Introduction
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Introduction
La part de l’environnement est substantielle dans la genèse des cancers. Et parmi les différents facteurs environnementaux qui contribuent à l’augmentation du nombre de cas de cancers diagnostiqués, les facteurs professionnels ont un rôle important.
La survenue des cancers professionnels dépend de nombreux facteurs. Les cancérogènes peuvent être des produits chimiques, mais aussi des agents biologiques, physiques,…
En effet, environ la moitié des agents chimiques et physiques, composés et procédés industriels actuellement classés cancérogènes pour l’Homme par le Centre International de Recherche sur le Cancer (CIRC), sont présents dans l’environnement professionnel.
Ainsi, les risques cancérogènes pourraient en grande partie être prévenus sur les lieux de travail par une élimination des substances les plus nocives et par une diminution des niveaux d’exposition grâce à l’amélioration des protections collectives et individuelles.
De plus, la faible proportion de cancers professionnels indemnisés résulte de l’absence de déclaration. Celle-ci est due en partie à un manque de sensibilisation des médecins qui souvent n’interrogent pas les patients sur leur passé professionnel, et à une information insuffisante des travailleurs eux-mêmes.
De fait, en raison du long délai entre l’exposition et le diagnostic du cancer (en général au moins 10 ans et jusqu’à plus de 40 ans), les cancers professionnels sont souvent diagnostiqués longtemps après cessation de l’activité professionnelle en cause.
Les organes les plus fréquemment concernés sont les voies respiratoires à cause de leur contact direct avec la substance cancérogène. Les autres cancers fréquemment associés à des expositions professionnelles sont les leucémies, les cancers de la vessie et de la peau. L’Institut national de recherche et sécurité (INRS) en France estime qu’environ 15 % des cancers du poumon, 10 % des cancers de la vessie, de la peau et des leucémies et 50 % des cancers du nez et des sinus de la face sont d’origine professionnelle. Ces proportions sont plus faibles chez les femmes, moins souvent exposées.
Le présent dossier propose une compilation de sources documentaires traitant de ce type de cancer :
- Ouvrages sous format papier ;
- E-Books ;
- Articles scientifiques ;
- Rapports scientifiques ;
- Brochures, Dépliants ;
- Liens utiles (associations, centres de recherche spécialisés….)
La recherche documentaire a été effectuée dans des bases de données scientifiques telles que ScienceDirect et Scopus.
Références générales
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Références générales
Les cancers professionnels (Tome 1)
Monographie
K. Pairon, P. Brochard, J-P. Le Bourgeois, P. Ruffié
Editeur : Ed. Margaux Orange, Paris, 2000
ISBN : 2-914206-02-X
Cote : 616.994/PAI
Disponible à la bibliothèque de l’IMIST
Les cancers professionnels (Tome 2)
Monographie
K. Pairon, P. Brochard, J-P. Le Bourgeois, P. Ruffié
Editeur : Ed. Margaux Orange, Paris, 2001
ISBN : 2-914206-03-8
Cote : 616.994/BOU
Disponible à la bibliothèque de l’IMIST
Atlas of occupational health and disease
Monographie
N. R. Williams, J. Harrison
Editeur: Arnold, London, 2004
ISBN: 0340740698
Cote: 616.9/WIL
Disponible à la bibliothèque de l’IMIST
Questions prioritaires en matière de recherche sur le cancer d’origine professionnelle : points de vue des intervenants en Ontario
Article
K. Hohenadel, M. Sc. (1); E. Pichora, M. Sc. (2); L. Marrett, Ph. D. (1,2,3); D. Bukvic, M.P.H. (1); J. Brown, M.S.O.D. (1); S. A. Harris, Ph. D. (1,2,3); P. A. Demers, Ph. D. (1,2,3); A. Blair, Ph. D. (1)
Journal : Maladies chroniques et blessures au Canada, vol. 31, n°4, septembre 2011 –
Résumé :
Introduction : En milieu de travail, les travailleurs peuvent être exposés à des agents
cancérogènes connus ou présumés, dont bon nombre n’ont pas fait l’objet d’une évaluation complète. La recherche sur le cancer d’origine professionnelle a connu une baisse au cours des dernières décennies, et ce, même si les besoins demeurent constants. Le Centre de recherche sur le cancer professionnel (CRCP) a été créé en vue de contrer cette tendance à la baisse en Ontario. Le CRCP a mené une enquête auprès de l’ensemble des intervenants pour connaître les questions prioritaires en matière de recherche sur le cancer d’origine professionnelle.
Méthodologie : Dans le cadre de l’enquête, le CRCP a reçu 177 réponses provenant d’intervenants du milieu universitaire, du milieu de la santé et de l’industrie, d’intervenants affiliés à des syndicats et de responsables des politiques. Les réponses ont été analysées en fonction de l’exposition en milieu de travail, des emplois à risque et du siège de cancer, et elles ont été stratifiées selon le poste occupé.
Résultats : Les questions prioritaires soulevées comprennent diverses catégories d’exposition en milieu de travail, notamment les catégories « produits chimiques », « particules et fibres inhalables » (p. ex. amiante), « rayonnements » (p. ex. champs électromagnétiques), « pesticides » et « travail par quarts », ainsi que divers types d’emplois, en particulier les mineurs, les travailleurs de la construction et les travailleurs de la santé. Un financement inadéquat et des données insuffisantes sur l’exposition ont été définis comme les principaux obstacles à la recherche sur le cancer d’origine professionnelle.
Discussion : Les résultats de cette enquête font ressortir le besoin criant de recherche sur le cancer d’origine professionnelle en Ontario et ailleurs. Ces données seront très utiles pour l’élaboration du programme de recherche du CRCP
The burden of cancer at work: estimation as the first step to prevention.
Article
Rushton L, Hutchings S, Brown T.
Occup Environ Med. 2008 Dec;65(12):789-800. Epub 2007 Dec 13.
Résumé:
Objectives: Work-related cancers are largely preventable. The overall aim of this project is to estimate the current burden of cancer in Great Britain attributable to occupational factors, and identify carcinogenic agents, industries and occupations for targeting risk prevention.
Methods: Attributable fractions and numbers were estimated for mortality and incidence for bladder, lung, non-melanoma skin, and sinonasal cancers, leukaemia and mesothelioma for agents and occupations classified as International Agency for Research on Cancer (IARC) Group 1 and 2A carcinogens with "strong" or "suggestive" evidence for carcinogenicity at the specific cancer site in humans. Risk estimates were obtained from published literature and national data sources used for estimating proportions exposed.
Results: In 2004, 78,237 men and 71,666 women died from cancer in Great Britain. Of these, 7317 (4.9%) deaths (men: 6259 (8%); women: 1058 (1.5%)) were estimated to be attributable to work-related carcinogens for the six cancers assessed. Incidence estimates were 13,338 (4.0%) registrations (men: 11,284 (6.7%); women 2054 (1.2%)). Asbestos contributed over half the occupational attributable deaths, followed by silica, diesel engine exhaust, radon, work as a painter, mineral oils in metal workers and in the printing industry, environmental tobacco smoke (non-smokers), work as a welder and dioxins. Occupational exposure to solar radiation, mineral oils and coal tars/pitches contributed 2557, 1867 and 550 skin cancer registrations, respectively. Industries/occupations with large numbers of deaths and/or registrations include construction, metal working, personal and household services, mining (not metals), land transport and services allied to transport, roofing, road repair/construction, printing, farming, the Armed Forces, some other service industry sectors and manufacture of transport equipment, fabricated metal products, machinery, non-ferrous metals and metal products, and chemicals.
Conclusion: Estimates for all but leukaemia are greater than those currently used in UK health and safety strategy planning and contrast with small numbers (200-240 annually) from occupational accidents. Sources of uncertainty in the estimates arise principally from approximate data and methodological issues. On balance, the estimates are likely to be a conservative estimate of the true risk. Long latency means that past high exposures will continue to give substantial numbers in the near future. Although levels of many exposures have reduced, recent measurements of others, such as wood dust and respirable quartz, show continuing high levels.
Cancer in Africa
Rapport
American Cancer Society, International Agency for Research on Cancer, 2011
Document en ligne
Cancers d’origine professionnelle : quelle reconnaissance en Europe ?
Rapport d’enquête
EUROGIP, Avril 2010
Document en ligne
http://www.eurogip.fr/fr/docs/EUROGIP_RapportRecoCancerspro_49F.pdf
Plan national de prévention et de contrôle du cancer 2010-2019
Rapport du plan d’action
ALSC (Association Lalla Salma de lutte contre le cancer), 2010
Document en ligne
http://www.contrelecancer.ma/site_media/uploaded_files/Synthese_PNPCC_2010-1019.pdf
اتفاقية بشأن الوقاية و السيطرة على الأخطار المهنية الناتجة عن المواد و العوامل المسببة للسرطان
اتفاقية
المؤلف: منظمة العمل الدولية
سنة الإصدار: 1989
http://www1.umn.edu/humanrts/arabic/ilo-c139.pdf :رابط الإصدار
الحماية من السرطان المهني
كتاب
المؤلف: خطيب، عبد الرزاق
الناشر: منظمة العمل العربية، المعهد العربي للثقافة العمالية وبحوث العمل،,
سنة الإصدار: 1979
غير متوفر في المكتبة
السرطان المهنى
كتاب
المؤلف: جاسم كاظم العجزان
الناشر: الحسينى للكمبيوتر و نظم المعلومات
سنة الإصدار: 1988
غير متوفر في المكتبة
الملخص: يعالج الكتاب تأثير عدد من المواد الكيماوية على صحة الأشخاص المعرضين لهذه المواد التي تكون سببا في أحداث أو احتمال إحداث سرطانات مختلفة في أجسام هؤلاء الأشخاص بحكم عملهم في تنجيمها أو تصنيعها.
وقد صنف المؤلف هذه المسرطنات إلى صنفين، وقسم كل صنف إلى ثلاث مجموعات وفيما يلي كل صنف ومجموعاته:
1 -الصنف الأول:
المجموعة الأولي(أ): المواد الكيماوية المسرطنة أو الطرق التي أثبتت كونها مسرطنة.
المجموعة الثانية(ب):المواد الكيماوية التي يحتمل أن تكون مسرطنة.
المجموعة الثالثة(جـ):المواد الكيماوية التي يشك في كونها مسرطنة.
2 -الصنف الثاني:
المواد الكيماوية العلاجية التي أثبتت كونها مسرطنة أو يعتقد أو يشك بكونها مسرطنة للجنس البشري.
)أ)المجموعة الأولى: وتشمل المواد التي أثبتت كونها مسرطنة للجنس البشري ومنها الميلفالان
(ب)المجموعة الثانية: وتشمل المواد التي يعتقد بكونها مسرطنة للجنس البشري ومنها السايكوفوسفاميد ودكستران الحديد.
(جـ)المجموعة الثالثة: وتشمل المواد التي يشك في كونها مسرطنة للجنس البشري ومنها الكلورأمفينيكول المستعمل لعلاج التهاب المجاري البولية، والأيزوينازيد المستعمل في علاج التدرن الرئوي.
ويختتم الكتاب بتعليمات صحية مهنية عن كيفية تداول المواد الكيماوية المسرطنة، ثم سرد لمواد اتفاقية السرطان المهني رقم (139) لعام 1974.
الموجز الارشادى عن الطب المهنى
كتاب
المؤلف: هـ ا غالب والدرون
الناشر: المركز العربى لتوزيع المطبوعات
سنة الإصدار: 1988
غير متوفر في المكتبة
الملخص: هذا الكتاب من إصدارات المركز العربي للوثائق والمطبوعات الصحية - مجلس وزراء الصحة العرب - جامعة الدول العربية ، كما أنه من سلسلة الموجزات الإرشادية المترجمة عن الكتاب الأصلي Lecture Notes on Occupational Medicine للناشر العالمي "بلاكويل: Blackwell".
ويقع الكتاب في أربعة عشر فصل بالإضافة إلى ملحق في آخر الكتاب شمل جداول تبين قيم الحدود الآمنة لتعرض الجسم لكثير من المواد الكيميائية المستعملة في الصناعات المختلفة مرتبة ترتيبا ألفبائيا.
وفي نهاية الكتاب مسرد للمصطلحات الطبية الأجنبية مترجم إلى اللغة العربية مرتب ترتيبا أبجديا.
ويشرح الفصل الأول التأثيرات المهنية على الصحة العامة ويحتوي على جداول تبين نسب الوفيات بين المجموعات المهنية وبين طبقات المجتمع بالإضافة إلى جداول أخرى تبين ارتباط نسب الوفيات وبعض المجموعات المهنية بسبب التهاب القصبات وكذلك عدد الأيام المفقودة بسبب المرض للرجال حسب الأعمار من خلال الشهادات المرضية .
والفصل الثاني مخصص للسموم الصناعية بما فيها المعادن كالرصاص والزئبق والكادميوم والبريليوم والمنجنيز والفسفور وغيرها، كما يشرح طرق استخدامات هذه المعادن ومخاطرها وكيفية التسمم بها والتأثيرات السامة على الجلد والعينين والجهاز الهضمي والمسالك البولية الأعضاء التناسلية بما في ذلك الأورام كسرطان ا لبروستاتة.
ويتابع الفصل الثالث السموم الصناعية بشرح للمذيبات العضوية كالبنزين والتولوين والزايلين و الهيدروكربونات المكلورة أمثال رابع كلوريد الكاربون وثلاثي كلورو الإيثان وثلاثي كلورو الإيثيلين وغيرها وكذلك المذيبات الأخرى كالأسيتون و الجليكولات ومشتقاتها والديوكسان والكحول الصناعي الأبيض كما يشرح طرق استخدامات هذه المذيبات ومخاطرها وكيفية التسمم بها والتأثيرات السامة على الأنف والعينين والجلد والجهاز الهضمي والمسالك البولية . . .الخ.
ويتابع الفصل الرابع وصف السموم الصناعية بشرح لتأثيرات المركبات العضوية أمثال كلوريد الفينيل والمبيدات الحشرية والمبيدات العشبية والمركبات العضوية الأخرى كمثيل البروميد المستخدم مع كلوريد الكربون في إطفاء الحرائق كمبيد حشري وثلاثي أورثوكريزيل الفسفات المستخدم في صناعة البلاستيك والراتنجات المستخدمة بكثرة في الصناعة كمكونات للبويات والورنيش وكمواد لاصقة في أعمال.
المشابك والقوالب، كما يشرح بعض مواد التخدير المستخدمة في غرف العمليات كأكسيد النيتروز والهالوثان وتأثيراتها على الأطباء والممرضات وكذلك تأثيرات الأدوية على القائمين بإنتاجها أو تداولها كالهرمونات الصناعية والمضادات الحيوية.
ويشرح الفصل الخامس السموم الصناعية ويختص بالغازات السامة ومنها الخانقة البسيطة كالنتروجين والميثان وثاني أكسيد الكربون، والخانقة الكيميائية كأول أكسيد الكربون وكريونيل النيكل وكبريتيد وسيانيد الهيدروجين والأرسين وغيرها، وتأثيراتها السامة على الجسم خصوصا في الأماكن المغلقة، والغازات المهيجة كالأمونيا وثاني أكسيد الكبريت و الكلورين والفوسجين كلوريد الكاريونيل والفلورين ومركباته، وتأثيراتها على الجسم وطرق استخداماتها في الصناعة كالأمونيا وفي المنازل كغاز الكلورين وفي الحروب كالفوسجين الذي استخدم في الحرب العالمية الأولى، وطرق العلاج لكل منها.
ويشرح الفصل السادس الأمراض الرئوية المهنية كالربو المهني والتغبر الرئوي Pneumoconiosis و السحار السيليسي Silicosis وداء الأسبست وغيرها وأعراضها والعلامات المرضية والمظاهر الشعاعية وطرق العلاج ومآل كل مرض.
ويشرح الفصل السابع الأمراض الجلدية المهنية ومسبباتها وأعراضها وطرق علاجها.أما الفصل الثامن فيشرح السرطان المهني وأسبابه وأنواع السرطانات المهنية وطرق الوقاية منها.
ويصف الفصل التاسع بعض المخاطر الطبيعية الناجمة من المهنة كداء الغوص بين الغواصين ورأرأة العينين بين عمال المناجم وتأثيرات الإشعاعات المؤينة لدى العاملين في هذا المجال في الصناعة وفي المستشفيات والوقاية منها، والإجهاد السمعي للعمال المعرضين للضوضاء الصناعية كعمال مطابع الصحف وآلات الطحن وآلات النسيج وعمال تحميل الطائرات النفاثة على الأرض وغيرهم.ويصف كذلك متلازمة داء المباني ومن أعراضها الصداع وتهيج العينين والأنف وآلام المفاصل والتي تصيب العاملين أو سكان المباني الشاهقة المكيفة الهواء.
ويشرح الفصل العاشر الأمراض المعدية الناجمة عن مزاولة بعض المهن الطبية والبيطرية، وكذلك يشرح الأخماج الأخرى التي قد تصيب ممارسي بعض المهن كمتداولي اللحوم والجلود الخام والصوف أو منتجات الحيوان كالمزارعين والأطباء البيطريين وغيرهم.
ويشرح الفصل الحادي عشر أخطار الحوادث والرضح في بعض المهن وأسباب حدوثها وكيفية تلافيها، ويشرح الفصل الثاني عشر كيفية التحكم في المخاطر المهنية، كالمعايرة الفيزيائية وتحديد قيم الحدود الآمنة والمعايرة البيولوجية كتعيين حدود الأمان البيولوجية والتحكم المركزي على المصانع والمزارع والمناجم وغيرها.
ويشرح الفصل الثالث عشر تأثير صحة العاملين في المجالات المختلفة على أعمالهم ومنها الصرع والداء السكري الاضطرابات النفسية وكذلك الكحولية وتوفير سجلات للعاملين لسهولة متابعة أحوالهم الصحية.
ويصف الفصل الرابع عشر الخدمات الصحية المهنية التي توفرها بعض المؤسسات لعمالها كتوفير خدمات التأهيل الطبي و العلاج الطبيعي وخدمات المختبر وخدمات الفحص بالأشعة السينية كما تقدم خدمات علاج الأسنان والخدمات المساعدة مجانا أو لقاء أجور مخفضة.
وفي نهاية الفصل وصف للتطورات الحاصلة في المستقبل والتي من شأنها تلافي أخطار المهنة على الصحة العامة للعاملين والمهنيين الممارسين على السواء.
Détection des cancers d’origine professionnelle : quelques clés pour agir
Brochure
Institut National du Cancer – France-, Octobre 2006
Document en ligne
Cancers professionnels : des clés pour agir
Brochure
Association pour la Recherche sur le Cancer (ARC) ; Association des accidentés de la vie (FNATH)
Document en ligne
Agir aujourd’hui pour éviter les cancers professionnels de demain
Brochure
Institut National de Recherche et de Sécurité pour la Prévention des Accidents de Travail et des Maladies Professionnelles, Octobre 2012
Document en ligne
http://www.inrs.fr/accueil/produits/mediatheque/doc/publications.html?refINRS=ED%20992
Références par substances cancérogènes
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Références par substances cancérogènes
Liste des principales substances cancérogènes et leurs cancers respectifs [1]
Substances cancérogènes Principaux cancers concernés Amiante poumon, plèvre (mésothéliome) Amines aromatiques vessie Arsenic poumon, peau, foie Benzène leucémies Bischlorométhylether poumon Cadmium (fumées et poussières) poumon Chlorure de vinyle foie Chrome (certains composés) poumon, nez et sinus Goudrons, huiles, brais de houille suies de combustion du charbon peau, poumon, vessie Huiles minérales peau Nickel (grillage des mattes) poumon, nez et sinus Nitrosoguanidines cerveau (glioblastome) Nitrosourées cerveau (glioblastome) Oxyde de fer (fumées et poussières) poumon Poussières de bois nez et sinus Rayonnements ionisants leucémies, poumon, peau, os Silice poumon
Les références citées ci-dessous sont classées par substances cancérogènes. Amiante
-
Amiante
L’amiante est une substance cancérogène avéré pour l’homme pour le poumon, la plèvre (mésothéliome), le larynx et les ovaires, toutes les variétés d’amiante étant classées cancérogènes.
L’exposition professionnelle à l’amiante persiste pour certains professionnels du bâtiment lors de travaux de démolition, de désamiantage, d’entretien et de maintenance des bâtiments (notamment si les repérages préalables de l’amiante sont absents ou inadaptés). Les populations avoisinantes peuvent également être exposées.
Références bibliographiques
Les manifestations respiratoires de l’exposition à l’amiante
Thèse
M. Kandil
Editeur: Université Mohammed V, Faculté de Médicine et de Pharmacie, 2001
Disponible à la bibliothèque de l’IMIST
Rare thoracic cancers, including peritoneum mesothelioma
Article
On behalf of the RARECARE working group --- Siesling, S. --- Zwan, J.M.v.d. ---Izarzugaza, I. --- et al.
Journal: European Journal of Cancer ISSN: 09598049 Year: 2012
Fournis par: Elsevier
Résumé: Rare thoracic cancers include those of the trachea, thymus and mesothelioma (including peritoneum mesothelioma). The aim of this study was to describe the incidence, prevalence and survival of rare thoracic tumours using a large database, which includes cancer patients diagnosed from 1978 to 2002, registered in 89 population-based cancer registries (CRs) and followed-up to 31st December 2003. Over 17,688 cases of rare thoracic cancers were selected based on the list of the RACECARE project. Mesothelioma was the most common tumour (19 per million per year) followed by epithelial tumours of the trachea and thymus (1.3 and 1.7, respectively). The age standardised incidence rates of epithelial tumours of the trachea was double in Eastern and Southern Europe versus the other European regions: 2 per million per year. Epithelial tumours of the thymus had the lowest incidence in Northern and Eastern Europe and UK and Ireland1 and somewhat higher incidence in Central and Southern Europe.2 Highest incidence in mesothelioma was seen in UK and Ireland23 and lowest in Eastern Europe.4 Patients with tumours of the thymus had the best prognosis (1-year survival 85%, 66% at 5years). Five year survival was lowest for the mesothelioma 5% compared to 14% of patients with tumours of the trachea. Mesothelioma was the most prevalent rare cancer (12,000 cases), followed by thymus (7000) and trachea (1400). Cancer Registry (CR) data play an important role in revealing the burden of rare thoracic cancers and monitoring the effect of regulations on asbestos use and smoking related policies.
Pulmonary Endpoints (Lung Carcinomas and Asbestosis) Following Inhalation Exposure to Asbestos
Article
Mossman Brooke --- Lippmann Morton --- Hesterberg Thomas --- Kelsey Karl --- et al.
Journal: Journal of Toxicology and Environmental Health, Part BISSN: 10937404 Year: 2011
Fournis par: informaworld
Editeur: Taylor & Francis
Résumé : Lung carcinomas and pulmonary fibrosis (asbestosis) occur in asbestos workers. Understanding the pathogenesis of these diseases is complicated because of potential confounding factors, such as smoking, which is not a risk factor in mesothelioma. The modes of action (MOA) of various types of asbestos in the development of lung cancers, asbestosis, and mesotheliomas appear to be different. Moreover, asbestos fibers may act differentially at various stages of these diseases, and have different potencies as compared to other naturally occurring and synthetic fibers. This literature review describes patterns of deposition and retention of various types of asbestos and other fibers after inhalation, methods of translocation within the lung, and dissolution of various fiber types in lung compartments and cells in vitro. Comprehensive dose-response studies at fiber concentrations inhaled by humans as well as bivariate size distributions (lengths and widths), types, and sources of fibers are rarely defined in published studies and are needed. Species-specific responses may occur. Mechanistic studies have some of these limitations, but have suggested that changes in gene expression (either fiber-catalyzed directly or by cell elaboration of oxidants), epigenetic changes, and receptor-mediated or other intracellular signaling cascades may play roles in various stages of the development of lung cancers or asbestosis.
Biomarkers for Early Detection of Malignant Mesothelioma: Diagnostic and Therapeutic Application
Article
Auteurs: Marco Tomasetti --- Lory Santarelli
Journal: Cancers ISSN: 20726694 Year: 2010
Fournis par: Molecular Diversity Preservation International-- DOAJ
Editeur: Molecular Diversity Preservation International
Résumé: Malignant mesothelioma (MM) is a rare and aggressive tumour of the serosal cavities linked to asbestos exposure. Improved detection methods for diagnosing this type of neoplastic disease are essential for an early and reliable diagnosis and treatment. Thus, focus has been placed on finding tumour markers for the non-invasive detection of MM. Recently, some blood biomarkers have been described as potential indicators of early and advanced MM cancers. The identification of tumour biomarkers alone or in combination could greatly facilitate the surveillance procedure for cohorts of subjects exposed to asbestos, a common phenomenon in several areas of western countries.
Suivi des retraités exposés à l’amiante ou aux poussières de bois pendant leur vie professionnelle : premier bilan de la phase pilote du projet Spirale
Article
Nachtigal M --- Bonnaud S --- Gaignon A --- Serrano A --- et al.
Journal: Pratiques et organisation des soins ISSN: 19529201 Year: 2009Fournis par: Société française de santé publique-- DOAJ
Editeur: Société française de santé publique
Résumé : On estime que surviennent annuellement en France 15 000 à 20 000 cancers imputables à des expositions professionnelles, et qu’environ 25 % des hommes retraités ont été exposés à l’amiante au cours de leur vie professionnelle, et 8 % aux poussières de bois. Il existe depuis 1995 un dispositif de suivi médical post professionnel (SPP) qui est largement méconnu.
Le programme Spirale poursuit un double objectif : de santé publique, en repérant les personnes éligibles au SPP et en les y accompagnant, et de recherche épidé-miologique sur les effets à long terme des expositions professionnelles et les bénéfices du SPP. Spirale est mis en œuvre par l’unité 687 INSERM/CNAMTS qui repère les anciens salariés exposés à des cancérogènes au cours de leur vie professionnelle par un autoquestionnaire, et par les Centres d’examens de santé (CES) de l’Assurance maladie qui évaluent et confirment les expositions puis accompagnent les personnes dans leurs démarches.
La phase pilote de Spirale s’est déroulée dans 13 CES en 2006 et 2007, auprès d’environ 50 000 nouveaux retraités masculins ; elle a permis de repérer 1 751 expositions professionnelles à l’amiante et 684 aux poussières de bois. Dans les Caisses primaires d’assurance maladie concernées, les demandes de SPP pour l’amiante ont augmenté de 45 % et celles de SPP pour le bois de 600 %. Par ailleurs, environ 85 % des personnes exposées ont accepté de participer au suivi épidémiologique.
Dans l’attente d’une décision de généralisation du dispositif, la Caisse nationale de l’assurance maladie des travailleurs salariés (CNAMTS) a décidé la poursuite de Spirale dans les 13 CES pilotes.
Risk of gastrointestinal cancers from inhalation and ingestion of asbestos
Article
Journal: Regulatory Toxicology and Pharmacology ISSN: 02732300 Year: 2008
Fournis par: Elsevier
Editeur: Academic Press
Résumé: This paper summarizes the weight of epidemiological evidence to evaluate the hypothesis that asbestos exposure is causally associated with increased risk of gastrointestinal (GI) cancers as suggested by Selikoff in an early study of insulation workers. This review looks at populations that develop GI cancers, namely stomach, colorectal, colon and rectal. Guidelines for assessing causality are strength of association, biological gradient and consistency of the associations. Exposure-response (E-R) was evaluated using three methods to estimate exposure. Rate Ratios (RRs) for lung cancer and percent of mesothelioma are used as surrogate measures of asbestos exposure for all the cohorts of exposed workers. Quantitative or semi-quantitative estimates of cumulative exposure to asbestos were also used to assess E-R trends and were compared to E-R trends for lung cancer and mesothelioma in individual studies. Surrogate measures are important since there are few individual studies that have assessed E-R. None of the various methods to estimate asbestos exposure yielded consistent E-R trends and the strength of the associations were consistently weak or non-existent for the four types of GI cancers. The epidemiological evidence detracts from the hypothesis that occupational asbestos exposure increases the risk of stomach, colorectal, colon, and rectal cancer. Findings are briefly summarized below.
Malignant mesothelioma
Article
Moore Alastair --- Parker Robert --- Wiggins John
Journal: Orphanet Journal of Rare Diseases ISSN: 17501172 Year: 2008
Fournis par: BioMed Central-- DOAJ
Editeur: BioMed Central
Résumé: Malignant mesothelioma is a fatal asbestos-associated malignancy originating from the lining cells (mesothelium) of the pleural and peritoneal cavities, as well as the pericardium and the tunica vaginalis. The exact prevalence is unknown but it is estimated that mesotheliomas represent less than 1% of all cancers. Its incidence is increasing, with an expected peak in the next 10–20 years. Pleural malignant mesothelioma is the most common form of mesothelioma. Typical presenting features are those of chest pain and dyspnoea. Breathlessness due to a pleural effusion without chest pain is reported in about 30% of patients. A chest wall mass, weight loss, sweating, abdominal pain and ascites (due to peritoneal involvement) are less common presentations. Mesothelioma is directly attributable to occupational asbestos exposure with a history of exposure in over 90% of cases. There is also evidence that mesothelioma may result from both para-occupational exposure and non-occupational "environmental" exposure. Idiopathic or spontaneous mesothelioma can also occur in the absence of any exposure to asbestos, with a spontaneous rate in humans of around one per million. A combination of accurate exposure history, along with examination radiology and pathology are essential to make the diagnosis. Distinguishing malignant from benign pleural disease can be challenging. The most helpful CT findings suggesting malignant pleural disease are 1) a circumferential pleural rind, 2) nodular pleural thickening, 3) pleural thickening of > 1 cm and 4) mediastinal pleural involvement. Involvement of a multidisciplinary team is recommended to ensure prompt and appropriate management, using a framework of radiotherapy, chemotherapy, surgery and symptom palliation with end of life care. Compensation issues must also be considered. Life expectancy in malignant mesothelioma is poor, with a median survival of about one year following diagnosis.
Amines aromatiques
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Amines aromatiques
Les amines aromatiques (AA) sont des composés solides ou liquides utilisés pour la synthèse des matières colorantes, des produits pharmaceutiques, dans l’industrie du caoutchouc et des matières plastiques. La principale voie d’exposition aux AA est la voie cutanée, surtout en milieu professionnel.
Références bibliographiques
Amines aromatiques
Article
Auteurs: Villa, A.-F. --- Conso, F.
Journal: EMC - Toxicologie-Pathologie ISSN: 17625858 Year: 2004
Fournis par: Elsevier
Editeur: Elsevier
Résumé: Les composés aromatiques aminés sont des hydrocarbures aromatiques dans lesquels au moins un hydrogène du cycle a été remplacé par un groupement amine. Ils sont regroupés dans une même famille chimique mais leur toxicité est variable d'une substance à l'autre. Les amines aromatiques sont utilisées dans de nombreuses industries. La population générale peut être également exposée à ces amines, en raison du tabagisme ou lors d'apports alimentaires. Les voies de contamination peuvent être cutanée, respiratoire et digestive. Les effets toxiques aigus retrouvés peuvent être une méthémoglobinémie (aniline), une anémie hémolytique, une hépatite (MDA), une rhabdomyolyse avec insuffisance rénale, une cardiomyopathie ou une atteinte oculaire. Les effets chroniques peuvent être une irritation, une sensibilisation cutanée ou respiratoire (paraphénylène diamine). Un certain nombre de ces composés (benzidine, 2-naphtylamine) sont connus pour être cancérogènes chez l'homme. Le cancer de vessie d'origine professionnelle est le plus fréquent des cancers dus aux amines aromatiques. L'utilisation de ces amines cancérogènes est très réglementée en milieu de travail : interdiction des amines cancérogènes pour l'homme, surveillance des personnels ayant été anciennement exposés.
N-Acetyltransferase 1 in Colon and Rectal Cancer Cases from an Industrialized Area
Article
Hermann C. Roemer --- Wobbeke Weistenhöfer --- Dietrich Löhlein --- Frank Geller --
Journal of Toxicology and Environmental Health, Part A: Current IssuesISSN: 15287394 Year: 2008
Pages: 902-905
Fournis par: informaworld Editeur: Taylor & Francis
Résumé: Colon and rectal cancers are both associated with genetic as well as nutritional, occupational, and environmental factors. Aromatic amines and heterocyclic amines are established colorectal carcinogens. The polymorphic enzyme N-acetyltransferase 1 (NAT1) contributes to heterocyclic amine metabolism in the human colon. Thereby, NAT1 may influence the risk for development of colorectal cancer. The distribution of NAT1 genotypes was determined in 107 colon cancer cases, 77 rectal cancer cases, and 185 controls (suffering from nonmalignant diseases) by standard methods. In addition, possible occupational and nonoccupational risk factors were determined by a personal interview. Cancer cases and controls were derived from an area of former coal, iron, and steel industries, which is known for elevated colon cancer mortality. The proportions of NAT1*4/*4 genotype were 72% in controls, 75% in rectal cancer cases, and 72% in colon cancer cases. The proportions of the NAT1*4/*10 genotype were 17.8% in controls, 12.9% in rectal cancer cases, and 14% in colon cancer cases. Combinations of the determined NAT1 alleles *3/*3, *3/*10, *4/*3, *4/*11, *10/*10 and*11/*11 contributed to 10.2% of the genotypes in controls, 12.1% in rectal cancer cases, and 14% in colon cancer cases. In contrast to another study on healthy German volunteers, the NAT1*4/*4 genotype (wild type) is overrepresented. This might be due to the variation in the proportion of NAT1 alleles in the general population. The present study does not support a relevant impact of the NAT1 genotype on colorectal cancer risk development in the study area
Comments on the history and importance of aromatic and heterocyclic amines in public health
Article
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis ISSN: 00275107 Year: 2002
Fournis par: Elsevier
Editeur: Elsevier
Résumé: The carcinogenic risk of aromatic amines in humans was first discovered when a physician related the occurrence of urinary bladder cancer to the occupation of his patients. They were employed in the dyestuff industry, chronically exposed to large amounts of intermediate arylamines. Laboratory investigations disclosed that rats and mice administered specific azo dyes arylamines or derivatives developed cancer, primarily in the liver. Also, at that time, a possible pesticide, 2-aminofluorene, was tested for chronic toxicity, revealing that it rapidly induced cancers in several organs of rodents. This led to investigations on the mode of action of this class of chemicals, including their metabolic conversion. Biochemical activation to more reactive N-hydroxy compounds was found to occur, mostly in the liver, through what is now known as the cytochrome P450 enzyme systems, and also through prostaglandin synthetases. There were species differences. Guinea pigs were resistant to carcinogenesis because of the low titer of the necessary activating enzymes. In target tissues, a second essential reaction was necessary, namely acylation or sulfate ester formation. The reactive compounds produced display attributes of genotoxicity in appropriate test systems. Interest in this class of compounds increased when of Sugimura and colleagues discovered the formation of mutagens at the surface of cooked meat or fish, that were identified as heterocyclic amines (HCAs). These compounds undergo the same type of activation reactions, as do other arylamines. Epidemiological data suggest that meat eaters may have a higher risk of breast and colon cancer. HCAs induced cancer in rats in these organs and also in the prostate and the pancreas. In addition, there is some evidence that they affect the vascular system. The formation of HCAs during cooking can be decreased by natural and synthetic antioxidants, by tryptophan or proline, or by removing the essential creatine through brief microwave cooking prior to frying or broiling. The amounts of HCAs in cooked foods are small, but other components in diet such as ω-6-polyunsaturated oils have powerful promoting effects in target organs of HCAs. On the other hand, the action of HCAs may be decreased by foods containing antioxidants, such as vegetables, soy, and tea. Some constituents in foods also induce phase II enzymes that detoxify reactive HCA metabolites. Additional mechanisms involved decreased growth of neoplasms by intake of protective foods. Possibly, the carcinogenic effect of HCAs is accompanied by the presence of reactive oxygen species (ROS), which are also inhibited by antioxidants. World-wide, there have been many contributors to knowledge in this field. Adequate information may permit now to adjust lifestyle and lower the risk of human disease stemming from this entire class of aryl and HCA.
Bladder cancer
Article
de Braud, F. --- Maffezzini, M. --- Vitale, V. --- Bruzzi, P. --- et al. Gatta, G. --- Hendry, W.F. --- Sternberg, C.N.
Journal: Critical Reviews in Oncology/Hematology ISSN: 10408428 Year: 2002
Fournis par: Elsevier
Editeur: Elsevier
Résumé: Bladder cancer is the second most frequent tumour of the urogenital tract. Tobacco smoke has been shown to increase the risk of bladder cancer two- to fivefold as well as the exposure to metabolites of aniline dyes and other aromatic amines. Seventy-five per cent of bladder cancers are superficial at initial presentation, limited to the mucosa, submucosa, or lamina propria. Recurrence rates after initial treatment are 50–80%, with progression to muscle-invading tumour in 10–25%. In muscle-invading bladder cancers, there is a 50% risk of distant metastases. Surgery is the mainstay of standard treatment both in the form of transurethral endoscopic resection, mainly for superficial disease, and in the form of open ablative surgery with urinary diversion for muscle invasive disease. Endovesical administration of BCG has been employed after endoscopic resection as the most effective agent for both prophylaxis of disease recurrence and progression from superficial to invasive disease. The accepted treatment for muscle infiltrative disease is radical cystectomy. Response rates to combination chemotherapy regimens of up to 70% in patients with advanced metastatic disease have led to an investigation of its use for locally invasive disease in combination with conventional modalities of treatment.
IARC Monographs : Some Naturally Occurring Substances: Food Items and Constituents, Heterocyclic Aromatic Amines and Mycotoxins
Ebook
International Agency for research on Cancer (IARC), Volume 56
Editeur : IARC, Lyon, France, 1993
Document en ligne
http://monographs.iarc.fr/ENG/Monographs/vol56/mono56.pdf
IARC Monographs: Some Aromatic Amines, Organic Dyes, and Related Exposures
Ebook
International Agency for research on Cancer (IARC), Volume 99
Editeur : IARC, Lyon, France, 2010
Document en ligne
http://monographs.iarc.fr/ENG/Monographs/vol99/mono99.pdf
Arsenic
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Arsenic
L'arsenic est un élément de l'environnement que l'on retrouve naturellement dans les roches et le sol, l'eau, l'air et dans les plantes et les animaux. Il peut également être disséminé dans l'environnement à partir des sources agricoles et industrielles.
Références bibliographiques
Interaction between chronic arsenic exposure via drinking water and plasma lactate dehydrogenase activity
Article
Karim, Md.R. --- Salam, K.A. --- Hossain, E. --- Islam, K. --- et al. Ali, N. --- Haque, A. --- Saud, Z.A. --- Yeasmin, T. --- Hossain, M. --- Miyataka, H. --- Himeno, S. --- Hossain, K.
Journal: Science of the Total Environment ISSN: 00489697 Year: 2010
Fournis par: Elsevier
Résumé: Arsenic is a potent environmental pollutant that has caused one of the largest public health poisonings in the history of human civilization, affecting tens of millions of people worldwide especially in Bangladesh. Lactate dehydrogenase (LDH) in blood plays an important role in predicting cell or organ damage and as an important clue to the diagnosis of a variety of cancers. However, effect of chronic arsenic exposure on the LDH level in blood has not yet been documented. Since the chronic arsenic exposure is associated with organ damages and multi-site cancers, this research aimed at assaying the plasma level of LDH activity in the population who were exposed to arsenic chronically in Bangladesh. A total of 185 individuals living in arsenic-exposed areas and 121 individuals living in non-exposed area in Bangladesh were recruited as study subjects. Arsenic content in drinking water, hair and nails were estimated by Inductively Coupled Plasma Mass Spectroscopy (ICP-MS) and LDH activity was assayed by a spectrophotometer. Significant increase in LDH activity was observed with increasing concentrations of arsenic in water, hair and nails. Further, the study subjects were split into four groups based on the three ways of each exposure metrics (water, hair and nail arsenic concentrations) where the study subjects in the non-exposed area were used as a reference (lowest exposure) group. LDH activity was found to be increased in the higher exposure groups of water and hair arsenic concentrations. LDH activity was also increased at low to medium exposure groups of nail arsenic concentrations.Thus, the elevated plasma LDH activity might be helpful for the early prognosis of organ or tissue damage in the individuals who were exposed to arsenic chronically.
Mechanisms and Immune Dysregulation in Arsenic Skin Carcinogenesis
Article
Chih-Hung Lee --- Wei-Ting Liao --- Hsin-Su Yu
Journal: Journal of Cancer Therapy ISSN: 21511934 Year: 2010
Fournis par: DOAJ
Editeur: Scientific Research Publishing
Résumé: Long-term exposure to arsenic is associated with cancers of lung, urinary bladder, kidney, liver and skin. Arsenic car-cinogenesis might result from oxidative stress, altered growth factors, chromosomal abnormality, immune dysregula-tion, and aberrant epigenetic regulations. Bowen’s disease (As-BD) is the most common form of arsenic-induces skin cancers and is characterized by chronicity, multiplicity, and predisposition in sun-spare skin. However, only about 1% of the population exposed to arsenic developped skin cancers, indicating the host immune response plays an important modulatory role in skin carcinogenesis. In this review, we review the pathomechanisms of arsenic skin carcinogenesis and the immune interactions. Arsenic affects innate and adaptive immune responses through CD4+ T cells, monocytes, macrophages, and Langerhans cells. In skin of As-BD, CD4+ T cells undergo selective and differential apoptosis via Fas-FasL interaction. Numbers and dendrites of Langerhans cells are reduced in As-BD lesions. There is a defective homeostasis and aberrant trafficking of Langerhans cells. Such information is essential to understand the molecular mechanism for arsenic carcinogenesis in both skin and in internal organs.
Assessing the cancer risk associated with arsenic-contaminated seafood
Article
Chen, B.C. --- Chou, W.C. --- Chen, W.Y. --- Liao, C.M.
Journal: Journal of Hazardous Materials ISSN: 03043894 Year: 2010
Fournis par: Elsevier
Résumé: Tens of millions of people worldwide ingest excessive amounts of arsenic (As) through drinking water and food. The dietary intake of seafood is the major As exposure route in humans and can cause As-related adverse health effects including cancers. The aim of this study was to quantify potential cancer risks of As exposure for children and adults through seafood consumption. By coupling the age-specific physiologically based pharmacokinetic (PBPK) model and a Weibull-based dose-response function, a more accurate estimate of urinary arsenic metabolites could be achieved to better characterize potential cancer risks. The simulation results show that the proportion of inorganic As, monomethylarsonic acid (MMA), and dimethylarsinic acid (DMA) in human urine are estimated to total 6.7, 26.9, and 66.4% for children, and 6.2, 27.4, and 66.4% for adults, respectively. The estimated median cumulative cancer incidence ratios were respectively 2.67x10-6 and 3.83x10-6 for children and adults, indicating a low cancer risk for local residents exposed to As through the consumption of seafood. However, it is necessary to incorporate other exposure routes into the model to make it more realistic. The methodology proposed here can not only be applied to calculate the concentrations of As metabolites in urine, but also to provide a direct estimation of adverse health effects caused by the calculated internal concentrations.
Aberrant immune responses in arsenical skin cancers
Article
Lee, C.H. --- Liao, W.T. --- Yu, H.S.
Journal: Kaohsiung Journal of Medical Sciences ISSN: 1607551X Year: 2011
Fournis par: Elsevier
Résumé: Arsenic is a well-known human carcinogen. It also impairs immune functions and activation in many aspects. However, only a small portion of arsenic-exposed population develops skin abnormalities, including Bowen's disease and skin cancers. Differential immune activation among the individuals might account for the different susceptibilities. In patients with arsenic-induced Bowen's disease, there is a selective CD4 T-cell apoptosis through tumor necrosis factor-alpha pathway, decrease in macrophage differentiation and phagocytosis, reduced Langerhans cell numbers and dendrites, altered regulatory T-cell distribution, and other immune alterations. Several lines of evidence from mouse and fish studies also confirmed the potent and multifaceted effects of arsenic in the immune system. The molecular bases of immunosuppression by arsenic in lymphocytes may include chromosomal and DNA abnormalities, decreased T-cell receptor activation, and the cellular status of oxidation and methylation. This article also reviews the causative and differential role of selective CD4 cell apoptosis and the carcinogenesis of arsenic-induced Bowen's disease.
Epidemiology of Skin Cancer: Role of Some Environmental Factors
Article
Gabriella Fabbrocini --- Maria Triassi --- Maria Chiara Mauriello --- Guglielma Torre --- et al. Maria Carmela Annunziata --- Valerio De Vita --- Francesco Pastore --- Vincenza D’Arco --- Giuseppe Monfrecola
Journal: Cancers ISSN: 20726694 Year: 2010
Fournis par: Molecular Diversity Preservation International-- DOAJ
Editeur: Molecular Diversity Preservation International
Résumé: The incidence rate of melanoma and non-melanoma skin cancer entities is dramatically increasing worldwide. Exposure to UVB radiation is known to induce basal and squamous cell skin cancer in a dose-dependent way and the depletion of stratospheric ozone has implications for increases in biologically damaging solar UVB radiation reaching the earth’s surface. In humans, arsenic is known to cause cancer of the skin, as well as cancer of the lung, bladder, liver, and kidney. Exposure to high levels of arsenic in drinking water has been recognized in some regions of the world. SCC and BCC (squamous and basal cell carcinoma) have been reported to be associated with ingestion of arsenic alone or in combination with other risk factors. The impact of changes in ambient temperature will influence people’s behavior and the time they spend outdoors. Higher temperatures accompanying climate change may lead, among many other effects, to increasing incidence of skin cancer.
Arsenic Exposure and the Induction of Human Cancers
Article
Victor D. Martinez --- Emily A. Vucic --- Daiana D. Becker-Santos --- Lionel Gil --- et al. Wan L. Lam
Journal: Journal of Toxicology ISSN: 16878191 Year: 2011
Fournis par: DOAJ
Editeur: Hindawi Publishing Corporation
Résumé: Arsenic is a metalloid that is considered to be a human carcinogen. Millions of individuals worldwide are chronically exposed through drinking water, with consequences ranging from acute toxicities to development of malignancies, such as skin and lung cancer. Despite well-known arsenic-related health effects, the molecular mechanisms involved are not fully understood; however, the arsenic biotransformation process, which includes methylation changes, is thought to play a key role. This paper explores the relationship of arsenic exposure with cancer development and summarizes current knowledge of the potential mechanisms that may contribute to the neoplastic processes observed in arsenic exposed human populations.
IARC Monographs: Some Drinking-water Disinfectants and Contaminants, including Arsenic
Ebook
International Agency for research on Cancer (IARC), Volume 84
Editeur : IARC, Lyon, France, 2004
Document en ligne
http://monographs.iarc.fr/ENG/Monographs/vol84/mono84.pdf
IARC Monographs: Arsenic, Metals, Fibres, and Dusts
Ebook
International Agency for research on Cancer (IARC), Volume 100C
Editeur : IARC, Lyon, France, 2012
Document en ligne
http://monographs.iarc.fr/ENG/Monographs/vol100C/mono100C.pdf
Benzène
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Benzène
Le benzène est classé comme cancérogène avéré pour l’homme sur la base de leucémies observées dans des études épidémiologiques et animales.
Ses sources d’émission sont les processus de combustion (dont le tabagisme), le transport routier, et les activités industrielles.
Références bibliographiques :
Benzene as a cause of lymphoproliferative disorders
Article
Goldstein, B.D.
Journal: Chemico-Biological Interactions ISSN: 00092797 Year: 2010Fournis par: Elsevier
Résumé : There is a long standing issue concerning the strength of evidence relating benzene to lymphocytic neoplasms. Because benzene is a known cause of human acute myelogenous leukemia there has been little reason for organizations such as the International Agency for Research on Cancer (IARC) or the US National Toxicology Program (NTP) to perform standard hazard identification reviews of benzene as a possible cause of other cancers such as lymphomas. Increased understanding of underlying mechanisms of carcinogenesis, as is reflected in the greater scope given to mechanistic evidence in assigning overall sufficiency of evidence for carcinogenicity by both IARC and NTP, suggests that the evidence supporting benzene as a cause of lymphoma likely has passed the threshold required for being listed as a known causal relationship. A broad range of genotoxic effects in the lymphocytes of benzene-exposed workers has been well documented, as has the role of chromosomal effects in carcinogenesis. There is also increasing evidence of a close relationship between lymphoid tumors and the types of myeloid tumors known to be caused by benzene. This includes the not infrequent finding of biphenotypic lineage as well as the formation of lymphoid as well as myeloid leukemias following chemotherapy. Studies of the mechanism of benzene toxicity are consistent with a relatively non-specific mechanism capable of producing multiple chromosomal changes, and there is evidence that the early hematopoietic stem cell, which is believed to be targeted by benzene in causing myeloid cancers, is also the progenitor of lymphocytic cell types. Furthermore, the classification of lymphomas has evolved so that non-Hodgkin lymphoma now includes such formerly distinct disorders as chronic lymphocytic leukemia and multiple myeloma, and there is less of a distinction between leukemia and non-leukemia forms of lymphoma.
Hydroquinone, a benzene metabolite, and leukemia: A case report and review of the literature
Article
Regev Lee --- Wu Michael --- Zlotolow Ronald --- Brautbar Nachman
Journal: Toxicology and Industrial Health ISSN: 07482337 Year: 2012
Fournis par: HighWire
Editeur: Sage
Résumé: Hydroquinone is a phenolic metabolite of benzene, a known human carcinogen. Hydroquinone is widely used in the industry. We report a case of a 43-year-old male diagnosed with antecedent myelodysplastic syndrome and acute myeloid leukemia following 16 years of occupational exposure to hydroquinone in radiographic developer solution. Cytogenetic studies revealed aberrations in chromosome 5 and chromosome 7. We review the literature on hydroquinone as a potential cause of hematolymphatic cancers and discuss the role of hydroquinone as a genotoxic and leukemogenic agent.
A retrospective cohort study of leukemia and other cancers in benzene workers
Article
S.-N. Yin, G.-L. Li, F.-D. Tain, Z.-I. Fu, C. Jin, Y.-J. Chen, S.-J. Luo, P.-Z. Ye, J.-Z. Zhang, G.-C. Wang, X.-C. Zhang, H.-N. Wu, and Q.-C. Zhong .
Journal: Environ Health Perspect. July 1989
Résumé : A retrospective cohort study was carried out in 1982–1983 among 28,460 benzene-exposed workers (15,643 males, 12,817 females) from 233 factories and 28,257 control workers (16,621 males, 12,366 females) from 83 factories in 12 large cities in China. All-cause mortality was significantly higher among the exposed (265.46/100,000 person-years) than among the unexposed (139.06/100,000 person-years), as was mortality from all malignant neoplasms (123.21/100,000 versus 54.7/100,000, respectively). For certain cancers, increased mortality was noted among benzene-exposed males in comparison with that among unexposed males; the standardized mortality ratios (SMR) were elevated for leukemia (SMR = 5.74), lung cancer (SMR = 2.31), primary hepatocarcinoma (SMR = 1.12), and stomach cancer (SMR = 1.22). For females only leukemia occurred in excess among the exposed. Risk of leukemia rose as duration to exposure to benzene increased up to 15 years, and then declined with additional years of exposure. Leukemia occurred among some workers with as little as 6 to 10 ppm average exposure and 50 ppm-years (or possibly less) cumulative lifetime exposure (based on all available measurements for the exposed work units). Among the 30 leukemia cases identified in the exposed cohort, the proportion of subjects with acute lymphocytic leukemia was substantially lower and the proportion with acute nonlymphocytic leukemias was higher than in the general population. During 1972 to 1981, the annual incidence of leukemia ranged from 5.83 to 28.33 per 100,000 with higher rates occurring in the interval 1977 to 1981 than in the earlier years of the study period. Future studies should evaluate more precisely the relationship between exposure levels, job title, and development of leukemia among cases and noncases within the exposed cohort.
Bischlorométhyléther
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Bischlorométhyléther
Bis (chloromethy1) éther (BCME) est un produit chimique synthétique avec un odeur forte et désagréable. C'est un liquide limpide à température ambiante, mais il s'évapore facilement dans l'air. BCME subit facilement des réactions chimiques, il se décompose très rapidement quand il entre en contact avec de l'eau.
Références bibliographiques
Reactive Chemicals and Cancer
Article
Aaron Blair --- Neely Kazerouni
Journal: Cancer Causes & Control ISSN: 09575243 Year: 1997Fournis par: JSTOR
Editeur: Rapid Science Editeurs
Résumé: Epidemiologic evidence on the relation between reactive chemicals and cancer is reviewed. These highly reactive chemicals (acrylonitrile; bis[chloromethyl]ether and chloromethyl methyl ether; 1,3-butadiene, ethylene oxide; formaldehyde; mustard gas; sulfuric acid; and vinyl chloride) vary in use and exposure. All are animal carcinogens that also have received considerable epidemiologic attention. Acrylonitrile is a chemical of current economic importance. The epidemiologic evidence is quite weak, but the available studies were very small. Epidemiologic studies clearly demonstrate that bis (chloromethyl) ether and chloromethyl methyl ether cause lung cancer. Continued follow-up of exposed workers is encouraged to provide information on risks for other cancers. Results from epidemiologic studies of butadiene-exposed workers are somewhat inconsistent, but the largest study with the best exposure assessment found the largest relative risk for leukemia. The failure of several larger studies to replicate the early Swedish findings of a very strong association between leukemia and ethylene oxide has not been adequately explained. Epidemiologic studies of formaldehyde provide limited evidence for an association with cancer of the nasopharynx and possibly with nasal cancer. These very rare tumors, however, are difficult to study epidemiologically. Mustard gas is a well-established lung carcinogen, but a recent follow-up of the English cohort suggests that other sites also may be affected. Sulfuric acid appears to cause laryngeal cancer. A suggested relationship with lung cancer in a few studies is of concern because of the widespread opportunity for exposure from ambient air pollution. Vinyl chloride causes angiosarcoma of the liver, but a large, multi-country study provided no clear evidence that other sites are affected.
Retrospective exposure assessment in a chemical research and development facility
Article
Chen, Y.C. --- Ramachandran, G. --- Alexander, B.H. --- Mandel, J.H.
Journal: Environment International ISSN: 01604120 Year: 2012
Fournis par: Elsevier
Résumé: The objective of this exposure assessment was to reconstruct cumulative historical exposures for workers who have been exposed to multiple chemicals and chemical groups to better understand a cluster of brain cancers within a research and development lab. Chemicals of interest, including acrylates, bis-chloromethyl ether (BCME), chloromethyl methyl ether (CMME), isothiazolones and nitrosoamines, were selected on the basis of the plausibility of penetrating the blood–brain barrier and the uniqueness of the chemical's biological activity.
In a complicated exposure setting such as a chemical R&D facility, multiple exposure estimation methods were needed. First, similarly exposure groups (SEGs) were created for these materials based on department group, time period of the department's existence and function associated with job titles. A probabilistic framework for assessing exposures was developed using Bayesian analysis of historical monitoring data, mathematical exposure modeling and professional judgments of current and former industrial hygienists at the facility were used to reconstruct the exposure history for acrylates, BCME and CMME for each SEG over the time period of interest. Since sufficient measurement data for isothiazolones and nitrosoamines were not available, the exposure histories for each SEG for these chemicals were estimated. This was done using objective formaldehyde levels and subjective employee interviews. The interviews assessed workplace determinants of exposure as distinct surrogates for estimating inhalation and dermal exposures. The exposure assessments by these methods were compared against each other to estimate the potential for exposure misclassification. A job exposure matrix (JEM) was constructed that contained the exposures obtained from above multiple approaches for each of these chemical groups for each SEG for each year of interest. The combination of methods used in this work is a unique and potentially helpful framework that can be used in analogous workplace settings involving multiple exposures with incomplete objective measurement information.
Benjamin L. Van Duuren
Journal : Environmental Research, August 1989,
Résumé: he α-chloroether carcinogen chloromethylmethyl ether (CME) and its impurity bis(chloromethyl)ether (BCME) are direct-acting alkylating agents. Vinyl chloride (VC) is an indirect-acting carcinogen but its accepted carcinogenic intermediate, chloroethylene oxide, is also an α-chloroether. Both CME-BCME and VC have been in industrial use since about 1950. Hence, they were selected for comparison of potency as human carcinogens using numerous epidemiologic reports. There were 115 deaths due to angiosarcoma of the liver among several hundred thousand VC-exposed workers on the basis of reports from 10 countries during 1955 and 1984. Reports from five countries cited a total of 87 respiratory cancer deaths among only 3024 CME-BCME-exposed workers. If a recent court settlement in the United States is taken into account, the number of respiratory cancer deaths due to CME-BCME rises to 117. On the basis of these numbers of cancer deaths, and the levels and durations of exposure, it is concluded that VC is a weak human carcinogen compared to CME-BCME.
Lung cancer caused by chloromethyl ether
ArticleAuteurs: Weiss, W., Moser, R. L. & Auerbach, O.
Journal: Food and Cosmetics Toxicology, 1981
Editeur : Elsevier
Pas de résumé disponible.
Cadmium
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Cadmium
Élément naturel de numéro atomique Z = 48, présent dans certains minerais sous forme d'impuretés. Il fût utilisé pour ses caractéristiques physico-chimiques notamment dans les batteries pour la protection de l'acier contre la corrosion (cadmiage) et comme stabilisant pour les plastiques et les pigments. C’est un métal argenté qui se ternit à l'air. Il est soluble dans les acides mais pas en milieu alcalin. C'est le 65ème élément naturel le plus abondant de la croûte terrestre. On le trouve dans les piles, soudures, accumulateurs, pigments de peinture, produits pour la photogravure, les engrais et les pesticides. L'intoxication au cadmium se manifeste par des vertiges, de l'anémie, des douleurs osseuses, et des lésions aux reins.
Références bibliographiques
Review of cadmium transfers from soil to humans and its health effects in the Jamaican environment
Article
Lalor, G.C.
Journal: Science of The Total Environment ISSN: 00489697 Year: 2008Fournis par: Elsevier
Editeur: Elsevier
Résumé: Concerns about the effects of cadmium on human health have led to numerous guidelines and regulations limiting its concentrations in soils and food and allowable human intakes. These have socio-economic consequences in terms of land use and the marketing of food. The bauxite soils in Jamaica, which are both aluminium ores and agricultural soils contain orders of magnitude higher than world normal concentrations of cadmium resulting in elevated Cd concentrations in several foodstuffs and significant transfers to humans, which would seem to represent a risk factor for increased mortality and/or morbidity in the local populations. But, as in Shipham and other examples, there is no evidence of cadmium-related human distress. Macro-indicators like life expectancy and median ages of death do not show cadmium related geographical distributions. The present review focuses on the soils and foods and illnesses of high incidence especially cancers and renal disease that have been traditionally associated with cadmium. In view of the remarkable concentrations of cadmium involved in Jamaica, and often contradictory reports in the literature, it appears that much remains to be learned about certain details of cadmium toxicity.
Long duration exposure to cadmium leads to increased cell survival, decreased DNA repair capacity, and genomic instability in mouse testicular Leydig cells
Article
Singh, K.P. --- Kumari, R. --- Pevey, C. --- Jackson, D. --- et al. DuMond, J.W.
Journal: Cancer Letters ISSN: 03043835 Year: 2009Fournis par: Elsevier
Editeur: Elsevier
Résumé: Epidemiological and experimental studies have shown that cadmium is carcinogenic to human and experimental animals, however, the mechanism of cadmium-induced carcinogenesis is not clear. The aberrant expression of cell cycle and DNA repair genes resulting in increased cell proliferation and genomic instability are the characteristic features of cancer cells. The purpose of this study was to determine if exposure to cadmium can perturb cell proliferation/survival and causes genomic instability in TM3 cells, a mouse testicular Leydig cell line. The results of this study revealed that short-duration exposure to lower doses of cadmium significantly increase the growth of TM3 cells, whereas, higher doses are toxic and cause cell death. The long duration exposure to higher doses of cadmium, however, results in increased cell survival and acquisition of apoptotic resistance. Gene expression analysis by real-time PCR revealed increased expression of the anti-apoptotic gene Bcl-2, whereas decreased expression of pro-apoptotic gene Bax. Decreased expression of genes for maintenance of DNA methylation, DNMT1, and DNA repair, OGG1 and MYH, was also observed in cells exposed to cadmium for 24h. The random amplified polymorphic DNA (RAPD) assay revealed genomic instability in cells with chronic exposure to cadmium. The findings of this study indicate that mouse testicular Leydig cells adapt to chronic cadmium exposure by increasing cell survival through increased expression of Bcl-2, and decreased expression of Bax. The increased proliferation of cells with genomic instability may result in malignant transformation, and therefore, could be a viable mechanism for cadmium-induced cancers.
Cadmium induces mitogenic signaling in breast cancer cell by an ER@a-dependent mechanism
Article
Brama, M. --- Gnessi, L. --- Basciani, S. --- Cerulli, N. --- et al. Politi, L. --- Spera, G. --- Mariani, S. --- Cherubini, S. --- d'Abusco, A.S. --- Scandurra, R. --- Migliaccio, S.
Journal: Molecular and Cellular Endocrinology ISSN: 03037207 Year: 2007Fournis par: Elsevier
Editeur: Elsevier
Résumé: Breast cancer (BC) is linked to estrogen exposure. Estradiol (E2) stimulates BC cells proliferation by binding the estrogen receptor (ER). Hormone-related cancers have been linked to estrogenic environmental contaminants. Cadmium (Cd) a toxic pollutant, acts as estrogens in BC cells. Purpose of our study was to evaluate whether Cd regulates MCF-7 cell proliferation by activating ERK1/2, Akt and PDGFR@a kinases. Cd increased cell proliferation and the ER-antagonist ICI 182,780 blunted it. To characterize an ER-dependent mechanism, ER@a/@b expression was evaluated. Cd decreased ER@a expression, but not ER@b. Cd also increased ERK1/2, Akt and PDGFR@a phosphorylation while ICI blocked it. Since stimulation of phosphorylation was slower than expected, c-fos and c-jun proto-oncogenes, and PDGFA were analyzed. Cd rapidly increased c-jun, c-fos and PDGFA expression. Cells were also co-incubated with the Cd and specific kinases inhibitors, which blocked the Cd-stimulated proliferation. In conclusion, our results indicate that Cd increases BC cell proliferation in vitro by stimulating Akt, ERK1/2 and PDGFR@a kinases activity likely by activating c-fos, c-jun and PDGFA by an ER@a-dependent mechanism.
Metallothionein protection of cadmium toxicity
Article
Klaassen, C.D. --- Liu, J. --- Diwan, B.A.
Journal: Toxicology and Applied Pharmacology ISSN: 0041008X Year: 2009
Fournis par: Elsevier
Editeur: Academic Press
Résumé: The discovery of the cadmium (Cd)-binding protein from horse kidney in 1957 marked the birth of research on this low-molecular weight, cysteine-rich protein called metallothionein (MT) in Cd toxicology. MT plays minimal roles in the gastrointestinal absorption of Cd, but MT plays important roles in Cd retention in tissues and dramatically decreases biliary excretion of Cd. Cd-bound to MT is responsible for Cd accumulation in tissues and the long biological half-life of Cd in the body. Induction of MT protects against acute Cd-induced lethality, as well as acute toxicity to the liver and lung. Intracellular MT also plays important roles in ameliorating Cd toxicity following prolonged exposures, particularly chronic Cd-induced nephrotoxicity, osteotoxicity, and toxicity to the lung, liver, and immune system. There is an association between human and rodent Cd exposure and prostate cancers, especially in the portions where MT is poorly expressed. MT expression in Cd-induced tumors varies depending on the type and the stage of tumor development. For instance, high levels of MT are detected in Cd-induced sarcomas at the injection site, whereas the sarcoma metastases are devoid of MT. The use of MT-transgenic and MT-null mice has greatly helped define the role of MT in Cd toxicology, with the MT-null mice being hypersensitive and MT-transgenic mice resistant to Cd toxicity. Thus, MT is critical for protecting human health from Cd toxicity. There are large individual variations in MT expression, which might in turn predispose some people to Cd toxicity.
Comparative genomic analyses identify common molecular pathways modulated upon exposure to low doses of arsenic and cadmium
Article
Benton Margaret --- Rager Julia --- Smeester Lisa --- Fry Rebecca
Journal: BMC Genomics ISSN: 14712164 Year: 2011
Fournis par: DOAJ
Editeur: BioMed Central
Résumé:
Background
Exposure to the toxic metals arsenic and cadmium is associated with detrimental health effects including cancers of various organs. While arsenic and cadmium are well known to cause adverse health effects at high doses, the molecular impact resulting from exposure to environmentally relevant doses of these metals remains largely unexplored.
Results
In this study, we examined the effects of in vitro exposure to either arsenic or cadmium in human TK6 lymphoblastoid cells using genomics and systems level pathway mapping approaches. A total of 167 genes with differential expression were identified following exposure to either metal with surprisingly no overlap between the two. Real-time PCR was used to confirm target gene expression changes. The gene sets were overlaid onto protein-protein interaction maps to identify metal-induced transcriptional networks. Interestingly, both metal-induced networks were significantly enriched for proteins involved in common biological processes such as tumorigenesis, inflammation, and cell signaling. These findings were further supported by gene set enrichment analysis.
Conclusions
This study is the first to compare the transcriptional responses induced by low dose exposure to cadmium and arsenic in human lymphoblastoid cells. These results highlight that even at low levels of exposure both metals can dramatically influence the expression of important cellular pathways.
The effects of changes in cadmium and lead air pollution on cancer incidence in children
Article
Absalon, D. --- Slesak, B.
Journal: Science of the Total Environment ISSN: 00489697 Year: 2010Fournis par: Elsevier
Résumé: This article presents the results of research on the effects of air pollution on cancer incidence in children in the region of Silesia (Poland), which has undergone one of the most profound anthropogenic transformations in Europe. The main objective of the research was to specify the impact of changes in cadmium and lead pollution in the years 1990-2005 on the incidence of cancers reported in children. Lead concentration ranged from 0 to 1490.10-9Gm-2/year, and cadmium concentration ranged from 0 to 33.7.10-9G m-2/year. There was no strong significant correlation (max 0.3) between air pollution and incidence rate (IR) in the general population of children in any particular year. Alongside the cartographic presentation of dependences, correlation coefficients between the variables in question were calculated. This made it possible to determine the relationship between the pollution levels and incidence rates in the area. There was a significant reduction in the level of pollution during the investigated period. The study of the relationship between the number of cancers reported and the condition of the natural environment revealed increased sensitivity to toxins in boys (correlation coefficient 0.3). In addition, the spatial distribution of the number of cases reported in boys suggests a correlation with the spatial distribution of the coefficients for the entire group of children included in the study. The yearly average IR of childhood cancer in specific districts ranged from 0 to 61.48/100,000 children under 18years of age during the 1995-2004 period.
IARC Monographs: Beryllium, Cadmium, Mercury, and Exposures in the Glass Manufacturing Industry
Ebook
International Agency for research on Cancer (IARC), Volume 58
Editeur : IARC, Lyon, France, 1993
Document en ligne
http://monographs.iarc.fr/ENG/Monographs/vol58/mono58.pdf
Chlorure de vinyle
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Chlorure de vinyle
Le chlorure de vinyle est un composé chimique de synthèse utilisé dans la fabrication de plastique (PVC). Souvent employé sous forme liquide, il se présente aussi sous forme de gaz inodore et incolore.
Il est classé cancérogène avéré pour l’angiosarcome hépatique et le carcinome hépatocellulaire, deux formes de cancers du foie.
Références bibliographiques
Update of the Follow-Up of Mortality and Cancer Incidence among European Workers Employed in the Vinyl Chloride Industry
Article
Elizabeth Ward --- Paolo Boffetta --- Aage Andersen --- Didier Colin --- et al. Pietro Comba --- James A. Deddens --- Marco De Santis --- Lars Hagmar --- Sverre Langard --- Ingvar Lundberg --- Damien McElvenny --- Roberta Pirastu --- Davide Sali --- Lorenzo Simonato
Journal: Epidemiology ISSN: 10443983 Year: 2001
Fourni par: JSTOR
Editeur: Lippincott Williams & Wilkins
Résumé: Although vinyl chloride is an established cause of liver angiosarcoma, the evidence is inconclusive on whether it also causes other neoplastic and nonneoplastic chronic liver diseases as well as neoplasms in other organs. Furthermore, the shape of the dose-response relation for angiosarcoma is uncertain. We have extended for approximately 8 years the mortality and cancer incidence follow-up of 12,700 male workers in the vinyl chloride industry in four European countries. All-cause mortality was lower than expected, whereas cancer mortality was close to expected. A total of 53 deaths from primary liver cancer (standardized mortality ratio 2.40, 95% confidence interval = 1.80-3.14) and 18 incident cases of liver cancer were identified, including 37 angiosarcomas, 10 hepatocellular carcinomas, and 24 liver cancers of other and unknown histology. In Poisson regression analyses we observed a marked exposure response for all liver cancers, angiosarcoma, and hepatocellular carcinoma. The exposure-response trend estimated for liver cancer in analyses restricted to cohort members with cumulative exposures of <1,500 parts per million-years was close to that estimated for the full cohort (relative risk of 2.0 per logarithmic unit of cumulative dose). No strong relation was observed between cumulative vinyl chloride exposure and other cancers. Although cirrhosis mortality was decreased overall, there was a trend with cumulative exposure.
Carcinogenic, mutagenic and teratogenic risks associated with vinyl chloride
Article
Infante, P.F. --- Wagoner, J.K. --- Waxweiler, R.J.
Journal: Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis ISSN: 00275107 Year: 1976
Fournis par: Elsevier
Résumé: The data presented demonstrate clearly that vinyl chloride (VC) is related to a significant excess of mortality from cancer of the liver, lung and brain among workers occupationally exposed to VC. The risk of dying from cancer of the lymphatic and hematopoietic system also appears to increase with an increase in latency. These cancer sites could have been predicted by the animal bioassay conducted by Maltoni. With regard to the liver, even the histopathologic type of cancer (angiosarcoma) was observed first in experimental animals. A sutdy of cancer mortality among populations residing proximate to VC polymerization facilities also demonstrated an increased risk of dying from CNS and lymphatic cancer. These latter findings raise cause for concern about out-plant emisssions of VC, but without further study these cancers obviously cannot be interpreted as being related to out-plant exposure to VC. Various test systems now have been elicited a positive mutagenic response to VC. Thus, our observations of a significant excess of fetal mortality among the wives of males, who were occupationally exposed to VC, raise public health concern that VC may be mutagenic in humas. With regard to the teratogenicity of VC, observations of a significant excess of children born with birth defects were reported among populations residing proximate to VC polymerization facilities. Additional epidemiologic study is needed to determine whether a repeated pattern of excessive numbers of children born with birth defects can be observed in other communities with VC polymerization facilities.
Angiosarcoma of the Liver: A Signal Lesion of Vinyl Chloride Exposure
Article
Nicholas J. Vianna --- Judith Brady --- Philip Harper
Journal: Environmental Health Perspectives ISSN: 00916765 Year: 1981
Fournis par: JSTOR
Editeur: National Institute of Environmental Health Sciences.
Résumé: Vinyl chloride (VCM) induced angiosarcoma of the liver (ASL) is a rare vascular tumor which might be associated with a wide range of disease states. The possibility that this tumor might be a signal lesion is supported by mortality studies suggesting that cancers of the digestive, respiratory, neurological and lymphatic systems have occurred more often than expected in VCM workers. There is also evidence that certain non-neoplastic disorders, such as pneumoconiosis and excess fetal deaths, may be associated with this chemical. It has been suggested that a gradual increase in the incidence of ASL might have occurred in recent years. This could be a reflection of the long latency period and/or the increased recognition of this entity. Several cases of ASL have occurred in people living in the vicinity of VCM plants. This raises the possibility that low-level exposure to this chemical over a long period might induce ASL.
Mortality patterns among industrial workers exposed to chloroprene and other substances
Article
Marsh, G.M. --- Youk, A.O. --- Buchanich, J.M. --- Cunningham, M. --- et al. Esmen, N.A. --- Hall, T.A. --- Phillips, M.L.
Journal: Chemico-Biological Interactions ISSN: 00092797 Year: 2007
Fournis par: Elsevier
Editeur: Elsevier
Résumé: We conducted an historical cohort study to investigate the mortality experience of industrial workers potentially exposed to chloroprene (CD) and other substances, including vinyl chloride (VC), with emphasis on cancer mortality, including respiratory system (RSC) and liver. In 1999, the International Agency for Research on Cancer (IARC) classified CD as a possible carcinogen (Group 2B); VC was classified in 1987 as a known human carcinogen (Group 1). Subjects were 12,430 workers ever employed at one of two U.S. industrial sites (Louisville, KY (n=5507) and Pontchartrain, LA (n=1357)) or two European sites (Maydown, Northern Ireland (n=4849) and Grenoble, France (n=717)), with earliest CD production dates ranging from 1942 (L) to 1969 (P). Two sites (L and M) synthesized CD with the acetylene process that produced VC exposures. We determined vital status through 2000 for 95% of subjects and cause of death for 95% of the deaths. Historical exposures for individual workers were estimated quantitatively for CD and VC. Workers ever exposed to CD ranged from 92.3% (M) to 100% (G); to VC from 5.5% (M) to 22.7% (L). We computed standardized mortality ratios (SMRs) (using national and regional standard populations) in relation to selected demographic, work history and exposure factors. We used worker pay type (white or blue collar) as a rough surrogate for lifetime smoking history. For the combined cohort, SMRs (95% CIs) for all causes combined, all cancers combined, RSC and liver cancer were, respectively, 0.72 (0.69-0.74), 0.73 (0.68-0.78), 0.75 (0.67-0.84) and 0.72 (0.43-1.13). Site-specific (L, M, P and G, respectively) SMRs were: for all cancers combined: 0.75 (0.69-0.80), 0.68 (0.56-0.80), 0.68 (0.47-0.95) and 0.59 (0.36-0.91); for RSC: 0.75 (0.66-0.85), 0.79 (0.58-1.05), 0.62 (0.32-1.09) and 0.85 (0.41-1.56); for liver cancer: 0.90 (0.53-1.44) (17 deaths), 0.24 (0.01-1.34) (1 death), 0.0 (0-2.39) (no deaths) and 0.56 (0.01-3.12) (1 death). Among all workers ever exposed to CD, SMRs were: for all cancers combined: 0.71 (0.66-0.76); for RSC: 0.75 (0.67-0.84); for liver cancer: 0.71 (0.42-1.14). We also observed no increased mortality risks among cohort subgroups defined by race, gender, worker pay type, worker service type (short/long term), time period, year of hire, age at hire, duration of employment, the time since first employment, and CD or VC exposure status (never/ever exposed). In summary, our study has many strengths and is the most definitive study of the human carcinogenic potential of exposure to CD conducted to date. We conclude that persons exposed to chloroprene or vinyl chloride at the levels encountered in the four study sites did not have elevated risks of mortality from any of the causes of death examined, including all cancers combined and lung and liver cancer, the cancer sites of a priori interest. This conclusion is corroborated by our detailed analyses of mortality in relation to qualitative and quantitative exposures to CD and VC at each of the four study sites, reported in our companion paper (Marsh et al., submitted for publication).
Chrome
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Chrome
Le chrome est un élément chimique de symbole Cr et de numéro atomique24. Son étymologie vient du grec chroma signifiant couleur, car les composés du chrome sont différemment colorés.
Son mode d'action n'est pas encore totalement élucidé, mais on sait que le chrome agit comme cofacteur de l'insuline, facilitant ainsi l'assimilation du glucose par les cellules.
Références bibliographiques
Elevated Frequencies of Micronuclei and other Nuclear Abnormalities of Chrome Plating Workers Occupationally Exposed to Hexavalent Chromium
Article
Sudha S --- Kripa S K --- Shibily P --- Shyn J
Journal: Iranian Journal of Cancer Prevention ISSN: 20082398 Year: 2011
Fournis par: DOAJ
Editeur: Shahid Beheshti University of Medical Sciences
Résumé:
Background: Biomonitoring provides a useful tool to estimate the genetic risk from exposure to genotoxic agents. The aim of this study was to assess the potential cytogenetic damage associated with occupational exposure to hexavalent chromium by using micronuclei (MN) as a biomarker.
Methods: This was a cross-sectional study and all participants were males. Both the exposed and control individuals were selected from Coimbatore, Southern India. Exfoliated buccal cells from 44 chrome plating workers and 40 age and sex matched control subjects were examined for MN frequency and nuclear abnormalities (NA) other than micronuclei, such as binucleates, broken eggs, karyorrhexis, karyolysis and pyknosis.
Results: Results showed statistically significant difference between chrome plating workers and control groups. MN and NA frequencies in chrome plating workers were significantly higher than those in control groups (p < 0.05) and also significantly related to smoking habit (P < 0.05). A significant difference in NA was observed in workers exposed to chromium for longer duration. In addition to this, a higher degree of NA was observed among smokers.
Conclusion: MN and other NA reflect genetic changes, events associated with carcinogenesis. Therefore the results of this study indicate that chrome plating workers are under risk of significant cytogenetic damage. Therefore, there is a need to educate those who work with heavy metals about the potential hazard of occupational exposure and the importance of using protective measures.
Epidemiologic studies of chrome and cancer mortality: A series of meta-analyses
Article
Cole, P. --- Rodu, B.
Journal: Regulatory Toxicology and Pharmacology ISSN: 02732300 Year: 2005Fournis par: Elsevier
Editeur: Academic Press
Résumé: We used 49 epidemiologic studies based on 84 papers published since 1950 to develop an array of meta-analyses relating exposure to chrome-six compounds with 10 causes of death. Most exposures occurred in occupational settings. Studies were assessed for quality, and for control of smoking or economic status if they related to lung or stomach cancer. There was no excess mortality from all causes combined among chrome-exposed persons. A minimal excess of cancer (SMR=112), overall, was due primarily to an excess of lung cancer (SMR=141) but the SMR was 112 among the better-quality, 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, kidney, and central nervous system cancer and leukemia, Hodgkin's disease and other lymphatohematopoietic cancer. This series of meta-analyses indicates that chrome-six is a weak cause of lung cancer and is not a cause of any of the other seven forms of cancer evaluated.
Occupational exposure to hexavalent chromium and cancers of the gastrointestinal tract: A meta-analysis
Article
Gatto, N.M. --- Kelsh, M.A. --- Mai, D.H. --- Suh, M. --- et al.
Journal: Cancer Epidemiology ISSN: 18777821 Year: 2010Fournis par : Elsevier
Résumé :
Introduction: We conducted a systematic literature review and meta-analysis of oral cavity, esophageal, stomach, small intestine, colon, and rectal cancers among workers occupationally exposed to Cr(VI).
Methods: Using PubMed, studies published from 1950 to 2009 evaluating the relationship between Cr(VI) exposure and GI cancers were identified. Measures of effect and variability were extracted from 32 studies meeting specific inclusion criteria, and meta-analysis summary relative risk measures were calculated using random effects models and inverse variance weighting methods.
Results: Meta-standardized mortality ratios (SMRs) were, for cancer of the: oral cavity [1.02 (95% CI=0.77-1.34)]; esophagus [1.17 (95% CI=0.90-1.51)]; stomach [1.09 (95% CI=0.93-1.28)]; colon [0.89 (95% CI=0.70-1.12)]; and rectum [1.17 (95% CI=0.98-1.39)]. Analyses of more highly exposed subgroups included in the studies or subgroups based on geographic region or by industry with recognized Cr(VI) exposures (welding, chrome plating, chromate production, and pigment production) did not result in elevated meta-SMRs except for esophageal cancer among US cohorts [meta-SMR=1.49 (95% CI=1.06-2.09)]. However, that finding was based on a subgroup of only four studies, one of which was a PMR study. Potential confounding by socioeconomic status (SES), diet and/or smoking, or limitations due to the healthy-worker effect (HWE) were evaluated, and while smoking, diet and SES may be important factors that may have upwardly biased the meta-SMRs, HWE is not likely to have significantly affected the summary results. None of three studies reporting small intestine cancers observed a statistically significant increased risk. Discussion: These meta-analyses and literature review indicate that Cr(VI)-exposed workers are not at a greater risk of GI cancers than the general population
Lung cancer in Yorkshire chrome platers, 1972-97
Article
Journal: Occupational and Environmental Medicine ISSN: 1351-0711Year: 2000
Editeur: The BMJ Publishing Group
Résumé :
OBJECTIVES To investigate mortality from lung cancer in chrome platers, a group exposed to chromic acid.
METHODS The mortality of a cohort of 1087 chrome platers (920 men, 167 women) from 54 plants situated in the West Riding of Yorkshire, United Kingdom, was investigated for the period 1972–97. All subjects were employed as chrome platers for 3 months and all were alive on 31 May 1972. Mortality data were also available for a cohort of 1163 comparison workers with no known occupational exposure to chrome compounds (989 men, 174 women). Information on duration of chrome work and smoking habits collected for a cross sectional survey carried out in 1969–72 were available for 916 (84.3%) of the chrome platers; smoking habits were available for 1004 (86.3%) comparison workers. Two analytical approaches were used, indirect standardisation and Poisson regression.
RESULTS Based on serial mortality rates for the general population of England and Wales, significantly increased mortality from lung cancer was observed (obs) in male chrome platers (obs 60, expected (exp) 32.5, standardised mortality ratio (SMR) 185, p<0.001) but not in male comparison workers (obs 47, exp 36.9, SMR 127). Positive trends were not shown for duration of employment exposed to chrome, although data on working after 1972 were not available.
CONCLUSIONS Confident interpretation is not possible but occupational exposures to hexavalent chromium may well have been involved in the increased mortality from lung cancer found in this cohort of chrome platers.
IARC Monographs : Chromium, Nickel and Welding
Ebook
International Agency for research on Cancer (IARC),Volume 49
Editeur : IARC, Lyon, France, 1990
Document en ligne
http://monographs.iarc.fr/ENG/Monographs/vol49/mono49.pdf
Goudrons, huiles, brais de houille suies de combustion du charbon
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Goudrons, huiles, brais de houille suies de combustion du charbon
Les goudrons de houille appelé aussi simplement goudron, sont des dérivés houillés de couleur marron à noire, très visqueux, voire solides (brai de goudron). Ce sont des sous-produits de la distillation de la houille lors de la fabrication du coke, ou de sa gazéfaction en gaz de houille.
Références bibliographiques
Meta-Analysis of Lung Cancer in Asphalt Roofing and Paving Workers with External Adjustment for Confounding by Coal Tar
Article
William E. Fayerweather
Journal: Journal of Occupational and Environmental Hygiene ISSN: 15459624Year: 2007
Publisher: Taylor & Francis
Résumé : The study's objectives were to update Partanen's and Boffetta's 1994 meta-analysis of lung cancer among roofing and paving asphalt workers and explore the role of coal tar in explaining the statistical heterogeneity among these studies. Information retrieval strategies and eligibility criteria were defined for identifying the epidemiologic studies to be included in the analysis. The relative risk ratio (RR) for lung cancer was selected as the effect measure of interest. Coal tar bias factors were developed and used to externally adjust each eligible study's published RR for confounding by coal tar. Confidence intervals on adjusted RRs were estimated by the Monte Carlo methods outlined by Steenland and Greenland (2004). The meta-Relative Risk (meta-RR) and its variance were estimated by general variance-based methods. Heterogeneity of the RRs was assessed by heterogeneity chi-square and I 2 tests. Also explored were the influences of study design; differences between internally and externally adjusted RRs; and the potential impact of coal tar misclassification. The results from this update were similar to those in Partanen's and Boffetta's original meta-analysis. The unadjusted meta-RR (random effects model) for the roofing studies was elevated (meta-RR = 1.67, 95% CI = 1.39–2.02, I 2 = 80%) and significantly greater than the meta-RR for the paving studies (meta-RR = 0.98, 95% CI = 0.81–1.18, I 2 = 59%). After adjustment for confounding by coal tar, however, the corrected roofers' meta-RR dropped to 1.10 (meta-RR = 1.10, 95% CI = 0.91–1.33, I 2 = 60%), while the corrected pavers' meta-RR was nearly unchanged at 0.96 (meta-RR = 0.96, 95% CI = 0.80–1.16, I 2 = 56%). Although the meta-RRs for the roofers and the pavers were no longer statistically significantly different from one another, significant heterogeneity remained within each of the coal tar-adjusted sectors. Stratifying the roofing and paving studies by study design revealed that statistical heterogeneity was concentrated in the weaker designs such as those relying on death certificates for work history. When the weaker studies were excluded, the remaining roofing and paving studies had a combined meta-RR close to 1.0 (meta-RR = 1.01, 95% CI = 0.88–1.17) with no significant heterogeneity (I 2 = 0%). Meta-analysis of non-experimental epidemiologic studies is subject to significant uncertainties as is externally correcting studies for confounding. Given these uncertainties, the specific quantitative estimates in this (or any similar) analysis must be viewed with caution. Nevertheless, this analysis provides support for the hypothesis proposed by several major reviewers that confounding by coal tar-related PAH exposures may explain most or all of the lung cancer risks found in the epidemiologic literature on asphalt roofing and paving workers.
Huiles minérales
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Huiles minérales
Les huiles minérales sont des mélanges d'hydrocarbures paraffiniques, alicycliques, naphténiques et aromatiques.
Toutes les huiles sont susceptibles de contenir des additifs comme des inhibiteurs de corrosion, des émulsifiants (colophane),des biocides (formaldéhyde), des anti-oxydants (tétraéthylènediamine...), des amines aliphatiques, des diluants chlorés.....
Références bibliographiques
Petroleum Mineral Oil Refining and Evaluation of Cancer Hazard
Article
Carl R. Mackerer --- Larry C. Griffis --- John S. Grabowski Jr. --- Fred A. Reitman
Journal: Applied Occupational and Environmental Hygiene ISSN: 1047322x
Year: 2003
Editeur: Taylor & Francis
Résumé: Petroleum base oils (petroleum mineral oils) are manufactured from crude oils by vacuum distillation to produce several distillates and a residual oil that are then further refined. Aromatics including alkylated polycyclic aromatic compounds (PAC) are undesirable constituents of base oils because they are deleterious to product performance and are potentially carcinogenic. In modern base oil refining, aromatics are reduced by solvent extraction, catalytic hydrotreating, or hydrocracking. Chronic exposure to poorly refined base oils has the potential to cause skin cancer. A chronic mouse dermal bioassay has been the standard test for estimating carcinogenic potential of mineral oils. The level of alkylated 3–7–ring PAC in raw streams from the vacuum tower must be greatly reduced to render the base oil noncarcinogenic. The processes that can reduce PAC levels are known, but the operating conditions for the processing units (e.g., temperature, pressure, catalyst type, residence time in the unit, unit engineering design, etc.) needed to achieve adequate PAC reduction are refinery specific. Chronic dermal bioassays provide information about whether conditions applied can make a noncarcinogenic oil, but cannot be used to monitor current production for quality control or for conducting research or developing new processes since this test takes at least 78 weeks to conduct.
Three short-term, non-animal assays all involving extraction of oil with dimethylsulfoxide (DMSO) have been validated for predicting potential carcinogenic activity of petroleum base oils: a modified Ames assay of a DMSO extract, a gravimetric assay (IP 346) for wt. percent of oil extracted into DMSO, and a GC-FID assay measuring 3–7–ring PAC content in a DMSO extract of oil, expressed as percent of the oil. Extraction with DMSO concentrates PAC in a manner that mimics the extraction method used in the solvent refining of noncarcinogenic oils. The three assays are described, data demonstrating the validation of the assays are shown, and test results of currently manufactured base oils are summarized to illustrate the general lack of cancer hazard for the base oils now being manufactured.
Article
AlanJ.P. Dalton, H.A. Waldron, J.A.H. Waterhouse, Hermann Grunwald
Journal: The Lancet, 10 April 1976
Pas de résumé disponible.
Article
Randell, R.A.
Journal: The Lancet, 6 January 1990
Pas de résumé disponible.
On the prevention of mineral oil and tar dermatitis and cancer
Article
C.C. Twort, J.M. Twort
Journal: The Lancet, 10 February 1934
Pages 286-287
Pas de résumé disponible.Induction of cancer by cracked mineral oils
Article
Twort, C.C. --- Twort, J.M.
Journal: The Lancet ISSN: 01406736 Year: 1935Pages: 1226-1228
Fourni par: Elsevier
Pas de résumé disponible.
Nickel
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Nickel
Le nickel est un composé qui est présent dans l'environnement qu'à des concentrations très faibles. L'homme utilise le nickel pour différentes applications, la plus commune est l'utilisation du nickel comme composants de l'acier ou d'autres produits métalliques. On peut le trouver dans des produits à base de métaux comme les bijoux.
Références bibliographiques
Nickel-related cancer in welders
Article
Journal: Science of the Total Environment ISSN: 00489697 Year: 1994
Pages: 303-309
Fourni par: Elsevier
Résumé : During stainless steel (SS) welding, solid aerosols are generated from elemental compounds which are generally considered to be human carcinogens; i.e. compounds of hexavalent chromium (Cr vl) and nickel. Epidemiological studies
among groups of SS-welders have indicated that they may carry a higher risk of acquiring lung cancer than mild steel (MS) welders using the same welding techniques. This excess risk has been demonstrated in cohort as well as by casecontrol studies. The present evidence does not support the view that exposure to SS-welding fumes poses a hazard of cancer at any other site. Exposure to asbestos and smoking are generally major confounders in these studies. The number of SS-welders world-wide seems to be increasing, thus these findings may be of significance to SS-welders and to the welding industry. Despite the information on the possible cancer hazard among SS-welders, current epidemiological data on cancer incidence and mortality do not offer clear evidence to determine whether exposure to nickel or Cr w compounds constitutes the more important risk factor for lung cancer.
Occupational exposure to chromium and nickel in the 1980s in Finland
Article
Journal: The Science of The Total Environment ISSN: 00489697 Year: 1997
Pages: 91-101
Fourni par: Elsevier
Editeur: Elsevier
Résumé : Two large data bases accumulated from the 1980s at the Finnish Institute of Occupational Health, one with results on urinary chromium and nickel analyses and the other with results on total and hexavalent chromium and nickel, were compiled and analysed in order to clarify the occupational exposure during the 1980s, and to reveal possible trends in the exposure of workers in different jobs. The data were processed in three batches: years 1980–1982, 1983–1985 and 1986–1989. The median values of urinary chromium exceeded the biomonitoring action level, BAL, in metal workers, and the mean values exceeded the BAL in both metal workers and plasma cutters. Among all worker groups the median values of urinary chromium remained quite stable during the study period. The median values of urinary nickel concentration did not exceed the BAL in any worker group studied, but an increasing trend was observed among moulders. In the breathing zone of grinders, the median value of total or trivalent chromium exceeded the occupational exposure limit, OEL. The median of hexavalent chromium concentration in the breathing zone of metal sprayers and spray painters was higher than the OEL. No decreasing trend in exposure could be observed during the 10-year period in breathing zone air.
Respiratory cancer risks associated with low-level nickel exposure: an integrated assessment based on animal, epidemiological, and mechanistic data
Article
Journal: Regulatory Toxicology and Pharmacology ISSN: 02732300
Year: 2003
Pages: 173-190
Fourni par: Elsevier
Editeur: Academic Press
Résumé : Increased lung and nasal cancer risks have been reported in several cohorts of nickel refinery workers, but in more than 90% of the nickel-exposed workers that have been studied there is little, if any evidence of excess risk. This investigation utilizes human exposure measurements, animal data from cancer bioassays of three nickel compounds, and a mechanistic theory of nickel carcinogenesis to reconcile the disparities in lung cancer risk among nickel-exposed workers. Animal data and mechanistic theory suggest that the apparent absence of risk in workers with low nickel exposures is due to threshold-like responses in lung tumor incidence (oxidic nickel), tumor promotion (soluble nickel), and genetic damage (sulfidic nickel). When animal-based lung cancer dose-response functions for these compounds are extrapolated to humans, taking into account interspecies differences in deposition and clearance, differences in particle size distributions, and human work activity patterns, the predicted risks at occupational exposures are remarkably similar to those observed in nickel-exposed workers. This provides support for using the animal-based dose-response functions to estimate occupational exposure limits, which are found to be comparable to those in current use.
Nitrosoguanidines
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Nitrosoguanidines
C’est un produit instable qui réagit violemment avec l'eau. Il peut exploser en cas d'impact. C'est un produit hautement inflammable. L'hydrolyse alcaline libère des gaz toxiques et explosifs
Références bibliographiques
Rebamipide induces dendritic cell recruitment to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-exposed rat gastric mucosa based on IL-1@b upregulation
Article
Yamamichi, N. --- Oka, M. --- Inada, K.i. --- Konno-Shimizu, M. --- et al.
Journal: Biochemical and Biophysical Research Communications ISSN: 0006291X Year: 2012
Pages: 124-129
Fourni par: Elsevier
Résumé : Rebamipide is usually used for mucosal protection, healing of gastric ulcers, treatment of gastritis, etc., but its effects on gastric malignancy have not been elucidated. Using Lewis and Buffalo rat strains treated with peroral administration of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), we evaluated the effect of rebamipide on the induction of tumor-suppressive dendritic cells, which are known to be heterogeneous antigen-presenting cells of bone marrow origin and are critical for the initiation of primary T-cell responses. Using CD68 as a marker for dendritic cells, the stomach pyloric mucosae of Lewis and Buffalo rats were immunohistochemically analyzed in the presence or absence of rebamipide and MNNG. After a 14-day treatment of rebamipide alone, no significant change in number of CD68-expressing cells was detected in either rat strain. However, after concurrent exposure to MNNG for 14days, treatment with rebamipide slightly increased CD68-positive cells in the Lewis strain, and significantly increased them in the Buffalo strain. Analysis of two chemotactic factors of dendritic cells, IL-1@b and TNF-@a, in the gastric cancer cells showed that expression of IL-1@b, but not TNF-@a, was induced by rebamipide in a dose-dependent manner. A luciferase promoter assay using gastric SH-10-TC cells demonstrated that an element mediating rebamipide action exists in the IL-1@b gene promoter region. In conclusion, rebamipide has potential tumor-suppressive effects on gastric tumorigenesis via the recruitment of dendritic cells, based on the upregulation of the IL-1@b gene in gastric epithelial cells.
Advances in carcinogenesis: A historical perspective from observational studies to tumor genome sequencing and TP53 mutation spectrum analysis
Article
Soussi, T.
Journal: BBA - Reviews on Cancer ISSN: 0304419X Year: 2011Pages: 199-208
Fourni par: Elsevier
Résumé : Tumor sequencing projects have been initiated over the last decade with the promising goal of identifying novel cancer genes and potential therapeutic targets. One of the unexpected findings of these projects was the discovery that cancer genomes contain thousands of passenger mutations that are irrelevant to tumor development and are coselected by a small number of driver mutations that constitute the true selection power in cancer progression. Although often discarded and considered to be irrelevant, the value of passenger mutations should not be underestimated, as they are the most important markers of the exposure to various carcinogens and are essential to assess the etiology of individual tumors. Over the last century, the history of cancer epidemiology evolved in different stages and concepts from occupational observational studies beginning in the 18th century, in vitro and in vivo experimental analyses and cancer gene analyses, such as Ha-ras or TP53. Mutation spectra of passenger mutations from various types of cancers not only confirm the findings of molecular epidemiology analysis, but also reveal novel profiles that will extend this knowledge to single tumors in all types of cancer.
Nitrosourées (nitrosoureas)
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Nitrosourées (nitrosoureas)
C'est un cancérogène mutagène ettératogène dont la toxicité provient de ce qu'il transfère son groupe méthyle aux bases nucléiques des acides nucléiques.
C'était un précurseur traditionnel dans la synthèse du diazométhane, mais son usage à cette fin est à présent obsolète du fait de sa trop grande instabilité au-dessus de 20 °C et de sa sensibilité aux chocs.
Références bibliographiques
Nitrosoureas Inhibit the Stathmin-Mediated Migration and Invasion of Malignant Glioma Cells
Article
Liang Xing-Jie --- Choi Yong --- Sackett Dan L. --- Park John K.
Journal: Cancer research : the official organ of the American association for cancer research ISSN: 00085472 Year: 2008
Pages: 5267-5272
Fourni par: HighWire
Editeur: American Association for Cancer Research
Résumé: Malignant gliomas are the most common primary intrinsic brain tumors and are highly lethal. The widespread migration and invasion of neoplastic cells from the initial site of tumor formation into the surrounding brain render these lesions refractory to definitive surgical treatment. Stathmin, a microtubule-destabilizing protein that mediates cell cycle progression, can also regulate directed cell movement. Nitrosoureas, traditionally viewed as DNA alkylating agents, can also covalently modify proteins such as stathmin. We therefore sought to establish a role for stathmin in malignant glioma cell motility, migration, and invasion and determine the effects of nitrosoureas on these cell movement-related processes. Scratch wound-healing recovery, Boyden chamber migration, Matrigel invasion, and organotypic slice invasion assays were performed before and after the down-regulation of cellular stathmin levels and in the absence and presence of sublethal nitrosourea ([1-(2-chloroethyl)-3-cyclohexyl-l-nitrosourea]; CCNU) concentrations. We show that decreases in stathmin expression lead to significant decreases in malignant glioma cell motility, migration, and invasion. CCNU, at a concentration of 10 mmol/L, causes similar significant decreases, even in the absence of any effects on cell viability. The direct inhibition of stathmin by CCNU is likely a contributing factor. These findings suggest that the inhibition of stathmin expression and function may be useful in limiting the spread of malignant gliomas within the brain, and that nitrosoureas may have therapeutic benefits in addition to their antiproliferative effects. [Cancer Res 2008;68(13):5267-72]
IARC Monographs: Printing Processes and Printing Inks, Carbon Black and Some Nitro Compounds
Ebook
International Agency for research on Cancer (IARC), Volume 65
Editeur : IARC, Lyon, France, 1996
Document en ligne
http://monographs.iarc.fr/ENG/Monographs/vol65/mono65.pdf
L'oxyde de fer (iron oxide)
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L'oxyde de fer (iron oxide)
Egalement appelé oxyde ferrique, est le composé chimique de formule Fe2O3. C'est un oxyde paramagnétique stable du fer, dont une forme hydratée constitue la rouille. Il est de couleur ocre à rouille sous forme pulvérulente — ce qui donne notamment sa couleur à la planète Mars — mais grise à noire sous forme cristallisée. Il est l'un des trois oxydes principaux du fer, les deux autres étant l'oxyde de fer(II) FeO, plutôt rare, et l'oxyde de fer(II,III) Fe3O4 (parfois écrit FeO·Fe2O3), qu'on trouve naturellement dans la magnétite.
Références bibliographiques
Multifunctional poly(aspartic acid) nanoparticles containing iron oxide nanocrystals and doxorubicin for simultaneous cancer diagnosis and therapy
Article
Yang, H.M. --- Oh, B.C. --- Kim, J.H. --- Ahn, T. --- et al.
Journal: Colloids and Surfaces A: Physicochemical and Engineering Aspects ISSN: 09277757 Year: 2011
Pages: 208-215
Fourni par: Elsevier
Résumé : Multifunctional poly(aspartic acid) nanoparticles for simultaneous cancer diagnosis and therapy were developed. First, iron oxide nanocrystals were loaded in poly(aspartic acid) nanoparticles through an emulsion method using octadecyl grafted poly(aspartic acid). The influence of the organic solvent, used to disperse the hydrophobic iron oxide nanocrystals, on the size and loading efficiency of iron oxide nanocrystals loaded poly(aspartic acid) nanoparticles was investigated. Next, an anticancer drug, doxorubicin (DOX), was incorporated in the magnetic poly(aspartic acid) nanoparticles (MPAN). The presence of iron oxide nanocrystals in the poly(aspartic acid) nanoparticles and their size distribution were confirmed by transmission electron microscopy (TEM), Fourier transform infrared spectroscopy (FT-IR), and dynamic light scattering (DLS), respectively. The drug release behavior was also observed for 3 days. From the results of T2 weighted MR imaging and MTT assays, the DOX loaded MPAN showed high T2 relaxivity coefficients and high cytotoxicity for cancer cells.
Poussières de bois (Wood dust)
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Poussières de bois (Wood dust)
Les poussières de bois sont des agents irritants et allergènes associés à certaines pathologies respiratoires (asthme, fibrose pulmonaire) et cutanées (eczéma). Il existe également un lien direct entre l’exposition répétée aux poussières de bois et la survenue de cancers des fosses nasales et de l’ethmoïde, deux types de cancers rares et graves. Ces deux affections liées à l’inhalation de poussières de bois sont d’ailleurs reconnues comme maladies professionnelles.
Références bibliographiques
Cancer and wood-related occupational exposure in the Amazon region of Brazil
Article
Helena Arias Bahia, S. --- Echenique Mattos, I. --- Koifman, S.
Journal: Environmental Research ISSN: 00139351 Year: 2005
Pages: 132-140
Fourni par: Elsevier
Editeur: Academic Press
Résumé : The occurrence of neoplasms, particularly nasal cavities and paranasal sinus tumors, has been associated with exposure to wood dust. The wood industry occupies an important place in the State of Para, Brazil, where are located 90% of all the wood-related companies in the Brazilian Amazon market as a whole. The aim of this study was an exploratory analysis of cancer occurrence in woodworkers in the State of Para. The proportional cancer incidence ratio (PCIR) was calculated for a group of 138 male woodworkers 20 years or older with a histological diagnosis of neoplasm treated at the Ofir Loyola Cancer Hospital in the state capital of Belem from 1991 to 1999. The cancer mortality odds ratio (CMOR) was also calculated in order to compare the cancer mortality among men 20 years or older residing in the State of Para whose occupations involved wood exposure with that of men of the same age and place of residence but with different occupations. High and statistically significant PCIRs were observed for tumors of the oral cavity/pharynx, 2.44 (1.44-3.85), and stomach, 3.57 (2.41-5.10), in comparison to the population of Goiania as well as in comparison to the population of Porto Alegre (oral cavity/pharynx, 1.97 (1.17-3.12), stomach, 3.12 (2.11-4.47)). We also observed a high and statistically significant PCIR for Hodgkin's disease, 5.30 (1.09-15.47), in comparison to the population of Goiania. A CMOR of 8.86 (5.26-14.83) was observed for liver cancer. CMORs greater than 1 but not statistically significant were observed for neoplasms of the larynx. In agreement with the literature, woodworkers in Para presented a high cancer incidence in specific anatomical sites. The results highlight the need for further epidemiological investigation to better evaluate this occupational exposure in the Amazon region.
Wood dust-related mutational profile of TP53 in intestinal-type sinonasal adenocarcinoma
Article
Perez-Escuredo, J. --- Martinez, J.G. --- Vivanco, B. --- Marcos, C.A. --- et al.
Journal: Human Pathology ISSN: 00468177 Year: 2012
Pages: 1894-1901
Fourni par: Elsevier
Résumé : Intestinal-type sinonasal adenocarcinoma represents 8% to 25% of all malignant sinonasal cancer and is etiologically related to occupational exposure to wood dust. Despite its clear etiology, the mechanisms behind the carcinogenic effects of wood dust are unclear. Because it is known that carcinogens can leave specific mutational fingerprints, we aimed to analyze the spectrum of TP53 mutations and to relate the findings to the wood dust etiology of the patients. Forty-four primary tumors were examined for TP53 mutations by direct sequencing. In addition, p53 protein expression was analyzed by immunohistochemistry using a tissue microarray consisting of 92 tumors. We report a frequency of 41% (18/44) TP53 mutations and 72% (66/92) p53 immunopositivity in intestinal-type sinonasal adenocarcinoma, significantly related to wood dust, but not to tobacco etiology. G->A transition (50%, 9/18 cases) was the most common alteration detected, almost exclusively found in nonsmokers, whereas G->T (27%, 5/18 cases) was detected in smokers only. These data point to wood dust exposure as the causal factor in the mutagenesis of TP53, possibly caused by reactive nitrogen species generated through a chronic inflammatory process.
Occupational exposure to wood dust and formaldehyde and risk of nasal, nasopharyngeal, and lung cancer among Finnish men
Article
Siew SS, Kauppinen T, Heikkila P, Pukkala E
Journal: Cancer Management and Research ISSN: 11791322 Year: 2012
Pages: 223-232
Fourni par: DOAJ
Editeur: Dove Press
Réumé : Sie Sie Siew,1,2 Timo Kauppinen,1 Pentti Kyyrönen,3 Pirjo Heikkilä,1 Eero Pukkala2,31Finnish Institute of Occupational Health, Helsinki, Finland; 2School of Health Sciences, University of Tampere, Tampere, Finland; 3Finnish Cancer Registry, Institute for Statistical and Epidemiological Cancer Research, Helsinki, FinlandAbstract: Controversy exists over whether or not occupational inhalation exposure to wood dust and/or formaldehyde increases risk for respiratory cancers. The objective of this study was to examine the risk of nasal, nasopharyngeal, and lung cancer in relation to occupational exposure to wood dust and formaldehyde among Finnish men. The cohort of all Finnish men born between the years 1906 and 1945 and in employment during 1970 was followed up through the Finnish Cancer Registry for cases of cancers of the nose (n = 292), nasopharynx (n = 149), and lung (n = 30,137) during the period 1971–1995. The subjects' occupations, as recorded in the population census in 1970, were converted to estimates of exposure to wood dust, formaldehyde, asbestos, and silica dust through the Finnish job-exposure matrix. Cumulative exposure (CE) was calculated based on the prevalence, average level, and estimated duration of exposure. The relative risk (RR) estimates for the CE categories of wood dust and formaldehyde were defined by Poisson regression, with adjustments made for smoking, socioeconomic status, and exposure to asbestos and/or silica dust. Men exposed to wood dust had a significant excess risk of nasal cancer overall (RR, 1.59; 95% confidence interval [CI], 1.06–2.38), and specifically nasal squamous cell carcinoma (RR, 1.98; 95% CI, 1.19–3.31). Workers exposed to formaldehyde had an RR of 1.18 (95% CI, 1.12–1.25) for lung cancer. There was no indication that CE to wood dust or formaldehyde would increase the risk of nasopharyngeal cancer. Occupational exposure to wood dust appeared to increase the risk of nasal cancer but not of nasopharyngeal or lung cancer. The slight excess risk of lung cancer observed for exposure to formaldehyde may be the result of residual confounding from smoking. In summary, this study provides further evidence that exposure to wood dust in a variety of occupations may increase the risk of nasal cancer.Keywords: job-exposure matrix, inhalation exposure, cumulative exposure, cancer risk
IARC Monographs: Wood Dust and Formaldehyde
Ebook
International Agency for research on Cancer (IARC), Volume 62
Editeur : IARC, Lyon, France, 1995
Document en ligne
Rayonnements ionisants (ionizing radiation)
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Rayonnements ionisants (ionizing radiation)
La radioactivité est un phénomène naturel lié à l’instabilité de certains atomes qui composent la matière. Ces atomes instables (les radioéléments) émettent des rayonnements qui, en interagissant avec la matière, peuvent enlever un ou plusieurs électrons à ses atomes. Ces rayonnements sont dits ionisants.
La radioactivité peut provenir de substances radioactives naturelles (uranium, radium, radon) ou artificielles (californium, américium, plutonium). Différents dispositifs et installations (accélérateurs de particules, générateurs électriques…) peuvent également émettre des rayonnements ionisants.
Références bibliographiques
Radiation exposure and image quality in X-Ray diagnostic radiology: physical principles and clinical applications
Monographie
H. Aichinger, J. Dierker, S. Joite-Barfus, M. Säbel
Editeur: Springer, Berlin, 2004
Cote: 616.075/AIC
Disponible à la bibliotheque de l’IMIST
Cancer de la thyroïde après exposition aux rayonnements ionisants
Article
M. Schlumberger, S. Chevillard, K. Ory, C. Dupuy, B. Le Guen, F. de Vathaire
Journal : Cancer/Radiothérapie, August 2011,
Pages 394-399
Résumé : L’exposition aux radiations ionisantes pendant l’enfance augmente le risque de cancer de la thyroïde. Les mêmes facteurs de risque sont mis en évidence pour l’irradiation externe et l’irradiation interne par les iodes radioactifs. En cas de contamination radioactive, l’administration d’iodure de potassium peut prévenir l’irradiation de la thyroïde.Combined action of celecoxib and ionizing radiation in prostate cancer cells is independent of pro-apoptotic Bax
Article
Handrick, R. --- Ganswindt, U. --- Faltin, H. --- Goecke, B. --- et al.
Journal: Radiotherapy and Oncology ISSN: 01678140 Year: 2009
Pages: 413-421
Fourni par: Elsevier
Editeur: Elsevier
Résumé: Background and purpose: The cyclooxygenase-2-inhibitor celecoxib has been shown to inhibit cell growth and to reduce prostatic intraepithelial neoplasia in mice. The drug was suggested to increase efficacy of ionizing radiation. However, extent and mechanisms of the suggested benefit of celecoxib on the radiation response are still unclear. The aim of the present study was to analyze cytotoxic efficacy of celecoxib in combination with irradiation on human prostate cancer cell lines and to define the importance of pro-apoptotic Bax in this process. Materials and methods: Induction of apoptosis and global and clonogenic cell survival upon irradation- (2-10Gy), celecoxib- (10-75@mM) or combined treatment were evaluated in prostate cancer cells by fluorescence microscopy, WST-1 assay and standard colony formation assays. Results: Celecoxib <25@mM caused morphological changes and growth inhibition without substantial apoptosis or radiosensitization in terms of decreased clonogenic cell survival. In contrast, celecoxib >=25@mM increased radiation-induced cell death and clonogenic kill. While radiation-induced clonogenic death was increased in the presence of Bax, effects of celecoxib or combined treatment were Bax independent. Conclusions: Our findings reveal Bax-independent beneficial effects of celecoxib on radiation-induced apoptosis and eradication of clonogenic prostate cancer cells in vitro providing a rationale for clinical evaluation of high-dose celecoxib in combination with irradiation in prostate cancer patients.
IARC Monographs: Ionizing Radiation, Part 1: X- and Gamma (g)-Radiation, and Neutrons
Ebook
International Agency for research on Cancer (IARC), Volume 75
Editeur : IARC, Lyon, France, 2000
Document en ligne
Silice (Silica)
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Silice (Silica)
La silice existe à l’état libre sous forme cristalline ou amorphe, et à l’état combiné sous forme de silicates. Elle se trouve dans les produits en brique et en béton, dans les pierres, les roches et les abrasifs. La poussière est dégagée de ces matières par coupage à sec, broyage, dégarnissage, projection et balayage.
Les travailleurs qui respirent la poussière de silice cristalline présentent un risque accru de développement de la silicose (une maladie respiratoire qui affecte les poumons), la tuberculose et le cancer des poumons.
Références bibliographiques
Pooled Exposure-Response Analyses and Risk Assessment for Lung Cancer in 10 Cohorts of Silica-Exposed Workers: An IARC Multicentre Study
Article
Kyle Steenland --- Andrea Mannetje --- Paolo Boffetta --- Leslie Stayner --- et al.
Journal: Cancer Causes & Control ISSN: 09575243 Year: 2001
Pages: 773-784
Fourni par: JSTOR
Editeur: Kluwer Academic Publishers
Résumé:
Objectives: Silica is one of the most common occupational exposures worldwide. In 1997 the International Agency for Research on Cancer (IARC) classified inhaled crystalline silica as a human carcinogen (group 1), but acknowledged limitations in the epidemiologic data, including inconsistencies across studies and the lack of extensive exposure-response data. We have conducted a pooled exposure-response analysis of 10 silica-exposed cohorts to investigate lung cancer.
Methods: The pooled cohort included 65,980 workers (44,160 miners, 21,820 nominees), and 1072 lung cancer deaths (663 miners, 409 nonminers). Follow-up has been extended for five of these cohorts beyond published data. Quantitative exposure estimates by job and calendar time were adopted, modified, or developed to permit common analyses by respirable silica (mg/m3) across cohorts.
Results: The log of cumulative exposure, with a 15-year lag, was a strong predictor of lung cancer (p = 0.0001), with consistency across studies (test for heterogeneity, p = 0.34). Results for the log of cumulative exposure were consistent between underground mines and other facilities. Categorical analyses by quintile of cumulative exposure resulted in a monotonic trend with odds ratios of 1.0, 1.0, 1.3, 1.5, 1.6. Analyses using a spline curve also showed a monotonic increase in risk with increasing exposure. The estimated excess lifetime risk (through age 75) of lung cancer for a worker exposed from age 20 to 65 at 0.1 mg/m3 respirable crystalline silica (the permissible level in many countries) was 1.1-1.7%, above background risks of 3-6%. Conclusions: Our results support the decision by the IARC to classify inhaled silica in occupational settings as a carcinogen, and suggest that the current exposure limits in many countries may be inadequate. These data represent the first quantitative exposure-response analysis and risk assessment for silica using data from multiple studies.
Lung Cancer Risk among Refractory Brick Workers Exposed to Crystalline Silica: A Retrospective Cohort Study
Article
Franco Merlo -- Massimo Costantini -- Giorgio Reggiardo -- Marcello Ceppi -- et al.
Journal: Epidemiology ISSN: 10443983 Year: 1991Pages: 299-305
Fourni par: JSTOR
Publisher: Blackwell Scientific Publications, Inc. and Epidemiol
Résumé: We conducted a retrospective cohort study among 1,022 refractory brick workers exposed to crystalline silica. Mortality from lung cancer (SMR = 1.77) and respiratory diseases (SMR = 3.15) was elevated in workers first employed ≤ 1957 who are likely to have shared the highest exposure to crystalline silica. Workers with at least 19 years of cumulative employment in the plant experienced particularly increased risks for lung cancer (SMR = 2.01) and respiratory diseases (SMR = 3.89). Relative mortality from these specific causes increased with years since first employment (that is, first exposure) and decreased with age at first employment. Indirect adjustment for smoking habits and the lack of excess mortality from cardiovascular diseases and emphysema indicated little effect of smoking on the increased risks for lung cancer and respiratory diseases.
Respirable Crystalline Silica (RCS) emissions from industrial plants - Results from measurement programmes in Germany
Article
Ehrlich, C. --- Noll, G. --- Wusterhausen, E. --- Kalkoff, W.D. --- et al.
Journal: Atmospheric Environment ISSN: 13522310 Year: 2013
Pages: 278-285
Fourni par: Elsevier
Résumé : Numerous research articles dealing with Respirable Crystalline Silica (RCS) in occupational health because epidemiological studies reveal an association between RCS-dust and the development of silicosis as well as an increased probability of developing lung cancer. Research activities about RCS in ambient air are known from US-measurements. However there is a lack of knowledge regarding RCS-emissions in several industrial sectors. Industrial sources of crystalline silica include construction, foundries, glass manufacturing, abrasive blasting or any industrial or commercial use of silica sand, and mining and rock crushing operations. This paper describes a RCS-emission measurement method for stack gases and report results from the German RCS-emission measurement programmes which were used to identify installations and types of industries with the highest concentration levels of RCS in stack gases. A two-stage cascade impactor was used for the measurements which separate particles into the following size fractions: >10 @mm, 10-4 @mm und <4 @mm of aerodynamic diameter. The measurements were carried out according to international sampling standards. The size of crystalline silica particles of most concern are those respirable particles that are smaller than four microns (millionths of a metre), also called particulate matter 4 (PM4). The analytical procedure of determining crystalline silica in emission samples (in the fraction below 4 @mm) consists of using x-ray diffraction and infrared spectroscopy methods which are the same methods as used in the field of occupational health. A total of 37 emission measurement campaigns were assessed (112 RCS-samples in nine industrial sectors). The investigated plants are located in different German states such as Bavaria, North Rhine Westphalia, Baden-Wuerttemberg, Rhineland-Palatinate and Saxony-Anhalt. The results of the measurements show that most of the investigated plants can achieve compliance with the newly developed German emission limit value (ELV) of 1 mg m-3. The ELV is expressed as the concentration of RCS in stack emissions. According to the German emission minimising principle and the precautionary principle it is assumed that by complying with the RCS-ELV there is no ambient air health risk for people living these plants. In the case of increased total dust concentration in the stack gas (more than 20 mg m-3) combined with increased percentage of crystalline silica in PM4 dust, a violation of the above mentioned ELV is more likely. This applies mostly to installations in the silica sand processing industry. To comply with the ELV of 1 mg m-3, efficient emission control technology should be implemented and should be well maintained.
IARC Monographs: Silica, Some Silicates, Coal Dust and para-Aramid Fibrils
Ebook
International Agency for research on Cancer (IARC), Volume 68
Editeur : IARC, Lyon, France, 1997
Document en ligne
Sitographie
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Sitographie
L’ALSC (l’Association Lalla Salma de lutte contre le cancer)
CIRC (Centre international de recherche sur le cancer)
INRS (Institut National de Recherche et de Sécurité pour la Prévention des Accidents du travail et des Maladies professionnelles)
Classification du CIRC des agents cancérogènes
Tableau des maladies professionnelles : guide d’accès et commentaires (INRS)
Congrès Mondial sur le Cancer (Melbourne, 2014)
CONAMET (Collège National des Médecins du Travail)
La base de données CAREX (CARcinogen Exposure)
[1] Cancers d’origine professionnelle : Comment les repérer, les déclarer, les faire reconnaître, les faire indemniser…. La ligue Nationale contre le cancer, Décembre 2008.
