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Oddiy odamga sigareta tutuni qanday saraton kasalligiga olib kelishi mumkinligini tushuntiring

Oddiy odamga sigareta tutuni qanday saraton kasalligiga olib kelishi mumkinligini tushuntiring



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Mening juda aqlli do'stim bor, u engil chekuvchi, shuningdek, biologiya fanidan.
Men sigaretaning saratonga olib kelishini aniq tushunish uni kamroq chekishga (yoki butunlay tashlashga) undashi mumkinmi, deb hayron bo'ldim.

Xo'sh, biologiya bo'yicha mutaxassisga sigaretaning saratonga olib kelishini qanday tushuntirasiz?

Aniqroq qilib aytganda, men oddiy odam uchun batafsil tushuntirish izlayapman, bu ular uchun sabab-oqibatni yanada aniqroq qiladi va shuning uchun aqlli odam chekish xavfini o'z ichiga oladi.

Men topgan Internet -resurslar juda oddiy javob berdi yoki statistikaga e'tibor qaratdi (odatda, agar men to'g'ri tushunsam, odamlarga ularni kiritish qiyin).
(Bunday tushuntirishlarda hech qanday yomon narsa yo'q, ular men izlayotgan narsa emas.)


Men darslikda quyidagi paragrafga duch keldim Hayot: Biologiya fani:

Ba'zi kimyoviy moddalar asoslarga guruhlar qo'shadi. Masalan, sigaret tutunining bir qismi bo'lgan benzopiren, guaninga katta kimyoviy guruh qo'shib, uni bazaviy juftlik uchun mavjud emas. DNK -polimeraza bunday o'zgartirilgan guaninga etib kelganida, u to'rtta asosdan birini tasodifiy kiritadi. Vaqtning to'rtdan uch qismi sitozin emas va mutatsiyaga olib keladi.

Vikipediyaning Benzo (a) piren sahifasida quyidagi taklifni topgach, men BaP qanday qilib saraton kasalligiga olib kelishi mumkinligini aniq tushuntirishga qaror qildim:

BaP shundan beri sigaret tutunida asosiy kanserogen sifatida tan olingan.

Mening tushuntirishim:

  • Protein molekulasi aminokislotalar zanjiridir. Proteinlar juda katta ahamiyatga ega, chunki ular uyali funktsiyalari uchun javobgardir.
  • DNK molekulasi nuklein kislotalarning zanjiridir. DNKda 4 turdagi nuklein kislotalar mavjud: A, G, C, T.
  • Buzilmagan DNK molekulalariga ega bo'lish juda muhim, chunki ular oqsillarni kodlashni o'z ichiga oladi, shunga ko'ra hujayralar oqsillarni sintez qiladi.
  • Mutatsiya - bu DNK molekulasining o'zgarishi.
  • Mutatsiya hujayralarimiz ishlamaydigan oqsil sinteziga olib kelishi mumkin. Agar hujayra bo'linishini tartibga soluvchi oqsil noto'g'ri ishlayotgan bo'lsa, natijada nazoratsiz bo'linish - saraton bo'lishi mumkin.
  • Chekish paytida kimyoviy BaP (sigaret tutunida mavjud) tanangizdagi ba'zi hujayralardagi DNK molekulasidagi G-nuklein kislotasini o'zgartirishi mumkin. Keyinchalik, bu hujayra bo'linishga harakat qilganda, u o'zining har bir DNK molekulasining nusxasini yaratadi, lekin u G-nuklein kislotasini (BaP o'zgartirilgan) aniqlay olmaydi, shuning uchun u nusxalangan hujayraga tasodifiy nuklein kislota qo'yadi. DNK molekulasi. Shunday qilib, mutatsiya uchun 3/4 imkoniyat mavjud.

Ikkinchi qo'l tutun va saraton

Ikkinchi darajali tutun (ba'zida passiv tutun, ekologik tamaki tutuni yoki beixtiyor tutun deb ataladi) - yonma -yon tutun (tamaki yoki boshqa chekilgan tamaki mahsulotining yonayotgan uchidan tutun) va asosiy tutun (tutun suyultirilgan tutun chiqarayotgan tutun) aralashmasidir. atrofdagi havo bilan) (1–3).

Chekilgan tutunga ta'sir qilishning asosiy parametrlariga ish joylari, jamoat joylari, masalan, barlar, restoranlar va dam olish joylari va uylar kiradi (4). Ish joylari va uylar, ayniqsa, odamlar bu muhitda qancha vaqt o'tkazgani uchun ta'sir qilishning muhim manbalaridir. Chaqaloqlar va yosh bolalar uchun uy ayniqsa ta'sirlanish manbai hisoblanadi. Bolalar va sigaret chekmaydigan kattalar, shuningdek, avtoulovlarda tutun tutuniga duch kelishi mumkin, bu erda ta'sir qilish darajasi yuqori bo'lishi mumkin. Restoranlar, barlar va kazinolar kabi chekishga ruxsat berilgan yopiq jamoat joylarida ham ekspozitsiya darajasi yuqori bo'lishi mumkin, bu esa ishchilarga ham, homiylarga ham katta ta'sir ko'rsatadi (3).

Qo'shma Shtatlarda ko'pchilik tutun sigaretadan, undan keyin quvurlar, sigaralar va boshqa dudlangan tamaki mahsulotlaridan kelib chiqadi.

Ikkinchi qo'l tutun ta'sirini qanday o'lchash mumkin?

Tutunning tutun ta'sirini nafas oladigan (nafas oladigan) to'xtatilgan zarrachalar (inson o'pkasining pastki nafas yo'llariga yetadigan darajada kichik zarrachalar) yoki nikotin yoki tamaki tutunining boshqa zararli va potentsial zararli tarkibiy qismlari kabi individual kimyoviy moddalar uchun ichki havoni tekshirish orqali o'lchash mumkin. 5).

Chekilmagan tutunga ta'sir qilish, chekmaydigan odamning qonida, tupurigida yoki siydigida kotinin (nikotin metabolizmining yon mahsuloti) kabi biomarkerlar darajasini o'lchash yo'li bilan ham baholanishi mumkin (1). Sigaret chekmaydigan odamlarning tana suyuqligida tutun tutunida mavjud bo'lgan nikotin, kotinin va boshqa kimyoviy moddalar topilgan.

Ikkinchi tutun tarkibida zararli kimyoviy moddalar bormi?

Ha. Chekuvchilar tomonidan nafas olayotgan tutun tarkibidagi ko'plab zararli kimyoviy moddalar, shuningdek, tutunda (1, 3, 6, 7), shu jumladan saraton kasalligini keltirib chiqaradigan (1, 3, 7, 8) ham mavjud.

Qaysi kimyoviy moddalar va ularning miqdori ikkinchi qo'l tutunida mavjudligiga ko'p omillar ta'sir qiladi. Bu omillarga ma'lum bir mahsulotni ishlab chiqarishda ishlatiladigan tamaki turi, tamaki tarkibiga qo'shilgan kimyoviy moddalar (shu jumladan mentol kabi aromatizatorlar), tamaki mahsulotining chekish usuli va tamaki, tamaki, kichik sigara va sigarillolar kiradi. tamaki o'ralgan material (1-3, 7).

Tamaki chekish saratonga olib keladimi?

Ha. AQSh atrof-muhitni muhofaza qilish agentligi, AQSh milliy toksikologiya dasturi, AQSh bosh jarrohi va Xalqaro saraton tadqiqotlari agentligi ikkinchi darajali tutunni odam kanserogenlari (saraton kasalligi) deb tasniflagan (1, 3, 7, 9). ). Bundan tashqari, Mehnatni muhofaza qilish va sog'liqni saqlash milliy instituti (NIOSH) ikkinchi darajali tutun kasbiy kanserogen (3) degan xulosaga keldi.

Bosh jarrohning hisob-kitoblariga ko'ra, 2005-2009 yillar mobaynida tutun tutuni har yili chekmaganlar orasida o'pka saratonidan 7300 dan ortiq o'limga olib kelgan (10).

Ba'zi tadqiqotlar shuni ko'rsatadiki, ikkinchi qo'l tutuni kattalarda ko'krak saratoni, burun sinus bo'shlig'i saratoni va nazofarengeal saraton (10) va bolalarda leykemiya, limfoma va miya shishi xavfini oshirishi mumkin (3). Tutun tutuni va bu saraton o'rtasida bog'liqlik bor yoki yo'qligini aniqlash uchun qo'shimcha tadqiqotlar o'tkazish kerak.

Ikkilamchi tutun ta'sirining boshqa sog'liqqa qanday ta'siri bor?

Sigaret chekadigan kattalar va bolalarda ikkinchi darajali tutun kasallik va erta o'lim bilan bog'liq (3, 7). Tutunning tutuni nafas yo'llarini bezovta qiladi va odamning yurak va qon tomirlariga darhol zararli ta'sir ko'rsatadi. Bu yurak xastaligi xavfini 25-30% ga oshiradi (3). Qo'shma Shtatlarda, tutun tutuni har yili 34 mingga yaqin yurak xastaligidan o'limga olib keladi (10). Ikkinchi tutunga ta'sir qilish ham insult xavfini 20-30% ga oshiradi (10).

Homiladorlik paytida ikkinchi darajali tutunning tutilishi tug'ilishning pasayishiga, homiladorlikning asoratlariga va tug'ilishning yomon natijalariga, shu jumladan o'pkaning rivojlanishining buzilishiga, kam vaznga va erta tug'ilishga olib kelishi aniqlandi [11].

Ikkilamchi tutunga duchor bo'lgan bolalarda to'satdan chaqaloq o'limi sindromi, quloq infektsiyalari, shamollash, pnevmoniya, bronxit va yanada og'ir astma xavfi ortadi. Ikkilamchi tutunga ta'sir qilish bolalar o'pkasining o'sishini sekinlashtiradi va ularda yo'talish, xirillash va nafas olish hissi paydo bo'lishiga olib kelishi mumkin (3, 7, 10).

Ikkinchi darajali tutunga ta'sir qilishning xavfsiz darajasi yo'q. Hatto past darajadagi chekish ham zararli bo'lishi mumkin.

O'zingizni va oilangizni tutundan qanday himoya qilish mumkin?

Chekmaydiganlarni tutun tutunidan to'liq himoya qilishning yagona yo'li - yopiq ish joylarida va jamoat joylarida chekishni tashlash va shaxsiy joylar, shu jumladan ko'p qavatli turar -joy binolari uchun chekishsiz siyosatni ishlab chiqish. Derazalarni ochish, ventilyatorlar va ventilyatsiya tizimlaridan foydalanish, chekishni uyning ayrim xonalarida yoki kunning ma'lum vaqtlarida cheklash, tutun tutunining ta'sirini yo'q qilmaydi (3, 4).

O'zingizni va oilangizni himoya qilish uchun qanday choralar ko'rishingiz mumkin:

  • uyingizda chekishga ruxsat bermang
  • mashinangizda, hatto derazalari pastda ham chekishga hech kimga ruxsat bermaslik
  • farzandlaringiz boqiladigan joylar tamakisiz ekanligiga ishonch hosil qiling
  • bolalarni chekishdan qochishga o'rgatish
  • restoran, bar va chekmaydigan boshqa joylarni qidirish (agar sizning davlatingiz hali ham jamoat joylarida chekishga ruxsat bersa)
  • chekish yoki tamaki mahsulotining boshqa turidan foydalanmaslik orqali o'z oilangizni tutun tutunidan himoya qilish va yaxshi namuna bo'lish. Chiqish uchun smokefree.gov saytiga qarang yoki 1-877-44U-QUIT raqamiga qo'ng'iroq qiling.

Elektron sigaret chekuvchi tutun chiqarmikan?

Elektron sigaret (elektron sigaret, vape qalam, vape va pod mod deb ham ataladi), odatda, nikotin o'z ichiga olgan suyuqlikni foydalanuvchi nafas olish uchun aerozolga qizdirish uchun mo'ljallangan batareyali qurilmalardir. Nafas olgandan so'ng, foydalanuvchi aerozolni chiqaradi (12).

Elektron sigaretdan foydalanish natijasida ikkinchi qo'l aerozollar (sigaret tutuni emas) ta'sir qiladi. Ikkinchi qo'l aerozollarda zararli va potentsial zararli moddalar, shu jumladan nikotin, qo'rg'oshin kabi og'ir metallar, uchuvchan organik birikmalar va saraton keltirib chiqaruvchi moddalar mavjud. Ushbu qurilmalar haqida qo'shimcha ma'lumotni CDC elektron sigaretalar sahifasida olish mumkin.

Chekmaydiganlarning ikkinchi qo'l tutuniga ta'sirini kamaytirish uchun nima qilinmoqda?

Federal darajada jamoat joylarida chekishni cheklovchi bir qancha siyosatlar amalga oshirildi. Federal qonun aviakompaniya reyslarida, davlatlararo avtobuslarda va poezdlarning ko'pchiligida chekishni taqiqlaydi. 1997 yil 13058-sonli farmonga binoan ko'pchilik federal binolarda chekish ham taqiqlangan. 1994 yilgi "Bolalarni himoya qilish to'g'risida" gi qonun bolalarga federal byudjetdan xizmat ko'rsatadigan muassasalarda chekishni taqiqlaydi. Uy -joy va shaharsozlik boshqarmasi 2016 yil dekabr oyida 2018 yil iyulda to'liq joriy qilingan yakuniy qoidani e'lon qildi, u 2018 yil iyul oyida to'liq joriy qilingan bo'lib, jamoat uy -joy idoralarida, shu jumladan, barcha turar -joy binolarida sigaret, tamaki, quvur va kalyan (suv quvurlari) ishlatishni taqiqlaydi. umumiy foydalanish joylari va ma'muriy idoralar, shuningdek, binolardan 25 fut narida joylashgan ochiq joylar.

Ko'plab shtatlar va mahalliy hukumatlar ish joylarida va jamoat joylarida, jumladan, restoranlar, barlar, maktablar, kasalxonalar, aeroportlar, avtovokzallar, bog'lar va plyajlarda chekishni taqiqlovchi qonunlarni qabul qilgan. Bu chekishsiz siyosatlar AQShning ko'plab ish joylarida chekuvchi tutun ta'sirini sezilarli darajada kamaytirdi [13]. Barcha shtatlarning yarmidan ko'pi ish joylari, restoranlar va barlarning yopiq joylarida chekishni taqiqlovchi keng qamrovli cheksiz qonunlarni amalga oshirdi va ba'zi shtatlar va jamoalar ham ko'p xonadonli uy-joy va avtomobillarda chekishni tartibga soluvchi qonunlarni qabul qildilar (14). Amerika chekmaydiganlar huquqlarini himoya qilish jamg'armasi shtat va mahalliy chekmaydigan havo siyosatlari ro'yxatini taqdim etadi.

Chekish tutunidan kelib chiqadigan sog'liq uchun xavflarni aniqlash uchun Milliy Saraton Instituti, agar maxsus holatlar istisno qilmasa, NCI tomonidan uyushtirilgan yoki asosan homiylik qiladigan yig'ilishlar va konferentsiyalarni chekishni cheklash bo'yicha keng qamrovli siyosatni qabul qilgan shtat, tuman, shahar yoki shaharchada o'tkazilishini talab qiladi. bu siyosatga.

AQSh Sog'liqni saqlash va odamlarga xizmat ko'rsatish departamenti (Sog'liqni saqlash vazirligi) tomonidan tuzilgan sog'liqni saqlash va kasalliklarning oldini olish bo'yicha butun mamlakat miqyosida tuzilgan "Sog'lom odamlar 2020" tamaki mahsulotlarini iste'mol qilish va tutun ta'siridan kelib chiqadigan kasallik, nogironlik va o'limni kamaytirishga qaratilgan bir nechta vazifalarni o'z ichiga oladi. 2020 yil uchun "Sog'lom odamlar" maqsadi sigaret chekmaydiganlarning sigaret chekadiganlar sonini 10 foizga kamaytirishdir. Bu maqsadga erishishda yordam berish uchun "Sog'lom odamlar 2020" jamoat tadbirlari g'oyalarini o'z ichiga oladi, masalan, barcha ish joylarida va jamoat bog'lari, sport maydonchalari va plyajlar kabi boshqa odamlar yig'iladigan joylarda chekishsiz siyosatni joriy etishni rag'batlantirish.

Ushbu siyosatlar va boshqa harakatlar tufayli chekmaydiganlar ulushi 1999–2000 yillarda 52,5% dan 2011–2014 yillarda 25,3% gacha qisqardi (15). Aholining barcha kichik guruhlari orasida ikkinchi qo'l tutuniga ta'sir qilish kamaydi, ammo nomutanosibliklar hali ham mavjud. 2011–2014 yillar mobaynida 3-11 yoshdagi bolalarning 38%, ispan bo'lmagan qora tanlilarning 50%, qashshoqlikdan pastda yashovchi odamlarning 48% va ijarada yashovchilarning 39% tutun tutuniga duchor bo'lgan (15) .

Tanlangan adabiyotlar

Milliy toksikologiya dasturi. Tamaki bilan bog'liq ta'sirlar. In: Kanserogenlar haqida hisobot. O'n to'rtinchi nashr. AQSh Sog'liqni saqlash va aholiga xizmat ko'rsatish departamenti, Jamoat sog'liqni saqlash xizmati, Milliy toksikologiya dasturi, 2016 yil.

Saraton tadqiqotlari xalqaro agentligi. Tamaki chekish, Ikkinchi qo'l tamaki tutuni va Tutunsiz tamaki. In: Shaxsiy odatlar va ichki yonishlar: inson kanserogenlarini ko'rib chiqish. IARC "Odamlarga kanserogen xavflarni baholash bo'yicha monografiyalar", Vol. 100E. Lion, Frantsiya: Saraton kasalligi bo'yicha xalqaro tadqiqot agentligi 2012. p. 43-318.

AQSh sog'liqni saqlash va odamlarga xizmat ko'rsatish vazirligi. Tamaki tutunining majburiy ta'sirining sog'liq uchun oqibatlari: Bosh jarroh hisoboti. Rokvil, MD: AQSh Sog'liqni saqlash va odamlarga xizmat ko'rsatish departamenti, Kasalliklarni nazorat qilish va oldini olish markazlari, Salomatlikni mustahkamlash bo'yicha muvofiqlashtiruvchi markaz, Surunkali kasalliklarning oldini olish va salomatlikni mustahkamlash milliy markazi, Chekish va salomatlik bo'yicha ofis, 2006.

Milliy saraton instituti. Saraton tendentsiyalari haqida hisobot. Bethesda, MD: AQSh sog'liqni saqlash va odamlarga xizmat ko'rsatish vazirligi, Milliy sog'liqni saqlash institutlari 2018.

AQSh oziq -ovqat va farmatsevtika idorasi. Tamaki mahsulotlari va tamaki tutunidagi zararli va potentsial zararli tarkibiy qismlar: belgilangan ro'yxat. Kumush bahor, MD: AQSh sog'liqni saqlash va odamlarga xizmat ko'rsatish departamenti, Oziq -ovqat va farmatsevtika idorasi, Tamaki mahsulotlari markazi 2012.

Rodgman A, Perfetti TA. Tamaki tarkibiy qismlari sifatida ishlatiladigan tamaki va/yoki tamaki tutuni komponentlari. In: Tamaki va tamaki tutunining kimyoviy komponentlari. Boka Raton, FL: CRC Press 2009. p. 1259.

AQSh sog'liqni saqlash va odamlarga xizmat ko'rsatish vazirligi. Tamaki tutuni qanday kasallikka olib keladi: chekish bilan bog'liq kasallikning biologiyasi va xulq-atvori: umumiy jarroh hisoboti.. Atlanta, GA: AQSh Sog'liqni saqlash va aholiga xizmat ko'rsatish departamenti, Kasalliklarni nazorat qilish va oldini olish markazlari, Surunkali kasalliklarning oldini olish va salomatlikni mustahkamlash milliy markazi, Chekish va salomatlik bo'yicha idora, 2010 yil.

Milliy saraton instituti. Atrof-muhit tamaki tutuniga ta'sir qilishning sog'liqqa ta'siri. Chekish va tamaki chekish monografiyasi 10. NIH Pub. 99-4645 raqami. Bethesda, MD: AQSh Sog'liqni saqlash va inson xizmatlari departamenti, Milliy saraton instituti 1999 yil.

AQSh atrof-muhitni muhofaza qilish agentligi. Passiv chekishning nafas olish tizimiga ta'siri: o'pka saratoni va boshqa kasalliklar. Vashington, Kolumbiya okrugi: AQSh Atrof -muhitni muhofaza qilish agentligi, Sog'liqni saqlash va atrof -muhitni baholash boshqarmasi, Tadqiqot va ishlab chiqish boshqarmasi 1992.

AQSh sog'liqni saqlash va odamlarga xizmat ko'rsatish vazirligi. Chekishning salomatlik oqibatlari - 50 yillik taraqqiyot: Bosh jarrohning hisoboti, 2014 yil. Atlanta, GA: AQSh Sog'liqni saqlash va aholiga xizmat ko'rsatish departamenti, Kasalliklarni nazorat qilish va oldini olish markazlari, Surunkali kasalliklarning oldini olish va salomatlikni mustahkamlash milliy markazi, Chekish va salomatlik bo'yicha idora, 2014 yil.

Milliy saraton instituti. Tamaki bilan bog'liq sog'liqdagi nomutanosibliklarni bartaraf etishga sotsioekologik yondashuv. Milliy saraton instituti tamaki nazorat monografiyasi 22. NIH Pub. № 17-CA-8035A. Bethesda, MD: AQSh Sog'liqni saqlash va inson xizmatlari departamenti, Milliy sog'liqni saqlash institutlari, Milliy saraton instituti 2017.

AQSh sog'liqni saqlash va odamlarga xizmat ko'rsatish vazirligi. Yoshlar va kattalar orasida elektron sigaretdan foydalanish: Bosh jarroh hisoboti. Atlanta, GA: AQSh Sog'liqni saqlash va aholiga xizmat ko'rsatish departamenti, Kasalliklarni nazorat qilish va oldini olish markazlari, Surunkali kasalliklarning oldini olish va salomatlikni mustahkamlash milliy markazi, Chekish va salomatlik bo'yicha idora 2016 yil.

Mehnat xavfsizligi va salomatligi milliy instituti. Ish joyidagi tamaki siyosati orqali sog'liqni saqlash va kasallik va shikastlanishlarning oldini olish. Hozirgi razvedka byulleteni. DHHS (NIOSH) Nashr No 2015-113. AQSh Sog'liqni saqlash va odamlarga xizmat ko'rsatish vazirligi, Kasalliklarni nazorat qilish va profilaktika markazi, Mehnat xavfsizligi va salomatligi milliy instituti 2015.

Tynan MA, Xolms CB, Promoff G va boshqalar. Ish joylari, restoranlar va barlar uchun shtat va mahalliy keng qamrovli chekmaydigan qonunlar - Amerika Qo'shma Shtatlari, 2015 yil. MMWR kasalligi va o'limi haftalik hisoboti 2016 65(24):623-626.


Oddiy odamga sigareta tutuni qanday saraton kasalligiga olib kelishi mumkinligini tushuntiring - Biologiya

Chekish-gaz almashinuvi va qon aylanish tizimining surunkali, hayot uchun xavfli kasalliklarining oldini olish mumkin bo'lgan asosiy xavf omillaridan biri.

Sigaretaning tutunida gaz almashinuvi tizimi va yurak-qon tomir tizimiga ta'sir qiluvchi bir nechta moddalar mavjud. Bularga quyidagilar kiradi:

qatron , moddalar aralashmasi, shu jumladan kanserogenlar sifatida ishlaydigan turli xil kimyoviy moddalar.
nikotin , miya va tananing boshqa qismlarida neyronlar (nerv hujayralari) retseptorlari bilan bog'lanib, asab tizimiga ta'sir qiluvchi, o'ziga qaram bo'lgan modda. Bu neyrotransmitterning chiqarilishini oshiradi dopamin miyada, bu lazzatlanish hissini beradi. ning chiqarilishini oshiradi adrenalin qonga kiradi, bu esa o'z navbatida nafas olish tezligini va yurak tezligini oshiradi. Bundan tashqari, nikotin qon pıhtılarının paydo bo'lish ehtimolini oshiradigan ba'zi dalillar mavjud.
CO , Hb bilan qaytarilmas birlashib, karboksiemoglobin hosil qiladi. Bu O. bilan birlasha oladigan Hb miqdorini kamaytiradi2, va shuning uchun O miqdorini kamaytiradi2 bu tana to'qimalariga ko'chiriladi.


Chekishning gaz almashinuv tizimiga ta'siri

Surunkali obstruktiv o'pka kasalligi (KOAH)

Bu odamda surunkali bronxit va amfizem bo'lgan holat. Bu juda o'chirib qo'yishi mumkin.

Surunkali bronxit

Sigaret tutunining turli tarkibiy qismlari, shu jumladan smola, ko'zoynak hujayralari balg'am ishlab chiqarishni ko'payishiga, siliya esa kamroq urilishiga olib keladi. Bu alveolalarni qisman to'sib qo'yishi mumkin bo'lgan mukus to'planishiga olib keladi. Bu gaz almashinuvini qiyinlashtiradi, chunki alveolalardagi havo va kapillyarlardagi qon orasidagi diffuziya masofasi kattaroqdir. Balg'am bakteriyalar bilan kasallangan bo'lishi mumkin bronxit . Chekuvchilar ko'pincha surunkali (uzoq davom etadigan) bronxitga ega.

Balg'am doimiy yo'talni rag'batlantiradi, bu nafas yo'llarining devorlaridagi to'qimalarga zarar etkazishi mumkin, ularni qattiqroq va nafas yo'llarini toraytiradi.

Emfizema

Chekish o'pkada yallig'lanishni keltirib chiqaradi. Bu oq qon hujayralari sonining ko'payishini o'z ichiga oladi, ularning ba'zilari elastik tolalarga zarar etkazadigan kimyoviy moddalarni chiqaradi. Bu alveolalarni kamroq elastik qiladi. Ular portlashi mumkin, natijada katta havo bo'shliqlari paydo bo'ladi. Bu gaz almashinuvi mumkin bo'lgan sirt maydonini kamaytiradi. Bu amfizem deb ataladi. Amfizem bilan og'rigan odamda nafas qisilishi bor, ya'ni ular kerak bo'lganda chuqur nafas olish uchun kurashadilar, ayniqsa mashqlar paytida.

O'pka saratoni

Qatronning turli komponentlari tana hujayralarida DNKning o'zgarishiga olib kelishi mumkin, shu jumladan saraton kasalligiga olib kelishi mumkin bo'lgan hujayralar bo'linishini boshqaruvchi genlar. Shuning uchun bu moddalar kanserogenlar . Sigaret tutunidan kelib chiqadigan saraton o'pkada paydo bo'lishi mumkin, ammo gaz almashinuvi tizimining istalgan joyida, shuningdek tananing boshqa qismlarida paydo bo'lishi mumkin. Chekish saratonning barcha turlarini rivojlanish xavfini oshiradi. O'pka saratonining alomatlariga nafas qisilishi, surunkali yo'tal kiradi
qon - ko'krak og'rig'i, charchoq va vazn yo'qotish.

Chekishning yurak -qon tomir tizimiga ta'siri

Tamaki tutunidagi nikotin va CO ning rivojlanish xavfini oshiradi ateroskleroz . Ateroskleroz - arteriyalar devorlarining qalinlashishi va elastikligining yo'qolishi. Bu qon tomirlari devorida blyashka to'planishi natijasida yuzaga keladi. Blyashka tarkibida xolesterin va tolalar mavjud. Ular qon pıhtılarının shakllanishini rag'batlantiradigan, arteriyani qoplaydigan qo'pol sirt hosil qiladi.

Qon pıhtı arteriya devoridan ajralib chiqishi va qon tizimining boshqa joylarida, masalan, o'pkada yoki miyada tor tomirga yopishib qolishi mumkin. Bu qon o'tishini oldini oladi, shuning uchun hujayralar O bilan ta'minlanmaydi2 va o'l. Agar bu miyada sodir bo'lsa, u a deyiladi insult.

Arteriya yoki arteriolada elastiklikning yo'qolishi, shuningdek, yuqori bosimli qon zarbasi paytida tomirning yorilishi ehtimolini oshiradi. Bu qon tomirining yana bir sababidir.

Agar yurak mushagini kislorodli qon bilan ta'minlaydigan koronar arteriyalarda ateroskleroz ro'y bersa, odamda shunday bo'ladi koroner yurak kasalligi (CHD). Mushak qismlari to'g'ri ishlamay qolishi mumkin, chunki ular etarli O ga ega emas2 aerob nafas olish uchun. Mushak o'lishi mumkin. Oxir-oqibat, yurakning bu qismi urishni to'xtatib, yurak xurujiga olib kelishi mumkin.


Chekishning salomatlikka ta'siri haqida dalillar

Chekishning sog'liqqa ta'sirini o'rganishning ikki yo'li mavjud.

Epidemiologik dalillar

Bu odamlarning chekish odatlari va ularning sog'lig'i haqida to'plangan ma'lumotlardan iborat. Tadqiqotga ko'p odamlar jalb qilinishi kerak. Tadqiqotchilar chekish va ma'lum kasalliklar o'rtasidagi bog'liqlikni izlaydilar. Garchi bu yondashuv chekish va kasallik o'rtasidagi sababiy bog'liqlik haqida hech qanday aniq dalil keltirmasa-da, u hech bo'lmaganda sababiy bog'liqlik mavjudligini ko'rsatishi mumkin. Agar bizda chekish qanday kasallikka olib kelishi mumkinligini ko'rsatadigan fiziologik dalillar bo'lsa, demak bu chekishning haqiqatan ham kasallikka olib kelishiga kuchli dalil qo'shadi.

Eksperimental dalillar

Bu nazorat ostida tajribalarni o'tkazishdan iborat. Masalan, mustaqil o'zgaruvchi subyekt sigaret chekadimi yoki yo'qmi (yoki qancha chekadi) bo'lishi mumkin va qaram o'zgaruvchi fiziologiyaning ba'zi jihatlari bo'lishi mumkin. Boshqa barcha o'zgaruvchilar doimiy bo'lishi kerak. Odamlarda bu mumkin emas, chunki odamlarni chekish axloqsiz bo'ladi. 1960 -yillarda bunday tajribalarda itlar va boshqa hayvonlardan foydalanilgan. Natijalar tamaki chekish o'pka saratoni rivojlanish xavfini sezilarli darajada oshirishini aniq ko'rsatdi. Tajribalar o'sgan hujayralar yordamida ham o'tkazilishi mumkin
to'qima madaniyati. Ushbu hujayralarga smolada topilgan kimyoviy moddalar ta'siri, bu kimyoviy moddalar DNKga zarar etkazishi mumkinligini ko'rsatadi.

CHDning oldini olish va davolash

CHD rivojlanish xavfi oshadi:

• genlarning alohida allellarini meros qilib olish
• to'yingan yog'lar va xolesteringa boy dietani iste'mol qilish
• etarli mashq qilmayapti
• semirib ketish
• chekish

Og'ir CHDni koronar bypass yordamida davolash mumkin, bunda kislorodli qonning aortadan yurak mushagiga oqishi uchun muqobil yo'lni ta'minlash uchun tananing boshqa qismidan qon tomirlari olinadi va joyiga tikiladi.

Agar yurak yurak-qon tomir kasalliklari yoki boshqa sharoitlar tufayli tuzatib bo'lmaydigan darajada shikastlangan bo'lsa, unda uzoq muddatli yagona variant yurak transplantatsiyasi bo'lishi mumkin. Yurak endigina vafot etgan (ko'pincha baxtsiz hodisada) va qabul qiluvchiga o'xshash to'qima turiga ega bo'lgan odamdan chiqishi kerak. Shunday bo'lgan taqdirda ham, qabul qiluvchi immunitet tizimining donor to'qimalariga hujum qilishiga va transplantatsiyani rad etishiga yo'l qo'ymaslik uchun, umrining oxirigacha immunosupressant dorilarni qabul qilishi kerak bo'ladi.

CHD va boshqa yurak kasalliklarining oldini olish murakkab jarrohlik amaliyotini o'tkazishdan ko'ra aniqroqdir. Yuqorida sanab o'tilgan xavflarni kamaytiradigan turmush tarzini tanlash mumkin (albatta, odamda mavjud bo'lgan genlardan tashqari). Biroq, tadqiqotlar shuni ko'rsatadiki, ozgina semirib ketgan odamlar, yupqa odamlarga qaraganda, yurak operatsiyasidan keyin yaxshi tiklanish ehtimoli ko'proq.


Chekish va saraton

Shakl (PageIndex<3>): AQShda erkaklar tomonidan sigaret chekish 1950-yillarda pasayishni boshladi, ammo 1970-yillarga qadar va taxminan 20 yil o'tgach, bu o'pka saratonidan o'limning bir vaqtning o'zida kamayishi bilan namoyon bo'ldi. erkaklar

Chekishning sog'liq uchun asosiy xavflaridan biri saraton, ayniqsa o'pka saratoni hisoblanadi. Chekish bilan o'pka saratoni xavfi ortib borayotganligi sababli, 85 yoshgacha o'pka saratonidan o'lish xavfi chekmaydigan erkaklarnikiga qaraganda 20 baravar yuqori. Chekish darajasi oshgani sayin o'pka saratonidan o'lim darajasi ham oshadi, garchi chekishning o'pka saratonidan o'limga ta'siri o'zini namoyon qilish uchun 20 yilgacha vaqt ketishi mumkin, rasmda ko'rsatilganidek, (PageIndex<3>).

O'pka saratoni bilan bir qatorda, sigaret chekmaydiganlarga qaraganda saratonning boshqa bir qancha shakllari, shu jumladan buyrak, halqum, og'iz, lab, til, tomoq, siydik pufagi, qizilo'ngach, oshqozon osti bezi va oshqozon saratoni ham sezilarli darajada ko'proq. Afsuski, bu saratonlarning ko'pchiligi juda past davolanishga ega.

Tamaki tutunining tarkibini ko'rib chiqsangiz, bu saraton xavfini oshirishi ajablanarli emas. Tamaki tutunida o'nlab kimyoviy moddalar mavjud bo'lib, ular kanserogenlar yoki saraton kasalligi sabablari isbotlangan. Bu kimyoviy moddalarning ko'pchiligi chekuvchi va rsquos hujayralarida DNK bilan bog'lanadi va hujayralarni o'ldirishi yoki mutatsiyaga olib kelishi mumkin. Agar mutatsiyalar dasturlashtirilgan hujayra o'limini inhibe qilsa, hujayralar saraton hujayralariga aylanish uchun omon qolishi mumkin. Tamaki tutunidagi eng kuchli kanserogenlar qatoriga benzopiren, akrolein va nitrozaminlar kiradi. Tamaki tutunidagi boshqa kanserogenlar radioaktiv izotoplar, shu jumladan qo'rg'oshin-210 va poloniy-210.


Chekish va saraton o'rtasidagi bog'liqlik


Xalqaro Saraton Tadqiqot Agentligi tamaki iste'molini og'iz bo'shlig'i, farenks, qizilo'ngach, oshqozon, ichak, jigar, o'pka, oshqozon osti bezi, burun bo'shlig'i va paranasal sinuslar, halqum saratoni uchun 1 -guruh kanserogen (IARCning eng yuqori tasnifi) deb tasniflagan. , bachadon, bachadon bo'yni, tuxumdon, siydik, siydik pufagi, buyrak, siydik va miyeloid leykemiya. Ώ ] Tamaki iste'moli ko'krak bezi saratoni bilan ham bog'liq bo'lishi mumkinligi haqida ko'plab dalillar mavjud (ayollarda). Ώ ]

Tamaki tutunida 60 dan ortiq kanserogenlar mavjud. Polisiklik aromatik uglevodorodlar (PAH), N- nitrozaminlar, masalan, 4- (metilnitrosamino) -1- (3-piridil) -1-butanon (NNK) va N'-nitrosonornikotin (NNN), aromatik aminlar, 1,3-butadien, benzol, aldegidlar va etilen oksidi kanserogenligi va sigaret tutunining yuqori darajasi tufayli eng muhim birikmalardan biridir. ΐ] 2010 yilda tashxis qo'yilgan barcha saraton kasalliklarining 13% tamaki bilan bog'liq bo'lib, o'pka saratoni saraton bilan bog'liq bo'lgan eng ko'p holatlarga ega. Α ]

Chekish 16 turdagi saraton kasalligining sababi ekanligi to'g'risida ishonchli dalillar va chekishni bir -biri bilan bog'laydigan cheklangan dalillar mavjud (1 -jadvalga qarang). Ώ ] Tadqiqotlar shuni ko'rsatdiki, tutunsiz tamaki (chaynash tamaki va tamaki kabi) bo'shliq, qizilo'ngach va oshqozon osti bezi saratoni xavfi ancha yuqori. Ώ ]

Chiqishdan keyin vaqt oshishi bilan saraton rivojlanish xavfi kamayadi. Β] Γ] Δ] Tadqiqotlar shuni ko'rsatdiki, hozirgi chekuvchilar orasida umr ko'rish davomiyligi 10 yil yoki undan ko'proqqa qisqaradi. Δ] Ε] 25 yoshdan 34 yoshgacha chekishni tashlagan kattalar uchun 10 yillik hayot tiklanadi, 35 yoshdan 44 yoshgacha bo'lganida to'qqiz yil va 45 yoshdan 54 yoshgacha olti yillik hayot tiklanadi. , chekishni davom ettirayotganlar bilan solishtirganda. Ζ ]

Tamaki iste'moli bilan bog'liq bo'lgan bir qator saraton turlari, masalan, oshqozon osti bezi saratoni ko'pincha rivojlangan bosqichda tashxis qilinadi va boshqa ma'lum turmush tarzini o'zgartirish yoki aralashuvlar orqali oldini olish mumkin emasligini hisobga olsak, tamaki tutuniga ta'sir qilishdan qochish mumkin bo'lgan yagona choralardan biridir. individual xavfni faol ravishda kamaytirish. Ζ] Tamaki iste'moli va saraton o'rtasida doza-javob o'zaro bog'liqligi bor, ya'ni vaqt o'tishi bilan qancha ko'p tamaki chekilsa, tamaki bilan bog'liq saraton rivojlanishi xavfi shunchalik yuqori bo'ladi. Β] Γ] Η] ⎖]


Jadval 1. Tamaki va saratonning har xil turlari o'rtasidagi bog'liqlikni isbotlovchi IARC darajalari

Xavf omili Kanserogenlikning etarli dalillari Kanserogenlik haqida cheklangan dalillar Kanserogenlik etishmasligidan dalillar
Tamaki chekish Og'iz bo'shlig'i, farenks, qizilo'ngach, oshqozon, ichak, jigar, oshqozon osti bezi, burun bo'shlig'i va paranasal sinuslar, halqum, o'pka, bachadon bo'yni, tuxumdon, siydik pufagi, buyrak, siydik pufagi, suyak iligi (miyeloid leykemiya) Ayol ko'krak Endometrium (postmenopozal), qalqonsimon bez
Ikkinchi qo'l tutun O'pka Tomoq, tomoq
Tutunsiz tamaki Og'iz bo'shlig'i, qizilo'ngach, oshqozon osti bezi
Ota -onalarning chekishi (bolalarda saraton) Gepatoblastoma Bolalardagi leykemiya

Chekish va spirtli ichimliklar

Chekish va spirtli ichimliklar oshqozon-ichak trakti va oshqozon-ichak saratoni xavfiga sinergik ta'sir ko'rsatadi. ⎗] Rivojlangan mamlakatlarda yuqori aero-ovqat hazm qilish tizimi saratonining 75% dan ortig'i shu ta'sir bilan bog'liq bo'lishi mumkinligi taxmin qilingan. Masalan, chekmaydiganlar ichmaydiganlar bilan solishtirganda, og'iz va tomoq saratoni rivojlanishining taxminiy nisbiy xavfi tamaki iste'mol qiladiganlar uchun etti baravar, spirtli ichimliklarni iste'mol qiladiganlar uchun olti baravar va 35 baravar yuqori. tamaki va spirtli ichimliklarni muntazam iste'mol qiladiganlar. ⎘ ]

Spirtli ichimliklar og'iz bo'shlig'i, faringeal, laringeal va qizilo'ngach saratoni xavfiga mustaqil ta'sir ko'rsatadi, ammo uning chekish bilan sinergik ta'siri muhimroqdir. ⎙ ]

Qo'shimcha ma'lumot olish uchun Milliy saraton profilaktikasi siyosatining Alkogol bo'limiga qarang.

Ikkinchi qo'l tutun

Dalillar shuni ko'rsatadiki, ikkinchi qo'l tutuni o'pka saratoniga olib keladi (2-jadvalga qarang). Ώ] ⎚] ⎛] ⎜] ⎜] Uyda yoki ish joyida uzoq muddatli tutunga ta`sir qilish chekmaydigan odamda o'pka saratoni xavfini 20-30% ga oshirishi mumkin. ⎛ ] Shuningdek, tutun tutuni va halqum va tomoq saratoni o'rtasidagi bog'liqlik borasida cheklangan dalillar mavjud (2-jadvalga qarang). Ώ ] ⎚ ]

Ikkinchi qo'l tutun ham burun sinusi, nazofarenks, ko'krak, bachadon bo'yni, qovuq va buyrak saratoni uchun xavf omili bo'lishi mumkin. ⎛ ] Tamaki tutunining tug'ruqdan oldingi va keyingi ta'siri bolalarda miya shishi, limfoma va o'tkir limfotsitik leykemiya xavfini oshirishi mumkin. ⎝ ] ⎞ ] ⎟ ]


Tamaki

Umuman chekish kamaygan, lekin yosh kattalar uchun profilaktikani kuchaytirish kerak.

Tamaki iste'moli saraton va saraton kasalligidan o'limning asosiy sababidir. Tamaki mahsulotlarini ishlatadigan yoki doimiy ravishda atrof-muhit tamaki tutuni atrofida bo'lgan (shuningdek, ikkinchi qo'l tutuni deb ataladi) odamlarda saraton xavfi ortadi, chunki tamaki mahsulotlari va tutunida DNKga zarar etkazadigan ko'plab kimyoviy moddalar mavjud.

Tamaki iste'moli ko'plab saraton turlarini keltirib chiqaradi, jumladan o'pka, halqum (ovozli quti), og'iz, qizilo'ngach, tomoq, siydik pufagi, buyrak, jigar, oshqozon, oshqozon osti bezi, yo'g'on va to'g'ri ichak va bachadon bo'yni saratoni, shuningdek o'tkir miyeloid leykemiya. Tutunsiz tamaki iste'mol qiladigan odamlarda og'iz bo'shlig'i, qizilo'ngach va oshqozon osti bezi saratoni xavfi ortadi.

Tamaki iste'mol qilishning xavfsiz darajasi yo'q. Tamaki mahsulotining har qanday turidan foydalanadigan odamlarni, albatta, chekishni tashlashga chaqirishadi. Chekishni tashlagan odamlar, yoshidan qat'i nazar, chekishni davom ettirayotganlarga qaraganda, umr ko'rish davomiyligi sezilarli darajada oshadi. Shuningdek, saraton tashxisi qo'yilganda chekishni tashlash o'lim xavfini kamaytiradi.

Tamaki ishlatishning zarari haqida ko'proq ma'lumot olish uchun qarang:

Shuningdek, NCI telefon orqali va onlayn rejimida tamakidan voz kechish haqida bepul, maxfiy ma'lumotlarni taqdim etadi:


Chekish o'pka bilan birga boshqa organlarda saraton kasalligini keltirib chiqaradi

Olimlar chekish nafaqat o'pka saratoni, balki 17 turdagi saraton xavfini oshirishini aniqladilar. Buning sababi shundaki, chekish tananing turli organlarida hujayra mutatsiyasini keltirib chiqaradi. So'nggi tadqiqot shuni ko'rsatadiki, bir quti sigaret chekish har bir chekish yili uchun o'pkaning har bir hujayrasida qo'shimcha 150 ta mutatsiyaga olib keladi.

Tadqiqot natijalariga ko'ra, ta'sirlanadigan boshqa organlarga har bir gırtlak hujayrasida o'rtacha 97 ta, farenksda 39 ta, og'izda 23 ta, siydik pufagida 18 ta va jigarning har bir hujayrasida 6 ta, yil.

Sigaret chekish har yili 6 milliondan ziyod odamni yo'qotadi. Cigarettes contain more than 60 carcinogens, all of which accelerate tumor growth by causing mutations in the tumor DNA.

The scientists analyzed somatic mutations which is the alteration of genes causing them to pass on in cell division and DNA methylation in 5,243 genomes for which tobacco smoking is known to increase risk of cancer.

They studied these cancers and compared them with cancers found in nonsmokers, in order to analyze biophysical differences between the two types, focusing on mutational signatures that vary in different cancers.

Smoking is linked with increased mutation burdens of a variety of different mutational signatures which cause the biologically different effects in different cancers. One of these signatures, mainly found in cancers derived from tissues directly exposed to tobacco smoke, is attributable to misreplication of DNA damage caused by tobacco carcinogens.

Others likely reflect indirect activation of DNA editing by APOBEC cytidine deaminases and of an endogenous clocklike mutational process. However, smoking causes DNA methylation in a limited amount. The results are consistent with the proposition that smoking increases cancer risk by increasing the somatic mutation frequency, although clear proof for this mechanism is lacking in some smoking-related cancer types.

Dr Ludmil Alexandrov, first author from Los Alamos National Laboratory, had this to say, “Before now, we had a large body of epidemiological evidence linking smoking with cancer, but now we can actually observe and quantify the molecular changes in the DNA due to cigarette smoking.

With this study, we have found that people who smoke a pack a day develop an average of 150 extra mutations in their lungs every year, which explains why smokers have such a higher risk of developing lung cancer.”

Even though it is a remarkable study in its own, it still remains unclear how exactly smoking causes increase in tumors in other parts of the body that are unaffected by smoke. However, this research points out that different mechanisms are at play by which tobacco smoking causes these mutations, depending on the area of the body affected.

Professor David Phillips, an author on the paper and Professor of Environmental Carcinogenesis at King’s College London, believed that the results were quite fascinating as they were a combination of predicted and unexpected theories, and laid out the direct and indirect effects.

The expected result was that mutations caused by direct DNA damage from carcinogens in tobacco were mostly observed in organs that were in direct contact of tobacco smoke such as mouth and lungs.

In contrast, the unexpected or surprising result was that the other cells of the body suffered from indirect damage, as tobacco smoking seems to affect key mechanisms in these cells that in turn cause DNA mutations, which could be why other organs got affected so frequently.

Consistent with the proposition that an increased mutation load caused by tobacco smoke causes an increased cancer risk, the total mutation burden is higher in smokers compared to nonsmokers, specifically in lung adenocarcinoma, larynx, liver and kidney cancers.

However, differences in total mutation frequency were not observed in the other cancer types linked with smoking and in some there were no statistically significant smoking-associated differences in mutation load, mutation signatures or DNA methylation.

The researchers warned that this does not mean that smokers will be safe from acquiring certain cancers and careful deliberation is required when analyzing such findings. Aside from statistical limitations to thoroughly study the invasive effects of cancer, multiple rounds of clonal expansion over many years are required.

Therefore, it is possible that in the normal tissues from which smoking-associated cancer types originate, there are more somatic mutations or differences in methylation in smokers than in nonsmokers that could have been missed by the scientists as these differences become obscured at the start of clonal evolution, as the immune system has not expanded as such to properly detect the tumors.

Further studies should also involve e-cigarette users as a majority of population is switching to them in the hope of quitting smoking. Teenagers and young adults especially are using e-cigarettes as a form of recreation.

If follow-up studies include e-cigarettes and find similar results of accelerated cancer growth, it is hoped that people will be able to quit smoking altogether in any form.


Effects of cigarette smoke on the human airway epithelial cell transcriptome

Cigarette smoke is the major cause of lung cancer, the leading cause of cancer death, and of chronic obstructive pulmonary disease, the fourth leading cause of death in the United States. Using high-density gene expression arrays, we describe genes that are normally expressed in a subset of human airway epithelial cells obtained at bronchoscopy (the airway transcriptome), define how cigarette smoking alters the transcriptome, and detail the effects of variables, such as cumulative exposure, age, sex, and race, on cigarette smoke-induced changes in gene expression. We also determine which changes in gene expression are and are not reversible when smoking is discontinued. The persistent altered expression of a subset of genes in former smokers may explain the risk these individuals have for developing lung cancer long after they have discontinued smoking. The use of gene expression profiling to explore the normal biology of a specific subset of cells within a complex organ across a broad spectrum of healthy individuals and to define the reversible and irreversible genetic effects of cigarette smoke on human airway epithelial cells has not been previously reported.

Raqamlar

Clustering of current- and never-smoker…

Clustering of current- and never-smoker samples. Hierarchical clustering of current ( n =…

Multidimensional scaling plot of current-,…

Multidimensional scaling plot of current-, never-, and former-smoker samples. Multidimensional scaling plot of…

Genes irreversibly altered by cigarette…

Genes irreversibly altered by cigarette smoke. Hierarchical clustering plot of 15 of the…


Materiallar va uslublar

Study Subjects.

We conducted a population-based case-control study of risk factors for prostate cancer in middle-aged men, including lifetime history of cigarette smoking. Case patients included Caucasian and African-American male residents of King County in northwestern Washington, 40–64 years old, who were diagnosed with biopsy-proven prostate cancer between January 1, 1993, and December 31, 1996. Eligible cases were identified from the Seattle-Puget Sound SEER cancer registry and included 100% ages < 60 years and a random 75% sample of those who were ages 60–64 years at diagnosis.

A comparison group (n = 703) without a history of prostate cancer was identified through random digit dialing using a clustering factor of five residences/sampling unit (11) . These individuals were male residents of King County, Washington, 40–64 years of age. Controls were frequency matched to case patient by age (same 5-year group) and recruited evenly throughout the ascertainment period of cases.

All study participants signed informed consent for participation. The Fred Hutchinson Cancer Research Center’s Institutional Review Board approved study forms and procedures. Study subjects completed a structured in-person interview administered by a trained male interviewer. The questionnaire addressed the following areas: social and demographic factors physical development, height, weight, and physical activity reproductive history detailed medical history, including history of BPH and prostate cancer screening family structure and cancer history dietary habits, including total dietary fat intake and servings of cruciferous vegetables consumed/week lifetime smoking and alcohol consumption lifetime sexual history and occupational history. Clinical patient data were available from the cancer registry, including tumor grade and stage of disease at diagnosis. A detailed smoking history before reference date (date of diagnosis for cases and a similar assigned date for controls) was collected, including ages at onset and cessation, duration, and dose of cigarette smoking.

Statistical Methods.

ORs were calculated to estimate the association between prostate cancer and the following smoking variables (continuous and categorized): smoking status (nonsmoker, current, former) duration of smoking (1–9, 10–19, 20–29, 30–39, ≥40 years) number of cigarettes smoked/day (1–10, 11–20, 21–30, 31–40, ≥41) total pack-years of smoking (>0–10, 11–20, 21–30, 31–40, >40) years since cessation in former smokers (>0–9, 10–19, 20–29, ≥30 years) and age first smoked (≤15, 16–17, 18–19, ≥20 years). Multivariate logistic regression (12) analysis was used to compute ORs and estimate 95% CIs adjusted for potential confounders such as age, race, family history of prostate cancer, body mass index, history of prostate cancer screening such as PSA testing (ever had a PSA, had a PSA > 1 year before reference date, number of PSA tests within the 5-years before reference date) or digital rectal examination > 1 year before reference date, dietary habits, physical activity, socioeconomic factors, and medical history. Any covariate that produced a change of >5% in the age-adjusted OR for the smoking status-prostate cancer association was included in the final model, ya'ni, race, family history of prostate cancer in a first-degree relative, history of PSA testing >1 year before reference date, and a history of BPH. To examine if a dose-response relationship existed between smoking and prostate cancer, trend tests were performed using only cases and controls that were exposed to smoking (13) .

To explore the hypothesis that smoking was associated with the development of more aggressive prostate cancer, additional analyses were completed using a polychotomous multivariate regression model (14) . These models compared controls to cases with less aggressive (localized stage and Gleason score ≤ 7) and more aggressive (regional or distant stage disease or Gleason score 8–10) prostate cancer.


The Biology of Smoking and AMD

Ivan J. Suñer , MD
Scott W. Cousins, MD
Durham, N.C.

As age-related macular degenera tion primarily affects the macula, it has a severe impact on many of the basic ac­tivities of daily living such as driving, recognizing faces and reading. Therefore, it robs af­fected in­dividuals of their independence in their retirement years. Fif­teen million people in the United States alone are affected by AMD, and current estimates project this figure to increase by 50 percent by the year 2020. Ap­proximately 1.75 million (10 percent) Am­er­icans have the advanced or late forms of the dis­ease, exudative/wet AMD and geographic atrophy. 1

Epidemiology of Smoking and AMD

AMD is a multifactorial disease with associated age, environmental, sys­tem­ic and genetic factors. Age is the major risk factor in AMD. The prevalence of all forms of AMD increases significantly with age. It affects approximately 17 percent of all individuals between the ages of 55 and 64, and the prevalence rises to approximately 37 percent in those 75 or older. 2 The more ad­vanced, disabling forms (ex­uda­tive/wet and geographic atrophy) affect 1 percent of Cau­casian patients in their 50s, rising to more than 15 percent of those in their 80s. 1

Figure 1. Representative transmission electron micrographs (TEM) of outer retina and choroid in 16-month-old female mice demonstrating dry AMD findings in mice exposed to cigarette smoke or hydroquinone, a major component of cigarette tar. Panel A. TEM of mouse fed high fat diet without exposure to cigarette smoke or hydroquinone specimen shows mild nodular sub-RPE deposits (white arrows) Bruch's membrane and choriocapillaris are normal thickness. Panel B. TEM of mouse fed high-fat diet and exposed to cigarette smoke there are sub-RPE deposits (white arrows) and thickening of Bruch's membrane with accumulation of a homogenous material (white asterisk). Panel C. TEM of mouse fed high-fat diet plus hydroquinone there are thick sub-RPE deposits (white asterisks) and marked thickening of Bruch' s membrane (white arrows).

Cigarette smoking is the single most important modifiable environmental risk factor for development of all forms of AMD. Multiple large, well-controlled, cross-sectional 3-6 and prospective 7,8 studies in the United States, Australia, France and the Neth­erlands have demonstrated a 2.5- to threefold increase in the risk of all forms of AMD in smokers. Of particular interest is an analysis of pooled data from cross-sectional studies carried out in North Am­erica, Eu­rope and Australia. This data shows an es­pecially large disparity between cur­rent and never smokers with a threefold increase in all forms of AMD, 2.5-fold increase in atrophic AMD, and 4.5-fold increase in neovascular AMD 9 ( See Table 1 ).

Figure 2. Representative flatmount preparation (propidium iodide stain) of the posterior pole of 11-month-old mouse eyes 4 weeks after laser treatment. Four laser spots centered on the optic nerve (D) were performed. Panel A. Control group. CNV lesions were small and circular with discrete borders (dotted lines). Panel B. Oral nicotine group. In this example there is coalescence of three laser injuries gives rise to a large CNV complex (dotted lines). Panel C. Oral nicotine and subconjunctival hexamethonium group. A reduction of the severity of CNV lesions can be clearly appreciated with concurrent administration of a nicotine antagonist, hexamethonium. CNV lesions (dotted line) were similar in size to the control.

An important factor, yet difficult to tease out of this association, is the in­fluence of pack years, current smoking status, ex-smoker and passive smoker. A recent study looked at these issues specifically. 10 It demonstrated a strong association between AMD and number of pack years smoked. The odds ratio in patients smoking greater than 40 pack years was 2.75 as compared to nonsmokers the odds ratio was 3.43 for geographic atrophy and 2.49 for choroidal neovascularization. Smoke cessation was associated with decreasing risk, reaching a similar risk to nonsmokers at 20 years of not smoking. Pas­sive smoking was associated with an odds ratio of 1.87.

An interesting observation is the trend towards earlier onset of AMD, including advanced forms, in Asian countries. This has been attributed in large part to the increased rates of smoking and environmental pollutants. 11

Why Study Smoking and AMD?

Despite the wealth of robust epidemiologic evidence associating smoking with AMD, there is a relative dearth of science to support it. Only now are we beginning to study and elucidate pathobiologic mechanisms of this association. This may be partly due to the concept that cigarette smoking is considered purely a modifiable risk factor. In other words, pa­tients with AMD should quit smoking, and, therefore, there is not more to be gained by further pursuing this association on a biologic level. However, studying the effects of smoking on AMD may provide us with insights into the pathobiology of this complex disease process. Furthermore, some of the lessons we learn may translate into therapies for smokers as well as for nonsmokers.

Composition of Cigarette Smoke

Cigarette smoke is a complex mixture of more than 4,000 chemical substances. Selecting which molecules to study within the daunting number of potential candidates is a difficult issue. The agents present in cigarette smoke are generally subdivided into particulate and gaseous phases. 12 The major components of the particulate phase are tar and nicotine, whereas the gas­eous phase is composed primarily of carbon monoxide, carbon dioxide and nitric oxide.

Various proposed mechanisms by which cigarette smoke may cause end-organ damage include direct effects from chemicals in the smoke, immune activation, secondary hypoxia from pulmonary damage, and secondary sequelae from smoking-induced vascular disease.

The exact pathogenesis of drusen remains an unresolved question. One paradigm, "the response to injury" hy­pothesis, proposes that the RPE cell is the target for specific injury stimuli, resulting in deposit accumulation. 13

Cigarette smoke tar contains nu­merous pro-oxidant compounds within the quinone family. 14 Within these, hydroquinone, a benzene derivative, is the most abundant quinone in cigarette tar. High levels are detected in the plasma and urine of smokers. 14

Our group tested this hypothesis in cultured human RPE cells. In­cu­bation of RPE cells with hydroqui­none induced a specific injury re­sponse called nonlethal blebbing, a process that is proposed to be related to sub-RPE deposit formation. 15 Fur­thermore, exposure to hydroquinone also resulted in decreased levels of matrix metalloproteinase-2 and in­creased levels of collagen IV as measured by zymography ( Suñer I, et al. In­vest Ophthalmol Vis Sci. 200445: ARVO E-Abstract 1810 ). This leads to a net decrease in extracellular matrix turnover, which would result in thickening of Bruch's membrane or formation of sub-RPE deposits.

This relationship was further studied in an animal model by exposing mice to whole cigarette smoke or oral hydroquinone. In mice fed a high-fat diet and exposed to either cigarette smoke in a smoking chamber or di­et­ary hydroquinone, Bruch's membrane was thickened and sub-RPE deposits developed in contrast to controls only receiving a high-fat diet ( See Figure 1 ). 16 Therefore, smoke-related oxi­dants, specifically tar, ap­pear to be a significant oxidative in­jury stimulus that leads to dry AMD in the context of other oxidative sources such as high-fat diet or blue light. It is also likely that while tar is a po­tent oxidant within cigarette smoke, it is not the only oxidant molecule in this pathway.

Nicotine is an attractive candidate molecule to explain an association of smoking with wet AMD. It has been shown to be mitogenic for vascular endothelial cells and smooth muscle pericytes, to reduce apoptosis of vascular endothelial cells, and to induce the formation of capillary tubes. 17,18

We explored the effects of nicotine in a laser model for CNV in mice. We compared CNV size in those receiving nicotine in the drinking water or cigarette smoke in a smoking chamber with control animals. Mice receiving nicotine or cigarette smoke had a statistically significant increase in CNV size (twice the di­ameter in aged mice). This effect was blocked by subconjunctival coadministration of a nonspecific nicotinic antagonist, hexamethonium ( See Figure 2 ). 17

The experiment was carried one step further, and bone-marrow transplantation was performed within the CNV mouse model. Mice that were exposed to cigarette smoke in a smoking chamber and subsequently had bone marrow ablation followed by bone marrow reconstitution from a control mouse had regression of CNV to control levels. Conversely, a control mouse receiving bone marrow from a cigarette smoke-exposed mouse de­monstrated increased CNV size com­parable to cigarette smoke-ex­posed mice ( Cousins S, et al. Invest Oph­thalmol Vis Sci. 200647:ARVO E-Ab­stract 4172 ). This suggests that bone marrow-derived cells, either endothelial or inflammatory precursor cells, may play a role in establishing or modulating choroidal neovascularization.

Immunohistochemical analysis of CNV in cigarette smoke-exposed or nicotine-exposed mice reveals an in­creased number of macrophages in these lesions as compared to controls. Furthermore, it demonstrated higher le­vels of macrophages expressing TNF-a and COX-2 ( Suñer I, et al. In­vest Ophthalmol Vis Sci. 200647: ARVO E-Abstract 1531 ). These are markers of activated macrophages, which supports current theories of in­flam­matory contributions to the path­ogenesis of AMD.

The immediate clinical implications of these findings are that we must continue to impress upon our patients that smoking is not only a significant risk factor for cancer, heart disease and pulmonary disease, but that it is the leading modifiable risk factor for the leading cause of blindness in pa­tients older than 50 years of age. It appears that risks correlate with total number of pack years, and that smoke cessation may result in risk reduction to that of never smokers at 20 years. Fur­thermore, second hand smoke also confers risk for AMD.

Dry AMD patients should be en­couraged to quit smoking. Those with higher-risk lesions per the Age-Re­lated Eye Disease Study should take the recommended vitamin supplementation with the exception of ß-ca­ro­tene, which has been demonstrated to increase rates of lung cancer. 20

Patients with active choroidal neovascularization should be especially encouraged to quit smoking. Fur­thermore, they should abstain from nicotine replacement therapies as nicotine may promote growth of the lesion.

We are entering an era of molecular therapies for retinal diseases. As we learn more about the pathobiologic mechanisms by which smoking im­pacts AMD, we may discover specific pathways of oxidation or im­mu­no­modulation in dry AMD and of vascular endothelial cell and smooth-muscle pericyte proliferation, matrix turnover or immunomodulation that are relevant to wet AMD.

It is also likely that these pathways will be relevant to the biology of AMD not only in smokers, but also nonsmokers. Taking the example of nicotine in wet AMD one step further, it may be that nicotinic receptors (which are also present in nonsmokers) may be a viable target for therapy.

Dr. Suñer is an associate professor of ophthalmology on the Retina Ser­vice at Duke University Eye Center and chief of ophthalmology, Durham Veterans Affairs Medical Center, Dur­­ham, N.C. Contact him at Duke Uni­versity Eye Center, DUMC 3802 Erwin Road, Durham, N.C. 27710, 919-6868-1876 (office), 919-681-6474 (fax), or [email protected]

Dr. Cousins is a professor of ophthalmology and director of the Duke Center for Macular Diseases, Duke Uni­versity Eye Center, Durham, NC. Contact him at Duke University Eye Center, DUMC 3802 Erwin Road, Durham, NC 27710, 919-684-3090 (office), 919-681-6474 (fax), or [email protected]

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