2011 Vol. 14 N o 3. W numerze: Contents: ISSN MEDYCYNA ÂRODOWISKOWA / ENVIRONMENTAL MEDICINE 2011 Vol. 14 N o 3

Transkrypt

1 ISSN Vol. 14 N o 3 MEDYCYNA ÂRODOWISKOWA / ENVIRONMENTAL MEDICINE 2011 Vol. 14 N o 3 W numerze: NeurotoksycznoÊç o owiu u dzieci RakotwórczoÊç kadmu urawka detoksykacja Pb, Cd, Zn gleby WWA w pyle i mutagennoêç Energooszcz dne oêwietlenie Uk ad krà enia u kierowców Stres u ratowników Przewlek a choroba (cukrzyca) dziecka XVII Konferencja Zdrowie Êrodowiskowe w Legnicy Contents: Lead neurotoxicity in children Cadmium carcinogenesis Coral bells soil Pb, Cd, Zn decontamination PAH in dust mutagenicity Energy-saving lighting Cardiovascular diseases in bus drivers Stress in paramedics Chronic disease (diabetes)of child XVII-th EHC Conference in Legnica

2 Medycyna Ârodowiskowa / Environmental Medicine Czasopismo Journal of Instytutu Medycyny Pracy Institute of Occupational Medicine and i Zdrowia Ârodowiskowego w Sosnowcu Environmental Health in Sosnowiec oraz Polskiego Towarzystwa and Polish Society Medycyny Ârodowiskowej of Environmental Medicine Ukazuje si cztery razy w roku It is published four times a year ZESPÓ REDAKCYJNY / EDITORIAL STAFF Redaktor Naczelny / Editor-in-Chief Zast pcy Redaktora Naczelnego / Deputy Editors Redaktor Tematyczny / Feature Editor Sekretarz Redakcji / Co-editor Prof. dr hab. med. Zbigniew Rudkowski Prof. dr hab. med. Jan Grzesik Prof. dr hab. med. Janusz Ha uszka lek. med. Maja Muszyƒska-Graca mgr Karina Erenkfeit RADA PROGRAMOWA / EDITORIAL BOARD Przewodniczàcy Rady Programowej / Chairperson Cz onkowie Rady Programowej / Members Dr n. med. Edmund Anczyk Prof. dr hab. n. med. Ryszard Andrzejak Dr n. med. Piotr Z. Brewczyƒski Dr n. med. Zdzis aw Brzeski Prof. dr hab. n med. Marian Dró d Prof. dr hab. n. med. Jerzy Filikowski Dr in. Janina Fuda a Dr hab. n. med. Rafa Górny Prof. dr hab. n. med. Jan Grzesik 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 Prof. dr hab. n. przyr. Jerzy Kwapuliƒski Cz onkowie Zagraniczni / International Editorial Board Prof. David Bellinger, M.D., PhD, USA Stephan Boese O Reilly, M.D., Germany Prof. Gyula Dura, M.D., Hungary Prof. Helmut Greim, M.D., Germany Prof. Philippe Hartemann, M.D., France Peter van den Hazel, M.D., Netherlands Hannu Komulainen, M.D., Finland Jan Koval, M.D., Slovakia Prof. Jean Krutmann, M.D., Germany Prof. Robert Malina, M.D., PhD, USA Prof. dr hab. med. Gerard Jonderko Prof. dr hab. n. med. Henryka 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 Olszowy Prof. dr hab. n. med. Janusz Pach Prof. dr hab. n. med. Krystyna Pawlas Prof. dr hab. n. med. W adys aw Pierzcha a Prof. dr hab. n. med. Zbigniew Rudkowski Prof. dr hab. Jerzy Boles aw Samoliƒski Dr hab. n. med. Andrzej Sobczak Prof. dr hab. Jerzy A. Sokal Prof. dr hab. n. med. Neonila Szeszenia-Dàbrowska Prof. dr hab. n. h. Beata Tobiasz-Adamczyk 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. Karl Ernst von Muehlendahl, M.D., Germany Peter Ohnsorge, M.D., Germany Anna Paldy, M.D., PhD, Hungary Prof. Roberto Ronchetti, M.D., Italy Prof. Tore Sannel, M.D., Norway Prof. Staffan Skerfving, M.D., Sweden Prof. Anne Steenhout, M.D., Belgium Loreta Strumylaite, M.D., PhD, Lithuania Andrzej Szpakow, M.D., PhD, Belorussia Prof. Gerhard Winnecke, M.D., Germany Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (2) 1

3 Adres Redakcji i Wydawcy: Instytut Medycyny Pracy i Zdrowia Ârodowiskowego oraz Polskie Towarzystwo Medycyny Ârodowiskowej ul. KoÊcielna Sosnowiec tel. (32) wew. 201, 202 fax (32) ms@ imp.sosnowiec.pl Editorial office and publisher s address: Institute of Occupational Medicine and Environmental Health and Polish Society of Environmental Medicine KoÊcielna 13 Str Sosnowiec, Poland Tel. +48 (32) ext. 201, 202 Fax: +48 (32) ms@ imp.sosnowiec.pl Warunki prenumeraty: Cena prenumeraty rocznej dla instytucji wynosi 105 z (26,25 z za jeden numer), dla odbiorców indywidualnych 63 z (15,75 z za jeden numer). Zamówienie prosimy kierowaç na adres: Redakcja Medycyny Ârodowiskowej Instytut Medycyny Pracy i Zdrowia Ârodowiskowego ul. KoÊcielna Sosnowiec Zakup numeru bie àcego i numerów archiwalnych mo liwy jest po dokonaniu wp aty na konto Instytutu Medycyny Pracy i Zdrowia Ârodowiskowego w Sosnowcu nr: Wp at tytu em op aty cz onkowskiej mo na dokonywaç na konto Polskiego Towarzystwa Medycyny Ârodowiskowej nr: Subscription conditions: Annual subscription for institutions: 105 z (26,25 z one volume) Annual subscription for individuals: 63 z (15,75 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 Sosnowiec, Poland People or institutions interested in subscribing should send an order to the address of editorial office. Payments could be made to the account no. MILLENIUM Bank S.S. Oddzia Katowice PL BIC/SWIFT: BIGBPLPWXXX of the Institute of Occupational and Environmental Medicine in Sosnowiec Czasopismo ukazuje si w wersji pierwotnej drukowanej oraz w wersji elektronicznej na stronie Journal is published in the original printed wersion and on webside Nak ad: 400 egz. Edition: 400 copies Punktacja czasopisma: MNiSW (Ministerstwo Nauki i Szkolnictwa Wy szego) 6,0 p. IC (Index Copernicus) 4,47 p. ISSN Medycyna Ârodowiskowa / Environmental Medicine 2010; 13 (1)

4 SPIS TREÂCI ARTYKU REDAKCYJNY Ostatnie badania nad neurotoksycznoêcià o owiu. Dawno znany metal nowe zagadnienia David C. Bellinger RakotwórczoÊç kadmu kluczowe zagadnienia Loreta Strumylaite, Kristina Mechonosina PRACE ORYGINALNE OkreÊlenie przydatnoêci trzech odmian urawki (Heuchera cvs.) do bioremediacji kadmu (Cd), o owiu (Pb) i cynku (Zn) z terenów pogórniczych Zag bia Dàbrowskiego Gabriela Sàkol, Patryk Ochota, Janusz Miros awski, Piotr Z. Brewczyƒski ZawartoÊç wielopierêcieniowych w glowodorów aromatycznych a mutagenne w aêciwoêci py owych zanieczyszczeƒ powietrza na obszarze województwa Êlàskiego Agnieszka Koz owska, Natalia Pawlas, Marzena Zaciera, Lucyna Kapka-Skrzypczak, Rafa Jasiƒski Wp yw powszechnego wdro enia energooszcz dnych êróde Êwiat a na sprawnoêç i komfort widzenia osób starszych El bieta Janosik, Stanis aw Marzec, Marcin aciak, Jolanta Nowicka, Jolanta Zachara Cz stoêç wyst powania i czynniki ryzyka chorób uk adu krà enia w populacji kierowców autobusów miejskich Renata Z otkowska, Piotr Z. Brewczyƒski, Beata Dàbkowska, Maja Muszyƒska-Graca, Magda Skiba, Pawe Wyl ek Nasilenie objawów stresu pourazowego u osób wykonujàcych zawód ratownika medycznego Ewa Og odek PRACE POGLÑDOWE Choroba przewlek a w yciu dziecka. Aspekt spo eczny oraz psychologiczny na przyk adzie cukrzycy typu 1 Lucyna Sochocka, Anna Noczyƒska, Aleksander Wojty ko SPRAWOZDANIA Notatki i wra enia z Jubileuszowej XVII Mi dzynarodowej Konferencji Naukowej Zdrowie Êrodowiskowe dzieci z uwzgl dnieniem czynników ywieniowych, chemicznych i metali toksycznych maja 2011 w Legnicy Zbigniew Rudkowski KOMUNIKATY X Mi dzynarodowa Konferencja Naukowa Polskiego Towarzystwa Medycyny Ârodowiskowej Cz owiek Zdrowie-Ârodowisko. Szczecin r I Szczeciƒska Mi dzynarodowa Konferencja Naukowa Polskiego Towarzystwa Medycyny Ârodowiskowej Cz owiek Zdrowie-Ârodowisko. Szczecin r Regulamin publikowania prac wskazówki dla Autorów Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3) 3

5 CONTENTS EDITORIAL Recent Studies of Lead Neurotoxicity in Children: Old Metal, New Questions David C. Bellinger Cadmium carcinogenesis some key points Loreta Strumylaite, Kristina Mechonosina ORIGINAL PAPERS Suitability of three cultivars of coral bells (Heuchera cvs.) to bioremediation of cadmium (Cd), lead (Pb) and zinc (Zn) from post-mining area in Zag bie Dàbrowskie Gabriela Sàkol, Patryk Ochota, Janusz Miros awski, Piotr Z. Brewczyƒski Policyclic aromatic hydrocarbons concentration and mutagenic effects of dust un outdoor environment in Silesian Region Agnieszka Koz owska, Natalia Pawlas, Marzena Zaciera, Lucyna Kapka-Skrzypczak, Rafa Jasiƒski Impact of energy-saving light sources on the efficiency and comfort vision of elderly people El bieta Janosik, Stanis aw Marzec, Marcin aciak, Jolanta Nowicka, Jolanta Zachara Prevalence and risk factors for the cardiovascular diseases in the population of municipal bus drivers Renata Z otkowska, Piotr Z. Brewczyƒski, Beata Dàbkowska, Maja Muszyƒska-Graca, Magda Skiba, Pawe Wyl ek Symptoms intensification of post-traumatic stress in individuals performing the job of a medical rescue worker Ewa Og odek REVIEW PAPERS Chronic disease in child s life. Social and psychological aspects in the context of type I diabetes Lucyna Sochocka, Anna Noczyƒska, Aleksander Wojty ko REPORTS Notes and impressions from the XVII International Conference Children s health impact of environment, nutrition, chemicals and toxic metals in Legnica, May Zbigniew Rudkowski ANNOUNCEMENTS X th International Scientific Conference of Polish Society of Environmental Medicine Man-Health-Environment, Szczecin I st Szczecin International Scientific Conference of Polish Society of Environmental Medicine Man-Health-Environment, Szczecin Instructions to authors Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3)

6 Od Redaktora Artyku redakcyjny autorstwa Davida Bellingera, profesora z Uniwersytetu Harvarda, omawia bardzo istotne zagadnienie, jakim jest wp yw obcià- enia o owiem w niskich st eniach w krwi dzieci. O ów znacznie poni ej st enia 100 µg/l (limit przyj ty dawniej przez WHO) mo e uszkadzaç centralny uk ad nerwowy, szczególnie we wczesnym okresie rozwoju dziecka; nie mo na okreêliç minimum st - enia o owiu nieszkodliwego. Kolejny artyku na podstawie danych z ostatnich lat przedstawia Êrodowiskowe karcinogenne dzia anie kadmu. Dzia prac oryginalnych rozpoczyna studium na temat u ycia urawki jako roêliny detoksykujàcej gleb z o owiu, kadmu i cynku. Nast pne doniesienie ma podobnie wa ne znaczenie nie tylko dla Âlàska, gdy wykazuje, e wielopierêcieniowe w glowodory aromatyczne zawarte wpy ach wzmagajà ich mutagennoêç. Problem bardzo aktualny w Êrodowisku domowym i b dàcy treêcià kolejnego oryginalnego artyku u to ocena wp ywu zamiany tradycyjnych arówek na energooszcz dne êród a Êwiat a i wp ywu na zdolnoêç widzenia przez osoby starsze. Kolejne doniesienie przedstawia, jak w Êrodowisku pracy kszta tujà si wskaêniki zdrowia, szczególnie uk adu krà enia i metaboliczne u kierowców autobusów (u ponad 80% nadwaga lub oty oêç!). W nast pnej pracy omówiono znaczenie stresu u ratowników medycznych, co uzasadnia podj cie dzia- aƒ profilaktycznych. Przewlek a choroba dziecka, np. coraz cz Êciej wyst pujàca obecnie cukrzyca (nb. w du ym stopniu z udzia em czynników Êrodowiskowych) wywiera znaczàcy wp yw psychologiczny i spo eczny zarówno na pacjenta jak i na jego otoczenie. Aspekty tego zagadnienia omawia publikowana praca poglàdowa. Numer zamyka sprawozdanie z Jubileuszowej XVII Konferencji Naukowej w Legnicy maja 2011 Zdrowie Êrodowiskowe dzieci z uwzgl dnieniem czynników ywieniowych, chemicznych i metali ci kich oraz ze sesji przedstawiajàcej post py pediatrii bia oruskiej. Redaktor Naczelny Prof. dr hab. n. med. Zbigniew Rudkowski Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3) 5

7 6 Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3)

8 ARTYKU REDAKCYJNY EDITORIAL RECENT STUDIES OF LEAD NEUROTOXICITY IN CHILDREN: OLD METAL, NEW QUESTIONS OSTATNIE BADANIA NAD NEUROTOKSYCZNOÂCIÑ O OWIU. DAWNO ZNANY METAL NOWE ZAGADNIENIA David C. Bellinger Children s Hospital Boston Harvard Medical School Harvard School of Public Health Abstract Many times in the history of lead toxicology the view has prevailed that the problem has been solved, and that exposure to lead is no longer a major public health concern. Each time, additional research has demonstrated the prematurity of this judgment. In the last decade, an extraordinary number of new studies have illustrated that the problem remains, and that it has dimensions never before considered. Children s intelligence has traditionally been considered to be the most sensitive endpoint and used as the basis for risk assessment and standard setting. For IQ, the dose-effect relationship appears to be supralinear, with greater deficits per µg/l increment below than above 100 µg/l. Recent studies have found that greater lead exposure in early childhood is also associated with a wide variety of other outcomes, with some associations evident at biomarker levels comparable to those at which IQ deficits are observed. Among these endpoints are poorer academic achievement, ADHD, conduct disorder, and antisocial behavior. In animals, early life lead exposure has been implicated in neurodegenerative disorders later in life, perhaps via epigenetic mechanisms. Studies employing neuroimaging modalities such as volumetric, diffusion tensor, and functional MRI are providing insights into the neural bases of the cognitive impairments associated with greater lead exposure. Several recent risk assessments (e.g., EFSA, JECFA) have concluded that research has yet to identify a threshold level below which lead can be considered safe. Keywords: lead, neurotoxicity, children, epidemiology Streszczenie Wiele razy w historii toksykologii o owiu przewa a poglàd, e problem ten zosta rozwiàzany a ekspozycja na o ów nie jest ju powa nym zagadnieniem zdrowia publicznego. Za ka dym razem dalsze dodatkowe badania wykazywa y, e taki poglàd jest przedwczesny. W ostatniej dekadzie nadzwyczajnie du a liczba nowych badaƒ ukaza a, e problem pozostaje i e jego rozmiary sà tak szerokie jak nigdy przedtem tego nie spodziewano si. Inteligencja dzieci tradycjonalnie by a uwa ana za najbardziej czu y koƒcowy wskaênik i by a u ywana jako podstawa dla oceny ryzyka i ustalania standardów. Dla IQ zwiàzek dawka skutek okaza si byç supra-linearnym z wi kszymi deficytami przez zwi kszenie µg/l o owiu poni ej ani- eli powy ej st enia 100 µg/l w krwi. Ostatnie badania wykaza y, e wi ksza ekspozycja na o ów we wczesnym okresie dzieciƒstwa jest równie zwiàzana z szerokà ró norodnoêcià wyst powania innych nast pstw, które sà skojarzone ewidentnie na poziomie biomarkerów porównywalnie do tych, przy których obserwuje si deficyty IQ. Nades ano: Zatwierdzono do druku: Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3) 7

9 WÊród tych koƒcowych nast pstw wymienia si gorszà zdolnoêç do uczenia si na poziomie akademickim, ADHD, zaburzenia zachowania i zachowania antyspo- eczne U zwierzàt wczesna ekspozycja w wieku rozwojowym ma zwiàzek z wyst powaniem chorób neurodegeneracyjnych w póêniejszym okresie ycia, byç mo e na drodze mechanizmów epigenetycznych. Badania z u yciem metod obrazowania uk adu nerwowego jak wolumetryczny tensor dyfuzyjny i czynnoêciowe MRI dostarczajà wglàdu w neurologiczne podstawy uszkodzenia poznawczego zwiàzanego z wi kszà ekspozycjà na o ów. Liczne ostatnie oceny ryzyka (np. EFSA, JECFA) Êwiadczà, e badania naukowe jeszcze nie zdo a y zidentyfikowaç takiego progowego poziomu o owiu w krwi, poni ej którego mo na by uwa aç, e jest on bezpieczny dla zdrowia. S owa kluczowe: o ów, neurotoksycznoêç, dzieci, epidemiologia Knowledge that lead is neurotoxic, especially to children, is more than a century old, yet remarkable advances in our understanding of the scope of its adverse effects continue to be made. Although great success has been achieved in reducing population exposures, recent research has identified surprising new dimensions of lead s toxicities. This commentary focuses specifically on lead neurotoxicity in children, broadly surveying epidemiologic literature from the past decade. Recent studies on lead s renal, cardiovascular, adult central nervous system, and reproductive effects are reviewed elsewhere [1]. The list of the aspects of brain function and development that are impaired as a result of lead exposure, and the mechanisms by which these impairments occur, is impressive. The latter include apoptosis and excitotoxicity, reduced energy production in the mitochondria, reduced oxygen transport due to interference with heme synthesis, increased oxidative stress, alteration of first, second, and third messenger systems, and alteration of patterns of gene expression and transcription [2]. In rodents exposed to environmentally-relevant levels of lead exposure, neurogenesis is reduced in the hippocampus, neurons that are born are less likely to survive, and those that do survive tend to have aberrant morphology [3]. In imaging studies of young adults for whom detailed histories of early life blood lead levels are available, greater early lead exposure is associated with reduced volumes in several brain regions [4, 5]. Reduced fractional anisotrophy and other changes in the white matter suggest altered myelination and reduced axonal integrity [6]. Lead-associated changes in brain metabolism are suggested by studies that found reduced levels of N-acetyl aspartate, creatine and phosphocreatine, glycerolphosphocholine and phosphocholines in several regions of grey and white matter [7]. Yuan et al. [8] reported significant lead-associated changes in activation patterns in the left frontal cortex and left middle temporal gyrus on a verb generation task. These changes in neuronal structure and function are accompanied by persistent impairments at the level of behavior. In a pooled analysis of 7 international prospective studies, involving 1,333 children, concurrent blood lead level was inversely related to covariate-adjusted IQ in childhood, with a supralinear form providing the best fit to the data [9]. Specifically, the reduction in IQ per µg/dl in blood lead level was greater at blood lead levels below 100 µg/l than it was at levels greater than 100. Although an explanation for this somewhat surprising finding has not been identified, it has since been found in several other studies [10, 11]. The IQ deficits appear to be long-lasting. A follow-up study of a cohort enrolled at birth showed that childhood blood lead level is a significant predictor of IQ at age 30 years [12]. While the lead-related deficits in IQ might be considered to be modest in magnitude, deficits are also apparent in outcomes that have clear implications for children s well-being. For example, Surkan et al. [13] found that children with a blood lead level of µg/l scored significantly worse than children with a blood lead level of µg/l on tests of reading and mathematics, even when the comparisons were adjusted for the children s Full-Scale IQ scores. This finding suggests that even among children with similar Full- Scale IQ scores, those with a higher blood lead level find academic tasks more challenging. Such adiscrepancy between aptitude (i.e., IQ) and ability (i.e., academic achievement) is a hallmark sign of a specific learning disability. Furthermore, children with greater lead exposure achieve reduced levels of success in meeting the goals set for learning in school. Miranda et al. [14] found, in a study involving 8,600 4th graders in the U.S., that the percentage of children who failed an end-of-grade reading test was monotonically related to blood lead level, with the association apparent down to ablood lead level of 10 µg/l. This finding was replicated in an even larger study of more than 56,000 children [15], and, furthermore, showed that the impact of lead was stronger among children who had other risk factors for neurodevelopmental impairment. 8 Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3)

10 It has been known for decades that greater lead exposure is associated with behaviors that suggest attentional deficits, including increased distractibility, poorer persistence, greater disorganization, and inability to follow directions. This observation has been explored in several recent studies that examined the association between blood lead level and Attention Deficit Hyperactivity Disorder (ADHD). Using the data of NHANES , Braun et al. [16] found that the odds ratio for parent-reported ADHD among children with a blood lead level greater than 20 µg/l was 4, using children with ablood lead level below 8 µg/l as the reference group. The odds ratios for children with a blood lead level of or were approximately 2 and 3, respectively, suggesting a roughly linear doseresponse relationship. The finding of an increased risk of ADHD among children with greater lead exposure has also been reported in other studies from the U.S. [17, 18], and in studies from Korea [19], Romania [20], and China [21]. A recent line of investigation involves the possible relationship between increased early lead exposure and aggression, including criminality. This is not a new hypothesis as an early case series [22] raised this possibility that one effect of lead poisoning is loss of the normal inhibitory function and the promotion of socially disruptive behaviors. Needleman et al. [23] reported that 11 year olds children with higher bone lead levels were rated by both their parents and teachers as more impaired on the Aggression and Delinquency scales of the Child Behavior Checklist. Needleman et al. [24] followedup this observation, comparing the bone lead levels of adolescents who were adjudicated delinquents to the levels of controls. Among both boys and girls, the delinquents were significantly more likely than the controls to have a detectable bone lead level. Other studies reporting a link between delinquency and lead exposure include Dietrich et al. [25], Stretesky and Lynch [26, 27], Nevin [28, 29], Fergusson et al. [30], Marcus et al. [31], and Olympio et al., [32]. Using data from NHANES , Braun et al. [33] reported significantly increased adjusted odds of meeting DSM-IV criteria for conduct disorder among 8 15 year old children with a concurrent blood lead level greater than 8 µg/l. The strongest epidemiological evidence for an association between early life lead exposure and criminality, however, comes from a prospective study conducted by Wright et al. [34] on a group of 250 socio-economically-disadvantaged children, years old, for whom blood lead level was measured several times between gestation and age 6 years. The median blood lead level through age 5 was 123 µg/dl (range ). The investigators obtained records, from the county criminal justice system, of the number of times the participants had been arrested since age 18 years. A variety of blood lead indices were developed, including prenatal, average childhood, and 6-year blood lead level. Using the number of arrests for violent offenses as the outcome, the covariate-adjusted rate ratios associated with each 50 µg/l increase in blood lead level were 1.34 (95% CI: ), 1.30 (95% CI: ), and 1.48 (95% CI: ), respectively, for the three blood lead indices. The reason that this study is persuasive is that the data on exposure and covariates were collected decades before the data on outcome were collected, eliminating the likelihood of selection bias and other biases that threaten the validity of cross-sectional or retrospective analyses. The plausibility of a role for childhood lead exposure as a risk factor for aggression is supported by experimental studies of rats, hamsters, cats, and monkeys. In rhesus monkeys, Laughlin et al. [35] showed that exposure to 1 mg of lead per kg per day in the first year of life resulted in persistent alterations in play behavior even after cessation of lead exposure. These alterations included reductions in rough-and-tumble play, and increases in self-stimulation and fear grimacing. The authors noted that these suggested, a pattern of inappropriate social interactions which are unlikely to promote social integration and reproductive success. Moore et al. [36] reported that lead-exposed monkeys demonstrated an increased propensity for impulsive responding, namely tactile defensiveness, expressed as increased fear and withdrawal in response to innocuous stimulation (i.e., stimulation of the face and neck with a feather). Finally, Li et al. [37] found that lead exposure reduced the amount of electrical stimulation of the lateral hypothalamus required to elicit predatory attack of an anesthetized rat in cats. In this study, the amount of stimulation required subsequently increased when lead exposure was stopped, but fell when exposure was resumed. In aggregate, the recent evidence on lead-associated neurological morbidity in children suggests that early life exposure results in a cascade of effects, involving deficits in IQ, executive function, impulse control, and ability to delay gratification and downstream effects such as reduced academic achievement, increased likelihood of incomplete schooling, disorders such as ADHD, conduct disorder, antisocial behavior, and, perhaps, substance abuse. The focus tends to be on developmental processes that are directly impacted by lead exposure, but it is important to consider a more complex model in which lead exposure is viewed as a predictor rather than an outcome. In animal models, early lead Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3) 9

11 exposure limits the capacity to respond successfully to a later insult. For example, rats exposed to lead in early life show a reduced capacity to recover beam walking and proprioceptive limb placing skills following the administration, in adulthood, of a photochemically-induced ischemic stroke in the hind limb parietal sensorimotor cortex [38]. Recent studies in rodents and non-human primates suggest that developmental exposure to lead might be a risk factor for neurodegenerative disease in adulthood. Animals exposed to lead only in early life show elevations, in adulthood, of beta-amyloid protein precursor (APP) mrna, APP, and its amyloidogenic product, Abeta, in old age [39]. In monkeys, Abeta staining and amyloid plaques accumulate most striking in the frontal cortex [40]. In addition, DNA methylation is decreased and oxidative damage to DNA is increased in lead-exposed animals, suggesting that an epigenetic process might underlie these delayed effects. An active but relatively undeveloped area of investigation concerns individual variation in susceptibility to lead neurotoxicity. In several studies, effect modification by socio-economic status (SES) has been noted, with poorer children suffering disproportionately from lead exposure [41]. Because SES is a complex construct that encompasses a variety of more proximal factors that can influence child neurodevelopment, considerable effort has been invested in identifying which component of SES, or more likely, components, influence response to lead exposure. Among the classes of components likely to be important are health co-morbidities (including exposure to other toxicants), genotype, the rearing environment, stress, access to health care, quality of schools, neighborhood characteristics, and nutrition. Some of these components, or aspects of them, have been investigated. For example, two studies suggest that the adverse effects of lead are greater if a child is co-exposed to higher levels of manganese [42, 43]. The learning deficits of lead-exposed rats are attenuated if they are raised in an enriched environment that includes exposure to other rats, larger spaces, and more toys [44]. An enriched environment also normalizes aspects of NMDA and BDNF gene expression in the hippocampus. Animals raised by dams subjected both to lead exposure and to stressful procedures show greater learning deficits as well as altered patterns of stress responsivity [45]. The evolution over the past forty years in the level of lead exposure at which important adverse effects appear continues unabated, and two recent risk assessments concluded that a level of lead exposure that is safe has yet to be identified [46, 47]. Although impressive reductions in population exposures have occurred in many developed countries as a result of interventions, lead exposure in developing countries remains an important public health problem. The World Health Organization estimated that in 2000, less than 10% of the world s children had a blood lead level of 200 µg/l or greater, but that 99% of them lived in developing countries and that nearly 1% of the global burden of disease could be attributed to lead exposure [48]. References 1. Bellinger, D.C. The protean toxicities of lead: New chapters in a familiar story. International Journal of Environmental Research and Public Health, 2011;8: Lidsky, T.I., Schneider, J.S. Lead neurotoxicity in children: Basic mechanisms and clinical correlates. Brain 2003; 126: Verina T, Rohde CA, Guilarte TR. Environmental lead exposure during early life alters granule cell neurogenesis and morphology in the hippocampus of young adult rats. Neuroscience 2007;145: Cecil, K.M.; Brubaker, C.J.; Adler, C.M.; Dietrich, K.N.; Altaye, M.; Egelhoff, J.C.; Wessel, S.; Elangovan, I.; Hornung, R.; Jarvis, K.; Lanphear, B.P. Decreased brain volume in adults with childhood lead exposure. PLoS Medicine 2008, 5, e Brubaker, C.J.; Dietrich, K.N.; Lanphear, B.P.; Cecil, K.M.. The influence of age of lead exposure on adult gray matter volume. Neurotoxicology 2010, 31, Brubaker, C.J.; Schmithorst, V.J.; Haynes, E.N.; Dietrich, K.N.; Egelhoff, J.C.; Lindquist, D.M.; Lanphear, B.P.; Cecil, K.M. Altered myelination and axonal integrity in adults with childhood lead exposure: a diffusion tensor imaging study. Neurotoxicology 2009, 30, Cecil, K.M.; Dietrich, K.N.; Altaye, M.; Egelhoff, J.C.; Lindquist, D.M.; Brubaker, C.J.; Lanphear, B.P. Proton magnetic resonance spectroscopy in adults with childhood lead exposure. Environmental Health Perspectives 2011, 119, Yuan, W.; Holland, S.K.; Cecil, K.M.; Dietrich, K.N.; Wessel, S.D.; Altaye, M; Hornung, R.W.; Ris, M.D.; Egelhoff, J.C.; Lanphear, B.P. The impact of early childhood lead exposure on brain organization: A functional magnetic resonance imaging study of language function. Pediatrics 2006, 118, Lanphear, B.P.; Hornung, R.; Khoury, J.; Yolton, K.; Baghurst, P.; Bellinger, D.C.; Canfield, R.L.; Dietrich, K.N.; Bornschein, R.; Greene, T.; Rothenberg, S.J.; Needleman, H.L.; Schnaas, L.; Wasserman, G.; Graziano, J.; Roberts, R. Low-level environmental lead exposure and children s intellectual function: an international pooled analysis. Environmental Health Perspectives 2005, 113, Tellez-Rojo, M.M.; Bellinger, D.C.; Arroyo-Quiroz, C.; Lamadrid-Figueroa, H.; Mercado-García, A.; Schnaas- Arrieta, L.; Wright, R.O.; Hernández-Avila, M.; Hu, H. Longitudinal associations between blood lead concentrations lower than 10?g/dL and neurobehavioral development in environmentally exposed children in Mexico City. Pediatrics 2006, 118, e323 e Kordas, K.; Canfield, R.L.; López, P.; Rosado, J.L.; Vargas, G.G.; Cebrián, M.E.; Rico, J.A.; Ronquillo, D.; Stoltzfus, R.J. Deficits in cognitive function and achievement in Mexican first-graders with low blood lead concentrations. Environmental Research 2006, 100, Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3)

12 12. Mazumdar, M.; Bellinger, D.C.; Abanilla, K.; Bacic, J.; Needleman, H.L. Low-level environmental lead exposure in childhood and adult intellectual function: a follow-up study. Environmental Health 2011, 10, Surkan, P.J.; Zhang, A.; Trachtenberg, F.; Daniel, D.B.; McKinlay, S.; Bellinger, D.C. Neuropsychological function in children with blood lead levels <10 µg/dl. Neurotoxicology 2007, 28, Miranda, M.L.; Kim, D.; Galeano, M.A.; Paul, C.J.; Hull, A.P.; Morgan, S.P. The relationship between early childhood blood lead levels and performance on end of grade tests. Environmental Health Perspectives 2007, 115, Miranda, M.L.; Kim, D.; Reiter, J.; Overstreet Galeano, M.A.; Maxson, P. Environmental contributors to the achievement gap. Neurotoxicology 2009, 30, Braun, J.M.; Kahn, R.S.; Froehlich, T.; Auinger, P.; Lanphear, B.P. Exposures to environmental toxicants and attention deficit hyperactivity disorder in US children. Environmental Health Perspectives 2006, 114, Nigg, J.T.; Knottnerus, G.M.; Martel, M.M.; Nikolas, M.; Cavanagh, K.; Karmaus, W.; Rappley, M.D. Low blood lead levels associated with clinically diagnosed attention deficit/hyperactivity disorder and mediated by weak cognitive control. Biological Psychiatry 2008, 63, Nigg, J.T.; Nikolas, M.; Knottnerus, G.M.; Cavanagh, K.; Friderici, K. Confirmation and extension of association of blood lead with attention-deficit/hyperactivity disorder (ADHD) and ADHD symptom domains at population-typical exposure levels. Journal of Child Psychology and Psychiatry 2010, 51, Ha, M.; Kwon, H.J.; Lim, M.H.; Jee, Y.K.; Hong, Y.C.; Leem, J.H.; Sakong, J.; Bae, J.M.; Hong, S.J.; Roh, Y.M.; Jo, S.J. Low blood levels of lead and mercury and symptoms of attention deficit hyperactivity in children: a report of the Children s Health and Environment Research (CHEER). Neurotoxicology 2009, 30, Nicolescu, R.; Petcu, C.; Cordeanu, A.; Fabritius, K.; Schlumpf, M.; Krebs, R.; Kramer, U.; Winneke, G. Environmental exposure to lead, but not other neurotoxic metals, relates to core elements of ADHD in Romanian children: Performance and questionnaire data. Environmental Research 2010, 110, Wang, H.L.; Chen, X.T.; Yang, B.; Ma, F.L.; Wang, S.; Tang, M.L.; Hao, M.G.; Ruan, D.Y. Case control study of blood lead levels and attention deficit hyperactivity disorder in Chinese children. Environmental Health Perspectives 2008, 116, Byers, R.K.; Lord, E.E. Late effects of lead poisoning on mental development. American Journal of Diseases of Children 1943, 66, Needleman, H.L.; Riess, J.A.; Tobin, M.J.; Biesecker, G.E.; Greenhouse, J.B. Bone lead levels and delinquent behavior. Journal of the American Medical Association 1996, 275, Needleman, H.L.; McFarland, C.; Ness, R.B.; Fienberg, S.E.; Tobin, M.J. Bone lead levels in adjudicated delinquents: a case control study. Neurotoxicology and Teratology 2002, 24, Dietrich, K.N.; Ris, M.D.; Succop, P.A.; Berger, O.G.; Bornschein, R.L. Early exposure to lead and juvenile delinquency. Neurotoxicology and Teratology 2001, 23, Stretesky, P.B.; Lynch, M.J. The relationship between lead exposure and homicide. Archives of Pediatrics and Adolescent Medicine 2001, 155, Stretesky, P.B; Lynch, M.J. The relationship between lead and crime. Journal of Health and Social Behavior 2004, 45, Nevin, R. How lead exposure relates to temporal changes in IQ, violent crime, and unwed pregnancy. Environmental Research 2000, 83, Nevin, R. Understanding international crime trends: the legacy of preschool lead exposure. Environmental Research 2007, 104, Fergusson, D.M.; Boden, J.M.; Horwood, L.J. Dentine lead levels in childhood and criminal behaviour in late adolescence and early adulthood. Journal of Epidemiology and Community Health 2008, 62, Marcus, D.K.; Fulton, J.J.; Clarke, E.J. Lead and conduct problems: A meta-analysis. Journal of Clinical Child & Adolescent Psychology 2010, 39, Olympio, K.P.K.; Oliveira, P.V.; Naozuka, J.; Cardoso, M.R.A.; Marques, A.F.; Gunther, W.M.R.; Bechara, E.J.H. Surface dental enamel lead levels and antisocial behavior in Brazilian adolescents. Neurotoxicology and Teratology 2010, 32, Braun, J.M.; Froehlich, T.E.; Daniels, J.L.; Dietrich, K.N.; Hornung, R.; Auinger, P.; Lanphear, B.P. Association of environmental toxicants and conduct disorder in U.S. children: NHANES Environmental Health Perspectives 2008, 116, Wright, J.P.; Dietrich, K.N.; Ris, M.D.; Hornung, P.W.; Wessel, S.D.; Lanphear, B.P. Association of prenatal and childhood blood lead concentrations with criminal arrests in early adulthood. PLoS Medicine 2008, 5, e Laughlin, N.K., Bushnell, P.J., Bowman, R.E. Lead exposure and diet: differential effects on social development in the rhesus monkey. Neurotoxicology and Teratology 1991;13: Moore, C.F.; Gajewski, L.L.; Laughlin, N.K.; Luck, M.L.; Larson, J.A.; Schneider, M.L. Developmental lead exposure induces tactile defensiveness in Rhesus monkeys (Macaca mulatta). Environmental Health Perspectives 2008, 116, Li, W.; Han, S.; Gregg, T.R.; Kemp, F.W.; Davidow, A.L.; Louria, D.B.; Siegel, A.; Bogden, J.D. Lead exposure potentiates predatory attack behavior in the cat. Environmental Research 2003, 92, Schneider, J.S., Decamp, E. Postnatal lead poisoning impairs behavioral recovery following brain damage. Neurotoxicology 2007;28: Basha, M.R., Murali, M., Siddiqi, H.K., Ghosal, K., Siddiqi, O.K., Lashuel, H.A., Ge, Y.W., Lahiri, D.K., Zawia, N.H. Lead (Pb) exposure and its effect on APP proteolysis and Abeta aggregation. FASEB Journal 2005;19: Wu, J., Basha, M.R., Zawia, N.H. The environment, epigenetics and amyloidogenesis. Journal of Molecular Neuroscience 2008;34: Bellinger, D.C. Lead neurotoxicity and socioeconomic status: conceptual and analytical issues. Neurotoxicology 2008;29: Kim, Y.; Kim, B.N.; Hong, Y.C.; Shin, M.S.; Yoo, H.J.; Kim, J.W.; Bhang, S.Y.; Cho, S.C. Co-exposure to environmental lead and manganese affects the intelligence of school-aged children. Neurotoxicology 2009, 30, Claus Henn, B., Ettinger, A.S., Schwartz, J., Téllez-Rojo, M.M., Lamadrid-Figueroa, H., Hernández-Avila, M., Schnaas, L., Amarasiriwardena, C., Bellinger, D.C., Hu, H., Wright, R.O. Early postnatal blood manganese levels and children's neurodevelopment. Epidemiology 2010, 21, Guilarte, T.R., Toscano, C.D., McGlothan, J.L., Weaver, S.AEnvironmental enrichment reverses cognitive and molecular deficits induced by developmental lead exposure. Annals of Neurology 2003;53:50 6. Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3) 11

13 45. Rossi-George, A., Virgolini, M.B., Weston, D., Thiruchelvam, M., Cory-Slechta, D.A.Interactions of lifetime lead exposure and stress: behavioral, neurochemical and HPA axis effects. Neurotoxicology 2011;32(1): European Food Safety Authority. Scientific Opinion on lead in food. EFSA Panel on Contaminants in the Food Chain. EFSA Journal 2010; 8: Joint FAO/WHO Expert Committee on Food Additives. Summary and Conclusions, Seventy-third meeting, June ( 48. Fewtrell, L.; Kaufmann, R.; Pruss-Ustun, A. Lead: Assessing the environmental burden of disease. Environmental burden of disease series No. 2, Geneva: World Health Organization, Address David C. Bellinger Children s Hospital Boston Harvard Medical School Harvard School of Public Health david.bellinger@childrens.harvard.edu 12 Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3)

14 CADMIUM CARCINOGENESIS SOME KEY POINTS RAKOTWÓRCZOÂå KADMU KLUCZOWE ZAGADNIENIA Loreta Strumylaite 1, Kristina Mechonosina 2 1 Laboratory for Environmental Health Research, Institute for Biomedical Research Head Assoc. Prof. DSc Olegas Abdrachmanovas Director of Institute for Biomedical Research Prof. dr. hab. Arimantas Tamasauskas 2 Department of Surgery, Medical Academy, Lithuanian University of Health Sciences, Kaunas, Lithuania Rector of Lithuanian University of Health Sciences Prof. dr. hab. Remigijus Zaliunas Abstract The article presents briefly the main mechanisms of cadmium carcinogenesis and the most important sites of cancer (lung, breast, prostate, testes, kidney) induced by cadmium. In spite of some evidence showing carcinogenic potential of cadmium, further research is still required to elucidate the relative contributions of various molecular mechanisms involved in cadmium carcinogenesis. Keywords: cadmium, cancer, carcinogenesis Streszczenie Przedstawiono w skrócie g ówne mechanizmy karcinogenezy wywo anej przez kadm oraz najbardziej cz ste miejsca wyst powania nowotworu indukowanego przez kadm (p uca, piersi, prostata, jàdra, nerki). Mimo wielu dowodów wykazujàcych dzia anie karcinogenne kadmu konieczne sà dalsze badania, aby wyjaêniç wzgl dny udzia ró nych mechanizmów molekularnych bioràcych udzia w karcinogenezie wywo anej przez kadm. S owa kluczowe: kadm, nowotwory, karcinogeneza Cadmium is a toxic, nonessential, and bioaccumulating heavy metal widely used in industry as a colour pigment, in several alloys and most commonly in re-chargeable nickel-cadmium batteries. Metallic cadmium has mostly been used as an anticorrosion agent. Production, consumption and emission of this metal to the environment worldwide have increased dramatically during 20th century [1, 2]. Since cadmium is highly persistent in the environment, it affects human health both through occupational and environmental exposures. Cadmium exerts multiple toxic effects, and has been classified as a human carcinogen by the International Agency for Research on Cancer [2]. Cadmium accumulates primarily in liver and kidney where it is bound to metallothioneins, a low molecular weight metal binding proteins thought to detoxify the metal through high affinity sequestration [3]. There is evidence, that the metal may play a role in the initiation of cancer, by increasing the metastatic potential of existing cancer cells. It has been demonstrated that cadmium induces cancer by multiple 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 Cdinduced aberrant gene expression, inhibition Nades ano: Zatwierdzono do druku: Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3) 13

15 of DNA damage repair, and apoptosis [4]. Results of experimental studies have shown that depending on the dose, route and duration of exposure, cadmium can cause damage to various organs including the lung, breast, liver, kidney, bones, testes and placenta [4]. Several studies show that inhaled cadmium is a potent pulmonary carcinogen in the rats, supporting its potential as a human carcinogen. Large numbers of studies found that occupational cadmium exposure is associated with lung cancer in humans [2]. It is estimated that workers in certain occupations are exposed to cadmium at significantly higher levels than the general public. Similarly, people living in areas contaminated with cadmium are exposed to higher amounts of the metal. In this way chronic inhalation of cadmium causes pulmonary adenocarcinomas [5, 6]. There is evidence that carcinogenicity due to metals is the result of the production of the reactive oxygen species. Inhaled metals are not biodegradable. Therefore, they are deposited and remain for long periods in various areas of the pulmonary tissue. Some studies have looked at the influence of cadmium as one of environment risk factor on breast cancer. There is evidence that cadmium may have estrogenicity [7, 8]. In vivo and in vitro studies show cadmium acting like an estradiol activating estrogens receptor a through a high-affinity interaction with the hormone binding domain of the receptor. Regulation of expression and activity of estrogens receptors plays an essential role in the growth, differentiation and prognosis of human breast cancer. Some studies reported that cadmium exposure increased uterine weight, induced the expression of progesterone receptor, increased the proliferation of the endometrium and promoted growth and development of the mammary glands increasing the formation of side branches and alveolar buds as well as the production of casein and whey acidic protein in mice [9]. Greater concentration of cadmium was determined in urine, blood, and breast tissue of breast cancer patients than in controls [10, 11]. Epidemiological study revealed twice as high risk of breast cancer in women with creatinine-adjusted urine cadmium 0.58 µg/g compare to those with cadmium *0.26 µg/g [12]. Cadmium exposure has also been linked to human prostate cancer [1]. Cadmium relation between cancer of the prostate or testes in humans is unclear in spite of suggestive results in rats. Parenteral administration or oral exposure to cadmium resulted in proliferative lesions or tumours of the prostate and testes in rats. The pathogenesis of cadmiuminduced prostate cancer involved the effect of cadmium on the testes manifested by a positive dose response with low doses of cadmium but not with high doses. High doses of cadmium produced testicular degeneration reducing testosterone production. Cadmium induced testicular hemorrhagic necrosis in rat testes if it was given parenterally, oral cadmium exposure resulted in testes tumours [2, 13, 14]. Recent studies suggest that cadmium may be a cause of renal cancer. It accumulates in kidney cells, particularly those of the proximal tubular epithelium, and the damage caused is associated with development of chronic kidney disease, characterized by proximal tubular necrosis and proteinuria. Some epidemiologic studies showed positive associations between occupational exposure to cadmium and the risk of renal cancer [13, 15, 16]. Other target sites for cadmium carcinogenesis in humans (liver, stomach) are still investigated [4]. In conclusion, large results of studies show carcinogenic potential of cadmium to experimental animals and human beings. However, further research is still required to elucidate relative contributions of various molecular mechanisms involved in cadmium carcinogenesis. References 1. Jarup L.: Hazards of heavy metal contamination. British Med Bull 2003; 68: International Agency for Research on Cancer (IARC). IARC Monographs on Monographs on the evaluation of carcinogenic risks to humans. IARC, Lyon, 1993: Waalkes M.P.: Cadmium carcinogenesis in review. J Inorg Bioch 2000; 79: Joseph P.: Mechanisms of cadmium carcinogenesis. Toxicol Appl Pharmacol 2009; 38: Satarug S., Baker J.R., Urbenjapol S., et al.: Global perspective on cadmium pollution and toxicity in non-occupationally exposed population. Toxicol Lett 2003; 137: Klaassen C.D., Liu J., Choudhuri S.: Metallothionein: an intracellular protein to protect against cadmium toxicity. Ann Rev Pharmacol Toxicol 1999; 39: Pearson C.A., Prosealeck W.C.: E cadherin, B catenin and cadmium carcinogenesis. Medical Hypothesis 2001; 56(5): Stoica A., Katzenellenbogen B.S., Martin M.B.: Activation of estrogen receptor-alpha by the heavy metal cadmium. Mol Endocrinol 2000; 14: Johnson M.D., Kenney N., Stoica A.: Cadmium mimics the in vivo effects of estrogen in the uterus and mammary gland. Nat Med 2003; 9: Strumylaite L., Bogusevicius A., Ryselis S., et al.: Association between cadmium and breast cancer. Medicina (Kaunas) 2008; 44: Strumylaite L., Bogusevicius A., Abrachmanovas O., et al.: Cadmium concentration in biological media of breast cancer patients. Breast cancer Res Treat 2011; 125: McElroy J.A., Shafer M.M., Trentham-Dietz A.: Cadmium exposure and breast cancer risk. J Natl Cancer Inst 2006; 98: Goyer R.A., Liu J., Waalkes M.P.: Cadmium and cancer of prostate and testis. BioMetals 2004; 17: Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3)

16 14. Achanzar W.E., Webber M.W., Waalkes M.P.: Altered apoptotic gene expression and acquired apoptotic resistance in cadmium transformed human epithelial cells. The Prostate 2002; 52: Curti B.D.: Renal cell carcinoma. JAMA 2004; 292: Hu J., Mao Y., White K.: Renal cell carcinoma and occupational exposure to chemicals in Canada. Occup Med 2002; 52: Address Dr Loreta Strumylaite Institute for Biomedical Research Medical Academy Lithuanian University of Health Sciences Eiveniu 4 LT Kaunas Lithuania loreta.strumylaite@med.kmu.lt Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3) 15

17 16 Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3)

18 PRACE ORYGINANE ORIGINAL PAPERS OKREÂLENIE PRZYDATNOÂCI TRZECH ODMIAN URAWKI (Heuchera cvs.) DO BIOREMEDIACJI KADMU (Cd), O OWIU (Pb) I CYNKU (Zn) Z TERENÓW POGÓRNICZYCH ZAG BIA DÑBROWSKIEGO SUITABILITY OF THREE CULTIVARS OF CORAL BELLS (Heuchera cvs.) TO BIOREMEDIATION OF CADMIUM (Cd), LEAD (Pb) AND ZINC (Zn) FROM POST-MINING AREA IN ZAG BIE DÑBROWSKIE Gabriela Sàkol 1, Patryk Ochota 2, Janusz Miros awski 3, Piotr Z. Brewczyƒski 1 1 Zak ad SzkodliwoÊci Biologicznych i Immunoalergologii Instytutu Medycyny Pracy i Zdrowia Ârodowiskowego, Kierownik Zak adu, Dyrektor Instytutu: dr n. med. Piotr Z. Brewczyƒski 2 Zak ad SzkodliwoÊci Chemicznych i Toksykologii Genetycznej Instytutu Medycyny Pracy i Zdrowia Ârodowiskowego, Kierownik Zak adu: dr hab. n. med. Andrzej Sobczak, Dyrektor Instytutu: dr n. med. Piotr Z. Brewczyƒski 3 Katedra i Zak ad Toksykologii, Wydzia Farmaceutyczny z Oddzia em Medycyny Laboratoryjnej, Âlàski Uniwersytet Medyczny, Kierownik Katedry i Zak adu: dr hab. Danuta Wierchu a, Dziekan Wydzia u: dr hab. n. farm. Stanis aw Boryczka Streszczenie Wst p: Wieloletnia p ytka eksploatacja w gla kamiennego w rejonie B dzina w Zag biu Dàbrowskim doprowadzi a do degradacji Êrodowiska. Profile gleb zosta y przemieszczone i zanieczyszczone ponadnormatywnie metalami ci kimi. Poniewa jest to region silnie zaludniony, ryzyko nara enia na szkodliwe dzia anie metali ci kich dotyczy du ej populacji osób. Przyspieszenie oczyszczania gruntów terenów pogórniczych mo na uzyskaç wykorzystujàc roêliny, które nie tylko tolerujà podwy szone iloêci tych metali ale potrafià je te gromadziç wswoich organach. Materia i metody: Przedmiotem badaƒ by y trzy kultywary urawki: Chatterbox, Purple Petticoats i Strawberry Swirl, uprawiane na terenie pogórniczym i na poletku kontrolnym w sezonie wegetacyjnym 2010 roku. ZawartoÊç pierwiastków metalicznych (Cd, Pb, Zn) oznaczono metodà absorpcyjnej spektrometrii atomowej (A- AS) przy u yciu spektrometru PU 9100 firmy Philips i Perkin ELMER 4100ZL. Wyniki: Wyniki przeprowadzonych badaƒ gleb na obecnoêç form ca kowitych i wyekstrahowanych 1M HCl kadmu (Cd), o owiu (Pb) i cynku (Zn) pokazujà, e zanieczyszczenie terenu pogórniczego jest nadal wysokie. ZawartoÊci form dost pnych dla roêlin w glebie poletka do- Êwiadczalnego, które wynoszà: kadm 1,92 mg kg 11, o ów 56,3 mg kg 11, cynk 153,7 mg kg 11, sà od 2 do 4 razy wi ksze ni zawartoêç naturalna w glebach o odczynie oboj tnym (ph 6,5), którym charakteryzuje si wi kszoêç gleb badanego terenu. Wybrane do badaƒ odmiany urawek: Chatterbox, Purple Petticoats i Strawberry Swirl pobra y znaczàce iloêci kadmu, o owiu i cynku. Wnioski: RoÊliny z terenu pogórniczego uprawiane wwarunkach nara enia na istotnie wy sze st enia metali (p 0,01), nie wykazywa y widocznej reakcji toksycznej na cz Êci nadziemne mimo, e gromadzi y kadm, o ów i cynk zarówno w korzeniach, jak i liêciach. Ró nice odmianowe stwierdzono na poziomie istotnoêci p 0,05. Odmianà, która przemieszcza a w swoim organizmie z korzeni do liêci najwy sze iloêci o owiu by a Palace Purple. Dwie pozosta e odmiany: Chatterbox i Strawberry Swirl gromadzi y metale w wi kszym stopniu w korzeniach wed ug zale noêci Cd Zn Pb. S owa kluczowe: teren pogórniczy, metale ci kie, bioakumulacja, urawki Nades ano: Zatwierdzono do druku: Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3) 17

19 Abstract Background: Long-term shallow exploitation of pitcoal in B dzin area (in mining district Zag bie Dàbrowskie) has degraded the environment. Profiles of soil were dislocated and contaminated with heavy metals above permissible standards. Due to the fact that Zag bie Dàbrowskie is densely populated, risk of harmful exposure to heavy metals affects high number of people. Decontamination of post-mining grounds is possible with planting plants which not only tolerate elevated heavy metals quantities but can also accumulate them in plant tissues. Materials and methods: The cultivars Chatterbox and Strawberry Swirl and Palace Purple of coral bells (Heuchera cvs.) were chosen to do the research. Cadmium, lead and zinc uptake in plants growing in contaminated and control fields was evaluated. Amount of heavy metals was determined by atomic absorption spectrometry (AAS). Results: Content of metals detected in plants in postmining soil was respectively: Cd 1,92 mg kg 11, Pb 56,3 mg kg 11, Zn 153,7 mg kg 11. Those metals value is from 2 to 4 times higher than natural content in neutral soil of ph 6,5 a typical ph in this region. The examined cultivars of coral bells accumulated significant amount of Cd, Pb, Zn even if concentration of those metals was low, what is characteristic for clean regions of Poland. Conclusions: The plants cultivated on contaminated soil of post-mining region didn`t show toxic response (damaged leaves) even though they accumulated cadmium, lead and zinc in their roots and leaves. Cultivars differences of coral bells found on significance level (p 0,05). The cultivar Palace Purple has transported the highest amount of lead from roots to leaves. Other cultivars Chatterbox and Strawberry Swirl have accumulated higher amounts of metals in their roots in a sequence Cd Zn Pb. Key words: post-mining region, heavy metals, bioaccumulation, Heuchera cvs. Wst p Wraz z rozwojem cywilizacyjnym zwi ksza si wp yw czynników antropogenicznych na naturalne Êrodowisko przyrodnicze. Teren zdegradowany, w potocznym zrozumieniu, obejmuje gleby, grunty iwody zmienione lub zniszczone przez dzia alnoêç przemys owà. Degradacja mo e byç skutkiem wieloletniej i wielorakiej dzia alnoêci cz owieka takiej jak eksploatacja kopalin, przetwarzanie surowców, sk adowanie odpadów przemys owych. Za zdegradowane uznaje si te tereny, które sà nieprzydatne do okreêlonego sposobu zagospodarowania bez wykonania dzia aƒ rekultywacyjnych. Czynniki szkodliwe wyst pujàce w Êrodowisku zdegradowanym oddzia owujà negatywnie na zdrowie cz owieka. Po udniowo-zachodnia cz Êç Polski obfituje w z o a surowców. Z o a w gla kamiennego w Zag biu Dàbrowskim sà eksploatowane od przesz o 250 lat. Skutkiem trwajàcej dziesi ciolecia emisji ogromnych iloêci zanieczyszczeƒ, spowodowanych wydobyciem i przetwórstwem surowców mineralnych (w gle, rudy metali) w skoncentrowanych tu zak adach przemys owych, jest m.in. ponad normatywne zanieczyszczenie gleb. Równie geomechaniczne przekszta cenia powodujà wad u ytkowà gruntów. Gleby na terenach pogórniczych charakteryzujà si, oprócz nienaturalnych wynios oêci i zapadlisk z przemieszanymi profilami glebowymi, zaburzonym sk adem granulometrycznym i wysokimi, cz sto ponadnormatywnymi zawartoêciami pierwiastków Êladowych. IloÊç fitodost pnych form zanieczyszczeƒ, g ównie metali ci kich oraz zakwaszenie wp ywa na obni enie ich wartoêci u ytkowej. Metale sà naturalnym komponentem gleb, a w Êladowych iloêciach stanowià niezb dne dla ro- Êlin mikroelementy. Metale ci kie to pierwiastki zdefiniowane jako posiadajàce okreêlone w aêciwo- Êci (metaliczne) i g stoêç w aêciwà wi kszà ni 4,5 g cm 13. Zagro enie dla cz owieka metalami ci kimi polega g ównie na wchodzeniu ich do wy szych ogniw aƒcucha pokarmowego. Szczególnie niebezpieczne dla organizmów ywych sà kadm (Cd), o ów (Pb), rt ç (Hg), chrom (Cr), miedê (Cu), nikiel (Ni), cynk (Zn) i arsen (As). Nadmiarowe zawartoêci fitodost pnych form metali toksycznych w glebie sà ich êród em w nast pnych ogniwach. Dlatego zanieczyszczenie metalami stanowi wspó czeênie jeden z najwa niejszych problemów Êrodowiskowych. Realizacja polityki zrównowa onego rozwoju wymaga eliminacji i przeciwdzia ania negatywnym skutkom procesów niszczàcych grunty i gleby [1]. Prawo ochrony Êrodowiska i Ustawa o ochronie gruntów rolnych i leênych nakazujà popraw warto- Êci u ytkowej gruntów m.in. przez zapobieganie procesom degradacji i dewastacji gruntów, rekultywacj i zagospodarowaniu ich na cele rolnicze i leêne. Rekultywacja ma na celu umo liwienie wykorzystania i u ytkowania terenu (np. zmiana terenów przemys owych i pogórniczych na tereny budownictwa mieszkaniowego). Celem rekultywacji biologicznej jest przywrócenie walorów produkcyjnych lub innych walorów u ytkowych terenom zniszczonym wskutek dzia alnoêci antropogenicznej. Obejmuje ona ró norodne zabiegi o charakterze agrotechnicznym, w tym fitoremediacj. Rola roêlin w rekultywacji gruntów jest nie do przecenienia: rozbudowanym systemem korzeniowym chronià 18 Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3)

20 gleb przed erozjà a dzi ki fotosyntezie zwi kszajà swojà biomas, jednoczeênie u yêniajàc pod o e. Jednym z problemów niskobud etowego zagospodarowania terenów pogórniczych dla celów zieleni miejskiej jest wybór roêlin, które, tolerujàc obecnoêç zanieczyszczeƒ, spe ni yby funkcje estetyczne [2 4]. Dotychczas opublikowano niewiele prac o roêlinach ozdobnych, które zastosowane do aran acji zieleni miejskiej, jednoczeênie oczyszcza yby gleb Êrednio zanieczyszczonà metalami toksycznymi i by y dekoracyjne przez ca y sezon wegetacyjny [5, 6]. Byliny ozdobne tzw. zadarniajàce ograniczajà ponadto erozj eolicznà i pluwialnà powierzchni gruntów, przez co zmniejszajà reemisj metali do atmosfery. urawka (Heuchera cvs.) jest ozdobnà, zimozielonà bylinà, która mo e byç stosowana jako roêlina rabatowa lub okrywowa na wi kszych powierzchniach [7]. Przeprowadzone badania mia y na celu sprawdzenie czy urawka mo e spe niaç rol bioakumulatora, przyczyniajàc si do dekontaminacji terenów pogórniczych o Êrednim stopniu zanieczyszczenia metalami ci kimi. Materia i metody Dost pne dane o tolerancji roêlin na fitotoksyczne st enia metali ci kich stanowià cz sto rezultat badaƒ prowadzonych w warunkach kontrolowanych w doêwiadczeniach wazonowych lub laboratoryjnych przy wzroêcie roêlin w roztworach po ywek. Tym samym nie w pe ni odzwierciedlajà Êrodowiskowà ró norodnoêç i zmiennoêç warunków polowych, co zmniejsza ich wiarygodnoêç. Eksperyment przeprowadzono w warunkach polowych. Wszystkie próbki pobrano po zakoƒczeniu eksperymentu. Miejsce doêwiadczenia Teren pogórniczy Aglomeracja Êlàsko-dàbrowska jest w skali kraju najbardziej uprzemys owionym i zurbanizowanym regionem, a jednoczeênie regionem o najbardziej zdegradowanym Êrodowisku. Zag bie Dàbrowskie jest cz Êcià wschodnià tego regionu (ryc. 1). Zajmuje obszar oko o 1800 km 2. Sà to w ca oêci tereny pogórnicze, o ró nym stopniu przekszta ceƒ geomechanicznych. Rycina 1. Schemat lokalizacji W glowego Zag bia Dàbrowskiego w GórnoÊlàskiej Niecce W glowej i w Polsce. Po o enie badanego terenu pogórniczego: d ugoêci geograficznej wschodniej, szerokoêci geograficznej pó nocnej. Figure 1. Location of Dàbrowski Mining Region in Upper Mining Basin and in Poland. Location of post mining site of east longitude, north latitude. Medycyna Ârodowiskowa / Environmental Medicine 2011; 14 (3) 19