Clinical detection of silicosis is currently dependent on radiological and lung function abnormalities, both late manifestations of disease. Markers of prediction and early detection of pneumoconiosis are imperative for the implementation of timely intervention strategies. Understanding the underlying mechanisms of the etiology of coal workers pneumoconiosis (CWP) and silicosis was essential in proposing numerous biomarkers that have been evaluated to assess effects following exposure to crystalline silica and/or coal mine dust. Human validation studies have substantiated some of these proposed biomarkers and argued in favor of their use as biomarkers for crystalline silica- and CWP-induced pneumoconiosis. A number of “ideal” biological markers of effect were identified, namely, Clara cell protein-16 (CC16) (serum), tumor necrosis factor-α (TNF-α) (monocyte release), interleukin-8 (IL-8) (monocyte release), reactive oxygen species (ROS) measurement by chemiluminescence (neutrophil release), 8-isoprostanes (serum), total antioxidant levels measured by total equivalent antioxidant capacity (TEAC), glutathione, glutathione peroxidase activity, glutathione S-transferase activity, and platelet-derived growth factor (PDGF) (serum). TNF-α polymorphism (blood cellular DNA) was identified as a biomarker of susceptibility. Further studies are planned to test the validity and feasibility of these biomarkers to detect either high exposure to crystalline silica and early silicosis or susceptibility to silicosis in gold miners in South Africa.

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Background. The rate of recurrent tuberculosis disease due to reinfection, compared with the incidence of new tuberculosis, in those with and without

Anaemia in pregnancy is a major public health and economic problem worldwide, that contributes to both maternal and fetal morbidity and mortality. The aim of the study was to calculate the prevalence of anaemia in early pregnancy in a cohort of ‘low risk’ women participating in a large international multicentre prospective study (n = 5 609), to identify the modifiable risk factors for anaemia in pregnancy in this cohort, and to compare the birth outcomes between pregnancies with and without anaemia in early gestation. The study is an analysis of data that were collected prospectively during the Screening for Pregnancy Endpoints study. Anaemia was defined according to the World Health Organization’s definition of anaemia in pregnancy (haemoglobin < 11g/dL). Binary logistic regression with adjustment for potential confounders (country, maternal age, having a marital partner, ethnic origin, years of schooling, and having paid work) was the main method of analysis. The hallmark findings were the low prevalence of anaemia (2.2%), that having no marital partner was an independent risk factor for having anaemia (OR 1.34, 95% CI 1.01-1.78), and that there was no statistically significant effect of anaemia on adverse pregnancy outcomes (small for gestational age, pre-tem birth, mode of delivery, low birth weight, APGAR score < 7 at one and five minutes). Adverse pregnancy outcomes were however more common in those with anaemia than in those without. In this low risk healthy pregnant population we found a low anaemia rate. The absence of a marital partner was a non-modifiable factor, albeit one which may reflect a variety of confounding factors, that should be considered for addition to anaemia’s conceptual framework of determinants. Although not statistically significant, clinically, a trend towards a higher risk of adverse pregnancy outcomes was observed in women that were anaemic in early pregnancy.

Background: HIV increases the risk of tuberculosis directly, through immunosuppression, and indirectly, through onward transmission of Mycobacterium tuberculosis from the increased caseload. We assess the contribution of these two mechanisms by time since seroconversion to HIV. Methods: The incidence of new pulmonary tuberculosis was estimated in a retrospective cohort study of South African gold miners over 14 years. HIV tests were done in random surveys in 1992–1993, and in clinics. One thousand nine hundred fifty HIV-positive men with seroconversion intervals of less than 3 years were identified and linked to medical, demographic and occupational records. They were compared with men who were HIV-negative in a survey, with no later evidence of HIV. Analyses were censored when men were diagnosed with tuberculosis, died or left the mine. Results: Tuberculosis incidence rose soon after HIV infection, reaching 1.4/100 person-years (95% confidence interval 1.1–1.9) within 2 years, and 10.0/100 person-years (95% confidence interval 6.5–15.5) at 10 or more years. By 11 years from seroconversion, nearly half the men had had tuberculosis. Among 5702 HIV-negative men, tuberculosis incidence was 0.48/100 person-years (95% confidence interval 0.33–0.70) in 1991–1993 and doubled over the period of the study (after adjusting for age). Age-adjusted model estimates suggest that half the increase in tuberculosis incidence by time since HIV infection was attributable to increasing incidence over calendar period – the indirect effect. Conclusion: For the first time, we have shown that the increase in tuberculosis risk by time since seroconversion reflects both direct effects of HIV increasing susceptibility, and indirect effects due to onward transmission. Innovative and sustained public health measures are needed to reduce Mycobacterium tuberculosis transmission.