Bagassosis

Article Author:
Alpha Madu
Article Editor:
Tariq Sharman
Updated:
5/8/2020 11:47:44 AM
PubMed Link:
Bagassosis

Introduction

Bagassosis belongs to the group of respiratory conditions classified as interstitial lung diseases or hypersensitivity pneumonitis. It presents similarly to other extrinsic allergic alveolitis, such as Farmer's Lung.[1] It develops in a patient as a result of exposure and inhalation of bagasse - the residual fibrous material following sugar extraction from sugar-cane.[2] This seemingly waste product of sugar production has now found use in the manufacturing of other end-products such as building materials, biofuel, pulp, paper, furniture, brick, ship, automobiles, and fertilizers.[1][2] Historically bagassosis was first described by Jamison and Hopkins in 1941 after it was reported in a hard-board factory in New Orleans, USA. Subsequently, other reports followed from other American states (mostly in the south) and other countries such as Italy, India, and the Philipines. Castleden and Hamilton-Paterson were the first to use the actual term 'bagassosis' after they reported it in four factory workers in London in 1942.[1] In the past, bagasse was processed manually, in a time-consuming process, before the technological revolution in the 1950s and '60s. However, the machine-processing of bagasse led to the dispersal of particle-laden dust around the machines. Soon after the introduction of these machines, the first cases of bagassosis were reported, predictably in those close to the machines such as the workers who fed the machines and the engineers who supervised them. Other workers, such as those who handled the finished products, were not affected.[2] 

Etiology

Bagassosis is an airborne disease caused by inhalation of the fibrous cane-sugar residue, bagasse.[3] It most commonly occurs in those who are frequently close to this material, e.g., sugar factory workers. A study showed that 11 out of 21 bagasse-shredding workers developed the disease over 15 months.[1]

Epidemiology

There is no mention of the prevalence of Bagassosis in recent literature, and its sex and age distribution are unknown. It is a relatively rare disease, first described in 1941. Most of the initially reported cases were in southern American states, especially Louisiana.[1] Few cases were reported in Europe and Asia.[1] Four reported cases came from a London factory in 1942. By 1958, the total number of cases reported globally in the literature was up to 60.[1] However, after 69 cases occurred in 140 Puerto Rican paper-mill workers in 1960, the disease was no longer regarded as very uncommon at the time.[1] 

Pathophysiology

The disease is an airborne disease caused by inhalation of the bagasse dust contaminated by thermophilic actinomycetes, most importantly, Thermoactinomycetes vulgaris.[3] This organism produces a hypersensitivity reaction characterized by widespread bronchoconstriction in the peripheral bronchopulmonary tree, resembling that seen in other extrinsic allergic alveolitis such as Farmer's lungs.[1][3] However, other mechanisms have also been postulated in the pathophysiology of the disease, including the irritant property of bagasse itself, its silica content, other micro-organisms including fungi, or a combination of these factors.[4]

Histopathology

Bronchoalveolar lavage specimens from patients suffering from bagassosis show hypercellularity and neutrophilia.[5] Other findings include increased levels of TNF-alpha, IL-1beta, IL-8, and IL-6.[5] Lung autopsy shows minute needle-like spicules in the pulmonary tissue. These spicules have the same semblance and characteristics as bagasse fiber when rotated in polarized light. Other findings are the presence of large cells with a foamy cytoplasm in the alveolar spaces and an interstitial fibroblastic tissue reaction.[4] 

History and Physical

The onset of the disease may be acute or insidious. The acute onset is usually after exposure to a very large concentration of the bagasse dust. In other cases, symptoms start to appear about four months to 12 years after exposure to the dust.[1] Classical presenting complaints include a worsening and severe shortness of breath, cough, fever, malaise, and weight loss.[1][3] The cough is usually dry but maybe productive of mucoid sputum. Cyanosis, clubbing, wheezing, and signs of consolidation are generally absent.[1]

Physical examination of these patients reveals crepitations, which are usually basal but may be generalized in severe cases.[1][3] 

The diagnosis is clinical and based on a positive occupational history, characteristic clinical features, and chest X-ray findings, and after the exclusion of other possible conditions.[4]

Evaluation

Blood tests are usually unremarkable; normal white cell counts, normal PCO2, and slightly elevated ESR.[1] The chest X-ray shows fine micronodular shadowing, but may be normal in some patients.[1][3] Pulmonary function tests show a restrictive picture, including reduced lung volumes, ventilatory capacity, and gas transfer.[3] FEV1 and FVC will both be reduced while the FEV1/FVC ratio will be normal.[1] There is no evidence of airway reversibility after inhalation of a bronchodilator.[1]

Treatment / Management

There is no role for drugs in the management of bagassosis. Being an occupational hypersensitivity pneumonitis resulting from exposure to the bagasse dust, avoiding the dust is usually all that is required to treat the condition. Re-exposure to the dust is associated with the re-occurrence of the disease.[4] Symptomatic treatment with antitussives, antipyretics, fluid rehydration, rest, nutrition, and in some cases, oxygen supplementation, may be required. In very severe forms of the disease, the use of steroids has shown to be beneficial.[4] 

Differential Diagnosis

The differential diagnoses of the disease are numerous. They include other causes of extrinsic allergic alveolitis, such as those occurring after exposure to other organic dust (such as silicon, hay, cotton, and compost dust) and other non-allergic types of pneumonia, such as infective causes.[6][7]

Examples of hypersensitivity pneumonia that could mimic bagassosis include Farmer's lung, suberosis, Pigeon breeder's/bird fancier's disease, and fungal pneumonitis.[8] Other differential diagnoses include asthma, chronic obstructive pulmonary disease (COPD), eosinophilic pneumonia, community-acquired pneumonia, miliary tuberculosis, silicosis, pulmonary edema, and idiopathic interstitial lung disease.[4][8] 

Prognosis

After stopping the patient from contact with the offending bagasse dust, complete resolution of symptoms usually occurs in 1 to 6 months. The chest X-ray returns to normal in 2 to 6 months while pulmonary function normalizes in 2 to 4 months.[1][3][4] The mortality rate of the disease is reported to be 7.5% but is likely much lower as much milder forms of the disease go undetected.[4]

Complications

Bagassosis usually resolves completely without any long-standing complications. However, similar to other pneumoconioses, several complications can arise in these patients, including interstitial lung fibrosis, chronic obstructive pulmonary disease, hemoptysis, pneumothorax, pleuritis, chronic interstitial pneumonia, and malignancy.[9]

Deterrence and Patient Education

Educating factory workers on the clinical symptoms and signs of the disease is very important in the prevention of bagassosis. Early recognition of the disease leads to immediate separation of the worker from the offending dust leading to complete recovery. Patients should be informed of warning symptoms of recurring disease or worsening features indicative of lung fibrosis and advised to seek medical care urgently. Workers should also receive training on the importance of personal protective equipment, and its use should be mandatory. Work schedules should encourage the rotation of patients working close to bagasse to limit contact.

Pearls and Other Issues

Bagassosis is now an 'almost non-existent' disease due to preventive control measures that were put in place to improve the storing process of bagasse.[10] For instance, dust control measures such as wetting the bagasse, thereby increasing its moisture content, improving ventilation, and the use of face masks led to a significant reduction in the incidence of the disease, especially in the 1970s.[4][11] As such, there is now little mention of bagassosis in recent literature.

Enhancing Healthcare Team Outcomes

The diagnosis of bagassosis is often clinical. Other investigations and radiological imaging studies are only supportive. Once diagnosed, the most effective treatment involves removing the patient from the offending dust. As an occupational health issue, the main focus is prevention. From an occupational and public health perspective, this involves a much broader multi-disciplinary team including clinicians, occupational therapists, public health workers, social workers, health and safety professionals, physiotherapists and even a medicolegal team. Since the management of the condition involves prolonged absenteeism from work, the social welfare of the patients becomes essential; this is why the disease is fraught with medicolegal issues. Unfortunately, due to the lack of information on the condition when it was first described, it was not covered under the Workman's Compensation Act; hence sufferers could not make any claims.[12] However, the American College of Occupational and Environmental Medicine (ACOEM) now updates its guidelines on the investigation and management of the disease every three years. [Level 1]


References

[1] Hearn CE, Bagassosis: an epidemiological, environmental, and clinical survey. British journal of industrial medicine. 1968 Oct;     [PubMed PMID: 5723350]
[2] Castleden LI,Hamilton-Paterson JL, Bagassosis: An Industrial Lung Disease. British medical journal. 1942 Oct 24;     [PubMed PMID: 20784500]
[3] Miller GJ,Hearn CE,Edwards RH, Pulmonary function at rest and during exercise following bagassosis. British journal of industrial medicine. 1971 Apr;     [PubMed PMID: 4995433]
[4] BUECHNER HA,PREVATT AL,THOMPSON J,BLITZ O, Bagassosis; a review, with further historical data, studies of pulmonary function, and results of adrenal steroid therapy. The American journal of medicine. 1958 Aug;     [PubMed PMID: 13559276]
[5] Zhai R,Ge X,Li H,Tang Z,Liao R,Kleinjans J, Differences in cellular and inflammatory cytokine profiles in the bronchoalveolar lavage fluid in bagassosis and silicosis. American journal of industrial medicine. 2004 Oct;     [PubMed PMID: 15376226]
[6] Hargreave FE,Pepys J,Holford-Strevens V, Bagassosis. Lancet (London, England). 1968 Mar 23;     [PubMed PMID: 4170904]
[7] Castranova V,Robinson VA,Frazer DG, Pulmonary reactions to organic dust exposures: development of an animal model. Environmental health perspectives. 1996 Mar;     [PubMed PMID: 8722109]
[8] Lacasse Y,Cormier Y, Hypersensitivity pneumonitis. Orphanet journal of rare diseases. 2006 Jul 3;     [PubMed PMID: 16817954]
[9] Jun JS,Jung JI,Kim HR,Ahn MI,Han DH,Ko JM,Park SH,Lee HG,Arakawa H,Koo JW, Complications of pneumoconiosis: radiologic overview. European journal of radiology. 2013 Oct;     [PubMed PMID: 23791520]
[10] Ueda A,Aoyama K,Ueda T,Obama K,Ueno T,Hokama S,Nomura S, Recent trends in bagassosis in Japan. British journal of industrial medicine. 1992 Jul;     [PubMed PMID: 1637710]
[11] Lehrer SB,Turer E,Weill H,Salvaggio JE, Elimination of bagassosis in Louisiana paper manufacturing plant workers. Clinical allergy. 1978 Jan;     [PubMed PMID: 627039]
[12] Gillison JA,Taylor F, Four Cases of Bagassosis. British medical journal. 1942 Nov 14;     [PubMed PMID: 20784538]