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AVALIAÇÃO DA EXPOSIÇÃO PROFISSIONAL AO FORMALDEÍDO E XILENO NO SERVIÇO DE ANATOMIA PATOLÓGICA DOS HOSPITAIS DA UNIVERSIDADE DE COIMBRA
... In hospital pathology and anatomical laboratories, formaldehyde is used as a fixative or preservative, in which the biological material is dipped in order to conserve it, and it is also considered a good disinfectant that does not cause excessive hardening of the tissues. Formaldehyde is an excellent medium for the preservation and storage of biopsy and surgical specimens [7]. ...
... In civil construction, formaldehyde is employed in the form of urea-methanal coating foams, which are among the most widely used systems for coating buildings [4,7]. ...
A evolução do conhecimento humano, referente ao estudo da fauna terrestre, demanda ações éticas que envolvem, entre outros, a preservação de animais e suas partes em coleções biológicas e o desenvolvimento de tecnologias inovadoras para tais procedimentos. Nesse contexto, este trabalho objetivou mapear os principais pedidos de patentes relacionadas com a preservação de animais e suas partes e identificar quais tecnologias envolvem acervos museológicos. Metodologicamente, combinaram-se pesquisas acadêmicas, no Portal de Periódicos da Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), e patentárias, na base de dados Espacenet, no período de 2000 a 2018. Os resultados evidenciaram tecnologias modernas, cujos maiores depositantes são: Estados Unidos da América (EUA), China (CN) e a própria Organização Mundial de Propriedade Intelectual (WIPO). As tecnologias envolvidas na preservação de animais e suas partes apresentaram as classificações cooperativas de patentes: C12N1/14, A01N1/02, A61K38/00, A01N3/00, A61K38/45, A23L3/3463 e A61K31/4178; e aquelas com enfoque em preservação de acervo museológico, A01N1/00 e A01N1/02. Concluiu-se que esta é uma temática ampla, com potencial de desenvolvimento tecnológico, porém ainda pouco explorada no mundo.
p>O presente artigo tem como objetivo mapear os principais pedidos de patentes depositados no mundo, relacionados com às tecnologias de preservação de animais e suas partes e que foram requeridos por universidades através da prospecção tecnológica no Espacenet. Este tema é relevante porque permite extrair informações das patentes, permitindo se identificar novas possibilidades e novos conhecimentos. Os resultados desta pesquisa demonstraram que os maiores depositantes são os que o fazem pela WO, seguido dos US e CN. As principais patentes da WO envolvem a preservação da função mitocondrial, dos US envolvem Cicatrização e reparo de feridas e Métodos de preservação de órgãos. As patentes da CN envolvem métodos para preservação de materiais no estado amorfo; Preservação da função mitocondrial; Preservação de tecidos; Preservação dos órgãos e método de preservação a baixa temperatura de acordo com os Códigos Internacionais C12N1/14, A01N1/02, A61K38/00, A01N3/00, A61K38/45, A23L3/3463, A61K31/4178.
Palavras-chave: Patente. Preservação. Prospecção tecnológica.</p
Resumo Pala a s-Ci~av~: Formaldeido, Compostos Orgánicos Voláteis, Ventilação, Qualidade do Ar Interior, Serviços de Anatomia Patológica.-INTRODUÇÃO O efeito mais facilmente detectável da exposição aos vapores de Formaldeído é o seu odor desagradável e o seu efeito irritante das mucosas dos olhos e aparelho respiratório superior. Os limites de detecção estão entre os valores de 0,1-0,3 mglm3. No entanto, alguns indi víduos podem sentir o cheiro de Formaldeido a concen trações inferiores (WHO, 1991). O contacto directo com soluções de Formaldeido a concentrações de 1 %-2% pode causar irritações da pele em alguns individuos. De uma forma geral, solu ções com concentrações entre 5% e 25% são irritantes, e com concentrações superiores a 25% são corrosivas. As exposições de longa duração da pele podem levar a dermatoses alérgicas por contacto. Esta situação foi demonstrada apenas para as soluções de Formaldeído e não para os vapores (WHO, 1991). Foi demonstrado através de estudos com células humanas (ri vitro que o Formaldeído interfere com a repa ração do ADN ÇWHO, 1991). Paralelamente, demons trou-se que a exposição a vapores induzida a duas espécies de ratos levou a uma significante incidência de carcinomas nas cavidades nasais ÇWHO, 1991). A Environmental Protection Agency (EPA) classificou o Formaldeido como agente cancerígeno no Grupo El, isto é, provável carcinogénico de médio risco (Crespo & Lourenço, 2000). Por seu lado, a lei portuguesa, segundo a Norma Portuguesa NP-1796 (1988), classi fica o Formaldeído como agente suspeito de ter efeito oncogénico (Crespo & Lourenço, 2000). No entanto a proposta de actualização desta norma aponta para o mesmo em relação à sua carcinogenicidade e para uma concentração de 0,3 ppm, que nunca deve ser excedida para qualquer período de exposição. Num estudo efectuado por Cain et aL (1986), um grupo de 33 individuos autoavaliou-se relativamente à irritação e detecção do cheiro quando expostos ao formaldeído a concentrações entre 0,3 e 2,4 mg/m3 (0,25 e 2 ppm) durante 29 minutos. A partir deste estudo verificou-se que a irritação sensorial aumentou com o tempo a baixas concentrações e diminuiu com o tempo a altas concentrações. Este efeito ocorreu a nível do nariz, olhos e garganta, nos quais a sensibilidade foi seme lhante. Weber-Tschoop et aI. (1977) e Bender et aI. (1983) mostraram que ocorre uma adaptação sensorial em exposições de longa duração. Em 1983, um grupo de estudo da OMS estudou o Formaldeido procurando encontrar um limite de expo sição ocupacional com base nos seus efeitos para a saúde. Desta investigação foi indicado um limite de exposição ocupacional de curto prazo (15 minutos) para uma concentração de Formaldeído no ar de 1 mg/m3. Foi também indicado como limite a concentração de Pretendeu-se com a realização deste estudo conhecer a Quali dade do Ar Interior dos Serviços de Anatomia Patológica, mais especificamente, ao nivel das suas Sala de Entradas. Sabe-se que nestes locais ocorre a utilização e manuseamento de produtos químicos potencialmente tóxicos e carcinogéneos, nomeadamente do formol, que é um fixador pouco dispendioso e bastante eficiente, o que implica a sua eleição para os trabalhos de rotina em anatomia patológica. A solução de trabalho habitual é constituida essencialmente por formaldeido em forma gasosa e água. Foi demonstrado através de estudos com células humanas in vitro que o Formaldeido interfere com a reparação do AON. Paralelamente, demonstrou-se que a exposição a vapores indu zida a duas espécies de ratos levou a uma significante incidência de carcinomas nas cavidades nasais. considerando as actividades que se desenvolvem nos referidos locais de trabalho e a utilização dada ao formol, julga-se que se não existirem as condições de ventilação adequadas e procedi mentos de trabalho correctos os individuos que ai desenvolvem a sua actividade profissional acabarão por estar expostos a vapores de formaldeido. Procurando determinar os valores de exposição dos trabalha dores, realizou-se a medição da concentração de compostos Orgánicos Voláteis (cOVs) em três momentos específicos exem plificativos das principais actividades que se desenvolvem na Sala de Entradas. Optou-se pela medição de cov's porque o formaldeido está enquadrado neste grupo de poluentes (U.S. consumer Product Safety commission. 1997) e porque, no local, e no momento da medição, não se utilizava mais nenhum produto quimico de características semelhantes. As medições foram efectuadas em 5 Hospitais da Grande Lisboa. Na maior parte das situações investigadas foram encontradas concentrações elevadas de cov's (até 50,6 ppm) que se julga puderem estar relacionadas com as condições de ventilação existentes nas salas de entradas que foram alvo do nosso estudo. No momento da realização das medições encontraram-se outras situações que devem também ser objecto de melhoramento e, para as quais, se tecem também algumas recomendações.
A abordagem das relações trabalho/saúde(doença) implica um conhecimento adequado das variáveis (factores) profis-sionais em jogo e das respectivas repercussões, positivas ou negativas, sobre a saúde dos trabalhadores. Tal conheci-mento adquire-se mediante análise das (sempre complexas) situações reais de trabalho. As substâncias químicas constituem o mais extenso dos grupos de factores de risco de natureza profissional. O número de substâncias químicas a que se encontram expostos os trabalhadores aumenta dia a dia, sendo actual-mente conhecidas mais de 100 000. Os autores procedem à revisão de alguns conceitos que, numa perspectiva de prevenção, são essenciais para o diag-nóstico das situações profissionais de risco. O trabalho — enquanto factor imprescindível ao desenvolvimento técnico, económico e social — tem representado um papel de transcendente importância ao longo de toda a história da humanidade. Actualmente, e de acordo com a definição preconi-zada pela Organização Mundial da Saúde (OMS, 1995), a chamada «força laboral mundial» abrange cerca de 45% da população do universo ou, numa outra perspectiva, aproximadamente 58% dos indiví-duos com idade superior a 10 anos. Trata-se de um avultado contingente de pessoas que dedicam uma parte apreciável da sua vida adulta (≅ 1/3) ao desem-penho de actividades profissionais nem sempre isen-tas de perigo e, muitas vezes, pouco gratificantes. Por isso, a salubridade dos ambientes de trabalho constitui um elemento relevante em matéria de saúde e bem-estar das populações. E não deve ser entendida como um mero problema de gestão de riscos profis-sionais confinado ao(s) local(is) de trabalho. Deve, isso sim — e de modo bem menos redutor —, ser equacionada na perspectiva (globalizante e integra-dora) que caracteriza as acções de promoção da saúde. A abordagem dos problemas do âmbito da saúde ocupacional é necessariamente influenciada por diversos elementos de índole contextual, entre os quais se destacam: a estrutura macroeconómica; o grau de desenvolvimento (sócio-económico e cultural); o nível (e o modelo) de industrialização; o modelo organizativo e as características dominantes dos serviços e da prestação de «cuidados» de segu-rança, higiene e saúde nos locais de trabalho. A estratégia mundial «Saúde ocupacional para todos», definida pela Organização Mundial da Saúde (OMS, 1995) (Beijing, China) em 1994, inclui — a par do enunciado das correspondentes acções, de
Estudo da exposição profissional a formaldeído em laboratórios hospitalares de Anatomia Patológica 06 Resumo (a) Professora Adjunta da Escola Superior de Tecnologia da Saúde de Lisboa / Instituto Politécnico de Lisboa (b) Professor Associado da Escola Nacional de Saúde Pública / Universidade Nova de Lisboa A exposição a formaldeído é reconhecidamente um dos mais importantes factores de risco pre-sente nos laboratórios hospitalares de anatomia patológica. Neste contexto ocupacional o for-maldeído é utilizado em solução, designada comummente por formol. Trata-se de uma solução comercial de formaldeído, normalmente diluída a 10%, sendo pouco onerosa e, por esse motivo, a eleita para os trabalhos de rotina em anatomia patológica. A solução é utilizada como fixador e conservante do material biológico, pelo que as peças anatómicas a serem processadas são pre-viamente impregnadas. No que concerne aos efeitos cancerígenos a primeira avaliação efectuada pela International Agen-cy for Research on Cancer data de 1981, actualizada em 1982, 1987, 1995 e 2004, considerando-o como um agente cancerígeno do grupo 2A (provavelmente carcinogénico). No entanto, a mais recente avaliação, em 2006, considera o formaldeído no Grupo 1 (agente carcinogénico) com base na evidência de que a exposição a este agente é susceptível de causar cancro nasofaríngeo em humanos. Constituiu objectivo principal do estudo desenvolvido caracterizar a exposição profissional a for-maldeído em laboratórios hospitalares de anatomia patológica.
Introduction – The widespread use of formaldehyde is mainly due to its high reactivity, lack of colour, purity in a commercial format, and also low cost. These characteristics put it among the 25 most abundant chemicals produced in the world. IARC, since 2006, classify formaldehyde in Group 1 (carcinogen) based on evidence that exposure to formaldehyde can cause nasopharyngeal cancer in humans. It was developed an explo ratory study with the purpose of obtaining information about the occupational exposure reality to formaldehyde in Portugal. Methodology – Several formaldehyde concentrations measurements were performed in 7 industrial units and in an anatomy and pathology laboratory. Environmental measurements were performed using Photo Ionization Detection (PID) equipment. Results – The anatomy and pathology laboratory have the highest concentration value recorded and larger than reference limit (0.3 ppm). Also, in 2 of 7 industrial units studied were recorded maximum concentration values above 0,3 ppm. Conclusions – The anatomy and pathology laboratory was the occupational setting where formaldehyde occupational exposure was more critics. The methodology used for environ mental monitoring seems appropriate to the study objectives and related to the chemical agent mode of action. RESUMO: Introdução – O formaldeído está enquadrado entre as 25 substâncias químicas mais abundantemente produzidas no mundo devendose essencialmente à sua elevada reactividade, ausência de cor, à sua pureza no formato comercial e, ainda, ao seu baixo custo. A IARC, desde 2006, classifica o formaldeído no Grupo 1 (agente carcinogénico) com base na evidência de que a exposição a formaldeído é susceptível de causar cancro nasofaríngeo em humanos. Desenvolveuse um estudo de natureza exploratóra com o objectivo essencial de obter informação sobre a realidade da exposição profissional a formaldeído em Portugal. Igualmente, pretendeuse conhecer a adequabilidade de uma nova metodologia de monitorização ambiental ao estudo da exposição ocupacional a formaldeído. Metodologia – Realizaramse várias medições das concentrações de formal deído em 7 unidades industriais e num laboratório hospitalar de anatomia patológica. As avaliações ambientais foram concretizadas com recurso a um equipamento de leitura directa que realiza a medição por Photo Ionization Detection (PID), com uma lâmpada de 11,7 eV. Resultados – No laboratório de anatomia patológica estudado foram registados valores de concentração superiores ao valorlimite de referência (0,3 ppm). Igualmente, em 2 das 7 unidades industriais estudadas foram registados valores de concentração máxima superiores a 0,3 ppm. Conclusões – Em consonância com outros estudos, o laboratório de anatomia patológica apresentouse como o contexto ocupacional onde a exposição a formaldeído apresenta as concentrações mais elevadas. A metodologia adoptada para monitorização ambiental parece adequarse aos objectivos da presente investigação e relacionada com o modo de actuação do agente químico em estudo. Palavraschave: formaldeído, exposição ocupacional, laboratório de anatomia patológica, monitorização ambiental
The 1980 report that inhaled formaldehyde induced nasal squamous cell carcinomas in rats had a significant societal impact and resulted in extensive research in the fields of rodent nasal pathology and human cancer risk assessment. This article presents an overview of the evolution of these events. It is concluded that the nasal passages of humans and rats are fundamentally identical biological target organs. Nevertheless, in the case of human health risk assessment, minor differences between these species may be critically important. Special attention should be paid to interspecies differences in nasal dosimetry and local metabolism; thus, chemical toxicity data derived from rats require careful interpretation when used for human risk assessments. In the case of formaldehyde, it is recommended that low-concentration (< or = 2 ppm airborne exposure) extrapolation, where no tissue damage is observed, be uncoupled from the responses at high concentrations (> or = 6 ppm), where epithelial degeneration, regenerative cell replication, and inflammation appear to be essential driving forces in formaldehyde carcinogenesis. The presence of treatment-related nasal lesions in rats following exposure to chemicals should always be treated as an indication of a potential human health risk, whether exposure is by the inhalation, oral, or dermal route.
Exposure assessment, the first step in risk assessment, has traditionally been performed for a variety of purposes. These include compliance determinations; management of specific programs that are implemented by comparison with an occupational exposure limit (such as medical surveillance, training, and respiratory protection programs); task/source investigations for determination of exposure control strategies; epidemiologic studies; worker compensation/toxic tort cases; health complaint or problem investigations; risk assessment and management; and evaluation of future changes in the workplace (e.g., introduction of a new chemical). Each purpose requires slightly different approaches, but there are also many similarities. The goal of this paper is to identify a general approach to assessing exposures that can be used for all purposes with only slight modifications. Five components of exposure assessments are identified: collection of data, identification of the hazard, selection of exposure metrics, definition of exposure groups and estimation of the exposures. The characteristics of these components for each type of assessment are discussed. From this review, it is clear that there is substantial overlap across the types of assessment. A single exposure assessment program is suggested that encompasses all the needs of these assessments and incorporates assessment of exposures for an entire workforce at a site at minimal cost by using prediction models and validation with measurements.
Although many questions remain unanswered, the general principle of the sequence of events leading to cancer after exposure to genotoxic carcinogens has become increasingly clear. This helps to understand the parameters that influence the shape of the dose-effect curve for carcinogenesis, including metabolic activation and inactivation of carcinogens, DNA repair, cell cycle control, apoptosis, and control by the immune system. A linear dose-response relationship with no observable threshold seems to be a conservative but adequate description for the carcinogenic activity of many genotoxic carcinogens, such as aflatoxin B1, the tobacco-specific nitrosoketone NNK, and probably N,N-diethylnitrosamine. However, extrapolation models connecting the high-level risk to the zero intercept have clearly resulted in overestimations of risk. Vinyl acetate is an example that is discussed extensively in this review. At extremely high and toxic doses, vinyl acetate is carcinogenic in rats and mice and causes chromosomal aberrations. In tissues of contact, vinyl acetate is converted to acetic acid and acetaldehyde. Only when threshold levels are achieved do critical steps in the mechanism ultimately leading to cancer become active, namely pH reduction in exposed cells of more than 0.15 units leading to cytotoxicity, damage to DNA, and regenerative proliferation. Consistent with the known exposure to endogenous acetic acid and acetaldehyde, tissues sustain a certain level of exposure without adverse effects. Physiological modeling shows that the conditions necessary for carcinogenesis are in place only when threshold levels of vinyl acetate are exceeded. The example of vinyl acetate underlines the importance of toxicological research that unequivocally identifies genotoxic carcinogens acting through a threshold process.
Interest is increasing in the role of variations in the human genome (polymorphisms) in modifying the effect of exposures to environmental health hazards (often referred to as gene-environment interaction), which render some individuals or groups in the population more or less likely to develop disease after exposure. This review is intended for an audience of environmental health practitioners and students and is designed to raise awareness about this rapidly growing field of research by presenting established and novel examples of gene-environment interaction that illustrate the major theme of effect modification. Current data gaps are identified and discussed to illustrate limitations of past research and the need for the application of more robust methods in future research projects. Two primary benefits of incorporating genetics into the existing environmental health research framework are illustrated: a) the ability to detect different levels of risk within the population, and b) greater understanding of etiologic mechanisms. Both offer opportunities for developing new methods of disease prevention. Finally, we describe a basic framework for researchers interested in pursuing health effects research that incorporates genetic polymorphisms.
This new book, written by two outstanding scientists in the field, describes the basic principles of toxic mechanisms and organ toxicity, providing detailed information on specific mechanisms or chemicals for exemplification. The goal is to provide sufficient information that the reader becomes familiar with the basic concepts in toxicology to enable him or her to understand the basic principles in toxicology and to evaluate the risks at given exposures. With this basic understanding the reader also will be able to critically evaluate the available information on a chemical and to identify data gaps. In addition to the introductory chapters the book will offer the following systematic information, presented in six special sections: Principles in Toxicology. Organ Toxicology. Methods in Toxicology. Risk Assessment. Risk Management. Toxicity of Chemicals. Fulfilling a demand for such a book, this will be a welcomed introductory text for students and non-experts alike to focus on and understand the principles of hazard identification and risk assessment of toxicants. Relevant to all those studying toxicology, biochemistry, biology, medicine and chemistry, as well as toxicologists in hospitals, universities and in industry.
Sumario: Current applications of risk assessment methods in the development of occupational regulations -- Methods and strategies for the use of epidemiological studies in risk assessment -- Animal bioassay data in the assessment of risks to worker health -- Use of scientific data on mechanisms of toxicity, toxicokinetics and biomarkers to assess occupational risks -- Special issues in occupational risk assessment: values, politics, ethics and uncertainty -- Conclusions: Strenghts and limitations of risk assessment approaches to occupational health and recommendations for the future Bibliografía: P. 237-260
Formaldehyde (FA) is a chemical traditionally used in pathology and anatomy laboratories as a tissue preservative. Several epidemiological studies of occupational exposure to FA have indicated an increased risk of nasopharyngeal cancers in industrial workers, embalmers and pathology anatomists. There is also a clear evidence of nasal squamous cell carcinomas from inhalation studies in the rat. The postulated mode of action for nasal tumours in rats was considered biologically plausible and considered likely to be relevant to humans. Based on the available data IARC, the International Agency for Research on Cancer, has recently classified FA as a human carcinogen. Although the in vitro genotoxic as well as the in vivo carcinogenic potentials of FA are well documented in mammalian cells and in rodents, evidence for genotoxic effects and carcinogenic properties in humans is insufficient and conflicting thus remains to be more documented. To evaluate the genetic effects of long-term occupational exposure to FA a group of 30 Pathological Anatomy laboratory workers was tested for a variety of biological endpoints, cytogenetic tests (micronuclei, MN; sister chromatid exchange, SCE) and comet assay. The level of exposure to FA was evaluated near the breathing zone of workers, time weighted average of exposure was calculated for each subject. The association between the biomarkers and polymorphic genes of xenobiotic metabolising and DNA repair enzymes was also assessed. The mean level of exposure was 0.44+/-0.08ppm (0.04-1.58ppm). MN frequency was significantly higher (p=0.003) in the exposed subjects (5.47+/-0.76) when compared with controls (3.27+/-0.69). SCE mean value was significantly higher (p<0.05) among the exposed group (6.13+/-0.29) compared with control group (4.49+/-0.16). Comet assay data showed a significant increase (p<0.05) of TL in FA-exposed workers (60.00+/-2.31) with respect to the control group (41.85+/-1.97). A positive correlation was found between FA exposure levels and MN frequency (r=0.384, p=0.001) and TL (r=0.333, p=0.005). Regarding the genetic polymorphisms studied, no significant effect was found on the genotoxic endpoints. The results of the present biomonitoring study emphasize the need to develop safety programs.
Formaldehyde is an economically important chemical, to which more than 2 million U.S. workers are occupationally exposed. Substantially more people are exposed to formaldehyde environmentally, as it is generated by automobile engines, is a component of tobacco smoke and is released from household products, including furniture, particleboard, plywood, and carpeting. The International Agency for Research on Cancer (IARC) recently classified formaldehyde as a human carcinogen that causes nasopharyngeal cancer and also concluded that there is "strong but not sufficient evidence for a causal association between leukemia and occupational exposure to formaldehyde". Here, we review the epidemiological studies published to date on formaldehyde-exposed workers and professionals in relation to lymphohematopoietic malignances. In a new meta-analysis of these studies, focusing on occupations known to have high formaldehyde exposure, we show that summary relative risks (RRs) were elevated in 15 studies of leukemia (RR=1.54; confidence interval (CI), 1.18-2.00) with the highest relative risks seen in the six studies of myeloid leukemia (RR=1.90; 95% CI, 1.31-2.76). The biological plausibility of this observed association is discussed and potential mechanisms proposed. We hypothesize that formaldehyde may act on bone marrow directly or, alternatively, may cause leukemia by damaging the hematopoietic stem or early progenitor cells that are located in the circulating blood or nasal passages, which then travel to the bone marrow and become leukemic stem cells. To test these hypotheses, we recommend that future studies apply biomarkers validated for other chemical leukemogens to the study of formaldehyde.
Formaldehyde exposure, acute pulmonary response, and exposure control options were evaluated in a group of 34 workers in a gross anatomy laboratory. Time-weighted average (TWA) exposure to formaldehyde ranged from 0.07-2.94 parts per million (ppm) during dissecting operations. More than 94% were exposed to formaldehyde in excess of the ceiling value of 0.3 ppm recommended by the American Conference of Governmental Industrial Hygienists (ACGIH). The eight-hour TWA exposure of 31.7% of the subjects exceeded the action level of 0.5 ppm set by the Occupational Safety and Health Administration (OSHA). Reported symptoms included irritation of eye (88%), nose (74%), throat (29%), and airways (21%). Forced vital capacity (FVC) and forced expiratory volume in 3 seconds (FEV3) decreased, and FEV1/FVC increased during the exposure. The changes of FEV3 were statistically different from those of the controls. The results strongly support the necessity for designing and testing special local exhaust-ventilated worktables with necessary flexibility for dissecting operations.
Formaldehyde is classified as a probable human carcinogen. DNA-protein crosslinks (DPCs) and sister chromatid exchanges (SCEs) may represent early lesions in the carcinogenic process. The authors examined the DPCs and SCEs in peripheral-blood lymphocytes of 12 and 13 workers exposed to formaldehyde and eight and 20 unexposed workers, respectively. The amounts of DPCs and SCEs in the exposed and the unexposed differed significantly after adjustment for smoking. There was a linear relationship between years of exposure and the amounts of DPC and SCE. The authors conclude that the data indicate a possible mechanism of carcinogenicity of formaldehyde, and that formaldehyde is mutagenic to humans. These results support the use of DPCs as a biomarker of occupational exposure to formaldehyde and to detect high-risk populations for secondary prevention.
Sister chromatid exchange (SCE) was measured in peripheral lymphocytes of 90 workers from 14 hospital pathology departments in Israel who were occupationally exposed to formaldehyde (FA) and of 52 unexposed workers from the administrative section of the same hospitals. The mean exposure period to FA was 15.4 years (range 1-39). The results of SCEs are expressed in two variables: (a) mean number of SCEs per chromosome and (b) proportion of high frequency cells (cells with more than eight SCEs). A high correlation was found between these two variables. The adjusted means of both SCEs variables were significantly higher among the exposed compared with that of the unexposed group (P<0.01). Adjustment was made for age, sex, smoking habits, education workers and origin. Evaluation of the influence of years of exposure on the frequency of SCEs showed that the two variables of SCEs were higher among those who were exposed to FA for 15 or more than among those with less than 15 years of exposure. Concerning levels of exposure, both variables of SCEs were the same in the low and in the high levels of exposure sub-groups. However, among the smokers, both variables of SCEs were higher in the high exposure sub-group than in the low exposure sub-group. Our finding of a significant increase of SCEs frequency in peripheral lymphocytes in pathology staff indicates a potential cytogenetic hazard due to FA exposure. We conclude that our data indicate that FA is mutagenic to humans.
Engineering or administrative methods are often insufficient or impractical to control exposure to chemicals in anatomy laboratories. This study explored the feasibility of wearing one or a combination of respirators and goggles used as personal protective equipment (PPE) to control exposure in one such laboratory.
A group of 28 subjects were briefly trained in wearing PPE, fit-tested, and asked to complete a questionnaire regarding their subjective reaction after wearing the assigned PPE ensemble while working in the laboratory. The subjects' exposure to formaldehyde was also measured and generally exceeded the recommended limits.
When a full-face respirator or the combination of a half-mask respirator and goggles was worn, a majority of subjects reported no odor problem and no irritation to eyes or upper respiratory system. Subjects accepted the PPE to certain degrees, but those using respirators encountered difficulties communicating with others.
The combination of a half-mask respirator and goggles was the most feasible ensemble to control exposure to air pollutants in an anatomy laboratory.
Biomarkers are becoming increasingly important in toxicology and human health. Many research groups are carrying out studies to develop biomarkers of exposure to chemicals and apply these for human monitoring. There is considerable interest in the use and application of biomarkers to identify the nature and amounts of chemical exposures in occupational and environmental situations. Major research goals are to develop and validate biomarkers that reflect specific exposures and permit the prediction of the risk of disease in individuals and groups. One important objective is to prevent human cancer. This review presents a commentary and consensus views about the major developments on biomarkers for monitoring human exposure to chemicals. A particular emphasis is on monitoring exposures to carcinogens. Significant developments in the areas of new and existing biomarkers, analytical methodologies, validation studies and field trials together with auditing and quality assessment of data are discussed. New developments in the relatively young field of toxicogenomics possibly leading to the identification of individual susceptibility to both cancer and non-cancer endpoints are also considered. The construction and development of reliable databases that integrate information from genomic and proteomic research programmes should offer a promising future for the application of these technologies in the prediction of risks and prevention of diseases related to chemical exposures. Currently adducts of chemicals with macromolecules are important and useful biomarkers especially for certain individual chemicals where there are incidences of occupational exposure. For monitoring exposure to genotoxic compounds protein adducts, such as those formed with haemoglobin, are considered effective biomarkers for determining individual exposure doses of reactive chemicals. For other organic chemicals, the excreted urinary metabolites can also give a useful and complementary indication of exposure for acute exposures. These methods have revealed 'backgrounds' in people not knowingly exposed to chemicals and the sources and significance of these need to be determined, particularly in the context of their contribution to background health risks.
This research was conducted to determine formaldehyde exposure of staffs in pathology laboratories, surgery rooms and endoscopy wards in eight large hospitals of Tehran University of Medical Sciences located at Tehran, Iran. Air sampling have been made by both long and short-term methods. Total numbers of samples were 160 for both methods. Nineteen samples of 160 samples were collected as blank in other non-exposed environments such as administrative sections. The mean (SD) levels of formaldehyde in long-term methods were 0.96 (0.74), 0.25 (0.21) and 0.13 (0.18) ppm, at pathology laboratories, surgery rooms and endoscopy wards, respectively. The results of measurements showed that mean (SD) concentration of formaldehyde in one hour sampling at short intervals were 0.83 (0.29), 0.23 (0.16) and 0.75 (0.25) ppm at pathology labs, surgery rooms and endoscopy wards, respectively. There were significant differences in the mean levels of formaldehyde (long-term) at surgery rooms (p < 0.02) and endoscopy wards (p < 0.005) in eight hospitals of this study. It is concluded that the concentration levels of formaldehyde at pathology laboratories exceeded recommended limit which established by the American Conference of Governmental and Industrial Hygienists ACGIH (TLV-C = 0.3 ppm). It is recommended that local exhaust ventilation should be installed to minimize the contact to formaldehyde in the staffs.
Objectives:
The critical health effects of formaldehyde exposure include sensory irritation and the potential to induce tumours in the upper respiratory tract. In literature, a concentration as low as 0.24 ppm has been reported to be irritating to the respiratory tract in humans. Nasal tumour-inducing levels in experimental animals seem to be 1-2 orders of magnitude larger. In this paper, the subjectively measured sensory irritation threshold levels in humans are discussed in line with findings obtained in animal experiments. In addition, a Benchmark dose (BMD) analysis of sensory irritation was used to estimate response incidences at different formaldehyde concentrations.
Methods:
Data on respiratory irritation and carcinogenicity of formaldehyde were retrieved from public literature and discussed. BMD analysis was carried out on human volunteer studies using the US-EPA BMD software.
Results:
Subjective measures of irritation were the major data found in humans to examine sensory (eye and nasal) irritation; only one study reported objectively measured eye irritation. On a normalized scale, mild/slight eye irritation was observed at levels 1 ppm, and mild/slight respiratory tract irritation at levels 2 ppm. With the BMD software, it was estimated that at a level of 1 ppm, only 9.5% of healthy volunteers experience 'moderate' (i.e., annoying) eye irritation (95% upper confidence limit). An important factor modulating the reported levels of irritation and health symptoms most probably includes the perception of odour intensity. In several studies, the 0-ppm control condition was missing. From the results of the long-term inhalation toxicity studies in experimental animals, a level of 1 ppm formaldehyde has been considered a NOAEL for nasal injury.
Conclusions:
Sensory irritation is first observed at levels of 1 ppm and higher. From both human and animal studies, it was concluded that at airborne levels for which the prevalence of sensory irritation is minimal both in incidence and degree (i.e., <1 ppm), risks of respiratory tract cancer are considered to be negligibly low.
A study was conducted to evaluate the genotoxic effect of occupational exposure to formaldehyde on pathology and anatomy laboratory workers. The level of exposure to formaldehyde was determined by use of passive air-monitoring badges clipped near the breathing zone of 59 workers for a total sampling time of 15min or 8h. To estimate DNA damage, a chemiluminescence microplate assay was performed on 57 workers before and after a 1-day exposure. Assessment of chromosomal damage was carried out by use of the cytokinesis-blocked micronucleus assay (CBMN) in peripheral lymphocytes of 59 exposed subjects in comparison with 37 controls matched for gender, age, and smoking habits. The CBMN assay was combined with fluorescent in situ hybridization with a pan-centromeric DNA probe in 18 exposed subjects and 18 control subjects randomized from the initial populations. Mean concentrations of formaldehyde were 2.0 (range <0.1-20.4ppm) and 0.1ppm (range <0.1-0.7ppm) for the sampling times of 15min and 8h, respectively. No increase in DNA damage was detected in lymphocytes after a one-workday exposure. However, the frequency of binucleated micronucleated cells was significantly higher in pathologists/anatomists than in controls (16.9 per thousand+/-9.3 versus 11.1 per thousand+/-6.0, P=0.001). The frequency of centromeric micronuclei was higher in exposed subjects than in controls (17.3 per thousand+/-11.5 versus 10.3 per thousand+/-7.1) but the difference was not significant. The frequency of monocentromeric micronuclei was significantly higher in exposed subjects than in controls (11.0 per thousand+/-6.2 versus 3.1 per thousand+/-2.4, P<0.001), while that of the acentromeric micronuclei was similar in exposed subjects and controls (3.7 per thousand+/-4.2 and 4.1 per thousand+/-2.7, respectively). The enhanced chromosomal damage (particularly chromosome loss) in peripheral lymphocytes of pathologists/anatomists emphasizes the need to develop safety programs.
In this paper carcinogenicity classification and evaluations case of formaldehyde made by national and international agencies and organizations (such as European Union, International Agency for Research on Cancer, World Health Organization) both in occupational (such as American Conference of Government Industrial Hygienists, National Institute of Occupational Safety and Health and Occupational Health and Safety Administration) and non occupational environment (such as United States Environmental Protection Agency) are proposed. The differences in the database and consequently in the conclusion are described in a short historical review since formaldehyde was considered for the first time as regard as health effects.
Formaldehyde and glutaraldehyde cause toxicity to the nasal epithelium of rats and mice upon inhalation. In addition, formaldehyde above certain concentrations induces dose-related increases in nasal tumors in rats and mice, but glutaraldehyde does not. Using the 2006 IPCS human framework for the analysis of cancer mode of action (MOA), an MOA for formaldehyde was formulated and its relevance was tested against the properties of the noncarcinogenic glutaraldehyde. These compounds produce similar patterns of response in histopathology and in genotoxicity tests (although formaldehyde has been much more extensively tested studied). The MOA is based on the induction of sustained cytotoxicity and reparative cell proliferation induced by formaldehyde at concentrations that also induce nasal tumors upon long-term exposure. Data on dose dependency and temporal relationships of key events are consistent with this MOA. While a genotoxic MOA can never be ruled out for a compound that is clearly genotoxic, at least in vitro, the nongenotoxic properties fundamental to the proposed MOA can explain the neoplastic response in the nose and may be more informative than genotoxicity in risk assessment. It is not yet fully explained why glutaraldehyde remains noncarcinogenic upon inhalation, but its greater inherent toxicity may be a key factor. The dual aldehyde functions in glutaraldehyde are likely to produce damage resulting in fewer kinetic possibilities (particularly for proteins involved in differentiation control) and lower potential for repair (nucleic acids) than would be the case for formaldehyde. While there have been few studies of possible glutaraldehyde-associated cancer, the evidence that formaldehyde is a human carcinogen is strong for nasopharyngeal cancers, although less so for sinonasal cancers. This apparent discrepancy could be due in part to the classification of human nasal tumors with tumors of the sinuses, which would receive much less exposure to inhaled formaldehyde. Evaluation of the human relevance of the proposed MOA of formaldehyde in rodents is restricted by human data limitations, although the key events are plausible. It is clear that the human relevance of the formaldehyde MOA in rodents cannot be excluded on either kinetic or dynamic grounds.
Setting standards, such as occupational exposure limits (OELs) for carcinogenic substances must consider modes of action. At the European Union level, the scientific committee on occupational exposure limits (SCOEL) has discussed a number of chemical carcinogens and has issued recommendations. For some carcinogens, health-based OELs were recommended, while quantitative assessments of carcinogenic risks were performed for others. For purposes of setting limits this led to the consideration of the following groups of carcinogens. (A) Non-threshold genotoxic carcinogens; for low-dose assessment of risk, the linear non-threshold (LNT) model appears appropriate. For these chemicals, regulations (risk management) may be based on the ALARA principle ("as low as reasonably achievable"), technical feasibility, and other socio-political considerations. (B) Genotoxic carcinogens, for which the existence of a threshold cannot be sufficiently supported at present. In these cases, the LNT model may be used as a default assumption, based on the scientific uncertainty. (C) Genotoxic carcinogens with a practical threshold, as supported by studies on mechanisms and/or toxicokinetics; health-based exposure limits may be based on an established NOAEL (no observed adverse effect level). (D) Non-genotoxic carcinogens and non-DNA-reactive carcinogens; for these compounds a true ("perfect") threshold is associated with a clearly founded NOAEL. The mechanisms shown by tumour promoters, spindle poisons, topoisomerase II poisons and hormones are typical examples of this category. Health-based OELs are derived for carcinogens of groups C and D, while a risk assessment is carried out for carcinogens of groups A and B. Substantial progress is currently being made in the incorporation of new types of mechanistic data into these regulatory procedures.
In the present study, the results of a measurement campaign aiming to assess cancer risk among two special groups of population: policemen and laboratory technicians exposed to the toxic substances, benzene and formaldehyde are presented. The exposure is compared to general population risk. The results show that policemen working outdoor (traffic regulation, patrol on foot or in vehicles, etc.) are exposed at a significantly higher benzene concentration (3-5 times) than the general population, while the exposure to carbonyls is in general lower. The laboratory technicians appear to be highly exposed to formaldehyde while no significant variation of benzene exposure in comparison to the general population is recorded. The assessment revealed that laboratory technicians and policemen run a 20% and 1% higher cancer risk respectively compared to the general population. Indoor working place air quality is more significant in assessing cancer risk in these two categories of professionals, due to the higher Inhalation Unit Risk (IUR) of formaldehyde compared to benzene. Since the origin of the danger to laboratory technicians is clear (use of chemicals necessary for the experiments), in policemen the presence of carbonyls in indoor air concentrations due to smoking or used materials constitute a danger equal to the exposure to traffic originated air pollutants.
The United States Environmental Protection Agency (EPA) recently proposed a hypothetical mode of action (MOA) to explain how inhaled formaldehyde (FA) might induce leukemia, lymphoma and a variety of other lymphohematopoietic (LHP) malignancies in occupationally exposed workers. The central hypothesis requires that B lymphocytes or hematopoietic progenitor cells (HPC) present at the "portal of entry (POE)" undergo sustained mutagenic change as a result of direct FA exposure. These modified cells would then migrate back to the bone marrow or primary lymphatic tissue and subsequently develop into specific LHP disease states. Chemical interaction at the POE is an absolute requirement for the hypothesized MOA as there is no convincing evidence that inhaled FA causes distant site (e.g., bone marrow) toxicity. The purpose of this review is to critically evaluate this proposed MOA within the context of the existing data concerning the toxicokinetic and biological properties of FA, the current understanding of the induction of chemically-induced leukemias and lymphomas, as well as within EPA's specific guidelines for evaluating the MOA of chemically-induced cancers. Specifically, we examine the scientific support for the hypothesis that FA exposure may induce carcinogenic transformation of localized lymphocytes or peripheral hematopoietic progenitor cells (HPC) in the absence of discernable systemic hematopoietic toxicity (i.e., peripheral transformation). While little or no empirical evidence exists upon which to fully evaluate the proposed hypothesis, available data does not support the proposed concept of "peripheral transformation" at the chemical entry site. Numerous animal bioassays evaluating chronic inhalation of FA clearly do not support this hypothesis since no properly conducted study as ever shown an increase in any LHP malignancy. Moreover, the notion that FA can cause any LHP malignancy is not supported with either epidemiologic data or current understanding of differing etiologies and risk factors for the various hematopoietic and lymphoproliferative malignancies. It is therefore concluded that existing science does not support the proposed MOA as a logical explanation for proposing that FA is a realistic etiological factor for any LHP malignancy.
Diversos estudos apontam os Laboratórios de Anatomia Patológica como um dos cenários ocupacionais onde os trabalhadores estão expostos a concentrações de Formaldeído superiores aos valores limite estabelecidos, o que indica uma situação de risco de exposição profissional
- Akbar-Khanzadeh
Diversos estudos apontam os Laboratórios de Anatomia Patológica como um
dos cenários ocupacionais onde os trabalhadores estão expostos a concentrações de
Formaldeído superiores aos valores limite estabelecidos, o que indica uma situação de
risco de exposição profissional (AKBAR-KHANZADEH et al., 1994; SHAHAM et al.,
1997; AKBAR-KHANZADEH & PULIDO, 2003).
Um outro estudo publicado anteriormente relatou que trabalhadores deste ramo profissional estavam expostos a concentrações médias de
- Costa
hospitais da zona do Porto e Aveiro estavam compreendidos entre 0.04 ppm e 1.58 ppm
(mínimo e máximo, respectivamente) e que a concentração média era de 0.44 ppm
(TWA) (COSTA et al., 2008). Um outro estudo publicado anteriormente relatou que
trabalhadores deste ramo profissional estavam expostos a concentrações médias de
Formaldeído compreendidas entre 0.1 e 0.7 ppm (mínimo e máximo, respectivamente)
(ORSIÈRE et al., 2006).
TLVs and BEIs : based on the documentation of the threshold limits values for chemical substances and physical agents and biological exposure indices
- American Conference
- Governamental
- Hygienists
AMERICAN CONFERENCE OF GOVERNAMENTAL INDUSTRIAL HYGIENISTS
(ACGIH). TLVs and BEIs : based on the documentation of the threshold limits values
for chemical substances and physical agents and biological exposure indices.
American Conference of Governmental Industrial Hygienists
- O H Cincinnati
Cincinnati, OH : American Conference of Governmental Industrial Hygienists; 2008.
Industrial Ventilation : a manual of recommended practice
- American Conference
- Governamental
- Hygienists
AMERICAN CONFERENCE OF GOVERNAMENTAL INDUSTRIAL HYGIENISTS
(ACGIH). Industrial Ventilation : a manual of recommended practice. Cincinnati OH :
American Conference of Governmental Industrial Hygienists, Inc; 1998. p. 1-512.
Guidelines for Design and Construction of Hospital and Health Care Facilities
- American Institute
- Architects
AMERICAN INSTITUTE OF ARCHITECTS. Guidelines for Design and Construction
of Hospital and Health Care Facilities. Washington DC : American Institute of
Architects Press, 2000.
Ventilation for Indoor Air Quality. ASHRAE Standard 62-1999
- American Society
- Heating
- Inc Engineers
AMERICAN SOCIETY OF HEATING, REFRIGERATION AND AIR-CONDITIONING ENGINEERS, INC. Ventilation for Indoor Air Quality. ASHRAE
Standard 62-1999. Atlanta GA : ASHRAE; 1999. p. 1-27.
Health and safety : risk management. 2nd revised ed. Leicestershire : IOSH Services
- T Boyle
BOYLE, T. Health and safety : risk management. 2nd revised ed. Leicestershire : IOSH
Services; 2003.
Exposição ao Xilol nos laboratórios de anatomia patológica
- Josianne Carriço
CARRIÇO, Josianne, et al. Exposição ao Xilol nos laboratórios de anatomia patológica.
Report nº 10. Effects of indoor air pollution on human health
- European
- Action
EUROPEAN CONCERTED ACTION. Report nº 10. Effects of indoor air pollution on
human health. Luxembourg : Office of publications of the European Communities;
Advances in risk assessment and communication. Annual Review of Public Health
- B D Goldstein
GOLDSTEIN, B. D. Advances in risk assessment and communication. Annual Review
of Public Health. 2005 ; 26 : 141-163.
Assessment of the carcinogenicity of formaldehyde (CAS No. 50-00-00)
- Von A S Herausgegeben
HERAUSGEGEBEN, Von A. S., et al. Assessment of the carcinogenicity of
formaldehyde (CAS No. 50-00-00). Berlim : Bundesinstitut fur Risikobewertun; 2006.
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER. Wood dust and
formaldehyde. Lyon : IARC; 1995. 217-362.
Formaldehyde : health and safety guide. Geneva : World Health Organization
Disponível em:
http://inchem.org/documents/ehc/ehc/ehc89.htm
INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY. Formaldehyde :
health and safety guide. Geneva : World Health Organization, 1991. [Consult. 11 Mar.
INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY. Biomarkers in risk assessment : validity and validation. Geneva : World Health Organization
Disponível em: http://www.inchem.org/documents/hsg/hsg/hsg057.htm
INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY. Biomarkers in risk
assessment : validity and validation. Geneva : World Health Organization; 2001.
In Hansen W. A Guide to Managing Indoor Air Quality in Health Care Organization
- Orme I. Patient
- Impact
ORME I. Patient Impact. In Hansen W. A Guide to Managing Indoor Air Quality in
Health Care Organization. Ed. Oakbrook Terrace IL : Joint Commission on
Accreditation of Healthcare Organizations Publications; 1997. p. 43-52.
Avaliação da exposição profissional ao formaldeído: efeito genotóxico. Porto : Instituto de Ciências Biomédicas Abel Salazar. Faculdade de Ciências da Universidade do Porto
- Carolina Pina
PINA, Carolina. Avaliação da exposição profissional ao formaldeído: efeito genotóxico.
Porto : Instituto de Ciências Biomédicas Abel Salazar. Faculdade de Ciências da
Universidade do Porto; 2010.
A qualidade do ar interior em instalações hospitalares
- Carlos Piteira
PITEIRA, Carlos. A qualidade do ar interior em instalações hospitalares. Lisboa : Lidel;
Exposição profissional a agentes químicos: os indicadores biológicos na vigilância de saúde dos trabalhadores
- J Prista
- A Uva
PRISTA, J.; UVA, A. Exposição profissional a agentes químicos: os indicadores
biológicos na vigilância de saúde dos trabalhadores. Revista Saúde e Trabalho. 2003 ; 4
: 5-12.
Diagnóstico e gestão do risco em saúde ocupacional
- A S Uva
UVA, A. S. Diagnóstico e gestão do risco em saúde ocupacional. Lisboa : IDICT; 2006.