World Health Organisation and Eradication of Polio

The discovery and use of polio vaccines have eliminatedpolio from America. In 1960, there were 2,525 cases of

paralytic polio in the United States. By1965, there were 61. Between 1980 and1990, cases averaged 8 per year, andmost of those were induced byvaccination. There has not been a singlecase of polio caused by the wild virus inUS since 1979, with a rare case reportedeach year from persons coming into thecountry carrying the virus. In 1994, poliowas declared eradicated from all ofAmerica. Once the Sabin and Salkvaccines were proven effective, thedisease was rapidly eradicated not onlyin US but also throughout most of theindustrialized world. The economic effecthas been enormous; it has beencalculated that the polio vaccine paysfor the costs of its developmentapproximately every three weeks. Thebenefit to the United States alone for

this single breakthrough runs into trillions of dollars. Thesocial impact has been incalculable. The crutches,wheelchairs, and iron lungs of polio victims have at lastbeen banished from children and parents’ nightmares, atleast in the developed world.

The results shown by the Polio vaccines on thedeveloped nations prompted the World Health Organisationin 1988 to set a goal of eradication of poliomyelitis fromthe entire world by the year 2000. The results speak forthemselves. The number of polio cases worldwide has beenreduced dramatically in just over a decade. In 1988,according to WHO, there were an estimated 350,000 cases,of which only 10 per cent were actually reported. By theend of 2001, the number of cases had dropped to 537.Although the number of reported cases increased during

One of the Popular billboards in supportof March of Dimes.

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Salk Polio vaccine was declared effective on April 12, 1955

2002, due to polio outbreaks in India and Nigeria, themajority of these cases were concentrated in isolated areasthus giving an optimistic view for a world free of polio.

Polio eradication efforts in IndiaIndia officially committed itself to eradicate polio,

supporting the WHO resolution to that effect in the verysame year 1988. India had more polio cases than any othercountry in the world. It was estimated that the Indian healthcare personnel officially reported to the government over24,000 cases of polio. In reality though, there were probablyas many as 10 times that number of cases that wentunreported. The sight of children and adults with witheredarms and legs throughout thecities, towns and villages of Indiawas routine, and some of the majorrisk factors for polio virustransmission- crowding, povertyand poor sanitation- were presentin India to a degree not seen inmost countries.

Progress towards eradicationof polio has been steady. Thegovernment of India, along with keypartners including WHO, UNICEFand Rotary International, hasspearheaded a massive effort. Theinitial attack on polio came withprovision of universalimmunization in 1985. Under theUniversal ImmunizationProgramme (UIP), more Indianchildren were provided oral poliovaccine (OPV) than ever before in history. The numbers ofreported polio cases have dropped from over 24,000 in 1988-89 to less than 5,000 in 1993-94. Although this wasencouraging, the government of India soon responded tothe need to intensify the polio eradication effort anddeveloped the Pulse Polio Immunization (PPI) strategy. Thekey innovation was utilisation of mass immunizationcampaigns to supplement the routine immunizationactivities. The state of Delhi was the first area to adopt aPPI component in 1994. The first round of NationalImmunization Day (NID) programme was held in late 1995,which was followed with a second round in early 1996. TheNIDs featured booths (fixed sites) to which children under5 were invited to take two oral polio drops. Over 500,000booths were set up nationally during the first NIDprogramme, and on a single day a total of 87 million childrenreceived oral polio vaccine. The scope and intensity ofmobilization utilized for this activity was unprecedented inthe annals of the health initiatives in India, and possibly,the world. To understand this remarkable achievement, itis important to comprehend the scale of the efforts made

to meet this gigantic challenge. At the same time as theNIDs were being initiated, it became clear to the governmentthat better information on polio cases was necessary tocomplete the job of polio eradication. The government ofIndia and the WHO developed a collaborative unit, theNational Polio Surveillance Project (NPSP), to provideaccurate and rapid surveillance information on polio casesin India. There is now a systematic methodical tracking ofcases, finding the source of the infection and floodinginfected area with massive doses of polio vaccines.Beginning in 1997, NPSP is now supporting over 200surveillance medical officers throughout India to coordinatepolio surveillance activities. In addition to NPSP network,

a regional laboratory network of9 highly qualified Indian researchcentres provides rapid andaccurate analysis of samplesfrom patients.

ConclusionThe poliovirus lives in the

human intestine, is ejected intothe environment through excreta,and spreads by contact with fecalmatter. The disease strikesmainly children, cripples thelimbs, and is sometimes fatal.Children living in unhygienicconditions without access toclean drinking water areparticularly vulnerable to it. Thisis why a bombardment of thevirus through a synchronised

mass immunisation of children in the zero to five age groupsuch as the one carried out nationally on January 4, 2004is considered the best way to ensure zero incidence. Indiahas done this since 1996 but a cutback in plannedimmunisation programmes in 2002 was the main factorbehind that year’s polio resurgence in Uttar Pradesh. Itpushed back the goal of a polio-free India and a polio-freeworld from 2005 to 2007. This year the Government isreported to be considering holding five nationwideimmunisation days as against the usual two annually. Thisdecision, despite the costs involved in conducting such anexercise, will be timely and appropriate in reaching thegoal. The benefits of total polio eradication, which willeventually include savings on the massive nationalexpenditure in fighting the disease, far outweigh theexpenditure. In order to be effective, national immunisationdays must cover as many as possible of India’s 165 millionchildren under the age of five years. Superstition andfallacies about the perceived side effects of the oral poliovaccine still deter many parents from getting their childrenvaccinated. Large-scale public awareness campaigns

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through mass media, using brandambassadors, like the ones that involvematinee idols Amitabh Bachhan andAishwarya Rai, should be continued for theefficacy of the polio eradication efforts. Theinvolvement of voluntary organisations suchas Rotary in a door-to-door campaign to buildawareness has helped immensely, howevereducating people about the disease and thevaccine still remains a key challenge for theGovernment.

Simultaneously, the Government mustalso ensure that the focus on plannedimmunisation does not distract attention fromroutine immunisation through which newbornchildren get four oral polio vaccine doses fromzero to three months. With 15.5 millionchildren born every year in India, routinevaccination is the only way to prevent gaps in immunityfrom developing. As Tamil Nadu has shown, much alsodepends on surveillance. The early detection of the twocases reported in Tamil Nadu enabled health officials

immediately to immunise all children in thosetwo areas. The Union Health Minister,Sushma Swaraj, wants zero incidences ofpolio in India in 2004, so that the countrycan be declared polio-free after the waitingperiod of three years. The goal is withinreach. It must not be allowed to slip awaythis time not after so much has already beendone.

The Government and other agenciesinvolved in the programme should thereforeemphasise on human cooperation and notlet their guard down in waging the final assaulton one of the world’s most debilitatingdiseases. They should intensify the NationalImmunisation Programme all through thisyear, specially targeting states like UttarPradesh and Bihar, which have accounted

for most reported cases of polio. They should also addressthe issues of the emergence of polio in Karnataka, WestBengal, and Andhra Pradesh. As long as the wild poliovirusexists anywhere in India, the risk of it spreading to areasconsidered free of the disease will remain. Since polio iscompletely eradicable, even one case of polio is a casetoo many and therefore we should not miss out on this lastopportunity to kill the virus before it can strike back.

Mother Teresa an Apostle ofpeace is seen administering oralpolio vaccine to an Indian child.

leading ophthalmologist of New Delhi for her interest, helpand for numerous discussions on the topic. She also wentthrough the manuscript and made suggestions for itsimprovement. Discussions with several doctors andophthalmologists are also gratefully acknowledged.

References

1. System of Ophthalmology Volume XIV (Injuries) Part II (Non-mechanical Injuries) edited by Sir Stewart Duke - Elder and PeterA. Mac Faul (1972).

2. Eclipse Blindness, Penner and MacNair, American Journal ofOphthalmology, 61 (1966) 1452.

3. Filter for Viewing, David G. Cogan, Archieves of Ophthalmology,70 (1964) 139.

4. Sun Gazing as the Cuase of Faveomacular Retinitis, Ewald andRitchey, American Journal of Ophthalmology, 70 (1970) 491.

5. Total Solar Eclipse of 1999 August 11, NASA ReferencePublication, No. 1398.

6. World Book Encylopaedia, Volume-V.7. Total Solar Eclipse of October 24, 1995, circumstances related

to India, issued by India Meteorological Department, 1994.8. Health and Environmental Effects of Ultraviolet Radiation

A Scientific Summary of Environmental Health Criteria 160Ultraviolet Radiation ((WHO/EHG/95.16).

9. Hazards to eyes from optical radiation http://www.hvbg.de/e/

bia/fac/strahl/augen_e.pdf

critically endangered, 113 endangered and 87 vulnerable.Amongst animals, 18 are critically endangered, 54endangered and 143 are vulnerable. India ranks second interms of the number of threatened mammals and sixth interms of countries with the most threatened birds. In India,poaching is another insidious threat as one of the primaryreasons for the decline in numbers of species, such as thetiger.

True, the underlying causes of biodiversity loss arepoverty, economic policies, international trade factors, policyfailures, poor environmental laws and / or their weakenforcement, unsustainable development projects and lackof local control over resources. Needless to say that it takesenormous efforts at all levels, from individual to global, tohalt species extinction. Data on species, their habitat andthreats would need to be periodically collected and analysedto evolve appropriate strategies to prevent their loss. Wemust act in right earnest now. The time is running out.

No doubt, in earlier extinctions life had always bouncedback firmly in all its multiplicity. But, it required millions ofyears to do so. That may be a blink in geological terms butis considerably longer when viewed against human life spanor even human civilization. Most ecologists accept that weare approaching the rates of extinction seen in the pastfive mass extinctions. The culprit for the current wipe-outis us. We need to quickly develop the capacity to foreseeand forestall the sixth extinction wave, or else we shallend by destroying the Earth.

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Eye, Vision ..... contd from page... 35

The Sixth Wave contd from page... 43

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Vacation Health and SafetyNine Practical TNine Practical TNine Practical TNine Practical TNine Practical Tips for the Summer Holidaips for the Summer Holidaips for the Summer Holidaips for the Summer Holidaips for the Summer Holidaysysysysys

❏ Dr. Yatish Agarwale-mail: [email protected]

With the children out of school and colleges enjoyinga vacation, it is time to pack your bags and escape

from the hustle and bustle of the killing city life into the lapof Mother Nature. A relaxing, fun-filledholiday is a perfect recipe for good health.It casts a magic effect on your physiologicaland psychological health. And that’s onegood way to recharge your batteries,cleanse your mind and body of stressesand strains and be at your best once again.Here are some basic mantras:

Just rest and relax : The word“vacation” has been coined from “vacate”,which means “to leave”, to go away. Youmust remember this to enjoy your holiday.Go away– not just physically, but mentallyas well. A sedentary desk-bound personmay wish to go out and stretch his musclesa bit, but a physically active worker may wish to take aquiet vacation. Let the vacation be a complete changefrom the routine.

Avoid strenuous schedule : The vacation should aimat resting and recreation. Tight, strenuous schedules spoilthe vacation, cause fatigue and are of no use. Always planthe itinerary in a way that each person feels comfortable,can relax and does not feel strained. Excessive hours ofdaily travel lead to fatigue and frayed tempers. An easyschedule ensures a more relaxed and enjoyable holiday.

Give a slip to heat : If you have a choice, travel duringthe early hours of the day before the sun reaches its zenith.Early evenings also make a good choice. That way youcan escape the high temperatures of the day.

Wear easy fitting clothes : Clothing for a trip shouldbe casual and comfortableand should provide for thechanges in weather. Weara T-shirt, shorts andsneakers. Cotton clothingis the best. It is easy onthe skin.

Eat at selectedplaces : The places whereyou plan to stay or go foryour meals must bechosen with care.Unhygienic places and substandard food must strictly beavoided. The risks of food poisoning and viral infectionsare very high during summer months, because high

temperatures promote growth of disease-causing germs.Avoid foods that are known to be suspect : It is

best to avoid foods which are more likely to be infected.These include dairy products, cream,potatoes, seafood, egg preparations,chicken and ham spreads, cold slicedmeats, and custard.

Carry a first-aid kit : It should consistof a sturdy box with a good catch; a first-aid manual you’re familiar with; a pair ofblunt-pointed scissors; a roll of one-inchfinger bandage; a roll of two-inch rollerbandage; a pack of sterile cotton; a packof sterilised gauze squares that come insealed envelopes; a roll of adhesive plaster,a small bottle of Savlon, or Dettol; and aclinical thermometer.

Pack in a small medicine kit : It isalways a good idea to carry some utility medicines, forinstance, paracetamol (Crocin, Calpol, Metacin) ornimisulide tablets for fever, promethazine (Avomine) fornausea, Norfloxacillin for diarrhoea and cetrizine for allergy.

Return a day early : You should neither start a tripon the first day of your vacation nor return on the last. Thiscauses unnecessary stress, and adds to fatigue. You canhave more fun in fewer days, than being under pressure allthe time.

TRAVEL SICKNESSTimely Prevention Works Best

Some people become miserable during travel. Soon asthe wheels roll in motion, their problems begin. There is firsta feeling of restlessness, which quickly progresses to a coldsweat, dizziness and then vomiting and that very sick feelingin the tummy. You wish you had never started on the trip. Ifthat’s how you feel, try these simple preventive steps:

Eat light : Go easy on your stomach. Eat less beforesetting out and avoid large meals on the way. That’sbecause a full stomach makes matter worse. Thegravitational inertia the stomach must suffer when the bodyis in movement can set it rolling.

Swallow anti emetic pill : Take an over-the-counterantihistamine pill that can check symptoms for the nextfour hours or so if taken 30 to 60 minutes before settingout for the trip. The best names in this line are Avomine,Phenergan, Benadryl and Migril. Remember however thatthese medicines could make you drowsy, so leave the

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1874 Transit of Venus Observations ofPathani Samanta Chandrasekhar

Pathani Samanta Chandrasekhar, of Orissa, is a poignantfigure of a classical Siddhantic Astronomer of India,

who survived into the 20th century (he died in 1904).The year 2004 is a very appropriate year to remember

his work and, in particular, to put together his observationsof the 1874 Transit of Venus. Not just observations –predictions too, as he was a Siddhantic Astronomer,completely un-influenced by the western schools ofAstronomy, and to some extent – unaware of it, during theearly phases of his Astronomical efforts.

Samanta Chandrasekhar was born on the 13th ofDecember 1835, at Khandapara, in Orissa. His full namewas Mahamahopadhya Chandrasekhar Singh HarichandanMohapatra Samant, but he was betterknown as Pathani Samanta. Hislifetime Astronomy efforts weresummarized by him in ‘SiddhantaDarpana’, which was published in1899, by Calcutta University. Theoriginal manuscript of 2500 Sanskritshlokas was written in Oriya script,on palm leaves, by SamantaChandrasekhar.

Samanta Chandrasekhar did nothave a formal University educationand his interest and efforts inAstronomy were completely selftaught, from manuscripts ofSiddhantic Astronomical treatises,that he had access to. It is veryevident that he had no exposure tothe revolutionary advances inAstronomy between the 17thand 19th

centuries, until rather late in his Astronomical career, andvery little, even towards the end of that. He remained acomplete Siddhantic Astronomer in the classical mould,uninfluenced by more recent developments.

Chandrasekhar was a keen observer and mademeticulous observations of celestial objects withinstruments that he had made himself. He was deeplyperturbed on finding that the ephemeral elements calculatedfrom classical siddhantic principles did not agree with hisobservations. The same perplexity had also been faced bySawai Jaisingh, early in the 18th century, and had givenrise to the construction of his gigantic masonryobservatories for the correction of ephemeral elements. Oneunderlying factor that had been responsible for theseperplexities was the freezing of classical Indian

astronomical calculations away from observationalverifications. The precession of equinoxes (Ayanamasa)had been noticed as far back as the Vedic times, by IndianAstronomers and had been entering the calculation ofephemeral elements as bija corrections – ad hoc correctionsthat needed to be applied with the passage of time, toincorporate the changes in ephemeral elements arising fromprecession. For about a thousand years before the time ofSawai Jai Singh or Pathani Samanta – the emphasis hadshifted away from observational verifications and ephemeralelements had remained uncorrected.

These perplexities led Samanta to make a life time ofobservations with simple handmade instruments, correct

the ephemeral elements from these,and create predicted ephemeralelements in the classical Siddhanticformat for future observations. Theresulting ephemeral elements wereamazingly accurate. Samanta’s workwas in the classical mould – with theassumption of a geocentric Universe,although his own model included theplanets other than Earth, as revolvingaround the Sun.

Equivalent mathematicalformulations exist for calculation ofephemeral elements in the two differentworld systems – Geocentric orHeliocentric – and many observedphenomena require only theappropriate framework of calculationsin order to accurately predict possiblecelestial events. Thus, Samanta’s

inability to envisage or accept the Copernican revolution,did not prevent him from making many accurate calculationsof contemporary celestial events in his lifetime and observingthem. The most interesting of the celestial phenomena inhis life time was the 09 December 1874 Transit of Venus.

This rare and inspiring event was visible from India andmany other parts of the world. The Transit of Venus 8 yearsfollowing that, in 1882, was not visible from India. Such anevent will again be visible on the 8th of June 2004, fromIndia and other parts of the world, and is generating a lot ofexcitement amongst the amateur astronomers andeducators. The underlying excitement of this event, beingthe possibility of recreating historical measurements ofthe Earth-Sun distance by students world wide, throughobservations of the timings of this transit.

Pathani Samanta Chandrasekhar

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❏ N. Rathnasreee-mail: [email protected]

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Going back to the year 1874 – there must have beenconsiderable excitement at that time too, with efforts fromAstronomers worldwide, making expeditions to India, asone of the locations from where, the event was visible. Therewere also efforts by Observatories under the then BritishGovernment in India, to study this event. And then, therewere observatories built by private individuals and princelystates where activities were intense, for the observationsof this event. Some popularizations efforts also seem tohave been in evidence. Chintamani Raghunathachary, ofMadras observatory, for instance, had made a popularbooklet on this event, that had been translated into manylanguages, including Urdu. In all probability, none of thisexcitement reached the remote Khandapara regions ofOrissa, where Samanta could have heard of this event.

Pathani Samanta observed the 1874 Transit of Venus– and reported it in his Siddhanta Darpana as

(P.C. Naik and L. Satpathy – Bulletin of Astronomicalsociety of India)

Arun Kumar Upadhyaya, in his translation of theSiddhanta Darpana – interprets this Shloka as –

“Solar eclipse due to Sukra (Venus) – To find the eclipseof the Sun due to Sukra, their bimba (angular diameter)and size of other tara graha is stated. In Kali year 4975(1874 AD) there was a Solar Eclipse due to Sukra inVrischika Rasi (Scorpio). Then Sukra bimba was seen as1/32 of solar bimba which is equal to 650 yojana. Thus it iswell proved that bimba of Sukra and planets is much smallerthan the Sun.”

Did Samanta hear that there was going to be a transitand set out to observe it – or did he find that there was to besuch an occurrence from his lifetime work of creating accurate

ephemeral elements? Most probably, the latter, as thereseems no evidence that there was any EuropeanAstronomical activity in the regions of Orissa, at that time.The Italian expedition from the Palermo Observatory was toMuddapur in Bengal a neighbouring state to Orissa and couldthere have been some information that reached toKandapara? It is not certain and there seems no evidence ofit. Even if the information did reach, Samanta would not haveaccepted it without his own calculations agreeing with that.

All in all, it seems possible that not only did Samantaobserve this Transit, but, he predicted it from his owncalculations, unaware, of the excitement in the rest of theworld arising from the Transits of Venus – in the 17th, 18th

and 19th centuries.The mention of the ratio of the bimba or apparent angular

diameters of Venus and Sun as 1/32 is very interesting.On the date of these observations – the 9th of December

1874, the apparent angular diameters of Sun and Venus,respectively, were – 32 minutes, 29 seconds of arc and 1minute, 3 seconds of arc. The ratio then would have beendiscernible as 1: 30.93. This ratio would have small variationsfrom one transit to another due to the ellipticity of orbitsinvolved. In the year 2004, for instance, the apparentdiameters are – 31 minutes, 31 seconds for Sun and 58seconds of arc, for Venus so that the ratio discernable, wouldbe 1:32.6 for the coming Transit of Venus.

Pathani Samanta’s observations were completely nontelescopic, and made with handmade instruments – andthe accuracy achieved seems extra ordinary. In theoreticalcalculations and observations of the Transit of Venus,Samanta’s achivement would be considered comparableto that of Jeremiah Horrocks, though poignantlyanachronistic.Dr. (Smt.) Rathnasree is Director, Nehru Planetarium, New Delhi and is activelyengaged in popularization of astronomy.

wheel to somebody else.Take the front seat : Sit in the comfort zone. In an

automobile, the front passenger seat is the bestplace to be in because the motion is at minimum.Ask the driver to be careful and desist from suddenacceleration or decelerations.

Look straight as an arrow : It is best tolook straight ahead. If you are in the hills, a movinghorizon can be most disturbing. Just concentrateon the road in front and stop in between, if youwish to soak in the natural beauty of the valleyand the hills.

Don’t read : Avoid activities that need closeeye attention. Reading, knitting or playing cardsmay aggravate or even cause motion sickness. Keep yourhead still, rested against a seat back.

Never be cramped for clean air : Always allow plenty

of fresh air to get in. A close and smelly environment canmake matters worse. Don’t smoke or sit near smokers.

Avoid bad air : Do not stop where the air hangs heavywith odour or is unpleasant to the nostrils. If atravel companion experiences motion sickness,stay away and let him clean himself thoroughly.

Stay relaxed : Keep yourself cool. A badmood can make matters worse, while a lightmood can ease the situation.

Injectables work, when other things fail :Once vomiting begins, there is little sense intaking the pill now. It’s like closing the stabledoor after the horse has bolted! At this stage, itis best to break journey and take rest. Restusually helps quieten matters. If you feel

particularly bad, the best course is to find a doctor. A shotof antihistamine injectables can check symptoms quickly.

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