Cancer asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Cancer asbestos exposure Biogarphy

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Although tobacco smoking affects the total lung cancer risk, this effect does not detract from the risk of lung cancer attributable to asbestos exposure. No attempt has been made in this report to apportion the relative contributions of asbestos exposure and tobacco smoking
Prevention and screening
Screening of asbestos-exposed populations can be carried out for practical and scientific purposes. There are 4 goals of screening: (i) to identify high risk groups, (ii) to target preventive actions, (iii) to discover occupational diseases, and (iv) to develop improved tools for treatment, rehabilitation and prevention. Screening should aim to prevent asbestos-related diseases and therefore lead to gained healthy years of life among the screened or among those in similar risk situations. The benefits to the individual person should be viewed cautiously. The substantial morbidity and mortality related to asbestos exposure argue for continued efforts to increase the preventive power of screening.
Any screening for purely scientific purposes requires appropriate methods and criteria (eg, low cost and high predictive value). Before a screening program is initiated, the ethical, financial, and legislative aspects need to be considered. These aspects may include patient notification, data protection, allocation of costs, and follow-up of identified abnormalities. In addition, provision should be made for epidemiologic analyses, quality control, primary and secondary prevention, and the assessment of program effectiveness.
As tools for screening, questionnaires and personal interviews should include items related to asbestos exposure, smoking, and other contributing factors. Questionnaires should preferably be validated for smoking habits and occupational histories. When possible, questionnaires should be applied nationally to permit epidemiologic analysis of the results.
Chest X-ray examinations can include frontal and lateral roentgenograms. Appropriate lung function tests can measure respiratory flow volumes and rates. In spirometry, attention should be given to careful calibration, acceptable performance efforts, and reproducibility.
The prevention strategies of asbestos-related diseases can be based on the identification of exposure sources and exposed people. There are 3 main targets for prevention: (i) an individual worker, (ii) a selected group of workers, and (iii) the work environment. At the level of the individual worker, the tools for prevention include health education and the introduction of safe work practices, the avoidance of tobacco smoking, and careful follow-up of health by surveillance. The group level methods are in part the same as at the individual level (ie, health information, education, and recommendations including the use of respiratory protective equipment).
The work environment is the most important target for preventive measures, starting from avoiding the use of asbestos, carefully controlling dust emissions using wet techniques, and controlling passive smoking at the workplace. Many countries have prohibited the use of asbestos, but there are still substantial amounts of asbestos in consumer products and in buildings that can expose workers in repair and removal work. Some countries have permitted asbestos work only under special authorization, training, and protective measures.
From the knowledge on potential exposures to asbestos, high-risk populations can be identified among persons exposed 10 or more years ago. The availability of registers—union, workers` compensation, and employment records—can be explored for this purpose.
Subjects can be assigned to subgroups for intervention or screening as defined by their risk (eg, the current risk of lung cancer and risk projected to given time windows in the future). Criteria for inclusion in each intervention or screening group should be established in the study protocol. Subsequently, the members of each subgroup can serve as separate targets for group-based and individual intervention programs.
Protocols for intervention should be designed in such a way that they serve each subject and subgroup optimally in terms of promoting individual health and the early detection of asbestos-related diseases. Data on these subgroups can also form a basis for more specific studies of disease outcome or various biomarkers. Identified abnormalities should be followed by the best clinical and occupational practices.
Reserach needs
There are several issues that still require clarification and further study. The following list of recommendations and future directions is not intended to be exhaustive.
• Improvement in the assessment and quantification of exposure to asbestos, to include specific worker groups, with collation of data and the development of an international standardized protocol for the assessment of exposure.
• Further analysis of job-exposure data and further studies on asbestos fiber burdens in tissue in relation to various asbestos-related disorders.
• Studies on chrysotile fiber burdens in lung tissue relative to the risk of lung cancer (also to include experimental investigations).
• Lung cancer relative to the lung tissue burdens of mineral fibers other than asbestos (eg, refractory ceramic fibers and zeolites).
• Improvement of the ILO system for the radiological diagnosis and categorization of pleural abnormalities.
• Development of a standardized system for the reporting of HRCT scans of asbestos-related disorders, analogous to the ILO system.
• Studies on the specificity of lesions of the pleura visualized by CT as markers of asbestos exposure and studies on the prognosis of diffuse pleural abnormalities.
• Improvement in ultrasound imaging of the pleura.
• Development of new digital imaging techniques for the investigation of asbestos-related diseases.
• Standardization of the approach to lung crepitations with the use of special auditory devices.
• Investigation of mesothelioma as a potential outcome of exposure to mineral fibers other than asbestos—such as refractory ceramic fibers—to include experimental studies and a series of mesothelioma patients without exposure to asbestos or erionite, supported by lung tissue fiber analysis.
• Multicenter studies on biomarkers for the detection of early asbestos diseases and the assessment of the response to new treatment modalities.
• Investigation of asbestos-associated tumors other than lung cancer and mesothelioma (eg, laryngeal carcinoma and renal carcinoma).
• Further studies on the effectiveness of screening programs.
Participants: Douglas W. Henderson (Flinders Medical Centre, Australia), Jorma Rantanen (Finnish Institute of Occupational Health, Finland), Scott Barnhart (University of Washington, United States), John M Dement (Duke University Medical Center, United States), Paul De Vuyst (Cliniques Universitaires de Bruxelles, Hopital Erasme, Belgium), Gunnar Hillerdal (Karolinska Hospital, Sweden), Matti S Huuskonen (Finnish Institute of Occupational Health, Finland), Leena Kivisaari (Helsinki University Central Hospital, Finland), Yukinori Kusaka (Fukui Medical School, Japan), Aarne Lahdensuo (Tampere University Hospital, Finland), Sverre Langård (The National Hospital, Norway), Gunnar Mowe (Department of Social Insurance Medicine, University of Oslo, Norway), Toshiteru Okubo (University of Occupational and Environmental Health, Japan), John E Parker (National Institute for Occupational Safety and Health, United States), Victor L Roggli (Duke University Medical Center, United States), Klaus Rödelsperger (Justus-Liebig University, Germany), Joachim Rösler (Justus-Liebig University, Germany), Antti Tossavainen (Finnish Institute of Occupational Health, Finland), Hans-Joachim Woitowitz (Justus-Liebig University, Germany).
The article by Mollo and coworkers[1] examines the criteria for attribution of lung cancers to asbestos exposure, suggesting that the number of asbestos-related lung cancers in Italy might be underestimated. Their review of 924 consecutive lobectomies and pneumonectomies for lung cancer in northwest Italy included light microscopic asbestos body counts for asbestos body concentration in addition to histologic examination for asbestosis and asbestos bodies. Their interpretation is that 6% of the lung cancers in their series are attributable to asbestos exposure because of histologic diagnosis of asbestosis. However, they also conclude that another 0.5% of their cases had interstitial fibrosis without asbestos bodies on histologic section but an elevated asbestos body concentration on digestion study. Mollo and coworkers[1] raise the possibility that these cases also may be asbestos-related lung cancers.
The great majority of lung cancers are caused by tobacco smoke, but a minority of lung cancers are caused by asbestos exposure, virtually always in association with tobacco smoke exposure. One reason to identify the lung cancers caused by asbestos exposure is for establishing occupational and public health policies regarding asbestos or for investigation of lung cancer pathogenesis that, in turn, may provide a basis for new lung cancer therapies. In the individual case, the major reason to determine whether asbestos contributed to the development of a lung cancer is for purposes of compensation, which, in the United States, often is through litigation. Accurate identification of patients deserving compensation is also a primary concern of Mollo and coworkers.[1]
Before proceeding, we should remind ourselves that risk of a disease and actually having a disease due to that risk are two different things. This is a rather simple observation, but it is important if one is addressing etiology of a disease. Risk has to do with populations studied for relative likelihood of disease due to a common factor not present in a control population. Any membes of the at-risk population may not develop the disease under investigation and may have many individual factors that may modify the risk from the studied factor, be a confounding factor for the risk factor under study, or put them at risk for other diseases. An example can be found with the relationship of tobacco smoke to lung cancer. On the one hand, about 10% of tobacco smokers develop lung cancer as a result of their tobacco smoking. This is a considerably greater risk than the population of never smokers who have a background risk of lung cancer that is less than 1%, probably considerably so. On the other hand, even though most smokers do not develop lung cancer, about 90% of all lung cancers are caused by tobacco smoking.[2]
A smoker has a risk of lung cancer because of smoking that is much greater than that of individuals who have never smoked, but, even so, that person has a fairly good chance of not developing a lung cancer based on the risk seen in the population of all smokers. If that smoker does develop lung cancer, the lung cancer will be caused by the tobacco smoke and could have been avoided if the person had never smoked. If we look closer at the population of smokers with a risk of lung cancer, we can identify criteria that select those with the most risk of developing lung cancer based on the cumulative dose of tobacco smoke that they are exposed to and to factors of individual susceptibility.[3-5] However, the causal association between tobacco smoke and lung cancer is so strong that we seldom do more than obtain a smoking history and do not require a detailed analysis of corroborating evidence to link a smokers lung cancer to tobacco smoke in the vast majority of cases.
As rightly pointed out by Mollo et al,[1] many studies examine only the risk of lung cancer for asbestos-exposed populations and do not investigate the criteria for ascribing an individuals lung cancer to asbestos exposure. Studies have demonstrated that certain occupations and populations of workers commonly have higher asbestos exposures and greater risks of asbestos-related diseases than others.[6,7] For compensation, however, a worker must substantiate the individual claim.
Unlike the situation with tobacco smoke and lung cancer, at least 2 factors necessitate clearly defined criteria for linking a lung cancer to asbestos in the individual case. First, most workers with asbestos exposures will not develop lung cancers, indicating that there are differences between workers and/or their asbestos exposures in regard to lung cancer risk. Second, as already noted, tobacco smoke is the primary cause of lung cancers and is sufficient by itself to cause the great majority of lung cancers. As a result, tobacco smoke exposure is a powerful confounding factor in most cases of lung cancers in workers with asbestos exposures.
In regard to the first factor, studies indicate that everyone is exposed to background levels of asbestos in the ambient air. Studies have shown that members of the general (nonoccupationally exposed) population have tens of thousands to hundreds of thousands of asbestos fibers in each gram of dry lung tissue, which translates into millions of fibers and tens of thousands of asbestos bodies in every persons lungs.[6,7] However, the general population does not have an increased risk of asbestos-related lung cancers despite these background levels. Individuals with occupational exposures to asbestos have tissue burdens of asbestos that are higher than background levels. A number of studies have failed to show an increased risk of lung cancer in populations with comparatively low levels of asbestos exposure.[8] Therefore, the level of cumulative asbestos exposure, reported as asbestos dose or asbestos tissue burden, must be one of the factors that determine lung cancer risk. However, considering that millions of workers have had occupational exposure to asbestos and that only some of these individuals develop lung cancer, there must be other factors that separate those who develop asbestos-related lung cancer from those who do not. As with other types of exposures that carry risk of disease, including tobacco smoke, factors related to individual susceptibility also must have a role in whether an asbestos-related lung cancer develops in an individual once the requisite asbestos tissue burden is present.
The second factor creating a need for attribution criteria is the confounding factor of tobacco smoke. As previously stated, current or former active tobacco smoking accounts for 90% of all lung cancers in the United States. Secondhand environmental smoke accounts for a sizable percentage of the remainder, for a total of more than 150,000 new lung cancers in the United States each year due to tobacco smoke.[2] In contrast, asbestos is estimated to account for 2% to 5%, or about 3,400 to 8,500 new lung cancers in the United States each year.[9,10] Thus, there are anywhere from 20 to 50 tobacco-related lung cancers for every asbestos-related lung cancer. Tobacco smoke contains some 4,000 to 5,000 chemicals, including many known and suspected carcinogens, both initiators and promoters. As a result, tobacco smoke is sufficient by itself to cause the great majority of lung cancers without the additional contribution of any other agent.
Virtually all workers with lung cancers and asbestos exposure also are tobacco smokers or former smokers and, therefore, have 2 potential etiologic agents for their lung cancers. There is a synergistic effect of asbestos with tobacco smoke, and both of these potential etiologic agents are responsible for lung cancers in some workers. Other workers may have had asbestos exposure, but their lung cancers are due exclusively to their tobacco smoke exposure, like the overwhelming majority of patients with lung cancer in the general population. Specific criteria are needed to separate workers with purely tobacco-related lung cancers from those with lung cancers attributable to both tobacco and asbestos.
As noted, no increased risk of asbestos-related lung cancer from background levels of asbestos has been demonstrated in the general population, and a number of studies have failed to demonstrate an increased risk of lung cancer in populations with increased but comparatively low levels of asbestos exposure.[6-8] Various tissue burden studies report thousands of asbestos bodies and millions of asbestos fibers per gram of dried lung tissue in asbestos workers with lung cancer. In industrial hygiene terms, cumulative asbestos exposure of 25 fibers per cubic centimeter yea

Cancer asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Cancer asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Cancer asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Cancer asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Cancer asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Cancer asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Cancer asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Cancer asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Cancer asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Cancer asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Cancer asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Exposure asbestos Wallpaper Photos Pictures Pics Images 2013

Exposure asbestos  Biogarphy

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authorities as a minimal dose for increased risk of lung cancer.[8,11] Some investigators estimate that the 25 fibers per cubic centimeter year dose doubles the risk of lung cancer.[12] To put this in perspective, a report from Florida indicated that increased intake of dietary fat doubles the risk of lung cancer (in multiple studies there is emerging evidence that dietary fat consumption increases the risk of lung cancer).[13] However, it should be noted that most workers with asbestos-related lung cancer have much more than the minimal asbestos dose or tissue burden and, therefore, potentially will have more than a doubling of risk. For purposes of establishing causation criteria, however, the diminishing risk with lower levels of exposure means that a worker may have had occupational exposure to asbestos but that exposure may be less than the minimal levels of asbestos required to produce an increased risk of lung cancer.
This observation has implications for some of the potential criteria that we might consider for attributing a lung cancer to asbestos exposure. Workers with asbestos-related lung cancers usually will have histories of asbestos exposure and are expected to have asbestos bodies on tissue sections of their lung parenchyma. Many also coincidentally will have pleural plaques because of their asbestos exposure. However, asbestos bodies can be seen in tissue sections when the asbestos tissue burden is less than the minimum for lung cancer risk. Pleural plaques also can occur at asbestos concentrations less than those required for a lung cancer risk and in tissue burden studies generally are associated with average tissue burdens that are much less than those for lung cancer. As a result, the presence of 1 asbestos body on tissue sections, or even a few asbestos bodies depending on circumstances, and the presence of pleural plaques are not reliable criteria by themselves for causally linking a lung cancer to asbestos exposure on the basis of tissue burden.[12] Either of these findings may provide evidence of an asbestos exposure but neither, by itself, quantitates the exposure. For similar reasons, a work history of asbestos exposure must be detailed and comprehensive before it can be used to estimate the asbestos dose.
Tissue burden analyses and work history analyses tell us that not everyone who has the requisite level of asbestos exposure will develop an asbestos-related lung cancer. As noted, individual susceptibility to the asbestos exposure is necessary before an individual will develop a disease from the exposure. Asbestos workers potentially are subject to the same nonasbestos risk factors and nonasbestos-related diseases to which the general population is subject. Since tobacco smoke is sufficient by itself to cause the majority of lung cancers, there is no reason that lung cancer in a tobacco-smoking asbestos worker should not be related purely to tobacco smoking. Obviously, if the worker has less than the minimal asbestos exposure to cause asbestos-related lung cancer, the cause of the lung cancer should not be an issue. However, even with sufficient dose or tissue burden of asbestos to create a risk of asbestos-related lung cancer, a tobacco smoker could have a purely tobacco-related lung cancer like most patients with lung cancer if the worker is not susceptible to the asbestos exposure.
Do we have any marker for both asbestos tissue burden and individual susceptibility to that exposure? Over the years, a number of investigators have concluded that the increased risk for lung cancer in asbestos-exposed workers occurs in workers with asbestosis. Detailed editorials and reviews of the studies supporting this conclusion have been written by several well-known authorities in the field, including Churg,[8,11] Jones et al,[14] and Weiss,[15] and will not be repeated here. It should be noted that, over the years, a great many epidemiologic studies of lung cancer risk and asbestos exposure do not provide information about presence or absence of asbestosis in the patients. An example is the classic work by Hammond et al[16] demonstrating an increased risk of lung cancer in insulators. Interestingly, when a histopathologic review was performed of the lung cancer cases with available lung parenchyma, the insulators in Selikoffs series with an increased risk of lung cancer from asbestos exposure above that of their smoking showed asbestosis in 100% of cases.[17] Evaluation of studies said to support an increased risk for asbestos-related lung cancer in the absence of asbestosis have been criticized for failing to show an increased risk when cases with asbestosis are excluded from their study populations.[8,14,15] Overall, there is a strong association between lung cancer risk and asbestos exposure with asbestosis that can be demonstrated more readily than an association with asbestos exposure without asbestosis.
However, in response to the aforementioned reviews and editorials, reviews and editorials by other authorities in the field, including Roggli et al,[18] Abraham,[19] Egilman and Reinert,[20] and Banks et al,[21] have challenged the premise that asbestosis is necessary to causally link a lung cancer to asbestos exposure, contending that a sufficient asbestos dose or tissue burden is enough evidence by itself to establish a causal link. Some of their positions are based on different conclusions from portions of the literature, but they also often are based on grounds of intuitive reasoning. Therefore, the primary debate about criteria for attributing a lung cancer to asbestos exposure has centered on whether sufficient asbestos tissue burden alone or sufficient asbestos tissue burden with accompanying asbestosis should be the criterion. As noted by Abraham,[19] litigation has provided much of the stimulus for this debate, and we already have observed that criteria for establishing cause of a lung cancer are largely for purposes of compensation in the individual case. The differences between those who require and those who do not require asbestosis may appear exaggerated in the adversarial context of litigation. No one disputes that most lung cancers are caused by tobacco smoking and that some lung cancers are caused or partly caused by asbestos exposure. No one disputes that there must be a basis for attributing a lung cancer to asbestos exposure, especially if the patient also is a smoker. No one disputes that a lung cancer in a patient with asbestosis is due to asbestos exposure. The debate is what to do with patients with lung cancer with the requisite asbestos tissue burden who do not have asbestosis, especially if they also are tobacco smokers or former smokers.
An intuitive question about the requirement of asbestosis for attributing lung cancer causation was raised in an editorial by Roggli et al[18] and then subsequently by other editorials: Since asbestos is the cause of the lung cancer, why would only patients with asbestosis have the increased risk of asbestos-related lung cancer? This question deserves further consideration.
Part of the relationship between asbestosis and lung cancer risk has to do with the dose or tissue burden of asbestos. The risk of asbestosis and the risk of asbestos-related lung cancer rise in a parallel manner with increasing tissue burden of asbestos.[7,8,22] The evidence indicates that the level of asbestos exposure required for a risk of asbestosis is in the same range as that for lung cancer risk. Asbestosis, thus, is a reliable marker that the patient has been exposed to the asbestos dose or tissue burden necessary to put that patient at risk for asbestos-related lung cancer.
Tissue burden alone does not fully explain why asbestosis should be the criterion for linking a lung cancer to asbestos exposure. There are a number of forms of diffuse lung fibrosis in which there is in an increased risk of lung cancer, including usual interstitial pneumonia/idiopathic pulmonary fibrosis (UIP/IPF) and collagen vascular diseases such as scleroderma.[23] In earlier decades, the theory was offered that asbestos-related lung cancers were so-called scar cancers as an explanation for the link between asbestosis and lung cancer risk. In regard to local scars, Cagle et al[24] have demonstrated that scar cancers do not arise from preexisting focal scars, but rather the cancers produce the so-called scars as a desmoplastic reaction. Similarly, lung cancer is not caused by diffuse fibrosis or scarring in the lungs, but rather lung cancer is caused by the same agent, for example asbestos, that also causes the fibrosis in susceptible patients with sufficient dose.
There are underlying similarities in the increased risk of lung cancer in patients with asbestosis and patients with other forms of chronic diffuse pulmonary fibrosis. It is now thought that tobacco smoking is a likely cause of UIP/IPF.[25] Tobacco smoke causes a variety of molecular events and inflammatory responses in the lung tissue with release of substances such as mediators and cytokines, some of which may have roles in the pathogenesis of both the neoplastic disease and the nonneoplastic disease producing what investigators have observed for several decades as an increased risk of lung cancer in patients with UIP/IPF. Interestingly, there is an increased risk of cancers of both the lung and skin in patients with systemic scleroderma.[26] These are the same tissues where the fibrosis of scleroderma most often occurs. This, too, is consistent with molecular events and inflammatory responses that have roles in the pathogenesis of both the neoplastic and nonneoplastic diseases in the lungs and the skin in scleroderma. As a result, investigators have observed for decades an increased risk of lung cancer in patients with scleroderma of the lungs.[26] Similar increases of primary cancers in organs affected by sarcoidosis (lymphoid tissues, skin, liver, and lung during the first decade of follow-up) have been reported with chronic inflammation as the putative mediator of the increased risk.[27]
Similar to other forms of chronic diffuse pulmonary fibrosis or inflammation associated with an increased risk of lung cancer, asbestosis develops when asbestos fibers stimulate inflammatory cells to produce a variety of mediators of fibrogenesiseg, growth factors, cytokines, and oxidative damage.[23,28-33] As suggested by Rom et al[34] a decade ago and observed by subsequent investigators, some of these mediators also can act as similar mediators for the growth of carcinomas. A component of the individual susceptibility that I have referred to would be related, for example, to whether the individual produces the mediators, how fast or how much the individual metabolizes the mediators, and how many receptors the individual has for the mediators. The role of these mediators in both fibrogenesis and carcinogenesis provides a basis for the simultaneous occurrence of asbestosis and asbestos-related lung cancers in the same individual and a basis for the increased risk of lung cancer in patients with asbestosis.
Of course, most tobacco smokers with lung cancer do not have UIP/IPF. However, there are other tobacco-related changes that can be observed more often in the lung tissue of patients with tobacco-related lung cancers. In particular, it is the subpopulation of smokers with chronic obstructive pulmonary disease who have the greatest risk of developing lung cancer, and the association of these diseases with lung cancer is so strong that emphysema and other forms of chronic obstructive pulmonary disease have been reported to be risk factors for lung cancer independent of tobacco smoking.[35-38] In the case of emphysema and other smoking-related changes in the lung tissue, we once again have a situation in which various inflammatory, oxidative, and growth factor mediators have a role that might impact carcinogenesis as well as the changes in other lung tissues, including remodeling of tissue in emphysema. However, as noted, the causal association between tobacco smoke and lung cancer is so strong that we do not require identification of other tissue markers of tobacco dose and susceptibility to that dose to attribute a lung cancer to tobacco smoking.
However, we still have largely been talking about risk in populations and, for assessing individuals, we would like to know how often a patient with lung cancer with the requisite level of asbestos exposure also has asbestosis. This fundamental question has been neglected in most studies, but Roggli and Sanders[39] recently reported on 234 lung cancer cases with data on asbestos tissue burden from digestion studies. Their cases were mostly medicolegal cases and, therefore, expected to have at least some asbestos exposure above background. In the series of Roggli and Sanders,[39] all patients with lung cancer with asbestos tissue burdens above 50,000 amphibole fibers per gram of wet lung tissue by scanning electron microscopy had histopathologic asbestosis in sections of their lung tissue except for 10 patients (based on their Table 6), or 6.5%, of the 155 patients without asbestosis. This finding indicates that the great majority of patients with lung cancer with asbestos tissue burden sufficient to increase lung cancer risk also have asbestosis on tissue sections. This is consistent with asbestosis as a marker of asbestos-related lung cancer, both as an indicator of the requisite tissue burden for increased lung cancer risk and as verification that the individual is susceptible to the fibrogenic-carcinogenic effects of that asbestos exposure.
There are some patients in the series of Roggli and Sanders[39] that have the requisite asbestos burdens for lung cancer risk but who do not have asbestosis. Do these patients have asbestos-related lung cancers or not? I do not think there is any way to really tell from the published data. Since we would expect that some people with excessive amphibole burdens would not be susceptible to those tissue burdens, we cannot say whether one, several, or all of these patients would have developed a lung cancer anyway. This is especially problematic in any who may have been tobacco smokers. Although 93% of the patients in the study by Roggli and Sanders[39] for whom information was available were smokers, it is not clear whether the 10 patients with the excessive amphibole burdens but without asbestosis were smokers.
The study by Mollo et al[1] in this issue of the Journal has some similarities to the study by Roggli and Sanders,[39] but it raises a different question of how to diagnose asbestosis. Generally, the number of asbestos bodies seen on tissue sections is proportionate to the total asbestos tissue burden. Of course, with relatively low tissue burdens, no asbestos bodies may be seen on tissue sections, even if the levels are above background. When someone has a tissue burden in the range seen with asbestosis and asbestos-related lung cancer, asbestos bodies should be readily identifiable in tissue sections, and, indeed, the presence of asbestos bodies on tissue sections is a component of the definition of asbestosis. The article by Mollo et al[1] raises a question that there may be a number of occult asbestosis cases with fibrosis and elevated asbestos burden on digestion study but no asbestos bodies on tissue sections. The literature indicates that occult asbestosis, if it exists, is extremely raremuch less frequent than the 0.5% of cases for which Mollo et al[1] raised the question.
One challenge in interpreting articles on asbestos-related diseases is that different investigators use different methods for determining asbestos tissue burden and report results differently, eg, asbestos bodies vs asbestos fibers, wet weight vs dry weight, and light microscopy vs electron microscopy. Some variability in ranges for different conditions is to be expected between different laboratories as well. Therefore, results must be interpreted for the methods used and the ranges established for the individual laboratory doing the study. The concentration of asbestos bodies per gram of dry tissue that Mollo et al[1] use as their cutoff for a level sufficient to produce asbestosis is lower than what others have reported, and Mollo et al[1] concur with this in the article. I wonder if Mollo et al considered that some of the fibrosis in their cases might be from causes other than occult asbestosis. Churg,[8] Roggli and Pratt,[40] Egilman and Reinhart,[20] and Hammar[41] all have pointed out potential pitfalls in the histopathologic diagnosis of asbestosis. There are many causes of lung fibrosis, and patients with lung cancer are subject to fibrosis from a variety of reasons related to their lung cancer. Lung cancers, of course, can cause peritumoral and postobstructive pneumonias or other reactions that result in interstitial fibrosis. Most of the patients in the study by Mollo et al[1] were smokers, and tobacco smoke can cause smokers bronchiolitis and fibrosis around bronchioles and may even cause respiratory bronchiolitisassociated interstitial lung disease, desquamative interstitial pneumonia, or Langerhans histiocytosis (eosinophilic granuloma) in some patients.[25]

Banks et al[21] pointed out that traditional epidemiologic studies may not convince all authorities that asbestosis is required to link a lung cancer to asbestos exposure. There also are differences in whether traditional studies of various types include all the information one would like to answer specific questions. Not only are there differences in reporting results owing to varying methods within the same discipline, as already noted, there are also differences in what can be determined within different disciplines (radiologic studies may sometimes not detect the lesions of minimal grade 1 asbestosis that can be seen under the light microscope, for example). If the increased lung cancer risk occurs in workers with asbestosis, then any study that includes workers with asbestosis is expected to show an increased risk of lung cancer, even if the parameter studied is asbestos dose or tissue burden. When comparing results between asbestos studies, these factors must be taken into account, in addition to usual issues such as cohort size and control of confounding factors. As Banks et al[21] point out, a molecular marker likely would be a superior tool to link lung cancers to asbestos exposure. In the case of tobacco smoke and lung cancer, the association is so strong that no special criteria are required to link a lung cancer to tobacco smoke. However, many mutations caused by tobacco smoke during the pathogenesis of lung cancer have been identified, and some of these are unique enough and frequent enough that they can be used as a fingerprint to demonstrate the link between a lung cancer and tobacco smoke. I agree with Banks et al[21] that what is needed is a molecular marker that is unique to asbestos, or at least not caused by tobacco smoke, that would allow us to link a lung cancer to asbestos exposure. So far, molecular markers like p53 and k-ras seen in patients with smoking-related cancers have been reported in lung cancers said to be due to asbestos, but a unique marker for asbestos-related lung cancer has not been identified.[42]
From the point of view of the pathologist, asbestosis is an unambiguous marker not only of a tissue burden of asbestos sufficient to cause a risk of lung cancer but also of individuals whose tissues are susceptible to the effects of that tissue burden. Asbestosis is the most consistent marker of asbestos-related lung cancer in the literature to date and has a basis in current molecular theories of disease similar to many other inflammatory or fibrotic diseases associated with an increased risk of lung cancer, including diseases caused by tobacco smoke. Tobacco smoke is sufficient by itself to cause the vast majority of lung cancers and is sufficient by itself to cause lung cancers in workers with asbestos exposures. Asbestosis establishes the link between a lung cancer and asbestos exposure even when the patient also was a tobacco smoker. Since there is no other marker, for example, a molecular genetic marker, available to link a lung cancer to asbestos exposure, currently there is no basis in the absence of asbestosis for assuming that an individual lung cancer is caused by asbestos or asbestos and tobacco smoke combined rather than by tobacco smoke alone. This also applies to the 0.5% of cases in which Mollo et al[1] raise the issue of occult asbestosis, to which we must add a debate about the histopathologic definition of asbestosis. Unless and until a better marker comes along, the only consistently reliable marker for an asbestos-related lung cancer is asbestosis, especially in asbestos workers who are also tobacco smokers.

Exposure asbestos Wallpaper Photos Pictures Pics Images 2013

Exposure asbestos Wallpaper Photos Pictures Pics Images 2013

Exposure asbestos Wallpaper Photos Pictures Pics Images 2013

Exposure asbestos Wallpaper Photos Pictures Pics Images 2013

Exposure asbestos Wallpaper Photos Pictures Pics Images 2013

Exposure asbestos Wallpaper Photos Pictures Pics Images 2013

Exposure asbestos Wallpaper Photos Pictures Pics Images 2013

Exposure asbestos Wallpaper Photos Pictures Pics Images 2013

Exposure asbestos Wallpaper Photos Pictures Pics Images 2013

Exposure asbestos Wallpaper Photos Pictures Pics Images 2013

Exposure asbestos Wallpaper Photos Pictures Pics Images 2013

Exposure to asbestos Wallpaper Photos Pictures Pics Images 2013

Exposure to asbestos  Biogarphy

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Lung cancer continues to be the leading cause of cancer among Canadian men, and in 2012, it was estimated that 13,300 men would be diagnosed with lung cancer and 10,800 would die of it [1]. While cigarette smoking is recognized as the leading cause of lung cancer, many occupational exposures, including asbestos, have also been shown to increase risk. Asbestos is a term used to describe six naturally fibrous minerals, and one of these, chrysotile, accounts for 95% of the asbestos ever used worldwide, and until recently was the only type produced in Canada [2]. All forms of asbestos have long been recognized as human carcinogens by the United States Environmental Protection Agency [3], the International Agency for Research on Cancer [4], and the National Toxicology Program [5]. This conclusion is based largely on unequivocal evidence assembled from epidemiological studies that have found excesses of lung cancer and mesothelioma in highly exposed textile workers, miners, and cement factory workers [4,6].
Today, more than 90% of the asbestos produced worldwide is used to manufacture asbestos sheets and pipes [7]. The World Health Organization has estimated that approximately 125 million individuals continue to be exposed to asbestos in the workplace [8]. Occupational exposure to asbestos in Canada has decreased dramatically over the past two decades due to provincial occupational health and safety controls that have been implemented. While those involved in the mining of asbestos are at higher risk of developing asbestos-related disease, the precautions offered to these workers to limit exposure are greater than those unwittingly exposed through other trades. Overall, the mining of asbestos in Canada has decreased dramatically, and in 2011, for the first time in over 130 years, production was halted [9], Today, in Canada, the most common sources of asbestos exposure arise from the repair, renovation, and demolition of older (pre-1980) buildings.
Relatively few studies have examined associations between workplace exposure to asbestos and lung cancer using a population-based design. Population-based designs provide important features that include an ability to estimate risks over a wider range of exposure levels than those typically reported in industry-specific studies. They provide the opportunity to characterize the frequency and nature of exposures in the general population. Moreover, because such studies cover diverse occupational groups, there is a reduced impact of confounders that may be specific to particular occupations. Recently, a population-based case–control study in Montreal found that workers with substantive exposure to asbestos had a greater risk of lung cancer, however, this finding did not achieve statistical significance (odds ratio (OR) =1.78, 95% CI=0.94, 3.36) [10]. Cumulative exposure was positively associated with lung cancer risk in a case–control study in Stockholm, Sweden [11], while a multi-center European case–control study found no association between occupational exposure to asbestos and lung cancer in six Central and Eastern European countries, but a nearly twofold (OR=1.85, 95% CI=1.07-3.21) increased risk was observed among UK workers [12].
While both cigarette smoking and asbestos are recognized lung carcinogens, there remain uncertainties about how they operate together to increase the risk of lung cancer. Attempts to understand the joint effects of smoking and asbestos on the risk of lung cancer extend back to Selikoff et al.’s seminal work in the late 1960s [13]. A subsequent review of this literature suggested that the interactive effects are multiplicative [14], which implies that asbestos exposure increases the risk of lung cancer by the same factor in smokers and non-smokers alike. An additive relationship, on the other hand, would assume that the effects of asbestos exposure and smoking are independent. Other reviews [15,16] and a meta-analysis [17] have suggested that the combined effects of smoking and asbestos are more than additive but less than multiplicative. This conclusion is consistent with very recent work by Frost et al. that revealed interactions that were greater than additive, although the multiplicative association could not be rejected [18]. Apart from the studies by Gustavsson et al. and Pintos et al., we know of no other research that has evaluated the joint relationship between asbestos and smoking on lung cancer risk in the general population where exposure levels are much lower than in asbestos workers, yet with fewer precautions and protections offered to reduce exposure. In the Gustavsson et al. study, the association between asbestos and smoking on lung cancer risk was found to be between additivity and multiplicativity [11]. In the Montreal study, the association was found to be sub-multiplicative [10]. To add to this knowledge, we examined the joint relationship between smoking and asbestos in this population-based case–control study.
With this background, the primary objective of our study is to build upon past research by reporting on the association between occupational exposure to asbestos and lung cancer among Canadian men. The secondary objective of the study is to evaluate the combined effects occupational exposure to of asbestos and cigarette smoking on the risk of lung cancer
Methods
Study population
A case–control study design was used to address the research objectives, and the data come from the lung cancer case–control component of the National Enhanced Cancer Surveillance System (NECSS). The overall objective of the NECSS was to improve our understanding of both environmental and occupational determinants of cancer [19]. The NECSS was a collaborative project between the Public Health Agency of Canada and cancer registries in eight Canadian provinces (British Columbia, Alberta,Saskatchewan, Manitoba, Ontario, Nova Scotia, Newfoundland, and Prince Edward Island). There were no subjects (cases or controls) from the province of Quebec. Detailed information was collected from cases and controls for a number of potential risk factors including: sociodemography, anthropometry, diet, smoking, exposure to second hand smoke, and participation in physical activities. Individuals were also asked to provide lifetime residential and occupational histories. Questionnaires were administered between 1994 and 1997.
The NECSS endeavoured to collect information for each incident cancer within three months of diagnosis. Among men, there were a total of 3,718 histologically confirmed lung cancer cases (ICD-9 rubric 162) identified between 1994 and 1997. Letters were sent to the physicians of 3,033 (81.6%) of these cases to solicit their participation. Physician consent was obtained and questionnaires were mailed to 2,548 (69%) of the cases; physician consent was refused for 229 (6%) of all eligible cases and 653 (18%) were deceased at the time of the request and therefore excluded. Completed questionnaires were returned by 1,736 of the 2,548 cases who were mailed a questionnaire yielding an overall response rate of 68.1%.
The NECSS assembled a series of controls from the general population. For 5 provinces, controls were identified through provincial health insurance plans (Prince Edward Island, Nova Scotia, Manitoba, Saskatchewan and British Columbia). These insurance plans cover more than 95% of residents in the province. Elsewhere, either random digit dialing (Newfoundland and Alberta), or property assessment data (Ontario) were used as the sampling frame to recruit controls. Frequency matching to the overall case grouping (19 types of cancers) was used to select controls with similar age and sex distribution, such that there would be at least one control for every case within each sex and 5-year age group for any specific cancer site within each province. In total, questionnaires were mailed to 4,270 men identified as possible controls in the 8 provinces. Approximately 7% of these (n=287) were returned because the address was incorrect, and no updated address could be found through publicly available sources. In all, 2,547 male controls returned completed questionnaires, representing 64% of those contacted and 60% of those ascertained
For the purposes of our analyses, we restricted the study population to only include men given that we expected few women to have been exposed to asbestos in the workplace. We used the same analysis file previously used to evaluate associations between diesel engine exhaust emissions and lung cancer which excluded individuals under the age of 40, and those who had not worked for at least one year [20]. In the NECSS, among all participating incident lung cancer cases only 0.7% (n=13) were diagnosed before the age of 40; the corresponding number of controls excluded to meet the age requirement was 438. A total of 42 cases and 56 controls were excluded because their reported length of employment was less than one year. After applying these exclusion criteria we were left with a total of 1,681 cases and 2,053 controls.
Occupational assignment of exposures
Cases and controls were asked to provide information for each job held in Canada for at least 12 months from the time they were 18 years old until the time of interview. Information sought for each job included: job title, main tasks, type of industry, location, and the start and end dates of employment. A total of 15,646 jobs were identified, of these 15,234 (97.4%) jobs contained sufficient information for exposure assessment. No exposures were assigned for jobs that were self-reported to be retirement (n=185), disability (n=10), and unemployment (n=8).
Occupations and industry titles were assigned by one of two hygienists, who were blinded to case–control status, using the Canadian Classification and Dictionary of Occupation codes (originally published in 1971 with revisions up until 1986), and Standard Industrial Codes [21]. The hygienist coded each job on the basis of exposure to known or suspected lung cancer carcinogens. These exposures included: asbestos, diesel and gasoline engine exhaust emissions, and crystalline silica. This assessment was guided by the scientific and technical literature, consultation with experts, and a review of existing databases of exposure assessment. The assignment of workplace exposures took into account the manner that asbestos was used over the years. For example, before 1976, drywall installers used dry-wall joint cement that contained asbestos, while after 1980 asbestos was banned in this cement.
The assignment of occupational exposures was done according to three dimensions: concentration, frequency and reliability. The frequency of exposure was assigned based on the proportion of work time during a normal work week that the subject was exposed; this assignment took into account whether the work was part-time or seasonal in nature. ‘Low’ frequency corresponded to less than 5% of the work time, ‘Medium’ between 5% and 30%, and ‘High’ represented more than 30%. Concentration was assessed on a relative scale. For each substance, benchmarks were established and exposures were coded with respect to these benchmarks. Non exposure was interpreted as exposure up to background levels found in the general environment. The relative benchmarks for concentration levels used by our team of hygienists were ‘Low’ for welders and boiler operators, ‘Medium’ for boiler and pipe insulators and marine firemen and ‘High’ for miners and insulation workers (blowers and sprayers). It is very difficult to provide a reliable estimate of the absolute number of fibres per unit of volume corresponding to the different exposure levels. However, as a crude indicator, we can suggest that our ‘Medium’ level corresponded roughly to the 1976 American Conference of Governmental Industrial Hygienists threshold limit values (TLV) given that these values were in force in Canada in 1983 at a time when our study subjects were working. Specifically, the TLV for chrysotile asbestos fibers over 5 microns was 5 fibres per/cc in these Quebec guidelines. Finally the third dimension of exposure, reliability, refers to the hygienists’ degree of confidence that the exposure was actually present in the job under evaluation; ‘Low’ refers to a possible exposure, ‘Medium’ to a probable exposure and ‘High’ to a certain exposure. Estimates of the inter-rater reliability of the exposure assignment method, which were based on the work of chemists from the group that conducted the exposure assessment our study, lend credibility to the validity of the approach we used. Specifically, Goldberg et al. reported that the percent agreement among raters was between 95% to 98% with a Cohen’s kappa from 0.5 to 0.7 [22].
Statistical analysis
We constructed several metrics to characterize occupational exposure to asbestos. These metrics included: ever exposed, highest attained concentration (high, medium, low), as well as a duration of exposure. Given the small number of individuals that had high concentrations of exposure, we combined medium and high into one group. Those with a low reliability score (“possibly exposed”) were assumed to have had no exposure.
Logistic regression was used to estimate the odds ratios (OR) and their corresponding 95% confidence intervals (CI) for the various exposure metrics. Adjustments were made for the potential confounders: age, cigarette smoking, socioeconomic status, exposure to second hand smoke, and occupational exposure to silica, and diesel exhausts. Occupational exposure to silica, and diesel engine exhausts were assigned to the cases and controls using the same methodology that was used for asbestos. Silica and diesel exposures were modelled as cumulative time-weighted measures. While gasoline engine emission exposure measures were also derived for the cases and controls, they did not confound the risk estimates for asbestos, and therefore, were not included in the models as adjustment factors. Multivariable models were adjusted for cigarette smoking through the use of a pack-years variable which incorporated aspects of both smoking duration and intensity. Cigarette pack-years were defined as the number of years of smoking an average of 20 cigarettes per day. For exposure to second-hand smoke, a composite measure was used that took into account lifetime exposures received both at home, and in the workplace [23]. It was derived as a function of the number of years of exposure that incorporated both the number of regular smokers that lived in each residence, and the number of smokers who smoked regularly in the subjects’ immediate work environment
The joint effect of smoking and occupational exposure to asbestos was first examined by estimating the odds ratios for cross-classification categories of cigarette pack-years (<10, 10 - <40, ≥40) and the highest attained occupational exposure to asbestos (none, low, medium/high). The small numbers of lung cancers among never smokers (n=34; 2% of all cases) precluded a separate evaluation of asbestos risks in this group. The odds ratios and 95% confidence intervals were estimated for eight cross-classification categories, while the ninth category (no asbestos exposure, < 10 cigarette pack-years) was used as the referent. The joint effects of smoking and asbestos on lung cancer risk were evaluated using two previously derived indices: the Synergy (S) [24] and Multiplicativity (V) [25]. We followed a similar approach that Frost et al. used to evaluate the relationship between asbestos and smoking and lung cancer in workers in Great Britain [18]. We used our derived odds ratios (ORs) to calculate the index S [24] as follows:
S=ORAS−OR0ORA+ORS−2OR0
Where ORA is the odds ratio of lung cancer exposed to ‘medium or high’ levels of asbestos among those with little to no smoking history (<15 pack-years), ORS is the odds ratio of lung cancer among smokers (≥ 40 pack-years) with no exposure to asbestos, ORAS is the odds ratio of lung cancer among smokers (≥ 40 pack-years) exposed to asbestos, where each odds ratio is estimated relative to the referent group of men who had accrued less than 10 cigarette pack-years and were not exposed to asbestos (OR0).The Multiplicativity index was calculated as:V=OR0ORASORAORS
A value that exceeds one for the S index suggests an interactive effect between smoking and asbestos exposure on lung cancer that could imply a multiplicative effect. In contrast, a value of S near one suggests that the two risk factors would operate in an additive fashion on the risk of lung cancer. For the V index, a value of one indicates a multiplicative interaction, whereas as values greater and less than one indicate an interaction that is more or less than multiplicative, respectively.
Ethics approval
The participating provincial cancer registries obtained approval of the NECSS study protocol through their respective ethics review boards. All participants provided informed consent.
Results
Of the 15,234 occupations ever held by the study subjects, a total of 801 were coded as having either ‘probable’ or ‘definite’ exposure to asbestos. The most commonly reported exposed occupations were mechanics and repairmen, stationary engine and utility workers, pipefitters, and construction workers (Table  1). Water transport operating occupations represented the only group deemed to have a high frequency of exposure to asbestos. Specific jobs included in this group that worked on ships included: deck officers, engineering officers, deck crew, engine and boiler room crew workers.
Table 1. Most frequent occupations among the 801 jobs held by subjects that were classified as having probable or definite exposure to asbestos
A total of 233 cases and 224 controls, respectively, were exposed to asbestos at some point during their lifetime occupational history (Table  2). Those who were ever exposed to asbestos had a 28% increased risk of lung cancer relative to those who were not (OR=1.28, 95% CI: 1.02, 1.61). The risks according to highest concentration of occupational exposure ever attained were more pronounced. Only two cases and one control reported working in a job with an assigned ‘high’ concentration of exposure. As a result, we combined ‘medium’ and ‘high’ concentrations into one category. Those who had ever been exposed to medium or high levels had a more than twofold increase in risk (OR=2.16, 95% CI=1.21-3.88).
Table 2. Adjusted odds ratios of lung cancer in relation to occupational exposure to asbestos
We found that duration of occupational exposure to asbestos was not related to the risk of lung cancer (Table  2). When we modeled duration of exposure as a continuous variable, the adjusted odds ratio of lung cancer for an increase in 10 years of exposure was 1.03 (95%% CI=0.94-1.13). This risk increased to 1.13 (95% CI=0.84-1.52) when analyses were restricted to those who were only exposed to medium or high concentrations; this result however was not statistically significant (p=0.44). The frequency of the jobs that were deemed to have ‘medium’ or ‘high’ concentrations of asbestos is presented in Figure  1. The most common of these jobs were pipefitters and boilermakers, and insulators.
thumbnailFigure 1. Most common occupations among mean with medium or high concentration levels of asbestos, NECSS lung cancer case-control study.
None of the first-order interaction terms between cigarette smoking pack-years and the three measures of asbestos exposure were statistically significant. The corresponding p-values for the smoking interaction terms with ‘ever’, ‘highest attained’ and ‘duration’ asbestos exposure were 0.33, 0.77, and 0.88, respectively.
Stratified analyses of highest attained asbestos exposure across cigarette pack years categories are presented in Table  3. There was an approximate two-fold increase in risk among those with ‘medium’ or ‘high’ occupational exposure to asbestos relative to those with no such exposure in each of the three pack-year categories. This is consistent with a multiplicative relationship between the two factors. Those who had at least 40 pack-years of smoking and were exposed to medium or high asbestos levels had the highest risk of lung cancer; relative to those with no asbestos exposure, and less than 10 cigarette pack-years, their risk nearly 38-fold higher (OR=38.59, 95% CI=10.78-138.08) (Table  4). The calculated values of the S and V indices were 2.10 and 0.99 respectively, supporting the notion that the interaction between asbestos and smoking is multiplicative.
Table 3. Adjusted odds ratios* and 95% C.I. according highest occupational exposure to asbestos across cigarette pack-year smoking categories
Table 4. Synergy and multiplicative indices between asbestos exposure and cigarette smoking
Discussion
This population-based study of men employed across a diverse range of jobs found that workplace exposure to asbestos was associated with an increased risk of lung cancer. This association persisted after adjusting for cigarette smoking, second hand smoke, and other occupational exposures previously implicated as possible risk factors for lung cancer. The approximate 28% increased risk observed among men ever exposed to asbestos is similar to the finding of Pintos et al. [10]. In their Montreal based case–control study, those who were exposed to asbestos had an odds ratio of 1.21, (95% CI=0.98-1.49) relative to those with no exposures. The population attributable risk (PAR) percent is often used to provide an estimate of the percentage of cases that be avoided if the putative exposure was eliminated [26] . We calculated the PAR in our study using the odds ratio of 1.28 among ever exposed, and an estimated prevalence of exposure of 11.3% (based on our control series). This yielded a PAR of 3.1% which suggests that a relatively small percentage of Canadian male lung cancer cases are due to occupational exposure to asbestos. Based on an estimated 13,300 incident lung cancers among men in Canada in 2012 [1] this would account for approximately 412 incident cases.
Our study provided support for a dose–response relationship between asbestos exposure and lung cancer as higher risks were observed among those who were ever exposed to ‘medium’ or ‘high’ concentrations of asbestos. Pipefitters accounted for nearly half of these cases and controls (41 of 87). While the limited number of subjects did not allow us to characterize risks for specific types of jobs, our results are consistent with a previously published study of Ontario pipe trade workers [27]. They reported a 53% increased risk of lung cancer mortality among pipefitters who had been registered trade members for at least 30 years, relative to the Ontario general population. However, their study was somewhat limited due to a lack of data on smoking. Our findings support the hypothesis that asbestos and cigarette smoking affect the risk of lung cancer in a multiplicative fashion.
In many occupational studies, duration of exposure is regarded as valid surrogate measure of cumulative exposure due to the inherent difficulties in retrospective studies to precisely characterize exposure intensity. In their Montreal case–control study, Pintos et al. found a higher risk of lung cancer among those exposed to asbestos for at least 20 years when compared to those exposed for shorter durations [10]. Duration of exposure was also positively associated with lung cancer risk in other industry-specific cohorts [28]. In contrast, we found that only intensity but not duration of exposure was associated with statistically significant increased risks of lung cancer. This observation is consistent with recently published findings on a cohort of workers employed in an asbestos reprocessing plant in the Calvados region of France [29]. In this study, Clin and colleagues observed that the average exposure to asbestos expressed in terms of fibers per ml was associated with pleuro-peritoneal mesothelioma, lung cancer, and colorectal cancer (p<0.05), however, no statistically significant associations were evident with duration of exposure for any of these three cancer sites. Other studies of asbestos workers have also found associations with intensity but not duration of exposure [12,30,31]. Our finding of a stronger positive association between duration of exposure at medium or high levels of asbestos when compared to durations spent at lower levels suggests that time exposed above a threshold level may be a relevant marker of risk. However, this finding should be interpreted cautiously as it based on a very small number of subjects who were exposed to either medium or high intensities.
It is well recognized that there is a lengthy latency period between the time of first exposure to an environmental carcinogen and the development of a solid tumour such as lung cancer. For example, the latency period associated with cigarette smoking and lung cancer has been estimated to be several decades following the initiation of smoking [32]. By extension, the increased risks of lung cancer due to exposure to asbestos observed in this study are a reflection of workplace exposures many years if not decades earlier. Indeed, among those classified has having ‘medium’ or ‘high’ concentrations to asbestos in the workplace, the start date of employment was after 1980 in only 6% of these jobs.
Participants in our study were asked to provide information for only those jobs that were held for at least one year. The exclusion of these short-term jobs raises the possibility that some exposure misclassification has been introduced. Previous analysis of 27.5 million workers found increased risks of lung cancer among those exposed to high levels of asbestos (20 to 40 fibers per cubic centimeter of air) for only a few months [33]. Under a classical error model where the possible exposure misclassification error arising from excluding these short term jobs is non-differential to case–control status, our risk estimates would be understated.

An important strength of this study was the availability of other risk factor data obtained through both the questionnaire, as well as expert-based coding of occupational histories. Unlike many other occupational case–control studies, we had extensive data on cigarette smoking, most notably, exposure to second hand smoke. This measure allowed our risk estimates to take into account lifetime exposure to second-hand smoke incurred at both home and workplace settings. In addition, the industrial hygienists also coded each job for possible exposure to other known or suspected lung carcinogens including: crystalline silica, gasoline and engine emissions. We recently found that occupational exposure to diesel but not gasoline engine emissions increased the risk of lung cancer; the risk of lung cancer was also increased among individuals exposed to crystalline silica [34]. The addition of these two covariates (diesel and silica) strengthened the association for asbestos by approximately 20%.

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Approximately 68% of eligible cases and 64% of eligible controls completed a questionnaire. This raises the potential to introduce some bias in our risk estimates, and our results should be interpreted cautiously because of this possibility. However, for several reasons, we do not believe this bias fundamentally changes our results. First, observed associations with known and suspected risk factors such as cigarette smoking, and exposure to second-hand smoke are similar in direction and magnitude to risk estimates reported in other epidemiological studies. Moreover, our published findings for other occupational exposures within the same study population [34] are also consistent with the epidemiological literature. Lastly, the distribution of lung cancers by histology in our study is remarkably similar to population-based figures for North America [35] and provides some support for the generalizeability of these results to incident lung cancers in Canada. Unfortunately, the NECSS did not collect data from those diagnosed with mesothelioma, and therefore, we were unable to investigate associations with this endpoint.
We were unable to distinguish asbestos on the basis of fiber type. Asbestos fibers can be described according to two broad classes serpentines (phyllosilicates) and amphiboles (inosilicates) that differ substantially with respect to biopersistence and physical and chemical properties. Serpentines include chrysotile asbestos which is the predominant type of asbestos in Canada. The International Agency for Research on Cancer has determined that there is sufficient evidence to conclude that all these forms of asbestos can cause cancer in humans [4,6]. There remains considerable uncertainty regarding differences in lung cancer risk resulting from exposure to different types of asbestos fibers. A review of cohort studies where quantitative measurements of asbestos exposure were available demonstrated clearer and consistent associations between exposure and lung cancer for crocidolite or amosite [36]. On the other hand, associations from cohorts exposed primarily to crysotile asbestos were less consistent [37,38]. It is generally accepted that amphibole fibers are more harmful than chrysotile fibers for mesothelioma [36,39]. However, it has been argued that these differences are not all that important given that chrysotile is the most commonly used type of asbestos [40,41]. In our study, those who were determined to have been exposed to asbestos were believed to have been exposed to chrysotile, however, it is possible that some exposure to less prevalent yet more potent types of fibers occurred and was unaccounted for.
Another limitation of our study was the relatively small number of study subjects who were ever exposed to medium or high levels of asbestos. In total, there were only 39 cases and 24 controls exposed at these levels. These small numbers hindered our ability to characterize the joint relationship between smoking and asbestos exposure on the risk of lung cancer. It also limited our examination of the risks of lung cancer with exposure to asbestos according to different histological subtypes. Several studies have found associations that were most pronounced for adenocarcinoma subtypes [28,42-44], however, others did not [45-47]. The three most common histological types of lung cancer in our study population were squamous cell carcinoma (35%), adenocarcinoma (28%), and small cell carcinoma (15.9%) [34]. When we restricted analysis to adenocarcinoma, the odds ratio among those exposed to medium or high levels of asbestos increased from 2.16 to 3.14 (95% CI=1.50 – 6.58). However, the latter estimate was based on only 13 incident cases and therefore, our study has very limited statistical power to make inferences by histological type.
Conclusions
In summary, the findings from this Canadian case–control study are consistent with the determination by international agencies that asbestos is a human lung carcinogen. While chrysotile asbestos is the predominant type of asbestos in Canada, it is possible that some of the workers in our study were exposed to other types of asbestos fibers. For this reason, and given the relatively small number of individuals exposed to medium and high exposure where the excess risks of lung cancer were found, we cannot conclusively attribute increased lung cancer risks to chrysotile. Despite the limitation, our findings provide further support that exposure to asbestos has contributed to an increased risk of lung cancer in Canadian workplaces
Asbestos exposure can cause a number of disabling and fatal diseases. The principal rout of exposure is by inhalation through the nose and mouth. Asbestos, traditionally valued for it's indestructibility, is especially resistant to the internal defenses of the human body. Once lodged inside the lungs, most fibers will not break up or dissolve, and they cannot be neutralized or removed.
AsbestosisAsbestosis is a disease which is characterized by pulmonary fibrosis, a progressive scarring of the lungs caused by the accumulation of asbestos fibers. Asbestosis is associated exclusively with chronic, occupational exposure. The build up of scar tissue interferes with oxygen uptake through the lungs and can lead to respiratory and heart failure. Often, asbestosis is a progressive disease, even in the absence of continued exposure. Symptoms include shortness of breath, cough, fatigue, and vague feelings of sickness. When the fibrosis worsens, shortness of breath occurs even at rest.
Pleural Plaques
Pleural plaques and pleural calcification are markers of exposure and may develop 10 to 20 years after initial exposure. Plaques are opaque patches visible on chest x-rays that consist of dense strands of connective tissue surrounded by cells. All commercial types of asbestos induce plaques. Plaques can occur even when fibrosis is absent and do not seem to reflect the severity of pulmonary disease.
Lung CancerOf all the diseases related to asbestos exposure, lung cancer has been responsible for over half of the excess deaths resulting from occupational exposure. Although tissues and cells react to the presence of asbestos immediately, detectable symptoms take years, or more often decades, to manifest themselves. Asbestos-induced lung cancer may not show up on x-rays for twenty years or more after the exposure began. This delay between exposure and onset is referred to as the "latency period". Even in cases of prolonged heavy exposure, abnormalities commonly appear on x-rays only after ten or more years following exposure.
Asbestos as a Co-Factor: Other substances appear to cooperate with asbestos to multiply the risk of lung cancer. Asbestos exposure in combination with cigarette smoking can multiply the risk of developing lung cancer as much as ninety times over the risk to a non-smoker with no history of exposure to asbestos.
Mesothelioma
Mesothelioma, a malignant nodular type cancer of the membranes which line the lung cavity, is another disease related to asbestos exposure. Malignant mesotheliomas of these membranes (the pleura and the peritoneum) are extremely rare in persons with no history of asbestos exposure, but may account for 10% to 18% of excess deaths in workers exposed to asbestos. Generally, a latency period of at least 25 to 30 years is required in order to observe mesotheliomas, and some victims have had a latency period of forty years since their initial exposure to asbestos. This form of cancer is incurable and is usually fatal within a year after diagnosis. Mesothelioma has been associated with short term, incidental exposure, but here is no evidence of a relationship between cigarette smoking and mesothelioma risk.
Other Cancers
Some health studies have observed increases in esophageal, stomach, colo-rectal, kidney, and possibly ovarian cancers as well as cancers in the nose and throat from exposure to asbestos. While the magnitude of increased cancer risk for these sites is not as great as for lung cancer and mesothelioma, the increased risk may be of considerable importance because of the high background rates of some of these tumors in the general population. By way of example, a 50% increase of risk in a common cancer such as colo-rectal cancer results in many more deaths than a similar 50% increase in a rare cancer.

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Late in 1985, asbestos contamination was discovered in the public water supply of the Town of Woodstock, Ulster County, New York. Contamination resulted from asbestos-cement (AC) pipes installed in the town water system in the mid to late 1950s and the corrosiveness of the local water. The New York State (NYS) Department of Health established the Woodstock Asbestos Exposure Registry (WAER) in 1986 to monitor rates of cancer among individuals who lived on the water supply between 1960 and 1985. Demographic, health, and residential information were collected on 2,936 registrants. The follow-up period for observation of cancer was 1980-1998, consistent with the expected lag of 20-30+ years for development of asbestos-related cancers. The NYS Cancer Registry was used to confirm cancer diagnoses and to identify unreported cancers. Standardized incidence ratios (SIRs) for gastrointestinal, respiratory, and total cancers were all approximately 1.00 or less and all 95% confidence intervals (CIs) included 1.00. For individual types of the gastrointestinal cancers, only the SIR for pancreatic cancer was marginally statistically significant at 2.19 (95% CI=1.00-4.16), based on a total of nine observed cases. The excess in pancreatic cancer occurred primarily among men (SIR=3.08; 95% CI=1.13-6.70), and was only slightly elevated among women (SIR=1.39; 95% CI=0.29-4.06). This association may be related to factors other than asbestos exposure such as cigarette smoking, or to chance. No cases of mesothelioma were observed among WAER participants. There was no increase in incidence by latency or duration of residence on the water supply, but the ability to detect these trends is limited by small numbers and unknown dates of initial exposure. The general pattern of results did not demonstrate a likely link between exposure to asbestos in drinking water and cancer occurrence among participants in the WAER. This is the final report for this study; follow-up of the Woodstock Asbestos Exposure Registry has ended.
Background
In November 1985, residents of the Town of Woodstock, Ulster County, NY, reported a decrease in water pressure following a temporary interruption in water service. Town and New York State (NYS) Department of Health (DOH) staff determined that strainers on faucets and showerheads were clogged with asbestos fibers. The source of the asbestos fibers was asbestos-cement (AC) pipes installed in the town water system in the mid to late 1950s. Examination of the pipe showed significant deterioration of its interior, probably due to the high corrosivity of the local water. All water delivered by the public water supply traveled through AC pipes located near the pumping stations. The time frame during which asbestos fibers started leaching into the water is unknown but the entire town water supply system may have contained some level of asbestos fibers since around 1960. A 10-year-old sample of water drawn in 1976 (tested in 1986) contained asbestos, confirming that leaching of asbestos into the water supply began as early as 1976.
A 1982 survey of 47 NYS public water supply systems performed by the United States Environmental Protection Agency (USEPA), which did not include the Woodstock water supply, found only one water system with an asbestos level greater than 10 million fibers per liter (MFL). Ulster County officials collected five water samples from different locations on the Woodstock water supply in November 1985, following flushing of the water mains. Four of the samples had asbestos levels greater than 10 MFL, with the maximum equaling 304.5 MFL.
To address the asbestos contamination problem, a variety of actions were taken. In December 1985, a water advisory was issued, cautioning people against use of the town water supply for drinking, cooking, food preparation, or mist-type humidifiers. Emergency procedures also included distribution of uncontaminated water and replacement of the AC pipes with ductile iron pipes. The majority of the AC pipe replacement was completed in early March 1986, with a few remaining sections replaced in early June. Extensive flushing of the water supply system, cleaning or replacement of water service meters, and repeated testing for asbestos were conducted before lifting the water use advisory in July of 1987.
Carcinogenicity of Asbestos
Asbestos has been classified as a human carcinogen by the USEPA and the International Agency for Research on Cancer (IARC) (USEPA, 1993), (IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 1987). Numerous studies have linked occupational exposure to airborne asbestos with excess risk of lung cancer and mesotheliomas of the pleura and the peritoneum (Selikoff, 1965), (Peto et al., 1985), (Enterline et al., 1987). A weak association between occupational exposure to airborne asbestos exposure and gastrointestinal cancer was first noted by Selikoff et al., (1964), and was supported by a meta-analysis of 31 occupational cohorts using a lung cancer standardized mortality ratio of 2.0 or greater as a proxy for asbestos exposure (Frumkin and Berlin, 1988). Investigators proposed that the increase in gastrointestinal cancers was the result of ingestion of airborne asbestos fibers that occurred following clearance from the airways. A more recent meta-analysis of 69 occupational cohorts does not support a causal relation (Goodman et al., 1999). Some investigators have speculated that the elevated rate of gastrointestinal cancer attributed to occupational asbestos exposure reflects misdiagnosis of mesothelioma and lung cancer (Peto, 1989), (Gamble, 1994). Peto (1989) noted that relative risks for cancers other than lung and gastrointestinal are correlated with relative risks for lung cancer in cohorts of male asbestos workers. An increase in risk for all other sites of cancer similar to that observed for gastrointestinal cancer supports the misdiagnosis theory.
Both huma and animal studies have examined the relationship between ingestion of asbestos fibers and cancer. Animal studies of ingested asbestos carcinogenicity have generally produced negative results (Chouroulinkov, 1989). However, based on the results of genotoxicity studies, Varga et al., (1999) suggest that combined exposure to asbestos fibers and waterborne asbestos may have a carcinogenic effect. Cancer incidence or mortality has been studied in eight populations exposed to asbestos in drinking water in the United States, Canada, and Norway (see Table 1). In several instances, the same study population was the subject of two or three investigations. A later study extended the scope or study period of the original investigation. The results of the most recent study of each population are summarized in Table 1.
Erosion of rock containing asbestos was the source of asbestos in several study locations: the Bay Area of California; Quebec, Canada; and the Puget Sound region of the state of Washington. Dumping of mine tailing wastes into Lake Superior resulted in asbestos in the water supply in Duluth, Minnesota. AC pipes were the source of asbestos in selected water supplies in Connecticut and Escambia County, Florida. Weathering of AC roof tiles by rainwater runoff used for drinking water was the source of asbestos exposure among lighthouse keepers in Norway. In some cases, asbestos levels were relatively low. Concentrations were less than 0.1 MFL in town water supplies in Connecticut (Meigs et al., 1980); in Escambia County, Florida, seven census tracts with detectable levels measured 0.11-0.7 MFL (Millette et al., 1983). Much higher concentrations were measured in lighthouse keepers' cisterns (range=1,760-71,350 MFL) (Andersen et al., 1993), in water supplies in two cities in Quebec, Canada (> 100 MFL) (Toft et al., 1981), and in the Puget Sound area of Washington (200 MFL) (Polissar et al., 1984). Intermediate levels were reported in water supplies in the Bay Area of California (up to 36 MFL) (Conforti et al., 1981) and Duluth, Minnesota (range=2-64 MFL) (Sigurdson, 1983).
As shown in Table 1, an excess of stomach cancer among males was observed in five study populations (Conforti et al., 1981), (Toft et al., 1981), (Sigurdson, 1983), (Polissar et al., 1984), (Andersen et al., 1993), and pancreatic cancer was associated with exposure among males in one population (Meigs et al., 1980) and among females in another (Conforti et al., 1981). A positive association was not reported for more than one study population for any other cancer site. Despite indications of increased risk in early investigations, the epidemiologic studies conducted to date generally do not provide strong evidence of an association between exposure to asbestos in drinking water and gastrointestinal or respiratory cancers. However, a number of study limitations prevent firm conclusions. Six of the eight studies employed an ecologic design. The most serious weakness of ecologic studies is the potential for bias in attempting to draw conclusions about individual-level risk based on group-level observations. The assignment of exposure status to all individuals in a region undoubtedly results in exposure misclassification. Geographic boundaries used to identify cases and controls often do not correspond perfectly with water system boundaries. In addition, migration can contribute to misclassification since residents who have recently moved into an "exposed" region would not be at risk of exposure-related cancer. Other considerations include inadequate latency (Meigs et al., 1980), (Sigurdson, 1983), (Howe et al., 1989) and small sample size.
The case-control study by Polissar et al. (1984) was able to avoid many of these limitations. Detailed information on residential and occupational history was used to estimate asbestos exposure, data were collected on personal risk factors for cancer, and latency was taken into account. Statistically elevated risk of cancers of the stomach and pharynx were reported among men. In view of the large number of statistical comparisons (84) in conjunction with nonsignificant protective effects observed among women for cancers of the stomach and pharynx, the authors suggested that positive findings were due to chance. The study had power to detect relative risks as low as 1.4-1.6 for cancers of the colon, lung, gastrointestinal system, and respiratory system.
A preliminary study of cancer incidence for the years 1973-1983 among Woodstock residents living in the census blocks that include the water district, conducted by the NYS DOH, is included among the studies summarized in Table 1 (Howe et al., 1989). No evidence of elevated gastrointestinal or respiratory cancer incidence was observed when rates of cancer for census blocks including the water district were compared to rates for NYS excluding New York City (NYC). Insufficient latency and the inclusion in the exposed population of individuals who did not live on the public water supply were limitations of the study.
Most of the community studies conducted to date did not have individual-level information on source of water and duration of residence. The exposure assessment for the present study improves on these studies. Only people who lived on the water supply were included and information on duration of residence was examined.Study Subjects and Methods
Construction of Cohort
In 1986, the NYS DOH began a prospective cohort study to monitor cancer incidence among individuals who lived in homes serviced by the Woodstock water supply. Specifically, NYS DOH established the Woodstock Asbestos Exposure Registry (WAER) to collect exposure and health status information on individuals who, between 1960 and 1985, had resided for six months or more in a home serviced by the Town of Woodstock water supply. Information on demographics, smoking history, drinking habits, occupation, family history of cancer, and residential history was obtained through questionnaires and interviews. The registrants were followed through 1998. Address and health information was updated every two years. The objectives of the WAER were:
To identify individuals who lived for six months or more in a residence served by the town water between January 1, 1960, and December 31, 1985.
To notify these individuals of their exposure.
To obtain demographic and medical history data on registered individuals and to periodically update this information.
To calculate cancer incidence rates among the WAER population for total cancers, mesothelioma, respiratory cancers and gastrointestinal cancers and compare these to cancer rates for NYS excluding NYC.
An in-person registration week was held in the Woodstock Town offices in June 1986. The following month, introductory letters and questionnaires were mailed out to an additional 565 households currently serviced by the public water supply. A variety of sources were used to identify and trace former property owners and tenants: tax assessor's records, voter records, city directories, post office change-of-address records, neighbor referrals, and Department of Motor Vehicle files. Extensive efforts were made to contact and recruit current and former residents. If possible, individuals who did not respond to mailed questionnaires were contacted by telephone and offered a telephone interview or remailing of the questionnaire. Those with non-published telephone numbers or otherwise not reachable by telephone were mailed registered letters.
The person-years of observation contributed by each person in the study cohort began at the start date of the follow-up period (January 1, 1980), or on the date of first residence on the water supply if residence began after 1980 (exceptions are noted below for the analyses accounting for latency and exposure beginning in 1976). Follow-up ended at the date of cancer diagnosis, date of death, last date before loss-to-follow-up or the end of the study period (December 31, 1998), whichever came first. An individual diagnosed with cancer no longer contributed person-years after his or her date of diagnosis. Similarly, accrual of person-years stopped as of date of death or loss-to-follow-up. Registrants for whom information was missing on duration of residence or date of birth were excluded from the study cohort. Since individuals who had a cancer diagnosis prior to 1980 would not be at risk of a first diagnosis of a primary cancer during the study follow-up period, persons with a confirmed diagnosis of cancer prior to 1980 were excluded from the study population.

Asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Asbestos exposure Wallpaper Photos Pictures Pics Images 2013

Asbestos exposure Wallpaper Photos Pictures Pics Images 2013