ISSN 1505-7054 2011 Vol. 14 N o 1 W numerze: Metale a nowotwor Bia aczka elektrownie atomowe Tlenek w gla u stra aków Bioaerozol morski Yersinioza ZdolnoÊci koordnacjne dzieci Postawa cia a u dzieci Ot oêç u dzieci Rozwój fizczn studentów Wapƒ w migda kach Ankiet w astmie Salmoneloz rzko Êrodowiskowe Sinice w wodzie Selen w krwi Fenole a zdrowie Contents: Metals and Cancer Leukemia Nuklear Power Plants Carbon Monoxide in Firefighters Marine Bioaerosol Yersiniosis Coordinational abilities in Children Posture Tpes in Children Overweight in Children Phsical Development of Students Calcium in Tonsils Questionnaires in Asthma Salmonella Infections environmental risk Canobacteria in Water Selenium in Blood Phenols and Health
Medcna Ârodowiskowa / Environmental Medicine Czasopismo Journal of Insttutu Medcn Prac Institute of Occupational Medicine and i Zdrowia Ârodowiskowego w Sosnowcu Environmental Health in Sosnowiec oraz Polskiego Towarzstwa and Polish Societ Medcn Ârodowiskowej of Environmental Medicine Ukazuje si czter raz w roku It is published four times a ear ZESPÓ REDAKCYJNY / EDITORIAL STAFF Redaktor Naczeln / Editor-in-Chief Prof. dr hab. med. Zbigniew Rudkowski Zast pc Redaktora Naczelnego / Deput Editors Prof. dr hab. med. Jan Grzesik Prof. dr hab. med. Janusz Ha uszka Sekretarz Redakcji / Co-editor Lek. med. Maja Muszƒska-Graca Redakcja Techniczna / Technical Staff RADA PROGRAMOWA / EDITORIAL BOARD mgr Karina Erenkfeit Przewodniczàc Rad Programowej / Chairperson Prof. dr hab. med. Gerard Jonderko Cz onkowie Rad Programowej / Members Dr n. med. Edmund Anczk Prof. dr hab. n. med. Rszard Andrzejak Dr n. med. Piotr Z. Brewczƒski Dr n. med. Zdzis aw Brzeski Prof. dr hab. n med. Marian Dró d Prof. dr hab. n. med. Jerz Filikowski Dr in. Janina Fuda a Dr n. med. Marek Ludwik Grabowski Prof. dr hab. n. med. Jan Grzesik Dr hab. n. med. Rafa Górn Prof. dr hab. n. med. Janusz Ha uszka Prof. dr hab. n. med. Wojciech Hanke Prof. dr hab. n. med. Marek Jakubowski Dr n. med. Dorota Jarosiƒska Prof. dr hab. n. med. Marcin Kamiƒski Prof. dr in. Roman Knapek Prof. dr hab. n. med. Aleksandra Kochaƒska-Dziurowicz Mgr Karol Kowal Cz onkowie Zagraniczni / International Editorial Board Stephan Boese O Reill, M.D., German Prof. Gula Dura, M.D., Hungar Prof. Helmut Greim, M.D., German Hannu Komulainen, M.D., Finland Prof. Jean Krutmann, M.D., German Peter Ohnsorge, M.D., German Prof. Roberto Ronchetti, M.D., Ital Prof. Karl Ernst von Muehlendahl, M.D., German Prof. dr hab. n. przr. Jerz Kwapuliƒski Prof. dr hab. n. med. Henrka Langauer-Lewowicka Prof. dr hab. Jan Ludwicki Prof. dr hab. n. med. Kazimierz Marek Prof. dr hab. n. med. Jacek Musia Prof. dr hab. n. med. Zofia Olszow Prof. dr hab. n. med. Janusz Pach Prof. dr hab. n. med. Krstna Pawlas Prof. dr hab. n. med. W ads aw Pierzcha a Prof. dr hab. n. med. Zbigniew Rudkowski Prof. dr hab. Jerz Boles aw Samoliƒski Dr hab. n. med. Andrzej Sobczak Prof. dr hab. Jerz A. Sokal Prof. dr hab. n. med. Neonila Szeszenia-Dàbrowska Prof. dr hab. n. h. Beata Tobiasz-Adamczk Prof. dr hab. n. med. Barbara Zahorska-Markiewicz Prof. dr hab. n. med. Jan E. Zejda Prof. dr hab. n. med. Brunon Zem a Dr hab. n. med. Renata Z otkowska Prof. Philippe Hartemann, M.D., France Peter van den Hazel, M.D., Netherlands Prof. Tore Sannel, M.D., Norwa Prof. Staffan Skerfving, M.D., Sweden Prof. Anne Steenhout, M.D., Belgium Dr n. med. Andrzej Szpakow, Bia oruê Prof. Gerhard Winnecke, M.D., German Loreta Strumlaite, MD PhD, Lithuania Medcna Ârodowiskowa / Environmental Medicine 2010 13 (1) 1
Adres Redakcji i Wdawc: Insttut Medcn Prac i Zdrowia Ârodowiskowego oraz Polskie Towarzstwo Medcn Ârodowiskowej ul. KoÊcielna 13 41-200 Sosnowiec tel. (32) 266-08-85 wew. 201, 202 fax (32) 266-11-24 e-mail: ms@ imp.sosnowiec.pl Editorial office and publisher s address: Institute of Occupational Medicine and Environmental Health and Polish Societ of Environmental Medicine KoÊcielna 13 Str. 41-200 Sosnowiec, Poland Tel. +48 (32) 266-08-85 ext. 201, 202 Fax: +48 (32) 266-11-24 e-mail: ms@ imp.sosnowiec.pl Warunki prenumerat: Cena prenumerat rocznej dla insttucji wnosi 100 z (25 z za jeden numer), dla odbiorców indwidualnch 60 z (15 z za jeden numer). Zamówienie prosim kierowaç na adres: Redakcja Medcn Ârodowiskowej Insttut Medcn Prac i Zdrowia Ârodowiskowego ul. KoÊcielna 13 41-200 Sosnowiec Zakup numeru bie àcego i numerów archiwalnch mo liw jest po dokonaniu wp at na konto Insttutu Medcn Prac i Zdrowia Ârodowiskowego w Sosnowcu nr: 13 1160 2202 0000 0000 7623 3258 Wp at ttu em op at cz onkowskiej mo na dokonwaç na konto Polskiego Towarzstwa Medcn Ârodowiskowej nr: 56 1020 2498 0000 8502 0172 1018 Subscription conditions: Annual subscription for institutions: 100 z (25 z one volume) Annual subscription for individuals: 60 z (15 z one volume). Subscription orders should be sent to the following address: Environmental Medicine Editorial Office Institute of Occupational Medicine and Environmental Health KoÊcielna 13 Str. 41-200 Sosnowiec, Poland People or institutions interested in subscribing should send an order to the address of editorial office. Paments could be made to the account no. MILLENIUM Bank S.S. Oddzia Katowice PL13 1160 2202 0000 0000 7623 3258 BIC/SWIFT: BIGBPLPWXXX of the Institute of Occupational and Environmental Medicine in Sosnowiec Nak ad: 400 egz. Edition: 400 copies PUBLIKACJA ZOSTA A DOFINANSOWANA ZE ÂRODKÓW MINISTERSTWA NAUKI I SZKOLNICTWA WY SZEGO THE PUBLICATION IS SUPPORTED BY MINISTRY OF SCIENCE AND HIGHER EDUCATION Punktacja czasopisma: MNiSW (Ministerstwo Nauki i Szkolnictwa W szego) 6,0 p. IC (Index Copernicus) 4,47 p. ISSN 1505-7054 2 Medcna Ârodowiskowa / Environmental Medicine 2010 13 (1)
SPIS TREÂCI ARTYKU REDAKCYJNY Cancer risk in relation to exposure to trace elements Rzko chorob nowotworowej w zwiàzku z ekspozcjà na metale Êladowe Loreta Strumlaite....................................................................... 7 PRACE ORYGINALNE Childhood leukaemia in children under 5 ears of age in close vicinit of nuclear power plants Bia aczka u dzieci w wieku poni ej 5 lat w bliskim sàsiedztwie elektrowni atomowej Karl Ernst von Mühlendahl, Stephan Böse-O Reill, Ursula Heudorf, Thomas Lob-Corzilius, Matthias Otto, Sabine Schmidt.......................................................................... 13 Ocena nara enia na tlenek w gla grup stra aków z jednostki ratowniczo-gaêniczej Jadwiga Lembas-Bogaczk, Anna D ugosz, Ilona Tokarczk........................................ 18 Bioaerozol morski w rejonie Zatoki Gdaƒskiej Ma gorzata Michalska, Maria Bartoszewicz, Monika Cieszƒska, Jacek Nowacki....................... 24 Nara enie ludzi na kontakt z ró nmi serotpami pa eczek Yersinia Nimfa Maria Stojek...................................................................... 29 Wp w wbranch cznników spo eczno-ekonomicznch rodzin na predspozcje koordnacjne dzieci Jaros aw Domaradzki..................................................................... 34 Zró nicowanie postaw cia a dzieci zamieszkujàcch Êrodowisko zagro one ekologicznie Jakub Pokrwka, Jaros aw Fugiel, Pawe Pos uszn.............................................. 43 Poziom ot uszczenia dzieci wiejskich w m odszm wieku szkolnm z Legnicko-G ogowskiego Okr gu Miedziowego Pawe Pos uszn, Jaros aw Fugiel, Jakub Pokrwka.............................................. 50 Rozwój fizczn studentów wchowania fizcznego - trzletnia obserwacja z uwzgl dnieniem Êrodowiska pochodzenia Agnieszka Wasiluk....................................................................... 58 ZawartoÊç wapnia w migda kach gard owch dzieci w zale noêci od p ci, miejsca zamieszkania i wp wu biernego palenia ttoniu Ewa Nogaj, Jerz Kwapuliƒski, Ma gorzata Suflita, Marcin Babula.................................. 67 PRACE POGLÑDOWE Cz krótki kwestionariusz mo e bç wiargodnm narz dziem badaƒ przesiewowch astm oskrzelowej wieku dzieci cego? Agata Wpch-Âlusarska, Jerz S owiƒski, Joanna Kasznia-Kocot................................... 75 Salmoneloz jako wcià aktualne zagro enie Êrodowiskowe dla ludzi i zwierzàt Teresa K apeç, Maria Stroczƒska-Sikorska.................................................... 79 Zasad ocen zagro eƒ zdrowotnch zwiàzanch z zakwitami sinic w kàpieliskach Agnieszka Stankiewicz, Ma gorzata Jamsheer-Bratkowska, Dorota Maziarka, Krzsztof Skotak............ 85 St enie selenu we krwi w ró nch populacjach osób zdrowch i chorch przeglàd piêmiennictwa z lat 2005 2010 Pawe Gaç, Krstna Pawlas................................................................ 93 Biochemiczne i fizjologiczne skutki oddzia wania zwiàzków fenolowch na organizm cz owieka Danuta Wojcieszƒska, Urszula Guzik, Katarzna Hupert-Kocurek, Julita Marsza ek.................... 105 KOMUNIKATY Regulamin publikowania prac wskazówki dla Autorów......................................... 113 Prace opublikowane w Medcnie Ârodowiskowej w 2010 r.................................... 120 Spis autorów (2010 r.)................................................................... 124 Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1) 3
CONTENTS EDITORIAL Cancer risk in relation to exposure to trace elements Loreta Strumlaite....................................................................... 7 ORIGINAL PAPERS Childhood leukaemia in children under 5 ears of age in close vicinit of nuclear power plants Karl Ernst von Mühlendahl, Stephan Böse-O Reill, Ursula Heudorf, Thomas Lob-Corzilius, Matthias Otto, Sabine Schmidt.......................................................................... 13 Assessment of exposure to carbon monoxide group of firefighters from fire fighting and rescue units Jadwiga Lembas-Bogaczk, Anna D ugosz, Ilona Tokarczk........................................ 18 Marine bioearosol in the area of Gdaƒsk Ba Ma gorzata Michalska, Maria Bartoszewicz, Monika Cieszƒska, Jacek Nowacki....................... 24 The risk on contact people with different serotpes of sticks the Yersinia Nimfa Maria Stojek...................................................................... 29 Impact of selected famil socio-economic factors on coordinational predispositions of children Jaros aw Domaradzki..................................................................... 34 Variabilit of posture tpes in children from polluted environment Jakub Pokrwka, Jaros aw Fugiel, Pawe Pos uszn.............................................. 43 Bod fat levels in rural children in ounger school age from Copper Basin from south-western Poland Pawe Pos uszn, Jaros aw Fugiel, Jakub Pokrwka.............................................. 50 Three-ear observation of phsical development of students of phsical education originating from various environments Agnieszka Wasiluk....................................................................... 58 The occurrence of calcium in pharngeal tonsils of children dependent on gender, living place and influence of passive smoking Ewa Nogaj, Jerz Kwapuliƒski, Ma gorzata Suflita, Marcin Babula.................................. 67 REVIEW PAPERS Short questionnaire a reliable tool for screening of childhood asthma? Agata Wpch-Âlusarska, Jerz S owiƒski, Joanna Kasznia-Kocot................................... 75 Salmonellosis as still present environmental hazards to humans and animals Teresa K apeç, Maria Stroczƒska-Sikorska.................................................... 79 Health risk assessment standards of canobacteria bloom occurrence in bathing sites Agnieszka Stankiewicz, Ma gorzata Jamsheer-Bratkowska, Dorota Maziarka, Krzsztof Skotak............ 85 Blood selenium concentration in various populations of health and sick people review of literature from the ears 2005 2010 Pawe Gaç, Krstna Pawlas................................................................ 93 Biochemical and phsiological effects of phenols on human health Danuta Wojcieszƒska, Urszula Guzik, Katarzna Hupert-Kocurek, Julita Marsza ek.................... 105 ANNOUNCEMENTS Instructions to authors................................................................... 115 Papers published in Environmental Medicine in 2010......................................... 122 List of authors (2010).................................................................... 124 4 Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1)
Od Redaktora W artkule wst pnm przedstawiono rol metali jak arsen, chrom i kadm w nara eniu Êrodowiskowm na powstawanie nowotworów. Publikowana praca jest oparta o dane z okresu ostatniego dziesi ciolecia. Orginalne prace przedstawione w niniejszm wdaniu MS/EnvMed rozpoczna sprawozdanie niemieckiej komisji na temat wst powania bia aczki u dzieci w zale noêci od odleg oêci zamieszkania od elektrowni atomowej. Wniki badania nie sà jednoznaczne, ale jednak udowadniaj zwiàzek zapadalnoêci z odleg oêcià od êród a ekspozcji, ale nie z intenswnoêcià radiacji. Praca jest obszernm fragmentem sprawozdania udost pnionego naszej Redakcji. Zawodowe nara enie na tlenek w gla ró ni si wnikami st enia hemoglobin tlenkow glowej po ekspozcji mi dz palàcmi a niepalàcmi to jeszcze jeden element wskazujàc na szkodliwoêç palenia i nara enie zawodowe stra aków. Bioaerosol morski tak cenion wêród pla owiczów przenosi tak e zanieczszczenia mikrobiologiczne, co jest zale ne od por roku i od kierunku wiatru, pozostaje otwarte ptanie, jakie mo e to mieç praktczne znaczenie dla zdrowia? Przeglàd serologiczn na Podlasiu wkazuje obecnoêç przeciwcia przeciw Yersinia u 30% populacji zdrowch ludzi, mo na uwa aç to za wnik przebtego zaka enia Êrodowiskowego, ze êród a zaka enia jakim jest gleba, woda lub zwierz ta (po- wienie). Wp w nierównoêci spo ecznej i ekonomicznej na zdrowie jest tak e przedmiotem badaƒ Êrodowiskowch. Doniesienia orginalne przedstawiajà wniki badaƒ grup dzieci reprezentujàcch ró ne Êrodowiska ekonomiczno-socjalne (badano cech jak predspozcje koordnacjne, zdolnoêci pami ciowe) albo przebwajàcch w Êrodowisku zanieczszczonm (badano postaw cia a, ot uszczenie, st enie wapnia w migda kach), tak e wniki badaƒ charakterzujàcch rozwój fizczn m odzie ze wsi i miasta w zwiàzku z aktwnoêcià motorcznà. Sà interesujàce odniesienia i porównania z innmi regionami kraju. Niestet w pracach Autorz nie podajà aktualnch danch na temat wskaêników zanieczszczenia Êrodowiska, a te zmieniajà si stale, zazwczaj w kierunku polepszenia Êrodowiska. Prace poglàdowe dotczà ró nch tematów. PrzdatnoÊç badaƒ ankietowch nad cz stoêcià astm u dzieci jest tematem bardzo aktualnm z powodu tzw. pochodu alergicznego i prób ocen szbkoêci tego fenomenu cwilizacjnego i narastajàcego odsetka chorujàcch. Wspó czeênie aktualne ska enia biologiczne to m.in. rozprzestrzenianie si salmoneloz odzwierz cch w populacji ludzkiej z powodu cznników cwilizacjnch, jak te inne zagro enie zdrowotne z powodu zakwitów sinic w kàpieliskach (zagadnienie ma o znane klinicstom!). Wst powanie i znaczenie dla zdrowia selenu, m.in. Êrednie st enie selenu we krwi wg ctowanch w prac ostatnich badaƒ, to treêç kolejnej publikacji. Ostatnia praca poglàdowa w tm wdaniu MS/EnvMed dotcz znaczenia zdrowotnego polifenoli, a tak e patologii z powodu chemicznego, cwilizacjnego ska enia Êrodowiska zwiàzkami fenolowmi. Redaktor Naczeln Prof. dr. hab. n. med. Zbigniew Rudkowski Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1) 5
6 Medcna Ârodowiskowa / Environmental Medicine 2010 14 (1)
ARTYKU REDAKCYJNY EDITORIAL Cancer risk in relation to exposure to trace elements Rzko chorob nowotworowej w zwiàzku z ekspozcjà na metale Êladowe Loreta Strumlaite Laborator for Environmental Health Research, Institute for Biomedical Research, Academ of Medicine, Lithuanian Universit of Health Sciences Head of Laborator for Environmental Health Research (Assoc Prof. ScD Olegas Abdrachmanovas) Director of Institute for Biomedical Research (Prof. dr. hab. Arimantas Tamasauskas) Rector of Lithuanian Universit of Health Sciences (Prof. dr. hab. Remigijus Zaliunas) Loreta Strumlaite MD, PhD, senior researcher Abstract Cancer is a major public health concern in man parts of the world. The genesis of cancer is multi-causal with some well known causal factors for some sites of cancer. However, some cancer causes are not clear up to nowadas. There are substantial geographic variations in mortalit of some sites of cancer in different regions of the world that could be in relation with some environmental factors and trace elements such as arsenic, chromium and cadmium. The review summarizes the recent studies on that matter. Kewords: cancer, trace elements, arsenic, chromium, cadmium Streszczenie Wwielu cz Êciach Êwiata nowotwor sà g ównm zagadnieniem zdrowia publicznego. Powstawanie nowotworu jest zale ne od wielu przczn, niektóre z nich sà znane, jednak przczn innch nie sà dotàd wjaênione. Istotne zró nicowanie geograficzne odnoênie ÊmiertelnoÊci nowotworów narzàdowch w ró nch regionach Êwiata mo e bç zwiàzane z cznnikami Êrodowiskowmi i ze Êladowmi metalami jak arsen, chrom i kadm. Niniejsz przeglàd przedstawia aktualne badania na ten temat. S owa kluczowe: cancer, trace elements, arsenic, chromium, cadmium Introduction Cancer is a major public health concern in man parts of the world accounting more than 10 million new cancer cases each ear and being the cause of approximatel 12% of all death. The lung, breast, colorectum, and stomach are the most common cancers worldwide [1]. Prostate cancer is the fifth most common cancer overall and the second most common among men, bladder cancer, ranks ninth in terms of incidence, and is more common in developed countries [1]. The genesis of cancer is multi-causal with some well known causal factors for some sites of cancer although some cancer causes are not clear up to nowadas. A substantial geographic variations in cancer mortalit in some regions of the world make us think about environmental factors of the disease. Among man environmental factors trace elements are of particular interest. Trace elements refer to chemical elements present or required in small quantities. Trace elements are found naturall in the environment and human exposure derives from a variet of sources, including air, drinking water, and food (Table I) [3]. Nades ano: 24.11.2010 Zatwierdzono do druku: 20.12.2011 Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1) 7
Table I. Average exposure to trace elements from environmental sources Trace Exposure b source element Air Water a Diet Arsenic 1 2000 ng [4, 5] *1 ng 7200 µg, depending on 50 200 µg (3.5 µg of geographic location [4, 7, 8] inorganic arsenic) [2, 4] Chromium 0.07 157 ng (200 ng in 0.8 16 µg [9] 50 200 µg [9] industrial areas ) [9] Cadmium 1 40 ng [6, 7] 0.01 0.2 µg (50 µg in heavil 3 160 µg, approximatel polluted areas) [6, 7] 1 3 µg is absorbed [6, 7] Sources [2, 4, 5, 6, 7, 8, 9] a Assuming an intake of 2 l water/da Arsenic Arsenic (As) is ubiquitous in the environment due to both anthropogenic and natural processes [10, 11]. The major sources of human exposure to As ma be through food, water, air and soil in that dietar intake is the major exposure route [12]. As species from drinking water are mainl found in the form of inorganic arsenicals, whereas organoarsenic compounds (e.g., arsenobetaine and arsenosugars) predominate in seafood [13, 14]. A high level of As in groundwater (up to 2 5000 µg/l) is found in areas of Argentina, Bangladesh, Bolivia, Chile, China (Xinjiang, Shanxi), India (West Bengal), Mexico, Mongolia, Taiwan, Thailand, the USA (Arizona, California, Nevada) and Vietnam. The most significant exposures, in terms of levels and populations, occur around the Gulf of Bengal, in South America and in Taiwan. In Europe, intermediate levels (not higher than 200 µg/l) are found in areas of Hungar and Romania in the Danube basin, as well as in Spain, Greece and German [15]. World Health Organization lowered the Maximum Contamination Level for As in drinking water from 0.05 to 0.01 mg/l [16], although dietar exposure to organic arsenicals was formerl neglected due to their relativel nontoxic nature. However, more and more studies have focused on As exposure through seafood rather than drinking water because some seafood contains high As concentrations [17, 18]. The toxicit of As in humans varies in its chemical form. It has been recognized that inorganic As is more toxic than its organic forms [13]. Inorganic trivalent arsenical, which reacts directl with protein-bound sulfhdrls, is considered more toxic than the inorganic pentavalent form [17]. Inorganic As is proposed to be metabolized to monomethlarsonic acid and dimethlarsinic acid of lower toxicit [18, 19]. The International Agenc for Research on Cancer recognized arsenic and arsenic compounds as carcinogenic to humans (Group I) [4]. There is strong evidence of an increased risk of bladder, skin and lung cancers following consumption of water with high As contamination [20, 21, 22, 23]. Ver limited data are available on the risk of other neoplasms at low or intermediate exposure levels. [15]. Although some authors support the possibilit of an increased risk of specific lung cancer histological tpes at lower levels of As exposure and recommend large-scale population-based studies [24]. The evidence for an increased risk of other cancers, such as those of the liver, colon and kidne, are weaker but suggestive of a sstemic effect [15]. Most of the available studies have been conducted in areas with elevated As content (above 200 µg/l). It has been determined median cumulative cancer incidence ratios 2.67210 16 and 3.83210 16 for children and adults, indicating a low cancer risk for local residents exposed to As after ingestion of seafood [25]. Epidemiologic data from regions of the world with ver high levels of As in drinking water ( 150 µg/l) show a strong association between As exposure and risk of several internal cancers. A causal interpretation of the data is mainl based on the strength and consistenc of stud findings. At lower levels of exposure (*100 µg/l), in the absence of unambiguous human data, extrapolation from the high exposure studies has been used to estimate risk. Misclassification of exposure usuall results in depressing observed levels of risk, and studies conducted in populations with exposures below 100 µg/l have been limited b the challenge of estimating past exposures, a criticall important aspect of studing relative small increases in risk [26]. 8 Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1)
Chromium Chromium (Cr) is the 21 st most abundant element in the Earth s crust [27]. While several valence states of Cr are possible, onl the trivalent (Cr 3& ) and hexavalent (Cr 6& ) forms have significant environmental stabilit. Most of the naturall occurring Cr is in the Cr 3& form as chromite ore [28], while Cr 6& tends to occur as a result of anthropogenic uses. These include pigments, metal finishing (including Cr plating) and wood preservatives [29]. Although the highest levels of exposure occur in industrial settings, lesser levels of exposure are also common in the general population. Cr is also constituent of tobacco smoke and has been suspected to pla a role in tobacco-induced carcinogenesis [30]. Cr is a human carcinogen primaril absorbed b inhalation exposure in occupational settings. The International Agenc for Research on Cancer declared in 1980 that Cr and some of its compounds are carcinogenic and, in 1987, concluded that Cr 6& is a human carcinogen but that Cr 3& was not et classifiable [31]. Adverse health effects of Cr have long been known and include skin ulceration, perforated nasal septum, nasal bleeding, and conjunctivitis. Recent studies updating chromium worker cohorts demonstrated an excess lung cancer risk from exposure to Cr 6& [32, 33]. Some epidemiological studies found elevated standardized mortalit ratios (SMR) for prostate, lmphoma, Hodgkin s, leukemia, stomach, renal, bladder, and genital cancer. This index for cancers of the brain varied from 2.5 to 8.44 in a number of studies [34]. According to the reported elevation of brain cancers, and knowledge that Cr gets into the central nervous sstem, there should also be concern about the possibilit that Cr 6& ma be neurotoxic [35]. Although Cr 6& is not generall considered to be a neurotoxin, perhaps this should be reconsidered since Cr gains entr into the central nervous sstem and ma be a carcinogenic at this site [36]. The meta-analses of 49 epidemiologic studies mostl relating exposure to Cr 6& compounds declared no excess mortalit from all causes combined among chrome-exposed persons. A minimal excess of cancer overall, was due primaril to an excess of lung cancer but SMR was 112 among the better-qualit, smoking-controlled studies. The overall SMR for stomach cancer was 113 but it was 82 among the studies that were controlled for economic status. Findings were unremarkable for the six other cancers evaluated: prostate, kidne, and central nervous sstem cancer and leukemia, Hodgkin s disease and other lmphatohematopoietic cancer. Finall, the authors concluded that Cr 6& is a weak cause of lung cancer and is not a cause of an of the other seven forms of cancer evaluated [37]. It has been stated that the relationship between Cr 6& and lung cancer is weak because of the great capacit of the lung to reduce Cr 6& to the non-carcinogenic Cr 3&. Onl ver heav exposure to Cr 6& could overwhelm the lung s reducing capacit and produce cancer [38]. Crump et al. [39] also inferred that Cr 6& was onl weakl carcinogenic for the lung. However, most of the evidence regarding lung cancer risks related to these agents comes from cohort studies in a narrow range of industries in which exposures have been relativel high. In the majorit of these studies, it has been difficult to rule out confounding b smoking or other occupational co-exposures as a possible explanation for the associations [40]. Although lung cancer has been established as a consequence of Cr 6& exposure in smokers and nonsmokers, some cancers of other tissues of the gastrointestinal and central nervous sstems have also been noted [36]. It has been shown that Cr 6& exposure, b either inhalation or ingestion, can have sstemic effects that are distant from the site of exposure. Since Cr 6& is isostructural with sulfate and phosphate at phsiological ph, it can be carried throughout the bod and even into the brain. Thus, if exposure is in sufficient amounts, the levels of Cr mabe elevated in man different organs. Depending on the genetic susceptibilit of an individual, this could pose significant risk to cancer induction in an organ. All cells and organs possess the abilit to take up hexavalent chromate, and an cell has the capacit to reduce the Cr 6& intracellularl to Cr 3&, which reacts with protein to produce toxicit and with DNA to potentiall cause cancer. The abilit of the stomach to reduce Cr 6& is limited, and even at relativel low doses, chromate escapes reduction and enters the bod, as illustrated b hairless mouse stud [41]. Experimental stud showed that the induction of malignant skin cancers in hairless mice exposed to 0.5 5.0 ppm Cr 6& in drinking water was dose dependent and highl statisticall significant [41]. In spite of Cr being a human carcinogen primaril b inhalation exposure, the experimental sstem representing an important new animal model developed for chromate-induced cancers b ingestion of drinking water developed, suggested that chromate could likel be considered a human carcinogen b ingestion as well [36]. Cadmium Cadmium (Cd) is a toxic, nonessential, and bioaccumulating heav metal widel used in industr. Cd affects human health both through occupational and environmental exposures. In general Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1) 9
population the primar sources of Cd are cigarette smoke, food, water, and ambient air particularl in urban areas and in the vicinit of industrial settings [42]. About 10% of inhaled Cd is deposited in lung tissues and 30 40% is absorbed into blood. Generall, Cd uptake in the gastrointestinal tract is 5 20% and depends on speciation of Cd, interactions between components in the diet affecting the bioavailabilit of Cd and the person s nutritional status. Approximatel, 75% of the total dietar Cd intake is from vegetable food with the highest contribution from cereals [43]. Owing to long half-life of Cd in the human bod, it accumulates in the kidnes. The urinar excretion of Cd is proportional to the bod burden and used as a dose of lifetime exposure to Cd, whereas concentration in blood represents recent exposure [44]. Cd exerts multiple toxic effects, and has been classified as a human carcinogen b the International Agenc for Research on Cancer [45]. Cd carcinogenesis can be explained b several mechanisms: (1) aberrant gene expression, (2) inhibition of DNA damage repair, (3) induction of oxidative stress, and (4) inhibition of apoptosis. The most important among them is oxidative stress because of its involvement in Cd-induced aberrant gene expression, inhibition of DNA damage repair, and apoptosis [46]. Although Cd is known as a human lung carcinogen [45], there is evidence that it ma be related to other cancers such as human prostate cancer [47, 48], renal cell carcinoma [49, 50], and breast cancer [51, 52]. The human mammar gland is a controversial target site for Cd. Epidemiological stud revealed twice the higher risk of breast cancer in women with creatinine-adjusted urine Cd more than 0.58 µg/g compare to those with Cd less than 0.26 µg/g [52]. Experimental studies suggest several pathwas to explain association of Cd with human breast cancer. There is evidence that Cd ma have estrogenicit [51]. According to some authors, the bivalent metal cations Cd belongs to a new class of potent environmental estrogens, referred to as metalloestrogens. The studies in vivo and in vitro show that Cd acts like an estradiol activating estrogen receptor (ER) a through a highaffinit interaction with the hormone binding domain of the receptor [53]. There is evidence that the effects of cadmium are mediated b the ER independent of estradiol [51]. Antila et al. [54] defined high content of Cd (3.2 86.9 µg/g) in breast samples from breast cancer patients, but the mean cadmium level did not differ from that of health controls. However, three other studies found significant difference between Cd in breast cancer and health breast tissue [55, 56, 57]. Multiple studies have linked occupational exposure to cadmium with pulmonar cancer, as well as prostate, renal, liver, hematopoietic sstem, urinar bladder, pancreatic, and stomach cancers [58, 59, 60, 61, 62]. Some authors concluded that pancreatic cancer in the East Nile Delta region is significantl associated with high levels of serum Cd and farming [63]. However, the data are nor consistent. In contrast to laborator studies, epidemiological studies do not convincingl implicate Cd as a cause of prostate cancer [64]. In conclusion, arsenic and its compounds, chromium (VI) compounds, cadmium and cadmium compounds are recognized human carcinogens. However, in spite of an association between chronic arsenic ingestion and internal cancers, epidemiologic studies have not produced convincing evidence of risks related to drinking-water concentrations of less than 100 µg As /liter. Compounds of chromium (VI) and cadmium are human carcinogens primaril b inhalation inducing lung cancer. However, due to inconsistenc of the data the relationships with the other sites of cancer are not proved finall. Relativel small stud size and misclassification of exposure usuall results in depressing observed levels of risk and contributes to the variabilit of findings in most studies and makes interpretation of results challenging. References 1. Parkin D.M., Bra F., Ferla J., et al.: Global cancer statistics, 2002. CA Cancer J Clin 2005 55: 74 108. 2. World Health Organization (WHO). Trace elements in human nutrition and health. World Health Organization, Geneva 1996. 3. Navarro Silvera S.A., Rohan T.E. Trace elements and cancer risk: a review of the epidemiologic evidence. Cancer Causes Control 2007 18: 7 27. 4. Agenc for Toxic Substances and Disease Registr (ATSDR). Toxicological profile for arsenic. US Department of Health and Human Services, Agenc for Toxic Substances and Disease Registr, Atlanta, GA, 2003: Report No.: 7440-38-2. 5. Rasmussen L., Andersen K.J.: Arsenic in drinking water (in:) World Health Organization, UNICEF (ed.): Environmental health and human exposure assessment. IWA, London, 2003: 67 168. 6. Agenc for Toxic Substances and Disease Registr (ATSDR). Toxicological profile for cadmium. United States Department of Health and Human Services Agenc for Toxic Substances and Disease Registr, Atlanta, GA, 1999: Report No.: 7440 43-9. 7. World Health Organization (WHO). Regional Office for Europe. Air qualit guidelines, Second Ed. World Health Organization, Copenhagen, Denmark 2000. 8. Lamm S.H., Engel A., Kruse M.B., et al: Arsenic in drinking water and bladder cancer mortalit in the United States: an analsis based on 133 U.S. counties and 30 ears of observation. J Occup Environ Med 2004 46:.298 306. 9. World Health Organization (WHO). Regional Office for Europe Air qualit guidelines. Europian series No. 23. Copenhagen, 1987. 221 230. 10 Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1)
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Contribution of environmental factors to cancer risk. Br Med Bull 2003 68:71-94. 16. El-Masri H.A., Kenon E.M.: Development of a human phsiologicall based pharmacokinetic (PBPK) model for inorganic arsenic and its mono- and dimethlated metabolites. J Pharmacokinet Pharmacodn 2008 35: 31 68. 17. Hughes M.F.: Biomarkers of exposure: a case stud with inorganic arsenic. Environ Health Perspect 2006 114: 1790 1796. 18. Hsueh Y.M., Hsu M.K, Chiou H.Y., et al.: Urinar arsenic speciation in subjects with or without restriction from seafood dietar intake. Toxicol Lett 2002 133: 83 91. 19. Clewell H.J., Thomas R.S., Gentr P.R., et al.: Research toward the development of a biologicall based dose response assessment for inorganic arsenic carcinogenicit: a progress report. Toxicol Appl Pharmacol 2007 222: 288 398. 20. Hsueh Y.M., Cheng G.S., Wu M.M., et al.: Multiple risk factors associated with arsenic-induced skin cancer: effects of chronic liver disease and malnutritional status. Br J Cancer 1995 71: 109-114. 21. Bates M.N., Re O.A., Biggs M.L., et al.: Case-control ctud of bladder cancer and exposure to arsenic in Argentina. Am J Epidemiol 2004159:.381 389. 22. Celik I., Gallicchio L., Bodet K. et al.: Arsenic in drinking water and lung cancer: A sstematic review. Environ Res 2008 108: 48 55. 23. Chen Ch.L., YiChiou H., IHsu L., et al.: Ingested arsenic, characteristics of well water consumption and risk of different histological tpes of lung cancer in northeastern Taiwan. Environ Res 2010 110: 455 462. 24. Heck J.E., Andrew A.S., Onega T., et al.: Lung Cancer in a U.S. Population with Low to Moderate Arsenic Exposure. Environ Health Perspect 2009 117(11): 1718-1723. 25. Chen B.C., Wei-Chun Choub, Wei-Yu Chenb, Chung-Min Liao. Assessing the cancer risk associated with arsenic-contaminated seafood. J Hazardous Materials 2010 181: 161 169. 26. Cantor K.P., Lubin J.H.: Arsenic, internal cancers, and issues in inference from studies of low-level exposures in human populations. Toxicol Appl Pharmacol 2007.22: 252 257. 27. Krebs R.E.: The histor and use of our Earth s chemical elements: A Reference Guide. Second Ed. Greenwood Publishing Group, Santa Barbara, CA 2006: 96. 28. Independent Environmental Technical Evaluation Group (IETEG) (in:) Guertin, J., Jacobs, J.A., Avakian, C.P. (ed.), Chromium (VI) Handbook. CRC Press, Boca Raton 2005. 29. Agenc for Toxic Substances and Disease Registr (ATSDR). Toxicological profile for chromium. Public health service, U.S. department of health and human services, Atlanta, GA 2000. 30. Stavrides J.C.: Lung carcinogenesis. Pivotal role of metals in tobacco smoke. Free Radic Biol Med 2006 41: 1017 1030. 31. International Agenc for Research on Cancer (IARC). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Volume 49: Chromium, Nickel and Welding. IARC Press: Lon, France 1990. 32. Sorahan T.J., Harrington J.M.: Lung cancer in Yorkshire chrome platers, 1972 97. Occup Environ Med 2000 57: 385 389. 33. Luippold R.S., Mundt K.A., Panko J., et al.: Lung cancer mortalit among chromate production workers. Occup Environl Med 2003 60: 451 457. 34. Costa M.: Toxicit and carcinogenicit of Cr (VI) in animal models and humans. Crit Rev Toxicol 1997 27(5): 431 442. 35. Wesseling C., Pukkala E., Neuvonen K., et al.: Cancer of the brain and nervous sstem and occupational exposures in Finnish women. J Occup Environ Med 2002 44(7): 663 668. 36. Costa M., Klein C.B.: Toxicit and Carcinogenicit of Chromium Compounds in humans Crit Rev Toxicol 2006 36: 155 163. 37. Cole P., Rodu B. Epidemiologic studies of chrome and cancer mortalit: A series of meta-analses. Regulator Toxicolog and Pharmacolog 2005 43: 225 231. 38. De Flora, S.: Threshold mechanisms and site specificit in chromium (VI) carcinogenesis. Carcinogenesis 2000 21: 533 541. 39. Crump C., Crump K., Hack E., et al.: Dose response and risk assessment of airborne hexavalent chromium and lung cancer mortalit. Risk Analsis 2003 23: 1147 1163. 40. Beveridge R., Pintos J., Parent M.E., et al.: Lung Cancer Risk Associated With Occupational Exposure to Nickel, Chromium VI, and Cadmium in Two Population-Based Case Control Studies in Montreal. Am J Indust Med 2010 53: 476 485. 41. Davidson T.L., Kluz T., Burns, F.J., et al.: Exposure to chromium (VI) in the drinking water increases susceptibilit to UV-induced skin tumors in hairless mice. Toxicol Appl Pharmacol 2004 196(3): 431 437. 42. The International Programme on Chemical Safet (IPCS). Cadmium. Environmental Health Criteria 134. World Health Organization, Geneva 1992. 43. EEC-European Council Regulation. Commission Regulation (EC) No 66/2001 of 8 March 2001 setting maximum levels for certain contaminants in food stuffs. Off J Eur Commun L 077:0001 0013. 2001. 44. The Centers for Disease Control and Prevention (CDC). Third national report on human exposure to environmental chemicals. Centers for Disease Control and Prevention, Atlanta 2005. 45. International Agenc for Research on Cancer (IARC). IARC Monographs on Monographs on the evaluation of carcinogenic risks to humans. IARC, Lon, 1993: 119 237. 46. Joseph P.: Mechanisms of cadmium carcinogenesis. Toxicol Appl Pharmacol 2009 238: 272 279. 47. Achanzar W.E., Diwan B.A., Liu J., et al.: Cadmium-induced malignant transformation of human prostate epithelial cells. Cancer Res 2001 61: 455 458. 48. Vinceti M., Venturelli M., Sighinolfi C., et al.: Case-control stud of toenail cadmium and prostate cancer risk in Ital. Sci Total Environ 2007 373: 77 81. 49. Pesch B., Haerting J., Ranft U., et al.: Occupational risk factors for renal cell carcinoma: agent-specific results from a case-control stud in German. Int J Epidemiol 2000 29: 1014 1024. 50. Hu J., Mao Y., White K.: Renal cell carcinoma and occupational exposure to chemicals in Canada. 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51. Garcia-Morales P., Saceda M., Kenne N., et al.: Effect of cadmium on estrogen receptor levels and estrogen-induced responses in human breast cancer cells. J BiolChem 1994 269: 16896 16901. 52. McElro J.A., Shafer M.M., Trentham-Dietz A., et al.: Cadmium exposure and breast cancer risk.j Natl Cancer Inst 2006 98:869 872. 53. Martin M.B., Reiter R., Pham T., et al.: Estrogen-like activit of metals in Mcf-7 breast cancer cells. Endocrinolog 2003 144: 2425 2436. 54. Antila E., Mussalo-Rauhamaa H., Kantola M., et al.: Association of cadmium with human breast cancer. Sci Total Environ 1996186: 251 256. 55. Ionescu J.G,. Novotn J., Stejskal V., et al.: Increased levels of transition metals in breast cancer tissue. Neuroendocrinol Lett 2006 27(Suppl. 1): 36 39. 56. Strumlaite L., Bogusevicius A., Rselis S., et al.,: Association between cadmium and breast cancer. Medicina (Kaunas) 2008 44: 415 420. 57. Strumlaite L., Bogusevicius A., Abdrachmanovas O., et al.: Cadmium concentration in biological media of breast cancer patients Breast Cancer Res Treat DOI 10.1007/s10549-010- 1007-8 58. Waalkes M.: Cadmium carcinogenesis in review. J Inorg Biochem 2000 79: 241 244. 59. Pesch B., Haerting J., Ranft U., et al.: Occupational risk factors for renal cell carcinoma:agent specific results from a case-control stud in German. Int J Epidemiol, 2000 29: 1014 1024. 60. Hu J., Mao Y., White K.: Canadian Cancer Registries Epidemiolog Research Group. Renal cell carcinoma and occupational exposure in Canada. Occup Med 2002 52: 157 164. 61. Waalkes M., Misra R.: Cadmium carcinogenicit and genotoxicit (in:) Chang L. (ed.): Toxicolog of Metals. CRC Press, Boca Raton, FL, 1996:. 231 244. 62. Schwartz G., Reis I. Is cadmium a cause of human pancreatic cancer? Cancer Epidemiol. Biomarkers Prev 2000 9: 139 145. 63. Kriegel A.M., Soliman A.S., Zhang Q., et al.: Serum cadmium levels in pancreatic cancer patients from the East Nile Delta region of Egpt. Environ Health Perspect 2006 114 (1): 113-119. 64. Sahmoun A.E., Case L.D., Jackson S.A., Schwartz G.G. Cadmium and prostate cancer: A critical epidemiologic analsis cancer investigation 2005 23:256 263. Address: Loreta Strumlaite MD.PhD Institute for Biomedical Research Medical Academ Lithuanian Universit of Health Sciences Eiveniu 4 LT-50009 Kaunas Lithuania e-mail: loreta.strumlaite@med.kmu.lt 12 Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1)
PRACE ORYGINANE ORIGINAL PAPERS Leukaemia in Children under 5 Years in the Close Vicinit of Nuclear Power Plants 1 Bia aczka u dzieci w wieku poni ej 5 lat w bliskim sàsiedztwie elektrowni atomowej Karl Ernst v. Mühlendahl, Matthias Otto, Stephan Böse-O Reill, Ursula Heudorf, Thomas Lob-Corzilius, Sabine Schmidt From the Commission for Environmental Issues of the Deutsche Akademie für Kinder- und Jugendmedizin (DAKJ)* Abstract The KiKK (Kinderkrebs in der Umgebung von Kernkraftwerken) stud shows that the relative risk (RR) for leukaemias in children under 5 ears of age in the 5 km region around the German nuclear power plants (NPP) is significantl correlated to the distance between the living place and the NPP. The reason is unclear. There exists a discrepanc between the radiation exposure, as measured around the NPPs, and the observed risk increase. Further investigations into pathogenesis for the development of leukaemias are necessar. Ke words: childhood leukaemia, nuclear radiation, leukaemia risk, KiKK German Streszczenie Studium KiKK (nowotwor u dzieci w otoczeniu elektrowni atomowch) wkaza o. e wzgl dne rzko (RR) bia aczki u dzieci w wieku poni ej 5 lat w promieniu 5 km wokó niemieckiej elektrowni atomowej (NPP) jest znaczàco zale ne od odleg oêci miejsca zamieszkania od elektrowni atomowej. Przczna jest niewjaêniona. Istnieje rozbie noêç pomi dz ekspozcjà na promieniowanie mierzone wokó elektrowni a wzmo eniem zaobserwowanego rzka. Konieczne sà dalsze badania przczn powstawania bia aczki. S owa kluczowe: bia aczka dzieci, promieniowanie jàdrowe, rzko bia aczki, KiKK Niemc 1 Essential parts of the Position of the Commission for Environmental Issues of the Deutsche Akademie für Kinder- und Jugendmedizin (DAKJ) regarding the KiKK Stud (Kinderkrebs in der Umgebung von Kernkraftwerken, Childhood Leukaemia in the Surrounding of Nuclear Power Plants) of the Kinderkrebsregister Mainz (German Childhood Cancer Registr) and regarding the ensuing discussions. The complete document is available in German language at http://www. dakj. de/. The literature citations at the bottom of the last refer to the original paper. Members of the Commission: Stefan Böse-O Reill, Ursula Heudorf, Thomas Lob-Corzilius, K. E. v. Mühlendahl (speaker), Matthias Otto, Sabine Schmidt * Published in MS/Env. Med. with the permission of chairman of the Commission Prof Dr. KE v. Mühlendahl. Nades ano: 18.01.2011 Zatwierdzono do druku: 16.02.2011 Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1) 13
Historical remarks B the end of the eighties of the last centur, British investigators reported an increased occurrence of childhood leukaemias in the vicinit of nuclear installations in England and Wales [1]. In overall contradictor findings, some studies reported an increase of leukaemias in under 5 ear old children in the close proximit of nuclear reprocessing plants and power plants (NPP). The German Childhood Cancer Registr (DKKR) in Mainz performed an ecological stud (comparing incidences), looking for malignant diseases in under 15 ear old children in the vicinit (15 km radius) of West German NPP [2], comparing the incidence to defined regions without NPP. For the period from 1980 to 1990, there was no increase of incidences [3]. However, consecutive, detailed explorations of the data showed an increased incidence of leukaemias in the age group of 0 5 in the 5 km proximit of NPP. Some ears later, a second stud of the DKKR was started, using the same design, with data of the period 1991 1995. Again, no relationship between the incidence of childhood leukaemias and residence within 15 km radius of NPP was found. Also, the data for the 0 5 ear old children of the first stud could not be confirmed [4, 5, 6]. Discordant results came from England [7, 8] and France [9]. A later metaanalsis [10] showed an increase of leukaemias in the vicinit of NPP, but correlations were mostl weak. Are-analsis of the Mainz data ielded again an increased relative risk (RR) for leukaemias in children under 5 ears in the vicinit of German NPP [11]. The KiKK (Kinderkrebs in der Umgebung von Kernkraftwerken) stud of the Mainzer Kinderkrebsregister (DKKR) With regard to the persisting controversies the German Ministr for Environment (Bundesumweltministerium) in 2001 invited applications for the performance of a case-control-stud, and the task was given to the DKKR, also with regard to the extensive data alread compiled there. The design of the new stud was, in advance, defined with the Bundesamt für Strahlenschutz (Radiation Protection Agenc, BfS) and a 12 person external expert committee [12]. The KiKK stud [13] investigated 16 West German NPP. Stud regions were the counties where the NPP were situated, and the counties neighbouring to the east, withouth NPP. Since the radiation exposure b other sources (background radiation, medicine, nutrition) could not be measured, the distance of residence to the NPP was taken as surrogate for a possible radiation exposure due to the NPP. Cases were children who, between 1980 and 2003, were diagnosed as having malignant diseases, who were not older than 5 ears and who lived in the stud regions. There were 1592 cases, among them 593 leukaemias (512 ALL, 75 AML), 242 tumours of the central nervous sstem (CNS), and 486 embronal tumours. For each case, three controls were added, taken from the person registries, with identical sex and with birth dates as close as possible to those of the cases (n44735). For cases and controls, residence was located b geo-coding (GPS) this was done for cases at the date of diagnosis, for controls at the time of attribution when the were defined as controls. Accurac of geographical location was 25 m. There existed neither for cases, nor for controls, data on previous residences, or on changes of residenc. The KiKK stud re-used data from cases that had made part of the previous DKKR studies, amounting to approximatel 70%. The median of the distance of residence to the NPP was 20.8 km in cases, and 21.1 km in controls (means: 23.4 and 24.1 km). The relative risk (RR) for malignant diseases was 1,61 for the under 5 ears old in the 5 km vicinit, and for leukaemias 2,19, reconfirming the previousl stated increase of incidences. Interpretations of these results Authors of the KiKK stud In German there is a relationship between the proximit of residence to a NPP and the frequenc b which children before their fifth birthda have malignant disease, above all leukaemia. The stud does not allow to sa which factor is responsible for this increase in the surrounding of German NPPs. According to the present state of knowledge, radiation emitted from the NPP cannot be held to be the reason for this increase in risk. Conceivabl, et unknown factors could be implicated, or it could be accidentall. External expert group The stud applies the absolutel best statistical methods for probing the hpothesis which had been defined a priori. Grave weaknesses of previous studies thus were avoided. The main result gives a definite answer to the question of the stud. The main result is the estimation of the regression curve, which alone answers the a priori given question of the stud. The application of categories of distance has onl limited power. 14 Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1)
Concerning the estimation of radiation related risk b international radiation protection agencies: Quantitative estimations of the risk of radiation b such commissions repeatedl had to be later corrected towards higher risk values. These reports focused mainl on quantative radiation risks caused b high doses of external gamma radiation, mainl with high dose rate and high energies. Therefore, the conclusions drawn from these reports necessaril can onl conditionall be applied to NPP.. Thus the exposition of people living close to NPP is marked b an additional radiation dose which is below the exposition from natural sources and b diagnostic X-ra, b exposition with low dose rate, a mixed exposition of direct gamma radiation, external gamma and beta radiation resulting from the deca of short lived radionuclides, and from gamma, beta, and alpha radiation resulting from the deca of incorporated radionuclides. Overall, a causal effect of radioactive emissions of German NPP cannot be excluded at the moment with regard to childhool leukaemia incidences. Strahlenschutzkommission (German Commission on Radiological Protection) [14, 15] The KiKK-Stud s new data confirm the results of earlier explorator studies that found an increased risk of leukaemia, for children ounger than five, within a 5 km radius around German nuclear power plants, relative to the risk in the outer areas around the relevant stud areas [16 20]. B virtue of its design, the KiKK-Stud exhibits numerous methodological weaknesses with regard to determination of exposure and surveing of influencing factors. Consequentl, the stud should not have been carried out in the manner in which it was carried out. In spite of such weaknesses, the stud s design is suitable for the task of analsing dependence on distance. The stud is thus not suited to the task of establishing a correlation with exposure to radiation from nuclear power plants. All of the radioecological and risk-based circumstances reviewed b the SSK indicate that exposure to ionising radiation caused b nuclear power plants cannot explain the results found b the KiKK-Stud. The additional radiation exposure caused b nuclear power plants is lower, b a factor of considerabl more than 1,000, than the radiation exposure that could cause the risks reported b the KiKK-Stud. The natural radiation exposure within the stud area, and its fluctuations, are both greater, b several orders of magnitude, than the additional radiation exposure caused b the relevant nuclear power plants. The reason for the increased leukaemia rate that the KiKK-Stud observed in children is unclear. Since leukaemia is caused b multiple factors, numerous influencing factors could have been responsible for the observed result. If the man relevant conflicting findings in the literature, and the finding of the KiKK-Stud, are to be understood, more extensive, interdisciplinar research into the causes and mechanisms of the development of leukaemias in children will have to be carried out. Commission for Environmental Issues of the German Acadam of Pediatrics (DAKJ) Lack of transparenc of DKKR data Deplorabl the Mainz data (which all come from German pediatricians and from the families of sick children) are not open to the public, nor to pediatricians or epidemiologists, hindering further analses and transparenc. Sufficient anonmisation of data to protect privac and conform to data protection regulations would be possible. The commission asks for a change in this practice, e.g. b offering a public use file, as has been done with the results from KiGGS (Kinder- und Jugend-Gesundheitssurve, Child and Youth Health Surve) and of the KUS (Kinderumweltsurve, Child Environmental Surve). Man questions remain open so far. Most historical data referring to places of residence are lacking for cases and controls. One should know where the mothers have lived before conception, and where during the pregnanc, and whether the or the fathers have worked in the NPP. The extensive and important data in the hands of the DKKR appear to be suitable to bring more differentiating and clarifing results. Further analsis of this material must go on, to be done either b the DKKR, or b another institution. Radiation biolog Background radiation (in German 2,1 msv/a with some variations) is 100 or 1000 fold higher than the anthropogenic radiation caused b NPP. If NPP related radiations were at reason for the increase in leukaemia risk, there should be, due to the local variabilit of background radiation, important local differences in leukaemia frequenc, which is not the case. Taking into account the calculations of radiation damage after the atomic bomb detonations in Hiroshima and Nagasaki, and the inductions of leukaemias b X ra investigations during pregnanc, the emissions from NPP are lower b two or Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1) 15
three orders of magnitude than those necessar for the induction of leukaemia. However, the dose calculations derived from the above mentioned sources have a ver limited applicabilit for the context discussed here. Also, it remains unclear whether this dosimetr is applicable for all radionuclides, or for those incorporated, e.g. for tritium. (see minorit vote 3 at the end of the text) Interpretation of results (b the Commission) The KiKK stud confirms the results of earlier explorative studies that had given partl contradictor results and shows that the relative risk for leukaemias for children up to 5 ears of age within a5 km radius around NPP is elevated (Kaatsch et al. 2008 13). The reason for this increase is not clear. The maximal possible additional radiation exposure, as calculated from the data of the surveillance sstems, appling a worst case scenario, is b two orders of magnitude lower than that which, according to our present state of knowledge, could explain on the basis of radiation biolog the observed effect. The distance of residences to the NPP show small differences between cases and controls (cases 20.8 km, median, controls 21.1 km). The majorit of the commission is of the opinion that it is not realistic to accept distances of residenc as indicator for different radiation exposures. The investigation of confounders which has been performed in a second part of the KiKK stud has shown no other significantl effective factors onto the induction of leukaemias (this second part has not made part of the KiKK stud, due to methodological reasons). The results do not permit to exclude ionising radiation as cause for the increased incidence of malignancies, as has been stated b the authors of the KiKK stud ( that the radiation emitted normall b NPP principall cannot be interpreted as cause ). Leukaemias in childhood are rare diseases, the mostl develop due to multifactorial influences, and in addition to ionising radiation, man other risk factors are defined. Within the KiKK stud, the influence of such other risk factors could not be established with statistical significance. None of the known risk factors is potent enough as to explain the result, and, additionall, such factors should correlate with the distance to the NPP. The results of the second part of KiKK (case control stud with questionnaires) give not an such indications. The Commission for Environmental Issues of the DAKJ, in accordance with most experts, sees the necessit for further investigations into the causes of leukaemia, taking into account the increase in frequenc of childhood leukaemias of 0.6 1.0% per ear. Attribution of risks According to the authors of the KiKK and also to the SSK the attribution of cases should be restricted to the 5 km distance around NPP. On this basis, around all German NPP and during the time period between 1980 2003, an additional number of 29 ALL cases have been observed. An extrapolation for the 50 km region is mathematicall possible, using a constant function, but is based on the unproven supposition that the function has an equal validit for all distances and that a supposed effect is present also in the more distant regions. This appears to be improbable if one takes into account the ver small difference (300 m) between cases and controls regarding the distances between living places and NPP. Minorit votes Two members of the commission, St. Böse- O Reill and Th. Lob-Corzilius add the following comments: As to the precision of monitoring in the surroundings of NPP: The model estimations were prone to remarkable uncertainties of at least one to two orders of magnitude, due to numerous biokinetic and phsical assumptions and simplifications. Additionall, the measurements have been done b the NPP operators themselves. The results presented as mean values have then be controlled b supervising authorities. It would be necessar to list and control all single results of measurement in order to control and better recognize peaks of radioactivit, e.g. during nuclear fuel rod exchange, because just short lived peaks radiation could ield radiobiological explanations. As to the special vulnerabilit of children: This statement takes into account onl adult, male persons, the so called reference man, and not to women in reproductive age, or to embros who have a considerabl higher radiation sensitivit. Furthermore, effects of ingested or inhaled fission products are neglected b this approach. References 1. Beral V. (1990): Leukaemia and nuclear installations. BMJ. Vol. 300 (6722) p. 411-2. 2. DKKR (2008): Stellungnahme des Deutschen Kinderkrebsregisters/Institut für Medizinische Biometrie, Epidemiologie und Informatik (IMBEI) zu dem von der Mitgliedern des BfS-Expertengremiums im Auftrag des BfS erstellten Bericht 16 Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1)
Epidemiologische Qualitätsprüfung der KiKK-Studien. Dtsch Arztebl 1999 96(14): A 918 24. 3.Michaelis J, Keller B, Haaf G, Kaatsch P. (1992): Incidence of childhood malignancies in the vicinit of west German nuclear power plants. Cancer Causes Control. 1992 Vol. 3 S. 255-63. 4.Kaatsch P, Kaletsch U, Meinert R, Michaelis J. (1998): An extended stud on childhood malignancies in the vicinit of German nuclear power plants. Cancer Causes Control. Vol. 5 S. 529-33. 5.Michaelis J, Kaatsch P, Kaletsch U (1999): Leukämien im Kindesalter - Epidemiologische Untersuchungen des Deutschen Kinderkrebsregisters. 6.Schulze-Rath R, Kaatsch P, Schmiedel S, Spix C, Blettner M (2006): Krebs bei Kindern in der Umgebung von Kernkraftwerken: Bericht zu einer laufenden epidemiologischen Studie. Umweltmed Forsch Prax 2006 11: 20 6. 7.COMARE (Committee on Medical Aspects of Radiation in the Environment) (1988): Investigation of the possible increased incidence of childhood cancer in oung persons near the Dounrea Nuclear Establishment, Caaiathness, Scotland. Her Majest s Stationar Office, London, UK, 1988. 8.COMARE (Committee on Medical Aspects of Radiation in the Environment) (1989): Report on the incidence of childhood cancer in the West Berkshire and North Hamshire Area, in which are situated the Atomic Weapons Research Establishment, Aldermason and Roal Ordnance Factor, Burghfield.. Her Majest s Stationar Office, London, UK, 1989. 9.Viel J. F, Pobel D, Carre A (1995): Incidence of leukaemia in oung people around the La Hague nuclear waste reprocessing plant: a sensitivit analsis. Statis Medicine 14, 2459-2472, 1995 10. Baker P. J., Hoel D. G. (2007): Meta-analsis of standardized incidence and mortalit rates of childhood leukaemia in proximit to nuclear facilities. Eur J Cancer Care Vol. 16 S. 355-363. 11. Körblein A, Hoffmann W (1999): Childhood Cancer in the Vicinit of German Power Plants. Med Global Surv, August 1999, Vol 6. 18-23 12. Expertengremium des BfS (2007): Stellungnahme vom 10. 12. 2007 zur KiKK-Studie. www. bfs. de/de/kerntechnik/kinder krebs/expertengremium. html 13. Kaatsch P, Spix C, Jung I, Blettner M, (2008): Leukämien bei unter 5-jährigen Kindern in der Umgebung deutscher Kernkraftwerke. Deutsches Ärztebl Vol. 105, S. 725-732, 2008 14. SSK (2008): Berichte der Strahlenschutzkommission (SSK) des Bundesministeriums für Umwelt, Naturschutz und Reaktorsicherheit. Bewertung der epidemiologischen Studie zu Kinderkrebs in der Umgebung von Kernkraftwerken (KiKK-Studie). Stellungnahme der Strahlenschutzkommission. Hoffmann Verlag, Berlin, Heft 57 (2008) 15. SSK (2009): Berichte der Strahlenschutzkommission (SSK) des Bundesministeriums für Umwelt, Naturschutz und Reaktorsicherheit, Bewertung der epidemiologischen Studie zu Kinderkrebs in der Umgebung von Kernkraftwerken (KiKK-Studie). Wissenschaftliche Begründung zur Stellungnahme der Strahlenschutzkommission. Hoffmann Verlag, Berlin, Heft 58 (2009) 16. Expertengremium des BfS (2007): Stellungnahme vom 10. 12. 2007 zur KiKK-Studie. www. bfs. de/de/kerntechnik/ kinderkrebs/expertengremium. html 17. Gesellschaft für Strahlenschutz e. V., Smposion (2008): Umwelt - Evidenz Kontroverse Konsequenz am 28. 9. 2008, Berlin. www. gfstrahlenschutz. de/docs/smpumwmed080829. pdf 18. Grosche B, Jung,T, Weiß W (2008): Häufigkeit von Krebs bei Kindern in der Umgebung von Kernkraftwerken. ATW 53, 174-178, 2008. 19. Jöckel KH, Greiser E, Hoffmann W (2008): Epidemiologische Qualitätsprüfung der KiKK-Studien im Auftrag des Bundesamts für Strahlenschutz (BfS) 19. 3. 2008 20. Nussbaum R. H. (2009): Childhood Leukemia and Cancers Near German Nuclear Reactors: Significance, Context, and Ramifications of Recent Studies. International Journal of Occupational and Environmental Health, Vol 15, No 3 (2009) p. 318-323 Address Prof. Dr. med. Karl Ernst v. Mühlendahl Kinderumwelt ggmbh der Deutschen Akademie für Kinder- und Jugendmedizin Westerbreite 7, D 49084 Osnabrück info@uminfo.de Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1) 17
Ocena nara enia na tlenek w gla grup stra aków z jednostki ratowniczo-gaêniczej Assessment of exposure to carbon monoxide group of firefighters from fire fighting and rescue units Jadwiga Lembas-Bogaczk, Anna D ugosz, Ilona Tokarczk Akademia Medczna im. Piastów Âlàskich we Wroc awiu, Katedra i Zak ad Tokskologii. Kierownik: Prof. dr hab. Anna D ugosz Praca wkonana w ramach dzia alnoêci statutowej nr ST-280. Streszczenie Badania zagro eƒ stra aków w warunkach po aru substancjami chemicznmi wkaza we wszstkich przpadkach obecnoêç tlenku w gla. Wch anian przez drogi oddechowe àczàc si z hemoglobinà blokuje transport tlenu w organizmie, co doprowadza do anoksji tkankowej, która jest bezpoêrednim zagro eniem cia stra aków. Celem prac b a ocena nara enia na tlenek w gla stra aków uczestniczàcch w akcji gaszenia po aru. Oszacowanie iloêci wch anianego tlenku w gla przez stra- aków wkonano w grupie 40 stra aków z Jednostki Ratowniczo-GaÊniczej Paƒstwowej Stra Po arnej w Nsie na podstawie pomiaru tlenku w gla w wdchanm powietrzu. Do pomiarów tlenku w gla w wdchanm powietrzu u to miernika Micro CO. Wniki analizowano oddzielnie dla niepalàcch (n425) i dla palàcch papieros (n415). Âredni poziom COHb % dla niepalàcch wkonan przed akcjà ratowniczo gaêniczà wniós 0,3950,30% i wzrós po akcji istotnie statstcznie do 0,6150,34%, natomiast w grupie palàcch poziom ten wniós 2,1750,64% przed akcjà i wzrós nieistotnie po akcji do 2,3350,63%. Poziom Êredni COHb% w tch samch grupach przed i po çwiczeniach sprawnoêciowch wnosi odpowiednio dla niepalàcch przed çwiczeniami 0,4850,28% i po çwiczeniach obni si statstcznie istotnie do 0,3050,27%, a w grupie palàcch przed çwiczeniami wnosi 2,23%50,61 i obni si istotnie statstcznie do 1,5450,71%. Stosujàc podzia zale nie od wieku i sta u prac nie stwierdzono ró nic. S owa kluczowe: poziom COHb we krwi, nara enie na CO, stra ac,akcja ratunkowo-gaênicza Abstract Firemen threat during fire burning of chemical substances indicated presence of carbon monoxide (CO) in all cases. Carbon monoxide causes death of fire. Inhaled through respirator sstem, links with hemoglobin, thus blocking transport and distribution of oxgen in the bod. This leads to tissue anoxia, which is a direct threat to firefighters life. The purpose of this stud was to assess the exposure to carbon monoxide of participating firefighters extinguishing fire. Estimation of carbon monoxide quantit absorbed b firefighters was isolated in a group of 40 firefighters from Fire Extinguishing and Rescue Unit of State Fire in Nsa. The stud was conducted b measuring carbon monoxide in exhaled air. For measurement of carbon monoxide concentration in exhaled air Micro CO meter was used. Results were demonstrated separatel for nonsmokers (n425) and smokers (n415). Mean COHb[%] levels in nonsmokers, measured prior the rescue action was 0,3950,3% and increased statisticall significant after the action to 0,6150,34%, while in the group smokers, this level was 2,1750,64% before the action and increased insignificantl after the action to 2,3350,63%. The average COHb level in the same groups before and after exercise, was respectivel: for nonsmokers prior to exercise was 0,4850,28% and after exercise decreased statisticall significant to 0,3050,27%. In the group of smokers before exercise was 2,2350,61% and decreased statisticall significant up to 1,5450,71%. It was no difference between the group of age and time of emploment. Ke words: COHb blood level, exposure to CO, firefighters, actions to extinguish the fire and rescue Nades ano: 30.07.2010 Zatwierdzono do druku: 30.09.2010 18 Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1)
Wst p Sk ad tokscznch gazów powstajàcch podczas po arów zale od rodzaju palàcch si materia ów i warunków procesu spalania. Badania sk adu substancji powstajàcch podczas po arów przeprowadzone w Stanach Zjednoczonch wkaza, e tlenek w gla b obecn we wszstkich przpadkach, a jego st enie oznaczane w powietrzu osiàga o wartoêci maksmalne od 1000 15.000mg/m 3 [1, 2]. Podobne badania przeprowadzone w Polsce, wkaza obecnoêç CO w pobranch próbkach powietrza bezpoêrednio w warunkach akcji gaêniczej i iloêç CO waha a si od 0 720mg/m 3 [3]. Nara enie stra- aków na tlenek w gla podczas akcji gaszenia po aru jest w ka dm przpadku mo liwe, ale iloêç tlenku w gla wch anianego przez stra aków nie jest dok adnie znana. Nieliczne badania st enia tlenku w gla w wdchanm powietrzu, potwierdzajà wi ksze jego wch anianie u stra aków po akcji gaszenia po aru oraz wi ksze st enie u palàcch papieros [4]. Podczas po arów dla podtrzmania palenia pobieran jest tlen z otaczajàcego powietrza, co powoduje zmniejszenie jego procentowej zawartoêci w sk adzie powietrza niezb dnego dla prawid owego funkcjonowania organizmu, a jednocze- Ênie wzrasta st enie substancji tokscznch, takich jak tlenek w gla. Szczególnà wra liwoêç na brak tlenu wkazuje uk ad nerwow i mi sieƒ sercow. Dopuszczalna granica obni enia zawartoêci tlenu, z normalnej 21% w powietrzu, wnosi maksmalnie do 17 16%. Prz tm st eniu prz normalnm ci- Ênieniu 1013 hpa, hemoglobina we krwi jest wscona tlenem w oko o 95%. Spadek zawartoêci tlenu w powietrzu powoduje spadek wscenia hemoglobin i wst powanie objawów ostrego g odu tlenowego. Prz st eniu tlenu w powietrzu 16 14% pojawia si wzmo ona cz stotliwoêç oddechów i przspieszenie t tna. Prz st eniu tlenu 14 10% wst pujà zaburzenia równowagi i koordnacji ruchów oraz zaburzenia ze stron uk adu nerwowego. Prz obni eniu tlenu w powietrzu do 10 6% objaw niedotlenienia wzmagajà si, wst pujà md oêci, wmiot, utrata zdolnoêci poruszania si, a po pewnm czasie dochodzi do utrat prztomnoêci i do Êpiàczki. Dalsze zmniejszanie si zawartoêci tlenu w powietrzu powoduje w kilka minut ustanie akcji serca. Przebwanie w obszarze po aru oko o 5 minut prz spadku zawartoêci tlenu o 3% jest jeszcze bezpieczne. Prz zawartoêci tlenku w gla w powietrzu 0,01% nawet kilka godzin, brak oznak zatrucia, prz st eniu 0,04% do 2 godzin wst pujà bóle g ow i nudnoêci. Prz 0,16% zawartoêci CO przez 20 minut pojawiajà si dodatkowo bóle i zawrot g ow, a st enie 0,5% w ciàgu 20 30 minut mo e spowodowaç zatrucie Êmiertelne, a zawartoêç 1% CO Êmierç w ciàgu 1 do kilku minut. [5, 6]. Podczas po arów, stra ac sà nara eni na podw szonà temperatur i strumieƒ promieniowania cieplnego. W strefie spalania gazów, ciecz i materia ów sta ch, Êrednia temperatura mo e wnosiç oko o 10.000 C. Toksczne produkt powstajàce wwarunkach po aru, oprócz CO 2 i CO sà to równie : tlenki siarki, pi ciotlenek fosforu, tlenki azotu, par cjanowodoru, chlorowodoru, siarkowodoru. Wiele ofiar zatrucia CO, umiera lub doêwiadcza ci kiego urazu neurologicznego pomimo leczenia. A oko o 50% uratowanch po odzskaniu prztomnoêci, mo e doznaç w ró nm stopniu l ejszch, lecz ograniczajàcch sprawnoêç, neuropschiatrcznch powik aƒ. Zadmienie skutkuje mi dz innmi ograniczeniem widocznoêci, co powoduje utrat orientacji, zawienie oczu i utrudnia ewakuacj ludzi zagro onch. W Polsce przeprowadzono badania przczn zachorowaƒ wêród stra aków wkonujàcch bezpoêrednie cznnoêci ratowniczo-gaênicze. Badania te wkaza, e najcz stszà przcznà czasowej niezdolnoêci do prac b chorob uk adu oddechowego (22,3%), chorob uk adu nerwowego i narzàdów zms ów (18,5%), chorob uk adu kostno-mi Êniowego i tkanki àcznej 18%, chorob uk adu krà enia (takie jak, nadciênienie, niedokrwienna choroba serca) stanowi 12,9% absencji chorobowej. Zaburzenia pschiczne to a 8,1%, chorob uk adu trawiennego 6,8%, nowotwor 1,5%, wêród pozosta ch przczn stwierdzono chorob krwi i narzàdów krwiotwórczch [7]. Oszacowanie jakie iloêci tlenku w gla sà wch aniane przez stra aków podczas akcji ratowniczo-ga- Êniczej zosta podj te przez badacz z Japonii, poprzez oznaczenie tlenku w gla w powietrzu wdchanm u stra aków po powrocie z akcji. Stwierdzono obecnoêç COHb Êrednio w iloêci 3,5% u niepalàcch i 5,7% u palàcch, po 5 dniach wolnch oznaczone st enie spad o odpowiednio u niepalàcch do 1,5% i do 3,8% u palàcch [8]. Badania amerkaƒskie ostrego dzia ania po tokscznej ekspozcji na uk ad oddechow stra aków, wkaza istotne zmian funkcjonalne u tch, którz nie chronili dróg oddechowch aparatem tlenowm. Nie zaobserwowano adnch zmian u stra aków stosujàcch ochron dróg oddechowch. Oznaczon poziom we krwi COHb% u stra aków nie stosujàcch ochron przed akcjà wnosi 1,5% i po akcji wzrós statstcznie nieistotnie do 2% [9]. Inne badania poprzez pomiar iloêci CO w wdchanm powietrzu wkaza poziom COHb% u stra aków stosujàcch ochron dróg oddechowch od 0% 3%, a bez zabezpieczenia otrzmano wartoêci od 4% do 14%. Oceniono, e ta metoda poêrednia jest bardzo przdatna do oszacowania nara enia stra aków na CO [10]. Medcna Ârodowiskowa / Environmental Medicine 2011 14 (1) 19