RR540 The HSE Grain Dust Study

2y ago
20 Views
2 Downloads
1.83 MB
108 Pages
Last View : 2m ago
Last Download : 2m ago
Upload by : Olive Grimm
Transcription

Health and SafetyExecutiveThe HSE Grain Dust Study workers'exposure to grain dust contaminants,immunological and clinical responsePrepared by the Health and Safety Laboratoryfor the Health and Safety Executive 2007RR540Research Report

Health and SafetyExecutiveThe HSE Grain Dust Study workers'exposure to grain dust contaminants,immunological and clinical responseJ R M Swan, D Blainey & B CrookHealth and Safety LaboratoryHarpur HillBuxtonDerbyshireSK17 9JNInhalation of airborne micro organisms and their associated contaminants in the workplace can cause a range ofimmunological and respiratory symptoms. The mechanisms through which these respiratory effects are caused are notall fully understood. The evaluation of worker exposure is essential for establishing causal relationships betweenoccupational disease and one or several specific micro organisms or their associated contaminants.This study investigated the role of micro organisms and their associated contaminants in the development ofimmunological and clinical response in workers exposed to grain dust. The objectives were: To assess the exposure of grain workers in the UK to inhalable grain dust, the microbial contaminants in grain dust,including identification of the predominant micro organisms involved, and to endotoxin (bacterial cell wall toxins).To measure the prevalence of immunological response to grain dust associated allergens in UK grain workers.To examine the long term clinical and immunological effects of workplace exposure to grain dust and itscontaminants in terms of its effect on respiratory health. This was done by establishing a cohort of 321 workersexposed to grain dust (farmers at 27 farms and dock workers at 2 docks in South East England) and maintainingas many as possible in the cohort for repeated immunoassay and clinical assessment over two study phases,Phase 1 from 1990 to 1993 and Phase 2 from 1997 to 2003.This report and the work it describes were funded by the Health and Safety Executive (HSE). Its contents, including anyopinions and/or conclusions expressed, are those of the authors alone and do not necessarily reflect HSE policy.HSE Books

Crown copyright 2007First published 2007All rights reserved. No part of this publication may bereproduced, stored in a retrieval system, or transmitted inany form or by any means (electronic, mechanical,photocopying, recording or otherwise) without the priorwritten permission of the copyright owner.Applications for reproduction should be made in writing to:Licensing Division, Her Majesty’s Stationery Office,St Clements House, 2 16 Colegate, Norwich NR3 1BQor by e mail to hmsolicensing@cabinet office.x.gsi.gov.ukii

CONTENTS1 INTRODUCTION. 11.1Organic dust, grain dust and respiratory disease . 11.2Grain Dust . 11.3The role of atopy in occupational allergy . 21.4Prevalence of allergic respiratory symptoms in UK workers . 21.5The role of endotoxin in respiratory disease . 31.6The UK maximum exposure limit (MEL) for grain dust . 51.7The Health and Safety Executive grain dust survey: aims. 52 MICROBIOLOGICAL EXPOSURE STUDY. 72.1Background . 72.2Study sites, Materials and Methods . 72.3Results summary and Discussion. 112.4Summary of microbiological exposure study . 232.5Conclusions . 303 IMMUNOLOGY STUDY . 313.1Aim . 313.2Study Population . 313.3Immunoglobulin G immunoassay . 323.4Immunoglobulin E immunoassay . 333.5Results. 373.6Discussion; immunology results . 454 CLINICAL STUDY . 514.1Introduction and Summary of Phase 1. 514.2Subjects. 514.3Methods. 534.4Results. 554.5Summary of findings – Clinical study . 705GENERAL DISCUSSION . 726 QUESTIONS ADDRESSED BY THE STUDY . 746.1Has the MEL reduced sensitisation? . 746.2Did anyone develop new IgG or IgE during the study?. 746.3Should the MEL be reduced to reduce sensitisation?. 746.4Does new sensitisation result in new symptoms?. 757OVERALL SUMMARY. 768MAIN RECOMMENDATIONS. 789ANNEX 1. 8010REFERENCES . 90iii

iv

EXECUTIVE SUMMARYObjectivesInhalation of airborne micro-organisms and their associated contaminants in the workplace cancause a range of immunological and respiratory symptoms. The mechanisms through whichthese respiratory effects are caused are not all fully understood. The evaluation of workerexposure is essential for establishing causal relationships between occupational disease and oneor several specific micro-organisms or their associated contaminants.This study investigated the role of micro-organisms and their associated contaminants in thedevelopment of immunological and clinical response in workers exposed to grain dust. Theobjectives were:1. To assess the exposure of grain workers in the UK to inhalable grain dust, the microbialcontaminants in grain dust, including identification of the predominant micro-organismsinvolved, and to endotoxin (bacterial cell wall toxins).2. To measure the prevalence of immunological response to grain dust associated allergensin UK grain workers.3. To examine the long term clinical and immunological effects of workplace exposure tograin dust and its contaminants in terms of its effect on respiratory health.This was done by establishing a cohort of 321 workers exposed to grain dust (farmers at 27farms and dock workers at 2 docks in South East England) and maintaining as many as possiblein the cohort for repeated immunoassay and clinical assessment over two study phases, Phase 1from 1990 to 1993 and Phase 2 from 1997 to 2003.Main FindingsUK grain workers were frequently found to be exposed to more than 1 million bacteria andfungi per m3 air. Airborne bacteria exceeded 106 per m3 air and fungi exceeded 105 per m3 air atall the work places sampled. Levels of airborne endotoxin of over 10,000 EU/m3 were recordedat all but one workplace visited and personal exposures reached over 600 EU/m3 at everyworkplace. The Maximum Exposure Limit (MEL) for grain dust is an average of 10 mg/m3 ofThe Maximum Exposure Limit (MEL) for grain dust is an average of 10 mg/m3 of totalrespirable dust in the air over an 8 hour period, and the maximum dust level should neverexceed 30 mg/m3 measured over a 10 minute period. The MEL was introduced between Phases1 and 2 of the study. Throughout both phases of the study, very high levels of dust wererecorded with levels equal to, or greater than, 30 mg/m3 recorded in all work situations at 17 ofthe 19 workplaces visited.The predominant micro-organisms present differed between freshly harvested grain and storedgrain and grain for human and animal consumption, but not between different types of grain.The microbial species identified were used to select relevant isolates for use in immunoassays.In the immunoassays, large numbers of sera were expected to show positive immunoglobulin G(IgG) response as the prevalent micro-organisms are also common environmental allergens tov

which everyone is exposed to some extent. Between 13 and 39% of dockers, 25 to 41% offarmers and 24 to 35 % of the controls tested positive to one or more of the work-relatedallergens throughout the study. IgE sensitisation to work related allergens among the grainworker cohort showed evidence of a decrease since the introduction of the grain dust MEL, i.e.,there was an overall trend towards a decrease in IgE positive responses across the study fromPhase 1 to Phase 2. However, the long term trend towards improvement may not be shownclearly in this study as the majority of the participants were occupationally exposed to grain dustfor many years before the MEL was introduced.Although some workers who remained in the study throughout developed new IgG response orpositive IgE response during the study, more workers lost their positive status than gained it.No dockworkers developed a sustained new positive status. There was a decrease in the numberof non atopic workers who tested IgE positive to the work-related allergens, and none of thenon-atopic dockworkers were IgE positive in Phase 2 of study. However, 11% of non atopicHowever, 11% of non atopic farmers were still testing positive to one or more of the workrelated allergens at the end of the study. This suggests that it is possible to reduce exposurelevels to below those required to trigger an IgE response in non-atopic workers, but that farmworkers continue to be exposed to levels of grain dust and its contaminants that could trigger ormaintain sensitisation.In the two phases of the clinical study, grain workers were found to have a high prevalence ofrespiratory symptoms and sensitisation to environmental allergens including microorganisms,the grain itself and storage mites.There was a close relationship between some respiratory symptoms (especially ‘wheeze in adusty place’) and the presence of specific IgE to environmental allergens. There was noassociation between specific IgG and symptoms or lung function. Not all respiratory symptomscould be explained by IgE mediated immunological sensitisation. The longitudinal exposure ofgrain workers to high doses of endotoxin may be contributing to the development of workrelated ill health.Lung function was found to be inversely related to the duration of exposure to grain dust in thefirst phase of the study, but the cause(s) of impaired lung function could not be identified fromthis phase. In the second phase of the study this relationship was not identified, and over thecourse of the study, both in those who took part in both phases, or those who just participatedthroughout Phase 2, there was no overall decline in lung function.Main RecommendationsAlthough fungal allergens are recognised components of grain dust, this study has shown thatnot all grain workers’ impaired lung function and respiratory symptoms could be linked withimmunological response. The study also highlighted the exposure of grain workers to largeconcentrations of endotoxin, which may contribute to respiratory symptoms but notimmunological response. Guidance/information on endotoxin exposure in the workplace isrecommended. The longitudinal health effects of high endotoxin exposure, and the adjuvanteffects of endotoxin inhalation with other contaminants, require further investigation.In many instances in grain handling, the use of respiratory protective equipment (RPE) is theonly control option. This study highlighted that exposure to large numbers of micro-organismsand their toxins may occur in apparently ‘clean’ areas, where currently RPE is not worn.Improved cleanliness is recommended in rest areas, offices and vehicle cabs. Vehicle cabs mayvi

not be offering enough protection and the use of. RPE inside the cabs should be considered.The levels of IgE response in non-atopic farmers indicates that farmers continue to be exposedto high levels of grain dust work-related allergens. Observations made during themicrobiological sampling indicated that better protection factor RPE, worn more frequentlyduring specific high dust exposure tasks, would help reduce the levels of exposure, particularlyduring harvesting in areas/situations where it is not practicable to reduce dust exposure in otherways. It would be important to ensure that such RPE offered suitable levels of protectionagainst endotoxin exposure.vii

viii

11.1INTRODUCTIONORGANIC DUST, GRAIN DUST AND RESPIRATORY DISEASERamazzini published work on the subject of occupational illness caused by grain dust over twocenturies ago. This paper ‘Diseases of sifters and measurers of grain’ was published in 1713. Henoted that the dust was made up ‘not only of the dust picked up from the threshing floor, but alsoanother less innocent sort which is shed from the grain itself which is kept for long’. He describedsome of the symptoms - ‘the throat, lungs and eyes are keenly aware of serious damage’, ‘intenseitching over the whole body of the sort sometimes observed in nettle rash’, ‘almost all who make aliving by sifting or measuring grain are short of breath, cachetic and rarely reach old age’ (Ramazzini,1713; cited in Becklake, 1980).There is no clear understanding of the variety of mechanisms by which the problems associated withgrain dust occur, though some have been identified. Organic dust from the grain itself can causerespiratory irritant effects and an immunological response. In addition to this, other biologicalmaterials present including fungi, actinomycetes, bacteria and their endotoxins, pollen, insects andarachnid mites and their debris are present in harvested and stored grain and may have effects on therespiratory system. The evaluation of worker exposure to microorganisms in the workplace in general,and of grain workers in particular, is essential for establishing causal relationships betweenoccupational disease and one or several specific microorganisms or their associated contaminants.The number of known allergens is continually rising and the list of microorganisms that can causeoccupational illness is increasing.1.2GRAIN DUSTGrain dust is the dust produced during harvesting, drying, handling, storage or processing of wheat,oats, barley, maize or rye. It is a complex mixture of fragments of grain, inorganic soil particles andassociated organic contaminants. These contaminants may include plant cell debris, insect parts andmites as well as viable and non-viable microorganisms (vegetative cells and spores of fungi,actinomycetes and bacteria, and their components such as endotoxins and mycotoxins). Thiscomplicated mixture makes the effects of the grain dust on the lungs difficult to define, (Burrell, 1995;Lacey, 1990; Rylander, 1994). When grain is handled, clouds of this complex dust mixture aredispersed in the air. Inhalation of these dusts can lead to decreased lung function and the developmentof immunological respiratory symptoms which may include allergic rhinitis and asthma, chronicbronchitis, granulomatous pneumonitis (extrinsic allergic alveolitis, hypersensitivity pneumonitis),toxic pneumonitis (organic dust toxic syndrome/grain fever) and decline in lung function. Themechanisms by which these occur are not yet well understood (Becklake, 1980; Dimich-Ward et al.,1995; Fonn et al., 1993a; Fonn et al., 1993b; Hurst and Dosman, 1990; Mcduffie et al., 1991;Rylander, 1994).The role of microbial exposure, the immunological effects and the relative importance of these graindust contaminants compared to grain itself have not been established by previous research. Many ofthe microorganisms found in grain dust both during harvesting and after storage are known respiratorysensitisers e.g. Cladosporium, Alternaria, Aspergillus spp., Penicillium spp. which are well known asallergens (Darke et al., 1976; Dutkiewicz et al., 1985; Dutkiewicz et al., 1989; Lacey 1995; Marx etal., 1993) while Enterobacter agglomerans may also be a source of endotoxin (Dutkiewicz, 1976). It1

is hard to define the precise effects of grain dust on the lungs because of the diversity of workerexposure and the range and diversity of symptoms involving different pathogenic mechanisms.1.3THE ROLE OF ATOPY IN OCCUPATIONAL ALLERGYAbout 20% of the population are atopic. Atopic people have a hereditary predisposition to produceIgE antibodies and respond to tiny amounts of exposure to common environmental allergens with thepersistent production of specific IgE antibodies. To determine atopic status, a subject is tested with aseries of allergens. A positive test is an indicator of predisposition to further sensitisation to otherallergens. Atopy is the single strongest risk factor for the development of asthma. Atopy can increasethe risk of developing asthma by 10-20 fold when compared with those who are non-atopic (Holgate,1997).Other factors that affect the development of allergic disease are those of infection and toxicity.Infection can stimulate the immune response to adjuvant action or inflammation. Toxic factors suchas tobacco smoke, air pollution and industrial exposures may enhance absorption of antigens as aresult of pulmonary inhalation and inflammation. Alternatively, the toxic factors may act as adjuvants,it has been suggested that endotoxin is involved as an adjuvant.1.4PREVALENCE OF ALLERGIC RESPIRATORY SYMPTOMS IN UK WORKERSThe overall frequency with which occupational asthma occurs in the UK is unknown but it has beenestimated that 2-6% of all the cases of adult asthma may be due to workplace exposures (HSE, 1998).In 1995 a survey of self reported work-related ill health was carried out. Information on self-reportedoccupational health data was collected from a representative national sample of adults in England andWales. From these data it was estimated that about 138,000 people believe they are affected by workrelated asthma. 62,000 of these people felt that their asthma was caused by, rather than made worseby, their work (HSE, 1998).The ‘Surveillance of work-related and occupational respiratory disease in the UK’ - SWORD 99 - is asurveillance scheme of chest physicians reporting cases to produce a national picture of occupationalrespiratory disease (Meyer, 2001). In 1999 there were 1168 cases of occupational asthma, 43 ofallergic alveolitis (13 cases of which were farmers lung) and 129 bronchitis reported (HSE,2001).There were 9 deaths from Farmers Lung in 1999 (HSE, 2001). Ross (1995) reported that follow-upstudies showed that most patients with occupational asthma failed to recover and half left theiremployer. Patients who were exposed continually for a year or more after diagnosis had a worseoutcome than those removed rapidly from exposure. In 1989 SWORD reported that 42% of cases ofoccupational asthma and 7% of allergic alveolitis were due to flour or grain dust. In 1999 8% of casesof asthma caused by sensitisation were attributed to flour and grain. In 2000 an estimated 797 newcases of occupational asthma was seen for the first time by occupational and chest physiciansreporting to SWORD/OPRA schemes (HSE, 2001). These figures probably underestimate the problemas not all cases of work-related respiratory symptoms are seen by a doctor, and an occupationalaetiology may not be considered in all cases. It is currently estimated by the Health and SafetyExecutive (HSE) that 1000 - 1500 new cases of occupational asthma occur every year in the UK(HSE, 1998).As well as the very high personal cost of respiratory disease, these figures represent an increasingfinancial cost to industry not only in loss of manpower, but also compensation. In 1996, 410 peoplewith occupational asthma were assessed as being disabled in order to qualify for benefit purposes(HSE, 1998).2

1.5THE ROLE OF ENDOTOXIN IN RESPIRATORY DISEASEEndotoxin is found in the outer layer of the cell walls of all Gram-negative bacteria and some bluegreen algae. Occupational exposure to airborne endotoxin causes short-term illness, and maycontribute to long-term worker ill-health. However at present there are no occupational exposurelimits in place for endotoxin. A great number of people may be exposed to airborne endotoxin becauseof the wide range of workplace sources. The general population is exposed to low levels of endotoxin.Gram-negative bacteria are present in the oral cavities and intestinal tracts of humans and animals;they also live on the surfaces of animals and plants. Endotoxin has also been found in house dust.Endotoxin is present in occupational settings, mainly as a component of organic dusts such as those ofvegetable origin contaminated with Gram-negative bacteria, grain dust, cotton dust, and dustscontaining animal faeces in swine confinement buildings, poultry houses and sewage sludge. Airconditioning units, contaminated process waters or water-mix oil emulsions can also containendotoxin.The short term effects of endotoxin inhalation include a febrile response with leucocytosis and flu-likesymptoms which resolve within 18 hours after initial intense exposure e.g. organic dust toxicsyndrome (ODTS) or inhalation fever. No prior sensitisation is needed, antibodies do not develop andrespiratory symptoms may or may not occur (Chan-Yeung et. al. 1992). Chronic effects occurfollowing repeated occupational exposure to endotoxin e.g. Chronic bronchitis and chronic obstructivepulmonary disease (Clapp et al.1994; Olenchock et al. 1990). Long term decline in lung function hasalso been measured (Schwartz 1996).Exposure to endotoxin in occupational environments and the resultant health consequences have beenwidely investigated. Several studies have investigated endotoxin exposure associated with grain dustand the subsequent health effects (Jagielo et al. 1996; Clapp et al. 1993 and 1994; Schwartz, 1996;Schwartz et al. 1995a; Smid et al. 1992 a and b; Blaski et al. 1996). These studies were reviewed inSwan and Crook (1999). These studies highlight the difficulties involved in determining which healtheffects resulting from the inhalation of organic dust mixtures are caused by the endotoxin componentof the dust. The wide range of epidemiological studies in the review suggest that chronic exposure toendotoxin present in occupational organic dusts may cause chronic inflammation leading to chronicbronchitis and reduced lung function, however, more data is required on the longitudinal health effectsof endotoxin exposure.The most common route of occupational exposure to endotoxin is through inhalation of airborneendotoxin. The amount of airborne endotoxin in different occupational environments varies widelySome typical examples are summarised in Table 1.1 and exposure to endotoxin in grain dust is inTable 1.2. There have been few UK studies of occupational endotoxin exposure.Although such investigation is outside the remit of this study, there is increasing recognition of thepotential role of endotoxin as a synergistic component to increase respiratory ill health effects. Forexample, animal studies have demonstrated the potential for the combination of diesel exhaustparticles and endotoxin (lipopolysaccharide) to aggravate endotoxin induced lung injury, asdemonstrated for example by pro-inflammatory cytokines (Yanagisawa et al, 2003; Arimoto et al,2005; Inoue et al, 2006). Other animal studies have shown the potential for exposure to a commonlyused organothiophosphate pesticide to alter inflammatory response to endotoxin (Singh and Jiang,2003), and a synergistic combination of the pesticide rotenone and endotoxin exposure has beenhypothesised as being an acceleratory factor in neural degeneration (Gao et al, 2003).3

Table 1.1. Summary of occupational exposure to airborne endotoxin.airborne cultureGrain handling0 - 54,900Animal feed0.1 - 1,870Swine houses31 - 75,000Poultry farm3.8 - 1,500Vegetable processing1 - 4,600IndustryCotton industry4 - 2,000Biotechnology0.07 - 162.85Machining MWF0.007 - 2,690Fibreglass wash water0.4 - 27,800Waste processingsewage processing0.08 - 310garbage handling0.02 - 131composting0.008 - 5,930OfficesOffices0.018 - 1,200Table 1.2 Endotoxin levels measured in grain dustIndustry/activity mean airborne endotoxin levelendotoxinin bulk sampleconcentration(ng/mg)(ng/m3)Grain handling54,900Grain handling#237.22x105 - 5x105Dutkiewitz et al., 86Blaski et al., 96#Grain handling2 - 23.7Grain handling*3 - 2,247Beard et al., 961 - 199 in dust Simpson et al., 98apgrain elevator0 - 0.74Grain dryingdrier emptying21416,100Liesivuori et al., 94105Liesivuori et al., 94Grain millsilo emptying22.5 - 187.5159 - 8,850DeLucca et al., 84Olenchock et al., 90b#wheat dustoat dust#Reference268.7283.3 #nanograms calculated from Endotoxin Units by dividing by 10ppersonal sampling* UK study4Olenchock et al., 89

1.6THE UK MAXIMUM EXPOSURE LIMIT (MEL) FOR GRAIN DUSTThe HSE guidance on the new maximum exposure limit (MEL) for grain dust came into effect on the1 January 1992 (HSE Agricultural Information Sheet no. 3). It applies to all dust, includingcontaminants, arising from harvesting, drying, handling, storage or processing of barley, wheat, oats,maize or rye. The MEL is an average of 10 mg/m3 of total respirable dust in the air over an 8 hourperiod. This is a maximum and not a target. Dust levels must be reduced as far below the MEL asreasonably practicable. Higher concentrations can be permitted if exposure times are shorter, but themaximum dust level should never exceed 30 mg/m3 measured over a 10 minute period.The MEL was set because of increasing evidence that exposure to high levels of grain dust causes illhealth. HSE recommends that, when taking on new workers who may be exposed to grain dust,employers should check whether they have any pre existing chest disorders such as asthma.Employees should be encouraged to report any respiratory problems. The MEL did not take intoaccount the fact that grain dust is a biologically active dust because, at the time, there had been nocomprehensive study of the effects of the individual components of grain dust on the health of thegrain workers. Consequently, there was a need to investigate these effects, and this study described inthis report forms part of this investigation.1.7THE HEALTH AND SAFETY EXECUTIVE GRAIN DUST SURVEY: AIMSThe Health and Safety Executive (HSE) Grain Dust Survey has been an on-going longitudinalcollaborative survey of worker exposure to grain dust in the UK. The survey involved assessments ofthe exposure to grain dust and its contaminants and clinical assessments of workers' respiratory healthfor workers handling grain in a range of occupational settings at 2 docks, 27 farms and, at the start,animal feed mills in the South East of England. The study population of 321 workers potentiallyexposed to grain dust was selected and recruited by a study team led by Dr David Blainey of theMedical Academic Unit, Broomfield Hospital, Chelmsford, who also carried out the clinicalassessments. HSL provided dust and microbial exposure measurement and immunoassays of exposedworkers’ sera.The purpose of this study was to assess the long term clinical and immunological effects of workplaceexposure to grain dust and its contaminants in terms of its effect on respiratory health, the prevalenceof respiratory symptoms and airflow limitation in grain workers, and to examine the role ofimmunological and cellular markers in predicting the link between exposure to grain dust and thedevelopment of occupationally acquired disease of the respiratory tract.A detailed examination was made of the exposure of a cohort of grain workers to microorganisms indust in order to relate this to the incidence of immunological response and health effects. Airbornemicroorganisms were studied, both quantitatively and qualitatively, while grain was being handled onfarms during harvest and after harvest; when stored grain was being moved and milled for feed onfarms, and also during bulk handling of grain that was being imported or exported at docksideterminals. The findings from the microbiological study were then used in the subsequent studies to5

measure the prevalence of immunological response to grain dust associated allergens in UK grainworkers. In the clinical study, a computer administered respiratory health questionnaire wascompleted by volunteer workers at the farms and grain handling docks. Lung function tests werecompleted to measure respiratory airway calibre and serum samples were collected for use in theimmunological studies.The study was divided into 2 phases. Phase 1 took place from 1990 to 1993 and Phase 2 from 1997 to2003, as far as possible using the same worker cohort.This final report describes the outcome of the study. As there were three main parts to the study, thereport will deal in separate sections with the assessments of workers’ mic

To assess the exposure of grain workers in the UK to inhalable grain dust, the microbial contaminants in grain dust, including identification of the predominant micro-organisms involved, and to endotoxin (bacterial cell wall toxins). 2. To measure the prevalence of immunological response to grain dust associated allergens in UK grain workers. 3.

Related Documents:

May 02, 2018 · D. Program Evaluation ͟The organization has provided a description of the framework for how each program will be evaluated. The framework should include all the elements below: ͟The evaluation methods are cost-effective for the organization ͟Quantitative and qualitative data is being collected (at Basics tier, data collection must have begun)

Silat is a combative art of self-defense and survival rooted from Matay archipelago. It was traced at thé early of Langkasuka Kingdom (2nd century CE) till thé reign of Melaka (Malaysia) Sultanate era (13th century). Silat has now evolved to become part of social culture and tradition with thé appearance of a fine physical and spiritual .

On an exceptional basis, Member States may request UNESCO to provide thé candidates with access to thé platform so they can complète thé form by themselves. Thèse requests must be addressed to esd rize unesco. or by 15 A ril 2021 UNESCO will provide thé nomineewith accessto thé platform via their émail address.

̶The leading indicator of employee engagement is based on the quality of the relationship between employee and supervisor Empower your managers! ̶Help them understand the impact on the organization ̶Share important changes, plan options, tasks, and deadlines ̶Provide key messages and talking points ̶Prepare them to answer employee questions

Dr. Sunita Bharatwal** Dr. Pawan Garga*** Abstract Customer satisfaction is derived from thè functionalities and values, a product or Service can provide. The current study aims to segregate thè dimensions of ordine Service quality and gather insights on its impact on web shopping. The trends of purchases have

Chính Văn.- Còn đức Thế tôn thì tuệ giác cực kỳ trong sạch 8: hiện hành bất nhị 9, đạt đến vô tướng 10, đứng vào chỗ đứng của các đức Thế tôn 11, thể hiện tính bình đẳng của các Ngài, đến chỗ không còn chướng ngại 12, giáo pháp không thể khuynh đảo, tâm thức không bị cản trở, cái được

All off-farm grain handling facilities are required to develop and implement a written housekeeping program—to reduce accumulations of fugitive grain dust on ledges, floors, equipment, and other exposed surfaces. Fugitive grain dust means combustible dust particles emitted from the grain handling system and of a size less than 400 microns.

API 653 Tank Inspection, Repair, Alteration and Reconstruction, 3rd 2005 American Petroleum Institute USA Current Inspection, repair, modification and reconstruction of tanks built edition incorporating addendum 1 to API 650 or API 12C and 2 4 . Standard Title Year Publishing body Country Status Primary focus BS EN 14015 Specification for the design and 2004 European Europe Current Design and .