Environmental exposures associated with early childhood recurrent wheezing in the mother and child in the environment birth cohort: a time-to-event study.

BACKGROUND: Antenatal factors and environmental exposures contribute to recurrent wheezing in early childhood. AIM: To identify antenatal and environmental factors associated with recurrent wheezing in children from birth to 48 months in the mother and child in the environment cohort, using time-to-event analysis. METHOD: Maternal interviews were administered during pregnancy and postnatally and children were followed up from birth to 48 months (May 2013-October 2019). Hybrid land-use regression and dispersion modelling described residential antenatal exposure to nitrogen dioxide (NO2) and particulate matter of 2.5 µm diameter (PM2.5). Wheezing status was assessed by a clinician. The Kaplan-Meier hazard function and Cox-proportional hazard models provided estimates of risk, adjusting for exposure to environmental tobacco smoke (ETS), maternal smoking, biomass fuel use and indoor environmental factors. RESULTS: Among 520 mother-child pairs, 85 (16%) children, had a single wheeze episode and 57 (11%) had recurrent wheeze. Time to recurrent wheeze (42.9 months) and single wheeze (37.8 months) among children exposed to biomass cooking fuels was significantly shorter compared with children with mothers using electricity (45.9 and 38.9 months, respectively (p=0.03)). Children with mothers exposed to antenatal ETS were 3.8 times more likely to have had recurrent wheeze compared with those not exposed (adjusted HR 3.8, 95% CI 1.3 to 10.7). Mean birth month NO2 was significantly higher among the recurrent wheeze category compared with those without wheeze. NO2 and PM2.5 were associated with a 2%-4% adjusted increased wheezing risk. CONCLUSION: Control of exposure to ETS and biomass fuels in the antenatal period is likely to delay the onset of recurrent wheeze in children from birth to 48 months.

Pneumococcal pneumonia on the job: Uncovering the past story of occupational exposure to metal fumes and dust.

The objectives of this study are to elucidate the early history of risk for pneumococcal pneumonia from occupational exposure to metal fumes and dusts, and to demonstrate the importance of searching older literature when performing reviews. We performed manual searching for articles in the Library of the Surgeon General's Office (the precursor to Index Medicus), in the Hathi Trust database, in PubMed, andby screening reference lists in literature appearing before the introduction of PubMed. An early body of literature, from the 1890s onward, recognized that pneumonia was linked to "Thomas slag," a steel industry byproduct containing iron, manganese, and lime. Researchers, mainly in Germany, showed that workers in metal-dust-exposed occupations, especially using manganese, manifested an increased incidence of pneumococcal pneumonia. An outbreak of pneumococcal pneumonia in the 1930s implicated manganese fume in its etiology. In the immediate post-World War II period, there was a brief flurry of interest in pneumonia from exposure to potassium permanganate that was soon dismissed as a chemical pneumonitis. After a hiatus of two decades, epidemiologic investigations drew attention to the pneumonia risks of welding and related metal fume exposure, bringing renewed interest to the forgotten role of pneumococcal pneumonia as an occupational disease. Occupational or environmental inhalation of manganese, iron, or irritants may be causally related to increased pneumococcal pneumonia risk. In particular, the risk associated with manganese seems to be overlooked in recent literature. An important conclusion is the importance of obtaining additional evidence through a deeper assessment of the literature in a broad historical context.

Prenatal Air Pollution Exposure and Placental DNA Methylation Changes: Implications on Fetal Development and Future Disease Susceptibility.

The Developmental Origins of Health and Disease (DOHaD) concept postulates that in utero exposures influence fetal programming and health in later life. Throughout pregnancy, the placenta plays a central role in fetal programming; it regulates the in utero environment and acts as a gatekeeper for nutrient and waste exchange between the mother and the fetus. Maternal exposure to air pollution, including heavy metals, can reach the placenta, where they alter DNA methylation patterns, leading to changes in placental function and fetal reprogramming. This review explores the current knowledge on placental DNA methylation changes associated with prenatal air pollution (including heavy metals) exposure and highlights its effects on fetal development and disease susceptibility. Prenatal exposure to air pollution and heavy metals was associated with altered placental DNA methylation at the global and promoter regions of genes involved in biological processes such as energy metabolism, circadian rhythm, DNA repair, inflammation, cell differentiation, and organ development. The altered placental methylation of these genes was, in some studies, associated with adverse birth outcomes such as low birth weight, small for gestational age, and decreased head circumference. Moreover, few studies indicate that DNA methylation changes in the placenta were sex-specific, and infants born with altered placental DNA methylation patterns were predisposed to developing neurobehavioral abnormalities, cancer, and atopic dermatitis. These findings highlight the importance of more effective and stricter environmental and public health policies to reduce air pollution and protect human health.

Maternal demographic and antenatal factors, low birth weight and preterm birth: findings from the mother and child in the environment (MACE) birth cohort, Durban, South Africa.

BACKGROUND: Low birthweight (LBW) and preterm birth (PB) remain the leading cause of morbidity and mortality in neonates worldwide. The aim of this study was to identify maternal demographic and antenatal factors associated with PB and LBW among low socio-economic communities. METHODS: Pregnant women (n = 1099) were recruited in the first trimester into the Mother and Child in the Environment (MACE) birth cohort in Durban, South Africa. Maternal factors such as demographic information, health status, residential area, occupational, personal and environmental smoking and biomass fuel use were obtained through standardised interviews, while clinical status was obtained in each trimester and antenatal information on HIV status and treatment, syphilis and conditions such as pregnancy induced hypertension, diabetes etc. was extracted from the antenatal assessments. Key outcomes of interest were preterm birth and low birthweight. The latter data was obtained from the clinical assessments performed by midwives at delivery. Logistic regression models identified factors associated with PB and LBW. RESULTS: Of the 760 live births, 16.4 and 13.5% were preterm and LBW, respectively. Mothers who delivered by caesarean section had an increased odds of having LBW babies (Adjusted odds ratio (AOR): 1.7; 95% CI: 1.1-2.7) and PB (AOR: 1.7, 95% CI: 1.1-2.7) versus normal vaginal deliveries. Mothers > 30 years (AOR: 1.8, 95% CI: 1.1-2.9) and current smokers (AOR: 2.7, 95% CI: 1.3-5.8) had an increased odds of having PB babies. Compared to younger mothers and non-smokers respectively. An effect of PB and LBW was seen among mothers with high BMI (25.0-29.9 kg/m2) (PB: AOR: 0.5, 95% CI: 0.3-0.9 and LBW: AOR: 0.5, 0.5, CI: 0.3-0.8), and obese BMI (> 30 kg/m2) (PB: AOR: 0.5, 95% CI: 0.3-0.9 and LBW: AOR: 0.4, CI: 0.2-0.7). Maternal HIV (PB AOR: 1.4 and LBW AOR: 1.2) and history of sexually transmitted infections (PB AOR: 2.7 and LBW AOR: 4.2) were not statistically significant. CONCLUSION: Maternal age, cigarette smoking and caesarean delivery were associated with LBW and PB. Findings highlight the need of maternal health interventions to improve new-born health outcomes.

Effect of maternal HIV infection, BMI and NOx air pollution exposure on birth outcomes in South African pregnant women genotyped for the p53 Pro72Arg (rs1042522).

Tumour suppressor protein, p53, plays a role in modulating innate immune responses, DNA repair, cell cycle arrest, senescence and apoptosis. Maternal nitrogen oxide (NOx) air pollution exposure, body mass index (BMI), human immunodeficiency virus (HIV) infection and p53 Pro72Arg (rs1042522) affect foetal growth. We investigated whether the aforementioned factors influence birth outcomes in a South African population. Pregnant women (n = 300; HIV -ve = 194 and HIV +ve = 106) were genotyped for the p53 rs1042522 using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), and further stratified based on HIV status, infants' birthweight (BW; NBW: normal BW [>2,500 g] and LBW: low BW [<2,500 g]) and gestational age (GA; NGA: normal GA [>37 weeks] and PTB: preterm birth [≤37 weeks]). A land use regression model was developed to characterize maternal NOx exposure. Pearson's correlation and multivariate regression analysis statistical tests were used to determine the effect of rs1042522 genotyped pregnant women's BMI and NOx exposure on maternal blood pressure and haemoglobin and iron levels, and infants' anthropometric measurements and Appearance Pulse Grimace Activity and Respiration (APGAR) scores. The prevalence of LBW and PTB was 14.7% and 18.7%, respectively. The LBW group had a higher frequency of the variant Arg-allele versus NBW group (47.7% vs. 31.4%, p = .0046, OR = 2.0, 95% CI = 1.26-3.17). No association was observed between NGA and PTB groups. A significant association between BMI and systolic blood pressure (r = .50, p = .00; B = 0.76, p = .002) and birth length (r = -.28, p = .01; B = -0.107, p = .011), and NOx and birth length (r = -.26, p = .08; B = -0.191, p = .046) and birthweight (B = -8.87, p = .048) was observed in HIV-infected mothers with the variant Pro/Arg + Arg/Arg genotypes. Mothers from the LBW group with the variant genotypes displayed an association between NOx and diastolic blood pressure (r = .58, p = .04), blood iron levels (r = -.60, p = .04; B = -0.204, p = .004), APGAR scores at 1 min (r = -.86, p = .00; B = -0.101, p = .003) and 5 min (r = -.75, p = .01) and birth length (r = -.61, p = .04), and BMI and diastolic blood pressure (r = .72, p = .01). In the PTB group, maternal variant genotypes and NOx were associated with blood haemoglobin levels (B = -0.132, p = .045) and APGAR scores at 1 min (B = -0.161, p = .045) and 5 min (B = -0.147, p = .043). Maternal rs1042522 Arg-allele, HIV infection, BMI and NOx exposure collectively play a role in lowering blood iron levels, gestational hypertension and LBW outcomes.

Occupational exposure to dust and to fumes, work as a welder and invasive pneumococcal disease risk.

OBJECTIVES: Occupational exposures to metal fumes have been associated with increased pneumonia risk, but the risk of invasive pneumococcal disease (IPD) has not been characterised previously. METHODS: We studied 4438 cases aged 20-65 from a Swedish registry of invasive infection caused by Streptococcus pneumoniae. The case index date was the date the infection was diagnosed. Six controls for each case, matched for gender, age and region of residency, were selected from the Swedish population registry. Each control was assigned the index date of their corresponding case to define the study observation period. We linked cases and controls to the Swedish registries for socioeconomic status (SES), occupational history and hospital discharge. We applied a job-exposure matrix to characterise occupational exposures. We used conditional logistic analyses, adjusted for comorbidities and SES, to estimate the OR of IPD and the subgroup pneumonia-IPD, associated with selected occupations and exposures in the year preceding the index date. RESULTS: Welders manifested increased risk of IPD (OR 2.99, 95% CI 2.09 to 4.30). Occupational exposures to fumes and silica dust were associated with elevated odds of IPD (OR 1.11, 95% CI 1.01 to 1.21 and OR 1.33, 95% CI 1.11 to 1.58, respectively). Risk associated with IPD with pneumonia followed a similar pattern with the highest occupational odds observed among welders and among silica dust exposed. CONCLUSION: Work specifically as a welder, but also occupational exposures more broadly, increase the odds for IPD. Welders, and potentially others with relevant exposures, should be offered pneumococcal vaccination.

The Occupational Burden of Nonmalignant Respiratory Diseases. An Official American Thoracic Society and European Respiratory Society Statement.

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. Results: Workplace exposures contribute substantially to the burden of multiple chronic respiratory diseases, including asthma (PAF, 16%); chronic obstructive pulmonary disease (PAF, 14%); chronic bronchitis (PAF, 13%); idiopathic pulmonary fibrosis (PAF, 26%); hypersensitivity pneumonitis (occupational burden, 19%); other granulomatous diseases, including sarcoidosis (occupational burden, 30%); pulmonary alveolar proteinosis (occupational burden, 29%); tuberculosis (occupational burden, 2.3% in silica-exposed workers and 1% in healthcare workers); and community-acquired pneumonia in working-age adults (PAF, 10%). Conclusions: Workplace exposures contribute to the burden of disease across a range of nonmalignant lung conditions in adults (in addition to the 100% burden for the classic occupational pneumoconioses). 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.

Association of childhood pulmonary tuberculosis with exposure to indoor air pollution: a case control study.

BACKGROUND: Crude measures of exposure to indicate indoor air pollution have been associated with the increased risk for acquiring tuberculosis. Our study aimed to determine an association between childhood pulmonary tuberculosis (PTB) and exposure to indoor air pollution (IAP), based on crude exposure predictors and directly sampled and modelled pollutant concentrations. METHODS: In this case control study, children diagnosed with PTB were compared to children without PTB. Questionnaires about children's health; and house characteristics and activities (including household air pollution) and secondhand smoke (SHS) exposure were administered to caregivers of participants. A subset of the participants' homes was sampled for measurements of PM10 over a 24-h period (n = 105), and NO2 over a period of 2 to 3 weeks (n = 82). IAP concentrations of PM10 and NO2 were estimated in the remaining homes using predictive models. Logistic regression was used to look for association between IAP concentrations, crude measures of IAP, and PTB. RESULTS: Of the 234 participants, 107 were cases and 127 were controls. Pollutants concentrations (µg/m3) for were PM10 median: 48 (range: 6.6-241) and NO2 median: 16.7 (range: 4.5-55). Day-to-day variability within- household was large. In multivariate models adjusted for age, sex, socioeconomic status, TB contact and HIV status, the crude exposure measures of pollution viz. cooking fuel type (clean or dirty fuel) and SHS showed positive non-significant associations with PTB. Presence of dampness in the household was a significant risk factor for childhood TB acquisition with aOR of 2.4 (95% CI: 1.1-5.0). The crude exposure predictors of indoor air pollution are less influenced by day-to-day variability. No risk was observed between pollutant concentrations and PTB in children for PM10 and NO2. CONCLUSION: Our study suggests increased risk of childhood tuberculosis disease when children are exposed to SHS, dirty cooking fuel, and dampness in their homes. Yet, HIV status, age and TB contact are the most important risk factors of childhood PTB in this population.

Indoor air quality of low and middle income urban households in Durban, South Africa.

INTRODUCTION: Elevated levels of indoor air pollutants may cause cardiopulmonary disease such as lower respiratory infection, chronic obstructive lung disease and lung cancer, but the association with tuberculosis (TB) is unclear. So far the risk estimates of TB infection or/and disease due to indoor air pollution (IAP) exposure are based on self-reported exposures rather than direct measurements of IAP, and these exposures have not been validated. OBJECTIVE: The aim of this paper was to characterize and develop predictive models for concentrations of three air pollutants (PM10, NO2 and SO2) in homes of children participating in a childhood TB study. METHODS: Children younger than 15 years living within the eThekwini Municipality in South Africa were recruited for a childhood TB case control study. The homes of these children (n=246) were assessed using a walkthrough checklist, and in 114 of them monitoring of three indoor pollutants was also performed (sampling period: 24h for PM10, and 2-3 weeks for NO2 and SO2). Linear regression models were used to predict PM10 and NO2 concentrations from household characteristics, and these models were validated using leave out one cross validation (LOOCV). SO2 concentrations were not modeled as concentrations were very low. RESULTS: Mean indoor concentrations of PM10 (n=105), NO2 (n=82) and SO2 (n=82) were 64µg/m3 (range 6.6-241); 19µg/m3 (range 4.5-55) and 0.6µg/m3 (range 0.005-3.4) respectively with the distributions for all three pollutants being skewed to the right. Spearman correlations showed weak positive correlations between the three pollutants. The largest contributors to the PM10 predictive model were type of housing structure (formal or informal), number of smokers in the household, and type of primary fuel used in the household. The NO2 predictive model was influenced mostly by the primary fuel type and by distance from the major roadway. The coefficients of determination (R2) for the models were 0.41 for PM10 and 0.31 for NO2. Spearman correlations were significant between measured vs. predicted PM10 and NO2 with coefficients of 0.66 and 0.55 respectively. CONCLUSION: Indoor PM10 levels were relatively high in these households. Both PM10 and NO2 can be modeled with a reasonable validity and these predictive models can decrease the necessary number of direct measurements that are expensive and time consuming.

Respiratory health effects of occupational exposure to charcoal dust in Namibia.

BACKGROUND: Charcoal processing activities can increase the risk of adverse respiratory outcomes. OBJECTIVE: To determine dose-response relationships between occupational exposure to charcoal dust, respiratory symptoms and lung function among charcoal-processing workers in Namibia. METHODS: A cross-sectional study was conducted with 307 workers from charcoal factories in Namibia. All respondents completed interviewer-administered questionnaires. Spirometry was performed, ambient and respirable dust levels were assessed in different work sections. Multiple logistic regression analysis estimated the overall effect of charcoal dust exposure on respiratory outcomes, while linear regression estimated the exposure-related effect on lung function. Workers were stratified according to cumulative dust exposure category. RESULTS: Exposure to respirable charcoal dust levels was above occupational exposure limits in most sectors, with packing and weighing having the highest dust exposure levels (median 27.7 mg/m3, range: 0.2-33.0 for the 8-h time-weighted average). The high cumulative dust exposure category was significantly associated with usual cough (OR: 2.1; 95% CI: 1.1-4.0), usual phlegm (OR: 2.1; 95% CI: 1.1-4.1), episodes of phlegm and cough (OR: 2.8; 95% CI: 1.1-6.1), and shortness of breath. A non-statistically significant lower adjusted mean-predicted % FEV1 was observed (98.1% for male and 95.5% for female) among workers with greater exposure. CONCLUSIONS: Charcoal dust levels exceeded the US OSHA recommended limit of 3.5 mg/m3 for carbon-black-containing material and study participants presented with exposure-related adverse respiratory outcomes in a dose-response manner. Our findings suggest that the Namibian Ministry of Labour introduce stronger enforcement strategies of existing national health and safety regulations within the industry.

The risk of pulmonary tuberculosis in underground copper miners in Zambia exposed to respirable silica: a cross-sectional study.

BACKGROUND: Pulmonary tuberculosis (PTB) among underground miners exposed to silica remains a global problem. Although well described in gold and coal mining, risk in other mining entities are not as well documented. This study aims to determine dust-related dose response risk for PTB among underground miners exposed to silica dust in Zambia's copper mines. METHODS: A cross sectional study of in-service miners (n = 357) was conducted at Occupational Health and Safety Institute (OHSI), Zambia. A systematic review of medical data over a 5-year period from assessments conducted by doctors at OHSI and statutory silica exposure data (n = 16678) from the Mine Safety Department (MSD) were analysed. Lifetime cumulative exposure metrics were calculated. Multivariate logistic regression analysis was used to determine the association between PTB and lifetime exposure to silica, while adjusting for various confounders. RESULTS: The median respirable silica dust level was 0.3 mg/m(3) (range 0.1-1.3). The overall prevalence of PTB was 9.5 % (n = 34). High cumulative respirable silica dust category showed a statistically significant association with PTB (OR = 6.4 (95 % CI 1. 8-23)) and a significant trend of increasing disease prevalence with increasing cumulative respirable silica dust categories was observed (ptrend < 0.01). Smoking showed a statistically significant association with PTB with OR = 4.3 (95 % CI 1.9-9.9). CONCLUSIONS: Our results demonstrate the association of increased risk for certified active TB with cumulative respirable dust in a dose related manner among this sample of copper miners. There is need to intensify dust control measures and incorporate anti-smoking interventions into TB prevention and control programmes in the mines.

Tumour necrosis factor α polymorphism (TNF-308α G/A) in association with asthma related phenotypes and air pollutants among children in KwaZulu-Natal.

BACKGROUND: The study of gene-environment interactions enables us to further understand the pathogenesis of asthma and inflammation. The TNF-α gene has been associated with airway pathology in asthma but there is limited information in relation to pollutant exposure and the TNF-α 308G/A polymorphism. OBJECTIVE: To determine the risk conferred by the TNF-α 308(G/A) polymorphism on respiratory outcome and to evaluate whether the association between exposure to ambient air pollutants such as SO2, NO2, NO, and PM10 and variation in lung function measures is modified by genotype. METHODS: The sample comprised 129 African children (between 9-11 years old). A questionnaire based on guidelines from the British Medical Research Council and the American Thoracic Society was administered to all caregivers to evaluate the prevalence of respiratory symptoms. Atopy was evaluated by skin prick testing. Bihourly measures of lung function (spirometry) were collected at school five days per week over three week periods in each of four seasons (2004-2005) using digital hand-held devices. During each of the four intensive 3-week phases, gaseous air pollutant concentrations were monitored continuously. Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-PFLP) analysis was used to detect the TNF-α 308 genotype and plasma TNF-α levels were measured using the human TNF-α Max Standard™ Enzyme-linked immuno-absorbent assay (ELISA) kit. RESULTS: The TNF-α variant A allele was common among this sample of African children (40% with an allelic frequency of 0.24). There was no significant association with the TNF-α G/A polymorphism and any respiratory linked phenotype, nor cytokine levels. However, when exposure to pollutants were analyzed with genotypic and phenotypic data, we found relatively modest interaction effects for the TNF-α 308 genotype. GEE models showed that children with the TNF-α 308 A allele had increased deterioration of lung function post pollution exposure to SO2 [ß=2.62, CI:0.51-4.71, p=0.02 and pint=0.03] and NO [ß=3.28, CI:0.68-5.89, p=0.01, pint=0.03]. CONCLUSION: The TNF-α 308 (G/A) polymorphism may be associated with increased pollutant-associated effects on FEV1 intraday variability for both SO2 and NO. The A allele may increase susceptibility to the adverse effects of air pollutants.

Model development including interactions with multiple imputed data.

BACKGROUND: Multiple imputation is a reliable tool to deal with missing data and is becoming increasingly popular in biostatistics. However, building a model with interactions that are not specified a priori, in the presence of missing data, presents a challenge. On the one hand, the interactions are needed to impute the data, while on the other hand, the data is needed to identify the interactions. The objective of this study was to present a way in which this challenge can be addressed. METHODS: This paper investigates two strategies in which model development with interactions is achieved using a single data set generated from the Expectation Maximization (EM) algorithm. Imputation using both the fully conditional specification approach and the multivariate normal approach is carried out and results are compared. The strategies are illustrated with data from a study of ambient pollution and childhood asthma in Durban, South Africa. RESULTS: The different approaches to model building and imputation yielded similar results despite the data being mainly categorical. Both strategies investigated for building the model using the multivariate normal imputed data resulted in the identical set of variables and interactions being identified; while models built using data imputed by fully conditional specification were marginally different for the two strategies. It was found that, for both imputation approaches, model building with backward elimination applied to the initial EM data set was easier to implement, and produced good results, compared to those from a complete case analysis. CONCLUSIONS: Developing a predictive model including interactions with data that suffers from missingness is easily done by identifying significant interactions and then applying backward elimination to a single data set imputed from the EM algorithm. It is hoped that this idea can be further developed and, by addressing this practical dilemma, there will be increased adoption of multiple imputation in medical research when data suffers from missingness.

Occupational exposures and chronic obstructive pulmonary disease: a hospital based case-control study.

BACKGROUND: Occupational exposures are associated with chronic obstructive pulmonary disease (COPD). This study investigated this association among a population with a high prevalence of tuberculosis and smoking. METHODS: Cases (n=110) diagnosed by pulmonologists were selected from specialist respiratory clinics. Frequency sex- and age-matched controls (n=102) were selected from other clinics at the same institutions. Lifetime occupational exposure histories were obtained through interviews. Exposure variables derived from the ALOHA Job Exposure Matrix (JEM) were used to complement the self-reporting variables. ORs were calculated from logistic regression models, adjusting for smoking and past history of tuberculosis. Percentage population attributable risk (PAR%) was also calculated. RESULTS: The adjusted ORs for COPD from the JEM-derived high cumulative biological dust exposure, high cumulative mineral dust exposure and high cumulative gas and fumes exposure were 2.1 (95% CI 1.1 to 4.2), 1.1 (95% CI 0.6 to 2.4) and 1.8 (95% CI 0.8 to 3.9), respectively. Self-reported occupational exposures were associated with higher risks, with adjusted ORs for high dust exposure-years and high chemical, gas and fumes exposure-years of 5.9 (95% CI 2.6 to 13.2) and 3.6 (95% CI 1.6 to 7.9), respectively. Among ever smokers, there was an increased risk for COPD, with ORs ranging from 5.0 to 5.5. Tuberculosis was a strong risk factor, with an OR ranging from 7.7 to 8.1. The PAR% was 25% for self-reported high exposures, but lower when the JEM variables were used. CONCLUSIONS: Lifetime occupational exposures contribute to the risk of COPD, adjusted for smoking. These risks are present in populations with a high burden of tuberculosis, which is considered an important causative factor.

Cross-shift peak expiratory flow changes are unassociated with respirable coal dust exposure among South African coal miners.

BACKGROUND: The objectives of this study were to determine whether cross-shift changes in peak expiratory flow rate (PEFR) were related to respirable dust exposure in South African coalminers. METHODS: Fifty workers were randomly selected from a cohort of 684 miners from 3 bituminous coalmines in Mpumalanga, South Africa. Peak expiratory efforts were measured prior to the commencement of the shift, and at the end of the shift on at least two occasions separated by at least 2 weeks, with full shift personal dust sampling being conducted on each occasion for each participant. Interviews were conducted, work histories were obtained and cumulative exposure estimates were constructed. Regression models examined the associations of cross-shift changes in PEFR with current and cumulative exposure, controlling for shift, smoking and past history of tuberculosis. RESULTS: There were marginal differences in cross-shift PEFR (ranging from 0.1 to 2 L/min). Linear regression analyses showed no association between cross-shift change in PEFR and current or cumulative exposure. The specific shift worked by participants in the study showed no effect. CONCLUSIONS: Our study showed no association between current respirable dust exposure and cross-shift changes in PEFR. There was a non-significant protective effect of cumulative dust exposure on the outcome, suggesting the presence of a "healthy worker survivor effect" in this data.

Respirable coal dust exposure and respiratory symptoms in South-African coal miners: a comparison of current and ex-miners.

OBJECTIVES: Dose-response associations between respirable dust exposure and respiratory symptoms and between symptoms and spirometry outcomes among currently employed and formerly employed South-African coal miners were investigated. METHODS: Work histories, interviews, and spirometry and cumulative exposure were assessed among 684 current and 212 ex-miners. RESULTS: Lower prevalences of symptoms were found among employed compared with ex-miners. Associations with increasing exposure for symptoms of phlegm and past history of tuberculosis were observed, whereas other symptom prevalences were higher in the higher exposure categories. Symptomatic ex-miners exhibited lower lung function compared to the nonsymptomatic. CONCLUSIONS: Compared with published data, symptoms rates were low in current miners but high in ex-miners. Although explanations could include the low prevalence of smoking and/or reporting/selection bias, a "survivor" and/or a "hire" effect is more likely, resulting in an underestimation of the dust-related effect.

Respiratory outcomes among South African coal miners at autopsy.

BACKGROUND: Studies of dose-response relationships between respiratory outcomes at autopsy and coal dust exposure are limited. The Pathology Automation System (PATHAUT) database of South African miners, is one of the largest autopsy databases of occupational lung disease. This study described the prevalence of respiratory outcomes among South African coal miners at autopsy, and determined whether dose response relationships existed between emphysema and exposure. METHODS: Autopsies conducted from 1975 to 1997 on coal miners with exclusive coal mining exposure and having exposure duration information (n = 3,167) were analyzed from PATHAUT. Logistic regression was used to determine relationships between exposure and outcomes, controlling for race, smoking and age on a subset for whom smoking history was available (n = 725). RESULTS: The mean duration of exposure was 11.0 years. Most were black miners (75.3%) with significant differences in the mean ages of black and white miners (37.9 and 55.3 years, respectively). Only 22.9% of cases had information on smoking. The prevalence of silicosis, tuberculosis (TB), coal workers' pneumoconiosis (CWP), and moderate and marked emphysema were 10.7%, 5.2%, 7.3%, and 6.4%, respectively. All diseases, except TB, were associated with exposure duration. Black miners had 8.3 and 1.2 fold greater risks for TB and CWP, respectively, than white miners. White miners had an increased risk of 1.4 and 5.4 for silicosis and moderate to marked emphysema, respectively. In models unadjusted for age, and including smoking, moderate to marked emphysema was strongly associated with exposure duration (OR = 3.4; 95% CI = 1.9-5.9 for highest tercile of exposure duration). Exposure-related risk estimates were reduced when age was introduced into the model. However, age and duration of exposure were highly correlated, (r = 0.68) suggesting a dilution of the exposure effect by age. CONCLUSIONS: There were significant dose related associations of disease, including emphysema, with coal dust exposure.

Differential respirable dust related lung function effects between current and former South African coal miners.

Dust-related dose-response decrements in lung function among coal miners have been reported in several studies, with varying magnitudes across populations. Few studies have compared differences between current and former coal miners. No studies on dose response relationships with lung function have been conducted in South African coal mines, one of the top three producers of coal internationally. The objectives of this study were (1) to describe the relationship between respirable dust exposure and lung function among current and former South African coal miners and to determine whether differential dust related effects were present between these employment categories; (2) to examine dust related dose response relationships, controlling for potential confounding by smoking and a history of tuberculosis (TB). Six hundred and eighty-four current and 188 ex-miners from three bituminous coal mines in Mpumalanga Province were studied. Interviews assessing work histories, smoking profiles and other risk factors were conducted. Work histories were also obtained from company records. Standardised spirometry was performed by trained technicians. Cumulative respirable dust exposure (CDE) estimates were constructed from company-collected sampling and measurements conducted by the researchers. Regression models examined the associations of CDE with per cent predicted FEV(1) and FVC, controlling for smoking, past history of TB and employment status. A statistically significant decline in FEV(1) of 1.1 and 2.2 ml/mg-year/m(3) was found in representative 40-year-old, 1.7-m tall current and former miners, respectively. Significant differences were found between the highest and medium exposure categories. Ex-miners had a lower mean per cent predicted lung function than current miners for each cumulative exposure category, suggesting a "healthy worker" effect. Past history of TB contributed to 21 and 14% declines in per cent predicted FEV(1) and FVC, respectively. Thus, in this cohort, a dose-related decline in lung function was associated with respirable dust exposure, with a magnitude of effect similar to that seen in other studies and important differences between current and former employees. A "healthy worker" effect may have attenuated the magnitude of this relationship. TB was a significant contributor to lung function loss.