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Will sewage workers with endotoxin related symptoms have the benefit of reduced lung cancer?
  1. J H Lange1,
  2. G Mastrangelo2,
  3. K W Thomulka3
  1. 1Envirosafe Training and Consultants, Inc., PO Box 114022, Pittsburgh, PA 15239, USA; john.pam.lange{at}
  2. 2Department of Environmental Medicine and Public Health, Section of Occupational Health, University of Padova, Via Giustiniani, 2-35128 Padova, Italy
  3. 3University of the Sciences in Philadelphia, 600 South 43rd Street, Philadelphia, PA 19104, USA

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    Thorn and colleagues1 reported that sewage workers suffer from various symptoms which can be related to bacterial endotoxin (lipopolysaccharide) exposure. Other studies2–5 have shown that some members of this occupational group are commonly exposed to endotoxin. However, there appears to be a large discrepancy in endotoxin exposure among those categorised within this group.2 Endotoxin exposure to some of these workers appears to be sufficient to induce a respiratory response characteristically associated with endotoxin.2 Workers that have the highest exposure in sewage treatment are suggested to be associated with the waste treatment process.3 Professor Rylander pointed out that endotoxin exposure to this occupational group is low overall (personal communication with Professor Rylander). Rapiti and colleagues6 suggested that the lack of an increased lung cancer rate in one study7 and reduced risk of lung cancer in another8 for sewage workers may be related to endotoxins in their occupational environment as was originally reported for cotton textile workers.9 Other studies10,11 that reported on lung cancer rates for sewage workers support these findings as suggested by Rapiti and colleagues.6 Rylander12 and Lange13 previously reviewed the epidemiological literature on reduced cancer rates in various occupations that are exposed to endotoxin.

    A number of epidemiological,12–16 experimental,17,18 and clinical19,20 studies have suggested that endotoxin is effective against cancer. A recent study in humans by Palmberg and colleagues21 reported that there is a rapid blood response of total leucocytes, monocytes, and granulocytes within seven hours followed by a dramatic decline within 24 hours. These findings are supported by an investigation by O'Grady and colleagues22 in humans, in which endotoxin was instilled into a lung segment; increased tumour necrosis factor (TNF) and interleukin 1 were found in the bronchoalveolar lavage fluid 2–6 hours afterwards. Cytokine levels returned to normal concentrations within 24–48 hours after treatment. An increase of TNF in lung fluids as a result of exposure to endotoxin and dust containing endotoxin has been reported by others conducting human investigations as well,23,24 including the suggestion of a dose-response relation.25 Thus, periodic exposure as would likely be experienced by those in sewage and dusty occupations may afford a continual or pulse stimulation of the immune system. Such stimulation may enhance production of anticancer mediator factors and cells26 that are suggested to be responsible for observed reduced lung cancer rates.13

    Experimental studies27 have suggested that benefit of endotoxin exposure is most effective during initiation of lung cancer with a finding of less benefit for established tumours. This, together with results from Palmberg and colleagues,21 supports the hypothesis14,27 that endotoxin in an occupational setting is effective against the early formation of lung cancer. This further suggests that endotoxin reduces the incidence of lung cancer by stimulating the immune system to guard against early lung cancer events.

    Additional studies are warranted on the relation of endotoxin and reduced lung cancer rates. This relation has been suggested for textile and agricultural workers.12–16 There is no reason to believe that it will not exist for other occupational groups exposed to endotoxin. Many have explained that the relation is not one of benefit, but rather methodology and bias, including differences in smoking rates.6–9 However, this explanation is not supported by experimental and clinical investigations involving endotoxin. The major influence on lung cancer is tobacco use (smoking). Although smoking is identified as one of the reasons for lower than expected rates in some populations, some studies6–9 have shown that smoking is not always an explainable factor or bias for reduced lung cancer. For example, Rapiti and colleagues6 reported that the consumption of cigarettes and prevalence of smoking in a population of municipal waste workers was higher than the general population, but the incidence of cancer deaths (standardised mortality ratio) for lung cancer in this group was 0.55. Epidemiological studies need to include and report not only detrimental outcomes but also potentially beneficial associations.