Background: Workers exposed to sewage may have an increased risk of infection by Helicobacter pylori and hepatitis E virus (HEV). Aims: To assess the prevalence of clinical hepatitis E (HE) and peptic ulcer disease as well as the seroprevalence of antibodies to H pylori and HEV in workers with and without sewage exposure and to look for symptoms due to exposure to endotoxin. Methods: In the first year of a prospective cohort study 349 sewage exposed workers and 429 municipal manual workers (participation: 61%) underwent a complete medical examination. Travelling to endemic areas, socioeconomic level, age, country in which childhood was spent, and number of siblings were considered as the main confounding factors. Results: Peptic ulcer disease and clinical HE did not occur more often in workers exposed to sewage. Prevalence of antibodies to HEV was 3.3% and overall prevalence of IgG antibodies to H pylori was 42% with large differences between subgroups. Logistic regression did not show an increased risk of seropositivity or antibodies to parietal cells in sewage exposed workers, but disentangling the effect of exposure from that of confounders was extremely difficult. No increase of symptoms due to exposure to endotoxin was found in sewage workers, with the exception of diarrhoea. Conclusions: No clear increased risk of infection by H pylori or by HEV in workers exposed to sewage was found in this cross-sectional study, but these results need to be confirmed by follow up.

Objectives: Inhalation of bioaerosols has been hypothesised to cause ''toxic pneumonitis'' that should increase lung epithelial permeability at the bronchioloalveolar level. Serum Clara cell protein (CC16) and serum surfactant protein B (SPB) have been proposed as sensitive markers of lung epithelial injury. This study was aimed at looking for increased lung epithelial permeability by determining CC16 and SPB in workers exposed to bioaerosols from wastewater or garbage. Methods: Subjects (778 wastewater, garbage and control workers; participation 61%) underwent a medical examination, lung function tests [American Thoracic Society (ATS) criteria], and determination of CC16 and SPB. Symptoms of endotoxin exposure and several potential confounders (age, gender, smoking, kidney function, obesity) were looked for. Results were examined with multiple linear or logistic regression. Results: Exposure to bioaerosols increased CC16 concentration in the wastewater workers. No effect of exposure on SPB was found. No clue to work-related respiratory diseases was found. Conclusions: The increase in CC16 in serum supports the hypothesis that bioaerosols cause subclinical ''toxic pneumonitis'', even at low exposure.

Objectives: Workers exposed to sewage may have an increased risk of infection by Helicobacter pylori (H. pylori) and hepatitis E virus (HEV). To assess the incidence of clinical hepatitis E (HE) and peptic ulcer disease as well as the seroconversion rate of antibodies to H. pylori and HEV in workers with and without sewage exposure.Methods: 332 workers exposed to sewage and a control group of 446 municipal manual workers (participation: 61 %) entered a prospective cohort study with clinical examination and determination of antibodies to H. pylori and HEV (immunoglobulins G and A or G and M, respectively). Survival curves were examined with log rank tests and Cox regressions. Travelling to endemic areas, socioeconomic level, age, country in which childhood was spent, number of siblings, and personal protective equipment were considered as the main confounding factors.Results: Incidence of clinical HE was not increased in sewage workers. One peptic ulcer and three eradications were recorded in sewage workers whereas no case of peptic ulcer and 12 eradications occurred in control workers. Incidence rates of about 0.01, 0.10, and 0.15 seroconversion / person-year for HE, H. pylori IgG, and H. pylori IgA, respectively, were found in both exposed and non exposed workers. Survival curves did not show an increased risk in sewage workers and no association with any exposure indicator was found. Sensitivity analyses did not alter these results.Conclusions: These results do not support the hypothesis of sewage as a source of occupational infection for H. pylori or HEV in sewage workers trained for this job with available personal protective equipment and working in a region with good sanitation.

In this population no effects of occupational exposure to bioaerosols were found, probably because of good working conditions.

Endotoxin causes an inflammation at the bronchial and alveolar level. The inflammation-induced increase in permeability of the bronchoalveolar epithelial barrier is supposed to cause a leakage of pneumoproteins. Therefore, their concentrations are expected to increase in the bloodstream. This study aimed at examining the association between occupational exposure to endotoxin and a serum pneumoprotein, surfactant protein A, to look for nonoccupational factors capable of confounding this association, and examine the relation between surfactant protein A and spirometry. There were 369 control subjects, 325 wastewater workers, and 84 garbage collectors in the study. Exposure to endotoxin was assessed through personal sampling and the Limulus amebocytes lysate assay. Surfactant protein A was determined by an in house sandwich enzyme-linked immunosorbent assay (ELISA) in 697 subjects. Clinical and smoking history were ascertained and spirometry carried out according to American Thoracic Society criteria. Multiple linear regression was used for statistical analysis. Exposure was fairly high during some tasks in wastewater workers but did not influence surfactant protein A. Surfactant protein A was lower in asthmatics. Interindividual variability was large. No correlation with spirometry was found. Endotoxin has no effect on surfactant protein A at these endotoxin levels and serum surfactant protein A does not correlate with spirometry. The decreased surfactant protein A secretion in asthmatics requires further study.