Prevalence and association factor of copd among textile factory worker in moroco pdf

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prevalence and association factor of copd among textile factory worker in moroco pdf

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Vol. 11 No. 3 (2020): Indian Journal of Public Health Research & Development

Rationale: Workplace inhalational hazards remain common worldwide, even though they are ameliorable. Previous American Thoracic Society documents have assessed the contribution of workplace exposures to asthma and chronic obstructive pulmonary disease on a population level, but not to other chronic respiratory diseases. The goal of this document is to report an in-depth literature review and data synthesis of the occupational contribution to the burden of the major nonmalignant respiratory diseases, including airway diseases; interstitial fibrosis; hypersensitivity pneumonitis; other noninfectious granulomatous lung diseases, including sarcoidosis; and selected respiratory infections.

Methods: Relevant literature was identified for each respiratory condition. The occupational population attributable fraction PAF was estimated for those conditions for which there were sufficient population-based studies to allow pooled estimates. For the other conditions, the occupational burden of disease was estimated on the basis of attribution in case series, incidence rate ratios, or attributable fraction within an exposed group. This burden has important clinical, research, and policy implications.

There is a pressing need to improve clinical recognition and public health awareness of the contribution of occupational factors across a range of nonmalignant respiratory diseases.

Occupational exposures are important, frequently overlooked, and modifiable contributors to the burden of respiratory disease. Quantifying the occupational contribution to this disease burden is critical to preventing disease and improving lung health. To date, the question of the occupational burden in respiratory disease at the population level has been addressed primarily in relation to asthma and chronic obstructive pulmonary disease COPD.

This document reviews and synthesizes existing data to quantify the occupational contribution to the burden of nonmalignant respiratory diseases across a range of conditions frequently unrecognized as potentially work related. Inhalation of vapors, gas, dust, or fumes VGDF in the workplace is common worldwide, and occupation is an important global contributor to the burden of respiratory disease 1. Occupational exposures also contribute to the disease burden in a number of other conditions, including interstitial disease diagnosed as IPF, HP, other noninfectious granulomatous lung diseases such as sarcoidosis, other interstitial lung diseases, and selected respiratory infections 5 — 9.

We synthesized data from multiple sources to quantify the occupational contribution to the burden of nonmalignant respiratory disease. The occupational burden in thoracic cancer lung and pleura has been well characterized elsewhere 10 — That does not detract, however, from their public health importance.

In this statement, we assess the occupational burden in four categories of respiratory conditions: airway disease asthma, COPD, and chronic bronchitis , interstitial lung disease IPF as well as PAP and other uncommon interstitial diseases , granulomatous processes HP and other noninfectious granulomatous diseases, including sarcoidosis , and selected respiratory infections tuberculosis [TB] and CAP.

We searched the PubMed and Embase databases from their respective start dates through December 31, , unless otherwise noted. A supplemental literature search was conducted covering January to September The search strategies, including start dates, rationale, and search terms, are shown in Table E1 in the online supplement.

We also reviewed reference citations in identified publications to identify relevant papers. Except when stated explicitly, all data were population based and were not limited to a specific industry or exposure.

We limited the analysis of asthma to incident data. For PAP, HP, and sarcoidosis, we extracted data from cases series in which the proportion of occupationally related cases was available.

For TB, we used World Health Organization and World Bank databases 21 — 23 for data on country-specific general population rates to estimate relative disease incidence by occupation. We pooled published or derived PAF values asthma, COPD, chronic bronchitis, and interstitial lung disease and the occupationally attributable burden PAP, HP, and sarcoidosis to obtain weighted summary estimates using the metaproportion command in Stata Because we recognized that the heterogeneity among the studies was high, we calculated the pooled PAF or proportion using random effects modeling with case numbers informing the weights.

We also estimated statistical heterogeneity using the I 2 statistic, which in each case was consistent with high heterogeneity, as we expected values not presented.

We also calculated the pooled estimate excluding the highest and lowest values in the group, as well as calculating the median of the observed PAF or occupational burden values. For TB and CAP, we did not calculate weighted pooled values, limiting summary data to the median values among the estimates considered.

Work-related asthma is now the most commonly reported work-related respiratory disorder in many industrialized countries. Cross-sectional prevalence studies have dominated previous estimates of the occupational burden of disease. To build on earlier estimates, we limited our search to longitudinal, population-based studies that reported incident asthma and occupational risk factors.

We identified nine studies with longitudinal data relevant to occupation and incident asthma for inclusion 25 — 33 Table 1. Three newer studies have been published since the previous review A third longitudinal study analyzed data from the United Kingdom. Overall, longitudinal data from which inferences can be drawn on the occupational burden of incident asthma are limited.

Of note, the studies considered were largely done in developed economic settings. Sex-stratified longitudinal data are even more limited; we identified only two such analyses, both with lower PAF estimates for women than for men. Asthma: population attributable fraction PAF. Forest plot of studies relevant to estimating the occupational contribution to asthma. Seven reviews published since the ATS statement 3 , 13 — 16 , 18 , 19 identified 33 papers relating to the occupational contribution to COPD or chronic bronchitis.

The additional literature search for publications published between and identified a further 15 relevant citations not among the 33 included in the reviews noted above. We retained population-based studies that included a range of potential occupations or case—control studies that clearly reflected the general population.

Studies were excluded if they lacked a clear definition of the disease endpoint e. When a study reported multiple endpoints or measures of exposure, we preferentially considered risk estimates for COPD defined by spirometry using lower limit of normal, if reported over self-reported COPD, and, similarly, we considered JEM-defined risk over self-reported exposure.

In studies stratified by smoking status, the ever-smoking stratum was the one used in the pooled analysis of PAF. When data from a never-smoking stratum were available in some cases the entire cohort analyzed , we used these in a separate pooled analysis of PAF among never-smokers.

Results presented only in a stratified manner e. We included 26 studies to estimate the contribution of occupational exposures to the burden of COPD 35 — 60 and 7 for the contribution to chronic bronchitis 39 , 40 , 50 , 51 , 61 — Table 2 summarizes the 26 COPD studies considered, including 28 estimates of risk taking into account sex-stratified data.

Forest plot of studies relevant to estimating the occupational contribution to COPD. Table 3 summarizes the seven chronic bronchitis studies used eight estimates of risk. Only two studies allowed estimation of the occupational PAF for chronic bronchitis among never-smokers, yielding values of 8. Several publications excluded from the tables nonetheless warrant mention.

An ecological analysis of three large international studies estimated a 0. Several large population-based studies have addressed the association between various occupations and COPD 11 , 69 , Also of note, other researchers have investigated large occupational cohorts, including construction workers exposed to dust 71 , Chronic bronchitis: population attributable fraction PAF.

Forest plot of studies relevant to estimating the occupational contribution to chronic bronchitis. In summary, an impressive body of new data on the occupational burden of COPD, and to a lesser degree chronic bronchitis, has been published since the original ATS statement. In aggregate, participant numbers are large and international in scope. IPF is a diagnosis of exclusion made in the presence of a usual interstitial pneumonia pattern on biopsy or with a consistent appearance on a high-resolution computed tomographic scan.

The IPF diagnosis presumes that known causes of interstitial lung disease have been excluded e. Therefore, studies of cohorts with a diagnosis of IPF presumably already exclude persons with a recognized occupational cause of fibrosis, such as asbestosis. We identified four reviews of occupational exposures in IPF 5 , 74 — 76 that collectively included 10 relevant case—control studies.

One of these, a meta-analysis of six studies, reported a PAF for several exposure categories ranging from 3. Four of the 15 publications were not included in our PAF estimates: one because data were not available on the proportion of cases with specific occupational exposures 78 , two because of methodological issues in exposure assignment 85 , 86 , and one because of overlap with an included study We initially included one publication that appeared in abstract form only 92 , because we were aware that the full paper was forthcoming The remaining 11 case—control studies provided data permitting analysis of occupational exposures in five exposure categories: VGDF, metal dust, wood dust, silica dust, and agricultural dust.

Thirty-nine risk estimates from 11 studies 1, IPF cases in total contributed to these pooled PAF estimates Table 4 77 , 79 — 84 , 87 , 88 , 91 , The burden of each pooled exposure type was based on 5—11 individual risk estimates Table 5. The pooled OR for agricultural work five studies was elevated but not statistically significant OR, 1. The pooled ORs for each of the remaining exposure categories were elevated and statistically significant. All studies had case—control designs, with most by interview-based self-reported exposure assessment Hubbard exposure by job category.

The study by Paolocci and colleagues, which estimated risk with two separate wood variables, later appeared as a full publication Forest plot of studies relevant to estimating the occupational contribution to IPF of VGDF combined categories of exposure considered in the studies included. A major challenge in assessing the occupational burden of IPF disease is differentiating between disease misclassification e. Another important challenge is exposure misclassification, especially when estimating chronic inhalational work exposures over many years.

For example, asbestos exposure was common in metal and wood industries and could have contributed to these exposure-associated PAFs for IPF. PAP has been categorized as primary idiopathic , secondary, or congenital 94 , Primary PAP involves autoantibodies to granulocyte—macrophage colony—stimulating factor 94 ; secondary PAP is attributed to a variety of occupational exposures, most notably silica 96 — Cases of autoimmune PAP have been reported in occupationally exposed persons 98 , 99 , — We included 29 relevant publications since subsuming 1, PAP cases with a range of 10— cases per series — , excluding overlapping reports — A range of exposures was reported, including vapors or gases cleaning fluids, gasoline, hairspray, paint, and pesticides , inorganic dusts asbestos, cement, chalk, coal, glass fiber, and silica , organic dusts cotton, flour, wood, and wool , and metal dusts or fumes aluminum, copper, indium, iron, and zirconium.

All studies are case series except four case—control studies , , , and one national registry Occupational burden is based on the prevalence among cases of occupations likely to involve inhalational exposures or inhalational exposures likely to be occupational. Although PAP has a more robust literature relevant to the occupational burden of disease, there are a number of other respiratory syndromes in which occupational associations have been observed in disease outbreaks, in certain work settings, or after suspect exposures , — We synthesized data from 15 relevant publications for HP, the earliest paper dating from see Table 7.

We excluded case series limited to a single avocation or occupation e. The studies included — were all case series or registries , except for one case—control design , but used variable criteria for diagnosing HP and assessing causation. For the case series, we considered the work-related cases within a larger series to represent the occupational burden of disease. Occupational burden is derived from the proportion of occupationally attributed cases in the series or, in the case of Cramer and colleagues , derived from the OR and proportion of exposed cases.

Hypersensitivity pneumonitis HP : occupational burden. Forest plot of studies relevant to estimating the contribution of work exposures to HP. In addition to HP, we also considered the occupational burden of other noninfectious granulomatous lung diseases.

Inhalation of beryllium can cause granulomatous lung disease that mimics sarcoidosis; other metals have also been associated with granulomatous responses; and sarcoidosis prevalence has been reported to be elevated among various occupational groups, including firefighters, navy recruits, workers in the lumber industry, rock or glass wool workers, salespeople, and World Trade Center disaster emergency responders , Several large case-referent studies of patients with sarcoidosis who were not beryllium sensitized have found that occupational exposures to organic dusts, bioaerosols, and metals increased risk of sarcoidosis —

BMC Public Health

Rationale: Workplace inhalational hazards remain common worldwide, even though they are ameliorable. Previous American Thoracic Society documents have assessed the contribution of workplace exposures to asthma and chronic obstructive pulmonary disease on a population level, but not to other chronic respiratory diseases. The goal of this document is to report an in-depth literature review and data synthesis of the occupational contribution to the burden of the major nonmalignant respiratory diseases, including airway diseases; interstitial fibrosis; hypersensitivity pneumonitis; other noninfectious granulomatous lung diseases, including sarcoidosis; and selected respiratory infections. Methods: Relevant literature was identified for each respiratory condition. The occupational population attributable fraction PAF was estimated for those conditions for which there were sufficient population-based studies to allow pooled estimates. For the other conditions, the occupational burden of disease was estimated on the basis of attribution in case series, incidence rate ratios, or attributable fraction within an exposed group.

To determine the incidence of pulmonary tuberculosis TB in inmates, factors associated with TB, and the time to sputum smear and culture conversion during TB treatment. Prospective cohort study. All prisoners with respiratory symptoms RS of any duration were evaluated. After participants signed consent forms, we collected three spontaneous sputum samples on consecutive days. TB cases were followed, and the times to smear and culture conversion to negative were evaluated.


The frequency of rhinitis was %, asthma %, chronic bronchitis % and chronic obstructive pulmonary disease (COPD) % (% for current and former.


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Chiang , R. Strunk, L. Louis Children's Hospital, St. Louis, MO. D'Ambrosio 1 , P. Pierimarchi 2 , M.

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