GS Magazine - - Climate Change: A Call To Action From Madrid - Dr. Ar­sè­ne Bien­ve­nu Loem­be Dr. Vi­cen­te Ló­pez-Ibor Ma­yor

Health, good health of cour­se, is the ne­ces­sary and im­per­cep­tibly prior con­di­tion for our sta­bi­lity and our phy­si­cal and emo­tio­nal well-being. Our qua­lity of li­fe, and that of our lo­ved ones, re­la­tes in many ways to the de­gree of strength of our health. That´s the reason why we fight all the en­do­ge­nous and exo­ge­nous ac­tions that dis­turb it or that de­te­rio­ra­te its nor­mal healthy and ba­lan­ced sta­te. The qua­lity of air, wa­ter, food, sa­ni­ta­tion ser­vi­ces and health ca­re at dif­fe­rent te­rri­to­rial and out­pa­tient le­vels, allows us to mea­su­re the ge­ne­ral phy­si­cal health around us and the healthy or per­ver­se ef­fects of the­se mat­ters over peo­ple and the so­cial com­mu­nity whe­re their li­ves un­fold. The fight against cli­ma­te chan­ge in­te­gra­tes many ele­ments of health de­fen­se and pro­tec­tion, as well as against di­sea­ses associated with the lack of ca­re for the na­tu­ral en­vi­ron­ment. Doc­tor Loem­bé is an ex­pe­rien­ced and well re­cog­ni­zed Me­di­cal Doc­tor and Scien­tist, gra­dua­ted from the “Free Uni­ver­sity Me­di­cal Cen­ter” in Ams­ter­dam, with mo­re than eigh­teen years of ex­pe­rien­ce in cli­ni­cal on­co­logy and can­cer drugs re­search and de­ve­lop­ment, and a gro­wing in­ter­est in the im­pact that cli­ma­te chan­ge has on the in­ci­den­ce and pre­ven­tion of can­cer. All this work, re­search and ex­pe­rien­ce, will be re­flec­ted, and be part, of a book of im­mi­nent pu­bli­ca­tion.

As a true and firm be­lie­ver of scien­ce but al­so of equal op­por­tu­ni­ties for all – all men are crea­ted equal-, I ad­mi­re Abraham Lin­coln, son of a far­mer and car­pen­ter and una­ni­mously con­si­de­red as one of the grea­test pre­si­dents of the Uni­ted Sta­tes of Ame­ri­ca. Thanks to his coura­ge and, con­vin­ced that a di­vi­ded hou­se could not stand, he sa­ved the Union.

Do­ris Kearns Good­win mas­ter­fully des­cri­bes Abraham Lin­coln’s po­li­ti­cal ta­lents and strengths in her Pu­lit­zer Pri­ze-win­ning book “Team of Ri­vals” whe­re she bri­lliantly wro­te how Lin­coln, unex­pec­tedly and against all odds, won the pre­si­den­tial elec­tion in 1860 abo­ve th­ree ac­com­plis­hed can­di­da­tes.

Un­for­tu­na­tely, fi­ve days af­ter Con­fe­de­ra­te Ge­ne­ral Ro­bert E. Lee su­rren­de­red his mas­si­ve army at Ap­po­mat­tox Court Hou­se, Virginia, of­fi­cially en­ding the Ame­ri­can Ci­vil War, on the eve­ning of April 14, 1865, John Wil­kes Booth, a fa­mous ac­tor and Con­fe­de­ra­te sym­pat­hi­zer, as­sas­si­na­ted Pre­si­dent Abraham Lin­coln at Ford’s Thea­tre in Was­hing­ton, D.C.

When I la­tely get to know mo­re about Lin­coln’s li­fe and le­gacy, among all ot­her sta­te­ments and quo­tes, the­re is one that I con­si­de­red as the most ins­pi­ring and which has gui­ded me along my pro­fes­sio­nal and per­so­nal li­fe. In the con­clu­sion on his first po­li­ti­cal an­noun­ce­ment on March 9, 1832, Abraham Lin­coln, whi­le see­king his first seat in the Illi­nois Ge­ne­ral As­sembly, men­tio­ned:

“Every man is said to ha­ve his pe­cu­liar am­bi­tion. Whet­her it be true or not, I can say for one that I ha­ve no ot­her so great as that of being truly es­tee­med of my fe­llow men, by ren­de­ring my­self worthy of their es­teem. How far I shall suc­ceed in gra­tif­ying this am­bi­tion, is yet to be de­ve­lo­ped.”

I ha­ve de­ci­ded to ren­der my­self worthy by mo­destly at­tem­pting to rai­se awa­re­ness on the im­pact of cli­ma­te chan­ge on health. I ho­pe that by the end of this chap­ter, I will un­pre­sum­ptuously suc­ceed to con­vin­ce you and my­self to ta­ke pre­ven­ti­ve ac­tions to re­du­ce the im­pact of cli­ma­te chan­ge on health and par­ti­cu­larly on can­cer- a fourt­hou­sand-year-old di­sea­se-, which is one of the lea­ding cau­ses of death world­wi­de.

I am at­tem­pted to think and pro­bably to ad­mit that the cri­sis, if we can talk about cri­sis, about the glo­bal war­ming is not (yet) des­pe­ra­te, as “des­pair ser­ves no pur­po­se when reality still of­fer ho­pes”, had taught us Al Go­re in Our Choi­ce [ 1]. Un­doub­tedly the­re is ho­pe, the­re are al­ways been ho­pes and ho­pes had al­ways gi­ven our hu­ma­nity a hand when we had to fa­ce dif­fi­cul­ties. Is not the young preacher from Geor­gia who was drea­ming that one day, “We will hew up from a moun­tain of des­pair a sto­ne of ho­pe” in that swel­te­ri­ng Au­gust in 1963 in Was­hing­ton DC? Is not the for­mer le­gen­dary pri­so­ner of Rob­ben Is­land, who ex­hor­ted us that “the­re we­re many dark mo­ments when my faith in hu­ma­nity was so­rely tes­ted, but I would not and could not gi­ve my­self up to des­pair. “Our faith is hu­ma­nity is com­monly tes­ted now, I be­lie­ve.

What should we do? Isn’t the young se­na­tor from Illi­nois, who af­ter a vic­tory for the de­mo­crats no­mi­na­tion for 2008 pre­si­den­tial elec­tion, ad­dres­sing to sup­por­ters af­ter the Io­wa Cau­cu­ses, on Jan 3, 2008, dis­cour­sed “that ho­pe is not a blind op­ti­mism, ho­pe is that thing inside us that in­sists, des­pi­te all the evi­den­ce to the con­trary, that so­met­hing bet­ter awaits us so long as we ha­ve the coura­ge to reach for it, to work for it , to fight for it.”

Af­ter we all, wi­llingly and un­wi­llingly, ha­ve ack­now­led­ged that our cli­ma­te is dra­ma­ti­cally chan­ging, my ho­pe is that we all to­get­her coura­geo­usly and un­daun­tedly will work to­get­her to rai­se awa­re­ness about the im­pact of cli­ma­te chan­ge on health; that we all to­get­her un­flin­chingly and lion­hear­tedly will fight for so­lu­tions to re­du­ce the im­pact of glo­bal war­ming and health; that we all to­get­her cons­ciously and au­da­ciously will reach for a bet­ter clean world.

The Uni­ted Sta­tes of Ame­ri­ca has an im­pres­si­ve num­ber of No­bel Pri­ze win­ners. In the 104 years of its exis­ten­ce, the No­bel Pri­ze has been awar­ded to clo­se to 1,000 lau­rea­tes and The Uni­ted Sta­tes is the hig­hest No­bel Pri­ze win­ning country, with 368 win­ners. The num­ber of scien­ce pu­bli­ca­tion in Chi­na has in­crea­sed and over­ta­ken the Uni­ted Sta­tes, ne­vert­he­less the Uni­tes Sta­tes re­mains a scien­ti­fic giant pro­du­cing out high pro­fi­le re­search and trans­la­ting scien­ce in­to va­lua­ble in­te­llec­tual pro­perty [ 2]. No­net­he­less, the Uni­ted Sta­tes has long been the world’s se­cond lar­gest con­su­mer of coal. Af­ter a sus­tai­na­ble hu­ge in­cli­ne in con­sum­ption has been ob­ser­ved, the US drop­ped to the 3rd pla­ce behind Chi­na and In­dia and is, as re­sult, lea­ding the world in re­du­cing car­bon dio­xi­de emis­sions. In 2015, US car­bon dio­xi­de emis­sions was re­du­ced by 145 mi­llion tons, by far the lar­gest de­cli­ne of any country in the world. This ef­fort is not a scorn­ful de­ri­sion and should, in con­trary, be com­men­ded. For the most re­cent 120 years, it co­mes forth that US emis­sions de­cli­ned by 622 mi­llion ton which clearly re­pre­sents a 10% de­cli­ne over 10 years. This could be ex­plai­ned by po­wer com­pa­nies swit­ching stea­dily from coal to na­tu­ral gas. Des­pi­te this de­cli­ne, ove­rall the US is still the world se­cond lar­gest emit­ter of car­bon dio­xi­de. In 2015 the US emit­ted 5.5 bi­llion tons of car­bon dio­xi­de re­pre­sen­ting 16% of the glo­bal to­tal behind Chi­na (9.2 bi­llion ton and 27% of the to­tal glo­bal emis­sion. [3]

The­re ha­ve been sig­ni­fi­cant gains in li­fe ex­pec­tancy du­ring the past half-cen­tury com­bi­ned with de­cli­ning fer­ti­lity ra­tes. It is fo­re­cas­ted that glo­bal li­fe ex­pec­tancy to in­crea­se by 4·4 years for men and for wo­men by 2040. In 2040, Ja­pan, Sin­ga­po­re, Spain, and Swit­zer­land ha­ve a fo­re­cas­ted li­fe ex­pec­tancy that will ex­ceed 85 years for both se­xes, and 59 coun­tries in­clu­ding Chi­na we­re pro­jec­ted to sur­pass a li­fe ex­pec­tancy of 80 years by 2040. At the sa­me ti­me, Cen­tral Afri­can Re­pu­blic, Le­sot­ho, So­ma­lia, and Zim­bab­we had pro­jec­ted li­fe ex­pec­tan­cies be­low 65 years in 2040 [ 4].

The pro­fi­le of ma­jor cau­ses of di­sea­se and death is being trans­for­med; the pat­tern of in­fec­tious di­sea­ses has be­co­me much mo­re un­ders­tood and cli­ni­cally ma­na­gea­ble, though health inequa­li­ties bet­ween rich and poor coun­tries un­for­tu­na­tely per­sist. The­re ha­ve been mo­re drugs dis­co­ve­red, re­vo­lu­tio­ni­zing ip­so fac­to the treat­ment of li­fe-th­rea­te­ning di­sea­ses. The world has be­co­me an im­men­sely clo­se neigh­bor­hood whe­re we eas

ily in­ter­act with each ot­her. No­net­he­less, today the pros­pects for fu­tu­re health de­pend to an in­crea­sing ex­tent, on the pro­ces­ses of glo­ba­li­za­tion and on the emer­gen­ce of glo­bal en­vi­ron­men­tal chan­ges and cha­llen­ges oc­cu­rring in res­pon­se to the great weight of man’s so­cio- eco­no­mic ac­ti­vi­ties. We are at a subs­tan­tial cross­roads whe­re our daily ac­tions ha­ve a sig­ni­fi­cant im­pact on the li­ving to­get­her to­mo­rrow; which im­plies to as­cer­tain that to­mo­rrow is, ve­ri­tably, today.

The­re are nu­me­rous of di­sea­ses which af­fect pu­blic health, and which could be di­rectly or in­di­rectly re­la­ted to cli­ma­te chan­ge. Among the­se di­sea­ses, we could, wit­hout blin­king an eye, na­me can­cer. We all know so­meo­ne with can­cer; we all ha­ve lost so­meo­ne or a be­lo­ved be­cau­se of can­cer. How of­ten didn’t we ask our­sel­ves whet­her the can­cer was not re­la­ted to this food, to this pla­ce or to this ha­bit? You would hear all uni­ma­gi­na­ble pos­si­ble and im­pas­sa­ble reasons that could be lin­ked to can­cer. The cau­ses of can­cer are mul­ti­ple and va­rious, well es­ta­blis­hed and dispu­table and con­tro­ver­sial at the sa­me ti­me. Among the well-es­ta­blis­hed are ge­ne­tic-he­re­di­tary pre­dis­po­si­tion, as well as en­vi­ron­men­tal-li­fe sty­le-to­bac­co, hu­man pa­pi­llo­ma vi­rus1 ex­po­su­re, sun ex­po­su­re. En­vi­ron­men­tal im­plies that the­se cau­ses are un­de­via­tingly, pre­ven­ta­ble. Ac­cor­ding to Can­cer Re­search UK, 4 in 10 can­cer can be pre­ven­ted. Pre­ven­tion mea­su­res in­clu­de not smo­king,

kee­ping a healthy body­weight, ea­ting healthy and ba­lan­ced, cut­ting back on al­cohol con­sum­ption, en­jo­ying the sun sa­fely and kee­ping ac­ti­ve. The­se evi­den­ces and the re­la­ted pre­ven­ti­ve ac­tions are not clearly un­ders­tood and not wi­dely sha­red. This holds true for cli­ma­te chan­ge and can­cer. What are the straight irre­vo­ca­ble evi­den­ces cu­rrently known and what are the uns­wer­vingly co­rrec­ti­ve and pre­ven­ti­ve mea­su­res im­ple­men­ted so far?

Be­fo­re ans­we­ring the­se ques­tion, it is of sig­ni­fi­cant im­por­tan­ce to ack­now­led­ge that, as off today, the­re is a cer­tain de­gree of skep­ti­cism in our so­ciety when it co­mes to cli­ma­te chan­ge and di­sea­ses. For ins­tan­ce, what do we know about the ba­bies born wit­hout arms in ru­ral Fran­ce? A mystery. The na­tio­nal health agency has laun­ched a na­tion­wi­de in­ves­ti­ga­tion and we are im­pa­tiently wai­ting for the out­co­me [ 109].

Yes, it ta­kes ti­me and tre­men­do­us ef­fort to ac­cept or es­ta­blish the car­ci­no­ge­ni­city of an agent. Let’s re­mem­ber the story of to­bac­co. Be­fo­re to­bac­co was ac­cep­ted as car­ci­no­ge­nic, many years as well as many li­ves re­gret­fully we­re lost.

Are the­re any si­mi­la­ri­ties bet­ween smo­king and cli­ma­te chan­ge?

Doc­tor Ja­mes Lee Gil­mo­re (1884 -1863), a pro­mi­nent smo­ker for years, was a 49 years old obs­te­tri­cian gy­ne­co­lo­gist from Pit­ts­burgh in Pennsyl­va­nia, who was ad­mit­ted on Fe­bruary 27, 1933, to the me­di­cal and sur­gi­cal chest ser­vi­ce of Bar­nes hos­pi­tal in St Louis, Mis­sou­ri. Be­fo­re this ad­mis­sion Dr Gil­mo­re had been hos­pi­ta­li­zed re­pea­tedly four ti­mes owed to pul­mo­nary com­plains.

Sin­ce Ja­nuary 1929, Dr Gil­mo­re had been diag­no­sed with pneu­mo­nia of the right lo­wer lo­be of the lung which re­co­ve­red only se­ve­ral weeks la­ter. Six months la­ter, on July 1932, he ex­pe­rien­ced ge­ne­ral dis­com­fort, chills, fe­ver and ele­va­ted whi­te blood cell count. A chest ra­dio­graphy per­for­med one month la­ter re­vea­led a sha­dow in the up­per lo­be of his left lung which (the­re is no re­cord of an ad­mi­nis­tra­ted treat­ment) re­gres­sed over the next days and re­cu­rred in Oc­to­ber. Af­ter a slight re­mis­sion, it re­cu­rred in December as an abs­cess lea­ding to de no­vo pneu­mo­nia.

On Fe­bruary 27, 1933, he was ad­mit­ted again with fe­ver, chest dis­com­fort that was sus­pi­cious for lung abs­cess. A per­for­med X-ray sho­wed a co­llap­se of up­per lo­be of his lung. He un­der­went a bron­chos­copy fo­llo­wed by a biopsy which re­vea­led a pre­sen­ce of car­ci­no­ma-ma­lig­nant tu­mor - ma­de up of epit­he­lial cells2. A fo­llow-up bron­chos­copy re­vea­led a wor­se­ning of the tu­mor; a new biopsy was ta­ken, which con­fir­med a squa­mous cell car­ci­no­ma of the left up­per lo­be. Dr Gil­mo­re went ho­me ta­king the biopsy sli­des with him for re­view, he got his den­tal ca­vi­ties fi­lled and pur­cha­sed a ce­me­tery plot.

On April 4, he was newly ad­mit­ted in the Bar­nes hos­pi­tal, in pre­pa­ra­tion for a left up­per lo­bec­tomy3 by Dr Evarts Graham.

The sur­gery star­ted at 10.00, pre­ci­sely 25 mi­nu­tes af­ter anest­he­sia be­gun. Af­ter in­ci­sion and ope­ning the tho­ra­cic ca­vity, Dr Graham found mul­ti­ple no­du­les obs­truc­ting the bron­chi* which ma­de a lo­bec­tomy un­ne­ces­sary. Then, against all ex­pec­ta­tion, he de­ci­ded to per­form a pneu­mo­nec­tomy af­ter dis­cus­sion with Dr. Gil­mo­re’s friend and brot­her-in­law. His­to­ri­cally, a pneu­mec­tomy has ne­ver been per­for­med in hu­mans, but suc­cess­fully in ani­mals and ob­viously not by Dr Graham him­self.

The day af­ter ha­ving un­der­go­ne the first pneu­mec­tomy in hu­man’s his­tory, Dr. Gil­mo­re con­di­tion was sa­tis­fac­tory. He had had 8 hours wit­hout opia­te but about 800 cc fluid had drai­ned from the chest cat­he­ter. He was la­ter ta­ken again to the ope­ra­ting room to re­mo­ve a por­tion of the se­cond rib. Initially ribs 5-6-7-8 to 11 we­re al­ready re­mo­ved. On Ju­ne 18, 10 weeks af­ter the sur­gery, Dr Gil­mo­re was dis­char­ged to go ho­me. Dr Graham reali­zed that he has for the first ti­me per­for­med a sur­gi­cal pro­ce­du­re which will ha­ve sig­ni­fi­can­ce con­se­quen­ces in the treat­ment of lung can­cer. (C Bar­ber Mue­ller, The li­fe, li­ves and ti­mes of the sur­gi­cal spi­rit of St Louis , chap­ter 7).

Dr Graham, con­si­de­red by his last re­si­dent C. Bar­ber Mue­ller as one of the th­ree most emi­nent Ame­ri­can sur­geons, him­self, was a te­na­cious smo­ker for mo­re than 50 years, quit­ted, 5 years be­fo­re he was diag­no­sed with bi­la­te­ral bron­cho­ge­nic car­ci­no­ma* in 1956. In 1920 Evarts Graham has iro­ni­zed when he was as­ked for the first ti­me whet­her to­bac­co cau­sed lung can­cer: ”so is the use of ny­lon stoc­kings.”

Dr Graham was one of tho­se who thought that “Bla­ming ci­ga­ret­tes for lung can­cer was li­ke bla­ming um­bre­llas for brin­ging on the rain. [5]

Th­ree years be­fo­re his death, Graham wro­te in 1954 an es­say in a book en­titled “Smo­king and Can­cer”. He won­de­red how to fight the spread of to­bac­co in our so­ciety in the fu­tu­re, Me­di­ci­ne was not po­wer­ful enough, da­ta we­re not enough, the so­lu­tion is po­li­ti­cal and should co­me from the po­licy­ma­kers and from all of us, from each of us in our daily li­ve. Whi­le his con­di­tion was de­te­rio­ra­ting pro­gres­si­vely, on Fe­bruary 14, 1957 he would wri­te to his dear friend and co­llea­gue Al­ton Ochs­ner- who was not awa­re of his con­di­tion-, la­ter that: “By the way my can­cer is a squa­mous cell can­cer ap­pa­rently li­ke all the ot­her smo­ker’s lung can­cers. I don’t think an­yo­ne can bring up a very for­ci­ble ar­gu­ment against the idea of a cau­sal con­nec­tion with smo­king be­cau­se af­ter all I had smo­ked for about 50 years be­fo­re stop­ping [ 6].

So­me aut­hors sug­ges­ted a link bet­ween ci­ga­ret­te smo­king and the in­crea­sing ca­ses of lung can­cer al­ready in the 1920s and 1930s, but the­se re­ports did not ha­ve a tan­gi­ble ef­fect on con­sum­ption [ 7].

The battle to of­fi­cially re­cog­ni­zed to­bac­co as car­ci­no­ge­nic star­ted in early 1940, when the Ox­ford epi­de­miolo­gist Ri­chard Pe­to won­de­red whet­her the­re could be a co­rre­la­tion.

Ma­jor epi­de­miolo­gi­cal stu­dies pu­blis­hed in 1950 by Doll and Hill [8] and Wyn­der and Graham [9] de­fi­ni­ti­vely es­ta­blis­hed that ci­ga­ret­te smo­king cau­ses lung can­cer; ad­di­tio­nal con­fir­ma­tory stu­dies fo­llo­wed la­ter and co­ming from the UK. In the win­ter of 1947 go­vern­ment sta­tis­ti­cians in Great Bri­tain, Doll and Hill, no­ti­ced that lung can­cer mor­bi­dity was ex­po­nen­tially in­crea­sing nearly fif­teen­fold in prior two de­ca­des (Sidd­hart­ha Muk­her­jee, The Em­pe­ror of all ma­la­dies, Scrib­ner 2010).

The hig­her mor­ta­lity ra­te was ob­ser­ved in ur­ban towns whe­re the ci­ga­ret­te con­sum­ption was much hig­her and per­cei­ved as co­ol.

In the US, Ernst Wyn­der, a me­di­cal stu­dent on a sur­gi­cal ro­ta­tion was a wit­ness of an un­for­get­ta­ble ca­se of a 42 years old pa­tient who had died from lung can­cer who­se au­topsy re­vea­led a ty­pi­cal smo­kers’ lungs. Wyn­der re­crui­ted a po­wer­ful men­tor- Evarts Graham-, to re­search the con­nec­tion bet­ween smo­king and lung can­cer. They both set up a trial in­clu­ding pa­tients with lung can­cer and a con­trol group of pa­tients wit­hout lung can­cer. All pa­tients we­re as­ked about their smo­king his­tory. This ca­se con­trol study de­mons­tra­ted that, in the lung can­cer group, smo­king his­tory was pro­mi­nent. Ne­vert­he­less, when Wyn­der pre­sen­ted the da­ta at a con­fe­ren­ce on lung bio­logy in Memp­his, the au­dien­ce was skep­ti­cal, and no ques­tions we­re as­ked in­si­nua­ting that the co­rre­la­tion was weak and the in­ter­est, mi­nor.

In Oc­to­ber 1951 Doll and Hill, ba­sed on early pre­sen­ted study from Ox­ford ge­ne­ti­cist Ed­mund Ford, who pros­pec­ti­vely de­mons­tra­ted that po­pu­la­tions un­der­go de­fi­ned ge­ne­tic chan­ges over­ti­me, which im­plies that the chan­ges should be cap­tu­red in the real world and in the real ti­me, set up a new pros­pec­ti­ve trial. They pros­pec­ti­vely co­llec­ted da­ta about smo­king his­tory and death cau­ses from mo­re than 60.000 doc­tors in a cen­tra­li­zed

re­gistry of all doc­tors in Great Bri­tain. From Oc­to­ber 1951 to March 1954, 789 deaths we­re re­por­ted, among them 36 we­re due to lung can­cer. All smo­kers!

It was when the frac­tion of smo­kers in the adult Ame­ri­can ca­ta­pul­ted to 45% that Ri­chard Doll and Brad­ford Hill pu­blis­hed their study in 1956. Con­cu­rrently, ad­ver­ti­sing from to­bac­co in­dus­tries was in­crea­sing as ne­ver; tar­ge­ting all po­pu­la­tion and even doc­tors. “Mo­re doc­tors smoke Ca­mels” would be said in a Ca­mel com­mer­cial. Shoc­kingly, at the an­nual con­fe­ren­ces of the Ame­ri­can Me­di­cal As­so­cia­tion in the early 1950, ci­ga­ret­tes we­re dis­tri­bu­ted free of char­ged to par­ti­ci­pants.

It is only in 1962, nearly 15 years af­ter Doll and Wyn­der stu­dies, the Ame­ri­can Can­cer So­ciety, the Ame­ri­can Heart As­so­cia­tion and the Na­tio­nal Tu­bercu­losis As­so­cia­tion sent a join let­ter to Pre­si­dent Ken­nedy re­ques­ting to crea­te a com­mis­sion to in­ves­ti­ga­te the con­nec­tion bet­ween smo­king and health. Luther Terry, the sur­geon ge­ne­ral was as­sig­ned as head of the com­mit­tee. He ap­poin­ted 10 mem­bers to his com­mit­tee. The com­mit­tee com­pri­sed of 5 smo­kers and 5 nons­mo­kers. They vi­si­ted do­zens of labs, re­views ton of da­ta, in­ter­views, opi­nions. 6000 ar­ti­cles, 1200 jour­nals we­re re­vie­wed. Mo­re than 1.123.000 men and wo­men we­re in­clu­ded in this me­ta-analy­sis.

Slowly but irre­fu­tably evi­den­ce of the link bet­ween smo­king and can­cer emer­ged. A 387 pa­ges re­port re­cog­ni­zing to­bac­co as cau­se of lung can­cer was fi­nally re­lea­sed on Ja­nuary 1964. It was now the task of the Fe­de­ral Tra­de Com­mis­sion to re­gu­la­te the abun­dant to­bac­co ad­ver­ti­se­ment. In 1965 a bill en­titled the Fe­de­ral Ci­ga­ret­te La­be­ling and ad­ver­ti­sing Act was is­sued [ 10].

In Great Bri­tain, the Ro­yal College of Phy­si­cians pu­blis­hed in 1962 the first re­port con­fir­ming the co­rre­la­tion bet­ween to­bac­co and lung can­cer and ot­her di­sea­ses.[ 11]

A new are­na of “bloody” battle bet­ween to­bac­co in­dustry and an­ti­to­bac­co lobb­yists was open. In this battle law­yers such as John Banz­haf had suc­cess­fully pla­yed a sig­ni­fi­cant ro­le to mi­ni­mi­ze the ad­ver­ti­se­ment ti­me for ci­ga­ret­tes on te­le­vi­sion.

Awa­re­ness star­ted stea­dily and no­ti­ceably to ri­se each year but re­mar­kably, it is from 1994 that a ci­ga­ret­te con­sum­ption in the US be­gun to drop for 20 straight years. Lung can­cer in­ci­den­ce as well is de­crea­sing.

What are the da­ta today about smo­king and lung can­cer? 5.5 per­cent of ma­le for­mer smo­kers and 2.6 per­cent of wo­men for­mer smo­kers; 15.9 per­cent of cu­rrent ma­le smo­kers; 9.5 per­cent for cu­rrent wo­men smo­kers and 24.4 per­cent for ma­le “heavy smo­kers” de­fi­ned as smo­king mo­re than fi­ve ci­ga­ret­tes per day; 18.5 per­cent for wo­men “heavy smo­kers de­ve­lop can­cer [ 108].

It has been es­ti­ma­ted that up to 20% of all can­cer deaths world­wi­de could be pre­ven­ted by the eli­mi­na­tion of to­bac­co smo­king [ 12]. It is ge­ne­rally known that ove­rall mor­ta­lity among both ma­le and fe­ma­le smo­kers in the Uni­ted Sta­tes is about th­ree ti­mes hig­her than that among si­mi­lar peo­ple who ne­ver smo­ked. Mo­re than 480,000 deaths an­nually 278,544 deaths an­nually among 201,773 deaths an­nually among wo­men in the US. [13]

So many years lost, so many li­ves could un­de­niably ha­ve been sa­ved, if we al­ready in the early 50’s had the coura­ge to ack­now­led­ge the car­ci­no­ge­nic ef­fect of to­bac­co. To help this awa­re­ness, the to­bac­co ad­ver­ti­sing could ha­ve been broadly ban­ned ear­lier and no­ne of us would ha­ve ever been wi­lling to iden­tify him­self to the Marl­bo­ro man with his hor­se, who was ack­now­led­gedly, the sym­bol of man­hood.

The cau­sal co­rre­la­tion bet­ween to­bac­co and lung can­cer has ma­de a long one­rous and bur­den­so­me jour­ney be­fo­re being uni­ver­sally ac­cep­ted, be­cau­se of dis­com­bo­bu­la­tion of the facts and de­nial of the reality. The­re is no worst blind that the one that do not want to see. What about the cli­ma­te chan­ge? Should the ha­zar­dous con­nec­tion bet­ween cli­ma­te chan­ge and health ha­ve to tra­vel the sa­me long pe­ri­lous jour­ney be­fo­re being ex­ten­si­vely ac­cep­ted?

Is it too la­te? Do we ha­ve a choi­ce? Who is to bla­me? Pas­si­vity is a choi­ce as such as ac­tion. What are the op­tions? Af­ter all, what are the evi­den­ces avai­la­ble for the cy­nics among us? Is it ap­pur­te­nant to ques­tion whet­her the­re is a cau­sal co­rre­la­tion bet­ween cli­ma­te chan­ge and health- can­cer-? The cy­nics among us, for a fact, would re­mem­ber Wi­lliam Ed­wards De­ming and ans­wer: “In God we trust. All ot­hers must bring da­ta”.

Cli­ma­te Chan­ge is hap­pe­ning

The­re are as­toun­ding amounts of da­ta that de­mons­tra­tes ma­ni­festly that the cli­ma­te is chan­ging. For se­ve­ral de­ca­des, the In­ter­go­vern­men­tal Pa­nel on Cli­ma­te Chan­ge- the IPCChas been do­cu­men­ting the world­wi­de re­search that shows con­clu­si­vely that the pla­net is war­ming from the ga­ses we are re­lea­sing ( 14). The­re­fo­re, the in­ten­tion, rat­her the ob­jec­ti­ve is to put for­ward as much evi­den­ces as pos­si­ble to help the ac­cep­tan­ce of cli­ma­te chan­ge as ha­ving a sig­ni­fi­cant im­pact on health. In the ho­pe that many li­ves could be sa­ved be­fo­re it

is too la­te, as it was too la­te as with to­bac­co. Cli­ma­te chan­ge amounts to the glo­bal shift in weat­her pat­terns oc­cu­rring over long pe­riods. The­se chan­ges could be -but not only- re­la­ted to tem­pe­ra­tu­re, rain­fall, winds speeds cloud co­ver and ozo­ne de­ple­tion.

Cli­ma­te chan­ge af­fects health di­rectly by ha­ving an ef­fect on clean air, safe drin­king wa­ter, suf­fi­cient food and last but not least ozo­ne de­ple­tion. It is ex­pec­ted that bet­ween 2030 and 2050, cli­ma­te chan­ge would cau­se ap­pro­xi­ma­tely 250.000 ad­di­tio­nal deaths per year, from malnu­tri­tion, ma­la­ria, diarrhea and heat wea­ves. The di­rect da­ma­ge cost could rai­se up to USD 2-4 bi­llion per year by 2030.

In or­der to as­sess the im­pact of cli­ma­te chan­ge on health, it is worthw­hi­le to ela­bo­ra­te ex­pli­citly on this im­pact with well-foun­ded evi­den­ces, by analy­zing which chan­ges ha­ve an ef­fect on health. Con­se­quently, it is ju­di­cious to co­me up with re­com­men­da­tions for us as in­di­vi­duals, po­licy­ma­kers, po­li­ti­cians, re­sear­chers, bu­si­ness lea­ders and key opi­nions lea­ders.

Cli­ma­te chan­ge has a very broad and di­ver­se un­ders­tan­ding and it is, ap­pro­pria­tely, not an easy task to clearly and un­de­niably de­fi­ne the ma­jor dri­vers of it and their con­se­quen­ces, among which the im­pact on health. It is com­men­da­ble as a mat­ter of facts, to fo­cus on few spe­ci­fic areas, which in my view re­qui­re mo­re at­ten­tion con­si­de­ring the re­la­ted bur­den.

Al Go­re gai­ned reign, as a cli­ma­te de­fen­der, af­ter the in­con­ve­nient truth witch ma­de him a world­wi­de ad­vo­ca­te of cli­ma­te chan­ge. His voi­ce was heard world­wi­de and the in­con­ve­nient truth has hel­ped to in­crea­se awa­re­ness of the con­se­quen­ces of cli­ma­te chan­ge.

Af­ter the suc­cess of An In­con­ve­nient Truth, and our Choi­ce, in “the Fu­tu­re”, he mas­ter­fully high­ligh­ted the six dri­vers of cli­ma­te chan­ge.

• The emer­gen­ce of deeply in­ter­con­nec­ted glo­bal eco­nomy

• The emer­gen­ce of pla­net-wi­de elec­tro­nic com­mu­ni­ca­tion grid

• The emer­gen­ce of com­ple­tely new ba­lan­ce of po­li­ti­cal, eco­no­mic and mi­li­tary po­wer in the world

• The emer­gen­ce of ra­pidly un­sus­tai­na­ble growth- in po­pu­la­tion, ci­ties; re­sour­ce con­sum­ption; de­ple­tion of top­soil, fresh­wa­ter sup­plies and li­ving spe­cies; po­llu­tion flows

• The emer­gen­ce of a re­vo­lu­tio­nary new set of po­wer­ful bio­lo­gi­cal, bio­che­mi­cal, ge­ne­tic and ma­te­rials scien­ce tech­no­lo­gies.

• The emer­gen­ce of a ra­di­cally new re­la­tions­hip bet­ween the ag­gre­ga­te po­wer off hu­man ci­vi­li­za­tion and the earth eco­lo­gi­cal sys­tems.

It is the ques­tion now which of the­se dri­vers im­pact our health? And how to align to fi­nd a com­mon ground to mi­ti­ga­te the ef­fect of the­se dri­vers?

The ef­fect of cli­ma­te chan­ge is va­riably im­men­se, dif­fe­rently per­cei­ved and li­ved, but all as­pects of the pu­blic health are con­cer­ned. Ac­cor­ding to the re­port from The In

te­ra­gency Wor­king Group on Cli­ma­te Chan­ge and Health pu­blis­hed in April 2010, glo­bal cli­ma­te chan­ge could in­crea­se the in­ci­den­ce of Asth­ma, Res­pi­ra­tory Aller­gies, and Air­way di­sea­ses; Can­cer, Car­dio­vas­cu­lar di­sea­se and Stro­ke, Food­bor­ne di­sea­ses and Nu­tri­tion, Heat-Re­la­ted Mor­bi­dity and Mor­ta­lity, Hu­man De­ve­lop­men­tal Ef­fects, Men­tal Health and Stress-Re­la­ted Di­sor­ders, Neu­ro­lo­gi­cal Di­sea­ses and Di­sor­ders, Vec­tor bor­ne and Zoo­no­tic Di­sea­ses, Wa­ter­bor­ne Di­sea­ses.

Cau­ses of deaths world­wi­de

In 2016, 56.9 mi­llion deaths world­wi­de we­re re­por­ted; among them 54% we­re cau­sed by the 10 most fa­tal di­sea­ses. Is­che­mic heart di­sea­se and stro­ke are the world’s lea­ding cau­se of death, ac­coun­ting for a com­bi­ned 15.2 mi­llion deaths in 2016.

Ch­ro­nic obs­truc­ti­ve pul­mo­nary di­sea­se clai­med 3.0 mi­llion li­ves in 2016, whe­reas lung can­cer (along with tra­chea and bron­chus can­cers) cau­sed 1.7 mi­llion deaths. Dia­be­tes ki­lled 1.6 mi­llion peo­ple in 2016, up from less than 1 mi­llion in 2000. Deaths due to de­men­tias mo­re than dou­bled bet­ween 2000 and 2016, ma­king it the 5th lea­ding cau­se of glo­bal deaths in 2016 com­pa­red to 14th in 2000.

Lo­wer res­pi­ra­tory in­fec­tions re­mai­ned the dead­liest com­mu­ni­ca­ble di­sea­se, cau­sing 3.0 mi­llion deaths world­wi­de in 2016 [ 15].

Pro­jec­ted glo­bal deaths in 2030 ran­ged from 64.9 mi­llion un­der the op­ti­mis­tic sce­na­rio to 80.7 mi­llion un­der the pes­si­mis­tic sce­na­rio, with a ba­se­li­ne pro­jec­tion of 73.2 mi­llion [ 16].

Ba­sed on the afo­re­men­tio­ned da­ta from WHO, it is ques­tio­na­ble what has been the con­tri­bu­tion of glo­bal cli­ma­te chan­ge on the­se pains­ta­kingly fi­gu­res. Though the­re are no straight da­ta from the WHO, but we could an­ti­ci­pa­te that the con­tri­bu­tion of cli­ma­te chan­ge is sig­ni­fi­cant ba­sed on the mor­ta­lity da­ta from the stu­died en­vi­ron­men­tal re­la­ted deaths.

It goes wit­hout sa­ying that, to co­ver all cli­ma­te chan­ges re­la­ted di­sea­ses, an en­ti­re book will be nee­ded ins­tead of a chap­ter in a book. The­re­fo­re, it ap­pears mo­re ap­pro­pria­te to con­cen­tra­te on the di­sea­se which cau­se the one hig­hest mor­ta­lity in the world: can­cer

Sin­ce 1998, the Ame­ri­can Cen­ters for Di­sea­se Con­trol and Pre­ven­tion, The Na­tio­nal Can­cer Ins­ti­tu­te and the North Ame­ri­can As­so­cia­tion of Can­cer re­gis­tries ha­ve been co­lla­bo­ra­ting an­nually to ge­ne­ra­te da­ta on can­cer in­ci­den­ce and mor­ta­lity. In the re­port com­pi­ling da­ta from 2010-2014, in­ci­den­ce and mor­ta­lity of spe­ci­fic can­cer si­tes such as fe­ma­le breast, Co­lo-rec­tal, lung and me­la­no­ma skin can­cer de­cli­ning. Can­cer in­ci­den­ce is de­cli­ning for 7 of the most 17 most com­mon can­cers among wo­men and the in­ci­den­ce is in­crea­sing for 8 can­cer si­tes among men and 10 si­tes among wo­men. The most sig­ni­fi­cant in­crea­se is ob­ser­ved for li­ver can­cer, mye­lo­ma, me­la­no­ma of the skin, thy­roid can­cer and leu­ke­mia. The cons­tant and con­ti­nue in­crea­se in me­la­no­ma ra­te is associated with the in­crea­se of sun ex­po­su­re and tan­ning bed use [ 17].

About 1.7 mi­llion new can­cer ca­ses we­re ex­pec­ted to be diag­no­sed in 2018 in the Uni­ted Sa­tes; and about 609,640 Ame­ri­cans we­re ex­pec­ted to die of can­cer which is dra­ma­ti­cally equal to about 1,670 deaths per day. Can­cer is the se­cond most com­mon cau­se of death in the Uni­ted Sta­tes of Ame­ri­ca af­ter heart di­sea­se. The Agency for Health­ca­re Re­search and Qua­lity es­ti­ma­tes that the di­rect me­di­cal costs (to­tal of all health ca­re costs) for can­cer in the US in 2015 we­re $80.2 bi­llion. Fifty-two per­cent of

tho­se costs we­re for hos­pi­tal out­pa­tient or of­fi­ce-ba­sed pro­vi­der vi­sits, and 38% we­re for in­pa­tient hos­pi­tal stays [ 18].

Can­cer bio­graphy and epi­de­miology

It is com­monly thought and wongly per­cei­ved in our so­ciety that can­cer is a mo­dern di­sea­se. Alt­hough, chro­no­lo­gi­cal as­sess­ment of the in­ci­den­ce and oc­cu­rren­ce of can­cer in early fos­sil ani­mal and hu­man re­mains sho­wed the scar­city of ma­lig­nan­cies in an­ti­quity, can­cer is an old di­sea­se. Pa­lae­pat­ho­lo­gi­cal fin­dings from Egypt and Gree­ce pro­vi­de evi­den­ces about the pos­si­ble diag­no­sis and treat­ment of can­cer in the an­ti­quity [ 111].

The first ca­se of can­cer was na­rra­ted by Im­ho­tep, one of world his­tory’s ge­niu­ses In­ven­tor of the py­ra­mid, aut­hor of an­cient wis­dom, ar­chi­tect, high priest, and es­sen­tially, a phy­si­cian and as­tro­no­mer who li­ved around 2625 BC. He des­cri­bed a fe­ma­le pa­tient with a bul­ging mass, lar­ge, hard, cold to the touch, den­se as a he­mat fruit and sprea­ding. For this ca­se, Im­ho­tep wro­te that the­re is no the­rapy avai­la­ble. Ba­sed on this des­crip­tion, it could reaso­nably be as­su­med that it was a ca­se of breast can­cer.

Around 440 BC, 2 mi­llen­nia af­ter the ca­se des­cri­bed by Im­ho­tep, the story of Atos­sa, queen of Per­sia told by the Greek his­to­rian He­ro­do­tus, emer­ged and was as in­tri­guing as it could des­cri­be Atos­sa suf­fe­ring be­lie­vably from breast can­cer. She has a blee­ding lump in the breast which was “to not avail”.

Pre­su­mably it was in the ti­me of Hip­po­cra­tes around 400 BC that a world can­cer ap­pears for the first ti­me in the me­di­cal li­te­ra­tu­re as kar­ki­nos from the Greek word for crab. Ac­cor­ding to Hip­po­cra­tes the tu­mor, li­ke the crab and his legs spread in a cir­cle, will in­va­de through the ves­sel with his legs [ 19]. Let’s re­mem­ber Ye­frem in Can­cer ward from Solz­he­nitsyn moc­king sha­me­lessly to Pa­vel Ni­ko­la­ye­vich, who was just ad­mit­ted in the Can­cer Ward of this filthy so­viet hos­pi­tal: “the crab lo­ves peo­ple. On­ce he’s grab­bed you with his pin­cers, he won’t let go till you croak” [110, pa­ge 19].

Can­cer has ins­pi­red aut­hors such as Ale­xan­der Solz­he­nitsyn to for­ce­fully and forth­rightly de­noun­ce the atro­ci­ties of the Sta­li­nism in 1955, 2 years af­ter the Sta­li­nin’s death. In Can­cer ward (110), Solz­he­nitsyn pain­ted a pic­tu­re of a deadly di­sea­se in re­la­tion to po­li­ti­cal re­pres­si­ve doc­tri­ne and lo­ve. He des­cri­bed the es­sen­ce and na­tu­re of can­cer in his most tra­gic forms, in­clu­ding it’s phy­si­cal ,men­tal and so­cial bur­dens; most im­por­tantly the par­ti­cu­lar re­la­tions­hip bet­ween can­cer pa­tients and the hos­pi­tal ca­re­gi­vers.

Can­cer is a di­sea­se which re­qui­res from the pa­tients to go be­yond hu­man li­mits du­ring treat­ment which, though be­ne­fi­cial in terms of sur­vi­val, but could al­so be im­pac­ting se­ve­rely the qua­lity of li­fe. Che­mot­he­rapy* is still the back­bo­ne of can­cer the­rapy. The first che­mot­he­ra­peu­tic agent was dis­co­ve­red by Syd­ney Far­ber, a pat­ho­lo­gist born in Buf­fa­lo, New York in 1903, who, on Sep­tem­ber 6, 1947 suc­cess­fully trea­ted a two year old child-let­har­gic Ro­bert Sand­ler with Leu­ke­mia, with Pte­roy­las­par­tic acid PAA, con­si­de­red to be an an­ti­fo­la­te*.[ 19, pa­ge 33]

Can­cer is one of most wi­des­pread di­sea­se in the world and of the lea­ding cau­ses of death world­wi­de. The to­tal num­ber of new ca­ses in 2018 was 18.078 mi­llion cau­sing 9.6 mi­llion deaths in 2018. The most com­mon can­cers are:

• Lung (2.09 mi­llion ca­ses, 11.6%)

• Breast (2.09 mi­llion ca­ses, 11.6%)

• Co­lo­rec­tal (1.85 mi­llion ca­ses, 10.2%)

• Pros­ta­te (1.28 mi­llion ca­ses 7,1%)

• Skin can­cer (non-me­la­no­ma) (1.04 mi­llion ca­ses) • Sto­mach (1.03 mi­llion ca­ses)

• Ot­her can­cers ( 7.75 mi­llion ca­ses)

The most com­mon cau­ses of can­cer death are can­cers of:

• Lung (1.76 mi­llion deaths, 18,4%)

• Co­lo­rec­tal (880792 deaths, 9.2%)

• Sto­mach (782685 deaths, 8.2%)

• Li­ver (781631 deaths, 8.2%)

• Breast (626679 deaths, 6.6%)

• Oe­sop­ha­gus (508585 deaths, 5.3%)

• Ot­her can­cers ( 3,42 mi­llion deaths, 35.8%) *(20)

It is ob­vious that can­cer is well es­ta­blis­hed as a deadly di­sea­se with di­sas­trous con­se­quen­ces for fa­mi­lies. The mor­ta­lity due to can­cer is de­crea­sing for so­me can­cer ty­pes and at the sa­me ti­me in­crea­sing for ot­hers. It is our per­ti­na­cious tasks to iden­tify the con­tri­bu­tion of cli­ma­te chan­ge in the in­crea­se of the in­ci­den­ce and mor­ta­lity of cer­tain ty­pes of can­cers.

How is cli­ma­te chan­ge con­tri­bu­ting to can­cer in­ci­den­ce and con­se­quently to can­cer re­la­ted mor­ta­lity?

Can­cer is a group of di­sea­se, which af­fects dif­fe­rent or­gans. It oc­curs when nor­mal cells initially un­der­go a trans­for­ma­tion and start gro­wing un­con­tro­llably, for­ming a mass ca­lled a tu­mor. Tu­mors are ca­lled can­cer only if they are ma­lig­nant. This means that they in­va­de neigh­bo­ring tis­sues (es­pe­cially lymph no­des) be­cau­se of their un­con­tro­lled growth. Ma­lig­nant tu­mors may al­so spread to dis­tant or­gans via the bloods­tream. This pro­cess of in­va­ding and sprea­ding to ot­her or­gans is ca­lled me­tas­ta­sis.

Ac­cor­ding to the Eu­ro­pean Cli­ma­te adap­tion Platform, it is ex­pec­ted that by 20502080 the lo­cal cli­ma­te In Corn­wal, South West En­gland will in­crea­se up to 3 de­grees war­mer, lea­ding lon­ger pe­riod of hot and dry weat­her. The in­crea­se in tem­pe­ra­tu­res will lead to in­crea­se ex­po­su­re to ul­tra vio­let ra­dia­tion and con­se­quently to in­crea­se in­ci­den­ce of skin can­cer.

It is com­monly ac­cep­ted in our so­ciety that too much sun is di­sa­greea­ble for our skin, How does it stand with the link bet­ween cli­ma­te chan­ge, UV ra­dia­tion- sun ex­po­su­re, and skin can­cer?

The ca­se of Zac­ki Murphy

From co­ver girl to skin can­cer pa­tient, Mo­del Zac­ki Murphy sha­res her story in skin can­cer foun­da­tion de­li­nea­ting her per­so­nal ex­pe­rien­ce at the ti­me when she was on the spotlights as a mo­del in “the Pur­suit of Fal­se Per­fec­tion “.

A native of Hills­bo­rough, North Ca­ro­li­na and a gra­dua­te of the Uni­ver­sity of North Ca­ro­li­na, Zac­ki Murphy was a po­pu­lar mo­del in 1970’s. Her fa­ce, hair and body we­re her pay­check, for this reason her skin had to look im­pec­cably good and spotless. She was cons­tantly as­ked to get a little mo­re co­lor by tan­ning and being re­gu­larly ex­po­sed in the sun. In her tee­na­gers’ years, she would spent sig­ni­fi­cant ti­me in the sun and smea­red her­self with io­di­ne and baby oil to am­plify the ef­fect of the sun. She al­ways had the dar­kest legs when la­ter she be­ca­me a cheer­lea­der. As a mo­del she had mul­ti­ple and num­ber­less sun ex­po­su­re spe­cially for Vo­gue cam­paign, for which the shoo­tings we­re ta­king pla­ce in very sunny exo­tic lo­ca­tions.

“Get­ting tan­ned is li­ke an ob­ses­sion” she na­rra­ted; and de­ca­des la­ter she star­ted to pay the pri­ce of the extreme sun ex­po­su­re with a spot on the no­se, which was diag­no­sed as skin can­cer in 2015. She wro­te furt­her that:

“On­ce you suf­fer sun da­ma­ge and es­pe­cially on­ce you ha­ve had skin can­cer, your odds of de­ve­lo­ping fu­tu­re skin can­cer go way up. Af­ter 28 years as a pro­fes­sio­nal mo­del, I look back and think about the countless ads I did for beauty com­pa­nies what the pu­blic did not know and see, was the sun da­ma­ge. I now know that avoi­ding tan­ning and prac­ti­cing sun pro­tec­tion are the best ways to avoid skin can­cer. Over the years I wor­ked with Avon, Co­ver Girl Shis­he­do, Co­tu, May­be­lli­ne, Mer­le Nor­man, Re­vlon, Oil of Olay and many ot­her com­pa­nies.” Be awa­re that the sun is a won­der­ful and ne­ces­sary part of our exis­ten­ce, but it is not our skin best friend. We used to as­so­cia­te being tan with being healthy, but now, with the sun’s ray mo­re in­ten­se than ever, we know bet­ter.” [21]

Ul­tra vio­let ra­dia­tion and skin can­cer

At the be­gin­ning of last cen­tury, the up­co­ming in­dus­trial re­vo­lu­tion, the mi­gra­tion of im­po­ve­ris­hed ru­ral mas­ses in­to ur­ban cen­ters, and the vir­tual chai­ning of the hu­man work for­ce to fac­to­ries far from any ray of sun­light, pa­ved the way for the de­si­re to go out­doors and spend mo­re ti­me ex­po­sed to the sun. This, to­get­her with the dis­co­very of the be­ne­fi­cial ef­fects of sun­light for so­me con­di­tions, even­tually crea­ted in­crea­sing last cen­tury’s dri­ve and ob­ses­sion to the bea­ches. Being tan­ned star­ted to be con­si­de­red as a hall­mark of beauty, fas­hion and so­cial pres­ti­ge in the West.

Many fas­hion hou­ses and de­sig­ners built on this by pus­hing the idea that, a sun­tan was be­ne­fi­cial and in­dus­triously at­trac­ti­ve in terms of fas­hion. Only in the se­cond half of last cen­tury did the ra­pid in­crea­se of bio­lo­gic da­ta help us to bet­ter un­ders­tand skin bio­logy, in­clu­ding pho­to­bio­logy. And only then a re­la­tion to pho­toty­pes was ma­de, lon­gi­tu­di­nal and epi­de­miolo­gic stu­dies we­re initia­ted, to in­ves­ti­ga­te the harm­ful ef­fect of the sun; and a mo­re dif­fe­ren­tia­ted pers­pec­ti­ve of the in­ter­ac­tion bet­ween sun and skin was set in [ 22].

Ul­tra­vio­let Ra­dia­tion ex­po­su­re was first lin­ked ex­pe­ri­men­tally to skin can­cer in the 1920s [23] In his pu­bli­ca­tion Find­lay, from the La­bo­ra­to­ries of the Im­pe­rial Can­cer Re­search Fund, Lon­don, no­ted that “It has long been known that pro­lon­ged ex­po­su­re to the weat­her may pro­du­ce, in the ex­po­sed skin, chan­ges which not in­fre­quently ter­mi­na­te in can­cer.” The­se chan­ges we­re first des­cri­bed in 1896 by Paul Ger­son Un­na, Ger­man der­ma­to­lo­gist from Ham­burg and one of the pio­neers of der­ma­to­pat­ho­logy, un­der the na­me “See­mans­haut,” or sai­lor’s skin; sin­ce the con­di­tion was es­pe­cially com­mon in sai­lors [ 24]. The Ame­ri­can Hy­de, in 1906 [25] and the French Du­breuil in 1907, pu­blis­hed the first evi­den­ces lin­king hu­man skin can­cer to sun­light. [26]

The­re are th­ree ma­jor ty­pes of skin can­cers dis­tin­guis­hed: ba­sal cell car­ci­no­ma (BCC), squa­mous cell car­ci­no­ma (SCC), and me­la­no­ma. The first two skin can­cers are grou­ped to­get­her as non-me­la­no­ma skin can­cers. SCC is mo­re dan­ge­rous and is res­pon­si­ble for the most skin can­cer re­la­ted deaths. Ove­rall, 80 % of skin can­cers are BCC, 16 % are SCC and 4 % are me­la­no­ma. [27]

Ge­ne­rally fair skin, red and blond hair, blue or green eyes are mo­re sus­cep­ti­ble to skin can­cer [ 28].

Ex­po­su­re to Ul­tra Vio­let ra­dia­tion is the main fac­tor that cau­ses skin cells to be­co­me can­cer cells.

Al­most all skin can­cers -ap­pro­xi­ma­tely 99% of non-me­la­no­ma skin can­cers and 95% of me­la­no­ma-, are cau­sed by ex­ces­si­ve UV ra­dia­tion from the sun or ot­her sour­ces such as so­la­ria (so­la­riums, sun­beds, and sun lamps).

What is Ul­tra­vio­let Ra­dia­tion?

UV ra­dia­tion is part of the elec­tro­mag­ne­tic (light) spec­trum that reaches the earth from the sun, a 6 bi­llion old star, and is in­vi­si­ble to the na­ked eye. The­se wa­ve­lengths are clas­si­fied as UVA, UVB, or UVC, with UVA the lon­gest of the th­ree at 320-400 na­no­me­ters. UVA is furt­her di­vi­ded in­to two wa­ve ran­ges, UVA I, which mea­su­res 340-400 na­no­me­ters (nm, or bi­llionths of a me­ter), and UVA II which ex­tends from 320-340 na­no­me­ters. UVB ran­ges from 290 to 320 nm. With even shor­ter rays, most UVC is ab­sor­bed by the ozo­ne la­yer and does not reach the earth [ 29].

Both UVA and UVB, ho­we­ver, pe­ne­tra­te the at­mosp­he­re and play an im­por­tant ro­le in con­di­tions such as pre­ma­tu­re skin aging, eye da­ma­ge (in­clu­ding ca­ta­racts), and skin can­cers. They al­so sup­press the im­mu­ne sys­tem-re­du­cing your abi­lity to fight off the­se and ot­her ma­la­dies.

It is es­ti­ma­ted that ul­tra­vio­let ra­dia­tion cons­ti­tu­tes only 7% of the so­lar energy that reaches the skin; 39% is in the vi­si­ble light spec­trum (400–760 nm). But 54% of so­lar energy con­sists of in­fra­red ra­dia­tion [ 30].

As de­fi­ned ear­lier, the­re are two ty­pes of UV ra­dia­tion. A and B; but the hig­hest risk of skin can­cer is re­la­ted to UVB ex­po­su­re by cau­sing mo­re ge­ne­tic da­ma­ge, whe­reby it con­tri­bu­tes to about 80% sun­burn, whe­reas UVA con­tri­bu­tes to the re­mai­ning 20% [ 31]. It is ob­vious that UV ra­dia­tion ex­po­su­re is the lea­ding cau­se of skin can­cer. It is well es­ta­blis­hed that the de­ple­tion of the one la­yer wor­sen the ef­fect of the sun ex­po­su­re on the skin.

Skin can­cer de­ve­lops in the cells in the epi­der­mis – the ou­ter la­yer of the skin. UV ra­dia­tion is ma­de up of two ty­pes of ra­dia­tions: UVA and UVB rays which are both able to pe­ne­tra­te the skin and cau­se per­ma­nent da­ma­ge to the skin cells.

UVA pe­ne­tra­tes mo­re deeply in­to the skin (the der­mis) cau­sing ge­ne­tic da­ma­ge to cells, such as wrin­kling, blot­chi­ness; and im­mu­ne-sup­pres­sion whe­reas UVB pe­ne­tra­tes in­to the epi­der­mis (top la­yer of the skin) cau­sing da­ma­ge to the cells.

Ex­ces­si­ve UV ra­dia­tion from the sun or sun­beds would even­tually da­ma­ge the ge­ne­tic ma­te­rial (DNA) of the skin cells. In ca­se sig­ni­fi­cant DNA da­ma­ge is built up over ti­me, it can lead to an un­con­tro­lled growth of cells lea­ding to skin can­cer.

Ex­po­su­re to so­lar UV ra­dia­tion de­pends on a num­ber of fac­tors, in­clu­ding la­ti­tu­de, ele­va­tion, the pre­sen­ce of re­flec­ti­ve sur­fa­ces, ozo­ne con­cen­tra­tion, cloud co­ver, and par­ti­cu­la­te mat­ter in the at­mosp­he­re [ 32].

Stra­tosp­he­ric Ozo­ne

Alt­hough they re­cei­ved the No­bel pri­ze to­get­her with Crut­zen in che­mistry only in 1995, for their work in at­mosp­he­ric che­mistry , Molina and Row­land, de­mons­tra­ted al­ready ear­lier that stra­tosp­he­ric ozo­ne might be des­tro­yed by in­dus­trially pro­du­ced chlo­ri­ne- and bro­mi­ne-con­tai­ning sta­ble subs­tan­ces, such as chlo­ro­fluo­ro­car­bons* com­monly used in spray cans, re­fri­ge­ra­tors and air con­di­tio­ners. The­se inert subs­tan­ces can reach the stra­tosp­he­re*, whe­re they are de­com­po­sed by high-energy UV ra­dia­tion; con­se­quently, reac­ti­ve chlo­ri­ne and bro­mi­ne are re­lea­sed [ 33].

Re­sul­tantly, the ozo­ne de­ple­tion will re­du­ce the dam­ping ef­fect of UV ra­dia­tion even if the sun ex­po­su­re will re­main the sa­me. It should be ack­now­led­ged that, nor­mally, peo­ple need reaso­na­ble daily ex­po­su­re to or­di­nary le­vels of UVB ra­dia­tion to main­tain their vi­ta­min D le­vels and their adap­ta­tion to sun ex­po­su­re, but ove­rex­po­su­re will con­tri­bu­te to ad­ver­se ef­fects such as im­mu­no­sup­pres­sion and skin can­cer [ 34]. Ex­po­su­re to sun is one of the sour­ce of vi­ta­min D which con­tri­bu­te to re­du­ce the risk of breast can­cer. Co­rres­pon­dingly, UV ra­dia­tion cau­ses da­ma­ge on DNA lea­ding to se­ve­ral mu­ta­tions of ge­nes; most im­por­tantly of the P53 which is con­si­de­red as the guar­dian of hu­man ge­no­me.

It has been de­mons­tra­ted, in ad­di­tion, that ge­ne­tic al­te­ra­tions wit­hin the p53 gene* ha­ve a di­rect co­rre­la­tion with can­cer de­ve­lop­ment and oc­cur in nearly 50% of all can­cers. p53 mu­ta­tions are par­ti­cu­larly com­mon in skin can­cers cau­sed by UV irra­dia­tion.[ 35]

As spe­ci­fic p53 gene mu­ta­tions associated with hu­man skin can­cer are in­du­ced in nor­mal skin by so­lar UV ra­dia­tion, it has been sug­ges­ted that mea­su­re­ment of the­se mu­ta­tions may be use­ful as a bio­lo­gi­cally re­le­vant mea­su­re of UV ex­po­su­re in hu­mans and as a pos­si­ble pre­dic­tor of risk for skin can­cer [ 36].

Ac­cor­ding to a study from Van der Leun, ba­sed on mou­se ex­pe­ri­ment, in­crea­sed room tem­pe­ra­tu­re en­han­ced ul­tra­vio­let (UV) ra­dia­tion-in­du­ced car­ci­no­ge­ne­sis; the ef­fec

ti­ve UV do­se was in­crea­sed by 3-7% per °C. Hen­ce, the aim of the study was to re­search the ef­fect of cli­ma­te chan­ge on the in­ci­den­ce of skin can­cer in the US, ba­sed on a sur­vey in 11 re­gions. It was de­mons­tra­ted that the in­crea­se of the in­ci­den­ce of non-me­la­no­ma skin can­cer was re­la­ted to the in­crea­se of tem­pe­ra­tu­re, thus of am­bient UV ra­dia­tion ex­po­su­re. For squa­mous cell car­ci­no­ma, the in­ci­den­ce was hig­her by 5.5% per °C and for ba­sal cell car­ci­no­ma by 2.9% per °C. The­se va­lues co­rres­pond to an in­crea­se of the ef­fec­ti­ve UV do­se by about 2% per °C. The study con­clu­ded that the tem­pe­ra­tu­re ri­ses associated with cli­ma­te chan­ge could un­doub­tedly in­crea­se the in­duc­tion of non-me­la­no­ma skin can­cers by UV ra­dia­tion in hu­man po­pu­la­tions. [37]

The­re­fo­re, the­re are in­ter­na­tio­nal agree­ments on ozo­ne-de­ple­ting subs­tan­ces, des­cri­bed in the Mon­treal Pro­to­col of 1987 and its la­ter amend­ments to re­du­ce the de­ple­tion of the ozo­ne la­yer [ 38].

The per­sis­tent de­gra­da­tion of the ozo­ne la­yer will li­kely lead to a dra­ma­tic in­crea­se in skin can­cer in­ci­den­ce, which is es­ti­ma­ted to in­crea­se four­fold by the year 2100 [ 39].

The in­ci­den­ce of both Me­la­no­ma and Non Me­la­no­ma Skin Can­cer is on the ri­se, with an an­nual in­crea­se in MM of 0.6% among adults over 50 years [ 40]. This is an un­con­ven­tio­nal and im­per­fect truth we ha­ve to fa­ce and to deal with. Daily!

The ob­ser­ved in­crea­ses in skin can­cer in­ci­den­ce could be associated, on one hand with the sig­ni­fi­cant ol­der po­pu­la­tions [41] and on the ot­her hand with the im­por­tant ro­le of in­crea­sed oc­cu­pa­tio­nal and re­crea­tio­nal UV light ex­po­su­re. [42]

For ins­tan­ce, wo­men <40 years ex­hi­bi­ted a cons­tant li­near in­crea­se in BCC in­ci­den­ce ra­tes of 6.3% bet­ween 1973 and 2009 [ 43].

Ot­hers aut­hors such as Lens et al ha­ve pu­blis­hed ex­ten­si­vely on the in­crea­se of the in­ci­den­ce of ma­lig­nant me­la­no­ma , res­pon­si­ble for 1-2% of all can­cers and 75% of all skin can­cer deaths [ 44]. For ins­tan­ce, in Ire­land from 1994-2012, the in­ci­den­ce of me­la­no­ma has in­crea­sed an­nually by 3% and 5% in fe­ma­les and ma­les, res­pec­ti­vely. Mor­ta­lity ra­tes are al­so on the in­cli­ne, with a 2.2% and 6% an­nual ri­se in me­la­no­ma re­la­ted deaths in fe­ma­les and ma­les, res­pec­ti­vely [ 45]. From all the­se da­ta, ul­tra­vio­let ra­dia­tion has been in­cri­mi­na­ted as the im­por­tant con­tri­bu­ting fac­tor, par­ti­cu­larly in­ter­mit­tent exposition to sun­light [ 46].

Nu­me­rous stu­dies with ani­mal’s mo­dels had con­vin­cingly de­mons­tra­ted that skin can­cer is associated with a fai­lu­re of the im­mu­ne sys­tem to re­cog­ni­ze tu­mor an­ti­gens and/ or to des­troy ma­lig­nant cells. In this con­text, UV-in­du­ced skin can­cers may be vie­wed as the re­sult of fai­led sur­vei­llan­ce sys­tem by the im­mu­ne sys­tem.

The scien­ti­fic da­ta abo­ve­men­tio­ned are, in my opi­nion, con­vin­cing enough that the­re is a fier­ce ur­gency that full com­plian­ce of all na­tions and in­dus­tries with the in­ter­na­tio­nal agree­ments will help to re­du­ce the ozo­ne de­ple­tion and to ac­ce­le­ra­te his re­co­very.

The in­di­vi­dual res­pon­si­bi­lity is al­so re­qui­red to help the na­tions and in­dus­tries. We are all con­cer­ned, and inac­ti­vity could be fa­tal and con­tri­bu­te to in­crea­se the in­ci­den­ce of skin can­cer.

In­ter­na­tio­nal con­fe­ren­ces on UV and skin can­cer pre­ven­tion

To rai­se awa­re­ness about the pre­ven­tion of skin can­cer, in­ter­na­tio­nal ex­perts in skin can­cer pre­ven­tion, UV ra­dia­tion scien­ce, der­ma­to­logy, allied beha­vio­ral and cli­ni­cal dis­ci­pli­nes and mem­bers of the en­vi­ron­men­tal planning and de­sign com­mu­ni­ties, gat­her for the in­ter­na­tio­nal con­fe­ren­ces on UV and skin can­cer pre­ven­tion. The 4th edi­tion was held in North Ame­ri­ca in To­ron­to from 1st May to 4th May, af­ter the suc­ces­ses of past con­fe­ren­ces in Co­pen­ha­gen (2011), Ber­lin (2013) and Melbourne (2015). Skin can­cer is the most com­mon can­cer in North Ame­ri­ca.The ob­jec­ti­ves of the 4th con­fe­ren­ce was:

• Bring to­get­her the lea­ding in­ter­na­tio­nal re­sear­chers and prac­ti­tio­ners in skin can­cer pre­ven­tion to show­ca­se the la­test re­search fin­dings and best prac­ti­ces in com­mu­nity-ba­sed in­ter­ven­tions

• Crea­te co­lla­bo­ra­ti­ve op­por­tu­ni­ties bet­ween the skin can­cer pre­ven­tion com­mu­nity and allied dis­ci­pli­nes such as ur­ban plan­ners, ar­chi­tects, and ra­dia­tion scien­tists

• Res­pond to cu­rrent con­cerns about gaps in the skin can­cer pre­ven­tion li­te­ra­tu­re

• Fos­ter dis­cus­sions about in­no­va­ti­ve emer­ging di­rec­tions in skin can­cer pre­ven­tion re­search and prac­ti­ce. [47]

Kris­tie L. Ebi, PhD, Jen­ni­fer Va­nos res­pec­ti­vely pro­fes­sor at Rohm & Haas En­do­wed Pro­fes­sor, Pu­blic Health Scien­ces and the Uni­ver­sity of Was­hing­ton (USA), in the ple­nary ses­sion 2 pre­sen­ted a to­pic on “En­vi­ron­men­tal Is­sues in Skin Can­cer Pre­ven­tion In­cor­po­ra­ting Cli­ma­te Chan­ge in Skin Can­cer Pre­ven­tion In­ter­ven­tions”. They high­ligh­ted that “in­ter­ac­tions among en­vi­ron­men­tal, so­cial, and eco­no­mic fac­tors could af­fect skin can­cer pre­va­len­ce, with the mag­ni­tu­de and pat­tern of chan­ges var­ying spa­tially

and tem­po­rally. The main path­ways are through chan­ges in eryt­he­mal irra­dian­ce and through chan­ges in hu­man ac­ti­vi­ties and beha­viors that could in­crea­se or de­crea­se UV ex­po­su­res and the risk of skin can­cer. “They ad­vo­ca­ted furt­her to re­du­ce green­hou­se gas emis­sions to ad­dress the im­pact of cli­ma­te chan­ge on the in­crea­sing eryt­he­mal irra­dian­ce. Ear­lier and war­mer springs in­vi­te peo­ple to spend mo­re ti­me out­doors, en­ga­ging in lei­su­re-ti­me phy­si­cal ac­ti­vity in clot­hing that could in­crea­se ex­po­su­re to UVA and UVB if suns­creen use. In fi­ne, in­crea­sing awa­re­ness of how cli­ma­te chan­ge could al­ter the risks of skin can­cers is nee­ded among health ca­re pro­vi­ders and the ge­ne­ral pu­blic to en­su­re that pre­ven­ti­ve mea­su­res are ti­mely and ef­fec­ti­ve. In­crea­sed mo­ni­to­ring and re­search are nee­ded to im­pro­ve es­ti­ma­tes of UVR ex­po­su­re, to bet­ter quan­tify UV ex­po­su­res, and to in­form ef­fec­ti­ve mo­di­fi­ca­tions of po­pu­la­tion-ba­sed in­ter­ven­tions in the fa­ce of a chan­ging cli­ma­te to pre­vent an in­crea­se in skin can­cers.

In her pre­sen­ta­tion en­titled: “Allian­ce for UV Pro­tec­tion: Pre­ven­tion of Health Da­ma­ge Cau­sed By The Sun - Struc­tu­ral Pre­ven­tion in Ur­ban and Ru­ral Areas” Cor­ne­lia Bal­der­mann from the Ger­man Fe­de­ral Of­fi­ce for Ra­dia­tion Pro­tec­tion in Neuher­berg, Ger­many, al­so no­ti­ced that “The num­ber of UV ra­dia­tion in­du­ced skin can­cer con­ti­nues to ri­se in Ger­many as well as world­wi­de. The si­tua­tion is furt­her exa­cer­ba­ted by cli­ma­te chan­ge. Cli­ma­te chan­ge is al­so the cau­se for mo­re high tem­pe­ra­tu­re days with in­crea­sed mor­bi­dity and mor­ta­lity “

What about fo­re­cas­ting the le­vel of UV ra­dia­tion? Yves Ro­chon from En­vi­ron­ment and Cli­ma­te Chan­ge Ca­na­da, To­ron­to, ON, and Jean de Grand­pré from En­vi­ron­ment and Cli­ma­te Chan­ge Ca­na­da, Dor­val, QC. emp­ha­si­zed that the de­ve­lop­ment of a com­prehen­si­ve Che­mi­cal Da­ta As­si­mi­la­tion (CDA) sys­tem which can be used for va­rious air qua­lity ap­pli­ca­tions and al­so UV index fo­re­cas­ting is being com­ple­ted. The ob­jec­ti­ves will be:

1. In­form the com­mu­nity of pro­gress at En­vi­ron­ment and Cli­ma­te Chan­ge Ca­na­da in UV index fo­re­cas­ting.

2. Pro­vi­de in­sight as to how the UV index is de­ter­mi­ned from ozo­ne and weat­her mo­del fo­re­casts with this new sys­tem.

3. Pro­vi­de in­sight on the re­lia­bi­lity of the­se new UV index fo­re­casts

De­ple­tion of stra­tosp­he­ric ozo­ne by man-ma­de ga­ses such as chlo­ro­fluo­ro­car­bons has been oc­cu­rring du­ring the past few de­ca­des and is li­kely to peak by about 2020. Am­bient ground-le­vel ul­tra­vio­let irra­dia­tion is es­ti­ma­ted to ha­ve in­crea­sed by up to 10% at mid-to-high la­ti­tu­des du­ring the past two de­ca­des [ 48].

Af­ter 8000 ge­ne­ra­tions of ho­mo sa­piens, our ge­ne­ra­tion is wit­nes­sing the una­voi­da­ble pro­cess of hu­man cau­sed de­ple­tion of stra­tosp­he­ric ozo­ne. Most of the ozo­ne re­si­des wit­hin the stra­tosp­he­re and the ozo­ne ab­sorbs most of the so­lar UV ra­dia­tion. Ne­vert­he­less at­mosp­he­ric ozo­ne is not ori­gi­nally part of the pla­net sys­tem but a pro­duct of li­fe on earth . About 2 bi­llion years ago as pho­tosynt­he­si­zing or­ga­nism emit­ted oxy­gen, a was­te gas ca­lled ozo­ne be­gun gra­dually to form wit­hin the at­mosp­he­re. The ozo­ne la­yer de­ple­tion is cau­sed by va­rious in­dus­trial ha­lo­ge­na­ted che­mi­cal such as chlor­fluo­car­bons (CFC) used in the re­fri­ge­ra­tion and in­su­la­ted pac­ka­ging and spray cans pro­pe­llants. (A.J Mi­chael, R Lu­cas A.L Pon­sonby, S J Ed­wards, Cli­ma­te chan­ge and hu­man health stra­tosp­he­ric ozo­ne de­ple­tion ul­tra­vio­let ra­dia­tion and health chap­ter 8.

As men­tio­ned ear­lier, UVR ex­po­su­re was first lin­ked ex­pe­ri­men­tally to skin can­cer in the 1920s in mou­se mo­dels (Find­lay, G.M. Ul­tra­vio­let light and skin can­cer. Lan­cet 2: 1070–1073 (1928). The as­so­cia­tion bet­ween stra­tosp­he­ric ozo­ne de­ple­tion and skin can­cer was first es­ta­blis­hed in the 1970s. Sub­se­quently the In­ter­na­tio­nal Agency for Re­search on Can­cer in 1992 con­clu­ded that so­lar ra­dia­tion is a cau­se of skin can­cer [ 49].

Mc Ken­zie et al ha­ve de­mons­tra­ted that sus­tai­na­ble de­crea­ses in sum­mer­ti­me ozo­ne over Lau­der in New Zea­land led to sig­ni­fi­cant in­crea­ses in peak ul­tra­vio­let (UV) ra­dia­tion in­ten­si­ties. In the sum­mer of 1998–99, the peak sun burning UV ra­dia­tion was about 12 per­cent mo­re than in the first years of the de­ca­de. [50]

We all re­mem­ber the co­lour-en­han­ced pic­tu­res of the win­ter-spring po­lar “ozo­ne ho­le” on the Uni­ted Sta­tes NASA web-si­te de­pict an ove­rall loss which had keppt up to around one third of to­tal An­tar­ctic ozo­ne, by the la­te 1990s, re­la­ti­ve to the pre-1975 fi­gu­re. Win­ter-spring los­ses in the Ar­ctic are sma­ller be­cau­se lo­cal stra­tosp­he­ric tem­pe­ra­tu­res are less cold than in the An­tar­ctic. Du­ring the 1980s and 1990s at nort­hern mid-la­ti­tu­des (such as Eu­ro­pe), the ave­ra­ge year-round ozo­ne con­cen­tra­tion de­cli­ned by around 4% per de­ca­de: over the sout­hern re­gions of Aus­tra­lia, New Zea­land, Ar­gen­ti­na and South Africa, the fi­gu­re has ap­pro­xi­ma­ted 6–7%. Long-term de­crea­ses in sum­mer­ti­me ozo­ne over New Zea­land are associated with sig­ni­fi­cant in­crea­ses in ground le­vel UVR, par­ti­cu­larly in the DNA-da­ma­ging wa­ve­band [ 51].

The Mon­treal pro­to­col

Two years af­ter the dis­co­very of the An­tar­ctic ozo­ne ho­le in 1985, na­tions of the world sig­ned the Mon­treal Pro­to­col on Subs­tan­ces that De­ple­te the Ozo­ne La­yer, which re­gu­la­ted ozo­ne-de­ple­ting com­pounds.

The Mon­treal Pro­to­col fi­na­li­zed on 26 Au­gust 1987 -and which en­te­red in for­ced 2 years la­ter, is a glo­bal agree­ment to pro­tect the stra­tosp­he­ric ozo­ne la­yer by pha­sing out the pro­duc­tion and con­sum­ption of ozo­ne-de­ple­ting subs­tan­ces. It was a pro­to­col to the Vien­na for the pro­tec­tion the ozo­ne la­yer.

The pro­to­col has had in to­tal eight re­vi­sions:

• in 1990 (Lon­don, Pha­se out of CFCs4 and ot­her harm­ful Ozo­ne de­ple­ting subs­tan­ces is set at 2000 for de­ve­lo­ped and 2010 for de­ve­lo­ping coun­tries),

• 1991 (Nai­ro­bi, The Mul­ti­la­te­ral Fund is es­ta­blis­hed to fi­nan­ce pha­seout pro­jects in de­ve­lo­ping coun­tries),

• 1992 (Co­pen­ha­gen, Pha­seout of CFCs is ac­ce­le­ra­ted to 1996 and hy­dro­chlo­ro­fluo­ro­car­bons (HCFC) pha­seout is tar­ge­ted to be­gin in 2004 for de­ve­lo­ped coun­tries),

• 1993 (Bang­kok, Pha­seout of HCFCs is ac­ce­le­ra­ted for de­ve­lo­ped coun­tries to start ten years ear­lier),

• 1995 (Vien­na, Pha­seout of methyl bro­mi­de is set to 2010 and HCFC pha­seout is mo­ved from 2030 to 2020 for de­ve­lo­ped coun­tries),

• 1997 (Mon­treal, Pha­seout of HCFCs is es­ta­blis­hed for de­ve­lo­ping coun­tries),

• 1998 (Aus­tra­lia, ozo­ne pro­tec­tion amend­ment bill to ma­ke the re­gu­la­tion of the im­por­ta­tion, ma­nu­fac­tu­re and ex­port of hy­dro­chlo­ro­fluo­ro­car­bons (HCFCs) and methyl bro­mi­de mo­re equi­ta­ble, ope­ra­ble and ef­fec­ti­ve),

• 1999 (Bei­jing, Con­trols on the pro­duc­tion and tra­de of methyl bro­mi­de and HCFCs are tigh­te­ned),

• 2016 (Ki­ga­li, Pha­se­down of HFCs is es­ta­blis­hed).

Full im­ple­men­ta­tion of the Mon­treal Pro­to­col is ex­pec­ted to re­sult in avoi­dan­ce of mo­re than 280 mi­llion ca­ses of skin can­cer, ap­pro­xi­ma­tely 1.6 mi­llion skin can­cer deaths, and mo­re than 45 mi­llion ca­ses of ca­ta­racts in the Uni­ted Sta­tes alo­ne by the end of the cen­tury, with even grea­ter be­ne­fits world­wi­de. The Mon­treal Pro­to­col’s Scien­ti­fic As­sess­ment Pa­nel es­ti­ma­tes that with im­ple­men­ta­tion of the Mon­treal Pro­to­col we can ex­pect near com­ple­te re­co­very of the ozo­ne la­yer by the midd­le of the 21st cen­tury.

The Mon­treal Pro­to­col has pro­ven to be in­no­va­ti­ve and suc­cess­ful, and is the first treaty to achie­ve uni­ver­sal ra­ti­fi­ca­tion by all coun­tries in the world in the his­tory of the

Uni­ted Na­tions [ 52]. For­mer Uni­ted Na­tions Se­cre­tary-Ge­ne­ral Ko­fi An­nan re­mar­ked on the suc­cess of this glo­bal res­pon­se by sa­ying, “per­haps the sin­gle most suc­cess­ful in­ter­na­tio­nal en­vi­ron­men­tal agree­ment to da­te has been the Mon­treal Pro­to­col.”

In No­vem­ber 2017, the EPA Uni­ted Sta­tes En­vi­ron­men­tal Pro­tec­tion Agency, is­sued a re­port on “Stra­tosp­he­ric Ozo­ne Pro­tec­tion: 30 Years of Pro­gress and Achie­ve­ments”. Ac­cor­ding to this re­port, the Uni­ted Sta­tes is ex­cee­ding its Pha­seout Obli­ga­tions. The Uni­ted Sta­tes has im­ple­men­ting a ran­ge of do­mes­tic ac­tions un­der Title VI that ha­ve led to meet and ex­ceed the ODS pha­seout outli­ned un­der the Mon­treal Pro­to­col.

Tech­no­lo­gi­cal Im­pro­ve­ments Sti­mu­la­ted by the Mon­treal Pro­to­col as men­tio­ned in the 30 years re­port from the EPA on the Mon­treal pro­to­col

1. Re­fri­ge­ra­tion and Air Con­di­tio­ning Equip­ment Ma­nu­fac­tu­rers. Ma­nu­fac­tu­rers of re­fri­ge­ra­tion and air con­di­tio­ning equip­ment re-de­sig­ned their equip­ment to im­pro­ve energy ef­fi­ciency and re­du­ce re­fri­ge­rant lea­ka­ge ra­tes, which al­so re­sul­ted in re­du­ced ope­ra­ting costs.

2. Ae­ro­sols In­dustry. This in­dustry de­ve­lo­ped “not-in-kind” al­ter­na­ti­ve de­li­very sys­tems to ODS-pro­pe­lled ae­ro­sol cans, such as spray pumps and roll-on deo­do­rants, which are safe for hu­man and en­vi­ron­men­tal health and mo­re cost-ef­fec­ti­ve than ae­ro­sols.

3. Sol­vents In­dustry. To re­du­ce the use of sol­vents to clean me­tal parts, de­flux wi­ring as­sem­blies, and re­mo­ve con­ta­mi­nants from pre­ci­sion me­cha­ni­cal parts in the elec­tro­nics in­dustry, the sol­vent clea­ning in­dustry de­ve­lo­ped new sol­der flu­xes and pas­tes that do not re­qui­re clea­ning or can be lea­ned with wa­ter.

4. Agri­cul­tu­ral Fu­mi­gants. High-ba­rrier tarps are now used in the agri­cul­tu­re in­dustry in res­pon­se to the pha­seout of methyl bro­mi­de. The­se tarps are laid on top of a fu­mi-

ga­ted field and sig­ni­fi­cantly re­du­ce at­mosp­he­ric emis­sions and bys­tan­der ex­po­su­re to fu­mi­gants whi­le achie­ving ef­fec­ti­ve pest con­trol.

In 2015 in his re­port titled, “Up­da­ting ozo­ne cal­cu­la­tions and emis­sions pro­fi­les for use in the at­mosp­he­ric and health ef­fects fra­me­work mo­del“, EPA mo­de­led the ef­fects of a de­ple­ted ozo­ne la­yer on Ame­ri­cans born bet­ween 1890 and 2100, a ti­me­fra­me that in­clu­des tho­se who we­re very old when the ozo­ne ho­le was dis­co­ve­red and tho­se who will be very young when the ozo­ne la­yer is fully re­co­ve­red. The mo­de­ling sho­wed that full im­ple­men­ta­tion of the Mon­treal Pro­to­col is ex­pec­ted to re­sult in the avoi­dan­ce of mo­re than 280 mi­llion ca­ses of skin can­cer, ap­pro­xi­ma­tely 1.6 mi­llion skin can­cer deaths, in the Uni­ted Sta­te [53] Up­da­ting Ozo­ne Cal­cu­la­tions and Emis­sions Pro­fi­les for Use in the At­mosp­he­ric and Health Ef­fects Fra­me­work Mo­de ) re­sul­ting in hun­dreds of bi­llions of do­llars in so­cie­tal health be­ne­fits in the Uni­ted Sta­tes over the pe­riod 1990 to 2165.

For the first ti­me, scien­tists ha­ve shown through di­rect ob­ser­va­tions of the ozo­ne ho­le by a sa­te­lli­te ins­tru­ment, built by NASA’s Jet Pro­pul­sion La­bo­ra­tory in Pasadena, Ca­li­for­nia, that le­vels of ozo­ne-des­tro­ying chlo­ri­ne are de­cli­ning, re­sul­ting in less ozo­ne de­ple­tion.

Mea­su­re­ments show that the de­cli­ne in chlo­ri­ne, re­sul­ting from an in­ter­na­tio­nal ban on chlo­ri­ne-con­tai­ning hu­man-pro­du­ce che­mi­cals ca­lled chlo­ro­fluo­ro­car­bons (CFCs), is re­sul­ting in about 20 per­cent less ozo­ne de­ple­tion du­ring the An­tar­ctic win­ter in 2005 - the first year that mea­su­re­ments of chlo­ri­ne and ozo­ne du­ring the An­tar­ctic win­ter we­re ma­de by NASA’s Au­ra sa­te­lli­te [ 54].

Eco­no­mics bur­den of skin can­cer

Health has in­dispu­tably been re­la­ted to high costs. Scree­ning, diag­no­sis and treat­ment are the most im­por­tant sour­ces of spen­ding. This par­ti­cu­larly holds true for can­cer. Non Me­la­no­ma Skin Can­cer has a sig­ni­fi­cant eco­no­mic bur­den. In Aus­tra­lia, it is the most costly can­cer, ac­coun­ting for ex­pen­di­tu­re of AUS$511 mi­llion in 2010. Non Me­la­no­ma Skin Can­cer treat­ments in­crea­sed by 86% bet­ween 1997 and 2010. It was an­ti­ci­pa­ted that the num­ber and the to­tal cost of NMSC treat­ments will in­crea­se by a furt­her 22% bet­ween 2010 and 2015. NMSC will re­main the most costly can­cer and pla­ce an in­crea­sing bur­den on the Aus­tra­lian health ca­re sys­tem ( 55).

In Uni­ted King­dom, it is es­ti­ma­ted that costs due to skin can­cer we­re in the ran­ge of £106–£112 mi­llion in 2008 and that the cost to the NHS due to skin can­cer will amount to over £180 mi­llion in 2020 (56) .The costs of treat­ment and mor­bi­dity associated with Ba­sal Cell Car­ci­no­mas pla­ce a heavy eco­no­mic bur­den on pu­blic health and pa­tients, their fa­mi­lies and al­so on go­vern­ments. We should all, in­clu­ding the po­licy­ma­kers, ma­ke mo­re ef­fort to un­der­pin the im­por­tan­ce of ef­fi­cient ma­na­ge­ment and pre­ven­tion ef­forts di­rec­ted to­ward this ma­lig­nancy.

In the USA, it has been es­ti­ma­ted that to­tal an­nual NMSC-re­la­ted ex­pen­di­tu­re is US$650 mi­llion, with Me­di­ca­re costs 6–7 ti­mes grea­ter than tho­se for trea­ting me­la­no­ma [ 57]. The analy­ses of a study by Ghent Uni­ver­sity in co­lla­bo­ra­tion with the Foun­da­tion

against can­cer, sho­wed that the to­tal eco­no­mic bur­den of skin can­cer in 2014 in Bel­gium, was es­ti­ma­ted at €103.2 mi­llion. The ma­jo­rity of this to­tal cost was due to Me­la­no­ma skin can­cer re­pre­sen­ting 62% of the costs.

Con­ver­sely costs for the pa­tient we­re hig­her in ca­se of non‐me­la­no­ma skin can­cer. It is es­ti­ma­ted that both pri­mary pre­ven­tion pro­grams (pre­ven­tion cam­paign and ban on sun­bed use), would be cost‐sa­vings. The bud­get im­pact analy­sis re­vea­led that for every eu­ro in­ves­ted in the pre­ven­tion cam­paign, €5.7 would be sa­ved on the long term (over 50 years). Both scree­ning stra­te­gies re­sul­ted in a gain in QALYs* over a pe­riod of 20 years [ 58].

An es­ti­ma­ted 2,846 (5.3%) of the 53,696 newly diag­no­sed ca­ses of ba­sal cell car­ci­no­ma (BCC) and 1,710 (9.2%) of the 18,549 newly diag­no­sed ca­ses of squa­mous cell car­ci­no­ma (SCC) in 2011 in Ca­na­da, we­re at­tri­bu­ta­ble to oc­cu­pa­tio­nal so­lar ra­dia­tion ex­po­su­re. The com­bi­ned to­tal for di­rect and in­di­rect costs of oc­cu­pa­tio­nal NMSC ca­ses is $28.9 mi­llion ($15.9 mi­llion for BCC and $13.0 mi­llion for SCC), and for in­tan­gi­ble costs is $5.7 mi­llion ($0.6 mi­llion for BCC and $5.1 mi­llion for SCC). On a per-ca­se ba­sis, the to­tal costs are $5,670 for BCC and $10,555 for SCC [ 59].

1.5 mi­llion Ca­na­dian wor­kers are ex­po­sed to so­lar UV at work, and ap­pro­xi­ma­tely 900,000 of them spent mo­re than 75% of their work­days out­doors (e.g., cons­truc­tion wor­kers, far­mers, and lands­ca­pers) and ha­ve a high le­vel of ex­po­su­re to so­lar UV ( 60).

The costs re­la­ted to skin can­cer are ad­mit­tedly very high; the most wes­tern coun­tries are fa­cing bud­get de­fi­cit and are ea­ger to cut on health costs. Ri­sing awa­re­ness for pre­ven­tion is less costly and should be worth our at­ten­tion and ef­fort. As it is “Bet­ter to pre­vent that to heal”, it should be crys­tal clear that pre­ven­ting is chea­per that trea­ting. We do not ha­ve anot­her choi­ce to act now as the­se costs could be allo­ca­ted to found mo­re

mo­dern struc­tu­res, to re­form so­cial and edu­ca­tion sys­tems. It is a man­da­te of cons­cien­ce to ha­ve a new vi­sion and to da­ringly ans­wer this call which im­pacts our own daily li­ves and which, at the sa­me ti­me goes be­yond our own boar­ders.

Lung can­cer

Ac­cor­ding to The Ame­ri­can Can­cer So­ciety, es­ti­ma­tion for lung can­cer in the Uni­ted Sta­tes for 2019 will be: about 228,150 new ca­ses of lung can­cer (116,440 in men and 111,710 in wo­men) and about 142,670 deaths from lung can­cer (76,650 in men and 66,020 in wo­men). World­wi­de it is es­ti­ma­ted that the­re we­re 2 093 876 new ca­ses of (ac­coun­ting for 11.6% of all ty­pes can­cer.

In 2018 the Glo­bo­can5 es­ti­ma­ted 1.761007 deaths due to lung can­cer and ac­coun­ting for 18,4% of all can­cer re­la­ted deaths whe­reas for co­lo­rec­tal it was :880.792 (9.2%), 626.679 (6.6%) for breast and 358.989 (3.8%) for pros­ta­te.

Lung can­cer is by far the lea­ding cau­se of can­cer death re­la­ted among both men and wo­men. Each year, mo­re peo­ple die of lung can­cer than of co­lon, breast, and pros­ta­te can­cers com­bi­ned.

The in­ci­den­ce ra­te has been de­cli­ning sin­ce the mid-1980s in men, but only sin­ce the mid-2000s in wo­men, be­cau­se of gen­der dif­fe­ren­ces in his­to­ri­cal pat­terns of smo­king up­ta­ke and ces­sa­tion. From 2005 to 2014, lung can­cer in­ci­den­ce ra­tes de­crea­sed by 2.5% per year in men and 1.2% per year in wo­men.

Lung can­cer im­po­ses a ma­jor di­sea­se bur­den on the world. World­wi­de, lung can­cer re­mains the most com­mon can­cer diag­no­sed and grea­test cau­se of can­cer-re­la­ted death.

Lung can­cer ra­tes vary around the world, re­flec­ting geo­grap­hi­cal dif­fe­ren­ces in to­bac­co use and air qua­lity.

Un­doub­tedly the in­ci­den­ce of lung can­cer has been de­cli­ning due to smo­king ces­sa­tion as re­sult of in­ten­se and strong pre­ven­ti­ve po­licy world­wi­de. un­for­tu­na­tely, the num­ber of ca­ses re­la­ted to en­vi­ron­men­tal fac­tors ex­clu­ding to­bac­co are in the ri­se. Mo­re ef­fort could be ma­de to re­du­ce the im­pact of ot­her fac­tors such as Ra­don and air po­llu­tion to re­du­ce the in­ci­den­ce ra­te of lung can­cer.

Cli­ma­te chan­ge and lung can­cer

En­vi­ron­men­tal risk fac­tors of lung can­cer

Though to­bac­co is con­si­de­red as the lea­ding cau­se of lung can­cer (80%), the fo­cus of lung can­cer in nons­mo­kers is gro­wing, ta­king in­to con­si­de­ra­tion that the­re are ot­her mul­ti­ple risk fac­tors that are associated with lung can­cer. Among the­se risk fac­tors, the­re are ra­don -is the se­cond lea­ding cau­se of lung can­cer-, and air po­llu­tion.

Re­si­den­tial ra­don from soil ac­counts for the se­cond most com­mon risk fac­tor for lung can­cer, ac­coun­ting for ap­pro­xi­ma­tely 10% of the ca­ses [ 61].

Ra­don ex­po­su­re

Ac­cor­ding to the En­vi­ron­men­tal Pro­tec­tion Agency, in the Uni­ted Sta­tes, Co­lo­ra­do is one of the Sta­tes with high re­si­den­tial ra­don con­cen­tra­tions. Con­ver­sely the in­ci­den­ce of lung can­cer was 54.7 ver­sus 67,7 na­tion­wi­de per 100.000. The an­nual death ra­te due to lung can­cer in Co­lo­ra­do (41.8 per 100.000 in the 1998-2002 pe­riod) whi­le the na­tio­nal death ra­te due to lung can­cer was hig­her (55.7%). Are then the risks are men­tio­ned by EPA spe­cu­la­ti­ve? [ 62].

Ever­yo­ne is ex­po­sed to ra­don, but so­me po­pu­la­tions as des­cri­bed in the li­te­ra­tu­re, are at hig­her risk of ex­po­su­re to in­crea­sed ra­don le­vels than ot­hers lea­ding to in­crea­se health risk. Ap­pro­xi­ma­tely 6 mi­llion ho­mes in the Uni­ted Sta­tes ha­ve ra­don le­vels abo­ve 4 pi­co­cu­ries per li­ter (pCi/L), which is the re­me­dia­tion le­vel EPA re­com­mends. ( * ATSDR, 2010). EPA es­ti­ma­tes that at its re­com­men­ded gui­de­li­ne of 4 pCi/L, the risk of de­ve­lo­ping lung can­cer for a li­fe­ti­me ex­po­su­re to ra­don is

• 1% for nons­mo­kers,

• 3% for for­mer smo­kers, and • 5% for smo­kers.

Ch­ro­nic ex­po­su­re to ra­don and his de­cay pro­ducts is a well know and es­ta­blis­hed se­cond lea­ding cau­se of lung can­cer. We know that alp­ha par­ti­cle emis­sions from in­ha­led ra­don

de­cay pro­duct cau­se lung can­cer [63] cau­sing mo­le­cu­lar da­ma­ge lea­ding to DNA mu­ta­tions and chro­mo­so­mal strands breaks (Bo­ris B.M. Me­llo­ni, Eu­ro­pean Res­pi­ra­tory jour­nal 2014 44: 850-852) and the risk for lung can­cer is sig­ni­fi­cantly hig­her for smo­kers than for nons­mo­kers. Mo­re than 85% of ra­don-in­du­ced lung can­cer deaths are among smo­kers.

What is Ra­don?

When you fight an in­vi­si­ble but known enemy, you ha­ve a chan­ce to win a battle even the war, with the right army and stra­tegy. The Chi­ne­se le­gend taught us in the Battle of Wuz­hang Plains, that “A dead Zhu­ge sca­red away a li­ving Zhong­da “. When the­re is an unk­nown enemy, we seat in our com­fort zo­ne and po­si­tion ig­no­ring the dan­ger that looms in the ho­ri­zon. Be­cau­se, un­ders­tan­dably, we do not even know how to fight and whom to fight, even when we ha­ve the best army and stra­tegy. So, know­led­ge and awa­re­ness are key. Kno­wing your enemy, if any, is car­di­nal and reg­nant.

Ra­don is a co­lor­less, odor­less, ra­dio­ac­ti­ve gas which is a brea­king down pro­duct of ra­dio­ac­ti­ve ele­ments, such as ura­nium, which a are found in dif­fe­rent amounts in soil and rock world­wi­de Ra­don gas in the soil and rock can mo­ve in­to the air and in­to un­der­ground wa­ter and surface wa­ter.

The­re is a con­tro­versy as to who dis­co­ve­red ra­don. The dis­co­very of Ra­don was alle­gedly, wrongly at­tri­bu­ted to the Ger­man phy­si­cist Frie­drich Ernst Dorn, (1848-1916), Pro­fes­sor from Frie­drichs Uni­ver­sihit, Ha­lle (Saa­le), whe­reas Er­nest Ruthr­hord (1871-1937), Pro­fes­sor of McGill Uni­ver­sity from Mon­treal, Ca­na­da seems to be the dis­co­ve­rer. Rut­her­ford first cha­rac­te­ri­zed ema­na­tion of a ra­don iso­to­pe (from tho­rium) as a gas and an ele­ment and should be cre­di­ted with the dis­co­very of ra­don. Dorn was the first to ob­ser­ve ema­na­tion from ra­dium spe­ci­fi­cally (the ety­mo­lo­gi­cal sour­ce of the na­me “ra­don”), but his ob­ser­va­tions we­re sub­se­quent to Rut­her­ford’s work [ 64]. Two of ra­don’s iso­to­pes* (ra­don-220 and ra­don-222) are pro­geny in two de­cay chains that be­gin with na­tu­rally oc­cu­rring tho­rium and ura­nium, res­pec­ti­vely, in rock, soil, wa­ter, and air. It is an inert gas of 86 with a mass of the most sta­ble iso­to­pe of 222. It is che­mi­cally an inac­ti­ve gas and is 7.6 ti­mes hea­vier than air and could readily be dis­sol­ved in wa­ter; slightly aci­dic and poor in mi­ne­ral, al­cohol and fatty acids. It emits alp­ha ra­dia­tion [ 65].

Ra­don breaks down in­to so­lid ra­dio­ac­ti­ve ele­ments ca­lled ra­don pro­geny* (such as po­lo­nium-218, po­lo­nium-214, and lead-214). Ra­don pro­geny can at­tach to dust and ot­her par­ti­cles and can be

breat­hed in­to the lungs. As ra­don and ra­don pro­geny in the air break down, they gi­ve off ra­dia­tion that can da­ma­ge the DNA inside the body’s cells. (Being ex­po­sed to ra­don for a long pe­riod of ti­me can lead to lung can­cer. Ra­don gas in the air breaks down in­to tiny ra­dio­ac­ti­ve ele­ments (ra­don pro­geny) that can lod­ge in the li­ning of the lungs, whe­re they can gi­ve off ra­dia­tion. This ra­dia­tion can da­ma­ge lung cells and even­tually lead to lung can­cer [ 40].

Ra­don is pre­sent not only out­doors but al­so in­doors. It is nor­mally found at very low le­vels in out­door air and in drin­king wa­ter from ri­vers and la­kes. It can be found at hig­her le­vels in the air in hou­ses and ot­her buil­dings, as well as in wa­ter from un­der­ground sour­ces, such as well wa­ter. When in­ha­led in­to the lung, alp­ha par­ti­cles emit­ted by shortli­ved de­cay pro­ducts of ra­don can da­ma­ge ce­llu­lar DNA. Ce­llu­lar mu­ta­ge­ne­sis stu­dies, ex­pe­ri­men­tal re­search in ani­mals, and oc­cu­pa­tio­nal epi­de­miolo­gic stu­dies ha­ve es­ta­blis­hed ra­don as a hu­man lung car­ci­no­gen [ 66].

Con­cen­tra­tion of ra­don are low out­doors but could be high in­doors spe­cially in ho­me. Ur­ban areas trends to ha­ve mo­re lo­wer ra­don con­cen­tra­tions than ru­ral ones as the un­derl­ying rock is usually

The nor­mal do­se of ra­don in the US is es­ta­blis­hed at 4 pi­co­cu­ries

Stu­dies ha­ve sho­wed that the­re is a sy­ner­gis­tic ef­fect bet­ween ra­don and to­bac­co smoke [ 67]. The­se stu­dies we­re con­duc­ted in Eu­ro­pe among 150 peo­ple with lung can­cer and 150 con­trol group in­cor­po­ra­ted de­tai­led smo­king his­tory and ra­don ex­po­su­re.

The U.S. En­vi­ron­men­tal Pro­tec­tion Agency (US EPA) and the Sur­geon Ge­ne­ral’s Of­fi­ce ha­ve es­ti­ma­ted that as many as 20,000 lung can­cer deaths are cau­sed each year by ra­don. Ra­don is the se­cond lea­ding cau­se of lung can­cer. Ra­don-in­du­ced lung can­cer costs the Uni­ted Sta­tes over $2 bi­llion do­llars per year in both di­rect and in­di­rect health ca­re costs.

Ra­don is the lea­ding en­vi­ron­men­tal cau­se of mor­ta­lity re­la­ted to can­cer. Ra­don in­du­ced lung mor­ta­lity is se­venth lea­ding cau­se of can­cer mor­ta­lity in the US,

In 1986 En­vi­ron­men­tal and pro­tec­tion agency (EPA) and the de­part­ment of health a and hu­man ser­vi­ces re­com­men­ded ra­don scree­ning for most ho­mes in the USA. In 1992 the re­com­men­da­tion was amen­ded re­qui­ring a dou­ble stra­tegy for mea­su­ring re­si­den­tial ra­don. First short-term mea­su­re­ment fo­llo­wed by a con­fir­ma­tory mea­su­re­ment if the scree­ning mea­su­re­ment was 4 pCi/L or grea­ter. The num­ber of pre­ven­ta­ble lung can­cer by the first scree­ning is es­ti­ma­ted to be 811 and by the se­cond scree­ning 527 [ 68]. But what has Ra­don to do with cli­ma­te chan­ge? Again, know your enemy and de­fi­ne align the stra­te­gies.

Cli­ma­te chan­ge is lea­ding to lon­ger spring and fall, and the sum­mer are ac­com­pa­nied with hit wa­ves which is in­dispu­tably ha­ving im­pact on in­door air ex­chan­ge.

Cli­ma­te chan­ge is un­doub­tedly af­fec­ting de­po­si­tio­nal en­vi­ron­ment wit­hin ho­me that is im­pact in do­se of ra­don de­cay pro­duct in ho­mes [ 69]. The do­se of Ra­don and his de­cays is im­pac­ted by the buil­ding ven­ti­la­tion ra­te.

To all ap­pea­ran­ces, ex­po­su­re risk sce­na­rio to ra­don is chan­ging as re­sult of cli­ma­te chan­ge. Cu­rrently buil­dings are bet­ter sea­led to ma­ke them mo­re energy ef­fi­cient to mi­ti­ga­te the cli­ma­te chan­ges ef­fects. The in­door con­cen­tra­tion of ra­don is un­de­via­tingly in­crea­sing with sea­led buil­ding. Coun­tries as US and UK ha­ve Ra­don mi­ti­ga­tion de­sign stan­dards and buil­dings co­des used for de­sign and cons­truc­tion of buil­dings whe­reas so­me ot­her coun­tries which are hea­vily con­fron­ted with cli­ma­te chan­ges ef­fects / New Zea­land and Aus­tra­lia-, do not ha­ve [ 70].

The in­crea­sed use of cei­ling fans for co­oling could im­pact the do­se of ra­don de­cay pro­ducts lea­ding to a re­du­ce do­se of ra­don to the lung [ 71].

Con­tra­rily, the use of air con­di­tio­ning may re­du­ce the use of cei­ling fans and the­re­fo­re en­han­ce the de­li­ve­red do­se by ra­don pro­geny.

The di­rect mea­su­re­ment of the do­se ra­tes pro­du­ced by ra­don pro­geny in air is hardly pos­si­ble in ra­don at­mosp­he­res with high ac­ti­vity con­cen­tra­tions, be­cau­se the ma­jor con­tri­bu­tion of mea­su­red do­se ra­tes is pro­du­ced by ra­don pro­geny on the hou­sing of the do­se ra­te ins­tru­ments. The ef­fect of the ra­don ef­fect lar­gely de­pends on the abi­lity of sur­fa­ces to ab­sorb ra­don pro­geny [ 72].

Most li­kely, the use of air con­di­tio­ning due to in­crea­se hit wa­ve will cau­se hig­her ra­don con­sul­ting as a re­sult of de­crea­se air ex­chan­ge ra­tes, par­ti­cu­larly in tightly sea­led ho­mes. Con­se­quently the use of AC will be lon­ger and will crea­te a clo­se hou­se con­di­tion (EPA).

It is re­por­ted that the con­cen­tra­tion of Ra­don in hig­her in the ba­se­ment than in ot­her rooms. In­crea­se tem­pe­ra­tu­re will in­crea­se the po­ten­tial to mo­ve to co­oler pla­ces in the hou­se whe­re the ra­don ex­po­su­re is hig­her (ba­se­ment). This was de­mons­tra­ted in a re­tros­pec­ti­ve study among wo­men in Io­wa [ 73].

Lo­ca­tions such as ho­mes, schools or of­fi­ce buil­ding ha­ve ge­ne­rally hig­her con­cen­tra­tion of Ra­don than out­door, es­pe­cially in new buil­dings which are mo­re energy ef­fi­cient

Cli­ma­te chan­ge re­la­ted fac­tors, such as high tem­pe­ra­tu­re, rain­fall. would irre­fu­tably in­fluen­ce ra­don ex­po­su­re. In­crea­se rain­fall as ob­ser­ved re­cently, will in­crea­se ra­don ema­na­tion by cap­ping the soil out­door and di­rec­ting it to­ward the un­sa­tu­ra­ted soil near or

un­der hou­se. In ca­se the soil are not sa­tu­ra­ted low and mo­de­ra­te le­vels of soil mois­tu­re pro­vi­de a grea­ter ra­don sour­ce that can en­ter through the ho­les in the buil­dings.

In all li­ke­lihood, the pri­mary weat­her fac­tors in­fluen­cing soil-gas ra­don con­cen­tra­tions are pre­ci­pi­ta­tion and ba­ro­me­tric pres­su­re, with les­ser ef­fects at­tri­bu­ted to tem­pe­ra­tu­re and, pos­sibly, wind. The cha­rac­ters and com­po­si­tion of the soil are highly sig­ni­fi­cant in de­ter­mi­ning the mag­ni­tu­de and ex­tent of the soil’s res­pon­se to weat­her chan­ge. Ob­viously me­teo­ro­lo­gi­cal con­di­tions ha­ve a mar­ked ef­fect on ra­don trans­port in soils. Of all na­tu­ral oc­cu­rren­ces, the most im­por­tant fac­tors ap­pear to be pre­ci­pi­ta­tion -by af­fec­ting soil mois­tu­re con­di­tions-, and ba­ro­me­tric pres­su­re. To less ex­tend, tem­pe­ra­tu­re and wind ha­ve less im­pact­ful ef­fects, and the­re are con­flic­ting ob­ser­va­tions in the li­te­ra­tu­re con­cer­ning the­se fac­tors.

De­ter­mi­ning the in­fluen­ce of in­di­vi­dual weat­her fac­tors and their ef­fects on ra­don mi­gra­tion and con­cen­tra­tion in soils could be os­ten­sibly com­pli­ca­ted for the sim­ple reason that se­ve­ral weat­her fac­tors are chan­ge cons­tantly. For exam­ple, storms are ge­nui­nely associated with pre­ci­pi­ta­tion, lo­wer ba­ro­me­tric pres­su­re, lo­wer tem­pe­ra­tu­res and of­ten­ti­mes, wind. Com­pa­ring plots of the­se fac­tors with soil-gas ra­don con­cen­tra­tions would be help­ful to lead to the con­clu­sion that all of the­se fac­tors cau­se soil-gas ra­don con­cen­tra­tions to in­crea­se [ 74].

It is com­monly ac­cep­ted now that we should re­du­ce our energy con­sum­ption to mi­ti­ga­te the re­lea­se of green­hou­se ga­ses. This ob­ser­va­tion leads pri­ma fa­cie to the buil­ding of energy ef­fi­ciency hou­ses. No­net­he­less the­se new hou­ses, which are mo­re toughly sea­led, are allo­wing ra­don gas to build up to grea­ter de­gree. This dou­ble-ed­ged sword needs to be ap­proa­ched and hand­le cau­tiously to fi­nd the midd­le way. For exam­ple, by re­gu­lar mea­su­re­ment of ra­don.

Re­si­den­tial ra­don is res­pon­si­ble for 10-15% of the 157.400 lung can­cer death oc­cu­rring an­nually in the US [ 75]. Stu­dies (in­clu­ding 7148 peo­ple with lung can­cer and 14 208 con­trol. Among con­trols, the per­cen­ta­ge who we­re li­fe­long non-smo­kers in­crea­sed as ra­don con­cen­tra­tion in­crea­sed. The avai­la­ble ra­don mea­su­re­ments co­ve­red a mean of 23 years show ap­pre­cia­ble ha­zards from re­si­den­tial ra­don, par­ti­cu­larly for smo­kers and re­cent ex-smo­kers, and in­di­ca­te that it is res­pon­si­ble for about 2% of all deaths from can­cer in Eu­ro­pe [ 76].

Ra­don is pre­sent in ho­mes. Ac­cor­ding to a re­port from EPA from 1994 ra­don en­ters our hou­se by dif­fe­rent rou­tes:

• The ra­don con­tent of the soil

• The dif­fe­ren­ce in pres­su­re bet­ween the in­te­rior of the ho­me and the soil

• The air ex­chan­ge ra­te in the ho­me

• The mois­tu­re con­tent su­rroun­ding the ho­me

• The pre­sen­ce and si­ze of entry rou­tes

As known all the­se 5 fac­tors could be af­fec­ted by cli­ma­te chan­ge.

Ra­don con­tent of the soil and cli­ma­te chan­ge.

High energy costs and cli­ma­te-chan­ge mi­ti­ga­tion ef­forts are crea­ting pres­su­res to de­crea­se ven­ti­la­tion ra­tes in buil­dings as a means of re­du­cing the energy used to co­ol or warm in­door air.

The Wa­tras in­ci­dent :

On December 2, 1984, a ca­se of Stan­ley. J Wa­tras, a cons­truc­tion en­gi­neer at the Li­me­rick nu­clear po­wer in Pot­ts­town in Pennsyl­va­nia, gai­ned na­tio­nal in­ter­est. A ra­dia­tion mo­ni­tor was ins­ta­lled at the plant which was still un­der cons­truc­tion, to en­su­re that wor­kers we­re not ac­ci­dently ex­po­se to un­sa­fe and to­xic ra­dia­tion le­vels from the plant. One day, Stan­ley Wa­tras en­te­red the plant and set off the ra­dia­tion alarm. He has a high le­vel of ra­dia­tion alt­hough the plant was still in cons­truc­tion and was not yet fi­lled with nu­clear fuel yet. The ori­gin of mis­ter Wa­tras ra­dia­tion was a co­nun­drum. La­ter a team of spe­cia­list re­lie­vedly dis­co­ver that Wa­tras was not pic­king up the ra­dia­tion at the plant but from his hou­se whe­re the le­vel of ra­don was 700 ti­mes hig­her than the ma­xi­mum le­vel con­si­de­red safe [ 77].

The in­ter­na­tio­nal Agency for Re­search on Can­cer has clas­si­fied 4 groups of agents ac­cor­ding to their ha­zar­dous car­ci­no­ge­nic ef­fect to hu­mans.

• Group 1: Car­ci­no­ge­nic to hu­mans: 120 agents

• Group 2A: Pro­bably car­ci­no­ge­nic to hu­mans: 82 agents

• Group 2B: Pos­sibly car­ci­no­ge­nic to hu­mans: 311 agents

• Group 3: Not clas­si­fia­ble as to its car­ci­no­ge­ni­city to hu­mans: 499 agents • Group 4: Pro­bably not car­ci­no­ge­nic to hu­mans: 1 agent

Ra­don is a class 1 car­ci­no­gen, which means that the evi­den­ces are strong that it cau­ses can­cer. Most peo­ple do not know that ra­don is the se­cond lea­ding cau­se of lung can­cer in the Uni­ted Sta­tes, re­sul­ting in ap­pro­xi­ma­tely 21,000 lung can­cer deaths in the US each year and 11.000 deaths in UK.

The­re are ot­her cli­ma­te chan­ge re­la­ted fac­tors which could lead to lung can­cer. High le­vels of in­door air po­llu­tion and fi­ne par­ti­cu­la­tes may in­crea­se the risk of lung can­cer. In­crea­sed pre­ci­pi­ta­tion or floo­ding has the po­ten­tial to in­crea­se the re­lea­se of to­xic che­mi­cal and heavy me­tal lea­ching from sto­ra­ge si­tes. Ex­po­su­re to che­mi­cals that are pre­sent in the en­vi­ron­ment may al­so in­crea­se, if ru­noff en­ters the wa­ter supply.

It is no se­cret at all, that cli­ma­te chan­ge has cau­sed last years an in­crea­se of am­bient tem­pe­ra­tu­res that we will wit­ness mo­re fre­quently in the near fu­tu­re. As re­sult, the trans­fer of vo­la­ti­le and se­mi-vo­la­ti­le com­pounds from wa­ter and was­te will in­crea­se, al­te­ri­ng the dis­tri­bu­tion of con­ta­mi­nants to pla­ces mo­re dis­tant from the sour­ces, chan­ging sub­se­quent hu­man ex­po­su­res [ 78].

Air po­llu­tion and can­cer :

“Every breath you ta­ke con­tains atoms for­ged in the blis­te­ri­ng fur­na­ces deep inside stars [ 79].

In the mor­ning of December 1952, re­si­dent of Lon­don wo­ke up with a fog which en­ve­lo­ped all Lon­don and re­si­dents did not gi­ve too much at­ten­tion to the fog as it hap­pe­ned every now and then. But over the cour­se of few days the con­di­tions de­te­rio­ra­ted lea­ding to the death of initially thought 4000, and la­ter ad­jus­ted to 12.000 and the hos­pi­ta­li­za­tion of 150.000 peo­ple. Sup­po­sedly, the fog could ha­ve been cau­se by emis­sions from coal burning. This fog has led to the he pas­sa­ges of the Clean Air Act in 1956. But the ori­gin and ex­pla­na­tion of this 5 days black smog re­mai­ned for years a mystery. It is only in 2016 that a team of re­sear­chers has de­cip­he­red the mystery through la­bo­ra­tory ex­pe­ri­ments and at­mosp­he­ric mea­su­re­ments in Chi­na, as sul­fa­te I big con­tri­bu­tor to the smog, sul­fu­ric acid par­ti­cles we­re for­med from sul­fur dio­xi­de re­lea­sed by coal burning for re­si­den­tial use and po­wer plants, and ot­her means. sul­fur dio­xi­de was tur­ned in­to sul­fu­ric acid. The re­sults from this team sho­wed that this pro­cess was fa­ci­li­ta­ted by ni­tro­gen dio­xi­de, anot­her co-pro­duct of coal burning. Anot­her key as­pect in the con­ver­sion of sul­fur dio­xi­de to sul­fa­te is that it pro­du­ces aci­dic par­ti­cles, which sub­se­quently in­hi­bits this pro­cess. Na­tu­ral fog con­tai­ned lar­ger par­ti­cles of se­ve­ral tens of mi­cro­me­ters in si­ze, and the acid for­med was suf­fi­ciently di­lu­ted. Eva­po­ra­tion of tho­se fog par­ti­cles, then left sma­ller aci­dic ha­ze

par­ti­cles that co­ve­red the city”. This hap­pe­ned re­cu­rrently in chi­na. The study shows that si­mi­lar che­mistry oc­curs fre­quently in Chi­na, which has battled air po­llu­tion for de­ca­des. “The dif­fe­ren­ce in Chi­na is that the ha­ze starts from much sma­ller na­no­par­ti­cles, and the sul­fa­te for­ma­tion pro­cess is only pos­si­ble with am­mo­nia to neu­tra­li­ze the par­ti­cles [ 80].

In the on­li­ne ver­sion of the in­de­pen­dent from 25 Fe­bruary 2016 Fio­na Os­gun won­de­red: “Air Po­llu­tion; How strong is the link to can­cer? [ 81]. She ba­sed her ar­ti­cle on the re­port of the Ro­yal College of Phy­si­cians and the Ro­yal College of Pae­dia­trics and Child Health form the Ro­yal Phy­si­cians high­ligh­ting the ro­le of air po­llu­tion. About eight in every 100 ca­ses of lung can­cer each year in the UK are at­tri­bu­ta­ble to PM2.5 air po­llu­tion ex­po­su­re, which is equal to ap­pro­xi­ma­tely 3,500 peo­ple. We do not know, ac­cor­ding to the re­port, how the par­ti­cu­la­te mat­ters exactly af­fect the lungs but the good thing is that they ha­ve sug­ges­ted se­ve­ral steps to coun­te­ract, rat­her re­du­ce the in­ci­den­ce of di­sea­ses cau­sed by air po­llu­tion.

We dis­cus­sed ear­lier the im­pact of cli­ma­te chan­ge on health. Ne­vert­he­less, it is worthw­hi­le to men­tion that the­re are mo­re fac­tors lea­ding un­ques­tio­nably to cli­ma­te chan­ge and glo­bal war­ming that are at the sa­me ti­me ha­ving an im­pact on health. Among the­se fac­tors, we could un­mis­ta­kably no­tify air po­llu­tant by dif­fe­rent subs­tan­ces that are re­lea­sed in the air daily due to our daily ac­ti­vi­ties. Polycy­clic aro­ma­tic hy­dro­car­bon(PAH) is among them.

Polycy­clic aro­ma­tic hy­dro­car­bons are pro­du­ced from the in­com­ple­te com­bus­tion of or­ga­nic ma­te­rial. They are a class of che­mi­cals that oc­cur na­tu­rally in coal, cru­de oil, and ga­so­li­ne. They al­so are pro­du­ced when coal, oil, gas, wood, gar­ba­ge, and to­bac­co are bur­ned. PAHs ge­ne­ra­ted from the­se sour­ces can bind to or form small par­ti­cles in the air (EPA).

Their pre­sen­ce in the air we breat­he has been sig­ni­fi­cant du­ring the past cen­tu­ries due to emis­sions from in­dus­trial pro­ces­ses and energy pro­duc­tion, mo­tor vehi­cu­lar traf­fic and re­si­den­tial hea­ting.

Air po­llu­tion plays an im­por­tant ro­le in the pro­cess of cli­ma­te chan­ge.

IARC re­por­ted that air po­llu­tants be­ca­me a car­ci­no­ge­nic agent sin­ce 2013. Many com­po­nents of air po­llu­tants are die­sel en­gi­ne ex­haust, sol­vent me­ta and dust and im­por­tantly Par­ti­cu­la­te mat­ter- in­clu­ding ex­tre­mely small so­lid par­ti­cles and li­quid dro­plets-, that are for­med in the air which in­crea­se the risk on lung can­cer.

Ac­cor­ding to the re­port from the wor­king party of Ro­yal college Phy­si­cians and the Ro­yal College of Pae­dia­trics and Child Health pu­blis­hed in 2016 and title Every breath you ta­ke, the li­fe­long im­pact of air po­llu­tion, the­re was 3.2 mi­llion deaths among them 223.00 lung can­cer. The re­port is ba­sed on the re­view of mo­re than 1000 scien­ti­fic pa­pers from stu­dies on dif­fe­rent con­ti­nents. From this analy­sis, it could be con­clu­ded that can­cer risks cau­sed by va­rious po­llu­tants pre­sent in out­door air po­llu­tion and par­ti­cu­larly par­ti­cu­la­te mat­ter and trans­por­ta­tion re­la­ted. It was a lar­ge epi­de­miolo­gic study that in­clu­ded mi­llions li­ving in Eu­ro­pe, Ame­ri­ca and Asia. It is evi­dently es­ta­blis­hed that the pre­do­mi­nant ar­ti­fi­cial cau­se of out­door po­llu­tion is trans­por­ta­tion and sta­tio­nary po­wer.

Long-term ex­po­su­re to out­door air po­llu­tion cau­sed the equi­va­lent of ap­pro­xi­ma­tely 29,000 deaths in 2008 in the UK.40. 000 deaths oc­cur each year due to ex­po­su­re on po­llu­tion. We are ex­po­sed to this da­ma­ge du­ring our en­ti­re li­fe­ti­me from first of the baby in the womb through to the years of ol­der age[ 82].

Par­ti­cu­la­te mat­ters; si­ze de­fi­ni­tely mat­ters!

Par­ti­cu­la­te mat­ter of PM are tiny dust-li­ke par­ti­cles just mi­llionths of a me­ter wi­de In par­ti­cu­lar, the sma­llest par­ti­cles ­­— less than 2.5 mi­llionths of a me­ter across, known as PM2.5 ­— ap­pear to be behind lung can­cers cau­sed by po­llu­tion.

Asia is con­si­de­red as one of the con­ti­nents whe­re the emis­sions of PAH is the hig­hest. The an­nual PAH emis­sion is 290.000 to­nes — in Chi­na with 114.000 tons per year fo­llo­wed by In­dia with 90.000 per year —, which re­pre­sents 55% of the glo­bal emis­sions whe­reas the emis­sions in the US is cal­cu­la­ted to be 32.000 tons per year. Eu­ro­pean coun­tries ac­count for only 9.5% of the to­tal PAH emis­sions an­nually [ 83].

The emis­sions from PAH and their car­ci­no­ge­nic ef­fect on hu­man health, are be­co­ming mo­re and mo­re stu­died. The­re are about 500 dif­fe­rent PAH which ha­ve been found in air. Ne­vert­he­less ben­zopy­re­ne, as the re­pre­sen­ta­ti­ve of the who­le PAH, is the most stu­died and do­cu­men­ted.

PAH ha­ve dif­fe­rent ori­gins. In­dus­trial and mo­bi­les such as from vehi­cles.

In­dus­trial pro­cess such as coal coc­king and oil re­fi­ning lead to the re­lea­se of PAH. Ac­cor­ding to Co­ri­nair [ 84], in­dus­trial sour­ces of PAH con­tri­bu­tes as much as mo­bi­les sour­ces. The con­tri­bu­tion of mo­tor vehi­cles, though sig­ni­fi­cant in the past, is being re­du­ced by the

in­tro­duc­tion of th­ree con­ver­ters in cars. In the past and wit­hout con­ver­ters, the emis­sions we­re 5-10 ti­mes hig­her than in mo­dern cars.

Com­pe­lling da­ta ha­ve sho­wed the mu­ta­ge­nic ef­fect of PAH by cau­sing the mu­ta­tion of P53 tu­mor sup­pres­sor that is one of the mu­ta­ted ge­nes in hu­man lung can­cer [ 85].

Peo­ple ta­ke thou­sands of breaths daily, lea­ding to a to­tal in­ta­ke of about 10 000 li­ters of air per day. Lungs re­cei­ve the most subs­tan­tial in­ha­led do­ses.

Air po­llu­tion is associated with the oc­cu­rren­ce of dif­fe­rent ty­pes of can­cer. Lung can­cer, again, is the most wi­des­pread and stu­died. Re­sear­chers from Hong Kong and Bir­ming­ham con­duc­ted a study that in­clu­ded 66280 re­si­dents from Hong Kong aged ol­der than 65 years, who we­re re­crui­ted bet­ween 1998 and 2001 and fo­llo­wed up till 2011. An­nual con­cen­tra­tions of PM 25 at their hou­se we­re mea­su­red using sa­te­lli­te and fi­xed mo­ni­tors da­ta. The study de­mons­tra­ted that for every 10 mi­cro­gram per cu­bic me­ter of in­crea­se ex­po­su­re to PM25, the risks of dying from any can­cer was 22% hig­her, and 42% for di­ges­ti­ve can­cer. Mor­ta­lity due to lung can­cer was 36% hig­her. The in­crea­se was at­tri­bu­ta­ble to air po­llu­tion [ 86].

In 2015 out­door air po­llu­tion ki­lled 4.2 mi­llion peo­ple, among them 42% we­re due to lung can­cer and ot­her res­pi­ra­tory di­sea­se. PM2.5 air po­llu­tion is res­pon­si­ble for up to 16.5 % of the es­ti­ma­te 1.7 mi­llion lung ca­ner deaths world­wi­de.

Am­bient PM2.5 was the fifth ran­king mor­ta­lity risk in 2015. Ex­po­su­re to it was res­pon­si­ble for 4.2 mi­llion deaths and 103 di­sa­bi­lity ad­jus­ted li­ve years in 2015,( in 1990 3.5 mi­llions) re­pre­sen­ting 7.6% of to­tal glo­bal deaths.59% of the­se we­re is Asia [ 87].

Anot­her study in­ves­ti­ga­ted the as­so­cia­tion bet­ween long term am­bient PM2,5 con­cen­tra­tions and lung can­cer among 188.699 li­fe long ne­ver smo­kers from the 12 mi­llion can­cer pre­ven­tion study par­ti­ci­pants en­ro­lled by the Ame­ri­can Can­cer So­ciety in 1982 and fo­llo­wed up pros­pec­ti­vely through 2008. 1100 lung can­cer deaths we­re ob­ser­ved du­ring 26 years fo­llow up pe­riod. Each 10 mi­cro­gram per me­ter cu­be in­crea­se in PM2.5 con­cen­tra­tions we­re associated with 15-27% in­crea­se in lung can­cer mor­ta­lity [ 88].

Ad­di­tio­nally, an analy­sis of the Har­vard six ci­ties study which en­ro­lled 8096 peo­ple­fo­llo­wing ci­ties: Wa­ter­town, MA; Kings­ton and Ha­rri­man, TN; St. Louis, MO; Steu­ben­vi­lle, OH; Por­ta­ge, Wyo­ce­na, and Par­dee­vi­lle, WI; and To­pe­ka, KS. Par­ti­ci­pants we­re re­crui­ted bet­ween 1974 and 1977 -, mo­ni­to­red for 14 to 16 yr du­ring the 1970s and 1980s found al­so a po­si­ti­ve as­so­cia­tion bet­ween PM 2.5 and lung can­cer mor­ta­lity. The mor­ta­lity ra­te ra­tio (RR) was 1.13 (95% con­fi­den­ce in­ter­val [CI], 1.04–1.73) for each 10-μg/m3 in­crea­se in city-spe­ci­fic PM2.5 con­cen­tra­tions.

The­re we­re 104,243 per­son-15 years of fo­llow-up and 1,364 deaths bet­ween 1974 and 1989 (Pe­riod 1) and an ad­di­tio­nal 54,735 per­son-8 years of fo­llow-up and 1,368 deaths bet­ween 1990 and 1998 (Pe­riod 2; Ta­ble 1). The ove­rall death ra­te was 13.1 deaths per 1,000 per­son-years in Pe­riod 1 and 25.0 in Pe­riod 2, re­flec­ting the aging of this cohort. As in pre­vious analy­ses, cru­de mor­ta­lity ra­tes we­re hig­hest in Steu­ben­vi­lle and St. Louis. Con­clu­si­vely they found lung can­cer mor­ta­lity po­si­ti­vely associated with ave­ra­ge PM2.5.

The es­ti­ma­ted ef­fect of par­ti­cu­la­te air po­llu­tion has been shown to in­crea­se as lon­ger ex­po­su­re pe­riods (up to 7 weeks) are con­si­de­red, in­di­ca­ting ex­po­su­res in the month(s) be­fo­re death may be im­por­tant.

Ex­po­su­re to PM2.5 was sta­tis­ti­cally sig­ni­fi­cantly associated with deaths due to car­dio­vas­cu­lar di­sea­se, and the as­so­cia­tion with lung can­cer mor­ta­lity was of bor­der­li­ne sig­ni­fi­can­ce. The num­ber of non­ma­lig­nant res­pi­ra­tory deaths was small (alt­hough com­pa­ra­ble to num­bers for lung can­cer), but the PM2.5-associated risk was po­si­ti­ve, alt­hough weak [ 89].

The analy­sis is ba­sed on da­ta co­llec­ted by the Ame­ri­can Can­cer So­ciety (ACS) as part of the Can­cer Pre­ven­tion Study II (CPS-II), an on­going pros­pec­ti­ve mor­ta­lity study of ap­pro­xi­ma­tely 1.2 mi­llion adults. Par­ti­ci­pants re­si­ded in all 50 sta­tes, the District of Co­lum­bia, and Puer­to Ri­co, and we­re ge­ne­rally friends, neigh­bors, or ac­quain­tan­ces of ACS vo­lun­teers. En­roll­ment was res­tric­ted to per­sons who we­re aged 30 years or ol­der and who we­re mem­bers of hou­seholds with at least 1 in­di­vi­dual aged 45 years or ol­der. This study de­mons­tra­ted as­so­cia­tions bet­ween am­bient fi­ne par­ti­cu­la­te air po­llu­tion and ele­va­ted risks of both car­dio­pul­mo­nary and lung can­cer mor­ta­lity. Each 10-μg/m3 ele­va­tion in long-term ave­ra­ge PM2.5 am­bient con­cen­tra­tions was associated with ap­pro­xi­ma­tely a 4%, 6%, and 8% in­crea­sed risk of all-cau­se, car­dio­pul­mo­nary, and lung can­cer mor­ta­lity, res­pec­ti­vely, the es­ti­ma­ted po­llu­tion ef­fect on both car­dio­pul­mo­nary and lung can­cer mor­ta­lity was stron­gest for ne­ver smo­kers vs for­mer or cu­rrent smo­kers [ 90].

The­re was al­so a po­si­ti­ve as­so­cia­tion found bet­ween mea­su­re of black smoke con­cen­tra­tions and traf­fic in­ten­sity and lung can­cer in­ci­den­ce in 40.114 ne­ver smo­kers par­ti­ci­pants in the Net­her­lands cohort study on diet and can­cer a to­tal of 252 lung can­cer ca­ses we­re ob­ser­ved in the 11 years fo­llow up ti­me pe­riod [ 91]. In this study da­ta from on­going Diet and can­cer study, in which 120.852 sub­jects , aged bet­ween 55 and 69 years old li­ving in 204 mu­ni­ci­pa­li­ties th­roug­hout the country-,we­re in­clu­ded , we­re used. Ex­po­su­re to black smoke, ni­tro­ge­ne dio­xi­de (No2), sul­fur dio­xi­de (SO2) and PM2.5 and traf­fic va­ria­bles we­re analy­zed. The fo­llow up was 11.3 years.

90% of par­ti­ci­pants ha­ve li­ved 10 years of lon­ger in their 1986 mu­ni­ci­pa­lity. Du­ring 11,3 years of fo­llow up, 2183 lung can­cer ca­ses we­re re­por­ted. Black smoke ave­ra­ge con­cen­tra­tion was 16.8, 16.6 and 16.3 mi­cro­gram per me­ter cu­be for cu­rrent, ex and ne­ver smo­kers res­pec­ti­vely. The as­so­cia­tion was strong among ne­ver smo­kers whe­reas no as­so­cia­tion was found among the smo­kers.

In many parts of the world, mo­ni­to­ring sys­tems for air po­llu­tants ha­ve been ins­ta­lled, usually wit­hin the fra­me­work of go­vern­men­tal re­gu­la­tory pro­grams. The ol­der and most ex­ten­si­ve of the­se are in North Ame­ri­ca and the Eu­ro­pean Union. The po­llu­tants most fre­quently mo­ni­to­red are:

The ga­ses: sul­fur dio­xi­de (SO2), ni­tro­gen

The PM in­di­ca­tors: to­tal sus­pen­ded par­ti­cles, black smoke, PM [ 92].

Ac­cor­ding to the World health Or­ga­ni­za­tion, the air we breat­he is la­ced with can­cer-cau­sing subs­tan­ces and is being of­fi­cially clas­si­fied as car­ci­no­ge­nic.

The In­ter­na­tio­nal Agency for Re­search on Can­cer (IARC) ci­ted da­ta in­di­ca­ting that in 2010, 223,000 deaths from lung can­cer world­wi­de re­sul­ted from air po­llu­tion, and inexo­rably con­clu­ded the­re was al­so con­vin­cing evi­den­ce it in­crea­ses the risk of blad­der can­cer.

The­re­fo­re, it is of sig­ni­fi­cant im­por­tan­ce to mo­ni­tor and as­sess the im­pact of air po­llu­tion wit­hin a fra­me­work with clear ob­jec­ti­ves.

The­re are se­ve­ral pro­jects which ha­ve been put in pla­ce to in­ves­ti­ga­te the ef­fects of air po­llu­tant on health. Exam­ples of such pro­jects in Eu­ro­pe are:

The Air Po­llu­tion Ex­po­su­re of Adult Ur­ban Po­pu­la­tions in Eu­ro­pe Study (EXPOLIS), Eu­ro­pean mul­ti­cen­ter study for mea­su­re­ment of air po­llu­tion ex­po­su­res of wor­king age ur­ban po­pu­la­tion du­ring work­days. The se­lec­ted ur­ban areas are At­hens, Ba­sel, Gre­no­ble, Hel­sin­ki, Mi­lan and Pra­gue. The main ob­jec­ti­ves of EXPOLIS are: - To as­sess the ex­po­su­res of Eu­ro­pean ur­ban po­pu­la­tions to ma­jor air po­llu­tants. - To analy­se the per­so­nal and en­vi­ron­men­tal de­ter­mi­nants and in­ter­re­la­tions­hips to the­se ex­po­su­res. - To de­ve­lop an Eu­ro­pean da­ta­ba­se for si­mu­la­tion of air po­llu­tion ex­po­su­res.

The Ex­po­su­re and Risk As­sess­ment for Fi­ne and Ul­tra­fi­ne Par­ti­cles in Am­bient Air Study (UL­TRA). It is a Eu­ro­pean co­lla­bo­ra­ti­ve pro­ject which aims to im­pro­ve know­led­ge on

hu­man ex­po­su­re to am­bient air par­ti­cu­la­te mat­ter of dif­fe­rent si­zes and dif­fe­rent che­mi­cal com­po­si­tion in Eu­ro­pe, and to eva­lua­te the associated health risks.

The Re­la­tions­hip bet­ween Ul­tra­fi­ne and Fi­ne Par­ti­cu­la­te Mat­ter in In­door and Out­door Air Pro­ject (RUPIOH), The study in­tends to im­pro­ve ex­po­su­re as­sess­ment for ul­tra-fi­ne par­ti­cles and as­sess the ef­fect of im­pro­ved ex­po­su­re cha­rac­te­ri­za­tion on es­ti­ma­ted health ef­fects. Mea­su­re­ments of par­ti­cle num­ber counts; The re­sults from this study show that im­pro­ved fil­tra­tion is wa­rran­ted in me­cha­ni­cally ven­ti­la­ted buil­dings, par­ti­cu­larly for ul­tra­fi­ne par­ti­cles, and that night­ti­me in­fil­tra­tion is sig­ni­fi­cant de­pen­ding on the buil­ding de­sign [ 93].

The Che­mi­cal and Bio­lo­gi­cal Cha­rac­te­ri­za­tion of Am­bient Air Coar­se, Fi­ne and Ul­tra­fi­ne Par­ti­cles for Hu­man Health Risk As­sess­ment Pro­ject (PAMCHAR)

The Air Po­llu­tion and In­flam­ma­tory Res­pon­se in Myo­car­dial In­far­ction Sur­vi­vors Gene–En­vi­ron­ment In­ter­ac­tions in a High-Risk Group Pro­ject (AIRGENE)

The In­ter­na­tio­nal Agency for Re­search on Can­cer (IARC) has put in pla­ce a list of Group 1 car­ci­no­gens which in­clu­ded ben­ze­ne, die­sel ex­haust, ben­zo[a]py­re­ne (a polycy­clic aro­ma­tic hy­dro­car­bon [PAH]), in­door emis­sions from coal com­bus­tion, and 1,3-bu­ta­die­ne. Com­bus­tion-re­la­ted sour­ces, such as au­to­mo­bi­les, in­door hea­ting and coo­king, are wi­des­pread and could lead to high po­ten­tial ex­po­su­res and health risks. Com­bus­tion is the reac­tion bet­ween a fuel and oxi­dant ac­com­pa­nied by the re­lea­se of heat: Fuel + Oxi­dant → Pro­ducts + Heat [ 94].

Dis­cus­sion and Con­clu­sion

What ha­ve we lear­ned? Or has my ef­fort been in vain? The­re are doubtlessl­y nu­me­rous and he­te­ro­ge­neo­us fac­tors which could be lin­ked to the­se cul­prits. Ho­we­ver, I ha­ve pur­po­sely de­ci­ded to draw the most at­ten­tion on sun, ra­don, air po­llu­tion, can­cer and ul­ti­ma­tely, pre­ven­tion and re­gu­la­tory ac­tions.

Be­yond the sha­dow of a doubt, it is clearly scien­ti­fi­cally es­ta­blis­hed and agreed that ex­ces­si­ve sun ex­po­su­re in­crea­se the risk of skin can­cer. Ne­vert­he­less, the sun is a known sour­ce of vi­ta­min D which at the sa­me ti­me re­du­ces the risk of breast can­cer. A me­ta-analy­sis – with 68 stu­dies pu­blis­hed bet­ween 1998 and 2018-, in­clu­ding all pa­pers pu­blis­hed with key­words breast can­cer and vi­ta­min D sho­wed that the­re is a pro­tec­ti­ve re­la­tions­hip bet­ween cir­cu­la­ting vi­ta­min D and breast can­cer de­ve­lop­ment, in pre­me­no­pau­sal wo­men [ 95].

A lar­ge po­pu­la­tion-ba­sed ca­se-con­trol study pu­blis­hed a year ear­lier, sho­wed that wo­men who spent a lot of ti­me out­doors, had a lo­wer risk of breast can­cer than tho­se who spent very short pe­riods of ti­me out­doors. A com­bi­ned so­lar vi­ta­min D sco­re*, in­clu­ding all the va­ria­bles re­la­ted to vi­ta­min D pro­duc­tion, was sig­ni­fi­cantly associated with re­du­ced breast can­cer risk. Vi­ta­min D is pro­du­ced in the skin through the con­ver­sion of 7-dehy­dro­cho­les­te­rol to pre­vi­ta­min D3 fo­llo­wing suf­fi­cient ex­po­su­re to ul­tra­vio­let B (UV-B)

ra­dia­tion from sun­light. A to­tal of 4,352 hou­seholds with eli­gi­ble wo­men we­re iden­ti­fied, and 3,420 wo­men com­ple­ted the study (79%). The ma­jo­rity of study par­ti­ci­pants re­si­ded in the Grea­ter To­ron­to Area [ 96].

One might then ask how much sun is too much and how much sun is enough? In point of fact, the quin­tes­sen­tial ques­tion is about ade­qua­tely quan­tif­ying and re­gu­la­ting sun ex­po­su­re. How much of sun ex­po­su­re would re­du­ce the risk on skin can­cer and how much of sun ex­po­su­re will pro­tect against breast can­cer by in­crea­sing the pro­duc­tion of vi­ta­min D from the sun­light? The tem­pe­ra­tu­res are ri­sing and ac­cor­ding to the ex­pec­ta­tion, the sum­mer will be lon­ger with shor­ter win­ter lea­ding to in­crea­se sun­light and sun ex­po­su­re. For this reason, it is pa­ra­mount to clearly de­ter­mi­ne the re­com­men­ded du­ra­tion of sun ex­po­su­re that is fa­vo­ra­ble for re­du­cing the risk of breast can­cer and ha­zar­dous for skin can­cer. This ad­vi­ce will cinch our de­ci­sion as to how long we need to en­joy the sun. I would strongly re­com­mend this to­pic in the pro­gram of the next mee­ting of the in­ter­na­tio­nal con­fe­ren­ces on UV and skin can­cer pre­ven­tion and Eu­ros­kin6.

I as­ked to one of my best friends and one of my mul­ti­ple nep­hews as to whet­her they ever heard about ra­don. Their ans­wer was pla­cidly, but not shoc­kingly, no!

Ra­don is the se­cond cau­se of lung can­cer af­ter to­bac­co and the 7th the cau­se of can­cer re­la­ted deaths. Though the safe le­vels of ra­don va­ries ac­cor­ding to the coun­tries, high ra­don

con­cen­tra­tions can be re­du­ced in exis­ting hou­ses at mo­de­ra­te cost, and low con­cen­tra­tions can usually be achie­ved at reaso­na­ble or low cost when new buil­dings are cons­truc­ted. Re­si­den­tial ra­don pro­du­ces subs­tan­tial ha­zards, par­ti­cu­larly among smo­kers, even at con­cen­tra­tions be­low the ac­tion le­vels cu­rrently re­com­men­ded in many coun­tries [ 76].

Air po­llu­tion con­tri­bu­tes to lung can­cer in­ci­den­ce. Am­bient PM2.5 was the fifth ran­king mor­ta­lity risk in 2015. Ex­po­su­re to it was res­pon­si­ble for 4.2 mi­llion deaths and 103 di­sa­bi­lity ad­jus­ted li­ve years in 2015. No­net­he­less most peo­ple spend around 85% of their ti­me in­doors and it is re­cog­ni­zed that a sig­ni­fi­cant por­tion of to­tal per­so­nal ex­po­su­re to par­ti­cu­la­te mat­ter (PM) oc­curs in in­door en­vi­ron­ments. Roughly 80% of the ti­me in­doors is spent in re­si­den­ces, whi­le the ot­her 20% is spent in of­fi­ces, res­tau­rants, schools, and ot­her in­door lo­ca­tions that are mostly me­cha­ni­cally ven­ti­la­ted buil­dings [ 97].

Al­so he­re, quan­tify the ti­me spent are out­si­de, des­pi­te the pre­sen­ce of PM, which is less risky for us is in the do­main of scien­ce fic­tion. No­net­he­less ma­king the air less po­llu­ted is rea­lis­tic on­ce we fi­nally “get” it.

We all know so­meo­ne who knows so­meo­ne who knows so­meo­ne who un­for­tu­na­tely died from can­cer. In­te­res­tingly in my 15 years of drug dis­co­very and re­search in on­co­logy, I am of­ten un­sur­pri­singly as­ked two ques­tions at birth­days par­ties, with friends or whi­le mee­ting new peo­ple: Do you think that can­cer will be cu­red one day? And whet­her can­cer has es­sen­tially to do with what we eat or breath. Ne­ver been as­ked what should be doing to pre­vent can­cer. No of­ten I ha­ve been as­ked about the mo­di­fia­ble cau­ses of can­cer. Let alo­ne about can­cer and cli­ma­te chan­ge. I am su­re that if we know mo­re about the cau­ses of can­cer, we will com­prehen­sibly do mo­re to pre­vent it. The le­vel of pre­ven­ti­ve ac­tions va­ries, ac­cor­ding to our own be­liefs and, no­te­worthy, are ba­sed on a kind of uni­ver­sal wis­dom. My brot­her in law told me this mor­ning that he eats only bio­lo­gi­cal pro­ducts sin­ce years to pre­vent can­cer and ot­her car­dio­vas­cu­lar di­sea­ses. The­re is so­mehow, at dif­fe­rent le­vels and in va­rious hou­seholds, a kind of cons­cien­ti­za­tion about the cau­se and ef­fect re­la­tions­hip but at the sa­me ti­me, un­cons­cious ig­no­ran­ce about pre­ven­tion.

With the dis­co­very of new mo­le­cu­les with new mo­de of ac­tion, the bet­ter un­ders­tan­ding of can­cer bio­logy and the early de­tec­tion of can­cer, by vir­tue of di­ver­se scree­ning pro­grams, the sur­vi­val ra­tes are wit­hout fail im­pro­ving. Ac­cor­ding to Ame­ri­can Can­cer So­ciety, the in­ci­den­ce ra­te as well as the mor­ta­lity ra­te from ma­jor can­cer ty­pes, na­mely Lung, breast, pros­ta­te, and co­lo­rec­tal can­cer, in the US has de­cli­ned stea­dily over the past 20 years. As of 2015, the can­cer death ra­te, for men and wo­men com­bi­ned, had fa­llen 26% from its peak in 1991. This de­cli­ne trans­la­tes to nearly 2.4 mi­llion deaths aver­ted du­ring this ti­me pe­riod [ 98].

In the an­nual re­port to the na­tion on the sta­tus on can­cer, pu­blis­hed in can­cer in 2018 it was trans­lu­cently men­tio­ned that can­cer in­ci­den­ce for all can­cer si­tes com­bi­ned is de­cli­ning. Par­ti­cu­larly, lung can­cer, breast can­cer, pros­ta­te can­cer and co­lo­rec­tal can­cer [ 99].

The con­ti­nuous de­cli­ne due to lung and bron­chus can­cer sin­ce the early 1990 among men and sin­ce the early 2000s among wo­men is at­tri­bu­ta­ble to the re­duc­tion in ci­ga­ret­te smo­king over the past 5 de­ca­des [ 100].

La­men­tably, pro­gress in de­cli­ning did not oc­cur for so­me ot­her ty­pe of can­cer such as skin can­cer. In con­trast, the in­ci­den­ce of skin can­cer due to in­crea­se re­crea­tio­nal ex­po­su­re to the sun- lon­ger fall, spring and high tem­pe­ra­tu­re in sum­mer-, is in­crea­sing [ 101]. The­re­fo­re, as it is un­doub­tedly re­cog­ni­zed, the de­cli­ne of lung can­cer is at­tri­bu­ta­ble to the re­duc­tion of to­bac­co con­sum­ption, the de­cli­ne of skin can­cer will oc­cur only when we will sig­ni­fi­cantly re­du­ce the re­crea­tio­nal sun ex­po­su­re, in light of the glo­bal war­ming that is cha­rac­te­ri­zed by in­crea­sed tem­pe­ra­tu­res. On the ot­her hand, as it has been de­mons­tra­ted that the bla­med glo­bal war­ming could be re­ver­si­ble, it is re­com­men­da­ble, un­re­len­tingly to put our ef­fort to­get­her to re­du­ce the glo­bal war­ming which, con­se­quently, will re­du­ce the sun ex­po­su­re and by pro­xi, skin can­cer.

The cru­cial ques­tion of cli­ma­te chan­ge and health is an exis­ten­tial one and it re­qui­red self-im­pro­ve­ment in our ways on thin­king and doing. Ralph Wal­do Emer­son- fat­her of exis­ten­tia­list et­hics of self-im­pro­ve­ment. -, taught us to “not go whe­re the path may lead, go ins­tead whe­re the­re is no path and lea­ve a trail (…) Every wall is a door”. The wall set up by the cli­ma­te chan­ge is un­bea­rably thick, wit­hin which we are all pri­so­ners. Pri­so­ners of a cri­me com­mit­ted by ot­hers? No, by all of ours. But I am still con­vin­ced that we are, to­get­her and if well or­ga­ni­zed, able to suc­cess­fully fi­nd a door. We should pres­singly fi­nd the door; the re­medy, but most im­por­tantly and fun­da­men­tally, the coura­ge. Not­hing has been achie­ved wit­hout coura­ge and bra­very and it will ta­ke mo­re ti­me as­su­redly to do right. ” Hu­man pro­gress ne­ver rolls in on wheels of inevi­ta­bi­lity; it co­mes through the ti­re­less ef­forts of peo­ple (…). We must use ti­me crea­ti­vely, in the know­led­ge that the ti­me is al­ways ri­pe to do right” [ 102].

Many di­sea­ses such as the Pla­gue, ha­ve been era­di­ca­ted from our pla­net in the last cen­tury. Would we be able to rid of can­cer? To cu­re can­cer or to era­di­ca­te all men re­la­ted risk fac­tors-en­vi­ron­men­tal fac­tors cau­sing can­cer? Ho­nestly, I don’t know. Can­cer in­vol­ves the mu­ta­tions of many ge­nes and even when suc­cess­fully trea­ted, the ac­ti­va­tion of dor­mant re­sis­tant ge­nes would help the can­cer cells to be treat­ment re­sis­tant, lea­ding in the most ca­ses, to fa­tal pro­gres­sion-out­co­me. The path is pe­ri­lously long, the goal far; very far; but im­pos­si­ble is not­hing and gi­ving up is not and ne­ver been an op­tion.

“We can rid our­sel­ves of can­cer, then only as much as we can rid our­sel­ves of the pro­cess in our phy­sio­logy that de­pend on growth-aging, re­ge­ne­ra­tion, hea­ling, re­pro­duc­tion” [ 103].

Al Go­re in “Our choi­ce” com­pe­tently told us that: “not too many years from now, a new ge­ne­ra­tion will look back at us in this hour of choo­sing and ask one or two ques­tions Eit­her they will ask,” What we­re you thin­king? Didn’t you see the en­ti­re North Po­lar ice cap, mel­ting be­fo­re your eyes? Didn’t you hear the war­nings from the scien­tists? Whe­re you dis­trac­ted? Did you not ca­re?

Or they will ask ins­tead, “how did you fi­nd the mo­ral coura­ge to ri­se up and sol­ve a cri­sis so many said was im­pos­si­ble to sol­ve?” We must choo­se which of the­se ques­tions we want to ans­wer, and we must gi­ve our ans­wer now- not in words but in ac­tions.”

Al Go­re, he­re is my ans­wer, in ac­tion, to mi­ti­ga­te the ba­le­ful con­se­quen­ces of cli­ma­te chan­ge! The chan­ge in cli­ma­te we cons­tantly talk about is nig­gardly loo­ming us though so­me might still be­lie­ve that it is an apocryp­hal story.

As it was the ca­se for lung can­cer af­ter the co­rre­la­tion with to­bac­co was es­ta­blis­hed for the first ti­me by Doll and Hill in 1950, des­pi­te the dis­may of the ma­jo­rity of the peo­ple in­clu­ding Evarts Graham him­self, who was in­vol­ved in the first re­search work, cli­ma­te chan­ge and can­cer are still fa­cing de­nial and dis­may [ 104].

Evarts Graham to­get­her with Wyn­der we­re one of the first to es­ta­blish de­ter­mi­na­tely and ines­ca­pably the re­la­tions­hip bet­ween smo­king and to­bac­co use. Be­si­de pneu­mo­nec­tomy, be­yond re­call, “Smo­king and Can­cer” is one of the most che­ris­hed le­gacy of Evarts Graham. He sta­ted that “aca­de­mic in­ves­ti­ga­tors could pro­vi­de da­ta about risks and ar­gue in­ces­santly about proof and cau­sa­lity, but the so­lu­tion had to be po­li­ti­cal”. It is in 2019, ap­pli­ca­ble for the cau­sa­lity bet­ween cli­ma­te chan­ge and health, in par­ti­cu­lar bet­ween cli­ma­te chan­ge and can­cer. Mo­re po­li­cies should be de­ve­lo­ped to pre­vent the de­ple­tion of stra­tosp­he­ric ozo­ne whe­reby re­du­cing as­su­redly sun ex­po­su­re re­la­ted skin can­cer.

How about ra­don ex­po­su­re in ot­her coun­tries then the US. Is the­re any re­gu­la­tion? Which re­gu­la­tions are exis­tent in Eu­ro­pe, es­pe­cially when we build energy ef­fi­ciency buil­dings? How would we crea­te energy ef­fi­ciency hou­se which would not in­crea­se the ema­na­tion of ra­don de­cays and pro­ge­nity? How should we mo­re ef­fi­ciently fight against air po­llu­tion by re­du­cing in­dus­trial and mo­bi­le po­llu­tion. Dri­ve an elec­tric car, bi­ke, ta­ke pu­blic trans­por­ta­tion; they re­com­mend to us.

Be­gin­ning of 2019, Aus­tra­lia re­cor­ded its hot­test month ever in Ja­nuary with ave­ra­ge tem­pe­ra­tu­re ex­cee­ding 30 de­grees and the Mid­west of the US is ha­ving one of the worst cold ever in de­ca­des be­cau­se of the po­lar vor­tex.

Cli­ma­te chan­ge is a fact!

It is ur­gent to act!

In light of pro­vi­ded evi­den­ces and wit­nes­sed and ack­now­led­ged th­reats, we can no lon­ger ig­no­re cli­ma­te chan­ge and his im­pact on health. Who should be bla­med?

The ti­me to in­ces­santly search for sca­pe­goats is over. The cul­prit is in our daily ac­tions. The so­lu­tion should be in our daily thin­king and ac­tion. We are all res­pon­si­ble and we should all to­get­her fi­nd the so­lu­tions.

Hans Ros­ling in Fact­ful­ness [105] - which Bill Ga­tes con­si­der as “one of the im­por­tant books he has ever read” in­tro­du­ced 10 ins­tin­cts which dis­tres­singly bia­ses our views on the world and on tho­se with whom we in­ter­act daily: he no­tably na­med: The gap ins­tinct, the ne­ga­ti­vity ins­tinct, the straight li­ne ins­tinct, the fear ins­tinct, the si­ze ins­tinct, the ge­ne­ra­li­za­tion ins­tinct, the des­tiny ins­tinct, the sin­gle pers­pec­ti­ve ins­tinct , the bla­me ins­tinct and the ur­gency ins­tinct. Among all the­se mul­ti­fa­rious ins­tin­cts, the bla­me ins­tinct would be mostly ap­pli­ca­ble to all of us in re­la­tion to the world­wi­de des­tro­ying si­tua­tion and his dis­tor­ted per­cep­tion. Ac­cor­ding to Hans Ros­ling: “The ins­tinct to fi­nd guilty party de­rails our abi­lity to de­ve­lop a true, fact ba­sed un­ders­tan­ding of the world: it steals our fo­cus as we ob­sess about so­meo­ne to bla­me, then blocks our lea­ning be­cau­se on­ce we ha­ve de­ci­ded who to punch in the fa­ce we stop loo­king for ex­pla­na­tions el­sew­he­re (…) To un­ders­tand most of the world’s sig­ni­fi­cant pro­blems we ha­ve to look be­yond a guilty in­di­vi­dual and to the sys­tem” [ 106].

It is only with te­na­cious coura­ge and ur­gency ins­tinct we will be able to re­lin­quish a clean earth to the next ge­ne­ra­tion. It is only with a her­cu­lean coura­ge that we could reali­ze our dream of era­di­ca­ting can­cer by re­du­cing the im­pact of cli­ma­te chan­ge. Hans Ros­ling again co­mes to our help by emp­ha­si­zing that sol­ving cli­ma­te chan­ge cha­llen­ges “re­qui­res so­me sen­se of glo­bal so­li­da­rity to­wards the needs of dif­fe­rent peo­ple on dif­fe­rent in­co­me le­vels.” [107]

The­re are se­ve­ral per­so­na­li­ties in the his­tory of the man­kind who had sho­wed his coura­ge, who­se ac­tion had had im­pact on bi­llion of peo­ple. Owing to her coura­ge and fir­mness, her pug­na­city and in­te­lli­gen­ce, her bright­ness and per­se­ve­ran­ce, her pers­pi­ca­city and es­sen­tially her self-ab­ne­ga­tion and hu­mi­lity; her dis­co­very had had im­pact on the li­ves of bi­llion peo­ple. Her his­tory will im­pact­fully fas­ci­na­te me li­fe­long: Ma­rie Sklo­dows­ka Cu­rie, first wo­men to win a No­bel pri­ze, first wo­men to win two No­bel pri­zes. I could not finish this hum­ble work wit­hout a deep and res­pect­ful thought for her. “We can­not ho­pe to build a bet­ter world wit­hout im­pro­ving the in­di­vi­dual. To­ward this end, each of us must work for his own hig­hest de­ve­lop­ment, ac­cep­ting at the sa­me ti­me his sha­re of res­pon­si­bi­lity in the ge­ne­ral li­fe of hu­ma­nity—our par­ti­cu­lar duty being to aid tho­se to whom we think we can be most use­ful.“[108]

As in the words of Tho­mas Kuhn, “a pa­ra­digm shift” is im­pe­ra­ti­vely re­qui­red to sol­ve the cli­ma­te chan­ge pro­blem by im­pro­ving the in­di­vi­dual. De­ci­dedly, “We can­not sol­ve our pro­blems with the sa­me thin­king we used when we crea­ted them.”, war­ned A. Einstein. No ifs ands or buts about it, af­ter years of in­de­fi­ni­te and he­si­tant dis­cus­sions, we ha­ve a lot to iron out now. A pa­ra­digm shift is re­qui­red, de no­vo, at all le­vels. In­di­vi­duals, po­licy­ma­kers, bu­si­ness/cor­po­ra­te lea­ders and key opi­nion lea­ders, should co­me to­get­her fre­quently and think about what we all , re­gard­less of our ori­gins and wealth, ha­ve in com­mon; earth and health. I could not agree mo­re with Ralph Wal­do Emer­son that “the first wealth is health “(Ralph Wal­do Emer­son (1883). “Es­says and Lec­tu­res”, p. 972, Li­brary of Ame­ri­ca).

The bu­si­ness mo­dels need to be tho­roughly re­vi­si­ted and ret­hought. For ins­tan­ce, the eco­no­mist pu­blis­hed re­cently an ar­ti­cle on 09 Fe­bruary 2019 with an eye-cat­ching ar­ti­cle : “The true about big oil and cli­ma­te chan­ge” and how “even as con­cerns about glo­bal war­ming grow, energy firms are planning to in­crea­se fos­sil-fuel pro­duc­tion … des­pi­te the fact that last week Chica­go was col­der than part of Mars.” Could the­se big oil firm rein­vent the wheel with new bu­si­ness mo­dels with less im­pact on the earth, con­se­quently on the cli­ma­te?

We are all, the­se days as many ot­hers in Eu­ro­pe, en­jo­ying the ni­ce warm weat­her. No­net­he­less do we the ti­me to re­flect about how the­se warm tem­pe­ra­tu­res are pos­si­ble in this pe­riod of the year? On 25 Fe­bruary 2019, The Net­her­lands re­gis­te­red the war­mest 25 Fe­bruary ever in their me­teo­ro­lo­gi­cal his­tory, with a ma­xi­mum tem­pe­ra­tu­re of 18.1 de­grees Cel­sius.

Just a whi­le ago, I had a plea­su­re, on a beau­ti­ful sunny Sa­tur­day af­ter­noon, to play ten­nis with my friend, his brot­her and his brot­her’s son! It was a great ga­me.; a min­gling of ge­ne­ra­tions to ma­ke the Ro­yal fa­mily jea­lous. At the end of the ga­me, my friend’s brot­her sud­denly de­ci­ded to show us the re­mains of the tree which was cut few days ago, be­cau­se, li­ke can­cer me­tas­ta­ses, the roots we­re in­va­ding the neigh­bor’s gar­den! Whi­le de­plo­ring this an­ti-en­vi­ron­men­tal pa­llia­ti­ve sur­gery, my at­ten­tion got cap­tu­red by a black li­mou­si­ne par­ked out­si­de the ga­ra­ge; pro­bably with an heavy en­gi­ne and sig­ni­fi­cant CO2 emis­sion!

-“What a ni­ce, but cer­tainly po­llu­ting car”, I said.

My friend’s brot­her proudly reac­ted by sa­ying that he al­so has an elec­tric car in the ga­ra­ge, which has mo­re rid­den mo­re ki­lo­me­ters than the li­mou­si­ne; implying os­ten­sibly that he dri­ves the elec­tric car mo­re of­ten than the li­mou­si­ne. Un­doub­tedly, he ca­res mo­re about his small elec­tric “je­welry” and that ex­plain as to why it was se­cu­rely par­ked in the ga­ra­ge.

In 1969, the Pu­blic Health Smo­king Act of 1969 re­qui­red all ci­ga­ret­tes pac­ka­ging con­tain the sta­te­ment: WAR­NING: THE SUR­GEON GE­NE­RAL HAS DE­TER­MI­NED THAT CI­GA­RET­TE SMO­KING IS DAN­GE­ROUS TO YOUR HEALTH. The war­nings ha­ve evol­ved du­ring the last de­ca­des and pic­tu­res of can­cer pa­tients we­re even put on the packs.

When are we ha­ving war­nings stic­kers/mes­sa­ges on po­llu­ting cars -, with a mes­sa­ge: this car cau­ses can­cer? Or pic­tu­res of lung can­cer pa­tients on trucks or air­pla­nes?

Awai­ting the qua­si unt­hin­ka­ble pa­ra­digm shift we, as in­di­vi­dual will need to exi­gently mo­de­ra­te the sun ex­po­su­re, im­pe­ra­ti­vely avoid any ac­tion which could lead to air po­llu­tion, whe­reby we will be able help to pre­vent can­cer; we shall al­ways ne­ver for­get that “so­la do­sis fa­cit ve­ne­num “-It is the do­se which ma­kes the poi­son. Again, and al­ways!

A Call to Ac­tion from Madrid Hu­man Pa­pi­lo­ma Virus: is a group of vi­ru­ses that are ex­tre­mely com­mon world­wi­de. The­re are mo­re than 100 ty­pes of HPV, of which at least 14 are can­cer-cau­sing (al­so known as high risk ty­pe).HPV is mainly trans­mit­ted through se­xual con­tact and most peo­ple are in­fec­ted with HPV shortly af­ter the on­set of se­xual ac­ti­vity. Cer­vi­cal can­cer is cau­sed by se­xually ac­qui­red in­fec­tion with cer­tain ty­pes of HPV.Two HPV ty­pes (16 and 18) cau­se 70% of cer­vi­cal can­cers and pre-can­ce­rous cer­vi­cal le­sions. The­re is al­so evi­den­ce lin­king HPV with can­cers of the anus, vul­va, va­gi­na, pe­nis and orop­harynx. (https://www.who.int/news-room/fact-sheets/de­tail/hu­man-pa­pi­llo­ma­vi­rus-(hpv)-and-cer­vi­cal-can­cer).

A Call to Ac­tion from Madrid

A Call to Ac­tion from Madrid

A Call to Ac­tion from Madrid

The Glo­bal Can­cer Ob­ser­va­tory (GCO) is an in­te­rac­ti­ve web-ba­sed platform pre­sen­ting glo­bal can­cer sta­tis­tics to in­form can­cer con­trol and re­search.

A Call to Ac­tion from Madrid

A Call to Ac­tion from Madrid

EUROSKIN is an in­de­pen­dent non-pro­fit ma­king scien­ti­fic so­ciety, who­se prin­ci­pal aims are to re­du­ce the in­ci­den­ce and mor­ta­lity of skin can­cer. It sets out to achie­ve this through the pro­mo­tion and co-or­di­na­tion of co­lla­bo­ra­ti­ve ac­tions bet­ween Eu­ro­pean pro­fes­sio­nals ac­ti­ve in the fields of pri­mary and/or se­con­dary pre­ven­tion. The­se in­clu­de, for exam­ple, der­ma­to­lo­gists, epi­de­miolo­gists, bio­lo­gists, phy­si­cists and ot­her pro­fes­sio­nals with an in­ter­est in the­se aims. https://www.euroskin.eu/en/

A Call to Ac­tion from Madrid

A Call to Ac­tion from Madrid

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