Occupational and Environmental Health

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Epidemiological and genetic risk factors associated with asthma among children in the south Durban region, KwaZulu-Natal.
(2008) Reddy, Poovendhree.; Naidoo, Rajen.; Naidoo, Richard.
Several genes are associated with an increased susceptibility to respiratory diseases, including asthma, which may be exacerbated by ambient air pollution. These genes include the Gluthathione-S-Transferase family (GSTM1 and GST1l) and the NAD(P)H quinone oxidoreductase (NQO1). This, the first genetic epidemiological study conducted in Sub-Saharan Africa had 2 main objectives: I) to evaluate whether the above genotypes confer susceptibility to asthma and related phenotypes; and 2) to investigate if polymorphisms in these genes known to modulate the response to or protect from epithelial oxidative damage modify pulmonary response to ambient air pollutants. A total of 369 schoolchildren from seven primary schools in a heavily industrialized region of south Durban and a demographically similar area in north Durban, Kwa-Zulu Natal, South Africa during the period May 2004 - October 2005, participated in the study. DNA was extracted from whole blood using the GENTRA Puregene kit. Genotyping for the GSTM1 (null vs present genotype) was done using multiplex PCR while the GSTP1 (I1e105Val; AA>AG/GG) and the NQO1(Pro/Ser; CC>CT/TT) genotypes were determined using real time PCR and Taqman probes (Applied Biosystems). Persistent asthma and asthma of "any severity" was determined by questionnaires based on the ATS and BRMC questionnaires. Positive atopy was determined by at least one positive skin test reaction to the seven allergens tested. Other health assessments included spirometry, methacholine challenge testing and four cycles of three-week serial peak flow measurements. Acute respiratory measures included within day variability in FEV1 and PF and the lowest valid values on a given day. SO2. NO2, NO and PM10 were measured over a year using ultraviolet fluorescence, gas-phase chemiluminescence and gravimetric methods respectively. STATA (version 9, College Station, TX, USA) was used for data analysis. Multiple logistic models and Pearson's chi-squared tests were used to evaluate the association between asthma, BHR, atopy and genotype. Covariate-adjusted generalised estimating equations (GEE) with lags of 1-5 days were used to evaluate genotype effect modification of exposure-response. The GSTM1 gene deletion (GSTM1null) was detected in 28.9% of the study population while the distribution of GSTP1 AG/GG and the NQO1 CT/IT polymorphisms were 64.9% and 36.0% respectively. Multiple regression with the adjustment for relevant covariates indicated that individuals carrying one or more copies of the GSTP 1 minor allele had a statistically significant risk for persistent asthma. GSTM1 and NQO1 genotypes showed no significant association with any of the respiratory outcomes tested. However, we found a protective effect for those individuals carrying the GSTM1null genotype and at least one Ser allele (NQO1 CT/TT) for persistent asthma and marked BHR (OR = 0.7, Cl: 0.3-1.5 and OR= 0.3, Cl: 0.0-1.9 respectively). This protective effect is consistent with the role of NQO1 in metabolic activation. Children from the south schools had almost twice the risk of persistent asthma (OR=2.0, Cl: 1.2-3.2, p<.005) and 3 times the risk of BHR (OR=3.5, Cl: 1.4-8.4, p<.005) than those from the schools in the north. Based on symptoms, 20.4% of children from the random sample had persistent asthma and 10.3% had marked BHR (PC20< 2mg/ml). The GEE model results were consistent with modification of air pollutant-pulmonary function relationships by oxidative stress associated genotypes. Statistically significant gene*environment interactions with NO2, NO, and PM10 using FEV1 and PEF outcomes in the expected direction were more frequent for GSTP1 AA and NQO1 CC genotypes (interaction p-values <0.05). There were very few gene*environment interactions for SO2 and any of the 3 SNPs tested. The most striking finding in our study was that pollutant exposure, especially oxides of nitrogen and PM10, even at levels below the recommended limits of South African guidelines, is associated with poorer lung function and that this association is significantly modified by an individual's genotype, particularly the GSTMlnull, GSTPIAA and NQOICC genotypes. Children with the GSTMlnull GSTPI AG/GG, GSTPI AG/GG NQOI CC and GSTMlpos NQOICC gene-gene combinations showed a significant interaction with NO2, NO, and PM10 with decrement in lung function measures. The increased risk to air pollution conferred by the GSTPI and GSTMl genotypes may have clinical and public health importance because this variant is common in most populations. The findings suggest that the risk of developing respiratory symptoms is increased when genetic susceptibility is included with environmental exposures. Our models suggest significant gene*environment interactions i.e the response to the level of air pollutants, as indicated by variability in pulmonary function measures, is modified by genotype. The heightened allergic airway response may be a consequence of a decreased capacity to mount an effective cytoprotective response to oxidative stress. Studying genes may inform us about the biology of asthma which may lead to new therapies or preventative strategies. This study supports the importance of further investigation on these and other genotype variants involved in oxidative stress and respiratory phenotypes in larger cohorts.
Occupational exposure and genotoxicity among Ethekwini Municipality petrol attendants.
(2013) Makwela, Mpho Hazel.; Naidoo, Rajen.
Background Benzene, a constituent of petrol, is classified as a Group 1 carcinogen. Once benzene enters the human body, its breakdown products, benzene oxide (BO) and 1.4 benzoquinone (BQ), have the ability to interact with DNA and proteins. Hydroquinone (HQ), a metabolite of benzene, has the ability to produce toxicity in the bone marrow once it interacts with phenol. The effects of genotoxicity are seen in a metabolizing gene (CYP2E1), detoxification genes (NQO1 and GSTT1), and in DNA-repair gene (XRCC1). Purpose To determine whether occupational exposure among eThekwini Municipality petrol attendants is associated with DNA damage. Methods This analytic cross sectional study included 151 participants that comprising of 75 high-exposed petrol attendants, 26 low-exposed workers from eight petrol stations within the city of Durban, and 50 office-based controls from University of KwaZulu-Natal. Researcher administered validated questionnaires were used to establish an association between DNA tail length via comet assay and the volume of petrol pumped in the past year, adjusting for various covariates through multivariate modelling. Results The median duration of employment in the petroleum industry was 4.5 years (range: 1-14 years) among the 26 low exposed and 5 years (range: 1-27 years) among 75 high-exposed pet-rol attendants. The median volume of petrol pumped by the 75 petrol attendants was 182 metric tons in the past year (range: 18-573 tons). The median tail lengths were 60.5μm (range: 18-149) for the high exposed, 89.5μm (range: 24-124) for the low exposed and 56 μm (range: 14-80) for the unexposed. Wilcoxin rank test, showed a statistically significant association between job title and tail length among the exposed and unexposed group. Mann Whitney test showed alcohol consumption to have a significant influence on the level of DNA damage. The multi-variate analysis showed a statistically significant association between job category, smoking, alcohol consumption and comet tail length. Conclusion Occupational exposure was associated with an increased comet tail length among the exposed group compared to the unexposed. Cumulative exposure of volume of petrol pumped over one year duration had no significant dose related risk and was not associated with an increase in DNA damage.
Tuberculosis in coal mine workers in Mpumalanga.
(2009) Mphofu, Obed.; Naidoo, Rajen.
Introduction Pulmonary tuberculosis (TB) is a disease which is both curable and preventable, with recognised complications such loss of lung function and progressive massive fibrosis (PMF). It is a major cause of pulmonary disability and mortality in the South Africa mining industry. Tuberculosis has a high social and economic cost, both for the individual concerned and for the industry as a whole. However, notwithstanding the extensive literature on TB in the mining industry, given the size and economic importance of coal mining in South Africa, there is surprisingly scanty information available on TB and other occupational lung diseases in coal mines. A strong correlation was reported in Canada, the USA and China between coal usage and TB. This highlights the possibility of the direct impact of coal usage on TB. Although black miners have historically done jobs with the highest exposure in the coal mining industry, there have been remarkably few studies reporting the prevalence of TB and the exposure response relationship in black coal miners in South Africa. Dust exposure in coal mines is a risk factor for occupational lung diseases such as coal workers' pneumoconiosis (CWP), chronic obstructive airways disease (COAD) and lung function deficiency. However, there are still doubts and debates about the risk in such work of tuberculosis. The aim of this study was to fill the gap in the literature by determining the prevalence and exposure response relationship of TB to coal dust exposure. Objective To determine, within a sample of coal miners: . Prevalence of tuberculosis (TB) . Prevalence of coal workers' pneumoconiosis and past TB . Association of outcome variables with exposure variables and underground coalmine workers' exposure as compared to that of surface workers . Association of TB with coal workers' pneumoconiosis and past TB . Exposure response relationship of TB, coal workers' pneumoconiosis and past TB to respirable coal dust. Method A cross-sectional study of 344 employed black male coal miners at a coal mining complex with fourteen mine shafts at Secunda in Mpumalanga, was done. The records from 1 January 2000 to 31 December 2005 were reviewed. The main outcome measure was the prevalence of current TB in coal miners. The sample consisted of 220 underground and 124 surtace coal miners. The exposure variables considered were lifetime mean exposure level (LMEL) (mgim3), cumulative dust exposure (CDE) in mg-years/m3, and coal mining years. Information was collected from multiple sources including hospital files, surveillance records and medical records, and crossvalidated with the information from the human resources department. Information was collected on the demographic profile, exposure, underground or surface work, area of work, smoking history, HIV status from medical records, dust exposure intensity, length of service, TB diagnosis and the methods of diagnosis and outcome of the treatment, and previous TB and CWP. Participants with current TB were either sputum culture positive or sputum culture negative TB. Results The mean age of the sample was 45.2 years, (range 2844 years; SD = 8.2).The mean duration of service was 16.1 years (range 4.1-27.7 years; SD 5.9). There were 34 (9.9%) cases of current TB in total, of which 31 were underground coal miners and three were surface coal miners. The prevalence of current TB reported by this study was 9.97o, with a mean age of 46J years and length of service of 16.2 years. The prevalence of current TB among the underground and surface workers was 14.1o/o and 2.4o/o rcspectively. The prevalence of CWP was 3.8o/o, with a mean age of 51.3 years and a mean length of service of 2Q.l years. The prevalence of past TB was also 3.8o/o, with a mean age and length of service of 44.9 and 1 6. 1 years respectively. Underground coal mines workers' exposure to coal dust was high, with a lifetime mean exposure level (LMEL) and cumulative dust exposure (CDE) of 2.4 mg/m3 and 33.4 mgyears/ m3 respectively. The difference in LMEL and CDE among underground vs. surface workers was significant, with underground exposure being higher than surface exposure, namely p<0.001 and p<0.001 respectively. The difference in length of service between underground and surface participants was not significant. The difference in exposure to coal dust (LMEL and CDE) among participants with current and previous TB, compared to those without current and previous TB, was statistically significant, p<0.008 and p<0.04. The difference between the coal dust exposure indices (LMEL, CDE exposure duration) for participants with and without CWP was significant. However, the difference between participants with current TB and previous TB compared to those with non-current TB and without previous TB in age and length of service years was not significant. This also applied to HIV status and smoking: the difference between participants with and without current TB was not significant. There was a strong significant association of underground mine work with current TB, with a prevalence odds ratio (POR) of 6.62 (p<0.001).This showed that the association of exposure to coal dust with current TB was strong and significant as underground mine workers were exposed to higher coal dust concentrations than surface workers. Workers with current TB were more likely to have co-existing CWP, with a POR of 1.7 (95Vo Cl:0.f7.1). The exposure-response relationship of LMEL and CDE in participants with current TB and CWP was significant. A significant trend was observed of increasing of LMEL and CDE with an increase in the prevalence of current TB, CWP and past TB. Conclusions There was a possible dose response relationship between coal dust exposure and the risk of development of pulmonary TB. The study showed that coal dust exposure was associated with pulmonary TB, and a dose response relationship with the trend of increasing coal dust exposure. lt has been shown that there is a more significant and stronger association of underground coal mine work with current TB than there is in surface work. This study has shown a significant exposure response relationship in the exposure indices (CDE and LMEL), age and length of service for CWP. This study found a high prevalence of pulmonary TB of 9.9% in black migrant coal mine workers who historically held jobs in the dustiest areas in the mining industry. The limitations of the study include the use of cumulative exposure calculated from current exposure, and the secondary healthy worker effect or survivor workforce. Dust control and HIV/AIDS programmes should be an integral part of a TB and occupational lung disease control strategy in the mining industry.
Workplace risk factors associated with extra-pulmonary tuberculosis among healthcare workers in eThekwini health district, KwaZulu-Natal.
(2022) Bhengu, Nontuthuzelo May.; Naidoo, Rajen.
Background Tuberculosis (TB) can be categorized as pulmonary tuberculosis (PTB) and extra-pulmonary tuberculosis (EPTB) involving other organs besides the lungs. Healthcare workers (HCWs) are at increased risk of tuberculosis exposure. The average burden among healthcare workers is 2% compared to 0.9% in the general population. EPTB constitutes about 16% of all TB cases. This study aimed to examine occupational, environmental, and demographic risk factors associated with EPTB among healthcare workers. Methods This was a retrospective case referent type study with two control groups (one without tuberculosis and the other with pulmonary tuberculosis) and cases defined as those with EPTB. 282 records of healthcare workers were reviewed from January 2009 to December 2017.The study reviewed available medical records of healthcare workers from various categories and departments, both clinical and non-clinical. in health facilities within eThekwini Health District, Durban, South Africa. Data was analysed using a chi-square test, t- test and multivariet analysis. Results The mean incidence of TB in 2016 was 908/100 000 and for EPTB, was estimated at 87.2/100 000 HCWs in eThekwini Health District. Cases without respiratory protective equipment (RPE) use were more than three-fold suceptible (aOR 3.5 95%CI 1.0 – 11.4) compared to a PTB control. Working in a clinical department increased the odds for developing EPTB almost three-fold when compared to those with PTB (aOR 2.9 95% CI 0.6 – 13.2) than among those with no TB (aOR 1.4 95%CI 0.1– 13.8). As expected, HCWs diagnosed with HIV were almost two-fold likely to be exposed to EPTB when compared to thosed with PTB (aOR: 1.9 95% CI 0.9 – 4.0), however, when comparing EPTB to no TB, HIV positivity had a wide confidence interval (aOR: 23.4 95% CI 8.1 – 67.7) rendering the results indeterminate. Conclusion Occupational risk factors for EPTB are similar to that of pulmonary tuberculosis, however, risk estimates may be greater than those for PTB. Human immunodeficiency virus/ acquired immunodeficiency syndrome (HIV/AIDS) infection increases the odds of exposure to EPTB in HCWs.

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